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BIO 421 > Chapter 12 > Flashcards

Chapter 12 Flashcards

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Biology 101 flashcards
1
Q

List parts of the vascular system

A
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2
Q

Dense connective tissue that surrounds the heart. What is it connected to? What is the function of this tissue?

A

Pericardium - contains a fluid-filled area with mucus-like fluid. Pericardium offers support and protection for heart, while the fluid lubricates the heart to relieve friction. Pericardium is connected to the diaphragm

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3
Q

Label the heart. What are the three layers? Also, trace blood flow.

A
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4
Q

Endocardium Label, and what is it comprised of?

A

Some connective tissue, but a lot of endothelium –> cells that are able to secrete some substances that can adjust heart rate and contractibility

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5
Q

Label Valves

A
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6
Q

Narrowing of the mitral valve? What causes it? What happens if someone has this?

A

Mitral stenosis - can be congenital problem or build up of scar tissue from previous damage (may or may not know about it).

Blood backs up in left atria so SV gets less efficient and decreases, start having pain from enlargement of atria, and if it continues it eventually backs up into lungs. So not getting oxygen efficiently from lungs. Can be corrected with surgery.

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7
Q

Damaged mitral valve or torn chordae tendineae. What does it cause?

A

Mitral insufficiency. Tendons are stretched or torn, so you get a regurgitation of blood from left ventricle to left atria. Not getting sufficient SV, depending on amount if may not be a problem, but you can hear it with stethoscope.

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8
Q

When a portion of the valve gets pushed up during ventricular contraction? What happens?

A

10% of pop. has some amount of this. It’s called mitral valve prolapse. It happens when the mitral valve gets pushed up during ventricular contraction, and lets some blood in, and when ventricule contracts it lets a little blood back into atria

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9
Q

Just like mitral stenosis, but between the left ventricle and aorta. What happens? Which valve are we dealing with here?

A

Aortic stenosis. Blood backs up in left ventricle. Aortic semilunar valve.

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10
Q

Weak, or damaged chordae tenineae which causes SV to decrease and allows blood to back up into left ventricle. Which valve does this deal with?

A

Aortic insufficiency. Aortic semilunar valve. Get flappy doors, so blood regurgitation.

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11
Q

List the nodes, and what are they/what is their function?

A

The SA node is the pacemaker for the entire heart. Its depolarization generates the action potential that leads to depolarization of all other cardiac muscle cells. Electrical excitation of the heart is coupled with contraction of cardiac muscle.

**Initial depolarization normally arises in a small group of conducting-system cells called the sinoatrial (SA) node

Everything in hot yellow in this figure has auto rhythmic potential, as you travel down these towards the AV nodes, etc there is less and less action potentials generated by these cells. Bundle branches (30), purkinje fibers (20 action potentials…).

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12
Q

The period of ventricular contraction and blood ejection?

A

Systole

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13
Q

Alternating period of ventricular relaxation and blood filling?

A

Diastole

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14
Q

A small fraction of cardiac muscle cells. What do they do, and what are they called?

A

1% of cardiac muscle cells. called autorhythmic (pacemaker) cells, and they determine the HR. These are specialized neurons that fire AP’s not due to any sensory input, but just due to autorhythmic firing

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15
Q

Much larger group of cardiac muscle cells. What percentage, and what are they called and what do they do?

A

99% contractile cells, and their activity determines the SV

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16
Q

Define cardiac output (CO). What is CO at rest?

A

amount of blood pumped per min by each ventricle

5L/Min

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17
Q

Define SV. What is determines SV? What is SV typically amount wise?

A

amount of blood pumper per beat by each ventricle. SV is determined by contractibility strength of heart muscle. SV is typically 70-75 ml/contraction

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18
Q

Average HR? Factors that influence resting heart?

A

70bmp (but there is a large range for normal)

Factors that influence resting heart: age, sympathetic/parasympathetic innervation, caffeine, physical fitness, medications.

The more active you are, the lower your resting HR, and the higher your SV.

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19
Q

If you suddenly become active how much can you increase HR and SV? If you’re active how much can you increase CO?

A

4-5 times. If healthy/active can increase CO by up to 8x but might not be able to sustain long.

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20
Q

People who are not physically fit rely more on what to increase CO? More active people rely more heavily on what to increase CO?

A

Inactive: rely more on increase in HR

Active: rely more on increase in SV

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21
Q

CO: What determines HR? What decreases HR, what increases HR? What else does increase in HR increase?

A

HR determined by autorhythmic cells rate of depolarization (90 action potentials per minute).

Parasympathetic innervation decreases HR. Sympathetic innervation and epinephrine increase HR.

Increase in HR increases venous constriction, and contractibility.

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22
Q

SV determined by what? This in turn is influenced by what?

A

SV is determined by contractibility of ventricular myocardium. This is influenced by contractibility, and EDV.

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23
Q

What influences EDV?

A

venous constriction –> venous return

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24
Q

What aids venous return?

A

skeletal muscle pump, and respiratory pump

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25
Q

A rapid assessment of blood composition. It is the percent of the blood volume that is composed of _______? What is the average composition?

A

Hematocrit - red blood cells (erythrocytes)

45% RBCs (hematocrit = 45%), Plasma 55%, and the rest leukocyctes, and platelets (buffy coat)

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26
Q

Composition of plasma? What is the one special protein that we discussed?

A

Water, ions, proteins, nutrients, hormones, wastes, etc.

-Albumin - osmotic solute that allows water to stay in the blood vessels so you don’t have wide fluctuations of blood volume

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27
Q

funtion of red blood cells

A

transport oxygen and CO2

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28
Q

What are the two systems that the heart pumps blood through?

A

systemic and pulmonary circuits

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29
Q

where does O2, CO2 exchange occur?

A

capillary beds

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30
Q

pericardium is comprised of what?

A

dense connective tissue that connects to diaphragm

31
Q

epicardium comprised of what? endocardium comprised of what?

A

epicardium - dense connective tissue for structural support

endocardium - some connective tissue, but a lot of epithelium that is capable of secreting some substances that can adjust HR and contractibility

32
Q

Innervating cells that trigger cardiac contraction?

A

authorhythmic cells: Sinoatrial node, atrioventricular node, bundle of His, bundle branches (left and right), and purkinje fibers. As you travel down from the SA node there are less and less action potentials generated.

33
Q

SA Nodes - how many action potentials per minute?

AV nodes - “ ?”

Bundle branches?

Purkinje fibers?

A

90 - SA nodes

50 - AV nodes

30 - Bundle Branches

20 - Purkinje Fibers

34
Q

Where are left and right bundle branches found?

A

interventricular septum

35
Q

electrical activity of the heart says that the atria depolarized. And then atria contracts.

A

P-wave

36
Q

electrical activity of the hearts says that ventricles depolarized. And right after that ventricles contract.

A

QRS Complex

37
Q

tells me that ventricles repolarize

A

T-wave

38
Q

How long is the absolute refractory period for skeletal muscle vs the duration of contraction for skeletal muscle? What does this mean?

A

Absolute refractory period 1 to 2 msec, vs actual contraction which is 20 to 100msec. This means that another action potential can be elicited while the contraction from the first action potential is still underway. This results in tetanus = prolonged contraction.

39
Q

Because of prolonged depolarized state, the absolute refractory period lasts almost as long as the contraction. What is the amount of time? What does this prevent?

A

250msec. This prevents sustained contraction = tetanus.

40
Q

What has to happen before muscle contraction?

A

electrical stimulation. Have to have action potential first before muscle contraction.

41
Q

What’s the time scale here? Is there anything wrong?

A

Normal ECG here, and this is 6-7 seconds in length

42
Q

Is there anything wrong here?

A

Additional P-waves, and less contractions here (depolarization events). This could mean that SA node is not able to communicate downstream, so attempting to fire more action potentials and therefore more atrial depolarization events in attempt to communciate downstream. Could be due to blockage in AV node or bundle branches.

43
Q

Is there anything wrong here?

A

Heart rate even slower, so more severe blockage. SA node isn’t driving contraction at all?

44
Q

1st heart beat sound is when? Which valve, and what is happening? What follows this?

A

mitral valve, bicuspid valve is closing.

After valve closes, pressure in ventricles increases rapidly, and aortic valve opens during ventricular ejection of systole.

45
Q

When does the aortic valve open? What happens after ventricular contraction?

A

It opens during ventricular ejection of systole. Following ejection/contraction of ventricle. Aortic valve closes.

46
Q

Second heart sound is associated with which valve closing?

A

Aortic valve closes

47
Q

At rest HR is under control of what? What can be done to speed up HR? All effects are exerted upon what?

A

At rest HR is under control of parasympathetic nervous system.

To speed up HR: 1. deliver the sympathetic hormone (epinephrine), and/or 2. release sympathetic neurotransmitter norepinephrine, and/or 3. reduce the release of parasympathetic neurotransmitter acetylcholine

All effects are exerted upon the SA node.

48
Q

How much can we increase HR, and for how long? As we age what happens to our max HR?

A

If sympathetic nervous system comes into play, we can increase HR significantly. From 65bpm, and with a shot of adrenaline, my HR can go up to a max of around 180bpm (can’t sustain it here).

It declines. 10bpm per decade

49
Q

What is the primary point exchange between the blood and the interstitial fluid (ISF)? What assists with this exchange?

A

the capillary, and intercellular clefts assist the exchange

50
Q

What are capillary walls comprised of? List parts of capillary cell from picture.

A

capillary walls are a single endothelial cell in thickness - the flat cells that constitute the endothelial wall of a capillary are not attached tightly to each other, but are separated by narrow, water-filled spaces termed intercellular clefts

51
Q

Capillary walls are very _____. Why is this? What does the capillary wall lack?

A

thin, for gas exchange

muscular layer or connective tissue layer

52
Q

Why do I need erythrocyte to be pliant (flexible)?

A

to squeeze into capillary (very large in comparison to capillary)

53
Q

Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle in upstream ______ and ________ determine the volume of blood each capillary receives.

A

precapillary sphincters, and metarterioles

54
Q

movement of fluid and solutes out of the blood…could be going where?

A

filtration. could be going to tissues.

55
Q

movement of fluid and solutes into the blood…could be taking these things from where?

A

absorption. could be taking them from tissues or ISF

56
Q

_______ function as sensors in the hemostatic maintenance of MAP by constantly monitoring pressure in the _______ and ________.

A

Baroreceptor neurons, in the aortic arch and carotid sinuses

57
Q

Expanded blood volume is detected by stretch receptors in left atrium, and causes release of ________. What does this do?

A

Atrial Natriuretic Peptide (ANP)

  • inhibits aldosterone, promoting salt and water excreation to lower blood volume
  • promotes vasodilation
  • protein hormone secreted by heart muscle cells in left atrium
58
Q

High blood pressure also called what?

A

hypertension

59
Q

Beta-adrenergic receptor blockers. what do they do?

A

(beta blockers) - blocking sympathetic neurotransmitter. Beta blockers are working to decrease HR primarily, which then decreases cardiac output.

60
Q

What do calcium channel blockers do? What is influenced? Risks involved?

A

Cause vasodilation. Way they do that is by inhibiting calcium diffusion into the vascular smooth muscle. These drugs may increase chance of a heart attack. Arteries supplying oxygen to the heart, coronary arteries aren’t contracting enough to send blood, nutrients, and oxygen to the heart it can potentially lead to a heart attack.

61
Q

ACE Inhibitor. What does it do? What is it called?

A

the enzyme being influenced here is a vasoconstrictor. An ace inhibitor is a drug that prevents vasoconstrictor from working. It is an angiotensin-converting enzyme (ACE) inhibitor

62
Q

ways to treat blocked coronary artery?

A
  1. coronary bypass (surgical intervention) - Sometimes they grab a vessel from another part of the body. Or tie off the blocked portion, and reroute around it. May have to do that in several places.
  2. if stopped blood flow - stint (tube inserted into blocked area) mesh tube that is inserted into the blocked area, is opened, and then holds blood vessel open, good solid mechanism for keeping that portion of coronary artery open, tougher to regulate it but can, at some point, dissolve or become ineffective
  3. angioplasty - Tiny balloon that flattens plaque on the side of walls. Plus, not leaving anything foreign in, and less risk. Must change life style that put them in that position in the first place. Significant risk of building back up again. If it’s a stable plaque then angioplasty might be the way to go.
63
Q

A stem cell that is an undifferentiated cell that can become many different types of cells, but it’s not like the first zygote.

A

Pluripotent hematopoietic stem cell

64
Q

Completely undifferentiated stem cell = first zygote

A

omnipotent stem cell

65
Q

happens when an Rh- mother has an Rh + child (second pregnancy) when she had an Rh+ child the first time. What does this cause?

A

erythroblastosis fetalis, causes hemolysis of fetal RBCs

66
Q

________ can be used right after a stroke to dissolves clots, and restore blood flow. How do they work?

A

synthetic plasminogen activators.

Plasminogen enzyme that is activated by plasminogen activators to plasmin which dissolves fibrin. Fibrin was originally created by thrombin.

67
Q

the enzyme being influenced here is a vasoconstrictor. An ________ is a drug that prevents vasoconstrictor from working.

A

ACE inhibitor - angiotensin-converting enzyme

68
Q

Where is SA node located?

A

Right atrial endothelium

69
Q

what is the formula for net filtration pressure?

A

…

70
Q

drugs that increase contractility strength. their heart may not be strong enough to handle the increased stimulation to pump, so in some people not that effective

A

cardiac inotropic drugs

71
Q

drugs that allow more volume to stay in veins

A

vasodilator drugs

72
Q

Decreased oxygen delivery to the kidney causes the secretion of ______, which does what?

A

erythropoietin, which activates receptors in bone marrow, leading to an increase in the rate of erythropoiesis

73
Q

where can cholesterol start to build up?

A

between endothelium and connective tissue layer

BIO 421 (5 decks)

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