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PR3152 Finals > Immune-related Toxicities > Flashcards

Immune-related Toxicities Flashcards

1
Q

Difference between true allergy and pseudoallergy in terms of components involved?

A

True allergy: mediators, lgE, lgG, lgM and T cells, formation of immune complexes

Pseudoallergy: mediators (histamine, PGs, kinins), does NOT involve immune system or any Ab

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2
Q

What are the drugs that can cause pseudoallergy? (3)

A
  • Vancomycin
  • ACE/ Sacubitril
  • NSAIDs
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3
Q

What are the different types of hypersensitivity reactions? (6)

Which type is SLE?

A
  1. Anaphylaxis
  2. Serum-sickness/ drug fever
  3. Drug-induced autoimmunity (SLE)
  4. Vasculitis
  5. Respiratory
  6. Hematologic
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4
Q

Drugs that can cause anaphylaxis? (3)

A

Penicillins, NSAIDs, insulins

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5
Q

Drugs that can cause serum-sickness/ drug fever? (1)

A

Antibiotics

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6
Q

Drugs that cause drug-induced autoimmunity? (2)

A

Methyldopa → hemolytic anaemia
Phenytoin → hepatitis

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7
Q

Drugs that cause vasculitis? (2)

A

Allopurinol, Thiazide

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8
Q

Drugs that cause respiratory hypersensitivity? (3)

A

NSAIDs, Bleomycin, Nitrofurantoin

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9
Q

Drugs that cause SCAR? (3)

A

Allopurinol, anticonvulsants and sulflonamides

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10
Q

First-line Tx for anaphylaxis and MOA?

What should we do if the pt manages to reach the hospital? (4)

A

Epinephrine (adrenaline)
MOA: counteracts bronchoconstriction and vasodilation

If pt reaches hospital:
- IV fluids (restore volume/ BP)
- Intubation to save airway (if necessary)
- Norepinephrine (noradrenaline) if in shock (severe hypotension)
- Steroids, glucagon, diphenhydramine (H1) + ranitidine (H2)

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11
Q

Tx for SCAR?
Non-pharmacological and pharmacological?

Use of which medication is controversial?

A

Supportive care (similar to burn pts):
- Wound care
- Nutritional support
- Fluids
- Temperature regulation
- Pain management
- Prevention of infections

May use intravenous immunoglobulin (IVIG) or cyclosporine

Steroid use controversial

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12
Q

In what type of people are SLE most prevalent?

A

More prevalent in females, non-white > white (African descent highest)

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13
Q

Which drugs have the highest risk of causing SLE? (3) (HPQ)

Other drugs?

A

Procainamide, hydralazine, quinidine

Others: minocycline, isoniazid, methyldopa, carbamazepine, TNFα inhibitors

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14
Q

What are the clinical presentation (labs) of SLE in terms of blood count?

A
  • Haemolytic anaemia: ↓ RBC
  • ↓ WBC / ↓ lymphocytes
  • ↓ PLT
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15
Q

What are the clinical presentation (labs) of SLE in terms of immunologic components?

A

Non-exhaustive:
- Antinuclear Ab (ANA)
- Antidouble-stranded DNA (dsDNA)
- Anti-Smith Ab (anti-Sm)
- Antinuclear ribonucleoprotein (anti-RNP)
- Low complement (C3, C4, CH50)

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16
Q

Name the drugs used for Tx of SLE (5) (BISHN)

A
  1. Hydroxychloroquine
  2. NSAIDs
  3. Steroids
  4. Biologics
  5. Immunosuppressants
17
Q

When do we use hydroxychloroquine for SLE? MOA?

How long to achieve effects?

A

ALL SLE patients

MOA:
- Prevents flare
- Improves long term survival
- Anti-inflammatory, immunomodulatory and anti-thrombotic effects

  • 4-8w to achieve effects
18
Q

Impt ADE of hydroxychloroquine?

What must we monitor?

A

Retinal toxicity > 10% prevalence after 20 years use

Need retinal checks

19
Q

Elaborate on NSAIDs for SLE and its ADEs

Hence what must we check before initiation?

A

First-line for acute s/sx

ADEs:
- Worsen kidney function
- ↑ cardiac risk
- GI bleed

Caution in worsening lupus nephritis, check kidney function beforehand

20
Q

Elaborate on use of steroids for SLE (what type of steroid used?)

MOA? ADEs (systemic and topical)?

A

Glucocorticoids

MOA:
- Control flares
- Maintain low disease activity

ADEs (systemic):
- Osteoporosis
- Cataracts
- Glaucoma
- Hyperglycemia/ diabetes
- HTN
- Dyslipidemia
- Skin thinning
- Weight gain
- Fat redistribution
- Sleep/ mood disturbances

Topical:
- Skin atrophy

21
Q

How do corticosteroids cause HPA axis suppression?

A
  1. Exogenous corticosteroids → ↓ secretion of Corticotropin-Releasing Hormone (CRH) from hypothalamus and Adrenocorticotropic Hormone (ACTH) from pituitary gland
  2. Overtime, HPA axis inactive (pts cannot produce own cortisols)
  3. End result: adrenal suppression
22
Q

How much steroid use before adrenal suppression occurs?

A
  • Doses > 5mg prednisone daily for > 3w (but actually IRL no clear “cut off”)
  • Maintain suspicion as long as pts have taken corticosteroids before/ are taking it currently
23
Q

Type of biologics used for SLE? (2)

MOA? What should we note about live vaccines?

A

Belimumab, Rituximab

MOA:
- Targets and disrupts functioning of B cells

DO NOT administer live vaccines in pts taking biologics

24
Q

Name the immunosuppressants used for SLE (6)

Note: immunosuppressants are steroid sparing :)

A
  1. Cyclophosphamide (PO, IV)
  2. Mycophenolate
  3. Azathioprine
  4. Methotrexate
  5. Mycophenolate Mofetil
  6. Cyclosporine
  7. Tacrolimus
25
Q

ADEs of cyclophosphamide? Who should avoid?

A
  • Hemorrhagic cystitis
  • Bladder malignancy
  • INFERTILITY*

Avoid if pt has Hx of cystitis/ bladder problems

26
Q

How often do you monitor labs for SLE?

What labs do you monitor?

A

Regular labs every 1-3 mths with active disease, 6-12 mths if stable

Monitor urinalysis, anti-dsDNA Ab, complement C3, C4 levels, C-reactive protein, full blood counts, liver function

27
Q

What is a complication of SLE?

What happens during SLE?

A

Antiphospholipid syndrome (APS)

  • High risk of clotting
  • High risk of pregnancy morbidity (no. of miscarriages can also be a diagnostic criteria)
28
Q

Tx of APS SLE?

  1. Primary thromboprophylaxis
  2. Secondary thromboprophylaxis
  3. Protective
A
  1. Primary thromboprophylaxis: aspirin
  2. Secondary thromboprophylaxis: thrombophylaxis
  3. Protective: hydroxychloroquine
29
Q

Drugs used for induction of immunosuppression?

  1. Lymphocyte-depleting agents
  2. Immune modulators which prevent activation & proliferation of T cells
A

Lymphocyte-depleting agents:
- Antithymocyte globulin
- Alemtuzumab (off-label)

Prevent activation & proliferation of T cells:
- Basiliximab

30
Q

Drug classes and drugs under each class that are used for maintenance Tx of immunosuppression?

Note: ALL need TDM!

A

Calcineurin inhibitors: cyclosporin, tacrolimus*

Anti-metabolites: mycophenolate*, azathioprine

Corticosteroids

mTOR inhibitors: sirolimus, everolimus

Biologics: adalimumab, belatacept

31
Q

What complications can azathioprine and mycophenolate cause? (2)

A
  • Bone marrow suppression
  • Hepatotoxicity
32
Q

What complications can steroids and CNI cause? (3)

A
  • HTN
  • Hyperlipidemia
  • Hyperglycemia
33
Q

What do we give pts for induction therapy for immunosuppression? Why?

A

Give biologic Tx to delay use of CNI (CNI is nephrotoxic)

34
Q

What is a common combination of maintenance agents for immunosuppression?

A

Calcineurin inhibitor + glucocorticoids + mycophenolate

35
Q

What is a combination we should avoid for maintenance agents for immunosuppression and why?

A

Calcineurin inhibitor + mTOR due to ↑ nephrotoxicity

36
Q

How should we treat CNI-induced renal toxicity?

What should we AVOID?

A

First-line: DHP CCB

Avoid ACEi or diuretics

37
Q

DDIs to take note of for drugs under immunosuppression maintenance Tx?

A

CNI (tacrolimus, cyclosporine) and mTORi → CYP3A4 and P-glycoprotein substrates

PR3152 Finals (8 decks)

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