Brainscape's Knowledge GenomeTM

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


See full index

MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE > MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE- Pharmacology > Flashcards

MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE- Pharmacology Flashcards

1
Q

Products of Arachidonic Acid

A

Lipoxygenase

Cyclooxygenase

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

Products of Arachidonic Acid

A

Lipoxygenase

Cyclooxygenase

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

What is the product of Phospholipase A2?

A

Arachidonic Acid

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

What produces Phospholipase A2?

A

Membrane lipid (eg. phosphatidylinositol)

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

Which drug inhibit Phospholipase A2 and protein synthesis to Cyclooxigenase?

A

Corticosteroids

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

Drug that inhibits Lipoxigenase pathway

A

Zileuton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which drugs inhibit Leukotrienes?

A

Zafirlukast

Montelukast

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

Which drugs inhibit just Cyclooxygenase?

A

NSAIDS, aspirin, acetaminophen, COX- 2 inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which pathway yields Leukotrienes?

A

Lipoxygenase

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

Effect of LTB4

A

Neutrophil chemotactic agent

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

Which is the function of LTC4, D4 and E4?

A

Bronchoconstriction, vasoconstriction, contriction of smooth muscle and ↑ vascular permeability

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

Products of Cyclooxygenase

A

Endoperoxides

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

Which are the products of Endoperoxides?

A

Prostacyclin
Prostaglandins
Thromboxane

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

PGI2

A

Prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Who forms Prostaglandins?

A

PGE2

PGF 2 α

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Before getting to leukotrienes, what is the product of Lipoxygenase?

A

Hydroperoxides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name effects of PGI2

A

↓ Platelet aggregation
↓ Vascular tone
↓ bronchial tone
↓ uterine tone

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

What is the effect of Prostaglandins?

A

↓ Bronchial tone

↑ Uterine tone

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

Main effects of Prostaglandins

A

↑ Platelet aggregation
↑ Vascular tone
↑ Bronchial tone

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

Mechanism of action of Aspirin

A

Irrevisbly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation, which ↓ synthesis of both thromboxane A2 (TXA2) and prostaglandins

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

Which cyclooxygenase are inhibited by Aspirin?

A

Both COX-1 and COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the effect of Aspirin related to bleeding?

A

↑ Bleeding time until new platelets are produced

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

How much time does it takes to produce new plateles?

A

7 days

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

How are coagulation time affected by Aspirin?

A

No effect on PT and PTT

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

How is Aspirin calssified?

A

A type of NSAID

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

Low dose of Aspirin

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the clinical use of Low dose Aspirin?

A

↓ low platelet aggregation

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

Intermediate dose of Aspirin

A

300-2400 mg/day

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

Clinical use for Intermediate dose of Aspirin

A

Antipyretic and analgesic

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

Dosis consider to be high of Aspirin

A

2400 - 4000 mg/ day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical use for High dose aspirin

A

As inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Toxic effects caused by Aspirin

A

Gastric ulceration

Tinitus (CN VIII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the risk of chronic use of Aspirin?

A

Acute renal failure, interstitial nephritis and upper GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Respiratory secondary effects caused by Aspirin use

A

Stimulates respiratory centers, causing hyperventilation and respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Respiratory secondary effects caused by Aspirin use

A

Stimulates respiratory centers, causing hyperventilation and respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the product of Phospholipase A2?

A

Arachidonic Acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What produces Phospholipase A2?

A

Membrane lipid (eg. phosphatidylinositol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which drug inhibit Phospholipase A2 and protein synthesis to Cyclooxigenase?

A

Corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Drug that inhibits Lipoxigenase pathway

A

Zileuton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Which drugs inhibit Leukotrienes?

A

Zafirlukast

Montelukast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which drugs inhibit just Cyclooxygenase?

A

NSAIDS, aspirin, acetaminophen, COX- 2 inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which pathway yields Leukotrienes?

A

Lipoxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Effect of LTB4

A

Neutrophil chemotactic agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which is the function of LTC4, D4 and E4?

A

Bronchoconstriction, vasoconstriction, contriction of smooth muscle and ↑ vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Products of Cyclooxygenase

A

Endoperoxides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which are the products of Endoperoxides?

A

Prostacyclin
Prostaglandins
Thromboxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

PGI2

A

Prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Who forms Prostaglandins?

A

PGE2

PGF 2 α

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Before getting to leukotrienes, what is the product of Lipoxygenase?

A

Hydroperoxides

50
Q

Name effects of PGI2

A

↓ Platelet aggregation
↓ Vascular tone
↓ bronchial tone
↓ uterine tone

51
Q

What is the effect of Prostaglandins?

A

↓ Bronchial tone

↑ Uterine tone

52
Q

Main effects of Prostaglandins

A

↑ Platelet aggregation
↑ Vascular tone
↑ Bronchial tone

53
Q

Mechanism of action of Aspirin

A

Irrevisbly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation, which ↓ synthesis of both thromboxane A2 (TXA2) and prostaglandins

54
Q

Which cyclooxygenase are inhibited by Aspirin?

A

Both COX-1 and COX-2

55
Q

What is the effect of Aspirin related to bleeding?

A

↑ Bleeding time until new platelets are produced

56
Q

How much time does it takes to produce new plateles?

A

7 days

57
Q

How are coagulation time affected by Aspirin?

A

No effect on PT and PTT

58
Q

How is Aspirin calssified?

A

A type of NSAID

59
Q

Low dose of Aspirin

A
60
Q

What is the clinical use of Low dose Aspirin?

A

↓ low platelet aggregation

61
Q

Intermediate dose of Aspirin

A

300-2400 mg/day

62
Q

Clinical use for Intermediate dose of Aspirin

A

Antipyretic and analgesic

63
Q

Dosis consider to be high of Aspirin

A

2400 - 4000 mg/ day

64
Q

Clinical use for High dose aspirin

A

As inflammatory

65
Q

Toxic effects caused by Aspirin

A

Gastric ulceration

Tinitus (CN VIII)

66
Q

What is the risk of chronic use of Aspirin?

A

Acute renal failure, interstitial nephritis and upper GI bleeding

67
Q

Risk of aspirin use in children

A

Reye syndrome when treating viral infections`

68
Q

Respiratory secondary effects caused by Aspirin use

A

Stimulates respiratory centers, causing hyperventilation and respiratory alkalosis

69
Q

NSAIDs

A

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac

70
Q

Mechanism of NSAIDs

A

Reversibly inhibit cyclooxygenase (both COX-1 and COX-2)

Block PG synthesis

71
Q

Clinical use of NSAIDs

A

Antypiretic, analgesic, anti-inflammatory

72
Q

NSAID use to close PDA

A

Indomethacin

73
Q

Alternative use of Indomethacin

A

NSAID use to close PDA

74
Q

Secondary effects of NSAIDs

A

Interstitial nephritis, gastric ulcer, renal ischemia

75
Q

Why NSAIDs cause gastric ulcer?

A

Because they inhibit PGs that protect gastric mucosa

76
Q

Why NSAIDs cause renal ischemia?

A

Because they inhibit PGs that vasodilate afferent arteriole

77
Q

COX-2 inhibitors

A

Celecoxib

78
Q

Mechanism of action of Celecoxib

A

Reversibly inhibits specifically the cyclooxygenase isoform 2

79
Q

Cellular effect of Colchicine

A

Impairing leukocyte chemotaxis and degranulation

80
Q

Which benefit do COX-2 inhibitors have compared to NSAIDs?

A

Spares COX-1, which helps maintain the gastric mucosa

Spares platelet function as TXA-2 production is dependent on COX-1

81
Q

When is recommended the clinical use of Celecoxib?

A

Rheumatoid arthritis and osteoarthritis; patiens with gastritis or ulcers

82
Q

What are the risks of COX-2 inhibitors use?

A

↑ risk of thrombosis

Sulfa allergy

83
Q

Mechanism of action of Acetaminophen

A

Reversibly inhibits cyclooxygenase, mostly in CNS

84
Q

Where is Acetaminophen inactivated?

A

Peripherally

85
Q

Effect of Acethaminophen

A

Antipyretic, analgesic, but not anti-inflammatory

86
Q

Used instead of aspirin to avoid Reye syndrome in children with viral infection

A

Acetaminophen

87
Q

Secondary effect of acetaminophen overdose

A

Hepatic necrosis

88
Q

How does acetaminophen produces hepatic necrosis?

A

Acetaminophen metabolite (NAPQI) deplets glutathione and forms toxic tissue adducts in liver

89
Q

Which is Acetaminophen metabolite?

A

NAPQI

90
Q

Antidote of Acetaminophen

A

N acetylcysteine is antidote

91
Q

What is the effect of N acetylcysteine in Acetaminophen overdose?

A

Regenerates Glutathione

92
Q

Biphosphonates drugs

A

Alendronate, other -dronates

93
Q

Pyrophosphate analogs

A

Biphosphonate

94
Q

Mechanism of action of Biphosphonates

A

Bind hydroxyapatite in bone, inhibiting osteoclast activity

95
Q

Clinical use of Biphosphonates

A

Osteoporosis, hypercalcemia, Paget disease of bone

96
Q

Toxic effect caused by biphosphonates

A

Corrosive esophagitis, osteonecrosis of the jaw

97
Q

In order to prevent corrosive esophagitis, what is recommended when indicating biphosphonates?

A

Patients are advised to take with water and remain upright for 30 minutes

98
Q

How is the treatment for Gout classified?

A

Chronic gout drugs (preventive)

Acute gout drugs

99
Q

Chronic gout drugs

A

Allopurinol
Febuxostat
Probenecid

100
Q

Mechanism of action of allopurinol

A

Inhibits xanthine oxidase, ↓ conversion of xanthine to uric acid

101
Q

Other clinical use for Allopurinol

A

Also used in lymphoma and leukemia to prevent tumor lysis associated urate nephropathy

102
Q

What is increased with allopurinol use?

A

Increases concetration of azathioprine and 6 MP

103
Q

What metabolizes Azathioprine and 6 MP?

A

By xanthine oxidase

104
Q

What is contraindicated when using allopurinol?

A

Salicylates

105
Q

Why Salicylates are contraindicated when using allopurinol?

A

All but the highest doses depress uric acid clearance

106
Q

High doses of Allopurinol

A

5-6 g/day

Have only minor uricosuric activity

107
Q

Mechanism of action of Febuxostat

A

Inhibits xanthine oxidase

108
Q

Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin)

A

Probenecid

109
Q

Drugs used for Acute gout

A

NSAIDs
Glucocorticoids
Colchicine

110
Q

NSAIDs recommended for acute gout

A

Naproxene, indomethacin

111
Q

Administration way of Glucocorticoids for acute gout

A

Oral or intraarticular

112
Q

Binds and stabilizes tubulin to inhibit microtubule polymerization

A

Colchicine

113
Q

Cellular effect of Colchicine

A

Impairing leukocyte chemotaxis and degranulation

114
Q

Risk of using TNF α inhibitors

A

Predispose to infection, including reactivation of latent TB

115
Q

Why TNF α inhibitors predisposes to infection?

A

TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes

116
Q

TNF α inhibitors

A

Etanercept

Infliximab, adalimumab

117
Q

Fusion protein (receptor for TNF α + IgG1 Fc), produced by recombinant DNA

A

Etanercept

118
Q

Clinical use of Etanercept

A

Rheumatoid arthritis, psoriasis, ankylosing spondylitis

119
Q

Mechanism of action of Infliximab, adalimumab

A

Anti TNF α monoclonal antibody

120
Q

Clinical use for Infliximab, adalimumab

A

Inflammatory Bowel disease
Rheumatoid arthritis
Ankylosing spondylitis
Psoriasis

MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE (3 decks)

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