Cardiac Path Zaman

Front 1

define CHF

Back 1

heart no longer able to eject venous blood return

Front 2

low output CHF failure is due to what

Back 2

decreased contractility

Front 3

most common causes of L sided failure (6)

Back 3

1. HTN
2. Mitral valve dz
3. aortic valve dz
4. ischemic heart dz
5. primary myocardial dz
6. myocarditis

Front 4

most common cause of R sided heart failure?

Back 4

LV failure

Front 5

other causes of RSHF

Back 5

1. lung dz
2. cor pulmonale
3. pulmonic/triscuspid valve dz
4. L --> R shunts (PFO)

Front 6

conditions causing volume overload

Back 6

1. valvular regurg
2. abnormal shunts

Front 7

volume overload causes what kind of hypertrophy

Back 7

eccentric

Front 8

pressure overload causes what kind of hypertrophy

Back 8

concentric

Front 9

conditions causing pressure overload

Back 9

1. valvular stenosis
2. HTN

Front 10

MAJOR cause of death in pts w/ untreated HTN

Back 10

CHF

Front 11

difference b/w compensated and decompensated heart failure

Back 11

compensated: F-S still applies and CO is OK

decompensated: heart is compromised and CO drops. F-S no longer applies

Front 12

what kind of failure is CHF, backward or forward

Back 12

backward

Front 13

why does aldosterone inc. in response to CHF?

Back 13

b/c CO is decreased in CHF t/f kidney is not being perfused so aldosterone inc's to turn up the RAS to inc. fluid

kidney releases renin. renin turns angiotensinogen to Ang 1. ACE converts Ang1 to Ang2. Ang2 turns up aldosterone.

Front 14

Most common clinical manifestation of LVF (which is most commonly caused by CHF) is what?

Back 14

dyspnea

Front 15

where is BNP secreted from

Back 15

ventricles

Front 16

what increases bnp (heart)

Back 16

increased stretch and inc. volume

Front 17

how does BNP work? (4)

Back 17

1. down reg's the RAS
2. dec's sympathetic heart activity
3. increases renal blood flow and
4. Na+ excretion

Front 18

BNP normal range

Back 18

<100 PG/mL

Front 19

BNP can also be found in what other fluid imbalance problem

Back 19

renal insufficiency

Front 20

can you use BNP to "rule in" CHF?

Back 20

NO; BNP is used to r/o CHF in an adjunctive way

Front 21

what situation is BNP best used?

Back 21

acute ER setting w/ SOB

Front 22

List 3 ACS's

Back 22

1. unstable angina
2. non-STEMI
3. STEMI

Front 23

List 2 types of Ischemic Heart Dz's (IHD) and describe each

Back 23

1. Transmural infarct-TI(full wall thickness)
2. Subendocardial infarct-SI(partial wall thickness)

Front 24

Which is more severe and more common, TI or SI?

Back 24

TI

Front 25

Where do TI's usually begin?

Back 25

least perfused subendocardium

Front 26

TI's almost all caused by combo of: (4 things)

Back 26

1. Marked stenosis
2. Thrombosis over the fissure, rupture, or hemorrhage into plaque
3. Plt activation/aggregation and release of thromboxane and other vasoactive products
4. vasospasms from vasoactive products (cocaine)

Front 27

Name 2 vasoactive substances

Back 27

1. thromboxane
2. cocaine

Front 28

Reperfusion injury majorly caused by what 2 things

Back 28

1. inc. Ca++ inflow
2. free radicals from segs

Front 29

Is it more common for TI to occure in R ventricle alone or in conjuction w/ LVI? Why?

Back 29

-RVI more commonly occurs w/ LVI than isolated RVI

-b/c the posterior septum may extend into the posterior R ventricle

Front 30

vascular distribution of TI's from greatest to least

Back 30

LAD > RCA > LCA
40-50% > 30-40% > 15-20%

Front 31

What walls of the heart are infarcted by LCA, LAD, RCA?

Back 31

LCA --> posterolateral LVFW infarct

LAD --> anterior LVFW infarct near apex and anterior 2/3 of septum

RCA --> Posterior (inferior or diaphragmatic) LVFW infarct and posterior 1/3 of septum

Front 32

what gross changes occur 0-12 hrs post TI

Back 32

no change

Front 33

what gross changes occur 18-24 hrs post TI

Back 33

pallor

Front 34

what gross changes occur 24-72 hrs post TI

Back 34

pallor, hyperemia

Front 35

gross changes at 3-7 days post TI

Back 35

hyperemic border, central yellow-brown softening

Front 36

gross changes 10 days post TI

Back 36

maximun yellow and soft w/ red-brown margins

Front 37

gross changes 7 weeks post TI

Back 37

scarring complete

Front 38

microscopic changes 0-2 hrs post TI

Back 38

Subtle: waviness at fiber border, fine cytosol lipid droplets, cellular swelling, band contraction in reperfused areas

Front 39

mircoscopic changes 4-12 hrs post TI

Back 39

coagulative necrosis begins, edema, hemorrhage, early PMN infiltration,chromatin margination

Front 40

microscopic changes 18-24 hrs post TI

Back 40

coagulative necrosis w/ loss of nuclei and striations, lots of PMN infiltrates

Front 41

microscopic changes 3-7 days post TI

Back 41

disintegration of dead fibers w/ macrophage activity, granulation tissue formation

Front 42

microscopic changes 3 weeks post TI

Back 42

inc'd collagen, dec'd cellularity

Front 43

what complication occurs in 4-15% of transmural AMI's (TAMI) b/w days 2-10

Back 43

rupture of infarct

Front 44

Do most ruptured TAMI's involve the free wall or interventricular septum

Back 44

free wall --> 90%

Front 45

Subendocardial infarcts begin where (layer of heart muscle)

Back 45

least well perfused myocardium --> subendocardium w/ advanced stenosis

Front 46

what is a big difference b/w subendocardial and transmural infarcts (layers of heart muscle)

Back 46

subendocardial --> localized to no more than 1/2 (usually 1/3) of myocardium

transmural --> all layers (endo, myo, epicardium)

Front 47

do most (80%) of Subendocardial infarcts occur w/ or w/o major trunk thrombosis

Back 47

w/o

Front 48

Name 3 things that are notorious for causing hypotensive episode leading to subendocardial infarct

Back 48

1. shock
2. arrhythmia
3. cardiac surg

Front 49

which is more likely to dvlp pericarditis, ventricular aneurysm, or rupture SI or TI

Back 49

TI

Front 50

___% of Asx AMI's are recognized by EKG or enzymes or both

Back 50

20%

Front 51

more than ___% of all IHD deaths are from ventricular arrhythmias

Back 51

50%

Front 52

what will rupture of the LVFW lead to

Back 52

hemopericardium --> cardiac tamponade

Front 53

What happens to 30% of the TCA's (transluminal coronary angio)

Back 53

re-stenosis in 2-3 yrs

Front 54

What happens to CABG vein grafts eventually? Which vein graft is the exception?

Back 54

-intimal thickening in 5-10 yrs or sooner

-internal mammary

Front 55

Define IHD

Back 55

imbalance b/w myocardial need for O2 and supply

Front 56

almost all O2 deficiency is d/t severe ____ and ____

Back 56

Aortic stenosis and CAD

Front 57

4 big causes of IHD

Back 57

1. inc'd demand
2. dec'd coronary artery perfusion
3. Anemia - dec'd O2 transport
4. sudden loss of BP

Front 58

4 clinical manifestations of IHD

Back 58

1. Angina pectoris (AP)
2. MI
3. Chronic ischemic heart dz
4. SCD

Front 59

T/F: AP is defined as paroxysmal episodes of precordial chest pain/discomfort caused by episodic ischemia which causes an infarction

Back 59

F--> ...which DOES NOT cause and infarction

Front 60

define stable AP

Back 60

provoked by exertion but relieved w/ rest

Front 61

define variant AP

Back 61

occurs at rest and relieved by vasodilators (nitroprusside, hydralazine)

Front 62

variant AP AKA

Back 62

Prinzmetal's AP

Front 63

define unstable or crescendo AP

Back 63

intense, prolonged sometimes worsening pain W/ SUBCLINICAL FINDINGS (mild enzyme/slight EKG changes) and pain responds slowly to vasodilators

Front 64

all angina can be caused by any combo of what 4 things

Back 64

1. fixed stenotic lesions
2. vasospasms
3. plt aggregation
4. inc'd myocardial demand

Front 65

chronic IHD AKA

Back 65

ischemic cardiomyopathy

Front 66

chronic IHD is caused by what specifically?

Back 66

- significant coronary artery stenosis

Front 67

older pts w/ h/o ____ or previous ____ are good candidates for chronic IHD

Back 67

- AP (fixed stenotic lesion)

- MI

Front 68

what are 3 normal gross morph wear and tear changes seen in chronic IHD (2 mitral, 1 aortic)

Back 68

1. thickened mitral leaflets --> from collagen
2. calcifications of mitral annulus
3. senile calcific aortic stenosis

Front 69

chronic IHD is a Dx of exclusion in elderly with a h/o? (3 things)

Back 69

1. angina
2. conduction defects
3. infarction

Front 70

what is the major DDx assoc. w/ chronic IHD?

Back 70

dilated cardiomyopathy

Front 71

microscopic morph of chronic IHD (5)

Back 71

1. diffuse myocardial fiber atrophy w/ dense perinuclear lipofuscin (fine granular yellow-brown pigments) in myocytes
2. perivascular interstitial fibrosis
3. patchy foci of scarring
4. Myocytolysis of cells -- interstitial perimysial (muscle) fibrosis
5. possible previous scarring

Front 72

how is SCD defined?

Back 72

sudden death w/in 24 hrs of symptoms

Front 73

Name some things that can cause SCD (4)

Back 73

1. PE
2. Heart Dz
3. Ruptured AA
4. CNS d/o

Front 74

What is the most common cause of SCD?

Back 74

chronic IHD

Front 75

chronic IHD can predispose you to what arrhythmia?

Back 75

V fib

Front 76

How often is SCD the initial manifestation of IHD?

Back 76

50%

Front 77

What is the 2nd most common cause of cardiac death?

Back 77

HHD (hypertensive heart dz)

Front 78

2 tests that can discover compensated HHD

Back 78

1. EKG
2. Echocardiogram

Front 79

what may be the first 2 signs of HHD

Back 79

1. A fib
2. CHF

Front 80

what is a major risk factor that accelerates CAD

Back 80

HHD

Front 81

minimum criteria for the Dx of HHD (2)

Back 81

Aortic Stenosis or Coarctation of the Aorta -->L vent hypertrophy in absence fo other CV path that can induce HHD
AND
hx of HTN

Front 82

How is LVH defined?

Back 82

wall thickness of >= 2cm

Front 83

Dz caused by pulmo HHD resulting from d/o of the lungs or pulmonary vasculature which causes RVH and dilation leading to failure

Back 83

cor pulmonale (CP)

Front 84

Acute CP cause causing sudden death? Is the heart grossly normal in this condition?

Back 84

PE

Yes

Front 85

chronic CP often follows prolonged pressure overload of _____ and _____

common causes of this

Back 85

pulmo arteries and arterioles

COPD, TB, pneumoconiosis, sarcoidisis, scleroderma, PF, kyphoscoliosis, Pickwickian syndrome (marked obesity)

Front 86

T/F: In CP, there is thickening of the muscle below the pulmonary valve which leads to obstruction.

Back 86

T

Front 87

Besides the pulmonary valve thickening, what are some other secondary issues (thickening, etc) in CP?

Back 87

- moderator band
- mild tricuspid regurg and secondary thickening

Front 88

T/F the LV remains unaffected in CP.

Back 88

False. It is compressed by the RV

Front 89

What Dz process is IHD mainly d/t?

Back 89

coronary atherosclerosis

Front 90

unstable angina can be d/t ____ of plaque w/ formation of _____ thrombus

Back 90

- fissuring
- mural

Front 91

Dx of AMI based on? (3)

Back 91

1. Symptoms
2. EKG
3. CK-MB and cTn's

Front 92

Impaired filling of LV w/ LA hypertrophy and dilation --> pulmonary congestion and RV hypertrophy and dilation --> inc'd venous pressure and dec'd periph perfusion ??CHF??describes what type of valvular dz

Back 92

Mitral stenosis

Front 93

Is LV hypertrophy found in pure mitral stenosis?

Back 93

No; however, the rigid mitral valves are often insufficient and may cause regurge --> LA & LV hypertrophy

Front 94

What is a deadly complication assoc. w/ the enlarged LA in mitral stenosis? (think systemic)

Back 94

multiple brain infarcts d/t possible mural thrombi

Front 95

where do the the mural thrombi assoc. w/ brain infarct usually hang out in Mitral Stenosis?

Back 95

atrial appendage

Front 96

List some external causes of Mitral Stenosis (3)

Back 96

1. Ergot alkaloids for migraines
2. Phen-fen
3. Radiation of CA

Front 97

LA and LV hypertrophy and dilation --> pulmonary congestion-->pulmonary HTN and RV hypertrophy and dilation describe what valvular dz

Back 97

Mitral Regurg (insufficiency)

Front 98

How can mitral regurg cause CHF later

Back 98

LA dilation reduces the load on the LV

Front 99

List some late complications assoc. w/ mitral regurg (3)

Back 99

1. thromboemboli
2. supraventricular tachycardia or arrhythmia
3. sudden death

Front 100

What is most common cause of mitral regurg?

Back 100

MVP (mitral valve prolapse) AKA "floppy valve"

Front 101

Age and gender MVP's are usually found

Back 101

20-40 yo; female

Front 102

connective tissure d/o assoc. w/ MVP

Back 102

marfans

Front 103

chromosome mutation and inheritance of MVP

Back 103

16p; AD

rarely X-linked recessive

Front 104

which mitral valve leaflet is most prone to balloon out?

Back 104

posterior

Front 105

what 2 things are heard w/ auscultation of MVP?

Back 105

1. midsystolic click
2. late systolic murmer

Front 106

Is there an inc'd chance of SCD arrhythmias and infective endocarditis w/ MVP

Back 106

Yes

Front 107

aortic stenosis results in ____ hypertrophy and eventual dilation

Back 107

LV

Front 108

what kind of overload is aortic stenosis pressure or volume? And what happens to the pulse pressure?

Back 108

- pressure

- pulse pressure narrows

Front 109

Why does the pulse pressure narrow?

Back 109

b/c the concentric LV hypertrophy inc's the diastolic pressure

Front 110

aortic stenosis more common in men or women?

Back 110

men

Front 111

is MOST aortic stenosis rheumatic (illness) related in origin?

Back 111

No

Front 112

is aortic stenosis MOST often calcific, senile, and degenerative?

Back 112

Yes

Front 113

Is the mitral valve usually involved in aortic stenosis?

Back 113

No

Front 114

Can congenital malformed valves calcify in the early teens?

Back 114

Yes

Front 115

Are bicuspid valves more common in men or women

Back 115

4:1 Men:Women

Front 116

Biscupid aortic stenosis inc's risk for (3) things

Back 116

1. ENDOCARDITIS
2. aortic dilation
3. dissection

Front 117

What accounts for 8-10% of all congenital outflow obstructions and has a gray white fibroelastic endocardial ridge

Back 117

subaortic (subvalvular) stenosis

Front 118

which is it supravalvular or subvalvular aortic stenosis, that is the least common and represents an arterial dysplasia?

Back 118

supravalvular

Front 119

couple of other causes of aortic stenosis?

Back 119

1. type II hyperlipidemia
2. glycogen storage diseases

Front 120

eccentric LVH and dilation w/ volume overload, a wide pulse pressure w/ failure to maintain diastolic pressure with ability to cause SCD d/t impaired coronary filling complicated by inc'd O2 demand of the extremely dilated LV describes what valvular insufficiency (regurg)?

Back 120

aortic regurg

Front 121

Aortic stenosis = wide or narrow pulse pressure

Aortic regurg = wide or narrow pulse pressure

Back 121

AS = narrow

AR = wide

Front 122

name given to oval defects in the valve above the lines of closure in mitral/aortic valve that have no funtional significance

Back 122

fenestrae

Front 123

define Lambl's excrescences

Back 123

fibrous bands in the centers of the valve

Front 124

type of deposits that can be found on the mitral/aortic valve after 30 yo

Back 124

lipid

Front 125

is Libman-Sacks a BTE or NBTE?

Back 125

NBTE

Front 126

what autoimmune dz is libman-sacks endocarditis assoc. w/?

Back 126

SLE

Front 127

"Rheumatoid" endocarditis assoc. w/ what dz

Back 127

ankylosing spondylysis

Front 128

define NBTE

Back 128

non-inflammatory accumulation of plts, fibrin, and collagen

Front 129

In autopsy ~75% of NBTE were assoc. w/ what type of CA

Back 129

colon adenocarcinoma

Front 130

2 immunologic mechanisms (general) in NBTE

Back 130

1. Ab's to tumors
2. Immune complex deposition

Front 131

is bacterial endocarditis vegetative or verucca like growths

Back 131

large vegetative, inflammatory

Front 132

bug rate(%) of occurance in acute bacterial endocarditis?

Back 132

Staph 33% > Strep 24% > pseudomonas 14% > Klebsiella 5% and Serratia 5%

Front 133

G- or G+ bugs common in IV drugies and diabetics

Back 133

G+ bugs

Front 134

4 predisposing factors for BE

Back 134

1. deformed valve (RHD)
2. in adults, transient bacteremia w/ dental surg heart caths, UTIs, abortions, endo procedures, IV durgs, etohism
3. kids, congenital heart dz
4. pre-existing NBTE

Front 135

2 extracardiac consequences of BE

Back 135

1. skin petechiae
2. Osler's nodes on fingertips

Front 136

what are janeway lesions

Back 136

hemorrhagicpainless immune complex deposits on the palms and soles

Front 137

what are Osler's nodes

Back 137

red, raised, tender lesions on pads of fingers and toes

Front 138

Dx of Be consist of: (6)

Back 138

1. + blood cultures
2. + serology
3. PCR
4. bugs in the lesions
5. Echocardiogram shows lesions
6. fistulas created from abcesses

Front 139

what layers of the heart does RHD effect?

Back 139

Pancarditis

Front 140

time frame for RHD following infxn

Back 140

10 days to 6 weeks

Front 141

what infxn causes RHD?

Back 141

group A strep (S pyogenes --> B hemolytic)

Front 142

3 NBTE's

Back 142

1. Rheumatic valvular endocarditis
2. Libman-Sacks endocarditis
3. "Rheumatiod" endocarditis

Front 143

what areas can RHD effect besides the heart?

Back 143

joints, skin, brain

Front 144

what is order of valvular involvement from greatest to least?

Back 144

mitral > mitral & aortic > aortic & tricuspid > mitral & tricuspid > all 4

Front 145

is pulmonic valve involvement w/ RHD common or rare?

Back 145

rare

Front 146

What are the Jones Major Criteria for Dx of RF? (5)

Back 146

1. Carditis
2. Migratory polyarthritis
3. Subcutaneous nodules
4. Cutaneous erythema marginatum
5. Sydenham chorea

Front 147

What are the Jones Minor Criteria for Dx of RF? (3)

Back 147

1. Fever
2. Arthralgia
3. inc'd acute phase proteins (CRP, ESR)

Front 148

What does it take to Dx RF w/ Jones criteria?

Back 148

2 majors OR 1 major and 2 minors

Front 149

what 2 things (lab test) indicate recent infxn of ~10 days-6wks?

Back 149

1. Anti streptolysin O (ASO)
2. DNAse B

Front 150

What is a MacAllum's patch?

Back 150

thickened fibrous plaque on posterior LA above posterior leaflet of mitral valve

Front 151

3 things related to gross examination of RF

Back 151

1. MacAllum's patch
2. Endocardial pocket on upstream side of an incompetent valve
3. LA mural thrombus w/ mitral stenosis

Front 152

Microscopic RF changes can be seen earliest at what structure?

Back 152

valve ring

Front 153

what are the earliest microscopic changes seen in RF path?

Back 153

edema --> vascularization of leaflets --> infiltration of lymphs, plasma cells, and PMNs

Front 154

what are 4 other microscopic changes seen in RF path?

Back 154

1. Fibrinoid change near surface
2. Anitschkov myocytes AKA Aschof cells
3. Aschoff bodies
4. Verrucae at lines of closure

Front 155

describe what Aschoff cells, Aschoff bodies, and the veruccae consist of in the microscopic changes of RF.

Back 155

Aschoff cells --> elongated "caterpillar" nuclei

Aschoff bodies --> aggretates of Aschoff cells w/ multinucleated giant cells AKA granuloma

Verrucae --> plt thrombi on altered valve surface at the lines of closure

Front 156

Why do Aschoff bodies form?

Back 156

Antibody (Ab) formation

Front 157

% of pts w/ RF have what Ab's to what? (4)

Back 157

1. streptolysins
2. Hyaluronidase
3. streptokinase
4. DNAses

Front 158

Which GAS subtype causes the xreactivity to cell wall antigens (Ag)

Back 158

type 5 GAS

Front 159

What are the 4 distinct tissue targets assoc. w/ the xreactivity of RF?

Back 159

1. subsarcolemmal cytoplasm of cardiac myofibers
2. smooth muscle of intracardiac vessel walls
3. heart valve fibroblast Ag's
4. CNS neuronal Ag's in subthalamic and caudate nucleus

Front 160

what do immunofluorescent studies correspond and what is the correlation with the severity?

Back 160

- IgG, IgA, IgM, complement
- proportional

Front 161

what % of pts w/ post strep glomerulonephritis is not assoc. w/ any carditis

Back 161

60%

Front 162

Will all pts w/ RF have detectable xreactive Ab's?

Back 162

No

Front 163

Will you have a higher % chance of having xreactive Ab's with recent strep infxns or RF/RHD

Back 163

RF--> 55%
RHD--> 58%
recent infxns--> 24%

Front 164

Mechanism by which immune response to strep Ag's in RF occur?

Back 164

delayed type hypersensitivity

BTW: in vitro stimulation macrophage inhibitory factor (MIF) or blastogenic response (triggering T cell proliferation w/ defined Ag)

Front 165

3 related COD's related to RF

Back 165

1. CHF
2. mural thrombotic emboli
3. BE

Front 166

term "tree barking" which is dilation and scarring of Aorta is used w/ what infective valvular dz

Back 166

syphilis

Front 167

Aortitis occurs in ___% of tertiary syphilis if left untx'd

Back 167

70-80%

Front 168

where does T pallidum like to lodge

Back 168

vasa vasorum

Front 169

"tree barking" can cause (3)

Back 169

1. aortic regurg
2. coronary ostial stenosis
3. aneyrysms (not common)

Front 170

where does coronary ostial stenosis assoc. w/ syphilis occur?

Back 170

just above aortic valve

Front 171

What kind of aneurysms are commonly found in cardiovascular syphilis?

Back 171

None; they are NOT common

Front 172

valvular causing dz assoc. w/ the HLA B-27 Ag?

Back 172

Ankylosing spondylitis

Front 173

Inflammation of the intima of an artery which leads to closure of the lumen

Back 173

endarteritis obliterans

Front 174

3 collagen d/o's assoc. w/ MV problems

Back 174

1. marfans
2. Ehlers-Danlos
3. Stickler syndrome

Front 175

stenosis of which 2 valves account for 2/3 of all valve dz's?

Back 175

aortic and mitral

Front 176

General acronym used to describe sterile vegetations of the valves which can cause embolic complications?

Back 176

NBTE