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  1. ECL cells
    • entero chromaffin like
    • in body/fundus of stomach
    • secrete HCL
  2. G Cells
    • in antrum of stomach
    • secrete Gastrin
  3. parietal cells
    • in fundus/body
    • secrete gastric acid in response to: Ach, gastrin, histamine
  4. acetylcholine (in stomach)
    directly stimulates H+ ion generation by binding to parietal cell muscarinic receptors --> activation of H-K ATPase secretion of stomach acid
  5. gastrin
    • 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
  6. Histamine
    binds to H2 receptor on parietal cell to activate cell --> activation of H-K ATP ase --> secretion of stomach acid
  7. gastric acid production
    comformational change of pump --> inc acid secretion
  8. peptic ulcer disease
    • ulcer in stomach lining r/t inc acid/pepsin secretion and impaired mucosal cytoprotection
    • causes: NSAID, H pylori, smoking, EtOH, stress
  9. h pylori
    • spiral bacteria
    • once infected, remain colonized until treated
    • releases toxins/proteases/phospholipase enzymes --> inflammation
    • -impair mucosal integrity
  10. h pylori treatment
    • 1 acid suppressive (usually PPI)+ 2 antibiotics X 7/14 days
    • -no stomach absorption, need something w/ activity in stomach
  11. GERD triggers
    • 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
  12. GERD treatment
    • 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
  13. chronic use of laxatives
    can --> dependency --> fluid/lyte imbalance, steatorrhea, osteomalacia, vit/mineral dificiencyes
  14. tartazine sensitivity
    • yelow dye
    • incidence greater in pt with ASA allergies
    • --> excess bowel activity, cramping, flatulence, bloating, perianal irritation
  15. laxatives in pregnancy
    • bulk forming
    • surfactant
  16. bowel prep
    polyethylene glycol
  17. neurotransmitter storage
    in vesicles at axon terminal
  18. neurotransmitter release
    • 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
  19. acetylcholine
    • PNS: activates skeletal muscle
    • CNS: arousal, reward, sensory perception, sustaining attention
  20. monoamines
    • dopamine
    • norepi
    • serotonin
  21. dopamine
    reward, reinforcement, motivation, motor function
  22. norepi
    sleep, arousal, pain, food intake, emotions, mood, temp, CV function
  23. serotonin
    sleep/arousal, pain, food intake, emotions, mood, temp, CV fcn
  24. GABA
    • inhibitory
    • alerts ion specific channels using hyperpolarization
    • --> sedation, muscle relaxation, CV/resp, spinal reflexes, pain perception
  25. glutamate
    • excitatory
    • 2 receptors: NMDA, AMPA
  26. schizophrenia
    too much serotonin and/or dopamine
  27. Parkinsonianism
    • EPS from antipsychotics
    • bradykinesia, rigid, tremors: usually responsive to anticholinergics like benadryl/benzotropin
  28. dyskinesia
    • EPS from antipsychotics
    • spasms of muscle groups
  29. Akathisia
    • EPS from antipsychotics
    • somatic restlessness, inability to stay still/calm
  30. tardive dyskinesia
    • EPS from antipsychotics
    • constantly chewing gum
    • only diagnosed after 6 mos of being on med
    • not acute, but can be irreversible
  31. neuroleptic malignant syndrome
    • serious complication of typical antipsychotics, more common w/ high potency
    • agitation, confusion, fever, tachy, labile BP, sweating, changing LOC
    • treat w/ Dopa Agonist
  32. sedative
    • moderates excitement and physical activity
    • depress consciousness
    • retain ability to respond purposely to external stimuli
  33. hypnotic
    induce and maintain sleep
  34. sedative-hypnotic
    depress CNS function
  35. anticonvulsants for BPD
    • valproic acid
    • lamotrigine
    • carbamezapine
  36. epilepsy management
    • silence neurons generating abnormal discharge
    • inhibit spread of discharge through CNS
    • inhibit voltage gated na/ca channels
    • antagonize glutamate/enhance GABA
  37. ezogabine
    • newer antiepileptic, fewer SE
    • activated voltage gated K channels
  38. vigabatrin
    • newer antiepileptic, fewer SE
    • prevents gaba inactivation
  39. rifunamide
    • newer antiepileptic, fewer SE
    • Na Channel blocker
  40. lacosamide
    • newer antiepileptic, fewer SE
    • Na Channel blockers
  41. parkinsons
    • destruction of the group of cells (substantia nigra) that make dopamine --> bradykinesia
    • imbalance b/w dopa and Ach --> too much GABA
  42. wearing off
    • gradual loss of effect of levodopa/carbidopa:
    • can add dopamine agonist or COMT inhibitor
    • or increase dose/frequency
  43. on-off
    • acute loss of effect of levodopa/darbidopa
    • add MAO-B inhibit, COMT inhibitor, dopamine agonist
    • limit dietary protein
    • changing dose wont help
  44. parkinson's tx
    • 1st line: sinimet, dopa agonist, COMT inhibitor alone or in compo
    • 2nd line: dopa releaser, MAO-B, anticholinergic
  45. somatic pain
    • from skin, bone, muscle, joint, CT
    • localized
    • dull, throbbing, aching, nagging, stabbing
  46. visceral pain
    • internal organs
    • diffuse
    • gnawing, cramping, aching
  47. neuropathic pain
    • injury to peripheral nerves
    • sharp, burning, shooting
    • management: antidepressants, anticonvulsants- try to solve underlying issue

    similar to visceral, but w/ subtle differences
  48. AB nociceptors
    • light touch, vibration, movement of hairs
    • fast
  49. C nociceptors
    • heat, warmth, mechanical stimuli, chemicals
    • slow
  50. nociceptor/pain response signal transduction
    • in dorsal horn
    • stimulation of receptor -->na/ca influx --> membrane depolarization --> voltage gated na threshold --> action potential --> release of NT
  51. inhibitory neurotransmitters in dorsal horn
    • stop transmission of pain signal
    • opioid peptides
    • NE
    • Serotonin
    • Glycine
    • Gaba
  52. sites of action of pain meds
    • 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
  53. mu receptors
    respiratory depression, euphoria, bradycardia, pruritis, miosis, n/v, inhibit gut motility, dependence
  54. delta receptors
    antidepressant, dependence
  55. kappa receptors
    sedation, psychomimetic, dysphoria, diuresis
  56. sigma receptors
    dysphoria, delirium, hallucinations
  57. opiate
    • naturally occuring
    • ie morphine, codeine
  58. opioids
    • all hepatically metabolized
    • agonists, partial agonists, antagonists
    • only nubain, butorphanol, buprenophine, pentazocine are not full agonists
  59. heroin
    • 3x morphine r/t lipid solubility
    • metabolized to morphine
  60. chine white
    • 1000X morphine
    • metabolites accumulate during chronic use
  61. tolerance
    • 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
  62. psychological dependence
    drug affects reward system of brain
  63. physical dependence
    • 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
  64. addiction
    physical dependance plus abuse or drug seeking behavior

    (but can be drug seeking and not dependent it no withdrawl)
  65. cox-2
    pathologic prostoglandins: vasdilate, inflammation, inhibit PLT
  66. cox-1
    physiologic prostoglandins: GI mucosa, platelet aggregation, vasoconstrict
  67. COX inhibitors
    • non anti-inflammatory: only APAP
    • anti inflammatory: NSAID
  68. 1st gen NSAID
    inhibit cox 1 and cox 2
  69. 2nd gen NSAID
    only inhibit cox 2
  70. acetylcysteine
    mucomyst: substitutes for glutathione in the rxn that converts toxic metabolite to non toxic form
  71. APAP metabolism
    • 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
  72. reye's
    • life threatening disorder in PEDS recovering from virus, higher risk from ASA
    • vomiting, lethargy, elevated liver enzymes, progressing to coma
  73. low risk NSAID
    low dose ibuprofen, naproxen
  74. mod risk NSAID
    • mod-high dose of ibuprofen, naproxen
    • diclofenac
  75. high risk NSAID
    • ASA
    • indomethacin
    • ketorolac
    • piroxicam
  76. renal sparing NSAID
    • sulindac
    • nabumetone
    • celecoxib
  77. adjunctive pain therapy: TCA
    amitryptyline, nortriptyline
    • neuropathy
    • also help w/ depression/insomnia of chronic pain
  78. adjunctive pain therapy: dual NE/ser reuptake inhibitors
    venlaflexine, duloxetine
    neuropathic pain, fibromyalgia
  79. adjunctive pain therapy: anticonvulsants
    • gabapentin: post op
    • pregablin: more bioavailable than gabapentin, euphoria in some pts
    • cabamazepine: FDA trigeminal neuralgia
    • lamotrogine: phantom limb, MS, stroke
  80. adjunctive pain therapy: clonidine
    • very limited use
    • --> postural hypotension
  81. monitored anesthesia care
    • low dose so pt remain responsive and breathe on their own. 
    • used during minor surgery
  82. general anesthesia
    • deep state of sleep
    • no sensory perception
    • lose consciousness
    • no recall
    • immobile
    • need assisted ventilation
  83. malignant hyperthermia
    • inc skeletal muscle oxidative
    • metabolism → overwhelms body's ability to regulate temp
  84. heroin
    • close structural analog to morphine
    • more hydrophobic --> crosses BBB --> sharper high
  85. cocaine/amphetamines
    • potentiate dopaminergic, adrenergic, serotinergic neurotransmission
    • fast high b/c dumps quickly, but long time for serotonin to go back in --> long high then downer
  86. EtOH receptors
    • GABA
    • NMDA
    • cannabinoid

Card Set Information

Author:
 ieast
ID:
 203003
Filename:
 pharm2
Updated:
2013-02-26 22:39:41
Tags:
pharm
Folders:

Description:
GI/Neuro
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