DM-Epidemiology, Etiology, & Pathophysiology Flashcards
About ___ in every 10 people have diabetes
1
about 1 in __ people don’t know they have diabetes
5
___ million american adults have prediabetes
96
T/F Type 1 diabetes can develop at any age
T
Risk factors for type 2 diabetes:
Being overweight
Having a family history
Being physically inactive
Being 45 or older
Diabetes =
Hyperglycemia
1 st century B.C. Greek physician, _____, named it diabainein, meaning “a
siphon” referring to the excessive urination
associated with the disease
Aretaeus the Cappadocian
The word diabetes was first recorded in ____
1425
In _____, the Greek mellitus, “like honey,” was added to reflect the sweet smell & taste of the patient’s urine
1675
the four major islet hormones & the cells secreting them:
- α cells making glucagon
- β cells making insulin
- δ cells making somatostatin
- PP or F cells making pancreatic polypeptide
Activation of these receptors suppresses chemoreflex-evoked sympathetic activity
GLP1R are found in chemosensory glomus cells of the carotid body
primary stimulus for insulin release from pancreatic β-cells
Glucose
Additional stimulatory & inhibitory factors that can also affect insulin release from the β-cell
- 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
____ separate C peptide from
insulin (orange- colored residues on proinsulin
Converting enzymes
Describe the Insulin Regulation process in β-Cells
- 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
In DM Type I: Ultimately, when β-cells are destroyed, there is not enough
endogenous insulin to prevent ____
Diabetic Ketoacidosis
~____% of T1D patients have circulating islet cell antibodies
85
How does Insulin resistence occur with Type II DM?
- To maintain euglycemia, pancreas ↑ insulin secretion (Compensatory hyperinsulinemia)
- As insulin resistance ↑ impaired glucose tolerance (IGT) develops (↑ postprandial glucose)
- ↓ insulin +/– ↑ glucagon → ↑ hepatic glucose (Fasting hyperglycemia)
Impaired Glucose Tolerance causes
- Sufficient insulin to prevent ketoacidosis
- Insufficient insulin to prevent hyperglycemia
The fundamental problem With DMII is NOT Hyperglycemia but what?
Insulin resistance & Beta cell dysfunction
Normal Pregnancy Carbohydrate Metabolism in Gestational Diabetes
- Mild fasting hypoglycemia
- Postprandial hyperglycemia
- Hyperinsulinemia
What percentage of pregnant women appear to get peripheral insulin resistance
About 30%
There is no known way to prevent this type of diabetes
T1
GLP1R are found in chemosensory glomus cells of the carotid body and Activation of these receptors______ chemoreflex-evoked
sympathetic activity
suppresses
Ultimately, when β-cells are destroyed, there is not enough endogenous insulin to prevent ____
Diabetic Ketoacidosis
