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3152 > HYPERSENSITIVITY > Flashcards

HYPERSENSITIVITY Flashcards

1
Q

drug/ food/ etc allergies

A

• Immunologically mediated hypersensitive reaction to sub in sensitised person

Response of immune system to antigenic sub leads to host tissue damage (organ specific// generalised systemic reaction)

6-10%

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2
Q

what is present in allergy

A

○ IgE released
○ Type 1 Immediate hypersensitivity
§ TH2 cells, IgE Ab, mast cells, eosinophils
§ Mast cell-derived mediators
§ Cytokine-mediated inflam
§ Eosino, neut

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3
Q

Immune response:

A

• Hives
• Rash
• Hypotension
• Bronchospasm
• Anaphylaxis
• Vasculitis

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4
Q

Drug hypersensitivity

A

• Adverse events that clinically resemble drug allergy
• Not proven to be associated with immune response

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5
Q

Drug hypersensitivity what is present

A

• Drug release mast cell
• Basophil derived mediators
• By pharmacologic or physical effect
•Not IgE

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6
Q

eg of drug hypersensitivity

A

• Vancomycin
• Red man syndrome
• Direct release of histamine when infused too quickly

• ACE/ sacubitril
• Angioedema
• Inhibit breakdown of bradykinin
• Inflammation, vasodilation, permeation

• NSAID
• Induced asthma
• Alter metabolism of prostaglandins
•Vasoconstriction

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7
Q

effector of allergic / DH reactions

A

○ Involve major components of INNATE/ ADAPTIVE immune
§ Cellular elements: macro, T, B lymph, mast cells
§ Ig E
§ Complements
§ Cytokines

○ Release of pharmacologically active chemical mediators
§ histamine
§ Platelet-activating factor – platelet aggregation
§ Prostaglandin
§ Thromboxane
§ Leukotrienes – bronchodilators

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8
Q

Clinical manifestation of drug allergies/ hypersensitive rxn

A

anaphylaxis
serum sickness (drug fever)
drug-induced autoimmunity
vasculitis
respiratory
hematologic
Serious cutaneous ADR

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9
Q

Anaphylaxis

A

Acute, life threatening reaction
Multiple organ systems involved
• Risk of fatality within first few hrs (acute)
○ Skin: hives, itch, flushed skin, swelling of lips, tongue, throat, face
○ Airway: bronchospasm, trouble breathing, chest tightness
○ CNS
○ CVS: low BP, fast HR
○ GIT

• Most reported: penicillin, NSAID, insulin
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10
Q

Serum sickness/ drug fever

A

• Circulating immune complexes (antigen in body, drug/ transplant)
• Systemic symptoms
• Fever, malaise, rash

Antibiotics

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11
Q

Drug induced autoimmunity

A

• Systemic lupus erythematosus (SLE)
• Hemolytic anemia: Methyldopa
•Hepatitis: phenytoin

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12
Q

vasculitis

A

• Inflammation and necrosis of blood vessel walls
• Limited to skin, or may involve multiple organs
• Kidney, liver etc

Allopurinol, thiazide (diuretic)

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13
Q

respiratory

A

• Asthma: NSAID
• acute infiltrative and chronic fibrotic pulmonary reactions: bleomycin (chemo)

• nitrofurantoin

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14
Q

Hematologic

A

• Eosinophilia common manifestation of DH
• Hemolytic anemia(RBC)
• Thrombocytopenia(PLT)
• Agranulocytosis
○ Low neut count
○ Low granulocytes

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15
Q

Serious cutaneous AD

A

• Drug rash with eosinophilia and systemic symptoms (DRESS)
•mucocutaneous disorders
•steven-Johnson syndrome
•toxic epidermal necrolysis

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16
Q

• Drug rash with eosinophilia and systemic symptoms (DRESS)

A

• Triad:
1) Rash
2) Eosinophilia
3) Internal organ involved
i. Hepatitis, carditis, interstitial nephritis, odynophagia

• Allopurinol, anticonvulsants
      • 10% mortality
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17
Q

Stevens-Johnson syndrome (SJS)

A

• Bullous or blistering disorders. Dermatologic emergencies
• Can progress to:
○ Mucous mem erosion
○ Epidermal detachment
○ <10% detachment of BSA

• Antibiotics (sulfonamides)
• 1-5% mortality
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18
Q

Toxic epidermal necrolysis (TEN)

A

• Bullous or blistering disorders. Dermatologic emergencies
• Can progress to:
○ Mucous mem erosion
○ Epidermal detachment
○ >30% detachment of BSA

• Antibiotics (sulfonamides)
• 10-70% mortality
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19
Q

Genetic disposition for drug A/ HS

A

1) HLA (human leukocyte antigen) alleles incr susceptibility to several DHS syndrome

2) Metabolic deactivation of drugs affected by genetics
§ Phase 1,2 metabolism

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19
Q

Genetic disposition for drug A/ HS

A

1) HLA (human leukocyte antigen) alleles incr susceptibility to several DHS syndrome

2) Metabolic deactivation of drugs affected by genetics
§ Phase 1,2 metabolism

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20
Q

Therapeutic agents for A/ HS rxn: anaphylaxis

A

• Restore resp and CVS function
1) Epinephrine (adrenaline)
• Hosp
• IV fluids – restore vol, BP
• Intubation – save airway collapse
• Norepinephrine – SHOCK
• Steroids, glucagon
• diphenhydramine, ranitidine
•Antihistamines

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21
Q

Therapeutic agents for A/ HS rxn: Serious cutaneous ADR

A

• Less defined, standardized
• Manage like burn pts
1) Supportive care
a. Wound care
b. Nutritional support
c. Fluids
d. Temp regulation (ice bathe)
e. Pain management
f. Prevent infections
2) Steroids use ?

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22
Q

Autoimmune diseases

A

condition where body attacked by own immune system

23
Q

Autoimmune diseases caused by:

A

○ Genetic background
○ Environmental stimuli: smoke, infections, drug use
= incr autoimmune disorder developed

24
Q

Autoimmune diseases difficult to treat

A

§ Do not respond to treatment/ lose response/ do not tolerate/ ADR

§ Drugs are poorly indicated, off-label
□ Not researched sufficiently on
□ Greater variability of treatment among centers and specialists

§ Costly drugs

§ Stigma, weakness, less likely to seek help/ diagnosis

25
Q

SLE Clinical manifestation

A

• Disease fluctuates with periods of remission, flares, progression
• BUTTERFLY Rash on face
• Muscle and joints
○ Joints swollen, tender
○ Arthritisaches
○ Swollen joints
• Heart
○ Endocarditis
○ Atheroclerosis
• Lung
○ Pneumonitis
○ Pul emboli
○ Pul hemorrhage
• Kidney
○ Blood in urine
• Blood
○ Anemia
○ High BP
○ Low blood counts: WBC, RBC, PLATELETS

26
Q

SLE assiociations

A

• Auto-Ab production (multi-system disease)
• More prevalent in females
• Genetic disposition + environ factors
• Smoke, infections, drugs
• Mortality 2.6-3x > general pop
• CVS, renal, infections

27
Q

Pathophysiology

A

• Disorder of innate & adaptive

• T, B lymph activation and signaling altered 

• Abnormal CL of apoptotic debris 
	○ (containing nuclear material)
	○ Not cleared fast enough  etc

• Stimulate immune response 
	○ Incr n.o. plasma cells inactive SLE
	○ Produce autoAb --> tissue damage
		§ Target nucleic acid
		§ Nuclear proteins
28
Q

Clinical presentation
(organs)

A

1) lupus nephritis
2) neuropsychiatric lupus
3) cardiovascular CVS

29
Q

1) lupus nephritis

A

• Class I - minimal mesangial
• Class II - mesangial proliferative
• Class III - focal
• Class IV - diffuse
•Class VI - advanced sclerosing (cancer)

30
Q

2) Neuropsychiatric lupus

A

• Cerebrovascular disease -stroke
• Anxiety+
• Seizure
• Cognitive dysfunction
• Confusion
• Peripheral neuropathy
• Psychosis

31
Q

Clinical presentation
(LABS)

A
  1. Full blood count
    a. Hemolytic anemia
    b. WBC, LYMPH, RBC, PLT
  2. Immunologic
    a. Anti(nuclear) Ab — ANA
    b. Anti(double stranded DNA) Ab — dsDNA
    c. Anti(smith)Ab —- Anti-Sm
    d. Anti(nuclear ribonucleoprotein) Ab – anti-RNP
    e. Low complement (C3,4, CH50)
    i. Used to monitor if pt responding to treatment
    ii. Try to incr back to normal lvls
32
Q

Clinical presentation
(LABS)

A
  1. Full blood count
    a. Hemolytic anemia
    b. WBC, LYMPH, RBC, PLT
  2. Immunologic
    a. Anti(nuclear) Ab — ANA
    b. Anti(double stranded DNA) Ab — dsDNA
    c. Anti(smith)Ab —- Anti-Sm
    d. Anti(nuclear ribonucleoprotein) Ab – anti-RNP
    e. Low complement (C3,4, CH50)
    i. Used to monitor if pt responding to treatment
    ii. Try to incr back to normal lvls
33
Q

SLE management OVERALL

A

• Remission is goal <– low disease activity
• Prevent flares, other organs
○ Slow disease activity
○ Reduce STEROIDS use
○ Improve QOL
○ Minimise ADR
• Treat other comorbidities
• Lifestyle, support grp
• No smoking

34
Q

Pharmacological
(General)

A

• Aspirin (NSAID)

• Prednisolone (steroids)

• Hydroxychloroquine (1st line SLE)
○ Immunomodulatory

• Belimumab (biologics)

• Immunosuppressants
• Steroid sparing (less reliance)
○ Induction therapy
§ Mycophenolate: induce + maintain
§ Azathioprine: maintain

35
Q

Aspirin

A

• 1st line for acute symptoms
Caution: lupus NEPHRITIS, incr cardiac risk, GI bleed

36
Q

Prednisolone (steroids)

A

• Mono/ adjunct
• Control flares, maintain low disease activity
• Rapid onset
•Concern: high dose, LT effect

37
Q

Hydroxychloroquine (1st line SLE)

antimalaria class of drugs

A

• Even preg
• Prevent flare
• LT survival
○ Anti-inflamm
○ Immunomodulatory
○ Anti-thrombotic effect
○ Minimal adverse effects
• 4-8wks to have effect

38
Q

Belimumab (biologics)

A

• Target, disrupt function of B cells, plasma cells
○ Belimumab/ rituximab
Ongoing trials for other biologics

39
Q

Immunosuppressants

A

• IV/PO cyclophosphamide
• Steroid sparing (less reliance)
○ Several organ involved
○ Induction therapy
§ Mycophenolate: induce + maintain
§Azathioprine: maintain

40
Q

Complications/ types of SLE

A

1) Antiphospholipid syndrome (SLE-APS)
2) drug-induced SLE

41
Q

1)Antiphospholipid syndrome (SLE-APS)

A

• Antiphospholipid Ab
○ Lupus anticoagulant, anticardiolipin, anti-b2 glycoprotein (+ve)
• High risk of clotting, preg morbidity

• Treatment:
	○ 1* thromboprophylaxis 
		§ Hydroxychloroquine + aspirin 
	○ 2* thromboprophylaxis (repeated clots) Warfarin
42
Q
  1. Drug-induced SLE

10-15% of SLE from drug use

A

• IDIOSYNCRATIC reactions: due to genetic, environment
• MOA:
○ Small mole induce immune resp
When bind to larger mole (albumin, proteins)

43
Q

Drug-induced SLE (high risk drugs)

A

○ Procainamide (anti arrhythmia)
○ Hydralazine
○ Quinidine
○ Minocycline, isoniazid, methyldopa, carbamazepine, others

44
Q

Drug-induced SLE 1st treatment

A

1* treatment:
○ STOP risk drug
○ SYMPTOMATIC TREATMENT
Maybe reversible, but SLE condition may also just start

45
Q

Evaluation and monitoring of SLE

A

• ADR
• Development of comorbidities
• Measure disease acitvity
• SELENA-SLEDAI
• BILAG
• Regular labs: (look at trend)
• ACTIVE = (1-3mnths)
• STABLE = 6-12mnths

46
Q

labs to monitor

A

○ Don’t need ANA, anti Sm, anti-RNP Ab to repeat at each visit
§ Do not fluctuate with disease activity

1) Urinalysis/ renal function
2) Anti-dsDNA Ab
	a. More uncontrolled condition = higher
	b. Aim for near 0 (normal)
3) Complement C3, 4 levels
	a. Responding to treatment? Try icnr lvls
4) C-reactive protein
	a. Inflammatory market 
5) Full blood count (WBC, RBC, PLT)
    6) Liver function test
47
Q

Immunosuppression in practice

A

○ Rest of life
§ Autoimmune conditions
§ Solid organ transplant
§ Stem cell/ bone marrow transplants
§ Blood disorders/ cancer

48
Q

INDUCTION of immunosuppression

A

§ High potency, short course therapy
§ Initiate asap to:
□ Reduce existing damage
□ Prevent worsening of autoimmune condition

§ Initiate to prevent:
□ Acute rejection with lymph depleting therapy
- Basiliximab, alemtuzumab

49
Q

MAINTENANCE of imunosuppression

A

§ Calcineurin inhibitors
□ Cyclosporin, tacrolimus
§ Antimetabolites
□ Mycophenolate, azathioprine
§ Corticosteroids
§ mtor inhibitors – transplants
□ Sirolimus, everolimus
§ Biologics
□ Adalimumab

50
Q

Complications with immunosuppression

A

§ Risk opportunistic infections
§ Risk cancers
§ Blood disorders
□ Leukopenia, thrombocytopenia, pancytopenia

§ Hepatotoxicity
□ Mycophenolate, aza (Antimetabolites)

§ Renal toxicity
□ Cyclo, tacro (Calcineurin inhibitors)

§ Hypertension, hyperlipemia, hyperglycemia
□ (Calcineurin inhibitors & mTOR inhibitors)

51
Q

opportunistic infections

A

□ Bacterial: Mycobacterium TB, listeria (meningitis), legionella

□ Viral: Cytomegalovirus, Epstein Barr, HV

□ Fungal: Cryptococcus (soil), Aspergillus, pneumocystis jiroveci 

□ Parasites: Toxoplasma gondii (cat)
52
Q

Corticosteroids

A

○ Long term use: anti-inflammatory, immunosuppressive effects
○ Conditions:
§ Asthma, COPD, autoimmune disease, transplant, IBD - CD/ UC, eczema, cancer, pain

53
Q

ADR with steroids

A

1) CVS risk
2) cataract, glaucoma
3) skin thinning, hirsutism (hair)
4) gastric ulcer
5) weight gain, fluid retention, CUSHING, b-cell dysfunciton/ insulin resistance

6) neuro-psychiatric symptoms, HPA insuff
7) osteoporosis
8) myopathy
9) infections

54
Q

HPA Axis suppression (reliant on corticosteroids)

§ Hypothalamic pituitary adrenal axis suppression
□ Common in pt on chronic CS therapy

A

1) Excess exogenous CS/ glucocorticoids
2) Decr secretion of CR, ACTH
3) HPA axis less active
a) Unable to recover function to produce endogenous steroids
b) Adrenal cortex atrophy (smaller)

55
Q

how to reduce Adrenal suppression

A

□ Supraphysiologic dose > 5mg pred daily (>3wks)
-May occur at lower dose/ lower duration too

□ Tapered withdrawal
□ Maintain suspicion of adrenal suppression when pt take CS

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