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Aneesha Flashcards BRS 2 > Type 1&2 Diabetes Mellitus > Flashcards

Type 1&2 Diabetes Mellitus Flashcards

1
Q

what is type 1 diabetes?

A

autoimmune disease in which insulin producing beta cells in pancreas are attacked and destroyed by the immune system resulting in partial/complete deficiency of insulin and hyperglycemia
This resultant hyperglycemia requires lifelong insulin treatment

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2
Q

WHO 2019 Diabetes classifiction

A

Type 1 Diabetes
Type 2 Diabetes
Hybrid forms
Other
Unclassified
During pregnancy

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3
Q

Dichotonomy of type nd type 2 diabetes

A
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4
Q

what is the onset of type 1 diabetes?

A

thought to be childhood but adulthood becoming more common
Autoimmune diabetes leading to insulin deficiency can present later in life = latent autoimmune diabetes in adults

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5
Q

Stages of development of type 1 diabetes in relation to beta cell mass

A
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6
Q

what are the stages of development for type 1 diabetes?

A
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7
Q

what can constitute a precipitating event?

A

viral illness

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8
Q

what is immune infiltration in T1DM

A

immune cells infiltrate islet cells in T1DM

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9
Q

what is the importance of understanding T1DMs immune basis?

A

Increased prevalence of other autoimmune disease
Risk of autoimmunity in relatives
More complete destruction of B-cells
Auto antibodies can be useful clinically
Immune modulation offers the possibility of novel treatments
Not there yet

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10
Q

Brief overview of immunology of T1DM

A

Primary step is the presentation of auto-antigen to autoreactive CD4+ T lymphocytes
CD4+ cells activate CD8+ T lymphocytes
CD8+ cells travel to islets and lyse beta-cells expressing auto-antigen
Exacerbated by release of pro-inflammatory cytokines
Underpinned also, by defects in regulatory T-cells that fail to supress autoimmunity

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11
Q

Are all beta cells destroyed in T1DM?

A

NO
Some people with type 1 diabetes continue to produce small amounts of insulin ((some B cells evade immune system))
Not enough to negate the need for insulin therapy

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12
Q

Genetic susceptibility for T1DM

A

HLA is the biggest
risk modulater

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13
Q

what are some environmental risk factors of T1DM?

A

Multiple factors implicated, but causality has not been established

enteroviral infections
cows milk protein exposure
seasonal variation
changes in microbiota

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14
Q

what are some detectable pancreatic autoantibodies?
Are these needed for diagnosis?

A

Insulin antibodies (IAA)
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
Insulinoma-associated-2 autoantibodies (IA-2A)-Zinc-transporter 8 (ZnT8)
Not generally needed for diagnosis in most cases

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15
Q

what are the symptoms of T1DM?

A

polyuria
nocturia
polydypsia
blurring of vision
recurrent infections
weight loss
fatigue

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16
Q

what are the signs of T1DM?

A

dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria

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17
Q

what are the physiological effects of insulin deficiency? T1DM

A

proteinolysis (amino acids)
increased hepatic glucose output
lipolysis- ketogenesis, NEFA and glycerol

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18
Q

Involvement of insulin and glucagon in generation of ketone

A
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19
Q

what are the ketone bodies?

A

3-beta-hydroxybutyrate
acetoacetate
acetone

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20
Q

what are the treatment aims for T1DM?

A

maintain glucose levels
restore close to physiological profile of insulin
prevent acute metabolic decompensation
prevent microvascular and macrovascular complications

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21
Q

what are the complications of hyperglycaemia?
Complication of treatment

A

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

of treatment- hypoglycemia

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22
Q

what is the management of T1DM?

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

Type 1 diabetes is a condition that is ‘self-managed’

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23
Q

Physiological insulin profile

A
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24
Q

what are the types of insulin treatments?

A

short insulin (with meals)
background/basal insulin

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25
Q

what are examples of short acting insulin?

A

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

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26
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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27
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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28
Q

what is insulin pump therapy?

A

Continuous delivery of short-acting insulin analogue e.g. novorapid via pump

Delivery of insulin into subcutaneous space

Programme the device to deliver fixed units / hour throughout the day (basal) ((useful if you do something like run a marathon- can adjust based on daily requirement))

Actively bolus for meals

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29
Q

what is the dietary advice for T1DM?

A

Dose adjustment for carbohydrate content of food.
All people with type 1 diabetes should receive training for carbohydrate counting

Where possible, substitute refined carbohydrate containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index)

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30
Q

What is DAFNE

A

Structured Education Programme (all people with T1DM should be offered one)
5 day course on skills and training in self-management

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31
Q

what is a closed loop/artificial pancreas?

A

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

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32
Q

what types of transplantation are available for T1DM?

A

islet cell transplants
simultaneous pancreas and kidney transplants

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33
Q

What happens during islet cell transplants?
Disadvantage of this?

A

Isolate human islets from pancreas of deceased donor
Transplant into hepatic portal vein
Requires life-long immunosuppression

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34
Q

Advantage and disadvantage of simultneous pancreas and kidney transplant

A

Better survival of pancreas graft when transplanted with kidneys
Requires life-long immunosuppression

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35
Q

Aim of transplantation in treating T1DM
Limitations

A

Aim: try to restore physiological insulin production to the extent that insulin can be stopped

Even if incomplete, often results in better control

Limitations: availability of donors, complications of life-long immunosuppression

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36
Q

how can glucose be monitored?

A

capillary finger prick blood glucose monitoring
continuous glucose monitoring

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37
Q

what is HbA1c?

A

reflects last 3 months of glycaemia
Biased to the 30 days preceding measurement
Glycated NOT glycosylated -enzymatic so linear relationship
irreversible

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38
Q

What are the limitations of HbA1c?

A

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

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39
Q

What is used to guide insulin doses?

A

Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months

Based on results, increase or decrease insulin doses

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40
Q

Acute complications of T1DM

A

Diabetic ketoacidosis
Uncontrolled hyperglycemia
Hypoglycemia

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41
Q

Diabetic ketoacidosis is often a presenting feature of new-onset type 1 diabetes but can occur in those with established T1DM- in what situation would this occur?

A

Acute illness
Missed insulin doses
Inadequate insulin doses

42
Q

Does diabetic ketoacidosis only occur in T1DM?

A

Can occur in any type of diabetes ((TYPE 2 ALSO SOMETIMES))
Commonly in T1 though

43
Q

What is diabetic ketoacidosis?

A

Acute life threatening complication of t1DM
pH less than 7.3, ketones increased (urine or capillary blood), HCO3- less than15 mmol/L and glucose >11 mmol/L

44
Q

Numerical definition of hypoglycemia
What is severe hypoglycemia?

A

below 3.6 mmol/L
Severe hypoglycaemia: any event requiring 3rd party assistance

45
Q

when does hypoglycaemia on insulin therapy become problematic?

A

excessive frequency
impaired awareness (unable to detect low glucose)
nocturnal hypoglycaemia
recurrent severe hypoglycaemia

46
Q

what are the risks of hypoglycaemia?

A

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

47
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

48
Q

how can problematic hypoglycaemia be supported?

A

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

49
Q

what are the treatments for hypoglycaemia but alert and oriented?

A

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

50
Q

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

A

buccal glucose e.g glucogel/hypostop
complex carbohydrate

51
Q

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

A

IV access 20% glucose IV

52
Q

what should you consider for a deteriorating / refractory /insulin induced /difficult IV access patient with hypoglycemia?

A

IM/SC 1mg glucagon

53
Q

what is type 2 diabetes?

A

a condition in which beta cell failure and insulin resistance result in hyperglycaemia
Associated with obesity but not always
The resultant chronic hyperglycaemia may initially be managed by changes to diet / weight loss and may even be reversible
With time glucose lowering therapy including insulin, is needed

54
Q

How can monogenic diabetes (MODY, mitochondrial diabetes) present?

A

As T1 or T2DM

55
Q

Can diabetes present following pancreatic damage or other endocrine disease

A

Yes

56
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

57
Q

what are normal fasting glucose levels?

A

less than/ equal to 6mmol/L

58
Q

what are normal 2hr glucose levels? (OGTT)

A

less than 7.7mmol/L

59
Q

what is normal HbA1c?

A

less than 42mmol/L

60
Q

how can random glucose readings confirm T2DM diagnosis?

A

above 11.1mmol/L WHEN SHOWING SYMPTOMS

61
Q

what fasting glucose levels indicate T2DM?

A

above/equal to 7mmol/L

62
Q

what 2hr glucose levels (OGTT) indicate T2DM?

A

above/ equal to 11mmol/L

63
Q

what HbA1c indicates T2DM?

A

over/equal to 48mmol/mol

64
Q

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

A

impaired fasting glycaemia

65
Q

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

A

impaired glucose tolerance

66
Q

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

A

prediabetes or non diabetic hyperglycaemia

67
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

68
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)

69
Q

Beta-cell function at diagnosis of T2DM

A
70
Q

what is known about the pathophysiology of T2DM?

A

Genes and intrauterine environment and adult environment.
Insulin resistance and insulin secretion defects
Fatty acids important in pathogenesis and complications

HETEROGENOUS
People develop T2D at variable BMI, ages and progress differently

71
Q

Why does hyperglycemia in T2DM not usually lead to ketosis?

A

Insulin is produced by pancreatic beta-cells but not enough to overcome insulin resistance
There is therefore a relative deficiency of insulin
However it is enough to suppress ketone body formation

72
Q

What happens to insulin production in long duration type 2 diabetes
What should we do then

A

In long-duration type 2 diabetes, beta-cell failure may progress to complete insulin deficiency
Usually on insulin at this point in any case, but important not to stop as at risk of ketoacidosis

73
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
(first phase insulin release is lost)

74
Q

Doesglucose just come from diet in T2DM?

A

No
In type 2 diabetes, reduced insulin action causes less uptake of glucose into skeletal muscle
Hepatic glucose production is also increased due to both a reduction in insulin action and increase in glucagon action

75
Q

what are the physiological consequences of insulin resistance?

A

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

76
Q

Relationship between insulin resistance and insulin secretion in people with T2DM

A
77
Q

Genetics of diabetes- monogenic vs polygenic

A

Monogenic- Single gene mutation ==> Diabetes (MODY)
‘Born with it, always going to develop diabetes’

Polygenic- Polymorphisms increasing risk of diabetes
‘Not born with it but high risk and may develop later depending on other factors’

78
Q

what have GWAS shown for T2DM?

A

each individual SNP has only mild effect on risk
cumulative SNPs have greater effect

79
Q

what is the role of obesity in T2DM?

A

Major risk factor for T2DM
Fatty acids and adipocytokines important
Central vs visceral obesity- visceral higher risk
80% T2DM are obese
Weight reduction useful treatment

80
Q

T2DM associations other than obesity

A

Perturbations in gut microbiota
Intra-uterine growth retrdation

81
Q

what is the presentation of T2DM like?

A

Hyperglycaemia
Overweight
Dyslipidaemia
Fewer osmotic symptoms
With complications
Insulin resistance
Later insulin deficiency

82
Q

what are the main risk factors for T2DM?

A

age
high BMI
PCOS
ethnicity
family history
inactivity

83
Q

what is first line diagnostic test for T2DM?

A

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

84
Q

Diagnosis of type 2 diabetes- how does this occur

A

Osmotic symptoms
Infections
Screening test: incidental finding
at presentation of complication
Acute; hyperosmolar hyperglycaemic state,
Chronic; ischaemic heart disease, retinopathy

85
Q

what is hyperosmolar hyperglycaemic state?

A

Presents commonly with renal failure.
Insufficient insulin (NOT ABSENT) for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis.
Absence of significant acidosis.
Often identifiable precipitating event (infection, MI).

unchecked gluconeogenesis leads to hyperglycemia and osmotic diuresis to dehydration

86
Q

what is the management for T2DM?

A

Diet
Oral medication
Structured education
May need insulin later
Remission / reversal

87
Q

what makes up a typical T2DM consultation?

A

Glycaemia: HbA1c, glucose monitoring if on insulin, medication review
Weight assessment
Blood pressure
Dyslipidaemia: cholesterol profile
Screening for complications: foot check, retinal screening

88
Q

what are the dietary recommendations for someone with T2DM?

A

Healthy eating or diet
Total calories control
Reduce calories as fat
Reduce calories as refined carbohydrate
Increase calories as complex carbohydrate
Increase soluble fibre
Decrease sodium

89
Q

Drug treatments for type 2 diabetes

A
90
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 severe liver, severe cardiac or moderate renal failure

91
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

92
Q

what is pioglitazone?

A

Peroxisome proliferator-actived receptor agonists PPAR-γ
Pioglitazone
Insulin sensitizer, mainly peripheral
Adipocyte differentiation modified, weight gain but peripheral not central
Improvement in glycaemia and lipids
Evidence base on vascular outcomes
Side effects of older types hepatitis, heart failure

93
Q

which diabetes drug increases weight gain the most?

A

thiozolidinediones - TZDs

94
Q

what is the role of GLP-1 in T2DM?

A

Gut hormone
Secreted in response to nutrients in gut
Transcription product of pro-glucagon gene, mostly from L-cell
Stimulates insulin, suppresses glucagon
↑ satiety (feeling of ‘fullness’)

95
Q

Why does GLP-1 have a short half life

A

Due to rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)

96
Q

What is the gastrointestinal incretin effect

A
97
Q

what are GLP-1 agonists?
How are they administered?
Effects?

A

Liraglutide, Semaglutide
Injectable –daily, weekly
Decrease [glucagon]
Decrease [glucose]
Weight loss

98
Q

what are DPPG-4 inhibitors?
Example

A

Increase half life of exogenous GLP-1
Increase [GLP-1]
Decrease [glucagon]
Decrease [glucose]
Neutral on weight

Gliptins

99
Q

what are SGLT-2 inhibitors?

A

Empagliflozin, dapagliflozin, canagliflozin
inhibits Na-glu transporter in kidney
increases excretion of glucose in urine
lowers HbA1c

Lowers all cause mortality, risk of hear failure and improves CKD

100
Q

What does the DIRECTstudy/ DROPLET study show?

A

very low-calorie diet (800 kcal/day) for 3-6 months has the potential to induce remission in T2DM, which appears to be sustained at 2 years

101
Q

Other than glucose lowering, what aspects of T2DM management are important

A

Blood Pressure management
Hypertension very common in T2DM
Clear benefits for reduction esp with use of ACE-inhibitors

Lipid management
Total cholesterol raised
Triglycerides raised
HDL cholesterol reduced!!!!!!!!!!!
Clear benefit to lipid-lowering therapy

102
Q

how can remission of T2DM be encouraged non medically?

A

surgery - gastric bypass (roux en y)

Aneesha Flashcards BRS 2 (47 decks)

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