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Pharmocology > Chapter 5 > Flashcards

Chapter 5 Flashcards

1
Q

Means by which body is made urgently aware of the presence of tissue damage

A

Sensation of pain

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2
Q

Protective reflex for self preservation

A

Pain

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3
Q

The physical component of pain

A

Perception

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4
Q

The psychological component of pain

A

Reaction

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5
Q

Where does pain go?

A

Cortex (brain)

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6
Q

Unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

A

IASP definition of pain

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7
Q

pain where the injury is

A

Nociceptive

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8
Q

Feeling pain in normal structures

A

Nociceptive

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9
Q

Is the site of pain always the source of pain?

A

NO

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10
Q

Classification of analgesic agents

A

Nonopiods, nonnarcotics

Opioids, narcotics

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11
Q

Salicylates, aspirin, nonaspirinxsalicylates

A

Nonopioids or nonnarcotics

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12
Q

Nonopioid analgesics act primarily at peripheral nerve endings, although their antipyretic effect is mediated centrally. Opioids act primarily in the central nervous system

A

Site of action

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13
Q

Nonopioid analgesics inhibit prostaglandin synthesis. Opioids affect the response to pain by depressing the CNS

A

Mechanism of action

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14
Q

Acetylsalicylic acid (aspirin) is broken down into

A

Acetic acid (HA) + salicylic acid (SA)

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15
Q

Acetylsalicylic acids mechanism of action

A

Inhibit prostaglandin synthesis, enzyme cycle-oxygenase (COX 1 and ll)

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16
Q

Sensitize pain receptors, lower pain threshold to painful stimuli, cause inflammation and fever, affect vascular tone and permeability

A

Prostaglandins

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17
Q

Where is acetylsalicylic acid absorbed?

A

Stomach and small intestine

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18
Q

With the addition of a buffer the half life of unhydrilyzed aspirin is

A

About 15 minutes

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19
Q

The half life of hydrolyzed aspirin is what?

A

Dose dependent

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20
Q

Half life of small doses of acetylsalicylic acid

A

2-3 hours

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21
Q

Half life of high doses of acetylsalicylic acid

A

15-30 hours

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22
Q

What has zero order kinetics

A

Acetylsalicylic acid

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23
Q

A constant amount rather than a constant percentage of the drug is metabolized per hour

A

Zero order kinetics

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24
Q

Addition of a buffer in aspirin facilitates what

A

Dispersing, dissolving, and absorption of the aspirin

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25
Q

Aspirin is poorly bound to what?

A

Plasma proteins

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26
Q

Pharmacologic effects of acetylsalicylic acid

A 
Analgesic effect 
Antipyretic effect
Anti inflammatory effect 
Uricosuric effect 
Antiplatelet effect
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27
Q

What is aspirins analgesic effect

A

Mild to moderate pain such as arthritis, headache, and toothache

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28
Q

The ability of aspirin to reduce fever (antipyretic) results from

A

Inhibition of prostaglandin syntheses in the hypothalamus

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29
Q

Aspirins antiinflammatory effect is derived from what

A

It’s ability to inhibit prostaglandin synthesis (COX l and ll). While prostaglandins are potent vasodilation agents, inhibition if prostaglandins causes decreased erythema and swelling of the inflamed area

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30
Q

Large doses of aspirin have a uricosuric effect which means

A

It can increase the elimination of uric acid

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31
Q

Aspirin irreversibly binds to

A

Platelets

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32
Q

Inhibits aggregation

A

Prostacyclin

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33
Q

Stimulates aggregation

A

Thromboxane A2

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34
Q

Acetylsalicylic acid adverse reactions

A 
GI effects
Bleeding
Reye’s syndrome 
Hepatic and renal effects
Pregnancy and nursing considerations
Hypersensitivity (allergy)
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35
Q

What is aspirins most frequent side effect?

A

GI Tract (dyspepsia, nausea, vomiting, gastric bleeding)

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36
Q

At usual therapeutic doses, aspirin irreversibly interferes with clotting mechanism by

A

Reducing platelet adhesiveness. Bleeding time is prolonged and each platelet is affected until new platelets are formed in 4-7 days

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37
Q

What is Reye’s syndrome associated with

A

Hepatotoxicity

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38
Q

Acetylsalicylic acid toxicity

A

Salicylism, tinnitus, headache, nausea, vomiting, dizziness, dimness of vision, hyperventilation , respiratory alkalosis, death

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39
Q

Tinnitus

A

Ringing in ear

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40
Q

When blood levels of salicylates reached a certain level, a toxic reaction occurs

A

Salicylism

41
Q

Cause of death from aspirin poisoning is usually what?

A

Acidosis and electrolyte imbalance

42
Q

Prevention of toxicity

A

Education of parents

43
Q

Lethal dose of acetylsalicylic acid for children and adults

A

Child: 4 gm
Adult: 10-30 gm

44
Q

Warfarin interaction with acetylsalicylic acid

A

Bleeding and hemorrhage

45
Q

Acetylsalicylic acid interaction with probenecid

A

Precipitates gout attack

46
Q

Acetylsalicylic acid interaction with methotrexate

A

Causes increased serum concentration and MTX toxicity

47
Q

Acetylsalicylic acid interaction with sulfonylureas

A

Hypoglycemia

48
Q

Aspirin interaction with antihypertensives

A

Reduce the effects of hypertensive agents

49
Q

Uses of aspirin

A

Analgesia for mild to moderate pain, antiinflammatory, low dose aspirin therapy

50
Q

Chemical classification of nonsteroidal antiinflammatory drugs

A 
Propionic acids
Acetic acids
Fenamates
Pyrazolones 
Oxicams
51
Q

What are NSAID’s similar to

A

Aspirin- inhibition of prostaglandin synthesis by inhibiting COX

52
Q

What enzymes do NSAID’s inhibit

A

COX l and ll

53
Q

NSAID mechanism of action results in

A

Reduction in formation of prostaglandin precursors and thromboxanes from arachidonic acid

54
Q

Most NSAID’s peak in

A

1-2 hours

55
Q

Where are NSAID’s metabolized

A

Liver

56
Q

Where are NSAID’s excreted

A

Kidneys

57
Q

NSAID’s are useful for treating what

A

Dysmenorrhea and gout

58
Q

Gastrointestinal effects of NSAID’s

A

Irritation, pain, bleeding, interfere with normal stomach protective mechanisms

59
Q

Central nervous system effects of NSAID’s

A 
Sedation 
Dizziness
Confusion
Mental depression
Headache
Vertigo 
Convulsions
60
Q

NSAID adverse reactions

A 
Blood clotting and myocardial infarction or stroke
Muscle weakness
Ringing ears
Hepatitis 
Hematologic problems 
Blurred vision 
Celecoxib
61
Q

Renal effects of NSAID’s

A 
Hypertension 
Renal failure
Cystitis 
Increased urinary tract infection 
Decrease in renal blood flow 
Decrease in glomerular filtration rate
62
Q

Oral effects of NSAID’s

A

Ulcerative stomatitis
Gingival ulceration
Dry mouth

63
Q

Hypersensitivity reactions of NSAID’s

A 
Hives or itching
Angioneurotic edema
Chills and fever
Steven Johnson’s syndrome
Exfoliative dermatitis 
Epidermal necrolysis
64
Q

Pregnancy and nursing considerations of NSAID’s

A

Prolong gestation
Delay parturition
Produce dystocia

65
Q

What drugs are FDA pregnancy category B

A

Fenoprofen
Ibuprofen
Naproxen

66
Q

What drugs are FDA pregnancy category c

A

Diflunisal
Tolmetin
Medenamic acid

67
Q

NSAID drug reactions

A 
Lithium
Digoxin
Antihypertensives 
Probenecid 
Cyclosporin and MTX
68
Q

Lithium

A

May increase lithium toxicity

69
Q

May increase effect of digoxin

A

Digoxin

70
Q

May decrease effects

A

Antihypertensives

71
Q

May increase serum levels of NSAID’s

A

Probenecid

72
Q

Increased toxicity

A

Cyclosporin and MTX

73
Q

NSAID medical therapeutic uses

A 
Osteoarthritis 
Rheumatoid arthritis 
Gouty arthritis 
Fever
Dysmenorrhea 
Pain
Bursitis and tendinitis
74
Q

NSAID dental therapeutic uses

A

Pain

Equivalent in analgesia efficacy to opioid analgesics in many clinical situations

75
Q

How long is the half life of ibuprofen (Advil, Motrin)

A

2 hours

76
Q

Onset of action for ibuprofen (Advil, Motrin)

A

1/2 hour

77
Q

Duration of ibuprofen

A

4-6 hours

78
Q

NSAID examples

A

Naproxen (naprosyn)
Naproxen sodium (anaprox)
Naproxen sodium otc (aleve)
Longer half life than ibuprofen!

79
Q

Other NSAID’s

A

Cyclo-oxygenase ll specific agent ( fewer adverse reactions)
Celecoxib (Celebrex)
(Less irritating to stomach)

80
Q

Member of the p-aminophenols

A

Acetaminophen (Tylenol)

81
Q

Where is acetaminophen absorbed from

A

GI Tract

82
Q

Peak plasma level of Tylenol

A

1-3 hours

83
Q

Half life of Tylenol

A

1-4 hours

84
Q

Tylenol is

A

Hepatotoxic possibly nephrotixic

85
Q

Tylenol does not..

A

Have antiinflammatory effects
Produce gastric bleeding
Affect platelet adhesiveness
Affect uric acid excretion

86
Q

Toxic dose of Tylenol

A

12 gm or more

87
Q

Adverse reactions of Tylenol

A

Hepatic necrosis

Nephrotoxicity

88
Q

Who should avoid Tylenol

A

Patients with hepatic disease or who ingest 3 or more alcoholic beverages a day (me on the weekends) 🍺

89
Q

Treatment of toxicity of Tylenol

A

Gastric lavage
Activated charcoal
Sulfhydryl groups- oral N-acetylcysteine

90
Q

Associated with long term consumption of acetaminophen

A

Nephrotoxicity

91
Q

Acetaminophen + aspirin or NSAID’s

A

Risk of analgesic nephropathy, renal papillary necrosis, end stage renal disease, and cancer of the kidney or bladder

92
Q

Skin reactions to Tylenol

A

Steven Johnson’s syndrome
Toxic epidermal necrolysis
Acute generalized exanthematous pustulosis

93
Q

Drug interactions of Tylenol

A

Hepatotoxicity can be potentiated by agents that induce hepatic microsomal enzymes
Chronic, large doses of alcohol

94
Q

Uses of Tylenol

A

Analgesic
Antipyretic
Patients with aspirin hypersensitivity
Patients with aspirin induced gastric irritation

95
Q

Regular adult dose of Tylenol

A

325 mg 2 tabs every4-6 hours

96
Q

Extra strength adult dose of Tylenol

A

650 mg 2 tabs every 6 hours

97
Q

Infant suspension of Tylenol

A

Per prescribing practitioner

98
Q

JR strength Tylenol for what ages

A

6-11 years

99
Q

Drugs used to treat gout

A

Colchicine
Allopurinol (zyloprim)
Probenecid (benemid)

Pharmocology (12 decks)

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