Quiz 1 Flashcards

1
Q

REVIEW: 4 main types of tissue

A

1) Muscular
2) Neural
3) Connective
4) Epithilial

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2
Q

T or F: Blood is a Connective Tissue?

A

True

Blood is a liquid, but it is a connective tissue.

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3
Q

Your blood can be separated out into 2 main categories (and % of each in blood):

A

FORMED ELEMENTS (cells) - about 45%

PLASMA (liquid) - about 55%

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4
Q

What is PLASMA composed of?

Plasma proteins role is:

A
90% water
Plasma proteins (7% ... albumins, globulins, fibrinogen)
Other solutes (1% ... electrolytes, nutrients, waste)

Plasma is composed of different proteins that play a role in immunity, clotting, inflammation, maintainingosmotic pressure, etc.

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5
Q

What are FORMED ELEMENTS COMPOSED of:

A

RBC’s (Erythrocytes) … about 44 of 45%
WBC’s (Leukocytes) … leukocytes and platelets are the other 1% of 45%
Platelets (Thrombocytes)

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6
Q

How much blood volume is in our bodies at one time

A

4-6 Liters

a little more for men, little less for women

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7
Q

What is pH

High concentrations of hydrogen ion have a low or a high pH?

pH levels in blood?

What is acidocis (and level)

What is alkalosis (and level)

A

pH is a measure of the hydrogen ion concentration of a solution.

Solutions with a HIGH concentration of hydrogen ions have a LOW pH, and solutions with a LOW concentration of H+ ions have a HIGH pH.

Should be between 7.35 and 7.45

Acidocis = Below 7.35
Alkalosis = Above 7.45
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8
Q

What is viscocity

Is blood or water more viscous

Temp of blood should be:

A

Viscocity is resistance to flow (thick)

Blood is 5x more viscus (thick) than water

100.4 degrees

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9
Q

What are the 2 main functions of blood:

Other functions of blood?

A

BLOOD FUNCTIONS:

1) Transports O2, nutrients, and hormones to our cells (and wastes out and CO2 out / away)
2) Regulates pH and ion regulation (ions are calcium, potassium, sodium) … ions are key to muscle contraction (like in the heart)

Other Functions:

  • Helps restricts blood / fluid loss through blood clots (platelets will form mesh-like clot at injured site)
  • Defense (WBC’s fight toxins and foreign materials)
  • Maintain body temp by absorbing heat from skeletal muscles.
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10
Q

Is there more O2 in arteries or veins

A

ARTERIES

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11
Q

What does deoxygenated mean?

Are veins or arteries deoxygenated?

A

Deoxygenated does NOT mean NO O2 in blood. It just means it is LESS O2 than oxygenated blood.

So venous (Veins) blood is deoxygenated compared to arterial blood.

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12
Q

Plasma is made up mainly of water, but it also has many protiens within fluid matrix. What are the main 3 protiens and their function:

A

Albumins: maintain OSMOTIC PRESSURE

Globulins are important for IMMUNITY (antibodies) and to transport substances … and important for clotting

Fibrinogen: Blood CLOTTING

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13
Q

What is osmotic pressure

A

Osmotic pressure can be thought of as the pressure that pulls fluid BACK INTO the intervascular space. It could be thought of as it would be required to STOP LIQUIDS FROM DIFFUSING through a barrier by osmosis. In other words, it refers to how hard the water would “push” to get through the barrier in order to diffuse to the other side.

Water moves from high to low water activity (high pressure to low pressure) due to osmosis. The pressure needed to stop the osmotic flow is the osmotic pressure.

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14
Q

Besides water making up 90% of plasma, and the 3 plasma proteins mentioned above, what are the other solutes (and examples of each) in blood plasma:

A
  • Electrolytes: sodium, potassium, calcium, magnesium
  • Nutrients: carbs, fats, proteins
  • Wastes
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15
Q

Why would someone need someone else’s plasma donation

Do RBC’s get donated as well during a plasma donation?

A

Replace nutrients and electrolytes for patient who needs them

No

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16
Q

What is Hematopoiesis / Hemopoiesis:

What is life span of blood cells

Where and when do blood cells form?

A

Formation of new blood cells and platelets that form in bone marrow.

100-120 days (average closer to 90-100 according to Dr. Paschall)

Originally occurs during the prenatal stage (e.g., in the yolk sac, liver, spleen and bone marrow) and then continuously in the postnatal periods (e.g., in the bone marrow)

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17
Q

Function of:

  • RBC’s
  • WBC’s
  • Platelets
A

RBC’s = transport gases (O2 and CO2)

WBC’s = Defense, to kill off bacteria, immunity, kill toxins/antigens, etc.

Platelets = help with clotting

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18
Q

What is the Hematocrit

About how much is it in blood?

What would a low hematocrit mean?

A

Hematocrit is the % of RBC’s compared to total blood.

Usually it is about 44% of blood makeup

You have less RBC’s so unable to deliver needed O2 to cells = anemia

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19
Q

Do RBC’s have a nucleus, mitochondria, and other organelles?

A

Originally they do, but over time they lose organelles. So they can’t replicate or produce energy/ATP … so that is partly why they die in 100-120 days.

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20
Q

RBC’s are shaped in a Biconcave disc. What are 3 reasons this is important?

Why is it biconcave shape?

A

1) Large surface area to absorb more oxygen
2) RBC’s can stack (called a rouleaux) so they can flow through capillaries (narrow vessels) easier
3) Flexibility, so they can flex and bend as they travel through vessels.

Because a RBC has no organelles within it

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21
Q

What helps transport gases (O2 and CO2) in RBC’s

What is it?

A

Hemoglobin

Hemoglobin is the protein molecule in red blood cells that O2 binds to (4 O2 molecules can bind to a hemoglobin molecule) and the HgB carries oxygen from the lungs to the body’s tissues … and it also returns carbon dioxide (CO2) from the tissues back to the lungs.

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22
Q

What is Hemoglobin A1c or HbA1c:

Why would we need to know this?

A

A 3 month view of how your body has been managing blood sugar. Average amount of glucose in blood over 3 months (since RBC’s live for about that long).

Because of how prevalent diabetes is. The blood test for HbA1c level is routinely performed in people with type 1 and type 2 diabetes mellitus. Blood HbA1c levels are reflective of how well diabetes is controlled. The normal range level for hemoglobin A1c is less than 6%. HbA1c also is known as glycosylated, or glycated hemoglobin.

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23
Q

What is blood doping?

Why would someone blood dope?

What are dangers of blood doping?

A

Taking your own RBC’s out and then inject them back into your blood before an event to give you ability to carry more O2 (increase VO2)

Can exercise / aerobic exercise / athletic performance much longer without fatiguing

Increased viscosity, so potential in clogging arteries because blood is thicker (thrombosis -> embolism). Increased risk for stroke or MI (myocardial infarction = heart attack). Increased BP.

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24
Q

What is EPO:

What is: hematopoiesis / Hemopoiesis

What is Anemia:

A

Erythropoietin. … EPO is a protein hormone produced by the KIDNEY (since the kidney filters blood and would know if RBC’s count is low). After being released into the blood stream it binds with receptors in the bone marrow, where it stimulates the production of red blood cells (erythrocytes).

EPO is hormone to stimulate hemopoiesis, which is creation of new RBC’s

Anemia is a low RBC count, so lack of O2 to tissues.

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25
Q

What is Sickle Cell disease

A

Sickle cell disease is when RBC’s change into a sickle shape (not biconcave shape), so they get clogged in arteries and vessels (blood clot), so O2 can’t get to tissues, so you get short of breath or fatigued due to lack of O2 = anemic.

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26
Q

What is function of WBC’s:

Accronym to remember 5 WBC’s:

5 main types of WBC’s:

Of these 5, which are granular, agranular (no granules), and which are phagocytes (eaters)

A

WBC’s (leukocytes) are for DEFENSE and IMMUNITY … to defend body against pathogens, toxins, debris, or abnormal cells.

B  ecause
N  obody
E  njoys
M ore
L  eukocytes

(Means you’d be more sick)

B  - Basophil
N  - Neutrophil
E  - Eosinophil
M  - Monocyte
L  - Lymphocyte

Granular: BNE
Agranular: ML
Phagocytes: NEM

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27
Q

T or F: WBC’s can travel out of bloodstream / vessels and are not always circulating in blood

Why

A

True

They travel through and out of bloodstream (between organs) to fight immunities and kill foreign particles, and send signals to other cells to fight toxin (so they don’t necessarily always circulate IN blood).

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28
Q

KEY to remember about Basophils

What is a Histamine

What is an anti-histamine

A
  • They have/release HISTAMINE

Histamine is like a bouncer at a club. It is a compound released by body to get foreign object out (like an allergy) So you sneeze, running nose, rash, or tear up to get it out.

An antihistamine causes body NOT to react that way (stop allergic reaction).

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29
Q

What are 3 KEYS to remember about Neutrophils … and MOST IMPORTANT

A

MOST IMPORTANT … First on scene during acute inflammation

Most abundant WBC’s

They eat and kill bacteria (Phagocytes)

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30
Q

KEY to remember about Eosinophils

A
  • Kill PARASITIC WORMS
  • Bilobed nucleus
  • Darker than neutrophils
  • Active in allergic reactions
  • Found in bronchi, GI tract, uterus
  • They eat and kill bacteria (Phagocytes)
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31
Q

KEY to remember about Monocytes

A

Main role is to PHAGOCYTIZE (eat)

Agranulocyte

C-shaped nuclues

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32
Q

KEY to remember about Lymphocytes

Lymphocytes are subdivided into 3 categories:

A

Most abundant agranulocyte

1) B lymphocytes – antiBody production
2) T lymphocytes – ATTACK antigen processing (two subsets … HELPERS and SUPPRESSORS. They either help fight, or suppress the process of WBC’s)
3) NK - Natural killer (NK) cells

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33
Q

What is Leukemia

How can you tell if someone has leukemia?

A

A cancer of the blood. Where body produces way more WBC’s than it needs, so the WBC’s don’t work right and kill other cells. It is a cancer of blood-forming tissues, hindering the body’s ability to fight infection.

Since there are way more WBC’s than RBC’s, you don’t have ability to get as much O2 to cells, so you are tired and lack energy often.

Elevated levels of WBC’s in a CBC test (bone marrow produces a lot)

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34
Q

How fast leukemia progresses … acute or chronic.

Acute means

Chronic means

A

Acute (fast growing) … it gets bad FAST!

Chronic (slow growing) … it takes a while for it to get bad.

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35
Q

Main function of platelets

A

HELP WITH CLOTTING to stop bleeding.

They form a platelet plug. If a problem arises (a cut) the platelets will aggregate together, a clot is formed (coagulation), clot contracts and hardens, and then eventually the clot dissolves.

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36
Q

SUMMARY.

Main function of these cells:

  • Erythrocytes
  • Leukocytes
  • Basophils
  • Neutrophils
  • Eosinophils
  • Monocytes
  • Lymphocytes
  • Platelets
A
  • Erythrocytes: RBC’s to transport O2 and CO2
  • Leukocytes: WBC’s for immunity, defense, etc. All the 5 different WBC’s (BNEML) help with body defense
  • Basophils: release histamine to get foreign body OUT
  • Neutrophils: First on site, most abundant, phagocytosis of bacteria
  • Eosinophils: defense against parasites / inflamation
  • Monocytes: phagocytosis (c shaped)
  • Lymphocytes: B and T lymphocytes and NK cells. Produce antibodies (B) and attack antigens (T) to kill viruses/infections/foreign bodies.
  • Platelets: clot blood
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37
Q

EVERYTHING BELOW HERE IS ON THE VASCULATURE SLIDES

A

ok

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38
Q

T or F: The circulatory system includes what two major systems

A

Cardiovascular

Lymphatic

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39
Q

The cardiovascular system can be subdivided into 2 sub systems:

A

Systemic

Pulmonary

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40
Q

What types of tissues are found in vascular walls?

A

All 4 types of tissue:

  • Muscular (smooth muscle)
  • Nervous
  • CT (blood)
  • Eptithilial (simple squamous for exchange of gases)
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41
Q

Walls of vessels consist of 3 layers:

A

1) Tunica Intima (inner)
2) Tunica Media (middle)
3) Tunica Adventitia (outer)

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42
Q

Which of the 3 layers of vessels is where endothilial cells are?

Which of 3 layers is where smooth muscle is?

Nerve fibers are in what layer of vessels?

Which of 3 layers is the thickest with LOTS of elastic fibers?

A

Tunica Intima

Tunica Media

Tunica Adventitia

*** Tunica media

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43
Q

*** T or F: Capillaries do NOT have smooth muscle in Tunica Media

A

***** (SOS)

TRUE

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44
Q

Explain route of blood through vessels:

A

Arteries > Arterioles > Capillaries > Venuoles > Veins

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45
Q

What is the lumen?

A

Inside space of a tube / vessel

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46
Q

Are the more elastic arteries the bigger arteries (aorta, pulmonary) or little arteries?

So is Tunica Media thick or thin in the elastic arteries?

Why are they so elastic?

A

Bigger arteries are more elastic, medium arteries are more smooth muscle.

Thick

Because bigger arteries have a lot of blood and PRESSURE, so they are more elastic, so need more ability to stretch.

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47
Q

Examples of muscular arteries:

Are they bigger than elastic arteries?

Do you see more elastic fibers or smooth muscle in the Muscular Arteries?

SO - Remember the bigger arteries (aorta) are ELASTIC, and slightly smaller (splenic/ulnar) are more muscular)

A

Coronary, splenic, ulnar

No, not as big. They are big, but not as big.

Smooth muscle

Ok

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48
Q

As arteries move AWAY from the heart there is more / less elastin and more / less smooth muscle

WHY?

A

LESS elastin

MORE smooth muscle

So smooth muscle can contract to move blood through arteries.

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49
Q

In our vessels, we have ________ that respond to or have the ability to detect PRESSURE changes in the blood. Our vessels also respond to chemical changes by __________

Examples of chemicals?

A

Baroreceptors

Chemorecptors

Examples of chemicals (O2, CO2, pH)

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50
Q

What is the unique thing about the smooth muscle in Arterioles?

A

The smooth muscle acts as sphincters to help close off vessels if needed. This is critical in regulating blood pressure and how much/where blood goes.

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51
Q

If sphincters in arterioles are relaxed, what happens?

If sphincters in arterioles are contracted, what happens?

Why?

A

Relaxed: blood passes through / filters through capillaries (like normal)

Contracted: blood goes right through to venuoles (does NOT pass through/filter through capillaries).

Regulation of blood pressure

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52
Q

What areas of the body deviate from the traditional arterioles > capillaries > venuoles path, and why?

A

Arteriovenus shunt = blood goes straight from arterioles to venuoles and bypass capillaries for purposes of temperature and blood pressure regulation.

Portal System = there are two capillary beds blood pass through. Arterioles > capillary > portal vein > capillary > venuoles

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53
Q

A lot of the regulation of blood pressure happens where?

A

Arterioles

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54
Q

What is Atherosclerosis

What is a stenosis

What is an aneurism
(how to remember)

What is a thrombus

What is an embolism

A

Atherosclerosis impacts larger arteries where you get plaque build up and it hardens vessels. It weakens the vessel walls which can lead to an aneurism which can burst artery.

Stenosis is a NARROWING of a vessel (or lumen) so it impacts blood flow, which limits O2 delivery to tissues / cells.

Aneyrism is a ballooned or weakened artery wall
(annual = week … anneurism = weak)

A blood clot

The obstruction of a blood vessel by a foreign substance or a blood clot (thrombus) that travels through the bloodstream, lodging in a blood vessel, plugging a distant vessel away from the thrombus originating atherosclerotic vessel.

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55
Q

What are capillaries, and their function

A

They are the smallest of vessels where gases / materials are exchanged at the cell level. Where gas exchange happens. Due to pressure gradient / diffusion, O2 diffuses out to tissue and CO2 diffuses back into capillaries.

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56
Q

T or F: Capillary beds are simply a layer of endothilial cells

Why?

Arterioles connect with capillary beds through many __________

A

True (there is no tunica media or tunica adventitia layers) … just intima of simple squamous endothilial cells for gas diffusion

They are so thin because all they do is gas / nutrient / waste exchange

Metarterioles

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57
Q

List the details of the 3 types of capillaries:

A

1) Continuous: don’t allow much movement across vessel wall (little permeatation). Blood vessel intact with not much permeability / fenestration, and continuous basement membrane over vessel.
2) Fenestrated: have holes in vessel, but has continuous basement membrane. Are located where there are lots/rapid exchange of materials … very permeable (brain, kidney, etc.)
3) Sinusoidal: larger openings (BIG holes) with larger fenestrations and a basement membrane that is NOT continuous (bone marrow, liver, spleen).

58
Q

What are venuals

A

VENUALS are the smallest of veins. Walls are thin, and lumen area is quite large. They take blood from capillaries and drain into larger veins.

59
Q

T or F: Adventitia is larger in arteries than it is in veins

A

False. Adventitia is THICK in veins, much thicker than the MEDIA in arteries. VEINS ARE THICK WITH ADVENTITIA

60
Q

Generally, larger arteries have higher/lower blood pressure?

Larger arteries have speed/flow of blood larger or smaller

Larger arteries have more elastic fibers or smooth muscle fibers?

Larger arteries are more permeable or less than capillaries

Veins have higher or lower blood pressure

Arterioles have more elastic fibers or smooth muscle fibers?

T or F: Velocity (speed) of blood actually increases in veins from capillaries towards heart?

A

Higher

Larger (BUT … as diameter of lumen decreases during a sympathetic response, velocity increases).

Elastic

Much less

Lower

Smooth muscle

True

An increased diameter means less resistance on vessel wall = increased blood flow. A decreased diameter means more resistance = less blood flow.

The velocity (speed) of blood flow DECREASES dramatically as the blood moves from arteries to arterioles to capillaries (away from heart). This slow flow rate allows more time for exchange processes to occur. As blood flows through the veins, the rate of velocity INCREASES, as blood is returned to the heart.

Blood pressure is HIGHER in the larger more elastic arteries, and decreases in pressure as you get towards capillaries (since we don’t want to burst capillaries).

61
Q

T or F: Capillaries are only epithilial for gas exchange, and have no smooth muscle

62
Q

I DID NOT DO FLASHCARDS ON THE MODULE 1 Heart Powerpoints. Go review that power point for quiz.

63
Q

T or F: PLATELETS are responsible for helping blood clot to prevent continued blood flow.

64
Q

Review the 5 steps in blood clotting:

A

1) Primary Aggregation: platelets adhere to collagen fibers and form a clot.
2) Secondary Aggregation: placelets release substances / granules to signal other platelets to come help form bigger clot
3) Blood coagulation: Meshwork forms to capture/stop RBC’s, WBC’s, other platelets (trap other cells passing by).
4) Clot Retraction: Platelets have actin and myosin in them so they contract to basically close off area.
5) Clot removal: clot dissolves and tissue is restored.

65
Q

What does ASPIRIN do … what does it counteract?

What does ASPIRIN do specifically related to blood?

A

Reduces pain and fever … so counteracts prostaglandins.

BUT … Aspirin helps PREVENT a blot clot from happening … it restricts platelets from clotting (blood thinner). So, it reduces chance of heart MI or heart attack.

66
Q

Circulatory system includes what two sub systems

A

Cardiovascular

Lymphatic

67
Q

T or F: Lymph vessels have capillaries?

Is pressure higher or lower in lymphatic vessels compared to blood vessels

A

True. These capillaries intersect with the blood vessel capillaries to pick up EXCESS fluid to filter it and return it to the heart.

LOWER (that is why higher pressure fluid goes into lymphatic vessels to lower pressure areas).

68
Q

MAIN role of lymphatic system

MAIN role of LYMPH

A

Lymphatic system filters and removes wastes from body, removes excess fluid (preventing edema), has WBC’s (lymphocytes) to fight toxins, has lymph nodes with lymphocytes that are filters to detect foreign invadors/bacteria.

Lymph carries PROTEINS and excess fluid back to heart
(the blood vessels do NOT do that). Lymph doesn’t have RBC’s, but has PROTEINS.

69
Q

EVERYTHING BELOW IS ON THE POWER POINT LECTURE OF INFLAMMATION

70
Q

Explain difference between

  • homeostasis
  • hemostasis
  • hematopoiesis / Hemopoiesis:
  • angiogenesis
A

Homeostasis: stable equilibrium physiologically

Hemostasis: stopping blood flow, or clotting to stop blood flow.

Hemopoiesis: formation of new blood cells

Angiogenisis: formation of new blood vessels

71
Q

Do cells get injured / damaged / die in our body?

Can damaged / injured cells repair or reverse to get back to normal?

Do some cells just die? And is that ok?

A

Yes, all the time

Yes

Cells die ALL THE TIME in our body. RBC’s have a 120 day life cycle, hair and skin cells die and regenerate all the time, etc. That is normal.

72
Q

2 types of cell injury:

When cells die (and can’t recover), two things can happen. What are they?

Which one is associated with inflammation?

A

2 types of cell injury = reversible and irreversible

DEATH OF CELLS:
Necrosis: is accidental or UNPLANNED cell death … a cell bursts and loses contents; the cell bursting open is associated with INFLAMMATION.

Apoptosis: is PLANNED or PROGRAMMED cell death (it’s beneficial) and NOT associated with inflammatory response (like dewebbing of fingers during development, RBC’s dying, hair cells die, dead skin cells, etc).

Necrosis

73
Q

How can cells get damaged or injured (or what causes an inflammatory response):

A
  • Ischemia: tissues not getting enough O2 / blood supply
  • Infectious Agents: Bacteria, worms, toxins, virus
  • Immune Reactions:
  • Genetic Factors: Change or mutation in Chromosomes
  • Nutritional Factors: Not enough vitamins or minerals, foods
  • Physical Factors: Injury, blunt trauma, heat, gun shot
  • Chemical Factors: Drugs, chemotherapy, metals, stress
74
Q

What is inflammation:

A

Inflammation is the body’s response to cell injury (INJURY TO CELLS). It works to heal wounds, cuts, infections. It is the body’s attempt to heal itself after an injury; defend itself against foreign invaders, such as viruses and bacteria; and repair damaged tissue.

75
Q

How the body responds (how much inflammation) is due to the _________ of the injury

A

SEVERITY

Cells don’t care if we are stabbed or a chemical agent kills cells … they care about the severity of cell death, and respond accordingly.

76
Q

Is inflammation good or bad? How?

Difference between acute and chronic inflammation

Does acute inflammation lead to chronic, or chronic inflammation lead to acute? Explain.

A

BOTH. Inflammation is needed to help heal damaged cells, initiate healing, remove debry, and kill foreign objects in body. But it can be bad if lymphatic system doesn’t work, or edema occurs, and thus chronic swelling results which causes pain and loss of function and leads to other issues.

Acute inflammation is GOOD - helps quickly heal a wound or cut.
Chronic Inflammation is BAD. It is WBC’s going and fighting a perfectly good tissue, or back up / damage in lymphatics system, long term edema.

Acute leads to chronic. So if you get a splinter, or damaged cells, or infection, then ACUTE inflammation will kick in to go heal area (cells) and remove foreign object. If it works, acute inflammation is all you need and you are done. If it persists or doesn’t work, it leads to chronic long term inflammation.

77
Q

What are the 5 s/s of inflammation:

A

Rubor (redness)

Tumor (swelling)

Dolor (PAIN)

Calor (Heat)

Functio laesa (Loss of function)

78
Q

So if a foreign object protrudes skin, a bacteria enters blood, a splinter happens, allergy, etc. - what is process of inflammation

A
  • HISTAMINES are released so we get VASODILATION and vessel PERMEABILITY. This brings more blood / plasma to area so WBC’s can get out (lets out more “stuff”).
  • Plasma leaks out (swelling) which actually SLOWS DOWN the foreign invader
  • This increased permeability / opening allows WBC’s to exit to fight bacteria or foreign object.
  • PLATELETS are also released from vessels and signal other platelets to come to area and help clot
  • WBC’s kill foreign invader.
  • Clot forms, tissue repairs (more cells form). HEALS
79
Q

2 types of ACUTE inflammation:

A

1) Edema (from leakage of plasma protiens from vessels)

2) Migration of Leukocytes (neutrophils) to affected area

80
Q

What are the FIRST responders in inflammation (or “migration of leukocytes”)?

A

NEUTROPHILS

81
Q

What is Increased Vascular Permeability

A

Vessels open up more (more holes / fenestrations) so that fluid/plasma, protiens, WBC’s, platelets can escape

82
Q

S/S (or s/s) =

Tx =

A

Signs and Symptoms

Treatments

83
Q

S/S of Chronic Inflammation:

A
  • Macrophages (eaters)
  • Lymphocytes
  • Plasma cells
  • Granulation tissues (fibroblasts = collagen)

ALL of these persisting can lead to scaring and potentially loss of function.

84
Q

What structures will be involved with Inflammation:

A

What will be involved with inflammation:

  • Blood vessels
  • Blood cells (Platelets, WBC’s)
  • Connective tissue cells
  • Chemical mediators (chemicals that help with a change process)
  • ECM: collagen and basement membrane
85
Q

What factors influence the TYPE of inflammation that will occur?

The nature of the inflammatory response is determined more by the _______ of the injury than by the actual cause.

A
  • Mechanism of injury
  • SEVERITY of injury
  • Location of injury (tissue involved)
  • State of the individual (age, gender, health, etc.)

SEVERITY

86
Q

3 Goals of Inflammation:

A

1) Get blood cells and plasma proteins to injured tissue
2) Remove the injurious stimulus / kill bacteria / remove splinter
3) Replace injured tissue with regenerated tissue and/or a scar

87
Q

*** 5 events happening with Inflammation:

A

1) Vasodilation
2) Increased vascular permeability
3) Vascular stasis (with RBC’s) and WBC emigration/leakage
4) Edema
5) Removal of exudate

88
Q

What is Vasodilation (#1) and why does it happen in inflammation:

S/S of vasodilation

What chemical is released to cause vasodilation? Or, vasodilation is a result of __________

A

Well we need to get more blood to that area to have WBC’s kill foreign object, and get platelets to clot area.

Heat and redness (since blood is red, and higher temperature)

Histamine

89
Q

Explain what is happening with increased vascular permeability (#2):

How is histamine involved in increased vascular permeability?

A

Plasma proteins, fluid, and WBC’s escape into the extravascular space (s/s=edema)

Histamine increases blood vessel permeability

*** Histamine causes vasodilation, and then endothelial cells contract, so gaps (fenestrations) occur, which increases permeability in vessels allowing plasma to leak (edema and slow down foreign invader) and WBC’s to escape (to kill foreign invader).

90
Q

2 main roles of Histamine

A

1) Causes vasodilation

2) Increases vessel permeability (allowing blood to exit vessels to clot and fight foreign object)

91
Q

Explain #3 of vascular stasis

Explain WBC emigration

A
  • As vessel becomes more permeable and endothelial cells contract causing a gap/hole, then proteins and plasma and WBC’s exit vessel (from the intervascular space/lumen into the extravascular or interstitial space). But RBC’s typically are too big / thick so they don’t exit vessel. This causes vascular STASIS (or slowage of blood in the vessel because the blood is now thicker and more viscosity/thick because a higher concentration of RBC’s in vessel).
  • WBC’s leave vessel into interstitial space to go fight infection / disease / foreign object, etc. due to the increased vessel permeability (from histamine).
92
Q

Explain phagocytosis and how it occurs during this entire inflammation process

What is Opsonization

   (how to remember)
A

Phagocytosis happens throughout the inflammation process. Neutrophils (eosonphils, monocytes are released to area to go kill and eat foreign body). Those WBC’s remove dead skin / cells / tissue / foreign objects (and excess plasma).

Basically foreign object is “tagged” (coated with a protien) so other WBC’s know to phagocytosis / eat it and destroy it.
(remember: the cop’s son will TAG the bad guy so
big cops can come kill)

93
Q

Now, what is Edema (#4) in the inflammation process

What is difference between Extracellular space/fluid and interstitial fluid/space?

Difference between INTRA and INTER

A

Because vessels are more permeable, protiens and plasma and WBC’s exit into interstitial spaces. This excess ‘exudate’ collects and causes swelling (edema is extreme case).

The cells have INTRAcellular fluid. But outside and between cells is the ECM with extracellular fluid. Part of the extracellular fluid in the ECM is the interstitial fluid (which makes up 80% of the Extracellular fluid).

Intra = within itself   (intra-capsular)
Inter = between others  (an intermediate)
94
Q

What is Exudate

4 different types of Exudate:

A

The “stuff” (plasma/fluid, proteins, blood) that escapes or is secreted out during inflammation as a result of increased permeability. Basically it is all the stuff that has escaped from inter-vascular to interstitial space.

1) Sanguineous (blood / red)
2) Serosanguineous (Pink … blood and fluid)
3) Serous (yellow / clear fluid)
4) Purulent (Puss … whitish … dead neutriphils)

95
Q

Finally the #5 step of inflammation process is Removal of Exudate. What is this?

A

Now we need to get rid of all this excess stuff. This is where lymphatic system comes in. Lymph vessels pull this in and lead back into venous system. If we can’t do this, we get lymphedema.

96
Q

Prostaglandins =

What drug reduces Prostaglandins =

A

Hormone in body to help create PAIN and FEVER to help in the healing/inflammation process.

NSAID’s: Non-steroidal anti-inflammatory drugs

97
Q

After inflammation process, the vessels need to repair themselves. So, what is Angiogenesis?

So proliferation and migration is essentially what?

A

Angiogenesis is the development of forming new blood vessels. Endothilial cells are created to form new capillaries (called ANGIOGENESIS … or formation of new vessels)

Cells migrate (proliferate) to the area to heal area / remove object, and start the process of creating new cell growth / repair.

98
Q

What is remodeling and maturation

A

Like bones remodel after a break, so do vessels. The vessels will remodel, form scar tissue, and slowly heal and go back to normal from formation of new endothelial cells.

99
Q

Great summary of the process of an injury, inflammation, and healing:

A

1) Histamines release and cause vasodilation and vessel permeability. WBC’s leak and exit to kill foreign object and heal tissue. As blood flows to the area, RBC’s clog and as soon as hemostasis occurs (blood flow thickens and clogs up artery), inflammatory process begins in response to chemicals released by platelets.
2) Increase in blood flow (vasodilation) and vessel permeability, so plasma and WBC’s are released, followed by phagocytosis of dead and damaged tissue in the area of injury.
3) Cell migration and proliferation follow.
4) Healing occurs by either regeneration or repair, depending on a number of factors. Foreign object eaten/removed.
5) Remodeling of vessel and maturation are the final steps.

100
Q

BELOW IS STARTING FLASHCARDS ON POWER POINT #4 on Cardiac Anatomy and Physiology Review

101
Q

What is PMI (with relation to the heart)

Where is it on the heart?

A

Point of Maximal Impulse

Apex (where it is most superficial where you can palpate it and feel and even see the beat in skinnier people).

102
Q

What is in the Mediastinum?

A

Heart
Great vessels (aorta, pulmonary trunk, SVC)
Trachea / Esophogus

103
Q

What is a pneumothorax?

Closed vs. open pneumothorax?

What is a tension pneumothroax?

Why are they so dangerous?

What is a hemothorax?

A

Air (blood, puss, object, fluid) gets in the pleural cavity (or pleural cavity gets ruptured). So air from lungs leaks, or air from outside seeps in. THIS CAUSES THE LUNG TO COLLAPSE.

Closed is chest is still in tact, open is from a gun shot wound or knife puncturing through thoracic wall into lung … so air gets into pleural space. THIS CAUSES THE LUNG TO COLLAPSE.

Tension Pneumothorax: when you don’t have an open wound, but maybe fractured rib punctures one lung, and air escapes into pleural cavity but then can’t get air out. So pressure and air keep building and building until it collapses lung, shifts the mediastinum over or causes heart valves to be pinched which effects entire cardiac cycle.

If air gets into pleural cavity, it will collapse lung (limiting how much air/O2 you can get into body … so you can’t breathe). But then collapsed lung often shifts mediastinum over which could injure or alter heart function by squeezing great vessels (and potentially puncture pericardial cavity) so heart can’t pump as much blood / O2 to body.

Hemothorax: when blood gets into pleural cavity.

104
Q

Review layers of the heart:

A
Fibrous pericardium
Parietal pericardium
Pericardial Cavity
Visceral Pericardium (same as epicardium)
Epicardium
Myocardium
Endocardium (inner layer of chamber)
105
Q

** What is Cardiac Tamponade:

How can you remember this :)

What is treatment to fix it?

A

When fluid gets into pericardial space. More fluid will
compress heart and vessels and be life threatening

(equivalent of a pneumothorax of the lung, but in the heart)

Put a tampon in the space of pericardial cavity to soak up the liquid that got in there.

Pericardiocentesis

106
Q

Which chamber has the LEAST amount of pressure … and why?:

Which chamber has the HIGHEST amount of pressure?

A

Least: Right Atrium. Because blood in veins is least pressure, and that blood just flows into RA with no resistance / valve (pressure build up).

Most: Left ventricle.

107
Q

What is COPD?

Examples?

If someone has COPD, which chamber will be most effected?

A

Chronic Obstructive Pulmonary Disease

It is many conditions that block airflow and make it difficult to breathe. (Ex: Emphazima, Bronchitis, Asthma)

Right Ventricle (RV)

108
Q

What is Cor Pulmunale:

A

Right sided heart failure

Most commonly arises out of complications from high blood pressure in the pulmonary arteries (pulmonary hypertension). It’s also known as right-sided heart failure because it occurs within the right ventricle of your heart.

109
Q

What opens and closes the AV valves?

What opens and closes the Semi-lunar valves?

A

Opens AV: PRESSURE (It is NOT the papillary muscles or chordae tenineae … those just hold cusps from retracting back into atria during systole)
Closes AV: As ventricles contract, the blood naturally forces valves closed. But the Chordae tendineae are pulled by papillary muscles to keep AV valves closed and not retracting back up into atria during systole.

Open Semilunar: Pressure from ventricular contraction
Closes Semilunar: Blood falling back down into cusps due to gravity and the valves naturally close.

110
Q

What is the purpose of the heart’s fibrous skeleton

A
  • Give support to whole heart
  • Fibrous ring around valves for support
  • Site for muscle attachment
111
Q

T or F: the muscle (myocardium) in ventricles is shaped in a spiral arrangement?

Why?

A

True

Squeeze the blood upward from the apex of the heart (contract to squeeze blood up and out).

112
Q

What does occluded / occlusion mean?

Occult means

If there is an occlusion of the heart, what would happen?

What is a ‘Collateral Route’ or ‘Collateral Circulation’ (for heart)

If an occlusion happens, and you don’t have an MI, how or what process repairs blood vessel?

A

Blockage or closing off of a blood vessel. Vessel won’t supply tissue with enough blood / O2

Occult means hidden

Heart wouldn’t get O2 (ishemia), so you’d get Myocardial Infarction (MI) or heart attack.

Collateral Routes: If a major coronary artery gets occluded, there is a work around (ANASTAMOSIS). New vessel will form or reroute blood around blocked vessel.

Collateral Circulation: Collateral circulation in the heart tissue will sometimes bypass the blockage in the main artery and supply enough oxygenated blood to enable the cardiac tissue to survive and recover.

Angiogenesis (new blood vessel formation / growth)

113
Q

Coronary arteries provide blood and O2 to what?

Is the myocardium mitochondria dense?

Do cardiac muscle cells (the heart) fatigue very easy?

A

The heart muscle itself.

Yes, MANY mitochondria … it needs lots of energy to constantly beat, thus needs a lot of O2 (thus creates a lot of ATP and has a lot of mitochondria)

NO (thank goodness)

114
Q

Explain what determines heart dominance?

How many are RC dominant?

Can it be both?

Acronym to remember coronary arteries and veins?

A

Which artery supplies the Posterior Interventricular Artery (or AV node).

If the posterior interventricular artery is supplied by the right coronary artery (RCA), then the coronary circulation can be classified as “right-dominant”.

2/3rds are right coronary dominant.

Possible to be co-dominant.

GAMP SR

115
Q

What are the main things that make myocardial cells unique?

4 main properties of cardiac muscle:

A
  • Gap Junctions (quick communication b/n cells)
  • Branched / Y (faster communication)
  • Desmosomes (allows force to be transmitted cell-cell)
  • T-Tubules and Sarcoplasmic Reticulum (increased surface area for CALCIUM to get in for contraction)
  • Lots of mitochondria
  • Involuntary
  • Striated (actin and myosin)
  • No Motor Units
  • It’s own unique conduction system
  • NO satelite cells

4 Properties:

  • Authorhythmicity (generate HB continuously)
  • Excitibility (respond to an action potential)
  • Contractility (can contract)
  • Conductivity (conduct an impulse)
116
Q

Are pace maker cells of heart different than myocardial cells? How?

Where are pacemaker cells located?

Do these different types of cells have the same RATE?

A

Yes.

Pacemaker cells are to conduct action potential, not to contract (contain no contractile fibers / sarcomere structure). Myocardial cells contract as a response to action potential

Located:

  • SA Node
  • AV Node
  • Bundle of His
  • R and L Bundle branches
  • Purkinjie fibers

NO - they each have their own RATE of contraction.
SA Node = 60-100 bpm
AV Node = 40-60
Bundle / Ventricles: 20-40

117
Q

Heart is autorhythmic due to what cells?

Another term for the heart being self-exciting?

A

Pacemaker cells

Myogenic

118
Q

What is resting potential

Is resting potential of a cell negative or positive?

What changes the resting potential of a cell?

What is depolarization?

What is repolarization?

A

The electrical potential (or charge) INSIDE of a neuron / cell relative to its surroundings.

Negative. It is -90mV

If a neuron initiates an action potential, then the cell membrane permeability changes (voltage gated channels open) and IONS (calcium, potassium, sodium) rush in / out to change resting potential or charge in the cell.

Depolarization is CONTRACTION … the state which the cell changes from a negative to a positive charge inside the cell (and thus a positive to negative charge outside the cell) as ions flow in and out. CAUSING A CONTRACTION

Repolarization then would be contraction stops and the cell returns to a NEGATIVE charge as ions flow out of cell and go back to resting potential of a negative charge. IT IS RELAXATION

119
Q

Slow depolarization =
Fast depolarization =
Repolarization =

A

Slow: Na+ rush into cell slowly through FUNNY channels
Fast: Ca+ channels open to have Ca+ rush in
Repolarization: K+ channels open and K+ goes in

Ca: +123
Na: +67
K+: -92

120
Q

Is contraction of heart ventricles depolarization or repolarization?

A

Depolarization

121
Q

All or nothing response means what?

Is all or nothing different for different chambers?

A

All cells depolarize and repolarize at same time. It is ALL cells or no cells (sysinctom).

BOTH atria are all or nothing and contract together. And BOTH ventricles are all or nothing and contract together. But they obviously contract at diff. times.

122
Q

Talk about the action potential of a cardiac contractile cell in 4 stages:

A

Ca: +123
Na: +67
K+: -92

Stage 4: resting membrane potential is -90mv
Stage 0: Action potential hits, Na+ comes in (goes from -90mv to +20mv) … a little Ca comes in too.
Stage 1: K+ EXITS cell, so charge decreases a bit.
Stage 2: Ca+ comes INTO cell, but K+ is still leaving, so it balances each other out … plateau
Stage 3: K+ flows OUT of cell at first. Then Na+ and Ca+ flow OUT while Potassium flows back in (resulting in a negative / repolarization).
Stage 4: back to resting potential

123
Q

Review …

Sympathetic stimulation does what to heart:

Parasympathetic stimulation does what to heart:

A

Sympathetic: Speeds up heart, increase HR, increased contractility

Parasympathetic: Slows down heart, decrease HR, decreased contractility

124
Q

Chronotropic =

Inotropic =

Dromotropic =

How to remember?

A

Chronotropic = speed of heart

Inotropic = strength of contraction

Dromotropic = # of action potentials

Ino (“I know) I am strong
Dromo = Drama = Acting = Action Potentials

125
Q

What is path of the conduction / conductivity of heart:

T or F: Depolarization is happening in atria as conduction goes from SA node down internodal branches to AV node?

A

SA node > internodal branches > AV node > bundle of his > Bundle Branches > Purkinjie fibers

True

126
Q

What is the primary pace maker of the heart?

If Pacemaker fails, is there a back up?

Does SA node and AV node have same conducting rate?

T or F: The conduction speeds up at the AV node?

A

SA node

If SA node fails, AV node can take over, just at a slower rate.

NO. Sa node is 60-100 b/p/m, and AV is 40-60 b/p/m

False: there is a slight pause to allow full contraction of atria before ventricles contract. The “atrial kick”

127
Q

What is:

  • Diastole
  • Systole
  • Atrial Kick
  • EDV
  • ESV
  • SV
  • Ejection Fraction (EF)
  • How to calculate EF
A
  • Diastole: Ventricles filling with AV valves open, and the ventricles are relaxed
  • Systole: Ventricles contracting (AV valves close, Semilunar valves open)
  • Atrial Kick: Extra little squeeze of blood from atria to ventricles (as AV node slightly delays) to give ventricles just a bit more blood
  • End Diastolic Volume is how much (mL) of blood in ventricles before ventricular contraction
  • End Systolic Volume is how much (mL) of blood after ventricular contraction
  • SV = EDV - ESV
  • Ejection Fraction is the % of blood ejected out of ventricles during systole (not amount - that is SV)

Calculate: EDV-ESV. Take that amount and divide by EDV = a %.

128
Q

Explain the heart sounds:

A

Lub = 1st heart sound when AV valves are closing during ventricular contraction

Dub = 2nd heart sound when semilunar valves are closing during atrial contraction / ventricular filling

129
Q

Where would you auscultate or listen to heart sounds for each of the 4 valves?

A

Tricuspid valve: 5th intercostal space just L of sternum
Pulmonary valve: 2nd intercostal space just L of sternal angle
Mitral valve: 5th intercostal space 2-3 inches L of sternum (mid clavicular line)
Aortic valve: 2nd intercostal space just R of sternal angle

130
Q

Cardiac output formula:

Average amount per min (in L)?

SV Formula =

HR =

A

Q = SV X HR

About 4-6 L of blood p/min

SV = Stroke Volume (EDV - ESV)

HR = beats/per/min

131
Q

What impacts Cardiac output:

A
  • HR
  • SV
  • EDV
  • Venous Return
  • Skeletal Muscle Pump
  • Sympathetic / Parasympathetic stimulation
  • Many various heart / health conditions and diseases
132
Q

With regards to stroke volume, what is:

  • Preload:
  • Contractility:
  • Afterload:

What is the Frank Starling Law:

A
  • Preload: amount ventricles are STRETCHED (by EDV amount) by contained blood (left ventricular length before systolic ejection)
  • Contractility: force during contraction of muscle cells
  • Afterload: ventricular PRESSURE on aorta at the end of systole (or resistance to ejection during systole)

FRANK STARLING:
- The greater the preload (EDV) the more blood the heart will pump (SV).

133
Q

T or F: the greater the diastolic filling (preload) the greater the quantity of blood pumped

T or F: the slower the heart beats, the more it can fill with blood, so you get a higher SV

134
Q

If vagus nerve gets damaged, how would that effect heart?

A

Parasympathetic innervation to heart comes from Vagus nerve, so it would NOT allow heart to slow down and relax.

135
Q

T or F: We have baroreceptors in our blood vessels (like Carotid and Aortic areas) to help with blood pressure regulation

What is the purpose of these baroreceptors … and what specific chemical signals does it send?

A

True

If BP is high, it sends a parasympathetic response (AcH) to slow down and relax heart to lower BP.

If BP is low, it send sympathetic response (norepinephron) to speed up heart to increase BP.

136
Q

Can body temperature impact HR?

A

Yes, increased temp increases HR (and visa versa)

137
Q

What is ejection fracture again?

What is a low or scary ejection fracture? Why?

What do you want your ejection fraction to be?

A

% of blood pumped out of ventricles during contraction compared to amount of blood in ventricles at EDV (not amount, that is SV).

15% or less. Means body isn’t getting enough blood and O2 … which can lead to anemia

About 60% or higher

138
Q

T or F: Blood flows from low pressure to high pressure

A

NO - it goes from HIGH pressure to LOW pressure.

139
Q

What is the difference between flow rate and flow velocity in regards to blood in a vessel

*** What determines whether blood will flow FAST or SLOW in a vessel?

*** Will a smaller diameter vessel cause faster or slower flow? How will it impact how much and how fast blood flows?

*** Does blood flow faster in capillaries or aorta?

A

Flow rate: how much blood flows past a fixed point in space.

Flow velocity: how far a given volume of blood will travel in a unit of time.

SLOWS:

  • Diameter of vessel
  • Viscosity of blood
  • Tube length

BLOOD FLOWS FASTER IN A SMALLER DIAMETER VESSEL. It goes faster in splenic or ulnar artery than it does in Aorta. Larger CSA means MORE blood flows, but slower.

But, blood goes very slow in capillaries because there are thousands so it spreads blood out. Technically blood goes faster in a smaller (more constricted) vessel, but capillaries are broken up into many, so if you put them together the CSA is actually bigger than the aorta.

140
Q

What has the MOST impact on blood flow

How does the body regulate for this?

A

Blood vessel diameter

When it comes to regulating blood pressure in our body, or amount of blood sent to tissues, the body will change diameter of vessel to regulate the pressure to shunt blood to different areas of body based on what we need.

141
Q

Remember the 1st quiz, and how there was the ? about the 25 year old who couldn’t stand or walk because he was sweaty, anxious, etc. and his CO was really low. Why would this happen?

A

He was probably hemorrhaging inside.