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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
chamomile tea... it cross reacts with ?
ragweed and mugwort FYI
26
what are screening tests for 1. drug induced vasculitis 2. serum sickness
1. CBC CRP pANCA and cANCA and ANA | 2. cryoglobylin or cold preictoable serum protein for immune complex
27
what is the advantage of LTA tests also what do you look for marker wise on BAT
LTA - bypass need for knowledge of metabolic determinants as check for LTA to drug itself CD63 for BAT
28
name 4 histologic findings with biosy of drug exantham
1) Eo 2) interface dermatitis 3) vacuolar alteration of keratinocyte 4) foci of spongiosis
29
name reasons why coombs are positive
presence of complement drug on RBC membrane Rh determinant autoanntibody
30
name 4 reasons drugs may be continued even tho you have allergy ie) medicatl condtion
``` DKA Tb neurosyphllis endocarditis IBD ```
31
5 contrainidcations to inudction of tolerance?
``` SJS TEN hemolytic anemia interstial nephritis hepatitis ``` drug reactions ACE inh angioedma
32
name four mechainsim of asa desens loss of tolerance ocucurs 2-4d wihtout asa
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
what is the diagnostic critetria for SWEET syndrome most ocmmon drug GCSF
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
whats SDRIFE (baboon syndrome)
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
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
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
four findings AFRS on CT
central hyperattenuation, heterogenous opacification with inspissated secretions in affected sinuses, nasal expansion, bony deminderalization, erosion of lamina papyacae or skull base
37
name 4 pre assessment and pre med before ASA desen 1-7 days before procedure
1) FEV >60 PRED 2) STARAT 10MG MONTEKULAST 3) continuse or start ICS and LABA 4) give sustemic steroid burst if feb1 low
38
what three cephalsopring share r1 with amox
cefprozil cefadroxil cefatrizine
39
what makes sulfonamide abx allergic in nature froma chemical structure pespective
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
name 5 reasosn to stop HIV patient on septra\ dapsone cross reactiivity is LOW but avoid if severe rxn like sjs on septra
persistnt of rash and fever for more then 5 d ANC <5000 hypotension dspynea a signs of blistering or desquam or mm involvement
41
what is IMMUNE RECONSITUTION INFLAMATORY SYNDROME
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
what is IMMUNE RECONSITUTION INFLAMATORY SYNDROME
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
what is the most common type of hypersneivity reaction inudced by steroids
contact derm allergic IV methylprednisoline and hydrocort are most implicated in anaphylaxsi
44
which med can put diabetics at higher risk of anaphylaxis
protamine | from salmon testes
45
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
GROUP 1: benzoic acid esters - procaine and benzocaine | GROUP 2: amides - lidocaine and mepivacaine
46
what do u do wiht patient prev anaphylacoitd to RCM RF, women, asthma, prev hx, beta blocer and CVD
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
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
ashtma 10% AR And astham 30% with the challemge- get dec PGE2, which inhibits 5 lipoxygnease -> hence they get more cysteinil leukotreine
48
what does ACE do
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
name a bad reaction to the following anti TNF meds 1) inflixmab 2) humira
inflix - progressive multifocular encelopathy, if N10yoGBS peripheral neuropathy and demylinating sndorme humira - asthma new onset (alsow ith enterncdept)
50
name three drugs gthat can cause cytokine storm syndorme fever rigos chillss and ARDS
ritux | her 2 trastuzamab and \anti cll alemtuxumab
51
1. Compare reactions between metabisulfite and ASA.
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
latex allergy spina vs HCP common foods
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
patient with RCM approach
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
discuss Gel coombs and examples
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
name mast cell pre formed mediators and then what is released with activation
``` 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
diagnostic criteria of MCAS tryptase 1.2x + 2 from baseline
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
in insulin HS rxn what are the top 3 allergens
protamine, cresol and latex, check additives if avail. Can SPT neat and use 1/100 dilution for IDT. IgE protamine, insulin and latex
58
findings in DRESS on bx
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
ddx for morbiliform rash
Ddx: measles, rubella, fifth disease, EBV, scarlet fever, mycplasma, JIA, acut ecutnaeous lupus erythematosus
60
distingush uritcaria from vasculitic urticaria
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
skin bx findings of UV
Skin bx: RBC extravasation, fragmented leukocyte, No predmoninance, swelling of endotheliall cellsesp post cap, fibrin deposits, leukocystoclasis and fibrinoid deposits
62
diagnostic criteria of HUVS
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
what would u find in bx of skin of HUV
Skin bx: RBC extravasation, fragmented leukocyte, No predmoninance, swelling of endotheliall cells esp post cap, fibrin deposits, leukocystoclasis and fibrinoid deposits Ddx: urticaria,
64
HUVS mcDUffe syndrome
``` 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
blood findings with SSLR
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
ddx for extensive dermatitis
Extensive dermatitis ddx SCALPID: seborrheic dermatitis C3: CD, CTD, cancer, AD, Lymphoma, P2 psoriasis piityriasis rubra pilaris, Infxn Idipathic, immunobulous, Drug related
67
list high risk and CI for desens
high risk: severe anaphlya, cardioresp disease, systemic diseas,e beta blocker, preg, ace inh contrai SCARS, SJS, DRESS< AGEP, Type 2 vasculitisn, SSLR
68
name vaccine component causing anaphylaxis
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
what are KNOWN vaccine rxns
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
MOA of ritux
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
MOA of Cyclophoshamide
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
five causes of secondary hypogam
``` steroids ritux Bone marrow failure CLL, myeloma protein losing eneterophaty neprhotic sx lymphagenetiactasia ```
73
taxane reaction mgt
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
four sjs HLA risk subsyptes
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 HLA b57 01- abcavir HLA b 13;01- dapsone in thai patients

Allergy and Immunology (10 decks)

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