General MEH Flashcards

1
Q

Where in the pancreas and in what cells are insulin and glucagon produced?

A

Islets of Langerhans
Alpha cells - glucagon
Beta cells - insulin

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2
Q

How many polypeptides is insulin and how many disulphide bonds are there?

A

2 polypeptide chains

3 disulphide bonds

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3
Q

What is the name of the protein that is cleaved from the middle of the insulin polypeptide to create 2 chains? What is its clinical significance?

A

C-peptide
C-peptide is released into the blood in equimolar amounts with mature insulin, so measurement of C-peptide is a good indication of endogenous insulin synthesis in the body.

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4
Q

What amino acids do disulphide bonds form between?

A

Form between 2 thiol groups of cysteine residues.

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5
Q

Which receptors does insulin bind to?

A

Tyrosine-kinase receptors

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6
Q

Which receptors does glucagon bind to?

A

GPCRs (Gs)

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7
Q

How is insulin stored in Beta cells in the pancreas?

A

Stored as crystalline zinc-insulin complex

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8
Q

What are the 3 main tissues in the body that insulin acts on?

A

Liver, skeletal muscle and adipose tissue (as well as being required for normal growth and development of most tissues).

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9
Q

Out of insulin and glucagon, which is anabolic and which is catabolic?

A

Insulin - anabolic

Glucagon - catabolic

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10
Q

What is diabetic ketoacidosis?

A

Lack of insulin body increases lipolysis, and fatty acids are converted to ketone bodies in a process called beta oxidation. The ketone bodies create a metabolic acidosis in the body (bicarbonate system tries to buffer this but eventually can’t) - creates life-threatening condition.

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11
Q

What is the triad of symptoms of diabetes? What causes each symptom?

A

Polyuria - excess glucose in kidney, not all of it can be reabsorbed, increases water loss.
Polydipsia - excess thirst due to water loss.
Weight loss - loss of insulin leads to unopposed glucagon and catabolic effects in the body.

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12
Q

Name some symptoms of diabetic ketoacidosis.

A
Vomiting
Nausea
Abdominal pain
Hyperventilation (to try to compensate for metabolic acidosis)
Dehydration
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13
Q

What are the glucose concentrations that would indicate a diagnosis of diabetes?

A

Venous plasma glucose concentration > 11.1mmol/L
Fasting plasma glucose concentration > 7mmol/L
Plasma glucose concentration > 11.1mmol/L 2 hours after 75g anhydrous glucose in an oral glucose tolerance test.

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14
Q

What does the drug metformin do?

A

Reduces gluconeogenesis.

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15
Q

What do sulphonylureas do?

A

Increase insulin release from remaining beta cells, and reduce insulin resistance.

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16
Q

What are the macroscopic consequences of diabetes/persistent hyperglycaemia?

A

Increased risk of stroke
Increased risk of MI
Poor blood supply to peripheries (especially feet)

17
Q

What are the microvascular complications of diabetes/persistent hyperglycaemia?

A

Diabetic retinopathy
Diabetic nephropathy
Diabetic neuropathy
Diabetic feet

18
Q

What causes the microvascular complications of diabetes?

A

In tissues such as retina, kidneys and peripheral nerves, glucose enters the cell based on [glucose] outside the cell (not insulin), therefore hyperglycaemia leads to increased glucose in the cell, which can damage the cell.

19
Q

What enzyme metabolises glucose?

A

Aldose reductase

20
Q

What is HbA1c? What is its clinical significance?

A

Glycated haemoglobin - produced when glucose in the blood reacts with Hb. The percentage of haemoglobin that is glycated is a good indicator of how effective blood glucose control has been.

21
Q

What is sorbitol?

A

Produced in the breakdown of glucose by aldose reductase (NADPH is used, meaning less protection against oxidative damage).

22
Q

What is Metabolic Syndrome?

A

A group of symptoms including insulin resistance, dyslipidaemia, glucose intolerance and hypertension associated with central adiposity.

23
Q

What are the 3 layers of the adrenal cortex and what does each layer produce?

A

Zona Glomerulosa (outermost) - mineralocorticoids e.g. Aldosterone
Zona Fasiculata - glucorticoids e.g. Cortisol
Zona Reticularis - androgens and some glucocorticoids

24
Q

What is produced in the medulla of the adrenal glands?

A

Adrenaline

Noradrenaline

25
Q

Describe the synthesis of noradrenaline and adrenaline.

A

Tyrosine - dopamine
Dopamine - noradrenaline
Noradrenaline - adrenaline

26
Q

In what cells does the tyrosine-dopamine-noradrenaline-adrenaline pathway occur?

A

Chromaffin cells

27
Q

What ion does aldosterone mainly have control over?

A

Na+

28
Q

What are all the steroid hormones synthesised from?

A

Cholesterol

29
Q

Name the hormones in the hypothalamus-pituitary-adrenal axis for the synthesis of cortisol.

A

Hypothalamus - Corticotropin releasing factor (CRF).
Anterior pituitary - Adrenocorticotropic hormone (ACTHH).
Adrenal cortex - cortisol.

30
Q

How is alpha-MSH related to ACTH?

A

Post-translational processing of POMC produces ACTH and alpha-MSH (alpha-MSH is contained within ACTH).

31
Q

Why do you get hyperpigmentation when there’s an over secretion of ACTH?

A

Due to alpha-MSH activity.

32
Q

What receptor does ACTH bind to?

A

GPCR

33
Q

Which transport protein transports cortisol around the blood (because it is lipophilic)?

A

Transcortin

34
Q

What are the effects of cortisol on the body?

A

Important component of the stress response.

Has catabolic effects on the body (similar to glucagon).