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3152 Immune and Endocrine System > IC15 Pharmacology of Women's and Men's health drugs > Flashcards

IC15 Pharmacology of Women's and Men's health drugs Flashcards

1
Q

What is tamsulosin?
What is the pathophysiology of BPH?
What is the MOA of tamsulosin?

A

MOA Alpha 1A adrenoreceptor antagonist

  • Specific alpha 1A (bladder and lower urinary tissues)
  • Does not affect adrenoreceptors on heart
  • Reversible inhibition of Alpha1A receptor, prevents vasoconstriction and muscle constriction of bladder sphincter, urethra and prostate
  • Reduce urinary obstruction, increase urinary flow rate
  • Significantly delay need for surgery or catherization

(Pathophysiology:

  • Adrenergic nerves releases noradrenaline
  • Noradrenaline released acts on adrenoreceptors and cause muscle constriction of bladder sphincter, urethra and prostate
  • Urinary obstruction, reduced urinary flow)
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2
Q

What is tamsulosin indicated for?

A

BPH

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3
Q

What is the PK profile of tamsulosin?

A

PK
A: oral, OD, Works in hours or days (fast onset)
D: minimal distribution, highly PPB
M: CYP3A4, CYP2D6
E: Urine

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4
Q

What are the ADRs of tamsulosin?

A

ADR:
1. Abnormal ejaculation
2. Back pain

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5
Q

What are the special considerations of tamsulosin?

A

Special Considerations

DDI:

  • Grapefruit, pomelo
  • CYP3A4 and CYP2D6 inhibitor and inducer

CI:

  • Avoid other a1-adrenoreceptor antagonist e.g. prazosin, epinephrine –> can cause excessive muscle relaxation and hypotension
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6
Q

What is finasteride?
What is the pathophysiology of BPH? (static component)
What is the MOA of finasteride?

A

MOA 5apha-reducatase inhibitor

  • Competitively inhibits 5a-reductase
  • Prevents conversion of testosterone to DHT
  • Reduces prostate size
  • Increase urine flow and reduce frequency of acute retention of urine
  • Reduce need for surgery
  • Lower PSA

Physiology:

  • 5a-reductase converts testosterone to dihydrotestosterone (DHT)
  • DHT leads to increase prostate size and hair loss in males
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7
Q

What is finasteride indicated for?

A

Clinical Indications
1. BPH
2. Hair loss (Propecia)
3. Hirsutism

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8
Q

What is the PK profile of finasteride?

A

PK
A: oral, OD, takes 6 months to exert effects (slow onset)
D: highly plasma protein bound
M: CYP3A4
E: urine and feces (NO need adjustment when renal impaired, liver impaired or elderly)

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9
Q

What are the ADRs of finasteride?

A

ADR
1. Loss of libido and sexual potency
2. Gynecomastia (rare)

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10
Q

What are the special considerations of finasteride?

A

Special Considerations

DDI:

  • Grapefruit, pomelo
  • CYP3A4 inhibitor and inducer

CI:

  • Avoid in women, children or pregnancy
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11
Q

What is sidanefil?
What is the pathophysiology of ED?
What is the MOA of sidanefil?

A

MOA Phosphodiesterase-5 inhibitor (PDE5i)

  • Specific to penis since PDE5 highly expressed in corpora cavernosa but poorly in myocardium
  • Inhibits PDE5 in penis which prevents degradation of cGMP
  • Increases cGMP
  • More can be used for smooth muscle relaxation
  • More blood flow to the corpora cavernosa

Physiology:

  • Sexual stimulation release NO
  • NO increases cGMP
  • cGMP triggers signal transduction
  • arteriole relaxation
  • a lot of PDE5 in corpora cavernosa
  • PDE5 degrades cGMP –> preventing arteriole relaxation –> less blood flow to the penis for erection
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12
Q

What is sidanefil indicated for?

A

ED

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13
Q

What is the PK profile of sidanefil?

A

PK
A: oral, OD, fast onset
D: widely distributed
M: CYP3A4 (major), CYP2C9 (minor)
E: Feces (NO need to adjust when renal impaired, liver impaired and elderly)

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14
Q

What are the ADRs of sidanefil?

A

ADR

  1. Headache
  2. Flushing
  3. Dyspepsia
  4. Dizziness
  5. Back pain
  6. Blur vision, blue-green tinting of vision (inhibit PDE6)
  7. Priapism (prolong erection)
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15
Q

What are the special considerations of sildanefil?

A

Special Considerations

DDI:

  • Grapefruit, pomelo
  • CYP3A4 and CYP2C9 inhibitor and inducer

CI:

  • Avoid in patients taking GTN (glyceryl trinitrate) –> both increase cGMP –> marked vasodilation and hypotension
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16
Q

What is the MOA of ethinyl estradiol?

A

MOA:
Estrogen receptor agonist

  • Binds to estrogen receptor
  • Inhibits FSH release –> prevents development of ovarian follicle
  • Create unsuitable endometrium for implantation of ovum
17
Q

What is ethinyl estradiol indicated for?

A

Clinical Indications:
1. Menopausal issues
2. Gynaecological disorders
3. Some hormone sensitive cancers

18
Q

What is the PK profile of ethinyl estradiol?

A

PK
A: oral, OD, fast onset
D: highly plasma protein bound
M:
Phase I: hydroxylation by CYP3A4
Phase II: glucuronidation, sulfation (EE sulfate undergo enterohepatic recirculation, increase t1/2)
E: urine and feces

19
Q

What are the ADRs of ethinyl estradiol?

A

ADR
1. Breast tenderness
2. Headache
3. Fluid retention (bloating)
4. Nausea
5. Dizziness
6. Weight gain
7. VTE
8. Myocardial infarction, stroke
9. Liver damage

20
Q

What are the special considerations of ethinyl estradiol?

A

Special Considerations

DDI:

  • CYP3A4 inhibitor and inducer

CI:

  1. Patients with arterial or venous thrombosis
  2. Advanced diabetes AND vascular disease
  3. Hypertension >160/100mmHg
  4. Breastfeeding (<21 days postpartum)
  5. Patients with breast cancer
21
Q

What is the MOA of norethindrone?

A

MOA:
Synthetic Progesterone

  • Progesterone receptor agonist
  • Inhibits LH secretion –> prevents ovulation
  • Create unsuitable endometrium for implantation of ovum
22
Q

What is the clinical indication of norethindrone?

A

Clinical Indications:
1. Contraception
2. Endometriosis
3. Abnormal periods

23
Q

What is the PK profile if norethindrone?

A

PK
A: oral, OD, fast onset
D: highly plasma protein bound
M: reduction, glucuronidation, sulfation
Some metabolized in liver become EE (take note of EE side effects)
E: urine and feces

24
Q

What are the ADRs of norethindrone?

A

ADR

  1. Headache
  2. dizziness
  3. bloating
  4. weight gain
  5. Breakthrough bleeding (initial)
  6. Amenorrhea
25
Q

What are the special considerations of norethindrone?

A

Special Considerations:

  • Not good for women planning pregnancy, since ovulation suppression may last up to 1.5 years
  • Take note of EE ADR e.g. VTE
26
Q

What is the absorption / ROA for all 5 drugs?

A

oral oral oral oral oral

27
Q

What is the PPB for all 5 drugs?

A

High High - High High

28
Q

How are all 5 drugs metabolised?

A
  1. CYP3A4
    CYP2D6
  2. CYP3A4
  3. CYP3A4 (major)
    CYP2C9 (minor)
  4. Liver (I & II)
    CYP3A4 Hydroxylation
    Glucuronidation
    Sulphation
  5. Liver (I & II)
    Reduction
    Glucuronidation
    Sulphation
29
Q

How are all 5 drugs excreted?

A
  1. Urine
  2. Urine and feces (no need renal/liver adjustment or elderly)
  3. Feces (no need renal/liver adjustment or elderly)
  4. Urine and feces
  5. Urine and feces

3152 Immune and Endocrine System (11 decks)

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