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YR2: Endocrinology > 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 2 monogenic causes of diabetes that may present phenotypically as T1/T2

A

Mitochondrial Diabetes

Maturity Onset Diabetes of the Young

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3
Q

Diabetes can also present with endocrine diseases. Name 3 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 leads to autoimmune attack of islet cells, resulting insulin + hyperglycaemia

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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

Gradual AI destruction of B cells resulting in gradually reducing levels of insulin (+ C-peptide)
An early sign = loss of 1st phase insulin
Eventually there is destruction of all B 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 AI diseases (e.g. rheumatoid arthritis, thyroid disease)
Increased risk of AI in relatives
More complete destruction of B cells

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10
Q

What are the histological features of T1DM?

A

Lymphocyte infiltration + destruction of B-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 + DR4 = significant risk

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13
Q

What are the 2 most significant markers of diabetes?

A

Islet Cell Antibodies (ICA)

Glutamic Acid Decarboxylase Antibodies (GADA)

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14
Q

State 2 antibody markers of diabetes that are not used in clinical practice?

A 
Insulin Autoantibodies (IAA) 
Insulinoma-associated-2 autoantibodies (IA-2A)- receptor like family
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15
Q

State 7 symptoms of T1DM.

A 
Polyuria 
Nocturia 
Polydipsia 
Blurring of vision  
Thrush (due to increased risk of infection) 
Weight loss 
Fatigue
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16
Q

What are 6 signs of T1DM?

A 
Dehydration 
Cachexia 
Hyperventilation (kussmaul breathing) 
Smell of ketones  
Glycosuria 
Ketonuria
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17
Q

What are the triglycerides in adipocytes broken down to?

A

Glycerol

Fatty Acids

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18
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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19
Q

What does insulin have a positive effect on?

A

Glucose uptake by tissues

20
Q

State 4 hormones that increase hepatic glucose output.

A

Catecholamines
Cortisol
Growth Hormone
Glucagon

21
Q

Describe how insulin deficiency leads to diabetic ketoacidosis (DKA). Why do DKA patients hyperventilate?

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.
Bicarbonate levels very low, as part of compensation they blow off lots of CO2

22
Q

What is a defining feature of insulin deficiency?

A 
Ketone Bodies  
(some cases of T2DM also get DKA but this is mainly a complication of T1DM)
23
Q

State 4 long-term complications of T1DM.

A

Neuropathy
Nephropathy
Retinopathy
Vascular Disease

24
Q

What is the main treatment for T1DM?

A

Exogenous insulin

25
Q

Describe 5 dietary changes recommended in T1DM.

A 
Decreased fat  
Decreased refined carbohydrates  
Increased complex carbohydrates  
Increased soluble fibre
Balanced distribution of food over course of day
26
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

27
Q

When are the following drugs given:
Lipsro
Aspart
Glulisine

A

With meals

28
Q

Describe the features of background insulin.

A

Long-acting

Non-C bound to zinc or protamine

29
Q

What type of insulin do the following drugs provide:
Glargine
Determir
Degludec

A

Background insulin

30
Q

What do insulin pumps do?

A

Continuous insulin delivery
Pre-programmed basal rates + boluses for meals
DO NOT measure blood glucose so the feedback loop isn’t complete

31
Q

Describe the use of islet cell transplants.

A

Islet cells harvested from donors + injected into the liver of a patient with diabetes
They must be on immunosuppressants for life

32
Q

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

A

Finger prick + test the blood drawn

It is a measure of capillary blood glucose

33
Q

What is HbA1c level used to gage?

A

Glycaemic control over the past 3 months

RBC life span = 120 days

34
Q

What HbA1c level are T1DM patients aiming for?

A

< 6.5%

35
Q

When might the HbA1c level not be accurate?

A

In cases of increased haemoglobin turnover e.g. haemolytic anaemia + haemoglobinopathies

36
Q

What are the main acute complications of T1DM?

A 
Hyperglycaemia (Reduced tissue glucose utilisation +increased HGO)
Metabolic acidosis (Osmotic dehydration + poor tissue perfusion)
37
Q

What are the 2 main ketones that circulate in metabolic acidosis caused by T1DM?

A

Acetoacetone

Hydroxybutyrate

38
Q

DKA tends to be in patients with T1DM, however, some subsets of T2DM also get ketoacidosis. What are these subsets?

A

Black and Asian patients with T2DM

May be due to pancreatic insufficiency at a time of stress

39
Q

Define hypoglycaemia.

A

Blood glucose < 3.6 mmol/L

40
Q

Define severe hypoglycaemia.

A

Any level of hypoglycaemia requiring another person to treat it

41
Q

What can recurrent hypos result in?

A

Loss of warning (hypoglycaemia unawareness)

This can lead to poor glycaemic control

42
Q

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

A

Pre-lunch

Nocturnal

43
Q

What can trigger a hypo?

A 
Unaccustomed exercise  
Missed meals  
Inadequate snacks 
Alcohol (may make you unaware of hypo symptoms) 
Inappropriate insulin regime
44
Q

State 5 signs and symptoms of hypoglycaemia due to increased autonomic activation

A 
Palpitations (tachycardia)
Tremor  
Sweating  
Pallor/ cold extremities 
Anxiety
45
Q

How is hypoglycaemia treated?

A 
Oral glucose  
Complex carbohydrate (to maintain BG after initial treatment) 
Parenteral (if consciousness impaired)
IV dextrose (e.g. 10% glucose infusion)
1 mg glucagon IM
46
Q

What do continuous glucose monitoring devices measure?

A

Glucose levels in interstitial fluid

Indicate pattern of increase/ decrease

47
Q

State 5 signs and symptoms of hypoglycaemia due to impaired CNS function

A 
Drowsiness 
Confusion
Altered behaviour  
Focal neurology  
Coma

YR2: Endocrinology (19 decks)

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