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Health Studies > reza last quiz > Flashcards

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
Q

ROS leads to?

A

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
Q

during myocardial ischemia or metabolic inhibition leads to decrease ATP levels, cells become acidic with ____

A

increase lactate levels, phosphate and magnesium

27
Q

decrease ATP levels and increase phosphate levels inhibit ____ leading to intracellular NA+ accumulation

A

Na+/K+ ATPase activity

28
Q

increase late Na+ currents contributes to increase intracellular sodium during ____

A

myocardial ischemia and heart failure

29
Q

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 ____

A

calcium overload

30
Q

The activity SR calcium:
-uptake: ___
-release:____

A
  1. through SERCA
  2. through RyR2
    *both are inhibited by myocardial ischemia
31
Q

_____: RyR2 is released from inhibition, producing spontaneous waves of calcium release

A

reperfusion or reoxygenation

32
Q

in a failing heart: ___glucose utilization to ATP production, this change is not matched with increase pyruvate oxidation in mitochondria

A

increase

33
Q

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

A

ketone bodies

34
Q

shuttling high energy phosphates via ___ is impaired in heart failure

A

creatine shuttle

35
Q

decrease in fatty acid oxidation is explained by the activation of hypoxia inducible factor Ialpha (HIF1alpha) PPAR gamma signaling axis which impairs ____

A

FA transport into mitcohndria and downregulated Fa oxidative

36
Q

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 ___

A

decrease in FA utilization

37
Q

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 ____

A

1.increase circulating free fatty acids
2. increase lipolysis and circulating fatty acids

38
Q

carnitine is a derivative of ____
-the main source is from the diet but it can be synthesized by liver and kidneys

A

lysine

39
Q

____ is caused by strict vegan diets, defects in hepatic synthesis of carnitine, defects in carntine uptake from blood stream or defects in renal reabsorption

A

primary carnitine deficiency

40
Q

what are symptoms primary carntine deficiency?

A

mild muscle cramping, severe muscle weakness and death

41
Q

____ its genetic, found in cardiac and skeltal muscle, leads to cardiomyopathy and myoglobinuria followed by prolonged exercise

A

carnitine palmitoyltransferase II deficiency (CPT II)

42
Q

____ in liver are rare and lethal at young age

A

CPT I or acylcarnitine translocase (CACT) deficiency

43
Q

In a diabetic heart, ATP production is reliant on _____

A

FA oxidation

44
Q

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

A

futile cycling

45
Q

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?

A

free coA and Fatty acid anions

46
Q

diabetes:
mitochondria can ____ regenerate acyl-coa, the fatty acid anion is proposed to be exported to cytosolic compartment by transport function of UCPs

A

NOT

47
Q

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: ___

A
  1. function of UCPs
  2. acyl-CoA synthase
  3. consumes 2 ATP as it releases AMP and PPi, not generate ADP
48
Q

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.

A
  1. 30%
  2. ATP dependent re-esterification
49
Q

diabetes:
futile cycling from these routes results in?

A

decrease cardiac efficiency by decrease efficiency of converting ATP hydrolysis to contraction when increase fatty acid utilization

50
Q

treatments for heart failure regarding ____, ___ and ____

A

ROS, glycolysis and fatty acid oxidation

51
Q

what are the treatment options for heart failure are?

A

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
Q

what is the target of B-blockers?

A

cardiac metabolism by inhibiting CPT 1 activity

53
Q

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

A

B-blockers

54
Q

ace inhibitors and angiotensin receptor blockers
-ang II damages mitochondria in failing heart thru generation of ____
-ang II reduces?

A
  1. ROS
  2. glucose oxidation, acetylcoa and ATP by upregulating PDK expression
55
Q

sodium glucose transport protein 2 (SGLT2) inhibitor
-pts with ___and ___ benefit from this medication
-SGLT2 inhibitors improve cardiac function by ______

A
  1. type 2 diabetes and heart failure
  2. increasing ketones, free fatty acids and BCAA
56
Q

what medication?
-shifts myocardial metabolism from FAO to glucose oxidation

A

inhibition of long chain 3-ketoacyl coa

57
Q

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

A

malonyl-coa decarboxylase (MCD) inhibitors

Health Studies (8 decks)

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