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Y2B3 - Reproductive πŸ“˜ > Pharmacology πŸ’Š > Flashcards

Pharmacology πŸ’Š Flashcards

1
Q

what are the types of estrogen?

A

Natural estrogens: estradiol, estrone and estriol

Semisynthetic estrogens: Ethinyl estradiol and mestranol.

Synthetic estrogens: diethyl stilbosterol.

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2
Q

Mechanism of action of estrogen

A
  • It acts via binding to Intracellular receptors which are ligand activated transcription factors that controls gene transcription.
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3
Q

whata re the pharmacological effects of estrogen?

A
  • Development of genital tract and breast.
  • Development of ♀ secondary sex characters.
  • Metabolic effects:
    1. Increase bone mass and prevent bone resorption.
    2. Increase blood glucose and TGs.
    3. Salt and water retention.
    4. Increase blood coagulation and platelet adhesiveness
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4
Q

absorbtion of estrogen

A

Oral, Parenteral, Transdermal or topical.

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5
Q

Distribution of estrogen

A

Bind to albumin and sex hormone binding globulin (SHBG).

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6
Q

Metabolism of estrogen

A

Metabolized by sulfate and glucuronide conjugation in the liver and undergo enterohepatic recycling.

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7
Q

Elimination of estrogen

A

Excreted via bile and urine.

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8
Q

what are the therapeutic uses of estrogen?

A
  1. Contraceptive pills.
  2. Dysfunctional uterine bleeding.
  3. Replacement therapy in ovarian hypofunction.
  4. Postmenopausal symptoms e.g. atrophic vaginitis and osteoporosis.
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9
Q

what are the adverse effects of estrogen?

A
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10
Q

Contraindications of estrogen

A
  • Hypertension or ischemic heart disease (IHD).
  • History of thrombosis.
  • History of cancer breast.
  • Migraine headache.
  • Depression
  • Diabetes mellitus.
  • Liver disease and gall stones.
  • Obese, smokers, or women over 35 years.
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11
Q

what is the mechanism of action of Clomiphene citrate (Clomid)?

A
  • Blocks estrogen receptors in hypothalamus and pituitary →↑ FSH and LH β†’ stimulate ovulation.
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12
Q

Uses of Clomiphene citrate (Clomid)

A

Infertility

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13
Q

Adverse effects of Clomiphene citrate (Clomid)

A
  • Ovarian cysts
  • Hot flushes.
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14
Q

what are Selective estrogen receptor modulators (SERMs)?

A
  • Tamoxifen
  • Raloxifene
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15
Q

Compare between Tamoxifen and Raloxifene in terms of (mechanism of action, uses & adverse effects)

A
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16
Q

what are Aromatase inhibitors?

A
  • Nonsteroidal competitive inhibitors
  • Steroidal, irreversible inhibitor
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17
Q

Nonsteroidal competitive inhibitors

A

Anastrazole and letrozole (Femara).

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18
Q

Steroidal, irreversible inhibitor

A
  • Exemestane
  • Used for treatment of postmenopausal women with estrogen- receptor positive breast cancer who have received two to three years of tamoxifen and are switched to them to complete five years of hormonal therapy.
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19
Q

Hormonal contraception

A
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20
Q

Mechanism of action of Hormonal contraception

A

They inhibit ovulation by exerting –ve feedback on LH and FSH secretion.

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21
Q

what are the Causes of failure of contraceptive pills?

A
  • Enzyme inducers e.g. rifampin, phenytoin
  • Broad spectrum antibiotics: e.g tetracycline
  • Laxatives: ↓ intestinal absorption of contraceptive pills.
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22
Q

Types of Progesterone

A

Natural: Progesterone injection

Synthetic: Medroxy progesterone acetate.

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23
Q

Mechanism of action and pharmacokinetics of Progesterone

A

Like estrogen

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24
Q

Therapeutic uses of Progesterone

A
  • Contraceptive pills.
  • Threatened abortion.
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25
Q

what are the adverse effects of Progesterone?

A
  • Menstrual irregularities: spotting bleeding, breakthrough bleeding, amenorrhea, and dysmenorrhoea.
  • Acne.
  • Hirsutism.
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26
Q

what is the mechanism of action of Antiprogesterone (Mifepristone)?

A

It is a competitive blocker of progesterone receptors.

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27
Q

what are the uses of Antiprogesterone (Mifepristone)?

A

It is used with PGF2Ξ± to induce medical abortion in the first trimester.

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28
Q

what are examples of Androgens and anabolic steroids?

A
  • Natural androgens: androsterone and testosterone
  • Synthetic androgens: testosterone propionate.
  • Anabolic steroids: Stanazol.
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29
Q

Mechanism of action & pharmacokinetics of Androgens and anabolic steroids

A

Like estrogen

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30
Q

what are the uses of Androgens and anabolic steroids?

A
  • Chronic debilitating diseases e.g renal failure.
  • Chronic refractory anemia
  • Illicit use by athletes: to increase muscle bulk
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31
Q

what are the adverse effects of Androgens and anabolic steroids?

A
  1. Reduction in spermatogenesis after stopping.
  2. Precocious puberty and premature closure of epiphysis in children.
  3. Cholestatic jaundice.
  4. Verilizing effects in females.
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32
Q

what are examples of Antiandrogens?

A
  • Ξ±-reductase inhibitors: Finasteride
  • Testosterone receptor blockers
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33
Q

what is the mechanism of action of Ξ±-reductase inhibitors (Finasteride)?

A

Inhibits 5 Ξ±-reductase enzyme responsible for conversion of testosterone into the active form di-hydro-testosterone (DHT).

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34
Q

Uses of Ξ±-reductase inhibitors (Finasteride)

A
  • Treatment of benign prostatic hyperplasia (BPH).
  • Treatment of male baldness.
  • Treatment of female hirsutism.
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35
Q

what are examples of Testosterone receptor blockers?

A
  • Cyproterone acetate
  • Flutamide
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36
Q

what are the uses of Testosterone receptor blockers?

A

Cyproterone acetate: Used in hirsutism in females.

Flutamide: Used in cancer prostate.

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37
Q

what are Oxytocic drugs? and what are they used for?

A
  • Oxytocin
  • Prostaglandins
  • Mifepristone
  • Ergot alkaloids

Used in induction of delivery.

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38
Q

what is the mechanism of action of oxytocin?

A
  • Stimulation of Oxytocin receptors (which are expressed by the uterus and myoepithelial cells of mammary gland):
  1. ++ contraction of uterine muscle (facilitate delivery).
  2. Stimulates smooth muscles of mammary glands (milk-ejection).
  3. Weak pressor and anti-diuretic activity.
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39
Q

Uses of Oxytocin

A

1. Induction of labor.
2. Control postpartum hemorrhage.
3. Stimulate milk ejection

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40
Q

Adverse effects of Oxytocin

A

Mother:
- Uterine rupture.
- HTN.
- Arrhythmia.
- Water intoxication.
- Afibrinogenemia.
- Death.

Fetus:
- Arrhythmia
- Fetal death

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41
Q

CI of Oxytocin usage

A
  • Fetal distress
  • Prematurity
  • If vaginal delivery is contraindicated.
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42
Q

when is vaginal delivery contraindicated?

A
  • Abnormal fetal presentation
  • Cephalopelvic disproportion
  • Invasive cervical cancer
  • Active genital herpes
  • Prolapse of the cord
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43
Q

what are examples of Prostaglandins?

A
  • Dinoprostone (PGE2)
  • Carboprost (PGF2Ξ±)
  • Misoprostol (PGE1 analogue)
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44
Q

mechanism of action of prostaglandins

A
  • Potent stimulation of uterine contractions.

- PG plays an important role in cervical ripening (Softening of the cervix ).

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45
Q

uses of prostaglandins

A
  1. Induction of abortion.
  2. Cervical ripening before induction of labor.
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46
Q

what are the adverse effects of prostaglandins?

A
  • Colic and diarrhea
  • Carboprost aggravate bronchial asthma.
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47
Q

what is the mechanism of action of Mifepristone?

A

Antagonize Progesterone at its receptor in the uterus.

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48
Q

uses of Mifepristone

A

Medical termination of intrauterine pregnancy

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49
Q

what are the adverse effects of Mifepristone?

A
  • GI cramps
  • Vaginal bleeding
  • Urticarial rash
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50
Q

examples of Ergot alkaloids

A

(Methylergometrine)

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51
Q

what is the mechanism of action of Ergot alkaloids?

A

Increases motor activity of the uterus results in forceful, prolonged contraction

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52
Q

Uses of Ergot alkaloids

A

Only for postpartum bleeding

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53
Q

what are the adverse effects of Ergot alkaloids?

A
  • Hypertension & tachycardia
  • Acute myocardial infarction
  • Nausea, vomiting and colic
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54
Q

what are tocolytic drugs?

A
  • Atosiban
  • Beta-sympathomimetics
  • Calcium channel blockers
  • Magnesium sulphate
  • Ethyl alcohol
  • Prostaglandin inhibiting agent
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55
Q

Mechanism of action of Atosiban

A
  • Modified form of oxytocin that competitively blocks oxytocin receptor leading to halting uterine contractions.
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56
Q

what are tyhe uses of Atosiban?

A

Prevention of premature labor

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57
Q

Adverse effects of Atosiban

A
  • Headache
  • Hypotension
  • Hot Flushing
  • Hypersensitivity
  • Tachycordia.
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58
Q

what are examples of Beta-sympathomimetics?

A
  • Ritodrine.
  • Isoxuprine.
  • Terbutaline.
  • Salbutamol.
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59
Q

<echanism of action of Beta-sympathomimetics

A

Increases cAMP via activation of B2- adrenoceptors leading to relaxation of uterine smooth muscle.

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60
Q

what are the uses of Beta-sympathomimetics?

A

Prevention of premature labor

61
Q

Adverse effects of Beta-sympathomimetics

A

Fetal:
* Tachycardia.
* Hypotension.
* Arrhythmia.

Maternal:
* Tachycardia
* Hypokalaemia
* Tremors
* Hypotension.
* Arrhythmia
* Flushing

62
Q

Contraindications of Beta-sympathomimetics

A

a. Hypotension.
b. Heart disease.
c. Hyperthyroidism.
d. Uterine bleeding : (dilatation of uterine arteries increase bleeding).

63
Q

what are examples of Calcium channel blockers?

A

Nifedipine

64
Q

what is the mechanism of action of Calcium channel blockers?

A

Block voltage gated Ca channel β€”> decrease Ca concentration within the myometrial cells and reduce its contractility.

65
Q

whata are the uses of Calcium channel blockers?

A

Prevention of premature labor

66
Q

Adverse effects of Calcium channel blockers

A
  1. Hypotension and reflex tachycardia.
  2. Gingival (gum) hyperplasia.
  3. Salt & water retention (ankle edema).
67
Q

Contraindications of Calcium channel blockers

A

a. Hypotension.
b. Angina
c. Tachycardia

68
Q

what is the mechanism of action of Magnesium sulphate?

A

Calcium efflux outside myometrial cells leading to uterine relaxation.

69
Q

what are the uses of Magnesium sulphate?

A
  • Prevention of premature labor
  • Prevention & It of seizures in preeclampsia
  • TTT of arrhythmia (torsade de pointes)
70
Q

Adverse effects of Magnesium sulphate

A
  • Shock and hypotension
  • Nausea and vomiting
  • Pulmonary edema
  • Cardiovascular collapse
  • Hypotonia (ms weakness)
71
Q

Contraindications of Magnesium sulphate

A

Myasthenia gravis is an absolute contraindication for magnesium sulfate.

72
Q

what reverses the side effects of magnesium sulphate?

A

ca gluconate

73
Q

what is the mechanism of action of Ethyl alcohol?

A
  1. Inhibits oxytocin release from posterior pituitary.
  2. Suppresses myometrial activity directly.
  3. Inhibits prostaglandin F2 synthesis.
74
Q

Adverse effects of Ethyl alcohol

A

a. Nausea, vomiting.

b. Drunken mother and foetus.

c. Maternal and foetal acidosis.

d. Congenital anomaly

75
Q

what is the mechanism of action of Prostaglandins inhibiting agents?

A

Inhibit uterine contraction by inhibiting PGs synthesis. e.g. indomethacin

76
Q

what are the uses of Prostaglandins inhibiting agents?

A
  • Relief of cramps associated with menstruation (dysmenorrhea)
77
Q

Contraindications of Prostaglandins inhibiting agents

A

Don’t administer NSAIDs during late 2nd or 3rd trimester of pregnancy β€”> premature closure of ductus arteriosus.

78
Q
A
79
Q

Absorbtion of drugs in pregnancy

A
  • Slow drug absorption does not occur except at term, Thus parenteral drug administration is preferred to obtain quick response.
  • Increased emesis is seen due to morning sickness.
80
Q

Distribution of drugs during pregnancy

A
  • Pregnancy is accompanied by a 30% increase in plasma volume, with consequent decrease in plasma albumin.
  • This may alter the Vd and plasma concentration of drugs given.
81
Q

Metabolism of drugs during pregnancy

A

Hepatic drug metabolising enzymes are induced during pregnancy.

81
Q

Execretion of drugs during pregnancy

A
  • During pregnancy, renal plasma flow increases by 100% and GFR by 70%.
  • Drugs are eliminated more rapidly than in the non-pregnant state.
82
Q

what are the Factors affecting transfer of drugs to fetus?

A

1. Physicochemical properties of the drug:

  • Molecular weight (size)
  • Lipid solubility

2. Rate & amount of drug reaching the fetus:

  • Protein binding
  • Variables affect uterine blood flow & rate of drug transfer

3. Genetic Fetal Predisposition

4. Stage of placental and fetal development at time of exposure to drug:

  • The human gestation period is approximately 40 weeks from first day of last menstrual period (38 weeks’ post-conception).
83
Q

Molecular size & its relation to placental transfer of drugs

A
  • Most drugs (MW <600) cross easily.
  • Drugs with very large MW (e.g Insulin & Heparin) have negligible transfer.
84
Q

Lipid solubility & ionization relation to placental transfer of drugs

A
  • Lipophilic, unionized drugs cross the placenta more easily than polar drugs.
  • Molecules that are ionized at physiological pH cross slowly (e.g. salicylates, tubocurarine)
  • Weakly basic drugs become β€˜trapped’ in fetal circulation due to slightly lower pH compared with maternal plasma.
85
Q

Protein binding relation to placental transfer of drugs

A
  • Drugs which are highly protein bound tend to achieve higher maternal and lower fetal concentrations.
  • The penetration of highly protein-bound drugs is inhibited
  • Only free unbound drugs, cross placenta.
86
Q

uterine blood flow & rate of drug transfer relation to placental transfer of drugs

A

Uterine & umbilical bl. Flow :
1. Maternal blood pressure
2. Cord compression
3. Drug therapy e.g. alpha-stimulant

Maternal diseases :
1. Pregnancy-induced hypertension
2. DM -> change permeability of placenta

87
Q

what are the 3 stages of development of embryo & fetus?

A
  1. Pre-embryonic Stage
  2. Embryonic stage
  3. Fetal stage
88
Q

what is another name for Pre-embryonic stage

A

fertilization and implantation period

89
Q

Duration of Pre-embryonic stage

A

0-14 days

90
Q

Effect of teratogenic drugs during Pre-embryonic stage

A
  • Drugs in this stage leads to death of fetus at a very early and sub-clinical stage.
91
Q

what is another name of Embryonic stage?

A

Organogenesis period

92
Q

Duration of Embryonic stage

A

14-56 days (weeks 3-8 post-conception)

93
Q

Effects of teratogenic drugs during Embryonic stage

A
  • The most sensitive period to Teratogenic effects therefore represents greatest risk of major birth defects.
  • Avoid or minimise all drug use in the first trimester.
94
Q

what is another name of fetal stage?

A

growth and development period

95
Q

Duration of fetal stage

A

57th day onward (weeks 9-38 post-conception)

96
Q

Effect of administration of teratogenic drug during fetal stage

A
  • Fetus remains susceptible to some drug effects..
  • NSAIDs β€”-β€Ί premature closure of fetal ductus arteriosus (inhibit prostaglandin synthesis).
97
Q

Results of trimethoprim adminstration in:

  • 3-4 weeks post-conception
  • after 32 weeks’ gestation
A
  • Folic acid antagonists (trimethoprim): are associated with an increased risk of neural tube defects if exposure occurs 3-4 week post-conception but not after this period
  • Trimethoprim: should be avoided after 32 weeks’ gestation in view of the theoretical risk of severe jaundice in the neonate (Kernicterus).
98
Q

what is a Teratogen?

A
  • Any agent that results in structural or functional abnormalities in fetus, or in child after birth, as a consequence of maternal exposure during pregnancy.
  • Agent that has the potential under certain exposure conditions to produce abnormal development in the fetus.
99
Q

what is the mechanism by which a teratogen causes its effect?

A

Direct effects of the drug on fetus and or as a consequence of indirect physiological changes in mother or fetus.

100
Q

Manifestations of congenital anomalies

A
  • Congenital anomalies are non-reversible birth defects.
  • Include 4 major manifestations of abnormal fetal development :
    1. Growth alterations.
    3. Structural malformations.
    2. Functional deficits.
    4. Fetal death.
101
Q

what are the types of congenital anomalies?

A
102
Q

Give examples for congenital anomalies at birth

A
  • Obvious at birth
  • Delayed many years to manifest clinically
103
Q

Give examples for congenital anomalies which delayed many years to manifest clinically

A
  • limb abnormalities.
  • Spina bifida.
  • Hydrocephalus.
104
Q

what is the first teratogen discovered?

A

Thalidomide

105
Q

what drugs were proven to be teratogenic?

A
  • ACE inhibitors
  • Corticosteroides
  • Warfarin
  • Androgens
  • Vitamin A (Isotritenoine)
  • Antithyroid drugs
  • Diethylstilbestrol
  • Phenytoin
  • Lithium
  • Valproic acid
  • Carbamazpine
  • Cyclophosphamide
  • NSAIDs
  • Trimethoprim
106
Q

Teratogenic effects of ACE inhibitors

A

Pulmonary hypoplasia.

(CAPTOPRIL) for example

107
Q

Teratogenic effects of Corticosteroids

A

Oral cleft lip and palates if used during organogenesis

108
Q

Teratogenic effects of Warfarin

A
  • Fetal warfarin syndrome with nasal hypoplasia, stippled epiphyses, and skeletal and CNS defects
109
Q

Teratogenic effects of androgens

A

Masculinization of female fetus

110
Q

Teratogenic effects of Vitamin A (Isotritenoine)

A
  • Microtia (under developed ear pinna).
  • Anotia (complete under developed ear pinnae).
  • Thymic aplasia.
  • Cardiovascular defects
111
Q

Teratogenic effects of antithyroid drugs

A
  • Fetal and neonatal goiter with iodine use.
  • Small risk of aplasia cutis with methimazole. (Atrophy of skin)
112
Q

Teratogenic effects of diethylsilbestrol

A
  • Vaginal carcinoma and other genitourinary defects
112
Q

Teratogenic effects of Phenytoin

A
  • Fetal hydantoin syndrome. (Cleft lip, Microcephaly, MR)
  • Growth retardation.
  • CNS deficits
113
Q

Teratogenic effects of Lithium

A
  • Ebstein anomaly (Tricuspid valve regurge)
114
Q

Teratogenic effects of Valproic acid

A
  • Neural tube defects, developmental delay and deficits
115
Q

Teratogenic effects of Carbamazpine

A
  • Neural tube defects, minor craniofacial defects.
  • Fingernail hypoplasia
116
Q

Teratogenic effects of Cyclophosphamide

A
  • Craniofacial, eye, and limb defects.
  • IUGR & Neurobehavioral deficits
117
Q

Teratogenic effects of NSAIDs

A
  • Constriction of the ductus arteriosus
  • Oral clefts, cardiac defects.
  • Spontaneous abortion
118
Q

Teratogenic effects of Trimethoprim

A
  • Neural tube defects and cardiac defects
119
Q

Adverse effects of ACE inhibitors during later stages in pregnancy

A
  • Fetal and neonatal hypoxia
  • Hypotension.
  • Fetal kidney anuria, neonatal renal failure, oligohydramnios β€œHypo renal”
  • Infra-uterine growth retardation. β€œHypo growth”

4 Hypo

120
Q

Adverse effects of phenothiazines during later stages in pregnancy

A
  • Neonatal withdrawal.
  • Transient extrapyramidal symptoms.
121
Q

Adverse effects of Benodiazepines during later stages in pregnancy

A
  • Floppy infant syndrome.
  • Withdrawal reactions.
122
Q

Adverse effects of opiods during later stages in pregnancy

A
  • Respiratory depression.
  • Withdrawal reactions.
123
Q

Adverse effects of B-blockers during later stages in pregnancy

A
  • Neonatal bradycardia.
  • Hypotension & hyperglycaemia.
124
Q

Adverse effects of corticosteroids during later stages in pregnancy

A
  • Fetal adrenal suppression
125
Q

Adverse effects of NSAIDs during later stages in pregnancy

A
  • Premature closure of ductus arteriosus
  • Fetal renal impairment (decreased urine output),
126
Q

Adverse effects of Tetracycline during later stages in pregnancy

A
  • Permanent discoloration of deciduous teeth
127
Q

Tips for prescribing during pregnancy

A
  • Minimize prescribing
  • Use the smallest effective dose
  • Remember that the fetus is most sensitive in the first trimester
  • Consider pregnancy in all women of childbearing potential
  • Discuss the potential risks of taking or withholding therapy with the patient
  • Warn the patient about the risks of smoking, alcohol, over-the-counter drugs and drugs of abuse.
128
Q

what are drug categories according to FDA?

A

A, B, C, D & X

129
Q

Definition of Category A drugs

A
  • Well controlled studies in human fail to demonstrate a risk to the fetus in all trimesters & possibility of fetal harm appears remote (no demonstrable risk)
130
Q

Definition of Category B drugs

A
  • Animal studies have not demonstrate a fetal risk But no controlled studies in human

OR

  • Animal studies have demonstrate adverse effect that not confirmed by Well controlled studies in human
131
Q

what are examples of category B drugs?

A
  • penicillin
  • Cephalosporin
  • Paracetamol
132
Q

Definition of Category C drugs

A
  • Animal studies positive (Teratogen) and no Well contralled studies in human

OR

  • Studies in human and animal are not available

(Drugs given only if potential benefits justifies potential risk)

133
Q

what are examples of category C drugs?

A
  • Anti-histaminic drugs
134
Q

Definition of Category D drugs

A
  • There is positive evidence of human fetal risk, but benefit from use may be acceptable despite risk ( life threatening situation)
135
Q

what are examples of category D drugs?

A

Lithium

136
Q

Definition of category X drugs

A
  • Studies in animals or human have demonstrated fetal abnormalities

OR

  • There is evidence of fetal risk based on human experience or both and risk of drug outweigh any possible benefit.

(Teratogenic &The drug is contraindicated)

137
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Anti-emetics
A
138
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Antacids
A
139
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Laxatives
A
140
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Analgesics
A
141
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Anti-bacterials
A
142
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Anti hypertensives
A
143
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Anti-diabeteic
A
144
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Anti thyroid
A
145
Q

Mention condition, Drugs prevented in pregnancy & Safer options in pregnancy

  • Anti-coagulants
A
146
Q

what are drugs that may cause problems at later stages of pregnancy?

A
  • ACE inhibitors
  • Phenothiazines
  • Benzodiazepines
  • Opioids
  • Beta blockers
  • Corticosteroids
  • NSAIDs
  • Tetracycline

Y2B3 - Reproductive πŸ“˜ (9 decks)

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