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Semester 2 - MEH > 14. Diabetes mellitus > Flashcards

14. Diabetes mellitus Flashcards

1
Q

What is diabetes characterised by and what can this be due to?

A

Chronic hyperglycaemia (elevated blood glucose concentration), due to insulin deficiency, insulin resistance, or both

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2
Q

What is type 1 diabetes characterised by and which age range does it mostly affect?

A

Characterised by the progressive loss of all or most of the pancreatic β-cells
- In ~90% of cases destruction of β-cells is caused by an autoimmune response

  • commonest type in the young
  • Is rapidly fatal if not treated.
  • Must be treated with insulin.
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3
Q

What is type 2 diabetes characterised by and which age range does it mostly affect?

A

Slow progressive loss of β-cells along with disorders of insulin secretion and tissue resistance to insulin
- affects a large number of usually older individuals

• May be present for a long time before diagnosis.
• May not initially need treatment with insulin but sufferers usually
progress to a state where they eventually do.

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4
Q

Describe the stages of type 1 diabetes.

A
  1. people can be found with the relevant human leucocyte antigen (HLA) markers and auto-antibodies but without glucose or insulin abnormalities
  2. impaired glucose tolerance
  3. diabetes (sometimes initially amenable to dietary control)
  4. total insulin dependence
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5
Q

Describe the stages of type 2 diabetes.

A
  1. insulin resistance
  2. impaired insulin production → glucose intolerance
  3. diabetes (initially managed with diet, tablets then insulin if lose all insulin production)
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6
Q

What does different rates of type 1 diabetes between different countries suggest?

A

Likely that a genetic predisposition to the disease interacts with an environmental trigger to produce immune activation

This leads to the production of killer lymphocytes and macrophages and antibodies that attack and progressively destroy β-cells (an auto-immune process)

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7
Q

Which genetic markers are involved in autoimmune destruction of β cells?

A

HLA DR3, HLA DR4

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8
Q

There is a seasonal variation of type 1 diabetes, what does this suggest?

A

Suggesting a link with a viral infection acting as a trigger to a rapid deterioration

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9
Q

What is a classic case of type 1 diabetes?

A

Lean, young person with a recent history of viral infection who presents a triad of symptoms

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10
Q

What are the triad of symptoms of type 1 diabetes?

A

Polyuria, thirst, weight loss

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11
Q

Why does a patient with type 1 diabetes experience polyuria?

A

Large quantities of glucose in the blood are filtered by the kidney not all of this glucose is
reabsorbed. The extra glucose remains in the nephron tubule. This places an extra osmotic load on the nephron, and means that less water is reabsorbed to maintain the isosmotic character of this section of the nephron. This extra water then remains with the glucose in the nephron tubule and is excreted as copious urine

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12
Q

Why does a patient with type 1 diabetes experience thirst?

A

Due to excess water loss and the osmotic effects of glucose on the thirst centres

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13
Q

Why does a patient with type 1 diabetes experience weight loss?

A

Fat and protein are metabolised by tissues because insulin is absent

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14
Q

What is it important to test for in the urine of diabetic patients?

A

Ketones and glucose

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15
Q

How do diabetic patients develop ketoacidosis?

A

High rates of β-oxidation of fats in the liver coupled to the low insulin leads to the production of huge amounts of ketone bodies
As this ketosis develops, the H+ associated with the ketones produce a metabolic acidosis

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16
Q

What are are the features of ketoacidosis?

A

Prostration (extreme physical, emotional weakness), hyperventilation, nausea, vomiting,
dehydration and abdominal pain

Keto-acidosis is a very dangerous condition.

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17
Q

Which type of diabetes is ketoacidosis more common in?

A

Type 1

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18
Q

What is glycosuria and why is it present in stir talks with diabetes?

A

Blood glucose is elevated because of the lack of insulin. The lack of insulin causes decreased uptake of glucose into adipose tissue and skeletal muscle, decreased storage of glucose as glycogen in muscle and liver and increased gluconeogenesis in liver. The high blood glucose will lead to the appearance of glucose in the urine (glycosuria also called glucosuria).

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19
Q

What symptoms might a type 2 diabetes patient present with?

A
  • classical triad of symptoms

But are more likely to present with a variety of symptoms:
- lack of energy, persistent infections, particularly thrush infections of the genitalia, or infections of the feet, slow healing minor skin damage, or visual problems

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20
Q

What is said to cause type 2 diabetes?

A

Obesity and a sedentary lifestyle is a massive risk factor in the development of type 2 diabetes.

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21
Q

Why is the difference in cause of type 1 and 2 diabetes?

A

Type diabetes 1 is due to autoimmune beta cell destruction

  • Beta Cells: secrete insulin… Autoantibodies made are directed against the beta cells and insulin producing cells destroyed
  • The pancreas does not produce enough insulin (absolute insulin deficiency)

Type 2:
- Your pancreas may not produce enough insulin (relative insulin deficiency)
- Or your cells do not use insulin properly. The insulin cannot fully
“ unlock” the cells to allow glucose to enter (insulin resistance) .

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22
Q

What is used to diagnose diabetes?

A

Symptoms plus:
• A random venous plasma glucose concentration ≥ 11.1 mmol/L or
• A fasting plasma glucose concentration ≥ 7.0 mmol/L (whole blood ≥ 6.1 mmol/L) or
• Plasma glucose concentration ≥ 11.1 mmol/L 2 hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).

• HbA1c
• You need symptoms and 1 abnormal test or 2 if
asymptomatic

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23
Q

How can diabetes be diagnosed in the absence of symptoms? What should you never use to diagnose diabetes?

A

With no symptoms diagnosis should not be based on a single glucose determination but requires confirmatory venous plasma glucose determination.

At least one additional glucose test result on another day with a value in the diabetic range is essential, either fasting, from a random sample or from the two hour post glucose load.

If the fasting or random values are not diagnostic the 2-hr value should be used.

A diagnosis should never be made on the basis of glycosuria or a stick reading of a finger-prick blood glucose alone

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24
Q

How is type 1 diabetes managed?

A
  • insulin injections
  • appropriate dietary control
  • regular exercise
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25
Q

Why is it important to educate patients on insulin injections?

A

Different forms of insulin with different time courses of actions
- patients must be educated to treat themselves at
appropriate times with appropriate doses and formulations so as to mimic as closely as possible the behaviour of pancreatic islets

26
Q

In what scenario might a type 1 diabetes patient need to increase their dose of insulin and why?

A

Infection, trauma

- risk of DKA

27
Q

Why do patients and associates need to be aware of sign and symptoms of hypoglycaemia?

A

Risk that blood glucose will fall too low

- can be fatal unless treated with glucose, either by mouth or by infusion

28
Q

How is type 2 diabetes treated?

A 
Three major components in the
treatment of Type 2 diabetes
• Diet and Exercise
• Oral hypoglycaemic B therapy (drugs)
• Insulin Therapy
29
Q

What drugs are used to treat type 2 diabetes?

A
  • metformin (reduce gluconeogenesis)
  • sulphonylureas (Modulates ATP sensitive K+ channel
    function by decreasing open probability –> increase insulin production)
  • thiazolidinediones (decrease insulin resistance)
30
Q

What are the major prevention methods of type 2 diabetes?

A

Exercise and diet management

31
Q

Why is persistent hyperglycemia harmful to some tissues? give examples.

A

Uptake of glucose into cells of tissues such as peripheral nerves, the eye and the kidney does not require insulin and is determined by the extracellular glucose concentration

32
Q

How is glucose metabolised in tissues during persistent hyperglycemia?

A

Metabolised via the enzyme aldose reductase which catalyses the reaction:

Glucose + NADPH + H+ → Sorbitol + NADP+

33
Q

What effects does glucose metabolism by aldose reductase have?

A

Depletion of NADPH: leads to increased disulphide bond formation in cellular proteins, altering their structure and function

Sorbitol accumulation causes osmotic damage

34
Q

What effects does persistent hyperglycaemia have on plasma proteins?

A

Increased glycation (non-enzymatic glycosylation)

35
Q

How does protein glycation occur and what effect does it have?

A

Glucose reacts with free amino groups in proteins to form stable covalent linkages.
Glycation changes the net charge and 3-D structure of the protein and therefore affects protein function.

36
Q

What does the extent of glycation depend on?

A

The extent of glycation depends on the glucose concentration and the half-life of the protein

37
Q

Which amino acid will glucose react with in haemoglobin and what does this form?

A

Terminal valine to produce glycated haemoglobin (HbA1c)

38
Q

What is HbA1c used as an indicator for?

A

The percentage of haemoglobin that is glycated
is a good indicator of how effective blood glucose control has been.
As red blood cells normally spend about 3 months in the circulation the % HbA1c is related to the average blood glucose concentration over the preceding 2-3 months

39
Q

What is the normal HbA1c and what can it rise to in diabetes?

A

Normal healthy individuals 4-6% of haemoglobin is glycated and in poorly controlled diabetics this value can increase above 10%

40
Q

What are the macrovascular complications of diabetes?

A
  • Increased risk of stroke.
  • Increased risk of myocardial infarction.
  • Poor circulation to the periphery - particularly the feet.
41
Q

What are the microvascular complications of diabetes?

A
  • Diabetic eye disease
  • retinopathy
  • nephropathy
  • neuropathy
  • diabetic feet
42
Q

What happens in retinopathy?

A

Damage to blood vessels in the retina which can lead to blindness:
- damaged blood vessels may leak and form protein exudates on the retina
- or they can rupture and cause bleeding in
to the eye
- new vessels may form (proliferative retinopathy), these vessels are very weak and can easily bleed

43
Q

What happens in Diabetic eye diseases?

A

Visual problems can arise from changes in the lens due to osmotic effects of glucose (glaucoma), and possibly cataracts

44
Q

What happens in nephropathy?

A

The kidney is affected by damage to the glomeruli, poor blood supply because of changes in kidney blood vessels, or damage from infections of the urinary tract which are more common in diabetics.

45
Q

What is an early sign of nephropathy?

A

Increase in the amount of protein in the urine (microalbuminuria).

46
Q

What happens in neuropathy?

A

Diabetes damages peripheral nerves in a number of ways producing a variety of effects, including:

  • changes of or a loss of sensation
  • and changes due to alteration in the function of the autonomic nervous system
47
Q

How does diabetes affects patients feet?

A

Poor blood supply, damage to nerves, and increased risk of infection all conspire to make the feet of diabetics particularly vulnerable. In the past loss of feet through gangrene was not uncommon
- foot ulcers, gangrene e

48
Q

What is metabolic syndrome?

A

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

The co-occurrence in the same individual of a number of cardiovascular risk factors such as dyslipidaemia and hypertension, usually in association with overweight or obesity and a sedentary life style is known as the ‘metabolic syndrome’

49
Q

Describe the association of insulin resistance with obesity

A

The major factors that predispose to insulin resistance are obesity and a sedentary life-style. Insulin resistance in turn, is associated with the development of a dyslipidaemic profile (↑ VLDL, ↑LDL & ↓HDL) that is highly atherogenic. It is also associated with an increased risk of hypertension

50
Q

What are the WHO criteria for metabolic syndrome?

A
  • waist: hip ratio above 0.9 for men and 0.85 for women
  • and/or a body mass index (BMI) above 30 kg/m2
  • blood pressure above 140/90 mmHg
  • triglycerides above 1.7 mmol/L
  • HDL cholesterol <0.9 mmol/L in men and <1 mmol/L in women
  • glucose fasting or 2 h after a glucose load above 7.8 mmol/L
51
Q

What are the symptoms of type 1 diabetes?

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • Tiredness
  • Acute onset in young patient
52
Q

Describe the Progression of Type 1 Diabetes mellitus

A
  • Autoimmune process occurring in individuals with a genetic predisposition to the disease.
  • Humoral autoantibodies indicate that disease process is underway
  • Progressive impairment of β-cell function manifested by progressive deterioration of glucose metabolism.
Insulin deficiency --> Catabolic state --> 
• Hyperglycaemia
• Ketoacidosis
• Dehydration
--> If untreated --> coma --> death
53
Q

Describe the effect of Untreated Type 1 DM

A

Lack of insulin and corresponding elevation in glucagon:

• Rapid Lipolysis in adipose tissue –> Excess fatty acids
converted to Ketone bodies in liver –> Ketoacidosis
• Hepatic glycogenolysis increases –>Hyperglycaemia
• Hepatic gluconeogenesis increases–>Hyperglycaemia
• Peripheral glucose uptake reduced–>Hyperglycaemia

54
Q

What are the symptoms of ketoacidosis?

A
  • Hyperventilation
  • Nausea
  • Vomiting
  • Abdominal pain
  • Ultimately Coma
  • Smell of acetone on breath
  • Ketonuria
55
Q

What are the symptoms of hyperglycaemia?

A 
Osmotic diuresis:
• Glucosuria
• Polyuria
• Dehydration
• Polydipsia
• Confusion
56
Q

What are the tests for diabetes?

A
  • Urine – glucose and ketones
  • Finger prick – glucose (glucometer) and ketones
  • Smell of acetone on breath
  • Blood sample for measurement of Glucose urea, electrolytes HbA1c
  • Check for signs of dehydration
  • BP, pulse, chest sounds.
  • Check respiration rate
57
Q

What are the Considerations needed in management of type 1 diabetes?

A
  • Type of insulin, units & frequency.
  • Regular meal times,
  • Unrefined carbohydrate in preference to refined
  • Once injected, effects of insulin are largely irreversible. Remind about the need for regular food.
  • Education – help groups, family & friends.
  • Carry sugar or sweets to avoid hypos.
  • Regular self-monitoring of blood glucose and feet (neuropathy).
  • Regular check-ups by GP – HbA1c, feet eyes, BP & kidneys
58
Q

What is type 2 diabetes?

A
  • Insufficient insulin production from β cells in the setting of insulin resistance.
  • Proportion of insulin resistance vs β cell dysfunction differs among individuals. Some have primarily insulin resistance with a minor defect in insulin secretion whilst others have slight insulin resistance and primarily a lack of insulin secretion.
  • > 85% of type-2 diabetics are obese.
59
Q

What are the differences of type 2 diabetes in comparison to type 1?

A 
• Late onset
• Ketoacidosis not usually present
• No acute weight loss – often obese
• Rate of fatality slower than type 1
• Insulin replacement not
immediate
60
Q

Describe the Clinical and biochemical features of

type-1 and type-2 diabetes

A 
type 1:
• Childhood
• Sudden onset
• Severe symptoms
• Recent weight loss
• Usually lean
• Spontaneous Ketosis
• No C-peptide
• Markers for auto-immunity
type 2:
• Middle age
• Gradual onset
• May be few acute symptoms but long term chronic effects may be severe
• Often no weight loss
• Usually Obese
• Non-ketotic
• C-peptide detectable
• No markers for autoimmunity
61
Q

Describe the HbA1c Test

A

• Measure of glycated haemoglobin reflects average
glycaemia over a period of weeks.
• Generally provides an accurate diagnosis of glycaemic control

62
Q

What’s the difference between glycosylation and glycation?

A

Glycosylation
• Post-translational modification mediated by enzymes
• Defined carbohydrate molecule added to a pre-determined region of the protein
• Carbohydrate plays natural role in protein function
• Not associated with disease process

Glycation
• Random non-enzymatic reaction
• Sugar covalently attached to protein creating unnatural glycated product.
• Glycation impairs protein function and stability,
• Associated with disease processes.

Chronic hyperglycaemia results in GLYCATION of proteins

Semester 2 - MEH (23 decks)

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