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ENDO- OBG > Pathophysiology and Treatment of Type I Diabetes Mellitus > Flashcards

Pathophysiology and Treatment of Type I Diabetes Mellitus Flashcards

1
Q

Name a form of type I diabetes that presents late.

A

Latent Autoimmune Diabetes in Adults (LADA)

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2
Q

State two monogenic causes of diabetes.

A

Mitochondrial Diabetes

Maturity Onset Diabetes of the Young

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3
Q

Diabetes can also present with endocrine diseases. Name three endocrine diseases that are associated with diabetes.

A

Phaeochromocytoma

Cushing’s Syndrome

Acromegaly

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4
Q

What conditions and triggers are required for the onset of type 1 diabetes mellitus?

A

Environmental trigger in the presence of a genetic predisposition –> autoimmune attack of islet cells

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5
Q

Which type of diabetes has a bigger genetic component?

A

Type 2 Diabetes Mellitus

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6
Q

What can be measured in the blood to give an indication of insulin function?

A

C-peptide

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7
Q

Describe the pathogenesis of T1DM.

A

You get gradual autoimmune destruction of beta cells resulting in gradually reducing levels of insulin (and C-peptide)

One of the first signs will be the loss of first phase insulin
There will be eventual destruction of all beta cells

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8
Q

Why is T1DM described as a ‘relapsing-remitting’ disease?

A

Over time the beta cell mass appears to reduce, then stabilise, then reduce again

There is a theory that this is due to the imbalance in effector T-cells and regulatory T-cells

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9
Q

What is the importance of the autoimmune basis of T1DM?

A

Increased prevalence of other autoimmune diseases (e.g. rheumatoid arthritis, thyroid disease)

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10
Q

What are the histological features of T1DM?

A

Lymphocyte infiltration of beta cells (which destroys the beta cells)

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11
Q

On which chromosome is the HLA found?

A

Chromosome 6

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12
Q

Which alleles convey a risk of diabetes? Which of these alleles is associated with the most significant risk?

A

DR alleles

DR3 and DR4 = significant risk

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13
Q

What are the two most significant markers of diabetes?

A

Islet Cell Antibodies (ICA)

Glutamic Acid Decarboxylase Antibodies (GADA)

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14
Q

State some symptoms of T1DM.

A

Polyuria

Nocturia

Polydipsia

Blurring of vision

Thrush (due to increased risk of infection)

Weight loss

Fatigue

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15
Q

What are the signs of T1DM?

A

Dehydration

Cachexia

Hyperventilation (kussmaul breathing)

Smell of ketones

Glycosuria

Ketonuria

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16
Q

What are the triglycerides in adipocytes broken down to?

A

Glycerol

Fatty Acids

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17
Q

What does insulin have a negative effect on?

A

Hepatic glucose output (HGO)

Protein breakdown in muscle

Ketone body generation by the liver

Glycerol release from the fat cells

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18
Q

What does insulin have a positive effect on?

A

Glucose uptake by tissues

19
Q

State 4 other hormones that increase hepatic glucose output.

A

Catecholamines

Cortisol

Growth Hormone

Glucagon

20
Q

Describe how insulin deficiency leads to diabetic ketoacidosis (DKA).

A

Insulin has a suppressive effect on hepatic ketone body generation.

In insulin deficiency, fatty acids from the breakdown of triglycerides, travel to the liver where they are used to produce ketone bodies.

21
Q

What is a defining feature of insulin deficiency?

A

Ketone Bodies

NOTE: some cases of T2DM can also get DKA but this is mainly a complication of T1DM

22
Q

State some long-term complications of T1DM.

A

Neuropathy

Nephropathy

Retinopathy

Vascular Disease

23
Q

What is the main treatment for T1DM?

A

Exogenous insulin

24
Q

Describe the dietary changes that are recommended in T1DM.

A

Decreased fat

Decreased refined carbohydrates

Increased complex carbohydrates

Increased soluble fibre

25
Q

Describe the features of the insulin that is given with meals.

A

Short-acting

Human Insulin

Insulin analogues are genetically engineered to mimic normal physiology

26
Q

State three forms of insulin that are given with meals.

A

Lipsro

Aspart

Glulisine

27
Q

Describe the features of background insulin.

A

Long-acting

Non-C bound to zinc or protamine

28
Q

State three forms of insulin that is given as background insulin.

A

Glargine

Detemir

Degludec

29
Q

What do insulin pumps do?

A

Continuous insulin delivery

There are pre-programmed basal rates and boluses for meals

But these DO NOT measure blood glucose so the feedback loop isn’t complete

30
Q

Describe the use of islet cell transplants.

A

Islet cells can be harvested from donors and injected into the liver of a patient with diabetes

They must be on immunosuppressants for life

31
Q

How is capillary monitoring done and what does it give a measure of?

A

Prick the finger and test the blood drawn

It is a measure of venous blood glucose

NOTE: you can also get continuous monitors, which aren’t as accurate (need to be calibrated with capillary glucose)

32
Q

What is HbA1c level used to gage?

A

Glycaemic control over the past 3 months (red cell life span = 120 days)

33
Q

What HbA1c level are T1DM patients aiming for?

A

< 7%

34
Q

When might the HbA1c level not be accurate?

A

In any case of increased haemoglobin turnover e.g. haemolytic anaemia and haemoglobinopathies

35
Q

What are the main acute complications of T1DM?

A

Hypoglycaemia

Metabolic acidosis

36
Q

What are the two main ketones that circulate in metabolic acidosis caused by T1DM?

A

Acetoacetone

Hydroxybutyrate

37
Q

Define hypoglycaemia.

A

Blood glucose < 3.6 mmol/L

38
Q

Define severe hypoglycaemia.

A

Any level of hypoglycaemia that requires another person to treat it

39
Q

What can recurrent hypos result in?

A

Loss of warning (hypoglycaemia unawareness)

This can lead to poor glycaemic control

40
Q

At what times during the day do hypos tend to happen?

A

Pre-lunch

Nocturna

41
Q

What can trigger a hypo?

A

Unaccustomed exercise

Missed meals

Inadequate snacks

Alcohol (may make you unaware of hypo symptoms)

Inappropriate insulin regime

42
Q

State some signs and symptoms of hypoglycaemia.

A 
Signs and symptoms are due to increased sympathetic activity and due to impaired CNS function  
Palpitations  
Tremor  
Sweating  
Pallor/cold extremities 
Anxiety  
Drowsiness 
Confusion
Altered behaviour  
Focal neurology  
Coma
43
Q

How is hypoglycaemia treated?

A

Oral glucose

Complex carbohydrate (to maintain blood glucose after initial treatment)

Parenteral – if consciousness impaired
 IV dextrose (e.g. 10% glucose infusion)
 1 mg glucagon IM

ENDO- OBG (17 decks)

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