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STEP 1 (2) > Cardiovascular- Pathology > Flashcards

Cardiovascular- Pathology Flashcards

1
Q

Describe how a right-left shunt might appear clinically

A

there is early cynaosis (aka ‘blue babies”) often seen/diagnosed at birth and usually requiring intervention

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2
Q

What are the five things that normally cause right-left shunts?

A

5T’s

Truncus arteriosus (1 vessel)

Transposition of the GVs (2 switched vessels)

Tricuspid atresia (Tri= 3)

Tetralogy of Fallot (tetra= 4)

TAPVR (5 letters)

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3
Q

Describe persistent truncus arteriosus

A

this occurs when the truncus arteriosis fails to divide into the pulmonary trunk and aorta ***due to lack of aorticopulmonary septum formation**

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4
Q

Most pts with persistent truncus arteriosus also have _____

A

a VSD

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5
Q

Transposition of the GVs is not compatible with life unless accompanied by what?

A

a shunt like a VSD, PDA, or a patent foramen ovale

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6
Q

What causes transpositon of the GVs?

A

failure of the aorticopulmonary septum to spiral

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7
Q

What are the 4 main parts of Tetralogy of fallot?

A

a VSD, a hole between the two ventricles

  • pulmonary stenosis
  • right ventricular hypertrophy
  • an overriding aorta, which allows blood from both ventricles to enter the aorta
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8
Q

What does this show?

A

the classic ‘boot-shaped heart’ on CXR as seen in tetralogy of Fallot due to right heart hypertrophy

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9
Q

What is the most common cause of early childhood cyanosis?

A

TOF

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10
Q

What are the risk factors for TOF?

A

Risk factors include a mother who uses alcohol, has diabetes, is over the age of 40, or gets rubella during pregnancy. It may also be associated with Down syndrome

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11
Q

What occurs with total anomalous pulmonary venous return (TAPVR)?

A

pulmonary veins drain into the RIGHT heart instead of the left

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12
Q

Late cyanosis is associated more with left-right shunts. What are some common LTR shunts?

A
  • VSD (most common)
  • ASD
  • PDA
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13
Q

What is the most common congenital cardiac defect?

A

VSD

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14
Q

What is the prognosis of a VSD?

A

most spontaneously resolve

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15
Q

How do heart sounds with an ASD?

A

there is a loud S1 with a wide, fixed split S2

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16
Q

How does a patent PDA present?

A

late onset lower extremity cyanosis (aka ‘differential’ cyanosis) and a continuous machine-like murmur

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17
Q

What can be used to close a patent PDA? Keep it open (as in the case of transposition of the GVs)?

A

Close- Indomethacin

KEEp open- PGEs 1 and 2

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18
Q

What is Eisenmenger syndrome?

A

An uncorrected LTR shunt will cause increased pulmonary blood flow leading to PAH and subsequently RVH causing the shunt to switch to the right to left shunt and causing late cyanosis

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19
Q

How does corarctation of the aorta appear clinically?

A

HTN in the upper extremities and weak,delayed pulses in the lower extremities (brachial-femoral delay). With age, collateral aa. erode the ribs giving them a notched appearance on CXR

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20
Q

What congenital defects can be caused by alcohol exposure in utero?

A

VSD, PDA, ASD (all LTRs)

TOF

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21
Q

What congenital defects can be caused by congenital rubella?

A

PDA, pulmonary a. stenosis

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22
Q

What congenital defects can be caused by down syndrome?

A

AV septal defects (endocardial cushion defects), VSD, ASD

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23
Q

What congenital defects can be caused by having a diabetic mother?

A

transposition of the GVs

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24
Q

What congenital defects can be caused by Marfan Syndrome?

A

MVP, thoracic aortic aneurysm and dissection, aortic regurg

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25
Q

What congenital defects can be caused by prenatal lithium exposure?

A

Ebstein anomaly

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26
Q

What congenital defects can be caused by Turner Syndrome?

A

Bicuspid aortic valve, coarctation of the aorta

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27
Q

What congenital defects can be caused by Williams Syndrome?

A

supravalvular aortic stenosis

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28
Q

What congenital defects can be caused by 2q11 Syndromes?

A

truncus arteriosus, TOF

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29
Q

What is HTN defined as?

A

Persistent systolic BP 140+ and/OR diastolic BP 90+

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30
Q

What is ‘hypertensive urgency’?

A

severe (180+/120+) HTN without acute end-organ damage

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31
Q

What is ‘hypertensive emergency’?

A

severe HTN with evidence of acute end-organ damage (e.g. encephalopathy, stroke, retinal dmaage, MI, HF, kidney damage, etc.)

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32
Q

What is this?

A

Hypertensive nephropathy

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33
Q

While the vast majority of HTN pts are primary, other things such as fibromuscular dysplasia can cause it. Describe this

A

a non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery. FMD has been found in nearly every arterial bed in the body. However, the most common arteries affected are the renal and carotid arteries

Below: classic ‘beads on a string’ appearance of the renal a.

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34
Q

What are some superficial signs of hyperlipidemia?

A
  • xanthomas
  • tendinous xanthomas
  • corneal acrus
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35
Q

What is xanthelasma?

A

xanthomas, or plaques/nodules of lipid-laden histiocytes, deposited periocularly

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36
Q

What is this?

A

corneal arcus, as seen in hyperlipidemia

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37
Q

What is arteriosclerosis?

A

HARDENING of the arteries, with arterial wall thickening and loss of elasticity

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38
Q

What are the two main types of arteriosclerosis?

A
  • hyaline
  • hyperplastic (onion-skin appearance)
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39
Q

What is Monckeberg (medial calcific sclerosis) arteriosclerosis?

A

uncommon type of arteriosclerosis affecting medium-sized aa. and marked by calcification of the elastic lamina of aa.

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40
Q

What is atherosclerosis?

A

a form of arteriosclerosis affecting elastic aa. and large- and medium-sized muscular aa. caused by buildup of cholesterol plaques

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41
Q

How does atherosclerosis occur?

A

endothelial cell dysfunction caused by inflammation/etc. causes macrophage and LDL accumulation leading to the formation of foam cells, subsequent fatty streaks, and smooth muscle cell migration and ECM deposition

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42
Q

Where is atherosclerosis most common?

A

abdominal aorta > coronary a. > popliteal a. > carotids

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43
Q

What are the two types of aortic dissection?

A

Stanford Type A: in the ascending aorta; tx is surgery

Stanford Type B: in the descending aorta/aortic arch; tx is B blockers, then vasodilators

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44
Q

What causes angina?

A

chest pain due to an ischemic myocardium (no myocyte necrosis)

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45
Q

What are the main causes of angina?

A
  • Stable
  • Variant (Prinzmetal)
  • Unstable
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46
Q

Describe stable angina

A

This usually occurs secondary to atherosclerosis with exerteional chest pain resolving with rest or nitroglycerin

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47
Q

How might angina appear on an ECG?

A

ST depression

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48
Q

Describe variant angina

A

this occurs at rest 2ndary to coronary a. spasm with transient ST ELEVATION on ECG. Triggers include tobacco, cocaine, and triptans

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49
Q

Describe unstable angina

A

there is usually thrombosis with incomplete coronary a. occlusion +/- ST depression and/or T wave inversion on ECG but no cardiac biomarker elevation

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50
Q

What is coronary steal syndrome?

A

a phenomenon where an alteration of circulation patterns lead to a reduction in the blood directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – “stealing” blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia.

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51
Q

MI is most often caused by what?

A

thrombosis of ruptured atherosclerotic plaque

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52
Q

What is the difference between a STEMI and NSTEMI?

A

STEMI- if transmural, ECG may show ST elevation

if subendocardial, ECG may show ST depression (NSTEMI)

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53
Q

What are the most commonly occluded vessels resulting in MI?

A

LAD > RCA > circumflex

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54
Q

What is the gold standard of MI diagnosis in the first 6 hrs?

A

ECG

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55
Q

How does cardiac troponin I respond to MI?

A

It rises after 4 hrs and is elevated for 7-10 days (specific to MI)

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56
Q

How does CK-MB respond to MI?

A

it rises after 6-12 hrs and is predominantly found in the myocardium but can also be released from skeetal muscle. Levels typically return to normal within 48 hrs (good for evaluating subsequent infarcts)

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57
Q

How does an ECG respond to an MI?

A

It can include ST elevation (STEMI, transmural infarct), ST depression (NSTEMI, subendocardial infarct), hyperacute (‘peaked) T waves, T-wave inversion, and pathologic Q waves

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58
Q

Describe the findings of a transmural infarct

A
  • elevated necrosis
  • ST elevation
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59
Q

MI of which artery would present with ST elevations or Q waves in leads V1-V2?

A

Anteroseptal (LAD)

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60
Q

MI of which artery would present with ST elevations or Q waves in leads V3-V4?

A

Anteroapical (distal LAD)

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61
Q

MI of which artery would present with ST elevations or Q waves in leads V5-V6?

A

Anterolateral (LAD or LCX)

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62
Q

MI of which artery would present with ST elevations or Q waves in leads I or aVL?

A

LCX

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63
Q

MI of which artery would present with ST elevations or Q waves in leads II, III, and aVF?

A

InFerior (RCA)

64
Q

When is cardiac arrhythmia one of the most common causes of death following MI?

A

first few days

65
Q

When is ventricular free wall rupture one of the most common causes of death following MI?

A

3-14 days post-MI

66
Q

When is ventricular aneursym one of the most common causes of death following MI?

A

2 weeks- several months post MI

67
Q

When is postinfarct fibrinous pericarditis common following MI?

A

1-3 days- resulting in a friction rub

68
Q

What causes Dressler Syndrome?

A

It is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of the MI. A similar pericarditis can be associated with any pericardiotomy or trauma to the pericardium or heart surgery.

69
Q

How does Dressler Syndrome present?

A

The disease consists of a persistent low-grade fever, chest pain (usually pleuritic in nature), pericarditis (usually evidenced by a pericardial friction rub), and/or a pericardial effusion. The symptoms tend to occur 2–3 weeks after myocardial infarction, but can also be delayed for a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade.[8] An elevated ESR is an objective, yet nonspecific, laboratory finding.

70
Q

How is unstable angina/NSTEMI tx?

A

anticoagulation (e.g. heparin), antiplatelet therapy (e.g. aspirin + clopidogrel), B-blockers, ACEIs, stains

symptom control with nitroglycerin and morphine

71
Q

How is STEMI tx?

A

same as unstable angina/NSTEMI + reperfusion therapy

72
Q

What is the most common cardiomyopathy?

A

dilated cardiomyopathy

73
Q

What are some causes of dilated cardiomyopathy?

A
  • idiopathic/familial
  • chronic Alcohol abuse
  • wet Beriberi
  • Coxsachie B vrus, chronic Cocaine use, or Chagas disease
  • Doxorubicin
  • hemochromatosis, sarcoidosis
74
Q

What are the findings of dilated cardiomyopathy?

A

HF, S3, systolic regurgitant murmur, balloon heart on CXR

SYSTOLIC dysfunction

75
Q

How is dilated cardiomyopathy tx?

A

Na+ restriction, ACEIs, BBs, diuretics, digoxin, ICD

heart transplant

76
Q

What are the main causes of hypertrophic cardiomyopathy?

A

60-70% are familial, AD (commonly a B-myosin heavy-chain mutation)

-Friedreich ataxia

77
Q

What are the findings of hypertrophic cardiomyopathy?

A

S4, systolic murmur, sudden death in young athletes common, mitral regurg

DIASTOLIC dysfunction

78
Q

How is hypertrophic cardiomyopathy tx?

A

cessation of high-intensity athletics, BBs or non-dihydropyridine CCBs (e.g. verapamil)

ICD for high risk pts.

79
Q

What are the main causes of restrictive/infiltrative cardiomyopathy?

A
  • sarcoidosis, amyloidosis
  • postradiation fibrosis
  • endocardial fibroelastosis in children
  • Loffler Syndrome
80
Q

What is Loffler Syndrome?

A

a disease in which eosinophils accumulate in the lung in response to a parasitic infection.

Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis and can be caused by idiopathic eosinophilia or eosinophilia in response to parasitic infection

81
Q

What are the clinical signs of left heart failure?

A
82
Q

Pathogenesis of left heart failure and edema

A

decreased LV function causes pulmonary venous congestion leading to pulmonary edema and decreased CO leading to increased renin activity, Na+/H2O reabsorption, and sympathetic activity all increasing preload and venous pressure contributing to peripheral edema

83
Q

What are the findings of right heart failure (most commonly due to left heart failure)?

A

-hepatomegaly (nutmeg liver), JVD, and peripheral edema

84
Q

What are the main types of shock?

A
  • hypovolemic
  • cardiogenic
  • obstructive
  • distributive
85
Q

What are the main causes of hypovolemic shock?

A

-hemorrhage, dehydration, burns (all leaving the skin cold and clammy)

86
Q

How are preload, CO, and afterload affected by hypovolemic shock?

A

preload- very decreased

CO- decreased

afterload- increased

87
Q

What is the tx of hypovolemic shock?

A

IV fluids

88
Q

What are some causes of cardiogenic shock?

A
  • acute MI, HF
  • valvular dysfunction
  • arrhythmia

(all leaving the skin cold and clammy)

89
Q

What are some causes of obstructive shock?

A

PE, cardiac tamponade (skin cold and clammy)

90
Q

How are preload, CO, and afterload affected by cardiogenic and obstructive shock?

A

preload- increased

CO- very decreased

afterload- increased

91
Q

How is cardiogenic shock tx?

A

inotropes and diuresis

92
Q

What are some causes of distributive shock?

A

-sepsis, CNS injury, and anaphylaxis (leaving the skin warm and dry)

93
Q

How are preload, CO, and afterload affected by cardiogenic and obstructive shock?

A

preload- decreased

CO- increased

afterload- very decreased

94
Q

What are the symptoms of bacterial endocarditis?

A

Bacteria FROM JANE

Fever

Roth Spots

Osler Nodes

Murmur

Janeway lesions

Anemia

Nail-bed (‘splinter’) hemorrhage

Emboli

95
Q
A
96
Q

What is the difference between Osler nodes and Janeway lesions?

A

Osler nodes are tender raised lesions on the finger or toe pads

Janway lesions are small, painless, lesions on the palm or soles

97
Q

T or F. Multiple blood cultures are needed for diagnosis of bacterial endocarditis

A

T.

98
Q

What is the major cause of acute bacterial endocarditis?

A

s. aureus

99
Q

What is the major cause of subacute bacterial endocarditis?

A

viridans streptococci (low virulence so valves are usually damaged)

100
Q

What is a common cause of bacterial endocarditis in colon cancer?

A

S. bovis

101
Q

What is a common cause of bacterial endocarditis in prosthetic valves?

A

S. epidermidis

102
Q

What is the most common valve for bacterial endocarditis?

A

mitral (Tricuspid with IVDU)

103
Q

Culture negative bacterial endocarditis is most likely due to what?

A

Coxiella burnetii, Bartonella spp.

HACEK (haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

104
Q

What causes Rheumatic fever?

A

group A B-hemolytic strep

105
Q

How does rheumatic fever present?

A

The disease typically develops two to four weeks after a throat infection. Symptoms include: fever, migratory polyarthritis, sydenham chorea, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of cases. Damage to the heart valves usually occurs only after multiple attacks but may occasionally occur after a single case of RF. The damaged valves may result in heart failure and also increase the risk of atrial fibrillation and infection of the valves

106
Q

What are the Jones criteria of Rheumatic fever?

A
  • Joint (migratory polyartritis)
  • Carditis
  • Nodules in skin (subQ)
  • Erythema marginatum
  • Sydenham chorea
107
Q

Erythem marginatum in RF

A
108
Q

The _____ valve is most commonly affected in rheumatic fever

A

mitral

109
Q

What is this?

A

Aschoff body as seen in RF

110
Q

Seen in RF

A
111
Q

Rheumatic fever is caused by molecular mimicry to the GAS ____ protein

A

M

112
Q

How does acute pericarditis present?

A

sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. Presents with friction rub

113
Q

What are some common causes of pericarditis?

A
  • idiopathic
  • infection (e.g.Coxsachivirus)
  • autoimmune (e.g. SLE, rheuamtoid arthritis)
  • uremia

STEMI or Dressler syndrome

114
Q

Cardiac tamponade is marked by the ____ triad, consisting of:

A

Beck triad: hypotension, distended neck veins, and distant heart sounds

as well as tachcyardia and pulsus paradoxus

115
Q

What is pulsus paradoxus?

A

a decreased in the amplitude of the systolic BP by 10+ mmHg during inspiration

116
Q

When else is pulsus paradoxus seen?

A

-asthma

obstructive sleep apnea

  • percarditis
  • croup
117
Q

Describe syhpillis related heart disease

A

Involvement of the vasa vasorum of the aorta resulting in a characteristic “tree-bark” appearance

118
Q

What is the most common cardiac tumor?

A

METs

119
Q

What is the most common primary cardiac tumor in adults?

A

myxomas

120
Q

Where do most myxomas occur?

A

in the left atria, commonly described as a ‘ball valve” obstruction

121
Q

What is the most common primary tumor in children?

A

rhabdomyomas, associated with tuberous sclerosis

122
Q

What is a Kussmaul sign?

A

Increase in JVP on inspiration instead of the normal decrease

123
Q

What are some common vascular tumors?

A
  • Angiosarcoma
  • bacillary angiomatosis
  • cherry hemangiomas
  • cystic hygromas
  • glomus tumors
  • Kaposi sarcoma
  • Pyogenic granulomas
  • Strawberry hemangiomas
124
Q

Describe angiosarcomas

A

rare blood vessel tumors typically occurring in the head, neck, and breast areas usually in elderly, on sun-exposed areas

associated with radiation therapy and chronic postmastectomy lymphedema

125
Q

Hepatic angiosarcomas are associated with what?

A

vinyl chloride and arsenic exposure

126
Q

What is this?

A

Bacillary angiomatosis, a benign capillary skin lesion found in AIDS pts.

127
Q

What causes Bacillary angiomatosis?

A

Bartonella henselae (neutrophilic infiltrate distinguishes from Kaposi sarcoma)

128
Q

What is this?

A

Cherry hemangioma, a benign capillary hemangioma of the elderly that does not regress

129
Q

What is this?

A

Cystic hygroma, a cavernous lymphangioma of the neck seen in Turner Syndrome

130
Q

What is this?

A

A glomus tumor

131
Q

What causes a glomus tumor?

A

modified smooth muscle cells of the thermoregulatory glomus body

132
Q

Describe Raynaud Phenomenon

A

Decreased blood flow to the skin due to arteriolar vasospasm in response to cold or stress

133
Q

How do you tx Raynaud Syndrome?

A

CCBs

134
Q

What are the large vessel vasculites?

A
  • Temporal (giant cell) arteritis
  • Takayasu arteritis
135
Q

Describe temporal arteritis

A

This is a disease mostly affecting elderly females and presenting as a unilaterla HA and jaw claudication that may lead to ophthalmic a. occlusion and blindness

136
Q

How is temporal arteritis tx?

A

high-dose steroids to prevent blindness

137
Q

How does Takayasu arteritis present?

A

usually in Asian females under 40 yo with granulomatous thickening of the aortic arch described as ‘pulseless disease’ (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules

138
Q

What are the medium-vessel vasculites?

A
  • Polyarteritis nodosa
  • Kawasaki disease
  • Buerger disease (thromboangiitis obliterans)
139
Q

Describe polyarteritis nodosa

A

vasculitis of the renal and visceral aa. (NOT pulmonary arteries) of young adults without ANCA association but with a high correlation of Hep B seropositivitiy

140
Q

How does polyarteritis nodosa present?

A

constitutional symptoms of fever, weight loss, malaise

GI disturbances

HTN, neurologic dysfunction, renal damage

141
Q

What causes polyarteritis nodosa?

A

deposits containing HBsAg-HBsAb complexes in affected vessels, indicating an immune complex–mediated etiology in that subset.

142
Q

Diagnosis criteria for polyarteritis nodosa

A

A patient is said to have polyarteritis nodosa if he or she has three of the 10 signs known as the 1990 American College of Rheumatology (ACR) criteria:

Weight loss greater than/equal to 4.5 kg

Livedo reticularis (a mottled purplish skin discoloration over the extremities or torso)

Testicular pain or tenderness (occasionally, a site biopsied for diagnosis)

Muscle pain, weakness, or leg tenderness

Nerve disease (either single or multiple)

Diastolic blood pressure greater than 90 mmHg (high blood pressure)

Elevated kidney blood tests (BUN greater than 40 mg/dl or creatinine greater than 1.5 mg/dl)

Hepatitis B or hepatitis C virus tests positive (for surface antigen or antibody)

Arteriogram (angiogram) showing the arteries that are dilated (aneurysms) or constricted by the blood vessel inflammation

Biopsy of tissue showing the arteritis (typically inflamed arteries):[9] The sural nerve is a frequent location for the biopsy.

143
Q

How is PAN tx?

A

corticosteroids and cyclophosphamide

144
Q

Describe Kawasaki Disease

A

this is a medium vessel vasculitis of asian children (under 4 yo) that can lead to coronary a. aneurysm

145
Q

What are the symptoms of Kawasaki Disease?

A

CRASH and burn

Conjunctival infection

Rash

Adenopathy (cervical)

Strawberry tongue

Hand-foot changes (edema, erythema)

fever

146
Q

What is this?

A

Strawberry tongue seen in Kawasaki disease

147
Q

How is Kawasaki disease tx?

A

IV immunoglobin and ASPIRIN (ONLY time in children)

148
Q

Describe Buerger Disease

A

Buerger’s disease (thromboangiitis obliterans) is a rare disease of the arteries and veins in the arms and legs. In Buerger’s disease, your blood vessels become inflamed, swell and can become blocked with blood clots (thrombi).

This eventually damages or destroys skin tissues and may lead to infection and gangrene. Buerger’s disease usually first shows in your hands and feet and may eventually affect larger areas of your arms and legs.

Virtually everyone diagnosed with Buerger’s disease smokes cigarettes or uses other forms of tobacco, such as chewing tobacco. Quitting all forms of tobacco is the only way to stop Buerger’s disease. For those who don’t quit, amputation of all or part of a limb is sometimes necessary.

149
Q

What are the main small-vessel vasculites?

A
  • Granulomatosis with polyangiitis (Wegener)
  • Microscopic Polyangiitis
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  • Henoch-Schonlein purpura

-

150
Q

Describe Wegeners

A

This is a small vessel vasculitis affecting the lungs and the kidneys associated with deposition of PR3(‘c’)-ANCA immune complexes

151
Q

How does Wegeners affect the URT?

A

can cause perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis

152
Q

How does Wegeners affect the LRT?

A

hemoptysis, cough, dyspnea

153
Q

How does Wegeners affect the kidneys?

A

hematuria, red cell casts

154
Q

What is the triad of histo findings with Wegener’s?

A
  • focal necrotizing vasculitis
  • necrotizing granulomas in the lung and upper airway
  • necrotizing glomerulonephritis
155
Q

How is Wegener tx?

A

-cyclophosphamide and corticosteroids

156
Q

Describe microscopic polyangiitis

A

necrotizing vasculitis commonly affecting the lungs, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura

Presents similar to Wegeners but without nasopharyngeal involvement or granulomas

157
Q

microscopic polyangiitis is associated with ___-ANCA

A

MPO (‘p’) (anti-myeloperoxidase)

STEP 1 (2) (16 decks)

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