DM part 3 Flashcards

1
Q

What does skeletal muscle and adipose tissue have receptors for?

A

insulin

-skeletal muscle and adipose is insulin dependent

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2
Q

What does insulin unlock?

A

receptors so glucose can move into the cell to be used for energy (from the blood to the cell??)

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3
Q

Other tissues (brain, liver, blood) dont require insulin for glucose glucose transport, but what do they require glucose for?

A

to function

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4
Q

Liver cells are not insulin dependent but why do they have receptor sites?

A

to facilitate uptake of glucose and convert it to glycogen

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5
Q

What are the counter-regulatory hormones?

A

glucagon, epinephrine, growth hormone, cortisol

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6
Q

The counter-regulatory hormones (glucagon, epinephrine, growth hormone, cortisol) oppose the effects of insulin and increase blood glucose levels by doing what?

A
  • stimulate glucose production and release by the liver
  • decrease movement of glucose into cell
  • this helps to maintain normal blood glucose levels
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7
Q

The counter-regulatory hormones (glucagon, epinephrine, growth hormone, cortisol) and insulin maintain blood glucose levels within the normal range by doing what?

A

regulating the release of glucose for energy during food intake and periods of fasting

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8
Q

What was type 1 diabetes formerly known as?

A
  • juvenile-onset

- insulin dependent

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9
Q

Who is generally affected by type 1 DM?

A

people under age 40

-but can occur at any age

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10
Q

What type of disorder is Type 1 DM?

A

autoimmune

  • the body develops antiboties against insulin and/or pancreatic beta cells that produce insulin
  • this results in not enough insulin to survive
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11
Q

What are 3 types of the genetic link of T1DM?

A
  • predisposition to type 1 related to human leukocyte antigens (certain HLA types who are exposed to a virus then the beta cells are destroyed directly or through autoimmune process)
  • Idiopathic diabetes which is strongly inherited (mostly hispanic, African, or Asian)
  • Latent autoimmune diabetes in adults which is a slowly progressing form of type 1 and is often mistaken for type 2.
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12
Q

In T1DM how long are the islet cell autoantibodies responsible for beta cell destruction present before onset of symptoms?

A

months to years

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13
Q

When will the manifestations of T1DM develop?

A

when the persons pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose levels

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14
Q

Once the manifestations of T1DM occurs (usually rapidly) what will the patient present with?

A
  • impedending or actual ketoacidosis
  • history of recent and sudden weight loss
  • polydipsia (excessive thirst)
  • polyuria (frequent urination)
  • polyphagia (excessive hunger)
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15
Q

Where is the bottom line with T1DM?

A

thye have to have insulin from an outside source (exogenous)
-or they will develop DKA: diabetic ketoacidosis which is a life threatening disease

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16
Q

What might patients with T1DM experience after treatment is initiated?

A

3-12 month remission

-the patient requires very little injected insulin because beta cell production remains sufficient for healthy insulin.