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LCRS Year 2 - Endocrinology > Type 1 Diabetes Mellitus > Flashcards

Type 1 Diabetes Mellitus Flashcards

1
Q

What are two reasons as to why there is some ambiguity in labelling patients as type 1 and type 2 diabetic?

A
  • There is a form of autoimmune “type 1” diabetes leading to insulin deficiency which can present in later decades of life - latent autoimmune diabetes in adults (LADA)
  • T2DM may present in childhood (when you’d usually expect them to be type 1)
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2
Q

What is monogenic diabetes and how can patients present in terms of type 1 or type 2 diabetes?

A

Genetic defect in the beta cells

- can present as EITHER type 1 or type 2

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3
Q

When might diabetes also present?

A

Following pancreatic damage or other endocrine diseases

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4
Q

How are the 4 types of diabetes (T1DM, T2DM, LADA, MODY) divided amongst the patients with diabetes?

A

T2DM - Large chunk (most common)
T1DM - Small chunk (rare)
LADA/MODY - Very small chunks (very rare)

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5
Q

How are type 1 and type 2 diabetes classified?

A

Based on aetiology - the causes of the disease

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6
Q

What is the series of events that causes type 1 diabetes?

A

There can be an environmental or genetic trigger

  • autoimmune destruction of beta cells follows
  • leads to insulin deficiency
  • leads to symptomatic hyperglycaemia
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7
Q

What is the series of events that causes type 2 diabetes?

A

There can be a genetic cause but also caused by obesity

  • leads to insulin resistance
  • this causes the hyperglycaemia

15-20 years later, the beta cells fail and stop producing insulin and patients require insulin replacement

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8
Q

What is the ‘honeymoon’ phase in type 1 diabetics?

A

This is a period of time where the beta cells aren’t totally destroyed

  • pancreas can sort of start working again before it switches off altogether
  • important for insulin dose calculation, patient can become hypoglycaemic if the dose is too high and the pancreas begins to produce insulin again
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9
Q

Why is the immune basis of type 1 diabetes important?

A

Increased prevalence of other autoimmune disease

  • increases your risk of developing other autoimmune diseases
  • risk of autoimmunity in relatives as well
  • the auto-antibodies can be useful clinically
  • immune modulation offers the possibility of novel treatments
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10
Q

What, genetically, can increase a patient’s susceptibility of developing T1DM?

A

Some DR1 to DR9 genes can increase risk of development

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11
Q

What is the hypothesis around different prevalences of diabetic ketoacidosis (and type 1 diabetes) in different periods of the year?

A

Winter highest - could be more that people are more susceptible to getting infections which may precipitate beta cell destruction
Summer lowest

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12
Q

What evidence supports the hypothesis that environmental factors can precipitate type 1 diabetes?

A

Specific regions around the world where incidence of specifically type 1 diabetes is very high
- may be due to the environment but we don’t really know

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13
Q

What are some measurable markers that we can measure to solidify whether the patient has type 1 or type 2 diabetes?

A

Islet cell antibodies (ICA)
Insulin antibodies (IAA)
Glutamic acid decarboxylase (GADA)
Insulinoma-associated-2 autoantibodies (IA-2A)

All you need to know about these is that they’re available to measure, they’re not usually needed, and, importantly, these markers don’t change the outcome or treatment option for the patient but can be used clinically to determine whether they are type 1 or type 2

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14
Q

What are the symptoms of diabetes?

A 
Polyuria 
Nocturia
Polydipsia
Blurring of vision
'Thrush' (female)
Weight loss
Fatigue
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15
Q

What are the signs of diabetes?

A 
Dehydration
Cachexia (weakness/wasting of the body due to severe chronic illness)
Hyperventilation
Smell of ketones
Glycosuria (glucose in urine)
Ketonuria
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16
Q

What three organs tightly regulate glucose in the body?

A

Liver
Muscle
Adipose tissue

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17
Q

How does insulin regulate serum glucose levels?

A
  • Inhibits release of glucose from liver
  • Inhibits release of amino acids from muscle to be converted to glucose in the liver
  • Inhibits release of glycerol from adipocytes to be converted to glucose in the liver
  • Stimulates glucose uptake into muscle

Overall decreases glucose in the blood.
Insulin deficient patients will have none of these processes working and the reverse occurring

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18
Q

What hormones oppose the effects of insulin?

A

Glucagon
Catecholamines
Growth hormone (somatotrophin)
Cortisol

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19
Q

What else can adipose tissue cells produce that insulin usually prevents the release of?

A

Fatty acids

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20
Q

What is the significance of fatty acids and what can they cause?

A

Fatty acids are taken up into the liver where they’re converted to ketone bodies
- can cause metabolic acidosis

21
Q

What are the aims of treatment in type 1 diabetes?

A

Reduce early mortality
Avoid acute metabolic decompensation
Prevent long term complications

22
Q

What are the long term complications of type 1 diabetes?

A

Retinopathy
Nephropathy
Neuropathy (these three are microvascular)
Vascular disease (macrovascular)

23
Q

What are the main principles of diet in patients with type 1 diabetes?

A
  • Reduce calories as fat
  • Reduce calories as simple (refined) carbohydrates
  • Increase calories as complex carbohydrates
  • Increase soluble fibre

Balanced distribution of food over course of the day with regular meals and snacks

24
Q

How was insulin discovered as a treatment?

A

Dogs with diabetes had their glucose levels restored to normal with insulin injections

25
Q

What happens to insulin levels in normal people when they eat and why is this relevant to insulin treatment plans?

A

Rise sharply after you eat, falls sharply once glucose has been regulated
- important as treatment attempts to mimic this as far as possible

26
Q

Where are all forms of modern insulin that is administered produced?

A

Genetic engineering, not from animals anymore

27
Q

What are the different forms of insulin treatment?

A

Short-acting insulin
- human insulin or insulin analogies (given with meals)

Background insulin

  • long-acting
  • non-c bound to zinc or protamine
  • or insulin analogue

A form of both short-acting and long-acting are usually in the treatment plan

28
Q

When is short-acting insulin given and what dictates the dose?

A

Given with meals so one dose per meal

- dosage dependent on what and how much food the patient is eating e.g. larger dose if patient eats a large evening meal

29
Q

What does the ‘classic’ type 1 diabetic patient treatment plan look like for a day?

A

Long-acting insulin given 1 a day or intermediate-acting insulin given 2 a day
- this is to maintain and simulate a background or basal level of insulin that would exist between meals in a healthy person

Short-acting insulin given whenever the patient has a meal
- provides the natural sharp rise and fall that would be seen after a meal in a healthy person

30
Q

What is an insulin pump and why is it sometimes necessary?

A

Some patients still have a poor glucose profile throughout the day and they experience severe hypoglycaemic episodes

  • allows continuous insulin delivery
  • has preprogrammed basal rates and bolus (bigger chunk) for meals
  • does not measure glucose so doesn’t self-regulate, up to the patient to set it
31
Q

What is one invasive treatment which is used and when is it used?

A

Islet cell transplants

  • islet cells harvested from dead person
  • islet cells travel round in the portal system and produce insulin
  • patients require immunosuppressants long-term

Used when patients have received treatment, including the insulin pump, but still have constant, severe hypoglycaemic episodes

32
Q

How do we know how successful our treatment is?

A

Measure glucose profile

33
Q

What are the two main ways the patient’s glucose profile can be measured?

A

Capillary monitoring
- prick the finger and enter blood sample into the machine method

Continuous glucose monitoring on abdomen which provides a good glucose profile

34
Q

What is more accurate than capillary glucose levels and why do we then still bother with capillary glucose measurements?

A

Venous glucose levels

  • more difficult to measure and more invasive
  • capillary glucose levels still provide a good idea of the patient’s glucose trends and a relative value they can use to determine how much insulin they need to inject before a meal
35
Q

What is the marker used to assess glucose levels on a longer-term basis and how does it work?

A

HbA1c red cells react with glucose
Irreversible non-covalent binding depending on
- lifespan of red cell, about 120 days
- rate of glycation

Usually a very good marker in most patients
- the higher the HbA1c, the higher the serum glucose

36
Q

What is important about HbA1c being low or lowering its levels?

A

The lower the HbA1c levels, the lower the glucose levels
- means that lowering HbA1c levels is associated with lower risk of complications, particularly microvascular complications (X-opathys)

37
Q

What is an acute complication of diabetes?

A

Ketoacidosis

38
Q

What is ketoacidosis and what happens in the body during an episode of this?

A

Hyperglycaemia

  • reduce tissue glucose utilisation
  • increased hepatic glucose production

Metabolic acidosis

  • due to circulating acetoacetate and hydroxybutyrate (two ketone bodies)
  • osmotic dehydration (vomiting as well then leads to severe hypotension) and poor tissue perfusion

Patients experiencing this can sometimes end up in ICU to be treated

39
Q

Does diabetic ketoacidosis occur more frequently in patients with type 1 or type 2 diabetes?

A

Usually type 1 diabetes (across all patients)

but can disparity between T1 and T2 can differ amongst ethnic groups

40
Q

What is the definition of hypoglycaemia?

A

Hypoglycaemia - plasma glucose of <3.6mmol/L

41
Q

What is the definition of severe hypoglycaemia?

A

Sever hypoglycaemia

- any hypoglycaemia requiring the help of another person to treat

42
Q

What are the 3 main benchmarks for loss in function in hypoglycaemia?

A

Most mental processes impaired at <3mmol/L
Consciousness impaired at <2mmol/L
Severe hypoglycaemia may contribute to arrhythmia and sudden death

43
Q

What are the longer-term effects of hypoglycaemic episodes?

A

May cause long-term effects on the brain

Recurrent hypos result in loss of warning symptoms a hypo is happening

44
Q

Who is at most risk of hypoglycaemic episodes?

A

Main risk is quality of glycaemic control

- More frequent in patients with low HbA1c

45
Q

When do hypoglycaemic episodes happen most often?

A

Can occur at anytime but often a clear pattern

  • pre-lunch hypos common
  • nocturnal hypos very common and often not recognised (high glucose in the morning due to catecholamine-induced glucose release in response to low glucose)
46
Q

Why do hypoglycaemic episodes happen?

A 
Unaccustomed exercise
Missed meals
Inadequate snacks
Alcohol
Inappropriate insulin regime (miscalculation of insulin injection amount required)
47
Q

What are the main symptoms and signs of hypoglycaemia?

A

Increased autonomic activation

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

Impaired CNS function

  • drowsiness
  • confusion
  • altered behaviour
  • focal neurology (symptoms attributed to specific part of the CNS)
  • coma
48
Q

How is hypoglycaemia treated?

A

If conscious:

  • Oral - FEED the patient
  • given glucose to be rapidly absorbed as solution or tablets
  • later on diet should contain complex carbohydrates to maintain blood glucose after initial treatment

If consciousness impaired:

  • IV dextrose e.g. 10% glucose infusion
  • 1mg glucagon IM - requires sufficient liver glucose store to work
  • avoid concentrated solutions if possible
49
Q

What are the main conclusions about type 1 diabetes mellitus?

A
  • Ketosis-prone diabetes type
  • due to beta-cell loss
  • all intermediary metabolism deranged (lots of metabolic changes
  • insulin therapy should be regarded as the main therapy for T1DM and as physiological treatment with pharmacological agents
  • hypoglycaemia almost inevitable
  • long-term complications can be prevented
  • diabetic ketoacidosis is a severe, acute complication of diabetes

LCRS Year 2 - Endocrinology (21 decks)

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