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Endocrinology > diabetes mellitus > Flashcards

diabetes mellitus Flashcards

1
Q

Define Type 1

A

autoimmune destruction of beta cells by T cells causing an absolute insulin deficiency

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2
Q

type 2 diabetes

A

caused by reduced insulin sensitivity (known as insulin resistance)

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3
Q

what is the most common type of diabetes

A

type 2

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4
Q

presentation of both type 1 and type 2

A
  • hyperglycaemia
  • polyphagia
  • glycosuria
  • polyuria
  • polydipsia
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5
Q

what is polyphagia

A

excessive hunger

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6
Q

what is glycosuria

A

glucose in the urine

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7
Q

what is polyuria

A

excessive urination

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8
Q

what is polydipsia

A

excessive thirst

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9
Q

what emergency complication can type 1 diabetes present with

A

diabetic ketoacidosis

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10
Q

what emergency complication can type 2 diabetes

A

hyperosmolar hyperglycaemic state

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11
Q

diagnosing diabetes

A

requires symptoms to be present and one of the following tests: if asymptomatic requires 2 abnormal test results

  • oral glucose tolerance test
  • random blood glucose test
  • fasting glucose
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12
Q

fasting glucose of

A

7mmol/l and above is diabetic

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13
Q

normal fasting glucose levels

A

6mmol/l and below

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14
Q

what is oral glucose tolerance test (OGTT)

A

measures the plasma glucose concentration 2 hours after 75g anhydrous glucose

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15
Q

Oral glucose tolerance test of

A

11.1 mol/l and above is diabetic

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16
Q

normal oral glucose tolerance test levels

A

7.7mmol/l and below

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17
Q

random venous glucose concentration of

A

11.1mmol/l and above is diabetic

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18
Q

what should a diabetes diagnosis never be made in the presence of

A

glycosuria or a finger prick test but these tests may be useful for screening people

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19
Q

HbA1c

A

not used to diagnose diabetes but is useful to measure a person glucose control over the past 2-3 months

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20
Q

what is HbA1C

A

a measure of the amount of glucose attached to haemoglobin which occurs via a process called glycosylation

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21
Q

target levels of HbA1c

A

48 in younger people, but in older people with co-morbidities the target is 53 because any lower than this and you risk hypoglycaemia

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22
Q

percentages of HbA1c

A

48m/m is 6.5% so anything above this is diabetic

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23
Q

what can be used to distinguish between type 1 and type 2 diabetes clinically

A

GAD auto-antibodies and anti-islet cell autoantibodies

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24
Q

anti-hyperglycaemic drugs used in the management of type 2 diabetes ladder

A

1st line= metformin
then if HbA1c still not controlled
2nd line= 2 drugs: metformin and sulfonylurea or pioglitazone or DPP-4 inhibitor
3rd line= triple therapy with metformin and any 2 of the above
4th line= insulin

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25
Q

what family does metformin belong to

A

biguanides

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26
Q

mechanism of action of metformin

A

increases peripheral tissue sensitivity to insulin, increases glucose uptake in skeletal muscle, reduces hepatic gluconeogenesis

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27
Q

contra-indications to using metformin

A

renal, cardiac, respiratory and hepatic failure due to the risk of lactic acidosis

28
Q

examples of sulfonylurea drugs

A

glipizide and glimepiride

29
Q

mechanism of action of sulfonylurea drugs

A

mimics the action of ATP at the potassium ATP channels which clocks the channel causing depolarisation of the cell membrane results in calcium influx and the exocytosis of insulin

30
Q

Side effects of sulfonylurea drugs

A

weight gain and hypoglycaemia

31
Q

contra-indications to using sulfonylurea drugs

A

renal and hepatic failure, porphyria, pregnancy and breastfeeding

32
Q

what family of drugs does pioglitazone belong too

A

thiazolidinedionees

33
Q

mechanism of action of pioglitazone

A

activates nuclear PPAR gamma, which is a transcription factor for genes which increase insulin sensitivity in adipose, muscle and hepatic cells

34
Q

contra-indications of using pioglitazone

A

heart failure

35
Q

side effects of pioglitazone

A

increase the risk of hip fractures

36
Q

examples of incretins

A

GLP-1 agonists

37
Q

GLP-1 agonist example

A

exenatide

38
Q

mechanism of action of GLP-1 agonists

A

directly stimulates the release of insulin by stimulating the action of GLP-1 which activates incretins and is an analogue of glucagon like peptide so inhibits the release of glucagon

39
Q

contra-indications for GLP-1 agonists

A

thyroid cancer

40
Q

side effect of GLP-1 agonists

A

diarrhoea, acute pancreatitis

41
Q

DPP-4 inhibitors example

A

saxagliptin

42
Q

mechanism of action of DPP-4 inhibitors

A

blocks the action of DPP-4, DDP-4 is an enzyme which destroys incretins, incretins serve to

43
Q

SGLT2 INHIBITORS example

A

dapagliflozin

44
Q

mechanism of action of SGLT2 inhibitors

A

reduces uptake of glucose in the kidneys so more glucose is excreted in the urine

45
Q

side effect of SGLT2 inhibitors

A

increased risk of UTIS

46
Q

insulin use

A

use for all people with type 1 diabetes and for those with type 2 who’s HbA1c levels have not responded to elevation through the ladder of anti-hyperglycaemic drugs

47
Q

what can type 1 diabetes initially present with in some cases

A

diabetic ketoacidosis

48
Q

pathophysiology of DKA

A

beta cells of the pancreas are destroyed so there is no insulin production, so even though there is high levels of glucose in the blood it cannot enter the cells, therefore the cells enter the starvation state and they have to generate energy by some means so they do this by the beta oxidation of fatty acids to produce acetyl-co-A, this processes produces ketone bodies which in turn results in a metabolic acidosis

49
Q

how does DKA commonly occur

A

non-compliance with insulin regime, infection and illicit drug use such as cocaine and ecstasy

50
Q

presentation of DKA

A

nausea, vomiting, abdominal pain, ketones smelt on breath, kausmals breathing, coma and eventually death

51
Q

investigations required for DKA

A
  • high blood glucose levels (in DKA average is about 40mmol/l)
  • ketones in blood/ urinalysis
  • high anion gap
  • hyperkalaemia, hyponatraemia
  • low bicarbonate
  • WCC is high in all cases but if shifted to left suggest infection is the cause
52
Q

management of DKA

A
  • IV fluids
  • IV insulin
  • potassium replacement
53
Q

IV fluids used in DKA

A

0.9% sodium chloride and then switch to dextrose when glucose levels reach about 15, give 1-3 litres in the first hour, another litre over the second hour and another litre over the subsequent 4 hours

54
Q

IV insulin dosage in DKA

A

0.1 units per kg per hour

55
Q

why is potassium replacement required

A

even though DKA initially causes hyperkalaemia the fluids required to treat DKA cause a hypokalaemia

56
Q

hyperosmolar hyperglycaemic state

A

occurs due to chronic dehydration in individuals with type 2 diabetes

57
Q

blood glucose levels in HHS

A

massively elevated at around 60mmol/l

58
Q

what else is high in HHS

A

high serum osmolality which is greater than 320 mosmol/kg

59
Q

what else doe HHS cause

A

hypovolaemia

60
Q

presentation of HHS

A
  • focal/ global neurological deficits
  • extreme thirst
  • excessive urination (polyuria)
61
Q

the primary goal in HHS

A

fluid replacement insulin therapy comes second

62
Q

initial management

A

1-2 litres of fluid over first hour and then over the next 12 hours replace half of the estimated fluid that has been lost

63
Q

secondary management

A

once azotemia has resolved start insulin and monitor potassium

64
Q

what is azotemia

A

elevated blood urea nitrogen and creatinine kinase levels

65
Q

what is azotemia

A

elevated blood urea nitrogen and creatinine kinase levels

66
Q

incretin effect

A

increased secretion of insulin elicited by oral glucose in comparison with IV glucose due to the action of incretin hormones

Endocrinology (15 decks)

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