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Pathology > P9- Shock and atheroma (atherosclerosis) > Flashcards

P9- Shock and atheroma (atherosclerosis) Flashcards

1
Q

what do all causes of shock result in?

A

acute circulatory failure with hypotension and inadequate tissue perfusion

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2
Q

what is a large component of the syndrome, regardless of aetiology?

A

failure of microcirculation

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3
Q

what happens if shock is not reversed quickly?

A

leads to multiorgan failure and death

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4
Q

Name the 5 major types of shock.

A
  • Hypovolaemic
  • septic
  • cardiogenic
  • anaphylactic
  • neurogenic
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5
Q

What are other causes of shock?

A

Include ‘Chemical’ shock eg

acute pancreatitis, acute peritonitis from perforated gastric ulcer

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6
Q

What is hypovolaemic shock due to?

A
  • Due to reduced blood volume
    eg haemorrhage,vomiting, diarrhoea,
    burns
  • Inadequate circulating volume
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7
Q

what is susceptibility to hypovolaemic influenced by?

A

age and prior health if patients

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8
Q

Who tolerate blood loss less well?

A

elderly and hypertensive patients

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9
Q

How much blood can be lost that is still asymptomatic?

A

10% in healthy adult

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10
Q

what does rapid loss of half blood volume lead to?

A

coma and death

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11
Q

What causes septic shock?

A
  • Severe infection, often Gram-negative bacilli that produce endotoxins
  • LPS, liopolysaccahride, from the outer cell wall of the bacilli binds to and activates macrophages and endothelial cells
  • TNF-α—IL-1- cytokine cascade
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12
Q

What does septic shock lead to?

A

Peripheral vasodilation, tissues underperfused, endothelial injury, fluid leakage, oedema, activated coagulation, DIC (disseminated intravascular coagulation)

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13
Q

Describe cariogenic shock.

A
  • Severe acute reduction in cardiac output due to pump failure
  • Massive myocardial infarct, arrhythmia, cardiac tamponade, pulmonary embolism, valve dysfunction
  • Failure to maintain perfusion pressure and flow
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14
Q

what type of reaction is anaphylactic shock?

A

Systemic Type I Hypersensitivity

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15
Q

What happens in anaphylactic shock?

A

Massive mast cell degranulation causes release of vasodilators and permeability factors

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16
Q

Name 2 types of neurogenic shock.

A
  • Acute brain injury

* Spinal cord injury

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17
Q

What role do compensatory mechanisms play?

A

In the early stages, compensatory mechanisms maintain blood flow to vital organs- CNS, heart, Kidneys- reduced perfusion to other tissues

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18
Q

Give examples of compensatory mechanisms.

A
  • Increased sympathetic activity
  • Renin-Angiotensin-Aldosterone system
  • CNS, heart and kidney autoregulate their own perfusion
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19
Q

What happens if tissue perfusion is not restored urgently after shock?

A

ischaemia causes multiorgan failure and death

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20
Q

what is the shock consequence to the lungs?

A

Diffuse alveolar injury (ARDS Adult Respiratory Distress Syndrome)

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21
Q

what is the shock consequence to the heart?

A

ischaemia and failure

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22
Q

what is the shock consequence to the gut?

A

ischaemia and endotoxaemia

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23
Q

what is the shock consequence to the adrenal?

A

initially stimulated then failing

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24
Q

what is the shock consequence to the brain and kidneys?

A
  • initially auto regulated blood supply

- later loss of consciousness and acute renal failure

25
Q

How do shocked patients present?

A
  • Restless
  • Confused
  • Pale
  • Cold
  • Sweaty skin
  • Rapid weak pulse
  • Low BP
  • Increased rate and depth of respiration
  • Eventually drowsy then comatose
26
Q

Give the layers of a normal artery from the inside out.

A
  • endothelium
  • intima
  • elastic lamina
  • media
  • adventitia
27
Q

what are artery structural adapted to?

A

pressure and flow of blood within them

28
Q

What does the aorta do?

A

multiple layers of elastic tissue to absorb impulse of cardiac systole and maintain blood flow in diastole

29
Q

what do the medium-sized arteries do?

A

Medium-sized arteries regulate distribution of blood to various organs by constriction and dilatation, so possess thick medial wall with less elastic tissue

30
Q

what is the most important disease of arteries?

A

Atheroma (Atherosclerosis)

31
Q

where is the atheroma a principal cause of death and inability ?

A

western countries

32
Q

what does atheroma cause?

A

ischaemic heart disease, stroke and peripheral vascular disease

33
Q

How doe atheroma arise and progress?

A

Arises and progresses as an inflammatory response of the vessel wall to chronic multifactorial injury

34
Q

what is an indicator of the extent of atherosclerosis in a community?

A

The incidence of ischaemic heart disease

35
Q

what have epidemiological studies identified?

A

many risk factors with increased or reduced risk of ischaemic heart disease

36
Q

Name atheroma risk factors

A
  • Family history
  • male
  • age
  • cigarette smoking
  • hypertension
  • diabetes
  • hyperlipidaemias
  • exercise level
37
Q

Name 3 atheroma risk factors that are not modifiable.

A
  • Family history
  • Male
  • age
38
Q

Name some atheroma risk reduction.

A
  • non - smoker
  • blood pressure control
  • diabetes control/prevention
  • diet
  • exercise
  • low/moderate alcohol
39
Q

what is atherosclerosis ?

A

focal accumulation of lipid in the intima of arteries with inflammation and fibrosis, forming atherosclerotic plaques

40
Q

What does atherosclerosis affect?

A

medium to large arteries, including Aorta, coronary, carotid, cerebral and iliofemoral arteries

41
Q

what does atherosclerosis cause?

A
  • It causes luminal narrowing, with ischaemia in brain, heart and lower limbs
  • Plaque rupture with thrombosis causes acute ischaemia and infarct
42
Q

Describe the pathogenesis of atherosclerosis.

A
  • fatty streak
  • early atherosclerotic plaque
  • advanced atherosclerotic
  • complicated atherosclerotic plaque
43
Q

what are lipoproteins?

A

fat + proteins

44
Q

what does lipoproteins allow?

A

Enable fat to be carried in bloodstream without separating out

45
Q

where do low-density lipoprotein (LDL) move?

A

from plasma moves freely in and out of intima

46
Q

what do a small proportion of LDLs undergo?

A

oxidative change

47
Q

what does oxidised LDL act as?

A
  • inflammatory stimulus and invokes
  • adhesion molecule expression by endothelial cells
  • monocyte migration
  • cytokine production
48
Q

what are oxidised LDL taken up by?

A

macrophages

49
Q

when does lipid uptake continue till?

A
  • until cytoplasm is packed to form “foamy macrophage”

- Foam cells die and release lipid

50
Q

what do monocytes tick to and what does this involve?

A
  • Monocytes stick to intact endothelial surface then enter intima
  • This involves endothelial dysfunction, influx of lipid macrophages and T lymphocytes, inflammation, smooth muscle proliferation, deposition of collagen and elastic tissue
51
Q

what are fatty streaks?

A
  • Fatty streak earliest lesion visible to naked eye
  • “ foam cells” in intima (ie foamy macrophages) with intact endothelial surface
  • Usual lesions seen in children up to 10 yrs
52
Q

what is fatty streaks the starting point in?

A

plaque development

53
Q

what happens when intimal lesions develop?

A
  • develop and acquire extracellular lipid, intracellular lipid in foamy macrophages, collagen and other connective tissue matrix produced by smooth muscle cells
  • These larger elevated lesions=atherosclerotic plaques
54
Q

what makes up atherosclerotic plaque?

A

Collagen cap, core of lipid and calcium deposits and vascularization from vasa vasorum

55
Q

where is early plaque confined to?

A

intima

56
Q

where does advanced plaque erode?

A

the media

57
Q

what does progression of the disease lead to?

A

narrowing of the artery lumen and to changes in the plaques “Complicated Plaque”

58
Q

Name 4 changes in the plaques.

A
  • Surface ulceration
  • Intraplaque haemorrhage
  • Rupture
  • Thrombosis- most important complication
59
Q

Name some complications of atheroma.

A

• Ischaemic Heart Disease (Sudden death, MI, heart failure)
• Cerebrovascular Disease (TIAs, cerebral infarction)
• Peripheral Vascular Disease (Intermittent claudication, gangrene
• Mesenteric Vascular Disease (Mesenteric claudication, intestinal infarction)
• Renovascular Disease (Hypertension, renal failure)
• Aneurysms
(At least 50% localised increase in luminal diameter of an artery Abdominal aorta, rupture)

Pathology (9 decks)

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