Brainscape's Knowledge GenomeTM

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


See full index

PR3152 (cleefy) > PR3152 IC16 > Flashcards

PR3152 IC16 Flashcards

1
Q

what is the mechanism of action of tamsulosin

A

block alpha adrenal receptors on smooth muscle of prostate, prostatic urethra, bladder neck

alpha adrenoreceptor antagonist

inhibits vasoconstriction induced by endogenous catecholamines

decrease muscle tone = relaxation of prostate smooth muscle / reduced tension
=
improvement in urodynamics: increases maximum urinary for rate from the decreased smooth muscle tension = decreased urinary obstruction

ULTIMATELY
= improve symptoms related to bladder instability e.g., urinary storage and voiding

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

selectivity of tamsulosin

A

affects a1A receptors (blood vessels and prostate) more than a1B (blood vessels and heart) receptors

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

absorption of tamsulosin (include dosing)

A

PO 0.4mg OD
well absorbed orally

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

distribution of tamsulosin?
protein binding and Vd?

A

highly protein bound >90%
small vd 0.2L/kg

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

metabolism of tamsulosin
enzyme and t1/2

A

cyp3a4 2d6
t1/2 - 10-15h

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

excretion of tamsulosin

A

~10% really excreted unchanged in urine

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

ADR of tamsulosin

A

abnormal ejaculation
backpain

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

contraindication of tamsulosin

A

concurrent admin with another a1 receptor antagonist like non selective prazosin
= may drastically decrease bp esp in patients w cvs issues

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

MOA of finasteride

A

5 alpha reductase inhibitor

bind to the 5 alpha reductase which is used to convert testosterone to DHT
= reducing the prostate size = improve flow and frequency of urinary retention.

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

counselling for finasteride

A

may take up to 6 months for clinical effects
test for PSA, should decrease with finasteride; ideally 1.5-1.

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

absorption of finasteride (include dose and F

A

PO 5mg OD
F = 0.65
no dose adjustment in renal or hepatic impairment

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

distribution of finasteride (protein binding and vd)

A

90% protein bound
poor apparent Vd

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

metabolism of finasteride (t1/2)

A

liver
e.g. 3a4.
t1/2 6hours

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

ADR of finasteride

A

gynaecomastia (raRE)
decreased libido/sexual potency

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

contraindications of finasteride

special population

A

women children and pregnancy

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

additional indication of finasteride (include dose)

A

1mg OD
also used in male pattern baldness and hirsutism in women

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

excretion of finasteride

A

50% excreted unchanged in faeces

metabolites = faeces and urine

18
Q

MOA of sildenafil

A

during sexual stimulation, NO released that causes increase in cGMP. cGMP is converted to 5-GMP via PDE5

sildenafil is a PDE5 inhibitor that prevents conversion to 5GMP = increase cGMP = increase smooth muscle relaxation and blood flow to the corpora cavernosa = erection

19
Q

special properties of PDE5

A

it is highly expressed by the corpora cavernosa in the penis compared to myocardium, allowing for tissue specificity

20
Q

absorption of sildenafil
including dosing, ONSET, F, DOA

A

pO 5mg OD
onset: 30-60MIN
F = 0.4
duration of action max 12h
no dosage adjustment

21
Q

metabolism of sildenafil include enzymes and t1/2

A

major 3a4
minor 2c9
t1/2 = 4 hours

22
Q

distribution of sildenafil

A

widely distributed

23
Q

excretion of sildenafil

A

metabolites: 80% by faces, 13% urine

unchanged: remaining via urine

24
Q

adr of sildenafil

A

flushing
back pain
headache, dizzy
blur vision (blue green tinting from inhibition of retinal PDE5)
priapism
dyspepsia

25
Q

contraindication of sildenafil

A

X admin with GTN = potentiate vasodilation effect of GTN via increased cGMP from concomitant blockade of degradation
= vasodilation and hypotension

26
Q

special dosage instruction for sildenafil

for special populations

A

start lowest dose esp elderly >65

27
Q

MOA of ethinyl estradiol

A

estrogen receptor agonist
synthetic estrogen
= decrease FSH release from anterior pituitary = decrease in development of follicle + make endometrium unsuitable for implantation

28
Q

indication for ethinyl estradiol

A

menopausal symptoms
gynaecological disorders
certain hormone sensitive cancers

29
Q

distribution of EE

A

98% protein bound (albumin)

30
Q

absorption of EE (F, onset)

A

oral (can also be parenteral, topical, transdermal)
F = 0.4
onset 30-60min

31
Q

excretion of EE

A

feces and urine

32
Q

metabolism of EE including t1/2

A

liver
phase I: hydroxylation by cyp3a4
phase II: conjugation by glucuronidation and sulphation

note that EE sulphate can undergo enterohepatic recirculation
this increases t1/2 to 13-27 hours

33
Q

ADR of EE

A

breast tenderness
VTE
MI stroke
liver damage
weight gain
fluid retention/bloating

nausea
dizziness
headache

34
Q

contraindications of EE

A

X venous or arterial thrombosis
X breastfeeding (<21 days post partum)
X breast cancer
X advanced diabetes with vascular disease
X HTN >160/100

35
Q

moa of norethindrone

A

synthetic progesterone
inhibit LH release = prevent ovulation and makes endometrium unsuitable for implantation

36
Q

indications of norethindrone

A

endometriosis
menstrual disorders

37
Q

absorption of norethindrone

A

OD
F = 0.64

38
Q

distribution of norethindrone

A

highly plasma protein e.g., albumin bound

38
Q

metabolism of norethindrone

include t1/2

A

Metabolized in liver by reduction follow by glucuronidation and sulfations
t1/2 = ~8h
some evidence of percentage of norethindrone metabolised in liver to EE

39
Q

excretion of norethindrone

A

metabolites: 50% urine 40% feces

40
Q

adr of norethindrone

A

headache
dizziness
fluid retention/bloating
weight gain

spotting episodes
amenorrhea

41
Q

notes for norethindrone

A

ovulation suppression may be up to 1.5 years = counsel women planning pregnancy soon after cessation therapy

partial conversion to EE (risk factor for EE complications

PR3152 (cleefy) (13 decks)

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