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Pharm 323 Spring 22 > Osteoporosis, Gout, RA > Flashcards

Osteoporosis, Gout, RA Flashcards

1
Q

3 causes for gout

A
  1. increased uric acid production
  2. decreased uric acid excretion
  3. increased intake of purine-containing foods
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2
Q

acute gout attacks are classified as how many a year? and what type of meds should they be on?

A

< 3 attacks/year

should be on ANTI INFLAMMATORY AGENTS

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3
Q

what is our 1st line tx for acute gout attack?

A

NSAIDs

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4
Q

name some of the main adverse effects of NSAID use

A
  1. GI ulceration/bleeding
  2. impair renal function
  3. CV events
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5
Q

what is 2nd line tx for acute gout attack? + what’s the prototype?

A

glucocorticoids : PREDNISONE

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6
Q

when treating acute gout attack (NSAIDs + glucocorticoids) when would we want to see results (decreased pain + inflammation)?

A

within 24 hours ◡̈

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7
Q

what’s our 3rd choice tx for acute gout attack?

A

ColChiCine

= aCute

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8
Q

what is our anti-inflammatory prototype for acute gout attack? (3rd choice, if NSAIDs and steroids are out)

A

colchicine

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9
Q

what is the unique thing about colchicine?

A

anti-inflammatory effects ONLY with gout

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10
Q

what is the MOA of colchicine?

A

inhibits leukocyte infiltration –> prevents destructive lysosomal enzymes

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11
Q

what is the MAIN adverse effect of colchicine and what should we do if this occurs?

A

GI effects –> discontinue drug!!!

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12
Q

describe the dosing for colchicine (initial + max)

A

1.2mg loading dose –> 0.6mg 1 hour later

MAX: 1.8mg/day

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13
Q

what are the 4 serious/rare AE of colchicine?

A
  1. bone marrow suppression
  2. rhabdomyolysis
  3. severe kidney disease
  4. severe liver disease
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14
Q

drug-food interaction with colchicine?

A

grapefruit juice

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15
Q

if someone has > 3 gout attacks/year, what medication plan should they be on?

A

PREVENTION of gout (allopurinol)

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16
Q

what is our prototype for drugs that inhibit uric acid formation?

A

allopurinol

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17
Q

in addition to reducing uric acid levels, allopurinol has 2 more actions r/t gout

A
  1. decrease tophi that’s already formed

2. decrease risk of urate crystals in kidneys

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18
Q

what is allopurinol known to do at the START of therapy?

A

can increase acute gout attacks

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19
Q

SE of allopurinol

A

GI (mild)

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20
Q

rare/serious AE of allopurinol

A

hypersensitivity syndrome

“ALL PUR drugs are sensitive”

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21
Q

drug-drug interaction with allopurinol

A

warfarin

“ALL PUR drugs are SENSITIVE (AE) and don’t like WAR[farin]”

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22
Q

what patient education should we include with allopurinol therapy?

A

H2O H2O H2O!!!

increase fluid intake to flush out kidneys

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23
Q

what is our “least invasive”/starting point for therapy for osteoporosis + also what all other drug therapies should be paired with?

A

vitamin supplementation: vit D + calcium

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24
Q

for osteoporosis therapy, what are the 5 classes of drugs that decrease bone resorption (osteoClast)?

A
  1. calcitonin-salmon
  2. biphosphonates*
  3. estrogen replacement
  4. SERMs
  5. Denosumab
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25
Q

for osteoporosis therapy, what is the prototype for drugs that increase bone formation (osteoBlast)?

A

teriparatide

“teri has this bone para ti (for you)”
“teri is super generous and wants to help you increase your bone formation”

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26
Q

vitamin supplementation for osteoporosis prevention + tx is based on what?

A

age + intake

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27
Q

how much calcium/day? (woman 51-70yrs)

A

1200mg

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28
Q

what’s the unique thing about calcium dosing?

A

body can only absorb 600mg at a time, so dosing should be divided

*calcium carbonate has HIGHEST % of Ca ◡̈ *

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29
Q

what food interactions should you know about with calcium? how can we work around this?

A

oxalic acid

spinach, beets, rhubarb, swiss chard, brain, whole grains

separate intake of Ca + these foods by 1 hour

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30
Q

how much vitamin D should be supplemented daily?

A

800-1000mg/day

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31
Q

what is the MOA of calcitonin-salmon?

A

prevents bone resorption (osteoClast activity) : keeps calcium in the bone + prevents pulling into bloodstream

“the salmon prevents you from being pulled into the stream”

32
Q

routes for calcitonin-salmon?

A

intranasal

SQ

33
Q

SE of calcitonin-salmon

A

nasal drying, nausea, increased malignancies (canada)

3rd choice drug

“snorting salmon through your nose causes you to be nauseated with a dry nose and get malignancies if you go to canada”

34
Q

what’s our gold star and 1st choice drug for TREATMENT of osteoporosis? + what is prototype?

A

biphosphonates : alendronate

35
Q

MOA of biphosphonates

A

prevents bone resorption + undergoes incorporation into bone (so effects of this drug can last a long time)

36
Q

what is the ending of biphosphonates / how can we recognize them?

A

“____ronates”

37
Q

patient education with PO alendronate (4 things)

A
  1. don’t take with ANY food - none will be absorbed
  2. take with FULL glass of H2O
  3. remain upright for 30 minutes - can cause severe esophagitis!
  4. don’t chew or suck on tablets
38
Q

what is most common SE of alendronate?

A

esophagitis

stay upright 30 mins after PO admin

39
Q

AE of alendronate (4)

A
  1. atypical femur fractures
  2. musculoskeletal pain
  3. ocular inflammation
  4. osteonecrosis of the jaw

“ALEN + NATE get weird fractures that give you MS pain, inflame your eyes and necrose your jaw”

40
Q

what is the prototype for estrogen replacement for tx of osteoporosis?

A

premarin

41
Q

what is MOA of premarin

A

suppresses osteoclast proliferation (decreases bone resorption)

“pregnant horse pee gives you strong bones”… gross

42
Q

risks associated with premarin therapy (4)

A
  1. breast CA
  2. endometrial CA
  3. MI
  4. stroke
43
Q

re: treatment of osteoporosis, what does SERM stand for?

A

selective estrogen-receptor modifiers

44
Q

what is the prototype for SERMs?

A

raloxifene

45
Q

what is the MOA of raloxifene?

A

decreases bone resorption (mimics estrogen effects on non-breast cells + / or blocks effects of estrogen on breast cells)

46
Q

what 3 things does raloxifene improve?

A
  1. bone density
  2. lipid profiles
  3. CV risk
47
Q

what are the 3 major risks associated with raloxifene therapy?

A
  1. DVT
  2. PE
  3. stroke
48
Q

for tx of osteoporosis, what is the prototype for the monoclonal antibody?

A

denosumab

“den = density”

49
Q

MOA of denosumab

A

prevents activation of RANK receptor

RANK receptors are on osteoClasts, so blocking this receptor decreases osteoclast activity

50
Q

route + frequency of denosumab

A

SQ q 6 months ◡̈

51
Q

what should also be taken with denosumab?

A

vitamin D + Calcium supps

52
Q

SEs of denosumab (4)

A
  1. injection site rxns
  2. pain (back, MS, extremity)
  3. UTI
  4. hypercholesterolemia
53
Q

what are the rare/serious AE of denosumab?

A
  1. serious infections
  2. derm rxns
  3. osteonecrosis of the jaw
54
Q

what is our prototype drug for increasing bone formation?

A

teriparatide

55
Q

MOA of teriparatide

A

increase bone deposits by osteoblasts

= increase bone formation

56
Q

route for teriparatide

A

SQ

$1500/month!

“teri is rich, but we love her b/c shes super generous and gives us all the bone deposits!”

57
Q

SEs of teriparatide (5)

A
  1. nausea
  2. HA
  3. back pain
  4. leg cramps
  5. initial ORTHOSTATIC HYPOTENSION
    (but generally, well tolerated)

teri’s got some period symptoms

58
Q

teriparatide therapy is associated with an increased risk of what?

A

osteosarcoma

“teri is so generous and gives gives gives, but sometimes this can be toxic”

59
Q

what are the 3 classes of antirheumatic drugs?

A
  1. NSAIDS
  2. glucocorticoids
  3. DMARDs
60
Q

which of the 3 classes for antirheumatic drugs reduces joint destruction?

A

DMARDS (disease modifying drugs)

glucocorticoids slow progression of joint damage

61
Q

which of the antirheumatic drugs should be started within 3 months of dx of RA?

A

DMARDs

62
Q

which of the antirheumatic drugs are really only for symptomatic relief?

A

NSAIDs

63
Q

DMARDs are broken up into 2 categories. what are they?

A

biologic + non-biologic

64
Q

prototype for non-biologic DMARD agent

A

methotrexate

65
Q

how long does methotrexate take to start working? what should be done until they kick in?

A

3-6 weeks to work

NSAID therapy until then

66
Q

what supplement should be given with methotrexate? what is dosing?

A

folic acid 5mg/week

67
Q

how is methotrexate working?

A

immunosuppressive

68
Q

SE of methotrexate (7)

A
  1. hepatic fibrosis
  2. bone marrow suppression
  3. GI ulceration
  4. pneumonitis
  5. CV disease (reduced life expectancy)
  6. infections
  7. Cancers
69
Q

what is the prototype for the biologic DMARD?

A

etanercept

70
Q

MOA of etanercept

A

immunosuppressive: targets specific parts of the inflammatory process (mostly tumor necrosis factor)

71
Q

ALL biologic DMARDs put patient at high risk of what?

A

INFECTIONS (b/c it’s an immunosuppressive)

72
Q

what should patients be tested for before beginning etanercept therapy?

A

TB

if positive TB test, patient should be treated first!!!

73
Q

route + frequency for etanercept

A

SQ twice a week

74
Q

special considerations for etanercept therapy (4)

A
  1. test for TB + treat if needed
  2. watch for Hep B reactivation
  3. no active infections
  4. no live vaccines
75
Q

etanercept therapy puts someone at risk for what 4 things?

A
  1. HF
  2. cancer
  3. CNS disorders
  4. serious skin rxns

brain, heart, cancer, skin

Pharm 323 Spring 22 (18 decks)

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