3 - Physiology (BusySPR 2016 SBAs)

This Copy is for Dr.
Mohamed ElHodiby
ACID-BASE, RENAL & BLADDER FUNCTION
Question 1 Bladder volume at first sensation to void

A 50-100 ml B 150-250 ml
C 300-330 ml D 400-600 ml
E 10-50 ml
A(Correct answer: B)
Explanation
Normal cystometric parameters

 Bladder capacity 400-600ml
 First sensation to void 150-250ml
 Rise in detrusor pressure less than 15cmH2O
 No leakage on coughing
 Voiding detrusor pressure less than 70cmH2O
 Peak urine flow rate > 15ml/sec
 Residual volume < 50ml
Question 2 Which one is typically associated with hypokalaemia?
A Release of urinary tract obstruction B Transfusion of stored blood

C Haemolysis D Vigorous exercise
E Digoxin poisoning
A(Correct answer: A)
Explanation
Hypokalaemia - causes include: *****
1) GI loss - prolonged vomiting, diarrhoea, fistulae, ileostomy, villous adenoma, ileus & intestinal
obstruction *
2) Increased renal excretion - diuretics (spironolactone is a potassium-sparing diuretic) *
3) Use of intravenous saline / dextrose
4) Re-distribution - beta-agonists, acute MI, insulin therapy, alkalosis *
5) Increased aldosterone secretion - liver / heart failure, Cushing's syndrome, Conn's syndrome, ACTH
producing tumours *
6) Exogenous mineralocorticoids - corticosteroids, carbenoxolone, liquorice *
7) Renal tubular acidosis type 1 & 2; renal damage from cytotoxic drugs, aminoglycosides,
amphotericin *
8) Release of urinary tract obstruction *
Clinical features include muscle weakness, arrhythmias, increased risk of digoxin toxicity. *
This Copy is for Dr. Mohamed ElHodiby

Question 3 The clearance of a solute can be calculated from the formula C = U x V/P.

A V = urine volume B U = urine volume
C P = plasma concentration of the solute D P = plasma flow rate
E V = volume of solute added
A(Correct answer: C)
Explanation
GLOMERULAR FILTRATION
· Clearance of a solute can be determined from the formula:??C = UxV/P??Where U =
urinary concentration of the solute, V = urinary flow rate and P = plasma concentration of the
solute
Question 4 With respect to the anatomy of the nephron

The glomerulus is a network of tubules which filter The proximal convoluted tubule arises directly
A B
solutes from Bowman’s corpuscle
The proximal convoluted tubule is connected to The proximal convoluted tubule is located in the
C D
the ascending limb of the loop of Henle renal medulla
The ascending limb of the loop of Henle is
E
connected to the glomerulus
Explanation
THE NEPHRON *****
· Functional unit of the kidney, ~1.25 million per kidney

· Bowman’s corpuscle - contains a tuft of capillaries - the Glomerulus, fed by an afferent
arteriole and drained by an efferent arteriole
· The Proximal convoluted tubule arises directly from Bowman’s corpuscle and is lined by
cuboidal cells with apical microvilli
· The proximal tubule connects with the descending loop of Henle lined by flattened cells.
Descends into the renal medulla and then turns and ascends towards the cortex as the thin
ascending limb of the loop of Henle
· Thin ascending limb connects with thick ascending limb lined by cuboidal cells with
extensive invaginations of the basolateral membrane
· Thick ascending limb connects to the distal convoluted tubule
· The terminal part of the thick ascending limb = the proximal part of the distal convoluted
tubule contact the respective afferent arteriole to form the juxta-glomerullar apparatus. The wall

of the arteriole is thickened to form the juxtaglomerullar cells, modified smooth muscle cells
which secrete renin. The tubular epithelial cells are modified to form the macula densa
· Distal tubules of several nephrons merge to form collecting tubules
· Collecting tubules merge to form collecting ducts
Question 5 Which one increases glomerular filtration rate?

A Sympathetic stimulation B Angiotensin II
C Dilatation of the afferent arteriole D Dilatation of the efferent arteriole
E Increased arterial blood pressure
Explanation
REGULATION OF GRF
· Glomerular filtration is determined by Starling forces -increased hydrostatic pressure
(dilatation of afferent arteriole / constriction of efferent arteriole) or decreased plasma oncotic
pressure will increase GFR *
· Sympathetic stimulation - constricts afferent arteriole, reducing renal plasma flow and
GFR *
· High concentrations of angiotensin II constrict both afferent and efferent arterioles, reduce
renal plasma flow and GFR *
· Atrial natriuretic peptide - increase GFR. Secretion increased with plasma volume
expansion *
· Between 90-180mmHg arterial pressure, GFR remains constant due to auto-regulation of
renal blood flow
· Haemorrhage results in sympathetic stimulation and reduced GFR *
· Dehydration and other causes of hypovolaemia reduce GFR. Activation of the renin-
angiotensin mechanism increases sodium retention *
· Glucocorticoids and nitric oxide cause dilatation of afferent arteriole and increase GFR *
· Prostaglandins do not regulate renal plasma flow or GFR in healthy individuals *
Question 6 Atrial natriuretic peptide

A Decreases glomerular filtration rate B Secretion is increased by acute haemorrhage
Secretion is increased by plasma volume
C Secretion is increased by dehydration D
expansion
E Has no effect on glomerular filtration rate
A(Correct answer: D)

Explanation
REGULATION OF GRF
· Glomerular filtration is determined by Starling forces -increased hydrostatic pressure
(dilatation of afferent arteriole / constriction of efferent arteriole) or decreased plasma oncotic
pressure will increase GFR *
· Sympathetic stimulation - constricts afferent arteriole, reducing renal plasma flow and
GFR *
· High concentrations of angiotensin II constrict both afferent and efferent arterioles, reduce
renal plasma flow and GFR *
· Atrial natriuretic peptide - increase GFR. Secretion increased with plasma volume
expansion *
Question 7 Renal plasma flow is measured by measuring

A Creatinine clearance B Inulin clearance
C Clearance of p-aminohippuric acid D Uric acid clearance
E Urea clearance
Explanation
MEASUREMENT OF GFR *****
· Requires a marker which is freely filtered by glomerulus, not absorbed/secreted by
nephron and not metabolized/produced by kidney - Inulin
· Creatinine is used in clinical setting instead of inulin, since muscle produces creatinine at
a constant rate proprtional to muscle mass. *
· However, creatinine is secreted by organic cation transporter in proximal tubule, leading to
~10% error in filtered amount.*
· The estimation method for plasma creatinine concentration introduces ~10% error, thus
cancelling out the overall error and rendering creatinine as a reliable marker for GFR *
· Plasma creatinine concentration, unlike urea concentration, is largely independent of diet *
· Renal plasma flow is measured by measuring clearance of p-aminohippuric acid *
Question 8 The proximal convoluted tubule

Reabsorbs almost all filtered glucose and amino
A Does not reabsorb potassium B
acids
C Does not reabsorb glucose D Reabsorbs almost all filtered sodium
E Secretes chloride

Explanation
TUBULAR ABSORPTION & SECRETION *****
· Proximal tubule *-reabsorbs about two thirds of filtered water, sodium, potassium,
chloride, bicarbonate and other solutes
· Reabsorbs virtually all filtered glucose, lactate and amino acids. Uptake of glucose and
amino acids is sodium dependent and saturable *
· The filtered glucose load is increased and may exceed the maximal tubular reabsorptive
capacity in pregnancy or poorly controlled diabetes mellitus, resulting in glycosuria
· Renal amino acid excretion is increased in pregnancy *
· Bicarbonate absorption is sodium dependent - and Na+-H+ antiporter exchanges tubular
Na+ for intracellular H+ which combines with HCO3- to form carbonic acid. Carbonic acid
dissociated to water + CO2 (Carbonic anhydrase) and CO2 is reabsorbed *
· Water absorption follows solute uptake while proteins are taken up by pinocytosis *
· Bile salts, creatinine, urate and drugs such as penicillin, quinine and salicylate are
secreted into the lumen of the proximal tubule *
Question 9 Amino acid excretion by the kidneys

A Does not occur in the absence of pathology B Is increased during pregnancy
C Is decreased during pregnancy D Is unchanged by pregnancy
In healthy kidneys, only occurs in pregnancies
E
complicated by pre-eclampsia
Explanation
Same as of Question 8
Which molecules are typically secreted into the lumen of the proximal
Question 10
convoluted tubule?

A Glucose and amino acids B Glucose and creatinine
C Bile salts and penicillin D Sodium ions and salicylates
E Glucose and salicylates
Explanation

Which segment of the nephron plays an important role in the regulation of ionic
Question 11
balance?

A The glomerulus only B The glomerulus and the proximal convoluted tubule
C The loop of Henle D The distal convoluted tubule and colleting duct
E The collecting duct only
Explanation
BICARBONATE BUFFERING SYSTEM
· Made up of carbonic acid and sodium bicarbonate in extracellular fluid*
· Made up of carbonic acid and potassium and magnesium bicarbonate in intracellular fluid
*
· 399 out of 400 parts of carbonic acid exists as dissolved carbon dioxide. Hence carbonic
acid is a weak acid and sodium bicarbonate is a weak base
· The pH of the bicarbonate buffer system is calculated from the Henderson-Hasselbalch

equation: pH = 6.1 + log[HCO3- / CO2]
· Hence the pH of a solution containing an equal concentration of bicarbonate and carbon

dioxide is 6.1 (log of 1 = 0) = pK of the buffer
Question 12 At physiological pH
The bicarbonate buffering system has its optimum The bicarbonate buffering system is less
A B
buffering capacity important than the phosphate buffering system
The bicarbonate buffering system is more The protein buffering system is more important
C important than the protein or phosphate buffering D than the bicarbonate or phosphate buffering
systems systems
The amino acid buffering system is more
E
important than the bicarbonate buffering system
Explanation
The bicarbonate buffer system is a poor buffer at physiological pH. However, it is more
important than the other buffers (phosphate and protein) because the concentrations of the two

components can readily be regulated – carbon dioxide by the respiratory system and
bicarbonate by the kidneys *
Question 13 Renin

Is produced as an inactive precursor called pro-
A B Is not produced by the ovaries or the decidua
renin
Secretion is inhibited by reduced extracellular Secretion is increased by a rise in sodium
C D
fluid volume concentration in the renal filtrate
E Is produced by the loop of Henle
Explanation
PHOSPHATE BUFFER SYSTEM *****
• Made up of Na2HPO4 (weak base) and NaHPO4 (weak acid)
• Has a pK of 6.8
• Low concentration of buffers in extracellular fluid therefore less important than bicarbonate
buffer
• Higher concentration in renal tubular fluid. In addition, pH of tubular fluid is closer to pK of

phosphate buffer system - therefore more important buffer
• Higher concentration in intracellular fluid and pH is closer to pK - becomes more important
Question 14 The intracellular pH is
A 7.0 B 7.2
C 7.4 D 7.6
E 7.8
Explanation
RESPIRATORY REGULATION OF pH
• Increased alveolar ventilation results in a fall in arterial CO2 concentration and a rise in pH
• The central and peripheral chemoreceptors are particularly sensitive to changes in pH and
regulate respiratory centre activity. A fall in pH increases respiratory centre activity, increasing
alveolar ventilation
• The respiratory system cannot, however, completely correct a metabolic acidosis as the
stimulus for increased ventilation decreases as the pH approaches normal.

Question 15 The normal anion gap is

A 1-2 mM B 3-5 mM
C 4-10 mM D 10-18 mM
E 20-32 mM
Explanation
RENIN
· Proteolytic* enzyme secreted by the kidneys (juxta-glomerular apparatus in the afferent
arteriol) in response to a fall in sodium concentration in the distal tubule
· Produced as an inactive precursor pro-renin
· Also produced in the uterus and chorion, decidua and ovary*
· Pro-renin is present in ovarian follicular fluid and its concentration (BUT NOT that of active
rennin) increases in plasma transiently by up to 2 fold during the LH surge and in response to
HCG to induce ovulation. After conception, it increases about 8 to 10-fold in parallel with plasma
HCG.
· Acts on angiotensinogen, an alpha-2-globulin*, converting it to angiotensin I
· Plasma concentration of active renin increases slightly early in the first trimester to reach a
plateau (five-fold basal value) at the 20th week of gestation which is then maintained throughout
pregnancy*.
· Renin secretion is increased by factors which reduce extracellular fluid volume or pressure
or reduce sodium concentration in the renal filtrate*
Question 16 The anion gap is calculated from the equation
A [Cl-] – [HCO3-] B [Na+] – [K+]

C [Na+] + [K+] – [Cl-] D [Na+] + [K+] – [Cl-] – [HCO3-]
E [Na+] – [Cl-]
Explanation
METABOLIC ACIDOSIS WITH NORMAL ANION GAP
· Anion gap = [Na+] + [K+] - [HCO3-] - [Cl-] = 10-18mM *
· Made up of negatively charged proteins, phosphate and organic acids *
· Normal anion gap acidosis - hyperchloraemic acidosis - occurs when bicarbonate is lost
by the gut or kidneys, or rarely when hydrogen ions are ingested as ammonium chloride.
Chloride ions are retained as bicarbonate is lost

Question 17 The anion gap is made up of

A Positively charged proteins B Bicarbonate ions
C Chloride and phosphate ions D Negatively charged proteins and phosphate ions
E Zinc and magnesium ions
Explanation
Occurs in:
· Diarrhoea, pancreatic fistulae
· Renal tubular acidosis - including vitamin D intoxication, hypergammaglobulinaemia,
hyperparathyroidism (PTH inhibits bicarbonate resorption by the proximal tubule)
· Ingestion of ammonium chloride or arginine hydrochloride or other cationic amino acids
· Rapid iv hydration
Question 18 Metabolic acidosis with a normal anion gap occurs in

A Diabetic keto-acidosis B Diarrhoea
C Uraemia D Starvation
E Alcohol poisoning
Explanation.
Question 19 Which one is not typically associated with metabolic acidosis with a high anion gap?

A Ingestion of ammonium chloride B Salicylate poisoning

C Methanol poisoning D Paraldehyde poisoning
E Diabetic keto-acidosis
Explanation

A 23 year old woman presents at 6 weeks gestation with a 48 hours history
Question 20
of severe nausea and vomiting. Her acid-base status is likely to show
A A metabolic acidosis with normal anion gap B A metabolic acidosis with increased anion gap
C A metabolic alkalosis with hyperchloraemia D A metabolic alkalosis with hypokalaemia
E A metabolic acidosis with hypokalaemia
Explanation
Question 21 With respect to respiratory failure

Arterial PO2 is low and PCO2 is high in type 1 Arterial PO2 is normal and PCO2 is high in type 2
A B
respiratory failure respiratory failure
Arterial PO2 is low and PCO2 is high in type 2 Arterial PO2 is low and PCO2 is normal in type 2
C D
respiratory failure respiratory failure
Arterial PO2 is low and PCO2 is low in type 2
E
respiratory failure
Explanation
METABOLIC ALKALOSIS *****
· Less common than metabolic acidosis
· Associated with potassium or chloride depletion
Caused by
· Vomiting -causes hypochloraemic alkalosis with hypokalaemia and potassium loss in
urine. *
· Urine is acidic despite systemic alkalosis - when alkalosis is associated with volume
depletion, bicarbonate is not excreted.
· Excretion of bicarbonate only occurs with restoration of extracellular fluid volume
· Diuretics -loop diuretics especially. Associated with hypochloraemia and hypokalaemia *
Question 22 With respect to the regulation of acid-base balance by the kidneys

Bicarbonate ions are secreted into the proximal The majority of filtered bicarbonate is reabsorbed
A B
tubule in the proximal tubule
Carbonic anhydrase plays a key role in the Hydrogen ions are absorbed from the tubular
C D
reabsorption of bicarbonate ions lumen coupled to sodium secretion
Hydrogen ions are secreted into the tubular lumen
E
coupled to potassium absorption

Explanation
RESPIRATORY ACIDOSIS *****

· Type I respiratory failure - arterial PO2 is low but PCO2 is normal or low - hypoxia may
cause a metabolic acidosis
· Type II respiratory failure - arterial PO2 is low and PCO2 is high - causes respiratory
acidosis *
· Chronic - associated with a compensatory metabolic alkalosis with raised plasma
bicarbonate
· Occurs in ventilatory failure, chronic bronchitis and emphysema
Question 23 The human body contains

A 75% water in males B 60% water in females
C 50% water in neonates D 75% water in neonates
E 55% water in males
Explanation
RESPIRATORY ALKALOSIS
· Spontaneous or induced hyperventilation causes a fall in arterial PCO2
· Although alveolar ventilation increases and arterial PCO2 falls in normal pregnancy,
alkalosis does not occur
· Type I but not type II respiratory failure is associated with respiratory alkalosis
· Renal compensation produces a metabolic acidosis with a fall in bicarbonate ion
concentration
Question 24 The plasma volume in females is
A 1.5 liters B 2 liters

C 2.5 liters D 3 liters
E 3.5 liters
Explanation
BODY WATER *****

• ? Males - 60% body weight = water *
• ? Females - more fat and body water = 50% *
• ? Neonate 75% water *

• ? Measured using the deuterium oxide dilution method *
• ? Extracellular fluid volume measured using inulin or mannitol dilution *
• ? Intracellular fluid volume calculated by total body water minus extracellular fluid
volume *
Question 25 With respect to the regulation of water balance, thirst is stimulated when osmolarity
A Falls by more than 4 mOsmol/kg B Rises by more than 4 mOsmol/kg

C Rises by more than 14 mOsmol/kg D Falls by more than 14 mOsmol/kg
E Rises by more than 10%
Explanation
Proteins contribute only ~0.5% to the osmolarity of plasma and much less to the osmolarity of
interstitial fluid which contains little protein. The osmotic pressure exerted by proteins is the
colloid osmotic pressure or oncotic pressure (~25mmHg) *
Question 26 Which one is a recognized cause of hyperkalaemia?
A Conn’s syndrome B Cushing’s syndrome

C Alkalosis D Acute myocardial infarction
E Infectious mononucleosis
A(Correct answer: E)
Explanation
Plasma osmolarity decreases by ~ 10mOsmol/kg in pregnancy *
• ? Water intake is dependent on body surface area
• ? Total daily water gain ~2600ml (1500ml drinking, 500ml from food and 500ml from
metabolism). Water loss = 2600ml / day (1500ml urine, 100ml faeces, 500ml lungs, 500ml skin)
• ? Urine osmolarity cannot exceed 1250 mOsmol/kg - the minimum volume of urine
required to excrete wastes is ~700ml/day (~30ml/h). Kidneys form ~180L of filtrate per day of
which 178.5L is reabsorbed *

Question 27 Which one is a recognized cause of salt-deficient hyponatraemia?
A Excessive vomiting or diarrhoea B Syndrome of inappropriate ADH secretion

C Psychogenic polydipsia D Oxytocin use
E Insulin therapy
Explanation
REGULATION OF BODY WATER *****
• ? Water balance is monitored by the osmoreceptors in the hypothalamus which
regulate ADH secretion by the posterior pituitary and water reabsorption in the collecting ducts
and tubules of the kidneys *
• ? When osmolarity of body fluid rises by over 4 mOsmol/kg, desire to drink is

stimulated and ADH secretion is increased with a reduction in urine volume *
Which one is a recognized cause of hyponatraemia with increased

Question 28
extracellular fluid volume?

A Unilateral renal artery stenosis B Hyperglycaemia
C Hypoalbuminaemia D Oxytocin use
E Excessive diuretic use
Explanation
POTASSIUM BALANCE ****
• ? Intake 80-150mmol per day
• ? Most of potassium is intracellular *
• ? Plasma concentration regulated by uptake into cells, renal excretion and extra-renal
losses (GI)
• ? Potassium uptake into cells is dependent on the activity of Na+K+ATPase -

stimulated by insulin, beta-agonists and theophyllines. Uptake is inhibited by alpha agonists,
acidosis and cell damage or death.*
• ? Renal potassium loss is stimulated by aldosterone which stimulates K+ and H+

secretion in exchange for Na+. Acidosis decreases while alkalosis increases K+ secretion (H+
and K+ are interchangeable) *

Question 29 Which one is not a typical clinical feature of hypercalcaemia?

A Muscle cramps and tetany B Abdominal pain
C Peptic ulceration D Polyuria
E Corneal calcification
Explanation
Hyponatraemia with normal extracellular fluid volume:
1) Syndrome of inappropriate ADH secretion

2) Psychiatric illness - psychogenic polydypsia, anti-depressant therapy
3) Use of ADH-like drugs - oxytocin, DDAVP
Question 30 Prolonged QT interval on ECG is a typical feature of

A Hypercalcaemia B Hypocalcaemia
C Hyponatraemia D Hypernatraemia
E Alkalosis
Explanation
Symptoms of hypocalcaemia
1) neuromuscular irritability
2) neoro-psychiatric manifestations
3) cramps
4) paraesthesia, circumoral numbness,
5) tetany followed by convulsions, laryngeal stridor, dystonia and psychosis
6) pappiloedema and prolonged QT interval on ECG

Question 31 The residual volume of the bladder

A 50-100 ml B 150-250 ml
C 300-330 ml D 400-600 ml
E 10-50 ml
Explanation

The time limit for the diagnosis of prolonged third stage of labour following
Question 32
physiological management
A Over 15 minutes B Over 30 minutes

C Over 60 minutes D Over 75 minutes
E Over 90 minutes
Explanation
The third stage of labour
Definition:
 Begins with the complete delivery of the fetus and ends with the complete delivery of the placenta and
membranes.
Duration
 The mean duration of the third stage following physiological management has been reported to be
between 12 – 21 minutes. A physiological third stage has duration of less than 60 minutes in 95% of
women.
 There is a moderate level of evidence that an actively managed third stage of 30 minutes or longer is
associated with increased incidence of PPH. PPH remains the most common cause of maternal mortality
globally. In addition, PPH is an important contributor to maternal morbidity including:
Post-natal anaemia
Impaired establishment of breastfeeding
Need for blood transfusion and risk of transfusion-acquired infection
Sepsis secondary to exploration of the uterus during treatment of haemorrhage
 The third stage of labour is diagnosed as prolonged if not completed within 30 minutes of the birth of the
baby with active management and 60 minutes with physiological management.
Question 33 The third stage of labour

Lasts on average about 1 hour following Begins with crowning of the fetal head in
A B
physiological management multiparous women
Is prolonged if it lasts more than 1 hour with Is prolonged if it lasts more than 2 hours with
C D
active management physiological management
Is prolonged if it lasts more than 30 minutes with
E
active management

Explanation
Active management of the third stage of labour does not include which one
Question 34
of the above interventions?
A Early clamping of the umbilical cord B Routine administration of uterotonic drugs

C Controlled cord traction D Uterine massage to stimulate uterine contraction
E Cutting the umbilical cord early
Explanation
Active management
Active management of the third stage involves a package of care which includes all of these three
components:
1. Routine use of uterotonic drugs
2. Early clamping and cutting of the cord
3. Controlled cord traction.
Early clamping of the cord contributes little to the benefits of active management of the third stage. It may
be indicated to enable neonatal resuscitation.
Physiological management of the third stage of labour includes which one

Question 35
of the above?
A Nipple stimulation to induce uterine contraction B Delivery of the placenta by maternal effort
No clamping of the cord until at least after 30
C D Routine use of uterotonic drugs
seconds
E Controlled cord traction
Explanation
Physiological management
Physiological management of the third stage involves a package of care which includes all of these three
components:
1. No routine use of uterotonic drugs
2. No clamping of the cord until pulsation has ceased
3. Delivery of the placenta by maternal effort.
Early suckling or nipple stimulation can increase uterine contractility. There is no evidence that early
suckling reduces the risk of PPH or other complications of the third stage.

Question 36 The proportion of pre-term babies who develop neonatal jaundice
A 1% B 10%
C 25% D 60%
E 80%
Explanation
Neonatal Jaundice
Yellow discolouration of the skin and the sclerae caused by a raised bilirubin concentration
Affects about 60% of term and 80% of preterm babies during the first week of life
About 10% of breastfed babies are still jaundiced at 1 month of age
Clinical recognition and assessment of jaundice is more difficult in babies with dark skin tones
Prolonged jaundice is jaundice lasting more than 14 days in term babies and more than 21 days in
preterm babies
Question 37 Enzyme that catalyses the rate-limiting step in bilirubin synthesis

A Cyclo-oxygenase B Cytochrome P450
C Bilirubin synthetase D Heme oxygenase
E Catalase
Explanation
Bilirubin metabolism
 Bilirubin (unconjugated / ‘indirect’) is produced from the breakdown of red blood cells
 The hemoglobin released is broken down to heme the globin chains are converted to amino acids
 Heme is converted to unconjugated bilirubin in the reticuloendothelial cells of the spleen
 In the first step, heme is converted to biliverdin by the action of heme oxygenase, the rate-limiting step in
the process. Iron and carbon monoxide are released.
 Carbon monoxide is excreted through the lungs and can be measured as an index of to bilirubin
production.
 In-utero, bilirubin crosses the placenta by passive diffusion, and excretion of bilirubin from the fetus
occurs through the mother
 Approximately 75% of bilirubin is derived from hemoglobin, but degradation of myoglobin, cytochromes,
and catalase also contributes
 Unconjugated bilirubin is insoluble and is transported in the circulation bound to albumin
 In the liver, unconjugated bilirubin is conjugated with glucuronic acid by the enzyme
glucuronyltransferase, making it water-soluble
 Bilirubin-glucuronide is excreted in bile. In the large bowel, conjugated bilirubin is metabolised by bacteria
into urobilinogen and then to stercobilin which gives faeces its brown colour

 Some of the urobilinogen is reabsorbed and excreted in the urine
 Bilirubin levels are higher in neonates than in adults because:
 Neonatal red cells have a shorter lifespan
 Neonates have a higher haematocrit
 Neonatal hepatic enzyme systems are immature and less effective at metabolizing bilirubin. Glucuronyl
transferase activity in neonatal liver is 0.1 – 1% that in adult liver but increases to adult values by 4-8
weeks of age
 There is increased entero-hepatic circulation of bilirubin in the neonate. In the absence of gut bacteria to
convert conjugated bilirubin to stercobilin, the bilirubin is de-conjugated
Jaundice may therefore occur in neonates as part of normal physiology
Question 38 The orientation of the long axis of the fetus to the long axis of the mother
A Lie B Presentation
C Engagement D Position
E Station
Explanation
Fetal Lie
 This refers to the orientation of the longitudinal axis of the fetus to that of the mother.
 The lie can be longitudinal (parallel to the mother), transverse (at right angles) or oblique
Presentation
 This describes that part on the fetus lying lowest in the maternal abdomen or pelvis.
 A distinction should be made between ‘cephalic’ and ‘vertex’ presentation, although these descriptions
are used interchangeably
 Cephalic presentation means the fetal head is lowest in the maternal abdomen or pelvis. However, the
precise presentation may be face, brow or vertex
 Vertex presentation is a more precise description indicating that the fetal neck is flexed with the top of the
fetal head (vertex) lying lowest in the abdomen or pelvis. A diagnosis of vertex presentation can only be
made with confidence on vaginal examination when the cervix is dilated
Denominator of the presenting part
 This is an arbitrary point on the presenting part used to orientate it to the maternal pelvis.
 In a vertex presentation, the denominator is the occiput. In a face or brow presentation, the denominator
is the mentum (chin). In a breech presentation, the denominator is the sacrum
Position
 This describes the orientation of the denominator of the presenting part to the maternal pelvis.
Engagement
 This occurs when the biparietal diameter is at or below the inlet of the true pelvis. Clinically, this occurs
when 2/5th or less of the fetal head can be palpated per abdomen.
 Engagement is an all-or-none phenomenon. The presenting part is either engaged or it is not. The
common description of ‘1/5th engaged’ is inaccurate

Question 39 Delivery of the fetal head from beneath the simphysis pubis
A Internal rotation B Restitution

C External rotation D Extension
E Asynclitism
Explanation
Internal rotation
 Occurs at the level of the ischial spines as a result of the combined effect of uterine contractions and the
tone & shape of the pelvic floor. Typically, the head rotates 45° from the occipito-transverse to the
occipito-anterior position. This brings the suboccipito-bregmatic diameter in line with the wider diameter of
the pelvic outlet – the antero-posterior diameter
Extension
 Following internal rotation and further descent, the base of the occiput is located at the inferior margin of
the symphysis pubis. The tone of the pelvic floor and the downward forces from uterine contractions
cause the neck to extend and the head is delivered beneath the symphysis pubis.
Restitution and external rotation
 When the fetal head is free of resistance, it untwists 45° left or right, returning to its original position in
relation to the body. This is restitution.
 The fetal shoulders enter the pelvis with the bis-acromial diameter aligned to the transverse diameter of
the pelvic inlet. When the shoulders reach the pelvic floor, ‘internal rotation’ also occurs to align the bis-
acromial diameter with the antero-posterior diameter of the pelvic outlet. This process is reflected in
further movement of the head and constitutes external rotation
Expulsion
 The anterior shoulder is then delivered under the symphysis pubis followed by the posterior shoulder
Question 40 With respect to cervical changes during normal pregnancy and labour
The cervix typically becomes shorter and softer

A The normal cervix is 1.5-2.0 cm long B
during the second trimester
Cervical ripening begins after the onset of labour Cervical effacement refers to shortening and
C D
in primigravidae thinning of the cervix
Cervical dilatation typically occurs before cervical
E
effacement in primigravidae
Explanation
Cervical changes
 The normal pregnant cervix is 3 – 3.5 cm long and is composed mainly of type 1 and type 3 collagen,
glycosaminoglycans and proteoglycans with only 10-15% being smooth muscle

 The cervix remains largely unchanged during most of pregnancy. In the late third trimester, cervical
ripening begins. This is followed by cervical effacement and dilatation which occur during labour.
Cervical ripening
 Softening of the cervix that usually begins before the onset of labour and is a prerequisite for cervical
dilation
 Caused by biochemical changes with rearrangement and realignment of the collagen molecules and
reduced bridging of collagen fibres. The activity of proteolytic enzymes contribute to these changes
 There is an increase in hyaluronic acid and water content while the amount of dermatan sulphate and
chondroitin sulphate decreases
Cervical effacement
 This is shortening and thinning of the cervix in response to uterine contractions
 In primigravidae, cervical effacement occurs before dilatation. In multiparous women, dilatation and
effacement may occur simultaneously
Cervical dilatation
 This occurs passively under the influence of uterine contractions and pressure from the presenting part.
The cervix is stretched and pulled over the presenting part. The elastin component of the cervix behaves
in a ratchet-like manner to maintain dilatation between contractions
Question 41 With respect to the fetal circulation
The mean arterial pressure is higher at 20 weeks

A The mean arterial pressure at term is ~ 15 mmHg B
compared to 40 weeks
Loss of blood flow to the placenta at delivery
The pressure in the pulmonary artery is lower
C D results in a marked reduction in systemic
than that in the aorta
resistance
The mean systemic venous pressure is higher in
E
the fetus than in adults
Explanation
Fetal arterial pressure is low and, importantly, pulmonary pressure is slightly higher than the aorta. Mean
arterial pressure is 15mmHg in mid-gestation and 40-50mmHg at term
The mean systemic venous pressure is higher in the fetus than in the adult resulting in increased flow
back to the heart and a consequent high cardiac output
The fetal circulation is characterised by a low pressure shunt through the placenta. Loss of blood flow
through the placenta at birth approximately doubles systemic resistance.
Question 42 With respect to the changes in the fetal circulation at the time of birth

There is a decrease in PaO2 and an increase in
A Pulmonary artery resistance rises rapidly B
PaCO2
Rise in PaO2 initiates constriction of the umbilical
C D The pressure in the left atrium falls
arteries
E The pressure in the right atrium increases

Explanation
Changes at birth
 Pulmonary arteriolar resistance falls rapidly due to vasodilation caused by lung expansion, increased
Pao2, and reduced Paco2
 Expansion of the chest wall also reduces pulmonary interstitial pressure, increasing blood flow
through pulmonary capillaries
 Air breathing increases the Pao2, which constricts the umbilical arteries
 Increased venous return from the lungs raises left atrial pressure while venous return from the placenta is
reduced and eventually stops, reducing right atrial pressure. The net result is a reduction in the pressure
gradient between left and right atria and functional closure of the foramen ovale
 Systemic resistance becomes higher than pulmonary resistance soon after birth and the direction of blood
flow through the ductus arteriosus reverses, creating left-to-right shunting (transitional circulation). This
is established moments after birth and lasts until about 24 to 72 h of age, when the ductus arteriosus
closes.
 High PO2 in blood entering the ductus from the aorta and alterations in prostaglandin metabolism, leads
to constriction and closure of the ductus arteriosus
 Soon after birth, a stressed neonate may revert to a fetal-type circulation due to hypoxia and hypercarbia.
This causes the pulmonary arterioles to constrict and the ductus arteriosus to dilate, reversing the
processes that resulted in functional closure of the ductus. The foramen ovale also re-opens.
 The neonate becomes severely hypoxemic (persistent pulmonary hypertension or persistent fetal
circulation)
Question 43 The production of red blood cells by the fetus
A Occurs in the liver at ter B Occurs in the spleen at term

Is dependent on maternal erythropoietin which
C D Occurs in the spleen from 20 weeks gestation
crosses the placenta
Is dependent on erythropoietin produced by the
E
fetal kidneys
Explanation
FETAL HAEMATOPOIESIS
 Begins in the yolk sac (2 -8 weeks) - progenitor cells migrate from the yolk sac to the liver at 5-8 weeks
gestation
 Only terminal differentiation of red cells occurs in the yolk sac
 Liver active from 5-8 weeks gestation - mainly red cells. Spleen also involved before 20 weeks
 Begins in the medullary cavity of the clavicle at about 10-12 weeks and in the medullary cavity of long of
bones at ~ 20 weeks gestation
 Some lymphocytes are produced in lymph nodes
 At term, all red cell production is in bones unless there is a reason for increased haematopoiesis
 Erythrocyte production in-utero is controlled exclusively by fetal erythropoietin produced in the liver and
maternal erythropoietin does not cross the placenta
 At birth erythropoietin production changes from the liver to the kidneys

 The increase in Po2 at birth causes serum erythropoietin to fall, and erythrocyte production shuts down
between birth and about 6 to 8 weeks
 This causes physiologic anaemia and contributes to anaemia of prematurity
Question 44 Surfactant

Is not produced by the fetus until 34 weeks Is not produced by the fetus until 37 weeks
A B
gestation gestation
Is not detectable in amniotic fluid until 34 weeks Production begins in the fetus at 24-28 weeks
C D
gestation gestation
E Production is stimulated by labour
Explanation
SURFACTANT
 Important role in reducing surface tension at the air-liquid interface in the lung
 Produced by type II alveolar epithelial cells
 Surfactant has a high rate of turnover and is replaced with a half life of about 10 hours
Contains the following:
1. Protein (5-10%) - four surfactant-associated proteins SP A-D
2. Neutral lipids including cholesterol, diacylglycerol (2-3%)
3. Phospholipids - sphingomyelin, phosphatidylinositol (7%)
4. Dipalmitoylphosphatidylcholine (36%)
5. Phosphatidylcholine (Lecithin - 33%)
6. Phosphatidylglycerol (10%)
7. Lecithin contains palmitic acid
 The lecithin: sphingomyelin ratio (L/S) test on amniotic fluid has been used to predict fetal pulmonary
maturity based on the principle that surfactant is rich in phospholipid, and that mature surfactant contains
high concentrations of lecithin
 Surfactant production begins in the fetus at 24-28 weeks gestation and detectable in amniotic fluid by 28-
32 weeks. By 35 weeks, most babies have developed adequate amounts of surfactant
 Surfactant production increased in: hypertensive disorders of pregnancy, malnutrition, placenta previa,
and drug addiction, premature rupture of membranes, intrauterine growth restriction, female fetus, and
hemoglobinopathy.
 Maternal glucocorticoid administration increases fetal pulmonary surfactant production and reduces the
risk of neonatal respiratory distress syndrome
 Surfactant production decreased in: maternal diabetes mellitus, anemia, polyhydramnios, hypothyroidism,
male fetus, twins, isoimmune disease, liver disease, renal disease, advanced maternal age, perinatal
infection, cold stress
 Albumin, bilirubin, meconium and inflammatory mediators act as surfactant inhibitors
Question 45 With respect to changes in maternal coagulation during pregnancy
A The concentration of factor VII decrease B The concentration of factor VIII decreases
The concentration of factor VIII does not change
C D The concentration of factor X increases
in haemophilia carriers
E The concentration of anti-thrombin III increases

Explanation
COAGULATION CHANGES IN PREGNANCY
Concentrations of clotting factors VII - X. fibrinogen increased in pregnancy and remain elevated in the
puerparium, accounting for the increased risk of thrombosis. This is true for carriers of haemophilia and
women with von Willebrand disease
Anticoagulants- Antithrombin III concentration is UNCHANGED
Protein C, Alpha-1 antitrypsin and alpha-2 macroglobulin concentrations increase
Protein S concentrations FALL
Fibrinolysis - increased inhibition of fibrinolysis - plasminogen activator inhibitor concentrations -
produced by the placenta
Fibrin degradation products - concentrations rise in the third trimester
Question 46 With respect to gastro-intestinal changes during pregnancy

A Gut motility is increased B Gastric acid secretion is increased
The risk of peptic ulceration is increased
C D The risk of gastro-oesophageal reflux is increased
especially during the third trimester
E The risk of constipation is reduced
Explanation
GI TRACT
 Decreased motility, probably due to influence of progesterone
 Reduced gastric acid secretion
 Peptic ulceration is rare during pregnancy and if present pre-pregnancy, may improve
 Relaxation of lower oesophageal sphincter - increased risk of reflux
 Constipation more common - compression of rectum by uterus, increased water absorption caused by
increased angiotensin II and reduced smooth muscle activity caused by progesterone
 Gall stones more common - smooth muscle relaxation cause sluggish flow of bile. Liver function and
bilirubin concentration unchanged
 Serum albumin concentration falls by 20% but there is a slight increase in total protein concentration
Change in serum creatinine concentration at 24 weeks gestation compared

Question 47
to pre-pregnancy

A 10% increase B 25% increase
C 10% decrease D 25% decrease
E 50% decrease

Explanation
RENAL SYSTEM
 Increase in kidney size and weight, ureteral dilatation (Right > left), bladder becomes an intra-
abdominal organ
 GFR increases 50%, renal plasma flow increases by 75%. Peak GFR reached ~16-24 weeks
gestation. GFR falls in late pregnancy
 Creatinine clearance increases to 150-200 ml/min
 Serum urea & creatinine decreases by about 25% to ~ 3.6mM and 60mM respectively
 Decreased uric acid concentration in early pregnancy due to increased clearance. Levels
increase in the third trimester
 Renal tubular secretion is unchanged
 Plasma osmolarity decreases about 10 mOsm/kg H2O. Colloid osmotic pressure falls by ~10%
 One mole of solute depresses the freezing point of water by 1.86C. Plasma (osmolarity
300mOsmol/kg H2O) has a freezing point of -0.56C. Pregnancy is associated with a 10% fall in
osmolarity and therefore plasma has a slightly higher freezing point (-0.5C)
 Marked increase in renin and angiotensin concentrations, but markedly reduced vascular
sensitivity to their hypertensive effects
 Aldosterone secretion increased as a consequence of activation of renin-angiotensin pathway - 6-
8x non-pregnant. Increases salt and water reabsorption from the renal tubules off-setting the
increase in GFR
 Progesterone has a natriuretic effect and stimulates potassium loss - this is balanced by the
effects of aldosterone. Overall, there is a small degree of salt and water retention in pregnancy
 Total body water increases by 6-8L. Extracellular fluid volume increased by 3L, about 1.5L of
which is plasma
 Increase in glucose excretion as filtered glucose load may exceed renal threshold for absorption
 Increased renal protein excretion - up to 300mg / 24h is normal. Amino acid excretion is
increased
 Thus, mild glycosuria (1-10 gm/day) and/or proteinuria (to 300 mg/day) can occur in normal
pregnancy
 Urine volume is not changed
Question 48 maternal nutritional requirement during pregnancy
Maternal vitamin A concentrations increase with

A Vitamin A requirements increase by ~ 40% B
increasing gestation age
Maternal concentrations of 1,25 dihydroxy- Maternal concentrations of 25-hydroxy-
C D
cholecalciferol increase during pregnancy cholecalciferol increase during pregnancy
Maternal vitamin C concentrations increase
E
during pregnancy
Explanation
VITAMINS
 Vitamin A requirement not increased in pregnancy and high intake may be terratogenic
 Blood vitamin A concentrations decline gradually in pregnancybecause of hemodilution
 The active metabolite of blood vitamin D (1,25-dihydroxycholecalciferol)increases in pregnancy whereas
the inactive form (25-hydroxycholecalciferol)decreases

 Vitamin E concentrations increaseduring gestation, probably because of the hyperlipidemic state
 During pregnancy, serum vitamin C progressively decreases ~50% because of the extra uptake by the
fetus and hemodilution
 Plasma thiamine, niacin and riboflavinconcentrations also decline during pregnancy
 Vitamin B-6 concentrations decline during pregnancy as a physiologicadjustment secondary to increased
blood volume or as a resultof increased requirements for active transport across the placenta
 Folate concentrations may decline in pregnancy as a resultof decreased intestinal absorption, inadequate
intake, or increaseddemand
 Serum vitamin B-12 concentrations progressivelydecline during pregnancy
 Vitamin B12 is not excreted into urine until the renal tubular reabsorptive capacity has been exceeded
 Biotin concentrations are significantly lower in pregnancy than in the non pregnant, non-lactating stateand
decrease progressively throughout pregnancy
Question 49 The storage temperature of cryoprecipitate

A -50 C B -30C
C -4C D 2-5 C
E 15C
Explanation
TRANSFUSION OF BLOOD & BLOD PRODUCTS
 Blood components such as red cells, platelets, fresh frozen plasma and cryo-precipitate are obtained
from a single donation of blood
 All blood used for transfusion is screened for HIV, Hep B&C and syphilis
 Clotting factors, albumin and immunoglobulins are prepared using plasma from many donors
 On average, 470ml of blood is obtained into 63ml anticoagulant and stored at 4C - shelf life = 5 weeks
and over 70% of red cells should be viable
 Whole blood is rarely used and packed red cells + crystalloid / colloid used
 Packed red cells - plasma is removed and replaced by optimal additive solution containing glucose,
adenine, mannitol and sodium chloride. Blood is leukocyte-depleted by filtration. Mean volume = 330ml,
haematocrit = 57%
 Washed red cells used in patients who have had urticarial or anaphylactic reactions
 Platelet concentrates - prepared from whole blood and may be stored at 22C for up to 5 days
 Fresh frozen plasma - plasma from one unit of blood frozen at -30C within 6h of donation. Volume
~200ml. Used to replace clotting factors in acquired bleeding disorders
 Cryoprecipitate - FFP from a single donation is allowed to thaw at 4-8C and removing the supernatant.
Volume ~20ml and stored at -30C. Contains factor VIII, vWF and fibrinogen. Used in the treatment of DIC
 Factor VIII & IX concentrates - freeze-dried from pools of plasma. Recombinant coagulation factors are
the treatment of choice for inherited bleeding disorders
A 34 year old woman had a post-partum haemorrhage following

Question 50 spontaneous vaginal delivery. Bleeding has been controlled using medical
therapy. Her HB is 6.8 g/dl
A Use type-specific blood B Use O Rhesus negative blood

C Use cross-matched blood D Use blood substitute
E Use salvaged blood

Explanation
BLOOD USE IN EMERGENCIES
 Blood required immediately use 2 units of O Rh negative blood (emergency stock)
 Blood required in 10-15 min use type-specific blood (same ABO and Rh type as the patient)
 Blood required in 45-60min use cross-matched blood
Question 51 With respect to the transfusion of blood and blood products

Immuno-suppression is a recognized complication Stored red blood cells have a high concentration
A B
of blood transfusion of 2,3-bisphosphoglycerate
Stored red blood cells have a lower oxygen
Hypercalcaemia is a recognized complication of
C affinity compared to freshly donated red blood D
rapid blood transfusion
cells
The plasma concentration of potassium in stored
E
blood is lower than in freshly donated blood
Explanation
Non-immunological complications of blood transfusion
 Transmission of infection- risk of Hep B or C ~ 1:200,000 units while risk of HIV ~ 1:3 million units
transfused. Risk of other infections including CMV and EBV. Clotting factor concentrates are treated to
inactivate viruses. Spirocheates do not survive for more than 72h in blood stored at 4C
 Bacterial contamination of blood components is one of the commonest causes of transfusion-associated
death
 Risk of vCJD transmission likely to be very small
 Volume over-load
 Air embolism
 Thrombophlebitis
 Transfusion-induced immuno-suppression - mechanism unknown
Oxygen Affinity Changes- Massive transfusion of stored blood with high oxygen affinity may adversely
affects oxygen delivery to the tissues - use fairly fresh red cell transfusions (<1 week old). 2,3 DPG levels
rise rapidly following transfusion and normal oxygen affinity is usually restored in a few hours.
DIC and electrolyte imbalance due to massive transfusion of stored blood
Hypocalcaemia- Each unit of blood contains approximately 3g citrate, which binds ionised calcium. The
healthy adult liver will metabolise 3g citrate every 5 minutes. Transfusion at rates higher than one unit
every five minutes or impaired liver function may thus lead to citrate toxicity and hypocalcaemia.
Hyperkalaemia- plasma potassium concentration of stored blood increases during storage and may be
over 30mmol/l. Hyperkalaemia associated with large amounts of blood are given quickly. Hypokalaemia is
more common as red cells begin active metabolism and take up potassium.
Hypothermia- leads to reduction in citrate and lactate metabolism (leading to hypocalcaemia and
metabolic acidosis), increase in affinity of haemoglobin for oxygen, impairment of red cell deformability,
platelet dysfunction and an increased tendency to cardiac dysrhythmias. Use blood warmers for large
transfusions.

Question 52 The erythrocyte sedimentation rate (ESR)

A Increases with increasing age B Decreases in pregnancy
C Is decreased in severe anaemia D Is increased in sickle cell disease
E Is increased in polycythaemia
Explanation
ESR & CRP
 Rate of fall of red cells in a column of blood = ESR
 Measure of acute phase response
 Raised ESR reflects increased plasma concentration of large proteins such as fibrinogen and
immunoglobulins which cause rouleux formation
 Increases with age, pregnancy, severe anaemia, heparinised blood, hypoalbuminaemia,
hypercholesterolaemia and higher in females
 Low in polycythaemia, sickle cell disease, hypofibrinigenaemia, hepatic necrosis, low molecular weight
dextran infusion, very high serum bile salt concentrations, congestive cardiac failure, treatment with
valproic acid
 ESR increases with temperature and refrigerated blood should not be used
 Plasma viscosity may be used instead of ESR - not different between males and females, only increases
slightly with age and not affected by Hb concentration. Results available within 15min
 ESR increased in sepsis, ischaemia, trauma, immunological disease and malignancy
 CRP is produced exclusively in the liver - acute phase protein - rises within 6h of acute event
 Follows clinical state of the patient more rapidly than ESR
 Not affected by Hb concentration
 Less helpful than ESR or plasma viscosity in monitoring chronic inflammatory processes
 Increased levels predict future cardiovascular disease
Question 53 With respect to alpha thalassaemia

Individuals with one alpha globin gene deleted Individuals with two alpha globin genes deleted
A B
have moderate anaemia have alpha thalassaemia trait
Individuals with two alpha globin genes deleted Individuals with one alpha globin gene deleted
C D
have severe anaemia typically have a microcytic blood picture
Individuals with two alpha globin genes deleted
E have an increased concentration of fetal
haemoglobin
Explanation
Alpha Thalassaemia
 Mainly caused by gene deletions, although mutations occur
 Two alpha chain genes on each chromosome 16 (4 genes total)
 Deletion of one (alpha+) or both (alpha0) genes on each chromosome may occur

 If all 4 genes deleted, no alpha chain and only gamma chain is produced in the fetus (gamma-4, Hb
Barts) - causes severe anaemia and fetal hydrops with intra-uterine or early neonatal death
 Three genes deleted - moderate anaemia, not transfusion dependent. Hb A, Hb Barts, Hb H (gamma-4)
are produced. Hb A2 is normal or reduced
 Two genes deleted - alpha thalassaemia trait - microcytosis with mild anaemia
 One gene deleted - normal blood picture
Question 54 Glomerular filtration rate

Is lower in the left lateral position compared to the
A Is unaffected by posture B
supine position
C Is increased if salt intake is increased D Is increased if salt intake is reduced
E Decreases by 20-25% in the first trimester
Explanation
GFR increases in pregnancy by 25-50% from 120ml/min to 160-170ml/min with a parallel increase in
renal plasma flow. GFR is altered by posture and is reduced in the supine or upright position compared to
a lateral position. Increased salt intake increases GFR *
· Plasma concentrations of creatinine, uric acid and urea are decreased in pregnancy *
The pH of the bicarbonate buffering system can be calculated from the

Question 55 equation pH = 6.1 + log [HCO3- / CO2]. When the concentration of HCO3-
is equal to the concentration of CO2, pH is
A 7.0 B 7.1
C 6.0 D 6.1
E 1.0
Explanation
· Made up of carbonic acid and potassium and magnesium bicarbonate in intracellular fluid *
· 399 out of 400 parts of carbonic acid exists as dissolved carbon dioxide. Hence carbonic acid is a
weak acid and sodium bicarbonate is a weak base
· The pH of the bicarbonate buffer system is calculated from the Henderson-Hasselbalch equation:
pH = 6.1 + log[HCO3- / CO2]
· Hence the pH of a solution containing an equal concentration of bicarbonate and carbon dioxide is
6.1 (log of 1 = 0) = pK of the buffer

Question 56 The physiological effects of angiotensin II include
Vasoconstriction and inhibition of anti-diuretic Stimulation of thirst and stimulation of anti-diuretic

A B
hormone secretion hormone secretion
Inhibition of thirst and stimulation of sodium and
C Potassium retention D
water retention
Inhibition of anti-diuretic hormone secretion and
E
increased renal potassium loss
Explanation
ANGIOTENSIN *****
· Angiotensin I is a decapeptide* produced by the action of renin on angiotensinogen

· Angiotensin I is a vasoconstrictor and stimulates catecholamine release from the adrenal medulla
and sympathetic neurons*
· Angiotensin I is converted to the more potent angiotensin II, an octapeptide* by the action of
angiotensin converting enzyme in the lungs and placenta*
· Angiotensin II stimulates aldosterone secretion, is a vasoconstrictor, stimulates thirst and ADH
secretion. Causes sodium and water retention with potassium loss*
· Angiotensin II has a half life of 90sec in plasma and is converted to angiotensin III by the action of
peptidases. Angiotensin III is a more potent stimulator of aldosterone secretion than angiotensin II
· Angiotensinogen is constitutively synthesized by the liver; its synthesis is up-regulated by
estrogens*.
· In pregnant women, or women taking estrogen-containing preparations, the plasma level of
angiotensinogen increases approximately 3 to 5-fold*.
Question 57 Which one is not a recognized cause of respiratory alkalosis?

A Anxiety-related hyperventilation B Acute asthma
C Pulmonary embolism D Pneumonia
E All listed items cause respiratory alkalosis
Explanation
Respiratory alkalosis
Causes include: *****
· Head Injury
· Stroke
· Anxiety-hyperventilation syndrome (psychogenic)
· Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
· Various endogenous compounds (e.g. progesterone during pregnancy, cytokines during sepsis,
toxins in patients with chronic liver disease) *
· Respiratory stimulation via peripheral chemoreceptors secondary to hypoxaemia
· Pulmonary Embolism

· Pneumonia
· Asthma
· Pulmonary oedema (all types) *
Question 58 With respect to the regulation of potassium balance

Aldosterone stimulates potassium retention by the Acidosis increases potassium secretion into the
A B
kidneys renal tubules
Alkalosis increases potassium secretion into the
C D Insulin inhibits potassium uptake into cells
renal tubules
Cell death results in increased uptake of
E
potassium into the cell
Explanation
• ? Potassium uptake into cells is dependent on the activity of Na+K+ATPase - stimulated by
insulin, beta-agonists and theophyllines. Uptake is inhibited by alpha agonists, acidosis and cell damage
or death.*
• ? Renal potassium loss is stimulated by aldosterone which stimulates K+ and H+ secretion in

exchange for Na+. Acidosis decreases while alkalosis increases K+ secretion (H+ and K+ are
interchangeable) *

ADAPTATION TO PREGNANCY
Question 1 With respect to maternal respiratory changes during pregnancy

A The FEV1 is increased B The peak expiratory flow rate (PEFR) is decreased
C The vital capacity is unchanged D The respiratory quotient decreases
E The tidal volume decreases by 15-20%
Explanation
RESPIRATORY CHANGES IN PREGNANCY
Progesterone increases the sensitivity of the respiratory centres to CO2
Respiratory rate unchanged
Minute volume - tidal volume X respiratory rate - increased by 50% in early pregnancy. Tidal volume
increases with little increase in respiratory rate
Residual volume - volume of air left in the lungs after the most forceful expiration decreased by 20% as
does functional residual capacity and expiratory reserve volume
Vital capacityand expiratory reserve are unchanged - unchanged
Physiological dead space increased by dilatation of small bronchioles
Respiratory quotient - ration of oxygen consumption to carbon dioxide production - increased from 0.76
to 0.83
Anatomical changesinclude an increase in the subcostal angle and elevation of the diaphragm
PEFR and FEV1are unchanged
There is a fall in arterial PCO2 with little change in PO2. The fall in PCO2 is matched by a fall in plasma
bicarbonate (renal compensation - compensated respiratory alkalosis) with no resultant change in pH.
pH= 7.44, pCO2=30, bicarbonate=20-25

The respiratory rate increases by 15% during the first The minute volume decreases by 15% during the first
A B
trimester trimester
The minute volume is the respiratory rate x the vital
C D The residual volume decreases by ~ 20%
capacity
Progesterone reduces the sensitivity of the respiratory
E
centres to CO2
Explanation

A There is a rise in arterial PCO2 B There is no change in arterial PO2
There is a compensatory rise in plasma bicarbonate
C D There is a 0.02-0.04 fall in pH
concentration
E There is a compensated respiratory acidosis

Explanation
Question 4 With respect to maternal haematological changes during normal pregnancy

A Plasma volume increases by 40-50% B There is a 10-15% increase in red cell mass
There is an increase in mean cell haemoglobin
C The red blood cell mean cell volume decreases D
concentration
E Plasma erythropoietin concentration falls
Explanation
HAEMATOLOGICAL CHANGES IN PREGNANCY
Increased plasma volume in the first trimester (40 - 50%) with a 25-30% increase in red cell mass
resulting in haemodilution
Mean cell volume is increased but mean cell Hb concentration is unchanged
Plasma and urinary erythropoietin concentrations are increased
Platelet count falls at term while the leucocyte count is increased slightly
Iron demand is increased with increased absorption from the gut. Total serum iron binding capacity is
increased with decreased serum iron and serum ferritin. Transferrin concentration increased
Erythrocyte free protoporphyrin is increased as haem synthesis produces this substrate ready for the
addition of iron
Reticulocyte count may increase in pregnancy
With respect to maternal haematological changes during normal

Question 5
pregnancy, which one of the above statements is not true?
There is a physiological reduction in haemoglobin

A B Urinary erythropoietin concentration increases
concentration
C Platelet count increases in the third trimester D Total serum iron binding capacity is increased
E Serum iron concentration decreases
Explanation

Question 6 With respect to changes in maternal coagulation during pregnancy

A The concentration of factor VII decrease B The concentration of factor VIII decreases
The concentration of factor VIII does not change in
C D The concentration of factor X increases
haemophilia carriers
E The concentration of anti-thrombin III increases
Explanation
COAGULATION CHANGES IN PREGNANCY
Concentrations of clotting factors VII - X. fibrinogen increased in pregnancy and remain elevated in the
puerparium, accounting for the increased risk of thrombosis. This is true for carriers of haemophilia and
women with von Willebrand disease
Anticoagulants- Antithrombin III concentration is UNCHANGED
Protein C, Alpha-1 antitrypsin and alpha-2 macroglobulin concentrations increase
Protein S concentrations FALL
Fibrinolysis - increased inhibition of fibrinolysis - plasminogen activator inhibitor concentrations -
produced by the placenta
Fibrin degradation products - concentrations rise in the third trimester
With respect to changes in maternal coagulation during pregnancy,
Question 7
which one of the above statements is not true?
A The concentration of protein C increases B The concentration of alpha-1 antitrypsin increases

Plasminogen activator inhibitor is produced by the
C The concentration of alpha-2 macroglobulin increases D
placenta
E The concentration of protein S increases
Explanation
Question 8 With respect to maternal cardiovascular changes during pregnancy
There is a decrease in pulse pressure by about 15

A Blood pressure falls to a nadir at ~ 36 weeks gestation B
mmHg
Pulmonary vascular resistance is unchanged during Stroke volume is increased by ~10% during the first
C D
pregnancy trimester
The apex beat of the heart is located at the sixth left
E
intercostal space during the third trimester
Explanation
CARDIOVASCULAR CHANGES IN PREGNANCY
CARDIAC OUTPUT - 40% increase by 12 weeks gestation from 4.5- 6L/min.

Current data do not favour a fall in cardiac output at term
Cardiac output falls rapidly after delivery and is not increased by breast-feeding. Both heart rate (10%
increases) and stroke volume are increased with increased myocardial contractility.
Peripharal resistance - falls, secondary to factors such as oestrogen and nitric oxide.
Blood pressure falls to a nadir at ~24 weeks gestation then rises to pre-pregnancy values at term.
There is a small increase in pulse pressure
Sphygmomanometry tends to overestimate BP in pregnancy by 7-12mmHg compared to direct
measurement.
No change in pulmonary capillary pressure. Pulmonary vascular resistance falls by ~35%
Heart position - elevated by diaphragm.
Apex beat moves to fourth left inter-costal space
ECG - deviation of electrical axis to the left by 15 degrees; other changes including S-T segment
depression and flattening or depression of T waves in III
Oxygenation - decreased Hb concentration but increased total oxygen carrying capacity of blood
(increased total Hb)
Increased cardiac output exceeds oxygen consumption hence the arterio-venous oxygen difference is
decreased.
Immediately following delivery, cardiac out-put increases by 10-20% as blood initially within the uterus is
returned as the uterus contracts
With respect to maternal cardiovascular changes during pregnancy,

Question 9
which one of the above statements is not true?
A Cardiac output increases following delivery B Myocardial contractility is increased

Sphygmomanometry tends to over-estimate blood
C There is a fall in total peripheral resistance D
pressure when compared to direct measurement
E ECG typically shows right axis deviation
Explanation

The risk of peptic ulceration is increased especially
during the third trimester
Explanation
GI TRACT


A Gall stones are less common B Serum bilirubin concentration is increased
There is a decrease in total plasma protein
C Serum albumin concentration increases by ~ 20% D
concentration
E Water absorption from the colon is increased
Explanation
Question 12 Change in GFR at 24 weeks gestation compared to pre-pregnancy

C 50% increase D 75% increase
E 50% decrease
Explanation
RENAL SYSTEM
abdominal organ
increase in GFR

which is plasma
increased
pregnancy

Question 13
to pre-pregnancy


E 50% decrease
Explanation
Change in serum urea concentration at 24 weeks gestation compared to pre-

Question 14
pregnancy

E 50% decrease
Explanation
Question 15 Change in colloid osmotic pressure during pregnancy compared to pre-pregnancy

E 50% decrease
Explanation

Question 16 With respect to changes in renal function during pregnancy
A The kidneys increase in size and weight B The left ureter becomes more dilated than the right
Renal plasma flow increases by 20-40% by 24 weeks
C D Creatinine clearance increases to ~ 90 ml/min
gestation
E Serum creatinine concentration increases by 25-40%
Explanation
Serum uric acid concentration increases during the first

A B There is a 50% increase in GFR by 24 weeks gestation
trimester
Serum uric acid concentration falls during the third There is a 25% increase in renal tubular secretion by 24
C D
trimester weeks gestation
E Plasma osmolarity increases by ~ 10 mOsm/kg
Explanation

A There is an increase in total urine volume B Plasma volume is increased by ~ 3L
C Total body water is increased by 1-2 L D There is an increase in serum angiotensin concentration
There is impaired glucose reabsorption from the renal
E
tubules resulting in glycosuria
Explanation

With respect to changes in renal function during pregnancy, which one of the
Question 19
above statements is not true?
There is increased salt and water re-absorption from the

A B There is a reduction in serum aldosterone concentration
renal tubules
Vascular sensitivity to the effects of angiotensin is
C D There is an increase in serum renin concentration
reduced
Renal clearance of uric acid is increased during the first
E
trimester
Explanation
Question 20 During uterine contraction

There is auto-transfusion of blood from the uterus into
A Maternal cardiac out-put decreases B
the maternal circulation
C Maternal heart rate decreases D Maternal stroke volume decreases
The changes in maternal cardiac output are more
E pronounced in the supine position compared to the left
lateral position
Explanation
Maternal physiological changes during labour
Cardiovascular
 There is auto-transfusion of 300-400 ml of blood from the uterus into the maternal circulation during
uterine contraction
 This results in a 10-40% increase in cardiac output brought about by an increase in heart rate and stroke
volume. The increase in cardiac output is more pronounced in the second stage of labour and greater in
the left lateral compared to the supine position
Question 21 With respect to maternal cardiovascular changes during labour and delivery

Venous return decreases markedly immediately Cardiac output returns to pre-labour values 24-48h after
A B
following normal birth birth
Immediately following delivery, maternal cardiac output
C D Systolic blood pressure falls during labour
increases up to 80% above pre-labour values
E Diastolic blood pressure falls during labour
Explanation

Following birth, cardiac output continues to increase to 80% above pre-labour values due to auto-

transfusion from the uterus and relief of inferior vena cava compression. Cardiac output returns to pre-
labour values about 1 hour post-partum.
 Basal BP increases during labour and is further increased with each contraction
Question 22 With respect to nutritional requirements during pregnancy
Maternal plasma triglyceride concentrations decrease in Serum cholesterol levels decrease with increasing
A B
the third trimester gestation age
Maternal protein requirement decreases during the third Maternal daily calcium intake needs to increase by
C D
trimester about 70% compared to pre-pregnancy values
Maternal fasting glucose levels are increased in the third
E
trimester
Explanation
 In the first half of pregnancy, there is a tendency to hypoglycaemia. Late pregnancy associated
with insulin resistance - decreasing maternal glucose utilisation and increasing plasma glucose
concentration for transfer to the fetus. Fasting glucose not increased
 Increased mobilisation of lipids as alternative maternal energy source - increased plasma
triglyceride concentration. Increased serum cholesterol and phospholipids with increasing
gestation
 Maternal protein requirement increases by ~6-10g per day at term
 Fetus requires 0.3g calcium per day in the third trimester and accumulated 28g during gestation.
Maternal daily calcium intake needs to increase by ~70%
Question 23 maternal nutritional requirement during pregnancy

Maternal vitamin A concentrations increase with
A Vitamin A requirements increase by ~ 40% B
Maternal concentrations of 1,25 dihydroxy- Maternal concentrations of 25-hydroxy-cholecalciferol
C D
cholecalciferol increase during pregnancy increase during pregnancy
Maternal vitamin C concentrations increase during
E
pregnancy
Explanation
VITAMINS
 Vitamin A requirement not increased in pregnancy and high intake may be terratogenic
 Blood vitamin A concentrations decline gradually in pregnancybecause of hemodilution
 The active metabolite of blood vitamin D (1,25-dihydroxycholecalciferol)increases in pregnancy whereas
the inactive form (25-hydroxycholecalciferol)decreases
 Vitamin E concentrations increaseduring gestation, probably because of the hyperlipidemic state
 During pregnancy, serum vitamin C progressively decreases ~50% because of the extra uptake by the
fetus and hemodilution
 Plasma thiamine, niacin and riboflavinconcentrations also decline during pregnancy

 Vitamin B-6 concentrations decline during pregnancy as a physiologicadjustment secondary to increased
blood volume or as a resultof increased requirements for active transport across the placenta
 Folate concentrations may decline in pregnancy as a resultof decreased intestinal absorption, inadequate
intake, or increaseddemand
 Serum vitamin B-12 concentrations progressivelydecline during pregnancy
 Vitamin B12 is not excreted into urine until the renal tubular reabsorptive capacity has been exceeded
 Biotin concentrations are significantly lower in pregnancy than in the non pregnant, non-lactating stateand
decrease progressively throughout pregnancy
Question 24 With respect to changes in maternal physiology during pregnancy
Serum alkaline phosphatase concentrations decrease

A Arterial PCO2 increases with increasing gestation age B
with increasing gestation age
Serum alanine transaminase concentration increases Serum gamma glutamyl-transferase concentration
C D
during pregnancy increases during pregnancy
E Arterial PO2 increases with increasing gestation age
Explanation
 Maternal arterial PO2 increases and PCO2 decreases with gestation age. Standard bicarbonate
decreases with gestation age
 Alkaline phosphatase increases in pregnancy - both placental and bone isoenzymes
 Serum gamma GT and transaminase levels decrease during pregnancy
 Bile acids cholic acid and deoxycholic acid levels do not change in pregnancy. Chenodeoxycholic
acid levels increase sharply at term
 Phosphate concentration falls during pregnancy
 Fasting glucose levels fall in pregnancy while insulin levels rise in the third trimester. The third
trimester is associated with decreased glucose tolerance
 Serum fructosamine concentrations are lower in the second and third trimester compared to non-
pregnant / first trimester. Glycosylated Hb concentration unchanged

Question 25 With respect to changes in maternal physiology during pregnancy

Serum alanine transaminase concentration increases
A Arterial PCO2 increases with increasing gestation age B
during pregnancy
There is a 40% fall in serum bile acid concentration Glycosylated haemoglobin concentration is unchanged
C D
during pregnancy during normal pregnancy
Maternal fasting insulin levels fall during the third
E
trimester
Explanation

Question 26 With respect to early fetal physiology
The fetal heart beat is not detectable by trans-vaginal

The crown-rump length is most useful in dating
A ultrasound scanning until at least 6 weeks after B
pregnancy between 14 to 16 weeks gestation
conception
Fetal umbilical venous pressure increases with Fetal mean umbilical artery pressure decreases with
C D
increasing gestation age increasing gestation age
At 20 weeks gestation, there is reverse flow in the
E
umbilical arteries during diastole
Explanation
 Fetal heart beat detectable by trans-vaginal ultrasound 28 days after conception. Fetal heart rate
increases from 90 / min to 145 / min by 7 weeks post-conception
 Crown-rump length useful for dating pregnancy only in the first trimester. Not affected by maternal age,
height or parity. Smaller in female fetuses
 Amniotic fluid pressure increases with gestation age with a plateau of 4-5mmHg in mid-gestation. Not
affected by maternal age or parity and similar in multiple and singleton pregnancies
 After 16 weeks gestation, there is forward flow in the umbilical arteries throughout the cardiac cycle
 Fetal cardiac out-put, umbilical venous pressure and mean umbilical arterial pressure increase with
 Fetal heart rate decreases with increasing gestation age while heart rate variability increases. The
frequency and amplitude of accelerations increases with gestation age. Spontaneous decelerations are
commonly found in the second and early third trimester
Question 27 Which one of the above statements is not true?

Between 5 and 9 weeks gestation, the fetal heart rate Between 20 and 37 weeks gestation, the fetal heart rate
A B
increases with gestation age variability increases with gestation age
Between 20 and 37 weeks gestation, the amplitude of Between 20 and 37 weeks gestation, the frequency of
C fetal heart rate accelerations decreases with gestation D fetal heart rate accelerations increases with gestation
age age
Between 20 and 37 weeks gestation, the fetal heart rate
E
decreases with gestation age
Explanation

Question 28 With respect to fetal biochemistry
Fetal haemoglobin concentration remains unchanged as Fetal blood oxygen content remains unchanged as
A B
gestation age increases gestation age increases
Blood in the inter-villous space has lower PO2 than Blood in the inter-villous space has lower PCO2 than
C D
umbilical venous blood umbilical venous blood
Blood in the inter-villous space has 2x the lactate
E
concentration of umbilical venous blood
Explanation

Umbilical arterial PO2 increases with increasing Umbilical venous PO2 increases with increasing
A B
gestation age gestation age
Umbilical arterial pH decreases with increasing Umbilical venous PCO2 decreases with increasing
C D
gestation age gestation age
Umbilical arterial PCO2 decreases with increasing
E
gestation age
Explanation
Fetal albumin concentration increases with increasing Fetal triglyceride concentration increases with
A B
gestation age increasing gestation age
Fetal bilirubin concentration decreases with increasing Fetal bilirubin concentration is lower than maternal
C D
gestation age concentration
Fetal cholesterol concentration is higher than maternal
E
concentration
Explanation

A 50-100 ml B 150-250 ml
C 300-330 ml D 400-600 ml
E 10-50 ml

Explanation
Question 32

E Over 90 minutes
Explanation
Definition:
 Begins with the complete delivery of the fetus and ends with the complete delivery of the placenta and
membranes.
Duration
 The mean duration of the third stage following physiological management has been reported to be
between 12 – 21 minutes. A physiological third stage has duration of less than 60 minutes in 95% of
women.
 There is a moderate level of evidence that an actively managed third stage of 30 minutes or longer is
associated with increased incidence of PPH. PPH remains the most common cause of maternal mortality
globally. In addition, PPH is an important contributor to maternal morbidity including:
Post-natal anaemia
 The third stage of labour is diagnosed as prolonged if not completed within 30 minutes of the birth of the
baby with active management and 60 minutes with physiological management.
Physiological management of the third stage of labour includes which one of

Question 33
the above?
A Nipple stimulation to induce uterine contraction B Delivery of the placenta by maternal effort
C No clamping of the cord until at least after 30 seconds D Routine use of uterotonic drugs

Explanation
Physiological management of the third stage involves a package of care which includes all of these three
components:
Early suckling or nipple stimulation can increase uterine contractility. There is no evidence that early
suckling reduces the risk of PPH or other complications of the third stage.
Question 34 The proportion of term babies who are jaundiced at birth
A 0% B 5%
C 8% D 12%
E 15%
Explanation
Neonatal Jaundice
Prolonged jaundice is jaundice lasting more than 14 days in term babies and more than 21 days in
preterm babies
Question 35 Enzyme that catalyses the rate-limiting step in bilirubin synthesis

E Catalase
Explanation
Bilirubin metabolism
 Bilirubin (unconjugated / ‘indirect’) is produced from the breakdown of red blood cells
 The hemoglobin released is broken down to heme the globin chains are converted to amino acids
 Heme is converted to unconjugated bilirubin in the reticuloendothelial cells of the spleen
 In the first step, heme is converted to biliverdin by the action of heme oxygenase, the rate-limiting step in
the process. Iron and carbon monoxide are released.
 Carbon monoxide is excreted through the lungs and can be measured as an index of to bilirubin
production.

 In-utero, bilirubin crosses the placenta by passive diffusion, and excretion of bilirubin from the fetus
occurs through the mother
 Approximately 75% of bilirubin is derived from hemoglobin, but degradation of myoglobin, cytochromes,
and catalase also contributes
 Unconjugated bilirubin is insoluble and is transported in the circulation bound to albumin
 In the liver, unconjugated bilirubin is conjugated with glucuronic acid by the enzyme
glucuronyltransferase, making it water-soluble
 Bilirubin-glucuronide is excreted in bile. In the large bowel, conjugated bilirubin is metabolised by bacteria
into urobilinogen and then to stercobilin which gives faeces its brown colour
 Some of the urobilinogen is reabsorbed and excreted in the urine
 Bilirubin levels are higher in neonates than in adults because:
 Neonatal red cells have a shorter lifespan
 Neonates have a higher haematocrit
 Neonatal hepatic enzyme systems are immature and less effective at metabolizing bilirubin. Glucuronyl
transferase activity in neonatal liver is 0.1 – 1% that in adult liver but increases to adult values by 4-8
weeks of age
 There is increased entero-hepatic circulation of bilirubin in the neonate. In the absence of gut bacteria to
convert conjugated bilirubin to stercobilin, the bilirubin is de-conjugated
Jaundice may therefore occur in neonates as part of normal physiology

E Asynclitism
Explanation
Internal rotation
 Occurs at the level of the ischial spines as a result of the combined effect of uterine contractions and the
tone & shape of the pelvic floor. Typically, the head rotates 45° from the occipito-transverse to the
occipito-anterior position. This brings the suboccipito-bregmatic diameter in line with the wider diameter of
the pelvic outlet – the antero-posterior diameter
Extension
 Following internal rotation and further descent, the base of the occiput is located at the inferior margin of
the symphysis pubis. The tone of the pelvic floor and the downward forces from uterine contractions
cause the neck to extend and the head is delivered beneath the symphysis pubis.
 When the fetal head is free of resistance, it untwists 45° left or right, returning to its original position in
relation to the body. This is restitution.
 The fetal shoulders enter the pelvis with the bis-acromial diameter aligned to the transverse diameter of
the pelvic inlet. When the shoulders reach the pelvic floor, ‘internal rotation’ also occurs to align the bis-
acromial diameter with the antero-posterior diameter of the pelvic outlet. This process is reflected in
further movement of the head and constitutes external rotation
Expulsion
 The anterior shoulder is then delivered under the symphysis pubis followed by the posterior shoulder

Question 37 With respect to the anatomy of the fetal / neonatal skull

The anterior fontanelle is bound posteriorly by the The anterior fontanelle is bound anteriorly by the two
A B
occipital bone halves of the frontal bone
The posterior fontanelle is bound anteriorly by the The posterior fontanelle is never overlapped by bone
C D
temporal bone during moulding
E The fetal skull has two fontanelles
Explanation
THE FETAL SKULL
 The frontal bone is in two halves separated by the frontal suture. The frontal bone is separated from the
parietal bones by the coronal suture
 Two parietal bones separated by the sagittal suture
 One occipital bone separated from the parietal bones by the lambdoid suture
 The parietal bones are separated from the temporal bone on each side by the temporal suture.
 In utero, the bones of the skull are not closely knit at the sutures like they are in the adult skull. The fetal /
neonatal skull bones are separated by six un-ossified membraneous intervals called fontanelles
 The anterior and posterior fontanelles are of greatest clinical use.
Anterior fontanelle (Bregma)

 Bound anteriorly by the two halves of the frontal bone
 Bound posteriorly by the two parietal bones
 Diamond shaped
 Has a membraneous base at term and remains clinically palpable until ~18 months of age
 Remains palpable even after moulding during labour and the surrounding bones will not overlap
Posterior fontanelle (Lambda)
 Bound anteriorly by the two parietal bones
 Bound posteriorly by the occipital bone
 Triangular in shape
 Has an ossified base at term and no longer palpable by the 12 months of age
 The surrounding bones overlap during moulding
Question 38 Presenting diameter in a fully flexed occipito-anterior position
A Suboccipito-bregmatic diameter B Occipito-bregmatic diameter

C Submento-frontal diameter D Bi-tronchanteric diameter
E Mento-vertical diameter
Explanation
Diameters of Fetal Skull
Suboccipito-bregmatic diameter
 9.5cm
 From below the occipital protuberance (sub-occiput) to the centre of the anterior fontanelle (bregma)
 The presenting diameter in the occipito-anterior position with complete flexion
Suboccipito-frontal

 10 cm +
 From below the occipital protuberance to the anterior end of the bregma
 The presenting diameter in occipito anterior with incomplete flexion
 With greater degrees of de-flexion, the anterior limit of this diameter extends further into the frontal bone,
presenting a wider diameter to the maternal pelvis
Occipito-frontal
 11.5 cm
 Form the occipital protuberance to the root of the nose
 The presenting diameter in the occipito-posterior position
 This diameter is different from the diameter that presents in the occipito-anterior position because of the
tendency of the head to be de-flexed in the occipito-posterior position
Submento-bregmatic
 9.5 cm
 From the junction of the chin and neck (sub-mentum) to the centre of the bregma
 The presenting diameter in face presentation when the head is completely extended
Submento-vertical
 11.5 cm
 From the junction of the chin and neck to the centre of the vertex (point on the sagittal suture midway
between anterior and posterior fontanelles)
 The presenting diameter in an incompletely extended face presentation
Mento-vertical
 13.5 cm
 From the tip of the chin to the centre of the vertex
 The presenting diameter in brow presentation
 The mento-vertical diameter is longer than any diameter of the pelvis so a bow presentation cannot be
delivered vaginally
Question 39 The presenting diameter in a fully flexed occipito-anterior position

A 9.5 cm B 10.5 cm
C 11.5 cm D 12.5 cm
E 13.5 cm
Explanation

Is dependent on maternal erythropoietin which crosses
the placenta
Is dependent on erythropoietin produced by the fetal
E
kidneys
Explanation

gestation
Question 41 Surfactant
A Is not produced by the fetus until 34 weeks gestation B Is not produced by the fetus until 37 weeks gestation
Is not detectable in amniotic fluid until 34 weeks
C D Production begins in the fetus at 24-28 weeks gestation
gestation
E Production is stimulated by labour
Explanation
SURFACTANT
 The lecithin: sphingomyelin ratio (L/S) test on amniotic fluid has been used to predict fetal pulmonary
maturity based on the principle that surfactant is rich in phospholipid, and that mature surfactant contains
high concentrations of lecithin
 Surfactant production begins in the fetus at 24-28 weeks gestation and detectable in amniotic fluid by 28-
32 weeks. By 35 weeks, most babies have developed adequate amounts of surfactant
 Surfactant production increased in: hypertensive disorders of pregnancy, malnutrition, placenta previa,
and drug addiction, premature rupture of membranes, intrauterine growth restriction, female fetus, and
hemoglobinopathy.
 Maternal glucocorticoid administration increases fetal pulmonary surfactant production and reduces the
risk of neonatal respiratory distress syndrome
 Surfactant production decreased in: maternal diabetes mellitus, anemia, polyhydramnios, hypothyroidism,
male fetus, twins, isoimmune disease, liver disease, renal disease, advanced maternal age, perinatal
infection, cold stress

Question 42 Blood for transfusion in the UK is screened for which of the above infections?
A HIV and malaria B HIV and hepatitis B

C HIV, hepatitis B, Hepatitis C D HIV, hepatitis B, Hepatitis C, hepatitis D
E HIV, syphilis, hepatitis B, hepatitis C
Explanation

Question 43 spontaneous vaginal delivery. Bleeding has been controlled using medical
therapy. Her HB is 6.8 g/dl


Explanation
Question 44 Prolonged prothrombin time is indicative of abnormalities in which clotting function?
A Abnormal platelet function B Abnormalities in the intrinsic pathway

C Abnormalities in the extrinsic pathway D Abnormalities in the intrinsic or common pathway
E Abnormalities in the extrinsic or common pathway
Explanation
COAGULATION STUDIES
 BLEEDING TIME - measures platelet plug formation - 3-10 minutes
 Blood for coagulation tests is collected into citrate to prevent clotting
 PROTHROMBIN TIME - prolonged with abnormalities in the extrinsic or common pathways

 PARTIAL THROMBOPLASTIN TIME WITH KAOLIN - PTTK - prolonged with abnormalities in the intrinsic
or common pathways
 THROMBIN TIME - prolonged with fibrinogen deficiency or the presence of inhibitors such as heparin or
fibrin degradation products

Prolonged partial thromboplastin time with kaolin (PTTK or APPT) is

Question 45
indicative of abnormalities in which clotting function?

Explanation

A Should be measured using heparinized blood B Is the rate of fall of red blood cells in a column of serum
C Is raised following ischaemic injury D Is decreased in the presence of malignant tumours
E Is raised in congestive cardiac failure
Explanation
ESR & CRP
 Low in polycythaemia, sickle cell disease, hypofibrinigenaemia, hepatic necrosis, low molecular weight
dextran infusion, very high serum bile salt concentrations, congestive cardiac failure, treatment with
valproic acid
 Plasma viscosity may be used instead of ESR - not different between males and females, only increases
slightly with age and not affected by Hb concentration. Results available within 15min

Which one of the above is not associated with an increase in erythrocyte
Question 47
sedimentation rate (ESR)?

A Hypoalbuminaemia B Pregnancy
C Severe anaemia D Sickle cell disease
E Hypercholesterolaemia
Explanation
Question 48 Which one of the above statements regarding iron metabolism is correct?
In healthy females, ~ 50-60% of ingested iron is

A B The majority of iron in the body is contained in ferritin
absorbed from the gut
The average daily iron loss in women of reproductive
C Iron is transported in plasma by ferritin D
age is 2mg
E Daily iron intake is ~ 1-2g
Explanation
IRON METABOLISM
 Body contains ~4.5g iron - 65% in Hb, 5% in myoglobin. Small amount in cytochrome-dependent
enzymes
 Transported in plasma as transferring and stored in tissues (liver mainly) as ferritin. Haemosiderin is a
very insoluble iron store only formed in iron overload
 Average daily iron loss is 1mg (males) and 2mg (females of reproductive age)
 Children and pregnant women require more iron
 Daily iron intake 15-20mg of which 0.5-2mg is absorbed (~10% of intake)
Absorption
 Iron absorption inhibited by phytates, phosphate, bicarbonate and tannins which form insoluble
complexes
 Iron absorption promoted by vitamin C and HCl. HCl solubilises iron while ascorbate reduces iron (3+) to
iron (2+) which is less likely to form insoluble complexes
 Heme iron better absorbed than non-heme iron
 Ferrous iron (2+) better absorbed than ferric iron (3+)
 Following absorption, ferrous iron (2+) is converted to ferric iron (3+) and bound to ferritin within intestinal
epithelial cells or transported into the plasma where it is bound to transferring - a beta-globulin
synthesised by the liver - transferin saturation ~33%
 Each transferring molecule binds two atoms of ferric iron
 Transferrin-bound iron becomes attached to specific receptors on erythroblasts and reticulocytes and the
iron is removed
 Iron stored as ferritin in gut epithelial cells is lost as the cells are shed
 Haemosiderin is an insoluble iron-protein complex in macrophages, hepatocytes and spleen
 Mostly absorbed in the duodenum and jejunum by carrier mediated transport
 Iron deficiency results in increased GI uptake - mechanism effective within 3-4 days

 Serum iron concentration 11-30 microM - levels higher in the morning
 The body cannot get rid of excess iron and absorption has to be matched to requirements. Excessive iron
may be removed by chealating agents such as desferrioxamine
Question 49 Serum ferritin concentrations
Fall if the woman develops an acute inflammatory

A B Are raised in iron deficiency anaemia
disease
Are a better indicator of iron stores than serum iron
C D Fall in the presence of malignancy
concentration
E Are typically low in sickle cell disease
Explanation
ANAEMIA
Iron deficiency
 Caused by blood loss (menorrhagia, PPH. GI bleed), increased demands (growth, pregnancy),
decreased absorption or poor intake. Commonest cause worldwide is hookworm infestation
 MCV reduced <80fl
 MCH (<27pg) - hypochromia
 Poikliocytosis (variation in shape), anisocytosis (variation in size) and target cells
 Serum iron falls with a rise in serum iron binding capacity. Transferrin saturation falls <19%
 Serum ferritin reflects iron stores better than serum iron - falls. However, ferritin is an acute phase
protein and concentrations increase in inflammatory or malignant disease
 Differential diagnoses include anaemia of chronic disease, thalassaemia
 Treat underlying cause. Iron replacement results in a rise in Hb by 1g per week. Ferrous sulphate
is best absorbed when the patient is fasting

Individuals with one alpha globin gene deleted have Individuals with two alpha globin genes deleted have
A B
moderate anaemia alpha thalassaemia trait
Individuals with two alpha globin genes deleted have Individuals with one alpha globin gene deleted typically
C D
severe anaemia have a microcytic blood picture
Individuals with two alpha globin genes deleted have an
E
increased concentration of fetal haemoglobin
Explanation
Alpha Thalassaemia


Question 51 equation pH = 6.1 + log [HCO3- / CO2]. When the concentration of HCO3-
is equal to the concentration of CO2, pH is
A 7.0 B 7.1
C 6.0 D 6.1
E 1.0
Explanation
· Made up of carbonic acid and potassium and magnesium bicarbonate in intracellular fluid *
· 399 out of 400 parts of carbonic acid exists as dissolved carbon dioxide. Hence carbonic acid is a
weak acid and sodium bicarbonate is a weak base
· The pH of the bicarbonate buffer system is calculated from the Henderson-Hasselbalch equation:
pH = 6.1 + log[HCO3- / CO2]
· Hence the pH of a solution containing an equal concentration of bicarbonate and carbon dioxide is
6.1 (log of 1 = 0) = pK of the buffer
Question 52 Plasma renin concentrations

A Fall during the first trimester B Fall from 20 weeks gestation
C Are unchanged throughout pregnancy D Increase in the first half of pregnancy
E Fall from 32 weeks gestation
Explanation
RENIN
· Proteolytic* enzyme secreted by the kidneys (juxta-glomerular apparatus in the afferent arteriol) in
response to a fall in sodium concentration in the distal tubule
· Pro-renin is present in ovarian follicular fluid and its concentration (BUT NOT that of active rennin)
increases in plasma transiently by up to 2 fold during the LH surge and in response to HCG to induce
ovulation. After conception, it increases about 8 to 10-fold in parallel with plasma HCG.
· Plasma concentration of active renin increases slightly early in the first trimester to reach a plateau
(five-fold basal value) at the 20th week of gestation which is then maintained throughout pregnancy*.

· Renin secretion is increased by factors which reduce extracellular fluid volume or pressure or
reduce sodium concentration in the renal filtrate*
Question 53 The anion gap is calculated from the equation
A [Cl-] – [HCO3-] B [Na+] – [K+]

C [Na+] + [K+] – [Cl-] D [Na+] + [K+] – [Cl-] – [HCO3-]
E [Na+] – [Cl-]
Explanation
Question 54 Metabolic acidosis with a normal anion gap occurs in

A Diabetic keto-acidosis B Diarrhoea
C Uraemia D Starvation
E Alcohol poisoning
Explanation
Occurs in:
Question 55 Which one is not a recognized cause of respiratory alkalosis?
A Anxiety-related hyperventilation B Acute asthma

C Pulmonary embolism D Pneumonia
E All listed items cause respiratory alkalosis
Explanation
Respiratory alkalosis
Causes include: *****

· Head Injury
· Stroke
· Anxiety-hyperventilation syndrome (psychogenic)
· Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
· Various endogenous compounds (e.g. progesterone during pregnancy, cytokines during sepsis,
toxins in patients with chronic liver disease) *
· Respiratory stimulation via peripheral chemoreceptors secondary to hypoxaemia
· Pulmonary Embolism
· Pneumonia
· Asthma
· Pulmonary oedema (all types) *
Question 56 Potassium uptake into cells is inhibited by
A Insulin B Beta agonists

C Theophyllines D Acidosis
E The activity of Na+K+ATPase
Explanation

or death.*

interchangeable) *

Aldosterone stimulates potassium retention by the Acidosis increases potassium secretion into the renal
A B
kidneys tubules
Alkalosis increases potassium secretion into the renal
C D Insulin inhibits potassium uptake into cells
tubules
Cell death results in increased uptake of potassium into
E
the cell
Explanation

Question 58 Which one is not a typical clinical feature of hypercalcaemia?
A Muscle cramps and tetany B Abdominal pain

C Peptic ulceration D Polyuria
E Corneal calcification
Explanation
Symptoms of hypercalcaemia
1) fatigue, malaise, dehydration, depression
2) renal colic, polyuria, nocturia, haematuria, hypertension
3) bone pain. Bone cysts may occur
4) abdominal pain & peptic ulceration
5) ectopic calcification including corneal calcification


HAEMATOLOGY
A woman has blood group A and her partner has blood group AB. Their
Question 1 daughter has blood group B. Which one of the above is the woman’s
genotype?

A OO genotype B OA genotype
C AA genotype D AB genotype
E BB genotype
Explanation
ABO BLOOD GROUP
 Under control of a pair of allelic genes H and h and three allelic genes A,B & O
 The A,B and H antigens are very similar in structure and differences in their sugars determine their
specificity
 The H gene codes for enzyme H which attaches fucose to the basic glycoprotein backbone to form H
substance, the precursor for A & B antigens
 The A & B genes control specific enzymes responsible for the addition of N-acetyl-galactosemine (Group A)
and D-galactose (Group B) to H substance
 The O gene does not transform H substance and therefore O is not antigenic
 The A,B & H antigens are found on most body cells and in the saliva and gastric juice of most individuals
 Inherited as co-dominant traits
 Blood group O individuals must have an OO genotype
 Group A individuals are AA or AO and group B individuals are BB or BO. Group AB individuals have both A
& B antigens
 Antibodies to the ABO antigens develop in childhood the titres peak at about the age of 10. Group O have
anti-A and anti-B antibodies; group A have anti-B and group B have anti-A while group AB have no
antibodies
 Group AB can receive blood from all other group types (universal recipients) while group O can donate to all
other groups (universal donors
 Caucasians: O = 47%; A = 41%, B = 9%, AB = 3%
 Anti-A and anti-B antibodies are IgM and cause severe intra-vascular haemolysis of incompatible red cells

A woman has blood group B and her son has blood group O. Which
Question 2
one of the above is the woman’s genotype?
A OO genotype B OA genotype
C AA genotype D AB genotype
E BO genotype
Explanation
ABO BLOOD GROUP
 Under control of a pair of allelic genes H and h and three allelic genes A,B & O
 The A,B and H antigens are very similar in structure and differences in their sugars determine their
specificity

 The H gene codes for enzyme H which attaches fucose to the basic glycoprotein backbone to form H
substance, the precursor for A & B antigens
 The A & B genes control specific enzymes responsible for the addition of N-acetyl-galactosemine (Group A)
and D-galactose (Group B) to H substance
 The O gene does not transform H substance and therefore O is not antigenic
 The A,B & H antigens are found on most body cells and in the saliva and gastric juice of most individuals
 Inherited as co-dominant traits
 Blood group O individuals must have an OO genotype
 Group A individuals are AA or AO and group B individuals are BB or BO. Group AB individuals have both A
& B antigens
 Antibodies to the ABO antigens develop in childhood the titres peak at about the age of 10. Group O have
anti-A and anti-B antibodies; group A have anti-B and group B have anti-A while group AB have no
antibodies
 Group AB can receive blood from all other group types (universal recipients) while group O can donate to all
other groups (universal donors
 Caucasians: O = 47%; A = 41%, B = 9%, AB = 3%
 Anti-A and anti-B antibodies are IgM and cause severe intra-vascular haemolysis of incompatible red cells
Question 3 With respect to Rhesus blood group

The child of two Rhesus negative individuals can be Rhesus The child of two Rhesus positive individuals cannot be
A B
positive Rhesus negative
The E antigen is a recognized cause of fetal haemolytic
C The C antigen does not cause fetal haemolytic disease D
disease
The child of a Rhesus positive mother and a Rhesus
E
negative father cannot be Rhesus negative
Explanation
RHESUS BLOOD GROUP
 Six antigens - C, D, E; c,d,e
 An individual with the C antigen cannot have the c antigen; same for D & E antigens
 D antigen is most antigenic - individuals with D antigen are Rhesus positive. 15% of Caucasians are
Rhesus negative.
 Immune response to Rhesus antigens is slow and peak antibody titres are attained 2-4 months after
exposure. Transfusion reaction in an unsensitized individual is therefore delayed
 D antigen causes severe Rhesus disease. C & E antigens can cause mild fetal haemolysis. Usually the
first pregnancy is not affected, but may be if the mother had received incompatible blood products
 The offspring of two Rh negative individuals must be Rh negative. The offspring of a Rh negative and a
Rh positive individual may be Rh negative as the Rh positive parent may be heterozygous


A An individual with the C antigen cannot have the D antigen B An individual with the D antigen cannot have the d antigen
Immune response to Rhesus antigens develops over 36-72
C D is the least antigenic Rhesus antigen D
hours
Following exposure to the D antigen, a Rhesus D negative
E
individual would produce antibodies within 72 hours
Explanation
RHESUS BLOOD GROUP
 D antigen is most antigenic - individuals with D antigen are Rhesus positive. 15% of Caucasians are
Rhesus negative.
 Immune response to Rhesus antigens is slow and peak antibody titres are attained 2-4 months after
exposure. Transfusion reaction in an unsensitized individual is therefore delayed
 D antigen causes severe Rhesus disease. C & E antigens can cause mild fetal haemolysis. Usually the
first pregnancy is not affected, but may be if the mother had received incompatible blood products
 The offspring of two Rh negative individuals must be Rh negative. The offspring of a Rh negative and a
Rh positive individual may be Rh negative as the Rh positive parent may be heterozygous
Question 5 The storage temperature of fresh frozen plasma
A -50 C B -30C
C -4C D 2-5 C
E 15C
Explanation
haematocrit = 57%

Question 6 The storage temperature of platelet concentrates

A -50 C B -30C
C 2-5 C D 15C
E 22 C
Explanation
haematocrit = 57%

Question 7 spontaneous vaginal delivery. Bleeding has been controlled using
medical therapy. Her HB is 6.8 g/dl

Explanation

Question 8 A delayed consequence of allo-immunisation following blood transfusion

A Urticaria B Haemolytic transfusion reaction
C Haemolytic disease of the newborn D Delayed transfusion reaction
E Non-haemolytic febrile reaction
Explanation
COMPLICATIONS OF BLOOD TRANSFUSION
Immunological
 Allo-immunisationto antigens present on red cells, platelets, leukocytes, plasma. Not a problem with first
transfusion but problems may arise with subsequent transfusions. Delayed consequences include
haemolytic disease of the newborn and rejection of tissue transplants
 Haemolytic transfusion reactions - due to ABO incompatibility. Associated with rigors, loin pain, SOB,
hypotension, haemoglobinuria, renal failure, DIC
 Delayed transfusion reaction - extra-vascular haemolysis presenting with anaemia and jaundice about
1 week after transfusion
 Non-haemolytic febrile reaction - common and due to leukocyte antibodies. Associated with flushing,
fever, tachycardia, rigors.
 Urticaria & anaphylaxis - common and managed by stopping or slowing transfusion with use of anti-
histamines. Severe anaphylaxis is rare
Question 9 Complication of blood transfusion which is caused by leucocyte antibodies

Explanation
Question 10 Which one of the above statements regarding platelets is true?
Concentration typically rises in the third trimester of

A They have a hyper-segmented nucleus B
pregnancy
C Contain both actin and myosin fibrils D Do not produce growth factors
E Are produced by the spleen

Explanation
PLATELETS
 2-4 microns in diameter, produced in bone marrow from megakaryocytes. Do not have a nucleus.
Concentration 150,000 - 350,000/ml. Count falls during pregnancy but remains within normal limits
 Half life 8-12 days, removed from circulation by splenic macrophages
 Adhere to injured endothelial cells / collagen to form platelet plug - important for haemostasis
 Contain actin and myosin important in clot retraction, a process by which the clot shrinks and serum is
extruded - occurs 30-60 minutes after clot formation
 Also produce thromboplastin which hastens blood coagulation
 Produce growth factors such as platelet derived growth factor - also produced by other tissues such as
liver and bone
 Attach to sites of endothelial injury, where sub-endothelial elements, particularly fibrillar collagen via
specific receptor glycoprotein Ia. Von Willebrand's factor is necessary for adhesion
Question 11 The half life of platelets

A 1-2 days B 3-5 days
C 8-12 days D 15-25 days
E 50-65 days
Explanation
Question 12 The normal platelet concentration

A 1,000 – 2,000 per ml B 100,000 – 200,000 per L
C 100,000 – 200,000 per ml D 150,000 – 350,000 per ml
E 150,000 – 300,000 per L
Explanation
Question 13 Which one of the above inhibits platelet aggregation?

A ADP B Thromboxane A2
C Serotonin D Endothelial injury
E Prostacyclin

Explanation
Platelet aggregation stimulated by:
 ADP
 Thromboxane A2
 Serotonin - causes vasoconstriction
Aggregation is inhibited by:
 Prostacyclin
 Cyclo-oxygenase inhibitors like aspirin

Question 14 With respect to blood coagulation
The extrinsic pathway is activated when blood comes into

A B The intrinsic pathway is activated by tissue damage
contact with glass
C Blood can clot in the absence of calcium D Prothrombin is converted to thrombin during coagulation
E Thrombin activates Factor X during coagulation
Explanation
COAGULATION
 Occurs via the INTRINSIC or EXTRINSIC pathways
 The intrinsic pathway is initiated by exposure of blood to negatively charged surfaces such as
collagen in vivo or glass in vitro
 The extrinsic pathway is initiated by tissue thromboplastin which is released after tissue damage
 Both pathways result in the activation of Factor X
 Prothrombin is then converted to thrombin
 Thrombin converts soluble fibrinogen into insoluble fibrin
 Apart from the first two steps of the intrinsic pathway, all steps of the coagulation cascade depend
on the presence of calcium. Blood does not clot in the absence of calcium.
 Citrate and oxalate remove calcium and prevent clotting. Aspirin prevents platelet aggregation but
not clot formation.
Question 15 Prolonged bleeding time is indicative of abnormalities in which clotting function?

Explanation
COAGULATION STUDIES
 PARTIAL THROMBOPLASTIN TIME WITH KAOLIN - PTTK - prolonged with abnormalities in the intrinsic
or common pathways

 THROMBIN TIME - prolonged with fibrinogen deficiency or the presence of inhibitors such as heparin or
fibrin degradation products
Question 16 Prolonged prothrombin time is indicative of abnormalities in which clotting function?

Explanation

Question 17

Explanation
Question 18 Which one of the above statements regarding red blood cells is true?

A The half life of red blood cells is 120 days B Haemoglobin synthesis occurs in reticulocytes
Red blood cells make up 45-55% of total blood volume in
C The normal mean cell volume of red blood cells is 96-126 fl D
females
E Red blood cells have a diameter of ~ 0.7 microns
Explanation
ERYTHROCYTES
 Red blood cells - biconcave discs with diameter of 7 microns and a thickness of 1-2
microns. 4.5-6.5 X 10E12/ L males; 4.0-5.5 X10E12/L females. Make up 40-54% of
blood in males (37-47% females; = haematocrit)
 Mean cell volume 76-96fl; mean cell Hb concentration 30-36g/dl; mean cell Hb = 27-
32pg
 Primitive red cells are produced by the yolk sac. Fetal red cells are produced in the
spleen and lymph nodes and mainly in the liver.

 In late gestation and after birth, red cells are produced only in bone marrow - almost all
bones initially then only in membraneous bones (ribs, sternum, vertebrae and iliac
bones) in adulthood.
 Produced from the pluripotent haemopoietic stem cells - first committed erythrocyte
precursor is the proerythroblast. The cells later form large quantities of Hb; the nucleus
condenses and is extruded and the most of the golgi apparatus and endoplasmic
reticulum are reabsorbed
 Enter the circulation as RETICULOCYTES - contain a small amount of basophilic
material - golgi and some mitochondria and ribosomal RNA - still able to synthesise Hb.
Develop into mature RBC within 1-2 days of release into the circulation
 Life span 120 days
 Production is stimulated by: tissue hypoxia (high altitude), anaemia, erythropoietin
Which one of the above is not associated with an increase in erythrocyte

Question 19
sedimentation rate (ESR)?
A Hypoalbuminaemia B Pregnancy
C Severe anaemia D Sickle cell disease
E Hypercholesterolaemia
Explanation
ESR & CRP

 Low in polycythaemia, sickle cell disease, hypofibrinigenaemia, hepatic necrosis, low molecular
weight dextran infusion, very high serum bile salt concentrations, congestive cardiac failure,
treatment with valproic acid
 Plasma viscosity may be used instead of ESR - not different between males and females, only
increases slightly with age and not affected by Hb concentration. Results available within 15min

A Increases with increasing age B Decreases in pregnancy
C Is decreased in severe anaemia D Is increased in sickle cell disease
E Is increased in polycythaemia

Explanation
Question 21 Plasma

A Has a lower protein content than serum B Has a lower protein content than interstitial fluid
C Contains clotting factors D Does not contain gamma globulins
E Does not contain beta globulins
Explanation
PLASMA
 Blood minus the cellular component. Makes up 58-62% of total blood volume
 Higher protein content than interstitial fluid or serum (does not contain clotting factors)
 Contains albumin, globulins and fibrinogen
 Globulins are divided into alpha and beta globulins which serve a transport function and gamma
globulins which are antibodies
 The osmotic pressure of the plasma proteins (colloid osmotic pressure or oncotic pressure) is
important in preventing leakage of fluid into the interstitial space
Question 22 Serum ferritin concentrations

A Fall if the woman develops an acute inflammatory disease B Are raised in iron deficiency anaemia
Are a better indicator of iron stores than serum iron
C D Fall in the presence of malignancy
concentration
E Are typically low in sickle cell disease
Explanation
ANAEMIA
Iron deficiency
 Caused by blood loss (menorrhagia, PPH. GI bleed), increased demands (growth,
pregnancy), decreased absorption or poor intake. Commonest cause worldwide is
hookworm infestation
 MCV reduced <80fl
 MCH (<27pg) - hypochromia
 Poikliocytosis (variation in shape), anisocytosis (variation in size) and target cells
 Serum iron falls with a rise in serum iron binding capacity. Transferrin saturation falls
<19%
 Serum ferritin reflects iron stores better than serum iron - falls. However, ferritin is an
acute phase protein and concentrations increase in inflammatory or malignant disease

 Differential diagnoses include anaemia of chronic disease, thalassaemia
 Treat underlying cause. Iron replacement results in a rise in Hb by 1g per week. Ferrous
sulphate is best absorbed when the patient is fasting
Question 23 Macrocytic anaemia
A Is always associated with megaloblastosis B Can be caused by vitamin B12 or vitamin C deficiency
C Can be caused by iron deficiency in pregnancy D Is diagnosed if the MCV is < 86fl
In severe cases, is associated with leucopaenia and
E
thrombocytopaenia
Explanation
MACROCYTIC ANAEMIA
 Megaloblastic and non-megaloblastic depending on bone marrow findings
Megaloblastic
 Bone marrow contains erythroblasts with delayed nuclear maturation because of defective DNA
synthesis
 Caused by vitamin B12 deficiency (pernicious anaemia, malabsorption, vegans), folate
deficiency
 Increased MCV > 96fl
 Hypersegmented polymorphs in peripheral blood with 6 or more lobes in the nucleus
 Leukopaenia and thrombocytopaenia may occur in severe cases
 Pernicious anaemia associated with autoimmune diseases including thyroid, Addison's disease
and vitiligo. Increased risk of gastric carcinoma
Question 24 Which one of the above is not associated with raised erythrocyte mean cell volume?

A Normal pregnancy B Chronic alcohol abuse
C Chronic liver disease D Alpha thalassaemia
E Reticulocytosis
Explanation
MACROCYTIC ANAEMIA
Megaloblastic
synthesis
deficiency

Macrocytosis without megaloblastosis
 Pregnancy
 Neonate
 Alcohol abuse
 Liver disease
 Reticulocytosis
 Aplastic anaemia
 Drugs like azathioprine
Question 25 Which one of the above is not a typical feature of haemolytic anaemia?

A Conjugated hyperbilirubinaemia B Reduced plasma haptoglobin concentration
C Increased serum lactate dehydrogenase concentration D Reticulocytosis
E Increased urinary urobilinogen concentration
Explanation
HAEMOLYTIC ANAEMIA
Increased red cell haemolysis associated with
 Hyperbilirubinaemia (unconjugated)
 Increased urinary urobilinogen
 Haemoglobinuria
 Reduced plasma haptoglobin
 Increased serum LDH
 Reticulocytosis
 Erythroid hyperplasia of the bone marrow
Causes
 Inherited - hereditary spherocytosis, sickle cell disease, thalassaemia, glucose-6-phosphate
dehydrogenase deficiency, pyruvate kinase deficiency
 Acquired - autoimmune & alloimmune haemolytic anaemia, transfusion reaction, drug-induced
haemolytic anaemia, prosthetic heart valves, infections (malaria, mycoplasma)
Question 26 Beta thalassaemia
Is associated with precipitation of globin chains within red

A Is not associated with red cell haemolysis B
cells
C Causes macrocytic anaemia D Causes megaloblastic anaemia
E Is typically caused by deletions of the globin gene
Explanation
THALASSAEMIAS
Defective synthesis of one globin chain in adult Hb causing precipitation of globin chains within
red cells and ineffective erythropoiesis and haemolysis

Beta Thalassaemia
 Homozygous - no normal beta chain produced (ß0) or reduced beta chain synthesis (ß+). Excess
alpha chain combines with whatever beta, gamma or delta chain is available or precipitates,
causing haemolysis and ineffective erythropoiesis
 Heterozygous beta-thalassaemia - usually asymptomatic microcytosis with mild anaemia
 Over 200 genetic defects - mainly point mutations
 Beta-thalassaemia minor - heterozygous carrier, low MCV and MCH but normal serum ferritin.
Hb electrophoresis shows raised HbA2 and HbF
 Beta-thalassaemia major - homozygous, severe anaemia from 3-6 months old when switch from
gamma to beta chain occurs.
 Extra-medullary haematopoiesis causes hepato-splenomegaly & bone expansion with typical
facies
 Requires regular blood transfusions and folate supplementation
 Iron overload from repeated transfusion treated with chelating agent desferrioxamine
Question 27 Which one of the above is not a recognized feature of beta thalassaemia major?

A Iron overload B Extra-medullary haematopoiesis
C Hepatomegaly and splenomegaly D Hydrops fetalis
E Low red cell mean cell volume and mean cell haemoglobin
Explanation
Question 28 The results of haemoglobin electrophoresis in a woman with beta thalassaemia minor

A Haemoglobin S B Haemoglobin A2 and Haemglobin F
C Haemoglobin A and haemoglobin S D Haemoglobin Barts and haemoglobin H
E Haemoglobin S and haemoglobin F
Explanation
Beta-thalassaemia minor - heterozygous carrier, low MCV and MCH but normal serum ferritin.
Hb electrophoresis shows raised HbA2 and HbF
Beta-thalassaemia major - homozygous, severe anaemia from 3-6 months old when switch from
gamma to beta chain occurs.
Question 29 Alpha thalassaemia

Is most commonly caused by point mutations of the alpha The individuals with normal haemoglobin have 4 alpha
A B
globin gene chain genes
C Does not cause anaemia until 3-6 months after birth D Causes macrocytic anaemia
E Is associated with an increased concentration of fetal

haemoglobin in adults
Explanation
Alpha Thalassaemia
 If all 4 genes deleted, no alpha chain and only gamma chain is produced in the fetus (gamma-4,
Hb Barts) - causes severe anaemia and fetal hydrops with intra-uterine or early neonatal death
 Three genes deleted - moderate anaemia, not transfusion dependent. Hb A, Hb Barts, Hb H
(gamma-4) are produced. Hb A2 is normal or reduced
Question 30 Sickle cell anaemia

A Is caused by a point mutation on the alpha globin gene B Is inherited as a co-dominant trait
C s typically associated with reduced reticulocyte count D Is a recognized cause of hydrops fetalis
E Is associated with shortened life-span of red blood cells
Explanation
SICKLE CELL SYNDROME

 Single base mutation of adenine to thymine producing a substitution of valine for glutamine at
the sixth codon of the beta-globin chain
 Autosomal recessive trait
 Homozygous (Hb SS) - both genes abnormal, sickle cell disease
 One abnormal gene - sickle cell trait: 25% prevalence in West Africans
 Deoxygenated HbS insoluble - polymerises causing sickling
 Red cell life-span is shortened and there is occlusion of the micro-circulation
 Sickling precipitated by: infection, dehydration, cold, acidosis, hypoxia
 HbS releases oxygen to tissues more readily than Hb A - patients feel well despite anaemia
 Degree of anaemia usually stable. Fall in Hb associated with
1) Aplasia - parvovirus infection
2) Acute sequestration - liver & spleen become engorged
3) Haemolysis - drugs, acute infection or associated Glucose-6-phosphate dehydrogenase
deficiency
 Hb 6-8 g/dl, reticulocyte count 10-20%, sickling of red cells on blood film induced by sodium
metabisulphite, Hb electrophoresis shows no Hb A, 80-95% Hb S and 2-20% Hb F
Beta chain not required for Hb F synthesis therefore disease does not manifest until about 6
months of age



A 50-100 ml B 150-250 ml
C 300-330 ml D 400-600 ml
E 10-50 ml
Explanation

Question 32

E Over 90 minutes
Explanation

Definition:
 Begins with the complete delivery of the fetus and ends with the complete delivery of the
placenta and membranes.
Duration
 The mean duration of the third stage following physiological management has been reported to
be between 12 – 21 minutes. A physiological third stage has duration of less than 60 minutes in
95% of women.
 There is a moderate level of evidence that an actively managed third stage of 30 minutes or
longer is associated with increased incidence of PPH. PPH remains the most common cause of
maternal mortality globally. In addition, PPH is an important contributor to maternal morbidity
including:
Post-natal anaemia

 The third stage of labour is diagnosed as prolonged if not completed within 30 minutes of the
birth of the baby with active management and 60 minutes with physiological management.
Question 33 In normal pregnancy at term

A The capacity of the uterus is about 2000 ml B Blood flow to the uterus is 5-8 L/min
C About 10-15% of cardiac output is directed to the uterus D The uterus weighs about 10kg
E Blood flow to the uterus is 200 – 300 ml/min
Explanation
Preventing blood loss

Pre-pregnancy uterine weight ~ 70 g and cavity capacity of ~10 ml. This increases to a weight ~
1.1 kg and capacity of ~ 5 L at term. Uterine growth occurs through hypertrophy and hyperplasia
under the influence of oestrogen. At term, uterine blood flow is ~ 500-800 mL/min (10-15% of
cardiac output).
Which one of the above mechanisms is important in controlling blood loss

Question 34
from the uterus during the third stage of labour?

A Relaxation of the myometrium B Retraction of the myometrium
C Increased fibrinolysis D Increased oxytocin secretion from the posterior pituitary gland
E Shedding of the decidua
Explanation
 The increase in maternal blood volume during pregnancy provides a reserve for the blood loss
that occurs at delivery. Changes also occur in the coagulation system, with an increase in
clotting factors and a decrease in fibrinolysis.
 Uterine contraction is initially responsible for controlling blood loss during the third stage. Clot
formation and fibrin deposition occur rapidly and are essential in subsequent maintenance of
hemostasis.
 As the placenta separates, the spiral arteries are exposed in the placental bed with the potential
for massive haemorrhage. The spiral arteries run through a latticework of crisscrossing muscle
bundles that occlude and kink-off the vessels as they contract and retract. This arrangement of
muscle bundles has been referred to as the "living ligatures" or "physiologic sutures" of the
uterus.
 Contraction and retraction of the myometrium is therefore central to the control of blood loss
during the third stage. Uterine atony is the most important cause of post-partum haemorrhage

Question 35 The bi-parietal diameter is at or below the level of the pelvic inlet

A Presentation B Engagement
C Position D Station
E Attitude
Explanation
Fetal Lie
Presentation
 A distinction should be made between ‘cephalic’ and ‘vertex’ presentation, although these
descriptions are used interchangeably
 Cephalic presentation means the fetal head is lowest in the maternal abdomen or pelvis.
However, the precise presentation may be face, brow or vertex
 Vertex presentation is a more precise description indicating that the fetal neck is flexed with the
top of the fetal head (vertex) lying lowest in the abdomen or pelvis. A diagnosis of vertex
presentation can only be made with confidence on vaginal examination when the cervix is
dilated
 In a vertex presentation, the denominator is the occiput. In a face or brow presentation, the
denominator is the mentum (chin). In a breech presentation, the denominator is the sacrum
Position
Engagement
 This occurs when the biparietal diameter is at or below the inlet of the true pelvis. Clinically, this
occurs when 2/5th or less of the fetal head can be palpated per abdomen.
 Engagement is an all-or-none phenomenon. The presenting part is either engaged or it is not.
The common description of ‘1/5th engaged’ is inaccurate
Station
 This relationship between the leading point of the presenting part to the level of the ischial
spines measured in plus or minus centimeters (or cm above / below the ischial spines)
 When the presenting part is above the ischial spines then the distance is negative (spines minus
2cm or 2cm above the spines)
 When the presenting part is below the ischial spines then the distance is positive (spines plus
2cm or 2cm below the ischial spines)

The anterior fontanelle is bound anteriorly by the two halves of
A The anterior fontanelle is bound posteriorly by the occipital bone B
the frontal bone
The posterior fontanelle is never overlapped by bone during
C The posterior fontanelle is bound anteriorly by the temporal bone D
moulding

Explanation
THE FETAL SKULL

 The frontal bone is in two halves separated by the frontal suture. The frontal bone is separated
from the parietal bones by the coronal suture
 In utero, the bones of the skull are not closely knit at the sutures like they are in the adult skull.
The fetal / neonatal skull bones are separated by six un-ossified membraneous intervals called
fontanelles

 Diamond shaped
Question 37 Presenting diameter in a brow presentation

Explanation

 9.5cm
 From below the occipital protuberance (sub-occiput) to the centre of the anterior fontanelle
(bregma)
Suboccipito-frontal
 10 cm +
 With greater degrees of de-flexion, the anterior limit of this diameter extends further into the
frontal bone, presenting a wider diameter to the maternal pelvis
Occipito-frontal

 11.5 cm
 This diameter is different from the diameter that presents in the occipito-anterior position
because of the tendency of the head to be de-flexed in the occipito-posterior position
Submento-bregmatic
 9.5 cm
Submento-vertical
 11.5 cm
 From the junction of the chin and neck to the centre of the vertex (point on the sagittal suture
midway between anterior and posterior fontanelles)
Mento-vertical
 13.5 cm
 The mento-vertical diameter is longer than any diameter of the pelvis so a bow presentation
cannot be delivered vaginally

A 9.5 cm B 10.5 cm
C 11.5 cm D 12.5 cm
E 13.5 cm
Explanation
Question 39 Umbilical venous blood

A Has an oxygen saturation of ~ 98% B Has a higher oxygen saturation than umbilical arterial blood
C Has a pH of ~ 7.47 D Has a PO2 which is higher than maternal arterial PO2
E Has a PCO2 of ~ 30 mmHg
Explanation
Oxygenation of fetal blood

 PO2 falls in umbilical arterial and venous blood as gestation age increases during the second half of
pregnancy
 Fetal haemoglobin concentration, red cell count, haematocrit however increases with increasing
gestation age
 As a result, the oxygen carrying capacity of fetal blood increases with gestation age
 Fetal red cell MCV and haemoglobin content decreases with gestation age

 During the last week of pregnancy, the % of adult haemoglobin increases to 20% at term. Fetal Hb - two
alpha and two gamma chains - more resistant to both acid and alkali elution than the maternal cells and
this forms the basis of the Kleihauer test
 Fetal Hb has a higher affinity for oxygen and its dissociation curve is shifted to the left of the adult curve -
this is a result of lower affinity for 2,3-bisphosphoglycerate (2,3-BPG). 2,3-BPG concentration increases
with increasing gestation age
 Oxygenated umbilical venous blood has an oxygen saturation of ~80%. pH = 7.34 (maternal arterial pH =
7.42), PCO2 = 45mmHg (maternal = 32mmHg) and PO2 = 30mmHg
 Anaemia, hypoxia and acidosis result in increased 2,3-diphosphoglycerate concentration which shifts the
oxygen dissociation curve to the right increasing oxygen release in tissues
 Fetal red cell has a mean life-span of 80 days (120 days for adult red cell)
 Hb concentration at term ~17g/dl, falling to 11-12g/dl by 12 months

Is dependent on maternal erythropoietin which crosses the
placenta
E Is dependent on erythropoietin produced by the fetal kidneys
Explanation
gestation

The risk of peptic ulceration is increased especially during the
third trimester

Explanation
GI TRACT

Question 42
to pre-pregnancy

E 50% decrease
Explanation
RENAL SYSTEM
abdominal organ
increase in GFR
which is plasma
increased
pregnancy

Question 43 Change in serum urea concentration at 24 weeks gestation compared to pre-pregnancy

E 50% decrease
Explanation
With respect to changes in renal function during pregnancy, which one of

Question 44
the above statements is not true?

There is increased salt and water re-absorption from the renal
A B There is a reduction in serum aldosterone concentration
tubules
C Vascular sensitivity to the effects of angiotensin is reduced D There is an increase in serum renin concentration
E Renal clearance of uric acid is increased during the first trimester
Explanation
Question 45 With respect to blood transfusion

A Most red cells are transfused in the form of whole blood B Blood for transfusion is usually stored at 0 C
C Blood for transfusion has a shelf life of 48-72h from donation D Packed red cells for transfusion have a haematocrit of ~ 35%
E The volume of one unit of blood is 330 ml
Explanation
RANSFUSION OF BLOOD & BLOD PRODUCTS

haematocrit = 57%

Question 46 Which one of the above statements regarding iron metabolism is correct?

In healthy females, ~ 50-60% of ingested iron is absorbed from
A B The majority of iron in the body is contained in ferritin
the gut
C Iron is transported in plasma by ferritin D The average daily iron loss in women of reproductive age is 2mg
E Daily iron intake is ~ 1-2g
Explanation
IRON METABOLISM
 Body contains ~4.5g iron - 65% in Hb, 5% in myoglobin. Small amount in cytochrome-dependent
enzymes
 Transported in plasma as transferring and stored in tissues (liver mainly) as ferritin. Haemosiderin is a
very insoluble iron store only formed in iron overload
 Average daily iron loss is 1mg (males) and 2mg (females of reproductive age)
 Children and pregnant women require more iron
 Daily iron intake 15-20mg of which 0.5-2mg is absorbed (~10% of intake)
Absorption
 Iron absorption inhibited by phytates, phosphate, bicarbonate and tannins which form insoluble
complexes
 Iron absorption promoted by vitamin C and HCl. HCl solubilises iron while ascorbate reduces iron (3+) to
iron (2+) which is less likely to form insoluble complexes
 Heme iron better absorbed than non-heme iron
 Ferrous iron (2+) better absorbed than ferric iron (3+)
 Following absorption, ferrous iron (2+) is converted to ferric iron (3+) and bound to ferritin within intestinal
epithelial cells or transported into the plasma where it is bound to transferring - a beta-globulin
synthesised by the liver - transferin saturation ~33%
 Each transferring molecule binds two atoms of ferric iron
 Transferrin-bound iron becomes attached to specific receptors on erythroblasts and reticulocytes and the
iron is removed
 Iron stored as ferritin in gut epithelial cells is lost as the cells are shed
 Haemosiderin is an insoluble iron-protein complex in macrophages, hepatocytes and spleen
 Mostly absorbed in the duodenum and jejunum by carrier mediated transport
 Iron deficiency results in increased GI uptake - mechanism effective within 3-4 days
 Serum iron concentration 11-30 microM - levels higher in the morning
 The body cannot get rid of excess iron and absorption has to be matched to requirements. Excessive iron
may be removed by chealating agents such as desferrioxamine
Question 47 Beta thalassaemia

A Is not associated with red cell haemolysis B Is associated with precipitation of globin chains within red cells
C Causes macrocytic anaemia D Causes megaloblastic anaemia
E Is typically caused by deletions of the globin gene

Explanation
THALASSAEMIAS
Defective synthesis of one globin chain in adult Hb causing precipitation of globin chains within red cells
and ineffective erythropoiesis and haemolysis
Beta Thalassaemia
 Homozygous - no normal beta chain produced (ß0) or reduced beta chain synthesis (ß+). Excess alpha
chain combines with whatever beta, gamma or delta chain is available or precipitates, causing
haemolysis and ineffective erythropoiesis
 Heterozygous beta-thalassaemia - usually asymptomatic microcytosis with mild anaemia
 Over 200 genetic defects - mainly point mutations
 Beta-thalassaemia minor - heterozygous carrier, low MCV and MCH but normal serum ferritin. Hb
electrophoresis shows raised HbA2 and HbF
 Beta-thalassaemia major - homozygous, severe anaemia from 3-6 months old when switch from gamma
to beta chain occurs.
 Extra-medullary haematopoiesis causes hepato-splenomegaly & bone expansion with typical facies
 Requires regular blood transfusions and folate supplementation
 Iron overload from repeated transfusion treated with chelating agent desferrioxamine

Individuals with one alpha globin gene deleted have moderate Individuals with two alpha globin genes deleted have alpha
A B
anaemia thalassaemia trait
Individuals with two alpha globin genes deleted have severe Individuals with one alpha globin gene deleted typically have a
C D
anaemia microcytic blood picture
Individuals with two alpha globin genes deleted have an increased
E
concentration of fetal haemoglobin
Explanation
Alpha Thalassaemia
Question 49 With respect to the electrolyte concentration of urine and plasma

A Normal plasma osmolarity is 300-315 mOsmol/kg B Urine osmolarity is typically higher than plasma osmolarity
Urine bicarbonate concentration is typically higher than plasma Urine creainine concentration is typically higher than plasma
C D
bicarbonate concentration creatinine concentration
Urine glucose concentration in non-pregnant women is 0.2-1.0
E
mM

Explanation
RENAL FUNCTION
Solute??? Plasma Urine

Na+??? 135-150mM *??? 50-130mM???
K+???
3.5 - 5.5mM??? 20-70mM???
Ca2+??? 1.35-1.50mM??? 10-24mM???
HCO3-??? 22-28mM??? 0???
Cl-??? 100-110mM??? 50-130mM???
Creatinine??? 0.06-0.12mM??? 6-20mM???
Urea??? 4-7mM??? 200-400mM???
NH4+??? 0.005-0.02mM??? 30-50mM???
Protein??? 65-80 g/L??? 0???
Uric acid??? 0.1-0.4mM??? 0.7-8.7mM???
Glucose ??? 3.5-5.5mM??? 0???
pH??? 7.36 - 7.46 *??? 4.8 - 7.5???
Phosphate??? 0.8-1.25mM??? 25-60mM???
Osmolality??? 281-297 mOsmol/kg *??? 50-1300 mOsmol/kg
Question 50 The phosphate buffer system

A Is not effective in the extracellular space B Is not effective in the intracellular space
C Is less effective in renal tubular fluid than in the extracellular fluidD Is more effective in intracellular fluid than in extracellular fluid
E Is only effective if pH is below 6.8
Explanation

• Has a pK of 6.8
• Low concentration of buffers in extracellular fluid therefore less important than bicarbonate buffer
• Higher concentration in renal tubular fluid. In addition, pH of tubular fluid is closer to pK of phosphate
buffer system - therefore more important buffer

.

Question 51 Which one is recognized to cause an increase in renal tubular hydrogen ion secretion?

A A rise in plasma pH B A rise in PCO2
C A rise in plasma [HCO3-] D Hyperkalaemia
E Hypertension
Explanation
RENAL TUBULAR HYDROGEN ION SECRETION

??increased by:
• Decreased plasma pH - fall in bicarbonate, a rise in hydrogen ion concentration or a rise in PCO2 -
creates a favourable cell - to -tubular fluid hydrogen ion gradient and promotes secretion through the
entire nephron *
• Hydrogen ion secretion in the proximal tubule and thick ascending limb of the loop of Henle is linked
to sodium resorption - factors which increase sodium resorption will increase hydrogen ion secretion *
• Angiotensin II and andosterone stimulate hydrogen ion secretion *
• Hypokalaemia stimulates and hyperkalaemia inhibits hydrogen ion secretion by the proximal tubule *
Question 52 Plasma renin concentrations

A Fall during the first trimester B Fall from 20 weeks gestation
C Are unchanged throughout pregnancy D Increase in the first half of pregnancy
E Fall from 32 weeks gestation
Explanation
RENIN
· Proteolytic* enzyme secreted by the kidneys (juxta-glomerular apparatus in the afferent arteriol) in
response to a fall in sodium concentration in the distal tubule
· Pro-renin is present in ovarian follicular fluid and its concentration (BUT NOT that of active rennin)
increases in plasma transiently by up to 2 fold during the LH surge and in response to HCG to induce
ovulation. After conception, it increases about 8 to 10-fold in parallel with plasma HCG.
· Plasma concentration of active renin increases slightly early in the first trimester to reach a plateau
(five-fold basal value) at the 20th week of gestation which is then maintained throughout pregnancy*.
· Renin secretion is increased by factors which reduce extracellular fluid volume or pressure or
reduce sodium concentration in the renal filtrate*
Question 53 The normal anion gap is

A 1-2 mM B 3-5 mM
C 4-10 mM D 10-18 mM
E 20-32 mM

Explanation

· Normal anion gap acidosis - hyperchloraemic acidosis - occurs when bicarbonate is lost by the gut
or kidneys, or rarely when hydrogen ions are ingested as ammonium chloride. Chloride ions are retained
as bicarbonate is lost
Question 54 Vitamin D intoxication is typically associated with

A Metabolic alkalosis with normal anion gap B Metabolic alkalosis with high anion gap
C Metabolic acidosis with normal anion gap D Metabolic acidosis with high anion gap
E Metabolic acidosis with low anion gap
Explanation

Occurs in: *****
Question 55 With respect to the regulation of acid-base balance by the kidneys

The majority of filtered bicarbonate is reabsorbed in the proximal
A Bicarbonate ions are secreted into the proximal tubule B
tubule
Carbonic anhydrase plays a key role in the reabsorption of Hydrogen ions are absorbed from the tubular lumen coupled to
C D
bicarbonate ions sodium secretion
Hydrogen ions are secreted into the tubular lumen coupled to
E
potassium absorption
Explanation
RENAL ACID-BASE REGULATION *****

· Bicarbonate: 90% of filtered bicarbonate is reabsorbed in the proximal tubule. Depending on acid-
base status, the rest of the bicarbonate may be reabsorbed distally *
· Hydrogen ions secreted into the lumen combine with filtered bicarbonate to form H2CO3 which
dissociates into CO2 and water catalysed by carbonic anhydase in the tubular cell brush border. CO2
diffuses into the cells and the reaction is reversed, generating hydrogen ions and bicarbonate *
· Hydrogen ions are secreted into the tubules coupled to sodium ion reabsorption *

Question 56 Osmoreceptors responsible for the regulation of water balance are located in

A The hypothalamus B The medulla oblongata
C The carotid sinus D The right atrium
E The left atrium
Explanation
REGULATION OF BODY WATER *****
• ? Water balance is monitored by the osmoreceptors in the hypothalamus which regulate ADH
secretion by the posterior pituitary and water reabsorption in the collecting ducts and tubules of the
kidneys *
• ? When osmolarity of body fluid rises by over 4 mOsmol/kg, desire to drink is stimulated and
ADH secretion is increased with a reduction in urine volume *

A Aldosterone stimulates potassium retention by the kidneys B Acidosis increases potassium secretion into the renal tubules
C Alkalosis increases potassium secretion into the renal tubules D Insulin inhibits potassium uptake into cells
E Cell death results in increased uptake of potassium into the cell
Explanation

or death.*

interchangeable) *
Question 58 Which one is not a recognized cause of hypocalcaemia?

A Chronic renal failure B Hypoalbuminaemia
C Massive transfusion with citrated blood D Hypoparathyroidism
E Chronic lithium therapy
Explanation
HYPOCALCAEMIA ******
May be caused by
• Increased phosphate levels - chronic renal failure

• Hypoparathyroidism
• Vitamin D deficiency

• Drugs such as bisphosphonates, calcitonin
• Acute pancreatitis, citrated blood in massive blood transfusion
• Malabsorption
• Low plasma albumin
Chronic lithium therapy associated with hypercalcaemia

Physiology of labour & Fetal assessment

Question 1 The orientation of the long axis of the fetus to the long axis of the mother
A Lie B Presentation
C Engagement D Position
E Station
Explanation
Fetal Lie
Presentation
dilated
Position
Engagement
E Attitude
Explanation

Fetal Lie
Presentation
dilated
Position
Engagement
Station
Question 3 The fetal attitude

Can be
Refers to the orientation of the fetal back
A B flexed or
to the maternal abdomen
extended
Can be
Has no effect on the diameter that
C D longitudinal
presents to the maternal pelvis
or oblique
E Can be anterior or posterior
Explanation

Fetal Attitude
 This refers to the posturing of the joints and relation of fetal parts to one another.
 The normal fetal attitude during labour is with all joints flexed.
 Of particular importance is the attitude of the fetal neck. Flexion of the neck results in the
smallest diameter of the fetal head presenting to the maternal pelvis.
 In a well flexed occipito-anterior position, the suboccipito-bregmatic diameter presents to the
maternal pelvis. This is ~9.5cm wide.
Which one of the above statements regarding the mechanism of labour is not
Question 4
true?
The head typically enters the pelvis with

The occipito-frontal diameter is wider the occipito-frontal diameter aligned to
A B
than the bi-parietal diameter the transverse diameter of the pelvic
inlet
When the fetal head is fully flexed and in
The head is engaged when the bi-
the occipito-anterior position, the
C D parietal diameter is at the level of the
presenting diameter is the suboccipito-
ischial spines
bregmatic diameter
When the head is fully flexed and in the
occipito-anterior position, the diameter
E
that presents to the maternal pelvis is
9.5 cm wide
Explanation
Flexion and Engagement
 During the first pregnancy, the head is usually engaged around 37 weeks gestation. In
multiparous women, the head may not become engaged until labour is established
 Engagement and flexion are brought about by the combined effect of pre-labour and labour
uterine contractions, the limitations of the pelvic inlet and the tone of the pelvic floor. When the
head begins to enter the pelvis, the degree of flexion is only partial. The occipito-frontal
diameter is wider than the bi-parietal diameter. The occipito-frontal diameter is therefore aligned
to the wider diameter of the pelvic inlet – the transverse diameter.
 The head enters the pelvis in an occipito-transverse position in the majority of women
 The head is engaged when the biparietal diameter enters the pelvis to a level below the plane of
the pelvic inlet. On vaginal examination, the head is at 0 station, or at the level of the ischial
spines. Uterine contractions push the head against the soft tissue of the pelvis and the pelvic
floor to encourage further flexion. The fetal chin is brought into contact with the thorax, and the
presenting diameter changes from occipitofrontal (11.0 cm) to suboccipito-bregmatic (9.5 cm).
Descent
 Progressive descent occurs during the last few weeks of pregnancy in primigravidae. During
labour, descent is intermittent with contractions. The rate is greatest during the second stage of
labor.

Question 5 With respect to the mechanism of normal labour
The head is usually engaged by 37 In multiparous women, the head is

A B
weeks gestation in primigravidae usually engaged by 36 weeks gestation
The head typically gets through the
The occipito-frontal diameter is narrower
C pelvic inlet in the occipito-anterior D
than the bi-parietal diameter
position
A flexed attitude results in a wider
E diameter of the head presenting to the
pelvis compared to an extended attitude
Explanation
Internal rotation typically results in the

Internal rotation occurs at the level of the suboccipito-bregmatic diameter being
A B
anterior superior iliac spines aligned to the transverse diameter of the
pelvic outlet
Internal rotation results in the fetal head
During internal rotation, the fetal head
C D moving from the occipito-transverse to
typically rotates by 180 degrees
the occipito-anterior position
Internal rotation typically occurs before
E
the head is engaged
Explanation
Internal rotation
 Occurs at the level of the ischial spines as a result of the combined effect of uterine contractions
and the tone & shape of the pelvic floor. Typically, the head rotates 45° from the occipito-
transverse to the occipito-anterior position. This brings the suboccipito-bregmatic diameter in
line with the wider diameter of the pelvic outlet – the antero-posterior diameter
Extension
 Following internal rotation and further descent, the base of the occiput is located at the inferior
margin of the symphysis pubis. The tone of the pelvic floor and the downward forces from
uterine contractions cause the neck to extend and the head is delivered beneath the symphysis
pubis.
 When the fetal head is free of resistance, it untwists 45° left or right, returning to its original
position in relation to the body. This is restitution.

 The fetal shoulders enter the pelvis with the bis-acromial diameter aligned to the transverse
diameter of the pelvic inlet. When the shoulders reach the pelvic floor, ‘internal rotation’ also
occurs to align the bis-acromial diameter with the antero-posterior diameter of the pelvic outlet.
This process is reflected in further movement of the head and constitutes external rotation
Expulsion
 The anterior shoulder is then delivered under the symphysis pubis followed by the posterior
shoulder
Movement of the fetal head from the occipito‐transverse to the occipito‐
Question 7
anterior position at the level of the ischial spines

Movement of the bis‐acromial diameter from the transverse to the
Question 8
antero‐posterior diameter of the maternal pelvis

E Asynclitism
Explanation
Question 9 Which one of the above statements regarding the mechanism of labour is not true?
The fetal shoulders enter the pelvis with

External rotation is a reflection of the
the bis-acromial diameter aligned to the B
A rotation of the fetal shoulders
transverse diameter of the pelvic inlet
Following external rotation, the bis-

The posterior shoulder is typically
C D acromial diameter is aligned to the antero-
delivered before the anterior shoulder
posterior diameter of he pelvic outlet
E Extension occurs after internal rotation
Explanation

Just before extension begins, the base
A Extension occurs before internal rotation B of the occiput is located at the inferior
margin of the simphysis pubis
Restitution is a reversal of the process Restitution is typically associated with
C D
that occurred during external rotation rotation through 90 degrees
Extension typically occurs before the
E
head is engaged
Explanation
Lateral or antero-posterior displacement of the fetal head can result in the
Question 12
saggital suture lying anterior, posterior or lateral to the median plane

E Asynclitism
Explanation
Question 13 With respect to myometrial function during normal labour
The uterus has two layers of smooth The uterus has specialised pace-maker
A muscle, an outer circular and an inner B fibres located around the the utero-tubal
longitudinal layer junction
The strength of uterine contractions is
Uterine contraction results in reduced
C D higher in the first stage of labour
blood flow to the placental bed
compared to the second stage
Braxton-Hicks contractions do not occur
E
before 30 weeks gestation
Explanation

Myometrial Contractions
 The musculature of the pregnant uterus is arranged in three layers:
 An external hood-like layer which arches over the fundus
 An internal layer consisting of sphincter-like fibers around the orifices of the tubes and the
internal os.
 An intermediate layer consisting of a dense network of muscle fibers perforated in all directions
by blood vessels. This forms the bulk of the myometrium. When the muscle cells contract, they
constrict the blood vessels and reduce blood flow to the placental bed. After delivery,
contraction of this layer plays a central role as ‘living ligatures’ to prevent post-partum
haemorrhage
 Uterine contractions are involuntary and driven by pacemakers to produce the rhythmic
coordinated contractions of labour. The pacemaker sites are located at the utero-tubal junctions
but are not structurally different from the rest of the myometrium
 Uterine contractions (Braxton-Hicks contractions) occur throughout normal pregnancy and
become stronger and more frequent with advancing gestation.
 These contractions play a key role in engagement of the presenting part and cervical
effacement. They may also cause cervical dilatation
 During normal labour, there is a progressive increase in the strength of contractions form
approximately 20 mmHg at the onset of labour to 50 to 80 mmHg late in the second stage. The
interval between contractions reduces from ~ every ten minutes in early labour to every two
minutes in the second stage
Which one of the above statements regarding cervical changes in pregnancy

Question 14
is not true?
In primigravidae, cervical effacement In multiparous women, cervical

A typically occurs before the onset of B effacement and cervical dilatation can
cervical dilatation occur simultaneously
Cervical effacement is associated with
Cervical effacement is associated with a
C an increase in hyaluronic acid content of D
decrease in water content of the cervix
the cervix
Cervical effacement is associated with
E increased activity of proteolytic enzymes
in the cervix
Explanation
Cervical changes
 The normal pregnant cervix is 3 – 3.5 cm long and is composed mainly of type 1 and type 3
collagen, glycosaminoglycans and proteoglycans with only 10-15% being smooth muscle
 The cervix remains largely unchanged during most of pregnancy. In the late third trimester,
cervical ripening begins. This is followed by cervical effacement and dilatation which occur
during labour.
Cervical ripening
 Softening of the cervix that usually begins before the onset of labour and is a prerequisite for
cervical dilation

 Caused by biochemical changes with rearrangement and realignment of the collagen molecules
and reduced bridging of collagen fibres. The activity of proteolytic enzymes contribute to these
changes
 There is an increase in hyaluronic acid and water content while the amount of dermatan
sulphate and chondroitin sulphate decreases
Cervical effacement
 This is shortening and thinning of the cervix in response to uterine contractions
 In primigravidae, cervical effacement occurs before dilatation. In multiparous women, dilatation
and effacement may occur simultaneously
Cervical dilatation
 This occurs passively under the influence of uterine contractions and pressure from the
presenting part. The cervix is stretched and pulled over the presenting part. The elastin
component of the cervix behaves in a ratchet-like manner to maintain dilatation between
contractions
Question 15 With respect to cervical changes during normal pregnancy and labour
The cervix typically becomes shorter and

A The normal cervix is 1.5-2.0 cm long B
softer during the second trimester
Cervical ripening begins after the onset Cervical effacement refers to shortening
C D
of labour in primigravidae and thinning of the cervix
Cervical dilatation typically occurs before
E
cervical effacement in primigravidae
Explanation
Which one of the above statements regarding the vertex of the fetal skull is
Question 16
not true?
Is bound anteriorly by the anterior Is bound posteriorly by the posterior

A B
fontanelle fontanelle
Is bound posteriorly by the lambdoid
C D Is bound laterally by the saggital suture
suture
E Is bound anteriorly by the coronal suture
Explanation
Regions of the skull
The vertex is the area of the vault bounded
 anteriorly by the anterior fontanelle and the coronal suture
 posteriorly by the posterior fontanelle and lambdoidal suture

 laterally by the parietal eminencies
The brow is the area from the tip of the nose and supra-orbital ridges to the anterior fontanelle
and coronal suture
The face is the area from the tip of the nose and supra-orbital ridges extending laterally to the
angles of the mandible and then to the mentum (chin)
During normal labour, the median plane of the fetal head (saggital suture) should lie on the
median plane of the maternal pelvis (either antero-posterior or transverse plane)
Lateral or antero-posterior displacement of the fetal head can result in the saggital suture lying
anterior, posterior or lateral to the median plane. This is ‘Asynclitism’ and occurs more
commonly with an occipito-posterior or occipito-transverse position
In Anterior asynclitism, the head is in the occipito-transverse position. The saggital suture is
displaced towards the sacrum and the anterior parietal bone presents on vaginal examination
(Naegele’s obliquity)
In posterior asynclitism, the head is in the occipito-transverse position. The saggital suture is
displaced towards the simphysis pubis and the posterior parietal bone presents on vaginal
examination (Litzman’s obliquity).
Asynclitism results in a wider diameter being presented to the maternal pelvis and may
contribute to slow progress in labour
Which one of the above statements regarding the mechanism of labour is not
Question 17
true?
The degree of flexion of the fetal head is

In the occipito-posterior position, the
more complete in the occipito-anterior
A occipito-frontal diameter presents to the B
position than in the occipito-posterior
maternal pelvis
position
The submento-bregmatic diameter is the
The submento-bregmatic diameter is
C D presenting diameter in a fully extended
9.5cm wide
face presentation
The suboccipito-bregmatic diameter is
E
12 cm wide
Explanation
 9.5cm
(bregma)
Suboccipito-frontal
 10 cm +
Occipito-frontal
 11.5 cm

Submento-bregmatic
 9.5 cm
Submento-vertical
 11.5 cm
Mento-vertical
 13.5 cm

The mento-vertical diameter is the
The mento-vertical diameter is 11.5cm
A B presenting diameter in a brow
wide
presentation
When the mento-vertical diameter is the
C presenting diameter, the fetus cannot be D
9.5cm wide
delivered vaginally
When the fetal head is de-flexed, a wider
E
diameter presents to the maternal pelvis
Explanation
Question 19 With respect to the mechanism of labour

In a fully flexed occipito-anterior position, In a well-flexed occipito-anterior position,
A the bi-parietal diameter is the presenting B the fetal diameter that presents to the
diameter maternal pelvis is 9.5cm wide
The suboccipito-frontal diameter is The occipito-frontal diameter is 13.5cm
C D
9.5cm wide wide
Because of the wide diameter, a face
E
presentation cannot deliver vaginally

Explanation
 Same as of Question 17

Question 20 Presenting diameter in a fully extended face presentation

Question 21 Presenting diameter in the occipito-posterior position

A Bi-parietal diameter B Suboccipito-bregmatic diameter
C Bis-acromial diameter D Occipito-frontal diameter
E Submento-bregmatic diameter
Explanation
Question 22 Presenting diameter in a fully flexed occipito-anterior position

Explanation
Question 23 Bi-parietal diameter

A 9.5 cm B 10 cm
C 10.5 cm D 11.5 cm
E 13.5 cm
Explanation


Question 24 Suboccipito-bregmatic diameter

Question 25 Submento-bregmatic diameter
Question 26 Mento-vertical diameter

A 9.5 cm B 10 cm
C 10.5 cm D 11.5 cm
E 13.5 cm
Explanation
Question 27 The presenting diameter in the occipito-posterior position

Question 28 The presenting diameter in a brow presentation

A 9.5 cm B 10.5 cm
C 11.5 cm D 12.5 cm
E 13.5 cm
Explanation

Question 30 The presenting diameter in a fully extended face presentation

A 9.5 cm B 10.5 cm
C 11.5 cm D 12.5 cm

E 13.5 cm
Explanation

Question 31
active management

E Over 90 minutes
Explanation

Definition:
Duration
95% of women.
including:
Post-natal anaemia
Physiological management of the third stage of labour includes which one

Question 32
of the above?

Nipple stimulation to induce uterine
A B Delivery of the placenta by maternal effort
contraction

No clamping of the cord until at least after
C D Routine use of uterotonic drugs
30 seconds
Explanation
Physiological management of the third stage involves a package of care which includes all of
these three components:
Early suckling or nipple stimulation can increase uterine contractility. There is no evidence that
early suckling reduces the risk of PPH or other complications of the third stage.

A The capacity of the uterus is about 2000 ml B Blood flow to the uterus is 5-8 L/min
About 10-15% of cardiac output is directed to

C D The uterus weighs about 10kg
the uterus
E Blood flow to the uterus is 200 – 300 ml/min
Explanation
cardiac output).

The anterior fontanelle is bound
The anterior fontanelle is bound
A B anteriorly by the two halves of the frontal
posteriorly by the occipital bone
bone
The posterior fontanelle is bound The posterior fontanelle is never
C D
anteriorly by the temporal bone overlapped by bone during moulding

Explanation
THE FETAL SKULL
 The frontal bone is in two halves separated by the frontal suture. The frontal bone is separated
from the parietal bones by the coronal suture
 In utero, the bones of the skull are not closely knit at the sutures like they are in the adult skull.
The fetal / neonatal skull bones are separated by six un-ossified membraneous intervals called
fontanelles

 Diamond shaped
Question 35 Presenting diameter in a brow presentation

Explanation

 9.5cm
(bregma)
Suboccipito-frontal

 10 cm +
Occipito-frontal
 11.5 cm
Submento-bregmatic
 9.5 cm
Submento-vertical
 11.5 cm
Mento-vertical
 13.5 cm

Has a higher oxygen saturation than
A Has an oxygen saturation of ~ 98% B
umbilical arterial blood
Has a PO2 which is higher than maternal
C Has a pH of ~ 7.47 D
arterial PO2
Explanation
 PO2 falls in umbilical arterial and venous blood as gestation age increases during the second
half of pregnancy
 Fetal haemoglobin concentration, red cell count, haematocrit however increases with

 During the last week of pregnancy, the % of adult haemoglobin increases to 20% at term. Fetal
Hb - two alpha and two gamma chains - more resistant to both acid and alkali elution than the
maternal cells and this forms the basis of the Kleihauer test
 Fetal Hb has a higher affinity for oxygen and its dissociation curve is shifted to the left of the
adult curve - this is a result of lower affinity for 2,3-bisphosphoglycerate (2,3-BPG). 2,3-BPG
concentration increases with increasing gestation age
 Oxygenated umbilical venous blood has an oxygen saturation of ~80%. pH = 7.34 (maternal
arterial pH = 7.42), PCO2 = 45mmHg (maternal = 32mmHg) and PO2 = 30mmHg
 Anaemia, hypoxia and acidosis result in increased 2,3-diphosphoglycerate concentration which
shifts the oxygen dissociation curve to the right increasing oxygen release in tissues
Question 37 With respect to the fetal circulation, which one of the above statements is not true?

Over 90% of the out-put from the right side
Pressure in the left atrium is lower than that
A B of the heart goes directly into the systemic
in the right atrium
circulation
Low systemic PO2 plays an important role in Prostaglandins play an important role in
C D
keeping the ductus arteriosus open keeping the ductus arteriosus open
Low systemic PO2 plays a key role in
E
keeping the foramen ovale open
Explanation
Fetal circulation
Fetal circulation is characterised by
 A patent ductus arteriosus connects the pulmonary artery to the aorta and the foramen ovale
connects the right and left atria
 The ductus arteriosus is kept open by low fetal systemic Pao2 (about 25 mm Hg) and the effect
of local prostaglandins
 The foramen ovale is kept open by pressure gradients. The left atrial pressure is low because of
low venous return from the lungs while right atrial pressure is higher due to higher venous return
from the placenta.
 90 to 95% of the right heart output bypasses the lungs and goes directly to the systemic
circulation

The peak expiratory flow rate (PEFR) is
A The FEV1 is increased B
decreased

Explanation
Minute volume - tidal volume X respiratory rate - increased by 50% in early pregnancy. Tidal
volume increases with little increase in respiratory rate
Residual volume - volume of air left in the lungs after the most forceful expiration decreased by
20% as does functional residual capacity and expiratory reserve volume
Respiratory quotient - ration of oxygen consumption to carbon dioxide production - increased
from 0.76 to 0.83
There is a fall in arterial PCO2 with little change in PO2. The fall in PCO2 is matched by a fall in plasma bicarbonate (renal
compensation - compensated respiratory alkalosis) with no resultant change in pH. pH= 7.44, pCO2=30, bicarbonate=20-25

The majority of the change in cardiac output
A Cardiac output increases by ~ 40% B
occurs during the third trimester
Cardiac output is increased by breast- Heart rate increases by 40% during the first
C D
feeding trimester
E
There is a fall in cardiac output to pre-
pregnancy levels after 40 weeks gestation
Explanation
CARDIOVASCULAR CHANGES IN PREGNANCY

CARDIAC OUTPUT - 40% increase by 12 weeks gestation from 4.5- 6L/min.
Current data do not favour a fall in cardiac output at term
Cardiac output falls rapidly after delivery and is not increased by breast-feeding. Both heart rate
(10% increases) and stroke volume are increased with increased myocardial contractility.
Peripharal resistance - falls, secondary to factors such as oestrogen and nitric oxide.
Blood pressure falls to a nadir at ~24 weeks gestation then rises to pre-pregnancy values at
term.
There is a small increase in pulse pressure
Sphygmomanometry tends to overestimate BP in pregnancy by 7-12mmHg compared to direct
measurement.
No change in pulmonary capillary pressure. Pulmonary vascular resistance falls by ~35%
Heart position - elevated by diaphragm.
Apex beat moves to fourth left inter-costal space
ECG - deviation of electrical axis to the left by 15 degrees; other changes including S-T
segment depression and flattening or depression of T waves in III

Oxygenation - decreased Hb concentration but increased total oxygen carrying capacity of
blood (increased total Hb)
Increased cardiac output exceeds oxygen consumption hence the arterio-venous oxygen
difference is decreased.
Immediately following delivery, cardiac out-put increases by 10-20% as blood initially within the
uterus is returned as the uterus contracts

Blood pressure falls to a nadir at ~ 36 weeks There is a decrease in pulse pressure by
A B
gestation about 15 mmHg
Pulmonary vascular resistance is unchanged Stroke volume is increased by ~10% during
C D
during pregnancy the first trimester
The apex beat of the heart is located at the
E sixth left intercostal space during the third
trimester
Explanation

The risk of peptic ulceration is increased The risk of gastro-oesophageal reflux is
C D
especially during the third trimester increased
Explanation
GI TRACT
 Constipation more common - compression of rectum by uterus, increased water absorption
caused by increased angiotensin II and reduced smooth muscle activity caused by
progesterone
 Gall stones more common - smooth muscle relaxation cause sluggish flow of bile. Liver function
and bilirubin concentration unchanged
 Serum albumin concentration falls by 20% but there is a slight increase in total protein
concentration

Change in serum creatinine concentration at 24 weeks gestation compared to pre-
Question 42
pregnancy

E 50% decrease
Explanation
RENAL SYSTEM
 Increase in kidney size and weight, ureteral dilatation (Right > left), bladder becomes an
intra-abdominal organ
 GFR increases 50%, renal plasma flow increases by 75%. Peak GFR reached ~16-24
weeks gestation. GFR falls in late pregnancy
 Decreased uric acid concentration in early pregnancy due to increased clearance.
Levels increase in the third trimester
 Plasma osmolarity decreases about 10 mOsm/kg H2O. Colloid osmotic pressure falls by
~10%
300mOsmol/kg H2O) has a freezing point of -0.56C. Pregnancy is associated with a
10% fall in osmolarity and therefore plasma has a slightly higher freezing point (-0.5C)
 Aldosterone secretion increased as a consequence of activation of renin-angiotensin
pathway - 6-8x non-pregnant. Increases salt and water reabsorption from the renal
tubules off-setting the increase in GFR
 Progesterone has a natriuretic effect and stimulates potassium loss - this is balanced by
the effects of aldosterone. Overall, there is a small degree of salt and water retention in
pregnancy
 Total body water increases by 6-8L. Extracellular fluid volume increased by 3L, about
1.5L of which is plasma
 Increase in glucose excretion as filtered glucose load may exceed renal threshold for
absorption
increased
 Thus, mild glycosuria (1-10 gm/day) and/or proteinuria (to 300 mg/day) can occur in
normal pregnancy

Question 43 Change in serum urea concentration at 24 weeks gestation compared to pre-pregnancy

E 50% decrease
Explanation
Question 44 With respect to maternal cardiovascular changes during labour and delivery

Venous return decreases markedly Cardiac output returns to pre-labour
A B
immediately following normal birth values 24-48h after birth
Immediately following delivery, maternal
Systolic blood pressure falls during
C cardiac output increases up to 80% D
labour
above pre-labour values
Diastolic blood pressure falls during
E
labour
Explanation
 Following birth, cardiac output continues to increase to 80% above pre-labour values due to
auto-transfusion from the uterus and relief of inferior vena cava compression. Cardiac output
returns to pre-labour values about 1 hour post-partum.
 Basal BP increases during labour and is further increased with each contraction
Question 45 The storage temperature of platelet concentrates

A -50 C B -30C
C 2-5 C D 15C
E 22 C
Explanation

 Blood components such as red cells, platelets, fresh frozen plasma and cryo-precipitate are
obtained from a single donation of blood
 On average, 470ml of blood is obtained into 63ml anticoagulant and stored at 4C - shelf life = 5
weeks and over 70% of red cells should be viable
 Packed red cells - plasma is removed and replaced by optimal additive solution containing
glucose, adenine, mannitol and sodium chloride. Blood is leukocyte-depleted by filtration. Mean
volume = 330ml, haematocrit = 57%
 Fresh frozen plasma - plasma from one unit of blood frozen at -30C within 6h of donation.
Volume ~200ml. Used to replace clotting factors in acquired bleeding disorders
 Cryoprecipitate - FFP from a single donation is allowed to thaw at 4-8C and removing the
supernatant. Volume ~20ml and stored at -30C. Contains factor VIII, vWF and fibrinogen. Used
in the treatment of DIC
 Factor VIII & IX concentrates - freeze-dried from pools of plasma. Recombinant coagulation
factors are the treatment of choice for inherited bleeding disorders

Most red cells are transfused in the form Blood for transfusion is usually stored at
A B
of whole blood 0C
Blood for transfusion has a shelf life of Packed red cells for transfusion have a
C D
48-72h from donation haematocrit of ~ 35%
The volume of one unit of blood is 330
E
ml
Explanation
Question 47 The half life of platelets
A 1-2 days B 3-5 days

C 8-12 days D 15-25 days
E 50-65 days
Explanation
PLATELETS

 2-4 microns in diameter, produced in bone marrow from megakaryocytes. Do not have a
nucleus. Concentration 150,000 - 350,000/ml. Count falls during pregnancy but remains within
normal limits
 Half life 8-12 days, removed from circulation by splenic macrophages
 Adhere to injured endothelial cells / collagen to form platelet plug - important for haemostasis
 Contain actin and myosin important in clot retraction, a process by which the clot shrinks and
serum is extruded - occurs 30-60 minutes after clot formation
 Also produce thromboplastin which hastens blood coagulation
 Produce growth factors such as platelet derived growth factor - also produced by other tissues
such as liver and bone
 Attach to sites of endothelial injury, where sub-endothelial elements, particularly fibrillar collagen
via specific receptor glycoprotein Ia. Von Willebrand's factor is necessary for adhesion

Question 48

Abnormalities in the intrinsic or common
C Abnormalities in the extrinsic pathway D
pathway
Abnormalities in the extrinsic or common
E
pathway
Explanation
COAGULATION STUDIES
 PARTIAL THROMBOPLASTIN TIME WITH KAOLIN - PTTK - prolonged with abnormalities in
the intrinsic or common pathways
 THROMBIN TIME - prolonged with fibrinogen deficiency or the presence of inhibitors such as
heparin or fibrin degradation products

Individuals with one alpha globin gene Individuals with two alpha globin genes
A B
deleted have moderate anaemia deleted have alpha thalassaemia trait
Individuals with one alpha globin gene
Individuals with two alpha globin genes
C D deleted typically have a microcytic blood
deleted have severe anaemia
picture
Individuals with two alpha globin genes
E deleted have an increased concentration
of fetal haemoglobin

Explanation
Alpha Thalassaemia
 If all 4 genes deleted, no alpha chain and only gamma chain is produced in the fetus (gamma-4,
Hb Barts) - causes severe anaemia and fetal hydrops with intra-uterine or early neonatal death
 Three genes deleted - moderate anaemia, not transfusion dependent. Hb A, Hb Barts, Hb H
(gamma-4) are produced. Hb A2 is normal or reduced
Question 50 With respect to the electrolyte concentration of urine and plasma

Normal plasma osmolarity is 300-315 Urine osmolarity is typically higher than
A B
mOsmol/kg plasma osmolarity
Urine bicarbonate concentration is Urine creainine concentration is typically
C typically higher than plasma bicarbonate D higher than plasma creatinine
concentration concentration
Urine glucose concentration in non-
E
pregnant women is 0.2-1.0 mM
Explanation
RENAL FUNCTION
Solute??? Plasma Urine

Na+??? 135-150mM *??? 50-130mM???
K+???
3.5 - 5.5mM??? 20-70mM???
Ca2+??? 1.35-1.50mM??? 10-24mM???
HCO3-??? 22-28mM??? 0???
Cl-??? 100-110mM??? 50-130mM???
Creatinine??? 0.06-0.12mM??? 6-20mM???
Urea??? 4-7mM??? 200-400mM???
NH4+??? 0.005-0.02mM??? 30-50mM???
Protein??? 65-80 g/L??? 0???
Uric acid??? 0.1-0.4mM??? 0.7-8.7mM???
Glucose ??? 3.5-5.5mM??? 0???
pH??? 7.36 - 7.46 *??? 4.8 - 7.5???
Phosphate??? 0.8-1.25mM??? 25-60mM???

Osmolality??? 281-297 mOsmol/kg *??? 50-1300 mOsmol/kg
Question 51 Glomerular filtration rate

Is lower in the left lateral position
A Is unaffected by posture B
compared to the supine position
C Is increased if salt intake is increased D Is increased if salt intake is reduced
Decreases by 20-25% in the first
E
trimester
Explanation
GFR increases in pregnancy by 25-50% from 120ml/min to 160-170ml/min with a parallel
increase in renal plasma flow. GFR is altered by posture and is reduced in the supine or upright
position compared to a lateral position. Increased salt intake increases GFR *
· Plasma concentrations of creatinine, uric acid and urea are decreased in pregnancy *
Question 52 The phosphate buffer system

A Is not effective in the extracellular space B Is not effective in the intracellular space
Is less effective in renal tubular fluid than Is more effective in intracellular fluid than
C D
in the extracellular fluid in extracellular fluid
E Is only effective if pH is below 6.8
Explanation
• Has a pK of 6.8
• Low concentration of buffers in extracellular fluid therefore less important than bicarbonate
buffer
• Higher concentration in renal tubular fluid. In addition, pH of tubular fluid is closer to pK of

phosphate buffer system - therefore more important buffer
Question 53 A 23 year old woman presents at 6 weeks gestation with a 48 hours history


A metabolic acidosis with normal anion A metabolic acidosis with increased

A B
gap anion gap
A metabolic alkalosis with
C D A metabolic alkalosis with hypokalaemia
hyperchloraemia
E A metabolic acidosis with hypokalaemia
Explanation
· Less common than metabolic acidosis
· Associated with potassium or chloride depletion
Caused by
urine. *
A 23 year old woman presents at 6 weeks gestation with a 48 hours history

Question 54

A A metabolic acidosis with acidic urine B A metabolic alkalosis with alkaline urine
C A metabolic alkalosis with acidic urine D A metabolic acidosis with alkaline urine
A compensated respiratory acidosis with
E
acidic urine
Explanation

Bicarbonate ions are secreted into the The majority of filtered bicarbonate is
A B
proximal tubule reabsorbed in the proximal tubule
Hydrogen ions are absorbed from the
Carbonic anhydrase plays a key role in
C D tubular lumen coupled to sodium
the reabsorption of bicarbonate ions
secretion
Hydrogen ions are secreted into the
E tubular lumen coupled to potassium
absorption

Explanation
RENAL ACID-BASE REGULATION *****
· Bicarbonate: 90% of filtered bicarbonate is reabsorbed in the proximal tubule. Depending
on acid-base status, the rest of the bicarbonate may be reabsorbed distally *
· Hydrogen ions secreted into the lumen combine with filtered bicarbonate to form H2CO3
which dissociates into CO2 and water catalysed by carbonic anhydase in the tubular cell brush
border. CO2 diffuses into the cells and the reaction is reversed, generating hydrogen ions and
bicarbonate *
· Hydrogen ions are secreted into the tubules coupled to sodium ion reabsorption *

Aldosterone stimulates potassium Acidosis increases potassium secretion
A B
retention by the kidneys into the renal tubules
Alkalosis increases potassium secretion Insulin inhibits potassium uptake into
C D
into the renal tubules cells
E
Explanation

Question 57 Which one is not a recognized cause of hypocalcaemia?

A Chronic renal failure B Hypoalbuminaemia
C Massive transfusion with citrated blood D Hypoparathyroidism
E Chronic lithium therapy
Explanation
HYPOCALCAEMIA ******

May be caused by
• Increased phosphate levels - chronic renal failure

• Hypoparathyroidism
• Vitamin D deficiency
• Drugs such as bisphosphonates, calcitonin
• Acute pancreatitis, citrated blood in massive blood transfusion
• Malabsorption
• Low plasma albumin
Chronic lithium therapy associated with hypercalcaemia

Third stage, Lactation & Neonate
Question 1 The third stage of labour

Lasts on average about 1 hour following Begins with crowning of the fetal head in
A B
physiological management multiparous women
Is prolonged if it lasts more than 1 hour Is prolonged if it lasts more than 2 hours
C D
with active management with physiological management
Is prolonged if it lasts more than 30
E
minutes with active management
Explanation
Definition:
Duration
95% of women.
including:
Post-natal anaemia
Active management of the third stage of labour does not include which one of
Question 2
the above interventions?

Routine administration of uterotonic
A Early clamping of the umbilical cord B
drugs
Uterine massage to stimulate uterine
C Controlled cord traction D
contraction
E Cutting the umbilical cord early
Explanation
Active management

Active management of the third stage involves a package of care which includes all of these
three components:
1. Routine use of uterotonic drugs
2. Early clamping and cutting of the cord
3. Controlled cord traction.
Early clamping of the cord contributes little to the benefits of active management of the third
stage. It may be indicated to enable neonatal resuscitation.
The most important physiological mechanism to minimize blood loss during

Question 3
the third stage of labour

Oxytocin release from the posterior Prostaglandin release from the
A B
pituitary myometrium
Contraction and retraction of the
C D Fibrin deposition
myometrium
E Withdrawal of beta-HCG support
Explanation
hemostasis.
uterus.
Question 4 A recognized benefit of delayed cord clamping in term pregnancies
Question 5 A recognized disadvantage of delayed cord clamping in term pregnancies

Decreased risk of post-partum Increased duration of the third stage of
A B
haemorrhage labour
Higher neonatal haemoglobin
C Shortening of the third stage of labour D
concentration
E Increased risk of neonatal jaundice

Explanation
In the term baby, delaying cord clamping until pulsations cease (2-4 mins) results in:
1. Higher neonatal hemoglobin and hematocrit
2. Higher iron stores (ferritin levels) in childhood
In addition, in pre-term babies, delayed cord clamping is associated with
1. Less need for blood transfusion in the neonatal period
2. Lower rates of neonatal intraventricular hemorrhage
3. Lower rates of neonatal sepsis
The risks of delayed cord clamping include an increased risk of neonatal polycythaemia and
jaundice.
Parents may have a preference regarding the timing of cord clamping and the position of the
baby immediately following delivery.
The RCOG recommends that the cord should not be clamped within 30 seconds of delivery
Question 6 With respect to controlled cord traction during the third stage of labour

The initial direction of traction should be As the placenta emerges through the
A at right angle to the axis of the birth B introitus, the direction of traction should
canal be upwards
Cord traction should only be applied The uterine fundus should be massaged
C D
between contractions during cord traction
At caesarean section, cord traction
should be applied while the non-
E
dominant hand is used to massage the
uterine fundus
Explanation
Controlled Cord Traction
 Gentle downward traction is applied along the axis of the birth canal with counter-traction on the
uterine body. Traction should initially be downward, then horizontal, and finally upward as the
placenta delivers.
 Counter-traction is performed by trapping the body of the uterus above the symphysis pubis and
directing it upwards into the abdomen and back.
 Cord traction should only be applied when the uterus is well contracted and manually supported
above the symphysis pubis with counter-traction (Brandt-Andrews maneuver). When the uterus
relaxes between contractions, cord traction should be discontinued
 Cord traction should not be applied in the absence of counter-traction otherwise uterine
inversion may occur. Uterine massage or fundal pressure should not be used before delivery of
the placenta.
 CCT alone does not reduce the incidence of PPH


The capacity of the uterus is about 2000
A B Blood flow to the uterus is 5-8 L/min
ml
About 10-15% of cardiac output is
C D The uterus weighs about 10kg
directed to the uterus
Blood flow to the uterus is 200 – 300
E
ml/min
Explanation
cardiac output).
Which one of the above mechanisms is important in controlling blood loss

Question 8
from the uterus during the third stage of labour?

A Relaxation of the myometrium B Retraction of the myometrium
Increased oxytocin secretion from the
C Increased fibrinolysis D
posterior pituitary gland
E Shedding of the decidua
Explanation
hemostasis.
uterus.
Question 9 The proportion of term babies who are jaundiced at birth

A 0% B 5%
C 8% D 12%
E 15%
Explanation
Neonatal Jaundice
Prolonged jaundice is jaundice lasting more than 14 days in term babies and more than 21 days
in preterm babies
Question 10 Neonatal jaundice

A Affects about 60% of term babies B Affects about 25% of pre-term babies
Is more easily recognized by clinical
Is prolonged if it lasts more than 28 days
C examination in babies with dark D
in a pre-term baby
compared to white skin tones
Typically presents within 24 hours of
E
birth
Explanation
Question 11 With respect to bilirubin metabolism

Bilirubin is a product of the breakdown of Heme is converted into bilirubin mainly in
A B
the globin chain of haemoglobin the liver
The rate-limiting step in the synthesis of
C D Bilirubin does not cross the placenta
bilirubin is catalyzed by heme oxygenase
Bilirubin is produced exclusively from the
E
breakdown of red blood cells
Explanation

Question 12 With respect to bilirubin metabolism

A Unconjugated bilirubin is water-soluble B Unconjugated bilirubin is fat-soluble
In the liver, conjugated bilirubin is Bilirubin is excreted into bile mainly in
C D
converted to unconjugated bilirubin the form of bilirubin-sulphate
Carbon monoxide is consumed during
E
the synthesis of bilirubin
Explanation
The breakdown of this enzyme contributes to the total concentration of

Question 13
bilirubin

E Catalase
Explanation
The breakdown of this protein makes the largest contribution to total bilirubin
Question 14
concentration
Product of bilirubin metabolism responsible for the brown colour of faeces
Question 15
A Urobilinogen B Stercobilin
C Catalase D Haemoglobin
E Myoglobin
Explanation
Question 16 Enzyme which catalyses the conjugation of bilirubin in the liver


A Glucuronyltransferase B Cytochrome P450
E Catalase
Explanation
With respect to bilirubin metabolism in the neonate Breast-fed neonates are

less likely to develop jaundice compared to bottle-fed neonates F Insufficient
breast milk intake by the neonate increases the risk of jaundice T Breast milk
Question 17
increases the conjugation of bilirubin F The risk of neonatal jaundice
increases with increasing gestation age F Active management of the third
stage of labour is associated with an increased risk of neonatal jaundice F

Breast-fed neonates are less likely to
Breast milk increases the conjugation of
A develop jaundice compared to bottle-fed B
bilirubin
neonates
Insufficient breast milk intake by the The risk of neonatal jaundice increases
C D
neonate increases the risk of jaundice with increasing gestation age
Active management of the third stage of
E labour is associated with an increased
risk of neonatal jaundice
Explanation
Physiological jaundice
 This is jaundice that develops in many newborn babies in the first weeks of life and for which
there is no underlying cause.
 Breastfed babies are more likely to develop physiological jaundice than bottle-fed babies.
 Jaundice may occur due to insufficient breast milk intake. There is stasis of conjugated bilirubin
in the GI tract allows greater entero-hepatic circulation. This is described as ‘breast-feeding
jaundice’ as opposed to ‘breast milk jaundice’
 Breast milk also contains enzymes that inhibit the conjugation of bilirubin causing breast milk
jaundice.
 The raised bilirubin in physiological jaundice is unconjugated
 Risk of developing significant neonatal jaundice is higher in male infants
 The risk of significant neonatal jaundice is inversely proportional to gestation age

A 5 days old term neonate is found to be jaundiced but well hydrated and
gaining weight. His mother is breast-feeding exclusively and breast milk
Question 18
production is thought to be adequate. No other cause of jaundice has been
identified. Which one is the most likely diagnosis?

A Neonatal jaundice B Breast milk jaundice
C Early jaundice D Breast-feeding jaundice
E Prolonged jaundice
Explanation
The following are associated with an increased risk of neonatal hyper-

Question 19
bilirubinaemia

A sibling with a history of neonatal
A Gestation age over 38 weeks B
jaundice requiring phototherapy
Maternal intention to bottle feed
C D Birth by elective caesarean section
exclusively
E Gestation age over 40 weeks
Explanation
Tests to predict significant hyperbilirubinaemia
 Serum bilirubin level within 2 hours in all babies with suspected or obvious jaundice in the first
24 hours of life
 Continue 6 hourly serum bilirubin levels for all babies with suspected or obvious jaundice in the
first 24 hours of life until the level is below the treatment threshold and is stable or falling
 Urgent medical review should be undertaken as soon as possible and within 6 hours for all
babies with suspected or obvious jaundice in the first 24 hours of life to exclude pathological
causes of jaundice.
 Bilirubin levels should be interpreted according to the baby’s postnatal age in hours and
managed using treatment threshold graphs
The following groups of babies are at increased risk of developing significant

hyperbilirubinaemia:
1. Gestational age under 38 weeks

2. A previous sibling with neonatal jaundice requiring phototherapy
3. Maternal intention to breastfeed exclusively
4. Visible jaundice in the first 24 hours of life.

Question 20 Which one of the above statements about fetal physiology is true?

Fetal blood makes up a larger proportion
Over 70% of fetal blood is within the
A of total body weight compared to adult B
umbilical cord and placenta
blood
The proportion of blood within the fetus
About 40% of fetal cardiac output goes
C decreases, while that within the placenta D
to the placenta
increases with increasing gestation ag
E
to the brain
Explanation
CARDIOVASCULAR PHYSIOLOGY
Blood volume
 Fetal blood volume is 10-12% of body weight (7-8% in adults) –large volume of blood in the
placenta
 Depending on the timing between birth and clamping of the cord, 65-85% of total blood volume
is contained within the neonate
 The % of total blood within the fetus increases while that contained within the placenta
decreases with increasing gestation age
 Distribution of fetal cardiac output: 40 % placenta, 35% trunk, 5% each - brain, gut and heart,
4% lungs, 2% each - kidney, liver and spleen
 Fetal heart does not metabolise free fatty acids - uses mainly glucose and lactate. The placenta
produces a large quantity of lactate. In the adult heart, long chain fatty acids are the main fuel
with glucose and lactate being minor fuels. Ketone bodies also metabolised
Question 21 With respect to the fetal circulation

The mean arterial pressure at term is ~ The mean arterial pressure is higher at
A B
15 mmHg 20 weeks compared to 40 weeks
Loss of blood flow to the placenta at
The pressure in the pulmonary artery is
C D delivery results in a marked reduction in
lower than that in the aorta
systemic resistance
The mean systemic venous pressure is
E
higher in the fetus than in adults
Explanation
Fetal arterial pressure is low and, importantly, pulmonary pressure is slightly higher than the
aorta. Mean arterial pressure is 15mmHg in mid-gestation and 40-50mmHg at term

The mean systemic venous pressure is higher in the fetus than in the adult resulting in
increased flow back to the heart and a consequent high cardiac output
The fetal circulation is characterised by a low pressure shunt through the placenta. Loss of
blood flow through the placenta at birth approximately doubles systemic resistance.
Question 22 Which one of the above statements regarding fetal physiology is not true?

The oxygen dissociation curve of fetal
The proportion of adult haemoglobin in
A B haemoglobin lies to the left of the
cord blood at 40 weeks gestation is 20%
curvefor adult haemoglobin
Fetal haemoglobin has a lower affinity The concentration of 2,3-
C for 2,3-bisphosphoglycerate compared toD bisphosphoglycerate in fetal blood
adult haemoglobin decreases with increasing gestation age
Fetal haematocrit increases with
E
Explanation
PO2 falls in umbilical arterial and venous blood as gestation age increases during the second
half of pregnancy
Fetal haemoglobin concentration, red cell count, haematocrit however increases with
As a result, the oxygen carrying capacity of fetal blood increases with gestation age
Fetal red cell MCV and haemoglobin content decreases with gestation age
During the last week of pregnancy, the % of adult haemoglobin increases to 20% at term. Fetal
Fetal Hb has a higher affinity for oxygen and its dissociation curve is shifted to the left of the
Question 23 With respect to fetal blood, which one of the above statements is not true?

Fetal red cells have a life-span of ~ 80
A B Umbilical venous pH is ~ 7.34
days
A shift of the oxygen dissociation curve
Hypoxia causes the oxygen dissociation
C to the left results in greater oxygen D
curve to shift to the right
release in tissues
Acidosis causes the oxygen dissociation
E
curve to shift to the right

Explanation

 PO2 falls in umbilical arterial and venous blood as gestation age increases during the second
half of pregnancy
 Fetal haemoglobin concentration, red cell count, haematocrit however increases with
 During the last week of pregnancy, the % of adult haemoglobin increases to 20% at term. Fetal
 Fetal Hb has a higher affinity for oxygen and its dissociation curve is shifted to the left of the
 Oxygenated umbilical venous blood has an oxygen saturation of ~80%. pH = 7.34 (maternal
arterial pH = 7.42), PCO2 = 45mmHg (maternal = 32mmHg) and PO2 = 30mmHg
 Anaemia, hypoxia and acidosis result in increased 2,3-diphosphoglycerate concentration which
shifts the oxygen dissociation curve to the right increasing oxygen release in tissues
Question 24 With respect to fetal blood

Haemoglobin concentration at birth is ~ Fetal red cells have a longer life-span
A B
17 g/dl than adult red cells
Acidosis results in a decrease in the
The life-span of fetal red cells is ~ 150
C D concentration of 2,3
days
bisphosphoglycerate
Hypoxia results in a decrease in the
E concentration of 2,3-
bisphosphoglycerate
Explanation


Has a higher oxygen saturation than
A Has an oxygen saturation of ~ 98% B
umbilical arterial blood
Has a PO2 which is higher than maternal
C Has a pH of ~ 7.47 D
arterial PO2
Explanation

A Begins from ~ 12 weeks gestation B Begins in the primitive streak
Begins in the clavicle from 30 weeks
C Occurs in the liver at 8 weeks gestation D
gestation
Begins in the medullary cavity of long
E
bones from 37 weeks gestation
Explanation
 Begins in the yolk sac (2 -8 weeks) - progenitor cells migrate from the yolk sac to the liver at 5-8
weeks gestation
 Begins in the medullary cavity of the clavicle at about 10-12 weeks and in the medullary cavity
of long of bones at ~ 20 weeks gestation
 Erythrocyte production in-utero is controlled exclusively by fetal erythropoietin produced in the
liver and maternal erythropoietin does not cross the placenta
 The increase in Po2 at birth causes serum erythropoietin to fall, and erythrocyte production
shuts down between birth and about 6 to 8 weeks


Is dependent on maternal erythropoietin Occurs in the spleen from 20 weeks
C D
which crosses the placenta gestation
Is dependent on erythropoietin produced
E
by the fetal kidneys
Explanation
Question 28 With respect to fetal glucose metabolism

The fetal liver can produce glucose from The majority of fetal hepatic glycogen is
A B
fatty acids stored during the first trimester
In healthy term neonates, glucose
Gluconeogenesis is stimulated once the
C concentrations peak 30-90 minutes after D
umbilical cord is clamped at birth
birth
Neonates born to women with type 1
E diabetes are at increased risk of
neonatal hyperglycaemia
Explanation
Fetal Glucose metabolism
 The fetus is totally dependent on the mother for glucose supply and gluconeogenesis does not
occur during fetal life
 The fetus begins to build a hepatic glycogen store from early gestation but the majority of
glycogen is accumulated in the second half of the third trimester
 Maternal glucose supply terminates at cord clamping
 This causes a rise in neonatal circulating adrenaline while glucose concentration falls.
Gluconeogenesis from hepatic glycogen is stimulated
 In healthy, term neonates, glucose levels reach a nadir 30 to 90 min after birth, after which
neonates are typically able to maintain normal glucose concentrations.
 The following are associated with an increased risk of neonatal hypoglycemia
1. Reduced glycogen stores (growth restricted and premature neonates)
2. Severely ill neonates (increased glucose metabolism)
3. Neonates of diabetic mothers (hyperinsulinemia)

Question 29 With respect to the fetal and neonatal immune system

Phagocytic cells are present in the fetus Granulocytes are not produced by the
A B
during the first trimester fetus until the third trimester
The thymus gland becomes functional at In the normal neonate, the thymus gland
C D
~ 32 weeks gestation should not be detectable on chest X-ray
B-cells are not produced by the fetal
E
bone marrow until after birth
Explanation
Fetal & Neonatal Immunology
Fetus
 Phagocytic cells are identifiable in the fetus at the yolk sac stage of development
 Granulocytes can be identified in the second month and monocytes can be identified in the
fourth month. The function of these immune cells increases with gestational age but is still low
at term.
 The thymus is functional by 14 weeks gestation and T cells are present in the fetal liver and
spleen
 The thymus grows rapidly in utero and is readily noted on chest x-ray in the neonate. Growth
continues in childhood reaching a peak size at ~10 years of age followed by involution
 The number of T cells in the fetal circulation increases during the second trimester and
approach adult numbers by 30 to 32 weeks gestation
 B cells are present in fetal bone marrow, blood, liver, and spleen by the 12th week
 Trace amounts of IgM and IgG are detected by the 20th week and trace amounts of IgA is
detected by the 30th week
 Only small amounts of predominantly IgM immunoglobulin are produced in utero in normal fetal
life
 Almost all fetal IgG is acquired through trans-placental transfer. After 20 weeks gestation,
placental transfer of IgG increases to reach maternal levels or greater at term.
Neonates
 Neonates are immuno-deficient relative to adults because most immunological systems are not
fully developed. Neonates are therefore at increased risk of overwhelming sepsis, especially
pre-term neonates
 At birth, the ultrastructure of neutrophils is normal but function is impaired especially in pre-term
neonates
 Neonates have a relative T lymphocytosis compared to adults but T-cell function is also
impaired
 IgA, IgM, IgD, and IgE do not cross the placenta and are detectable only in trace amounts at
birth.
 Passive transfer of maternal immunity through breast milk (IgG, IgA, white blood cells,
complement proteins, lysozyme, lactoferrin) confers immunity to many bacteria and viruses
 Passive immunity wanes with time, reaching a nadir at 3 to 6 months of age

Question 30 Which one is associated with increased fetal surfactant production

A Meconium aspiration B Hypertensive disorders of pregnancy
C Obstetric cholestasis D Hypothyroidism
E Chorioamnionitis
Explanation
SURFACTANT
 The lecithin: sphingomyelin ratio (L/S) test on amniotic fluid has been used to predict fetal
pulmonary maturity based on the principle that surfactant is rich in phospholipid, and that
mature surfactant contains high concentrations of lecithin
 Surfactant production begins in the fetus at 24-28 weeks gestation and detectable in amniotic
fluid by 28-32 weeks. By 35 weeks, most babies have developed adequate amounts of
surfactant
 Surfactant production increased in: hypertensive disorders of pregnancy, malnutrition, placenta
previa, and drug addiction, premature rupture of membranes, intrauterine growth restriction,
female fetus, and hemoglobinopathy.
 Maternal glucocorticoid administration increases fetal pulmonary surfactant production and
reduces the risk of neonatal respiratory distress syndrome
 Surfactant production decreased in: maternal diabetes mellitus, anemia, polyhydramnios,
hypothyroidism, male fetus, twins, isoimmune disease, liver disease, renal disease, advanced
maternal age, perinatal infection, cold stress
Which one of the above is a characteristic feature of placental separation

Question 31
during the third stage of labour?

A Descent of the uterus B After-pains
C Gush of blood D Shortening of the umbilical cord
Cessation of pulsation in the umbilical
E
cord

Explanation
Signs of placental separation
1. Lengthening of the umbilical cord as the placenta separates and is pushed into the lower uterine
segment by progressive uterine retraction.
2. A gush of blood. The retroplacental clot typically forms centrally and escapes following complete
separation of the placenta. However, blood within the clot may escape before complete
separation and a gush of blood is not a reliable sign of complete separation
3. The uterus takes on a more globular shape and becomes firmer. This occurs as the placenta
descends into the lower segment and the body of the uterus continues to retract.
4. The uterus rises in the abdomen. The descent of the placenta into the lower segment, and
finally into the vagina, displaces the uterus upward.
(3) and (4) are not clinically useful signs
During the third stage, periodic assessment of the uterus should occur to detect signs of
placenta separation and evidence of an atonic uterus becoming distended with blood.

E Attitude
Explanation
Fetal Lie
Presentation
dilated
Position
Engagement

Station

The degree of flexion of the fetal head is
In the occipito-posterior position, the
more complete in the occipito-anterior
A occipito-frontal diameter presents to the B
position than in the occipito-posterior
maternal pelvis
position
The submento-bregmatic diameter is the
The submento-bregmatic diameter is
C D presenting diameter in a fully extended
9.5cm wide
face presentation
E
12 cm wide
Explanation
 9.5cm
(bregma)
Suboccipito-frontal
 10 cm +
Occipito-frontal
 11.5 cm
Submento-bregmatic
 9.5 cm

Submento-vertical
 11.5 cm
Mento-vertical
 13.5 cm

The mento-vertical diameter is the
The mento-vertical diameter is 11.5cm
A B presenting diameter in a brow
wide
presentation
When the mento-vertical diameter is the
C presenting diameter, the fetus cannot be D
9.5cm wide
delivered vaginally
When the fetal head is de-flexed, a wider
E
diameter presents to the maternal pelvis
Explanation
Question 35 With respect to the mechanism of labour

In a fully flexed occipito-anterior position, In a well-flexed occipito-anterior position,
A the bi-parietal diameter is the presenting B the fetal diameter that presents to the
diameter maternal pelvis is 9.5cm wide
The suboccipito-frontal diameter is The occipito-frontal diameter is 13.5cm
C D
9.5cm wide wide
Because of the wide diameter, a face
E
presentation cannot deliver vaginally
Explanation

Question 36 Occipito-frontal diameter

A 9.5 cm B 10 cm
C 10.5 cm D 11.5 cm
E 13.5 cm
Explanation
Question 37 Submento-bregmatic diameter

A 9.5 cm B 10 cm
C 10.5 cm D 11.5 cm
E 13.5 cm
Explanation
Question 38 The presenting diameter in the occipito-posterior position

A 9.5 cm B 10.5 cm
C 11.5 cm D 12.5 cm
E 13.5 cm
Explanation
Question 39 The presenting diameter in a fully extended face presentation

A 9.5 cm B 10.5 cm
C 11.5 cm D 12.5 cm
E 13.5 cm

Explanation
Question 40 Which one of the above statements about fetal cardiovascular physiology is true?

The fetal heart metabolises free fatty Fetal blood makes up about 2% of total
A B
acids body weight
About 4% of fetal cardiac output goes to About 20% of fetal cardiac output goes
C D
the lungs to the heart
E
to the placenta
Explanation
CARDIOVASCULAR PHYSIOLOGY
Blood volume
 Fetal blood volume is 10-12% of body weight (7-8% in adults) –large volume of blood in the
placenta
 Depending on the timing between birth and clamping of the cord, 65-85% of total blood volume
is contained within the neonate
 The % of total blood within the fetus increases while that contained within the placenta
decreases with increasing gestation age
 Distribution of fetal cardiac output: 40 % placenta, 35% trunk, 5% each - brain, gut and heart,
4% lungs, 2% each - kidney, liver and spleen
 Fetal heart does not metabolise free fatty acids - uses mainly glucose and lactate. The placenta
produces a large quantity of lactate. In the adult heart, long chain fatty acids are the main fuel
with glucose and lactate being minor fuels. Ketone bodies also metabolised

The peak expiratory flow rate (PEFR) is
A The FEV1 is increased B
decreased
Explanation

Minute volume - tidal volume X respiratory rate - increased by 50% in early pregnancy. Tidal
volume increases with little increase in respiratory rate
Residual volume - volume of air left in the lungs after the most forceful expiration decreased by
20% as does functional residual capacity and expiratory reserve volume
Respiratory quotient - ration of oxygen consumption to carbon dioxide production - increased
from 0.76 to 0.83
There is a fall in arterial PCO2 with little change in PO2. The fall in PCO2 is matched by a fall in
plasma bicarbonate (renal compensation - compensated respiratory alkalosis) with no resultant
change in pH. pH= 7.44, pCO2=30, bicarbonate=20-25

Question 42
to pre-pregnancy

E 50% decrease
Explanation
RENAL SYSTEM
 Increase in kidney size and weight, ureteral dilatation (Right > left), bladder becomes an
intra-abdominal organ
 GFR increases 50%, renal plasma flow increases by 75%. Peak GFR reached ~16-24
weeks gestation. GFR falls in late pregnancy
 Decreased uric acid concentration in early pregnancy due to increased clearance.
Levels increase in the third trimester
 Plasma osmolarity decreases about 10 mOsm/kg H2O. Colloid osmotic pressure falls by
~10%
300mOsmol/kg H2O) has a freezing point of -0.56C. Pregnancy is associated with a
10% fall in osmolarity and therefore plasma has a slightly higher freezing point (-0.5C)
 Aldosterone secretion increased as a consequence of activation of renin-angiotensin
pathway - 6-8x non-pregnant. Increases salt and water reabsorption from the renal
tubules off-setting the increase in GFR
 Progesterone has a natriuretic effect and stimulates potassium loss - this is balanced by
the effects of aldosterone. Overall, there is a small degree of salt and water retention in
pregnancy

 Total body water increases by 6-8L. Extracellular fluid volume increased by 3L, about
1.5L of which is plasma
 Increase in glucose excretion as filtered glucose load may exceed renal threshold for
absorption
increased
 Thus, mild glycosuria (1-10 gm/day) and/or proteinuria (to 300 mg/day) can occur in
normal pregnancy
Question 43 Change in colloid osmotic pressure during pregnancy compared to pre-pregnancy

E 50% decrease
Explanation

Fetal haemoglobin concentration
Fetal blood oxygen content remains
A remains unchanged as gestation age B
unchanged as gestation age increases
increases
Blood in the inter-villous space has lower Blood in the inter-villous space has lower
C D
PO2 than umbilical venous blood PCO2 than umbilical venous blood
Blood in the inter-villous space has 2x
E the lactate concentration of umbilical
venous blood
Explanation

Fetal albumin and total protein concentration increases with gestation age . Triglyceride levels
fall while bilirubin concentration increases with gestation. Fetal bilirubin concentration higher
than maternal concentration while cholesterol and triglyceride concentrations are lower
 Umbilical arterial and venous PO2 and pH decrease while PCO2 increases with gestation age.
Fetal Hb concentration increases with gestation age so blood oxygen content remains constant.
Intervillous blood has higher PO2 and lower PCO2 than umbilical venous blood but similar
lactate concentration.

 In the second and third trimesters, fetal red cell count increases while white cell and platelet
count remain unchanged. Lymphocytes form the main population of white cells in the fetus.
Reticulocyte count falls with increasing gestation age. Fetal Hb makes up 80% of total Hb in
mid-pregnancy and 70% at term
 Fetal iron concentration, total iron binding capacity and transferrin saturation increases with
 Amniotic fluid bilirubin concentrations fall during the third trimester

Fetal albumin concentration increases Fetal triglyceride concentration increases
A B
with increasing gestation age with increasing gestation age
Fetal bilirubin concentration decreases Fetal bilirubin concentration is lower than
C D
with increasing gestation age maternal concentration
Fetal cholesterol concentration is higher
E
than maternal concentration
Explanation

The child of two Rhesus negative The child of two Rhesus positive
A B
individuals can be Rhesus positive individuals cannot be Rhesus negative
The C antigen does not cause fetal The E antigen is a recognized cause of
C D
haemolytic disease fetal haemolytic disease
The child of a Rhesus positive mother
E and a Rhesus negative father cannot be
Rhesus negative
Explanation
RHESUS BLOOD GROUP
 D antigen is most antigenic - individuals with D antigen are Rhesus positive. 15% of Caucasians
are Rhesus negative.
 Immune response to Rhesus antigens is slow and peak antibody titres are attained 2-4 months
after exposure. Transfusion reaction in an unsensitized individual is therefore delayed
 D antigen causes severe Rhesus disease. C & E antigens can cause mild fetal haemolysis.
Usually the first pregnancy is not affected, but may be if the mother had received incompatible
blood products

 The offspring of two Rh negative individuals must be Rh negative. The offspring of a Rh
negative and a Rh positive individual may be Rh negative as the Rh positive parent may be
heterozygous
Question 47 The storage temperature of packed red cells for transfusion

A -50 C B -30C
C 2-5 C D 15C
E 22 C
Explanation
 Blood components such as red cells, platelets, fresh frozen plasma and cryo-precipitate are
obtained from a single donation of blood
 On average, 470ml of blood is obtained into 63ml anticoagulant and stored at 4C - shelf life = 5
weeks and over 70% of red cells should be viable
 Packed red cells - plasma is removed and replaced by optimal additive solution containing
glucose, adenine, mannitol and sodium chloride. Blood is leukocyte-depleted by filtration. Mean
volume = 330ml, haematocrit = 57%
 Fresh frozen plasma - plasma from one unit of blood frozen at -30C within 6h of donation.
Volume ~200ml. Used to replace clotting factors in acquired bleeding disorders
 Cryoprecipitate - FFP from a single donation is allowed to thaw at 4-8C and removing the
supernatant. Volume ~20ml and stored at -30C. Contains factor VIII, vWF and fibrinogen. Used
in the treatment of DIC
 Factor VIII & IX concentrates - freeze-dried from pools of plasma. Recombinant coagulation
factors are the treatment of choice for inherited bleeding disorders

Most red cells are transfused in the form Blood for transfusion is usually stored at
A B
of whole blood 0C
Blood for transfusion has a shelf life of Packed red cells for transfusion have a
C D
48-72h from donation haematocrit of ~ 35%
The volume of one unit of blood is 330
E
ml

Explanation
Complication of blood transfusion which is caused by extra-vascular

Question 49
haemolysis and typically presents ~ 1 week after transfusion

Explanation
COMPLICATIONS OF BLOOD TRANSFUSION
Immunological
 Allo-immunisationto antigens present on red cells, platelets, leukocytes, plasma. Not a
problem with first transfusion but problems may arise with subsequent transfusions. Delayed
consequences include haemolytic disease of the newborn and rejection of tissue transplants
 Haemolytic transfusion reactions - due to ABO incompatibility. Associated with rigors, loin
pain, SOB, hypotension, haemoglobinuria, renal failure, DIC
 Delayed transfusion reaction - extra-vascular haemolysis presenting with anaemia and
jaundice about 1 week after transfusion
 Non-haemolytic febrile reaction - common and due to leukocyte antibodies. Associated with
flushing, fever, tachycardia, rigors.
 Urticaria & anaphylaxis - common and managed by stopping or slowing transfusion with use
of anti-histamines. Severe anaphylaxis is rare
Question 50 Which one of the above inhibits platelet aggregation?

Options for Questions 22-22
Explanation
Platelet aggregation stimulated by:

 ADP
 Thromboxane A2
 Serotonin - causes vasoconstriction
Aggregation is inhibited by:
 Prostacyclin
 Cyclo-oxygenase inhibitors like aspirin

Question 51 Which one of the above statements regarding red blood cells is true?

The half life of red blood cells is 120 Haemoglobin synthesis occurs in
A B
days reticulocytes
The normal mean cell volume of red Red blood cells make up 45-55% of total
C D
blood cells is 96-126 fl blood volume in females
Red blood cells have a diameter of ~ 0.7
E
microns
Explanation
ERYTHROCYTES
 Red blood cells - biconcave discs with diameter of 7 microns and a thickness of 1-2
microns. 4.5-6.5 X 10E12/ L males; 4.0-5.5 X10E12/L females. Make up 40-54% of
blood in males (37-47% females; = haematocrit)
 Mean cell volume 76-96fl; mean cell Hb concentration 30-36g/dl; mean cell Hb = 27-
32pg
 Primitive red cells are produced by the yolk sac. Fetal red cells are produced in the
spleen and lymph nodes and mainly in the liver.
 In late gestation and after birth, red cells are produced only in bone marrow - almost all
bones initially then only in membraneous bones (ribs, sternum, vertebrae and iliac
bones) in adulthood.
 Produced from the pluripotent haemopoietic stem cells - first committed erythrocyte
precursor is the proerythroblast. The cells later form large quantities of Hb; the nucleus
condenses and is extruded and the most of the golgi apparatus and endoplasmic
reticulum are reabsorbed
 Enter the circulation as RETICULOCYTES - contain a small amount of basophilic
material - golgi and some mitochondria and ribosomal RNA - still able to synthesise Hb.
Develop into mature RBC within 1-2 days of release into the circulation
 Life span 120 days
 Production is stimulated by: tissue hypoxia (high altitude), anaemia, erythropoietin
Question 52 Which one of the above is not associated with raised erythrocyte mean cell volume?

A Normal pregnancy B Chronic alcohol abuse
C Chronic liver disease D Alpha thalassaemia
E Reticulocytosis
Explanation
MACROCYTIC ANAEMIA
Megaloblastic

synthesis
deficiency
Macrocytosis without megaloblastosis

 Pregnancy
 Neonate
 Alcohol abuse
 Liver disease
 Reticulocytosis
 Aplastic anaemia
 Drugs like azathioprine
Question 53 Which molecules are typically secreted into the lumen of the proximal convoluted tubule?

A Glucose and amino acids B Glucose and creatinine
C Bile salts and penicillin D Sodium ions and salicylates
E Glucose and salicylates
Explanation
TUBULAR ABSORPTION & SECRETION
· Proximal tubule *-reabsorbs about two thirds of filtered water, sodium, potassium,
chloride, bicarbonate and other solutes
· Reabsorbs virtually all filtered glucose, lactate and amino acids. Uptake of glucose and
amino acids is sodium dependent and saturable *
· The filtered glucose load is increased and may exceed the maximal tubular reabsorptive
capacity in pregnancy or poorly controlled diabetes mellitus, resulting in glycosuria
· Renal amino acid excretion is increased in pregnancy *
· Bicarbonate absorption is sodium dependent - and Na+-H+ antiporter exchanges tubular
Na+ for intracellular H+ which combines with HCO3- to form carbonic acid. Carbonic acid
dissociated to water + CO2 (Carbonic anhydrase) and CO2 is reabsorbed *
· Water absorption follows solute uptake while proteins are taken up by pinocytosis *
· Bile salts, creatinine, urate and drugs such as penicillin, quinine and salicylate are
secreted into the lumen of the proximal tubule *

Question 54 The bicarbonate buffering system

Is made up of bicarbonate ions and
Is made up of carbonic acid and carbon
A potassium bicarbonate in the B
dioxide in the extracellular fluid
extracellular fluid
Is made up of carbonic acid and sodium Is made up of carbonic acid and sodium
C D
bicarbonate in the intracellular fluid bicarbonate in the extracellular fluid
E Is not functional in the intracellular space
Explanation
· Made up of carbonic acid and potassium and magnesium bicarbonate in intracellular fluid
· 399 out of 400 parts of carbonic acid exists as dissolved carbon dioxide. Hence carbonic
acid is a weak acid and sodium bicarbonate is a weak base
· The pH of the bicarbonate buffer system is calculated from the Henderson-Hasselbalch

equation: pH = 6.1 + log[HCO3- / CO2]
· Hence the pH of a solution containing an equal concentration of bicarbonate and carbon

dioxide is 6.1 (log of 1 = 0) = pK of the buffer

Question 55
equation pH = 6.1 + log [HCO3- / CO2]. This is

A The Michaelis-Menten equation B The Henderson-Hasselbalch equation
C The Niels Bohr equation D The acid-base dissociation equation
E The Nernst equation
Explanation
Question 56 Hyperaldosteronism is typically associated with

Metabolic acidosis with normal anion
A B Metabolic acidosis with raised anion gap
gap
C Metabolic alkalosis with hypokalaemia D Metabolic alkalosis with hyponatraemia
E Metabolic acidosis with hyperkalaemia

Explanation

Caused by
urine. *
· Hyperaldosteronism, liquorice / carbenoxolone ingestion (aldosterone-like effects) -

increase renal bicarbonate reabsorption and cause moderate chloride and potassium depletion
*
· Massive blood transfusion - due to metabolism of citrate
· Laxative abuse *
· Therapeutic doses of magnesium trisilicate do not cause alkalosis but excessive use may
cause alkalosis because of the sodium bicarbonate content *
Question 57 Oncotic pressure

Is the plasma osmotic pressure exerted Is the plasma osmotic pressure exerted
A B
by small molecules such as glucose by amino acids
C Is about 2-5 mmHg D Is about 25 mmHg
Is the intracellular pressure needed to
E
maintain cell membrane stability
Explanation
Proteins contribute only ~0.5% to the osmolarity of plasma and much less to the osmolarity of
interstitial fluid which contains little protein. The osmotic pressure exerted by proteins is the
colloid osmotic pressure or oncotic pressure (~25mmHg) *

Aldosterone stimulates potassium Acidosis increases potassium secretion
A B
retention by the kidneys into the renal tubules
Alkalosis increases potassium secretion Insulin inhibits potassium uptake into
C D
into the renal tubules cells
E

Explanation



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This Copy is for Dr.

Question 1 Bladder volume at first sensation to void

Normal cystometric parameters

Question 2 Which one is typically associated with hypokalaemia?

A Release of urinary tract obstruction B Transfusion of stored blood

This Copy is for Dr. Mohamed ElHodiby

C P = plasma concentration of the solute D P = plasma flow rate

E V = volume of solute added

Question 4 With respect to the anatomy of the nephron

· Functional unit of the kidney, ~1.25 million per kidney

This Copy is for Dr. Mohamed ElHodiby

Question 5 Which one increases glomerular filtration rate?

Question 6 Atrial natriuretic peptide

This Copy is for Dr. Mohamed ElHodiby

Question 7 Renal plasma flow is measured by measuring

Question 8 The proximal convoluted tubule

This Copy is for Dr. Mohamed ElHodiby

Question 9 Amino acid excretion by the kidneys

This Copy is for Dr. Mohamed ElHodiby

· The pH of the bicarbonate buffer system is calculated from the Henderson-Hasselbalch

· Hence the pH of a solution containing an equal concentration of bicarbonate and carbon

This Copy is for Dr. Mohamed ElHodiby

• Higher concentration in renal tubular fluid. In addition, pH of tubular fluid is closer to pK of

• Higher concentration in intracellular fluid and pH is closer to pK - becomes more important

Question 14 The intracellular pH is

This Copy is for Dr. Mohamed ElHodiby

Question 16 The anion gap is calculated from the equation

A [Cl-] – [HCO3-] B [Na+] – [K+]

This Copy is for Dr. Mohamed ElHodiby

Question 18 Metabolic acidosis with a normal anion gap occurs in

A Ingestion of ammonium chloride B Salicylate poisoning

This Copy is for Dr. Mohamed ElHodiby

Question 21 With respect to respiratory failure

Question 22 With respect to the regulation of acid-base balance by the kidneys

This Copy is for Dr. Mohamed ElHodiby

RESPIRATORY ACIDOSIS *****

Question 23 The human body contains

Question 24 The plasma volume in females is

A 1.5 liters B 2 liters

BODY WATER *****

This Copy is for Dr. Mohamed ElHodiby

A Falls by more than 4 mOsmol/kg B Rises by more than 4 mOsmol/kg

Question 26 Which one is a recognized cause of hyperkalaemia?

A Conn’s syndrome B Cushing’s syndrome

Plasma osmolarity decreases by ~ 10mOsmol/kg in pregnancy *

• ? Water intake is dependent on body surface area

This Copy is for Dr. Mohamed ElHodiby

A Excessive vomiting or diarrhoea B Syndrome of inappropriate ADH secretion

• ? When osmolarity of body fluid rises by over 4 mOsmol/kg, desire to drink is

Which one is a recognized cause of hyponatraemia with increased

• ? Most of potassium is intracellular *

• ? Potassium uptake into cells is dependent on the activity of Na+K+ATPase -

• ? Renal potassium loss is stimulated by aldosterone which stimulates K+ and H+

This Copy is for Dr. Mohamed ElHodiby

1) Syndrome of inappropriate ADH secretion

Question 30 Prolonged QT interval on ECG is a typical feature of

Question 31 The residual volume of the bladder

This Copy is for Dr. Mohamed ElHodiby

A Over 15 minutes B Over 30 minutes

Question 33 The third stage of labour

This Copy is for Dr. Mohamed ElHodiby

A Early clamping of the umbilical cord B Routine administration of uterotonic drugs