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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
Difference in mono/bi/triphasic preperation of the Combined oral contraceptive pill?
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)
26
Other combined hormonal methods that are not pill-based?
Combined transdermal patch Combined vaginal ring
27
S/E associated with combined contraceptive methods?
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
28
What do single contraceptice methods contain?
Progestin only
29
Examples of single hormonal methods?
Progestin only pill Subdermal implant Injectables Intra-uterine coils
30
Contraceptive effects of single hormonal methods?
Fallopian tubes: reduced cilia bet frequency and contractions Inhibits GnRH release and LH surge Cervix: thick mucus plug Endometrium: thick mucus induction
31
Benefits to single hormonal contraceptive methods?
No effect on thromboembolism and blood clotting No increased risk of cancer Return to fertility more rapid Good tolerance
32
S/E's of single hormonal methods?
Altered menstrual pattern Nausea/mood changes Hypertension Atherosclerosis
33
Mechanism of action of the copper IUD?
Inhibits fertilisation as copper is toxic to sperm and Oocytes Endometrial inflammation has anti-implantation effects Inhibit sperm penetration
34
Reasons the copper IUD could be contra-indicated?
UKMEC3:
35
Examples of barrier methods to contraception?
Male condoms Female condoms Diaphragms Cervical cap Dams
36
Do diaphragms reduce risk of STI?
No
37
Methods of sterilisation?
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
Choice for emergency hormonal contraception?
Levonorgestrel Ulipristal Taken 3-5 days post-coital
39
Choices for non-hormonal contraception?
Copper IUD - 120 hours after
40
Method of Levonorgestrel to prevent pregnancy?
Inhibits ovulation
41
Method of Ulipristal function?
Selective progesterone receptor modulator
42
5 points of Fraser guidance to prescribing contraception to teenagers?
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
What age is sex considered rape regardless of consent?
44
Signs of grooming/sexual exploitation in a young person asking for contraception?
Reluctance to say partners name Repeat STI testing Repeat pregnancies Expensive clothes/gifts
45
Where can you refer to if you believe teen is in danger?
Specialist sexual Health nurses/safeguarding nurse Children's social care Police
46
Changes in pharmacokinetics in pregnancy?
Greater Vol. of distribution means a higher loading dose may be required Increased clearance means higher maintenance doses are needed
47
Drugs of concern in pregnancy?
Lithium Anti-convulsants Iodine Sex hormones NSAIDS Tetracycline ACE inhibitors Aminoglycoside antibiotics
48
Recommendations on prescribing new drugs in pregnancy?
Avoid in first trimester Use lowest effective dose Use for shortest possible time
49
Potentially harmful drugs in lactation?
Metronidazole Barbituates BDZ Opioids Lithium Immunosuppressants
50
Main drug treatments for Type 2 diabetes?
Sulphonylureas Post-prandial glucose regulators Insulin sensitisers Metformin and Thiazolidinediones Alpha glucosidase inhibitors New therapies: GLP-1 analogues/ DDP4 inhibitors SGLT-2 inhibitors
51
How do sulphonylureas work in diabetes?
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
S/E's of sulphonylureas?
Hypoglycaemia | Weight gain
53
Example of a post-prandial glucose regulator?
Repaglinide
54
Mechanism of action of post-prandial glucose regulator?
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
S/Es of Repaglinide (post-prandial glucose regulator)
Hypoglycaemia - less so than sulphonylureas Quite well tolerated
56
Mechanism of action of metformin?
Increased glucose uptake in skeletal muscle and adipocytes Decreased hepatic gluconeogenesis Decreased glucose absorption in intestines (only at high concentrations
57
How is metformin used in diabetes? Prescribing patterns.
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
Metformin S/Es?
Lactic acidosis GI upset
59
Thiazolidinedione mechanism of action?
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
S/Es of Thiazolidinediones?
Weight gain Cardiac failure Anaemia and oedema Hepatotoxicity
61
Alpha glucosidase inhibitors mechanism of action?
Inhibit alpha glucosidase involved in glucose absorption in the gut - so reduce post-prandial glucose peaks
62
Alpha glucosidase S/Es?
Flatulence and diarrhoea
63
GLP-1 analogues mechanisms of action?
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
Why is GLP-1 of limited use? What other drug is more useful due to this?
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
Examples of DPP-4 inhibitors?
Sitagliptin
66
Drug combinations in Hodgkins Lymphoma and the way to remember it?
ABDV: Adriamycin Bleomycin Dacarbazine Vinblastine
67
Breast cancer combinations and way to remember it?
CMF: Cyclophosphamide Methotrexate Fluorouracil Followed by tamoxifen
68
Examples of direct DNA targeting drugs in anti-cancer therapies?
``` Alkylating agents Platinum compounds Cytotoxic antibiotics Topoisomerase I inhibitors Topoisomerase II inhibitors ```
69
Example of a cytotoxic alkylating agent? Mechanism?
Cyclophosphamide - pro-drug, damages DNA causes guanine ring opening
70
Cyclophosphamide S/Es?
Destruction of high turnover normal tissue - bone marrow, gut epithelium, hair Sterility Teratogen Cardiac and bladder toxicity
71
Example of cytotoxic platinum compound? Mechanism?
Cisplatin - Cross-links DNA
72
Example of Cytotoxic antibiotics? Mechanism?
Doxorubicin (adriamycin) - blocks DNA polymerase by forming a complex with DNA
73
Example of topoisomerase I inhibitor? Mechanism?
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
Example of topoisomerase II inhibitor? Mechanism?
Etoposide - Binds to topoisomerase II and prevents DNA replication and causes strands breaks
75
Cytotoxic antimetabolite examples?
Methotrexate Leucovorin Hydroxyurea
76
Methotrexate mechanism?
Inhibits dihydrofolic acid reductase and therefore inhibits the formation of folic acid
77
What cytotoxic drugs affect microtubule function as their mechanism? Example
Vinca alkaloids: Vincristine
78
Mechanism of action of Vincristine?
Bind to tubulin, block division at metaphase and stimulate depolymerisation of tubulin
79
What cytotoxic drug affects protein assembly? Mechanism of action?
Asparaginase - Asparagine is essential in cancer cells as they cannot produce it, asparaginase breaks down asparagine
80
Example of a monoclonal antibody used in cancer treatment?
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
What cytotoxic drugs cause high, moderate and low nausea and vomiting?
Mild: Fluorouracil, etoposide, low dose methotrexate, vinca alkaloids Moderate: Doxorubicin, high dose methotrexate, low/intermediate dose cyclophosphamide High: cisplatin, high dose cyclophosphamide
82
Acute nausea and vomiting treatment in cancer
Domperidone/metaclopramide Lorazepam/dexamethosone (potentiate 5-HT antagonists e.g. ondansetron)
83
What antibiotic might you use for pneumonia, what might you use for hospital acquired pneumonia?
Pneumonia - amoxicillin Hospital acquired - Vancomycin
84
What factors might the success of chemotherapy depend on?
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
What is addisons disease?
Autoimmune destruction of adrenal cortex, reducing the amounts of all corticoid hormones
86
What tests can you do to diagnose phaeochromocytoma?
Metadrenaline and clonidine suppression tests
87
Two theories behind PCOS?
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
Macroscopic hallmarks of cancer?
Autonomous growth Evasion of apoptosis Angiogenesis Insensitive to growth inhibitors
89
Two branches for treatment of PCOS, and the drugs within them?
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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