Wednesday, 7 July 2010
BOF
1-What is the mechanism of action of tacrolimus?
A.A Mercaptopurine antagonist
B.A Interferes with purine synthesis
C.A Inhibits inosine monophosphate dehydrogenase
D.A Monoclonal antibody against IL-2 receptor
E.A Decreases IL-2 release by inhibiting calcineurin
2-Which one of the following is least associated with thymomas?
A.A Syndrome inappropriate ADH
B.A Myasthenia gravis
C.A Red cell aplasia
D.A Dermatomyositis
E.A Motor neurone disease
3-Which one of the following statements is true regarding autosomal recessive polycystic kidney disease?ia
A.A Onset is typically in the third decade
B.A Liver involvement is rare
C.A Is due to a defect on chromosome 16
D.A More common than autosomal dominant polycystic kidney disease
E.A May be diagnosed on prenatal ultrasound
4-Each one of the following features is seen in phenylketonuria, except:
A.A Learning difficulties
B.A Seizures
C.A Eczema
D.A Recurrent infections
E.A 'Musty' urine
phenylalanine hydroxylase deficiency,AR, Guthrie test 5-9day after birth
5-Each one of the following predisposes to cataract formation, except:
A.A Down's syndrome
B.A Hypercalcaemia
C.A Diabetes mellitus
D.A Long-term steroid use
E.A Uveitis
6-Which one of the following causes of delayed puberty is associated with short stature?
A.A Klinefelter's syndrome
B.A Turner's syndrome
C.A Polycystic ovarian syndrome
D.A Androgen insensitivity
E.A Kallman's syndrome
7-Which of the following types of renal stones are said to have a semi-opaque appearance on x-ray?ia
A.A Calcium oxalate
B.A Cystine stones
C.A Urate stones
D.A Xanthine stones
E.A Triple phosphate stones
8-What is the most common clinical pattern seen in motor neuron disease?
A.A Progressive muscular atrophyia (best prognosis)
B.A Bulbar palsyia (worst prognosis)
C.A Spinocerebellar ataxia
D.A Relapsing-remitting
E.A Amyotrophic lateral sclerosis
9-Which one of the following is least recognised as a cause of clubbing?ia
A.A Grave's disease
B.A Empyema
C.A Cyanotic congenital heart disease
D.A Coeliac diseasei
E.A Cystic fibrosis
10-Which of the following congenital heart defects may progress to Eisenmenger's syndrome
A.A Tetralogy of Fallot
B.A Coarctation of the aorta
C.A Patent ductus arteriosus
D.A Tricuspid atresia
E.A Transposition of the great arteries
A.A Mercaptopurine antagonist
B.A Interferes with purine synthesis
C.A Inhibits inosine monophosphate dehydrogenase
D.A Monoclonal antibody against IL-2 receptor
E.A Decreases IL-2 release by inhibiting calcineurin
2-Which one of the following is least associated with thymomas?
A.A Syndrome inappropriate ADH
B.A Myasthenia gravis
C.A Red cell aplasia
D.A Dermatomyositis
E.A Motor neurone disease
3-Which one of the following statements is true regarding autosomal recessive polycystic kidney disease?ia
A.A Onset is typically in the third decade
B.A Liver involvement is rare
C.A Is due to a defect on chromosome 16
D.A More common than autosomal dominant polycystic kidney disease
E.A May be diagnosed on prenatal ultrasound
4-Each one of the following features is seen in phenylketonuria, except:
A.A Learning difficulties
B.A Seizures
C.A Eczema
D.A Recurrent infections
E.A 'Musty' urine
phenylalanine hydroxylase deficiency,AR, Guthrie test 5-9day after birth
5-Each one of the following predisposes to cataract formation, except:
A.A Down's syndrome
B.A Hypercalcaemia
C.A Diabetes mellitus
D.A Long-term steroid use
E.A Uveitis
6-Which one of the following causes of delayed puberty is associated with short stature?
A.A Klinefelter's syndrome
B.A Turner's syndrome
C.A Polycystic ovarian syndrome
D.A Androgen insensitivity
E.A Kallman's syndrome
7-Which of the following types of renal stones are said to have a semi-opaque appearance on x-ray?ia
A.A Calcium oxalate
B.A Cystine stones
C.A Urate stones
D.A Xanthine stones
E.A Triple phosphate stones
8-What is the most common clinical pattern seen in motor neuron disease?
A.A Progressive muscular atrophyia (best prognosis)
B.A Bulbar palsyia (worst prognosis)
C.A Spinocerebellar ataxia
D.A Relapsing-remitting
E.A Amyotrophic lateral sclerosis
9-Which one of the following is least recognised as a cause of clubbing?ia
A.A Grave's disease
B.A Empyema
C.A Cyanotic congenital heart disease
D.A Coeliac diseasei
E.A Cystic fibrosis
10-Which of the following congenital heart defects may progress to Eisenmenger's syndrome
A.A Tetralogy of Fallot
B.A Coarctation of the aorta
C.A Patent ductus arteriosus
D.A Tricuspid atresia
E.A Transposition of the great arteries
Wednesday, 16 June 2010
lung fibrosis
LUNG FIBROSIS >> Localized Systemic sclerosis, Sarcoidosis, Tuberculosis, Berylliosis and Asbestosis >>Diffuse Idiopathic lung fibrosis, Rheumatoid lung, Langerhans’ cell histiocytosis ( exclusive in smoker), Tuberous sclerosis, Neurofibromatosis
Idiopathic pulmonary fibrosis (IPF) , >> High-resolution CT scan (HRCT) 90% accurate in diagnosis. Bronchalveolar lavage > increase neutrophil and macrophage, ANA and RF +ve in 30%. Lung biopsy may needed to DD from othe causes
Pneumonia
Pneumonia:
- Hospitalized ‘ill’ patients –Gram negative organisms.
- Alcohol excess ass with aspiration pneumonia (anaerobes>> add metronidazol to antibiotic regimen) and klebsila ( upper lobe + gelatinous sputum).
- Immunosuppression (e.g. AIDS or treatment with cytotoxic agents) – organisms include Pneumocystis jiroveci, Mycobacterium avium-intracellulare,cytomegalovirus.
- Intravenous drug users (may be multiple abcesses in x ray)>> Staph. aureus infection, G+ve cocci. Chlamydia psittaci exposed to infected birds, especially parrots and has chronic course.
- Persistent changes on the chest X-ray after 6 weeks suggest a bronchial abnormality, usually a carcinoma. No improvement with copious sputum >> abscess and empyema.
- Diagnosis of L. pneumophila (shower in hotels) suggested by: a prodromal virus-like illness, a dry cough, confusion or diarrhea, lymphopenia without marked leucocytosis, hyponatraemia., Hypoalbuminaemia and high serum levels of liver aminotransferases. Urinary antigen test and confirmed by direct immunofluorescent staining of the organism. ttt Azithromycin + add rifampicine in sever case.
- CRUB-65 if =2 hospitals and if > 2 ICU
Monday, 7 June 2010
Endocarditis
Endocarditis (Fever, murmur, malaise and petechia or heamaturia)
A definite diagnosis of endocarditis (Duke's criteria) is achieved when 2 major criteria are present, or 1 major and 3 minor criterias. Major criteria: blood culture positive for typical organisms persistent bacteremia positive ECHO for vegetations abscess or valve dehiscence Minor criteria: valvular heart disease or IV drug user fever greater than 38°C vasculitis skin lesions suggestive ECHO (but not definite) positive blood culture
MC organism Strep.viridans, post prothetic valve operation is Staph epidermitis within 60 days is MC organism. IV drug user, pt. with prolonged vascular cath>> Staph. Aureau. genitourinary disease or procedures Enterococc . GIT malignancy, strep.bovis
One of the major dangers with aortic valve endocarditis is an aortic root abscess. This can lead to prolonging of the PR interval by erosion into the adjacent AV node, hence daily ECGs are useful for monitoring. Use CRP or plasma viscosity for monitoring
1st investigation of choice TTEho, but the investigation of choice specially prothetic valve TOE
Antibiotic: start with penicillin and gentamicin, vancomycin if staph. Suspected or penicillin allergy.after culture result, if strept continue with same antibiotic, if staph use flucxacillin or vancomycin + gentamicin. If enterococci use ampicillin + gentamicin
Fever persistant search cause, drug, Infection, pulmonary embolism or cardiac abcess formation
Patients at risk of endocarditis should beno antibiotic required unless the procedure in infective focus)
– Advised to maintain good oral hygiene
– Told how to recognize signs of infective endocarditis and advised when to seek expert advice
ECG
ECG manifestations of chamber enlargement:
A-Left atrial enlargement:
a. P wave duration equal or more than 0.12 sec.
b. Notched, slurred P wave in lead I and II (P mitrale).
c. Biphasic P wave in lead V1 wit ha wide ,deep and negative terminal component.
d. Mean P wav axis shifted to the left ( between +45 to – 30 degree ).
B-Right atrial enlargement:
a. P wave duration equal or less than 0.11 sec.
b. Tall, peaked T wave equal or more than 2.5 mm in amplitude in lead II,III or aVF (P pulmonale).
c. Mean P wave axis shifted to the right( more than +70 degree).
C-Left ventricular enlargement :
a. "Voltage criteria":
1-R or S wave in limb lead equal or more than 20mm
2-S wave in V1,V2 or V3 equal or more than 30mm
3-R wave in V4,V5 or V6 equal or more than 30mm.
b. Depressed ST segment with inverted T waves in lateral leads(strain pattern ;more reliable in the absence of digitalis therapy.
c. Left axis of -30 degree or more.
d. QRS duration equal or more than 0.09 sec.
e. Time of onset of the intrinsicoid deflection ( time from the beginning of the QRS to the peak of the R wave ) equal or more than 0.05 sec in lead V5 or V6.
D-Right ventricular enlargement :
a. Tall R waves over the right precordium and deep S waves over the left precordium ( R:S ratio in lead V1 > 1.0)
b. Normal QRS duration (if no bundle branch block)
c. Right axis deviation.
d. ST-T "strain" pattern over the right precordium.
e. Late intrinsicoid deflection in lead V1 or V2.
ECG manifestations of bundle branch block (BBB):
A-Left bundle branch block :
a. QRS duration equal or more than 0.12 sec.
b. Broad , notched or slurred R wave in lateral leads( I, aVL , V5,V6 )
c. QS or rS pattern in the anterior precordium.
d. Secondary ST-T wave changes ( ST and T wave vectors are opposite to the terminal QRS vectors).
e. Late intrinsicoid deflection in lead V5 and V6.
B-Right bundle branch block:
a. QRS duration equal or more than 0.12 sec.
b. Large R' wave in lead V1( rsR' ).
c. Deep terminal S wave in lead V6.
d. Normal septal Q wave.
e. Inverted T wave in lead V1 ( secondary T wave changes ).
f. Late intinsicoid deflection in lead V1 and V2.
ECG manifestations of fascicular blocks:
A-Left anterior fascicular block:
a. QRS duration equal or more than 0.10 sec.
b. Left axis deviation ( -45 degree or greater ).
c. rS pattern in lead II, III and aVF.
d. qR pattern in lead I and aVL.
B-Left posterior fascicular block:
a. QRS duration equal or more than 0.10 sec.
b. Right axis deviation ( +90 degree or greater ).
c. qR pattern in lead II,III ands aVF.
d. rS pattern in lead I and aVL.
e. Exclusion of other causes of right axis deviation ( COPD, RVH, lateral MI ).
Localization of myocardial infarction:
Infarct location Leads depicting primary ECG changes Likely vessel * involved
Inferior II,III,aVF RCA
Septal V1-V2 LAD
Anterior V3-V4 LAD
Antero-septal V1-V4 LAD
Extensiveanterior I,aVL,V1-V6 LAD
Lateral I,aVL,V5-V6 CIRC
High Lateral I, aVL CIRC
Posterior ** Prominent R in lead V1 RCA or CIRC
Right ventricular*** ST elevation in lead V1,and more specifically, V4R in the setting of inferior infarction RCA
*this is a simple generalization, variations occur.
** Usually in association with inferior or lateral infarctions.
***Usually in association with inferior infarctions.
Some observations on abnormal rhythms:
Remember: A slow regular ventricular rhythm might be due to :
1-Sinus bradycardia.
2-Complete AV block with idioventricualr rhythm.
3-Normal sinus rhythm with 2:1 AV block.
4-Normal sinus rhythm with 2:1 SA block (very rare).
5-Atrial flutter with high grade 4:1 AV block.
6-Sinus default with idionodal escape rhythm.
7-Sinus default with idioventricualr escape rhythm.
Remember: Causes of IRREGULAR ventricular rhythm:
1-Atrial fibrillation.
2-frequent and irregularly occurring atrial and or ventricular extrasystoles.
3-Atrial flutter with second degree AV blockand varying AV conduction ratios.
4-Paroxysmal atrial tachycardia with variable second degree AV block .
5-Marked respiratory sinus arrhythmia.
"SLOW' atrial fibrillation:
Slow atrial fibrillation usually reflects treatment with digitalis ; or in the absence of digitalis therapy , a structural nodal disease ( sick sinus syndrome ).A more correct description is " atrial fibrillation with slow or diminished ventricular response".
Remember: Common causes of bigeminal rhythm:
1-alternate ventricular extrasystoles( the commonest cause ).
2-alternate atrial or nodal extrasystoles.
3-any form of 3:2 AV block.
4-atrial flutter with alternating 4:1 and 2:1 AV block.
Remember: Absent P wave might be due to :
1-SA block.
2-Atrial fibrillation.
3-Severe hyperkalemia.
4-AV nodal rhythm ( the P wave might be hidden within the QRS complexes).
Remember: A long PAUSE interrupting a regular rhythm might be caused by:
1-a dropped beat as a result of 2nd degree AV block.
2-a dropped beat as a result of SA block.
3-a blocked or non conducted atrial extrasystole.
NB: extrasystoles occur PREMATURELY , escape beats occur LATE.
NB: when the PR interval becomes progressively shorter, AV dissociation is usually present.
Remember: Paroxysmal atrial rhythm (tachycardia, paroxysmal or flutter fibrillation ) in a young person without obvious evidence of cardiac disease rises the possibility of :
1-Thyrotoxicosis.
2-WPW syndrome.
3-Lone atrial fibrillation .
Remember: TALL symmetrical T waves in the precordial leads might be due to :
1-acute subendocardial ischemia , injury or infarction.
2-recovering inferior wall myocardial infarction.
3-hyperacute phase of anterior wall myocardial infarction.
4-Prinzmetal 's angina.
5-true posterior wall myocardial infarctions.
6-hyperkalemia.
Remember: Generalized LOW voltage might be due to :
1-incorrect standardization.
2-emphydema.
3-marked obesity or thick chest wall.
4-pericardial effusion.
5-myxedema.
6-hypopituitarism.
7-Cardiac Amyloid.
8-Severe cardiomyopathy
9-Global Myocardial iscehmia.
Remember: Acute rheumatic frequently associated with :
1-sinus tachycardia.
2-non paroxysmal AV nodal tachycardia( idionodal tachycardia).
3-prolonged PR interval.
4-2nd degree AV block .
5-prolonged QT interval.
NB: it is NEVER associated with 3rd degree AV block
Some ECG finding in heart diseases:
Mitral stenosis:
1-atrial fibrillation
2-RVH ,right axis deviation
3-P mitrale, P pulmonale
Mitral reflux:
1-P mitrale
2-atrial fibrillation
3-left ventricular "diastolic" overload
4-RVH, Right axis deviation.
Tricuspid stenosis:
1-VERY TALL right atrial P wave in standard lead II.
2-1st degree AV block
3-normal QRS axis
Hypertensive heart disease:
1-left atrial P wave
2-left ventricular "systolic " overload
Arrhythmias associated with HYPERthyroidism:
1-sinus tachycardia
2-atrial extrasystoles
3-paroxysmal atrial tachycardia
4-paroxysmal atrial flutter
5-paroxysmal atrial fibrillation
6-idionodal tachycardia
7-paroxysmal nodal tachycardia
NB: Ventricular rhythms are NOT usually associated with hyperthyroidism unless there is a cardiac DECOMPENSATION.
Pulmonic styenosis:
1-P congenitale
2-right ventricular systolic overload
3-right axis deviation
Tricuspid atresia:
1-left axis deviation
2-left ventricular dominance
NB: MOST cases of cyanotic congenital heart disease are associated with RIGHT ventricular dominance and RIGHT axis deviation ; tricuspid atresia is a notable exception .
Ebstein's anomaly:
1-TALL peaked P waves in standard lead II
2-RBBB with small amplitude QRS complexes
3-WPW syndrome type B, ie the QRS complex is negative in the right precordial leads
4-paroxysmal supra-ventricular tachycardia
Mirror image dextro-cardia:
1-Inverted P waves in standard lead I
2-all other deflections –QRS complex and T wave- are also negative in standard lead I.
2-This lead now resembles a normal lead aVR.
3-the normal appearances of standard leads II and lead III are interchanged .
4-the QRS complexes are tallest in the right precordial leads –V1 and V2- and diminished progressively towards the left.
Limb lead reversal:
This will manifest as a mirror image dextro-cardia but the precordial lead complexes are NORMAL.
Anomalous left coronary artery:
When the left coronary artery arises from the pulmonary artery ,the ECG reflects the pattern of ANTERO-LATERAL myocardial infarction, viz pathological q waves, raised coved ST segments and inverted T waves in standard lead I and aVL and the left precordial leads.
Causes of SA block:
SA block is a rare ECG finding and might be caused ny:
1-marked sinus bradycardia
2-marked sinus arrhythmia
3-highly trained young athletes
4-digitalis toxixity
5-ureamia
6-hypokalemia
7-sick sinus syndrome
1st degree AV block is associated with:
1-coronary artery disease
2-acute rheumatic carditis
3-Beta blockers
4-digitalis
5-cardiomyopathy
Small intestin
• Iron and Ca absorbed from proximal Small intestine but B12 absorbed from ileum and need intrinsic factor that secreted from funds of stomach
• Coeliac disease: investigation of choice endoscopy and biopsy from prx.Small intestine (never diagnose it without biopsy) >> increase interaepithilium lymphocyte, subtotal villous atrophy and absence of Small intestine folds.
• Coeliac disease Screening by antiendomyseal Ab and anti tissue transglutiminase antibodies also used for follow up and evaluation of ttt. HLA-DQ2 in 90% and can used for rule out the diagnosis of coeliac disease if no response to ttt.
• Coeliac disease Iron and folate deficiency so there is macro and micro RBCs in blood film and MCV can be N/low or high
• Coeliac disease, Spleen atrophy what u will do for? Also DXA should do even in ttt as osteoporosis ass with it and dosent decrease with ttt
GIT bleeding
• Upper GIT bleeding: finding ass with high risk of bleeing are>> endoscopic adherent clot (black), Blood in stomach or duodenum and high Rockall score. Do urgent endoscopy if patient in shock, continuing bleeding And Suspect varices.
• In bleeding ulcer do 2 from the following: adrenalin injection, thermal coagulation,laser or clipping
• Omepral decrese rebleeding and need of surgery.triplressin decrease mortality in varicealk bleeding
• Varices prophylactic : BB (cost effective) or banding (better)
• Iron deficiency anemia d2 GIT> hoock worm (stool analysis) or chronic bleeding (upper then lower endoscopy then capsule endoscopy then celiac and mesenteric angio)
• Lowe GIT bleeding investigation>> proctoscopy> flexible sigmiodoscopy> colonoscopy> angiography
GIT 2 stomach
• PU>> do endoscopy (age>55 ys or progressive course) and H.pylori test> If DU medical ttt for 2 month and don’t repeat endoscopy unless still symptomatic or there was perforation in 1st endoscopy. If GU u have to take biopsy and repeat endoscopy
• ZES: multiple PU in stomach, duodenum and jejunum. High gastrin, CT abd. ttt by high dose PPI
• H.pylori: Ass. With PU, Gastric adenocarcinoma and gastric lymphoma (ttt by PPI in 1st stages) for screening>> rapid urea breath test (best), or serum IgG. For diagnosis stool antigens for it (patient off PPI for 2 ws), Biopsy (urea test, histopathology and culture)
GIT 1
GIT notes
• Dyspepsia (upper GIT symptoms) + alarm symptoms >> do upper GIT endoscopy
• Alarm symptoms: Anorexia, Dysphagia, heamatemsis or Melina, sever vomiting, Abdominal pain or unexplained iron deficiency anemia
• Vomiting don’t forget Drug causes, increase ICT, MI and pneumonia
• Oral whit patches>> Candida (HIV, Steroids), Leucoplekia (take biopsy) and Lichen planus (precancerous)
• Gum swelling: Drugs (nifidipin, phyntoin and ciclosporn), pregnancy, Vit C deficiency, infection and acute leukemia
• Oral pigmentation>> peutz-Jegher syn. (AD), Addisons disease, ant malaria drugs and bithmus
• Parotid enlargement >> Bilateral in Sarcoidosis, Lymphoma and alcohol. Unilateral in tumors
• GERD: if no alarm symptoms try PPI >> No improvement do Endoscopy and PH monitoring. Before surgery u should do PH monitoring and Manomertry to exclude motility disorders (Scleroderma). DD misdiagnosis of uncontrolled asthma
• Barretes esophagus: d2 long standing GERD, Squamous cell replaced by columner cells, premalignant 30-50x, Central Obesity increase its malignancy
• Achalasia: Investigation of choice is esophageal manometry (noncontractil LOS and Poor peristalsis in the wall of esophagus), But UGIT endoscopy is mandatory
• Esophageal tumor sq.cc > adeno.c
COPD
- COPD: smoking, pollution and alph 1 antitrypsin deficiency (under 40ys, basal emphysema). Usually clinical diagnosis, PFT with no or limited <15% reversibility
- In moderate to sever COPD Prednisolone trial should be done: 30 mg daily should be given for 2 weeks, with measurements of lung function before and after the treatment period. If FEV1 increase > 15%, prednisolone should be discontinued and replaced by inhaled corticosteroids.
Long-term continuous domiciliary oxygen therapy will benefit patients who have:
A Pao2 of < 7.3 kPa (55 mmHg) when breathing air. Measurements should be taken on two occasions at least 3 weeks apart after appropriate bronchodilator therapy or
A Pao2 7.3–8 kPa with secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or evidence of pulmonary hypertension.and
Carboxyhaemoglobin of less than 3% (i.e. patients who have stopped smoking).
LTOT for 15h/day decrease Pulmonary pressure, 19h/day improve survival
- COPD Surgery, Some patients with large emphysematous bullae can benefit from bullectomy, selected patients with severe COPD (FEV1 < 1 L) may benefit from lung volume reduction surgery.
- Obstructive sleep apnea syndrome: The Epworth Sleepiness Scale then confirmed by oximetry and polysomnographic studies> The diagnosis of sleep apnoea/hypopnoea is confirmed if there are more than 10–15 apnoeas or hypopnoeas in any 1 hour of sleep. Management consists of correction of treatable factors, if necessary, nasal continuous positive airway pressure (CPAP) delivered by a nasal mask during sleep
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