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2 - MEH > Endocrine Kidney & Diabetes > Flashcards

Endocrine Kidney & Diabetes Flashcards

1
Q

Explain the half life and solubility properties of insulin and glucagon

A
  • Water soluble
  • Short half life to allow constant monitoring and changing of glucose concentration
  • Once binds to receptor and enters cell, internalised and inactivated
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2
Q

Which cells are insulin and glucagon made in

A

Insulin made in pancreatic ß-cell

Glucagon made in pancreatic α cells

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3
Q

Describe the structure of insulin

A
  • Structure - α helix with A and B chains, and C-peptide
    • A and B chains linked covalently by two disulphide bonds
    • Another inter-chain disulphide bond within A chain to maintain curve
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4
Q

Describe how insulin is synthesized

A
  • Preproinsulin made in ribosomes associated with RER
  • Signal peptide removed to become proinsulin when it enters ER and folds
  • Proinsulin travels to Golgi and packaged into storage vesicles
  • Proteolysis removes C-peptide, forming two chains connected by disulphide bridge
  • Vesicles contain insulin and C peptide separately and marginate to cell surface and remain there
  • When needed, insulin and C peptide released from vesicles
  • C peptide - helps prevent vascular damage in patients with diabetes
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5
Q

What happens when insulin binds to its receptor on target cell surface

A
  • Insulin binds to target cells through insulin receptor
    • Stimulates insertion of glucose transporter (GLUT-4) onto target cell membrane
    • Glucose moves from plasma inside the cell
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6
Q

How is glucagon synthesized

A
  • Synthesised from pre-proglycogen in RER and stored in vesicles until release (similar to insulin)
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7
Q

Describe the structure of glucagon

A

Structure - single chain with no disulphide bonds

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8
Q

What happens when glucagon binds to its receptor on target cell surface

A
  • Glucagon binds to GPCR receptors which activate adenylyl cyclase
    • Increases cyclic AMP which activates protein kinase A
    • Phosphorylates and thereby activates important enzymes in target cells
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9
Q

Describe how the structure of the ß-cell relates to the synthesis and storage of insulin

A
  • Contain ATP sensitive potassium channels (KATP) - allows efflux of potassium
    • Channels hyperpolarise cell membrane
    • Inhibited by ATP
  • In presence of high plasma glucose:
    • Glucose increases ATP which closes channel to cause depolarisation
    • By depolarising membrane, voltage gated calcium channels open to increase intracellular calcium
    • Cause vesicles containing insulin to fuse with membrane of ß cell and released
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10
Q

How does ATP sensitive-potassium channels regulate insulin synthesis

A
  • Process also regulates insulin synthesis
    • In low metabolism, KATP channels open so insulin not secreted
    • In high metabolism, ATP causes KATP to close so insulin secreted
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11
Q

What are the effects of insulin

A
  • Stimulated at glucose concentration > 5mmol/L
  • Increase glucose transport into adipose tissue and skeletal muscle
  • Increase glycogenesis and decrease glycogenolysis in liver and muscle
  • Increase lipogenesis and decrease lipolysis in adipose tissue
  • Decrease ketogenesis in liver
  • Increase amino acid uptake and protein synthesis in liver, muscle and adipose tissue
  • Decrease proteolysis in liver, muscle and adipose tissue
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12
Q

What are the effects of glucagon

A
  • Stimulated at glucose concentration > 5mmol/L
  • Increase glycogenolysis and decrease glycogenesis in liver
  • Increase gluconeogenesis in liver (synthesize glucose from amino acids)
  • Increase ketogenesis in liver
  • Increase lipolysis in adipose tissue
  • Stimulated in high amino acid in starvation - digestion of muscle
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13
Q

Explain the timing response of the effects of insulin and glucagon

A
  • Glucose uptake rapid response to insulin
  • Glycogen synthesis/breakdown intermediate response to hormones
  • Gluconeogenesis intermediate response to glucagon
  • Lipogenesis/lipolysis/ketogenesis delayed response to hormones
  • Amino acid uptake rapid response to insulin
  • Protein synthesis intermediate response to insulin
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14
Q

What is normal glucose concentration

A

Normally 3.3-6mmol/L

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15
Q

At what glucose concentration does polyuria occur

A

Plasma glucose > 10mmol/L

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16
Q

Define diabetes mellitus

A
  • Diabetes mellitus is a group of metabolic disorders characterized by chronic hyperglycaemia
    • Prolonged elevation of glucose > 6mmol/L
17
Q

Describe Type 1 diabetes

A
  • Type 1 - insulin deficiency
    • Common in young people
    • Autoimmune destruction of ß cells
      • Absolute - pancreatic ß cells destroyed
      • Relative - ß cells not responding properly leading to relative deficiency in insulin
    • Insulitis - inflammation of Islet’s of Langerhans
      • Chronic inflammation leading to infiltration of T lymphocytes and macrophages
    • Mutation of 2 subunits in ATP sensitive potassium channel which becomes insensitive to ATP
      • Insulin not released so plasma glucose does not decrease
    • Presence of high ketone bodies - breakdown product of fat
18
Q

Describe Type 2 diabetes

A
  • Type 2 - normal insulin secretion but peripheral tissue resistant to insulin
    • Common in older or obese individuals
    • Slow progressive loss of ß-cells along with defective insulin secretion and tissue resistance to insulin
    • Defective insulin receptor mechanism
    • Or Excessive or inappropriate glucagon secretion
    • Normal ketone bodies
19
Q

Distinguish between Type 1 and Type 2 diabetes

A
  • Type 1 is autoimmune destruction of ß cells, Type 2 is defective insulin receptor mechanism
  • Type 1 has high ketone bodies, Type 2 has normal
  • Type 1 more common in young people, Type 2 more common in adults
20
Q

Describe the presentation of Type 1 diabetes

A
  • Polyuria - large amount of glucose not reabsorbed into blood
    • Increases osmotic pressure inside nephron so less water is reabsorbed
  • Polydipsia - due to excess water loss
  • Weight loss - fat and protein metabolised by tissues as glucose not entering cells
  • Ketoacidosis - hyperventilation, nausea, vomiting, dehydration, abdominal pain, coma, prostration (collapse)
    • Acetone smell in patient’s breath
21
Q

Describe the presentation of Type 2 diabetes

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • Lethargy
  • Persistent infections - particularly thrush infections in genitalia (infection thrives on glucose from polyuria)
    • Infections on feet
  • Slow healing minor skin damage
  • Visual problems
22
Q

Explain the sequence of events leading to ketoacidosis in the uncontrolled diabetic

A
  • High rates of ß-oxidation of fats in the liver coupled with low insulin leads to vast production of ketone bodies
  • Acetone can be breathed out - patients breath
  • Increased ketone body production leads to keto-acidosis
  • Presents as prostration, hyperventilation, nausea, vomiting, dehydration, abdominal pain
23
Q

What are consequences of hyperglycaemia

A
  • Uptake of glucose into peripheral nerves, eye and kidney do not require insulin - determined by plasma glucose concentration
    • Glucose metabolised which needs NADPH - causes NADPH depletion
    • Increased disulphide bone formation - alter cellular protein struture and function
    • Osmotic changes in cells
  • Increased glycation of plasma proteins - affects protein function
  • Ketoacidosis - leading to coma
  • Glucosuria
  • Polyuria - dehydration - polydipsia and confusion
24
Q

What tests do you do on suspected diabetic patient

A
  • Fasting glucose concentration > 7mmol/L
  • Random venous plasma glucose concentration > 11.1mmol/L
  • Oral glucose tolerance test - plasma glucose concentration > 11.1mmol/L 2 hours after glucose given
  • HbA1c > 10%
  • Urine dipstick - test glucose and ketone
  • Finger prick - test glucose and ketone
25
Q

What are treatments of Type 1 diabetes

A
  • Subcutaneous insulin injection - life long
    • Need to maintain regular eating schedule
  • Exercise and diet
    • Exercise increases insulin sensitivity
26
Q

What are treatments of Type 2 diabetes

A
  • Exercise and diet
    • Exercise increases insulin sensitivity
  • Metformin - reduces gluconeogenesis
  • Sulphonylureas - makes KATP more sensitive to ATP, so more insulin released
  • Increase glucose excretion through urine - however causes vagina thrush
27
Q

Explain the principle and practice of measuring glycated haemoglobin as an index of blood glucose control in the diabetic

A
  • HbA1c test > 10%
  • Test measures 3 month average glucose concentration (red blood cell life time = 120 days)
  • Normally only a small percentage of plasma glucose is bound to haemoglobin
  • For diabetes, glycated haemoglobin levels high
28
Q

What are macrovascular complications of diabetes

A
  • Increased risk of stroke
  • Increased risk of myocardial infarction
  • Poor circulation to the periphery - particularly to feet
29
Q

What are microvascular complications of diabetes

A
  • Diabetic eye disease - osmotic changes in glucose
    • Cataracts
  • Retinopathy - damage to blood vessels in retina leading to blindness
    • Vessels may leak and form protein exudates, or rupture
  • Diabetic kidney disease (nephropathy)
    • Damage from infections of urinary tract
    • Damage to glomeruli
    • Poor blood supply because of changes in kidney blood vessels
  • Diabetic neuropathy
    • Diabetes damages peripheral nerves
    • Loss of sensation
  • Diabetic feet
    • Poor blood supply, damage to nerves and increased risk of infection
30
Q

Discuss the aetiology of metabolic syndrome and its consequences for health

A
  • Cluster of most dangerous risk factors associated with cardiovascular disease
    • Diabetes and raised fasting plasma glucose
    • Abdominal obesity
    • High cholesterol
    • High blood pressure
  • To have metabolic syndrome
    • Waist measurement > 94cm for men and > 80cm for women + any 2 of the following
      • Raised triglyceride levels
      • Reduced HDL cholesterol
      • Raised blood pressure
      • Raised fasting glucose level
  • Causes - insulin resistance and central obesity, genetics, physical inactivity, aging

2 - MEH (16 decks)

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