Chronic IHD, ARRYTHMIAS< HTN Heart disease

Question 1

Chronic IHD

Answer 1

progressive heart failure secondary to ischemic myocardial damage. it appears when the compensatory mechanisms begin to fail

Question 2

severe CAD

Answer 2

cause diffuse diffuse myocardial dusfunction and even micro infarction and replacement fibrosis,without any clinically evident episode of frank infarction

Question 3

HF

Answer 3

chronic IHD is typically seere and is occassionally severe and punctuated by new episodes of angina or infarction

Question 4

Arrythmias

Answer 4

Abberant

,ischemic injury is te most common cause

Question 5

Types

Answer 5

the SA node is damaged (e.g., sick sinus syndrome),
other fibers or even the atrioventricular (AV) node can
take over pacemaker function, albeit at a much slower
intrinsic rate (causing bradycardia).
• If the atrial myocytes become “irritable” and depolarize
independently and sporadically (as occurs with atrial
dilation), the signals are variably transmitted through
the AV node leading to the random “irregularly irregular”
heart rate of atrial fibrillation.
• If the AV node is dysfunctional, varying degrees of heart
block occur, ranging from simple prolongation of the P-R
interval on the ECG (first-degree heart block), to intermittent
transmission of the signal (second-degree heart block),
to complete failure (third-degree heart block

Question 6

Hypertension

Answer 6

ventricular hypertrophy
myocardial dadaptive capacity
cardiac dilation
CHF
sudden death

Question 7

systemic I(left sided)hypertensive heart disease

Answer 7

left ventricular hypertrophy in the absence of other cvs pathology and a pathology evidence

Question 8

CLINICAL FEATURES OF HHD

Answer 8

Atrial fibrillation(secondary to left atrial enlargement)

Question 9

Cor Pulmonale

Answer 9

right ventricular hypertrophy and dilation-frequently accompanied by right sided heart failure-pulmonary HTN because of primary disorders of lung parenchyma or pulmonary vasculature

Question 10

valvular heart disease

Answer 10

failure of a valve to open completely obstructing forward flow
that is because of a cuspal abnormality, scarring or fibrosis

Question 11

insufficiency

Answer 11

results from failure of a valve completely, allowing regurgitation

Question 12

causes of insufficiency

Answer 12

endocarditis
aorta
mitral stenosis

Question 13

Bicuspid aortic valve(2 cusps)

Answer 13

one large one small
1 to two perecnt of all
more prone to calcification

Question 14

degenerative ECM changes

Answer 14

calcification
cuspal(aortic)
annular(mitral)
alterations in the ECM
increased proteoglycans and diminished proteoglycans and diminished fibrillar collagen and elastin(myxomatous)
changes in the generation of matrix ma

Question 15

calcific aortic stenosis

Answer 15

heaped up calcific masses on the outflow side of the cuspswhich protrude into the sinuses of valsalva and impede valve opening

Question 16

clinical features

Answer 16

high left ventricular pressures because of hypertrophy 200 mmhg

Question 17

sequence of events

Answer 17

hypertrophied muscle prone to ischemia and angina CHF and cardiac decompensation

Question 18

myxomatous mitral valve

Answer 18

floppy and prolapse
balloon back into LA during systole
CT defect like Marfan syndrome

Question 19

Rheumatic Valvular Disease

Answer 19

acute,immunologically mediated disease
Group A Beta hemolytic streptococci(pharyngitis)
but also occasionally infections at other sites RHF
RHD deforming mitral stenosis

Question 20

pathogenesis

Answer 20

antibodies directed against classically attributed to antibodies against group A streptococci that cross react with host myocardial antigens
antigens bind to M proteins against the myocardium and cardiac valves and cause injury through the activation of complement and Fc receptor-bearing cells
CD4+ t cells that recognize streptococci cross react w antigens and elicit cytokine mediated inflammatory responses

Question 21

Acute rheumatic fever morphology

Answer 21

Discrete inflammatory foci
Aschoff bodies
T cells+plasma cells+plump activated macrophages Anitschkow cell(zones of fibrinoid necrosis)
In any 3 layers

Question 22

chronic rheumatic heart disease

Answer 22

organization of acute inflammation and subsequent scarring aschoff bodies replaced by scar
create fishmouth stenosis

Question 23

JONES CRITERIA

Answer 23

carditis
migratory polyarthritiss
subcutaneous nodules
erythematous annular rash
Sydenham chorea

Question 24

Infective Endocarditis

Answer 24

microbial infection of the heart valves that has vegetations composed of thrombotic debris like organisms

Question 25

types

Answer 25

acute destructive on injured

Question 26

subacute

Answer 26

previously injured
cardiac anomalies predispose to such infections
prosthetic heart valves and Ipacemakers
S viridians
HACEK

Question 27

signs

Answer 27

fever
fatigue weight loss flu like syndrome
splenomegaly
fever chills lassitude
microemboli
splinter hemorrhages
Roth spots(retinal hemorrhages)
painful palm or sole erythema(Janeway lesions)
painful fingertip nodules(Osler nodules)

Question 28

NBTE

Answer 28

deposition of sterile thrombi non destructive
hypercoagulable state causes predisposition
DIC, hyperestrogenic

Question 29

Libman-Sacks Endocarditis

Answer 29

characterized by the presence of sterile vegetations on the valves of patients with SLE

Question 30

Cardiomyopathies

Answer 30

diverse group
immun ologic diseases
systemic metabolic disorders