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Diabetes Flashcards

0
Q

What is the main cause of type 1 diabetes?

A

-Autoimmune progressive B-cell destruction via autoantibodies, macrophages and killer lymphocytes

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1
Q

Describe Diabetes Mellitus

A

Condition where blood glucose levels can become elevated, which over years leads to damage to the small and large blood vessels causing premature death from cardiac diseases

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2
Q

Where is insulin produced and secreted?

A

In the b-cells in the islets of langerhans in the pancreas

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3
Q

What is the triad of symptoms for type 1 diabetes and why do these symptoms occur?

A

Polyuria - Increased urination - as blood glucose levels rise they surpass the renal threshold meaning that more glucose is excreted in the urine. As levels of glucose in the urine rise, water is drawn in to the tubules and is thus not reabsorbed, increasing the amount of urine being formed
Polydipsia - increased thirst as a result of water loss due to polyuria
Weight Loss - as there is an absolute deficiency of insulin, fat mobilistation occurs, followed by lipolysis. Proteolysis also occurs. This occurs so that the stored energy within lipid and protein can be used in cells

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4
Q

Why are people with diabetes susceptible to recurrent urogenital infections, particularly thrush?

A

High levels of glucose within the blood means bacteria can thrive

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5
Q

Why do people with diabetes experience tiredness, weakness and lethargy?

A

Due to inadequate energy utilisation

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6
Q

Why do people with diabetes experience blurred vision during a hyperglycaemic episode?

A

Hyperglycaemia causes swelling in the lens of the eye

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7
Q

In late presentation of Type 1 Diabetes, how may a patient present and why?

A
  • Ketoacidosis
  • Nausea/Vomiting
  • Confusion
  • Slurred speech
  • Dizziness
  • Acetone on breath
  • Ketoacidosis occurs due to fat mobilisation and lipolysis. Glucose utilisation is inadequate due to no insulin, thus fat mobilisation occurs. Lipolysis breaks the fats down into glycerol and FAs. FAs undergo B-oxidation into Acetyl CoA. This Acetyl Co A is then converted into an excessive amount of ketones. Accumulation of ketones lowers the pH of the blood leading to ketoacidosis
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8
Q

At what age do Type 1 diabetes patients usually present?

A

Usually before the age of 30 but not always.

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9
Q

What is the treatment for Type 1 Diabetes?

A
  • Exogenous insulin via subcutaneous injection
  • Patient must be educated into appropriate times and doses
  • Appropriate dietary management and exercise
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10
Q

What causes type 2 diabetes?

A

Insulin resistance leading to insulin deficiency

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11
Q

Why does insulin resistance develop?

A
  • The cells become non-responsive and down-regulate insulin receptors due to the continually high circulating levels of glucose
  • Also the high circulating free FAs interferes with insulin sensitivity
  • Associated with obesity
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12
Q

How old do type 2 patients usually present?

A

Usually above 40 years, however it is becoming increasingly common in children

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13
Q

Why do people with type 2 diabetes not experience weight loss and ketoacidosis?

A

-There is an insulin resistance/deficiency not an absolute lack of insulin. -The body doesn’t enter the starvation catabolic state and thus fat metabolism, lipolysis and proteolysis does not occur. Therefore there is no weightloss. Ketoacidosis does not occur as there is no increase in free FAs so no ketones are produced

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14
Q

What is the treatment of type 2 diabetes?

A
  • 3 levels of treatment
    1) Diet and lifestyle changes
    2) Non-insulin therapies, eg sulphonylureas (increase insulin from remaining B cells and reduce gluconeogenesis) and metformin (reduces gluconeogenesis)
    3) insulin (rare)
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15
Q

What are the acute complications of hyperglycaemia?

A
  • Massive metabolic decompensation
  • Diabetic Ketoacidosis in type 1
  • Hyper-osmolar non-ketotic syndrome in type 2
16
Q

What is hyper-osmolar non-ketotic syndrome?

A

A relative insulin deficiency leads to a serum glucose and a resulting increase in serum osmolarity. This leads to polyuria which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level .Hyperglycemia and hyperosmolarity result in an osmotic diuresis and an osmotic shift of fluid to the intravascular space, resulting in further intracellular dehydration. This diuresis also leads to loss of electrolytes, such as sodium and potassium

17
Q

What are the acute complications of hypodlycaemia?

A

Diabetic coma due to lack of insulin to the brain

18
Q

What macrovascular chronic complications can occur in diabetes?

A
  • Stroke
  • MI
  • Gangrene
19
Q

What microvascular chronic complications can arise in diabetes?

A
  • Retinopathy-> Very small blood vessels in the eye get damaged by consistent high levels of glucose, causing leakage of protein exudate onto retina potentially leading to blindness. Changes in osmotic pressure due to glucose accumulation can cause blurred vision
  • Nephropathy -> Damage is sustained to the small capillaries of the glomerulus due to chronic high glucose levels, potentially leading to renal failure
  • Neuropathy -> damage to peripheral nerves by chronic high glucose leads to loss of feeling at the periphery. Can cause diabetic foot ulcers; skin more prone to damage (dehydrated) and patient lost sensation in the foot. Also high glucose levels in the blood result in bacteria being able to thrive resulting in an ulcer
20
Q

Why can insulin resistance lead to insulin deficiency in T2 diabetes?

A

-Amyloid deposits begin to form in the islet cells causing B cell failure

21
Q

Define ketoacidosis

A

-State of absolute insulin deficiency aggravated by ensuing hyperglycaemia, dehydration and acidosis

22
Q

How does ketoacidosis develop?

A
  • Insulin defeciency leads to cells not being able to utilise glucose as a source of fuel
  • Patient become hyperglycaemic with polyuria and glycosuria leading to dehydration and decreased blood volume
  • Body enters catabolic state and begins fat mobilisation and lipolysis
  • High levels of free FA are converted into acetyl coA and then ketones (so brain can use them and also because the lack of insulin means lyase is not inhibited)
  • Excessive ketone formation surpasses renal threshold and effects buffering capacity of the blood leading to acidosis
23
Q

What is the cause of hypoglycaemia in diabetics?

A

-Administration of too much insulin

24
Q

What are the symptoms of hypoglycaemia?

A

-Headache, blurred vision, mental confusion, dizziness, trembling, axiety, coma, seizures

25
Q

List some non-diabetic causes of hyperglycaemia

A
  • Pancreatitis
  • Cushing’s disease
  • Glucagonoma
26
Q

How can cushing’s disease cause hyperglycaemia?

A

-High glucocorticoid levels stimulates gluconeogenesis, promotes lipolysis and proeolysis which contributes to insulin resistance and interferes with insulin receptors

27
Q

Why does sorbitol accumulate in the lens of the eye in diabetes?

A
  • Glucose uptake into the eye does not require insulin
  • Persistent hyperglycaemia causes accumulation of glucose in the lens of the eye
  • Aldose reductase catalyses Glucose->Sorbitol
28
Q

Why is glucose conversion to sorbitol in the eye a problem?

A
  • The reaction uses NADPH and depletes it leading to increased DSB formation through oxidation of proteins due to lack of reducing power of NADPH. This alters protein structure and function
  • Also accumulation of sorbitol causes a change in osmotic pressure of the cells in the lens of the eye leading to damage
29
Q

What is non-enzymatic glycosylation of plasma proteins?

A

-Glucose spontaneously reacts with free a’a on plasma proteins forming stable covalent bonds leading to disturbances in function

30
Q

What is non-enzymatic glycosylation of RBCs and how can it be useful?

A
  • Spontaneous reaction of glucose with the terminal valine of Hb producing HbA1c
  • Indicates how effective blood glucose control has been over the past 2-3 months due to RBC lifespan
  • HbA1c>6.5% is indicative of diabetes
31
Q

Describe the diagnosis of diabetes

A
  • Triad of symptoms plus one of the following:
  • random venous blood plasma>11.1mmol/L
  • Fasting plasma glucose >7.0mmol/L
  • OGTT plasma glucose > 11.1mmol/L 2hours after 75g anhydrous glucose
32
Q

How can acromegaly lead to diabetes?

A

-Increased GH can lead to insulin resistance

Metabolism (14 decks)

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