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study guide exam 1
| Question | Answer |
|---|---|
| Define pharmacokinetics | Study of drug distribution rates. Includes absorption, distribution, metabolism and excretion. ADEM is kinetic |
| Define pharmacodynamics | Study of biochemical and physiologic interactions of drugs (dynamics BP-biochem and physiology drugs) |
| Pharmacotherapeutics | Treatment of pathological conditions through use of drugs (therapeutic=treatment) |
| Pharmacognosy | Study of drugs derived from natural sources |
| Therapeutic class | Drug group by USE of medication |
| 5 rights? | Patient, drug, route, time, dose. Documentation |
| What are the enteral routes? | Oral, gastic, rectal |
| What are characteristics of enteral administration? | Easy to administer and self-administer; low cost. Slower onset b/c needs to be absorbed. Gastric acid and other GI enzymes can inactivate the drug, and it may cause nausea and other irritations. Water soluble, little flavor. |
| What are the parenteral routes? | IV, IM, sub-Q |
| What are characteristics of IV administration? | Directly into venous blood, fast onset, quicker elimination, precise control, large volumes of fluid can be adm with poor solubility. Expensive, irreversible, difficult to adm. Poss infection, fluid overload and embolism. Must be water soluble. |
| What are characteristics of IM/sub-Q administration? | Minimal barriers to absorption: rate determined by flow of blood to site and water solubility of drug. Can be used for poorly soluble drugs (unlike IV), can be used for depot preparations. Potential for injury, inconvenience, discomfort. |
| Biotransformation | Changing of a drug to an inactive metabolite, a more soluble compound, or more potent metabolite. |
| Absorption | Rate at which a drug leaves its site of administration and the extent to which it occurs. |
| What factors effect absorption? | Rate of dissolution, surface area, blood flow, lipid solubility and pH partitioning |
| Distribution | The transport of a drug in the bloodstream to its site of action, or movement of drugs throughout the body. |
| What factors effect distribution? | Blood flow, exit from vascular system, entering process into cell, protein binding. |
| How are drugs eliminated from the body? | Primarily eliminated in the urine, but also the liver, bowl, lungs and exocrine glands. |
| What medical illnesses would be concerning in regard to the proper elimination of medications from the body? | Problems with the liver and/or kidneys are of primary concern |
| Maintenance dose | Dose needed to replace drug at the rate it is eliminated |
| Plateau level | Time of constant drug level, when dose administration equals elimination |
| Loading dose | Large, initial dose of drug that reduces time to plateau |
| Peak of action | Time needed for drug to reach maximum response |
| Half-life | Time needed for amount of drug in the body to decrease by 50% |
| Beta-1 receptors | Located in heart and kidney. Activation of cardiac beta receptors increase HR, force of contraction, and velocity of impulse conduction through the AV node. Activation of kidney receptors cause synthesis of angiotensin, a vasoconstrictor increasing BP |
| Beta-2 receptors | Arterioles of heart, lung, skeletal muscle; bronchi, uterus, liver and skeletal muscle. Activation causes bronchial dilation, relaxation of uterine smooth muscle, vasodilation in arterioles, glycogenolysis, contraction of skeletal muscle |
| Side effect | Secondary drug effect caused by therapeutic doses. Nearly unavoidable and expected. (Normal) |
| Adverse reaction | Noxious, unintended, undesired effect occurring at normal doses |
| Iatrogenic effect | Diseases caused by drug/physician, or damage to patient's organs due to drug therapy. |
| What would be a "good statement from a pt" when patient education regarding allergic reaction is assessed by the nurse? | S/E: GI upset like nausea, vomiting and diarrhea.AE: (signs of hypersensitivity or allergic reaction) skin rashes, itching, anaphylaxis. Patient should know the difference between the common side effects and more serious adverse effects. |
| What is important to teach a patient receiving an enteric coated medication? | The medication has a coating to protect it from the acid in the stomach. Med may not work until reaching intestine, effect may be delayed until stomach empties (up to 12 hrs). Should not be chewed or crushed. |
| What actions should be taken if a nurse questions the validity of a medication order? | Double-check it. Check order with prescriber. Ensure 5 rights. |
| What is the correct technique for giving a sub-Q injection? | |
| Agonist | Drug displays affinity for recpetor and enhances the functional properties of receptor |
| Antagonist | Prevents response from occuring |
| Teratogenic effects | Drug induced birth defect. Effects of drug on fetus |
| Maximal efficacy | Greatest effect drug can have. Even if you add more of the drug, it will not have a greater effect. |
| What should the nurse do in case of medication error? | Ensure patient safety and assess for adverse reaction. Check with physician to see if further action if needed, chart medication administration and changes to care plan, report medication error, inform patient. |
| Describe actions of synthroid (Levothyroxine)and management strategies for its administration | Levothyroxine is a T4 analog that is used to treat hypothyroidism. It increases thyroid hormone level and increases cell metabolism. Usually given PO, IV poss for pt unable to take orally. Should be taken on empty stomach to increase absorption |
| Hyperthyroidism | Too much thyroid hormones produced. Can be due to thyroid/pituitary/hypothalamus dysfunction, too much iodine, Graves'. Nervousness, weight loss, increased appetite, insomnia, anxiety, heart palpitations or arrhythmia, and fine motor tremors. inc. metabol |
| Hypothyroidism | Not enough thyroid hormone produced. Iodine deficiency, thyroid/pituitary/hypothalamus problems. |
| Hypothyroidism signs/symptoms? | Lowered metabolic rate, which may manifest as a general lethargy, sleepiness, and hypertrophy of the adipose tissue. Other signs/symptoms include hair loss, intolerance to cold, pale skin, and fatigue. |
| Salicylate beneficial effects? | Inhibit cox-1 and cox-2. Relief of moderate to mild pain, reduces fever, protects against thrombotic disorders, r/a & other infammatory conditions. Protection against MI & ischemic stroke. |
| Salicylate adverse effects? | Gastric ulceration, bleeding and renal impairment |
| Salicylate absorption? | All are absorbed by in the small intestine, and are extensively metabolized in the liver and excreted by the kidneys |
| Salicylate contraindications? | sensitivity to salicylates, bleeding disorders or thrombocytopenia,and children or adolescents with viral infections. Cautious use with GI bleeding history or ulcer, alcohol abuse, and renal or hepatic disease |
| Salicylate SE/AE? | GI bleeding, tinnitus, dyspepsia, epigastric distress, nasuea, dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis. Allergic reactions can cause anaphylaxis and laryngeal edema |
| Salicylate pt ed? | Minimize alcohol use when using. Take with full glass of water after meals. |
| Type 1 diabetes? | Juvenile onset diabetes. Insulin-dependent. Autoimmune process destroys beta-cells of pancreas that produce insulin. No/not enough insulin inhibits glucose uptake in cells, resulting in hyperglycemia. |
| What are some symptoms of Type 1 diabetes? | Polyuria, polydipsia, polyphagia, weight loss. Body usually thin and malnourished |
| Oral hypoglycemic agents are effective on...? | Diabetes type II only |
| Treatment of Type 1? | Insulin replacement is mandatory, along with strict dietary control |
| Type 2 diabetes? | caused by body's cells resistance to insulin, inhibiting their ability to take up glucose. |
| Type II symptoms? | May be asymptomatic. Frequently obese. |
| Type II treatment? | Caloric and carb restriction, exercise and weight loss. Oral hypoglycemic alone, or in combination with insulin. More than one oral agent, or insulin alone. |
| What effects do diabetes (both type) have on vasculature and nerves? | Both types can cause damage to vascular system and nerve degeneration, causing poor circulation and loss of feeling (neuropathy), which can lead to severe damage and amputation of extremities. Renal failure and blindness (retinopathy) are also concerns. |
| What is hypoglycemia? | Condition of low blood glucose. Side effect of diabetic treatments such as insulin replacement, but can also be caused by not eating or metabolic abnormalities. |
| How is hypoglycemia treated? | By resoring blood glucose back to normal by the ingestion or administration of dextrose or carb foods. Injection/infusion of glucagon in severe cases. |
| What are signs and symptoms of hypoglycemia? | chills, cold sweats, hunger, anxiety, nervousness, numbness, pallor, palpitations, tachycardia, headache, nausea and confusion |
| What is insulin? | Insulin is a hormone produced by the pancreatic beta cells. Insulin causes cells to take up glucose, which can be stored as glycogen in the liver and muscle. Usually administered as sub-Q injection, can be given IV (rare) in emergencies. |
| What are the rapid acting insulins? | Lispro (humalog), Aspart (Novolog), Glulisine (Apidra) (5-15, 30-90, <5) |
| Peak of rapid-acting insulins? | 30-90 min |
| Onset of rapid-acting insulins? | 5-15 min |
| Duration of rapid-acting insulins? | < 5 hrs |
| What are the short-acting insulins? | Regular insulin (Humulin R, Novolin R) (1/2-1, 2-3, 5-8) |
| Peak of short-acting insulin? | 2-3 hrs |
| Onset of short-acting insulin? | 1/2 to 1 hr |
| Duration? | 5-8 hrs |
| What are the intermediate-acting insulins? | NPH (Lente, Humulin N, Novolin N), Detemir (Levemir) (2-4, 4-10, 10-16) |
| Peak of intermediate-acting insulins? | 4-10 hrs |
| Onset of intermediate-acting insulins? | 2-4 hrs |
| Duration of intermediate-acting insulins? | 10-16 hrs |
| What are the long-acting insulins? | Glargine (Lantus) |
| Peak of long-acting insulins? | NO PEAK |
| Onset of long-acting insulin? | 2-4 hrs |
| Duration of long acting insulin? | 20-24 hrs |
| What are pre-mixed insulins? | Usually a short-acting insulin in combination with a longer acting one. Humalog mix 75/25; Humalog mix 50/50; Novolog mix 70/30 |
| What is the onset of premixed insulins? | usually 30-60 min |
| Duration of premixed insulin? | up to 24 hrs |
| What are the oral agents used to treat Type II diabetes? | Sulfonylureas, biguanides, meglitinides, alpha-glucosidase inhibitors, thiazolidinediones |
| Sulfonylureas: Action? | Stimulate pancreas to produce insulin |
| Sulfonylureas: Indication? | Lower blood glucose, by increasing insulin secretion by pancreas- after diet and exercise modifications fail. |
| Sulfonylureas: Contraindications? | Known drug allergy, active hypoglycemia, renal or liver failure |
| Sulfonylureas: SE/AE? | HYPOGLYCEMIA, Hemolytic anemia, thrombocytopenia, GI |
| Sulfonylureas: Drug interactions? | BATA: beta-blockers, alcohol, thyroid preps, anabolic steroids |
| Sulfonylureas: Prototype? | Glyburide |
| Biguanides: Action? | RIL: Increase sensitivity of receptors to insulin, increase glucose absorption by intestine, decrease glucose production by liver |
| Biguanides: Indication? | Lower blood glucose, after diet and exercise modifcations fail (like sulfonylureas). Drug of choice for DMII |
| Biguanides: Contraindications? | Known drug allergy, active hypoglycemia, renal or liver failure. |
| Biguanides: SE/AE? | Hemolytic anemia, thrombocytopenia, erythema, HI, heartburn, N/V, diarrhea, decreased appetite. Can cause lactic acidosis (rare) |
| Biguanides: Drug interactions? | BATA. Beta-blockers, alcohol, thyroid preps, anabolic steroids (like sulfonylureas) |
| Biguanides: Prototype? | Metformin |
| Megaglitinides/glinides: Action? | Increased insulin secretion by pancreas |
| Megaglitinides/glinides: SE/AE? | HYPOGLYCEMIA (esp in liver failure pts), wt. gain. |
| Megaglitinides/glinides: Prototype? | Repaglinide (Prandin) Nateglinide (Starlix) |
| Alpha-glucosidase Inhibitors: Action? | Inhibit carbohydrate digestion and absorption (intestine). Decreases postprandial rise in blood glucose |
| Alpha-glucosidase Inhibitors: SE/AE? | HYPOGLYCEMIA (if used with insulin or sulfonylurea). Flatulence, cramps, adbominal distension, borborygmus, GI. May cause liver damage in long term, high dosage. |
| Alpha-glucosidase Inhibitors: Prototype? | Acarbose (Precose) Miglitol (Glyset) |
| Thiazolidinediones (Glitazones or TZD): Action? | Decreases insulin resistance. Increases glucose uptake by muscle/adipose tissue. Decrease glucose production by liver. (z-did/rul) |
| Thiazolidinediones(Glitazones or TZD): Indication? | Lower blood glucose |
| Thiazolidinediones (Glitazones or TZD): SE/AE? | HYPOGLYCEMIA (in presence of excessive insulin), wt. gain, hepatotoxicity, fluid retention, congestive heart failure, bone effects |
| Categories of beta-lactam antibiotics? | PCCM. Penicillin, cephalosporin, carbapenem, monobactam |
| Cephalosporin: Prototype? | Cefazolin |
| Cephalosporin: Prototype: Indications? | Gram-pos bacteria. Skin infections, penumonia, UTI, bone/joint infections, septicemia, perioperative prophylaxis, billiary tract/genital infections. Bacterial endocarditis, prophylaxis for dental and upper resp tract procedures. |
| Adverse effects of administering Vancomycin for MRSA? | OTOTOXICITY. Flushing, rash, pruritis, uticaria, tachycardia, hypotension, thrombophlebitis, thrombocytopenia. |
| Macrolide: Prototype? | Erythromycin |
| Macrolide: Prototype: Indications? | Diptheria, pneumonia, strep throat. Legionnaires’ disease, Bordatella pertussis (cause of whooping cough), urethritis, cervicitis, respiratory infections, rheumatic fever, bacterial endocarditis |
| Tetracycline: Prototype? | Doxycycline |
| Tetracycline: Prototype: SE/AE? | discoloration of teeth, photosensitivity, candida; diarrhea, pseudo colitis, vestibular toxicity: lightheadedness, dizziness, unsteadiness. |
| Types of MRSA? | Hospital asssociate, community associated |
| What is MRSA? | Methicillin resistant staphylococcus aureus. |
| HA-MRSA? | Hospital associated MRSA. More prevalent (85%). More serious, harder to treat. Acq from health-care setting. Person-person contact (health care worker-patient) |
| HA-MRSA Risk factors? | Old age, recent surgery or hospitalization, dialysis, treatment in ICU, prolonged antibiotic therapy, indwelling catheter, residence in long-term care facility. |
| Treatment of choice of HA-MRSA? | IV Vancomycin |
| CA-MRSA? | Community-associated MRSA. Distinct strain, less common (15%). Many are asymptomatic carriers (20-30 % of pop) on skin/nostrils. Generally less dangerous. Usually affects young, healthy persons with no recent exposure to health care settings. |
| CA-MRSA infections? | Can cause mild infections of skin & soft tissues- boils, impetigo. More serious infections: necrotizing fasciitis, severe necrotizing pneumonia, severe sepsis |
| CA-MRSA transmission? | Skin to skin, or contact with contaminated objects. Athletes, men who have sex with men, close quarters. Sports equipment, razors |
| Treatment of choice for CA-MRSA? | trimethoprim/sulfamethoxazole, doxycycline, clyndamycin. Severe cases: vancomycin. |
| HA-MRSA and CA-MRSA are resistant to what class of antibiotics? | Beta-lactams |
| NSAIDs: Action? | Anti-inflammatory and analgesic effects due to prostglandin synthesis inhibition. Anti-pyretic effects are also due to prostaglandin inhibition, but also vasodilation. |
| NSAIDs: SE/AE? | Nausea, heartburn, vomiting, tinnitis, mucosal lesions |
| NSAIDs: Indications? | Moderate pain, fever, inflammatory conditions (RA, OA) |
| Metformin: Action? | Increases sensitivity of insulin receptors. Increases glucose absorption by intestines. Decreases glucose production by liver. |
| Metformin: SE/AE? | Decreased appetite, nausea, diarrhea. May cause lactic acidosis (rare). Possible vitamin deficiency. |
| Metformin: Contraindications? | Impaired renal function. |
| Metformin: Indications? | Does not actively lower blood glucose, so used on patients who tend to skip meals, as it will not exacerbate hypoglycemia. It is used prophylactically in high risk patients to prevent diabetes type 2.Gestational diabetes, polycystic Ovary Syndrome (PCOS) |
| Acetaminophen (Tylenol) | No inflammation, poses liver damage w/ overdose. Does not prevent, nor impose risk of MI and stroke. Does not pose risk of gastric ulceration |
| Aspirin | Prevents MI and stroke |
| Which NSAIDs pose risk of gastric ulceration? | All except Acetaminophen (Tylenol) |
| Which NSAIDs pose risk of renal impairment? | All except Acetaminophen (Tylenol) |
| Should aspirin be used to treat fever in children? | No. Can cause Reye's Syndrome |
| Most common side effects of aspirin? | Gastric distress, heartburn and nausea |
| Long term effects of aspirin? | Gastric ulceration, perforation and bleeding. |
| Does acetaminophen (Tylenol)increase bleeding time? | NO |
| Does acetaminophen (Tylenol) pose risk of renal impairment? | NO |
| Which drug is ok for pregnancy? (Which "NSAID") | Tylenol |
| Which drug poses risk of liver damage w/ overdose? | Tylenol |
| Who should not receive aspirin? | Those with peptic ulcer, bleeding disorders, pregnant women, children. |
| What drugs interact with aspirin? | Warfarin, heparin (anticoags). Alcohol |
| True/false: Non-aspirin first-generation NSAIDs promote MI/stroke | True |
| What is the trade name for Naproxen? | Aleve |
| Which drug can interact with alcohol to cause major liver damage? | Acetaminophen (Tylenol) |
| Which analgesic is preferred to use for children without chickenpox/influenza? | Acetaminophen (Tylenol) |
| What cautions should you take when administering Naproxen? | Caution when giving to elderly patients |
Created by:
kangaloo
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