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the use of drugs to diagnosis, prevent or treat disease or to prevent pregnancy.
2. Bipolar disorder
3. Migraine prophylaxis
1. : Cefdinir, cefditoren, cefixime, cefotaxime, cefpodoxime, ceftazidime, ceftibuten, ceftizoxime, ceftriaxone; gram positive (staph and strep, but not enterococcus) and gram negative coverage
associated with s specific drug molecule
Study of drug movement throughout the body. What the body does to the drug.
A. Cannot be given orally; short half-life (1.5 hours)
The study of the biochemical and physiologic effects of drugs
the study of the biochemical and physiological effects of drugs and the molecular mechanisms by which those effects are produced
What the drug does to the body
a pre-existing condition that precludes use of a particular dugs
factors that prevent the use of a drug or treatment
When plasma levels rise above resting levels, they promote energy mobilization and glucose sparing.
- Decreased uptake of glucose and amino acids
- Stimulate lypolysis in adipose tissue (raising fatty acids and glycerol)
- Stimulate protein breakdown in muscle tissues, inhibit protein synthesis, and stimulate gluconeogenesis.
1. Hypokalemic Alkalosis
-inhibitsfunction and secretions of antigen-presenting cells
-inhibitssynthesis of pro-inflammatory eicosanoids-decreases release of histamines by basophilsand mast cells
a. Includes epinephrine, norepinephrine, isoproterenol, dopamine, and dobutamine
b. Three common features
a. Cannot be taken orally
b. Brief duration of action
c. Cannot cross blood-brain barrier
c. Destroyed by MAO and COMT
d. Use the drug solution only if colorless because a discoloration indicates oxidation of the drug
a. Lack a catechol group
b. Not substrates for COMT and metabolized slowly by MAO so longer half-lives
c. Can be given orally
d. Penetrate blood-brain barrier
a. Where are a1 receptors located and what happens when you stimulate them?
a. blood vessels (vasoconstriction)
b. prostatic capsule (contraction)
c. bladder (contraction of trigone and sphincter)
d. eye (mydriasis)
1. : Identify patients at higher risk for norepinephrine adverse effects. Baseline BP and HR
A. : Agonist at dopamine receptors at low doses, beta1 at moderate doses, at high doses-alpha1; Catecholamine
A. (maintain renal function through dopamine receptors and increase cardiac output and blood pressure through beta-1 and alpha-1 receptors); limited use in heart failure
A. Tachycardia, dysrhythmias, and anginal pain, necrosis if extravasation
A. Use caution in patients with heart disease, hyperthyroidism, hypertension, angina
1. : Baseline cardiovascular status. Identify patients at higher risk for adverse effects.
1. : Monitor cardiovascular status very carefully.
A. Nonselective beta receptor agonist; Receptors b1 and b2; Catecholamine
CV disorders (ie, AV heart block)Bronchospasm: Can be used to treat bronchospasm during anesthesia; no longer used for asthma
A. : Cardiac effects of dysrhythmias and angina pectoris and hyperglycemia in diabetics (b2 mediated glycogenolysis)
A. Use caution in patients with hyperthyroidism, cardiac dysrhythmias, heart disease, hypertension, angina, diabetes
B. Drug Interactions: Similar to epinephrine
1. Baseline cardiovascular status. Identify patients at higher risk for adverse effects.
1. Monitor cardiovascular status very carefully. Blood glucose in diabetics.
A. Reduce nasal congestion, elevate blood pressure in hypotensive states, adjunct to local anesthesia, mydriasis
c. Identify patients at higher risk for adverse effects (patients with uncontrolled high blood pressure). Watch in patients with BPH or other problems initiating urination.
1. Identify patients at higher risk for adverse effects.
A. Reduce firing of sympathetic neurons that decrease release of NE from sympathetic nerves to decrease blood pressure; Decreases sympathetic outflow to blood vessels and the heart
Causes bradycardia, decrease in cardiac output, and vasodilation, which decreases blood pressure; effect is not posture dependent
Hypertension – Vasodilation and decrease in cardiac output contribute to decrease in blood pressure
Treatment of severe pain – Blocks nerve impulses in pathways that transmit pain signals from the periphery to the brain
ADHD – Mechanism of action unknown
Clonidine also has other investigational uses such as migraines, menopausal flushing, Tourette’s syndrome, and withdrawal from opioids, alcohol, and tobacco
A. Do not use during pregnancy. Do not abruptly stop clonidine. It should be tapered off when stopping due to rebound hypertension.
A. Monitor cardiovascular function and for CNS effects. Treatment is largely supportive care.
A. Very lipid soluble. Half-life 12-16 hours. Eliminated by a combination of hepatic metabolism and renal excretion.
1. Baseline BP and HR. Determine pregnancy status.
1. : Oral, transdermal. Transdermal patch should be applied to a hairless, intact skin on the upper arm or torso every 7 days.
1. hypertension, reversal of toxicity from alpha1 agonists, benign prostatic hyperplasia (BPH), pheochromocytoma, and Raynaud’s disease
a. a1 blockade adverse effects—Orthostatic hypotension, reflex tachycardia, nasal congestion, inhibition of ejaculation, and sodium retention with increased blood volume
b. a2 blockade adverse effects—Potentiation of the reflex tachycardia
A. Beta-Adrenergic Antagonists or beta-blockersTherapeutic Applications
1. Major consequences of blocking b1 receptors are reduced heart rate, reduced force of contraction and reduced velocity of impulse conduction through AV node; used to treat angina pectoris, hypertension, cardiac dysrhythmias, myocardial infarction, heart failure, hyperthyroidism, migraine, stage fright, pheochromocytoma, and glaucoma
A. Beta-Adrenergic Antagonists or beta-blockers Adverse Effects
a. Effects of b1 blockade—Bradycardia, reduced cardiac output, precipitation of heart failure, AV block, and rebound cardiac excitation; can mask symptoms of hypoglycemia
1. NOTE: b1 blockers can precipitate heart failure or make heart failure worse. However certain b1 blockers (like metoprolol or carvedilol) are used to treat heart failure.
b. Effects of b2 blockade—Bronchoconstriction (contraindicated in patients with asthma) and inhibition of glycogenolysis (can delay recovery from a hypoglycemic episode in diabetic patients)
PT - as ratio of pateint's PT to normal PT
less problem with bleeding
standard dose 2.0-3.0 INR
A. Physiologic process by which bleeding is stopped
1. Formation of a platelet plug—Begins when platelets come in contact with collagen on exposed surface of damaged vessel and adhere to area; mediators of platelet aggregation include adenosine diphosphate (ADP) and thromboxane A2; platelet aggregation ends with fibrinogen bridges using glycoprotein IIb/IIIa receptors (see Figure 52-1 in the text)
1. : coagulation (reinforcement of platelet plug with fibrin)—Occurs in series of cascading reactions (see Figure 52-2 in the text) from extrinsic and/or intrinsic pathways; four coagulation factors (II [prothrombin], VII, IX, X) require vitamin K for synthesis
1. Antithrombin prevents widespread coagulation by forming a complex with clotting factors
1. Uses plasmin to break down clot (precursor is plasminogen)
1. Begins with platelet adhesion to arterial wall; result is localized tissue injury owing to lack of perfusion
1. Usually develops when blood flow is slow; this initiates coagulation cascade; part can break off and become embolus
A. Helps antithrombin inactivate thrombin, factor Xa, and other factors; fibrin formation is then suppressed; acts in minutes (Figure 52-3)
A. : Preferred during pregnancy and for situations requiring rapid onset: for pulmonary embolism, evolving stroke, and massive deep vein thrombosis (DVT), as well as patients undergoing open heart surgery and renal dialysis; low-dose heparin to prevent venous thrombosis; also used for treating disseminated intravascular coagulation (DIC) and as adjunct therapy in acute MI
A. Hemorrhage, thrombocytopenia (HIT), spinal or epidural hematoma, hypersensitivity reactions; local irritation and hematoma from subcutaneous administration
A. Contraindicated for patients with thrombocytopenia; uncontrollable bleeding; during and immediately after eye, brain, or spinal cord surgeries and lumbar puncture and regional anesthesia. Warnings include patients with high likelihood of bleeding or liver or kidney disease.
A. Protamine sulfate for heparin overdose—A small protein with positive charges which interacts with negative charges of heparin
1. CBC, platelets, hematocrit, and activated partial thromboplastin time (aPTT)
1. Parenteral only (IV intermittent or continuous or SC); dosage varies with application and blood levels. Prescribed in terms of units not milligrams.
1. aPTT - normal value for aPTT is 40 seconds; therapeutic levels increase aPTT by 1.5 to 2 times. Monitor platelets and for signs of bleeding.
1. In general the low molecular weight heparins are used for:
a. Prevention of DVT following abdominal surgery, hip replacement surgery or knee replacement surgery
b. Treatment of established DVT, with or without PEPrevention of ischemic complications in patients with unstable angina, non-Q-wave MI, acute ST-segment elevation myocardial infarction.
A. Patients with thrombocytopenia; uncontrollable bleeding; during and immediately after eye, brain, or spinal cord surgeries and lumbar puncture and regional anesthesia
A. Higher bioavailability and longer half-life than unfractionated heparin.
1. No specific laboratory monitoring required unless patient is obese or has poor renal function. Monitor platelets and for signs of bleeding.
A. Antagonist of vitamin K; decreases synthesis of vitamin K dependent clotting factors (factors VII, IX, X and prothrombin)
1. Prevention of venous thrombosis and associated PE
2. Prevention of thromboembolism with prosthetic heart valves
3. Prevention of thrombosis during atrial fibrillation
A. : Hemorrhage; fetal hemorrhage and teratogenesis with use during pregnancy; not for use during breastfeeding; other (skin necrosis, alopecia, urticaria, dermatitis, fever, GI disturbances, and red-orange urine)
given orally or IV; avoid SC injection; IV can cause anaphylactoid reactions; large doses can cause warfarin resistance
Use whole blood, fresh frozen plasma, or concentrates of vitamin K-dependent clotting factors if vitamin K fails to control bleeding
A. Readily absorbed after oral administration; 99% bound to albumin; hepatic metabolism and excretion in urine and feces; doesn’t affect clotting factors already present, only those being synthesized; effects take several days to develop; after discontinuing drug, effects still present for 2–5 days.
First generation NSAID
Irreversible nonselective COX inhibtor
A. Used to reduce thrombotic events (MI and ischemic stroke) in patients with acute coronary syndrome or previous event or peripheral arterial disease; prevent blockage of coronary artery stents; can be used as an alternative to or in combination with aspirin (depending on indication)
A. Increases conversion of plasminogen to convert it to plasmin, an enzyme that digests fibrin meshwork of clot
1. Bleeding, intracranial hemorrhage (1%)
A. : Long list of contraindications associated with use of thrombolytics (See Table 52-9) – list includes any prior intracranial hemorrhage, ischemic stroke within last 3 months (except within last 4.5 hours), active internal bleeding, suspected aortic dissection, and many others. Always double check contraindication list prior to administration.
1. Carefully assess patient for contraindications. Streptokinase can only be used in a patient once due to antibody production.
1. : Monitor for signs of bleeding, blood pressure, body temperature
1. Sources of cholesterol include diet and endogenous cholesterol (made in liver)
2. Hydroxymethylglutaryl coenzyme A (HMG CoA) reductase necessary in synthesis
a. Carriers for transporting lipids, which are not water soluble, in blood
a. Hydrophobic core of cholesterol and triglycerides surrounded by hydrophilic shell
a. All lipoproteins have at least one of these embedded in shell; apolipoproteins function as recognition sites for cell-surface receptors, activate enzymes that metabolize lipoproteins, and increase structural stability of lipoproteins
1. Contain triglycerides and some cholesterol; function to deliver triglycerides from liver to adipose tissue and muscle; unclear role of VLDL in atherosclerosis; increased triglycerides increases risk of pancreatitis
1. )—“Bad cholesterol”; delivers cholesterol to nonhepatic tissues; cells requiring cholesterol engulf LDLs; major contributor to atherosclerosis
1. cholesterol”; carry cholesterol from peripheral tissues back to liver (aid in cholesterol removal)
A. Increase in LDL increases risk for CAD, while increase of HDL decreases the risk of CAD
1. Initiates and fuels development of atherosclerosis
i. Positive risk factors: Advancing age, family history of premature coronary artery disease, hypertension, cigarette smoking, low HDL
ii. Negative risk factors: High HDL
1. Therapeutic Lifestyle Changes
a. Weight control
c. Smoking cessation
2. Drug Therapy
A. Secondary Treatment Targets
1. Metabolic syndrome
2. High triglycerides
A. : Inhibits the enzyme HMG-CoA Reductase which is involved in cholesterol synthesis; this inhibition of cholesterol synthesis causes an increase in LDL receptors in the liver so the liver takes up more cholesterol from the blood
1. Reduction of LDL cholesterol
2. Elevation of HDL cholesterol
3. Promote plaque stability, reduce inflammation, enhance blood vessel dilation, decrease risk of thrombosis
1. Hypercholesterolemia, dyslipidemia – Reduces LDL and increases HDL
2. Primary and secondary prevention of cardiovascular events – Statins decrease risk of stroke and cardiac events
3. Diabetes (even if patient doesn’t have high cholesterol) – Reduces risk of cardiovascular events in patients with diabetes
A. : generally well tolerated; adverse effects include headache, rash or GI disturbances; serious effects of hepatotoxicity and myopathy
A. Category X, contraindicated during pregnancy. Caution or contraindication with liver diseases.
A. : Fibrates and inhibitors of P450 enzyme 3A4
1. : Liver function tests, lipid panel. Remember to continue lifestyle modifications.
A. : Vitamin that in pharmacologic doses reduces LDL and triglyceride levels and increases HDL
A. Intense flushing of the face; hepatotoxicity; hyperglycemia and gouty arthritis. Note that the extended release niacin (Niaspan) has less adverse effects, including decreased incidence of flushing and decreased risk of hepatotoxicity.
Intense flushing of the face; hepatotoxicity; hyperglycemia and gouty arthritis
Extended release form (Niaspam) has less side effects
A. Caution in diabetics and patients with hyperuricemia and history of gout. Contraindicated with active liver disease or severe gout.
1. : Lipid panel, liver function tests
A. : Reduces triglycerides, increases HDL, small reduction in LDL (in some patients may actually increase LDL)
A. Well tolerated; rashes and GI disturbances most common; increased risk of gallstones; can cause myopathy; hepatotoxic
A. : Contraindicated in patients with liver disease, severe renal dysfunction, and gallbladder disease.
1. lipid panel, liver function tests
A. Inhibits absorption of cholesterol from GI tract
A. Indicated to reduce total cholesterol, LDL, and apolipoprotein B; can be given alone or with a statin
A. Contraindicated in patients with active liver disease. Do not use during pregnancy.
1. Lipid panel, liver function tests
1. Colesevelam (Welchol) – also approved for improvement of glycemic control in type II diabetes mellitus
2. Cholestyramine (Questran, etc)
3. Colestipol (Colestid)
A. Bind bile acids in the intestine, which prevents their reabsorption; body then uses cholesterol to make more bile acids so the liver expresses more LDL receptors
A. Constipation, abdominal discomfort and bloating; may decrease absorption of fat-soluble vitamins
A. Can form complexes with other drugs; drugs that bind cannot be absorbed (thiazide diuretics, digoxin, warfarin, and some antibiotics); take other medications that can form complex with bile acid sequestrant 1 hour before or 4 hours after
when lots lactate in blood (over 5 mM...normal is 1.2 mM); blood pH can be less than 7.1 if severe; will cause tissue hypoxia, severe anemia, mitochondrial enzyme defects, liver disease; give HCO3- to treat; happens if over exercise
short or regular insulin doses adjusted according to blood glucose test results
* Typically used in hospitalized diabetic patients or those on TPN or enteral tube feedings
* Disadvantage: delays insulin administration until hyperglycemia occurs: results in large swings in glucose control
Pathophysiology of Diabetes
A. A disorder of carbohydrate metabolism; characterized by hyperglycemia
B. Also affects protein and lipid metabolism
C. Caused by failure to produce insulin, development of insulin resistance, and/or impaired insulin secretion
1. Type 1 diabetes mellitus
2. Type 2 diabetes mellitus
3. Gestational diabetes: diabetes that appears during pregnancy and subsides after delivery
A. Short term complications of diabetes
4. Hyperglycemic hyperosmolar nonketotic syndrome
A. Long term complications of diabetes
1. Macrovascular disease
a. Increased risk of heart disease hypertension, and stroke
b. Glycemic control alone is not enough to reduce macrovascular complications; must be combined with other treatments such as medications to treat hypertension and dyslipidemia
2. Microvascular disease: Due to damage to small blood vessels and capillaries
a. Fasting plasma glucose test
a. Casual plasma glucose test (nonfasting plasma glucose)
a. Should be less than 200 mg/dL
b. If patient has symptoms of diabetes with high nonfasting plasma glucose, diabetes can be diagnosed
a. Oral glucose tolerance test
a. Give oral glucose load and measure plasma glucose levels 2 hours later
b. If 2-hour plasma glucose is ≥200 mg/dL, diabetes is indicated
a. Impaired fasting glucose (100-125 mg/dL) or impaired glucose tolerance (140-199 mg/dL at 2 hours during an oral glucose tolerance test
a. Plasma glucose and A1C
b. Self-monitoring of blood glucose
c. Treatment targets for most patients
a. Preprandial plasma glucose 70-130 mg/dL
b. Postprandial plasma glucose peak <180 mg/dL
c. A1C <7%
1. Beef or pork pancreas—No longer available in US; had problems with antibody production to these since they were foreign proteins
2. Recombinant DNA technology
a. Insulin lispro
b. Insulin aspart
c. Insulin glulisine
a. Regular insulin
a. Insulin glargine
Human insulin analog
U-100 (100 units/mL)
Human insulin analog
Human insulin analog
Humulin R; Novolin R
Humulin N; Novolin N
Human insulin; conjugated with protamine
Human insulin analog
Human insulin analog
1. NPH can be mixed with shorter acting insulins to decrease number of injections; draw up short acting insulin into syringe first, then draw up NPH; several premixed combinations are available for convenience
a. Subcutaneous injection
b. Insulin pumps
d. Inhaled insulin (Exubera) – removed from market by manufacturer in 2007
1. Maintaining glucose levels within the normal range
a. Benefits - Reduces long-term complications
b. Drawbacks—Concern for hypoglycemia, patients gain more weight, increased complexity of therapy, expense
1. Match to insulin needs based on calories, stress, growth spurts, and pregnancy; dosed in units
2. Dosing schedules—Helps determine extent to which tight control is achieved (See table 57-10 for examples of conventional and tight control schedules)
a. Conventional therapy—Dosing does not provide tight control
b. Intensified conventional therapy (ICT)—Significant feature is adaptability using long-acting and regular insulin
c. Continuous subcutaneous insulin infusion (CSII)—Basal level of insulin using pump
1. Hypoglycemia—Glucose of <50 mg/dL; symptoms include tachycardia, palpitations, sweating, nervousness, shakiness, headache, confusion, drowsiness, fatigue; symptoms depend on how rapid the change in glucose level occurs
2. Other complications—Lipohypertrophy, weight gain
1. Hypoglycemic agents—Intensify hypoglycemia; drugs include oral diabetic agents, beta-blockers, and alcohol
2. Hyperglycemic agents—Thiazide diuretics, glucocorticoids, and sympathomimetics counter effects of insulin (may need increased dosage of insulin with these drugs)
3. Beta-adrenergic blocking agents—Delays awareness of insulin-induced hypoglycemia by masking symptoms associated with sympathetic activation; delays recovery from hypoglycemia
1. Glipizide (Glucotrol, Glucotrol XL) mechanism of action
1. — Lowers glucose levels by stimulating release of insulin from the pancreas; generally well tolerated but can get hypoglycemia
1. : GI effects, lactic acidosis; cannot be used in patients with poor renal function (need to monitor serum creatinine)
1. fluid retention, heart failure, effects on plasma lipids (increases LDL), heart attack, increased risk of heart-related death, hypoglycemia
1. Delays absorption of dietary carbohydrates
1. GI, liver dysfunction
1. Inhibits dipeptidyl peptidase 4 (DPP-4) and thus enhances the actions of incretin hormones; incretin stimulates release of insulin and suppresses glucagon release
1. upper respiratory tract infection, headache, inflammation of nasal passages and throat, hypoglycemia
mimics the effects of amylin, reduces postprandial glucose. Adverse effects: hypoglycemia, nausea, injection site reactions.
– analog of glucagon-like peptide, slows gastric emptying, stimulates insulin release, inhibits postprandial release of glucagons, and suppresses appetite. Adverse effects: hypoglycemia, GI, pancreatitis
Inactivates thrombin and factor Xa
Used for PE, stroke, massive DVT, open heart surgery, renal dialysis
Adverse: hemorrhage, HIT
Measured in units
A. Medication Class: Low molecular weight heparin
B. Mechanism of Action: Same process as standard heparin except LMW preferentially inactivates factor Xa and fewer effects to inactivate thrombin
A. Medication Class: Oral anticoagulant; antagonist of vitamin K
B. Mechanism of Action: Antagonist of vitamin K; decreases synthesis of vitamin K dependent clotting factors (factors VII, IX, X and prothrombin)
A. Medication Class: First oral direct thrombin inhibitor
B. Mechanism of Action: Binds directly to thrombin and inhibits its activity
C. Therapeutic Uses: Reduction of risk of stroke and systemic embolism in patients with nonvalvular atrial fibrillation
A. Medication Class: Oral antiplatelet agent; nonselective, irreversible COX inhibitor
B. Mechanism of Action: Causes irreversible inhibition of cyclooxygenase (COX) (enzyme that synthesizes thromboxane A2, a promoter of platelet aggregation)
C. Therapeutic Uses: Acute MI, prevention of MI, patients who have had a previous MI, unstable angina, coronary stenting, ischemic stroke, TIA
A. Medication Class: Adenosine diphosphate (ADP) receptor antagonist; oral antiplatelet agent
B. Mechanism of Action: Causes irreversible blockade of ADP receptors on platelet surface which prevents ADP mediated platelet aggregation
A. Medication Class: Glycoprotein IIb/IIIa receptor antagonist; IV antiplatelet
B. Mechanism of Action: Causes reversible blockade of platelet glycoprotein IIb/IIIa receptors thereby inhibiting the final step in platelet aggregation
C. Therapeutic Uses: Acute coronary syndrome, patients undergoing percutaneous coronary intervention
A. Medication Class: Thrombolytic; fibrinolytic
B. Mechanism of Action: Increases conversion of plasminogen to convert it to plasmin, an enzyme that digests fibrin meshwork of clot
C. Therapeutic Uses: Acute MI, acute ischemic stroke, acute pulmonary embolism
A. Medication Class: Phenothiazine; low potency typical antipsychotic
B. Mechanism of Action: Dopamine receptor antagonist
C. Therapeutic Uses: Schizophrenia, psychotic disorders, suppression of emesis and relief of intractable hiccups
A. Medication Class: Butyrophenone; high potency typical antipsychotic
B. Mechanism of Action: Dopamine receptor antagonist
C. Therapeutic Uses: Schizophrenia, acute psychoses, Tourette’s syndrome
A. Medication Class: Atypical antipsychotic-second generation-newer agents
B. Mechanism of Action: Blocks sertonin receptors; affinity for dopamine receptors is relatively low; also blocks norepinephrine, histamine and acetylcholine
C. Therapeutic Uses: Treatment refractory schizophrenia
1. Uses: schizophrenia and acute bipolar mania; autistic disorder
2. Blocks serotonin and dopamine receptors, also blocks histamine and alpha-1 receptors
3. Low risk of EPS at normal doses, higher doses can cause EPS; does increase prolactin levels; other adverse effects include weight gain, and diabetes; can increase the risk of stroke and mortality in elderly dementia patients
A. Medication Class: Tricyclic antidepressant (TCA)
B. Mechanism of Action: Exact mechanism unknown; blocks reuptake of serotonin and norepinephrine; also affects other receptors such as cholinergic (muscarinic) receptors (Figure 32-2)
1. inhibits the enzyme HMG-CoA Reductase which is involved in cholesterol synthesis
1. Preadministration Assessment: Baseline CBC, platelets, hematocrit, and activated partial thromboplastin time (aPTT)
2. Administration: Parenteral only (IV intermittent or continuous or SC); dosage varies with application and blood levels. Prescribed in terms of units not milligrams.
3. Monitoring: aPTT - normal value for aPTT is 40 seconds; therapeutic levels increase aPTT by 1.5 to 2 times. Monitor platelets and for signs of bleeding.
Mast cell stabilizers