Week 1

Question 1

What is the endocrine system responsible for ?

Answer 1

Maintaining metabolism for growth, development, hemostasis, reproduction, stress. Utilises chemical signals to communicate that maintains homeostasis, produces and stores hormones which when released bind to target cells to illicit a response.

Question 2

Where are the alpha and beta cells located, what are their roles

Answer 2

Location: Pancreas —> pancreatic islets —> cluster of cells —> ( p-p cells, delta cells, beta cells, alpha cells)
Beta: main one that produce hormone insulin. Insulin is release when we have high BGL to reduce it
Alpha: produce hormone glucagon, every time our BGL drops our alpha cells release glucagon to increase BGL

Question 3

What is the function of glucose and insulin in metabolism when there’s high BGL

Answer 3

When we eat we break down foods into glucose to produce ATP.
Glucose travels to small intestine where it is absorbed into blood and increases BGL.
Blood then travels to pancreas to signal beta cells to release insulin = insulin binds to insulin receptors on call membrane, triggers glut4 vesicles to move to cell membrane and to open up cell and allow glucose to enter cells and be used for ATP. Left over glucose is stored in the form of glycogen as insulin signal liver to convert glucose to glycogen. Insulin also inhibits the liver from producing excess glucose - no need to release stored glucose. Insulin also stimulates excess glucose to be converted to triglyceride and stored in adipose tissue.

Question 4

What is the function of glucose and insulin metabolism for low BGL

Answer 4

Reduced BGL in blood goes by the pancreas and stimulates alpha cells to release glucagon. Glucagon stimulates glyconeogenesis (amino acids —> glucose) glycogenolysis (glycogen —> glucose) in liver to release stored glucose.

Question 5

What are non insulin dependent cells ?

Answer 5

RBC, Brain cells, kidney cells, lens of the eye that use a different transport vesicle

Question 6

What is diabetes mellitus

Answer 6

Group of metabolic diseases characterised by hyperglycaemia, due to defects with insulin secretion, insulin action or both

Question 7

Type 1 DM cause, onset, risk factors, age of onset, body weight

Answer 7

Cause: auto immune destruction of beta cells - severe absolute insulin deficiency
Onset of symptoms: sudden
Risk factors: genetics, environmental, drugs, ethnicity
Age of onset: usually <18
Body weight: normal BMI/ thin

Question 8

Type 2 DM cause, onset, risk factors, age of onset, body weight

Answer 8

Cause: insulin resistance at target tissues and relative insulin deficiency, insulin doesn’t work as well as it should + reduced insulin production, decreased beta cell responsiveness
Onset: gradual
Risk factors: non-modifiable are genetics/age, modifiable: obesity, sedentary lifestyle, poor diet, intake>expenditure
Age of onset: usually >40 years
Body weight: usually overweight

Question 9

Type 1 DM clinical manifestations (initial/late), management, acute complications

Answer 9

Initial symptoms: 3 P’s = polyphagia/polyuria/polydipsia. Fatigue/weight loss(no glucose entering/breakdown of fat), polyuria: excess glucose exerted through kidneys, polydipsia: glucose pulls water when excreted, polyphagia: break down glucose stores —> deplete stores cell starve.
Late symptoms: N&V from ketone build up, abdo pain, tachycardia/pnoea, ketones breath, seizure
Management: insulin
Acute complications: diabetic ketoacidosis, hypoglycaemia

Question 10

Type 2 DM clinical manifestations (initial/late), management and acute complications

Answer 10

Initial symptoms: 3 P’s polyphagia, polydipsia, polyuria, fatigue, blurred vision, hyperglycaemia
Late symptoms: repeated infections (hyperglycaemia is conductive to organism growth + damage to BV) poor wound healing, weight change
Management: diet+ exercise, oral hypoglycaemic agents
Acute complications: hyperosmolar hyperglycaemic state, hypoglycaemia

Question 11

Pathophysiology of type 1 DM

Answer 11

1. Genetic/viral causative agent that produces an immune response against beta cells.
2. Beta cell destruction
3. Lack of insulin released
4. Glut 4 are not activated
5. Glucose unable to be take up by cells = hyperglycaemia
6. Release of glucagon as body thinks we aren’t taking it up, liver continues to release = hyperglycaemia

Question 12

Pathophysiology of type 2 DM

Answer 12

Modifiable/non-modifiable causes that create:

1. Increased adipose tissue = increases free fatty acids = chronic inflammation = damage to insulin receptor/binding site
2. Increased insulin resistance at cells = excess glucose produced by liver/muscle = hyperglycaemia
3. Beta cell dysfunction= less insulin produced = hyperglycaemia

Question 13

How is insulin measured

Answer 13

In units: 1ml of insulin = 100 units

Question 14

What are the types of insulin

Answer 14

Rapid acting (novalog) - onset 10-30mins and duration 3-5hrs. Takes immediately prior to eating
Short acting - (actrapid) - onset 30-60mins and duration 6-8 hours. Take 30 min before meal
Intermediate acting - onset 1.5-4 hrs and duration is up to 24hr. Basal
Long acting - onset 1-4 hours and duration is 24 hours. Slow and steady taken 1 or 2 a day
Mixed insulin: short acting with intermediate or rapid acting and intermediate

Question 15

What insulin regimen is the best

Answer 15

One that suits the patients lifestyle/age. Usually basal bolus regime is the best as it best replicates the physiological insulin.

Question 16

Type 2 DM treatment

Answer 16

1. Diet
2. Exercise
3. Closely monitor BGL
4. Oral hypoglycaemic agents (OHA) and or insulin
5. Prevention t and long term complications

Question 17

Types of OHA for type 2 DM and why they might need insulin

Answer 17

Biguanides (metformin) - reduces hepatic release of glucose + reduces intestinal absorption of glucose + improves insulin sensitivity by increasing peripheral uptake
Sulphonylureas (glicazide) - stimulates insulin secretion from beta cells

Insulin: acute stress/illness increasing need for insulin (energy) + OHA become less effective + overtime pancreas unable to produce sufficient insulin + non adherence to diet/exercise can lead to persistent hyperglycaemia

Question 18

Acute complications of type 1 & 2 DM - hypoglycaemia causes/early signs/later signs

Answer 18

Causes: 1. medication overdose 2. Not eating enough carbs/skipping meals 3. Excessive alcohol consumption (doesn’t allow liver to release stored glucose) 4. Excessive exercise 5. Malnutrition
Early signs: BGL < 4mmol/L, sweating, pale, hunger,headache, dizziness (activation of SNS)
Late signs: difficulty concentration, anxiety, seizures, ALOC, coma (brain dysfunction)

Question 19

Examples of fast and slow acting carbohydrates

Answer 19

Fast: glass of orange juice, 1/2 can of fizzy soda, 6-7 jelly beans, 3 tbsp honey
Slow: 1 slice of bread, half. Bowl of cereal, glass of milk. Medium size fruit, 1 pot of yogurt

Question 20

Manage of mild hypoglycaemia vs severe hyperglycaemia

Answer 20

Mild: check BGL, eat fast acting carbs, recheck BGL, follow by slow acting carbs to not have severe drop in BGL
Severe: medical emergency - call help, position patient on side for aspiration, IV dextrose bolus, if no IV access IM glucagon then IV dextrose, once stabilised then follow with slow acting carbs

Question 21

How does hyperglycaemia progress in type 1 & 2 DM

Answer 21

Acutely unwell —> inflammatory process —> body release hormones as a stress mechanism —> causes impaired insulin function/increase glycogenolysis (glucose release by liver) because when unwell you need more energy —> lots of glucose = hyperglycaemia

Question 22

DKA lab markers, early symptoms and later symptoms

Answer 22

Lab markers: BGL > 11mmol/L, ketones present in blood and urine, pH < 7.3, HCO3 < 15mmol/L, K+ and Na+ changes, high serum osmolarity

Early symptoms: fruity breath (ketones), polyuria, polydipsia, increase RR to compensate

Later: all dehydration signs: sunken eyes,tachycardia, fatigue, abdo, N&V

Question 23

Pathophysiology of DKA

Answer 23

1. Absolute/severe relative insulin deficiency
2. Hyperglycaemia
3. Glucsouria, urinary loss of water+electrolytes
4. Dehydration + hypovolemia (water loss)
5. Increased counterregulatory hormones (glucagon, epinephrine) + increase lactate = acidosis
6. Break down fat tissue —> build up of byproduct called ketones that are acidic
7. Acidotic state which worsen dehydration by loosing Na/K = metabolic acidosis
8. Body tries to compensate —> kidneys try to help filter out ketones + use lungs to remove the excess (increase RR to blow off CO2 - acid - sweet breath)

Question 24

Risk factors and management of DKA

Answer 24

Risk factors: new diagnosis, acute stress/illness, omission of insulin, lack of access to medical care
Management: 1. Correct dehydration of fluid to restore BV and cell volume. Not to quick = oedema risk. 2. Reverse ketones: insulin + dextrose infusion. 3. Acid base and electrolyte corrections 4. Regular BGL monitoring, ABG, Na/K, bed rest, FBC, cardiac monitor, treat underlying cause

Question 25

Hyperosmolar hyvperglycemic state lab markers, earlier signs, later signs

Answer 25

Lab markers: BGL > 30mmol/L, ketones can be present/absent, pH > 7.3, HCO3 > 15mmol/L, Na/K changes due to water loss, high serum osmolarity
Earlier signs: polyuria, polydipsia
Later signs: dehydration/electrolyte imbalance, sunken eyes, tachycardia. Dry skin, hypotension, N&V, ALOC

Question 26

HHS pathophysiology

Answer 26

1. Severe hyperglycaemia
2. Glucose lost through urine
3. Osmotic dieresis = dehydration
4. Na>water = hyperosmolarity (blood more concentrated)
5. Body tries to draw water out from cells - further water loss
6. Electrolyte imbalance + hypovolemia + hypotension
7. Impaired tissue perfusion / ALOC / seizure

Question 27

HHS risk factors and management

Answer 27

Risk factors: elderly (reduced thirst), non-compliance/missed doses, poorly controlled diabetes, infection/illness, drugs that deuce insulin
Management: 1. Correction of dehydration slowly to allow fluids to shift back into cells, 2. Reverse hyperglycaemia 3. Acid base/electrolyte corrections, regular BGL monitoring, ABG, cardiac monitoring, treat underlying cause

Question 28

DKA vs HHS

Answer 28

Both hyperglycaemia occurs
DKA: absolute lack of insulin causes breakdown of fat - ketone production as by product = acidosis
HHS: still has insulin just not working effectively, instead of breaking down fat continue to build up BGL = dehydration