DANIL HAMMOUDI, MD

 

DANIL HAMMOUDI, MD                          

SINOE MEDICAL ASSOCIATION

2/1/04

USMLE GENERAL QUESTION ANSWERS FOR STEP 1 AND 2

CARDIOLOGY

 

 

1.        NON OPERATIVE THERAPY OF PATENT DUCTUS ARTERIOSUS IS BY INHIBITION OF:

***PROSTAGALANDIN E1

2.        ASYMPTOMATIC PATIENTS WITH PATENT DUCTUS ARTERIOSUS SHOULD HAVE LIGATION :

***BY AGE 4-5 YEARS

3.        THE HIGHEST OVERALL OPERATIVE MORTALITY IS IN :

***TRICUSPID VALVE REPLACEMENT

4.        THE MOST COMMONLY USED PROCEDURE IN THE OPERATIVE TRT OF CORONARY ARTERY OCCLUSIVE DISEASE IS:

***AUTOGENOUS SAPHENOUS VEIN AORTO-CORONARY BYPASS

 

5.        FACTORS ASSOCIATED WITH POOR PROGNOSIS IN CORONARY ARTERY DISEASE:

***SEX [ERLER HIGH IN FEMALE]

***ADVANCED AGE

***POOR LEFT VENTRICULAR FUNCTION

***DIFFUSE CORONARY DISEASE

***ADVANCE FUNCTIONAL STATUS

***SERIOUS ASSOCIATED DISEASE

***HIGH LEFT VENTRICULAR END DIASTOLIC PRESSURE

***PRIOR CONGESTIVE HEART FAILURE

***MYOCARDIAL INFARCTION WITHIN 1 WEEK PRIOR TO OPERATION

***STENOSIS OF LEFT MAIN CORONARY VESSEL

 

6.        ETIOLOGY OF CORONARY  ARTERY DISEASE:

***ATHEROSCLEROSIS [COMMONEST CAUSE OF DEATH IN USA]

***UNCOMMON CAUSE :

a.        +++VASCULARITIS [OCCURING WITH COLLAGEN VASCULAR DISORDER]

b.       +++RADIATION INJURY

c.        +++TRAUMA

 

 

1.        RISK FACTORS FOR CORONARY ARTERY DISEASE:

***HTA

***SMOKING

***HYPERCHOLESTEROLEMIA

                              ***FAMILY HISTORY OF HEART DISEASE

***DIABETES

***OBESITY

2.        PATHOPHYSIOLOGIC EFFECTS OF ISCHEMIC CORONARY ARTERY DISEASE ON THE MYOCARDIUM INCLUDE:

***DECREASE VENTRICULAR COMPLIANCE

***DECREASE CARDIAC CONTRACTILITY

***MYOCARDIAL NECROSIS

CLINICAL PRESENTATION :

***ANGINA PECTORIS

***MYOCARDIAL INFARCTION

***CONGESTIVE HEART FAILURE

***SUDDEN DEATH.

3.        THE MOST SERIOUS THREAT [SIGNAL] TO LIFE IN ADULTS WITH CONGENITAL HEART DISEASE IS:

*** SUBACUTE BACTERIAL ENDOCARDITIS

 

4.        THE USUAL TRT OF VENTRICULAR SEPTAL DEFECT IN INFANTS:

***MEDICAL

VSD [ventricular septal defect ] often regress and close spontaeously.

 

5.        THE INTRINSIC CLOTTING [COAGULATE] SYSTEM IS TRIGGERED BY ACTIVATION OF FACTOR :

***XII

BLEEDING DISORDERS

CAUSED BY VESSELS WALL ABNORMALITIES

 

 

 

RELATED TO REDUCED PLATELET NUMBER: THROMBOCYTOPENIA

 

·         IDIOPATHIC THROMBOCYTOPENIC PURPURA [IPT]

·         ACUTE IDIOPATHIC THROMBOCYTOPENIC PURPURA

·         DRUG INDUCED THROMBOCYTOPENIA

·         HIV-ASSOCIATED THROMBOCYTOPENIA

 

 

THROMBOTIC

·         MICROANGIPATHIES THROMBOTIC

·         THROMBOPENIC

·         PURPURA AND HEMOLYTIC UREMIC SYNDROME

 

 

RELATED TO DEFECTIVE PLATELET FUNCTIONS

 

 

HEMORRAGIC DIATHESES RELATED TO ABNORMALITIES IN CLOTTING FACTORS

·         DEFICIENCY IN FACTOR VIII- Vvw COMPLEX

·         VON WILLEBRAND DISEASE

·         HEMOPHILIA A [FACTOR VIII DEFICIENCY]

·         HEMOPHILIA B [CHRISTMAS DISEASE, FACTOR IX DEFICIENCY]

 

 

DISSEMINATED INTRACASCULAR COAGULATION [DIC].

BLEEDING DISORDERS

 

Bleeding disorders

Description and causes

Presentation

 

 

o        family history of bleeding after minor surgical procedures, dental procedures, childbirth, or other trauma

o        Can be an isolated event bleeding episodes

o        medications that can cause a bleeding problem

1.         semisynthetic penicillins,

2.         cephalosporins,

3.         dipyridamole,

4.        thiazides,

5.         alcohol,

6.         quinidine,

7.        chlorpromazine,

8.        sulfonamides,

9.         INH,

10.      rifampin,

11.      methyldopa,

12.      phenytoin,

13.     barbiturates,

14.      warfarin,

15.     heparin,

16.      thrombolytic agents,

17.      NSAIDs

18.      ASA,

19.      diuretics,

20.      allopurinol,

21.     TMP/SMX.

o        capillary bleeding and fragility.

22.     Cushing syndrome

23.      Marfan's syndrome.

24.     senile purpura,"

25.      petechiae secondary to coughing,

26.     sneezing,

27.     Valsalva maneuver, blood pressure measurement, vasculitis ("palpable purpura"), scurvy (vitamin C deficiency), or exogenous steroids.

o        Telangiectasias are suggestive of Osler-Weber-Rendu syndrome.

 

 

Differentiation of Platelet Versus Coagulation Defect

.

1.        Platelet defects.

2.        Generally have immediate onset of bleeding after trauma.

3.        Bleeding is predominantly in :

4.        skin,

5.        mucous membranes,

6.        nose,

7.        GI

8.         urinary tracts.

9.        Bleeding may be observed as:

10.      petechiae (<3 mm)

11.      ecchymoses (>3 mm).

12.      Must differentiate from vasculitic "palpable purpura."

13.     Coagulation system defects.

14.     "Deep" bleeding (in the joint spaces, muscles' and retroperitoneal spaces) is common.

15.     Observed on exam as hematomas and hemarthroses

 

1.        Bleeding caused by qualitative platelet disorders.

i.    Von Willebrand's disease.

ii.    Defective aggregation.

iii.    Defective activation or secretion

1.        Bleeding caused by quantitative platelet disorders.

i.    Thrombocytosis

ii.    Thrombocytopenia.

iii.    Idiopathic thrombocytopenic purpura (ITP).

iv.    Disseminated intravascular coagulation (DIC).

1.        Bleeding caused by defects of the intrinsic pathway.

i.    Products available for factor replacement.

·         Fresh frozen plasma

·         Cryoprecipitate

·         Factor VIII concentrate.

·         Genetically engineered factor VIII

·         Prothrombin complex concentration.

ii.    Hemophilia A. Deficiency of factor VIII

iii.    Hemophilia B

iv.    Factor XI deficiency.

1.        Bleeding caused by defects of the extrinsic and common pathway.

i.    Hepatocellular insufficiency

ii.    Vitamin K deficiency

iii.    Coumarin anticoagulants.

1.        Bleeding caused by vascular defects.

2.        Paraproteinemias.

3.         Cryoglobulinemia,

4.        macroglobulinemia,

5.        myeloma.

6.        Thrombotic thrombocytopenic purpura

a.        Hemolytic uremic syndrome.

b.       Henoch-Schönlein purpura.

c.        Causes of vascular defects include:

i.     SLE,

ii.     rheumatoid arthritis,

iii.    Sjögren syndrome,

iv.     Amyloidosis

a.        Bleeding caused by heparin.

 

Differentiation of Platelet Versus Coagulation Defect  

Bleeding can be attributable to either platelet problems or coagulation defects.

.Platelet defects.

1.        immediate onset of bleeding after trauma.

2.        Bleeding is predominantly in:

i.    skin,

ii.    mucous membranes,

iii.     nose, GI

iv.     urinary tracts.

1.        Bleeding may be observed as:

·         petechiae (<3 mm)

·          ecchymoses (>3 mm).

·          Must differentiate from vasculitic "palpable purpura."

Coagulation system defects.

 "Deep" bleeding in:

·         the joint spaces,

·         muscles'

·         retroperitoneal spaces.

 

 Observed on exam as hematomas and hemarthroses.

 

 

 

Differential Diagnosis of Abnormal Bleeding

 

Bleeding caused by qualitative platelet disorders.

Von Willebrand's disease.

Defective aggregation.

Defective activation or secretion.

·         Most common hereditary coagulation disorder.

·         Autosomal dominant.

·         Abnormal synthesis of von Willebrand's factor (vWf) causing decreased platelet adhesion and decreased serum levels of factor VIII:C (vWf is carrier for factor VIII:C).

·         Type I is absent vWf; type II is abnormal, nonfunctional vWf.

 

rare

1.        Ingestion of aspirin or NSAIDs.

2.        High-dose penicillin.

3.        Storage pool defects. Vary rare. The platelet's are activated but secrete "inactive" granules, that is, gray platelet syndrome and dense granule deficiency syndrome.

4.        Can treat these with platelet transfusion

 

Bleeding caused by quantitative platelet disorders.

 

Thrombocytosis

Thrombocytopenia.

Idiopathic thrombocytopenic purpura (ITP).

Disseminated intravascular coagulation (DIC).

Occurs in:

 

v      myeloproliferative disease

 

v      polycythemia vera,

v      myeloid metaplasia with myelofibrosis,

v      essential thrombocytosis).

 

 

In these states platelets are often poorly functioning with abnormal aggregation leading to a bleeding disorder.

 

The platelets in those with a reactive thrombocytosis (such as cancer, inflammation) function well.

Causes include:

v      decreased production,

v      increased splenic sequestration,

v      increased platelet destruction.

v      Consider also HELLP syndrome and preeclampsia in pregnant females.

 

 

a.Decreased production can be caused by:

Marrow aplasia.

 Infiltration secondary to malignancy or fibrosis.

 vitamin deficiency.

Diagnose by bone marrow biopsy.

 

 

Multiple drugs including :

 

ethanol,

estrogens,

 thiazides,

 cytotoxic drugs (cytosine arabinoside, daunorubicin, cyclophosphamide, busulfan, methotrexate, 6-mercaptopurine, .).

 

 

1.        Infectious causes including

 

sepsis,

AIDS,

 EBV,

ehrlichiosis,

Colorado tick fever,

Rocky Mountain spotted fever, babesiosis,

malaria, .

 

2.        Increased sequestration in spleen secondary to portal HTN

secondary to cirrhosis),

 

myeloproliferative disease.

 

 

b.Increased platelet destruction caused by:

3.        Immunologic destruction.

 

After bacterial or viral infections,

 

 drugs (sulfonamides, quinidine, INH, sedative or hypnotics, chlorpromazine, digoxin, methyldopa, heparin),

 

idiopathic thrombocytopenic purpura (ITP).

 

 

4.        Nonimmunologic destruction

 

. Vasculitis,

 DIC,

 thrombotic thrombocytopenic purpura (TTP),

 hemolytic uremic syndrome (HUS),  prosthetic heart valves.

 

Antibodies form against platelets.

Frequently preceded by:

v