Diabetes medications

Revision as of 05:20, 13 March 2011 by Rossdonaldson1 (talk | contribs) (Source)

Hypoglycemics- sulfonylureas, benzoic acid derivatives

Antihyperglycemics- biguanides, alpha glucosidase inhibitors and thiazolidinediones


- type 2 dm- overproduction and under utilization of glucose

- diet and exercise best

- if sugar not controlled with one agent, add bedtime insulin or second agent

- if still not controlled p 2 meds either do 2 orals + nighttime insulin, or mixed split insulin regimen or third oral agent


- increase insulin secretion and enhance activity

- second and third gen sulfonyls are lipid soluble so penetrate cell mem better and have selective binding

- stimulate insulin release from panc beta cells by inhibiting atp dependent potassium channel.

- Decrease hepatic insulin clearance= increase insulin conc

- Elevated insulin level feeds back to liver and causes decrease hepatic gluc prod

- Secondary treatment failure from noncompliance, wt gain, desensitized beta cells, and escalating insulin resistance and increased insulin deficiency

- Sulfon has hepatic metab, renal exretion and prolonged activity

- Toxicity related to hypoglycemia

- Risk factors for hypoG- elderly, poor diet, alcohol, renal/ hepatic dz, polypharmacy

- Time to peak effect and duration of effect important in OD

- Chlorpropamide, glyburide and glypizide most likely to cause hypoG

- Do not use glyburide in pt with CRI since renally excreted

- If pt well and young, will not get hypoG during fast due to counterregulatory hormones for glucose homeostasis

- Chlorpropamide can cause hyponatremia regardless of dose- induces ADH secretion- risk increases with elderly and if on thiazide diuretics

- Chlorpropamide can also give cholestatic jaundice, resolves with discontinuation

- Glypizide- enterohepatic recirculation- prolonged action if liver dz. Long duration of action since metabolite still active. All metabolites renally cleared


- metformin, phenformin and buformin

- phenformin no longer used due to lactic acidosis

- metformin does not cause wt gain like sulfonyls

- effect is to decrease hep glucose prod, inhibit intestinal glucose absorption

- also decreases fatty acid oxidation

- increases insulin sensitivity and decreases insln resis

- decrease sugar of dm pt not normal person- so is antihyperglycemic agent not hypoglycemic agent

- 100% renal excretion

- most serious side effect is lactic acidosis- aerobic type by increased lactate production- not tissue hypoxia

- signs of lactic acidosis- nonspecific- nvd, abd pain, sleepy, tachypnia, lethargy- seen mostly if renal/ liver dz, alcohol, heart dz, infection

- metformin exclusion criteria- CRI, cardiac/ pulm insuff, h/o lactosis, profound infc, liver dz, alcohol, iv contrast agents

- fatality from metformn lactosis not related to lactate levels or metformin level but rather to concomitant condition (hypoxia) resulting in elevated lactate

- OD- hypoglycemia rare, can get lactosis- obs for 6-8 hr and tx c bicarb and consider hemodialysis

Alpha Glucosidase Inhibitors

- acarbose, miglitol, voglibose

- competitively and reversibly inhibit alpha glucosidase brush border hydrolase enzyme- makes postprandial decrease in carbohydrate absorption since complex polysaccharides not broken down into absorbable monosaccharides

- does not affect lactose absorption

- if hypoG- sucrose/ table sugar will not work- use glucose- po or iv

- take these meds with each meal with first bite

- since limited aborption, stays in gut and side effects mostly GI- bloating, gas, diarrhea

- contraindications- cirrhosis, IBD, malabsorption synd

- alpha glucs do not cause hypoG when used as monotx

- acarbose- can cause transaminitis/ liver inj

- since min absorption- systemic tox from OD unlikely


- rosiglitazone and poiglitazone

- enhance insulin effect on muscle, fat, liver without increasing panc insulin secretion

- protein bound and hep metab- not good if liver dz

- side effects- induce ovulation, increase plasma vol bad if CHF, decrease effectiveness of OCP's

Benzoic Acid Derivatives

- repaglinide- mono or combo tx c metformin

- binds to atp dependent potassium channel like sulfonyls but at different site.

- Unlike sulfonyls, it decreases insulin lvls

- Dose 30 min before meal to decrease post prandial hyperglycemia