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Aint nobody go time for that, Iv got diabetes!!! > 1 > Flashcards

1 Flashcards

1
Q

insulin chromosome

A

11

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2
Q

insulin creation to excretion pathway

A

beta cells in pancrease > portal blood > liver 50% degraded) > remainder excreted by kidneys

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3
Q

what does C-peptide indicate

A

rate of insulin secretion

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4
Q

what are normal glucose levels

A

3.5-8.0 mmol/L

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5
Q

liver stores glucose as _____

A

glycogen

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6
Q

what is gluconeogenisis

A

liver makes 6 carbon glucose from combining 3 carbon molecules from fat (glycerol), muscle glycogen (lactate), protein (alanine)

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7
Q

90% of daily glucose comes from?

A

liver glycogen & gluconeogenisis

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8
Q

insulin progression pathway

A

preproinsulin > proinsulin (disulphide bond & stored in vesicles) > insulin ( C-peptide cleaved as secreted)

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9
Q

what role does insulin have in fasting state

A

controls glucose release from liver

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10
Q

what role does insulin have in post feeding state

A

promotes glucose uptake into muscle and adipose

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11
Q

GLUT 1 receptor does what

A

basal non-insulin-stimulated glucose uptake

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12
Q

GLUT 2 receptor does what

A

transports glucose into beta cells

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13
Q

GLUT 3 receptor does what

A

non-insulin mediated glucose uptake into brain

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14
Q

GLUT 4 receptor does what

A

peripheral action of insulin, channel glucose taken up into muscle and adipose following stimulation of insulin receptors

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15
Q

sequence in beta cell for insulin release

A

glucose taken up into beta cell by GLUT2 > glucokinase phospohorylates glucose into gluco-6-phosphate > ATP > inc ATP closes potassium channels > = depolarisation (calcium ion influx) > release of insulin

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16
Q

glucose production in liver ___ as insulin levels fall

A

rises

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17
Q

insulin receptors are made up of what sub units

A

alpha (outer) and beta (inner)

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18
Q

insulin binds which part of insulin receptor

A

alpha

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19
Q

what happens when insulin binds insulin receptor

A

GLUT 4 receptor which are in intracellular vesicles translocate to membrane and start taking up glucose

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20
Q

type 1 diabetes due to

A

auto immune pathogenesis = insulin deficiency (peaks around puberty)

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21
Q

type 2 diabete due to

A

insulin resistance and less severe insulin deficiency

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22
Q

LADA stands for

A

latent autoimmune diabetes in adults (slow progression)

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23
Q

HLA associated with type 1

A

HLA-DR3/DR4

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24
Q

C-peptide presence will vary between type 1 compared to type 2 how

A

type 1 it will vanish (cos insulin not being produced)

type 2 it persists

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25
Q

type 1 is associated with which conditions

A

autoimmune thyroid disease, coeliacs, addisons, pernicious anaemia

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26
Q

what will histology in type 1 show

A

infiltrates of mononuclear cells called insulits

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27
Q

type 2 associated with

A

family history
central obesity
hyper secretion of insulin by depleted beta cells

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28
Q

what is MODY

A

maturity onset diabetes of young (also called monogenic diabetes)

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29
Q

age of MODY onset

A

before 6 months of age

  • acute onset 2-6 wks
  • chronic months-yrs
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30
Q

WHO diagnostic criteria for diabetes

A

fasting glucose >7
random plasma glucose >11.1
HbAC1 >6.5

  • 1 value is diagnostic in symptomatic person
  • 2 values in non symptomatic person
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31
Q

type 2 treatment (6)

A

metformin
sulfonylureas
thiazolidinedione (glitazones)

other: dideptidyl peptidase-4 (DPP4) inhibitors
GLP-1 agonist
meglitinides

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32
Q

how does metformin work (3)

A

activates AMP-kinase (involved in GLUT4 metabolism & fatty acid oxidation), reduces rate of gluconeogensis, inc insulin sensitivity

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33
Q

how does sulfonylureas work

A

acts on beta cells and promotes insulin secretion

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34
Q

side effects of sulfonylureas

A

weight gain

hypos

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35
Q

who dont you give sulfonylureas to

A

pregnant woman

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36
Q

thialidinedione (TZDs)/glitazone work how

A

reduce insulin resistance, regulates transcription, activate PPARs (nuclear receptors that acts as transcription factors)

37
Q

who dont you give metformin to

A

renal and hepatic failure

38
Q

hypo is blood glucose of ___

A

<3

39
Q

features of hypo

A

sweating
tremor
pounding heart

40
Q

when does injected insulin hit peak

A

60-90 mins post injection

41
Q

examples of rapid acting insulin

A

USPRO/ASPART/GLUSIN

42
Q

Examples of long acting insulin

A

NPH (isophane), glargin, determin

43
Q

what do you give person who is hypo and unconscious

A

1mg glucagon IM OR IV glucose 25-50ml of 50% glucose solution + 0.9% saline to preserve vein

44
Q

fatty lumps at over used injection site is called

A

lipohypertrophy

45
Q

how does glucagon work

A

mobilises hepatic glycogen, works as rapidly as glucose

46
Q

how does islet transplantation work

A

from cadaver, injected into portal vein, seeds in liver

** requires immuno suppresion **

47
Q

2 steps lead to glcosylation of Hb (giving HbA1C), what changes occur

A

covalent bonds forms between glucose and terminal valine of B-chain of Hb

48
Q

normal range of HbA1c

A

4-6.1% (20-44 mmol/l)

49
Q

average Hb life span is

A

6 weeks

50
Q

target HbA1c in type 1

A

7% (53)

51
Q

target BP in type 1

A

130/80

52
Q

target LDL, HDL and triglicerides in type 1

A

LDL: < 2
HDL: >1.1
triglicerides: <1.7

53
Q

features of DKA

A

no insulin, uncontrolled catabolism, hormone excess, fluid depletion

54
Q

what does lack of insulin (in DKA) lead to

A

accelerated hepatic glucose production & reduced glucose uptake

55
Q

increased blood glucose leads to what

A

osmotic diuresis = loss of fluids and electrolytes (dehydration)
increased osmolarity and reduced renal perfusion

56
Q

what is osmotic diuresis

A

glucose in urine = inc osmotic pressure within kidney tubules causing water retention in lumen and reduced reabsorption of water, so, inc urination

57
Q

fasting glucose:
2h after glucose

in normal person

A

fasting glucose: <7.8

58
Q

fasting glucose:
2h after glucose:

in impaired glucose tolerance

A

fasting glucose: <7

2h after glucose: 7.8-11.0

59
Q

fasting glucose:
2h after glucose:

in diabetic

A

fasting glucose: >7

2h after glucose: 11.1 or more

60
Q

other than blood glucose, what tests do you want to do in a diabetic (5)

A
  • urinalysis for protein
  • FBC
  • U & E
  • liver biochemistry
  • random lipids (rule out hyperlipidaemia)
61
Q

sequence of how ketones are produced

A

in DKA rapid lipolysis occurs > inc circulating free fatty acids > broken down to acyl-CoA in liver > ketone bodies in mitochondria = accumulation causes metabolic acidosis

62
Q

symptoms of DKA

A 
collapse
hyperventilation
nausea
vomiting
abdominal pain
63
Q

kidney hypo perfusion occurs in DKA what does this lead to

A

reduces excretion of ketones & hydrogen ions

64
Q

how do you diagnose DKA

A

demonstrate hyperglycaemia + ketonaemia OR heavy ketonuria and acidosis

65
Q

in DKA what will the levels be for:
ketones:
bicarb:
PH:

A

ketones: >6
bicarb: <7

66
Q

how do you manage DKA

A
  • fluids 0.9% saline
  • electolytes (potassium)
  • insulin
  • rarely give bicarb if PH <7
67
Q

why must you give electrolytes in DKA

A

because insulin leads to potassium uptake by cells

68
Q

what must you be careful of when giving fluids to someone with DKA

A

can cause cerebral oedema (especially in kids)

69
Q

what is condition that type 2 diabetics can get if poor glucose control

A

hyperosmolar hyperglycaemia state

70
Q

what is hyperosmolar hyperglycaemia state

A

severe hyperglycaemia WITHOUT ketone formation (there is enough circulation insulin to prevent ketones)

71
Q

who tends to get hyperosmolar hyperglycaemia state

A

mid/late life people with undiagnosed type 2

72
Q

what leads to hyperosmolar hyperglycaemia state

A

dehydration/hyperosmolarity + insulin deficiency = hepatic glucose production

73
Q

investigations for hyperosmolar hyperglycaemia state

A

plasma osmolarity (2(Na+ K+)+glucose + urea) in mmol/L

74
Q

what is a normal anion gap

A

40

75
Q

who gets lactic acidosis

A

those on metformin (low risk)

76
Q

what is absent in lactic acidosis

A

hyperglycaemia and ketones

77
Q

lactic acidosis treatment

A

rehydration and infusion with isotonic 1.26% bicarbonate

78
Q

list complications of diabetes (4)

A

retinopathy
nephropathy
neuropathy
cataracts

79
Q

nephropathy aslo called what

A

kimmelstein-wilson syndrome

80
Q

pathophysiology of nephropathy

A

afferent arteriole leading to glomerulous vasodilates more then efferent arteriole, this incr intre-glomerular pressure. this causes sheering force which causes mesangial cell hypertrophy and incr secretion of extracellular mesangial matrix material = glomerular sclerosis. loss of protein cross linkage so leakage of large molecules into urine.

81
Q

what precedes proteinuria

A

microalbuminoria > intermittent albuminuria > proteinuria

82
Q

what indicates late stage kidney disease

A

incr plasma creatinine (fall in glomerular filtration)

83
Q

normal albumin creatine ratio (ACR)

A

< 2.5 in men

< 3.5 in woman

84
Q

what 3 things rise in nephropathy

A

plasma creatinine
proteinuria
mean BP

85
Q

what drops in nephropathy

A

glomerular filtration rate

86
Q

things that autonomic neuropathy can lead to (6)

A
  • gustratory sweating
  • cardiac denervation
  • postural hypotension
  • gastrophoresis
  • diarrhoea
  • atonic bladder/erectile dysfundtion
87
Q

things that somatic neuropathy can lead to (6)

A
  • occular palsies
  • carpal tunnel
  • small muscle wasting
  • painful neuropathy
  • neuropathic foot
88
Q

which nerves usually affected in occular palsies

A

3rd and 6th

Aint nobody go time for that, Iv got diabetes!!! (1 decks)

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