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Med School Year 2 Flash Cards > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the effect of corticosteroids?

A

Inhibit the production and release of many different cytokines that normally would stimulate the proliferation and function of B and T lymphocytes
Block the phospholipase 2

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2
Q

What are the corticosteroids used for asthma?

A

Beclomethasone
Budesonide
Triamcinolone

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3
Q

What is the toxicity associated with systemic administration of corticosteroids?

A 
HPA suppression
Immunosuppression - poor wound healing, opportunistic infection
Cushing's syndrome
Hyperglycemia 
Hypertension
Peptic ulcers 
Myopathy
Behavioral changes 
Cataracts
Osteoporosis 
Growth retardation
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4
Q

What are the therapeutic considerations for a short course of corticosteroids?

A

Insomnia and hyperactivity

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5
Q

When do you use pulse therapy with corticosteroids?

A

When the person has a serious or life-threatening disease

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6
Q

What is the treatment for anaphylactic reaction?

A

Epinephrine

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7
Q

What are topical corticosteroids used for?

A

Dermatologic conditions

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8
Q

What is a COX 2 Inhibitor?

A

Celecoxib

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9
Q

What is a non-NSAIDs antipyretic / analgesic?

A

Acetaminophen

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10
Q

What is the MOA of NSAIDs?

A

Non-selectively Blocks the action of COX 1 and 2 so it ultimately stops the production of prostaglandins which are involved in inflammation

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11
Q

What are the 5 prostanoids?

A
  1. Prostacyclin
  2. Thromboxane A2
  3. Prostaglandin D2
  4. PGE2
  5. PGF2
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12
Q

Where is COX1 expressed?

A

In most tissues - it is constitutively active

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13
Q

What is COX2 induced by?

A

Induced by cytokines and other inflammatory mediators

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14
Q

What are the contraindications to Celebrex?

A

Aspirin allergy and 3rd trimester

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15
Q

What was the reason for taking COX 2 inhibitors off the market?

A

Increased risk for cardiac events

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16
Q

What are some of the advantages to NSAIDs over aspirin?

A

More potent
More efficacious
Less GI problems
Have longer duration of action

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17
Q

What are the disadvantages to new NSAIDs compared to aspirin.?

A

More expensive
More toxic
No CV benefit or anti-cancer usage

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18
Q

What level of pain are NSAIDs effective for?

A

Low-to-moderate intensity

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19
Q

What are the GI effects of prostaglandins?

A

Inhibit gastric acids secretion
Stimulate synthesis of bicarbonate and mucus
Promotes mucosal blood flow

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20
Q

What are the GI effects of NSAIDs?

A 
Epi gastric distress
Nausea
Vom
Microhemorrhage 
Ulceration
Anemia
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21
Q

What does thromboxane A2 do?

A

Vasoconstrictor

Activates platelet aggregation and release

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22
Q

How is aspirin good for prophylaxis of CVD?

A

It inhibits TXA2 so inhibits vasoconstriction and platelet aggregation

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23
Q

How can NSAIDs cause renal failure?

A

In the setting of diseases with high levels of circulation vasoconstrictors, it can cause acute renal failure by decreasing renal blood flow because it is inhibiting prostacyclin which normally opposes vasoconstrictor action on the efferent arterioles in the kidney
Diseases to be careful with using NSAIDs: liver failure, CHF,

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24
Q

What are the anti-cancer effects of COX2 inhibitors and aspirin?

A

Reduces occurrence and mets of cancer by 1/3

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25
Q

What is Reyes’s syndrome?

A

Consequence of flu virus of chicken pox and using salicylates in children.
Liver damage and encephalopathy

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26
Q

What is indomethacin?

A

The most efficacious NSAID. But causes high rates of GI bleeding so not used chronically.

Used to tx patent ductus arteriosus

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27
Q

What are the side effects of NSAIDs?

A

Epi gastric distress, naus/vom, microscopic bleeding, ulceration, anemia, prolonged bleeding time, hypersensitivity,

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28
Q

What are the sign of salicylism?

A

Naus/vom, tinnitus, hyperventilation, headache, mental confusion, dizziness

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29
Q

What are the signs of overdose of a salicylate?

A

Fever, dehydration, delirium, hallucination, convulsions, coma, respiratory and metabolic acidosis, death

Children are especially vulnerable!!!

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30
Q

What are adverse effects of salicylates during pregnancy?

A 
Low birth weight
Increased perinatal mortality
Anemia
Antepartum and postpartum hemorrhage
Prolonged gestation
Premature closure of ductus arteriosus
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31
Q

What is ketorolac used for?

A

Post op pain

Can be given parenterally

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32
Q

What is celecoxib approved for?

A

Osteoarthritis and rheumatoid arthritis

Menstual pain and acute post op pain

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33
Q

What is the MOA of acetaminophen?

A

Metabolized in the brain to COX inhibitor.

This drug is mostly effective in the CNS - not for peripheral anti inflammatory activity.

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34
Q

What are the adverse effects of acetaminophen?

A

Depletes glutathione — hepatic damage

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35
Q

What is used to treat toxicity of acetaminophen?

A

N-acetylcysteine (sub for glutathione)

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36
Q

What are dynorphins?

A

Usually associated with kappa receptor activation

Cause dysphoria and hyperalgesia in animal studies

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37
Q

What are mu receptors important for?

A 
Analgesia
Euphoria
Miosis
Respiratory depression
Physiological dependence
Reduced GI motility
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38
Q

What are the delta receptors for?

A

Euphoria

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39
Q

What are the kappa receptors responsible for?

A 
Dysphoria
Psychotomimetic responses
Analgesia
Sedation
Vasodilation
Increased urinary output
Less miosis and respiratory depression than mu
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40
Q

What is an advantage to kappa receptors?

A

Less involvement in abuse potential and physical dependence

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41
Q

What is the use of opioids in analgesia?

A

They hit the mu and kappa receptors. They diminish the sensory and reactive component of pain, but the reactive component more.

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42
Q

What is morphine useful in treating and how does it work?

A

Pulmonary edema
It is a great vasodilator because it makes the brain stem less responsive to pCO2 so there is less sympathetic activation. Flid is shifted from the central to the peripheral compartment

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43
Q

How do opioids cause constipation?

A

They cause increased tone in the intestine

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44
Q

What are the high efficacy mu opioids?

A 
Morphine
Meperidine
Methadone
Fentanyl
Oxycodone
Heroin
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45
Q

What are the main points about morphine?

A

Binds of all opioid receptors
Highest affinity for mu
Highly polar - less potent thru the oral route
High efficacy for analgesia

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46
Q

Which mu opioid has a metabolite that can cause seizures?

A

Meperidine

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47
Q

What is the MOA of methadone?

A

Blocks NMDA receptors and mono amine uptake pumps so it also acts as an antidepressant
Long Elimination half life

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48
Q

What is the mu opioid with the highest potency?

A

Fentanyl

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49
Q

What is fentanyl used for?

A

Naus/vom - lipid soluble so used as a patch

Surgery

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50
Q

What is the side effect of fentanyl if given IV?

A

Truncal rigidity

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51
Q

What are the high efficacy kappa opioids?

A

Butorphanol

Nalbuphine

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52
Q

What is butorphanol used for?

A

Post surgery because less potential for respiratory suppression

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53
Q

Who does butorphanol work better on?

A

Women

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54
Q

What is nalbuphine used for?

A

Post surgery to remove the depressant effects of mu agonists

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55
Q

What are the intermediate efficacy opioids?

A

Hydrocodone
Oxycodone
Pentazocine

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56
Q

What schedule drug is oxycodone?

A

Schedule 2

Highly addictive

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57
Q

What are the attempts to limit abuse of oxycodone?

A

Add a matrix

Add naloxone - not absorbed orally very well

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58
Q

What is the cornerstone drug for pain clinics?

A

Amitriptyline - an antidepressant

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59
Q

Which intermediate opioid has an effect on kappa receptors?

A

Pentazocine

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60
Q

What are the low efficacy opioids?

A

Buprenorphine

Codeine

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61
Q

What are the characteristics of burprenorphine?

A

Long duration of action
Slow to dissociate from my receptors
Ideal for preventing high efficacy compounds in narcotic tx programs

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62
Q

What is the opioid of choice for cough?

A

Codeine

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63
Q

What is the limitation of codeine?

A

At higher doses it hits non-mu receptors producing unpleasant psychotomimetic effects

64
Q

What is the MOA of codeine in analgesia?

A

It is converted to morphine in the liver by CYP2D6 by demethylation

65
Q

What is CYP450 ?

A

A family of Microsomal enzymes located in the ER of liver cells

66
Q

What subfamily of P450 enzymes does CYP2D6 come from?

67
Q

What is CYP2D6 responsible for?

A

Demethylation reactions : metabolism of beta blockers and codeine to morphine

68
Q

What is the consequence of missing CYP2D6?

A

High level of parent drug - codeine. No analgesic effects

69
Q

What is the opioid that is not classified according to efficacy?

A

Tramadol - not a good mu agonist

70
Q

What is the MOA of tramadol?

A

Weak mu agonist
Serotonin releases
Norepinephrine reuptake inhibitor

71
Q

What are the uses of tramadol?

A

Good for pain in moderate range
Good for neuropathic pain
Outpatient therapy

72
Q

What are the potential side effects of tramadol?

A

High doses can cause seizures
Dependence/withdrawal
Enhances respiratory depression of other drugs - be careful

73
Q

What are the drug interactions with tramadol?

A

SSRIs - risk of serotonin syndrome
Alcohol
Barbiturates

74
Q

What are the sx of serotonin syndrome?

A

Tremor
Clonus
Hyperreflexia
Hyper pyresis

75
Q

What are the opioid antagonists?

A

Naloxone - short acting, injected
Naltrexone - long acting, oral
Nalmefene

76
Q

What is the prototype antagonist?

77
Q

When does dependence become clinically relevant?

A

After 2-3 weeks of use

78
Q

What is the primary triad of sign for opioid overdose?

A

Lethargy or coma
Depressed respiration
Pinpoint pupils

79
Q

What are secondary signs of opioid overdose?

A 
Hypotension
Hypothermia with cold or clammy skin
Pulmonary edema
Convulsions
Dilated pupils (near death)
80
Q

What is the DOC for tx of opioid OD?

81
Q

What is the tx for opioid OD?

A

Naloxone
Support of respiration and vitals
Identify drug

82
Q

What is a non-opioid OTC drug used for cough?

A

Dextromethorphan

83
Q

What are the opioids used for diarrhea?

A

Loperamide
Diphenoxylate
Difenoxin

84
Q

What is the MOA of MTX?

A

Inhibits dihydrofolate reductase. Prevents DNA and RNA synthesis - immunosuppressive
Used in low doses for RA

85
Q

What are the most common side effects of MTX when given in low doses?

A

Nausea and mucosal ulcers

86
Q

What are the most common side effects of MTX at higher doses?

A

Drop in WBC
Cirrhosis
Pneumonitis

87
Q

What are the effects of TNF-alpha?

A

Release of inflammatory mediators

Kill intra cellular organisms

88
Q

What are the TNF- alpha antagonists?

A 
Inflict ab
Etanercept
Adalimumab
Golimumab
Certolizumab
89
Q

What is infliximab?

A

A chimeric mouse/human monoclonal antibody that binds to TNF-alpha.
Given IV every several weeks

90
Q

What is the most common side effect of infliximab?

91
Q

What is etanercept?

A

A recombinant protein that binds two molecules of TNF-alpha.
Injected subq twice weekly

92
Q

What is adalimumab?

A

An entire human monoclonal Ab.

An attempt to decrease the immunoreactivity of infliximab.

93
Q

What is golimumab?

A

A once monthly injection approved for RA, anklyosing spondylitis, and psoriatic arthritis

94
Q

What is leflunomide ?

A

What is an alternative to MTX. Mech in RA is not entirely clear - may inhibit tyrosine kinase and production of pyrimidines.

95
Q

What are the side effects of leflunomide?

A

Elevated liver enzymes
GI problems
Alopecia

96
Q

What is abatacept?

A

It is a drug approved for use in severe RA for patients that don’t respond to TNF inhibitors

97
Q

What is the MOA of abatacept?

A

Constimulation modulators that renders T cells inactive because it interferes with the process that turns them on.
It binds to CD 80 and CD 86 on the APC so that the T cell can’t be activated via interaction with CD 28.

98
Q

In what disease condition is abatacept contraindicated in?

99
Q

What other drug can abatacept not be used with?

A

MTX - too many incidences of infection

100
Q

What is rituximab?

A

It is a monoclonal Ab that reduces B cells.

Approved for moderate to severe RA.

101
Q

What are the side effects of rituximab?

A

Flu-like sx

Possible breathing problems, cardiac rhythm disturbances, cardio genic shock

102
Q

What is sulfalazine?

A

Drug used to treat IBD and autoimmune diseases (RA, anklyosing spondylitis, seronegative spondyloarthropathy)

103
Q

What are the side effects of sulfalazine?

A

Hypersensitivity rxns

GI problems

104
Q

Who is sulfalazine a good alternative for?

A

Patients with liver disease who need MTX

105
Q

How does sulfalazine work in the body?

A

It is poorly absorbed. Bacteria metabolize it to antibiotic and anti inflammatory metabolites.

106
Q

What are hydroxychloroquines?

A

They are antimalarials used to treat RA that is mild to moderate.

107
Q

What are the toxicity was associated with hydroxychloroquines?

A

Corneal deposits
Extra ocular muscle weakness
Loss of accommodation
Retinopathy —loss of vision

108
Q

How do gold salts work?

A

They suppress RA by inhibiting maturation and function of mononuclear phagocytes and T cells.

109
Q

At what stage of RA, are gold salts used?

A

In the early active phase

110
Q

What are the gold salts?

A

Gold sodium thiomalate
Aurothioglucose
Auranofin

111
Q

Which gold salts are water soluble?

A

Aurothioglucose

Gold sodium thiomalate

112
Q

Which is the hydrophobic gold salt?

A

Aurofin - better tolerated, less efficacy

113
Q

What are the most common side effects of gold salts?

A

Lesions on skin and mucous membranes, mostly in the mouth

Other less frequent:
Kidney damage
Severe blood dyscrasias

114
Q

What is D-penicillamine?

A

An cysteine analog used in RA to slow bone destruction.

115
Q

What are the long term effects of D-penicillamine?

A

Nephritis
Aplastic anemia
Dermatological problems

116
Q

When is D-penicillamine used?

A

In severe disease after every other treatment has failed

117
Q

What are the actions of IL-1?

A

Stimulates own production
Causes secretions of prostaglandins, NO, metalloproteinases - promotes joint degradation
Inhibits collagen synthesis - inhibits joint repair

118
Q

What is anakinra?

A

A recombinant for of human IL-1ra, IL-1 receptor antagonist

119
Q

What drugs should anakinra not be prescribed with?

A

TNF inhibitors - higher rate of infection

120
Q

What is tocilixumab/actemra?

A

Antibody that binds to and inactivates IL6 receptors

Approved for patients who fail TNF inhibitor therapy

121
Q

What does IL-6 do?

A

Secreted by macrophages and T cells

Stimulates immune response, osteoclasts formation

122
Q

What are the side effects of tocilixumab?

A

URI, headache, high bp, liver enzyme elevation, increased LDL, decreased neutrophils and platelets.

123
Q

What are the serious adverse side effects of tocilixumab?

A

Infection
GI perforation
Anaphylaxis

124
Q

What is cyclosporine?

A

Complex cyclic peptide isolated from fungus

Immunosuppressant

125
Q

What is the MOA of cyclosporine?

A

Selectively inhibits T lymphocytes

126
Q

Who is cyclosporine reserved for?

A

Patients who fail to respond to other therapies with severe disease

127
Q

What are the disadvantages to cyclosporine?

A

Expensive

Renal toxicity

128
Q

What is azathioprine?

A

A purine anti metabolite that interferes with purine synthesis and causes DNA damage through formation of false nt substrates for DNA synthesis

Immunosuppressant

129
Q

What are the side effects of azathioprine?

A

BM suppression

Hepatotoxicity

130
Q

What are the uses of azathioprine?

A

Transplant rejection
Cancer
Severe refractory RA
SLE

131
Q

What is cyclophosphamide?

A

Nitrogen mustard, alkylation agent.

132
Q

What is the MOA of cyclophosphamide?

A

Alkylate a DNA interfering with its synthesis and function.

Causes t and B cell suppression

133
Q

What is cyclophosphamide used in?

A

Cancer

Severe autoimmune disease with vasculitis

134
Q

What is capsaicin?

A

Derived from plants

135
Q

What is the MOA of capsaicin?

A

Local depletion of substance P

136
Q

How is capsaicin uses?

A

As a cream for RA and OA

137
Q

What are the non-pharm ways to control gout?

A

Avoid organ means, high fructose corn syrup, alcohol
Avoid large meals with meat
Stay hydrated

138
Q

What are the foods that are encouraged in gout?

A

Low-non fat dairy

Vegetables

139
Q

What is the DOC for acute attacks of gout?

A

Indomethacin

140
Q

Which NSAIDs should not be used in gout?

A

Aspirin or salicylates because it inhibits phagocytosis of urea crystals and excretion of uric acid into the urine.

141
Q

Which drug used to be used for acute gout attacks binds Tubulin in mitotic spindles causing cell cycle arrest?

A

Colchicine

142
Q

How does colchicine relieve the sx of gout?

A

By causing cell arrest, it prevents the migration of granulomatous into the inflamed area

143
Q

What are the side effects of colchicine?

A

Diarrhea
Nausea/vom
Ab pain

144
Q

What can long term use of colchicine cause?

A

Myopathy
Agranulocytosis
Aplastic anemia
Alopecia

145
Q

What are the 2 drugs used in standard care of gout?

A

Allopurinol and Febuxostat

146
Q

What is allopurinol?

A

A purine analog that competitively inhibits the last 2 steps in uric acid production

147
Q

What are the most common side effects of allopurinol?

A

Hypersensitivity rxns

148
Q

What is Febuxostat?

A

A xanthine oxidase inhibitor

Better at lowering uric acid levels, but no benefit wi lesser attacks

149
Q

Why must you begin with a low dose of allopurinol with colchicine?

A

Because allopurinol can precipitate a gout attack. Once uric acid levels fall, colchicine can be stopped

150
Q

How do uricosuric agents work?

A

Prevent tubular reabsorption of uric acid

151
Q

What is probenecid?

A

A uricosuric agent used for treating chronic gout.

152
Q

Who is the use of probenecid contraindicated in?

A

Impaired renal function

Patients prone to stone formation.

153
Q

What is sulfinpyrazone?

A

A uricosuric agent.

May induce hypoglycemia

154
Q

What are bisphosphonates?

A

Pyrophosphate analogs that are not hydrolyzed

155
Q

What is the MOA of bisphosphonates?

A

Inhibit bone resorption

Prevent formation and dissolution of hydroxyapatite crystals

156
Q

What are the side effects of bisphosphonates?

A

Esophagitis

Osteonecrosis of the jaw

157
Q

What are the bisphosphonates used?

A

Alendronate - weekly oral

Ibandronate. - monthly oral

Med School Year 2 Flash Cards (18 decks)

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