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69 Cards in this Set
- Front
- Back
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Opiods act on which receptors? |
-mu -kappa -sigma -delta -epsilon |
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Opioid agonist drugs do what? |
-stimulate receptors |
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Opioid antagonists do what? |
-block receptors |
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Which kind of opioid is Morphine Sulfate? |
pure opiod agonist |
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which kind of opioid is Buprenorphine |
-mixed opiod agonist (mu) |
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which kind of opioid is pentazocine butorphanol? |
mixed opiod agonist (kappa) |
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which kind of opioid is naloxone |
-pure opioid antagonist |
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Cell receptor "mu" does what? |
-analgesia -decreases GI motility -respiratory depression -sedation -physical dependence |
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Cell reeptor "kappa" does what? |
-analgesia -decreased GI motility -sedation |
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NSAIDs: prototype? MOA? primary use? adverse effects? |
-motrin -inhibit ccyclooxygenase and prevents formation of prostoglandins -for mild - moderate pain and to reduce inflammation -GI upset, acute renal failure |
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Selective Cox-2 Inhibitors: prototype? MOA? Primary use? Adverse effects? |
-Celecoxib (celebrex) -similar to NSAIDS -releave pain, fever, and inflammation -mild and related to GI system |
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Nursing implications of Nonopiod analgesics |
-monitor clients condition and educate -assess for hypersensitivity and bleeding disorders -assess for gastric ulcers and renal/hepatic disease and pregnany -renal and lab tests |
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Tension HAs |
-most common -muscles of head and neck are tight d/t stress -steady lingering pain -treated with OTC analgesics |
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Migraine HAs |
-throbbing or pulsating -unilateral -may have aura |
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Med classes to treat migraine |
-antiseizure drugs -beta-adrenergic blockers -Ca channel blockers -tricyclic antidepressants |
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Meds to stop migraines in process -MOA? |
-triptans and ergot alkaloids -stimulate serotinin (5-HT) |
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Ergot Alkaloids: MOA? Primary use? Adverse effects? |
-interact with adrenergic, dopaminergic, and serotinin receptors to promote vasoconstriction -terminate ongoing migraines -GI upset, weakness in legs, myalgia numbess and tingling in fingers and toes, angina-like pain tachycardia |
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Functional divisions of nervous system |
-CNS (brain and spinal cord) -PNS (montor and sensory neurons) |
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Autonomic nervous system action: |
-action potential travels along first nerve -encounters first synapse (ganglionic) -ex: nerve travels from preganglionic neuron, reaches ganglionic synapse, then travels to postganglionic neuron |
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preganglionic neuron |
nerve carrying impulse exiting spinal cord |
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postganglionic neuron |
nerve on other side of ganglionic synaps waiting to reveive impulse |
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How do drugs affect the autonomic function? |
altering neurotransmitter activity at the 2nd synapse |
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what can drugs affecting the sutonomic system do? |
-prevent normal destruction or reuptake of neurotransmitter -bind to receptor site on the postsynaptic target tissue |
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Primary neurotransmitter of autonomic nervous system: |
-Norepinephrine (adrenergic) -released by most postganglionic nerves in sympathetic nervous system |
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Adreneric receptors |
receptors at the end of postganglionic sympathetic neurons |
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Autonomic drugs are classified based on what 4 possible actions? |
1. stimulation of the sympatheric nervous system 2. inhibition of the sympatheric nervous system 3. stimulation of the parasympatheric nervous system 4. inhibition of the parasympathetic nervous system |
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Autonomic drugs that stimulate the sympathetic nervous system: |
-adrenergic agents (sypathomimetics) -stimulate "fight or flight" |
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autonomic drugs that inhibit sympathetic nervous system: |
-adrenergic-blocking agents (adrenergic antagonists) -produce actions opposite of "fight or flight" |
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autonomic drugs that stimulate parasympathetic nervous system |
-cholinergic agents (parasympathomimetics) -produce symptoms of "rest, and digest response) |
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autonomic drugs that inhibit parasympathetic nervous system: |
-cholinergic-blocking agents (anticholinergics) -produe actions opposite of cholinergic agents (anti rest and digest) |
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CVA |
impairment of one or more vessels in the cerebral circulation which interupts blood supply and leads to ischemia of brain tissue |
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CVA causes |
-thrombosis -embolus -stenosis -hemorrhage |
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CVA risks: |
-age (>65) -atherosclerotic risk factors -HTN and diabetes -smoking (50% ^) -A-Fib (6 fold risk) |
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Thrombotic stroke |
-most often from atherosclerosis with thrombus formation -inflammatory disease process damage arterial walls (arteritis) |
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conditions causing inadequate cerebral perfusion: can cause: |
-dehydration -Hypotension -prolonged vasoconstriction from malignant HTN -thrombotic CVA |
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TIA |
-preceeds about 80% of thrombotic strokes -temporary -causes changes in vision, speech, motor function, dizziness, or LOC |
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Embolic stroke |
-involves fragments that break from a thrombus formed outside the brain or int he heart, aorta, or common carotid |
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Risk factors for embolic stroke |
-MI -A-fib -valvular disease -endocarditis -hypercoaguability -air or fat emboli |
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Hemorrhagic stroke common causes |
-10% of all CVAs -HTN -ruptured aneurisms -bleeding into tumor -hemorrhage associated with bleeding disorders -anticoagulation -head trauma -illicit drug use |
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Lacuna stroke |
-20% of CVAs -occurs where small perforating arterioles branch off large cerebral vessels in basal ganglia, internal capsule, and brainstem -small arterioles exposed to constant high pressure flow of large arteries leads to thickenen, thrombosed, eventual obstructed small arterios |
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Lacuna strokes symptoms and causes: |
-motor and sensory deficits -smoking, HTN, and diabetes |
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Ischemic stroke treatment: |
-thrombolytic drugs: tissue plasminogen activator (TPA) -restablishes blood flow to brain by disolving clots -should be given within 3 hours |
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Hemorrhagic stroke treatment |
-focuses on stopping or reducing the bleed -neurosurgical consult |
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Secondary prevention of stroke |
-Statins, antiHTNives, antiplatelets, Anticoagulants |
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Antiplatelets used in prevention of another stroke |
-aspirin combined with dipyridamole (aggrenox) -clopidogrel (plavix) -aspirin 81 mg |
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INtracranial Aneurism: |
-most occur near circle of willis -results from: -arteriosclerosis -congenital abnormality -trauma and inflammation -cocaine |
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Intracranial Aneurism is classified by: |
-shape and form 1. Saccular aneurysms (berry) 2. Fusiform aneuryss (giant) |
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Saccular aneurysms |
-result from congenital abnormalities -highest incidence of ruptureing or bleeding 20-50 y/o |
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Fusiform Aneurysms |
-result of diffues arteriosclerotic changes -mostly found terminal portion of internal carotid arteries |
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Clinical manifestations of Intracranial Aneurisms |
-acute subarachnoid hemorrhage, intracerebral hemorrhage, or both -CN III, IV, VI most often affected -surgical management to treat |
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Subarachnoid Hemorrhage: etiology and risks |
-blood escapes from defect or injured vessel into the subarachnoid space -existing intracranial aneurism, existing intracranial arteriovenous malformation -prior head injury -HTN |
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Clinical manifestations of Subarachnoid hemorrhage |
-seizures (25% of time) -leaking vessel: HA, Lowered lOC, N/V, focal neurologic defets -ruptured vessel: sudden, throbbing explosive HA, N/V, visual disturbances, motor deficits, LOC due to ^ ICP, neck stiffness, photophobia, blurred vision, irritability, reslessness, low grade fever |
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Esters |
-Local anesthetic -incidence of allergic reaction is low -ex: benzocaine |
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Amides |
-local anesthetic -longer duration of action and fewer side effects than esters |
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Adverse effects of local anesthetics |
-uncommon -CNS stimulation earlier -CNS depression later -Cardiovascular effects |
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epinephrine |
-agent that can be added to local anesthesia -constricts blood vessels -increases duration of anesthetic |
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sodium hydroxide |
-can be added to local anesthesia -used in areas of infection that may be acidic (from bacteria) |
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General anesthetics |
-block flow of sodium into neurons -delays nerve impulses and reduces neural activity -produces unconsciousness -produces lack of responsiveness to painful stimuli |
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Types of general anesthesia |
-inhalation anesthesia -intravaneous: thipental (pnthonal |
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Inhalation anesthesia: ex's and adverse effects |
-gases: Nitrous oxide, volatile liquids (halothane, enflurane, isoflurane) -N/V, CNS depression, respiratory difficulty, vital sign changes |
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Intravenous General Anesthesia |
-Thipental -barbituate and barbiturate-like agents, opioids, benzos -act within a few seconds -used alone or in combo with inhalation agents: balanced anesthesia |
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Barbituate and barbiturate-like agents |
-can be used with general anesthesia -etomidate -methohexital sodium -propofol |
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Benzodiazepines and anesthesia |
-diazepam, larazapam, midazolam |
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general anesthetic Adverse effects: |
-allergic reactions -dysrhythmia -respiratory depression -CNS depression (shivering, HA) -N/V and vital sign changes POSTOP: hallucinations, confusion, excitability |
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Seizures |
-abnormal or uncontrolled neuronal discharges in the brain -disturbance of electrial activity in the brain that may affect: consciousness, motor activity, sensation |
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paroxysmal episodes |
-sudden, involuntary muscle contractions -alterations in consciousness, behaviour, sensation, and autonomic functioning |
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Seizure episodes may be: |
1. partial (simple or complex) 2. generalized (absence, myoclonic, tonic, clonic, or tonic-clonic) 3. unclassified |
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pathophysiology of seizures |
-internal and external stimulus causes abnormal hypersynchronous discharges in a focal area in the cerebrum -neuropeptides and neurotransmitters released and blood flow is increased -extracellular concentrations change |
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Simple Partial clinical manifestations |
-motor: recurrent involuntary muscle contractions of one body part (face, hand, arm, legs) that may spread to other, same side of body -sensory: auditory or visual hallucinations -psychic: Deja vu, complex hallucinations or illusions, unwarranted anger or fear, sweating |
