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p.cology exam 2
pharmacology exam 2
| Question | Answer |
|---|---|
| inventor & revelar of anasthetic inhalation | William Morton |
| General Anesthesia requirements | hypnosis, analgesia, amnesia, muscle relaxation, homeostasis |
| stages of anesthesia | 1. analgesia, 2. excitement/delirium, 3. surgical anesthesia, 4. medullary depression |
| what stage do we want to get to quickly | surgical anesthesia--> regular respiration is gained |
| all inhaled anesthetics are complete anesthetics except | nitrous oxide |
| names of inhaled anesthetics | NO, Halothane, Enflurane, Methoxyflurane, Isoflurane, Desflurane, Sevoflurane |
| characteristic of general anethesia | slightly water soluble, very oil soluble |
| 1st inhaled anesthetics | diethyl ether & chloroform |
| MAC | minimum Alveolar concentration prevents purposeful mvmt in 50% of pts in response to painful stimuli |
| goal MAC | 1.2-1.3 |
| what drugs reduce MAC of inhaled anesthetics | narcotics, sedatives, alpha 2 antagonists, local anesthetics |
| more soluble inhaled anesthetics = | high blood gas partition coefficient--slower onset due to large Vd in blood--we want more lipophilic drugs |
| concentration of inspired air | increased concentration will increase speed of onset |
| volume of pulmonary ventilation | increased pulm ventilation rate will increase onset & speed of offset |
| inhaled anesthetics are eliminated mainly via... | exhalation |
| what inhaled anesthetic is 20% metabolized | halothane |
| which inchaled anesthetic is not metabolized at all | NO |
| if an inhaled anesthetic is more lipophilic... | has higher oil: water partition coefficient & is there form more potent |
| MOA of inhaled anesthetics | stabilize the membrane of cells & inhibit ion fluxes |
| what is the most potent/ most lipophilic inhaled anesthetic | Methoxyflurane |
| what inhaled anesthetics decrease MAP in direct proportion to their alveolar conc | reduce CO= halothane & enflurane reduce TPR = isoflurane, desflurane, & sevoflurane |
| inhaled anesthetics cause HR changes by... | altering rate of SA node depolarization or by shifting autonomic balance (more para=decrease HR) |
| which inhaled anesthetics cause tachycardia | desflurane & isoflurane |
| all inhaled anesthetics do what to right atrial pressure? | increase R atrial pressure via depression of myocardial function--halothane = greatest increase |
| respiratory effects of inhaled analgesics | all except NO decrease tidal vol. & increase respiratory rate = overall decrease in minute ventilation |
| @ ____ MAC is there no response to hypoxia | 1.1 MAC |
| brain effects of inhaled anesthetics | increase cerebral blood flow & cranial pressure |
| how can you minimize increased cerebral blood flow & intracranial pressure caused by inhaled anesthetics | hyperventilate patient |
| which inhaled anesthetic is associated w/ seizure-like EEG & myoclonic activity | Enflurane |
| inhaled anesthetic that cause nephrotoxicity & why | Methoxyflurane, Enflurane, Sevoflurane, Isoflurane--form flouride ions |
| what causes malignant hyperthermia | increase in free calcium concentration in muscle cells |
| treatment for malignant hyperthermia | Dantrolene--reduces free Ca release from SR, reduce body temp, & restore acid-base balance |
| Generalized anesthetics- Barbiturates | loss of consiusness--no analgesia or muscle relaxation |
| generalized anesthetics- BZDs | pre-op drugs to lessen anxiety sedative, reduces anxiety, amnestic NO analgesia!!! |
| what drug can be used to accelerate recovery from BZDs | Flumazeril |
| opioid analgesics as general anesthetics | morphine, fentanyl, sufentanil--mu opioid R AGONISTS--potent analgesics, no muscle relax or amnesia |
| main AE of opioid analgesics | respiratory depression |
| Propofol | GABAa agonist, inhibits M1 Rs rapid unconsciouness--no analgesia, not amnestitic |
| AE of Propofol | reduces bp by vascular resis, respiratory depression, reduces cerebral blood flow, metab rate, intracranial pressure |
| Etomidate | faciliates GABAnergic neurotransmission by increasing the # of available GABA Rs--rapid unconsciousness |
| AE Etomidate | myoclonic activity (no EEG effect), post-op nausea, adrenal steroidgenesis inhibition if prolonged sedation |
| Ketamine | not general anesthetic--produces dissociative anesthesia via NMDA ANTAGONISM |
| AE Ketamine | stim symp nervous system (inc HR, MAP, CO), increase cerebral blood flow & intracranial press, dec RR |
| Local Anesthetics MOA | block impulse conduction along nerve axons via motor & sensory fibers |
| 1st LA | Cocaine |
| LA structure | lipophilic group (aromatic ring) linked by alkyl chain (ester or amide) to a hydrophilic domain (tertiary amine) |
| pka of most LA is _____? this means they are _____ @ physiologic pH | pka= 8-9 so they are charged @ phys pH |
| cationic vs uncharged form | cationic is most active @ R site but cant penetrate mem---uncharged penetrates mem rapidly so allows entry into cell mem where Rs are |
| ester links are more prone to... | hydrolysis via esterases in plasma, so have a shorter DOA |
| amides are degraded via.. | microsomes in liver |
| when esters are degraded by esterases they produce? | PABA which causes allergies |
| common ester LA | procaine= most potent, short DOA Benzocaine=topical use only |
| common amide LA | Lidocaine & Bupivicaine |
| onset of LA is determined by | DOA & toxicity |
| if LA if inj into more vascular area... | absorbed faster & shorter DOA |
| what class can be used to reduce systemic absorption of LAs & prolong DOA | Vasoconstrictors (alpha 1 agonists)--epinephrine |
| CSF has no.... | esterases, so intrathecial inj of ester LA persists until drug is absorbed into bloodstream |
| LAs preferentially bind what type of channels | activated or inactivated Na channels b/c more mem + (occurs during depolarization)--mem is rapidly firing AP |
| LAs preferentially block what types of fibers | myelinated, small fibers (must block 3+ node section) |
| effects of LA on nerves | threshold is increased/ slower depolarization to peak/ peak actually gets lower/ no longer able to fire AP |
| surface anesthesia | mucous mem, cornea, skin |
| infiltration anesthesia | inj of LA into tissue w/out regard for location of nerve tracts |
| nerve block | inj of LA into or adjacent to peripheral nerves/plexuses to block entire area distal to inj (do consider where nerves are) |
| Spinal (intrathecal) anesthesia | inj LA into CSF (subdural space) to anesthetize a large fraction of body |
| epidural anesthesia | inj LA into epidural space (above dural space) before hit meninges--LA can be absorbed into bloodstream from here |
| wet tap | accidentally puncture dura instead of space right above dura--causes bad headaches |
| spinal nerve block | inject LA into sub-arachnoid space, above surface of spinal cord |
| CV toxicity of LA | slow conduction in atria & ventricles, reduce excitability of cardiac muscle, depress strength of contraction, cause arteriolar dilation |
| spasticity | certain muscles are continuously contracted causing: stiffness/tightness that may interfer w/ mvmt, speech, & walking |
| symptoms of spasticity | hypertonicity, muscle weakness, exaggerated deep tendon reflexes, muscle spasms, scissoring, fixed joings |
| parallel pathway | motor cortex OR brain stem --> Spinal Cord --> Muscle |
| Hierarchial pathway | motor cortex-->brain stem--> SC--> skeletal muscle |
| where are sensory receptors found | in skeletal muscle responding to motor neurons, tendons, joints, skin of body assoc w/ mvmt of muscle |
| what do sensory Rs do | monitor length & tension of muscles, mvmt of joints, effects of mvmt on overlying skin |
| Extrafusal fibers | form bulk muscle, generate force & movement to allow for contraction & relaxation |
| intrafusal fibers | in muscle spindle--communicate info about how much muscle is relaxing/contracting |
| nuclear chain fibers | innervated by type II neurons--transmit info about length |
| nuclear bag fibers | innervated by type Ia neurons--transmit info about length & velocity |
| efferent fibers | take motor info out via ventral horn of SC |
| afferent fibers | bring in sensory info via dorsal horn |
| where are alpha motor neurons located | in ventral horn of SC |
| stretch reflex arc | sensory neuron of muscle-->type 1a afferent fibers-->alpha motor neuron in SC--> efferent fibers-->muscle |
| spasticity is due to... | overactivation of alpha motor neuron via type 1a afferents that innervate nuclear bags |
| goal for spasmolytics | decrease activation of alpha motor neuron by: reduce activity of Ia afferents, reduce excitation of motor neurons by enhancing IPSPs via inhibitory interneurons |
| Diazepam (spasmolytic) | binds GABAa R on alpha neuron increasing freq of channel opening to increase amplitude of IPSP--produces sedation @ doses required to reduce muscle tone |
| Baclofen MOA (spasmolytic) | GABAb R AGONIST--opens K+ channels letting K+ out causing IPSP--also causes hyperpolarization to decrease Ca release to decrease NT release (Glutamate in this case) |
| GABAb Rs are... | metabotropic Rs |
| Glutamate interneurons originate from? | corticospinal (parallel)pathway--glutamate is an excitatory NT |
| main AE of Baclofen | increased seizure activity in epileptic patients |
| Tizanidine MOA (spasmolytic) | alpha 2 R AGONIST--reinforces pre & post-synaptic inhibition in SC & inhibits nociceptive transmission in dorsal horn |
| Dantrolene (spasmolytic) | blocks Ryanodine Rs in SR preventing Ca release so skeletal muscle cant contract |
| AE of Dantrolene | muscle weakness, sedation, hepatitis |
| Carisoprodol & Cyclobenzaprine (spasmolytic) | centrally acting skeletal muscle relaxant that acts in brain stem--helps w/ pain 2ndary to localized muscle spasm--used for acute spasms |
| Carisprodol metabolite | meprobamate--causes AE of drug abuse, dependence/withdrawl |
| Parkinson's Disease | no cure--combo of rigidity, bradykinesia, resting tremors, postural instability |
| what is main NT assoc w/ PD | Dopamine |
| death of what pathway results in PD | nigrostriatal pathway (motor control) |
| pathophysiology of PD | DA input into striatum is lost--syx dont appear until 50-60% lost & DA in striatum is reduced 70-80% |
| retrograde degeneration | terminals degrade first, then cell bodies degrage--occurs in PD |
| drugs that cause PD | Dopamine R antagonists (neuroleptics) & MPTP |
| PD treatment strategy | supplement DA or use DA agonists |
| normal action of DA | normally inhibits GABA neuron causing an EPSP (remember: Ach neuron is also exciting GABA to produce IPSP) |
| what happens in PD... | lose DA block on GABA, causing it to only be excited by Ach to produce IPSP |
| Levodopa | DA supplement--delayed absorption if taken on full stomach--enters blood as L-dopa which can cross BBB to be turned into DA if isnt degraded in periph fist |
| what turns L-dopa into DA | dopa-decarboxylase--located in brain and periphery (b/c we need to make NE) |
| Sinemet | Levodopa + Carbidopa (dopa decarboxylase inhibitor) blocks peripheral conversion of Levodopa allowing 10% to enter brain |
| AE of L-dopa | anxiety, agitation, insomnia, hallucinations, delusions, schizophrenia like SE, dyskinesias, ortho hypo, arrhythmias, N/V |
| long term "wearing off" | loss of dopa decarboxylase over time due to terminals degenerating typically after 3-5yrs--predictable fluctuations in motor fxn |
| how do we combat wearing off | reduce fluctuations in L-dopa by increasing freq of dosing |
| on-off phenomenon | represents end stage of L-dopa therapy--unpredicatble fluctuations in motor fxn |
| to decrease on-off phenomenon... | delay L-dopa therapy by using MAO & COMT inhibitors to increase DA levels by preventing degredation |
| as PD progresses, what happens to therapeutic window | it gets smaller so pts experience dyskinesia b/c too high OR akinesia b/c too low |
| Entacapone | peripheral COMT# that crosses BBB (used in PD)--allows more L-dopa to get into brain & doubles half-life if used w/ carbidopa--also limits L-dopa fluctuations |
| Stalevo | levodopa + carbidopa + entacapone |
| Selegiline & Rasagiline | MAO#s mainly block MAOb (DA metabolism)--both irreversibly bind MAOb to inhibit intracell degradation of DA |
| cheese effect | seen w/ MAO#s--causes hypertensive crisis in foods w/ tyramine b/c it releases monoamines in periphery & if MAO is blocked it cant get broken down causing increased NE |
| MAOa vs MAOb | MAOa= degrades NE & 5-HT MAOb= degrades DA |
| Pramipexole & Ropinirole | DA R AGONISTS--D2 & D3 pramipexole=excreted unchanged in urine ropinirole=metabolized by CYP1A2 |
| Benztropine & Trihexyphenidyl | Muscarinic R ANTAGONISTS--inhibit Ach from exciting GABA decreasing IPSPs--improve tremor NOT bradykinesia |
| Amantadine | antiviral agent used in PD that may influence synthesis, release or reuptake of DA |
| Huntington's Disease | autosomal dominant disorder--chromosome 4 (to many CAG repeats)--characterized by chorea dance |
| what happens in Huntington's Disease | degeneration of neurons in striatum (mvmt) & cortex (memory, thought) |
| what drugs often alleviate chorea | those that impair DA neurotransmission |
| Reserpine & Tetrabenazine | deplete DA & other monoamines by preventing intraneuronal storage via # DMAT--only treats symptoms not progression |
| main AE of Reserpine & Tetrabenazine | depression/suicidal thoughts |
| drug used to tx restless leg syndrome | ropinirole |
| risk of AD increases w/ | age |
| early onset AD | symptoms appear before age 60, progress rapidly |
| late onset Ad | occurs in those over 60, most common form |
| what happens in AD | loss of cholinergic neurons in striatum & nucleus basalis--cortex shrivles up (conversion of short to long term mem & mem storage)--ventricles grow larger |
| what part of brain is susceptible to degeneration in AD | basal forebrain (learning & memory) |
| what protein is present in neurons that organizes micro tubules & transports nutrients | TAU |
| TAU in AD | problem w/ TAU allows neurofibrillary tangles to form causing decrease in transport of nutrients (glucose) causing neuron death |
| plaques in AD | made of B amyloid protein that builds up interrupting communication btwn neurons or targets them for immune cell attack |
| Donepezil | Anticholinesterase- treat mild to mod AD--inhibits Ach esteraases allowing Ach to stay in synapse longer & have more of an effect (IPSP) |
| main NT assoc w/ AD | Acetylcholine |
| Memantine | NMDA antagonist (weak nicotinic antagonist)--blocks pathological activation of NMDA s to decrease noise allowing brain to see signal--tx of mod to severe AD |
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heljmaso
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