Week 3 Block 6: PCR

Question 1

(1) Most prevalent collagen in body (2) Primary collagen in mature scars (3) Type of collagen in granulation tissue (4) Places these types of collagen found

Answer 1

(1) Type I collagen most prevalent collagen in human body and is (2) primary collagen in mature scars (3) Granulation tissue composed primarily of type III collagen. (4) Type I found in Dermis, bone tendons, ligaments, dentin, cornea, blood vessels, & scar tissue; Type III in skin, lungs, intestines, blood vessels, bone marrow, lymphatics, & granulation tissue

Question 2

(1) Embryologic abnormality/mechanism behind Tetralogy of Fallot (2) Other cyanotic heart diseases sharing this mechanism/abnormality

Answer 2

(1) Abnormal migration of neural crest cells through primitive truncus arteriosus and bulbus cordis (2) TOF, transposition of great vessels, & Truncus arteriosus

Question 3

Compensation in CHF & consequences

Answer 3

Compensatory activation of renin-angiotensin-aldosterone pathway and sympathetic nervous system results in increased afterload (from excessive vasoconstriction), excess fluid retention, and deleterious cardiac remodeling

Question 4

(1) Dx: progressive exertional sob, coronary sinus dilation on echocardiographic (2) Explain mechanism & significance of findings

Answer 4

(1) Pulmonary hypertension (2) Coronary sinus (carrying deoxygenated blood) communicates freely with right atrium and therefore may become dilated secondary to any factor that causes right atrial dilatation. The most common factor is pulmonary artery hypertension, which leads to elevated right heart pressures. Coronary sinus not usually visible by echocardiography in most normal, healthy patients.

Question 5

(1) Part of heart that forms diaphragmatic surface of heart (2) Artery that supplies it (3) Artery that usually feeds into artery in #2

Answer 5

(1) Inferior wall of left ventricle (2) Posterior descending artery (PDA) (3) In 85-90% of individuals, PDA derives from right coronary artery

Question 6

Acute left ventricular heart failure : (1) CXR findings (2) Mechanistic cause of findings (3) Common triggers for acute heart failure (4) Sx (5) PE findings

Answer 6

Cardiomedgaly (heart > 1 hemithorax in size), Kerley B lines (short horizontal lines situated perpendicularly to pleural surface that represent edema of interlobular septa), pleural effusions (blunting of costophrenic angles), & increased vascular shadowing (alveolar edema) bilaterally (2) Result from increased left atrial and ventricular filling pressure (increased preload). Increased pressure transmitted to pulmonary capillaries, causing fluid transudation into pulmonary interstitial and alveolar spaces (cardiogenic pulmonary edema) (3) MI, severe hypertension, arrhythmias (e.g., atrial fibrillation), & drug use (e.g., cocaine) (4) cough, dyspnea, and fatigue, which can rapidly become more severe. (5) typically tachypneic and may be using accessory muscles to breathe. Chest exam reveals crackles, and sometimes wheezing (cardiac asthma) due to edema of the bronchial airways

Question 7

(1) Holosystolic murmur that increases in intensity on inspiration (2) Other holosystolic murmurs

Answer 7

(1) Tricuspid regurgitation (2) Mitral regurgitation, VSD (which do not typically increase during inspiration)

Question 8

Nerves transmitting from baroreceptors in the following: (1) Carotid sinus (2) Aortic arch (3) Termination of fibers from carotid sinus and aortic arch baroceptors (4) Triggers & Effect of stimulating baroreceptors in carotid sinus

Answer 8

(1) Glossopharyngeal (CN IX) branch, Hering’s nerve(2) Vagus (CN X) (3) Solitary nucleus of medulla (4) Blood pressure increases or external pressure on carotid sinuses stimulation baroeceptors in the carotid sinus walls, leading to vasodilatation, decrease in heart rate and contractility, & decrease in blood pressure. “Carotid sinus syncope” tends to occur in patients with very sensitive carotid sinuses.

Question 9

Give predominant light microscopic changes at following times after MI: (1) 0-4 hrs (2) 4-12 hrs (3) 12-24 hrs (4) 1-5 days (5) 5-10 days (6) 10-14 days (7) 2 wks-2 mo.

Answer 9

(1) minimal change (2) early coagulation necrosis, edema, hemorrhage, wavy fibers (3) coagulation necrosis and marginal contraction band necrosis (4) coagulation necrosis and neutrophilic infiltrate (5) macrophage phagocytosis of dead cells (6) granulation tissue and neovascularizaton (7) collagen deposition/scar formation

Question 10

(1) Dx: MI, mitral valve leaflet thickening, several small masses attached to both sides, coronary arteries appear normal on coronary angiography (2) Associated condition & frequency (3) Unique presentation/finding relating this Dx & associated condition (4) Ddx: MI in setting of normal coronary arteries

Answer 10

(1) Verrucous endocarditis (Libman-Sacksendocarditis) occurs in (2) up to 25% of patients with systemic lupus erthematosus (SLE). This condition can cause small cardiac valvular vegetations on either side of a valve, resulting in fibrotic valve thickening and deformity. (3) SLE may cause an acute coronary syndrome at a young age even with angiographically normal coronary arteries. (4) coronary arteritis, hypercoagulability with acute thrombosis (e.g., SLE thromobosis due to hypercoagulable antiphospholipid antibody syndrome), or coronary vasopasm

Question 11

Heart pressure(s) changed in isolated mitral stenosis & its effects

Answer 11

Elevates atrial diastolic pressure & can therefore cause elevated pulmonary capillary wedge pressure, pulmonary hypertension, decreased pulmonary vascular compliance, right ventricular dilatation, and functional tricuspid regurgitation. Diastolic pressure in left ventricle usually near normal or even decreased with severe mitral stenosis.

Question 12

(1) Diastolic heart failure diagnostic findings in: a) Left ventricular end-diastolic pressure b) Left ventricular end-diastolic volume c) Left ventricular ejection fraction (2) Explain (3) Contrast to systolic heart failure

Answer 12

(1) a) Increased b) Normal c) Normal (2) Diastolic heart failure characterized by decrease in ventricular diastolic compliance but normal ventricular compliance performance. As a result, LVEDP must be increased in order to achieve normal LVEDV and stroke volume. (3) Systolic heart failure results from decrease in ventricular contractile performance (decreased ejection fraction) and requires an increase in both LVEDP and LVEDV to improve stroke volume.

Question 13

(1) Verapamil mechanism/drug type & effects (2) How skeletal muscle reacts to it, and why

Answer 13

(1) Calcium channel blocker - Vasodilatory, also affects cardiac contractility but has minimal effect on skeletal muscle (2) Skeletal muscle resistant to effect of calcium channel blockers because it does NOT require an influx of extracellular calcium for excitation-contraction coupling, whereas cardiac and smooth muscle depend on extracellular calcium entering the cell via voltage-gated L-type calcium channels for excitation-contraction coupling. These voltage-gated calcium channels are target of verapamil and other calcium channel blockers.

Question 14

List cardiac tissue conduction velocities from fastest to slowest

Answer 14

Purkinje system => Atrial muscle (from SA node) => Ventricular muscle => AV node; Mnemonic: “Park at Ventura Avenue”

Question 15

(1) General causes of palpitations & it’s most common cause(2) Most likely Dx: irregularly regular tachyarrhythmia in conscious patient (3) EKG signs of this dx (4) Precipitating factors of this dx

Answer 15

(1) Any significant acute change in heart rate or rhythm or force of ventricular contraction may cause palpitations; Most common cause of palpitations is anxiety (2) Atrial fibrillation, the most common chronic arrhythmia (3) In AF, EKG shows absent p waves (because atrial contractions do not occur) and irregularly spaced ventricular contractions (QRS complexes) evidenced by variable R-R interval (4) Precipitating factors for isolated episodes of AF include binge alcohol consumption (“holiday heart syndrome”), increased cardiac sympathetic tone, and pericarditis.

Question 16

Nitroprusside: (1) drug type (2) mechanisms (3) effects

Answer 16

(1) Short-acting balanced venous and arterial vasodilator (2) Decreases both preload and afterload (3) Since these changes balanced, stroke volume maintained

Question 17

(1) Dx: nocturnal episodes of chest pain found to be accompanied by transient ST segment elevations in leads I, AVL, and V1-V4 on 24-hour ECG monitoring, PMH significant for migraines (2) Med that provokes chest pain in this pt & its clinical utility (3) Tx

Answer 17

(1) Prinzmetal’s (variant) angina is characterized by episodic, transient attacks of coronary vasospasm, typically occurring at rest and during midnight-to-early morning hours. These episodes generally produce temporally transmural myocardial ischemia with ST-sgement elevation. (2) Ergonovine (ergot alkaloid that constricts vascular smooth muscle by stimulating both alpha adrenergic and serotonergic receptors) can provoke this coronary vasospasm, and can aid in dx (3) Tx with vasodilating nitrates and calcium channel blockers

Question 18

Patient with chronic aortic stenosis and concentric left ventricular hypertrophy: (1) Role of Atrium(-) (2) Consequences of Atrial fibrillation (3) Significance of this condition

Answer 18

(1) Contributes significantly to left ventricular filling (2) In these patients, loss of atrial contraction due to atrial fibrillation can reduce left ventricular preload and cardiac output sufficiently to result in dangerous systemic hypotension. Decreased forward filling of left ventricle can also result in increased left atrial pressure, leading to acute pulmonary edema.

Question 19

(1) 2 factors stimulating transcription/release of ANP (2) What else do they release

Answer 19

(1) Both ventricular hypertrophy and volume overload cause release of both ANP and (2) BNP from the ventricular myocytes to facilitate natriuresis and diuresis

Question 20

Signs of constrictive pericarditis (other than pericardial friction rub)

Answer 20

(1) Kussmaul sign - although JVP normally drops on inspiration, paradoxical rise in JVP (2) may also be pericardial knock, which occurs earlier in diastole than S3 heart sound

Question 21

(1) Dx: child w/ toe cyanosis, and clubbing, no finger abnormalities, congenital heart defect (2) Explain this case (3) Distinguish from related/opposite/alternative cases

Answer 21

(1) Patent ductus arteriosus (2) Differential cyanosis restricted to lower body in child most suggestive of PDA with late-onset reversal of shunt flow (from left-to-right to right-to left). (3) Whole-body cyanosis result when there is shunt reversal in patients with septal defects or tetralogy of fallot. Coarctation of aorta can limit lower-extremity exercise tolerance but does not cause cyanosis in children or adults.

Question 22

(1) Dx: murmur w/ bounding femoral pulses and carotid pulsations plus Head bobbing (2) Name these signs

Answer 22

(1) Aortic regurgitation (2) “Water hammer” pulses and head-bobbing with each heart beat (de Musset sign)

Question 23

Ateriovenous (AV) shunts: (1) causes (2) effect on hemodynamics/heart & why (3) Complication of shunts, and what kind of shunts

Answer 23

(1) Congenital or acquired; acquired forms can result from med interventions or penetrating injuries (2) increase preload and decrease afterload by routing blood directly from arterial system to venous system, bypassing arterioles (3) High-volume AV shunts can eventually result in high output cardiac failure

Question 24

PDA: (1) type of murmur (2) heard best where/when (3) effects of small PDA (4) most common patient population(s)

Answer 24

(1) continuous murmur (2) heard best in left infraclavicular region with maximal intensity at S2 (3) small PDA often asymptomatic and usually detected incidentally during routine cardiac auscultation (4) occurs most commonly in patients born prematurely and those with cyanotic congenital heart disease

Question 25

(1) Dx: 14 yo girl, short and thick neck, broad chest, shortened fourth metacarpals bilaterally, several episodes of otitis media as a young child, heart abnormality (2) most likely cardiac abnormality (3) relation to other heart defects (4) presentation of the most likely cardiac abnormality

Answer 25

(1) Turner syndrome (2) Bicuspid aortic valve (3) usually isolated, but may occur in combo with other anomalies, particularly aortic coarctation (4) nonstenotic bicuspid aortic valve can manifest as early systolic, high frequency click over cardiac apex and/or right second interspace

Question 26

Damage most likely done by penetrating injury at left sternal border in 4th intercostal space

Answer 26

Puncture anterior surface of heart; The right ventricle composes most of the heart’s anterior surface.

Question 27

(1) Dx: constitutional sx (i.e., fever, weight loss), mid-diastolic rumbling murmur heard best at apex, positional cardiovascular symptoms (e.g., dyspnea and syncope), embolic sx, & large pedunculated mass in L. atrium (2) Histology

Answer 27

(1) Typical findings of atrial myxoma (2) Scattered cells within mucopolysaccharide stroma, abnormal blood vessels, and hemorrhaging

Question 28

(1) What time after onset of total ischemia = loss of cardiomyocyte contractility (2) Point at which ischemic injury becomes irreversible

Answer 28

(1) Within 60s (2) AFter 30 minutes

Question 29

Developmental cardiovascular abnormalities in the following sex chromosomal-inherited disorders: (1) Down syndrome (2) DiGeorge syndrome (3) Friedreich’s ataxia (4) Marfan syndrome (5) Tuberous sclerosis (6) Turner’s syndorme

Answer 29

(1) Endocardial cushion defects (ostium primum ASD, regurgitant AV valves) (2) Tetralogy of Fallot and aortic arch abnormalities (3) Hypertrophic cardiomyopathy (4) Cystic medial necrosis of aorta (5) Valvular obstruction due to cardiac rhabdomyomas (6) Coarctation of aorta

Question 30

(1) Name sign: bp cuff inflated to 130 mmHg & pressure very slowly decreased, at 100 mmHg, intermittent Korotkoff sounds heard only during expiration. At 78 mmHg, Korotkoff sounds heard throughout respiratory cycle. (2) Definition (3) Explain sign (3) Clinical signs

Answer 30

(1) Pulsus paradoxus (2) defined by decrease in systolic blood pressure of greater than 10 mmHg with inspiration (3) Detected by inflating bp cuff above systolic pressure then slowly releasing it. Korotkoff sounds first become audible during expiration & subsequently become audible during all phases of respiration. Inspiration causes increase in systemic venous return, resulting in increased right heart volumes. Under normal conditions, results in expansion of right ventricle into pericardial space with little impact on left side of heart. However, in conditions that impair expansion into pericardial space, increased right ventricular heart volume occurring with inspiration pushes interventricular septum toward left. Consequently, left heart diastolic volume and stroke volume are reduced, resulting in decreased systemic blood pressure during inspiration. (4) Acute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease, and restrictive cardiomyopathy

Question 31

(1) Dx: Patient with Pulsus paradoxus, tachypneic, cannot speak in full sentences, expiration prolonged, prominent bilateral wheezes (2) Tx & mechanism

Answer 31

(1) Acute asthma exacerbation (note: pulsus paradoxus can occur in severe obstructive pulmonary disease) (2) Beta-adrenergic agonists control acute asthma exacerbations by causing bronchial smooth muscle relaxation via increased intracellular cAMP

Question 32

(1) Patient’s own maneuver assisting with cyanosis of Tetralogy of Fallot (2) Mechanism

Answer 32

(1) Squatting (2) Increases SVR & decreases right to left shunting, thereby increasing pulmonary blood flow. Squatting thus counteracts arterial desaturation during hypoxemic spells.

Question 33

Pericarditis: (1) Characterize/Distinguish pain (2) Relation to MI (i.e., contexts) & Mechanism(s)

Answer 33

(1) Unlike angina, sharp and pleuritic chest pain, and may be exacerbated by swallowing or relieved by leaning forward (2) EARLY-ONSET pericarditis develops in about 10 to 20% of patients between days 2 and 4 following transmural MI. It represents an inflammatory reaction to cardiac muscle necrosis that occurs in adjacent visceral and parietal pericardium. (3) LATE-ONSET post-MI pericarditis (Dressler’s syndrome) begins 1 week to a few months following MI & affects less than 4% of cases. Thought to be be an autoimme polyserositis.