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Disease And Defense > Glucocorticoid and NSAIDs > Flashcards

Glucocorticoid and NSAIDs Flashcards

1
Q

what synthesizes Arachidonic Acid?

A

Phospholipase A2 breaks down membrane phospholipids

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2
Q

Arachidonic acid is the precursor for…

A

prostaglandins, thromboxane, and leukotriene

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3
Q

Cycooxygenase -1

A

constitutive enzyme, path of arachidonic acid break down involved in prostaglandin and thromboxane synthesis

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4
Q

Cycooxygenase -2

A

enzyme that is both induced with inflammation and constitutive, part of arachidonic acid break down, involved in prostaglandin synthesis

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5
Q

COX-1 ubiquitously located and has these functions …

A

Gastroprotection, platelet aggregation, renal function

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6
Q

COX-1 gastroprotection

A

Decreased pepsin/acid synthesis; increase mucosa and bicarbonate synthesis. This COX1 pathway is gastro-protective. (prostaglandin)

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7
Q

Cox-1 Platelet aggregation

A

pro aggregatory, increased clot formation (thromboxane)

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8
Q

Renal Function - Cox 1

A

Increase renal blood flow to promote diuresis (prostaglandin)

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9
Q

Side effects when COX-1 is inhibited?

A

Gi ulceration and dyspepsia (bleeding), prolonged bleeding, acute renal failure

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10
Q

COX 2 has these functions..

A

Pain, Fever, Inflammation, Renal Function, Endothelial vasodilation, Uterine contractions, Ductus Arteriosus prolongation

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11
Q

COX-2 Pain

A

potentiation of bradykinin (prostaglandin)

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12
Q

COX-2 Fever

A

Increased heat generation and decreased heat loss (prostaglandin)

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13
Q

Cox -2 Inflammation

A

Enhanced edema and leukocyte infiltration

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14
Q

Cox-2 Renal Function

A

Maintenance of renal blood flow

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15
Q

Endothelial Cells - Cox2

A

Vasodilation and antiaggregatory;

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16
Q

Uterus - Cox 2

A

Labor contraction

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17
Q

Ductus arteriosus

A

prolonged opening

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18
Q

Side Effects when COX2 is inhibited?

A

Acute renal failure, thrombosis/increased risk of MI and stroke, prolonged gestation, premature closure of ductus arteriosus

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19
Q

Therapeutic Effect of COX2 inhibition?

A

Antipyretic, anti-inflammatory, analgesic

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20
Q

Aspirin CoX 1 or 2? Reversible or Irreversible?

A

Cox 1/2 Irreversible

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21
Q

NSAIDs CoX 1 or 2? Reversible or Irreversible?

A

Cos 1/2, Reversible

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22
Q

Acetaminophen CoX 1 or 2? Reversible or Irreversible?

A

COX 2 reversible in the CNS

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23
Q

Celecoxib

A

COX2 reversible

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24
Q

Therapeutic Analgesia

A

inhibition of inducible COX2 at site of injury

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25
Q

Antipyretic Therapeutic Effect

A

inhibition of inducible COX2 in hypothalamus

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26
Q

Anti-inflammaotry Therapeutic Effect

A

Inhibition of inducible COX-2 at sites of inflammation

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27
Q

Anti-thrombogenesis Therapeutic Effect

A

Inhibition of constitutive COX1 in platelets

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28
Q

GI side effects are due to…

A

inhibition of constitutive COX-1 in gastric cells

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29
Q

Increased bleeding is due to…

A

inhibition of constitutive COX-1 in in platelets

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30
Q

Renal Side Effects are due to..

A

Inhibition of constitutive COX-1 or Induced COX-2 in kendey cells

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31
Q

Uterine side effects are due to..

A

inhibition of induced COX-2 in uterine smooth muscle

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32
Q

Increased thrombotic events are due to..

A

unopposed inhibition of COX3 in vascular endothelial cells

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33
Q

Aspirin Therapeutic Effects

A

Analgesic, Antipyretic, Anti-inflammatory, Anti-plaetlet

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34
Q

NSAIDs therapeutic effects

A

Analgesic, Antipyretic, Anti-inflammatory

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35
Q

Acetaminophen therapeutic effects

A

Analgesic, Antipyretic,

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36
Q

Celecoxib therapeutic effects

A

Analgesic, Antipyretic, Anti-inflammatory

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37
Q

which COX1 and COX 2 inhibitors are analgesic?

A

ALL

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38
Q

which COX1 and COX 2 inhibitors are antipyretic?

A

All

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39
Q

which COX1 and COX 2 inhibitors are antiinflammatory?

A

All except acetaminophen

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40
Q

which COX1 and COX 2 inhibitors are anti—platelet?

A

Only aspirin

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41
Q

Aspirin side Effects

A

GI Upset, Increased bleeding, Renal Failure, Decreased Labor

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42
Q

NSAIDs Side Effects

A

GI upset, Increased Bleeding, Renal Failure, Decreased Labor

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43
Q

Acetaminophen Side Effects

A

None

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44
Q

Celecoxib Side Effects

A

Renal Failure, Decreased labor, increased clotting, closure of ductus arteriosus

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45
Q

Which medications cause GI upset?

A

Aspirin and NSAIDs

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46
Q

Which medications cause Increased bleeding?

A

Aspirin and NSAIDs

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47
Q

Which medications cause increase renal failure?

A

Aspirin, NSAIDs, Cox-2 selective

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48
Q

Which medications cause decreased labor/contractions?

A

Aspirin, NSAIDS, COX-2 selective

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49
Q

What medications cause increased clotting?

A

COX-2 selective

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50
Q

NSAID dose for Pain/Fever reducer

A

Moderate

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51
Q

NSAID dose for Inflammation

A

high

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52
Q

Which is more effective for acute pain - NSAID, Aspirin, Acetaminophen?

A

NSAIDs

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53
Q

Toradol

A

IM or IV NSAID used to treat post-surgical pain

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54
Q

what should dysmenorrhea be treated with?

A

NSAIDs

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55
Q

Which is more effective for fever - NSAID, Aspirin, Acetaminophen?

A

all equal

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56
Q

Contraindications of NSAIDs

A

Advanced age, prior NSAID gastropathy or history of peptic ulcer disease, concurrent glucocorticoid use; anti-coagulent agent, patients with heart failure, hypertension, diabetes

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57
Q

Solutions of GI upset of NSAIDs

A

food or antacids; PPI to protect against gastroduodenal toxicity

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58
Q

Bleeding Effects Aspirin vs. NSAID

A

less bleeding in NSAID (around 2 days active); Aspirin is active 4-7 days

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59
Q

GI upset Aspirin vs. NSAID

A

Less GI upset compared to aspirin

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60
Q

Renal dysfunction Aspirin vs. NSAID

A

greater for NSAID, causes Renal blood flow, increased fluid retention and BP

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61
Q

What NSAID would you prescribe to a person at risk of GI bleed?

A

Ibuprofen because it has greater COX2 inhibition than COX1

62
Q

What NSAID would you prescribe to a person at risk of cardiac problems?

A

Naprozen because it has greater COX1 inhibition over COX2

63
Q

NSAID use in pregnancy

A

not established, not recommended especially in 3rd trimester

64
Q

Celecoxib - what is selectivity of COX2 compared to COX 1?

A

5-7x more inhibition of COX2

65
Q

Celecoxib metabolism

A

in liver with renal excretion; metabolized by CYP2C9; long half life allowing 1-2 times per day dosing

66
Q

Clinical uses of Celecoxib

A

rheumatoid arthritis, osteoarthritis, dysmenorrhea, acute pain; benefits outweigh risks for those who cannot use NSAIDs due to GI bleeding risk

67
Q

Adverse Reactions with Celecoxib

A

prothrombotic potential to increase MI risk

68
Q

Pain reflief Celecoxib vs. NSAIDs

A

less effective for acute pain than NSAIDs

69
Q

Inflammation relief Celecoxib vs. NSAIDs

A

equal for osteo and rheumatoid arthritis

70
Q

GI upset in Celecoxib vs. NSAIDs

A

Less than NSAIDs at low dose, but equal at high dose.

71
Q

avoid use of Celecoxib in these patients…

A

Chronic renal insufficiency, severe heart disease, volume depletion, hepatic failure

72
Q

Celecoxib in pregnancy

A

not recommended, especially in 3rd trimester

73
Q

Acetaminophen limitations

A

Not-antiinflammatory; limited to 4g/day due to hepatotoxicity.

74
Q

Pain/fever dose for acetaminophen

A

moderate; less effective than NSAIDs for moderate pain

75
Q

Adverse Effects of Acetaminophen

A

Hepatotoxicity - liver damage

76
Q

what dose of acetaminophen causes toxicity

A

single 6 mg dose; also 5-8 mg/day for several weeks or 3-4 g/dy for 1 year

77
Q

How does alcohol influence acetaminophen toxicity

A

alcohol induces CYP2E1 to produce toxic metabolite; thus may achieve toxicity at lower doses

78
Q

Treatment of acetaminophen toxicity

A

N-Acetylcysteine (substitute glutathione in inactive toxic metabolite)

79
Q

Max dose for acetaminophen

A

4000 mg/24 hours

80
Q

Pregnancy and acetaminophen

A

safe in all stages, but only for therapeutic short term use

81
Q

Aspirin - what type of pain does it work with?

A

inflammatory origin, less effective in visceral pain

82
Q

Antipyretic effect of aspirin

A

reduced elevated body temperature (not normal)

83
Q

Aspirin Anti-platelet function

A

low dose aspirin has larger effect on circulating platelet COX1 than tissue endothelial COX 2 - resulting in decreased tendency for clotting

84
Q

Warfarin and Heparin interactions

A

inhibit platelet function - hemorrhage

85
Q

Alcohol with additive gastric irritation

A

internal bleeding

86
Q

Glucocorticoids

A

principally involved in carbohydrate and protein metabolism and anti-inflammatory response through cortisol

87
Q

Mineralcorticoids

A

principally involved in Na Retention through Aldosterone

88
Q

Dihydroandrostenedione (DHEA)

A

works with androstenedione to have weak androgenic active, but some DHEA is converted to testosterone and estradiol outside of adrenal gland.

89
Q

ACTH

A

Adrenocorticopropic hormone - release from pituitary and under the control of the Corticotropin release factor from hypothalamus. Controls synthesis and secretion of clutocorticoids

90
Q

Negative feedback in the hypothalamic pituitary adrenal axis

A

circulating corticosteroids (both endogenous and exogenous) act on hypothalamus AND pituitatary to decrease ACTH release.

91
Q

Adrenal Crisis

A

chronic glucocorticoid can suppress HPA axis and results in adrenal atrophy and insufficient adrenal release

92
Q

Stress and the HPA axis

A

injury, hemorrhage, infection, surgery, hypoglycemia, cold, pain, fear, override negative feedback loop to produce increased levels of steroid.

93
Q

Cortisol Binding Globulin

A

binds to free cortisol in plasma and enters cells as free molecule.

94
Q

What does cortisol in cytoplasm bind to?

A

HSP90

95
Q

what does binding to HSP90 to cortisol do?

A

allows dimerization of S-R complex and entry into the nucleus to bind to glucocorticoid response element on DNA.

96
Q

What genes dos Gluccocortcoid Response Element control?

A

transcription of genes that bring about the delayed hormone response.

97
Q

Secretion of natural cortisol is highest…

A

during the early AM and after meals

98
Q

Which is more active, bound cortisol or free?

A

Free, 75% of cortisol is bound

99
Q

Half life of Cortisol

A

60-90minutes; prolonged in stress

100
Q

changes to cortisol in glucocorticoid drugs?

A

altered protein binding, prolonged half life, separation of mineralocorticoid activity from glucocorticoid activity

101
Q

Metabolic Effects of Glucocorticoids

A

Stimulates gluconeogenesis to increase blood glucose and glyocogen synthesis; increase Amino acid uptake in liver and kidney for decreased protein synthesis (transfer of AA to liver) can lead to muscle wasting; inhibit glucose uptake by fat to stimulate glycolysis (increased lipogenesis); net result maintenance of glucose supply to brain

102
Q

Carbohydrate effect of glucocorticoids

A

increased blood sugar and glyocogen synthesis for diabets like state

103
Q

Protein effect of glucocorticoids

A

increased uptake of AA into liver and kidney for overall decreased protein synthesis and muscle wasting

104
Q

Lipid effect of glucocorticoids

A

inhibit uptake of glucose by fat cells to stimulate lipolysis (net effect though is lipogenesis) that leads to centripetal obesity (abdominal fat)

105
Q

Mechanism of Mineralocorticoids

A

aldosterone binds to cytosolic receptor and migrate to nucleus to induce formation of mRNA for synthesis of Na/K ATPase channels for reabsorption of Na and increased secretion of H and K.

106
Q

Pharmocologic reasoning for glucocorticoids

A

suppress inflammation and immune response

107
Q

Anti-inflammatory Glucocorticoids

A

decreased synthesis of inflammatory and immune mediators; decreased production/action of cytokines; reduced generation of leukotrienes and prostalandinds vis decreased COX-2 and inhibition of phospholipase A2

108
Q

Immunosuppresive Effects of Glucocorticoids

A

reduction in chronic inflammation and autoimmune reactions, but decreased healing and diminution of protective aspects of immune system

109
Q

Four actions of glucocorticoids

A

1) suppress Tcell activation 2) suppress cytokine production 3) preventing mast cells and eosinophils form release chemical mediators of inflammation

110
Q

Mast cells release

A

histamine, prostaglandins, leukotrienes

111
Q

Eosinophils release

A

histamine, leukotrienes, cationic proteins

112
Q

What do mediators of inflammation cause

A

tissue damage, vasodilation, edema

113
Q

Glucocorticoid vascular effects

A

reduced vasodilation, decreased fluid exudation

114
Q

GLucocorticoid effects on cellular events

A

decrease in accumulation and activation of cells

115
Q

glucocorticoids on acute inflammation

A

decrease number and activity of leukoctyes; neutrophils increase in circulation, but movement into peripheral tissues is decreased

116
Q

Glucocorticoids on chronic inflammation

A

decreased activity of monocytes and lymphocytes, decreased proliferation of Blood vessles, less fibrosis

117
Q

Glucocorticoids on lymphoid areas

A

decreased clonal expansion of T and B cells, decrease cytokine secreting cells

118
Q

11-hydroxy

A

glucocorticoids are physiologically active

119
Q

11-keto

A

glucocorticoids are prodrugs that must be activated - prednisone and cortisone

120
Q

11Beta-Hydrozysteroid dehydrogenase

A

converst to active or inactive glucocorticoids depending on lcoations

121
Q

11Beta-HSD1 in liver

A

converts cortisone to cortisol (prednisone to prednisolone) in Activating step

122
Q

11Beta-HSD2 in kidney

A

converts Cortisol to cortisone - inactivating step

123
Q

11Beta-HSD2 in fetus

A

inactivating form is active in fetus, but 11Beta HSD1 is not functional in liver. Thus can treat mother with glucocorticoids without effect on fetus because placental enzymes can covert active drug back to prodrug

124
Q

Treating fetus with glucocorticoids

A

poor substrate for 11beta-HSD2 (betamethasone)

125
Q

Cortisol

A

hydrocortisone - use in physiologic doses for replacement therapy and emergencies; activated from cortisone in liver

126
Q

Cortisol Glucocorticoid:mineralcorticoid acitivty

A

1 to 1

127
Q

Cortisol forms

A

Orally, injectable, topical

128
Q

Prednisone

A

use for steroid burst therapy; not activated until first pass from liver

129
Q

Prednisone Glucocorticoid:mineralcorticoid acitivty

A

13 gluco to 1 mineral

130
Q

Prednisone forms

A

Orally

131
Q

Methylprednisolone

A

use of parenteral administration during steroid burst

132
Q

Methylprednisolone Glucocorticoid:mineralcorticoid acitivty

A

NO mineralcorticoid activity

133
Q

Methylprednisolone forms

A

Oral, Injectable

134
Q

Dexamethasone

A

most potent antiinflammaotry, used in cerebral edema, chemo induced vomiting

135
Q

Dexamethasone Glucocorticoid:mineralcorticoid acitivty

A

most potent antiinfalmmatory, no mineralocorticoid

136
Q

Triamcinolone

A

potent systemic agent, excellent topical, no mineralcorticoid

137
Q

Dosage of Glucocorticoid

A

determined by trial and error; considered by minimal amount for desired effect, duration of therapy; alternative day schedule; tapered otherwise might cause rebound of disease or adrenal insuffienciency

138
Q

Acute affects of mineralocorticoid overdose

A

edema, increased BP, hypokalemia

139
Q

Acute affects of glucocorticoid overdose

A

glucose intolerance, mood changes, insomnia, GI upset

140
Q

High dose sustained Glucocorticoid therapy >2 weeks

A

Iatrogeni cushing’s syndrome, hypothalamic pituitary adrean axis suppression, mood disturbance, impaired wound healing; increased suseptabillty to infection

141
Q

Iatrogenic Cushing Syndrome

A

hyperglycemia, protein wasting in muscle, lipid deposion (weight gain) in diabetes like state.

142
Q

Hypothalamic-Pituitary Adrenal Axis Suppresion

A

insufficient response to stress, decreased ACTH, GH, TSH, LH, sex steroids

143
Q

Possible side effects of large cumulative doses of glucocorticoids

A

Osteoporosis; posteror capsular cataracts, skin atrophy, growth retardation in children, peptic ulceration

144
Q

Osteoporosis in glucocorticoid use

A

decrease in osteoblast, blockage of Vitamin D3, decrease calcium aborsption and increase PIH release.

145
Q

Skin atrophy in glucocorticoid use

A

loss of collagen support

146
Q

Growth retardation in children with glucocorticoids

A

decreased growth hormone secretion and impaired somatomedins.

147
Q

Fludrocortisone

A

glucocorticoid with high anti-inflammatory (10), but extra high mineralocorticoid activity (250). only available in oral form.

148
Q

Which glucocorticoids have no topical activity?

A

cortisone and prednisone

149
Q

Potency of Glucocorticoids.

A

most potent is dexamethasome, leas is hydrocortisone; in between is methylprednisolone and triamcinolone.

150
Q

which glucocorticoids have topical activity

A

hydrocortisone, triamcinolone, dexamethasone

Disease And Defense (7 decks)

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