CARDIOVASCULAR USMLE QUESTION BANK REVIEW

CARDIOVASCULAR USMLE QUESTION

BANK
CARDIOVASCULAR USMLE QUESTION
BANK - EMBRYOLOGY
Q:1: What is the first functional organ in vertebrate embryos that beats spontaneously by
week 4 of development?
Ans: Heart.
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Q:2: What is Cardiac looping?
Ans: Primary heart tube loops to establish left-right polarity; begins in week 4 of
development.
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Q:3: What can lead to Dextrocardia?
Ans: Defect in left-right dynein (involved in left-right asymmetry) can lead to dextrocardia,
as seen in Kartagener syndrome.
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Q:4: How foramen ovale is sealed soon after birth?
Ans: Septum primum closes against septum secundum, sealing the foramen ovale soon
after birth because of increased Left atria pressure and decreased Right atria pressure.
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Q:5: What is potent foramen ovale?
Ans: It is caused by failure of septum primum and septum secundum to fuse after birth and
most are left untreated.
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Q:6: What can potent foramen ovale lead to?
Ans: It can lead to paradoxical emboli (venous thromboemboli entering the systemic
arterial circulation through right-to-left shunt) as can occur in atrial septal defect (ASD).
Q:7: What is the most common congenital cardiac anomaly?
Ans: Ventricular septal defect is the most common congenital cardiac anomaly, usually
occurs in membranous septum.
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Q:8: How aorticopulmonary septum is formed?
Ans: Neural crest cell migrations that leads to truncal and bulbar ridges that spiral and
fuse to form aorticopulmonary septum.
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Q:9: What is Conotruncal cardiac anomalies?
Ans: A group of congenital cardiac outflow tract anomalies that include such defects as
tetralogy of Fallot, pulmonary atresia with ventricular septal defect, double-outlet right
ventricle (DORV), double-outlet left ventricle, truncus arteriosus and transposition of the
great arteries (TGA).
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Q:10: What are the 4 defects found in tetralogy of Fallot?
Ans: 1. Pulmonary Stenosis. 2. Right ventricular hypertrophy. 3. Ventricular septal defect.
4. Overriding aorta.
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Q:11: How heart valves are derived?
Ans: Aortic/pulmonary: derived from endocardial cushions of outflow tract.
Mitral/tricuspid: derived from fused endocardial cushions of the AV canal
Q:12: What is the derivative of first aortic arch?
Ans: Part of maxillary artery (branch of external carotid). 1st arch is maximal.
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Q:13: What are the derivatives of second aortic arch?
Ans: Stapedial artery and hyoid artery. Second = stapedial.
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Q:14: What are the derivatives of third aortic arch?
Ans: Common carotid artery and proximal part of internal carotid artery. C is 3rd letter of
alphabet.
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Q:15: What are the derivatives of fourth aortic arch?
Ans: On left, aortic arch; on right, proximal part of right subclavian artery.
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Q:16: What are the derivatives of sixth aortic arch?
Ans: Proximal part of pulmonary arteries and (on left only) ductus arteriosus. 6th arch =
pulmonary and the pulmonary-to-systemic shunt (ductus arteriosus).
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Q:17: What embryonic structure Truncus arteriosus give rise to?
Ans: Ascending aorta and pulmonary trunk.
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Q:18: What embryonic structure bulbus cordis give rise to?
Ans: Smooth parts (outflow tract) of left and right ventricles.
Q:19: What embryonic structure primitive ventricle give rise to?
Ans: Trabeculated part of left and right ventricles.
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Q:20: What embryonic structure primitive atrium give rise to?
Ans: Trabeculated part of left and right atria.
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Q:21: What embryonic structure left horn of sinus venosus give rise to?
Ans: Coronary sinus.
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Q:22: What embryonic structure right horn of sinus venosus give rise to?
Ans: Smooth part of right atrium (sinus venarum).
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Q:23: What embryonic structure endocardial cushion give rise to?
Ans: Atrial septum, membranous interventricular septum; AV and semilunar valves.
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Q:24: What embryonic structure right common cardinal vein and right anterior cardinal
vein give rise to?
Ans: Superior vena cava (SVC).
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Q:25: What embryonic structure posterior cardinal, subcardinal, and supracardinal veins
give rise to?
Ans: Inferior vena cava (IVC).
Q:26: What embryonic structure primitive pulmonary vein give rise to?
Ans: Smooth part of left atrium.
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Q:27: What are four key adaptations of fetal circulation system?
Ans: 1. Foramen Ovale. 2. Ductus arteriosus. 3. Umbilical arteries and veins. 4. Ductus
Venosus.
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Q:28: What is the pressure of Blood in umbilical vein and is how much saturated with O2
concentration?
Ans: Blood in umbilical vein has a Po2 of ≈ 30 mm Hg and is ≈ 80% saturated with O2.
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Q:29: What are the 3 structures that forms the 3 important shunts in fetal circulation?
Ans: 1. Ductus Venosus. 2. Foramen Ovale. 3. Ductus arteriosus.
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Q:30: Which drugs help close the patent ductus arteriosus?
Ans: NSAIDs (eg, indomethacin, ibuprofen) or acetaminophen help close the patent ductus
arteriosus.
“Endomethacin” ends the PDA.
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Q:31: Which chemicals keep PDA(Patent ductus arteriosus) open?
Ans: Prostaglandins E1 and E2 kEEp PDA open..
12
Q:32: What is postnatal derivative of Ductus arteriosus?
Ans: Ligamentum arteriosum.
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Q:33: What is postnatal derivative of Ductus venosus?
Ans: Ligamentum venosum.
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Q:34: What is postnatal derivative of Foramen ovale?
Ans: Fossa ovalis.
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Q:35: What is postnatal derivative of Allantois?
Ans: Median umbilical ligament.
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Q:36: What is postnatal derivative of Umbilical arteries?
Ans: Medial umbilical ligaments.
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Q:37: What is postnatal derivative of Umbilical vein?
Ans: Ligamentum teres hepatis (round ligament).
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Q:38: Part of umbilical arteries becomes which arteries?
Ans: Superior Vesical arteries that supply either side of bladder.
CARDIOVASCULAR USMLE QUESTION
BANK - ANATOMY
Q:1: What is the most posterior part of Heart?
Ans: Left Atrium.
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Q:2: Name one disease that can cause enlargement of Left atrium and what are the two
complications of it?
Ans: The disease that cause Left atrium enlargement is Mitral valve(Bicuspid valve) stenosis.
Two complications due to this are:
1. Dysphagia: Due to compression of esophagus.
2. Ortner syndrome: Due to compression of the left recurrent laryngeal nerve, a branch of
the vagus nerve, causing hoarseness.
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Q:3: What is the most anterior part of the heart and most commonly injured in trauma?
Ans: Right Ventricle.
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Q:4: What parts of heart forms the inferior (diaphragmatic) cardiac surface?
Ans: Left Ventricle is about 2/3 and Right Ventricle is about 1/3 of the inferior
(diaphragmatic) cardiac surface.
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Q:5: Pericardium consists of how many layers from outside to inside?
Ans: 1. Fibrous Pericardium. 2. Parietal Pericardium. 3. Epicardium(Visceral pericardium).
Q:6: Pericardial cavity is situated between which two layers of pericardium?
Ans: Pericardial space lies between parietal pericardium and epicardium.
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Q:7: Pericardium is inverted by which nerve?
Ans: Phrenic nerve.
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Q:8: Pericarditis can cause referred pain to the which parts of the body?
Ans: Pericarditis can cause referred pain to the neck, arms, or one or both shoulders (often
left).
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Q:9: What are the two main branches of left coronary artery and one optional branch that
is present in some individuals?
Ans: 1. Left anterior descending artery. 2. Left circumflex artery.
3. Obtuse marginal artery.
Optional.
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Q:10: What are the two main branches of right coronary artery?
Ans: 1. PDA(Posterior descending artery). 2. Acute marginal artery.
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Q:11: Left anterior descending artery(LAD) and it's branches supply which parts of the
heart?
Ans: Anterior 2/3 of interventricular septum, anterolateral papillary muscle, and anterior
surface of LV.
Q:12: Which is the most common occluded artery in heart?
Ans: LAD(Left anterior descending artery): Branch of left coronary artery.
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Q:13: PDA(Posterior descending artery) supplies which structures of the heart?
Ans: PDA supplies posterior 1/3 of interventricular septum, posterior 2/3 walls of
ventricles, and posteromedial papillary muscle.
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Q:14: SA node and AV node are supplied by which artery?
Ans: Right coronary artery.
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Q:15: What is Right-dominant circulation, Left-dominant circulation and codominant
circulation in heart for different individuals and which is the most common?
Ans: Right-dominant circulation = PDA arises from right coronary artery.
Left-dominant circulation = PDA arises from left circumflex artery(branch of left coronary
artery).
Codominant circulation = PDA arises from both LCV and RCA.
Right-Dominant circulation is the most common.
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Q:16: What are the four main cardiac veins of the heart?
Ans: 1. Great cardiac vein. 2. Middle cardiac vein. 3. Small cardiac vein. 4. Anterior
cardiac veins.
Q:17: Where these main veins drain to?
Ans: Great cardiac vein, Middle cardiac vein, Small cardiac vein = drain into coronary sinus
and then into right atrium.
Anterior cardiac veins drain directly into right atrium.
CARDIOVASCULAR USMLE QUESTION
BANK - PHYSIOLOGY
Q:1: Stroke volume is affected by which three factors?
Ans: CAP = Contractility(eg, Anxiety, exercise), Afterload, Preload(eg, early pregnancy).
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Q:2: What are the factors that increase the contractility of heart hence increasing Stroke
Volume?
Ans: 1. Catecholamines : Acting on Beta-1 receptor: Activated protein kinase A leads to
Ca2+ channel phosphorylation that leads to Ca2+ entry and that causes Ca2+-induced Ca2+
release.
2. Digoxin: Digoxin inhibits the Na+/K+ ATPase pump. So sodium can not move outside the
cell through this transporter and accumulates inside the cell. To compensate this sodium
has to move through another transporter called Sodium/Calcium exchanger. So as the
more sodium is intracellularly, more calcium is to be exchanged inside the cell and
increased calcium leads to increased contractility.
3. Increased Intracellular Calcium ions: Increases contractility.
4. Decreased extracellular sodium ions: So it causes Sodium/Calcium exchanger to work
more to move sodium from inside the cell to extracellularly and calcium to be exchanged
inside the cell, so more calcium more contractility.
Q:3: What are the factors that decrease the contractility of heart hence the stroke
volume?
Ans: 1. β1-blockade (decreased cAMP).
2. Heart failure (HF) with systolic dysfunction.
3. Acidosis.
4. Hypoxia/hypercapnia (Decreased Po2/ Increased Pco2).
5. Nondihydropyridine Ca2+ channel blockers.
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Q:4: What is preload and what are the factors it depends on?
Ans: Preload is defined as the stretch of myocardium or end-diastolic volume of the
ventricles(Approximated) and most frequently refers to the volume in a ventricle just
before the start of systole. It depends on venous tone and circulating blood volume.
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Q:5: Which drugs decrease preload and tell me one example?
Ans: Vasodilators(eg, nitroglycerin).
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Q:6: What is afterload?
Ans: Afterload is the pressure that the heart must work against to eject blood during
systole. Afterload is proportional to the average arterial pressure. As aortic and pulmonary
pressures increase, the afterload increases on the left and right ventricles respectively.
Q:7: How Left ventricle compensates for increased afterload?
Ans: Left Ventricle compensates for increased afterload by thickening (hypertrophy) in
order to decrease wall stress.
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Q:8: Which drugs decrease afterload alone and which drugs decrease both preload and
afterload?
Ans: Arterial vasodilators (eg, hydralazine) decreases afterload.
ACE(Angiotensin converting enzyme) inhibitors and ARBs(Angiotensin receptor blockers)
decreases both preload and afterload.
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Q:9: Myocardial O2 demand is increased by which factors?
Ans: C = Increased contractility.
A = Increased Afterload.
R = Increased heart rate.
D = Increased diameter of ventricle (increased wall tension).
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Q:10: Which structure contains the most deoxygenated blood in the body?
Ans: Coronary sinus.
Q:11: What is Stroke volume?
Ans: The definition of stroke volume is the volume of blood pumped out of the left
ventricle of the heart during each systolic cardiac contraction.
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Q:12: How to calculate Stroke volume?
Ans: Stroke Volume = End-Diastolic Volume - End-systolic volume.
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Q:13: How to calculate Ejection fraction?
Ans: Ejection fraction(%): Stroke Volume/End-Diastolic Volume.
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Q:14: What is the status of Ejection fraction in systolic Heart failure and diastolic heart
failure?
Ans: Ejection fraction is decreased in systolic heart failure.
And Ejection fraction is normal in diastolic heart failure; hence called diastolic ejection
fraction preserved heart failure.
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Q:15: How to calculate Cardiac output?
Ans: Cardiac output = Stroke Volume x Heart rate.
Cardiac output by Fick principle: rate of O2 consumption/(arterial O2 content-Venous O2
content).
Q:16: How Cardiac output is maintained during Exercise?
Ans: In early stages: Increased Heart rate and Increased Stroke volume both.
In late stages: Increased HR only because Stroke Volume plateaus.
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Q:17: What happens to Cardiac output in Ventricular Tachycardia?
Ans: Diastole is shortened with a lot of increase in HR (eg, ventricular tachycardia) causing
a lot of decrease in diastolic filling time causing decrease in SV hence decrease in CO.
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Q:18: How to calculate pulse pressure?
Ans: PP = systolic blood pressure (SBP) – diastolic blood pressure (DBP)
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Q:19: How Stroke volume and arterial compliance are related to Pulse pressure?
Ans: Pulse pressure is directly proportional to stroke volume and inversely proportional to
arterial compliance.
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Q:20: What are the diseases or factors that increase pulse pressure?
Ans: Mnemonic: Vowels. A. E. I(hi). O. (pUlse pressure).
1. A = Aortic regurgitation : As the blood regurgitates back into the left ventricle during
diastole, the diastolic pressure in the aorta decreases, thereby leading to an increase in the
pulse pressure. 2. A = Aortic stiffening (isolated systolic hypertension in older adults). 3.
Anemia. 4. Exercise. 5. Hyperthyroidism: by increasing systolic BP. 6. Obstructive sleep
apnea (increased sympathetic tone).
Q:21: What are the diseases or factors that decrease pulse pressure?
Ans: Mnemonic: AC = (1. Aortic stenosis. 2.Advanced Heart failure.) = Stroke volume
decrease; PP is directly proportional to SV).
3. Congestive heart failure. 4. Cardiac tamponade(Cardiac tamponade happens when extra
fluid builds up in the space; pericardial sac around the heart).
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Q:22: How to calculate Mean arterial pressure?
Ans: 1. MAP = CO × total peripheral resistance (TPR).
2. MAP (at resting HR) = 2/3 DBP + 1/3 SBP.
3. MAP = DBP + 1/3PP.
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Q:23: Examples of drugs that increase contractility of heart?
Ans: 1.Catecholamines.
2. Positive inotropes (eg, dobutamine, milrinone, digoxin).
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Q:24: What are the diseases or drugs that decrease contractility of heart?
Ans: 1. Loss of functional myocardium (eg, MI). 2. β-blockers (acutely).
3. Nondihydropyridine Ca2+ channel blockers. 4. Heart failure.
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Q:25: How much Stroke volume is usually there?
Ans: 70ml(120ml-50ml).
Q:26: How much End-diastolic volume is usually there?
Ans: 120ml.
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Q:27: How much End-systolic volume is usually there?
Ans: 50ml.
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Q:28: Systolic pressure is highest in which vessels in the body?
Ans: Large arteries.
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Q:29: Mean Arterial pressure(MAP) is highest in which vessels in the body?
Ans: Aorta.
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Q:30: What are the disorder that can increase or decrease the viscosity of the blood?
Ans: Viscosity is increased in: 1. hyperproteinemic states (eg, multiple myeloma). 2.
Polycythemia.
Viscosity is decreased in anemia.
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Q:31: Which blood vessels have highest total cross-sectional area and lowest flow velocity?
Ans: Capillaries have highest total cross-sectional area and lowest flow velocity.
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Q:32: Which blood vessels account for most of Total peripheral resistance?
Ans: Arterioles account for most of TPR.
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Q:33: Which blood vessels provide most of blood storage capacity?
Ans: Veins.
Q:34: What is the relation of blood flow and resistance to radius of vessels?
Ans: Q ∝ r4. R ∝ 1/r4.
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Q:35: How to calculate blood flow?
Ans: 1. Volumetric flow rate (Q˙) = flow velocity (v) × cross-sectional area (A).
2. Q = Change in driving Pressure x Resistance.
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Q:36: How to calculate Resistance in vessels?
Ans: R= 8η(viscosity) × length/πr4
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Q:37: How to calculate total resistance in series vessels?
Ans: RT = R1 + R2 + R3.
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Q:38: How to calculate total resistance in parallel vessels?
Ans: 1/RT = 1/R1 + 1/R2 + 1/R3.
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Q:39: What are the examples of drugs/factors that increase inotropy?
Ans: Catecholamines, dobutamine, milrinone, digoxin, exercise.
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Q:40: What are the examples of drugs/factors that decrease inotropy?
Ans: Heart failure with reduced Ejection fraction, narcotic overdose, sympathetic inhibition.
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Q:41: What are the examples of factors that increase venous return?
Ans: Fluid infusion, sympathetic activity, arteriovenous shunt.
Q:42: What is arteriovenous shunt?
Ans: Arteriovenous shunts are abnormal connections between coronary arteries and a
compartment of the venous side of the heart. The abnormal connection may originate in
the right or left coronary artery, or, more rarely, multiple shunts originating in both arteries
may be present.
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Q:43: What are the examples of factors that decrease venous return?
Ans: Acute hemorrhage, spinal anesthesia.
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Q:44: Which drugs increases Total peripheral resistance?
Ans: Vasopressors.
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Q:45: Which factors decrease total peripheral resistance?
Ans: Exercise, arteriovenous shunt.
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Q:46: What are the phases of LV in Pressure-volume loops and cardiac cycle?
Ans: 1. Isovolumetric contraction: period between mitral valve closing and aortic valve
opening; period of highest O2 consumption. 2. Systolic ejection: period between aortic
valve opening and closing. 3. Isovolumetric relaxation: period between aortic valve closing
and mitral valve opening. 4. Rapid filling: period just after mitral valve opening. 5. Reduced
filling: period just before mitral valve closing.
Q:47: What are the two normal heart sounds?
Ans: S1 = Mitral and tricuspid valve closure. Loudest at mitral area.
S2 = Aortic and pulmonary valve closure. Loudest at left upper sternal border.
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Q:48: What is the S3 heart sound?
Ans: In early diastole during rapid ventricular filling phase. Best heard at apex with patient
in left lateral decubitus position. Associated with increased filling pressures (eg, MR, AR,
HF, thyrotoxicosis) and more common in dilated ventricles (but can be normal in children,
young adults, athletes, and pregnancy). Turbulence caused by blood from LA mixing with
increased ESV.
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Q:49: What is S4 heart sound?
Ans: In late diastole (“atrial kick”). Turbulence caused by blood entering stiffened LV. Best
heard at apex with patient in left lateral decubitus position. High atrial pressure. Associated
with ventricular noncompliance (eg, hypertrophy). Can be normal in older adults.
Considered abnormal if palpable.
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Q:50: Right atrial pressure is also called?
Ans: Jugular venous pulse.
Q:51: Right atrial pressure/Jugular venous pulse consists of which waves and descent and
what they indicate?
Ans: a wave:atrial contraction. Absent in atrial fibrillation.
c wave: RV contraction (closed tricuspid valve bulging into atrium).
x descent: atrial relaxation and downward displacement of closed tricuspid valve during
rapid ventricular ejection phase. Reduced or absent in tricuspid regurgitation and right HF
because pressure gradients are reduced.
v wave: Increased RA pressure due to increased volume against closed tricuspid valve.
y descent: RA emptying into RV. Prominent in constrictive pericarditis, absent in cardiac
tamponade.
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Q:52: What are the effects of AORTIC STENOSIS on heart?
Ans: 1. Left ventricle pressure increases: because heart tries hard against this stenosis.
2. End-systolic Volume increases: because heart can compensate little volume to be ejected
with increasing pressure.
3. Stroke Volume decreases: As heart can not eject the normal blood volume even with
increasing left ventricle pressure.
4. End-diastolic volume remain same, but end-diastolic pressure increases due to
ventriclular hypertrophy.
Q:53: What are the effects of AORTIC REGURGITATION on heart?
Ans: 1. No true Isovolumetric phase(both Isovolumetric contraction and Isovolumetric
relaxation) : Because Blood always leaks through aortic valve.
2. End-diastolic Volume increases : Due to Aortic blood leaks back into ventricle.
3. Stroke Volume increases : As more End-diastolic volume, more strong contraction, more
stroke volume ejected.
4. Loss of Dicrotic notch: As aortic valve never closes.
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Q:54: What are the effects of MITRAL STENOSIS on heart?
Ans: 1. Increased LA pressure: As left atrium tries hard to pump blood from atrium to
ventricle.
2. Decreased EDV because of impaired ventricular filling: Despite of Increased LA pressure,
blood pumped from LA to LV is not compensated to normal values.
3. Decreased ESV: Heart tries to pump whatever End-diastolic volume it gets.
4. Decreased SV: Because of Low End-diastolic volume.
Q:55: What are the effects of MITRAL REGURGITATION on heart?
Ans: 1. No true isovolumetric phase: Because blood always leaks through mitral valve.
2. Decreased ESV due to decreased resistance and increased regurgitation into LA during
systole
3. Increased EDV due to increased LA volume/pressure from regurgitation leads to
increased ventricular filling: As mitral valve never closes completely, whatever blood comes
into atrium goes into ventricle.
4. Inreased SV (forward flow into systemic circulation plus backflow into LA).

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Q:56: What is physiological splitting of S2 sound?
Ans: 1. Inspiration causes drop in intrathoracic pressure that leads to increased venous
return leads to increased RV filling leads to increased RV stroke volume leads to increased
RV ejection time causing delayed closure of pulmonic valve.
2. Decreased Pulmonary impedance (Increased capacity of the pulmonary circulation) also
occurs during inspiration, which contributes to delayed closure of pulmonic valve.
Q:56: What is Wide splitting of S2 sound?
Ans: Seen in conditions that delay RV emptying (eg, pulmonic stenosis, right bundle branch
block). Causes delayed pulmonic sound (especially on inspiration). An exaggeration of
normal splitting.
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Q:57: What is Fixed splitting of S2 sound?
Ans: Heard in ASD. ASD causes left-to-right shunt leads to increased RA and RV volumes
leads to increase flow through pulmonic valve causing delayed pulmonic valve closure
(independent of respiration: S2 heard at same time in expiration aswell inspiration).
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Q:58: What is paradoxical splitting of S2 sound?
Ans: Heard in conditions that delay aortic valve closure (eg, aortic stenosis, left bundle
branch block). Normal order of semilunar valve closure is reversed: in paradoxical splitting
P2 occurs before A2. On inspiration, P2 closes later and moves closer to A2, “paradoxically”
eliminating the split. On expiration, the split can be heard (opposite to physiologic splitting).
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Q:59: What type of murmer is produced due to Aortic stenosis?
Ans: Crescendo-decrescendo ejection murmur, loudest at heart base, radiates to carotids.
Soft S2 +/– ejection click “Pulsus parvus et tardus”— weak pulses with delayed peak.
Q:60: What is clinical association of aortic stenosis?
Ans: 1. In older (>60 years old) patients, most commonly due to agerelated calcification.
2. In younger patients, most commonly due to early-onset calcification of bicuspid aortic
valve.
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Q:61: Aortic stenosis can lead to which diseases on exertion?
Ans: S = Syncope.
A = Angina.
D = Dyspnea.
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Q:62: What type of murmer is produced due to Mitral/tricuspid regurgitation?
Ans: Holosystolic, high-pitched “blowing” murmur.
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Q:63: Mitral valve regurgitation murmer is heard loudest at which area of body?
Ans: Loudest at apex, radiates toward axilla.
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Q:64: Tricuspid valve regurgitation murmer is heard loudest at which which area of body?
Ans: Loudest at tricuspid area.
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Q:65: What are the clinical associations with Mitral valve regurgitation(MR)?
Ans: Mnemonic: MR LoVe Dilation: M = Mitral valve prolapse(MVP). Ischemic heart
disease(post MI). Rheumatic fever. LV dilation.
Q:66: What are the clinical associations with Tricuspid valve regurgitation(TR)?
Ans: RV dilation.
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Q:67: Which infection can cause either MR or TR?
Ans: Infective endocarditis.
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Q:68: What type of murmer is produced due to mitral valve prolapse?
Ans: Late crescendo murmur with midsystolic click (MC) that occurs after carotid pulse.
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Q:69: Mitral valve prolapse murmer is heard at which part of the body?
Ans: Best heard over apex Loudest just before S2.
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Q:70: What are the clinical associations with Mitral valve prolapse murmur/late crescendo
murmer?
Ans: Mnemonic: MCR(Mitral Crescendo) = Myxomatous degeneration, Chordae rupture,
Rheumatic fever.
Myxomatous degeneration is a progressive, non-inflammatory disarray of the structure
involved caused by a defect in the integrity of the structure, due to the alteration in the
synthesis and remodelling of the tissue.
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Q:71: How mid-systolic click(MC) is produced in Mitral valve prolapse murmer?
Ans: Due to sudden tensing of chordae tendineae as mitral leaflets prolapse into LA
(chordae cause crescendo with click).
Q:72: Which type of murmer is heard due to VSD(Ventral septal defect)?
Ans: Holosystolic, harsh-sounding murmur.
Larger VSDs have lower intensity murmur than smaller VSDs.
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Q:73: VSD murmer is heard best at which part of body and what is it's clinical association?
Ans: Loudest at tricuspid area. And it is congenital.
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Q:74: What are the four systolic murmers?
Ans: 1. Aortic stenosis murmer/Crescendo-decrescendo ejection murmer.
2. Mitral/Tricuspid regurgitation murmers/Holosystolic high-pitched “blowing” murmur.
3. Mitral valve prolapse(MVP) murmer/Late crescendo murmur with midsystolic click (MC).
4. Ventricular septal defect(VSD) murmer/Holosystolic, harsh-sounding murmur.
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Q:75: What are the two diastolic murmers?
Ans: 1. Aortic Regurgitation murmer/Early diastolic, decrescendo, high-pitched “blowing”
murmur.
2. Mitral stenosis murmer/Delayed rumbling mid-to-late murmur.
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Q:76: Aortic regurgitation murmer is heard best at which part of body?
Ans: Base(aortic root dilation) or left sternal border (valvular disease).
Q:77: What are the causes of the aortic regurgitation murmer?
Ans: Mnemonic: BEAR.
B = Bicuspid aortic valve.
E = Endocarditis.
A = Aortic root dilation.
R = Rheumatic fever.
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Q:78: What are the pulse changes that occur in aortic regurgitation murmer?
Ans: 1. Wide pulse pressure.
2. Pistol shot femoral pulse.
3. Pulsing nail bed (Quincke pulse).
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Q:79: What are the complications of Aortic regurgitation?
Ans: 1. Hyperdynamic pulse and head bobbing when severe and chronic.
2. Can progress to left HF.
--------------------------------------------------------------------------------------------------------
Q:80: Which murmur Follows opening snap (OS)?
Ans: Mitral stenosis murmer.
--------------------------------------------------------------------------------------------------------
Q:81: What is the cause of Mitral stenosis?
Ans: Late and highly specific sequelae of rheumatic fever.
Q:82: What are the complications of chronic Mitral stenosis?
Ans: 1. LA dilation and pulmonary congestion.
2. Atrial fibrillation. 3. Ortner syndrome. 4. Hemoptysis. 5. Right HF
--------------------------------------------------------------------------------------------------------
Q:83: Which murmer is also called Continuous machinelike murmur and where in body it is
best heard?
Ans: Patent ductus arteriosus murmer. Best heard at left infraclavicular area Loudest at S2.
--------------------------------------------------------------------------------------------------------
Q:84: What are the causes of Continuous machine like murmur/Patent ductus murmur?
Ans: 1. Congenital Rubella. 2. Prematurity.
--------------------------------------------------------------------------------------------------------
Q:85: What cardiovascular changes happens with inspiration maneuver?
Ans: Increased venous return to right heart, decreased venous return to left heart.
--------------------------------------------------------------------------------------------------------
Q:86: Which MURMURS THAT INCREASE/become louder WITH MANEUVER inspiration?
Ans: Most right-sided murmurs. Remember by RINSPIRATION.
--------------------------------------------------------------------------------------------------------
Q:87: Which MURMURS THAT DECREASE/become softer WITH MANEUVER inspiration?
Ans: Most left-sided murmurs.
--------------------------------------------------------------------------------------------------------
Q:88: Which MURMURS THAT INCREASE/become louder WITH MANEUVER expiration?
Ans: Left-sided murmers. Remember by: LEXPIRATION.
Q:89: What happens to murmers with increasing or decreasing preload? And what are the
two exceptions?
Ans: 1. Increased preload = louder murmers.
Exceptions =1. HOCM(Hypertrophic obstructive cardiomyopathy) : Because increased
blood cause the septum to move to normal size due to pressure. 2. Mitral valve
prolapse(MVP).
2. Decreased preload = softer murmers.
Exceptions = 1. HOCM. 2. MVP.
--------------------------------------------------------------------------------------------------------
Q:90: Which two maneuver increase preload?
Ans: Squatting and leg raise.
--------------------------------------------------------------------------------------------------------
Q:91: Which two maneuver decrease preload?
Ans: Valsalva and standing.
--------------------------------------------------------------------------------------------------------
Q:92: Which murmer become louder with increasing afterload and which murmers become
softer?
Ans: Aortic regurgitation become louder.
HOCM and MVP become softer.
Q:93: What maneuver can increase afterload?
Ans: Handgrip.
--------------------------------------------------------------------------------------------------------
Q:94: Which murmer become louder with decreasing afterload?
Ans: HOCM and MVP.
--------------------------------------------------------------------------------------------------------
Q:95: Which drug decrease afterload?
Ans: Amyl nitrite.
--------------------------------------------------------------------------------------------------------
Q:96: Which valve is damaged primarily because of Intravenous drug abuse?
Ans: Tricuspid valve resulting into Tricuspid valve regurgitation; as it is the first valve that is
exposed to pathogen. Mnemonic: Wanna TRI some drugs?
--------------------------------------------------------------------------------------------------------
Q:97: Opening snap is heard in which murmur?
Ans: Mnemonic: The Operating system is MicroSoft. The OS is MS. OS= Opening snap. MS =
Mitral stenosis.
--------------------------------------------------------------------------------------------------------
Q:98: Midsystolic click is found in which murmur?
Ans: Mnemonic: To win MVP, your team has to click.
MVP= Mitral valve prolapse murmer/Myxomatous valve disease.
Q:99: What is the resting potential of cardiac myocytes?
Ans: -85mv.
--------------------------------------------------------------------------------------------------------
Q:100: What happens in phase 0 myocardial action potential?
Ans: Rapid upstroke and depolarization— voltage-gated Na+ channels open.
--------------------------------------------------------------------------------------------------------
Q:101: What happens in phase 1 myocardial action potential?
Ans: Initial repolarization—inactivation of voltage-gated Na+ channels. Voltage-gated K+
channels begin to open.
--------------------------------------------------------------------------------------------------------
Q:102: What happens in phase 2 myocardial action potential?
Ans: Plateau (“platwo”)—Ca2+ influx through voltage-gated Ca2+ channels balances K+
efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte
contraction (excitation-contraction coupling).
--------------------------------------------------------------------------------------------------------
Q:103: What happens in phase 3 myocardial action potential?
Ans: Rapid repolarization—massive K+ efflux due to opening of voltage-gated slow
delayed-rectifier K+ channels and closure of voltage-gated Ca2+ channels.
--------------------------------------------------------------------------------------------------------
Q:104: What happens in phase 4 myocardial action potential?
Ans: Resting potential—high K+ permeability through K+ channels.
Q:105: Pacemaker action potential occurs in which cells of heart?
Ans: SA node and AV node.
--------------------------------------------------------------------------------------------------------
Q:106: What happens in phase 0 in pacemaker action potential?
Ans: Upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels
are permanently inactivated because of the less negative resting potential of these cells.
Results in a slow conduction velocity that is used by the AV node to prolong transmission
from the atria to ventricles.
--------------------------------------------------------------------------------------------------------
Q:107: What happens in phase 3 in pacemaker action potential?
Ans: Repolarization—inactivation of the Ca2+ channels and increased activation of K+
channels causing increased K+ efflux.
--------------------------------------------------------------------------------------------------------
Q:108: What happens in phase 4 in pacemaker action potential?
Ans: Slow spontaneous diastolic depolarization due to If (“funny current”). If channels
responsible for a slow, mixed Na+ inward/K+ outward current; different from INa in phase
0 of ventricular action potential.
--------------------------------------------------------------------------------------------------------
Q:109: In which phase of pacemaker action potential accounts for automaticity of SA and
AV nodes?
Ans: Phase 4.
Q:110: The slope of which phase of pacemaker potential in the SA node determines HR?
Ans: Phase 4.
--------------------------------------------------------------------------------------------------------
Q:111: Which drugs decrease the rate of diastolic depolarization and decrease HR?
Ans: ACh/adenosine.
--------------------------------------------------------------------------------------------------------
Q:112: What is the resting potential of pacemaker cells?
Ans: -60mv.
--------------------------------------------------------------------------------------------------------
Q:113: What is Threshold potential of pacemaker cells?
Ans: -40mv.
--------------------------------------------------------------------------------------------------------
Q:114: What is the extension of SA node into left atrium is called?
Ans: Bachmann bundle.
--------------------------------------------------------------------------------------------------------
Q:115: What is the sequence of pacemaker rates of conduction pathway of Heart?
Ans: SA > AV > bundle of His/ Purkinje/ventricles.
--------------------------------------------------------------------------------------------------------
Q:116: What is the sequence of Speed of conduction of conduction pathway of Heart?
Ans: He Parks At Ventura AVenue.
His-Purkinje > Atria > Ventricles > AV node.
--------------------------------------------------------------------------------------------------------
Q:117: What P-wave indicate in ECG?
Ans: Atrial depolarization.
Q:118: What PR interval indicate in ECG?
Ans: Time from start of atrial depolarization to start of ventricular depolarization (normally
120-200 msec).
--------------------------------------------------------------------------------------------------------
Q:119: What QRS complex indicate in ECG?
Ans: Ventricular depolarization (normally < 100 msec).
--------------------------------------------------------------------------------------------------------
Q:120: What T-wave indicate in ECG?
Ans: Ventricular repolarization.
--------------------------------------------------------------------------------------------------------
Q:121: What T-wave inversion indicate?
Ans: T-wave inversion may indicate ischemia or recent MI.
--------------------------------------------------------------------------------------------------------
Q:122: What is J-point in ECG?
Ans: Junction between end of QRS complex and start of ST segment.
--------------------------------------------------------------------------------------------------------
Q:123: What is the ST-segment in ECG?
Ans: Isoelectric, ventricles are in depolarized state.
--------------------------------------------------------------------------------------------------------
Q:124: What is U wave in ECG?
Ans: Prominent in hypokalemia (think hyp“U”kalemia), bradycardia.
--------------------------------------------------------------------------------------------------------
"Whenever a doctor cannot do good, he must kept from doing harm." ~ Hippocrates.
Q:125: Atrial natriuretic peptide(ANP) is released from atrial myocytes in response to what
changes in body?
Ans: Increased blood volume and increased atrial pressure.
--------------------------------------------------------------------------------------------------------
Q:126: What is the mechanism of action of ANP?
Ans: Acts via cGMP.
--------------------------------------------------------------------------------------------------------
Q:127: What is the effect of ANP on body?
Ans: ANP causes vasodilation and decreases Na+ reabsorption at the renal collecting
tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting
diuresis and contributing to “aldosterone escape” mechanism.
--------------------------------------------------------------------------------------------------------
Q:128: B-type (brain) natriuretic peptide(BNP) is released from ventricular myocytes in
response to what changes in body?
Ans: Increased Tension.
--------------------------------------------------------------------------------------------------------
Q:129: What is the difference between ANP and BNP in their physiologic action?
Ans: Similar physiologic action to ANP, with longer half-life.
--------------------------------------------------------------------------------------------------------
Q:130: BNP blood test used for diagnosing which disease?
Ans: BNP blood test used for diagnosing HF(heart failure).
Q:131: Aortic baroreceptors and Aortic chemoreceptors in Aortic arch transmits via which
nerve to solitary nucleus of medulla (responds to changes in BP)?
Ans: Vagus nerve.
--------------------------------------------------------------------------------------------------------
Q:132: Carotid sinus baroreceptors and carotid body chemoreceptors transmits via which
nerve to solitary nucleus of medulla (responds to changes in BP).
Ans: Glossopharyngeal nerve.
--------------------------------------------------------------------------------------------------------
Q:133: Peripheral chemoreceptors: carotid and aortic bodies are stimulated by what
changes in the body?
Ans: Increase PCO2, Decreased pH of blood, and Decreased PO2 (< 60 mm Hg).
--------------------------------------------------------------------------------------------------------
Q:134: Central chemoreceptors are stimulated by what changes in the body?
Ans: Stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are
influenced by arterial CO2 as H+ cannot cross the blood-brain barrier.
--------------------------------------------------------------------------------------------------------
Q:135: Which chemoreceptors do not directly respond to Po2?
Ans: Central chemoreceptors.
--------------------------------------------------------------------------------------------------------
Q:136: What are the factors that cause chemoreceptors to be less responsive?
Ans: Central chemoreceptors become less responsive with chronically increased Pco2
(eg, COPD) leads to increased dependence on peripheral chemoreceptors to detect 
O2 to drive respiration.
Q:137: How baroreceptors responds to hypotension?
Ans: Decreased arterial pressure leads to decreased stretch leads to increased afferent
baroreceptor firing that leads to increased efferent sympathetic firing and decreased
efferent parasympathetic stimulation causing vasoconstriction, increased HR, increased
contractility, increased BP.
--------------------------------------------------------------------------------------------------------
Q:138: Baroreceptors response to hypotension is important in which shock?
Ans: Hypovolemic Shock.
--------------------------------------------------------------------------------------------------------
Q:139: What is the response of baroreceptors to carotid massage?
Ans: Increase in carotid sinus pressure causes increased afferent baroreceptor firing leads
to increased AV node refractory period that causes decreased HR leads to decreased CO.
Also leads to peripheral vasodilation.
--------------------------------------------------------------------------------------------------------
Q:140: What can be caused by carotid massage?
Ans: Presyncope/Syncope.
--------------------------------------------------------------------------------------------------------
Q:141: What are the conditions exaggerate the carotid massage reflex?
Ans: Exaggerated in underlying atherosclerosis, prior neck surgery, older age.
--------------------------------------------------------------------------------------------------------
Q:142: What is Cushing reflex?
Ans: Triad of hypertension, bradycardia, and respiratory depression.
Q:143: What happens due to cushing reflex?
Ans: Increased intracranial pressure constricts arterioles causing cerebral ischemia leads to
increased pCO2 and decreased pH leads to central reflex sympathetic increase in perfusion
pressure (hypertension) causing increased stretch activating peripheral reflex
baroreceptor– induced bradycardia.
--------------------------------------------------------------------------------------------------------
Q:144: What are the factors that determine the autoregulation of lungs?
Ans: Hypoxia causes vasoconstriction.
The pulmonary vasculature is unique in that alveolar hypoxia causes vasoconstriction so
that only well-ventilated areas are perfused. In other organs, hypoxia causes vasodilation.
--------------------------------------------------------------------------------------------------------
Q:145: What are the factors that determine the autoregulation of heart?
Ans: Local metabolites (vasodilatory): NO, CO2, decreased O2.
--------------------------------------------------------------------------------------------------------
Q:146: What are the factors that determine the autoregulation of Brain?
Ans: Local metabolites (vasodilatory): CO2 (pH).
--------------------------------------------------------------------------------------------------------
Q:147: What are the factors that determine the autoregulation of kidneys?
Ans: Myogenic (stretch reflex of afferent arteriole) and tubuloglomerular feedback.
--------------------------------------------------------------------------------------------------------
" No beauty shines brighter than that of a good heart. "
Q:148: What are the factors that determine the autoregulation of skeletal muscles in
response to wide range of perfusion pressures?
Ans: Local metabolites during exercise (vasodilatory): CHALK: CO2, H+, Adenosine, Lactate,
K+.
At rest: sympathetic tone in arteries.
--------------------------------------------------------------------------------------------------------
Q:149: What are the factors that determine the autoregulation of skin in response to wide
range of perfusion pressures?
Ans: Sympathetic vasoconstriction most important mechanism for temperature control.
--------------------------------------------------------------------------------------------------------
Q:150: How to calculate the net capillary exchange fluid flow?
Ans: Jv = net fluid flow = Kf [(Pc − Pi) − σ(πc − πi)].
Kf = capillary permeability to fluid. σ = reflection coefficient (measure of capillary
impermeability to protein).
--------------------------------------------------------------------------------------------------------
Q:151: What are the examples that increase capillary pressure?
Ans: HF(Heart failure).
--------------------------------------------------------------------------------------------------------
Q:152: What are the examples that increase capillary permeability?
Ans: Toxins, infections, burns.
Q:153: What are the examples that increase interstitial fluid oncotic pressure?
Ans: Lymphatic blockage.
--------------------------------------------------------------------------------------------------------
Q:154: What are the examples that decrease plasma proteins oncotic pressure?
Ans: Nephrotic syndrome, liver failure, protein malnutrition.
--------------------------------------------------------------------------------------------------------
Q:155: What is the systolic/diastolic pressure in systemic circulation?
Ans: 120/80.
--------------------------------------------------------------------------------------------------------
Q:156: What is the systolic/diastolic pressure in pulmonary circulation?
Ans: 25/8.
CARDIOVASCULAR USMLE QUESTION
BANK - PATHOLOGY
Q:1 Classify the congenital heart diseases?
Ans: 1. RIGHT-TO-LEFT SHUNTS.
2. LEFT-TO-RIGHT SHUNTS.
3. Coarctation of the aorta.
--------------------------------------------------------------------------------------------------------
Q:2: Examples of Right-to-left shunts?
Ans: The 5 T’s: 1. Truncus arteriosus ( 1 vessel). 2. Transposition ( 2 switched vessels). 3.
Tricuspid atresia ( 3 = Tri). 4. Tetralogy of Fallot ( 4 = Tetra). 5. TAPVR ( 5 letters in the
name).
TAPVR = Total anomalous pulmonary venous return.
Also Ebstein Anomaly.
--------------------------------------------------------------------------------------------------------
Q:3: Patients with Persistent truncus arteriosus also has mostly which heart defect
accompanying?
Ans: VSD(Ventricular septal defect).
--------------------------------------------------------------------------------------------------------
Q:4: Types of transposition of great Vessels(TGA)?
Ans: 1. Dextro-TGA(Complete TGA). = Not compatible with life unless a shunt is present to
allow mixing of blood (eg, VSD, PDA, or patent foramen ovale).
2. Levo-TGA. = Compatible with life but will lead to Heart failure later in life.
Q:5: What are the risk factors that will cause a mother to have infant with TGA?
Ans: Mothers having: 1. Diabetes. 2. Rubella. 3. Poor nutrition.
Mothers consuming: 4. Alcohol.
Mothers age: greater than 40 years.
--------------------------------------------------------------------------------------------------------
Q:6: Absence of tricuspid valve(Tricuspid atresia) and hypoplastic RV; requires which two
other heart defects to be viable for life?
Ans: 1. ASD. 2. VSD.
--------------------------------------------------------------------------------------------------------
Q:7: Which congenital heart disease is the most common cause of early childhood cyanosis?
Ans: Tetralogy of Fallot.
--------------------------------------------------------------------------------------------------------
Q:8: Tetralogy of Fallot is associated with which syndrome?
Ans: 22q11 syndromes(DiGeorge syndromes).
--------------------------------------------------------------------------------------------------------
Q:9: Name the 4 abnormalities in Tetralogy of fallot?
Ans: Mnemonic: PROVe.
1. Pulmonary infundibular stenosis (most important determinant for prognosis).
2. Right ventricular hypertrophy (RVH)— boot‑shaped heart on CXR.
3. Overriding aorta.
4. VSD.
Q:10: What are Tet spells?
Ans: Babies who have tetralogy of Fallot will suddenly develop deep blue skin, nails and
lips after crying or feeding, or when agitated. These episodes are called tet spells. Tet spells
are caused by a rapid drop in the amount of oxygen in the blood.
--------------------------------------------------------------------------------------------------------
Q:11: What is the treatment for a tet spell?
Ans: Place infants with hypercyanotic spells in the knee-chest position(Squatting) and give
oxygen; sometimes, opioids (morphine or fentanyl), volume expansion, sodium
bicarbonate, beta-blockers (propranolol or esmolol), or phenylephrine may help.
--------------------------------------------------------------------------------------------------------
Q:12: What is Total Anomalous Pulmonary Venous Return(TAPVR)?
Ans: Pulmonary veins drains into right atrium instead of left atrium.
--------------------------------------------------------------------------------------------------------
Q:13: TAPVR is associated with which other heart abnormalities?
Ans: ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.
--------------------------------------------------------------------------------------------------------
Q:14: What is Ebstein's anomaly and which element exposure can cause it?
Ans: 1. Tricuspid valve defect resulting in regurgitation.
2. ASD.
It can be caused by lithium exposure in utero.
Q:15: Examples of cyanotic congenital heart defects?
Ans: 1. Truncus arteriosus. 2. Transposition of great vessels. 3. TAPVR. 4. Tetralogy of
fallot. 5. Hypoplastic left heart syndrome.
--------------------------------------------------------------------------------------------------------
Q:16: Examples of Acyanotic congenital heart defects?
Ans: 1. ASD. 2. VSD. 3. PDA. 4. Coaraction of aorta.
--------------------------------------------------------------------------------------------------------
Q:17: Examples of LEFT-TO-RIGHT SHUNTS?
Ans: 1. ASD. 2. VSD. 3. PDA. 4. Eisenmenger syndrome.
--------------------------------------------------------------------------------------------------------
Q:18: What is the frequency sequence of LEFT-TO-RIGHT SHUNTS?
Ans: VSD > ASD > PDA.
--------------------------------------------------------------------------------------------------------
Q:19: Two types of Coarctation of aorta?
Ans: 1. Infantile(70%). 2. Adult(30%).
--------------------------------------------------------------------------------------------------------
Q:20: In which heart defect shunts there is early cyanosis and late cyanosis?
Ans: Right-to-left shunts: early cyanosis. Left-to-right shunts: “later” cyanosis.
--------------------------------------------------------------------------------------------------------
Q:21: Eisenmenger syndrome causes which symptoms?
Ans: Causes late cyanosis, clubbing, and polycythemia.
Q:22: What are complications of coarctation of aorta?
Ans: Complications include HF, Increased risk of cerebral hemorrhage (berry aneurysms),
aortic rupture, and possible endocarditis.
--------------------------------------------------------------------------------------------------------
Q:23: Fetal Alcohol syndrome causes which cardiac defects?
Ans: 1. ASD. 2. VSD. 3. PDA. 4. Tetralogy of Fallot.
--------------------------------------------------------------------------------------------------------
Q:24: Congenital Rubella causes which cardiac defects?
Ans: 1. ASD. 2. VSD. 3. PDA. 4. pulmonary artery stenosis.
--------------------------------------------------------------------------------------------------------
Q:25: Down syndrome causes which cardiac defects?
Ans: 1. ASD. 2. VSD. 3. AV septal defect (endocardial cushion defect).
--------------------------------------------------------------------------------------------------------
Q:26: Mother with diabetes will have baby with which cardiac defects?
Ans: 1. Transposition of great vessels. 2. VSD.
--------------------------------------------------------------------------------------------------------
Q:27: Marfan syndrome can cause which congenital cardiac defects?
Ans: MAT = 1. MVP. 2. Aortic regurgitation. 3. Thoracic aortic aneurysm and dissection.
--------------------------------------------------------------------------------------------------------
Q:28: Ebstein anamoly is caused by?
Ans: Prenatal lithium exposure.
--------------------------------------------------------------------------------------------------------
Q:29: Bicuspid aortic valve is caused in which syndrome?
Ans: Turners syndrome.
Q:30: Coarctation of aorta is caused in which syndrome?
Ans: Turners syndrome.
--------------------------------------------------------------------------------------------------------
Q:31: 22q11 syndromes is causes which cardiac defects?
Ans: Mnemonic, give hyphen hat to 11 to become TT: Truncus arteriosus, tetralogy of
Fallot.
--------------------------------------------------------------------------------------------------------
Q:32: Tetralogy of fallot is caused by which two syndromes?
Ans: 1. 22q11 syndrome. 2. Fetal Alcohol syndrome.
--------------------------------------------------------------------------------------------------------
Q:33: What is hypertension?
Ans: Persistent systolic BP ≥ 130 mm Hg and/or diastolic BP ≥ 80 mm Hg.
--------------------------------------------------------------------------------------------------------
Q:34: What are the risk factors for hypertension?
Ans: Mnemonic: SAD TOP family.
S = High sodium intake. A = Increased Age, Excess Alcohol intake. D = Diabetes. T = Tobacco
smoking. O = Obesity. P = Physical inactivity. Family history.
--------------------------------------------------------------------------------------------------------
Q:35: What is the incidience rate of hypertension in different populations?
Ans: Black > White > Asian populations.
--------------------------------------------------------------------------------------------------------
Q:36: What are the two types of Hypertension?
Ans: Primary(Essential) hypertension(90%) and Secondary hypertension.
Q:37: What are the causes of secondary hypertension?
Ans: Mnemonic: RENALS.
R = Glomerulonephritis, renal artery stenosis.
E = Endocrine -> Cushing's disease, Conn's syndrome, pheochromocytoma, acromegaly,
corticosteroids, oral contraceptive pills.
N = Neurogenic -> Raised intracranial pressure.
A = Aortic coarctation.
L = Little people -> pregnancy induced hypertension.
S = Stress -> Trauma, white coat hypertension.
--------------------------------------------------------------------------------------------------------
Q:38: What are the two main causes of renal artery stenosis?
Ans: 1. Fibromuscular dysplasia (characteristic “string of beads” appearance of renal artery,
usually seen in adult females).
2. Atherosclerotic renal artery stenosis.
--------------------------------------------------------------------------------------------------------
Q:39: What is hypertensive urgency?
Ans: Severe (≥ 180/≥ 120 mm Hg) hypertension without acute end-organ damage.
Q:40: What is Conn's syndrome?
Ans: Primary aldosteronism (also called Conn's syndrome) is a rare condition caused by
overproduction of the hormone aldosterone that controls sodium and potassium in the
blood. Conn's syndrome is most often caused by an adrenal tumor, such as
aldosterone-producing adenomas.
--------------------------------------------------------------------------------------------------------
Q:41: What is Hypertensive emergency?
Ans: Severe hypertension with evidence of acute end-organ damage;
Brain: Encephalopathy, Stroke, Eclampsia.
Eyes: Retinal hemorrhages and exudates, papilledema.
Heart: Coronary artery disease(CAD), Heart failure, Myocardial Infarction, Atrial fibrillation,
microangiopathic hemolytic anemia.
Vessels and blood: Aortic aneurysms, aortic dissection.
Kidney: Chronic kidney disease.
--------------------------------------------------------------------------------------------------------
Q:42: What is Pre-eclampsia?
Ans: 1. Preganancy Induced hypertension. 2. Proteinuria. 3. Edema.
Q:43: What is Eclampsia?
Ans: Convulsions on a background of Pre-Eclampsia.
--------------------------------------------------------------------------------------------------------
Q:44: What is papilledema?
Ans: Optic disc swelling that is secondary to elevated intracranial pressure.
--------------------------------------------------------------------------------------------------------
Q:45: What are Xanthomas and xanthelasmas?
Ans: Plaques or nodules composed of lipid-laden histiocytes in skin, especially the eyelids
(xanthelasma).
--------------------------------------------------------------------------------------------------------
Q:46: What is Tendinous xanthoma?
Ans: Lipid deposit in tendon, especially Achilles tendon and finger extensors.
--------------------------------------------------------------------------------------------------------
Q:47: What is Corneal arcus?
Ans: Lipid deposit in cornea. Common in elderly (arcus senilis), but appears earlier in life
with hypercholesterolemia.
--------------------------------------------------------------------------------------------------------
Q:48: What is Arteriosclerosis?
Ans: Hardening of arteries, with arterial wall thickening and loss of elasticity.
--------------------------------------------------------------------------------------------------------
Q:49: What are three types of Arteriosclerosis?
Ans: 1. Atherosclerosis(Very common). 2. Arteriolosclerosis(Common). 3. Monckeberg
sclerosis(Uncommon).
Q:50: What is Atherosclerosis?
Ans: Disease of elastic arteries and large- and medium-sized muscular arteries; a form of
arteriosclerosis caused by buildup of cholesterol plaques in intima.
--------------------------------------------------------------------------------------------------------
Q:51: What are the locations of Atherosclerosis according to incidence?
Ans: Mnemonic: A COP CAR chasing Willis in circles. Willis shouts Atherosclerosis.
A = Abdominal aorta. > CO= Coronary artery. > P= Popiliteal artery. > Car = Carotid arteries.
> Circle of Willis.
--------------------------------------------------------------------------------------------------------
Q:52: What are the modifiable risk factors of Atherosclerosis?
Ans: Diabetes, dyslipidemia (Increased LDL, decreased HDL).
Hypertension and Tobacco smoking.
--------------------------------------------------------------------------------------------------------
Q:53: What are the non modifiable risk factors of Atherosclerosis?
Ans: MAP of family history: Male sex, Increasing age, Postmenopausal women, family
history.
--------------------------------------------------------------------------------------------------------
Q:54: What are the symptoms of Atherosclerosis?
Ans: Angina, claudication, but can be asymptomatic.
--------------------------------------------------------------------------------------------------------
Q:55: What are the complications of Atherosclerosis?
Ans: 1. Thrombus. 2. Emboli. 3. Ischemia. 4. Infarct. 5. Peripheral Vascular disease.
Q:56: What are the pathogenesis of Atherosclerosis?
Ans: Inflammation important in pathogenesis: endothelial cell dysfunction leads to
macrophage and LDL accumulation leads to foam cell formation leads to fatty streaks leads
to smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular
matrix deposition leads to fibrous plaque leads to complex atheromas leads to calcification
(calcium content correlates with risk of complications).
--------------------------------------------------------------------------------------------------------
Q:57: Arteriolosclerosis affects which vessels in the body?
Ans: Small vessels and arterioles.
--------------------------------------------------------------------------------------------------------
Q:58: What are the two types of Arteriolosclerosis?
Ans: 1. Hyaline arteriolosclerosis. 2. Hyperplastic Arteriolosclerosis.
--------------------------------------------------------------------------------------------------------
Q:59: What is Hyaline arteriolosclerosis?
Ans: Thickening of vessel walls 2° to plasma protein leak into endothelium in essential
hypertension or diabetes mellitus.
--------------------------------------------------------------------------------------------------------
Q:60: What is Hyperplastic arteriolosclerosis?
Ans: “Onion skinning” in severe hypertension with proliferation of smooth muscle cells.
Q:61: What is Monckeberg sclerosis?
Ans: Calcification of internal elastic lamina and media of arteries causing vascular
stiffening without obstruction.
--------------------------------------------------------------------------------------------------------
Q:62: What Monckeberg sclerosis is also called and affects which sized arteries?
Ans: It is also called medial calcific sclerosis. Medium Sized arteries.
--------------------------------------------------------------------------------------------------------
Q:63: What type of appearance occurs in Monckeberg sclerosis on X-ray?
Ans: “Pipestem” appearance on x-ray.
--------------------------------------------------------------------------------------------------------
Q:64: What is aortic aneurysm?
Ans: Localized pathologic dilation of the aorta. May cause abdominal and/or back pain,
which is a sign of leaking, dissection, or imminent rupture.
--------------------------------------------------------------------------------------------------------
Q:65: What are two types of aortic aneurysm?
Ans: 1. Thoracic aortic aneurysm. 2. Abdominal aortic aneurysm.
--------------------------------------------------------------------------------------------------------
Q:66: What is Cystic medial necrosis (CMN)?
Ans: Cystic medial necrosis (CMN) is a disease of large arteries, especially the aorta, caused
by collagen linking defects leading to deposition of basophilic ground substance in the
media, creating cyst-like lesions that weaken the artery wall.
Q:67: Thoracic aortic aneurysm is associated with which disease?
Ans: Cystic medial necrosis or degeneration.
--------------------------------------------------------------------------------------------------------
Q:68: What are the risk factors for Thoracic aortic aneurysm?
Ans: 1. Hypertension. 2. Bicuspid aortic valve. 3. Connective tissue disorders(e.g Marfan
syndrome). 4. Tertiary syphillis(obliterative endarteritis of the vasa vasorum). 5. Aortic root
dilation.
--------------------------------------------------------------------------------------------------------
Q:69: Abdominal aortic aneurysm is associated with which disease?
Ans: Atherosclerosis.
--------------------------------------------------------------------------------------------------------
Q:70: What are the risk factors for abdominal aortic aneurysms?
Ans: 1. Increased age. 2. Male sex. 3. Family history.
--------------------------------------------------------------------------------------------------------
Q:71: What is the most common location of abdominal aortic aneurysm?
Ans: Most often infrarenal (distal to origin of renal arteries).
--------------------------------------------------------------------------------------------------------
Q:72: At what part of aorta, Traumatic aortic rupture most commonly occurs?
Ans: Aortic isthmus, proximal descending aorta just distal to left subclavian artery.
--------------------------------------------------------------------------------------------------------
Q:73: What is aortic dissection?
Ans: Longitudinal intimal tear forming a false lumen.
Q:74: Aortic dissection is associated with which diseases?
Ans: 1. Hypertension. 2. Bicuspid aortic valve. 3. Inherited connective tissue disorders (eg,
Marfan syndrome).
--------------------------------------------------------------------------------------------------------
Q:75: What are the symptoms of aortic dissection?
Ans: Sudden-onset chest pain radiating to the back +/− markedly unequal BP in arms.
--------------------------------------------------------------------------------------------------------
Q:76: What are the complications of aortic dissection?
Ans: 1. Organ ischemia. 2. Aortic rupture. 3. Death.
--------------------------------------------------------------------------------------------------------
Q:77: What are the two classifications that classify the aortic dissection?
Ans: 1. Stanford Classification. 2. DeBakey Classification.
--------------------------------------------------------------------------------------------------------
Q:78: In Stanford type A, aortic dissection can result in what complications?
Ans: Acute aortic regurgitation or cardiac tamponade.
--------------------------------------------------------------------------------------------------------
Q:79: What is the treatment for Stanford type A aortic dissection?
Ans: Surgery.
--------------------------------------------------------------------------------------------------------
Q:80: What is the treatment for Stanford type B aortic dissection?
Ans: Beta blockers then vasodilators.
Q:81: What is subclavian steel syndrome?
Ans: Stenosis of subclavian artery proximal to origin of vertebral artery leads to
hypoperfusion distal to stenosis leads to reversed blood flow in ipsilateral vertebral artery
leads to reduced cerebral perfusion on exertion of affected arm.
Q:82: What are the symptoms of subclavian steal syndrome?
Ans: It causes 1. Arm ischemia. 2. Pain. 3. Paresthesia. 4. Vertebrobasilar insufficiency
(dizziness, vertigo). 5. >15 mm Hg difference in systolic BP between arms.
Q:83: With what subclavian steal syndrome is associated with?
Ans: 1. Associated with arteriosclerosis. 2. Takayasu arteritis. 3. Heart surgery.