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Endocrinology > Diabetes Revision > Flashcards

Diabetes Revision Flashcards

1
Q

what are the 4 roles of insulin

A

facilitation of glucose transport into cells (via GLUT4)

stimulation of glycogenesis

inhibition of glycogenolysis

inhibition of gluconeogenesis

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2
Q

what effect does insulin have on fatty acids

A

encourages entry of fatty acids into adipose tissue

promotes chemical reactions that use fatty acids for triglyceride synthesis

inhibits lipolysis

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3
Q

what is insulins effect on amino acids

A

promotes uptake bu muscles and other tissues

stimulates protein synthesis

inhibits the degradation of proteins

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4
Q

what other than blood glucose can trigger the release of insulin

A

GI hormones (glucose dependent insulinotrophic peptide) stimulate release in anticipation of food being ingested

elevated blood amino acids

parasympathetic nervous system stimulates pancreas to secrete insulin (sympathetic decreases secretion e.g. adrenaline)

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5
Q

do babies of mother with diabetes have low birth weight

A

no tend to be higher than (have usual length)

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6
Q

what birth defect is seen in babies from diabetic mothers

A

spina bifida, anencephaly, caudal regression
abnormalities of the great vessels
increased fat and skeletal growth and organomegaly

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7
Q

what are the chances of a child developing diabetes if one parent or sibling has it

A

5-6%

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8
Q

diabetes is teratogenic, when is the risk highest

A

in the first 8 weeks

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9
Q

why does hyperglycaemia affect the foetus so much

A

as glucose can cross placenta but insulin cant

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10
Q

is metformin safe in pregnancy

A

yes

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11
Q

what are diabetic mothers at increased of during pregnancy

A

still birth and pre eclampsia

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12
Q

what vitamin should diabetic mothers take in pregnancy

A

folic acid

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13
Q

what four hormones increase blood glucose

A

glucagon, adrenaline, cortisol, growth hormone

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14
Q

what causes the release of adrenaline

A

sympathetic stimulation of the adrenal gland

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15
Q

how does adrenaline increase blood glucose

A

inhibits secretion of insulin, increases synthesis of glucose by inhibiting uptake

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16
Q

how does growth hormone increase blood glucose

A

stimulated in response to hypoglycaemia, stress, exercise, deep sleep

decreases glucose uptake, increases protein synthesis

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17
Q

why do tissues rely on fat metabolism in type 1DM

A

as glucose cant enter the cells

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18
Q

what type of diabetes is there amyloid deposition within islets

A

non insulin dependent diabetes (type 2)

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19
Q

what type of diabetes in insulinitis seen in

A

type 1- beta cell destruction

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20
Q

what are the diagnostic criteria for diabetes

A

Fasting plasma glucose >= 7.0 mmol/L

And/or a plasma glucose 2 hours after a 75g oral glucose load OR a random glucose >= 11.1 mmol/L

(one +ve test + symptoms= diagnosis or 2 + tests
Other terms:
Impaired glucose tolerance: 2 hour glucose between 7.0 and 11.1 mmol/L
Impaired fasting glucose: Fasting glucose between 6.0 and 7.0 mmol/L

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21
Q

what is gestational diabetes

A

diabetes that develops in pregnancy- resolves post natally

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22
Q

what is secondary diabetes

A

occurs secondary to other pathology (e.g. endocrinopathies- cushings, acromegaly. haemachromatosis, post pancreatitis, cystic fibrosis)

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23
Q

what is monogenic diabetes

A

due to mutation in gene regulating insulin secretion or action e.g.
maturity onset diabetes of the young

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24
Q

what are the chances of getting type 1 diabetes if your parent or twin has it

A

parent 25%
MZ twins 35%
siblings 6%

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25
Q

what are the chances of getting type 2 diabetes if your parent or twin has it

A

MZ twins 80-90%
DZ twins 30-40%
sibling 3/4x risk of normal population
if both parents have it then 70-80%

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26
Q

what type of diabetes is more genetic

A

type 2 (polygenic)

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27
Q

what would you expect insulin concentrations to be in a T1DM patient

A

low to none

some retain small amounts of insulin secretion

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28
Q

what would you expect insulin concentrations to be in a T2DM patient

A

normal to high

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29
Q

what antibodies are tested in T1DM/ young T2DM

A

GAD and IA-2

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30
Q

what HbA1c should T2DM aim for

A

53

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31
Q

what might precipitate T2DM presentation

A

infectino

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32
Q

what are the features of secondary diabetes

A

cushingoid
bronze pigmentation (haemachromatosis)
acanthosis

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33
Q

what should you ask for in PMH in T1DM

A

pancreatitis, autoimmune conditions, heavy alcohol consumption

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34
Q

what is the relationship between diabetes and corticosteroids

A

increase blood sugar

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35
Q

how do you calculate plasma osmolarity

A

2 x (plasma Na+ + plasma K+) + plasma urea + plasma glucose

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36
Q

what is the purpose of the anion gap

A

evalutaes metabolic acidosis (high= metabolic acidosis)

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37
Q

what is the anion gap formula

A

= (Na+ + K+) - (Cl- + HCO3-)

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38
Q

what has more microvascular complications T2 or T2 DM

A

Type 2

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39
Q

what causes the temporary blurry vision seen in diabetes

A

high blood sugar causes lens of eye to swell
or
blurry/ double vision in hypos

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40
Q

what can cause hypos in T1DM controlled with insulin

A

too much insulin, exercise not enough carb intake, alcohol., insulin, vomiting/ illness, coeliac, addisons (cortisol deficient), pituitary disease (reduce ACTH reduce cortisol)

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41
Q

even when not eating why when ill might T1DM need more insulin

A

as stress hormones released when ill will increase blood glucose

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42
Q

what is addisons

A

a primary renal disease

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43
Q

why are patients with pituitary disease are greater risk of hypos

A

as also release GH

44
Q

what is the prevelance of coeliac in normal population and in diabetics

A

1 in 100 in pop

1 in 20 in diabetics

45
Q

what can reduce HbA1c

A

conditions that increase cell turnover

46
Q

what can cause DKA

A

infection, surgical abdomen, silent MI

47
Q

what is the management for DKA

A

ABC
HX and exam for cause
cardiac monitor + other monitoring if required
IV fluids
IV insulin (no bolus)
watch K+, replace aggressively to prevent hypokalaemia and cardiac arrest

48
Q

what is the relationship between insulin and potassium

A

insulin drives K+ into the cells and blood K can drop

49
Q

should eggs be avoided if you have high cholesterol

A

no

50
Q

what are the treatment steps for T2DM

A

1- metformin

2- metformin + SGLT 2
metformin + GLP-1 
metformin + DDP-4 inhibitor 
metformin + TZD
metformin + insulin

(metformin - SGLT 2 - GLP- 1)

51
Q

what shouldnt be given with TZDs

A

GLP-1 analogues and DPP-4 inhibitors

52
Q

what does GLP-1 do

A

is secreted when food ingested- increases insulin secretion

53
Q

what does DPP-4 do

A

breaks down GLP-1

54
Q

when should metformin be avoided

A

patient with renal failure or lactic acidosis

55
Q

what are the main side effects of SUs

A

hypos (especially in elderly as renal function decreases with age), weight gain, stimulates appetite

56
Q

what do TZDs

A

promote fatty acid uptake and adipogenesis

57
Q

should people with fatty liver disease be given TZD

A

yes reduce lipid content in the liver and act as insulin sensitisers

58
Q

who should you not get TZDS to

A

elderly slim females, heart failurem osteoporosis, bladder cancer

59
Q

what acts faster gliclazide or metformin

A

gliclazide 2-3 days

metformin 2-3 weeks

60
Q

why do you not give fix mix insulin to young people

A

does not allow flexibility of meals

61
Q

what do you recommend doing for T1DM ill patients

A

keep giving insulin, check BG and ketones, get carbs in the patient

62
Q

what do you recommend a T1DM wanting to do exercise

A

eat before or reduce insulin dose

63
Q

what does increased body Na predispose to

A

hypertension

64
Q

what does the AGE pathway interfere with

A

proteoglycans, basement membranes, enzyme activity, cellular receptors, increases nucleic acid damage

65
Q

what is the relevance of microalbuminuria

A

shows presence of albumin in urine, suggestive of diabetic nephropathy or hypertension

66
Q

how do you manage micoralbuminuria

A

tackle hypertension if present - ace inhibitors

67
Q

what bad effects might tight glycaemic control cause

A

hypos, weight gain, worsen vascular complications (ischaemia)

68
Q

what are the stages of retinal grading

A

none, background, moderate, severe, proliferative

69
Q

what is metabolic syndrome

A

glucose intolerance, impaired glucose tolerance or DM and/or insulin intolerance along with any two of:

  • impaired glucose regulation/ diabetes
  • insulin resistance
  • raised arterial BP
  • raised plasma triglycerides and/or low HDL
  • central obesity
  • microalbuminuria
70
Q

how is insulin resistance linked to T2DM

A

is a predisposing factor

71
Q

what is acromegaly and its link to diabetes

A

condition caused by excess GH, GH can also cause insulin resistance

72
Q

what is cushings link to diabetes

A

excess cortisol can inhibit the uptake of glucose in the muscles- hyperglycaemia and insulin resistance

73
Q

what names do SUs end in

A

ide (tolbutamide)

74
Q

how do SUs work

A

action dependent on beta cell function (no use in T1DM), depolarise beta cells stimulating the release of insulin

75
Q

what is the risk in SUs

A

hypos

76
Q

what drug has an additive effect when used with SUs

A

biguanides (metformin)

77
Q

what impedes the effectiveness of SUs

A

corticosteroids, thiazide diuretics

78
Q

how does metformin cause weight loss

A

suppresses appetite

reduced absorption of glucose from the gut

79
Q

how does glucose work

A

reduced absorption of glucose from the gut
facilitates non insulin dependent entry of glucose into tissues
inhibits liver gluconeogenesis
enhances anaerobic glycolysis

80
Q

what is the most serious side effect of metformin

A

lactic acidosis

81
Q

what are the less serious side effects of metformin

A

nausea, vomiting, diarrhoea, metallic taste in the mouth

82
Q

who should not get metformin

A

patients with:

  • renal failure
  • alcoholism
  • cirrhosis
  • chronic lung disease
  • cardiac failure
  • serious current illness
  • mitochondrial myopathy
83
Q

what are glitazones

A

thiazolidinediones (TZDs)

84
Q

how do TZDs work

A

bind to receptors within the cell nucleus and affect gene expression decreasing insulin resistance

85
Q

what is the only glitazone licensed in the UK

A

pioglitazone

86
Q

how do GLP-1 analogues work

A

mimic the actions GLP-1 which:

  • increases secretion of glucagon
  • decreases secretion of glucagon
  • increases insulin sensitivity in the peripheral tissues
87
Q

how do DDP-4s work

A

inhibit DDP which inhibit GLP-1

88
Q

what are the possible side effects of insulin

A

hypos
hypers (overcompensation in response to slight hypo after dose- somogyi effect)
reactions at injection site
insulin resistance

89
Q

what is the poyol/ aldose-reductase pathway

A

series of biochemical reactions which occur in the presence of raised intracellular glucose (esp in insulin dependent tissues)

attempt to reduce glucose level in insulin dependent tissues that cannot regulate influx of glucose (insulin allows movement of glucose into the cell)

90
Q

when does the poyol pathway become active

A

when there is very high intracellular glucose

91
Q

what is the enzyme in the poyol pathway

A

aldose reductase

92
Q

what is the role of aldose reductase

A

coverts glucose into sorbitol (sugar alcohol)

not all glucose is converted- some go into methylglyoxal and acetol (glycating sugars)

93
Q

what does sorbitol do

A

exerts osmotic pressure on the cell (too large to diffuse out) which can cause damage to the cell so sorbitol dehydrogenase converts the sorbitol into fructose which diffuses out

94
Q

what is AGE

A

advanced gylcation end products
these are synthesised in the aldose reductase pathway- can cause damage to cells

formed by glycating sugars and excess glucose binding to proteins

95
Q

why is proteinuria done in diabetes

A

shows kidney damage either due to hypertension (diabetics more likely to get) or nephropathy

96
Q

describe the process of nephropathy

A

the kidneys hypertrophy due to increased glomerular filtration rate- causes the afferent arteriole to dilate which leads to increased intraglomerular pressure = shearing forces which cause glomerular sclerosis (thickening of basement membrane and disruption of protein cross links) = kidney is no longer an effective filter

97
Q

what is increased creatine a sign of in diabetes

A

renal failure

98
Q

what pathway is responsible for the vascular complicationsin T2DM

A

poyol pathway (sorbitol-aldose-reductase pathway)

99
Q

why is hypertension predisposed in diabetes

A

vasodilator effect of insulin blunted in diabetes
action of insulin which increase BP- sodium and water reabsorption
BMI of diabetic patients

100
Q

patients with nephropathy should target their BP to be what

A

less than 130/80

101
Q

how much more common is HPX in diabetics

A

2x normal population

102
Q

what size monofilament for foot exams

A

10 g

103
Q

how many areas are examined with monofilament on the feet

A

10 together

104
Q

how does hyperglycaemic neuropathy present and resolve

A

discomfort in lower legs

regain glycaemic control

105
Q

when does acute painful neuropathy occur

A

rapid weight loss and poor glycaemic control (severe burning and contact sensitivity)

106
Q

what causes retinopathy

A

capillary microangiopathy- proteins of vessel wall get more glycosylated, membrane thickens and becomes MORE permeable, increased transduction of protein which has a fibrous response with the retina damaging the retinas neural network

small vessels also dilate causing micro-aneurysms

also thrombosis of some capillaries - promotes neoangiogenesis which also damages the retinae

107
Q

where do neuropathic food ulcers most commonly occur

A

high pressure areas e.g. metatarsal heads, big toe

Endocrinology (46 decks)

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