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endo y3s1 > IC9 Immune-mediated toxicities > Flashcards

IC9 Immune-mediated toxicities Flashcards

1
Q

types of allergy

A

immune (allergy)
non-immune (pseudoallergy)

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2
Q

immune (allergy): types of hypersensitivity reactions

A
  1. Immediate → IgE mediated; atopy
    Type I, II, III hypersensitivity reactions → occurs within 24 hours of exposure
  2. Delayed → IgM, IgG, T cell mediated
    Type IV hypersensitivity reaction
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3
Q

immune (allergy): prevalence

A

~10-15% of all ADR

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4
Q

cause of non-immune (pseudoallergy)

A

Drugs causing release of mediators: histamine, prostaglandins, bradykinins → often mast cell & basophil derived
By pharmacologic/ physical effect

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5
Q

non-immune (pseudoallergy): prevalence

A

~77% of hypersensitivity reactions

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6
Q

Effectors of drug hypersensitivity reactions

A

Involving major components of innate & adaptive immune systems
Involving release of pharmacologically active chemical mediators

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7
Q

Effectors of drug hypersensitivity reactions: innate & adaptive components

A

Cellular elements: macrophages T & B lymphocytes, platelets, mast cells
Immunoglobulins: especially IgE (associated to type I AR, immediate reaction)
Complements: activation of mast cells & inflammatory mediators
Cytokines

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8
Q

Effectors of drug hypersensitivity reactions: pharmacologically active chemical mediators

A

Histamine, platelet-activating factor (PAF), prostaglandins (PG), thromboxanes, leukotrienes

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9
Q

clinical manifestations (main ones)

A

anaphylaxis
severe cutaneous adverse reactions

others:
serum sickness/ drug fever
drug induced autoimmunity
vasculitis
haematologic
respiratory

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10
Q

clinical manifestations: anaphylaxis definition

A

Acute & life-threatening, involves multiple organ systems
First few hours ⇒ highest risk of fatal anaphylaxis

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11
Q

clinical manifestations: anaphylaxis organs involved

A

skin, CNS, GIT
respiratory - bronchoconstriction: difficulty breathing, SOB, chest tightness
CVS: low BP, high HR, chest pain

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12
Q

clinical manifestations: anaphylaxis first line treatment + how does it work

A

epinephrine

Acts on ⍺ & β receptors
Counteracts bronchoconstriction & vasodilation

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13
Q

clinical manifestations: anaphylaxis hospital treatment

A

IV fluids → restore volume/ BP
Intubation PRN → to save airway
Norepinephrine (noradrenaline) → if shock

Others:
possible agents:
Steroids → suppresses later reactions
Glucagon (if patient currently on BB) → helps with chronotropic & inotropic effects, for regular heart beat
H1 [diphenhydramine] + H2 [ranitidine] → blocks all histamine receptors, to slow down reactions

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14
Q

clinical manifestations: SCAR types

A

DRESS, TEN, SJS

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15
Q

clinical manifestations: SCAR (DRESS presentation)

A

Triad of rash, eosinophilia & internal organ involvement

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16
Q

clinical manifestations: SCAR (DRESS mortality)

A

10%

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17
Q

clinical manifestations: SCAR (SJS & TEN presentation)

A

Progressive bullous or “blistering” disorders → dermatologic emergencies
Progress to include mucous membrane erosion & epidermal detachment

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18
Q

clinical manifestations: SCAR (SJS & TEN extent of symptoms)

A

SJS: less than 10% detachment of body surface area
TEN: greater than 30%

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19
Q

clinical manifestations: SCAR (SJS & TEN mortality)

A

SJS: 1% to 5%
TEN: 10% to 70%

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20
Q

clinical manifestations: SCAR treatment guide

A
  1. No defined cure; important to stop taking causative drug
  2. Supportive care (similar to burn patients): Wound care, nutritional support, fluids, temperature regulation, pain management & prevention of infection
  3. Possible steroid use (not first line)
  4. IV immunoglobulin, cyclosporin
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21
Q

SLE
how it is a multisystem disease

A

Associated with auto-Ab production
immune-mediated complex can be anywhere in the body

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22
Q

SLE
how is it a multifactorial disease

A
  1. Strong genetic disposition
    Present in first degree relatives ⇒ 20x more likely
  2. environmental factors
    smoking, infection, drugs, pollution, UV light, Epstein-Barr virus (herpes)
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23
Q

SLE
clinical presentation

A
  1. Lupus nephritis
    Kidney disease; requires transplant
    4 classes (stages of disease)
  2. Neuropsychiatric lupus
    Cerebrovascular disease (stroke), anxiety, seizures, cognitive dysfunction, confusion, peripheral neuropathy, psychosis
  3. CVS
    Pericarditis, myocarditis
    Accelerated atherosclerosis
24
Q

SLE
labs

A
  1. Full blood count
    Hemolytic anaemia (↓ RBC)
    ↓ WBC or ↓ lymphocytes
    ↓ Platelet
  2. Immunologic
25
Q

SLE
treatment: goals

A

achieve low disease activity & treat complications

To prevent flares & other organ involvement, slow disease activity, reduce use of steroids, improve QOL & minimise AE

26
Q

SLE
treatment: drugs involved

A

hydroxychloroquine
steroids
NSAIDs
biologics
immunosuppresants

27
Q

treatment of SLE: hydroxychloroquine dose

A

5mg/ kg/ day

28
Q

treatment of SLE: hydroxychloroquine effect

A

Prevents flare & improve long term survival ⇒ have anti-inflammatory, immunomodulatory & anti-thrombotic effects
- ↓ activation of T & B cells ⇒ no production of auto Ab
- ↓ APC & receptors on T cell ⇒ suppression of T cell activation

29
Q

treatment of SLE: hydroxychloroquine indication

A

ALL patients to receive (including pregnant women)

30
Q

treatment of SLE: hydroxychloroquine AE

A

Minimal AE but retinal toxicity > 10% prevalence after 20 years
Important to conduct eye exams

31
Q

treatment of SLE: hydroxychloroquine time for effects

32
Q

treatment of SLE: NSAIDs indication

A

1st line for acute symptoms

33
Q

treatment of SLE: NSAIDs cautionary

A

worsening lupus nephritis, increase cardiac risk & GI bleed

34
Q

treatment of SLE: Steroids dose

A

Low-dose monotherapy/ adjunctive therapy

35
Q

treatment of SLE: Steroids purpose

A

controlling flares & maintain low disease activity
Rapid onset

36
Q

treatment of SLE: Steroids concerns

A

high dose and/ or long term use

37
Q

treatment of SLE: Steroids AE (PO)

A

hyperglycemia, HTN, pre-eclampsia (for pregnancy), gestational diabetes & osteoporosis, weight gain, dyslipidemia

38
Q

treatment of SLE: Steroids AE (topical)

A

skin atrophy

39
Q

treatment of SLE: biologics (agents)

A

Belimumab & Rituximab (for severe disease)

40
Q

treatment of SLE: biologics MOA

A

Targets & disrupts functioning B cells

41
Q

treatment of SLE: immunosuppresants (agents & therapy type)

A

IV/ PO cyclophosphamide (severe disease) → severe organ involvement; induction therapy

Mycophenolate → induction & maintenance therapy

Azathioprine → alternative to mycophenolate (maintenance)

42
Q

treatment of SLE: immunosuppresants
cyclophosphamide - AE

A

cystitis, bladder malignancy, infertility

43
Q

treatment of SLE: immunosuppresants
Mycophenolate - AE

A

GI SE might limit use & compliance

44
Q

treatment of SLE: immunosuppresants
Azathioprine - requirement before use

A

Test for thiopurine methyltransferase (TPMT) before initiation → should be able to work & metabolise drug

45
Q

treatment of SLE: guide (according to severity)

A

ALL:
hydroxychloroquine
steroids (PO/IM - mild & PO/IV - moderate and severe)

MILD: methotrexate/ azathioprine
MODERATE: benlimumab/ mycophenolate
SEVERE: cyclophosphamide/ rituximab

46
Q

SLE
Evaluation of therapeutic outcomes

A

ADR
Development of comorbidities
Measure disease activity
Regular labs every 1-3 months with active disease; 6-12 months if stable
- urinalysis/ renal function, anti-dsDNA Ab, Complement C3, C4 levels, CRP, FBC, LFT
- other tests dont need repeat –> does not fluctuate with disease state

47
Q

Immunosuppression: reasons

A

Autoimmune conditions
Solid organ transplants
Stem cell/ bone marrow transplants
- Involves development of new cell lines → impt to suppress existing immune cells to produce new cells

48
Q

Immunosuppression: cell targets

A

T cells, B cells, mediators (cytokines), APC

49
Q

Immunosuppression: Purpose in autoimmune diseases
(induction)

A

To stop immune system from exerting effects
High potency, short-course therapy ASAP → reduce existing damage & prevent worsening of condition

To suppress/ lyse/ prevent activation & proliferation of T cells

50
Q

Immunosuppression: agents used for induction (autoimmune diseases)

A
  1. Lymphocyte-depleting agents causing cell lysis
    * Antithymocyte globulin → targets T cells
    * Alemtuzumab → longer duration of action; binds to CD52 surface Ag on T cells ⇒ triggers apoptosis & destroys T cells
  2. Immune modulators preventing activation & proliferation of T cells: Basiliximab
51
Q

Immunosuppression: Purpose in autoimmune diseases
(maintainence)

A

To keep immune system from functioning

52
Q

Immunosuppression: use in transplant

A
  1. Patient selection: match HLA & blood type as closely as possible → reduce risks of rejection
  2. Use intensive induction therapy to avoid initial rejection
  3. Multiple maintenance agents used to target different mechanisms
  4. Reduce dosage/ withdraw if toxicity > benefits
53
Q

Immunosuppression: autoimmune diseases
(importance of TDM)

A

to prevent toxicity, depending on type of transplant & when transplant

54
Q

Use of steroids

A

Essential for chronic conditions due to powerful anti-inflammatory & immunosuppressive effects

55
Q

Dose of HPA-axis suppression

A

Generally supraphysiologic doses of >5mg prednisone daily for more than 3 weeks

Also possible in <5mg prednisone daily after <4 weeks of exposure and tapered withdrawal

56
Q

Effects of steroid use

A

reduce pain, swelling, stiffness & physical disability

57
Q

HPA-axis suppression
process of occurrence

A
  1. Exogenous GC → decreased secretion of CRH & ACTH
  2. Over time, whole HPA axis becomes inactive ⇒ cannot produce own cortisol
  3. Unable to recover function quickly if exogenous steroids are stopped

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