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Pathology > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What is the most common cause of ischemic heart disease?

A

Atherosclerosis of coronary arteries = decreases blood flow to myocardium

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2
Q

What is stable angina?

A

Chest pain that arises with exertion or emotional stress

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3
Q

What is the underlying cause of stable angina?

A

Atherosclerosis of coronary arteries w/ >70% stenosis = decreased blood flow is unable to meet metabolic demands of myocardium during exertion

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4
Q

Is stable angina a reversible or irreversible process? What is a hallmark finding in this kind of damage?

A
  • Reversible injury to myocytes (no necrosis)
  • Cellular swelling
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5
Q

What is the clinical presentation of stable angina?

A

Chest pain lasting <20 mins that radiates to left arm or jaw, diaphoresis, and SoB

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6
Q

EKG in a pt w/ stable angina would show what change? Why?

A
  • ST-segment depression
  • Subendocardial ischemia = ST-segment depression
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7
Q

What Rx is given to treat stable angina? How does this drug work?

A
  • Nitroglycerin (or just relieved by rest)
  • NG can vasodilate both arteries and veins; most importantly is NG’s effect on veins, which would decrease preload and therefore the stress on the heart
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8
Q

What is unstable angina?

A

Unstable angina is chest pain that occurs @ rest

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9
Q

What is the most common underlying cause of unstable angina?

A

Rupture of atherosclerotic plaque w/ thrombosis –> incomplete occlusion of a coronary artery

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10
Q

Is unstable angina an irreversible or reversible process?

A

Reversible injury to myocytes (no necrosis)

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11
Q

What changes would EKG show in a pt w/ unstable angina?

A

ST-segment depression (due to subendocardial ischemia)

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12
Q

What Rx is used to treat unstable angina?

A

Nitroglycerin

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13
Q

What is a complication that a patient w/ unstable angina may develop?

A

Myocardial infarction (pt w/ unstable angina has high risk of progression to MI)

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14
Q

What is Prinzmetal angina? What is it caused by?

A
  • Episodic chest pain (unrelated to exertion)
  • Coronary artery vasospasm (causes ischemia to all layers of vessel wall)
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15
Q

Is Prinzmetal angina a reversible or irreversible process?

A

Reversible injury to myocytes (no necrosis)

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16
Q

What EKG changes would be present in a pt w/ prinzmetal angina? Why?

A
  • ST-segment elevation
  • Transmural ischemia causes ST-segment elevation
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17
Q

What Rx’s can be used to treat prinzmetal angina?

A
  • Nitroglycerin or Ca2+ channel blockers (to relieve vasospasms)
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18
Q

Is myocardial infarction a reversible or irreversible process?

A

Irreversible (necrosis of cardiac myocytes)

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19
Q

What is usually the underlying cause of myocardial infarction?

A

Rupture of an atherosclerotic plaque w/ thrombosis and complete occlusion of a coronary artery

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20
Q

What are 3 other possible causes for myocardial infarction aside from that involving atherosclerosis?

A
  • Prolonged ( > 20mins) coronary artery vasospasm (e.g. Prinzmetal angina or cocaine use)
  • Emboli
  • Vasculitis (e.g. Kawasaki disease)
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21
Q

How does myocardial infarction present clinically?

A

Severe, crushing chest pain ( > 20 mins) that radiates to the left arm or jaw, diaphoresis, dyspnea

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22
Q

What part of the heart is usually affected by myocardial infarction?

A
  • Left ventricle (RV and both atria are usually spared)
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23
Q

What are the 3 most common blood vessels involved in myocardial infarction?

A
  • Left Anterior Descending (most common; 45% of cases); Right coronary artery (2nd most common); Left circumflex artery
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24
Q

Occlusion of the LAD in MI causes infarction in what areas of the heart?

A

LAD: infarction of ant. wall and ant. IV septum

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25
Q

Occlusion of the right coronary artery leads to infarction of what areas of the heart?

A

RCA: Post. wall; post. IV septum; papillary muscles of the LV

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26
Q

Occlusion of the LCX in MI causes infarction of what part of the heart?

A

LCX: Laterall wall of the LV

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27
Q

Where in the heart is necrosis seen in the initial phase of MI? What changes would EKG show?

A
  • Initial phase of MI = subendocardial necrosis (involving <50% of mycardium)
  • ST-segment depression
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28
Q

If MI persists, where in the heart is necrosis seen? What changes in the EKG would be seen?

A
  • Transmural necrosis; involving most of the myocardial wall (this is the most common type of infarction)
  • ST-segment elevation
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29
Q

What are 2 cardiac enzymes that are elevated in MI? Which is useful to detect reinfarction and why?

A
  • Tropinin I (most sensitive and specific marker for MI; peaks @ 24 hrs and returns to normal 7-10 days later) and CK-MB
  • CK-MB is useful for detecting reinfarction that occur days after an initial MI b/c CK-MB levels rise and peak @ 24 hrs and return to normal by 72 hrs
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30
Q

What are the different treatment options for MI? (Hint: limit thrombosis, minimize ischemia, vasodilate, slow HR, decrease LV dilation, open blocked vessels)

A
  • Aspirin and/or heparin - limit thrombosis
  • Supplemental O2 - minimize ischemia

Nitrates - vasodilate veins and arteries

B-blocker - slow HR (decreases O2 demand and risk of arrhythmia)

ACE Inhibitor - decrease LV dilation

Fibrinolysis or angioplasty - open blocked vessel

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31
Q

What are 2 complications to be concerned of when openning a blocked vessel?

A
  • Contraction Band Necrosis (Reperfusion of irreversibly-dmg’d cells causes Ca2+ influx –> hypercontraction of myofibrils)
  • Return of O2 + inflammatory cells –> free radical generation –> further dmg myocytes (Pt will present w/ rising cardiac enzymes despite opening occluded vessel)
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32
Q

Describe the gross changes, microscopic changes, and complications: < 4hrs from MI

A

Gross: none

Microscopic: non

Complications: Cardiogenic shock (if large infarct causes heart to stop beating all together), CHF, and arrhythmia

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33
Q

Describe the gross changes, microscopic changes, and complications: 4 - 24 hrs after MI

A

Gross: dark discoloration

Microscopic changes: coagulative necrosis (pyknosis –> karyorhexis –> karyolysis)

Complications: Arrhythmia (if MI dmgs conducting system)

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34
Q

Describe the gross changes, microscopic changes, and complications: 1 - 3 days after MI

A
  • Gross: yellow pallor
  • Microscopic: neutrophil invasion
  • Complications: Fibrinous pericarditis (only if transmural infarction had occurred –> inflamm exudate extends out from the epicardium into pericardium)
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35
Q

Describe the gross changes, microscopic changes, and complications: 4 - 7 days after MI

A

Gross: yellow pallor

Microscopic: Macrophages

Complications: Rupture of ventricle –> cardiac tamponade; Rupture of IV septum –> leads to shunt; Rupture of papillary muscle –> leads to mitral insufficiency

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36
Q

Describe the gross changes, microscopic changes, and complications: 1 - 3 weeks after MI

A

Gross: red border emerges as granulation tissue enters

Microscopic: Granulation tissue w/ fibroblasts, collagen, and bv’s

Complications: none

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37
Q

Describe the gross changes, microscopic changes, and complications: Months after MI

A

Gross: white scar

Microscopic: fibrosis

Complications: Aneurysm; mural thrombus; Dressler Syndrome (Autoimmune pericarditis that happens 6-8wks after MI)

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38
Q

What is Dressler Syndrome? When does it occur?

A

Dressler Syndrome is an autoimmune pericarditis that happens 6-8 wks after MI; transmural infarction + inflamm w/n pericardium –> exposure of pericardial antigens to immune system –> pt can devo Abs agains pericardium

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39
Q

What is sudden cardiac death? What is usually the cause?

A
  • Unexpected death due to cardiac disease; occurs w/o symptoms or <1 hr after symptoms arise
  • Usually due to fatal ventricular arrhythmia
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40
Q

What is the most common etiology of sudden cardiac death? What are 3 other less cammon causes of sudden cardiac death?

A
  • acute ischemia (90% of pts have preexisting severe atherosclerosis)
  • Other less common causes: mitral valve prolapse; cardiomyopathy; cocaine abuse
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41
Q

What is chronic ischemic heart disease? What complication can this lead to?

A
  • CIHD is poor myocardial fxn due to chronic ischemic dmg (w/ or w/o infarction)
  • Progresses to CHF
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42
Q

What is the process by which pulmonary symptoms arise in CHF? What are 4 sypmtoms that can be seen?

A
  • Pumonary congestion due to blood being back up –> leads to pulmonary edema
  • Dyspnea, paroxysmal nocturnal dyspnea (due to increased venous return when lying flat; this is dyspnea that happens after lying down for a few hours); orthopnea (dyspnea that occurs after lying down for a few minutes); and crackles (due to edema)
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43
Q

What are “heart-failure” cells? How do they arise?

A

In Left-sided heart failure, small capillaries in the lungs get congested and may burst –> intraalveolar hemorrhage –> macrophages eat this up and become hemosiderin-laden macrophages = heart-failure cells

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44
Q

How does the RAA system exacerbate left-sided heart failure? What is therefore a mainstay Rx for left-sided heart failure?

A
  • Decreased flow to kidneys –> activation of RAA system –> ANG II constricts arterioles (increase TPR) and facilitates release of Aldosterone (increase fluid retention) = exacerbate CHF
  • ACE Inhibitors
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45
Q

What is the most common cause of right-sided heart failure? What are 2 other important causes of right-sided heart failure?

A
  • Most commonly due to left-sided heart failure
  • Other important causes:
    1. L –> R shunt
    2. Cor pulmonale (Chronic lung disease –> hypoxia –> bv in lungs constrict –> RH has to pump against this increased pressure)
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46
Q

What are 3 clinical features of right-sided heart failure due to congestion?

A
  1. Jugular vein distension
  2. Painful hepatosplenomegaly w/ characteristic “nutmeg” liver –> may lead to cardiac cirrhosis (when cirrhosis occurs due to chronic congestion of hepatic vein due to RH failure)
  3. Dependent pitting edema (due to increased hydrostatic pressure)
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47
Q

What is Eisenmenger syndrome? How does it arise?

A
  • Eisenmenger syndrome is a reversal of a L –> R shunt into a R –> L shunt
  • L –> R shunt increases flow through pulm. circulation –> results in pulm hypertrophy and pulm HTN –> increased pulm resistance reverses shunt from L –> R to R –> L
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48
Q

What is the most common congential heart defect? What syndrome is it closely associated with?

A
  • Ventricular Septal Defect (VSD)
  • Fetal Alcohol Syndrome
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49
Q

What are 3 clinical symptoms due to a reversal of shunt in Eisenmenger syndrome?

A
  1. RV hypertrophy (due to Pulm HTN)
  2. Polycythemia (due to EPO release from the hypoxemia)
  3. Clubbing of fingers (due to cyanosis)
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50
Q

What is the treatment of large VSD? What is treatment of small VSD?

A
  • Surgicial closure
  • Small defects may close spontaneously
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51
Q

What is the most common form of Atrial Septal Defect?

A

Ostium secundum (90%)

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52
Q

What syndrome is ostium primum closely assoc with?

A

Down Syndrome

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53
Q

What kind of shunting is seen in ASD?

A

L –> R

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54
Q

What is heard on auscultation of ASD? Why does this occur?

A
  • Split S2
  • Increased blood in RH delays closure of pulm valve
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55
Q

What is an impt complication that can arise from ASD? Give an example.

A
  • Paradoxical emboli
  • DVT embolus usually lodge into pulm circuit and cause PE, but due to ASD, it may escape into systemic circuit into an uncommon area (e.g. brain or distal extremities)
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56
Q

What congenital heart defect is associated w/ congenital rubella?

A

Patent Ductus Arteriosus (PDA)

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57
Q

What kind of shunt does patent ductus arteriosus cause? Between which 2 vessels?

A
  • L –> R shunt
  • Aorta and pulm artery
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58
Q

What is the use of ductus arteriosus in the developing fetus?

A

During devo, ductus arteriosus shutns blood from pulm artery to aorta in order to bypass the uninflated lungs

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59
Q

What characteristic murmur is heard with PDA at birht?

A

A continuous “machine-like” murmur can be heard

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60
Q

If Eisenmenger syndrome arises in PDA, what clinical symptoms arise?

A

Lower extremity cyanosis

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61
Q

Why is cyanosis only seen in lower extremities if Eisenmenger syndrome occurs in PDA?

A

Ductus arteriosus arises after the proximal major branches of aortic arch (which supplies upper extremities)

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62
Q

What is the treatment for PDA? Why?

A
  • Indomethacin
  • Indomethacin decreases PGE; elevated PGE is responsible for keeping PDA open
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63
Q

What are the 4 symptoms of Tetralogy of Fallot?

A
  1. Stenosis of RV outflow tract
  2. RV hypertrophy
  3. VSD
  4. Aorta that overrides the VSD
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64
Q

What kind of shunting is seen in Tetralogy of Fallot? What determines the extend of shunting?

A
  • R –> L shunt
  • Degree of RV outflow tract stenosis determines extent of shunting
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65
Q

In pts w/ Tetralogy of Fallot, what physical manipulation do they do to reduce cyanotic spells? Why does this alleviate cyanotic spells?

A
  • Patients learn to squat in response to cyanotic spells
  • Squatting increases arterial resistance –> decreases R -> L shunting and allows more blood to reach the lungs
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66
Q

What cardiac defect is classically described as having a “boot-shape” on x-ray?

A

Tetralogy of Fallot

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67
Q

What is transposition of great vessels?

A

Cardiac defect where pulm artery arises from LV and aorta arises from RV

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68
Q

What cardiac defect is assoc w/ maternal diabetes?

A

Transposition of great vessels

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69
Q

What are 2 treatments used for Transposition of Great Vessels?

A
  1. Surgical creation of shunt (in order to allow blood to mix) is required for survival
  2. PGE can be administered to maintain a PDA until surgical repair is performed
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70
Q

What changes to heart morphology is seen in Transposition of Great Vessels?

A

Hypertrophy of RV and Atrophy of LV

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71
Q

What is truncus arteriosus?

A

Cardiac defect where a single large vessel arises from both ventricles (truncus fails to divide durign devo)

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72
Q

What cardiac defect results in RV hypoplasia due to failure of devo of tricuspid valve?

A

Tricuspid atresia

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73
Q

What morphological change in heart is seen in tricuspid atresia?

A

RV hypoplasia

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74
Q

What other cardiac defect is Tricuspid Atresia assoc w/?

A

ASD

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75
Q

What is coarctation of the aorta? What are the 2 subtypes?

A
  • Narrowing of the aorta
  • Subtypes:
    1. Infantile form
    2. Adult form
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76
Q

What other cardiac defect is the infantile form of Coarctation of the Aorta assoc w/?

A

Infantile form is assoc w/ a PDA

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77
Q

Where is the coarctation of the aorta seen in the infantile form, specifically?

A

Coarctation lies after (distal to) the aortic arch, but before (proximal to) the PDA

78
Q

What clinical symptom is seen in coarctation of the aorta infantile form?

A

Lower extremity cyanosis, since it happens after major proximal branches of the aortic arch

79
Q

What syndrome is assoc w/ the infantile coarctation of the aorta?

A

Turner syndrome

80
Q

Which form of aortic coarctation is assoc w/ PDA?

A

Only infantile form

81
Q

Where is the aortic coarctation seen in the adult form?

A

Distal to the aortic arch

82
Q

What clinical symptoms are seen in the extremities of pts w/ the adult aortic coarctation?

A

Presents as HTN in upper extremities and hypotension w/ weak pulses in lower extremities

83
Q

What radiographic finding is assoc w/ adult aortic coarctation? What causes this?

A
  • “notching” of ribs are seen on x-ray
  • collateral circulation develops across the intercostal arteries in an attempt to bypass the coarctation –> engorged arteries compress against the ribs and make it look notched on x-ray
84
Q

What valvular defect is assoc w/ adult form of aortic coarctation?

A

Bicuspid aortic valve

85
Q

Generally when you have a valvular lesion, what 2 clinical complications arise?

A
  1. Stenosis –> decreased caliber of the valve orifice (less blood can pass through)
  2. Regurgitation (backflow)
86
Q

What precipitates acute rheumatic fever?

A

Pharyngitis due to group A Beta-hemolytic strep (i.e. strep pyogenes)

Acute Rheumatic Fever is a systemic complication of this pharyngitis that arises 2-3 weeks after

87
Q

Why does the infxous etiology of acute rheumatic fever lead to the autoimmune symptoms seen in pts?

A

Molecular mimicry - Bacterial M protein resembles proteins in human tissue

88
Q

The JONES criteria is a mneumonic for what disease? What does it entail?

A
  • Acute Rheumatic Fever
  • J (Joints): migratory polyarthritis
  • O (looks like a heart): pancarditis (inflamm of all layers of heart)
  • N (Nodules): subcutaneous nodules
  • E (Erythema marginatum)
  • S (Sydenham chorea)
89
Q

What is a MSK symptom that is seen in acute rheumatic fever? Explain its clinical presentation.

A
  • Migratory polyarthritis
  • Pt will have swelling and pain in a large joint (e.g. wrist, knees, ankles) that resolves w/n days and then migrates to another large joint
90
Q

In the endocarditis seen in acute rheumatic fever, which valve is most commonly affected? 2nd most common? What does this look like grossly?

A
  • Mitral valve is most commonly affected; Aortic valve is 2nd (but if aortic valve is affected, it will be in conjxn w/ mitral)
  • Small vegetations will be seen on the lines of closure on the valve
91
Q

What is the characteristic histological finding in myocarditis due to Acute Rheumatic Fever? What does it consist of (just name the pathognomic cell found here)?

A
  • Aschoff bodies
  • Aschoff bodies is a foci of chronic inflammation that contains: special reactive hisitiocytes w/ slender, wavy nuclei (Anitschkow cells)
92
Q

What is the most common cause of death in acute rheumatic fever?

A
  • Myocarditis
93
Q

What is a physical finding that can be used to diagnose pericarditis in acute rheumatic fever?

A
  • Friction rub (audible extra heart sound due to pericarditis)
94
Q

What is a dermatologic symptom seen in acute rheumatic fever? What part of the body does it commonly affect?

A
  • Erythema marginatum
  • Commonly involves trunk and limbs
95
Q

What cardiac disease is classically referred to as having “fish-mouth” appearance of valves? What causes this appearance of the valves?

A
  • Chronic rheumatic heart disease
  • Acute rheumatic fever may progress to chronic RF, which leads to valve scarring –> fusion of commissures occurs (since this was where the vegetations were seen in the acute phase) leading to a fish-mouth appearance
96
Q

What is a cardiac complication that can arise from persistent chronic rheumatic fever?

A

Infectious endocarditis

97
Q

What is aortic stenosis usually caused by?

A

Usually due to fibrosis and calcification from “wear and tear”

98
Q

What patient population is most affected by aortic stenosis?

A

Late adulthood ( > 60 years)

Makes sense this is a disease of wear and tear

99
Q

What morphological abnormality leads to an increased risk for aortic stenosis?

A

Bicuspid aortic valve (normal has 3; only have 2 increases wear and tear on each cusp)

100
Q

How can you differentiate aortic stenosis from being due to “wear and tear” or from being a complication of chronic rheumatic heart disease?

A

In classic aortic stenosis due to “wear and tear,” the valve will look fibrotic and irregular, but there will be no fusion b/w commisures.

In chronic RF, you will see fusion of commissures leading to the classic “fish-mouth” appearance in the valve (and you’d prob see this on mitral valve too)

101
Q

Aortic stenosis has an insidious progression with a prolonged asymptomatic stage. Why is this the case? What physical finding can be detected during the asymptomatic stage?

A
  • Cardiac compensation prevents clinical manifestation of aortic stenosis for a long time
  • a systolic ejection click (due to the blood being forced out the stenotic valve until it blows open) followed by a crescendo-decrescendo murmur is heard (due to blood rushing out initially and slowing down as the stenotic valve closes back)
102
Q

How can cardiac failure arise from aortic stenosis?

A

Persistent elevated afterload will cause concentric LV hypertrophy –> heart doesn’t contract as effectively –> cardiac failure may develop

103
Q

What is a complication that can arise w/ exertion (e.g. exercise) in a Pt w/ aortic stenosis? Why would this happen?

A
  • Angina and syncope
  • Due to stenosis, there is limited ability to increase blood flow across the valve –> decreased perfusion of myocardium and brain
104
Q

What kind of anemia can arise from aortic stenosis? Why?

A
  • Microangiopathic hemolytic anemia
  • RBCs are sheared as they cross the stenotic valve (produces schistocytes)
105
Q

Once complications arise, what is the treatment for aortic stenosis?

A

Valve replacement

106
Q

What is aortic regurgitation?

A

Backflow of blood from aorta –> LV during diastole

Recall that diastolic pressure begins as soon as aortic valve closes

107
Q

What is the most common cause of aortic regurgitation? How does this cause regurgitation?

A
  • Aortic root dilation is the most common cause of aortic regurg
  • By dilating the aortic root, you are physically stretching out the valve so that it can’t close tightly
108
Q

Give 2 examples that lead to the most common cause of aortic regurgitation.

A

Most common cause of aortic regurg is aortic root dilation: tertiary syphillis and aortic dissection

109
Q

What is the 2nd most common etiology of aortic regurg? Give 1 example of what may cause it.

A
  • Valve dmg
  • Infectious endocarditis (e.g. complication of chronic RF)
110
Q

What characteristic murmur can be heard in aortic regurg? What is it caused by?

A
  • A blowing diastolic murmur can be heard
  • A blowing sound is often heard when there is backflow of blood
111
Q

What happens to the pulse pressure in aortic regurg? Why?

A
  • Pulse pressure (difference b/w systolic and diastolic pressures) increases
  • In aortic regurg, blood flows backwards into LV during diastole = decreased diastolic pressure; In the next systole, the heart pumps out the regurgitant blood + the blood that filled normally during diastole = increased systolic pressure
112
Q

What clinical symptoms would the hyperdynamic circulation due to aortic regurg cause the patient to present?

A

Bounding pulse (water-hammer pulse); pulsating nail bed (Quincke pulse); and head bobbing (aka De Musset’s Sign, where Pt bobs his head in accordance to the systolic pressure)

113
Q

Aortic regurg can lead to heart failure. How does this occur/what morphological changes would be seen in the heart?

A

Regurgitation leads to LV dilation due to volume overload –> LV will undergo eccentric hypertrophy (lumen enlarges but thickness of myocardium remains same) –> unable to effectively pump blood

114
Q

What is the treatment for aortic regurgitation? When is it implemented?

A
  • Valve replacement
  • Once LV dysfxn develops
115
Q

What is mitral valve prolapse?

A

Ballooning of mitral valve into LA during systole

116
Q

What histological change is attributed to mitral valve prolapse?

A

In mitral valve prolapse, myxoid degeneration and accumulation of ground substance of the valve –> makes it floppy

117
Q

What genetic abnormalities is associated w/ mitral valve prolapse?

A

Marfan Syndrome or Ehlers-Danlos

118
Q

What abnormal heart sounds are heard in mitral valve prolapse? What is it caused by?

A
  • Mid-systolic click followed by a regurgitation murmur can be heard in mitral valve prolapse
  • The degenerative mitral valve parchutes backwards during systole (mid-systolic click); some blood may flow backwards into the parachuted mitral valve flap (regurgitant sound)
119
Q

The abnormal heart sounds heard in mitral valve prolapse is lessened when the patient squats. Why?

A

When Pt squat, there is an increase in systemic resistance –> less blood is emptied from the LV –> the heart places more tension on the chordae to try to keep it closed –> click and murmur become less audible.

Also, think of it as if there’s more liquid in the LV, it’s harder to hear things

120
Q

What are some complications that can arise from mitral valve prolapse?

A

Complications from mitral valve prolapse is rare, but they include: infectious endocarditis (since the valve will get dmged over time and is susceptible to subacute infxn); arrhythmia, and severe mitral regurgitation (over time as valve keeps flapping and getting stretched, it won’t be able to close as tightly)

121
Q

What is the treatment for mitral valve prolapse?

A

Valve replacement

122
Q

What is mitral regurgitation?

A

Backflow of blood from LV to LA during systole

123
Q

What is the most common cause of mitral regurg? What are 4 other possible causes?

A
  • Most common cause is when it arises as a complication of mitral valve prolapse
  • Other possible causes:
    1. LV dilation –> left-sided heart failure
    2. infective endocarditis
    3. acute RF (since it predom affects mitral valve)
    4. papillary muscle rupture (e.g. post-MI)
124
Q

What abnormal heart sound is heard in mitral valve regurgitation?

A

Holosystolic blowing murmur (You’ll hear it all throughout systole)

125
Q

If a Pt w/ mitral regurgitation does something that increases venous return or increases diastolic filling (e.g. squatting or expiration), how would the abnormal heart sound change?

A

In mitral regurg, you’d hear a holosystolic blowing murmur: when systemic resistance increases (squatting) or more blood is returned to the left heart (expiration), more blood will regurgitate backwards.

This is different from mitral valve prolapse, where you would see decrease in the murmur sound. The reason for this is that the chordae increases tension and thereby prevents backflow. However, in mitral regurgitation, the valve is already very leaky –> even if the chordae tense up, the blood would still be able to escape

126
Q

What is the most common cause of mitral stenosis?

A

Chronic RF

127
Q

What would be heard on auscultation in a Pt w/ mitral stenosis?

A

Opening snap w/ diastolic rumble (due to forcibly opening the stenotic valve and turbulent inital flow through it as blood enters LV during diastole)

128
Q

How do pulm symptoms arise in mitral stenosis?

A

Mitral stenosis causes volume overload in LA and dilatation –> backup of blood into pulm circuit –> pulm HTN causes pulm congenstion w/ edema and alveolar hemorrhage –> eventually this will extend into RV and cause right-sided failure

129
Q

Why is atrial fib and mural thrombus a possible complication of mitral stenosis (explain how it happens)?

A
  • A-fib can arise b/c stretching of LA causes dysfxn of conduction system
  • Mural thrombus can arise due to stasis of blood since LA isn’t contracting properly
130
Q

What is endocarditis? What is the etiology usually due to?

A
  • Endocarditis is inflamm of endocardium that lines the surface of cardiac valves
  • Usually due to bacterial infxn
131
Q

What is the most common bacterial cause of endocarditis? What is a precursory step before the infxn can cause endocarditis?

A
  • Strep viridans
  • Strep viridans is a low-virulence org = infects previously dmged vessels (subacute)
  • Previous dmg can be from chronic RF or mitral valve prolapse*
132
Q

What gross changes occur due to strep viridans in the heart?

A

Small vegetations can be seen on valves (subacute endocarditis)

The valve is not destroyed by it

133
Q

How does previous dmg to the endocardium allow for subacute endocarditis due to strep viridans?

A

Dmged subendocardial surface activates coag cascade –> devo thrombotic vegetations –> transient bacteremia (e.g. during dental procedure) allows some bacteria to get trapped w/n those vegetations

134
Q

In a Pt who has a Hx of endocardial dmg, what precautionary step should be taken to decrease the risk of endocarditis?

A

Prophylactic antibiotics

135
Q

What is the most common cause of endocarditis in IV drug users?

A

Staph aureus: contaminated skin is pierced –> allows entry for s. aureus into blood

136
Q

Do IV drug users require a previously dmged endocardium to develop endocarditis? Why?

A
  • No, staph aureus can infect normal valves; it is a high-virulence organism
137
Q

Which valve is most commonly affected by infxous endocarditis in IV drug users? What gross changes would be seen?

A
  • Tricuspid valve is most commonly affected (first valve staph aureus would come in contact w/ once it enters blood stream)
  • Large vegetations would be seen around the valve that destroys it (acute endocarditis)
138
Q

What organism is associated w/ endocarditis in prosthetic valves?

A
  • Staph epidermidis
139
Q

Which organism is associated w/ endocarditis in Pts w/ an underlying cancer? What underlying cancer could this Pt have?

A
  • Strep. bovis
  • Colorectal carcinoma
140
Q

If a Pt w/ endocarditis returns w/ negative blood cultures, what other organisms should be suspected? (Also, state the mneumonic)

A
  • “HACEK” organisms (usually come w/ neg cultures b/c they are hard to grow)
    1. Haemophilus
    2. Actinobacillus
    3. Cardiobacterium
    4. Eikenella
    5. Kingella
141
Q

Septic embolization of infectious endocarditis causes what 4 clinical symptoms?

A
  1. Janeway lesions (erythematous nontender lesions on palms and soles) Think of it liek a highway and you’re driving = palms and soles are affected
  2. Osler nodes (tender lesions on fingers or toes) Ouch Osler
  3. Splinter hemorrhages in nail bed (black streaks on nail bed)
  4. Roth spots (small retinal hemorrhages w/ white centers)
142
Q

Pts w/ infxous endocarditis would get what kind of anemia? Explain how the Hb, MCV, ferritin, TIBC, serum Fe2+, and % saturation would be affected.

A
  • Anemia of chronic disease (microcytic anemia)
  • Hb: decrease
  • MCV: decrease
  • Ferritin: increase (Hepcidin is released as an acute phase reactant and prevents iron release from ferritin; cell is technically in Fe2+ overload, but simply can’t release it from ferritin)
  • TIBC: decrease (since body is technically in Fe2+ overload)
  • Serum Fe2+: decrease (body tries to use up Fe2+ in the blood since it can’t get it from ferritin storage)
  • % sat: decrease (due to decrease serum Fe2+ = not many can bind w/ transferrin)
143
Q

What imaging technique is useful for detecting lesions on valves in Pts w/ suspected infxous endocarditis?

A

Transesophageal echo

144
Q

What gross change does nonbacterial thrombotic endocarditis cause? Which valve is most commonly affected?

A
  • Nonbacterial thrombotic endocarditis causes sterile vegetations
  • the mitral valve is most commonly affected along the lines of closure
145
Q

What underlying conditions is nonbacterial thrombotic endocarditis associated with?

A

Hypercoagulable state or underlying adenocarcinoma

146
Q

What is Libman-Sacks endocarditis?

A

Sterile vegetations of endocardium that arise in association w/ SLE

147
Q

What unique gross presentation is assoc. w/ Libman-Sacks endocarditis?

A

Sterile vegetations are seen on the surface and undersurface of the mitral valve

148
Q

Why can mitral regurg occur in nonbacterial thrombotic endocarditis?

A

Vegetations arise on the mitral valve along lines of closure –> valve can’t close properly –> mitral regurg

149
Q

Why can mitral regurg occur in Libman-Sacks endocarditis?

A

Vegetations are present on surface and undersurface of mitral valve –> valve can’t close properly –> mitral regurg

150
Q

What is dilated cardiomyopathy?

A

Where all 4 chambers of the heart becomes massively dilated

151
Q

What is the most common form of cardiomyopathy?

A

Dilated cardiomyopathy

152
Q

What type of heart failure would be seen in dilated cardiomyopathy? Explain the process by which this happens.

A

Dilation of all chambers of the heart –> systolic dysfxn as ventricles can’t pump properly –> Biventricular CHF (both RV and LV fail together)

153
Q

What kind of valvular problems could be expected in dilated cardiomyopathy?

A

Mitral and Tricuspid valve regurg could develop as the chambers enlarge

154
Q

What is the most common cause of dilated cardiomyopathy?

A

Dilated cardiomyopathy is most commonly idiopathic

155
Q

What infectious etiology can cause dilated cardiomyopathy?

A

Coxsackie A or B

156
Q

How can a viral infxn cause dilated cardiomyopathy?

A

Coxsackie A or B can cause myocarditis –> dilated cardiomyopathy is a late complication

157
Q

What is the treatment for dilated cardiomyopathy?

A

Heart transplant (there’s no other way to fix a dilated heart)

158
Q

What kind of cardiomyopathy can develop in a pregnant patient? When would it develop?

A
  • Dilated Cardiomyopathy
  • During late prego or soon (weeks to months) after childbirth
159
Q

What hematologic condn can cause dilated cardiomyopathy?

A

Hemochromatosis

160
Q

What is hypertrophic cardiomyopathy?

A

Massive hypertrophy of LV

161
Q

If dilated cardiomyopathy is inherited, what pattern of inheritance would it follow?

A

AD

162
Q

What is the most common cause of hypertrophic cardiomyopathy?

A

Genetic mutation (AD) in sarcomere proteins

163
Q

What changes in the cardiac output could be expected from hypertrophic cardiomyopathy? Why?

A
  • Decreased CO
  • LV becomes so thick w/ muscle that it loses its compliance –> diastolic dysfxn (ventricle can’t fill)
164
Q

What histological changes may be seen in a Pt who developed dilated cardiomyopathy after being infected w/ coxsackie A/B virus?

A

Coxsackie A/B viruses cause myocarditis which can precipitate dilated cardiomyopathy:

  • Lymphocytic infiltrate in the myocardium can be seen histologically
165
Q

A young athlete develops sudden death due to a cardiomyopathy. What kind of cardiomyopathy would most likely be responsible? What complication could this cardiomyopathy have caused that led to sudden death?

A
  • Hypertrophic cardiomyopathy is a common cause of sudden death in young athletes
  • Hypertrophy of the ventricle would disrupt the conduction system –> ventricular arrhythmia –> sudden death
166
Q

How does syncope w/ exertion arise in hypertrophic cardiomyopthy?

A

Hypertrophy of the ventricular septum (subaortic hypertrophy) may block the aortic valve –> functional aortic stenosis –> blood is difficult to eject out

167
Q

What histological change would be seen upon biopsy in hypertrophic cardiomyopathy? How is it supposed to look?

A
  • Myofiber hypertrophy that are disorganized would be seen on biopsy
  • Normally, myofibers should be lined up in an organized, parallel pattern
168
Q

What is restrictive cardiomyopathy?

A

Decreased compliance of ventricular endomyocardium –> restricts filling during diastole (diastolic dysfxn)

169
Q

What is a way by which children can develop restrictive cardiomyopathy?

A

Children w/ endocardial fibroelastosis (where pt has fibrosis and elastic tissue in endocardium) would restrict the compliance of the ventricular endomyocardium

170
Q

What is Loeffler syndrome? What kind of cardiomyopathy can this precipitate?

A
  • Loeffler syndrome is a disease in which there is endomyocardial fibrosis w/ eosinophilic infiltrate + eosinophilia
  • Loeffler syndrome can lead to restrictive cardiomyopathy
171
Q

What is the most common primary cardiac tumor in adults?

A

Myxoma

172
Q

What EKG changes would be present in restrictive cardiomyopathy?

A

Low-voltage EKG w/ dimished QRS amplitude (decreased electrical conduction due to fibrous connective tissue)

173
Q

What is a myxoma?

A

Benign mesenchymal tumor w/ gelatinous appearance and abundant ground substance (gel-like substance that surrounds cells)

174
Q

What gross changes does a myxoma cause in the heart? What clinical symptoms can arise from this?

A
  • Myxomas grow as a pedunculated (growing off of a stalk) mass in the LA –> obstructs the mitral valve
  • Syncope since obstruction of mitral valve causes diastolic dysfxn –> not enough blood perfuses brain
175
Q

What is the most common primary cardiac tumor in children? What genetic disease is it assoc w/?

A
  • Rhabdomyoma
  • Tuberous sclerosis (AD)
176
Q

What is a rhabdomyoma?

A

It is a hamartoma (malformation that looks like a tumor, but is actually just made of the normal tissue growing in a disorganized way) of cardiac muscle

177
Q

Where do rhabdomyomas usually arise in the heart?

A

Ventricles

178
Q

What is the most common malignant tumor of the heart?

A

Metastatic tumors are more common in the heart than primary tumors

179
Q

Give 4 primary tumors that can metastasize into the heart.

A
  1. Breast
  2. Lung
  3. Melanoma
  4. Lymphoma
180
Q

In metastatic cancer to the heart, what part of the heart is most commonly affected? What clinical symptoms does this cause?

A
  • Metastases most commonly involve the pericardium
  • This leads to pericardial effusion (these cells secrete proteins that increase leakiness –> effusion)
181
Q

What type of heart failure are Pts w/ Graves Disease most likely to develop?

A

High-Output heart failure (One of the symptoms of Graves Disease is flushing = vasodilation –> causes decreased peripheral resistance –> Heart has to increase CO in order to maintain MAP –> high-output heart failure)

182
Q

What is high-output heart failure? What change in BP would be seen?

A
  • High-output heart failure is a condn where CO is higher than normal, which causes circulatory overload
  • Diastolic Pressure would be increased
183
Q

What is marantic endocarditis?

A

Fancy word for nonbacterial thrombotic endocarditis

184
Q

What are the 3 main causes of aortic stenosis?

A
  1. Rheumatic disease
  2. Senile aortic stenosis
  3. Congenital aortic bicuspid valve
185
Q

What histological changes to the nuclei would be seen in ventricular hypertrophy?

A

Hypertrophic cardiac cell nuclei would be enlarged, hyperchromatic and rectangular (“boxcar”)

186
Q

What is Carcinoid Syndrome? How is the heart affected in this disease process (and what changes to the heart would be seen)?

A
  • Malignant proliferation of neuroendocrine cells (normally in small bowel) that release Serotonin into the portal circulation
  • Metastasis of carcinoid tumor to liver allows it to bypass liver metabolism (liver usually metabolizes 5-HT into 5-HIAA) –> active serotonin release can cause right-sided valvular fibrosis (increased collagen) –> tricuspid regurgitation and pulmon valve stenosis
187
Q

What side of the heart is affected by Carcinoid Syndrome? Why?

A
  • Carcinoid heart disease affects the Right-sided valves only (hence you see tricuspid regurg and pulmon valve stenosis)
  • Left-sided valvular lesions are not seen since MAOs (which metabolize serotonin) are present in the lung
188
Q

What is the most common cause of death in heart transplant patients after the 1st year of transplantation?

A

Chronic vascular rejection (aka Accelerated Coronary Artery Disease)

189
Q

What are the histological changes that would be observed in chronic vascular rejection (accelerated coronary artery disease) in a transplant patient?

A

Concentric intimal proliferation in the proximal and distal coronary arteries –> leads to MI

190
Q

What is constrictive pericarditis?

A

A chronic fibrosing disease of the pericardium that compresses the heart and restricts inflow

191
Q

Explain the pathogenesis of constrictive pericarditis.

A

Acute pericardial injury (e.g. TB, radiation therapy and surgery, chronic infxn) –> aggressive healing response causes pericardial space to become obliterated and visceral and parietal layers fuse in a dense mass of fibrous tissue

192
Q
A

Pathology (5 decks)

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