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Cardiology Flashcards

1
Q

Stable Angina

A

= chest pain that arises w/ exertion or emotional stress; represents reversible injury to myocytes (no necrosis)

Due to atherosclerosis of coronary arteries w/ >70% stenosis = ↓ blood flow not able to meet metabolic needs of the myocardium during exertion

Pw/ chest pain (lasting <20 min) that radiates to the left arm or jaw, diaphoresis & SOB

EKG = ST depression due to subendocardial ischemia

Relieved by rest or nitroglycerin (↓ preload = ↓ stress)

**hallmark of reversible injury is cellular swelling

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2
Q

Unstable angina

A

= chest pain that occurs at rest; represents reversible injury of the myocytes (no necrosis)

Usually due to rupture of an atherosclerotic plaque w/ thrombosis & incomplete occlusion of a coronary artery

EKG = ST depression due to subendocardial ischemia

Relieved by nitroglycerin

**high risk of progression to MI

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3
Q

Prinzmetal angina

A

= episodic chest pain unrelated to exertion; represents reversible injury to myocytes (no necrosis)

Due to coronary artery vasospasm

EKG = ST elevation* due to transmural ischemia (cutting blood flow to entire wall for short period of time)

Relieved by nitroglycerin or CCB (relieve vasospasm)

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4
Q

Myocardial Infarction

A

= Necrosis of cardiac myocytes (irreversible injury); usually involves the left ventricle and septum

Usually due to rupture of an atherosclerotic plaque w/ thrombosis & complete occlusion of a coronary artery (other = vasospasm, emboli & vasculitis)

= Severe, crushing chest pain (>20 min) that radiates to the left arm/jaw, diaphoresis & dyspnea
symptoms not relieved by nitroglycerin

Initially ST depression leading to ST elevation and patholigic Q waves as infarction moves from subendocardial to transmural and then tissue death

Labs = Troponin I (rise 2-4 hr, peak 24hr, stay 7-10 day) most sensitive & specific marker (gold standart)
- CK-MB (rise 4-6 hr, peak 24hr, return to normal by 72 hr = useful in detecting reinfarction)

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5
Q

MI Treatment

A

Aspirin &/or heparin - limits thrombosis
Supplemental O2 - minimizes ischemia
Nitrates - vasodilate veins (↓ preload) & coronary arteries
β-blockers - ↓ HR = ↓ O2 demand & arrhythmia risk
ACEI - ↓ LV dilation
Fibrinolysis or angioplasty = open blocked vessels
-reperfusion may lead to contraction band necrosis (from calcium influx) or reperfusion injury (from free radical generation)

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6
Q

MI Morphologic changes

A

< 4 hours = cardiogenic shock, CHF, arrhythmia
2-24 hours = Coagulative necrosis w/ arrhythmia risk = dark discoloration
1-3 days = Neutrophils w/ risk of fibrinous pericarditis = yellow pallor
4-7 days = Macrophages w/ risk or rupture = yellow pallor
1-3 weeks = granulation tissue w/ plump fibroblasts, collagen & blood vessels = Red border from edge
Months = Fibrosis w/ risk or aneurysm, mural thrombosis or Dressler syndrome (pericarditis 6-8 wks post infarction from pericardial Ab formation) = white scar

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7
Q

Sudden Cardiac Death

A

Unexpected death due to cardiac disease; occurs w/out symptoms or < 1 hour after symptoms arise (before biological markers appear)

Usually due to fatal ventricular arrhythmia

Most common etiology = acute ischemia (90% of patients have preexicting severe atherosclerosis); less commonly MVP, cardiomyopathy & cocaine abuse

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8
Q

Chronic Ischemic Heart Disease

A

Poor myocardial function due to chronic ischemic damage (w/ or w/out infarction)

Progresses to CHF

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9
Q

Congestive Heart Failure

A

= pump failure; divided into right- & left-sided failure

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10
Q

Left-sided Heart Failure

A

Causes = ischemia, dilated or restrictive cardiomyopathy, MI, or HTN

  • pulmonary congestion leads to pulmonary edema = dyspnea, paroxysmal nocturnal dyspnea, orthopnea & crackles; congested capillaries may burst resulting in hemosiderin-laden macrophages (“HF cells”)
  • ↓ forward perfusion = ↓ flow to kidneys & activation of the Renin-angiotensin system = fluid retention exacerbates CHF

ACEI = mainstay of treatment

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11
Q

Right-sided Heart Failure

A

Most commonly due to Left-sided heart failure (other causes = L->R shunt & chronic lung disease)

Clinical features due to congestion
= JVD
=Painful hepatosplenomegaly w/ ‘nutmeg’ liver; may lead to cardiac cirrhosis
=Dependent pitting edema (due to ↑ hydrostatic pressure)

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12
Q

Ventricular Septal Defect (VSD)

A

Defect in the septum that divides the ventricles
-Most common CHD; associated w/ fetal alcohol syndrome

= R -> L shunt; small defects often asymptomatic, Large defects can = Eisenmenger syndrome (late cyanosis when shunt reverses w/ RV hypertrophy, polycythemia & clubbing)

Tx = surgical closure; small defects may close spontaneously

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13
Q

Atrial Septal Defect (ASD)

A

Defect in the septum that divides the atria

  • most common type = ostium secundum (foramen ovale)
  • ostium primum associated w/ Down Syndrome

= R -> L shunt & fixedly split S2; Paradoxical emboli (venous thrombus moving into systemic circulation) are an important complication

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14
Q

Patent Ductus Arteriosus (PDA)

A

Failure of ductus arteriosus to close; associated w/ congenital rubella

= L -> R shunt between aorta and pulmonary artery

Asymptomatic at birth w/ continuous ‘machine-like’ murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis (shunts after branches of the aortic arch)

Tx = indomethacin which ↓ PGE resulting in PDA closure
**PGE maintains patency of ductus arteriosus

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15
Q

Tetralogy of Fallot

A

1 - stenosis of right ventricular outflow tract
2 - right ventricular hypertrophy
3 - VSD
4 - Overriding aorta

= R -> L shunt leading to early cyanosis; degree of stenosis determines the extent of shunting & cyanosis

“boot-shaped” heart on x-ray

Pt learns to squat in response to cyanotic spell (↑ arterial resisitance ↓ shunting & allows more blood to reach lungs)

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16
Q

Transposition of the Great Vessels

A

Pulmonary arises from LV, and aorta arises from RV
-Associated w/ early cyanosis as pulmonary and systemic circuits do not mix
=creation of shunt after birth is required for survival (need to allow blood to mix) - PGE to maintain PDA until definitive surgical repair is performed

= hypertropy of the RV & atrophy of LV

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17
Q

Truncus Arteriosus

A

Single large vessel arising from both ventricles as truncus fails to divide

Pw/ early cyanosis; deoxygenated blood from RV mixes w/ oxygenated blood from LV before circulations separate = mixed blood systemically

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18
Q

Tricuspid Atresia

A

Tricuspid valve orifice fails to develop; right ventricle is hypoplastic

Often associated w/ ASD = R -> L shunt

Pw/ early cyanosis

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19
Q

Coarctation of the Aorta

A

Narrowing of the aorta

Infantile form - associated w/ PDA & coarc lies after the aortic arch, but before PDA
= Pw/ lower extremity cyanosis
- associated w/ Turner syndrome

Adult form - not associated w/ PDA & coarc lies after the aortic arch, associated w/ bicuspid aortic valve
= Pw/ HTN in upper & HoTN/weak pulses in lower extremities; classically discovered in adulthood
- Collateral circulation develops across the intercostal arteries & engorged arteries cause ‘notching’ of ribs on X-ray

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20
Q

Acute Rheumatic Fever

A

systemic complication of pharyngitis due to group A β-hemolytic strep; affects children 2-3 weeks after an episode of strep pharyngitis

caused by molecular mimicry; bacterial M protein resembles proteins in human tissue

Acute attack usually resolves, but may progress to chronic rheumatic heart disease; repeat exposure to group A β-hemolytic strep results in relapse of the acute phase & increases risk for chronic disease

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21
Q

Jones Criteria

A

For diagnosis of acute rheumatic fever1-evidence of prior group A β-hemolytic strep infection2- Minor criteria (nonspecific & include fever, ↑ ESR)3- Major Criteria: Joints (Migratory polyarthritis)
: Pancarditis (does not resolve overtime) = endocarditis involving the mitral valve; Myocarditis w/ Aschoff bodies & Anitschkow cells
: Subcutaneous Nodules
: Erythema marginatum (annular, nonpruritic rash w/ erythematous borders0
:Sydenham chorea - rapid involuntary muscle movement

Major criteria = J<3NES

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22
Q

Chronic Rheumatic Heart Disease

A

Valve scarring that arises as a consequence of rheumatic fever

Results in stenosis w/ a classic ‘fish-mouth’ appearance & almost always involves the mitral valve (leads to thickening of chordae tendinaea & cusps); occasionally involves the aortic valve (leads to fusion of the commissures)

Complications include infectious endocarditis

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23
Q

Aortic Stenosis

A

Narrowing the aortic valve orifice - usually due to fibrosis/calcification from wear & tear

Cardiac compensation leads to a prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard

Complications include Concentric LV hypertrophy; Angina & syncope w/ exercise; Microangiopathic hemolytic anemia

Bisucpid aorta valve ↑ risk & hastens disease onset; May also arise as a consequence of chronic rheumatic valve disease

Tx = valve replacement after onset of complications

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24
Q

Aortic Regurgitation

A

Backflow of blood from aorta into the LV during diastole

Arises due to aortic root dilation (most common), or valve damage

=Early, blowing diastolic murmur

=hyperdynamic circulation due to ↑ PP; LV dilation & eccentric hypertorphy (due to volume overload)

Tx - Valve replacement once LV dysfunction develops

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25
Q

Mitral Valve Prolapse

A

Ballooning of mitral valve into LA during systole

Due to myxoid degeneration of the valve making it floppy

Pw/ incidental mid-systolic click followed by a regurgitation murmur (usually asymptomatic)

**Click/murmur become SOFTER w/ squatting (↑ systemic resistance = ↓ LV emptying)

Complications rare = infectious endocarditis, arrhythmia & severe mitral regurge

Tx = valve replacement

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26
Q

Mitral Regurgitation

A

Reflux of blood from the LV into the LA during systole

Usually arises as a complication of MVP; other causes include LV dilation, Infective endocarditis, Acute rheumatic heart disease, papillary muscle rupture after MI

= Holosystolic ‘blowing’ murmur; louder w/ squatting & expiration
= results in volume overload and left-sided HF

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27
Q

Mitral Stenosis

A

Narrowing of the mitral valve orifice usually due to chronic rheumatic valve disease

= Opening snap followed by diastolic rumble

Volume overload leads to dilatation of the LA =

  • Pulmonary congestion w/ edema & alveolar hemorrhage
  • Pulmonary HTN & right-sided HF,
  • A Fib w/ associated risk for mural thrombi
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28
Q

Endocarditis

A

Inflammation of the endocardium that lines the surface of cardiac valves; usually due to bacterial infection

= Fever (due to bacteremia), Murmer (due to vegetations), Janeway lesions (erythematous nontender lesions on palms & soles), splinter hemorrhages in nail bed & Roth spots (seen fundoscopically) (both due to embolization of septic vegetations)

Labs - + Blood Cultures; Anemia of chronic disease
- transesophageal endocardiogram is useful for detecting lesions on valves

29
Q

Streptococcus viridans Endocarditis

A

= most common,

infects previously damaged valves, resulting in small vegetations that do not destroy the valve

30
Q

S. Aureus Endocarditis

A

most common in IV drug abusers

= affects normal valves (tricuspid most commonly), results in large vegetations that destroy the valve

31
Q

S. Epidermidis Endocarditis

A

associated w/ endocarditis of prosthetic valves

32
Q

Streptococcus bovis endocarditis

A

associated w/ endocarditis in Pt w/ underlying colorectal carcinoma

33
Q

HACEK organisms endocarditis

A

(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

Associated w/ endocarditis w/ negative blood cultures

34
Q

Nonbacterial thrombotic endocarditis

A

due to sterile vegetations that arise in association w/ a hypercoagulable state or underlying adenocarinoma

Vegetations arise on the mitral valve along lines of closure & result in mitral regurgitation

35
Q

Libman-Sacks endocarditis

A

due to sterile vegetations that arise in association w/ SLE

Vegetations are present on the surface & undersurface of the mitral valve & result in mitral regurgitation

vegetation present on both sides of the valve

36
Q

Dilated Cardiomyopathy

A

Dilation of all 4 chambers; most common cardiomyopathy

Most commonly idiopathic; Genetic mutation (AD), myocarditis (coxsackie A/B), Alcohol abuse, Drugs, Pregnancy (late), or Hemochromatosis are also possible causes

= systolic dysfunction leading to biventricular CHF
-complications = mitral & tricuspid valve regurgitation & arrhythmia

Tx = heart transplant

37
Q

Hypertrophic Cardiomyopathy

A

Massive hypertorphy of the Left Ventricle

Usually due to genetic mutations in sarcomere proteins (most common form is AD)

= diastolic dysfunction & ↓ CO; Sudden death due to ventricular arrhythmias; syncope w/ exercise (subaortic hypertrophy of septum = functional aortic stenosis)

common cause of sudden death in young athletes

*Biopsy shows myofiber hypertrophy w/ disarray

38
Q

Restrictive Cardiomyopathy

A

↓ compliance of the ventricular endomycardium that restricts filling during diastole

Causes = amyloidosis, sarcoidosis, endocardial fibroelastosis & Loeffler syndrome (=endocardial fibroelastosis w/ eosinophilic infiltate & eosinophilia)

Pw/ CHF; classic finding = low-voltage EKG w/ diminished QRS amplitude

39
Q

Myxoma

A

Benign mesenchymal tumor w/ gelatinous appearance & abundant ground substance on histology

Most common primary cardiac tumor of adults

Usually forms as a pedunculated mass in the LA that causes syncope due to obstruction of the mitral valve

40
Q

Rhabdomyoma

A

Benign hamartoma of cardiac muscle

Most common primary cardiac tumor in children (associated w/ tuberous sclerosis)

Usually arises in the ventricle

41
Q

Metastasis

A

Metastatic tumors are more common in the heart than primary tumors

Most commonly involve the pericardium, resulting in pericardial effusion

Common metastases to the heart include breast & lung carcinoma, melanoma, & lymphoma

42
Q

Vasculitis

A

Inflammation of the blood vessel wall

Etiology usually unknown, most causes are not infectious

=Nonspecific Sx of inflammation (fever, fatigue, weight loss, myalgias)
=Sx of organ ischemia (due to luminal narrowing or thrombosis of the inflamed vessel)

Large vessel = aorta & its major branches
Medium vessel = Muscular arteries that supply organs
Small vessel = arterioles, capillaries & venuoles

43
Q

Temporal (Giant Cell) Arteritis

A

LVV = Granulomatous vasculitis that classically involves branches of the carotic artery

Most common form in older adults (>50), usually females

Pw/ headache (temporal a.), visual distrubances (ophthalmic a.), & jaw claudification. Flu-like Sx w/ joint & muscle pain often present

ESR is elevated (>100)
Biopsy = inflamed vessel wall w/ giant cells & intimal fibrosis (lesions are segmental = negative biopsy doesn’t exclude disease)

Ts = corticosteroids; *high risk for blindness w/out Tx

44
Q

Takayasu Arteritis

A

LVV = Granulomatous vasculitis that classically involves the aortic arch at branch points

In adults )

ESR is elevated

Tx = corticosteroids

45
Q

Polyarteritis Nodosa

A

MVV = necrotizing vasculitis involving multiple organs (lungs are spared)

Classically in young adults; Pw/ HTN (renal a.), ab pain w/ melena (mesenteric a.), neurologic disturbances & skin lesions.

Associated w/ serum HBsAg

Lesions of varying stages are present. Early lesion consists of transmural inflammation w/ fibrinoid necrosis; eventually heals w/ fibrosis, producing ‘string-of-pearls’ appearance

Tx - corticosteroids & cylcophosphamide (fatal if not Tx)

46
Q

Kawasaki Disease

A

MVV - classically affects Asian children < 4 yo

Pw/ nonspecific signs including fever, conjunctivitis, erythematous rash of palms & soles, and enlarged cervical lymph nodes

Coronary artery involvement is common and leads to risk for thrombosis w/ MI, & aneurysm w/ rupture

Tx = aspirin** and IVIG; disease is self-limited

**need to make sure it is not viral infection before giving aspirin (due to risk of Reye’s syndrome)

47
Q

Buerger Disease

A

MVV - Necrotizing vasculitis involving digits

Pw/ ulceration, gangrene, autoamputation of fingers & toes; Raynaud phenomenon is often present

Highly associated w/ heavy smoking; and classically seen in younger males

Tx = smoking cessation

48
Q

Wegener Granulomatosis

A

SVV = Necrotizing granulomatous vasculitis involving nasopharynx, lungs & kidneys

Classic presentation is a middle-aged male e/ sinusitis/nasopharyngeal ulceration, hemoptysis w/ bilateral nodular lung infiltrates, & hematuria due to rapidly progressive glomerulonephritis

Biopsy reveals reveals large necrotizing granulomas w/ adjacent necrotizing vasculitis

Serum c-ANCA levels correlate w/ disease activity

Tx = cyclophosphamide & steroids; relapses are common

WeCener Granulomatosis - c-ANCA, Cyclophsphamide

49
Q

Microscopic Polyangiitis

A

SVV - necrotizing vasculitis involving multiple organs, especially lung & kidney

Pw/ similar to Wegener (but nasopharyngeal involvement & granulomas are absent)

Serup p-ANCA levels correlate w/ disease activity

Tx - corticosteroids & cyclophosphamide; relapses are common

50
Q

Churg-Strauss Syndrome

A

SVV - necrotizing granulomatous inflammation w/ eosinophils involving multiple organs, especially lungs & heart

*Asthma & peripheral eosinophilia are often present

Serum p-ANCA levels correlate w/ disease activity

51
Q

Henoch-Schonlein Purpura (HSP)

A

SVV - due to IgA immune complex deposition; most common vasculitis in children

Pw/ PALPABLE purpura on buttocks & legs, GI pain & bleeding, & hematuria (IgA nephropathy); usually occurs following an URTI

Disease is self-limited, but may recur;
Tx w/ steroids if severe

52
Q

Hypertension

A

↑ blood pressure; may involve pulmonary or systemic circulation

Systemic HTN is defined as pressure > 140/90 mm Hg (normal < 120/80)
- can have isolated systolic or diastolic HTN

Divided into primary and secondary types based on etiology

53
Q

Primary HTN

A

HTN of unknown etiology (95%)

Risk factors include:
- age, race (↑ AA, ↓ Asian), obesity, stress, lack of physical activity & high-salt diet

54
Q

Secondary HTN

A

HTN due to an identifiable etiology (5%)

Renal artery stenosis is a common cause (renovascular HTN)
- ↓ blood flow to glomerulus
= JGA secretes renin = ANGI -> ANGII (by ACE)
-> ANGII ↑ BP by contracting arteriolar AM (↑ TPR) &
promoting adrenal release of aldosterone (↑ Na
reabsorption = expanding plasma volume)
=↑ plasma renin & unilateral atrophy of affected kidney (neither seen in primary HTN)
- Atherosclerosis (elderly males) & fibromuscular dysplasia (young females) = important causes

55
Q

Benign HTN

A

mild or moderate elevation in BP

= Clinically silent; vessels & organs are damaged slowly over time

Most causes of HTN are benign

56
Q

Malignant HTN

A

severe elevation in BP (>200/120)

May arise from preexisting benign HTN or de novo

Pw/ acute end-organ damage (acute renal failure, headache, & papilledema)
Is a medical emergency

comprises <5% of cases

57
Q

Atherosclerosis

A

Intimal plaque that obstructs blood flow (in medium & large sized vessels)

Modifiable RF = HTN, hypercholesterolemia (LDL), smoking & diabetes

Nonmodifiable RF = age, gender (estrogen is protective), & genetics

Damage to endothelium allows lipids to leak into the intima, lipids are oxidized & then consumed by macrophages via scavenger receptors = foam cells

=Results in fatty streaks that progress to atherosclerotic plaques

58
Q

Complications of Atherosclerosis

A

account for >50% of disease in Western countries

Stenosis of medium-sized vessels results in impaired blood flow and ischemia, leading to
= Peripheral vascular disease, Angina, Ischemic bowel disease

Plaque rupture w/ thrombosis results in MI & stroke

Plaque rupture w/ embolization results in atherosclerotic emboli, **characterized by cholesterol crystals w/in the embolus

Weakening of vessel wall results in aneurysm

59
Q

Arteriolosclerosis

A

Narrowing of small arterioles

diveded into hyaline & hyperplastic types

60
Q

Hyaline Arteriolosclerosis

A

caused by proteins leaking into the vessel wall, producing vascular thickening; proteins are seen as pink hyaline on microscopy

*Consequence of long-standing benign HTN or Diabetes

= reduced vessel caliber w/ end-organ ischemia; classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure

=reason that Pt w/ HTN or Diabetes get renal failure

61
Q

Hyperplastic arteriolosclerosis

A

Thickening of vessel wall by hyperplasia of smooth muscle (‘onion-skin’ appearance)

  • Consequence of malignant HTN

= reduced vessel caliber w/ end-organ ischemia

May lead to fibrinoid necrosis of the vessel wall w/ hemorrhage; classically causes acute renal failure w/ a characteristic ‘flea-bitten’ appearance (pin-point hemorrhages from blowing out small vessels)

62
Q

Monckeberg Medial Calcific Sclerosis

A

Calcification of the media of muscular (medium-sized) arteries nonobstructive

Not clinically significant; seen as an incidental finding on x-ray or mammography

63
Q

Aortic Dissection

A

Intimal tear w/ dissection of blood through media of the aortic wall

Most common cause is HTN; also associated w/ inherited defects of CT (Margan or Ehlers-Danlos Syndrome)

Occurs in the proximal 10cm (high stress region) w/ preexisting weakness of the media

Pw/ sharp, tearing chest pain that radiates to the back

Complications = pericardial tamponade (most common cause of death), rupture w/ fatal hemorrhage, & obstruction of branching arteries w/ resultant end-organ ischemia

64
Q

Thoracic Aortic Aneurysm

A

Balloon-like dilation of the thoracic aorta

Due to weakness in the aortic wall *Classically seen in tertiary syphilis; endarteritis of the vasa vasorum results in luminal narrowing, ↓ flow & atrophy of the vessel wall
= ‘tree bark’ appearance of the aorta

Complications = dilation of the aortic valve root resulting in aortic valve insufficiency; compression of mediastinal structures; & thrombosis/embolism

65
Q

Abdominal Aortic Aneurysm

A

Balloon-like dilation of the abdominal aorta; usually arises below the renal arteries, but above the aortic bifurcation

Primarily due to atherosclerosis; classically seen in male smokers >60yo w/ HTN

Pw/ a pulsatile abdominal mass that grows w/ time

Complications = rupture (esp when >5cm) (pw/ triad of HTN, Pulsatile ab mass & flank pain); compression of local structures & thrombosis/embolism

66
Q

Hemangioma

A

Benign tumor comprised of blood vessels

Commonly present at birth; often regresses during childhood

Most often involves skin & liver

**will blanch when pressed on (vs a bleed into the skin (ex a purpura))

67
Q

Angiosarcoma

A

Malignant proliferation of endothelial cells; highly aggressive

Common sites include skin, breast & liver
- Liver angiosarcoma is associated w/ exposure to polyvinyl chloride (PVC), arsenic, & Thorotrast

68
Q

Kaposi Sarcoma

A

Low-grade malignant proliferation of endothelial cells; associated w/ HHV-8

Pw/ purple patches, plaques, & nodules on the skin; may also involve visceral organs

Classically seen in:

  • Older Eastern European males - tumor remains localized to skin; Tx w/ surgical removal
  • AIDS - tumor spreads early; Tx - antiretroviral agents
  • Transplant recipients - tumor spreads early; Tx - ↓ immunosuppression

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