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YEAR 5: Histopathology - PK Edited > Histo: Vascular and Cardiac Pathology > Flashcards

Histo: Vascular and Cardiac Pathology Flashcards

(56 cards)

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1
Q

What is atherosclerosis?

A

A disease characterised by atheromatous deposits in and fibrosis of the inner layer (tunica intima) of arteries

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2
Q

List some risk factors for atherosclerosis.

A
  • Age
  • Gender
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
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3
Q

Outline the pathogenesis of atherosclerosis.

A
  • Endothelium gets injured and *LDLs accumulate in the tunica intima
  • LDLs oxidised causing inflammation
  • Macrophages consuming fat to become foam cells
  • Apoptosis of foam cells causes inflammation and cholesterol core of plaque
  • Platelet adhesion makes the issue worse, smooth muscle cells are accumulated and form the fibrous cap
  • Lipid accumulates and the plaque grows

plaque has three principle components:
- Cells (smooth muscle, macrophages and leukocytes)
- ECM including collagen
- intracellular and extracellular lipid

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4
Q

What is a fatty streak?

A
  • Earliest change in atherosclerosis
  • Lipid filled foamy macrophages deposit in the intima but they do not disturb flow

NOTE: presence in pretty much everyone > 10 years old

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5
Q

What is critical stenosis?

A

When oxygen demand is greater than supply

This occurs at around 70% occlusion and causes stable angina

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6
Q

List three types of acute plaque change.

A
  • Rupture - exposes prothrombogenic plaque contents
  • Erosion - exposes prothrombogenic subendothelial basement membrane
  • Haemorrhage into plaque - increases size
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7
Q

In which patients does acute plaque change tend to happen?

A

Patients with mild-to-moderate atheroma (large plaques tend to be very stable)

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8
Q

List some features of vulnerable plaques.

A
  • Lots of foam cells and extracellular lipids
  • Thin fibrous cap
  • Few smooth muscle cells
  • Adrenaline increases BP and causes vasoconstriction
  • Circadian rhythm (more likely to have an infarct in the morning)
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9
Q

List the possible presentations of ischaemic heart disease.

A
  • Angina pectoris
  • MI
  • Chronic ischaemic heart disease with heart failure
  • Sudden cardiac death
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10
Q

What are the most common sites for atheromatous plaques within the coronary circulation?

A
  • First few centimetres of the LAD and left circumflex
  • Entire length of right coronary artery
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11
Q

What is angina pectoris?

A

Transient ischaemia that does not produce myocyte necrosis

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12
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

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13
Q

Outline the pathogenesis of myocardial infarction.

A
  • Sudden change in plaque
  • Platelet aggregation
  • Vasospasm
  • Coagulation
  • Thrombus evolves
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14
Q

What is the most common cause of death in post-menopausal women?

A

Myocardial infarction

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15
Q

Outline the myocardial response to plaque rupture.

A
  • Loss of contractility occurs within 60 seconds
  • So, heart failure may precede myocyte death (so patients could get an arrhythmia and die before any histological changes take place)
  • Irreversible after 20-30 mins
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16
Q

Which arteries tend to be involved in myocardial infarction (in order of most to least frequent)?

A
  • LAD - 50%
  • RCA - 40%
  • LCX - 10%
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17
Q

Describe the microscopic changes that take place in myocardial infarction.

A
  • Under 6 hours - normal histology
  • 6-24 hours - loss of nuclei, homogenous cytoplasm, necrotic cell death
  • 1-4 days - infiltration of polymorphs then macrophages
  • 5-10 days - removal of debris
  • 1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
  • Weeks to months - strengthening and decllularising the scar
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18
Q

What is reperfusion injury?

A
  • Consequence of letting blood go back into the area of myocardial necrosis
  • Oxidative stress, calcium ovrload and inflammation caus further injury
  • Arrhythmias are common
  • It can cause stunned myocardium - reversible cardiac failure lasting several days
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19
Q

What is hypernating myocardium?

A
  • Chronic sublethal ischaemia leads to lower metabolism in myocytes which can be reversed with vascularisation
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20
Q

List some complications of MI.

A

DARTH VADER

Death

Arrythmia

Rupture

Tamponade

Heart failure

Valve disease

Aneurysm

Dressler’s (chest pain, fever, pericarditis, pleural effusion - weeks/months after MI)

Embolism

Recurrence

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21
Q

What is the 1-year mortality after an MI?

A

30%

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22
Q

What is chronic ischaemic heart disease?

A

Progressive heart failure due to ischaemic myocardial damage

NOTE: there may be no prior infarction, usually due to atherosclerosis

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23
Q

What is sudden cardiac death?

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A

Unexpected death from cardiac causes in individuals without symptomatic heart disease or early after the onset of symptoms (e.g. 1 hour)

Usually due to lethal arrhythmia (ischaemi-induced electrical instability)

24
Q

List some causes of heart failure.

Study These Flashcards
A
  • Ischaemic heart disease
  • Valve disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
25
List some complications of heart failure.
* Sudden death * Arrhythmias * Systemic emboli * Pulmonary oedema with superimposed infection
26
Outline the histology of heart failure.
* Dilated heart * Scarring and thinning of the walls * Fibrosis and replacement of ventricular myocardium
27
What are cardiomyopathies?
Intrinsic problems of the heart muscle
28
What is dilated cardiomyopathy?
Caused by progressive loss of myocytes leading to a dilated heart
29
List some causes of dilated cardiomyopathy.
* Idiopathic * Infective * Toxic (e.g. alcohol) * Hormonal * Genetic (e.g. haemochromatosis) * Immunological (e.g. myocarditis)
30
What is hypertrophic cardiomyopathy?
* Thickening of the heart muscle * Family history in 50% of cases NOTE: some are associated with a specific abnormality in the beta-myosin heavy chain
31
What is restrictive cardiomyopathy?
* Impaired ventricular compliance * Results in a normal sized heart with big atria
32
What is chronic rheumatic valvular disease caused by?
Caused by immune cross-reactivity with cardiac valves
33
Which valve is most commonly affected in rheumatic valvular disease?
Left-sided valves (almost always mitral)
34
What is the most common cause of aortic stenosis?
Calcified aortic stenosis
35
List some causes of aortic regurgitation.
* Rigidity (rheumatic, degenerative) * Destruction (endocarditis) * Disease of the aortic valve ring (dilatation, dissectin, Marfan's, syphilis, ankylosing spondylitis)
36
Which valves are most commonly affected by endocarditis?
Left-sided valves (unless you are an IVDU)
37
What are the two different types of true aneurysms?
Fusiform Saccular
38
What is Dressler's syndrome?
It consists of fever, pleuritic pain, pericarditis and/or pericardial effusion. Happens weeks-months following MI
39
Compensatory mechanisms for heart failure?
Activation of RAS to increase BP Activation of sympathetic nervous system to increase TPR
40
Symptoms of LV failure
Lung problem
41
causes of RV failure symptoms of RV failure
commonly due to LV failure but can be from chronic severe pulmonary hypertension nutmeg liver peripheral oedema ascites
42
Ix for heart failure
BNP/NT-proBNP CXR ECG Echo
43
Inheritance of HCM + gene
Autosomal domiant Beta myosin gene
44
What is acute rheumatic fever
Untreated strep throat/scarlet fever/impetigo Develops 2-4w after the strep throat infection Occurs at 5-15y, affecting: - heart (pancarditis - endocarditis, myocarditis, pericarditis) - joints (arthritis, synovitis) - skin (erythema marginatum) - CNS (encephalopathy)
45
Explain the criteria for rheumatic fever
Jones' Major Criteria Diagnosis: Group A strep + 2 majors or 1 major + 2 minors MAJOR CRITERIA- CASES Carditis Arthritis Sydenham's chorea Erythema Marginatum Subcutaneous nodules MINOR CRITERIA Fever Raised ESR/CRP Migratory Arthralgia Prolonged PR Previous rheumatic fever Malaise Tachycardia EVIDENCE OF GAS INFECTION Positive throat culture Elevated ASO titre
46
Which valves do rheumatic fever affect? What about in IVDU?
Mitral valve only (70%) Mitral and aortic (25%) Then right sided valves (tricuspid and pulmonary)
47
What is the main pathogen for rheumatic fever valve vegetation? And what is the pathophysiology
Lancefield group A strep Antigenic mimicry - cross reaction of anti-strep antibodies with heart tissue
48
Histology of rheumatic fever valve vegetation?
Beady fibrous vegetation (**verrucae**), **Aschoff Bodies** (small giant-cell granulomas), **Anitschkov myocytes**
49
Treatment for rheumatic fever?
Benzylpenicillin or erythromycin if pericillin-allergic
50
Pathogens for acute and subacute infective endocarditis?
Acute - staph aures (30-45%) or strep pyogenes Subacute - strep viridans, staph epidermis
51
Immune vs thromboembolic phenomenon of infective endocarditis?
Immune - roth spots - oslers nodes - haematuria due to glomerulonephritis Thromboembolic - Janeway lesions - Septic abscess - splinter haemorrhages - splenomegaly
52
What is the diagnosis - nonspecific FLAWS symptoms and haematuria
infective endocarditis
53
What criteria for infective endocarditis and explain it
Duke's criteria, diagnosis by: - 2 major - 1 minor + 3 major - 5 minor MAJORS - positive blood culture growing typical IE organisms or 2 positive cultures for something >12hrs apart - evidence of vegetation/abscess on echo or new regurigtant murmur MINORS - risk factor for it - fever >38 - Thromboembolic phenomenon - Immune phenomena - +ve blood cultures but not meeting major criteria
54
order the valves in order of most likely to be affected by chronic rheumatic fever
Mitral > aortic > tricuspid > pul
55
What is beck's triad and what does it indicate
Pericardial effusion Muffled heart sounds, raised JVP, hypotension
56
Causes of pericarditis
Viral and idiopathic (90%)

YEAR 5: Histopathology - PK Edited (29 decks)

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