First Edition

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بطIا 2qIm _s Iasاوaأ و Iaaاوaإ ..
دnµ و ..

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ةدIz IæaوI¡wq _sIا 2Iawtا

نIm دJ و ل,nIا بIzأ ¿Iz ازmر,s, ءاز,Iا رqa uIIا Iyاز, 2aو,q, ةروsmدIا سورد

رa Iaµsm و Ian,, I,qs ةدaIsIا اود,s نأ او, . _s حI,aIا و قqsوsIا مmI ¿a,sa و
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ءIzدIا ¿IIæ ن, Iaوwas x

مmsاوaأ و مmaاوaإ
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مmaار¡ و مmsIaارsJا : MedKnightsSona3Project@gmail.com

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نو,yIw,Iا ءIaztا :
ةIqaIا عIaæ
Kia Ora
angelic_doc
DR.JENEFER
N.S.G
amoona
asphora
ocash
doctor_ology
Dr.Noura
Dr.ambition
Dr. ShoSho
Dr-E
Da_joker
The One
Konvict
KAU Dr.X
ن,زIا سرIs
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, VSD…etc.
* 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
ﺖﻗﻮﻟا ﻊﻣ ، حوﺮﺗ ﻪﺗﺪﻳﺎﻓ ÷ لوأ ﻲﻓ ﺪﺧﺄﺘﻳ مزﻻ ٦ تﺎﻋﺎﺳ .. ﺪﻌﺑ ٢٤ ﺔﻋﺎﺳ
ةﺪﻳﺎﻓ ﻪﻟﺎﻣ ﺮﯿﺴﻳ
ﻧ ﺎﻧﺮﺧﺄﺗا اذإ ﻢﻗر ﻲﻓ رﻮﻛﺬﻤﻟا يﻮﺴ ٤
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 disease…and 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 disease…MI.
4- No compliance with medications.
5- Arrhythmia.
6- Taking NSAID. Which cause salt and water retention.
7- Taking ca channel blocker…Negative 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,
ﺐﺒﺴﻤﻟا و ﺔﻟﺎﺤﻟا ﺐﺴﺣ غﺎﺼﻳ مﻼﻜﻟا ﻦﻜﻟ
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: Sydenham’s 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"
ﻢﮫﻣ

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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:
 К+
- Conn's
- Pheochromocytoma
- Cushing
 К+ ¬ 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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-25 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-26 -
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GENE
RAL
Vasodilators

Β-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
ﺺﻗﺎﻧ ®



¬ α-methyl dopa ¬ poor or pregnant
ACE inhibitors
Β-blockers
Hydralazine
¬ Thiazide

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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-27 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-29 -
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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 ¬ don’t 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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-30 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-31 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-32 -
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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.

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-33 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-34 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-35 -
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R es pir at o r y
dis eas es

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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-36 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-37 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-38 -
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INVESTIGATIONS: {FOR ALL ASTHMATICS}
1- CBC ¬ LEUCKOCYTOSIS + EOSONEPHILIA
2- ABG
3- U+E
a- Hyperventilation ¬ dehydration
b- β2-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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-39 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-40 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-41 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-42 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-43 -
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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 don’t
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)

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-44 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-45 -
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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
*****************

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-46 -
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-47 -
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R en al dis eas es

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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
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-48 -
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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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-49 -
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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. Wilson‘s 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 Chron’s:
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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Crohn’s 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 (ﺔﻳاﺪﺒﻟا ﻲﻓ) 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 ulcer…etc.
- 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) α-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/ µl ¬ 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- β-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 :
¬ It’s Definitive autoimmune hepatitis
 If the score of the criteria is 10 – 15 before ttt & 12 – 17 after ttt
¬ It’s 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 donor’s 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
α-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 ¬ α -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
α-IF.
2. Left ¬ synthetic function ( PT – PTT – Albumin )
¬ Excretory function (bilirubin)
 α-IF should not be given to any autoimmune pt. e.g. SLE , RA.
Because it will worse the condition.
 α-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 shouldn’t ever be given to
patient with hemolytic anemia.
 Rebavirine until now doesn’t 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
α-IF for 6 months ¬ response ¬ 6 %
After 1994 ¬ extended monotherapy ¬ for 1y ¬ 15 %
In 1998 α-IF + Rebavirin ¬ response ¬ 41 %
HCV ¬ 6 genotypes ¬ type I & IV (requires a year) disresponse to
α-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 + α-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 μ.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- post–partum 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.
K–iodine
β–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 ¬ ﻈﺘﻧﺎﺑ بﻮﺒﺤﻟا ﺬﺧﺄﺗ ﻰﺴﻨﺗ مﺎ
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 ¬ doesn’t cross nasolabial fold
because if it does we’ve to think ¬ hypothyroidism, polycythemia ….
Dr. Fatah Aldien said,, it could be found in the buccal mucosa and labia
majora.
Also doesn’t leave scar... and it’s erythematous.
2- Discoid rash ¬ it’s 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 this…any proteinuria (frothy bubbles
seen with the urine) or New Hypertension…or 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.
Let’s go through each system:
1- CNS: 60%.
-Convulsion and seizure.
-Psychosis ¬ we’ve 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 they’ll have
esophageal dismotility and atonic intestine and blind loop syndrome…also
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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
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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: arthritis…fever, 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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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 +
فوﺮﺤﻟا جرﺎﺨﻣ :
فوﺮﺤﻟا ﺾﻌﺑ ﻖﻄﻧ ﻰﻠﻋ ةرﺪﻘﻟا :
ﻢﯿﻣ .. ﻢﯿﻣ .. جﺮﺨﻤﻟا :
Lips
مﻼﻟا .. ﻞﺜﻣ : ﷲا ﻻا ﻪﻟا ﻻ .. جﺮﺨﻣ ـﻟا ﻦﻣ فﺮﺤﻟا
Tongue
فﺎﻜﻟا فﺮﺣ .. ﻻﻮﻛ ﺎﻛﻮﻛ ﻞﺜﻣ .. جﺮﺨﻤﻟا :
Palate
- hearing problem: (8)
- Difficulty in swallowing, choking sensation + hoarseness: (9, 10, 12)

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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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# Motor:
- Weakness
- Proximal:
جرﺪﻟا دﻮﻌﺻ – سﻮﻠﺠﻟا ﺔﯿﻌﺿو ﻦﻣ فﻮﻗﻮﻟا – ﺬﺧأ وا ﺮﻌﺸﻟا ﺢﻳﺮﺴﺘﻛ ﺪﯿﻟا ﻊﻓر ﻦﻣ ضﺮﻏ
ﺪﯿﻌﺑ يﻮﻠﻋ فر

- Distal:
ا ءاﺬﺤﻟا لﺎﻌﺘﻧ – نود ءاﺬﺤﻟا جوﺮﺧ ﻗ ﻪﻣﺪﻗ ﻦﻣ ﺪﺼ – ﺐﻠﻌﻟا ﺢﺘﻓ – بﺎﺒﻟا ﺪﻳ ﺢﺘﻓ

- 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:
ﻪﺴﻔﻧ ﻰﻠﻋ ﺾﻳﺮﻤﻟا دﺎﻤﺘﻋا ىﺪﻣ / هﺮﯿﻏ ﻰﻠﻋ وا
ا ﻞﺒﻗ هﺪﻌﺑو ضﺮﻤﻟ ﺪﻌﺑو جﻼﻌﻟا
# 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 patient’s complains.
Do not forget important review of systems for differential.
e.g.: (fever indicates infection, vomiting indicates increase intracranial
pressure)

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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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, temp¬ntralateral.
-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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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.
أ ةﺪﺣاو ﺔﻣﺰﺣ ي
= 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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
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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
- Huntington’s 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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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:
Thrombo–embolic: 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 (α-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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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- Neck rigidity ¬ If there hasn’t 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 doesn’t 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.

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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O t h er

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ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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 ﺔﯿﺣﺎﯿﺴﻟا ﺔﺟرﺪﻟا ( ) 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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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 ………… تﺎﺒﺒﺴﻤﻟا دﺪﻌﻧ
(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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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
لﻮﻘﻧ ﻦﻳﺪﻌﺑ :
No history of fever or loss of weight
)) ﻲﺷ لوأ نذإ exclude causes of DVT ـﻠـﻟ حوﺮﻧ ﻦﻳﺪﻌﺑ complications ((
No history of ………
ﻪﻠﻛ ﻪﻧإ هﺎﻨﻌﻣ ﺶﻣ NO ـﻟا لﺎﻘﻨﻳ مزﻻ ﻪﻧإ ﺪﺼﻘﻟا ﺲﺑ Hx اﺪﻛ 
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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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
ﻦﯿﻛﺎﺷ ﺔﺴﻟ و ﻲﺷ نﺎﺑ ﺎﻣ اذإ ، يد يﻮﺴﻧ :
2- Venography: gold standard ¬ if negative: no DVT
A dye is injected in the (vein) dorsum of foot
ًﺄﻄﺧ اﻮﻟﻮﻘﻳ ﻪﺒﻠﻄﻟا ﻦﻣ ﺮﯿﺜﻛو angiogram ﻊﺒﻄﻟﺎﺑ اﺬھو صﺎﺧ ﺺﺤﻓ ﻪﻧﻻ ﻲﻃﺎﺧ
ﺪﻳرﻮﻟا ﺲﯿﻟو نﺎﻳﺮﺸﻟﺎﺑ for artery
* ﺎھﺪﻨﻋ ﺔﻟﺎﺣ ﺎﻨﺗﺎﺟ اذإ stroke for 10 years ﺔﻤﻳﺎﻧ ﺎﮫﺘﻗو لﻮﻃ و ، ﺎﮫﻟ يﻮﺴﻧ ﺎﻣ
investigations ﻢھﺪﻨﻋ ﻲﻠﻟا ﻲﺸﻟا ﺲﻔﻧ و fractures ﻦﻳﺎﺑ ﺐﺒﺴﻟا ﻪﻧﻷ ©

ـﻟا ﻞﻛ يﻮﺴﻧ ﺐﺒﺴﻟا ﺎﻨﻓﺮﻋ ﺎﻣ اذإ ﻦﻜﻟ investigations :
Blood work:  certain blood tests are done for specific history
3 – CBC ¬ lycyciemia , malignancy , cytopenia
4- Peripheral blood film ¬ SCA

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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
تﺎﻔﺻ ثﻼﺜﻟا ﺪﺠﻧ ﺪﻗ ﺐﻠﻘﻟا ﻂﯿﻄﺨﺗ ﻲﻓ يأ ﻚﯿﺳﻼﻜﻟا
S1 Q3 T3
ﺐﻠﻏﻻا ﻦﻜﻟ ﻂﻘﻓ ﺪﺠﻧ
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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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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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 -

ﺮﺘﻤﻟا ماﺪﺨﺘﺳﺎﺑ ، ﺲﯿﻘﻨﺳ ﻞﺟﺮﻟا ﻂﯿﺤﻣ
ﺪﻨﻋ نﻮﻜﯿﺳ سﺎﯿﻘﻟا نﺎﻜﻣ نﺎﻜﻣ ضﺮﻋا / ﺮﺜﻛﻷا ﺎﺧﺎﻔﺘﻧا
ﺔﻄﻘﻧ ﺪﻳﺪﺤﺗ ﻦﻣ ﺪﺑﻻ ﻚﻟذ ﻞﻌﻔﻟو ﺔﺘﺑﺎﺛ سﺎﯿﻘﻠﻟ ، ﺲﯿﻘﻨﻟ ﺎﮫﻨﻣ ةﺮﻤﻟا ﺔﻣدﺎﻘﻟا ﺲﻔﻧ ﻲﻓ
ﻂﯿﺤﻤﻟا ﻲﻓ ﺮﯿﻐﺘﻟا ﺔﻧرﺎﻘﻤﻟ نﺎﻜﻤﻟا
ﺔﻄﻘﻧ ﺪﻳﺪﺤﺘﻟ ﺔﺘﺑﺎﺛ سﺎﯿﻗ :
ﺔﻄﻘﻧ مﺪﺨﺘﺴﻧ ﺔﺘﺑﺎﺛ ﻞﺟﺮﻟا ﻦﻣ
Bony prominence
ﺎﻨھ نﻮﻜﺘﺳو لا
Tibial tuberosity
و اﻮﮫﺒﺘﻧا ﻻ ﻼﯿﺗﺎﺒﻟا ماﺪﺨﺘﺳا ﺢﺼﻳ
Patella
ﻪﻄﻘﻨﻛ ﺔﺘﺑﺎﺛ ﺎﮫﻧﻷ ﺔﻛﺮﺤﺘﻣ




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ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
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ﻠﻋ ﺮﺘﻤﻟا ﺖﺒﺜﻧ ﻰ ﺪﻨﻋ ﻲﺘﯿﺳوﺮﺑﻮﯿﺗ لﺎﺒﯿﺘﻟا 0 ﻢﺳ
ﻞﺼﻧ ﻰﺘﺣ قﺎﺴﻟا داﺪﺘﻣا ﻰﻠﻋ ﺎھﺪﻤﻧو ﺮﺒﻛﻷ ةءاﺮﻘﻟا ﻞﺠﺴﻧو ﺦﻔﺘﻨﻣ ﻂﯿﺤﻣ
ﻼﺜﻣ ﺎھﺎﻧﺪﺟو ١٢ ﻢﺳ )) ﺐﻠﻏﻷا مﺪﺨﺘﺴﻳ ١٠ ﻢﺳ ( ( ÷ ﻨﻟا ﻲھ نﻮﻜﺘﺳو ﺔﻄﻘ ﺔﺘﺑﺎﺜﻟا
مﻮﻳ ﻞﻛ ﺎﮫﻨﻣ ﺲﯿﻘﻨﺳ ﻲﺘﻟا

)) مﺪﺨﺘﺴﻳ ﺐﻠﻏﻷا ١٠ ﻼﯿﺗﺎﺒﻟا ﺪﻨﻋ ﻦﻣ ﻻوﺰﻧ ﻦﯿﻗﺎﺴﻟا ﻼﻛ ﻲﻓ ﻢﺳ ((
هﺬھ ﺪﻨﻋ ﻦﻣ ﺔﻄﻘﻨﻟا ﻟا ـ ١٢ ﻢﺳ )) ﺐﻠﻏﻷا مﺪﺨﺘﺴﻳ ١٠ ﻢﺳ (( ﺬﺧﺄﻧ قﺎﺴﻟا ﻂﯿﺤﻣ
ةءاﺮﻘﻟا ﻞﺠﺴﻧو
ﻼﺜﻣ ﺎھﺎﻧﺪﺟو ٣٤ ﺳ ﻢ ÷ ﻂﯿﺤﻤﻟا ةءاﺮﻗ ﻲھ نﻮﻜﺘﺳو ﺔﺑﻮﻠﻄﻤﻟا
نﻵا ﺐھﺬﻧ ﻰﻟإ ا ﺔﯿﻧﺎﺜﻟا قﺎﺴﻟ
رﺮﻜﻧو ﺔﯿﻠﻤﻌﻟا
ﺎﮫﻨﻣ لﺰﻨﻧو ﻲﺘﺴﻳﺮﺑﻮﯿﺗ ﺎـﯿﺒـﯿــﺘﻟا نﺎﻜﻣ دﺪﺤﻧ ﻂﺒﻀﻟﺎﺑ ﺮﺘﻤﻟﺎﺑ ١٢ ﻢﺳ )) ﺐﻠﻏﻷا مﺪﺨﺘﺴﻳ
١٠ ﻢﺳ ((
قﺎﺴﻟا سﺎﯿﻗ ﺔﻄﻘﻧ ﺲﻔﻧ نﻮﻜﯿﻟ ىﺮﺧﻷا
ﻢﺛ ﻦﻣو ﺬﺧﺄﻧ ةءاﺮﻗ ﺎھﺎﻧﺪﺟو ضﺮﻔﻨﻟ ﺎﮫﻠﺠﺴﻧو ﻂﯿﺤﻤﻟا ٣٠ ﻢﺳ
ةﺪﻋﺎﻘﻟا لﻮﻘﺗ اذإ ﻦﯿﻄﯿﺤﻤﻟا ﻦﯿﺑ قﺮﻔﻟا ﺮﺜﻛأ ﺳ ﻒﺼﻧ ﻦﻣ ﻢ ﺳ نﻮﻜﺘ
Abnormal
ﺖﻧﺎﻛ ﺎﻨھو ﻰﻟوﻷا ٣٤
ﺔﯿﻧﺎﺜﻟاو ٣٠
ﻟا قﺮﻔ ٤ ﻢﺳ ، نذإ ﻲﻌﯿﺒﻃ ﺮﯿﻏ
قﺎﺴﻟا ﻂﯿﺤﻣ ﺲﯿﻘﻨﺳ ﺎﯿﻣﻮﻳو ﺔﺑﺎﺼﻤﻟا ﺲﻔﻨﺑ ﺔﻘﻳﺮﻄﻟا ﻲﺸﻤﻧ ﺎﯿﺒﯿﺘﻟا ﺪﻨﻋ ﻦﻣ ١٢ ﻢﺳ
ﺬﺧﺄﻧو مﻮﻳ ﻦﻋ مﻮﻳ قﺮﻔﻟا فﻮﺸﻧو ﻂﯿﺤﻤﻟا ةءاﺮﻗ
اذإ ﺬﺨﻔﻟا ﺖﻧﺎﻛ ﺎﻀﻳأ ﺲﻔﻨﺑ ﺎﮫﺴﯿﻘﻨﺳ ﻪﺑﺎﺼﻣ ﺔﻘﻳﺮﻄﻟا
ﻪﺘﺑﺎﺛ ﺔﻄﻘﻧ دﺪﺤﻧ ﻊﻠﻄﻧو ﻢﻈﻌﻟا ﻦﻣ ﺮﺘﻤﻟﺎﺑ ﺎﮫﻨﻣ ﺮﺜﻛﻷ ﺦﻔﺘﻨﻣ نﺎﻜﻣ ﺬﺧﺄﻧو ﻂﯿﺤﻤﻟا سﺎﯿﻗ
قﺎﺴﻟا ﻲﻓ رﺮﻜﻧ ىﺮﺧﻷا ﺔﻧرﺎﻘﻤﻠﻟ
ﺬﺨﻔﻟا ﻂﯿﺤﻣ ﺲﯿﻘﻧ ﺎﯿﻣﻮﻳو ﺔﺑﺎﺼﻤﻟا ﺔﻧرﺎﻘﻤﻠﻟ
ﻲﻓ حﺮﺸﻟا ﺢﯿﺿﻮﺗ ﻟا ةرﻮﺼﻟا ﺔﯿﻟﺎﺘ :

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-159 -
MKSf or um.net


MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-160 -
MKSf or um.net
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

MKSf or um.net

ﺐﻄﻟا نﺎﺳﺮﻓ ﻰﻘﺘﻠﻣ
ﻲﺒﻄﻟا ﻊﻤﺘﺠﻤﻠﻟ لوﻷا ﻰﻘﺘﻠﻤﻟا
-161 -
MKSf or um.net
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 2–2 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

MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

..‫طب‬‫ ا‬  ‫وا‬‫ و أ‬‫وا‬‫إ‬ ..‫د‬ ‫و‬ ‫طب‬‫ ا‬ ‫ب‬‫م ط‬‫م و ز‬‫ؤ‬‫ ز‬ ‫م‬ ‫ود‬ ‫ج‬ ‫م‬‫د‬‫ن أ‬  ‫ن‬‫ن ا‬ ‫طب‬‫ن ا‬‫ر‬  ‫ء‬‫ن أ‬ ،‫دة‬ ‫ز‬‫ز‬‫د ا‬ ‫ك‬‫ ا‬ ‫ و‬‫ط‬ ‫ء‬‫ط‬‫ ا‬‫د‬  ‫ب‬‫ أ‬‫ط‬ ‫، و‬‫دروس ا‬‫ ا‬ ‫ن‬  ‫ب‬‫ذا ا‬ ‫دة‬ ‫و‬ ‫ ا‬‫ا‬ ‫زاء‬‫ر ا‬ ‫ ا‬‫زا‬ ‫و‬ ‫ورة‬‫د‬‫ دروس ا‬ ‫زا‬‫ر‬ ‫ل‬‫ب ا‬‫ن أ‬ ‫د‬ ‫و‬  ‫ح‬‫ق و ا‬‫و‬‫م ا‬  ‫. و‬ ‫ و‬  ‫دة‬‫دوا ا‬ ‫وا أن‬‫ر‬ ‫ و ا‬‫م ا‬ ‫ء‬‫د‬‫ ا‬ ‫ن‬ ‫و‬  ‫م‬‫وا‬‫م و أ‬‫وا‬‫إ‬ ‫طب‬‫ن ا‬‫ر‬

MedKnightsSona3Project@gmail.com ‫م‬‫را‬‫م و ا‬‫را‬

MKSforum.net

-1-

eyelash dr.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫ون‬‫ء ا‬‫ا‬ ‫ة‬‫ع ا‬ Kia Ora angelic_doc DR.MKSforum. ShoSho Dr-E Da_joker The One Konvict KAU Dr.Jet December 2007 MKSforum.net -2- .ambition Dr.X ‫ن‬‫ز‬‫رس ا‬ Dr.S.JENEFER N.Noura Dr.G amoona asphora ocash doctor_ology Dr.

. 56 IV. 48  Nephrotic syndrome ……………………………………….Akbar ....…….. 99  Addison's disease …………………………………………….......Maimoona .Endocrinology:  Hypothyroidism ……………………………………………… 97  Hyperthyroidism ………………………………………….net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Contents I. 105 MKSforum....Cardiovascular diseases:  Myocardial infarction ……………………………......Gastroenterology & Liver disease:  Diarrhea ………………………………………….………… 6  Stable angina ………………………………………………. 39  Respiratory failure ………………………………………….Respiratory diseases:  Asthma …………………………………………………….…………………. 17  Rheumatic Heart Disease …………………………………. 17  Dilated Cardiomyopathy …………………………………. 17  Hypertrophic Cardiomyopathy ……………………………. 22  Atrial fibrillation …………………………………………… 27 II..MKSforum..net -3- ..….. 12  Prinzmetal's angina ………………………………………… 12  Heart failure ……………………………………………..…………. 82 V.………….………..72  Chronic Liver Disease....……. Hepatitis – Dr. 14  Restrictive Cardiomyopathy ……………………………….. 18  Hypertension ……………………………………………….. 36  COPD ……………………………………………………….64  Chronic Liver Disease – Dr.. 11  Unstable angina …………………………………………….103  Diabetic ketoacidosis (DKA) ...... 58  Inflammatory Bowel Disease ……………………...…..………….…....Renal diseases:  Renal failure ……………………………………………….... 42 III...

………….…………………………….net -4- .. 146 VIII – Other:  Deep Venous Thrombosis …………………………………… 150 MKSforum.….. 110  Septic arthritis..………………………………..history …………………… 123  Localization of site of lesion .. 144  Acute Confusion State ……………………………………….net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ VI. 110  Seronegative arthritis.Rheumatology:  Arthritis / connective tissue diseases………………….…………110  Seropositive arthritis . 126  Stroke / CVA ………………………………………………… 129  Upper Motor Neuron Lesion ………………………………… 139  Polyneuropahties …………………………………………….………………………………………..Neurology:  How to take: quick perfect neuro.113  Smart Rheumatology Questions…………………..120 VII.……...……....……………………………………….112  SLE ………………………………………………………....MKSforum..…112  Rheumatoid Arthritis…………………………………….

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Cardiovascular diseases MKSforum.MKSforum.net -5- .

Pericarditis.re infarction 2.Maimoona 12345Stable angina. Chronic complications: .Thromboembolism manifestation ( blood stagnant). Suspected ventricular aneurysm: 1. 3.net -6- . Valvular heart disease (papillary muscle.Ventricular aneurysm:  ST elevation > 6 weeks after MI: Differential: 1. Myocardial Infarction. MKSforum.MKSforum.ECG > 6 weeks ST elevation.developed ventricular aneurysm. o shoulder joint pain .Dressler's syndrome: o muscle necrosis  antigen antibody reaction  autoimmune disease. Unstable angina. serositis.Recurrent HF not responding to medication. Hypotension. Prinzmetal's angina. o ttt: steroid. Arrhythmia.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Dr. 2. Heart Failure. IHD MI Acute complications: 12345Heart failure. . ventricular septum).

Look for: * Heart failure evidence: Increase JVP. VSD…etc.Family history of IHD.net -7- . 3.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ History: You should include in HPI: * 1-DM.HTN.Look for underlying disease: .: sometimes increase in MI. 3.DM complications. * Pericardial rub on auscultation.MKSforum. basal lung crepitations. ascites.Vitals: Blood Pressure: high Blood Pressure in HTN. 3RD heart sound. Pulse: Arrhythmia. lower limb edema. * Valvular heart disease evidence: valve incompetence. MKSforum. 2.Hyperlipidemia. Examination: 1. Temp. . * Chest pain duration > 30 minutes. hepatomegaly. 5. 2. 4. MI may cause low BP.Atherosclerosis.Smoking.

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

But now all patients i. MKSforum.(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. Relief pain: morphine & antiemetic.net -9- . *review the contraindication from textbook* After stabilized: Before discharge: 1.e. vasodilation. generalized in cardiomyopathy. should have angiogram angioplasty dilation or bypass surgery….Echocardiogram for: (why do we do echo?) * Valvular heart disease. It should be around 50  normal. 2. MI. * Ejection fraction abnormality < 50  low. & start tridine infusion to relief pain. The earlier.MKSforum. the better the prognosis. & will benefit + O2. * Wall motion abnormality  hypokinesia: Heart not contract at site of infarction. antithrombolytic therapy if no contraindication.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Treatment: Typical history of retrosternal chest pain. 1234Chewable aspirin before investigation. will not kill pt.arrhythmia 2-hypotension This was done before to decide if argent angiogram will done or delayed 4-5 weeks.

Aspirin 2.discharge on: 4 medications: 1.Statin. 2.Admit patient to the ICU & give O2  oxy-bed rest.MKSforum. ﺑﻌﺪ ٤٢ ﺳﺎﻋﺔ‬ ‫ﻣﻊ اﻟﻮﻗﺖ، ﻓﺎﻳﺪﺗﻪ ﺗﺮوح‬ ‫ﻳﺴﯿﺮ ﻣﺎﻟﻪ ﻓﺎﻳﺪة‬ ٤ ‫إذا اﺗﺄﺧﺮﻧﺎ ﻧﺴﻮي اﻟﻤﺬﻛﻮر ﻓﻲ رﻗﻢ‬ 4.Lasix.Statin. in good centers.Thrombolytic therapy  streptokinase  resolve the thrombus ‫ ﻻزم ﻳﺘﺄﺧﺪ ﻓﻲ أول ٦ ﺳﺎﻋﺎت.Prescribe painkillers.ACE Inhibtors. MKSforum. 3. & good primary care units) 5.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Role of thrombolytic therapy & angiogram: If the time from ER door to angiogram more than 90 minutes. 4. Management of MI (briefly for 5th year): 1. don't waste time give thromolytic therapy. +/.B-blocker. 2.B-blocker. Home medication: 2ry prevention of MI  4 medication 1.ACE Inhibitors. 3.lasix. If the time within 90 minutes immediately for angiogram. +/. 4.net -10- .Aspirin. 3..angiogram & angioplasty (if possible.

3.Statin.net -11- .Nature. 2.Typical angina: have 3 things : a. Examination. 4.Site.B-blocker. b.ACE Inhibitors.Atypical angina: have got two out three.Non-Anginal chest pain: just one thing. If NO MI. Nabeel likes to ask about angina? 1.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Stable Angina ER. Same History.  Send home Dr.MKSforum.Increased by exertion and decreased by rest. MKSforum. 2. Investigation of MI. c. 3. Sublingual nitroglycerin & 4 drugs: 1.Aspirin.

no HTN. 2. ECG no change  Q wave  for 6 hrs  for 24 hrs. Examination. then every day. . Q6 hrs. 1.ACE Inhibitors. Start by: 1. Until angiogram shows normal coronary. ttt: put on calcium channel blocker.net -12- . .Same History.MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Unstable angina . Angioplasty& pain control.Heart enzymes not rise & evidence of ST segment depression ischemia on ECG.ST elevation.Aspirin.Normal cardiac enzymes.B-blocker. If the pain does not improve  a cardiologist orders an urgent angiogram. Investigation of MI. no DM. MKSforum. Examination. 4. 2. 3. Investigation of MI. Cardiac enzyme no rise. TREATMENT: Tridile infusion & heparin infusion.Statin.No risk factors of MI. **BUT** IT SHOULD BE TRATED AS ANGINA unless proven otherwise. Prinzmetal's angina Same History.

net -13- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 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 MKSforum.MKSforum.

if he's bedridden. Like in Thyrotoxicosis. Thyrotoxicosis. 10.P. 4.net -14- . 2. 8.Constrictive pericarditis. Like in anemia. Nabeel Eight Causes are preferable to be Heard by any Students when Dr.: what are the precipitating factors for HF? 1.Taking ca channel blocker…Negative inotropic agent.HTN or Hypertensive Heart disease with end Organ damage.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Heart Failure (HF) Dr. 7. 9.MKSforum.High salt intake..Valvular Heart disease…and the commonest cause is Rheumatic heart disease.Cardiomyopathy.Uncontrolled HTN. 2. MKSforum.embolism esp.Ongoing Ischemic heart disease…MI.. 8... 6.. 6.Core-pulmonale. Nabeel Al-a3ma asks about the causes of HF? 1.Arrhythmia. 5.Heart failure with high cardiac Output. Also He loves to ask this Question: Patient is known having HF. 3.Hyperdynamic circulation. 7. anemia….Taking NSAID. 5. 4. Which cause salt and water retention. What are the causes that push him to a failure and to the ER… i.Ischemic Heart disease (IHD) which is the commonest.No compliance with medications.Congenital heart disease.Infection (pneumonia). 3...e.

No compliance to drugs. Known case of HF. History in ER: No History suggestive of IHD.MKSforum. Increased salt intake. 1234567IHD.. ‫ﻟﻜﻦ اﻟﻜﻼم ﻳﺼﺎغ ﺣﺴﺐ اﻟﺤﺎﻟﺔ و اﻟﻤﺴﺒﺐ‬ Examination: Same of MI.. That is important to mention in History. HTN. Thyrotoxicosis.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Same Q with Dr. Valvular heart disease.infection -underlying cause. Look for evidence of – heart failure . but she only mentioned these: This way. No History of palpitation. Pt was compliant to his medications. Investigation: like MI MKSforum.arrhythmia .net -15- . Hyperdynamic circulation  anemia. Arrhythmias. Maimoona. No change in diet. the pt got acute HF.

liver failure  low kidney perfusion  activate renineangiotensin system.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Management: On admission: 1.net -16- .Start loop diuretic fursemide 40 mg TID. + 4 drugs: (1) Aspirin. 2. Spironolactone will block it so no Na/H2O retention & not used as K sparing. (3) ACEI. (4) Statin. nephrotic $.Start spironolactone 25 mg  take 3 days to work in HF. (2) B-blocker. Note: moderate/sever HF do not give B-blocker. MKSforum. If echo show ejection fraction below 25% you have to give anticoagulant.MKSforum.

.Amiodarone.Alcoholic.Diuretic 4 drugs: 1.Aspirin.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Restrictive Cardiomyopathy Infiltration of myocardium: TB.MKSforum.Statin. 4.Thiamin deficiency.ACEI. 2. MKSforum. Dilated Cardiomyopathy As heart failure. ttt: treat underlying cause. hemochromatosis. .net -17- . 3.anticoagulants Causes: 1. Hypertrophic Cardiomyopathy ttt: B-blocker & . 2.B-blocker.Ischemic. amyloidosis. 3.

MKSforum. Maimoona 2006 (1) - Major: Carditis Arthritis Erythema marginatum Chorea Subcutaneous nodules minor: (2)      History of tonsillitis Fever Raised C-reactive protein Raised ESR Arthralgia MKSforum.net -18- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Rheumatic Heart Disease RHD Session with Dr.

MKSforum.Synovial fluid analysis elevated white blood cell count with no crystals or organisms .X-ray of joints only when there is mono joint involvement [] MKSforum. IV Penicillin monthly.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ * ask about: rheumatism.ESR & C-reactive protein  high .ECG  PR interval prolongation .X-ray  cardiomegaly or evidence of heart failure .Echocardiography  establishing cordites . hotness  improvement But before cure  involvement of another joint [4] Erythema marginatum: rash w/ very clear margins Investigations: .Streptococcal antibody tests . recurrent tonsillitis.CBC  show leukocytosis .blood culture & throat culture looking for group A streptococcal infection . long bed rest … [1] Carditis: if all 3 layers are involved  Heart Failure  Tachycardia [2] Chorea: Sydenham’s chorea (abnormal movement) [3] Arthritis: fleeting arthritis: redness.net -19- .

Heart failure 3. jaundice.Thromboembolic manifestations MKSforum.MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Complications of rheumatic fever: 1.net -20- .Valvular Heart Disease:  (1) Mitral  (2) Aortic  (3) Tricuspid  (4) Pulmonary  Infective endocarditis  most important Infective endocarditis  multisystem disease Renal failure. brain involvement (Multiorgan failure) 2. heart failure.Arrhythmias 4.

Bed rest . It is effective and may be easier to use than aspirin.High dose aspirin.Haloperidol may be helpful in controlling chorea.Penicillin  then long term to patient with persistent cardiac damage .Heart failure may require digitalis .net -21- . MKSforum. .MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Treatment . The nonsteroidal anti-inflammatory drug (NSAID) naproxen has also been studied.

Maimoona 1424 H 95%  essential HTN 5%  R: Renal: .MKSforum.Congenital adrenal hyperplasia C: Corticosteroids Contraceptive pills Clonidine withdrawal Coarctation of aorta MKSforum.net -22- .Primary hypothyroidism .Hyperparathyroidism .Cushing's .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Hypertension (HTN) Session with Dr.Acromegaly .GlumeruloNephritis .Conn's .Renal Cell Carcinoma E: Endocrine: .Thyrotoxicosis .Carcinoid tumor .Pheochromocytoma .Polycystic Kidney Disease .CRF .Renal Artery Stenosis .

Pregnancy .MKSforum.Renal "for polycystic" .Sympathomimitics * Refractory "Resistant" HTN:  ‫ﻣﮫﻢ‬ 3 anti-HTN medications with maximum dose.Alcohol .Thyroid  Palpations: .net -23- .Acromegaly . Takaiaso) .NSAIDs .Cushing .Polycythemia rubra vera (PRV) P: D: Drugs: .Radio femoral artery "Coarctation" MKSforum. One of them is Diuretic for 3 months Examination:  Inspection: .Arteritis (eg.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ A: .

MKSforum.Coarctation of aorta MKSforum.RBC cast . renal aneurysm  Then look for an end organ damage  Heart "apex beat"  Eye for papilloedema Investigations: in all patients with HTN (1)  К+  К+ U & E: Conn's Pheochromocytoma Cushing  CRF Blood glucose  hyperglycemia  DM Urinalysis (Active sediments): (2) (3) .Proteinuria (4) (5) Lipid profile  atherosclerosis CXR .Cardiomegaly .net -24- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬  auscultation: Renal bruit for tumor.Haematuria .

do adrenal venous sampling to localize MKSforum. Main diagnosis for renal artery stenosis: (The most common cause of HTN in young patient) 1234Doppler US INP = delayed uptake Captopril renogram Angiogram Pheochromocytoma:  Investigation:  Chatecholamines either in urine or blood CT for the abdomen  localize the tumor If not localized.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (6) (7) ECG  Left ventricular hypertrophy 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.MKSforum.net -25- .

IHD: ACE inhibitor &/or B-Blocker .DM: Diltiazam – verapamil Never use Dihydro__?_____ in HTN & DM patient.net -26- .Nifidipin HTN Emergency: HTN + Brain Hemorrhage  don't lower the Blood Pressure rapidly HTN + HF  lower the Blood Pressure  ‫ﻧﺎﻗﺺ‬ MKSforum. because they worsen proteinuria: .Amlodipin .MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Treatment: step one management GENE RAL  α-methyl dopa  poor or pregnant ACE inhibitors Β-blockers Hydralazine Vasodilators Β-blocker diuretic  Thiazide .

9. B.Cardiomyopathy.IHD (including acute MI).WPW syndrome (wolf Parkinson white). MKSforum.MKSforum.net -27- . 5.HTN. myocarditis".Inflammatory heart disease "pericarditis.Valvular heart disease esp.VSD. 8.Pheochromocytoma.Sick sinus syndrome "tachy-Brady syndrome". 2.Thyrotoxicosis. 3. MR.Cardiovascular : 1.Cardiac surgery.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Atrial fibrillation (AF) Definition: It's totally chaotic atrial activity caused by simultaneous discharge of multi atria foci. 4. 6. Rheumatic "Ms.Left atrial myxoma. AS.Endocrinological causes: 1. Causes: A. 2. 10. AR". 7.

MKSforum.net -28- . no HTN and no CAD. 2.Symptoms vary from Palpitation and SOB and aggravating of HF.Asymptomatic. D. no DM.Pneumonia.Embolization symptoms.COPD 4.Theophylline toxicity.E.Ca of the Bronchus.Idiopathic: Lone AF in which no cardiac cause can be identified. Symptoms of AF: 1. 3. 2.MKSforum.Pulmonary causes: 1. E .P. 3.Acute or chronic alcohol. 2.Drugs: 1.Co poising. 5.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ C.

The pericardium. 7.Assess etiology and recurrence of: 1. 3.U and E  if hypo K  don’t give digoxin because it will lead also to arrhythmias. 2. 2.: left atrium.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Investigation: 1. 4.Echo  so in here we're doing: A.Cardiac chamber size and function  i.The myocardium.Identification of patient at high risk of thromboembolism complication of AF. 3.Thyroid function test. 4. edema.Cardiac enzymes.e. 5.ECG  absence P wave + Irregular R-R interval more than 100. 6. B.MKSforum.CXR  p.PT and PTT.Valvular function. MKSforum.net -29- .

2. MKSforum. 1.When and How to use anticoagulant and antiplatlets? Types of AF: 1. So.How to convert to sinus rhythm? 4.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Management of AF: 1.How to maintain sinus rhythm? 5.Isolated one “single".Sustained one  chronic.Treat the cause. If stable follow that previously mentioned points.MKSforum.Paroxysmal  don't give digoxin. 2. 3.How to Control Ventricular rate ( VR)? 3. So the Management: If the Patient is not stable  Do DC cardioversion.net -30- .Treat the cause.

HOCM. B.125 .Digoxin dose: in Normal Patient: 0.Control Ventricular rate By A-V node blocking Drugs: A.Digoxin: .Contraindication of Digoxin: 1.Loading dose: 0. If you want to give verampil + digoxin  decrease digoxin dose.25 mg.5 mg IV  followed by IV bolus 1 mg every 5 mints till …??? The contraindication of B-blocker is: Asthma. . .B-Blocker: Usually given with Ca channel blocker  because more rapid control. and in renal disease: 0.Maintenance: 0.5 mg/30mints IV. 3.0. But digoxin is more preferable in the setting of LVF or HF. So.125 mg.06 0. C.0. MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 2.25 mg/6h.net -31- . Dm and HF.25 .MKSforum.Ca Channel blocker: Verampil 5 – 10 mg bolus / 10 mints.Narrow QRS  atrial tachycardia. propranolol 0.WPW so in here use procainamide. . 2.

Hold Digoxin and check its serum level.propafenone . MKSforum. The drugs used in here: .Dm.net -32- .MKSforum.Class 1c: Flecainide .Class 1a: Quinidine .Previous MI or Stroke. 2.procainamide. Indications for anticoagulation: Clinically and ECG: Clinically: 1. 3.Previous MI.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 3- Convert to Sinus Rhythm: Indicated when VR is more than 140 B/m.Anticoagulant  3 weeks before and after if there's thrombus shown in echo.Thyrotoxicosis  in here. 2.Class 3: Amiodarone So the preparation: 1. .HTM +/. 3.Start Quinidine at least 24 h before to help maintain NSR once it's achieved. 4. decrease the Warfarin dose because of increased clearance of vitamin K in Hyperthyroidism.

Low risk: age less than 65. Complications of cardioversion: 1.Left Ventricle aneurysm.Intermediate: age more than 65 or RF.MKSforum.Large Left Ventricle. 2.High: when Mitral valve disease seen: previous Mi or stroke.net -33- .Intracardiac Thrombus. . 3. . MKSforum. 3.Large Left atrium or Left atrium dysfunction.MI damage due to the Current. Risk of Systemic Embolization with AF is divided to: . 4.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ EchoCardioGraphically: 1.Erythema on the chest wall.Ventricular fibrillation.Thromboembolism. 4. 2.

3.Maintenance of sinus rhythm is better with: 1.Short AF. MKSforum.MKSforum.Left atrium less than 60 mm.net -34- . 4.Conversion with drug only. Please see the classes of anti-arrhythmic drugs.Absence of mitral valve dis. 2.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 4.

net -35- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Respiratory diseases MKSforum.MKSforum.

[1] Drugs 1.net -36- . 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 MKSforum.MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Management of asthma in ER HISTORY:  mainly history of the etiology of the disease. B-blockers o Propranolol o Atenolol o metoprolol 2.

net -37- .Blood pressure.Accessory muscles 3.Cyanosis c.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ EXAMINATION: 1.General examination a.Pulse  tachycardia. arrhythmias b.Tachypnea d. palsus paradoxes c.Signs of Pneumothorax  You fail if you don't mention them!! 4.Temperature  increase  infection 2.Vital signs a.MKSforum.Tremor b.Severity of asthma (1) Signs of infection (2) Signs of status asthmaticus 12345Silent chest Drowsiness Cyanosis Tachycardia > 120 Pulsus paradoxus MKSforum.

U+E a.Hyperventilation  dehydration b. PNEUMOTHOARX 5-ECG  ARRHYTHMIA + hypertrophy 6-Pulmonary function test 7-Peak flow meter  drop inonter base …… 8-Sputum culture 9-Positive skin Note: Mg.MKSforum. Ca. and Ph are not part of U-E MKSforum.ABG 3.Sputum + steroid 4-CXR  INFECTION.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ INVESTIGATIONS: {FOR ALL ASTHMATICS} 1.Theophyllin d.β2-agonist c.net -38- .CBC  LEUCKOCYTOSIS + EOSONEPHILIA 2.

B2 agonist b.Bed rest 2.KCL  DECREASE K 5.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 MKSforum.I.V FLUID 4.Anti-cholenergic drugs Ventolin/atrovent Ibratropum promide Decrease mucus secretion f.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ MANAGEMENT: 1.terbutaline  SlE: TACHYCARDIA FOR 24hours / hourly d.Oxygen according to blood gases  (1) DecreaseO2+decrease CO2 (2) DecreaseO2+normal CO2 (3) DecreaseO2+IncreaseCO2 3.Salbutamol .net -39- .I.Nabulizar c.MKSforum.Pharmacological medications (1) Bronchodilator a.

so. when you admit the patient you must increase the conc.Antibiotics: If there are sought of infection mainly  H.MKSforum. In patient with COPD  chronic hypercapnia  chronic stimulation of respiratory center.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 O2 to be delivered to the patient.net -40- . 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 O2 (24-28%) THEN ADJUST ACCORDING TO "ABG" ASTHMA  NO CHRONIC HYPERCAPNIA  SAFE TO GIVE INCREASE CONCONCENTRATION OF O2 (60%) MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (2) +/.

RESPIRATORY FAILUER MKSforum.net -41- .Tachycardia 5.MKSforum.Use of accessory muscles of respiratory 7.R >33 8.Cyanosis COMPLICATION: 1.EXHAUSTION 3.Drowsiness .exhaustion 9.Pulse>120 6. inability to complete sentences 2.Pulses paradoxus 4.Patients are unable to speak (cannot give history).net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ SIGNS OF SEVERE ASTHMA "STATUES ASTHMATUCUS" 1.PNUMOTHORAX 4.DEHYDRATION 2.R.Silent chest 3.

Hyperthermia Sedative Drugs Benzodiazepin opiates Hypercapnia = P CO2 > 6 kPa = > ~ 5 mmHg (1) Hypoventilation = Depression in Respiratory center in medulla (2) Ventilation. pulmonary). (1) (2) (3) (4) Voluntary → hold breathing Brainstem lesion. muscles.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Respiratory failure ** Influence on respiratory center Stimulation Depression (1) Voluntary → over breathing. (2) Upper brainstem lesion. and joints.MKSforum. (5) ↑ PaCO2 (6) ↓ Pa O2 (7) ↑ Arterial H+ concentration.perfusion mismatching = COPD MKSforum.net -42- . (4) Pyrexia. (3) Input from receptors (pain.

MKSforum.  Brainstem lesion = CNS depression (Narcotic drugs) * COPD * Chest wall ds * Ankylosing Spondylitis MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ** Respiratory Failure: A disorder of the lungs where the lungs don’t function accordingly to match the metabolic requirements. edema ARDS Pneumothorax Pneumonia **Emphysema Lung fibrosis R → L shunt Anemia Type 2 (hypoxia & hypercapnia) Acute PaO2 ↓ Pa CO2 ↑ HCO3 ↔ Chronic PaO2 ↓ PaCO2 ↑ HCO3 ↑  Severe acute asthma (life threatening)  Respiratory muscle paralysis (Kyphoscoliosis) + fractured rib + intercostals ms tear.net -43- . Type 1 (hypoxia & hypo or normal CO2) Acute Pa O2 ↓↓ Pa CO2 ↓ or ↔ HCO3 ↔ Chronic Pa O2 ↓ Pa CO2 ↔ HCO3 ↔ ***Asthma (severe) PE P.

GIT hemorrhage Pneumothorax Bronchial Obstruction.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Other Causes of Type 1 Failure:  Extrinsic allergic alveolitis. MKSforum. 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. LVF Pulmonary Embolism Convulsion.  Interstitial fibrosing alveolitis.net -44- .MKSforum.

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 ***************** MKSforum. infection.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 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.net -45- . sepsis.MKSforum.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (3) Theophyllin ( improve muscle contraction * Diuretics LVF * Chest physiotherapy * Hydration & mucolytic (Danse) ****************** (4) Mechanical Ventilation  Failure to provide adequate oxygenation without marked hypercapnia. MKSforum.net -46- .  Decrease level of conconcentaration  Failure of Respiratory stimulant.MKSforum.

‫‪MKSforum.net‬‬ ‫-74-‬ .net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫‪Renal diseases‬‬ ‫‪MKSforum.

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.MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Renal failure Classification: a) according to duration  acute (6 w-6 m)  chronic (>6 m) b) according to etiology Pre 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 Renal (most important) a) DM  diabetic nephropathy b) HTN  hypertensive nephrosclerpsis c) Glomerulonephritis d) Infection:  E.net -48- . e) drugs  amino glycosides  NSAIDs  Diuretics  Contrast agents  Gold (heavy metal that treat RA.)  nephrotoxins  Penicillamine Post renal Mainly obstruction due: Stone Radiation Tumor Lymph. Node Infection:  TB  Bilhariziasis MKSforum.

systemic sclerosis. orthopnea. nausea. Hemochromatosis 4. Hypercalcemia 2. Wilson‘s ds.. Hypercalcemia 2. polyarteritis nodosa g) Tumor  Renal cell carcinoma  Multiple myloma: 1. connective tissue dis. Hyperurecemia I) Polycystic kidney Complication: 1) Uremia: o Uremic gastropathy  loss of appetite. Recurrent infection 4.MKSforum. constipation o Leg swelling o Respiratory symptoms  SOB. problems in concentration. impaired memory. vomiting. cough. 3.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ f) Vasculitis SLE.net -49- . yellowish sputum o Uremic pericarditis o Symptoms of cardiac overload (HF)  dyspnea. loss of wt. PND… o Generalized skin itching o fatigability o Uremic encephalopathy  disturbance of sleep. RA. Deposition of paraprotein h) Metabolic causes: 1. Hyperuracemia 3. confusion in advaced RF MKSforum.

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) MKSforum.MKSforum.net -50- . insulin  lead to gynecomastia in male & dysfunction in female & improve DM (or hypoglycemia) Decrease: Erythropoietin factor& 1.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ RF of transplanted Kidney presenting with uremic symptoms  the cause is Renal Artery Stenosis 2) HTN 3) Edema (fluid overload) 4) In the endocrine: 3 (increase) 3 (decrease) 2 abnormal Increase: LH. prolactine.

Kyperkalemia (should be treated to protect the heart) 5) Blood sugar: increase with DM 6) HBV & HCV screen  Urine analysis: 1) 2) 3) 4) Oligouria Proteinuria Hematouria casts: RBC MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 7) Electrolyte disturbance: (Hyperkalemia) Brain: confusion & mental dullness CVS: arrest GIT: atony (nausea. urea . paraesthesia Investigation:  Blood Work 1) CBC: HB  anemia MCV. vomiting. constipation) Muscle: weakness. flaccid paralysis.net -51- . MCH  or (nomocytic normochromic) Pancytopenia… WBC  infection 2) ESR: increase with infection 3) ABG: metabolic acidosis 4) U & E (renal function): increase creatinine.MKSforum. Pi.

MKSforum.US: 1) Kidney size Enlarged: DM. HIV. Amylodosis Shrunken:  Chronic GN  (evidence of obstruction) LN. tumor  Hepatosplenomegaly 2) Collection over kidney 2.net -52- . Pulmonary edema pleural effusion  uremia TB Metastatic kidney  ECG. Cardiac Enzymes  if patient has cardiac symptoms  Band screen  if pt is on line dialysis & febrile urine sputum culture blood MKSforum. polycystic kidney. stone. Echo.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬  Radiology: 1.Urgent US + Doppler  for transplanted kidney  to reveal renal artery stenosis 3.CXR: Heart.

MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

Important Points in RF: 1- Underlying cause:  DM  how long? does pt has retinopathy (because nephropathy occur at same time)  Swelling – renal biopsy – controlled?  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  Do you expect this pt to have retinopathy? No, because his diabetes is controlled  HTN  How long?  Control HF  Unknown etiology  SLE (pt knows about it)  medications, ……. etc

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MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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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MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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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2ry causes: . Complication: 1.5 g\day.Infection.Systemic: DM – HTN – SLE – amyloidosis.net -56- .Drugs: NSAIDs – heroin – captopril – gold – penicillamine .crescentic GN. 2.membranoproliferative GN.Edema.probenecide . 3. .malaria . .MKSforum. . . .Allergy. Hyperlipidemia ( cholesterol.Hypercoagulability.Focal segmental Glomerulosclerosis. LDL). Hypoalbuminemia < 30g\L (< 3g\dl) 3. 2. Evidence of fluid retention and edema. Proteinuria > 3. . 2.Infection: HBV – HIV. Causes: 1.Malignancy: carcinoma – lymphoma – MM. 4.Minimal change disease.1ry renal: . MKSforum. . 4.Membranous GN.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Nephrotic syndrome Definition: 1.Hypercholesterolemia.

net -57- .MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Gastroenterology & Liver disease MKSforum.

MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Diarrhea Session with Dr.net -58- . Giardia MKSforum. Infections:  Protozoa: Amoeba  . Maimoona Diarrhea Acute & Chronic   2 weeks more Causes: I.

botulinium  botulism (preserved food) C. Aureus (milk products) Campylobacter  (pets at home) Yersinia  C. Klibsiella .net -59- . pseudomembranous colitis Note: C. Perfringins  food poisoning / gas gangrene C. salmonella  Vibrio cholera  watery diarrhea Staph. tetini  tetanus Note: Algid Malaria: malaria superimposed by Salmonella  Common cause of septic shock  Viruses: HIV (common cause)   3 months + lymphadenopathy + wt loss Rota virus.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬  Bacteria: E.MKSforum. adenovirus  Fungal in immunocompromised Cryptosporidium  Lyme disease  Liptospirae  Mycobacteria: intestinal TB The underlined words are important causative organisms   Means Bloody MKSforum. difficile   diarrhea. Shigella  . Coli .

Colon carcinoma. Inflammatory Bowel Disease  Crohn's – Ulcerative colitis III. Malabsorption: 1.MKSforum.Whipple's disease (malabsorption due to trophyrhyma whipple "bacteria") MKSforum.D.net -60- . Malignancy: Intestinal lymphoma.Tropical sprue (hot humid countries) Probably due to E.Celiac disease (not all patients present with diarrhea) *malabsorption* CBC: dimorphic picture Microcytosis & macrocytosis Hypochromic & hyperchromic D. coli (traveler's diarrhea) 3. Celiac Disease Combined deficiency (folate – Fe) They have hypo Ca+2 Note Hemolytic anemia  peripheral blood film  reticulocytosis 2.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ II. Medullar carcinoma of thyroid IV. Pancreas carcinoma.

diverticular disease MKSforum.Pancreatic (chronic) malabsorption Chronic pancreatitis – cystic fibrosis .Post-gastrectomy . hepatosplenomegaly.carcinoma 6. skin pigmentation. malabsorption and.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Usually patients also suffer Lymphadenopathy. short loop 5. Drugs:  Antibiotics  mainly clindamycin  Laxatives  Cytotoxic VII.net -61- .Blind loop syndrome (malabsorption) .MKSforum. Endocrine:         Thyrotoxicosis Addison's (hypotension & diarrhea) DM (autoimmune neuropathy) Glucagonoma VIP tumor Pheochromocytoma Hypoparathyroidism Carcinoind (flushing face) VI. Idiopathic: Irritable bowel syndrome. arthritis. Tetracycline should be prescribed for 1 year Periodic acid Sheff (PAS)  positive (+) 4. resection of colon V.

Serology: HIV+ for ulcerative colitis pANCA. house hold diarrhea (ACUTE) Investigations of a patient with diarrhea: 1. E.ESR 4U and E Hypo K+ Hyper Na+ Renal failure (due to fluid loss) 5. ASCA + CMV IgM MKSforum. Coli Fever: Infections. Shigella. and malignancy Family History Laxatives. IBD. eat outside the house.Stool analysis: Blood – Mucus – Protozoa e. trophozoid Cuture  bacteria & Sensitivity 2CBC Anemia Leukocytosis Thrombocytosis: bone marrow  to confirm safe anemia 3. Salmonella.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ In History: The amount and frequency Consistency: watery Associates with bleeding: Amoeba.net -62- .Left: hypoalbuminemia 6. IBD.g.MKSforum. IBD Tenesmus or not: Giardiasis & Amoebiasis Abdominal Pain  IBD and malignancy Loss of weight: HIV.

Endoscopy 8.Salmonella titer 10.MKSforum.Abdominal X-Ray:  toxic mega colon Differential Diagnosis of Diarrhea: 1234567Infection IBD Malignancy Malabsorption Endocrine Drugs Idiopathic MKSforum.net -63- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 7.Enema 9.

MKSforum.Thromboembolic disease 6. sacroilitis.Ulcerative Colitis 1. Presentation: mainly diarrhea.Skin: erythema nodosum.MKSforum. autoimmune hepatitis.Fatty liver.Intestine: diarrhea (bloody) . Uveitis.Amylodosis. 4. sclerosing cholangitis 7.pain .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Inflammatory Bowel Disease Clinically we cannot differentiate between ulcerative colitis and Crohn's unless fistula develops.malabsorption .Arthropathy 5. pyoderma gangrnosum 3.tenesmus 2. iritis. ankylosing spondylitis.Both: ant. I. episcleritis.net -64- . conjectivitis.

hypotension.Severe Diarrhea > 10/day Fever Tachycardia Hypotension Hypoabuminia (edema) MKSforum.Moderate (In between) III.Toxic megacolon (most severe complication) Tachycardia.MKSforum.Amylodosis (in both) 4. anemia. dilated transverse colon more than 6cm If not improved in 24 to 48 hours -> total Colonectomy should be preformed immediately.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Complications: 1. II. 3.net -65- . Perianal (abscess .Chron's Terminal ilium  B12 deficiency Intestinal obstruction . (Chest x-ray) 2.stricture Fistula (entero .Malignancy: More with Ulcerative Colitis A patient with Ulcerative Colitis for more than 10 years must have an annual endoscopy.tags) Grading I.enteric or vesical).Mild Diarrhea > 5/day No anemia No fever Normal albumin II.Thrombosis.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Treatment I. * Exudates stones Crohn's (Child) MKSforum.Salphasalazine (Paraaminosalicylic acid) II.Steroids (Pridnisolone) If the patient suffers Chron’s: Add metronidazole (antibiotic covers anaerobes) Investigations 12345678CBC U&E Left Barium enema Endoscopy (Chron's skiplesion) coplet stones Biopsy Stool (to exclude infections) Abdominal x-ray * Vitamin deficiency (B12)  numbness.MKSforum.net -66- . * Gallstone (both).

5.Abdominal pain (lower). leukonychia.Skin: erythema nodosum.If fulminant: diarrhea mixed with blood & mucus.Constipation.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (Non-smokers) Ulcerative Colitis Symptoms: 1.Tenesmus.Fever 5. episcleitis.MKSforum. 2.Bloody diarrhea. 2. 6.Weight loss. hypoalbuminemia. If only rectum (proctitis). 2. iritis.Blood in stool.More frequent diarrhea more than 10 times per day 4. Pyoderma gangrinosum. 1. 6.Eye: uvitis.Abdominal tenderness . 3. distention (toxic megacolon) Extra-intestinal signs: 1.Arthropathy.Signs of anemia. 4.Mouth: aphtous ulcer. 2. Signs: 1.Amyloidosis. 3. MKSforum. 3.Clubbing. If severe: .Thromboembolic disease. conjunctivitis.net -67- .

autoimmune hepatitis.Bleeding  dehydration.Perforation. 2.Amyloidosis. 5. 6.Fatty liver.Ankylosing spondylitis.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Other unrelated to disease activity: 1. 3.Toxic megacolon. sacroilitus.Thrombosis. 2. Complications: 1.MKSforum. MKSforum. 4.net -68- .Sclerosing cholangitis. 3.Malignancy.

Extra-intestinal: as in Ulcerative Colitis Complications: 123456Stricture (intestinal obstruction). vescal or vaginal). Weight loss.MKSforum. abscess. Fe.B12 deficiency.net -69- . abdominal pain. fever. right iliac fossa pain. fistula. rectal bleeding (less than U C). Renal disease due to ureteric compression. Abdomen: tender. Perianal skin tags.folate. MKSforum. Fever. malabsorption. stricture.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Crohn’s Disease Granulomatous – transmural – skip lesion. Anemia Hypoproteinemia. weight loss. Amyloidosis. Fistula (enteroenteric . Malignancy. Signs: 123456Clubbing. mass. Terminal ilium (any where) Symptoms: Diarrhea.

Peritonitis  severe abdominal pain 5.net -70- .Intestinal obstruction:  abdominal pain  abdominal distention  vomiting (repeated attacks)  constipation 2.Relapsing of Crohn's 3. what might be the causes of his complains? 1.Colon cancer  weight loss MKSforum.MKSforum.Gastric or duodenal ulcer  heart burn 4. presents to the ER with vomiting & abdominal distention.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Relapsing of Crohn's Session with Dr. Faiza Qari (5th year tutor) ► A known case of Crohn's dis.

Times admitted to hospital . abdominal distension.Skin rash  Erythema Nodosum ► Crohn's affect  small intestine ↓ Vomiting Weight loss > large intestine ► Most important investigations: .Any ICU admissions * Last colonoscopy * Abdominal pain.Any relapses . repeated mouth ulcer. gall stone … . bleeding/rectum. repeated fissures & fistulae * Intestinal manifestations of Crohn's: .ESR  activity of disease .Arthritis  sacroiliac joint  back pain Or mono-arthritis .Appendicitis (Right Iliac mass) * Extra-intestinal manifestations of Crohn's: .Procedures (what happened?) . bleeding diarrhea.MKSforum.CBC: WBC normal Hb ↓  microcytic hypochromic anemia Platelet ↑↑↑  (1) postsplenectomy (↑) (2) Relapse of Crohn's .LFT MKSforum. weight loss.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ► Relapsing of Crohn's  other important history: * Past history  since the time of 1st diagnosis .net -71- .Renal stones .Phlebitis  DVT… . loss of appetite.Liver  hepatitis.Anemia (iron deficiency)  chronic illness .

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Dr.Hydatid cyst  by compression. MKSforum. . People working at port of entry. ETIOLOGY: (1) infection: .Maimoona CLD When a patient presents with hepatic symptoms. 1st search for acute causes of illness then ask about chronic.MKSforum. but chronic if patient lives long enough.TB  most common in KSA.hepatitis  B  sexually  C  blood transfusion / vertical from mother to child . REMEMBER! These infections are causes of acute.net -72- .HIV  usually acute. not hepatocellular. * Most likely jobs to be alcoholic & drug abusers: Cops & Army.Schistosomiasis (Bilharziasis) . . not chronic liver disease: CMV Toxoplasmosis EBV Malaria (2) Alcohol  always take History of alcohol.

Primary biliary cirrhosis: (6) Classically pt present with:  Young female .  High 24 hr urine cupper. ferretin. Diagnosed by:  Serum iron.  Liver biopsy  diagnostic.  High ALP.  hemochromatosis  autosomal recessive. RA. Diagnosed by:  Anti-Mitochondrial Abs. Diagnosed by:  Low ceruloplasmin (serum). Metabolic:  Wilson's disease  autosomal recessive. All these 3 are raised in these patients. (7) (8) Malignancy  metastasis. Wegner's Granulomatosis.  Itching 1 or 2 years before any liver involvement.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (3) (4) Autoimmune  all CTD: SLE.MKSforum. tegretol.  Methotrexate. Causes:  all causes of DVT MKSforum. budd chiare syndrome: Hepatic vein thrombosis. 90% of pt  IgM Abs.  Anti-epileptics  sodium valporate. (5) Drugs  remember 1 or 2 only  Anti-Tuberculosis. phenytoin.net -73- .

Dr Maimoona will tell you to talk about something that is more important. because it is TOO RARE. Hepatic encephalopathy. Bleeding tendency.  Splenomegaly. SBP.MKSforum.  pancytopenia. Do liver scan  find  uptake in caudate lobe. (9) Cardiac cirrhosis. (2) (3) (4) (5) (6) (7) MKSforum. Hepatocellular Ca. (11) fatty liver  NEVER say it.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Present:  acute abdominal distention  main  Others. (10) Idiopathic. (spontaneous bacterial peritonitis) Hepatorenal syndrome  if you mentioned this.net -74- . Decompensation of CLD shows up by Complications: (1) Portal Hypertension:  variceal Hrg. & if you mentioned it in the exam (‫ )ﻓﻲ اﻟﺒﺪاﻳﺔ‬you will lose marks Dr Maimoona says "don't remember it".  Ascites.  this is #1 Hypersplenism.

burn. . of a patient to have an encephalopathy: History of precipitating factor: .Dehydration: vomiting. . who is known case of CLD secondary to HCV.Vital signs: -Temp  infection. . diarrhea. -Pulse  tachycardia due to infection or loss of fluid. . sedatives & tranquilizers. respiratory. . leg ulcer…etc. . (2) Examination of pt who already has CLD & came with hepatic encephalopathy: 1.High protein diet  high urea.Hemorrhage (bleeding): Upper/Lower GI bleeding  globulin  high urea. C/O: altered level of conciseness (complaint & HPI)  Hepatic encephalopathy How do you manage? (1) Take History of what ppt.Constipation.MKSforum. .Glasgow coma scale (1st)  consciousness.Infection:  SBP: spontaneous bacterial peritonitis   Sore throat.Hepatoma (hcc). UTI.net -75- .Causes of electrolytes imbalance:  Overuse of diuretics.Heart failure. 2. .Drugs: analgesics.  Gastroenteritis  vomiting & diarrhea. MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Hepatic Encephalopathy: 50 years old lady admitted through ER. .Excess alcohol. -Blood Pressure  look for postural hypotension (Ascites).

1. postural hypotension. .  Leucopenia.PR = per rectum Ex (digital rectal Ex) (3rd)  bleeding: 'melena' in all hepatic encephalopathy. 4. 6.  Thrombocytopenia.Obstructive (primary biliary cirrhosis)  ALP. MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 3. 3.Evidence of infection: (4th)  Chest. auxiliary sweating. lower limb edema. Investigations: That should be done to all patients: (1) CBC: .net -76- .Hepatocellular Ca   enzymes.Cytopenia  hypersplenism & vasculitis (CTD). (2) LFT: In cirrhotic liver: cells are distorted  enzymes not secreted = normal LFT.  Dehydration  mucus membrane.Constructional apraxia: draw a 5 pointed star (better) or draw a square. Ascites. (3) Everyday follows up: 1.Flapping tremor (asterixis).Fluid status: (2nd)  Fluid overload (from liver failure)  pleural effusion.  Anemia.Leukocytosis  infection. 2.  SBP (spontaneous bacterial peritonitis) abdominal tenderness. + CLD stigma.MKSforum.Hepatic bruit 'hepatoma'. 2.Glasgow-coma scale. 5.

 Fluids overload  pulmonary edema. (5) Hepatitis B & C serology  most common in KSA. 1° tumor.Ascites.Spleen  enlarged  hypersplenism. hydatid cyst. 2. 4.  3rd  lesion (masses)  metastasis.prerenal failure  increase urea & creatinine. if US didn't help: do CT) 1. MKSforum.  2nd  macronodular (alcohol) or micronodular. (3) Urea & electrolytes: 1. tumor. 5.Any other masses  LN / metastasis.Bilirubin.MKSforum.Dilatation of biliary tract  obstruction  stones … etc. 2. you have to write them all)  (7) Abdominal US/CT (only 1.PT. 3.Liver:  1st  size of liver?  If shrunken  order a biopsy. because there is no gluconeogenesis in liver. *NOTE: If all these didn't help you. 3.net -77- . (4) Blood glucose  hypoglycemic.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 3. then you'll do the other tests if symptoms are suggestive (but in a written exam.  Malignancy  metastasis. (8) CXR:  Evidence of infection.Albumin level  if <13  pt is prone to develop SBP.Low K  diuretic. 5. 4. PTT (coagulation profile) clotting factors.  HF.Low Na  dilutional or diuretic. (6) α-fetoprotein (AFP) & abdominal US  every 6 months  for hepatoma.

fever. Only in patient with non-shrunken liver & he has Hepatitis B or C. (10) Liver biopsy: (invasive procedure. worsening hepatic encephalopathy. culture & sensitivity. . Urine analysis.Abdominal pain Diagnosis: P/C: Abdominal pain. do: -HBV. -ANA profile. ECG in electrolytes disturbance. SBP: . Others: Blood culture. distention. presented with hepatic encephalopathy.net -78- . . & treatment. (11) ascitic tap: diagnostic/relief  for gram stain . (12) If Pt. cytology. endogenous gastrin  ttt: PPI (proton pump inhibitor). -Young Pt: metabolic causes. Or in the absence of signs: MKSforum.MKSforum.Oesophageal varices. keep it at last).net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (9) UGI endoscopy: to know source of bleeding.CLD . HCV. protein.Patient should have Ascites to develop it . tenderness.Peptic ulcer  because liver can't metabolize. Ammonia. decrease bowel sounds. glucose "see below".  To know activity of the virus. not known to have CLD. Urine culture & sensitivity.

Intake/output chart. pt. 3. After tap. 5. then if +ve SBP (SBP is documented)  life-long prophylactic antibiotic. MKSforum. 2. flapping tremor asterixis: see if improver with ttt.Bed rest.Low salt/low protein diet. antialdosteron (aldosterone cause Na & water retention)  take 3 days to work.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Ascetic tap: 1.Daily weighting: the goal of diuretic therapy is daily weight loss of 0. .Gram staining.Daily examination of 2 signs: constructional apraxia.Daily urea & electrolytes if disturbed.MKSforum.Culture  E. coli  most common. .  spironolactone. aldactone. neutrophil >250 neutrophils/ µl  diagnostic. 4.5-1 mg/day. . Management: . lactic acid lactose disaccharide change pH of colon flora  no overgrowth of bacteria. quick action till spironolactone takeover. Aim: 2-3 bowel motion daily.Proton pump inhibitor 'prophylaxis'.Antibiotic  3rd generation cephalosporin SBP.net -79- .Fluid status management: o Dehydration  give fluid. . will be on antibiotic empirically. 1. 2. .laxative: lactulose. 3. o Fluid overload  diuretic:  loop diuretic.WBC >500.β-blocker inderal decrease portal pressure.

If total protein < 10g give antibiotic as prophylaxis even if no SBP.MKSforum.Diuretic: loop diuretic & spironolactone.therapeutic paracentesis Q 2/52.Urea & electrolytes. 2. or quinolone( ciprofloxacin).Lasix. MKSforum.In refractory ascites: fluid overload that is none responsive to a sodiumrestricted diet & high-dose diuretic: -TIPS -shunt .In GI bleeding start antibiotic prophylaxis 2nd generation cephalosporin or quinolone.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ If patient out of encephalopathy: Discharge on: 1.In large volume paracentesis: concomitant administration of IV colloid (5-8g albumin/L ascites removed). . If it is not diuretic albumin. SBP management: -ttt: empiric IV antibiotic therapy 3rd generation cephalosporin (ceftriaxone or cefotaxime) depending on renal function.Then long life/2ry prophylaxis: norfloxacin 400 mg PO qd. . . . 2. If child C >>liver transplant.Salt restriction.Proton pumps inhibitor.Alpha-fetoprotein Q 6 months.Diagnostic paracentesis. . 3. .Spironolactone. & the following investigation: 1.net -80- . . 4-CBC Ascites Management: .Abdominal U/S Q 6 months. 3.

. .Octreotide infusion.Vit. . GI bleeding management: . shunt surgery: if child B not responding to therapeutic endoscopy to relief portal hypertension. U & E. improving the diagnostic & therapeutic success of subsequent endoscopy.Endoscopy every year.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Coagulopathy management: . cross matching.Lab tests CBC. sclerotherapy.TIPS. .net -81- .Balloon tamponade: dangerous esophageal rupture. bolus then infusion acutely reduces portal pressures & controls variceal bleeding with very few side effects. cardiac monitoring. . .Endoscopy for variceal ligation banding.Discharge on b-blocker Propranolol : reduce portal pressure & lower the risk of recurrent bleeding. .In active bleeding or invasive procedure: fresh frozen plasma & platelets transfusion.Vasopressin: cardiovascular risk in ICU w. coagulation profile.MKSforum. then liver transplant. .NGT.ICU admission. .ABC  resuscitation with IV fluid fast drip till blood available. K IV 10mg/day for 3 consecutive days. . . + nitroglycerin. MKSforum.

Metavir 3. According to etiology: 1. Traditional:  Chronic persistent  Chronic lobular  Chronic active  Liver cirrhosis 2. Necrotic 2.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Chromic liver disease Dr. Hisham Akbar      Definition Types Causes Manifestations Treatment Types: A. According to pathology: 1.net -82- . Post necrotic MKSforum. Knodells Depends on taking liver specimen to show:  Degree of inflammation  Staging = of the degree of fibrosis B.MKSforum.

net -83- . 3. isonizaid. 8. a patient with hepatic cirrhosis is more liable to develop HCC. … ) Metabolic  fatty liver Cholestatic  1ry & 2ry biliary cirrhosis  sclerosing cholangitis Infiltrative Vascular problem ( cardiac cirrhosis ) Neoplastic  benign  Malignant  1ry  2ry Idiopathic To establish the diagnosis For the detection or exclusion of other diseases For grading For staging Evaluation of therapeutic effect MKSforum.MKSforum. Classification of CLD according to the cause: 1. C. 6.  The liver histological specimen is usually stained with H&E. Infection : viral hepatitis ( B. 4.  Cirrhosis: is the complete distraction of hepatic nodules.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Role of liver biopsy in chronic hepatitis: 1. 9. 5. 5. 2. Moreover. D ) Autoimmune hepatitis Alcoholic Drugs ( methotrexate. methyldopa. Note:  Initially the inflammatory cells limited in the portal tract  then in a lobule  then spreads to the portal vein. 2. 7. 10. 3. 4.

HBVs Abs  (Positive + ) 3.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 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.net -84- . CLD MKSforum.MKSforum. he has the same chance of infection with HCC as a patient who is Symptomatic. 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.

Anti liver & kidney LK 2.In liver disease not fully defined action.Double stranded DNA in some but target Ags. Microsomal ( Abs type I LKM ) Antisoluble liver Ag Auto Ag .MKSforum.  Type II & III more in children  If the score of the criteria is 15 before ttt and greater than 17 after ttt :  It’s Definitive autoimmune hepatitis  If the score of the criteria is 10 – 15 before ttt & 12 – 17 after ttt  It’s 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 MKSforum. . .net -85- . anti-smooth Abs II III 1.Cytochrome P450 11D . Serum anti nuclear 2. Anti mitochondria 3.Cytochrome 8 + 18 - The interpretation of aggregated score is:  Type I in female at menopause and teenage years.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Classification of autoimmune hepatitis: Types Serum auto Abs I 1.

Angioneuretic edema MKSforum. Vasculitis 6. Glumerulonephritis  membranoproliferative 3. Gynecomastia  the most common cause is diuretics ( Spironolactone / Aldactone ) . Rash 2. Enlarged spleen 5. Xanthelasma 9.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Manifestations of CLD:  Asymptomatic  Symptomatic   Extra abdominal manifestation 1. Enlarged or Shrunken liver 4. Collapsing pulse 7.net -86- . 12. Fatigue 2. Kayser-Fleischer ring 8. Palmer erythema  Hypothenar  Pulp of fingers 11.MKSforum. Spider nevi 3. porphyria cutanea tarda hepatocellular ca 4. Advanced disease  Ascites  Bruising  Esophageal varices  Extra hepatic manifestation of hepatitis: mixed cryoglobulinemia 1. 13. Dupetrine contraction (common cause is occupational – manual working). Arthritis 5. Parotid swelling  alcoholic  Thenar 10. Finger clubbing 6.

net -87- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Persistent infection Chronic hepatitis Asymptomatic carrier Cirrhosis HCC Death Acquisition of HDV infection:  Co-infection: simultaneous introduction of HBV – HDV  Super infection: introduction of HDV into HBVs Ag (positive) host MKSforum.MKSforum.

MKSforum.net -88- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Clinical Sequelae : HDV / HBV Co-infection Acute hepatitis Chronic HBV / HDV hepatitis Fulminant hepatitis HDV super infection to HBV Natural Hiostory of HCV : Acute infection < or = 15 % Resolution ( Risk for subsequent infection is unknown ) > or = 85 % Persistent infection MKSforum.

coli )  neutrophile 6. must have cirrhosis to develop HCC HCC Fibrosis & Cirrhosis Death Treatment  Treat the cause  Treat the complications : 1. Bleeding  a. flagel ) 3. Ascites ( diuretic ) 5.net -89- . TIPS for  bleeding  ascites 4. b. SBP (most common E. Hepatorenal syndrome 2. ABC first. Encephalopathy ( lactose.MKSforum. Endoscopy: sclerotherapy c.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Persistent infection Normal ALT Non-Progressive liver injury Elevated ALT Progressive liver injury HBV pt. Hepatoma MKSforum. might develop HCC without cirrhosis but HCV pt.

Pegylated INF B. It's effective in treatment if the infection is recent (not more than 2 years). which does not apply to Saudi patients. 5. Nucleoside MKSforum.INF + Ribavirine .net -90- . Most of the viruses here in Saudi Arabia are pre-coremutant viruses which are resistant to INF  so.MKSforum. 4. Also it should not be prescribed to patients with leukopenia and thrombocytopenia (CBC). RA. 1. Interferon (INF ) : But not in Saudi patients since they fulfill the criteria for ttt with INF.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Treatment of chronic hepatitis: A. (They have high liver enzymes but not as twice). 3. but most Saudi patients have established the infection since childhood (more than 30 years). Fibrosis Moderate to severe necroinflammation HCV RNA ( + ve) INF Persist elevated ALT New combination: . once you stop the ttt viremia it will rise again. 2. INF is effective only if the liver enzymes are elevated twice the normal. It should not be given to a patient with an autoimmune disease such as SLE.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ C.Nowadays.Only in case of Liver failure . .Most of deaths occur  early = infection Late = rejection . MKSforum.MKSforum. The donor’s liver will grow another left lobe to replace the donated lobe. transplantation of the left lobe enhances the liver to be a complete one within 6 months. Liver transplantation : .net -91- .Not all HCC are sent for assessment of liver transplantation.

Incubation period for HCV ( 30 – 90 days ) . Q: PCR (+) increase in liver enzymes.If liver enzymes > 1000 it means the infection is acute. Alpha IF or Rebavirine is contraindicated for a reason or the other. ELISA : detect HCV Abs  Generation 1  Generation 2  Generation 3 . MKSforum.g.MKSforum. reaching the stage of Ascites – varices 2. .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ How to diagnose HCV? 1. RIBA: Recombinant Immuno Blotting Assay = detects Abs earlier than ELISA.net -92- . 3.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. Decompensate CLD e. what is to be done? We cannot start the treatment for any patient with HCV unless: 1.If ELISA is (positive) that means the patient has the Abs  has the infection for at least 6 months. .

Baseline CBC  because  α -IF cause  leukopenia ( neutropenia )  Thrombocytopenia .net -93- . 4. 6. Left  synthetic function ( PT – PTT – Albumin )  Excretory function (bilirubin)  α-IF should not be given to any autoimmune pt. when we discover HCV infections we should decide in which stage is the patient by taking History & physical examination. SLE .g. 5.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ So.If the patient is already leukopenic. 2. 7. Because it will worse the condition.MKSforum. 2. . e. That's why we need to do TFT ( T3 – TSH ).So we need to know his baseline. Jaundice Hematemesis Asterixis Lower limb edema Epistaxis Bleeding gum Abdominal pain & distention α-IF ( S.varices) Investigations: 1. 3. 1.  α-IF can cause thyroid dysfunction  hypo ( common )  & hyperthyroidism & this S/E is the only S/E of a-IF which is not reversible. he is not a good candidate for α-IF. MKSforum. Decompensation (Ascites .C ) + Ribavirine ( tablets ) = ttt of HCV + CLD Could be used with any patient with compensated CLD and has no contraindication to medication. RA.Encephalopathy.

 Rebavirine until now doesn’t have an exact defined dose. So.  Rebavirine could cause impaired renal function.MKSforum. a baseline should be done on RFT. a follow-up is need.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬  Rebavirine should not be given to a pregnant patient can't control her because it is teratogenic.net -94- .  Rebavirine could cause hemolysis so it shouldn’t ever be given to patient with hemolytic anemia. 1st time the HCV was discovered was in 1989 α-IF for 6 months  response  6 % After 1994  extended monotherapy  for 1y  15 % In 1998 α-IF + Rebavirin  response  41 % HCV  6 genotypes  type I & IV (requires a year) disresponse to α-IF – Rebavirine  While genotype II & III (requires 6 months) cause better response 60%.  At this time it's (SVR). So.  Some patients could have co-infection of I & II 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. MKSforum.

that is why we give pegylated IF.MKSforum. 2. Factors affecting response: 1. Female better than male.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ It fails many times due to mutation in genotype. Genotype II is & III better than I & IV. EVR = Early Virologic Response MKSforum. 3. Viral load.net -95- . Younger than 40 years.  In type IV after 1y Polyethylene glycol + α-IF  pegylated IF (41 % response). 4. Degree of cirrhosis.  In type II / III (~ 80 % response). 5.

net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫‪Endocrinology‬‬ ‫‪MKSforum.‫‪MKSforum.net‬‬ ‫-69-‬ .

Drugs (amiodarone – lithium) 2.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Hypothyroidism Primary hypothyroidism: 1. ↑TSH  1ry ↓FT3.net -97- .Autoimmune (e.Radio isotope scanning   uptake .Anti-thyroglobulin antibodies . ↓FT4.Thyroid peroxidase antibodies .US: multinodular + cystic + solid o Cold  malignant  biopsy o hot  benign MKSforum.TFT  ↓FT3.Post surgical  ttt of thyrotoxicosis 4.g. Hashimoto thyroiditis) 3. ↓FT4.Post radiation  ttt of thyrotoxicosis 5. ↓TSH  2ry . Secondary hypothyroidism Investigations: .MKSforum.Post – partum thyroiditis: transient hyperthyroid  euthyroid  hypothyroditis then return back to euthyroid.

MKSforum.Better not to operate on hypothyroid patient till 3 months. The heart cannot cooperate with this & might infarct. .net -98- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Management .Need to give thyroxin gradually because the heart in hypothyroidism is functioning slowly. so if we give ↑thyroxin this would ↑ metabolic demand. MKSforum.0. If it is an emergency operation order it.5 μ. She will not die from hypothyroidism but from operation. ** In elderly start with low dose WHY?? ↓metabolic rate  can go in infarction .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 .

MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

Hyperthyroidism
1- post–partum 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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MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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. K–iodine β–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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MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

- 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  ‫ﺗﻨﺴﻰ ﺗﺄﺧﺬ اﻟﺤﺒﻮب ﺑﺎﻧﺘﻈﺎم‬ So, we are emphasizing on compliance & NO dose change – with regular use & thyroxin symptoms improve by 2-3 weeks.

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Goiter The patient is symptomatic. This group will develop hypothyroidism later on and so. will need treatment.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Sub clinical hypothyroidism ↑ TSH + T3 / T4 ( N ) 12345TSH > 10 Um / L Family history with thyroid problem Positive thyroid antibodies. MKSforum.net -102- .MKSforum.

Hyper pigmentation (creases + press areas) 5.Most common: autoimmune 2-Infections: TB .Dizziness 4.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Addison's disease Primary  adrenal failure Secondary  failure to the axis Causes of primary: 1.Sheehan syndrome  post – partum hemorrhage 2.MKSforum. fungal (histoplasmosis .Postural hypotension 6.Drugs: ketoconazol + metinapol ( used to test for Cushing's disease ) 5.Any tumor compressing the pituitary Symptoms: 1. coccidiomycosis) 3. meningococcal . HIV .Nausea.Infiltration  by amyloidosis + heamochromatosis + Wilson's Causes of secondary: 1.Vitiligo  can be associated with Addison's MKSforum.net -103- . vomiting 3.Diarrhea 2.Malignancy: tumor of adrenal or metastasis 4.Radiation 6.Adrenalectomy 7.

DM type I 7.MKSforum.Addison's 2.Pernicious anemia  affecting parietal diseases 4-Graves disease 5.Hypothyroidism 3.net -104- .Premature ovarian failure MKSforum.Vitiligo 6.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Organ specific disease ( autoimmune ) 1.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 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 + HCO3 ) 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 MKSforum.MKSforum.net -105- .

5 K+  no k+ @ 4. Required in the 1st 4-6hrs * Normal saline 2) Insulin: short acting insulin (lispro) = 0.5  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 1st 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 MKSforum.net -106- .MKSforum.V  bolus #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+ : @ 5.14 /Kg (bolus) then 0.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Treatment : 1) Fluid: 1/2 the amount of 24hours.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 # 6 unit I.V  infusion #5 unit I.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ [3] Acidosis & HCO3: Only correct if H < 7 . his HCO3 = 6  deficient = 24 – 6 = 13 Deficient x 1/6 body weight = 18 x 10 = 180 Give half of it only i. MKSforum. HCO3 < 5 before correction & after correction < 10 Normal HCO3 (24 – 28).net -107- .e.MKSforum. = 90 give it we are not aim to ideal level over 1/2 hour Therapeutic output depends on the patients opinion & what he feels.

net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫‪Rheumatology‬‬ ‫‪MKSforum.net‬‬ ‫-801-‬ .‫‪MKSforum.

Pain on rest. (Wt. hips in elderly & obese). Bamboo spine & Syndesmophyes (Tramline appearance) in an x-ray.MKSforum. Synovial NF > 50.000.net -109- . RA.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Arthritis 1234Septic. bearing knee. Seronegative. [1] Septic arthritis: All monoarthritis is septic arthritis until proven other wise. improved on exercise. Aortic regurge. Achilles tendonitis. Acute onset. More commonly in knee. Seropositive  SLE. Positive culture. Anterior uveitis. HLA-B27 Spine – sacroiliac joints. [2] SERONEGATIVE: 1* Ankylosing spondylitis:  4 As: Apical lung fibrosis. With fever & chills. Osteoarthritis. MKSforum.

MKSforum.Psoriatic spondylitis: like ankylosing spondylitis. 3* Psoriatic arthritis: . . Recurrent thrombi: CVA.Predominant distal interphalangeal joint arthritis. -Circinate balanitis: on glans & prepuce. DVT. . Skin: scaling on extensor.net -110- . 4* (Enteropathic Arthritis) Arthritis with inflammatory bowel disease (IBD): Ankylosing spondylitis & sacroiliitis with diarrhea. Extra articular: Nail: onycholysis. arthritis).net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 2* Reactive arthritis (Reiter's Syndrome): 1. conjunctivitis. (urethritis. horizontal ridging.STD. . Rash: Keratoderma blennorrhagica: on palm & sole. sublingual hyperkeratosis. 6* Whipple's disease: Arthritis + Hyperpigmentation + LN + Splenomegaly. . 2.non STD. optic.Arthritis mutilans. 5* Bachet syndrome: Recurrent oral / genital ulcer.Symmetrical polyarthritis: like RA. pitting. MKSforum.A symmetrical inflammatory oligoarthritis.

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. X-ray (chest). . ECG.RF  present in 70% of cases  RA. cast). . Urea & electrolyte  to assess kidneys.ANA  SLE may be for the other also. a rheumatologist will require it). hematuria. LFT. (1) BASE LINE INVETIGATION: 12345678CBC  cytopenia. INVESTIGATION: 1.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ [3] Seropositive: 1. cervical atlantoaxial joint)  RA. . anti-Sm Abs  SLE. Urine analysis (protein.Anti-Scl 70  Scleroderma.Specific. .RA: Significant morning stiffness or joint pain must be more than an hour.Motility test  scleroderma. MKSforum.Upper GI endoscopy.Anti-ds DNA.P-ANCA  if chest pain + hemoptysis / antiglomerular basement membrane (anti-GBM). HCV  cryoglobulinemia.X-ray (hands. . (2) SPECIFIC: . . . ESR. knee. feet.Base line for all patients 2. . HBV.net -111- . CRP.MKSforum.

net -112- .MKSforum.. . Fatah Aldien said.Discoid rash  it’s raised erythematous found more commonly in the scalp area… also leave scar. 8. 5.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ .If u suspects complement  Do: C3.. and it’s erythematous. pericardium. 2. or new redness formed in exposed area.Oral ulcer.. 2. Dr. polycythemia ….Serositis  pleura. 6.All patients with hematuria & proteinuria more than 1g  DO Renal Biopsy regardless of renal function test. Also doesn’t leave scar. 7.Renal disorder  can be asked like this…any proteinuria (frothy bubbles seen with the urine) or New Hypertension…or lower limb edema or any edema. C4..Arthritis  non erosive  small (peripheral) joints. 3.Photo sensitivity means the redness increase when exposed to sun. it could be found in the buccal mucosa and labia majora.Neurological disorder  seizure or psychosis not depression. MKSforum..Butterfly molar rash cross the nasal bridge  doesn’t cross nasolabial fold because if it does we’ve to think  hypothyroidism. Remember this word  SOAP Brain Md Four out 11 is considered ok to diagnose SLE: 1. 4.SLE: Criteria to diagnose SLE.

anti phospholipids' Abs.anti-Ds DNA Abs.eye: (1) Anterior Uveitis but more with RA. Let’s go through each system: 1. if it's wetted by tear  change the color. C. 10Immunological disorder: a.Lymphopenia less than 1500. MKSforum.False positive syphilis serology.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 9. 2.000. Schirmer's test  put litmus paper strip. 11ANA positive > 95% of cases. c – anti-Sm. -Convulsion and seizure.Thrombocytopenia less than 100. B-leucopenia less than 4000.Hematological disorder: A-Hemolytic anemia. (2) Dry eye plus dried mouth  sjogren syndrome. b. D.net -113- . Abs. -Psychosis  we’ve to know is it due to SLE or Cortisone treatment side effect?  By: -myopathy  due to cortisone side effect. -depression and vasculitis  stroke.  15 mm is normal.MKSforum. d.CNS: 60%.

thrombosis (lung infarction).Effusion. . . Abeer Kawther: 1) 2) 3) 4) 5) Vasculitis  fibrosis. Recurrent DVT  pulmonary embolism. 8) Shrunken lung syndrome  due to bilateral fibrosis (fibrosing alveolitis). edema. 4. In Lupus Pneumonitis: .MKSforum.Anemia  autoimmune (hemolytic). due to vasculitis)  like lobar pneumonia.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (3) Cystoid bodies (on microscopy) / by ophthalmoscope  cotton wool spots. 9) obliterative bronchiolitis. .lung:  Dr. Pleurisy. In Lung Fibrosis: Patients may take bronchodilators  may benefit or may not.S.Pneumonitis.B.Fever  might present or not (suppressed by medications). 10) Dyspnea (analyze it & see if it's related to SLE or not)  due to: .Myositis of respiratory muscles.net -114- . 7) Pleural effusion  transudate. (4) Subconjunctival hemorrhage. 6) Pneumonitis (non-bacterial. . MKSforum.Lung fibrosis. Immunosuppression (immunity) by SLE or steroids (drugs)  prone to infection  Tb or atypical infection. .O. 3-Neck: Thyroiditis.Pulmonary infarction. Pulmonary edema due to secondary HF. .

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 5.Renal failure. but more with RA. c.MKSforum. Peptic ulcer  due to drug or vasculitis. 6.  Mesangeal lupus GN. -Pericarditis and pericardial effusion.. MKSforum.Heart: -Aseptic endocarditis (libman sack $).Kidney: 50% Lupus Nephritis  classes. Diarrhea. Remember  felty's syndrome: Splenomegaly + RA + leucopenia + leg ulcer.  Focal proliferative GN. d.  Membranous GN.Abdomen: Autoimmune hepatitis  high liver enzymes either due to drug or hepatitis.  Diffuse proliferative GN.Glomerulonephritis  5 stages (patterns):  Minimal change GN. It could be: a.net -115- . -Mitral regurge is more with SLE and Aortic regurge with RA. Splenomegaly. 7. e.Normal b. Pancreatitis  due to drug.Amyloidosis. because it can be associated with scleroderma  so they’ll have esophageal dismotility and atonic intestine and blind loop syndrome…also crest syndrome..UTI. 3 signs of peritonitis: fever – turbid drain – vomiting – abdominal pain (may be).

Any cytopenia.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 8.Joints: >90% -None deforming. 9.High ESR / CRP is normal in SLE. 10.Low complements. -No morning stiffness.Hematologically: . Livedo reticularis especially associated with antiphospholipid syndrome and Pancreatitis Alopecia. Discoid lupus erythematous (DLE).Skin: 80% Butterfly rash. -Affect small joint. MKSforum. -Distal interphalangeal joint.net -116- . .MKSforum. .

pericarditis Loin pain can be presented in SLE due to: -Infraction (vasculitis). Signs of active disease: 1. 5.MKSforum.Clinically: arthritis…fever. 9. 8. 2.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Investigations: 1.CXR  Cardiomegaly. 6. Normal ESR level up to 20mml/h Zero ESR is seen in polycythemia.ANA which is sensitive / Anti-Ds DNA Antibodies which is diagnostic for SLE AND Anti-sm Antibodies 4.ECG because of conduction abnormality and arrhythmia. -Renal vein thrombosis which is noticed as antiphospholipid syndrome (APS) MKSforum.High ESR which is indictor for reactivity.net -117- . rash. Chest pain in a SLE patient is due to serositis  pleural effusion.Complements level  low. Normal CRP in SLE  used in Differential Diagnosis 3.LFT for chronic active hepatitis. Also active sediments in urine  hematuria or red cast cells. pericardial and lung effusion. -Infection.Biochemical: cytopenia. high ESR and normal CRP. low complements. 7.U & E for lupus nephritis.Echo.Urine test  red cell cast And proteinuria  do 24h. 10.CBC  cytopenia … 2.

. Causes of death in a SLE patient? 1Infections (opportunistic). -Scleroderma. 2Renal /CNS involvement (active SLE).What criteria are they based on?  Clinical & Laboratory.MKSforum. -Chronic active hepatitis.net -118- .When was it diagnosed? . -Rheumatic heart disease. thus upon them the diagnosis made and was diagnosed by dr. if the patient doesn't know  ask about: an expensive tablets or drugs taken through IV once every month. ____ 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. Differential diagnosis of SLE: -RA. 3Accelerated atherosclerosis  MI. because if she has Lupus nephritis  class VI is usually treated by chemo.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 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).Complicated with what? Always ask about chemotherapy. -Drug induced lupus. . MKSforum.Treated with what? .

she was diagnosed in Harvard as RA because she has High ANA and High sky RF. Then she was diagnosed to have parvovirus infection which causes symptoms similar to RA & SLE. So the doctor said “I don't trust Harvard University. 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. with symptoms similar to RA (joint pain).. amurosis fugax.net -119- . How to differentiate that psychosis in SLE pt. Side effect: Increased skin pigmentation and deposit in retina  and all these seen only in high dose. Anti-phospholipids' Syndrome: Diagnosed by Having Low platelets and prolonged PTT and in the Hx they've abortions and Migraine. 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.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Smart Rheumatology Qs by Dr. Fat'h Al-deen. A patient came to Dr. MKSforum.. Fat'h Aldeen and then he swore when any student answered them.. 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.MKSforum. TIA. And in examination they've levido reticularis. stroke..

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Causes of prolonged PTT: Either  coagulopathy or auto Abs like antiphospholipid $.IsoNiazid. 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 the result was corrected (PTT not prolonged). 3Anti-Beta 2 glycoprotein 1 Abs (beta2GP1)  very important for the diagnosis. Methotrexate is hepatotoxic  it's given once weekly. *In summary: PTT: -If corrected  factor deficiency. So to investigate anti-phospholipids' $  by three tests [ELISA]: 1Lupus anticoagulant (its mechanism is very important)  see below: 2Anti-Cardiolipin. Drug induced SLE: -Usually by hydralazine – procainamide . -Anti-ds DNA negative. we take patient serum (50%) & mix it with serum from a normal person (50%). has prolonged PTT. -Normal complements and ANA positive.MKSforum.net -120- . If Prolongation of PTT is still the same  not corrected  Ag/Abs reaction (autoimmune). MKSforum. So. -They've Positive anti-Histone. -If not corrected  Ag/Abs. 50/50 fixed test for Lupus Anticoagulant: Antiphospholipid pt.

‫‪MKSforum.net‬‬ ‫-121-‬ .net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫‪Neurology‬‬ ‫‪MKSforum.

.hearing problem: (8) . speech difficulty + :‫ﻣﺨﺎرج اﻟﺤﺮوف‬ :‫اﻟﻘﺪرة ﻋﻠﻰ ﻧﻄﻖ ﺑﻌﺾ اﻟﺤﺮوف‬ :‫ﻣﯿﻢ .Facial muscle: (7) asymmetry. ﻣﺜﻞ : ﻻ اﻟﻪ اﻻ اﷲ . choking sensation + hoarseness: (9. 12) MKSforum..net -122- .MKSforum. food accumulation...... ﻣﺜﻞ ﻛﻮﻛﺎ ﻛﻮﻻ.Double vision… (3. in ability to close the eye.Aishah Al-Shareef # Higher functions: .Headache . 4. ﻣﺨﺮج اﻟﺤﺮف ﻣﻦ اﻟـ‬ Tongue : ‫ﺣﺮف اﻟﻜﺎف .. اﻟﻤﺨﺮج‬ Lips ‫اﻟﻼم . (2) .Loss of conciseness . ﻣﯿﻢ .Smelling problem…(1) . saliva drooling.Facial numbness or hypersensitivity. 6) . 10.Confusion .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ How to take: A quick perfect neuro-history Dr.Difficulty in swallowing.Seizure # Cranial nerves: .Decrease in vision acuity. اﻟﻤﺨﺮج‬ Palate .. (5) ..

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ # Motor: .Urine control (Either retention or incontenence) MKSforum.MKSforum. decrease in sensation or increase) Analysis: site .Stool control .Distal: ‫اﻧﺘﻌﺎل اﻟﺤﺬاء – ﺧﺮوج اﻟﺤﺬاء دون ﻗﺼﺪ ﻣﻦ ﻗﺪﻣﻪ – ﻓﺘﺢ اﻟﻌﻠﺐ – ﻓﺘﺢ ﻳﺪ اﻟﺒﺎب‬ Double vision Speech difficulty Voice hoarseness Facial asymmetry Food accumulation Inability to close the eye Difficulty in swallowing neck stiffness # Sensory: Pain (dull.Weakness .Unstable gait # Autonomic: .Proximal: ‫ﺻﻌﻮد اﻟﺪرج – اﻟﻮﻗﻮف ﻣﻦ وﺿﻌﯿﺔ اﻟﺠﻠﻮس – رﻓﻊ اﻟﯿﺪ ﻛﺘﺴﺮﻳﺢ اﻟﺸﻌﺮ او أﺧﺬ ﻏﺮض ﻣﻦ‬ ‫رف ﻋﻠﻮي ﺑﻌﯿﺪ‬ . distribution … # Cerebellar functions: .net -123- .Tremor . numbness.

exposure to sunlight ( osteomalasia and generalized weakness) .net -124- .Anticoagulant .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ # Risk factors: (Depend upon your case) .Family history of the same condition.Similar condition in the past .Intubation .DM.. .: .ICU (why?? ttt) .Smoking .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. HTN. # Social: .g. vomiting indicates increase intracranial pressure) MKSforum. or specific neuro cases .Degree of disability: ‫ﻣﺪى اﻋﺘﻤﺎد اﻟﻤﺮﻳﺾ ﻋﻠﻰ ﻧﻔﺴﻪ/او ﻋﻠﻰ ﻏﯿﺮه‬ ‫ﻗﺒﻞ اﻟﻤﺮض وﺑﻌﺪه وﺑﻌﺪ اﻟﻌﻼج‬ # Hospital course: . You will reach to this aim if you write the complete history (both positive and negative symptoms) Start with the patient’s complains..MKSforum. hyperlipidemia. e.…….g.Food type. diarrhea . IHD . e.………. Do not forget important review of systems for differential. URTI.: (fever indicates infection.fever.

Dysphagia: IX. 2.net -125- . MKSforum.4 Ds: at least 2 of them: 1.CN: ipsilateral. 4. 3. proprioception vibration silateral -Brown square syndrome. -Sensory: pain.Diplopia: III.Crossed phenomena (sensory or motor): .Aisha Al-Shareef Weakness pattern: -Hemiparesis. VI.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Localization Dr.Dysarthria CNS IX. Hemiparesis: 1.MKSforum.Cranial nerve CNS involvement: Any CN involvement is in brain stem except facial nerve could be cortical or subcortical. 3. dysphagia).Where is the lesion? 2. -Generalized ( cranial nerve involvement motor part: double vision. tempntralateral. -Quadriparisis. -Deep sensation. IV.What is the lesion? * Spinal cord hemiparesis: -Face not involved.Disequilibrium cerebellar peduncle. -Paraparesis. Brain stem: 1. X. 2. XII. -Body: contralateral. X. -No CN involvement.

Cortical: -Cognitive impairment e. Except: facial nerve – lower part – -Hemiparesis. -Facial + weakness = all is ipsilateral to each other.g. leg). trunk. MKSforum. hand.MKSforum.g. -Distribution of lesion: Internal capsule is a dense fiber.: upper power 0/5 wer 4/5 Seizure = cortex irritation.net -126- . = e. ‫أي ﺣﺰﻣﺔ واﺣﺪة‬ = 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.: aphasia. memory. language problem.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Subcortical / Cortical: -No cranial nerve involvement.

. mononeuritis multiplex.Cervical spinal cord lesion. arefelxia etc… In cortical: cognitive impairment. internal capsule. 2.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Paraparesis: Upper power 5/5 lower weakness: 1. no UMNL only weakness normal reflexes.Spinal cord lesion. -In muscle myopathy: normal sensory.g.Parasagittal tumor. Weakness normal reflexes. proximal > distal. lambert-eaton. early polyneuropathy  later on hands affected). any nerve above L1 can give sensory level but below it not consider a spinal cord lesion e.C: . after exercise 4/5.MKSforum. 4. In spinal cord: sensory level. 3. in myopathy the power is the same even after exercise. distal > proximal. Quadriparesis: Big insult.NMJ: myasthenia. 1.Muscle.Motor neuron disease. stock distribution in diabetes is not a spinal cord. If no UMNL.net -127- ..Late stage GBS. CNS.H.In polyneuropathy (gloves & stock) LMNL. A.Mixed UMNL +LMNL. fatigability: fluctuation in power 5/5 in the beginning.In NMJ: normal sensory. 3. MKSforum. In polyneuropathy LMNL fasciculation. 2. no UMNL only. . proximal > distal. .In spinal cord: motor UMNL.Peripheral nerve (mononeuritis. sensory level. .

Space Occupying Lesion (SOL) 4.Infarction 3. warfarin.net -128- .Hyperlipidemia .Smoking MKSforum.MKSforum. we don't call it vascular CAUSES: 1 .Demyelinating disease 5.Metabolic disease Hemorrhage: AV malformation most common in young patients Ruptured berry aneurysm Hypertension (HTN) in old patients Patient on anticoagulant: aspirin. heparin Trauma Infarction: (1) Atherosclerosis: .Hemorrhage 2.Maimoona CVA is only vascular Stroke.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ STROKE / CVA Dr.Diabetes Mellitus (DM) .Degenerative disease 6.Hypertension (HTN) .

due to any arrhythmia: .MKSforum.net -129- . just remember Multiple Sclerosis (MS) MKSforum.IHD .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ (2) Thromboembolism: 1.Thyrotoxicosis 2.Rheumatic heart disease  Valvular heart disease .Infections: Tuberculosis #1 Meningitis Hydatid cyst Abscess whatever the cause is Fungal HIV Toxoplasmosis CMV Demyelinating disease : They are many.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.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Degenerative disease: .Hemochromatosis .MKSforum.Cerebral palsy .Wilson's disease Pediatrics MKSforum.Huntington’s disease Metabolic: When there's a heavy metal deposition in the brain.net -130- . depending on site of deposition .

abscess ) MKSforum.Infective endocarditic (drug abuse) Arrhythmia due to any cause DM & HTN  in young & elderly In elderly: 12345678Diabetes mellitus Hypertension Anticoagulant Space occupying lesion  tumor. S . III .MKSforum. vasculitis Thyrotoxicosis any other cause : infection :  abscess . HIV . mainly metastatic Hyperlipidemia ( atherosclerosis . TB . V ) CTD connective tissue disease . smoking ) Ischemic Heart Disease (IHD) Arrhythmia Infection ( TB .net -131- . meningitis Sickle Cell Anemia (SCA) 9.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ In HISTORY: Causes according to age group: In young (< 45y) The commonest cause is hemorrhage 12345678AV malformation Rupture berry aneurysm MS (demyelinating) Valvular heart disease Thrombophilia ( decrease protein C .

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‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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: Thrombo–embolic: 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 MKSforum.net
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‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

(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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‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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 ………..) MKSforum.net
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If CTS.net -135- .if demyelination on CT  LP  increase protein oligoclonal band . 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) MKSforum.cerebellum STROKE MANAGEMENT: In general: . diaper [1] Hemorrhagic stroke: .COAGULATION profile: PT.MKSforum. X lesion  NGT .Incontinence  catheter.U & E  HTN 8.Optic Nerve . PTT 9.SEPTIC CULTURE  infective endocarditis 10.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 7.HG electrophoresis  SCA 11.CNC IX.Physiotherapy .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 MS  diagnosed mainly by relapse & remission  2 attacks Affect mainly: .

HTN.Hemorrhage resolves on its own & patient improves 2. but if survives  less morbidity than ischemic in ischemic stroke: less mortality but high morbidity compared to hemorrhagic stroke [3] If demyelination: steroids + alpha interferon (α-IF) MKSforum.net -136- . VHD. AF  anticoagulation .Angiogram to be available before calling neurosurgeon to confirm which artery [2] Infarction type: Treat according to the cause: .In arrhythmias.If not any of these  just put patient on aspirin & plavix (Usually patient is DM.call neurosurgeon to clip the aneurysm because it will re-bleed in 10 days .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 . not below 180/100 because it will causes decreased perfusion Dextamethasone: would not work Observe the patient: either: 1. hyperlipidemia. smoker  treat the comorbiditiy) in hemorrhagic stroke : high mortality.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ If there is midline shift  give manitol to decrease ICP If no midline shift  then decrease BP very slow.MKSforum.

Complete stroke MKSforum. in primary malignancy some times surgery depends on the type [6] Carotid artery stenosis 70 .80%  neurological deficit. usually in immunocompromized patient . 2 weeks neurological deficit 3.RIND: reversible ischemia.If infection is not HIV & the chest is clear  empirically give Anti-TB . CMV & toxoplasmosis are very rare.If there is a middle ear infection then give broad spectrum antibiotic [5] If malignancy: biopsy.net -137- .TIA: improve in 24 hrs 2.MKSforum.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ [4] If infection: find the source  erode the infection . radiotherapy. TIA  end artery surgery [7] Metabolic  specific treatment Notes: Classification of neurological deficit: 1.If not HIV.

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 MKSforum. breast.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 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. lung.net -138- .MKSforum. MM. prostate.

MKSforum. Growth of nerve \ can affect any nerve 11) Granuloma → syringomylia → sarcoidosis →T.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ → → → → → 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.B 12) Congenital spastic paraplegia 13) MKSforum. Spinal cord thrombosis Myocardial infarction 7) Subacute combined degeneration of spinal cord 8) B12 deficiency 9) Lymphoma 10) Neurofibromatosis Exc.net -139- .

disc prolapse .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ *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 .MKSforum.net -140- . trauma Renal pain and haematuria → renal cell carcinoma Brachial plexus compression: → Cervical rib → Any mass at the apex (lymphoma. TB) MS → relapse & remission MKSforum.

and cyst) 3. Lumbar puncture ↑ Protein (infections. MRI → Specific for demyelinating disease → Demyelinating plaque → Look for space occupying lesions (tumor. Fundoscopy → Papilloedema C.net -141- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Investigations: A) Definite: 1.T scan (if no papilloedema we can perform a lumbar puncture) 2. MS) ↓ Glucose (bacterial infection) ↑ Lymphocytes (TB) ↑ Neutrophils (bacterial infection) Malignant cells Single P band  mono/oligoclonal P band (MS) MKSforum. abscess.MKSforum. X-Ray → → → → TB Disc prolapse Fracture Cervical spondyelitis 4.

ANA 5. ESR → ↑ (infection. EMG (delayed conduction in MS) *For Infection: 1. CBC → leukocytosis 2. Biopsy → Pott's → Tumors B) Supportive: 1.net -142- .MKSforum. ECG 4. Auditory evoke response 7. …… (B12) MKSforum. Visual evoke response 6. PPD ( TB) 2. malignancy) 3.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 5.

hypothyroidism. B6. HIV 2) Inflammation: Guillan-Barre . wegeners .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Polyneuropahties (PN) Causes: 1) Infection: Leprosy . INH. lyme . or increase B6 MKSforum. polycythemia . anticancer 8) Vitamins: Low B1. disease: PAN. renal failure 5) Malignancy : PNS. syphilis . arsenic 7) Drugs: Alcohol. multiple myeloma 6) Toxines: Lead.net -143- .T.MKSforum. RA 4) Metabolic: DM. Folate. B12. hypoglycemia.sarcoidosis 3) C. chronic inflammatory demyelinating PN .

MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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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MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

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    3rd nerve palsy - Blood pressure  Low  septicemia High hypertensive hemorrhage - Temperature - Pulse

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MKSforum.net
‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬

- Neck rigidity  If there hasn’t 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 doesn’t 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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Glumerlonephritis 4.net -147- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ CNS: 1.Splinter hemorrhage MKSforum.Acute abdomen Skin: 1.MKSforum.Amyloidosis 5.Psytotic body with SLE 2.Scleritis – Episcleritis CVS: Respiratory: Abdomen: 1.Mono neuritis multiplex Eye: 1.Primary sclerosing cholyngitis 3.Stroke 4.Skin ulcer 2.Psychosis 2.Chronic active hepatitis 2.Seizure 3.

net‬‬ ‫-841-‬ .net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫‪Other‬‬ ‫‪MKSforum.‫‪MKSforum.

MKSforum.Abnormal blood flow *The most important points in order. paralysis. CVA.MKSforum.Immobility* (due to traveling "the most important”.Compression by pregnancy or tumor & economic class (‫ )اﻟﺪرﺟﺔ اﻟﺴﯿﺎﺣﯿﺔ‬syndrome DVT Because vessels are kinked during the flight causing blood stasis.Heart failure* .net -149- . pregnancy) . Maimoona Etiology of DVT: Virchaw's triad 1-Abnormal blood flow 2-Abnormal constituents of blood (hypercoagulability) 3-Abnormal vessel wall 1. you can then mention the others according to order .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ DVT Session with Dr. post operative. fracture.

Polycythemia . factor V (recurrent & positive FH) .CLD (chronic liver disease)  prot.Para protienemia (multiple myloma) .Pancreas carcinoma .Thrombophilia: is the deficiency of protein C & S.Antiphospholipid antibodies in APLS (in females ask about recurrent abortion) .Abnormal constituents .net -150- .Hypercoagulopathy . lymphomatic .OCP = oral contraceptive pills .SCA (sickling crisis) 2.MKSforum.Thrombocytopenic purpura MKSforum. leukemic ) The most common malignancies causing hypercoagulable state are: .Nephrotic Syndrome  loss of antithrombin III .Lung carcinoma .Prostate carcinoma . pancreatic.SCA . diarrhea) .Dehydration due to any reason: (fever.Polycythemia . Anti-Thrombin III deficiency Never say "nephrotic syndrome & CLD are causes of DVT" but "they are causes of protein deficiency" . antithrombin III.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ . C & S.Any malignancies: (prostatic.IBD is Inflammatory Bowel Disease: hypofibrogenemia .

hemoptysis.. good pasture. palpitations. ulceration.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.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 3-Abnormal vessel wall .Trauma*  IV cannulation (either in hospital or in IV drug abusers) . HSP = henoch shonleinn purpra) . discoloration History Presentation: The Patient presented with ……. C MKSforum.Chronic: post phelebitic limb >> stagnation of blood >> not return normally to heart >> leg edema. or syncope . RA. (Occupation) He/she has no history of ………… ‫ﻧﻌﺪد اﻟﻤﺴﺒﺒﺎت‬ (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.Vasculitis*: (SLE.net -151- .MKSforum.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ No history of (protein loss) No previous history of DVT No history of recurrent abortion  I think this is due to APLAS :‫ﺑﻌﺪﻳﻦ ﻧﻘﻮل‬ No history of fever or loss of weight (( complications ‫ ﺑﻌﺪﻳﻦ ﻧﺮوح ﻟـﻠـ‬exclude causes of DVT ‫))إذن أول ﺷﻲ‬ No history of ………  ‫ ﻛﺪا‬Hx ‫ ﺑﺲ اﻟﻘﺼﺪ إﻧﻪ ﻻزم ﻳﻨﻘﺎل اﻟـ‬NO ‫ﻣﺶ ﻣﻌﻨﺎه إﻧﻪ ﻛﻠﻪ‬ Note: Patient < 45 yr-old  traveling.T.net -152- .MKSforum. Disease. 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 MKSforum. C. pregnancy. malignancy. OCPs Patient > 45 yr-old  immobilization.

Venography: gold standard  if negative: no DVT A dye is injected in the (vein) dorsum of foot ‫ وھﺬا ﺑﺎﻟﻄﺒﻊ ﺧﺎﻃﻲ ﻻﻧﻪ ﻓﺤﺺ ﺧﺎص‬angiogram ً‫وﻛﺜﯿﺮ ﻣﻦ اﻟﻄﻠﺒﻪ ﻳﻘﻮﻟﻮا ﺧﻄ‬ ‫ﺄ‬ for artery‫ﺑﺎﻟﺸﺮﻳﺎن وﻟﯿﺲ اﻟﻮرﻳﺪ‬ ‫ و ﻃﻮل وﻗﺘﮫﺎ ﻧﺎﻳﻤﺔ، ﻣﺎ ﻧﺴﻮي ﻟﮫﺎ‬stroke for 10 years ‫* إذا ﺟﺎﺗﻨﺎ ﺣﺎﻟﺔ ﻋﻨﺪھﺎ‬  ‫ ﻷﻧﻪ اﻟﺴﺒﺐ ﺑﺎﻳﻦ‬fractures ‫ و ﻧﻔﺲ اﻟﺸﻲ اﻟﻠﻲ ﻋﻨﺪھﻢ‬investigations : investigations ‫ﻟﻜﻦ إذا ﻣﺎ ﻋﺮﻓﻨﺎ اﻟﺴﺒﺐ ﻧﺴﻮي ﻛﻞ اﻟـ‬ Blood work:  certain blood tests are done for specific history 3 – CBC  lycyciemia .ECG ---------------Diagnostic Tests: 1 .net -153- .MKSforum.D-dimer 6. malignancy .Peripheral blood film  SCA MKSforum.Coagulation profile 5. cytopenia 4. DO the following: 1 .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ Investigations: For every patient.Doppler 2.Doppler  1st line to document DVT  if negative :‫إذا ﻣﺎ ﺑﺎن ﺷﻲ و ﻟﺴﺔ ﺷﺎﻛﯿﻦ، ﻧﺴﻮي دي‬ 2.CBC 4.Venogram 3.CXR 7.

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) MKSforum. but NOT specific may increase in pregnancy . PTT (BEFORE starting the treatment for monitoring) Or Anti-Cardiolipin Abs 6.Wedge shaped infarction.Protein electrophoresis  multiple myeloma Radiology: 11. malignancy.net -154- .Coagulation profile: PT.D-dimer  increase in thrombosis & PE.Chest X-Ray (CXR): for pulmonary embolism(PE).Ag-Ab profile 9.post operative 7. pulmonary edema. 3.ESR & C .Works for thrombophilia 8.Oligemic lung  decrease blood flow 12.MKSforum. etc 1-Normal 2.infection .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 5.reactive protein 10.

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 ‫أي ﻓﻲ ﺗﺨﻄﯿﻂ اﻟﻘﻠﺐ ﻗﺪ ﻧﺠﺪ اﻟﺜﻼث ﺻﻔﺎت اﻟﻜﻼﺳﯿﻚ‬ S1 Q3 T3 ‫ﻟﻜﻦ اﻻﻏﻠﺐ ﻧﺠﺪ ﻓﻘﻂ‬ Sinus tachycardia 15.net -155- . MKSforum. 18.Pulmonary Angiogram 20.Spiral CT scan.Ventilation/Perfusion scan (VQ scan) ---------------SPECIFIC Investigation According to History: e.g. if the cause is not CVA.d-dimer (end product of breakdown of thrombus  increases in blood) 17.: ANA in CTD In elderly patient.ABG 19.Doppler US 16.MKSforum. immobilization always screen for malignancy. or post operative or.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 14.

net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ If PE  1. ultrasound abdomen In both do an ECG. antithrombin III I the patient is > 45  chest X-Ray.MKSforum. ulcer in mouth Legs:  Inspection: Swelling & determine the exact site Scar (IV. O/Ex.ventilation perfusion VQ scan PULMONARY ANGIOGRAPHY is the definitive test for pulmonary embolism Supporting: If the patient is < 45  protein C & S.: Vital. general Hands: C.T. rashes Cyanosis (heart failure) Pulse (tachycardia: Pulmonary Embolism.spiral CT scan. no active arthritis. disease. APL Abs. 2. drug abuse) Pigmentation Shiny skin Edematous MKSforum. unequal pulse: Vasculitis) Postural hypotension Face: Rashes. no ulcer. pallor.net -156- .

Homan's signs = increasing resistance & pain on forced foot Dorsiflexion : say it but DON'T do it  dislodge thrombus .MKSforum.Phlegmasia alba / white leg .Pulse : vasculitis unequal .net -157- .net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ .Edema ( DVT = pitting .Redness .Phlegmasia dolens / milk leg  Palpitations .g.: till the knee or the thigh . lymphoedema = non pitting ) & do it up & up to see till where no more pitting edema e.Tense calf muscle .Temperature is down and up and compare both .Tenderness . . if absent: why? Because edema compresses the artery.Measurements: ‫ﺑﺎﺳﺘﺨﺪام اﻟﻤﺘﺮ ، ﺳﻨﻘﯿﺲ ﻣﺤﯿﻂ اﻟﺮﺟﻞ‬ ‫ﻣﻜﺎن اﻟﻘﯿﺎس ﺳﯿﻜﻮن ﻋﻨﺪ اﻋﺮض ﻣﻜﺎن / اﻷﻛﺜﺮ اﻧﺘﻔﺎﺧﺎ‬ ‫وﻟﻔﻌﻞ ذﻟﻚ ﻻﺑﺪ ﻣﻦ ﺗﺤﺪﻳﺪ ﻧﻘﻄﺔ ﺛﺎﺑﺘﺔ ﻟﻠﻘﯿﺎس ، ﻟﻨﻘﯿﺲ ﻣﻨﮫﺎ اﻟﻤﺮة اﻟﻘﺎدﻣﺔ ﻓﻲ ﻧﻔﺲ‬ ‫اﻟﻤﻜﺎن ﻟﻤﻘﺎرﻧﺔ اﻟﺘﻐﯿﺮ ﻓﻲ اﻟﻤﺤﯿﻂ‬ :‫ﻟﺘﺤﺪﻳﺪ ﻧﻘﻄﺔ ﻗﯿﺎس ﺛﺎﺑﺘﺔ‬ ‫ﻧﺴﺘﺨﺪم ﻧﻘﻄﺔ ﺛﺎﺑﺘﺔ ﻣﻦ اﻟﺮﺟﻞ‬ Bony prominence ‫وﺳﺘﻜﻮن ھﻨﺎ ال‬ Tibial tuberosity ‫و اﻧﺘﺒﮫﻮا ﻻ ﻳﺼﺢ اﺳﺘﺨﺪام اﻟﺒﺎﺗﯿﻼ‬ Patella ‫ﻛﻨﻘﻄﻪ ﺛﺎﺑﺘﺔ ﻷﻧﮫﺎ ﻣﺘﺤﺮﻛﺔ‬ MKSforum.

net‬‬ ‫-851-‬ .net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫ﻧﺜﺒﺖ اﻟﻤﺘﺮ ﻋﻠﻰ اﻟﺘﯿﺒﺎل ﺗﯿﻮﺑﺮوﺳﯿﺘﻲ ﻋﻨﺪ 0 ﺳﻢ‬ ‫وﻧﻤﺪھﺎ ﻋﻠﻰ اﻣﺘﺪاد اﻟﺴﺎق ﺣﺘﻰ ﻧﺼﻞ ﻷﻛﺒﺮ ﻣﺤﯿﻂ ﻣﻨﺘﻔﺦ وﻧﺴﺠﻞ اﻟﻘﺮاءة‬ ‫ﻣﺜﻼ وﺟﺪﻧﺎھﺎ ٢١ ﺳﻢ )) اﻷﻏﻠﺐ ﻳﺴﺘﺨﺪم ٠١ ﺳﻢ (( ‪ ‬وﺳﺘﻜﻮن ھﻲ اﻟﻨﻘﻄﺔ اﻟﺜﺎﺑﺘﺔ‬ ‫اﻟﺘﻲ ﺳﻨﻘﯿﺲ ﻣﻨﮫﺎ ﻛﻞ ﻳﻮم‬ ‫)) اﻷﻏﻠﺐ ﻳﺴﺘﺨﺪم ٠١ ﺳﻢ ﻓﻲ ﻛﻼ اﻟﺴﺎﻗﯿﻦ ﻧﺰوﻻ ﻣﻦ ﻋﻨﺪ اﻟﺒﺎﺗﯿﻼ ((‬ ‫ﻣﻦ ﻋﻨﺪ ھﺬه اﻟﻨﻘﻄﺔ اﻟـ ٢١ ﺳﻢ )) اﻷﻏﻠﺐ ﻳﺴﺘﺨﺪم ٠١ ﺳﻢ (( ﻧﺄﺧﺬ ﻣﺤﯿﻂ اﻟﺴﺎق‬ ‫وﻧﺴﺠﻞ اﻟﻘﺮاءة‬ ‫ﻣﺜﻼ وﺟﺪﻧﺎھﺎ ٤٣ ﺳﻢ ‪ ‬وﺳﺘﻜﻮن ھﻲ ﻗﺮاءة اﻟﻤﺤﯿﻂ اﻟﻤﻄﻠﻮﺑﺔ‬ ‫اﻵن ﻧﺬھﺐ إﻟﻰ اﻟﺴﺎق اﻟﺜﺎﻧﯿﺔ‬ ‫وﻧﻜﺮر اﻟﻌﻤﻠﯿﺔ‬ ‫ﻧﺤﺪد ﻣﻜﺎن اﻟﺘــﯿـﺒﯿـﺎ ﺗﯿﻮﺑﺮﻳﺴﺘﻲ وﻧﻨﺰل ﻣﻨﮫﺎ ﺑﺎﻟﻤﺘﺮ ﺑﺎﻟﻀﺒﻂ ٢١ ﺳﻢ )) اﻷﻏﻠﺐ ﻳﺴﺘﺨﺪم‬ ‫٠١ ﺳﻢ ((‬ ‫ﻟﯿﻜﻮن ﻧﻔﺲ ﻧﻘﻄﺔ ﻗﯿﺎس اﻟﺴﺎق اﻷﺧﺮى‬ ‫وﻣﻦ ﺛﻢ ﻧﺄﺧﺬ ﻗﺮاءة اﻟﻤﺤﯿﻂ وﻧﺴﺠﻠﮫﺎ ﻟﻨﻔﺮض وﺟﺪﻧﺎھﺎ ٠٣ ﺳﻢ‬ ‫اﻟﻘﺎﻋﺪة ﺗﻘﻮل إذا اﻟﻔﺮق ﺑﯿﻦ اﻟﻤﺤﯿﻄﯿﻦ أﻛﺜﺮ ﻣﻦ ﻧﺼﻒ ﺳﻢ ﺳﺘﻜﻮن‬ ‫‪Abnormal‬‬ ‫وھﻨﺎ ﻛﺎﻧﺖ اﻷوﻟﻰ ٤٣‬ ‫واﻟﺜﺎﻧﯿﺔ ٠٣‬ ‫اﻟﻔﺮق ٤ ﺳﻢ، إذن ﻏﯿﺮ ﻃﺒﯿﻌﻲ‬ ‫وﻳﻮﻣﯿﺎ ﺳﻨﻘﯿﺲ ﻣﺤﯿﻂ اﻟﺴﺎق اﻟﻤﺼﺎﺑﺔ ﺑﻨﻔﺲ اﻟﻄﺮﻳﻘﺔ ﻣﻦ ﻋﻨﺪ اﻟﺘﯿﺒﯿﺎ ﻧﻤﺸﻲ ٢١ ﺳﻢ‬ ‫وﻧﺄﺧﺬ ﻗﺮاءة اﻟﻤﺤﯿﻂ وﻧﺸﻮف اﻟﻔﺮق ﻳﻮم ﻋﻦ ﻳﻮم‬ ‫إذا ﻛﺎﻧﺖ اﻟﻔﺨﺬ أﻳﻀﺎ ﻣﺼﺎﺑﻪ ﺳﻨﻘﯿﺴﮫﺎ ﺑﻨﻔﺲ اﻟﻄﺮﻳﻘﺔ‬ ‫ﻧﺤﺪد ﻧﻘﻄﺔ ﺛﺎﺑﺘﻪ ﻣﻦ اﻟﻌﻈﻢ وﻧﻄﻠﻊ ﻣﻨﮫﺎ ﺑﺎﻟﻤﺘﺮ ﻷﻛﺜﺮ ﻣﻜﺎن ﻣﻨﺘﻔﺦ وﻧﺄﺧﺬ ﻗﯿﺎس اﻟﻤﺤﯿﻂ‬ ‫ﻧﻜﺮر ﻓﻲ اﻟﺴﺎق اﻷﺧﺮى ﻟﻠﻤﻘﺎرﻧﺔ‬ ‫وﻳﻮﻣﯿﺎ ﻧﻘﯿﺲ ﻣﺤﯿﻂ اﻟﻔﺨﺬ اﻟﻤﺼﺎﺑﺔ ﻟﻠﻤﻘﺎرﻧﺔ‬ ‫ﺗﻮﺿﯿﺢ اﻟﺸﺮح ﻓﻲ اﻟﺼﻮرة اﻟﺘﺎﻟﯿﺔ:‬ ‫‪MKSforum.‫‪MKSforum.

‫‪MKSforum.net‬‬ ‫-951-‬ .net‬‬ ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ ‫‪MKSforum.

Start with heparin IV 80 – 100 U/kg bolus 20 U/kg/hour infusion maintenance dose 2.net -160- . OK 30-40 MKSforum.MKSforum.INR re measure * PTT  heparin * PT. INR ratio  warfarin 2-2 1/2 time control After heparin of 4 hours   PTT e.Warfarin either with heparin or on 3rd day or on 7th day 10 mg every day for 3 day 3.: patient control 100 sec. : 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.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ OTHER Ex.g.

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.If the cause is hereditary cause  ttt life long .Vitamin K 3.  high  decrease heparin dose 60 sec  increase heparin dose Warfarin: PT INR  used usually Patient control 2.Warfarin t1/2 = 72 hr = 3 days we measure it 3 days after start ttt if over dose: 1. or antidote= protamine sulfate  but it is not given to the patient.net ‫ﻣﻠﺘﻘﻰ ﻓﺮﺳﺎن اﻟﻄﺐ‬ ‫اﻟﻤﻠﺘﻘﻰ اﻷول ﻟﻠﻤﺠﺘﻤﻊ اﻟﻄﺒﻲ‬ 200 sec.5 1 5  decrease dose 1  increase dose .If the cause is malignancy  life long MKSforum.ONCE warfarin 2–2 1/2  Stop heparin If the patient takes an OVER DOSE: .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 . .Antidote 2.net -161- .MKSforum.

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