Endocrine deck 3 Flashcards

1
Q

Age of diabetics type I vs type 2

A

type 1 - children/young adults

type II - Usually after age 40, Incidence increases with age

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2
Q

onset of DM - type 1 vs type II

A

Type I - Generally abrupt

Often diagnosed after an infection

Often first sign is DKA

Type II - Usually insidious

Often obese

HHNK

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3
Q

treatment of DM - type I vs type II

A

type I - Insulin

Type II - Diet, exercise, medication
Insulin may be required

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4
Q

complications of DM - type I vs type II

A

type I - Occur early, often severe

type II - Full range of complications may be present at diagnosis

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5
Q

Insulin levels of DM - type I vs type II

A

type I - low or absent

Type II - Frequent normal or high

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6
Q

Type I DM develops when …..

A

Type 1 DM develops when the body’s immune system destroys pancreatic beta cells, leading to progressive loss of insulin secretion.

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7
Q

What causes Type I DM

A

). The exact cause of type 1 diabetes is unknown, but most likely a viral or environmental trigger in genetically susceptible people causes an autoimmune reaction. Initially in the course of the disease, there may be a short period (sometimes 1–2 years) termed the honeymoon phase where there are still residual beta cells producing insulin, but as more and more insulin is needed, as during an infection or puberty, the insulin reserve disappears and insulin becomes near absent to absent.

. With type 1 DM, beta cells are destroyed by the immune system (e.g., cytotoxic CD8 and T lymphocytes), and while there is sparing of other pancreatic cells (e.g., alpha and delta cells), hormonal patterns from these cells are altered

Cannot be prevented

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8
Q

What is Type II DM

A

This form of diabetes usually begins as insulin resistance, a disorder in which the body’s cells do not use insulin properly. As the need for insulin rises, the pancreas gradually loses its ability to produce insulin. Type 2 DM is associated with advancing age, obesity, family history of DM, history of gestational DM, impaired glucose metabolism, and physical inactivity

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9
Q

explain the pathogenesis of Type II DM

A

type 2 DM starts with insulin resistance, which refers to insulin’s inability to act upon target tissues (fat, muscle, and liver, which are insulin sensitive tissue). The lack of glucose use causes the liver to produce more glucose in response. Both these processes, lack of use and increased production) lead to hyperglycemia. Hyperinsulinemia occurs as a compensatory response. Ultimately, the beta cells struggle with maintaining the hyperinsulinemic state, so insulin secretion decreases, hepatic glucose production increases, and beta cell failure occurs. Glucagon additionally increases hepatic glucose production due to the inadequate insulin suppression further compounding the hyperglycemia.

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10
Q

Adipocytes and type II DM

A

Adipocytes (cells that store fat) release adipokines such as leptin, adiponectin, resistin, and other chemicals such as tumor necrosis factor-alpha, which stimulate inflammatory activity. These various factors released from adipose tissue may be increased or decreased and contribute to the development of type 2 DM e.g., leptin is increased while adiponectin is decreased).
Adiponectin is a protective adipokine that reduces free fatty acid and is associated with glycemic control, reduced inflammation, and improved lipid profiles

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11
Q

Diabetic symptoms

A
  • Glucosuria (glucose is excreted in the urine to lower serum levels)
  • Polyuria (increased urine output because of the osmotic effects of the glucosuria)
  • Polydipsia (increased thirst because of the dehydration caused by the increased urine output)
  • Polyphagia (increased appetite because of the energy loss as glucose is excreted)
  • Weight loss (from increased fat catabolism)
  • Blurred vision (excessive glucose changes the shape and flexibility of the lens of the eye, decreasing the ability to focus and causing blurred vision)
  • Fatigue (because of a lack of an energy source)
  • Nausea, vomiting, and abdominal pain (associated with sudden onset of type 1 diabetes)
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12
Q

Diabetic complications

A
  • Coronary artery disease
  • Peripheral artery disease
  • Cerebral vascular disease
  • Hypertension
  • Hypercholesterolemia
  • Diabetic retinopathy
  • Diabetic neuropathy
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13
Q

Diagnostics for DM

A

history and physical examination. The various glucose tests include fasting blood glucose test, oral glucose tolerance test (most accurate for diagnosis in pregnancy), random blood glucose test, and hemoglobin A1c (HgbA1c; an average of glucose control for the previous 2–3 months).

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14
Q

Glucose for Criteria for Diagnosis of Diabetes

A

HgbA1c ≥ 6.5%
or
Fasting plasma glucose ≥ 126 mg/dL*

or
2-hour plasma glucose ≥ 200 mg/dL* post 75 g glucose challenge

or
Random plasma glucose ≥ 200 mg/dL with symptoms (polyuria, polydipsia, and
and unexplained weight loss)

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