Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 BRS Neuro > ischemic heart disease > Flashcards

ischemic heart disease Flashcards

1
Q

causes of IHD
MI

when blood flow to a region is reduced?

A 
usually obstruction 
due to 
- atheroma
-thrombosis 
-Spasm
-Embolus
-Coronary ostial stenosis
-Coronary arteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

why could IHD occur when blood flow is not obstructed?

A

could be a general decrease of OXYGENATED blood flow to myocardium due to

anemia
Carboxyhaemoglobulinaemia
Hypotension causing decreased coronary perfusion pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MI due to decrease in oxygenated blood occurs with what?

A

anemia

hypotension = decreased coronary perfusion pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what triggers atherogenesis?

A

endothelial dysfunction
mechanical sheer stresses

Genetic alteration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what triggers atherogenesis?

Biochemical abnormalities

A

(elevated and modified LDL, DM, elevated plasma homocysteine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what triggers atherogenesis?
Immunological factors
Inflammation

A

(free radicals from smoking) (infection such as chlamydia, Helicobacter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

atherosclerosis can be defined as a

A

inflammatory process

- cytokine storm in covid -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

plaques build in adventitia in atherosclerosis

T/F?

A

False

build in Tunica intima in large and medium sized coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why do atherosclerotic plaques cause IHD?

A

narrow artery lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

features of Atherosclerotic plaque

A

necrotic rich core
SMC [these proliferate]
fibrous cap around
foam cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how are foam cells created

A

lipoproteins [such as LDL] are retained into dysfunctional endothelium

these then form foam cells - this process is mediated by macrophages, immune cells

there is increased expression for monocyte interaction into dysfunctional endothelium intimal space

via increased selectins on endothelium which attract chemokines on monocytes - VCAM;ICAM-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why do the tunica media smooth muscle cells proliferate?

A

response to injurv [plaque formation w necrotic core is injury]

SMC’s are recruited to the luminal side of the lesion to form a barrier between lesional prothrombotic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

tunica of vessel wall? from lumen

A

intima ; endothelium
media ; smooth muscle cells , internal +external elastic membrane
adventitia ; vasa vasorum ; nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is an important regulator of fibrous cap formation?

why?

A

TGF-B - Transforming Growth Factor
IL-10
produced by T-reg cells and macrophages

potent stimulator of collagen production in SMC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why is formation of a fibrous cap good for an atherosclerotic plaque?

A

= stable plaque - avoid rupture
contains necrotic core
limits thrombus formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how is a necrotic core produced?

A

noninternalized apoptotic macrophage foam cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why is plaque rapture bad?

A

necrotic core comes into contact with blood exposing it to prothrombotic components to platelets and pro-coagulation factors

stimulates inflammatory state in blood = increasing thrombus formation
DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why doe plaque rupture happen?

A

thinning of the fibrous cap

this occurs due to no resolution of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

chronic stable angina defined as?

A

fixed atherosclerotic plaque
= reduced blood flow through narrowed lumen
but stable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acute

coronary syndromes?

A

Unstable angina
Non Stemi
STEMI

platelet aggregation
thrombus formation

21
Q

progression of events in IHD?

A 
Asymptomatic 
Chronic stable angina 
Acute Coronary syndromes 
HF
Sudden death
22
Q

Acute coronary occlusion

A

plaque breaks through endothelium [from intima]

> pro-thrombotic factors introduced to blood so platelets aggregate; adhere
haemostasis does its thing
= fibrin clot formation
= thrombus/ blood clot
artery occludes vessel = hypoxia of that region
= infarct - necrosis / death of region if oxygen supply not restored

if it moves away - emboli of distal vessels

23
Q

collaterals are?

A

local anastamosis of heart arteries

dilate within seconds of acute episode
= aim to reach normal coronary flow

24
Q

chronic atherosclerotic patients

A
  • slow occlusion-collateral vessels develop as atherosclerosis develops
    collaterals cannot cope with demand
25
Q

why do you still get ACS with role collaterals play?

A

The collaterals can also get atherosclerosis or the damage become so extensive that even the collaterals can not help

collaterals dilate = HF as weakens the heart and cannot maintain blood supply

26
Q

infarction defn?

A

area that in ischemic state has zero or little flow of blood[oxygen]
infarcted

27
Q

Pathogenesis: Soon after infarction

A

Small amount of collaterals open and blood seep into the infarcted area
Local blood vessels dilate and area becomes overfilled with stagnant blood
Muscle fibres use all the remaining oxygen, hemoglobin becomes totally deoxygenated giving bluish brown hue & blood vessels appear engorged despite lack of blood flow

28
Q

later stages of infarction?

A

Vessels walls permeability increases, fluid leak and local tissue oedematous
Cardiac muscle cells swell and due to no blood supply die within few hours

29
Q

causes of death after MI

A

decreased CO
damming of blood in bodys venous system
V fibrillations
rupture of infarcted area

30
Q

why does decreased cardiac output occur after MI?

A

loss of elasticity of infarcted smooth muscle ; cannot contract just forced outwards by pressure inside

lack of pumping force > cardiac failure = peripheral ischemia , cardiac shock

31
Q

Damming of blood in body’s venous system

A

Can die after few days of doing well.—-because of low cardiac flow —low blood flow to kidneys a –fail to excrete add to blood volume and congestive symptoms—-pulmonary oedoma die after few hours of symptoms

32
Q

after an acute MI will CO remain the same?

A

technically yes due to reserves; collaterals
normal areas of heart hypertrophy to compensate

but exertional CO will not be the same

33
Q

what biomarkers are most informative with CVD?

A

B-type natriuretic peptide

urinary albumin-to-creatinine ratio

34
Q

IHD clinical history?

A

chest pain
age,sex,ethnicity,smokinh,alcohol
SES
family history

35
Q

lab tests for CVD/IHD?

A

basics lipid profile

LDL, HDL, Triglycerides, lipoprotein a, C-reactive proteins etc

36
Q

Serum markers in patients with suspected acute cardiac events (ACS, MI)

A

Troponins(I or T)
Creatine kinasewith MB isozymes
Lactate dehydrogenase and lactate dehydrogenase isozymes
Serumaspartate aminotransferase

37
Q

biomarkers for predicting death after an MI?

A 
B-type natriuretic peptide
CRP
Homocysteine
Renin
Urinary albumin-to-creatinine ratio
38
Q

unstable angina?

ECG changes

A

st depression and t wave inversion

39
Q

acute MI ecg changes?

A

infarct - transmural so

ST elevation with T wave inversions

40
Q

pharmacological treatments for IHD?

targeting LDL

A

HMG-CoA reductase inhibitors:
These agents lower LDL-C levels. They also lower triglyceride levels and raise serum HDL levels.
ATORVASTATIN

41
Q

what do Bile acid sequestrants do?

Cholestyramine

A

prevent recycling of bile acids

so you use up more cholesterol - fecal

42
Q

ACE inhibitors and CCB?

A

Hypertension and atherosclerosis may be intimately linked through their effects on vascular endothelial dysfunction

CCB : amlodipine
dilatory effect on coronary SMC - vasodilation
= improves myocardial oxygen delivery

43
Q

CABG?

coronary artery bypass grafting

A

A vessel from another part of your body to create a graft that allows blood to flow around the blocked or narrowed coronary artery. This type of open-heart surgery is usually used only for people who have several narrowed coronary arteries.

44
Q

Percutaneous coronary Intervention

A

Involves angiography and stent placement:
Common to treat stable CAD
Improves blood flow by placing a stent and compressing the plaque

45
Q

acute anginal symptoms

pharmacological treatment?

A

anti-ischemic effect of nitrates is to decrease myocardial oxygen demand by producing systemic vasodilation

46
Q

“reducing myocardial cellular sodium and calcium overload via inhibition of the late sodium current of the cardiac action potential”

what drug does this?

A

ranolazine

antianginal agents

47
Q

how do B-blockers work

A

Beta-blockers inhibit sympathetic stimulation of the heart, reducing heart rate and contractility; this can decrease myocardial oxygen demand and thus prevent or relieve angina in patients with CAD

48
Q

which drug inhibits platelet function

why is this useful in IHD?

A
  • prevents atherosclerosis
    antiplatelet drugs

aspirin
clopidogrel

Year 2 BRS Neuro (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions