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Histopathology > Histopathology 6 - Vascular and Cardiac pathology > Flashcards

Histopathology 6 - Vascular and Cardiac pathology Flashcards

1
Q
  • Progression of an atheroma:
A
  1. Raised lesion which projects into the lumen (preceded by fatty streak)
  2. Soft lipid core
  3. White fibrous cap
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2
Q

Recall the 7 steps of atheroma pathophsyiology

A
  1. Endothelial injury - this happens because of the risk factors discussed later. Turbulent blood flow due to hypertension etc also contributes
  2. LDL enters intima and gets trapped in intimal space
  3. LDL is converted into oxidised LDL –> inflammation
  4. Macrophages take up OxLDL via scavenger receptors –> foam cells
  5. Foam cell apoptosis –> inflammation and cholesterol deposition to form plaque core
  6. Endothelium expresses more adhesion molecules –> more macrophages and T cells enter plaque
  7. VSMCs form fibrous cap
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3
Q

What % atheroma of a vessel lumen is considered ‘critical stenosis’?

A

70%

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4
Q

What is prinzmental angina?

A

Coronary artery spasm

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5
Q

Which parts of the cardiac muscle are affected by an infarction of the LAD?

A

Anterior wall of left ventricle, anterior septum and apex

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6
Q

Which parts of the cardiac muscle are affected by an infarction of the RCA?

A

Posterior wall of left ventricle, posterior septum and posterior wall of right ventricle

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7
Q

Which parts of the cardiac muscle are affected by an infarction of the LCx?

A

Lateral wall of left ventricle

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8
Q

What are the 4 most important complications of MI?

A
  1. Contractile dysfunction (eg cardiogenic shock)
  2. Arrhythmia >> most common cause of acute death after MI
  3. Myocardial rupture >> can result in cardiac tamponade
  4. Pericarditis
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9
Q

What is Dressler’s syndrome?

A

Pericarditis occuring weeks-months post-MI

autoimmune

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10
Q

What is the average time between MI and myocardial rupture?

A

4-5 days

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11
Q

What is the prognosis of papillary muscle rupture following MI?

A

Rubbish - very high mortality

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12
Q

What is the most common cause of sudden cardiac death?

A

Lethal arrhythmia

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13
Q

What is restrictive cardiomyopathy + causes

A

Normal size heart but with large atria - due to amyloidosis + sarcoidosis

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14
Q

Recall 3 possible causes of aortic regurgitation

A

MAIN CAUSE: RHEUMATIC FEVER

Infective endocarditis
Marfan’s
Ankylosing spondylitis

  • Rigidity- rheumatic, degenerative
  • Destruction- microbial endocarditis
  • Disease of the aortic valve ring
    • Dilation means the valve leaflets are insufficient to cover the increased area
    • Marfan’s syndrome
    • Dissecting aneurysm
    • Syphilitic aortitis
    • Ankylosing spondylitis
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15
Q

What is Monckeberg atherosclerosis?

A

Focal calcification of the media of small-medium sized vessels; no associated inflammation

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16
Q

What histological findings would be found within 6 hours of an MI?

A

Normal histology and normal CK-MB

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17
Q

What histological findings would be found 6 -24 hours following an MI?

A

Loss of nuclei
Homogenous cytoplasm
Necrotic cell death

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18
Q

What histological findings would be found 1-4 days following an MI?

A

Infiltration of polymorphs (monocytes + lymphocytes) and macrophages

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19
Q

What histological findings would be found 5-10 days following an MI?

A

Removal of debris

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20
Q

What histological findings would be found 1-2 weeks following an MI?

A

Granulation tissue
New blood vessels
Myofibroblasts
Collagen synthesis

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21
Q

What histological findings would be found in the months following an MI?

A

Strengthening, de-cellularising scar tissue

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22
Q

Recall the possible complications of MI

A

Mnemonic = PACE MAKERED

Papillary muscle dysfunction/rupture >> mitral regurgitation
Arrhythmia >>> most common cause of acute death after MI
Ccf
Effusion (pericardial)

Mural thrombus
Aneurism (ventricular) >> late complication
(K)ontractile dysfunction >> cardiogenic shock secondary to reduced contractility
Early pericarditis
Rupture of venticular wall/myocardial rupture >> cardiogenic shock

  • most common- free wall
  • septum- less common: VSD + right to left shunt
  • papillary mscule: mitral regurgitation

Elevation of ST segment
Dressler’s syndrome

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23
Q

What types of cardiomyopathy can be caused by sarcoidosis?

A

Dilated

more commonly restrictive

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24
Q

Which type of cardiomyopathy is associated with alcohol misuse?

A

Dilated

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25
Q

Is the pathology of cardiomyopathy systolic or diastolic dysfunction in

a) dilated CM
b) hypertrophic CM
c) restrictive CM?

A

Dilated: systolic

Hypertrophic and restrictive: diastolic

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26
Q

What is the HOCM?

A

Hypertrophic obstructive CM = septal hypertrophy + Thickening of the heart muscle, usually left ventricular hypertrophy

resulting in an outflow tract obstruction: narrowing of the LV outflow tract

offen causes sudden death

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27
Q

What mutation is associated with Hypertrophic CM?

A

Beta-myosin heavy chain

  • autosomal dominant

(Beta-HMC - HMC is HCM rearranged)

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28
Q

Recall the major criteria for Rheumatic fever diagnosis

A

CASES
Carditis
Arthritis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules

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29
Q

What is the main pathogen in rheumatic fever?

A

Lancefield group A strep

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30
Q

How is ‘antigenic mimicry’ involved in rheumatic heart fever?

A

Cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens

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31
Q

How are vegetations seen on heart valves in rheumatic fever described?

A

Small and warty, “verrucae”

beady vegestations,

Aschoff bodies (small giant- cell granulomas),

Anitschkov myoocytes (regenerating myocytes)

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32
Q

What is Libman-Sacks endocarditis

A

Unknown pathogenesis - associated with SLE and anti-phospholipid syndrome

NON-INFECTIVE form of endocarditis >>> inflammatory endocarditis

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33
Q

Differentiate the likely causative organisms in acute vs subacute infective endocarditis

A

Acute: Staph aureus/ pyogenes

Subacute: strep viridans/ epidermis/ HACEK/ coxiella/ candida/ mycoplasma

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34
Q

Recall the major and minor Duke criteria for infective endocarditis

A

Major:

  • Pos BC growing typical IE organism OR 2 pos BCs >12hrs apart
  • Evidence of vegetation/ abscess on echo or new regurgitant murmur

Minor:

  • RF: e.g. prosthetic valve, IVDU, congenital valve abnormalities
  • Fever >38
  • Thromboembolic phenomena:
  • Janeway lesions
  • Septic abscesses in lungs/ brain/ spleen/ kidney
  • Microemoboli
  • Splinter haemorrhage
  • Splenomegaly
  • Immune phenomena:
  • Roth spots
  • Osler’s nodes
  • Haematuria due to glomerulonephritis
  • Pos BCs not meeting major criteria
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35
Q

How many of Duke’s criteria are needed for diagnosis of infective endocarditis?

A

2 major

1 major and 3 minor

5 minor

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36
Q

What abnormality in the mitral valve might be caused by rheumatic fever vs IE?

A

RhF: mitral stenosis

IE: mitral regurgitation

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37
Q

How many deaths are caused by coronary heart disease?

A

men under 75: 25%

women under 75: 16%

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38
Q

Where in the world is ischaemic heart disease increasing?

A

Japan - because of increase in adoption of the western diet

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39
Q

Definition of atherosclerosis?

A

Arteriosclerosis charactersed by atheromatous deposits in and fibrosis of inner layer of the arteries

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40
Q

Risk factors for atherosclerosis

A

Unmodifiable

  • genetics - family history is the largest risk factor i.e. familial hypercholestrolaemia
  • age - increasing age
  • gender - postmenopausal women at higher risk

Modifiable

  • smoking
  • hyperlipidamiea
  • hypertension
  • diabetes mellitus

Risk factors are multiplicative

Other risk factors: (commonly in those without any of the above risk factors)

  • Inflammation
  • Hyperhomocysteinaemia
  • Metabolic syndrome
  • Lipoprotein (a)
  • Haemostasis (procoagulation)
  • Lack of exercise
  • Stress
  • Obesity
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41
Q

important studies

A
  1. framingham heart study
  2. atherosclerosis risk in communities study
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42
Q

What age group is most likely to get MIs?

A

40-60

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43
Q

What is the earliest change in atherosclerosis? What is it?

A

Fatty streak

  • lipid filled foamy amcorphages
  • don’t obstruct lumen flow
  • seen in children above the age of 10
    *
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44
Q

What is an atheroscleortic plaque?

A
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45
Q

What is the main difference between fatty streak and atherosclerotic plaque?

A

Fatty streak - no disturbance to blood flow

Atherosclerotic plaque: disturbs blood flow

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46
Q

Where in arteries do atheroscleortic plaques tend to occur?

A

At branch points where there is turbulent blood flow

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47
Q

What are the two main consequences of atheroma?

A

1. obstruction of lumen - stenosis

>70% of occlusion/diameter of <1mm –> critical stenosis–> stable angina –> chronic ischaemic heart disease

(crtical stenosis- demand outgrows the supply)

2. acute plaque change

a) rupture - exposes prothrombogenic plaque contents
b) erosion - exposes prothrombogenic subendothelial basement membrane
c) haemorrhage into the plaque - plaque therefore gets bigger >>>artery occlusion, subsequent ischaemia and death)

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48
Q

Who does acute plaque change occur in?

A

Can occur in people with mild-moderate stenosis so lots of asymptomatic people with risk of plaque rupture

i.e. plaque does not have to be big to undergo these acute changes : big ones are usually quite stable

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49
Q

What makes plaques vulnerable to rupture

A
  • Lots of foam cells or extracellular fluid
  • Thin fibrous cap
  • Few smooth muscle cells
  • Clusters of inflammatory cells
  • Adrenaline increases blood pressure and causes vasoconstriction
    • which leads to increased physical stress within the plaque
    • Therefore, emotional stress can increase the risk of sudden death
  • anything that causes vasoconstriction
    • Adrenergic agonists
    • Platelet contents
    • Reduced endothelial relaxing factors
    • Mediators from perivascular cells
  • Circadian rhythm
    • more likely to infarct in the early morning (6am- noon)
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50
Q

When are you most likely to have an infarction?

A

6 am to noon

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51
Q

WHat % of IHD is caused by atherosclerosis?

A

90%

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52
Q

What % stenosis do you need for pain on rest?

% needed for pain on exercise?

A

90%

75%

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53
Q

What causes acute coronary syndromes?

A

When stable plaque becomes unstable

This happens because of rupture, erosion or haemorrhage

Generally leads to superimposed thrombus which occludes the lumen further

54
Q

Types of angina

A

Stable - comes on with exertion and relieved on rest: no plaque disrupion

Unstable - more frequent and longer lasting pain. present at rest or with lower levels of activity. Due to plaque disruption with superimposed thrombus. Impending MI.

Prinzmetal: due to coronary artery vasospasm - uncommon

55
Q

What does Non‐reperfused MI show?

A

Typical ischaemic coagulative necrosis

56
Q

How quickly does loss of contractility occur after plaque rupture?

A

Within 60 seconds

heart failure can precede myocyte death (so they could get an arrhythmia and die before any histological changes take place

57
Q

When does heart failure occur in relation to myocyte death and what is the consequence of this?

A

Heart failure can precede myocyte death - because loss of contractility occurs within 60 seconds of plaque rupture

This means patient can die before any histological changes take place

58
Q

When does MI become irreversible?

A

It is reversible before myocyte death occurs

Once myocyte death occurs it becomes irreversible - usually within 20-30 mins

**obviously, if the patient hasn’t already died before myocyte death occured…*

59
Q

Which coronary artery is most affected by MI?

A

LAD - 50%

RCA - 40%

LCx- 10%

60
Q

Changes wthin first 6 hours of MI

A

Normal histology

Normal CK-MB

61
Q

What happens 6-24 hours post MI?

A
  • loss of nuclei
  • homogenous cytoplasm
  • necrosis
62
Q

What happens 1-3 days post MI?

A
  • polymorph cells infiltrate (moth-eaten neutrophils eating the damaged myocardium)
  • loss of nuclei and striations
  • coagulative necrosis
63
Q

What happens 1-2 weeks following MI?

A

Granulation tissue

New blood vessels

Myofibroblasts

Collagen synthesis

Over time, macrophages appear

64
Q

What happens weeks-months after MI?

A

STrengtheining

decellularising scar formation

65
Q

WHich type of MI does not cause ST changes?

A

Subendocardial infarct - does not affect the full thickness

66
Q

Which factors cause worse prognosis from MI?

A
  • age
  • female
  • DM
  • previous MI
67
Q

When do half of deaths from MI occur?

A

Within an hour

68
Q

Why does reperfusion injury occur?

A

Reperfusing blood to area of died cardiac cells>>>> oxidative stress, calcium overload and inflammation can cause further injury>>> can lead to arrythmias etc.

Can cause STUNNED MYOCARDIUM: reversible cardiac failure lasting several days

69
Q

What is the name given to reversible cardiac failure as a result of reperfusion injury?

A

Stunned myocardium

70
Q

What is hibernating myocardium?

A
  • The concept that chronic sublethal ischaemia
  • → lower metabolism (i.e. hibernating) in myocytes
  • which can be reversed with revascularisation
71
Q

Complications of MI

A
72
Q

When do arrythmias occur post MI

A

First few hours - days

73
Q

When does persistent pain following MI occur?

A

12 hours to few days

74
Q

When does angina following MI occur?

A

Can be immediate or delayed

75
Q

When does cardiac failure post MI occur?

A

Variable

76
Q

When does mitral incompotenece post MI occur?

A

First few days

77
Q

When does pericarditis post MI occur?

A

2-4 days

78
Q

When does cardiac rupture post MI occur?

A

3-5 days

79
Q

When does mural thrombus post MI occur?

A

>Week

80
Q

When does ventricular anueyrsm post MI occur?

A

>4 weeks

81
Q

When does Dressler’s syndrome post MI occur?

A

Weeks to months

82
Q

When do pulmonary emboli post MI occur?

A

>1 week

83
Q

Anterolateral MI leads

A

aVL, V2, V3, V4, V5, V6

**remove the 1s**

84
Q

Anterior MI leads

A

Left Anterior Descending artery

V1-V4

85
Q

Lateral MI leads

A

Left Circumflex artery

V5, V6, Lead I, aVL

86
Q

Inferior MI leads

A

Right Coronary artery

Lead II, III, aVF

87
Q

Septal MI leads

A

V1 and V2

88
Q

What is sudden cardiac death?

A

unexpected death from cardiac causes in individuals:

WITHOUT symptomatic heart disease

or early (1 hour) after the onset of symptoms

COMMONLY due to LETHAL ARRYTHMIA: thought to occur due to ischaemia-induced electrical instability

other causes: aortic stenosis, mitral valve prolapse and pulmonary hypertension

Most have underlying atherosclerosis

89
Q

CHF vs RHF vs LHF

A

CHF: both sides

RHF: peirpheral oedema and nutmeg liver

LHF: SOB and pulmonary oedema - water logged lungs

90
Q

MOst common cause of RHF

A

LHF

91
Q

Histology of heart failure

A

LVF = iron laden macrophages

Dilated heart

Scarring and thinning of walls

Fibrosis and replacement of ventricular myocardium with scar tissue

92
Q

Definition of cardiomyopathy

A

Intrinsic problems of the heart not due to ischaemic or valvular causes etc.

93
Q

Histology of rheumatic fever

A

beady vegetations

Aschoff bodies:

small giant-cell granulomas

Anitschkow myocytes:

94
Q

Which valves are affected in rheumatic fever?

A

Most commonly mitral

Followed by aortic

Then tricuspid then pulmonary

95
Q

Complication of chronic rheumatic valvular disease

A

Aortic stenosis

96
Q

Most common cause of aortic stenosis +AGE OF ONSET

A

Calcific aortic stenosis - impairs the opening and compromises the orifice >>>outflow tract obstruction + REDUCED BLOOD FLOW

occurs in 70s-80s

97
Q

Main cause of aortic regurgitation

A

Rheumatic fever

98
Q

Most likely causative organisms of infective endocarditis

A
  1. acute: staph aureus. mostly in IVDU. can occur on healthy or damaged valves
  2. subacute: strep viridans. usually affects pre-existing damaged valves
99
Q

Treatment of rheumatic fever

A

Benzylpenicillin

100
Q

Treatment of infective endocarditis

A

Acute: flucloxacillin

Subacute: benzylpencillin

101
Q

Most commonn location for atheroscleortic anueyrsm

A

Abdominal region below renal arteries

102
Q

Types of anuerysms

A
  1. saccular: only one side of vessel wall affected
  2. fusiform: both sides of vessel wall affected

** anuerysms involve all layers of the wall unlike false anueyrsms where only particular layers of the wall are invovled

  • False- extravascular haematoma (i.e. a rupture and haematoma that forms)
103
Q

2 main complications of aneurysms

A
  1. rupture: more likely in lower portion (ABDOMINAL) of the aorta
  2. dissection: more likely in upper portion of the aorta ie aortic arch

can tear and get a false lumen + false lumen causes problems >> Can get blockage and poor flow, leading to ischaemia distally

104
Q
A
105
Q
A
106
Q

3 principcal components of atheroscleortic plaques

A

Cells - including SMC, macrophages and other leukocytes; 2. ECM including collagen; 3. Intracellular and extracellular lipid

107
Q

WHich part of aorta is more affected by atheroscleorsis ?

A

**abdominal aorta** - confirm

  • An atherosclerotic aneurysm typically occurs in the abdominal portion below the renal arteries
108
Q

What type of blood flow makes you more suspcetible to atheroscleoriss?

A

Laminar is protective

Low shear stress is dangerous (especially at origins of major branches–>turbulent blood flow)

109
Q

Duration of MI that leads to irreversible injjury

A

20-40 mins

110
Q

What % of patients develop arrythmia following an MI? and which type of aarythmia is of most concern

A

90%

*VF: usually in first 24 hours, common cause of sudden death

111
Q

What complication of MI causes persistent ST elevation?

A

Ventricular aneurysm

112
Q

Histology of HCM

A

Myocyte disarray - arrythmogenic

113
Q

Large, irregular masses on valve cusps,
extending into the chordae.

A

Infective endocarditis

114
Q

Small, warty vegetations found along the heart disease
lines of closure of valve leaflet - ‘verrucae’

A

Rheumatic heart disease

115
Q

Small, bland vegetations attached to thrombotic lines of closure. Formed of thrombi.

A

Non-bacterial thormbotic enodcarditis

116
Q

Small (up to 2mm), warty vegetations that are sterile and platelet-rich.

A

Libman Sacks endocarditis

SLE

117
Q

Acute vs subacute endocarditis

A
118
Q

Which valves are affected in chronic hreumatic valve disease?

A

Mitral>aortic>tricuspid>pulmonary

119
Q

Mid-systolic click + late systolic murmur

A

Mitral prolapse

*usually middle aged women, SOB, chest pains

120
Q

Types of pericarditis

A

Fibrinous (MI, uraemia)

● Purulent (Staphylococcus)

● Granulomatous (TB)

● Hemorrhagic (tumour, TB, uraemia)

● Fibrous (a.k.a. Constrictive) (arises from any of above)

121
Q
  • Consequences of Atheromatous Plaques:
A
  • Obstruct- keeps growing and blocks the artery
  • Rupture- suddenly tear/ rupture
122
Q

define Angina Pectoris

A

Transient ischaemia that does NOT produce myocyte necrosis

123
Q

Myocardial Infarction (MI) define

A

Death of myocardial muscle due to prolonged ischaemia

124
Q

describe how the effect of MI depends on severity and duration of injury

A
125
Q

Morphological and Microscopic Changes in MI with time

A
126
Q

changes in cell type in MI over tim

A
127
Q

complication of cardiac failure

A
  • Sudden death (usually due to arrhythmias)
  • Arrhythmias
  • Systemic emboli (as the heart is not pumping well so its prone to having clots within the walls so they can fly off)
  • Pulmonary oedema with superimposed infection (lungs are full of water so more likely to get an infection)
128
Q

what does this hsow

A

Dilated Cardiomyopathy

129
Q

what does this show

A

Hypertrophic Cardiomyopathy (HOCM)

130
Q
  • There is thickening, shortening and fusion of the chordae tendinae
  • The valves look like buttonholes- tight, thick and sclerosed
A
  • Chronic Rheumatic Valvular Disease
131
Q

which valves are affected in endocarditis

A
  • Left sided >>> damaged valve
  • Right sided >>> drugs
  • IVDU: more likely to get it on the right side of the heart
  • Most people tend to get it on the left side (aortic or mitral) unless they are IVDUs
132
Q

what type of valves do we have in the heart?

A

all are tricuspid except for the mitral valve which is bicuspid

Histopathology (18 decks)

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