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Pharmacology AP > IVIG > Flashcards

IVIG Flashcards

1
Q

What does the IVIG contain (Spurlock, 2020)

A

-90% IgG
-traces: IgA, IgM, CD8, CD4 and leukocyte antigen

+ altered pH (to decerase bacterial contamination)

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2
Q

What is the half life of IVIG?

A

-human: 21-33 days
-canine: 7-9 days

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3
Q

By wich mechanisms do IVIG modulates immune system (Spurlock, 2020)

A
  1. Fc receptor disruption
  2. Pathologic autoAb neutralisation
  3. Complement inhibition
  4. Fas-FasL binding interference
  5. Cytokine syntesis downregulation
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4
Q

Where are Fc receptors found (Spurlock, 2020)

A
  1. neutrophils
  2. NK cells
  3. macrophages
  4. eosinophils
  5. Mast cells
  6. platelets
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5
Q

How does IVIG block the Fc receptor?

A

-IVIG blocks transient Fc receptors, interferes with Ag presentation and downregulates the immune response
+IVIG initiates self-inhibition in inflammatory cells ( in presence of IVIG macrophages upregulate inhibitory receptors, which block FcR normally activated by immune complexes /dont release inflammatory mediators)

(Ab-Ag complex bind to Fc receptor and initiate phagocytosis)

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6
Q

Within what time frame IVIG works in humans and dogs?

A

-in humans- Fc blockade is conc dependent and immediate - clinical effects within 3 days
-canine- within 24-48 h

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7
Q

How does the autoAb neutralization works with IVIG (Spurlock, 2020)

A

-anti-idiotype Ab in hIVIG solutions- bind both Ag binding sites and non-binding site idiotypes on B cell Ig or circulating autoAb
-via this mech- IVIG can help regulate immune response by neutralising pathogenic autoAb

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8
Q

Why is autoAb neutralization less effective in canine than in humans (Spurlock, 2020)

A

-because interspecies Ab binds poorly and rarely yields anti-idiotypic Ab

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9
Q

What is the MOA of IVIG and complement inhibition?

A

-transfused Ig binds C3b and C4b
- subsequently inhibits generation of MAC (C5b-C9)
-prevents complement -Ig interaction and limits tissue damage

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10
Q

To wich family Fas receptors belong?

A

TNF superfamiliy

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11
Q

How does the IVIG block FAS-FASL mediation?

A

-blocks their interaction and prevents epidermal apoptosis
-they promote proinflammatory cytokines

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12
Q

How does the IVIG downregulates cytokines?

A

-in the presence of IVIG , mononuclear cells and activated T cell produce less proinflammatory cytokines (IL-1, TNF-beta, INF-gamma) in response to lipopolysaccharide or bacterial superantigens
-the same cells produce antiinflammatory cytokine- IL-1 R anatagonis

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12
Q

What are other immunomodulatory effects of IVIG?

A

-modulate adhension molecules, B and T cells
-modifications of innate and adaptive immunity
-dependant on dose or specific inflammatory conditions
-BUT effects are synergistic, and not mutually exclusive

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13
Q

For wich conditions is hIVIG beeing used in vet med?

A
  1. IMHA
  2. ITP
  3. Evans syndrome
  4. Cutaneous autoimmune disease-EM (cat), SJS, TEN, PF
  5. MG
  6. Sudden acquired retinal degeneration syndrome
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14
Q

Which drug is recommened in refractory ITP?

A

vincristine

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15
Q

What are the dosages used in cutaneous diseases ?

A

1 g/kg over 4 h for 2 consecutive days

= 0.5-2.2 g/kg
-start slow at 0.01 mL/kg/min
-increase over 30-60 min
-max 0.8 mL/kg/min
-over 4 to 8 h

-reaction: stop +adminiter antihistamines

16
Q

What are the most common complications in human and vet medicine?

A

-people 5-15 %
-hypersensitiovity reactions- especially in dogs XENOPROTEIN
-thromboembiolism
-renail failure
-hypotension
-asepctic meningitis
-intravascular fluid overload
-transient neutropenia
-serum sickness

16
Q

What is the most common complication of hIVIG?

A
  1. Acute hypersensitivity /anaphylaxis
    -rate of administration is correlated with complication rate
    -start slow then incerase
    -signs often reslove after slowing or temporarly disoctinuiting
  2. type III hypersensitivity
17
Q

What are the most common symptoms of acute hypersnitivity of hIVIG?

A

-pyrexia, flushing, facial edema, tachycardia, vomiting, diarrhoea
-dysthythmias, dyspnea, hypotension, seizures
-anaphylaxis

18
Q

With type III hypersensitivity, what are symtoms and is it documented in canines?

A

-Ag-Ab complex deposition in renal basement membrane and glomerulonephritis
-NOT

19
Q

How does hIVIG promotes thromboembolic disease?

A

-because it stimulates inflammation, promotes hyper coagulability
-activates platelets
-especially be careful in IMHA (prothrombitic condition) - pretreatment with antithrombotic therapy
+ the hIVIG is a hyperosmolar fluid

20
Q

What is patomechanims of renal failure in hIVIG?

A

-sucrose is used as a stabilizer in hIVIG preparations
= cause osmotic damage to prox tubules , cellular swelling, tubular occlusion, cytoplasmic vacuolisation
-azotemina- within 5 days (can be transient)
-also available sucrose free Ig products

Pharmacology AP (10 decks)

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