Diabetes Flashcards
Describe how glucose trigger insulin secretion from pancreatic beta cells.
GLUT2 transporter glucose into cell of pancreatic beta
glucose is broken down and increases the ATP
High ATP inhibits K+ channel.
Depolarization.
Voltage-gated Ca++ channel opens, and Ca++ comes in.
Ca++ causes the release of insulin vesicles
Which tissues in the body have insulin-dependent glucose transporters? What is the effect of insulin on these?
adipose tissue
skeletal muscle
**insulin also increases the amount of GLUT4 receptors on the surface
Describe the basic symptoms of diabetes?
hyperglycemia polyuria polydipsia polyphagia (can't get glucose you do have in your cells!) weight loss (if Type I)
What is the dangerous thing to watch out for w/ Type I and Type II diabetes?
Type 1: diabetic ketoacidosis
Type II: HHS: hyperosmolar hyperglycemic state
Where are the beta cells and alpha cells located within the pancreas?
beta cells are inside. Think: insulin is inside.
alpha cells are on the periphery
delta cells are interspersed.
What is a strange thing that glucagon stimulates?
the release of insulin
T/F Insulin crosses the placenta.
False. it does not. glucose does
What are 2 weird functions of insulin?
Na+ retention in the kidneys
increased cellular uptake of K+ and amino acids (be are building things here, people!)
WHere is GLUT1 found?
brain, RBCs, cornea
Where is GLUT2 found?
pancreatic beta cells
kidney
liver
SI
Where is GLUT3 found?
brain
Where is GLUT5 found?
this is the fructose one
spermatocytes
GI tract
Which antibody is found in Type 1 diabetes?
islet cell antibody
for glutamic acid decarboxylase (GAD)
What is the genetic association w/ Type I diabetes?
HLA-DR3, HLA-DR4
What histo is seen in Type II diabetes?
islet amyloid polypeptide deposits
What are some different treatment options for neuropathic pain from diabetes?
gabapentin
pregabalin
duloxetine
amitriptyline
What are the 2 main categories of complications in diabetes?
non-enzymatic glycosylation
osmotic damage
what types of damage do you see with non-enzymatic glycosylation?
small vessel disease: retinopathy, glaucoma, neuropathy, nephropathy. leaky vessels. thickening of basement membrane
large vessel atherosclerosis contributor. Gangrene. MI.
What’s the deal with the retinopathy produced by diabetes?
nonprolif phase and then proliferative phase where you get the growth of a ton of blood vessels
leaky vessels. hemorrhage. blindness possible.
**may also see cotton wool spots (non-specific)
What types of damage do you see with osmotic damage in diabetes?
neuropathy (motor, sensory, autonomic)
cataracts
**think about sorbitol accumulation in tissue w/ aldolase reductase and without sorbitol dehyrogenase
Which tissues have aldolase reductase, but not sorbitol dehydrogenase? What is this MOA and damage?
Glucose–>Sorbitol via aldolase reductase
Sorbitol–>Fructose via sorbitol dehydrogenase
**schwann cells, lens, retina, kidney
Describe what is going on with DKA in T1DM emergencies.
insulin deficiency-determines severity
glucagon increases–>glucose increases & ketone bodies increase
**glucose leads to polyuria and dehydration
**ketone bodies are acids, leads to anion gap metabolic acidosis
get kussmaul respirations to try to compensate
no serum hyperosmolarity
Describe what is going on w/ HHS in T2DM emergencies.
no ketoacidosis
roughly normal insulin levels
this insulin inhibits lipolysis and ketone body formation
no kussmaul
extreme hyperglycemia>800
serum hyperosmolar>340!
Presenting symptoms: may be confusion, coma
What is the treatment for diabetic ketoacidosis?
ICU
IV Fluids (To fix dehydration)
Insulin drip (for the purpose of inhibiting lipolysis and ketone formation)
Monitor anion gap acidosis
Give insulin or even insulin and glucose until gap is closed
fix potassium and magnesium
