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ELC > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Precursor of all steroids?

A

Cholesterol

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2
Q

Where are the steroid receptors located? How do they produce effects?

A

Cytoplasm of cells - act as gene transcription factor

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3
Q

Where is oestrogen produced, what stimulates production?

A

Produced in ovarian follicles stimulated by FSH and LH

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4
Q

Where is oestrogen produced, what stimulates production?

A

Produced in ovarian follicles stimulated by FSH and LH

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5
Q

Main enzyme involved in oestrogen synthesis?

A

17β-oestradiol

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6
Q

Actions of oestrogen

A

Development of secondary sexual characteristics

Positive effect on the ovulatory cycle (low blood conc)

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7
Q

Progesterone actions?

A

Negative feedback on FSH and LH

Prepares endometrium for implantation by thickening cervical mucus, suppresses lactation and inhibits uterine contractility (pregnancy hormone)

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8
Q

Mechanism of the combined oral contraceptive pill?

A

Suppresses LH and FSH

Prevents ovulatory surge of LH

Thickens cervical mucus

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9
Q

Progestin only contraceptive S/E?

A

Ectopics, menorrhoea (breakthrough bleeding)

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10
Q

Non-contraceptive uses of progestin?

A

HRT

Dysmenorrhoea/menorrhoea

Abortion (morning-after)

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11
Q

Growth of 60% of breast tumours driven by what?

A

Oestrogen

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12
Q

Common treatments for oestrogen driven breast cancer? Examples?

A

Aromatase inhibitors (Reduce oestrogen synthesis)

Irreversible: Exemestane
Reversible: anastrazole

Anti-oestrogens (ER antagonist): Tamoxifen

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13
Q

S/Es of Aromatase inhibitors?

A

osteoporosis

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14
Q

What cells mainly produce testosterone, where?

A

Leydig cells in testes (also in adrenals)

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15
Q

Testosterone functions?

A

Primary and secondary sexual characteristic development

Spermatogenesis

Increased bone and lean muscle mass

Aggression, libido

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16
Q

Anti-androgen uses? examples?

A

Used in benign prostatic hyperplasia and prostate cancer

Finasteride, Flutamide

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17
Q

Anabolic steroids actions?

A

Increase lean muscle mass, accelerate recovery from injury

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18
Q

What are anabolic steroids?

A

testosterone derivatives e.g. nandrolone

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19
Q

What are anabolic steroids?

A

testosterone derivatives e.g. nandrolone

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20
Q

What do combined hormonal methods include in them?

A

Combination of synthetic oestrogen and progesterone

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21
Q

Effects of combined hormonal methods?

A

Reduced contractions and frequency of cilia beat in the fallopian tube

Ovary: Progestin inhibits LH surge and inhibits FSH release

Cervix: progestin produces a thick mucus plug

Thick mucus in endometrium

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22
Q

What is Ethinylestradiol, and oestradiol valerate

A

Ethinylestradiol - synthetic oestrogen

oestradiol valerate - prodrug metabolised to oestrogen

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23
Q

What are synthetic progesterones called?

A

Progestins

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24
Q

What receptor to progestins bind to?

A

Progesterone receptors (induce thick mucus and create mucus plug) - good effect

Others include: GnRHR, Androgen Receptors, Oestrogen Receptors, Glucocorticoid Receptors, Mineralocorticoid receptors

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25
Q

Difference in mono/bi/triphasic preperation of the Combined oral contraceptive pill?

A

Monophasic - steady levels of bothe oestrogen and progestins

Biphasic and triphasic have constant oestrogen levels and increase the progestin component once (biphasic) and twice (triphasic)

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26
Q

Other combined hormonal methods that are not pill-based?

A

Combined transdermal patch

Combined vaginal ring

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27
Q

S/E associated with combined contraceptive methods?

A

Increased anti-clotting factors and decreased anti-thrombin can lead to venous thrombosis/MI/stroke

Nausea/mood changes

Hypertension (water/sodium retention)

Androgenic effects (Oily skin/acne/weight gain)

Rare increased risk of breast cancer

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28
Q

What do single contraceptice methods contain?

A

Progestin only

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29
Q

Examples of single hormonal methods?

A

Progestin only pill

Subdermal implant

Injectables

Intra-uterine coils

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30
Q

Contraceptive effects of single hormonal methods?

A

Fallopian tubes: reduced cilia bet frequency and contractions

Inhibits GnRH release and LH surge

Cervix: thick mucus plug

Endometrium: thick mucus induction

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31
Q

Benefits to single hormonal contraceptive methods?

A

No effect on thromboembolism and blood clotting

No increased risk of cancer

Return to fertility more rapid

Good tolerance

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32
Q

S/E’s of single hormonal methods?

A

Altered menstrual pattern

Nausea/mood changes

Hypertension

Atherosclerosis

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33
Q

Mechanism of action of the copper IUD?

A

Inhibits fertilisation as copper is toxic to sperm and Oocytes

Endometrial inflammation has anti-implantation effects

Inhibit sperm penetration

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34
Q

Reasons the copper IUD could be contra-indicated?

A

UKMEC3:

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35
Q

Examples of barrier methods to contraception?

A

Male condoms

Female condoms

Diaphragms

Cervical cap

Dams

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36
Q

Do diaphragms reduce risk of STI?

A

No

37
Q

Methods of sterilisation?

A

Female - Tubal occlusion:

  • Laparoscopic: 1 in 200 failure rate, reversible
  • Hysteroscopic: 1 in 500 failure rate, irreversible

Male: Vasectomy failure rate 1 in 2000

38
Q

Choice for emergency hormonal contraception?

A

Levonorgestrel

Ulipristal

Taken 3-5 days post-coital

39
Q

Choices for non-hormonal contraception?

A

Copper IUD - 120 hours after

40
Q

Method of Levonorgestrel to prevent pregnancy?

A

Inhibits ovulation

41
Q

Method of Ulipristal function?

A

Selective progesterone receptor modulator

42
Q

5 points of Fraser guidance to prescribing contraception to teenagers?

A
  1. Understand implications and advice
  2. Cannot be persuaded to involve parent/guardian
  3. Likely to have sex with/without treatment
  4. Physically/mentally likely to suffer
  5. In best interest to proceed
43
Q

What age is sex considered rape regardless of consent?

A
44
Q

Signs of grooming/sexual exploitation in a young person asking for contraception?

A

Reluctance to say partners name

Repeat STI testing

Repeat pregnancies

Expensive clothes/gifts

45
Q

Where can you refer to if you believe teen is in danger?

A

Specialist sexual Health nurses/safeguarding nurse

Children’s social care

Police

46
Q

Changes in pharmacokinetics in pregnancy?

A

Greater Vol. of distribution means a higher loading dose may be required

Increased clearance means higher maintenance doses are needed

47
Q

Drugs of concern in pregnancy?

A

Lithium

Anti-convulsants

Iodine

Sex hormones

NSAIDS

Tetracycline

ACE inhibitors

Aminoglycoside antibiotics

48
Q

Recommendations on prescribing new drugs in pregnancy?

A

Avoid in first trimester

Use lowest effective dose

Use for shortest possible time

49
Q

Potentially harmful drugs in lactation?

A

Metronidazole

Barbituates

BDZ

Opioids

Lithium

Immunosuppressants

50
Q

Main drug treatments for Type 2 diabetes?

A

Sulphonylureas

Post-prandial glucose regulators

Insulin sensitisers Metformin and Thiazolidinediones

Alpha glucosidase inhibitors

New therapies:

GLP-1 analogues/
DDP4 inhibitors
SGLT-2 inhibitors

51
Q

How do sulphonylureas work in diabetes?

A

Bind to ATP-sensitive K+ channel on beta cells in the pancreas, which then closes. Causes a depolarisation wjich then opens Ca++ channels causing increased insulin exocytosis

52
Q

S/E’s of sulphonylureas?

A

Hypoglycaemia

Weight gain

53
Q

Example of a post-prandial glucose regulator?

A

Repaglinide

54
Q

Mechanism of action of post-prandial glucose regulator?

A

Binds to a site on Beta cell distinct from sulphonylurea binding site and also acts on K+ channels

Stimulates early insulin secretion without prolonged stimulation during later periods of fasting

55
Q

S/Es of Repaglinide (post-prandial glucose regulator)

A

Hypoglycaemia - less so than sulphonylureas

Quite well tolerated

56
Q

Mechanism of action of metformin?

A

Increased glucose uptake in skeletal muscle and adipocytes

Decreased hepatic gluconeogenesis

Decreased glucose absorption in intestines (only at high concentrations

57
Q

How is metformin used in diabetes? Prescribing patterns.

A

1st line in patients with an increased BMI or normal BMI

Reduce appetite and can lead to weight loss

Given with food 2-3 times daily

58
Q

Metformin S/Es?

A

Lactic acidosis

GI upset

59
Q

Thiazolidinedione mechanism of action?

A

Causes increased transcription of insulin-sensitive genes in adipose tissue/liver/skeletal muscle

Adipose:

  • Increased glucose uptake
  • Fatty acid uptake and utilisation

Liver:
- Decreased glucose output

Skeletal muscle:
- Increased glucose uptake

60
Q

S/Es of Thiazolidinediones?

A

Weight gain

Cardiac failure

Anaemia and oedema

Hepatotoxicity

61
Q

Alpha glucosidase inhibitors mechanism of action?

A

Inhibit alpha glucosidase involved in glucose absorption in the gut - so reduce post-prandial glucose peaks

62
Q

Alpha glucosidase S/Es?

A

Flatulence and diarrhoea

63
Q

GLP-1 analogues mechanisms of action?

A

Decreased hepatic glucose production

Increased pancreatic insulin secretion and decreased glucagon secretion

Increased glucose uptake in muscle cells

Decreased gastric emptying and decreased hunger

64
Q

Why is GLP-1 of limited use? What other drug is more useful due to this?

A

It is rapidly broken down by DPP-4

DPP-4 inhibitors are therefore quite useful and have similar effects to GLP-1 receptor agonists

65
Q

Examples of DPP-4 inhibitors?

A

Sitagliptin

66
Q

Drug combinations in Hodgkins Lymphoma and the way to remember it?

A

ABDV:

Adriamycin
Bleomycin
Dacarbazine
Vinblastine

67
Q

Breast cancer combinations and way to remember it?

A

CMF:

Cyclophosphamide
Methotrexate
Fluorouracil

Followed by tamoxifen

68
Q

Examples of direct DNA targeting drugs in anti-cancer therapies?

A 
Alkylating agents
Platinum compounds
Cytotoxic antibiotics
Topoisomerase I inhibitors
Topoisomerase II inhibitors
69
Q

Example of a cytotoxic alkylating agent? Mechanism?

A

Cyclophosphamide - pro-drug, damages DNA causes guanine ring opening

70
Q

Cyclophosphamide S/Es?

A

Destruction of high turnover normal tissue - bone marrow, gut epithelium, hair

Sterility

Teratogen

Cardiac and bladder toxicity

71
Q

Example of cytotoxic platinum compound? Mechanism?

A

Cisplatin - Cross-links DNA

72
Q

Example of Cytotoxic antibiotics? Mechanism?

A

Doxorubicin (adriamycin) - blocks DNA polymerase by forming a complex with DNA

73
Q

Example of topoisomerase I inhibitor? Mechanism?

A

Topotecan - DNA needs breaks during replication, so forms gap, will block the reformation of this gap and therefore lead to a halt in DNA synthesis

74
Q

Example of topoisomerase II inhibitor? Mechanism?

A

Etoposide - Binds to topoisomerase II and prevents DNA replication and causes strands breaks

75
Q

Cytotoxic antimetabolite examples?

A

Methotrexate

Leucovorin

Hydroxyurea

76
Q

Methotrexate mechanism?

A

Inhibits dihydrofolic acid reductase and therefore inhibits the formation of folic acid

77
Q

What cytotoxic drugs affect microtubule function as their mechanism? Example

A

Vinca alkaloids:

Vincristine

78
Q

Mechanism of action of Vincristine?

A

Bind to tubulin, block division at metaphase and stimulate depolymerisation of tubulin

79
Q

What cytotoxic drug affects protein assembly? Mechanism of action?

A

Asparaginase - Asparagine is essential in cancer cells as they cannot produce it, asparaginase breaks down asparagine

80
Q

Example of a monoclonal antibody used in cancer treatment?

A

Trastuzumab - herceptin:

HER-2 recruits EGF (human epidermal growth factor)

20% of patients over-express HER-2 and Herceptin binds to receptors inactivating them

81
Q

What cytotoxic drugs cause high, moderate and low nausea and vomiting?

A

Mild: Fluorouracil, etoposide, low dose methotrexate, vinca alkaloids

Moderate: Doxorubicin, high dose methotrexate, low/intermediate dose cyclophosphamide

High: cisplatin, high dose cyclophosphamide

82
Q

Acute nausea and vomiting treatment in cancer

A

Domperidone/metaclopramide

Lorazepam/dexamethosone (potentiate 5-HT antagonists e.g. ondansetron)

83
Q

What antibiotic might you use for pneumonia, what might you use for hospital acquired pneumonia?

A

Pneumonia - amoxicillin

Hospital acquired - Vancomycin

84
Q

What factors might the success of chemotherapy depend on?

A

Size of the tumour

Number of cells dividing at any one time

Endocrine environment of the cell

Rate of recovery of normal tissue from the effect of treatment

85
Q

What is addisons disease?

A

Autoimmune destruction of adrenal cortex, reducing the amounts of all corticoid hormones

86
Q

What tests can you do to diagnose phaeochromocytoma?

A

Metadrenaline and clonidine suppression tests

87
Q

Two theories behind PCOS?

A

ACTH theory:

High aromatase results in incraesed breakdown of cortisol, results in feedback resulting in increased ACTH release

DHEA conversion to testosterone is increased by ACTH

High aromatase in adipose converts androgen to oestradiol (E2)

Feedback of oestradiol decreases GnRH and therefore LH, leading to amenorrhoea and cysts in ovaries

Insulin theory:

Increased peripheral adiposity

Insulin resistance causes hyperinsulinaemia

Insulin stimulates androgen release

Which is converted to E2 by aromatase, the negative feedback again decreases the amount of GnRH and LH

88
Q

Macroscopic hallmarks of cancer?

A

Autonomous growth

Evasion of apoptosis

Angiogenesis

Insensitive to growth inhibitors

89
Q

Two branches for treatment of PCOS, and the drugs within them?

A

Management of hirsutism:

  • Oral contraceptive pill
  • Anti androgens e.g. spironolactone

Management of infertility:

  • Clomiphene (blocks oestrogen)
  • Gonadotrophin therapy

ELC (9 decks)

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