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endocrine > principles > Flashcards

principles Flashcards

1
Q

define diabetes

A

hyperglycasemia above a fasting glucose of 7mmol/L

-> a threshold set in relation to risk of diabetic retinopathy

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2
Q

main mechanism of metformin

A

inhibits complex 1 in respiratory chain causing a fall in cellular ATP, results in -

  • reduction in hepatic gluconeogenesis
  • activation of AMP-activated protein kinase (AMPK)
  • increases gut glucose utilisation + metabolism
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3
Q

what organs does metformin highly concentrate in?

A

intestine, liver, kidney

Organic Cation Transporters (OCTs) are found here which metformin needs to get into cells as its hydrophillic

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4
Q

benefits of metformin

A
  • weight neutral / negative
  • v cheap
  • potent glucose monitoring
  • generally well tolerated
  • CV benefit ish
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5
Q

metformin side effects

A

GI upset - diarrhoea, nausea, abdo pain (20%)
lactic acidosis - in liver disease / renal failure, metformin increase lactate
reduced B12 absorption

*modified release formula available (better tolerated)

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6
Q

how can metformin side effect be reduced?

A

starting - should be titrated up slowly to reduce incidence of GI side effects

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7
Q

sulphonylureas MoA

A

act directly on pancreatic beta-cells to increase insulin secretion

glucose independent = insulin secretion even when not needed (glucose low/norma) –> results in HYPOglycaemia

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8
Q

suphonylurea side effects

A

hypoglycaemia risk
weight gain

cheap but lack of CV benefit (compared to metformin)

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9
Q

thiazolidinediones side effects

A

weigh gain
fluid retention - peripheral oedeam
fracture risk - increase fat in bones + decrease bone density

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10
Q

thiazolidinediones (TZDs) MoA

A

TZD = pioglitazone

PPAR-gamma rceptor agonist
reduces peripheral insulin resistance (insulin sensitiser)

increase fat mass - “suck out” fat from liver, pancreas + muscle
increases adiponectin + reduced inflam cytokines

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11
Q

Dipeptidyl peptidase-4 (DDP-4) inhibitors

A

increases levels of incretins (GLP-1 + GIP) by decreasing their peripheral breakdown
–> increase insulin secretion but only when needed (unlike sulphonylureas)

well tolerated - minimal SE
moderate cost
weight neutral
weak glucose lowering

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12
Q

GLP-1 like molecules

A

promote insulin secretion when needed (glucose dependent)
lowers glucagon

reduces appetite (weight loss) + gastric emptying + BP
potent at glucose lowering
expensive
SE - N+V, gallstones

(subcutaneous)

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13
Q

SGLT-2 inhibitors MoA

A

inhibits reabsorption of glucose in the kidney
–> makes you pee sugar - increase thrush risk

(oral)

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14
Q

describe the structure of insulin

A

polypeptide composed of an A chain + B chain linked by disulfide bonds

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15
Q

how is insulin synthesised?

A

in the rough endoplasmic reticulum of beta-cells

preproinsulin -> proinsulin + single peptide -> C-peptide + insulin

C-peptide = no function
preproinsulin = single chain preprohotmone
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16
Q

what do alpha-cells of the pancreatic islets secrete?

A

glucagon

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17
Q

what do delta-cells of the pancreatic islets secrete?

A

secrete somatostatin

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18
Q

comment on insulins physiological window

A

NARROW

death by causing hypoglycaemic coma

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19
Q

how does glucose enter pancreatic beta-cells?

A

via GLUT2 glucose transporter

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20
Q

what is glucose phosphorylated by in the pancreatic beta cell?

A

glucokinase

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21
Q

list the steps of insulin release from an increase in glucose metabolism

A
  1. increase in glucose metabolism in beta cell leads to increase in intracellular ATP
  2. ATP inhibits ATP-sensitive channel K channel leading to depolaristaion of beta cell membrane
  3. depolarisation causes opening of voltage-gated Ca2+ channels allowing Ca2+ to enter
  4. increase in Ca2+ leads to fusion of secretory vesicles with the cell membrane –> release of insulin
22
Q

what can be said about the amount of glucose that enters the beta-cell compared to the amount of insulin released?

A

directly proportional

23
Q

glucokinase activity in patients with type 2 diabetes

A

glucokinase is maximally active at all times

  • > post meal (increase glucose) won’t stimulate more insulin = glucose insensitive
  • > chronically secreting insulin (high levels) = mitochondrial exhaustion = reduced ATP production
24
Q

the release of insulin is biphasic, what are the differences between the 2 wves?

A

1st = short, sharp peak = prevents sharp increase in glucose (hypo)

2nd = broader, shorter = more tuned to insulin requirement, related to glucose intake (amount, duration)

25
Q

3 key healthy lifestyle behaviours to prevent obesity

A

limiting energy dense food
reducing sedentary time
increase physical activity

26
Q

why is prevention difficult in the NHS?

A

not easy
not cheap

requires constant reinforcement by education

27
Q

what is the evidence that T2DM can be prevented?

A

weight reduction - calorie reduction + improved exercise

28
Q

what are the barriers to prevention of T2DM + how can they be overcome?

A

identify + engage people at risk - screen for impaired glucose tolerance (HbA1C)
political - sugar tax
low income at highest risk but poorest engagement
evaluate if programme working - high quality data collection

29
Q

is it posiible to reverse hyperglycaemia?

A

yes - weight reduction

**less need for medication

30
Q

how do you measure insulin resistance?

A

gold standard = hyperinsulinemic-euglycemic clamp

sample taken from artery

insulin constantly effused, glucose variably depending on levles in sample, RBCs effused to replace

31
Q

alpha cells + glucagon

A

secrete glucagon inversly proportional to blood glucose

glucagon acts on liver to promot hepatic glucose production - raising blood glucose

32
Q

glucagon secretion during fed state in T2DM

A

glucagon secretion is elevated in the fed state in T2D + contributes to hyperglycaemia

33
Q

how do alpha cells respond to low glucose

A

K-ATP channels open

voltage-gated sodium channels contribute to action potentials

P/Q type volgated gated calcium channels enable calcium influx

glucagon exocytosis is triggered

34
Q

how do alpha cells respond to high glucose?

A

K-ATP channels closed, cell depolarised

presence of SGLT 2 glucose transporter contributes to non-voltage regulated sodium ion influx

NaV + CaV channels closed, glucagon not exocytosed

35
Q

current guidlines recommend prioritising what percentage weight loss in individual living with type 2 diabetes who are overweight or obese?

A

> 5%

36
Q

name 2 benefits of physical activity for individual with type 2 diabetes?

A

improved glycaemic control

reduction in cadiovascular risk

37
Q

where are the thyroid hormone receptors typically found in a cell?

A

nucleus

Thyroid hormones enter cells by diffusion or by carriers, once inside they bind to a thyroid hormone receptor. These are intracellular DNA-binding proteins found in the nucleus. Once bound they form a complex which then binds to the thyroid hormone responsive element on DNA.

38
Q

what are the 3 different types of hormone structure?

A
  1. steroids e.g. oestrogen
  2. amine-derived e.g. adrenaline
  3. proteins e.g. insulin, ADH, oxytocin
39
Q

effect of insulin on proteolysis, lipolysis + glycogen synthesis?

A

decreases proteolysis
decreases lipolysis

increases glycogen synthesis

40
Q

what hormone stimulates ACTH production?

A

CRH corticotropin-releasing hormone

–> ACTH then stimulates cortisol

41
Q

what does GnRH stimulate?

A

stimulates release of LH/FSH which goes on to stimulate estrogen / testosterone depending

42
Q

what controls prolactin secretion?

A

dopamine inhibits prolactin secretion

43
Q

which hormones released by the hypothalamus are stored in the posterior pituitary?

A

vasopress + oxytocin

44
Q

what hormones in the hypothalamus + pituitary stimulate production of thyroxine?

A

TRH –> TSH –> thyroxine

45
Q

what type of drug is orlistat?

A

lipase inhibitor

46
Q

what is the max time orlistat is safe to prescribe?

A

4yrs - 2yrs recommeded tho

47
Q

definition of a very low calorie diet

A

under 800kcal

! under close supervision
never first line + only BMI >30

48
Q

what is the BMI referral criteria for bariatic surgery?

A

BMI > 40

or 35-40 if co-morbitidies
have tried everything else
can cope with surgery shiz

49
Q

which bariatric surgery is viewed as a malabsorptive procedure?

A

gastric bypass

bilio-pancreatic diversion

50
Q

why is it difficult to maintain weight loss?

A

adaptive thermogenesis - weight loss seen as threat to survival

the lower the resting metabolic rate (RMR) - the harder it is to lose weight

endocrine (15 decks)

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