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FD1 > Haemodynamic abnormalities and shock > Flashcards

Haemodynamic abnormalities and shock Flashcards

1
Q

What is an oedema?

A
  • accumulation of excess interstitial fluid
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2
Q

What are the 5 mechanisms of oedema formation?

A
  1. increased vascular permeability
  2. increased vascular hydrostatic pressure
  3. decreased vascular oncotic pressure
  4. decreased lymohatic drainage
  5. neurogenic pulmonary oedema
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3
Q

What is this showing?

A
  • gross apearance of oedema
    • clear to yellow coloured fluid
    • small amount of protein (transudate)
    • fluid may be forced into the body cavities/ open spaces
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4
Q

What is pulmonary oedema?

A
  • fluid in alveoli
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5
Q

What is hydrothorax

A
  • fluid in thorax
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6
Q

What is hydropericardium?

A
  • fluid in pericardium
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7
Q

What is ascites (hydroperitoneum)?

A
  • fluid in abdominal cavity
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8
Q

What is Anasarca?

A
  • generalised oedema
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9
Q

What is this showing?

A
  • severe pulmonary oedema
    • quite a bit of protein (pink)
    • air spaces in alveolar
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10
Q

Describe the mechanism of increased vascular permeability

A
  • associated with inflammation/ immunological stimuli
  • release of mediators which cause endothelial cell contraction and widening of interendothelial spaces
    • histamine, bradykini, substance P
  • movement of fluid from the vascular lumen into the interstitium through these gaps causes oedema
  • localised/ general
  • E.g.
    • viruses, bacteria
    • immune mediated
    • toxins
    • neovascularisation
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11
Q

Describe the mechanism of increased vascular hydrostatic pressure

A
  • increased pressure in vessels
  • due to increased blood vol in the microvasculature
    • hyperaemia (increased blood flow in inflammation)
  • forces fluid out of vessel (increased filtration through vessel wall) and reduced reabsorption leading to oedema
  • localised/ generalised
  • E.g.
    • heart failure
    • portal hypertension
    • pulmonary hypertension
    • localised venus obstruction
    • fluid overload
    • hyperaemia
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12
Q

Describe the mechanism of decreased vascular oncotic pressure

A
  • low levels of plasma proteins (albumin)
  • results in reduced reabsorption of interstitial fluid back into the vessel by osmosis
  • typically generalised oedema
  • hypoalbuminaemia can be caused by decreased production of albumin or increased loss of albumin from plasma
  • decreased production of albumin
    • malnutrition: inadequate protein in diet/ failure to absorb
    • sever liver disease: inadequate albumin production
  • increased loss of albumin (GI disease)
  • water intoxication (haemodilution)
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13
Q

Describe the mechanism of decreased lymphatic drainage

A
  • lymphatic vessels: contribute to balance of interstitial fluid by draining the slight excess of fluid which has not been reabsorbed by blood vessels
  • reduced ability of lymphatic vessels to drain excess interstitial fluid results in oedema
  • Causes:
    • lymphatic compression or obstruction e.g. neoplasia, inflam
    • lymphangitis
    • congenital lymohatic aplasia/ hypoplasia
    • intestinal lymohangiectasia
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14
Q

Describe the mechanism of neurogenic pulmonary oedema

A
  • thought to be due to catecholamine release following CNS injuries resulting in increased intracranial pressure
  • leads to pulmonary oedema
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15
Q

What is Hyperaemia (erythema)?

A
  • INCREASED blood flow
  • active engorgment of vascular beds caused by increased inflow of blood with a normal or decreased outflow of blood
    • increased metabolic activity
    • heat dissipation
    • inflam
  • hyperaemic tissues appear bright red and warm
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16
Q

What is congestion and what is the appearance of congested tissues?

A
  • DECREASED blood flow
  • Passive engorgement of vascular beds caused by decreased outflow of blood with normal or increased inflow of blood
    • passive congestion can happen acutely or chronically
  • appear enlarged, dark red, swollen (oedema) and cooler
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17
Q

What does this show and why?

A
  • ACUTE congestion
  • occurs in liver and lungs in acute heart failure
  • after euthanasia by barbiturate overdose
  • tissue appears enlarged and dark red, oozing blood from cut surface
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18
Q

When would localised chronic congestion occur?

A
  • due to obstruction of venous outflow e.g. neoplasia, inflam
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19
Q

When would generalised chronic congestion occur?

A
  • due to reduced blood flow through the heart/ lungs
  • most commonly heart failure or conditions which limit blood flow in lungs e.g. pulmonary fibrosis
  • may be fibrosis caused by hypoxia and cell injury that accompanies congestion
20
Q

How does decreased tissue perfusion occur?

A
  • decreased cardiac output results in decreased inflow of blood to tissues
  • local congestion results in decreased outflow of blood from tissues
  • obstruction to a vessel supplying/ draining a tissue results in decreased inflow or outflow of blood
21
Q

When does ischaemia occur?

A
  • when the perfusion becomes inadequate to meet the metabolic needs of the tissue (reduced oxygen delivery and waste removal)
22
Q

Give examples of how ischaemia occurs

A
  • arterial disease
    • incomplete luminal blockage by an embolus or thrombus
    • decreased flow of oxygenated blood into an area
  • arteriolar vasoconstriction
    • if prolonged and result in decreased flow of oxgenated blood into an area
  • venous obstruction
    • luminal blockage/ extravascular compression
    • congestion- reduced oxygen

Heart and brain are most susceptible to ischaemia

23
Q

What is a reperfusion injury and how does it happen?

A
  • if blood is returned after brief ischaemia - tissue returns to normal
  • if blood is returned after prolonged- reperfusion injury
  • reflow into tissue after prolonged =
    • oedema
    • haemorrhage
    • release of TF - thrombus formaton
    • ATP degradation to hypoxathine during ischaemia
    • further reactive oxygen species are created by superoxide anions
24
Q

What is infarction?

A
  • coagulative necrosis due to peracute ischaemia
    • caused by same events that cause ischaemia
    • secondary to thromosis
  • complete arterial blockage = immediate infarction
  • venous obstruction = extensive congestion and oedema preceding and promoting infarction
25
Q

What is happening at 1 and 2?

A
  • 1 = normal arterial flow
  • 2 = thrombus occluding artery
  • black area - necrosis
26
Q

What is happening at 1 and 2 and M?

A
  • M = mass compressing vein 1
  • 2 = normal venous flow
27
Q

What tissues are most prone to infarction?

A
  • tissues with a single blood supply
  • e.g. brain, heart, kidney, spleen
  • occlusion of nearly any sized vessel results in infarction of the dependent tissue
28
Q

How likely is infarction in tissue with parallel blood supply with anastomoses?

A
  • less likely than single
  • e.g. skeletal muscle, GIT
  • occlusion less serious
29
Q

Which tissues are least prone to infarction?

A
  • tissues with dual blood supply e.g. liver/ lung
  • not susceptible unless concurrent underlying disease compromises whole blood supply
30
Q

What is this showing?

A
  • acute renal infarction
  • haemorrhage results in dark red discolouration
31
Q

What does this show?

A
  • acute cellular swelling causes buldging of infarction
  • acute renal infarction
32
Q

What does this show?

A
  • acute venous infarction in volvulus of a portion of intestine
  • can lead to endotoxic shock - bacteria travel through more permeable gut
33
Q

What is this showing?

A
  • acute renal infarction
  • central coagulation necrosis bordered by inflammatory cells (blue)
34
Q

What is shown here?

A
  • chronic renal infarction
  • replacement of necrotic tissue by fibrosis, with contraction- resulting in an indented appearance
35
Q

What is this showing?

A
  • chronic myocardial infarction
  • replacement of necrotic tissue by fibrosis disrupting myofibre bundles
36
Q

What is shock?

A
  • cardiovascular shock
    • circulatory dyshomeostasis
  • loss of circulating blood vol, reduced CO and/ or inappropriate peripheral resistance
    • results in hypotension, reduced tissue perfusion, cellular hypoxia, degeneration and death
37
Q

What are the 3 categories of shock?

A
  1. cardiogenic
  2. hypovolaemic
  3. maldistributive
    • septic
    • anaphylatic
    • neurogenic
38
Q

Describe cardiogenic shock

A
  • failure of heart to adequately pump blood e.g. inadequate CO
  • caused by cardiac failure:
    • myocardial infarction
    • ventricular tachycardia
    • fibrillation
    • cardiomyopathies
    • obstruction of outflow of blood from the heart
39
Q

Describe hypovolaemic shock and its causes

A
  • reduced circulating blood vol leading to hypotension and hypoperfusion
  • caused by:
    • haemorrhage
    • fluid loss
      • vomiting
      • diarrhoea
      • burns
40
Q

What are the compensation mechanisms of hypovolaemic shock?

A
  • peripheral vasoconstriction
  • fluid movement into plasma
41
Q

What % of blood volume do you need to lose to cause a dramatic fall in pressure and CO?

A
  • 35-45%
42
Q

What is maldistributive shock?

A
  • decreased peripheral resistance
  • pooling of blood in peripheral tissues
    • hypotension and hypoperfusion
43
Q

What is anaphylatic shock?

A
  • generalised type I hypersensitivity
  • widespread mast cell degranulation leading to systemic vasodilation and increased vascular permeability
44
Q

What is neurogenic shock?

A
  • CNS trauma, electrocution, emotional stress
  • autonomic discharges leading to systemic vasodilation
45
Q

What is septic shock?

A
  • components of microorganisms such as endotoxin
  • activates endothelial cells, leukoctres, platelets releasing cytokines
  • results in actvation of myriad vascular, proinflam and procoagulant pathways
  • systemic vasodilation, hypotension and hypoperfusion
46
Q

How might shock progress?

A
  • may be compensated for (non-progressive shock)
  • may result in organ failure- due to prolonged hypotension and hypoperfusion
  • may progress to disseminated intravascular coagulation (DIC)

FD1 (31 decks)

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