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ADV. Human Phys > Test 3 Study Guide Part 5 > Flashcards

Test 3 Study Guide Part 5 Flashcards

1
Q

If other pacemakers exist why does the SA node get to dictate what happens?

A

SA node natural pace: ~72 bpm
AV node natural pace: ~50 bpm
Purkinje fibers: ~30

The fastest pacemaker overrides the other, by firing them before they have a chance to fire themselves

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2
Q

any pacemaker other than the SA node is called?

A

an Ectopic pacemaker

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3
Q

Myocardial action potential:

A

Stage one: fast Na+ channels cause sudden spike
Stage two: voltage gated Ca2+ channels (DHP) slow depolarization (leads to a long plateau)
Stage three: voltage gated potassium channels repolarize the cell

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4
Q

What does the plateau depolarization effect of the Ca do for the cell?
- It does two things

A

It causes there to be an elongated refractory phase, so muscles cannot summate, and the heart will relax before excepting another action potential.
It also is needed for the muscles themselves to contract. The Ca2+ plateau will correspond to contraction.

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5
Q

How depolarization reach the ventricles?

A

The AV is depolarized (with a brief delay). This depolarizes the bundle of his, which depolarizes the right and left bundle branches, which depolarizes the purkinje fibers

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6
Q

Electrical conduction path throughout the heart:

A

SA -> AV (slight delay) -> bundle of his -> left/right bundle branch -> purkinje fibers

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7
Q

What mechanism causes a cardiac muscle contraction?

A

(note this is the myocardial action potential)

Na+ motor plate potential -> DHP open -> RyR2 open (Ca2+ ligand activated) -> contration

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8
Q

How is Ca2+ removed from the heart?

A

SERCA into sarcoplasmic reticulum

Na/Ca exchanger (rate 3 Na for 1 Ca) into the extracellular space

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9
Q

Who created the first electrocardiograph?

A

Dr. Augustus Waller

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10
Q

What does the S-T segment relate to?

A

The amount of time between polarization and depolarization of the ventricle. Corresponds to the plateau phase

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11
Q

Three layers of veins/arteries:

A
  • Tunica externa:
  • Tunica media:
  • Tunica intima (interna):
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12
Q

Tunica Externa:

A

Outermost layer, contains collagen and elastin (structural fibers)
- Veins have thicker tunica externa’s then arteries

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13
Q

Tunica Media:

A

Muscular tissue (circular smooth muscle). Arteries have a much thicker tunica media, resulting in arteries having much thicker walls overall

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14
Q

Tunica Intima (interna):

A

three layers:

  • endothelium (innermost)
  • basement membrane (outermost)
  • internal elastic lamina (elastin)
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15
Q

Do veins or arteries have more elastin?

What correlates to higher elastin?

A

Arteries

Thicker arteries

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16
Q

What is the purpose for elasticity in arteries?

A

It helps to propel blood forward. It also allows there to be a storage, so the blood flow does not stop when the semilunar valves close

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17
Q

Elastic arteries:

A

The largest arteries. Example: aorta

Elastin in all three layers, tunica externa, tunica media, tunica intima

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18
Q

Muscular arteries:

A

medium sized vessels.
Thick tunica media (better ability to vasoconstrict/dilate)
Elastin confined between tunica media and tunica externa

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19
Q

Arterioles:

A

Smallest arteries.
Smaller tunica media.
Still, by vasoconstrict/dilate they provide greatest resistance to blood flow in arterial system.

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20
Q

After load:

A

The resistance which your heart must pump against.

- Arterioles greatest contributors

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21
Q

Arteriovenous anastomoses:

A

Bypass capillaries. Arterioles flow directly to venules.

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22
Q

What allows arterioles to flow directly to venules in some systems?

A

Arteriovenous anastomoses

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23
Q

Capillaries:

  • Wall structure:
  • Explanation:
A
  • Wall structure:
    Tunica interna only.
    Tunica interna is also just basement membrane and endothelium (no elastin)
  • Explanation:
    Thin to allow flow of nutrients out of capillaries .
    Cannot vasoconstrict or dilate
24
Q

How might the depolarization or hyperpolarization of the tunica media spread after a signal is instantiated by norepinephrine or acetylcholine?

A

There is evidence of gap junctions between smooth muscle cells.

25
Q

What is the maximum distance a cell can be from a capillary

A

60 to 80 um away from a blood capillary

26
Q

How much can vasoconstriction of arterioles and small arteries reduce blood flow of the capillaries to?

A

5 - 10 % of its maximal flow

27
Q

Precapillary sphincters:

  • Define/purpose:
  • Location:
A
  • Define/purpose:
    Can modify blood flow through an artery (does not cut it off, but reduces blood flow), and shift the blood to arteriovenous shunts
  • Location:
    At the base of arteriole branching into capillary beds
28
Q

arteriovenous shunts:

A

When the precapillary sphincters close, blood is sent instead to these pathways.

29
Q

How many cells thick are the capillary walls?

A

1

30
Q

Types of capillaries:

A

Continuous capillaries:
Fenestrated capillaries:
Sinusoid capillaries:

31
Q

Continuous capillaries:

A

Most common type.
Continuous lining with tight junctions.
Lack of intercellular channels, contributes to the blood brain barrier (nutrients can cross by pinocytosis)

32
Q

Fenestrated capillaries:

A

Have fenestrations, which allow fluid to directly exit capillaries.
Have an intact basement membrane which retains proteins.
Located where there is a great deal of fluid transport (kidney, endocrine glands, intestine)

33
Q

Sinusoid capillaries:

A

Discontinous capillary. Wide openings which allow transport of large proteins or cells. Incomplete basement membrane.
Important in spleen, bone marrow, and liver

34
Q

What is the only mechanism of capillary exchange in the nervous system?

A

Pinocytosis.

35
Q

Angiogenesis:

A

Generation of new blood supply.

36
Q

What growth factor promotes angiogenesis:?

A

Vascular Endothelial Growth Factor. (VEGF)

37
Q

What types of tissues may produce Vascular Endothelial Growth Factor?

A

Ischemic (deoxygenated) tissues

Cancerous tissues

38
Q

Skeletal muscle pump:

A

Propels blood through veins.
The massaging action of the skeletal muscles. The squish the muscle towards your heart (one way valves in veins, made from the tunica intima)

39
Q

What happens if you stand to stiff?

What happens if you lay down for too long?

A

You can pass out because of blood collection in the legs.

You can have thrombi form in your legs, and end up with pulmonary emboli

40
Q

Respiratory (breathing) pump:

A

Breathing in causes negative pressure in the thoracic cavity, making it easier for blood to flow into it.

This is not counteracted by increased pressure when breathing out because of one way valves.

41
Q

Where does atherosclerosis cause a build up?

What causes clot formation associated with atherosclerosis?

A

In the tunica intima, between the endothelium and basal lamina.
Clot formation is caused by exposure of collagen as the atherosclerosis eats through the epithelium

42
Q

What is currently believed to start atherosclerosis?

A

An insult/damage to the endothelium (smoking, hypertension, high blood cholesterol, diabetes, some infectious agents)

43
Q

What is the first visual sign of atherosclerosis?

A

Fatty streaks! These are macrophages which are filled with fatty acids! These are located within the tunica interna.

44
Q

What happens in atherosclerosis after fatty streak formation?

A

A fibrous plaque forms! Cap of connective tissue with the smooth muscle cells and macrophages.
If this cap ruptures thrombosis is likely (exposure to collagen)

45
Q

Foam Cells:

A

Macrophages present in the fibrous plaque which are engorged because they have consumed LDL. Their progression is hindered by HDL (which is good)

46
Q

What acts to prevent the progression of atherosclerosis?

What can counteract this?

A

Endothelial cells.

Hypertension, high cholesterol other risk factors.

47
Q

High cholesterol is associated with increased risk of atherosclerosis. What causes high cholesterol?

A 
Diet high in cholesterol (debatable)
Inherited condition (familial hypercholesteremia)
48
Q

Good or bad?
LDL:
HDL:

A

LDL: Bad!
HDL: Good!

49
Q

Explain LDL:

A

Bind to cholesterol. Normally removed by binding to apolipoproteins in the liver.
Can also be removed by receptors apolipoprotein B which can become present in the inner endothelium. This causes intake of cholesterol. (apolipoprotein b is a predominant apolipoprotein of the chylomicrons and low density lipoproteins)

50
Q

High risk individuals for atherosclerosis have what?

A

High levels of apolipoprotein B receptors in the arteries.

Low levels of LDL (apolipoprotein B) receptor in liver (liver can handle it, arteries cannot.)

51
Q

Explain HDL:

A

Protects by carrying cholesterol away from the arterial wall and to the liver.

52
Q

What contributes to naturally high HDL:

A

Genetics (larger determination)
Exercise increases HDL.
Women prior to menopause have high HDL

53
Q

What else can raise HDL:

A

Statins
Fibrates (don’t learn this one)
Vitamin Niacin

54
Q

What makes LDL worse (hint: why are antioxidants good for you):

A

Oxidized LDL is considered worse for you.

55
Q

Inflammatory disease atherosclerosis:

  • Why do people think this?
  • What test aligns with this?
A
  • Why do people think this?
    Important role played by monocytes, lymphocytes.
  • What test aligns with this?
    C-reactive protein, a marker for inflammation is a stronger predictor of atherosclerotic heart disease than blood LDL cholesterol levels.

ADV. Human Phys (51 decks)

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