Flashcards in Diabetes Deck (57):
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.
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?
**insulin also increases the amount of GLUT4 receptors on the surface
Describe the basic symptoms of diabetes?
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
Where is GLUT3 found?
Where is GLUT5 found?
this is the fructose one
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?
What histo is seen in Type II diabetes?
islet amyloid polypeptide deposits
What are some different treatment options for neuropathic pain from diabetes?
What are the 2 main categories of complications in diabetes?
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)
**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.
roughly normal insulin levels
this insulin inhibits lipolysis and ketone body formation
Presenting symptoms: may be confusion, coma
What is the treatment for diabetic ketoacidosis?
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
What is the treatment for HHS?
insulin--for the purpose of decreasing serum glucose
What are some common triggers of DKA in T1DM patients?
undiagnosed diabetes-first presentation!
missed insulin doses
alcohol or drug abuse
Severe medical illness (MI, CVA, trauma)
infection (pneumonia, gastroenteritis, UTI)
What are the short-acting insulins used with meals?
What are the long-acting 24 hour insulins?
Regular insulin is usu depleted at about ___ hours.
NPH is a type of insulin that lasts ___ hours.
12 hours, fully gone by 18 hours
What are incretins?
made in GI
increase insulin secretion
messed up in T2DM
What is the MOA of DPP-4 inhibitors?
inhibit DPP-4, which inhibits GLP-1 and other incretins
What is the effect of incretin?
delays gastric emptying
What are the DPP-4 inhibitors?
What is the MOA of GLP-1 agonists?
act like an incretin
exenatide is made from a hormone found in Gila monster saliva
**increase satiety and may even cause weight loss!
What are the SE of GLP-1 agonists?
increased risk for acute pancreatitis
What are the GLP-1 agonists?
What is the MOA of SGLT-2 inhibitors?
inhibit sodium glucose linked transporter in the kidney
blocks reabsorption of glucose
**can also cause weight loss
What is the SE of SGLT-2 inhibitors?
need normal kidney
can increase risk of UTIs b/c of increased glucose down there
What are the SGLT-2 inhibitors?
Which diabetes meds have hypoglycemia as an SE?
Which drugs are not safe in patients with fluid balance problems, such as CHF?
Which drugs should not be used in patents with kidney dysfunction?
Which drugs may actually help w/ weight loss?
What is a useful diabetes med for patients with kidney dysfunction,b /c it is metabolized by the liver?
Which drugs decrease hepatic gluconeogenesis?
What is a possible non-insulin treatment for patients with organ failure?
What are possible fatal effects of DKA?
cardiac arrhythmias b/c of altered K+ & Mg
-include Vtach and torsades de point(mg)
Mucormycosis-->brain abscess if sinus infection
What are the biguanides and their MOA?
basically, decrease gluconeogenesis, increase glycolysis, increase peripheral glucose uptake and increase insulin sensitivity
**can be used if patients don't have islet cell function
What are the SE & contraindications of metformin?
lactic acidosis--watch for patients w/ renal insufficiency
What is the MOA of sulfonylureas? And the 2nd gen drugs?
inhibit K+ pump on pancreatic beta cells. Cause depolarization, ca++ influx and release of insulin
What are the SE of the 2nd gen sulfonylureas?
What are the 1st gen sulfonylureas and their potential side effects?
What is the MOA of TZDs? What are they?
increase insulin sensitivity by binding to PPARgamma
regulates fatty acid storage and glucose metabolism
What are the SE of TZDs?
Edema->bad for CHF
What is the MOA of amylin analogs?
decrease gastric emptying
**amylin usu released w/ insulin