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reza last quiz Flashcards

1
Q

what is the phase?
____: begins with the activation of Na+ channels, leading to rapid depolarization.

A

phase 0

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2
Q

what is the phase?
___: followed by inward repolarizing OUTward K+ currents, forming the notch of the AP waveform

A

Phase 1

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3
Q

what is the phase?
___: the balance between Inward L-type Ca2+ current and OUTward delayed rectifier K+ contributes to the plateau

A

phase 2

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4
Q

what is the phase?
___:outward delayed rectifier K+ currents continue to repolarize the membrane potential and the INwardly rectifying K+ currents contribute to later part of phase ___ repolarization

A

phase 3

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5
Q

what is the phase?
____: the INwardly recitifying K+ currents contributes to the maintenance of resting membrane potential

A

phase 4

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6
Q

during the AP Ca2+ influx via leak triggers the release of Ca2+ ions from the ____

A

sarcoplasmic reticulum

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7
Q

diastolic phase; sarcoplasmic reticulum/endoplasmic reticulum Ca2+ ATPase (___) retrices cytosolic Ca2+ to SR and Na+/Ca2+ exchanger (____) extrudes Ca2+ from the cell, bringing cytosolic calcium back to baseline

A

SERCA; NCX

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8
Q

Sarcolemmal KATP channels (SARKATP) is gated by?

A

intracellular ATP/ADP and acidosis

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9
Q

Sarcolemmal KATP channels (SARKATP) roles?

A

regulating cellular metabolism and electrophysiological responses to metabolic and oxidative stress

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10
Q

____: consumes ATP to pump Na+ outside of cell in exchange for K+, this is critical for maintenance of Na+ and K+ gradients across plasma membrane

A

Na/K ATPase

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11
Q

____: indicates connexin 43

A

Cx43

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12
Q

ATP production in heart tissue:
-greater than 90% of ATP is produced in cardiac myocytes is supplied by the ______
-remainder comes from ____

A
  1. mitochondria via oxidative phosphorylation
  2. glycolysis and GTP from the TCA cycle
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13
Q

In a healthy adult myocardium:
-60% to 90% of acetyl coa comes from ___
-10%-40% comes from oxidation of pyruvate from ____

A
  1. B-oxidation of fatty acids
  2. glycolysis and lactate oxidation
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14
Q

majority of cardiac ATP is consumed by ____

A

myofilaments

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15
Q

25% of cardiac ATP hydrolysis is used to fuel ____ and ___
-the mismatch between ATP supply and use can disrupt the cardiac rhythm through decrease energy supply to these channels and transporter

A

ion channels and transporters

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16
Q

mitochondrial ETC efficiency is impaired under myocardial ischemia and heart failure resulting in _____

A

increase electron leak and ROS production

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17
Q

Mitochondrial ROS induced ROS release: accumulating ROS levels trigger the opening of mitochondrial channels, mitochondrial permeability transition pore (PTP) and inner membrane anion channel (IMAC), leading to depolarization of delta psim and _____

A

increase ROS production

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18
Q

______: is nonselective channel residing on the inner mitochondrial membrane

A

mitochondrial permeability transition pore (PTP)

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19
Q

PTP opens from?

A

increase matrix calcium, increase ROS, increase phosphate levels, and by decrease adenine nucleotides ADP or ATP

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20
Q

ROS in cardiac myocytes:
____: superoxide and hydroxyl radicals

A

radical forms

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21
Q

ROS in cardiac myocytes:
___: hydrogen peroxide, hypochlorite, nitric oxide and peroxynitrite

A

nonradical forms

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22
Q

what are the main sources of ROS in cardiac myocytes?

A

NADPH oxidases, Xantine oxidase, nitric oxide synthase (NOS), and mitchondria

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23
Q

Excessive ROS causes damage ETC complex ___, impairing ATP generation and aggravate electron leakage

A

I, II, IV and ATP synthase

24
Q

oxygen activates mitochondrial uncoupling proteins, resulting in ___

A

increase electron leak and uncoupled oxygen consumption from ATP synthesis

25
ROS leads to?
abnormal electric function directly by ROS-mediated signaling and oxidative damage, as well as indirectly decrease ATP generation that is required for normal ion channel/transporters functions
26
during myocardial ischemia or metabolic inhibition leads to decrease ATP levels, cells become acidic with ____
increase lactate levels, phosphate and magnesium
27
decrease ATP levels and increase phosphate levels inhibit ____ leading to intracellular NA+ accumulation
Na+/K+ ATPase activity
28
increase late Na+ currents contributes to increase intracellular sodium during ____
myocardial ischemia and heart failure
29
increase intracellular sodium leads to increase cytosolic calcium, through decrease extrusion of calcium or through actual calcium entry with NCX activity in reverse mode (sodium out and calcium in) causing ____
calcium overload
30
The activity SR calcium: -uptake: ___ -release:____
1. through SERCA 2. through RyR2 *both are inhibited by myocardial ischemia
31
_____: RyR2 is released from inhibition, producing spontaneous waves of calcium release
reperfusion or reoxygenation
32
in a failing heart: ___glucose utilization to ATP production, this change is not matched with increase pyruvate oxidation in mitochondria
increase
33
In a failing myocardium: ___are a more relevant source of energy, the associated decrease in fatty acid oxidation is not matched with decrease in fatty acid uptake resulting in accumulation of toxic lipid intermediates
ketone bodies
34
shuttling high energy phosphates via ___ is impaired in heart failure
creatine shuttle
35
decrease in fatty acid oxidation is explained by the activation of hypoxia inducible factor Ialpha (HIF1alpha) PPAR gamma signaling axis which impairs ____
FA transport into mitcohndria and downregulated Fa oxidative
36
shift towards glucose oxidation is beneficial because of its high energetic efficiency than that FA oxidation in end stage heart failure, this shift is unlikely to compensate fully for ___
decrease in FA utilization
37
How diabetes affect cellular metabolism causing heart failure: -main contributers to the accelerated cardiac fatty acid flux in diabetes ____ -increase in circulating free fatty acids is due to insulin resistance in adipose tissue, which ____
1.increase circulating free fatty acids 2. increase lipolysis and circulating fatty acids
38
carnitine is a derivative of ____ -the main source is from the diet but it can be synthesized by liver and kidneys
lysine
39
____ is caused by strict vegan diets, defects in hepatic synthesis of carnitine, defects in carntine uptake from blood stream or defects in renal reabsorption
primary carnitine deficiency
40
what are symptoms primary carntine deficiency?
mild muscle cramping, severe muscle weakness and death
41
____ its genetic, found in cardiac and skeltal muscle, leads to cardiomyopathy and myoglobinuria followed by prolonged exercise
carnitine palmitoyltransferase II deficiency (CPT II)
42
____ in liver are rare and lethal at young age
CPT I or acylcarnitine translocase (CACT) deficiency
43
In a diabetic heart, ATP production is reliant on _____
FA oxidation
44
Diabetes: uncoupling protein upregulation leads to export of fatty acid anions from the mitochondrial matrix this effect contributes to ____ of fatty acid intermediates and hence ATP wasting in presence of increase FA oxidation
futile cycling
45
Diabetes: when fatty acyl coa to mitochondria exceeds capacity to utilize it via fatty acid beta oxidation mitochondrial thioesterase enzymes can hydrolyze surplus fatty acyl-coa yielding?
free coA and Fatty acid anions
46
diabetes: mitochondria can ____ regenerate acyl-coa, the fatty acid anion is proposed to be exported to cytosolic compartment by transport function of UCPs
NOT
47
Diabetes: ____: in conjunction with mitochondrial thioesterase may protect against accumulation of harmful Fatty acid anions in the matrix, as well as preventing depletion of matrix coA -this is associated with ATP wasting effect as the exported Fatty acid anion requires activation/esterification prior to furthur metabolism -require: ___ -RXN: ___
1. function of UCPs 2. acyl-CoA synthase 3. consumes 2 ATP as it releases AMP and PPi, not generate ADP
48
diabetes: fatty acid can also cycle between acyl-coa moietes and intracellular triacylglycerol -this cycling accounts for ___ of total cellular energy expenditure -requires ______ of fatty acid liberated from triacylglycerol pool prior to B-oxidation or reincorporation into triacyclglycerol pool.
1. 30% 2. ATP dependent re-esterification
49
diabetes: futile cycling from these routes results in?
decrease cardiac efficiency by decrease efficiency of converting ATP hydrolysis to contraction when increase fatty acid utilization
50
treatments for heart failure regarding ____, ___ and ____
ROS, glycolysis and fatty acid oxidation
51
what are the treatment options for heart failure are?
beta blockers, ace inhibitors and angiotensin receptor blockers, sodium glucose transpport protein 2 (SGLT2) inhibitor, inhibition of long chain 3-ketoacyl coA, malonyl-coa decarboxylase (MCD) inhibitors
52
what is the target of B-blockers?
cardiac metabolism by inhibiting CPT 1 activity
53
what medication? -results in increase glucose oxidation and more efficient oxygen use for ATP production -other findings: have been found to inhibit fatty acid oxidation, which is beneficial in failing heart as shifting from fatty acid oxidation to glucose oxidation is more oxygen efficient
B-blockers
54
ace inhibitors and angiotensin receptor blockers -ang II damages mitochondria in failing heart thru generation of ____ -ang II reduces?
1. ROS 2. glucose oxidation, acetylcoa and ATP by upregulating PDK expression
55
sodium glucose transport protein 2 (SGLT2) inhibitor -pts with ___and ___ benefit from this medication -SGLT2 inhibitors improve cardiac function by ______
1. type 2 diabetes and heart failure 2. increasing ketones, free fatty acids and BCAA
56
what medication? -shifts myocardial metabolism from FAO to glucose oxidation
inhibition of long chain 3-ketoacyl coa
57
what medication? -works by increasing cardiac malonyl coa levels leading to inhibition of CPT 1, resulting in reduced mitochondrial fatty acid uptake and favoring glucose oxidation pathways -not available on market
malonyl-coa decarboxylase (MCD) inhibitors

Health Studies (8 decks)

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