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Pharmacology > Anti Inflammatory Drugs: NSAIDS & Acetaminophen (75) > Flashcards

Anti Inflammatory Drugs: NSAIDS & Acetaminophen (75) Flashcards

1
Q

Tissue injury causes the relapse of (5)

A

-prostaglandins
-bradykinin
-histamine
-leukotriennes
-serotonin

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2
Q

Most importantly tissue injury causes release of…

A

Prostaglandins

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3
Q

What are signs of inflammation

A

-vasodilation
-increased vascular permeability
-chemotaxis
-pain

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4
Q

A stimulus like damage causes release of phospholipase A2 which interacts with ____ to create ___

A

Interacts with PHODPHOLIPIDS to create ARACHIDONIC ACID

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5
Q

ARACHIDONIC acid is metabolized by _____ to create PGH2 or different variations

A

Cyclooxygenase

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6
Q

What are the two versions of cyclooxygenase

A

COX-1 and COX-2

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7
Q

PG stands for

A

Prostaglandin

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8
Q

What does COX-1 do

A

Physiological functions
-GI, renal, platelet function, blood vessels

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9
Q

What does COX-2 do

A

Inflammation

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10
Q

Which of the COX is inhibition undesirable?

A

COX-1 since it is related to regular physiological functions

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11
Q

NSAIDS stands for

A

Non steroidal anti inflammation drugs

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12
Q

Where do NSAIDS work in the action of creating prostaglandins?

A

NSAIDS stop the metabolism of ARACHIDONIC acid, by competition inhibition of COX

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13
Q

Is the inhibition of COX reversible or permanent?

A

Reversible

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14
Q

NSAIDS can block

A

Either one or both COX

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15
Q

What are the properties of NSAIDS groups

A

-analgesic
-anti inflammatory
-antipyretic

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16
Q

Indications of NSAIDs

A

-relief of mild to moderate pain
-fever
-gout, RA, osteoarthritis

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17
Q

Non selective NSAIDs target

A

Inhibitbition of both COX 1 and 2

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18
Q

Non selective NSAIDs are used for

A

-alleviating mild to moderate pain
-inflammatory disorders

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19
Q

The downside of non selective NSAIDs are

A

That they suppress inflammation but pose risks of serious harm

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20
Q

Examples of non selective NSAIDs

A

-acetylsalicylic acid (ASA or ASPRIN)
-ibuprofen (Advil)
-naproxen (Aleve)

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21
Q

NSAIDs can be used in

A

Combination
-codeine, caffeine

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22
Q

Acetylsalicylic acid is the

A

Standard NSAID agains which all others are compared

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23
Q

Acetylsalicylic acid is created from

A

Salicylic acid- Willow bark, and other plants ‘

Acetyl- added on in that era to create a drug

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24
Q

Where does the name ASPRIN come from

A

Acetalation spiraea

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25
Q

Acetylsalicylic acid properties

A

-anti inflammatory
-analgesic
-antipyretic
-antiplatelet

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26
Q

Antiplatelet properties of Acetylsalicylic acid

A

A special property of Acetylsalicylic acid
-COX will be inhibited for the life time of the platelet (eight days)

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27
Q

Positives of Acetylsalicylic acid being an antiplatelet

A

Heart attack
-prolonged use can reduce the risk of heart attack

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28
Q

Acetylsalicylic acid is different to other NSAIDs because it

A

Irreversibly inhibits COX

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29
Q

Daily dose for prophylactic use of Acetylsalicylic acid

A

80 to 160mg

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30
Q

Contraindications and cautions Acetylsalicylic acid

A

-pregnancy
-bleeding disorders
-operations
-renal dysfunction
-gastrointestinal

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31
Q

Contraindications and cautions Acetylsalicylic acid: pregnancy

A

In late trimester connected with low weight, intracranial bleed, and even death

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32
Q

Contraindications and cautions Acetylsalicylic acid: bleeding disorders

A

Hemophilia, as it is an ntiplatelet

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33
Q

Contraindications and cautions Acetylsalicylic acid: operations

A

Discontinue one week before operations (antiplatelet)

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34
Q

Contraindications and cautions Acetylsalicylic acid: renal

A

Renal dysfunction
-relies on PG in kidney dysfunction
-can exacerbate function

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35
Q

Contraindications and cautions Acetylsalicylic acid: gastrointestinal

A

Increases ulcerations and bleeding

36
Q

How does Acetylsalicylic acid cause bleeding and ulcers

A

-increases acidity in stomach
-deeper ulcer causes bleeding
-can vomit up coffee grounds or have dark stool

37
Q

Why does someone develop ulcers on Acetylsalicylic acid

A

The stomach has ow pH but intact stomach wall

-this is due to PGE2 and PGI2 which increase protective mucus and dilate blood to increase cell health

-the loss of PG in the Acetylsalicylic acid properties will get rid of this stomach wall health

38
Q

AE of Acetylsalicylic acid

A

-Reyes syndrome
-renal

39
Q

Reye’s syndrome

A

Viral infections, being young, and taking Acetylsalicylic acid can increase risk of Reye’s syndrome
-which causes vomiting, liver damage, CNS encephalopathy

40
Q

AE of Acetylsalicylic acid: renal

A

Reduction in creatinine clearance

41
Q

AE of Acetylsalicylic acid: renal

A

Reduction in creatinine clearance

42
Q

Salicylate toxicity

A

Use of several NSAIDs
-adults: tinnitus, hearing loss
-children: hyperventilation

43
Q

Acetylsalicylic acid is not given too

A

Children generally

44
Q

Interactions with Acetylsalicylic acid

A

-anticoagulants increase bleeding
-glucocorticoids increase gastric ulcers
-non ASA NSAIDs can reduce antiplatelet effects

45
Q

Important not to mix NSAIDs if Acetylsalicylic acid is being used for

A

Antiplatelet effect

46
Q

Non Acetylsalicylic acid NSAIDs have fewer

A

-fewer GI, renal, hemorrhagic effects
-many different types

47
Q

Non ASA NSAIDs inhibit COX 1 and 2, is it reversible or permanent

A

Reversible unlike ASA

48
Q

Non ASA NSAIDs do not

A

Protect against MI and stroke

49
Q

Selective NSAIDs are able to target just one COX, which one is that

A

COX 2, which is good because this will stop inflammation and hopefully not affect the physiological functions with COX 1 inhibition

50
Q

What was the purpose of creating selective NSAIDs

A

Hoping to solve GI problems associated with non selective NSAIDs

51
Q

COX 2 inhibitors example

A

Celecoxib

52
Q

Selective NSAIDs are just as effective as

A

Traditional NSAIDS in suppressing inflammation and pain

53
Q

Selective NSAIDs have a lower risk of

A

GI adverse effects
-but would be better to just not take the drug in general

54
Q

Selective NSAIDs can impair

A

Renal function and cause hypertension and edema

55
Q

Selective NSAIDs can increase the risk of

A

MI and stroke

56
Q

How can someone reduce GI ulceration when using NSAIDs

A

Misoprostol

57
Q

How are NSAIDs antipyretic

A

Inhibit prostaglandin E2 production within the area of the brain that control temperature

58
Q

Before beginning NSAID therapy, nurses should assess for

A

-GI lesions or peptic ulcer disease
-bleeding disorders

—> especially long term

59
Q

Clients taking NSAIDs long term, for the occurrence of

A

Any unusual bleeding
-dark or black, color, tarry stool

60
Q

Enteric coated tablets should not

A

Be crushed or chewed

61
Q

Salicylates are NOT to be given to

A

Children under age 12

62
Q

Non opioid analgesics

A

Acetaminophen

63
Q

Acetaminophen

A

Analgesic and antipyretic
-but is NOT an anti inflammatory
-no antiplatelet

64
Q

Mechanism and action of acetaminophen

A

We dont really know

65
Q

acetaminophen inhibits

A

COX
-but only in the CNS

66
Q

acetaminophen has no

A

-peripheral therapeutic sites of action
-no AE associated with NSAIDs like GI ulceration or excessive bleeding

67
Q

Maximum dosage of acetaminophen per day for an adult

A

4000 mg

68
Q

Maximum acetaminophen for 11 to 12 year olds

A

2400

69
Q

acetaminophen should be used in extreme caution in

A

Alcohol absorbers

70
Q

Single tablet amount of acetaminophen

A

325, 500, 650mg

71
Q

Tylenol combinations with codeine

A

All have 300mg of acetaminophen

72
Q

Contraindications of acetaminophen

A

-severe hepatic disease
-renal disease
-alcoholism
-drug allergy

73
Q

Toxicity of acetaminophen

A

OTC prescription which can risk overdose both intentionally or unintentional use

74
Q

Overdose is usually due to

A

Hepatic necrosis
-drug induced hepatitis

75
Q

Long term ingestion of large doses also causes

A

Nephropathy

76
Q

acetaminophen should not be used with other drugs containing

A

acetaminophen
-easy to overdose since many drugs need/contain acetaminophen

77
Q

What other warning is found on acetaminophen bottles

A

Liver warning- severe or possibly fatal liver damage if
-taking more than recommend dose
-other drugs with acetaminophen
-while drinking thee or more alcoholic drinks every day

78
Q

Symptoms of liver damage may include

A

-yellowing of skin, eyes, dark urine
-sweating, nausea, vomiting, stomach pain
-unusual tiredness, loss of appetite

79
Q

How is acetaminophen metabolized normally

A

acetaminophen had a major pathway which creates non toxic metabolites

80
Q

How is acetaminophen metabolized when taken with alcohol

A

when taking alcohol with acetaminophen, it creates toxic metabolites that are broken down by glutathione creating a non toxic metabolite

81
Q

How are toxic metabolites turned into nontoxic metabolites

A

Glutathione

82
Q

What do toxic metabolites do

A

-alter proteins
-damage DNA
-death of cells

83
Q

Glutathione is depleted by

A

Alcohol and acetaminophen overdose

84
Q

What can be done when someone is overdosing on acetaminophen

A

Take acetylcysteine to increase amounts of glutathione

85
Q

Acetylcysteine must be taken in what amount of time

A

8 to 10 hours

86
Q

Dangerous interactions may occur if acetaminophen is taken with

A

Alcohol

87
Q

Acetaminophen should not be take in the prescience of

A

-liver dysfunction, chronic Alcoa is
-possible liver failure or severe renal disease
-taking other hepatotoxic drugs

Pharmacology (37 decks)

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