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Endo, Cardio and Neuro > Type 1&2 Diabetes Mellitus > Flashcards

Type 1&2 Diabetes Mellitus Flashcards

1
Q

what is type 1 diabetes?

A

autoimmune destruction of insulin producing beat cells in pancreas resulting in partial/complete deficiency of insulin

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2
Q

what is the onset of type 1 diabetes?

A

thought to be childhood but adulthood becoming more common

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3
Q

what are the stages of development for type 1 diabetes?

A

genetic predisposition
potential precipitating event/immune activation
immune response
stage 1 - normal blood sugar
stage 2 - abnormal blood sugar
stage 3 - clinical diagnosis
stage 4 - long standing T1D

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4
Q

what can constitute a precipitating event?

A

viral illness

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5
Q

what is immune infiltration in T1DM

A

immune cells infiltrate islet cells in T1DM

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6
Q

what is the importance of understanding T1DMs immune basis?

A

autoantibodies important clinically
immune modulation as possible treatment?
increased likelihood of other autoimmune disease & FH
more complete destruction of beta cells

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7
Q

which genes carry the highest susceptibility for T1DM?

A

DR3 DR4

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8
Q

what genes carry protection against T1DM?

A

DR2 and possibly DR6

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9
Q

what are some environmental risk factors of T1DM?

A

enteroviral infections
cows milk protein exposure
seasonal variation
changes in microbiota

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10
Q

what are some detectable pancreatic autoantibodies?

A

insulin autoantibodies IAA
glutamic acid decarboxylase
insulinoma associated 2 autoantibodies
zinc transporter 8

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11
Q

what are the symptoms of T1DM?

A

polyuria
nocturia
polydypsia
blurring of vision
recurrent infections
weight loss
fatigue

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12
Q

what are the signs of T1DM?

A

dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria

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13
Q

what are the physiological effects of insulin deficiency? T1DM

A

proteinolysis
increased hepatic glucose output
lipolysis- ketogenesis

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14
Q

what are the ketone bodies?

A

3-beta-hydroxybutyrate
acetoacetone
acetone

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15
Q

what are the treatment aims for T1DM?

A

maintain glucose levels
restore close to physiological profile of insulin
prevent acute metabolic decompensation
prevent micro¯ovascular complications

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16
Q

what are the complications of hyperglycaemia?

A

diabetic ketoacidosis (mostly T1DM)
microvascular - retinopathy, neuropathy, nephropathy
macrovascular - ischaemic heart disease, cerebrovascular disease, peripheral vascular disease

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17
Q

what is the management of T1DM?

A

insulin treatment
dietary support & education programs
technology
transplantation

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18
Q

what are the types of insulin treatments?

A

short insulin (with meals)
background/basal bolus insulin

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19
Q

what are examples of short acting insulin?

A

human insulin - actrapid
insulin analogues - lispro, aspart, glulisine

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20
Q

what are the types of basal insulin?

A

bound to zinc/protamine - neutral protamine hagedorn (NPH)
insulin analogues - glargine, determir, degludec

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21
Q

what are the typical bolus regimes for insulin?

A

once daily long acting
three times daily short acting
OR
twice daily intermediate acting insulin
three times daily actrapid

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22
Q

what is insulin pump therapy?

A

continuous delivery of short acting insulin fixed units/hr into subcutaneous space
then actively bolus for meals

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23
Q

what is the dietary advice for T1DM?

A

dose adjustment for carbs
training for carb content
substitute refined carbs for complex carbs

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24
Q

what is a closed loop/artificial pancreas?

A

real time continuous glucose sensor with algorithm to calculate insulin requirement and delivers dose
however lags around 15mins

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25
Q

what types of transplantation are available for T1DM?

A

islet cell transplants
simultaneous pancreas and kidney transplants

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26
Q

how can glucose be monitored?

A

capillary finger prick blood glucose monitoring
continuous glucose monitoring

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27
Q

what is HbA1c?

A

reflects last 3 months of glycaemia
enzymatic so linear relationship, irreversible

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28
Q

What are the limitations of HbA1c?

A

Affected by red cell turnover, only can be done by 3 months

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29
Q

What are the acute complications o type l diabetes

A

Diabetic ketoacidosis
Uncontrolled hyperglycaemia
Hypoglycaemia

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30
Q

What is diabetic ketoacidosis?

A

Acute life threatening complication of t1DM
blood pH <7.3 and high ketones

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31
Q

when does hypoglycaemia on insulin therapy become problematic?

A

excessive frequency
impaired awareness (unable to detect low glucose)
nocturnal hypoglycaemia
recurrent severe hypoglycaemia (need 3rd party assistance)

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32
Q

what are the risks of hypoglycaemia?

A

seizure/coma/death
impacts on: emotional wellbeing
driving
day to day function
cognition

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33
Q

what are the risk factors for hypoglycaemia with t1dm?

A

exercise
missed meals
inappropriate insulin regime
alcohol intake
lower HbA1c
lack of training dose-adjustment around meals

34
Q

how can problematic hypoglycaemia be supported?

A

insulin pump therapy
different insulin analogues
revisit carb counting/education
behavioural psychology support
transplantation

35
Q

what are the treatments for hypoglycaemia but alert and oriented?

A

oral carbohydrates
juice/sweets - fast acting
sandwich - slow acting

36
Q

what are the treatments for hypoglycaemia but drowsy/confused but swallowing intact?

A

buccal glucose e.g glucogel/hypostop
complex carbohydrate

37
Q

what are the treatments for hypoglycaemia when unconscious/concerned about swallowing?

A

IV access 20% glucose IV

38
Q

what should you consider for a deteriorating hypoglycaemic patient with difficult IV access?

A

IM/SC 1mg glucagon
especially if insulin induced

39
Q

what is type 2 diabetes?

A

a condition in which beta cell failure and insulin resistance result in hyperglycaemia

40
Q

what is the epidemiology and trend of T2DM?

A

increasing prevalance
increasing in younger adults
greatest in ethnic groups moving from rural to urban lifestyles

41
Q

what are normal fasting glucose levels?

A

less than 6mmol/L

42
Q

what are normal 2hr glucose levels? (OGTT)

A

less than 7.7mmol/L

43
Q

what is normal HbA1c?

A

less than 42mmol/L

44
Q

how can random glucose readings confirm T2DM diagnosis?

A

above 11.1mmol/L WHEN SHOWING SYMPTOMS

45
Q

what fasting glucose levels indicate T2DM?

A

above 7mmol/L

46
Q

what 2hr glucose levels (OGTT) indicate T2DM?

A

above 11mmol/L

47
Q

what HbA1c indicates T2DM?

A

over 48mmol/mol

48
Q

what does a fasting glucose of between 6-7mmol/L indicate?

A

impaired fasting glycaemia

49
Q

what does a 2hr glucose OGTT reading between 7.7-11mmol/L indicate?

A

impaired glucose tolerance

50
Q

what does an HbA1c of between 42-48mmol/L indicate?

A

prediabetes or non diabetic hyperglycaemia

51
Q

what indicates impaired fasting glucose, impaired glucose tolerance and pre-diabetes in terms of glucose tests?

A

IGF - fasting glucose level between 6-7mmol/L
IGT - 2hr glucose OGTT between 7.7-11mmol/L
pre-diabetes - HbA1c between 42-48mmol/mol

52
Q

how do insulin levels change over the course of developning T2DM?

A

normal for normal people
intermediate stage - production increases to compensate as resistance is increasing
full blown T2DM - insulin production much reduced and body is maximally insulin resistant

53
Q

how does insulin production differ in T1 and T2DM?

A

T1 - no/little production of insulin due to cell death
T2- insulin still produced by beta cells but tissues are resistant, therefore a relative insulin deficiency (not enough produced to overcome resistance)

54
Q

how may T2DM progress if there is a long duration of the disease?

A

there may be complete insulin deficiency as the pancreas is exhausted, too much beta cell failure
may cause ketoacidosis at this point - patient usually on insulin by now

55
Q

what is known about the pathophysiology of T2DM?

A

internal adiposity, proinflammatory state, production of adipocytokines
makes tissues resistant to insulin action
insulin resistance and secretion defects occur at different points in disease
fatty acids related
heterogenous - diff ethnicity at diff ages etc

56
Q

how do glucose clamp tests differ between impaired glucose tolerance and T2DM in terms of insulin release?

A

IGT - blunted response to glucose
T2DM- no response to glucose, first phase of insulin response lost

57
Q

what is the role of the liver in T2DM?

A

makes things worse
less insulin means hepatic glucose output is increased due to less insulin (inhibition of gluconeogenesis normally) and more glucagon action

58
Q

what are the physiological consequences of insulin resistance?

A

increased hepatic glucose output
increased fatty acid uptake from gut by adipocytes, increased triglycerides and unhealthy lipids
in muscle less glucose uptake

59
Q

what is maturity onset diabetes of the young? MODY

A

monogenic diabetes - born with it and will lead to developing diabetes

60
Q

what have GWAS shown for T2DM?

A

cumulative SNPs have greater effect

61
Q

what is the role of obesity in T2DM?

A

major risk factor
central vs visceral obesity - visceral highest risk
80% T2DM obese

62
Q

what is the presentation of T2DM like?

A

unlikely to be acute presentation
hyperglycaemia
non-specific symptoms (tiredness etc)
overweight
dyslipidaemia
fewer osmotic symptoms
complications, frequent infections
insulin resistance

63
Q

what are the main risk factors for T2DM?

A

age
high BMI
PCOS
ethnicity
family history
inactivity

64
Q

what are the other main associations of T2DM besides obesity?

A

pertubations in gut microbiota
growth retardation intra-uterine (smaller - more likely to have T2DM)

65
Q

what complications often cause presentation of T2DM?

A

acutely - metabolic decompensation (hyperosmolar hyperglycaemic state)
chronically - ischaemic heart disease, retinopathy, neuropathy, nephropathy

66
Q

what is first line diagnostic test for T2DM?

A

HbA1c - above 48mmol/L
either with symptoms
or twice above 48 with no symptoms

67
Q

what is hyperosmolar hyperglycaemic state?

A

metabolic decompensation due to insulin resistance
dehydration
commonly presents with renal failure
often with precipitating event - MI, infection

68
Q

what is the management for T2DM?

A

initially diet modification, lifestyle changes
then oral medications - metformin etc
structured education
focus on prevention of diabetes related complications

69
Q

what makes up a typical T2DM consultation?

A

glycaemia - HbA1c, glucose monitoring (if on insulin), med review
weight assessment
blood pressure
dyslipidaemia- cholesterol profile
complication screeening

70
Q

what are the dietary recommendations for someone with T2DM?

A

total calorie control
reduce fat, refined carb calories
increase complex carb calories and soluble fibre
decrease sodium intake

71
Q

what is metformin?

A

biguanide - insulin sensitiser
first line treatment if lifestyle hasnt made diff
reduces insulin resistance, reduces hepatic glucose output, increased peripheral glucose disposal
has GI side effects
contraindicated in liver, cardiac or renal failure

72
Q

what are sulphonylureas?

A

glicazide
bind to ATP K+ channel on pancreatic b cells and close it, independent of glucose - causes insulin production
helps insulin release, increase insulin production

73
Q

what is pioglitazone?

A

thiazolidinedione insulin sensitiser - mainly peripheral
improves glycaemia and lipids, modifies adipocyte differentiation (peripheral weight gain)

74
Q

which diabetes drug increases weight gain the most?

A

thiozolidinediones - TZDs

75
Q

what is the role of GLP-1 in T2DM?

A

L cell gut hormone stimulates insulin and suppresses glucagon, increases satiety
used in treatment of T2DM via incretin effect - GLP-1 agonists

76
Q

what are GLP-1 agonists?

A

liraglutide, semaglutide injectables
decrease glucagon, glucose and encourage weight los

77
Q

what are DPPG-4 inhibitors?

A

gliptins
increase half life of exogenous GLP-1
decrease glucagon
decrease glucose
neutral on weight

78
Q

what are SGLT-2 inhibitors?

A

empagliflozin
inhibits Na-glu transporter in kidney
increases excretion of glucose in urine
lowers HbA1c

79
Q

how can remission of T2DM be encouraged non medically?

A

surgery - gastric bypass

80
Q

what is LADA?

A

latent autoimmune diabetes in adults
autoimmune slow progressing type 1 diabetes
presents later in life

Endo, Cardio and Neuro (22 decks)

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