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PR3152 Immune and Endocrine (NUS Pharmacy) > IC5 Management of Immune-mediated Toxicity > Flashcards

IC5 Management of Immune-mediated Toxicity Flashcards

1
Q

What is the difference between drug allergies and hypersensitivity reactions?

A

Drug Allergies = Immunologically mediated response in a sensitized person

Hypersensitivity = Not proven to be immunologically mediated but can involve mediators released from mast cells and basophils caused by drugs

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2
Q

3 Examples of Drug Hypersensitivity Reactions

A

Vancomycin - Red Man Syndrome (Histamine)

ACEi/ARB - Angioedema (Bradykinin)

NSAIDs - Asthma (Prostaglandin)

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3
Q

What effectors of Allergic/Hypersensitivity reactions can be involved?

A

Innate and Adaptive - IgE, Cytokines, Complements, Cellular elements

Mediators released - Histamine, PAF, PG, Thromboxanes, Leukotrienes

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4
Q

4 Classifications of Allergic Reactions

A
  1. Immediate Hypersensitivity (Mast cells, IgE, eosinophils)
  2. Antibody-mediated Diseases (IgM, IgG)
  3. Immune Complex-mediated Diseases (IgM and IgG complexes deposit in vascular basement membrane)
  4. T Cell-mediated Diseases (CD4 and CD8)
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5
Q

3 Most reported drugs causing anaphylaxis

A
  1. Penicillin
  2. NSAID
  3. Insulin
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6
Q

What is anaphylaxis?

A

Acute, life-threatening reaction

Involves multiple organ systems

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7
Q

When is the risk of fatal anaphylaxis the greatest?

A

Within the first few hours

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8
Q

Signs of Anaphylaxis - Where do they normally present?

A

Skin - Urticaria (Hives), Itch/flush skin, swelling lips/tongue/throat/face

Airway - Tight/Swelling throat, hoarseness, scratchy throat, SOB, wheeze, chest tight

CVS - Chest pain, Low BP, Rapid HR

GIT - N/V/D, abdominal cramp

CNS - Tunnel vision, confusion, dizziness

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9
Q

Other clinical manifestations of allergy/hypersensitivity

A
  1. Serum sickness (Drug Fever) - Abx
  2. Drug induced autoimmunity (SLE)
  3. Vasculitis - Allopurinol, thiazide
  4. Asthma/Acute infiltrative & chronic fibrotic pulmonary reactions - Bleomycin, Nitrofurantoin
  5. Hematologic (Eosinophilia - Drug Hypersensitivity; Hemolytic anemia, thrombocytopenia, agranulocytosis)
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10
Q

What is SCAR? Three types of SCAR?

A

Serious Cutaneous Adverse Reactions
1. Drug Rash with Eosinophilia and Systemic Symptoms (Dress)
2. Mucocutaneous Disorders (SJS and TEN)

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11
Q

The DRESS Triad

A

Rash, Eosinophilia, Internal Organ involvement (Hepatitis, Interstitial Nephritis, Carditis, Adenopathy, Pneumonia)

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12
Q

Big culprits of DRESS

A

Allopurinol

Anticonvulsants

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13
Q

Presentation of SJS and TEN

A

Progressive bullous or “blistering” disorders (Dermatologic emergencies)

Progression - Mucus membrane erosion, Epidermal Detachment

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14
Q

Which is more severe? SJS or TEN?

A

TEN is more severe than SJS
1) >30% vs <10% detachment of body surface area
2) Mortality rate of TEN is higher (10-70% vs 1-5%)

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15
Q

What drugs cause SJS and TEN?

A

Antibiotics (Sulfonamides especially)

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16
Q

4 Common drugs that have been more genetically disposed to drug allergy or hypersensitivity

A
  1. Abacavir
  2. Allopurinol
  3. Phenytoin
  4. Carbamazepine
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17
Q

Which drug requires compulsory pharmacogenomic testing?

A

Carbamazepine

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18
Q

5 Therapeutic Actions for Anaphylaxis Treatment

A
  1. Epinephrine - HR and BP
  2. IV fluid - BP / Blood volume
  3. Intubation - Airway
  4. Norepinephrine - If shock
  5. Others: Steroids, glucagon, diphenhydramine (H1) + Ranitidine (H2)
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19
Q

How is SCAR treated?

A

Supportive care (Similar to burn patients)
- Wound care
- Nutritional support
- Fluids
- Temperature regulation
- Pain management
- Prevention of infections

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20
Q

What is controversial in the use of SCAR treatment?

A

Steroids

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21
Q

Why are autoimmune diseases difficult to treat?

A
  1. Patient response - Poor tolerance
  2. Drug cost
  3. Poor drug indications (Off-label use)
  4. Seen as weakness, people are less likely to seek help
22
Q

What is autoimmune disease associated with?

A

Autoantibody production resulting in multisystem disease

23
Q

Most autoimmune diseases including SLE are more prevalent in ______

A

Females

24
Q

Factors leading to SLE

A

Genetic disposition is strong

Environment (Smoking, infection, drugs)

25
Q

Which patient population has a standardized mortality ratio for SLE that is 2.6 to 3 times higher than the general population?

A

Cardiovascular

Renal

Infections

26
Q

How does autoantibody production in SLE occur? (Pathophysiology)

A

T and B lymphocyte activation and signaling are altered

Abnormal clearance of apoptotic debris containing nuclear material ==> Immune response stimulated

27
Q

4 Signs and Symptoms in the Clinical Presentations of SLE

A
  1. Butterfly rash and red skin patches
  2. Lupus Nephritis (Kidney)
  3. Neuropsychiatric Lupus (Stroke, seizures, peripheral neuropathy)
  4. Cardiovascular inflammation (Myocarditis) and accelerated atherosclerosis
28
Q

Lab Clinical Presentation of SLE

A

Full Blood count drop (RBC, WBC, PLT)

Immunologic Nuclear Material Present (ANA, Anti-dsDNA, Anti-Sm, Anti-RNP, low complement)

29
Q

SLE Treatment goal

A

Remission or at least low disease activity (Prevent flares and other organ damage)

30
Q

What 4 drugs are used for SLE? (Labelled indications)

A
  1. NSAIDs (Aspirin)
  2. Steroids (Prednisone)
  3. Biologics (Belimumab)
  4. Immunosuppressants
31
Q

Which drug should all SLE patients, including pregnant women use? Why? (Efficacy, Toxicity, Timeframe)

A

Hydroxychloroquine
- Prevent flare
- Improve long term survival (Anti-inflammatory, immunomodulatory, anti-thrombotic effects)
- Minimal ADR
- 4 to 8 week effect

32
Q

What is used as 1st line for acute symptoms of SLE? What needs to be taken for caution?

A

NSAIDs

When Lupus nephritis worsens, cardiac risk increases, GI bleeding occurs

(Recall ADRs of non-selective COX inhibitors)

33
Q

How are steroids used in SLE?

A

Monotherapy or adjunctive to control flares and maintain low disease activity

34
Q

What are the concerns of using high dose or long term corticosteroids?

A

HPA Suppression

35
Q

Biologics Mode of action

A

Target and disrupt functioning B cells

36
Q

3 Immunosuppressants and uses

A

IV/PO Cyclophosphamide - Severe organ involvement / Induction therapy

Mycophenolate - Induction / Maintenance

Azathioprine - Maintenance alternative

37
Q

What is Antiphospholipid Syndrome?

A

Antiphospholipid antibody positive found in 40% of SLE patients but < 40% of these experienced thrombotic events

38
Q

Primary and Secondary Thromboprophylactic Treatment of APS?

A

Hydroxychloroquine + Aspirin

Warfarin

39
Q

What is the mechanism of drug-induced lupus?

A

Small molecules from drugs can induce immune response by binding to larger molecules like proteins

40
Q

3 cardio drugs at highest risk for drug-induced lupus

A

Hydralazine, Procainamide, Quinidine

41
Q

How to evaluate therapeutic outcomes of SLE?

A
  1. ADR
  2. Comorbidity development
  3. Measures of disease activity
  4. Regular labs (1-3 mth) for active disease
  5. 6-12 mth for stable disease
42
Q

What lab values to look at to evaluate therapeutic outcomes for SLE?

A
  1. Urinalysis / Renal function
  2. Anti-dsDNA antibodies
  3. Complement C3, C4 levels
  4. C-reactive protein
  5. Full blood count
  6. Liver function tests
43
Q

What lab values do not need to be repeated at each visit for SLE therapeutic outcome evaluation? Why?

A

ANA, Anti-SM and Anti-RNP Antibodies

They don’t correlate well with activity

44
Q

When is immunosuppression necessary?

A

Autoimmune conditions, Solid organ transplants, Stem cell/bone marrow transplants

45
Q

Characteristics of induction therapy for
1) Autoimmune conditions
2) Preventing Acute Rejection

A

1) High potency short course therapy ASAP

2) Lymphocyte-depleting therapy (Basiliximab, Alemtuzumab)

46
Q

5 types of maintenance therapy

A
  1. Calcineurin inhibitors (Cyclosporin, Tacrolimus)
  2. Antimetabolite (Mycophenolate, Azathioprine)
  3. Corticosteroids
  4. mTOR inhibitors (Sirolimus, Everolimus)
  5. Biologics (Adalimumab)
47
Q

6 Complications of Immunosuppression

A
  1. Opportunistic infections
  2. Cancers
  3. Blood disorders (-penias)
  4. Hepatotoxicity (Antimetabolites)
  5. Renal Toxicity (Calcineurin)
  6. Cardio - HTN, Hyperlipidemia, Hyperglycemia (Calcineurin, mTOR)
48
Q

4 Main therapeutic effects of Corticosteroids

A
  1. DMARD effect reducing joint damage
  2. Anti-allergy
  3. Anti-inflammatory (Pain, swelling)
  4. Reduced endothelial dysfunction by reducing permeability
49
Q

9 Adverse Reactions of Corticosteroids

A
  1. Infection
  2. Myopathy
  3. Osteoporosis/Osteonecrosis
  4. Neuropsychiatric symptoms (HPA insufficiency)
  5. Metabolism - Weight gain, obesity, fluid retention, edema, Cushing syndrome, Insulin resistance, Beta cell dysfunction
  6. Gastric ulcer (if concomitant NSAIDs)
  7. Skin thinning and hirsutism
  8. Cataract and Glaucoma
  9. Increased Cardiovascular risk
50
Q

How does HPA Axis suppression occur with corticosteroid therapy?

A

Exogenous glucocorticoids can inhibit CRH and ACTH secretion ==> Reduced cortisol secretion by adrenal cortex ==> Atrophy occurs ==> HPA axis becomes inactive ==> Cannot recover function quickly if corticosteroid stopped immediately

51
Q

How much steroid to be used before adrenal suppression occurs?

A

Supraphysiologic doses of greater than 5mg prednisone equivalents daily for > 3 weeks

< 5mg prednisone equivalent dose daily after less than 4 weeks of exposure and even following tapered withdrawal

PR3152 Immune and Endocrine (NUS Pharmacy) (10 decks)

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