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Module 7: Urogenital > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Oestrogen:

Effects, clinical uses and adverse effects

A

Effects: Female sexual maturation and growth (breast/endometrium/uterus); increased coagulation; metabolic and CV effects; increased progesterone receptor synthesis

Clinical uses: Contraception; HRT; primary hygonadism: decreasing levels to decrease dysmenorrhoea, hirsutism and amenorrhoea

Adverse effects: Migraines; nausea; hyperpigmentation; endometrial/breast cancer; hyperpigmentation; breast tenderness; metabolic effects

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2
Q

Outline the M.O.A. of oestrogen/progesterone/androgens

A

Transported bound to a transport protein. Dissociation allows diffusion to target cell.

Bind to a cell surface receptor (ER/PR/AR)

Chaperone proteins (hsp) are displaced and the hormone:receptor is translocated to the nucleus

The hormone:receptor complex associates with the hormone responsive element

Co-regulator molecules are recruited

Gene transcription is altered

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3
Q

Progesterone:

Effects, clinical uses and side effects

A

Effects: Breast and endometrial development; ↓ Na+ absorption; prompts decidualisation of endometrium in secretory phase; weak androgenic effects; inhibit gonadotropins; fat and carb. metabolism

Clinical uses: Contraception; HRT; conceiving difficulties; long term ovarian suppression; use in dysmenorrhoea, endometriosis and PMS when oestrogen is contraindicated

NOTE: May take a while for ovulatory function to return following cessation of the therapy

Side effects: May ↑ BP; ↓ HDL and increase risk of breast cancer

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4
Q

Androgens:

Effects, clinical uses and side effects

A

Effects: Foetal sexual differentiation; development of male sexual characteristics; spermatogensis; ↑ erythropoietin synthesis; stimulates/maintains sexual function and behaviour; metabolic actions (anabolic effects on muscle and bone, ↑ hepatic protein synthesis, ↓ HDL)

Clinical uses: Primary hypogonadism; delayed puberty; anabolic steroids

Side effects: Prostate cancer; gynaecomastia; ↑ Na+ retention (↑ BP); hirsutism, male baldness and acne; cholestatic jaundice; anxiety and depression

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5
Q

Gonadal hormone synthesis inhibitors: GnRH agonists and antagonists

A

Agonists:

Suppressive function indications: Endometriosis; uterine fibroids; precocious puberty; amenorrhoea and infertility (PCOS)

Adverse effects of suppression: Menopausal like symptoms; decreased bone density → osteoporosis

NOTE - may also be used for stimulatory functions: Female and male infertility.

Initial administration leads to a surge in FSH and LH - may require drug to counteract. Following this the increased levels cause negative feedback, creating suppression.

Pulsatile administration = stimulatory function

Continuous administration = suppressive function

Antagonists: Decrease FSH and LH levels. ‘Quicker’ inhibition and easier to withdraw

Indications: Controlled ovarian hyperstimulation; advanced prostate cancer

THINK OF ‘DOWNSTREAM’ HORMONES - Production stimulus is now removed

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6
Q

Gonadal hormone synthesis inhibitors: 5α-reductase inhibitors

A

M.O.A.: Blocks testosterone synthesis (conversion of testosterone to dihydrotestosterone) through high affinity binding of the androgen receptor

Indications: Benign prostate hyperplasia (BPH); androgenic alopecia

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7
Q

Gondal hormone synthesis inhibitors: Aromatase inhibitors

A

M.O.A.: Inhibit aromatase, preventing the conversion of testosterone to oestrogen

Indications: Metastatic breast cancer; preventing cancer reoccurence; precocious puberty; excessive aromatase production

CAUTION: Suppresion of protective oestrogen (osteoprotegerin) may lead to decreased bone density and osteoporosis

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8
Q

Receptor antagonists/modulators: SERM

M.O.A., examples (tamoxifen, raloxifen, clomiphene) and their indications/cautions

A

SERM: Selective oestrogen receptor modulators

M.O.A.: Display a mixed agonist/antagonist function, which is tissue dependent. Tissue specificity is acheived through the tissue specific oestrogen receptor and through interactions with ligand associated transcription factors (TFs).

Tamoxifen:

  • Antagonist in breast tissue
  • Partial agonist in the endometrium and bone

Indications: Treatment/prevention of breast cancer

Cautions: Treatment > 5 years increases risk of endometrial cancer (due to partial agonist function)

Raloxifen:

  • Antagonist in breast and endometrium
  • Agonist bone

Indications: Breast cancer prevention; delays osteoporosis

Clomiphene:

  • Antagonist in hypothalamus and antierior pituitary (competitive antagonist of ER, ↓ negative feedback inhibition, ↑ GnRH, FSH and LH release)
  • Agonist in ovaries

Indications: Ovulation inducing agent

Cautions: Can increase ovary size

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9
Q

Receptor antagonists/modulators: SPRM

M.O.A., examples (Mifepristone and asoprisnil) and their indications/cautions

A

SPRM: Selective progesterone receptor modulators

Mifepristone

Indications: Admistered alongside misoprostol/gemeprost for the stimulation of uterine contractions

Cautions: May induce first trimester abortion (with progesterone inhibited the decidua decay/die and the embryo has no nutritional support)

Asoprisnil: Inhibits the growth of endo- and myometrial derived tissues

Indications: Endometriosis; uterine fibroids

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10
Q

Receptor antagonists/modulators: Androgen receptor antagonists

M.O.A., indications and examples

A

M.O.A.: Block the action of testosterone and dihydrotestosterone (DHT)

Indications: Hirsutism; prostate cancer; ‘chemical castration’; hyperandrogenism in females

Examples

Flutamide and bicalutamide: Non-steroidal pure antagonist. Block gene transcription initiation

Cyproterone acetate: Anti-androgen at high doses

Drospirenone: Derived from spironolactone

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11
Q

Contraception: COCP

M.O.A., benefits, adverse effects

A

M.O.A.:

1. Prevent ovulation: The presence of oestrogen suppresses GnRH, and subsequently FSH and LH, release. This means the follicle does not mature (no FSH) and ovulation does not occur.

Oestrogen inhibits FSH secretion (via negative feedback), progesterone inhibits LH secretion (?decreases GnRH pulsatile release, this in turn favours FSH?)

2. Prevents pregnancy: Changes in uterine tube peristalsis, endometrial receptivity and cervical mucus secretions

Benefits: Decreased incidence of enodmetrial and ovarian cancer

Adverse effects: Increased risk of DVT, PE, gallbladder disease and breast cancer

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12
Q

Contraception: Progesterone only pill (POP)

M.O.A.,

A

M.O.A.:

1. Ovulation inhibition: The progesterone acts to decreasing the pulsatile release of GnRH (this favours secretion of FSH). It also causes decreased sensitivitiy of the anterior pituitary to GnRH.

2. Inhibits endometrial proliferation and endometrial secretions.

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13
Q

Contraception: Emergency contraception

A

A progesterone receptor modulator

Levonorgestrel - Upto 96 hours

Ulipristal - Upto 120 hours

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14
Q

HRT

Indications

A

Suppresses menopausal symptoms e.g. hot flushes, urogenital tissue atrophy

Oestrogen and progesterone can be used to prevent the induction of endometrial cancer.

*Use lowest possible dose for shortest amount of time*

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15
Q

Infertility and ovulation inducing agents

Examples, possible adverse effects

A

Examples:

Clomiphene and gonadotropins: Enhance fertility through causing the maturation of multiple eggs per cycle

Possible ADR: Multiple pregnancies

Pulsatile GnRH: Less likely to cause multiple pregnancies or ovarian hyperstimulation syndrome

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16
Q

State the effect of impaired kidney function on pharmacokinetics and pharmacodynamic processes

A

Pharmacokinetics:

  • ↓ Absorption: Increased gastric pH, phosphate binding drugs, vomiting and diarrhoea, decreased intestinal CytP450 activty
  • Distribution: Affected by changes in hydration status (Vd changed for water soluble drugs); less albumin (less binding of acidic drugs); urea displaces drugs from plasma proteins; tissue binding changed (e.g. digoxin)
  • ↓ Metabolism: Hepatic metabolism also reduced. Reduced clearance of insulin → insulin resistance
  • Excretion: Filtration, secretion and reabsorption are all affected
    • Filtration: ↓ GFR → decreased clearance and therefore more change of toxicity and ADRs
    • Reabsorption: May be reduced
    • Secretion: Increased levels of metabolites lead to saturation of transporters
  • Reduced metabolism of medicines
  • Impaired distribution of drugs due to the fluid retention associated with renal disease

Pharmacodynamics:

  • Increased sensitivity to CNS drugs
  • Increased risk of GI bleeds (with GI irritant drugs)
  • Increased risk of hyperkalaemia
  • Increased toxicity and decreased efficacy
  • Increased incidence of ADRs
17
Q

Impaired kidney function: Effects on absorption

A

Reduced due to:

  • Reduced gastric empyting
  • Reduced gastric acidity
  • Treatment with phosphate binding drugs - that are able to bind various medications

As a consequence of this the therapeutic level is not achieved.

18
Q

Impaired kidney function: Effects on distribution

A
  • The fluid retention associated with renal failure leads to reduced effective drug concentration for water soluble drugs with low protein binding
  • Organic acids accumulate in kidney disease. These acids compete with medicines for binding to albumin and other plasma proteins. This decreased availabilty of proteins for binding leads to an increased proportion of free drug.
  • Decreased albumin levels lead to an increased level of free drug
  • Urea is able to displace drugs from plasma proteins subsequently increasing the concentration of free drug
  • Tissue binding of digoxin is changed (due to altered cardiac muscle:plasma ratio) leading to increased displacement of digoxin. Dose must be reduced.
19
Q

Impaired kidney function: Effects on metabolism

A
  • Reduced renal metabolism
  • Liver:
    • Enzymatic reactions altered
  • Decreased clearance of insulin
  • Changes in mineral and bone metabolism
20
Q

Impaired kidney function: Effects on excretion

A
  • The reduction of renal clearance seen in kidney disease causes an increase in drug half-life. Resultantly, the dose interval must be widened. However, this means that the time taken for the drug to reach steady state is increased.
  • Excretion of acidic drugs is increased by increased urinary pH
    • The opposite is true for alkaline drugs
21
Q

Describe 3 mechanisms responsible for drug excretion by the kidneys, how they can be altered and the implications of the alteration

A
22
Q

Understand how to assess and identify patients with imapired kidney function (dose adjustment)

A
  • Reduced GFR
  • Increased serum creatinine or urea (BUN)
  • Proteinuria
  • Oedema
23
Q

Describe how drugs reduce kidney function: Pre-renal, renal and post-renal

A
24
Q

Give key examples of how specific drugs/drug classes cause nephrotoxicty

A

Module 7: Urogenital (29 decks)

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