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PHAL304 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

The endocrine system

A

Different parts if the brain/body create hormones which travel through the blood as chemical messages

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2
Q

Histamine

A

A hormone and neurotransmitter that acts on receptors H1-H4
Produced from mast cells, basophils (stored in granules) and neurons produced from decarboxylation of L-histidine
Stored as a complex with heparin as inactive

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3
Q

Mast cells and basophils

A

Sentinels for the immune system originating from bone marrow and released into tissues

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4
Q

Release of histamine from cells

A

Antibody mediated IgE binds to FceR1 receptors resulting in an increase of intracellular calcium, releasing granules

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5
Q

Histamine receptors

A

GPCRs
H1 - Ca2+ second messenger
H2 - cAMP/PKA
H3 - decrease cAMP
H4 - probably Ca2+
levels decrease with age

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6
Q

Allergic reaction

A

H1 dilates blood vessels via NO resulting in flushed face, decreases blood pressure and increase skin temp
As well as contracting veins, increasing vascular permeability, itchiness/pain (sensory nerves), exocrine excretion (mucus secretion)

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7
Q

Triple response

A

Wheal - swelling of hive from epithelial cels
Flare - redness from blood flow
Itch - nerves sensitised

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8
Q

Response to allergen

A

IgE antibodies produced, recruit mast cells
Second exposure -> release histamine
Type I - quick, 20-30% pop, nose, bronchial tree, skin

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9
Q

Anti-histamines

A

First generation - cross BBB = sedation, dizziness, fatigue, cognitive effects. Anti-cholinergic, Muscarinic, serotonin and K+ ions in heart
Second generation - faster onset (~50 min), don’t cross BBB, minimal anti-cholinergic, H1 selective

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10
Q

First generation antihistamine examples

A

Diphenhydramine, chlorpheniramine, promethazine

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11
Q

Second generation antihistamine examples

A

Terfenadine (withdrawn as bind to Ca2+ channels in heart, CYP3A4), fexofenadine (best), loratadine, cetirizine

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12
Q

H2R use

A

Gut acid management (GERD)
Food -> gastrin -> enterochromffin-like cell receptors
Histamine antagonists stop parietal cell from producing gastric acid
Dimaprit = agonist (research only)
antagonists = cimetidine (CYP), ranitidine, famotidine = 70% suppression of gastric acid, tolerance, not as good as proton pump inhibitors but cheaper

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13
Q

Sex hormones

A

Oestrogen, testosterone, GnRH, FSH, LH, progesterone
Estrogen = 30-400 pg/mL females, 10-40 males
Testosterone = 150-700 pg/mL females, 3000-10000 males

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14
Q

GnRH

A

Gonadotropin releasing hormone
Binds to anterior pituitary gland to provoke release of FSH (follicle stimulating) and LH (luteinising)

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15
Q

Famale sex hormone cascade

A

FSH triggers release of oestrogen
LH triggers ovulation as well as progesterone release - negative feedback on ant-pituitary and hypothalamus
Oestrogen has negative feedback on ant-pituitary

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16
Q

Oestrogen receptors

A

Nuclear receptors and GPCRs
increase proliferation of normal and neoplastic breast epithelium, prevent cardiomyocyte dysfunction, regulate bone turnover/growth, prevent inflammation in brain, no effect on muscle

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17
Q

Combined oral contraceptives

A

Oestrogens and progestogens
Cause negative feedback on hypothalamus and anterior pituitary, no release of GnRH, no ovulation
Weight gain, nausea, depression, irritability, skin changes, amenorrhoea
Progesterone only - 96-97.5% effective (rigid compliance)
Combination pill (levonorgestrel/ethinylestradiol) - 97-98%
3rd Gen - ethinylestradiol and progesterone (deep vein thrombosis)

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18
Q

SERMs

A

Selective estrogen receptor modulators
Reduce harmful effects of oestrogen’s and don’t increase risk of breast cancer

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19
Q

Severe risks of COCs

A

DVT and pulmonary embolism - highest risk in first 3 months
Increased risk in third gen (and in pregnancy)
1-2% fatal - risk factors (age, smoking, history of disease)
Lots of contraindications - diabetes mellitus, breast cancer, history of liver disease
Carcinogenic - increase risk of breast cancer RR 1.24 (reverses after 5 years w/o)
Thus need medical history before prescribing

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20
Q

Pharmacokinetics of COCs

A

Estradiol binds to serum album and steroid hormone bonding globulin (SHBG) = lipophilic, metabolised
Progesteron is 100% bioavailable, lipophilic

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21
Q

SERMs examples

A

Raloxifene, tamoxifen, clomiphene

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22
Q

Raloxifene

A

Antiestrogenic in the breast and uterus, estrogenic in bone
used in post-menopausal women with high risk of breast cancer
Reduced risk of ER+ cancer (not -)

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23
Q

Tamoxifen

A

Antiestrogenic on breast, estrogenic on plasma lipids, endometrium and bone. Decreases risk of all breast cancer (ER+ particular). Increases risk of thromboembolism and endometrial cancer
Partial agonist, high efficacy in estrogenic places

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24
Q

Clomiphene

A

Antagonist (ish), used to treat infertility, prevents binding at anterior pituitary to prevent negative feedback (increasing ovulation)
may increase testosterone in males due to increasing GNRH, FSH and ICSH

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24
Q

Testosterone

A

Ant-pituitary stimulates leydig cells (ICSH) and Sertoli cells (FSH) in the testis
Testosterone released by ICSH
Dihydotestosterone has potent androgenic effects = increase bone growth, deepen voice, muscles and facial hair
Negative feedback can create oestrogen via aromatase

25
Q

Testosterone modulators

A

Finasteride - inhibits 5a-reductase (decrease dihydrotestosterone concentrations) = prevent prostate cancer
Nandralone - androgen receptor agonist = treat aplastic anaemia
Clomiphene - inhibit negative feedback
Testosterone - replacement therapy

26
Q

Low testosterone

A

Decreased mood, weight gain, increase risk of cardiovascular disease
TRT 0 decrease risk of death and stroke but increase risk of plaques

27
Q

Erectile dysfunction

A

Vaodilation of penile vascular smooth muscle via NO -> cGMP
PDEV - inactivates cGMP (inhibit this)

28
Q

Corticosteroids

A

Stress hormones, inflammation and immune system effects, regulated via HPA axis
Release of CRF from hypothalamus -> anterior pituitary gland -> ACTH -> adrenal cortex -> glucocorticoids (negative feedback) and mineralocorticoids

29
Q

Glucocorticoids

A

hydrocortisone/cortisol
Carbs, fat and protein metabolism, suppress inflammatory and immune response

30
Q

Mineralocorticoids

A

Aldosterone
Stimulated secretion via angiotension, blood K+ conc and ACTH
Salt retaining and water balance

31
Q

Glucocorticoid therapy

A

Hydrocortisone, prednisolone and dexamethasone
(prednisone and cortisone are prodrugs)
Used in adrenal failure (Addisons), anti-inflammatory/immunosuppressive, neoplastic disease

32
Q

Hydrocortisone

A

Oral, IV and topical
Replacement therapy, asthmaticus/anaphylactic shock, eczema

33
Q

Prednisolone

A

Glucocorticoid activity
Allergy and inflammatory disease

34
Q

Dexamethasone

A

Most potent
Glucocorticoid activity (inside mineralo)
Oral and IV - suppress inflammatory and allergic disorders and reduce cerebral oedema

35
Q

Betamethsone

A

Potent = with dexamethasone
Glucocorticoid
Topically - eczemas unresponsive and psoriasis

36
Q

Beclometasone

A

Potent glucocorticoid
Aerosol in asthma, topical in eczeme (avoid systematic effects)

37
Q

Triamcinolone

A

Glucocorticoid
Anti-inflammatory and intra-articular rheumatoid arthritis

38
Q

Flurocortisone

A

sodium retaining properties and anti-inflam
Short acting

39
Q

Aldosterone

A

Not used as a drug - high sodium retaining

40
Q

Adverse effects of glucocorticoids

A

Fat metabolism - lipolysis, redistribute fat -> buffalo hump
Carb metabolism - reduce glucose uptake, increase gluconeogenesis -> hyperglycaemia
Protein metabolism - decrease synthesis, increase protein break down -> muscle wasting and skin thinning
Immune response - inhibited -> infection, wound healing
Calcium regeneration - decrease absorption and increase excretion -> osteoperosis
Kidney - Na+ reabsorption and K+ excretion -> hypertension and hypokalaemia (heart disease)

41
Q

Corticosteroid precautions

A

Heart disease, infections, diabetes, osteoporosis
Use for less than two weeks
Adrenal crisis from suppression of the HPA axis and adrenal atrophy

42
Q

Corticosteroid deficiency

A

Addisons disease or deficient ACTH
Use oral hydrocortisone (add flurocortisone in Addisons)

43
Q

Glucocorticoid excess

A

Cushings syndrome = excess ACTH
Use synthesis inhibitors - metyrapone (inhibit 11-B-hydroxylation, also increases ACTH production), ketoconazole (inhibits conversion of cholesterol to pregnenolone)

44
Q

Short term corticosteroid ADRs

A

insomnia, behavourial changes, peptic ulcers

45
Q

Diabetes

A

Type 1 - Failure to produce insulin IDDM
Type 2 - Insensitivity to insulin NIDDM - resistance via increase in insulin plasma conc

46
Q

Blood glucose regulation

A

Insulin decreases,
Glucagon increased
Somatostatin supresses both
Released from pancreas via Ca2+ release

47
Q

Insulin

A

Produced by B-cells in pancreas and released into portal circulation
Broken down in liver (80%) and kidney by insulinase
Uptake of sugar by GLUT4
receptors -> gene expression and growth regulation, glucose utilisation and glycogen/lipid/protein synthesis

48
Q

Insulin therapy

A

Both type 1 and 2
Human analogue - substitute aas
ADRs = hypoglycaemia, weight gain, oedema, lipotrophy, allergy

49
Q

Short acting insulin therapy

A

Novorapid (aspart - repulsion), Humalog (lispro - steric hinderance) reduce hexameter formation = easy diffusion

50
Q

Long acting insulin therapy

A

Insulin glargine - increase pI, reduce solubility and clearance
Insulin detemir - add fatty acid chain to bind to albumin = depot release

51
Q

Type 2 diabetes treatment

A

Lifestyle change and metformin as mono therapy
Non-obese can add empaglifozin/sitaglipin/suphonylureas

52
Q

Biguanides

A

Metformin (must be taken with food), half life 4-6 hr, no hepatic metabolism
Increases insulin sensitivity, decreasing blood glucose by 1-4 mmol/L
Transported into cell via OCT1, inhibits mitochondrial electron complex 1, increasing AMPK, thus pyruvate and decreasing gluconeogenesis, increasing GLP-1 secretion
Can increase lactic acid build up (acidosis, decrease B12 absorption)

53
Q

Sulphonylureas

A

Gliclazide (short) or glibenclamide (long)
Increase insulin secretion and suppress glucagon production, blocks K+ ATP channel causing Ca2+ depolarisation and secretion.
May promote obesity

54
Q

Glicazide

A

Short acting sulphonylurea
Oral, rapid absoprtion, metabolised by CYP2C9, half life 8-12 hours, present after 1-2 hours
ADR - hypoglycemia, weight gain, plasma protein binding

55
Q

Incretins

A

Hormones released when food is eaten by intestinal cells, increasing insulin secretion and decrease glucagon secretion
Metabolised by DPP-IV
GIP - glucose dependant insulinotropic peptide (small intestine K-Cells)
GLP-1 - glucagon like peptide-1 (large intestine L-cells)

56
Q

Exenatide

A

GLP-1 agonist, synthetic exendin-4
Subcutaneous injection twice daily, half life 2-4 hours, eliminated in kidneys
ADRs - nausea, hypoglycaemia, pancreatitis
Promotes weight loss, cardiac benefits

57
Q

Sitagliptin

A

DPP-IV inhibitor, prevent GLP-1 breakdown, increase insulin response to glucose and decrease glucagon secretion
Oral, well absorbed, excreted in urine (mostly unchanged)
ADRs - resp tract infection, headache

58
Q

SGLT-2

A

Sodium-glucose cotransporter in the kidney
Increased in type 2 diabetes = inhibit
SGLT-2 bad to block due to heart, intestine etc

59
Q

Gliflozins

A

Empaglifozin
Inhibit SGLT-2, reduce Na+ absorption, cause osmotic stress and pee out more glucose
Long half life 13h, good bioavailability, metabolised via glucoronidatio,n, need to drink lots, UTIs common and diabetic ketoacidosis
(because of decrease in plasma volume it appears glucose volume hasn’t changed)

PHAL304 (4 decks)

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