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YR2 LCRS Endocrinology > 15. Type I diabetes mellitus > Flashcards

15. Type I diabetes mellitus Flashcards

1
Q

what are the 2 classifications of diabetes and who is affected?

A
  • type 1 diabetes - lean, young individuals

- type 2 diabetes - older, obese individuals

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2
Q

what is LADA?

A

latent autoimmune diabetes in adults which requires insulin as treatment

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3
Q

what is a feature of T2DM?

A

diabetic ketoacidosis

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4
Q

what can present phenotypically as type 1/2 diabetes?

A

monogenic diabetes e.g. MODY, mitochondrial diabetes

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5
Q

how does type 1 diabetes arise?

A

an environmental trigger and genetic influences lead to the autoimmune destruction of islet cells leading to insulin deficiency which results in hyperglycaemia

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6
Q

how does type 2 diabetes arise?

A

a stronger genetic influence associated with diabetes leads to insulin resistance which causes B-cell failure, resulting in hyperglycaemia

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7
Q

what is the pathogenesis (development) of type 1 diabetes?

A
  • pre-diabetes followed by overt diabetes as the b-cells start to malfunction
  • steady progression of b-cell failure
  • patients are admitted as sick from diabetic ketoacidosis
  • T1DM is a relapsing remitting disease
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8
Q

which type of diabetes has greater genetic susceptibility?

A

T2DM

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9
Q

abnormalities in which haplotypes can result in an increased risk of developing T1DM?

A

DR3 and DR4 of the HLA-DR allele

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10
Q

what suggests there is an environmental influence on T1DM?

A
  • there is a higher prevalence of T1DM in winter

- certain places in the world have a higher prevalence of T1DM

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11
Q

what can be done when a clinician is unsure of whether a patient has T1DM or T2DM?

A

antibody tests

  • measure islet cell antibodies (ICA)
  • measure insulin antibodies (IAA)
  • measure glutamic acid decarboxylase antibodies (GADA)
  • measure insulinoma-associated-2 autoantibodies (IA-2A)
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12
Q

what are the symptoms of diabetes?

A
  • polyuria
  • nocturia
  • polydipsia
  • blurred vision
  • thrush
  • weight loss
  • fatigue
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13
Q

what are the signs of diabetes?

A
  • dehydration
  • cachexia
  • hyperventilation
  • smell of ketones
  • glycosuria
  • ketonuria
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14
Q

what is the role of insulin?

A
  • reduce hepatic glucose output
  • drive uptake of glucose by muscle
  • prevent protein destruction in muscle
  • prevent fatty acids/glycerol from leaving adipose
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15
Q

what happens in insulin deficiency?

A
  • glucose in the liver is released into the circulation
  • glucose in the circulation is not taken up by muscle
  • proteins are broken down into amino acids and released from muscle
  • amino acids are taken up by the liver and result in glucose production
  • fatty acids in adipose tissue are broken down so triglycerides start to release lots of fatty acids
  • fatty acids released are taken up by the liver and ketone bodies are produced

LEADS TO HYPERGLYCAEMIA

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16
Q

what are the aims of treatment in T1DM?

A
  • reduce early mortality
  • avoid acute metabolic decompensation
  • prevent long-term complications (retinopathy, nephropathy, neuropathy, vascular disease)
17
Q

what is the diet of individuals with T1DM?

A
  • reduce calories as fat
  • reduce calories as refined carbohydrates
  • increase calories as complex carbohydrates
  • increase soluble fibre
  • balanced distribution of food over the course of the day with regular meals and snacks
18
Q

what short-acting insulin treatment is administered?

A

human insulin, insulin analogues (lispro, aspart, glulisine) taken with meals

19
Q

what long-acting insulin treatment is administered?

A

protamine zinc insulin (obtained from cow pancreas), insulin analogues (glargine, determir, degludec)

20
Q

what is a basal bolus regimen?

A

taking short acting insulin at meal times, taking long acting insulin to cover the day

21
Q

what is an insulin pump?

A

a device that administers continuous insulin

the pump has pre-programmed basal rates and bolus for meals

the pump does not measure glucose

22
Q

what do islet cell transplants involve?

A

a transplant team taking some b-cells from a donor pancreas (after death of donor), isolating the cells and injecting them into the liver

through hepatic veins the b-cells migrate around the body and produce insulin

patients need to be on immunosuppressive agents after

(rare)

23
Q

how can the success of treatment be determined?

A
  • patients can measure capillary glucose levels (though this varies depending on tissue perfusion)
  • doctors can monitor glucose levels by taking a blood sample
  • use a glucose monitor
24
Q

how can blood glucose be measured over time?

A
  • continuous glucose monitor
  • HBA1C: a blood sample that relies on red cells attaching to the glucose monitor. red cells have a lifespan of approx. 120 days so the test gives an idea of glucose levels over 3 months
25
Q

in which cases will HBA1C not be as accurate?

A
  • patients with a haemoglobinopathy (SCA, thalassaemia)

- patients with renal failure or blood loss

26
Q

what is an acute complication of T1DM and how does it occur?

A

ketoacidosis

  • patients are hyperglycaemic: reduced tissue glucose utilisation, increased HGP
  • patient therefore has a metabolic acidosis: circulating ketone bodies, osmotic dehydration and poor tissue perfusion
27
Q

what is hypoglycaemia defined as?

A

plasma glucose <3.6mmol/l

28
Q

what are the effects of hypoglycaemia?

A
  • blood glucose <3mmol/l: most mental processes impaired
  • blood glucose <2mmol/l: conciousness impaired
  • severe hypoglycaemia may contribute to arrhythmia and sudden death
  • long-term effects include cognitive problems
29
Q

who is at risk of hypoglycaemia?

A

patients with low HBA1C

30
Q

when do hypoglycaemic episodes happen?

A

can occur at any time but pre-lunch episodes and nocturnal episodes are common

31
Q

why does hypoglycaemia occur?

A
  • going to the gym while not changing insulin dose
  • missing meals or having inadequate snacks
  • drinking lots of alcohol
  • inappropriate insuline regime
32
Q

what are the hypoglycaemic symptoms and signs due to increased autonomic activation?

A
  • palpitations
  • tremor
  • sweating
  • pallor/cold extremities
  • anxiety
33
Q

what are the hypoglycaemic symptoms and signs due to impaired CNS function?

A
  • drowsiness
  • confusion
  • altered behaviour
  • focal neurology
  • coma
34
Q

how is hypoglycaemia treated orally?

A
  • if the patient is conscious feed the patient
  • give quick acting glucogels (rapidly absorbed as a solution or as tablets)
  • complex carbohydrates to maintain blood glucose after initial treatment
35
Q

how is hypoglycaemia treated parenterally?

A
  • done if the patient has impaired consciousness
  • intravenous dextrose (10%) glucose infusion
  • 1mg glucagon (intramuscular)
  • avoid concentration solutions as these can cause severe skin reactions

YR2 LCRS Endocrinology (18 decks)

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