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Human Physiology > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

What are three main components of the cardiovascular system?

A
  1. Heart
  2. Vasculature (blood vessels)
  3. Blood
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2
Q

What are the six functions of the cardiovascular system?

A
  1. Transports nutrients, wastes, hormones, etc.
  2. Blood pressure regulation
  3. Water homeostasis
  4. Hemopoiesis (formation of blood)
  5. Immunity
  6. Blood clotting
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3
Q

In blood flow, what is the pulmonary circuit?

A

Pulmonary circuit sends blood to lungs for oxygenation.

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4
Q

In blood flow, what is the systemic circuit?

A

Systemic circuit sends oxygen rich blood to all other tissues of the body.

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5
Q

What are the four chambers of the heart?

A

Right and left atria; Right and left ventricles.

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6
Q

Which one of the heart’s two ventricles is thicker?

A

The left ventricle is 3-4 times thicker than the right ventricle because the left ventricle needs more power to pump to rest of body (right ventricle only pumps to lungs).

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7
Q

What are the chambers of the heart separated by?

A

Fibrous connective tissue that impulses cannot cross.

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8
Q

What do the heart valves do?

A

Direct the flow of blood through the heart.

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9
Q

What makes cardiac cells similar to skeletal muscle cells?

A

Both contain myofibrils, filaments, t-tubules, and sarcoplasmic reticulum.

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10
Q

What are gap junctions?

A

Interconnections found within intercalated discs. They aid in impulse transmission between contractile cells (quick spread or transmission of impulses from myocardial cell to myocardial cell).

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11
Q

The heart uses what process for ATP?

A

Aerobic respiration.

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12
Q

What are three types of specialized cardiac cells?

A
  1. Contractile cells (myocardial cells)
  2. Nodal cells
  3. Specialized conduction cells or fibers
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13
Q

What do contractile cells do?

A

They are responsible for the contraction of the chambers and the formation of pressure to move blood out of ventricles and into arteries.

99% of cardiac cells are contractile cells.

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14
Q

What do nodal cells do?

A

They are auto-rhythmic (myogenic) and generate their own action potentials or impulses. That’s why the heart can still beat outside of the body.

Two nodes include the sinoatrial (SA) node and the atrioventricular (AV) node.

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15
Q

What do specialized conduction cells or fibers do?

A

They’re fast action potential conducting systems. It’s a system for the rapid movement of the impulse between the chambers and also within the ventricles.

Ex: internodal pathways, Bundle of His (AV bundle), bundle branches, Purkinje fibers.

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16
Q

What node in the heart has the fastest firing rate?

A

Pacemaker (SA node).

Faster than AV node. It dictates the pace of the heart.

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17
Q

How does the pacemaker (SA node) propagate its impulse?

A

Impulses from the pacemaker located at the upper surface of the right atrium can spread out and stimulate other right atrial contractile cells and left atrial contractile cells by impulse propagation over gap junctions.

Pacemaker impulses CANNOT reach ventricles by gap junctions b/c of the non-conducting fibrous tissue that separates the chambers.

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18
Q

How do impulses spread from atria to ventricles?

A

Step 1: Impulses spread from SA node to AV node along the internodal pathways (where there is a 1/10 second delay at AV node).

Step 2: Impulses from AV node are sent to apex of ventricles by way of Bundle of His (AV bundle), bundle branches, and Purkinje fibers.

Step 3: Using gap junctions between cells alows for the excitation of the contractile cells of the ventricles.

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19
Q

Explain the three steps for electrical activity in NODAL or PACEMAKER cells?

A

Step 1: Gradual depolarization from increase Na+ and decrease K+ permeability at first, followed by opening of Ca2+ gates. (More Na, less K, and more Ca)

Step 2: Rapid opening of the Ca gates causes depolarization of the action potential b/c Ca flows into cell. (More Ca)

Step 3: Closing of Ca gates and opening of K gates cause repolarization. This causes K to flow out of cell. (Less Ca, more K)

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20
Q

How does the autonomic system influence the electrical activity in NODAL or PACEMAKER cells?

A

Sympathetic stimulation: speeds up depolarization (increase Na and Ca permeability).

Parasympathetic stimulation: slows down by hyperpolarizing cell (increase K) and slowing depolarization (decrease Ca).

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21
Q

Explain the three steps for electrical activity in CONTRACTILE cells?

A

Step 1: Depolarization caused by increase in Na permeability. (-90mV to +30mv)

Step 2: Plateau from decrease Na and increase Ca permeability.

Step 3: Repolarization from decrease Ca and increase K permeability.

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22
Q

What four things make contractile cells different from skeletal muscle cells?

A
  1. Ca ions play an important role.
  2. Depolarization is longer.
  3. Refractory period is longer.
  4. No tetanus.
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23
Q

Electrical stimulation of cardiac muscle is similar to skeletal muscle except for these five factors:

A
  1. Action potential is longer around 200 milliseconds, with a longer refractory period in cardiac muscle.
  2. There is no tetanus in heart due to muscle relaxation during refractory period.
  3. Impulse on contractile cell is generated from its excited neighboring cell by using gap junctions.
  4. Action potential opens Ca channels on the sarcolemma so there is an influx of Ca into the cell from the ECF.
  5. Influx of Ca into ICF activates release of Ca from sarcoplasmic reticulum. This is a chemically activated gate in cardiac muscle and NOT votage activated gate as in skeletal muscle.
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24
Q

What is an electrocardiogram (ECG)?

A

A way to measure electrical currents of the heart by placing electrodes on the body’s surface.

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25
Q

What are P-waves, QRS complexes, and T-waves of an ECG strip?

A

P-wave: atrial depolarization

QRS complex: ventricular depolarization

T-wave: ventricular repolarization

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26
Q

What are the three standard limb leads?

A

Lead I: right arm, left arm

Lead II: right arm, left leg

Lead III: left arm, left leg

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27
Q

What are the three augmented vector leads?

A

aVR (right arm)

aVL (left arm)

aVF (left foot)

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28
Q

What are the six chest leads?

A

V1 - V6

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29
Q

What is the heart’s main function?

A

To receive blood from the veins and to create enough pressure to pump blood out the arteries to the body’s system.

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30
Q

What does systole mean?

A

Contraction (receives blood).

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31
Q

What does diastole mean?

A

Relaxation (gives blood).

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32
Q

What three major things happen during the cardiac cycle?

A
  1. Pressure changes (force behind blood flow) in the atria, ventricles, and arteries (aorta).
  2. Ventricular volume changes (amt of blood the ventricles receive and pump).
  3. Valve actions fill and empty the heart and to direct flow of blood.
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33
Q

What happens during Phase 1A (Ventricular Filling) during the cardiac cycle?

A

Atrial diastole and Ventricular diastole.

  1. Ventricles receive blood from atria via gravity and pressure before atria contracts. At rest, 80% of blood is in ventricles before atria contracts.
  2. Pressure in ventricle at this time is 0-5mm Hg.
  3. Atrial pressure > ventricular pressure, so AV valves are OPEN.
  4. Aortic pressure > ventricular pressure, so semilunar valves are CLOSED.
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34
Q

What happens during Phase 1B (Ventricular Filling w/ Atrial Systole) of the cardiac cycle?

A

Atrial systole and Ventricular diastole.

  1. P-wave causes atria to contract.
  2. Atria contracts and deliver 20% more blood into ventricles
  3. Maximum volume of blood in each ventricle is 135 mL (EDV)
  4. Pressure and valves similar to Phase 1A b/c we’re still filling
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35
Q

What happens during Phase 2 (Isovolumetric Contraction) of the cardiac cycle?

A

Ventricular systole and Atrial diastole.

  1. QRS complex causes contraction in ventricles.
  2. Ventricular depolarization activates systolic phase, which starts to rapidly build up ventricular pressure from 0mm Hg to 80mm Hg. Ventricular pressure > Atrial pressure, so AV valves are CLOSED.
  3. AV valves closing produces S1 or Lub sound.
  4. Aortic pressure > Ventricular pressure, so semilunar valves are still CLOSED.
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36
Q

What happens during Phase 3 (Ventricular Ejection) of the cardiac cycle?

A

Ventricular systole.

  1. Ventricular pressures increases. Ventricular pressure > aortic pressure, so semilunar valves OPEN above 80mm Hg.
  2. Ejection of blood occurs when semilunar valve opens and continues as long as ventricular pressure > arterial pressure.
  3. Ventricular contraction does not eject all the blood and the amt remaining is 65 mL (ESV).
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37
Q

What happens during Phase 4 (Isovolumetric Relaxation) of the cardiac cycle?

A

Ventricular diastole.

  1. After systole, heart returns to diastolic phase and ventricular pressure < aortic pressure, so semilunar valves CLOSE and make S2 or Dub sound.
  2. Ventricular pressure still > atrial pressure, so AV valves are CLOSED.
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38
Q

What are heart murmurs?

A

Turbulence in blood flow within OR outside the heart.

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39
Q

What is normal cardiac output at rest?

A

5000 mL (5 Liters) per minute.

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40
Q

How does cardiac output change depending on different physiological states?

A

Cardiac output depends on body’s oxygen requirement. During exercise, cardiac output can increase to 15-20 L/min or 30-40 L/min in well-trained athletes.

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41
Q

What is cardiac output?

A

Cardiac output = heart rate x stroke volume.

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42
Q

What are three extrinsic controls (outside heart) for heart rate?

A
  1. Increase sympathetic firing to pacemaker (SA node).
  2. Decrease parasympathetic firing to pacemaker.
  3. Epinephrine on pacemaker.
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43
Q

Stroke volume is influenced by what three factors?

A
  1. Ventricular contractility
  2. End diastolic volume or preload
  3. Mean arterial pressure or afterload
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44
Q

What is ventricular contractility and how does it influence stroke volume?

A

Extrinsic control b/c it’s controlled by nerves and hormones.

Sympathetic stimulation (epinephrine) to the contractile cells increases strength of contractility, thus increasing stroke volume.

Parasympathetic doesn’t do anything for ventricular contractility. There’s NO dual innervation.

This causes more Ca to enter cells and more to be released from sarcoplasmic reticulum. More Ca binding to troponin and more cross-bridges available for muscle contraction.

So epi and norepi cause more of these Ca gates to open, so there’s more strength.

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45
Q

What is the end diastolic volume and how does it influence stroke volume?

A

Intrinsic control.

Increase in EDV (preload… loading heart w/ blood before contraction) will increase SV.

Length-Tension relationship.

More cross-bridge overlap.

An increase in cardiac muscle distension from more blood increases force of contraction.

Venous return: more venous return, more SV.

Length of diastole: longer filling time, more blood in heart, more SV.

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46
Q

What is the mean arterial pressure (afterload) and how does it influence stroke volume?

A

Decrease in MAP, increase in SV.

Vasodilation of arterioles decreases mean arterial pressure. So heart doesn’t have to work too hard to get blood in.

Increase in compliance in arteries, decreases in MAP, so increase in SV.

Arteriosclerosis (hardening of arteries), means less compliance so heart works harder to get blood out.

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47
Q

What is bradycardia?

A

Heart rate < 60 per min.

Decrease in heart rate, decrease cardiac output.

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48
Q

What is tachycardia?

A

Heart rate > 100 per min.

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49
Q

What is a flutter?

A

Heart rate 200-300 per min.

Disadvantage is that with an increased heart rate, filling time decreases, thus decreases SV and cardiac output.

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50
Q

What is fibrillation?

A

An uncoordinated contraction of the heart causes a quivering of muscle, thus no pumping.

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51
Q

What are heart blocks?

A

Impulses from SA node are slwoed or completely blocked from reaching AV node.

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52
Q

What is a myocardial infarction?

A

Heart attack.

Starts w/ decrease in blood supply to muscle, called tissue ISCHEMIA. This causes decrease in oxygen supply to muscle that shifts metabolism from aerobic to anaerobic.

Damage is reversible within 30-45 min. Afterwards tissue necrosis occurs followed by a replacement w/ connective tissue.

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53
Q

What three things can cause myocardial infarction?

A
  1. Vascular spasms
  2. Emboli from heart chambers or from veins
  3. Atherosclerosis
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54
Q

What are eight predisposing factors for a myocardial infarction?

A
  1. Family history
  2. Diabetes
  3. Weight
  4. Gender
  5. Smoking
  6. Nutrition
  7. Lack of exercise
  8. Stress
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55
Q

What are five treatments for myocardial infarction?

A
  1. Coronary bypass
  2. Angioplasty
  3. Stents
  4. Atherectomy
  5. Drugs
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56
Q

What is a coronary bypass?

A

Arteries or veins from elsewhere in the patient’s body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the myocardium (heart muscle).

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57
Q

What is angioplasty?

A

Mechanically widening narrowed or obstructed arteries. An empty and collapsed balloon on a guide wire, known as a balloon catheter, is passed into the narrowed locations and then inflated to a fixed size. The balloon forces expansion of the inner white blood cell/clot plaque deposits and the surrounding muscular wall, opening up the blood vessel for improved flow, and the balloon is then deflated and withdrawn.

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58
Q

What are stents?

A

A mesh ‘tube’ inserted into a natural passage/conduit in the body to prevent or counteract a disease-induced, localized flow constriction.

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59
Q

What is an atherectomy?

A

Surgical method of removing the plaque burden within the vessel.

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60
Q

What are vessels?

A

Vessels contain an inner single layer of cells called the endothelium surrounding by blood vessel walls consisting of smooth muscle and elastic connective tissue.

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61
Q

What is the relationship between the total surface area and diameter of vessels?

A

Inverse relationship. Total surface area increases as vessel diameter increases.

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62
Q

What is the relationship between the blood velocity and diameter of vessels?

A

Direct relationship. Blood velocity decreases as vessel diameter decreases.

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63
Q

Which blood vessels have the slowest blood flow?

A

Capillaries.

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64
Q

Which blood vessels have the fastest blood flow?

A

Arteries.

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65
Q

How does blood pressure change from arteries to veins?

A

Blood pressure dereases from arteries to veins.

66
Q

What is blood flow?

A

Blood flow is equal to pressure difference divided by resistance.

F = P/R

67
Q

What is resistance influenced by?

A

Length, viscosity, and vessel radius.

R = 1/r4

A small change in diameter (or radius) causes large change in blood flow (and resistance).

68
Q

What are arteries?

A

Large vessels w/ mostly elastic walls.

69
Q

What are the two functions of arteries?

A
  1. They act as low resistance conducting vessels (b/c they’re large) due to their large diameter (b/c they’re elastic).

The blood pressure throughout the arterial is similar and is usually written as 120/80, where 120 is the systolic pressure and 80 is the diastolic pressure.

Mean arterial pressure = diastole + 1/3(systolic-diastolic)pulse pressure

Pulse pressure = 40mmHg

  1. Act as PRESSURE reservoirs. Elastic recoil of blood vessels maintains diastolic pressure.
70
Q

What are arterioles?

A

Smaller vessels (more resistance to blood flow) that contain a high amount of smooth muscle in their walls. No connective tissue.

71
Q

What are the three functions of the arterioles?

A
  1. Involved w/ TOTAL peripheral resistance and blood pressure regulation.
  2. Offer resistance to blood flow and are involved in distributing blood to the tissues that have a greater requirement at that time.
  3. Change blood flow patterns in response to physiological demands.

Vasodilation: visceral muscle relaxation, more blood flow

Vasoconstriction: visceral muscle contraction, less blood flow

72
Q

What are three intrinsic controls over arteriolar diameter?

A
  1. Metabolic changes
  2. Autoregulation
  3. Local chemical messengers
73
Q

Explain metabolic changes as an intrinsic control over arteriolar diameter.

A

Low O2, high CO2, and high acidity vasodilate. These factors are powerful during exercise and cause vasodilation in coronary and skeletal muscle arterioles.

Vasodilation → resistance → blood flow → more O2 → remove CO2

Low CO2 level causes vasoconstriction.

Hypercapnia: high CO2

Hypocapnia: low CO2

74
Q

Explain autoregulation as an intrinsic control over arteriolar diameter.

A

Keeps blood flow to an organ constant.

High blood pressure in the cerebral arterioles causes vasoconstriction in order for precise blood flow to the brain. Increases resistance to keep flow constant.

Low blood pressure causes less vessel stretching that causes the muscles to relax and vasodilate the arterioles.

75
Q

Explain local chemical messengers as an intrinsic control over arteriolar diameter.

A

Paracrines that cause vasodilation: histamine, prostaglandins, nitric oxide (NO)

76
Q

What are two extrinsic controls over arteriolar diameter?

A
  1. Nerves
  2. Hormones
77
Q

Explain nerves as an extrinsic control over arteriolar diameter.

A

Sympathetic stimulation (norepi) activates the ALPHA receptors in visceral, skin, coronary, and skeletal muscle arterioles that causes VASOCONSTRICTION.

Sympathetic stimulation can also activate BETA2 receptors in skeletal muscle and coronary arterioles that cause a minor VASODILATION.

There is NO parasympathetic innervation to arterioles except in erectile tissue.

78
Q

Explain hormones as an extrinsic control over arteriolar diameter.

A
  1. Epinephrine:
    - Constricts vessels w/ alpha receptors
    - Dilates vessels w/ beta2 receptors
  2. Angiotensin constricts:
    - Angiotensin converting enzyme (ACE) turns angiotensin active

Angiotensin1 (inactive form) → Angiotensin2 (active form)

  • An ACE inhibitor is called lotensin
    3. ADH (vasopressin) constricts
79
Q

What are capillaries?

A

Small vessels that contain only a layer of endothelium in their walls.

They’re very numerous, resulting in a large total surface area (larger than veins and arteries). B/c of large total surface area, there’s little resistance through vessels.

Capillaries have slowest blood flow.

Oxygen demands of tissues can be met by changing arteriolar diameter, thoroughfare channels activity, and pre-capillary sphincter activity. So to increase blood flow through capillary, arterioles vasodilate and pre-capillary sphincter relaxes.

80
Q

What are the two functions of capillaries?

A
  1. Molecular exchange by diffusion.
    - Via concentration. Blood moving slowly, lots of total surface area, and thin epithelium makes molecular exchange efficient.
  2. Fluid exchange.
    - Extracellular fluid mixes every 10-30 minutes in the body by rapid transport within the blood stream and fluid exchange between plasma and interstitial fluid.
81
Q

What are the two pressures used to create fluid exchange within capillaries?

A
  1. Hydrostatic pressure (blood pressure): this pressure causes FILTRATION of fluid OUT of the bloodstream.
  2. Capillary colloidal osmotic pressure aka COP (due to concentration difference of impermeable proteins): this pressure causes REABSORPTION or ABSORPTION of fluid INTO the bloodstream.
82
Q

What is edema?

A

Tissues become more swollen from fluid accumulation.

83
Q

What is tissue dehydration?

A

Not enough fluid in tissues.

84
Q

What are two factors that change the fluid balance between capillaries and interstitial fluid?

A
  1. A change in blood pressure:
    - Increase in BP: increase filtration, decrease reabsorption, congestive heart failure, edema
    - Decrease in BP: decrease filtration, increase reabsorption, tissue dehydration
  2. A change in plasma protein levels the colloidal osmotic pressure
    - Increase in COP: increase reabsorption, decrease filtration, tissue dehydration. Lactated Ringers brings extra salt in bloodstream and draws water into bloodstream. Mannitol (sugar that helps get rid of extra fluids in body).
    - Decrease in COP: decrease reabsorption, increase filtration, edema (high BP, low BP)
85
Q

What is the lymphatic system?

A

Includes one-way vessels that originate in the tissues and drain into the veins. They contain valves.

Fluid moves slowly (3L/day). Can be enhanced by skeletal muscle activity.

86
Q

What is the function of the lymphatic system?

A

Returns water and proteins to bloodstream, so you always have the same concentration of COP.

87
Q

What are veins?

A

Large thin-walled vessels that have a low resistance to blood flow and enable the blood to return to the heart. Their thin walls are easily stretched and compliant. Veins also contain one-way valves. They have smooth muscle in their walls.

88
Q

What are two functions of veins?

A
  1. Return blood from tissues to heart
  2. VOLUME reservoirs. Holds 60% of blood. Can be used for the heart when needed.
89
Q

Explain venous flow.

A

Valves: muscle contractions pump blood up to heart, and valves help prevent the blood from flowing the wrong way.

90
Q

What are varicose veins?

A

Twisted enlarged veins near surface of skin. Caused by weakened valves and veins.

Risk factors: heredity, overweight

91
Q

Explain venous return.

A

Venous pressure and atrial pressure influences venous return.

  • As venous pressure increases, more return
  • As atrial pressure increases, less return
92
Q

What are three factors that increase venous pressure?

A
  1. Venomotor tone: vasoconstriction by sympathetic nerves causes more blood to go back to heart.
  2. Skeletal muscle pump: skeletal muscles squeeze veins and moves blood to heart
  3. Respiratory pump: take breath, squeezes veins, moves more blood to heart.
93
Q

What two factors increase atrial pressure?

A
  1. Congestive heart failure: pressure in heart increases = less cardiac output and less stroke volume.
  2. Bad tricuspid valve: blood flowing from ventricle to right atrium.
94
Q

What is mean arterial pressure (MAP)?

A

Cardiac output and total peripheral resistance.

If blood pressure drops, either put more CO in or put in more TPR by tightening blood vessels.

95
Q

How does blood pressure homeostasis work?

A

Receptors: baroreceptors (stretch receptor) are located in the aortic arch, carotid sinus, arteries, veins, and right atrium.

Integration center: increased pressure → increased AP frequency;
decreased pressure → decreased AP frequency
(Processing center = medulla oblongata)

Output: autonomic neurons (parasympathetic and sympathetic)

Effectors: heart and vessels

96
Q

Describe neural controls over mean arterial pressure.

A

Step 1: A drop in blood pressure causes less stretch of the baroreceptors.

Step 2: Sensory neurons activate the integrating center and compare the stimulus to the set point.

Step 3: Autonomic neurons send info to the effectors for their responses to raise the blood pressure.

97
Q

What are the effectors and their responses to raise blood pressure?

A

1) Increase sympa stim to SA node
↑ heart rate
↑ cardiac output
↑ mean arterial pressure

2) Decrease parasympa stim to SA node
↑ heart rate
↑ cardiac output
↑ mean arterial pressure

3) Increase sympa stim to ventricular myocardium (contractile cells)
↑ force of contraction
↓ end systolic volume
↑ stroke volume
↑ cardiac output
↑ mean arterial pressure

4) Increase sympa stim to smooth muscles in veins (vasoconstriction)
↑ venous pressure & venous return
↑ end diastolic volume
↑ stroke volume
↑ cardiac output
↑ mean arterial pressure

5) Increase sympa stim to smooth muscle in arterioles (vasoconstriction)
↑ total peripheral resistance
↑ mean arterial pressure

NOTE: 3-5 do NOT have parasymp involvement.

98
Q

What is blood?

A

Blood consists of formed elements (hematocrit) that are cellular in origin and make up about 45% of the total blood. The remaining component of blood is plasma.

99
Q

What are the three components of plasma?

A
  1. Water (90%)
  2. Plasma proteins (8%)
  3. Solutes (1%)
100
Q

What is serum?

A

Plasma minus the clotting agents.

Given to patients w/ clotting probs.

101
Q

What are the three formed elements?

A
  1. Erythrocytes (red blood cells): carries oxygen
  2. Thrombocytes (platelets): blood clotting
  3. Leukocytes (white blood cells): part of immunity or body’s defense
102
Q

How many red blood cells are in females and how many are in males?

A

Females: 4.3—5.2 million RBC per microliter

Males: 5.1—5.8 million RBC per microliter

103
Q

What is the function of erythrocytes?

A

To carry oxygen and carbon dioxide in the blood.

104
Q

Describe the structure of erythrocytes.

A

The cell is a biconcave disk that facilitates gas exchange. It has no nucleus.

105
Q

What is hemoglobin?

A

Hemoglobin is a biomolecule that consists of four separate protein chains, each of which consist of a heme group (contains iron and carries oxygen in the cell) and a protein globin.

106
Q

Where in the body can iron be found?

A

65% found in the blood and the ramining is found in the liver, spleen, and bone marrow.

107
Q

What five locations does erythropoiesis (formation of red blood cells) occur?

A
  1. Bone marrow of the ribs
  2. Sternum
  3. Vertebrae
  4. Pelvis
  5. Ends of long bones
108
Q

What is needed for the production of red blood cells?

A

Vitamin B-12, folic acid, iron, and amino acids are needed.

109
Q

Explain the five stages of red blood cell formation.

A

Stage 1: Stem cell hemocytoblast

Stage 2: Erythroblast (hemoglobin is produced)

Stage 3: Reticulocyte (loses its nucleus)

Stage 4: Erythrocyte (goes to bloodstream from bone marrow)

Stage 5: Goes into peripheral bloodstream

110
Q

What helps with controll red blood cell production?

A

Growth hormone, thyroxine, estrogen, testosterone.

Most importantly, a hormone called erythropoietin that’s made in the kidney and secreted into blood.

111
Q

Describe the reflex for control over erythrocyte production.

A

Step 1: A decrease in tissue oxygen (hypoxia)

Step 2: Activated the kidney to produce erythropoietin

Step 3: Erythropoietin journeys to the bone marrow to stimulate the RBC formation, thus decreasing hypoxia.

112
Q

How many days do RBC’s generally live in males and females?

A

Males: 120 days

Females: 109 days

113
Q

What are reticuloendothelial system macrophages?

A

They are what destroy old, abnormal, or damaged cells. They’re located in the spleen, liver, some bone marrow, and other tissues.

114
Q

What happens to iron in the body after awhile?

A

Iron travels to the liver and spleen for storage or to bone marrow for reuse. The body recycles 99% of its iron.

115
Q

What happens to bilirubin?

A

It goes to the liver for excretion in bile.

116
Q

What is anemia?

A

A condition due to a low concentration of hemoglobin or RBC in the blood.

117
Q

What is hemorrhagic anemia?

A

Caused by a substantial amount of blood loss form the body.

118
Q

What is iron deficiency anemia?

A

Due to an excessive loss of iron fmor the body, due to blood loss from menstruation or bleeding ulcers; or dietary deficiency of iron.

119
Q

What is pernicious anemia?

A

Due to the inability of the body to absorb Vitamin B-12 from the digestive tract into the body for RBC production.

Vitamin B-12 normally attaches to an intrinsic factor (glycoprotein) produced by the stomach’s lining. Individuals with pernicious anemia lack the intrinsic factor, thus they can’t absorb Vitamin B-12.

Treatment: Vitamin B-12 shot that bypasses the digestive system and intrinsic factor.

120
Q

What is aplstic anemia?

A

Caused by inadequate production of mature or normal RBC’s due to bone marrow destruction. The agents that can cause this are radiation, benzene, gold salts and DDT.

121
Q

What is sickle cell anemia?

A

The result of abnormal hemoglobin production due to a genetic defect in the sequence of amino acids in the beta chain (valine for glutamic acid).

When these cells are exposed to low oxygen tension they undergo a sickle cell crisis and become distorted into sickle shapes causing the fragile membranes to rupture. Sickled cells can also pule up and block capillaries.

Carrier is more resistant to malaria than normal… thus their numbers would increase at the expense of normal individuals.

122
Q

What are thrombocytes (platelets)?

A

Small cytoplasmic fragments pinched off of megakaryocytes located in the bone marrow.

There’s 200k-500k per microliter.

They are involved in blood clotting.

123
Q

What is the homeostasis process of blood clotting?

A

It’s the stopping or slowing bleeding from a ruptured vessel. Too little versus too much coagulation.

Damage to the blood vessel exposes the underlying connective tissue or collagen and releases a variety of chemicals.

124
Q

What are the four stages of thrombocyte homeostasis?

A
  1. Vascular spasm
  2. Platelet plug
  3. Blood clot (fibrin) formation
  4. Vessel repairs
125
Q

Describe the vascular spasm stage of thrombocyte homeostasis?

A

Platelet factors cause a local vasoconstriction that reduces blood flow and loss.

126
Q

Describte the platelet plug stage of thrombocyte homeostasis.

A

Platelets adhere to the collagen and form a platelet plug. Platelets release chemicals that attract more platelets, a positive feedback of platelet recruitement.

127
Q

Describe the blood clot (fibrin) formation stage of thrombocyte homeostasis.

A

Exposed collagen and tissue factors stimulate a cascade of chemicals that produce fibrin or a strong fibrous plug.

Fibrin formation has three pathways:

  1. Intrinsic: activated by exposure of blood to collagen. Makes Factor VIII.
  2. Extrinsic: activated by tissue damage and release of chemicals into bloodstream.
  3. Common (both intrinsic and extrinsic): Active Factor X converts prothrombin into thrombin. Thrombin converts inactive fibrinogen into active fibrin to make fibers.
128
Q

Describe the vessel repairs stage of thrombocyte homeostasis.

A

Plasmin (fibrinolysin) and other chemicals slowly dissove the clot. Connective tissue and endothelium repairs itself w/ fibroblasts.

129
Q

What three things prevent clotting in normal vessels?

A
  1. Thrombomodulin
  2. Plasmin
  3. Protein C and S
130
Q

What is thrombosis?

A

A problem that comes from excessive clotting. Clot breaks off a vessel and forms embolus, which can cause problems.

131
Q

What two types of treatment can be used for excessive clotting?

A
  1. Coumadim: slows down blood clotting
  2. Heparin: used in surgery
132
Q

What is hemophilia?

A

Lack of Factor VIII, a clotting protein.

133
Q

What is Vitamin K Deficiency?

A

Caused by antibiotics that mess up microorganisms that make Vitamin K (Vitamin K helps w/ blood clotting proteins.

Take a Vitamin K shot to rectify the problem.

134
Q

What is aspirin?

A

“Thins” your blood by interfering w/ platelet formation. This causes you to bleed longer.

135
Q

Why is the QRS complex’s amplitude larger than the P-wave?

A

Because the QRS complex amplitude is caused by the ventricles, which ahve a greater mass of muscles, thus a greater number of cellular depolarizations, thus a larger amplitude than the P-wave.

136
Q

What is the specific aspect of ventricular depolarization that produces that S-wave?

A

The larger left ventricle and the presence of more Purkinje fibers than the right ventricle affect the size of the R-wave and the presence of the S-wave.

137
Q

What’s the PR interval?

A

The time it takes electrical impulse to spread from the beginning of atrial depolarization to the beginning of ventricular depolarization.

138
Q

What happens to the PR interval w/ a first-degree block?

A

A prolonged PR interval may be caused by longer delay at the AV node as seen in a first-degree heart block.

139
Q

What does the QT interval represent?

A

The time it takes to complete depolarization within the ventricles.

140
Q

Why might a very fit person have a slower heart rate than someone of average fitness?

A

A trained athlete, whose heart rate is slower than someone of average fitness, has a larger stroke volume.

Note: cardiac output = stroke volume x heart rate

141
Q

What is the normal angle range for the electrical axis of the heart?

A

The electrical axis is normally between -30 degrees and +90 degrees.

142
Q

What factors can cause a left axis deviation and a right axis deviation?

A

Left axis deviation: electrical axis is less than -30 degrees b/c left ventricular hypertrophy, COPD, obesity, or an inferior myocardial infarction.

Right axis deviation: electrical axis is greater than +90 degrees b/c right ventricular hypertrophy, an anterior-lateral myocardial infarction, pulmonary emboli, or normally occurs in tall thin adults.

143
Q

How would a fibrillating heart influence the pumping action or efficiency of the heart?

A

It would lower the efficiency of the heart.

144
Q

Which of the four phases of the normal frog heart cycle is the longest in duration?

A

Atrial diastole.

145
Q

Which ventricular phase of the normal frog heart cycle is the shortest in duration?

A

Ventricular systole.

146
Q

How does the frog’s heart rate change from the warm Ringer’s solution to the cold Ringer’s solution.

A

From warm to cold, the heart rate decreases.

147
Q

How does the kinetic energy relate to changes seen in heart rate after the aplication of the Ringer’s solution at different temperatures?

A

The higher the temperature, the more kinetic energy. Change from cold to warm increases kinetic energy.

148
Q

How does the length of ventricular diastole change from the warm Ringer’s solution to the cold Ringer’s solution?

A

From warm to cold, the length of ventricular diastole increases.

149
Q

Define Sterling’s law of the heart.

A

The strength of the heart’s systolic contraction is proportional to its diastolic expansion with the result that under normal physiological conditions, otherwise known as the length-tension relationship.

150
Q

How does strength or amplitude of muscle contraction change from warm Ringer’s solution to cold Ringer’s solution?

A

From warm to cold, the amplitude increases.

151
Q

How could Sterling’s law of the heart explain the amplitude change from the warm Ringer’s solution to the cold Ringer’s solution?

A

Longer refractory with cold solution allows for longer filling time. More blood increases distension of the heart, so the cold solution causes a stronger contraction of the heart (and higher amplitude) than the warm solution.

152
Q

How does tension data of the frog heart support Starling’s law of the heart?

A

Stretching of the ventricular wall causes cardiac muscle to contract more forcefully, so more tension leads to higher amplitude or contractile force.

153
Q

What causes the extrasystole in the frog’s heart?

A

Stimulation outside of the refractory period causes the extrasystole in the heart.

154
Q

At what point in the frog’s cardiac cycle did an extrasystole occur?

A

After the contraction and after the refractory period.

155
Q

What happened to the frog’s heartbeat interval after the extrasystole?

A

The heartbeat interval increased.

156
Q

What causes the frog’s heart to be insensitive to its normal pacemaker impulse after the extrasystole?

A

The heart is intensitive to its normal pacemaker impulse after the extrasystole because the heart is in refractory.

157
Q

Compared to skeletal muscle, what feature of the refractory period and heart cycle prevents the heart muscle from entering tetanus?

A

The refractory period is longer in the heart muscle, which keeps the heart from entering tetanus.

158
Q

What’s the significance of keeping the heart from entering tetanus?

A

If the heart were to enter tetanus, then the heart would not receive the blood it needs during relaxation, which would cause the ventricles to not pump blood efficienctly to the rest of the body.

159
Q

Which three chemicals could be used to elevate cardiac output?

A
  1. Epinephrine
  2. Digitalis
  3. Atropine
160
Q

Which three chemicals could be used to decrease cardiac output?

A
  1. Beta1 receptor blocker (propanolol)
  2. Cholinergic agonist (pilocarpine)
  3. Calcium channel blocker (verapamil)

Human Physiology (5 decks)

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