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drug allergy Flashcards

1
Q

pseudoallergic (anaphylactoid):

A

immediate systemic rxn that mimic anaphylaxis but non IgE mediated - release mediator from mast and basophil

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2
Q

Drug intolerance vs

drug idiosyncrasy

A

: undesriable pharma effect - occur at low/usual dose - no underlying abn in metbaolism, excretion or bioavail - T and B cell not involved and cant understand mechanism - ie) tinnitus with aspirin

Drug idiosyncrasy: abn and unexpected effect unrelated t drug, and uknown why, not T or B cell mediated but is repdocuble - could be due to metabolism or bioavail - ie) fever from quinidine or g6pd and hemolytic anemia with dapsone

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3
Q

name gel and coombs types and subtype of 4

A

1-ige
2-igg or igm directed at hapten coated _ autoimm anemia

3- tissue deposited of drug ab complex with complement activation and inflm (serum sickness, vasculitis)

4: T cell medaited MCH presentinh drtug
METN
(1a - macro, 1b, eo, 4c T cell, iv d neotrphil)

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4
Q

type 4 reactions for gel coombs, subtypes and ex

A

4a- Macrophage, Infn gamma, TNFalpha Th1 medaited, APC presented ie) TB

4b: Eo, il5,/23, Eo and chronic AR and athma, dress?
4c: T cell perforin granzyme, contact dermatitis, and macolpop bullous

4d- No, ILbeta GMCSf
AGEP and bechets

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5
Q

what is pi concept

A

Pharmacologic interaction with immune receptors
Drug binds non covalantly to the TCR and this leads to immune rxn via interaction with major histocombatability receptor
No sensitization needed as its direct stimulation of the memory and effector T cell (like a superantigen)

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6
Q

name RF for drug allergy

A

patient: middle age adult more then infant, women more then men, genetic polymorphihsm , HIV herpeps, and prev rxn

Drug: HMW compound, topical>iv>oral, dose frequnt>single dose

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7
Q

give examples of drugs causing

1) Type 2 cytotoxic
2) serum sickness
3) type 4 contact dermatitis

hyoersensitivty vasculitis

pulm DRUG hypersensitve

SYSTEMIC sle

CUTANEOUS sle

granuloma

blistering

neophropathy

A

1) Type 2 cytotoxic
penicilline, sulga

2) serum sickness
penicillin, thymo, inflixmab

3) type 4 contact dermatitis
0 neomycin, pen, sulfonamide

hypersensitivty vasculitis: hydralazine

pulm DRUG hypersensitve: bleo, MTX, nitrofuranton

SYSTEMIC sle: hydralazine, procainamde, isonazid

CUTANEOUS sle: HZT, CCB, AE inh

granuloma: PTU

blistering
: NSAID, sulfonamide,
anticonvulsant

neophropathy: gold, penicillin, sulfonamide

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8
Q

Contraindications for drug desensitization

A

SJS, TEN, interstitial nephritits, hepatitis and hemolytic anemia

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9
Q

what is in pen testing

A

major determinant (PRE-penicilloylpolylysine)

MINOR

  • pen G
  • penicilloate and penilloate
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10
Q

List 4 types of reactions to NSAIDS

A

AERD, worsening of CSU, IgE mediated anaphylaxis/urticarial,

urticarial/angioedema to all cox-1 inhibitors (no hx of CSU)

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11
Q

Underlying mechanism of AERD?

A

aberrant arachidonic acid metabolism. Before administration of
aspirin, compared with non–aspirin-sensitive asthmatic patients,
patients with AERD have higher levels of both COX and 5-
lipoxygenase products, such as increased urinary leukotriene E4 and
throm- boxane B2, and increased leukotriene E4 and thromboxane B2
in bronchoalveolar lavage fluid.602-604 Patients with AERD also have
increased respiratory tract expression of the cystei- nyl leukotriene 1
receptor and heightened responsiveness to inhaled leukotriene
E A number of genetic polymor- phisms involving the
leukotriene pathway have been reported to be associated with
AERD, including the leukotriene C4 promotor, cysteinyl
leukotriene receptor 1 promotor,606 prostanoid receptor related
genes,607 and thromboxane A2 receptor genes. Administration of
aspirin leads to inhibition of COX-1 with resultant decrease in
prostaglandin E2. Prostaglandin E2 normally inhibits 5-lipoxygenase,
but with a loss of this modifying effect, arachidonic acid molecules
are preferen- tially metabolized in the 5-lipoxygenase pathway,
resulting in increased production of cysteinyl leukotrienes.

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12
Q

name 5 ways to prevent drug reactions

A

1) careful hx for host factors
2) avoid of cross reactive drugs
3) use of oral abx
4) use predictive tests when u can
5) proper prescribing of drugs when needed
6) document thr ADR in the chart

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13
Q

name an example of using induction of tolerance with drug in an non-Ige drug reaction

A

imatanib (tyrosine kinase inhibitor) for malignant tumors

gernally it is contraidncated tho - ie_ with SJS or TEN

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14
Q

Lupus (cutaneuso vs systemic) drug indue

A

Cutaneous
more freq- 4-8w in onset, no systmic signs, photsensitive ertyhema, scaly anular plaques,
drug: CCB, HZT, ACE, antifungal

vs systemic is rare and take months to get tehre with photosensitivty and erythema nodosum as skin
(procainamide, minocycline, isonaizide, methldopa)

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15
Q

causes of elevated tryptase

A

Familial tryptasemia, AML, refractory anemia’s, myelodysplastic syndrome, SCF (stem cell factor) administration, ESRD with elevated SCF
anaphylaxis

Mastyoctosis
anaphylaxis
myeloid HES

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16
Q

give three common drugs implicated in type 2 rxn

complement MEDIATED cytotoxi c IgM or IgG formed to drug altered cell surface membranes

A

pencillin, quinidine, and alpha methyl dopa - cause anemia
usu when treatment with pen for a long time

can get low plt with quinidine as well, and quinine, tylenol, PTU

low granulocyte anticonvulsant , sulfonamide

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17
Q

type 3 rxn example of drugs

remember from slight antigen excess

A

penicillin
sulfonamdie
phenytoin
mabs

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18
Q

name 5 common topical allergic contact dermatitis antigegns

A 
neomycin
parabens
bactiracin
thimerosal
lanolin
formaldehyde

remmeber - photoallergic ones: sulfonamide, thaizide, quinidine, and chlorporamazine and fluoroquinolones

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19
Q

five risk factor for radiocontrast anaphylactoid reaction

A

usually ionic is worst

but 
female
asthma
hx of prec fxn
beta blocker - higher risk
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20
Q

steps for pt who has possible anaphylactoid

A 
Management: 
Determine if its essential
Patient understands risk
Hydration
Use NON ionic, iso osmolar RCM
Pretreatment regime that works
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21
Q

Lupus (cutaneuso vs systemic) drug indue

A

Cutaneous

more freq- 4-8w in onset, no systmic signs, photsensitive ertyhema

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22
Q

causes of elevated tryptase

A

Familial tryptasemia, AML, refractory anemia’s, myelodysplastic syndrome, SCF (stem cell factor) administration, ESRD with elevated SCF
anaphylaxis

Mastyoctosis
AERD
anaphylaxis
myeloid HES

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23
Q

name high risk drugs for EM/SJS

A

sulfonamide. cephalosporine, imidazole and oxicam derivative

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24
Q

name two drugs causing bllous pemphigoid

and two causing pemphigus

A

furosemide and penicillin and sulfasalazine cause bullous pemphifoid

THIOL group meds like captoprile and penicillamine

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25
Q

chamomile tea… it cross reacts with ?

A

ragweed and mugwort FYI

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26
Q

what are screening tests for

  1. drug induced vasculitis
  2. serum sickness
A
  1. CBC CRP pANCA and cANCA and ANA

2. cryoglobylin or cold preictoable serum protein for immune complex

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27
Q

what is the advantage of LTA tests

also what do you look for marker wise on BAT

A

LTA - bypass need for knowledge of metabolic determinants as check for LTA to drug itself

CD63 for BAT

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28
Q

name 4 histologic findings with biosy of drug exantham

A

1) Eo
2) interface dermatitis
3) vacuolar alteration of keratinocyte
4) foci of spongiosis

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29
Q

name reasons why coombs are positive

A

presence of complement

drug on RBC membrane

Rh determinant autoanntibody

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30
Q

name 4 reasons drugs may be continued even tho you have allergy

ie) medicatl condtion

A 
DKA
Tb
neurosyphllis
endocarditis
IBD
31
Q

5 contrainidcations to inudction of tolerance?

A 
SJS
TEN
hemolytic anemia
interstial nephritis
hepatitis

drug reactions ACE inh angioedma

32
Q

name four mechainsim of asa desens

loss of tolerance ocucurs 2-4d wihtout asa

A

1) reduction of urinary leukotriene e4
2) intenralization of cysteinail leukotriene receptor 1 receptor

330 release of mast cell trpytase

monitor for lung issues

33
Q

what is the diagnostic critetria for SWEET syndrome

most ocmmon drug GCSF

A

Diagnostic criteria for Sweet syndrome
Classical*
1. Abrupt onset of painful erythematous plaques or nodules
2. Histopathologic evidence of a dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis
3. Pyrexia >38°C
4. Association with an underlying hematologic or visceral malignancy, inflammatory disease, or pregnancy, or preceded by an upper respiratory or gastrointestinal infection or vaccination
5. Excellent response to treatment with systemic corticosteroids or potassium iodide
6. Abnormal laboratory values at presentation (three of four): erythrocyte sedimentation rate >20 mm/hr; positive C-reactive protein; >8,000 leukocytes; >70 percent neutrophils

Drug-induced¶
A. Abrupt onset of painful erythematous plaques or nodules
B. Histopathologic evidence of a dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis
C. Pyrexia >38°C
D. Temporal relationship between drug ingestion and clinical presentation, or temporally-related recurrence after oral challenge
E. Temporally-related resolution of lesions after drug withdrawal or treatment with systemic corticosteroids

34
Q

whats SDRIFE (baboon syndrome)

A

symetrical drug related interginous and flexural exanthema
Tend to be near lips, hands and genitalaia - can occur with NSAID cabamazipine and tetraclcyine
Few hours to days after administration of the drug
Treat with stopping drug and then topical steroids

35
Q

name 3 upper and lower resp effects of ASA desn

for acute urtcaira- 2-5 h protocol
if its CSU worsened by nsaid it dont help

A

1) upper
- dec nasal symptoms
- dec INCS
- less polyp
better smell
dec polpyectomy

lower - dec asth,a, dec inh steroids, dec hos and ED

36
Q

four findings AFRS on CT

A

central hyperattenuation, heterogenous opacification with inspissated secretions in affected sinuses, nasal expansion, bony deminderalization, erosion of lamina papyacae or skull base

37
Q

name 4 pre assessment and pre med before ASA desen

1-7 days before procedure

A

1) FEV >60 PRED
2) STARAT 10MG MONTEKULAST
3) continuse or start ICS and LABA
4) give sustemic steroid burst if feb1 low

38
Q

what three cephalsopring share r1 with amox

A

cefprozil
cefadroxil
cefatrizine

39
Q

what makes sulfonamide abx allergic in nature froma chemical structure pespective

A

There is NH2 S02 in sulfonamide, but the abx have aromatic amine at N4 and substituted ring at N1 which make it more allergic in nature

40
Q

name 5 reasosn to stop HIV patient on septra\

dapsone cross reactiivity is LOW but avoid if severe rxn like sjs on septra

A

persistnt of rash and fever for more then 5 d

ANC <5000
hypotension
dspynea a
signs of blistering or desquam or mm involvement

41
Q

what is IMMUNE RECONSITUTION INFLAMATORY SYNDROME

A

its when hiv ppl get TB and are n HAARD and anti tb drugs - causes

1) induction of p450 and recuces HAART med effeciy
2) toxic effects of drugs overlap
4) increased risk of anaphylaxis as it skews towards th2

42
Q

what is IMMUNE RECONSITUTION INFLAMATORY SYNDROME

A

its when hiv ppl get TB and are n HAARD and anti tb drugs - causes

1) induction of p450 and recuces HAART med effeciy
2) toxic effects of drugs overlap
4) increased ris =k of anaphylaxis as it skews towards th2

43
Q

what is the most common type of hypersneivity reaction inudced by steroids

A

contact derm allergic

IV methylprednisoline and hydrocort are most implicated in anaphylaxsi

44
Q

which med can put diabetics at higher risk of anaphylaxis

A

protamine

from salmon testes

45
Q

groups of topical anestehics?

remember when testing takng out paraben, epi and sulfites

SPT then subcut
0.1ml 1:100 and then go up every 15 min till u get 1ml of undilutes

A

GROUP 1: benzoic acid esters - procaine and benzocaine

GROUP 2: amides - lidocaine and mepivacaine

46
Q

what do u do wiht patient prev anaphylacoitd to RCM

RF, women, asthma, prev hx, beta blocer and CVD

A

can try SPT if neg
then non ionic iso osmolar agent to be used and pre med with steroid and anthistamine, 13h, 7 h and 1 h before *50mg
diphenhydramine 1h before 25mg
DONT give ranitidine

can get deayed reaction 1w after in 2%

47
Q

what % patients have AERD

baseline they have higher COX asnd 5 lipoxygenase products like uirintary leukotriene e4 and thromboaxane B2, with increased expression of of cysteineyl leukortirene 1 receptor.

w

A

ashtma 10%

AR And astham 30%

with the challemge- get dec PGE2, which inhibits 5 lipoxygnease -> hence they get more cysteinil leukotreine

48
Q

what does ACE do

A

it breaksd down bradykinin which if its inhibitors can get angioedema and also its known bradykinin can stumulate vagal efferent nerver and produce cough as well as aa metaboites and NO wehivh can cause inflammation

49
Q

name a bad reaction to the following anti TNF meds

1) inflixmab
2) humira

A

inflix - progressive multifocular encelopathy, if N10yoGBS peripheral neuropathy and demylinating sndorme

humira - asthma new onset (alsow ith enterncdept)

50
Q

name three drugs gthat can cause cytokine storm syndorme

fever rigos chillss and ARDS

A

ritux

her 2 trastuzamab and \anti cll alemtuxumab

51
Q
  1. Compare reactions between metabisulfite and ASA.
A

ASA
Can cause 4 types of ‘pseudoallergic reactions’, which is related to the pharmacologic ability of NSAIDs to inhibit COX-1 enzyme
(1) AERD
(2) urticaria/angioedema in patients who already have chronic urticaria
(3) urticaria/angioedema in patients without underlying disease
(4) respiratory reaction + cutaneous symptoms (either in patients with AERD or patients with no underlying disease)
NSAIDs can also cause allergic reactions (presumed to be IgE-mediated), but these are NOT reported with aspirin

metabisulfite
(1) Asthma
Sulfites are the only additives that have been convincingly demonstrated to provoke asthmatic reactions (for other additives- evidence limited to case reports)
Up to 5% of asthmatics may experience adverse reactions to sulfites
Affected patients typically have severe, steroid-dependent asthma, and sulfites can cause serious / life-threatening asthmatic reactions

(2) Anaphylaxis
Small number of cases
Epinephrine autoinjectors contain small amounts of metabisulfite, but this is not a contraindication to their use

(3) Urticaria
(4) Contact dermatitis

52
Q

latex allergy

spina vs HCP
common foods

A

Latex allergy
Health care workers react Hev b 5, 6 and 7 - 5 and 6 are inhaled or direct contact
Spina bifida: hev b 1 and 3 are most frequent and need direct mucosal exposure
Cross reactive with BACK fruits (banana, avocado, chestnut, and kiwi) - potato, green pepper, fig, apple, cherry and some nuts → can cause anaphylaxis

53
Q

patient with RCM

approach

A

Radiocontrast - want non ionic iso osmolar
Can be anaphylactoid, physologic (warm, chills, CP, seizure), IgE, delayed type 4 (2%)
RF for RCM rxn: female, atopy, asthma CVD, beta blocker (NOT IODINE and SEAFOOD)
JACI 2018 SPT with undilated RCM and intradermal 1:10 can be done NPV high
Treat
Prednisone 50mg - 13, 7 and 1 hour prior
Diphenhydramine 50mg - 1 hour prior
ephedrine/albuterol, H2 antagonists → controversial (as per ACAAI slides… but previous groups said to give ventolin 1 hour prior)

54
Q

discuss Gel coombs and examples

A

Type 1: Ige mediated: anaphylaxis
Type 2: Ag:Ab mediated: hemloytic anemia (NSAID, beta lactam), thrombocytopenia (heparin) and neutropenia (PTU)
Type 3: immune complex mediated: serum sickness, vasculitis (beta lactam), arthrus reaction
Type 4: delayed T cell mediated (METN): SDRIFE, AGEP, SJS, DRESS, allergic contact

55
Q

name mast cell pre formed mediators and then what is released with activation

A 
Preformed:
Histamine
Tryptase
Chymase
Carboxypeptidase
heparin

Synthesized/released after activation:
PAF
PGD2
LTB4/C4/D4

And then also cytokines/chemokines hours later
IL3/4/5/13, TNFalpha, GMCSF, RANTES

56
Q

diagnostic criteria of MCAS

tryptase 1.2x + 2 from baseline

A

1) symptoms of mast cell activation with two organs
2) objective evidence like elevated tryptase , Elevated 24 hr urine N-methylhistamine, PGD2, or 11beta-PGF2alpha on at least two occasion
3) responds to meds that inhibit mast cell

57
Q

in insulin HS rxn what are the top 3 allergens

A

protamine, cresol and latex, check additives if avail. Can SPT neat and use 1/100 dilution for IDT. IgE protamine, insulin and latex

58
Q

findings in DRESS on bx

A

Considered to be type 4b. Common drug antiepileptic, septra, minocycline and alluprinol.
Reactivation of hhv6, 2-6w get rash, usu fever, skin, liver, kidney and lung. Can try for patch
Ddx: SJS, AGEP, HES, T cell lymphoma, cutaneous lymphoma, acute cutaneous lupus erythematosus
Inv: CBC, blood film, high Eo, LFTs, elevated Cr consider skin bx (mild spongiosis, perivascular infiltrate with lympcyte and Eo and dermal edema). Ebv hhv6 and 7 serology, CXR and trop for heart
Manage by stopping drug, and steroids, very slow taper

59
Q

ddx for morbiliform rash

A

Ddx: measles, rubella, fifth disease, EBV, scarlet fever, mycplasma, JIA, acut ecutnaeous lupus erythematosus

60
Q

distingush uritcaria from vasculitic urticaria

A

Distinguish from normal urticaria: painful, duration >48h, purpura, hyper pigm, can have EM, raynaud, livido reticularis, arthritis, renal proteinuria, hematuria, pulmonary SOB, asthma COPD, GI diarrhea or vx or pain
angiodedema, annular eryhtema

61
Q

skin bx findings of UV

A

Skin bx: RBC extravasation, fragmented leukocyte, No predmoninance, swelling of endotheliall cellsesp post cap, fibrin deposits, leukocystoclasis and fibrinoid deposits

62
Q

diagnostic criteria of HUVS

A

More severe and associated with COPD in 50%
Diagnostic Criteria (Schwartz)
Major: need both of Urticaria >6 months + low complement
Minor: need 2 or more
Dermal venulitis by biopsy
arthralgia/arthritis
uveitis/episcleritis
Mild GN
Recurrent abdo pain
Positive C1q precipitins test (same as antibodies to C1q) with suppressed C1q level

63
Q

what would u find in bx of skin of HUV

A

Skin bx: RBC extravasation, fragmented leukocyte, No predmoninance, swelling of endotheliall cells esp post cap, fibrin deposits, leukocystoclasis and fibrinoid deposits
Ddx: urticaria,

64
Q

HUVS mcDUffe syndrome

A 
Diagnostic Criteria (Schwartz)
Major: need both of Urticaria >6 months + low complement
Minor:  need 2 or more
Dermal venulitis by biopsy
arthralgia/arthritis
uveitis/episcleritis
Mild GN
Recurrent abdo pain
Positive C1q precipitins test (same as antibodies to C1q) with suppressed C1q level
65
Q

blood findings with SSLR

A

Inv: CBC lymphocytosis, neutorpehnia, low plt, inc Eo, ESR CRP, urine proteinuria mild and mild hematuria, elevated Cr, low Alb. r/u HBV. C3,C4CH50 can be low. No need skin bx

66
Q

ddx for extensive dermatitis

A

Extensive dermatitis ddx
SCALPID: seborrheic dermatitis C3: CD, CTD, cancer, AD, Lymphoma, P2 psoriasis piityriasis rubra pilaris, Infxn Idipathic, immunobulous, Drug related

67
Q

list high risk and CI for desens

A

high risk: severe anaphlya, cardioresp disease, systemic diseas,e beta blocker, preg, ace inh

contrai
SCARS, SJS, DRESS< AGEP, Type 2 vasculitisn, SSLR

68
Q

name vaccine component causing anaphylaxis

A

Gelatin: Flu, MMRV, zoster, rabies, yellow fever.
Egg protein (influenza, yellow fever)
Latex
Yeast (saccharomyces cerevisiae: Hep B and quadrivalent HPV)
Actual vaccine component (eg. tetanus/diphtheria)
Thimerosal: Hep B and influenza
Neomycin: Varivax and MMR
Aluminum

69
Q

what are KNOWN vaccine rxns

A

Febrile seizure if MMRV given together at 12-15 mo
MMR can cause thrombocytopenia
Rubella acute arthritis if adult women and transient arthralgia in children
Pertussis can cause other less severe neurological events: febrile seizure, crying and hypotonic-hyporesponsive episodes
Tetanus causing arthus reaction, GBS, brachial neuritis (shoulder pain with weakness)
Varicella can cause local versicle
Absolute contraindications
Influenza vaccine causing gullain barree syndrome within 6w of vaccine
Encephalopathy with pertussis vaccine
Yellow fever can cause encephalitis and should not be given in infants

70
Q

MOA of ritux

A

B cell-depleting monoclonal anti-CD20 antibody, comprised of both mouse and human portions.
Depletion occurs through one or more of several antibody dependant mechanisms including:
Fc receptor gamma-mediated antibody-dependent cytotoxicity and phagocytosis, complement-mediated cell lysis, growth arrest, B cell apoptosis

71
Q

MOA of Cyclophoshamide

A

An alkylating agent, is one of the most potent immunosuppressive therapies available.
Prodrug that is converted to its active form in the liver
Alkylating agents exert their biologic activity via covalent binding and crosslinking of a variety of macromolecules including DNA, RNA, and proteins.
DNA crosslinking, probably the most important biologic action of these drugs, impairs DNA replication and transcription, ultimately leading either to cell death or to altered cellular function.
Alkylating agents are cytotoxic. Absolute lymphopenia is frequently seen following their administration, with reductions in the number of B cells and T cells of both CD4+ and CD8+ types
3 side effects
Cytopenia
Gonadal toxicity
Malignancy (leukemia and skin)
Bladder toxicity - hemorrhagic cystitis, bladder cancer
Hyponatremia due to SIADH

72
Q

five causes of secondary hypogam

A 
steroids
ritux
Bone marrow failure
CLL, myeloma
protein losing eneterophaty
neprhotic sx
lymphagenetiactasia
73
Q

taxane reaction mgt

A

Taxane reactions
Paclitaxal and Docetaxel - 10-15min direct mast cell
Can pretreat and slow the infusion
If doesnt work can desnsitize
REMEMBER with platinum compound (CISplatin and carboplatin, CANNOT pre-treat and need SPT before coure) can try desensitize but does not always work

74
Q

four sjs HLA risk subsyptes

A

Three derm features: mm erosions, target lesion and epidermal necrosis with detachment
Ill defines, coalescing, erythematous macules with itchy center, nikolsky sign, bulla spread sign, mm invovlement, urethritis ocular involvement
Drugs: sulfa, phenytoin, pb, allopruinol, carbamazepine, NSAID
Ethrnicity:
HLA b1502 - carbamaezpine ASIAN
Hla b58:01 allopriuinol in asian
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Allergy and Immunology (10 decks)

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