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Pharmacology II > Osteoarthritis (exam 1) > Flashcards

Osteoarthritis (exam 1) Flashcards

1
Q

cardinal features of osteoarthritis

A

progressive cartilage loss
subchrondral thickening
marginal osteophytes

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2
Q

what type of disease is OA

A

degenerative joint disease

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3
Q

osteoarthritic is characterized by

A

degeneration of cartilage that cushions the ends of bones

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4
Q

treatment for osteoarthritis

A

exercise
pain medication

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5
Q

is there a drug that can reverse OA?

A

no

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6
Q

initial drug of choice for OA

A

acetaminophen

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7
Q

what types of medication can be used to treat OA?

A

acetaminophen
NSAIDs
capsaicin
tramadol
glucocorticoids
opioids

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8
Q

when does OA begin and how long does it develop compared to RA?

A

RA: 25-50 yrs; weeks-months

OA: 40 yrs; years

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9
Q

are osteophytes present in RA and OA?

A

ONLY osteoarthritis

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10
Q

is RF present in RA and OA?

A

ONLY rheumatoid arthritis

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11
Q

major sign of RA and OA

A

RA: inflammation
OA: pain

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12
Q

how long does morning stiffness last in RA and OA?

A

RA: over an hour
OA: under 20 minutes

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13
Q

are fatigue, weight loss and anemia present in RA and OA?

A

ONLY rheumatoid arthritis

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14
Q

rheumatoid arthritis is a _____________ response while osteoarthritis is a _______________

A

autoimmune

loss of cartilage matrix

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15
Q

eicosanoids

A

prostaglandins, thromboxanes, leukotrienes
short lives, extremely potent
formed in almost every tissue of the body

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16
Q

COX1 pathway is ___________ and COX2 pathway is ___________

A

constitutive (expressed at all times)

inducible (expressed by inflammatory stimuli)

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17
Q

which COX pathway is NSAID sensitive?

glucocorticoid sensitive?

A

both COX1 and COX2

only COX2

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18
Q

types of prostaglandins in COX-1 pathway

A

stomach - PGE2
Kidneys - PGE2, PGI2
platelets - TxA2
vascular endothelium - PGI2

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19
Q

COX-1 pathway activation leads to ___________ while COX-2 pathway activation leads to _______________

A

physiological homeostasis

inflammation

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20
Q

NSAIDs MOA

A

inhibit the product of eicosanoids by inhibiting the activity of cyclooxygenases

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21
Q

NSAIDs are what type of antagonist?

A

noncompetitive

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22
Q

NSAIDs posses what type of effects?

A

anti-inflammatory
analgesic
antipyretic

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23
Q

aspirin MOA

A

irreversibly acetylates COX1 and COX2

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24
Q

how are NSAIDs antipyretic?

A

PGE2 crosses BBB to increase body temperature

when this is decreased, body temp lowers

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25
Q

chief metabolic products of aspirin

A

salicyluric acid (glycine conjugate)
phenolic glucuronide
acyl glucuronide

26
Q

how is aspirin exerted in the urine?

A

75% - free salicyluric acid
10% - salicylic acid
10% - salicylic phenolic
5% - acyl glucuronide

27
Q

aspirin is contraindicated in

A

vitamin K deficiency and hemophilia

28
Q

ADRs of aspirin

A

increase gut irritation
gastric distress
N/V
prolonged bleeding time
nephropathy

29
Q

where is aspirin metabolized?

A

hepatic ER and mitochondria

30
Q

Pharmacokinetics of acetaminophen

A

extensive 1st pass metabolism in luminal cells of intestine
conjugated in liver to form inactive glucuronidated/sulfated metabolites

31
Q

part of acetaminophen is hydroxylated to from

A

N-acetyl-p-benzoiminoquinoneimine (NAPQI)

32
Q

NAPQI

A

highly reactive
potentially dangerous metabolite that reacts with sulfhydryl groups

33
Q

acetaminophen converts into _________________ which can be therapeutic or toxic doses

A

toxic intermediate

34
Q

adverse effects of acetaminophen

A

acute overdoses - fatal liver damage (from NAPQI)
renal tubular damage

35
Q

are there adverse effects at normal doses of acetaminophen?

36
Q

antidote for acetaminophen

how it works?

A

n-acetylcysteine

contains sulfhydryl groups which interact with NAPQI and detoxify it

37
Q

MEOS compromises

A

CYP4502E1 (major)
1A2
3A4

38
Q

why acetaminophen intake can be toxic after alcohol consumption?

A

increase liver damage due to increased production of NAPQI

39
Q

NSAID nonselective antagonists

A

piroxicam
tolmetin
indomethacin
ibuprofen
naproxen
meloxicam

40
Q

most potent nonselective antagonist NSAID to inhibit COX1

41
Q

most potent nonselective antagonist NSAID to inhibit COX2`

42
Q

which nonselective antagonist NSAIDs are more selective at inhibiting COX2 pathway?

A

meloxicam
naproxen

43
Q

celecoxib and parecoxib are what type of antagonist?

A

reversible
selective COX-2

44
Q

how is parecoxib administered?

A

by injection

45
Q

adverse effects of selective COX-2 antagonists

A

risk of myocardial infarction and stroke
hypertension and edema due to inhibition of PG production in kidney
protective effects
thrombosis

46
Q

acetaminophen MOA

A

poor inhibitor of COX1 and COX2 in presence of peroxides
inhibits a novel COX splice variant in the brain (COX3)

47
Q

what type of effects does acetaminophen have?

A

antipyretic and analgesic

48
Q

is acetaminophen an anti inflammatory?

49
Q

NAPQI is considered a

A

BRI
biological reactive intermediate

50
Q

acetaminophen undergoes _______________ to form NAPQI

A

CYP450 oxidation

51
Q

2 classes of DMARDs

A

traditional
biologic

52
Q

traditional DMARDs

A

MTX
leflunomide
hydroxychloroquine
sulfasalazine
cyclophosphamide
cyclosporine
tacrolimus

53
Q

biologic DMARDs

A

abatacept
etanercept
infliximab
rituximab
tocilizumab

54
Q

methotrexate is the ___________ for DMARD therapy

A

gold standard

55
Q

treatment and care for osteoarthritis

A

protecting joints
medication and lifestyle changes
knee injections
knee replacement
joint fusion injury
corticosteroid injections
joint replacement

56
Q

joint replacement are sometimes considered

A

treatment of last resort

57
Q

inflammasome

A

multiprotein intracellular complex that detects pathogens and sterile stressors
activates highly pro-inflammatory cytokines I-1b and IL-18

58
Q

what is the best characterized inflammasome?

59
Q

what does APAP stand for?

A

N-acetyl-para-aminophenol

60
Q

acetaminophen is found to inhibit _____________ in the canine brain but its role in humans is not confirmed

A

COX-1 isoenzyme COX3

Pharmacology II (11 decks)

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