1. which corticosteroid isadminsitered by inhalation totreat 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 enhancesbronchodilating effects of the beta 2 adrenergic agonists.- disadvantage of inhaled steroids is a cause of fungal infection of the mouth and throat.

2. the major naturalmineralcorticoid in humans is ?

ALDOSTERONE.- cortisol, prednisone and dexamethasone are glucocorticoids.

3. 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 ofhte sodium in the kidney tubules. Due to this increased blood aldosterone levels result in high sodium and low potassium levels inthe 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 whichin turn stimulates the adrenal cortex to release aldosterone.- ADH (Vasopressin - antidiuretic hormone) decreases urine production by increasing thereabsorption of water by renal tubule (increases permeability of collecting ducts and distaltubules).------ at high concnetrations ADH can cause arterioles to constrict (increases blood pressure) .

4. Name a disease that is caused bythe hyposecretion of aldosteroneand cortisol?

Addison's disease is caused by the hyposecretion of aldosterone and cortisol. Addisonian crisis isan 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 andneurotransmitter. crh stimulates ACTH

5. name two types ofcorticosteroids:

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. Contraindicationsinclude 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 aerosolcorticosteroids like triamcinolone (Azmacort), beclomethasone (Beconase), fluticasone (Flovent)and budesonide (Pulmicort) can lead to localized infections and Candida albicans .

6. Alprazolam (Xanax) andTriazolam (Halcion) are whattype 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 inhibitorneurotransmitter gamma-amino-butyric acid (GABA) found in the brain. - adverse effects are: fatigue, slurred spech, drowsiness, DRY MOUTH, nausea as well ashypotension and muscle relaxation.- tolerance nad phys dependence can occur with prolonged high dosage.

Dental Decks NDB Exam Part 2 pharmacologyStudy online at quizlet.com/_4qfnf

7. which benzodiazepine comes as a liquid for pre opsedation in children and injectable for IV conscioussedation?

Midazolam (Versed) - flurazepam (Dalmane), temazepam, and midazolam (Versed) areprescribed for treatment of insomnia.

8. the most common adverse effects associated withbenzodiazepines 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 seriouspotentiation of sedative effects leads to respiratory depression).- with normal dosing benzos have little effect on respiraotry systems.- benzodiazepines, barbiturates, and narcotic analgesics all prodcuesedation 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 riskof overdose. pentobarbital and phenobarbital are examples.phenobarbital used for anti-convulsants.

9. Name a benzodiazepine antagonist that may be used toreverse the residual effects of benzodiazepines in theevent of an overdose.

Flumazenil (Mazicon).

10. Busprione (BuSpar) is clasified as a minor trnaguilizerwhich 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 musclerelaxant properties.- does NOT impair psychomotor function and does NOT causesedation or physical dependence.- slow onset of action (couple weeks), probably acts on 5-hydroxytryptamine (serotonin) receptors to diminish serotonergicaction.- side effects are restlessness, dizziness, headache, nausea, diarrhea,and paresthesias.Long term risk --- tardive dyskinesia.

11. 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 localanesthtic overdose. - if given intravenously use a large vein to decrease the risk ofthrmobophlebitis.(thrombo - vein inflammation, phlebitis - bloodclot) . propylene glycol in the IV mix is hte main cause ofthrombophlebitis.

12. the barbiturates phenobarbital (Luminal),mephobarbital (mebaral), and Primidone (Mysoline) areclassified as what type of barbiturate (wrt duration ofaction)?

Long acting- relates to lipid solubility. ultrashort being the most lipid soluble andlong acting the least lipid soluble. - metabolized by liver. -- ultrashort - 5-20 minutes for induction of general anesthsia. iethiopental (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)

13. do barbiturates possessanalgesic 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.

14. the brief duration of generalanesthetic action of an ultra-short-acting barbituate isdue 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 theyrapidly 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.

15. All of the following arepharmacologic effects ofglucocorticoids except:- decrease in gluconeogenesis- decrease in utilization ofglucose- inhibition of proteinsynthesis- an increase in proteincatabolsim- impaired wound healing- a decreased resistance toinfection

answer: a decresae in gluconeogenesis!- glucocorticoids ENHANCE gluconeogenesis through the breakdown of endogenous proteins toamino 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 toedema and hypertension if excessive.

16. beclomethasone, budesonide,and flunisolide are what typeof 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 andtoxicity is greatly reduced.

17. the major naturalglucocorticoid is?

Cortisol (hydrocortisone)- corticosteroids produced by adrenal cortex...two groups...glucocorticoids and mineralocorticoids. - glucocorticoids - metabolism, catabolism, immunes repsone, and inlammation. they act onarachidonic acid metabolism, induce syntheis of a protein that inhibits phospholipase A2 , thusdecreasing the production of both prostaglandins and leukotrienes. Synthetic glucocoritcoids areprednisone, prednisolone, dexamethasone, and triamcinolone.- mineralcorticoids regulate Na and K+ reabsorption in collecting tubules of the kidney. The majornatural mineralocorticoid is ALDOSTERONE. - corticosteroids don't cure, just replace. - may cause peptic ulcers. - toxic effects of corticosteroids include growth inhibition, hyperglycemia, osteoporosis, psychosisand salt retention.

18. posoning with anorganophosphatecholinesterase inhibitor canbe treated with?

Pralidoxime (Protopam)- a cholinesterase reactivator used as an antidote to reverse muscle paralysis resulting fromorganophosphate 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 msfasciculations (twitching)

19. isoflurophate andechothiophate are examplesof ?

organophosphates (inhibit cholinesterase) - tx glaucoma.malathion nad parathion are cholinesterase inhibitors used as insecticides.

20. all are true of edrophonium except?- direct acting cholinergic agonist(cholinomimetic)- rapid acting, short duration, injectablecholinesterase inhibitor- drug of choice for dx myasthenia gravisbecause of rapid onset and reversibility.- useful in differentiating a myasthenic crisisform a cholinergic crisis

It is false that it is a direct acting cholinomimetic.It is an indirect action cholinergic agonist (no cholinesterase - more cholinergicaction).....cholinomimetic.- other cholinomimetics are neostigmine, pyridostigmine, and physostigmine- allcholinesterase inhibitors)------ cholinergic crissi: bradycardia (decreased heart rate), lacrimation, extremesalivation, vasodilation, and muscle weakness.

21. why is it difficult to distinguish myastheniagravis and cholinergic crisis?

they both result in muscle weakness.- administration of short acting cholinomimetic such as edrophonium willimprove myasthenic crisis but worsen the cholinergic crisis!

22. 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 acetylcholinereceptors (cholinergic receptors)

mydriasis is dilation (more vivid images at night)

23. in dentistry a cholinergic drug is used to? - treat a dry mouth by inducting salivation

24. name two cholinergic drugs used in dentistry. - pilocarpine (Salagen) - indicated for xerostomia caused by salivary glandhypofunction resulting form radiotherapy for cancer of hte head nad neck. It is acholinergic agonist. Side effects are excess weating, nausea, heartburn, anddiarhea

- cevimeline (Evoxac) - tx of symptoms of xerostomia in patieths with Sjogren'ssyndrome. It is a cholinergic agonist. Side effects are sweating, nausea, hearburnnad diarrhea

25. 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 nadactivity of GI and urinary tractis. These drugs tend to cause miosis and decreaseintraocular pressure. Carbachol used in ophthalmology to produce miosis.

26. Name a non-dental use for pilocarpine? - pilocarpine is the most useful alkaloid employed as a miotic and to treat openangle glaucoma. - glaucoma associated with optic nerve damage often due to increased pressure inthe eye (aqueous humor).open v closed angle often differentiated by speed of onset (closed is rapid andoften painful, open is slower and people often put off tx until irreversible damageoccurs).

- cholinesterase inhibitors like physostigmine, neostigmine, edrophium,pyridostigmine, malathion, and parathion inhibit acetylcholinesterase at BOTHmuscarinic and nicotinic sites. indirect acting cholinomimetic agents.

27. True or False: All the following drugs have anaction which results in increased effects ofacetylcholine within the autonomic nervoussystem 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 neuromuscularjunctions but the excess acetylcholine eventually results in muscle paralysis.

28. The prototypedepolarizingneuromuscular blockingagent is?

Succinylcholine (Anectine)- neuromuscular blockign drugs prodcue complete skeletal muscle relaxation and facilitate endotrachealintubation. adjunt for surgical anesthesia.

- **** succinylcholine may cause MUSCARINIC responses such as bradycardia and increased glandularsecretions.

29. what type of receptors toneuromuscular blockingdrugs work on?

these neuromuscular blocking drugs interact with nicotinic receptors at the skeletal neuromuscularjunction. The two classes are nondepolarizing and depolarizing.- nondepolarizing - competitive compete with acetylcholine at hte nicotinic receptor. prevent Ach fromstimulating so result is muscle paralysis. - depolarizing (non-competitive) - Sucinylcholine (anectine) only one used in US. It desensitizes theneuromuscular end plate. it binds to the ACh receptor and stimulates depolarization causing initialexcitation followed by block of neurotransmission and muscle paralysis.

30. name a currentlyavailable ganglionicblocker for clinical use:

mecamylamine (Inversine) and Trimethaphan (Arfonad)---- when would you use mecamylamine and or trimethaphan.....an emergency hypertension.

31. ganglion blocking drugsfall into what larger classof 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......

32. list the cholinergicactions:

- 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 parasympatheticpostganglionic synapses. It is also the transmitter substance of the neuromuscular junction in skeletalmuscle (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 appropriatebodily actions.

33. Methyldopa (Aldomet) &Clonidine (Catapres) arewhat types of drugs?

centrally acting antihypertensives.

- methyldopa produces alpha-methylnorepinephrine which replaces norepinephrine in the vesicularstorage sites and is released by the nerve impulse.Leads to hypotension and bradycardia.

34. Tolazoline (Priscoline) iswhat 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.

35. sympathetic is to_____ asparasympatheticis to ____

sympathetic is to * adrenergic * as parasympathetic is to " muscarinic".

--- At the effector organs, sympathetic ganglionic neurons release noradrenaline (norepinephrine), along with othercotransmitters such as ATP, to act on adrenergic receptors, with the exception of the sweat glands and the adrenalmedulla:--- sweat glands are part of sympathetic nervous system but have muscarinic receptors. --- In the parasympathetic system, ganglionic neurons use acetylcholine as a neurotransmitter, to stimulatemuscarinic receptors.

-- At the adrenal cortex, there is no postsynaptic neuron. Instead the presynaptic neuron releases acetylcholine to acton nicotinic receptors.

---- t he adrenal medulla is the center part of the adrenal gland (surrounded by adrenal cortex) .

36. Tolazolien(Priscoline) iswhat type ofdrug?

parenteral antihypertensive moderate alpha-2 adrenergic blocking drug.

Antiadrenergic agents inhibit the signals of epinephrine and norepinephrine. They are primarily adrenergicantagonists, (Alpha Blockers and Beta Blockers) inhibiting adrenergic receptors, but there are exceptions: clonidineis an adrenergic agonist on the α2 receptor, since this receptor is located presynaptically to inhibit further release ofadrenaline and noradrenaline. (other exceptions are clonidine, guanfacine, and guanabenz)...stim central alpha-2adrenergic 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.

37. what is aclinicallysignificantadverse reactionto metoprolol?

drowsiness:metoprolol (Lopressor) is a competitive beta-1 selective blocker.

**** the most common side effects of beta blockers are weakness and drowsiness.

38. if a drug isselective beta 1blocker it can besaid 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 arecardioselective. ----- this is important....non-selective like propranolol have higher cns side effects and are a higher risk for pt's witha history of asthma or bronchitis.

39. describe theautonomicfunction ofsalivary 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 ofstarches during mastication. It breaks down amylose (straight chain starch) and amylopectin (branched starch) byhydrolyzing alpha 1,4 bonds.

The secretory viscous cells of the submandibular gland have distinct functions. The mucous cells are the most activeand therefore the major product of the submandibular glands is saliva. In particular, the serous cells producesalivary amylase, which aids in the breakdown of starches in the mouth. Mucous cells secrete mucin which aids inthe 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 andsublingual glands account for the remaining 30%. (Sublingual gland via sublingual duct - Bartholin)

40. epinephrine reversal is apredictable result of the use ofepinephrine in a patient whohas 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 pressureto rise. If the alphas are blocked...effect of norepinephrine is reduce/abolished while epinephrinebrings about a FALL in blood pressure.

why would epi cause a fall?......epinephrine stimulate both alpha nad beta receptores in thecardiovascular 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 andaction at SA and AV nodes and contractility....no alpha adrenergic action...to relax it isparasympathetic and mostly M2 receptors to relax....---- beta - 2's relax vascular smooth ms and dilate veins. and dilate arteries to skeletal ms. alpha'sconstrict the veins and vascular smooth ms.

----- a pressor response (inc blood pressure) mediated by alpha receptors and a depressor response(decrease blood pressure) is mediated by beta-2 receptors.

41. somebody is having ananaphylactic reaction at thedental office.......what is a typeof drug you could give andwhy?

give the patient EPINEPHRINE:---- possibly sublingually.

this stimulates both the alpha nad beta adrenergic receptors. alpha receptors stimulate vasopressorresponse (elevate blood pressure) and beta receptors stimulate air way dilation and increased cardiacoutput. 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 muscleconstriction. they cause vasodilation and increased permeability.

remember- in the pulmonary system fight or flight sympathetic reaction...you would want more air tofight....beta 2 response is to relax (alpha - 1 contracts but that is a minor effect --- the maor effect isthe beta-2). Here the parasympathetic contracts ....M3 stuff.

42. this agent producesphysiologic actions oppositeto 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.

43. Salmeterol andmetaproterenol are ?

beta 2 adrenergic receptor AGONISTS.

bronchodilators....along with albueterol (proventil) and epinephrine. stim beta recepotrs in airwayto cause bronchodilation. take via aerosol inhalers and nebulizer.

aminophylline is a "theophylline compound" ....administered orally as bronchodilators in reversibleairway obstruction due to asthma or copd. theophylline relax bronchial smooth muscle to improveairway function.

44. all of the following neurons arecholinergic except?preganglionic sympathetic neuronspreganglionic parasympatheticneuronspostganglionic sympathetic neuronspostganglionic parasympatheticneurons

postganglionic sympathetic neurons are adrenergic and secrete norepinephrine.

- preganglionic of both sympathetic and parasympathetic are cholinergic neurosn thatsecrete acetylcholine.

---- adrenergic blockign agents block the effect of impulses transmitted by the adrenergicpostganglionic nerusons of hte sympathetic branch. alpha and beta adrenergic blockingagents act by "COMPETITIVE INHIBITION"

45. alpha adrenergic receptors are locatedon?- vascular smooth muscle-presynaptic nerve terminals- blood platelets- fat cells- neurons in the cns- all of the above.

all of the above- alpha receptors mostly responsible for excitatory effects - beta recepotrs mostly inhibitory effects like vasodilation and relaxation of respiratorysmooth muscles.**** two important exceptions.- alphas mediate relaxation of GI smooth ms.- betas increase force and rate of contraction of heart.

alphas are postjunctional alhpa1 and prejunctional alpha 2-postjunction alpha 1 in radial smooht ms of the iris, arteries, arterioles, and veins...inthe GI tract.-prejunction alpha 2 mediate the inhibition of relesae of norepinephrine.

betas are postjunctional beta1 and postjunctional beta 2- postjunctional beta 1 in myocardium, intestinal tract smoooth muscle, and adiposetissue.-- postjunctional beta 2 in bronchiolar and vascular smooth ms.

46. 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 cardiacconditions.

- nonselective alpha antagonsists block both receptors . can cause tachycardia andpalpitations. sometimes used to treat raynaud's phenomenon.

47. tyramine and methamphetamine are? indirect-acting adrenergic agonists.- cause release of stored norepinphrine at the post ganglioncic nerve endings to producetheir effects.

direct acting:phenyleprine - alpha 1 agonistalbuterol - beta 2 agonistepinephrine - alpha 1,2 and beta 1,2norepinephrine - alpha 1,2 and beta1 (no beta 2!)

48. 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.

49. if you need to control superficialhemorrhage what could you use?

use an adrenergic agonist: specifically an alhpa 1 adrenergic agonist... avsoconstricotr....epinephrine (adrenalin)

- for a nasal decongestant use an alhpa 1 adrenergic agonsit as well...a vasoconstrictor...phenylephrine (neosynephrine) is a good option ...

50. list the four types ofsympatholytic 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 andin the brain. - reserpine- guanethidine

51. the following foursymptoms resultfrom what type ofdrug?- lower bloodpressure- vasodilation- tachycardia- orthostatichypotension

alpha adrenergic blocker.- doxazosin, prazosin and terazosin are all selective alpha 1 blockers to treat hypertension...terazosin also usedto treat benign prostate hyperplasia.

52. list three therapeuticuses ofamphetamines?

- 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 andrespiratory stimulants.- they have a HIGH POTENTIAL FOR ABUSE...they readily pas into the cns nad cuase a rapid release ofnorepinephrine in the brain.

treat:1 - adhd (amphetamine (adderall)2 - narcolepsy (dextroamphetamine) to prevent daytime sleepiness3 - weight loss

53. T/F epinephrine isideal to preventangina pectoris?

false- i tis contraindicated in angina conditions becasue its cardiostimulatory effects would aggravate thiscondition. - epinephrine could though restore cardiac activity in a cardiac arrest.

epinephrine is ideal to reverse an anaphylactic rxn. anaphylaxis ischaractehttp://quizlet.com/7951803/edit/rized by rapid, exreme reduction in blood presure nadbronchospsms. epi would reverse hypotesion via alpha 1 stim, dilate bronchial tubes via beta 2 and increasecardiac output via beta 1.

54. halothane andisoflurane are?

inhalational anesthetics- simple lipohilic molecules.

55. What is consideredthe first symptom ofNO2

- tingling in the hands - main tehrapeutic effect of nitrous oxide (N20) is relaxation/sedation. Mild analgesia is a secondary effect.

56. what color tank isnitrous oxide storedin?

blue (oxygen is green)

57. what is the failsafemechansim fornitrous oxide delivery?

mechanism doesn't allow less tan 20% oxygen to the patient.

58. List the typical bodilyresponses to nitrousoxide at both 10-20%and 20-40% nitrous.

10-20: tingling of hands, feet, and body warmth20-40: mild sleepiness, relaxation, some analgesia, mind dissociation, heightened audiotry perception.

above 50 --- too much nitrous leads to nausea and sweating

59. list three reasons whyepinephrine isincluded in dentalanesthetics?

epinephrine is a vasoconstrictor so it:1. prolongs duration of local anesthetic2. provides hemostasis3. delay absorption of anesthetic into the systemic circulation thus reducing hte chance of systemic toxicities

60. name the four stages ofgeneral anesthesiawith respect toinhalants.

1. amnesia/anelgesia2. delirium (dilated pupils, tachycardia, hypertension) 3. surgical (four planes)4. medullary paralysis (cessation of respiration)

some inhalants are desflurane, sevoflurane, halothane, isoflurane, and enflurane

61. name the only amide-type local anestheticthat is metabolized inthe bloodstreamrather 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 uponby plasam cholinesterase to render it ineffective.

62. which component oflidocaine localanesthetic solutioncauses 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 rarethan allergic reactions to the bisulfites.

63. Name a localanestheticpreparation that doesnot havevasoconstrictor.

mepivacaine 3% (carbocaine 3%)-- no epi..therefore no bisulfites....therefore less chance of a hypersensitivity reaction.

64. why do you give 100%oxygen followingnitrous oxygen use?

prevent diffusion hypoxia

65. namecontraindications fornitrous 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 causedby 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 orresting on something to help them breathe.)

66. a "bluebloater" issaid to have?

chronic bronchitis.

Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined inclinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.[12] Inthe 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 theairways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there isinfiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling thatthickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamousmetaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening andscarring of the airway wall). The consequence of these changes is a limitation of airflow.[13]

Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referredto as "Blue Bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them.[14] The hypoxia and fluidretention leads to them being called "Blue Bloaters".[edit] EmphysemaMain article: emphysema

Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargementof the air spaces distal to the terminal bronchioles, with destruction of their walls.[12] The destruction of air spacewalls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It alsoreduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung.These airways are more likely to collapse causing further limitation to airflow. The effort made by patients sufferingfrom emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them,"Pink Puffers".

There are 4 types of emphysema:

Centriacinar / centrilobular: proximal to central parts of acini (air spaces closer to bronchioles) are affectedPanacinar / panlobular: enlargement of all air spaces (from bronchioles to terminal blind alveoli). This type isassociated with alpha-1-antitrypsin deficiencyDistal acinar / paraseptal: proximal acinus normal, distal acinus affectedIrregular: various parts of acinus involved. Associated with fibrosis.[15]

67. what is themax dose inmg/kg forarticaine forchildren?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 , 4carps 272, 7 carpules is 476 mg. Also remember .017 mg epi per carpule for 1.7 mL......all other anesthetics are 1.8 mLcarpules..

my math: 7mg/kg divided by 2.2 lb/kg equals 3.18 mg/lb.......approx 3mg/lb......safety factor.....150 lbperson......450mg

68. localanestheticsdepresswhich type ofnerve fiberfirst?

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 wythey have a rapid onset of action).

69. list thegeneral orderof loss offunction dueto use of localanesthetics.....

1. pain2. temp3. touch4. proprioception5. skeletal muscle tone.

70. describe in general terms, howlocal anesthetics work.

they appear to become incorporated within hte nerve membrane or to ind to specific membranesodium ion channels- restric sodium permeability in response to PARTIAL DEPOLARIZATION.

71. max dose of local anesthetic to achild less than 10 years ld isdetermined by?

weight.

for lidocaine...don't exceed 4.4 mg/kg with max of 300 mg.

72. the max recommended adult doseof lidocaine is 300 mg. How manymilliliters of 2% lido is needed toreach 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

73. what are the max recommendeddoses for lidociane, mepivacaine(Carbocaine), prilocaine(Citanest), and bupivacaine(Marcaine)?

lidocaine (Xylocaine) 300 mgmepivacaine (Carbocaien) 300 mgprilocaine (Citanest) 400mg Bupivacaine (Marcaine) 90 mg

74. local anesthetics theoreticallyshould be less effective in acutelyinflamed tissue than normal tissuebecause?

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 portionnon-ionized (no proton attached). The part that is ionized has difficulty penetrating the nerveand 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 apparentlyenough for anesthesia)

75. name a local anesthetic that has noplace in the routine practice ofdentistry?

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 membranesof hte oral, laryngeal, and nasal cavities.

- despite being an excellent local anesthetic, risk of abuse and intense local vasoconstrictionprevent cocaine from being a more widely used clinical anesthetic.

- cocaine pharmacology is different as well.... it inhibits the uptake of catecholamines byadreneric nerve terminals. it therefore potentiates the action of endogenously released andexogenously administered sympathomimetic amines such as dobutamine, dopamine, orepinephrine. an increased risk of developign cardiac arrhythmias and hypertension.

76. list a contraindication / precautionfor the use of prilocaine.

- hepatic diseasealso - prilocaine (citanest) is metabolized to orthotoluidine which prodcuedmethamoglobinemia...characterized by increased levels of methamoglobin in the blood whichis less effective than hemoglobin in carrying oxygen in the blood.** all amides are metabolized primarily in the liver, and the metabolites are then renallyexcreted.

77. where are ester type localanesthetics 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.

78. what are ester type localanesthetics mainly used for today?

topical anesthetics. -- benzocaine, tetracaine, and dibucaine. medical anesthetic preparations to inclupropoxycaine (ravocaine).

79. describe why a patient isallergic to procaine(Novocaine)

plasma cholinesterase breaks the ester into a compound called paraminobenzoic acid (PABA). manypatietns develped an allergy to paba.

80. Name the onlynonbarbiturate sedative-hypnotic agent that isindicated 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 hydratedoesn'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 thehypoprothrombinemic response to warfarin. - sedative effects and or respiratory depression with chloral hydrate may be aditive with other cnsdepressants. montior for increased effect ... includeds ethanol, antidepressants, narcotic analgesics,and benzodiazepines.

81. which form of a localanesthetic can readilypenetrate tissuemembranes?

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 thefree base.

82. describe the mechanism ofaction of local anesthetics onthe nerve axon.

decreases sodium uptake through sodium channels of the axon. this decreases the nerves excitabilitybelow a critical level and nerve impulses fail to propagate along the axon.

**** local anesthetics have no effects on potassium at the nerve axon.

83. what are some adverse sideeffects of local anesthetic?

toxicities and allergies.toxicity: too much leads to toxicities to the cns and cardiovascular system. CNS effects includerestlessness, stimulation, tremors, convulsive seizures, followed by cns depresion, slowed respirationand even coma. Cardiovascular effects include bradycardia and reduction of cardiac output.

allergy: hypersensitivities or allergic reactionsot local anesthetics, particularly from amides are rare.usually manifested as dermatological reactions and edema at injection site. asthmatic wheezingsyndromes have occured. allergic reaction are more prevalent with ester-type rahter htan amide-type.

- ester local anesthetic allergic manifestations include nasolabial swelling, itchinga nd oral mucosalswelling.

84. the amide local anestheticsare metabolized primarily inthe ?

liver - use with caution for all patients with compromised liver function.

85. which amide type localanesthetic has the longestduration of action?

bupivacaine (marcaine) has the longest duration of action of any dental local anesthetic presentlyavailable.

carbocaine (mepivacaine) 3% has 20 minutes or 40 minutes duration depending on route (infiltrationand IAN block)

citanest plain (prilocaine) 4% has 20 min & 2.5 hr.

citanest forte w/ epi (prilo) 4% has 2.25 hrs and 3 hrs.

lido 2% w/ epi has 60 and 90 minutes

marcaine (bupivacaine) 0.5% w/ epi has 60 min and 5-7 hrs.

articaine 4% w/ epi has 60 min and 60 min.

86. the following drugs belong to whatpharmaceutical class of agents:darbepoetin alfa, pegfilgrastim, andsargramostin

answer: colony stimulating factors

darbeoetin: induces erythropoiesis by stim division and differentiation of erythroidprogenitor cells. used to treat anemia associated with chronic renal failure

pegfilgrastim: stim production, maturation, and activation of neutrophils. decreasesthe incidence of infection by stimulation of granulocyte production in patients iwthnonmyeloid malignancies.

sargramostin: used for myeloid reconstitution after autologous bone marrowtransplantation.

(myeloid cells describe any cells that are leukocytes but not lymphocytes)

87. exemestane (Aromasin) and letrozole(Femara) are anticancer drugs classifiedunder what category?

aromatase inhibitors

-- exemestane is an irreversible steroidal aromatase inactivator. prevents theconversion of androgens to estrogens by tying up the enzyme aromatase. in breascancers wehre the growth is estrogen dependent, this drug will lower circulatingestrogens.

--- letrozole (Femara) works like exemestane. it is used as a first line treatment ofhormone receptor positive or metastatic breast cancer in postmenopausal women. it isalso indicated as an extend adjuvant treatment of early breast cancer in postmenopausal women who hae received 5 years of adjuvant tamoxifen therapy.

88. your patient has a history of breast cancerand is undergoing chemotherapy with adrug called cisplatin (platinol). What arethe drug's expected adverse effects?

nausea and vomiting (75-100% dose related)hair lose (alopecia)xerostomiachanges within the tissues of hte oral cavity such as mucositis.

mucosisits is a common reaction to cancer chemotherapy. it is an inflammation of htemucousmembranes. during chemo and radiation therapy, mucosal tissues begin todesquamate and develop into ulcerations. the mucosal integrity is broken and issecondarily infected by the oral flora.

palliative tx is indicated for mucositis.

89. What type of drugs are methotrexate,doxorubicin, and 5-fluorouracil?

anti-neoplastics

*** these are commonly associated with the development of oral mucositis

90. which complication is most likely seenwith chemotherapy treatment?

alopecia.

this occurs one to two weeks after treatment. other common side effects include GIupset, increaed incidence of infection (especially candidiasis) and degeneration oflymphatic tissue.

most chemotherapy agents have shown to be teratogenicin humans and should beavoided by pregnant women

91. name the 8 classes of drugs used in cancerchemotherapy.

1. alkylating agents - alkylate DNA so it can't replicate.--- ie Cisplatin and cyclophosphamide.2. anthracyclines - destroy DNA so ca'nt replicate--- ie daunorubicin and doxorubicin3. antibiotics--- ie dactinomycin4. antimetabolites - interfere with biochem rxn needed for cell growth.--- ie 5-FU (fluorouracil), 6-Mercaptopurine and methotrexate.5. antimicrotubular inhibits cell mitosis--- ie pupular agent is paclitaxel (taxol)6. antiestrogen - blck tumors on which estrogen has a stimulatory effect.--- ie tamoxifen (Nolvadex)7. vinca alkaloids - these are mitotic spindle posons-- ie vinblastine and vincristine8. gonadotropin hormone releasing antigen - inhibits gonadotropin secretionwhich is effective in reducing certain carcinomas. -- ie leuprolide.

- asparaginase deprievs tumor cells of certain amino acids such that proteinproduction is blocked.- interferon boos the immune system.

92. antimetabolites are cell cycle specific drugsacting primarily in which phase of the cellcycle?

S phase of the cell cycle. The S phase of the cell cycle = DNA synthesis. - these antimetabolites attack the cells in the S phase of reproduction cycle byinterfering with the biosynthesis of the purine and pyrimidine bases.

Go phase is the resting phase of the cell cycle.

methotrexate is a folic acid analog - choriocarcinoma, leukemia in spinal fluid,osteogenic sarcoma, beast cancer and head and neck cancer.

flurorouracil (5-FU) and floxuridine are pyrimidine analogs. 5-FU used in somehead and neck cancers.

mercaptopurine and thioguanine are purine analogs. used to treat leukemias.

93. alkylating agents are most effective intreating?

chronic leukemias, lymphomas, myelomas, and carcinomas of the breast andovary.

- alkylating agents are a diverse group of compoundswhich all form alkyl bonds tonucleic acids. these agents share similar mech of action and mech of resistance. - the alkylating agents form covalent bonds with nucleic acids and prtien. the N7position of guanine is a common binding site.

- mechlorethamine, cyclophosphamide, chlorambucil, and melphalan arenitrogen mustards.- carmustine, lomustine, and semustine are nitrosureas.- myleran is a busulfan

94. name thecommonpharmalogicantagonist ofaldosterone inthe collectingtubule.

spironolactone (aldactone)

- potassium-sparing diuretcs result in increased sodium and decreased potassium concentrations at hte end ofhtedistal convuluted tubules. there are two categories of potassium spariing diuretics.

1. antagonist of aldosterone in the collecting tubules. spironolactone has been found to be effective in the treatmentof primary aldosteronism. it may be useful in the treatment of heart failure because hyperaldosteronism is commonlyseen in this condition.2. block the osdium channels in the collecting tubules. triamterene (dyrenium) and amiloride (midamor)

*** toxic side effect of these potassium sparing diuretics is hyperkalemia.

Aldosterone is a hormone that increases the reabsorption of sodium ions and water and the release (secretion) ofpotassium in the collecting ducts and distal convoluted tubule of the kidneys' functional unit, the nephron. Thisincreases blood volume and, therefore, increases blood pressure. Drugs that interfere with the secretion or action ofaldosterone are in use as antihypertensives. One example is spironolactone, which lowers blood pressure byblocking the aldosterone receptor. Aldosterone is part of the renin-angiotensin system.

95. name the threecategories ofwidely useddiuretics

- treats chf by relieving edema and symptoms of dyspnea arising from pulmonary congestion.

1. thiazides - inhibit soidum reabsorption in the distal portion of hte rneal tubule within the kidney causing increaedexcretion of sodium and water. --- ie hydrochlorothiazide (HCTZ) 2. loop diuretics - inhibits reabsorption of sodium and chloride in the ascending loop of henle, thus causingincreased secretion of water, sodium, and chloride. --- prototype agent is flurosemide (lasix)3. potassium sparing diuretics - conserve potassium while causing diuresis. thus no potassium is lost from the bodyas is the case with other diuretics such as the thiazides and the "loops." --- ie spironolactone (aldactone) and triamterene (dyrenium)- triamterene promotes sodium and water excretion while retaining potassium.- spironolactone (aldactone) which competes with aldosteone receptor sites in renal tubules causing increasedsecretion of sodium, chloride, and water while conserving potassium.

96. what type ofdrug is dyazide

brand name for the combination of triamterene (Dyrenium) and hydrochlorothiazide (HCTZ)

97. how does insulinaffect proteinsynthesis?

insulin increases protein synthesis.

(also increases triglyceride storage, increases glycogen synthesis, and decreases gluconeogenesis).

insulin is secreted by the pancreatic beta-cells of hte islets of Langerhans an dis essential for hte metabolism ofglucose and for hte homeostasis of blood glucose.

the four types of insulin are ultra-rapid acting, rapid acting, immediate acting, and long acting.

98. How do mostdrugs travelthrough theblood stream?

Most drugs travel through the blood steram by binding to ALBUMIN PROTEIN. this is abundant in plasma. thisway drugs are carried toall the tissues and organs.

- a drug which is bound to plasma albumin always has some fraction which is not bound. the unbound portion isfree to leave the blood compartment and to be taken up by tissues wehre they elicit hte pharmacological effect. thereamining bound fraction of hte drug then coninuously releases mroe free drug to be taken up by the tissues.

- this is important to understand for drug interactions!. if drug A is administered first and then drug B (which hhas astronger binding affinity to albumin than A) is administered later it will displace drug A from albumin resulting inlarge amounts of UNBOUND drug A whihc could lead to adverse reactions.

99. oral contraceptives blockovulation by inhibitingwhich anterior pituitaryhormones?

follicle stimulating hormone (FSH) and luteinizing hormone (LH).

- they also produce alterations in the genital tract, including changes in cervical mucus, rendering itunfavorable for sperm penetration even if ovulation occurs. changes in the endometrium also occurrendering it unfavorable for nidation (implantation of the fertilized ovum)

100. oral contraceptive agentsusually contain both an______ agent and a_______ agent.

estrogenic agent and a progestational agent.

- estrogenic are ethinyl estradiol and mestranol.- progestational agents include levonorgestrel, norethindrone, norgestimate, and norgestrel

101. all of the following arecentralneurotransmitters. whichelicit major excitatoryeffects within the cns?- acetylcholine- dopamine- norepinephrine- serotonin- gamma-aminobutyricacid- opioid pepieds like beta-endorphin, enkephalins,dynorphin- glutamate- aspartate

- glutamate and aspartate*** both of these amino acids have powerful excitatory effects on neurons in virtually every region ofhtecns.

- GABA is the major inhibitory transmitter in the cns.

- dopamine, norepinphrine, and epinephrine are all CATECHOLAMINEs.

102. list the prominent toxiceffects of mercury.

- loosened teeth, excessive saliva, gum disorders, slurred speech, tremors, and irritability.

- these are all the chronic form! - Hg in body is determined by urien test. British Antie-Lewisite (BAL) or Dimercaprol forms a stable complex with mercury and allows it to beexcreted as an inactive compound.

- mercury is not collected irreversibly in human tissues.average half life of 55 days for transport through the body to the point of excretion.

103. name a drug used to treatdiarrhea (reduce GImotility)

- Loperamide (Imodium) and Diphenoxylate and atropine (lomotil)

- Loperamide (Imodium) is an anti-diarrheal which acts on the intestinal muscles to inhibit peristalsis.It is a member of the OPIOID family. It does NOT cross the blood brain barrier like codeine. - Lomotil requires a prescription due to the atropine.

atropine It is a competitive antagonist for the muscarinic acetylcholine receptor.

Atropine increases firing of the sinoatrial node (SA) and conduction through the atrioventricular node(AV) of the heart, opposes the actions of the vagus nerve, blocks acetylcholine receptor sites, anddecreases bronchial secretions.

In general, atropine lowers the parasympathetic activity of all muscles and glands regulated by theparasympathetic nervous system. This occurs because atropine is a competitive antagonist of themuscarinic acetylcholine receptors (acetylcholine being the main neurotransmitter used by theparasympathetic nervous system). Therefore, it may cause swallowing difficulties and reducedsecretions.

104. dexmethylphenidateand atomoxetine(Strattera) is usedto treat whatcondition?

attention deficity hyperactivity disorder (ADHD)

- Methylphenidate (Ritalin) - mild cns stimulant. rsults in an increase in attention psan, reduction inhyperactivity, and improvement in behavior.- focalin - a new form of methylphenidate called dexmethylphenidate- concerta - a long acting form of methyphenidate- adderall -brand name for mixed amphetamine salts which as the same as methylphenidate in treating adhd- strattera - brand name for atomoxetine, first non-stimulant approved for treating adhd.- metadate cr - brand name for a controlled delivery methylphenidate, another long acting form of the drug.

105. amphetaminedescription fromwikipedia

Substituted amphetamines are a chemical class of stimulants, entactogens, hallucinogens, and other drugs.They feature a phenethylamine core with a methyl group attached to the alpha carbon resulting inamphetamine, along with additional substitutions. Examples of amphetamines are amphetamine (itself),methamphetamine, ephedrine, cathinone, MDMA ("Ecstasy"), and DOM ("STP").

Amphetamine derivatives occur in nature, for example in the leaves of Ephedra and khat plants. These havebeen used since antiquity for their pharmacological effects. Amphetamines were first produced synthetically atthe end of the 19th century. By the 1930s such synthetic amphetamines found use as decongestants in thesymptomatic treatment of colds and also occasionally as psychoactive agents. Their effects on the centralnervous system are diverse, but can be summarized by three overlapping types of activity: psychoanaleptic,hallucinogenic and empathogenic. Various amphetamines may cause these actions either separately or incombination. Improper consumption of amphetamine derivatives may result in addiction and aggressiveness,as well as in rapid deterioration of basic body functions and death. Therefore, production and distribution ofmost related drugs are controlled by the authorities both nationally and internationally

106. chronic caffeineconsumption cancause the followingsymptoms:

- feelings of anxiety and nervousness- sleep disruption- irritability- diuresis- stomach complaints- palpitations and arrhythmias

Caffeine toxicity is thought to occur if intake is around 600-750 mg/day. A cup of coffee has 100-150 mg ofcaffeine. A soda has abotu 50 mg. Vivarin has around 200 mg per serving.

107. all are CNSstimulants except:pentylenetetrazol(metrazol)doxapram(dopram)phenobarbital nikethamide(coramine)picrotoxinstrychnine

answer : phenobarbital!***** phenobarbital is a barbituate (sedative -hypnotic)

the others listed are analeptics and respiratory stimulants (pulmonary disease or hasten recovery form generalanesthetic)

108. define the termanaleptic

refers to a cns stimulant which has the ability to overcome drug-induced respiratory depression and hypnosis.In the past cns stimulants were widely used, but today limited clinical application.

109. caffeine,theophylline, andtheobromine are allwhat type of drug?

xanthines.

- stimulants that improve mental alertness, reduce the urge to sleep and elevate mood. - theophylline and theobromein are weaker cns stimulants than caffeine. - theophylline is hte only xanthine impoortnat i the treatme of asthma...stimulates respiratory centers of themedulla nad is able to cause bronchial dilation in patients w/ asthma.

sympathomimetic amines include amphetamines and other related agents like methylphenidate andphennmetrazine which are potent cns stimulants. used to treat narcolepsy, obesity and attention deficitdisorder.

110. Bromocriptine (Parlodel) and Pergolide(Permax) are prescribed to treat?

Parkinson's disease.- In parinson's - nerve cells in the basal ganglia degenerate, resulting in lowerproduction of dopamine. Treated but not cured.

- levodopa is the precursor to dopamine. It is the MAIN treatment for pt's withParkinson's diseae. It is given in combination with carbidopa.- bromocriptine or pergolide are dopamine agonsits which are often given inadditio to levodopa early in tx to enhancelevodopa..or alter when levodopa's sideeffects are more of a problem.- selegiline is a selective inhibitor of MAO type B , this enzyme is responsible forthe oxidative deamination of dopamine in the brain.- amantadine - appears to potentiate dopaminergic responses.- anticholineric drugs like benztropine and trihexyphenidyl .

111. all of the following are skeletal musclespasmolytic drugs except:- methocarbamol (Robaxin)- cyclobenzaprine (Flexeril)- Baclofen (Lioresal)- Succinylcholine (Anectine)- Carisoprodol (Soma)

all except : succinylcholine*** this is the prototype depolarizing neuromuscular blocking drug.

spasmolytic drugs relieve muscle spasms wihtout paralysis. they act in the cns orin the skeletal muscle cell rather then the neuromuscular end plate!!!- they are used in certain chronic diseases of hte cns like ms, cerebral palsy andcerebrovascular accidents. the drugs used to treat chronic and acute musclespasms.

chronic- baclofen is a derivative of gaba..reduce spasms in spinal cord...tx ms and otherspinal cord diseases.- carisoprodol (soma) used to treat ms spasms and pain associated with acutetemporomandiublar joint pain.

acute muscle spasms- cyclobenzaprine - central action ...relieves acute, painful musculoskeltalconditions. it is NOT effective for muscle spasms secondary to cerebral or spinalcord disease.- methocarbamol - used in mgnt of tetanus and used ot relieve acute, painfulmusculoskeletal conditons.

112. name a popular drug to help relieve acute,painful musculoskeletal pain associated withacute temporomandibular joint pain:

carisoprodol (Soma)- for chronic pain that has acute tmj affects.

113. define and list catecholamines. catecholamines are any one of a group of symapthomimetic compoundscomposed of a catechol molecule and the aliphatic portion of an amine. some areproduced naturally and are calle dendogenous (epi, norepi, dopa).

*** epinephrine, norepinephrine and isoproterenol are considered to be directacting catecholamines.

sympathomimetics that ar ecatecholamines are:epi, norepi, dopamine, dobutamine, and isoproterenol.

sympathomimetics that are not catecholamines are:amphetamine/phenmetrazine, ephedrine, phenylephrine, albuterol /metaproterenol / terbutaline, and oxymetazoline / xylometazoline.

114. the following drugs areuseful in the treatment ofwhat medical condition?- colchicine, probenecid

GOUTgout meds are colchicine, indomethacin, sulfinpyrazone, probenecid, allopurinol.

- three aspects of disease1. reduce inflammation during acute attacks. - colchicine may be used (serious side effects) and nsaid's like indomethacin may be used.2. decrease uric acid production..... allopurinol ( Zyloprim) drug of choice for chronic gout. it inhibitsxanthine oxidase, an enzyme that converts hypoxanthine to xanthine, and xanthine to uric acid....3. enhance uric acid clearane-- probenecid (Benemid) and sulfinpyrazone (anturane). act on kidney and inhibit the secretion ofother weak acids and inhibit reabsorption of uric acid.

115. a pt needs antibiotics for anoral infection. this pt alsohas chronic gout. whatconcerns might you have?

one concern is if the patient is taking the drug probenecid (Benemid) to increase uric acid clearance.While this helps clear uric acid, it inhibits secretion of other weak acids like penicillin. Normallycephalosporins and penicillins have to be given in high and frequen doses due to their high rate ofelimination by the kidneys. Their excretion is SLOWED by giving probenecid!

116. somatotropin is producedby?

somatotropin (aka growth hormone GH) is produced by and secreted form the anterior pituitary gland.- inc rate of protein synthesis- decreased rate of carbo utilization- inc mobilization of fats and use of fat for energy.

- gh usually given subcut inj or intramuscular injection 3x/week

117. ethyl alcohol cuases a well-marked diuresis byinhibiting the production ofwhich hormone?

vasopressin .... aka antidiuretic hormone (ADH).

- ADH decreases urine y inc reabsorption of water by the renal tubules. w/out adh there would beextreme loss of water into the urine.- ethanol (ethyl alcohol) inhibits the adh production.

- ethyl alcohol also dilates blood vessels of hte skin and depresses the cns.

118. inhaled ammonia is thedrug of choice for actingagainst?

syncope- it irritates the trigeminal nerve sensory endings, resulting a reflex stimulation of medullaryrespiratory and vasomotor centers. *** oxygen will aid in combating tisue anoxia

symptoms of syncope include beads of sweat on the upper lip, a weak thready pulse, cold clammy skin,pallor and dzzy feeling. loss of norma vasomotor tonus produces pooling of blood peripherally sonormal blood volume becomes insufficient.*** place patietn in a supine position and elevate the feet to give the pt a transfusion of whole blood .

119. list thetypes ofsyncope

-vasovagal- neurogenic- orthostatic- hyperventilation syndrome

----- tx vaasovagal, neurogenic, and orthostatic with 100% high flowing oxygen!----- 100% oxygen is contraindicated for a person who suffers from copd.

In healthy people, high levels of carbon dioxide is what triggers respiration (to help get rid of the carbon dioxide), butbecause people with COPD are used to having high levels of carbon dioxide their bodies become immune to it andrespiration in this case is triggered by low levels of oxygen. Therefore if you give a person with COPD high concentrationsof oxygen, you are removing their trigger to breath, leading to respiratory depression or even arrest (stop breathingcompletely). This is known as hypoxic drive (hypoxia means low levels of oxygen)

The respiratory drive is normally largely initiated by PaCO2 but in chronic obstructive pulmonary disease (COPD) hypoxiacan be a strong driving force and so if the hypoxia is corrected then the respiratory drive will be reduced. There will also bea loss of physiological hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of grossalveolar hypoventilation.1Therefore, oxygen therapy in COPD must be used with care in the acute setting but it can have distinct benefits in the long-term.

120. list thealuminumsalts usedasantacids:

hydroxidecarbonatephosphateaminoacetate

*** aluminum hydroxide is themsot potenet of these but has less neutralizing capacity than calcium carbonate or sodiumbicarbonate (the only systemic antacid). sodium bicrabonate - alka-seltzercalcium carbonate - tumsaluminum hydroxide - amphojelmagnesium hydroxide - milk of magnesiabismuth salt products - pepto biasmamagnesium and aluminum - Maalox and Mylanta

121. disulfiramis used inthe mgmtof ?

ETHANOL ABUSE- it isn't a cure for alcoholism, but a deterrent. it is an antioxidant that interferes with hepatic oxidation of acetaldehydemetabolized from alcohol. it inhibits aldehyde dehydrogenase (mitochondrial enzyme found in the liver). it is adeterrent....even small amounts of ethanol results in high concentrations of acealdehyde and unpleasant reaction calleddisulfiram-ethanol reaction or DER...... throbbing headache, dyspnea, throbbin in neck, nausea, copious vomiting, thirst,tachycardia, and hypotension. metronidazole also inhibits aldehyde dehydrogenase.

ethanol is a sedative...other alcohols are methanol and ethylene glycol. drugs synergistic with ethanol include diazepam, meperidine, pentobarbital and chlorpromazine.diazepam - aka valium - a benzodiazepammeperidine -aka demerol - fast acting opioid analgesicpentobarbital - short acting barbituate (seizures/sedation)chlorpromazine - first phenothiazine antipsychotic (sedates)

122. which substance is an enzymeformed in the kidney and releasedinto the bloodstream where it hasan important role in theformation of angiotensin?

renin- reniin is a proteolytic enzyme produced by and stored in the juxtaglomerular apparatus thatsurrounds each arteriole as it enters a glomerulus. Renin acts on the precursor substanceangiotensinogen, which is manufactured by the liver and is present in the blood.

- Renin converts angiotensinogen to angiotensin 1. In turn, angiotensin 1 is converted toangiotensin II by a converting enzmye associated with the walls of capillaries, paricularly inthe lungs (ACE) .- Angiotensin II is a POTENT VASOPRESSOR. It is note only increases in total peripheralresistance but, by stimulating aldosterone release, leads to an increase in plasma volume,venous return, stroke volume, and ultimately cardiac output.

- wrong answers were plasmin, lysozyme, and heparin. Heparin come from the word "hepar ....liver....coagulation stuff."

Heparin is a naturally occurring anticoagulant produced by basophils and mast cells.[10]Heparin acts as an anticoagulant, preventing the formation of clots and extension of existingclots within the blood. While heparin does not break down clots that have already formed(unlike tissue plasminogen activator), it allows the body's natural clot lysis mechanisms towork normally to break down clots that have formed. Heparin is generally used foranticoagulation for the following conditions:

123. name the high molecular weightheteropolysaccharide that isfound especially in the lungs andinactivates thrombin and othercoagulation factors and thusprevents blood clotting.

heparin

- wrong answers were prothrombin, fibrin, and plasmin.

- Heparin is contained within mast cells and basophils. these cells occur in connective tissueand in extracellular spaces near blood vessels, particularly the lungs. Heparin neutralizes tisuethromboplastin and blocks thromboplastin generation.

- administering heparin to a pt increases bleeding time (antithrombin III inactivates thrombinso prevents fibrinogen to fibrin.

- Plasmin is a serine protease that acts to dissolve fibrin blood clots. Apart from fibrinolysis,plasmin proteolyses proteins in various other systems: It activates collagenases, somemediators of the complement system and weakens the wall of the Graafian follicle (leading toovulation). It cleaves fibrin, fibronectin, thrombospondin, laminin, and von Willebrand factor.Plasmin, like trypsin, belongs to the family of serine proteases.

124. Your pt's medication historyincludes modafinil (Provigil)......why is your patient taking thisdrug ?

- improve wakefulness during daytime sleepiness

- a cns stimulant. also treats atha (attention deficit/hyperactivity disorder)

- mechanism unknown...likely decreases GABA mediated neurotransmission.

- it is also thought to increase high frequency alpha waves while decreasing both delta andtheta activity, thus increasing mental alertness.

125. The following drugs belong to whatpharmaceutical class of agents:adalimumab, alefacept,infliximab, trastuzumab

- monoclonal antibodies

adalimumab (Humira) is a recombinant monoclonal antibody that binds to human tumornecrosis factor alpha receptor sites. it is used to treat active rheumatoid arthritis.

alefacept (amevive) treats severe plaque psoriasis

126. the following drugs belong to what pharmaceutical class ofagents: pimecrolimus; sirolimus, tacrolimus?

immunosuppressants

- Pimecrolimus (Elidel) tx mild to moderate atopic dermatitis

- Sirolimus (rapamune) tx prophylaxis of organ rejection inpatients receiving renal transplants.

- tacrolimus (protopic) is an imunosuppressant agent used to treatmod to severe atopic dermatitis in patients not responsive toconventional therapy.

127. Granisetron (Kytril) and ondansetron (Zofran) areselective 5-HT3 receptor antagonists used to treat whatcondition?

- emesis caused by cancer chemotherapy.

- 5-HT3 receptor is a serotonin receptor which when activatedduring chemo for cancer, causes emesis (nausea and vomiting).Both granisetron and ondansetron are indicated for proophylaxischemo related emesis,

- also treats PONV ----- post operative nausea and vomiting.

- 5HT3 stands for 5-hydroxytrypamine type 3 receptor.

128. carbidopa is used to treat what disease? what must it beused with.

Carbidopa us used in conjuction with levodopa to treatParkinson's disease.

- carbidopa reduces the levodopa needed because levodopa wouldbe quickly metabolized before it could reach the brain. carbidopainhibits the peripheral decarboxylation of levodopa. this reducslikelihod of peripheral side effects and allows more levodopa toreach the brain.

- carbidopa does not cros the blood-brain barrier. levodopa isconverted to dopamine in the brain.

129. which antiarrhythmic agent is effective only on theventricle and is often administered IV to treat lifethreatening ventricular arrhythmias?

lidocaine utilized IV

- acts on fibrillating ventricles to decrease the cardiac excitabilityand spares the atria. it can effectively reverse a life threateningsituation.

- Quinidine is a prototype anti-arrhythmic used primarily to treatatrial fibrillation. it is not effective in treating life threateningventricular fibrillation.

130. Triazolam (Halcion) is a pre-operative sedative used indentistry, it is metabolized in theliver by the P-450 isoformCYP3A4 enzyme. Drugs which inhibit the actions ofCYP3A4 would affect triazolam in which way? (hint - relateto serum levels)

- cause in increase in serum levels of triazolam

- drugs that inhibit hte metabolic pathway may have a profoundeffect on the clearance of triazolam. could result in unexpectedincrease in actions of triazolam.

131. which drugs are common contraindications for triazolam? antifungal agents can significantly elevate the serum levels oftriazolam resulting in toxicity with therapeutic doses. theseantifungal agents inhibit the cyp3a4 isoform responsible forhepatic metabolsim of triazolam.

(ie itraconazole, ketoconazole, fluconazole, miconazole, andvoriconazole)