Ahmeds appetite

Part A
It almost noon when Ahmed, 50-year old retired construction engineer, closed his private
office which he started a few years after his retirement and went home.
Oh, Im so tired! Honey, have you finished lunch yet? said Ahmed while smoking his
cigarette for what seemed the fifth time. Yes, its ready! said Mona, Ahmed`s wife.
So, how is your stomach pain? Is it better? asked Mona. It comes and goes, but I feel
less nauseated today. answered Ahmed, while eating his second bite.
Shortly after starting his lunch, Ahmed stands to wash his hands. Just as usual, you have
not finished your plate! Are you sure you did not eat at work, because I spent time in the
kitchen making this meal and now you're barely eating! said Mona. He looked over at
her I'm sorry, I feel somewhat full and a little of discomfort ... He stepped out to the
balcony to have a smoke.
The next day, Ahmed woke up early on the weekend to take some ibuprofen for his
nagging knee pain. Monas voice came I am sorry about yesterday; Ill cook your favorite
meals for dinner tonight. Ahmed replied, Honey, I know that you didnt mean it.
Ahmeds pain increased in the following months, he kept skipping meals and felt
nauseated more often. It reached to a point where Mona became worried about his
weight, seeing that he has lost about kg. Ahmed I am really worried; I think you should
go to the hospital said Mona, but Ahmed refused and thought it was unnecessary.
Two weeks later, Ahmed panicked when he noticed that his stool was black and with
Mona constantly demanding that he visit the doctor, Ahmed finally relented and booked
an appointment.
During the doctors visit, Ahmed was very anxious but once the doctor smiled at him, he
relaxed. I cant eat very well; my stomach pain is very annoying especially after meals. I
feel nauseated very often and my appetite is nonexistent! said Ahmed. I am not my self
anymore.
Dont worry Ahmed, we are going to figure it out. Just relax. said Dr. Nada. Now I need
you to answer some questions, is that OK?

Questions
1- You are a general practitioner in a primary health care clinic and Ahmed has came to
you complaining of the previously mentioned symptoms. Take a thorough history of his
presenting complaint, including his past medical, family, and social history. (Year 2&3) 8 minutes

a. Introduction:
o Introduce yourself name/role, Confirm patient ID, Gain consent,
Ensure the patient is comfortable.
b. Hx of presenting complaint:
o So whats brought you in today?
o WWAAQQ+B and ICE (where, when, aggravating and alleviating
factors, associated symptoms, + beliefs) and (Ideas, Concerns,
Expectations) Or SOCRATE
c. Past medical history:
o Gastrointestinal disease IBD/IBS/malignancy/GERD
o Surgical history e.g. appendectomy/colectomy/c-section
o Travel Hx.
d. Drug and allergy history:
o Laxatives, Proton pump inhibitors, H2 receptor antagonists, Sodium
alginate/calcium carbonate e.g. Gaviscon.
o Recreational drug use, IV drugs.
o NSAIDS, Steroids, Bisphosphonates, contraceptives?
o Any allergies?
e. Family history
o Gastrointestinal disease malignancy/IBD/GERD
o Hereditary bowel conditions HNPCC/FAP
o Other significant medical conditions
f. Social history:
o Smoking, Alcohol, Sexual history.
o Occupation
o Housing, lives with who?
g. Diet Hx:
o Lack of fiber constipation/Gluten celiac disease/Fatty foods.
h. Systematic review:
o Cardiovascular Chest pain/Palpitations/Dyspnea/
Syncope/Orthopnea/Peripheral edema
o Respiratory Dyspnea/Cough/Sputum/Wheeze/Hemoptysis/Chest
pain
o GI Appetite/Nausea/Vomiting/Indigestion/Dysphagia/Weight
loss/Abdominal pain/ Bowel habit
o Urinary Volume of urine
passed/Frequency/Dysuria/Urgency/Incontinence

o CNS Vision/Headache/Motor or sensory disturbance/Loss of

consciousness/ Confusion
o Musculoskeletal Bone and joint pain/Muscular pain
o Dermatology Rashes/Skin breaks/Ulcers

2- After taking the history from Mr. Ahmed you have made a differential diagnosis list.
What are the possible differential diagnoses for Mr. Ahmed's symptoms? (year 3) (10
minutes)

Gastric cancer.
Acute ulcers (occur at times of severe physiological stress e.g. severe
burns/head injury).

GERD. (Gastro esophageal reflux disease)

Drug-induced dyspepsia.

Crohn's disease.

Zollinger-Ellison syndrome (if H. pylori is negative, or has been eradicated

and ulceration is refractory/recurrent).

Irritable bowel syndrome.

Hepatitis.

Chronic pancreatitis.

Gallstones.

Diverticular disease.

Abdominal aortic aneurysm.

Coronary heart disease.

3- After listing your differentials you had to perform physical examination to rule
out some conditions and reach a diagnosis. Perform a physical examination on
Mr. Ahmed and make sure to take consent and ensure his privacy and
confidentiality. Dont forget to take the vital signs (year3) (10 minutes)

As with other systems, positioning of the patient and adequate exposure of

their abdomen is critical when examining the abdomen. When you come to
palpate the abdomen, it is essential that the patient be lying flat with legs
straight and arms by their side. Supporting the patients head with a pillow
will make them more comfortable. It is important to examine the abdomen
from the right side of the patient, even when the examiner is left-handed!
It is virtually impossible to accurately palpate the liver and spleen from the
left side.
The routine for examining the abdomen consists of the same components
used in the examination of the chest and other systems.
o
o
o
o

INSPECTION
PALPATION
PERCUSSION
AUSCULTATION

INSPECTION:
o Make sure that your subject is suitably positioned (i.e. lying flat),
then examine as follows:
o ANY SCARS (note type and position)
o STRIAE (stretch marks)
o DISTENSION
o CONTOURS
o UMBILICUS
o VEINS
o PULSATIONS
o VISIBLE PERISTALSIS
o PAIN ON COUGHING
o PAIN ON STRAIGHT LEG RAISING
PALPATION:
o Start by identifying the regions which the abdomen is divides.
o Different organs and intra-abdominal structures can
characteristically be palpated in each of these regions. Before
commencing palpation, the subject should be: relaxed, Warm and
dont forget to ask the patient to point to any area that is tender.
o Usually the routine palpation moves in an orderly fashion through
each of the regions or quadrants. However, if the patient identifies
an area of tenderness it is best to start AWAY from that point and
finish with the tender region.
o When palpating look for:
- Areas of guarding/rigidity

Cross tenderness
Rebound tenderness
Palpable masses

PERCUSSION:
o Percussion is used to:
Define the sites of major organs (liver, spleen, kidneys and
bladder)
Detect the presence of ascites (fluid in the peritoneal cavity)
i.e. shifting dullness
AUSCULTATION:
o Using your stethoscope, listen to your subject's abdomen and
identify the following:
BOWEL SOUNDS: Normal abdominal sounds are soft, gurgling,
intermittent and their frequency varies depending on when the
last meal have been eaten. Loud, high pitch sound, with
tinkling quality indicates obstructed bowel. Complete absence
of bowel sound for 4 min indicates paralytic ileus.

SITE OF AORTIC AND RENAL BRUITS: Renal bruits heard above

umbilicus ~2-2.5cm to right or left of midline using the
diaphragm of the stethoscope. The presence of bruits may
indicate narrowing of these arteries that would require further
investigation.

4- You had finished examining Mr. Ahmed and ruled out some differentials. You
have requested some lab investigations. After getting the results you have
made a certain diagnosis which is "peptic ulcer. What do you know about peptic
ulcers? (year 2&3) (-7 minutes).
Definition: It is a condition of painful sores or ulcers in the superficial epithelial
cells penetrating down to the muscularis mucosa in the stomach or duodenum .
Causes:
-

infection by Helicobacter pylori (H. pylori)

Frequent use of nonsteroidal anti-inflammatory drugs (NSAIDs)( NSAIDs can

cause damage to the gastroduodenal mucosa via several mechanisms:
impairment of the barrier properties of the mucosa, suppression of gastric
prostaglandin synthesis, reduction of gastric mucosal blood flow and interference
with the repair of superficial injury, impairing the restitution process, interfering
with hemostasis and inactivating several growth factors that are important in
mucosal defense and repair.)
-

smoking

- Excessive drinking of alcohol

- radiation therapy
- Excess acid production from stomach cancer
- what are the signs and symptoms of peptic ulcer disease ( not necessary all
present in the case) ?
Burning sensation or pain in the area between the chest and umbilicus (
epigastria)
dull pain in the stomach
Loss of appetite.
bloating
burping or acid reflux
Heartburn (burning sensation in the chest.
Other signs and symptoms
Less often, but ulcers may cause severe signs or symptoms such as:

Vomiting of blood which may appear red or black

Dark blood in stools or stools that are black or tarry

Epigastric tenderness.

Nausea or vomiting

Unexplained weight loss

Appetite changes

5- After you have made your diagnosis, you received a call from your consultant
and he was very high tempered he is the type that wants everything to be
perfect he won't allow any mistakes. he asked you to come by his office
and asked you the following questions:( year 3) ( 15-20 minutes)
- what is the pathophysiology of peptic ulcer disease?
Ulcers may occur with hypersecretion of hydrochloric acid and pepsin, causing
imbalance between gastric luminal factors and degradation in the defensive
function of the gastric mucosal barrier, when acid and pepsin invade a weakened
area of the mucosal barrier, histamine is released. Histamine will stimulate
parietal cells to secrete more acid. With the continuation of this vicious cycle,
erosion occurs to form the ulcer.

- He showed you the following picture and asked you to briefly describe the
anatomy of the stomach and duodenum:

Present in left hypocondrium, and

epigastrium (pain felt here).
4 parts: fundus, body, antrum and pylorus.
2 opening: cardiac and pyloric orifices.
Cardiac orifice have only physiological
sphincter. However, the pyloric orifice have
both anatomical and physiological sphincter.
2 curvatures: greater and lesser curvatures.
2 Surfaces: Anterior and posterior Surfaces.

Boundaries:

Anteriorly: liver, diaphragm and anterior

abdominal wall.
Posteriorly (stomach bed): transverse colon, transverse mesocolon, pancreas +
splenic artery, spleen, left kidney and suprarenal gland left part of diaphragm
and the lesser sac.
Blood supply: right and left gastric arteries supply the lesser curvature.
Right and left gastroepipolic arteries supply the
.greater curvature
.Short gastric artery which is derived from splenic artery supply the fundus
Venous drainage into the portal circulation.
Lymphatic drainage: left and right gastric node, left and right
gastroepipolic node and short gastric node. Eventually, all lymphatic from
the stomach reach celiac node.
Ascending
L3-L2
Duodenojejunal
.flexure

Duodenum parts
Inferior
Descending
L3
L1-L3
Cross the
Around the
inferior vena
head of the
.cava and aorta
.pancreas
Posterior to Major duodenal
superior
papilla
mesenteric
ampulla
.artery

Superior
L1
Duodenal ulcer
.common site

Blood supply:
Upper part of duodenum by superior pancreaticoduodenal Artery. Its
vein drainage to portal vein.
- Lower part of the duodenum by inferior pancreaticoduodenal artery. Its
vein drainage to superior mesenteric vein which also drains into the
portal vein.
Lymphatic drainage:
Upper part: pancreaticoduodenal nodes => gastroduodenal nodes =>
celiac nodes
Lower part: pancreaticoduodenal nodes=> superior mesenteric nodes
-

- he asked you also on how acid is secreted?

The stomach parietal cells secrete H+ and Cl- by the action of two separate
pumps. H+ is secreted to the lumen by mean of H+ K+ ATPase active transporter
pump, the H+ secreted is coming from breaking down of H2O into OH- and H+.
The OH- combines CO2 -either from cellular metabolism or plasma- to form HCO3.
Cl- is secreted by secondary active transport. Driven by the HCO3- concentration
gradient HCO3- is transmitted into the plasma while Cl- get into the parietal cell
and then to gastric lumen.

- The consultant pinpointed on the mechanism of referred pain of peptic ulcer

and asked you to explain the mechanism:
The nerves which supply pylorus and first part of duodenum relay on the same
segments by which the nerves that sxsq `upply skin of epigastria thus when pain
is produced in pylorus or duodenum the afferent will travel to spinal cord

segments and from there the efferent will travel to the epigastria so pain is
sensed there.

6- Luckily you have answered all of the consultant's questions correctly and was
allowed to be dismissed from his office. He also gave you the permission to start
treating the patient. ( year 2&3) (15-20 minutes).
what are your first line options of treatment:
1-reduce stress
2- quit smoking
3- lose weight
4- avoid eating heavy greasy meals
5- avoid eating before sleeping
- but since Mr. Ahmed is already has a bleeding stool, you should evaluate his
hemodynamic status and start treating him immediately. list the available drugs, and
what will be the first line:

Treatment: A- antisecretory agents:

1- H2 receptor antagonist: revesible competitive inhibition of H2 receptors.
Very effective in inhibiting nocturnal acid secretion. Inhibit histamine, gastrin
& Ach (less than PPI).
Promotes healing of duodenal ulcers. Drugs end with tidine.
.Cimetidine may interfere with hepatic metabolism. Renal excretion
2- *Proton-pump inhibitor: block acid secretion by irreversibly inactivating H/K
ATPase pump at the parietal cell surface. Weakly basic, activated in canaliculi
of parietal cells. Most effective treatment. Drugs end with prazole. Not
administred with other acid suppressors. Extremely safe, inhibits CYP450.
Pantroprazole & rebeprazole have no significant interactions.
3- Others: antimuscarinics (significant SE), Gastrin antagonist (low
effectiveness) & somatostatin analogues (require parenteral administration)
:B-Cytoprotective agents & mucosal strengtheners
1- Sucralfate: adheres to ulcer & acts as a barrier. Stimulates mucosal
protective mechanisms. Antacids & meals shouldnt be taken within30 min of
administration. AE: constipation & inhibits absorption of some drugs.
2- PG analogues: E & I PGs generally protective, inhibit acid secretion &
increase mucus & blood flow. Misoprostol: PGE analogue, used in patients
using NSAIDs w/high risk of ulcer. AEs pain sensitization, uterine contraction
(CI in pregnancy), diarrhea, headacheetc.
3- Bismuth Chelate: not 1st line, used in combination. Forms precipitate which
binds to ulcer forming a barrier; enhance PG synthesis, stimulate mucus &
bicarbonate secretion. Also has moderate direct antimicrobial activity against

H.pylori. SEs inc. black stool & tongue, damage to kidney & CNS (bismuth
toxicity). Dont take w/meals, antacids or other meds.
4- Carbenoxolone: derived from liquorice root. Accelerate healing of gastric
ulcers & promotes the production of mucus. Significant SEs: mineralcorticoid
effect (Na & H2O retention) hypertension, alkalosis, & hypokalemia.
Precipitate to glaucoma & urinary retention.
5- Antacids: simplest, weak base to raise pH & inhibit formation of pepsin. Most
effective against duodenal ulcers. AlCl 3(constipation) or MgCl2(diarrhea) or
both. Take antacids 2h before of after other drugs. Some additives are added
with antacids including:
Alginatesfoam layer over gastric contents to reduce reflux.
Simeticonereduce bubble formation to prevent reflux.
.OxethazaineSurface anaesthetic
since he is using NSAIDs, He should continue using PPIs or +
,prostaglandin analogues
.or replace NSAIDs with COX-2 inhibitors to avoid reoccurrence
.If the patients Hb level is low start resuscitation
You also ordered Urea breath test, to investigate for helicobacter pylori infection, and it came back positive. What is the treatment

?plan now
Bismuth, Amoxicillin, clarithromycin, tetracycline, &
.metronidazole
Triple regime of PPI, Metrondiazole, & amoxicillin or clarithromycin is used
with >90%
- why antibiotics are used in combinations?
Natural (Biological) Causes
Selective Pressure
In the presence of an antimicrobial, microbes are either killed or, if they carry
resistance genes, survive. These survivors will replicate, and their progeny will
quickly become the dominant type throughout the microbial population.
Mutation
Most microbes reproduce by dividing every few hours, allowing them to evolve
rapidly and adapt quickly to new environmental conditions. During replication,
mutations arise and some of these mutations may help an individual microbe
survive exposure to an antimicrobial.

Gene Transfer
Microbes also may get genes from each other, including genes that make
the microbe drug resistant.
Societal Pressures

The use of antimicrobials, even when used appropriately, creates a selective

pressure for resistant organisms. However, there are additional societal
pressures that act to accelerate the increase of antimicrobial resistance.
Inappropriate Use
Selection of resistant microorganisms is exacerbated by inappropriate use of
antimicrobials. Sometimes healthcare providers will prescribe antimicrobials
inappropriately, wishing to placate an insistent patient who has a viral infection
or an as-yet undiagnosed condition.
Inadequate Diagnostics
More often, healthcare providers must use incomplete or imperfect information
to diagnose an infection and thus prescribe an antimicrobial just-in-case or
prescribe a broad-spectrum antimicrobial when a specific antibiotic might be
better. These situations contribute to selective pressure and accelerate
antimicrobial resistance.
Hospital Use
Critically ill patients are more susceptible to infections and, thus, often require
the aid of antimicrobials. However, the heavier use of antimicrobials in these
patients can worsen the problem by selecting for antimicrobial-resistant
microorganisms. The extensive use of antimicrobials and close contact among
sick patients creates a fertile environment for the spread of antimicrobialresistant germs.
Agricultural Use
Scientists also believe that the practice of adding antibiotics to agricultural feed
promotes drug resistance. More than half of the antibiotics produced in the
United States are used for agricultural purposes.1, 2 However, there is still much
debate about whether drug-resistant microbes in animals pose a significant
public health burden.
- How does H. pylori cause ulcers?
H. pylori are adapted to live in the harsh, acidic environment of the stomach.
These bacteria can change the environment around them and reduce its acidity
so they can survive. Which allows them to penetrate the stomach lining and
cause ulcers.

- Mr. Ahmed asked you about the possible complications of peptic ulcer if it
was untreated, so you answered him by:

1-obstruction
2- perforation (posterior wall of the stomach => perforate to pancreas =>
erosion to splenic artery => back pain and fatal hemorrhage)
3- atrophy gastritis
4- gastric malignancy
- He also asked you how come in normal conditions gastric acid don't cause
damage to stomach lining?