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Year 2 CV > Exam 2, heart gomez > Flashcards

Exam 2, heart gomez Flashcards

1
Q

what causes foramen ovale to be a problem

A

when the R ventricular pressure overcomes the L

like in pulmonary HTN

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2
Q

a

A

a

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3
Q

what is unique about cardiac muscle cells

A

intercalated discs with gap junctions etc

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4
Q

what occurs in heart chambers with age

A

increased left atrial size
decreased ventricula size
sigmoid shaped venricular septum

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5
Q

what occurs in heart valves with age

A

aortic valve calcific deposits
mitral valve annular calcific deposits
fibrous thickening

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6
Q

what occurs to the epicardial coronary arteries in an aging heart

A

tortuosity

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7
Q

what happens to the myocardium in an aging heart

A 
decreased pass, brown atrophy
lipofuscin deposition (aging pigment)
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8
Q

what happens to the aorta with an aging heart

A

dilated ascending aorta

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9
Q

What are the five basic categories of cardiac disease

A 
congenital heart disease
HTN heart disease
ischemic heart disease
valvular heart disease
nonischemic primary myocardial disease
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10
Q

what is the cardiac reserve

A

the CO that is not used at rest

use 10-20% maximal output

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11
Q

What are the six general causes of cardiac dysfunction

A
  • pump failure
  • obstruction to blood flow through the heart
  • regurgitant flow
  • shunted flow
  • disorders of cardiac conduction
  • disruption of continuity of circulatory system
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12
Q

What are the six general causes of cardiac dysfunction

A
  • pump failure
  • obstruction to blood flow through the heart
  • regurgitant flow
  • shunted flow
  • disorders of cardiac conduction
  • disruption of continuity of circulatory system
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13
Q

what are examples of pump failure

A

primary myocardiopathy

ischmic cardiac disease

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14
Q

what are causes of obstruction blood flow through heart

A 
valvular disease (stenosis)
HTN disease
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15
Q

what is an example of regurgitant flow

A

valvular disease (insufficiency)

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16
Q

what is an example of shunted flow cardiac dysfunction

A

congenital heart disease (PDA ASD and VSD)

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17
Q

what are examples of disruption to continuity of circulatory system

A

gunshot, ventricular rupture

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18
Q

what are examples of disruption to continuity of circulatory system

A

gunshot, ventricular rupture

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19
Q

what can cause an increased workload resulting in hypertrophy

A

increased physiologic need by a normal heart
or
overall decreased intrinsic myocardial contractility

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20
Q

what is the difference of cardiac hypertrophy and cardio megaly

A

megaly is heart size and weight, hypertrophy is ventricular thickness or weight

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21
Q

what is the normal weight for male and femal hearts

A

male 300-500 female 250-300

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22
Q

what can cause a heart to weigh >800 gm

A

aortic regurgitation or hypertrophic cardiomyopathy

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23
Q

what can cause a heart to weigh >400

A

pulmonary HTN, IHD, systemic HTN aortic stenosis, mitral regug, dilated cardiomyopathy

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24
Q

what is the definition for cardiac dysfunction

A

inability to pump blood at a rate necessary for metabolizing tissues

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25
Q

What catecholamine is released in cardiac dysfunction

A

NE, neurohumoral stimulation, leads to more work for the heart. not good

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26
Q

What catecholamine is released in cardiac dysfunction

A

NE, neurohumoral stimulation, leads to more work for the heart. not good

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27
Q

What is the hearts response to pressure overload?

volume overload?

A 
pressure= concentric Hypertrophy
volume= eccentric
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28
Q

what are causes of concentric hypertrophy in each ventricle

A

L– systemic HTN or aortic stenosis

R– cor pulmonale

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29
Q

what can cause a volume overload that results in eccentric hypertrophy

A

valve disorders and congenital heart disease

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30
Q

What can lead to CHF

A

insufficient pump rate

pump can only meet demands with increase in filling pressure

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31
Q

What 2 type of dysfunction can lead to decreased CO (forward failure) leading to CHF

A

systolic dysfunction from progressive deterioration of myocardial contractility
diastolic dysfunction from inability of heart chambers to relax sufficiently to fill during diastole

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32
Q

describe fluid accumulation differences in left sided heart failure versus right

A

left leads to accumulation of fluid within the lungs and pleural cavities
right sided leads to accumulation of fluid in all other body sites and all body cavities

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33
Q

describe fluid accumulation differences in left sided heart failure versus right

A

left leads to accumulation of fluid within the lungs and pleural cavities
right sided leads to accumulation of fluid in all other body sites and all body cavities

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34
Q

L sided heart fialure is most commonly caused by

A

ischemic heart disease
HTN heart disease
aortic and mitral valvular disease
primary nonischemic myocardial disease (cardiomyopathy)

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35
Q

What are common physical findings in left-sided heart failure

A

cardiomegaly, hypertrophy, chamber dilation

secondary enlargement of left atrium

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36
Q

what can lead to left atrial enlargement

A

atrial fib

mural thrombus

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37
Q

What heart sound is heart with left sided heart failure

A

third heart sound S3 (gallop)
diastolic ventricular filling
mitral regurg will have systolic murmur

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38
Q

What occurs in lungs because of left sided heart failure

A

pulmonary congestion and edma that is heard as rales or crackles and possible effusions
flash pulmonary edema- extremely rapid onset
dyspnea, orthopnea, paroxysal nocturnal dyspnea

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39
Q

what occurs in kidney because of left sided heart failure

A

decreased CO leads to renal hypoperfusion
activates RAAS (fluid retention and expansion of vascular volume- a vicious cycle)
severe: prerenal azotemia

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40
Q

what occurs in brain because of left sided heart failure

A

hypoxic encephalopathy

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41
Q

when does right sided heart failure usually occur

A

consequence of left sided heart failure

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42
Q

what are examples of isolated right sided heart failure

A

cardiac hypertophy and dilation confined to right sides

sequela of severe pulm HTN

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43
Q

what are the systemic effects of right sided heart failure

A

pitting edema in subcut tissue
liver and portal system congestion and slpeen leadting to HSM
pleural and pericardial cavities (effusions)

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44
Q

what are the systemic effects of right sided heart failure

A

pitting edema in subcut tissue
liver and portal system congestion and slpeen leadting to HSM
pleural and pericardial cavities (effusions)

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45
Q

What is BNP

A

produced by ventricles from increased P used to determine CHF

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46
Q

what is C type natriutetic peptide

A

made by endothelial cells from shear stress

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47
Q

what is the effect of natriutetic peptides

A

vasodilation, natriuresis and diuresis

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48
Q

What level of BNP makes it unlikely to be CHF

A

<100 pg/ml

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49
Q

what other conditions can cause an increase in BNP

A

right filling P increase, primary pulm HTN, end stage renal failure, cirrhosis, hormone replacement therapy

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50
Q

what other conditions can cause an increase in BNP

A

right filling P increase, primary pulm HTN, end stage renal failure, cirrhosis, hormone replacement therapy

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51
Q

when do ehart defects occur in development

A

between 3 and 8 weeks gestational age

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52
Q

what are envrironmental factors that can cause congenital heart disease

A

congenital rubella infection

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53
Q

what are the genetic contributions to congenital heart disease

A

familial forms

trisomies 13 18 21 and turner syndrome

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54
Q

which trisomy has 40% associated with heart defects

A

21

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55
Q

What are the 3 most common congenital cardiac malformations

A

bicuspid aortic valve- 2% population!!!
ventricular septal defect
atrial septal defect

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56
Q

what is the most common cardiac anomaly first diagnosed in adulthood and more comman than VSD in adult population

A

ASD

commonly Dx with onset pulmonary HTN

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57
Q

which gene is associated with cardiav outflow tract defects

A

TBX1 del 22q11.2

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58
Q

what gene is mutated in marfan syndrome

A

fibrillin

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59
Q

what gene is mutated in marfan syndrome

A

fibrillin

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60
Q

What gene is affected in digeorge syndrome

A

TBX1 del 22q11.2

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61
Q

what are the Sx of Digeorge syndrome

A 
catch 22
cardiac
abnormal facies
thymic aplasia
cleft palate
hypocalcemia
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62
Q

what are the Sx of Digeorge syndrome

A 
catch 22
cardiac
abnormal facies
thymic aplasia
cleft palate
hypocalcemia
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63
Q

what are examples of left to right shunt

A

ASD, VSD, PDA, AVSD

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64
Q

Are babies cyanotic with left to right shunts?

A

not initally once the pulmonary HTN gets high enough (shunt reversal) there is a shift from right to left and causes cyanosis

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65
Q

Describe a ventricular septal defect

A 
pressures same in both ventricles
pressure ypertrophy in R ventricle
Volume hypertrophy in L 
90% involve membranous septum
sypmtpms depend on size of anomaly
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66
Q

Describe a ventricular septal defect

A 
pressures same in both ventricles
pressure ypertrophy in R ventricle
Volume hypertrophy in L 
90% involve membranous septum
sypmtpms depend on size of anomaly
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67
Q

What are the 3 major types of ASD

A

secundum, primum and sinus venosus

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68
Q

what is the msot common ASD

A

secundum, involving patent foramen ovalis

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69
Q

untreated ASD coyld lead to what

A

pulmonary HTN

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70
Q

untreated ASD coyld lead to what

A

pulmonary HTN

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71
Q

what causes ductus arteriosus to close

A

increase in O2
dec pulm vasc R
dec PGE2

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72
Q

describe findings of PDA

A

90% isolated defets
continous harsh machine-like murmur
chornic= pulm HTN and cyanosis

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73
Q

What is a complete artioventricular septal defect

AVSD

A

large combined AV septal defect and large common AV valve
all 4 chambers comunicating and 4 chamebr hypertrophy
1/3 have down syndrome

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74
Q

What is a complete artioventricular septal defect

AVSD

A

large combined

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75
Q

What is the main cardiac defect associated with downs syndrome

A

AVSD>VSD>ASD>PDA>tetralogy of Fallot

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76
Q

what type of shunts cause cyanosis

A

right to left shunts

decreased amount of blood going to lungs to be oxygenated

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77
Q

what are signs of right to left shunts

A

clubbing of tips of fingers and toes and polycythemia due to hypoxia
paradoxical embolism- emboli from periphery bypass lungs through cardiac defect and enter systemic circulation

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78
Q

what is the shape of the heart and why in tetralogy of fallot

A

embryologically anterosuperior displacement of infundibular septum so result is a boot shaped heart

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79
Q

what is the shape of the heart and why in tetralogy of fallot

A

embryologically anterosuperior displacement of infundibular septum so result is a boot shaped heart

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80
Q

the direction of shunting in tetralogy of fallot depends on what

A

severity of subpulmonic stenosis

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81
Q

What is pink tetralogy of fallot

A

when the subpulmonic stenosis is mild and so the lungs are perfused, behave slike VSD

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82
Q

what causes transposition of the great arteries

A

defect with truncal and aortapulmonary septae

separation of pulmonary and systemic circulations

83
Q

What makes transposition of great arteries somewhat compatibile with lfe

A

VSDm patent foramen ovale, or PDA

84
Q

what is the most important thing to do in a patient with transposition of great arteries and PDA

A

give PGE2 to keep PDA open until surgery because keeping them alive

85
Q

What is the infantile form of coarctation of aorta

A

hypoplasia of aorta prior to PDA (cyanosis of inferior body and weak femoral pulses)

86
Q

What is the adult form of coarctaion of aorta

A

ride like fold opposite ligamentum arteriosus (HTN upper extremities with low P and pulses in lower extremities)

87
Q

what are the types of congenital aortic stenosis or atresia

A

valvular- hypolastic dysplastic or abnormal # cusps
subaortic- ring or collar below cusps
aupravalvular- elastin gene mutation with aortic dysplasia (thickening)q

88
Q

What is williams beuren syndrome

A

deletion of 28 genes from chrom 7 with elastin causing haploinsufficiency, hyperCa, glucose intolerance, facial and cognitive defects
have supravalvular aortic stenosis

89
Q

coarcation of the aorta is mroe common in what pipulation

A

M:F 2:1 and more common in turners syndrome

90
Q

coarctaion of arota is associated with what valvular defect

A

bicuspid aortic valve

91
Q

what happends to the intercostal aa in coarctation of aorta

A

dilated

92
Q

what type of murmur is heard in adult coarctaion of aorta

A

pansystolic mrumur from renatl HTN and blood flow through collaterals

93
Q

What is the definition of cardiac ischmia

A

imbalance between the supply and demand of the hear for oxygenated blood

94
Q

90% of IHD is due to what

A

atherosclerotic coronary arterial obstruction

95
Q

What are common causes of IHD

A 
athersclerosis narrowing of coronaries
thrombosis from dirupted plaque
localized platelel aggregation
vasospams
emboli
hypotension
coronary artery vasculitis
96
Q

What are common causes of IHD

A 
athersclerosis narrowing of coronaries
thrombosis from dirupted plaque
localized platelel aggregation
vasospams
emboli
hypotension
coronary artery vasculitis
97
Q

what percent of fixed obstruction leads to Sx with exercise in IHD? what aobut lead to ischemia at rest?

A

with exercise >75%

at rest >90%

98
Q

What are the characteristics of unstable plaques

A

the ones with large cores and thin caps

99
Q

what are the acute plaque changes

A

rupture.fissuring
erosion/ulceration
hemorrhage into atheroma (plaque)

100
Q

where does acute plaqu change not usually occur

A

in severely stenoic portions of aa

101
Q

What aa to plaques tend to involve

A

proximal LAD and LCX

entire RCA

102
Q

what syndrome has an occlusive plaque-associated thormbus

A

transmural myocardial infarction

103
Q

plaque disruption is common in what coronary artery syndromes

A

unstavle angina and transmural MI

104
Q

stenoses is severe in what coronary artery syndrome

A

sudden death

105
Q

What are the levels of moderate risk CRP

A

1-3mg/L

106
Q

what is prinzmetal angina (variant)

A

sustained vasospasm causing angina

107
Q

What is cardiac raynaud

A

cold or emotion induced cardiac vasospasm

if vasospasm >20 minutes can lead to myocardial infarction

108
Q

what is takotsubo cardiomyopathy

A

dilated cardiomyopathy secondary to emotional or physical stress with normal coronary angiogram

109
Q

what is apprpriate Tx for angina pectoris of any etiology

A

nitro

110
Q

What is the definition of sudden cardiac death

A

unexpected death from cardiac causes early afeter onset of symptoms (1-24 hours) or sudden death from cardiac cause without antecedent acute symptoms

111
Q

what is the mechanism of death in sudden cardiac death

A

lethal arrhythmia from electrical instability (irritability) v fib (80%) or asystole

112
Q

what is the most common cause of sudden cardiac death

A

IHD

113
Q

Channelopathies of heart are most likely what inheritance pattern

A

autosomal dominant

114
Q

What channelopathies can lead to long QT syndrome

A

K channel KCNQ1 of KCNH2

SCN5A Na channel

115
Q

what channelopathies can lead to short QT syndrome

A

K channels KCNQ1

KCNH2

116
Q

What channelopathies can lead to catecholamingergic polymorphic ventricular tachycardia

A

RYR2
CASQ2
diastolic Ca release

117
Q

What channelopathies can lead to catecholamingergic polymorphic ventricular tachycardia

A

RYR2
CASQ2
diastolic Ca release

118
Q

What population is non ishchemic sudden cardiac death seen in

A

<40 y/o

young people

119
Q

What are common causes of SCD in young adults

A

hypertrophic cardiomyopathy
coronary artery anomalies
myocarditis

120
Q

What is chronic ischemic heart disease

A

insidious onset of CHF in patients with past MIs or anginas
cardiomegaly with L ventricular hypertophy and dilation
evidence of previous MIs (myocardial fibrosis)
arrhythmias

121
Q

chronic ischemia that does not lead to necrosis can lead to what other remodeling

A

hypokinetic myocardium with myocyte hibernation

122
Q

Angina PEctoris usually presents how

A

paroxysmal and usually recurrent substernal or precordial chest discomfort

123
Q

What can cause angina pectoris

A

transient MI that falls short of causing necrosis

124
Q

What is a stable angina

A

decreased perfusion from narrowing
most common
provoked by exercise or emotion
relived by rest or sublingual nitro

125
Q

what is unstable angina

A

cresendo, have acute plaque change
progressive increase in frequency and severity of attacks
provoked by less effort and sometimes at rest
relieved by sublingual nitro and sometimes rest

126
Q

what is prinzmetal angina

A

episodic angina from coronary artery spasm

relieved by rests, nitro, or CaChblockkers CCBs

127
Q

what is the definition of a MI

A

death of cardiac muscle from ischemia

128
Q

what factors account for 50-60% MIs

A

lipid risk factors

129
Q

what genetic risk factors account for 10-20% MIs

A

prothrombin mutations, hyperhomocystenemia

130
Q

What is a transmural infarction

A

ishcemic necrosis that involves more than 50% centricular thickness (acute plaque changes)

131
Q

what is a subendocardial infarction

A

area of ischemic necrosis liminted to the inner 1/3 or at most the inner 1/2
may occur as resul tof acute plaque change and thrombosis or prolonged and severe recution in systemic blood pressure

132
Q

What is the typical sequence of events in an MI

A

sudden change in plaque
formation initial platelet plug over plaque
vasospasm from platelet adhesion
propagation of platelt plug into stable clot from extrinsic clotting system
clot occludes lumen of involved vessel

133
Q

Describe causes of transmural MI with NO atherosclerosis

A

vasospasm (cocaine)
embolie L atrium (a fib) ventricl (mural thrombus), valve vegetations, paroxysmal embolie
vasulitis, hemoglobinopathy

134
Q

What type and when does adrenergic stimualtion induce MI

A

intense emotional stress

peak incidenc between 6 am and noon

135
Q

When does dec in ATP occur in I

A

within seconds

136
Q

whtn does irreversible cell injury occur in MI

A

20-40 minutes

137
Q

when does microvascular injury occur in MI

A

> 1 hr

138
Q

when is there complete unsalvageable necrosis in I

A

6 hours

139
Q

When are gross features seen in MI

A

around 12 hours. sometimes between 4 and 12 but usually around 12 hours or more (dark discoloration

140
Q

what is the earliest light microscopy can pick up on MI

A

4 hours, variable waviness of fibers at border

141
Q

With MI how does neutrophilia help Dx

A

because around 12-24 hours the first cells to infiltrate are the neutrophils

142
Q

When does granulation tissue begin to form in MI duration

A

7-10 days

143
Q

can pathologist tell how long ago MI occured if scarring already done

A

no

144
Q

can pathologist tell how long ago MI occured if scarring already done

A

no

145
Q

What days of MI are neutrophils bery prominent

A

3-4 days

146
Q

What coronary a is most commonly obstrcuted second?

A

first is LAD

2nd is RCA

147
Q

What is the goal of reperfusion after MI

A

salvage ischemic myocardium from potential infarction by restoration of tissue perfustion as quickly as possive

148
Q

what are problemes with cardiac reperfusion after MI

A

can cause an increase release of ROS and cause damage
can lead to arrhythmias
myocardial hemorrhage iwth contraction bands
endothelial swelling
reversible :myocardial stunning”

149
Q

What are the intervention techniques for MIs

A

lysis of thrombus with fibrinolytic meds like streptokinase, urokinase or tPA
balloon angioplasy
coronary artery bypass graft

150
Q

what is myocardial stunning

A

when there is prolonged ischemic dysfuntiong.

although reeprfused wll take mycardiocytes longer to recover and gain function

151
Q

what are the clinical Sx of an MI

A

severe substernal chest pain with radiation of pain down left arm, neck, jaw, epigastrium, weak rapid pulse, sweating, nausea, dyspnea

152
Q

How are asymptomatic MIs detected

A

STEMI and NSTEMI on EKG

153
Q

What are the most useful cardiac markers

A

troponins

154
Q

what cardiac markers do you use to detect MI a few days ago

A

troponins

TnT can go longer than TnI

155
Q

what percent of MI patients have one or more complications of acute MI

A

75%

156
Q

what are the physiologic complications of acute MI

A

contractile dysfunction: severe pump failure in 10-15% patients
arrhythmias: conduction distrubances along myocardial irritability
papillary muscle dysfunction with mitral regurgitation

157
Q

what are the pathologic complications of acute MI

A 
fmyocardial rupture
pericarditis
right ventricular infarction
infarct extension and expansion
mural thrombus
ventricular aneurysm
progressive late heart failuer
158
Q

what are the types of myocardial ruptures that are complications of acute MI

A 
free wall (anterior) leading to cardiac tamponade
interventricular septum leading to VSD and ASD
papillary muscle leading to acute valvular regurg
159
Q

what is the criteria for Dx of left sided HTN heart disease

A

have to have Hx of systemic HTN and then also L ventricular hypertrophy without other CV path that could induce it

160
Q

L sided HTN heart disease may present clinically with what other syndromes.signs

A

CHF and atrial arrhythmias

161
Q

R sided HTN heart disase occurs with what disorders

A

pulmonary parenchyma disorders (COPD and diffuse interstitial lung disease)
pulmonary vessel disorders (recurrent pulmonary embolism, primary pulmonary HTN)
chest movement disorders (kyphoscoliosis)

162
Q

what is an example of right sided HTN heart disease

A

cor pulmonale from pulmonary disorders with chornic severe pulm HTN

163
Q

What disease of pulm parenchyma presdispose to core pulmonale

A 
COPD
diffuse pulm interstitial fibrosis
pneumoconioses
cystiv fibrosis
bronchectasis
164
Q

what diseases of pulm vessels could lead to cor pulmonale

A 
recurrent pulm thromboembolism
orimary puml HTN
extensive pulmonary aa (wegener)
drug, toxin or radiation induced obstruction
extensibe pulmonary tumore microembolis
165
Q

what disorders infcuing pulm arterial constrction may predispose to cor pulmonale

A 
metabolic acidosis
hypoxemia
chronic altitiude sickness
obstruction major airways
idiopathic alveolar hypoventilation
166
Q

what disorders infcuing pulm arterial constrction may predispose to cor pulmonale

A 
metabolic acidosis
hypoxemia
chronic altitiude sickness
obstruction major airways
idiopathic alveolar hypoventilation
167
Q

What are the 2 major types of cardiac valve dysfunctions

A

stenosis and insufficiency

168
Q

stenosis is always what type of disease

A

chronic

169
Q

what is functional regurgitation

A

normal valve leaflets but there is a dilated annulu from ventricular dilation that spreads apart valve leaflets

170
Q

what is a pure vs mixed cardiac valve dysfunction

A

pure is only stenosis or insufficiency present

mixed is when both are present in same valve

171
Q

what is the most common acquired heart valve disease

A

mitral stenosis from rheumatic heart disease

172
Q

What stenoses account for 2/3 valvular diseases

A

aortic and mitral valves

173
Q

what is most frequent cause of aortic stenosis

A

calcification of anatmoically normal and congenital bicuspid aortic valves

174
Q

what is most common cause aortic insufficiency

A

dilation of ascending aorta due to HTN and agin

175
Q

what is most common cause mitral stenosis

A

rheumatic heart disease

176
Q

what is most common cause mitral insufficiency

A

myxomatous degeneration

177
Q

What is the most common of all valvular abnormalities

A

calcific aortic stenosis from aging

178
Q

what are the pathologic findings of calcific aortic stenosis (Senile)

A

nodular masses of Ca are heaped up within sinuses of valsalva

179
Q

what are the clincal features of calcific aortic stenosis

A

around 60s-80s
pressure hypertrophy from flow obstruction and patient has Lconcentric hypertrophy
L ventricular cardiac mass tends to be ischemic and leads to CHF syncope and angina pectoris

180
Q

bicuspid aortic valves are more prone to what

A

progressive degenerative calcification, develops earlier

181
Q

What types of patients does mitral annular calcification occur in

A

women over 60
individuals with myxomatous mitral valves
patients with elevated L ventricular P (HTN)

182
Q

What condition is mitral annular calcification

A

associated with arrhythmias

183
Q

when are mitral annular calcifications Dx

A

with radiography done for other reasons

184
Q

What is myxomatou degeneration of mitral valve

A

mitral valve prolapse

185
Q

What murmur do you hear with mitral valve prolapse

A

mid systolic click and regurgitant murmu

186
Q

is mitral valve prolpase more commoin in young women or men

A

7:1 W:M

187
Q

mitral valve prolapse is seen in what other condition assocaited with cardiac anomlalies

A

marfans

188
Q

What are the serious complicatinos with mitral valve prolapse

A

infective endocarditis, mitral insufficiency, strok or other systemic infarct, arrhythmias, atypical chest pain

189
Q

when is mitral valve prolapse Dx

A

Echocardiography

190
Q

what are the pathologic changes in mitral valve prolapse

A

intercordal ballooning of mitral valve leaflets
affected ones are enlarged thick and rubbery
concomitant involvemnt tricuspid valve
thinned fibrosa lyaer with thickend spongiosa layer and depsition of mucoid or (myxoid) material

191
Q

what are jet leasions

A

fibrosis of valve leaglets and endocardial surfaces of atrium and ventricl in mitral valve prolapse form wehre it hits close

192
Q

what are jet leasions

A

fibrosis of valve leaglets and endocardial surfaces of atrium and ventricl in mitral valve prolapse form wehre it hits close

193
Q

what are the steps of rheumatic carditis

A

begins with strep pharyngitis that leads to production of Ab against self and then infects all layers of heart, pancarditis

194
Q

when does chronic rheumatic valvular heart disease begin

A

10 days-6 weeks post strep throat

195
Q

what cells are pathoneumonic of rheumatic heart valve disease

A

aschoff bodies which are colelcitons of activated histocytes
antischkow cells (mononuclear)
aschoff cells- multinucleated forms
caterpillar cells- unique linear chromatin pattern

196
Q

what 5 major clinical signs are assoc with acute rheumatic fever

A

migratoyr polyarthritis of large joints
acute carditis with cardiac enlargement and diminshed fucntion
subcutaneous nodules
erythema marginatum of skin
sydenham chorea (involuntary, purposeless movements of extremities)

197
Q

what is criteria for Dx acute rheumatic fever

A

evidence of prior group A strep infection with either 2 major sytem findings or 1 major finding plus 2 minoe

198
Q

what are the minor findings with acute prheumatic fever

A

fever, arthralgia, evidence of acute phase reactants( inc sed rate or inc CRP

199
Q

After intial attack of acute rheumatic fever what is risk and Tx

A

risk for repeat group A strep infections

should receive long term PCN prophylaxid well into adulthood and perhaps life

200
Q

When does rheumatic heart disease occur

A

years of decades ater episodes of acute rheumatic fever

201
Q

what valves are commonlay affected by rheumatic valvular disease

A

mitral and aortic valves
uncommonly tricuspid
rarely pulmonic

202
Q

99% of all mitral stenosis is caused by what

A

Rheumatic heart disease

203
Q

what percent of RHD patients have mitral and aortic valve problems

A

25%

204
Q

what are hallmarks of rheumatoid heart disease

A

cardiac involvemtn in 20-40% cases rheumatoid arthritis
fibrinous pericarditis is most common
rheumatoid nodules in myocardium, endocardium, valves and aortic root may be present
rheumatoid valvulitis with fibrous thickeing and calcificaiton of aortic valve cusps

Year 2 CV (31 decks)

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