Week 7 - Hypoglycaemia

Question 1

1. Explain the pathophysiology of Type 1 Diabetes:

Answer 1

• Autoimmune destruction of pancreatic beta cells that produces absolute deficiency in insulin production
• Peak incidence between 9 months and 14 years
• Patients require insulin injections

Question 2

2. Explain the pathophysiology of Type 2 Diabetes:

Answer 2

• Associated with insulin resistance, may initially have increased plasma insulin levels
• Obesity decreases the relative number of insulin receptors on target cells, insulin released by less effective

Question 3

3. What are the risk factors for Gestational Diabetes?

Answer 3

• > 30 years of age
• Family Hx of T2DM
• Overweight
• ATSI background
• Vietnamese, Chinese, Middle Eastern, Polynesian
• GDM during previous pregnancy
  Complicates 4% of pregnancies

Question 4

4. Explain the pathophysiology of Hypoglycaemia-associated autonomic failure (HAAF):

Answer 4

• Decrease in adrenaline release and sympathetic responses, resulting in defective glucose counter-regulation and patients are unaware of hypoglycaemia
• Recent episodes of hypoglycaemia can worsen HAAF
• Cardiovascular implications including reduced baroreflex sensitivity - predisposing patients to ventricular arrhythmias

Question 5

5. Explain the pathophysiology of Diabetic Ketoacidosis:

Answer 5

• Lack of insulin results in increase BGL - fatty acids are released from adipose tissue - unsuppressed lipase activity of triglyceride breakdown
• Metabolic breakdown of stored fat results in build up of ketones
• Increased accumulation of keto acids results in low blood pH

Question 6

6. Explain the pathophysiology of Hyperosmolar Hyperglycaemic state (HHS):

Answer 6

• Hyperglycaemia develops but not enough to promote metabolism of fatty acids, no production of ketones
• Excessive diuresis results in severe hyperosmolarity and dehydration
• Precipitated by increased resistance to effect of insulin, excessive carbohydrate intake

Question 7

7. What is the function and cellular action of Insulin?

Answer 7

• Essential role in carbohydrate, fat and protein metabolism
• Release stimulated by increase in BGL
• Facilitates diffusion of carbohydrates into cells
• Causes excess carb to be stored as glycogen, mainly in liver and skeletal muscle
• Activates membrane receptors on target cells causing most body cells to become permeable to glucose
• Inhibits gluconeogenesis and the release of fat from adipose tissue
• Lack of insulin causes fat breakdown, which is used as primary source of energy

Question 8

8. What is the function and cellular action of Glucagon?

Answer 8

• Rapidly converts liver glycogen to glucose
• Increases gluconeogenesis
• Released in response to decreasing BGLs

Question 9

9. What are the S/S for Hypoglycaemia?

Answer 9

• Autonomic clinical finding: hunger, tremor, anxiety, palpitations, sweating, pallor, pupil dilation
• CNS clinical finding: headache, irritability, confusion, ataxia, seizures, coma, brain damage-death

Question 10

10. What are the s/s of DKA?

Answer 10

• Tachycardia
• Hypotension - severe dehydration
• Hyperventilation - Kussmaul’s
• Frequent vomiting
• Polyuria
• Polydipsia - thirst
• Fatigue
• Acetone detected on breath
• BSL > 13

Question 11

11. What are the key features and s/s of HHS?

Answer 11

• More common among Type 2 diabetics (elderly) - high mortality
• No hyperventilation
• Significant dehydration
• Can mimic a stroke

Question 12

12. What hormones do the following cells produce:
    - Alpha cells
    - Beta cells
    - Delta cells

Answer 12

• Alpha cells - glucagon
• Beta cells - insulin
• Delta cells - somatostatin (inhibits insulin and glucagon secretion)
  alphabetical order

Question 13

13. What are some complications of Diabetes Mellitus?

Answer 13

• Arterioles hardening
• Capillary - basement membrane thickens leading to diffusion
• Arteries - deposits - stroke and MI
• Diabetic retinopathy - blindness
• Kidney damage - dialysis
• Peripheral neuropathy - ulcers