22241522
Beschreibung
Karteikarten von Evian Chai, aktualisiert more than 1 year ago
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Erstellt von Evian Chai
vor mehr als 4 Jahre
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| Frage | Antworten |
| Electrical signals transmit through the heart from the ....cardium to the ...cardium | Endocardium to Epicardium |
| What is the conduction pathway through the heart, starting from the SA node? | 1. SA node 2. Atrial systole 3. Atria 4. AV node 5. Bundle of His 6. Left/right bundle 7. Purkinje Fibers |
| Excitation Contraction coupling refers specifically to | events at the neuromuscular junction where a motor fibre excites a muscle cell |
| When an AP arrives at the T-tubule, which channels open? What happens after? | L-Type Ca2+ channels Ca2+ binds RyR receptors on sacroplasmic reticulum, Ca2+ release bu Sacro.retic, causing contraction |
| How is Ca2+ reuptaken? | Circle pump and Na+/Ca2+ exchanger |
| In the first phase of depolarisation in the pacemaker potential (SA node), why is depolarisation so slow? | 1. Lack of Na+ channels, so Ca2+ depolarises instead 3. Transient Ca2+ channels open first 4. Then L-type Ca2+ channels open (slower) 5. Delayed rectifier K+ channel also slows |
| What initiates spontaneous depolarisation in the SA node? | The funny currents, which are streams of Na+ that enable spontaneous depolarisation |
| What channel is responsible for depolarisation (phase 0) of Pacemaker potential? | L-type Ca2+ channels |
| What channel is responsible for repolarisation (phase 3) of Pacemaker potential? | Rectifier K+ channels |
| What causes depolarization (phase 0) of the ventricular action potential? | Opening of voltage gated Ca2+ channels |
| After depolarisation (phase 0) in the ventricular action potential, why is there a partial repolarisation? | Na+ channels close |
| After partial repolarisation (phase 1) in the ventricular action potential, why is there a plateau (phase 2)? | L type Ca2+ channels open, Ca2+ enters |
| What eventually causes repolarisation (phase 3) in the ventricular action potential? What is phase 4? | 1. K+ outward current 2. Resting membrane potential |
| What is the ventricular action potential? What is the unique feature about its shape and why is it important? | The spontaneous electrical activity in cardiac muscle cells It is longer with a plateau (300ms) to PREVENT tetany in cardiac muscle |
| What is the rate of distribution of AP in the heart determined by? (2) | 1. Membrane capacitance 2. Number of connexons |
| How does AP distribute through myocytes? | They are electrically coupled due to their intercalated discs Ions move through the connexons |
| How do ionotropic factors (eg. noradernaline, B agonist) affect HR? | They impact contractility |
| How does noradernaline affect HR? | Increases Ca2+, HR |
| How do B-adrenergic agonists impact HR? | Mimic SNS, increase HR |
| How does ischemia hypoxia impact the heart? | Lowers contractibility |
| What do chronotropic drugs do? What is an example of a sympathetic drug? What about examples of parasympathetic drugs? | Impact heart rate 1. Noradrenaline 2. Ach, B-blockers, Adenosine receptors |
| How do sympathetic chronotropic drugs increase HR? | Creates a steeper pacemaker potential by incresing adenylyl cyclase, which increases activity of K+, funny, and Ca2+ channels |
| What is the Staircase/Trepple Effect? | Increase in HR means less time to remove Ca2+, which in turn increases contractile force |
| How do parasympathetic chronotropic drugs decrease HR? | Create a flatter pacemaker potential by inhibiting adenylyl cyclase, which lowers K+/funny/Ca2+ channels |
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