Pharmacology Study Guide – Test 2

Pharmacology Study Guide – Test 2

Analgesic Agents Ch. 10

¨  Analgesic: relives pain w/o causing unconsciousness

¨  Pain: most commonly described as unpleasant sensory & emotional experience associated w/either actual or potential tissue damage.

¨  Pain threshold: level of stimulus to produce perception of pain

¨  Pain tolerance: amount of pain a PT can endure w/o it interfering w/normal fx.

¨  Acute pain: sudden in onset; subsides w/tx

¨  Chronic pain: persistent & recurring

¨  Somatic pain: originates from skeletal muscles, ligaments & joints

¨  Visceral pain: originates from organs/smooth muscles (superficial) skin, mucous membranes

o   Visc/superficial tx = opiods

o   Somatic pain tx = nonopiods

¨  Vascular pain: originates from some pathology of the vascular or peripheral tissues

¨  Referred pain: visceral never fibers synapsing at a level in the spinal cord close to fibers that supply specific subQ tissues in the body

¨  Neuropathic pain: injury/damage to peri nerve fibers or damage to CNS

¨  Phantom pain: removed body part (burning, itching, tingling)

¨  Cancer pain: many causes, i.e. pressure on tissues, organs or nerves, hypoxia, blockage to an organ, matastisis, pathologic fractures, muscle spasms, side efx of radiation, surg & chemo

¨  Phsychogenic pain: psychological factors that actually stimulates nerve pain impulses

¨  Central pain: tumors, trauma, inflammation of brain and may occur with any condition that induces CNS damage

Type of Fiber	Myelin sheath	Fiber size	Conduction speed	Type of pain
A	Yes	Large	Fast	Sharp/local
C	No	Small	Slow	Dull/nonlocalized

Neuron regulation:

1. Conducting an action potential
2. releasing neurotransmitter
3. binding transmitter molecules to receptors

Pain Gate Theory

Massage to area relieves pain…large sensory fibers from peri receptors carry impulses to spinal cord…this causes impulse transmission to be inhibited & gate closed, which reduces the recog of pain impulses arriving by means of the small fibers. Opiods work in this way. p. 149

Steps in Junctional Transmission

Synthesis: a transmitter substance is needed

Storage: this transmitter must be stored until released

Release: triggered by an action potential at the axon terminal

Receptor binding: after release, transmitter undergoes reversible binding to receptor site

Termination: removal of transmitter occurs

PNS RX

• Cholinergics: either block or stimulate actions of Ach
• Blockers: muscarinics, ganglionics, neuromuscular blockers, cholinesterase inhibitors
• Adrenergic agonists (epi) vs. antagonists block or stimulate SNS
• Indirect acting antiadrenergics

• Neurologic Rx: patho of disorder is depletion of dopamine (inhib transmitter) i.e. Levodopa; carbidopalevodopa

• Epilepsy TX: reduce rate of d/c of neurons; prevent spread of seizures to rest of brain i.e. phenytoin; Phenobarbital; tegretol; diazapam
• Muscle spasm/spasticity RX i.e. analgesics (ASA), centrally acting relaxants (Diazapam)

Opioid Analgesics (only 3 clinically useful, morphine, codeine, papaverine)

Mechanism of action & DE

¦  Agonist binds to opioid pain receptor in brain & causes an analgesic response

¦  Partial agonist: binds to pain receptor and causes only limited actions

¦  Antagonist: reverses the efx of these on pain receptors

¦  Primarily bind to mu, kappa & delta receptors

¦  Many opiods have affinity for CNS…suppress medullary cough center

¦  Strong opiods for surgery: fentanyl, sufentanil, alfentanil (balanced anesthesia)

¦  Post-op pain TX: Morphine, meperidine, oxycodone, MS Contin …long acting

¦  Analgesia: codeine (also antitussive)

NSAIDS

¦  Lodine: dental

¦  Ibuprofen: only OTC NSAID

¦  Indocin: if ASA or Tylenol doesn’t work

¦  Naprosyn: for tx of O/A (monitor effectiveness)

Mixed Narcotics & Non-narcotics:

¦  Percoset: mixed with Tylenol

¦  Perdocan: mixed with ASA

¦  Darvon & Darvon N: weaker in action, analgesic, sedative?

¦  Vicodin: Tylenol & narcotic

¦  Stadol: used in MCH, pre-op, watch for OD, change in alertness, hallucinations

NARCOTIC ANTAGONIST: NARCAN: used IV for immediate action, blocks mu & kappa receptors; reverses opiod works in mins, used when resp are below 10/R per minute, minimal toxicity

CONTRAINDICATIONS: allergy, asthma, RT insufficiency, elevated ICP, pregnancy

SE/AE: euphoria, dependence, tachycardia, “ BP, mental agitation, nausea, vomiting constipation, urinary retention, pruritis (due to his release), flushing, orthostatic hypotension…serious side efx=CNS depression which leads to R. dep

Non-Opioid Analgesics (primary: Acetominophen (all drugs in NSAID class)

Mechanism of action & DE

¦    Similar to Salicylates…blocked pain impulses peripherall via response to prostaglandin inhibition

¦    Acetaminophen: ↓ fever by acting on the hypothalamus; vasodilation & heat loss

No effect on platelets, cardiovascular or respiratory system, or acid-base changes

¦  Fever, moderate pain TX

NOT SURE IF THIS DRUG WILL BE ON TEST

CNS Depressents & Muscle Relaxants Ch. 12

Sedatives: reduce nervousness, excitability & irritability w/o causing sleep

Hypnotics: more potent than sedatives; causes sleep

Sedative-hypnotics: barbiturates; benzodiazepines, etc.

Barbituates

¦  First used for tx of insomnia & producing sedation; narrow therapeutic index

Mechanism of action & DE

¦  CNS depressant L works in the reticular formation

¦  Inhibits nerve impulse transmission traveling to areas of brain due to ability to potentiate an inhibitory amino acid GABA

¦  Low doses act as sedatives

¦  High doses act as hypnotics

¦  Cause enzymes in liver to metabolize drugs more quickly, which shortens their actions.

¦  Capable of raising the seizure threshold

¦  Used as hypnotics, sedatives, anticonvulsants & anesthesia for surgical procedures. Differ in potency, onset, duration of action

o   Ultrashort: anesthetics

o   Short: sedative-hypnotic

o   Intermediate: anticonvulsant & sedative-hypnotic

o   Long: sedative-hypnotic; anticonvulsant

¦  Long acting: Phenobarbital & short acting Pentobarbital (Nembutal)

CONTRAINDICATIONS: pregnancy, significant respiratory difficulties & severe liver disease

SE/AE: drowsiness, lethargy, dizziness, hangover, restlessness or excitement; affect normal sleep by depriving REM. Adverse reaction: respiratory depression; CNS depression

Toxicity: activated charcoal, assisted respiration, interactions w/alcohol, antihistamines, benzodiazepines, opioids & tranquilizers…most are secondary to efx on hepatic enzyme system i.e. MAOI coadmin…can result in ↓ anticoagulation response and clot formation

Benzodiazapines (most commonly prescribed sedative-hypnotics)

Mechanism of action & DE

¦  Depress CNS (hypothalamus, thalamus & limbic systems) by inhibiting stimulation of brain

¦  Receptors thought to be those of inhibitory transmitter GABA

¦  They do NOT suppress REM sleep or induce hepatic microsomal enzyme activity, so safe to admi to PT taking meds metabolized by this enzyme system

¦  Calming effect; controls agitation & anxiety by inhibition of hyperexcitable nerves

¦   Skeletal muscle relaxation

¦  Used in Tx of alcohol withdrawal, agitation, depression and epilepsy

¦  Tx is symptomatic & supportive

CONTRAINDICATIONS: pregnancy, narrow angle glaucoma & other CNS depressants & coadmin w/MAOIs

SE/AE: drowsiness, headache, excitement or nervousness; dizzy & lethargy Adverse efx: can lead to falls in elderly, also effect normal sleep cycle “hangover effect”

Toxicity: confusion/coma; diminished reflexes, somnolence, syrup of ipecac generally used, gastric lavage

Muscle Relaxants  (needed for conditions such as trauma, inflammation, anxiety, pain…can be assoc w/ acute muscle spasms)

Mechanism of action and DE

¦    Work w/ CNS & actions come from sedative efx rather than direct muscle relaxation…act on nerve transmission in spinal cord..enhance GABA’s central inhibitory efx @ spinal cord

¦    Only ONE works directly on skeletal muscle: dantrolene

¦    Effects are a result of CNS depression in brain at level of brainstem, thalamus & basal ganglia

¦    Tx of muscle-skeletal conditions (spasms, chorea … Involuntary dancing or writhing of the limbs or facial muscles, spasticity), such as MS, cerebral lesions, cerebral palsy or rheumatic disorders. Huntingtons chorea, ↓ rigidity in parkinsonian syndrome or pain assoc w/trigeminal neuralgia

¦  Flexeril, baclofen (aka Lioresal, Atrofen) for TX of hiccups

CONTRAINDICATIONS: severe renal impairment

SE/AE: euphoria, lightheadedness, dizzy/drowsiness, fatigue, muscle weakness…short lived. Dantrolene = hepat tox

Toxicity: NO specific tx!!! Supportive therapy

CNS Stimulant Agents Ch. 16 (stimulate a  specific area of brain or spinal cord)

¨  Amphetamines: CNS stimulants that elevate mood or euphoria, “ mental alertness and “ capacity to work, ↓ fatigue & drowsiness

¨  Analeptics: CNS stimulants that have generalized efx on brainstem & spinal cord (“ response to ext. stimuli)

¨  Anorexiants: suppress appetite

¨  Cataplexy: abrupt attacks of muscle weakness & hypotonia triggered by emotional stimuli such as anger, fear, surprise…often associated w/narcolepsy

¨  Narcolepsy: syndrome charx by sudden sleep attacks, cataplexy, sleep paralysis & visual/auditory hallucination

¨  Seratonin agonist: new class of CNS stimulants used to tx migraines… stimulate 5-HT1 receptors

¨  Sympiomymetic agents: another name for CNS stimulants (aka amphet., caff., cocaine)

¦  Oldest known: cocaine & amphetamine; also caffeine

¦  Anorexiants for tx of exogenous obesity; appetite control via suppression of appetite ctrl centers in brain

¦  Analeptics: generalized efx on brainstem & spinal cord

¦  Amphetamines for tx of narcolepsy & ADHD by “ the amt & duration of nore and dopamine

CONTRAINDICATIONS: marked anxiety/agitation, glaucoma, tourette’s MAOI’s p276

SE/AE: “speed up” body systems; “ CV, hypertension, restless/nervousness; get VITAL SIGNS for baseline

Assess for OTC! i/e. ephedra/ginseng

Adrenergic Agents Ch. 17 (drugs that stimulate the CNS…mimic nore & e)

¦  Adrenergic receptors: receptor sites for the sympathetic neurotransmitters nore & e

¦  Adrenergics: drugs that stimulate the SNS; they mimic the efx of nore & e

¦  Alpha adrenergics: further classified into alpha1 & alpha2, differentiated by loci on nerves

¦  Autonomic fx: involuntary, result from physiologic activity of the ANS. Occur in pairs of opposing actions between the SNS & PNS divisions of the NS.

¦  ANS: controls autonomic bodily fx. Consists of PNS & SNS

¦  B-adrenergic receptors: located on post synaptic effector cells…the cells, muscles & organs that the nerves stim.

¦  B1= Y B2= smooth muscle, bronchioles, arterioles & visceral organs for tx of asthma/COPD

¦  Catecholamines: induce SNS response, “ CO & “ HR and ↓ GI; either endogenous (nore & e) or synthetic (dobutamine)

¦  Dopaminergic receptors: when stimulated by dopamine cause the renal, mesenteric, coronary & cerebral arteries to dilate the blood flow to “

¦  Catecholamines: specifically metabolized by two enzymes: MAO (monomine oxidase) & COMT (catechol O methyltransferase)

¦  Noncatecholamines: structurally dissimilar & have a longer duration of action than the endogenous or synthetic cathechol

Adrenergic Drugs (cause biologic response similar to SNS catecholamines & noncatecholamines)

Mechanism of Action & DE

¦  Rapid onset/distributed widely; systemic/local efx (alpha tx hypotension, beta tx bradycardia)

¦  Bathe the synaptic cleft (area between nerve & effector organ)

¦  Bathe the synaptic cleft (area between nerve & effector organ)

¦  Work by direct stimulation, indirect stimulation or a combo

¦  B2-adrenergic: bronchodialator = epi, ephedrine, pseudoephedrine

o   Used for tx of asthma, anaphylaxis; CPR, hypotension/shock; allergies, eye exams

¦  Alpha agonist: vasoconstriction of arterioles in skin, kidneys, mesentery

¦  A1-receptor: pupil dilation, nasal decongestion, mesentery

¦  A2-receptor: work on presynaptic nerve terminals: cause release of nore and ↓ BP

¦  Dopamine agonists for tx of parkinson’s disease

¦  Epinephrine for tx of bronchodilation & potentiate anesthesia

¦  Dobutamine “ CO; used in acute CHF (nursing indication: monitor BP, RR, inhalant usage)

Noncatecholamines: longer duration, given PO, works directly & indirectly for tx of hypertension, congestion, asthma, bronchitis

¦  Epinephrine for tx of bronchodilation, Albuterol (B-2) for tx of bronchospasms

¦  Ephedrine: activates both A & B, similar to epi but slower onset, longer acting, less potent for tx of nasal decongestion, bronchodialator, narcolepsy

CONTRAINDICATIONS: severe hypertension

SE/AE: alpha-adrenergics:h/a, tachycardia, palpitations, dry mouth. Beta-adrenergics: mild tremors, h/a, nervousness, dizziness, unwanted side effects on CV syste, “ HR, palpitations Toxicity: stop drug quickly

Adrenergic-Blocking Agents Ch. 18 (interrupt or block stimulation of the SNS)

↓ nore or prevents action of cholinergics…alpha blockers, beta blockers, autonomic ganglion blockers

¦  Alpha blockers: interrupt/block stimulation of the SNS which leads to:

o   Vasodilation, “ BP, constriction of pupil (miosis), suppressed ejaculation

Mechanism of Action and DE

¦   Have a higher affinity for a-adrenergic receptors than nore & occupy the receptor site before they can

¦   ↓ response to stimulation of the SNS

¦   effect depends on agent’s selectivity for certain tissues/cells in body (i.e. by blocking fight flight/allowing breed/feed= uterine contractions, GI, bladder)

¦   Ergotamine for tx of migraine headaches by constricting blood flow (a/e=orthstatic hypo; fatigue)

CONTRAINDICATIONS: peri vascular disease, hepatic/renal disease, coronary artery disease, peptic ulcer, sepsis

SE/AE: orthostatic hypotension, tachycardia, vertigo, watch VS, chest pain and avoid alcohol/caffeine….most severe interactions are ones that potentiate the a-blockers effects Toxicity: syrup of ipecac or gastric lavage, then activated charcoal

¦  Beta blockers: compete with catecholamines e and nore

o    B1 = heart ↓ myocardial stimulation, ↓ HR, slows conduction of the AV node, ↓ myocardial O2 demand

o    B2 = smooth muscles contracts (i.e. bronchioles) and airway narrows “ peripheral vascular resistance

Mechanism of Action and DE

¦  Comepete with and block nore & e @ beta-adrenergic receptors, then SNS stimulation is blocked

¦  For tx of hypertension, ↓ cardiac output: Atenelol

¦  B-1 blocker, second-step antihypertensive: Lopressor

¦  For tx of angina, hypertension, MI, onselective blocker: Inderol

CONTRAINDICATIONS: uncompensated heart failure, heart block, bradycardia, pregnancy, severe pulm disease, Raynaud’s disease SE/AE: Acute withdrawl can cause worst effects (rebound hypertension); ATROPINE for crisis; hypotension, cough, sleepiness, bradycardia (AV block), CHF

Autonomic Ganglionic Blockers: inhibit Ach, prevent or ↓ impulses transmission in ANS; used in emergencies to lower BP (antihypertensive)

¦  Given PO, not too stable, uses are limited and not very safe. Pt must be carefully assessed frequently

Cholinergic Agents Ch. 19 (promote action of PNS & acetylcholine)

Ach: neurotransmitter responsible for transmission of nerve impuses to effector cells in PNS

Cholinergic agents: stimulate PNS

Cholinesterase: breaks down Ach

Direct-acting cholinergic agents: bind to chol receptors to activate them

Indirect acting cholinergic agonists: make more Ach available at receptor site

Muscanaric receptors: cholinergic receptors located postsynaptically in the smooth muscle, cardiac muscle and glands of the PS fibers & in effector organs of the cholinergic symp fibers; can be stimulated by alkaloid muscarine.

Nicotinic receptors: cholinergics receptors located in the ganglia of both PNS & SNS; can be stimulated by alkaloid nicotine

Cholinergic agents

¦  Tx of smooth muscle of GI/bladder & mgmt of urinary retention: Urecholine

¦  Tx for intraocular pressure (↓) & mgmt of glaucoma, MG: Pilocarpine

Anticholinesterase agents: inhibit destruction of acetylcholine; short term & reversible action

¦  Absorbed readily from GI, sq & mucous membranes

¦  “ effects of Ach, reduces intraocular pressure, stimulates peristalsis & promotes muscular contraction

¦  For tx of glaucoma, urinary retention, paralytic ileus, MG: Prostigmine

Cholinergic blockers: (block the actions of the PNS)

Mechanism of Action & DE

¦  NARROW Therapeutic index!!!!!!!!

¦  compete with Ach & cholinergic agonists @ muscarinic receptors & increase SNS efx

¦  Tx of spastic conditions of GI/urinary tract; asthma, parkinsons (ach short supply in parkinsons pt), motion sickness

¦  Tx…can stimulate or depress CNS, depending on does…bradycardia, spastic GI, asthma: ATROPINE

o   ATROPINE primarily used for CV disorders i.e. dx of sinus node dysfx, tx of PT w/ symptomatic 2^nd degree AV block & adv life support for tx of sinus bradycardia accomp by hemodynamic compromise

o   Know the next 3 drugs only as chol. Blockers for test

¦  Tx of parkinsons: 1)Cogentin

¦  Tx of peptic ulcer, preanesthetic; reduces arrhythmias: 2)Robinul

¦  Tx of motion sickness, ↓ salivation, amnesia, euphoria: 3)Scopalamine

CONTRAINDICATIONS: GI or GU obstruction, bradycardia, defects in cardiac impulse conduction, hyperthyroidism, epilepsy, hypotension, COPD, parkinsons Toxicity: sludge: Salivation, Lacrimation, Urinary incont, Diarrhea, GI cramps, Emesis

Neuromuscular blockers: disrupt neuro transmission; do NOT cross blood-brain barrier

¦  Tx to relax smooth muscle, redu ce muscle spasm, manage ventilator PTs

¦  Neurotransmission: impulse…nm jct…release of Ca+…Ach release…depolarize & Na+ enters…result: muscle contracts

Nonpolarizing blocking agents: produce prolonged muscle relaxation

¦  Competes with Ach; rapid…relaxes/paralyzes skeletal muscle

¦  Tx adjunct to general anesthesia; minimal histamine releasing efx, doesn’t ↓ BP, causes “ BP, HR, CO: Pavulon

Depolarizing blocking agents:

¦  Action: short term muscle relaxion (i.e. intubation), metabolized in liver/plasma A/E: apnea, CV alterations

¦  Tx for ventilated PT, ultra short acting skeletal muscle relaxat: succinyulcholine

Acid-Controlling Agents Ch. 49 (neutralize acid, or inhibit overproduction of acid)

Hcl: secreted by the parietal cells & maintains stomach pH of 1-4

Pepsin: pepsinogen converts to this, secreted by chief cells in stomach

Antacids

Three forms: aluminum, magnesium & Ca+ based

Mechanism of action & DE

¦  Stimulating mucosal defensive mechanisms…stimulate mucus, PG & bicarbonate secretion from the cells inside the gastric glands…protective barrier

¦  Tx for hyperacidity from gastritis, PUD, pyrosis

o   Bicarbonate buffers acidic properties of Hcl

o   Neutralizers mixed w/ aluminum: Mylanta

o   Neutralizers mixed w/magnesium: MOM

o   Neutralizers mixed w/ Ca+: Maalox & Tums

CONTRAINDICATIONS: severe renal failure or GI obstruction SE/AE: diarrhea, renal impairment (i.e. mg levels = toxicity) constipation, interactions w/other RX, can change absorption/excretion of other drugs

H2 Agonists

Blocks H+ secretion from parietal cells by binding to receptors; ↓ but do NOT eliminate acid secretion

Mechanism of action  & DE

¦  Blocks acid production by blocking parietal cell secretion

¦  Tx of PUD, GERD, esophogitis, upper GI bleed

¦  Zantac, Pepcid

CONTRAINDICATIONS: very few; minimal CNS effects; h/a, lethargy, depression AE: h/a, NV, diarrhea, confusion

PPI

Mechanism of action & DE:

¦  Binds to the H+/K+ ATPase which is responsible for last step in acid secretion from parietal cells

¦  More effective than H2 agonists in their inhibition of acid secretion

¦  TOTAL inhibition of acid secretion

¦  Prilosec (nexium, protronix, acphex)

CONTRAINDICATIONS: long term use a concern; predispose to GI infx SE/AE: not many!

Sucralfate

Mucosal protective agent, acts locally

Mechanism of action & DE

¦  Binds to surface of ulcers…disassociates into aluminum hydroxide & sulfate anions.

¦  Tx of PUD: sucralfate (carafate)

SE/AE: may affect absorption; causes dry mouth, some constipation/nausea

Antidiarrheals & Laxatives Ch. 50

¦  Adsorbent: AD agent that acts by coating the walls of the GI tract, absorbing the bacteria/toxins i.e. Kaopectate

¦  Anticholinergic: AD agent ↓ tone of muscle in intestine and ↓ peristalsis

¦  Bulk-forming laxatives: adsorb H₂0 into intestine which “ bulk & distends bowel to initiate reflex bowel mvmt i.e. Metamucil

¦  Cathartic: any substance that causes emptying of bowels

¦  Emollient laxative: stool softener/lubricant laxative works by ↓ the surface tension of fluids resulting in more H20 & fat to be absorbed into stool & intestines (lubes fecal material)…i.e. Surfak & Colace

¦  Hyperosmotic laxatives: “ fecal H20 content which results in distention “ peristalsis & evacuation

¦  IBS: periods of bloating/flatulence/diarrhea alternating w/periods of constipation

¦  Laxative: promotes bowel evacuation by “ bulk of feces, softening the stool or lubricating intestine wall

¦  Opiate: narcotic based AD agent that ↓ motility of bowel & reduces assoc pain w/diarrhea..i.e.

o   Opium tincture: Paregoric (onset 1 h, duration 4 hrs) contraindicated w/ETOH, resp depression, barbs, tranqs

o   OTC=, lomotil, OTC = immodium

¦  Saline laxative: a salt w/one or more ions that are poorly absorbed from intestine..the na+ draws into the intestinal lumen

¦  Stimulant laxative: (irritant to intestinal mucosa) agent that stimulates mvmt of intenstine by stimulating nerves that innervate the intestine which “ peristalsis activity in the intestine i.e. Dulcolax (can cause constipation, used for pre-op exams)

Antiemetic & Antinausea Agents Ch. 51

Induce vomiting by activating CTZ center; irritate gastric mucosa

¦  Neuroleptic agent: a drug that prevents nausea/vomiting by blocking dopamine receptors in CTZ & may also block Ach; i.e. Thorazine, Compazine, Phenergan, Reglan

¦  Anticholinergics: work by binding to and blocking ACH receptors on vestibular nuclei (labyrinth)

o   Tx of motion sickness: Scopalamine

¦  Antihistamine: inhibits action of histamine, some prevent nausea via inhibition of vestibular stimulation (H1 & H2 receptors)

o    Tx of motion sickness, n/v, allergies, rhinitis i.e. Meclizine, Antivert (antihistamines w/antichol. behaviors) i.e. Dramamine (low SE), Benedryl (ltd use d/t sedation), Tigan (post op)

¦  Seratonin blockers: block Seratonin receptors located in GI tract, CTZ & VC

o   for tx of n/v severe nature (chemo agents) i.e. Zofran

¦  Prokinetic agents: block dopamine in CTZ tx for delayed gastric emptying, n/v GERD: i.e. Metocoopramide, Reglan, Clopa

Review (from Rick)

§  CNS drugs: dep stim, sedative, hypotic…know the difference

§   

§  Different RX i.e. phenobarbitol, what meds NOT to take with

§   

§  Stimulation of CNS system, indications, why stimulate someone?

§   

§  CNS stimulation, what nursing dx you would have

§  Imbalanced nutrition

§  Ritilin, indicators, responses when child takes it: positive & negative

§   

§  Clinical manifestations of adrenergics & cholinergics, SNS vs. PNS…know the GI fight/flight how it effects pupils and other effects, bronchodilation/constriction

§   

§  Efx in bronchi…rebound efx with one of the types…afrin nose spray

§   

§  B-blockers, know S/A & A/E….what do you do?

§   

§  Complications of certain heart changes, pulse, HR, what does nurse do? Call MD? Prioritize.

§   

§  Atropine…why do you give it?

§   

§  What conditions exist for this drug?

§   

§  Sjojens syndrome…causes changes in the way you salivate: EVOXAC

§   

§  Scopalamine: know

§  ID the B-blocker

§   

§  Synthetic derivative…what does that mean? Does it work as well? Define.

§   

§  GI meds. ID this disorder and tx by this med

§   

§  Tagamet & Cimetodine…some things that a PT could do that are CONTRAINDICATED

§   

§  Laxatives…know different types, stimulants, emollients, how do they work, what do they do?

§   

§  GI raglan, zantac

§  Classifications of antiemetics, Why would you use one vs. the other in the way they are chosen to be used

§  H2 antagonists, etc. ↓ of acid production

§   

§  Define: iatrogenic (disease arising from complication of med or surg intervention) , tiatrogenic, antimicrobial, disinfectant

Analgesics (opioids, nsaids): MCQs for pharmacology review

These questions have been created by the Department of Pharmacology, UMKC School of Medicine. The use I suggest is to review your knowledge of the subject for USMLE or other pharma test. Did you find them useful? Too hard ? Too easy? Use the comment form to comment what did you think of them!

Item Number: 1684 correct answer: 5 category: Analgesics
1. A child has ingested an unknown substance and has evidence of
respiratory depression. This symptom is usually found with poisoning
due to:
1. amphetamines
2. atropine
3. mushrooms
4. kerosene
5. opioids

Item Number: 2534 correct answer: 3 category: Analgesics
2. The use of methadone in the treatment of heroin addiction continues
to be controversial. It would therefore be advantageous to find a substance
with the beneficial effects of methadone, but without its undesirable
characteristics. The correct statement is that:
1. methadone is not physically addicting and therefore very useful in
treating heroin addicts
2. the withdrawal syndrome of methadone is of shorter duration than that of
heroin
3. propoxyphene may successfully suppress the withdrawal syndrome in
heroin-addicted individuals
4. although propoxyphene does block heroin withdrawal, it itself is not
physically addicting
5. propoxyphene may be successfully substituted for heroin in the addicted
individual and abruptly discontinued after three to four weeks without
signs of an abstinence syndrome

Item Number: 2799 correct answer: 3 category: Analgesics
3. Chronic renal damage resulting from the ingestion of analgesics has
been suggested. The FALSE statement is:
1. phenacetin has been implicated
2. salicylates have been implicated
3. meperidine has been implicated
4. acetaminophen is a metabolite of phenacetin
5. combinations may be more harmful

Item Number: 3460 correct answer: 4 category: Analgesics
4. A 20-month old infant is brought to the emergency room with fever,
vomiting, stupor, and hyperpnea of 12 hours’ duration. His leukocyte count
is 6,000/cu mm. The chest roentgenogram is clear. Urinalysis shows albuminuria,
a positive test for reducing substance, and acetonuria. Ferric chloride added
to the boiled acidified urine shows a persistent purple color. The most likely
diagnosis is:
1. acute glomerulonephritis
2. diabetic acidosis
3. acute bacterial meningitis
4. salicylate poisoning
5. phenothiazine poisoning

Item Number: 3870 correct answer: 5 category: Analgesics
5. The gastric mucosa has the important ability to prevent movement of gastric
acid from the stomach lumen into the gastric wall. Some diseases and drug
regiments have been implicated as causes of increased gastric mucosal
permeability to hydrogen ion. Drugs which may increase gastric wall permeability
include:
1. erythromycin
2. indomethacin
3. nitrofurantoin
4. aspirin
5. 2,4

Item Number: 3871 correct answer: 4 category: Analgesics
6. In normal patients, the so-called gastric mucosa barrier protects the
mucosal lining from back diffusion of hydrogen ions and subsequent destruction.
In some patients even small changes in the gastric barrier allows back diffusion
of significant hydrogen ion and subsequent destructive action. Which of the
following pharmacologic agents have been implicated as causes of gastric
barrier breakdown?
1. caffeine
2. ethanol
3. aspirin
4. 2,3
5. All of the above

Item Number: 3907 correct answer: 5 category: Analgesics
7. Patients with normal platelet counts and normal bleeding time may
still bleed severely as a result of aspirin ingestion prior to a dental or
surgical procedure. The aspirin interference with normal platelet function may
last as long as:
1. 4 hours
2. 12 hours
3. 2 days
4. 5 days
5. 7 days

Item Number: 4099 correct answer: 3 category: Analgesics
8. The appropriate antidote in the treatment of pentazocine overdosage is:
1. nalorphine
2. levallorphan
3. naloxone
4. Any of the above
5. None of the above

Item Number: 4587 correct answer: 4 category: Analgesics
9. Acute hemorrhagic gastritis is one of the most frequent causes of severe
upper gastrointestinal bleeding. It is frequently related to recent ingestion of
ethanol and/or aspirin and may be life-threatening. Bleeding secondary to aspirin
is mainly due to:
1. inhibition of gastric prostaglandin synthesis
2. decreased renal excretion of the salicylate with attendant longer half-
life in serum
3. back diffusion of hydrogen ions across the gastric mucosa
4. 1,3
5. None of the above

Item Number: 4639 correct answer: 3 category: Analgesics
10. Many stimuli may cause vomiting. The chemoreceptor trigger zone of the
central nervous system is:
1. located in the cerebral cortex
2. stimulated in all forms of vomiting
3. stimulated by morphine and its congeners
4. All of the above
5. 1,3

Item Number: 5275 correct answer: 1 category: Analgesics
11. A pharmacologic agent which has the potential to cause increased
biliary tree pressure is:
1. morphine
2. warfarin
3. phenytoin
4. acetazolamide
5. carbon tetrachloride

Item Number: 6260 correct answer: 4 category: Analgesics
12. Many commonly utilized medications are subject to abuse. Normally nontoxic
medications, if ingested in excessive amounts, may cause end-organ damage.
Analgesic nephropathy has been associated with:
1. prolonged abuse of phenacetin
2. prolonged abuse of phenacetin-aspirin combinations
3. acetaminophen derived from phenacetin
4. All of the above
5. 1,3

Item Number: 6765 correct answer: 4 category: Analgesics
13. All of the following statements regarding acetaminophen toxicity are
true EXCEPT:
1. acetaminophen is the principal metabolic product of phenacetin
2. an overdose of 10 grams or more may produce hepatic necrosis in adults
3. acetaminophen overdose may produce transient azotemia or renal failure
4. forced diuresis may be a useful form of therapy for acetaminophen overdose
5. liver pathology is centrilobular and midzonal necrosis

Item Number: 9774 correct answer: 1 category: Analgesics
14. Opioid analgesics are sometimes associated with the production of
pulmonary disease. The most common pulmonary complication after oral ingestion is:
1. pulmonary edema
2. interstitial fibrosis
3. pulmonary calcification
4. bronchoconstriction
5. pleural effusion

Item Number: 6707 correct answer: 1 category: Analgesics
15. Characteristically observed in individuals following acute overdose of
opioids.
A. pinpoint pupils
B. depressed respiration
C. coma
D. convulsions
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 6708 correct answer: 2 category: Analgesics
16. TRUE statement concerning the actions of opioids on the secretion of pituitary
hormones.
A. suppress the secretion of luteinizing hormone and thyrotropin
B. reduce the release of prolactin
C. act as a stimulus for ADH secretion
D. inhibit the secretion of ACTH
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 6728 correct answer: 4 category: Analgesics
17. The duration of analgesia is one important characteristic which differentiates
one opioid from another. Which opioid possesses the shortest duration of
analgesia?
1. morphine
2. hydromorphone
3. codeine
4. meperidine
5. methadone

Item Number: 6733 correct answer: 5 category: Analgesics
18. Which of the following possess(es) some antagonist activity at opioid
receptors?
A. naloxone
B. pentazocine
C. butorphanol
D. nalorphine
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 6740 correct answer: 1 category: Analgesics
19. TRUE statements concerning the pharmacologic properties of salicylates
include:
A. high dose aspirin therapy can lower the serum urate concentration
B. aspirin is metabolized by a combination of 1st and zero order
kinetics
C. aspirin exerts its actions primarily by inhibition of
cyclooxygenase
D. aspirin overdose causes significant hepatic toxicity if ingested
in sufficient quantities
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 6754 correct answer: 2 category: Analgesics
20. The opioid expected to have the shortest duration of action following
subcutaneous administration of equianalgesic doses:
1. hydromorphone
2. meperidine
3. methadone
4. morphine
5. codeine

Item Number: 6756 correct answer: 2 category: Analgesics
21. A patient you follow in clinic has a well-known heroin abuse problem. Drugs
which could potentially prevent an abstinence withdrawal syndrome during
hospitalization include:
A. morphine
B. nalbuphine
C. methadone
D. butorphanol
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 6760 correct answer: 1 category: Analgesics
22. TRUE statement concerning the pharmacologic effects of salicylates include:
A. salicylates are thought to exert their activity at least partially
by inhibiting prostaglandin synthetase
B. high-dose salicylate therapy (> 5 grams/day) lowers the serum uric
acid concentration
C. the effect of salicylates upon platelet aggregation is
irreversible unlike that of other nonsteroidal anti-inflammatory
drugs
D. salicylate overdose is potentially fatal; however, prompt
administration of acetylcysteine will avert this danger
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 6990 correct answer: 5 category: Analgesics
23. The analgesic most apt to produce dysphoria:
1. morphine
2. meperidine
3. methadone
4. codeine
5. pentazocine

Item Number: 6998 correct answer: 1 category: Analgesics
24. Morphine’s affects the eye by:
1. producing miosis through an action on the oculomotor nerve
2. producing mydriasis through an action on the sympathetic system
3. decreasing pupillary responses to light
4. directly acting on the smooth muscles of the iris
5. directly acting on extrinsic muscles of the eye

Item Number: 7004 correct answer: 3 category: Analgesics
25. Aspirin is a nonopioid analgesic which is thought to work by inhibiting:
A. prostaglandin reductase
B. prostaglandin synthetase
C. thromboxane synthetase
D. cyclooxygenase
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 7006 correct answer: 3 category: Analgesics
26. Aspirin may be fatal if taken in sufficient quantity. The syndrome of acute
salicylate overdose in children is characterized by:
A. marked hypothermia secondary to an antipyretic effect
B. fever
C. peripheral edema
D. disturbance in acid-base and electrolyte balance
1. A,B,C
2. A,C
3. B,D
4. D only
5. All of the above

Item Number: 11217 correct answer: 3 category: Analgesics
27. Acetaminophen has been used as a safe and effective analgesic/ antipyretic
agent for over 80 years. Since it may be purchase without a prescription, it
is readily available and as such the recommended dose may be exceeded. The
primary toxicity leading to death from an acetaminophen overdose is:
1. papillary necrosis and chronic interstitial nephritis
2. pancytopenia
3. hepatocellular necrosis
4. myocarditis
5. hemolytic anemia

Item Number: 11645 correct answer: 4 category: Analgesics
28. The pharmacologic effects of morphine include all EXCEPT:
1. behavioral changes
2. miosis
3. respiratory depression
4. diarrhea
5. postural hypotension