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Winter P2 > Exam 2 - Medchem 753, Cardio Kioussi > Flashcards

Exam 2 - Medchem 753, Cardio Kioussi Flashcards

1
Q

What is the leading killer in the US?

A

CVD, 50% of all deaths

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2
Q

Describe blood flow through the hearts chambers/valves

A
  1. Blood enters from superior vena cava/Inferior vena cava and enters into the right atrium. 2. Blood travels through the Tricupsid valve into the Right Ventricle. 3. Blood flows from right Ventricle through pulmonary valve to the Pulmonary artery 4. Blood flows from pulmonary artery to Lungs to Pulmonary veins 5. Blood flow from pulmonary veins into Left Atrium 6. Blood flows from left atrium through mitral (bicuspid) valve to the Left Ventricle. 7. Blood flows from Left ventricle through aortic valve into Aorta.
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3
Q

What outer fibrous layer surrounds the pericardial cavity? What is composed of?

A

The Parietal Pericardium - Areolar tissue - Epithelium - Dense fibrous layer

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4
Q

What is the space inside the parietal pericardium called?

A

Pericardial cavity

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5
Q

What is the layer deep to the pericardial cavity? What is it composed of?

A

Epicardium - Epithelium - Areolar tissue

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6
Q

What resides between the Epicardium and Endocardium?

A

Myocardium (Cardiac muscle tissue)

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7
Q

What is the innermost layer of the heart? What is it composed of?

A

Endocardium

  • Areolar Tissue
  • Endothelium
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8
Q

What are the fusions between cardiac muscle cells?

A

Intercalated disks

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9
Q

What is the role of gap junctions in cardiac muscle?

A

They allow electrical signals to pass rapidly form cell to cell

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10
Q

What are microfibrils?

A

Bundle of protein filaments

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11
Q

What fraction of cell volume do mitochondria occupy on a contractile cardiac fiber?

A

1/3

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12
Q

What is the function of Intercalated disks? What components allow them this function?

A

They allow the synchronized contraction of cardiac cells. They contain desmosomes that transfer force from cell to cell, and fasciae adherens which are ribbon like junctions stabilize the muscle

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13
Q

What two areas of the heart can initiate electrical activity?

A

Sinoatrial Node

Atrioventricular Node

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14
Q

What Node begins electrical activity of the heart?

A

Sinoatrial Node (pace maker)

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15
Q

What transmits electrical signal from SA node to AV node?

A

The internodal tract

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16
Q

Where can the electrical signal from the SA node also be sent?

A

To the Atria via Bachmann’s bundle, allows simultaneous depolarization of the atrias

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17
Q

What is the role of Purkinje Fibers?

A

to send nerve impulses to the cells in the ventricles of the heart and cause them to contract and pump blood either to the lungs or the rest of the body.

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18
Q

How is the electrical signal from the AV node directed?

A

It is directed towards the apex by the bundle branches, before coming back around by the way of the conduction pathways

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19
Q

Channel in which gates randomly alternate between open and closed positions

A

Leakage Channels

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20
Q

Channel in which they open in response to change in membrane potential

A

Voltage gated channels

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21
Q

Channels which open and close in response to specific chemical stimuli

A

Ligand Gated channels

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22
Q

Channels which open or close in response to mechanical action such as sensory receptors

A

Mechanically gated channels

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23
Q

Stages of Atrial/Ventricular Action Potential

A

4 - Resting Membrane (K leaks out)

0 - Threshold reached, Voltage gated Na open and sodium rushes in (Depolarizes)

1 - Sodium channels close, Voltage gated potassium channels open and potassium leaves cell (Repolarizes)

2 - Voltage gated Ca open and keeps the AP from rapidly repolarizing.

3 - Voltage gated Ca close, and cell begins to repolarize back to resting potential

4 - Voltage gated K close, Resting membrane.

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24
Q

What allows the depolarizing current to travel from contractile or autorhythmic cells?

A

Gap Junctions

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25
Q

Once a depolarizing current has entered a contractile cell, how does it travel along the cell?

A

The Plasma Membrane and T tubules

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26
Q

What happens once Ca channels on the plasma membrane and SR open?

A

The Ca influx induces Ca release from the SR

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27
Q

How do myosin-binding sites become exposed?

A

Ca binds to troponin, which causes tropomysin to pull and expose the myosin binding sites

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28
Q

Once muscle fiber contraction finishes, what happens to calcium?

A

Ca is actively transported back into SR and ECF

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29
Q

Once Ca leaves the SR and muscle fibers, what happens to the muscle fiber?

A

Tropomyosin reblocks myosin binding site and muscle fiber relaxes

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30
Q

Describe the phases of nodal action potential

A

4 - Spontaenous depolarization of pacemaker potential

0 - Depolarization phase continues, increase of Ca conductance

3 - Repolarization occurs, K channels open and L type Ca channels inactivate, (decline is long lasting)

4 - Spontaneous depolarization of pacemaker potential occurs

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31
Q

How does the Ventricular Action potential compare to the atrium’s action potential?

A

The Ventricle Action potential is longer lasting than the Atrium

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32
Q
A
33
Q

What is the difference in membrane potential between Contractile myocardium and Autorhytmic myocardium?

A

Contractile = Stable @ -90mV

Autorhythmic = @ -60mV

34
Q

What is the difference in events that lead to threshold potential in Contractile myocardium and Auto-rhythmic myocardium?

A

Contracile - Depolarization enters through gap junctions

Auto-Rhythmic - Na entry through If channel, and is reinforced by Ca entry

35
Q

What is responsible for the rising phase of the action potential in contractile myocardium vs Autorhthmic myocardium?

A

Contractile - Na entry

Autorhythmic - Ca entry

36
Q

What is responsible for the repolarization phase in Contractile myocardium vs Autorhymic myocardium?

A

Contractile - Extended plateau caused by Ca entry, and rapid phase caused by K efflux

Auto-rhythmic - Rapid repolarization by K efflux

37
Q

What is the difference in the duration of the action potential in Contractile myocardium vs the autorhythmic myocardium?

A

Contractile - 200ms (extended)

Autorhythmic - ~150ms (variable)

38
Q

What is the difference in the refractory period between Contracile Myocardium vs Autorhythmic myocardium?

A

Contracile - long refractory period in which restting Na channels gates are delayed until the end of the AP

Autorhythmic - No refractory period

39
Q

What electrical event is responsible for the P wave of an EKG?

A

Sinoatrial node depolarization

40
Q

What electrical event is responsible for the QRS complex of an EKG?

A

Ventricular Repolarization

41
Q

What electrical event is responsible for the T wave on an EKG?

A

Ventricular repolarization

42
Q

What electrical event is responsible for tthe ST segment on an EKG?

A

The segment is seen due to the period during ventricular depolarization (plateau)

43
Q

What event is responsible for the small u wave following the T wave on an EKG?

A

It is seen due to repolarization of the papillary muscle

44
Q

What is the significance of the P-R interval?

A

It is the time taken from the first atrial depolarization to the first ventricular depolarization

45
Q

What is the Q wave on an EKG?

A

The first downward deflection of the QRS, and may or may not be present/visible on an EKG

46
Q

According to the Wiggers Diagram, when does ventricular pressure become greatest?

A

During Systole, prior to ejection into aorta

47
Q

What happens when there is a change in the electrical activity of action potentials?

A

Cardiac Arrythmias

48
Q

In a delay after depolarization, what occurs to action potential following 1st depolarization?

A

A new action potential appears qujickly after the first. This abnormal depolarization of cardiac myocytes can interrupt phase 2, phase 3, or phase 4 of the cardiac action potential

49
Q

When does accelerated normal automaticity (reentry) occur?

A

Re-entry occurs when an action potential fails to extinguish itself and reactivates a region that has recovered from refractoriness

50
Q

When do early after-depolarization often occur?

A

depolarizing shifts in the membrane potential can reactivate the L-type calcium channel, resulting in increased ICa,L that further depolarizes the membrane. This can continue to create a positive feedback loop.

51
Q

DAD

A

Delayed afterdepolarization, spontanes release of calcium from the SR produces extra Ca removal from Na-ca exchanger, thich causes production of Na influx which depolarizes the cell

52
Q

EAD

A

Early afterdepolarization, occurs due to interruption of phase 3 repolarization, where reactivation of Ca channels during AP prolongs it out further.

53
Q

In Wolff-Parkinson-White Syndrome, What type of depolarization event occurs and how is it treated?

A

There is a premature atrial impulse which blocks in the acessory pathway, and on reaching the accessory pathway, the impulse re-enters the atrium, which then re-enters the ventricle via the AV node and becomes self-sustaining. This causes a short P-R interval which prolongs the QRS.

Treatment: Drugs that prolong refratoriness

54
Q

What is the event when there is an obstruction of blood flow in the myocardium by partial or complete blockage of a coronary artery?

A

Myocardial Ischemia

55
Q

A sudden severe blockage of coronary artery may lead to what event?

A

Myocardial Infarction

56
Q

What types of events may lead to serious abnormal hearth arrhythmias?

A

Acidosis

Catecholamine release

Efflux of K from myocyte to ECS

Intracellular Ca accumulation

57
Q

What is atherclerosis?

A

hardening and narrowing of the arteries

58
Q

In acute ischemia, what is generally the cause of the event?

A

a mechanical or oxidative stress such as cell death which increases cytokine release resulting in inflammation and obstruction

59
Q

in mild and severe ischemia, what happens to the threshold for AP?

A

The more severe the ischemia, the less negative the resting potential needed to reach threshold, and there is a delayed recovery period for AP depolarization.

60
Q

What is the most common type of heart failure?

A

Enlargement, where the body tries to compensate fo heart’s reduced pumping ability by retaining salt and water to increase the amount of blood in bloodstream, which increases heart rate, and the size of the heart.

61
Q

What are some common causes of fibrosis/heart failure?

A
  • Changes in activity of some ion channels/ion transporters
  • Increased sympathetic activity
  • Mechanical stretch
  • Electrolyte disturbances
62
Q

Increasing the activity of delayed rectifier K channels has what effect on AP?

A

Shortens the AP

63
Q

Decreasing the activity of delayed rectififier K channels does what to AP?

A

Prolongs the AP

64
Q

The delayed inactivation of Na channels does what to AP?

A

Prolongs the AP

65
Q

What is the type of heart rate defined by <60 beats/min

A

Bradycardia

66
Q

What is the type of heart rate defined by >100 beats/min

A

Tachycardia

67
Q

What heart arrhythmia occurs when there is an increased rate that arises in the ventricles?

A

Ventricular Tachycardia, (life threatening)

68
Q

What is a Supra-ventricular arrhythmias?

A

An arrythmia that occurs above the ventricles

69
Q

What is an atrial flutter?

A

A rapid regular beating of the atria

70
Q

What is fibrillation?

A

A very rapid irregular beating of the atria or ventricles

71
Q

What is a block arrhythmia?

A

A failure of heart conduction to occur

72
Q

What non-pharmaceutical anti-arrhythmic interventions may be taken in the heart?

A

Cardioverter/defibrillator

Ectopic pacemaker

73
Q

What are the Class I Anti-arrhythmic drugs and what subclasses are there?

A

Na Channel Antagonists (slow conduction velocity

1a: Intermediate rate
1b: Fast rate
1c: slow rate

74
Q

What are the Class II anti-arrhythmic drugs?

A

B-adrenergic receptor antagonists (blunt sympathetic effects)

75
Q

What are the Class III anti-arrhythmic drugs and what is there goal?

A

K channel antagonists (increase Action potential duration)

76
Q

What are the Class IV antagonists and what is there goal?

A

Ca2+ channel antagonsits, affect the SA and AV nodes

77
Q

What are the Class V anti-arrhythmic drugs?

A

Cl-channel antagonists

78
Q

What are the disadvantages of anti-arrhythmic drugs?

A

Potential to be pro-arrhythmic

  1. Toxic
  2. Depress automaticity
  3. Depress conduction velocity
79
Q

What are the advantages of anti-arrhythmic drugs?

A

They may be selective for abnormally fast heart rhythms

Winter P2 (6 decks)

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