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PR3152 IC9 Flashcards

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1
Q

Define drug hypersensitivty reactions.

A

Activation of the immune or inflammtory cells leading to adverse reactions to a drug

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2
Q

What are the two types of hypersensitivity reactions?

A

Immune

Non immune

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3
Q

What are the types of immune-mediated hypersx reactions?

A

Immediate: IgE (atopy)
Delayed: IgG, IgM, T cell.

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4
Q

What are non-immune hypersx reactions?

A

They are pseudoallergies, and usually account for appx 77% of hypersx reactions.

usually from mast cell or basophil derived mediators eg histamine, prostaglandins, kinins AND NOT FROM IgE.

OR

other chemical mediators like platelet activating factor, thromboxanes.

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5
Q

what is a drug allergy?

A

defined as immunologically mediated hypersensitivity reaction to a drug (antigenic substance) causing host tissue damage and leading to organ-specific or generalised-systemic reaction.

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6
Q

what are type 1 hypersensitivity reactions?

A

immediate hypersx

igE, Th2, mast cell, eosinophil

1) mast cell derived mediators (vasoactive amines, lipid mediators, cytokines)
and
2) cytokine derived inflammation (eosinophil, neutrophils)

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7
Q

what are type 2 hypersensitivity reactions?

A

antibody mediated hypersx

igM, igG

complement and Fc receptor mediated recruitment and activation of leukocytes (neutrophils, macrophage)

opsonisation and phagocytosis

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8
Q

what are type 3 hypersensitivity reactions?

A

immune complex mediated

igG and igM + immune complexes of circulating antigens

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9
Q

what are type 4 hypersensitivity reactions?

A

t cell mediated

cd4 and cd8

macrophage activation, cytokine mediate inflammation
direct cell lysis by cytokine mediated inflammation

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10
Q

Role of PG in hypersx reactions?

A

NSAID allergy result in altered metabolism of prostaglandins
(pulmonary smooth muscle contraction)

also involved in platelet aggregation

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11
Q

Prostaglandin source?

A

mast cell breakdown

synthesis by neutrophils and macrophages

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12
Q

Role of histamine in hypersx reactions?

A

vasodilation,
bronchial smooth muscle contraction

vessel permeability,

mucus production
itching
sneezing

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13
Q

Histamine source?

A

mast cell and basophil granules

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14
Q

Role of serotonin in hypersx reactions?

A

vasodilation

bronchial smooth muscle contraction

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15
Q

serotonin source?

A

mast cell and basophil granules

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16
Q

Role of protease in hypersx reactions?

A

mucus production
basement membrane digestion
BP elevation

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17
Q

protease source?

A

mast cell and basophil granules

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18
Q

Role of platelet activating factors in hypersx reactions?

A

platelet aggregation and degranulation

pulmonary smooth muscle contraction

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19
Q

source of PAF

PLATELET ACTIVATING FACTORS

A

mast cell breakdown
eosinophil granules
synthesis by neutrophils, macrophages

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20
Q

source of prostaglandins

A

mast cell breakdown
synthesis by neutrophils and macrophages.

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21
Q

ROLE of prostaglandins

A

platelet aggregation,
pulmonary smooth muscle contraction

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22
Q

Role of leukotrienes in hypersx reactions?

A

vasodilation
increased vessel permeability
bronchial smooth muscle breakdown
mucus production

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23
Q

source of leukotrienes

A

mast cell membrane breakdown
eosinophil granules
synthesis by neutrophils, macrophages

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24
Q

what are the clinical manifestations of hypersensitivity reactions?

A

drug fever

hematologic

drug induced autoimmunity

vasculitis

respiratory

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25
what causes drug-induced fevers?
circulating immune complexes causing systemic symptoms like fever, malaise, rash. antibiotics
26
what causes/manifestations of drug-induced autoimmunity?
SLE hematolytic anemia (methyldopa) hepatitis (phenytoin)
27
what causes/manifestations of vasculitis
vasculitis caused by the inflammation and necrosis of blood vessel walls. (allopurinol, thiazide)
28
what causes/manifestation of respiratory hypersx reactions?
asthma acute infiltrative and chronic fibrotic pulmonary reactions (nitrofurantoin, bleomycin)
29
what causes/manifestation of hematologic hypersx reactions?
eosinophillia (very common) hemolytic anemia, thrombocytopenia, agranulocytosis.
30
what are the serious cutaneous allergic reactions (SCAR)
DRESS - drug rash with eosinophilia and systemic symptoms SJS and TEN all can lead to mortality
31
Explain DRESS and the likely drug causes
usually a triad of eosinophilia, rash, and internal organ involvement - involving lungs, kidney, etc inflammation most commonly caused by allopurinol and anticonvulsants
32
Explain difference between SJS and TEN
TEN detachment rate >30% while SJS is less than <10%
33
SJS and TEN progression?
bullous/blisters on skin > mucous membrane erosion (involves internal organ also) and epidermal detachment
34
what are the likely cause of SJS and TEN
sulfonamides e.g., bactrim and sulfonylurea
35
what is the treatment for severe allergic reactions ie anaphylaxis ?
first line agent: epinephrine - counteracts bronchoconstriction, vasodilation if reach ambulance/hospital: 1) fluids to restore BP/blood vol 2) intubation to save airway (if needed) 3) norepinephrine for shock 4) others: - steroids = suppress latent reaction - glucagon = stop inotropic and chronotropic effects to allow heart to beat properly - diphenhydramine (H1) + ranitidine (H2) = block histamine receptors
36
what are the risk factors for systemic lupus erythematous?
genetic disposition -> first degree relatives have 20x risk environment: UV light may alter the structure of the skin and activate SLE infection: epstein barr virus drugs smoking
37
what is the epidemiology for systemic lupus erythematous?
more frequently occuring in females than males more frequent in non-whites (esp hispanics) vs whites
38
description of autoimmune diseases
multifactorial; difficult to treat genetic disposition and environmental stimuli (smoking, infection) increase risk.
39
what are examples of autoimmune diseases
organ specifc -> non-organ specific psoriasis, graves, t1dm, rheumatoid arhtritis, sjogren syndrome, multiple sclerosis, SLE, scloroderma,
40
what is the pathophysiology for SLE
apoptosis of self -cell releases nucleic acid. SLE forms complexes with the nucleic acid impaired clearance of nucleic acid lymphocyte activation and signalling activates T cell with presentation of MHC defective T regulatory cell function formation and proliferation of B cell auto antibodies.
41
what is the clinical presentation of SLE
fluctuating symptoms with periods of remission and flares. typically most present with chronic cutaneous lupus and rheumatoid arthritis
42
what are the FBC results for a patient with SLE?
low RBC, WBC and platelets due to auto antibodiesw
43
what are the immunologic tests for a patient with SLE?
ANA (antinuclear) dsDNA (antidouble-stranded) anti-sm (anti-smith) anti-RNP (antinuclear ribonucleoprotein) low complement C3,C4, CH50)
44
what are the 4 FDA approved agents for SLE?
hydroxychloroquine belimumab aspirin prednisolone
45
what are the indications, drug profile of hydroxychloroquine?
hydroxychloroquine recommended in all populations including pregnant women. minimal adr profile besides retinal toxicity after around 20 years of use. takes about 4-8 weeks for effects to show. has anti thrombotic, anti immunomodulatory, and anti-inflammatory properties which reduces the number of flares in the patient.
46
what are the general 4 classes of agents used for the treatment of SLE
STEROIDS NSAIDS IMMUNOSUPPRESSANTS BIOLOGICS
47
what is the indication for NSAIDS in SLE treatment
first line agent for acute symptoms caution in worsening lupus nephritis, increased cardiac risk and GI bleed
48
what is the indication for STEROIDS in SLE treatment
adjunctive for management of flares do not use long term, might have long term problems
49
what is the indication for BIOLOGICS in SLE treatment
consists of belimumab and rituximab to disrupt B Cell function
50
what is the indication for IMMUNOSUPPRESSANTS in SLE treatment
THREE TYPES: IV/PO cyclophosphamide: severe organ involvement, induction therapy mycophenolate: induction and maintenance therapy azothiopine: alternative for maintenance therapy. **note that the latter 2 are steroid sparing.**
51
how to classify mild SLE?
1) mild arthritis/constitutional symptoms/rash BSA≤9% 2) PLT 50-100 x 103/mm3 3) SLEDAI ≤6% 4) BILAG C or ≤1 BILAG B
52
how to classify moderate SLE?
1) RA-like arthritis/cutaneous vasculitis ≤18% /rash 9-18% 2) PLT 20-50 x 103/mm3 / serostitis 3) SLEDAI 7-12% 4) ≥2 BILAG B
53
how to classify severe SLE?
1) organ involvement (nephritis, cerebritis, mesenteric vasculitis, myelitis, pneumonitis 2) thrombocytopenia PLT < 20x103/mm3 3) SLEDAI >12% or TPP-like disease or acute hemophagocytic syndrome 4) ≥1 BILAG A
54
how to manage mild SLE?
1st line: HCQ and PO/IM GC add on refractory: AZA/MTX
55
how to manage moderate SLE?
1st line: HCQ and PO/IV GC add on for 1st line: AZA/MTX, MMF, CNI add on refractory: BEL, MMF, CNI
56
how to manage severe SLE?
1st line: HCQ and PO/IV GC add on for 1st line: MMF or CYC add on refractory: RTX or CYC
57
what is the remission target for SLE
SLEDAI = 0 HCQ stop GC
58
what is the target for low disease activity in SLE
HCQ GC pred <7.5mg/d SLEDAI ≤4 immunosuppresives doses stable and well tolerated
59
what are some non-phx recommendations for SLE?
stop smoking body weight control diabetes, CV, lipid control vaccinations photo-Resistance exercise if antiphospholipid positive, to start on antiplatelets or anticoagulants.
60
which drugs to avoid in SLE management in pregnant women
AZA/MTX CYC (avoid in the first trimester) MMF caution diabetes for GC in pregnant women caution ADR preclampsia and HTN
61
what are some adr for systemic glucocorticoids
eyes: * glaucoma * cataract chronic conditions: * HTN * Hyperglycemia * dyslipidemia lifestyle: * fat redistribution * sleep/mood disturbance others: * osteoporosis * skin atropy
62
what are some adr for CYC
cystitis bladder malignancy infertility
63
what are some counselling points for mmf
gi side effects which might affect adherence
64
what are some counselling points for AZA
need to test for TPMT thiopurine methyltransferase before starting
65
what is the possible MOA causing drug induced lupus
small drug molecules that bind to large molecules like proteins
66
what are the top 3 drugs causing drug induced lupus
hydralazine procainamide quinidine
67
other drug causes of lupus?
MIMC minocycline isoniazide methyldopa carbamazepine TAILS TNF alpha inhibitor induced lupus like syndrome
68
what are the antiphospholid antibodies in antiphospholipid syndrome?
ACA: anticardiolipin antibodies LA: lupus anticoagulants anti-B2GPI
69
what are the risks of APA?
high risk of clotting, recall virchow's triad high risk of pregnancy morbidity - if more than 3 unexplained miscarriages, to test for underlying SLE
70
what are the treatment options for APA? (non preg)
primary thromboprophylaxis: aspirin secondary: warfarin HCQ for protective function
71
what are the treatment options for APA? (preg)
parenteral heparin.
72
what are the lab paremeters to monitor for SLE and how frequent
1-3 months if active 6-12 months if stable urinalysis/renal fbc lft complement c3 c4 antidsDNA CReactive protein
73
immunosuppression in transplantation (induction therapy)
ASAP high potency and short course 1) immune modulators to prevent proliferation of t cells: basiliximab 2) lymphocyte depleting agents (b and t cell) - antithymocyte globulin (ATG) - alemtuzumab
74
immunosuppression in transplantation (maintenance therapy)
CNI (cyclosporin, tacrolimus) anti metabolites (mycophenolate, azathioprine) CSC mTOR inhibitors (sirolimus, everolimus) biologics (adalimumab, belatacept)
75
what is the approach to transplant
1) match HLA to patient blood type 2) initiate high potency induction therapy ASAP to avoid initial rejection 3) maintenance agents (combination therapy) - encourage use of CNI + CSC + mycophenolate - avoid CNI + mTOR due to risk of nephro (substrates of cyp450 3a and p glycoprotein) 4) withdraw or reduce if toxic
76
complications of immune suppression
immune related: infections, cancers non-immune related: Bone marrow suppression (esp antimetabolites: azathioprine and mycophenolate) Hepatotoxicity (esp antimetabolites: Mycophenolate, Azathioprine) Renal toxicity (esp Cyclosporin, Tacrolimus, worse when combined with mTOR inhibitors) Hypertension, hyperlipidaemia, hyperglycemia (esp steroids, calcineurin inhibitors)
77
immunosuppression maintenance drugs that need TDM
CNI: cyclosporin, tacrolimus MMF mTORi: sirolimus, everolimus
78
what are the long term effects of steroid use
HPA axis suppression causing adrenal insufficiency/suppression - decrease crh (corticotropin) and acth (adrenocorticotropin) | hypothalamic pituitary adrenal

PR3152 (cleefy) (13 decks)

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