CEP WK4 - DIABETES

Question 1

GLUCOSE LEVELS IN DAY

Answer 1

peak after breakfast & after evening meal

Question 2

BLOOD GLUCOSE TARGETS

Answer 2

• 4-7 = pre-meal
• 5-7 = waking
• 5-9 (>90 after meal)

Question 3

SYMPTOMS

Answer 3

weight loss, fatigue, infection, osmotic symptoms (coma, thirst, tiredness, polyuria)

Question 4

WHY DIABETES LEADS TO POLYURIA

Answer 4

high glucose level in urine (as kidneys can’t drain it all out) so urine draws water (osmosis) which leads to excess urination

Question 5

HbA1C test for diagnosing

Answer 5

take blood test & see glucose amount stuck on each blood cell (above 48mmol/l = diabetic) (every 12 weeks as lifetime of RBC is 10-12 & each RBC has glucose imprinted on it so no need to weekly measure)

Question 6

BLOOD GLUCOSE LEVEL TEST FOR DIAGNOSING

Answer 6

random test (>11.1 mmol/l = diabetic) or fasting glucose (>7 = diabetic) BUT if in range & no symptoms we do repeat

Question 7

URINE ANALYSIS TEST FOR GLUCOSE

Answer 7

cheap, not painful, useful but not enough to make a diagnosis, not great as threshold changes (e.g. lower in pregnancy)

Question 8

INSULIN

Answer 8

• made by B-cells in islets of langerhans by proinsulin (has a C-peptide which detaches when insulin released to expose binding sites on insulin)
• brings down blood glucose
• protein synthesis, inhibit fat breakdown, metabolism in muscles

Question 9

TYPES

Answer 9

• 1 (immune attacks & destroys B-cells) (rapid onset of symptoms)
• 2 (body doesn’t produce enough insulin)
• gestational (women in pregnancy have so much blood glucose they can’t absorb it all (lose diabetes after pregnancy))(due to poor diet, ethnicity)

Question 10

TYPE 1

Answer 10

• caused by insulitis (auto-immune response to B-cells making insulin)
• has ketone release as we don’t have insulin to breakdown the glucose so we need to find energy from other sources so we break down ketones for energy (put it into TCA) (too much ketone = acidosis (acidic blood) = coma)
• treated by lifestyle changes & giving insulin

Question 11

TYPE 2

Answer 11

• due to not responding to insulin & also not producing enough insulin
• treated by lifestyle changes, increasing insulin (tablets or injection)

Question 12

INSULIN PROFILE

Answer 12

HEALTHY PERSON (insulin made after each meal & also randomly in low concs to maintain blood glucose levels)
DIABETIC (we tell patient to take insulin after every meal based on carbohydrate level in meal)

Question 13

INCRETIN

Answer 13

produced by gut & goes to kidney to make insulin

Question 14

MEDS TO LOWER GLUCOSE LEVELS

Answer 14

• injection
• metformin increases sensitivity to insulin
• incretin breakdown inhibitors (tablets to stop incretin breakdown)

Question 15

EFFECT OF HIGH BLOOD GLUCOSE

Answer 15

• platelet dependent thrombosis (platelets stick to vessel walls & narrow them) = blood vessel damaged (can damage any part of body & even give gangrene (tissue decay due to lack of blood supply = amputation)
• controlled by controlling blood glucose levels (for controlling small vessel diseases e.g. neuropathy) & controlling lifestyle (for controlling large vessel diseases e.g. stroke, heart disease)

Question 16

LEVELS DIABETICS SHOULD AIM FOR

Answer 16

• lifestyle changes
• glucose control
• BP (130/80)
• cholesterol (4mmol/L)

Question 17

HOW INSULIN REGULATES GLUCOSE (what happens when glucose enters)

Answer 17

• 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
• biphasic release - 1st phase (due to Ca2+) & 2nd phase (type 1 have no phases & type 2 lack first phase)

Question 18

INSULIN RECEPTOR

Answer 18

• has 2 extracellular a-subunits (binding site) & 2 transmembrane b-subunits
• 1 insulin binds to each a-receptor & activates tyrosine kinase enzyme (B-unit) = phosphorylate IRS proteins = enzyme activation = gene transcription for higher glucose uptake & glycogen synthesis

Question 19

ORAL HYPOGLYCAEMIC AGENTS (METFORMIN)

Answer 19

• activates protein kinase which inhibits gene expression of gluconeogenesis genes = less gluconeogenesis = less glucose made in liver
• used for obese diabetics as decreased apetite

Question 20

SULPHONYLEREAS (SU)

Answer 20

• e.g. tolbutamide (short), glibenclamide (long)
• bind to SU receptor = kATP channels close = less potassium efflux = depolarisation = Ca2+ channels open = insulin secreted
• increase tissue sensitivity to insulin
• side effects are hypoglycaemia & stimulated appetite

Question 21

THIAZOLIDINEDIONES

Answer 21

• e.g. pioglitazone
• binds to TF to affect gene expression
• primary function is increasing fatty acid uptake & secondary function is lower plasma fatty acids & increase glucose uptake but lower gluconeogenesis