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KPE 260 Human physiology > Blood Circulation L 13 > Flashcards

Blood Circulation L 13 Flashcards

1
Q

what are the 2 plasma proteins?

A
  1. Globulins
    -) Alpha and beta globulins - transport lipids and fat-soluble vitamins
    -) Gamma globulins - antibodies that function in immunity
  2. Fibrinogen: helps in clotting after becoming fibrin
    -) Serum - blood without fibrinogen
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2
Q

what is plasma volume?

A

regulatory mechanisms that maintain plasma volume to maintain blood pressure

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3
Q

what happens if fluid is lost?

A

Osmoreceptors in the hypothalamus cause the release of ADH from the posterior pituitary gland

-lose water = lose pressure source=heart has to pump harder to maintain pressure = need pressure for perfusion to keep things moving

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4
Q

what are the 3 functions of the circulatory system?

A
  1. Transportation
    -respiratory gases, nutrients, wastes
  2. Regulation
    -hormonal and temp
  3. protection
    -immunity
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5
Q

septal defects are holes in …..

A

holes in interventricular or interatrial septa which allows blood to cross sides.

-Patent ductus arteriosus results from a failure of the foramen ovale to close after birth

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6
Q

what are erythrocytes? and their features

A

red blood cells,
a. Flattened, biconcave discs (disease: sickle cell)
b. Carry oxygen
c. Lack nuclei and mitochondria
d. Count - approximately 5 million/mm3 blood
e. Have a 120-day life span
f. Each contain about 280 million hemoglobin molecules
g. Iron heme is recycled from the liver and spleen; carried by transferrin in the blood to the red bone marrow
h. Anemia - abnormally low hemoglobin or RBC count

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7
Q

what are the 2 erythrocyte enzymes?

A

glycolytic enzymes and carbonic anhydrase

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8
Q

what are glycolytic enzymes and what do they do

A

-type of erythrocyte enzyme
- generate energy needed to fuel active transport mechanisms involved in maintaining proper ionic concentrations within cell
- Rely on glycolysis for ATP formation

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9
Q

what is carbonic anhydrase and what does it do?

A

-type of erythrocyte enzyme
- Critical in CO2 transport
- Catalyzes reaction that leads to conversion of metabolically produced CO2 into bicarbonate ion (HCO3-)
* Primary form in which CO2 is transported in blood

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10
Q

what are the 2 parts hemoglobin consists of?

A
  1. heme group
    * Four iron-containing non-protein groups
    * Each is bound to one of the polypeptides
  2. Globin portion
    * Protein composed of four highly folded polypeptide chains
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11
Q

erythropoiesis
-where does it occur?
-what removes old rbcs from circulation?

A

production of red blood cells(erythrocytes)
-rbcs survive 120 days
-SPLEEN removes old rbcs from circulation
-replaced at rate of 1-3 million rbcs/second
-occurs in bone marrow
- Pluripotent stem cells in red bone marrow differentiate into the different types of blood cells

Hematopoiesis
blood cell formation

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12
Q

Hematopoiesis

A

blood cell formation

a. Hematopoietic stem cells - embryonic cells that give rise to all blood cells

b. Process occurs in myeloid tissue (red bone marrow) and lymphoid tissue

c. As cells differentiate, they develop membrane receptors for chemical signals

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13
Q

Erythropoeisis

A

production of red blood cells

  • red bone marrow produces 2.5 million RBCs/second
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14
Q

Regulation of erythropoiesis

-stimulated by:
-how long does process take?

all iron travels in blood bound to:

what hormone regulates iron homeostasis?

A

1) Process stimulated by erythropoietin from the kidneys that respond to low blood O2 levels
2) Process takes about 3 days

Most iron is recycled from old RBCs, the rest comes from the diet

1) Intestinal iron secreted into blood through ferroportin channels

2) All iron travels in blood bound to transferrin

3) Major regulator of iron homeostasis is the hormone hepcidin which removes ferroportin channels to promote cellular storage of iron and lowers plasma iron levels

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15
Q

Polycythemia

A

A disorder characterized by an abnormal increase in the number of red blood cells circulating in the blood (elevated hematocrit)

2 types primary and secondary

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16
Q

what are the 2 general types of polycythemia?

A
  1. primary polycythemia
    * Caused by tumorlike condition of bone marrow
    * Erythropoiesis proceeds at uncontrolled rate
  2. Secondary polycythemia
    * Erythropoietin-induced adaptive mechanism to improve blood’s oxygen-carrying capacity in response to prolonged reduced oxygen delivery to the tissues
    * Occurs normally in people living at high altitudes
    * Sometimes called relative polycythemia
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17
Q

hematocrit percentage under normal conditions

A

45%

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18
Q

hematocrit percentage under anaemia

A

30%

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19
Q

hematocrit percentage under polycythemia

A

70%

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20
Q

hematocrit percentage under dehydration

A

70%

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21
Q

more hematocrit makes blood more

A

viscous

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22
Q

anemia is characterized by:
causes:

A

low hematocrit
- Nutritional anemia
- Pernicious anemia
- Aplastic anemia
- Renal anemia
- Hemorrhagic anemia
- Hemolytic anemia

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23
Q

Platelets

  • clot blood with ….
  • have nuclei?
    -Lifespan?
    -how many?
  • removed from circulation by?
A

-clot blood with fibrinogen
-smallest
-dont have nuclei
-5-9 day lifespan
- release serotonin that stimulates vasoconstriction
- Count: 130,000 to 400,000/mm3 blood
* Thrombocytes
* Cell fragments shed from megakaryocytes
- Have organelles and cytosolic enzymes for generating energy and synthesizing secretory products
- High concentrations of actin and myosin
* Remain functional for an average of 10 days
* Removed from circulation by tissue macrophages
* Do not leave blood as WBCs do
- About ⅓ are stored in blood-filled spaces in spleen
- Released when needed by sympathetically induced splenic contraction
* Thrombopoietin
- Hormone produced by liver increases number of megakaryocytes and therefore increases platelet production

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24
Q

Leukocytes
- have nuclei and mitos?
- how many?
2 main categories :

A

white blood cells
- HAVE nuclei AND mitos
-Move in amoeboid fashion
- Diapedesis - movement through the capillary wall into connective tissue
- Count - approximately 5000 to 9000/mm3 blood
-. Types of leukocytes
1) Granular leukocytes: neutrophils, eosinophils, and basophils
2) Agranular leukocytes: monocytes and lymphocytes

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25
Q

What are the 3 granular leukocytes? Neb

A

neutrophils, eosinophils, basophils

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26
Q

What are the 2 agranular leukocytes?

A

lymphocytes and monocytes

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27
Q

Neutrophils

A

A granular type of white blood cell(leukocyte) that engulfs invading microbes

  • Phagocytic specialists* Release web of extracellular fibres called neutrophil extracellular traps (NETs) that contain bacteria-killing chemicals
  • Can also destroy bacteria by phagocytosis
  • Functions
  • First defenders on scene of bacterial invasion
  • Very important in inflammatory responses
  • Scavenge to clean up debris
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28
Q

Eosinophils

-granular or agranular
-what does it fight and kill?
-involved in what type of reaction?

A

a granular leukocyte that secretes chemicals that fights parasites, involved in allergic reactions

  • Increase in circulating eosinophils (eosinophilia) is associated with
  • Allergic conditions such as asthma and hay fever
  • Internal parasite infestations, such as worms
  • Attach to worm and secrete substances to kill it
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29
Q

Basophils

A

granular leukocyte

-release histamine and heparin
-involved in allergic reactions

  • Least numerous and most poorly understood of the leukocytes
  • Quite similar structurally and functionally to mast cells
  • Synthesize and store
  • Histamine
  • Release is important in allergic reactions
  • Heparin
  • Speeds up removal of fat particles from blood after fatty meal
  • Can also prevent clotting of blood samples drawn for chemical analysis
  • Used extensively as anticoagulant drug
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30
Q

monocytes

A

agranular leukocyte
-transformed into macrophages

  • Emerge from bone marrow while still immature and circulate for day or two before settling down in various tissues in body
  • Mature and enlarge in resident tissue and become known as macrophages
  • Life span can range from several months to years
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31
Q

lyphocytes

A

agranular leukocytes
-B lymphocytes(transformed into plasma cells that secrete antibodies
-T lymphocytes(cells)(responsible for cell-mediated immunity)

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32
Q

Lymphocytes
-what are the 2 types
-where do they each form?
-what do they each attack?
lifespan

A

B and T
The two types of white blood cells that are part of the body’s immune system
B lymphocytes form in the bone marrow
- release antibodies that fight bacterial infections;

T lymphocytes
- form in the thymus and other lymphatic tissue and
- attack cancer cells, viruses, and foreign substances.

  • Provide immune defense against targets for which they are specifically programmed
  • Live about 100 to 300 days
  • Two types of lymphocytes
  • B lymphocytes
  • Produce antibodies
  • Responsible to antibody-mediated or humoral immunity
  • T lymphocytes
  • Do not produce antibodies
  • Directly destroy specific target cells by releasing chemicals that punch holes in the victim cell (cell-mediated immunity)* Target cells include body cells invaded by viruses and cancer cells
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33
Q

Red Blood Cell Antigens and Blood Typing

  1. Antigens are found ?
  2. Antibodies are secreted by ? In response to?
  3. ABO system: antigens on ……..
A

3 types:
1. Antigens: found on the surface of cells to help immune system recognize self cells

  1. Antibodies: secreted by (B) lymphocytes in response to foreign cells
  2. ABO system: antigens on erythrocyte cell surfaces
    a. Type A - has the A antigen
    b. Type B - has the B antigen
    c. Type AB - has both the A and B antigens
    d. Type O - has neither the A nor the B antigen
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34
Q

blood group types

A

-form of passive immunity

  • ABO blood types are named for presence of antigens on surface of erythrocytes
  • Type A has A antigens and anti-B antibodies
  • Type B has B antigens and anti-A antibodies
  • Type AB has both A and B antigens and no antibodies related to the ABO system
  • Type O does not have A or B surface antigens and both anti
    -A and anti-B antibodies
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35
Q

transfusion reaction

A

reaction of the body to a transfusion of blood that is not compatible with its own blood

-If a person receives the wrong blood type, antibodies bind to erythrocytes and cause agglutination.

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36
Q

Universal blood donor

A

o

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37
Q

Universal blood recipient

A

ab

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38
Q

Rh factor

-what is it?
-what does RH + and Rh- mean?
-what is Erythroblastosis fetalis? when does it occur?

A

Refers to the presence or absence of the Rh antigen on red blood cells.
- Rh-positive individual has Rh factor
- Rh-negative individual lacks Rh factor
- Erythroblastosis fetalis (hemolytic disease of the newborn)blood disorder that occurs when the blood types of a mother and baby are incompatible

  • Occurs when Rh-negative mother develops antibodies against the erythrocytes of an Rh-positive fetus
  • Approximately 12 other minor human erythrocyte antigen systems
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39
Q

heart murmur

A

an abnormal sound from the heart produced by defects in the chambers or valves(abnormal blood flow in heart)
-caused by defective heart valves

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40
Q

mitral stenosis

A

Mitral valve calcifies and impairs flow between left atrium and ventricle.
- may result in pulmonary hypertension

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41
Q

incompetent valves are valves that:
caused by:
-most common cause of chronic mitral regurtitation:

A

do not close properly
-cause: damaged papillary muscle

-mitral valve prolapse is most common cause of chronic mitral regurgitation
-mitral=bicuspid=left

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42
Q

cardiac cycle

A

A complete heartbeat consisting of contraction and relaxation of both atria and both ventricles
a. Repeating pattern of contraction and relaxation of the heart.
b. Systole: contraction of heart muscles
c. Diastole: relaxation of heart muscles

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43
Q

end-diastolic volume

A

total volume of blood in the ventricles at the end of diastole

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44
Q

End-systolic volume

A

the amount of blood left in the left ventricle after systole (1/3 of the end-diastolic volume

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45
Q

Pressure Changes During the Cardiac Cycle

A
  1. Ventricles begin contraction, pressure rises, and AV valves close (lub); isovolumetric contraction
  2. Pressure builds, semilunar valves open, and blood is ejected into arteries.
  3. Pressure in ventricles falls; semilunar valves close (dub); isovolumetric relaxation
  4. Dicrotic notch - slight inflection in pressure during isovolumetric relaxation
  5. Pressure in ventricles falls below that of atria, and AV valve opens. Ventricles fill.
  6. Atria contract, sending last of blood to ventricles
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46
Q

How does electrical activity of the heart work?

A
  1. Cardiac muscle cells are interconnected by gap junctions called intercalated discs.
  2. Once stimulation is applied, the impulse flows from cell to cell.
  3. The area of the heart that contracts from one stimulation event is called a myocardium or functional syncytium.
  4. The atria and ventricles are separated electrically by the fibrous skeleton.
47
Q

electrical activity of the heart
-what is pacemaker of heart and where is it located?

-what are the 2 secondary pacemakers?

A

Contraction of the heart depends on electrical stimulation of the myocardium

  1. Automaticity - automatic nature of the heartbeat
  2. Sinoatrial node (SA node) - “pacemaker”; located in right atrium
  3. AV node and Purkinje fibers are secondary pacemakers of ectopic pacemakers; slower rate than the “sinus rhythm”
48
Q

ECG and heart sounds

Lub occurs …..
Dub occurs…..

A

a. “Lub” occurs after the QRS wave as the AV valves close
b. “Dub” occurs at the beginning of the T wave as the SL valves close

49
Q

electrocardiogram records:

A

electrical activity of the heart by picking up the movement of ions in body tissues in response to this activity.
a. Does not record action potentials, but results from waves of depolarization
b. Does not record contraction or relaxation, but the electrical events leading to contraction and relaxation

50
Q

ECG waves and intervals
P
P-Q interval
QRS wave
ST segment
T wave

A

a. P wave - atrial depolarization
b. P-Q interval - atrial systole
c. QRS wave - ventricular depolarization
d. S-T segment - plateau phase, ventricular systole
e. T wave - ventricular repolarization

51
Q

ECG leads

A

a. Bipolar limb leads record voltage between electrodes placed on wrists and legs
.1) Lead I: between right arm and right leg
2) Lead II: between right arm and left leg
3) Lead III: between left arm and left leg

b. Unipolar leads record voltage between a single electrode on the body and one built into the machine (ground).1) Limb leads go on the right arm (AVR), left arm (AVL), and left leg (AVF).2) There are six chest leads.

52
Q

Arrhythmias

A

abnormal patterns of electrical activity that result in abnormalities of the heartbeat

53
Q

drugs used to treat arrhythmias

A

affect the nature and conduction of cardiac action potentials, and have been classified into four different groups:
Group 1: drugs that block the fast Na+ channels (quinidine, procainamide, lidocaine).
Group 2: drugs are beta-blockers (propranolol, atenolol) Group 3: drugs block K+ channels (amiodarone)
Group 4: drugs block the slow Ca2+ channels (verapamil, diltiazem).

54
Q

Heart Arrhythmias Detected by ECG:
Abnormal heart rhythms

Bradycardia detected by:

Tachycardia detected by:

A

a. Bradycardia: slow heart rate, below 60 bpm
b. Tachycardia: fast heart rate, above 100 bpm
c. These heart rhythms are normal if the person is active, but not normal at rest.
d. Abnormal tachycardia can occur due to drugs or fast ectopic pacemakers.
e. Ventricular tachycardia occurs when pacemakers in the ventricles make them contract out of synch with the atria.
f. This condition is very dangerous and can lead to ventricular fibrillation and sudden death.

55
Q

Heart Arrhythmias Detected by ECG:
Flutter vs Fibrillation (difference)
-which is coordinated and uncoordinated

A

a. Flutter: extremely fast (200 to 300 bpm) but coordinated contractions

b. Fibrillation: uncoordinated pumping between the atria and ventricles

56
Q

Atherosclerosis and Cardiac Arrhythmias

A

Most common form of arteriosclerosis (hardening of the arteries)
a. Contributes to 50% of the deaths due to heart attack and stroke
b. Plaques protrude into the lumen and reduce blood flow.
c. Serve as sites for thrombus formation
d. Plaques form in response to damage done to the endothelium of a blood vessel.
e. Caused by smoking, high blood pressure, diabetes, high cholesterol

57
Q

how atherosclerosis is developed:
1. Lipid-filled __________ and _________ assemble at the site of damage within the _________ ___________.
2. Next, layers of _________ _______ are added.
3. Finally, a cap of ________ _______ covers the layers of smooth muscle, lipids, and cellular debris.
d. Progress promoted by inflammation stimulated by cytokines and other __________regulators.

A

a. Lipid-filled macrophages and lymphocytes assemble at the site of damage within the tunica interna (fatty streaks).
b. Next, layers of smooth muscle are added.
c. Finally, a cap of connective tissue covers the layers of smooth muscle, lipids, and cellular debris.
d. Progress promoted by inflammation stimulated by cytokines and other paracrine regulators.

58
Q

atherosclerosis: cholesterol and lipoproteins

a. Low-density lipoproteins (LDLs) carry cholesterol to ________.
1) People who consume or produce a lot of cholesterol have more ____.
2) This high LDL level is associated with increased development of ___________

b. High-density lipoproteins (HDLs) carry cholesterol away from the arteries to the ______ for metabolism.

1) This takes cholesterol away from the macrophages in developing plaques (foam cells).

2) Statin drugs (for example, Lipitor), fibrates, and niacin increase HDL levels.

A

a. Low-density lipoproteins (LDLs) carry cholesterol to arteries.
1) People who consume or produce a lot of cholesterol have more LDLs.
2) This high LDL level is associated with increased development of atherosclerosis

b. High-density lipoproteins (HDLs) carry cholesterol away from the arteries to the liver for metabolism.

1) This takes cholesterol away from the macrophages in developing plaques (foam cells).

2) Statin drugs (for example, Lipitor), fibrates, and niacin increase HDL levels.

59
Q

inflammation in atherosclerosis

-what is a good predictor for atheroscelrosis?
-treatments?

A

a. Atherosclerosis is now believed to be an inflammatory disease.
b. C-reactive protein (a measure of inflammation) is a better predictor for atherosclerosis than LDL levels.
c. When endothelial cells engulf LDLs, they become oxidized LDLs that damage the endothelium
d. Antioxidants may be future treatments for this condition.

60
Q

Pacemaker potential
-what is it?
- AKA?
-triggered by?

-how many mV do voltage gated Ca2+ channels open? what does this trigger?

-how does repolarization occur?

A

a. A slow, spontaneous depolarization; also called diastolic depolarization - between heartbeats, triggered by hyperpolarization
b. At −40mV, voltage-gated Ca2+ channels open, triggering action potential and contraction.
c. Repolarization occurs with the opening of voltage-gated K+ channels.

61
Q

electrical activity of heart and

What is responsible for pacemaker potential

What increases cAMP production that keeps cardiac pacemakers channels open

Heart rate speed increases due to inflow of

A

Pacemaker cells in the sinoatrial node depolarize spontaneously, but the rate at which they do so can be modulated
1) Epinephrine and norepinephrine increase the production of cAMP, which keeps cardiac pacemaker channels open.
a) Called HCN channels - hyperpolarization -activated cyclic nucleotide-gated channels
b) Speeds heart rate due to Na+ inflow
2) Parasympathetic neurons secrete acetylcholine, which opens K+ channels to slow the heart rate.

62
Q

Myocardial action potentials

a. Cardiac muscle cells have a resting potential of _____
b. They are depolarized to threshold by action potentials from the __ ________.
c. Voltage-gated Na+ channels (fast Na+) open, and membrane potential plateaus at -15mV for 200 to 300 msec.
1) Due to balance between slow influx of ____ and efflux of __
d. More K+ are opened, and ___________ occurs.
e. Long plateau prevents ________ and _________

A

a. Cardiac muscle cells have a resting potential of −85mV.
b. They are depolarized to threshold by action potentials from the SA node.
c. Voltage-gated Na+ channels (fast Na+) open, and membrane potential plateaus at -15mV for 200 to 300 msec.
1) Due to balance between slow influx of Ca2+ and efflux of K
d. More K+ are opened, and repolarization occurs.
e. Long plateau prevents summation and tetanus

63
Q

Conducting tissues of the heart

A

-Action potentials spread via intercalated discs (gap junctions).
-SA node to AV node to stimulate atrial contraction
-AV node at base of right atrium and bundle of His conduct stimulation to ventricles.
-In the interventricular septum, the bundle of His divides into right and left bundle branches.
-Branch bundles become Purkinje fibers, which stimulate ventricular contraction.

64
Q

Conduction of Impulses

A

Action potentials from the SA node spread rapidly
0.8-1.0 meters/second
At the AV node, things slow down.
0.03−0.05 m/sec
This accounts for half of the time delay between atrial and ventricular contraction.
The speed picks up in the bundle of His, reaching 5 m/sec in the Purkinje fibers.
Ventricles contract 0.1-0.2 seconds after atria.

65
Q

Excitation-Contraction Coupling

A

a. Ca2+-stimulated Ca2+ release
b. Action potentials conducted along the sarcolemma and T tubules, open voltage-gated Ca2+ channels
c. Ca2+ diffuses into cells and stimulates the opening of calcium release channels of the SR
d. Ca2+ (mostly from SR) binds to troponin to stimulate contraction
e. These events occur at signaling complexes on the sarcolemma where it is close to the SR

66
Q

electrical activity of heart: repolarization

A

a. Ca2+ concentration in cytoplasm reduced by active transport back into the SR and extrusion of Ca2+through the plasma membrane by the Na+-Ca2+exchanger
b. Myocardium relaxes

67
Q

electrical activity of heart: refractory periods

A

a. Because the atria and ventricles contract as single units, they cannot sustain a contraction.

b. Because the action potential of cardiac cells is long, they also have long refractory periods before they can contract again.

68
Q

plasma is

A

clotted

69
Q

serum is

A

non clotted

70
Q

hematocrit is

A

the amount of blood from rbcs (45%) percent of blood formed from blood cells

71
Q

hematocrit is

A

the amount of blood from rbcs (45%) percent of blood formed from blood cells

72
Q

what % of plasma is made of plasma proteins?

A

7-8%

73
Q

function of albumin

A

creates osmotic pressure to help draw water from tissues into capillaries to maintain blood volume and pressure

-transport substances, contribute most to colloid osmotic pressure

74
Q

function of alpha and beta globulins in blood plasma

A

transport water insoluble molecules
-clotting factors
-inactive precursor molecules

75
Q

what happens to ur blood when u go to high altitude(less oxygen)

A
  1. kidneys detect rduced O2 carrying capacity of blood
  2. when less O2 is delivered to kidneys, they secrete hormone erythropoietin(EPO) into blood
  3. EPO stimulates erythropoiesis by bone marrow(make more rbcs)
  4. additional circulating erythrocytes(rbcs) increase O2 carrying capacity of blood
  5. increased O2 carrying capacity relieves initial stimulus that triggered EPO secretion
76
Q

globulins(plasma proteins) types

A

1) Alpha and beta globulins – transport lipids and
fat-soluble vitamins
2) Gamma globulins – antibodies that function in
immunity
Fibrinogen: helps in clotting after becoming
fibrin
1) Serum – blood without fibrinogen

77
Q

what are the Erythrocyte Enzymes(2)

A
  1. Glycolytic enzymes
    – Necessary for generating energy needed to fuel active
    transport mechanisms involved in maintaining proper
    ionic concentrations within cell
    – Rely on glycolysis for ATP formation
  2. Carbonic anhydrase
    – Critical in CO2 transport
    – Catalyzes reaction that leads to conversion of
    metabolically produced CO2 into bicarbonate ion
    (HCO3-)
    * Primary form in which CO2 is transported in blood
78
Q

Arteries and veins are composed of 3 tissue layers.
what type is tissue is each made of?
Tunica Externa:
Tunica Media:
Tunica Interna:

A

connective tissue
smooth muscle tissue
3 parts:
1. innermost simple squamous endothelium
2. basement membrane(layer of glycoproteins)
3. layer of elastic fibres

79
Q

what tissue layer are capillaries composed of?

A

single layer of simple squamous epithelium tissue
permeable

80
Q

whats the pathway of blood out of the heart?

A

arteries
arterioles
capillaries
venules
veins

81
Q

what are the 2 types of arteries

A

elastic (gets blood from heart bfor passing it on to other arteries) closer to heart
ex. aorta and pulmonary artery
muscular(blood going to body’s tissues) further from heart
ex. femoral, radial, and brachial arteries

82
Q

what is an aneurysm?
where does it occur

A
  • is a balloon-like swelling in an artery or in a weakened
    ventricular wall
    -ost commonly occurs in the aorta - either as a thoracic aortic
    aneurysm or an abdominal aortic aneurysm; but can occur in cerebral
    and other arteries
    *A dissected aorta is a tear in the wall of the aortic aneurysm, which
    often can be detected and corrected before it completely bursts
    *Aneurysms may result from congenital causes and atherosclerosis,
    but conditions such as hypertension and diabetes can increase the
    risk
83
Q

how big are capillaries

A

smallest blood vessel
7-10 mm diameter (each micrometer is 0.001 mm)

84
Q

what is the function of capillaries

A

where gases and nutrients are exchanged between blood and tissues
“microcirculation”

85
Q

blood flow to capillaries is regulated by (2):

A

-vasoconstriction and vasodilation of arterioles
-precapillary sphincters(circular muscle bands)

86
Q

what are the 3 types of capillaries

A
  1. continuous
  2. fenestrated
  3. discontinuous(sinusoidal)
87
Q

what are continous capillaries
features
where are they found

A

*Continuous capillaries have no perforations (cells are close together)
*They allow only small molecules to pass through
*Found in muscles, adipose tissue, and central nervous system (add to blood-
brain barrier)

88
Q

what are fenestrated capillaries features?
where are they found

A

*Fenestrated capillaries have pores in
vessel wall
*Found in kidneys, intestines, and
endocrine glands

89
Q

what are discontinuous(sinusoidal) capillaries
where are they found
features

A

*Discontinuous (or Sinusoidal) capillaries have gaps between cells
*These gaps are large enough to allow proteins or blood cells through
*Found in bone marrow, liver, and spleen

90
Q

what are venules

A

*The smallest veins and receive blood from capillaries
*Have much larger lumina and thinner walls than arterioles
*Conduct the blood into the veins, which transport it back to the heart

91
Q

where are veins located?

A

Veins are closer to the surface of your body, and arteries are deep
inside your muscles

92
Q

3 Characteristics of Veins

A
  1. large w biggest lumens of any blood vessel
  2. thin walls w small layers of elastic fibers and smooth muscle
  3. blood is carried at low pressures so walls dont need to be strong
93
Q

what % of total blood volume do veins contain?

A

70% and are 30x more compliant than arteries

94
Q

how do veins get help to carry blood upwards against gravity when were standing to return blood to the heart?

A

Skeletal muscle pumps
venous valves(ensure one directional flow of blood(prevents backflow)

95
Q

what are varicose veins

A

Varicose veins are enlarged surface veins, generally in the lower
limbs, which occur when venous congestion stretches the veins to the
point that the venous valves no longer close effectively

96
Q

what are 5 risk factors for varicose veins?

A

Genetic susceptibility
Long periods of standing
Older age
Obesity
Pregnancy

97
Q

how to prevent/treat varicose veins?

A

walking
avoiding sitting/standinf for long periods of time
-shedding excess pounds to take pressure off veins
-compession socks
-leg elevation
-surgical treatment:
Sclerotherapy
* Where chemicals are injected into the vein causing it to collapse
*Laser Therapy
* Using laser to destroy the veins
*Ligation & stripping
* Tying off and removing the veins

98
Q

what are surgical treatments for varicose veins?

A

Sclerotherapy
* Where chemicals are injected into the vein causing it to collapse
*Laser Therapy
* Using laser to destroy the veins
*Ligation & stripping
* Tying off and removing the veins

99
Q

what is deep vein thrombosis(DVT)

A

Inadequate venous flow in a bedridden patient increases the risk of
deep vein thrombosis which can lead to a venous thromboembolism
(a traveling blood clot)

100
Q

how to reduce risk of deep vein thrombosis(DVT)

A

*Walking around as soon as possible after a surgery reduces the risk,
as does the use of compression stockings and devices that compress
the leg
*Anticoagulant drugs or thrombolytic agents may sometimes be
necessary to prevent or treat a thromboembolism so that it doesn’t
result in a potentially fatal pulmonary embolism

101
Q

what is the most common form of ateriosclerosis

A

atherosclerosis

102
Q

how may deaths does atherosclerosis contribute to

A

31% of deaths due to heart attack
Buildup of plaque (atheroma) in the tunica interna that
protrudes into the lumen and reduces blood flow

103
Q

what causes atherosceleosis

A

Buildup of plaque (atheroma) in the tunica interna that
protrudes into the lumen and reduces blood flow

104
Q

causes of Atherosclerosis(4)

A

a. Smoking
b. High blood pressure
c. Diabetes
d. High cholesterol
Plaques form in response to damage done to the
endothelium of a blood vessel.

105
Q

describe plaque formation in atherosclerosis

A

a.Lipid-filled macrophages and lymphocytes assemble at the site of damage within the tunica interna (fatty streaks).
b.Next, layers of smooth muscle are added.
c.Finally, a cap of connective tissue covers the layers of smooth muscle, lipids, and cellular debris.
d.Progress promoted by inflammation stimulated by cytokines and other paracrine regulators.
* Plaque serves as a site for thrombus formation

106
Q

what happens in thrombus formation
-what are the clotting agents recruited

A
  • Once the fibrous cap ruptures and vulnerable plaque is exposed, clotting agents are recruited:
  • Platelets
  • Fibrin
  • Together, these form the
    blood clot
107
Q

what lipoprotein caries cholerstrol to arteries?

A

LDLs =BAD
1) People who consume or produce a lot of cholesterol have more LDLs.
2) This high LDL level is associated with increased development of
atherosclerosis.

108
Q

what lipoprotein carries cholestrol away from arteries into the liver for metabolism?

A

HDLs = GOOD
1) This takes cholesterol away from the macrophages in developing plaques (foam cells).
2) Statin drugs (for example, Lipitor), fibrates, and niacin increase HDL levels.

109
Q

what is a good predictor for atherosclerosis?

A

C-reactive protein (a measure of inflammation) is a better predictor for atherosclerosis than LDL levels

110
Q

When endothelial cells engulf LDLs, they
become :

A

oxidized LDLs that damage the endothelium
-antioxidant can be future treatment for atherosclerosis

111
Q

Ischemic Heart Disease
-most common cause

A

a condition characterized by inadequate oxygen due to reduced blood flow.
-atherosclerosis
Associated with increased production of lacticacid and resulting pain, called angina pectoris(referred pain).
3) Eventually, necrosis of some areas of the heartoccurs, leading to a myocardial infarction (heart attack or MI).
-Nitroglycerin producesvasodilation
a) Improves blood flow
b) Dead myocardial cells can not be replaced by mitosis of
neighboring cells
c) Infarct may cause death of neighboring cells to
enlarge the infarct

112
Q

how to detect ischemia(2)

A

1) Depression of the S-T segment of an electrocardiogram
2) Plasma concentration of blood enzymes
a) Creatine phosphokinase – 3 to 6 hours, return to normal in 3 days
b) Lactate dehydrogenase – 48 to 72 hours, elevated about 11 days
c) Troponin I –most sensitive test
d) Troponin T

113
Q

ischemic vs hemorrhagic stroke

A

ischemic: blocked blood vessel
hemorrhagic: ruptured blood vessel

KPE 260 Human physiology (4 decks)

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