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Musculoskeletal and Connective Tissue > Musculoskeletal,skin,and connective tissue drugs > Flashcards

Musculoskeletal,skin,and connective tissue drugs Flashcards

1
Q

Membrane phospholipids to arachidonic acid - pathways (and steps)

A

2 pathways:
1. (leukotriene synthesis) arachidonic acid –> 5-HPETE
(5-lipoxygenase) –> Leukotrienes
2. (endoperoxide synthesis) arachidonic acid –> cyclic endoperoxides (COX1/2) –> prostacyclin/prostagladins/thromboxane

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2
Q

5-HPETE

A

5-hydroperoxyeicosatetraenoic acid

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3
Q

Leukorienes - types and action

A

LTB4–> increased neutrophil chemotaxis
LTC4 –> increased bronchial tone
LTD4 –> increased bronchial tone
LTE4 –> increased bronchial tone

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4
Q

5-Lipoxygenase inhibitor

A

Zileuton

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5
Q

Zileuton - clinical use / side effects

A

asthma

SE: hepatotoxicity

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6
Q

Leukotriene receptor antagonists (which receptor)

A

Montelukast
Zafirlukast
(LTC4, LTD4, LTE4)

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7
Q

Montelukast, Zafirlukast - clinical use

A

aspirin-induced asthma

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8
Q

Thromboxane - types and action

A

TXA2 –> increased aggregation, increased vascular tone

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9
Q

COX -2 inhibitor (only)

A

celecoxib

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10
Q

COX - 1/2 inhibitor

A

ASPIRIN (irreversible) and other NSAIDs

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11
Q

Membrane phospholipids to arachidonic acid - pathways

A
  1. leukotriene syntehsis

2. Endoperoxide synthesis

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12
Q

Prostacyclin types and action

A

PGI2 –> decreases aggregation and vascular tone (vasodilation)

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13
Q

Prostagladins types and action

A

PGE1 –> decrease vascular tone (vasodilation)
PGE2 –> increases uterine tone
PGF2 –> increases uterine tone

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14
Q

PGI2 is a

A

prostacyclin

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15
Q

TXA2 is a

A

thromboxane

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16
Q

PGI2 analog

A

epoprostenol

iloprost

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17
Q

PGE1 analog

A

alprostadil

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18
Q

PGE2 analog

A

Dimopristone

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19
Q

PGF2 analog

A

carboprost

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20
Q

acetaminophen - mechanism of action

A

reversible inhibits cycloxygenase, mostly in CNS. INACTIVATED PERIPHERALLY

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21
Q

acetaminophen action in periphery

A

INACTIVATED PERIPHERALLY

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22
Q

clinical use of acetaminophen

A

antipyretic and analgesic

NOT ANTI - INFLAMMATORY

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23
Q

acetaminophen action against inflammation

A

NOT ANTI - INFLAMMATORY

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24
Q

acetaminophen vs aspirin in children with viral infection

A

acetaminophen is used to avoid Reye syndrome

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25
Q

acetaminophen toxicity

A

overdose produce hepatic necrosis

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26
Q

acetaminophen toxicity - mechanims

A

overdose –> acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue byproducts in liver –> hepatic necrosis

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27
Q

antidote of acetaminophen toxicity and mechanism

A

N-acetylcysteine –> regenerates glutathione

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28
Q

N-acetylcysteine -clinical use

A
  1. cystic fibrosis (mucolytic)

2. antidote of acetaminophen toxicity

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29
Q

acetaminophen - reversible or irreversible inhibition of COX

A

REVERSIBLE

30
Q

Aspirin - mechanism of action

A

irreversible inhibits COX (both 1/2) via covalent acetylation, which decreases synthesis of TXA2 and prostaglandins. Effects lasts until new new platelets produced
ITS A TYPE OF NSAID

31
Q

Aspirin - PT, PTT

32
Q

Aspirin - bleeding time

33
Q

Clinical use of aspirin (and doses)

A 
Low dose, under 300 (inhibits platelet aggregation)
Intermediate dose (300-2400mg/day) --> antypyretic and analgesic
High dose (2400-4000mg/day) --> anti-inflammatory
34
Q

Aspirin - side effects

A
  1. Gastric ulceration 2. tinnitus (CN VIII)

3. Acute renal failure (chronic use) 4. interstitial nephritis 5. GI bleeding 6. Reye syndrome 7. pH disturbances

35
Q

Aspirin - pH disturbances

A

respiratory alkalosis early (hyperventilation)

transition to mixed metabolic acidosis-respiratory alkalosis

36
Q

COX-2 - area

A

inflammatory cells and vascular endothelium

37
Q

COX-2 mediates

A

inflammation and pain

38
Q

Celecoxib - mechanism of action

A

reversible inhibition of COX-2 (only)

39
Q

Celecoxib spares COX-1 - clinical importance

A

maintain gastric mucosa

40
Q

celecoxib vs other NSAID according side effects

A

celecoxib does not have the corrosive effects of ther NSAID on the GI lining

41
Q

beside gastric mucosa, celecoxib spares …. function (why)

A

it spares platelet function as TXA2 production is depended on COX-1

42
Q

TXA2 production is depended on

43
Q

NSAID - drugs

A
  1. ibuprofen 2. naproxen 3. indromethacin 4. ketorolac 5. diclofenac 6. meloxicam 7. piroxicam
44
Q

NSAID - mechanism

A

REVERSIBLE inhibit cyclooxygenase (both COX 1 and 2)

–> block prostaglandin synthesis

45
Q

clinical use of NSAID

A
  1. antipyretic 2. analgesic 3. anti-inflammatory

4. Indomethacin is uded to close PDA

46
Q

toxicity of NSAID

A
  1. interstitial nephritis 2. gasrtic ulcers 3. renal ischemia
47
Q

NSAID can cause renal ischemia - mechanism

A

prostagladins vasofilate afferent arteriole

48
Q

Bisphosphonates - drugs

A

alendronate and other -DRONATES

49
Q

Bisphosphonates - mechanism

A

pyrophosphate analogs –> hydroxyapatite in bone –> inhibition of osteoclasts

50
Q

Bisphosphonates - clinical use

A
  1. osteoporosis
  2. hypercalcemia
  3. Paget disease of bone
  4. metastatic bone disease
  5. osteogenesis imperfecta
51
Q

Teriparatide - mechanism of action

A

Recombinant PTH analog –> increases osteoblastic activity

52
Q

Teriparatide - administration

A

subcutaneously/daily

53
Q

Teriparatide - clinical use (explain)

A

osteoporosis –> causes increased growth compared to antirepsorptive therapies (eg. biphosphanates)

54
Q

Teriparatide - toxicity

A
  1. transient hypercalcemia

2. May increase risk of osteosarcoma (seen in rodent studies)

55
Q

TNF-a inhibitors - drugs and mechanism of action

A
  1. etanercept - fusion protein (receptor for TNF-A+IgG1 FC) produced by recombinant DNA
  2. infliximab - anti-TNF-a monoclonal antibody
  3. adalimumab - anti-TNF-a monoclonal antibody
  4. certolizumab - anti-TNF-a monoclonal antibody
56
Q

all TNF-a inhibitors predispose to

A

infection, including reactivation of latent TB

57
Q

TNF-a inhibitors predispose to TB reactivation - mechanism

A

TNF is important in granuloma formation and stabilization

58
Q

infliximab - mechanism of action

A

anti-TNF-a monoclonal antibody

59
Q

abalimunab - mechanism of action

A

anti-TNF-a monoclonal antibody

60
Q

Etanercept - mechanism of action

A

fusion protein (receptor for TNF-A+IgG1 FC) produced by recombinant DNA

61
Q

Etanercept - clinical use

A
  1. Rheumatoid arthritis
  2. psoriasis
  3. ankylosing spondylitis
62
Q

infliximab and adalimumab - clinical use

A
  1. inflammatory bowel disease
  2. rheumatoid arthritis
  3. ankylosing spondylitis
  4. psoryasis
63
Q

bisphosphonates - side effects

A
  1. corrosive esophagitis (patients are advised to take with water and remain upright for 30 mins)
  2. osteonecrosis of jaw
64
Q

bisphosphonates - vs Teriparatide according action on osteoporosis

A

bisphosphonates –> anti-resorptive

Teriparatide –> induce bone growth

65
Q

celecoxib - side effects

A
  1. increased risk of thrombosis

2. sulfa allergy

66
Q

celecoxib - clinical use

A
  1. Rheumatoid arthritis

2. osteoarthritis

67
Q

Rasburicase - mechanism of action

A

Recombinant uricase that catalyzes metabolism of uric acid to allanotin

68
Q

Rasburicase - clinical use

A

Prevention and treatment of tumor lysis syndrome

69
Q

Rasburicase - mechanism of action / clinical use

A

Recombinant uricase that catalyzes metabolism of uric acid to allanotin
Clinical use: Prevention and treatment of tumor lysis syndrome

70
Q

Leflunamide - mechanism of action

A

Reversibly inhibits dihydroorotate dehydrogenase –> prevent pyrimidine synthesis –> suppresses T-cell proliferation

71
Q

Leflunamide - clinical use

A
  1. RA

2. psoriatic arthritis

72
Q

Leflunamide - adverse effect

A
  1. Diarrhea
  2. hypertension
  3. hepatotoxicity
  4. teratogenicity

Musculoskeletal and Connective Tissue (19 decks)

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