Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

77 Cards in this Set

  • Front
  • Back
anesthetics, analgesics, antipsychotics

are drugs that act on:
the CNS
sympathomimetics, antihypertensives, cholinergic agents, NOS inhibitors

are drugs taht act on:
the PNS
Describe the CNS effects seen with increasing dosage
what do you call a drug, that's efficacy produces no GABA-Shift (neither inhibition, nor stimulation)
drugs that are less efficacious than the pure agonist, result in GABA-shift in what direction?
inhibitory shift
drugs that a partial agonists or full agonists, cause what type of GABA-shift
stimulatory shift
more efficacious than the pure agonist
Full agonist
Drug which mimics the action of NT;
binds to receptor and produces a biological response
Partial agonist
binds with equal affinity to the receptor but is less efficacious than the full agonist
mixed agonist-antagonist:
opioid analgesic, pentazocine
Inverse agonist
produces a post-synaptic effect which is opposite to that induced by an agonist
bind to receptor, does not later membrane potential, but prevents the effect of an agonist and the NT at that receptor
SNARE proteins are involved in:
protein-protein interactions that tether synaptic vesicles close to the plasma membrane of the presynaptic neuron

SNARE proteins in both the vesicle membrane and plasma membrane
What allows extracellular Ca2+ to enter the pre-synaptic cell?
Voltage-gated Ca channel opens in response to an action potential, allowing Ca2+ into the cell
what triggers vesicle release?
increase in intracellular Ca2+ triggers fusion of vesicles with the plasma membrane, releasing NT into the synaptic cleft
GLIA inlucde what types of cells?
Glia constitute what % of the cell population in the CNS?
once thought to be "supporting cells" of CNS, glia are now recognized as playing a major role in what?
-regulates LTP and LTD
-Astrocytes regulate synaptic [Ca], intrinsic Ca oscillations
what type of cell regulates Calcium concentration at the neuronal synapse?
ASTROCYTE (glial cell)
Ach: Nicotinic
Glutamate: Ionotropic
Serotonin: 5:HT
Purines: P2Y
NTs that act via Metabotropic receptors
Glutamate, GABA, dopamine, NE, Histamine, Serotonin, Adenosine, Ach;Muscharinic
Glutamic Acid
Aspartic Acid
GABA and its agonist improved visual cortical function in senescent monkeys

this suggests that cortical function decline may result from degradation of what during senescence?
degradation of INTRACORTICAL INHIBITION during senescence
xanax and valium are both
Benzodiazepines and barbiturates affect what NT?

Clinical Action:

anxlolytic, muscle relaxation, anesthesia, anti-seizure and sedation
Effector pathway of GABA-A
Chloride channel
effector pathway of GABA-B
cAMP, Ca, K+
IONOTROPIC RECEPTORS with excitatory action in response to glutamate and aspartate
NMDA (high Ca permeability)
AMPA/Kainate: low Ca permeability
Mechanisms of Motor Neuron degeneration
1) Faulty gene
2) Excess glutamate
3) Free radicals
4) neurofilaments
5) Antibodies
= cell damage and nuerofilament tangles
Memantine (Namenda)
Tx for moderate to severe AD

affects GLUTAMATE action on Metabotropic GPCR

(also stroke, epilepsy, ALS, Huntington's, AIDS Dementia, Neuropathic pain)
an Oral AchE inhibitor may be useful in treating what disease?
mild to moderate AD

(more ACh available for longer in teh synapse)
drugs that affect ACh in the CNS
NICOTINE: agonist??
ATROPINE: prototypical muscarinc receptor antagonist- used to dilate pupils, inhibit secretions during
surgery, can cause delirium
3) DONEPEZIL: AChE inhibitor
Biogenic Amines
cocaine's mechanism of action
prevents dopamine reuptake, allowing enhanced effect in synapse
Sinemet is used to treat what?

a combination of carbidopa, MSD, an aromatic amino acid decarboxylase inhibitor, and levodopa, MSD, the metabolic precursor of dopamine, for the treatment of Parkinson's disease and syndrome.

Levodopa relieves the symptoms of Parkinson's disease by being decarboxylated to dopamine in the brain. Carbidopa, which does not cross the blood-brain barrier, inhibits the extracerebral decarboxylation of levodopa, making more levodopa available for transport to the brain and subsequent conversion to dopamine.
Dopamine acts through receptors D1a, D1b-D(2-4)

effector pathways:
cAMP-adenylate cyclase
prototopic drugs that affect dopamine:
antipsychotics (block D2 receptors)
reserpine disrupts what?
noradrenaline storage granules
tricyclic antidepressants inhibit
reuptake of noradrenaline
imipramine is the prototypic...
prototypic tricyclic antidepressant
often used for chronic pain treatment
drugs that affect NE:
tricyclic antidepressants
(Tx of depression and pain)
Norepinephrine effector pathway
mainly intracellular mediation of cAMP
Prozac (fluoxetine) is what class of drug?
a 5-HT (serotonin) uptake blocker
How do tricyclic antidepressants differ from drugs like Prozac?
classic tricyclic antidepressants favor blockade of NE reuptake,

whereas fluoxetine (prozac) favors blockade of 5-HT (SEROTONIN)
drugs that affect serotonin
Hallucinogens (LSD)
Tricyclic Antidepressants
MAO inhibitors
cinical action of drugs affecting serotonin:
depression, migraine, anxiety, sleep disorders and pain
most serotonin receptors are what type?
metabotropic (5-HT1, 5-HT2)
5-HT3 (ionotropic)
primary psychoactive ingredient in cannabis
how does THC affect the brain?
mainly by activating a specific cannabinoid receptor CB1
CB1 is expressed where?
at high levels in many brain regions

ANANDAMIDE = endogenous CB1 ligand
THC = exogenous CB1 ligand
where are CB2 receptors found?
in the periphery, immune cells and glia
cannabinoids affect
pain perception
The activity produced in the nervous system by potentially tissue-damaging stimuli
physiological (acute) pain
mediated at nociceptors widely distributed in cutaneous tissue, bone, muscle, CT, vessels and vsicera
classes of nociceptors
physiological (acute) pain is response to:
opioids and NSAIDs
examples of acute pain
bone pain, pain elicited by tissue injury, colicky pain, pressure pain
examples of Pathological (chronic) pain
Cancer pain
Low Back pain
Neuropathic Pain
Neuropathic pain is elicited by damage to what?
the PNS or CNS
Neuropathic pain is often resistant to what drug?
usual clinical doses of opioids
examples of neuropathic pain
post herpetic neuralgia
HIV-associated neuropathy
diabetic neuropathy
Complex regional Pain syndromes I and II
Areas of Pain transmission and modulation
Peripheral sites (NOCICEPTORS)

Spinal cord

Supraspinal: BRAIN
what was the classic picture of pain mechanism?
hard-wired, line labeled, modality-specific, single pathway
current model of pain
dynamic interlocking series of biological reactive mechanisms
Basic strategies of pain control
1) attenuation or blockade at the PERIPHERY
2) activation of inhibitory processes that "gate" pain at SPINAL CORD
3) Interference with PERCEPTION of pain
TRP Channels
are the heat and capsaicin sensitive receptors associated with nociceptive afferent endings

resemble voltage gated K+ or nucleotide-gated channels
what are the key mediators produced by peripheral tissues in response to injury?
How can pain be attenuated or blocked by intervention at the periphery?
regional analgesia
neural ablative procedures
Opioids (both Peripheral and CNS axns)
Prototypic Opioid "Gold standard of analgesia"
Opioid receptors:
-present in the periphery, spinal cord and brain
Mu: prototype agonist- Morphine
What interventions activate the inhibitory processes that "gate" pain at the spinal cord and brain?
Opioids, a-adrenergic agonists, TCAs, TENS, acupuncture
Role of perception in severity of pain
reaction to painful stimulus, more severe when told that stimulus will be more unpleasant
psychological factors rarely cause pain, but they may:
trigger or exacerbate a pain episode
contribute to the distress and disability experienced with chronic pain disroders
Interference with perception of pain might involved:
-complementary medicine, psychotherapy, hypnosis, relaxation techniques, biofeedback

-opioids "feel good effect" may contribute to interference

-Placebo effect
Celebrex and Vioxx are what type of analgesics?
Cox-2 inhibitors
Gabapentin (Neurontin), Pregabalin (Lyrica)
anticonvuslants, mainstays for a lot of neuropathic pain
Tramadol (Ultram)
has a ceiling effect, not great for severe pain, developed as weak opioid

works like tricyclic antidepressant to increase norepi
Spinal Cord Stimulators
-implanted where?
-work similarly to what?
implanted into epidural space

idea is similar to accupuncture, to stimulate large fibers to gate pain at spinal cord?