advanced pharm
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| Osteoarthritis you take | simple pain medication like acetaminophen
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| RA has severe pain d/t | inflammation in the synovial membrane in the join so you need anti-inflammatory and steroid- NSAIDS (analgesia too)
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| 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
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| 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
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| Neuropathic pain | nothing stimulating the receptor- nothing peripherally- it’s all in the nerve- abnormal signal processing in the nerve itself
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| 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
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| Transmission is what | the nerve impulse is carried to the brain- depolarization- Na+ gets in
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| 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
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| 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
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| 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
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| Slow fibers | visceral- deep organs- type C- unmyelinated- will wake up the pt-
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| 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.
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| 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
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| What do you need to address in type C pain fibrous pain | sleep (emotion/depression)
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| Pain pathway neurotransmitters, what are they and what helps | Glutamate, Prostaglandins, Substance P, Bradykinin, Histamine, Serotonin→ NSAIDs help
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| What are the neurotransmitters that block pain in the modulating phase? | Opioids (endorphins & enkephalins), Serotonin, Norepinephrine, GABA (SNRI, TCA, morphine…etc)
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| Opioids work where | centrally in the brain
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| 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
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| Acute pain | be aggressive in tx it b/c it causes sensitization- 1 month later will cause pain d/t irritability/inflammation
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| Peripheral Sensitization | trauma was not tx appropriately and prostaglandins, substance P etc keep irritating it and surrounding neurons
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| 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
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| Transduction- what do you want to do in this phase | for prostaglandins released here→NSAIDs & ASA by inhibiting COX enzyme
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| Transmission what works here | local anesthetics by blocking sodium channels
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| Perception- what works here | CBT, imagery, anxiolytics,….etc.
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| 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
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| 2 s/e that don’t disappear with opioid use | miosis and constipation- you become tolerant to everything else (except Demerol dilates)
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| Where do we find the mu receptor | in the SC, brain stem, thalamus, cortex- opioids work centrally- modulation phase
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| NSAIDS work where | peripherally- where you have the nociceptors- nerve endings- transduction phase
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| 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
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| 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
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| Morphine has excessive first pass metabolism | you’d have to give high doses in oral but parental it’s much lower
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| Morphine metabolite | Active metabolite morphine-6-glucuronide- contributes to analgesia, and is possibly nephrotoxic (fentanyl and methadone are safer for patients with kidney disease)
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| Parenteral morphine is used for | pulmonary edema- hemodynamic action- veno-dialator- relieves congestion in lungs- in MI helps with O2 consumption
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| Codeine | weaker than morphine but best for cough- a prodrug- needs 2D6- some people don’t have 2D6- are not drug seekers
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| 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
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| 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
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| Meperidine/Demerol | do not constrict eyes- mydriasis because anticholinergic- blocks muscarinic receptors in the iris- also can cause seizures
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| Agonist/antagonist drugs | Buprenorphine, Pentazocine (Talwin), Nalbuphine (Nubain)- for OB, butorphanol, morphine/naloxone (Embeda), buprenorphine/naloxone (Suboxone).
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| Methadone | long acting opioid- helps addicts with withdrawal-also chronic neuropathic pain/phantom pain- will not test + on opioid test
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| 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
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| 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
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| Trigeminal neuralgia pain you use what med | carbamazepine
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| Aspirin is good for | analgesic, antipyretic, anti-inflammatory, antiplatelet- good for MI
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| Acetaminophen is good for | analgesic, antipyretic- NOT FOR RA
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| NSAIDS is good for | analgesic, antipyretic, anti-inflammatory- good for RA-
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| NSAIDS does what? | blocks COX 1 and 2- works on arachidonic acid- prostaglandins (pain)- celebrex works on cox 2
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| 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
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| 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
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| Tylenol and anti-inflammatory effect | has weak or none- damages the liver- takes 3g/day- antidote is mucomyst/Acetyl-cysteine
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| If you have acute pain | treat aggressively with opioids to avoid sensitization and avoid it turning into chronic pain
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| RA problem is | inflammation- start tx as early as possible- 1st 3 months for good results- use combination drugs instead of just methotrexate
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| 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
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| 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
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| 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
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| 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
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| Best combo for RA | methotrexate with Leflunomide because inhibits pyrimidine synthesis, and methotrexate inhibits purine synthesis- so both inhibit inflammatory cells
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| Those who have RA are more prone to get | septic arthritis- the sick joint- also because they get immunomodulators
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| When pts on methotrexate develop dyspnea or cough… | refer to pulmonologist or rhemotologist– mey be d/t drug or rheumatoid lung dz
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| 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
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| What precipitates a gouty attack and what do you give | mild trauma- start with NSAIDS, then steroids, then colchicine (liver toxicity)
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| Chronic gout, what do you give | allopurinol- it inhibits production uric acid
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| If a pt has high uric acid levels, but not symptomatic, do you tx? | no
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| If you have a pt with an acute gout attack, is allopurinol going to help? | no- give ibuprofen
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| Uricosuric agents like probenecid and methotrexate given together | drug-drug interaction- ↑ amount of methotrexate in the blood- not used for chronic gout
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| Allopurinol can cause | allergic interstitial nephritis
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| 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
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| 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
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| 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)
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| 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
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| 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)
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| 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
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| 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
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| Kids with migraines | ibuprofen, acetaminophen, promethazine/phenargine (anti-histamine), propranolol, periactin
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| Cluster HA tx | sumitripan in the beginning but then tx w/O2- repeated attacks you tx with lithium, CCB- stop smoking
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| 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
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| 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)
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| 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
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| Keppra and other anticonvulsants in especially younger pts can cause | depression and SI
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| When you use an anticonvulsant medication, you use the | brand name
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| Anticonvulsants can be used for what off- label things (test) | carbamazepine→ trigeminal neuralgia- bipolar- lamictal gabapentin→ neuropathic pain, Topamax for →migraine, Lyrica→ fibromyalgia
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| When dopamine is deficient in basal ganglia | high activity of acetylcholine takes the upper hand
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| Tx for parkinsons | either is dopaminergic or anticholinergic (bad for the elderly > 60)
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| 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
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| Start with DA agonists for parkinsons and save levodopa for when necessary- what are the DA agonists? | - Bromocriptine (Parlodel) - Pramipexole (Mirapex)- Ropinirole (Requip)
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| Amantadine (Symmetrel) does what | Parkinson’s medications- ↑DA by unknown mechanism- squeezes it- mild parkinsons
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| 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
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| Anticholinergics in Parkinsons are used in what type of pts? | younger <60 with mild fx impairment → Benzatropine (Cogentin) Trihexyphenidyl (Artane)
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| Mild functional impairment in a parkinsons pt >65 | Amantadine (Symmetrel)
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| Severe functional impairment in a parkinsons pt | use a dopaminergic drug
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| Alzheimers is | ↓Ach in the limbic system, you start losing memory. Ach is destroyed by acetylcholinesterase- use an inhibitor
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| 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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