DSF Cardio

Question 1

Long QT Syndrome

Answer 1

“Channelopathy”
Most commonly results from a loss-of-function mutation involving a K+ channel gene.
Prolong myocyte repolarization, leaving myocytes vulnerable to early after-depolarizations - can induce ventricular arrythmias and sudden death.

Question 2

Excitation-Contraction coupling

Answer 2

Ca2+ induced Ca2+ release
Involves the conduction of Ca2+ ions into the cell triggering further release of Ca2+ into the cytoplasm.
About 75% of Ca2+ present in the cytoplasm during contraction is released from the SR (via RyR).
Ca2+ drives contraction

Question 3

SERCA pumps (SR Ca2+ ATPase)

Answer 3

Pumps Ca2+ from cytoplasm back into SR

Question 4

Digoxin

Answer 4

Cardiac glycoside
Inhibit Na+-K+ pump, which results in intracellular Na+ accumulation
Also increases cardiac contractility by retaining Ca2+

Question 5

Catecholamines

Answer 5

Through beta receptor activity, can enhance cardiac contractility by phosphorylation (b/c cause increased cAMP)

Question 6

Phosphorylation of phospholamban

Answer 6

causes SERCA to pump more Ca2+ in the SR

Question 7

Troponin

Answer 7

Essential for cardiac contractility

Phosphorylation of troponin I decreases its Ca2+ affinity , causing the muscle to relax faster

Question 8

What 3 factors determine stroke volume (SV)?

Answer 8

Preload
Afterload
Contractility

Question 9

What regulates arteriolar tone?

What do the arterioles control?

Answer 9

Arterial tone regulated by: 
Local agents (autoregulation)**** (most important determinant of local blood flow)
Direct innervation (autonomics)
Circulating catecholamines/hormones
Arterioles control: SVR

Question 10

Autoregulation

Answer 10

Refers to the balance of supply/demand driven by the tissue itself
Vasodilator theory
O2 lack theory