DB Pharmacology

jmanderson's version from 2015-11-08 19:03

Section 1

Question Answer
Glucagonincrease cCAMP (heart ionotropy and chronotropy), bypasses beta receptors, tx of beta-blocker induced cardiac depression
Insulin Glargine (Lantus) long-lasting insulin (24 h), onset 1-2 h, for basal use
Detemirlong-lasting insulin (17-32 h), onset 1-2 h, dose-dependent t1/2, given 1-2x/d
basal and bolus of insulin 0.5kg/units x pt wt (kg) / 3 per day
7 units TID bolus of insulin for 84 kg pt
Insulin detemir (Levemir) long-lasting insulin (17-32 h), onset 1-2 h, less acidic than glargine (won’t burn w/ IV), don’t mix syringe w/ other insulins
hyperglycemia sx polydipsia, polyuria, fatigue
correction (supplemental) insulin corrects hyperglycemia before/between meals, corrects hyperglycemia due to mismatch of nutritional intake or illness related factors or scheduled insulin admin., given w scheduled insulin doses to tx blood glucose above desired targets (does not replace scheduled insulin)
correction (supplemental) insulin do NOT hold if pt is NPO, can still use to correct hyperglycemia
carbs (glucose) to tx hypoglycemia (tachycardia, tremulousness, sweating)
hypoglycemia sx tachycardia, tremulousness, sweating
Glucagon SC tx severe hypoglycemia (confusion, agitation, LOC), stimulates gluconeogenesis and glycogenolysis
Lipodystorphy repeated insulin injections at same site
pramlinitideamylin analoge; suppresses glucagon secretion, slows gastric emptying, increases satiety
pramlinitideuse for DB1 or DB2 when using insulin w/o optimal control (add-on), ave HBA1C reduction of 0.6%, AE (hypoglycemia, N/V, anorexia, HA), reduce insulin dose by 30-50% when adding on
pramlinitideamylin analog; DI = delay absorption of other meds (could be problem in those w/ DB gastroparesis)
DB pts w/ COPD exacerbation must tx COPD exacerbation w/ steroids, but steroids increase serum glucose (monitor)
Aspart (novolog), lispro (Humalog), glulisine (apirdra) rapid-acting insulins
rapid-acting insulinsonset <15 min, duration 3-4 h, expensive, early hypoglycemia if erratic eating
rapid-acting insulinsanalogs preferred to regular insulin due to reduced risk of “stacking” doses
GLP-1 incretin hormone from L-cells in distal intestinal mucosa w/in min of eating, increase insulin,, suppresses glucagon, slows gastric emptying, increases satiety
GIPincretin hormone from K-cells of the intestine, increases insulin secretion, no effect on glucagon, gastric motility or satiety
DDP4 enzyme that breaks down incretins (decreases insulin, increases glucagon)
Saxagliptin2nd line for DB2, DDP4 inhibitor, concern for immunological rxn (DDP4 has a role in Tcell activation), decreases WBC count, associated w/ HF
GLP1 analogs for DB2, increase satiety, wt loss, admin subQ, AE (nausea, risk of THYROID C-CELL TUMORS)
LiraglutideGLP1 analog, risk of c-cell tumors
Metformin first line for DB2, reduced macrovascular complications in obese pts, fewer MIs/CVAs, decreases all cause mortality despite similar A1C levels
Metformin most common AE = diarrhea
Metformin most severe AE = lactic acidosis (rare, fatal)
Metformin avoid w/ renal dysfxn, liver failure, decompensated HF, alcoholism
Metformincimetidine inhibits tubular secretion w/ this
Sulfonylureas2nd line for DB2, inhibits ATP-sensitive K+ channels on beta-cells to increase insulin secretion (insulin goes from pancreas to portal vein and suppresses gluconeogenesis)
Glyburidesulfonylurea, metabolized by kidneys (avoid in pts w/ renal problems)
Sulfonylureas1st line in DB2 pts who can’t take metformin, reduces microvascular complications
Gemfibrozil lowers cholesterol, doubles t1/2 of repaglinide (prolongs hypoglycemia)
TZDsbind to PPAR-gamma on fat/vascular cells, causes preadipocytes to differentiate into mature fat cells, more sensitive to insulin, able to stor FFAs, increase # of glucose transporter cells
TZDsAE = HF (CI in class III/IV HF)
alpha-glucosidase inhibitors 3rd line for DB2, inhibit enzymes at brush border of small intestine, delays breakdown of sucrose to complex carbs, reduce rise in postprandial blood sugar, AE = flatulence
Acarbose alph-glucosidase inhibitor
Bromocriptine 3rd line for DB2, dopamine agonist, metabolized by CYP3A4 (DI w/ inhibitors [cimetidine, clarithromycin] and inducers [carbamazepine])
canagliflozinSGLT2 inhibitor
SGLT2 inhibitor AE = female genital fungal infections, UTI, increase urination, risk of symptomatic hypotension
3 months how long to wait before adding 2nd DB drug when target A1c is not achieved
insulin give this when A1c is really high (drops A1c by 3.5)
Sulfonylureas and meglitinides avoid w/ pts that have complex insulin regime (e.g., prandial insulins)

Section 2

Question Answer
LisproShort acting insulin
basal NPH + regular insulinConventional therapy for DM
Somogyi phenomenon Early morning hyperglycemia (ie: 7 am) secondary to late evening (ie: 2 am) hypoglycemia
Long- or intermediate-acting insulin causes 2 am hypoglycemia. --> stimulates counter regulatory (glucagon) hormones to increase blood glucose
Somogyi phenomenon If this develops the physician should decrease long-acting insulin
Sulfonylureaused in T2DM; adverse effects= hypoglycemia and SIADH, disadvantages=potential for severe, prolonged hypoglycemia and weight gain
alpha glucose inhibitorsused in T2DM; disadvantage= increased delivery of CHO to colon resulting in flatulence and diarrhea
Mechanism of action of gliptinsincreases incretins by inhibiting DPP-4 (enzyme that inactivates incretins) thus increasing glucose mediated insulin secretion and suppresses glucagon secretion
Site of action of sulfonylureabind to pancreatic islet cell membrane --> decrease K+ permeability --> membrane depolarization --> increase intracellular Ca2+ --> exocytosis of insulin containing secretory granules
Acarbose (alpha glucosidase inhibitor) mechanism of actioncomplex oligosaccharide that decreases digestion of ingested CHO; competitive, reversible inhibition of intestinal brush border enzymes (hydrolyze polysaccharides to glucose)
Metformin serious side effect lactic acidosis; CI in renal failure

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