Past year System by System

M100 M200 M101 M201 M102 M202 M203 M104 (why no 03?!)

CVS
Anatomy
1. Layers of pericardium. Fibrous pericardium, parietal serous pericardium, pericardial cavity, visceral
serous pericardium (aka epicardium)

2. 2 functions of Lymph node

i. filters lymph & remove microorganisms & debris
ii. activates (trigger) immune system
iii. site of maturation for lymphocytes

Physiology
1. Ejection Fraction: Stroke volume/ End Diastolic Volume
2. What’s sinus tachycardia: more than 100beats/min for sinus rhythm
3.What’s respiratory sinus arrhythmia (RSA)?
Ans: R-R interval of ECG is reduced during inspiration (I) for young normal person compared to
expiration (E) because of increase HR. RSA due to inspiration that impede(hamper) the vagus nerve
from exerting it’s inhibitory effect on SA node. E:I ratio in ECG will detect the absence of sinus
arrhythmia.( test for sympathetic underactivity)… can also be due to the increase intra thoracic
pressure causing an increase in venous return incease the preload and hence arrhythmia…
4.What does the heart use for energy? Creatinine Phospate
5.What is the energy yield for aerobic and anaerobic respiration? 36 ATP and 2 ATP
6.What is Blood Pressure?
Dorlands: The pressure of the blood on the walls of the arteries, dependent on the energy of the heart
action, the elasticity o f the walls of the arteries, and the volume and viscosity of the blood.
Normally measured as Systolic and Diastolic Blood Pressure

MCQ:
1.
a. Acetylcholine increase the force of contraction in the heart (B1 receptor by noradrenaline)
b. The heart muscle can undergo spontaneous depolarization (autorhymic cell aka non – contractile
cardiac cells, prepotential by leaky Na channel)
c. The heart muscles uses potassium to contract (depo by opening of fast Na channel, repo by K
channel)
d. Calcium is taken up by sarcoplamic reticulum after muscle contraction
e. The heart muscle can undergo tetany (it has absolute refractory period)
Ans: D

2. Cardiac cycle= 1 systole + 1 diastole

Diastasis-slow filling 70% (P wave) Atrial contraction 20% ( after Pwave) Ventricle isometric
contraction (QRS)  Rapid ejection, sharp decrease in ventri volume. T wave at the end when ventri
repolarise isometric relaxation  rapid ventricle filling (10%)
a. Most of the Ventricular filling occurs upon Atrial contraction.
b. Atrial Contraction occurs during P wave ( after Pwave diastasis)
c. All valves are closed during Ventricle isometric filling
d. All valves are opened during isometric relaxation (closed)
e. Rapid ventricle filling is called Diastasis
Ans : C

3.
a. Adenosine cause Heart contraction ( cause transient heart block at AV node to treat
supraventricular tachycardia)
b. Adenosine and Ach decrease HR (chronotropic) and contractility (ionotropic) .. coffee is a
adenosine antagonist…
c. Adrenaline/Noradrenaline decrease HR and contractility
d. Histamine(H2 receptor) decrease HR and CO
Ans: B
* sym NA ( B1 adrenergic receptor), parasym Ach (M2 muscarinic receptor), Histamine( H2 receptor)

Pathology/Clinicals
Myocardial Infarction
1i.Characteristic of pain in MI: severe, crushing substernal pian, radiate to neck, jaw, epigastrium,
shoulder, left arm
-Angina Pectoris: intermittent chest pain on exertion lasting for 16 seconds to 15 minutes.
Characterised by crushing pain and relieved by resting.

1ii. Differentiate pain of AP and AMI

AP: pain < 15 min
AMI: pain > 15 min

1iii. Other cause of chest pain other than MI: chest trauma, aortic dissection, angina, GERD

Atherosclerosis
1) endothelial injury, 2) monocyte localize in intima, transform to macrophage 3) macrophage engulf
oxidize LDL (lipoprotein) foam cell 4) Macrophage activation smooth muscle cell(SMC) migrate from
media to intima 5) SMC proliferate and deposit ECM in intima, convert fatty streak into mature
atheromatous plaque
Ishaemic Heart Disease
1. Acute plaque changes- disruption of initially stenosing plaques, hemorrhage into atheroma,
rupture and expose thrombogenic plaque constituent
2. Coronary artery thrombosis – platelet aggregation, mayb superimposed
3. Coronary artery vasospasm
 If thrombus superimposed will cause total occlusion chronic hypoxia cell death

1iv. why pain is referred: dermatomal rule (T1-2), facilitation theory, convergence theory

2i.Pathophysiology of MI: artherosclerosis  IHD -Angina Pectoris (incomplete occlusion)Acute

Myocardiac infarction (complete occlusion)

2ii.How MI happen in HPT: HPT endothelial injury atherosclerosis narrowing of coronary

arteries hypoxiaMI

2iii.How smoking causes MI? smoking decrease antioxidant injury to the bld vessels…
atherosclerosis
How MI cause stroke? MI arrhythmia (atrial fibrillation)  emboli  stroke

2iv.Modifiable risk factors of MI: , Hypertension (control), Lifestyle (diet), obesity(wt reduction),
smoking

2v.DD: Unstable Angina, Peptic ulcer (epigastric pain), gallstone(right shoulder pain), reflux esophagitis
( heart burn), aortic dissection (chest pain)

2vi. give the definition of isoenzymes: A group of family of structurally related enzyme with similar function
but different physical, immunological and chemical properties.

List 2 isoenzymes that you would order and why ? ( if they are referring to enzymes)
 1) CKMB Creatinine kinase myocardium bound – specific,Rise and fall quickly ( good for
reinfarction)
2) CKMM Creatinine kinase muscle and myocardium bound – not as specific
Range 12-24 hrs

other possible cardiac markers.

-Lactate Dehydrogenase(LDH1)- LDH 1>LDH2 after MI. Long period so good for long time infarct.
LDH 1 for Heart & RBC, LDH 2 for WBC
-Cardiac troponin will be another preferred one after CKMB as it’s most sensitive (found only in cardiac
tissue), elevated parallel to CKMB and has longer period

3. Acute Complications of MI:

a. Contractile dysfunction of LV due to LVF with hypotension, pulmo congestion/edema  dyspnoea
b. lead to cardiogenic shock (severe pump failure massive infarct)
c. arrhythmia syncope
d. stroke (either arrhythmiaemboli or ischaemic stroke )
Late Cx: myocardial rupture, pericarditis, LV aneurysm

4.Coronary arteries distribution

RCA: Right marginal and posterior descending branch
LCA: Left circumflex and anterior descending branch
Post IVS by RCA, Ant IVS by LCA

5.list 4 cardiovascular advantages of exercise

1.Metabolic:
i) increase HDL production, decrease TG, less atherosclerosis plaque
ii) decrease blood stasis, decrease platelet coagulation
2.Morphological: increase myocardial mass and coronary artery size
3. Hemodynamic: Decrease resting HR and BP
4. Physiologically: increase maximal oxygen uptake ( adaptation – stamina)

Ischemic Heart Disease

Diminished coronary perfusion relative to myocardial demand
1. 4 syndromes: Angina pectoris, AMI, sudden cardiac death, Chronic IHD with congestive Heart failure

2.Characteristic of angina (3 types)

1. Stable AP, assoc with exertion/stress
2. Printzmetal, Variant angina, at rest, assoc with coronary artery spasm
3. Unstable angina (btw Stable angina and MI) aka preinfarction angina
-increase freq of angina pain, ppt by progressively less exertion
- induced by acute plaque chages with superimposed partial thrombosis

3.Why is angina more prone in smokers?

Smoking ( decrease anti oxidant) risk to coronary atherosclerosis  reduce myocardial oxygen supply or
Reduce lung capacity thus reduce oxygen carrying capacity to the heart.

Rheumatic Fever
1. What is rheumatic fever?
Hypersensitivity reaction induced by GAS, Antibody against M protein of GAS cross react with normal
protein in heart and joint. against M protein of GAS
2. Name 2 pathological features seen in the joints?
Skin :Subcutaneous nodules ; large joint (hip/knee) migratory polyarthritis
3. Name 2 other organs affected besides the heart and joints?
skin: erythema marginatum ; CNS: Sydenham chorea PAUL CHEN SINGS EVERYDAY SUNDAY…
migratory polyarthritis, Carditis , subcutaneous nodules, erythema marginatum, syndenham
chorea…

4. Name the most common causative organism. Group A Streptococcus

5. Name 2 investigation you would do
ASOT (antistreptolysin O titre),biochemical test, Blood agar culture

6. What are aschoff bodies?

Foci of fibrinoid degeneration surrounded by lymphocytes, plasma cells & Anitschkow cell
Anitschkow cells are plump macrophage, multinucleated to form Aschoff Giant cells

Valvular Disorder
1.
1st Heart Sound S1 2nd Heard Sound S2
Produced by Closure of Tricuspid/Mitral Valve Closure of Semilunar/Aortic Valve
Low/High pitch Low High
2. What is cardiac murmur?
Dorlands: an auscultatory sound, benign or pathologic, particularly a periodic sound of short duration of
cardiac or vascular in origin.
My own : Murmurs are abnormal heart sounds caused by turbulent blood flow .

3.
Systole/Diastole
Mitral Stenosis Diastole
Aortic Regurgitation Diastole
4.Auscultatory Areas and their location
Aortic: Right Parasternal border and 2nd intercostals space
Pulmonary: Left Parasternal Border and 2nd intercostal space
Tricuspid: Left Parasternal Border and 4th intercostals space
Mitral: Mid clavicular line and left 5th intercostals space

5i. position of apex beat: ~2cm medial to midclavicular line, left 5th intercostals space

5ii.what valvular disease causes apex beat displacement

Aortic stenosis left heart hypertrophy, cardiomegaly ( cause: RHD)

5 iii. In what condition is apex beat not palpable? Which valve can cause this?
Ans: Left heart hypertrophy, aortic valve ( stenosis); if respi cause: pleural effusion

6. Heart diseases cause valvular dysfunction

h : Rheumatic Heart Disease, Infective endocarditis, congenital Mitral Valve Prolapse due to connective
tissue disorder ( complication of Marfan)

7.Which valvular heart disease is most common in RHD/IE

RHD: aortic/mitral stenosis and regurgitation (fish mouth appearance)
IE: Aortic/Mitral commonest site  Aortic/Mitral Regurgitation

5.Congenital Heart Diseases

Tetralogy of Fallot ( right to left shunt) Morphology Boot shaped heart
Patient has blue spells when he cries
1i.What is blue spells?
Ans: blue discoloration of the skin, tongue mucosa due to deoxygenated blood.

1ii.Pathogenesis of cyanosis
Ans: presence of deoxygenated blood in systemic circulation due to entry of venous blood into aorta
(rt to left shunt).

1iii.Pathogenesis on why the baby has

a. Blue spell on crying
Ans: exertion increase RV outflow obstruction due to adrenergic stimulation  therefore low oxygenation
of Hb, also rate of deoxygenation increase  more increase in deoxygenated Hb

b. Dyspnoea on exertion
ans: exertion increase deoxygenation rate  shunting lead to V/Q mismatch
Dyspnea appeared to be related to the inappropriateness of the level of ventilation relative to the
metabolic needs of exercise (not sure of the ans)
Also receptor will lead to reflex bronchoconstriction  dyspnoea

c. Relief on squatting
ans: to increase systemic resistance to decrease right to left shunt  increase after load of heart

1iv. Name 4 components of Tetralogy of Fallot (results from anterosperior displacement of infundibular
septum by alcoholism) most common cyanotic CHD
Subvalvular pulmonary Stenosis, ,Right ventricle Hypertrophy, Ventricle Septal Defect , Dextraposed
aortic root that overrides the VSD

Patent Ductus Arteriosus (left to right shunt)bld fr aorta flow to pulmo art
2i. Name 2 congenital defects of Rubella
Ans: PDA, cataracts

2ii.How does Rubella affect the first 12 weeks of pregnancy

The rubella virus crosses the placenta and spreads through the fetus's circulatory system damaging
blood vessels and organs, including the heart. Affect the physiological closure Ductus Arteriosus at birth.
*machinery like murmur
Acynotic: pulmo HT +LV load  Lft to Rt shunt
Cynotic: prolong pulmo HT RVH Rt to Lft shunt

3.Name 2 congenital heart disease without shunt

Coarctation of Aorta
Ebstein malformation
Pulmo/Aortic stenosis/atresia

4.List 2 conditions predispose to congenital heart disease

Rubella infections, exposure to radiation, alcoholism

Pharmacology
1.Drugs that prevent Angina pectoris and its MOA?
GTN Glyceryl trinitrite
MOA:
1. NO3 & NO activates guanylate cyclase in Smooth muscles of vessels
2. increase cGMP
3. activated cGMP dependent protein kinase
4. smooth muscle relaxation
5. venodilation decrease venous return
6. decrease preload  decrease ventricle filling
7. decrease SV  decrease ventri wall tension
8 decrease myocardial oxygen demand

2. What is Renin Angiotensin System

RAS are long term blood pressure regulation system
When low BP, RAS activated
Ag II is a vasoconstrictor to increase BP, also increase blood volume by reabsorption of water(ADH) and
Na(aldosterone)

3.What is ACE inhibitor?

Angiotensin converting enzyme inhibitor. Prevent formation of Ag II and thus no vasoconstriction and
prevent high blood pressure(vasodilation)
i.Explain the mechanism of action (MOA)of Losartan & ACE inhibitors
Losartan is a angiotensin receptor antagonist. Prevent vasoconstrictive effect of AT
ACE inhibitor inhibit Angiotensin II synthesis

ii.Why does ACE inhibitor lead to cough?

ACE inactivate bradkinin. So ACEi lead to decrease of inactivation of bradykinin ( potent vasodilator by
pdcing NO) lead to accumulation of bradykinin  dry cough

end