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2a- Endocrinology > Intro to diabetes > Flashcards

Intro to diabetes Flashcards

1
Q

What happens in the fasting state?

A
  • Glycolysis
  • Gluconeogenesis
    • Glucose delivered to insulin
      independent tissues, brain and
      RBCs
  • Insulin ↓
  • Muscles use FFA
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2
Q

What happens after feeding?

A
  • Rising glucose (5-10 min after eating) stimulates insulin secretion and suppresses glucagon
  • 40% of ingested glucose goes to liver and 60% to periphery, mostly muscle
  • Ingested glucose helps to replenish glycogen stores both in liver and muscle
  • High insulin and glucose levels suppress lipolysis and levels of non-esterified fatty acids (NEFA or FFA) fall
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3
Q

What occurs in between alpha and beta cells in islets of langerhan?

A

Paracrine ‘cross talk’
Local insulin release inhibits glucagon, effect lost in diabetes

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4
Q

Describe the steps of insulin secretion by beta cells

A
  1. Glucose enters cell by GLUT-2 transporter
  2. Glucose either aerobically respired to produce ATP or converted into glycogen by glucokinase
  3. ATP binds to K+ channels, K+ channel closes (some K+ leave passively)
  4. Depolarisation of cell membrane
  5. VG Ca2+ channel open, Ca2+ influx
  6. Insulin vesicles fuse with membrane and are released
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5
Q

Describe the steps of insulin action in muscle and fat cells

A
  1. Insulin binds to receptor
  2. Intracellular signalling cascades causing intracellular GLUT4 vesicles to move to membrane
  3. Glucose can enter cells through GLUT4
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6
Q

What are the roles of insulin?

A
  • Supresses hepatic glucose output:
    • Glycogenolysis
    • Gluconeogenesis
  • Increases glucose uptake into insulin sensitive tissues (muscle, fat)
  • Suppresses
    • Lipolysis
    • Breakdown of muscle
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7
Q

What are the roles of glucagon?

A
  • Increases hepatic glucose output
    • Glycogenolysis
    • Gluconeogenesis
  • Reduce peripheral glucose uptake
  • Stimulate peripheral release of gluconeogenic precursors (glycerol, AAs)
    • Lipolysis
    • Muscle glycogenolysis and breakdown
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8
Q

What are other counterregulatory hormones to insulin?

A

adrenaline, cortisol, growth hormone

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9
Q

What is diabetes mellitus?

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia

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10
Q

How can diabetes mellitus cause morbidity and mortality?

A
  • Acute hyperglycaemia which if untreated leads to acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State)
  • Chronic hyperglycaemia leading to tissue complications (macrovascular and microvascular)
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11
Q

What are macrovascular tissue complications that chronic hyperglycaemia can cause?

A

heart, brain, nerves affected→ can lead to stroke, CVD, amputations

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12
Q

What are microvascular tissue complications that chronic hyperglycaemia can cause?

A

Blindness, end stage renal disease

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13
Q

Which type of diabetes is gestational and medication induced diabetes a part of?

A

Type 2

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14
Q

What is diabetes defined as?

A
  • Symptoms and random plasma glucose > 11 mmol/l
  • Fasting plasma glucose > 7 mmol/l
  • No symptoms - GTT (75g glucose test) fasting > 7 or 2h value > 11 mmol/l (repeated on 2 occasions)
  • HbA1c of > 48mmol/mol (6.5%)
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15
Q

Describe the pathogenesis of type 1 diabetes

A

An insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction

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16
Q

What happens due to the failure of insulin secretion?

A
  • Continued breakdown of liver glycogen
  • Unrestrained lipolysis and skeletal muscle breakdown providing gluconeogenic precursors
  • Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake
17
Q

What is the renal threshold of glucose concentration before there is urinary glucose losses?

A

10mM

18
Q

What does failure to treat no insulin lead to?

A
  • Increase in circulating glucagon (loss of local increases in insulin within the islets leads to removal of inhibition of glucagon release), further increasing glucose
  • perceived ‘stress’ leads to increased cortisol and adrenaline
  • progressive catabolic state and increasing levels of ketones
19
Q

Describe the pathogenesis of type 2 diabetes

A

Insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

20
Q

What does impaired insulin action lead to?

A
  • Reduced muscle and fat uptake after eating
  • Failure to suppress lipolysis and high circulating FFAs
  • Abnormally high glucose output after a meal
21
Q

What are the principles of treatment in diabetes?

A
  • Control of symptoms
  • Prevention of acute emergencies, ketoacidosis, hyperglycaemic hyperosmolar states
  • Identification and prevention of long-term microvascular complications
  • Limited evidence yet that glucose control reduces cardiovascular events in the short-term
  • But long-term follow-up indicates a modest reduction in IHD from tight glucose control if started at diagnosis
  • HbA1c 50mmol/mol (6.5%) (as low as possible in those not on insulin or sulphonylureas)
22
Q

What do sulphonylureas do?

A
  • Binds to potassium receptors that cause depolarisation to allow Ca to enter
  • Stimulate insulin release by binding to b-cell receptors
  • Improve glycaemic control (1-2% in HbA1c)
23
Q

What are the disadvantages of sulphonylureas?

A
  • significant weight gain
  • Do not prevent the gradual failure of insulin secretion
  • Can cause hypoglycaemia (occasionally prolonged and fatal, particularly in the elderly and when renal function is impaired)
24
Q

What is an example of sulphonylureas?

A

gliclazide

25
Q

What would an ideal type 2 diabetes drug do?

A
  • Reduce appetite and induce weight loss
  • Preserve b-cells and insulin secretion
  • Increase insulin secretion at meal time
  • Inhibit counterregulatory hormones which increase blood glucose such as glucagon
  • Not increase the risk of hypoglycaemia during treatment
26
Q

What is the first line drug for diabetes type 2?

A

Metformin

2a- Endocrinology (17 decks)

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