ACAAI Review Book Ch 7: Pharmacology and Therapeutics Flashcards

1
Q

Potential mechanisms and immunologic changes associated with immunotherapy include all of the following except:

A. increased IFNy/IL-4 ratio
B. decreased IgA in respiratory secretions
C. initial increase (month) then a steady decrease (years) in allergen-specific IgE
D. decreased seasonal rise in allergen-specific IgE
E. decreases basophil hyperreactivity

A

B. decreased IgA in respiratory secretions

INcreased IgA in respiratory secretions

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2
Q

Potential mechanisms and immunologic changes associated with immunotherapy include increases in all of the following except:

A. IgG blocking antibody (initially IgG1 and IgG2 -> IgG4)
B. CD4+CD25+ regulatory (IL-10, TGF-B) and percent of CD8+ T cells
C. allergen-specific lymphocyte proliferation
D. Th1 cytokines (IFNy, IL-12), shift from Th2 cytokines (IL-4, IL-5, and IL-13); Th1/Th2 ratio
E. IFNy/IL-4 ratio

A

C. allergen-specific lymphocyte proliferation

DECREASED allergen-specific lymphocyte proliferation

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3
Q

Potential mechanisms and immunologic changes associated with immunotherapy include decreases in all of the following except:

A. modified allergic response to allergens over time (early and late response to NAC, bronchial sensitivity to histamine)
B. low affinity IgE receptor, FcERII (CD23)
C. basophil hyperreactivity
D. recruitment of eosinophils, basophils and mast cells in nose/lung
E. Th1 cytokines (IFNy, IL-12), shift from Th2 cytokines (IL-4, IL-5, and IL-13); Th1/Th2 ratio

A

E. Th1 cytokines (IFNy, IL-12), shift from Th2 cytokines (IL-4, IL-5, and IL-13); Th1/Th2 ratio

this INCREASES

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4
Q

Standardized extracts include all of the following except:

A. cat
B. dog
C. dust mites
E. grasses
F. weeds
A

B. dog

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5
Q

All of the following allergens cross react except:

A. timothy grass
B. bermuda grass
C. Kentucky blue grass
D. orchard grass
E. perennial rye
F. sweet vernal
A

B. bermuda grass

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6
Q

Which two of the following do not cross react with the rest?

A. timothy grass
B. Bahia 
C. Kentucky blue grass
D. orchard grass
E. johnson
F. sweet vernal
A

B. Bahia & E. johnson

cross react with each other, not the others

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7
Q

All of the following ragweed allergens cross react except which 2:

A. short 
B. giant
C. southern
D. slender
E. false
F. western
A

C. southern
D. slender

cross react with each other and cocklebur & marsh elder

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8
Q

All of the following weed allergens cross react except:

A. Russian thistle
B. sage
C. lambs quarter
D. burning bush
E. Kochia
A

B. sage

cross reacts with wormwood & mugwort

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9
Q

All of the following tree allergens cross react except:

A. birch
B. juniper
C alder
D. hazel
E. hornbeam
A

B. juniper

cross reacts with cedar & cypress

other trees:

  • Oak, Beech, Chestnut OBC
  • Pecan, Hickory PH
  • Ash, Olive, Privet AOP
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10
Q

Dust mite extract in >10% glycerin is safe to mix with which of the following extracts:

A. cat
B. dog
C. pollen
D. cockroach
E. mold
F. all of the above
A

F. all of the above

  • ragweed & cat extracts in >50% glycerin resist degradation when mixed with high protease extracts
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11
Q

Mold and cockroach extracts should not be mixed with pollen because they contain:

A. high glycerin content
B. higher IgE binding affinity
C. non standardized extracts
D. proteolytic enzymes that degrade pollen

A

D. proteolytic enzymes that degrade pollen
= reduced IgE binding affinity

glycerin = inhibitor of proteolytic activity

phenol = antibacterial property

Venoms contain proteases that can degrade each other and should NOT be mixed
(except vespids hornets & yellow jackets)

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12
Q

effective maintenance dose for most inhalant allergens is:

A

5-20 ug of the major allergen per 0.5 mL mainenance dose

1000-4000 BAU/AU

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13
Q

All of the following are true about systemic reactions except:

A. they occur in approximately 2% of patients
B. they are more likely to occur in patients who experience a large local reaction
C. they are more likely to occur in patients who frequently experience large local reactions
D. most occur within the first 30 minutes
E. they occur in approximately 0.2% of injections

A

B. they are more likely to occur in patients who experience a large local reaction

  • greater risk of fatal reactions in patients taking beta blockers.
  • fatal reaction risk 1 in 2.5 million
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14
Q

All of the following incur a greater risk of systemic reactions except:

A. unstable asthma
B. history of previous SR
C. after"priming" of pollen season
D. during build up phase
E. first injection from new vial
F. during accelerated or rush protocols
A

C. after”priming” of pollen season

DURING priming

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15
Q

All of the following are relative contraindications to starting/build up IT except:

A. immunodeficiency
B. pregnancy
C. malignancy
D. mild, well controlled asthma
E. significant cardiovascular disease
F. ACE inhibitors in VIT
A

D. mild, well controlled asthma

  • poorly controlled or severe asthma
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16
Q

All of the following are relative contraindications to SLIT except:

A. prior severe SR to SLIT
B. HS reactions to inactive ingredients
C. significant cardiovascular disease
D. severe asthma
E. eosinophilic esophagitis
A

C. significant cardiovascular disease

EPI for all

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17
Q

tbale 7-5 page 361 for 4 types of histamine receptors

A

H1-antihistamines are INVERSE AGONISTS

which bind the receptor and stabilize it in the inactive form, shifting equilibrium to inactive state

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18
Q

Antiallergic and antiinflammatory effects of H1-antihistamines include all of the following except:

A. inhibit release of mast cell and basophil mediators through inhibition of calcium ion channels
B. reduce early allergen response via fewer ahesion molecules, eos, neutros, cytokines, LTs, and PGs in lavage fluid in when pretreatement in allergen challenge
C. upregulate NFkB
D. inhibit expression of cell adhesion molecules
E. inhibit eosinophil chemotaxis

A

C. upregulate NFkB

DOWNregulate to cause:

D. inhibit expression of cell adhesion molecules
E. inhibit eosinophil chemotaxis

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19
Q

All of the following antihistamines would require consideration of dose adjustment in a patient with hepatic impairment except:

A. cetirizine
B. diphenhydramine
C. chlorpheniramine
D. fexofenadine
E. doxepin
F. hydroxyzine
G. desloratidine
A

D. fexofenadine

  • the only one that is only RENALly metabolized

RENAL + hepatic =
A. cetirizine
G. desloratidine
levoceterizine

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20
Q

All of the following antihistamines would require consideration of dose adjustment in a patient with renal impairment except:

A. cetirizine
B. levoceterizine
C. loratidine
D. fexofenadine
E. desloratidine
A

C. loratidine

only HEPATIC metabolism

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21
Q

Potential adverse effects of H1 antihistamines due to blocking effects on receptors and ion channels include all of the following except:

A. ion channels: QT prolongation
B. antiserotonergic: decreased appetite
C. anti-alpha-adrenergic: hypotension, dizziness, reflex tachycardia
D. antimuscarinic/anticholinergic: dry mouth, urinary retention, sinus tachy
E. anti-H1 receptor: sedation, incr. appetite, decreased cognitive and psychomotor performance

A

B. antiserotonergic: decreased appetite

INCREASED appetite (cyproheptadine/periactin)

A. ion channels: QT prolongation
- blockade of the rapid component of the delayed rectifier potassium current (IKr) and long QT can -> torsades de pointes

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22
Q

Mechanism of beta agonists:

A

binds B2-beta GPCR and increases cAMP

  • activates protein kinase A
  • phosphorylation & muscle relaxation
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23
Q

Salmeterol has a slower onset of action (30 min) compared to formoterol (2-3 min) due to:

A

more lipophilic

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24
Q

Actions of beta-agonists include all of the following except:

A. increases mucociliary clearance
B. protect epithelium againts bacteria
C. binds B2-beta GPCR and increases cAMP leading to muscle relaxation
D. potentiate microvascular permeability
E. inhibit cholinergic neurotransmission
A

D. potentiate microvascular permeability

SUPPRESS

see page 366 for more actions & studies ICS/LABAs & B-agonist adverse effects

& page 367 for tachyphylaxis

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25
Q

Patients with what mutations may be at an increased risk of worsening lung function with regular use of albuterol:

A

B2-adrenergic receptor polymorphisms

  • B16 Arg/Arg homozygotes
  • agonist receptor downregulation
  • induces resistance to SM-relaxing effects of B2 agonists
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26
Q

All of the following may increase a patient’s risk during an asthma exacerbation except:

A. labetalol
B. nadolol
C. pindolol
D. propranolol
E. timolol
F. metoprolol
A

F. metoprolol
& atenolol are cardioselective (B1>B2)
= less risk for bronchoconstriction

the others are nonselective a/w blunted response to B2-agonists

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27
Q

CysLT1 receptors are expressed on inflammatory cells, bronchial epithelium, muscles and have the highest affinity for which leukotriene:

A. LTA4
B. LTB4
C. LTC4
D. LTD4
E. LTE4
A

D. LTD4
>LTC4 > LTE4

mediate pro-asthmatic actions- sustained bronchoconstriction, mucus secretions, and increase vascular permeability

leukotriene antagonists:

  • – attenuate EPR & LPR in Ag challenge
  • – AERD: improved FEV1, less B-agonist, decreased exac.

blocked by CysLT1R-antagonists:
montelukast (highest affinity), zafirlukast (dose-dep liver toxicity & warfarin interaction ^PTT), pranlukast. pg 368 for chart

asthmatics:

  • higher levels of cysLT production
  • sputum cysLTs correlate w/ severity
  • high levels in AERD
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28
Q

Adverse effects of Zileuton

A

5-LO & cytochrome CYP1A2 inhibitor

  • elevated ALT (monitor Q3mo, avoid in pts w/ hepatic dysfunction or heavy alcohol use)
  • headache, dyspepsia, myalgias, leukopenia
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29
Q

Doses of all of the following medications should be reduced if a patient is starting zafirlukast or zileuton except:

A. warfarin
B. fexofenadine
C. propranolol
D. theophylline

A

B. fexofenadine

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30
Q

All of the following are mechanisms of mast cell stabilizers cromolyn sodium and nedocromil sodium except:

A. inhibits IgE mediated calcium channel activation & mast cell degranulation
B. blocks eos activation
C. blocks neutros activation, chemotaxis, and mediator release
D. inhibits local IgE production
E. modulates parasympathetic nerve reflexes

A

E. modulates parasympathetic nerve reflexes

SYMPATHETIC

  • prevents EPR & LPR athmatic reactions
  • protects against exercise, cold, irritants, chemical, saline, mannitol challenges
  • NOT METHACHOLINE OR HISTAMINE
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31
Q

Anticholinergics:
- increased parasympathetic tone in asthma & COPD releases ACH -> stimulates muscarinic receptors -> bronchoconstriction, mucus secretion, vasodilation

A

M2: inhibitory R on parasympathetic nerves decreases ACH release

M3 GPC-ACH-R: primary mediator of SM contraction in airways

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32
Q

Ipratropium bromide can cause a paradoxical bronchoconstriction via what receptor:

A. M1
B. M2
C. M3

A

B. M2

  • blocking M2 -> increased ACH release from vagus -> may ^ bronchoconstriction
  • synergistic w/ B-agonists and decreases hospitalization rate in asthmatics
  • tiotropium has longer duration of action 2/2 100x slower dissociation from M1 & M3
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33
Q

All of the following are mechanisms of action of theophylline except:

A. inhibition of phosphodiesterases leading to increased cAMP
B. decreased HDAC2
C. antagonism of adenosine receptors, preventing mast cells from releasing histamine and LT and causing bronchoconstriction
D. increased IL-10
E. inhibition of phosphoinositide-3-kinase-delta (PI3K-d)

A

B. decreased HDAC2

E. inhibition of phosphoinositide-3-kinase-delta (PI3K-d) leads to INCREASED HDAC2

= can reverse corticosteroid resistance due to reduced HDAC2 activity

PDE inhibitors = incr. cAMP = bronchodilation & antiinflammatory effects

metabolized in liver by cytochrome p450 - adverse effects @ plasma levels >20 mg/L

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34
Q

All of the following can lead to an increased serum level (decreased clearance) of theophylline except:

A. macrolide antibiotics
B. ranitidine
C. zileuton
D. ciprofloxacin
E. allopurinol
F. CHF
A

B. ranitidine

NOT ranitidine, CIMETIDINE

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35
Q

All of the following can lead to an decreased serum level (increased clearance) of theophylline except:

A. rifampin
B. tobacco and marijuana use
C. ethanol
D. older age
E. carbamazepine, phenobarbital, phenytoin
A

D. older age

YOUNGER AGE

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36
Q

Steroids inhibit the LPR but NOT EPR of Ag challenge

ICS does not prevent progressive loss of lung function

GC-RBeta dominant negative effect = inhibits glucocorticoid response elements & antiinflammatory protein synthesis = incr expression a/w fatal & nocturnal asthma

A

effects in inflammatory cells & side effects pg 375

SUBCAPSULAR POSTERIOR cataracts

protease inhibitors (ritonavir) + ICS (fluticasone) -> high systemic concentrations & Cushing’s

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37
Q

IgE binds what chain of the FcERI receptor on mast cells and basophils?

A. alpha
B. beta
C. gamma

A

A. alpha

Omalizumab binds the CH3 domain (Fc portion) of FREE IgE molecule, preventing it from binding to FcεRI

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38
Q

Omalizumab is associated with a decrease in all of the following except:

A. free IgE and eosinophils
B. expression of FcERI on effector cells
C. circulating IL-13 and FENO
D. total IgE
E. mediator release from mast cells and basophils
F. B lymphocytes
A

D. total IgE

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39
Q

Mepolizumab mechanism of action:

A. IgG4/κ monoclonal antibody
B. IgG1/κ monoclonal antibody
C. IgG1k monoclonal antibody that binds α chain of human IL-5R Fcγ RIIIa region

A

B. IgG1/κ monoclonal antibody

inhibits bioactivity of IL-5 by blocking IL-5 from binding the alpha chain of the IL-5 receptor complex expressed on eosinophils

40
Q

Benralizumab mechanism of action:

A. IgG4/κ monoclonal antibody
B. IgG1/κ monoclonal antibody
C. IgG1k monoclonal antibody that binds α chain of human IL-5R

A

C. IgG1k monoclonal antibody that binds α chain of human IL-5R via its Fab fragments = preventing the interaction between IL-5 and its receptor

mechanism of activating ADCC & eosinophil apoptosis?
- through its Fc constant region, benralizumab binds to the FcγIIIRa receptor expressed by natural killer cells, thus inducing eosinophil apoptosis operated by the release of proapoptotic proteins such as granzymes and perforins

41
Q

All of the following are true about AERD except:

A. it is a non-IgE mediated reaction
B. increased expression of leukotriene C4 synthase and cysLT1 receptor
C. increased LTD4 causes acute bronchocontstriction and increased vascular permeability
D. urine LTD4 can be measured to reflect the increase production of cysLTs
E. PGE2 is an inhibitor of the 5-lipoxygenase pathway, which is decreased by COX1 inhibition but COX2 inhibitors are tolerated

A

D. urine LTD4 can be measured to reflect the increase production of cysLTs

LTE4!!! in urine

42
Q

ratio of chest compressions to breaths in an adult and child

A

adult 30:2
<8 yo 15:2

EPI: 0.01 mg/kg
SC/IM 1:1K
IV 1:10K

p 397

43
Q

Recommendations for vaccine administration include all of the following except:

A. live vaccines must be separated by 28 days if not given on the same day
B. all vaccines can be given on the same day
C. wait at least 6 months after IVIG or RBC product before giving live vaccines
D. wait at least 6-8 months after IVIG or RBC product before giving non-live vaccines
E. wait at least 2 weeks after live vaccine before giving IVIG or RBC product

A

C. wait at least 6 months after IVIG or RBC product before giving live vaccines

3 MONTHS!

Arthus reactions: Type 3 IC HS- common w/ 4-5 dose DTaP

LMNOP and RSV live vaccines:
Live vaccines include:
MMR
Nasal flu
Oral polio
Rotavirus
Smallpox, Shingles
Varicella
44
Q

table 7-20 page 403 topical corticosteroids

A

table 7-21 page 405 opthalmic treatments

45
Q

Risk factors for drug allergy include all of the following except:

A. history of prior drug allergy
B. higher dose
C. IV route
D. low-molecular weight agents
E. frequent, repetitive, or longer courses
F. female gender
A

D. low-molecular weight agents

HIGH MW

Atopy- a/w latex and RCM

46
Q

Which of the following mutations is associated with abacavir reactions in caucasians and is an indication for testing before initiating therapy?

A. HLA-A3101
B. HLA-B
5701
C. HLA-B1502
D. HLA-B
5801

A

B. HLA-B*5701

47
Q

Which of the following mutations is associated with carbamazepine reactions in Han Chinese that can result in SJS/TEN?

A. HLA-A3101
B. HLA-B
5701
C. HLA-B1502
D. HLA-B
5801

A

C. HLA-B*1502

A. HLA-A*3101- Carb in Europeans

D. HLA-B*5801- allopurinol in Asians, SCARs

48
Q

What is the major determinant of penicillin?

A. Penicillin G
B. penicilloate
C. penilloate
D. benzylpenicilloyl polylysine

A

D. benzylpenicilloyl polylysine (Pre-Pen)

  • most PCN allergy related to MAJOR determinant
  • 97% NPV of PCN SPTs
  • PCN IgE abs decrease 10%/yr = 50% will have negative SPT @ 5 years = 80% @ 10 years

10% pts have delayed non-IgE MP rash w/ AMP/AMOX
+ EBV = 80% get rash

49
Q

A patient with a history of penicillin allergy needs a cephalosporin. What is the next best step?

A. skin test to cephalosporin
B. give the cephalosporin
C. direct challenge with amoxicillin
D. perform penicillin skin testing; if negative, can safely receive cephalosporin

A

D. perform penicillin skin testing; if negative, can safely receive cephalosporin

50
Q

Penicillin has cross reactivity with which of the following drugs on skin testing, with much rarer rates of clinically important cross reactivity?

A. aztreonam
B. ceftazidime
C. sulfonamides
D. carbapenems

A

D. carbapenems (imipenem & meropenem)

CEFTAZ & AZTREOnam!!! cross react

TMP/SMX:

  • HIV = T cell mediated delayed MP rash
  • Type I HS = N4 sulfonamidoyl hapten major determinant
51
Q

The following are associated with increased incidences of radiocontrast adverse reactions except:

A. women
B. asthma or atopy
C. cardiovascular disease
D. prior history of reaction
E. multiple prior radiocontrast events
A

E. multiple prior radiocontrast events

  • nonspecific mast cell degranulation 2/2
    MRGPRX2-receptor
52
Q

High risk agents associated with SJS include all of the following except:

A. PCN
B. sulfonamides
C. aromatic anticonvulsants
D. allopurinol
E. vancomycin
F. NSAIDs
G. pantoprazole &amp; tramadol
A

E. vancomycin
(can cause linear IgA bullous dermatitis w/ tense blisters & RMS 2/2 direct MC activation)

mechanism: reactive metabolites cause Fas/FasL mediated apoptosis of epidermal cells & CTL activation & perforin release
sx: mucous membranes, epidermal necrosis, target lesiosn
- steroids CONTRAINDICATED in TEN

53
Q

What is the most likely timing between exposure to therapy and onset of reaction in drug rash with eosinophilia and systemic symptoms?

A. immediate (minutes to 1-2 hours)
B. delayed (4-6 hours)
C. days (>24 hours)
D. 1 week 
E. weeks (2-3 weeks)
A

E. weeks (2-3 weeks)

  • SX: fever, LAD, hepatitis, facial edema, can worsen after d/c drug
54
Q

What is the most likely hypersensitivity mechanism in drug rash with eosinophilia and systemic symptoms?

A. Type I
B. Type II
C. Type III
D. Type IVa
E. Type IVb
F. Type IVc
G. Type IVd
A

E. Type IVb

  • drug specific CD4/CD8 T cells
  • mechanism a/w reactivation of chronic persistent HHV viruses, CMV, and EBV
  • can be a/w autoimmune complications up to 4 years later
55
Q

What is the most likely hypersensitivity mechanism in fixed drug eruption?

A. Type I
B. Type II
C. Type III
D. Type IVa
E. Type IVb
F. Type IVc
G. Type IVd
H. vagal reaction
A

F. Type IVc

  • blue purple macule in same location w/ each drug exposure
  • a/w TMP/SMX bactrim and phenolphthalein, tetracyclines, NSAIDs
56
Q

What is the most likely mechanism of reaction in a patient at the dentist’s office who experiences flushing, hypotension, chest tightness, SOB, and bradycardia after local injection of lidocaine?

A. Type I
B. Type II
C. Type III
D. Type IVa
E. Type IVb
F. Type IVc
G. Type IVd
H. vagal reaction
A

H. vagal reaction

BRADYcardia (vs tachy in ANA)

no SPT, use graded challenges

57
Q

MCC perioperative ANA in:

  • US
  • non US
A
  • US = abx (cefazolin)

- non US = NMBA (quaternary ammonium agents, succinylcholine)

58
Q

What is the most likely mechanism of reaction in a patient receiving biologic therapy who experiences fever, rash, bronchospasm, GI sx, with elevated LFTs, LDH and uric acid?

A. Type I
B. Type II
C. Type III
D. Type IVa
E. Type IVb
F. Type IVc
G. Type IVd
H. vagal reaction
I. cytokine release syndrome (type alpha)
A

I. cytokine release syndrome (type alpha)

see DK slide 78, page 413

59
Q

Patient with IgE antibodies to galactose-alpha-1,3-galactose are at a higher risk for anaphylaxis with what medication

A

Cetuximab

60
Q

Immune mediated hemolytic anemias are classically due to all of the following drugs except:

A. quinidine
B. methyldopa
C. penicillin
D. heparin

A

D. heparin

  • heparin a/w THROMBOCYTOPENIA (HIT)
  • specific IgG to heparin platelet factor 4 -> immune complex formation -> HIT
  • immune thrombo also a/w: quinidine, PTU, gold, sulfa, vanc
61
Q

A patient with cough, migratory infiltrates, peripheral eosinophilia, and pulmonary fibrosis after drug exposure is most likely classically due to all of the following drugs except:

A. bleomycin
B. nitrofurantoin
C. vancomycin
D. methotrexate
E. NSAIDs
F. Amiodarone
A

C. vancomycin

Pulm drug HS:
A. bleomycin
B. nitrofurantoin - IP and pleural effusion
D. methotrexate

Eosinophilic PNA:
E. NSAIDs

IP:
F. Amiodarone

62
Q

What is the most likely timing between exposure to therapy and onset of reaction with fever, rash, urticaria, LAD, arthralgias, in serum sickness reactions?

A. immediate (minutes to 1-2 hours)
B. delayed (4-6 hours)
C. days (>24 hours)
D. 1 week 
E. weeks (1-3 weeks)
A

E. weeks (1-3 weeks)

SSR:

  • causes: heterologous antiera, snake antivenom
  • labs: low complement, high C1q binding assay
  • mechanism: immune complex formation, Type III HS rxn
  • TX: steroids & AH, no desensitization
63
Q

A child presents with fever, rash, urticaria, LAD, arthralgias, after receiving a medication 2 weeks ago. What is the most likely implicated agent?

A. penicillin
B. sulfonamide
C. cefaclor
D. phenytoin
E. a monoclonal antibody
A

C. cefaclor

MCC SSLR in KIDS!!!
- due to altered metabolism -> toxic intermediates

The other answers all cause SSR, too, but less in kids

64
Q

A patient presents with photodistributed erythema and annular, scaly plaques 4-8 weeks after starting hydrochlorothiazide. What is the most likely associated antibody profile?

A. antihistone antibodies
B. anticentromere antibodies
C. anti-Ro (SSA) and anti-La (SSB) antibodies
D. anti-HCTZ drug specific antibodies

A

C. anti-Ro (SSA) and anti-La (SSB) antibodies

  • drug induced CUTANEOUS lupus
  • cutaneouS = SSA + SSB (S = Skin)
65
Q

A patient presents with myalgias and arthralgias which have gradually progressed over the last few months after starting procainamide. What is the most likely associated antibody profile?

A. antihistone antibodies
B. anticentromere antibodies
C. anti-Ro (SSA) and anti-La (SSB) antibodies
D. anti-HCTZ drug specific antibodies

A

A. antihistone antibodies

  • drug induced SYSTEMIC lupus
  • sySTemic = antihiSTone ab
66
Q

A patient presents with photodistributed erythema and annular, scaly plaques 4-8 weeks after starting a new medication, and is found to have anti-Ro (SSA) and anti-La (SSB) antibodies. The most likely implicated medication can include all of the following except?

A. hydrochlorothiazide
B. procainamide
C. calcium channel blockers
D. ACE inhibitors
E. antifungals
A

B. procainamide (DI systemic lupus)

  • this case is drug induced CUTANEOUS lupus
67
Q

A patient presents with myalgias and arthralgias which have gradually progressed over the last few months after starting a new medication, and is found to have anti-histone antibodies. The most likely implicated medication can include all of the following except?

A. hydralazine
B. procainamide
C. phenytoin
D. isoniazid
E. ACE inhibitors
A

E. ACE inhibitors (DI cutaneous lupus)

  • this case is drug induced SYSTEMIC lupus
68
Q

Which 2 of the following chemotherapeutic agents can cause anaphylactoid reactions that may be treated or prevented with steroids and antihistamines?

A. taxanes
B. platinum compounds
C. aspariginase
D. excipients

A

A. Taxanes (paclitaxel, docetaxel)
D. Excipients (cremophor-EL)

C. aspariginase- can cause anyphylactoid or IgE med.

69
Q

All but which of the following chemotherapeutic agents can cause IgE mediated reactions that may be desensitized if necessary?

A. taxanes
B. carboplatin
C. cisplatin
D. oxiplatin

A

A. taxanes

PLATINUM compounds = DESENS.

MC reactions s/p 7 cycles

carbo > cis > oxo

70
Q

see DK’s slide on contrast reactions

A

risk for contrast reactions w/ atopy

71
Q

All of the following are contraindications to desensitization except:

A. hemolytic anemia
B. nephritis
C. hepatitis
D. immune complex-mediated reactions (serum sickness)
E. antibody dependent cytotoxic reactions
F. cell mediated exfoliative or blistering skin reactions (DRESS, SJS/TEN)

A

E. antibody dependent cytotoxic reactions

72
Q

Antihistamines and antileukotrienes decrease LRs what schedule of IT?

A

RUSH and cluster AIT

Might reduce frequency of systemic reactions in conventional, rush and cluster

73
Q

Consider discontinuation of what med only for venom IT

A

ACE-I

74
Q

All of the following can increase steroid metabolism, and may require higher doses of steroid therapy, except:

A. rifampin
B. carbamazepime
C. phenobarbital
D. OCPs
E. phenytoin
F. antacids
A

D. OCPs (DECREASE)

Also:

  • ketoconazole
  • methylpred affected by: clarithromycin

might need to increase steroid dose if patient is on RIPE therapy

75
Q

which major form of the glucocorticoid receptor mediates steroid resistance?

A

GRbeta is an inactive form of the receptor that is involved in steroid resistance

76
Q

Glucocorticoids influence gene transcription using 2 distinct pathways. Which pathway mediates the drugs adverse side effects?

A

All the unwanted effects of steroids come from trans-activation

(Trans-repression inhibits transcription factor function (NKkB, NF-AT), inflammatory cytokines, chemokines, enzymes, etc)

77
Q

Glucocorticoids can directly enhance gene expression via trans-activation (target gene activation) and increase transcription of all of the following anti-inflammatory genes except:

A. IL-10
B. GILZ
C. NFkB
D. MKP-1
E. IkBa
A

C. NFkB- inhibited

A. IL-10- basically the only cytokine NOT inhibited
B. GILZ- GCC_induced leucine zipper protein)
D. MKP-1 (Map kinase phosphatase-1)
E. IkBa- inhibits NFkB

78
Q

true or false: The major pathway thought to suppress inflammation is trans-activation and direct suppression of gene expression rather than transcription factor interference (trans-repression).

A

false.

used to think that, but now we think:

Steroids are a sponge that soak up transcription factors that enhance inflammatory reactions for gene transcription and their upregulation. Also binds TF on its response element and sterically inhibits its promotor (see page 168 of notes for picture)

79
Q

All of the following are mechanisms by which GCC mediate anti-inflammatory functions except:

A. Destabilize mRNA before it can be translated into DNA and make inflammatory factors
B. influence gene transcription by altering chromatin structure = prevent DNA from unwinding, and promotors aren’t available for gene transcription
C. activate HAT activity in low concentrations
D. recruit HDAC in low concentrations
E. repression of genes for RANTES, eotaxins, ICAM-1, VCAM-1, E-selectin, NOS, COX-2, PLA2, bradykinin B2-receptors

A

C. activate HAT activity in HIGH concentrations
= increased anti-infl. gene transcription (IkBa, IL-10)

B. influence gene transcription by altering chromatin structure = prevent DNA from unwinding, and promotors aren’t available for gene transcription
D. recruit HDAC in low concentrations = repression of pro-infl. gene transcription

80
Q

The glucocorticoid receptor beta (GRb) does not bind to GC, but may bind GRalpha and inhibit GRE via what effect?

A

dominant negative

increased expression of GRb a/w:

  • steroid resistant asthma
  • fatal asthma
  • nocturnal asthma
  • NP
81
Q

true or false: inhaled glucocorticoids affect the late and early phase bronchial response and airway hyperresponsiveneness

A

FALSE, only LATE

82
Q

All of the following are beta-2 selective, non-catecholamine bronchodilators except:

A. terbutaline
B. albuterol
C. fenoterol
D. salmeterol
E. formoterol
F. vilanterol
G. indacaterol
A

C. fenoterol - and metaproterenol (non-selective)

SHORT:
A. terbutaline
B. albuterol

LONG (>12 hrs):
D. salmeterol- SLOW (30 min). PARTIAL agonist = cant result in maximal bronchodilation
E. formoterol- FAST onset (2-3 min). FULL agonist- >80% maximal B2-agonist receptor activation = dose dependent effect

VERY LONG (>24 hrs):
F. vilanterol
G. indacaterol
carmoterol

Catecholamine:

  • isoproterenol
  • epinephrine
83
Q

true or false: B2-receptor desensitization results in diminished responsiveness that develops over weeks when receptors are repeatedly exposed to agonists, and downregulation of the B2-adrenergic receptor, affecting the ability of agonists to bronchodilate.

A

false: Tachyphylaxis doesn’t affect ability to bronchodilate, but does shorten duration/bronchoprotective affect of BDL ex. 12 hrs vs 6-8 hrs

84
Q

ipratropium mechanisms

A

blocks M2 & M3 receptors with equal affinity

1) blocking M3 decreases Ach-induced bronchoconstriction
2) M2 receptors can be inhibitory and excitatory:
- excitatory: comprise majority of MR in airway and stimulation = bronchoconstriction.
- inhibitory: agonist (Ach) = inhibit Ach release. antagonist (anticholinergic) = blocking inhibitory receptors = increased Ach release from vagus = paradoxical bronchospasm

85
Q

tiotropium mechanism

A

equal binding affinity for M2 & M3 receptor

  • dissociates from M2 receptor 10x faster than M3
  • dissociates from M3 receptor 100x slower than ipratropium

= overall more M3 selective -> more blocking M3 bronchoconstriction, and less paradoxical M2 bronchoconstriction

  • longer duration of action
86
Q

Which of the following results in reduced production of LTB4?

A. zafirlukast
B. zileuton
C. montelukast
D. pranlukast

A

B. zileuton

  • blocks 5-LO = blocks LTB4 & cysLTs
87
Q

Which is more potent in causing bronchoconstriction-histamine or cysteinyl leukotrienes?

A

LTE

88
Q

All of the following antagonize the cysLT1 receptor except:

A. zafirlukast
B. zileuton
C. montelukast
D. pranlukast

A

B. zileuton

LTD4 > LTC4 > LTE4

do not antagonize the cysLT2 receptor

89
Q

true or false: anti-leukotriene therapies attenuate both the late and early phase response to antigen challenge

A

TRUE

90
Q

Which histamine receptors are not mast cell mediated?

A

H3 & H4

1st gen AH- smaller, polar, hydrophobic = lipophilic = enter blood brain barrier, sedation

2nd gen-opposite

91
Q

Which of the following drugs is incorrectly matched with their non-H1-AH effects?

A. 1st generation AH- antimuscarinic and anticholinergic effects
B. promethazine- beta adrenergic blocking
C. diphenhydramine- local anesthetic effects
D. cyproheptadine- antiserotinergic effect

A

B. promethazine- ALPHA adrenergic blocking

1st gen AH are extensively metabolized by the hepatic CYP450 system = potential interactions with drugs that inhibit CYP450 (Ex. macrolides)

92
Q

Which of the following are mechanisms of action of theophylline is responsible for many of its seriously adverse effects:

A. inhibition of phosphodiesterases leading to increased cAMP
B. decreased HDAC2
C. antagonism of adenosine receptors, preventing mast cells from releasing histamine and LT and causing bronchoconstriction
D. increased IL-10
E. inhibition of phosphoinositide-3-kinase-delta (PI3K-d)

A

C. antagonism of adenosine receptors, preventing mast cells from releasing histamine and LT and causing bronchoconstriction

because it also leads to CNS stimulation, cardiac arrythmias, gastric hypersecretion, GE reflux, diuresis

93
Q

Reslizumab mechanism of action:

A. IgG4/κ monoclonal antibody
B. IgG1/κ monoclonal antibody
C. IgG1k monoclonal antibody that binds α chain of human IL-5R Fcγ RIIIa region

A

A. IgG4/κ monoclonal antibody

94
Q

nephelometry mechanism

A

measure immune complex formation in the liquid phase

measures scattered light to detect concentration of antibodies and levels of immunoglobulins

95
Q

HAE treatment guidelines for testing in the asymptomatic child of a parent with HAE?

A

C1INH testing be delayed until 1 year of age

96
Q

antihypertensives that can worsen rhinitis

A
  • β-blockers
  • ACE-I
  • ameloride
  • hydralazine
  • reserpine
  • calcium channel blockers
  • methyldopa
  • α-receptor antagonists (prazosin)
  • phospophodiesterase-5 inhibitors (sildenafil)