essential notes in internal medicine - 1st ed

First Edition

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ملتقى فرسان الطب الملتقى األول للمجتمع الطبي

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..إوا و أوا اطب

..و د

ب اطب ود م زؤم و زم طن ان ن أدم ج

رن اطب أءن، اك د ازز دة

دروس اا ن بذا ا ، و ط ءطا د بأ ط و

ا ا و دة

دروس ادورة و زا ا ر ازاءرزا أب الو د ن

و م اوق و اح . وا أن دوا ادة و ر

و ا م ا

و ن ادء

إوام و أوام

رن اطب

[email protected] ارامو رام

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اء اون

ع اة

Kia Oraangelic_docDR.JENEFER

N.S.Gamoona asphora

ocashdoctor_ology

Dr.NouraDr.ambitionDr. ShoSho

Dr-EDa_jokerThe OneKonvict

KAU Dr.Xرس ازن

Dr.eyelashdr.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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Cardiovascular diseases

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IHDDr.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, 3RD 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, 2nd 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 raisedtime of each enzyme is important & common question in exams troponine immediate 30 minutes- 1 hour (earliest to rise + more sensitive). CPK 4 hours + CPK-MB ratio. 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 30minutes) to see if complications develop: 1- arrhythmia2-hypotension

This was done before to decide if argent angiogram will done or delayed 4-5weeks.

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 medication1- Aspirin2- B-blocker.3- ACE Inhibitors.4- Statin.+/- lasix.

Management of MI (briefly for 5th year):

1- Admit patient to the ICU & give O2 oxy-bed rest.2- Prescribe painkillers.3- Thrombolytic therapy streptokinase resolve the thrombus

ساعة ٢٤بعد .. ساعات٦ الزم يتأخد في أول فايدته تروح ، مع الوقت يسیر ماله فايدة

٤سوي المذكور في رقم إذا اتأخرنا ن4- 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 depressionCardiac Enzymes Normal

[2] Unstable angina:

T-wave changesCardiac Enzymes Normal

[3] Prinzmetal's angina:

ST elevation due to spasmCardiac Enzymes Normal

[4] MI:

ST elevationCardiac 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, لكن الكالم يصاغ حسب الحالة و المسبب

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 DiseaseRHD

Session with Dr. Maimoona2006

(1) Major:

- Carditis- Arthritis- Erythema marginatum- Chorea- Subcutaneous nodules

(2) minor:

History of tonsillitis Fever Raised C-reactive protein Raised ESR 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 diseaseRenal 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. Maimoona1424 H

95% essential HTN5%

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 3months

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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(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 testOr 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 US2- INP = delayed uptake3- Captopril renogram4- Angiogram

Pheochromocytoma: Investigation:

Chatecholamines either in urine or bloodCT for the abdomen localize the tumor

If not localized, do adrenal venous sampling to localize

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GENERAL

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 rapidlyHTN + HF lower the Blood Pressure

ناقص

α-methyl dopa poor or pregnant

ACE inhibitorsΒ-blockersHydralazine

Thiazide

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Atrial fibrillation (AF)Definition: It's totally chaotic atrial activity caused by simultaneous discharge of multi atria foci.

Causes:

A- Cardiovascular :

1- HTN.

2- IHD (including acute MI).

3- Valvular heart disease esp. Rheumatic "Ms, MR, AS, AR".

4- VSD.

5- Cardiac surgery.

6- Inflammatory heart disease "pericarditis, myocarditis".

7- Cardiomyopathy.

8- Left atrial myxoma.

9- Sick sinus syndrome "tachy-Brady syndrome".

10- WPW syndrome (wolf Parkinson white).

B- Endocrinological causes:

1- Thyrotoxicosis.

2- Pheochromocytoma.

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C- Pulmonary causes:

1- P.E.

2- Pneumonia.

3- COPD

4- Co poising.

5- Ca of the Bronchus.

D- Drugs:

1- Acute or chronic alcohol.

2- Theophylline toxicity.

E - Idiopathic:

Lone AF in which no cardiac cause can be identified, no DM, no HTN and no CAD.

Symptoms of AF:

1- Asymptomatic.

2- Symptoms vary from Palpitation and SOB and aggravating of HF.

3- Embolization symptoms.

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Investigation:

1- Thyroid function test.

2- ECG absence P wave + Irregular R-R interval more than 100.

3- U and E if hypo K 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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Management of AF:

1- Treat the cause.

2- How to Control Ventricular rate ( VR)?

3- How to convert to sinus rhythm?

4- How to maintain sinus rhythm?

5- When and How to use anticoagulant and antiplatlets?

Types of AF:

1- Isolated one “single".

2- Paroxysmal don't give digoxin.

3- Sustained one chronic.

So the Management:

If the Patient is not stable Do DC cardioversion.

If stable follow that previously mentioned points.

So,

1- Treat the cause.

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2- Control Ventricular rate By A-V node blocking Drugs:

A- Digoxin:

- Loading dose: 0.25 - 0.5 mg/30mints IV.

- Maintenance: 0.125 - 0.25 mg/6h.

- Contraindication of Digoxin:

1- HOCM.

2- WPW so in here use procainamide.

3- Narrow QRS atrial tachycardia.

- Digoxin dose: in Normal Patient: 0.25 mg, and in renal disease: 0.06 -0.125 mg.

B- B-Blocker:

Usually given with Ca channel blocker because more rapid control. But digoxin is more preferable in the setting of LVF or HF.

So, propranolol 0.5 mg IV followed by IV bolus 1 mg every 5 mints till …???

The contraindication of B-blocker is:

Asthma, Dm and HF.

C- Ca Channel blocker:

Verampil 5 – 10 mg bolus / 10 mints.

If you want to give verampil + digoxin decrease digoxin dose.

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3- Convert to Sinus Rhythm:

Indicated when VR is more than 140 B/m.

The drugs used in here:

- Class 1a: Quinidine - procainamide.

- Class 1c: Flecainide - propafenone

- Class 3: Amiodarone

So the preparation:

1- Start Quinidine at least 24 h before to help maintain NSR once it's achieved.

2- Hold Digoxin and check its serum level.

3- Anticoagulant 3 weeks before and after if there's thrombus shown in echo.

Indications for anticoagulation: Clinically and ECG:

Clinically:

1- Previous MI or Stroke.

2- HTM +/- Dm.

3- Previous MI.

4- Thyrotoxicosis in here, decrease the Warfarin dose because of increased clearance of vitamin K in Hyperthyroidism.

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EchoCardioGraphically:

1- Large Left atrium or Left atrium dysfunction.

2- Large Left Ventricle.

3- Left Ventricle aneurysm.

4- Intracardiac Thrombus.

Complications of cardioversion:

1- Ventricular fibrillation.

2- Thromboembolism.

3- MI damage due to the Current.

4- Erythema on the chest wall.

Risk of Systemic Embolization with AF is divided to:

- High: when Mitral valve disease seen: previous Mi or stroke.

- Intermediate: age more than 65 or RF.

- Low risk: age less than 65.

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4- Maintenance of sinus rhythm is better with:

1- Left atrium less than 60 mm.

2- Absence of mitral valve dis.

3- Short AF.

4- Conversion with drug only.

Please see the classes of anti-arrhythmic drugs.

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Respiratory

diseases

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Management of asthma in ER

HISTORY: mainly history of the etiology of the disease.

[1] Drugs

1. B-blockerso Propranololo Atenololo metoprolol

2. NSAID

o ASPIRIN (acetylsalicylic acid)

o VOLTARINNE (DICLOFENAc)

[2] CHEST INFECTION

[3] Irritants animals + dust + fumes + house dust mite

[4] Newly changed furniture + painting

[5] Exercise

[6] Occupation

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EXAMINATION:

1- Vital signs

a- Pulse tachycardia, arrhythmias

b- Blood pressure, palsus paradoxes

c- Tachypnea

d- Temperature increase infection

2- General examination

a- Tremor

b- Cyanosis

c- Accessory muscles

3- Signs of Pneumothorax You fail if you don't mention them!!

4- Severity of asthma

(1) Signs of infection

(2) Signs of status asthmaticus

1- Silent chest2- Drowsiness3- Cyanosis4- Tachycardia > 1205- Pulsus paradoxus

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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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MANAGEMENT:

1- Bed rest

2- Oxygen according to blood gases (1) DecreaseO2+decrease CO2

(2) DecreaseO2+normal CO2

(3) DecreaseO2+IncreaseCO2

3- I.V FLUID

4- KCL DECREASE K

5- Pharmacological medications

(1) Bronchodilator

a- B2 agonistb- Nabulizarc- Salbutamol - terbutaline SlE: TACHYCARDIA FOR 24hours / hourlyd- Anti-cholenergic drugs Ventolin/atrovent Ibratropum promide Decrease mucus secretionf- I.V Theophyllin "narrow therapeutic index" bronchodilatorincreases 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 minMaintenance 0.2-0.6 mg/kg/hourIF AFTER 4 HOURS THE PATIENT DOES NOT IMPROVE MECHANICAL VENTILATION

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(2) +/- Antibiotics:

If there are sought of infection mainly H.influenza + streptococci We USE AMPICILLIN G (positive) OR G (negative)

(3) Anti inflammatory

Hydrocortisone 100-200mg/4hours for 24 hours (IV)Then prednisone 60mg/orally daily for 2 weeks

Discharge on B-agonist in halor +steroid inhalorPresent to the CLINIC History: exercise tolerance decrease and change color of sputumInvestigation 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.

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 O2 (24-28%) THEN ADJUST ACCORDING TO "ABG"

ASTHMA NO CHRONIC HYPERCAPNIA SAFE TO GIVE INCREASE CONCONCENTRATION OF O2 (60%)

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SIGNS OF SEVERE ASTHMA "STATUES ASTHMATUCUS"

1- Patients are unable to speak (cannot give history), inability to complete sentences

2- Silent chest

3- Pulses paradoxus

4- Tachycardia

5- Pulse>120

6- Use of accessory muscles of respiratory

7- R.R >33

8- Drowsiness - exhaustion

9- Cyanosis

COMPLICATION:

1- DEHYDRATION

2- EXHAUSTION

3- PNUMOTHORAX

4- RESPIRATORY FAILUER

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Respiratory failure

** Influence on respiratory center

Hypercapnia = P CO2 > 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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AcuteChronic

PaO2 ↓ Pa CO2 ↑ HCO3 ↔

PaO2 ↓PaCO2 ↑HCO3 ↑

** Respiratory Failure: A disorder of the lungs where the lungs don’tfunction 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 O2 ↓↓Pa CO2 ↓ or ↔HCO3 ↔

Pa O2 ↓Pa CO2 ↔HCO3 ↔

Severe acute asthma (life threatening) * COPD Respiratory muscle paralysis * Chest wall ds

(Kyphoscoliosis) + fractured rib + intercostals ms tear. Brainstem lesion = CNS depression * Ankylosing Spondylitis

(Narcotic drugs)

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Other Causes of Type 1 Failure:

Extrinsic allergic alveolitis. Interstitial fibrosing alveolitis.

Other Causes of Type 2 Failure:

Neuromuscular disease ( gullain barre syndrome ) Pulmonary Embolism Inhaled foreign body Pneumothorax Retention of secretion

☺ Refer to the Oxford hand book of Medicine

Complication of type 2 Respiratory Failure:

Cardiac Arrythmias. GIT hemorrhage Pneumothorax Bronchial Obstruction. LVF Pulmonary Embolism Convulsion.

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Management of Type 1 Respiratory Failure:

High flow O2 Maintain adequate O2 and O2 Saturation > 90 % Mechanical ventilation Avoid O2 toxicity PO2 > 55 mmHg Control underlying problem (pneumonia, infection, sepsis, pancreatitis)

☻YOU should know the indication for CAOT(chronic ambulatory oxygen therapy)

Management of Type 2 Respiratory Failure:

(1) Oxygen supply ( venture mask )

Start with 1 liter/min = 24% 2 liter/min = 28% 3 liter/min = 35% 4 liter/min = 40% 5 liter/min = 50%

** then titrate the requirement according to ABG** Provide O2 to keep the O2 saturation >90% but < 93% withoutinducing marked hypercapnia

*****************(2) Treat underlying causes:

*Antibiotic in case of infection/pneumonia*Bronchodilator in case of COPD/ Asthma*Anticholenergic in case of COPD/Asthma*Corticosteroid in case of severe bronchospasm

*****************

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(3) Theophyllin ( improve muscle contraction

* Diuretics LVF * Chest physiotherapy * Hydration & mucolytic (Danse)

****************** (4) Mechanical Ventilation

Failure to provide adequate oxygenation without marked hypercapnia. Decrease level of conconcentaration Failure of Respiratory stimulant.

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Renal diseases

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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 nephropathyb) HTN hypertensive

nephrosclerpsisc) Glomerulonephritisd) Infection: E. Coli HUS(hemolytic uremic syndrome) HIV HBV & HCV TB Schistosomiasis Malariaa) 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:

StoneRadiationTumorLymph. NodeInfection:

TB Bilhariziasis

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f) VasculitisSLE, RA, connective tissue dis., systemic sclerosis, polyarteritis nodosa

g) Tumor Renal cell carcinoma Multiple myloma:

1. Hypercalcemia2. Hyperuracemia3. Recurrent infection4. Deposition of paraprotein

h) Metabolic causes:1. Hypercalcemia2. Wilson‘s ds.3. Hemochromatosis4. Hyperurecemia

I) Polycystic kidney

Complication:

1) Uremia:o Uremic gastropathy loss of appetite, loss of wt, nausea, vomiting,

constipationo Leg swellingo Respiratory symptoms SOB, cough, yellowish sputumo Uremic pericarditiso Symptoms of cardiac overload (HF) dyspnea, orthopnea, PND…o Generalized skin itchingo fatigabilityo 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 skin5p+ 1EPallorPigmentationPruritisPurpuraPopular skin rashEdema

6) MusculoskeletalBone:Renal osteodystophyJoint: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 dullnessCVS: arrestGIT: 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 infection3) ABG: metabolic acidosis4) U & E (renal function): increase creatinine, urea , Pi, Kyperkalemia

(should be treated to protect the heart)5) Blood sugar: increase with DM6) HBV & HCV screen

Urine analysis:

1) Oligouria2) Proteinuria3) Hematouria4) 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 edemapleural effusion uremiaTBMetastatic 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

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

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2- Duration of RF

3- Dialysis through fistula or line How many times per week?

4- Symptoms of uremiaIf 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 anemia2- Calcium & vitamin D for low vitamin D3- Dialysis4- Renal transplant* Low salt diet* Low protein diet

Dialysis:Peritoneal dialysis if the patient can do aseptic techniquehemodialysis

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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 weeks10-25 weeks CRF OBSERVEIf 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- Infection2- Drugs: NSAID e.g.: for osteoarthritis,3- Contrast angiogram4- 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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Gastroenterology&

Liver disease

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Diarrhea

Session with Dr. Maimoona

Diarrhea

Acute & Chronic

2 weeks more

Causes:

I. Infections:

Protozoa:

Amoeba , Giardia

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Bacteria:

E. Coli , Klibsiella , Shigella , salmonellaVibrio cholera watery diarrheaStaph. Aureus (milk products)Campylobacter (pets at home)Yersinia C. difficile diarrhea, pseudomembranous colitis

Viruses:

HIV (common cause) 3 months + lymphadenopathy + wt lossRota virus, adenovirus

Fungal in immunocompromised

Cryptosporidium

Lyme disease Liptospirae

Mycobacteria: intestinal TB

Note:

C. botulinium botulism (preserved food)C. Perfringins food poisoning / gas gangreneC. 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 & hyperchromicD.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")

NoteHemolytic 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. trophozoidCuture 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- Endoscopy8- Enema9- Salmonella titer

10- Abdominal X-Ray: toxic mega colon

Differential Diagnosis of Diarrhea:

1- Infection2- IBD3- Malignancy4- Malabsorption5- Endocrine6- Drugs7- 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 - tenesmus2- Skin: erythema nodosum, pyoderma gangrnosum3- Amylodosis,

4- Arthropathy5- Thromboembolic disease6- Both: ant. Uveitis, conjectivitis, episcleritis, iritis, ankylosing spondylitis, sacroilitis, sclerosing cholangitis7- Fatty liver, autoimmune hepatitis.

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Complications:

1- Toxic megacolon (most severe complication)Tachycardia, anemia, hypotension, dilated transverse colon more than 6cmIf 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 - strictureFistula (entero - enteric or vesical).Perianal (abscess - tags)

Grading

I- Mild Diarrhea > 5/dayNo anemia No feverNormal albumin

II- Moderate(In between)

III- SevereDiarrhea > 10/day FeverTachycardiaHypotensionHypoabuminia (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- CBC2- U&E3- Left4- Barium enema5- Endoscopy (Chron's skiplesion) coplet stones6- Biopsy7- 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- Fever5- 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- Anemia6- 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 (5th 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 historys 'elapsing of CrohnR►

* Past history since the time of 1st 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 , lossweight, loss of appetite, outh ulcermrepeated

* 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 intestines affect'Crohn► ↓ Vomiting Weight loss

:Most important investigations►

- CBC:WBC normalHb ↓ microcytic hypochromic anemiaPlatelet ↑↑↑ (1) postsplenectomy (↑) (2) Relapse of Crohn's- ESR activity of disease- LFT

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CLDDr.Maimoona

When a patient presents with hepatic symptoms, 1st 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 (في البداية) 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 (1st) 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: (2nd) 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) (3rd) bleeding: 'melena' in all hepatic encephalopathy.5- Evidence of infection: (4th)

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: 1st size of liver? If shrunken order a biopsy. 2nd macronodular (alcohol) or micronodular. 3rd 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 0.5-1mg/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 3rd 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 3rd 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 2nd 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 diseaseDr. Hisham Akbar

Definition Types Causes Manifestations Treatment

Types:

A. According to pathology:1. Traditional:

Chronic persistent Chronic lobular Chronic active Liver cirrhosis

2. Metavir3. Knodells

B. According to etiology:1. Necrotic2. 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 diagnosis2. For the detection or exclusion of other diseases3. For grading4. For staging5. 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 hepatitis3. Alcoholic4. Drugs ( methotrexate, isonizaid, methyldopa, … )5. Metabolic fatty liver6. Cholestatic 1ry & 2ry biliary cirrhosis sclerosing cholangitis7. Infiltrative 8. Vascular problem ( cardiac cirrhosis )9. Neoplastic benign Malignant 1ry 2ry10. 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 AgI 1. Serum anti nuclear

2. Anti mitochondria3. anti-smooth Abs

- Double stranded DNA in some but target Ags.- In liver disease not fully defined action.

II 1. Anti liver & kidney LK2. 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 nevi3. Enlarged or Shrunken liver4. Enlarged spleen5. Finger clubbing6. Collapsing pulse7. Kayser-Fleischer ring8. Xanthelasma9. Parotid swelling alcoholic10. 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. Rash2. Glumerulonephritis membranoproliferative 3. porphyria cutanea tarda hepatocellular ca4. Arthritis5. Vasculitis6. 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

Chronichepatitis

Asymptomatic carrier

CirrhosisHCC

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 syndrome2. Encephalopathy ( lactose, flagel )3. Bleeding a. ABC first. b. Endoscopy: sclerotherapy c. TIPS for bleeding

ascites4. Ascites ( diuretic )5. SBP (most common E.coli ) neutrophile6. Hepatoma

Persistent infection

Non-Progressive liver injury

Elevated ALTNormal ALT

Progressive liver injury

Fibrosis & Cirrhosis Death

HCCHBV 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 2years), 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

FibrosisHCV 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. Jaundice2. Hematemesis3. Asterixis4. Lower limb edema5. Epistaxis6. Bleeding gum7. 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).

1st time the HCV was discovered was in 1989α-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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Endocrinology

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Hypothyroidism

Primary hypothyroidism:

1- Drugs (amiodarone – lithium)2- Autoimmune (e.g. Hashimoto thyroiditis) 3- Post surgical ttt of thyrotoxicosis4- 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 biopsyo 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 anemergency 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- Hashimoto4- thyrotoxic gravidarum.

No ttt for these only symptomatic ttt1- Beta blocker2- Analgesic

Investigations:

1- TFT : antibodies Graves disease ↓↓TSH ↑↑T3 & T42- Thyroid ultrasound diffuse enlargement Graves3- Cold or hot4- ECG atrial fibrillation5- CXR retrosternal goiter

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HOW TO DIFFERENTIATE BETWEEN THE DIAGNOSIS OF GRAVESDISEASE & SUB-ACUTE THYRODITIS?

Isotope scanning ↑ uptake Graves ↓uptake sub acute thyroiditis

Surgery with thyrotoxicosisPotassium iodine inhibit conversion & release ( 5 ml Tds ) with following up TFTBeta blocker about 3-4 days before operation.+ anti-thyroid but it will take long time thyroid stormdexamethsone 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 3-4days 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 امتنسى تأخذ الحبوب بانتظ

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 / L2- Family history with thyroid problem3- Positive thyroid antibodies.4- Goiter5- 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 failureSecondary failure to the axis

Causes of primary:

1- Most common: autoimmune2-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- Radiation6- Adrenalectomy7- Infiltration by amyloidosis + heamochromatosis + Wilson's

Causes of secondary:1- Sheehan syndrome post – partum hemorrhage2- Any tumor compressing the pituitary

Symptoms:1- Diarrhea2- Nausea, vomiting 3- Dizziness4- Hyper pigmentation (creases + press areas)5- Postural hypotension6- Vitiligo can be associated with Addison's

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Organ specific disease ( autoimmune )

1- Addison's2- Hypothyroidism3- Pernicious anemia affecting parietal diseases4-Graves disease5- Vitiligo6- DM type I7- Premature ovarian failure

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DKA

Causes of DKA aggravating factor :

EmotionMedical problemMedical dose of insulin Infection (URTI ,UTI )Trauma or surgeryNew undiagnosed casesHeavy meal

C/O:

Confusion comaAbdominal pain + vomiting because dilated stomachHyperventilation 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 stenosis5) Hyperchloremia

# high anion gab acidosisNot written

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Treatment :

1) Fluid: 1/2 the amount of 24hours. Required in the 1st 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 2hoursPut 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

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[3] Acidosis & HCO3:

Only correct if H < 7 , HCO3 < 5 before correction & after correction < 10Normal HCO3 (24 – 28), his HCO3 = 6 deficient = 24 – 6 = 13Deficient x 1/6 body weight = 18 x 10 = 180Give 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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Rheumatology

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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-B27Spine – 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 patients2- 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 foldbecause 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- Normalb- Glomerulonephritis 5 stages (patterns):

Minimal change GN. Mesangeal lupus GN. Focal proliferative GN. Diffuse proliferative GN. Membranous GN.

c- Renal failure.d- Amyloidosis, but more with RA.e- UTI.

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8- Joints: >90%

-None deforming.-Affect small joint.-Distal interphalangeal joint.-No morning stiffness.

9- Skin: 80%

- Butterfly rash.- Discoid lupus erythematous (DLE).- Livedo reticularis especially associated with antiphospholipid syndrome and

Pancreatitis- Alopecia,

10- Hematologically:

- Any cytopenia.- High ESR / CRP is normal in SLE.- Low complements.

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Investigations:

1- CBC cytopenia … 2- High ESR which is indictor for reactivity.

Normal CRP in SLE used in Differential Diagnosis

3- ANA which is sensitive / Anti-Ds DNA Antibodies which is diagnostic for SLE

AND Anti-sm Antibodies4- 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/hZero ESR is seen in polycythemia.

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In History:

Dr Fat'h Al-deen likes this scenario when a student presents the History:

Is a patient is known to have SLE for 10 years Based on (mention the criteria that was presented by the patient), thus upon them the diagnosis made and was diagnosed by dr. ____ then she was admitted to the hospital with flare up of her SLE complaining of ____

Dr Fatmah Al-Beladi says "never say SLE alone"

Known as SLE, - When was it diagnosed? - What criteria are they based on? Clinical & Laboratory.- Treated with what?- Complicated with what?

Always ask about chemotherapy, if the patient doesn't know ask about: an expensive tablets or drugs taken through IV once every month, because if she has Lupus nephritis class VI is usually treated by chemo.

Causes of death in a SLE patient?1- Infections (opportunistic).2- Renal /CNS involvement (active SLE).3- Accelerated atherosclerosis MI.

Differential diagnosis of SLE:

-RA. -Scleroderma. -Drug induced lupus.-Rheumatic heart disease.-Chronic active hepatitis.

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Smart Rheumatology Qs by Dr. Fat'h Aldeen and then he swore when any student answered them... He gave them almost a full mark

SLE patient takes an anti-Malarial drug like HydroxyChloroQuine?The function of this medication is to suppress the high level of ANA and RF.Side effect: Increased skin pigmentation and deposit in retina and all these seen only in high dose.

A patient came to Dr. Fat'h Al-deen, with symptoms similar to RA (joint pain), she was diagnosed in Harvard as RA because she has High ANA and High sky RF.

So the doctor said “I don't trust Harvard University... I only trust in my knowledge and trust excellent doctors" & told his patient that she doesn't have RA & gave her anti-Malaria drug (hyrdoxyChloroQunine) because it suppresses for High ANA and RF which then the symptoms subsides.

Then she was diagnosed to have parvovirus infection which causes symptoms similar to RA & SLE.

How to differentiate that psychosis in SLE pt, whether it's a side effect of cortisone or due to SLE it self?

By test of Anti-Ribosomal B Abs If positive so it is due to SLE.So in both situations we've to decrease steroid because of psychosis that's worsening.

Anti-phospholipids' Syndrome:

Diagnosed by Having Low platelets and prolonged PTT and in the Hx they've abortions and Migraine, TIA, stroke, amurosis fugax. And in examination they've levido reticularis.

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Causes of prolonged PTT:

Either coagulopathy or auto Abs like antiphospholipid $.

So to investigate anti-phospholipids' $ by three tests [ELISA]:1- Lupus anticoagulant (its mechanism is very important) see below:2- Anti-Cardiolipin.3- Anti-Beta 2 glycoprotein 1 Abs (beta2GP1) very important for the

diagnosis.

50/50 fixed test for Lupus Anticoagulant:

Antiphospholipid pt. has prolonged PTT.

So, we take patient serum (50%) & mix it with serum from a normal person (50%).

If the result was corrected (PTT not prolonged), then the cause of prolongation is a deficit in the blood itself (factor deficiency), not APLS. Because the defected blood earned factors from the healthy blood.

If Prolongation of PTT is still the same not corrected Ag/Abs reaction (autoimmune).

*In summary:

PTT:-If corrected factor deficiency.-If not corrected Ag/Abs.

Drug induced SLE:

-Usually by hydralazine – procainamide - IsoNiazid.-They've Positive anti-Histone.-Normal complements and ANA positive.-Anti-ds DNA negative.

Methotrexate is hepatotoxic it's given once weekly.

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Neurology

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How to take: A quick perfect neuro-historyDr.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 +

:مخارج الحروف : القدرة على نطق بعض الحروف

: المخرج.. میم .. میم Lips

الحرف من الـمخرج.. ال اله اال اهللا : مثل .. الالم Tongue

: المخرج.. مثل كوكا كوال.. حرف الكاف Palate

- hearing problem: (8)- Difficulty in swallowing, choking sensation + hoarseness: (9, 10, 12)

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# Motor:- Weakness- Proximal:

غرض من رفع الید كتسريح الشعر او أخذ– الوقوف من وضعیة الجلوس –صعود الدرج رف علوي بعید

- Distal:

فتح يد الباب–فتح العلب –صد من قدمهق خروج الحذاء دون –نتعال الحذاء ا

- 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:

او على غیره/مدى اعتماد المريض على نفسه العالجوبعدلمرض وبعده قبل ا

# 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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LocalizationDr.Aisha Al-Shareef

Weakness pattern:-Hemiparesis.-Paraparesis.-Quadriparisis.-Generalized ( cranial nerve involvement motor part: double vision, dysphagia).

Hemiparesis:1- Where is the lesion?2- What is the lesion?

* Spinal cord hemiparesis:-Face not involved.-No CN involvement.-Sensory: pain, tempntralateral.-Deep sensation, proprioception vibration silateral-Brown square syndrome.

Brain stem:1- Crossed phenomena (sensory or motor):

- CN: ipsilateral. -Body: contralateral.

2- Cranial nerve CNS involvement:Any CN involvement is in brain stem except facial nerve could be cortical or subcortical.

3- 4 Ds: at least 2 of them:1- Dysarthria CNS IX, X, XII.2- Dysphagia: IX, X.3- Disequilibrium cerebellar peduncle.4- Diplopia: III, IV, VI.

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Subcortical / Cortical:-No cranial nerve involvement.Except: facial nerve – lower part –-Hemiparesis.-Facial + weakness = all is ipsilateral to each other.

Cortical: -Cognitive impairment e.g.: aphasia, memory, language problem.-Distribution of lesion: Internal capsule is a dense fiber.

ي حزمة واحدة أ= upper & lower limp same power:If: Upper limp 0/5 lower limp 0/5: Upper limp 1/5 lower limp 1/5: Upper limp 2/5 lower limp 2/5: Upper limp 3/5 lower limp 3/5: Upper limp 4/5 wer limp 4/5

In cortex: no equal distribution (face, trunk, hand, leg).= e.g.: upper power 0/5 wer 4/5

Seizure = cortex irritation.

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Paraparesis:

Upper power 5/5 lower weakness:1- Spinal cord lesion.2- Parasagittal tumor.3- Peripheral nerve (mononeuritis, mononeuritis multiplex, early polyneuropathy later on hands affected).

In polyneuropathy LMNL fasciculation, arefelxia etc…In cortical: cognitive impairment, CNS.In spinal cord: sensory level, any nerve above L1 can give sensory level but below it not consider a spinal cord lesion e.g.; stock distribution in diabetes is not a spinal cord.

Quadriparesis:

Big insult, internal capsule.1- Cervical spinal cord lesion.2- Late stage GBS.3- NMJ: myasthenia, lambert-eaton.4- Muscle.

- In spinal cord: motor UMNL, sensory level.- In polyneuropathy (gloves & stock) LMNL, distal > proximal.- In NMJ: normal sensory, proximal > distal, no UMNL only. Weakness normal reflexes, fatigability: fluctuation in power 5/5 in the beginning, after exercise 4/5.-In muscle myopathy: normal sensory, proximal > distal, no UMNL only weakness normal reflexes, in myopathy the power is the same even after exercise.

A.H.C:- Motor neuron disease.If no UMNL.- Mixed UMNL +LMNL.

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STROKE / CVADr.Maimoona

CVA is only vascularStroke, we don't call it vascular

CAUSES:

1 - Hemorrhage 2- Infarction3- Space Occupying Lesion (SOL) 4- Demyelinating disease5- Degenerative disease6- Metabolic disease

Hemorrhage:

- AV malformation most common in young patients

- Ruptured berry aneurysm- Hypertension (HTN) in old patients

- Patient on anticoagulant: aspirin, warfarin, heparin- Trauma

Infarction:

(1) Atherosclerosis:- Diabetes Mellitus (DM)- Hypertension (HTN)- Hyperlipidemia- Smoking

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(2) Thromboembolism:1- due to any arrhythmia:

- Rheumatic heart disease Valvular heart disease- IHD- Thyrotoxicosis

2- Infective endocarditis(3) Thrombophilia(4) Sickle cell anemia(5) Polycythemia(6) Oral countraceptive pill (OCP)(7) Carotid stenosis due to atherosclerotic plaque commonest in elderly

(8) Connective tissue disease

Space occupying lesions: sudden decrease in BP

1- Tumors:

Primary tumors young patientsSecondary tumors due to metastasis elderly

2- Infections:

Tuberculosis #1MeningitisHydatid cystAbscess whatever the cause isFungalHIVToxoplasmosisCMV

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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In HISTORY:

Causes according to age group:

In young (< 45y)

The commonest cause is hemorrhage

1- AV malformation2- Rupture berry aneurysm3- MS (demyelinating)4- Valvular heart disease5- Thrombophilia ( decrease protein C , S , III , V )6- CTD connective tissue disease , vasculitis7- Thyrotoxicosis8- 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 mellitus2- Hypertension3- Anticoagulant4- Space occupying lesion tumor, mainly metastatic5- Hyperlipidemia ( atherosclerosis , smoking ) 6- Ischemic Heart Disease (IHD)7- Arrhythmia 8- Infection ( TB , abscess )

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Risk factors:

1- Increase in Blood Pressure2- Smoking 3- DM4- Heart diseases ( 1- valvular 2- IHD 3- AF)5- Peripheral vascular disease 6- Past TIA = transient ischemic attack7- Increase packed cell volume8- Carotid bruit9- Pills in smoker10 -Lipids increase 11- Excess alcohol12- Increase clotting ( increase fibrinogen decrease antithrombin III)

Important points in history:

Thrombo–embolic: suddenHemorrhagic: 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 infectionPulse 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 knee5 - 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 itValvular lesion, ejection fraction (dilated atria or ventricle )

Certain Investigations, only According to History & Examination.:

1- SCREEN FOR VASCULITIS: ANA, RF2- THROMBOPHILIA screen potien S, C, antithrombin III, factor V 3- screening for malignancy4- HIV5- LUMPER PUNCTURE if NORMAL CT, No cerebral HTN, No papilloedema6- Angiogram if you suspect AV malformation or Berry aneurysm rupture (not if pt has ………..)

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7- U & E HTN8- COAGULATION profile: PT, PTT9- SEPTIC CULTURE infective endocarditis10- HG electrophoresis SCA11- if demyelination on CT LP increase protein oligoclonal band - for multiple sclerosis : 1) Lumbar puncture (LP)2) Visual evoked potentials (VEP) optic nerve3) Auditory cerebellar evoked response4) EMG5) 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 improves2- 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 ischemicin 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 stenosis70 - 80% neurological deficit, TIA end artery surgery

[7] Metabolic specific treatment

Notes:

Classification of neurological deficit:

1- TIA: improve in 24 hrs2- RIND: reversible ischemia, 2 weeks neurological deficit3- Complete stroke

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Upper Motor Neuron LesionUMNL

Causes of paraplegia:

1) Demyelinating diseases: MS: → Cranial nerve palsy – eye problems → Upper motor neuron lesion → Hemiplegia and paraplegia (spastic) → Optic atrophy → Cerebellar signs

2) Trauma

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

4) Infections → T.B (brain – spinal cord) \ Guillain Barre Syndrome → Syphlysis (taboparesis) → Meningitis

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→ Viral infection \ herpes → transverse myelitis → Brucella → Abscess → HIV → Schistosoma

5) Vasculitis of spinal cord

→ Primary vasculitis of brain arteritis → Secondary vasculitis of connective tissue diseases → (vascular) SLE – (autoimmune) RA

6) Ant. Spinal cord thrombosis

Myocardial infarction

7) Subacute combined degeneration of spinal cord

8) B12 deficiency

9) Lymphoma

10) Neurofibromatosis

Exc. Growth of nerve \ can affect any nerve 11) Granuloma

→ syringomylia → sarcoidosis →T.B

12) Congenital spastic paraplegia

13)

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*Most Common Causes in young age group:

MS TB Transverse myelitisVasculitis *Most Common Causes in old age group:

Compression Disc Prolapse Cervical spondylitisMetastasis

*Notes: Sacral spinal nerves are affected Palpitation → AS, Arrhythmias Back pain → Brucella , disc prolapse , trauma Renal pain and haematuria → renal cell carcinoma Brachial plexus compression: → Cervical rib → Any mass at the apex (lymphoma, TB) MS → relapse & remission

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Investigations:

A) Definite:

1. Fundoscopy → Papilloedema

C.T scan (if no papilloedema we can perform a lumbar puncture) 2. MRI → Specific for demyelinating disease → Demyelinating plaque → Look for space occupying lesions (tumor, abscess, and cyst)

3. X-Ray → TB → Disc prolapse → Fracture → Cervical spondyelitis

4. Lumbar puncture ↑ Protein (infections, MS) ↓ Glucose (bacterial infection)

↑ Lymphocytes (TB)

↑ Neutrophils (bacterial infection)

Malignant cells

Single P band mono/oligoclonal P band (MS)

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5. Biopsy → Pott's

→ Tumors B) Supportive:

1. CBC → leukocytosis 2. ESR → ↑ (infection, malignancy)

3. ECG

4. ANA

5. Visual evoke response

6. Auditory evoke response

7. EMG (delayed conduction in MS)

*For Infection:

1. PPD ( TB) 2. …… (B12)

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Polyneuropahties (PN)

Causes:

1) Infection:Leprosy , lyme , syphilis , HIV

2) Inflammation:Guillan-Barre , chronic inflammatory demyelinating PN ,sarcoidosis

3) C.T. disease:PAN, wegeners , RA

4) Metabolic:DM, hypoglycemia, hypothyroidism, renal failure

5) Malignancy :PNS, polycythemia , multiple myeloma

6) Toxines: Lead, arsenic

7) Drugs:Alcohol, INH, anticancer

8) Vitamins:Low B1, B12, B6, Folate, or increase B6

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9) Other:Amyloidosis

10) Inherited:Refsum's , charcot-marie-tooth syndrome , prophyria , leukodystrophies

Symptoms:

1) Sensory & motor neuropathy

2) Cranial dysphasia, deafness, speech difficulty, diplopia

3) Autonomic neuropathy

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Acute Confusion State

Causes of acute confusion state:

A: alcoholE: encephalopathyI: insulin (hyper, hypo)O: overdoseU: uremiaT: tumor / traumaI: infectionS: seizureM: 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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- 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 leukocytosis2 – Blood glucose 3 – U & E, Ca++, Mg4 – Liver function test5 – Renal function test6 – 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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CNS: 1- Psychosis2- Seizure 3- Stroke4- Mono neuritis multiplex

Eye: 1- Psytotic body with SLE2- Scleritis – Episcleritis

CVS:

Respiratory:

Abdomen:1- Chronic active hepatitis2- Primary sclerosing cholyngitis 3- Glumerlonephritis4- Amyloidosis5- Acute abdomen

Skin: 1- Skin ulcer2- Splinter hemorrhage

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Other

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DVTSession with Dr. Maimoona

Etiology of DVT:

Virchaw's triad

1-Abnormal blood flow2-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 الدرجة السیاحیة( ) syndrome DVT Because vessels are kinked during the flight causing blood stasis.

*The most important pointsin order, you can then mention the others according to order

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- Dehydration due to any reason: (fever, diarrhea) - Polycythemia- SCA (sickling crisis)

2- Abnormal constituents

- Thrombophilia: is the deficiency of protein C & S, antithrombin III, factor V (recurrent & positive FH) - Nephrotic Syndrome loss of antithrombin III - CLD (chronic liver disease) prot. C & S, Anti-Thrombin III deficiency

- Polycythemia- SCA- Hypercoagulopathy - OCP = oral contraceptive pills- Antiphospholipid antibodies in APLS (in females ask about recurrent abortion) - Any malignancies: (prostatic, pancreatic, lymphomatic , leukemic )

- Para protienemia (multiple myloma) - IBD is Inflammatory Bowel Disease: hypofibrogenemia- Thrombocytopenic purpura

Never say "nephrotic syndrome & CLD are causes of DVT" but "they are causes of protein

deficiency"

The most common malignancies causing hypercoagulable state are:- Prostate carcinoma- Lung carcinoma- Pancreas carcinoma

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3-Abnormal vessel wall

- Vasculitis*: (SLE, RA, good pasture, HSP = henoch shonleinn purpra)- Trauma* IV cannulation (either in hospital or in IV drug abusers)- Varicose vein*

Complications of DVT:

-Acute: PE = pulmonary embolism: the most important Sudden onset chest pain (pleuritic) sharp and related to respiration Associated with SOB, palpitations, hemoptysis, or syncope

- Chronic: post phelebitic limb >> stagnation of blood >> not return normally to heart >> leg edema, ulceration, discoloration

History Presentation:

The Patient presented with ……..

(Occupation)

He/she has no history of ………… 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, C

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No history of (protein loss)

No previous history of DVT

No history of recurrent abortion I think this is due to APLAS

:بعدين نقول

No history of fever or loss of weight

))complications بعدين نروح لـلـ exclude causes of DVTإذن أول شي ((

No history of ………

كدا Hx بس القصد إنه الزم ينقال الـ NOمش معناه إنه كله

Note:

Patient < 45 yr-old traveling, C.T. Disease, pregnancy, OCPs

Patient > 45 yr-old immobilization, malignancy, Heart Failure

Differential diagnosis:

- Cellulites- Ruptured Baker's cyst (synovium in popliteal fossa as in RA) - DVT (pitting unless of extensive edema)- Hematoma- Lymphoedema (non-pitting)- Ruptured muscle due to trauma

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Investigations:

For every patient, DO the following:

1 - Doppler 2- Venogram3- CBC 4- Coagulation profile 5- D-dimer 6- CXR 7- ECG

----------------

Diagnostic Tests:

1 - Doppler 1st line to document DVT if negative: نسوي دي، إذا ما بان شي و لسة شاكین

2- Venography: gold standard if negative: no DVT

A dye is injected in the (vein) dorsum of foot خاطي النه فحص خاص وھذا بالطبعangiogram وكثیر من الطلبه يقولوا خطًأ

for artery بالشريان ولیس الوريد

ما نسوي لھا ، و طول وقتھا نايمة stroke for 10 yearsإذا جاتنا حالة عندھا* investigations و نفس الشي اللي عندھم fractures ألنه السبب باين

: investigationsلكن إذا ما عرفنا السبب نسوي كل الـ

Blood work: certain blood tests are done for specific history

3 – CBC lycyciemia , malignancy , cytopenia

4- Peripheral blood film SCA

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5- Coagulation profile: PT, PTT (BEFORE starting the treatment formonitoring)

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 RBBBArrhythmia (atrial) Sinus tachycardia S1 Q 3 T 3 CLASSICAL Lead I: deep S waveLead III: Q3 inverted T3

الكالسیكأي في تخطیط القلب قد نجد الثالث صفاتS1 Q3 T3نجد فقطلكن االغلب

Sinus tachycardia

15- Doppler US

16- d-dimer (end product of breakdown of thrombus increases in blood)

17- Spiral CT scan.

18- ABG

19- Pulmonary Angiogram

20- Ventilation/Perfusion scan (VQ scan)

---------------- SPECIFIC Investigation

According to History: e.g.: ANA in CTD

In elderly patient, if the cause is not CVA, or post operative or, immobilization always screen for malignancy.

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If PE 1- spiral CT scan, 2- ventilation perfusion VQ scan PULMONARY ANGIOGRAPHY is the definitive test for pulmonary embolism

Supporting:

If the patient is < 45 protein C & S, APL Abs, antithrombin IIII 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, rashesCyanosis (heart failure) Pulse (tachycardia: Pulmonary Embolism, unequal pulse: Vasculitis)Postural hypotension

Face:

Rashes, pallor, ulcer in mouth

Legs:

Inspection:

- Swelling & determine the exact site- Scar (IV, drug abuse) - Pigmentation- Shiny skin- Edematous

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- Redness- Phlegmasia alba / white leg- Phlegmasia dolens / milk leg

Palpitations

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

:Measurements-

محیط الرجلسنقیس ، باستخدام المتر انتفاخااألكثر/ اعرض مكان مكان القیاس سیكون عند

في نفس القادمة المرةمنھا لنقیس، للقیاس ثابتةولفعل ذلك البد من تحديد نقطة المكان لمقارنة التغیر في المحیط

:قیاس ثابتةلتحديد نقطة من الرجلثابتةنستخدم نقطة

Bony prominenceالوستكون ھنا

Tibial tuberosity

يصح استخدام الباتیال الانتبھوا وPatella متحركة ألنھا ثابتةكنقطه

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سم0 التیبال تیوبروسیتي عندىنثبت المتر عل

محیط منتفخ ونسجل القراءةألكبرونمدھا على امتداد الساق حتى نصل الثابتةقطة وستكون ھي الن)) سم ١٠ يستخدم األغلب(( سم ١٢وجدناھا مثال

التي سنقیس منھا كل يوم

)) سم في كال الساقین نزوال من عند الباتیال ١٠األغلب يستخدم ((

محیط الساق نأخذ)) سم ١٠ يستخدم األغلب(( سم ١٢ ـ الالنقطةمن عند ھذه ونسجل القراءة

المطلوبةوستكون ھي قراءة المحیط م س٣٤وجدناھا مثال

لساق الثانیةاإلى نذھب اآلنالعملیةونكرر

يستخدم األغلب(( سم ١٢بالمتر بالضبط نحدد مكان التــیـبیـا تیوبريستي وننزل منھا)) سم ١٠

األخرىلیكون نفس نقطة قیاس الساق سم٣٠المحیط ونسجلھا لنفرض وجدناھا قراءةنأخذومن ثم

تكونسم من نصف سأكثر الفرق بین المحیطینإذا تقول القاعدةAbnormal

٣٤ األولىوھنا كانت ٣٠ والثانیة

غیر طبیعيإذن ، سم٤فرق ال

سم ١٢من عند التیبیا نمشي الطريقة بنفس المصابةويومیا سنقیس محیط الساق قراءة المحیط ونشوف الفرق يوم عن يومونأخذ

الطريقة مصابه سنقیسھا بنفس أيضاكانت الفخذ إذا قیاس المحیطونأخذ مكان منتفخ ألكثرمنھا بالمتر من العظم ونطلعنحدد نقطة ثابته للمقارنةاألخرىنكرر في الساق

للمقارنة المصابةويومیا نقیس محیط الفخذ

:تالیةالصورة التوضیح الشرح في

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OTHER Ex. :

- Chest signs of pulmonary embolism- JVP Right side heart failure- Atrial fibrillation- Chest creptation- Hepatosplenomegaly- Lymph node- Abdominal mass- Vasculitis sings- Fullness of popliteal fossa ruptured Baker cyst

Management

1- Start with heparin IV80 – 100 U/kg bolus 20 U/kg/hour infusion maintenance dose

2- Warfarineither with heparin or on 3rd dayor 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 controlAfter heparin of 4 hours PTTe.g.: patient control100 sec. OK 30-40

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200 sec. high decrease heparin dose60 sec increase heparin dose

Warfarin: PTINR used usually

Patient control2.5 15 decrease dose1 increase dose

- ONCE warfarin 2–2 1/2 Stop heparin If the patient takes an OVER DOSE: - heparin t1/2 = 30 min – 1 hourIf over dose and bleed: stop heparinIf 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- Antidote2- Vitamin K3- Stop warfarin if bleeding occurs then FFP

PE & DVTWhatever 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

essential notes in internal medicine - 1st ed

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