TIDE Long Case PRO III Short Notes

~

S

H

O

R

T

N

O

T

ES

~

INDEX

MEDICAL BASED

MEDICAL

2

PAEDIATRIC

30

PSYCHIATRIC

53

SURGERY

BASED

SURGERY

59

O & G

80

ORTHOPAEDIC

108

“Ya Allah, Kuatkan Ingatan Kami Terhadap Apa Yang Kami Baca

Ya Allah, Tutuplah Segala Kesalahan Jawapan Kami Semasa Dalam Peperiksaan

Ya Allah, Berikanlah Ilham kpd Kami Untuk Menjawab Sepertimana Yang Pensyarah Kami Mahukan

Ya Allah, Kurniakan Pensyarah Yang Baik Hati Dan Pemurah Sebagai Pemeriksa Kami

Ya Allah, Kurniakanlah Pesakit Yang Baik Hati Dan Dapat Memberi Kerjasama Kepada Kami Nanti

Ya Allah, Semoga Apa Yang Kami Baca Dan Paham Sahaja Yang Ditanya Dalam Peperiksaan Nanti”

Aamiin….

MEDICAL

Notes

Approach to Chest Pain [IQbaL] HISTORY 1. Nature of chest pain ( SOCRATES )

 Constricting (cardiac ischemic or oesophageal spasm)

 Dull, central & crushing, last for 20min (MI)

 Radiates to jaw & upper extremities (cardiac cause)

 Sharp pleuritic pain that catch on inspiration (pleura or pericardium) & suggest pneumonia, pul. embolism or pericarditis

 Sudden substernal tearing & radiate to back ( aortic dissection )

2. Pain brought on by food, lying down, hot drinks, or alcohol, and relieved by antacids – GIT causes (eg GERD, PUD, oesophaeal spasm)

3. PMHx – known cardiac dz, HPT, HPL, smoking, FHx can support diagnosis

4. Acute cholecyctitis & pancreatitis can cause pain referred to chest

5. Associated Sx dyspnoea – cardiac ischemia, PE, pneumothorax or pneumonia

PHYSICAL EXAMINATION

1. Abnormality of pulse rate and heart sound (cardiac) 2. Crepitation – pneumonia or HF

3. Reduced breath sound in one side – pneumothorax or lung collapsed

4. Tenderness on chest – may causes from MSS however MI can present with chest tenderness

5. GIT origin in normal cardiac and respi system

INVESTIGATION Basic Ix

1. 12 lead ECG unless non-cardiac causes is confidently being diagnosed eg pneumothorax

 ST, QRS, arrhymias, tachy/brady

 Pericarditis – widespread concave ST, PR depression 2. CXR

 can confirm respi disorder eg pneumothorax, pneumonia

 can provide clues in cardiac dz (widened mediastinum in aortic dissection or a large globular heart in cardiac tamponade)

3. Echocardiograhy Laboratory

a) Cardiac biomarker – CK-MB, Troponin I & T b) FBC – infection & screen for anaemia c) RFT – baseline

d) TFT

# some DDx can be excluded/confirmed after basic Hx, PE and these Ix – STEMI, pneumothorax, pneumonia, pericarditis

MANAGEMENT

1) Management will depends on diagnosis 2) Psychological tx may be helpful in some pt

Diagnostic Approach for Dyspnoea [IQbaL]

Diagnostic Hypothesis Clinical Clues Test Treatment History Physical Pulmonary Etiologies

COPD >20 pack years tobacco Chronic cough +sputum Progressive/persistent dyspnea Exposure to occupational

dust/chemical

 Dec breath sounds, wheezing  Clubbing – superimposed bronchogenic CA, chronic infection  Spirometry (FEV1/FVC <70%)  Bronchodilator response – largely irreversible  CXR – hyperinflation,

bullous changes, pul HPT  ECG – cor pulmonale ( peak

P wave @ L2,L3 and AVF )  ABG  Nebulizer bronchodilator, O2  Antibiotic (H. influenza, Strep pneumonia)  Steroid ( beneficial in acute exacerbation of COAD) Asthma

Cold, exercise, allergen, pets  symptoms worsening Fmly Hx (atopic)

 Wheezing  Assessing for severe

asthma and life-threatening Sx  PFT  Bronchodilator response  Methacholine induced  CXR – TRO pneumothorax  ABG

 O2, nebulizer (B-agonist)  High dose steroid  For severe attack – IV

aminophylline, consider ventilation

Pulmonary embolism

Sudden onset of dyspnea, peuritic chest pain Hx of cancer Hx of surgery, immobilization Estrogen therapy  Tachypnea, cyanosis  JVP, loud P2, gallop rhythm  Unilateral leg swelling  D-dimer – exclude PE if normal  CT angiopraphy  Leg Duplex  O2 100%  Morphine + antiemetic  Immediate thrombolysis in massive PE ( bolus alteplase or surgery)  IV Heparin Pneumonia (CAP, TB, Pneumocystic jiroveci pneumonia)

Fever, productive cough Drug injection

High-risk sexual exposures

 Crackles, fever thrush  Kaposi sarcoma  Skin pop marks  Severity – “CURB-65”

 CXR

 FBC, Blood culture  HIV, CD4 (when

appropriate)

 O2, treat shock  Empirical antibiotic  IV fluid

 PRN analgesic

Intertitial lung disease (ILD)

Known connective tissue

disease (CTD)

Raynaud phenomenon Occupational exposure –

asbestos, silica Sarcoidosis

 Fine basal Crackles  Clubbing

 Sx of pul HPT, cor pulmonale & CTD

 CXR - Honeycombing  PFT

 High resolution chest  CT  Lung biopsy  Steroid / cyclophosphamide  Tx of underlying Dz Cardiac Etiology ACS  Chest pain  CAD risk factor

 JVP  S3  crackles  ECG  Biomakers  Stress test  Angiography  “MONA” Valvular heart

disease  Rheumatic heart disease  Significant murmurs

 Echo

Arrhythmias

 Palpitation _ Irregular pulse Variable intensity of S1

 ECG – absent P wave  Holter – paroxysmal AF  Echo – valvular defect, Lt

atrial thrombus  TFT

 Identify underlying cause  Cardioversion (electrical

or pharmacological)  Control ventricular rate

(digoxin)

 Antocoagulation – to prevent

thromboembolism

Heart failure

 CAD or risk factor  Poorly controlled HPT  PND  Alcohol abuse  JVP  S3  Crackles  Peripheral oedema  CXR  Echo  BNP  Sit pt upright  O2 100%, IV access  Treat any arrhythmias  Monitor ECG  Furosemide, dimorphine Anaemia  Melaena  Menorrhagia  Rectal bleeding  Pallor, cachexia  Pale conjunctiva  Thalassemic facies  Gum hypertrophy  HCT level (low)

Careful Hx-taking is very important 1) Time course

 Acute (within min) – life-threatening eg. Acute pul Embolism, MI, pneumothorax, anaphylaxis, FB aspiration, pul. oedema or cardiac temponade

 Subacute (hours-days) – AEBA, exacerbation of COPD, pul. oedema.

 Chronic (weeks-months) – CCF, COPD, cardiomyopathy, pul. HPT, valvular heart dz, anaemia 2) Severity

3) Associated Sx

 Fever - pneumonia, bronchitis, laryngitis, viral causes, sepsis

 Fever + cough – community-acquired pneumonia or opportunistic infection in immunocompromised host (need CXR to exclude pneumonia)

 Central chest pain – suggest CAD, pul embolism, pneumothorax, FB aspiration

 Pleuritic chest pain – suggest pleuritis, pneumonia, pneumothorax

 Palpitation – paroxysmal tachyarrhythmias, pul. embolism, valvular heart dz or anxiety attack

 Wheezing – Asthma, COPD, pul. oedema, bronchiolitis, FB aspiration

 Haemoptysis – exacerbation of bronchiectasis, bronchitis, chest malignancies, tuberculosis, cocaine toxicity

 Dysphagia – FB aspiration, tetanus, epiglottitis (+drooling saliva), GERD (+heart burn)

 Bone pain – sickle cell anaemia or fat embolism (a/w long bone #)

4) Position

 Orthopnea – CCF, COPD

 Dyspnea on standing, relieve by supine – pattern foramen ovale 5) Pattern

 Appear during working, resolve during period off work – occupational exposure

 Seasonal – asthma or reactive airway disease 6) Smoking Hx – COPD, lung Ca, interstitial lung disease

Questions

1. Common causes of chest pain?

ACS, Stable angina, pul embolism, pneumonia, viral pleuritis, GERD, anxiety & panic disorder 2. Life threatening chest pain? [PETAAA]

Acute Coronary Syndrome [Julea] HISTORY

NSTEMI/UA : incomplete occlusion, occur at rest STEMI: complete occlusion, not relieved by rest/GTN Chest pain (LORDSANFARO)

 Retrosternal/central/left chest

 Crushing/pressing/burning in nature

 Radiate to jaw/left upper limb

 A/w profuse sweating, n&v, sob, palpitation Atypical sx: fatigue, SOB, epigastric discomfort, n&v

Risk fx:

 Prev hx of IHD, CVA

 DM,HPT,HPL

 Smoking, physical inactivity, obese

 Family hx of heart dz, stroke DDX chest pain + SOB:

 MI

 Aortic dissection (sudden severe pain, tearing sensation, radiate to neck,back,abd,leg)

 Pulm embolism (period of immobility?)

 Pneumothorax (hx of trauma to chest?)

 Gerd (burning sensation in chest, sour taste, obesity)

 Esophageal rupture (chest pain after vomiting)

 Pneumonia (pleuritic chest pain, fever, cough)

PHYSICAL EXAMINATION CVS examination

Diagnosis of ACS:

I. Hx of ischemic type chest pain II. Ecg changes

III. Cardiac biomarkers

INVESTIGATION Diagnostic ix:

1. ECG

 NSTEMI: ST depression, T inversion

 STEMI: ST elevation, T inversion, Q wave 2. Cardiac enzymes: trop T, Trop I, CKMB

 NSTEMI:increase enzymes

 UA: normal 3. Echocardiography 4. Angiography Supportive ix:

 FBC (low hb can precipitate MI)  LFT/BUSE/CREAT

 Glucose lvl  Lipid profile  PT/APTT

 CXR: cardiomegaly, p.effusion, sign of LV failure  ABG

MANAGEMENT 1. Assess ABC

2. Bed rest, v/s, continuous ECG monitoring 3. O2 by nasal prong/facemask

4. Analgesic: S/L GTN, IV morphine +antiemetic 5. Pharmacological rx:

6. Antithrombotic(antiplatelet, anticoagulants), 7. B-blockers, nitrates, acei/ARB, statin

8. Non pharmaco: stop smoking, exercise, diet, control HPT, DM, HPL

Specific mx for STEMI: reperfusion therapy

thrombolytics ( iv streptokinase) @ PCI if C/I to thrombolytic

MONA

Common/Possible Question in Exam + Answer ECG interpretation !!

Advice before discharge:

-diet lifestyle, exercise, stop smoking, compliance to meds and f/up Cx of MI:

 Cardiac arrhythmia

 Heart failure & cardiogenic shock

 Thromboembolism (d/t bed rest,cardiac failure)  Cardiac rupture

 Pericarditis

 Post infarction angina  LV aneurysm

 Complex regional pain syndrome (pain at l arm after weeks,months following mi)  Dressler’s syndrome (pericarditis, fever, pericardial effusion)

Indicators of successful reperfusion:  Reduce chest pain

 ST segment isoelectric

 Restoration of hemodynamic/electrical stability Contraindications for thrombolytics in STEMI:

Congestive Cardiac Failure [Dalilah] HISTORY 1. Risk factors :

CAD, HPT, renal failure, valvular/congenital heart disease, pericardial disease (TB, effusion, tamponade), arrhythmia and anemia

2. Symptoms of pulmonary edema :

Acute breathlessness, orthopnea, PND, dry cough/ coughing with sputum, frothy sputum

3. Symptoms of right sided heart failure :

Lower limb edema, abdominal distension due to ascites 4. Symptoms of cardiogenic shock :

Cool, diaphoretic skin, cyanosis, dyspnea, altered sensorium, reduced urine output

5. Assess further based on NYHA to get the class of heart failure

PHYSICAL EXAMINATION GENERAL

- Respiratory distress

- Decreased alertness ( cardiogenic shock) - Tachypneic

- Tachycardia

- Cold peripheries, delayed CRT - Hypotension

- Sign of valvular heart lesion - Raised JVP

- Pitting edema SPECIFIC

- Apex beat shifted to left side ( cardiomegaly ) - Gallop rhythm ( pulmonary edema )

- Loud P2 ( pulmonary edema) - Third and forth heart sound

- Lung crepitation ( pulmonary edema) - Sign of pleural effusion

- Ascites

- Tender hepatomegaly

INVESTIGATION

1. FBP,LFT, BUSE & creatinine, cardiac enzyme, ABG 2. ECG – Ischaemic changes

3. Echocardiography – cardiac chamber dimension, systolic n diastolic function, valvular heart disease,

cardiomyopathies

4. Regular BP monitoring or intra-arterial BP monitoring 5. Urine output (renal perfusion), alertness and conscious

level (cerebral perfusion) and general wellbeing 6. Assessment of venous pressure

 CVP (only reflect right ventricular filling pressure)

 Pulmonary capillary wedge pressure (PCWP) with Swan-Ganz catheter ; useful in suspected ARDS, exclusion of VSD, associated hypotension requiring treatment with inotrope to guide therapy

MANAGEMENT 1. Priorities

a) Sit pt upright

b) Oxygen (35 to 100%) via facemask to maintain PaO2 more than 60 mmHg and SPO2 more than 90% c) Treat underlying arrthymia

d) IV canula large bore :

 IV morphine (2.5-5 mg) + IV /IM 10 mg metoclopromide

 frusemide 40-80mg IV

e) Sublingual nitrate if systolic BP > 100 mmHg 2. Oxygenation

3. Fluid challenge ( Hartmann’s solution ) 4. Diuretics

5. Venodilators 6. Inotropic agent

Details on Management 1. Oxygenation

- Increase inspired oxygen to keep SPO2 more than 90%

- Mechanical ventilation : if hypercapnia persist despite high flow oxygen (eg NIPPV)

- Correct severe metabolic acidosis (pH less than 7.2 ) as it has negative inotropic and proarrthymogenic effect 2. Fluid challenge ( Hartmann’s solution )

- If invasive hemodynamic monitoring is not available , fluid should be administered in small volumes (100ml ) over 5-10 min interval with reassessment of BP, heart rate, peripheral perfusion n breath sound. If BP does not responds to fluid (after 500-1000 ml), start vasopressor

- If invasive hemodynamic monitoring is available, volume should be administered until a PCWP of 18 mmHg is attained

3. Diuretics

- IV frusemide 40 mg or bumetanide 1 mg at 20 min interval if initial therapeutic response is inadequate 4. Venodilators

- Sublingual nitroglycerin 0.3-0.5 mg up to 3 tabs every 5 min interval

- IV nitroglycerin 5-10 microgram/min increased by 5-10 microgram/min every 5 -10 min - IV isoket ( isosorbide dinitrite) 2-10 mg/hr

5. Inotropic agent

- Dopamine 5-10 microgram/kg/min. low dose stimulates systemic vasodilation; high dose stimulates heart rate and contractility

- Dobutamine 15-20 microgram/kg/min. acts at beta adrenergic receptor , no alpha adrenergic receptor activity 6. Noradrenaline/adrenaline

- Beta and alpha adrenergic agonist. Increase heart contractility and peripheral vasoconstriction - Noradrenaline : 8 -12 microgram/kg/min

- Adrenaline : 0.05 – 0.1 microgram /kg/min QUESTIONS

1. Medications ( MOA, dose and side effect ) 2. Chest xray finding

Cardiogenic pulmonary edema; cardiomegaly, widened mediastinum, bat wings, upper lobe diversion, kerley A,B,C, blunted costophrenic angle.

3. PE finding for pulmonary edema

4. Sign of right heat failure vs left heart failure

ECG findings ( ischaemic changes ST elevation, T inversion, Q wave ), duration and onset. Localization of infarction area. ( sbb associated dengan CAD )

Rheumatic Heart Disease [Ain]

HISTORY

- RHD : A chronic heart condition caused by rheumatic fever that can be prevented and controlled. Rheumatic fever is caused by a preceding group A streptococcal (strep) infection.

- Multisystem disease affecting connective tissue particularly of the heart, joints, brain, cutaneous and subcutaneous tissues

1. Age ? - 5-15 yrs school-age children living in closed community (high risk group)

2. Any history of fever or URTI preceeding to the complaint 3. Any joint pain or others ass. symptoms

eg.malaise,pallor,fatique ?

4. Which joint affected,nature of the pain,is it migratory or localized?

5. Any skin lesions or rash noted in the body? 6. Any abnormal movement noted?

7. Any swelling anywhere or nodule especially over bony prominence?

8. Assess risk factor – overcrowding,poor sanitation, poverty,poor housing.

9. Any complication symptoms eg.heart failure,atrial fibrillation

#

The knees, ankles, elbows, and wrists are the joints most likely to become swollen from rheumatic fever. The pain often migrates from one joint to another.

PHYSICAL EXAMINATION

Carditis in RHD :

- Mitral valve (90 %) : MR –children,adolescent

MS – adult,later can get AF as cx. Aortic valve : AR,AS

Less common affected : pulmonary, tricuspid INVESTIGATION

1. FBC – anemia,leucocytosis

2. Inflammatory marker – ESR/CRP positive 3. Throats swab for group A streptococcus 4. Anti-streptolysin O titre (ASOT) - elevated 5. Investigations for evidence of carditis

• Chest x-ray – cardiomegaly, pulmonary venous congestion

• ECG- First degree A-V block, T wave changes, low voltage QRS

• Echocardiogram – cardiac dilatation, valve involvement, pericardial effusion

MANAGEMENT Principle of management :

- Step I - primary prevention (eradication of streptococci) - Step II - anti inflammatory treatment (aspirin,steroids) - Step III- supportive management & management of

complications

- Step IV- secondary prevention (prevention of recurrent attacks)

- Step v – tertiary prevention

1. Bed rest until CRP normal for 2 weeks (maybe by 3 months) 2. Benzylpenicillin 0.6-1.2g IM or Penicillin V 250-500 mg 2-3 times

daily for 10 days.

(if allergic give erythromycin or azithromycin for 10 days) 3. Analgesia for carditis/arthritis :aspirin 100 mg/kg/d in divided

dose (max 8g/d) for 2 day then 70 mg/kg/d for 6 weeks.  if moderate to severe carditis : add prednisolone

4. Immobilize joint in severe arthritis – rest and supportive splinting 5. Treatment of chorea - Haloperidol (0.5 mg/8h) or diazepam 6. Secondary Prevention of Rheumatic Fever- aims to prevent illness

or progression of disease once a problem has been identified  Benzathine penicillin G 1 200 000 U every 3 weeks*

Intramuscular

 Penicillin V 250 mg twice daily Oral

# For individuals allergic to penicillin : Erythromycin 250 mg twice daily

7. Tertiary prevention–aims to prevent complications once a disease is established. Reducing symptoms to minimise disability and prevent premature death. Eg.heart valve surgery, medication to manage heart failure eg.diuretics and preventing stroke.

1. Diagnosis of RHD

JONES criteria : evidence of recent strep infection plus 2 major criteria or 1 major criteria + 2 minor

# Exceptions to Jones Criteria

- Chorea alone, if other causes have been excluded - Insidious or late-onset carditis with no other explanation

- Patients with documented RHD or prior rheumatic fever,one major criterion,or of fever,arthralgia or high CRP suggests recurrence 2. Duration of Secondary Rheumatic Fever Prophylaxis

 Fever without carditis - At least 5 y or until age 18 y

 Rheumatic fever with carditis and heart disease (persistent valval lesion) - At least 10 y since last residual episode and at least until age 40 y,sometimes lifelong prophylaxis

 Rheumatic fever with carditis & heart disease (no valvar lesion) -10 y or well into adulthood  More severe valvular disease,post-valve surgery cases - lifelong

COPD [Rozana]

HISTORY Epidemiology :

> 35 yo, 10-20% in over 40s

Chronic bronchitis : defined clinically as cough, sputum production, on most days for 3 months of 2 sucessive years, sx improvise if pt stop smoking

Emphysema : define histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls Risk factor :

Genes (alpha-1 antitrypsin enzyme deficiency causes panlobular emphysema), Exposure to particles, Tobacco smoke, Organic and inorganic occupational dusts, Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings, Outdoor air pollution, Lung growth and development, Oxidative stress, Respiratory infections, Socioeconomic status

Sx :

 chronic cough, sputum, dyspnoea(interfere daily activities), wheeze, chest tightness

 extrapulmonary : LOW, cor pulmonale sx

Complication : acute infection +/- infection, polychythaemia, respi failure, cor pulmonale, pneumothorax, lung carcinoma, osteoporosis

PHYSICAL EXAMINATION General :

Tachypnoea, use of accessory muscle, wheeze, cyanosis Specific :

 sign of airflow limitation and air trapping in advanced stage (barrel chest, loss of cardiac and liver dullness, prolonged expiration, reduced breath soundhyperinflation, reduce expansion)

Cx : cor pulmonale: edema, ↑ JVP, pneumothorax

MANAGEMENT

Mx of acute COPD

 Controlled oxygen therapy

 Nebulized bronchodilators (salbutamol and ipratropium)

 Steroids (IV hydrocortisone and oral prednisolone)

 Antibiotics, if evidence of infection

 Physiotherapy to aid sputum expectoration

 If no response  repeat nebulizers and consider iv aminophlline

 If no respone

1) Consider nasal intermittent positive pressure ventilation. 2) Consider intubation & ventilation

Mx of stable COPD

Non pharmaco/ general : smoking cessation, encourage exercise, treat poor nutrition or obesity, influenza and pneumococcal vaccination

Pharmaco

 Mild (FEV1 50-80% predicted) : antimuscarinic

eg. Ipratropium/ B2 agonist inhaled PRN

 Moderate (FEV1 300-49% predicted) : regular

anticholinergic eg. Ipratropium or long acting inhaled B2 agonist eg. salmeterol + inhaled corticosteroid eg. beclamethasone

 Severe (FEV1 ) : LABA + inhaled steroid,

anticholinergic.

Pulmonary HPT : Assess the need of LTOT(long term 02 therapy), treat edema with diuretics

INVESTIGATION

Laboratory : FBC =anemia of chronic disease, PCV ↑(chronic hypoxemia)

Others :

 Spirometry : post bronchodilator FEV1/FVC ratio < 0.7 = not fully reversible airflow limitation

 Peak expiratory flow rate : low

 ECG :detect pulmonary HPT ( advanced disease) right atrial and ventricular hypertrophy (cor pulmonale)

 ABG : PaO2 ↓+/- hypercapnia Imaging :

 Hyperinflation (flattened diaphragm and increased lung volume), large central pulmonary arteries, ↓ peripheral vascular marking, bullae, hyperlucency of lung

 Exclude other diagnosis eg. Lung cancer, heart failure, bronchiectasis and TB

Pink puffers & blue bloaters (end of a spectrum)

 Pink puffers have ↑ alveolar ventilation, a near normal PAO2 and normal or low PCO2, breathless but not cyanosed, may progressed to type 1 respi failure

 Blue bloaters have ↓ alveolar ventilation, with low PAO2 and high PACO2, cyanosed but not breathless and may go on to dev. Cor pulmonale

Tuberculosis [Fatin]

HISTORY o Epidemiology

 Mycobacterium tuberculosis

 Transmit through microscopic droplet ( cough, sneeze, speaking)

o Risk factor

 Immunocompromise (DM, chronic dz, HIV, steroid, malnutrition)

 Travelling to endemic area

 Substance abuse (drug/alcohol)

 Contact with TB pt (occupation, family member)

 Living in overcrowded area

 Prev TB infection o S&S

 Chronic cough >2w

 Blood stained cough

 LOW, LOA

 Fever, night sweat

 SOB, chest pain, pleuritic chest pain

 Extra-pulmonary : hematuria (renal), back pain (spine), seizure (meninges)

o Complication (lymphatohematogenous spread)

 Extra-pulmonary TB

-bone, brain, liver&kidney, heart

 ARDS  Lung failure  Relapse of disease PHYSICAL EXAMINATION o General  Cachexic  Fever  Muscle wasting o Specific  Lung :

 Consolidation =↓chest expansion, dull percussion, bronchial BS, crepitation  Pleura effusion = trachea deviated if massive,

↓chest expansion, stony dull, absent BS, ↓vocal resonance

 Lung collapse = trachea deviation ipsilateral mediasternal shift, ↓chest expansion, dull, absent/reduce BS  Other : lymphadenopathy ∆∆ 1) pneumonia 2) lung carcinoma 3) lung abscess 4) fungal infection INVESTIGATION o Laboratory

 FBC –leucocytosis as sign of infection or anaemia due to chronic disease

 Sputum direct smear for AFB

 Mantoux test- result read after 72H

 Sputum c+ sensitivity –3 morning specimen

 Sputum cytology- to look for any abnormal cells to suggest malignancy

 Blood culture + sensitivity :to detect any microorganism

 Broncoscopy - tumour, foreign body, inflammation

 Pleura fluid analysis (pleura tapping) o Imaging

 X-ray :

 Primary TB: perihilar and paratracheal

lymphadenopathy, patchy area of consolidation, pleura effusion feature

 Post 1® TB: consolidation at post segment of upper lobe @ sup segment of lower lobe, tuberculoma at Rt upper lobe, cavitation

 Milliary TB : millet seed nodule (1-3mm) evenly distributed

MANAGEMENT Anti-TB therapy

 Intensive phase (2M) -> 2EHRZ

 Maintainence phase (4M) -> 4HR 1ST LINE : Rifampicin (R)-hepatitis

Isoniazid (H)- hepatitis

Pyrazinamide (Z) –joint and ms pain Ethambutol (E)- visual disturbance Streptomycin (S) – ototoxicity DOTS –directly observed therapy short case

Common/Possible Question in Exam + Answer 1) Screening of high risk group

 HIV pt

 Immigrant

 Person in prison/drug rehab centre

 Pt with dm, renal dz, steroid, immune sup drug

 Hemato malignancy

2) Classification of TB

 PTB +ve smear : * 2 sputum smear positive AFB

* 1 sputum +ve AFB and +ve radiological finding * 1 sputum +ve AFB and +ve culture

 PTB –ve smear : * 3 sputum smear –ve

* sputum smear –ve but subsequent culture +ve 3) TB meningitis Tx

 The duration of anti –tb is longer which for 12 months duration

 Intensive(2 months) maintenance (10 months)

 Other drug to give is steroid (6 weeks or longer)

4) Preventive measures

Primary intervention

 Identification + immediate isolation

 Herd immunity-BCG vaccination

 Contact tracing of individual who are in close contact with cases

 Reduce risk of transmission by using ppe(personal protective equipment), cough etiquette 5) Why hemoptysis occur?

Due to erosion of vessel located in the wall of cavity or rupture of dilated vessel in cavity 6) Mantoux test

7) Follow up : every 2 months, take CXR and sputum smear AFB

Lung Cancer ( Bronchogenic Carcinoma)[Zuraidah]

HISTORY

Def : malignancy of the lung arising from the epithelium of the bronchial tree.

Prevalence : 2nd after prostate ca in men , breast ca in women. Aetiology : smoking, asbestos exposure, radon gas exposure, familial predisposition (genetic), HIV infection, air pollution (pesticide), lung diseases.

History :

1. Sx related to 10 tumor: cough, dyspnea, hemoptysis, chest pain, postobstructive pneumonia

2. Sx related to mediastinal spread:

- Hoarness of voice with left sided lesion (caused by recurrent laryngeal nerve palsy

- Obstructive of svc with right sided tumor or asso lymphadenopathy

- Elevation of hemidiaphragm from phrenic nerve palsy - Dysphagia from esophageal obs and pericardial temponade 3. Sx related to mets: sites liver, brain, pleural cavity, bone,

adrenal glands, contralateral lung & skin 4. Paraneoplastic synd:

- Pain in arm/legs caused by hypertrophic osteoarthropathy - Sx of hypercalcemia caused by scc

5. Systemic effects: fever, anorexia, low/loa, weakness, profound fatigue

PHYSICAL EXAMINATION

General

- Hoarseness of voice, Cachexic, alopecia (chemo), nicotine staining, cyanosis, clubbing, flaps, cervical l/n, raised JVP + sign of SVC obstruction, leg edema

- Vital sign – tachypnea

* Horner syndrome (ptosis), paraneoplastic synd ( wasting of small ms of hand)

Specific (Respiratory system) Inspection

Barrel shaped, mvmnt of chest reduce on affected, use of accessory ms

Palpation

Trachea deviation, apex beat, chest wall tenderness (mets), inc tactile fremitus

Percussion - dullness, liver span enlarged (mets) Auscultate - bronchial bs, rhonchi, rub

DDx 1. Pulmonary TB 2. Pneumonia 3. Lung abscess 4. Bronchiectasis 5. Sarcoidosis INVESTIGATION Laboratory

- FBC: WBC raised in concomitant infection

- ABG: hypoxia with respi acidosis in severe endobronchial obs - ESR: > 100 in 1hour

- Serum sodium, calcium

- Sputum examination – malignant cell cytology, c+s for any u/l lung infection

- Lung fx test: FEV1 of 1000ml after planned resection

- Invasive: pleural fluid cytology, percutaneous transthoracic needle biopsy

Imaging - CXR:

 10 tumor - hilar mass or coin lesion, rib erosions, raised hemidiaphragm (phrenic nerve palsy), lymphangitis carcinomatosis, any lung collapse

 if 20 tumor – cannon ball appearance - CT scan TAP: metastasis, staging

- Bronchoscopy (+washing & brushing): endobronchial tumor - Bone scan: staging

MANAGEMENT

Depends on multiplicity factors: - It is a 10 or mets lesion - Hilar or mediastinal infiltration - Chest wall involvement

- Asso with complication- massive pleural effusion, svc obstruction, collapse-consolidation

- Phrenic nerve involvement - Paraneoplastic syndromes Treatment :

1) Surgery

Lobectomy- the most effective type of surgery, even when the lung tumor is very small.

A wedge- remove the tumor, surrounded by a margin of normal lung.

Segmentectomy- removes the portion of the lung where the cancer developed.

Pneumonectomy. If the tumor is close to the center of the chest, remove the entire lung.

Radiofrequency ablation-needle inserted into the tumor to destroy the cancer with an electrical current

* SCLC is not recommended for surgery d/t aggressive & micromets. Go for chemo

2) Medical – chemotherapy or radiotherapy 3) Treatment for sx such as infection & breasthless 4) Pain management & quality of life

Common/Possible Question in Exam + Answer

1. Cx of lung ca? i. Hemoptysis

ii. Acute breathlessness d/t endobronchial narrowing iii. Massive, recurrent hemorrhagic pleural effusin iv. SVC obstruction

v. Paraneoplastic syndrome

3. Contraindication for surgery? i. Metastatic carcinoma ii. FEV1 < 15000ml

iii. Severe pulmonary hpt

iv. Uncontrolled major cardiac arrhythmias v. Co2 retention

vi. Myocardial infarction in the past 3 months 2. Aim of staging?

To identify candidates for surgical resection, since this approach offers highest potential cure

4. Which tumor respond well to chemo?

Small cell lung ca (SCLC), combination of cisplatin & etoposide is the best therapeutic index of ay regime

Role for chemo in non small cell ca (NSCLC) suggested that bnefits are small

Notes Types :

Small cell lung ca (SCLC) – 20%, rapid growing, strong correlation with smoking, mets rapidly to various organ (liver, brain, bone, git, adrenal glands ), histologically- keratinization

Non small cell lung ca (NSCLC) – 80%

I. Adenocarcinoma (50%), commonly seen in non smoker, arises from bronchial mucosal glands in the outer, or peripheral area of lungs, histo-gland formation

II. Squamous cell carcinomas (30%), aka epidermoid carcinomas, centrally located, cavitary lesion, histo- presence of keratin pearls and has tendency to exfoliate.

III. Large cell carcinomas (20%), undifferentiated ca, large peripheral mass on cxr, histo-highly atypical cell with focal necrosis

Bronchiectasis [Rafidah]

HISTORY

Definition: Abnormal and permanent dilated airways resulting from Inflamed thickened and irreversibly damage bronchial walls cause mucociliary transport mechanism become impaired and frequent bacterial infection ensues.

Aetiology:

 Congenital: cystic fibrosis,  Primary ciliary dyskinesia,

Kartagener’s syndrome

 Post-infection: measles, pertussis, Bronchiolitis, pneumonia, HIV, TB

 Bronchial obstruction: tumour, foreign body

 Rheumatoid arthritis, IBD

 Allergic bronchopulmonary aspergillosis

S&S

 Cough with copious purulent sputum

 Recurrent hemoptysis

 SOB

 Intermittent fever and night sweat

 History of recurrent infection

 Weight loss

Complication

 Pneumonia  Pleural effusion  Pneumothorax  Hemoptysis  Cerebral abscess  amyloidosis PHYSICAL EXAMINATION General: - Respiratory distress - Finger clubbing Specific:

- Coarse crackles over affected area, usually basal lung - Sign of collapse, fibrosis or pneumonia

INVESTIGATION Laboratory

- Full blood count – white cell count (infection) - Sputum culture

Imaging

- Chest radiograph: cystic shadow, thickened bronchial walls(tramline and ring shadow)

- High resolution CT scan – thickened, dilated bronchi and cyst at the end bronchioles.

- Bronchoscopy – to locate site of hemoptysis or exclude obstruction

MANAGEMENT Non surgical:

Non pharmacological

1) Postural drainage at least 3 times daily for 10 – 20min

Pharmacological

1) Antibiotic: according bacterial sensitivities 2) Bronchodilator: may be useful in asthma, copd,cf,

allergic bronchopulmonary aspergillosis 3) Corticosteroid: eg. prednisolone Surgical : resection of the affected lobe

Common/Possible Question in Exam + Answer

1) What are the major respiratory pathogens in bronchiectasis?

Staph. Aureus, pseudomonas aeruginosa, H. influenza, and anerobes

2) What are the common site for localized disease? Left lower lobe and lingula

3) What is the indication of surgery in bronchiectasis?

Bronchiectasis localized to a single lobe or a segment without clinical, bronchographic, ct evidence of bronchiectasis of bronchitis affecting other parts of the lungs.

Pleural Effusion [Farhan]

HISTORY

 Accumulation of fluids in the pleural space

 Transudates (<25g/L):

 Due to increase venous pressure (CCF, constrictive pericarditis, fluid overload)

 Hyponatremia (cirrhosis, nephrotic syndrome, malabsorption)

 Hypothyroidism (right pleural effusion)

 Meig’s syndrome (benign ovarian tumor, ascites, pleural effusion)

 Exudates (>35g/L):

 Increased leakiness of pleural capillaries due to  Infection (pneumonia, tuberculosis)

 Ischemia (pulmonary infarction, SLE, rheumatoid arthritis)  Malignancy (bronchogenic ca, malignant mets, lymphoma)

 Common complaints: dyspnea, cough, pleuritic chest pain.

 Ask about associated symptoms e.g. dyspnea with bilateral leg swelling, orthopnea, and PND  CCF; or night sweats, fever, and weight loss  TB

 Ask about occupation; might give a clue to illness

PHYSICAL EXAMINATION

 General examination (look for signs of associated disease):  Malignancy (cachexia, clubbing, lymphadenopathy,

mastectomy scar)

 Stigmata of CLD (Dupuytren contracture, spider naevi)  Cardiac failure (displaced apex beat, ↓BP, cyanosis,

tachycardia)

 Hypothyroidism (dry skin, thin hair, cold hands, round puffy face)

 SLE (malar rash, discoid rash, oral ulcers, alopecia)  RA (symmetrical joint swelling)

 Chest examination (only apparent if effusion > 300ml):  Inspection: asymmetrical chest movement

 Palpation: reduced chest expansion, mediastinal shift, trachea deviation (>1000ml), decreased tactile fremitus,  Percussion: stony dullness

 Auscultation: Reduced or absent breath sound, reduced vocal resonance

INVESTIGATION

 CXR (PA):

 Blunted costophrenic angle (small effusion)  Clear air fluid level with concave upper border  Air fluid level with flat upper border (presence of

pneumothorax)

 Lateral decubitus film is useful to detect smaller effusion; layering of an effusion indicates free flowing effusion

 Pleural fluid analysis (send for):

 Clinical chemistry (protein, glucose, pH, LDH, amylase)  Bacteriology (microscopy & culture, TB culture)  Cytology

 Immunology (RF, ANA, complement) – if indicated

 Pleural biopsy

 If pleural fluid analysis is inconclusive

MANAGEMENT

 Transudative effusions are managed by treating underlying causes

 If effusion is symptomatic (exudative/transudative) drainage can be done to provide relief

 Drain fluid slowly (max 2L/24h)

 If drain large amount quickly; it can cause re-expansion pulmonary edema

 Pleurodesis (pleural sclerosis)

 Talc, tetracycline, bleomycin sulfate, zinc sulfate  Thoracoscopic talc pleurodesis most effective for

malignant effusions

 S/E: fever, chest pain, nausea

 Surgery

 Persistent collections and increasing pleural thickness (on ultrasound) requires surgery – pleurectomy

Light’s criteria

To differentiate between transudate and exudate for proteins ranged in between 25 – 35g/L According to Light’s criteria, the fluid is exudate if:

 Effusion protein : serum protein ratio > 0.5

 Effusion LDH : serum LDH ratio >0.6

 Effusion LDH level is greater than 2/3 of the upper limit of serum LDH

Pleural fluid analysis

Normal pleural fluid characteristics

 Clear ultrafiltrate of plasma that originates from the parietal pleura

 A pH of 7.60-7.64

 Protein content of less than 2% (1-2 g/dL)

 Fewer than 1000 white blood cells (WBCs) per cubic millimeter

 Glucose content similar to that of plasma

 Lactate dehydrogenase (LDH) less than 50% of plasma

Sample Causes

Clear, straw-coloured Turbid, yellow Haemorrhagic

Transudate, exudate

Empyema, parapneumonic effusion Trauma, malignancy, pulmonary infarction Clinical chemistry

Glucose <3.3mmol/L pH <7.2

LDH ↑ (pleural:serum >0.6) Amylase ↑

Empyema, malignancy, TB, RA, SLE

Pancreatitis, carcinoma, bacterial pneumonia, oesophageal rupture

Chest drain

Safe triangle for chest drain insertion: 1. Lateral border of pectoralis major 2. Anterior border of latissimus dorsi 3. Horizontal line at nipple level

Indication:

 Pneumothorax

 Malignant pleural effusion, complicated parapneumonic effusion, empyema

 Pleural effusion compromising ventilation

 Traumatic haemopneumothorax

Complication:

 Thoracic or abdominal organ injury

 Lymphatic drainage  chylothorax

Chronic Kidney Disease (Kidney Damage >3 Months) [Khiru] HISTORY

In history: i) Past UTI

ii) known BP, DM, FHx

iii) Drug hx (NSAIDS, gentamycin, sulphonamides, tetracyclines, vancomycin,amphotericin, cisplatin, ACEi, ARB, methotrexate, heavy metal poisoning)

iv) Fatigue, weakness

v) Anorexia, vomiting, metallic taste vi) Pruritus

vii) Bone pain viii) Dyspnea ix) Ankle swelling

Causes

 Acute kidney injury  DM

 HPT

 Glomerulonephritis/ pyelonephritis  Polycystic kidney disease

 Renal vascular disease

 Analgesic nephropathy (antipyretics, caffeine, NSAIDs)  Med

Complication

 Electrolyte: hyperk,hypoCa,hyperphosphatemia

 Haematological: anemia, bleeding tendency (plt dysfunction)  CVS: cardiac failure, HPT, pericarditis, accelerated atherosclerosis  Neurological: drowsy, seizure, peripheral neuropathy

 Metabolic/ endocrine: hyperlipid, renal osteodystrophy  GIT: anorexia, N&V, bleeding

 Skin: pruritus, easy bruising

PHYSICAL EXAMINATION

Signs: pallor, yellow skin pigmentation, brown nails, purpura, bruising, excoriation, increase BP,cardiomegaly, pericardial rub, peural effusion, pulmonary or peripheral edema, proximal myopathy

INVESTIGATION

1. Blood: Hb reduced (normochromic normocystic), ESR, Urea & electrolyte (increase urea & creatinine), glucose (DM), reduced calcium, increase phosphate, increase alkaline phosphate (renal osteodystrophy), increase PTH

2. Urine: microscopic culture & sensitivity, dipstick, 24H urinary protein

3. Imaging: renal ultrasound-renal size small, <9cm, but normal or large with CRF in DM, PKD, amyloidosis, myeloma, systemic sclerosis, asymmetric renal vascular disease

4. CXR-cardiomeegaly, pleural effusion, pulmonary edema 5. Bone xray- renal osteodystrophy

6. Renal biopsy- consider if cause is unclear & normal size kidneys

MANAGEMENT

1.Refer nephrologist treat reversible causes: relieve obstruction, stop nephrotoxic drugs, deal hypercalcemia & cardiovascular risk.

2.Lifestyle advice. Should exercise, healthy weight & stop smoking. Sodium restriction, moderate protein diet. Potassium restriction only if hyperkalemia; bicarbonate supplements to correct acidosis.

3.HPT. Target BP <140/85 (<130/80 if diabetic or >1g proteinuria/d). In diabetic kidney disease, even with normal BP, treat with ACEi or ARA. 4.CVS: statins & aspirin

5.Renal bone disease (osteodystrophy): treat if increase hyperparathyroidism. Phosphate rises in CRF, which increase PTH further, & also precipitates in kidney & vasculature. Restrict dietary phosphate. Give binders (calcichew) to bind phosphate in gut to reduce absorption. Vit D (alfacalcidol) & Ca2+ supplements reduce bone disease & hyperparathyroidism

6.Edema. High dose loop diuretics (frusemide) restrict on fluid & sodium intake

7.Restless legs. Clonazepam or gabapentin 8.Prepare for dialysis/ transplantation

Common/Possible Question in Exam + Answer 1. Definitions

 Azotemia: accumulation of nitrogenous product (chiefly urea) in blood as indicated by raised serum urea & creatinine  Uremia: manifestations of organ dysfunction a/w azotemia

 ARF: significant deterioration in renal function occurring over hours or days, clinically manifestation as an abrupt & sustained rise in serum urea & creatinine.

 CRF: permanent reduction in GFR (5-25ml/min) sufficient to produce detectable alteration in well-being & organ function. (>3 months)

 ESRF: final stage of CRF (GFR<5ml/min) when pt cnt survive w/o transplantation or long term dialysis  Normal GFR:90-120ml/min

2. Classification of CKD

3. Indications for dialysis

 Acid base imbalance (severe metabolic acidosis pH<7.2 or base excess <10)  Electrolyte imbalance (Resistant hyperK >7mmol/L)

 Intoxication (ingestants/toxins-lithium)

 Overload (Fluid overload not responsive to diuretics, refractory pulmonary edema, volume overload causing respi distress)  Uremic symptoms (uremic encephalopathy, uremic pericarditis)

4. Indication for renal biopsy

 Unexplained acute renal failure or chronic renal insufficiency  Acute nephritic syndrome

 Unexplained proteinuria & hematuria

 Previously identified & treated lesions to plan for future therapy

 Systemic diseases a/w kidney dysfunction e.g SLE, Foodpasture syndrome, wegener’s granulomatosis t0 confirm extent of renal involvement & to guide management

 Suspected transplant rejection, to differentiate it from other causes of acute renal failure  To guide treatment

5. Renal Osteodystrophy

 Skeletal complications of CRF characterized by:

i. osteomalacia, osteitis fibrosa (caused by hypocalcemia, hyperphosphatemia & reduced synthesis of 1,25-DHCC) ii. osteoporosis

iii. osteosclerosis (increased density at upper & lower ends of vertebra/ ‘jugger jersey’ spine) 6. Causes of Anemia in CRF

Chronic Liver Disease [Sofia]

HISTORY

1. Duration of jaundice

2. Ass symptoms :

Dyspepsia , fat intolerance or biliary colic, arthralgia,

myalgias, rash, anorexia, abdominal pain, fever,

pruritus

3. Changes in color of urine and stools

4. Social hx: sexual activity and alcohol history

5. Complication: bleeding tendency, easily bruising

6. Constitutional hx : LOW or LOA

7. Risk factors:

Recent travel history, Exposure of patients with

jaundice, Parenteral exposures-transfusions, IV

abuse, tattoos

8. Occupational history-contact with rats.

9. Exposure to contaminated foods or water. Recent

eat shellfish (HAV), any water sport activity, source

of water

10. Drug hx: Use or exposure to medication-OTC,

physician prescribed, Complementary or alternative

medicine-herbal or vitamin preparations or steroids.

11. Family history- hemolytic anemias, congenital

hyperbilurbinemias and hepatitis.

*basically a lot can be asked, need to rule out other

causes

PHYSICAL EXAMINATION A. Hand:

Leukonychia, clubbing, palmar erythema, bruising, asterixis, scratch mark

B. Face:

Jaundice, fetor hepaticus C. Chest:

Gynecomastia, loss of axillary hair, spider naevi D. Abdomen:

Hepatosplenomegay, ascites, testicular atrophy E. PR exmntn:

Stool colour

INVESTIGATION

1. FBC- low Hb (hemolysis), increased retic count, serum bilirubin, LDH & urobiliogen, decreased plasma haptoglobulin (hemolysis)

2. FBP- bite cells, blister cells , Heinz bodies 3. Clotting factor- deranged in liver dz 4. Liver function tests.

5. Viral serology for HAV, HBV, HCV 6. Tumor marker- alpha fetoprotein

7. Liver biopsy.- in case of hepatocellular carcinoma 8. ERCP-in case of post hepatic jaundice

9. Ultrasound – in case of post hepatic jaundice

MANAGEMENT For Viral Hepatitis B:

1. For acute hepatitis mainly supportive mx & monitor HBV markers

2. For chronic

 mostly observed unless had high viral load

 antiviral: interferon, entecavir, tenofovir. Lamivudine. Response is judged by HBV DNA level, or if HBeAg is present by seroconversion to anti-HBe

3. Pt w chronic hep should had routine lifelong f/up. Fr every 6 month or 1 year check for LFT, alpha-fetoprotein, u/s of liver

4. High risk group shud be screen for HepB and given vaccination

Causes of jaundice: Prehepatic:

 Malaria

 Hemolytic anemia: sickle cell anaemia, G6PD deficiency,

 Hereditary spherocytosis Intrahepatic:

 The viral hepatitis group of infections

 Alcoholic liver dz

 Leptospirosis

 Paracetamol overdose

 Primary biliary cirrhosis

 Gilbert's syndrome

 Liver cancer

 Autoimmune hepatitis

 Primary sclerosing cholangitis Posthepatic:

 Gallstones

 Pancreatic Cancer

 Gallbladder Cancer Or Bile Duct Cancer

 Pancreatitis

Child Pugh score (ABCDE)

Parameters 1 point 2 points 3 points

Albumin (g/L) <34 34-51 >51

Bilirubin (micromol/L) >35 28-35 <28

Coagulation (Prothrombin time) 1-3 4-6 >6

Distention (ascites) None Slight Moderate

Encephalopathy none 1-2 3-4

Grade A: 5-6 Grade B: 7-9 Grade C: >10

*risk of variceal bleeding is higher if score >8 *can also predict mortality:

1 year survival 5 years survival

Grade A 84 % 44%

Grade C 42% 21%

Hepatic encephalopathy

 As liver fails, nitrogenous waste (eg: ammonia) builds up in circulation and passes to the brain, where astrocytes clear it (by process involving the conversion of glutamate to glutamine).

 This excess glutamine causes osmotic imbalances and shift fluid into the cell  cerebral edema. Grading:

I. Altered mood/behavior, sleep disturbance (eg: reversed sleep pattern) , dyspraxia (pls copy this 5 pointed star), poor arithmetic, no liver flap

CAUSES OF HEPATOSPLENOMEGALY

 Infection:

 Acute viral hepatitis

 Infectious mononucleosis  Cytomegalovirus  Rubella  Malaria  Schistosomiasis or filariasis  Haematological disease:  Myeloproliferative disease  Leukaemia  Lymphoma  Pernicious anaemia

 Sickle cell anaemia

 Thalassaemia  Myelofibrosis  Metabolic disease:  Niemann-Pick disease  Gaucher's disease  Hurler's syndrome

 Chronic liver disease and portal hypertension

 Amyloidosis

 Acromegaly

 Systemic lupus erythematosus

Approach To Anemia [Baisyatul] HISTORY 1. Presenting symptoms:

- Weakness, lethargy, shortness of breath, fatigue, postural dizziness

2. Further history:

- History of GIT bleed ( hematemesis, PR bleed) - Heavy menstrual blood loss

- Bleeding after tooth extraction - Bruising, Heamathrosis - Bone pain,Recurrent infection - Jaundice

- Lymph gland swelling (lymphoma) 3. Past medical/surgical history

- History of gastric surgery/malabsorption

- Underlying RA, Underlying OA (required NSAIDs), chronic kideney disease

- History of previous blood transfusion, chemotherapy

4. Social history

- Strict vegetarian diets (B12 def)

- Exposure to toxins(benzene) risk of leukemia - Alcoholic

5. Family history- thalassemia, sickle cell dzs, colon ca, haemophilia, G6PD

6. Drug history-NSAIDs, anticoagulant

PHYSICAL EXAMINATION General

- Pallor

- Thalassemic facies - Cachexic (malignancy) - Pallor of palmar, koilonychia - Bruising, scratchmark (pruritus) - Conjunctiva pallor, jaundice

- Angular stomatitis, gum hypertrophy, glossitis Specific

Abdomen

- Surgical scar (gastrectomy, stoma) - Hepatosplenomegaly

Lymph node

- Lymphadenopathy at neck and inguinal Complete examination

- PR examination - Stool occult blood - Hematuria

INVESTIGATION Blood investigations:

1. FBC : Hb (low)

Total white cell count and differential count - leukocytosis (basohilia): CML

- leukocytosis (eosinophilia): lymphoma - lymphocytosis: lymphoma, CLL Platelet count

Mean cell volume (MCV) - low MCV-microcytic - normal MCV-normochromic - high MCV-macrocytic

Reticulocyte count (reticulocytosis)

2. Peripheral blood film: target cells, tear drop RBCs, poikilocytosis, blast cells, hypersegmented polymorph, pencil cells

3. Serum iron, serum ferritin, TIBC 4. Coagulation study: PT, aPTT, INR 5. Factor assay for factor deficiency 6. Hb electrophoresis for thalassemia

MANAGEMENT 1. Blood transfusion

- For actively bleed patient - Severe and symptomatic anemia - Hb<8

2. Ferrous sulphate therapy - IDA

3. Nutritional therapy and dietary folate - B12 and folate deficiency 4. Splenectomy

- Hypersplenism 5. Bone marrow transplant 6. Chemotherapy : leukemia

COMMON QUESTIONS 1. Anemia classification

Morphology

Hypochromic microcytic Normochromic normocytic Macrocytic

Thalassemia IDA

Sideroblastic anemia

Haemolytic anemia Bone marrow failure Anemia of chronic dzs

B12 deficiency Folate deficiency Alcoholism Causes

Blood loss Inadequate production Excessive destruction

-Trauma -Colon ca

-Bleeding oesophageal varices

-B12 and folate deficiency -Thalassemia, IDA

-Leukemia, aplastic anemia -Renal failure

-G6PD

-Haemolytic spherocytosis -AIHA,malaria,sepsis

2. Lab result

Iron deficiency anemia Thalassemia Anemia of chronic disease

Ferritin: low Iron: low Microcytic hypochromic TIBC: increased Ferritin: normal Iron: normal Microcytic hypochromic TIBC: normal Ferritin: normal Iron: low Normochromic normocytic TIBC: normal Reference:

1. Xpress revision short case UM 2. Oxford handbook

3. Student notes medical 4. Medscape

Systemic Lupus Erythematosus [Aiman] HISTORY Age: 20-40 years old

Gender: Female predominat (10x) +ve Family hx

Diagnostic features:

(at least 4 features, or 2 features in separate occasion) 1. Malar rash (spared nasolabial fold)

2. Discoid rash 3. Photosensitivity

4. Oral ulcer (initially painless – unless infected) 5. Arthritis (2 or more, involve peripheral joint) 6. Serositis (pleuritic or pericarditis – chest pain) 7. Renal disorder (persistant proteinuria – frotty urine) 8. Neurological disorder (seizure or psychosis – with absent of

offending drugs or metabolic derangement) 9. Haematological disorder (anemia, leucopenia,

thrombocytopenia)

10. Immunological (anti dsDNA antibodies, antibody to SM antigen, antiphospholipid antibodies)

11. Antinuclear antibody (ANA)

Complication:

 HPT – due to renal disorder

 Thromboembolism and recurrent miscarriage (in +ve of antiphospholipid antibodies)

 Bleeding tendency (easy bruises)  Anemic symptom (SOB, lethargy)

 HOW and when diagnose + on what medication, how many flare episode

PHYSICAL EXAMINATION General Examination

 Skin : pallor (anemia), petechae (thrombocytopenia), discoid rash, subacute cutaneous erythematosus

 Face : butterfly rash, oral ulcer, pale conjunctiva (anemia)

 Pitting oedema

 generalised oedema

 high BP Others

 Small joint arthritis (rarely with swelling)

 chorea

Differential Diagnosis : Depends on the presentation Discoid skin lesions

Erythematous macules Leukemia

Nephrotic syndrome

INVESTIGATION Bedside:

-urine dipstic : proteinuria Lab:

- FBC : anemia, leucopenia, thrombocytopenia – pancytopenia (hemolytic anemia – normocytic normochromic)

ESR – raised (CRP normal unless there is serositis/arthritis/infection present)

- BUSE : renal function (urea – creatinine), electrolyte imbalance - Urinalysis : RBC, proteinuria, cast on the urine microscopy) Specific:

- Identification of autoantibody 1. Antinuclear antibody (ANA)

– if negative unlikely to be SLE

unless Extractable nuclear antigen is positive (exp: Ro antigen, Sm antigen, La aantigen)

2. Anti dsDNA antibodies (+ve in 20-30%) 3. Antiphphospholipid antibody

- C3 C4 level : low in active disease (during flare) - Renal biopsy : in Lupus nephritis

- Skin biopsy : deposition of IgG and complement

MANAGEMENT 1. Avoid the flare

Sunlight exposure (UV light) by using sunblock, clothing 2. Medical therapy

Depends on severity:

Mild : require analgesic and NSAIDs

+troublesome cutaneous and joint symptom : Hydrochloroquine (200-400mg/day)

Mild-moderate disease : short course of oral corticosteroid (rash, synovitis, serositis)

Acute/life-threatening disease : high dose corticosteroid (oral prednisolone 40-60mg/day) or (methylprednisolone 500mg-1g/day) + pulse IV cyclophophomide

Then change to other immunosuppressive drug (azathioprine, methotrexate, ciclosporin) for the step down after cyclophosphamide or used with corticosteroid

(in renal and cerebral involvement)

+antiphospholipid antibody syndrome (thrombosis) : require lifelong warfarin

(in recur thrombosis despite on warfarin => target INR 2.5-3.5) Diuretic

1. Definition : chronic, remitting and relapsing multisystem autoimmune disease in which organ and cell undergo damage mediated by tissue-binding autoantibodies and immune complex

2. Exacerbation or flares usually follows: (all cause apoptosis of cell) o Sun exposure

o Viral or bacterial infection (esp: epstein-bar virus)

o Sex hormone status(on hormonal therapy, pregnancy-however there is fertility problem in sle patient and no contraindication for pregnancy unless in severe cases)

o Oxidative stress

o Drugs [hydralazine(anti-HPT), isoniazid(anti-TB), procainamide(anti-arrhythmia) 3. Immunosuppressive drugs

a. Cyclophosphamide(to achieve remission)

MOA:cross linking with cell DNA-not specific/SE:myelosuppressive, infertility in male who receive high dose as children b. Ciclosporin

MOA:interfere with activity and growth of T celss/SE: nephrotoxic, neurotoxic c. Methotrexate

MOA:inhibit Dihydrofolic acid reductase(antifolate), interfere with DNA synthesis specific for S phase/SE: cranial nerve palsy, hepatotoxicity

d. Azathioprine(to maintain remission)

MOA:purine analogues(affect more to proliferative cells such as T cells and B celss/SE:bone marrow suppression 4. Exacerbation, complete remission and chronic persistant condition. Early death associated with renal, cerebral or infection.

Later age stroke and coronary artery disease become more prominent. Deformity due to joint destruction is rare compare with OA or RA. Increased long term risk to developed lymphoma.

PAEDIATRIC

Notes

Acute Exacerbation of Bronchial Asthma (Alliah) HISTORY

Definition

Chronic airway inflammation leading to increase airway

responsiveness leads to recurrent episodes of wheezing,SOB,chest tightness & coughing particularly at night and early morning.

Important history

 Current sxpattern of sxpresent tx (response & compliancy)  Previous hosp.admission  Typical exacerbation  Precipitating factor  Infection (URTI)  Non-compliance to drug  Home/school environment (allergen:cat,bedsheet,smoking,insects)  Predisposing fctr

 Hx of atopy (eczema, allergic rhinitis, conjunctivitis)  Aggravating fctr

 Rhinosinusitis

 GERD

 Sensitive to NSAIDs (esp.aspirin)  Family hx of allergy and asthma  Personal impact to lifestyle

 School performance : attendance,academic,co-curiculum  Impact to family

 Financial?parents quarrel?

 Who take care pt/who send pt to hosp during attack? Complication  Status asthmaticus  Respiratory failure  Pneumothorax  Lung collapse PHYSICAL EXAMINATION  Tachypnea  Tachycardia  Cough  Drowsy  Wheezing, rhonchi  Prolonged expiratory phase As attack progress  Cyanosis  Tight chest  Sternal retraction  Agitation  Inability to speak  Tripod sitting position  Diaphoresis

 Pulsus paradosus Signs of chronic illness

 Barrel chest

 Generalized polyphonic expiratory wheeze  Prolonged expiratory phase

 Harrison’s sulci

 Crepitation (d/t segmental atelectasis)  Reduce liver and cardiac dullness  Eczema/dry skin

 Hypertrophied turbinates MANAGEMENT Principle

To allow child to lead as normal life as possible by :  Controlling sx

 Prevent exacerbation  Optimize pulmonary function  Minimize treatment and side effects Drug

Reliever (Short-acting B-agonist )

Controller/preventer : Corticosoteroids, LABA,Combination (Inhaled c/steroid+LABA) , anti-leukotrienes

Acute

 Close monitor pulse,color,PEFR,ABG & SpO2 for at least 4H  High flow oxygen via face mask

 Nebulised bronchodilator (salbutamol)

 Prednisolone 1-2mg/kg body wt orally (max 40mg)  If life-threatening features present :

- give IV aminophylline 5mg/kg over 20min followed by maintenance infusion then IV hydrocortisone 100mg 6hrly - add Ipratropium bromide 0.25mg to nebulised B-agonist  Reassess patient with pulse oximetryresponse to tx INVESTIGATION

a) Lung function test : PEFR > 5y/o or Spirometry b) Brochodilator reversibility test (improve 10-15% post

brochodilator)

c) Skin prick test (to aid dx of atopy)

d) CXR - particularly to exclude foreign body or chronic chest infection or to exclude complications in severe acute episode

Common/Possible Question in Exam + Answer Assessment of severity Intermittent  Daytime sx  Nocturnal sx  Exercise induced sx  Exacerbation affect

sleep & activity  PEFR/FEV1 < 1x a week < 1x a month NO NO Normal lung fx Persistent Mild > 1x a wk > 2x a mth YES 1x a month >80% Moderate Daily > 1x a wk YES > 2x a mth 60-80% Severe Daily Daily Daily > 2x a mth <60%

Monitoring (each f/up)

1) Assessment of asthma control  Interval sx

 Frequency & severity of acute exacbtn  Morbidity 2’ asthma

 Quality of life

 PEFR/FEV1 monitoring 2) Compliance to asthma therapy

 Frequency  Technique 3) Asthma education

 Understanding asthma in childhood  Reemphasize compliance to therapy  Written asthma action plan

Rheumatic Fever [Sofia]

HISTORY

1. History of preceded sore throat

2. Risk factor: low socioeconomic status, overcrowding, poor housing, genetic susceptibility

3. Carditis Pericarditis: audible friction rub

4. Arthritis: migratory polyarthritis, large joints usully affected (shoulder, elbow, knee, ankle), a/w fever

5. Syndenham chorea (SC): are involuntary movements, hypotonia, and mild muscular weakness. Chorea can be generalized or unilateral, predominantly involving the face, hands, and arms. Movements are present at rest, aggravated by stress, and usually cease during sleep. interfere with volitional movements and result in a clumsy gait, dropping and spilling, and explosive bursts of dysarthric speech.

6. Erythema marginatum: bright pink macule/ papule that spread outward in circular serpiginous pattern, multiple, appear at trunk / proximal extremities, rarely distal, never on face, non pruritic, painless, blanch on pressure, brought out by warmth

7. Subcutaneous nodules: non pruritic,painless round, firm, freely movable, elbows, wrist, knee, ankle, Achilles tendon, on extensor surface

MANAGEMENT

Aim: to suppress inflammatory response to minimize cardiac damage, provide symptomatic relief, & eradicate pharyngeal infection

1. Bed rest until acute phase protein return normal 2. Anti inflammatory:

if no/mild carditis- oral aspirin 80-100mg /kg/day in 4 doses for 4 weeks, taper over 4 weeks

If pericarditis/ moderate to severe carditis- oral

prednisolone 2mg/ kg/day in 2 divided doses for 4 weeks, taper w addition of aspirin as above

3. Anti failure: diuretics & ACE inhibitors

4. Anti streptococcal therapy: IV C.Penicillin 50 000 U/kg/dose 6H, give oral erythromycin if allergic to penicillin

5. Chorea: control w haloperidol or valproic acid, diazepam Secondary prophylaxis

 IM benzathine penicillin every 3 – 4 weeks (<30 kg – 0.6 mega unit, >30kg – 1.2mega unit)

 Oral penicillin 250 mg twice daily

 If allergic to penicillin give oral erythromycin 250mg twice daily

Duration of prophylaxis

 Until age of 21 or 5 years after last attack of ARF whichever was longer,

 Lifelong if got carditis or valvular involvement * The main symptoms of SC are believed to arise from an imbalance among the dopaminergic system, intrastriatal cholinergic system, and inhibitory gamma-aminobutyric acid (GABA) system. Evidence of this imbalance has been

suggested by the successful control of chorea by dopaminergic antagonists and valproic acid, a drug known to enhance GABA levels in the striatum and substantia nigra.

PHYSICAL EXAMINATION

General:

Fever, rashes, nodules, involuntary jerky movement, protruding of tongue revealed ‘bag of worm’

CVS:

Murmur, pericardial rub, cardiomegaly, sign of cardiac failure Examination of joints involved: red, swollen, warm, synovial aspiration revealed leukocytosis

To test for syndenham chorea:

- pronator sign when raising hand above head, if + pt may pronate 1 or both hand,spoon configuration occur when hand are extended, milking grip elicit by putting ur finger at pt grip hand

DDX - JRA - Leukemia - SLE

INVESTIGATION

1) FBC- leukocytosis, ESR/CRP – raised, throat swab 2) Anti-streptolysin O titre- >240 Todd U

3) Anti-DNAase B

4) Imaging : ECG, CXR, Echo- to look for carditis

5) Histo: Aschoff bodies in heart (granulomatous structures consisting of fibrinoid change, lymphocytic infiltration, occasional plasma cells, and abnormal macrophages surrounding necrotic centres)

Anitschkow cells are enlarged macrophages found within granulomas (called Aschoff bodies) associated with the disease. Ovoid nucleus and chromatin that is condensed toward the center of the nucleus in a wavy rod-like pattern

RHEUMATIC FEVER- d/t delayed immunologic rxtn of group A Beta hemolytic streptococcal infection of pharynx HISTORY

1 Required Criteria and 2 Major Criteria and 0 Minor Criteria 1 Required Criteria and 1 Major Criteria and 2 Minor Criteria Required criteria:

Evidence of antecedent Strep infection: ASO / Strep antibodies / Strep group A throat culture / Recent scarlet fever / anti-deoxyribonuclease B / anti-hyaluronidase

Major criteria (CASES)

 Carditis  Arthritis  Subcutaneous nodules  Erythema marginatum  Syndenham chorea Minor  Fever  Raised ESR/CRP  Arthralgia  Prolonged PR  Leukocytosis

 Previous Rheumatic Fever

Infective Endocarditis [Baisyatul] HISTORY Presenting complain

- Symptoms of systemic infection ( fever, malaise, anorexia, loss of weight, headache, myalgia, arthralgia)

- Congestive heart failure ( SOB, orthopnoea, PND, leg swelling)

- Emboli symptoms ( neurological deficit, haematuria, acute renal failure)

Predisposing factor:

- 50% occur in normal valve (acute IE) - Dental procedure

- Dermatitis - IVDU (subacute IE) - Prosthetic valve

- Chronic rheumatic valvular disease - Nosocomial infection (IV line) - Elderly

PHYSICAL EXAMINATION General examination

- Thin, poor nutrional status (anorexia) - Septic sign ( feverish, tachycardia) - Finger clubbing

- Splinter hemorrhage

- Osler’s node (tender nodules on finger pulp)

- Janeway lesion (non tender macule on palms or sole) - Pale conjunctiva, subconjuctival petechiae

- Dental hygiene Specific examination (chest)

- Changing cardiac murmur - Cardiac failure ( gallop rhythm ) - Pericardial rub

- TR/MR

- Lung crepitations (abdomen)

- splenomegaly (if emboli and cause abscess formation/ heart failure)

Complete examination by

- Fundoscopy to look for Roth’s spot (central pale area with surrounding)

- Urine dipstick to look for haematuria (microscopic) INVESTIGATION

For diagnosis: DUKE criteria

1. Blood investigations

- FBC (normocytic normochromic anemia, leucocytosis, high ESR and CRP)

- Blood culture n sensitivity ( 3 samples from different sites)

2. Urine FEME

- Microscopic haematuria 3. CXR (cardiomegaly)

4. ECG (prolonged PR interval, regular rhythm) 5. Echocardiography- transthoracic or transesophageal

(to look for vagetations)

*transesophageal more sensitive, better for visualizing mitral lesion

MANAGEMENT General management

- Asses ABC

- Heart failure management (oxygen, diuretics,monitor input output chart)

Antibiotic therapy

- Duration 2-4 weeks

- Empirical therapy: benzylpenicillin + gentamicin - Adjust according to culture

- Streptococci (as above)

- Staphylococci (cloxacillin or vancomycin + gentamicin)

Indication for surgery

- Persistent bacteremia or fever despite optimal antibiotic

- Extensive valve ring infection

- Prosthetic valve endocarditis esp staph aureus - Recurrent ep of systemic embolism