PBL 3: Understanding your Illness

Question 1

What is Type 1 diabetes?

Answer 1

Autoimmune T cell mediated destruction of the beta cells in the islets of Langerhans resulting in deficient insulin production

Question 2

What is the pathophysiology of type 1 diabetes?

Answer 2

Low insulin due to beta cell destruction = no glucose uptake into the cells so levels remain high in the blood and so are always hyperglycaemic
Always in starvation as no glucose uptake in the cells to use for energy
Glycolysis and gluconeogenesis not inhibited by insulin = hyperglycaemia
Glucagon not inhibited by anything = hyperglycaemia
Fructose-2,6-phosphate inhibited which regulates phospho-fructo-kinase to change fructose-6- phosphate into fructose-2,6, phosphate in glycolysis

Question 3

What are the risk factors of type 1 diabetes?

Answer 3

• 1st degree family history
• identical twins more likely to get it than non-identical twins
• genetic

Question 4

When is the normal onset for T1D?

Answer 4

Young

5-14 years

Question 5

What are some signs and symptoms of T1D?

Answer 5

Dehydration, thirst, tired, fatigue, bet wetting, hunger, increased urination, weight loss

Question 6

What are some common complications of diabetes?

Answer 6

Diabetic retinopathy
Diabetic neuropathy
Renal disease

Question 7

How is T1D treated?

Answer 7

Give insulin injections:

• Humalog
• Glargine

Question 8

What is the difference in types of insulin administrations?

Answer 8

Humalog - fast acting, give 5-10 minutes after a meal

Glargine - long acting, microcrystals, slowly releases insulin over 18-26 hours

Question 9

What are the main complications with being in a hyperglycaemic state?

Answer 9

Severe dehydration
Glycosuria
Hyperosmolarity
Dilutional Hyponatremia

Question 10

Why do you get severe dehydration?

Answer 10

Loss of fluid from the IC space as goes to the ECS where glucose levels are high due to osmosis and lost in urine/vomiting (osmotic diuresis)
Need to replace this fluid loss

Question 11

Why do you get glycosuria?

Answer 11

Excess of glucose saturates transporters in the PCT so doesn’t all get reabsorbed after filtration
Ends up in the urine instead

Question 12

Why do you get hyperosmolarity?

Answer 12

Osmotic diuresis

Water and electrolytes lost in urine

Question 13

Why do you get dilutional hyponatremia?

Answer 13

Low sodium as water is shifted into the ECS from the ICS due to osmosis
Sodium concentration doesn’t actually decrease but more water dilutes it

Question 14

How should T1D be managed?

Answer 14

• don’t starve yourself to decrease glucose levels as body will use your other stores of glucose from liver/muscle/fat and will still be hyperglycaemic whilst losing more weight and muscle wasting
• If vomiting it is important to monitor glucose levels and adjust insulin correctly as this will change
• Stay hydrated as dehydration is severe
• Alcohol will increase make you become hypoglycaemic so be careful
• Managing stress is important as big factor in glucose release due to adrenaline release/cortisol/GH

Question 15

How is T1D diagnosed?

Answer 15

HbA1C
Urine glucose test (asymptomatic vs symptomatic)
Oral glucose test (starvation)
C peptide test (true test to see insulin output)

Question 16

Why is her bicarbonate levels low?

Answer 16

Metabolic acidosis due to ketoacidosis

Question 17

Why is her CO2 low?

Answer 17

Compensation for metabolic acidosis = respiratory alkalosis through hyperventilation blowing off Co2

Question 18

How does ketoacidosis occur?

Answer 18

Low insulin levels means lipolysis is not inhibited and instead hormone sensitive lipase is activated to breakdown TG into FFA and glycerol. FFA got through beta oxidation to form ketone bodies such as acetoacetate and beta-hydroxybutyrate.

High glucagon allows this. Glucagon also turns off supply of pyruvate to Krebs so it is used for ketogenesis instead.

Essentially in a state of prolonged starvation.

Question 19

What are the symptoms/complications of ketoacidosis? How do they occur?

Answer 19

High anion gap
Vomiting (high sodium and potassium due to pancreatitis)
Hyperosmolarity (osmotic diuresis)
Hypokalaemia (K+ pulled out of cells into the blood then into urine to replace H+)
Enzymes become defective (fewer ketones metabolised and conditions worsen)
Hyperventilation/Kussmaul’s breathing (H+ stimulate respiratory centre of the brain causing panting)

Question 20

What is Kussmaul’s breathing?

Answer 20

Depp laboured breathing pattern

Question 21

How is ketoacidosis treated?

Answer 21

IV to replace lost fluid from diuresis/vomiting/sweating (Isotonic saline)
Administer insulin (short acting as want to act straight away)
Give potassium for hypokalaemia
Urinary catheter to drain bladder

Question 22

Why should an isotonic saline be given?

Answer 22

To restore electrolyte balance and osmotic balance

Should not be hypotonic as may cause brain cells to swell

Question 23

How is alcohol metabolised?

Answer 23

By alcohol dehydrogenase

Converts NAD+ to NADH

Question 24

What is the result of alcohol metabolism in diabetes?

Answer 24

Build up of NADH inhibits malate dehydrogenase which is needed to oxidase malate to oxaloacetate in gluconeogenesis

Inhibited gluconeogenesis means you become hypoglycaemic

Get an increase in acetyl-coA so get alcoholic ketoacidosis (worsens problem)

Worsened by lactic acid from drinking