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Cardiology > pathophysiology of acs > Flashcards

pathophysiology of acs Flashcards

1
Q

acs with st elevatoon?

A

troponin & ck elevated

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2
Q

nonstemi?

A

troponin elevated or not

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3
Q

coronary artery disease?

A

Most commonly due to coronary artery atheroma
Other coronary artery diseases:
Coronary artery spasm
Arteritis
Embolism
Congenital anomaly
Coronary artery dissecting aneurysm
Syphilitic aortitis

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4
Q

aha type 1?

A

non specific intimal thickening

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5
Q

aha type 2. fatty streaks

A
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6
Q

ulcerated complicated plaque?

A

thrombosis of plaque, involvement of media, thrombus

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7
Q

3 mechhanisms of atheroma occlusion?

A
  1. Thrombosis on complicated atheroma
  2. Haemorrhage into plaque
  3. Rupture of “vulnerable plaque”
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8
Q

recanalised thrombus?

A

Recanalized thrombus
End-stage of a thrombus. The blood clot (thrombus) is replaced by connective tissue with many newly formed channels. If these channels reestablish the continuity of the original vessel, blood may flow at a rate adequate to maintain perfusion. Note calcification

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9
Q

haemorrhage into plaque?

A

bleeding in the moddle of a plaque

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10
Q

ruptureof vulnerable plaque?

A

Stable plaque
Vulnerable plaque

Concept of remodelling

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11
Q

stable plaque?

A

thick fibrous collagen cap, few inflammatory cells

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12
Q

vulnerable plaque?

A

Loss of collagen and smooth muscle= thin fibrous cap Inflammation-

matrix degrading proteases
Weaken fibrous cap

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13
Q

glagov phenomenon?

A

Positive remodelling outward = compensatory remodeling : Glagov phenomenon
lumen diameter retained. no angina. thin fibrous cap

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14
Q

negative remodelling?

A

negative remodelling no dilatation

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15
Q

angina?

A

more than 70% narrowing

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16
Q

Stary Fuster classification

A
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17
Q

growing of arterial brnaches in atherosclerosis to accomodate?

A

adventitial vasa-vasorum

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18
Q

macrophage quantification score

A

score 0 - <5 macs

Score 1 - 6-25 macs

Score 2 - >25 macs

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19
Q

signs of intra plaque hemorraheg?

A

lipid core hemorrhage

re blood cells and fibrin

erythrocytes

inflammation

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20
Q

intraplaque hemorraheg?

A

Conversion of a stable, asymptomatic lesion to an unstable, ruptured plaque involves many processes, the most studied of which is inflammation, cellular breakdown, and expansion of the acellular, lipid rich, necrotic core.
Commonly believed that death of macrophages and SM foam cells, in addition to the aggregation of lipoproteins, contribute to the accumulation of extracellular free cholesterol within unstable plaques.
Intraplaque hemorrhage plays a role in the expansion of core of plaques though the relative importance of this vs. other mechanisms by which plaque burden increases is uncertain

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21
Q

how does the vessel respond to a plaque formation?

A

As plaque accumulates, the arterial wall often reacts by remodeling. As atherosclerosis progresses toward the more severe stages pictured on the right, the lumen remains constant because of compensatory expansion of the arterial wall. Eventually, however, in more severe stages of the disease, the artery is unable to expand further and the lumen begins to narrow.
The same process may work in reverse with disease regression. That is, plaque can be removed from the arterial wall with little change in lumen size. Therefore, the mildly narrowed lumen may be a less sensitive marker for the progression or regression of disease than direct estimates of plaque size.

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22
Q

postivie remodelling?

A

EEM and contour increases and allows the plaque to push against the walls and keep the luemn enlarged. I.E. plaque isn’t a [problem.

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23
Q

negative remodeling?

A

as he plaque grows the walls cave in and the lumen narows. looks like a christmas cracker (narrowing of arterial wall in places

24
Q

remodeling properties?

A

Plaques with Remodeling
More Macrophages
More Lipid-rich Atheroma
Less Collagen
Less Smooth Muscle Cells
More Metalloproteinases (MMP 2 and MMP-9)

25
Q

unstabe and stable

A

more positive remodeling in unstable, and more negative remodeling in stable

26
Q

ruptue

A

The Thin Cap Fibroatheroma (TCFA) has been identified as being often the atheromatous lesion responsible for an acute coronary event

27
Q

components of thin-cap atheroma?

A
28
Q

types of plaques?

A

fibrous atheroma

thin cap

hemorrhage

ruptur

heled rupture

29
Q

morphological change

A
30
Q

vulnerable plaque, what we do not know

A

We do not know the length or the circumference of a thin cap nor the volume of the necrotic core that will lead to rupture
We do not know the density of macrophages needed to cause a rupture if rupture is mainly determined by macrophage infiltration.
We do not know the quantity or the density of vasa vasorum that may predict rupture
We do not know the clinical or morphologic or hemodynamic parameters that will lead to rupture ?
There are no established laboratory methods of how to recognize a vulnerable lesion and therefore no longitudinal epidemiologic studies are available that identify vulnerable lesion are likely to rupture and at what time.
There is no proof today that a thin cap fibroatheroma (as defined today) will definitely rupture
Above all no good animal models of vulnerable plaque exist.

31
Q

what we know abot plaques?

A

Definition (based on ruptured plaques)
Frequency is higher in AMI than SCD, males than females
Higher prevalence in the presence of high TC, low HDL-C, high TC/HDL-C ration, high hs CRP (>3.2 mg/dl)
Location in SCD, proximal and mid LAD, RCA, and LCX
Length 2-22 mm (mean 8 mm)
% luminal narrowing (80% of TCFAs occur in lesions <50% diameter stenosis)
% necrotic core is <25% of plaque area in 70% of TCFAs
Calcification is not a marker of TCFA

32
Q

coronary stenosis and risk?

A

Plaques with >70% stenosis have a greater numerical probability of causing events than non haemodynamically significant lesions, but since there are vastly more mild, even non angiographically visible plaques than severe lesions, this leads to the observation that a mild lesion is more likely to cause sudden occlusion
Acute coronary syndrome more often results from rupture of a vulnerable plaque with thrombosis in mild <60% stenosis
Large lipid core, thin fibrous cap, inflammation
Rupture may be precipitated by isometric exertion

33
Q

advanced, obstructive disease: healed plaque rupture?

A
34
Q

development of athrosclerosis?

A
35
Q

medical treatet aimed at?

A

Medical treatment is aimed at
reducing lipid (LDL)
Stabilise plaque reducing inflammation
increasing collagen in fibrous cap

36
Q

distriobution of MI withi the heart?

A 
Regional (90% of cases)
 Diffuse subendocardial (10%)
37
Q

regional MI?

A

Regional (90% of cases)
Transmural
Wedge-shaped

Left ant. descending (LAD) cor. art. 50%
Right main cor. art. 30%
Circumflex cor.art. 20%

38
Q

diffuse MI?

A

Diffuse subendocardial (10% of cases)

No coronary thrombus
Partial stenosis of 2-3 coronary arteries
Associated with hypotension & left ventricular
hypertrophy

39
Q

left coronary artery occlusion

A

massive antero-lateral MI

40
Q

left anterior edscending coronary artery

A

antero-septal MI

41
Q

right coronary artery

A

postrerior inferiro MI

42
Q

circumflex coronary artery occlusion?

A

lateral MI

43
Q

sbendocardial MI?

A

inner 1/3

44
Q

when does a regional subendocardial MI occur?

A

if flow is restored after occlusion (rest of tissue is saved, only 1/3 of the inner wall affected).

45
Q

massive subendocardial MI around all of te left ventricle endocardium?

A

Severe stenosis of all arteries
Acute (hypotension sudden anaemia/shock)= infarction

46
Q

cronic subendocardial MI?

A
47
Q

myocardial changes after MI?

A

Muscle necrosis (SOFTENING)
Acute inflammatory response
REPAIR of defect in heart wall
Demolition of dead tissue by macrophages
Organisation of necrotic area
Repair by GRANULATION TISSUE
END RESULT = HEALING BY SCARRING

48
Q

changes after 0-12hr of MI?

A

ischemia/necrosis of muscle

macro-no macro changes

micro - intercellular oedema, subtle change in colour of fibres

49
Q

changes after 6-12 hrs?

A

muscle fibre eosinophilia oedema

50
Q

chages after I 12-24 hr?

A

macro- pale with small haemorrhages blotchy

micro- oedema, fibre eosinophilia, focal haemorrhage, few neutrophils

51
Q

microscpy 12-24 hr

A

necrosis, oedema, neutrophils

52
Q

changes after MI 24-72 hr?

A

necrosis, inflammation

maro- soft and plae

micro-muscle fibre necrosis, acute inflmmation

53
Q

microscopy 24-72hours?

A

necrosis, oedema, neutrophils

54
Q

changes after MI - 3-10 days

A

organisation of infart begins - ingrowth of new vessels

macro- pale area with red hyperaemic border

micro-necrosis, demolition, granulation tissue at edge

55
Q

chages after MI - 10+ days?

A

macro- white fibrous scar

Micro-vascular collagenous scar

later- avascular scar

Cardiology (23 decks)

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