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DT1 Exam 2 > Pharm/Bioterrorism > Flashcards

Pharm/Bioterrorism Flashcards

1
Q

physiological cause of gout

A

increased uric acid in the blood (hyperuricemia)

above 6-7 mg/dl serum

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2
Q

risk factors of gout

A

higher in men

women increased risk after menopause

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3
Q

idiopathic causes of gout

A

renal retention of urate
hypertension, obesity, hyperlipidemia
increased urate production

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4
Q

causes of renal retention

A

drug-diuretics, aspirin (could also cause increase in cell turnover)
renal damage
metabolic

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5
Q

enzyme defects related to gout

A

increased phosphoribosylpyrophosphate synthetase

decreased hypoxanthine guanine phsophoribosyl transferase

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6
Q

local causes of gout

A

low temperature

low pH

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7
Q

role of immune system in gout

A

granulocytes phagocytize urate crystals
release kinins and lysosomal enzymes from granulocytes
increased lactic acid production and local decrease in pH
leads to increased deposition of urate crystals

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8
Q

excretion of urate in kidneys

A

filtered at glomerulus
actively reabsorbed in PT (S1 100%)
active secretion in PT (S2 50%)
active reabsorption in late PT and DT (S3 80%)
overall 10% initially filtered at glomerulus is excreted

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9
Q

non-drug therapy of gout

A

avoid obesity-foods high in purine content
avoid dehydration-keep concentration in serum lower through proper hydration
avoid alcohol-decrease in ADH leads to increased concentration

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10
Q

MOA colchicine

A

antimitotic, anti-inflammatory
decrease leukocyte mobilization
decrease lactic acid and histamine
decrease release of inflammatory glycoprotein
inhibition of leukotriene synthesis by inhibiting lipoxygenase pathway

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11
Q

toxicity colchicine

A 
GI disturbance (N/V/D)
chronic-risk of aplastic anemia, agranulocytosis, myopathy, alopecia
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12
Q

uses colchicine

A 
acute attacks (DOC with NSAIDs)
prophylactic use to prevent acute attacks
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13
Q

MOA allopurinol

A

antimetabolite of hypoxanthine which inhibits xanthine oxidase
competitive at low concentrations, noncompetitive at high concentrations (metabolite alloxanthine is noncompetitive at all concentrations)

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14
Q

uses allopurinol

A

preferred in patients with impaired renal function (does not increase urate levels)
chronic gout
secondary hyperuricemia

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15
Q

allopurinol and 6MP

A

inhibits biotransformation of 6MP

should reduce dose of 6MP when both drugs are being used

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16
Q

toxicity allopurinol

A

rash, fever, vasculitis, hepatotoxicity, bone marrow toxicity

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17
Q

acute attacks with allopurinol

A

fluctuations in serum urate levels

colchicine or NSAID to prevent acute attacks

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18
Q

MOA febuxostat

A

inhibition of xanthine oxidase, non-purine drug that forms a stable complex with xanthine oxidase

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19
Q

pharmacokinetics febuxostat

A

absorption reduced by magnesium hydroxide and aluminum hydroxide antacids
slightly reduced absorption by food

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20
Q

uses febuxostat

A

hyperuric patients

not for patients with asymptomatic hyperuricemia

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21
Q

toxicity febuxostat

A

liver function abnormalities, nausea, joint pain and rash

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22
Q

acute attacks with febuxostat

A

fluctuations in serum urate levels

colchicine or NSAID to prevent acute attacks

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23
Q

MOA rasburicase

A

recombinant urate oxidase enzyme that catalyzes the oxidation of uric acid into soluble allantoin; lowers levels better than allopurinol

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24
Q

uses rasburicase

A

pediatric patients with leukemia, lymphoma, and solid tumors who are receiving cancer chemo that result in cell lysis and hpyeruricemia

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25
Q

decreased efficacy rasburicase

A

antibody against enzyme

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26
Q

toxicity rasburicase

A

hemolysis in G6PD, methemoglobinemia, acute renal failure and anaphylaxis

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27
Q

MOA uricosuric agents (probenecid and sulfinpyrazone)

A

competitively inhibits active reabsorption of urate by primarily URAT-1 in proximal tubule of nephron to increase urate excretion

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28
Q

low doses probenecid

A

inhibit active secretion (more sensitive system) of urate to cause UA retention

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29
Q

toxicity probenecid

A

GI irritation with aggravation of peptic ulcer

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30
Q

intrarenal urate stone formation probenecid

A

increase fluid intake or alkalinize urine

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31
Q

uses probenecid

A

chronic gout
hyperuricemic states
sufinpyrazone may decrease platelet aggregation (MI prophylaxis)

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32
Q

benzbromarone

A

increases urate excretion without urate retention
not in US
good for patients with decreased renal function or patients allergic to probenecid

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33
Q

acute attacks with probenecid

A

may precipitate an acute attack

colchicine or NSAID can be used prophylactically

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34
Q

NSAID MOA

A 
selective cox2 inhibitors
decrease inflammation (except acetaminophen)
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35
Q

FDA approved NSAIDs for gout

A

indomethacin, naproxen, sulindac

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36
Q

aspirin for gout

A

DO NOT USE

decrease urate secretion but increase risk of renal calculi

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37
Q

elderly gout treatment

A

NSAIDs or glucocorticoids over colchicine if patient has cardiac, renal, or GI diseases

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38
Q

glucocorticoids for gout

A

acute gout when other treatments fail

ex. prednisone

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39
Q

percutaneous absorption

A

exclusively diffusion process

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40
Q

rate limiting step in percutaneous absorption

A

permeation through stratum corneum

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41
Q

ways to increase amount of drug in receptor phase

A

increase diffusion coefficient
increase concentration of donor drug
increase solubility (Km)
(direct relationship)

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42
Q

ways to decrease amount of drug in receptor phase

A

increase thickness of skin

inverse relationship

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43
Q

tachyphylaxis

A

diminished biological effect after repeated usage-occurs after repeated steroid application

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44
Q

most common allergic reaction

A

dermatologic reactions

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45
Q

drug idiosyncrasy and drug intolerance MOA and side effects

A

nonimmune mediated
thrombocytopenia (ranitidine, linezolid, vanco)
GI side effects (N/D) with ABX

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46
Q

pseudoallergic MOA

A

nonimmune mediated

release of mediators from mast cells and basophils (opioids)

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47
Q

risk factors for allergic reactions

A

chemical structure-similar structures may cause cross sensitivity
molecular weight-high molecular weight increases change or low with hapten/carrier
route of administration-paraenteral vs. topical
reaction may present on repeat exposures

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48
Q

carrier and hapten as immunogenic compound

A

carrier and hapten are immunogenic compound
requires covalent binding
hapten-reacts with a specific antibody (low molecular weight prevents it from being immunogenic by itself)
can undergo biotransformation or photoactivation to become activated and immunogenic
insulin does not require binding for immune response

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49
Q

type I hypersensitivity

A

anaphylactic (IgE mediated)

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50
Q

type II hypersensitivity

A

cytotoxic antibodies

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51
Q

type III hypersensitivity

A

immune complexes

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52
Q

type IV hypersensitivity

A

cell mediated (delayed)

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53
Q

anaphylaxis

A

acute, life threatening allergic reaction
skin-pruritis, urticaria, erythema, angioedema
GI-N/V/D, abdominal pain
resp-chest tightness, stridor, bronchospasm
CV-hypotension, tachy, dysrhythmias

onset 30-120 mins after exposure

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54
Q

fatal anaphylaxis

A

asphyxia due to laryngeal edema or CV collapse

55
Q

serum sickness

A

resulting from soluble circulating immune complexes that form under conditions of antigen excess
onset-7 to 14 days
presentation-fever, malaise, lymphadenopathy

56
Q

common causes of serum sickness

A

cephalosporins, antivenim (equine serum leads to allergic reaction)

57
Q

drug fever

A

CNS-alters temperature or stimulate release of endogenous pyrogens from WBC (TNF and IL1)
direct-tumor cell destruction
onset-7 to 10 days
temperature pattern is highly variable

58
Q

common agents for drug fever

A

amphotericin B, antimicrobials

59
Q

Jarisch-Herxheimer Reaction

A

follows antibiotic treatment for spirochetal and bacterial infections
sudden release of bacterial components from injured and/or killed bacteria
symptoms-rigors, fever, hypotension

60
Q

classic causes of JHR

A

louse borne relapsing fever or tick borne refractory fever

61
Q

common agents causing JHR

A

TCN, doxy, Pen G

62
Q

drug induced autoimmunity

A

SLE
hemolytic anemia
renal interstitial nephritis
hepatic hypersensitivity reaction/toxic hepatitis

63
Q

SLE

A

drugs with hydrazine or amino group linked to aromatic ring (procainamide, hydralazine, isoniazide, phenytoin)
common-fever, rash, malaise, arhralgias, myalgias
several months after beginning drug

64
Q

common agents of SLE

A

procainamide, hydralazine, isoniazid, phenytoin, quinidine, penicillamine

65
Q

Interstitial nephritis

A

fever, rash and eosinophilia

proteinuria, hematuria, eosinophiluria

66
Q

mechanism interstitial nephritis

A

antibodies to drug-basement membrane complex

67
Q

common agents of interstitial nephritis

A

antistaphylococal penicillins (methicillin, ox, clox, diclox, nafcillin), cimetidine, sulfonamides

68
Q

hepatic hypersensitivity reaction

A

drug or metabolite acts as hapten to induce an autoimmune reaction
eosinophilia, fever, rash, granulomas

69
Q

common agents of hepatic hypersensitivity

A

erythromycin, penicillins

70
Q

vasculitis

A

inflammation and necrosis of blood vessels
limited to skin but can involve multiple organs
most common-palpable purpuric lesions
usually over lower extremities

71
Q

dermatologic reactions

A 
erythematous maculopapular rash (most common)
urticaria/angioedema
fixed drug eruptions
phototoxicity/photoallergy
eczematous contact dermatitis
erythema multiforme
SJS
TEN
72
Q

maculopapular rash

A

symmetrical, flat red rash
begins on extremities in ambulatory or back of bedridden patients
spares palms and soles

73
Q

common causes of maculopapular rash

A

penicillins, antibiotics, anticonvulsants

74
Q

urticaria/angioedema

A

blood plasma leaking out of small blood vessels due to histamine release
wheals with surrounding eryhtema
angioedema-facial and periorbital

75
Q

common agents of urticaria/angioedema

A

antibiotics, NSAIDS, anticonvulsants

lisinopril/ACEi can also cause angioedema

76
Q

fixed drug eruptions

A

single or multiple edematous, pigmented lesion
frequently dark red, violet or brownish pink
reappear in same location when drug reinitiated

77
Q

common agents fixed drug eruptions

A

PCN, TCN, cipro, bactrim

NSAIDs, quinidine, sulfonamides

78
Q

phototoxicity

A

immediately after drug treatment after a short exposure to sunlight
UV light results in drug emitting energy that can damage tissue

79
Q

photoallergy

A

activated by long wavelength sunlight
erythema/edema progress to urticarial, eczematous papulovesicular or exudative eruptions
UV light+drug or metabolite as hapten+ tissue antigen=complete antigen

80
Q

common causes of phototoxicity/photoallergy

A

TCN, carbamazepine, griseofulvin, coal tar derivatives, oral contraceptives

81
Q

eczematous contact dermatitis

A

new rash develops
normally during topical treatment of pre-existing dermatosis
new rash becomes eryhtematous, indurated, and vesicular

82
Q

erythema multiforme

A

begins as round, small, erythematous macule
target lesions on hands, feet, limbs, mucous membranes, and face
often preceded by mild upper respiratory symptoms

83
Q

common causes of erythema multiforme

A

antibiotics, anticonvulsants, NSAIDs

84
Q

Stevens Johnson syndrome

A

mucosal and conjunctival edema
high fever, myalgias, arthralgias
more severe erythema multiforme

85
Q

complications of Stevens Johnson syndrome

A

keratitis
conjunctival scarring
blindness

86
Q

common causes of SJS

A

sulfas, anticonvulsants, NSAIDs

87
Q

Toxic epidermal necrolysis

A

begins with malaise and fever
erythematous rash progresses to large flaccid bullae-become confluent, epidermis sloughs in large sheets, leaving exposed raw dermis

88
Q

common causes of TEN

A

antibiotics, anticonvulsants, NSAIDs

89
Q

Rhinitis/asthma

A

possibly IgE mediated allergy from agents that can cause anaphylaxis

90
Q

causes of rhinitis/asthma

A

NSAIDs, sulfites

91
Q

acute infiltrative and chronic fibrotic pulmonary reaction

A

cough and dyspnea

92
Q

causes of fibrotic pulmonary reaction

A

nitrofurantion, bleomycin

93
Q

hematological reactions

A 
eosinophilia
bone marrow aplasia (aplastic anemia)
hemolytic anemia (drug induced antibody)
thrombocytopenia
granulocytopenia (agranulocytosis)
94
Q

common causes of eosinophilia

A

antibiotics

digitalis

95
Q

aplastic anemia

A

pancytopenia
signs/symptoms-fatigue, weakness, stomatitis, easy bruising, petechiae
may appear after the drug has been discontinued

96
Q

common causes of aplastic anemia

A

dose dependent-chemotherapy
idiosyncratic-chloramphenicol
drug binding (IgG antibodies attack)
antibiotics, anticonvulsants, NSAIDs

97
Q

hemolytic anemia-drug/drug metabolite

A

IgG antibodies attack and destroy through complement

penicillins, cephalosporins

98
Q

hemolytic anemia-immune complexes

A

adsorb to erythrocyte surface
innocent bystander
quinidine

99
Q

hemolytic anemia-IgG antidrug metabolite

A

antibody binds eryhtrocyte
antibody coated cells phagocytized
coombs positive
methyldopa, penicillin

100
Q

thrombocytopenia-drug/drug metabolite

A

heparin

101
Q

thrombocytopenia-innocent bystander

A

quinidine, antibiotics

102
Q

thrombocytopenia-drug+HLA antigens

A

drug-platelet combination is recognized as non-self resulting in destruction by autoantibodies
gold salts

103
Q

symptoms of thrombocytopenia

A

petechiae, blisters in mouth
risk of bleed higher
intervention must occur

104
Q

symptoms of agranulocytosis

A

chills, fever, sore throat

105
Q

management of drug allergies

A

discontinuation of the agent when possible
treatment of adverse clinical signs and symptoms
substitution of another drug or agent
desensitization
skin testing for penicillin allergy
enter allergic reaction into patient chart-avoid mistakes in future
report ADR to FDA-medwatch program to collect phase IV info

106
Q

Naranjo scale

A

probability of allergic rxn related to medication in question
definite, probable, possible, doubtful

107
Q

cause of smallpox

A

variola major

108
Q

importnat subfamily of poxviridae

A

chordopoxvirinae

109
Q

orthopoxvirus genus members

A

vaccina, variola, cowpox

110
Q

molluscipoxvirus genus members

A

molluscum contagiosum

not seen until AIDS comes along

111
Q

structural characteristics of vaccinia

A

largest and most complex
oval or brick shape
double stranded DNA with covalently linked termini
envelope, biconcave core, lateral bodies

112
Q

importance of vaccinia in viruses

A

can accommodate a genome with additional DNA sequences artificially or naturally added (25 kb)

113
Q

Guarnieri bodies

A

cytoplasmic inclusion bodies that correspond to viral replication sites

114
Q

location of replication

A

entirely in cytoplasm

115
Q

Attachment

A

receptor-GAG (glycan amino glycan)

internalize through viropexis

116
Q

Uncoating

A

host cell enzyme remove outer envelope and lateral bodies
activation of core enzymes including viral DNA-RNAP to make immediate early mRNA
immediate early proteins for second step of uncoating

117
Q

early proteins

A

enzymatic activities for viral DNA replication

includes DNA dependent DNAP, thymidine kinase, exonucleases

118
Q

late proteins

A

from progeny DNA

form structural proteins

119
Q

maturation and assembly

A

MT allow virus particles to move to surface to egress

one layer synthesized, one from cell

120
Q

clinical manifestations of variola

A

enters through UR tract
transient viremia to internal organs and bone marrow
second viremia-first on face and then spreading centrifugally

121
Q

lesions of variola

A

macule to papule to umbilicated vesicle to pustule to crust and scarring
involves dermis and epidermis
umbilicated
lesions are on palms of hand and soles of feet

122
Q

benefit of incubation period

A

can vaccinate

severe fever 1-4 days prior to rash (important prodromal symptom)

123
Q

detection of variola

A

eosinophilic cytoplasmic inclusions in SPV infected skin cells
IF specifically directed to SPV antigens (hemagglutinin) for early detection
later-antibodies directed against viral antigens detected in patient serum

124
Q

transmission of variola

A

only in man
person to person contact-not infectious during incubation period and first day of prodrome
infectious when rash appears and progresses to crust

125
Q

vaccination

A

live attenuated vaccine

each generation becomes more avirulent

126
Q

vaccinia gangrenosa

A

low T cell

spreading lesion with necrosis of skin and muscles

127
Q

generalized vaccinia

A

occurs in patients with agammaglobulinemia or normal children
often fatal
resembles generalized herpes virus infections

128
Q

eczema vaccinatum

A

localize vesicles in areas of acne, eczema

129
Q

fetal vaccinia

A

vaccination of mother

still births or recovers

130
Q

postvaccinal encephalitis

A

hypersensitivity or viral invasion of CNS sudden onset at 12 day
often fatal
complications may be greater than risk of smallpox

131
Q

vaccinia immune globulin

A

administered to immunocompromised individuals with vaccinia infections

132
Q

Rifamyacin

A

inhibits morphogenesis by preventing proteolytic processing of precursor protein to smaller protein product (P4A to 4A)

133
Q

molluscum contagiosum

A

wart like, umbilicated
usually found in genital region
must remove central core of lesion to eliminate infection

DT1 Exam 2 (6 decks)

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