Endocrinology Flashcards

1
Q

Define Gylcogenolysis.

A

Breakdown of glycogen to glucose-1-phosphate and glycogen.

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2
Q

Define gluconeogenesis.

A

Transformation of lactate, amino acids and glycerol into glucose.

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3
Q

Define Lipolysis.

A

Hydrolysis of triglycerides into glycerols and fatty acids.

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4
Q

Define ketogenesis.

A

Production of ketones by breakdown of fatty acids and amino acids

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5
Q

Which organ produces insulin?

A

Pancreas

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6
Q

Where is insulin produced?

A

Beta cells in the islets of Langerhans.

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7
Q

State 5 functions of insulin.

A
⬇️ glycogenesis
⬇️ gluconeogenesis
⬇️ lipolysis
⬇️ ketogenesis
⬆️ glucose uptake
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8
Q

Explain the process of insulin secretion.

A
  1. Glucose moves into beta cells via GLUT2 channels
  2. ATP produced
  3. ATP binds to ATP sensitive K+ channel and closes it
  4. K+ ions cannot leave the cell, so it is depolarised
  5. Voltage-gated Ca2+ channels open, allowing Ca2+ ions in
  6. Ca2+ ions bind to insulin secretory granules (containing insulin) causing them to move to the cell membrane and release insulin via exocytosis
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9
Q

Explain the action of insulin.

A
  1. Insulin binds to insulin receptors on muscle and fat cells
  2. Intracellular signalling cascade is triggered
  3. Intracellular GLUT4 vesicles move to the cell membrane
  4. GLUT4 vesicle integrates into cell membrane:
    ⬆️ number of membrane glucose transporters
    ⬆️ rate of glucose facilitated diffusion into the cell
    ⬇️ blood glucose level
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10
Q

By which channels does glucose move into beta cells?

A

GLUT2 channels

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11
Q

By which channels does glucose move into muscle and fat cells?

A

GLUT4 channels

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12
Q

Name 5 effects of reduced insulin levels.

A
⬆️ glycogenolysis
⬆️ gluconeogenesis
⬆️ lipolysis
⬆️ ketogenesis
⬇️ glucose uptake
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13
Q

Define acidosis.

A

A condition in which the blood is too acidic

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14
Q

Define ketoacidosis.

A

Acidosis resulting from increased levels of ketone bodies in the blood

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15
Q

What is the pH of blood in acidosis?

A

pH < 7.35

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16
Q

Define glycogenesis.

A

Pathway which breaks down glucose

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17
Q

Define glycosuria.

A

Presence of glucose or other sugars in urine

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18
Q

Define polyuria.

A

Excessive urination

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19
Q

Define polydipsia.

A

Extreme thirstiness

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20
Q

Are ketones acidic or alkaline?

A

Acidic

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21
Q

Define ketonaemia.

A

Presence of abnormally high ketone concentrations in the blood

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22
Q

Define ketonuria.

A

High levels of ketones in urine

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23
Q

State 3 triggers of diabetic ketoacidosis.

A
  1. Undiagnosed diabetes mellitus
  2. Untreated type 1 diabetes mellitus
  3. Stress of illness or infection
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24
Q

Why does diabetic ketoacidosis occur in type 1 diabetes mellitus but not type 2?

A

Insulin levels in type 2 diabetes mellitus are reduced, but high enough to suppress ketogenesis and lipolysis.

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25
Q

How does low insulin lead to hyperglycaemia?

A
  1. Gluconeogenesis and glycogenolysis are not regulated so new glucose is formed and released into the blood.
  2. Glycolysis is inhibited so glucose molecules remain in the blood and are not broken down.
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26
Q

How does low insulin lead to ketonaemia?

A
  1. Low insulin means lipolysis can occur (especially when the body doesn’t have enough energy, e.g. illness)
  2. Lipolysis releases fatty acids into the blood
  3. Free fatty acids undergo ketogenesis in the liver
  4. Ketone bodies are released into the blood
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27
Q

What is the major cause of diabetic ketoacidosis?

A

Low insulin

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28
Q

What 2 signs is diabetic ketoacidosis characterised by?

A

High blood glucose and high blood ketones

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29
Q

Is CO2 acidic or alkaline?

A

Acidic

30
Q

State 2 ways in which the body responds to high blood acidity.

A
  1. Hyperkalaemia

2. Kussmaul respiration

31
Q

Why does Kussmaul respiration occur in diabetic ketoacidosis?

A
  1. Blood acidity is high due to ketones

2. In an attempt to raise blood pH, the body starts to respire quickly and deeply to remove CO2 from the blood

32
Q

Why does hyperkalaemia occur in diabetic ketoacidosis?

A
  1. Blood acidity is high due to ketones
  2. H+ ions are sent into cells via H+/K+ transporters, so K+ is sent into extracellular fluid
  3. Normally, insulin stimulates the Na+/K+ ATPases which help K+ enter cells, low insulin means this doesn’t happen, so K+ remains outside of cells
  4. Large amounts of K+ ions enter the blood
33
Q

State 4 symptoms of diabetic ketoacidosis.

A
  1. Nausea and vomiting
  2. Rapid weight loss
  3. Drowsiness and confusion
  4. Abdominal pain
34
Q

State 9 signs of diabetic ketoacidosis.

A
  1. Kussmaul’s respiration
  2. Sunken eyes/Reduced tissue turgor/Dry tongue
  3. Polyuria
  4. Polydipsia
  5. Dehydration
  6. Subnormal body temperature
  7. Hypotension
  8. Tachycardia
  9. Breath/Urine smells sweet
35
Q

What 4 investigations should be done to confirm diabetic ketoacidosis?

A
  1. Hyperglycaemia
  2. Ketonaemia
  3. Acidosis
  4. Urine dipstick
36
Q

What is a normal blood glucose level?

A

Approx. 7.8 mmol/L

37
Q

What is considered to be a hyperglycaemic random plasma glucose level?

A

Random plasma glucose > 11 mmol/L

38
Q

If a patient has diabetic ketoacidosis what will their urine dipstick show?

A

Glycosuria and ketonuria

39
Q

What bicarbonate level is considered to be acidosis?

A

Bicarbonate < 15 mmol/L

40
Q

What is considered to be a ketoamaemic plasma ketone level?

A

Plasma ketones > 3 mmol/L

41
Q

What 4 steps should be taken to treat diabetic ketoacidosis?

A
  1. Get bloods for investigation
  2. Administer IV fluids (0.9% saline)
  3. Restore electrolyte balance (K+ especially)
  4. IV insulin
42
Q

State 6 complications of diabetic ketoacidosis.

A
  1. Coma
  2. Cerebral oedema
  3. Thromboembolism
  4. Aspiration pneumonia
  5. Hypothermia
  6. Death
43
Q

State 3 risk factors of a hyperosmolar hyperglycaemic state.

A
  1. Infection
  2. Consumption of glucose rich fluids
  3. Medication
44
Q

How does a hyperosmolar hyperglycaemia state develop in type 2 diabetes mellitus?

A
  1. Insulin levels are high enough to prevent hepatic ketogenesis but do not inhibit hepatic glucose production
  2. Blood glucose increases
  3. Water leaves body cells and enter the blood to reduce the osmolality
  4. Blood vessels full of eater cause increased urination
  5. Cells become dry and shrivelled, causing total body dehydration
45
Q

Define osmotic diuresis.

A

Urination caused by an excess of urinary solute

46
Q

State 6 clinical presentations of a hyperosmolar hyperglycaemic state.

A
  1. Decreased level of consciousness or coma
  2. Severe dehydration
  3. Osmotic diuresis leading to polyuria
  4. Hyperglycaemia
  5. Hyperosmolality
  6. No ketones in blood or urine
47
Q

What causes a hyperosmolar hyperglycaemic state?

A

Uncontrolled type 2 diabetes mellitus

48
Q

What 3 investigations would confirm a hyperosmolar hyperglycaemic state?

A
  1. Hyperglycaemia
  2. Urine dipstick
  3. Plasma osmolality
49
Q

What would a urine dipstick show in a hyperosmolar hyperglycaemic state?

A

Heavy glycosuria

50
Q

Would plasma osmolality be high or low in a hyperosmolar hyperglycaemic state?

A

High

51
Q

State 4 ways to manage a hyperosmolar hyperglycaemic state.

A
  1. Fluid replacement with 0.9% saline
  2. Low molecular weight heparin to reduce the risk of stroke, myocardial infarction, thromboembolism and arterial thrombosis
  3. Restore electrolyte loss
  4. Insulin infusion (at low rate because of increased sensitivity)
52
Q

What is low molecular weight heparin?

A

A class of anticoagulant medication

53
Q

How does a hyperosmolar hyperglycaemic state cause mental status changes?

A

Total body dehydration can cause brain cells to dehydrate

54
Q

Below what level is classed as hypoglycaemia?

A

Plasma glucose < 3 mmol/L

55
Q

What are the most common causes of diabetic hypoglycaemia?

A

Insulin or sulphonylurea mixed with:

  • increased activity
  • missed meal
  • accidental/non-accidental overdose
56
Q

What are the 7 causes on non-diabetic hypoglycaemia?

A
Exogenous drugs
Pituitary insufficiency
Liver failure
Addison’s disease
Islets cell tumour
Immune hypoglycaemia
Non-pancreatic neoplasm
57
Q

State 9 risk factors of hypoglycaemia.

A
  1. Insulin dependent diabetes
  2. Previous history of hypoglycaemic episodes
  3. Lack of hypoglycaemia awareness
  4. Impaired renal function
  5. Dementia/Cognitive dysfunction
  6. Alcohol misuse
  7. Profound starvation
  8. Increased exercise
  9. Food malabsorption issues
58
Q

State 5 autonomic clinical presentations of hypoglycaemia.

A
  1. Trembling
  2. Palpitations
  3. Sweating
  4. Anxiety
  5. Hunger
59
Q

State 9 neurological clinical presentations of hypoglycaemia.

A
  1. Difficulty concentrating
  2. Confusion
  3. Drowsiness
  4. Dizziness
  5. Seizures
  6. Coma
  7. Vision changes
  8. Difficulty speaking
  9. Weakness
60
Q

State 2 non-specific clinical presentations of hypoglycaemia.

A
  1. Nausea

2. Headache

61
Q

If tests for hypoglycaemia show hypoglycaemic hyperinsulinaemia, what could the cause be?

A

Insulinoma
Sulphonylurea or insulin injection
Congenital

62
Q

If blood tests for hypoglycaemia show low insulin and no excess ketones, what could the cause be?

A

Non-pancreatic neoplasms

Anti-insulin receptor antibodies

63
Q

If blood tests for hypoglycaemia show low insulin and increased ketones, what could the causes be?

A

Alcohol
Pituitary insufficiency
Addison’s disease

64
Q

What does a HbA1c value tell you?

A

Average blood glucose level for the past 2 or 3 months

65
Q

Glucagon is secreted by which type of cell?

A

Alpha cell

66
Q

What cells are responsible for thyroid hormone synthesis?

A

Follicular cells

67
Q

True or False: the inferior suprarenal artery is a branch of the renal artery.

A

True

68
Q

True or False: insulin release is part of the homeostatic response to hypoglycaemia.

A

False

69
Q

What major vessel supplies blood to the body and tail of the pancreas?

A

Splenic artery

70
Q

What is parathyroid hormone released in response to?

A

Hypocalcaemia

71
Q

Is inhibition of aldosterone an effect of angiotensin II?

A

No

72
Q

True or False: the zona fasciculata mainly secretes gluocorticoids.

A

True