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Vicky's Cards - Exam 1 > Third > Flashcards

Third Flashcards

1
Q

Inflammatory compounds are all derived from_____________ which is broken down by _____________

A

membrane phospholipids

phospholipase

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2
Q

Phospholipase breaks down phospholipids to produce _____________

A

arachidonic acid

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3
Q

Arachidonic acid can enter two cycles…what are they?

A

lipoxygenase

cyclo-oxygenase

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4
Q

Leukotrienes are derived from what pathway?

A

lipoxygenase

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5
Q

Prostaglandins are derived from what pathway?

A

cyclo-oxygenase

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6
Q

Thomboxane are derived from what pathway?

A

cyclo-oxygenase

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7
Q

Prostacyclin are derived from what pathway?

A

cyclo-oxygenase

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8
Q

Prostacyclins counteract the action of _____________

A

thromboxanes

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9
Q

LTB4 is involved in ___________

A

chemotaxis

hyperalgesia

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10
Q

LCT4, LTD4, LTE4 are involved in _______________

A

bronchoconstriction
edema
*produced in asthma

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11
Q

Zafirlukast, montelukast block activity of which leukotrienes?

A

LCT4, LTD4, LTE 4

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12
Q

Acetaminophen is _______________ an NSAID

A

NOT

*tylenole ?

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13
Q

Is aspirin an NSAID?

A

yep

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14
Q

Is acetaminophen an NSAID?

A

nope

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15
Q

MOA of NSAIDs

A

blocks cyclo-oxygenase pathway

*cox 1 and cox 2

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16
Q

What are the selective COX2 inhibitors?

A

celecoxib

rofecoxib

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17
Q

Why would you prefer selective cox2 inhibitors over common nsaids?

A

COX1 remains intact, allowing for the production of gastric cytoprotection

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18
Q

COX1 pathway is known as the ___________ pathway

A 
constitutive 
physiologically active (always on) -gastric protection
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19
Q

COX2 pathway is known as the ____________pathway

A

inducible

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20
Q

Why would the COX2 pathway be turned on?

A

it kickstarts the inflammatory process, including pain

makes you mores sensitive to pain

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21
Q

What turns of COX2 pathway?

A

glucocorticoids
NSAIDs
growth factors, gut peptides
COX 2 inhibitors

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22
Q

_____________is located predominantly located in the vascular endothelium

A

prostacyclin

PGI2

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23
Q

TxA2 is found ________________

A

in the platelets

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24
Q

What are the main effects of PGI2?

A

vasodilation

inhibition of platelet aggregation

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25
Q

What are the main effects of TxA2?

A

platelet aggregation

vasoconstriction

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26
Q

PGE2 causes________________

A

inhibitirion of gastric acid secretion
contraction of uterus
contraction of GI smooth muscles

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27
Q

PGF2-a main effects are ________________

A

contraction of bronchi

contraction of myometrium in uterus

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28
Q

The cyclooxygenase (COX) is found ____________________________

A

bound to the endoplasmatic reticulum

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29
Q

__________ acts in physiological conditions

A

COX1

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30
Q

___________ is induced by inflammatory cells by pathological stimulus

A

COX2

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31
Q

____________ is located only in the brain

A

COX3

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32
Q

Which COX provides gastric protection?

A

COX1

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33
Q

What are the nonselective NSAIDs?

A 
salicylates
pehnylacetates
ndolacetates
enolates
fenamates
propionates 
butylpyrazo----- ugh
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34
Q

Phenylacetates:______________

A

diclofenac

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35
Q

indolacetates:__________________

A

indomethacin, sulindac

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36
Q

Enolates:____________________

A

piroxicam….. I dont think we need to know these.

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37
Q

___________connected with influence of thermoregulatoy centre in the hypothalamus

A

antipyresis

*benefit of NSAID

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38
Q

_________________mainly anti-exudative effect

A

anti-inflammatory

*benefit of NSAID

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39
Q

_______________ in very low daily doses

A

anti-thrombotic action

*benefit of NSAID

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40
Q

__________ of ductus arteriosus

A

Closure

*benefit of NSAID-specifically INDOMETHACIN

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41
Q

Which NSAID can be used to close the ductus arteriosus?

A

indomethacin

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42
Q

Toxicities of NSAIDs

A 
gastric mucosal damage 
bleeding
limitation of renal blood flow
delay/prolongation of labor 
asthma and anaphylactoid reactions
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43
Q

__________ arises from the inhibition of platelet function (TxA2 synthesis)

A

bleeding

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44
Q

Limitation of renal blood flow results in what?

A

Na and water retention

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45
Q

Asthma and anaphylactoid reactions associated with NSAIDS are connected with __________ inhibition

A

PGF2-a

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46
Q

How NSAIDs cause mucosal injury

A

ion trapping - direct toxicity from NSAID use

47
Q

Aspirin when metabolized is split into what 2 compounds?

A

acetic acid

salicylate

48
Q

What can salicylate conjugate with?

A

glucuronic acid

glycine

49
Q

When salicylates are oxidized they become __________

A

gentisic acid

50
Q

Aspirin resets the ___________________

A

hypothalmic? thermastat

51
Q

dont need to know slide 25-31

52
Q

___________ increases GI toxicity of NSAIDs

53
Q

Aspirin in high dose reduces renal tubular excretion of _____________

A

urate

*is harmful to the tubules-causes damage

54
Q

What are the uses of Aspirin?

A

analgesic
antipyretic
acute rheumatic fever
rheumatoid arthritis

55
Q

____________ is the DOC for acute rheumatic fever

56
Q

What two drugs are safer than aspirin in the treatment of a fever?

A

paracetamol
metamizole
*these are preferred over aspirin

57
Q

When treating RA with aspirin, when should the medication be given?

A

after meal

58
Q

Aspirin in children with a viral infection can result in what?

A

Reyes syndrome

59
Q

What is reyes syndrome

A

Aspirin in children w/viral infection

hepatic encephalopathy seen in children

60
Q

Aspirin should not be given to children under the age of ________

61
Q

What is a possible AE of being on chronic aspirin?

A

blood thinning

*higher risk of hemorrhagic stroke

62
Q

NSAIDs + cyclosporines

A

increase nephrotoxicity

63
Q

NSAIDs+ ACEi or BB

A

decrease antihypertensive effect

64
Q

NSAIDs + sulfonylureas

A

increased risk of hypoglycemia

65
Q

NSAIDs+ GCS

A

increase risk of GI bleeding

66
Q

NSAIDs+alcohol

A

increase of GI bleeding

67
Q

Ibuprofen (advil) is a derivative of ______________

A

phenylpropionic acid

68
Q

What is the effect of oral ibuprofen in lower doses?

A

analgesic but not inflammatory effect

69
Q

A liquid form of __________ provides prompt relief in post surgical dental pain

70
Q

Aspirin is ______ potent than ibuprofen

71
Q

In addition to indomethacin, what other NSAID is effective in closing the ductus arteriosus?

72
Q

In comparison to indomethacin, ibuprofen ________ urine output less and causes ________ fluid retention

A

decreases urine output

less fluid retention

73
Q

________________ is a propionic acid derivative

A

ketoprofen

74
Q

____________ inhibits both COX (non-selectively) and lipoxygenase

A

ketoprofen

75
Q

Ketoprofen has a dual effect on ________ and __________

A

prostaglandins
leukotrienes
* is no better than any other NSAID

76
Q

_______________ is a non selective cox inhibitor and may also inhibit phospholipase A and C, reduce neutrophil migration and decreases production of T and B cells

A

indomethacin

77
Q

Give _________ to prolong the life of indomethacin

A

probenecid

*inhibits both renal and biliary clearance

78
Q

Indications of indomethacin

A

juvenile RA, gout, ankylosing spondylitis, postepisiotomy pain

79
Q

There is an ophthalmic preparation of ___________

A

indomethacin

80
Q

_________ comes in an oral formulation

A

indomethacin

81
Q

Diclofenac is a ____________ derivative

A

phenylacetic

82
Q

____________ in a rectal suppository form can be considered and DOC for analgesia and postoperative nausea

A

diclofenac

83
Q

A combination of diclofenac and ___________ decreases upper GI ulceration

A

misoprostol (PGE1)

84
Q

___________ is a non-selective COX inhibitor that at high concentrations inhibits polymorphonuclear leukocyte migration, decreases oxygen radical production and inhibits lymphocyte function

85
Q

Piroxicam has a ______ half life

A

long

*can give only once a day

86
Q

In doses >20 mg/d of piroxicam you have a higher incidence of ______________

A

peptic ulcer and bleeding

*this drug has a higher risk than other NSAIDs

87
Q

Selective COX 2 inhibitors

88
Q

Preferential COX 2 inhibitors

A

meloxicam

nabumetone

89
Q

What is meloxicam?

A

preferential cox 2 inhibitor

90
Q

What is nabumetone?

A

preferential cox 2 inhibitor

91
Q

What is celeboxib?

A

selective cox 2 inhibitor

92
Q

___________are selective cox 2 inhibitors

93
Q

What is the only benefit of coxibs?

A

ulcerogenic potential is lower

94
Q

Celecoxib is a _____________

A

sulfonamide

95
Q

Celecoxib may cause _____________

96
Q

Celecoxib __________ effect platelet aggregation

A

does not (within normal doses)

97
Q

_____________ is an enolcarboxamide

98
Q

Meloxicam is ___________ selective

A

preferentially

99
Q

_____________ is associated with fewer GI symptoms and complications than piroxicam, diclofenac and naproxen

100
Q

________ can cause infertility.

101
Q

_________ have prothrombotic cardiovascular risk

102
Q

Acetaminophen is different than NSAIDs d/t its lack of ________________

A

anti-inflammatory effects

103
Q

Acetaminophen _______ effect uric acid levels

104
Q

Acetaminophen is preferential to aspirin in patients with ______________ or a history of ________ and_________

A

hemophilia
peptic ulcers
bronchospasm

105
Q

You have a kid with a viral infection, what do you give him? Aspirin or acetaminophen?

A

acetaminophen

*no risk of Reye’s syndrome

106
Q

NABQI is detoxicated by _________________

A

conjugation with glutathione

107
Q

_____________is a highly reactive arylating metabolite of acetaminophen

108
Q

Why is NABQI bad?

A

it binds covalently to proteins in the liver and causes necrosis

109
Q

What can you give in an acute gout situation?

A

colchicine
diclofenac, indomethacin
naproxen , piroxiam

110
Q

What are the uricostatics?

A

xanthine oxidase inhibitors

-allopurinol, febuxxostat

111
Q

What are the uricosurics?

A

probenecid, benzbromarone

sulfinpyrazone

112
Q

What are the uricolytics?

A

uricase, rasburicase

113
Q

Allopurinol + benzbromarone

114
Q

_________increase the release of uric acid, preventing buildup, preventing gout

A

uricosurics

Vicky's Cards - Exam 1 (4 decks)

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