Brainscape's Knowledge GenomeTM

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


See full index

Pharm Exam 4 > NSAIDS and Gout Treatment > Flashcards

NSAIDS and Gout Treatment Flashcards

1
Q

Salicylate drugs:

A

aspirin

salicylic acid

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

Non-specific NSAID drugs:

A

HIT BOTH COX1 and 2

  • *aspirin
  • *ibuprofen -
  • *indomethacin - gout
  • *ketorolac
  • *naproxen
  • *oxaprozin
  • *piroxicam
  • *sulindac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

COX2 Inh drugs:

A

CeleCOXIB
EtorlCOXIB
Meloxicam

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

Analgesic/Antipyretic (not anti-inflammatory) drugs:

A

acetaminophen

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

Acute gout Tx drugs:

A
  • NSAIDS=Indomethacin - primary for severe

- Colchicine

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

Gout prophylaxis drugs (lower uric acid levels):

A

1) xanthine oxidase inh (des UA production:
- allopurinol
- febuxostat
2) uricosuric drugs (inc renal excretion of UA):
- probenecid
- sulfinpyrazone

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

Classic inflammatory symptoms:

A

1) redness
2) swelling
3) heat
4) pain

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

Molecular inflammatory mediators:

A

1) kinins- BRADYKININ
2) neuropeptides- Substance P
3) vasoactive amines- Histamine & 5-HT
4) Arachidonic acid metabolites
- COX (prostaglandin, tromboxanes, prostacyclin)
5) Cytokines- TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • ACETAMINOPHEN IS NOT AN NSAID! –> NO ANTI-INFLAMMATORY PROPERTIES!
  • ONLY HAS ANALGESIC AND ANTIPYRETIC PROPERTIES
A
  • ACETAMINOPHEN IS NOT AN NSAID! –> NO ANTI-INFLAMMATORY PROPERTIES!
  • ONLY HAS ANALGESIC AND ANTIPYRETIC PROPERTIES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NSAIDs - Functional Characteristics:

A
  • analgesia
  • antipyretic
  • anti-inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

NSAIDs -Primary target/MOA:

A

Dec prostaglandin production by inh COX1 and COX2

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

Products of arachodonic acid pathway that mediate inflammation & immunity?

A

PGE2 and PGI2 ==> Inc edema and vascular permeability

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

COX1:

A

always expressed and widely distributed–>keeping everything in check …such as in the stomach to protect mucosa via Prostaglandin production
–»PROTECTIVE!!!!

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

COX2:

A
  • INDUCIBLE –> PRODUCTION OF INFLAMMATORY MOLECULES

- essential for kidney function

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

Leukotrienes primarily affect:

A

airways = inflammation = asthma and allergic rhinitis

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

NSAID uses:

A 
pain (analgesic)
fever (antipyretic
inflammation (arthritis)
-antithrombotic
-->>bnch of other stuff
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Original NSAID - prototype:

A

aspirin

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

Aspirin

-Pharmacokinetics:

A
  • significant amount is hydrolyzed to salicylic acid (reversible COX inh) in the blood
  • dose dependent uses (low=fever/pain and high=antiinflammatory)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Aspirin - why potential for drug interactions?

A

80% bound to plasma proteins

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

Low dose aspirin effects:

elimination?

A
  • analgesic & antipyretic

- first order

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

High dose aspirin effects:

elimination?

A

Anti-inflammatory

-zero order

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

Aspirin works on primarily which enzyme?

A

COX2

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

Aspirin

-Antipyretic effect MOA?

A
  • Inh of PGE2 via COX in the hypothalamus ==> resent temperature control
  • drop in temperature causes dilation of superficial blood vessel + profuse sweating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Aspirin

-Anti-inflammatory MOA?

A

-inhibit COX2 –> no PG synthesis

== inh inflammatory cell migration

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

Aspirin

-Analgesic effects MOA?

A

-inhibit COX2 –> no PG synthesis

==> most effective for muscular, vascular or inflammatory conditions

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

ASpirin

-Anti-coag effect MOA?

A
  • prolongs bleeding time
  • inh thromboxane synthesis via COX
  • irreversible inh of platelet COX1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ASpriin prophylactic for:

A

MI

coronary artery disease

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

Aspirin

-advrse effects:

A
  • GI upset and ulcers due to COX1 inh-protective COX (related to dose and duration)
  • PGI2 and PGE2 decrease gastric acid secretion
  • platelet inhibiton = prolonged bleeding time
  • hepatitis
  • renal tox- dec kidney function
  • hypersensitivity–>pruritus
  • tinnitus
  • reyes syndrome - encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Similarities and differences bw NSAIDs and non-specific NSAIDs:

A

Same: pretty much everything - anti-pyretic, inflammatory, analgesic, side effects, effect on platelets

DIFFERENCE IS IN DURATION OF ACTION AND POTENCY

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

Which nonselective NSAID is popular for gout and ankylosing spondylitis?

A

indomethacin

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

COX2 selective inh were developed to:

A

not effect COX1 protective effect on GI but still have anlgesic, antipyretic, anti-inflammatory effects!
-NO IMPACT ON PLATELET AGGREGATION

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

Rofecoxib adverse event:

A

-cardiovascular thrombotic events

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

Celecoxib-drug type?

A

-COX2 selective inh

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

Etoricoxib -drug type?

A

-COX2 selective inh

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

Meloxicam-drug type?

A

-COX2 selective inh

36
Q

Synthetic DMARD (disease modifying anti-rheumatic drugs) – LIST DRUGS:

A
  • methotrexate
  • leflunomide
  • chloroqine
  • hydroxychloroquine
37
Q

Biologic DMARD (disease modifying anti-rheumatic drugs) – LIST DRUGS:

A
  • etanercept
  • infliximab
  • anakinra
38
Q

Betablockers

  • list drugs
  • for what?
A
  • propranolol
  • metoprolol

-for preventative migrane therapy

39
Q

Antidepressants

  • list drugs
  • for what?
A
  • amitriptyline

- for preventative migrane therapy

40
Q

Anticonvulsants

  • list drugs
  • for what?
A
  • divaproex (valproic acid)
  • topiramate

-for preventative migrane therapy

41
Q

Ergot Alkaloid

  • list drugs
  • for what?
A
  • ergotamine
  • dihydroergotamine +derivs

-for acute migrane attacks

42
Q

Triptans

  • list drugs
  • for what?
A
  • sumaTRIPTAN
  • zolmiTRIPTAN

-for acute migrane attacks

43
Q

Acetaminopen

  • use?
  • what population?
A
  • pain reliever
  • fever reducer
  • NO ANTI INFLAMMATORY PROPERTIES

-ESP IN CHILDREN AND THE OLD

44
Q

Acetaminophen

-adverse effects:

A

1) liver toxicity at high doses
a) Narrow therapeutic index = -15mg/kg=ok
- 150mg/kg=centrilobular liver necrosis
- 350mg/kg=liver failure

45
Q

Acetaminophen interacts with what other major drug?

A

EtOH

46
Q

Gout

-what is?

A

1) acute arthritis due to the deposit of monosodium urate (uric acid crystals)
a) increased production
- metabolic imbalance
- diet intake of purine rich foods
- inc tissue destruction
b) decreased excretion by kidney
2) associated with hyperuricemia

47
Q

Therapeutic goals for gout tx:

A
  • stop gout attack
  • CONTROL PAIN AND INFLAMMATION
  • prevent future attacks
48
Q

First line treatment for gout?

A

NSAID–>indomethacin

aspirin would NOT be used - causes renal retention of uric acid at low dose

49
Q

Tx options for gout?

A
  • NSAID
  • corticosteroids - if cant tolerate NSAID
  • intra-articular steroid injection-benefits one of2 large joints
50
Q

Acute gout tx drug

A

Colchicine

51
Q

Colchicine

  • uses?
  • MOA?
A
  • reduces pain and inflammation of gout

- inh leukocyte migration and phagocytosis (inh microtubule aggregation)

52
Q

Colchicine

-AE?

A

DIARRHEA!

53
Q

Gout prophylaxis:

A

1) use xanthine oxidase inh drugs to prevent production of uric acid
- –> febuxostat & allopurinol
2) inc renal excretion by blocking tubular reabsorption –> probenecid or sulfinpyrazone

54
Q

Allopurinol

  • use?
  • type?
  • MOA?
A
  • gout prophylaxis
  • xanthine oxidase inh
  • blocks conversion of xanthine to uric acid
55
Q

Febuxostat

  • use?
  • type?
  • MOA?
A

-gout prophylaxis
-new xanthine oxidase inh
(more selective and well tolerated if cant use allopurinol)
-blocks conversion of xanthine to uric acid

56
Q

Probenecid/ Sulfinpyrazone

  • use?
  • type?
  • MOA?
  • AE?
A
  • gout prophylaxis
  • uricosuric drug
  • inc renal clearance of uric acid by inh tubular absorption
  • kidny and GI stones
  • not for acute attacks
57
Q

Stages of RA?

A
  • initiation –> nonspecific inflammation
  • amplification –> t-cell activation
  • FINAL STAGE: CHRONIC INFLAMMATION AND TISSUE INJURY
58
Q

First line tX for RA?

A

NSAIDs–> aspirin, acetominophen, indomethacin, ibuprophen, ….

REDUCE INFLAMMATION AND PAIN

59
Q

Tx options for RA?

A

1) NSAIDs-REDUCE INFLAMMATION AND PAIN (does not cahnge progression)
2) glucocorticoids-reduce inflammation and cause improvement (does not cahnge progression)
3) Disease modifying antirheumatic drugs (DMARDs) - reduce inflammation and slow bone damage == improve prognosis!

60
Q

issue with DMARDs?

A
  • SLow onset of therapeutic effects! could take 6weeks to 6months
  • more toxic!
61
Q

First line DMARD for RA tx?

A

methotrexate

62
Q

Methotrexate

  • drug type and what for?
  • MOA?
A
  • SYNTHETIC DMARD for RA
  • inhibits AICAR transformylase –> inc extracellular adenosine and inh T-cell activation, cytotoxic to proliferating lymphocytes following antigen exposure

FIRST LINE RA TX

63
Q

Lefunomide

  • drug type and what for?
  • MOA?
A
  • Synthetic DMARD for RA

- nih ribonucleotide synthesis and causes cell cycle arrest

64
Q

Chloroquine and hydroxychloroquine

  • drug type and what for?
  • MOA?
A
  • antimalarial drug for RA

- MOA UNK

65
Q

first agent for RA for both symptomatic improvement and retardation of structural joint damage?

A

leflunomide -synth DMARD

66
Q

Etanercept

  • drug type and what for?
  • MOA?
A
  • Anti-TNF-alpha agent for RA

- cytokine receptor fusion protein -binds to receptor so TNF-a cant

67
Q

Infliximab

  • drug type and what for?
  • MOA?
A
  • Anti-TNF-alpha agent for RA
  • anti-TNF-alpha chimeric monoclonal antibody
  • binds TNF-a and marks it for destruction/elimination
68
Q

Anakinra

  • drug type and what for?
  • MOA?
A
  • IL1 inhibitor for RA

- IL1 cytokine receptor decoy - so IL1 cant bind

69
Q

*Pathophys of migranes?

A

1) originates deep in brain
2) electrical impulse spread to other regions of brain
3) changes in nerve cell activity and blood flow = visual disturbance, numbness, tingling, dizziness
4) chemicals in brain cause blood vessel dilation and inflammation of surrounding tissue
5) inflammation irritates the trigeminal nerve = severe/throbbing pain

70
Q

Migrane Tx

  • non-pharm?
  • pharmacological?
A

1) Avoid triggers=regular SLEEP/meals/exercise
2) a) preventative therapy - prevent frequency and severity
b) acute migrane management
- nonspecific pain meds = aspirin, acetaminophen, NSAIDs, opiates
- speicific migrane drugs= ergotamine, dihydroergotamine, triptans

71
Q

Specific migrane drugs:

A

ergotamine
dihydroergotamine
triptans

72
Q

beta-blockers

  • what for?
  • drugs?
  • contraindication?
A

1) preventative therapy of migranes
2) propranolol (B1&2)
metoprolol (B1)
3) not to be used in asthmatics

73
Q

**tx of choice for migrane prevention?

A

metoprolol

74
Q

Antidepressants

  • what for?
  • drugs?
  • AE?
A
  • preventative therapy of migranes
  • amitriptyline
  • drowsiness
75
Q

Anticonvulsants

  • what for
  • drugs?
A
  • -preventative therapy of migranes
  • divalproex (varproic acid)
  • topiramate
76
Q
  • Acute tx of migriane attacks - non-specific - drugs:

- what should be avoided with these gys?

A
  • aspirin
  • Naproxen (NSAID)
  • ibuprophen (NSAID)
  • acetaminophen

-avoid OVERUSE —> might transform migriane into a more severe chronic disorder

77
Q

metoclopramide

  • what kind of drug?
  • what for?
  • how used to tx?
  • MOA?
A
  • antiemetic
  • for acute migrane attacks
  • -adjunct therapy to combat nasuea and vomiting due to migraine or ergot alkaloid tx
  • central D2 antagonist
  • weak 5-HT3 antagonist
78
Q

Chlorpormazine

  • what kind of drug?
  • what for?
  • how used to tx?
  • MOA?
A
  • antiemetic
  • for acute migrane attacks
  • -adjunct therapy to combat nasuea and vomiting due to migraine or ergot alkaloid tx

-central D2 antagonist

79
Q

Prochlorperazine

  • what kind of drug?
  • what for?
  • how used to tx?
  • MOA?
A
  • antiemetic
  • for acute migrane attacks
  • -adjunct therapy to combat nasuea and vomiting due to migraine or ergot alkaloid tx

-central D2 antagonist

80
Q

Ergotamine

  • what kind of drug?
  • what for?
  • MOA?
A
  • migrane specific drug - ergot derivative
  • acute migrate attacks
  • VASOCONSTRICTION due to stimulation of alpha and 5-HT receptors

VASODILATION IS THE PROBLEM

81
Q

Dihydroergotamine + derivs

  • what kind of drug?
  • what for?
  • MOA?
A
  • migrane specific drug - ergot derivative
  • acute migrate attacks
  • VASOCONSTRICTION due to stimulation of alpha and 5-HT receptors
82
Q

Ergot derivative - pros/cons

A

Pros: effective, used for a long time, and low cost

Cons: GI disturbance

  • complex pharmacology and kinetics - variable absorption, metabolism, and shit
  • inc risk of vascular effects due to vasoconstriction
83
Q

SumaTRIPTAN

  • what kind of drug?
  • what for?
  • MOA?
A

1) migraine specific - Triptan drug
2) for acute migraine attacks
3) MOA:
- selective 5-HT1D and 5-HT1B agonist = VASOCONSTRICTION
- inh activation of trigeminal affarent nociceptors

84
Q

triptan adv/disadv over ergots:

A
  • selective pharmacology
  • established and safe
  • fewer adverse effects
  • expensive
  • cant use if cardiovascular disease
85
Q

Triptans - safety?

A
  • safe but 5HT1B constricts coronary arteries = anginal pain

- irritating adverse effects – tingling, warm feeling, dizzy…

86
Q

Triptans - contraindications:

A

-ischemic heart disease
-HTN
cerebrovascular disase

Pharm Exam 4 (10 decks)

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