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ESA1 - Metabolism > Diabetes > Flashcards

Diabetes Flashcards

1
Q

List 3 differences between Type I and Type II DM

A
  • Type I is insulin dependant, Type II is non-insulin dependant
  • Type I is defined by an absolute lack of insulin, Type II can still produce insulin but cells are less responsive
  • Type I can cause ketoacidosis
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2
Q

What can cause a rise in blood glucose?

A
  • Inability to produce insulin due to β cell failure or autoimmune destruction
  • Insulin resistance of cells so glucose cannot be utilised
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3
Q

Name 4 typical symptoms of hyperglycaemia

A
  • Polyuria
  • Polydipsia
  • Urogenital infections
  • Blurring of vision
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4
Q

What are the symptoms of inadequate energy utilisation?

A
  • Tiredness
  • Lethargy
  • Weakness
  • Unexplained weight loss (due to increased metabolism of fatty acids)
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5
Q

What tests could you perform to help diagnose diabetes?

A
  • Fasting blood glucose
  • Oral glucose tolerance test
  • HbA1c (Type II only)
  • Need symptoms and 1 abnormal test (2 if asymptomatic) to be diagnosed
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6
Q

What is the advantage of performing a HbA1c test on a person with Type II DM?

A
  • GLYCATION of Haemoglobin in RBC due to high plasma glucose
  • Lifespan of RBC is ~120 days
  • Gives % reading of blood glucose levels (glucose saturation) over the past 120 days
  • Can monitor if diet/lifestyle modifications in Type II are effective
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7
Q

What are the diagnostic criteria that define diabetes?

A
  • Fasting venous plasma glucose of >7mmol/L
  • Random venous plasma glucose of >11.1mmol/L
  • HbA1c of >6.5%
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8
Q

Why can HbA1c NOT be used to diagnose Type I diabetes?

A

Patients have a short history of symptoms (onset is about 2-3 weeks)

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9
Q

What defines Type I diabetes mellitus?

A
  • Autoimmune destruction of β cells in islets of pancreas so no insulin production
  • Insulin deficiency
  • Hyperglycaemia
  • Lipolysis leads to increased production of ketone bodies which can cause KETOACIDOSIS (fatal)
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10
Q

Explain why Type II diabetes can be as a result of insulin resistance AND insulin deficiency

A
  • Insulin resistance of cells means glucose cannot be utilised so plasma levels rise
  • β cells secrete more insulin to compensate for high blood glucose
  • Eventually β cells wear out (exhaustion) which leads to relative lack of insulin
  • Type II diabetics can also require the administration of insulin
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11
Q

List 3 factors (other than β cell failure) that can contribute to the cause of diabetes

A
  • Drug induced e.g. Steroids
  • Genetic defects of β cell or insulin action
  • Pancreatitis (acute or chronic)
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12
Q

Explain the presentation of Type I diabetes in a patient

A
  • Patient usually
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13
Q

Describe the effects of insulin on cell metabolism

A
  • PROMOTES glycogenesis, lipogenesis, protein synthesis

- INHIBITS glycogenolysis, lipolysis, proteolysis, gluconeogenesis

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14
Q

Explain how insulin deficiency can lead to weight loss and ketoacidosis

A
  • Absolute lack of insulin so cells cannot utilise glucose
  • Signals stress response so lipolysis is activated to produce ketone bodies for brain metabolism (as glucose is unable to enter)
  • Fat metabolised so patient loses weight
  • Ketone bodies can accumulate in blood altering the buffering mechanisms and causes ketoacidosis - fatal
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15
Q

What factors can diagnose Type I diabetes straight away?

A
  • Elevated venous plasma glucose >10mmol/L
  • Presence of KETONES (smell acetone on breath)
  • High blood pressure
  • Family history
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16
Q

How is Type I diabetes treated?

A
  • Exogenous insulin injections (MUST)
  • Subcutaneous insulin injections several times per day
  • Fluids (saline, water)
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17
Q

What percentage of people with Type II overweight or obese?

A

90%

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18
Q

Describe the aetiology of Type II diabetes

A
  • Insulin resistance due to obesity
  • β cell failure which leads to relative lack of insulin
  • Genetic and environmental factors
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19
Q

Describe how obesity can lead to insulin deficiency

A
  • First leads to insulin resistance
  • Secretion of more insulin due to increase in circulating fatty acids (need to be stored)
  • Pancreatic exhaustion
  • Hyperglycaemia causes pancreas to secrete more insulin
  • Eventually β cell failure occurs
  • Can also have amyloid type deposits in islets which leads to β cell failure
20
Q

Explain why diet modification is the primary treatment method for Type II diabetes

A
  • Has been shown to drastically reduce blood glucose within a short period of time
  • Coupled with moderate exercise this is very effective
  • If diet changes and exercise do not work, drugs can be administered
21
Q

What are the effects of a hypo-calorific diet on insulin resistance?

A
  • Under hypo-calorific conditions fat is metabolised first from the LIVER (followed by other ectopic and subcutaneous sites)
  • Decrease in fat around liver results in normal hepatic insulin sensitivity
  • Glucose can slowly be utilised more so fasting glucose levels decrease
22
Q

Explain why a patient presenting with Type II diabetes may not have a presence of ketones

A
  • Still producing some insulin

- Fatty acid oxidation is inhibited by insulin so no ketones produced

23
Q

Describe the presentation of a patient with Type II diabetes

A
  • Most are >40 yrs however increasing in younger population
  • Variable and slower rise in blood glucose
  • Polyuria, Polydipsia, weight loss, lack of energy, persistent infections, blurred vision
  • NO KETONES
  • May be ASYMPTOMATIC
24
Q

What happens if Type I diabetes is left untreated?

A
  • Severe hyperglycaemia
  • KETOACIDOSIS
  • Coma/DEATH
25
Q

What happens if Type II diabetes is left untreated?

A
  • Gradual worsening of symptoms e.g. Inadequate energy utilisation leading to sedentary behaviour
  • Onset or worsening of complications related to diabetes e.g. Severe morbidity, mortality, susceptibility to CVDs
26
Q

Explain the treatment methods of Type II diabetes

A
  • PRIMARY treatment includes diet modification (low kcal) and moderate exercise
  • If hyperglycaemia persists, can use drugs such as biguanides (Metformin), sulphonylureas and INSULIN
  • Requires patient education for monitoring blood glucose
27
Q

Describe the action of sulphonylureas

A
  • Increase insulin release from (remaining) β cells

- Reduce insulin resistance

28
Q

Explain how the autoimmune destruction of β cells can be triggered

A
  • Genetic predisposition associated with genetic markers HLA DR3 and HLA DR4
  • Environmental trigger e.g. Viral infection that triggers immune response (activation of T lymphocytes and macrophages)
29
Q

Explain how increased plasma glucose can lead to Polyuria and Polydipsia

A
  • Glucose normally reabsorbed in PCT after ultrafiltration in glomerulus
  • Reabsorption is ISOSMOTIC (same osmotic pressure)
  • Increased plasma glucose filtered out is not all absorbed so some glucose remains in nephron - EXTRA OSMOTIC LOAD
  • Less water reabsorbed to maintain isosmotic character so extra water is excreted along with glucose
  • Leads to increased thirst as DEHYDRATION occurs
30
Q

Explain why people with hyperglycaemia are more susceptible to urogenital and thrush infections

A
  • Increased glucose concentration attracts bacteria

- Growth environment for broth turbidity/Biofilms

31
Q

Describe the presentation of a patient with KETOACIDOSIS

A
  • Severely ill
  • Hyperventilation (KUSSMAUL BREATHING)
  • Prostration (elevated chest and abdomen)
  • Nausea/vomiting
  • Dehydration
  • Abdominal pain
32
Q

Describe how you could test for the presence of ketones

A
  • Presence in urine using a KETOSTIK

- Smell of acetone on breath

33
Q

Explain why a person with diabetes may have blurred vision

A
  • Hyperglycaemic

- Increased plasma glucose causes lens of eye to swell, affecting the refractive index of the eye

34
Q

Describe the steps of an oral glucose tolerance test

A
  • Take fasting blood sample from patient
  • Administer 75g glucose orally e.g. 395ml Lucozade
  • Take another sample of blood after 2 hrs of administration
  • If plasma glucose is >11.1mmol/L indicates hyperglycaemia
35
Q

Explain how persistent hyperglycaemia may leave some tissues susceptible to ROS damage

A
  • Uptake of glucose in some tissues is regulated by extracellular concentration e.g. Peripheral nerves, eye and kidney
  • If plasma glucose is high, it leads to increased intracellular concentration
  • Excess glucose metabolised by ALDOSE REDUCTASE into SORBITOL
  • NADPH —> NADP+ in the process
  • Depletion of NADPH stores leaves cells more susceptible to oxidative damage as it is needed to recycle glutathione
36
Q

How does GLYCATION differ from GLYCOSYLATION?

A

GLYCATION is non-enzymatic

37
Q

Describe how glycation can affect protein function

A
  • Glucose binds to free amino acid residues on proteins

- Change in overall NET CHARGE and 3D structure of protein so disrupts functioning

38
Q

What is diabetes mellitus?

A
  • Blood glucose is too high (HYPERGLYCAEMIA) due to either absolute lack of insulin or decrease in cell sensitivity to insulin
  • Can lead to problems such as ketoacidosis and micro/macrovascular damage
  • Can cause premature death from CVD
39
Q

Explain the significance of the HbA1c test

A
  • GLYCATION of Haemoglobin in blood at terminal valine due to elevated blood glucose
  • RBC have a lifespan of ~120 days
  • Related to the average blood glucose over the preceding 120 days from when it was taken
  • Can indicate how well blood glucose has been monitored in diabetics
40
Q

List 3 MICROVASCULAR complications associated with diabetes

A
  • Diabetic retinopathy
  • Diabetic neuropathy
  • Diabetic nephropathy
41
Q

Explain why it is essential that the feet of diabetics are checked regularly

A
  • Feet particularly vulnerable in diabetics
  • Poor circulation
  • Damage to nerves
  • Increased risk of infection
  • Failure to examine feet and detect changes may result in amputation (e.g. Gangrene)
42
Q

What visual problems may be associated with diabetes?

A
  • Glaucoma -> osmotic effects of glucose draw water into eye
  • Cataracts -> production of sorbitol depletes NADPH stores which is needed for protection from ROS damage
  • Retinopathy - damage to blood vessels (may rupture causing bleed; leakage leads to formation of protein exudates on retina)
  • All can lead to BLINDNESS
43
Q

Describe the cause and detection of diabetic nephropathy

A
  • Damage to glomeruli due to high blood glucose
  • Damage from infection of urinary tract
  • Detected by increased amount of proteins such as ALBUMIN in urine
44
Q

Explain how diabetic neuropathy can affect the feet of diabetics

A
  • Damage to periphery nerves by increased intracellular concentration of glucose
  • Depletion of NADPH stores, production of SORBITOL (causes osmotic damage to cells)
  • Leads to loss of sensation and changes due to alteration of autonomic nervous system
  • Damage to feet may go undetected
45
Q

Explain how sorbitol is produced and what it’s effects on the tissue is

A
  • In some cells glucose uptake is determined by extracellular concentration
  • In patients with hyperglycaemia the intracellular concentration of glucose increases (due to increased uptake) so glucose is converted to SORBITOL using aldose reductase
  • Sorbitol causes OSMOTIC DAMAGE to cells and tissues
46
Q

What are the MACROVASCULAR complications of diabetes?

A
  • Increased risk of STROKE
  • Increased risk of MYOCARDIAL INFARCTION
  • Poor circulation to periphery - particularly in feet

ESA1 - Metabolism (20 decks)

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