32203537
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Flashcards by ACAPUN INSTITUTE, updated more than 1 year ago
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Created by ACAPUN INSTITUTE
almost 3 years ago
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| Question | Answer |
| Acyclovir has selective toxicity mechanism of action b/c: inhibits viral mRNA inhibits cellular mRNA in infected cells only phosphorylated and activated in infected cells | only phosphorylated and activated in infected cells |
| Which of the following is not properly matching the anti-viral med with the virus that caused the disease? | Retrovir was matched with coxsackie or varicella zoster both are false (retrovir is used for HIV/AIDS) |
| HIV patient with sinusitis due to what? | Murcomycosis |
| Most reliable measure of HIV progression? | CD4 count |
| CD4 count and T-cell count for HIV symptoms? | pt had HIV CD4 less than 200 |
| Pt has viral load of 100,000, which means? | pt has high virus load and prone to infection |
| T cell count was 50. What is the right statement? | Pt's T cell count is too low Healthy T-cell count: 500-1500 units/ml |
| Which of the following is not a risk of oral cancer a. Tobacco b. Alcohol c. HPV d. HIV | HIV |
| Which of the following agents is used for HIV infection? a. amantadine b. acyclovir c. zidovudine d. ribavirin e. isoniazid | C. amantadine (Parkinson's) acyclovir (Herpes) zidovudine (also called AZT) ribavirin (Hep C) isoniazid (TB) |
| Fungal agent for HIV? | Fluconazole or ketoconazole |
| Candidiasis & HIV, what do you give for systemic/topical anti-fungal? | Nystatin |
| How to take nystatin? | "swish & swallow" |
| Systemic antifungal? | Fluconazole |
| Medication for angular chelitis? | nystatin |
| Oral anti-fungal infection? | Nystatin |
| Griseofulvin used for? | athlete's foot |
| Clotrimazole mechanism of action? | Alter the enzyme for synthesis of ergosterol |
| Mechanism of miconazole (antifungal)? | inhibits the synthesis of ergosterol |
| Best topical antifungal? | Mycelex |
| which corticosteroid is adminsitered by inhalation to treat asthma? hydrocortisone, prednisone, cortisone, fluticasone (Flonase), or Methylprednisolone (Medrol) | Fluticasone (Flonase) - others inhaled are Triamcinolone (azmacort), Beclomethasone (Beconsase), and Budesonide (Pulmicort) - adv of inhaled are decrease inflammatio in airway in asthma. lower inflammation enhances bronchodilating effects of the beta 2 adrenergic agonists. - disadvantage of inhaled steroids is a cause of fungal infection of the mouth and throat. |
| the major natural mineralcorticoid in humans is ? | ALDOSTERONE. - cortisol, prednisone and dexamethasone are glucocorticoids. |
| which gland secretes aldosterone ? | secreted by cells in the ZONE GLOMERULOSA of the adrenal cortex. - secretion is regulated by the ACTH and by the renin-angiotensin system. - aldosterone promotes the reabsorption of sodium into the blodo from the glomerular filtrate. potassium is lost in the urine becsue of the electronegativey that is created by the reabsorption of hte sodium in the kidney tubules. Due to this increased blood aldosterone levels result in high sodium and low potassium levels in the plasma.......if this were lacking: decreased sodium concentration causes the juxtaglomerular cells of the kidneys to secrete renin, which converts angiotensinogen to angiotensin 1. angiotensin 1 converts to angiotensin II which in turn stimulates the adrenal cortex to release aldosterone. - ADH (Vasopressin - antidiuretic hormone) decreases urine production by increasing the reabsorption of water by renal tubule (increases permeability of collecting ducts and distal tubules). ------ at high concnetrations ADH can cause arterioles to constrict (increases blood pressure) . |
| Name a disease that is caused by the hyposecretion of aldosterone and cortisol? | Addison's disease is caused by the hyposecretion of aldosterone and cortisol. Addisonian crisis is an illness wherethere may be very low blood pressure (low Na in blood) and a coma. - ACTH is produced by the pituitary gland. adrenocorticotropic hormone. (stress rises -> acth up --> cortisol up) - CRH released by hypothalamus (corticotropin releasing hormone) - polypeptide hormone and neurotransmitter. crh stimulates ACTH |
| name two types of corticosteroids: | 1. glucocorticoids: affect carbo, lipid and protein metabolism. used as anti-inlammatory agnets. 2. mineralocorticoids regulate sodium and potassium metabolsim. Adverse reactions include Cushing's syndrome (obesity and weakening of muscles), hyperglycemia, osteoporosis, peptic ulcers, and increased risk of infection. Contraindications include latente infections (fungal,viral, or bacterial), AIDS, herpes, gastric ulcers, and CHF. Inhaled corticosteroids do not achieve sig blood levels to cause adverse effects but aerosol corticosteroids like triamcinolone (Azmacort), beclomethasone (Beconase), fluticasone (Flovent) and budesonide (Pulmicort) can lead to localized infections and Candida albicans . |
| Alprazolam (Xanax) and Triazolam (Halcion) are what type of drugs? | Tranquilizers (Benzodiazepines) others are chlordiazepoxide (Librium), diazepam (Valium), flurazepam (Dalmane), midazolam (Versed), lorazepam (Ativan). - IV benzos cause conscious-sedatio for outpatient surgery. - depress limbic system and reticular formation through potentiation of the inhibitor neurotransmitter gamma-amino-butyric acid (GABA) found in the brain. - adverse effects are: fatigue, slurred spech, drowsiness, DRY MOUTH, nausea as well as hypotension and muscle relaxation. - tolerance nad phys dependence can occur with prolonged high dosage. |
| which benzodiazepine comes as a liquid for pre op sedation in children and injectable for IV conscious sedation? | Midazolam (Versed) - flurazepam (Dalmane), temazepam, and midazolam (Versed) are prescribed for treatment of insomnia. |
| the most common adverse effects associated with benzodiazepines include all of the following except: - cns depression (drowsiness and sedation) - gi disturbances (nausea, vomitting and diarrhea) - confusion - respiratory depression - disorientation - ataxia | Answer: respiratory depression. (if taken w/ alcohol serious potentiation of sedative effects leads to respiratory depression). - with normal dosing benzos have little effect on respiraotry systems. - benzodiazepines, barbiturates, and narcotic analgesics all prodcue sedation and have the ability to produce dependence! - ataxia is the gross lack of coordination of muscle movements. ( movement coordinated in the cerebellum). - barbituates are largely replaced by benzodiazepines due to less risk of overdose. pentobarbital and phenobarbital are examples. phenobarbital used for anti-convulsants. |
| Name a benzodiazepine antagonist that may be used to reverse the residual effects of benzodiazepines in the event of an overdose. | Flumazenil (Mazicon). |
| Busprione (BuSpar) is clasified as a minor trnaguilizer which works by what mechanism? -GABAmimetic - diminish serotonergic activity - Cholinomimetic - diminish glutamate activity | Buspirone diminishes serotonergic activity. - oral anxiolytic - distinct pharmacology and also no anticonvulsant or muscle relaxant properties. - does NOT impair psychomotor function and does NOT cause sedation or physical dependence. - slow onset of action (couple weeks), probably acts on 5-hydroxytryptamine (serotonin) receptors to diminish serotonergic action. - side effects are restlessness, dizziness, headache, nausea, diarrhea, and paresthesias. Long term risk --- tardive dyskinesia. |
| Most common side effect of diazepam (Valium) is? | drowsiness, fatique. - tx nervous tension, ms spasm, and anticonfulsant. - contraindications: acute narrow angle glaucoma and psychoses. - agent of choise to reverse status epilepticus induced by a local anesthtic overdose. - if given intravenously use a large vein to decrease the risk of thrmobophlebitis.(thrombo - vein inflammation, phlebitis - blood clot) . propylene glycol in the IV mix is hte main cause of thrombophlebitis. |
| the barbiturates phenobarbital (Luminal), mephobarbital (mebaral), and Primidone (Mysoline) are classified as what type of barbiturate (wrt duration of action)? | Long acting - relates to lipid solubility. ultrashort being the most lipid soluble and long acting the least lipid soluble. - metabolized by liver. -- ultrashort - 5-20 minutes for induction of general anesthsia. ie thiopental (Pentothal) and methohexital (Brevital). -- short acting - 1-3 hrs for treating insomnia like secobarital (Seconal) and pentobarbital (Nembutal). -- intermediate 3-6 hrs - also insomina and include amobarbital (Amytal) and butabarbital (Butisol) -- Long acting for daytime sedation and as an anticonfulsant. examples are phenobarbital (Luminal) and mephobarbital (Mebaral) and primidone (Mysoline) |
| do barbiturates possess analgesic properties? | No, barbiturates do not posses analgesic properties. - barbiturates are from barbituric acid. - act on GABA receptors but different than benzos.. a GABA potentiator..... - also acts on AMPA which is a non- NMDA type -ionotropic transmembrane receptor for glutamate (major neurotransmitter of the body). - barbituate poisoning - respiratory failure - assure adequtae respiration. |
| the brief duration of general anesthetic action of an ultra-short-acting barbituate is due to what factor? | - rapid rate of redistribution for the brain to peripheral tissues. - these agents maintain anesthesia only while in the brain. because of their high lipid solubility they rapidly leave the brian. - examples of ultra short are thiopental (Penthothal) and methohexital (Brevital). - these durges have hte ability to produce dependence! - contraindications: porphyria (porphyrin is the main precursor to heme), liver dysfunction, emphysema, previous sedative addition. |
| All of the following are pharmacologic effects of glucocorticoids except: - decrease in gluconeogenesis - decrease in utilization of glucose - inhibition of protein synthesis - an increase in protein catabolsim - impaired wound healing - a decreased resistance to infection | answer: a decresae in gluconeogenesis! - glucocorticoids ENHANCE gluconeogenesis through the breakdown of endogenous proteins to amino acids, when are then converted to glucose for storage in the liver. - other effects: anti-inflammatory action, immunosuppression, anti-alergenci. Mineralocorticoidds: increase sodium retentions and increase potassium deplection can lead to edema and hypertension if excessive. |
| beclomethasone, budesonide, and flunisolide are what type of drugs? | they are special glucocorticoids (inhalers). developed for chrnoic asthma and bronchial disease. penetrate the airway mucosa but very short half-lives after they enter the blood so systemic effects and toxicity is greatly reduced. |
| the major natural glucocorticoid is? | Cortisol (hydrocortisone) - corticosteroids produced by adrenal cortex...two groups...glucocorticoids and mineralocorticoids. - glucocorticoids - metabolism, catabolism, immunes repsone, and inlammation. they act on arachidonic acid metabolism, induce syntheis of a protein that inhibits phospholipase A2 , thus decreasing the production of both prostaglandins and leukotrienes. Synthetic glucocoritcoids are prednisone, prednisolone, dexamethasone, and triamcinolone. - mineralcorticoids regulate Na and K+ reabsorption in collecting tubules of the kidney. The major natural mineralocorticoid is ALDOSTERONE. - corticosteroids don't cure, just replace. - may cause peptic ulcers. - toxic effects of corticosteroids include growth inhibition, hyperglycemia, osteoporosis, psychosis and salt retention. |
| posoning with an organophosphate cholinesterase inhibitor can be treated with? | Pralidoxime (Protopam) - a cholinesterase reactivator used as an antidote to reverse muscle paralysis resulting from organophosphate anticholinesterase pesticide poisoning. - used if overdose of anti-cholinesterase agents used to treat myasthenia gravis (ie neostigmine, pyridostigmine, and ambenonium) - MG is muscle weakness and fatigue. - organophosphate poisoning: excessive salivation, bronchoconstriction, diarrhea, and skeletal ms fasciculations (twitching) |
| isoflurophate and echothiophate are examples of ? | organophosphates (inhibit cholinesterase) - tx glaucoma. malathion nad parathion are cholinesterase inhibitors used as insecticides. |
| all are true of edrophonium except? - direct acting cholinergic agonist (cholinomimetic) - rapid acting, short duration, injectable cholinesterase inhibitor - drug of choice for dx myasthenia gravis because of rapid onset and reversibility. - useful in differentiating a myasthenic crisis form a cholinergic crisis | It is false that it is a direct acting cholinomimetic. It is an indirect action cholinergic agonist (no cholinesterase - more cholinergic action).....cholinomimetic. - other cholinomimetics are neostigmine, pyridostigmine, and physostigmine- all cholinesterase inhibitors) ------ cholinergic crissi: bradycardia (decreased heart rate), lacrimation, extreme salivation, vasodilation, and muscle weakness. |
| why is it difficult to distinguish myasthenia gravis and cholinergic crisis? | they both result in muscle weakness. - administration of short acting cholinomimetic such as edrophonium will improve myasthenic crisis but worsen the cholinergic crisis! |
| list typical cholinergic effects? | - salivation, miosis (constriction of the pupil), excessive sweating, flushing, increased GI motility, and bradycardia. - remember cholinergic effects are caused by the stimulation of acetylcholine receptors (cholinergic receptors) mydriasis is dilation (more vivid images at night) |
| in dentistry a cholinergic drug is used to? | - treat a dry mouth by inducting salivation |
| name two cholinergic drugs used in dentistry. | - pilocarpine (Salagen) - indicated for xerostomia caused by salivary gland hypofunction resulting form radiotherapy for cancer of hte head nad neck. It is a cholinergic agonist. Side effects are excess weating, nausea, heartburn, and diarhea - cevimeline (Evoxac) - tx of symptoms of xerostomia in patieths with Sjogren's syndrome. It is a cholinergic agonist. Side effects are sweating, nausea, hearburn nad diarrhea |
| All of the following are choline esters except? pilocarpine (Pilocar) methacholine (Provocholine) Bethanechol (Urecholine) Carbechol (Isopto-Carbachol) | -- Pilocarpine (Pilocar) ------- pilocarpine is a cholinergic alkaloid. - choline esters lower blood pressure attributable to generalized vasodilation, flushing of hte skin, and slowing of hte heart rate. There is increased tone nad activity of GI and urinary tractis. These drugs tend to cause miosis and decrease intraocular pressure. Carbachol used in ophthalmology to produce miosis. |
| Name a non-dental use for pilocarpine? | - pilocarpine is the most useful alkaloid employed as a miotic and to treat open angle glaucoma. - glaucoma associated with optic nerve damage often due to increased pressure in the eye (aqueous humor). open v closed angle often differentiated by speed of onset (closed is rapid and often painful, open is slower and people often put off tx until irreversible damage occurs). - cholinesterase inhibitors like physostigmine, neostigmine, edrophium, pyridostigmine, malathion, and parathion inhibit acetylcholinesterase at BOTH muscarinic and nicotinic sites. indirect acting cholinomimetic agents. |
| True or False: All the following drugs have an action which results in increased effects of acetylcholine within the autonomic nervous system AND at hte neuromuscular junctions: -neostimine -physostigmine - edrophonium - pyridostigmine | True. cholinestarase inhibitors - acetylcholine not broken odwn.... direct cholinergic effect are choline esters (methacholine, carbachol, bethanechol) and choline alkaloids (pilocarpine). - acetylcholine does stimulate skeletal ms contractions at the neuromuscular junctions but the excess acetylcholine eventually results in muscle paralysis. |
| The prototype depolarizing neuromuscular blocking agent is? | Succinylcholine (Anectine) - neuromuscular blockign drugs prodcue complete skeletal muscle relaxation and facilitate endotracheal intubation. adjunt for surgical anesthesia. - **** succinylcholine may cause MUSCARINIC responses such as bradycardia and increased glandular secretions. |
| what type of receptors to neuromuscular blocking drugs work on? | these neuromuscular blocking drugs interact with nicotinic receptors at the skeletal neuromuscular junction. The two classes are nondepolarizing and depolarizing. - nondepolarizing - competitive compete with acetylcholine at hte nicotinic receptor. prevent Ach from stimulating so result is muscle paralysis. - depolarizing (non-competitive) - Sucinylcholine (anectine) only one used in US. It desensitizes the neuromuscular end plate. it binds to the ACh receptor and stimulates depolarization causing initial excitation followed by block of neurotransmission and muscle paralysis. |
| name a currently available ganglionic blocker for clinical use: | mecamylamine (Inversine) and Trimethaphan (Arfonad) ---- when would you use mecamylamine and or trimethaphan.....an emergency hypertension. |
| ganglion blocking drugs fall into what larger class of drugs? | nicotinic receptor antagonists (nicotinic blocking agents) - there are two types: ganglion-blocking drugs and neuromuscular blocking drugs. - neuromuscular at at neuromuscular junction of hte somatic system - gnaglionic blockers act at the autonomic ganglia (both symp and parasympathetic) ***side effects of blocking parasympathetic are severe xerostomia, constipation, and hypotension. therefore, used for rapid and reversible fall in blood pressure..... an emergency hypertensive crisis...... |
| list the cholinergic actions: | - cholinergic ----- "the colon is urgent!" --- stim sweat, salivary, tear and bronchial glands --- stim smooth muscles of the bronchi, GI tract, gallbladder, bilde duct, bladder and ureters (urination) ---slowing of the heart (bradycardia) ---constriction of the pupils (miosis) *** Acetylcholine is the chem mediator at ALL autonomic ganglia and at the parasympathetic postganglionic synapses. It is also the transmitter substance of the neuromuscular junction in skeletal muscle (local anesthetics prevent or reduce the liberation of Ach at the NMJ and sweat glands). Acetylcholine causes an alteration in CELL MEMBRANE PERMEABILITY to produce the appropriate bodily actions. |
| Methyldopa (Aldomet) & Clonidine (Catapres) are what types of drugs? | centrally acting antihypertensives. - methyldopa produces alpha-methylnorepinephrine which replaces norepinephrine in the vesicular storage sites and is released by the nerve impulse.Leads to hypotension and bradycardia. |
| Tolazoline (Priscoline) is what type of drug? | moderate alpha-2 adrenergic blocking activity. --- leads to direct peripheral vasodilation. remember peripheral nervous system--> somatic and autonomic. autonomic nervous system ---> parasympathetic nervous system and sympathetic nervous system. |
| sympathetic is to _____ as parasympathetic is to ____ | sympathetic is to ** adrenergic ** as parasympathetic is to " muscarinic". --- At the effector organs, sympathetic ganglionic neurons release noradrenaline (norepinephrine), along with other cotransmitters such as ATP, to act on adrenergic receptors, with the exception of the sweat glands and the adrenal medulla: --- sweat glands are part of sympathetic nervous system but have muscarinic receptors. --- In the parasympathetic system, ganglionic neurons use acetylcholine as a neurotransmitter, to stimulate muscarinic receptors. -- At the adrenal cortex, there is no postsynaptic neuron. Instead the presynaptic neuron releases acetylcholine to act on nicotinic receptors. ---- t he adrenal medulla is the center part of the adrenal gland (surrounded by adrenal cortex) . |
| Tolazolien (Priscoline) is what type of drug? | parenteral antihypertensive moderate alpha-2 adrenergic blocking drug. Antiadrenergic agents inhibit the signals of epinephrine and norepinephrine. They are primarily adrenergic antagonists, (Alpha Blockers and Beta Blockers) inhibiting adrenergic receptors, but there are exceptions: clonidine is an adrenergic agonist on the α2 receptor, since this receptor is located presynaptically to inhibit further release of adrenaline and noradrenaline. (other exceptions are clonidine, guanfacine, and guanabenz)...stim central alpha-2 adrenergic receptors...thereby inhiitni gsympathetic nervous system outflow. Other ways of inhibiting adrenergic signaling is by catecholamine synthesis blocking, e.g. by methyltyrosine. Reserpine works by inhibiting transport into synaptic vesicles of noradrenaline by inhibiting the VMAT. |
| what is a clinically significant adverse reaction to metoprolol? | drowsiness: metoprolol (Lopressor) is a competitive beta-1 selective blocker. **** the most common side effects of beta blockers are weakness and drowsiness. |
| if a drug is selective beta 1 blocker it can be said that it is _____? | cardioselective..... the most common cardioselective drug is Atenolol. - Atenolol has a long plasma half life. It has low lipid solubility and minimally metabolized. -- due to low lipid soluble beta blockers has a low potential for CNS side effects --- Metoprolol and atenolol are cardioselective. ----- this is important....non-selective like propranolol have higher cns side effects and are a higher risk for pt's with a history of asthma or bronchitis. |
| describe the autonomic function of salivary glands: | sympathetic nervous system (adrenergic) --- beta stimulates viscous, amylase secretions --- alpha-1 stimulate potassium secretions parasympathetic (muscarinic) --- M3 stimulates watery secretions. The parotid gland secretes alpha-amylase ( via Stensen's duct) which is the first step in the decomposition of starches during mastication. It breaks down amylose (straight chain starch) and amylopectin (branched starch) by hydrolyzing alpha 1,4 bonds. The secretory viscous cells of the submandibular gland have distinct functions. The mucous cells are the most active and therefore the major product of the submandibular glands is saliva. In particular, the serous cells produce salivary amylase, which aids in the breakdown of starches in the mouth. Mucous cells secrete mucin which aids in the lubrication of the food bolus as it travels through the esophagus. The submandibular gland's highly active acini account for approximately 70% of salivary volume. The parotid and sublingual glands account for the remaining 30%. (Sublingual gland via sublingual duct - Bartholin) |
| epinephrine reversal is a predictable result of the use of epinephrine in a patient who has received a/an.......? | alpha- blocker --- alpha blocker is an antiadrenergic - these have the ability to reverse the actions of adrenaline (epinephrine) ....sometimes called pressor actions because epi and norepi both cause blood pressure to rise. If the alphas are blocked...effect of norepinephrine is reduce/abolished while epinephrine brings about a FALL in blood pressure. why would epi cause a fall?......epinephrine stimulate both alpha nad beta receptores in the cardiovascular system!! Norepinephrine ("Nope Two Beta fun") has no beta 2 effects - just beta 1 . So, epinephrine only effects beta receptors in this case. --- remember beta-1's generally have to do with heart.... beta -1 bascially increase heart rate and action at SA and AV nodes and contractility....no alpha adrenergic action...to relax it is parasympathetic and mostly M2 receptors to relax.... ---- beta - 2's relax vascular smooth ms and dilate veins. and dilate arteries to skeletal ms. alpha's constrict the veins and vascular smooth ms. ----- a pressor response (inc blood pressure) mediated by alpha receptors and a depressor response (d |
| somebody is having an anaphylactic reaction at the dental office.......what is a type of drug you could give and why? | give the patient EPINEPHRINE:---- possibly sublingually. this stimulates both the alpha nad beta adrenergic receptors. alpha receptors stimulate vasopressor response (elevate blood pressure) and beta receptors stimulate air way dilation and increased cardiac output. In this way, epinephrine counteracts the vascular effects of a histamine related anaphylaxis. anaphylaxis results in throat rash, itchy rash, and low blood pressure. Four types of histamine receptors. H1-H4. H1 causes bronchoconstriction and smooth muscle constriction. they cause vasodilation and increased permeability. remember- in the pulmonary system fight or flight sympathetic reaction...you would want more air to fight....beta 2 response is to relax (alpha - 1 contracts but that is a minor effect --- the maor effect is the beta-2). Here the parasympathetic contracts ....M3 stuff. |
| this agent produces physiologic actions opposite to that of histamine? | epinephrine: - alleviate symptoms of an acute astham attack. - tx bronchospasm associated with hypotension as in anaphylzx --- treat hypersensitiivty reactions - prolong activity of local anesthetic - restore cardiac activity in a cardiac arrest - relieve congestion of nose, sinus, and throat. -.... common side effects are headaches, agitation and tachycardia. use in caution w/ pt's who have high blood pressure, hyperthyroidism, etc. |
| Salmeterol and metaproterenol are ? | beta 2 adrenergic receptor AGONISTS. bronchodilators....along with albueterol (proventil) and epinephrine. stim beta recepotrs in airway to cause bronchodilation. take via aerosol inhalers and nebulizer. aminophylline is a "theophylline compound" ....administered orally as bronchodilators in reversible airway obstruction due to asthma or copd. theophylline relax bronchial smooth muscle to improve airway function. |
| all of the following neurons are cholinergic except? preganglionic sympathetic neurons preganglionic parasympathetic neurons postganglionic sympathetic neurons postganglionic parasympathetic neurons | postganglionic sympathetic neurons are adrenergic and secrete norepinephrine. - preganglionic of both sympathetic and parasympathetic are cholinergic neurosn that secrete acetylcholine. ---- adrenergic blockign agents block the effect of impulses transmitted by the adrenergic postganglionic nerusons of hte sympathetic branch. alpha and beta adrenergic blocking agents act by "COMPETITIVE INHIBITION" |
| Tolazoline (Priscoline) and doxazosin (Cardura) and Prazosin (Minipress) are what type of drugs? | alpha blockers. - alpha blockers competitively inhibit action of catecholamines at the alpha receptor sites. they act on blood vessels causing them to relax. - selective alpha antagonissts only block alpha-1 receptors are are common for cardiac conditions. - nonselective alpha antagonsists block both receptors . can cause tachycardia and palpitations. sometimes used to treat raynaud's phenomenon. |
| tyramine and methamphetamine are? | indirect-acting adrenergic agonists. - cause release of stored norepinphrine at the post ganglioncic nerve endings to produce their effects. direct acting: phenyleprine - alpha 1 agonist albuterol - beta 2 agonist epinephrine - alpha 1,2 and beta 1,2 norepinephrine - alpha 1,2 and beta1 (no beta 2!) |
| adrenaline stimulates? | both alpha 1,2 and beta 1,2 receptors. alpha 1 is the most common alpha receptor and beta 2 is the most common beta receptor. --- remember .. norepeinphrine doesn't interact with the most common beta receptor. |
| if you need to control superficial hemorrhage what could you use? | use an adrenergic agonist: specifically an alhpa 1 adrenergic agonist... a vsoconstricotr....epinephrine (adrenalin) - for a nasal decongestant use an alhpa 1 adrenergic agonsit as well...a vasoconstrictor ...phenylephrine (neosynephrine) is a good option ... |
| list the four types of sympatholytic drugs: | sympatholytic = anti-adrenergic.....all use to treat hypertension. 1. beta adrenergic blockers - propranolol - beta 1 and beta 2 blocker. atenolol adn metoprolol are selective beta 1 blockers. 2. alpha adrenergic blockers - tolazoline blocks alpha 2 receptors. - phentolamine blck alpha 1 and alpha 2. - prazosin block alpha 1 3. centrally acting agents...inihibit nerve transmission through cns actions - clonidine, guanfacine, guanabenz, and methyldopa 4. neuronal depleting agents - deplete catecholamine (NE) and serotonin stores from adrenergic terminals and in the brain. - reserpine - guanethidine |
| the following four symptoms result from what type of drug? - lower blood pressure - vasodilation - tachycardia - orthostatic hypotension | alpha adrenergic blocker. - doxazosin, prazosin and terazosin are all selective alpha 1 blockers to treat hypertension...terazosin also used to treat benign prostate hyperplasia. |
| list three therapeutic uses of amphetamines? | - they are sympathomimetic amines that effect both peripheral and sympathetic nervous systems. - amphetamines INCREASE systolic and diastolic blood pressures and they act as weak bronchodilators and respiratory stimulants. - they have a HIGH POTENTIAL FOR ABUSE...they readily pas into the cns nad cuase a rapid release of norepinephrine in the brain. treat: 1 - adhd (amphetamine (adderall) 2 - narcolepsy (dextroamphetamine) to prevent daytime sleepiness 3 - weight loss |
| T/F epinephrine is ideal to prevent angina pectoris? | false - i tis contraindicated in angina conditions becasue its cardiostimulatory effects would aggravate this condition. - epinephrine could though restore cardiac activity in a cardiac arrest. epinephrine is ideal to reverse an anaphylactic rxn. anaphylaxis is charactehttp://quizlet.com/7951803/edit/rized by rapid, exreme reduction in blood presure nad bronchospsms. epi would reverse hypotesion via alpha 1 stim, dilate bronchial tubes via beta 2 and increase cardiac output via beta 1. |
| halothane and isoflurane are? | inhalational anesthetics - simple lipohilic molecules. |
| What is considered the first symptom of NO2 | - tingling in the hands - main tehrapeutic effect of nitrous oxide (N20) is relaxation/sedation. Mild analgesia is a secondary effect. |
| what color tank is nitrous oxide stored in? | blue (oxygen is green) |
| what is the failsafe mechansim for nitrous oxide delivery? | mechanism doesn't allow less tan 20% oxygen to the patient. |
| List the typical bodily responses to nitrous oxide at both 10-20% and 20-40% nitrous. | 10-20: tingling of hands, feet, and body warmth 20-40: mild sleepiness, relaxation, some analgesia, mind dissociation, heightened audiotry perception. above 50 --- too much nitrous leads to nausea and sweating |
| list three reasons why epinephrine is included in dental anesthetics? | epinephrine is a vasoconstrictor so it: 1. prolongs duration of local anesthetic 2. provides hemostasis 3. delay absorption of anesthetic into the systemic circulation thus reducing hte chance of systemic toxicities |
| name the four stages of general anesthesia with respect to inhalants. | 1. amnesia/anelgesia 2. delirium (dilated pupils, tachycardia, hypertension) 3. surgical (four planes) 4. medullary paralysis (cessation of respiration) some inhalants are desflurane, sevoflurane, halothane, isoflurane, and enflurane |
| name the only amide-type local anesthetic that is metabolized in the bloodstream rather than the liver. | articaine (septocaine) - an amide-type local but it is unique due to the ester group attached to its molecule which can be acted upon by plasam cholinesterase to render it ineffective. |
| which component of lidocaine local anesthetic solution causes an allergy? | bisulfites - other components are water, lidocaine, and epinephrine. - sodium metabisulfite preetns the oxidation of epi vasoconstrictor in thos ecomercial preps containing epi. most patients reacting to bisulfites have a hisory of asthma nad the airway is hyperactive to hte sulfite.s allergic rxn usually is an asthmatic syndrome of whezing and bronchial constriction. **** hypersensitivity or allergic reactions ot local anesthetics, particularly the amides, are much more rare than allergic reactions to the bisulfites. |
| Name a local anesthetic preparation that does not have vasoconstrictor. | mepivacaine 3% (carbocaine 3%) -- no epi..therefore no bisulfites....therefore less chance of a hypersensitivity reaction. |
| why do you give 100% oxygen following nitrous oxygen use? | prevent diffusion hypoxia |
| name contraindications for nitrous oxide use? | upper respirotry infections, emphysema, bronchitis, and first trimester of pregnancy. Emphysema is called an obstructive lung disease because the destruction of lung tissue around smaller sacs, called alveoli, makes these air sacs unable to hold their functional shape upon exhalation. It is often caused by long-term exposure to air pollution or smoking. (The anteroposterior diameter of their chest may increase; this symptom is sometimes referred as "barrel chest." The patient may lean forward with arms extended or resting on something to help them breathe.) |
| a "blue bloater" is said to have? | chronic bronchitis. Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.[12] In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.[13] Patients with advanced COPD that have primarily chronic bronch |
| what is the max dose in mg/kg for articaine for children? adults? | 7 mg/kg for both. for a 70 kg adult male (a bit over 150lb) would be 490 mg.....if 1.7 mL carpule.... then 68 mg/carpule 2 carp 136 , 4 carps 272, 7 carpules is 476 mg. Also remember .017 mg epi per carpule for 1.7 mL......all other anesthetics are 1.8 mL carpules.. my math: 7mg/kg divided by 2.2 lb/kg equals 3.18 mg/lb.......approx 3mg/lb......safety factor.....150 lb person......450mg |
| local anesthetics depress which type of nerve fiber first? | small unmyelinated fibers (they conduct pain and temperature) --- they depress the large myelinated fibers last.......the small nerves have the greater surface-volume ration (thisis wy they have a rapid onset of action). |
| list the general order of loss of function due to use of local anesthetics..... | 1. pain 2. temp 3. touch 4. proprioception 5. skeletal muscle tone. |
| describe in general terms, how local anesthetics work. | they appear to become incorporated within hte nerve membrane or to ind to specific membrane sodium ion channels - restric sodium permeability in response to PARTIAL DEPOLARIZATION. |
| max dose of local anesthetic to a child less than 10 years ld is determined by? | weight. for lidocaine...don't exceed 4.4 mg/kg with max of 300 mg. |
| the max recommended adult dose of lidocaine is 300 mg. How many milliliters of 2% lido is needed to reach this? | 15 mL 2% lido so 20mg for every milliliter. 300 mg is max dose so 300/20 = 15...therefore 15mL's. and 300mg / 36 mg per carpule ....leaves 8.3 carpules...max |
| what are the max recommended doses for lidociane, mepivacaine (Carbocaine), prilocaine (Citanest), and bupivacaine (Marcaine)? | lidocaine (Xylocaine) 300 mg mepivacaine (Carbocaien) 300 mg prilocaine (Citanest) 400mg Bupivacaine (Marcaine) 90 mg |
| local anesthetics theoretically should be less effective in acutely inflamed tissue than normal tissue because? | the pH decreases, thus decreasing hte available free base. body pH of 7.4 - locals have a portion ionized (proton attached - aka a H+ atom) and a portion non-ionized (no proton attached). The part that is ionized has difficulty penetrating the nerve and wil not be effective. The non-ionized portion (free base) is more effective. at pH of 7.4 then 10-20% of a local anesthetic is in the form of the free base (this is apparently enough for anesthesia) |
| name a local anesthetic that has no place in the routine practice of dentistry? | Cocaine! - a naturally occurring ester of benzoidc acid. first local anethetic used in dentistry and medicine. - cocaine is commercially available in a variety of forms and is applied ot mucous membranes of hte oral, laryngeal, and nasal cavities. - despite being an excellent local anesthetic, risk of abuse and intense local vasoconstriction prevent cocaine from being a more widely used clinical anesthetic. - cocaine pharmacology is different as well.... it inhibits the uptake of catecholamines by adreneric nerve terminals. it therefore potentiates the action of endogenously released and exogenously administered sympathomimetic amines such as dobutamine, dopamine, or epinephrine. an increased risk of developign cardiac arrhythmias and hypertension. |
| list a contraindication / precaution for the use of prilocaine. | - hepatic disease also - prilocaine (citanest) is metabolized to orthotoluidine which prodcued methamoglobinemia...characterized by increased levels of methamoglobin in the blood which is less effective than hemoglobin in carrying oxygen in the blood. ** all amides are metabolized primarily in the liver, and the metabolites are then renally excreted. |
| where are ester type local anesthetics metabolized? | plasma - by the plasma enzyme plasma cholinesterase (aka pseudocholinesterase) ....it splits the ester - procaine (Novocaine) was the original ester-type anestheti. - an ester grouping is essentially a bridge or link containing the - COOCH2 configuration. |
| what are ester type local anesthetics mainly used for today? | topical anesthetics. -- benzocaine, tetracaine, and dibucaine. medical anesthetic preparations to inclu propoxycaine (ravocaine). |
| describe why a patient is allergic to procaine (Novocaine) | plasma cholinesterase breaks the ester into a compound called paraminobenzoic acid (PABA). many patietns develped an allergy to paba. |
| Name the only nonbarbiturate sedative-hypnotic agent that is indicated in dentistry. | chloral hydrate - traditionally used as an oral preoperative managemnt of the anxious pediatric patient...bad odor, bitter, and caustic tase..... onset in 15 minutes and lasts 4 hours. - children often enter a period of excitement and irritability before becoming sedated. chloral hydrate doesn't relieve pain. - chloral hydrate is a prodrug and is metabolized to the active metabolite trichloroethanol - trichloroethanol may displace warfarin from its protein binding sites resulting in an increase in the hypoprothrombinemic response to warfarin. - sedative effects and or respiratory depression with chloral hydrate may be aditive with other cns depressants. montior for increased effect ... includeds ethanol, antidepressants, narcotic analgesics, and benzodiazepines. |
| which form of a local anesthetic can readily penetrate tissue membranes? | nonionized free-base form. free bases are fat soluble lipophilic drugs. the potential action of all local anesthetics depends on the ability of hte anesthetic salt to liberate the free base. |
| describe the mechanism of action of local anesthetics on the nerve axon. | decreases sodium uptake through sodium channels of the axon. this decreases the nerves excitability below a critical level and nerve impulses fail to propagate along the axon. **** local anesthetics have no effects on potassium at the nerve axon. |
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