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Year 5 Path Charis > Histopathology - CVD > Flashcards

Histopathology - CVD Flashcards

1
Q

Most important independent RF for atherosclerosis/ CVD

A

FHx

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2
Q

What is the role of the factor released after platelets adhere to the injured endothelium?

A

Intimal smooth muscle proliferation
ECM deposition
Fatty streak - mature atheroma + growth

PDGF, FGF, TGF-alpha implicated

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3
Q

Early atheroma arises in ___ epithelium

A

intact

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4
Q

What does endothelial damage cause

A

Increase in permeability
Altered gene expression
Adhesion

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5
Q

Where do atheromatous plaques form?

A

In areas where there is flow disturbance

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6
Q

What do we mean by acute plaque change?

A

 Rupture - exposes prothrombogenic plaque contents
 Erosion - exposes prothrombogenic subendothelial basement membrane
 Haemorrhage - into plaque (increases size)

 Majority of plaques which show acute change only show mild to moderate luminal stenosis prior to acute change not enough narrowing to cause ischaemia – therefore, there are numerous asymptomatic potential victims

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7
Q

Characteristics of vulnerable plaques

A
  • Thin fibrous cap
  • Lots of foam cells and extracellular lipid
  • Clusters of inflammatory cells
  • Few smooth-muscle cells
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8
Q

What causes sudden death in people with vulnerable palques?

A

Emotional stress

  • Adrenaline increases BP and causes vasoconstriction
  • Increases physical stress on plaque

• Circadian periodicity to sudden death (6am-noon)

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9
Q

What is IHD

A

Group of conditions arising from myocardial ischaemia

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10
Q

% of stenosis required for

stable
unstable
angina

A

stable - 75%

unstable - > 90%

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11
Q

In which coronary arteries are plaques mainly found?

A

First few cm of LCA, LCX

Entire length of RCA

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12
Q

What happens during ACS?

A

Stable plaque undergoes acute plaque change and a thrombus forms which increases occlusion

(due to rupture, erosion, haemorrhage)

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13
Q

Most common death in postmenopausal women

A

IHD

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14
Q

Coronary arteries affected during MI

A

LAD > RCA > LCx

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15
Q

During an MI when is there

loss of nuclei
necrotic cell death
infiltration by neutrophils and then macrophages
new blood vessel formation + collagen synthesis + granulation tissue + myofibroblasts

A

loss of nuclei
6-24h

necrotic cell death
6-24h

infiltration by neutrophils and then macrophages
1-4 DAYS

new blood vessel formation + collagen synthesis + granulation tissue + myofibroblasts
1-2 WEEKS

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16
Q

Gross change in the heart after an MI

1-18h
24h
3-4D
1-3W
3-6W
A

1-18h
No change

24h
Pale, edema
inflammation, edema

3-4D
Haemorrhage
necrosis

1-3W
thin yellow
granulation tissue

3-6W
tough white
fibrosis

17
Q

Temporal sequence in the appearance of cells infiltrating a MI

A

neutrophils –> macrophages –> angioblasts –> fibroblasts + collagen

18
Q

What is a reperfusion injury

A

reversible cardiac failure post MI lasting a few days
arrhythmias

due to oxidative stress, Ca overload, inflammation

19
Q

What is hibernating myocardium?

A

Chronic sublethal ischaemia –> lower metabolism in myocytes

reversed with revascularisation

20
Q

Myocardial rupture post MI which places are the most common

A

free wall > septum > papillary muscle

21
Q

What is a mural thrombus and why is it dangerous?

A

 Infarct expansion – necrotic muscle stretches -> mural thrombus

can form a clot that can fly out in the heart –> clots/emboli from ventricular aneurysm can also block other capillaries/arteries in the body (e.g. bowel ischaemia, stroke, embolic damage to other organs)

rupture can lead to hemopericardium

22
Q

MI complications

A 
o	Complications (DARTH VADER)
	D	Death				
	A	Arrhythmia			
	R	Rupture (papillary muscle)		
	T	Tamponade			
	H	Heart Failure	
V	Valvular disease
A	Aneurysm of ventricle	
D	Dressler’s syndrome (pericarditis; 2nd or 3rd day)
E	Embolism (i.e. bowel ischaemia) 
R	Recurrence
23
Q

Chronic IHD w HF causes

A

previous MI or previous ischaemic myocardial damage e.g. severe obstructive coronary artery disease

24
Q

Define sudden cardiac death

A

o “Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1 hour) after onset of symptoms”

 Usually due to lethal arrhythmia (from ischaemia-induced electrical instability)

 Usually on background of IHD (90%)

 Acute myocardial ischaemia is usual trigger

 Usually causes electrical instability at sites distant from conduction system (near scars from old MIs)

50% have plaque rupture
10% non atherosclerotic cause e.g. long QT

25
Q

Commonest cause of left sided HF

A

RHF

26
Q

HF pathlogy

A

dilated myocardium

scarring
thinning of the wall
fibrosis + replacement of ventricular myocardium

27
Q

LHF

A

SOB

pulmonary oedema

28
Q

RHF

A

NUTMEG liver

peripheral oedema

29
Q

Restrictive HF

causes
heart size

A

idiopathic or secondary to heart disease (amyloidosis, sarcoidosis)

normal heart size
big atria

impaired ventricular compliance - heart is too stiff

30
Q

Order with which valves are affected in rheumatic heart disease

A

mitral > aortic > tricuspid > pulmonary

almost always MS

31
Q

rheumatic heart disease pathophysilogy

A

thickening of valve leaflet esp. along lines of closure

fusion of commissures

shortening, fusion, thickening of chordae tendineae

32
Q

commonest cause of AS

A

Calcification

33
Q

Causes of AR

A

Rigidity - rheumatic heart disease, degeneration

destruction -IE

disease of aortic valve ring (dilation means valve insufficient to cover increased area)

marfan’s
ankylosing spondylitis
dissecting aneurysm
syphilitic aortitis

34
Q

True vs false aneurysm

A
  • True – all layers of the wall
  • False – extravascular haematoma

https://as2.ftcdn.net/v2/jpg/03/02/87/29/1000_F_302872912_nIgwYTdh9ARRvW1OFPVmNO4xLJ1sePDI.jpg

35
Q

Causes of aneurysms

A

• Causes – weak wall of large arteries
o Marfan’s
o Atherosclerosis
o Hypertension

Year 5 Path Charis (44 decks)

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