Diabetes Key Points Flashcards

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1
Q

What four hormones can increase blood glucose

A

Glucagon
Cortisol
Epinephrine/adrenaline
Growth hormone

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2
Q

Define diabetes mellitus

A

The term diabetes mellitus describes a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism. Resulting from defects in insulin secretion, insulin action or both.

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3
Q

Define HbA1c

A

‘Long term bloods’

Formed by non-enzymatic attachment of glucose to haemoglobin A

Formed slowly and continuously

Normally less than 42 (6%) but in diabetics it can increase 2-3 times

Can be used diagnostically if over 6.5% or 48mmol/mol

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4
Q

What would indicate impaired fasting glycaemia

A

Fasting glucose equal to or between 6.1 and 7

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5
Q

What would indicate impaired glucose tolerance

A

OGTT between 7.8 and 11.1

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6
Q

Define type 1

A

Autoimmune destruction of pancreatic cells, usually occurs early in life
Characterised by low insulin output, high blood glucose, glucose in urine, excess urine flow, switch to fat metabolism
Treated with insulin injections, careful balance of diet and exercise
10% of diabetics

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7
Q

Define type 2 diabetes

A

Associated with obesity, usually starts later in life.
Insulin may be normal, but is ineffective (insulin resistance)
Many of symptoms the same, but less severe

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8
Q

What conditions may be associated with type 4

A

Genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas (endocrinopathies)
Drug-or chemical induced
Infections
Uncommon forms of immune-mediated diabetes
Other genetic syndromes sometimes associated with diabetes

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9
Q

How does type 1 present

A

Acute with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection

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10
Q

What is the pathophysiology behind type 2

A

A group of metabolic diseases characterised by hyperglycaemia resulting from defects in insulin secretion, insulin action or both

The chronic hyperglycaemia of diabetes is associated with long-term damage, dysfunction and failure of various organs, especially the eyes, kidneys, nerves, heart and blood vessels

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11
Q

How does type 2 present

A

Insidious presentation with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection

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12
Q

What are the three macrovascular complications of diabetes

A

Coronary artery disease (MI)
Cerebrovascular disease (stroke)
Peripheral vascular disease

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13
Q

What are the three microvascular complications of diabetes

A

Retinopathy
Nephropathy
Neuropathy

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14
Q

What are the five complications of poor glycaemic control

A

Neuropathy (nerve damage) -> impotence is commonly a presenting symptom

Cataracts

Kidney damage (nephropathy)

Arthritis -> damage to collagen in joints

Capillary damage -> circulatory defects and damage to retina

Abnormal plasma lipoprotein metabolism -> increased risk of cardiovascular disease

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15
Q

How does diabetes cause cataracts

A

Damage to a-crystallin protein

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16
Q

What are the three mechanisms of damage in hyperglycaemia

A

Glucose is converted to sorbitol by aldose reductase - Sorbitol accumulates in tissues -> disturbs control of intracellular osmotic pressure

Glucose is converted into ketones

Glycation of collagen - stiffening of the collagen in the blood vessel walls leading to high bp

17
Q

Why is ketoacidosis an emergency

A

If a diabetic lets their blood glucose get too high he may develop ketoacidosis, a life-threatening emergency
Most of the problems in ketoacidosis are due to:
- Dehydration (due to excessive urine production)
- Low pH (due to excessive lipid metabolism)
- Large amounts of ketoacids in the blood (also due to excessive lipid metabolism)

18
Q

How is the OGTT interpreted
(2

A

Patient has diabetes if OGTT 2h greater than 11.0 and or a fasting glucose of greater than/equal to 7.0 mmol/L

Patient has IGT if OGTT 2h between 7.8 and 11.1 and a fasting glucose less than 7.0 mmol/L

19
Q

What is fructosamine and how is it measured

A

Fructosamine is a glycation product that forms when glucose binds to proteins1. It measures average blood glucose levels over the past two to three weeks and is used to help manage diabetes

It is an earlier indicator of diabetes control compared to haemoglobin A1c (HbA1c), which measures average blood sugar over the previous two to four months

20
Q

What is microalbuminaemia

A

The excretion of a small amount of albumin in urine

Diabetic nephropathy is a major complication in 35-45% of IDDM which may progress to end stage renal failure

Microalbuminuria is the excretion of 50-200mg albumin in 24 hours

Its detected by sensitive immunoassays (using antibodies directed against human albumin)

Early detection can allow reversal of nephropathy through good glycaemic control, hypotensives and a low protein diet

However once proteinuria has developed then improving glycaemic control may transiently slow down progression but will not reverse it

What are four acute metabolic complications of diabetes mellitus

21
Q

What are four acute metabolic complications of diabetes mellitus

A

Diabetic ketoacidosis (DKA)
Hyperosmolar non-ketotic coma (HNC)
Lactic acidosis (LA)
Hypoglycaemia

22
Q

What cause DKA

A

Altered lipid metabolism
Increased concentrations of total lipids, cholesterol, triglycerides and free fatty acids

Free fatty acids are shunted into ketone body formation due to lack of insulin

The rate of formation of these ketone bodies exceeds the capacity for their peripheral utilisation and renal excretion leading to accumulation of ketoacids and therefore metabolic acidosis

Caused by:
Not enough insulin
Skipping insulin
Stress, trauma
Insulin resistance

23
Q

Symptoms of DKA

A

Dehydration
Acidosis
Hyperosmolality
Diminished cerebral oxygen utilisation
Consciousness becomes impaired
Ultimately patient becomes comatose

24
Q

How does someone present if they have DKA

A

Early manifestations are mild and include vomiting, polyuria and dehydration

More severe cases include Kussmaul respirations (acetone breath)

Abdominal pain or rigidity may be present and mimic acute appendicitis or pancreatitis

Cerebral dehydration and coma ultimately ensure

25
Q

What is a hyperosmolar non-ketotic coma

A

Presence of relative insulin deficiency and hyperglycaemia with associated elevated serum osmolality, dehydration and stupor progressing to coma if uncorrected without the presence of ketosis or acidosis

These patients have sufficient circulating insulin to prevent lipolysis and ketosis

Caused by:
Dehydration
Medications such as steroids and thiazides
Acute illness
Cerebral vascular disease
Advanced age

26
Q

What is lactic acidosi

A

Elevated lactic acid with acidosis and without ketoacidosis

There may be low levels of ketones present

Half of the reported cases of LA have been in diabetics

Rarely seen in diabetic patients particularly since the withdrawal of phenformin from the market

27
Q

What causes LA

A

Hypoxia
Medications such as phenoformin

28
Q

What is hypoglycaemia

A

Common in insulin-treated diabetics and occasionally seen in those treated with oral hypoglycemic sulfonylurea agents

Can range from very mild (3.3 to 3.9) with minimal or no symptoms

To severe (<2.2 mmol/L) where there is neurologic impairment

Associated with insulin therapy, may be related to errors in dosage, delayed or skipped meals, exercise and/or intensity of glycaemic control