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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
acetaminophen toxicity
overdose produce hepatic necrosis
26
acetaminophen toxicity - mechanims
overdose --> acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue byproducts in liver --> hepatic necrosis
27
antidote of acetaminophen toxicity and mechanism
N-acetylcysteine --> regenerates glutathione
28
N-acetylcysteine -clinical use
1. cystic fibrosis (mucolytic) | 2. antidote of acetaminophen toxicity
29
acetaminophen - reversible or irreversible inhibition of COX
REVERSIBLE
30
Aspirin - mechanism of action
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
Aspirin - PT, PTT
no effect
32
Aspirin - bleeding time
increased
33
Clinical use of aspirin (and doses)
``` Low dose, under 300 (inhibits platelet aggregation) Intermediate dose (300-2400mg/day) --> antypyretic and analgesic High dose (2400-4000mg/day) --> anti-inflammatory ```
34
Aspirin - side effects
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
Aspirin - pH disturbances
respiratory alkalosis early (hyperventilation) | transition to mixed metabolic acidosis-respiratory alkalosis
36
COX-2 - area
inflammatory cells and vascular endothelium
37
COX-2 mediates
inflammation and pain
38
Celecoxib - mechanism of action
reversible inhibition of COX-2 (only)
39
Celecoxib spares COX-1 - clinical importance
maintain gastric mucosa
40
celecoxib vs other NSAID according side effects
celecoxib does not have the corrosive effects of ther NSAID on the GI lining
41
beside gastric mucosa, celecoxib spares .... function (why)
it spares platelet function as TXA2 production is depended on COX-1
42
TXA2 production is depended on
COX-1
43
NSAID - drugs
1. ibuprofen 2. naproxen 3. indromethacin 4. ketorolac 5. diclofenac 6. meloxicam 7. piroxicam
44
NSAID - mechanism
REVERSIBLE inhibit cyclooxygenase (both COX 1 and 2) | --> block prostaglandin synthesis
45
clinical use of NSAID
1. antipyretic 2. analgesic 3. anti-inflammatory | 4. Indomethacin is uded to close PDA
46
toxicity of NSAID
1. interstitial nephritis 2. gasrtic ulcers 3. renal ischemia
47
NSAID can cause renal ischemia - mechanism
prostagladins vasofilate afferent arteriole
48
Bisphosphonates - drugs
alendronate and other -DRONATES
49
Bisphosphonates - mechanism
pyrophosphate analogs --> hydroxyapatite in bone --> inhibition of osteoclasts
50
Bisphosphonates - clinical use
1. osteoporosis 2. hypercalcemia 3. Paget disease of bone 4. metastatic bone disease 5. osteogenesis imperfecta
51
Teriparatide - mechanism of action
Recombinant PTH analog --> increases osteoblastic activity
52
Teriparatide - administration
subcutaneously/daily
53
Teriparatide - clinical use (explain)
osteoporosis --> causes increased growth compared to antirepsorptive therapies (eg. biphosphanates)
54
Teriparatide - toxicity
1. transient hypercalcemia | 2. May increase risk of osteosarcoma (seen in rodent studies)
55
TNF-a inhibitors - drugs and mechanism of action
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
all TNF-a inhibitors predispose to
infection, including reactivation of latent TB
57
TNF-a inhibitors predispose to TB reactivation - mechanism
TNF is important in granuloma formation and stabilization
58
infliximab - mechanism of action
anti-TNF-a monoclonal antibody
59
abalimunab - mechanism of action
anti-TNF-a monoclonal antibody
60
Etanercept - mechanism of action
fusion protein (receptor for TNF-A+IgG1 FC) produced by recombinant DNA
61
Etanercept - clinical use
1. Rheumatoid arthritis 2. psoriasis 3. ankylosing spondylitis
62
infliximab and adalimumab - clinical use
1. inflammatory bowel disease 2. rheumatoid arthritis 3. ankylosing spondylitis 4. psoryasis
63
bisphosphonates - side effects
1. corrosive esophagitis (patients are advised to take with water and remain upright for 30 mins) 2. osteonecrosis of jaw
64
bisphosphonates - vs Teriparatide according action on osteoporosis
bisphosphonates --> anti-resorptive | Teriparatide --> induce bone growth
65
celecoxib - side effects
1. increased risk of thrombosis | 2. sulfa allergy
66
celecoxib - clinical use
1. Rheumatoid arthritis | 2. osteoarthritis
67
Rasburicase - mechanism of action
Recombinant uricase that catalyzes metabolism of uric acid to allanotin
68
Rasburicase - clinical use
Prevention and treatment of tumor lysis syndrome
69
Rasburicase - mechanism of action / clinical use
Recombinant uricase that catalyzes metabolism of uric acid to allanotin Clinical use: Prevention and treatment of tumor lysis syndrome
70
Leflunamide - mechanism of action
Reversibly inhibits dihydroorotate dehydrogenase --> prevent pyrimidine synthesis --> suppresses T-cell proliferation
71
Leflunamide - clinical use
1. RA | 2. psoriatic arthritis
72
Leflunamide - adverse effect
1. Diarrhea 2. hypertension 3. hepatotoxicity 4. teratogenicity

Musculoskeletal and Connective Tissue (19 decks)

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