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pain & neuro
advanced pharm
| Question | Answer |
|---|---|
| Osteoarthritis you take | simple pain medication like acetaminophen |
| RA has severe pain d/t | inflammation in the synovial membrane in the join so you need anti-inflammatory and steroid- NSAIDS (analgesia too) |
| Fibromyalgia | pain in the neck d/t pain r/t the nerves- hyperirritable- need something that works centrally in the SC/brain- give TCAs/Elavil or meds with GABA- Lyrica |
| Nociceptive pain | when you put your hand on a fire and nerve/pain fibers turn into impulse→ depolarize to the SC- you’re stimulating the nociceptive nerve endings |
| Neuropathic pain | nothing stimulating the receptor- nothing peripherally- it’s all in the nerve- abnormal signal processing in the nerve itself |
| Transduction is what | when nociceptors receive damaging stimuli and convert them into a nerve impulse- occurs peripherally-releases chemicals→ prostaglandins, substance P…transduced into nerve impulses-positive charges |
| Transmission is what | the nerve impulse is carried to the brain- depolarization- Na+ gets in |
| Perception is what | how the pain messages coming from the periphery will finally be interpreted by the brain- what else is going on in your mind- CBT- perception |
| Modulation is what | where the most analgesics work- when Dr. Hanna was stabbed- survival mode- during its transmission, the pain impulse can be suppressed by signals descending from the brain to SC |
| 2 types of nerve fibers | 1) A-delta nerve fibers (fast/myelinated)- feel the pin-prick in finger- will maybe feel it 10 minutes later in the whole hand and 2) Type C pain fibers (unmyelinated)- visceral |
| Slow fibers | visceral- deep organs- type C- unmyelinated- will wake up the pt- |
| Fast pain- A delta travel which way | taken to SC to the dorsal horn- cross to the opposite side to the brain stem uninterrupted- to the Thalamus- the whole impulse goes the spinal-Thalamus tract & knows exactly where the injury’s at. |
| Type C fibers travel which way | to the reticular formation (sleep and awakening)- wake you up- visceral pain (like MI)address sleep in this type of pain- also effects limbic system- depression/ emotion |
| What do you need to address in type C pain fibrous pain | sleep (emotion/depression) |
| Pain pathway neurotransmitters, what are they and what helps | Glutamate, Prostaglandins, Substance P, Bradykinin, Histamine, Serotonin→ NSAIDs help |
| What are the neurotransmitters that block pain in the modulating phase? | Opioids (endorphins & enkephalins), Serotonin, Norepinephrine, GABA (SNRI, TCA, morphine…etc) |
| Opioids work where | centrally in the brain |
| Fast pain travels… | to the thalamus uninterrupted- no crying, does not interrupt sleep- but the pain that follows will stop at the RF will awaken sleep go to the limbic system and make you cry and = vague pain |
| Acute pain | be aggressive in tx it b/c it causes sensitization- 1 month later will cause pain d/t irritability/inflammation |
| Peripheral Sensitization | trauma was not tx appropriately and prostaglandins, substance P etc keep irritating it and surrounding neurons |
| Pain components are | Sensory→ (sharp, aching, heavy…..pain),Affective→mood & emotion, upsetting, Autonomic→tachycardia, hypertension, sweating, tachypnea, Motor→ withdraw, writhe around (wiggle), lie still, vocalize |
| Transduction- what do you want to do in this phase | for prostaglandins released here→NSAIDs & ASA by inhibiting COX enzyme |
| Transmission what works here | local anesthetics by blocking sodium channels |
| Perception- what works here | CBT, imagery, anxiolytics,….etc. |
| Modulation- what drugs work here | opioids: by acting on μ receptors→ (TCAs, SSRIs, SNRIs) by 5-HT & NE levels →Anticonvulsants (Gabapentin): by acting on GABA receptors |
| 2 s/e that don’t disappear with opioid use | miosis and constipation- you become tolerant to everything else (except Demerol dilates) |
| Where do we find the mu receptor | in the SC, brain stem, thalamus, cortex- opioids work centrally- modulation phase |
| NSAIDS work where | peripherally- where you have the nociceptors- nerve endings- transduction phase |
| When you give opioids, what happens to the ca+ channels, and the K+ channels? | ca+ channels close, open K+ channels and K+ leaves- loses + charges and the person becomes sedated |
| Opioids shut down the gut completely by… | μ2 receptors- Loperamide & diphenoxylate, Enhancement of non-propulsive contractions in the small intestine and Inhibition of propulsive contractions, augments tone of the anal sphincter, ↓acid secretions |
| Morphine has excessive first pass metabolism | you’d have to give high doses in oral but parental it’s much lower |
| Morphine metabolite | Active metabolite morphine-6-glucuronide- contributes to analgesia, and is possibly nephrotoxic (fentanyl and methadone are safer for patients with kidney disease) |
| Parenteral morphine is used for | pulmonary edema- hemodynamic action- veno-dialator- relieves congestion in lungs- in MI helps with O2 consumption |
| Codeine | weaker than morphine but best for cough- a prodrug- needs 2D6- some people don’t have 2D6- are not drug seekers |
| Hydrocodone | norco or Vicodin- most commonly used opioid- in combo with acetaminophen and NSAIDS- short term pain control- 2D6 codeine derivative - schedule II- need triplicate- no calling it in- one month at a time scripts |
| Fentanyl (Duragesic) and Congeners | can be used for patients during surgery so that they do not wake up- for longer acting use the patch- Sufentanil (Sufenta), and Alfentanil (Alfenta) are intraoperative and even more short-acting |
| Meperidine/Demerol | do not constrict eyes- mydriasis because anticholinergic- blocks muscarinic receptors in the iris- also can cause seizures |
| Agonist/antagonist drugs | Buprenorphine, Pentazocine (Talwin), Nalbuphine (Nubain)- for OB, butorphanol, morphine/naloxone (Embeda), buprenorphine/naloxone (Suboxone). |
| Methadone | long acting opioid- helps addicts with withdrawal-also chronic neuropathic pain/phantom pain- will not test + on opioid test |
| Tramadol | partially works on the mu receptor- serotonin and NE reuptake- do not give with SSRI- serotonin syndrome- physical dependence- x in those with seizures |
| Tapentadol (Nucynta and Nucynta ER) | least GI s/e- least constipation- A newer synthetic μ-receptor agonist-strong NE reuptake-inhibiting activity-implicated in the serotonin syndrome and should be used with caution in patients with seizure disorders |
| Trigeminal neuralgia pain you use what med | carbamazepine |
| Aspirin is good for | analgesic, antipyretic, anti-inflammatory, antiplatelet- good for MI |
| Acetaminophen is good for | analgesic, antipyretic- NOT FOR RA |
| NSAIDS is good for | analgesic, antipyretic, anti-inflammatory- good for RA- |
| NSAIDS does what? | blocks COX 1 and 2- works on arachidonic acid- prostaglandins (pain)- celebrex works on cox 2 |
| Cox 1 is good for | PGE for our stomach- mucous barrier or else you get peptic ulcer- good for the kidneys- produces vasodilator PGE- improves renal blood flow |
| COX 2 develops where | in inflamed tissues- produces prostaglandins that cause pain- goal is to block this one- NSAIDS usually block this one- Celebrex works here |
| Tylenol and anti-inflammatory effect | has weak or none- damages the liver- takes 3g/day- antidote is mucomyst/Acetyl-cysteine |
| If you have acute pain | treat aggressively with opioids to avoid sensitization and avoid it turning into chronic pain |
| RA problem is | inflammation- start tx as early as possible- 1st 3 months for good results- use combination drugs instead of just methotrexate |
| Drugs for RA | need something for s/s- NSAID for acute- and DMARDS- disease modifying anti-rheumatic drugs- very potent anti-inflammatory- takes 3-6 months to start working so need a steroid as a bridge- short term DMARD |
| Actual DMARD MEDS | synthetics (old) methotrexate and biological (living) ends with a mab- works faster- immunosuppressant- s/e infection- skin test TB- INH for + 9 months |
| Methotrexate | most effective single agent- hepatotoxicity- screen LFTs- CBC, lowers WBC, oral mucosal damage, bone marrow depression d/t anti-folate- do not give w/Bactrim |
| Biological DMARDS | Entercept, Adalimumab, Infliximab, certolisumab pegol, goliumab- 5 that are approved and go well with methotrexate- given SQ- work faster-weeks- A/E infection, ↓WBC, pregnancy category x- GI most common |
| Best combo for RA | methotrexate with Leflunomide because inhibits pyrimidine synthesis, and methotrexate inhibits purine synthesis- so both inhibit inflammatory cells |
| Those who have RA are more prone to get | septic arthritis- the sick joint- also because they get immunomodulators |
| When pts on methotrexate develop dyspnea or cough… | refer to pulmonologist or rhemotologist– mey be d/t drug or rheumatoid lung dz |
| Pre op with RA pts | Watch out for atlanto-axial subluxation (neck) -Withhold the biologics 2 t1/2 pre- and 2 t1/2 post- surgery |
| What precipitates a gouty attack and what do you give | mild trauma- start with NSAIDS, then steroids, then colchicine (liver toxicity) |
| Chronic gout, what do you give | allopurinol- it inhibits production uric acid |
| If a pt has high uric acid levels, but not symptomatic, do you tx? | no |
| If you have a pt with an acute gout attack, is allopurinol going to help? | no- give ibuprofen |
| Uricosuric agents like probenecid and methotrexate given together | drug-drug interaction- ↑ amount of methotrexate in the blood- not used for chronic gout |
| Allopurinol can cause | allergic interstitial nephritis |
| Other drugs that can be taken for fibromyalgia that weren’t discussed in previous lecture | Norepinephrine/Serotonin Reuptake Inhibitors (NSRIs) Milnacipran (Savalla) or flexeril/Cyclobenzaprine |
| Know 3 underlying issues for headache | 1) subarachnoid/meningitis) altered LOC- do CT- neck stiffness, fever, headache) 2) neurologic deficit/brain tumors 3) tenderness along temporal artery- unilateral w/eye- give steroid to prevent loss of vision |
| Tension headache | most common- non-vascular- d/t HALT- band around the head- may be tender- give NSAIDS or acetaminophen- if chronic- tx as if neuropathic (TCA) |
| Migraine | vascular- give vasoconstrictor to↓ spasm- or give CCB or propranolol or mag sulfate to ↓ chronic attack – unilateral- throbbing- photophobia- n/v- aura, ↓ in pregnancy, in boys and adult women |
| Cluster | vascular- give vasoconstrictor to ↓ spasm or give CCB to ↓ frequency- icepick in eye- unilateral- eye manifestations- red, lacrimation eye, rhinorrhea, Horner’s syndrome (ptosis, myosis) |
| Acute attack for migraine | for acute vasoconstrictors- sumitriptan/Imitex and dihydroergotamine (Migranal)may cause angina and ↑BP→serotonin agonists and can give NSAIDS also topiramate (preventive)- also propranolol |
| In pregnant women with migraines | avoid dihydroergotamine (Migranal), ibuprofen, Imitrex- give acetaminophen, avoid anticonvulsants (Cat D)- give propranolol, BB or verapamil CCB- but they do not get migraines |
| Kids with migraines | ibuprofen, acetaminophen, promethazine/phenargine (anti-histamine), propranolol, periactin |
| Cluster HA tx | sumitripan in the beginning but then tx w/O2- repeated attacks you tx with lithium, CCB- stop smoking |
| 4 mechanisms of actions by which seizures wrk | calm ↓ the brain 1) Na+Channel Blockade-brain sleeps- keep it negative- phenytoin, carbamazepine, lamictal 2) GABA related 3) calcium channel blockade- Ethosuximide for petit mal4) glutamate NMDA antagonism w/Felbamate |
| Carbamazepine | induces 3A4- induces its own metabolism- destroys itself- you need to ↑ dose also those with Asian descent with the gene HLA-B1502 may precipitate severe hypersensitivity rx Toxic Epidermal Necrosis (TEN) |
| Phenytoin/Dilantin has what | zero order kinetic- A constant amount of drug is lost per unit time. The higher the concentration of the drug, the longer the half life- like etoh- causes gingival hyperplasia |
| Keppra and other anticonvulsants in especially younger pts can cause | depression and SI |
| When you use an anticonvulsant medication, you use the | brand name |
| Anticonvulsants can be used for what off- label things (test) | carbamazepine→ trigeminal neuralgia- bipolar- lamictal gabapentin→ neuropathic pain, Topamax for →migraine, Lyrica→ fibromyalgia |
| When dopamine is deficient in basal ganglia | high activity of acetylcholine takes the upper hand |
| Tx for parkinsons | either is dopaminergic or anticholinergic (bad for the elderly > 60) |
| Levodopa works well with carbidopa because | it prevents dopa dexarboxylase from becoming dopamine which will have s/e, it will cross BBB to produce it in the brain- but the drug has on/off phenomenon- stops at 5 years- start w/DA agonists |
| Start with DA agonists for parkinsons and save levodopa for when necessary- what are the DA agonists? | - Bromocriptine (Parlodel) - Pramipexole (Mirapex)- Ropinirole (Requip) |
| Amantadine (Symmetrel) does what | Parkinson’s medications- ↑DA by unknown mechanism- squeezes it- mild parkinsons |
| MAOI and COMTIs | prevent DA breakdown→ MAOIs - Selegiline (Emsam) - Rasagiline (Azilect) and COMTIs: Entecapone (Comtran), Tolcapone (Tasman)→ need to give with sinemet b/c you need DA to preserve- they don’t create DA |
| Anticholinergics in Parkinsons are used in what type of pts? | younger <60 with mild fx impairment → Benzatropine (Cogentin) Trihexyphenidyl (Artane) |
| Mild functional impairment in a parkinsons pt >65 | Amantadine (Symmetrel) |
| Severe functional impairment in a parkinsons pt | use a dopaminergic drug |
| Alzheimers is | ↓Ach in the limbic system, you start losing memory. Ach is destroyed by acetylcholinesterase- use an inhibitor |
| Drug management of Alzheimer’s | 1) AChE inbitiors: Donepezil (Aricept)- cytochrome interactions also Rivastigmine (Exelon) is better 2)NMDA glutamate receptor antagonist: Memantine HCl (Namenda) |
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arsho453
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