Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Robbins systemic pathology > Chapter 12: Heart > Flashcards

Chapter 12: Heart Flashcards

1
Q

What are Lambl excrescences?

A

-filiform projections on the closure lines of aortic and mitral valves, probably related to fibrosed thrombi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Main mechanisms of cardiac dysfunction

A
  • pump failure
  • outflow obstruction
  • regurgitation
  • rupture of heart or a major vessels
  • conduction abnormalities
  • shunts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the main dysfunction in congestive heart failure?

A

-the heart is not able to pump at a rate sufficient to keep up with metabolic demand; or does so at the expense of increased filling pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the Frank-Starling mechanism?

A

-mechanism to maintain arterial pressure and perfusion by which increased filling volumes dilate the heart, increase functional cross-bridges between sarcomeres, and thereby increase contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens to hypertrophied myocytes?

A
  • a response to pressure or volume overload or other trophic signals
  • increased protein synthesis permitting assembly of more sarcomeres
  • increased mitochondrial
  • enlarged nuclei
  • not accompanied by a sufficient increase in capillary synthesis such that oxygen supply is more tenuous than in the normal heart
  • increased metabolic demands make the hypertrophied heart more vulnerable to decompensation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Morphology of pressure overload hypertrophy?

A
  • concentric wall thickening

- due to sarcomeres assembled parallel to the long axes of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Morphology of volume overload hypertrophy?

A

-chamber dilatation due to sarcomeres arranged in series to existing ones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Main causes of left sided heart failure

A
  • ischemic heart disease
  • mitral and aortic valvular diseases
  • myocardial disease
  • hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Consequences of left heart failure

A
  • pulmonary congestion
  • stasis of blood in left side of heart
  • decreased perfusion of organs leading to their dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diastolic failure

A
  • relatively preserved pump function but failure of heart to relax due to stiff ventricle
  • heart unable to increase its output in response to increased demand
  • can cause flash pulmonary edema
  • most common cause: hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Morphologic features of right sided heart failure

A

-hypertrophy and dilatation of right atrium and ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most common congenital cardiac malformations

A

-VSD>ASD>pulmonary stenosis>PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the main categories of cardiac congenital anomalies

A
  • right to left shunts
  • left to right shunts
  • obstructions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are secundum ASDs?

A
  • most common type
  • occur near the centre of the atrial septum
  • usually not associated with other abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are sinus venosus ASDs?

A
  • less common type
  • located near opening of SVC
  • may be associated with anomalous pulmonary venous return
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes persistent truncus arteriosus?

A

Failure of the truncus to separate into the aorta and pulmonary artery resulting in a single artery receiving bilateral blood flow and giving flow to systemic, pulmonary and coronary circulations
-associated with VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which gender more often gets coarctation?

A

-males, but females with Turner syndrome are at high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Four clinical syndromes by which IHD presents

A
  • myocardial infarction
  • angina pectoris
  • sudden death
  • chronic IHD with heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the primary cause of IHD syndromes?

A

-insufficient coronary perfusion for myocardial demand due to chronic, progressive atherosclerotic narrowing of the coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What event generally precipitates acute coronary syndromes?

A

-change from a stable plaque to an unstable plaque through rupture, erosion or hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe Prinzmetal angina

A
  • caused by coronary spasm
  • symptoms unrelated to exercise
  • may coexist with coronary atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are causes of transmural MI in the absence of the usual coronary artery pathology?

A
  • vasospasm (sometimes in connection with cocaine)
  • emboli from the left atrium or paradoxical emboli from the right heart
  • disorders of small vessels in the heart such as due to vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is a subendocardial infarct?

A
  • involves the inner 1/3 of the myocardium
  • least perfused area of the myocardium
  • possible causes include a thrombus that becomes lysed before causing more damage (in the territory of that thrombus), systemic hypoperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Potential causes of infarct extension

A
  • retrograde propagation of a thrombus
  • proximal vasospasm
  • impaired contractility rendering flow through stenoses inadequate
  • arrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Gross and microscopic appearance of a reperfused infarct?

A

Gross: hemorrhagic
Micro: irreversibly injured myocytes contain contraction bands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of acute MI

A
  • arrhythmia
  • pericarditis (Dressler syndrome; fibrinohemorrhagic)
  • contractile dysfunction (heart failure; cardiogenic shock)
  • myocardial rupture (VSD, free wall, papillary muscle rupture)
  • RV infarction
  • infarct extension
  • infarct expansion
  • ventricular aneurysm
  • papillary muscle dysfunction
  • mural thrombus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Microscopic features of chronic IHD

A
  • patchy myocardial fibrosis, sometimes with distinct old infarcts
  • subendocardial vacuolar change
  • mural thrombi
  • myocyte hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Non-atherosclerotic causes of sudden cardiac death?

A
  • congenital structural or coronary artery anomalies
  • aortic stenosis
  • mitral valve prolapse
  • dilated/hypertrophic cardiomyopathy
  • pulmonary hypertension
  • congenital or acquired arrhythmias
  • cardiac hypertrophy of any cause (e.g. hypertension)
  • drugs of abuse (cocaine, methamphetamine)
  • metabolic/catecholamine causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What electric abnormalities of the heart predispose to sudden cardiac death?

A
  • long QT syndrome
  • Brugada syndrome
  • short QT syndrome
  • Wolff-Parkinson-White
  • congenital sick sinus syndrome
  • catecholaminergic polymorphic ventricular tachycardia
  • isolated cardiac conduction disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are channelopathies?

A
  • mostly autosomal dominant mutations in genes for normal channel function
  • e.g. genes encoding K, Na or Ca channels, or accessory proteins
  • e.g. long QT syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

4 main categories of disorders predisposing to cor pulmonale (not including left heart failure)

A
  • primary pulmonary disorders (e.g. fibrosing, COPD, etc)
  • pulmonary vascular disorders (e.g. recurrent PE, primary pulmonary HTN)
  • chest wall abnormalities (e.g. kyphoscoliosis, obesity/sleep apnea)
  • disorders inducing pulmonary arterial vasoconstriction (metabolic acidosis, obstruction of large airways, etc)
32
Q

Pathologic features of cor pulmonale

A
  • RV hypertrophy, sometimes isolated to the outflow tract or moderator band thickening (connects ventricular septum to anterior RV papillary muscle)
  • fibrous thickening of tricuspid valve
  • myocytes appear more concentrically arranged compared to their usual more haphazard arranged
  • RV dilatation
33
Q

What is functional valve regurgitation?

A

-regurgitation resulting from instability of one of its support structures, e.g. ventricular dilatation pulling the valve muscles downwards and causing regurg

34
Q

Commonest causes of aortic stenosis?

A

-calcification of normal or bicuspid valves

35
Q

Commonest cause of aortic regurg?

A

-dilatation of ascending aorta, usually related to htn and age

36
Q

Commonest cause of mitral regurg?

A

-MVP (myxomatous degeneration)

37
Q

Commonest cause of mitral stenosis?

A

Rheumatic heart disease (post inflammatory scarring)

38
Q

Acquired aortic stenosis

A
  • most common valvular disorders
  • age related wear-and-tear of normal or bicuspid valves
  • may have relation to atherosclerosis but differs in morphology with valves having osteoblastic cells that synthesize bone matrix proteins and deposit calcium salts
39
Q

Morphology of acquired aortic stenosis

A
  • heaped up calcific masses protruding through outflow tracts into the sinuses of Valsalva, preventing valve opening
  • usually does not involve the free edges of the valve cusps
  • unlike rheumatic and congenital causes, no commissural fusion is seen
  • unlike rheumatic disease, mitral valve is usually normal
  • eventually associated with LV hypertrophy, ischemic damage, and heart failure
40
Q

What is the most frequent cardiovascular anomaly in humans and what is its prevalence?

A
  • bicuspid aortic valve

- 1% prevalence

41
Q

What is the morphology of a bicuspid aortic valve?

A
  • two cusps, usually of unequal size, with the larger cusp having a midline raphe
  • raphe is a major site for calcific deposits
  • mitral valve usually normal in these patients
42
Q

Mitral annular calcification

A
  • calcific deposits around the annulus, most common in elderly women
  • usually does not affect valve function but may rarely lead to regurg or stenosis
43
Q

Mitral valve prolapse

A
  • ballooning of the mitral leaflets, which are enlarged, redundant, thickened and rubbery
  • attenuation of the collagenous fibrosa layer with thickening of the spongiosa and deposition of mucoid (myxomatous) material
  • secondary changes include fibrous thickening of the valve leaflets where the contact, linear thickening of the LV endocardium where the valves contact it, thrombi and calcifications
44
Q

Causes of mitral valve prolapse

A
  • unknown in most

- Marfan syndrome

45
Q

Clinical features of MVP

A
  • most asymptomatic
  • mid-systolic click
  • complications include: infective endocarditis, mitral regurg, stroke or infarct from embolism of leaflet thrombi, arrhythmia
46
Q

What is an Aschoff body?

A
  • cardiac lesion in acute rheumatic fever
  • T cells, plasma cells and Anitschkow cells (activated macrophages)
  • may be present in any layer of the heart (endocardium, myocardium, pericardium = pancarditis)
47
Q

What acute valvular lesion occurs in rheumatic fever?

A

-small verrucous deposits along lines of closure, overlying necrotic foci in valves

48
Q

What are MacCallum plaques?

A

-subendocardial plaques, most often in left atrium, seen in rheumatic fever caused by regurgitant jets

49
Q

Mitral valve changes in chronic rheumatic heart disease?

A
  • leaflet thickening
  • commissural fusion and shortening
  • thickening and fusion of tendinous cords
  • mitral valve always involved, with aortic valve in 25% of cases, and occasional involvement of tricuspid and pulmonic valves
50
Q

What is the pathogenesis of rheumatic fever?

A
  • antibodies against the M protein of group A strep cross-reacts with cardiac proteins
  • T cells specific for M protein also react with self-proteins in the heart
  • therefore, a combination of antibody and cell-mediated immunity
51
Q

5 major manifestations of rheumatic fever?

A
  • sydenham chorea
  • erythema marginatum
  • pancarditis
  • migratory polyarthritis
  • subcutaneous nodules
52
Q

Major organisms responsible for endocarditis

A
  • Strep viridans
  • Staph aureus (especially IVDU)
  • enterococci
  • HACEK
  • Staph epidermidis (most often in prosthetic valves)
53
Q

Clinical features in infective endocarditis

A
  • fever
  • murmur
  • splinter hemorrhages
  • Janeway lesions (erythematous non-tender, palms and soles)
  • Osler nodes (subcutaneous in pulp of digits)
  • Roth spots (retinal hemorrhages)
54
Q

What are the Duke criteria?

A
  • criteria for diagnosing infective endocarditis

- clinical and pathologic criteria

55
Q

Nonbacterial thrombotic endocarditis

A
  • small sterile vegetations along lines of closure
  • non-infective/invasive, but may embolize
  • often in debilitated patients (cancer, sepsis, aka marantic endocarditis), and may be associated with DVT, PE, etc
  • may be associated with endocardial trauma
56
Q

What part of the heart is most often involved by carcinoid heart disease?

A

-right heart valves and endocardium

57
Q

What are the gross features of carcinoid heart disease?

A
  • plaque like fibrous thickening in right heart

- microscopically, smooth muscle, collagen and mucopolysaccharides

58
Q

Most common clinical manifestation of carcinoid heart disease?

A

Tricuspid insufficiency>Pulmonic insufficiency

59
Q

Complications of artificial valves

A
  • thromboembolic complications (main problem with mechanical valves)
  • infective endocarditis
  • structural deterioration (bioprosthetics»mechanical)
60
Q

What is the fundamental dysfunction in each type of cardiomyopathy

A

Dilated: contractile dysfunction

Restrictive and hypertrophic: diastolic dysfunction

61
Q

Pathologic features of hypertrophic cardiomyopathy

A
  • disproportionate septal hypertrophy (free wall:septum=1:3) with septal thickening most prominent in the subaortic region
  • banana shaped ventricle
  • endocardial thickening/mural plaque formation of outflow tract with anterior mitral valve leaflet thickening
62
Q

Histologic features of hypertrophic cardiomyopathy

A
  • myocyte disarray
  • increased myocyte diameter (40 microns)
  • interstitial fibrosis
63
Q

Genetic defects in hypertrophic cardiomyopathy

A
  • genes encoding sarcomeric proteins

- most commonly autosomal dominant with variable penetrance

64
Q

Causes of restrictive cardiomyopathy

A
  • idiopathic
  • radiation fibrosis
  • amyloidosis
  • sarcoidosis
  • metastatic tumors
  • inborn errors of metabolism with metabolite accumulation
65
Q

Gross features of restrictive cardiomyopathy

A
  • normal ventricular size and thickness

- often biatrial dilatation

66
Q

Etiologies of myocarditis

A
  • viral (most common, coxsackie and enterovirus)
  • parasitic (chagas disease, toxo)
  • bacteria (diphtheria)
  • hypersensitivity (e.g. to drug)
  • connective tissue disease (e.g. lupus)
  • sarcoid
  • poststrep

basically: infectious, immune, other

67
Q

Most common chemotherapeutic drugs to the heart

A

-doxorubicin and danorubicin (anthracyclines): often lead to dilated cardiomyopathy; dose dependent

68
Q

Cardiac effects of iron overload

A
  • systolic dysfunction, possibly due to ROS generation
  • perinuclear deposition of iron
  • rust brown heart resembling dilated cardiomyopathY
69
Q

Cardiac effects of thyroid disease

A

Hyperthyroidism: nonspecific hypertrophy with ischemic foci

Hypothyroidism (myxedema heart): flabby, dilated heart with interstitial mucopolysaccharides

70
Q

Three categories of causes of pericarditis

A

Infectious
Immune-mediated
Other

71
Q

Causes of serous pericarditis

A
  • usually non-infectious immune mediated
  • lupus
  • scleroderma
  • tumors
  • uremia
72
Q

Causes of fibrinous pericarditis

A
  • post MI
  • lupus
  • radiation
  • trauma
  • uremia
  • rheumatic fever
73
Q

Most common cardiac tumors

A
  • myxoma
  • fibroma
  • lipoma
  • papillary fibroelastoma
  • rhabdomyoma
  • angiosarcoma
  • other sarcomas
74
Q

Chromosomal abnormalities in cardiac myxoma

A

-abnormalities of chr 12 or 17

75
Q

Clinical manifestation of cardiac myxomas

A
  • obstruction
  • embolization
  • generalized fatigue, malaise due to elaboration of cytokines by the tumor
76
Q

Carney complex

A
  • autosomal dominant mutation of PRKAR1, chr 17 (acts as a tumor suppressor)
  • cardiac and cutaneous myxomas
  • pigmented skin lesions
  • endocrine hyperactivity
77
Q

What is graft arteriopathy?

A
  • diffuse stenosing intimal proliferation of coronary arteries in cardiac transplants
  • major cause of graft failure
  • may be related to low-level chronic rejection
  • may result in silent MI because the transplanted heart is denervated

Robbins systemic pathology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions