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Year 2 - LCRS - Endocrinology > Type 1 Diabetes Mellitus incl. DKA > Flashcards

Type 1 Diabetes Mellitus incl. DKA Flashcards

1
Q

How do people with T1DM typically present?

A
  • skinny / lean
  • young
  • DKA
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2
Q

What is the cause of T1DM?

A
  • environmental trigger (e.g. viral, bacterial infection) -> more new cases in the winter
  • AI destruction of cells
  • Insulin deficiency
  • Genetics
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3
Q

What are symptoms of diabetes?

A 
polyuria 
nocturia
polydipsia 
blurring of vision
‘thrush’ (candida infection)
weight loss
fatigue
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4
Q

What are signs of diabetes?

A 
dehydration 
cachexia
hyperventilation (kussmaul respiration due to metabolic acidosis)
smell of ketones
glycosuria 
ketonuria
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5
Q

What are some forms of T1DM?

A
  • LADA (latent autoimmune diabetes in adults)

- MODY (monogenic diabetes mellitus can present with features of types one and types 2)

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6
Q

Why is the immune basis of T1 diabetes important?

A
  • Increased prevalence of other autoimmune disease (e.g. Addison’s, b12 problems)
  • 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
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7
Q

What is the role of genetics in diabetes?

A
  • There is a genetic link

- certain HLA markers are linked to an increased T1 diabetes risk.

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8
Q

What are some markers in T1DM?

A
  • Islet cell antibodies (ICA)- grp O human pancreas
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase (GADA) – widespread nuerotransmitter
  • Insulinoma-associated-2 autoantibodies (IA-2A)-receptor like family

T1DM patients have higher levels of these.

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9
Q

What are the most important tissues in the metabolism of glucose?

A
  • muscle
  • liver
  • adipose tissue
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10
Q

What are the aims in treatment of T1DM?

A
  • reduce early mortality

- avoid acute metabolic decompensation

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11
Q

What are long term complications of T1DM?

A
  • retinopathy
  • nephropathy
  • neuropathy
  • vascular disease

Can lead a pretty good life but are more at risk of stroke, MI and peripheral arterial disease

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12
Q

What is the recommended diet in 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
  • eating simple sugars makes it difficult to regulate glucose levels, even with insulin.
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13
Q

What is the insulin release pattern in healthy individuals?

A
  • peaks when eating

- also there is basal insulin and glucose

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14
Q

What is insulin treatment like?

A

a) With meals
- short acting
- human insulin
- insulin analogue (Lispro, Aspart, Glulisine)

b) Background insulin
- long acting
- Non-c bound to zinc or protamine
- Insulin analogue (Glargine, Determir, Degludec)

They have to take short acting insulin with meals and also take long acting baseline insulin.

Also: Genetic engineering to alter absorption,
distribution, metabolism and excretion

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15
Q

Insulin Pump

A
  • Continuous insulin delivery
  • Preprogrammed basal rates and bolus for meals
  • Does NOT measure glucose, no completion of feedback loop
  • it gives basal insulin and you can programme it to give insulin after meals.
  • there are problems with financing it
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16
Q

Islet cell transplants

A
  • only been done a few times in the UK
  • have to take immunosuppressant drugs for the rest of their life
  • have to have very sever hypoglycaemia
  • Islets of langerhans into the portal vein
17
Q

How can you test if the treatment is working?

A
  • monitoring capillary glucose
  • not as accurate as venous glucose
  • gives you a trend of levels throughout the day
18
Q

What is CGM?

A
  • continuous glucose monitoring

- gives a better feel of someones glucose and insulin levels throughout the day

19
Q

HbA1c levels

A
  • HbA1c red cells react with glucose, as it does with all proteins. Irreversible, non-covalent depends on;
  • Lifespan of red cell, about 120 days
  • Rate of glycation, faster in some individuals
  • Hb opathy, renal failure etc
  • Level of glucose
  • Forms ideal measure of long term glycaemic control and has been shown to be related to risk of complications.
  • Furthermore lowering HbA1c associated lower risk of complication particularly microvascular complication

in patients with SCD or thalassemia it may not be the best measurement, their RBCs have a shorter lifespan.

20
Q

What are acute complications in T1DM?

A
  • hyperglycaemia (reduced tissue glucose utilisation; increased hepatic glucose production; high glucose production due to lack of insulin.
  • metabolic acidosis (circulating acetoacetate & hydroxybutyrate; osmotic dehydration and poor tissue perfusion)
21
Q

Does all diabetic ketoacidosis occur in T1DM?

A

No, can also occur in other types

22
Q

“hypos”

A
  • occasional hypos inevitable as a result of treating diabetes
  • major cause of anxiety in patients & families
  • source of major misconceptions in media
  • Big problem: patients tend to have a high glucose level because they try to avoid hypos.

Definitions

  • hypoglycaemia - plasma glucose of < 3.6 mmol / l
  • severe hypoglycaemia - any hypo requiring help of another person to treat
23
Q

What are symptoms during a hypoglycaemic event?

A
  • Disorientation, sweatiness, confusion
  • can lead to a coma
  • most people become aware, eat something and try to control it.

most mental processes impaired at <3 mmol/l
consciousness impaired at <2 mmol/l
severe hypoglycaemia may contribute to arrhythmia and sudden death

may have long-term effects on the brain
recurrent hypos result in loss of warnings
‘hypoglycaemia unawareness’

24
Q

Hypo unwareness

A

If you have a lot of themy ou might not have all the symptoms and become unawawre, changes in the autonomic drive leads to loss of awareness.

25
Q

Who is likely to have a hypoglycaemic events?

A
  • main risk factor is quality of glycaemic control

- more frequent in patients with low HbA1c

26
Q

When are hypoglycaemic events likely to occur?

A
  • can occur at anytime but often a clear pattern
  • pre-lunch hypos common
  • nocturnal hypos very common and often not recognised
  • pre dinner is quite common as well
27
Q

Why do hypos occur?

A
  • unaccustomed exercise (you should eat more when you exercise)
  • missed meals
  • inadequate snacks
  • alcohol (when you go out drinking you might forget to inject insulin)
  • inappropriate insulin regime
28
Q

What are signs and symptoms of hypoglycemia?

A

Due to increased autonomic activation:

  • palpitations (tachycardia)
  • tremor
  • sweating
  • pallor / cold extremities
  • anxiety

Due to impaired CNS function:

  • drowsiness
  • confusion
  • altered behaviour
  • focal neurology
  • coma
29
Q

How due you treat hypoglycaemia?

A

Oral:
- feed the patient!!
- glucose
- rapidly absorbed as solution or tablets
complex CHO
- to maintain blood glucose after initial treatment

Parenteral:

  • give if consciousness is impaired
  • IV dextrose e.g 10% glucose infusion
  • 1mg Glucagon IM
  • avoid concentrated solutions if possible (e.g 50% glucose)
30
Q

Glucagon

A

A hormone that causes glucose release from the liver

31
Q

Would you give glucagon to a cachexia patient?

A

No because if they are very skinny and have fasted for a few days their glucose stores in the liver will have become very low sop the glucagon would not work -> you should give glucose i.v.

Year 2 - LCRS - Endocrinology (18 decks)

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