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Pathopharm Final > NSAIDS, Serotonin, Kinins & Histamines > Flashcards

NSAIDS, Serotonin, Kinins & Histamines Flashcards

1
Q

Anti-inflammatory dose of Ibuprofen

A

600mg

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2
Q

IV dose form of Ibuprofen

A

Caldolor

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3
Q

will increase serum digoxin levels

A

ibuprofen

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3
Q

High protein binding but only occupies a fraction of total drug-binding sites, so less drug interactions (warfarin, oral hypoglycemics)

A

ibuprofen

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4
Q

T/F
Ibuprofen can increase BP and decrease effectiveness at chronic high doses

A

T

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4
Q

T/F
best to use high doses of ibuprofen for dysmenorrhea

A

False
use low doses for dysmenorrhea

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5
Q

Available OTC as Aleve

A

Naproxen (naprosyn)
(250 - 500 mg BID).

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6
Q

half life of Naproxen

A

14 hrs

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7
Q

T/F
peak plasma conc are slower with naproxen sodium (anaprox.)

A

False
they are more rapid

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8
Q

absorption characteristics of Fenoprofen

A

Fenoprofen (Nalfon) is readily absorbed but incompletely, and its absorption is delayed by food

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9
Q

dose should ne individualized with this drug

A

ketoprofen

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10
Q

Extended release tablet releases drug in higher pH of small intestine

A

ketoprofen

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11
Q

dosages of ketoprofen for RA or osteoarthritis

A

75 mg TID or 50 mg QID or ER form 200 mg once daily

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12
Q

dosages of ketoprofen for analgesia or dysmenorrhea

A

25-50 mg Q6-8 hr.

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13
Q

T/F
Ketoprofen does not inhibit leukotriene synthesis

A

False
it appears to inhibit leukotriene synthesis

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14
Q

Almost equally inhibits COX-1 and COX-2

A

Flurbiprofen

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15
Q

Very long t1/2 (40-60 hr) so can be given once a day (600 - 1200 mg once daily)

A

Oxaprozin (Daypro)

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16
Q

Very long t1/2 (57 hr) so can be given once daily (20 mg)

A

Piroxicam (Feldene)

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17
Q

t1/2 ~ 20 hrs. Main use is osteoarthritis

A

Meloxicam (Mobic)

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18
Q

May cause hemolytic anemia

A

Meclofenamate

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19
Q

Not recommended for initial treatment of RA or osteoarthritis

A

Meclofenamate

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20
Q

Indicated only for analgesia, especially for primary dysmenorrhea bec too toxic for chronic use

A

Mefenamic Acid (Ponstel)

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21
Q

Has central and peripheral actions.

A

Mefenamic Acid (Ponstel)

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22
Q

A prodrug converted to an active metabolite with t1/2 ~ 24 hr, so can be given once a day (1000 mg)

A

Nabumetone

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23
Q

somewhat selective inhibitor of COX-2 (much lower incidence of GI side effects)

A

Nabumetone

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24
Q

Difluorophenyl derivative of salicylic acid but is not metabolized to salicylic acid

A

Diflunisal

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25
Q

Newer agents selectively inhibit the ________ , which is found mainly in tissues other than the GI tract

A

COX II enzyme

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26
Q

benefit of cox-II inhibitors

A

GI ulceration and symptoms can be avoided (at least in theory), while still having potent anti-inflammatory and analgesic effects

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27
Q

name the 3 COX-11 inhibitors

A

Celecoxib (Celebrex)
Rofecoxib (Vioxx) (voluntarily recalled from US market)
Valdecoxib (Bextra)

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28
Q

Well tolerated and w/lower stomach S/E than other anti-inlfamm. drugs

A

COX-11 inhibitors

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29
Q

name the 4 “other analgesics” that are not classified as NSAIDs

A

Clonidine
Local anesthetics (e.g. Lidocaine)
Gabapentin
Corticosteroids (e.g. Decadron)

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30
Q

Where is serotonin (5-HT) primarily found in the body

A
  • throughout the body
  • 90%: GIT in enterochromaffin cells
  • remainder mainly CNS neurons

functions:

  • vomiting center
  • migraines
  • sleep, cognition, mood
  • sensory perception
  • GIT stimulation & inhibition
  • platelet aggregation
  • vasoconstriction
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31
Q

serotonin functions in the body?

A
  • vomiting center
  • migraines
  • sleep, cognition, mood
  • sensory perception
  • GIT stimulation & inhibition
  • platelet aggregation
  • vasoconstriction
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32
Q

Serotonin Synthesis

A
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33
Q

Serotonin receptors

A

14 subtypes currently identified
5-HT1 – 5-HT7 and subtypes

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34
Q

T/F
all serotonin receptors belong to G-protein family

A

False
All except 5-HT3 belong to G-protein family
5-HT3 receptors are non-selective Na+ - K+ ionophores

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35
Q

Serotonin subtype response:
Increase K+ conductance

A

5-HT1A,B

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36
Q

Serotonin subtype response:
Hyperpolarization
Decrease K+ conductance

A

5-HT2A

37
Q

Serotonin subtype response:
Slow depolarization
Gating of Na+, K+

A

5-HT3

38
Q

Decrease K+ conductance
Slow depolarization

A

5-HT4

39
Q

Name action, RX example & clinical disorder for the following serotonin receptor:
5-HT1A

A

Action: partial agonist
RX example: Buspirone (buspar)
Clinical d/o: anxiety, depression

39
Q

Name action, RX example & clinical disorder for the following serotonin receptor:
5-HT1D

A

Action: agonist
RX example: Sumatriptan (Imitrex)

Clinical d/o: Migraine

40
Q

Name action, RX example & clinical disorder for the following serotonin receptor:
5-HT2A/2C

A

Action: antagonist
RX example: Trazodone (Desyrel), Risperidone (Risperdal)
Clinical d/o: Migraine, depression, schizophrenia

41
Q

Name action, RX example & clinical disorder for the following serotonin receptor:
5-HT3

A

Action: antagonist
RX example: Ondansetron (Zofran)
Clinical d/o: Chemotherapy-induced emesis

42
Q

Name action, RX example & clinical disorder for the following serotonin receptor:
5-HT4

A

Action: agonist
RX example: Cisapride (Propulsid –DC’ed)
Clinical d/o: Gastrointestinal disorders

43
Q

Name action, RX example & clinical disorder for the following serotonin receptor:
5-HT transporter

A

Action: inhibitor
RX example: Fluoxetine (Prozac), (SSRI’s)
Clinical d/o: Depression, obsessive-compulsive disorder, panic disorder, social phobia, posttraumatic stress disorder

44
Q

5-HT pre- and post-synaptic receptors and recurrent collaterals

A
45
Q

main use of serotonin in anesthesia

A

antiemetic

46
Q

receptors in GI tract blocked by

A

5-HT3 Antagonists

47
Q

N/V triggered by release of serotonin from enterochromaffin cells of small intestine which then activates 5-HT3 receptors on vagal afferents, triggering the vomiting reflex on this receptor

A

5-HT3 Antagonists

48
Q

can be administered orally or intravenously and can prevent emesis due to cisplatin or radiation

A

Ondansetron (Zofran)

49
Q

has an oral bioavailability of about 60%, w/effective blood levels appearing 30-60 min after admin

A

Ondansetron (Zofran)

50
Q

metabolized extensively by the liver, with a plasma half-life of 3 to 4 hours

A

Ondansetron (Zofran)

51
Q

Ondansetron (Zofran):
total daily dose and IV infusion divide dose for acute emesis

A

total daily dose of 32 mg, administered by intravenous infusion or by divided doses (0.1 to 0.15 mg/kg each)

52
Q

Ondansetron transient, mild adverse effects

A

headache, constipation, and dizziness

53
Q

why does zofran not cause extrapyramidal side effects a/w metoclopramide?

A

bec it isn’t an antagonist of dopamine receptors

54
Q

available for oral, transdermal or intravenous administration to minimize chemotherapy-induced emesis

A

Granisetron HCl

55
Q

where is Granisetron HCl metabolized

A

in liver

56
Q

Granisetron HCl elimination

A

Approx. 11% to 12% of the admin. dose is eliminated unchanged in the urine;
the rest is eliminated as metabolites in the urine (48%) and the feces (34%).

57
Q

A single intravenous infusion of 10 ug/kg of _________ is effective in preventing n/v induced by cisplatin chemo

A

Granisetron HCl

58
Q

Granisetron HCl is a _____ antagonist

A

5-HT3

59
Q

Intravenous administration of ___ ug/kg of granisetron has been demonstrated to be effective in the prevention of n/v during repeat-cycle chemo

A

40

60
Q

oral admin of 1.0mg of ______ 2x a day prevents n/v in initial/repeated emetogenic CA therapy

A

Granisetron HCl

61
Q

Granisetron HCl mild adverse effects (4)

A

HA, somnolence, and diarrhea or, constipation

62
Q

admin of dexamethasone w/this drug improves acute antiemetic efficacy

A

Granisetron HCl

63
Q

only approved for last chance in women w/IBS d/t severe potential GO S/E’s

A

Alosetron (Lotronex)

64
Q

for chemotherapy-induced N&V, blocks vagal input to medullary vomiting center but doesn’t block motion sickness N&V

A

Dolasetron (Anzemet)

65
Q

used for chemo induced N/V and more effective than granisetron

A

Palonosetron (Aloxi)

66
Q

what are kinins

A

Polypeptide structures
Produced from plasma precursor proteins (kininogens) that are cleaved by kininogenases (trypsin, plasmin, etc).

67
Q

May act at specific receptors or trigger release of other compounds such as histamine or prostaglandins

A

kinins

67
Q

half life of kinins

A

Very short half-lives (< 30 seconds), being metabolized primarily in the lungs

68
Q

kinin vasodilator properties

A

increase capillary permeability
cause edema
stimulate/augment intense burning pain at nerve endings

69
Q

CO and HR is increased reflexively d/t ↑venous return and ↓TPR due to arteriolar vasodilation

A

kinins

70
Q

May trigger histamine release from mast cells & have direct effects similar to histamine

A

kinins

71
Q

named because it produces slow GI contractions

A

bradykinins

72
Q

excessive production of bradykinins linked to

A

Hereditary angioedema
Septic shock
Allergic reactions
Carcinoid syndrome

73
Q

decreased production of _____may lead to essential hypertension

A

bradykinins

74
Q

ACEI inhibit the enzyme responsible for metabolism (peptidyl dipeptidase) which can lead to ↓BP from increased concentrations

A

bradykinins

75
Q

Serine protease inhibitor that decreases activation of plasminogen and plasmin formation

A

Aprotinin (DC’ed in US but may be reapproved)

76
Q

Decreases bleeding by decreasing plasmin destruction of clot (fibrinolysis)

A

Aprotinin

77
Q

Aprotinin anti-inflamm. effects due to…..

A

decreased interleukin and nitric oxide production

78
Q

Aprotinin elimination

A

primarily by renal excretion with half-life of approx 8 hrs

79
Q

can accumulate in tubular cells and cause proteinuria

A

Aprotinin

80
Q

Used for the prevention and treatment of surgical hemorrhage and decreases additional blood needs

A

Aprotinin

81
Q

Aprotinin and when it was removed from market

A

Use in Cardiac Surgery a “Hot” topic
Manufacturer removed from US market in 2008
Europe (2012) approved its re-release for some use
Other markets never removed
Some literature suggest risks outweigh benefits, others disagree
CRASH-2 study showed increased mortality risk
Read:
http://www.jtcvsonline.org/article/S0022-5223(08)00085-8/fulltext

82
Q

Examples of ____ include histamine, serotonin, prostaglandins, and leukotrienes

A

autacoids

*they all have ability to be formed by certain tissues, and then act on those same tissues

83
Q

considered to be “local hormones”

A

Autacoids

*differs from circulating hormones, which are produced primarily by endocrine glands and are then transported to their site of action

84
Q

histamine distribution

A

Found in all tissues with highest concentrations in lung, skin, and intestinal mucosa

85
Q

Synthesized from histadine and stored intracellularly in vesicles complexed w/heparin

A

Histamine

86
Q

Storage sites of histamine (4)

A
  • principal sites: mast cells (tissue phagocytes) & basophils (blood phagocytes)
  • GI mucosa
  • nerve endings in certain brain areas
  • cells of rapidly growth/regeneration tissue
87
Q

histamine release for allergic rxn’s

A

release is initiated in allergen-sensitized mast cells when an antigen bridges adjacent molecules of IgE attached to the cell surface

88
Q

released w/Cellular injury (mechanical, thermal, radiation)

A

histamine

89
Q

histamine release w/drugs and other factors (4)

A
  • morphine & other opioids (peripheral arteriolar & venous dilation)
  • succinylcholine
  • radio contrast media (iodine containing worse?)
  • vancomycin
  • anti-protozoals
90
Q
A

Pathopharm Final (8 decks)

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