CEP --> DR

Question 1

HORMONAL REGULATION OF GLYCOGEN

Answer 1

1. glucagon binds to G-protein = adenyl cyclase= cAMP = AMP (by phosphodiesterase) = protein kinase A
2. protein kinase A phosphorylates (activates) glycogen synthase (forms glycogen) & then forms p-glycogen synthase (inactive)
3. protein kinase A also phosphorylates kinase (inactive) to glycogen phosphorylase B (inactive) which is activated to glycogen phosphorylase A (active)
4. OVERALL glycogen + Pi = glucose

Question 2

TSH RECEPTOR ROLE IN THYROID

Answer 2

TSH released from pituitary = binds to GPCR = adenyl cyclase = cAMP = pKA (rep. of thyroid cells & induces release of thyroid hormones)

Question 3

0 ORDER DRUG KINETICS

Answer 3

constant amounts of drugs lost per time

Question 4

HOW GLUCOSE AFFECTS INSULIN SECRETION

Answer 4

glucose enters B-cells & is metabolised -> increased ATP in cell -> lower activity of ATP sensitive K+ channels -> less potassium efflux -> depolarisation -> Ca2+ channels open -> insulin secretion

Question 5

HOW INSULIN MADE

Answer 5

in B-cells in islets of Langerhans by proinsulin (has a C-peptide which detaches when insulin released to expose binding sites on insulin)

Question 6

GRAVES DISEASE

Answer 6

autoimmune disorder on TSH receptors so no -ve feedback & always active

Question 7

HYPERTHYROIDISM TREATMENT

Answer 7

thionamides e.g. carbimazole inhibit TPO enzyme to block iodine uptake so no thyroid hormones made

Question 8

OXYTOCIN

Answer 8

stimulates contraction of smooth muscle of breast & uterus

Question 9

HOW INSULIN RECEPTOR WORKS

Answer 9

has 2 extracellular a-subunits & 2 b-subunits
- 1 insulin binds to each a-receptor & activates tyrosine kinase enzyme (on the b-unit) -> phosphorylate IRS proteins -> enzyme activation -> gene transcription for higher glucose uptake & glycogen synthesis

Question 10

METFORMIN

Answer 10

activates protein kinase which inhibits gene expression of gluconeogenesis genes -> less glucose made in liver

Question 11

CYTOKINE RECEPTOR

Answer 11

no catalytic activity & no naturally bound kinases but has a JAK2 protein kinase near the receptor (with high affinity) so when EPO dimerises the receptor, the small intracellular bits come closer together so JAK2 can phosphorylate receptor to cause response

Question 12

TYROSINE KINASES

Answer 12

ligand binds & then the receptors phosphorylate each other

Question 13

PROOF THAT AGONISTS OPEN RECEPTORS

Answer 13

patch-clamp, GFP into unstable gene & look for fluorescence

Question 14

FIRST PASS METABOLISM

Answer 14

P450 enzyme introduces hydroxyl groups to make compounds more hydrophilic then, these charged OH- groups linked to other compounds to be more hydrophilic (to form excretable watery solution)
- P450 usually in Fe3+ state but when reduced to Fe2+ state it can bind ligands

Question 15

1 ORDER DRUG KINETICS

Answer 15

drug loss proportional to drug concentration

Question 16

ANATOMY OF ANTERIOR PITUITARY

Answer 16

split into pars anterior (large & for hormone secretion) pars intermedia (separates pars anterior from posterior lobe) pars tuberalis (surrounds anterolateral of infundibulum)

Question 17

CALCITONIN

Answer 17

produced by C-cells in response to hypercalcaemia & works by inhibiting bone reabsorption

Question 18

OSTEOPOROSIS

Answer 18

normal bone but just less of bone density
- Treated by hormone replacement, bisphosphonates (disrupt enzymes needed for osteoclast activity), denosumab (blocks RANK receptor so less differentiation of pre-osteoclasts)

Question 19

OSTEOMALACIA

Answer 19

vitamin D & calcium deficiency leading to lack of mineralisation of collagen compartment of bone
- Leads to bow-knees, swollen joints

Question 20

LINK BETWEEN K INGESTION & ALDOSTERONE

Answer 20

excess K ingestion -> depolarisation of juxtaglomerular kidney cells -> Ca channels open & Ca enters -> aldosterone produced -> Na reabsorption & K excreted

Question 21

DIAGNOSING ADDISON

Answer 21

ACTH stimulation test (expect cortisol to shoot up but if <450)