DPT 6521 Pharmacology - Exam 2
what are the four main steps of neuronal regulation of physiology
1) transmission of action potential down axon
2) release of neurotransmitter from axon
3) binding of neurotransmitter to post-synaptic cell
4) post-synaptic cell changes action
list the ways medications can interfere with neuronal regulation of physiology
- alter axonal conduction (local anesthetics blocking ACh)
- alter synaptic transmission
- receptor agonism or antagonism
define agonist drug
- causes same effect as it occurs in nature --> receptor activation
define antagonist drug
- drug reduces or causes opposite effect --> receptor deactivation / blockade
list the steps in synaptic transmission
1) NT synthesis and storage vesicles
2) release of NT into cleft
3) post-synaptic receptor binding (reversible)
4) inactivation of NT (reuptake, enzymatic degradation, diffusion)
list agonist drug effects
- drug increases synthesis of NT molecules
- drug increases number of NT molecules by destroying degrading enzymes
- drug increases relay of NT molecules from terminal buttons
- drug binds to auto receptors and blocks their inhibitory effect on neurotransmitter release
,-drug binds to postsynaptic receptors and either activates them or increases the effect on the
neurotransmitter molecules
- drug blocks the deactivation of neurotransmitter molecules by blocking degradation or
reuptake
list antagonist drug effects
- drug blocks the synthesis of neurotransmitter molecules
- drug causes the neurotransmitter molecules to leak from the vesicles and be destroyed by
degrading enzymes
- drug activates autoreceptors and inhibits neurotransmitter release
- drug is a receptor blocker; it binds to the postsynaptic receptors and blocks the effect of the
neurotransmitter
list the central neurotransmitters
- acetylcholine (excitatory amino acid)
- norepinephrine (excitatory monoamine)
- glutamate (excitatory amino acid)
- aspartate (excitatory amino acid)
- substance P (excitatory peptide)
- enkephalins (excitatory peptide)
- dopamine (inhibitory monoamine)
- serotonin (inhibitory monoamine)
- GABA (inhibitory amino acid)
- glycine (inhibitory amino acid)
list the peripheral neurotransmitters
- acetylcholine
- catecholamines and monoamines (epinephrine and norepinephrine)
list some possible effects that drugs affecting the CNS can have
- affect movement (limit or cause involuntary)
- induce sleep or arousal, impact cognitive function
- treat anxiety, depression or other psychiatric conditions
- affect memory (positive and negatively)
- increase focus and attention
,what is the main problem for CNS drugs
- must cross blood brain barrier (BBB)
what is the function of the BBB
- effectively protects against passage of foreign substances into the brain
- prevents the entry of damaging and therapeutic substances
- barrier is achieved by structure and function of CNS capillaries (tight junctions and basement
membranes) --> impermeability
list general principles pertaining to crossing the BBB
- large molecules do not pass easily
- low lipid-soluble molecules do not pass BUT lipid soluble pass
- highly charged molecules do not pass easily
AKA we <3 small, non polar and lipid soluble drugs
how / when is the BBB affected and thereby allowing easier entry
- at birth b/c not fully formed
- post-radiation
- if infectious agents are present
- trauma, ischemia, inflammation
list the mechanism by which compounds are able to cross the BBB
- passive diffusion (for non-polar, lipid soluble drugs like morphine and ETOH)
- facilitated diffusion (glucose)
- active transport (carrier molecules used)
what is a transient ischemic attack (TIA)
- mini stroke, can occur without permanent damage
- could be due to bleeding in the brain, but more commonly due to blood clots
, list pharmacological interventions to decrease risk of future stroke post-TIA
- anti-platelet agents = aspirin (ASA) mono therapy; combo of aspirin and extended-release
dipyridamole; clopidogrel (Plavix) monotherapy
- works by ASA irreversibly acetylates COX-1 to prevent synthesis of TXA2, which is key to
platelet aggregation
what criteria must be considered for tPA administration
- time (3 hours), patient age and medical hx (BP, DWI-PWI) MRI
what is the affect of tPA
- produces local clot breakdown
list side effects of tPA
- hemorrhage, usually into region
- mild systemic bleeding (internal of GI or GU)
what should be monitored post tPA administration
- vascular system and neuro checks every 15 min for 2 hours, then every 30 min for 6 hours,
then every hour for 24 hours
- no other anticoags for 24 hours
- if you have decreased platelet aggregation, monitor due to increase risk of bleeding -->
consideration for PT intervention planning
discuss blood pressure control and management for patients post- ischemic stroke
recommendation = < 185/110
- preserve cerebral perfusion and minimize risk of bleed
list meds common post ischemic stroke responsible for BP control
(IV)
- labetalol (Trandate): alpha and beta blocker that blocks epinephrine)
- hydralazine (Apresoline): direct smooth muscle relaxation
what are the four main steps of neuronal regulation of physiology
1) transmission of action potential down axon
2) release of neurotransmitter from axon
3) binding of neurotransmitter to post-synaptic cell
4) post-synaptic cell changes action
list the ways medications can interfere with neuronal regulation of physiology
- alter axonal conduction (local anesthetics blocking ACh)
- alter synaptic transmission
- receptor agonism or antagonism
define agonist drug
- causes same effect as it occurs in nature --> receptor activation
define antagonist drug
- drug reduces or causes opposite effect --> receptor deactivation / blockade
list the steps in synaptic transmission
1) NT synthesis and storage vesicles
2) release of NT into cleft
3) post-synaptic receptor binding (reversible)
4) inactivation of NT (reuptake, enzymatic degradation, diffusion)
list agonist drug effects
- drug increases synthesis of NT molecules
- drug increases number of NT molecules by destroying degrading enzymes
- drug increases relay of NT molecules from terminal buttons
- drug binds to auto receptors and blocks their inhibitory effect on neurotransmitter release
,-drug binds to postsynaptic receptors and either activates them or increases the effect on the
neurotransmitter molecules
- drug blocks the deactivation of neurotransmitter molecules by blocking degradation or
reuptake
list antagonist drug effects
- drug blocks the synthesis of neurotransmitter molecules
- drug causes the neurotransmitter molecules to leak from the vesicles and be destroyed by
degrading enzymes
- drug activates autoreceptors and inhibits neurotransmitter release
- drug is a receptor blocker; it binds to the postsynaptic receptors and blocks the effect of the
neurotransmitter
list the central neurotransmitters
- acetylcholine (excitatory amino acid)
- norepinephrine (excitatory monoamine)
- glutamate (excitatory amino acid)
- aspartate (excitatory amino acid)
- substance P (excitatory peptide)
- enkephalins (excitatory peptide)
- dopamine (inhibitory monoamine)
- serotonin (inhibitory monoamine)
- GABA (inhibitory amino acid)
- glycine (inhibitory amino acid)
list the peripheral neurotransmitters
- acetylcholine
- catecholamines and monoamines (epinephrine and norepinephrine)
list some possible effects that drugs affecting the CNS can have
- affect movement (limit or cause involuntary)
- induce sleep or arousal, impact cognitive function
- treat anxiety, depression or other psychiatric conditions
- affect memory (positive and negatively)
- increase focus and attention
,what is the main problem for CNS drugs
- must cross blood brain barrier (BBB)
what is the function of the BBB
- effectively protects against passage of foreign substances into the brain
- prevents the entry of damaging and therapeutic substances
- barrier is achieved by structure and function of CNS capillaries (tight junctions and basement
membranes) --> impermeability
list general principles pertaining to crossing the BBB
- large molecules do not pass easily
- low lipid-soluble molecules do not pass BUT lipid soluble pass
- highly charged molecules do not pass easily
AKA we <3 small, non polar and lipid soluble drugs
how / when is the BBB affected and thereby allowing easier entry
- at birth b/c not fully formed
- post-radiation
- if infectious agents are present
- trauma, ischemia, inflammation
list the mechanism by which compounds are able to cross the BBB
- passive diffusion (for non-polar, lipid soluble drugs like morphine and ETOH)
- facilitated diffusion (glucose)
- active transport (carrier molecules used)
what is a transient ischemic attack (TIA)
- mini stroke, can occur without permanent damage
- could be due to bleeding in the brain, but more commonly due to blood clots
, list pharmacological interventions to decrease risk of future stroke post-TIA
- anti-platelet agents = aspirin (ASA) mono therapy; combo of aspirin and extended-release
dipyridamole; clopidogrel (Plavix) monotherapy
- works by ASA irreversibly acetylates COX-1 to prevent synthesis of TXA2, which is key to
platelet aggregation
what criteria must be considered for tPA administration
- time (3 hours), patient age and medical hx (BP, DWI-PWI) MRI
what is the affect of tPA
- produces local clot breakdown
list side effects of tPA
- hemorrhage, usually into region
- mild systemic bleeding (internal of GI or GU)
what should be monitored post tPA administration
- vascular system and neuro checks every 15 min for 2 hours, then every 30 min for 6 hours,
then every hour for 24 hours
- no other anticoags for 24 hours
- if you have decreased platelet aggregation, monitor due to increase risk of bleeding -->
consideration for PT intervention planning
discuss blood pressure control and management for patients post- ischemic stroke
recommendation = < 185/110
- preserve cerebral perfusion and minimize risk of bleed
list meds common post ischemic stroke responsible for BP control
(IV)
- labetalol (Trandate): alpha and beta blocker that blocks epinephrine)
- hydralazine (Apresoline): direct smooth muscle relaxation
