Anaphylaxis Flashcards

1
Q

What type of hyerpsensitivity reaction is anaphylaxis?

A

type I

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2
Q

What can cause nonimmune-mediated anaphylaxis?

A

heat, exhaustion, drugs/chemicals

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3
Q

What are the 2 most important cells in the pathogenesis of anaphylaxis?

A

mast cells
basophils

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4
Q

List 6 mediators released during anaphylaxis

A
  • histamine
  • Platelet activating factor
  • eosinophil-chemotactic factor
  • heparin
  • prostaglandins
  • tryptase
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5
Q

What are the effects of platelet activating factor in anaphylaxis

A

platelet aggregation
increased vascular permeability
bronchoconstriction
vasodilation

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6
Q

What are the effects of tryptase in anaphylaxis?

A

activates complement

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7
Q

What is the name of the receptor on mast cells’ and basophils’ surface that IgE binds to?

A

Fc-epsilon-R1

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8
Q

What are the different histamine receptors and what are each of their effects when activated?

A

H1 - vasodilation and extravasation
H2 - gastric acid secretion and modulation of cardiac myocytes
H3 and H4 - neurotransmitter release

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9
Q

How soon after exposure do signs of anaphylaxis occur?

A

different resources but say 15 min to hours - CCM within 30 min and progression over next hours

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10
Q

How is the hepatic/portal circulation affected in dogs with anaphylaxis?

A

hepatic arterial vasodilation and hepatic venous congestion - portal hypertension –> fluid transudation and decreased venous return to the heart

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11
Q

What is “biphasic” anaphylaxis?

A

occurence of delayed signs (usually respiratory and cutaneous) - hours to days later

reported in 1-20% of human anaphylaxis patients

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12
Q

How sensitive and specific are ALT elevations and gall bladder wall edema in dogs suspected to have anaphylaxis?

A

both almost 100% specific (98%), ALT 85% sensitive, Gall bladder edema 93% sensitive

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13
Q

How is epinephrine suspected to help reduce further progression of CS in anaphylaxis?

A

reduces further histamine release by stabilizing mast cells

beta - 2 effects - bronchodilation
alpha -1 effects - vasoconstriction
beta - 1 effects - improving CO

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14
Q

What is the main benefit of anti-histamine administration in anaphylaxis (e.g., diphenhydramine)

A

shown to reduce cutaneous signs - so really mostly indicated to help with that

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15
Q

How long does the onset of action take after administering glucocorticoids and what is their main benefit in anaphylaxis?

A

minimum 30 min - likely hours

downreguate the late phase eosinophilic response, block arachidonic acid pathway, delayed inflammatory cascades

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16
Q

describe the alternative IgG mediated pathway of anaphylaxis

A

IgG binds via Fc-gamma-RIII receptors

mediated mostly by PAF

17
Q

Explain how hepatocellular necrosis may happen in anaphylaxis

A

from sinusoidal and venous congestion - ischemia

18
Q

How much fluid can leave the IV space and move into the interstitial space during anaphylaxis?

19
Q

How common are cutaneous signs in anaphylaxis in dogs and cats and how do these signs compare to milder allergic reactions?

A

different studies - Drobatz says 57%
in anaphylaxis cutaneous signs are actually milder than in mild allergic reactions that are primarily cutaneous

20
Q

What has been associated with death in dogs with severe anaphylaxis in Smith et al, 2020?

A
  • hyperphosphatemia (>12)
  • elevated PT
  • concurrent PT and aPTT > 50% RI
  • hypglycemia within 6 hours of presentation
  • need for dextrose supplementation

serum phosphorous and PT times were significantly higher in nonsurvivors
temperature was significantly lower in nonsurvivors

21
Q

How common were coagulopathies, peritoneal effusion, and gall bladder halo signs in dogs with severe anphylaxis in Smith et al., 2020?

A
  • 85%
  • 65%
  • 85%

(approximate values)

22
Q

How common were GI, respiratory, and cutaneous signs in dogs with severe anaphylaxis in Smith et al, 2020?

A
  • 94%
  • 67%
  • 27%
23
Q

What was the overall mortality rate in dogs with severe sepsis in Smith et al, 2020?

24
Q

What is the proposed mechanism for hypothermia in dogs with severe anaphylaxis Smith et al, 2020? (3)

A
  • peripheral vasodilation
  • decreased CO
  • histamine affecting hypothalamic temperature regulation
25
What is the proposed mechanism for hyperphosphatemia in severe anaphylaxis in Smith et al, 2020?
liver injury: P release from cell death, decreased uptake and utiliation of P by hepatic cells
26
What is the proposed mechanism for hypoglycemia in severe anaphylaxis in Smith et al, 2020?
* decreased hepatic gluconeogenesis * increased cellular utilization * sepsis-induced - GI bacterial translocation
27
What was the estimated incidence of anaphylaxis or mild hypersensitivity reactions in Fosset et al, 2023?
* 0.04% * 0.15%
28
What was the most common cause for hypersensitivity reactions and anaphylaxis in Fosset et al, 2023?
* most common known trigger: vaccines * in hypersensitivity reactions: unknown trigger more common than known vaccine trigger
29
How did hemostatic derangements compare between severe versus mild and moderate cases of anaphylaxis in Smith et al, 2022?
VCM: * longer CT and CFT * decreased alpha angle, MCF prolonged PT and aPTT lower platelet counts
30
What was the association between anaphylaxis induced spontaneous hemoperitoneum and coagulopathies in Summers et al, 2021
did not seem to be the contributing factor, however, only 5/16 dogs had clotting times evaluated * only 1 patient prolonged PT and another one prolonged aPTT * all platelet counts were normal