Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PR3152 > Pharmacology - Women's and Men's Health > Flashcards

Pharmacology - Women's and Men's Health Flashcards

1
Q

What is tamsulosin indicated for?

A

Moderate-severe symptomatic BPH
(regardless of prostate size)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the MOA of tamsulosin?

A

MOA: reduces vasoconstriction induced by endogenous catecholamines by blocking the α-adrenoreceptors on the smooth muscle
- Decreases muscle tone
- Reduces bladder obstruction – relaxes prostate smooth muscle to improve urinary flow rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is tamsulosin selective for the prostate?

A

selective for α1A receptors (prostate) over α1B receptors (cardiac), so it favors selectivity for the prostate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is tamsulosin administered?

A

PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Does tamsulosin bind to plasma proteins?

A

> 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the Vd of tamsulosin?

A

0.2L/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is tamsulosin metabolised?

A

by CYP enzymes in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the half life of tamsulosin?

A

10-15h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is tamsulosin eliminated?

A

10% excreted unchanged in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How long does it take for the onset of tamsulosin’s effects?

A

Fast, takes days to weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the adverse effects associated with tamsulosin?

A

Abnormal ejaculation, back pain, muscle weakness, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the contraindications for tqmsulosin?

A

Concurrent use of another α1-adrenoreceptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the MOA of finasteride?

A

Competitively inhibits 5α reductase (Type II), which decreases conversion of testosterone to DHT, resulting in ↓prostate size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is finasteride indicated for?

A

Moderate or severe LUTS w large prostate (>40g)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How long does it take for the onset of finasteride’s effects?

A

Slow, may take up to 6-12 months to decrease prostate size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is finasteride administered?

A

PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the bioavailability of finasteride?

A

65%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Does finasteride need dose adjustments?

A

No - renal, liver, old age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Is finasteride highly protein bound?

A

Yes (~90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is finasteride metabolised?

A

By liver CYP enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the half life of finasteride?

A

~6h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is finasteride excreted?

A

50% excreted unchanged in faeces
Metabolites are excreted in urine and faeces

23
Q

What are the adverse effects of finasteride?

A
  • Ejaculatory disorders (reduced semen or delayed) – more common than α1 antagonists
  • Decreased libido (3-8%)
  • Erectile dysfunction (3-16%)
  • Gynecomastia and breast tenderness (1.0%)
  • Lesser risk of hypotension
  • More hair growth – reducing conversion of testosterone to DHT means testosterone levels are higher, resulting in increased hair growth
24
Q

What are the contraindications for finasteride?

A

Women and children, pregnancy

25
Q

What is the MOA of sildenafil?

A

Inhibit PDE5 enzyme (breaks down cGMP), resulting in increased cGMP activity, inducing smooth muscle relaxation to cause an erection

26
Q

Why is sildenafil v selective for the penis?

A

PDE5 is highly expressed in the corpora cavernosa of the penis and its vasculature, but poorly in the myocardium, which provides tissue specificity for the penis

27
Q

How is sildenafil administered?

A

PO

28
Q

What is the bioavailability of sildenafil?

A

~40%

29
Q

How long does it take for the onset of sildenafil?

A

30-60min

30
Q

How long can the effects of sildenafil last?

A

maximum of 12h

31
Q

Does sildenafil need dose adjustments?

A

No - renal, liver, old age

32
Q

Is sildenafil distributed by the body well?

A

Yes

33
Q

How is sildenafil metabolised by the body?

A

Liver - mainly CYP3A4 (and a bit of CYP2C9)

34
Q

How long is the half-life of sildenafil?

A

~4h

35
Q

How is sildenafil excreted?

A

Metabolites largely excreted in faeces (~80%), minorly in urine (13%)
Unchanged drug excreted in urine

36
Q

What are the adverse effects associated with sildenafil?

A
  • Headache
  • Flushing
  • Dyspepsia
  • Dizziness
  • Back pain
  • Blur vision/Blue green tinting of vision
  • Priapism
37
Q

What are the contraindications for sildenafil?

A

Any patient on GTN should not be taking any PDE-5i
- potentiates vasodilation effect of GTN via inc cGMP due to concomitant blockade of cGMP degradation by sildenafil
- results in potentially life-threatening hypotension

38
Q

What is the MOA of ethinyl estradiol?

A

Synthetic estrogen
- reduces FSH release from anterior pituitary to suppress the development of the ovarian follicle (endometrium unsuitable for ovum implantation)

39
Q

How is ethinyl estradiol administered?

A

PO, parenterally, transdermal or topically

40
Q

What is the bioavailability of ethinyl estradiol?

A

45%

41
Q

How long does it take for the onset of ethinyl estradiol?

A

30-60min

42
Q

Does ethinyl estradiol exhibit high plasma protein binding?

A

Very high plasma potein binding (~98%)

43
Q

How is ethinyl estradiol metabolised>

A

Metabolised by liver via
Phase I – hydroxylation by CYP3A4
Phase II – conjugation w glucuronide and sulfation into hormonally inert Ethinylestradiol glucuronides and Ethinylestradiol sulfate

Ethinylestradiol sulfate undergoes enterohepatic recirculation

44
Q

What is the half-life of ethinyl estradiol?

A

13-27h

45
Q

How is ethinyl estradiol excreted?

A

Metabolites excreted in faeces and urine

46
Q

What are the adverse effects associated with ethinyl estradiol?

A
  • breast tenderness
  • headache
  • fluid retention (bloating)
  • nausea
  • dizziness
  • weight gain

rare:
- venous thromboembolism
- MI
- liver damage

47
Q

What is ethinyl estradiol contraindicated for?

A
  • Patients w known Hx or at high risk for VTE
  • Advanced diabetes w vascular disease
  • Hypertension (>160/100mmHg)
  • Avoid in breastfeeding (<21 days postpartum) and breast cancer
48
Q

What is the MOA of norethindrone

A

Synthetic progesterone
- reduces LH release to prevent ovulation (makes endometrium unsuitable for ovum implantation)
- progesterone receptor agonist

49
Q

How is norethindrone administered?

A

PO

50
Q

What is the bioavailability of norethindrone?

A

64%

51
Q

Is norethindrone highly plasma protein bound?

A

Yes

52
Q

How is norethindrone metabolised?

A

Metabolised in liver by reduction, followed by glucuronidation and sulfation

53
Q

What is the half-life of norethindrone?

A

8h

54
Q

How is norethindrone excreted?

A

Metabolites excreted in urine (~50%) and faeces (~40%)

PR3152 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions