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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)

Created by: arsho453

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