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Endo > T1DM > Flashcards

T1DM 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 (MODY)

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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

Why is there ambiguity in the diagnosis of T1DM?

A

Diseases like LADA and MODY present later than typical T1DM, and MODY can phenotypically resemble T2DM.

T2DM in youth and keto acidosis in T2DM are also rising.

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5
Q

Broadly what are the mechanism of T1 and T2 diabetes?

A

T1DM - AI Beta cell destruction (requires environmental trigger and genetic predisposition)

T2DM - Insulin resistance followed by Beta destruction (has larger genetic component than T1)

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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

How does the pathology of T1DM effect insulin and C-peptide levels?

A

Gradual AI destruction of beta cells leads to decline in insulin (and C-peptide) First phase insulin lost early.

There will be eventual destruction of all beta cells, however it is ‘relapsing-remitting’ as 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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8
Q

What is the relevance of T1DM’s autoimmune basis?

A

Increases risk of other AI diseases
Increases risk in family members
Auto antibodies useful clinically
Immune modultion may offer novel treatment

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9
Q

What are the histological features of T1DM?

A

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

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10
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

Found on the HLA in chromosome 6

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11
Q

What are some ‘diabetes markers’ and their relevance?

A

Markers most not needed but can improve certainty in diagnosis
Common:

ICA (Islet cell antibodies)

GADA (Glutamic acid decarboxylase)

Rare:

IAA (Insulin antibodies)

IA-2A (Insulinoma-associated-2-auto antibodies)-receptor like family

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12
Q

What are some symptoms of T1DM?

A 
polyuria 
polydipsia 
blurred vision from hyperglycaemia 
thrush or other vaginal infections 
weight loss 
fatigue
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13
Q

What are the signs of T1DM?

A 
Dehydration 
Cachexia (wasting)
Hyperventilation (kussmaul breathing) 
Smell of ketones 
Glycosuria 
Ketonuria
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14
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 (Product of triglycerade break down)

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15
Q

What does insulin have a positive effect on?

A

Glucose uptake by tissues

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16
Q

State 4 other hormones that increase hepatic glucose output.

A

Catecholamines
Cortisol
Growth Hormone
Glucagon

17
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.

18
Q

State some complications of T1DM.

A

ACUTE:
Hypoglycaemia
Metabolic acidosis (Acetoacetone and Hydroxybutyrate circulate)

CHRONIC:
Neuropathy 
Nephropathy 
Retinopathy 
Vascular Disease
19
Q

What is the main treatment for T1DM?

A

Exogenous insulin

20
Q

Describe the dietary changes that are recommended in T1DM.

A

Decreased fat
Decreased refined carbohydrates
Increased complex carbohydrates
Increased soluble fibre

21
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

22
Q

State three forms of insulin that are given with meals.

A

Lipsro
Aspart
Glulisine

23
Q

Describe the features of background insulin.

A

Long-acting Non-C bound to zinc or protamine

24
Q

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

A

Glargine
Detemir
Degludec

25
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

26
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.

27
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)

28
Q

What is HbA1c level used to gauge?

A

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

29
Q

What HbA1c level are T1DM patients aiming for?

A

< 7%

30
Q

When might the HbA1c level not be accurate?

A

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

31
Q

Define hypoglycaemia.

A

Blood glucose < 3.6 mmol/L

Severe hypoglycaemia is any level where the patient needs someone else to treat it because they cannot themselves

32
Q

What can recurrent hypos result in?

A

Loss of warning (hypoglycaemia unawareness) This can lead to poor glycaemic control

33
Q

What can trigger a hypo?

A

Unaccustomed exercise
Missed meals
Inadequate snacks
Alcohol (may make you unaware of hypo symptoms) Inappropriate insulin regime

Due to these hypos are most common pre-lunch and during sleep.

34
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
35
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 (17 decks)

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