Brainscape's Knowledge GenomeTM

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


See full index

Pharma - MSK > Pharma 2: NSAIDs > Flashcards

Pharma 2: NSAIDs Flashcards

1
Q

NSAIDs exhibit 3 actions, these are:

A
  1. Reduce fever
  2. Reduce inflammation
  3. Reduce pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Eicosanoids definition + what are they derived from

A
  • Endogenous compounds which consist of oxygenated unsaturated 20-carbon fatty Also, (eg: prostanoids and leukotrienes)
  • mainly by arachidonic acid. Also, pro inflammatory mediators can be produced by “eicosapentaenoic acid” or “ dihomolinolenic acid”, since they are the precursor of the formation of Arachidonic acid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Eicosanoids or pro-inflammatory mediators are mainly derived from …(a)… which is released from cell membrane by …(b)… enzyme

A

(a): Arachidonic acid
(b): phospholipase A2

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

What triggers phospholipase A2?

A

Once phospholipase A2 is triggered by a stimulus, viruses, bacteria, or any antigen, Arachidonic acid is released.

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

arachidonic acid subjected to oxidation whether enzymatically or non enzymatically to give you two parts (mention the pathway and product)

A

1- “Cyclooxygenase pathway“ —> Prostanoids (Prostaglandins & Thromboxanes).
2- “Lipoxygenase pathway” —> Leukotrienes (mediators in asthma mainly).

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

What does the name “eicosanoid” mean?

A
  • Eicosa: in latin means 20
  • noid: 4 conjugated double bonds in their chemical structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Eicosanoid (slide)

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

Prostaglandins eg: where are they extracted from?
- PGE2 from ?
- PGF2a from?

A
  • PGE2 is extracted from Ethanol
  • PGF2a is extracted from phosphate buffer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s the function of thromboxane?

A

Aggregate platelets

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

Eicosanoids receptors are exitatory? Inhibitory? Both?

A

Once they are released, they act on their own specific receptors of the cell membrane whether an excitatory or inhibitory action.

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

Eicosanoids biosynthesis (slide)

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

What’s the difference between COX1 and COX2 in terms of:
1- production
2- action
3- inhibition

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

What is the effect of non-selective inhibition of COX?

A

inhibition of COX-1 is responsible for adverse effects of NSAIDs

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

What are the effects of prostaglandins on reproductive system?

A
  • PGE2 inhibits motility & tone of non-pregnant uterus, & increase that of pregnant uterus
  • PGF2a increase the motility & tone of both the non-pregnant & pregnant uterus
  • induction of abortion & labor (bcz it contracts uterus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the effects of prostaglandins on CVS?

A
  • PGE: increase capillary permeability + decrease systemic atrial pressure & venous pressure + increase coronary & regional arterial blood flow
  • PGI/PGH: increase systemic arterial & venous pressure + decrease regional arterial blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the effects of prostaglandins on respiratory system?

A
  • PGEs: bronchial dilation
  • TXA2 & PGF2a: bronchial constriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the effects of prostaglandins on nervous system?

A

PGEs: pulsating headache + pyrexia + increase ACTH, TSH, LH, FSH,prolactin, GH

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

What are the effects of prostaglandins on renal system?

A

PGE: increase blood flow & induces natriuresis & water diuresis + increase ureter & bladder motility

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

What are the effects of prostaglandins on GI system?

A

PGE: decrease gastric acidity + increase gastric & intestinal motility & may induce vomiting & diarrhea + stimulate mucus secretion

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

PGE2 has been used as tablets to treat gastric ulcers by decreasing …….?

A

gastric acidity

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

What are the effects of prostaglandins on haematological system?

A
  • PGI2: inhibition of platelet aggregation & adhesives by stimulation of platelet adenyl cycles
  • TXA2: stimulation of platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes bronchial dilation

A

PGEs

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

Increase motility & tome of both pregnant & non-pregnant uterus

A

PGF2a

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

Effect of PGE on uterus of pregnant vs non-pregnant

A

Inhibits motility & tone @non-pregnant uterus

Increases motility & tone @pregnant uterus

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

What two prostaglandins have opposite actions of haematological system (platelets specifically)

A

PGI2 and TXA2

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

What PGs are used in obsterics (induction of labor, termination of pregnancy)?

A
  • PGE2 (dinoprostone)
  • PGF2a (dinoprost)
    Note: name not in drug list
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What PGs are used in GIT (treat peptic ulcers)?

A

PGE2

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

What PGs are used in paediatrics (maintain patency of ductus arteriosus in infants)

A

PGE1

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

What PGs are used in inhibiting platelet aggregation and used for pulmonary hypertension?

A

PGI2 (epoprostenol or Ilprost)
Note: name of drug not in drug list

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

Clinical uses of PGs (slide)

A
31
Q

Pharmacological actions of NSAIDs

A
32
Q

What are the non-selective cox inhibitors?

A
  • aspirin
  • paracetamol
  • indomethacin
  • ibuprofen
  • Napraxen
  • piroxicam (this one is not on drug list)
33
Q

Selective COX2 inhibitors

A
  • celecoxib
  • etoricoxib
  • rofecoxib (not on drug list)
  • valdecoxib (not on drug list)
34
Q

From the selective COX2 inhibitors, which drugs drugs have been withdrawn due to their serious side effects?

A

Rofecoxib, valdecoxib, etoricoxib

35
Q

has only 2 effects: a good analgesic & antipyretic.

A

Paracetamol (acetaminophen)

36
Q

Nowadays, we don’t use ………….. as an anti inflammatory since it has serious side effects.
We use it as:
- a prophylactic for myocardial infarction
- for colon cancer
- to reduce hypertension

A

Aspirin (Acetylsalicylic acid)

37
Q

T/F: panadol can be used as an anti inflammatory?

A

False. You can’t use Panadol as an anti inflammatory. You can use it to reduce fever or pain.

Note: It’s a weak anti inflammatory bcz it can’t compete during inflammation with mediators like prostaglandins & lysosomal enzymes or peroxidase.

38
Q

What’s the MOA of aspirin?

A

Irreversible inhibition of COX1&2.

The main action of Aspirin is due to its acetyl group. Acetyl group interacts with cyclooxygenase
—> (Cox becomes inactive) therefore prevents synthesis of prostanoids. You need to synthesize a new enzyme to be active that’s why it’s an irreversible inhibition of cyclooxygenase 1 & 2.

39
Q

What’s the pharmacological action of aspirin?

A

Analgesic, antipyretic, anti-inflammatory (its effects mediated by inhibition of PGs)

40
Q

What drug increases alveolar respiration at therapeutic doses?

A

Aspirin

41
Q

What can happen in case of high doses of aspirin?

A

Hyperventilation & respiratory alkalosis

42
Q

Aspirin (slide)

A
43
Q

What are therapeutic uses of aspirin?

A
44
Q

What are side effects of mild intoxication Vs. Severe intoxication of salicylates?

A
45
Q

Effects of aspirin on:
- GIT?
- Blood?
- respiratory?
- two more effects?

A
46
Q

Acetaminophen (paracetamol) is metabolized into .…. Or .….. or ……?

A
  • 95% of Acetaminophen is
    Metabolized to Glucuronoide or sulfate
  • 5% of Acetaminophen is metabolized to Toxic intermediate.
47
Q

After metabolism of acetaminophen how is it excreted?

A

@urine

(95% of Acetaminophen is metabolized to glucuronide or sulfate and exerted in urine.)

48
Q

What detoxifies the toxic intermediate of acetaminophen metabolism at therapeutic doses?

A

Glutathione (AA contains glycine, cysteine, & glutamic acid) will detoxify the toxic intermediate leading to Mercapturic acid (non toxic).

49
Q

What happens at toxic doses of acetaminophen?

A

if there is higher dose (toxic dose) —> depletion of glutathione that can interact with intracellular proteins —> cell death (liver necrosis).

50
Q

What’s the Paracetamol poisoning antidote?

A

intravenous acetylcystine or methionine (bcz their action is to produce glutathione in the body).

51
Q

Metabolism of acetaminophen (slide)

A
52
Q

Aspirin (advantages & disadvantages)?

A

Aspirin:
- Advantages: low cost & long history of safety.
- Disadvantages: Upper GI disturbances.

53
Q

Indomethacin disadvantages?

A

1-Upper GI disturbances.
2- Very potent; should be used only after less toxic agents have proven ineffective.
3- CNS disturbances.

54
Q

Ibuprofen & Naproxen advantages?

A

Advantages: lower toxicity and better acceptance in some patients.

55
Q

Advantages & disadvantages of NSAIDs (slide)

A
56
Q

What drug causes respiratory alkalosis at high doses?

A

Aspirin

57
Q

Which of the following is a sside effect of aspirin?
A. Decrease BT
B. Respiratory acidosis
C. Fever
D. Reye’s syndrome

A

D. Reye’s syndrome

58
Q

Used externally as counterritang

A

Methyl salicylate

59
Q

Route of administration of salicylic acid to treat corn & calluses

A

Topical

60
Q

What is the effect of selective COX2 inhibition on platelets? Why?

A

No effect on platelets, which lack cox2

61
Q

Adverse effects of selective COX2 inhibitors?

A
62
Q

Which isoform of COX is constitutive & maintain normal function?

A

COX1

63
Q

Which isoform of COX is induced during inflammation?

A

COX2

64
Q

used as a prophylactic for myocardial infarction?

A

Aspirin

65
Q

treat peptic ulcer, induce abortion and labor, & as a powerful vasodilator or bronchodilator?

A

Prostaglandins

(We use pro inflammatory mediators also in medicine such as prostaglandins: we can treat peptic ulcer, induce abortion and labor, & as a powerful vasodilator or bronchodilator).

66
Q

Why we use Aspirin and not any other NSAIDs as a prophylactic for MI ?

A

Bcz only aspirin has an irreversible action of cyclooxygenase.

67
Q

form prostanoids

A

COX

68
Q

vasoconstrictors & bronchoconstrictors

A

Thromboxane

69
Q

Why aspirin gives vasodilator effect?

A
70
Q

What drug is contraindicated in gout patients and why?

A

Aspirin because it interacts with probenecid (which is used to treat gout) causing decreased urate excretion

71
Q

Salicylates interact with ….. which reduces rate of aspirin absorption

A

Antacids

72
Q

Why aspirin may be contraindicated in patients with heart burn?

A

For example: if he’s taking antacids (for the heart burn), this will reduce the rate of aspirin absorption (accumulated in his body).

73
Q

What other drugs interact with salicylates?

A
74
Q

I didn’t understand a word from this slide :) مخي قفل

A

Pharma - MSK (2 decks)

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