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Cardiovascular > Pathology > Flashcards

Pathology Flashcards

1
Q

What is arteriosclerosis?

A

Intimal damage and thickening
- fibrous change in the intima (thickening and fibrosis with lots of collagen), arteries are less elastic and can get lumen narrowing

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2
Q

What are sequelae of arteriosclerosis?

A
  • impairs artery’s role in controlling BP

- can impair blood supply to downstream tissues

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3
Q

How do you get intimal damage and thickening in arterioles?

A

Smooth muscle cells produce too much matrix

  • proteins from the blood can leak from the lumen across the damaged endothelium into the wall of the arteriole
  • smooth, clear, glassy, hard surface
  • hyaline arteriolosclerosis
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4
Q

What are sequelae of hyaline arteriolosclerosis?

A
  • ischaemia
  • microaneurysms and haemorrhage
  • cerebral haemorrhage
  • benign nephrosclerosis
  • hypertensive retinopathy
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5
Q

What is atherosclerosis?

A

A build up of inflammatory, fibrotic, necrotic and fatty material in arteries

  • an atheroma with a fibrous cap and a necrotic lipid core
  • can slowly narrow arteries or can rupture catastrophically
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6
Q

What are the stages of formation of atherosclerosis?

A
  1. Fatty streaks
  2. Damage, inflammation, cholesterol and fibrosis
  3. Stable atherosclerotic plaque
  4. Unstable atherosclerotic plaque
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7
Q

What are the microscopic features of atherosclerosis?

A

Foam cells, inflammatory cells, cholesterol clefts, calcification, thickened intima, narrowed lumen, fibrous cap, necrotic core, thinned media, neovascularisation

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8
Q

What is an acute plaque event?

A 
When something goes wrong in the plaque causing:
- plaque rupture 
- haemorrhage into the plaque 
- erosion of endothelium 
Leading to:
- thrombosis 
- thromboembolism 
- atheroembolism
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9
Q

What makes a plaque vulnerable to rupture?

A

Plaques which rupture often have:

  • thinner fibrous cap
  • larger necrotic core
  • more inflammatory cells
  • less than 50% stenosis (likely to be asymptomatic)
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10
Q

What are other sequelae of atherosclerosis?

A

Chronic ischaemia when the lumen is >70% stenosed
- stable angina
- peripheral vascular disease (claudication)
Aneurysm
- due to weakened media, risk of rupture/haemorrhage

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11
Q

What are the non-modifiable risk factors for atherosclerosis?

A
  • age
  • gender
  • family history
  • certain genes
  • already having atherosclerosis
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12
Q

What are the modifiable risk factors for atherosclerosis?

A
  • hypertension
  • smoking
  • diabetes
  • cholesterol
  • sedentary lifestyle
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13
Q

What role does the endothelium have in the start of atherosclerosis?

A

Normal epithelium does not interact with inflammatory cells, but “activated” epithelium behaves differently

  • becomes “leaky”
  • expresses adhesion molecules
  • produces cytokines and growth factors
  • changes from anti-coagulant to pro-coagulant
  • takes up LDLs into the intima which become oxidised and pro-inflammatory
  • allows monocytes into the intima which become macrophages
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14
Q

What role do the macrophages play in atherosclerosis?

A

Phagocytose the oxidised LDL and produce inflammatory cytokines
- they become foam cells –> accumulate and form the lipid core

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15
Q

What is the role of smooth muscle cells in atherosclerosis?

A

They migrate into the intima and change phenotype:

  • can proliferate
  • can produce ECM
  • produce collagen and the thick, fibrous cap
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16
Q

What is an aneurysm?

A

Abnormal dilation of blood vessels due to a weakness in the media
- risk of rupture and haemorrhage

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17
Q

What is a AAA?

A

Abdominal Aortic Aneurysm
- associated with atherosclerosis –> inflammatory environment weakens ECM, intimal thickening interferes with wall perfusion

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18
Q

What is a Berry aneurysm?

A

In the cerebral circulation, weakening of a congenital defect
- major cause of subarachnoid haemorrhage

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19
Q

What is a dissection?

A

A rupture in the intima bleeding into the media

  • very strong association with hypertension
  • generally affects the aorta (particularly ascending)
  • can rupture into the pericardium (cardiac tamponade) or into the thorax (exsanguination)
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20
Q

What is cardiac remodelling and hypertrophy?

A

Changes in size, shape and function of the heart after cardiac injury
- hypertrophy is when there is an increase in LV mass

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21
Q

What are some causes of cardiac remodelling/hypertrophy?

A
  • myocardial infarction
  • cardiac damage
  • volume overload
  • pressure overload
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22
Q

What is concentric hypertrophy?

A

Increase in LV mass with increased relative wall thickness

  • often due to pressure overload (compensation)
  • have more sarcomeres in parallel
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23
Q

What is eccentric hypertrophy?

A

Increase in LV mass with normal relative wall thickness

  • whole size of the heart increases - dilation of the ventricle
  • often due to volume overload (compensation)
  • myocyte stretching, more sarcomeres in series
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24
Q

What is decompensation?

A

The heart can compensate initially but long term decompensates

  • LV dilation, increased LVEDV, increased LVESV, decreased EF
  • reduced systolic function and CO
  • increased LVEDP
  • eventual cardiac failure
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25
Q

How do you identify LVH?

A 
Clinically - forceful apex beat, S4 and S3
ECG - fall voltages, T wave inversion 
CXR - large heart in eccentric 
Echo
MRI 
Cardiac CT
26
Q

What is diastolic dysfunction?

A

Thick muscle is stiff - harder for ventricle to relax and fill on each beat

  • increased LVEDP required to achieve same LVEDV (preload), so increased LA and pulmonary vein pressure
  • more likely to have pulmonary congestion, more sensitive to fluid loading or dehydration
  • atrial “kick” more important
27
Q

How do you treat LVH?

A

Treatment of the underlying condition

  • valves
  • hypertension
  • weight loss
28
Q

What are some causes of right ventricular hypertrophy?

A

Congenital
Pulmonary hypertension
- lung disease, pulmonary embolus, chronic L heart failure
Right heart valves

29
Q

What is hypertrophic cardiomyopathy?

A

An autosomal dominant condition which codes for a mutation in genes for sarcomere proteins

  • get increased LV wall thickness, especially of the septum
  • cellular hypertrophy, myocyte disarray, LV outflow tract obstruction, diastolic dysfunction
30
Q

What is a thrombus?

A

A clotted mass of blood within the unruptured cardiovascular system, during life
- forms in FLOWING blood

31
Q

What are the components of arterial thrombi?

A

“White” thrombus

  • contain a higher proportion of platelets and fibrin
  • associated with endothelial dysfunction/damage
  • aspirin more useful for preventing arterial thrombosis
32
Q

What are the components of venous thrombi?

A

“Red” thrombus

  • contain a higher proportion of blood cells and fibrin
  • associated with blood stasis and hypercoagulability
  • warfarin more useful for preventing venous thrombosis
33
Q

What are the components of Virchow’s triad?

A
  • abnormal endothelium
  • abnormal blood flow
  • abnormal blood contents
34
Q

How does abnormal endothelium contribute to thrombus formation?

A

Loss of endothelium exposes collagen and vWF

  • endothelial activation or dysfunction may be caused by inflammatory cytokines, toxins, hypertension etc
  • reduces anti-coagulant activity and increases pro-coagulant activity
35
Q

How does abnormal blood flow contribute to thrombus formation?

A

Genetic
- “primary” –> Factor V Leiden, etc
Not genetic
- “secondary” –> OCP, cancer, smoking

36
Q

What are the possible outcomes of a thrombus?

A
  1. Dissolution - fibrinolysis: tPA, protein C and S
  2. Organisation and recanalization - granulation tissue, can get new vessels opening up
  3. Propagation - grow longer and crumblier
  4. Embolisation
37
Q

What is an embolus?

A

An intravascular mass carried in the blood stream

  • can be solid, liquid or gaseous
  • blocks the vessel it lodges in
38
Q

What is ischaemia?

A

A deficiency, real or relative, of oxygenated blood in a tissue causing a shortage of oxygen and impaired aerobic respiration

39
Q

What are some causes of ischaemia?

A
  • local vascular narrowing or occlusion
  • increased demand for O2 that is not met
  • systemic reduction in tissue perfusion
40
Q

What is infarction?

A

Tissue death due to inadequate blood supply

- often wedge shaped

41
Q

What is a red infarction?

A

Where there is haemorrhage into the infarcted tissue, due to:
- dual blood supply or collateral blood supply

42
Q

What is a pale infarction?

A

Where there is no haemorrhage, due to:

- a blocked “end artery”

43
Q

What are some causes of valvular heart disease?

A
  • previously due to rheumatic fever but this is now uncommon

- mostly due to degenerative conditions

44
Q

What does the onset of symptoms mean in regurgitation and stenosis?

A
  • in regurgitation irreversible LV changes occur about the time symptoms develop
  • in stenosis the onset of symptoms indicates time to intervene and LVH changes usually regress
45
Q

Describe aortic stenosis, the compensatory response and the decompensation

A

Progressive narrowing of aortic valve (fibrosis, calcification), leading to a reduction in valve area ad a pressure gradient across the valve
The response is concentric hypertrophy from the left ventricle eventually leading to diastolic dysfunction
- an increased LVEDP is needed to fill the LV

46
Q

Describe aortic regurgitation, the compensatory response and the decompensation

A

Damage to the aortic leaflets/aortic root dilated so the leaflets don’t close causing part of each SV to leak back into the LV during diastole
To maintain normal CO, LV has to pump greater SV each beat (increased EDV and EF, normal ESV)
Eventual decompensation - LV diastolic volume increases, LV function decreases, LV systolic volume increases

47
Q

What are some causes of mitral regurgitation?

A

Myxomatous degeneration - mitral valve prolapse
Ruptured chordae tendinae
Infective endocarditis
Myocardial infarct –> ruptured papillary muscle
Rheumatic fever
Collagen vascular disease
Cardiomyopathy

48
Q

Describe mitral regurgitation, the compensatory response and the decompensation

A

A portion of SV is ejected into low pressure LA, to maintain normal CO, L has to pump greater SV each beat (increased EDV, EF, normal ESV, increased LA volume and pressure)
Eventual decompensation - LV diastolic volume increases, reduced EF, increased LV systolic volume

49
Q

Describe mitral stenosis, the compensatory response and the decompensation

A

Fibrotic, narrowed mitral vale with a pressure gradient across it. Leads to reduced filling of the LV, LA contraction more important
- LV systolic function now affected, but increased LA pressure and volume

50
Q

What is ischaemic heart disease?

A

An imbalance between myocardial oxygen supply and demand
Acute: unstable angina, myocardial infarction, sudden cardiac death
Chronic: stable angina, chronic myocardial ischaemia

51
Q

What factors limit coronary blood flow?

A
  • perfusion pressure
  • coronary vascular resistance
  • external compression
  • intrinsic regulation (prostacyclin/NO etc)
52
Q

What is a myocardial infarction?

A

An imbalance between the supply and demand of the myocardium resulting in ischaemia and cell death
- most commonly caused by an acute plaque event with rupture/haemorrhage of atherosclerotic plaque and formation of an occlusive thrombus within a coronary vessel

53
Q

When do you start to get irreversible injury in MI?

A

30 minutes to 12 hours

  • disruption of the cell membrane and leaking of cardiac proteins - TROPONIN/CK
  • STEMI/NSTEMI
54
Q

At what time do cardiac enzymes start to become detectable in the blood?

A

3-4 hours post infarction

55
Q

What are the potential complications 30mins - 4 hours after an MI?

A

Arrhythmia - damaged myocytes are unstable

Cardiac failure - damaged myocytes cannot contract properly

56
Q

What are the potential complications 1 - 3 days after an MI?

A

Arrhythmia - damaged myocytes unstable
Cardiac Failure - damaged myocytes being destroyed
Mural Thrombus - damaged wall not moving properly
Rupture - wall is necrotic and weakened
Pericarditis - inflammatory mediators abundant

57
Q

What are the 3 ways of rupturing?

A
  1. Rupture of free ventricle wall –> blood into the pericardium
  2. Rupture of papillary muscle
  3. Rupture of IV septum
58
Q

What is angina?

A

Transient ischaemia, symptomatic with chest pain

59
Q

What is stable angina?

A

Presents as chest pain that occurs on exertion and goes away with rest, due to atherosclerotic narrowing of a vessel
- symptoms generally start around 70% stenosis

60
Q

What is unstable angina?

A

Presents as cardiac chest pain that may occur at rest or minimal exertion

  • acute plaque event, coronary artery thrombosis
  • resolves with no irreversible damage
61
Q

What is sudden cardiac death?

A

Unexpected death due to cardiac causes, in a short period of time (

Cardiovascular (8 decks)

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