6.1 Diabetes Flashcards
What is DMI?
inability to produce insulin
immune-related, or idopathic
What is DMII?
inability to respond to insulin
with or without Beta-cell exhaustion
What is gestational diabetes?
Glucose intolerance during pregnancy
What is diabetes insipidus?
is NOT high blood sugar, but high urine output due to ADH deficiency and is named for excessive production of dilute urine (diabetes = siphon, insipidus = “not tasty”)
How does glucose enter the cell?
glucose is a simple sugar (monosaccharide) has to enter the cell through facilitated diffusion (transporter, down concentration gradient, no ATP)
GLUT= glucose transporter
What is glycogen? Where is it made?
carbohydrate, a starch made up of many glucose molecules linked together
glucose storage molecule mainly in liver and skeletal muscle
about 12-24 hours of glucose reserve via glycogen
How is the liver involved with glucose regulation?
break down glycogen, build up glucose, or store glycogen
Increase blood glucose:
glycogenolysis: breakdown of glycogen to yield glucose
gluconeogenesis: formation of glucose from amino acids (protein breakdown) or glycerol (fat breakdown)
Store glucose as glycogen:
glycogenesis: formation of glycogen by linking glucose molecules together
What are 4 stimuli that increase insulin production?
High blood glucose, high amino acids, PNS activation, GI Hormones
How does high blood glucose stimulate insulin release?
(ex: after high carbohydrate meal) sensed by the pancreatic Beta cells, directly stimulate insulin secretion
high blood glucose high insulin
low blood glucose low insulin
How do high amino acids stimulate insulin?
(ex: after high protein meal) sensed by the pancreatic Beta cells, directly stimulates insulin secretion
How does the PNS stimulate insulin?
parasympathetic activity (Ach) stimulates secretion of insulin sympathetic nervous system (Epi) inhibits insulin, related to need to mobilize glucose to muscle
How do GI hormones stimulate insulin?
“incretins”, stimulate insulin secretion in response to food in GI tract
gastrointestinal insulinotropic peptide (GIP)
glucagon-like peptide (GLP-1)
What is the difference between anabolic/catabolic?
Anabolic = storage Catabolic = breakdown
Is insulin anabolic or catabolic? Explain.
storage of nutrients when plentiful (ex: just absorbed after a meal)
increases glycogen formation (glycogen storage), triglyceride formation (fat storage), protein synthesis
decreases fat breakdown (lipolysis), inhibits protein breakdown (proteolysis)
decreases blood glucose, fatty acids, amino acids
lowers blood glucose, lowers amino acids, and lowers fatty acids in the blood
helps cells use and store nutrients
What is GLUT-4?
mechanism?
Glucose transporter, essential for bringing glucose into the cell
GLUT 4–>glucose txp molecule –> facilitated diffusion to enter the cell
What organs do not need GLUT-4?
Brain, liver
What are normal/prediabetes/diabetes fasting blood glucose ranges?
Random plasma glucose?
Normal: 70 to 99 mg/dL
Prediabetes: 100 to 125 mg/dL
Diabetes: 126 mg/dL or higher
Random: >200
During a 2-hour plasma glucose trial, what are the ranges for pre-diabetes? Diabetes?
Prediabetes: 140 to 199 mg/dL
Diabetes: 200 mg/dL or higher
What are the HbA1C ranges for pre-diabetes/diabetes?
Prediabetes: 5.7% to 6.4%
Diabetes: 6.5% or higher
What do the different cells of the pancreas make?
Alpha- Glucagon
Beta- Insulin
Delta- somatostatin (GH)
F-cells- pancreatic polypeptide
What hormone(s) lower blood glucose?
ONLY INSULIN
What hormone(s) raise blood glucose?
Glucagon, cortisol, GH, epi
What are the effects of glucagon?
Increase blood glucose by glycogenolysis (breakdown of glycogen)
Increase fat breakdown
Increase amino acid uptake
What causes polydipsia and polyuria in DM?
high glucose raises osmolarity of blood, water leaves cells –> polydipsia
kidneys reach threshold for glucose, excess is eliminated –>glucosuria
excess glucose in kidney tubules pulls water into urine –> polyuria, polydipsia
What causes blurred vision in DM?
glucose accumulates in fluid surrounding eyes, alters osmolarity of aqueous fluid, light refraction into eye is changed
What causes electrolyte derangement in DM?
water leaving cells can cause dilutional hyponatremia (low blood sodium vs. water)
potassium leaves cells with water: temporary hyperkalemia (high blood potassium), that can mask true hypokalemia (low blood potassium) when potassium returns to cell
What causes polyphagia in DM?
body cells are not able to use/take in glucose “starvation amidst plenty”
glycogen pathway is activated higher blood glucose, lipolysis, ketone production
What is the mechanism of DKA? In DMI, DMII?
low insulin –> lipolysis –> ketone formation –> decrease blood pH (acidosis)
In DM II can happen when Beta cells are exhausted
What is HHS? What causes it? Complications leading to it?
Hyperosmolar hyperglycemia syndrome
Extreme blood glucose 600+ leads to high blood osmolarity. Tx is aggressive rehydration. Complications include ETOH, infection, stress, cocaine
