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54 Cards in this Set
- Front
- Back
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Name the CNS neurotransmitters
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amino acids (neutral -Glycine and GABA; Acidic- glutamate and aspartate- involved in memory)
Acetylcholine: arousal memory, motor, speech in peripheral nvs system, lack in parkinsons, overabundance in parkinsons Monamines: in peripheri (Dopamine- movement; Norepinephrine- exitatory low level= depression; 5HT Serotonin- inhibitory affects sleep, depression/aggression mood appetite low levels seen in depession Neuropeptides; made in cell bodies function as NT, increas or decrease synthesis release or breakdown of NT, neurohormones, neuromodulators ex= endorphins-suprress pain opoid like |
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define analgesic
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pain reliever without loss of consciousness (opiods and non opiods)
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define Narcotic
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analgesic/cns depressant that could cause phsyical dependance illegal use includes drugs like cocaine, marijuana LSD and opiods
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define opiods
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natural or syntehtic drugs that have similar actions to MORPHINE (MS)
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what does neuropathic mean?
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pain due to injury or damage of nerve fiber
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What is nocioceptic?
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(activation of A or C fibers)
CATEGORIZED BY SPEED OF TRANSMISSION acute pain- fast pain activation of myelinated A delta fibers, travels these fibers in periphery to the spinal cord (sharp, prickling, electrical sensation, a deep boring type of pain) chronic pain- slow pain, long lasting elicited by nonmyelinated delta C fibers transmit impulses to spinal cord - dull burning or throbbing sensation hard to treat CATEGORIZED BY LOCATION Somatic- skeletal muscles, ligaments, joints; better relief with nonopioids; superficial or deep, well localized, constant, aching, throbbing or burning Visceral- organs; poorly localized bc few pain receptors, better relief with opiods; deep boring diffuse |
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What is a local anesthetic?
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causes a loss of pain in a designated area without depressing the CNS.
often includes- epinephrine nonselective blocks impulse conduction by blocking sodium nonspecific affects sensory and motor neurons 2 chemical compositions: -ESTER: low incidenece in allergic reaction, metabolized by enzymes in blood - AMIDE: very low incidence of reaction, metabolized in liver |
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what is a general anesthetic?
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CNS depressant used in production of loss of conciousness, skeletal muscle, and visceral smooth muscle relaxation
inhaled- isoflurane, haloflurane parenteral -propofol thiopental |
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what is balanced anethesia?
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combo of drugs --> anesthesia
combine sedative-hypnotics, antianxiety agents, analgesic, antiemetics, anticholinergics, to eneable use of lesser amount of anetheic with fewer side effects |
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what are opiod analgesics
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from unripe seed of poppy plant
act by occupying the opiod receptors in the CNS, prototype= MORPHINE |
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What are the Opiod receptors?
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Mu
Kappa Delta Sigma |
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What are the effects and opiod peptides for mu receptor for opiods?
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rapid onset; pain blocking glutamate (ACIDIC AMINO ACID)
1)euphoria (exagerated feeling of wellbeing/intense happiness) 2) physical dependence 3) RESPIRATORY DEPRESSION 4) Supraspinal analgesia 5) GI SE 6) PUPIL CONSTRICTION examples include: MORPHINE, Merperdine, methadone, CODEINE, FENTANYL, buprenorphine, naloxone |
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what are the effects and opiod peptides for the kappa receptor for opiods?
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LESS ANALGESIA THAN MU; MORE SEDATION
effects: 1) miosis (constriction of pupil) 2) sedation 3) SPINAL ANALGESIA 4) RESPIRATORY DEPRESSION Examples: MORPHINE, pentazosine, NALOXONE |
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What are the effects and opiod peptides for the Delta receptor for opiods?
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1) DYSPHORIA - restlessness, anxiety, discomfort, unhappiness
2) HALLUCINATIONS 3) Respiratory STIMULATION 4) Vasomotor stimulation ex: enkephalins, ENDORPHINES |
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what are the effects and opioid peptides for the SIGMA receptors for the opioids?`
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1) DYSPHORIA,
2) HALLUCINATIONS 3) RESPIRATORY STIMULATION 4) VASOMOTOR STIMULATION |
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what are the pure opiod agonists?
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MU and KAPPA
-strong narcotic agonists: MORPHINE OXYCODONE FENTANYL HYDROCODONE MEPERIDINE METHADONE all produce: euphoria, respiratory depresison, miosis, constipation, sedation and depression moderate narcotic agonists: CODEINE use: chronic and acute pain managment, antitussives (prevent coughing), |
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what do narcotic antagonists- agonists do?
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stimulate some receptors (kappa) and block others (Mu)
synthetics- same analgesia as Morphine but less abuse and same side effects : buprenorphine (Buprenex); butorphanol (Stadol)—mainly used in L & D, |
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what is the narcotic ANTAGONIST?
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NARCAN = antidote but reverses pain control
#1 opioid antagonist lasts 1 hour |
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what are the side effects from OPIOID MORPHINE?
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respiratory depression,
depresses cough reflex (may cause increase buildup), hypotension Euphoria Drowsiness Mental Confusion Nausea Vommiting Itching (release of histamine) Flushing (release of histamine) miosis constipation biliary colic urinary retention |
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Do natural or synthetic opioids release histamine?
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What are some drugs that are NONOPIODS for pain?
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TRAMODOL- blocks reuptake of norepinephine and serotonin
CLONIDINE: binds to alpha 2 receptors and blocks transmission of pain signals - also used EPIDURALLy for SURGICAL PAIN |
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NSAIDS (nonopioids)
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1) Salicytates (CNS AND PERIPHERY) Aspirin
2) prostaglandin synthetase inhibitors (CNS AND PERIPHERY) (IBUPROFEN)- propionic acids, Acetic acids, Pyrazolone dirivitves, fenamates, oxlcams, alkanones, Cox-2 inhibitors 3) Para-aminophenol derivites (ONLY CNS) |
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what does NSAID mean?
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anti steroidal anti inflammatory drugs
used for: pain, fever, inflammation all NSAIDS: inhibit cyclooxygenase COX enzyme (which syntehsizies prostaglandinase) (you want to block the COX enzyme because they make prostaglaninds which attract white blood cells to repair, to set off inflammation, pain, high temperature, redness and swelling; so if you are in pain and have this mechanism inhibitied-->nsaids decrease this enzyme (COX)that makes this prostaglandin |
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what are the most used drugs in the world?
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NSAIDS
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what are prostaglandins?
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chemical mediators in numerous cell functions
and forms when cell injury occurs cox 1- noninflamed cells- reggulates normal cell activity Cell injury → arachidonic acid released which is metabolized by cyclooxygenase (COX) enzyme → prostaglandins formed → act as pyrogens, activates pain receptors COX 2 in inflamed cells (pain, inflammation) |
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cox 1
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non inflamed cells (physiologic functions)
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cox 2
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inflamed cells (
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what are the effects of prostaglandins?
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activation results in:
pain edema fever vasodilation of inflammation uterine contraction platelet aggregation protect gi by mucous secretion maintains adequate renal profusion by vasodilation of the kidneys uterine contraction protects inner ear |
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Salicylates- aspirin what are the actions?
originally derived from willow bark tree |
inflammation (decreases erthema, edema, hyperalgesia due to release of PG, histamine and and all other cell mediators)
INHIBITS PROSTAGLANDINS SO INFLAMMATION DECREASES DECREASES SENSITIVITY OF PAIN FIBERS INHIBITIONOF CYTOKINES AND PROSTAGLANDIN FORMATION-->fever drops |
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What are the side effects of Aspirin?
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Gi irritation,
tinnitus vertigo (toxic levels) increased bleeding times hypersensitivity use: pain (mild-mod) inflammation (joint extermities), fever prevent platelet aggregation toxicity= mild=surem concentration of 50mg/dl --halmark= tinnitus sever- over 100 mg/dl |
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prostaglandin synthesis inhibitors
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ALL INhibit by binding to Cox which-->prevents prostaglandin synthesis
propinoic acids: COX nonspecific; ibuprofen (advil, nuprin, motrin) Side effects: gastric irritation, nausea, bleeding (prolongs bleeding time but less than ASA), dizzy, H/A, tinnitus Can cause renal toxicity |
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oxicams
prostiglandin synthesis inhibitors |
qd dosing, long half life $$$$$$
pain releif properties like ASA |
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Acetics (prostiglandin synthesis inhibitors)
PSI's |
indomethacin (Indocin); etodolac (Lodine)
Use: short-term acute inflammatory conditions, GOUT More potent than ASA Side effects: GI and CNS, high risk for bone marrow depression (leukopenia, anemias) Long half-life, expensive ketrolac (Toradol); commonly used as opioid alternative; good analgesic properties |
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What class of drugs is under scrutuiny by FDA
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COX 2 inhibitors -reduce pain and inflammation without affecting the stomach lining or causing blood clotting
VIOXX REMOVED FROM MARKET for increased heart attack and stroke |
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Aspirin and NSAIDS do what to the COX receptors?
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COX1block loss of stomach lining--> ulcers; prevents blood clotting
COX2- reduce pain and inflammation |
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what are the para aminophenol derivitives?
TECHNICALLY NOT AN NSAID-- do not decrease inflammation; MAY act on COX 3 which is only found in brain |
ACETOMEPHRIN (tylenol) aka APAP
- no peripheral inflammatory effect (inhibits prostaglanidn effect in CNS only) - weak inhibitor of prostaglandins -good analgesic -good antipyretic - GOOD GI TOLERANCE! (good for people with ulcers) - TOXIC WITH ALCOHOL |
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agents that arent nsaids
ANTI ARTHRITICS |
antiarthritics: Potent antiinflammatory drugs used in the treatment of rheumatoid arthritis (RA).
Also act as immune response modulators by INHIBITING MOVEMENT OF CELLS into an inflamed, damaged area so disease progression is slowed. |
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DMARDS?
for rheumatic arthritis |
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BIOLOGIC RESPONSE MODIFIERS (BRMS)
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What is GOUT?
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acute management of gout
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indomethacin
colchicine: Action: reduces inflammatory response to urate crystals deposited in joints; no analgesic effect Used in acute attack but is extremely toxic; severe GI SE in 80% of patients and causes renal toxicity PO (0.6 to 1.2 mg initially and then 0.6 mg 1 hr later hours till symptoms subside or GI symptoms appear; not to exceed 1.8 mg in 1 hr) and IV |
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what is epilepsy?
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chronic, reoccurent seizures
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what is a seizure?
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antielipeptics
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AEDS?
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antielipidemics
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what are the main categories for antilipidemics?
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what are benzodiazepines
(EPAMS) |
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SUCCINIMIDES
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raise seizure threshold;
used in absence seizures almost exclusively; decrease calcium influx ethosuximide (Zarontin) |
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broad spectrum;
inhibits sodium channels of hyperactive neurons; old drug; SE = CNS, facial hypertrophy (“Dilantin facies”), gingival hyperplasia; measles-like rash; osteoporosis; CV collapse if rapid IV infusion; mainly generalized seizures Can be teratrogenic |
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(enhance effects of GABA by binding to GABA receptors)-phenobarbital
old (since 1912); cheap; used in partial seizures, generalized seizures, status epilepticus CNS SE (sedation) mainly teratrogenic |
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other seizure drugs
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GABAPENTIN (Neurontin);
structurally similar to GABA also used in neuropathic pain management CNS SE expensive |
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the second most perscribed antiseizure drug
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CARBAMAZIPINE (Tegretol);
suppresses neuronal discharges around seizure foci; decreases sodium influx broad spectrum (not absence) CNS (see tolerance) and bone marrow suppression TERATROGENIC (neural tube defects) #2 most frequently prescribed antiseizure drug |
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valproic acid (Depakote)
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suppresses influx of calcium and sodium;
increases availability of GABA labeled for absence seizures but used in all rare to see SE Also TERATROGENIC Monitor liver enzymes-esp in kids |
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New antisezure drugs
have lesser risk to fetus have interactoins with other drugs better dosing schedule |
vigabatrin (newest acts by inhibiting breakdown of GABA)
oxcarbazepine (a derivative of carbamazepine) lamotrigine (Lamictal)-blocks sodium channels pregabalin (Lyrica)-a GABA analog topiramate (Topamax)-potentiates GABA and blocks sodium and calcium channels Tiagabine (Gabitril Filmtabs)-blocks reuptake of GABA |
