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Y3 > Atherosclerosis and Ischaemic Heart Disease > Flashcards

Atherosclerosis and Ischaemic Heart Disease Flashcards

1
Q

effects of atherosclerosis

A

elastic arteries - aorta, carotid, iliac arteries

large and medium muscular arteries - coronary and popliteal

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2
Q

which layer of the blood vessel does this affect

A

there is an intimal lesion - forms an atheromatous plaque underneath

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3
Q

distribution of atherosclerotic plaques

A

decreasing order of frequency

  • abdominal aorta
  • coronary arteries
  • popliteal arteries
  • descending thoracic aorta
  • internal carotid arteries
  • circle of willis
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4
Q

when can atheromatous plaques develop

A

develop throughout life with a fatty streak beginning in childhood
becomes symptomatic in middle age or later

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5
Q

consequences of athersclerosis

A 
MI/ chronic IHD/ suddne death 
stroke/ CVA
AAA
gangrene of legs - critical limb ischaemia  
gut ischaemia
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6
Q

what can happen to the vessel as a result of a plaque formation

A

narrowing as increase in plaque size - there can be an overlying thrombus which can dislodge and form a clot in a smaller vessel - lead to ischeamia of that beyond the vessel
haemorrhages
dilation of the vessel - aneurysm - rupture, mural thrombi

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7
Q

features of an atheromatous plaque

A

fibrous cap
cells - smooth muscle and inflammatory - foamy macrophages common feature
lipids
connective tissue and extracellular matrix
healing response - platelets can be found with the inflammatory cells

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8
Q

types of plaque

A

stable and unstable
stable - thick fibrous cap
unstable plaque - no thick cap - at risk of rupture/fissure, emboli +/- thrombosis
increased risk of a haemorrhage into the plaque

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9
Q

risk factors for atherosclerosis

A 
non modifiable
- increasing age 
- male
- family history 
- genetic abnormalities
modifiable
- hyperlipidaemia 
-hypertension
- smoking 
- diabetes
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10
Q

pathogenesis of atherosclerosis

A
  • response to injury hypothesis

chronic inflammatory response of arterial wall initiated by chronic endothelial injury

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11
Q

what is ischaemic heart disease

A

characterised by - myocardial ischaemia = imbalance between the supply and demand of the heart fro oxygenated blood
90% due to atherosclerosis of coronaries
remaining 10% due to congenital defects, anaemia, lng disease
can be aggrevated by :
- hypertrophy
- hypotension
- hypoxaemia
- increased heart rate

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12
Q

what increases the risk of developing ischaemia heart disease ( athersclerotic things)

A
  • no of vessels involved
  • distribution of the vessels
    the degree of narrowing of the vessels
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13
Q

how can you decrease the risk and effects of ischaemic heart disease

A

1) prevention: modification of the risk factors - smoking, hypercholesterolaemia, sedentry life style
2) therapeutic advances: new medications, CCU, angioplasty, stents, CABGs, improved control of arrythmias

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14
Q

4 syndromes associated with athersclerosis

A
  • MI
  • angina
  • chronic IHD
  • sudden cardiac death
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15
Q

what is the difference between angina and an MI

A

is cell death - no necrosis in angina
in MI - necrosis - myocyte necrosis, elevated enzymes - creatinine kinase, elevated cardiac specific proteins - troponins

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16
Q

what are the enzymes that rise in MI and how long for

A

creatinine kinase - rise within 4-8 hours and elevated for 3 days

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17
Q

what are the cardiac specific proteins that rise in MI and how long for

A

troponins - rise in 4-8 hours and last for 7-10 days

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18
Q

when does the stenosis of a vessel become critical

A

when it reaches less than 75% of the cross sectional area so compensatory vasodialtion is not enough to meet the demands

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19
Q

vessels that are involved

A

= proximal left anterior descending

  • proximal left circumflex
  • entire length of the RCA
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20
Q

where does the left anterior descending supply

A

septum; anterior, lateral and apical wall of the left ventricle; most of the left and right bundle branches; and the anterior papillary muscle of the bicuspid valve (left ventricle)

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21
Q

where does the left circumflex supply

A

most of the left atrium the posterior and lateral free wall of the left ventricle and part of the anterior papillary muscle

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22
Q

where does the right coronary artery supply

A 
right atrium and right ventricle
inf/post wall LV
posterior IV septum 
AV node 
SA node
23
Q

what are the most dangerous lesions

A

where there is 50-75% stenosis with a lipid rich core and a minimal fibrous cap - alone this is not enough to produce symtpmatic angina, but there is risk of acute plaque change -
also no development of colaterals and potentially a lack of preconditioning

24
Q

types of MI

A

transmural and subendocardial
- transmural is full thickness of the wall
usually associated with acute thrombosis/occlusion of the vessel
occasionally related to vasospasm or emboli
- subendocardial
inner 1/3 -1/2 of myocardium
may extend beyond the perfusion territory of a single artery
subendothelila zone is the least well perfused so most as risk when there is reduced coronary flow
usually critical stenosis but no acute plaque change

25
Q

How long after can you histologically see there has been an MI

A

4hours

26
Q

How long after can you see microscopically there has been an MI

A

12 hours

27
Q

What allows it to be seen earlier

A

Some dyes

28
Q

What can salvage the heart

A

Early reperfusion, thrombolysis

29
Q

What does earlier reperfusion do

A

Salvages sublethally injured myocytes and minimises infarct size, haemorrhage into the area

30
Q

What risk with reperfusion

A

Reperfusion injury

Induces a new element of injury due to free radicals

31
Q

Why might not the myocytes function for a few days

A

Stunned myocardium

So may not function

32
Q

What may be protective to the myocardium

A

Repetitive short lived ischamia may be protective
Preconditioning mechanisms
Collateral development

33
Q

Complications of MI

A

Contractile dysfunction - heart failure- cardiogenic shock
Arrhythmia
Myocardial rupture
- of the free wall - tamponade
- IVS left to right shunt
- papillary muscle - acute severe mitral regurgitation
Pericarditis early or several weeks (Dressler syndrome=autoimmune)
Mural thrombosis - at risk of embolising
Ventricular aneurysm
Papillary muscle dysfunction - MR
Progressive late heart failure

34
Q

Normal heart role and weight

A

Pump
250-300g female
300-350g males

35
Q

What is increased size weight called

A

Cardiomegaly

Hypertrophy

36
Q

Increased chamber size is

A

Dilated

37
Q

Role of cardiac myocytes

A

Cell of contraction

38
Q

What are the specialised myocytes for conduction

A

SAN
AVN
bundle of His

39
Q

Heart failure is also called

A

CCF
congestive cardiac failure
It is failure of the pump

40
Q

What are the adaptive mechanisms to prevent/ postpone failure

A
  • dilation - inc preload - frank starling mechanisms
  • hypertrophy - inc size of cardiac myocytes
  • activation of neural humoral mechanisms
    • NA released from adrenergic cardiac nerves
    • activation of RAA system
    • release atrial natriuretic peptide
41
Q

What causes heart failure

A

Usually due to systolic function - heart can’t contract enough
Occasionally due to diastolic function - chamber walls stiff and unable to stretch to allow filling with blood

42
Q

Left heart failure what happens

A

LV can’t pump to the body
Leading to organ ischaemia - impaired renal function
Pulmonary oedema due to back pressure

43
Q

What happens in right heart failure

A

RV can’t pump to the lungs
Leading to a back pressure in the body causing peripheral oedema
Congestion in the organs
As cites/ pleural effusion

44
Q

What is usually heart failure

A

Left
Right usually occurs secondary
Pure right heart failure income - cor pulmonale

45
Q

What is the response of the heart to increased demands

A

Inc pressure - left sided - systemic hypertension

Pulmonary hypertension - right sided cor pulmonale

46
Q

What does hypertension lead to

A

Hypertrophy

Adaptive response to pressure overload

47
Q

What can hypertrophy lead to

A

Myocardial dysfunction
Cardiac dilation
Congestive heart failure
Sudden death

48
Q

Diagnostic criteria for systemic hypertensive heart disease

A

Left ventricular hypertrophy (concentric)
History/pathological evidence of hypertension
Even prolonged mild hypertension can lead to hypertrophy

49
Q

Presentation of systemic hypertensive heart disease

A

Asymptomatic
ECG/echo - show increased size
Atrial fibrillation - left atrial enlargement
CCF

50
Q

What is the gross morphology of systemic hypertensive heart disease

A 
Circumferential LV hypertrophy 
No dilation of LV 
Inc heart weight
Thick wall
Thick wall = stiff --> impaired diastolic filling --> left atrial enlargement
51
Q

Histology of systemic hypertensive heart disease

A

Inc myocytes size
Increased nuclear size
Interstitial fibrosis

52
Q

What is cor pulmonale

A

Pulmonary hypertensive heart disease
Secondary to pulmonary hypertension
Is caused by a lung abnormality/lung vasculature abnormalities

Need to EXCLuDe pulmonary hypertension secondary to congenital heart disease
Diseases of the left side of the heart

53
Q

Acute cor pulmonale

A

Sudden increase in pulmonary blood pressure
E.g. Massive PE
–> marked dilation of the right ventricle
No hypertrophy

54
Q

Chronic cor pulmonale

A

Prolonged pressure overload

Right ventricular hypertrophy

Y3 (22 decks)

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