Pharmacology Flashcards
Are pre- and/or post-gangionic neurons myelinated?
Pre-ganglionic are myelinated, post ganglionic are not
In general, where is the gangion and synapse located for the parasympathetic vs. sympathetic nervous systems
Parasympathetic: near the effector tissue Sympathetic: in the sympathetic chain, near the spinal cord
What are the 3 tissue types controlled by the autonomic nervous system?
- Cardiac tissue (muscle, nodes, and conduction system) 2. smooth muscle 3. glands
Contrast miosis and mydriasis. What autonomic nervous system causes each?
Miosis: pupil constriction due to contraction of the sphincter muscle, caused by parasymathetic innervation Mydriasis: pupil dialation due to contraction of the radial muscle, caused by sympathetic innervation
What are the neurotransmitters associated with the pre- and post-ganglionic synapses of the parasympathetic vs. sympathetic nervous systems?
Pre-ganglionic: ACh for both para and symp Post-ganglionic: ACh for para, Epinephrine and Norepinephrine for symp
Contrast the parasympathetic and sympathetic effects on blood vessel dilation/constriction.
Parasympathetic: weak (not significant) dilation Sympathetic: strong constriction to unnecessary tissues (skin and GI), dialation to liver and skeletal muscle
Name the peptides that sometimes coexist with ACh and NE in their respective post-ganglionic nerves.
Vasoactive intestinal peptide with ACh in parasympathetic Neuropeptide Y with NE in sympathetic
Where is ACh synthesized?
in the pre-synaptic terminal (Extra detail: after ACh is broken down in the synapse by AChE, the choline is transported back into the pre-synaptic neuron so it can be used to make more ACh.)
Where in a cholinergic synapse are nicotinic and muscarinic receptors found (if present)?
On the post-synaptic neuron
Identify the excitatory and inhibitory muscarinic receptors and contrast their effects.
M1, M3, M5: excitatory; stimulate IP3 and eventually increase intracellular Ca++ M2, M4: inhibitory; decrease cAMP, open K+ channels (hyperpolarizes the cell)
Name the 5 important molecules in the catecholamine synthesis pathway.
- tyrosine 2. L-dopa 3. dopamine 4. norepinephrine 5. epinephrine (last step only happens in adrenal medulla)
Identify the two types of nicotinic receptors, where they are found, and their general effects.
nAChRn (autonomic gangia - N for nerve) nAChRm (skeletal muscle - M for muscle) They cause stimulation and then blockade of their end tissue
What is the most important mechanism for termination of the action of NE?
Reuptake from the junctional space into the pre-synaptic nerve and storage vessels (requires ATP and Mg^2+) - Drugs like cocaine, tricyclic antidepressants, & methylphenidate inhibit this. (Impt exception: in blood vessels, excess NE is broken down by enzymes and/or diffused away.)
Describe the mechanism of reuptake blockers, and give examples (3).
They block reuptake of NE from the synpase (keeps stimulating the post-synaptic neuron) e.g.: cocaine, tricyclic antidepressants, methylphenidate
What class of drugs includes cocaine and methylphenidate?
Indirect acting sympathomimetic amines
What is the function of enzymes such as monoamine oxidase (in mitochondria) and catechol-O-methyl transferase (in cytoplasm)
Breaks down catecholamines (like NE) in synapse to terminate the effects.
what heart rate represents tachycardia? bradycardia?
tachy: 100
brady: 60
what effect do catecholamines have on action potential velocity?
increases action potential velocity. catecholamines include epinephrine and norepinephrine.
what arrhythmia is depicted here?
premature atrial contraction: the wave are normal but there is less distance between waves two and three
what arrhythmia is seen here?
supraventricular tachycardia the waves are regular but close together, really fast
what arrhythmia is seen here?
Accessory Pathway tachycardia: the delta wave is seen here which indicates that the signal has found another route to excite the ventricles before the normal path (example: WPW)
what arrhythmia is seen here?
Atrial tachycardia: there is a decreased PR interval
what arrhythmia is seen here?
atrial fibrillation: the QRS complex looks normal but there is no distinct P wave because there are too many atrial impulses
what arrhythmia is seen here?
atrial flutter: re-entry circuit that circulates in the atrium shows rapid, back-to-back atrial depolarization waves (ex. “saw-tooth” appearance)
what arrhythmia is seen here?
ventricular tachycardia: the ventricles are contracting too often so they can’t fill up all the way. therefore this lowers cardiac output.
what arrhythmia is seen here?
ventricular fibrillation with big coarse waves and small, frequent fine waves: the QRS is rapid and indistinguishable.
what is happening during ventricular fibrillation? what is the immediate treatment?
the ventricles are quivering and can’t pump enough blood to the body
CPR and defibrillate
what part of the cardiac cycle does long QT sydrome delay? what dangerous ECG pathology can this lead to?
delays repolarization. this can lead to Torsades de Pointes which can lead to ventricular tachycardia and death
whatare the three requirements for re-entry?
- unidirectioncal conduction block
- conduction time slows so the refractory tissue can recover (while other tissue is still depolarizing)
- adjacent cardiac tissue with many parallel pathways and different refractory periods
what arrhythmia is seen here?
bradycardia: distance between R peaks is extended (Hr approx 50)
what arrhythmia is seen here?
First degree heart block: fixed long PR interval
what arrhythmia is seen here?
second degree heart block type 1 (Wenckenbach): PR interval continues to get larger and larger and then the QRS is dropped
what arrhythmia is seen here?
2:1 Mobitz type 2: the PR interval is stable and the P wave arrives regularly. For every two normal beats, 1 QRS complex is dropped.
what arrhythmia is seen here?
third degree heart block: the P, QRS and T are all out of synchronization
