pharm2

• entero chromaffin like
• in body/fundus of stomach
• secrete HCL

• in antrum of stomach
• secrete Gastrin

• in fundus/body
• secrete gastric acid in response to: Ach, gastrin, histamine

directly stimulates H+ ion generation by binding to parietal cell muscarinic receptors --> activation of H-K ATPase secretion of stomach acid

• directly stimulates H+ ion generation by binding to parietal cell receptors --> activation of H-K ATPase  secretion of stomach acid
• also stimulates histamine release from ECL cells

binds to H2 receptor on parietal cell to activate cell --> activation of H-K ATP ase --> secretion of stomach acid

comformational change of pump --> inc acid secretion

• ulcer in stomach lining r/t inc acid/pepsin secretion and impaired mucosal cytoprotection
• causes: NSAID, H pylori, smoking, EtOH, stress

• spiral bacteria
• once infected, remain colonized until treated
• releases toxins/proteases/phospholipase enzymes --> inflammation
• -impair mucosal integrity

• 1 acid suppressive (usually PPI)+ 2 antibiotics X 7/14 days
• -no stomach absorption, need something w/ activity in stomach

• chocolate/mint/def/fat/carbs/EtOH: dec LES tone
• acid/caffeince: inc gastric acid
• fat: delay gastric emptying
• tobacco: dec LES tone and inc acid
• anticholinergics, theophyline, CCB, meperidine: dec tone

• PPI: dec acid by ~100%, improve esophageal healing- good for chronic
• H2B: improve esophageal healing
• Antacid*: inc LES tone and pH
• Sucralfate/misoprostol
• metoclopramide/betanechol: inc LES tone, prokinetic

can --> dependency --> fluid/lyte imbalance, steatorrhea, osteomalacia, vit/mineral dificiencyes

• yelow dye
• incidence greater in pt with ASA allergies
• --> excess bowel activity, cramping, flatulence, bloating, perianal irritation

• bulk forming
• surfactant

polyethylene glycol

in vesicles at axon terminal

• triggered by arrival of action potential at axon terminal
• then can: bind to post synaptic cell, be taken back up, or broken down by enzymes in synapse

• PNS: activates skeletal muscle
• CNS: arousal, reward, sensory perception, sustaining attention

• dopamine
• norepi
• serotonin

reward, reinforcement, motivation, motor function

sleep, arousal, pain, food intake, emotions, mood, temp, CV function

sleep/arousal, pain, food intake, emotions, mood, temp, CV fcn

• inhibitory
• alerts ion specific channels using hyperpolarization
• --> sedation, muscle relaxation, CV/resp, spinal reflexes, pain perception

• excitatory
• 2 receptors: NMDA, AMPA

too much serotonin and/or dopamine

• EPS from antipsychotics
• bradykinesia, rigid, tremors: usually responsive to anticholinergics like benadryl/benzotropin

• EPS from antipsychotics
• spasms of muscle groups

• EPS from antipsychotics
• somatic restlessness, inability to stay still/calm

• EPS from antipsychotics
• constantly chewing gum
• only diagnosed after 6 mos of being on med
• not acute, but can be irreversible

• serious complication of typical antipsychotics, more common w/ high potency
• agitation, confusion, fever, tachy, labile BP, sweating, changing LOC
• treat w/ Dopa Agonist

• moderates excitement and physical activity
• depress consciousness
• retain ability to respond purposely to external stimuli

induce and maintain sleep

depress CNS function

• valproic acid
• lamotrigine
• carbamezapine

• silence neurons generating abnormal discharge
• inhibit spread of discharge through CNS
• inhibit voltage gated na/ca channels
• antagonize glutamate/enhance GABA

• newer antiepileptic, fewer SE
• activated voltage gated K channels

• newer antiepileptic, fewer SE
• prevents gaba inactivation

• newer antiepileptic, fewer SE
• Na Channel blocker

• newer antiepileptic, fewer SE
• Na Channel blockers

• destruction of the group of cells (substantia nigra) that make dopamine --> bradykinesia
• imbalance b/w dopa and Ach --> too much GABA

• gradual loss of effect of levodopa/carbidopa:
• can add dopamine agonist or COMT inhibitor
• or increase dose/frequency

• acute loss of effect of levodopa/darbidopa
• add MAO-B inhibit, COMT inhibitor, dopamine agonist
• limit dietary protein
• changing dose wont help

• 1st line: sinimet, dopa agonist, COMT inhibitor alone or in compo
• 2nd line: dopa releaser, MAO-B, anticholinergic

• from skin, bone, muscle, joint, CT
• localized
• dull, throbbing, aching, nagging, stabbing

• internal organs
• diffuse
• gnawing, cramping, aching

• injury to peripheral nerves
• sharp, burning, shooting
• management: antidepressants, anticonvulsants- try to solve underlying issue

similar to visceral, but w/ subtle differences

• light touch, vibration, movement of hairs
• fast

• heat, warmth, mechanical stimuli, chemicals
• slow

• in dorsal horn
• stimulation of receptor -->na/ca influx --> membrane depolarization --> voltage gated na threshold --> action potential --> release of NT

• stop transmission of pain signal
• opioid peptides
• NE
• Serotonin
• Glycine
• Gaba

• brain: alpha agonists, opioids --> highest addiction potential
• dorsal horn: opioids, alpha agonists, local --> most action here
• peripheral nerve: local
• site of trauma: local, anti inflammatory
• action is more direct post dorsal horn

respiratory depression, euphoria, bradycardia, pruritis, miosis, n/v, inhibit gut motility, dependence

antidepressant, dependence

sedation, psychomimetic, dysphoria, diuresis

dysphoria, delirium, hallucinations

• naturally occuring
• ie morphine, codeine

• all hepatically metabolized
• agonists, partial agonists, antagonists
• only nubain, butorphanol, buprenophine, pentazocine are not full agonists

• 3x morphine r/t lipid solubility
• metabolized to morphine

• 1000X morphine
• metabolites accumulate during chronic use

• PK: ability to metabolize/excrete increases over time
• PD: change in drug-receptor interaction
• -dec number of receptors, confirmational change, signal transduction pathway change
• Learned: pt alters behavior to hide effects

drug affects reward system of brain

• abrupt cessation of agent --> withdrawal
• can develop after a few weeks
• dependant on physical, emotional, social, psychological factors
• 3 factors: tolerance, withrawal, giving up other things

physical dependance plus abuse or drug seeking behavior

(but can be drug seeking and not dependent it no withdrawl)

pathologic prostoglandins: vasdilate, inflammation, inhibit PLT

physiologic prostoglandins: GI mucosa, platelet aggregation, vasoconstrict

• non anti-inflammatory: only APAP
• anti inflammatory: NSAID

inhibit cox 1 and cox 2

only inhibit cox 2

mucomyst: substitutes for glutathione in the rxn that converts toxic metabolite to non toxic form

• major pathway --> non toxic metabolite
• minor pathway --> toxic metabolite, then converted to non-toxic by glutathione.

• -Minor pathway(P45) induced by ETOH
• -EtOH/APAP OD deplete glutathione

• life threatening disorder in PEDS recovering from virus, higher risk from ASA
• vomiting, lethargy, elevated liver enzymes, progressing to coma

low dose ibuprofen, naproxen

• mod-high dose of ibuprofen, naproxen
• diclofenac

• ASA
• indomethacin
• ketorolac
• piroxicam

• sulindac
• nabumetone
• celecoxib

• neuropathy
• also help w/ depression/insomnia of chronic pain

neuropathic pain, fibromyalgia

• gabapentin: post op
• pregablin: more bioavailable than gabapentin, euphoria in some pts
• cabamazepine: FDA trigeminal neuralgia
• lamotrogine: phantom limb, MS, stroke

• very limited use
• --> postural hypotension

• low dose so pt remain responsive and breathe on their own. 
• used during minor surgery

• deep state of sleep
• no sensory perception
• lose consciousness
• no recall
• immobile
• need assisted ventilation

• inc skeletal muscle oxidative
• metabolism → overwhelms body's ability to regulate temp

• close structural analog to morphine
• more hydrophobic --> crosses BBB --> sharper high

• potentiate dopaminergic, adrenergic, serotinergic neurotransmission
• fast high b/c dumps quickly, but long time for serotonin to go back in --> long high then downer

• GABA
• NMDA
• cannabinoid