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PBL SEM 2 > PBL 5 - pathology of atheroma > Flashcards

PBL 5 - pathology of atheroma Flashcards

1
Q

what is an atheroma?

A

an accumulation of intracellular and extracellular lipid in the INTIMA of large and medium sized arteries

= an inflammatory condition

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2
Q

what are the 3 stages of the development of atheroma?

A
  1. fatty streak
  2. simple plaque
  3. complicated plaque
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3
Q

what is arteriosclerosis?

A

the thickening of the walls of arteries and arterioles usually as a result of hypertension or diabetes

(some would include atheroma as a form of arteriosclerosis)

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4
Q

what would a cross section of an atheromatous plaque look like?

A
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5
Q

what are blood vessels that are unsupported by surrounding cells prone to? what is the effect on the plaque?

A

prone to rupture and bleed into the plaque — increases the size of the plaque

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6
Q

how can bleeding into the plaque lead to thrombosis?

A

you can bleed into a plaque and rupture the surface so the extracellular lipid gets in contact with factors in the bloodstream, leading to thrombosis

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7
Q

what happens to the fibrous cap as it matures and what are the effects of this?

A

= becomes thicker and thicker as the plaque matures

  • less likely to rupture
  • accumulates fibrous tissue — reduces diameter of the lumen
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8
Q

describe a simple atheromatous plaque

A
  • fat in intima — extracellular or within modified smooth muscle cells
  • fibrous cap
  • blood vessel proliferation
  • inflammatory cells
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9
Q

why do you get blood vessel proliferation in a simple atheromatous plaque?

A
  • in response to low oxygen environment

- because initially there is no blood supply

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10
Q

describe a complicated atheromatous plaque

A
  • calcification
  • plaque disruption = rupture of surface
  • haemorrhage into plaque — small blood vessels bleed into plaque structure
  • thrombosis
  • aneurysm formation
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11
Q

how do you get calcification in a complicated atheromatous plaque?

A
  • breakdown of fat — WBCs come along to deal with it
  • release fatty acids from triglycerides
  • fatty acids bind to circulating calcium = calcification
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12
Q

how can an aneurysm form in a complicated atheromatous plaque?

A

inflammation causes weakening of elastic tissue in wall — can lead to blood clot formation

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13
Q

what is the typical site of an aneurysm caused by atheroma?

A

lower end of the abdominal aorta, immediately above the bifurcation into the common iliac arteries

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14
Q

what happens to a bulging aneurysm?

A

wall gets thinner and thinner until it ruptures

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15
Q

name some common sites of atheroma

A
  • aorta — especially abdominal
  • coronary arteries
  • carotid arteries
  • cerebral arteries
  • leg arteries
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16
Q

name some risk factors for atheroma

A
  • smoking
  • male sex
  • menopause
  • diet (high in fat)
  • alcohol
  • obesity
  • familial hyperlipidaemia (can cause atheromas in early adult life)
  • acquired hyperlipidaemia
  • diabetes mellitus
  • lack of exercise
  • type A personality
  • stress
  • infection
  • oral contraceptives
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17
Q

why do some people say red wine can be protective?

A

contains salicylates — prevent platelet aggregation so considered protective — however don’t actually drink enough for it to be protective

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18
Q

name 5 hypotheses/mechanisms of atheroma

A
  • encrustation of platelets
  • insulation of lipid from blood
  • monoclonal proliferation of smooth muscle cells (lysonisation = suggests proliferation from a patch of cells that themselves have a single cell ancestor)
  • response to injury (endothelial damage)
  • infection with Ag-Ab complexes deposition
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19
Q

what is ischaemia?

A

reduced delivery of blood to an organ, or part of an organ, sufficient to compromise function

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20
Q

what is infarction?

A

reduced delivery of blood to an organ, or part of an organ, sufficient to lead to its death

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21
Q

what are some major consequences of atheroma around the body?

A
  • brain — cerebral infarct, vascular dementia
  • gut — small bowel infarction
  • kidney — chronic renal failure
  • limbs — peripheral vascular disease - largely the legs - number of failures in the function of the muscles of the limbs
  • heart — IHD (ischaemic heart disease)
22
Q

what is a small bowel infarction dye to obstruction of? what can it cause?

A
  • superior mesenteric artery

- can cause sufficient mucosal defect

23
Q

what is ischaemic colitis and why does it gradually appear?

A
  • ischaemia in the large intestine
  • less common consequence of atheroma than small bowel infarction but is also disasterous
  • creeps up gradually because if the blood supply to the colon is poor, it can be bypassed to a degree because of the anastomotic connections between the branches of the superior mesenteric and inferior mesenteric arteries
24
Q

what is intermittent claudication?

A

= the pain in the muscles caused by exercise in the context where the blood supply is insufficient and causes an individual to stop walking
- pain walking a sufficient distance

25
Q

what can intermittent claudication (peripheral vascualar disease) lead to when obstruction gets worse?

A

ischaemic rest pain and gangrene (deaths of body tissue due to lack of blood flow)

26
Q

what is the cause of 99% of IHD?

A

coronary artery atheroma

27
Q

what are some other causes of IHD?

A
  • a few rare diseases eg. Kawasaki disease

- stimulant misuse (eg. cocaine — causes accelerated atheroma in coronary arteries. also damages cardiac muscle)

28
Q

what are some possible clinical consequences of IHD?

A
  • nothing
  • cardiac arrhythmia
  • acute coronary syndromes — angina pectoris, acute MI
  • acute LV failure
  • chronic heart failure
  • sudden unexpected death
29
Q

name 3 cardiac arrhythmias possible from IHD

A
  • atrial fibrillation — common and treatable if detected
  • heart block
  • ventricular fibrillation
30
Q

what is heart block?

A

a disruption in the flow of electrical impulse that causes systolic contraction

31
Q

what is ventricular fibrillation?

A

causes ventricles to pump in sufficiently with lots of little contractions (several hundred a minute)

32
Q

what is angina pectoris?

A
  • chest pain induced by exercise and relieved by rest
  • pain emanating from ischaemia in the heart because it has been pushed to the limit because it doesn’t have enough O2 to function in response to exercise — can only walk a particular distance, stop to relieve pain, then repeat
  • major forms = stable and unstable
33
Q

describe stable angina

A
  • symptoms stereotypic

- lowish risk of infarct

34
Q

describe unstable angina

A
  • pain at rest
  • increasing severity of attack — each attack lasts longer than the last
  • pain lasting over 15 minutes
  • medical emergency
  • very high risk of infarct
35
Q

how is acute myocardial infarction classified according to its distribution?

A
  • REGIONAL (occupying only a proportion of the diameter of the LV) or CIRCUMFERENTIAL (more likely to be clinically silent or difficult to diagnose as ECG changes are less prominent)
  • TRANSMURAL (endocardium to epicardium) or SUBENDOCARDIAL (typically limited to 1/3 of the myocardium of the LV)
  • regional are usually transmural
  • circumferential are usually subendocardial
36
Q

what are transmural MIs typically associated with?

A

coronary artery thrombosis

37
Q

what are subendocardial MIs typically associated with?

A

increased demand on the heart eg. tachycardia, AF — circumferential subendocardial

38
Q

is there always an infarction in STEMI and NSTEMI?

A

no

39
Q

which is more serious: STEMI or NSTEMI?

A

STEMI

40
Q

STEMI vs NSTEMI on an ECG

A

STEMI has ST elevation

41
Q

why would an infarct be not fully transmural?

A

oxygen diffuses in from adjacent structures, sparing often in subendocardial zone

42
Q

where is it more dangerous to have an infarct than in the free wall of the heart and why?

A

septum — where conducting tissue runs

43
Q

complications of an acute MI

A
  • cardiac arrhythmia
  • cardiac failure — acute or chronic
  • cardiac rupture — free wall or septum
  • sudden unexpected death
44
Q

what causes cardiac tamponade?

A
  • rupture in free wall of heart
  • blood fills pericardium
  • pericardium doesn’t stretch therefore get cardiac tamponade
45
Q

describe acute LV failure

A
  • pump failure of LV
  • increases pressure in pulmonary capillaries
  • rapid fluid accumulation in alveolar walls, and then air spaces — pulmonary oedema
  • symptoms come on suddenly
46
Q

describe chronic heart failure + symptoms

A
  • more gradual onset than acute LV failure
  • pump failure on both ventricles
  • inadequate systemic blood supply
  • tiredness, ankle swelling, minor liver dysfunction
47
Q

why do you get ankle swelling in chronic HF and what may it be indicative of?

A
  • may be indicative of elevated central venous pressures

- due to increased pressure in the tiny capillaries in the lower part of the body

48
Q

why do you get minor liver dysfunction in chronic HF?

A

liver gets congested with blood so can’t get rid of toxic substances

49
Q

describe sudden unexpected death

A
  • IHD is the most common cause of sudden unexpected death
  • a few are acute MI
  • moire are acute LV failure
  • most are (probably) cardiac arrhythmia
50
Q

describe how a plaque forms due to hyperlipidaemia (from pharmacology lecture)

A
  • excess LDL in circulation enters the intima of a blood vessel
  • monocytes migrate to the intima and transform into macrophages
  • macrophages take up oxidised LDL and transform into foam cells
  • foam cells attach to the endothelium and form the fatty streak
  • foam cells release cytokines and other growth factors that recruit smooth muscle cells
  • migrating smooth muscle cells thicken the streak into a stable plaque

PBL SEM 2 (44 decks)

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