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84 Cards in this Set

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Regular Insulin (Novolin-R, Humulin-R) ;
Humalog (Lispro) ;
Novolog (Aspart)
Onset: rapid
Duration: short-acting
NPH Insulin (Novolin-N, Humulin-N)
Intermediate-acting
Levemir (Detemir) and Lantus (Glargine)
Onset: Slow
Duration: Long-acting
how is Regular Insulins, Lispro, and Aspart administered?
Soluble - used IV in emergencies OR subQ for glycemic maintenance
how is NPH insulins administered
Not Very Soluble - subQ injection
Directions: once in the morning and once in the evening to provide basal level of insulin for 24 hours
how are Detemir and Glargine administered
Not Very Soluble - subQ injection
Directions: once a day to provide a basal level of insulin for 24hrs
Insulin Secretory Drugs (Insulin Secretagogues)
1. Glyburide (Diabeta, Micronase)
2. Glipizide (Glucotrol)
3. Repaglinide (Prandin)
4. Nateglinide (Starlix)
Insulin-Sensitizing Drugs
1. Metformin (Glucophage, Fortamet, Riomet)
2. Rosiglitazone (Avandia)
3. Pioglitazone (Actos)
alpha-Glucosidase Inhibitors
Acarbose (Precose)
Incretin Mimetics
Exenatide (Byetta)
Dipeptidyl Peptidase IV Inhibitors
Sitagliptin (Januvia)
Amylin Analogs
Pramlintide (Symlin)
Type 1 Diabetes Mellitus
deficiency of insulin production
1. destruction of beta cells due to autoimmune antibodies, viruses, or chemical toxins
2. not associated with obesity
3. high incidence of ketoacidosis
Type 2 Diabetes Mellitus
extrapancreatic peripheral tissues show resistance to certain actions of insulin
1. genetically determined and associated with obesity
Main functions of endogenous insulin in the liver
1. increased synthesis and insertion of additional glucose transporters into liver cell membranes which would then FACILITATE GLUCOSE UPTAKE
2. decreased hepatic output of glucose
3. decreases the conversion of fatty acids to keto acids in the liver
Main functions of endogenous insulin in skeletal muscle
1. increases glucose transport into muscle cells by causing more synthesis and insertion
Main function of endogenous insulin in adipose tissue
1. increasing glucose transport into the fat cells via increased synthesis and insertion of additional glucose transporters into fat cell membranes
Unwanted Effects of Insulin Use
1. Severe Hypoglycemia
2. allergy
3. Local Lipodystrophy
4. Weight gain
How do you take care of severe hypoglycemia associated with insulin
rapid administration of glucose or of glucagon
Mechanism of Action of Glyburide and Glipizide
stimulate the release of endogenous insulin
1. close certain potassium channels in pancreatic beta cell membrane - opens calcium channels (Independent of the level of blood glucose)
2. 2nd generation - more potent - work in T2D
Mechanism of Action of Repaglinide and Nateglinide
stimulate the release of endogenous insulin
1. close potassium channels in pancreatic beta cells - opens calcium channels (Dependent of the level of blood glucose)
2. work in T2D
Metabolism and duration of Glyburide and Glipizide
metabolized: liver
Excreted: liver or kidney
Duration: a few hours to many hours
Metabolism and duration of Repaglinide and Nateglinide
Metabolized: liver
Duration: rapid-acting
Unwanted effects of Glyburide, Glipizide, Repaglinide, Nateglinide
1. too much hypoglycemia
2. Weight gain
3. drug allergy (skin reaction)
Mechanism of Action of Metformin
Antihyperglycemic agent (not hypoglycemic)
1. reduces blood glucose by improving sensitivity of peripheral tissues to insulin action on glucose uptake and storage
2. decreases hepatic glucose output (PRIMARY MECHANISM)
3. decrease absorption of glucose and lower blood pressure and serum lipids)
Metabolism of Metformin
rapid renal excetion unchanged and requires good renal function
Unwanted Effects of Metformin
1. Gastrointestinal (nausea, anorexia, diarhea) common
2. Lactic Acidosis - rare
Mechanism of Action of Rosiglitazone and Pioglitazone
ANTIHYPERGLYCEMIC AGENT
1. activation of nuclear receptors known as peroxisome proliferator-activated receptors (PPARs)
2. leads to increased glucose uptake and decreased circulating glucose
Metabolism of Rosiglitazone and Pioglitazone
Require good liver function
Metabolism: Hepatic
Excretion: Biliary/Fecal
Unwanted Effects of Rosiglitazone and Pioglitazone
1. Vascular flui retention and some edema
2. increase risk of bone fractures in women
3. Weight Gain
Black Box Warning of Rosiglitazone
increase incidence of myocardial infarction
Mechanism of Action of Acarbose
USED AS ADJUNCTIVE THERAPY
1. lower plasma glucose by inhibiting intestinal alpha-glucosidase enzymes responsible for digestion of complex carbs
2. delay postprandial absorption of glucose = attenuation of postprandial increases in plasma glucose
BENEFITS: "smooth out" postprandial glucose peaks
Metabolism of Acarbose
minimally absorbed
Metabolized: by intestinal digestive enzymes
Excreted: in the urine
Duration: a few hours
Doses: no fixed dose, should be titrated per individual
Unwanted Effects of Acarbose
1. GI disturbances (flatulence, cramping, distension, diarrhea) = due to fermentable unabsorbed carbs)
Mechanism of Action of Exenatide (Byetta)
1. binds to and activates human GLP-1 receptors
2. enhances glucose dependent insulin secretion
3. inhibits glucagon secretion
4. slows gastric emptying
5. increases the sensation of satiety
Administration of Exenatide (Byetta)
SubQ before meals
Unwanted Effects of Exenatide (Byetta)
1. Hypoglycemia (when combined with a sulfonylurea)
2. high incidence of GI effects
Mechanism of Action of Sitagliptin (Januvia)
1. Rapidly inactivates endogenous incretin hormones after they are released from the intestines
2. increase glucose dependent insulin release
3. decrease glucagon release from the pancreas
Administration of Sitagliptin (januvia)
taken orally once daily
Unwanted effects of Sitagliptin (Januvia)
1. Hypoglycemia (combined with a sulfonylurea)
2. Upper respiratory infection, headache
3. hypersensitivity (RARE)
Mechanism of Action of Pramlintide (Symlin)
stable injectable peptide analog of amylin
1. slows gastric emptying
2. inhibits glucagon secretion
3. increases the sensation of satiety
*Used as adjunctive therapy in both T1D and T2D
Administration of Pramlintide (Symlin)
SubQ before meals
Unwanted Effects of Pramlintide (Symlin)
1. Hypoglycemia (combined with insulin)
2. GI side effects
General Treatment Considerations of Type 1 Diabetes
1. Dietary Instruction
2. parenteral Insulin administration
3. careful attention by the patient to things that change insulin requirements
2 Medications often recommended in Type 1 Diabetes
1. alpha-glucosidase inhibitor in combo with insulin taken orally before meals
2. injectable amylin analog Pramlintide
General Treatment Considerations of Type 2 Diabetes
1. Reduce Obesity
2. Lower Blood glucose by dietary means
Medications often recommended in Type 2 Diabetes
1. start with a sulfonylurea
2. add metformin, a glitazone, or insulin
3. can add on an alpha-glucosidase inhibitor if postprandial glucose peaks are still high
4. Exenatide, Pramlintide, Sitagliptin can be added
Congestive Heart Failure
Ventricles are unable to pump out all the blood normally being returned to them. Blood backs up in the lungs and systemic veins, left ventricle fails initially
Signs and Symptoms of Left-Ventricular CHF
1. Respiratory Wheezing (first indication)
2. nonproductive cough
3. dyspnea on exertion
4. fatigue, weakness, exercise intolerance
Signs and Symptoms of Right Ventricular CHF
1. Pitting Edema
2. Sacral Edema
3. Hepatomegaly & Hepatic Engorgement
Factors that can influence Cardiac Output
1. Intrinsic Contractility
2. Preload
3. Afterload
4. Heart Rate
Compensatory Mechanisms in CHF
1. Cardiac Hypertrophy
2. Increased Sympathetic Nervous System Activity
3. RAAS Activity
Primary Objective of therapeutic management of CHF
relieve symptoms and prolong life
2 most important actions of digitalis glycosides for treatment of CHF
1. increased myocardial contraction
2. decreased heart rate
Primary mechanism of digitalis glycosides when increasing myocardial contractility
1. inhibit Na/K pump, increases intracellular Na
2. blocks Na/Ca exchanger, increased intracellular Ca
3. increased contractility, increased cardiac output
4. excretion of Na and water, decreased congestion
Vagal slowing in how digitalis glycosides decrease heart rate
*reversal of SNS-induced reflex tachycardia*

can involve several sites (autonomic ganglia and cardiac sites and carotid baroreceptors
Diuretic action of digitalis glycosides
*produce copious urine output
*no notable direct effect on the renal tubules
*increased urine output is secondary consequence of improved hemodynamics due to cardiac actions
Drug Interactions with Digitalis Glycosides
1. Quinidine = increases levels of digoxin
2. Verapamil = inhibit renal clearance
3. antacid gels, sulfasalazine, bile acid binding resins
General Digitalis Toxicity
manifest toxicity on virtually all systems due to too much inhibition of Na/K-ATPase, thus too much intracellular concentration of free calcium
Digitalis Toxicity
1. GI = anorexia, nausea, vomiting, diarrhea
2. Cardiac = arrhythmia, tachycardias, fibrilliations
3. CNS = delirium
4. Blurred Vision
Treatment of Digitalis Toxicity
*Pay attention to Potassium levels*
1. potassium chloride orally or IV
2. Discontinue medication or decrease dose
3. Digoxin Antibody
Digoxin Immune Fab (Digibind)
*antigen binding fragments that bind to digoxin and form complex.......complex excreted in urine
Dobutamine
synthetic catecholamine-like B1 agonist given only IV in intensive care to treat severe, refractory congestive heart failure
Side effects of Dobutamine and Dopamine
tachycardia and increase in cardiac oxygen demand
*tolerance can develop*
Dopamine
endogenous catecholamine given only IV in intensive care to treat severe, refractory congestive heart failure
Inamrinone and milrinone
used intravenously for treatment of severe, refractory CHF or after tolerance to dopamine or dobutamine develops
Mechanism of Action of Inamrinone and milrinone
1. inhibition of cAMP inaction = increases ventricular cel cAMP content = increased free Ca availability
2. stimulates more SR Ca uptake during diastole
*little or no tolerance develops
ACE Inhibitors used for CHF
1. Captopril
2. Enalapril
3. Fosinopril
4. Quinapril
problem with some ACE inhibitors in congestive heart failure
some are prodrugs that are activated in the liver which may be congested in CHF
Side effects of ACE inhibitors in CHF
1. Non-Productive Cough (due to high levels of bradykinin)
drug interactions with ACE inhibitors in CHF
use with diuretics = too much reduction in arterial BP
Angiotensin 2 Receptor Blockers used in CHF
1. Losartan
2. Valsartan
3. Candesartan
Mechanism of action of ACE inhibitors and ARBs
decreases in vasoconstriction and aldosterone levels
Diuretics used in CHF
1. Thiazides
2. Loops
3. K-sparers
how diuretics work in CHF
1. marked retention of sodium and water
2. reduce extracellular fluid volume
3. reduce preload, relieve pulmonary congestion, and reduce peripheral edema
Spironolactone and Epleronone
multiple benefits in patients with CHF because aldosterone levels are very high
how direct vasodilators work in CHF
1. can inhibit vasoconstriction and reduce the impedance(afterload) and improve hemodynamic effect
2. can also decrease preload by increasing venous capacitance through venodilation
Direct Vasodilators that work by reducing preload
1. Nitroglycerin
2. Isosorbide Dinitrate
Direct Vasodilators that work by reducing afterload
1.hydralazine
Direct Vasodilator that works by reducing preload and afterload
Nitroprusside
Direct Vasodilator and a diuretic
Nesiritide = decreases arterial and venous smooth muscle tone by increasing intracellular levels of cGMP
CHF patients most benefited from Vasodilators
1. severe CHF refractory to other therapies
2. right after acute myocardial infarction with preexisting chronic CHF
Beta Blockers used in CHF
1. Bisoprolol
2. Metoprolol
3. Carvedilol
why are Beta Blockers effective in CHF
prevent chronic adverse effects of high endogenous catecholamines like:
1. prevent down regulation of beta receptor numbers and related functions
2. prevent excessive tachycardia and arrhythmias