First Edition

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,yIw,I Iazt :
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angelic_doc
DR.JENEFER
N.S.G
amoona
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doctor_ology
Dr.Noura
Dr.ambition
Dr. ShoSho
Dr-E
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The One
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Dr.eyelash
dr.Jet
December 2007

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Contents


I- Cardiovascular diseases:
Myocardial infarction . 6
Stable angina . 11
Unstable angina . 12
Prinzmetal's angina 12
Heart failure ....... 14
Restrictive Cardiomyopathy .. 17
Hypertrophic Cardiomyopathy .. 17
Dilated Cardiomyopathy .... 17
Rheumatic Heart Disease ... 18
Hypertension .. 22
Atrial fibrillation 27
II- Respiratory diseases:
Asthma ... 36
COPD . 39
Respiratory failure .. 42
III- Renal diseases:
Renal failure .. 48
Nephrotic syndrome .. 56
IV- Gastroenterology & Liver disease:
Diarrhea .... 58
Inflammatory Bowel Disease ....64
Chronic Liver Disease Dr.Maimoona ............72
Chronic Liver Disease, Hepatitis Dr.Akbar .............. 82
V- Endocrinology:
Hypothyroidism 97
Hyperthyroidism ... 99
Addison's disease ..103
Diabetic ketoacidosis (DKA) ...... 105

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VI- Rheumatology:
Arthritis / connective tissue diseases... 110
Septic arthritis...... 110
Seronegative arthritis....110
Seropositive arthritis ....112
SLE ..112
Rheumatoid Arthritis....113
Smart Rheumatology Questions...120
VII- Neurology:
How to take: quick perfect neuro- history 123
Localization of site of lesion .... 126
Stroke / CVA 129
Upper Motor Neuron Lesion 139
Polyneuropahties .. 144
Acute Confusion State .. 146
VIII Other:
Deep Venous Thrombosis 150

























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C ar dio v as c ul ar
dis eas es

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IHD
Dr.Maimoona
1- Stable angina.
2- Unstable angina.
3- Prinzmetal's angina.
4- Myocardial Infarction.
5- Heart Failure.
MI
Acute complications:
1- Heart failure.
2- Arrhythmia.
3- Pericarditis.
4- Hypotension.
5- Valvular heart disease (papillary muscle, ventricular septum).
Chronic complications:
- Ventricular aneurysm:
ST elevation > 6 weeks after MI:
Differential: 1- re infarction 2- developed ventricular aneurysm.
- Dressler's syndrome:
o muscle necrosis antigen antibody reaction autoimmune disease.
o shoulder joint pain , serositis.
o ttt: steroid.
Suspected ventricular aneurysm:
1- ECG > 6 weeks ST elevation.
2- Thromboembolism manifestation ( blood stagnant).
3- Recurrent HF not responding to medication.

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History:
You should include in HPI:
* 1-DM.
2- HTN.
3- Hyperlipidemia.
4- Smoking.
5- Family history of IHD.
* Chest pain duration > 30 minutes.
Examination:
1- Vitals:
Blood Pressure: high Blood Pressure in HTN, MI may cause low BP.
Pulse: Arrhythmia.
Temp.: sometimes increase in MI.
2- Look for:
* Heart failure evidence:
Increase JVP, 3
RD
heart sound, basal lung crepitations, ascites,
hepatomegaly, lower limb edema.
* Valvular heart disease evidence: valve incompetence, VSDetc.
* Pericardial rub on auscultation.
3- Look for underlying disease:
- DM complications.
- Atherosclerosis.

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Investigations:
1-ECG:
*- type of MI: anterior, posterior, inferior etc.
*- pericarditis.
*- arrhythmias: AF, ventricular ectopic, ventricular tachycardia, LBBB, RBBB,
2
nd
degree heart block, complete heart block.
*- evidence of previous ischemia if pt. has previous MI, the new ECG
changes will NOT show then do Cardiac Enzymes.
2- Cardiac enzymes: to be raised
time of each enzyme is important & common question in exams
C troponine immediate 30 minutes- 1 hour (earliest to rise + more
sensitive).
C CPK 4 hours + CPK-MB ratio.
C LDH 72 hours.
3-chest x-ray cardiomegaly, HF: pulmonary edema, pleural effusion.
4- Blood sugar.
5- Lipid profile.
6- PT, PTT (base line).
7- Urea & electrolytes: baseline ttt. or complication.
8- CBC: leukocytosis.

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Treatment:
Typical history of retrosternal chest pain.
1- Chewable aspirin before investigation, will not kill pt. & will benefit + O2.
2- Relief pain: morphine & antiemetic.
3- & start tridine infusion to relief pain, vasodilation.
4- antithrombolytic therapy if no contraindication.
*review the contraindication from textbook*
After stabilized:
Before discharge:
1- Echocardiogram for: (why do we do echo?)
* Valvular heart disease.
* Ejection fraction abnormality < 50 low.
It should be around 50 normal.
* Wall motion abnormality hypokinesia:
Heart not contract at site of infarction, generalized in cardiomyopathy.
2- (Before not nowadays) submaximal stress ECG.
This is to do exercise for 10 minute= submaximal (maximal test is 30
minutes) to see if complications develop: 1- arrhythmia
2-hypotension
This was done before to decide if argent angiogram will done or delayed 4-5
weeks.
But now all patients i.e. MI. should have angiogram angioplasty dilation or
bypass surgery. The earlier, the better the prognosis.

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Role of thrombolytic therapy & angiogram:
If the time from ER door to angiogram more than 90 minutes, don't waste
time give thromolytic therapy.
If the time within 90 minutes immediately for angiogram.
Home medication:
2ry prevention of MI 4 medication
1- Aspirin
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
+/- lasix.
Management of MI (briefly for 5
th
year):
1- Admit patient to the ICU & give O
2
oxy-bed rest.
2- Prescribe painkillers.
3- Thrombolytic therapy streptokinase resolve the thrombus
..


4- angiogram & angioplasty (if possible, in good centers, & good
primary care units)
5- discharge on:
4 medications:
1- Aspirin.
2- B-blocker.
3- ACE Inhibtors.
4- Statin.
+/- Lasix.


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Stable Angina
ER.
Same History, Examination, Investigation of MI.
If NO MI.
Sublingual nitroglycerin & 4 drugs:
1- Aspirin.
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
Send home
Dr. Nabeel likes to ask about angina?
1- Typical angina: have 3 things :
a- Site.
b- Nature.
c- Increased by exertion and decreased by rest.
2- Atypical angina: have got two out three.
3- Non-Anginal chest pain: just one thing.

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Unstable angina
- Same History, Examination, Investigation of MI.
- Heart enzymes not rise & evidence of ST segment depression ischemia on
ECG.
TREATMENT:
Tridile infusion & heparin infusion.
Start by:
1- Aspirin.
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
If the pain does not improve a cardiologist orders an urgent angiogram.
Angioplasty& pain control.
Prinzmetal's angina
Same History, Examination, Investigation of MI.
1- ST elevation.
2- Normal cardiac enzymes.
- No risk factors of MI, no DM, no HTN.
ttt: put on calcium channel blocker.
**BUT** IT SHOULD BE TRATED AS ANGINA unless proven otherwise.
ECG no change Q wave for 6 hrs for 24 hrs, then every day.
Cardiac enzyme no rise, Q6 hrs.
Until angiogram shows normal coronary.

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ECG differences:
[1] Angina:
ST depression
Cardiac Enzymes Normal
[2] Unstable angina:
T-wave changes
Cardiac Enzymes Normal
[3] Prinzmetal's angina:
ST elevation due to spasm
Cardiac Enzymes Normal
[4] MI:
ST elevation
Cardiac Enzymes elevated

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Heart Failure (HF)
Dr. Nabeel
Eight Causes are preferable to be Heard by any Students when Dr. Nabeel
Al-a3ma asks about the causes of HF?
1- Ischemic Heart disease (IHD) which is the commonest.
2- HTN or Hypertensive Heart disease with end Organ damage.
3- Valvular Heart diseaseand the commonest cause is Rheumatic heart
disease.
4- Cardiomyopathy.
5- Congenital heart disease.
6- Core-pulmonale.
7- Constrictive pericarditis.
8- Heart failure with high cardiac Output... Like in Thyrotoxicosis,
anemia.
Also He loves to ask this Question:
Patient is known having HF... What are the causes that push him to a failure
and to the ER i.e.: what are the precipitating factors for HF?
1- Infection (pneumonia).
2- P.embolism esp. if he's bedridden.
3- Ongoing Ischemic heart diseaseMI.
4- No compliance with medications.
5- Arrhythmia.
6- Taking NSAID. Which cause salt and water retention.
7- Taking ca channel blockerNegative inotropic agent.
8- High salt intake.
9- Uncontrolled HTN.
10- Hyperdynamic circulation.. Like in anemia... Thyrotoxicosis.

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History in ER:
No History suggestive of IHD.
Known case of HF.
No History of palpitation.
Pt was compliant to his medications.
No change in diet.
That is important to mention in History,

Examination:
Same of MI.
Look for evidence of heart failure - arrhythmia - infection -underlying
cause.
Investigation: like MI
Same Q with Dr. Maimoona, but she only mentioned these:
This way, the pt got acute HF...
1- IHD.
2- Hyperdynamic circulation anemia, Thyrotoxicosis.
3- Valvular heart disease.
4- HTN.
5- Arrhythmias.
6- Increased salt intake.
7- No compliance to drugs.

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Management:
On admission:
1- Start loop diuretic fursemide 40 mg TID.
2- Start spironolactone 25 mg take 3 days to work
in HF, nephrotic $, liver failure low kidney perfusion activate renine-
angiotensin system.
Spironolactone will block it so no Na/H2O retention & not used as K sparing.
+ 4 drugs:
(1) Aspirin.
(2) B-blocker.
(3) ACEI.
(4) Statin.
Note: moderate/sever HF do not give B-blocker.
If echo show ejection fraction below 25% you have to give anticoagulant.

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Restrictive Cardiomyopathy
Infiltration of myocardium: TB, hemochromatosis, amyloidosis.
ttt: treat underlying cause.
Hypertrophic Cardiomyopathy
ttt: B-blocker & - Amiodarone.
Dilated Cardiomyopathy
As heart failure.
- Diuretic
4 drugs:
1- Aspirin.
2- B-blocker.
3- ACEI.
4- Statin.
- anticoagulants
Causes:
1- Ischemic.
2- Alcoholic.
3- Thiamin deficiency.

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Rheumatic Heart Disease
RHD
Session with Dr. Maimoona
2006
(1) Major:
- Carditis
- Arthritis
- Erythema marginatum
- Chorea
- Subcutaneous nodules
(2) minor:
C History of tonsillitis
C Fever
C Raised C-reactive protein
C Raised ESR
C Arthralgia

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* ask about: rheumatism, recurrent tonsillitis, IV Penicillin monthly, long bed
rest
[1] Carditis: if all 3 layers are involved Heart Failure
Tachycardia
[2] Chorea: Sydenhams chorea (abnormal movement)
[3] Arthritis: fleeting arthritis: redness, hotness improvement
But before cure involvement of another joint
[4] Erythema marginatum: rash w/ very clear margins
Investigations:
- CBC show leukocytosis
- Streptococcal antibody tests
- blood culture & throat culture looking for group A streptococcal
infection
- ESR & C-reactive protein high
- ECG PR interval prolongation
- Echocardiography establishing cordites
- Synovial fluid analysis elevated white blood cell count with no crystals or
organisms
- X-ray cardiomegaly or evidence of heart failure
- X-ray of joints only when there is mono joint involvement []

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Complications of rheumatic fever:
1- Valvular Heart Disease:
(1) Mitral (2) Aortic (3) Tricuspid (4) Pulmonary
Infective endocarditis most important
Infective endocarditis multisystem disease
Renal failure, heart failure, jaundice, brain involvement
(Multiorgan failure)
2- Heart failure
3- Arrhythmias
4- Thromboembolic manifestations

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Treatment
- Bed rest
- High dose aspirin. The nonsteroidal anti-inflammatory drug (NSAID)
naproxen has also been studied. It is effective and may be easier to use than
aspirin.
- Penicillin then long term to patient with persistent cardiac damage
- Heart failure may require digitalis
- Haloperidol may be helpful in controlling chorea.



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Hypertension (HTN)
Session with Dr. Maimoona
1424 H
95% essential HTN
5%
R: Renal:
- Polycystic Kidney Disease
- CRF
- GlumeruloNephritis
- Renal Artery Stenosis
- Renal Cell Carcinoma
E: Endocrine:
- Cushing's
- Pheochromocytoma
- Acromegaly
- Thyrotoxicosis
- Conn's
- Carcinoid tumor
- Hyperparathyroidism
- Primary hypothyroidism
- Congenital adrenal hyperplasia
C:
- Corticosteroids
- Contraceptive pills
- Clonidine withdrawal
- Coarctation of aorta

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A:
- Arteritis (eg. Takaiaso)
- Alcohol
P:
- Pregnancy
- Polycythemia rubra vera (PRV)
D: Drugs:
- NSAIDs
- Sympathomimitics
* Refractory "Resistant" HTN:
3 anti-HTN medications with maximum dose. One of them is Diuretic for 3
months
Examination:
Inspection:
- Acromegaly
- Cushing
- Thyroid
Palpations:
- Renal "for polycystic"
- Radio femoral artery "Coarctation"

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auscultation:
Renal bruit for tumor, renal aneurysm
Then look for an end organ damage
Heart "apex beat"
Eye for papilloedema
Investigations: in all patients with HTN
(1) U & E:
+
- Conn's
- Pheochromocytoma
- Cushing
+ CRF
(2) Blood glucose hyperglycemia DM
(3) Urinalysis (Active sediments):
- RBC cast
- Haematuria
- Proteinuria
(4) Lipid profile atherosclerosis
(5) CXR
- Cardiomegaly
- Coarctation of aorta

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(6) ECG Left ventricular hypertrophy
(7) Echo Left ventricular hypertrophy
------------------
Serum urea & Creatinine: RF
Serum uric acid before ttt with diuretics:
If the patient has hyperuricemia diuretic therapy is contraindicated
Cushing:
Overnight suppression test
Or
24 hrs urine cortisone
If you're suspecting it's secondary to a Connective Tissue disease
screening must be made.
Main diagnosis for renal artery stenosis:
(The most common cause of HTN in young patient)
1- Doppler US
2- INP = delayed uptake
3- Captopril renogram
4- Angiogram
Pheochromocytoma: Investigation:
Chatecholamines either in urine or blood
CT for the abdomen localize the tumor
If not localized, do adrenal venous sampling to localize

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GENE
RAL
Vasodilators

-blocker
diuretic
Treatment: step one management


- IHD: ACE inhibitor &/or B-Blocker
- DM: Diltiazam verapamil
Never use Dihydro__?_____ in HTN & DM patient, because they worsen
proteinuria:
- Amlodipin
- Nifidipin
HTN Emergency:
HTN + Brain Hemorrhage don't lower the Blood Pressure rapidly
HTN + HF lower the Blood Pressure




-methyl dopa poor or pregnant
ACE inhibitors
-blockers
Hydralazine
Thiazide

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Atrial fibrillation (AF)
Definition: It's totally chaotic atrial activity caused by simultaneous
discharge of multi atria foci.
Causes:
A- Cardiovascular :
1- HTN.
2- IHD (including acute MI).
3- Valvular heart disease esp. Rheumatic "Ms, MR, AS, AR".
4- VSD.
5- Cardiac surgery.
6- Inflammatory heart disease "pericarditis, myocarditis".
7- Cardiomyopathy.
8- Left atrial myxoma.
9- Sick sinus syndrome "tachy-Brady syndrome".
10- WPW syndrome (wolf Parkinson white).
B- Endocrinological causes:
1- Thyrotoxicosis.
2- Pheochromocytoma.

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C- Pulmonary causes:
1- P.E.
2- Pneumonia.
3- COPD
4- Co poising.
5- Ca of the Bronchus.
D- Drugs:
1- Acute or chronic alcohol.
2- Theophylline toxicity.
E - Idiopathic:
Lone AF in which no cardiac cause can be identified, no DM, no HTN and no
CAD.
Symptoms of AF:
1- Asymptomatic.
2- Symptoms vary from Palpitation and SOB and aggravating of HF.
3- Embolization symptoms.

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Investigation:
1- Thyroid function test.
2- ECG absence P wave + Irregular R-R interval more than 100.
3- U and E if hypo K dont give digoxin because it will lead also to
arrhythmias.
4- PT and PTT.
5- Cardiac enzymes.
6- CXR p. edema.
7- Echo so in here we're doing:
A- Assess etiology and recurrence of:
1- Cardiac chamber size and function i.e.: left atrium.
2- Valvular function.
3- The pericardium.
4- The myocardium.
B- Identification of patient at high risk of thromboembolism
complication of AF.

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Management of AF:
1- Treat the cause.
2- How to Control Ventricular rate ( VR)?
3- How to convert to sinus rhythm?
4- How to maintain sinus rhythm?
5- When and How to use anticoagulant and antiplatlets?
Types of AF:
1- Isolated one single".
2- Paroxysmal don't give digoxin.
3- Sustained one chronic.
So the Management:
If the Patient is not stable Do DC cardioversion.
If stable follow that previously mentioned points.
So,
1- Treat the cause.

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2- Control Ventricular rate By A-V node blocking Drugs:
A- Digoxin:
- Loading dose: 0.25 - 0.5 mg/30mints IV.
- Maintenance: 0.125 - 0.25 mg/6h.
- Contraindication of Digoxin:
1- HOCM.
2- WPW so in here use procainamide.
3- Narrow QRS atrial tachycardia.
- Digoxin dose: in Normal Patient: 0.25 mg, and in renal disease: 0.06 -
0.125 mg.
B- B-Blocker:
Usually given with Ca channel blocker because more rapid control. But
digoxin is more preferable in the setting of LVF or HF.
So, propranolol 0.5 mg IV followed by IV bolus 1 mg every 5 mints till
???
The contraindication of B-blocker is:
Asthma, Dm and HF.
C- Ca Channel blocker:
Verampil 5 10 mg bolus / 10 mints.
If you want to give verampil + digoxin decrease digoxin dose.

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3- Convert to Sinus Rhythm:
Indicated when VR is more than 140 B/m.
The drugs used in here:
- Class 1a: Quinidine - procainamide.
- Class 1c: Flecainide - propafenone
- Class 3: Amiodarone
So the preparation:
1- Start Quinidine at least 24 h before to help maintain NSR once it's
achieved.
2- Hold Digoxin and check its serum level.
3- Anticoagulant 3 weeks before and after if there's thrombus shown
in echo.
Indications for anticoagulation: Clinically and ECG:
Clinically:
1- Previous MI or Stroke.
2- HTM +/- Dm.
3- Previous MI.
4- Thyrotoxicosis in here, decrease the Warfarin dose because of
increased clearance of vitamin K in Hyperthyroidism.

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EchoCardioGraphically:
1- Large Left atrium or Left atrium dysfunction.
2- Large Left Ventricle.
3- Left Ventricle aneurysm.
4- Intracardiac Thrombus.
Complications of cardioversion:
1- Ventricular fibrillation.
2- Thromboembolism.
3- MI damage due to the Current.
4- Erythema on the chest wall.
Risk of Systemic Embolization with AF is divided to:
- High: when Mitral valve disease seen: previous Mi or stroke.
- Intermediate: age more than 65 or RF.
- Low risk: age less than 65.

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4- Maintenance of sinus rhythm is better with:
1- Left atrium less than 60 mm.
2- Absence of mitral valve dis.
3- Short AF.
4- Conversion with drug only.
Please see the classes of anti-arrhythmic drugs.

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R es pir at o r y
dis eas es

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Management of asthma in ER
HISTORY: mainly history of the etiology of the disease.
[1] Drugs
1. B-blockers
o Propranolol
o Atenolol
o metoprolol
2. NSAID
o ASPIRIN (acetylsalicylic acid)
o VOLTARINNE (DICLOFENAc)
[2] CHEST INFECTION
[3] Irritants animals + dust + fumes + house dust mite
[4] Newly changed furniture + painting
[5] Exercise
[6] Occupation

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EXAMINATION:
1- Vital signs
a- Pulse tachycardia, arrhythmias
b- Blood pressure, palsus paradoxes
c- Tachypnea
d- Temperature increase infection
2- General examination
a- Tremor
b- Cyanosis
c- Accessory muscles
3- Signs of Pneumothorax You fail if you don't mention
them!!
4- Severity of asthma
(1) Signs of infection
(2) Signs of status asthmaticus
1- Silent chest
2- Drowsiness
3- Cyanosis
4- Tachycardia > 120
5- Pulsus paradoxus

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INVESTIGATIONS: {FOR ALL ASTHMATICS}
1- CBC LEUCKOCYTOSIS + EOSONEPHILIA
2- ABG
3- U+E
a- Hyperventilation dehydration
b- 2-agonist
c- Theophyllin
d- Sputum + steroid
4-CXR INFECTION, PNEUMOTHOARX
5-ECG ARRHYTHMIA + hypertrophy
6-Pulmonary function test
7-Peak flow meter drop inonter base
8-Sputum culture
9-Positive skin
Note:
Mg, Ca, and Ph are not part of U-E

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MANAGEMENT:
1- Bed rest
2- Oxygen according to blood gases
(1) DecreaseO
2
+decrease CO
2
(2) DecreaseO
2
+normal CO
2
(3) DecreaseO
2
+IncreaseCO
2
3- I.V FLUID
4- KCL DECREASE K
5- Pharmacological medications
(1) Bronchodilator
a- B2 agonist
b- Nabulizar
c- Salbutamol - terbutaline SlE: TACHYCARDIA
FOR 24hours / hourly
d- Anti-cholenergic drugs
Ventolin/atrovent
Ibratropum promide
Decrease mucus secretion
f- I.V Theophyllin "narrow therapeutic index" bronchodilator
increases contractility and diaphragm
{A} IF PATIENT RECEIVES ORAL THIOPHYLIN AT HOME
MANTINANCE DOSE SHOULD BE STARTED IMMEDIATILY
{B} IF PATIENT DOES NOT TAKE THIOPHYLIN AT HOME
BOLUES 5-6 Mg/kg/30 min
Maintenance 0.2-0.6 mg/kg/hour
IF AFTER 4 HOURS THE PATIENT DOES NOT IMPROVE
MECHANICAL VENTILATION


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(2) +/- Antibiotics:
If there are sought of infection mainly H.influenza + streptococci
We USE AMPICILLIN G (positive) OR G (negative)
(3) Anti inflammatory
Hydrocortisone 100-200mg/4hours for 24 hours (IV)
Then prednisone 60mg/orally daily for 2 weeks
Discharge on B-agonist in halor +steroid inhalor
Present to the CLINIC History: exercise tolerance decrease and change
color of sputum
Investigation PEAK Flow meter
COPD
The management of COPD is the same as that of bronchial asthma
EXCEPT the concentration of O
2
to be delivered to the patient.
In patient with COPD chronic hypercapnia chronic stimulation of
respiratory center, so, when you admit the patient you must increase
the conc. Of O2
YOU should wash out the remnant of hypoxemia which stimulates the
drive for ventilation worsening hypercapnia
Note:
A PATIENT WITH HYPERCAPNIA CHRONIC COPD SHULD RECEIVE LOW
CONCENTRATION OF O
2
(24-28%) THEN ADJUST ACCORDING TO "ABG"
ASTHMA NO CHRONIC HYPERCAPNIA SAFE TO GIVE INCREASE
CONCONCENTRATION OF O
2
(60%)

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SIGNS OF SEVERE ASTHMA "STATUES ASTHMATUCUS"
1- Patients are unable to speak (cannot give history), inability to complete
sentences
2- Silent chest
3- Pulses paradoxus
4- Tachycardia
5- Pulse>120
6- Use of accessory muscles of respiratory
7- R.R >33
8- Drowsiness - exhaustion
9- Cyanosis
COMPLICATION:
1- DEHYDRATION
2- EXHAUSTION
3- PNUMOTHORAX
4- RESPIRATORY FAILUER

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Respiratory failure
** Influence on respiratory center
Hypercapnia = P CO
2
> 6 kPa = > ~ 5 mmHg


Stimulation Depression
(1) Voluntary over breathing.
(2) Upper brainstem lesion.
(3) Input from receptors (pain,
muscles, and joints,
pulmonary).
(4) Pyrexia.
(5) PaCO2
(6) Pa O2
(7) Arterial H+ concentration.
(1) Voluntary hold breathing
(2) Brainstem lesion.
(3) Hyperthermia
(4) Sedative Drugs
opiates Benzodiazepin
(1) Hypoventilation = Depression in Respiratory center in medulla
(2) Ventilation- perfusion mismatching = COPD

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Acute
Chronic
PaO
2

Pa CO
2

HCO
3

PaO
2

PaCO
2

HCO
3

** Respiratory Failure: A disorder of the lungs where the lungs dont
function accordingly to match the metabolic requirements.
Type 1 (hypoxia & hypo or normal CO2)


Type 2 (hypoxia & hypercapnia)


***Asthma (severe) **Emphysema
PE Lung fibrosis
P. edema R L shunt
ARDS Anemia
Pneumothorax
Pneumonia
Acute Chronic
Pa O
2

Pa CO
2
or
HCO
3

Pa O2
Pa CO2
HCO3
Severe acute asthma (life threatening) * COPD
Respiratory muscle paralysis * Chest wall ds
(Kyphoscoliosis) + fractured rib + intercostals ms tear.
Brainstem lesion = CNS depression * Ankylosing Spondylitis
(Narcotic drugs)

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Other Causes of Type 1 Failure:
Extrinsic allergic alveolitis.
Interstitial fibrosing alveolitis.
Other Causes of Type 2 Failure:
Neuromuscular disease ( gullain barre syndrome )
Pulmonary Embolism
Inhaled foreign body
Pneumothorax
Retention of secretion
Refer to the Oxford hand book of Medicine
Complication of type 2 Respiratory Failure:
- Cardiac Arrythmias.
- GIT hemorrhage
- Pneumothorax
- Bronchial Obstruction.
- LVF
- Pulmonary Embolism
- Convulsion.

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Management of Type 1 Respiratory Failure:
- High flow O2
- Maintain adequate O2 and O2 Saturation > 90 %
- Mechanical ventilation
- Avoid O2 toxicity PO2 > 55 mmHg
- Control underlying problem (pneumonia, infection, sepsis, pancreatitis)
YOU should know the indication for CAOT
(chronic ambulatory oxygen therapy)

Management of Type 2 Respiratory Failure:
(1) Oxygen supply ( venture mask )
Start with 1 liter/min = 24%
2 liter/min = 28%
3 liter/min = 35%
4 liter/min = 40%
5 liter/min = 50%
** then titrate the requirement according to ABG
** Provide O2 to keep the O2 saturation >90%but < 93% without
inducing marked hypercapnia
*****************
(2) Treat underlying causes:
*Antibiotic in case of infection/pneumonia
*Bronchodilator in case of COPD/ Asthma
*Anticholenergic in case of COPD/Asthma
*Corticosteroid in case of severe bronchospasm
*****************

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(3) Theophyllin ( improve muscle contraction
* Diuretics LVF
* Chest physiotherapy
* Hydration & mucolytic (Danse)
******************

(4) Mechanical Ventilation
Failure to provide adequate oxygenation without marked hypercapnia.
Decrease level of conconcentaration
Failure of Respiratory stimulant.

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R en al dis eas es

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Renal failure
Classification:
a) according to duration
acute (6 w-6 m)
chronic (>6 m)
b) according to etiology
Pre renal Renal (most important) Post renal
Hypo volemic cause:
a) decrease amount
of fluid in vessels
( decrease
intravascular fluid)
loss of
blood(hrg)
burn
vomiting and
diarrhea
diuretic drug
b) decrease amount
of fluid by
extra vastion:
(causes of
edema)
nephrotic
syndrome
hepatic
failure
congestive
heart
failure
c) renal artery
Stenosis
d) sepsis
a) DM diabetic nephropathy
b) HTN hypertensive
nephrosclerpsis
c) Glomerulonephritis
d) Infection:
E. Coli HUS
(hemolytic uremic syndrome)
HIV
HBV & HCV
TB
Schistosomiasis
Malaria
a) Malaria (Ag-Ab)
b) Malaria falciparum
(black water fever)
Urine will be dark
Syphilis
Chronic recurrent
pyelonephritis.
e) drugs
amino glycosides
NSAIDs
Diuretics
Contrast agents
Gold (heavy metal that treat
RA.) nephrotoxins
Penicillamine
Mainly obstruction
due:
Stone
Radiation
Tumor
Lymph. Node
Infection:
TB
Bilhariziasis

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f) Vasculitis
SLE, RA, connective tissue dis.,
systemic sclerosis, polyarteritis
nodosa
g) Tumor
Renal cell carcinoma
Multiple myloma:
1. Hypercalcemia
2. Hyperuracemia
3. Recurrent infection
4. Deposition of paraprotein
h) Metabolic causes:
1. Hypercalcemia
2. Wilsons ds.
3. Hemochromatosis
4. Hyperurecemia
I) Polycystic kidney
Complication:
1) Uremia:
o Uremic gastropathy loss of appetite, loss of wt, nausea, vomiting,
constipation
o Leg swelling
o Respiratory symptoms SOB, cough, yellowish sputum
o Uremic pericarditis
o Symptoms of cardiac overload (HF) dyspnea, orthopnea, PND
o Generalized skin itching
o fatigability
o Uremic encephalopathy disturbance of sleep, impaired memory,
problems in concentration, confusion in advaced RF

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2) HTN
3) Edema (fluid overload)
4) In the endocrine:
3 (increase) 3 (decrease) 2 abnormal
Increase:
LH, prolactine, insulin lead to gynecomastia in male & dysfunction in
female & improve DM (or hypoglycemia)
Decrease:
Erythropoietin factor& 1.25-DHCC (active vititamin D) & testosterone
Abnormal:
GH secretion & action (impaired growth in child)
Thyroid H. level (myxedema)
5) In skin
5p+ 1E
Pallor
Pigmentation
Pruritis
Purpura
Popular skin rash
Edema
6) Musculoskeletal
Bone:
Renal osteodystophy
Joint:
Gout (uric acid deposition) \ Pseudogout (Ca pyrophosphate deposition)
RF of transplanted Kidney presenting with uremic symptoms the
cause is Renal Artery Stenosis

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7) Electrolyte disturbance:
(Hyperkalemia)
Brain: confusion & mental dullness
CVS: arrest
GIT: atony (nausea, vomiting, constipation)
Muscle: weakness, flaccid paralysis, paraesthesia
Investigation:
+ Blood Work
1) CBC: HB anemia
MCV, MCH or (nomocytic normochromic)
Pancytopenia
WBC infection
2) ESR: increase with infection
3) ABG: metabolic acidosis
4) U & E (renal function): increase creatinine, urea , Pi, Kyperkalemia
(should be treated to protect the heart)
5) Blood sugar: increase with DM
6) HBV & HCV screen

+ Urine analysis:
1) Oligouria
2) Proteinuria
3) Hematouria
4) casts: RBC

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+ Radiology:
1- US:
1) Kidney size
Enlarged:
DM, polycystic kidney, HIV, Amylodosis
Shrunken:
Chronic GN
(evidence of obstruction)
LN, stone, tumor
Hepatosplenomegaly
2) Collection over kidney
2- Urgent US + Doppler for transplanted kidney to reveal renal
artery stenosis
3- CXR:
Heart, Pulmonary edema
pleural effusion uremia
TB
Metastatic kidney
+ ECG, Echo, Cardiac Enzymes if patient has cardiac symptoms
+ Band screen if pt is on line dialysis & febrile
- urine
- sputum culture
- blood

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Important Points in RF:
1- Underlying cause:
DM how long? does pt has retinopathy (because nephropathy
occur at same time)
Swelling renal biopsy controlled?
HTN How long?
Control
HF
Unknown etiology
SLE (pt knows about it) medications, . etc
E Type II diabetic patient for a long time on oral
hypoglycemic, without changing his diet or medications.
How did his DM became controlled? Even sometimes he
has hypoglycemia
Due to development of renal failure
As the insulin is metabolized in kidney, it will be preserved
insulin
This will lead to control of sugar
So, Oral hypoglycemic should be stopped
E Do you expect this pt to have retinopathy?
No, because his diabetes is controlled

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2- Duration of RF
3- Dialysis through fistula or line
How many times per week?
4- Symptoms of uremia
If a patient doesn't have symptoms of uremia,
In HPI write: no symptoms of uremia
5- Line sepsis / we have to exclude other causes
6- UTI
Itching:
- Uremia uremic toxin (we don't know what it is)
- Uremic dryness
- Hyperphosphatemia major cause especially in Nephrotic syndrome
Renal failure management:
Replacement therapy:
1- Erythropoietin for anemia
2- Calcium & vitamin D for low vitamin D
3- Dialysis
4- Renal transplant
* Low salt diet
* Low protein diet
Dialysis:
Peritoneal dialysis if the patient can do aseptic technique
hemodialysis

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Dialysis indication:
- Hyperkalemia not responding to medical therapy
- Fluid over load not responding to medical therapy
- Uremic encephalopathy
- Uremic pericarditis
- Uremic gastropathy
- Rapid increasing in creatinine e.g 100-200
- Metabolic acidosis
- Uremic bone dystrophy (earlier better)
* In ARF pt treated by dialysis recover in 6 weeks
10-25 weeks CRF OBSERVE
If creatinine is maintained e.g.: 300 during his life & not increasing no
need for dialysis, only replacement therapy
Acute on Chronic Renal Failure:
e.g.: creatinine=300 after 2 weeks creatinine=800
Search for the cause, why developed?
1- Infection
2- Drugs: NSAID e.g.: for osteoarthritis,
3- Contrast angiogram
4- Obstruction BPH (benign prostatic hyperplasia)
5- Any fluid loss, dehydration vomiting, sun (sweating) , diuretic , heart
failure

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Nephrotic syndrome
Definition:
1. Proteinuria > 3.5 g\day.
2. Hypoalbuminemia < 30g\L (< 3g\dl)
3. Hyperlipidemia ( cholesterol, LDL).
4. Evidence of fluid retention and edema.
Causes:
1- 1ry renal:
- Minimal change disease.
- Membranous GN.
- Focal segmental Glomerulosclerosis.
- membranoproliferative GN.
- crescentic GN.
2- 2ry causes:
- Systemic: DM HTN SLE amyloidosis.
- Drugs: NSAIDs heroin captopril gold penicillamine - probenecide
.
- Infection: HBV HIV- malaria
- Malignancy: carcinoma lymphoma MM.
- Allergy.
Complication:
1- Edema.
2- Hypercoagulability.
3- Hypercholesterolemia.
4- Infection.

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Gas t r o en t er o l o gy
&
L iv er dis eas e

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Diarrhea
Session with Dr. Maimoona
Diarrhea
Acute & Chronic

2 weeks more
Causes:
I. Infections:
E Protozoa:
Amoeba , Giardia

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E Bacteria:
E. Coli , Klibsiella , Shigella , salmonella
Vibrio cholera watery diarrhea
Staph. Aureus (milk products)
Campylobacter (pets at home)
Yersinia
C. difficile diarrhea, pseudomembranous colitis
E Viruses:
HIV (common cause) 3 months + lymphadenopathy + wt loss
Rota virus, adenovirus
E Fungal in immunocompromised
Cryptosporidium
E Lyme disease Liptospirae
E Mycobacteria: intestinal TB
Note:
C. botulinium botulism (preserved food)
C. Perfringins food poisoning / gas gangrene
C. tetini tetanus
The underlined words are important causative organisms
Means Bloody
Note:
Algid Malaria: malaria superimposed by Salmonella
Common cause of septic shock

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II. Inflammatory Bowel Disease Crohn's Ulcerative colitis
III. Malignancy:
Intestinal lymphoma, Colon carcinoma, Pancreas carcinoma, Medullar
carcinoma of thyroid
IV. Malabsorption:
1- Celiac disease (not all patients present with diarrhea)
*malabsorption*
CBC: dimorphic picture
Microcytosis & macrocytosis
Hypochromic & hyperchromic
D.D. Celiac Disease
Combined deficiency (folate Fe)
They have hypo Ca
+2
2- Tropical sprue (hot humid countries)
Probably due to E. coli (traveler's diarrhea)
3- Whipple's disease (malabsorption due to trophyrhyma whipple
"bacteria")
Note
Hemolytic anemia peripheral blood film reticulocytosis

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Usually patients also suffer Lymphadenopathy, hepatosplenomegaly, arthritis,
malabsorption and, skin pigmentation.
Tetracycline should be prescribed for 1 year
Periodic acid Sheff (PAS) positive (+)
4- Blind loop syndrome (malabsorption) , short loop
5- Pancreatic (chronic) malabsorption
Chronic pancreatitis cystic fibrosis - carcinoma
6- Post-gastrectomy , resection of colon
V. Endocrine:
Thyrotoxicosis
Addison's (hypotension & diarrhea)
DM (autoimmune neuropathy)
Glucagonoma
VIP tumor
Pheochromocytoma
Hypoparathyroidism
Carcinoind (flushing face)
VI. Drugs:
Antibiotics mainly clindamycin
Laxatives
Cytotoxic
VII. Idiopathic: Irritable bowel syndrome, diverticular disease

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In History:
- The amount and frequency
- Consistency: watery
- Associates with bleeding: Amoeba, IBD, Shigella, Salmonella, E. Coli
- Fever: Infections, IBD
- Tenesmus or not: Giardiasis & Amoebiasis
- Abdominal Pain IBD and malignancy
- Loss of weight: HIV, IBD, and malignancy
- Family History
- Laxatives, eat outside the house, house hold diarrhea (ACUTE)
Investigations of a patient with diarrhea:
1- Stool analysis: Blood Mucus Protozoa e.g. trophozoid
Cuture bacteria
&
Sensitivity
2- CBC
- Anemia
- Leukocytosis
- Thrombocytosis: bone marrow to confirm safe anemia
3- ESR
4- U and E
- Hypo K
+
- Hyper Na
+
- Renal failure (due to fluid loss)
5- Left: hypoalbuminemia
6- Serology:
HIV
+
for ulcerative colitis pANCA, ASCA + CMV IgM

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7- Endoscopy
8- Enema
9- Salmonella titer
10- Abdominal X-Ray: toxic mega colon
Differential Diagnosis of Diarrhea:
1- Infection
2- IBD
3- Malignancy
4- Malabsorption
5- Endocrine
6- Drugs
7- Idiopathic

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Inflammatory Bowel Disease
Clinically we cannot differentiate between ulcerative colitis and Crohn's unless
fistula develops.
Presentation: mainly diarrhea.

I- Ulcerative Colitis
1- Intestine: diarrhea (bloody) - pain - malabsorption - tenesmus
2- Skin: erythema nodosum, pyoderma gangrnosum
3- Amylodosis,
4- Arthropathy
5- Thromboembolic disease
6- Both: ant. Uveitis, conjectivitis, episcleritis, iritis, ankylosing spondylitis,
sacroilitis, sclerosing cholangitis
7- Fatty liver, autoimmune hepatitis.

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Complications:
1- Toxic megacolon (most severe complication)
Tachycardia, anemia, hypotension, dilated transverse colon more than 6cm
If not improved in 24 to 48 hours -> total Colonectomy should be preformed
immediately.
(Chest x-ray)
2- Malignancy:
More with Ulcerative Colitis
A patient with Ulcerative Colitis for more than 10 years must have an annual
endoscopy.
3- Amylodosis (in both)
4- Thrombosis.
II- Chron's
Terminal ilium B12 deficiency
Intestinal obstruction - stricture
Fistula (entero - enteric or vesical).
Perianal (abscess - tags)
Grading
I- Mild
Diarrhea > 5/day
No anemia
No fever
Normal albumin
II- Moderate
(In between)
III- Severe
Diarrhea > 10/day
Fever
Tachycardia
Hypotension
Hypoabuminia (edema)

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Treatment
I- Salphasalazine (Paraaminosalicylic acid)
II- Steroids (Pridnisolone)
If the patient suffers Chrons:
Add metronidazole (antibiotic covers anaerobes)
Investigations
1- CBC
2- U&E
3- Left
4- Barium enema
5- Endoscopy (Chron's skiplesion) coplet stones
6- Biopsy
7- Stool (to exclude infections)
8- Abdominal x-ray
* Vitamin deficiency (B12) numbness.
* Gallstone (both).
* Exudates stones Crohn's (Child)



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Ulcerative Colitis
(Non-smokers)
Symptoms:
1- Bloody diarrhea.
2- Tenesmus.
3- Abdominal pain (lower).
If severe:
- More frequent diarrhea more than 10 times per day
4- Fever
5- Weight loss.
6- Signs of anemia, hypoalbuminemia.
If only rectum (proctitis).
1- Constipation.
2- Blood in stool.
Signs:
1- Clubbing, leukonychia.
2- If fulminant: diarrhea mixed with blood & mucus.
3- Abdominal tenderness , distention (toxic megacolon)
Extra-intestinal signs:
1- Skin: erythema nodosum, Pyoderma gangrinosum.
2- Eye: uvitis, conjunctivitis, iritis, episcleitis.
3- Mouth: aphtous ulcer.
4- Arthropathy.
5- Amyloidosis.
6- Thromboembolic disease.

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Other unrelated to disease activity:
1- Sclerosing cholangitis.
2- Fatty liver, autoimmune hepatitis.
3- Ankylosing spondylitis, sacroilitus.
Complications:
1- Toxic megacolon.
2- Malignancy.
3- Thrombosis.
4- Bleeding dehydration.
5- Perforation.
6- Amyloidosis.

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Crohns Disease
Granulomatous transmural skip lesion.
Terminal ilium (any where)
Symptoms:
Diarrhea, malabsorption, abdominal pain, right iliac fossa pain, rectal
bleeding (less than U C), weight loss, fever.
Signs:
1- Clubbing.
2- Perianal skin tags, fistula, stricture, abscess.
3- Weight loss.
4- Fever.
5- Anemia
6- Hypoproteinemia.
Abdomen: tender, mass.
Extra-intestinal: as in Ulcerative Colitis
Complications:
1- Stricture (intestinal obstruction).
2- Fistula (enteroenteric , vescal or vaginal).
3- Renal disease due to ureteric compression.
4- Fe- folate- B12 deficiency.
5- Malignancy.
6- Amyloidosis.

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Relapsing of Crohn's
Session with Dr. Faiza Qari (5
th
year tutor)
A known case of Crohn's dis. presents to the ER with vomiting &
abdominal distention, what might be the causes of his complains?
1- Intestinal obstruction:
abdominal pain
abdominal distention
vomiting (repeated attacks)
constipation
2- Relapsing of Crohn's

3- Gastric or duodenal ulcer heart burn
4- Peritonitis severe abdominal pain
5- Colon cancer weight loss

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: other important history s ' elapsing of Crohn R
* Past history since the time of 1
st
diagnosis
- Times admitted to hospital
- Procedures (what happened?)
- Any relapses
- Any ICU admissions
* Last colonoscopy
, abdominal distension , rectum / bleeding , bleeding diarrhea , Abdominal pain *
fistulae & repeated fissures , loss weight , loss of appetite , outh ulcer m repeated
* Intestinal manifestations of Crohn's:
- Anemia (iron deficiency) chronic illness
- Appendicitis (Right Iliac mass)
* Extra-intestinal manifestations of Crohn's:
- Arthritis sacroiliac joint back pain
Or mono-arthritis
- Liver hepatitis, gall stone
- Phlebitis DVT
- Renal stones
- Skin rash Erythema Nodosum
large intestine > small intestine s affect ' Crohn

Vomiting
Weight loss
: Most important investigations
- CBC:
WBC normal
Hb microcytic hypochromic anemia
Platelet (1) postsplenectomy ()
(2) Relapse of Crohn's
- ESR activity of disease
- LFT

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CLD
Dr.Maimoona
When a patient presents with hepatic symptoms, 1
st
search for acute causes of
illness then ask about chronic.
ETIOLOGY:
(1) infection:
- hepatitis
B sexually
C blood transfusion / vertical from mother to child
- Schistosomiasis (Bilharziasis)
- Hydatid cyst by compression, not hepatocellular.
- TB most common in KSA.
- HIV usually acute, but chronic if patient lives long enough.
(2) Alcohol always take History of alcohol.
* Most likely jobs to be alcoholic & drug abusers:
- Cops & Army.
- People working at port of entry.
REMEMBER! These infections are causes of acute, not chronic liver
disease:
- CMV
- Toxoplasmosis
- EBV
- Malaria

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(3) Autoimmune all CTD: SLE, RA, Wegner's Granulomatosis.
(4) Metabolic:
Wilson's disease autosomal recessive.
Diagnosed by:
Low ceruloplasmin (serum).
High 24 hr urine cupper.
hemochromatosis autosomal recessive.
Diagnosed by:
Serum iron, ferretin.
Liver biopsy diagnostic.
(5) Drugs remember 1 or 2 only
Anti-Tuberculosis.
Methotrexate.
Anti-epileptics sodium valporate, phenytoin, tegretol.
(6) Primary biliary cirrhosis:
Classically pt present with:
Young female .
Itching 1 or 2 years before any liver involvement.
Diagnosed by:
Anti-Mitochondrial Abs.
IgM Abs.
High ALP.
All these 3 are raised in these patients.
(7) Malignancy metastasis.
(8) budd chiare syndrome:
Hepatic vein thrombosis.
Causes: all causes of DVT
90% of pt

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Present:
acute abdominal distention main
Others.

Do liver scan find uptake in caudate lobe.
(9) Cardiac cirrhosis.
(10) Idiopathic.
(11) fatty liver NEVER say it, because it is TOO RARE, & if you mentioned it in the
exam ( ) you will lose marks
Dr Maimoona says "don't remember it".
Decompensation of CLD shows up by Complications:
(1) Portal Hypertension:
variceal Hrg.
Splenomegaly.
Ascites.
(2) Hepatocellular Ca. this is #1
(3) Hypersplenism. pancytopenia.
(4) Bleeding tendency.
(5) Hepatic encephalopathy.
(6) SBP. (spontaneous bacterial peritonitis)
(7) Hepatorenal syndrome if you mentioned this, Dr Maimoona will tell you
to talk about something that is more important.

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Hepatic Encephalopathy:
50 years old lady admitted through ER, who is known case of CLD secondary to
HCV.
C/O: altered level of conciseness (complaint & HPI)
+
Hepatic encephalopathy
How do you manage?
(1) Take History of what ppt. of a patient to have an encephalopathy:
History of precipitating factor:
- Infection:
SBP: spontaneous bacterial peritonitis ---
Sore throat, respiratory, UTI, leg ulceretc.
- Constipation.
- Hemorrhage (bleeding):
Upper/Lower GI bleeding globulin high urea.
- High protein diet high urea.
- Drugs: analgesics, sedatives & tranquilizers.
- Causes of electrolytes imbalance:
Overuse of diuretics.
Gastroenteritis vomiting & diarrhea.
- Dehydration: vomiting, diarrhea, burn.
- Excess alcohol.
- Heart failure.
- Hepatoma (hcc).
(2) Examination of pt who already has CLD & came with hepatic
encephalopathy:
1- Glasgow coma scale (1
st
) consciousness.
2- Vital signs:
-Temp infection.
-Blood Pressure look for postural hypotension (Ascites).
-Pulse tachycardia due to infection or loss of fluid.

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3- Fluid status: (2
nd
)
Fluid overload (from liver failure) pleural effusion, Ascites, lower limb
edema.
Dehydration mucus membrane, auxiliary sweating, postural
hypotension.
4- PR = per rectum Ex (digital rectal Ex) (3
rd
) bleeding: 'melena' in all hepatic
encephalopathy.
5- Evidence of infection: (4
th
)
Chest.
SBP (spontaneous bacterial peritonitis) abdominal tenderness.
6- Hepatic bruit 'hepatoma'.
+ CLD stigma.
(3) Everyday follows up:
1- Glasgow-coma scale.
2- Flapping tremor (asterixis).
3- Constructional apraxia: draw a 5 pointed star (better) or draw a square.
Investigations:
That should be done to all patients:
(1) CBC:
- Leukocytosis infection.
- Cytopenia hypersplenism & vasculitis (CTD).
Anemia.
Leucopenia.
Thrombocytopenia.
(2) LFT:
In cirrhotic liver: cells are distorted enzymes not secreted = normal LFT.
1- Hepatocellular Ca enzymes.
2- Obstructive (primary biliary cirrhosis) ALP.

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3- Bilirubin.
4- PT, PTT (coagulation profile) clotting factors.
5- Albumin level if <13 pt is prone to develop SBP.
(3) Urea & electrolytes:
1- Low K diuretic.
2- Low Na dilutional or diuretic.
3- prerenal failure increase urea & creatinine.
(4) Blood glucose hypoglycemic, because there is no gluconeogenesis in liver.
(5) Hepatitis B & C serology most common in KSA.
(6) -fetoprotein (AFP) & abdominal US every 6 months --- for hepatoma.
*NOTE:
If all these didn't help you, then you'll do the other tests if symptoms are suggestive (but
in a written exam, you have to write them all)
(7) Abdominal US/CT (only 1, if US didn't help: do CT)
1- Liver:
+ 1
st
size of liver? If shrunken order a biopsy.
+ 2
nd
macronodular (alcohol) or micronodular.
+ 3
rd
lesion (masses) metastasis, tumor, hydatid cyst.
2- Dilatation of biliary tract obstruction stones etc.
3- Ascites.
4- Spleen enlarged hypersplenism.
5- Any other masses LN / metastasis.
(8) CXR:
Evidence of infection.
Fluids overload pulmonary edema.
HF.
Malignancy metastasis, 1 tumor.

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(9) UGI endoscopy: to know source of bleeding.
- Oesophageal varices.
- Peptic ulcer because liver can't metabolize. endogenous gastrin
ttt: PPI (proton pump inhibitor).
(10) Liver biopsy: (invasive procedure, keep it at last).
Only in patient with non-shrunken liver & he has Hepatitis B or C.
To know activity of the virus, & treatment.
(11) ascitic tap: diagnostic/relief for gram stain , culture & sensitivity,
cytology, protein, glucose "see below".
(12) If Pt. not known to have CLD, presented with hepatic encephalopathy, do:
-HBV, HCV.
-ANA profile.
-Young Pt: metabolic causes.
Others:
- Blood culture.
- Urine analysis.
- Urine culture & sensitivity.
- Ammonia.
- ECG in electrolytes disturbance.
SBP:
- Patient should have Ascites to develop it
- CLD
- Abdominal pain
Diagnosis:
P/C:
Abdominal pain, distention, fever, decrease bowel sounds, worsening hepatic
encephalopathy, tenderness.
Or in the absence of signs:

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Ascetic tap:
1- WBC >500, neutrophil >250 neutrophils/ l diagnostic.
2- Gram staining.
3- Culture E. coli most common.
After tap, pt. will be on antibiotic empirically, then if +ve SBP (SBP is
documented) life-long prophylactic antibiotic.
Management:
- Bed rest.
- Low salt/low protein diet.
- Intake/output chart.
- Daily weighting: the goal of diuretic therapy is daily weight loss of 0.5-1
mg/day.
- Daily examination of 2 signs: constructional apraxia, flapping tremor asterixis:
see if improver with ttt.
- Daily urea & electrolytes if disturbed.
1- laxative: lactulose.
Aim: 2-3 bowel motion daily, lactic acid lactose disaccharide change pH of colon
flora no overgrowth of bacteria.
2- Antibiotic 3
rd
generation cephalosporin SBP.
3- Fluid status management:
o Dehydration give fluid.
o Fluid overload diuretic:
loop diuretic, quick action till spironolactone takeover.
spironolactone, aldactone, antialdosteron (aldosterone cause Na &
water retention) take 3 days to work.
4- Proton pump inhibitor 'prophylaxis'.
5- -blocker inderal decrease portal pressure.

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If patient out of encephalopathy:
Discharge on:
1- Lasix.
2- Spironolactone.
3- Proton pumps inhibitor.
If it is not diuretic albumin.
& the following investigation:
1- Urea & electrolytes.
2- Alpha-fetoprotein Q 6 months.
3- Abdominal U/S Q 6 months.
4-CBC
Ascites Management:
- Salt restriction.
- Diuretic: loop diuretic & spironolactone.
- Diagnostic paracentesis.
- In refractory ascites: fluid overload that is none responsive to a sodium-
restricted diet & high-dose diuretic: -TIPS -shunt - therapeutic paracentesis Q
2/52. If child C >>liver transplant.
- In large volume paracentesis: concomitant administration of IV colloid (5-8g
albumin/L ascites removed).
SBP management:
-ttt: empiric IV antibiotic therapy 3
rd
generation cephalosporin (ceftriaxone or
cefotaxime) depending on renal function, or quinolone( ciprofloxacin).
- Then long life/2ry prophylaxis: norfloxacin 400 mg PO qd.
- If total protein < 10g give antibiotic as prophylaxis even if no SBP.
- In GI bleeding start antibiotic prophylaxis 2
nd
generation cephalosporin or
quinolone.

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Coagulopathy management:
- Vit. K IV 10mg/day for 3 consecutive days.
- In active bleeding or invasive procedure: fresh frozen plasma & platelets
transfusion.
GI bleeding management:
- ICU admission.
- ABC resuscitation with IV fluid fast drip till blood available.
- Lab tests CBC, U & E, coagulation profile, cross matching.
- NGT.
- Octreotide infusion, bolus then infusion acutely reduces portal pressures &
controls variceal bleeding with very few side effects, improving the diagnostic &
therapeutic success of subsequent endoscopy.
- Vasopressin: cardiovascular risk in ICU w. cardiac monitoring, + nitroglycerin.
- Endoscopy for variceal ligation banding, sclerotherapy.
- TIPS, shunt surgery: if child B not responding to therapeutic endoscopy to
relief portal hypertension, then liver transplant.
- Balloon tamponade: dangerous esophageal rupture.
- Discharge on b-blocker Propranolol : reduce portal pressure & lower the risk of
recurrent bleeding.
- Endoscopy every year.

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Chromic liver disease
Dr. Hisham Akbar
Definition
Types
Causes
Manifestations
Treatment
Types:
A. According to pathology:
1. Traditional:
Chronic persistent
Chronic lobular
Chronic active
Liver cirrhosis
2. Metavir
3. Knodells
B. According to etiology:
1. Necrotic
2. Post necrotic
Depends on taking liver specimen to show:
Degree of inflammation
Staging = of the degree of fibrosis

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Role of liver biopsy in chronic hepatitis:
1. To establish the diagnosis
2. For the detection or exclusion of other diseases
3. For grading
4. For staging
5. Evaluation of therapeutic effect
Note:
Initially the inflammatory cells limited in the portal tract then in a
lobule then spreads to the portal vein.
The liver histological specimen is usually stained with H&E.
Cirrhosis: is the complete distraction of hepatic nodules. Moreover, a
patient with hepatic cirrhosis is more liable to develop HCC.
Classification of CLD according to the cause:
1. Infection : viral hepatitis ( B, C, D )
2. Autoimmune hepatitis
3. Alcoholic
4. Drugs ( methotrexate, isonizaid, methyldopa, )
5. Metabolic fatty liver
6. Cholestatic 1ry & 2ry biliary cirrhosis
sclerosing cholangitis
7. Infiltrative
8. Vascular problem ( cardiac cirrhosis )
9. Neoplastic benign
Malignant 1ry
2ry
10. Idiopathic

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Note:
4 months are needed to develop HBVs Abs
1-2 weeks are needed to develop HBVc Abs IgM then IgG
Therefore 1. HBVs Abs remains for 4 months or more
2. HBVs Abs (Positive + )
3. Persistent vireamia detected by PCR
Natural History of hepatitis B in adult by:
Acute HBV
95 % recovery & immunity
5 % chronic hepatitis
Note:
If the patient becomes jaundiced feverish ill , that signifies that his
immune system is intact and is trying to defend the body against the
disease
Chronicity risk by aging ( age chronicity )
Mode of transmission :
Neonate : vertical infection from the mother to the fetus ( 90%
chronic )
Adult: horizontal infection
Even if the patient is Asymptomatic but has persistent viremia, he has
the same chance of infection with HCC as a patient who is
Symptomatic.
CLD

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Classification of autoimmune hepatitis:
Types Serum auto Abs Auto Ag
I 1. Serum anti nuclear
2. Anti mitochondria
3. anti-smooth Abs
- Double stranded DNA
in some but target Ags.
- In liver disease not fully
defined action.
II 1. Anti liver & kidney LK
2. Microsomal ( Abs type I
LKM )
- Cytochrome P450 11D
- Cytochrome 8 + 18
III Antisoluble liver Ag -
The interpretation of aggregated score is:
Type I in female at menopause and teenage years.
Type II & III more in children
If the score of the criteria is 15 before ttt and greater than 17 after ttt :
Its Definitive autoimmune hepatitis
If the score of the criteria is 10 15 before ttt & 12 17 after ttt
Its Probably autoimmune hepatitis
Alcoholic Liver Disease
Depends on:
Amount per day
More than 10 years consumption
Genetic predisposition
Results in:
Acute alcoholic hepatitis
Fatty liver change
Cirrhosis

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Manifestations of CLD:
Asymptomatic
Symptomatic Extra abdominal manifestation
1. Fatigue
2. Spider nevi
3. Enlarged or Shrunken liver
4. Enlarged spleen
5. Finger clubbing
6. Collapsing pulse
7. Kayser-Fleischer ring
8. Xanthelasma
9. Parotid swelling alcoholic
10. Palmer erythema Thenar
Hypothenar
Pulp of fingers
11. Gynecomastia the most common cause is
diuretics ( Spironolactone / Aldactone ) .
12. Dupetrine contraction (common cause is occupational
manual working).
13. Advanced disease Ascites
Bruising
Esophageal varices
Extra hepatic manifestation of hepatitis: mixed cryoglobulinemia
1. Rash
2. Glumerulonephritis membranoproliferative
3. porphyria cutanea tarda hepatocellular ca
4. Arthritis
5. Vasculitis
6. Angioneuretic edema

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Acquisition of HDV infection:
Co-infection: simultaneous introduction of HBV HDV
Super infection: introduction of HDV into HBVs Ag (positive) host
Chronic
hepatitis
Asymptomatic
carrier
Cirrhosis
HCC
Persistent infection
Death

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Natural Hiostory of HCV :
Acute infection
Clinical Sequelae :
Acute hepatitis
Chronic HBV / HDV
hepatitis
Fulminant hepatitis
HDV / HBV
Co-infection
HDV super
infection
to HBV
< or = 15 %
Resolution ( Risk
for subsequent
infection is
unknown )
> or = 85 %
Persistent
infection

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Treatment
Treat the cause
Treat the complications :
1. Hepatorenal syndrome
2. Encephalopathy ( lactose, flagel )
3. Bleeding a. ABC first.
b. Endoscopy: sclerotherapy
c. TIPS for bleeding
ascites
4. Ascites ( diuretic )
5. SBP (most common E.coli ) neutrophile
6. Hepatoma
Persistent infection
Non-Progressive
liver injury
Elevated ALT Normal ALT
Progressive
liver injury
Fibrosis &
Cirrhosis Death
HCC
HBV pt. might develop
HCC without cirrhosis
but HCV pt. must have
cirrhosis to develop HCC

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Treatment of chronic hepatitis:
A. Interferon (INF ) :
But not in Saudi patients since they fulfill the criteria for ttt with INF.
1. It's effective in treatment if the infection is recent (not more than 2
years), but most Saudi patients have established the infection since
childhood (more than 30 years).
2. INF is effective only if the liver enzymes are elevated twice the normal,
which does not apply to Saudi patients. (They have high liver enzymes
but not as twice).
3. Most of the viruses here in Saudi Arabia are pre-coremutant viruses
which are resistant to INF so, once you stop the ttt viremia it will
rise again.
4. It should not be given to a patient with an autoimmune disease such as
SLE, RA.
5. Also it should not be prescribed to patients with leukopenia and
thrombocytopenia (CBC).
New combination: - INF + Ribavirine
- Pegylated INF

B. Nucleoside
INF
Moderate to
severe
necroinflammation
Fibrosis
HCV RNA ( + ve)
Persist elevated
ALT

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C. Liver transplantation :
- Not all HCC are sent for assessment of liver transplantation.
- Only in case of Liver failure
- Most of deaths occur early = infection
Late = rejection
- Nowadays, transplantation of the left lobe enhances the liver to be a
complete one within 6 months. The donors liver will grow another left lobe to
replace the donated lobe.

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How to diagnose HCV?
1. ELISA : detect HCV Abs Generation 1
Generation 2
Generation 3
- If ELISA is (positive) that means the patient has the Abs has the
infection for at least 6 months.
- If liver enzymes > 1000 it means the infection is acute.
- Incubation period for HCV ( 30 90 days )
- After 1 month the patient starts to have an increase in liver enzymes
either clinical
Or subclinical
2. PCR (positive): only after 2 weeks of the infection.
3. RIBA: Recombinant Immuno Blotting Assay = detects Abs earlier than
ELISA.
Q: PCR (+) increase in liver enzymes, what is to be done?
We cannot start the treatment for any patient with HCV unless:
1. Decompensate CLD e.g. reaching the stage of Ascites varices
2. Alpha IF or Rebavirine is contraindicated for a reason or the other.

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So, when we discover HCV infections we should decide in which stage is the
patient by taking History & physical examination.
1. Jaundice
2. Hematemesis
3. Asterixis
4. Lower limb edema
5. Epistaxis
6. Bleeding gum
7. Abdominal pain & distention
-IF ( S.C ) + Ribavirine ( tablets ) = ttt of HCV + CLD
Could be used with any patient with compensated CLD and has no
contraindication to medication.
Decompensation (Ascites - Encephalopathy- varices)
Investigations:
1. Baseline CBC because -IF cause leukopenia ( neutropenia )
Thrombocytopenia
- So we need to know his baseline.
- If the patient is already leukopenic, he is not a good candidate for
-IF.
2. Left synthetic function ( PT PTT Albumin )
Excretory function (bilirubin)
-IF should not be given to any autoimmune pt. e.g. SLE , RA.
Because it will worse the condition.
-IF can cause thyroid dysfunction hypo ( common )
& hyperthyroidism
& this S/E is the only S/E of a-IF which is not reversible. That's why we
need to do TFT ( T3 TSH ).

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Rebavirine should not be given to a pregnant patient can't control
her because it is teratogenic.
Rebavirine could cause hemolysis so it shouldnt ever be given to
patient with hemolytic anemia.
Rebavirine until now doesnt have an exact defined dose. So, a
follow-up is need.
Rebavirine could cause impaired renal function. So, a baseline
should be done on RFT.
End ttt Response ( ETR )
Sustained Viral Response ( SVR )
After finishing ttt (6 or 12 months),
& liver enzymes (negative)
& PCR (negative)
It is ETR
But my aim is to have PCR (negative) after 6 months of stopping ttt.
At this time it's (SVR).
1
st
time the HCV was discovered was in 1989
-IF for 6 months response 6 %
After 1994 extended monotherapy for 1y 15 %
In 1998 -IF + Rebavirin response 41 %
HCV 6 genotypes type I & IV (requires a year) disresponse to
-IF Rebavirine
While genotype II & III (requires 6 months)
cause better response 60%.

Some patients could have co-infection of I & II

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It fails many times due to mutation in genotype, that is why we give
pegylated IF.
Polyethylene glycol + -IF pegylated IF In type IV after 1y
(41 % response).
In type II / III
(~ 80 % response).
Factors affecting response:
1. Younger than 40 years.
2. Female better than male.
3. Genotype II is & III better than I & IV.
4. Degree of cirrhosis.
5. Viral load.
EVR = Early Virologic Response

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E n do c r in o l o gy

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Hypothyroidism
Primary hypothyroidism:
1- Drugs (amiodarone lithium)
2- Autoimmune (e.g. Hashimoto thyroiditis)
3- Post surgical ttt of thyrotoxicosis
4- Post radiation ttt of thyrotoxicosis
5- Post partum thyroiditis: transient hyperthyroid euthyroid
hypothyroditis then return back to euthyroid.
Secondary hypothyroidism
Investigations:
- TFT FT3, FT4, TSH 1ry
FT3, FT4, TSH 2ry
- Thyroid peroxidase antibodies
- Anti-thyroglobulin antibodies
- Radio isotope scanning uptake
- US: multinodular + cystic + solid
o Cold malignant biopsy
o hot benign

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Management
- Need to give thyroxin gradually because the heart in hypothyroidism is
functioning slowly, so if we give thyroxin this would metabolic demand.
The heart cannot cooperate with this & might infarct.
- 0.5 .g thyroxin ( as starting point then gradually for life as replacement )
& follow her up within 6-8 weeks to see the stabilization of thyroid level
because it is half life is ( 6-8 ) weeks .
** In elderly start with low dose WHY??
metabolic rate can go in infarction
- Better not to operate on hypothyroid patient till 3 months. If it is an
emergency operation order it. She will not die from hypothyroidism but from
operation.

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Hyperthyroidism
1- postpartum thyroditis
Radiation induced thyroditis
Drugs ( amiodaron )
2- sub acute thyroditis " De Quevare "
3- Hashimoto
4- thyrotoxic gravidarum.
No ttt for these only symptomatic ttt
1- Beta blocker
2- Analgesic
Investigations:
1- TFT : antibodies Graves disease
TSH
T3 & T4
2- Thyroid ultrasound diffuse enlargement Graves
3- Cold or hot
4- ECG atrial fibrillation
5- CXR retrosternal goiter

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HOW TO DIFFERENTIATE BETWEEN THE DIAGNOSIS OF GRAVES
DISEASE & SUB-ACUTE THYRODITIS?
Isotope scanning uptake Graves
uptake sub acute thyroiditis
Surgery with thyrotoxicosis
Potassium iodine inhibit conversion & release ( 5 ml Tds ) with following
up TFT
Beta blocker about 3-4 days before operation.
+ anti-thyroid but it will take long time
thyroid storm
dexamethsone inhibit conversion of T3 to T4.
Kiodine
blocker
TTT of Grave's disease:
1- Radioactive iodine (no increased risk of malignancy & need only one
setting for adjusted dose) method of choice better than anti-thyroid &
surgery WHY?

At last 1.5 2 years + recurrence
1- Low recurrence rate.
2- Better compliance.
3- Not needed to be taken for long duration.

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- The only percussion is conception.
- Need to stop radiation by at least 2 months.
- Rare complication is inducing thyroiditis.
- Rare complication in Grave's with eye sign is aggravation
- Of the eye sign that why we start them on oral corticosteroid about 3-4
days before isotope radiation for 3-4 weeks ( 30 40 mg / day )

3- Neumercazole :
The most important side effect is neutropenia so warn the patient if they
develop any fever to come to ER & report that they are taking anti-thyroid
drug, stop medication & shift to other type.
After starting the patient on a big dose (35 -30 mg / day Neumercazole)
then, see him in 6-8 weeks & give her the maintenance dose.
If she gets pregnant: follow-up with her & adjust the dose according to her
TFT & continue normally on Neumercazole with no problem.
- Once level of TSH stabilized follow her up every 3-6 months by TSH, even if
N don't change the dose!!
- If a patient admits with T4 but TSH is N that means she has poor
compliance
So, we are emphasizing on compliance & NO dose change with regular use
& thyroxin symptoms improve by 2-3 weeks.

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Sub clinical hypothyroidism
TSH + T3 / T4 ( N )
1- TSH > 10 Um / L
2- Family history with thyroid problem
3- Positive thyroid antibodies.
4- Goiter
5- The patient is symptomatic.
This group will develop hypothyroidism later on and so, will need
treatment.

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Addison's disease
Primary adrenal failure
Secondary failure to the axis
Causes of primary:
1- Most common: autoimmune
2-Infections: TB , meningococcal , HIV , fungal (histoplasmosis ,
coccidiomycosis)
3- Malignancy: tumor of adrenal or metastasis
4- Drugs: ketoconazol + metinapol ( used to test for Cushing's disease )
5- Radiation
6- Adrenalectomy
7- Infiltration by amyloidosis + heamochromatosis + Wilson's
Causes of secondary:
1- Sheehan syndrome post partum hemorrhage
2- Any tumor compressing the pituitary
Symptoms:
1- Diarrhea
2- Nausea, vomiting
3- Dizziness
4- Hyper pigmentation (creases + press areas)
5- Postural hypotension
6- Vitiligo can be associated with Addison's

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Organ specific disease ( autoimmune )
1- Addison's
2- Hypothyroidism
3- Pernicious anemia affecting parietal diseases
4-Graves disease
5- Vitiligo
6- DM type I
7- Premature ovarian failure

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DKA
Causes of DKA aggravating factor :
Emotion
Medical problem
Medical dose of insulin
Infection (URTI ,UTI )
Trauma or surgery
New undiagnosed cases
Heavy meal
C/O:
Confusion coma
Abdominal pain + vomiting because dilated stomach
Hyperventilation kussmaul breathing

# Normal anion gab acidosis (hypercholaridemia)
Anion gab = 140 (Ch + HCO
3
)
1) acetozolamide (carbonic anhydrate inhibitor [diuretics] ) used in benign
intracranial HTN (Pseudotumor cerebri (PTC))
2) Road Traffic Accident (RTA)
3) Severe diarrhea
4) Renal artery stenosis
5) Hyperchloremia
# high anion gab acidosis
Not written

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Treatment :
1) Fluid: 1/2 the amount of 24hours. Required in the 1
st
4-6hrs
* Normal saline
2) Insulin: short acting insulin (lispro) = 0.14 /Kg (bolus) then 0.1/Kg as
infusion / hour
# monitoring blood sugar hourly & the dropping of the blood glucose
occur gradually in rate of 75-120 m mol/L
* IM 6-10 v/h * Iv 4-6 v/h
#5 unit I.V bolus # 6 unit I.V infusion
#check glucose hourly
If > 120 drop reduce by 2 unit
If < 75 drop increase by 1 unit
#Then monitoring blood glucose hourly & adjust accordingly
# Very rapid decrease of glucose cerebral edema
3) Electrolytes: monitoring the ECG
[1] K+ :
@ 5.5 K+ no k+
@ 4.5 10 meqev/ 500 cc
@ 4.4 3 20 meqev / 500 cc
@ < 3 30 meqev /500 cc
Not concentrate K+ in 500 cc more than 40 & should given slowly over 2
hours
Put in 1
st
hour because hyperkalemia
[2] ph
+4
: usually corrected by it self unless who develop hypo
phosphatemia in form of muscle weakness give 20 m mol of phosphate &
respiratory failure

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[3] Acidosis & HCO
3:
Only correct if H < 7 , HCO
3
< 5 before correction & after correction < 10
Normal HCO
3
(24 28), his HCO
3
= 6 deficient = 24 6 = 13
Deficient x 1/6 body weight = 18 x 10 = 180
Give half of it only i.e. = 90 give it we are not aim to ideal level over 1/2 hour
Therapeutic output depends on the patients opinion & what he
feels.

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R h eumat o l o gy

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Arthritis
1- Septic.
2- Osteoarthritis. (Wt. bearing knee, hips in elderly & obese).
3- Seronegative.
4- Seropositive SLE, RA.
[1] Septic arthritis:
All monoarthritis is septic arthritis until proven other wise.
- Synovial NF > 50,000.
- Acute onset.
- With fever & chills.
- Positive culture.
- More commonly in knee.
[2] SERONEGATIVE:
1* Ankylosing spondylitis: 4 As:
- Apical lung fibrosis.
- Aortic regurge.
- Anterior uveitis.
- Achilles tendonitis.
HLA-B27
Spine sacroiliac joints.
Pain on rest, improved on exercise.
Bamboo spine & Syndesmophyes (Tramline appearance) in an x-ray.

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2* Reactive arthritis (Reiter's Syndrome):
1- STD.
2- non STD.
(urethritis, conjunctivitis, arthritis).
Rash:
Keratoderma blennorrhagica: on palm & sole.
-Circinate balanitis: on glans & prepuce.
3* Psoriatic arthritis:
- A symmetrical inflammatory oligoarthritis.
- Symmetrical polyarthritis: like RA.
- Predominant distal interphalangeal joint arthritis.
- Psoriatic spondylitis: like ankylosing spondylitis.
- Arthritis mutilans.
Extra articular:
Nail: onycholysis, pitting, sublingual hyperkeratosis, horizontal ridging.
Skin: scaling on extensor.
4* (Enteropathic Arthritis) Arthritis with inflammatory bowel disease
(IBD):
Ankylosing spondylitis & sacroiliitis with diarrhea.
5* Bachet syndrome:
Recurrent oral / genital ulcer.
Recurrent thrombi: CVA, DVT, optic.
6* Whipple's disease:
Arthritis + Hyperpigmentation + LN + Splenomegaly.

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[3] Seropositive:
1- RA:
Significant morning stiffness or joint pain must be more than an hour.
INVESTIGATION:
1- Base line for all patients
2- Specific.
(1) BASE LINE INVETIGATION:
1- CBC cytopenia.
2- ESR, CRP.
3- Urea & electrolyte to assess kidneys.
4- LFT.
5- HBV, HCV cryoglobulinemia.
6- Urine analysis (protein, hematuria, cast).
7- X-ray (chest).
8- ECG.
(2) SPECIFIC:
- ANA SLE may be for the other also.
- Anti-ds DNA, anti-Sm Abs SLE.
- RF present in 70% of cases RA.
- The most specific test for RA is anti-CCP Abs which is anti-cyclic citrullinated
peptide positive > 95% (new & still not written in text books, a rheumatologist will require it).
- X-ray (hands, knee, feet, cervical atlantoaxial joint) RA.
- Upper GI endoscopy,
- Motility test scleroderma.
- Anti-Scl 70 Scleroderma.
- P-ANCA if chest pain + hemoptysis / antiglomerular basement membrane
(anti-GBM).

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- All patients with hematuria & proteinuria more than 1g DO Renal Biopsy
regardless of renal function test.
- If u suspects complement Do: C3, C4.
2- SLE:
Criteria to diagnose SLE;
Remember this word SOAP Brain Md
Four out 11 is considered ok to diagnose SLE:
1- Butterfly molar rash cross the nasal bridge doesnt cross nasolabial fold
because if it does weve to think hypothyroidism, polycythemia .
Dr. Fatah Aldien said,, it could be found in the buccal mucosa and labia
majora.
Also doesnt leave scar... and its erythematous.
2- Discoid rash its raised erythematous found more commonly in the scalp
area also leave scar.
3- Photo sensitivity means the redness increase when exposed to sun... or
new redness formed in exposed area.
4- Oral ulcer.
5- Arthritis non erosive small (peripheral) joints.
6- Serositis pleura, pericardium.
7- Renal disorder can be asked like thisany proteinuria (frothy bubbles
seen with the urine) or New Hypertensionor lower limb edema or any
edema.
8- Neurological disorder seizure or psychosis not depression.

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9- Hematological disorder:
A-Hemolytic anemia.
B-leucopenia less than 4000.
C- Lymphopenia less than 1500.
D- Thrombocytopenia less than 100.000.
10- Immunological disorder:
a- anti phospholipids' Abs.
b- anti-Ds DNA Abs.
c anti-Sm. Abs.
d- False positive syphilis serology.
11- ANA positive > 95% of cases.
Lets go through each system:
1- CNS: 60%.
-Convulsion and seizure.
-Psychosis weve to know is it due to SLE or Cortisone treatment side effect?
By:
-myopathy due to cortisone side effect.
-depression and vasculitis stroke.
2- eye:
(1) Anterior Uveitis but more with RA.
(2) Dry eye plus dried mouth sjogren syndrome.
Schirmer's test put litmus paper strip.
if it's wetted by tear change the color.
15 mm is normal.

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(3) Cystoid bodies (on microscopy) / by ophthalmoscope cotton wool spots.
(4) Subconjunctival hemorrhage.
3-Neck:
Thyroiditis.
4- lung: Dr. Abeer Kawther:
1) Vasculitis fibrosis, thrombosis (lung infarction).
2) Pleurisy.
3) Recurrent DVT pulmonary embolism.
4) Pulmonary edema due to secondary HF.
5) Immunosuppression (immunity) by SLE or steroids (drugs) prone to
infection Tb or atypical infection.
6) Pneumonitis (non-bacterial, due to vasculitis) like lobar pneumonia.
7) Pleural effusion transudate.
8) Shrunken lung syndrome due to bilateral fibrosis (fibrosing alveolitis).
9) obliterative bronchiolitis.
10) Dyspnea (analyze it & see if it's related to SLE or not) due to:
- Pneumonitis.
- Effusion, edema.
- Pulmonary infarction.
- Lung fibrosis.
- Myositis of respiratory muscles.
- Anemia autoimmune (hemolytic).
In Lupus Pneumonitis:
- S.O.B.
- Fever might present or not (suppressed by medications).
In Lung Fibrosis:
Patients may take bronchodilators may benefit or may not.

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5- Heart:
-Aseptic endocarditis (libman sack $).
-Pericarditis and pericardial effusion.
-Mitral regurge is more with SLE and Aortic regurge with RA.
6- Abdomen:
- Autoimmune hepatitis high liver enzymes either due to drug or hepatitis.
- Pancreatitis due to drug.
- Peptic ulcer due to drug or vasculitis.
- Splenomegaly.
- Remember felty's syndrome: Splenomegaly + RA + leucopenia + leg
ulcer.
- Diarrhea... because it can be associated with scleroderma so theyll have
esophageal dismotility and atonic intestine and blind loop syndromealso
crest syndrome.
- 3 signs of peritonitis: fever turbid drain vomiting abdominal pain (may
be).
7- Kidney: 50%
Lupus Nephritis classes.
It could be:
a- Normal
b- Glomerulonephritis 5 stages (patterns):
Minimal change GN.
Mesangeal lupus GN.
Focal proliferative GN.
Diffuse proliferative GN.
Membranous GN.
c- Renal failure.
d- Amyloidosis, but more with RA.
e- UTI.

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8- Joints: >90%
-None deforming.
-Affect small joint.
-Distal interphalangeal joint.
-No morning stiffness.
9- Skin: 80%
- Butterfly rash.
- Discoid lupus erythematous (DLE).
- Livedo reticularis especially associated with antiphospholipid syndrome and
Pancreatitis
- Alopecia,
10- Hematologically:
- Any cytopenia.
- High ESR / CRP is normal in SLE.
- Low complements.

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Investigations:
1- CBC cytopenia
2- High ESR which is indictor for reactivity.
Normal CRP in SLE used in Differential Diagnosis

3- ANA which is sensitive / Anti-Ds DNA Antibodies which is diagnostic for SLE
AND Anti-sm Antibodies
4- LFT for chronic active hepatitis.
5- U & E for lupus nephritis.
6- Complements level low.
7- Urine test red cell cast And proteinuria do 24h.
8- CXR Cardiomegaly.
9- Echo.
10- ECG because of conduction abnormality and arrhythmia.
Signs of active disease:
1- Clinically: arthritisfever, rash, pericardial and lung effusion.
2- Biochemical: cytopenia, low complements, high ESR and normal CRP. Also
active sediments in urine hematuria or red cast cells.
Chest pain in a SLE patient is due to serositis pleural effusion, pericarditis
Loin pain can be presented in SLE due to:
-Infraction (vasculitis).
-Infection.
-Renal vein thrombosis which is noticed as antiphospholipid syndrome (APS)
Normal ESR level up to 20mml/h
Zero ESR is seen in polycythemia.

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In History:
+ Dr Fat'h Al-deen likes this scenario when a student presents the History:
Is a patient is known to have SLE for 10 years Based on (mention the criteria that
was presented by the patient), thus upon them the diagnosis made and was
diagnosed by dr. ____ then she was admitted to the hospital with flare up of her
SLE complaining of ____
+ Dr Fatmah Al-Beladi says "never say SLE alone"
Known as SLE,
- When was it diagnosed?
- What criteria are they based on? Clinical & Laboratory.
- Treated with what?
- Complicated with what?
Always ask about chemotherapy, if the patient doesn't know ask about: an
expensive tablets or drugs taken through IV once every month, because if she has
Lupus nephritis class VI is usually treated by chemo.
Causes of death in a SLE patient?
1- Infections (opportunistic).
2- Renal /CNS involvement (active SLE).
3- Accelerated atherosclerosis MI.
Differential diagnosis of SLE:
-RA.
-Scleroderma.
-Drug induced lupus.
-Rheumatic heart disease.
-Chronic active hepatitis.

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Smart Rheumatology Qs by Dr. Fat'h Aldeen and then he swore when any
student answered them... He gave them almost a full mark
SLE patient takes an anti-Malarial drug like HydroxyChloroQuine?
The function of this medication is to suppress the high level of ANA and RF.
Side effect: Increased skin pigmentation and deposit in retina and all these seen
only in high dose.
A patient came to Dr. Fat'h Al-deen, with symptoms similar to RA (joint pain), she
was diagnosed in Harvard as RA because she has High ANA and High sky RF.
So the doctor said I don't trust Harvard University... I only trust in my knowledge
and trust excellent doctors" & told his patient that she doesn't have RA & gave her
anti-Malaria drug (hyrdoxyChloroQunine) because it suppresses for High ANA and
RF which then the symptoms subsides.
Then she was diagnosed to have parvovirus infection which causes symptoms
similar to RA & SLE.
How to differentiate that psychosis in SLE pt, whether it's
a side effect of cortisone or due to SLE it self?
By test of Anti-Ribosomal B Abs If positive so it is due to SLE.
So in both situations we've to decrease steroid because of psychosis that's
worsening.
Anti-phospholipids' Syndrome:
Diagnosed by Having Low platelets and prolonged PTT and in the Hx they've
abortions and Migraine, TIA, stroke, amurosis fugax. And in examination they've
levido reticularis.

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Causes of prolonged PTT:
Either coagulopathy or auto Abs like antiphospholipid $.
So to investigate anti-phospholipids' $ by three tests [ELISA]:
1- Lupus anticoagulant (its mechanism is very important) see below:
2- Anti-Cardiolipin.
3- Anti-Beta 2 glycoprotein 1 Abs (beta2GP1) very important for the
diagnosis.
50/50 fixed test for Lupus Anticoagulant:
Antiphospholipid pt. has prolonged PTT.
So, we take patient serum (50%) & mix it with serum from a normal person (50%).
If the result was corrected (PTT not prolonged), then the cause of prolongation is a
deficit in the blood itself (factor deficiency), not APLS. Because the defected blood
earned factors from the healthy blood.
If Prolongation of PTT is still the same not corrected Ag/Abs reaction
(autoimmune).
*In summary:
PTT:
-If corrected factor deficiency.
-If not corrected Ag/Abs.
Drug induced SLE:
-Usually by hydralazine procainamide - IsoNiazid.
-They've Positive anti-Histone.
-Normal complements and ANA positive.
-Anti-ds DNA negative.

Methotrexate is hepatotoxic it's given once weekly.

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N eur o l o gy

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How to take: A quick perfect neuro-history
Dr.Aishah Al-Shareef
# Higher functions:
- Headache
- Confusion
- Loss of conciseness
- Seizure
# Cranial nerves:
- Smelling problem(1)
- Decrease in vision acuity... (2)
- Double vision (3, 4, 6)
- Facial numbness or hypersensitivity... (5)
- Facial muscle: (7) asymmetry, in ability to close the eye, food accumulation,
saliva drooling, speech difficulty +
:
:
.. .. :
Lips
.. : ..
Tongue
.. .. :
Palate
- hearing problem: (8)
- Difficulty in swallowing, choking sensation + hoarseness: (9, 10, 12)

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# Motor:
- Weakness
- Proximal:



- Distal:


- Double vision
- Speech difficulty
- Voice hoarseness
- Facial asymmetry
- Food accumulation
- Inability to close the eye
- Difficulty in swallowing
- neck stiffness
# Sensory:
Pain (dull, numbness, decrease in sensation or increase)
Analysis: site , distribution
# Cerebellar functions:
- Tremor
- Unstable gait
# Autonomic:
- Stool control
- Urine control
(Either retention or incontenence)

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# Risk factors:
(Depend upon your case) , e.g.:
- Similar condition in the past
- fever, URTI, diarrhea
- Food type, exposure to sunlight ( osteomalasia and generalized weakness)
- DM, HTN, hyperlipidemia, IHD
- Anticoagulant
- Family history of the same condition, or specific neuro cases
- ..
# Social:
- Smoking
- Degree of disability:
/

# Hospital course:
- Intubation
- ICU (why?? ttt)
- ..
- Investigation
---------------------------
Note: The aim is by the end of the history you know should have known the
cause of this condition (or differentiate and then be able to determine the
site of lesion.
You will reach to this aim if you write the complete history (both positive and
negative symptoms)
Start with the patients complains.
Do not forget important review of systems for differential.
e.g.: (fever indicates infection, vomiting indicates increase intracranial
pressure)

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Localization
Dr.Aisha Al-Shareef
Weakness pattern:
-Hemiparesis.
-Paraparesis.
-Quadriparisis.
-Generalized ( cranial nerve involvement motor part: double vision,
dysphagia).
Hemiparesis:
1- Where is the lesion?
2- What is the lesion?
* Spinal cord hemiparesis:
-Face not involved.
-No CN involvement.
-Sensory: pain, tempntralateral.
-Deep sensation, proprioception vibration silateral
-Brown square syndrome.
Brain stem:
1- Crossed phenomena (sensory or motor):
- CN: ipsilateral.
-Body: contralateral.
2- Cranial nerve CNS involvement:
Any CN involvement is in brain stem except facial nerve could be
cortical or subcortical.
3- 4 Ds: at least 2 of them:
1- Dysarthria CNS IX, X, XII.
2- Dysphagia: IX, X.
3- Disequilibrium cerebellar peduncle.
4- Diplopia: III, IV, VI.

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Subcortical / Cortical:
-No cranial nerve involvement.
Except: facial nerve lower part
-Hemiparesis.
-Facial + weakness = all is ipsilateral to each other.
Cortical:
-Cognitive impairment e.g.: aphasia, memory, language problem.
-Distribution of lesion:
Internal capsule is a dense fiber.

= upper & lower limp same power:
If: Upper limp 0/5 lower limp 0/5
: Upper limp 1/5 lower limp 1/5
: Upper limp 2/5 lower limp 2/5
: Upper limp 3/5 lower limp 3/5
: Upper limp 4/5 wer limp 4/5
In cortex: no equal distribution (face, trunk, hand, leg).
= e.g.: upper power 0/5 wer 4/5
Seizure = cortex irritation.

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Paraparesis:
Upper power 5/5 lower weakness:
1- Spinal cord lesion.
2- Parasagittal tumor.
3- Peripheral nerve (mononeuritis, mononeuritis multiplex, early
polyneuropathy later on hands affected).
In polyneuropathy LMNL fasciculation, arefelxia etc
In cortical: cognitive impairment, CNS.
In spinal cord: sensory level, any nerve above L1 can give sensory level but
below it not consider a spinal cord lesion e.g.; stock distribution in diabetes is
not a spinal cord.
Quadriparesis:
Big insult, internal capsule.
1- Cervical spinal cord lesion.
2- Late stage GBS.
3- NMJ: myasthenia, lambert-eaton.
4- Muscle.
- In spinal cord: motor UMNL, sensory level.
- In polyneuropathy (gloves & stock) LMNL, distal > proximal.
- In NMJ: normal sensory, proximal > distal, no UMNL only. Weakness normal
reflexes, fatigability: fluctuation in power 5/5 in the beginning, after exercise
4/5.
-In muscle myopathy: normal sensory, proximal > distal, no UMNL only
weakness normal reflexes, in myopathy the power is the same even after
exercise.
A.H.C:
- Motor neuron disease.
If no UMNL.
- Mixed UMNL +LMNL.

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STROKE / CVA
Dr.Maimoona
CVA is only vascular
Stroke, we don't call it vascular
CAUSES:
1 - Hemorrhage
2- Infarction
3- Space Occupying Lesion (SOL)
4- Demyelinating disease
5- Degenerative disease
6- Metabolic disease
Hemorrhage:
- AV malformation most common in young patients
- Ruptured berry aneurysm
- Hypertension (HTN) in old patients
- Patient on anticoagulant: aspirin, warfarin, heparin
- Trauma
Infarction:
(1) Atherosclerosis:
- Diabetes Mellitus (DM)
- Hypertension (HTN)
- Hyperlipidemia
- Smoking

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(2) Thromboembolism:
1- due to any arrhythmia:
- Rheumatic heart disease Valvular heart disease
- IHD
- Thyrotoxicosis
2- Infective endocarditis
(3) Thrombophilia
(4) Sickle cell anemia
(5) Polycythemia
(6) Oral countraceptive pill (OCP)
(7) Carotid stenosis due to atherosclerotic plaque commonest in elderly
(8) Connective tissue disease
Space occupying lesions: sudden decrease in BP
1- Tumors:
Primary tumors young patients
Secondary tumors due to metastasis elderly
2- Infections:
Tuberculosis #1
Meningitis
Hydatid cyst
Abscess whatever the cause is
Fungal
HIV
Toxoplasmosis
CMV
Demyelinating disease :
They are many, just remember Multiple Sclerosis (MS)

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Degenerative disease:
- Cerebral palsy
- Huntingtons disease
Metabolic:
When there's a heavy metal deposition in the brain, depending on site of
deposition
- Hemochromatosis
- Wilson's disease
Pediatrics

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In HISTORY:
Causes according to age group:
In young (< 45y)
The commonest cause is hemorrhage
1- AV malformation
2- Rupture berry aneurysm
3- MS (demyelinating)
4- Valvular heart disease
5- Thrombophilia ( decrease protein C , S , III , V )
6- CTD connective tissue disease , vasculitis
7- Thyrotoxicosis
8- any other cause :
infection : abscess , HIV , TB , meningitis
Sickle Cell Anemia (SCA)
9- Infective endocarditic (drug abuse)
Arrhythmia due to any cause
DM & HTN in young & elderly
In elderly:
1- Diabetes mellitus
2- Hypertension
3- Anticoagulant
4- Space occupying lesion tumor, mainly metastatic
5- Hyperlipidemia ( atherosclerosis , smoking )
6- Ischemic Heart Disease (IHD)
7- Arrhythmia
8- Infection ( TB , abscess )

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Risk factors:
1- Increase in Blood Pressure
2- Smoking
3- DM
4- Heart diseases ( 1- valvular 2- IHD 3- AF)
5- Peripheral vascular disease
6- Past TIA = transient ischemic attack
7- Increase packed cell volume
8- Carotid bruit
9- Pills in smoker
10 -Lipids increase
11- Excess alcohol
12- Increase clotting ( increase fibrinogen decrease antithrombin III)
Important points in history:
Thromboembolic: sudden
Hemorrhagic: progressive headache, blurred vision, neck pain
EXAMINATION:
Concentrate on the following:
(1) Level of consciousness according to Glasgow Coma Scale
(2) Vital signs
- Blood Pressure (BP) HTN
- Temperature infection
Pulse arrhythmias
(3) Cranial Nerve Examination

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(4) Site of lesion (type of paralysis) complete neuro-examination
- mono
- Hemi
- quadri
- .
(5) Looking for underlying etiology:
- CVS: arrhythmias valvular heart disease (murmurs)
- Respiratory: evidence of:
- Crepitations HF
- Consolidation TB
- Hepatosplenomegaly & Lymphadenopathy malignancy
- Signs of Connective Tissue Disease (CTD):
1 - Vasculitis
2- Arthritis
3 - Photosensitivity
4- Swollen knee
5 - Alopecia
- Listen for:
* Carotid bruit
* Renal bruit (renal artery stenosis)
- Meningeal irritation (neck stiffness)

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INVESTIGATIONS:
All patients should have:
(1) CT scan or MRI for the diagnosis:
(Hemorrhage, infarction, space occupying lesion, demyelinating,
degenerative)
(2) Chest x-ray (CXR) TB, HF, cardiomyopathy, tumors
(3) ECG* Lt. ventricular hypertrophy or Right. Ven. Hypertrophy, block
arrhythmia
(4) GLUCOUSE: random blood sugar DM
(5) CBC
- Leukocytosis (high WBC) infection (meningitis)
- Hb Polycythemia
- Cytopenia CTD (SLE)
(6) Lipid profile* hyperlipidemia
(7) DOPLLER of the CAROTID **very important**
(9) ECHOCARDIOGRAM* all patients with stroke should have it
Valvular lesion, ejection fraction (dilated atria or ventricle )
Certain Investigations, only According to History & Examination.:
1- SCREEN FOR VASCULITIS: ANA, RF
2- THROMBOPHILIA screen potien S, C, antithrombin III, factor V
3- screening for malignancy
4- HIV
5- LUMPER PUNCTURE if NORMAL CT, No cerebral HTN, No papilloedema
6- Angiogram if you suspect AV malformation or Berry aneurysm rupture
(not if pt has ..)

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7- U & E HTN
8- COAGULATION profile: PT, PTT
9- SEPTIC CULTURE infective endocarditis
10- HG electrophoresis SCA
11- if demyelination on CT LP increase protein oligoclonal band
- for multiple sclerosis :
1) Lumbar puncture (LP)
2) Visual evoked potentials (VEP) optic nerve
3) Auditory cerebellar evoked response
4) EMG
5) Nerve conduction study delay
STROKE MANAGEMENT:
In general:
- Physiotherapy
- CNC IX, X lesion NGT
- Incontinence catheter, diaper
[1] Hemorrhagic stroke:
- If CTS, MRI show: hemorrhage then find the cause
(1) If it is due to Hypertension:
Look if there is a midline shift or no (in massive midline shift: consciousness
affected & respiratory distress)
MS diagnosed mainly by relapse & remission 2 attacks
Affect mainly:
- Optic Nerve
- cerebellum

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If there is midline shift give manitol to decrease ICP
If no midline shift then decrease BP very slow, not below 180/100 because
it will causes decreased perfusion
Dextamethasone: would not work
Observe the patient: either:
1- Hemorrhage resolves on its own & patient improves
2- Bore hole & remove the hemorrhage if it is MASSIVE but usually not
needed
(2) If the cause of hemorrhagic stroke not known: then it is
AV malformation / ruptured berry aneurysm
- call neurosurgeon to clip the aneurysm because it will re-bleed in 10 days
- Angiogram to be available before calling neurosurgeon to confirm which
artery
[2] Infarction type:
Treat according to the cause:
- In arrhythmias, VHD, AF anticoagulation
- If not any of these just put patient on aspirin & plavix
(Usually patient is DM, HTN, hyperlipidemia, smoker treat the
comorbiditiy)
[3] If demyelination: steroids + alpha interferon (-IF)
in hemorrhagic stroke : high mortality, but if survives less
morbidity than ischemic
in ischemic stroke: less mortality but high morbidity
compared to hemorrhagic stroke

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[4] If infection: find the source erode the infection
- If not HIV, CMV & toxoplasmosis are very rare, usually in
immunocompromized patient
- If infection is not HIV & the chest is clear empirically give
Anti-TB
- If there is a middle ear infection then give broad spectrum antibiotic
[5] If malignancy: biopsy, radiotherapy, in primary malignancy some times
surgery depends on the type
[6] Carotid artery stenosis
70 - 80% neurological deficit, TIA end artery surgery
[7] Metabolic specific treatment
Notes:
Classification of neurological deficit:
1- TIA: improve in 24 hrs
2- RIND: reversible ischemia, 2 weeks neurological deficit
3- Complete stroke

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Upper Motor Neuron Lesion
UMNL
Causes of paraplegia:
1) Demyelinating diseases:

MS: Cranial nerve palsy eye problems
Upper motor neuron lesion
Hemiplegia and paraplegia (spastic)
Optic atrophy
Cerebellar signs
2) Trauma
3) Compression of spinal cord

Secondary tumor metastasis (lymphoma, MM, breast,
lung, prostate, renal)
Primary tumors (Meningioma or any brain
tumor compresses the
internal capsule)
Disc prolapse
Hemorrhage (blood)
Pott's disease
Cervical spondylosis
RA atlanto-axial dislocation
Syringomyelia (cyst)
4) Infections

T.B (brain spinal cord) \ Guillain Barre Syndrome
Syphlysis (taboparesis)
Meningitis

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Viral infection \ herpes transverse myelitis
Brucella
Abscess
HIV
Schistosoma
5) Vasculitis of spinal cord
Primary vasculitis of brain arteritis
Secondary vasculitis of connective tissue diseases

(vascular) SLE (autoimmune) RA
6) Ant. Spinal cord thrombosis
Myocardial infarction
7) Subacute combined degeneration of spinal cord
8) B12 deficiency
9) Lymphoma
10) Neurofibromatosis
Exc. Growth of nerve \ can affect any nerve

11) Granuloma
syringomylia
sarcoidosis
T.B
12) Congenital spastic paraplegia
13)

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*Most Common Causes in young age group:
MS
TB
Transverse myelitis
Vasculitis

*Most Common Causes in old age group:
Compression
Disc Prolapse
Cervical spondylitis
Metastasis
*Notes:
Sacral spinal nerves are affected
Palpitation AS, Arrhythmias
Back pain Brucella , disc prolapse , trauma

Renal pain and haematuria renal cell carcinoma

Brachial plexus compression:
Cervical rib
Any mass at the apex (lymphoma, TB)

MS relapse & remission

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Investigations:
A) Definite:
1. Fundoscopy

Papilloedema
C.T scan (if no papilloedema we can perform a lumbar
puncture)
2. MRI
Specific for demyelinating disease
Demyelinating plaque
Look for space occupying lesions (tumor,
abscess, and cyst)
3. X-Ray
TB
Disc prolapse
Fracture
Cervical spondyelitis
4. Lumbar puncture

Protein (infections, MS)

Glucose (bacterial infection)
Lymphocytes (TB)
Neutrophils (bacterial infection)
Malignant cells
Single P band mono/oligoclonal P band (MS)


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5. Biopsy

Pott's
Tumors

B) Supportive:
1. CBC leukocytosis

2. ESR (infection, malignancy)
3. ECG
4. ANA
5. Visual evoke response
6. Auditory evoke response
7. EMG (delayed conduction in MS)
*For Infection:
1. PPD ( TB)

2. (B12)

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Polyneuropahties (PN)
Causes:
1) Infection:
Leprosy , lyme , syphilis , HIV
2) Inflammation:
Guillan-Barre , chronic inflammatory demyelinating PN ,sarcoidosis
3) C.T. disease:
PAN, wegeners , RA
4) Metabolic:
DM, hypoglycemia, hypothyroidism, renal failure
5) Malignancy :
PNS, polycythemia , multiple myeloma
6) Toxines:
Lead, arsenic
7) Drugs:
Alcohol, INH, anticancer
8) Vitamins:
Low B1, B12, B6, Folate, or increase B6

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9) Other:
Amyloidosis
10) Inherited:
Refsum's , charcot-marie-tooth syndrome , prophyria , leukodystrophies
Symptoms:
1) Sensory & motor neuropathy
2) Cranial dysphasia, deafness, speech difficulty, diplopia
3) Autonomic neuropathy




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Acute Confusion State
Causes of acute confusion state:
A: alcohol
E: encephalopathy
I: insulin (hyper, hypo)
O: overdose
U: uremia
T: tumor / trauma
I: infection
S: seizure
M: metabolic
If no history (Hx):
- Hypo or hyperthyroid
- Hypercalcemia
- Hyperglycemia
- Hypo or hypernatremia
Examination:
- Glasgow coma scale
- Pupil size dilated pupil hemorrhage in brain stem
3
rd
nerve palsy
- Blood pressure Low septicemia
High hypertensive hemorrhage
- Temperature
- Pulse

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- Neck rigidity If there hasnt been any clinical evidence of trauma
If there is an evidence of trauma do not move the neck
- CVS
- Evidence of liver failure
- Evidence of uremia
Investigations:
1 CBC Pancytopenia
High leukocytosis
2 Blood glucose
3 U & E, Ca
++
, Mg
4 Liver function test
5 Renal function test
6 Septic screening
Throat culture
Urine culture
Blood culture
Sputum
After a CT scan of the brain Infarction or hemorrhage
Space occupying lesion
If the CT scan is normal order a coagulation profile then L.P
**Remember...
If CT scan doesnt show any infraction (blackish in brain CT)
so there is no infraction.
But in a hemorrhagic case (whitish) sometimes it initially looks
normal but repeat the scan after 12 h to make sure.

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CNS:
1- Psychosis
2- Seizure
3- Stroke
4- Mono neuritis multiplex
Eye:
1- Psytotic body with SLE
2- Scleritis Episcleritis
CVS:
Respiratory:
Abdomen:
1- Chronic active hepatitis
2- Primary sclerosing cholyngitis
3- Glumerlonephritis
4- Amyloidosis
5- Acute abdomen
Skin:
1- Skin ulcer
2- Splinter hemorrhage

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O t h er

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DVT
Session with Dr. Maimoona


Etiology of DVT:
Virchaw's triad
1-Abnormal blood flow
2-Abnormal constituents of blood (hypercoagulability)
3-Abnormal vessel wall
1- Abnormal blood flow
- Immobility* (due to traveling "the most important, fracture,
paralysis, post operative, CVA, pregnancy)
- Heart failure*
- Compression by pregnancy or tumor
& economic class ( ) syndrome DVT
Because vessels are kinked during the flight causing blood stasis.
*The most
important points
in order, you can
then mention the
others according
to order

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- Dehydration due to any reason: (fever, diarrhea)
- Polycythemia
- SCA (sickling crisis)
2- Abnormal constituents
- Thrombophilia: is the deficiency of protein C & S, antithrombin III, factor V
(recurrent & positive FH)
- Nephrotic Syndrome loss of antithrombin III
- CLD (chronic liver disease) prot. C & S, Anti-Thrombin III
deficiency
- Polycythemia
- SCA
- Hypercoagulopathy
- OCP = oral contraceptive pills
- Antiphospholipid antibodies in APLS (in females ask about recurrent
abortion)
- Any malignancies: (prostatic, pancreatic, lymphomatic , leukemic )
- Para protienemia (multiple myloma)
- IBD is Inflammatory Bowel Disease: hypofibrogenemia
- Thrombocytopenic purpura
Never say "nephrotic syndrome & CLD are
causes of DVT" but "they are causes of protein
deficiency"
The most common malignancies causing
hypercoagulable state are:
- Prostate carcinoma
- Lung carcinoma
- Pancreas carcinoma

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3-Abnormal vessel wall
- Vasculitis*: (SLE, RA, good pasture, HSP = henoch shonleinn purpra)
- Trauma* IV cannulation (either in hospital or in IV drug abusers)
- Varicose vein*
Complications of DVT:
-Acute: PE = pulmonary embolism: the most important
Sudden onset chest pain (pleuritic) sharp and related to respiration
Associated with SOB, palpitations, hemoptysis, or syncope
- Chronic: post phelebitic limb >> stagnation of blood >> not return normally
to heart >> leg edema, ulceration, discoloration
History Presentation:
The Patient presented with ..
(Occupation)
He/she has no history of
(Immobilization)
No history of traveling
No suggestive history of Connective Tissue Disease (musculoskeletal)
No history of OCP use
No history of malignancy
No family history of deficiency of protein S, C

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No history of (protein loss)
No previous history of DVT
No history of recurrent abortion I think this is due to APLAS
:
No history of fever or loss of weight
)) exclude causes of DVT complications ((
No history of
NO Hx
Note:
Patient < 45 yr-old traveling, C.T. Disease, pregnancy, OCPs
Patient > 45 yr-old immobilization, malignancy, Heart Failure
Differential diagnosis:
- Cellulites
- Ruptured Baker's cyst (synovium in popliteal fossa as in RA)
- DVT (pitting unless of extensive edema)
- Hematoma
- Lymphoedema (non-pitting)
- Ruptured muscle due to trauma

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Investigations:
For every patient, DO the following:
1 - Doppler
2- Venogram
3- CBC
4- Coagulation profile
5- D-dimer
6- CXR
7- ECG
----------------
Diagnostic Tests:
1 - Doppler 1st line to document DVT if negative
:
2- Venography: gold standard if negative: no DVT
A dye is injected in the (vein) dorsum of foot
angiogram
for artery
* stroke for 10 years
investigations fractures

investigations :
Blood work: certain blood tests are done for specific history
3 CBC lycyciemia , malignancy , cytopenia
4- Peripheral blood film SCA

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5- Coagulation profile: PT, PTT (BEFORE starting the treatment for
monitoring)
Or Anti-Cardiolipin Abs
6- D-dimer increase in thrombosis & PE, but NOT specific may increase in
pregnancy ,infection ,post operative
7- Works for thrombophilia
8- Ag-Ab profile
9- ESR & C - reactive protein
10- Protein electrophoresis multiple myeloma
Radiology:
11- Chest X-Ray (CXR): for pulmonary embolism(PE), pulmonary edema,
malignancy, etc
1-Normal
2- Wedge shaped infarction,
3- Oligemic lung decrease blood flow
12- Ultrasound (US) of pelvis & abdomen for compression:
Abdomen hepatosplenomegaly enlarged LN
Pelvis tumor pregnancy (maybe the patient doesn't know that she's
pregnant)
13- Pregnancy tests (due to increased hormones & compression)

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14- ECG:
Right Ventricular hypertrophy
RBBB
Arrhythmia (atrial)
Sinus tachycardia
S1 Q 3 T 3 CLASSICAL
Lead I: deep S wave
Lead III: Q3 inverted T3

S1 Q3 T3

Sinus tachycardia

15- Doppler US
16- d-dimer (end product of breakdown of thrombus increases in blood)
17- Spiral CT scan.
18- ABG
19- Pulmonary Angiogram
20- Ventilation/Perfusion scan (VQ scan)
----------------

SPECIFIC Investigation
According to History: e.g.: ANA in CTD
In elderly patient, if the cause is not CVA, or post operative or, immobilization
always screen for malignancy.

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If PE 1- spiral CT scan, 2- ventilation perfusion VQ scan
PULMONARY ANGIOGRAPHY is the definitive test for pulmonary embolism
Supporting:
If the patient is < 45 protein C & S, APL Abs, antithrombin III
I the patient is > 45 chest X-Ray, ultrasound abdomen
In both do an ECG.
O/Ex.:
Vital, general
Hands:
C.T. disease, no ulcer, no active arthritis, rashes
Cyanosis (heart failure)
Pulse (tachycardia: Pulmonary Embolism, unequal pulse: Vasculitis)
Postural hypotension
Face:
Rashes, pallor, ulcer in mouth
Legs:
Inspection:
- Swelling & determine the exact site
- Scar (IV, drug abuse)
- Pigmentation
- Shiny skin
- Edematous

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- Redness
- Phlegmasia alba / white leg
- Phlegmasia dolens / milk leg
Palpitations
- Temperature is down and up and compare both
- Tenderness
- Tense calf muscle
- Edema ( DVT = pitting , lymphoedema = non pitting ) & do it up & up to
see till where no more pitting edema e.g.: till the knee or the thigh
- Homan's signs = increasing resistance & pain on forced foot Dorsiflexion :
say it but DON'T do it dislodge thrombus
- Pulse : vasculitis unequal , if absent: why? Because edema compresses the
artery.
: Measurements -


/


:

Bony prominence

Tibial tuberosity

Patella





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0

)) ( (


)) ((
)) ((




))
((



Abnormal









:

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OTHER Ex. :
- Chest signs of pulmonary embolism
- JVP Right side heart failure
- Atrial fibrillation
- Chest creptation
- Hepatosplenomegaly
- Lymph node
- Abdominal mass
- Vasculitis sings
- Fullness of popliteal fossa ruptured Baker cyst
Management
1- Start with heparin IV
80 100 U/kg bolus
20 U/kg/hour infusion maintenance dose
2- Warfarin
either with heparin
or on 3rd day
or on 7th day
10 mg every day for 3 day
3- INR re measure
* PTT heparin
* PT, INR ratio warfarin
2-2 1/2 time control
After heparin of 4 hours PTT
e.g.:
patient control
100 sec. OK 30-40

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200 sec. high decrease heparin dose
60 sec increase heparin dose
Warfarin:
PT
INR used usually
Patient control
2.5 1
5 decrease dose
1 increase dose
- ONCE warfarin 22 1/2 Stop heparin
If the patient takes an OVER DOSE:
- heparin t1/2 = 30 min 1 hour
If over dose and bleed:
stop heparin
If the patient is bleeding can use FFP=fresh frozen plasma,
or antidote= protamine sulfate but it is not given to the patient.
- Warfarin t1/2 = 72 hr = 3 days
we measure it 3 days after start ttt
if over dose:
1- Antidote
2- Vitamin K
3- Stop warfarin
if bleeding occurs then FFP
PE & DVT
Whatever there is PE or not ttt will continue for 6 months If the cause
known
- If the cause is hereditary cause ttt life long
- If the cause is malignancy life long