Exam (elaborations)
Rush - Advanced Pharmacology - NSG 531 - Exam 3 already graded A+ 2024/2025
- Course
- Institution
Rush - Advanced Pharmacology - NSG 531 - Exam 3 already graded A+ 2024/2025
[Show more]
Content preview
Rush - Advanced Pharmacology - NSG531 - Exam 3
what is the difference between cardiac myocyte action potential and that of the CNS or ANS? -
ANSnerve cell action potential is very short
cardiac action potential is much longer
they are longer to have adequate filling time in order to get a good contraction for a reasonable
bolus of blood
the only way this can happen is if the action potential is longer
this will also mean that the refractory period will be longer
What are the 5 phases of the non-pacemaker action potential? - ANS0 - depolarization
1 - partial repolarization
2 - plateau
3 - repolarization
4 - resting membrane potential
what happens during phase 0 of the non-pacemaker action potential - ANSdepolarization
voltage gated sodium channels are opening up until we get past threshold
what happens during phase 1 of the non-pacemaker action potential - ANSpartial repolarization
what happens during phase 2 of the non-pacemaker action potential - ANSplateau
calcium channels open (L-type because they are long)
potassium is still open
potassium out and calcium in - they are opposing each other in voltage giving the plateau
this is when the ventricles are filling
what happens during phase 3 of the non-pacemaker action potential - ANSrepolarization
calcium channels are closed
potassium channels are the only thing open taking their positive charge with them making the
interior more negative
what happens during phase 4 of the non-pacemaker action potential - ANSresting membrane
potential where we are in between action potentials there is no net change in ovltage inside the
cell
When does contraction take place? - ANSbegins towards the end of repolarization and ends at
some point during repolarization
,refractory period - ANSduring phase 0, 1, 2, and part of phase 3 the cell is refractory to the
initiation of new action potentials
many antiarrhythmic drugs increase the Refractory period which reduces myocyte excitability
what are the benefits of the refractory period - ANSlimits frequency of cardiac contractions
allows for adequate filling time
prevents sustained contractions
how are pacemaker cells different from non-pacemaker cell - ANSno resting membrane
potential - no point where it is flat
there are very few sodium channels in pacemaker - sodium channels are not driving
depolarization - calcium is
only 3 phases
comprised of cells within the SA node
generate regular, spontaneous action potentials
what are the phases of pacemaker action potential - ANS0 - rapid depolarization
3 - repolarization
4 - slow depolarization
what happens during phase 0 of the pacemaker action potential - ANSRapid depolarization
something is coming to open voltage gated calcium channels (L-type) calcium comes rushing in
what happens during phase 3 of the pacemaker action potential - ANSrepolarization
potassium channels now open up, potassium rushes out, repolarizes
what happens during phase 4 of the pacemaker action potential - ANSslow depolarization
with potassium rushing out we are all the way down at -60
funny sodium channels open up until voltage reaches -50
T-type (transient) calcium channels open up until voltage reaches -40
L-type calcium channels then open back up
Describe how non-pacemaker APs can mimic pacemkaer APs - ANSHypoxia and ischemia
when the resting membrane potential is not getting enough oxygen it is going to become more
positive because you need oxygen to produce ATP. If we are deficient in ATP then the NA K
ATPase pump wont be functioning
if someone is hypoxic in a focal area - say they have a resting membrane potential at -45 - the
fast sodium channels won't open - they start using calcium to open - so they would convert into
action potentials that use calcium (hence how they mimic pacemaker APs)
excitation-contraction coupling - ANSsequence of events from motor neuron signaling to a
skeletal muscle fiber to contraction of the fiber's sarcomeres
conversion of depolarizing currents into contractile force
, L-type calcium channels open up in phase 2 in nonpacemaker - calcium comes flooding into
myocytes, so we now have calcium in the cell and a sarcoplasmic recticulum (a resovior for
calcium)
receptors called RYR (ligand gated calcium channels)
calcium then comes out - coming int the cell from the calcium channels and the sarcoplasmic
recticulum
describe how calcium binds to cause contraction - ANSwhen there is an influx of calcium in the
cell there is a myosin head separated by troponin. little binding sites for the myosin exist on the
aktin but it can't get to it because of the troponin. calcium therefore binds to the tropinin causing
a confirmational change in troponin so it will move and take the tropomyosin with it. the myosin
can then bind to the aktin molecules when it binds it activates ATP
the ATP will be used to generate the sliding of the aktin and the myosin filaments against each
other shortening the muscle cell causing contraction
Describe how adrenergic stimulation increases the force of contraction through inotropic effects
- ANSNE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
leads to phosphorylation of Ca channels and opens them
increases inward movement of Ca
there is also increased release of Ca from the SR
increases actin/myosin interaction
increases force of contraction
Describe how adrenergic stimulation increases the force of contraction through chronotropic
effects - ANSNE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
results in phosphorylation of Ca2 channels and opens them
increases inward movement of Ca2
shortens phase 0 by increasing the opening of L-type calcium in pacemaker
heightened sympathetic state
shortens effective refractory period
increases rate of contraction
how do catecholamines effect the NaK ATPase Pump - ANSepi to beta 1 - g coupled protein
receptor
increase in cAMP
activate protein kinase
phosphorylate and increase in ATPase proteins available on the cell surface
this is why we give epi during hypoxia - cardiac arrest - so that we can initiate more action
potentials
how does cholinergic stimulation work to decrease heart rate - ANSeffects on m2 receptors
acetylcholine binds to g coupled, alpha subunit comes off
can bind to t-type calcium channel - opens after funny sodium and before L-type - if it binds it
will inhibit it which will decrease the heart rate
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller Ashley96. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for $9.99. You're not tied to anything after your purchase.
Can Stuvia be trusted?
4.6 stars on Google & Trustpilot (+1000 reviews)
85169 documents were sold in the last 30 days
Founded in 2010, the go-to place to buy study notes for 14 years now