Term
|
Definition
| Amylin agonist administered via subcutaneous injection to suppress gastric emptying, decrease glucagon release, and reduce appetite. Pramlintide is given in addition to insulin and can cause hypoglycemia, N/V, and anorexia. Therefore, insulin dosages should be reduced by approximately 50%. |
|
|
Term
|
Definition
| An alpha-glucosidase inhibitor, which competively inhibits intestinal alpha-glucosidases and reduces post-meal glucose excursions by delaying the digestion and absorption of starch and disaccharides. |
|
|
Term
|
Definition
| Reduces the conversion of starch and disaccharides to monosaccarides. This enzyme inhibition leads to a decrease in upper intestinal digestion and defers digestion of the ingested starchees and disaccarides to the distal small intestine, thereby lower post-meal glycemic excursions as much as 45-60mg/dL and creating an insulin-sparing effect. |
|
|
Term
| Acarbose: Uses and adverse effects |
|
Definition
| Used in Type 2 Diabetes. Side effects: GI symptoms. Cannot use if impaired renal/hepatic function, or with intestinal disorders. |
|
|
Term
|
Definition
| Lowers blood glucose concentrations by stimulating the release of insulin from functioning beta cells of pancreatic islet tissue. This is accomplished by a selective ion channel mechanism. Repaglinide inhibits adenosine triphosphate (ATP)-potassium channels on the beta cell membrane and potassium efflux. The resulting depolarization and calcium influx induces insulin secretion. |
|
|
Term
| Repaglinide Pharmacokinetics |
|
Definition
| Absorption to peak 1 hr, 56% bioavailability, distribution- protein binding greater than 98%, Metabolism- hepatic via P450, excretion- 90% fecal, Half-life 1 hour |
|
|
Term
| Repaglinide Administration and Use |
|
Definition
| Take up to 30 minutes prior to meal, if meal is skipped then skip dose. Given twice a day or up to four times a day based on response to therapy. Hypoglycemic-Given to improve fasting blood glucose and HbA1c for type 2 DM. Monitor blood glucose levels, HbA1c, signs and symptoms of hypoglycemia and hyperglycemia. |
|
|
Term
| Repaglinide Toxicity & ADE |
|
Definition
| Toxicity- Hypoglycemia, seizures, confusion, metabolic acidosis, coma and death. ADE- mild GI upset (nausea, vomiting, diarrhea, constipation), acute hepatitis in elderly patients. |
|
|
Term
|
Definition
| MOA: antidiabetic, dipeptyl Peptidase-IV inhibitor that increases and prolongs incretin hormone activity which are inactivated by DPP-4 enzyme. SE: Hypoglycemia, HA, URI ADR: Pancreatitis-acute, Anaphylaxis, angiodema, generalized exfoliative dermatitis, Steven Johnson Syndrome, Rhabdomyolysis, Abnml renal fxn, Acute renal failure. Dosing:100mg daily. CrCl 30-50 mL/min give 50mg daily, for less than 30 give 25mg daily. Severe drug/drug intxn:Nilotinib and Lomitapide- increase absorption of P-glycoproteine substrates. |
|
|
Term
|
Definition
| An insulin secretagogue in the second generation sulfonylurea family. MOA= increase insulin release from the pancreas. Onset 30 min, take right before meals. Reduces HbA1c 1.5-2%. Can be used in combination. ADRs= hypoglycemia, weight gain, GI upset. Posssibility for allergy in pt.s allergic to sulfa. |
|
|
Term
|
Definition
| 1st line drug for DMII. Biguanide.Started as soon as DMII diagnosis is made.Used alone or in combination with other antihyperglycemics. |
|
|
Term
|
Definition
| MOA: 1. inhibits glucose production in the liver. 2. Slightly reduces glucose absorption in the gut. 3. sensitizes insulin receptors in target tissues (skeletal muscle) and therefore increases glucose uptake in response to any insulin available. Does Not stimulate insulin release from pancreas. |
|
|
Term
|
Definition
| Slowly absorbed in small intestine, not metabolized, excreted unchanged by kidneys, can accumulate to toxic levels in renal impairment. |
|
|
Term
|
Definition
| Good for use in people who skip meals because it does not lower blood glucose. |
|
|
Term
|
Definition
| ADRs- decreased appetite, nausea, diarrhea, decreases in folic acid and B-12 absorption, Lactic acidosis in people with HF, renal impairment, infection, liverdisease or chronic ETOH use. |
|
|
Term
|
Definition
| Drug interactions- ETOH, cimetidine H2 blocker (lactic acidosis), IV contrast (renal impairment and lactic acidosis), |
|
|
Term
|
Definition
| A thiazolidinedione (glitazone) that works by enhacing insulin sensitivity in muscle, fat, and liver tissues. Overall effect of a decrease in insulin resistance by increased glucose uptake by muscles and adipose tissue. Pioglitazone is associated with a decrease in serum glucose levels by 30-60mg/dl and less secondary failure in the beta cells. May take weeks to months to see an improvement in glucose levels. ADR include liver dysfunction, edema, weight gain, and ovulation. May be associated with an increased risk for MI. Has a once daily dosing regimen but is very expensive. This medication is contraindicated in those with CHF as Pioglitazone increases plasma volume (edema). Use cautiously in those with liver impairement. |
|
|
Term
|
Definition
Synthetic version of exendin-4, a hormone found in the saliva of the Gila
monster. It displays biological properties similar to human glucagon-like
peptide-1 (GLP-1), a regulator of glucose metabolism and insulin secretion. |
|
|
Term
|
Definition
enhances
glucose-dependent insulin secretion by the pancreatic beta-cell, suppresses
inappropriately elevated glucagon secretion, and slows gastric emptying,
although the mechanism of action is still under study. |
|
|
Term
|
Definition
Exenatide is approved as adjunctive therapy to improve
glycemic control in patients with type 2 diabetes mellitus who are taking
metformin, a biguanide, or a combination of metformin and a sulfonylurea, but
have not achieved adequate glycemic control. |
|
|
Term
|
Definition
The main side effects of Exenatide use are gastrointestinal
in nature, including acid or sour stomach, belching, diarrhea, heartburn,
indigestion, nausea, and vomiting; Exenatide is therefore not meant for people
with severe gastrointestinal disease. Other side effects include dizziness,
headache, and feeling jittery. Severe side effects are necrotizing and hemorrhagic
pancreatitis. |
|
|
Term
| Exenatide Administration and dosage: |
|
Definition
Exenatide is administered as a subcutaneous injection (under
the skin) of the abdomen, thigh, or arm, any time within the 60 minutes before
the first and last meal of the day. Therapy is initiated at 5 mcg twice daily
with a max of 10 mcg twice daily. |
|
|
Term
|
Definition
| A bisphosphonate used in osteoporosis that inhibits bone resorption by suppressing activity of osteoclasts. |
|
|
Term
|
Definition
| An insulin secretagogues, its MOA is similar to sulfonylureas. It binds to receptors on beta cells of the pancreas and inhibits the efflux of potassium ions into the cell. This depolarizes the cell and open calcium channels resulting in a calcium influx and release of preformed insulin. The release of insulin lowers blood sugar levels. |
|
|
Term
|
Definition
| Very fast onset of action. Peak concentrations within 1 hour on ingestion. Half-life of 1 hour with a duration of 4-7 hours. It is hepatically cleared. |
|
|
Term
|
Definition
| Stimulates insulin production to lower blood glucose levels after a meal. Only for type 2 diabetes 0.25 to 4mg dose should be taken just before meals. Should not be taken without a meal because of risk of hypoglycemia. |
|
|
Term
| Repaglinide Adverse Effects |
|
Definition
| Headache, hypoglycemia, upper respiratory infection, ischemia, chest pain, constipation, diarrhea, back pain, and urinary tract infection |
|
|
Term
| Repaglinide Contraindications |
|
Definition
| Impaired liver fiction because it is hepatically cleared, type 1 or insulin dependant diabetes. Patients taking gemfibrozil |
|
|
Term
|
Definition
| regulates gene expression by binding to peroxisome proliferator-activated receptor (PPAR)-γ and PPAR-α, causing a reduction in insulin resistance |
|
|
Term
|
Definition
| fluid retention, edema, anemia, weight gain, macular edema, bone fractures in women; do NOT use in patients with CHF or hepatic disease |
|
|
Term
| Pioglitazone Clinical Use |
|
Definition
|
|
Term
|
Definition
| An inhibitor of cGMP specific phosphodiaterase type-5 (PDE5) in smooth muscle. Sildenafil increases cGMP within vadcular smooth muscle resulting in vasodilation and relaxation.In erectile dysfunction PDES5 is inhibitied with release of nitric oxide during sexual stimulation causing increased levels of cGMP and inflow of blood flow to the corpus cavernosum resulting in erection. |
|
|
Term
|
Definition
| Mean delay in Tmax of 60 minutes with ingestion of high fat meal, protein binding, Hepatic metabolism, excretion - fecal, elimination 1/2 life=4 hr. |
|
|
Term
|
Definition
| headach, insomnia, indigestion, visual disturbances, hearing disturbances, flushing, epistaxis, cardiovascular morbidity, myocardial infarction, priapism, prolonged erection |
|
|
Term
|
Definition
| reduce hepatic glucose production through activation of the enzyme AMP-activated protein kinase. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| lactic acidosis, N/V, anorexia, diarrhea. Also metformin is contraindiacted in patients with renal disease, alcoholism, hepatic disease, or conditions predisposing to tissue anoxia. |
|
|
Term
|
Definition
| inhibitor of DPP-4, the enzyme that degrades incretin hormones; increases circulating levels of native GLP-1 and glucose-dependent GIP. |
|
|
Term
| Sitagliptin Pharmakentics |
|
Definition
| bioavailibility of over 85% and achieves peak concentrations with 1-4 hours. Half life is about 12 hours. |
|
|
Term
| Sitagliptin Clinical Uses |
|
Definition
| For use in Type II Diabetes |
|
|
Term
| Sitagliptin Adverse Effects |
|
Definition
| Rhinitis, upper respiratory infections, headaches, pancreatitis |
|
|
Term
|
Definition
| Synthetic analog of amylin (hormone that modulates appetite, gastric emptying, and glucagon and insulin secretion); Amylin agonist which suppress glucagon release via an undetermined mechanism |
|
|
Term
| Pramlintide Clinical Uses |
|
Definition
| Type 1 and Type 2 diabetes |
|
|
Term
| Pramlintide Pharmacokinectics |
|
Definition
| Should be injected immediately before eating; It is rapidly absorbed after subcutaneous administration; levels peak within 20 minutes adn the duration of action is not more than 150 minutes; Renally metabolized and excreted |
|
|
Term
|
Definition
| Nausea, anorexia, hypoglycemia, headache |
|
|
Term
|
Definition
| Glucagon-Like Polypeptide-1 Receptor Agonists with multiple actions such as the potentiation of glucose mediated insulin secretion, suppression of postprandial glucagon release, slowed gastric emptying, and a central loss of appetite. |
|
|
Term
|
Definition
| Used in conjunction with metformin (or metformin and a sulfonylureas) in people with Type II DM. |
|
|
Term
|
Definition
| Weight loss, nausea, anorexia, necrotizing and hemorrhagic pancreatitis. Antibodies to exenatide are formed with chronic use. |
|
|
Term
|
Definition
| Biphosphonate that has many effects on bone mineral homeostasis such as increasing bone mineral density and slowing bone resorption. Inhibits farnesyl pyrophosphate synthase which is critical for osteoclast survival. Also inhibit 1,25(OH)2D production and intestinal calcium transport, cause metabolic changes in bone cells such as inhibition of glycolysis and cell growth and changes in acid and alkaline phosphatase activity. |
|
|
Term
| Alendronate pharmacokinetics |
|
Definition
| Less than 10% oral absorption (administer on empty stomach). Half of absorbed drug accumulates in bone and is often retained in bone for months. Drug is excreted in urine unchanged. |
|
|
Term
| Alendronate adverse effects |
|
Definition
| Esophageal and gastric irritation. Take with full glass of water and remain upright for 30 minutes to decrease irritation. Otherwise free of adverse effects. Rare femur fractures may occur in patients on long-term treatment. |
|
|
Term
| Alendronate clinical uses |
|
Definition
| Hypercalcemia associated with malignancy, Paget's disease, osteoporosis |
|
|
Term
|
Definition
| Alpha-glucosidase inhibitor-Only monosaccharides can be transported out of the intestinal lumen and into the bloodstream.This enzyme inhibitor inhibits intestinal alpha glucosidase which minimizes upper intestinal digestion, and defers digestion of the ingested starch and disaccharides to the distal small intestine lowering postmeal glycemic excrsions. |
|
|
Term
|
Definition
|
|
Term
|
Definition
GI symptoms: flatulence, diarrhea, abdominal pain d/t undigested carbohydrates in the colon that is fermented into short-chain fatty acids. These symptoms tend to diminish with ongoing use.
Hypoglycemia
Contraindicated in patients who have Inflammatory bowel disease, intestinal disorders, and impaired renal or hepatic function |
|
|
Term
|
Definition
| Reduces conversion of starch and disaccharides to monosaccharides and reduces post prandial hyperglycemia |
|
|
Term
|
Definition
| second generation sulfonylureas |
|
|
Term
|
Definition
| sulfonylureas increase insulin relaease from the pancreas, there is also a reduction of serum glucagon levels |
|
|
Term
|
Definition
| short 1/2 life of 2-4 hours, (less side effects such as serious hypoglycemia) ingest 30 minutes before breakfast, start with 5mg/d single dose, up to 15mg/day Contraindicated in patients with significant hepatic or renal impairment |
|
|
Term
|
Definition
| Supporesses glugagon release via undetermined mechanisms, delays gastric emptying, and has CNS mediated anorexic effects |
|
|
Term
|
Definition
| Hypoglycemia, nausea, vomiting, and anorexia |
|
|
Term
| Pramlintide administration considerations |
|
Definition
| Should be injected immediately before eating; patients taking concurrent rapid acting meal time insulin should have this dose decreased by 50% or more to reduce the risk of hypoglycemia. Cannot be combined with other insulins, needs to be administerd in a seperate syringe. |
|
|
Term
| Pramlintide class and indications |
|
Definition
| Amylin synthetic analog; amylin modulates appetite, gastric emptying, and glucagon and insulin secretion. It is an injectable antihyperglycemic agent that modulates postprandial glucose levels. Approved for patients with type 1 and 2 diabetes. |
|
|
Term
|
Definition
Diabetes Drug
MOA:
Thiazolidinedione (TZD)- ligand of PPAR (peroxisome prliferator-activated receptor) gamma receptors that DECREASE INSULIN RESISTANCE
*part of the steroid family (thus they modulate/alter gene expression)
* Bind to peroxisome proliferator activated receptors involved in transcription of insulin response genes
**decreases insulin resistance & promotes glucose uptake in liver, muscle & adipose tissue |
|
|
Term
Pioglitazone
(clinical uses) |
|
Definition
-NIDDM
(these drugs need insulin to work, therefore they can't be used in IDDM pts b/c these pts don't make insulin)
*do NOT use in IDDM pts w/ ketoacidosis
(do NOT use in CHF or liver disease pts either) |
|
|
Term
|
Definition
Liver Dysfunction (check LFTs at baseline & periodically)... do NOT use in pts w/ liver disease
-can cause ovulation
-wt gain
-edema
-causes expansion of plasma volume & edema... lead to MI... do NOT use in CHF pts
$$$$Very Expensive$$$ |
|
|
Term
|
Definition
| Glucagon-like polypetide-1 receptor agonist. Works by binding to receptors of GLP-1 (glucagon-like peptide-1) to potentiate glucose-mediated insulin secretion or inhibit postprandial glucagon release Administered as subcutaneous injection for single treament or adjunct to oral hypoglycemics. If administered as adjunct with oral hypoglycemics, the oral hypoglycemic dose should be reduced to prevent hypoglycemia. |
|
|
Term
|
Definition
| Major: nausea, vomiting and diarrhea caused by the other action the medication does: delay gastric emptying and reduction of appetite. Serious/fatal: necrotizing and hemorrhagic pancreatitis |
|
|
Term
|
Definition
competitively and reversibley inhibits pancreatic alpha-amylase and membrane-bound intestinal alpha-glucoside hydrolases; does not enhance
insulin secretion and when used as monotherapy should not cause
hypoglycemia; decreases the insulinotropic and weight-increasing effects of sulfonylureas when used concurrently |
|
|
Term
|
Definition
lowers postprandial blood glucose concentrations in patients with
DM II |
|
|
Term
|
Definition
| Abdominal pain, Diarrhea, Flatulence |
|
|
Term
| Repaglinide Clinical Uses |
|
Definition
| Oral agent used in addition to diet and exercise as a treatment for diabetes mellitus. In the catagory of medications called secretagogues, it causes release of insulin from the pancreas. |
|
|
Term
|
Definition
| By closing potassium channels and causing a calcium influx in beta cells, insulin secretion is stimulated. Share 2 common binding sites for stimulation with sulfaonylureas. Have one unique site.. |
|
|
Term
|
Definition
| Hypoglycemia, weight gain. |
|
|
Term
|
Definition
| relates to mealtime.... pre-prandial= before meals, post-prandial= after meals |
|
|
Term
|
Definition
Dipaptidyl Peptidase- 4 (DPP-4) Inhibitor: BLOCKS the breakdown of GLP-1 (glucagon-Like Polypeptide-1) which raises the amount of GLP-1 in circulation
This causes:
--decreased post meal glucose excursion
--INcreases glucose-mediated insulin release
--Lowers Glucagon levels
--Slows Gastric Emptying
--Decreases Apetite |
|
|
Term
| Sitagliptin (Clinical Indices) |
|
Definition
| Adjunct therapy for people with DM-2 who have failed to show glycemic control with diet and exercise |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Biguinide euglycemic; 1st line therapy for DMII; activates AMPK; ↓ hepatic glucose production; ↓ intestinal glucose absorption; ↑ insulin sensitivity; does not ↑ insulin secretion and should not cause hypoglycemia; GI related ADRs are common; contraindicated in liver or renal dysfunction, EtOH abuse, or predisposition to tissue anoxia (risk of lactic acidosis) |
|
|
Term
|
Definition
| Inhibitor of cGMP specific phosphodiesterase type-5 (PDE5) in smooth muscle, where PDE5 is responsible for degradation of cGMP. Sildenafil increases cGMP within vascular smooth muscle cells resulting in relaxation and vasodilation. In patients with pulmonary hypertension, this leads to vasodilation of the pulmonary vascular bed and, to a lesser degree, vasodilation in the systemic circulation. In patients with erectile dysfunction, sildenafil enhances the effect of nitric oxide (NO) by inhibiting PDE5 in the corpus cavernos. |
|
|
Term
| Sildenafil (Clinical Uses) |
|
Definition
| Viagra – Erectile dysfunction: Revatio – Pulmonary hypertension |
|
|
Term
| Sildenafil (drug interactions) |
|
Definition
| Potentiates the action of nitrates used for angina, and hypotensive effects. |
|
|
Term
|
Definition
| Flushing, Indigestion, Headache, Insomnia, Visual disturbance, Epistaxis,Myocardial infarction have been reported in men taking nitrates and sildenafil. Recommendation: Wait at least 6 hours between use of a nitrate and ingestion of sildenafil. Also effects color vision with blue/green discrimination. |
|
|
Term
|
Definition
Prevent bone resorption
Supress the activity of osteoclast
Indirect stimulation of osteoblast |
|
|
Term
| alendronate (Fosamax) Uses |
|
Definition
Osteoporosis
bone metastases, hypercalemia |
|
|
Term
| alendronate (ADR and clinical implications) |
|
Definition
GI Upset - Take in AM on empty stomach with full glass of water and remain upright for 30 minutes to prevent reflux.
Atypical fractures
bone pain |
|
|
Term
|
Definition
| Oral antidiabetic agent, alpha Glucosidase Inhibitor |
|
|
Term
|
Definition
| Delays digestion/absorption of ingested Carbohydrates by inhibiting alpha-glucosidase, resulting in a smaller rise in postprandial blood glucose after meals; however does NOT increase insulin production. |
|
|
Term
|
Definition
| Type 2 diabetes - can be used alone or in combination with Metformin or a Sulfonylurea |
|
|
Term
| Acarbose Contraindications |
|
Definition
| Pregnancy B, breast feeding, IBS, Ileus, cirrhosis, diabetic ketoacidosis |
|
|
Term
|
Definition
| Abdominal pain, diarrhea, flatulence, increased serum transaminase level |
|
|
Term
| Acarbose Pharmacokinetics |
|
Definition
| Poor systemic absorption, peak of 1 hour, metabolized in the GI tract, excreted as intact product in the urine; Half life of 2 hours. |
|
|
Term
| Acarbose Interactions / Increases effects of: |
|
Definition
| acetaminophen toxicity when combined with ETOH, decreases the effects of digoxiin, Increases hypoglycemia when used with sulfonylureas, insulin, MAOI's, salicylates, ACE Inhibitors, angiotension II receptor antagonists, Beta Blockers |
|
|
Term
|
Definition
| Increases: ALT, AST, bilirubin. Decreases: Calcium, Vitamin B6, HGB, HCT |
|
|
Term
| Acarbose Interactions / Decreases effects of: |
|
Definition
| increase hyperglycemia, digestive enzymes, thiazide diuretics, loop diuretics, corticosteroids, estrogen, progestins, oral contraceptives, sympathomimetics, atypical antipsychotics |
|
|
Term
| Acarbose Nursing Considerations |
|
Definition
| Monitor foy S/S of hypoglycemia & hyperglycemia when used in combination of sulfonylureas. Dosage may need adjustment when under stress, surgery, or trauma. |
|
|
Term
|
Definition
| 2nd generation sulfonylureas |
|
|
Term
|
Definition
| hypoglycemia; wt. gain; GI effects (nausea, epigastric fullness, heartburn); skin reactions; disulfiram-like reactions (unpleasant symptoms when consumed w/alcohol) |
|
|
Term
| Glipizide clinical application |
|
Definition
|
|
Term
|
Definition
|
|
Term
| advantages of 2nd generation sulfonylureas over 1st generation |
|
Definition
| fewer ADR; fewer drug/drug interactions; less expensive |
|
|
Term
|
Definition
|
|
Term
|
Definition
| kinetics: PO, T1/2=2-4 hrs; onset= 30 "; duration=10-24 hrs; ingest 30" before meals since absorption delayed w/food; if need >15mg/day (daily dose)- give in divided doses before meals; 90% metabolized into inactive products in liver; 10% excreted unchanged in urine |
|
|
Term
| Glipizide contraindications |
|
Definition
| hepatic or renal impairment |
|
|
Term
| Glipizide clinical effects |
|
Definition
| decreases FBS 60-70 mg/dl & decreases HbA1c 1.5-2 % points |
|
|
Term
| Glipizide effectiveness considerations |
|
Definition
| relative lack of effectiveness in higher doses- 75% of hypoglycemic action is @ 1/2 max. dose- if no effect @ 1/2 max. dose- unlikely any increase in dose will decrease BG |
|
|
Term
|
Definition
| 1) insulin secretagogue- close K+ channels in beta cells to increase pancreatic insulin secretion from beta cells; 2) w/long term use- decreases serum glucagon levels; 3) increase glycogen, fat, & protein formation; 4) gene regulation |
|
|
Term
|
Definition
| Requires good pancreatic beta cell function- secondary failure 5-10%/year (hyperglycemia is toxic to beta cells) |
|
|
Term
| Pramlintide (Symlin) MOA: |
|
Definition
| A synthetic analog of amylin: binds to amylin receptors |
|
|
Term
|
Definition
| Reduces post-meal glucose excursions: lowers glucagon levels, delays gastric emptying, decreases appetite |
|
|
Term
| Pramlintide clinical applications |
|
Definition
| Type 1 and type 2 diabetes |
|
|
Term
|
Definition
| Parenteral (SC), rapid onset - peak level within 20 minutes, 1/2 life ~ 48 minues. |
|
|
Term
| Pramlintide considerations |
|
Definition
Is administered in addition to insulin in those who are unable to achieve their target postprandial blood sugar levels.
Renally metabolized and excreted, but even at low creatine clearance there is no significant change in bioavailability.
Most reliable absorption is from the abdomen & thigh; arm administration is less reliable.
Sould be injected immediately before
Should be injected by itself in a seperate syringe and cannot be mixed with insulin. |
|
|
Term
|
Definition
| Hypoglycemia, headache & GI symtoms including nausea, vomiting & anorexia |
|
|
Term
| Metformin belongs to which drug category? |
|
Definition
| Antidiabetic agent; biguanides |
|
|
Term
|
Definition
| Decreases hepatic glucose production by activating the enzyme AMP-activated protein kinase (AMPK); decreases intestinal absorption of glucose; enhances insulin sensitivity in muscle and the periphery. NO direct affect the pancreas so does not stimulate insulin secretion |
|
|
Term
| Clinical effects of Metformin |
|
Definition
| Decrease in fasting BG by 60-70 mg/dL, decrease in HgbA1C by 1.5-2%, effective in preventing new onset type 2 DM. Does NOT cause weight gain or hypoglycemia in monotherapy. Also used to treat polycystic ovarian syndrome (PCOS) |
|
|
Term
|
Definition
| Most common are transient GI-related effects (dose-dependent); decreased B12 absorption, lactic acidosis (rare but fatal in 50% of patients with it) |
|
|
Term
| Contraindications of Metformin |
|
Definition
| renal impairment (SCr > 1.5), alcoholism, liver disease, septicemia, conditions associated with anoxia (acute MI, CHF, cardiopulmonary dysfunction) d/t increased risk of lactic acidosis |
|
|
Term
| Metformin may be combined with what other drug? |
|
Definition
|
|
Term
| Metformin pregnancy category |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Aldendronate Clinical Applications |
|
Definition
| Osteoporosis, bone metastases and hypercalcemia |
|
|
Term
|
Definition
| Suppress the activity of osteoclasts in part via inhibition of farnesyl pyrophosphate synthesis. It prevents bone reabsorption. Osteoclasts effects consist of inhibiting recruitment and apoptosis (Cell Suicide). It has indirect stimulation on osteoblast effects. |
|
|
Term
|
Definition
| Inhibit bone resorption and secondarily bone formation |
|
|
Term
| Aldendronate Adverse Effects |
|
Definition
| GI upset or ulceration, bone pain, atypical fractures, possible renal failure, rare osteonecrosis of the jaw |
|
|
Term
| How should Aldendronate be administered? |
|
Definition
| With a full glass of water on an empty stomach and should remain upright for 30 minutes after administration to prevent reflux of the medication |
|
|
Term
|
Definition
|
|
Term
|
Definition
| An analog of the hormone incretin, increases insulin secretion, decreases glucagon secretion, increases B-cell growth, slows gastric emptying, decreases food intake |
|
|
Term
|
Definition
| Decreases A1C by 0.5%-1% in immediate release, 1.5%-1.9% in extended release |
|
|
Term
|
Definition
| Used in the treatment of type 2 diabetes (non-insulin dependant) |
|
|
Term
|
Definition
| Thiazolidinediones (Tzds) |
|
|
Term
|
Definition
| Decreases insulin resistance by regulating gene expression by binding to peroxisome proliferator-activated receptor-gamma (PPRA-gamma). These genes are involved in lipid and glucose metabolism, insulin signal transduction, and adipocyte and other tissue differentiation |
|
|
Term
| Pioglitazone Clinical Uses and Contraindications |
|
Definition
| Type 2 Diabetes - can be used as monotherapy or in combination with metformin and sulfonylureas. Not to be used in pregnant patients, heart failure, or hepatotoxicity |
|
|
Term
|
Definition
| Fluid retention, increase risk of heart failure, and bone demineralization |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Modulates beta cell insulin release by regulating potassium efflux through the potassium channels |
|
|
Term
|
Definition
| Hypoglycemia if meals are delayed, skipped, or have insufficient carbohydrates. Use cautiously in renal and hepatic impairment (CYP3A4 enzyme cleared) |
|
|
Term
| Repaglinide Administration |
|
Definition
| Fast onset of action: peak effect 1 hr after administration. Take directly before a meal |
|
|
Term
|
Definition
| An oral gycemic agent; sitagliptin is a dipeptidyl peptidase-4 (DPP-4) enzyme inhibitor that protects endogenous incretin hormones from being broken down. Incretin hormones are released in response to a meal to maintain glucose homeostasis. |
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Term
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Definition
| Type 2 Diabetes (Trade name is Januvia) |
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Term
| What needs to be monitored in the patient taking sitagliptin? |
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Definition
| Monitor HbA1c levels and fasting blood glucose for drug effectiveness, monitor for signs/sx of hypoglycemia and renal function |
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Term
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Definition
| Hypoglycemia, headache, pharyngitis/URI |
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Term
| Sitagliptin Serious ADR's |
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Definition
| Pancreatitis, Anaphylaxis, Acute Renal Failure |
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