CVS PATHOLOGY Flashcards
Normal weight in female and male
250-300
300-350
changes in lungs
increased hydrostatic pressure
pulmonary edema and congestion
heart failure cells
brown induration of the lungs
Changes in Kidneys
Stimulation of RAAS
salt and water retention
acute tubular necrosis
Pro-renal azotaemia
Changes in liver
central hemorrhagic necrosis
Nutmeg appearance
cardiac sclerosis
spleen changes
congestive splenomegaly
siderofibrotic nodules - Ghandygamma bodies
hypertension values
greater than 140 and 90
types of hypertension
essential
secondary
cause of essential
genetics - genetic deffect in renal excretion and family cluster
environment - stress, obesity, increased salt intake
cause of secondary
renal diseases
endocrine
vasucular
neurogenic
blood pressure formula
C0 TIMES PR
what disease in hyptn usually associated with?
coronary atherosclerosis
characteristics of compensated hptn heart disease
steady cardiac output
concentric LVH
no dilatation
no vascular lesions
characterisitcs of decompensated hptn heart disease
cardiac dilatiion
hypertrophy
lv dilation
cardiomegaly
what organism causes rheumatic fever
group Aa B hemolytic streptococci
which part of the layers of the heart are aschoff bodies common
myocardium
diagnostic anatomic lesions of rheumatic fever
Aschoff body
what are ashcoff body
Foci or fibrinoid necrosis surrounded by lymphocytes, macrophages, occasional plasma cells and plump activated histiocytes called Anitschkow cells
what are verrucae in rheumatic endocarditis
small friable vegetations deposited along the free edge of the cusps
McCallum plaques in rheumatic endocarditis
fibrous plaques seen on the subendocardium of the left atrium
which cells are pathognomonic of RH
and what is another name for it
Anitschkow’s cells
Caterpillar cells
difference between infective endocarditis an rheumatic fever in terms of verrucae
IE have bulk friable bacterial laden vegetation
Organisms causing acute IE
S. Aureus
S. pneumonia
organisms causing subacute IE
S. viridans
s. epidermitis
E.coli
HACEK
Factors predisposing one to development of IE
Seeding of blood with microbes
Hemodynamic disturbance occuring across deformed heart valve
Activation of clotting cascade
Production off agglutinating antibodies leading to clumping of organism within the vegetation
is there fragmentation and embolisation of septic vegetation in IE
YES
Spleen
brain
coronary arteries
kidneys
Types of non-infective endocarditis
- Marantic endocarditis or non bacteria thrombotic endocarditis
- Libman-Sacks dx or non - bacteria verrucous endocarrditis
what’s the most common souce of coronary emboli
Marantic endocarditis
X’tics of verrucae in Libman-Sacks Endocarditis
Granular flat verucae on both surfaces of valves
4 clinicopathologic syndromes in ischemic heart disease```
Angina pectoris
Myocardial infarction
Chronic ischaemic heart disease
Sudden cardiac death
causes of coronary insufficiency
coronary atherosclerosis coronary vasospasm coronary artery embolism ostial stenosis coronary thrombosis aneurysms congenital anomalies
pathogenesis of mi
occlusive intrancoronary thrombus
vasospasm with or without atheroscelorosis
Emboli from
left sided mural thrombus
vegetative endocarditis
paradoxical emboli rom right side of heart via fromen ovale
left atrium in association with atrial fibrillation
which of the enzymes is useful in re infarction
CK MB
which enzyme or protein is much more specific in the diagnosis of MI
Troponin
Which enzyme or protein is elevated before CKMB but it’s not specific
Myoglobin
how to use ldh in diagnosing MI
Normally isoenzyme is higher than 1 but in MI, this is reversed
