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Pharmacology > Msk > Flashcards

Msk Flashcards

1
Q

Indications for NSAIDS

A

Osteoarthritis
Bursitis
Gout flare
Ankylosis spondylitis

Dysmenorrhea, HA

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2
Q

Same COX1 and 2

A

Same substrate-AA
Same products-PG
Same role in inflammation
Same physiological role in renal function

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3
Q

COX 1 only

A

Constitutive
In alll tissues alt he time

Prominent role in responding to physiological stimuli

Contributes to response to any pathological stimuli that release AA

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4
Q

How does COX1 work

A

Inflammation stimulates AA release
COX1 converts AA into PGE2
PGE2 causes symptoms

Constitutive: COX1 PGE2-erythema edema pain

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5
Q

COX2 only

A

Induced in some tissues some times

Physiological role in kidney complications and complements COX1

Prominent role in response to any pathological stimuli that release AA

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6
Q

How COX2 work

A

Inflammation induces COX2 expression

Cox2 also converts AA into PGE2

COX2 derived PGE2 amplifies symptoms

Induced COX2 increase PGE2 and worsen erythema, edema, pain

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7
Q

Asprin MOA

A

Inhibits COX1 and 2 cant cause beneficial effects

IRREVERSIBLE

Platelets cant make new COS

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8
Q

Bad effects asprin

A

Gastric ulceration, bleeding and renal impairment

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9
Q

Indication asprin

A

Anti-inflammatory doses higher than analgesic or antipyretic

RA

Chronic inflammatory conditions

Analgesic

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10
Q

Minimize risk asprin

A

Test for eliminate h pylori

Give PPI

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11
Q

When take asprin for primary prevention

A

Reduce risk of first MI in men is first ischemic stroke in women

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12
Q

Non asprin nsaids that antagonize the antiplatelet actions of asprin

A

Ibuprofen, naproxen antagonize the antiplatelet actions of asprin

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13
Q

Increased risk of bleeding from asprin when take what

A

Warfain, heparin or other

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14
Q

When see renal function issue with asprin

A

Advanced age, preexisting renal dysfunction, hypovolemia, HTN, hepatic cirrhosis, heart failure

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15
Q

Asprin induced asthma

A

PG and LT balance toward LT

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16
Q

BAD risk asprin

A

Papillary necrosis
Reye syndrome

Reduce spontaneous uterine contractions , indue premature closure of ductus arteriosus, and intensify uterine bleeding in labor and delivery

Asprin poisoning in kids lethal

Hypersensitivity reactions

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17
Q

Difference from asprin and non asprin nsaids

A

Others are reversible

Increase risk MI and stroke

Use lowest effective dose for shortest time

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18
Q

Coxibs second generation NSAIDS

A

Celecoxib-blocks COX2

Suppresses inflammation, pain, and fever

Less gastric ulceration

Does not inhibite platelet aggregation, so does not pose risk of bleeding and increase risk MI and stroke

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19
Q

NSAIDs

A 
Asprin 
Celecoxib
Diclofenac
Ibuprofen
Indomethacin
Ketorolac
Naproxen
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20
Q

Cardiovascular AHA on nsaids

A

All , espicially COX2 avoided if cardiovascular risk factors and used only with sufficient pain relief is not achieved with their therapies and the benefit outweighs the increased cardiovascular risk

-use naproxen if have to

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21
Q

Contraindications NSAIDS

A

CKD
Ulcer
Heart failrue or uncontrollable HTN

NSAID allergy

Ongoing anticoagulant

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22
Q

Acetaminophen

A

Suppresses pain and fever BUT NOT inflammation

Lacks antiinflammatory actions
No GI ulcers
No platelet aggregation
No renal impairement

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23
Q

Bad acetaminophen

A

Hepatic necrosis from acetaminophen overdose when glutathione is depleted

Treated withacetylcysteine

Inhibits metabolism of warfarin and increase risk of bleeding

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24
Q

Tricyclic antidepressants

A

Independent analgesic effects can relieve depressive symtpoms

Usually amitryptyline

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25
Q

SNRI

A

Venlafaxine, duloxetine

Beneficial with concurrent depression
Weaker evidence for effectiveness of pain relief as TCA

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26
Q

Pregabalin

A

GABA analog bind alpha2 delta subunit of voltage gated calcium channels

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27
Q

What pregabalin used for

A 
Neuropathic pain
Diabetic neuropathy
Postherpetic neuralgia
Partial seizures
Fibromyalgia
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28
Q

Gabapentin moa

A

Bind alpha2delta subunit of voltage gated ca channels

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29
Q

Indications gabapentin

A

Anti seizure

Post hepatic neuralgia, diabetic neuropathy, prophylaxis for migraine, fibromyalgia, restless leg

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30
Q

Tramadol

A

Weak mu agonist but works by blocking NE and 5-HT reuptake
-naloxone only partially blocks

Activates monoaminergic spinal inhibiton of pain

Used by millions for moderate to moderately severe pain

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31
Q

Side effects tramadol

A

Sedation, dizziness, HA, dry mouth constipation

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32
Q

Ketamine

A

NDMA antagonist used for maintain anesthesia

Common side effects include psychological reactions

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33
Q

Dexmedetomidine

A

Alpha 2 adrenergic agonist for analgesia and sedation

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34
Q

Clonidine

A

Alpha2 adrenergic agonist

for HTN and relief of severe pain

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35
Q

MOA centrally acting muscle relaxants

A

Unclear, relieve muscle spasm for low back pain

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36
Q

Ziconotide

A

For chronic severe pain in whom intrathecal administration si warranted and when refractory to other treatments

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37
Q

Capsaicin

A

Heat red pepper TPRV1

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38
Q

Camphor

A

TRPV1 heat

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39
Q

Methanol

A

TRPM8 cold

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40
Q

Topical NSAIDS

A

Yup

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41
Q

Topical Na channel blockers

A

Ok

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42
Q

Acute vs chronic gout

A

A-precipitation of uric acid in tubules

Chronic-monosodium urate in medullary interstitium

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43
Q

IMP and GMP are dephosphorylated and ribose cleaved from the base to give )) and ))0

A

Hypoxanthine and guanine

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44
Q

Xanthine formation

A

From hypoxanthine by xanthine oxidase and from guanine deamidation

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45
Q

Xanthine is converted to what by what

A

Uric acid by xanthine oxidase

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46
Q

Preformed nucleotide from diet or breakdown of endogenous nuclei acids is salvaged by

A

APRT

HGPRT

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47
Q

Lesch Nyhan

A

Defiency HGPRT
Intellectual defiency
Self utilization
Severe gout

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48
Q

Treat gout

A

Anti-inflammatories
Acute-intercritical period <2 years
Prophylactic

If recur-increase uric acid renal excretion ith uricosuric drugs and or reduce uric acid production with xanthine oxidase inhibitors and recombinant uricase

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49
Q

Treat acute gout

A

NSAIDS naproxen, indomethacin, celecoxib

Glucocorticoids-systemic/intra-articular

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50
Q

MOA coaching

A

Diffuse into cells to bind to tubules, blocks formation of microtubules

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51
Q

Effects coaching

A

Leads to inhibiton of leukocyte migration and phagocytosis

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52
Q

Clincial colchinen

A

If NSAIDS intolerance or contraindication

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53
Q

How colchicine given

A

Orally

HL 30 hours

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54
Q

AE colchicine

A

Very common is gastrointestinal distress, diarrhea, vomiting, nausea

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55
Q

If underexcreted with good GFR no tophi or stones

A

Urate lowering therapy with allopurinol, febuxostat, or uricosuric agent

OtherwiseUrate lowering therapy with low allopurinol and otherwise allopurinol

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56
Q

If allopurinol not tolerated

A

Febuxostat

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57
Q

Last resort

A

Pegloticase

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58
Q

Allopurinol MOA

A

Competitive inhibitor of xanthine oxidase

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59
Q

Effects allopurinol

A

Hypoxanthine and xanthine are excreted

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60
Q

AEA allopurinol

A

Rash

Hypersensitivity Stevens johnson syndrome can be fatal

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61
Q

Febuxostat OMA

A

Inhibitor of xanthine oxidase

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62
Q

Effects febuxostat

A

Hypoxanthine and xanthine are excreted

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63
Q

Clincial febuxostat

A

Those who cant tolerate allopurinol

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64
Q

Pegloticase moa

A

Recombinant mammalian uricase

Methoxy polyethylene glycol

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65
Q

Effects pegloticase

A

Converts uric acid the far more soluble allantoin

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66
Q

Rasburicase

A

No PEGylated recombinant uricase for acute uric acid nephorpathy due to tumor lysis syndrome with high risk lymphoma or leukemia

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67
Q

Probenecid moa

A

Organic acid blocks urate reabsorption more than urate secretion

Low dose asprin promotes urate reabsorption

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68
Q

Effects probenecid

A

Increases the fractional excretion of urate

Decreases plasma urate concentration

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69
Q

Clincial probenecid

A

Underexreters with GFR>60 ml/min and no stone !!!!!

Hyperuricemia
Frequent attacks
Tophi

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70
Q

AE probenecid

A

Kidney stones
Gouty arthritis flare
Suffer containg drug may cause hypersensitivity

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71
Q

Acute gout

A

NSAIDS colchinie glucocorticoids

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72
Q

Prevent recurrent gout

A

Urate lowering
Diet, weight reduction

Allopurinol, febuxostat, probenecid, pegloticase

73
Q

How treat RA

A

Stop inflammation
Relieve symptoms
Prevent joint and organ damage

74
Q

RA non pharm

A

Exercise, PT, OT< nutrition, bone protection, CVD risk , vaccination

75
Q

RA need pain relief addition

A

Acetaminophen

76
Q

First drug of choice for RA

A

NSAIDS
Anti inflammation and pain relief-naproxen and celecoxib
-doesnt alter disease progression

77
Q

Opioids with RA

A

No

78
Q

MOA glucocorticoids

A

Complexing with NFKB and AP1 transcription factors is a major indirect mechanism for immunosuppression

Lipocorticin, and inhibitor or PLA2

79
Q

Clincial glucocorticoids

A

Autoimmune disease like RA

Relieves pain and inflammation while waiting for DMARD effects

Treats flares

80
Q

Pharmacokinetics glucocorticoids

A

Others for RA, can be give PO, IM or intra articularly

81
Q

Prednisone

A

No effect until make to prednisolone in liver

82
Q

Side effects of glucocorticoids

A

Psychosis depression impaired glucose tolerance, salt water retention, buffalo hump, osteoporosis

83
Q

Abruptly stop glucocorticoids

A

Deadly

84
Q

Use of glucocorticoids

A

In sicker patient with RA prednisone is frequently added for a short period while awaiting a clincial repsonse to a slower acting disease modifying drug

85
Q

Chronic use of glucocorticoids

A

No

And keep <5 mg/day can generally be taken without significant adverse effects but no reduction in disease progression

86
Q

MILD RA

A

<5 inflated joints
Increase erythrocyte sedimentation rate and CRP
No extra articular disease
No evidence of erosions
Low levels of measures of disease activity

Most lack poor prognostic features such as rheumatoid factor or antibodies to cyclic citrullinated peptides

87
Q

Moderate RA

A

> 5 inflamed joints
Increase ESR and CRP

Rheumatoid factor and or anticyclic citrullinated peptide antibodies
Evidence of inflammation

Minimal joint space narrowing and small peripheral erosions

88
Q

Methotrexate MOA

A

Inhibitos of dihydrofolate reductase
Thymineless death

Undergoes polyglutamation to MTX whihc accumulates in cells over multiple weeks and also blocks thymidylate synthase and 5 aminoimidazole 4 carboxamide ribonucleotide transformylase

AICAR accumulation leads to adenosine efflux which binds to purinergic GPCR on cell surface to exert anti inflammatory effects

89
Q

Effects MTX

A

Faster than all other DMARDS in 3-6 weeks

For 80%

90
Q

Clincila MTX

A

Drug of first choice for RA due to its efficacy relative safety low cost and extensive use

Combination with other
Continued when patient is switched to biological DMARD

91
Q

Pharmacokinetics MTX

A

Once per week oral or injection

92
Q

AR MTX

A

Low doses

Well tolerated

Weekly folate supplements

Life threatening major toxicities

Higher doses include bone marrow suppression, hepatic fibrosis GI ulceration and pneumonitis

Fetal death and congenital abnormalities

93
Q

Hydroxychloroquine

A

Liphilic weak base

Accumulates in lysosomes

94
Q

Effects hydroxychloroquine

A

Higher pH of these lysosomal vesicles in antigen presenting cells limits the association of peptides with class II MHC molecules

Delayed onset 3-6 months

95
Q

Clincial hydroxychloroquine

A

Antimalarial

Combined with TMX

Safe in pregnancy

96
Q

Pharmacokinetics hydroxychloroquine

A

Half life of 23 days

Loading doses

97
Q

Toxicities hydroxychloroquine

A

Retinal damage

Low dosages carry little risk

98
Q

MOA sulfasalazine

A

Sulfapyridine active with RA unlike in IBD where 5-ASA

99
Q

Clincial sulfasalazine

A

Alone or in combination with hydroxychloroquine and/or MTX in triple therapy

Seems ok in pregnancy less studies

100
Q

AE sulfasalazine

A

Sulfa drug

GI side effects

101
Q

MOA leflunomide

A

Inhibiton of a mitochondrial enzyme dihydroorate dehydrogenase to block the synthesis of pyramiding rUMP

102
Q

Effects leflunomide

A

Inhibits T cell proliferation

103
Q

Clincial leflunomide

A

Alternative nonbiological DMARD to MTX second choice due to cost

In combination with MTX , sulfasalazine or hydroxychloroquine

104
Q

Pharmacokinetics leflunomide

A

16.5 days HL so loading doses needed

105
Q

AE leflunomide

A

Common adverse effects

106
Q

Biological DMARDS

A

Never be combined

But faster onset of action, high rate of response, more expensive, increased risk for severe adverse effects

107
Q

TNF antagonist MOA

A

Work by neutralizing TNF

108
Q

Effects TNF antagonist

A

Highly effective at reducing RA symptoms and disease progression

109
Q

Clincial TNF antagonist

A

Moderate to severe RA after DMARDS have proven ineffective

In combination with TMX

110
Q

AE TNF antagonist

A

All agents pose risk of developing serious infections

TB

Severe allergic reaction

111
Q

Etanercept

A

Of two p75 TNF receptors bound to the Fc portion of IgG

Once of trice weekly via SQ injection

112
Q

Infliximab

A

Chimeric mAb directed against TNF

IV infusion approximately every six weeks

113
Q

Adalimumab

A

Recombinant fully human anti TNF mAb SQ every 2 weeks

Best selling in world

114
Q

Rituximab MOA

A

B cell lineage

Surface expression of CD20

Beginning at the pre B cell state

CD20 lost as B cells differentiate into plasma

115
Q

Effects rituximab

A

Plasma cell resistance
Ig levels in normal range, despite profound B cell lymphopenia that persists for months following a single course

Autoantibodies

Affected by B cell depletion

116
Q

Clincial rituximab

A

With MTX for RA

Positive testing for Rheumatoid factor or anti cyclic citrullinated peptide greater likelihood of responsiveness

117
Q

AE rituximab

A

Infusion related hypersensitivity reactions

118
Q

Abatacept MOA

A

Prevents CD28 from binding to its counter receptor CD80/CD86

119
Q

Clincal abatacept

A

Moderate ot severe RA

Used in combination with nonbiological DMARDS like MTX

120
Q

AE abatacept

A

Generally well tolerated

Can increase the risk of serious infections

121
Q

Tocilizumab MOA

A

Anti human il6 receptor antibody

Competes for both the membrane bound and soluble forms of humans il6 receptor

122
Q

Effects tocilizumab

A

Blocking the binding of il6 to its receptor

Limits hepatic acute phase response and activation of T cells, B cells, macrophages and osteoclasts

123
Q

Clincial tocilizumab

A

IL6 levels are abnormally high in autoimmune disease

Moderate to severe RA if other DMARDS and TNF a blockers have proven to be ineffective

Can be used with or without MTX

124
Q

AE tocilizumab

A

Most common URI

Life threatening infections

125
Q

Tofacitinib MOA

A

Inhibitor of enzyme janus kinase 3

126
Q

Effects tofacitinib

A

Directly suppressed hte production of il17 and IFNy and ther proliferation of CD4 T cells

127
Q

Clincial tofacitinib

A

Moderately to severely active RA

With or without NTX

128
Q

Pharmacokinetics

A

Overpriced

129
Q

AE tofacitinib

A

Serious and sometimes fatal infections

Opportunistic pathogens

Increased malignancies

130
Q

MOA anakinra

A

Recombinant, non glycosylated version of IL1 receptos antagonist

131
Q

Effects anakinra

A

Endogenous il1ra are low in RA

Blocks the proinflamamtory activity of naturally occurring il1

132
Q

Clincial anakinra

A

Moderate to severe RA

Considered less efficacious

133
Q

AE anakinra

A

Increased incidence of serious infections

Hypersensitivity reactions

134
Q

Calcium salts

A

Oral for hypocalcemia, as dietary supplements in adolescents, elderly and postmenopausal women, but take too much and get hypercalcemia, GI disturbances, CNS, and renal dysfunction

Parenteral-given to rapidly increase calcium levels in patents with severe hypocalcemia

135
Q

What are vitamin D

A

Ergocalciferol D2 and cholecalciferol D3

Shiitake mushrooms and oily fish

Not in lots of foods
Fortified!

136
Q

MOA calcitonin-salmon

A

Similar in structure to human calcitonin but longer HL and potency

137
Q

Effects calcitonin salmon

A

Decrease bone resorption by inhibiting osteoclasts

Inhibits renal tubular resorption of calcium to increase calcium excretion

138
Q

Use of calcitonin

A

Osteoporosis

Paget disease

Hypercalcemia

139
Q

Pharmacokinetics calcitonin

A

Intranasal spray as parenteral for SC or IM administration

140
Q

Toxicities calcitonin

A

Sade
Nasal dry

Injection site reactions

May develop neutralizing antibodies

141
Q

Bisphosphonates MOA

A

Pyrophosphate analog

142
Q

Effects bisphosphates

A

Incorporate into bone and inhibit resorption by decreasing both the number and activity of osteoclasts

143
Q

Clincila use of bisphosphonates

A

Osteoporosis, paget, hypercalcemia of malignancy

144
Q

Pharmacokinetics aldronate

A

PO

145
Q

AE alendronate

A

Esophagitis, osteopetrosis of jaw, atypical femur fractures

146
Q

Risedronate

A

PO

147
Q

Ibandronate

A

PO IV

148
Q

Tiludronate

A

PO

149
Q

Zolendronic acid

A

IV

150
Q

Zolendronic acid

A

IV -osteopetrosis of jaw after tooth extraction

Dose dependent kidney damage and rarely atrial fibrillation

151
Q

SERMS

A

Raloxifene

Tamoxifen

152
Q

Raloxifene MOA

A

SERM

153
Q

Effects raloxifene

A

Blocks in breast and uterus

Estrogen effect in bone

154
Q

Raloxifene clincial

A

Due to its estrogen agonist effects on bone, prevent and treat postmenopausal osteoporosis

Antiestrogen effects in the breast, used to reduce the risk for estrogen dependent breast cancer

155
Q

Pharmacokinetics raloxifene

A

Administrated orally
Extensive first pass

Excreted in feces

HL 28 hrs

156
Q

AE raloxifene

A

DVT, pulmonary embolism, stroke

Discontinue at 72 hours before planned/prolonged immobilization

Pregnancy risk

Hot flashes

157
Q

Tamoxifen

A

Not for osteoporosis

158
Q

Teriparatide MOA

A

Truncated version of PTH from recombinant DNA

159
Q

Effects teriparatide

A

Increases bone formation!

Osteoclasts and osteoblasts

Continuously-resorption

Pulsed-osteoblast predominant

160
Q

Clincial teriparatide

A

Treatment of osteoporosis

161
Q

Pharmacokinetics teriparatide

A

20mcg is injected once daily with 28 doses

162
Q

Toxicities teriparatide

A

Nausea, HA, back pain leg cramps

Ca Mg uric acid rise but then back to normal

163
Q

Denosumab moa

A

Monoclonal antibody that is a first in class RANKL inhibitor

164
Q

Effects denosumab

A

Bind RANKL decreases formation of osteoclasts decrease bone resorption

165
Q

Clincial denosumab

A

Osteoporosis, prevent skeletal related events in patients with bone metastases from solid tumros, should be taken with ca and VD

166
Q

Pharmacokinetics denosumab

A

Injected every 6 months
For osteoporosis

Bone metastases SQ injected every 4 weeks

167
Q

Toxicities denosumab

A

Back pain, msk pain, UTI, hypercholestermia

In bone metastases fatigue, hypophosphatemia, nausea

Delays fracture healing, increase risk new fracture and osteopetrosis of jaw

Severe infections

168
Q

Osteoporosis in men treat

A

Terosterone replacement

Glucocorticoids, androgen deprivation therapy

Bisphosphonates , denosumab

169
Q

Drugs for hypercalcemia

A

Furosemide, glucocorticoids, gallium nitrate, bisphosphnates, inorganic phosphates, edetate disodium

170
Q

Cinacalcet moa

A

Calcimimetic drug

171
Q

Effects cinacalcet

A

Binds to calcium sensing receptors on the parathyroid gland

Increase their sensitivity to extracellular calcium

Decrease PTH secretion

172
Q

Clincial cinacalcet

A

Primary hyperparathyroidism

Secondary hyperparathyroidism due to CKD

173
Q

Pharmacokinetics cinacalcet

A

Dosing is oral with food

30-40 hrs HL

174
Q

AE cinacalcet

A

Nausea, vomiting, diarrhea

175
Q

Joint mice

A

Osteoarthritis

176
Q

OTC osteoarthritis

A

Glucosamine, chondroitin, DMSO, SAMe failed to prove benefit

Devil claw, stinging nettle, rose hips, avocado, soybean, lack reliable evidence of benefit and consistency in preparation

177
Q

Pain treatment OA

A

Acetaminophen
NSAIDS
Topical NSAIDS or capsaicin
-topical is 1% diclofenec gel

Resistant to opioid, intraarticular hyaluronans

178
Q

Osteomyelitis treatment

A

Based on pathogens
-clindamycin, rifampin, TMP SMX, fluoroquinolone
For 4-6 weeks

Pharmacology (52 decks)

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