67: Antidiabetic Agents Flashcards
alpha cell –>
beta cell –>
glucagon
insulin and amylin
d cell - somatostatin
g cell - gastrin
F cell - pancreatic polypeptide
+ regulation of insulin release
glucose amino acids incretins epi/B2 adrenergic stimulation vagus stimulation
- regulation of insulin release
NE/a2 adrenergic stimulation
amylin
which glucose transported is associated with insulin mediated uptake of glucose?
glut 4
found in muscle and adipose tissue
\+ or - with insulin: gluconeogenesis glycogenolysis glcogenesis glycolysis
+
+
s/s type I DM
polyuria/nocturnal enuresis thirst blurred vision WL/polyphagia weakness/dizziness paresthesia level of consciousness
s/s type II DM
asymptomatic initially infections neurpathy severe insulin deficiency signs obesity and metabolic syndrome
FPG – DM range
greater than 126 mg/dL
pre-diabetes is 110-125
CPG greater than 200
oral glucose tolerance test greater than 200
insulin is absolutely required for…
type I DM
therapeutic goal with insulin
FPG between 90-120
28 U equals =
1 mg
rapid acting insulins
lispro
aspart
glulisine
inhaled insulin
short acting insulin
regular insulin (pump type)
intermediate acting insulin
NPH
long acting insulin
glargine
determir
key feature rapid acting insulins
aa alteration in c-terminal tail of B peptide preventing insulin complex formation
key feature short acting insulins
identical to human insulin, forms complexes
key feature intermediate acting insulin
protamine-insulin complex
key feature long acting insulin
aa substitiutions that result in precipitate formation at more neutral pH in the body
duration of insulins: rapid short intermediate long
3-5 hr
4-12 hr
10-20 hr
12-20 h (glargine) r or 22-24 hr (detemir)
most common adverse effect to insulin therapy
hypoglycemia
tx: give glucose or give glucagon
s/s tahcycardia, sweating, tremors, nausea, hunge, coma, loss of consciousness
adverse effects of insulin therapy
hypoglycemia (insulin therapy too effective)
hypersensitivity (immune response to noninsulin prtn contaminants)
resistance (anti-insulin antibodies)
lipohypertrophy (fat deposition at injection site)
lipoatrophy (fat loss at injection site)
MOA glucagon and use
treat hypoglycemia
injected peptide
catabolism of stored glycogen to increase blood glucose levels
key points metformin
- first line agent
- doesn’t produce hypoglycemia
- not dependent upon B cell function