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Pharm final
| Question | Answer |
|---|---|
| Pharmacology | study of drugs and their effects |
| Pharmacodynamics | action of drugs on living organisms |
| Pharmacokinetics | what the body does in response to drugs |
| trade name i.e. | Tylenol |
| generic name | official name of drug (acetaminophen) |
| Which color are nitrous oxide cylinders | blue |
| the properties that make nitrous oxide conscious sedation popular in dental offices include all except | long period of onset and recovery |
| which Guedel's stage is absolutely contraindicated because of severe respiratory depression leading to possible death | stage IV |
| Which is not a component of general anesthesia | respiratory paralysis |
| Which anesthetic would be indicated for a lengthy dental procedure | Bupivacaine 0.5% with 1:200,000 epinephrine |
| What is the major advantage of amide local anesthetics over esters | lack of allergenicity |
| Vasoconstrictors are added to local anesthetics for all reasons execpt | shorten duration of action |
| which must occur for a local anesthetic to be absorbed into the tissue | weak base and primarily nonionized |
| T or F: amides are hydrolyzed in the blood plasma by the enzymes pseudocholinesterase and liver esterases | False |
| All considerations should be made when prescribing Nystatin execpt | cultures should be performed before prescribing |
| What is the most common adverse reaction associated with the antifungal agent ketoconazole | GI distress, nausea, vomiting |
| What is the mechanism of action of the imidazole's in treatment of fungal infections | increased cell membrane permeability |
| which medication is NOT used in the management of oral herpes simplex | Zidovudine |
| Which are cardiac conditions that are indications for prophylactic antibiotic premedication before a dental procedure | prosthetic heart valve and previous infective endocarditis |
| the current AHA prophylactic premed dosage for prevention of infective endocarditis in the pt that can have penicillin | 2 gram/2000mg amoxicillin taken one hour before treatment |
| which group of anti-infective is commonly used to treat oral infections of periodontal origin | tetracyclines |
| Which is not a common adverse effect of antiinfectives | central nervous system depression |
| The antiinfective Rx of choice for premed for a pt w/artificial heart valves if the pt is not allergic to penicillin is | amoxicillin |
| which antiinfective drug is contraindicated in a pregnant pt | tetracycline |
| log dose effect curve | represents relationship between dose of drug and its response |
| Therapeutic index | LD/ED higher TI is safter |
| potency | measure of strength related to dose of drug. its greater when dose is smaller |
| efficacy | max. response regardless of dose |
| onset | time it takes to have effect |
| duration | length of time drug has an effect |
| half-life | measures duration. time necessary for drug to fall to 1/2 of its original blood level |
| how many half-lives does it take for most drugs to be removed from circulation | 4 to 5 |
| FDA | promote and protect the public by helping safe and effective products get to the consumer. grants approval and determines what drugs are sold by prescription |
| DEA | determines degree of control for substances with abuse potential |
| Enteral route of administration | placed into GI tract, oral/rectal route |
| Parenteral ROA | bypasses GI tract, IV IM subcutaneous intradermal topical and sublingual |
| which ROA is the safest and least expensive | oral |
| which ROA has the most rapid drug response | IV |
| SANS characteristics | "fight or flight" increase BP, HR, dilates bronchioles, adrenergic |
| what is the preganglionic neurotransmitter for SANS | acetylcholine |
| what is postganglionic neurotransmitter for SANS | NE |
| what are the receptors for adrenergic drugs | a1, B1, and B2 |
| a1 | arteries, produce constriction of smooth muscles and blood vessels, increases BP |
| B1 | heart, stimulates cardiac output, increases BP |
| B2 | relaxes smooth muscles, dilation of blood vessels and bronchodilation |
| when should you avoid adrenergic drugs | pt's with angina, uncontrolled HTN, uncontrolled hyperthyroidism |
| a adrenergic blockers | Tx of hypertension, "-zosin" |
| B adrenergic blockers | Tx of hypertension, angina, arrhythmias, CHF, glaucoma, can be selective or non-selective beta blockers, "-olol" |
| agonist | has affinity for a receptor and combines with the receptor and produces an effect |
| antagonist | counteracts and competes with the agonist for the receptor |
| what are the cholinergic PANS receptors | muscarinic and nicotinic |
| what do muscarinic impact | smooth muscle, cardiac muscle, gland cells |
| what do nicotinic impact | postganglionic neurons |
| what are the neurotransmitters for cholinergic receptors | ACh |
| direct acting (cholinergic) | act as ACh at receptor site |
| indirect acting (cholinergic) | increase ACh by inhibiting AChE |
| what are the pharmacological effects of cholinergic agents | smooth muscle stimulation- GI motility, bronchoconstriction glands- increase secretion of saliva eye- decreased intraocular pressure |
| what is the toxic reaction of cholinergic agents | SLUD |
| what is the most common problem with supplements | bleeding |
| acemannan (aloe vera) | topical for aphthous ulcers |
| what is the most effective way for a pt to receive systemic fl2 | municipal water supply |
| how much ppm is OTC toothpaste | 1500 |
| how much ppm is prescription toothpaste | 5000 |
| function of vitamin A | prevents night blindness and maintains bone health |
| function of vitamin D | absorbs calcium and phosphorous, provides bone health |
| function of vitamin E | antioxidant and stimulated immune response |
| function of vitamin K | aids in blood clotting and bone health |
| function of vitamin B1 (thiamine) | coenzyme needed for nerve function and energy |
| deficiency of vitamin B1 (thiamine) | beriberi, damages nervous and cardiovascular systems |
| function of vitamin B2 (riboflavin) | coenzyme in energy metabolism |
| deficiency of vitamin B2 (riboflavin) | cheilosis and glossitis |
| function of vitamin B3 (niacin) | coenzyme in energy metabolism |
| deficiency of vitamin B3 (niacin) | pellagra (four D's) |
| function of folate | assist in forming DNA/RNA and RBC's |
| deficiency of folate | anemia, glossitis, diarrhea, spina bifida |
| function of vitamin B12 (cyanocobalamin) | essential for RBC development, needed for folate metabolism |
| deficiency of vitamin B12 | pernicious anemia, weakness and sore tongue/apathy |
| function of vitamin C (ascorbic acid) | promotes synthesis of protein collagen and antioxidant |
| deficiency of vitamin C | scurvy |
| another word for ANUG | trench mouth |
| what does ANUG look like in the oral cavity | ulceration, gingival pain, bleeding, malaise |
| how to manage ANUG | antibiotics (penVK), rinses, NSAIDS, nutritional support |
| characteristics of primary herpetic gingivostomatitis | children, diffuse erythema, crusted vessels, fever |
| characteristics of recurrent herpes labialis | "cold sore" triggered by sunlight, lop trauma, illness, and is contagious in vesicle stage |
| management of herpes | swishing, topicals, acyclovir |
| management of candidiasis | nystatin, ketoconazole, fluconazole |
| angular cheilitis | red, fissures, crusting at commissures |
| predisposing factors for angular cheilitis | sun, allergy, chronic moisture and drooling |
| management of angular cheilitis | topicals |
| management of alveolar osteitis (dry socket) | analgesics, prophylaxis |
| what are recurrent aphthous ulcers known as | canker sores |
| what is the first line of treatment for recurrent aphthous ulcers | topical cortiocosterioids |
| tetracycline stain | intrinsic in developing teeth |
| minocycline stain | blue/gray in fully mineralized teeth |
| chlorhexidine liquid iron stain | extrinsic stain |
| what is the most common dental emergency | syncope |
| signs of hypoglycemia | rapid pulse, decreased respiration, overly talkative |
| treatment for angina | nitroglycerin |
| signs for cardiac arrest | no pulse and BP is unobtainable |
| what causes an adrenal crisis | pts who are taking steroids in doses high enough to suppress adrenal gland |
| what triggers malignant hyperthermia | general anesthetics (most notable sign is rapid rise in body temp) |
| treatment of opioid overdose | naloxone (narcan) |
| level 1 emergency | critical drugs (epi, O2, nitro, glucose, albuterol, etc) |
| level 2 emergency | optional drugs (benzos, morphine, atropine, beta-blockers, etc) |
| level 3 emergency | additional agents (naloxone, flumazenil, antiarrhythmics) |
| what drugs are safe to use during pregnancy | antiinfectives |
| which local anesthetic is safest during pregnancy | lidocaine |
| stage 1 withdrawal of alcohol | agitation |
| stage 2 withdrawal of alcohol | hallucinations |
| stage 3 withdrawal of alcohol | delirium and seizures |
| dental considerations for alcohol | poor healing, increased bleeding, candidiasis, and parotid enlargement |
| acute overdose of opioids | pinpoint pupils, respiratory depression, hypotension, coma |
| withdrawal of opioids | yawning, sweating, irritability, tremors, GI upset |
| GERD definition | stomach acid flows backward through cardiac sphincter and irritates the esophagus |
| what is Barrett's esophagus | complication of GERD, cells in lower esophagus change due to acid exposure, look for taste changes and enamel erosion |
| lifestyle modifications for someone with GERD | small frequent meals, elevate bed, avoid eating 4 hrs BF bed |
| what is the primary cause of peptic ulcer disease | helicobacter pylori infection |
| what causes NSAID induced ulcers | inhibition of protective prostaglandins |
| dental management for GERD and PUD | avoid aspirin and NSAID, semi supine position, avoid alcohol, manage xerostomia |
| mechanism of H2 receptor blocking agents | inhibit gastric acid secretion by blocking H2 receptors |
| examples of H2 receptor blocking agents | cimetidine, famotidine, nizatidine |
| adverse effects of H2 receptor blocking agents | CNS effect, gynecomastia, dry mouth, tase alteration |
| mechanism of PPI's | inhibit enzymes to reduce acid (heal ulcers faster than H2 blockers) |
| what to PPI's end in | "prazole" |
| adverse effects of PPI's | headache, diarrhea, dry mouth, osteoporosis |
| misoprostol | prevents NSAID induced ulcers |
| sucralfate | protective coating over ulcers |
| metoclopramide | increases gastric motility and is a dopamine antagoinst |
| simethicone | relieves flatulence |
| examples of laxatives | bulk forming, stool softeners, stimulants, osmotic, Mu receptor antagonists |
| antiemetics | used for nausea and vomiting due to motion sickness, drugs, or illness |
| first line defense for IBD | anti-inflammatory drugs |
| celiac disease | autoimmune reaction to gluten |
| treatment of celiac disease | strict gluten-free diet |
| noninfectious respiratory diseases | asthma and COPD |
| infectious respiratory diseases | viral/bacterial URI |
| asthma | reversable airway obstruction |
| COPD | irreversible airway obstruction |
| biggest risk that causes COPD | smoking |
| pros of MDI's | direct to bronchioles, low dose and side effects, rapid onset, portable |
| cons of MDI's | technique dependent, potential overuse |
| short acting B2 agonists | albuterol, quick relief |
| long acting B2 agonists | not for monotherapy in asthma |
| what is the first controller for persistent asthma | inhaled corticosteroids |
| what is cromolyn for | prevention only, NOT for acute attacks |
| theophylline | oral bronchodilator medication |
| what is the first line defense for COPD | antimuscarinics |
| what to antihistamines do | help with allergy symptoms. they block histamine |
| what are antineoplastic agents used for | suppressing the growth and spread of malignant cells |
| what is the mechanism of action based on for antineoplastic agents | the ability to interfere with the metabolism or reproductive cycle of tumor cells |
| metastasis | migration to distant sites |
| antimetabolites | works in the S phase (when DNA is being copied) |
| vinca alkaloids and taxanes | work in the M phase (when cells divide) |
| bleomycin | works in the G2 phase (just before cell division) |
| topoisomerase inhibitors | work in the S and G2 phases |
| what are monoclonal antibodies | lab-engineered antibodies that target tumor antigens |
| why combine antineoplastic agents | to get different mechanisms, potential synergy, and lower individual doses = fewer side effects |
| bisphosphonates action when working with MRONJ | inhibit osteoclast activity |
| management of oral mucositis | analgesics such as acetaminophen, saline/baking soda rinses, cryotherapy, hydration |
| tumor lysis syndrome | when cancer cells die quickly and cause high levels of uric acid |
| allopurinol | a medicine used before treatment to prevent high uric acid levels |
| when is the best time for antineoplastic treatment | before chemo or in the early cycle |
| adrenocorticosteriods | naturally occurring steroidal components released from the adrenal cortex |
| glucocorticoids | affect carbohydrate metabolism |
| mineralocorticoids | influence sodium and H2O balance |
| adrenocorticotropic hormone | agent secreted by the pituitary that causes release of hormones from the adrenal cortex |
| Addison's disease | deficiency of adrenocorticosteroids |
| Cushing's syndrome | excessive production of adrenocorticosteroids |
| cortisol | involved in stress response and metabolism |
| routes of adrenocorticosteroids | oral, intramuscularly, intravenously, rarely topically |
| what kind of action do adrenocorticosteroids have | anti-inflammatory |
| adverse reactions to adrenocorticosteriods | peptic ulcers, impaired wound healing, CNS effects, adrenal crisis, hypokalemia, etc |
| insulin function | promotes fuel storage and its main function is to lower blood glucose levels |
| glucagon function | promote fuel mobilization and main function is to raise blood glucose levels |
| type 1 diabetes | lack of insulin, rapid onset, fruity breath, usually person younger than 30, increased glucagon secretion |
| type 2 diabetes | most common, obesity, does not secrete enough insulin to normalize plasma glucose |
| what is the first line of treatment for type 2 diabetes | diet and exercise |
| normal hemoglobin level | <7 |
| what is the primary treatment for type 1 diabetes | insulin |
| how is insulin administered | subcutaneously |
| what were the first drugs used to treat type 2 diabetes | sulfonylureas |
| sulfonylureas | stimulate insulin release (oral agent) |
| biguanides | reduce liver glucose output (oral agent) |
| meglitinides | rapid, short acting insulin releasers (oral agent) |
| thiazolidinediones | increase insulin sensitivity (oral agent) |
| DPP-4 inhibitors | preserve incretin hormones (oral agent) |
| a-glucosidase inhibitors | slow carbohydrate digestion (oral agent) |
| SGLT-2 inhibitors | increase urinary glucose excretion (oral agent) |
| bile acid sequestrants | reduce glucose via liver effect (oral agent) |
| GLP-1 receptor agonists | mimic incretion hormones to increase insulin and reduce appetite (injectable agent) |
| insulin | replaces or supplements natural insulin (injectable agent) |
| what is the most commonly prescribed medication for type 2 diabetes | metformin |
| anterior pituitary gland | regulates growth, metabolism, reproduction, and stress responses |
| what does bromocriptine act like | dopamine |
| posterior pituitary major hormones | ADH and oxytocin |
| posterior pituitary gland | vasopressin, induce labor |
| what do thyroid hormones do | control energy metabolism, growth, and development |
| what is a goiter | when you don't get enough iodine, your body makes too much TSH which causes the thyroid to swell |
| children with hypothyroidism may have | delayed tooth eruption, crooked teeth, gum problems |
| treatment for hypothyroidism | levothyroxine |
| hyperthyroidism effects | early tooth eruption, bone loss, heart becomes more active |
| should you treat someone who has a thyroid condition | only if it is under control |
| treatment for hyperthyroidism | antithyroid meds, radioactive iodine, surgery |
| what do antithyroid agents do | slow down the thyroid when it's making too much hormone |
| uses of estrogen | contraception, menstrual disorders, menopause, osteoporosis |
| adverse effects of estrogen | uterine bleeding, edema, weight gain |
| what does progestin do | prepare uterus for pregnancy, develop milk |
| what does progestin treat | painful periods, endometriosis, hormone replacement therapy |
| adverse effects of birth control | gum inflammation and increase dry socket risk |
| what does testosterone do | helps with male traits and building body tissues, used for hormone replacement |
| what should you avoid when a pt has hyperthyroidism | epinephrine |
| what should you limit with cardiovasular conditions | vasoconstrictors |
| cardiac glycosides | increases the force and efficiency of contraction of the myocardium |
| uses of cardiac glycosides | CHF |
| adverse effects of cardiac glycosides | profuse salivation, anorexia, nausea |
| arryhthmia | ineffective beating of the heart resulting in poor ciruculation |
| what to antiarrhythmic agents do | decrease myocardial excitability |
| why is nitroglycerine used to treat cardiovascular problems | it relaxes the smooth muscle |
| what is the action of propranolol | blocks beta response to catecholamine stimulation which reduces myocardial oxygen demand |
| what is verapamil | a calcium channel blocker used to treat angina and HTN |
| what are antihypertensives | used to control elevated blood pressure |
| what is secondary hypertension associated with | endocrine or renal disease |
| what is the most commonly prescribed agent for treatment of HTN | thiazide diuretics |
| mechanism of action of diuretics | increases urine output by stopping the kidneys from reabsorbing sodium and water. blocks Cl ions which reduces cardiac output and decreases PVR |
| most common adverse effects of diuretics | hyperuricemia, hyperglycemia, hypokalemia |
| function of vitamin K | nerve conduction, renal maintenance |
| mechanism of action of sympatholytics | reduce peripheral resistance through a CNS mediated action on alpha receptors. reduces HR |
| mechanism of action of adrenergic receptor blockers | lowers BP by blocking action on alpha 1 receptors |
| non-selective beta blocker example | propranolol |
| selective beta blocker example | metoprolol (greater action on beta 1 than 2) |
| alpha and beta blockers end in | "alol" |
| mechanism of action of neuronal blockers | blocks release of NE and reduces BP |
| mechanism of action of direct acting vasodilators | acts directly on arterioles to reduce PVR |
| mechanism of action of calcium channel blockers | block Ca ions which relaxes smooth muscle and decreases PVR |
| mechanism of action of angiotensin 1 | converted to angiotensin 2 by the enzyme ACE |
| mechanism of action of angiotensin 2 | creates vasoconstriction and produces aldosterone. |
| what do ACE inhibitors result in | drop of BP |
| what do ACE inhibitors end in | "pril" |
| mechanism of action of angiotensin 2 blockers | blocks the vasoconstrictor and aldosterone-secreting effects. is a selective and competitive antagonist |
| what do angiotensin 2 blockers end in | "sartan" |
| mechanism of action of DRI's | inhibits release of renin which reduces angiotensin 1 levels |
| what is gingival hyperplasia most notable with | calcium channel blockers |
| mechanism of action of antihyperlipidemics | inhibits HMG-CoA reductase and absorption of cholesterol |
| mechanism of action of anticoagulants (heparin) | increases the action of antithrombin III which inactives thrombin and factors IX, X, XI, and XII |
| mechanism of action of anticoagulants (warfarin) | interferes with hepatic synthesis of vitamin K factors II, VII, IX, and X |
| antagonist of heparin | protamine sulfate (intrinsic) |
| antagonist of warfarin | vitamin K (extrinsic) |
Created by:
sarawright