Chapter 5 Flashcards

(99 cards)

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
Aspirin is poorly bound to what?
Plasma proteins
26
Pharmacologic effects of acetylsalicylic acid
``` Analgesic effect Antipyretic effect Anti inflammatory effect Uricosuric effect Antiplatelet effect ```
27
What is aspirins analgesic effect
Mild to moderate pain such as arthritis, headache, and toothache
28
The ability of aspirin to reduce fever (antipyretic) results from
Inhibition of prostaglandin syntheses in the hypothalamus
29
Aspirins antiinflammatory effect is derived from what
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
30
Large doses of aspirin have a uricosuric effect which means
It can increase the elimination of uric acid
31
Aspirin irreversibly binds to
Platelets
32
Inhibits aggregation
Prostacyclin
33
Stimulates aggregation
Thromboxane A2
34
Acetylsalicylic acid adverse reactions
``` GI effects Bleeding Reye’s syndrome Hepatic and renal effects Pregnancy and nursing considerations Hypersensitivity (allergy) ```
35
What is aspirins most frequent side effect?
GI Tract (dyspepsia, nausea, vomiting, gastric bleeding)
36
At usual therapeutic doses, aspirin irreversibly interferes with clotting mechanism by
Reducing platelet adhesiveness. Bleeding time is prolonged and each platelet is affected until new platelets are formed in 4-7 days
37
What is Reye’s syndrome associated with
Hepatotoxicity
38
Acetylsalicylic acid toxicity
Salicylism, tinnitus, headache, nausea, vomiting, dizziness, dimness of vision, hyperventilation , respiratory alkalosis, death
39
Tinnitus
Ringing in ear
40
When blood levels of salicylates reached a certain level, a toxic reaction occurs
Salicylism
41
Cause of death from aspirin poisoning is usually what?
Acidosis and electrolyte imbalance
42
Prevention of toxicity
Education of parents
43
Lethal dose of acetylsalicylic acid for children and adults
Child: 4 gm Adult: 10-30 gm
44
Warfarin interaction with acetylsalicylic acid
Bleeding and hemorrhage
45
Acetylsalicylic acid interaction with probenecid
Precipitates gout attack
46
Acetylsalicylic acid interaction with methotrexate
Causes increased serum concentration and MTX toxicity
47
Acetylsalicylic acid interaction with sulfonylureas
Hypoglycemia
48
Aspirin interaction with antihypertensives
Reduce the effects of hypertensive agents
49
Uses of aspirin
Analgesia for mild to moderate pain, antiinflammatory, low dose aspirin therapy
50
Chemical classification of nonsteroidal antiinflammatory drugs
``` Propionic acids Acetic acids Fenamates Pyrazolones Oxicams ```
51
What are NSAID’s similar to
Aspirin- inhibition of prostaglandin synthesis by inhibiting COX
52
What enzymes do NSAID’s inhibit
COX l and ll
53
NSAID mechanism of action results in
Reduction in formation of prostaglandin precursors and thromboxanes from arachidonic acid
54
Most NSAID’s peak in
1-2 hours
55
Where are NSAID’s metabolized
Liver
56
Where are NSAID’s excreted
Kidneys
57
NSAID’s are useful for treating what
Dysmenorrhea and gout
58
Gastrointestinal effects of NSAID’s
Irritation, pain, bleeding, interfere with normal stomach protective mechanisms
59
Central nervous system effects of NSAID’s
``` Sedation Dizziness Confusion Mental depression Headache Vertigo Convulsions ```
60
NSAID adverse reactions
``` Blood clotting and myocardial infarction or stroke Muscle weakness Ringing ears Hepatitis Hematologic problems Blurred vision Celecoxib ```
61
Renal effects of NSAID’s
``` Hypertension Renal failure Cystitis Increased urinary tract infection Decrease in renal blood flow Decrease in glomerular filtration rate ```
62
Oral effects of NSAID’s
Ulcerative stomatitis Gingival ulceration Dry mouth
63
Hypersensitivity reactions of NSAID’s
``` Hives or itching Angioneurotic edema Chills and fever Steven Johnson’s syndrome Exfoliative dermatitis Epidermal necrolysis ```
64
Pregnancy and nursing considerations of NSAID’s
Prolong gestation Delay parturition Produce dystocia
65
What drugs are FDA pregnancy category B
Fenoprofen Ibuprofen Naproxen
66
What drugs are FDA pregnancy category c
Diflunisal Tolmetin Medenamic acid
67
NSAID drug reactions
``` Lithium Digoxin Antihypertensives Probenecid Cyclosporin and MTX ```
68
Lithium
May increase lithium toxicity
69
May increase effect of digoxin
Digoxin
70
May decrease effects
Antihypertensives
71
May increase serum levels of NSAID’s
Probenecid
72
Increased toxicity
Cyclosporin and MTX
73
NSAID medical therapeutic uses
``` Osteoarthritis Rheumatoid arthritis Gouty arthritis Fever Dysmenorrhea Pain Bursitis and tendinitis ```
74
NSAID dental therapeutic uses
Pain | Equivalent in analgesia efficacy to opioid analgesics in many clinical situations
75
How long is the half life of ibuprofen (Advil, Motrin)
2 hours
76
Onset of action for ibuprofen (Advil, Motrin)
1/2 hour
77
Duration of ibuprofen
4-6 hours
78
NSAID examples
Naproxen (naprosyn) Naproxen sodium (anaprox) Naproxen sodium otc (aleve) Longer half life than ibuprofen!
79
Other NSAID’s
Cyclo-oxygenase ll specific agent ( fewer adverse reactions) Celecoxib (Celebrex) (Less irritating to stomach)
80
Member of the p-aminophenols
Acetaminophen (Tylenol)
81
Where is acetaminophen absorbed from
GI Tract
82
Peak plasma level of Tylenol
1-3 hours
83
Half life of Tylenol
1-4 hours
84
Tylenol is
Hepatotoxic possibly nephrotixic
85
Tylenol does not..
Have antiinflammatory effects Produce gastric bleeding Affect platelet adhesiveness Affect uric acid excretion
86
Toxic dose of Tylenol
12 gm or more
87
Adverse reactions of Tylenol
Hepatic necrosis | Nephrotoxicity
88
Who should avoid Tylenol
Patients with hepatic disease or who ingest 3 or more alcoholic beverages a day (me on the weekends) 🍺
89
Treatment of toxicity of Tylenol
Gastric lavage Activated charcoal Sulfhydryl groups- oral N-acetylcysteine
90
Associated with long term consumption of acetaminophen
Nephrotoxicity
91
Acetaminophen + aspirin or NSAID’s
Risk of analgesic nephropathy, renal papillary necrosis, end stage renal disease, and cancer of the kidney or bladder
92
Skin reactions to Tylenol
Steven Johnson’s syndrome Toxic epidermal necrolysis Acute generalized exanthematous pustulosis
93
Drug interactions of Tylenol
Hepatotoxicity can be potentiated by agents that induce hepatic microsomal enzymes Chronic, large doses of alcohol
94
Uses of Tylenol
Analgesic Antipyretic Patients with aspirin hypersensitivity Patients with aspirin induced gastric irritation
95
Regular adult dose of Tylenol
325 mg 2 tabs every4-6 hours
96
Extra strength adult dose of Tylenol
650 mg 2 tabs every 6 hours
97
Infant suspension of Tylenol
Per prescribing practitioner
98
JR strength Tylenol for what ages
6-11 years
99
Drugs used to treat gout
Colchicine Allopurinol (zyloprim) Probenecid (benemid)