9. Heart 2 Flashcards

1
Q

Arrhythmia from atrium = supraventricular

What is choatic depolarization without functional ventricular contraction?

A

Ventricular fibirillation

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2
Q

What is the most common cause of arrhythmias?

A

Ischemic injury

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3
Q

What occurs when the SA node is damaged leading to bradycardia?

A

Sick sinus syndrome

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4
Q

What occurs when myocytes depolarize independently and sporadically (atrial dilation) with variable transmission through AV node w/ irregular irregular HR?

A

Atrial fibrillation

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5
Q

When the AV node is dysfunctional, it is known as heart block
First degree: prolonged PR interval
Second degree:
Third degree: ?

A

Second: intermittent transmission

Third Degree heart block: complete failure

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6
Q

The following can be due to what?

Ischemic heart dz, dilated cardiomyopathy, myocyte hypertrophy, inflammation (myocarditis) and amyloid…

A

Gap junction abnormalities

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7
Q

Most hereditary heart conditions are autosomal dominant. What are mutations in genes that are required for normal ion channel function? (sometimes assoc w skeletal muscle DOs and diabetes)

A

Channelopathies

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8
Q

What is the most common arrythmogenic syndrome manifests as arryhthmias associated with excessive prolongation of the cardiac repolarization, presenting with stress induced syncope, SCD, assoc w swimming?

A

Long QT syndrome

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9
Q

What syndrome presents with patients having arrhythmias associated with abbreviated repolarization intervals, have palpitations, syncope and SCD?

A

Short QT syndrome

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10
Q

What syndrome manifests as ECG abnormalities (St segment elevations and right bundle branch block) in the absence of a heart DO?

A

Brugada Syndrome

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11
Q

Sudden cardiac death SCD is unexpected deeath from cardiac cause, either without symtpoms or within 1-24 hours of symptom onset. 80-90% of successively resuscitated patients have no?

A

lab or ECG changes

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12
Q

What is the most common underlying etiology, causing 80-90% of SCD?

A

Coronary artery disease CAD

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13
Q

Pt usually have >75% stenosis of 1+ of the coronary As, prior MIs are seen in 40% of the cases… WHat is the first manifestation of Ischemic heart dz? IHD

A

SCD

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14
Q

SCD is typically due to what, which is most frequently a consequence of CAD/ ischemia induce myocardial irritability?

A

fatal arryhtmia/ ventricular fibrillation

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15
Q

Systemic left sided hypertensive heart disease (HHD) occurs when?

A

there is a pressure overload resulting in left ventricular hypertrophy (LVH)

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16
Q

In left sided HHD, the LV wall is concentrically (septum and wall same) thickened (>1.5cm, weight >500gm). The earliest morphologic change of system HHD is?

A

that myocytes show and increase tranverse diameter

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17
Q

What dysnfunction can result in left atrial enlargement leading to atrial fibirillation?

A

diastolic dysfunction

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18
Q

Systemic or left sided HHD may lead to CHF and is a risk factor for?

A

SCD

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19
Q

Pulmonary right sided HHD is isolated right sided HHD that arises in the setting of?

A

pulmonary hypertension

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20
Q

Acute cor pulmonale may arise from a large pulmonary embolus, what can be seen in the heart in this case?

A

marked dilation of RV without hypertrophy (if chronic cor pulomonale will have hypetrophy)

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21
Q

What is the most common cause of pulmonary hypertension?

A

Left sided heart disease

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22
Q

What are two ways one can tell the difference grossly between left sided and right sided hypertensive heart disease?

A

Right sided wall thickened and will be the new apex of the heart in some cases
Left sided wall thickened concentrically

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23
Q

PAthologic changes of cadiac valves are largely of 3 types…
1) damage to collagen weakens leaflets (MVP)
2) Nodular calcification beginning in interstitial cells (calcific aortic stenosis)
3)

A

Fibrotic thickening as seen in rheumatic heart dz (mitral stenosis)

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24
Q

Because cardiac valves are thin enough to be nourished by diffusion from the blood, normal leaflets and cusps have only scant blood vessels limited to?

A

the proximal portion of the valve

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25
Q

When does valvular disease come to clinical attention? 2

A

due to stenosis and insufficiency/ regurgiation / incompetence

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26
Q

What is used to describe the incompetence of a valve stemming from an abnormality in one of its support structures as opposed to a primary valve defect?

A

function (mitral valve) regurgitation

*common in IHD and dilated cardiomyopathy

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27
Q

Stenosis is when a valve doesnt open completely occuring chronically, impeding forward flow, sometimes resulting in?

A

pressure overload hypertrophy (CHF)

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28
Q

Insufficiency is when a valve doesnt close completely, occuring acutely and chronically, allowing reversed flow or regurgitation, chornically causing?

A

volume overload hypertrophy and CHF

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29
Q

What is the only cause of mitral stenosis?

A

Posinflammatory scarring due to rheumatic heart disease***

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30
Q

What are two causes of aortic valve disease?

A

postinflammatory scarring d/t rheumatic heart dz

Calcification of congenitally deformed valve

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31
Q

What are two causes of aortic regurgitation?

A

Rheumatic heart dz

Aortic insufficiency: dilation of the ascending aorta secondary to HTN/aging

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32
Q

Syphilitic aortitis and marfan syndrome cause what valvle disease?

A

Aortic valve disease

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33
Q

Abnormalities of tensor apparatus and of the left ventricle and or annulus can lead to?

A

mitral valve disease

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34
Q

What are the two MCC of mitral regurgitation?

A

Abnormalities of leaflets and commissures

Mitral valve prolapse (myxomatous degen)

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35
Q

Calcific aortic stenosis is the most common of all valvular problems whose prevalence increases with age (60-80) and is caused by wear and tear associated with what? 3

A

chronic HTN
hyperlipidemia
inflammation

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36
Q

Calcific aortic stenosis has a HUGE association with what, which shows an accelerated course due to mechanical stress?

A

Bicuspid arotic valve (BAV)

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37
Q

If someone has a bicuspid aortic valve, there will be clinical sx 1-2 decades earlier.. Affected valves contain osteoblast like cells which deposit?

A

an osteoid-like substance and ossifies

**no commisural fusion (as seen in rheumatic and congential aortic stenosis)

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38
Q

Calcific aortic stenosis has mounded calcification in cusps which prevent complete opening of the valve. What are 3 common sx?

A

angina CHF and syncope

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39
Q

LVH develops due to increase pressure of the valve not opening, most pts die in 5 years of devloping angina, in 3 of developing syncope and 2 in developing?

A

CHF

*tx with surgical replacement

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40
Q

Biscuspid valves are prone to calcification. Patients can remain asymptomatic until stenosis reaches a critical point when?

A

CHF ensues.

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41
Q

In mitral annular calcification calcific deposits occurs in the?

A

fibrous annulus-at the base of the leaflets

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42
Q

annular calcification normally does not affect valve function however there are expections including regurg, stenosis and?

A

**arrhythmias and occasionally sudden death by penetration of calcium deposits to a depth sufficient to impinge on the atrioventricular conduction system

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43
Q

patients with mitral annular calcification are at an increased risk for thrombus formation or infective endocarditis.. Where is this most commonly seen? 3

A

Females more than Males
greater than 60 y/o
WITH mitral valve prolapse

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44
Q

Myxomatous degeneration of the mitral valve, OR mitral valve prolapse MVP is where the valve leaflets prolapse BACK into the left atrium during systole. Affects 2-3% of adults affecting M/F more? and what type of murmur?

A

7Females to 1 Male

*mid systolic click

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45
Q

Marfan syndrome (FBN1) causes loss of CT support in the MV leaflets making them floppy. The leaflets in MVP become thickened and rubbery due to?

A

proteoglycan deposits (myxomatous degeneration) in spongiosa layer and elastic fiber disruption

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46
Q

What is the characteristic anatomic change in MVP?

A

interchordal ballooning of the leaflets

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47
Q

Most MVPs are asymptomatic but a minority may experience what two sx?

A

chest pain mimicking angina

dyspnea

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48
Q

MVP has rare complications including infective endocarditis, mitral insufficiency, thromboembolism and?

A

arrhythmias=SCD

*tx with valve replacement

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49
Q

Rheumatic fever is a multisystem inflammatory disorder following pharyngeal infection with?

A

group A streptococcus

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50
Q

Incidence of rheumatic fever has decreased with more rapid dx and tx of strep. Acute rheumatic fever may include carditis component and overtime may evolve into?

A

chronic rheumatic heart disease

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51
Q

The pathogenesis of rheumatic fever include immune response to streptococcall M proteins that cross react with?

A

cardiac self antigens (among others)

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52
Q

Acute RF occurs 10 day to 6 weeks after group a strep infection and can be determined by what two titers?

A

Anti-streptolysin O

Anti-DNAse B

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53
Q

acute RF symptoms include pancarditis, migratory polyarthritis, subcutaneous nodules and erythema marginatum (rash). It also involves a neuro DO with involuntary rapid purposeless movements known as?

A

Sydenham chorea

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54
Q

Cardiac features of RF include pancarditis (inflamm of entire heart) with Aschoff bodies contain T cells, plasma cells and plump activated macrophages known as?

A

Anitschkow cells ***** pathognomonic for RF

central wavy ribbon of chromatin- looks like catepillar

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55
Q

Inflammation and fibrinoid necrosis of endocardium on left sided valves seen with what?*

A

verrucae (vegetations) is seen in RF.

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56
Q

What causes mitral leaflet thickening, fusion of commissures with shortenin, fusion and thickening of cords?

A

Chronic Rhematic Heart disease

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57
Q

What is the ONLY cause of mitral stenosis?

A

chronic RHD

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58
Q

RHD causes left atrial enlargement leading to Afib and thromembolic events. It also causes right heart failure leading to?

A

right ventricular hypertrophy

*infective endocarditis as well

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59
Q

What is marked by a form of granulomatous inflammation “aschoff nodules’ centered around vessels?

A

acute rheumatic myocarditis

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60
Q

Where can one find maccallum plaques as seen in the heart in RHD?

A

Left atrium

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61
Q

Neovascularization is seen in RHD as well as what? which occurs due to calcification and fibrous bridging across the valvular commissures

A

Fish mouth or button hole stenosis

62
Q

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

A

Infective endocarditis (IE) (acute and subacute)

63
Q

What type of infectious endocarditis is a RAPIDLY progessing destructive infection of a previously normal valve?

A

ACUTE Infective endocarditis

*requries surgery and abx

64
Q

What type of infectious endocarditis is a slower-progressing infection of a previously DEFORMED valve (such as in chronic RHD)

A

SUBACTE infective endocarditis

*tx abx alone

65
Q

Predisposing conditions to IE including valvular abnormalities (RHD, prosthetic valves, MV prolapse) and bacteremia - including?4

A

***dental work/surgery
site infection
contaminated needle (IVDU)
Compromised epithelium

66
Q

Classic features of IE are friable, bulky, destructive valvular vegetations with what side valves being more common?

A

Left sided valves EXCEPT in IV drug users- right side more common

67
Q

The friability of the vegetations lead to septic emboli or what if they are on the right side valve?

A

pulmonary embolism

68
Q

The vegetations are mixtures of fibrin, inflammatory cells and organism, note subacte veges may have?

A

granulation tissue component

69
Q

Patients with IE present with fever weightloss fatigue and flu-like symptoms. What are the sx for acute endocarditis?

A

fever, chills, weakness, lassitude

70
Q

What organism affect previouslt damaged or abnormal valves *dental organisms?

A

Strep Viridans- subacute-not as bad

71
Q

What organism is highly virulent and seen in IV drug users and normal valves?

A

Staph Aureus ***acute-bad

72
Q

What organism is commonly infecting prothestic valves?

A

S. Epidermidis

73
Q
What is the significance of the following?
haemophilus
actinobacillus
cardiobacterium
kingella
eikenalla
A

HACEK organisms = commensal bacteria in the oral cavity

74
Q
What are the different forms of vegetative endocarditis (warty lesions) in the following?
Rheumatic Heart disease
Infective endocarditis
Nonbacterial thrombotic Endocarditis
Libman-Sacks disease
A

Rheumatic Heart disease: warty line along line of closure
Infective endocarditis: large and irregular masses on the valve cusps
Nonbacterial thrombotic Endocarditis: small, bland vegetations along line of clousre
Libman-Sacks disease: small/medium sized on either or BOTH sides of the valve leaflet

75
Q

What is present in 90% of patients with left sided infective endocarditis?

A

Heart murmur

76
Q

acute IE can cause mortality in less than 6 weeks (50%) and necrotizing ulcerative lesions. Its emboli can cause mycotic aneurysms and what is an outcome grossly?

A

RING ABSCESS : vegetation erode into underlying myocardium

77
Q

The duke criteria is used for dianosing infective endocarditis which include?

A

system of labs, clinical, echo and cultures that identify IE

78
Q

What are 4 COMMON important signs of infective endocarditis?

A
subungal splinter hemorrhages (d/t emobli)
janeway lesions (red lesions hands/feet)
osler nodes (subq painful nodules hands/feet)
roth spots (retinal hemorrhaging)
79
Q

What is characterized by small, STERILE thrombi on cardiac valve leaflets along the line of closure; loosely attached, not invasive, do NOT illicit inflam reaction?

A

nonbacterial thrombotic endocarditis (NBTE)

80
Q

NBTE may be a source of emboli (produces infarcts in brain/heart). What is the IMP* malignancy it is associated with? along with spesis or catheter induced endocardial trauma

A

MUCINOUS ADENOCARCINOMAS

81
Q

nonbacterial thrombotic endocarditis occurs on previously normal valves due to?

A

a hypercoaguable state

82
Q

Libman sacks endocarditis is due to SLE, mitral valve is more commonly involved causing regurgitation. The cause is due to antiphospholipid syndrome associated with lupus

A

Not on the test

83
Q

What is a systemic disorder marked by flushing, diarrhea, dermatitis and bronchoconstriction?

A

Carcinoid syndrome (eg caused by serotonin released from GI carcinoid tumor) - paraneoplastic syndrome!

84
Q

Severity of the cardiac carcinoid symdrome lesions correlate with plasma levels of serotonin and urinary excretion of the serotonin metabolite..?

A

5-hydroxindoleacetic acid

85
Q

What occurs when 50% of patients with carcinoid syndrome develop cardiac manifestations?

A

Carcinoid Heart disease

86
Q

Carcinoid heart disease does not occur until there is a massive hepatic burden or damage since the liver normally does what?

A

catabolizes circulating mediatiors before they effect the heart

87
Q

What heart valves are affects in carcinoid heart disease and why?

A

The right heart valves (and endocardium) since they are first in contact with the mediators, left side valves are protected due to pulmonary vascular bed degredation of mediators

88
Q

The valvular plaques seen are similar to those in patients taking fenfluramine (appetite suppresant) or ergot alkaloids for migraines - both affect systemic serotonin metabolism. Why serotonin?

A

it has not been proven why this occurs or if serotonin inhibitors can fix the problem

89
Q

carcinoid heart disease associated with carcinoid syndrome has intimal thickening (acid mucopolysaccharide-rich) and what other characteristic finding?

A

glistening white intimal plaque like thickenings of endocardial surfaces of the cardiac chambers and valve leaflet

90
Q

What are the two types of valvular prosthese to replace damaged cardiac valves?

A
mechanical valves (nonphysologic material)
tissue valves (porcine/bovine)
91
Q

60% of valve recipients have serious problems within 10 years. What is a specific complication to mechanical valves?

A

thromboembolism due to the disruption of laminar flow (long time anticoags)

92
Q

What is a specific complication to tissue valve replacements?

A

structural deterioration which is the most common for bioprosthetic valves (calcification and tear)

93
Q

Cardiomyopathy means heart muscle disease. What are the three types of cardiomyopathies?

A

Dilated (MC-90%)
Hypertrophic
Restrictive

94
Q

What is charcterized by progression cardiac dilation and systolic dysfunction, usually with dilated hypertrophy?

A

Dilated Cardiomyopathy DCM - most common

95
Q

DCM is thought to be familial in 30-50% of cases (TTN titin mutations may account for 20%- AD). What is strongly linked to DCM? 2

A

Alcohol

Myocarditis (esp. prior evidence of Coxsackie B Virus)

96
Q

Cardiotoxic drugs and substances are also known to cause DCM including doxorubicin (chemo), cobalt, and iron overload. How does iron do this?

A

Iron overload from hereditary hemochromatosis (HFE mutation) or multiple transfusions

97
Q

What stain is used to see iron in heart cells?

A

Prussian blue iron stain

98
Q

DCM causes a large, heavy flabby heart due to dilation of all four chambers, What is common? 2

A

**mural thrombi and embolism = stroke

Also, functional regurgitation of valves

99
Q

DCM usually manifests between ages 20-50yo causing progressive CHF with what sx? 3

A

dyspnea
exertional fatigue
dec. ejection fraction by 25%(end stage)

100
Q

What are two important consequences/ outcomes of dialted cardiomyopathy? 2

A

arrhythmias (sudden death)

embolism

101
Q

Another type of dilated cardiomyopathy which is caused by excess catecholamines from extreme emotional or physiological stress?

A

Takotsubo cardiomyopathy OR

broken heart syndrome

102
Q

Broken heart syndrome occurs in mainly women aged 58-75. Symptoms are like acut myocardial infarction. What can be seen grossly?

A

apical ballooning of the left ventricle with abnormal wall motion and contractile dysfunction (octopus trap like)

103
Q

Histologically in DCM, there is hypertrophied muscle cells with nelard nuclei but some are stretched and attenuated, along with a variable degree of?

A

interstitial and endocardial fibrosis

104
Q

What is the main difference between start and end point of DCM and HCM?

A

DCM only has 20-50% genetic causes (TITIN) while HCM is caused 100% by genetic mutations in sarcomere patients. Also in HCM, you will see myofiber disarray.

105
Q

What is an inherited disease of myocardium causing right ventricular failure and rhythym distrubances (ventricular tachycardia/ fibrillation) with SUDDEN DEATH?

A

arrhythmogenic right ventricular cardiomyopathy ARVC

106
Q

in ARVC, myocardium of the right ventricular wall is replaced by adipose and fibrosis no muscle left. How do you get this disease?

A

familial, autosomal dominant - defective cell adhesion proteins in the desmosomes that link adjacent cardiac myocytes

107
Q

What syndrome is ARVC with hyperkeratosis of plantar and palmar skin surfaces?

A

Naxos Syndrome

108
Q

Naxos syndromes is specifically associated with mutations in the gene encoding the desmosome-associated protein ______?

A

plakoglobin

109
Q

What is a genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to dec. stroke volume and often ventricular outflow obstruction?

A

Hypertrophic cardiomyopathy HCM

110
Q

There are numerous mutations known involving sarcomeric proteins, the most common one is?

A

B-MHC : b-myosin heavy chain

111
Q

HCM presents with massive myocardial hypertrophy often with marked septal hypertrophy, without dilation. What is important of this hypertrophy?

A

it is not concentric, instead eccentric asymetric septal hypertrophy (ventricular septum more thick than ventricular wall)

112
Q

Microscopically, HCM shows myocyte/fiber disarray (haphazard disarray). What else can be seen?

A

interstitial and replacement fibrosis and fibrous endocardial plaques

113
Q

What is said about the lumen in HCM, which is due to disproportionate septal and wall thickening without ventricular dilation?

A

Banana Lumen

114
Q

What symptom of HCM is caused by the ventricular outflow obstruction as the anterior mitral leaflet moves toward the ventricular septum during systole?

A

HARSH systolic ejection murmur

hypertrophied ventricular septum BLOCKs aorta

115
Q

Consequences of HCM include foci of myocardial ischemia, dec CO and inc pulomnary congestion leading to exertional dyspnea, arrhythmias and what other two important things?

A
SUDDEN DEATH (MC cause of sudden unexplained death in athletes)
left atrial dilation & mural thrombus
116
Q

What is caused by decreased ventricular compliance (inc stiffness), leading to diastolic dysfunction (impaired filling), while systolic function of the LV remains normal?

A

Restrictive Cardiomyopathy

117
Q

Restrictive Cardiomyopathy may be secondary to deposition of material within the wall or increased fibrosis, each due to? 2

A

amyloid (deposition in wall)

radiation (increase fibrosis)

118
Q

Restrictive Cardiomyopathy has patchy diffuse interstitial fibrosis and has normal sized ventricles but?

A

both atria can be enlarged

119
Q

What is extracellular deposition of proteins which form an insoluble B pleated sheet, sometimes systemic (myeloma) or restricted to the heart (transthyretin)?

A

Amyloid

120
Q

Certain mutations of transthyretin are more amyloidogenic, and it can involve different parts of the heart but when deposits are in the interstitium of the myocardium….?

A

resctrictive cardiomyopathy occurs

121
Q

Amyloid can be seen in myocardial interstitium using what stain and light?

A

congo red stain and using polarized light which shows the amyloid as apple green color

122
Q

Myocarditis is inflammation of the myocardium most commonly due to a virus in the US. Whats the most common virus?

A

Coxsackie A and B viruses

note viral=lymphocytes/bacterial=neutrophil

123
Q

What disease causes 10% to die during acute attacks, progressing to cardiac insufficiency in 10-20yrs, and causing myocarditis?

A

Trypanosoma Cruzi (chagas dz)

124
Q

Chagas can be seen with mixed inflammatory cell infiltrate (PMN, lymps, mø, and eosinophils), what can be seen in the myofibers?

A

parasitization of scattered myofibers (amastigotes to trypomastigotes in the heart muscle)

125
Q

Some noninfectious causes of myocarditis include immune mediated reactions like RH, drug hypersensitivity and?

A

SLE

126
Q

Active myocarditis is characterized by interstitial inflammatory infiltrate with focal myocyte necrosis, commonly lymphocytic. What can be seen histologically in hypersensitivity myocarditis?

A

interstitial infiltrates, principally perivascular composed of lymphocytes mø and eosinophils

127
Q

What type of myocarditis is characterized by widespread inflammatory cellular infilitrate containing multinucleate giant cells with lympocytes, eosinophils, mø and plasma cells?

A

Giant cell myocarditis

128
Q

Normal pericardial fluid is less than 50mL of clear, yellow colored fluid. Slow accumulation of fluid will allow how much and still be asymptomatic?

A

less than 500mL if slow enough = no sx

*globular enlargement of heart on CXR

129
Q

Acute accumulation of 200-300mL rapidly fast is clinically devastating and can cause?

A

Cardiac tamponade (pericardial effusion)

130
Q

What are the two most common types of pericarditis?

A

fibrinous and serofibrinous

131
Q

Both sero and fibrinous pericarditis can be due to AMI, post infarction (dresslers), chest irradiation, RF, SLE, trauma and most importantly?

A

UREMIA

132
Q

Serofibrinous pericarditis is a yellow-brown turbid fluid (chunky) with WBC, RBC and fibrin while fibrinous pericarditis is?

A

dry, finely granular/rough

133
Q

Some sx of sero/fibrinous pericarditis includ pain (sharp, pleuritic and position dependent), fever, +/- CHF. what is the MOST COMMON feature seen?

A

** LOUD pericardial friction rub **

134
Q

What pericarditis is characteristically produced by noninfectious inflammatory diseases including rheumatic fever, SLE, sleroderma, tumors and uremia?

A

Serous pericarditis

135
Q

What pericarditis is an active infection caused by microbial invasion of the pericadial space (direct extension, seeding from the blood, lympathic extension, direct introduction)?

A

Purulent or suppurative pericarditis

136
Q

What pericarditis has an exudate composed of blood mixed with a fibrinous or suppurative effusion?

A

Hemorrhagic pericarditis

MC d/t spread of malignant neoplasm

137
Q

What pericarditis is tuberculous in origin and infrequently fungal infections evoke the same reaction?

A

Caseous pericarditis

138
Q

What pericarditis occurs when the heart is encased in a dense, fibrous or fibrocalcific scar that limits diastolic expansion and cardiac output, features that mimic a restrictive cardiomyopathy?

A

constrictive pericarditis (limits diastole relaxation)

139
Q

Primary cardiac tumors are rare, the top 5 most common are all benign. What are the two most important?

A

Myxoma

Angiosarcoma

140
Q

Metastatic tumors occur only in 5% of people. What is the most common primary, pedunculated (sessile (on stalk) ) tumor usually in the fossa ovalis (foramen ovale)?

A

Myxoma (left atrium MC)

141
Q

Familial syndromes associated with myxomas have activing mutations in the GNAS1 gene, encoding what?

A

subunit of G protein Gsa (associated with mccune albright syndrome)

142
Q

Myxomas range from a globular hard mass mottled with hemorrhade to soft, translucent, papillary, or villous lesion with a ?

A

gelatinous appearance ***UNIQUE

143
Q

Sx of myxomas include constitutional symptoms (fever malaise d/t IL6), embolization and?

A

Ball-valve obstruction

144
Q

Pedunculated form of myxoma can cause obstruction during systole of AV valve, which can do what ?

A

‘wrecking ball’ does damage to the leaflets

ausculation = tumor “plop”

145
Q

On histology, myxomas are composed of stellate or globular myxoma cells embedded with an abundant acid mucopolysacchride groud substance.. Whats the buzz work for histo?

A

Multinucleated myxoma cells / giant cells

146
Q

What cardiac tumor is usually incidental, sea-anemone-like lesions, most often identified at autopsy and 80% are located on valves?

A

Papillary fibroelastoma (look like laml excresecences)

147
Q

What is a tumor of the pediatric heart, 50% due to sporadic mutations and 50% associated with tuberous sclerosis (mut in TSC1 hamartin or TSC2 tuberin)?

A

Rhabdomyoma

148
Q

What is the only malignant endothelial neoplasm that primarily affects older adult hearts?

A

Angiosarcoma

149
Q

Cardiac transplants occur about 3000/yr, mostly due to dilated cardiomyopathy and ischemic heart disease. What is the major complication?

A

Allograft rejection (check via endomyocardial bx)

150
Q

Allograft arteriopathy is the most important long term limitation for cardiac transplant because there is late…?

A

progressive, diffusely stenosing intimal proliferation

151
Q

Allograft arteriopathy develops in 50% of people in 5 years, and virtually all patients in 10 years. This leads to what?

A

silent myocardial infarctions (because of the denervated transplanted heart (no angina) )

152
Q

Along with arteriopathy, what is common due to chronic T cell immunosupression?

A

EBV associated B cell lymphomas