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House Pharmacology > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

The inflammatory process is the response to __________ evoked by a wide variety of noxious agents (e.g., infections, antibodies, or physical injuries).

A

an injurious stimulus

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2
Q

The ability to mount an inflammatory response is essential for survival in the face of environmental pathogens and injury

T/F

A

T

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3
Q

For eicosanoid synthesis to occur, ________ must first be released or mobilized from ___________ by one or more lipases of the _________ (PLA2) type

A

arachidonate

membrane phospholipids

phospholipase A2

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4
Q

At least ____ phospholipases mediate arachidonate release from membrane lipids

List them

A

three

cytosolic (c) PLA2, secretory (s) PLA2, and calcium-independent (i) PLA2.

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5
Q

Common Pharmacological Effects of NSAIDs to be covered below

______
Anti________
Anti- __________
Some are ____________

A

Analgesic

pyretic

inflammatory

Uricosuric

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6
Q

Common Pharmacological Effects of NSAIDs to be covered below

Analgesic (______________ effect)

Antipyretic (_____ effect)

Anti-inflammatory (except __________)

A

CNS and peripheral

CNS

acetaminophen

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7
Q

Common Pharmacological Effects of NSAIDs to be covered below

Analgesic : may involve _____ related effects

Anti-inflammatory : due mainly to _________

A

non-PG

PG inhibition.

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8
Q

Pharmacological Effects of NSAIDs

Diverse group of chemicals, but all inhibit ___________.

Resultant inhibition of ____ synthesis is largely responsible for their therapeutic effects.

But, inhibition of ________ in _____ mucosa leads to GIT damage (_______,________).

A

cyclooxygenase

PG

PG synthase; gastric

dyspepsia, gastritis

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9
Q

Common Adverse Effects of NSAIDs

________ Dysfunction

_____________ and ________ ulceration with bleeding

___________ Failure in susceptible

__________ retention and _____

A

Platelet

Gastritis and peptic

Acute Renal

Sodium+ water; edema

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10
Q

Common Adverse Effects of NSAIDs

________ nephropathy
Prolongation of _______ and ________

____________

GIT _______ and _______

A

Analgesic

gestation and inhibition of labor.

Hypersenstivity

bleeding and perforation

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11
Q

Hypersenstivity resulting from use of NSAIDs is immunologic

T/F

A

F

not immunologic but due to PG inhibition

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12
Q

COX

Exists in the tissue as ______ isoform (COX-__).

At site of inflammation, cytokines stimulate the induction of the ____ isoform (COX-____).

A

constitutive ; 1

2nd; 2

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13
Q

COX

Inhibition of COX-2 is thought to be due to the ___________ actions of NSAIDs.

Inhibition of COX-___ is responsible for their GIT toxicity.

A

anti-inflammatory

1

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14
Q

COX

Most currently used NSAIDs are somewhat selective for COX-___, but selective COX-___ inhibitors are available.

A

1

2

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15
Q

COX

________,________,_________– selective COX-2 inhibitors.

A

Celecoxib, etoricoxib, valdecoxib

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16
Q

COX

selective COX-2 inhibitors.

Have similar efficacies to that of the non- selective inhibitors, but ________________________________

And

no _________ and there is actually increased ———-

A

the GIT side effects are decr by ~50%.

cardioprotection

MI.

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17
Q

The Salicylates - Aspirin
Effect on Respiration: triphasic

•Low doses: ___________→____ CO2 →______ respiration.

•Direct stimulation of respiratory center → ______ventilation → resp._______ → ____ compensation

•Depression of respiratory center and cardiovascular center →____ BP, respiratory ________ , ______ compensation + metabolic ________ also

A

uncoupling phosphorylation ; ↑; stimulates

Hyper; alkalosis; renal

↓; acidosis; no; acidosis

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18
Q

The Salicylates - Aspirin

Duration of action ~_____.

______ taken.

A

4 hr

Orally

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19
Q

The Salicylates - Aspirin

Weak (acid or base?) (pKa ~____)

So it is non-ionized in _________ and easily absorbed.

It is also ______ by _______ in tissues and blood to ______ (active) and acetic acid.

A

Acid ; 3.5

stomach

Hydrolyzed ; esterases

salicylate

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20
Q

The Salicylates - Aspirin

Most salicylate is converted in _____ to H2O-soluble conjugates that are rapidly excreted by _____

A

liver

kidney

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21
Q

Effect of Aspirin

On GI System

Dose dependent _______
______ syndrome

A

hepatitis

Reye’s

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22
Q

Effect of Aspirin

Metabolic
___________ of _______

_______glycemia and depletion of ______ and ______ ———-

A

Uncoupling of Oxidative Phosphorylation

Hyper

muscle and hepatic glycogen

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23
Q

Effect of Aspirin

Endocrine: corticosteroids, thyroid

A

Okay?

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24
Q

Cardiovascular effects of Aspirin

• Platelets: Inhibition of platelet COX-1-derived _____ with the net effect of increasing ______ (inhibition of _________)

• Endothelial COX-2 derived _____ can inhibit platelet _______ (inhibition ______ ———— by ______).

A

TxA2; bleeding time; platelet aggregation

PGI2; aggregation; augments aggregation by TxA2

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25
Q

Cardiovascular effects of aspirin

Aspirin (__________________) (covalently or non-covalently?) modifies and, (reversibly or irreversibly?) inhibits platelet COX.

The enzyme is inhibited for the _____ of the platelet (~____-___days).

Effect achieved at very (low or high?) dose.

A

acetylsalicylic acid

Covalently; irreversibily

lifetime; 8 -11

Low

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26
Q

Cardiovascular effects of aspirin

PLATELTS:

• Basis of therapeutic efficacy in _____ and ——— (reduces mortality and prevents recurrent events).

A

stroke and MI

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27
Q

Additional Cardiovascular effects of aspirin

• Blood vessels/smooth muscle
COX-2 derived PGI2 can antagonize ________ and _________ induced vaso_______ (NSAIDs can ______ bp).

A

catecholamine- and angiotensin II-

constriction

elevate

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28
Q

Additional Cardiovascular effects of aspirin

• Atherosclerosis
Inhibition of COX-____ can destabilize atherosclerotic plaques (due to its ________________ actions)

A

2

anti- inflammatory

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29
Q

NSAIDs can elevate Blood pressure

T/F

A

T

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30
Q

Renal effects of nsaidS

COX-1 and COX-2 – generated PGs (TxA2, PGF2 , PGI2 (_____), PGE2 (______), powerful vaso______) can both increase and decrease Na+ retention (_________ predominates), usually in response to changes in _____________, extracellular tonicity or (low or high?) bp.

A

Glomerular; medulla

dilators; natriuresis

tubular Cl-; low

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31
Q

Renal

NSAIDs tend to promote Na+ ________ and can therefore _____ease bp.

L

A

retention; incr

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32
Q

Renal

PGs have (minimal or maximal?) impact on normal renal blood flow, but become important in ____________ kidney.

A

Minimal

the compromised

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33
Q

Renal

Patients (particularly ________ and _________ ) are at risk of renal ischemia with NSAIDs.

A

elderly and volume depleted

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34
Q

Gastrointestinal effects of NSAIDs

PGs (generated via COX-1)
1)inhibit ________ secretion,
2) stimulate _____________ secretion, vaso_________ and therefore,
3) are _________ for the gastric mucosa.

A

stomach acid

mucus and HCO3-

dilation; cytoprotective

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35
Q

NSAIDs Can counteract effects of many anti-hypertensives like diuretics, ACE inhibitors and -AR antagonists

T/F

A

T

36
Q

Gastrointestinal effects of NSAIDs

Therefore, NSAIDs with COX-1 inhibitory activity will produce opposite effects, leading to:
Gastric ______ , gastric ______, sudden ___________ (effects are dose-dependent)

A

distress

bleeding

acute hemorrhage

37
Q

Gestation
PGs (generated from COX-___) are involved in the initiation and progression of labor and delivery. Therefore, inhibition of their production by NSAIDs can _____________

A

2

prolong gestation.

38
Q

Respiratory system
(Low or High?) doses (salicylates) cause _____________________ with ___eased CO2 production (COX-______ effects).

A

Low

partial uncoupling of oxidative phosphorylation

incr; independent

39
Q

Respiratory system

Increase in plasma CO2 leads to _______. Even higher doses cause ________ of respiration.

A

hyperventilation; depression

40
Q

Other uses of NSAIDs (mechanisms less understood) - Decreased risk of fatal ____________

A

colon carcinoma

41
Q

Aspirin - Therapeutic Uses

_______,_______

_______________ due to platelet aggregation (CAD, post-op DVT)

A

Antipyretic, analgesic

Prophylaxis of diseases

42
Q

Aspirin - Therapeutic Uses

Anti-inflammatory: ____________,____________, other rheumatological diseases.

(Low or High?) dose needed (5-8 g/day).

But many patients cannot tolerate these doses (GIT); so, ________ derivatives, ______,_______ tried first.

A

rheumatic fever, rheumatoid arthritis (joint dis)

High; proprionic acid

ibuprofen, naproxen

43
Q

Aspirin - Therapeutic Uses

__________ and ________ of pregnancy (?excess TXA2)

A

Pre-eclampsia and hypertension

44
Q

Paracetemol (______) has significant anti- inflammatory effect

T/F

A

Tylenol

F

no significant anti- inflammatory effect,

45
Q

Paracetemol (tylenol) – used for its ______ ———- effect.

(Poorly or Well?) -absorbed and (with or without?) GIT irritation.

A

Mild analgesic

Well

Without

46
Q

Paracetemol (tylenol)

Serious disadvantage: at high doses, _______________ results.

A

severe hepatotoxicity

47
Q

Mechanism of action of NSAIDs

Analgesia
– works (centrally or peripherally?)

-associated with ___________ actions that results from ______ of ________ in inflamed tissues.

A

Works both centrally and peripherally.

anti-inflammatory

inhibition of PG synthesis

48
Q

Mechanism of action of NSAIDs

PGs cause little pain relief themselves

T/F

A

T

But

potentiate the pain caused by other mediators of inflammation (e.g., histamine, bradykinin).

49
Q

Mechanism of action of NSAIDs

Anti-inflammatory action –

Normally, PGs in inflammation leads to vaso______ and ____eased vascular permeability.

  • Inhibition of PGs by NSAIDs _______, not ________, inflammation
  • Very _________ from pain, stiffness, swelling for RA  often prescribed for their anti-inflammatory actions.
A

dilation; incr

attenuates, not abolish

modest relief

50
Q

NSAIDs inhibit mediators of inflammation

T/F

A

F

NSAIDs do not inhibit mediators of inflammation

51
Q

Mechanisms of Action of NSAIDs

Antipyretic actions – Fever, heat stroke, increased T° are _________ problems.

  • So, NSAIDs _________ body T°.
A

hypothalamic

do not decr

52
Q

Mechanisms of Action of NSAIDs

Antipyretic actions

  • Fever occurs due to release of _______ (e.g., interleukin-1) released from ______ and acts directly on the ________ in _________ , leading to an increase in body T°.
  • This is associated with increase in brain ____ (pyrogenic).
  • Aspirin prevents the T°-rising effects of interleukin-1 by ____________
A

endogenous pyrogens

leucocytes; thermoregulatory centers

hypothalamus; PGs

preventing the incr in brain PGs

53
Q

Mechanisms of Action

Aspirin prevents the T°-rising effects of interleukin-___ by _______________

A

1

preventing the incr in brain PGs

54
Q

Mechanism of Action on the Active Site of COX

Possess a (short or long?) channel

Non-selective NSAIDs enter channel (but not ______).

_____ channels by _____________________ half of the way in.

This (reversibly or irreversibly ?) inhibits the COX by preventing ______________

A

Long ; aspirin

Block; binding with H- bonds to an arg

reversibly; arachidonic acid from gaining access.

55
Q

Whose Channel is wider

COX-1 or COX-2

A

COX-2 channel is wider than in COX-1

56
Q

Mechanism of Action on the Active Site of COX

Aspirin ______ COX (at _____) and is, therefore, irreversible.

A

acetylates

ser530

57
Q

Selective COX-2 inhibitors generally (more or less?) bulky molecules

A

More

58
Q

Selective COX-2 inhibitors can enter and block the channel of COX-2, but not that of COX-1.

T/F
With reason

A

T

Because Selective COX-2 inhibitors are generally more bulky molecules - can enter and block the channel of COX-2, but not that of COX-1.

59
Q

Paracetamol – reduces _______________:

Recall: _______ is necessary to activate _____ enzyme to the ____.
.

A

cytoplasmic peroxide

peroxide

heme; Fe

60
Q

Paracetamol –

Acute inflammation: paracetamol is not very effective because _________________________________, which overcome the actions of the drug.

A

neutrophiles and monocytes produce much H2O2 and lipid peroxide

61
Q

Selective COX-2 Inhibitors

Anti-inflammatory with (more or less?) adverse effects, especially ___ events.

Potential toxicities: ______ and _______ , leading to increased risk of ______ events.

A

Less; GI

kidney and platelets

thrombotic

62
Q

Selective COX-2 Inhibitors

Associated with MI and stroke because _________________.

Thus,.. should not be given to patients with ____ disease

A

they do not inhibit platelet aggregation

CV

63
Q

Selective COX-2 Inhibitors

Has a Role in ______ prevention

Has a Role in ________ disease

A

Cancer

Alzheimer’s

64
Q

Lipoxins – (Anti or Pro?) -inflammatory Mediators

During inflammation, cells die by ______.

A

Anti-

apoptosis

65
Q

Lipoxins signal _______ to clean up.

During the acute inflammatory process, cytokines (e.g., IFN-γ and IL-1β) can induce the expression of anti-inflammatory mediators (_______ and _______), which promote the _______ phase of inflammation.

A

macrophages

lipoxins and IL-4

resolution

66
Q

Aspirin Toxicity - Salicylism

________-________-________– ____ impairment – ____ vision

Confusion and drowziness
________ and _____ventilation
Nausea, vomiting

A

Headache - timmitus - dizziness

Hearing ; dim

Sweating and hyper

67
Q

Aspirin Toxicity - Salicylism

Marked _____ disturbances
Hyper______
Dehydration
_________ and _________ collapse, coma convulsions and death

A

acid-base

pyrexia

Cardiovascular and respiratory

68
Q

Aspirin Toxicity - Treatment

Decrease absorption - _______,_______,______

Enhance excretion – ion trapping (_________ urine), forced ______, _______

Supportive measures - fluids, decrease temperature, bicarbonate, electrolytes, glucose, etc…

A

activated charcoal, emetics, gastric lavage

alkalinize; diuresis; hemodialysis

69
Q

Other NSAIDs

Phenylbutazone: additional _____ effect. Can cause ________ anemia.

A

uricosuric

Aplastic

70
Q

Other NSAIDs

_______________: has additional uricosuric effect. Aplastic anemia.
.

A

Phenylbutazone

71
Q

Other NSAIDs

Indomethacin: Common adverse rxns: ______,__________, CNS most common: hallucinations, depression, seizures, headaches, dizziness.

A

gastric bleeding, ulceration

72
Q

Other NSAIDs

___________: Common adverse rxns: gastric bleeding, ulceration, CNS most common: hallucinations, depression, seizures, headaches, dizziness.

A

Indomethacin

73
Q

Other NSAIDs

Proprionic acids: (better or worse?) tolerated. Differ in pharmacokinetics; ________,________,_______ widely used for inflammatory joint disease and (few or plenty?) side-effects.

A

better

ibuprofen, fenbufen, naproxen

Few

74
Q

Other NSAIDs

__________ : better tolerated. Differ in pharmacokinetics; ibuprofen, fenbufen, naproxen widely used for inflammatory joint disease and few side-effects.

A

Proprionic acids

75
Q

Other NSAIDs

Acetaminophen: differs in effects and adverse reaction from rest. Main toxicity: ________ due to toxic intermediate which ________ ————-.

Treat with _____________

A

hepatitis

depletes glutathione

N-acetylcysteine.

76
Q

Other NSAIDs

___________ : differs in effects and adverse rxn from rest. Main toxicity: hepatitis due to toxic intermediate which depletes glutathione. Treat with N-acetylcysteine.

A

Acetaminophen

77
Q

Other NSAIDs

_________
___________
__________
____________

A

Proprionic acids
Acetaminophen
Phenylbutazone
Indomethacin

78
Q

Drug reaction between NSAIDs and Lithium

The effect on lithium

A

NSAIDs inhibits renal elimination of lithium

Elevated serum lithium levels

79
Q

Drug reaction between NSAIDs and anti hypertensives

Effect on the anti hypertensives

A

NSAIDs may cause fluid retention and edema

Decreased antihypertensive effect

80
Q

Drug reaction between NSAIDs and anticoagulants

Effect on the anti coagulants

A

Displacement/additive effect

Increased anticoagulant activity

81
Q

Gout Characterized by deposition of _______ in the joint leading to painful ______.

A

Na urate crystals; arthritis

82
Q

Gout

Acute attacks treated with _______, ________, or other _______, but not with _________ because it ___________________________ by ________________ in the renal tubules

A

indomethecin; naproxen; NSAIDs

aspirin

increases plasma urate levels at low doses

inhibiting uric acid secretion

83
Q

Gout

Colchicine – bonds ________ in leukocytes that prevents ___________ In _________ which inhibits the ____________ and __________ of leukocytes to the area of _____________ thereby decreasing _________

A

tubulin

polymerization in microtubules

phagocytic activity and migration

uric acid deposition; inflammatory repsonse.

84
Q

Prophylactic treatment of Gout

Allopurinol lowers plasma urate by ________________

Uricosuric drugs inhibit ____________ thereby increasing ________.

Should drink plenty of _____ to prevent _________________

But These drugs (more or less?) effective and (more or less?) toxic than allopurinol.

A

inhibiting xanthine oxidase

renal tubular reabsorption of uric acid ; excretion

H2O; crystallization of urate in the urine.

Less; more

85
Q

Uricosuric drugs (_________,_________)

A

sulfinpyrazone, probenicid

86
Q

Period purr

A

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