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MFSRH part 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what does SERMs stand for, can you name three SERMS

A

SERMS = selective oestrogen receptor modulators

e.g. tamoxifen, raloxifene, clomiphene

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2
Q

in general how do SERMs work

A

SERMS work to target oestrogen receptors - they can have agonist or antagonist effects on the oestrogen receptors

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3
Q

what is the primary licence for tamoxifen

A

Treatment of breast cancer

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4
Q

what is another secondary indication for tamoxifen other than Rx of breast cancer

A

anovulatory induction

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5
Q

describe tamoxifen MOA in breast tissue

A

Tamoxifen is an ER antagonist in breast tissue however it is an agonist in the endometrial ER receptors, bone and lipids

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6
Q

what are the risks associated with tamoxifen

A

increase VTE risk, increase thickness of endometrial lining (agonist here) - increased risk of endometrial cancer

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7
Q

are any SERMs in the UK licences for Rx of postmenopausal symptoms

A

no

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8
Q

what is raloxifene liscenced indication

A

treatment of osteoporosis in PMW but not considered first line

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9
Q

How does raloxifene work to treat osteoporosis

A

ER agonist in bone - prevents bone resorption by osteoclasts

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10
Q

what is the liscenced indication for clomiphene

A

Induction of ovulation

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11
Q

where does clomiphene work to increase gonadotrophin release

A

directly on the hypothalamus

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12
Q

what are the known risks associated with using clomiphene for treatment of infertility

A

multiple gestations
after 12 cycles or more increases risk of ovarian cancer
ovarian cysts
hot flushes

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13
Q

Clomiphene, raloxifene and tamoxifen all increase the risk of VTE

True or false

A

False - clomiphene is not a/s with any increased risk of VTE

Tamoxifen and raloxifene both increase risk of VTE

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14
Q

SERMs work to improve postmenopausal symptoms
true or false

A

false - can actually worsen them

specifically tamoxifen and clomiphene commonly worsen hot flushes, not sure about raloxifene

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15
Q

what effect does tamoxifen and raloxifene have on cholesterol

A

decreases total cholesterol and LDL, no effect on HDL

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16
Q

what class of medication should be avoided in women on SERM

A

SSRIs - specifically avoid paroexteine with tamoxifen

SSRIs can reduce the effectiveness of SERMs

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17
Q

can you list the classes of antibiotics that are bactericidal

A

Penicillins & cephalosporins are very cidal for real microbes

Penicillins
cephalopsporins
Aminoglycosides
Vancomycin
Cephalosporins
Fluroquinolones
Rifampicin
Metronidazole

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18
Q

can you name the antibiotics which are bacteriostatic (i.e. halt the growth of the bacteria but don’t kill them)

A

trimethoprim
macrolides
chloramphenicol
tetracyclines
clindamycin
linezolid

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19
Q

what is the best choice antidepressant in postpartum women BF

A

sertraline
(but ultimately choice of anti-depressant PP will be determined by which drug they have been on during pregnancy)

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20
Q

which class of anti-depressants is best to avoid during pregnancy and pp period and why?

A

TCA due to risk associated with OD

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21
Q

is warfarin considered safe when breastfeeding

A

yes - switch to warfarin usually around day 5 PP purely to reduce risk of PMH

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22
Q

which anticoagulants out of the following list are considered safe when BF

  • warfarin
    LMWH
    DOACs
A

LMWH and warfarin are considered safe whilst BF
not enough evidence on DOACs so advised to avoid/ not use first line

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23
Q

which antihypertensives are safe to use in BF women

A

enalapril
labetalol
nifedipine (and other CCB e.g amlodipine)

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24
Q

which classes of antihypertensive drugs are best avoided in breastfeeding women

A

diuretics and ARBs (angiotensin receptor blockers) other ace-inhibitors except for enalapril

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25
Q

what dosing schedule is preferred for women using antihypertensives when BF

OD
BD
TDS
QDS

A

OD

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26
Q

out of the following anti-hypertensives which are considered safe when breastfeeding?

  • Sodium Valporate
    -Phenobarbital
    -Lamotrogine
  • Keppra
    -Primodone
A

sodium valproate (unlike in pregnancy), lamotrigine and keppra all safe

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27
Q

in terms of EC what would your advice be to a breast feeding woman in terms of taking UPA (ella one)

A

would need to discard milk for 1 week following taking UPA (express and discard)
whereas for levonorgestrel no need to do this
Cu-IUD also fine but would need to check >4 weeks pp

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28
Q

Which analgesia is it best to avoid in BF women

A

codeine due to risk of bradycardia, apnoea and cyanosis

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29
Q

which analgesia are considered safe for BF women

A

paracetamol, ibuprofen and dihydrocodeine

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30
Q

what enzyme metabolises codeine

A

CP450 - 2D6 (CYP2D6)

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31
Q

What condition is aspirin associated with causing in children

A

Reye’s syndrome

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32
Q

For how long in the neonatal period should nitrofurantoin be avoided for and why

A

avoid using in the first 8 days of life due to risk of haemolysis, avoid altogether in people with G6PD deficiency

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33
Q

mifepristone works in termination of pregnancy by:

A) prostaglandin e1 receptor agonist
B) inhibin receptors agonist on the smooth muscle to cause urterine contractions
C) progesterone receptor agonist
D)progesterone receptor antagonist

A

D - mifepristone works by blocking progesterone receptors i.e. it is an antagonist

This decreases progesterone. Progesterone is responsible for maintaining the lining of the endometrium for pregnancy and also desensitises the body to prostaglandin. without progesterone there is increased prostaglandin that causes disruption of the endometrium and uterine bleeding

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34
Q

mifepristone would be contra-indicated in patients with which medical conditions

A

long term steroids, adrenal insufficiency
severe asthma on steroids

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35
Q

mifepristone belongs to what class of medications

A) alpha blocker
B) glucorticoid receptor antagonist
C) prostaglandin E1 receptor agonist
D) progesterone receptor agonist

A

b

mifepristone is a progesterone and glucocorticoid receptor antagonist

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36
Q

misoprostol belongs to what class of medications

A) alpha blocker
B) glucorticoid receptor antagonist
C) prostaglandin E1 receptor agonist
D) progesterone receptor agonist

A

C - prostaglandin E1 receptor agonist

(misoPROSTol = PROSTaglandin)

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37
Q

can you explain how misoprostol works to cause termination of pregnancy or expulsion of RPOC/incomplete miscarriage

A

misoprostol is a prostglandin E1 receptor agonist. It binds to prostaglandin receptors on the smooth muscle of the uterus and this leads to uterine contractions.

In the cervix it helps to prime the cervix by decreasing the collagen in the cervical stroma and decreased cervical tone from increased amplitude and frequency of contractions

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38
Q

how does misoprostol work to cause cervical ripening

A

In the cervix it helps to prime the cervix by decreasing the collagen in the cervical stroma and decreased cervical tone from increased amplitude and frequency of contractions

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39
Q

how long after a patient stops acretin should they wait before conceiving

1 month
1 year
2 years
3 years

A

2 years!

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40
Q

how long after a patient stops isotretinoin or aitretinoin should they wait before trying to conceive

1 month
1 year
2 years
3 years

A

1 month

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41
Q

how long after a patient receives methotrexate for medical management of ectopic pregnancy should they wait before trying to conceive?

1 month
3 months
6 months
1 year

A

3 months

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42
Q

what is the success rate for methotrexate in the treatment of ectopic pregnancies

80%
85%
90%
95%

A

95%

43
Q

what class of medications does methotrexate to treat ectopic pregnancies

Folic acid agonist
folic acid antagonist
progesterone receptor agonist
progesterone receptor antagonist

A

folic acid antagonist

44
Q

what is the main mechanism of action for methotrexate when used for treatment of ectopic pregnancies

A) inhibits meiosis
B) inhibits apoptosis
C) inhibits dna synthesis
D) inhibits RNA synthesis

A

C - inhibits DNA synthesis

45
Q

what is the name of the enzyme that methotrexate inhibits

A) cGMP
B) dihydrofolate reductase
C) aromatase
D) dihydrofolate oxidase

A

B - dihydrofolate reductase

dihydrofolate reductase is an enzyme essential for purine production, DNA synthesis and cell replication. Any cell lacking this weill be effected. trophoblasts are rapidly dividing by mitosis and so this process is inhibited and leads to cell death.

46
Q

what enzyme converts aciclovir into aciclovir monophosphate

A) granulate kinase
B) thymidine kinase
C) CK
D) Adenosine kinase

A

B - thymidine kinase

47
Q

in patients with aciclovir resistance where are mutations commonly found

A) granulate kinase
B) thymidine kinase
C) CK
D) Adenosine kinase

A

B - thymidine kinase

48
Q

what is the end metabolite of aciclovir that works to inhibit DNA synthesis

A) aciclovir monophosphate
B) aciclovir triphosphate
C) aciclovir diphosphate

A

B - aciclovir triphosphate

49
Q

what class of drug is aciclovir

A

nucleotide analogue

50
Q

when performing a pudenal nerve block what anatomical bony landmark should you first identify when performing PV examination

A

ischial spine

51
Q

what ligament runs 1cm medial and posterior to the ischial spine that you want to try and identify when performing a pudenal nerve block

A

sacrospinous ligament

52
Q

once you puncture the sacrospinous ligament and continue to advance your needle you will feel resistance. This is the point where you should aspirate and inject your LA when performing a pudendal nerve block. What artery could you infiltrate if you fail to aspirate

A

pudendal artery

53
Q

What is the location of the pudendal vessels in relation to the pudendal nerve at the point when you are injecting LA if you have punctured the sacrospinous ligament advanced your needle and felt resistance?

A

artery lies medial to the pudendal vein

54
Q

you are consenting a patient during second stage of labour for a pudendal block. can you name three complications you should inform her about

A

haematoma
puncture of the rectum
LA toxicity/anaphylaxis
trauma to the sciatic nerve

55
Q

where does phase 1 metabolism of first pass metabolism occur?

A) smooth endoplasmic reticulum of the liver
B) smooth endoplasmic reticulum of the intestines
C) cytoplasm of the liver hepatocytes
D) cytoplasm of the intestines

A

A - smooth endoplasmic reticulum of the liver hepatocytes

56
Q

what reactions occur in phase 1 of first pass metabolism

A) oxidation
B) conjugation
C) reduction

A

phase 1 involves oxidation and reduction

57
Q

what reactions occur in phase 2 of first pass metabolism

A) oxidation
B) conjugation
C) reduction

A

B - conjugation

58
Q

what is the aim of first pass metabolism

A

to change a lipophilic drug into a hydrophilic drug that is more easily excreted

59
Q

Which of the following drug routes undergoes first pass metabolism

A) IV drugs
B) oral drugs
C) transdermal drugs
D) rectal drugs

A

B and D - both undergoe first pass metabolism

60
Q

Which of the following drug routes do not undergoe first pass metabolism

A) IV drugs
B) oral drugs
C) transdermal drugs
D) rectal drugs

A

C - transdermal and and A - IV route

61
Q

what are the names of the three forms of oestrogen a female body can produce

A
  1. 17 beta estradiol
  2. Estrone
  3. Estriol
62
Q

which type of oestrogen do we make during reproductive years

  1. 17B estradiol
  2. Estrone
  3. Estriol
A
  1. 17 beta estradiol
63
Q

which type of oestrogen do we produce when pregnant?

  1. 17B estradiol
  2. Estrone
  3. Estriol
A
  1. Estriol (E3) - produced by the placenta
64
Q

which type of oestrogen do we produce once we are post-menopausal

  1. 17B estradiol
  2. Estrone
  3. Estriol
A
  1. Estrone (e1)
65
Q

can you list the oestrogens in order of their strength, starting with most potent to the least potent

Estrone
17B estradiol
Estriol

A
  1. 17 b estradiol (most potent)
  2. Estrone (10 times less potent than estradiol)
  3. Estriol ( 100 times less potent than estradiol)
66
Q

what type of oestrogen is most commonly used in HRT

1.estradiol
2. Estrone
3. Estriol
4. ethinyl estradiol

A
  1. estradiol ( as it resembles the closest form of natural oestrogen)
67
Q

synthetic estradiol used in HRT is converted into what type of oestrogen by the liver

A

estrone

68
Q

why is the risk of VTE higher with oral estrogens compared to oestrogens delivered transdermally

A

oral oestrogens have to undergo first pass metabolism. When they pass through the liver it activates the clotting cascade, whereas transdermal preparations avoid first pass metabolism and so won’t activate clotting cascade

69
Q

what type of oestrogen does the human fetal liver produce

  1. 17B estradiol
  2. Estrone
  3. Estriol
  4. estetrol
A
  1. Estetrol
70
Q

if concerned about anti-cholinergic effects in someone diagnosed with OAB which of the following drugs should you choose as treatment?

A) solifenacin
B) mirabegron
C) tolterodine
D) oxybutynin

A

b - mirabegron - is a B3 agonist (improves parasympathetic activity by increasing relaxation of the bladder and detrusor muscle)

71
Q

out of the following list which is the most selective anti-cholinergic

A) solifenacin
B) mirabegron
C) tolterodine
D) oxybutynin

A

A - solifenacin (m3 receptor antagonist)

72
Q

which is the least selective anti-cholingeric out of the following list

A) solifenacin
B) mirabegron
C) tolterodine
D) oxybutynin

A

c - tolterodine (non selective)

73
Q

what receptors does oxybutynin exert its action on

A

M1 and M3 receptors in the SM

74
Q

what is the purpose of the extra ethinyl group on EE

A

the 17 alpha ethinyl group prevents oxidation of the c17Beta position of EE by 17 Beta HSD.

therefore EE is not converted to estrone and has higher oestrogen effects at target tissues

75
Q

what is estradiol metabolised into by the liver

A

estrone

76
Q

what enzyme is responsible for metabolising estradiol to estrone

A

17 beta HSD (hydroxysteroid dehydrogenase)

77
Q

what happens to SHBG levels in a patient on COCP

A

SHBG increases and therefore less free testosterone so anti-androgenic effects

78
Q

what happens to LH secretions on someone on the COCP

A

decrease LH therefore decrease testosterone production

79
Q

what dose of hormone is contained in the implant (nexplanon)

A

68 mg etonogestrel (metabolite of desogestrel)

80
Q

what is the release rate of etonogestrel per day in the implant at week 5-6

A

60-70 ug (mcg)/ day in week 5-6

81
Q

what is the release rate of etonogestrel per day in the implant in

A) year 1
B) year 2
c) year 3

A

a - year 1 - 35-45ug (mcg/day)
b) year 2- 30-40ug (mcg/day)
c) year 3 - 25-30ug (mcg/day)

82
Q

what are the two hormones and their respective doses contained in the CHC patch

A

EE 33.9 mcg + nolgestromin 203 mcg

83
Q

what are the two hormones and their respective doses contained in the CHC ring

A

EE 15mcg + etonogestrel 120mcg

84
Q

what is the fetal mortality rate of women with mechanical heart valves

1 in 2
1in 3
1in 5
1 in 10

A

1 in 3

85
Q

if warfarin is used during pregnancy what is the risk of the baby developing fetal warfarin syndrome

10%
20%
30%
50%

A

30%

86
Q

what is the most critical time period for the fetus if mum is taking warfarin

A

6-12 weeks

87
Q

what are some of the signs of fetal warfarin encephalopathy

A

stippled epiphyses
nasal hypoplasia
short limbs and digits

88
Q

what number of units of alcohol if drunk continuously is associated with fetal alcohol syndrome

A

> 5 units/day chronic usage

89
Q

are statins teratogenic?

A

yes - should be stopped 3 months prior to conception

90
Q

is retinoid acid safe in pregnancy

A

no teratogenic - contains vitamin A - ear malformations

91
Q

when should ARBs (candesartan, losartan and valsartan) and ace-inhibitors e.g. ramipril be avoided in pregnancy

A

avoid in second and third trimester

92
Q

which drug if used for hyperthyroidism should be avoided in pregnancy

A

carbimazole can cause chonal atresia, GI abnormalities and abdominal wall defects

PTU is safe

93
Q

MOA of penicillins and cephalosporins

A

inhibit pepitidoglycoan in cross links in cell walls

94
Q

MOA of macrolide

A

inhibit pepitdylotransfer, bind to 50s ribosomal unit

95
Q

MOA of tetracyclines

A

bind to 30s ribosomal unit

96
Q

MOA of quinolones

A

inhibit DNA gyrase

97
Q

MOA of trimethoprim and sulfonamides

A

Dihydrofolate reductase inhibitor

98
Q

MOA nitrofurantoin

A

inhibits citric acid cycle , damages bacterial DNA via multiple reactive intermediaries

99
Q

MOA of metronidazole and tinidazole

A

inhibit nucleic acid synthesis in the cell wall

100
Q

MOA aminoglycosides

A

bind to 30s ribosomal unit

101
Q

regarding COCP mechanism of action, where in the HPO axis does progestogen act

A
  1. progestogen acts on the hypothalamus to inhibit GnRH pulses
  2. pituitary to inhibit the oestrogen induced LH surge
102
Q

where does oestrogen act on the HPO axis in COCP to prevent ovulation

A

oestrogen decreases the pituitary response to GnRH and in the follicular phase inhibits the FSH surge

103
Q

How does the depo inhibit ovulation

A

slows down the GnRH pulse generator which prevents the LH surge required for ovulation

104
Q

how does CHC increase risk of VTE

A

decreases antithrombin III and plasminogen activator therefore increased platelet activation ==> increased VTE

MFSRH part 1 (20 decks)

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