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Y2 - ENDO > T1DM > Flashcards

T1DM Flashcards

1
Q

What type of diabetes is more common in young and lean individuals and which is more common in old and obese individuals?

A

T1DM - young and lean

T2DM - old and obese

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2
Q

Give the different types and causes of diabetes

A
  • T1DM
  • T2DM
  • Monogenic diabetes (e.g. MODY)
  • LADA - latent autoimmune diabetes in adults
  • Pancreatic damage
  • Endocrine disease (e.g. Cushing’s)
  • NOTE the last 4 manifest as either T1DM / T2DM
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3
Q

Whats more common, T1DM or T2DM?

A

T2DM

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4
Q

Outline very generally, the pathophgysiology of T1DM, including 2 general causative factors and how they cause hyperglycaemia

A
  1. Environment
  2. Genetics
  • Leads to autoimmune destruction of ß-cells in Islets of Langerhans
  • So insulin deficient
  • So hyperglycaemia
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5
Q

Outline very generally, the pathophgysiology of T1DM, including general causative factors, and how they cause hyperglycaemia

A
  1. Genetics
  2. Obesity
  • These lead to insulin resistance
  • Subsequent ß-cell failure as ß-cells try to produce loads of insulin to compensate but its just not working
  • Hyperglycaemia
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6
Q

Describe the development of T1DM

A
  • Pre-diabetes
  • Overt diabetes
  • Patients often present upon diabetic ketoacidosis symptoms
  • Diabetes is a relapsing remitting disease
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7
Q

What other risks exist in T1DM?

A
  • Because it is an autoimmune condition, you are at risk of other autoimmune conditions
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8
Q

What do the ß-cells look like in T1DM, what will you see under microscopy?

A
  • Inflammatory cells visible (plasma cells)
  • T-cells visible - play a role in beta-cell destruction
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9
Q

In which diabetes is there greater ß-cell destruction - T1DM or T2DM?

A

T1DM

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10
Q

How can you determine genetically if someone is at risk of developing T1DM, and what is particularly critical?

A
  • HLA-DR allele haplotype analysis - if there are abnormalities, then you can see this here
  • Especially important haplotypes are DR3 and DR4 - there is a significant risk of developing T1DM
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11
Q

2 things that suggests environmental influences on T1DM?

A
  1. There is a higher prevalence in the winter months
  2. There is a varying prevalenves between countries
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12
Q

1) Why is measuring antibodies as a means to clinically diagnose T1DM not really used, and when is it useful in particular though?
2) What are 4 types of antibodies that can be measured to clinically diagnose T1DM?

A

1)

  • You can just diagnose it just on presentation and other means
  • Useful when you’re not sure whether someone has T1DM or T2DM - particularly in LADA

2)

  1. Islet cell antibodies (ICA) - grp 0 human pancreas
  2. Insulin antibodies (IAA)
  3. Glutamic Acid Decarboxylase Antibodies (GADA)
  4. Insulinoma-associated-2-autoantibodies (IA-2A)-receptor like family
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13
Q

1) 7 symptoms of T1DM?
2) 6 signs of T1DM?

A

1)

  1. Polyuria
  2. Nocturia
  3. Polydipsia
  4. Vision blurring
  5. Thrush
  6. Weight loss
  7. Fatigue

2)

  1. Dehydration
  2. Cachexia
  3. Hyperventilation
  4. Smell of ketones
  5. Glycosuria
  6. Ketonuria
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14
Q

Label the diagram on a piece of paper 10 times

A
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15
Q

4 total actions that insulin has at the liver, muscles, adipose tissue

A
  1. Reduce hepatic glucose output
  2. Increases muscle’s uptake of hepatic glucose
  3. Inhibits the release of amino acids from muscle which would otherwise be taken into liver and enter glucoeogenic pathways here (so indirectly lowers hepatic glucose output in this way)
  4. Inhibits the release of glycerol and fatty tissues (breakdown products from triglyceride breakdown) from adipose tissue which would otherwise be taken into the liver and enter gluconeogenic pathways (or krebs eventually for F.A’s in muscle) here (so indirectly lowers hepatic glucose output in this way)
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16
Q

Which hormones oppose 3 of the actions of insulin at the liver, muscle and adipose tissue and what actions do they have?

A
  1. Increase hepatic glucose output against insulin - glucagon, catecholamines, growth hormones, cortisol
  2. Stimulate the release of amino acids from muscle against insulin to indirectly increase hepatic glucose output - cortisol
  3. Stimulate the release of glycerol from adipose tissue which indirectly increases hepatic glucose output as this glycerol is taken up into the liver and enters gluconeogenic pathways here - catecholamines, growth hormones
17
Q

Why are ketones used in T1DM, and why does diabetic ketoacidosis occur?

A
  • Because insulin deficiency causes fatty acid breakdown for some reason in adipose tissue so there is also higher tryglyceride tissue to replenish it
  • Lots of fatty acid released and taken up into the liver uninhibited by insulin as insulin deficient
  • Enters liver and ketone bodies are formed in lipolysis to form acetyl CoA eventually - this process in the liver is also normally inhibited by insulin, but this does not happen in T1DM
  • So lots of ketone bodies then travel through blood to the muscles where they become AcetylCoA to then feed into the Kreb’s cycle
  • So you’ll have high [ketone body] in the blood
18
Q

What complications can occur with T1DM?

A
  • Diabetic retinopathy
  • Diabetic nephropathy
  • Diabetic neuropathy
  • Vascular disease
19
Q

What are the aims of T1DM treatment?

A
  • Reduce early mortality
  • Avoid acute metabolic decompensation
  • Prevent long term complications
20
Q

What do you give in T1DM treatment?

A

Exogenous insulin

21
Q

What are the dietary advices for someone with T1DM?

A
  • Reduce calories as fat
  • Reduce calories as refined carbohydrate
  • Increase calories as complex carbohydrate
  • Increase soluble fibre
  • Balanced distribution of food over course of day with regular meals and snacks
22
Q

What exogenous insulin analogues are given in the treatment of T1DM, and are they slow or fast acting

1) With meals?
2) In the background?

A

1)

  • Human insulin
  • Insulin analogues (lispro, aspart, glulisine)
  • Short-acting

2)

  • Non c-bound to zinc/protamine
  • Insulin analogues (glargine, determir, degludec)
  • Long-acting
23
Q

1) How are insulin pumps use to administer exogenous insulin in T1DM treatment?
2) What is one weakness of insulin pumps - i.e. why they’re still not comparable to the glycaemic control your body can naturally possess?

A

1)

  • Pre-programmed basal and bolus rates
  • So continous insulin release basally but also increases dosage upon eating food
24
Q

1) Apart, from providing exogenous insulin, what is another form of treatment for T1DM that is only reserved for patients with particulary bad glycaemic control - name and describe the process
2) What do we need to give concurrently to avoid adverse affects?

A

1)

  • Islet cell transplants
  • Take ß cells from the donor pancreas, isolate them, inject them into the liver via hepatic vein
  • They migrate around the body, producing insulin

2)

  • Immunosuppresive agents
25
Q

4 ways to measure glucose levels - note this is useful in monitoring treatment efficacy

A
  1. Measure capillary glucose levels
  2. Blood sample (patients can’t do this)
  3. Glucose monitor
  4. HbA1C
26
Q

1) How does HbA1C glucose level measurement work?
2) Therefore why is it a useful measure?
3) In what cases can it be innacurate and why?
4) What is lowering HbA1C associated with?

A

1)

  • Red cells attach to the glucose monitor and react with glucose to be glycated irreversibly and non-covalently, measure the rate of glycation, knowing the life-span of the RBC is 120 days so it gives us an idea of glucose over 3 months

2)

  • Ideal measure of long-term glycaemic control

3)

  • If the patient has renal failure or blood loss
  • If the patient has has haemoglobinopathies e.g. SCA, thalassaemia, the red-cell half life will change, therefore HbA1C won’t be as accurate

4)

  • Lowering HbA1C is associated with lower risk of complications (particularly microvascular complications)
  • Risk of hypoglycaemia
27
Q

What occurs in metabolic acidosis that people with T1DM have?

A
  • Circulating ketone bodies
  • Osmotic dehydration
  • Poor tissue perfusion
28
Q

1) At what point is someone considered hypoglycaemic (what blood glucose level)?
2) What symptoms occur if you have blood glucose < 3 mmol / L?
3) What symptoms occur if you have blood glucose < 2 mmol / L?
4) At what point is hypoglycaemia considered severe, and what can it contribute to?

A

1) < 3.6 mmol / L
2) Impaired mental processes
3) Imparied consciousness
4) When a hypoglycaemic episode requires the help of another person to treat it, can contribute to arrythmia and sudden death

29
Q

When do hypoglycaemic episodes often occur (time of day)?

A
  • Pre-lunch
  • Nocturnal
30
Q

Some triggers of hypoglycaemia?

A
  • Patients going to the gym while not changing their insulin dose (unaccustomed exercise)
  • Missing meals or inadequate snacks
  • Drinking lots of alcohol
  • Inappropriate insulin regime
31
Q

5 symptoms classified within the causes being increased autonomic activation and impaired CNS function

A
  • Increased autonomic activation
  1. Palpitations (tachycardia)
  2. Tremor
  3. Sweating
  4. Pallor / cold extremities
  5. Anxiety
  • Impaired CNS function
  1. Drowsiness
  2. Confusion
  3. Altered behaviour
  4. Focal neurology
  5. Coma
32
Q

How and when to treat T1DM hypoglycaemic episodes by…

1) Oral administration?
2) Pareneteral administration? And what must you avoid
3) Otherwise, and when is this particular treatment not as effective?

A

1)

  • Give if the patient is conscious
  • Quick acting glucogels - rapidly absorbed as solutions and tablets
  • Give complex carbohydrates - to maintain blood glucose after initial treatment

2)

  • Give if the patient has impaired consciousness
  • I.V dextrose (10%) glucose infusion
  • i.m - 1mg glucagon

3)

  • Glucagon kit
  • Only effective when liver has enough glucose - if glycogen stores are depleted, the treatment won’t be as effective

Y2 - ENDO (18 decks)

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