Brainscape's Knowledge GenomeTM

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


See full index

CPR Exam 1 > Heart Pt 2 > Flashcards

Heart Pt 2 Flashcards

1
Q

What is the most common cause of rhythm disorders?

A

ischemic injury

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

What is sick sinus syndrome?

A

SA node damaged -> bradycardia

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

What is atrial fibrillation?

A

irregular heart rate

- myocytes depolarize independently and sporadically (atrial dilation) with variable transmission thru AV node

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

What is heart block?

A

DYSFUNCTIONAL AV NODE

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

What is first degree heart block?

A

prolonged PR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is second degree heart block?

A

intermittent transmission

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

What is third degree heart block?

A

complete failure

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

What do abnormalities in gap junction or spatial relationship lead to?

A
  • ischemic heart dz
  • dilated cardiomyopathies
  • myocyte hypertrophy
  • inflammation
  • amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a channelopathy?

A

mutations in genes required for normal ion channel function

- can be associated with skeletal muscle disorders and diabetes, but most commonly isolated to heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common inherited arrhythmogenic disease listed?

A

Long QT syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What genes are affected in Long QT syndrome?

A
  • KCNQ1 (K+ channel LOF)
  • KCNQ2 (K+ channel LOF)
  • SCN5A (Na+ channel GOF)
  • CAV3 (Na channel GOF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is sudden cardiac death?

A

unexpected death from cardiac cause, either without symptoms, or within 1-24 hours of symptom onset
- 80-90% of successively resuscitates pts show no lab or ECG changes

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

What is often the first manifestation of ischemic heart disease?

A

sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes sudden cardiac death?

A

a fatal arrhythmia most often arising from ischemia-induced myocardial irritability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is hypertensive heart disease?

A

a left-sided hypertensive disease
- pressure overload results in LV hypertrophy

NOTE: LV wall is concentrically thickened (septum and free wall same thickness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does diastolic dysfunction in left-sided hypertensive disease result in?

A

left atrial enlargement -> atrial fibrillation

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

What can left-sided hypertensive disease lead to?

A

CHF, and can be a risk factor for sudden cardiac death

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

What is right-sided (pulmonary) hypertensive disease?

A

isolated right-sided hypertensive disease arises in the setting of pulmonary HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What might arise from a large pulmonary embolus in right-sided heart disease?

A

acute cor pulmonale (right sided heart failure)

- marked dilation of RV without hypertrophy

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

What is the most common cause of pulmonary HTN?

A

left-sided heart disease

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

What are the three types of pathologic changes to heart valves?

A
  1. damage to collagen (MVP)
  2. nodular calcification (aortic stenosis)
  3. fibrotic thickening (Rheumatic heart disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does damage to collagen in valves lead to?

A

it weakens leaflets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does nodular calcification cause?

A

calcific aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is functional regurgitation?

A

described the incompetence of a valve stemming from an abnormality in one of it’s support structures, as opposed to a primary valve defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

When is functional mitral valve regurgitation clinically important?

A

IHD and dilated cardiomyopathy

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

What is stenosis?

A

valve doesn’t OPEN completely

  • impedes FORWARD flow
  • chronic stenosis may cause PRESSURE* overload hypertrophy -> CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is insufficiency?

A

valve doesn’t CLOSE completely, may occur acutely or chronically

  • allows REVERSE flow
  • chronic insufficiency may cause VOLUME* overload hypertrophy -> CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the common cause of mitral stenosis?

A

postinflammatory scarring from Rheumatic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the common causes of aortic stenosis?

A

calcification of congenitally deformed valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the common causes of mitral regurgitation?

A

mitral valve prolapse, abnormalities of leaflets and commissures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the common causes of aortic regurgitation?

A

aortic insufficiency, syphilitic aortitis, Marfan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is calcific aortic stenosis? Which valve commonly affected?

A

wear and tear associated with chronic HTN, hyperlipidemia, inflammation
-Bicusped valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When do you see mounded calcifications in valve cusps? What does it prevent? What are the symptoms?

A

calcific aortic stensosis

  • prevents complete opening of the valve
  • angina, CHF, or syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is annular calcification?

A

calcific deposits occur in the fibrous annulus

- irregular, stony, hard, occasionally ulcerated nodules at the base of the leaflets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the examples given of mitral annular calcification affecting valve function?

A
  • arrhythmia (Ca+ deposits fuck up conductivity)
  • regurgitation (fucks with valve ring contraction)
  • stenosis (impairs opening of mitral leaflets)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What demographic is mitral annular calcification most commonly seen?

A

F>M, >60 years old, with MVP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is mitral valve prolapse?

A

valve leaflets prolapse back into LA during systole “floppy valve”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is MVP sound described?

A

Mid-systolic click***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What happens to the leaflets in MVP?

A

they become thickened and rubbery, due to proteoglycan deposits*** (myxomatous degeneration), and elastic fiber disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is a characteristic anatomic change in MVP?

A

interchordal ballooning (hooding) of the mitral leaflets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the rare, but serious complications of MVP mentioned?

A
  • infective endocarditis
  • mitral insufficiency
  • thromboembolism
  • arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is Rheumatic fever (RF)?

A

inflammatory disorder following pharyngeal infections with Group A Strep***
- over time may evolve to chronic rheumatic heart disease

43
Q

What is the pathogenesis of RF?

A

immune response to Strep M proteins cross react with cardiac self-Ags

44
Q

When does acute RF occur?

A

10 days - 6 weeks after Group A strep infection

45
Q

What Ab titers can be drawn for RF?

A

Anti-streptolysin O and anti-DNAse B

46
Q

What are the symptoms of RF?

A

pancarditis (heart inflam), migratory polyarthritis (of large joints), subQ nodules, erythema marginatum rash, sydenham chorea (neurologic involuntary mvmnts)

47
Q

What are the cardiac features seen in acute RF?

A
  • pancarditis with aschoff bodies** (T-cells, plasma cells and activated macrophages called anitschkow cells)
48
Q

When would you expect to see inflammation and fibrinoid necrosis of endocardium and left-sided valve vegetations (verrucae)

A

acute RF

49
Q

What are the cardiac features of chronic RHD?

A

mitral leaflet thickening, fusion of commissures, with shortening/fusion/thickening of cords -> MITRAL STENOSIS**

  • LA enlargement -> atrial fib
  • RV hypertrophy
  • infective endocarditis
50
Q

What is virtually the only cause of mitral stenosis?

A

chronic RHD

51
Q

What is infective endocarditis?

A

an infection of valves or endocardium, characterized by vegetations consisting of microbes and debris, associated with underlying tissue destruction

52
Q

What is acute infective endocarditis?

A

a rapidly progressing destructive infection of a previously normal valve
- requires surgery and antibiotics

53
Q

What is subacute infective endocarditis?

A

a slower-progressing infection of a previously deformed valves (such as chronic RHD)
- can often be cured with antibiotics alone

54
Q

What are the predisposing conditions of infective endocarditis?

A
  • valvular abnormalities (prosthetics valves, RHD)

- bacteremia (DENTAL WORK**)

55
Q

What is the classic feature of IE?

A

friable, bulky, destructive valvular vegetations (can lead to septic emboli)

  • left-sided valves more commonly affected
  • right-sided valves often involved in IV DRUG ABUSERS**
56
Q

What are the symptoms of acute endocarditis?

A

fever, chills, weakness

- murmurs usually present (90%) with left-sided lesions

57
Q

What organisms are often involved in IE?

A
  • ** S. viridans
  • S. aureus
  • S. epidermidis
58
Q

Which type of endocarditis?

  • <6 weeks with 50% mortality
  • normal valves
  • highly virulent organisms
  • rapid onset of sx
  • necrotizing, ulcerative destructive lesions
  • requires surgery
  • right heart valves if IV drug user
A

Acute bacterial endocarditis

59
Q

Which type of endocarditis?

  • > 6 weeks, most survive with tx
  • less virulent orgs, insidious
  • ABnormal valves
  • less destructive lesions
  • clacification, chronic inflamm cells
  • vague flu-like sx
  • resolved with antibiotics
A

SUBacute bacterial endocarditis

60
Q

What is the Duke Diagnostic criteria for IE?

A

need 2/3:

  • blood cultures positive for organisms
  • echocardiographic ID of valve-related/implant-related mass
  • new valvular regurgitation
61
Q

What are the minor criteria for IE?

A
  • subungual (under nailbed) splinter hemorrhages
  • janeway lesions
  • Osler nodes (painful red lesions on hands/feet)
  • roth spots (retinal hemorrhages)
62
Q

What is nonbacterial thrombotic endocarditis?

A

small, sterile thrombi on cardiac valve leaflets, along the line of closure

  • loosely attached, NOT invasive, do NOT illicit inflammatory rxn
  • may be a source of emboli
  • associated with malignancies (esp MUCINOUS ADENOCARCINOMAS)
63
Q

What is carcinoid syndrome

A

systemic disorder marked by flushing, diarrhea, dermatitis, bronchoconstriction
- serotonin released by carcinoid tumors

64
Q

What is carcinoid heart disease?

A

50% of pts with carcinoid syndrome develop cardiac symptoms

- affects right endocardium and valves (left side protected due to pulmonary vascular bed degradation of mediators)

65
Q

What are the five complications of cardiac valve prostheses mentioned?

A
  1. thrombosis/thromboembolism
  2. anticoagulant-related hemorrhage
  3. prosthetic valve endocarditis
  4. structural deterioration (ball valve failure)
  5. inadequate healing (leak)/too much healing (obstruction)
66
Q

What is the most common cardiomyopathy?

A

dilated cardiomyopathy

67
Q

What causes dilated cardiomyopathy?

A

hemochromatosis**, genetic (30-50% of cases, TTN gene mutation), alcohol (STRONGLY linked), chronic anemia, sarcoidosis (swollen lungs/LNs)

68
Q

What is the least common type of cardiomyopathy?

A

Restrictive cardiomyopathy

69
Q

What cardiotoxic drugs were mentioned to be pathogenic in dilated cardiomyopathy?

A

doxorubicin, cobalt, iron overload from hereditary hemochromatosis (HFE mutation)

70
Q

What chambers are affected in DCM?

A

ALL chambers

71
Q

What is commonly seen in DCM?

A
  • mural thrombi

- functional regurgitation of valves

72
Q

What is the presentation of DCM?

A
  • manifests between ages 20-50 years old
  • progressive CHF -> dyspnea, fatigue
  • arrhythmias (sudden death)
  • embolism
73
Q

What is Takotsubo cardiomyopathy?

A

a type of DCM, “Broken Heart syndrome”

  • excess catecholamines following extreme emotional/ psychological stress
  • 90% women, ages 58-75
  • sx similar to acute MI
  • apical ballooning of LV
74
Q

What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

right ventricular failure/arrhythmias

  • myocardium of the RV wall replaced by ADIPOSE** and FIBROSIS**
  • familial, AD
75
Q

What does ARVC cause?

A

ventricular tachycardia or fibrillation -> sudden death

76
Q

What is Naxos syndrome

A

ARVC with hyperkeratosis of plantar palmar skin surfaces

77
Q

What gene is associates with Naxos syndrome?

A

mutations in the gene encoding the desmosome-associated protein plakoglobin

78
Q

What is hypertrophic cardiomyopathy?

A

genetic disorder leading to myocardial hypertrophy and diastolic function, leading to decrease in stroke volume and often ventricular outflow obstruction

79
Q

What gene mutations associated with hypertrophic cardiomyopathy?

A

numerous mutations involving sarcomeric proteins

- most commonly beta-myosin heavy chains (b-MHC)

80
Q

What is the morphology of hypertrophic cardiomyopathy?

A

massive myocardial hypertrophy, often with marked septal hypertrophy

81
Q

What can be seen histologically in hypertrophic cardiomyopathy?

A

myocyte disarray**

82
Q

What are the symptoms of hypertrophic cardiomyopathy?

A

harsh systolic ejection murmur** caused by ventricular outflow obstruction as the anterior mitral leaflet moves toward the ventricular septum during systole

83
Q

What are the consequences of extensive hypertrophy?

A
  • left atrial dilation and mural thrombus

- sudden death

84
Q

What is restrictive cardiomyopathy?

A

decreased ventricular compliance, leading to diastolic dysfunction, which systolic function of LV remains normal
- may be secondary to deposition of material within the wall (amyloid), or increased fibrosis (radiation)

85
Q

What type of cardiomyopathy would you see ventricles of normal size, but both atria enlarged?

A

restrictive cardiomyopathy

86
Q

What is amyloid restrictive cardiomyopathy?

A

extracellular deposition of proteins which form an insoluble beta-pleated sheet
- may be systemic (myeloma) or restricted to heart (usually transthyretin gene - leads to deposits in the interstitium of myocardium)

87
Q

What type of stain is used to test for amyloid restrictive cardiomyopathy?

A

Congro red stain

- amyloid shows up as apple green birefringence

88
Q

What is myocarditis?

A

inflammation of the myocardiu, most commonly due to Coxsackie A & B viruses

  • can also be caused by Trypanosoma cruzi (Chagas dz)
  • or immune mediated reactions, including RF, SLE, drug hypersensitivity
89
Q

What is the most common pericardial disease?

A

fibrinous and serofibrinous, slow accumulation of fluid

- AMI, post-infarction (Dressler’s pericarditis), uremia, chest irradiation

90
Q

What are the symptoms of fibrinous and serofibrinous pericardial disease?

A

sharp, pleuritis pain

* loud pericardial friction rub most striking feature

91
Q

What is the most common cause of hemorrhagic pericarditis?

A

the spread of a malignant neoplasm to the pericardial space

92
Q

What is the origin of caseous pericarditis?

A

Tuberculosis

93
Q

What are the 5 primary cardiac tumors?

A

myxoma, fibroma, lipoma, papillary fibroelastoma, rhabdomyoma, angiosarcoma

94
Q

What is a myxoma?

A

the most common primary cardiac tumor, pedunculated (elongated), usually in the region of fossa ovalis

95
Q

What genes are mutates in myxoma?

A

GNAS1, PRKAR1A

96
Q

What is the unique description of a myxoma?

A

globular hard mass, mottled with hemorrhage to soft, translucent, papillary or villous with gelatinous appearance

97
Q

What are the symptoms of a myxoma?

A

“ball-valve” obstruction, embolization or constitutional sx (fever, malaise)
** tumor “plop” is hallmark **

98
Q

What is the major mediator of acute-phase response seen with a myxoma?

A

IL6

99
Q

What is the most frequent primary tumor of the pediatric heart?

A

rhabdomyoma

  • 50% sporadic mutations
  • 50% associated with tuberous sclerosis
100
Q

What is an angiosarcoma?

A

malignant endothelial neoplasm that primarily affects older adults

101
Q

What is the most important long term imitation of cardiac transplantation?

A

allograft arteriopathy

  • late, progressive, diffusely stenosing intimal proliferation
  • 50% develop in 5 years, virtually at pt develop within 10 years
102
Q

What is the major complication of cardiac transplantation?

A

allograft rejection

- monitor with routine endomyocardial biopsies

103
Q

What causes Estein Barr virus associated with B-cell lymphoma in cardiac transplantation?

A

chronic T-cell immunosuppression

CPR Exam 1 (18 decks)

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