Diabetes Flashcards

1
Q

what is diabetes

A

Syndrome of carbohydrates, proteins and fat metbbolisms. Problem with how the pt process them.
Caused by either an insuffiency T1 or insulin resistance T2

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2
Q

What happens in a normal situation

A
  • pancreas produces insulin
  • On the muscles + tissues receptors for insulin and high levels of glucose stimulate insulin secretion
  • Insulin targets organs by binding to the recpetors decrease BGL.
  • This binding triggers cells to uptake glucose by producing more glucose channels on the surface of cells allowing glucose to move from the blood into the cells of the organs
  • Insulin promotes glucose storage into the liver to store as glycogen and fat.
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3
Q

What is T1

A

Destruction of beta cells
insuffiency of insulin

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4
Q

Describe the pathophysiology

A
  • A complete insuffiency of insulin or no insulin is produced
  • 80-90% of beta cells in pancreas are destroyed before symptoms
  • Is a inflammatory condition, degree of inflammation in the pancreas causes beta cell fibrosis and destruction
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5
Q

What causes the inflammation and destruction?

A

Non immune: enviromental factors
Immune: degree of genetics

Both of these lead to inflammation of islets where insulin is secreted, beta cell inflammation and fibrosis

Without this glucose cannot enter, blood glucose increase so pt is hyperglycameic.

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6
Q

What are complications of T1 diabetes

A
  • DKA, diabetes acidosis
  • presented as tachypnoea, unconcious, COMA and low pH
  • When in a hyperglycamic state, with a complete insulin deficency the body needs to compensate by breaking down fatty acids.
  • The liver tries to modify fatty acids into sugar but becomes overloaded and as a result forms ketones.
  • The ketones cause an acidotic state so the pH drops
  • The person can then develop metanbolic acidosis
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7
Q

Clinical signs of T1

A
  • Increased urine output - loss of electrolytes
  • Sugar in urine
  • Increased thirst and hunger
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8
Q

What is T2

A

Resistance to insulin

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9
Q

Patho of T2

A
  • Process starts with insulin resistance from genetic link or fat
  • As that process occurs we have hyperglycaemia so the pancreas tries to work hard and release more insulin to counteract
  • Insulin is an anabolic hormone so it increases storage of fatty acid, growth and feedback to the fat cell which increases BMI
  • This increases resistance
  • Inceases hyperglycameia
    -Increases insulin release
  • This process leads to beta cell exhaustion

Insulin doesnt work on beta receptors and glucose cannot be taken up

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10
Q

Risks of t2

A
  • Strong genetic link/predisposition
  • BMI/fat: the more fat, the more insulin, the more likely to have a resistance
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11
Q

Signs of T2

A
  • Kidney problems
  • Nerve problems
    Problems with retinas
    Increased thirst and hunger
    frequent urination
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12
Q

Complication of hyperglycamia

A

Over years leads to age ( advanced glycoylated end products) which is a sugary molecule jumping onto other things causing detrimental effects in other systems

  1. Eyes: retina, blood vessels grow over the retina leading to retinopathy
  2. Kidneys: changes the regulation of filtration- leading to renal failure

3.NS: a breakdown in myelin sheaths causing loss of sensation in legs which can lead to ulcer development

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