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Endocrinology > Diabetes basics > Flashcards

Diabetes basics Flashcards

1
Q

What is diabetes mellitus?

A

An elevation of blood glucose above a diagnostic criteria

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1
Q

What are the 2 mechanisms of diabetes cause?

A

Failure to produce insulin
Sensitivity to insulin

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2
Q

What are some examples of disorders of insulin production?

A

Type I diabetes
Genetic disorders (E.g. MODY, Neonatal diabetes)
Pancreatic disease

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3
Q

What are some examples of disorders of insulin action?

A

Genetic disorders
Insulin reisstance (E.g. T2DM, Obesity, NAFLD)
Endocrinopathies
Steroids

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4
Q

What are some genetic disorders that cause disordered insulin action?

A
  • Donohue sundrome
  • Rabson-Mendenhall syndrome
  • Familial partial lipodystrophy
  • Congenital lipoatrophy
  • Acquired lipoatrophy
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5
Q

What are some endocrinopathies that cause disordered insulin action?

A
  • Cushing’s syndrome
  • Acromegaly
  • Pheochromocytoma
  • Glucagonoma
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6
Q

What is the average blood glucose concentration?

A

5mmol/L

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7
Q

What is the fasting glucose threshold for diabetes diagnosis?

A

≥7mmol/L

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8
Q

What is the 2hr plasma glucose threshold for diabetes diagnosis?

A

≥11.1mmol/L

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9
Q

What is the HbA1c threshold for diabetes diagnosis?

A

≥48mmol/mol

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10
Q

How are the thresholds for diabetes diagnosis formed?

A

Based on risk of developing diabetic retinopathy

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11
Q

How are 2hr plasma glucose levels measured?

A

Having the patient drink a 75g oral glucose dose and waiting 2 hours before testing blood sugar

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12
Q

What is pre-diabetes?

A

This is the name given to impaired glucose tolerance, before the development of diabetes

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13
Q

What fasting plasma glucose is defined as pre-diabetic?

A

6.1 - 6.9 mmol/L

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14
Q

What 2hr plasma glucose is defined as pre-diabetic?

A

7.8 - 11 mmol/L

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15
Q

What HbA1c is defined as pre-diabetic?

A

6 - 6.4% or 42 - 47 mmol/mol

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16
Q

What is shown by C-peptide levels?

A

How much insulin the body is producing, even with exogenous insulin injections, as it is cleaved from insulin during its production

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17
Q

Why is measuring blood glucose at a single time not effective in diagnosing diabetes?

A

Blood glucose varies widely in response to meals and exercise throughout the day

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18
Q

What are the 2 ways to gain an accurate measure of long-term blood glucose changes?

A

HbA1c
Continuous glucose monitoring

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19
Q

How does continuous glucose monitoring work?

A

This involves continuous monitoring of glucose throughout many points during the day using a device in the arm (e.g. Free style libre)

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20
Q

What is HbA1c?

A

Glycated haemoglobin (Glucose in the blood is absorbed into erythrocytes and binds to haemoglobin)

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21
Q

What time-frame can HbA1c show glucose levels over?

A

Around 2-3 months, as this is the lifespan of a red blood cell

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22
Q

In what condition will HbA1c measurement not be useful or accurate?

A

Conditions with high red blood turnover such as haemolytic anaemia

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23
Q

Where is insulin produced?

A

In the RER of pancreatic ß-cells

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24
Q

Describe the formation of insulin

A

It is synthesised in the RER of pancreatic ß-cells as a larger, single chain pre-hormone called pre-proinsulin

This is then cleaved by Ca2+ dependant endopeptidases, PC2 and PC3 into insulin and C-peptide

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25
Q

Describe the release of insulin

A
  1. Glucose enters cell via GLUT2
  2. Increases glucokinase activity (Oxidation)
  3. Increased ATP release
  4. Closure of ATP-dependant K+ channels
  5. Build up of K+ in the cell
  6. Depolarisation of the membrane
  7. Opening of V-gated Ca2+ channels
  8. Ca2+ allows for release of insulin
26
Q

What are the 2 peaks of insulin release?

A

1st phase in which there is a release of insulin immediately from the readily releasable pool (RRP)

2nd phase caused by preparatory action to produce more insulin

27
Q

What are some other molecules that ß-cells can respond to with insulin production?

A

Nutrients, hormones, neurotransmitters, including leptin, GLP1, GIP, IL6, adiponectin and fatty acids

28
Q

What is the region in the pancreas responsible for blood glucose control?

A

Islets of Langherans

29
Q

What are the 5 main cells of the Islets of Langerhans?

A
  • a-cells (10-20%)
  • ß-cells (60-80%)
  • ∂-cells (5%)
  • PP-cells (<1%)
  • e-cells
30
Q

What is secreted by a-cells in the pancreas?

A

Glucagon

31
Q

What is secreted by ß-cells in the pancreas?

A

Insulin

32
Q

What is secreted by ∂-cells in the pancreas?

A

Somatostatin

33
Q

What is secreted by PP-cells in the pancreas?

A

Pancreatic polypeptide

34
Q

What is secreted by e-cells in the pancreas?

A

Ghrelin

35
Q

What is meant by exocrine secretion?

A

Release of secretions into ducts

36
Q

What is meant by endocrine secretion?

A

Release of secretions into the blood

37
Q

What is meant by paracrine secretion?

A

Release of secretions into neighbouring cells

38
Q

What is meant by autocrine secretion?

A

Release of secretions into the same cell (Itself)

39
Q

What is meant by juxtacrine secretion?

A

Release of secretions onto the cell surface as a receptor

40
Q

What is secreted when BCG increases?

A

Insulin

41
Q

What is secreted when BCG decreases?

A

Glucagon

42
Q

What are some of the functions of insulin?

A

Inhibits gluconeogenesis in the liver
Promotes glycogenesis in muscle, liver and adipose tissue

43
Q

What are some of the functions of glucagon?

A

Increased gluconeogenesis
Stimulation of lipolysis (Fat breakdown)

44
Q

How does exercise cause increased lipolysis and glucose production

A

Exercise leads to production of adrenaline and cortisol, which cause glucagon release from the pancreas

45
Q

How is glucagon formed?

A

The glucagon gene is one gene but codes for many hormones forming pre-proglucagon

This can then be cleaved into a number of hormones, depending on where it is cleaved

This depends on which enzyme is cleaving it, either PSCK2 or PCSK1

46
Q

How is glucagon secreted?

A
  1. Glucose enters cell via GLUT2
  2. Increases glucokinase activity (Oxidation)
  3. Increased ATP release
  4. Closure of ATP-dependant K+ channels and opening of Na+ channels
  5. No depolarisation of the membrane
  6. Closure of V-gated Ca2+ channels
  7. No secretion of glucagon
  8. Lower glucose, means less opening of Na+ channels so depolarisation means secretion of glucagon
47
Q

What is meant by insulin resistance?

A

The reduced ability to respond to physiological insulin levels

48
Q

What are some causes of insulin resistance?

A

Obesity
Excess caloric intake
Sedentary lifestyle
Genetic conditions

49
Q

What are some diseases that can occur as a result of insulin resistance?

A
  • Diabetes
  • Hypertension
  • Neurodegenerative disease
  • Liver disease
  • Sleep apnoea
  • Acne
  • Polycystic ovarian disease
  • Cancer
  • Hyperlipidaemia
50
Q

How can insulin resistance lead to impaired memory in Alzheimer’s disease?

A

Insulin signalling in the brain is responsible for synaptic plasticity and thus memory, therefore insulin resistance can lead to synaptic dysfunction

51
Q

What are some risk factor for developing insulin resistance?

A
  • Physically inactive
  • FHx of diabetes
  • Genetics
  • Race (African Americans, Hispanic/Latinos)
  • PCOS
  • Gestational diabetes
  • High blood pressure
  • Low HDL
  • High blood triglyceride
  • Heart disease
  • Smoking
52
Q

How does skeletal muscle insulin resistance occur?

A

In insulin resistant patients, skeletal muscle insulin receptors undergo decrease in tyrosine kinase activity

This causes a decrease in IRS1, PI3K and AKT phosphorylation, leading to a decrease in glycogen synthesis and a decrease in GLUT4 translocation, meaning less glucose is taken into the cell and even less is stored as glycogen

53
Q

How does adipose and muscle tissue insulin resistance occur?

A

Obesity-induced inflammation occurs with JNK and NF-kB activation in adipocytes, causing release of pro-inflammatory cytokines and free fatty acids, leading to local insulin resistance of the adipose tissue, and systemic inflammation of the skeletal muscle and liver

Inflammation leads to increased collagen levels on the cell membrane, with increased extra-cellular matrix receptor signalling, resulting in muscle insulin resistance

54
Q

How does hepatic insulin resistance occur?

A

In hepatic insulin resistance, there is a decrease in uptake of glucose, leading to lower levels of glycogenesis

Increased FFA and glycerol, means more is available in the liver fr gluconeogenesis (Formation of more glucose), as well as release of VLDL, therefore causing hyperglycaemia and hyperlipidaemia

55
Q

What are some ways in which insulin resistance can be reversed?

A
  • Eating less
  • Moving more
  • Medication
56
Q

How is insulin resistance measured?

A

Hyperinsulinaemic-eugycaemic clamp

57
Q

What is another name for Donoghue syndrome?

A

Leprechaunism

58
Q

Describe the genetics of Donoghue syndrome

A

Rare autosomal genetic trait involving mutations in the insulin receptor

59
Q

How does Donoghue syndrome present?

A

Severe insulin resistance
Developmental abnormalities:
- Growth retardation
- Abscence of SC fat

60
Q

Is Rabson Medenhall sydrome autosomal dominant or recessive?

A

Autosomal recessive

61
Q

How does Rabson Medenhall syndrome present?

A

Severe insulin resistance
Hyperglycaemia
Compensatory hyperinsulinaemia
Developmental abnormalities
Acanthosis nigricans

62
Q
A

Endocrinology (42 decks)

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