Histopathology 7: Vascular and cardiac pathology Flashcards

1
Q

Describe dressler’s syndrome ?

A

Pericarditis weeks-months after an M.I

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2
Q

What histological findings are seen < 6 hours post MI ?

A

normal histology

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3
Q

What histological findings are seen 6- 24 hours post MI ?

A
  • loss of nuclei
  • Homogenous cytoplasm
  • necrotic cell death
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4
Q

What histological findings are seen 1-4 days post MI ?

A

-infiltration of polymorphs and macrophages to clear debris

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5
Q

What histological findings are seen 5-10 days post MI ?

A

-debris cleared

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6
Q

What histological findings are seen 1-2 weeks post MI ?

A
  • granulation tissue
  • myelofibroblasts depositing collagen
  • revascularistation
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7
Q

What histological findings are seen weeks - months post MI ?

A

-scar tissue

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8
Q

What does Nutmeg liver indicate ?

A

hepatic cirrhosis most likely due to right sided heart failure

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9
Q

List 5 causes of dilated cardiomyopathy ?

A
  • Alcohol
  • post partum
  • sarcoidosis
  • Haemochromatosis
  • genetic: Duchenne’s muscular dystrophy
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10
Q

List 2 causes of Hypertrophic cardiomyopathy ?

A
  • Genetic

- storage diseases

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11
Q

List 3 causes of restrictive Cardiomyopathy ?

A
  • Sarcoidosis
  • Amyloidosis
  • Radiation
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12
Q

Which type of cardiomyopathy shows myocyte disarray ?

A
  • Hypertrophic
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13
Q

Describe what is meant by HOCM ?

A
  • Hypertrophic obstructive cardiomyopathy

- Septal hypertrophy leading to outflow tract obstruction

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14
Q

Crescendo - decrescendo murmur heard over the left lower sternal edge and bifid pulse.

Most likely diagnosis

A

HOCM

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15
Q

List 5 features of acute rheumatic fever ?

A

CASES

Carditis (pancarditis)
Arthritis 
Sydenham's chorea 
Erythema marginatum
Subcutaneous nodules
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16
Q

Which valve is most commonly affected by rheumatic fever ?

A

Mitral valve

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17
Q

What is the most common causative organism of rheumatic fever ?

A

Group A streptococcus (tonsillitis)

18
Q

Histology of the mitral valve and heart shows beady fibrous vegetations, Aschoff bodies and Anitschkov myocytes.

Most likely diagnosis ?

A

Rheumatic heart disease

19
Q

Which pathological mechanism leads to Rheumatic heart disease ?

A) Antigenic mimicry
B) Auto-immune
C) Inborn error of metabolism
D) Bacterial colonisation

A

A) antigenic mimicry

20
Q

Which type of endocarditis is associated with SLE ?

A

Libman-sacks endocarditis

caused by antigen-antibody complex deposition

21
Q

Which organism is the most common cause of acute infective endocarditis in IVDU ?

A

S.Aureus

22
Q

Which organism is the most common cause of subacute infective endocarditis ?

A

Strep. Viridans

23
Q

Which valve tends to be affected in IVDU with infective endocarditis ?

A

Right sided valves

24
Q

Which genetic syndrome is associated with bicuspid aortic valve ?

A

Turner’s syndrome

25
Q

Which valve disorder is associated with a mid systolic click and late systolic murmur ?

A

Mitral valve prolapse

26
Q

RF for atherosclerosis

A
age (40-60)
gender - postmenopausal women 
genetics
hyperlipidaemia
hypertension
smoking 
diabetes mellitus
27
Q

describe the pathogenesis of atherosclerosis

A

response to injury hypothesis - chronic inflammatory and healing response of the arterial wall to endothelial injury
endothelial injury - LDL accumulation in the intima
myocytes move to the intima - macrophages - foam cells
cytokine release + lipid accumulation
smooth muscle proliferation also important
GF - PDGF, FGF, TGF-alpha

fatty streak = earliest change

atherosclerotic plaques occur most at points of disturbed flow - ie where arteries branch

consequences = obstruction + rupture

28
Q

define critical stenosis

A

when demand>supply
occurs at around 70% occlusion
causes stable angina

29
Q

describe acute plaque change

A

rupture - exposes prothrombitic plaque contents
erosion - exposes prothrombotic subendothelial BM
haemorrhage into plaque - increases size

30
Q

describe IHD

A
leading cause of death worldwide
group of conditions resulting from myocardial ischaemia 
presents as:
- angina
- MI
- chronic ischaemic HD with HF 
- sudden cardiac death 

plaque sites:

  • first few cm of LAD or LCX
  • entire length of LCA
31
Q

what is ACS

A

stable plaque becomes unstable

generally leads to superimposed thrombus

32
Q

what is angina pectoris

A

transient ischaemia that does not produce myocyte necrosis
types = stable, prinzmetal, unstable
stable = no plaque disruption
prinzmetal = due to coronary artery spasm
unstable - disruption of plaque with a superimposed thrombus

33
Q

define MI

A

death of cardiac muscle due to prolonged ischaemia

  • myocardial blood supply compromised
  • loss of contractiliy within 60s
  • HF can preceded myocyte death
  • potentially reversible
  • irreversible after 20-30 mins

LAD > RCA > lateral LV

34
Q

describe histological changes post MI

A

under 6 hrs - nomal
6-24 - loss of nuclei, homogenous cytoplasm, necrotic cell death
1-4 days - infiltration of polymorphs then macrophages (clear up debris)
5-10 days - removal of debris
1-2 weeks - removal of granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
weeks - months - strengthening, decellularisisng scar

35
Q

cinical features of MI

A

10-15% asymptomatic (elderly, diabetes)

  • CK, troponins
  • 1/2 deaths within 1 hr

reperfusion injury - can cause stunned myocardium

hibernating myocardium - lower metabolusm

36
Q

complications of MI

A
contractile dysfunction - cardiogenic shock 
arrhythmia
myocardial rupture - can cause cardiac tamponade
pericarditis 
RV infarction 
infarct extension 
ventricular aneurysm 
papillary muscle rupture 
chronic ischaemic heart disease
37
Q

what is sudden cardiac death

A

unexpected death from cardiac causes in individuals without symptomatic heart disease
usually due to lethal arrhythmia

often caused by ischaemia-induced electrical instability

38
Q

featres of cardiac failure

A

congestive - both sides
left sided - SOB, pul oedema
right sided - peripheral oedemia, nutmeg liver

histology:

  • dilated heart
  • scarring and thinning of walls
  • fibrosis and replacement fo ventricular myocardium
39
Q

types of cardiomyopathy

A

dilated (too thin) - progressive loss of myocytes (idiopathic, infective, toxic, hormonal, genetic)

hypertrophic (too thick) - LVH, beta myosin heavy chain ab in some cases

restrictive (too stiff) - impaired ventricular compliance, normal size but big atria

40
Q

causes of cardiac valve disease

A

chronic rheumatic valvular disease - immune cross reactivity

  • almost always mitral
  • M>A>T>P
  • button holes

Calcified aortic stenosis - most common
- outflow obstruction

Aortic regurg
- caused by: rigidity (rheumatic, degenerative), destruction (microbial endocarditis), disease of AV ring (eg marfans)

Endocarditis - usually LS unless IV drug users

41
Q

difference between true and false aneurysm

A

true - all layers of the wall dilate
false - extravascular hematoma

causes: congenital (marfans), atherosclerosis, hypertension

dissection more common high up
lower more likely to rupture