Week 7: Type 2 DM Flashcards
DKA in which type of DM
Either Type 1 or 2 DM
Antibody testing negative for Type 1 or 2 DM
C-peptide testing for Type 1 or 2 DM
C-peptide testing
Injected insulin does not have C-peptide
Type 1 DM shouldn’t have C-peptide
if you don’t know what type of DM they have
Low C-peptide levels at Dx DM1 or DM2
could be either if DM1 in early Dx
DM2 late in Dx can be low
Epidemiology of DM
Increased adiposity in DM2
Type 2 DM mechanism
increased adiposity
increased energy intake
ectopic FAs accumulation
so what happens is there are breakdown products from FA deposition and interfere with insulin signaling leading to insulin resistance and can lead to DM2
ability for pancreas to keep up with excess insulin secretion can decrease leading to DM2
Risk for DM2
Methods for Dxing DM2
- Fasting glucose level (1 day)
- oral glucose tolerance (1 day)
- HbA1c (~ 3 months) (glycosylated Hb)
*
Diagnostic criteria for DM2
Also random glucose of >200 mg/dL
Treatment options for DM2
- Metformin
w/ Heart disease
- SGLT-2 inhibitors
- GLP-1 inhibitors
- TZDs
- Sulfonylureas
1st line therapy for DM2
Metformin
Metformin Effects
- Suppresses hepatic glucose production (gluconeogenesis)
- Increase insulin sensitivity
- Increase peripheral glucose uptake
- Decrease GI absorption of glucose
Metformin Side effects
GI intolerance/Diarrhea
Natural history of DM
aging is a bitch
SGLT-2 Inhibitors effects
inhibits SGLT-2 channel in the proximal tubule of the nephron
prevents reabsorption of Glucose and Na
loses calories in the urine and diuretic effect for blood pressure
List of SGLT-2 Inhibitors
GLP-1 Agonists effects
Normally when we eat carbohydrates the L cells of the small intestines secrete GLP-1 and it acts on a variety of receptors
GLP-1 receptors in the:
- β cells of the pancreas ((augment glucose-dependent insulin secretion *only increased insulin secretion during meals preventing low blood sugars* unlike sulfonylureas)
- Alpha cells of the pancreas (reduce postprandial glucagon secretion reducing glucose output from the liver)
- Stomach (slows down emptying of the stomach helping them feel full sooner and also slows down the absorption of carbohydrates)
- CNS (promotes satiety and reduces appetite)
Glucose lowering and reduction of weight
Don’t see a lot of hypoglycemia,
Caveat of GLP-1 agonists
When GLP-1 is secreted from the small intestines, it is rapidly inactivated by DPP-4
GLP-1 agonists are resistant to DPP-4 degradation)
DPP-4 inhibitors
inactivate DPP-4 preventing the inactivation of endogenous GLP-1
don’t see a lot of hypoglycemia
List of GLP-1 agonists
List of DPP-4 inhibitors
Sulfonylureas effects
help the pancreas make more insulin
Glucose in glucose transporter and glycolysis and TCA to generate ATP
ATP less K+ leaves islet cell and depolarizes cell and voltage-gated Ca2+ channel opens causing Ca2+ influx and causes insulin exocytosis and secretion
Sulfonylureas inhibits the K+ channel in substitution of ATP to cause depolarization and insulin secretion
Problem is that it doesn’t matter if the patient is eating or not
