Oral cardiology

HF
1. What is the most common cause of left ventricular failure?
- CAD
- systemic hypertension

2. What is the most common cause of RVF?
- LVF
- pulmonary disease

3. Which one leads to decrease C.O.P? LVF or RVF?
- Both LVF and RVF leads to decreased C.O.P., patient with left ventricular failure  ex: decreased
C.O.P and was controlled, but sudden pulmonary embolism  decrease blood flow to right ventricle 
decrease BL in lungs decrease blood in LV  decrease C.O.P

4. In which case there is decreased HR with HF?
- In patient who take digitalis or B blockers

5. Renin secreted only from kidney during:
- 1) Ischemia
- 2) hypoxia
- 3) renal disease

6. Kidney is endocrinal organ secretes :
- rennin -erythropoeitin - metabolites of vit D

7. Heart is endocrinal organ also secretes:
- Atrial natrueritic peptide (ANP) - BNP

8. S3 gallop ‫?امتى هنسمعه‬
a) ‫ دم طبيعى على عضله ضعيفه‬HF
b) ‫دم كتير على عضله كويسه‬ volume overloads (hyperdynamic circulation & MR)
NB: a & b must be with increased HR

9. Causes of enlarged tender liver?
- Congestion
- inflammation
- malignancy
- fatty liver (may be tender or not)

10.Causes of (tissues need more increase CO) :
a) General causes: (irrespective of causes of hyperdynamic circulation)  decreased transient time
( time of exchange of blood with tissue) due to quick circulation

b) Specific cause:
• Thyrotoxicosis  increase metabolites, increase needs of body
• anemic: decrease quality of HB of the blood

11.why increased velocity and blood flow in :
a) Anemia:
1. decreased HB-decrease velocity-increase blood flow
2. decreased O2-hypoxia which is anaerobic-increased lactate, pyruvate-VD decrease
peripheral resistance increase blood flow

Oral Questions & Answers of Cardiology Page 1

b) A-V fistula: this fistula leads to bypass the resistance (between artery & vein) so there is shorter and
faster circulation

 Types of A-V fistula?
• Congenital
• Acquired
o traumatic accidental :injury during surgery
o Iatrogenic: intentionalchronic renal failure to increase venous pressure in dialysis.

Rheumatic fever
1. R .F is a cause of :
- Polyarthritis
- Polyserositis

2. What are the diseases which cause Aschoff nodules?
- R.F
- T.B  Granuloma
 Caseous at center
- Sarcoidosis ( non caseating granuloma )

3. How to differentiate between arthritis and arthralgia?
- In arthritis there is LIMITATION OF THE MOVEMENT.

4. What is the only major criteria may be as asymptomatic?
- Carditis.

5. Which comes 1st as a result of endocarditis in R.F, mitral stenosis or
regurge ?
- M.R as it can occur by damage which is very quick.

6. What are medical causes of acute abdomen?
- R.F
- Aseptic
- Diabetic
- Hemolytic crisis
- Familial meditterian fever
- Pleurisy

7. What are the nodules which may be on shin of tibia?
- T.B
- Streptococcal infection
- Sarcoidosis
- Sulfonamide

8. What are conditions in which acute phase reactants are increased?


(ESR – CPR – leukocytosis)
- Tissue inflammation
- Tissue damage
So, it is non specific, used for follow up & diagnosis

9. What are other acute phase reactants?
Hepatoglobin, ferritin, transferrin, fibrinogen.

10.What are the diseases which present with subcutaneous nodules?
- Rheumatoid arthritis (commonest) than:
- Rheumatic fever

11.What are the skin manifestations of R.F?
- Major: erythema marginatum - S.C nodule.
- Minor: erythema nodosum

12.Elevated ESR in ….
- Inflammation
- Malignancy
- Anemia

13.Most common cause of very high ESR is : T.B , malignancy

14.Decreased ESR in ….. :
- Polycythemia
- Cryoglobulinemia

15.What are the causes of anemia in R.F?
- Due to anemia of chronic disease (ACD) also in:
- Chronic infection, chronic inflammation & malignancy.

16.Why in ttt of R.F, cortisol is withdrawn gradually?
- To avoid acute adrenal insufficiency (Addison disease) which may lead to shock  death.

17.What are other drugs which shouldn't stop suddenly?
- Antiepileptics
- Anticoagulants  rebound thrombosis.

18.Causes of clubbing?
- Toxic
- Hypoxic
- Non toxic, non hypoxic in bronchogenic carcinoma

19.Mechanism of embolic hemiplegia and subarachnoid hemorrhage
infective endocarditis?
- Embolic hemiplegia: stroke, is due to acute injury of brain (frontal lobe) due to thrombosis rupture of
blood vessels.
- Subarachnoid hemorrhage: is due to rupture of mycotic cerebral aneurysm.

20. Mention some diseases having double etiology? = (diseases where
infection predispose to autoimmune disease?)
- Rheumatic fever
- Immuno thrombocytopenic purpura (ITP)

- Henoch Schnolien purpura
- Post streptococcal glomerulonephritis
- Guillian baree syndrome ( antibodies against myelin sheath of peripheral nerves  PN)
- Diabetes ( type I diabetes)

21.Mention the site of affection in CNS in rheumatic fever?
- Basal ganglia

22.Why does myocarditis cause arrhythmia?
- Because
1) Inflammatory increase the excitability of normal cells turning it into autonomic focus
2) Myocarditis cause cardiac enlargement as a compensatory mechanism and this enlargement
cause stretch and stretch also excitability causing arrhythmia
3) Inflammatory blocks a-v node causing delay in conduction causing arrhythmia

23. Why does myocarditis cause tachycardia disproportionate to the degree
of fever?
- Because myocarditis cause impending heart failure and tachycardia is a compensatory mechanism in
case of heart failure so tachycardia in this case is not related to fever

24. Why does myocarditis cause tc-tac rhythm?
- Due to loss of muscular component of S1 (ventricular contraction which becomes very weak ) so S1
becomes similar to S2 which lacks the muscular component

25.What are the functional murmurs occurring in case of myocarditis?
- Mitral regurge and tricuspid regurge due to ventricular dilatation

26. Why doesn’t constrictive pericarditis occur with rheumatic fever?
- Because inflammation of serous tissues e.g. pericardium is the exudative type that resolves
completely without fibrosis

27. Define acute phase reactants?
- They are substances that increase in blood in acute conditions e.g. inflammation and tissue damage
they can be also called inflammatory markers these reactants are leukocytosis , positive crp , high
erythrocyte sedimentation rate

28. Causes of erythema nodosum?
- TB
- Streptococcal infection
- Sulphonamides
- Sarcoidosis

29. What is the difference between erythema nodosum and erythema
marginatum?
- Erythema nodusm (Painful - Appear at chin of tibia)
- Erythema marginatum (Painless - Trunk and proximal extremities)

30. Mention causes of anemia?
- Anemia of chronic disease
- Toxic inhibition of bone marrow

31. What are chronic conditions that can cause anemia?
- 1-chronic inflammation e.g. rheumatic fever


- 2-chronic infection
- 3-malignancy

32. Mention some drugs that if the patient stop them suddenly death
occurs?
- Cortisol “cortisone"
- Anti epileptic drugs
- Anti coagulants

33. Why do we withdraw cortisone gradually?
- For fear of Addisonian crisis which may cause death
- Its mechanism: cortex release cortisol in response to "ACTH"adrenocorticotrophic hormone which
released from antipituitary so when we use exogenous cortisol it cause -ve feed back inhibition that
stops formation of endogenous cortisol so if you suddenly stop the cortisone treatment there will be
no cortisol in the body so we have to break the inhibition gradually by gradual withdrawal

34.How can we be sure that the gland is active again producing
endogenous cortisol?

- To ensure the gland activity we give the patient 2 shots of ACTH at the 8th weak in the last week of
gradual withdrawal of cortisone "8th weak"

35.IF we gave cortisol for less than 2 weeks is gradually withdrawal
important measure?
- Gradual withdrawal won`t be important measure in this case as inhibition of the cortex doesn`t occur
before 2 weeks but there will be no harm if you stopped the cortisone gradually

Infective
endocarditis
1. Causes of enlarged tender spleen?
- I.E " only cause in cardiology "
- Typhoid
- Brucella
- Infectious mononucleosis
- Malaria
- Viral hepatitis
- Septicemia
- Splenic abscess
- Chronic myeloid leukemia

2. What are the possibilities in which blood culture become –ve in I.E?
- Prior use of antibiotics
- Infection with other organism ( fungi and rickettsia )

3. What is the most important investigation in I.E?
- Echocardiography especially transesophageal echo as it can detect small vegetations.

4. Define acute endocarditis?


- Its bacterial infection affecting normal heart. It is very rare and severe case.

5. Why are valvular lesion and prosthetic valves considered parts of
etiology of infective endocarditis?
- Because injury of the valve or prosthetic valve makes the valve surface rough so vegetations can
easily adhere to it.

6. Why infective endocarditis is rare in heart failure and atrial
fibrillation?
- Because infective endocarditis needs a high pressure gradient and in these 2 conditions myocardial
contractility is impaired and there is decrease in turbulence of blood so there is no high pressure
gradient.
7. Why infective endocarditis is more common in small VSD than big VSD?
- Because small VSD cause more turbulence of blood as blood passes through a very narrow orifice.

8. Why infective endocarditis is more common in left side valves than
right side valves?
- Because pressure is higher in left side of the heart.

9. Why does infective endocarditis aggravate heart failure?
- As it increases the tissue needs due to exaggerated metabolism with infection.
- And because of the valvular damage.

10.Why does it cause anemia?
- Due to toxic inhibition of bone marrow.

11. Explain the etiology of ROTH SPOTS with infective endocarditis?
- It is oval hemorrhages + pale center in the retina. It is caused by deposition of immune complex in
retinal vessels damaging it. The pale centre is infracted area of the retina and the red is hemorrhage.

12.Explain the cause of OSLER’S nodules?
- Toxic hyperplasia of the capillary endothelium this is caused by inflammation and deposition of the
immune complex that cause release of growth factors that cause proliferation of smooth muscle s in
the wall of the capillaries.

13.Mention the cause of endocarditis in intravenous drug abusers ?
special form of inf. Endocarditis?
- As they use unsterile water to take the injection through the vein so it passes to the right side of the
heart causing affection of the tricuspid valve.

14.Why is fungal endocarditis of bad prognosis?
- Because fungal infection usually don’t attack anyone except the immune suppressed.

Ischemic heart
disease
How can Anemia cause ischemic heart disease?
- Through double etiology
a) Decrease the quality of coronary blood.

b) Increase myocardial oxygen demand (hyperdynamic circulation).

Atherosclerosi
1. Is Vitamin B deficiency a risk factor for atherosclerosis?
- Vitamins B6, B9 & B12 are needed for the breakdown of homocystein. So deficiency of these
vitamins + + homocystein in blood homocysteinemia, which is a risk factor for atherosclerosis.
- ttt: multivitamin B

2. What are the foam cells?
- Macrophages engulfing oxidized LDL.

3. What are the substances produced by endothelium?
- Endothelins
- PAF
- Endothelial derived cofactor.
- Growth factor : secreted due to injury of endothelium by foam cells :
a) Smooth muscles proliferation
b) Fibrous cap.

4. What are the investigations which determine stages of
atherosclerosis?
- Multislice CT scan
- Intravascular u/s ( IVUS )
- By determining the thickening of the fibrous cap.

5. What are the factors which accelerate formation of thrombus during
plaque rupture?
- collagen
- tissue factor

Angina

1. What are the types of angina?
- Stable – classic
- Unstable
- Variant

2. Can angiography show normal coronaries in some cases of angina? yes
- In variant angina: may occur due to spasm in a normal artery
- In angina due to Vasculitis e.g. PAN, SLE

3. When are ‘exercise ECG’ +ve for myocardial ischemia? And when is it a
strong +ve test?

- Its +ve for myocardial ischemia if:
a) Typical anginal pain occurs
b) ST segment depression occurs
c) Ventricular arrhythmia occurs

- And it is a strong +ve test, if all 3 findings above are +ve.

4. What are the contraindications of Exercise ECG?
- Significant aortic stenosis (syncope)
- Severe hypertension
- Congestive heart failure (ttt is rest)
- Unstable angina and recent myocardial infarction.

5. What are the indications of cardiac catheterization & coronary
angiography?
- Angina not responding to medical ttt (most probably, will be indicated for revascularization, also to
assess condition of coronaries)
- Angina indicated for coronary revascularization (pre-operative)
- Angina which is unstable, variant or post-infarction (need to assess the condition of the rest of the
coronaries)
- Angina with a strong +e ex. ECG test
- Recurrent chest pain of unknown etiology
- Refractory ventricular arrhythmia (could be caused by ischemia)

6. What are the complications of catheterization?
- Myocardial infarction (injury of a coronary)
- Arrhythmia
- Embolization (mobilization of an atheroma)
- Arterial dissection

7. What are the benefits of regular exercise?
- Decreases heart rate, blood pressure & myocardial O2 demand (better cardiac reserve)
- Improves collateral blood flow
- Improves lipid profile
- ↓ platelets aggregation, ↑ fibrinolytic activity

8. Do calcium channel blockers cause tachycardia? Or bradycardia?
- Verapamil & Diltiazem: bradycardia (inhibition of conduction in AVN
- Nifedipine: Tachycardia (reflex due to severe hypotension –Mareys law)

9. What is the ergonovine provocative test?
- Ergonovine is α adrenergic stimulant ( VC )
- In variant angina  increased V.C. ??????? to anginal pain

10. What are the uses of B blockers?
- HF
- MVP
- Fallot
- Angina
- HTN
- Arrhythmia


11. How to avoid side effects of nitrates in ttt of CAD?
- Use the smallest effective dose.
- allow nitrates – free intervals ( ≈ 8 hrs )

12.What is the choice of drug therapy in ttt of CAD?
- begins with nitrates , if there is poor response then :
- for stable angina  add BB or CCB to nitrates
- for recurrent on 2 drug therapy  triple therapy
- for variant  add CCB to nitrates
- For unstable angina heparin and aspirin are the most important.

13. What are the indications of revascularization in CAD?
- I – GENERAL : a- angina not responding to medical ttt
b- Post infarction angina
- II – SPECIFIC : a- PTCA and stent :
i. Stenosis of 1 or 2 vessels only except left main coronary artery.
ii. stenosis of bypass graft after CABG
b- CABG:
i. Stenosis of 3 or more vs.
ii. Stenosis of left main coronary artery

14. What is the decapitated blood pressure?
- Marked drop of SBP with slight drop in DBP in MI

Myocardial
infarction
15. Cause of sudden death in M. I?
- VF , rupture of soft myocardium and occlusion of left main C.A

16.What are the causes of tall peaked T wave ?
- Hyperkalemia
- Early MI

17. Mention diseases that flare up in the morning?
- Bronchial asthma
- Infarction

18.Why are symptoms of myocardial infarction usually present in the
early morning?
- Because it is related to catecholamines and cortisol. And the level of both increases at the morning.

19. Mention the role of catecholamines and cortisol and increased
platelet aggregation in the etiology of the symptoms of AMI?
- Catecholamines produce vasoconstriction……increase afterload…….increase demand.
- Cortisol causes salt and water retention……hypervolemia that increases the preload.
- Platelet aggregation is produced by catecholamine that’s why it increases in the morning.


20. When do we use corticosteroids in ttt in infarction?
- In post cardiotomy syndrome (anti inflammatory + Immunosuppressed)
- Frozen shoulder syndrome(anti fibrotic)

21. Describe the etiology of frozen shoulder syndrome?
- Pain stimulating sympathetic leading to spasm in arterioles of the shoulder or arm leading to
ischemia which reduce release of
a- Free radicals
b- Growth factors
 Which stimulate fibroblasts present in the ligaments of the joints causing fibrosis.

22. Mention use of cortisone in cardiology?
- Non –cardiogenic pulmonary edema
- Angioneuretic edema
- ttt of rheumatic fever
- Post cardiotomy syndrome in infarction
- Frozen shoulder syndrome in infarction

23. Does pathological Q wave of ECG disappear with treatment?
- Usually it persist after treatment

24. Mention another name for non –transmural myocardial infarction?
- Non-transmural ST elevation myocardial infarction
- "NSTEMI"
- And it`s old name was subendocardial infarction

25. Why Troponin I is more specific than Troponin T?
- Because Troponin T can arise from skeletal muscles while Troponin I is specific to cardiac muscle

26. By using leads of ECG how can u detect the anatomical site of AHI?

-anterior infarction if ECG changes in lead v1-v6
-inferior infarction if ECG changes in v2 v3avf
lateral infarction if ECG changes in I1avl v5 v6

27. Why is old age considered as bad prognostic criteria of AMI?
- As patient might already have :
a- distended heart
b- atherosclerosis
c- bad collaterals

 NB.:75% of deaths in infarction occur in 1st 24 hours

Cardiomyopathies
1. How do we usually diagnose Cardiomyopathy?
- By exclusion

2. Causes of arrhythmia in dilated Cardiomyopathy?


- Due to stagnation of blood causing stretch which increase the excitability of the heart causing any
type of arrhythmia but most commonly AF, ventricular tachycardia

3. What is cause of sudden death in dilated Cardiomyopathy?
- Usually arrhythmia e.g. ventricular tachycardia that may be worsen to be VF

4. In investigations of dilated Cardiomyopathy how can we detect impaired
*****contractile function of the heart?
- By echocardiography we can measure shortening fraction "SF" &ejection fraction

5. Can we use corticosteroids indilated Cardiomyopathy?
- We can use it if there is no other choice but corticosteroid is used undercover of heart failure drugs

6. In auscultation of case of hypertrophic Cardiomyopathy, why is
systolic ejection murmur heard along sternal border instead of aortic
area?

- It changed it`s position because in this case it is not due to defect in aortic valve but it is due to
increase in thickness of septal wall below the valve

Pulmonary
embolism
1. How can factor V affect the etiology of pulmonary embolism?
- Normally protein C causes inhibition of factor V which is needed for clot formation.
- Genetic abnormality which is inborn resistance to protein C, where factor V is resistant to protein C
is due to mutation in factor V  called factor V Leyden or Abnormal factor V.

2. Protein C can cause pulmonary embolism through double etiology?
- congenital deficiency of protein c
- protein c resistance

3. What is the c/p of acute massive pulmonary embolism?
- acute chest pain
- acute dyspnea
- acute RVF
- shock

4. What is plasma D –Dimer?
- It is a sensitive but not a specific protein for pulmonary embolism.
 It is a substance that is released when a clot breaks up, it is reflects the break down of fibrin by
plasmin .

5. DD of wedge shaped opacity?
- Lobar pneumonia
- Bronchogenic tumor
- Mesothelioma of pleura
- Hydatid cyst
- Encysted pleural effusion
- Pulmonary embolism


6. What is the function of the lung?
- Ventilation
- Perfusion
- Diffusion

Mitral-stenosis
1- Most common cause of mitral stenosis?
- Rheumatic fever.

2- Mechanism of MS in Austin flint murmur (severe aortic regurge)?
- Regurge of blood from aorta  elevates the cusps of mitral during diastole.

3- When the left ventricle affected in mitral stenosis?
- In case of aortic valve disease
- Associated with M .R

4- What is the most common symptom in pulmonary congestion in MS?
- Dyspnea

5- What is the finding you will find during auscultation of the heart
in stage III?
- S4 due to pulmonary HTN ++ RV pressure  strong atrial contraction

6- What are the findings if calcifications occur in M .S?

- decreased S1
- no opening snap
- calcified valves in x ray
7- Loss of presystolic accentuation occurs in M.S in case of…?
- A.F due to loss of atrial contraction.

8- Changes occur if MS + AF?
- Murmur No presystolic accentuation.
- L.A No a wave
No S 4
Increased incidence of thromboembolism by 40%
- lung  Acute pulmonary edema
- ECG  Absent P wave

9- Most important investigations in M.S?
- Echocardiography

10-Complications of artificial valves?
- I.E
- Thromboembolism
- Mechanical dysfunctions
- Hemolytic anemia


11-How to investigate hemolytic anemia?
- By blood film  by fragmented RBC'S ( schistocytes )
-
12-Cause of hemolytic anemia?
- Due to premature rupture of RBC'S on valves

13-Most common cause of TR?
- Functional due to dilatation of the tricuspid ring 2ry to RV dilatation.

Mitral valve
prolapse
14-What are the causes of atypical chest pain?
- Sudden tension of papillary muscles causes ischemia due to compression of small vessels
- Reflex coronary spasm
- Pain of cardiac neurosis
- ttt: B - blocker

15-What are the causes of palpitation?
- Arrhythmia
- Neurosis
- Volume overload due to Mitral regurge (last to be said as it is not significant)

16-Why there is mid-systolic click with MVP?
- During Mid-systole, where there is the highest pressure in the ventricle, sudden stretch of
cordae tendinae occurs, so prolapse of mitral valve occure click

17-Why MVP may be associated with systemic Embolization?
- Deposition of mucopolysaccharides on the cusp surface, so it becomes rough & liable for
thrombus formation
- If associated with infective endocarditis, it may be septic emboli
- stagnation of blood, with arrhythmias

18-What are the causes of sudden death?
- Fatal ventricular arrhythmia (VF)
- Embolus in brain
- Sudden coronary spasm.

Aortic valvular
diseases
19-Which valvular disease is associated with angina?
- Aortic valvular disease

20-What are the causes of angina associated with aortic stenosis?
- Reduction of coronary blood flow due to low cardiac output & shortened diastole
- Left ventricular hypertrophy → increased myocardial oxygen demand
- Associated coronary atherosclerosis, especially with calcified AS

21-Why aortic stenosis may be complicated with heart block?
- In case of calcific AS, extension of calcification to the AV bundle may occur.

22-What’s angina of Lewis?
- Nocturnal angina, associated with autonomic disturbance e.g. sweating & tachycardia. It occurs
with aortic regurge.

23-General signs of aortic regurge?(v imp)
- De Musset sign
- Corrigan’s sign
- Systolic thrill
- Water hammer pulse
- Capillary pulsation
- Pistol shots
- Duroziez’s sign
- Blood pressure: ● Wide pulse pressure
● Hill’s sign

24-What’s Muller sign?
- Strong pulsations of uvula (capillary pulsations)

25-What’s Becker’s sign?
- Retinal pulsations, detected by ophthalmoscope

26- Mention 3 diseases in cardiology that affect retina
- Hypertension
- Infective endocarditis
- Aortic regurge

27-What are the causes of blood pressure discrepancy between upper and
lower limbs?
- Coarctation of aorta: pressure in UL › LL’s
- Hill’s sign of aortic regurge: pressure if LL › UL’s

28-What’s the valvular disease that causes murmur all through the
cardiac cycle?
- Aortic regurge
- Over the apex you’ll hear:
a) Propagated murmur of AR: early diastolic
b) Pansystolic murmur of functional MR
c) Mid-diastolic murmur of relative MS (Austin Flint murmur)

Pericardium

1. What is the most common cause of dry pericarditis?
- Idiopathic: viral: coxsakie v or echo v.

2. What are the other diseases which caused by viral infection?
- Cardiomyopathy, DM, meningitis & pleurisy

3. What are the complications of radiotherapy?
- Dry pericarditis ,enteritis (malabsorption syndrome) ,leukemia

4. What are the causes of pulsus paradoxicus?
- pericardial effusion ,constrictive pericarditis, restrictive Cardiomyopathy, copd, sever bronchial
asthma, pulmonary embolism

5. What are causes of dullness in the RT border of the sternum?
- RAE is most common cause
- pericardial effusion

6. What is the indication of corticosteroid therapy in pt diseseased
with T.B?
* In pericardial effusion to decrease inflammation & prevent C.P.
* TB meningitis
* TB adrenal gland
* Fulminant TB
* TB polyserositis

7. What is the role of tetracycline in medicine?
- Gm +ve, Gm-ve antibiotics
- Pericardesis in pericardial effusion
- Antimalarial drug

8. Causes of absent apex?

- Normally: under rib
- Disease :
• weak in __
• myocarditis , Cardiomyopathy, myocardial infarction
• hidden in__
• obesity
• Lt pleural effusion & pericardial effusion
• Lt Pn. thorax & emphysema

9. What is the amount necessary to produce cardiac tamponade?
- 2000ml if the fluid collects slowly.
- 200ml if the fluid collects rapidly.

Systemic HTN

1. What is JNC7?
- The seventh report of the joint national committee on prevention, evaluation, detection and ttt of high
blood pressure.

2. What is white coat HTN?
- It is a phenomenon in which patients have elevated BP in clinical sitting but not when recorded at
home, due to anxiety at clinic visit so ambulatory BP monitoring is required.

3. Etiology of essential HTN?
- UNKNOWN, but there are:
a) Predisposing factors like: genetic, obesity, stress, salt sensitivity and smoking.
b) Theories :
i. Activation of RAAS.
ii. Activation of adrenergic nervous system.
iii. Vascular hypertrophy (and endothelial dysfunction).
iv. Insulin resistance.

4. What are the drugs which cause secondary HTN?
- Corticosteroids : ttt of bronchial asthma and ttt of autoimmune diseases
- Catecholamines : ttt of bronchial asthma
- Cyclosporine : ttt of cancer as chemotherapy and autoimmune diseases
- Contraceptive pills
- Carbenoxolone : for ttt of peptic ulcer

5. What are the types of hypertensive emergency?
- Accelerated HTN : associated with retinopathy ( hemorrhage and exudates ) stage III
- Malignant HTN : associated with retinopathy ( papilledema ) stage IV

6. BERNHEIM EFFECT & REVERSED BERNHEIM EFFECT?

- BERNHEIM effect : one of the CVS complication of HTN as concentric hypertrophy of
interventricular septum cause bulging of the septum in RV cavity leading to slight impairment of
filling and giant a wave in neck veins .
- Reversed BERNHEIM effect: 1- one of the causes of left side heart failure in COPD (PHT) 
hypertrophy of R V causes bulging in septum of left ventricular cavity).

7. What are the similarities and differences between cerebral hemorrhage
and HTN encephalopathy?

* Similarities:
- Both are HTN emergencies
- Both with target organ damage.
- Both with severe HTN
- Both with deterioration of conscious
- Both with elevated I.C.T

* Differences:
- ( clinically ) :
 In cerebral hemorrhage  signs of lateralization
 In HTN encephalopathy  no lateralization

- (imaging CT scan ) :

 There is brain edema in HTN encephalopathy

8. What is the relation between HTN and renal failure?
- HTN  atherosclerosis  renal failure  elevated renin  HTN

9. Drugs induced lupus?
- anti  HTN (hydralazine )
- anti  TB
- anti arrhythmic

Arrhythmias
1. What is the type of rhythm of pulse in atrial flutter?
- Most commonly regular, less common irregular.

2. What is the most drug used in ttt of A. Flutter? How it works?
- Digitalis through increasing atrial automaticity ,converting atrial flutter into (A.F) , if drug
stopped , sinus rhythm may be restored

3. What are the most important 2 causes of ventricular tachycardia?
- CAD especially Acute MI
- Digitalis

4. What are causes of sudden death (in cardiology)?
- Acute MI
- Tachycardia
- A.S
- Cardiomyopathy
- Mitral valve prolapse

5. Causes of wide QRS?
- any ventricular arrhythmia
- BBB
- Hyperkalemia
- WPW syndrome

6. Shape of QRS complex in ventricular tachycardia?
- Wide and deformed ( similar to ventricular premature beats )
- Regular and rapid at a rate more than 120 / m

7. What is ICD (implantable cardiovertor defibrillator)?
- it creates new focus with higher excitability than the presenting focus to stop it , after stopping it ,
the new focus will stop , it used in prevention of future attacks of ventricular tachycardia.

8. Most imp causes of atrial fibrillation (A.F)?
- RHD especially M.S
- CHD especially A.S.D
- coronary H.D. especially AMI
- hyperthyroidism

- lone A,F ( idiopathic )

9. Difference between A.F and extrasystole?

A.F extrasystole
marked irregularity Occasional
Pulse deficit > or = 10 < 10
Exercise : worse it Decrease due to decreased diastolic period
Neck veins : absent a wave , Occasional irregularity
systolic expansion

10.Ventricular beats with associated structural heart disease should
treated if :
- Multiple , multifocal and ( R on T )
- If associated with AMI

11.Pro – arrhythmic drugs?
- As quinidine ( class I A )
- Propafenone ( class I c )

- Arrhythmia is caused as a side effect
- This reaction is occurring in therapeutic doses not toxic doses .
- Effect:

 Production of new arrhythmia
 Aggravation of present arrhythmia
- Mechanism:
 Include hypokalemia
Slow down conduction of myocardium ( re – entry)


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