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MSC CNS Pharm Test
187 test #3 3/24/10
| Question | Answer |
|---|---|
| What is the nervous sys responsible for | controlling functions of the human body, it analyzed incoming stimuli and intergrated internal and external responses |
| What makes up the CNS | brain and spinal cord |
| what makes up the PNS (peripheral nervous system) | sensory receptors and motor nerves |
| what does PSNS stand for | parasympathetic nervous system |
| what is the soma | body of the nerve cell |
| what is the dendrite | branches that bring info into neuron |
| what is the axon | elongated process from nerve to effector cells or to another nerve |
| what are afferent fibers | fibers that run from peripherial receptors to the CNS (in box) |
| what are efferent fibers | fibers that carry nervel impulses away form CNS to the periphery to stimulate action (out box) |
| what is action potential | messages that nerves send |
| what does the stimulation of a nerve cause | depolarization |
| what has to happen for depolarization to occur | Na rushes into cell, K leaves cell, cell now + charged |
| what is repolarization | return to the resting, Na leaves cell and K enters cell, cell now - charged |
| nerves need energy and the correct balance of electrolytes to maintain action potentials | electrolyte imbalance affects the ability of nerve cells to function properly |
| What so you need to assess if pt is confused | resp sys/O2 satCV sys/perfusionslucose levelelectrolyte labsmeds |
| where are schwann cels provided | in myelinated periphery nerve cells |
| what does the myelin sheath do | speeds electical conduction and protects nerves from fatigue |
| what happens at ther nerve synapse that is at the end of an axon | the electrical action stops |
| what is secreted across axon to continue impulse | neurotransmitter |
| neurotransmitters are receptor specific | neurotransmitters eithe excit of inhibit postsynaptic celss |
| what had to happen to a neurotransmitter so that the nerve cell can return to its resting state | it has to me inactivated by either reabsorbtion (reuptake) or broken down by enzymes |
| what is acetycholine | it communicates between nerves and muscles, works in ANS, PSNS, and found in brain pathways |
| what is norepinphrine and epinephrine | carecholamines released by nerves in the sympatheic branch of ANS, released from adrenal medulla |
| what is dopamine | involved in coordination of impulses and respons (motor and intellectual) |
| what does the vertebrae and the mennges provide for the CNS | protection |
| what does the blood brain barrier (BBB) do | keeps toxins, proteins, and other large structures out of brain protecting neurons |
| Protein bound drugs cannot reach the brain | Mannitol can be used to temorarily disrupt BBB, some drugs can be piggybacked into brain |
| what does the brain need to function properly | O2 and glucose from blood and CO2 has to be removed |
| glucose is not stored in the nerves has to be in constant supply | the carotids and vertebral deliver blood to the circle of willis, of carotids become occluded blood supply to brain can still be provided by the circle of willis |
| what is the hindbrain | pons and medulla, primitive, controls resp and cardiac, also controls vomiting and swallowing reflex, |
| what is the midbrain | higher brain stem, thalamus, hypothalamus and limbic |
| where does learning and communication take place | forebrain |
| how many pairs of nerves are in the spinal cord | 31 |
| what type of movement is the pyramidial sys responsible for coordinating | voluntary |
| what type of movementis the extrapyramidial sys responsible for | involuntary |
| what are symptoms of drugs interfering with the extrapyramidial system (EPS) | involuntary movementstremorsrigiditybody restlessnessmuscle contractionschanges in breathing and HR |
| what are the functions of the right side of the brain | artistic, forms and shapes |
| what are the functions of the left side of the brain | analytical, names, numbers, processes |
| when learning takes place there is an actual membrane change what is it called | an engram |
| what is needed for an engram to become part of permanent memory | O2, glucose, sleep |
| the release of extra ADH due to stress can increase learning, too much though can impair learning | oxytocin during childbirth can increase memoryemotions can enhance memory. |
| anxiolytic angents do what | alter pt response to the environment (reduced tension/anxiety) |
| sedative agents do what | make pt unaware of their environment (clams pt) |
| hypnotic agents do what | cause sleep |
| what are the 6 types of anxeity | 1. OCD2. PTSD3. GAD (generalized anxiety disorder)4. panic disorder5. social phobias6. simple phobia |
| what is OCD | obsessive compulsive disorder, repetive behviors that are compulsive |
| what is PTSD | stress after and event |
| what is GAD | generalized anxiety disorder, non specific cause |
| what is panic disorder | extreme anxiety that occurs suddenly with physiologic manifestations |
| what is social phobias | fear in social situation |
| what is simple phobia | fear of a particular thing |
| what can cause anxiety | illness, stress form a specific event |
| when should anxiety be treated with meds | when it interfers with normal function |
| what are symptoms of an anxiety attack | sweating, rapid breathing, tense muscles, fast HR, elevated BP, decreased concentration |
| anxiety is a feeling of what | tension, nervousness, apprehension, or fear that involves unpleasant reactions to a known or unknown stimulus |
| what is sedation characterized by | loss of awarenss and reaction to environmental stimuli |
| what is an important consideration for pts with anxiolytic and hyponotic agents | SAFETY |
| what does hypnotics work on | the RAS (reticular activating system which blocks the brain from being stimulated |
| the reticular formation (RAS) is a loosley arranged network of neurons that are distributed throughout the brainstem where ever there are no specific neurajl tracts or nuclei | hypnotics interfere with the RAS by preventing incomig stimuli which inhibits arousal |
| what are benzodiazepines | the most freq used class, does not have as many probs with sedation, are less adicitives |
| what is the theraputic action of benzodiazepines | work in the limbic sys and the RAS to make GABA (inhibitory transmitter), cause inhibition of neural arousal, at low dose is anxiolytic high doses causes sedation and hypnosis |
| what are the theraputic indications of benzodiazepines | various forms of anxiety, ETOH w/drawal, hyperexcitability, agitation, preoperative anxiety, balanced anesthesia |
| what are the pharmacokinetics of benzodiazepines | well absorbed in GI tract, peak in 30 minutes, lipid soluable, well distributed, metabolized in the liver (smaller doses w/ liver ds) |
| benzos may casue children to be aggressive, cry, and be irritable, monitor for CNS depression | adults may receive benzos for insomnia and should only be used short term, monitor liver function |
| older adults may be more susceptible to AE monitor for toxicity | benzos end with pam |
| what are the C/I for benzos | allergy, hx of psychosis, glaucoma, shock, coma, acute ETOH intoxication, PG/lactation, caution with kids, elderly and debilitated, renal/hepatic pts, african amer pop needs lower doses |
| what are the AE of benzos | sedation, drowsiness, depression, lethargy, blurred vision, HA, apathy, light headedness, confus, dry mouth,n/v/c, elevated liver enzymes, hypotension, HTN, heart rhyt changes, palpitations, resp dif, uriniary retent, sex dys do not stop abruptly. |
| drug interactions for benzos | do not mix with ETOH or other CNS depressants, effects may increase with oral contrceptives, effects my decrease with theophylines or ranitidine |
| what is the benzo prototype | diaxepam (valium) |
| what is the antidote for benzos | flumazenil |
| what are babiturates | class of drug with significant sedation adn addiction problems |
| what is the therapeutic action of barbiturates | depresses CNS: slow neuronal impulse conduction, depresses cerebral cortex and cerebral function and motor output resulting in sedation, hypnosis, anesthesia and coma. |
| what are the therapeutic indications for barbiturates | anxeity, sedation, insomnia, pre-anesthesia, and seizures |
| what are the pharmacokinetics of barbiturates | absorbed well reaching peak in20-60 min duration of 4-16 hrs, metabolized in the liver and excreted in urine. It is lipid soluable so elderly with less muscle and more fat will continue to have effects after it is dc's |
| what are the C/I for barbiturates | allergy, hx of addiction, significant kidney or liver impairment, cardiac and resp distress/dysfunction, PG/lactating |
| what are the AE of barbiturates | drowsiness, somnolence, lethargy, ataxia, vertigo, hangover, abn thought process, paradoxical excitment, anxiety, hallucinations, bradycardia, hypotension, syncope, Stevens Johnson syndrome |
| what is stevens johnson syndrome | a severe inflammatory eruption of the skin and mucous membrane usually occuring in children and young adults following resp infection or as an allergic reaction to drugs or other substances, there is skin necrosis/sloughiwng, can result in death |
| what drugs have interactions with barbiturates | other CNS depressants, phenytoin(dilantin), MAOI, drugs affected by liver enzyme induction systems |
| what is the prototype for barbiturates | phenobarbital |
| name 2 other anxiolytic/hypnotic agents | zolpidem (ambien) and buspirone (BuSpar) |
| what is the most prevalent neurologic disorder | epilepsy |
| what is epilepsy | a collection of different syndromes all characterized by the same manifestation of sudden discharge of excessive electrical discharge from nerve cells w/in the brain, occurs randomly and ia a chronic, recurrent patter of seizures |
| what is primary epilepsy | epilepsy that has no identifiable cause is determined |
| what is secondary epilepsy | epilepsy that results from trauma, infection, CVA, or illness |
| epilepsy is a state of hyper-excitability of the neurons, these disturbances can occur in a single region of the brain (partial seizure) or affect the entire brain (generalized seizure) | seizures can result in a loss of bodily functions such as movement, sensation, and consciousness |
| what are generalized seizures | seizure that begin in one area of the brainand rapidly spread through both hemispheres, usuall involves loss of consciousness |
| what are the 3 types of generalized seizure | tonic-clonic (grand mal seizures)atonic seizures (drop attacks)absence seizures (petit mal seizures) |
| name the 3 type of epileptic syndromes | myoclonic seizures (muscle jerks)febrile seizuresstatus epilepticus (life threatening) |
| what is a partial seizure | involves one are of the brain and does not spread thorughout the brain (also called focal) |
| what are the 2 types of partial seizures | simple partial seizure: single muscle movement or sensory alteration.complex parital seizures: complex sensory changes and motor changes |
| what is a seizure | a brief episode of abn electrical activity in the nerve cells of the brain |
| what is a convulsion | spasmodic contractions of voluntary muscles (convulsions are not always present with a seizure) |
| what is status epilepticus | starts out as a partial of generalized seizures and then develop into a pattern of no recovery between attacks, is life threatening, treated with barbiturates and benzodiazepines. |
| make sure you observe pt suring seizure and make note of what happens during the seizure | drugs are very specific to the type of seiuzure |
| what are anticonvulsants | drugs that are used to manage all types of epilepsy and not just convulsions. |
| the goal of antiepileptic drug therapy is to control or prevent seizures while maintaining quality of life | Anitepileptic drugs must be tried one at a time to see it which ones and in what does provides control. |
| antiepiletic drug doses are titrated up until a theraputic dose is found, drugs have to be weaned off, cannot stop abruptly. | another goal of anitepileptic drug therapy is to help protect the normal cells surrounding the seizure activity |
| there can be an influx of Ca coming into cells during a seizure which can cause destruction of brain tissue, what is the rescue drug given to help preserve brain tissue from damage | Ca channel blocker |
| multiple drugs are used to treat tonic-clonic seizures: hyda toins, barbituratesm and benzodiaepines, these drugs stabilze nerve membrane by blocking channels or altering receptor sites | teh RAS (reticular activating system) is the attention center of the brain, this center is depressed with antiepileptic drugs |
| hydotoin and phenytoin like drugs are generally effective in partial and generalized seizures by stabalizing nerve membranes and limiting the spread of excitabliity fr the initiating focus | hydantoins are less sedating, there is liver toxicity, these drugs end in toin. |
| barbirurates work as a general CNS suppressant, it inhibits impulse conduction in the ascending RAS, depressing the cerebral cortex, alters cerebellar function, depresses motor output and can produce excitation sedation hypnosis anesthesia and deep coma | phenobarbital is a barbiturate agent |
| Benzodiazapines potentiate teh effects of GABA which is an inhibitory neurotransmitter to stabalize teh nerve membrane, work in limbic sys and RAS, can cause muscle relax, and relieve anxiety. | Diazepam (valium) and Clonazepam (Klonopin) are benzodiazapine agents |
| what are the therapeutic actions of benzodiazapines and barbiturates | stabalize nerve membrane to decrease excitablilty and hyperexcitability |
| what are the therapeutic indicatoins of benzodiazapines and barbiturates | indicated for tonic-clonic seizures, status epilepricus and prevention of seizures as well as for adjunct therapy for muscle relaxation |
| what are the C/I for benzodiazapines and barbiturates | allergy, PG, elderly, debilitated pt, renal/liver dysfunction |
| waht are the adverse effects of cns depression | depression, confusion, drowsy, lethargy, fatigue, dry mouth, cardiac dysrhythmias, BP changes, urinary retention, loss of libido, anorexia, constipation |
| what are the adverse effects of hydatoins | liver toxicity, bone marrow suppression, gingival hyperplasis, dermatoligical reasctions, ataxia |
| what are the adverse effects of barbiturates and benzodiazapines | physical dependence and w/drawal symptoms, can develop a tolerance over time |
| what does benzodiazapines and barbiturates interact with | other cns depressants, primrose, ginko |
| what is the hydatonin prototype | dilantin |
| what is the prototype for barbiturates | phenobarbital |
| what is the prototype for benozodiazapines | diazepam (valium) |
| what type class of drug is used most often to treat petit mal seizures | succinimides (they supress the abnormal electrical activity that occurs with petit mal seizures) |
| what are the adverse effects of succinimides | cns effects, blood dycrasias, stevens-johnson syndrome |
| what is the prototype for succinimides | ethosuximide (zarontin) |
| what is the prototype drug to treat partial seizures | tegertol (carbamazipine) |
| what is gabapentin (neurontin) given for | partial seizures and neuropathic pain |
| give antiepileptic drugs at the same time each day | with antiepileptic drugs you need to monitor CBC, renal/hepatic effects (liver labs, ALT, AST), monitor drug levels for toxicity |
| what adverse effects do you need to monitor pt on antiepileptic drugs for | CNS changes, GI, GU, cardiac, bone marrow suppression, severe dermatological reactions) |
| what is parkinson's ds | a chronic and progressive degenerative disorder of dopaminergic neurons |
| what is the primary cause of parkinson's ds | an imbalance of 2 neurotransmitters: dopamine and acetylcholine |
| what type of neurotransmitter is dopamine | it is an inhibitory neurotransmitter in regards to muscle movement |
| what type of neurotransmitter is acetylcholine | it is excitatory in regard to muscle movement |
| what is parkinson's ds characterized by | movement disorders and pathological changes in the extrapyramidal system (EPS) which controls involuntary or inconscious movements |
| where are the substantia nigra and corpus striatum located | midbrain, they help regulate aned coordinate movements |
| what does dopamine do | influences the initiation, modulation, and completion of movement and regulates unconscious autonomic movements |
| what does the lack of dopamine result in | retarded transmission of neuronal impulses between the subtantia nigra and teh corpus striatum resulting in a chemical imblance that manifests itself as a movement disorder |
| what does a lack of dopamine or increased levels of acetylcholine result in | parkinson's like symptoms |
| In parkinson's ds there is a decreased # of dopaminergic neurons in the substantia nigra | due to the decline of dopamine the is an increase in the # of acetylcholine and it becomes domninant in the corpus striatim which controls involuntary movement, balance, posture, and muscle tone |
| retraded transmission of dopamine results in the inability to regulate and coordinate mivement | Parkinson's ds usually manifests itself between teh ages 45 and 65 |
| what are the 2 forms of parkinson's ds | idiopathic and parkinsonism |
| what is idiopathic parkinson's ds | it has an unknown cause, could be from trauma, virus, infection, atherosclerosis, drugs, or environmental factors |
| what is parkinsonism parkinson's ds | resutls from pathological events such as encephalitis or from the effects of drug therapy |
| when do parkinson's ds symptoms begin to occur | when 80% of the dopamine has been depleted |
| what are the symptoms of parkinson's ds | mask like face, tremor, shuffling, drooling, muscle rigidity/extreme slowness, difficulty w/ intentional movements, postural instability, pill rolling of hands/head shaking, depression, dementia in 10% of pts |
| what 4 drug classes are used to treat parkinson's ds | dopaminergics, anticholinergics, MAO-B Inhibitors, COMT inhibitors |
| what do dopaminerigics do (drug = levadopa) | convert levadopa to dopamine increasing the amount available |
| what do anticholinergics do (drug = bezotropine) | block cholinergic receptors and reduce the amount of acetylchoine |
| what do MAO-B inhibitors do (drug = selegiline) | inhibit monoamine oxidase-B which breaks doen dopamine which spares destruction of dopamine (neuroprotective and slow downs ds progression) |
| what do COMT inhibitors do (drug = entacapone or tolcapone) | inhibit COMT enzyme that inactivates dopamine making more avaiable |
| what are the 2 available COMT inhibitor agents | tolcapone and entacopone |
| which of the 2 COMT inhibitors is hard on the liver so it is reserved for later stages or PD | tolcapone |
| what is pain | whatever the pt says it is existing when adn where the pt says it does.Pain is subjective |
| Pain caused discomfort, disturbs sleep and may interfere with normal everdayday activities | Pain can be a warning sine of a disease process or impending danger |
| what are some objective signs that we can look for in regards to pain | contorted facial expression, changes is posture, increased VS, sweating, restlessness, lethargy/fatigue, self-focused/depression, irritable/anxious |
| what is pain threshold | the level of stimulus needed to produce the prerception of pain |
| what is pain tolerance | the amount of apin a pt can edure w/o it interfering w/ normal function |
| what are nociceptors (sensory fibers) | afferent neurons that feel pain, located in skin, muscle, CT, circulatory sys, adn deep visera. |
| what are the type of sensory nociceptor fibers | A deltaC deltaA beta |
| What are A delta fibers | fast traveling, respond to sharp, stinging, cutting, pinching pian as a result of mechanical stimulation, they open the gate and enhance perception of pain, small and large fibers |
| what are A beta fibers | respond to pressure and temp, closes the gate and inhibits the perception of pain, small fibers |
| what are C delta fibers | slow traveling, respond to dull, burning, aching pain as a result of mechanical, chemical, or thermal stimulaiton, opens the gate and enhances teh perception of pain. |
| pain is received from the sensory nerves and travels to the dorsal or posterior horn of the spinal cord | in the spinal cord these nerves form synapses with spinal cord nerves that then send impulses to the brain, the A and C delta fibers open the gates and send the signal of pain. |
| transmission of pain impulses can be modulated by interneurons that act as gates | gates can be closed by stimulation of large A beta finbers and descending impulses coming down the spinal cord from higher levels. |
| when you rub or massage an injured area of he body it stimulated the large A beta fibers resulting in pain relief | endorphins and enkephalins are known as natural painkillers, they close the gate and stop perception of pain |
| acupuncture is based on the gate control theory by stimulating the large delta fibers, closing the gate and blocking pain | natural endorphins can close the gate as well as out state of mind |
| what is transduction | initiation of pain signal at th epain receptor |
| what is transmission | pain info carried from pain receptor to the spinal cord |
| what is perception | brain;s perception of pain, influenced by anxiety, feat, apprehension, etc. |
| what is modulation | information sent from CNS back to the periphery |
| what is somatic pain | bone, muscle, and soft tissue pain |
| what is visceral pain | deep tissue or organ pain |
| what is superficial pain | skin or mucous pain |
| what is neuropathic pain | shooting, burning, nerve pain |
| what is acute pain | immediate phose of injury |
| what is chronic pain | pain lasting longer thatn 6 mos |
| what is cancer pain | progressive, deblitiating pain. |
| what is vascular pain | pain in the vascular system (ie migraine HA) |
| what is regerred pain | pain in differect location from injury |
| what is phantom pain | pain in a limb that was amputated |
| what is psychogenic pain | real pain r/t psychological factors, not physical factors |
| what is central pain | pain resulting from tumors, trauma to brain such as a CVA |
| what is around-the-clock dosing | basline amount of drug administered over 24 hrs ot treat bain before it begins |
| what is breakthrough pain | transitoy flare-ups of pain over the baseline pain |
| what is incidental pain | pain r/t a specific movement or results from an injury at taht specific moment |
| what is tolerance | capacity for enduring a large amount of a substance w/o adverse effects/decreased sensitivity to the substance |
| what is cross tolerance | one drug or substance such as ETOH causing a decrease inteh effect of morphine |
| what is physical dependence | pt will have pysical w/drawal symptoms when taken off a drug (there is no psychoplogical need to the drug) |
| what is addiction | physical and psychologiacl dependence on a drug |
| Always ask your pt to give you their pain as a number between 1-10 | also have them describe their pain and tell location, ask them if it is new or old pain |
| what are some non-pharmacological interventions for pain | relaxation, guided imagery, biofeedback, music, massage, TENS |
| pts may need higer dosing of narcotics due cross tolerance | opioid analgesics are the most effective pain relievers but are often underused due to pt/caregiver fear or misconceptions |
| what is an agonist | causes a response |
| what is a partial agonist | causes only a limited response (not good for pts with drug addiction hx) |
| what is an antagonist | reverses teh effects of an agonist |
| analgesics work in the CNS, bind to opiate receptors | opioid analgesics also act outside CNS, peripherally and this is what is responsible for many of the AE |
| what are the primary opioid receptors | Mu, kappa, and delta |
| what are the therapeutic actions of analgesics | act at specific opioid receptor sites in the CNS to produce analgesia, sedation, euphoria, hallucinations |
| what are the therapeutic indications of analgesics | releive mod-severe pain, often used with other pain relievers, cough suppression, treat diarrhea, used with anesthesia |
| what are the pharmacokinetics of analgesics | IV most therapeutic, IM an dSW absorption rates vary, met liver, excreted urine and bile |
| analgesics are C/I in | allergy, PG.lactating, resp dysfun, depressed GI function, GI/GU surgery, head injury (increase ICP), alcoholism, cerebral vasculat ds, liver/renal dysfun |
| what are the AE of analgesics | RESP DEPRESS euphoria, itching, hypotension, lightheadedness, psychosis, seadation, disorientation, N/C, constipation, urinary retention, hypersensitvity |
| always use smallest dose that gives effective pain reief w/o resp function being affected | use w/ caution in pts with resp conditions such as asthma or COPD |
| waht is the antagonist or antidote | Narcan |
| what is the level for severe resp depression and intervention is needed | <10 resp/min |
| Do not mix analgesics with other CNS depressants | prototypes: morphine, meperidine hydrochloride (demerol), codine, fantanyl (duragesic) |
| what is a migraine HA | severe throbbing HA on one side fo the head, involves dilation of cranial arteries, may or may not be preceded by an aura. |
| what is a tension HA | usually occur at times of stress and feel like a dull band of pain around the entire head and can last 30 min to 1 week, muscles of head and neck tighten in response to stress |
| what is a cluster headache | usually begin during sleep and involve sharp eye pain that radiates to neck and shoulder with sweating, flushing, tearing, and nasal congestion lasting 15-90 min, dilation of blood vessels cause pressure on trigeminal nerve |
| what are the 2 major classes of drugs that treat migraine HA | ergot derivatives and triptans |
| what is the prototype for HA meds | sumatriptan (imitrex)ergotamine |
| what is the therapeutic action of acetaminophen | mechanishm of action for analgesia is not understood |
| how does it lower body temp | acts on hypothalamus to cause vasodilation, increase peripheral blodd flow and cool boyd by dissipating heat |
| what are the pharmacokinetics of acetaminophen | met in liver, excreted in urine, caution in pts with renal/liver impairment |
| what are acetaminophen AE | HA, hemolytic anemia, blood dyscrasias, renal dysfunction, rash, fever, hepatotoxic |
| what are teh drug interactions with acetaminophen | increased bleeding risk with anticoagulants |
| what are the therapeutic actions of NSAIDS | works by blocking teh undesirable effects of prostaglandins in teh arachidonic acid pathway |
| what are the therapeutic indications of NSAIDS | treat mild-mod pain, inflammation, and fever, RA, OA, primary dysmenorrhea. Can b eused to prevent stroke, MI (inhibits paltelet formation) |
| what are the pharmacokinetics of NSAIDS | met liver, excreted urine |
| what are the C/I of NSAIDS | allergy, HTN, peptic ulcer, Pg/lactation |
| what are the AE of NSAIDS | GI upset and bleeding, HA, dizziness, fatigue, platelet inhigition, bone marrow supression |
| what are the drug interactions for NSAIDS | any drug thaqt affects platelets or coagualtion |
| What is the NSAIDs prptotype | ASA, ibuprophen |
| what is rheumatoid arthritis (RA) | autoimmune ds causede by substances in blood called rheumatoid factor to the body's own immunoglobulin |
| what are the s/s and RA | joint stiffness, swelling, pain adn of fusion of joints |
| RA is a cyclical inflammatory process that repeats itself and eventually leads to destruction of the entire joint space | RA can affect lungs, heart, nerves, and blood vessels |
| what is osteoarthritis (OA) | breakdown of cartilage in joints, can result from trauma, or aging, spurs of bone like material develop on the edges of joints and causes pain, stiffness, and inflammation |
| OA and RA prototype | celecoxib (celebrex) |
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shellyrbrooks
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