Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

IC5 Management of Immune-mediated Toxicity Flashcards

(51 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 Examples of Drug Hypersensitivity Reactions

A

Vancomycin - Red Man Syndrome (Histamine)

ACEi/ARB - Angioedema (Bradykinin)

NSAIDs - Asthma (Prostaglandin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 Most reported drugs causing anaphylaxis

A
  1. Penicillin
  2. NSAID
  3. Insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is anaphylaxis?

A

Acute, life-threatening reaction

Involves multiple organ systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When is the risk of fatal anaphylaxis the greatest?

A

Within the first few hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The DRESS Triad

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Big culprits of DRESS

A

Allopurinol

Anticonvulsants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Presentation of SJS and TEN

A

Progressive bullous or “blistering” disorders (Dermatologic emergencies)

Progression - Mucus membrane erosion, Epidermal Detachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What drugs cause SJS and TEN?

A

Antibiotics (Sulfonamides especially)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which drug requires compulsory pharmacogenomic testing?

A

Carbamazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is controversial in the use of SCAR treatment?

A

Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why are autoimmune diseases difficult to treat?

Study These Flashcards
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?

Study These Flashcards
A

Autoantibody production resulting in multisystem disease

23
Q

Most autoimmune diseases including SLE are more prevalent in ______

24
Q

Factors leading to SLE

Study These Flashcards
A

Genetic disposition is strong

Environment (Smoking, infection, drugs)

25
Which patient population has a standardized mortality ratio for SLE that is 2.6 to 3 times higher than the general population?
Cardiovascular Renal Infections
26
How does autoantibody production in SLE occur? (Pathophysiology)
T and B lymphocyte activation and signaling are altered Abnormal clearance of apoptotic debris containing nuclear material ==> Immune response stimulated
27
4 Signs and Symptoms in the Clinical Presentations of SLE
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
Lab Clinical Presentation of SLE
Full Blood count drop (RBC, WBC, PLT) Immunologic Nuclear Material Present (ANA, Anti-dsDNA, Anti-Sm, Anti-RNP, low complement)
29
SLE Treatment goal
Remission or at least low disease activity (Prevent flares and other organ damage)
30
What 4 drugs are used for SLE? (Labelled indications)
1. NSAIDs (Aspirin) 2. Steroids (Prednisone) 3. Biologics (Belimumab) 4. Immunosuppressants
31
Which drug should all SLE patients, including pregnant women use? Why? (Efficacy, Toxicity, Timeframe)
Hydroxychloroquine - Prevent flare - Improve long term survival (Anti-inflammatory, immunomodulatory, anti-thrombotic effects) - Minimal ADR - 4 to 8 week effect
32
What is used as 1st line for acute symptoms of SLE? What needs to be taken for caution?
NSAIDs When Lupus nephritis worsens, cardiac risk increases, GI bleeding occurs (Recall ADRs of non-selective COX inhibitors)
33
How are steroids used in SLE?
Monotherapy or adjunctive to control flares and maintain low disease activity
34
What are the concerns of using high dose or long term corticosteroids?
HPA Suppression
35
Biologics Mode of action
Target and disrupt functioning B cells
36
3 Immunosuppressants and uses
IV/PO Cyclophosphamide - Severe organ involvement / Induction therapy Mycophenolate - Induction / Maintenance Azathioprine - Maintenance alternative
37
What is Antiphospholipid Syndrome?
Antiphospholipid antibody positive found in 40% of SLE patients but < 40% of these experienced thrombotic events
38
Primary and Secondary Thromboprophylactic Treatment of APS?
Hydroxychloroquine + Aspirin Warfarin
39
What is the mechanism of drug-induced lupus?
Small molecules from drugs can induce immune response by binding to larger molecules like proteins
40
3 cardio drugs at highest risk for drug-induced lupus
Hydralazine, Procainamide, Quinidine
41
How to evaluate therapeutic outcomes of SLE?
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
What lab values to look at to evaluate therapeutic outcomes for SLE?
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
What lab values do not need to be repeated at each visit for SLE therapeutic outcome evaluation? Why?
ANA, Anti-SM and Anti-RNP Antibodies They don't correlate well with activity
44
When is immunosuppression necessary?
Autoimmune conditions, Solid organ transplants, Stem cell/bone marrow transplants
45
Characteristics of induction therapy for 1) Autoimmune conditions 2) Preventing Acute Rejection
1) High potency short course therapy ASAP 2) Lymphocyte-depleting therapy (Basiliximab, Alemtuzumab)
46
5 types of maintenance therapy
1. Calcineurin inhibitors (Cyclosporin, Tacrolimus) 2. Antimetabolite (Mycophenolate, Azathioprine) 3. Corticosteroids 4. mTOR inhibitors (Sirolimus, Everolimus) 5. Biologics (Adalimumab)
47
6 Complications of Immunosuppression
1. Opportunistic infections 2. Cancers 3. Blood disorders (-penias) 4. Hepatotoxicity (Antimetabolites) 5. Renal Toxicity (Calcineurin) 6. Cardio - HTN, Hyperlipidemia, Hyperglycemia (Calcineurin, mTOR)
48
4 Main therapeutic effects of Corticosteroids
1. DMARD effect reducing joint damage 2. Anti-allergy 3. Anti-inflammatory (Pain, swelling) 4. Reduced endothelial dysfunction by reducing permeability
49
9 Adverse Reactions of Corticosteroids
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
How does HPA Axis suppression occur with corticosteroid therapy?
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
How much steroid to be used before adrenal suppression occurs?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions