Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Mod 2 Exam > Analgesic, Antipyretic and Anti-Inflammatory Drugs > Flashcards

Analgesic, Antipyretic and Anti-Inflammatory Drugs Flashcards

1
Q

What does inflammation start with

A

Tissue Damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What chemicals are released to cause inflammation

A

histamines, kinins and prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Vasoactive amines

A

histamine and serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

plamsa protein systems

A

complement and clotting/fibrinolysis systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acetyl Glycerol Ether Phosphocholine (AGEPC)

A

platelet activating factor (PAF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the mediator systems of inflammation

A

vasoactive amines
plasma protein systems
prostaglandins and leukotrienes (Eicosinoids)
AGEPC= PAF
cytokines
Nitric oxide - vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Eicosinoids

A

prostaglandins and leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What mediates inflammation

A

Vasodilation
increase permeability
chemotaxis
pain
fever
tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what class of drugs inhibit the phospholipase

A

glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of antihistamine inhibit the Calcium and beta2 receptors

A

second generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

First and second generation antihistamines inhibit what

A

histamine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do “selective inhibitors” inhibit

A

COX-1 and COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do non-selective inhibitors inhibit

A

prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does PGI2 cause

A

vasodilation, and inhibits platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does Thromboxane A2 (TXA2) cause

A

vasoconstriction, and promotes platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is part of the Prostaglandin G2 (PGG2)

A

PGI1 and TXA2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

types of nonselective COX inhibitors

A

ibuprofen (Motrin, advil)
Naproxen (Naprosyn)
Diclofenac
Ketorolac (Toradol)
Indomethacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Type of selective COX-2 inhibitor

A

Celecoxib (celebrex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the MOA of NSAIDs

A

inhibits COX-1 and COX-2 enzymes that break down the first step in prostaglandin synthesis. This results in a decreased prostaglandin level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are prostaglandins synthesized from

A

Arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the two cycloocygenaze enzymes

A

COX-1 and COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the purpose of COX-1 and COX-2

A

prostaglandin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does COX-1 do

A

physiologic production of prostaglandins
“house keeping” enzyme
regulates homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does COX-2 do

A

unregulated during inflammation
induced by oxidative stress, injury, ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the physical differences between COX-1 and COX-2

A

larger and more flexible substrate channel and a larger space at the site where inhibitors bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What NSAID irreversibly inhibits the enzymes

A

Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does low dose aspirin inhibit

A

COX-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does higher dose aspirin inhibit

A

both COX-1 and COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is ASA and what are its properties

A

Aspirin - analgesic, antipyretic and anti-inflammatory effects at higher doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

where is aspirin hydrolyzed

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is aspirin hydrolyzed into

A

salicylic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

due to the hydrolysis of aspirin what are the plasma concentrations

A

always low and rarely exceed 20mcg/ml at ordinary therapeutic doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

describe the half life of aspirin

A

it is relatively short, but lengthens as the dose increases by Zero-order kinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is aspirins antiplalet effect

A

8-10 days (the life of the platelet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does ASA inhibit

A

TXA2 production in platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what happens when TXA2 production is inhibited by ASA

A

decreases platelet aggregation and prevents the first step in thrombus formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the anti-inflammatory effect of ASA

A

inhibits prostaglandin synthesis by inhibiting the function of COX enzymes. result in inhibiting granulocyte adherence to damaged vasculature and inhibiting the chemotaxis of PMN leukocytes and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the analgesic effect of ASA

A

through its effect on inflammation and probably because it inhibits pain stimuli at a subcortical(Central) site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the antipyretic effects of ASA

A

probably mediated by both COX inhibition in CNS and inhibition of IL-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is aspirin not effective for

A

severe visceral pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

when is IL-1 released

A

released by macrophages during episodes of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the adverse effects of theraputic doses of ASA

A

GI upset and ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are adverse effect of higher doses of ASA

A

vomiting, tinnitus, decreased hearing and vertigo (reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

define Salicylism

A

vomiting, tinnitus, decreased hearing and vertigo that is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are adverse effects to very large doses of ASA

A

hyperpnea (hyperventilating) through a direct effect on respiratory centers int he medulla resulting in respiratory alkalosis
and
elevated body temperature due to uncoupling of oxidative phosphorylation which can result in sever hyperthermia

46
Q

What is the primary concern with ASA toxicity

A

Respiratory alkalosis - early

47
Q

what occurs with ASA toxicity

A

lactic acidosis and hyperpyrexia
metabolic acidosis
ketone bodies - wide anion gap
respiratory alkalosis

48
Q

what are the common signs of ASA toxicity

A

nausea, vomiting, diaphoresis, tinnitus, deafness, vertigo, agitation, delirium, hallucinations

49
Q

what does increased renal bicarbonate exceretion due to ASA lead to

A

metabolic acidosis

50
Q

What does the inhibition of oxidative phosphorylation lead to with ASA

A

lactic acidosis hyperpyrexia

51
Q

What does the increase in fatty acid metabolism with ASA lead to

A

ketone bodies and wide anion gap

52
Q

What is an anion gap

A

a larger space in the NMJ space

53
Q

what is the effect of renal and cardiovascular disease

A

decreased renal blood flow

54
Q

what is the effect of cirrhosis, nephrosis, heart failure and diuretics

A

decreased blood volume

55
Q

What patients should you avoid NSAIDs in

A

Kidney disease, Cardiovascular disease, Liver disease and those on a diuretic

56
Q

what are the FDA black box warnings for non-ASA NSAIDS

A

increased risk of serious and potentially fatal cardiovascular thrombotic event and increased risk of serious or potentially fatal GI adverse events including bleeding, ulcer, stomach or intestine perforation

57
Q

What cardiac patients have a contraindication for NSAID use

A

CABCG peri-operative pain

58
Q

AHA NSAID recommendations

A

lowest effective dose
avoided in patients with cardiovascular risk factors
avoid in patients with history of hypersensitivity to NSAIDs
no recommended during pregnancy or children with viral diseases

59
Q

What is the risk of ASA in kids with viral diseases

A

it increases the risk of Reyes Syndrome

60
Q

what is Reyes Syndrome

A

a rare but serious illness thought to be preciptated by aspirin that causes cognitive impairement

61
Q

what is the effect of ASA on a fetus

A

damages fetal vasculature

62
Q

what cardiovacular risk factors for NSAID use

A

hypertension, hypercholesteremia, angina, edema, recent cardiac bypass surgery and a history of MI or other CV events

63
Q

What do COX-2 inhitors bypass

A

most side effects of COX -1 inhibitors
- less GI adverse effects

64
Q

what is an example of a COX-2 inhibitor

A

Celebrex (celecoxib)

65
Q

Where are COX-2 inhibitors metabolized

A

Liver (CYP2C9)

66
Q

what is the half life of COX-2 inhibitors

A

about 11 hours

67
Q

when do you avoid COX-2 inhibitor use

A

severe renal and hepatic disease and patients with anaphylactoid reactions to ASA and NSAIDs

68
Q

what are common drug type interactions with Celebrex

A

elevation of beta-blockers, antidepressants and antipsychotic drugs

69
Q

What is the mechanisms of action for ASA

A

irriversibly inhibits both COX-1 and COX-2, which decreases TSA2 and prostaglandin synthesis

70
Q

what is the clinical use of low dose aspirin

A

decreased platelet aggregation

71
Q

what is the clinical use for intermediate dose ASA

A

antipyretic and analgesic

72
Q

what is the clinic use for high dose ASA

A

Anti-inflammatory

73
Q

what are the most common NSAIDS

A

ibuprofen, naproxen, indomethacin, ketorolac, diclofenac

74
Q

what is the mechanism of action for NSAIDs

A

reversibly inhibits both COX-1 and COX-2. blocks prostaglandin synthesis

75
Q

what is the clinical use for NSAIDs

A

antipyretic, analgesic, anti-inflammatory, gout (indomethacin)

76
Q

what are signs of NSAID toxicity

A

interstitial nephritis, gastric ulcer and renal ischemia

77
Q

What is the MOA for Celebrex

A

reversibly inhibits COX-2. mediated inflammation and pain. spares COX-1 which helps maintain gastric mucosa. spares platelet function as TXA2 production is dependent on COX-1.

78
Q

what are toxicity concerns with Celebrex

A

increased risk of thrombosis, avoid in sulfa allergy and renal ischemia

79
Q

APAP

A

Tylenol/acetaminophen

80
Q

what does APAP inhibit

A

prostaglandin synthesis in CNS

81
Q

what does APAP have minimal effect on

A

antiiflammatory effects

82
Q

what are the primary effects of APAP

A

antipyretic and analgesia

83
Q

what is APAPs effect on platelets

A

none

84
Q

Where is APAP absorbed

A

GI tract - rapidly
hepatocytes and luminal cells of intestines

85
Q

what type of metabolism does APAP go through

A

first pass metabolism

86
Q

where is APAP conjugated

A

in the liver to form inactive metabolites

87
Q

what is the potentially damaging metabolite that APA is hydroxylated into

A

N-acetyl-p-benzoquinoneimine (NAPQI)

88
Q

at normal doses what does NAPQI react with

A

glutathione and forms a nontoxic metabolite

89
Q

where are APAP and its metabolites excreted

A

urine

90
Q

what happens when there is not enough glutothione

A

NAPQI does not react and lead to covalent binding of amino acids in proteins and enzymes leading to cell death

91
Q

what is the MOA of acetaminophen

A

reversibly inhibits cyclooxygenase in CNS. inactivated peripherally

92
Q

what is the clinical use for APAP

A

antipyretic, analgesic but no anti-inflammatory effect. used instead of ASA in children with viral infection

93
Q

what does overdose of APAP produce

A

hepatic necrosis and cell death

94
Q

Most common oral corticosteroids (4)

A

prednisone
methylprednisolone
dexamethasone
hydrocortisone

95
Q

most common IV corticosteroids (3)

A

Methylprednisolone
hydrocortisone
dexamethasone

96
Q

most common inhaled corticosteroids (4)

A

beclomethasone
fluticasone
budesonide
triamcinolone

97
Q

most common opthalmic corticosteroids (3)

A

dexamethasone
prednisolone
fluorcinolone

98
Q

most common topical corticosteroids (10)

A

hydrocortisone
triamcinolone
fluocinolone
desonide
fluticasone
mometasone
fluorandrenolide
fluorcinonide
betamethasone
clobestasol

99
Q

what is corticosteroids considered

A

immunosuppressive

100
Q

what do corticosteroids bind to

A

glucocorticoid receptor

101
Q

what do corticosteroids regulate

A

Translation of DNA as it is passed into the nucleus

102
Q

what do corticosteroids decrease

A

the expression of genes involved in inflammatory response

103
Q

what does the decrease in gene expression cause

A

decrease COX-2 up-regulation and inhibits various inflammatory cytokines

104
Q

What effect do corticosteroids have on inflammatory cells

A

decrease numbers of eosinophils (apoptosis)
decrease cytokines from T lymphocytes
decrease number of mast cells
decrease cytokines from macrophages decrease number of dendritic cells

105
Q

What effects do corticosteroids have on structural cells

A

decrease cytokines and mediators of epithelial cells
decrease leakage of endothelial cells
increase B2 receptors and decrease cytokines in smooth muscle (airway)
and decrease mucus secretion in the mucous glands

106
Q

why is tapering a corticosteroid necessary

A

it may cause adrenal suppression with prolonged use with greater than 20 mg/day being at higher risk

107
Q

what affects do corticosteroids have on blood glucose

A

increase blood glucose

108
Q

What can corticosteroids cause

A

insomnia, mood swings, psychiatric disturbances including euphoria, personality changes, severe depression or frank psychotic manifestations

109
Q

what patients require caution when using corticosteroids

A

renal impairment and osteoporosis

110
Q

what is the correlation between osteoporosis and corticosteroid use

A

high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures

111
Q

what is the correlation between renal impairment and corticosteroids

A

fluid retention may occur

Pharmacology Mod 2 Exam (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions