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PR3152 Finals > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is carbimazole used for?

A

Hyperthyroidism

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2
Q

What is carbimazole’s MOA?

A

inhibit thyroid peroxidase resulting in less T3/T4 precursors –> decreased thyroid hormones output

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3
Q

What is carbimazole dosing frequency and ROA?

A

PO once daily

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4
Q

What happens to carbimazole after absorption?

A

Converted into active methimazole in the serum

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5
Q

What is carbimazole’s (or its metabolites’) half life?

A

Methimazole’s half-life 4-6 hour

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6
Q

Does carbimazole (or its metabolites) bind to plasma proteins?

A

No

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7
Q

How long does it take for carbimazole to exert its effect?

A

> 90% inhibition achieved within 12 hours, however clinical response may take 3-6 weeks after initiation due to thyroid stores in the body and T4’s long half life.

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8
Q

How is carbimazole metabolized?

A

CYP450 and FMO enzymes

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9
Q

How is carbimazole excreted?

A

> 90% excreted in urine as methimazole or its metabolites

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10
Q

What are adverse effects of carbimazole?

A

Rashes
Joint pains
Nausea
Jaundice
Agranulocytosis (rare)

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11
Q

What is levothyroxine used for?

A

Hypothyroidism

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12
Q

What is levothyroxine’s MOA?

A

Synthetic thyroid hormone

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13
Q

What can affect levothyroxine’s absorption?

A

Increased absorption with fasting
Erratic absorption with dietary fiber
Affected by gastric pH

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14
Q

What is levothyroxine’s bioavailability?

A

70-80%

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15
Q

How long does it take for levothyroxine to exert its effect?

A

PO: 3-5 days
IV: 6-8H

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16
Q

What is levothyroxine’s half-life?

A

7 days

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17
Q

Does levothyroxine bind to plasma proteins?

A

Yes, >99%

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18
Q

How is levothyroxine being metabolized?

A

Liver - glucuronidation, sulphation
Kidney - deiodination

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19
Q

How is levothyroxine being excreted?

A

Primarily by kidneys

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20
Q

What are adverse effects of levothyroxine?

A

Reduced appetite
Anxiety, insomnia
Hair loss
Diarrhea

Rare and serious:
Heart issues
Seizures

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21
Q

When is IV form of levothyroxine used?

A

Myxoedema coma (severe form of hypothyroidism)
Cannot use PO levothyroxine as there is reduced blood flow to GI
Can also use IV Liothyronine (synthetic T3)

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22
Q

What should you monitor after initiation of levothyroxine therapy?

A

Serum TSH every 6-8 weeks after initiation or dose titration

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23
Q

What does persistently elevated TSH levels indicate after levothyroxine therapy has been started?

A

Inadequate dosing, poor compliance, malabsorption, DDI or food-drug interaction

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24
Q

What is tamoxifen used for?

A

Breast cancer in both pre- and post- menopausal women

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25
Q

What is tamoxifen’s MOA?

A

selective estrogen receptor modulator (SERM)

competitively blocks endogenous estrogen binding to the estrogen receptor in the target tissue

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26
Q

Does tamoxifen have stereoisomers?

A

Yes

Tamoxifen exists in cis- (estrogenic) and trans- (anti-estrogenic) stereoisomers

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27
Q

How is tamoxifen’s absorption profile like?

A

Rapidly and extensively absorbed in intestine
F ~100%
Css typically reached after 3-4 weeks (max 16 weeks)
Tmax is 3-7 hours

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28
Q

Does tamoxifen bind to plasma protein?

A

> 98%

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29
Q

What is tamoxifen’s Vd?

A

50-60 L/kg

high concentrations found in tissues especially uterus (2-3 fold higher than serum) and breast (10 fold higher than serum)

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30
Q

How is tamoxifen metabolized?

A

Phase 1: hydroxylation, N-oxidation, dealkylation
Phase 2: glucuronidation, sulphation
Major pathway: N-demethylation

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31
Q

What is tamoxifen’s major metabolite and its half-life?

A

N-desmethyltamoxifen (t1/2 ~14 days)

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32
Q

How is N-demethylation of tamoxifen catalyzed? And what’s the consequences?

A

By CYP3A4
Should not take with grape gruit or CYP3A4 inhibitors

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33
Q

What are tamoxifen’s minor metabolites?

A

4-hydroxytamoxifen
4-hydroxy-N-desmethyltamoxifen (endoxifen)

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34
Q

Which of the tamoxifen’s metabolites has greater affinity for the estrogen receptor?

A

Minor metabolites

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35
Q

What catalyzes metabolism of tamoxifen into its minor metabolites? And what are its consequences?

A

CYP2D6
Do not take with diphenhydramine or inhibitors of CYP2D6

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36
Q

How is tamoxifen excreted?

A

Mainly through feces

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37
Q

What are side-effects of tamoxifen therapy?

A

Anti-estrogenic
- Hot flushes
- Menstrual irregularities

Estrogenic
- Risk of endometrial cancer
- DVT
- Vaginal bleed and discharge
- Nausea/vomiting

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38
Q

Overdose of tamoxifen can lead to?

A

Acute neurotoxicity eg. tremor, hyperreflexia, unsteady gait, dizziness

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39
Q

How do you treat tamoxifen overdose?

A

Supportive treatment

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40
Q

What is pembrolizumab used for?

A

Breast cancer

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41
Q

What is pembrolizumab’s MOA?

A

PD-1 inhibitor
Binds to PD-1 and prevents PD-L1 on tumor cells binding to it, thus allowing activation of immune response to fight the tumor cells

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42
Q

What type of antibody is pembrolizumab?

A

Humanized antibody (-zumab)

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43
Q

How is pembrolizumab administered?

A

IV infusion over 30 mins

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44
Q

What is pembrolizumab’s dose?

A

IV 200mg every 3 weeks

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45
Q

What is pembrolizumab’s Vd?

A

~7L

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46
Q

How is pembrolizumab metabolized?

A

non-specific catabolism (general protein degradation routes) into small peptides and single amino acids

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47
Q

How is pembrolizumab excreted?

A

No studies done

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48
Q

What is pembrolizumab’s half-life?

A

~27 days

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49
Q

When will pembrolizumab reach Css?

A

after ~19 weeks

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50
Q

What can cause slower clearance of pembrolizumab?

A

Cervical cancer in women

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51
Q

What are S/E of pembrolizumab?

A

Infusion-related S/Es, immune-related inflammation, joint pain, fatigue, diarrhea, nausea

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52
Q

What are C/I of pembrolizumab?

A
  • On immunosuppressants or corticosteroids
  • Pregnancy
  • Hypersensitivity
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53
Q

List 4 ways to achieve androgen deprivation

A
  • Inhibition of pituitary gonadotropin release (by using GnRH analogs)
  • Inhibition of androgen synthesis
  • Inhibition of androgen binding (by using androgen receptor blockers)
  • Surgical extirpation of the glands (by castration and adrenalectomy)
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54
Q

What is leuprorelin used for?

A

Prostate cancer

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55
Q

What is leuprorelin’s MOA?

A

GLP-1 agonist
It is a synthetic GnRH which activates the pituitary GnRH receptors

Continuous GnRH causes negative feedback on the pituitary leading to reduced FSH and LH levels

Reduced FSH and LH levels suppresses testosterone production in the testes and causes prostate cancer cells (androgen-sensitive cells) to undergo apoptosis

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56
Q

What should you monitor after starting leuprorelin?

A

Measure PSA in first few weeks of therapy
Measure LH, FSH, and serum testosterone after 4 weeks of therapy

Reduction in levels of these substances indicates that the treatment works

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57
Q

How is leuprorelin administered?

A

SC or IM, given as single-dose long acting depot (1, 3, or 4 months interval)

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58
Q

What is leuprorelin’s time to Cmax and Css?

A

Cmax: 1-3 hours post injection
Css typically after 4 weeks

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59
Q

What is leuprorelin’s Vd?

A

~27L after IV
No data after SC or IM

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60
Q

Does leuprorelin binds to plasma protein?

A

~45% plasma protein binding (in vitro)

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61
Q

How is leuprorelin metabolized?

A

degraded proteolytically (peptidases) into inactive peptides

not metabolized in liver CYP450

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62
Q

What is leuprorelin’s half-life?

A

~ 3 hours

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63
Q

How is leuprorelin excreted?

A

<5% via urine

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64
Q

What are side effects of leuprorelin?

A
  • Hot flushes (first few weeks)
  • Injection site reaction
  • Headache/dizziness
  • Altered mood
  • Hyperglycemia
  • Decreased libido
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65
Q

What are C/I to leuprorelin?

A

Hypersensitivity
Pre-existing heart disease
Pts with risks for osteoporosis

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66
Q

What is bicalutamide used for?

A

Prostate cancer

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67
Q

What is bicalumatide’s MOA?

A

Androgen receptor antagonist

Steps:
- Competitive antagonist of androgen receptor
- Inhibits nuclear translocation of the androgen receptors
- Inhibits transcription processes
- Impairing cell proliferation
- Triggers apoptosis of the cancer cells.

68
Q

Can bicalumatide be used as a monotherapy? Why or why not?

A

No

Can cause initial surge of testosterone levels, which can lead to the prostate tumor flare

To be used in conjunction with GnRH analogue to alleviate those effects

69
Q

Does food interferes with bicalutamide’s absorption?

A

No

70
Q

Does bicalumatide bind to plasma protein?

A

> 99%

71
Q

How is bicalumatide metabolized?

A

By liver
Active metabolite - slow hydroxylation (CYP3A4) followed by glucuronidation

72
Q

Which isomer of bicalutamide is active? And its half-life?

A

R-isomer ~6 days

73
Q

How is bicalumatide excreted?

A

Via bile and urine

74
Q

What is bicalumatide’s S/E?

A

Constipation/diarrhea
Decreased libido
Fatigue
Hot flushes
Mild swelling of ankles/legs/feet
Nausea/vomiting

75
Q

What are C/I to bicalutamide?

A

Hypersensitivity
Women and children

76
Q

What are oral pharmacotherapy options for managing BPH?

A
  • Alpha adrenergic antagonists (alpha blockers)
  • 5-alpha-reductase inhibitors (5ARIs)
  • Muscarinic receptor antagonists (MRAs)
  • Phosphodiesterase 5 inhibitors (PDE5i)
77
Q

What is tamsulosin’s MOA?

A

reversible alpha-1A adrenoreceptor blocker

blocks the contraction of internal sphincter resulting in relaxation of bladder & urethra’s smooth muscle and allowing urine to flow

78
Q

Can tamsulosin be used on patients with enlarged prostate size?

A

Tamsulosin can be used for symptomatic BPH regardless of prostate size

79
Q

What is tamsulosin’s Vd?

A

0.2L/kg

80
Q

Does tamsulosin bind to plasma proteins?

A

> 90%

81
Q

How is tamsulosin metabolized?

A

CYP3A4 and CYP2D6

82
Q

What is tamsulosin’s half-life?

A

10-15 hours (OD dosing)

83
Q

How is tamsulosin excreted?

A

~10% excreted unchanged in urine

84
Q

What are adverse effects of tamsulosin?

A

Abnormal ejaculation
Back pain

85
Q

What are C/I to tamsulosin?

A

Concurrent use of another alpha-1-receptor antagonist

86
Q

What is finasteride’s MOA?

A

5-alpha reductase inhibitor (competitive and specific)

Inhibits the conversion of testosterone to DHT, hence decreasing prostate size

87
Q

What is finasteride’s bioavailability?

A

F ~0.65

88
Q

Is there any dose adjustment of finasteride required for renal/liver failure or elderly patients?

A

No dose adjustment required

89
Q

Is finasteride bound to plasma protein?

A

~90%

90
Q

How is finasteride metabolized?

A

CYP3A4

91
Q

What is finasteride’s half-life?

A

~6 hours

92
Q

How is finasteride excreted?

A

50% unchanged in feces
Metabolites in urine and feces

93
Q

What are S/E of finasteride?

A

Decreased libido and sexual potency
Gynecomastia (rare)

94
Q

What are C/I to finasteride?

A

Women and children
Pregnancy

95
Q

What is sildenafil used for?

A

Erectile dysfunction

96
Q

What is the MOA of sildenafil?

A

PDE5 inhibitor (specific to PDE5 in penis)

Inhibits PDE5 to decrease degradation of cGMP

Increased cGMP levels results in smooth muscle relaxation and increased blood flow to the corpora cavernosa

97
Q

What is the onset of sildenafil?

A

30-60 mins

98
Q

What is the bioavailability of sildenafil?

A

F ~0.4

99
Q

Is there any dose adjustment of sildenafil required for renal/liver failure or elderly patients?

A

No

100
Q

What is the maximum duration of action of sildenafil?

A

~12 hours

101
Q

How is sildenafil metabolized?

A

Major - CYP3A4
Minor - CYP2C9

102
Q

What is sildenafil’s half-life?

A

~4 hours

103
Q

How is sildenafil excreted?

A

Metabolites: 80% in feces, 13% in urine
Unchanged: in urine

104
Q

What are S/E of sildenafil?

A
  • Headache
  • Flushing
  • Dizziness
  • Blurred vision
  • Blue-green tinting of vision (retinal PDE6 inhibition)
  • Priapism
  • Back pain
  • Dyspepsia
105
Q

What are C/I to sildenafil?

A

Cardiac patients on GTN or nitrates

106
Q

What is ethinyl estradiol’s MOA?

A

Synthetic estrogen (estrogen receptor agonist)

Causes decreased FSH release from anterior pituitary and hence suppresses the development of ovarian follicle

Make endometrium unsuitable for implantation of ovum

107
Q

What is ethinyl estradiol used for?

A
  • Menopausal symptoms
  • Gynecological disorders
  • Certain hormone sensitive cancers
108
Q

What is the onset and bioavailability of ethinyl estradiol?

A

30-60 min
F ~0.45

109
Q

Is ethinyl estradiol protein bound?

A

~98%

110
Q

How is ethinyl estradiol metabolized?

A

Phase I - hydroxylation by CYP3A4
Phase II - glucuronidation (ethinyl estradiol glucuronide) and sulfation (ethinyl estradiol sulfate)

Ethinyl estradiol sulfate undergoes enterohepatic recirculation

111
Q

What is the half-life of ethinyl estradiol?

A

13-27 hours

112
Q

How is ethinyl estradiol excreted?

A

Feces and urine

113
Q

What are the adverse effects of ethinyl estradiol?

A
  • Breast tenderness
  • Headache
  • Dizziness
  • Nausea
  • Fluid retention
  • Weight gain
  • Risk of VTE
  • Risk of MI/stroke
  • Liver damage
114
Q

What are C/I to ethinyl estradiol?

A
  • Breastfeeding and <21 days postpartum
  • Breast cancer
  • Hx of DVT
  • Advanced diabetes with vascular disease
  • HTN ≥ 160/100
115
Q

What is norethindrone’s MOA?

A

Synthetic progestin (progesterone receptor agonist)

Reduces LH release which prevents ovulation + make endometrium unsuitable for implantation of ovum

116
Q

What is norethindrone used for?

A
  • Endometriosis
  • Abnormal periods or bleeding
117
Q

What is norethindrone’s bioavailability?

A

F ~64%

118
Q

Does norethindrone bind to plasma protein?

A

Yes, highly bound

119
Q

How is norethindrone metabolized?

A

Phase I - reduction
Phase II - glucuronidation and sulfation

120
Q

What is norethindrone’s half-life?

A

~8 hours

121
Q

How is norethindrone excreted?

A

Metabolites excreted 50% in urine and 40% in feces

122
Q

What are S/E of norethindrone?

A
  • Headache
  • Dizziness
  • Bloating
  • Weight gain
  • Amenorrhea
  • Initial spotting and bleeding
123
Q

Why is norethindrone to be used with caution in ppl with cardiovascular risk?

A

Partial conversion of norethindrone to ethinyl estradiol

124
Q

What is the MOA of metformin?

A

Biguanides

Decreases gluconeogenesis in the liver
Enhance tissue sensitivity to insulin

125
Q

What is the bioavailability of metformin?

A

40-60%

126
Q

What is the duration of action of metformin?

A

8-12 hours

127
Q

Does metformin bind to plasma protein?

A

Minimal

128
Q

What is the half-life of metformin?

A

3 hours

129
Q

How is metformin excreted?

A

Unchanged in the urine

130
Q

What are the S/E of metformin?

A

Anorexia
GI disturbances
Increased risk of vit B12 malabsorption

131
Q

Does metformin cause weight loss or gain?

A

Weight loss

132
Q

In which patients should metformin be used cautiously?

A

Patients who experienced lactic acidosis
Patients with renal problems

133
Q

What is glipizide’s MOA?

A

Sulfonylureas

Binds to SU receptor protein (found at the K(ATP) channels, inhibiting K+ efflux and hence triggering a calcium-dependent exocytosis of insulin granules from the pancreatic beta cells

134
Q

What is glipizide’s oral bioavailability?

A

> 95% (delayed with food intake)

135
Q

What is glipizide’s onset of action?

A

0.5 hours

136
Q

What is glipizide’s duration of action?

A

12-24 hours

137
Q

Does glipizide bind to plasma proteins?

A

Yes, 99%

138
Q

What is glipizide’s half-life?

A

4 hours

139
Q

How is glipizide metabolized?

A

Hydroxylation in the liver

140
Q

How is glipizide excreted?

A

<10% excreted unchanged in urine and feces
Metabolites are excreted in urine and feces

141
Q

What is the S/E of glipizide?

A

Weight gain
Hypoglycemia (less than 1st gen, more likely in elderly)

142
Q

What is the MOA of sitagliptin?

A

DPP-4 inhibitor

Inhibit DPP-4 to prevent enzymatic degradation of GLP-1 and prolong the action of endogenous incretins

Incretins stimulate insulin secretion at the beta pancreatic cells WHEN there is presence of hyperglycemia, suppresses alpha pancreatic cells mediated glucagon release and hepatic glucose production

Incretins also delay gastric emptying at the gut and induce satiety

143
Q

What is the oral bioavailability of sitagliptin?

A

F = 87%

144
Q

What is sitagliptin’s half-life?

A

10-12 hours

145
Q

How is sitagliptin metabolized?

A

low liver metabolism

146
Q

How is sitagliptin excreted?

A

80% excreted unchanged in urine, rest in feces

147
Q

What are S/E of sitagliptin?

A

GI disturbances
Flu-like symptoms
Skin reactions

148
Q

In which patients should sitagliptin be used cautiously?

A

In patients with history of pancreatitis

149
Q

What is liraglutide’s MOA?

A

GLP-1 agonist

Activates GLP-1 receptor on pancreatic beta cells to increase insulin secretion, and on alpha cells to decrease glucagon release (GLUCOSE DEPENDENT)
Delays gastric emptying and induces satiety (reduce appetite)

It is a long acting peptide (C16 fatty acid) and hence is resistant to degradation by DPP-4 enzymes in the body.

150
Q

What is liraglutide’s bioavailability after SC injection?

A

F = 55%

151
Q

How is liraglutide dosed?

A

Week 1 - 0.6 mg SC daily
Week 2 - 1.2 mg SC daily
Week 3 - 1.8 mg SC daily
Week 4 - 2.4 mg SC daily
Week 5 onwards - 3 mg SC daily

152
Q

Does liraglutide bind to plasma protein?

A

Yes (C16 fatty acid binds to plasma protein)

153
Q

What is the half-life of liraglutide?

A

13 hours (due to plasma protein binding)

154
Q

How is liraglutide metabolized?

A

Non-specific, similar to endogenous polypeptides

155
Q

How is liraglutide excreted?

A

Little or none excreted unchanged

156
Q

What are S/E of liraglutide?

A

Nausea, vomiting
Diarrhea, constipation
Headache, tiredness

157
Q

Who should liraglutide not be used on?

A

Pregnant women

158
Q

What are other benefits of liraglutide?

A
  • Weight loss
  • Reduces risk of CV death, non-fatal MI, and HF (IN DM2 LECTURE SAY NEUTRAL EFFECT) among T2DM patients
159
Q

What is the MOA of empagliflozin?

A

SGLT2i

Binds to SGLT2 at the proximal tubule of the nephron and decrease reabsorption of filtered glucose, increasing urinary glucose excretion

160
Q

What is the oral bioavailability of empagliflozin?

A

60-80%

161
Q

When is the Cmax achieved for empagliflozin?

A

1-2 hours

162
Q

What is the half-life of empagliflozin?

A

12 hours

163
Q

Does empagliflozin bind to plasma protein?

A

~90%

164
Q

How is empagliflozin metabolized?

A

Minimal metabolism
Glucuronidation in the liver

165
Q

How is empagliflozin excreted?

A

40% unchanged in feces
27% unchanged in urine

166
Q

What are the S/E of empagliflozin?

A
  • UTI
  • increased urination
  • female vaginal thrush
  • diabetic ketoacidosis
167
Q

What are additional benefits of empagliflozin?

A
  • Reduced risk of major cardiac event (ASCVD and HF)
  • Reduced risk for composite endpoint of worsening renal function (CKD)

PR3152 Finals (4 decks)

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