Final Version Flashcards

1
Q

MOA: inhibits phospholipase A2 and COX2 and works on concentration, distribution and function of peripheral leukocyte and macrophages?

A

Prednisone

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2
Q

What category does prednisone being in?

A

Corticosteroids

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3
Q

Other corticosteroids that work like prednisone

A

Methylprednisolone and dexamethasone

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4
Q

MOA: alkylating agent and signal 3 inhibitor
Non cell cycle specific
Inhibits b and T cells

A

Cyclophosphamide

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5
Q

MOA:
Antimetabolite and signal 3 inhibitor
Cell cycle specific
Inhibits T cells more than B cells

A

Azathiorpine

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6
Q
MOA: 
Antimetabolite and signal 3 inhibitor 
Cell cycle specific 
Inhibits B and T cells 
Used for Crohn's disease
A

Methotrexate

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7
Q

Mao: inhibits the synthesis of purines and signal 3 inhibitor.
Inhibits B and T cells

A

Mycophenolate

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8
Q

MOA:
Calcineurin phosphatase and signal 1 inhibition
T cell suppression

A

Cyclosporine

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9
Q

MOA:
CD3 receptor and signal 1 inhibition
T cell suppression

A

Muromonab-CD3

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10
Q

MOA:

T cell suppression

A

Lymphocyte immune globulin

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11
Q

Murine immunoglobulin

A

Muromonab-CD3

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12
Q

Horse immune globulin

A

Lymphocyte immune globulin.

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13
Q

Human IgG1 monoclonal antibody

A

Daclizumab

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14
Q

IL-2 receptor and signal inhibition

A

Daclizumab

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15
Q

Human immune globulin that helps passive immunity increase and helps prevent certain infection diseases in susceptible individuals

A

Gammagard

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16
Q

Suppresses immune response of Rh-negative individuals to Rh-positive blood cells

A

Rh0Gam

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17
Q

Antiviral and immunoregulatory activity but is not completely understood

A

Interferon beta

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18
Q

MOA:

Has phagocyte activating effects and antibody dependent cellular toxicity

A

Interferon gamma

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19
Q

Types of cytotoxic and proliferative agents

A

Cyclophosphamide, azathiorpine, methotrexate, mycophenolate

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20
Q

Category of T cell suppressants and other antibody immunosuppressive

A
Cyclosporine, micromanab-CD3, lymphocyte immune globulin, Daclizumab, Rh0
Immune globulin (Rh0Gam), immune globulin (gammagard)
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21
Q

Immunomodulators and immunostimulants

A

Interferon bets and interferon gamma

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22
Q

Used for relapsing/remitting multiple sclerosis

A

Interferon beta

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23
Q

Used for chronic granulomatoses disease and osteoporosis

A

Interferon gamma

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24
Q

ADRs:
nephrotoxicitt
hypertension
embryotoxic

A

cyclosporine

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25
Q

ADRs:
fever and chills
sensitivity for Murine products

A

Muromonab-CD3

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26
Q

used for hemolytic disease of the newborn

A

Rh0Gam

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27
Q

used for hypogammaglobulinemia and to prevent infections in HIV patientes

A

imuune globulin (Gammagard)

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28
Q

used for renal, liver, and heart trasnplant rejections and may be used with corticosteroids and azathiorpine
used for rheumatoid arthritis

A

cyclosporine

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29
Q

used for renal, liver, pancreas, an heart trasnplant rejection

A

muromonab-CD3

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30
Q

used for renal trasnplant rejection

A

lymphocyte immune globulin and daclizumab

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31
Q

used for rheumatoid arthritis, leukemias, and other tumors

A

cyclophosphamide

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32
Q

used for renal allotransplantation and rhumatoid arthrits in adults only

A

azathiorpine

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33
Q

used for Crohn’s disease, rheumatoid arthritis, leukemias and other tremors

A

methotrexate

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34
Q

used for renal, liver, and heart transplant rejections. used with cyclosporine and other corticosteroids

A

mycophenolate

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35
Q

used for allergic disorders, hematalogic disorders, hepatic and renal disease, and collagen disorders

A

corticosteroids

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36
Q
ADR: 
no serious effects for short period
long period: latogenic
cushing's syndrome
osteoporosis, infections, and ulcers
A

corticosteroids

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37
Q

ADR:
N/V/D
bone marrow suppression
aspermia

A

cyclophosphamide

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38
Q

ADR:
N/V
bone marrow suppression
infections

A

azathiorpine

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39
Q

ADR:
N/V
bone marrow suppression
Hepatotoxicity

A

methotrexate

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40
Q

ADR:
GI
neutropenia
infections

A

mycophenolate

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41
Q

ADR: fever and chills

sensitivity for equine products

A

lymphocyte immune globulin

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42
Q

ADR:

GI disorders

A

daclizumab

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43
Q

ADR:
mild side effects
contraindicated in Rh+ patients

A

Rh0 immune globulin (Rh0Gam)

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44
Q

ADR:

mild side effects

A

Immune Globulin (Gammagard)

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45
Q
ADR:
flu-like symptoms
depression
suicidal ideation
injection site reactions
A

interferon beta

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46
Q

ADR:

flu-like symptoms

A

Interferon Gamma

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47
Q

why can some immunosuppressives go in and activate the immune system?

A

drug allergy and drug hypersensitivity

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48
Q

what are the types of drug allergy/hypersensitivity?

A
anaphylaxis
serum sickness
drug fever
vasculitis
drug induced lupus
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49
Q

what factors affects the incidence of allergic reactions?

A
age and gender
genetic factors
associated illness (AIDS)
previous drug administration
drug-related factors
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50
Q

Anaphylactic (immediate response drug allergy)

A

Type 1

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51
Q

serum sickness or Arthus reaction drug allergy

A

Type 3

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52
Q

cytotoxic reaction

A

Type 2

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53
Q

in this type of reaction, the initial exposure to drugs makes IgE antibodies and IgE gets fixed to tissue mast cells and blood basophils. when re-exposed, mast cells and basophils release histamine, leukotrienes, and other mediators

A

Type 1/ anaphylactic (immediate response reaction)

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54
Q

this type of drug allergy requires IgG and IgM antibodies that activate complement cascade
antibodies to tissue constituents or drug can be demonstrated

A

type 2 or cytotoxic reactions

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55
Q

The antagonists for this type of allergic reactions are prednisone, isoproterenol, epinephrine, and thephylline and even though desensitization can be tried, it may be hazardous

A

Type 1 or anaphylactic reaction

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56
Q

this type of drug allergy is most common and manifestations occur 7-21 days after exposure of drug through fever, urticaria, arthralgia, and lymphadenopathy but go away when drug is stopped. corticosteroids can be used to help

A

type 3 or serum sickness

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57
Q

this type of drug reaction involves IgM and IgG but NOT IgE.

these generate drug-antibody complexest that deposit in the blood vessels after activating complement

A

type 3 or serum sickness

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58
Q

type of drug reaction that mainly targets cells in the circulatory system. the reaction may disappear after stopping the drug for several months and corticosteroids may suppress severe reactions

A

type 2 or cytotoxic

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59
Q

in this type of drug reaction, vascular permeability increases and neutrophils after aggregating and invading the cell wall, induce a hemorrhagic vasculitic lesion

A

serum sickness

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60
Q

this type of drug reaction is mediated by sensitized T lymphocytes and macrophages and cause contact dermatitis. can be helped with corticosteroids

A

Type 4 or cell-mediated (delayed) hypersensitivity reaction

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61
Q

MOA:
irreversible inhibition of COX-1 and COX-2
inhibits prostaglandin synthesis but not lipoxygenase

A

Aspirin

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62
Q

MOA:

reversible inhibition of COX-1 and COX-2

A

diflusinal, indomethacin, sulindac, diclofenac, tolemetin, ketorolac, naproxen, ibuprofen, ketoprofen, fenoprofen, flurbiprofen, oxaprozin, piroxicam, meloxicam, meclofenamate, mefenamic, nabumetone, etodolac, meloxicam and salicylate salts

(basically all drugs but aspirin)

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63
Q

MOA: same as the other drugs but just have MORE COX-2 selectivity than COX-1

A

Etodolac, Nabumetone and Meloxicm

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64
Q

this drug is not a true salicylate

A

diflusinal

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65
Q

This drug is only taken once daily

A

oxaprozin

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66
Q

this drugs is activated by the liver

A

nabumetone

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67
Q

MOA:

only inhibits COX-2

A

celecoxib

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68
Q

MOA:
analgesia by elevating pain threshold by weakly inhibiting COX-1, COX-2 and COX-3
antipyresis by acting on hypothalamic heat-regulating centers

A

acetaminophen

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69
Q
Use:
analgesic
antipyretic
antiinflammatory
antirheumatic (suppresses antigen-antibody reactions and prostaglandin mediated autoantibodies)
A

aspirin and salicylate salts

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70
Q

use:
analgesic
antiinflammatory
weak antipyretic (recommended not to be used as one)

A

diflusinal

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71
Q

use:
rheumatoid arthritis NOT for juvenile RA
osteoarthrits
tocolytic agent (suppress premature labor)

A

indomethacin

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72
Q

use:

rheumatoid arthritis and osteoarthrits

A

sulindac

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73
Q

use:
rheumatoid arthritis
osteoartritis
post-op analgesia

A

etodolac

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74
Q

use:
rheumatoid arthritis
osteoarthritis
analgesia/dysmenorrhea

A

diclofenac, ibuprofen, keoprofen and meclofenamate

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75
Q

use:
rheumatoid arthritis
Juvenile arthritis
osteoartritis

A

tolmetin

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76
Q

use:

moderate to severe acute pain

A

ketorolac (toradol)

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77
Q
use:
rheumatoid arthritis
Juvenile RA
osteoarthritis
analgesia
dymenorrhea
A

naproxen

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78
Q

use:
rheumatoid arthritis
osteoarthritis
analgesia

A

fenoprofen

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79
Q

use:
rheumatoid arthritis
osteoarthritis

A

flurbiprofen, oxaprozin, piroxicam and nabumetone

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80
Q

Use:

osteoarthritis

A

meloxicam

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81
Q

use:
analgesia and dysmenorrea
NOT for RA or osteoarthritis

A

mefenamic acid

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82
Q
use: 
osteoarthritis
RA
dymenorrhea
acute pain
familial adenomatous polyposis
A

celecoxib

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83
Q

use:
antipyretic and analgesic
osteoarthrits (relief of pain)

A

acetaminophen

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84
Q

ADR:
Minor (rash) rare
potential hepatotoxicity and nephrotoxicity

A

acetaminophen

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85
Q

ADR:

minor disturbances for GI, CNS, respiratory rash and sulfonamide allergy

A

celecoxib

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86
Q

ADR:
GI
CNS: headaches

A

nabumetone

ketorolac

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87
Q

ADR:
contraindicated for GI inflammation
pre-existing renal problems
autoimmune and hemolytic anemia

A

mefenamic acid

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88
Q

ADR:
GI
CNS: headaches
rahs/dermatitis

A

meclofenamate

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89
Q

ADR:

GI

A

meloxicam
piroxicam
oxaprozin

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90
Q

ADR:
GI
CNS: dizziness and headache

A

flurbiprofen

diclofenac

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91
Q

ADR:
GI: 30% of patients
CNS: headache

A

ketoprofen

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92
Q
ADR:
GI
pre-existing renal 
hypersensitivity
CNS: headache
A

fenoprofen

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93
Q

ADR:
GI < indomethacin
CNS < indomethacin
hypersensitivit

A

naproxen

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94
Q
ADR:
GI less than aspirin or indomethacin 
ocular disturbances
hypersensitivity (rash/dermatitis)
chronic use inhibits renal prostaglandin production
A

ibuprofen

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95
Q

this drug should be avoided during pregnancy or breast-feeding

A

ibuprofen

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96
Q

ADR:
GI
CNS: headache
causes Anaphylactoid reactions (caution!!)

A

tolmetin

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97
Q

ADR:
GI: less severe than indomethacin

A

etodolac

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98
Q
ADR:
GI: less severe than indomethacin
rash/dermatitis
potential fatality
pancreatitis
A

sulindac

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99
Q
ADR:
GI: severe
prolonged gestation
renal
CNS: headache and aggravate depression
A

indomethacin

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100
Q
ADR:
GI: mild
headache
renal
hypersensitivity
A

diflusinal

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101
Q

ADR:
GI: not too bad
no effect on platelets
hypermagnesemia

A

salicylates

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102
Q
ADR:
GI
hepatic
hypersensitivity
reyes syndrome
salicylism
A

Aspirin

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103
Q

category:

salicylic acid derivatives

A

aspirin
salicylate salts
diflusinal

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104
Q

category:

acetic acid derivatives

A
indomethacin
etodolac
diclofenac
tolmetin
ketorolac
sulindac
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105
Q

category:

propionic acid derivatives

A
ibuprofen
naproxen
ketoprofen
oxaprozin
fenoprofen 
flurbiprofen
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106
Q

category:

enolic acid derivatives

A

piroxicam

meloxicam

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107
Q

category:

anthranilic acid derivatives

A

meclofenamate

mefenamic acid

108
Q

category:

alkanones

A

nabumetone

109
Q

this drug may prolong bleeding time because irreversible acetylation and inactivation of cyclooxygenase in platelets and megakaryocytes. the platelets cyclooxyenase is not resynthesized

A

aspirin

110
Q

this drug is highly protein bound, ready crosses placental and BBB and is distributed in all tissues of the body

A

aspirin

111
Q

this drug causes gastric mucosal damage, reactive latent gastric and duodenal ulcers and should be used in caution with patients that have active GI lesions

A

aspirin

112
Q

this drug should not be taken with alcohol because in increases GI bleeding

A

aspirin

113
Q

this drug has antiulcer effects and is a prostaglandin analogue

A

Misoprostol

114
Q

hepatotoxicity occurs after 1-4 weeks when blood levels reach 200-250 micrgrams/mL
hepatic function MUST be monitored in these patients

A

aspirin/salicylates

115
Q

rarely any renal problems but in overdose situations, may cause acute tubular necrosis and a reduced renal clearance
still should be very carefully monitored in patients that have renal problems

A

aspirin/salicylates

116
Q

in patients with congestive heart failure, this drug should be avoided

A

highly buffered aspirin with high sodium content

117
Q

this drug should be discontinued 5-7 days before surgery and is contraindicated in patients with bleeding problems

A

aspirin.salicylates

118
Q

what is the aspirin triad?

A

asthma and nasal polyps because off aspirin sensitivity

119
Q

true or false

salicylates should not be used in children/teenagers with varicella or influenza

A

true because it increases the chance of getting Reye’s syndrome

120
Q

can salicylates be used in pregnancy?

A

has shown to have teratogenic and embryocidal effects in animals and may lead to maternal and fetal hemorrhagic complications

121
Q

what is salicylism?

A

chronic salicylate intoxication from prolonged therapy with high doses

122
Q

what is acute salicylate

A

overdosage from a single toxic dose of salicylate

123
Q

what symptoms does salicylism present with?

A

tinnitus and hearing loss in adults
hyperventilation and CNS effects in children
metabolic acidosis and respiratory alkalosis

124
Q

what is a salicylate jag?

A

when there is an increase in CNS stimulation becaue of salicylate intoxication and then is later replaced by CNS depression

125
Q

how do you know if there is a salicylate overdose?

A

acid base disorders
dehydration
hyperpyrexia
hyperglycemia/hypoglycemia

126
Q

drug interactions to salicylates

A

protein-bound drugs since salicylates are highly protein bound
anticoagulants
thrombolytic agents
uricosuric agents
antidiabetic agents (enhanced effect)
corticosteroids (increase renal clearance of salicylates)
alcohol (GI bleeding and ulcers/erosions)
NSAIDs (GI effects are increased)

127
Q

these drugs inhibit lipoxygenase pathway and inhibit lysosomal enzyme release and inhibit neutrophil activation
reduces prostaglandins and thomboxane B2

A

NSAIDs

128
Q

which NSAIDs do not treat RA?

A

ketorolac, meloxicam, ad mefenamic acid

129
Q

which NSAIDs do not treat osteoarthritis?

A

ketorolac and mefenamic acid

130
Q

which NSAIDs treat juvenile RA?

A

tolmetin and naproxen

131
Q

which NSAIDs should not be used in children under 14?

A

indmethacin
mefenamic acid
meclofenamate

132
Q

what are the major GI problems with the use of chronic NSAIDs?

A

ilcers (gastric, duodenal, intestinal, and gingival)

133
Q

which NSAID causes autoimmune hemolytic anemia?

A

tolmetin

134
Q

how are NSAIDs excreted?

A

renally and that’s why renal should be monitored

135
Q

renal problems associated with NSAIDs

A

interstitial nephritis (inhibition of prostaglandin)
hyperkalemia
hypernatremia
papillary necrosis

136
Q

contraindications for celecoxib

A

patients that are allergic to celecoxib
patients that are allergic to sulfonamides
patients that have asthma, urticaria, or allergic reactions to aspirin or NSAIDs

137
Q

this drug is toxic to both the liver and the kidney

A

acetaminophen

138
Q

how to relieve acetaminophen toxicity

A

gastric lavage and mucomyst (protects liver by restoring glutathione levels)

139
Q

how do you inhibit the release reaction (degranulation)

A

cromolyn sodium
agents that increase cyclic AMP and stabilize mast cells (not primary effect)
corticosteroids

140
Q

this drug inhitbits the lipoxygenase enzyme and decreases the formation of leukotrienes

A

zileuton

141
Q

these drugs block leukotriene receptors

A

zafirlukast and monteleukast

142
Q

hwo do you block receptors for autocoid or broncoconstrictors?

A

H1 antihistamines
anticholinergic (ipratropium and tiotropium)
autocoid antagonist like the antagonists for leukotrienes

143
Q

how do you dilate the bronchioles?

A

physiologic antagonists like beta adrenergic agonists (epinephrine, isoproterenol, terbutaline, salmeterol)
methylxantines (theophylline and aminophylline)

144
Q

how do you prevent inflammation and cell-mediated immunologic reactions?

A

corticosteroids and immunosuppressives

145
Q

how do you neutralize IgE?

A

olizumab…monoclonal antibody

given parenterally and allergic reactions are common

146
Q

overview approaches to treat hypersensitivity, anaphylaxis, and asthma

A

inhibit release reaction
inhibit formation of generated autocoids
block receptors for autocoids or bronchoconstrictors
bronchodilate through physiologic antagonists
prevent inflammation and cell-mediated immunologic reactions
neutralize IgE

147
Q

what are autocoids?

A

ex: kinins, leukotrienes, superoxides, platelet activating factor

148
Q

this drug is mainly used for the prophylactic treatment of bronchial asthma
not effective in acute attacks

A

cromolyn sodium

149
Q

how does cromolyn sodium work?

A

inhibit release of histamine and other autocoids from sensitized mast cells

150
Q

what are cromolyn and similar drugs most useful for and how are they used?

A

treat extrinsic asthma that’s caused by specific allergens

used in conjunction with other therapy like bronchodilators

151
Q

what can cromolyn sodium be used for?

A

allergic rhinits
allergic conjuntivitis
GI allergies

152
Q

what are H1 antagonists used for?

A
allergic rhinitis
allergic dermatitis (urticaria)
153
Q

these drugs are not effective in treating bronchospastic conditions like asthma and anaphylaxis

A

H1 antihistamines

154
Q

these drugs inhibit bronchospasms induced by acetylcholine and nothing else so limited effectiveness
dries secretions so not well liked

A

anticholinergic agents

ipratropium, atrovent, tiotropium, spiriva

155
Q

____ is a quaternay ammonium so not well absorbed (limited effect)

A

ipratropium

156
Q

these drugs act bronchodilators and inhibit release of autocoids from mast cells
fairly effective in treating acute asthma attacks

A

Beta adrenergic agonists

157
Q

______ and otehr adrenergic bronchodilators are drugs of choice in treating life-threatening anaphylactic reactions

A

epinephrine

158
Q

true or false

tolerance can occur and rebound bronchoconstriction is possible with beta agonists

A

true

159
Q

these drugs cause bronchodilation and inhibit release of mediators from mast cells

A

methylxanthines (theophylline and aminophylline)

160
Q

MOA:

inhibits phosphodiesterase –> increased cAMP

A

methylxanthines

161
Q

type of methylxanthine that is taken orally with other agents for severe asthma

A

theophylline

162
Q

type of methyxanthine that is given IV that is given for severe asthma

A

aminophylline

163
Q

what do we have to watch out for with methyxanthines?

A

they have a narrow therapeutic window and so monitor blood levels carefully

164
Q

ADRs:
N/V
headache, insomnia, nervousness
in severe toxicity cardiac arrythmias and seizures

A

methyxanthines

165
Q

these drugs have anti-inflammatory activity and they inhibit recruitment of leukotrienes and other autocoids like prstaglandins

A

corticosteroids

166
Q

very effective as prophylactic agents but not as effective in acute attacks because they reduce the severity of cell mediated immunological damage

A

corticosteroids

167
Q
ADRS:
cataracts (from inhaled)
cushings syndrome
immune system suppression
osteoporosis
peptic ulceration
suppression of growth in children (systemic)
menstrual and reproductive problems
A

corticosteroids

168
Q

these agents interfere with production/actions of leukotrienes and help treat asthma

A

leukotriene modulators

169
Q

cysteinyl leukotriene receptor antagonist
not for acute attacks
less effective than corticosteroids

A

zafirelukast and montelukast

170
Q

5-lipoxygenase inhibitor
reduces frequency of attacks
elevates liver enzymes and hepatotoxicity

A

zileuton

171
Q

drug of choice for treatment of mild allergies

A

H1 antihistamines but mast cell stabilizers or corticosteroids may be used in severe allergies

172
Q

_____ are commonly used to treat COPD

A

anticholinergics:
tiotropium (spiriva)
aclidinum (tudorza)

173
Q

category:

adrenergic bronchodilators

A
epinephrine
isoproterenol
metaproterenol 
albuterol
levalbuterol
salmeterol
terbutaline
pirabuterol
174
Q

category:

methylxanthine bronchodilators

A

theophylline and aminophylline

175
Q

category:

corticosteroids

A
beclomethasone
flunisolide
triamcinolone
fluticasone
budesonide
prednisone
mometasone
ciclesonide
methylprednisolone
176
Q

category:

mast cell stabilizers

A

cromolyn sodium

177
Q

category:

leukotriene modulators

A

monteleukast
zafirleukast
zileuton

178
Q

category:

antimuscarinic

A

ipratropium
tiotropium
aclidinum (COPD)

179
Q

catergory:

combination products for asthma

A

advair diskus
combivent
symbicort
duera

180
Q

category:

anti IgE

A

omaizumab

181
Q

category:

H1 histamine antagonist

A

diphenhydramine
fexofenadine
cetirizine
loratadine

182
Q

short-acting glucocorticoids

A

hydrocortisone

183
Q

long-acting glucocorticoid

A

dexamethasone

184
Q

intermediate acting glucocorticoid

A

prednisone and triamcinolone

185
Q

short acting mineralocorticoid

A

fludricortisone and spironolactone

186
Q

this corticoid stimulate the adrenal cortex and secretion of glucocorticoids, andronergic substance and aldosterone

A

cosyntropin

187
Q

3 zones in the adrenal cortex

A

zona glomerulosa
zona fasiculata
zona reticularis

188
Q

what hormone is secreted from zona glomerulosa?

A

mineralocorticoids (aldosterone)

189
Q

what hormone is secreted from zona fasiculata?

A

glucocorticoids (cortisol)

190
Q

what hormone is secreted from zona reticularis?

A

androgens, progesterones, and estrogens

191
Q

what components are involved in the biosynthesis of cortisol and other hormones?

A

ACTH and MC2R and several cytochrome P450 enzyme

cholesterol

192
Q

what are the 2 types of negative feedback systems to control ACTH secretion of glucocorticoids

A

fast feedback system

delayed feedback system (suppresses basal CRH and ACTH)

193
Q

how do mineralocoticoids regulate secretion?

A

aldoseterone works with the renin system
no significant feedback on ACTH
serum concentrations peak in the morning

194
Q

how doe glucocorticoids and mineralocorticoids affect carbohydrate, protein, and fat metabolism?

____ glucose production and insulin release
_____ hepatic gluconeogenesis
______ peripheral glucose utilization (insulin resistance in muscle cells)
_____proteolysis and amino acids
______fatty acid mobilization, lipolysis, and ____ release of fatty acids and glycerol

all this is done to maintain an adequate supply of glucose to _____

A
increase
stimulates
decrease
increase
enhance 
increases 

brain

195
Q

how do mineralocorticoids keep water and electrolyte balance?

A

through control of renal excretion ions

they promote reabsorption of small amounts of sodium but excrete potassium and hydrogen ions

196
Q

glucocorticoids regulate blood cells and cardiovasuclar by:

_____ vasoconstriction on small vessels
______ capillary permeability by _____histamine release by basophils and mast cells
____ plasma hemoglobin concentration, ____ erythrocytes and neutrophils in blood and ______wthite blood cell count
_____number of eosinophils, basophils, monocytes, and lymphocytes

A
potentiate
decrease
reducing
increase
increase
decrease
197
Q

mineralocorticoids regulate blood cells and cardiovascular by:

A

retaining sodium and maintaining normal blood volume

198
Q

glucocorticoids maintains the immune system by:

A

inhibiting prostaglading and leukotrienes by inducing production of lipocortins that inhibit phospholipase A2
reduce inflammation
suppress cytokines and chemokines

199
Q

role of corticoids in CNS

A

influence mood, sleep patterns and EEG

200
Q

mood changes (irrtability and depression) are associated with what?

A

adrenal insufficiency

201
Q

corticoids are needed for skeletal muscle…but what happens when there is a large amount present?

A

stimulate proteolysis in myocytes causing pain and muscle weakness

202
Q

secretion of which corticoid is increased with stress?

A

cortisol

has protective effect

203
Q

what are the non-endocrine uses for glucocorticoids?

A

inflammatory
allergic
immunological disorders

204
Q

what kind of doses do you need to use for chronic diseases such as chronic asthma

A

need suppressive doses and a therapuetic regimen after careful consideration

205
Q

what allergic disorders are corticoids used for?

A
seasonal allergies (systemic)
mild-moderate asthma (inhaled steroids)
206
Q

what type of cerebral edema are treated with glucocorticoids?

A

vasogenic type edema (brain tumors)

brain abcesses…closed head injury so less responsive

207
Q

corticoid treatments for allergic disorders

A

prednisone
methylprednisolone
triamcinolone
dexamethasone

208
Q

corticoid treatments for cerebral edema

A

prednisone

209
Q

how is bacterial meningitis treated with corticoids

A

anti-inflammatory effects of glucocorticoids reduces brain edema, TNF-alpha, IL-1, and prostaglandins E2. help treat acute, non-tb bacterial meningitis

210
Q

how do glucocorticoids help collagen disorders?

A

beneficial for acute exacerbations
used for systemic lupus erythematosus
polymyositis and dermatomysostitis use glucocorticoids as drugs of choice
polyarteritis nodosa (combination therapy)
polymyalgia rheumatica (high dose steroid therapy)

211
Q

corticoid treatments for collagen disorders

A

prednisone, methylprednisolone, triamcinolone, and dexamethasone

212
Q

hematological disorders treated with glucocorticoids

A

autoimmune hemolytic anemia
initial therapy for idiopathic thrombocytopenic purpura
inhibit phagocytosis and icrease platelet lifespan

213
Q

corticoid treatments for hematalogic disorders

A

prednisone
triamcinolone
dexamethasone

214
Q

glucocorticoids in hepatic diseases

A

initial therapy for subacute hepatic necrosis and autoimmune chronic hepatits

215
Q

corticoid treatments for hepatic disease

A

prednisone and azathiorpine

216
Q

corticoid in renal diseases

A

idiopathic nephrotic syndrome in pts <16

217
Q

corticoid treatments for renal disorder

A

methyprednisolone

218
Q

corticoids in respiratory disorders

A

treat pulmonary sarcoidosis (prednisone)

respiratory stress syndrome especially in premature neonates (betamethasone and dexamethasone)

219
Q

These drugs have variable mineralocorticoid activity so they can cause sodium and potassium retention

A

hydrocortisone, cortisone, prednisone, and prednisolone

220
Q

different routes of administration for corticosteroids

A
nonsystemic (intraarticular)
local (can have side effects)
depot preps (intralesion, intra/extra articular)
intrasynovial injection
rectal (inflammatory bowel)
parenteral (septic shock)
oral (chronic use)
221
Q

how do you pick a glucocorticoid?

A
look for
severity
anticipated dose and duration of therapy
factors predisposing to complications
alternative drug therapy
222
Q

what do the ADRs for corticosteroids correlate with?

A
dose
frequency
duration
route
age and condition of patient
underlying disease
223
Q

GI ADRs for corticosteroids

A
increase gastric acid and pepsinogen production
gastric ullcers (steroid should be slowly removed and start on antiulcer therapy
gastric bleeding (look in stools)
224
Q

Edema ADRs for corticosteroids:

A
fluid retention (bad for heart/kidney disease patients)
to treat: restrict dietary sodium
225
Q

carb and lipid metabolism ADRs for corticosteroids:

A
hyperglycemia
enhanced gluconeogenesis
aggravate diabetes 
triglycerides are elevated
elevated lipoproteins so increased risk of atherosclerosis vascular disease
226
Q

electrolyte ADRs for corticosteroids:

A

hypokalemia and metabolic acidosis leading to paralysis, arrhythmias and cardiac arrest
avoid by restricting sodium and eat potassium rich foods (spinach, raisins, OJ) and steroid with low mineralocorticoid therapy

hypophosphatemia (rare) severe muscle weakness. consume dairy to treat

227
Q

bone ADRs for corticosteroids:

A

osteonecrosis from fat embolism and swelling of fat cells and increase in intraosseous pressure
joint pain and stiffness
from prolonged corticosteroid treatmetn

228
Q

nitrogen ADRs for corticosteroids:

A

negative nitrogen balance from excessive protein breakdown.

eat high protein diet to treat

229
Q

CNS ADRs for corticosteroids:

A

personality and behavioral changes. euphoria
insomnia, increased appetite, nervousness, irritability, psychotic and manic episodes and paranoid state
symptoms disappear after a while

230
Q

growth ADRs for corticosteroids:

A

suppression of growth so should be restricted in children or alternate day therapy

231
Q

muscle ADRs for corticosteroids:

A

causes myopathy because of protein catabolism

associated with triamcinolone and is reversible

232
Q

skin and soft tissue ADRs for corticosteroids:

A

skin thinning and purpura
non-melanoma skin cancer (oral glucocorticoids)
acne, alopecia, hypertrichosis, striae
cushingoid syndrome: truncal obesity, buffalo hump, moon face, weight gain

233
Q

ocular ADRs for corticosteroids:

A

elevates intraocular pressure. exaggerated in diabetics and myopes
enhance development of secondary ocular infections by fungi or viruses
ocular herpes pts at risk for corneal perforation

234
Q

infection ADRs for corticosteroids:

A

decreases resistance to infections because inflammation mechanisms are depressed

235
Q

HPA ADRs for corticosteroids:

A

suppresses HPA (hypothalamic-petuitary-adrenal axis) through negative feedback

236
Q

pregnancy ADRs for corticosteroids:

A
placenta can metabolize glucocorticoids 
fetal adrenal hypoplasia
hypoadrenalism
cleft palate in offspring
category C
237
Q

withdrawal from glucocorticoid therapy leads to

A

malaise, fever, myalgia, arthralgia, fatigue, and restlessness

238
Q

why is dose reduction therapy needed to taken off of glucocorticoid

A

because coticoid causes HPA suppression so you will need to get that started up as well

239
Q

____promotes reabsorption of sodium

A

aldosterone

240
Q

what is the reabsorption of sodium coupled to?

A

excretion of potassium and hydrogen ions

241
Q

what happens when there is excess in aldosterone?

A

leads to hypokalemia, metabolic alkalosis, increase in plasma volume and hypertension

242
Q

this drug (potent steroid) has both glucocorticoid and mineralocorticoid

A

fludricortisone

243
Q

what does fludricortisone used for?

A

treat adrenocortical insufficiency associated with mineralocorticoid deficiency

244
Q

hypercortisolism or hyperadrenocortism

A

cushings syndrome

245
Q

what is cushings disease?

A

a tumor in the pituitary gland and it releases large amounts of ACTH and so there is an excessive release of cortisol

the pituitary gland does not respond to negative feedback and just continues to produce ACTH

246
Q

ACTH independent cortisol hyper secretion

A

patients present with benign adrenal adenomas and adrenocortical carcinomas

247
Q

Conn’s syndrome

A

hyperaldosteronism

248
Q

what happens when there is increased aldosterone?

A

there is decreased plasma renin activity, hypokalemia, metabolic alkalosis, and hypertension

249
Q
functions:
mediator for tissue/cell injury
mediator of inflammatory response in allergic reactions
regulator of cell growth and repair
regulator of gastric acid secretion
neurotransmitter in the CNS
regulator of cardiac function (possibly)
A

histamine

250
Q

what are the mechanisms that histamine is released by?

A

drug chemical induced
response to cell tissue/damage
immunologic stimulation (mas cells with IgE antibodies)
neuronal and endocrine stimulation (neuronal stimulation through Ach at muscarinic receptors and when histamine is released, it binds to H2 receptors (endocrine) and stimulates secretion of HCl

251
Q

what is the “triple response” of histamine?

A

when histamine is injected into the skin, you get:
red spot (local) – from dilation of minute blood vessels
flare – dilation of neighboring arterioles
wheal – increased capillary permeability

252
Q

what is histamine shock?

A

when histamine is given in a large doses or released during anaphylaxis and you have a huge drop in BP because of the vasodilation and leakage of fluid in the Extravascular space – resembles other shocks

253
Q

the effect of histamine on acid secretion is initiated by what receptor?

A

H2

254
Q

in blood vessels, what does histamine do?

A

causes intense dilation

can cause pulsatory headaches

255
Q

what are the effects of histamine on the heart?

A

increases force of contraction

slows AV conduction

256
Q

what are the different types of histamine receptors and where are they located?

A

H1: skin, blood vessels, heart, airway, CNS
H2: GI tract, heart, brain, blood vessels
H3: CNS
H4: hematopoetic cells

257
Q

what do H1 receptors do?

A

mediate rapid vasodilation, increased capillary permeability, bronchoconstriction, irritation of peripheral nerve endings

258
Q

what do H2 receptors do?

A

mediate gastric acid secretion

MAY have some effect in hypersensitivity reactions

259
Q

what do H3 receptors do?

A

presynaptic autoreceptors to regulate release of histamine

260
Q

what do H4 receptors do?

A

may be involved in inflammation

261
Q

what kind antihistamines do we use for H1 receptors?

A

“antihistamines”

262
Q

what do we use to block H2 receptors?

A

H2 antagonist like cimetidine and it reduces gastric acid secretion.
widely used to treat peptic ulcer disease

263
Q

what are the first generation of antihistamines that are very sedating?

A

doxylamine
promethazine
hydroxyzine

264
Q

what are the first generation of antihistmines that are sedating?

A

diphenhydramine
dimenhydrinate
chlorpheniramine
meclizine

265
Q

second generation, non sedating H1 antagonists

A

loratadine/desloratadine
cetirizine/levocetirizine
fexofenadine