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Pharmacotherapeutics with Sepik > Drugs for Mobility > Flashcards

Drugs for Mobility Flashcards

1
Q

What is gout?

A

Recurrent inflammatory disorder

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2
Q

Name 3 ways that gout can occur

A
  • Increased uric acid production
  • Under excretion of UA
  • Increased intake of foods containing purines
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3
Q

WTF is heckin’ purine?

A

Chemical compound in food known to cause gout. Forms UA when metabolized.

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4
Q

Who is most at risk for gout?

A

Males, ETOH, folks on diuretics, people who are immunosuppressed.

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5
Q

True or false: Stress cannot induce a gout attack.

A

FALSE. It sure can.

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6
Q

Three main anti-inflammatory agents used in an acute gout attack:

A

NSAIDS
Glucocorticoids
Colchicine

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7
Q

3 main NSAIDS used to treat an acute gout attack:

A

Indomethacin
Naproxen
Diclofenac Sodium

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8
Q

If the patient has less than 3 gout attacks a year, how will we treat when s/s arise?

A

Symptomatically (versus preventative)

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9
Q

What are those same ol’ SE for NSAIDs (just a refresher here)?

A

GI ULCERATION/BLEEDS, impaired renal function, fluid retention, increased risk of CV issues.

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10
Q

If NSAIDS aren’t effective, what do we try next?

A

Glucocorticoids

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11
Q

Which glucocorticoid is used for gout?

A

Prednisone

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12
Q

What are those same ol’ SE for glucocorticoids (just a refresher here)?

A

GI ULCERATION, hyperglycemia, decreased wound healing, fluid retention

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13
Q

Re: Using glucocorticoids for gout. Do we normally do a short or long course of therapy? And why?

A

SHORT. That shit’s bad for you long term.

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14
Q

Using NSAIDs or glucocorticoids, how soon should the patient get relief?

A

within 24 hours

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15
Q

If NSAIDs and GCs aren’t cutting it, what is next for anti-inflammatory agents for gout?

A

Colchicine

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16
Q

Why don’t we use colchicine first?

A

Not a great risk/benefit ratio

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17
Q

True or false: Colchicine ONLY works on inflammation related to gout.

A

True

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18
Q

What is the MOA of colchicine?

A

Inhibits leukocyte infiltration –> prevents the destruction of lysosomal enzymes that cause the pain and inflammation in joint

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19
Q

SE of colchicine? What do we do if this happens?

A

GI (25%). Discontinue if occurs.

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20
Q

Why did the GI SE used to be 80% of patients?

A

We used to use higher doses

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21
Q

How do we dose colchicine these days? What is the max dose/24 hours?

A

1.2 mg loading dose
then
0.6 mg given 1 hour later
Max dose over 24 hours = 1.8 mg

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22
Q

Rare/serious SE of colchicine?

A

BM suppression, rhabdomyolysis, severe kidney or liver disease.

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23
Q

Patient education alert! What drug/food interaction do we need to tell patients about when taking colchicine?

A

NO GRAPEFRUIT

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24
Q

Colchicine drug/drug interactions

A

PGP or CYP3A4 drugs

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25
Q

Name three ways we PREVENT gout (hyperuricemia):

A
  • Inhibit uric acid formation
  • Increase uric acid excretion
  • Convert uric acid
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26
Q

What is the prototype for drugs that inhibit uric acid formation?

A

Allopurinol (Zyloprim)

Also mentioned: Febuxostat (Uloric)

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27
Q

What is the medication mentioned that increases uric acid excretion?

A

Probenecid

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28
Q

How does probenecid work to increase UA excretion?

A

Works on renal tubules to increase UA excretion.

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29
Q

What else can probenecid be used for?

A

Used with abx because it manipulates excretion and allows drug to stay in the body longer

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30
Q

What are the two last ditch effort drugs mentioned that convert UA to help prevent gout?

A

Pegloticase and resburicase

they expensive and given IV tho

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31
Q

How does allopurinol work?

A

Decreases UA levels by inhibiting the enzyme that is required for UA formation.

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32
Q

What is tophi?

A

Deposits of uric acid crystals that develop into hard visible lumps that damage your joints and bones. Tophi can be microscopic or large and, though rarely, may need to be surgically removed.

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33
Q

How does allipurinol effect tophi? How long will you need to take it to see these results?

A

Decreases tophi that has already formed. Might take 6 months to see results!

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34
Q

How does allopurinol work with the kidneys?

A

Decreases risk of urate crystals in the kidneys

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35
Q

What can happen when patient first starts taking allopurinol for gout?

A

May increase acute gout attacks

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36
Q

When else might allopurinol be used?

A

As an adjunct medication with other issues that can cause an increase of UA (cancer, chemo, blood dycrasias)

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37
Q

Why can gout occur with chemo?

A

When cells die and break down, UA is released

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38
Q

What is the lab value of UA that is too high?

A

7 mg/dL

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39
Q

Most common SE of allopurinol?

A

GI

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40
Q

Rare and serious SE of allopurinol?

A

Hypersensitivity syndrome

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41
Q

Drug/drug interaction with allopurinol?

A

Warfarin (of course)

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42
Q

Patient teaching when taking allopurinol?

A

Increase fluids to flush kidneys!

Al needs to learn to flush to keep the toilet pure

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43
Q

What is osteoporosis?

A

Condition in which bone becomes weak and brittle

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44
Q

What t-score indicates osteoPENIA?

A

-1 to -2.5

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45
Q

What t-score indicates osteoPEROSIS?

A

-2.5 or mo’ negative

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46
Q

What is a FRAXX score?

A

10 year risk of experiencing a fracture

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47
Q

What three kinds of medications do we give for osteoporosis?

A
  • Vitamin supplements
  • Drugs that decrease bone resorption
  • Drugs that increase bone formation
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48
Q

Name the drugs that decrease bone resorption (5)

A
  • Calcitionin-Salmon
  • Biphosphonates
  • Estrogen replacement (Promarin)
  • SERMs
  • Denosumab (Prolia)
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49
Q

What is the one medication that increases bone formation?

A

Teriparatide, a form of parathyroid hormone (Forteo)

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50
Q

Let’s talk calcium. How much should you take/day, how should you take it, and which kind is best?

A
  • 1200 mg/day (needs base on age and intake – this is for women age 51-70 usually)
  • Take in divided doses (600 am, 600 pm)
  • Calcium carbonate is best, highest percentage of Ca
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51
Q

Drug/food interactions with oxalic acid (Calcium oxalate)?

A

Spinach, rhubarb, swiss chard, beets

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52
Q

Drug/food interactions with phytic acid (Calcium phytate)?

A

Whole grain cereals, bran

53
Q

Patient education for folks taking calcium oxalate or calcium phytate?

A

Separate meds from meals by 1 hour. There are a bunch of food-food interactions.

54
Q

How much vitamin D should we be taking for osteoporosis prevention?

A

Oral supplement of 800 - 1000 mg daily

amounts may need to be increased if deficient

55
Q

To what hormone does vitamin D act similarly?

A

Parathyroid hormone. Helps increase plasma Ca level.

56
Q

How does vitamin D help increase plasma Ca level?

A
  • Increases Ca absorption from bone
  • Decreases Ca excretion from kidneys
  • Increases Ca absorption from intestines
57
Q

What is our drug that treats osteoporosis by preventing bone resorption?

A

Calcitonin-Salmon

58
Q

How does Calcitonin-Salmon work to treat osteoporosis?

A

It keeps Ca in the bone and prevents pulling into the bloodstream
(Salmon won’t pull you into the ‘stream)

59
Q

How is Calcitonin-Salmon given?

A

IN or SQ

ew, fish up yr nose

60
Q

SE of Calcitonin-Salmon?

A

Nausea, nasal drying, increased malignancies (pulled in Canada)

(Snorting the The Great Canadian Salmon dries your nose and makes you nauseated.)

61
Q

How do biphosphates work?

A

They prevent bone absorption by actually going into the bone and decreasing osteoclast activity

62
Q

What are some other uses of biphosphates?

A

Padget’s disease, hypercalcemia of malignancy, bone mets

63
Q

Biphosphate prototype?

A

Alendronate (Fosamax)

Alan uses a drone to get inside the bone to decrease osteoclast activity

64
Q

How do you give alendronate?

A

PO

IV q 1 month or q 6 months (yay for compliance!)

65
Q

What is a big thing we need to teach patients about taking alendronate?

A

NO FOOD with meds, Like, none. Not even coffee. Zero of the drug will be absorbed because it already has a low bioavailability.

Can carry on 30 minutes later.

66
Q

True or false? Once alendronate is in the bone it is there for less than a month.

A

FALSE. It’s there for decades.

67
Q

SE of alendronate?

A

Esophagitis is the big one.

Also, atypical fracture of the femur, musculoskeletal pain, ocular inflammation and osteonecrosis of the jaw (whaa?)

68
Q

Re: Esophagitis as a SE of alendronate, what do we need to teach patients about taking this medication?

A
  • Take on empty stomach 1st thing in the morning (no coffee!)
  • Nothing to drink for 30 minutes
  • Remain upright for 30 minutes
  • Take with a full glass of water
  • Don’t chew or suck on tablets (WHO DOES THAT ANYWAY)
69
Q

What else should you take with alendronate?

A

Calcium and Vit D

70
Q

This drug is no longer standard therapy for preventing bone resorption probably because it is made from preggo horse piss.

A

Premarin

PREgnant MARe urINe

71
Q

How does premarin work?

A

Suppresses osteoclast proliferation (bone breakdown)

72
Q

Estrogen is ______ protective.

A

Bone

73
Q

Bad things that happen when you use pee from preggo horses?

A

Increased risk of BC and endometrial cancer, cholecystitis, MI, stroke

74
Q

What does SERM stand for and what is the prototype?

A

Selective Estrogen Receptor Modifiers

Raloxifen (Evista)

75
Q

MOA of SERMs/Raloxifen?

A

Block estrogen receptors on breast
cancer cells, but have estrogen effects
on non-breast cells

(Those non-breast cells can’t be RALOXin’)

76
Q

SERMs/Raloxifen improve ____ _________ and reduce ________ fractures.

A

bone density, spinal

77
Q

What other things do SERMs/Raloxifen improve?

A

Lipid profiles and CV risk

78
Q

AE of SERMs/Raloxifen?

A

DVT and PE risk

79
Q

True or false, SERMs/Raloxifen help with hot flashes

A

Nope, they can actually cause them

80
Q

What is the SERM used to help prevent BC recurrence for estrogen positive BCs?

A

Tamoxifen (Nolvadex)

81
Q

Can preggos take SERMs/Raloxifen?

A

No

82
Q

Prototype for monoclonal antibody that decreases bone resorption.

A

Denosumab (Prolia)

83
Q

MOA of denosumab?

A

Prevents the activation of RANK receptor.
RANK receptor is found of the surface of osteoclasts and their precursor cells. RANK stimulates the formation of osteoclasts.

SO this drug BLOCKS RANKL from activating RANK, thus inhibiting osteoclast formation. Also called a RANKL inhibitor.

84
Q

How do we take denosumab?

A

SQ q 6 months

Take with Ca and Vit D

85
Q

SE of denosumab?

A

Back pain, MS pain, pain in extremities, UTI, hypercholesteremia

86
Q

What imbalance do you need to correct before starting denosumab?

A

hypocalcemia

87
Q

What are the rare/serious SE of denosumab?

A

Serious infections, derm reactions, osteonecrosis of the jaw

88
Q

What is the only drug that helps increase bone formation?

A

Teriparatide (Forteo)

89
Q

What TF is teriparatide and what does it do?

A

A form of PTH made by recombinant DNA technology that increases bone deposits by osteoblasts.

90
Q

How do we give teriparatide?

A

SQ

91
Q

Some real bad things about teriparatide (2):

A

Expensive AF and increased risk of osteosarcoma

92
Q

SE of teriparatide

A

Generally well tolerated but some nausea, back pain, and leg cramps. INITIAL orthostatic hypotension.

93
Q

What is rheumatoid arthritis?

A

Autoimmune process where the immune system attacks synovial tissue.

94
Q

The immune system activates what immune cells in RA? Name a few for me.

A

Macrophages, t-lymphocytes, cytokines, TNF

95
Q

Types of anti-rheumatic drugs (3).

A

NSAIDS
Glucocorticoids
DMARDS

96
Q

NSAIDs are great, but what happens with them and RA?

A

They give rapid relief but don’t prevent joint damage. Might need to use higher doses and people switch which ones they use.

97
Q

How do glucocorticoids work with RA?

A

Rapid relief, slow progression. BUT long term use = toxic, so we have to do short courses.

98
Q

Let’s talk DMARDs! Tell me about them, good and bad (4).

A
  • Decrease joint destruction!
  • More toxic than NSAIDs :(
  • Come in a biologic and non-biologic form
  • Patient should start these early – within 3 months of initial diagnosis
99
Q

Prototype for non-biologic agent for DMARDs:

A

Methotrexate (Rhumatrex)

100
Q

OMG y’all

A

We are almost done with this effing deck

101
Q

What does methotrexate do?

A

Suppress immune system

102
Q

How long does it take methotrexate to work?

A

3-6 months. Tx with NSAIDs until it kicks in.

103
Q

What supplement should we take with methotrexate and why?

A

Folic Acid.

Methotrexate causes body to get rid of folate. Also, FA can help with GI side effects.

104
Q

Why do we love methotrexate?

A

Efficacious in 80% of patients, low cost, relatively safe

105
Q

Why do we hate methotrexate (4 SE) (3 shitty things)?

A

Hepatic fibrosis
BM suppression
GI ulceration
Pneumonitis

Reduced life expectancy from CV disease, infection, and certain cancers

106
Q

Can preggos take methotrexate?

A

Nope. Category X

107
Q

What do biologic DMARDs do?

A

Immunosuppressive drugs that target the specific parts of the inflammatory process

108
Q

What parts of the inflammatory process do DMARDs target (3)?

A

– Tumor Necrosis Factor
– Promotes destruction of B cells
– Inhibits activation of T cells

109
Q

All biologic DMARDs have this concern. Because of this, what should we do before starting these medications?

A

High risk of serious infections

• Test for TB, fungal infection (coccidioidomycosis), Hep B

110
Q

How are biologics DMARDs made (THINK OF THE NAME, MY FRIEND)?

A

Made with recombinant DNA

111
Q

For what other autoimmune infections are biologic DMARDs used?

A

Psoriasis, ankylosing spondylitis, Chron’s disease

112
Q

Big drawback of biologics: DMARDs?

A

$$$ ($14,000-$35,000 per year)

113
Q

Biologic DMARD prototype?

A

Etanercept (Enbrel)

114
Q

What is the category of etanercept? Like, how does it work?

A

Tumor Necrosis Factor Antagonists

115
Q

Main NBD SE of etanercept?

A

Injection site reactions

116
Q

Special considerations when giving etanercept?

A
  • Test for TB before tx
  • Watch for Hep B reactivation
  • No active infection
  • No live vaccines
117
Q

More serious SE of etanercept (Knowlton listed them as ‘risks’)?

A

Risk of heart failure, cancer, CNS disorders and rarely serious skin reactions

118
Q

GUESS WHAT TIME IT (ALMOST) IS?!

A

SPRING HECKIN’ BREAK

119
Q

Which of the following gout medications is used for an acute attack and may cause gastric upset?

A

Colchicine

120
Q

These drugs used to be reserved for advanced rheumatoid arthritis, but are now being used within 3 months of rheumatoid arthritis diagnosis because they can delay joint degeneration.

A

DMARDs

121
Q

What is calcium carbonate?

A

A calcium supplement

122
Q

What is calcitrol?

A

Vitamin D therapy

123
Q

What is alendronate (Fosamax)?

A

Biphosphonate

124
Q

What is raloxifene (Evista)?

A

SERM

125
Q

What is methotrexate (Rheumatrex)?

A

DMARD

non-biologic

126
Q

What is the MOA of allopurinol (Zyloprim)?

A

Decreases uric acid levels

127
Q

What does colchicine do?

A

Anti-inflammatory gout agent

128
Q

Methotrexate can be used to treat rheumatoid arthritis. What other condition is it used for?

A

Cancer

Pharmacotherapeutics with Sepik (7 decks)

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