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32 Cards in this Set
- Front
- Back
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How does the sympathetic system work to increase HR |
NA released - increase Na conductance - increases pacemaker potential If up I ca. Up - increases force of contraction Ik - delayed rectifier up shortens AP faster HR |
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What is If |
Funny current - the net current inward HCN channel |
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Gq |
PLC PIP2 - IP3 + DaG IP3 - Ca+ |
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GI |
Inhibits adenylyl cyclase No Camp produced |
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What neurotransmitter is released by the parasympathetic system |
Ach |
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What does Ach activate to slow HR |
Inwardly rectifying K+ channel (Gi coupled/ muscarinic) Girks |
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How does atropine work |
Stops Vegal slowing of HR |
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Why is it important that the muscarinic receptor is Gi |
It’s stops production of Camp and hence Ca and contractility |
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Why is voltage after hyperpolarization more negative than at rest |
Both inwardly rectifying K+ and delayed rectifiers are open (increased k+ permeability) makes cell more negative Decreased Na permeability |
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What’s the ERP |
The effective refractory period |
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Why is the ERP important in cardiomyocytes |
It prevents extra action potentials starting new heart beats - (arrythmias) |
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What’s a T tubule |
An invagination of the plasma membrane into myocyte found adjacent to SR |
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Purpose of t tubules |
So membrane currents can be near contractile machinery. Depolarisation in T tubule detected by terminal cisterna |
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What’s the terminal cisternae |
Enlarged area of ST specialised for storing and releasing calcium |
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What’s a triad |
1 T tubule surrounded by terminal cisternae |
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What are sodium channels on the cell membrane called |
DHPR |
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What are the calcium channels on the SR |
RYR |
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What’s SERCA |
A ca channel in membrane of SR that pumps calcium back into SR using ATP |
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What is calcium overload |
Excessive intracellular calcium - May cause ectopic beats/ arrhythmias |
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What can cause calcium overload |
Sympathetic drive |
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Name a calcium channel blocker that works on blood vessels (name it’s channel) |
Amlodipine DHPR |
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When to use calcium channel blockers for heart |
Angina and arrhythmias (NOT HF) |
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Which calcium channel blocker is most likely to be used as an antianginal |
Diltiazem |
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Which calcium channel blocker is most likely to be used as an antiarrhythmic |
Verapamil |
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How does verapamil work |
Slows conduction through AV node |
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Why is diltiazem used more as an antianginal |
It blocks both heart and vessel channels (vaso dilates coronary arteries and slows nodal rate) |
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What’s digoxin |
A cardiac glycoside which increases stroke volume and contractility (used HF - only improves symptoms not mortality) |
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Best treatment for heart failure |
Beta blockers |
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How does endothelium control vascular tone |
Release of NO Bradykinin |
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Describe activation of contraction in SM cells |
Myosin must be phosphorylated by MLCK MLCK is activates by calmodulin |
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What causes relaxation in SM cells |
Phosphatase activated by NO cascade No- gyaunyl cyclase- cGMP- PKG -inactivation of MLCK |
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Effects of Bradykinin |
Loosens capillaries Constructs bronchi/ GI tract muscles Also the factor which causes dry cough with ACE inhibitors |
