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P9- Shock and atheroma (atherosclerosis) Flashcards

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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?

Study These Flashcards
A
  • initially auto regulated blood supply

- later loss of consciousness and acute renal failure

25
How do shocked patients present?
- Restless - Confused - Pale - Cold - Sweaty skin - Rapid weak pulse - Low BP - Increased rate and depth of respiration - Eventually drowsy then comatose
26
Give the layers of a normal artery from the inside out.
- endothelium - intima - elastic lamina - media - adventitia
27
what are artery structural adapted to?
pressure and flow of blood within them
28
What does the aorta do?
multiple layers of elastic tissue to absorb impulse of cardiac systole and maintain blood flow in diastole
29
what do the medium-sized arteries do?
Medium-sized arteries regulate distribution of blood to various organs by constriction and dilatation, so possess thick medial wall with less elastic tissue
30
what is the most important disease of arteries?
Atheroma (Atherosclerosis)
31
where is the atheroma a principal cause of death and inability ?
western countries
32
what does atheroma cause?
ischaemic heart disease, stroke and peripheral vascular disease
33
How doe atheroma arise and progress?
Arises and progresses as an inflammatory response of the vessel wall to chronic multifactorial injury
34
what is an indicator of the extent of atherosclerosis in a community?
The incidence of ischaemic heart disease
35
what have epidemiological studies identified?
many risk factors with increased or reduced risk of ischaemic heart disease
36
Name atheroma risk factors
- Family history - male - age - cigarette smoking - hypertension - diabetes - hyperlipidaemias - exercise level
37
Name 3 atheroma risk factors that are not modifiable.
- Family history - Male - age
38
Name some atheroma risk reduction.
* non - smoker * blood pressure control * diabetes control/prevention * diet * exercise * low/moderate alcohol
39
what is atherosclerosis ?
focal accumulation of lipid in the intima of arteries with inflammation and fibrosis, forming atherosclerotic plaques
40
What does atherosclerosis affect?
medium to large arteries, including Aorta, coronary, carotid, cerebral and iliofemoral arteries
41
what does atherosclerosis cause?
* It causes luminal narrowing, with ischaemia in brain, heart and lower limbs * Plaque rupture with thrombosis causes acute ischaemia and infarct
42
Describe the pathogenesis of atherosclerosis.
- fatty streak - early atherosclerotic plaque - advanced atherosclerotic - complicated atherosclerotic plaque
43
what are lipoproteins?
fat + proteins
44
what does lipoproteins allow?
Enable fat to be carried in bloodstream without separating out
45
where do low-density lipoprotein (LDL) move?
from plasma moves freely in and out of intima
46
what do a small proportion of LDLs undergo?
oxidative change
47
what does oxidised LDL act as?
- inflammatory stimulus and invokes - adhesion molecule expression by endothelial cells - monocyte migration - cytokine production
48
what are oxidised LDL taken up by?
macrophages
49
when does lipid uptake continue till?
- until cytoplasm is packed to form “foamy macrophage” | - Foam cells die and release lipid
50
what do monocytes tick to and what does this involve?
* 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
what are fatty streaks?
* 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
what is fatty streaks the starting point in?
plaque development
53
what happens when intimal lesions develop?
- 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
what makes up atherosclerotic plaque?
Collagen cap, core of lipid and calcium deposits and vascularization from vasa vasorum
55
where is early plaque confined to?
intima
56
where does advanced plaque erode?
the media
57
what does progression of the disease lead to?
narrowing of the artery lumen and to changes in the plaques “Complicated Plaque"
58
Name 4 changes in the plaques.
* Surface ulceration * Intraplaque haemorrhage * Rupture * Thrombosis- most important complication
59
Name some complications of atheroma.
• 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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