Heart Pt 2 Flashcards
(103 cards)
1
Q
What is the most common cause of rhythm disorders?
A
ischemic injury
2
Q
What is sick sinus syndrome?
A
SA node damaged -> bradycardia
3
Q
What is atrial fibrillation?
A
irregular heart rate
- myocytes depolarize independently and sporadically (atrial dilation) with variable transmission thru AV node
4
Q
What is heart block?
A
DYSFUNCTIONAL AV NODE
5
Q
What is first degree heart block?
A
prolonged PR interval
6
Q
What is second degree heart block?
A
intermittent transmission
7
Q
What is third degree heart block?
A
complete failure
8
Q
What do abnormalities in gap junction or spatial relationship lead to?
A
- ischemic heart dz
- dilated cardiomyopathies
- myocyte hypertrophy
- inflammation
- amyloidosis
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
10
Q
What is the most common inherited arrhythmogenic disease listed?
A
Long QT syndrome
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)
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
13
Q
What is often the first manifestation of ischemic heart disease?
A
sudden cardiac death
14
Q
What causes sudden cardiac death?
A
a fatal arrhythmia most often arising from ischemia-induced myocardial irritability
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)
16
Q
What does diastolic dysfunction in left-sided hypertensive disease result in?
A
left atrial enlargement -> atrial fibrillation
17
Q
What can left-sided hypertensive disease lead to?
A
CHF, and can be a risk factor for sudden cardiac death
18
Q
What is right-sided (pulmonary) hypertensive disease?
A
isolated right-sided hypertensive disease arises in the setting of pulmonary HTN
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
20
Q
What is the most common cause of pulmonary HTN?
A
left-sided heart disease
21
Q
What are the three types of pathologic changes to heart valves?
A
- damage to collagen (MVP)
- nodular calcification (aortic stenosis)
- fibrotic thickening (Rheumatic heart disease)
22
Q
What does damage to collagen in valves lead to?
A
it weakens leaflets
23
Q
What does nodular calcification cause?
A
calcific aortic stenosis
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
25
When is functional mitral valve regurgitation clinically important?
IHD and dilated cardiomyopathy
26
What is stenosis?
valve doesn't OPEN completely
- impedes FORWARD flow
- chronic stenosis may cause PRESSURE* overload hypertrophy -> CHF
27
What is insufficiency?
valve doesn't CLOSE completely, may occur acutely or chronically
- allows REVERSE flow
- chronic insufficiency may cause VOLUME* overload hypertrophy -> CHF
28
What is the common cause of mitral stenosis?
postinflammatory scarring from Rheumatic heart disease
29
What are the common causes of aortic stenosis?
calcification of congenitally deformed valve
30
What is the common causes of mitral regurgitation?
mitral valve prolapse, abnormalities of leaflets and commissures
31
What are the common causes of aortic regurgitation?
aortic insufficiency, syphilitic aortitis, Marfan syndrome
32
What is calcific aortic stenosis? Which valve commonly affected?
wear and tear associated with chronic HTN, hyperlipidemia, inflammation
-Bicusped valve
33
When do you see mounded calcifications in valve cusps? What does it prevent? What are the symptoms?
calcific aortic stensosis
- prevents complete opening of the valve
- angina, CHF, or syncope
34
What is annular calcification?
calcific deposits occur in the fibrous annulus
| - irregular, stony, hard, occasionally ulcerated nodules at the base of the leaflets
35
What are the examples given of mitral annular calcification affecting valve function?
- arrhythmia (Ca+ deposits fuck up conductivity)
- regurgitation (fucks with valve ring contraction)
- stenosis (impairs opening of mitral leaflets)
36
What demographic is mitral annular calcification most commonly seen?
F>M, >60 years old, with MVP
37
What is mitral valve prolapse?
valve leaflets prolapse back into LA during systole "floppy valve"
38
How is MVP sound described?
Mid-systolic click***
39
What happens to the leaflets in MVP?
they become thickened and rubbery, due to proteoglycan deposits*** (myxomatous degeneration), and elastic fiber disruption
40
What is a characteristic anatomic change in MVP?
interchordal ballooning (hooding) of the mitral leaflets
41
What are the rare, but serious complications of MVP mentioned?
- infective endocarditis
- mitral insufficiency
- thromboembolism
- arrhythmias
42
What is Rheumatic fever (RF)?
inflammatory disorder following pharyngeal infections with Group A Strep***
- over time may evolve to chronic rheumatic heart disease
43
What is the pathogenesis of RF?
immune response to Strep M proteins cross react with cardiac self-Ags
44
When does acute RF occur?
10 days - 6 weeks after Group A strep infection
45
What Ab titers can be drawn for RF?
Anti-streptolysin O and anti-DNAse B
46
What are the symptoms of RF?
pancarditis (heart inflam), migratory polyarthritis (of large joints), subQ nodules, **erythema marginatum rash**, sydenham chorea (neurologic involuntary mvmnts)
47
What are the cardiac features seen in acute RF?
- pancarditis with aschoff bodies** (T-cells, plasma cells and activated macrophages called anitschkow cells)
48
When would you expect to see inflammation and fibrinoid necrosis of endocardium and left-sided valve vegetations (verrucae)
acute RF
49
What are the cardiac features of chronic RHD?
mitral leaflet thickening, fusion of commissures, with shortening/fusion/thickening of cords -> MITRAL STENOSIS**
- LA enlargement -> atrial fib
- RV hypertrophy
- infective endocarditis
50
What is virtually the only cause of mitral stenosis?
chronic RHD
51
What is infective endocarditis?
an infection of valves or endocardium, characterized by vegetations consisting of microbes and debris, associated with underlying tissue destruction
52
What is acute infective endocarditis?
a rapidly progressing destructive infection of a previously normal valve
- requires surgery and antibiotics
53
What is subacute infective endocarditis?
a slower-progressing infection of a previously deformed valves (such as chronic RHD)
- can often be cured with antibiotics alone
54
What are the predisposing conditions of infective endocarditis?
- valvular abnormalities (prosthetics valves, RHD)
| - bacteremia (DENTAL WORK**)
55
What is the classic feature of IE?
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
What are the symptoms of acute endocarditis?
fever, chills, weakness
| - murmurs usually present (90%) with left-sided lesions
57
What organisms are often involved in IE?
- ** S. viridans
- S. aureus
- S. epidermidis
58
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
Acute bacterial endocarditis
59
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
SUBacute bacterial endocarditis
60
What is the Duke Diagnostic criteria for IE?
need 2/3:
- blood cultures positive for organisms
- echocardiographic ID of valve-related/implant-related mass
- new valvular regurgitation
61
What are the minor criteria for IE?
- subungual (under nailbed) splinter hemorrhages
- janeway lesions
- Osler nodes (painful red lesions on hands/feet)
- roth spots (retinal hemorrhages)
62
What is nonbacterial thrombotic endocarditis?
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
What is carcinoid syndrome
systemic disorder marked by flushing, diarrhea, dermatitis, bronchoconstriction
- serotonin released by carcinoid tumors
64
What is carcinoid heart disease?
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
What are the five complications of cardiac valve prostheses mentioned?
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
What is the most common cardiomyopathy?
dilated cardiomyopathy
67
What causes dilated cardiomyopathy?
hemochromatosis**, genetic (30-50% of cases, TTN gene mutation), alcohol (STRONGLY linked), chronic anemia, sarcoidosis (swollen lungs/LNs)
68
What is the least common type of cardiomyopathy?
Restrictive cardiomyopathy
69
What cardiotoxic drugs were mentioned to be pathogenic in dilated cardiomyopathy?
doxorubicin, cobalt, iron overload from hereditary hemochromatosis (HFE mutation)
70
What chambers are affected in DCM?
ALL chambers
71
What is commonly seen in DCM?
- mural thrombi
| - functional regurgitation of valves
72
What is the presentation of DCM?
- manifests between ages 20-50 years old
- progressive CHF -> dyspnea, fatigue
- arrhythmias (sudden death)
- embolism
73
What is Takotsubo cardiomyopathy?
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
What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?
right ventricular failure/arrhythmias
- myocardium of the RV wall replaced by ADIPOSE** and FIBROSIS**
- familial, AD
75
What does ARVC cause?
ventricular tachycardia or fibrillation -> sudden death
76
What is Naxos syndrome
ARVC with hyperkeratosis of plantar palmar skin surfaces
77
What gene is associates with Naxos syndrome?
mutations in the gene encoding the desmosome-associated protein plakoglobin
78
What is hypertrophic cardiomyopathy?
genetic disorder leading to myocardial hypertrophy and diastolic function, leading to decrease in stroke volume and often ventricular outflow obstruction
79
What gene mutations associated with hypertrophic cardiomyopathy?
numerous mutations involving sarcomeric proteins
| - most commonly beta-myosin heavy chains (b-MHC)
80
What is the morphology of hypertrophic cardiomyopathy?
massive myocardial hypertrophy, often with marked septal hypertrophy
81
What can be seen histologically in hypertrophic cardiomyopathy?
myocyte disarray**
82
What are the symptoms of hypertrophic cardiomyopathy?
harsh systolic ejection murmur** caused by ventricular outflow obstruction as the anterior mitral leaflet moves toward the ventricular septum during systole
83
What are the consequences of extensive hypertrophy?
- left atrial dilation and mural thrombus
| - sudden death
84
What is restrictive cardiomyopathy?
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
What type of cardiomyopathy would you see ventricles of normal size, but both atria enlarged?
restrictive cardiomyopathy
86
What is amyloid restrictive cardiomyopathy?
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
What type of stain is used to test for amyloid restrictive cardiomyopathy?
Congro red stain
| - amyloid shows up as apple green birefringence
88
What is myocarditis?
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
What is the most common pericardial disease?
fibrinous and serofibrinous, slow accumulation of fluid
| - AMI, post-infarction (Dressler's pericarditis), uremia, chest irradiation
90
What are the symptoms of fibrinous and serofibrinous pericardial disease?
sharp, pleuritis pain
| *** loud pericardial friction rub** most striking feature
91
What is the most common cause of hemorrhagic pericarditis?
the spread of a malignant neoplasm to the pericardial space
92
What is the origin of caseous pericarditis?
Tuberculosis
93
What are the 5 primary cardiac tumors?
**myxoma**, fibroma, lipoma, papillary fibroelastoma, rhabdomyoma, **angiosarcoma**
94
What is a myxoma?
the most common primary cardiac tumor, pedunculated (elongated), usually in the region of fossa ovalis
95
What genes are mutates in myxoma?
GNAS1, PRKAR1A
96
What is the unique description of a myxoma?
globular hard mass, mottled with hemorrhage to soft, translucent, papillary or villous with gelatinous appearance
97
What are the symptoms of a myxoma?
"ball-valve" obstruction, embolization or constitutional sx (fever, malaise)
** tumor "plop" is hallmark **
98
What is the major mediator of acute-phase response seen with a myxoma?
IL6
99
What is the most frequent primary tumor of the pediatric heart?
rhabdomyoma
- 50% sporadic mutations
- 50% associated with tuberous sclerosis
100
What is an angiosarcoma?
malignant endothelial neoplasm that primarily affects older adults
101
What is the most important long term imitation of cardiac transplantation?
allograft arteriopathy
- late, progressive, diffusely stenosing intimal proliferation
- 50% develop in 5 years, virtually at pt develop within 10 years
102
What is the major complication of cardiac transplantation?
allograft rejection
| - monitor with routine endomyocardial biopsies
103
What causes Estein Barr virus associated with B-cell lymphoma in cardiac transplantation?
chronic T-cell immunosuppression
