sig for different types of insulin
rapid: 5-15 mins before meals
short: 30 mins pre meal
intermediate: bid (before bfast and dinner)
long: od to bid
longest acting insulin
newest: insulin degludec
types of insulin based on use
basal: nph, long acting insulin
prandial: regular, rapid-acting
combination
what is nph + regular insulin
3 total injections
- morning: bolus of regular + nph
- afternoon: regular
- night: regular + nph
what is long acting + rapid acting insulin
4 total injections
- 1 basal insulin
- 3 prandial rapid acting
what is pramlintide
- other agent approved for t1dm
- amylin agonist
- moa: causes appetite suppression, slows gastric emptying (satiety), inhibits release of glucagon (dec glycogenolysis)
glycemic targets
hba1c <7%
pre meal 80-130
post meal 180
three pronged approach to t2dm management
- individualized glycemic control
- treat associated conditions
- screen for dm complications
drug classes for treating dm
1 biguanides 2 sulfonylureas 3 non-su insulin secretagogues 4 a-glucosidase inhibitors 5 dpp-4 inhibitors 6 sglt-2 inhibitors 7 glp-1 receptor antagonists 8 thiazolidinediones 9 insulin
what are biguanides
- moa: reduced hepatic glucose production
- lowers fbs
- contra: discontinues if hospitalized, on npo, or radiocontast given
- metformin
what are sulfonylureas
- moa: stimulate insulin secretion (atp sensitive k channels on beta cells)
- dec in fbs and ppbs
- most effective for recent onset dm
- “g-ide”s (glipizide, glyburide, gliclazide)
- ades: hypoglycemia, weight gain
what are glinides/non-su
- moa: stimulate insulin secretion (sur1 portion)
- dec ppbs
- “glinide”s (repaglinide, mitiglinide)
- ae: hypoglycemia
what are incretin based therapies: glp1 receptor agonists
- moa: mimic endogenous incretins
- dec fbs and ppbs
- promotes weight loss
- contra: medullary thyroid ca, pancreatic disease
- “tide”s
- injectable
what are incretin based therapies: dpp4 inhibitors
- moa: prevent degradation of endogenous glp1
- reduce ppbs
- “liptin”s
- oral
what are alpha glucosidase inhibitors
- moa: reduce glucose absorption in small intestines
- dec ppbs
- “bose”
- contra: gi problems
what are thiazolidinediones
- moa: reduce insulin resistance by binding to nuclear receptor ppary, increased expression of glut4
- promotes glucose uptake, redistribution of fat
- “glitazone”
what are sglt2 inhibitors
- moa: urinary glucose excretion (only insulin independent drug)
- weight loss and bp reduction (diuretic)
- “aglifiozin”
- ade: genital mycotic and uti, orthostatic hypotension
strongest hba1c reduction agent
insulin, then mnt and lifestyle change
other therapies
read: colesevelam and bromocriptine
indications for insulin therapy in t2dm
initial therapy for
- very high baseline glucose with possible glucotoxicity
- hypercatabolic diabetics
- renal and liver patients
- hospitalized or acutely ill
insulin therapy strategies
- start with bedtime basal insulin
- can combine with ohas except sus
initiation of oral medication for t2dm
- <200 mgdl = 1 oral agent
- 200-250 mgdl = 2 oral agents/dual therapy
- > 250 mg = insulin agad
unite for diabetes philippines cpg
- hba1c <9 AND fbs <250 = monotherapy
- hba1c >9 AND fbs >250 = combination OR insulin
guidelines of aa endo
- first line: lifestyle therapy
- hba1c <7 = monotherapy, metformin
- hba1c 7.5-9 = dual or triple therapy with metformin as primary
- > 9, no symptoms = dual or triple therapy
- > 9, with symptoms = insulin +/- others
