DM-Epidemiology, Etiology, & Pathophysiology Flashcards

1
Q

About ___ in every 10 people have diabetes

A

1

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2
Q

about 1 in __ people don’t know they have diabetes

A

5

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3
Q

___ million american adults have prediabetes

A

96

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4
Q

T/F Type 1 diabetes can develop at any age

A

T

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5
Q

Risk factors for type 2 diabetes:

A

Being overweight
Having a family history
Being physically inactive
Being 45 or older

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6
Q

Diabetes =

A

Hyperglycemia

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7
Q

1 st century B.C. Greek physician, _____, named it diabainein, meaning “a
siphon” referring to the excessive urination
associated with the disease

A

Aretaeus the Cappadocian

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8
Q

The word diabetes was first recorded in ____

A

1425

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9
Q

In _____, the Greek mellitus, “like honey,” was added to reflect the sweet smell & taste of the patient’s urine

A

1675

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10
Q

the four major islet hormones & the cells secreting them:

A
  1. α cells making glucagon
  2. β cells making insulin
  3. δ cells making somatostatin
  4. PP or F cells making pancreatic polypeptide
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11
Q

Activation of these receptors suppresses chemoreflex-evoked sympathetic activity

A

GLP1R are found in chemosensory glomus cells of the carotid body

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12
Q

primary stimulus for insulin release from pancreatic β-cells

A

Glucose

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13
Q

Additional stimulatory & inhibitory factors that can also affect insulin release from the β-cell

A
  • Stimulatory
  • Glucose synergizes with other
    mediators & enhances the
    secretory response of the β-cell to
    these factors.
  • GLP-1, CCK, Glucagon,
    Acetylcholine, Sulfonylurea drugs
  • Inhibitory
  • Epi-/norepinephrine, somatostatin
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14
Q

____ separate C peptide from
insulin (orange- colored residues on proinsulin

A

Converting enzymes

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15
Q

Describe the Insulin Regulation process in β-Cells

A
  • Glucose Enters β-cell cell via glucose transporter protein (GLUT-2) & undergoes glycolysis → ATP
  • ↑ ATP/ADP ratio → closure of the ATP-sensitive K + channels → Plasma membrane depolarizes & opens voltage-dependent Ca 2+ channels
  • ↑ Ca 2+ influx + mobilization of intracellular stores of Ca 2+ → fusion of insulin-containing secretory granules with the plasma membrane & release of insulin (& C-peptide) into circulation
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16
Q

In DM Type I: Ultimately, when β-cells are destroyed, there is not enough
endogenous insulin to prevent ____

A

Diabetic Ketoacidosis

17
Q

~____% of T1D patients have circulating islet cell antibodies

A

85

18
Q

How does Insulin resistence occur with Type II DM?

A
  1. To maintain euglycemia, pancreas ↑ insulin secretion (Compensatory hyperinsulinemia)
  2. As insulin resistance ↑ impaired glucose tolerance (IGT) develops (↑ postprandial glucose)
  3. ↓ insulin +/– ↑ glucagon → ↑ hepatic glucose (Fasting hyperglycemia)
19
Q

Impaired Glucose Tolerance causes

A
  • Sufficient insulin to prevent ketoacidosis
  • Insufficient insulin to prevent hyperglycemia
20
Q

The fundamental problem With DMII is NOT Hyperglycemia but what?

A

Insulin resistance & Beta cell dysfunction

21
Q

Normal Pregnancy Carbohydrate Metabolism in Gestational Diabetes

A
  • Mild fasting hypoglycemia
  • Postprandial hyperglycemia
  • Hyperinsulinemia
22
Q

What percentage of pregnant women appear to get peripheral insulin resistance

A

About 30%

23
Q

There is no known way to prevent this type of diabetes

A

T1

24
Q

GLP1R are found in chemosensory glomus cells of the carotid body and Activation of these receptors______ chemoreflex-evoked
sympathetic activity

A

suppresses

25
Q

Ultimately, when β-cells are destroyed, there is not enough endogenous insulin to prevent ____

A

Diabetic Ketoacidosis