A quiz reviewing the material for Quiz 3. Sympathomimetics, Calcium channel blockers, Antiarrhythmics
Acetylcholine
Norepinephrine
Epinephrine
Tyrosine
Acetylcholine
Norepinephrine
Epinephrine
Tyrosine
Dopamine
Norepinephrine
Epinephrine
Acetylcholine
Post-synaptic neurons
Pineal Body
Posterior Lobe of Pituitary
Synaptic Vessicles
Dopa
Phenylalanine
Norepinephrine
Epinephrine
N-methyltransferase
Dopamine B-Hydroxylase
DOPA decarboxylase
Dopamine does not directly turn into norepi… you’re missing a step.
Re-uptake
Diffusion from receptor sites
Irreversible protein binding
Enzyme degredation
Opening of an ion channel
Activation of a second messenger such as cAMP or inositol phosphate
Depolarization
All of above.
Vanillymandelic Acid
3,7-dicarboxyvandelic acid
Nelson-Mandelic Acid
4,6-Pheocomtic acid
Dopamine
Tyrosine
COMT
Phenylalanine
Mitochondria
Synaptic cleft
Synaptic Vessicles
Storage Vessicles
Decrease SVR
Vasoconstriction
Increase LV afterload
Increase arterial BP
Alpha 1
Alpha 2
Beta 1
Beta 2
Dopa-b hydroxylase
Tyrosine
Adenylate cyclase
COMT
Increase Contractility
Increase HR
Increase CO
Decreased SVR
Hypokalemia
Hypochloremia
Hyponatremia
None of above
Phenylephrine
Amphetamine
Isoproterenol
Dobutamine
Epinephrine
Dobutamine
Phenylephrine
Isoproterenol
Norepinephrine
Ephedrine
Phenylephrine
Epinephrine
Increased renal blood flow
Increase rate of phase IV depolarization
Bronchodilation
Increase cerebral perfusion pressure
1:1000 solution .1-.5 ml SQ/IM
0.05 -1mg IV
2-20 ug/min
Racemic inhalation 0.5 ml of 2.25% solution
10
5
100
20
Dysrhythmias
Renal Failure
COPD
Hypertensive ischemic heart disease
Alpha
Beta 1
Beta 2
All are equal
Increase myocardial O2 demand
Increase CO
Bradycardia
Increase Afterload
Phenylephrine
Dopamine
Dobutamine
Norepinephrine
2 mcg/kg/min
8 mcg/kg/min
15 mcg/kg/min
All of above
16 mcg/kg/min
24 mcg/kg/min
5 mcg/kg/min
16 mcg/kg/min
24 mcg/kg/min
5 mcg/kg/min
They are not metabolized by MAO or COMT
Higher degree of protein binding
Increase volume of distribution
All of above
Beta 2
Alpha 1
Beta 1
Alpha 2
Norepinephrine
Amphetamine
Ephedrine
Phenylephrine
Epinephrine
Amphetamine
Dopamine
Ephedrine
Increase MAC
Decrease MAC
No effect on MAC
Increase MAC
Decrease MAC
No Effect
Phenylephrine
Norepinephrine
Clonodine
Dopamine
Maintaining respiratory stability
Sedation
Reduces brain Noradrenergic Activity
Increase pt BP
It won’t effect it… only hepatic impairment will.
You will need to decrease the dose
You will need to increase the dose
Pt will be more prone to bradycardia and hypotension
Altered sympathetic nervous system activity
Venous Hypoxia
Myocardial Ischemia
Bradycardia
Repolarization to resting potential results from outward K current
Rapid phase of repolarization caused by inactivation of Na influx and activation of a transient outward K current
Voltage dependent Na channel opens and rapid sodium influx depolarizes cell
Plateau phase, characterized by low membrane conductance and the activation of slow inward Ca current
Outward K current is deactivated and an inward Na current reduces transmembrane potential
Repolarization to resting potential results from outward K current
Rapid phase of repolarization caused by inactivation of Na influx and activation of a transient outward K current
Voltage dependent Na channel opens and rapid sodium influx depolarizes cell
Plateau phase, characterized by low membrane conductance and the activation of slow inward Ca current
Outward K current is deactivated and an inward Na current reduces transmembrane potential
Repolarization to resting potential results from outward K current
Rapid phase of repolarization caused by inactivation of Na influx and activation of a transient outward K current
Voltage dependent Na channel opens and rapid sodium influx depolarizes cell
Plateau phase, characterized by low membrane conductance and the activation of slow inward Ca current
Outward K current is deactivated and an inward Na current reduces transmembrane potential
Repolarization to resting potential results from outward K current
Rapid phase of repolarization caused by inactivation of Na influx and activation of a transient outward K current
Voltage dependent Na channel opens and rapid sodium influx depolarizes cell
Plateau phase, characterized by low membrane conductance and the activation of slow inward Ca current
Outward K current is deactivated and an inward Na current reduces transmembrane potential
Repolarization to resting potential results from outward K current
Rapid phase of repolarization caused by inactivation of Na influx and activation of a transient outward K current
Voltage dependent Na channel opens and rapid sodium influx depolarizes cell
Plateau phase, characterized by low membrane conductance and the activation of slow inward Ca current
Outward K current is deactivated and an inward Na current reduces transmembrane potentialt
By antagonizing adrenergic receptors
Through blockade of Na channels.
By blocking the slow inward calcium driven current
By prolonging repolarization
By antagonizing adrenergic receptors
Through blockade of Na channels.
By blocking the slow inward calcium driven current
By prolonging repolarization
By antagonizing adrenergic receptors
Through blockade of Na channels.
By blocking the slow inward calcium driven current
By prolonging repolarization
By antagonizing adrenergic receptors
Through blockade of Na channels.
By blocking the slow inward calcium driven current
By prolonging repolarization
Calcium, Magnesium
Potassium, Sodium
Magnesium, Calcium
Sodium, Potassium
Class IB
Class IA
Class IC
All the above have profound effects upon Phase O depolarization.
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