Questions Flashcards

1
Q

What does the cardiovascular system consist of? (3 answers)
-what
- main role:
- function

A
  1. blood (moving blood around the body)
  2. main role: transport substances
  3. the substance transported in vessels via blood
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2
Q

Blood roles (3 answers)

A

Transport: nutrients, dissolves gases, hormones, wastes

Regulation (homeostasis): pH, ions, water, temp.

Defence: It fights against fluid loss, pathogens, and toxins

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3
Q

What is special about blood? (3 answers)

A
  • specialized connective tissue
  • contains plasma (aqueous matrix)
  • contains cells and platelets
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4
Q

Blood is a fluid connective tissue containing what? (3 answer)

A
  • Cells: RBCs and WBCs (platelets)
  • Extracellular matrix: plasma
  • Extracellular protein: plasma protein
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5
Q

what is the ratio of blood? (remember!)

A

Red blood cells (45%)
Plasma(55% - range 46%-63%)
-> plasma protein (7%):
-> Albumins: transport and fluid balance
-> Globulins: immune and transport
-> Fibrinogen: clotting
-> Enzymes and hormones
-> Other Solutes (1%)
-> Electrolytes
-> Organic nutrients
-> Organic wastes
-> Water (92%)

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6
Q

What do the non-protein components of plasma do?

A
  • constantly circulate and mix w/ other extracellular fluid
  • in more tissues, h20 and small solutes can move freely from blood vessels into the interstitial fluid (ISF) between cells
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7
Q

Hemostasis (3 phases and notes under each)

A
  1. Vascular Phase
    -> rapid change to cells in the blood cells in the blood vessel wall
    - 1. contraction (vascular spasm)
    - 2. Increases endothelial ‘stickiness’
    -> exposes connective tissue and basement layer to the blood
    -> The vascular and platelet phases are collectively (also known as ‘primary hemostasis’)
  2. Platelet Phase
    -> Platelets aggregate at the exposed endothelial surface plus the broken vessel
    -> Platelets attach to the stick endothelial cells and basement membranes and become activated
    -> Activated platelets change shape and release chemicals that attract other platelets & help them stick to each other
  3. Coagulation Phase
    -> A fibrin mesh network forms around platelets, producing a clot
    -> The ultimate effect of coagulation (2nd hemostasis) is to create stands of insoluble fibrin
    -> a protein which binds aggregated platelets (and blood cells) into clots
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8
Q

A positive feedback loop (related to the circulatory system)

A
  • the accumulation and aggregation of platelets = pos feedback loo

IMPORTANT
- the only phase of blood clotting that is a pos feedback loop is the platelets phase
- the interaction between activated platelets and chemicals that attract more platelets

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9
Q

More about Coagulation phases (and notes) (2 steps total)

A
  1. involved a cascade of enzymes that catalyze the formation of fibrin from solvable fibrinogen
    -> Coagulation is triggered by tissue damage or exposed connective tissue
    -> It take at least 30 sec after bessel damage to begin and involves many enzymes
  2. Involved many clotting factors: enzymes that are linked in a complex cascade that produces fibrin
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10
Q

After the vessel wall is repaired, what happens?

A

As the clot forms, repair of the blood vessel begins. When the wall is repaired the fibrin will be cleaves and thus the clot dissolves

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11
Q

Steps of Fibrinolysis (3 steps)

A
  1. tissue plasminogen activator (t-PA) is released from the repaired vessel wall
  2. t-PA convert plasminogen) plasma protein to plasmin
  3. Plasmin degrades fibrin
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12
Q

What produces blood cells and platelets

A

red bone marrow = found in the space around the spongy bone

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13
Q

What are the 2 main potent lineages that come from hematopoietic stem cells?

A

lymphoid and myeloid

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14
Q

what is the lifespan of a typical RBC?
What happens to the dead RBC?

A
  • around 4 months
  • is recycled into new RBCs and/ or excreted
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15
Q

How does blood flow through vessels?

A
  • they flow through based on differences in pressure
  • contractions of the heart create a pressure gradient that drives blood movements
  • as a fluid, blood moves (flow from areas of high -> low pressure)
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16
Q

Blood flow direction…

A

heart-> arteries-> capillaries -> veins
- this is true for both systemic and pulmonary circuits
- but there is an exception: portal veins (sends blood to liver rather than veins)

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17
Q

Are the pulmonary and systemic circuits connected?

A

they are not directly connected, except through the heart

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18
Q

what is the function of smooth muscle in the vessel walls?

A
  • they allow arteries and veins to change their diameter, altering blood flow
  • they respond to the ANS and to different hormones
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19
Q

How does the blood flow in the circulatory system
-systemic veins empty into…
- pulmonary veins empty into…

A
  • blood flow from each atrium into the corresponding ventricles, and from ventricles into arteries
  • systemic veins empty into the right atrium
  • pulmonary veins empty into the left atrium
  • when the ventricle contracts, blood only flows into the arteries, NOT back into the atria
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20
Q

What is the function of the heart tissue?
Who is its supplier?

A

Supplier:
- is supplied w/ blood through a separate (coronary) blood supply
- has high metabolic demands, thus requires it own arteries and veins (not blood sitting inside its chambers)

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21
Q

What must happen in order for the heart to contract?

A
  • cardiac myocytes must be (electrically) excited in order to contract
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22
Q

what do cardiac muscle cells lack?

A

NMJs; instead, excitation is myotonic

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23
Q

Anatomy of the heart (2 points)

A
  1. the right ventricle has a thinner wall than the left
  2. the greater vessels of the systemic circuit are larger and thicker than those of the pulmonary circuit
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24
Q

What happens at a resting heart rate?

A
  • full diastole
  • both sets of chambers being relaxed
  • lasts for about half the duration of each cardiac cycle
  • pressure changes in heart chambers and arteries carry predictably across a single cardiac cycle
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25
Q

What is the difference between cardiac and skeletal muscle cells? (3 points)

A
  • Cardiomyocytes usually only have a single central nucleus, and branched structures, and are about 0.2 mm long
  • they have the same organelles but they may be indifferent locations (ex: nucleus)
  • there is no NMJ in cardiac myocytes
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26
Q

What is the difference between myofibres and cardiac myocytes?

A
  • ## cardiac myocytes have reduced T-tubules and sarcoplasmic reticulum and lack specialized neuromuscular junction
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27
Q

which action potential is faster skeletal myofibres or cardiac myocytes?

A
  • cardiac myocytes (prolonged plateau of depolarization) are slower and last about 200x longer than skeletal myofibres APs
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28
Q

what does the contraction cycle in cardiac myocytes involve? (2 points)
- steps for calcium-induced calcium release (2 points)

A
  • interactions between sliding filaments, similar to myofibres
  • once Ca+2 is present, the interaction cycle in cardiac myocytes closely resembles what occurs in a skeletal myofibre (involves calcium-induced calcium release)

Steps
1. some calcium ions enter the cytoplasm from the ECF
2. the elevated (CA+2) triggers the release of more calcium from cellular stores (the SR)

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29
Q

what is the difference between skeletal muscle cells and cardiac muscle cells (in regards to EC coupling)
(6 points total -> 3 each)

A

Skeletal muscle cell: Mechanical coupling
- no ion flow through DHPR (dihydropyridine receptor)
- DHPR pulls open the RyR (Ryanodine receptor)

Cardiac muscle cells: biochemical coupling
- calcium floes through DHPR into the cytosol
- concentration of calcium increases = opens the RyR

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30
Q

What happens from depolarization from SA node (2 points)

A
  • spreads through the atrial myocardium and the conduction pathway
  • SA node cells are electrically coupled to cardiac myocytes, and to the conducting cells of the intermodal fibres, = depolarization to rapidly spread across both atria
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31
Q

what are the conduction pathways cells specialized for?

A
  • for rapid electrical conduction; they can conduct APs up to several meters per sec
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32
Q

When is depolarization faster, conduction system or cardiac myocytes?

A

conduction system

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33
Q

How in the Purkinje fibres involved in depolarization?

A
  • the depolarization travels rapidly through the interventricular bundle to the Purkinje fibres, then back up the ventricle wall
  • the Purkinje fibres will be excited (and contracted) before the base
  • this allows for efficient emptying into the arteries
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34
Q

What does the cardiac cycle describe?

A
  • the sequences of contraction and relaxation of the heart chambers
  • a cardiac cycle is one heartbeat and its relaxation period
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35
Q

What is the resting heart rate (Hr) of the entire cardiac cycle?

A

800ms -> represented by about 75 beats per min (bpm)

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36
Q

Heart and valves, what pressure makes the heart?
Relaxation=
Contraction=

A

Relaxation= low pressure (valves closed)
Contraction= high pressure (valve open)

think of a pipe with a lid at the end

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37
Q

What does the cardiac cycle generate and what does that lead to?

A

The cardiac cycle generates pressure to produce cardiac output (blood flow into and through the blood vessels)

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38
Q

What does the pressure in the heart drive out and into what?

A

It drives blood out of the heart and into the systemic and pulmonary circuits

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39
Q

What is the cardiac output (CO) formula?
- include units for each element

A

CO = SV x HR = mL/min

SV = stroke volume (mL/beat)
HR= heart rate (bpm)

40
Q

Where does the cardiac cycle end (and begins)?

What else happens during this time?

A
  • The ventricular and atrial diastole, when the passive filling of the ventricles occurring
  • During this time, blood returning form the veins can flow through the atria and into the ventricles
41
Q

What happens during End Diastolic Volume (EDV) (2 points)

A
  • atrial systole completes the filling of the ventricles, which reach their End Diastolic Volume (EDV)
  • during this time, blood is squeezed from the atria to the ventricles and the ventricles achieve their maximum volume (End Diastolic Volume)
42
Q

What is the End Diastolic Volume (EDV) affected by

A

venous return and by ventricular filling time

43
Q

What initiates afterload?

A

is directly affected by resistance (pressure) in the blood vessel

44
Q

When do semilunar valves open?

A

they ONLY open when the ventricular pressure exceeds the pressure in its artery (pulmonary or aorta)

45
Q

If arterial pressure increases what happens to afterload?

A

the afterload of that side of the heart increases

46
Q

What happens if valve opening is delayed?

A

the time for ventricular ejection is reduced

47
Q

What happens when less blood is released at SV?

A

thus more remains as ESV

48
Q

What does NE or E signalling use?

A

they use receptors created by biochem signals that enhance multiple parts of cardiac excitation-contraction coupling, increasing the tension produced for each excitation (AP)

49
Q

What happens to cardiac output during exercise?

A
  • skeletal muscle uses more oxygen and nutrients from systemic blood circulations
  • skeletal muscles produce more waste products (and heat)
  • thermal homeostasis needs to be maintained by radiating heat away at the dermis
50
Q

What happens when contractility is enhanced?

A

= a higher stroke volume is produced for the same EDV
- proportional to the intensity of the exercise

51
Q

What happens to the sympathetic activity and epinephrine section during exercise?

A

they both increase
- epinephrine secretion is from the adrenal medulla

52
Q

What affects stroke volume?

A

muscle activity, vessel blood flow patterns, sympathetic activity and hormones

53
Q

As Hr (heart rate) increases what happens to diastole?
- what could also be affected due to Hr increase

A

the % of time spent in diastole drops

  • the loss of filling time only slightly reduced EDV, bc/ most passive filling happens very early in diastole
54
Q

What can aerobic training lead to in regard to your health? (3 points)

A
  • increase stroke volume due to both physiological and structural changes
  • can elevate cardiac output regularly for prolonged periods of time
  • induces hypertrophy of cardiac myocytes, adding sarcomeres in a way that increases the volume of the ventricles
55
Q

List the type of blood vessel walls and their difference (10 points)

  • 3 options
    Categories:
  • Lumen Diameter:
  • Smooth Muscle Layer:
  • Endothelial Layer:
  • Tunics (tissue layer):
A
  1. Arteries
    - Lumen Diameter: intermediate
    - Smooth Muscle Layer: thick
    - Endothelial Layer: tight
    - Tunics (tissue layer): 3
  2. Capillaries
    - Lumen Diameter: Smallest
    - Smooth Muscle Layer: Absent
    - Endothelial Layer: Leaky (gaps)
    - Tunics (tissue layer): 1
  3. Veins
    - Lumen Diameter: Largest
    - Smooth Muscle Layer: Thin
    - Endothelial Layer: Tight
    - Tunics (tissue layer): 3
56
Q

Larger pressure gradient =?

A

more force

57
Q

what slows down the velocity of liquid and thus volume flow rate?

A

resistance (caused friction between the walls of the tube and the fluid)

58
Q

The longer the vessel =?

A

more surface that is in contact w/ the blood -> thus more friction that blood will encounter

59
Q

Vessel luminal diameter is inversely and proportional to?

A
  • inversely to resistance
  • proportional, more of the blood inside a small diameter vessel will be in contact w/ or near the vessel wall (source of most friction)
60
Q

What will happen in the change in vessel diameter and explain why?

A

will always produce a larger change in resistance than an equivalent change in length this is bc/ the resistance associated w/ diameter is proportional to the radius

61
Q

When the liquid is more viscous =?

A

its molecules (and materials suspended within it) interact w/ each other, causing internal friction which slows down the overall flow

62
Q

how is Venule involved with the connection of…?
- what do they lack?

A

venules connect capillary beds to veins
- they lack tunica media

63
Q

What do arterioles have but also lack?

A

have tunica media but lack a true tunica externa

64
Q

When is arterial pressure highest and lowest?

A

highest during and just after ventricular systole
- lowest during diastole

65
Q

Blood pressure is reported as?

A

Systolic Pressure/ Diastolic Pressure

66
Q

The pressure drop-off is largest through?

A

arterioles= that these vessels provide the highest total resistance to volume flow

67
Q

Blood pressure reduces each time when?

A

blood flow must overcome resistance from a vessel
- therefore, the more vessels are from the ventricles (the source of the pressure gradient), the lower the average pressure w/ in them

68
Q

Where is the cross-sectional area of all blood vessels highest in? and lowest in?

A

highest in capillaries and lowest in elastic arteries

69
Q

Factors affecting blood flow through circuits and factors affecting cardiac output are interrelated. There are 4

A
  • Cardiac output affects pressure
  • Pressures affect blood flow
  • Blood flow affects venous return
  • Venous return affects cardiac output
70
Q

The relationship between arteries, veins and gravity

A

Arteries
- supply blood to the head must generate enough pressure to push blood directly against the force of gravity, as well as against vascular resistance
- supply blood to regions below the heart get an assist from the force of gravity

Veins
- the limbs contain valves to help prevent backflow of blood due to gravity

71
Q

How does skeletal muscle work w/ valves?

A
  • they work together to provide a secondary pump that helps propel blood toward the heart
  • muscles contracting around the vein compress the vein, providing extra pressure which helps squeeze blood upward toward the heart, countering the force of gravity
72
Q

Capillary Exchange
- definition
- 3 components

A
  • it’s the bidirectional movements of substance into or out of the blood from body tissues

3 components to capillary exchange
1. Diffusion
2. Filtration
3. Osmosis

73
Q
A
74
Q

Near an arteriole there is…

A
  • pos NFP, favouring filtration
  • BCOP is a constant value; related to the concentration of colloidal (large suspended) particles in plasma
  • CHP is initially (relatively) high in the proximal part of the capillary, as blood enters from the arteriole
  • CHP > BCOP = +ve NFP, meaning a pressure gradient that favours fluid movement into the ISF
75
Q

Filtration step

A
  • occurs along a capillary, CHP will decreased but BCOP will not change
  • near the middle of the capillary bed, the 2 forces are balanced
  • CHP = BCOP = 0 NFP
  • no more fluid moves into the ISF ( through solute diffusion does still occur)
  • CHP is reduced if filtration has already occurred bc/ of resistance, and also bc/ there is less fluid removing inside the capillary
  • BCOP remains the same (all the larger particles are still present in plasma)
76
Q

Near a venule

A
  • there is a neg NFP, favouring reabsorption
  • CHP decreasing further (still slowed by resistance)
  • CHP < BCOP = -ve NFP
  • meaning a pressure gradient that favours fluid movement from ISF back to plasma
77
Q

What are the blood pressure (effectors for short-term alterations)?

A
  • the heart and the blood vessel walls
78
Q

What does the cardiac centres in the medulla oblongata dive change?

A
  • they change the cardiac output by altering activity in ANS inputs to the SA node of the heart and the myocardium
79
Q

How do vasomotor centres initiate change in blood vessel diameter (in both arteries and veins)?

A

by altering activity in sympathetic vasomotor fibres

80
Q

What happens during increased metabolic demands?

A
  • forms peripheral tissues can lead to changes in the overall chem composition of blood in the systemic circuit
  • chem changes from globally elevated metabolic demands (or metabolic demands> current levels of Cardiac output)
  • decrease PO2
  • Increase PCO2
  • Decrease pH
81
Q

When is blood pressure (BP) homeostasis and allostasis

A

Homeostasis: when BP is disturbed, BP is restored to set point

Allostasis: when blood chem is disturbed, BP is moved to a new set point

82
Q

what are the mechanisms we’ve seen so far not ideal for long-term regulation?

A

1) energy intensive
2) maintain central pressure

83
Q

What need to be regulated/ changes in order to maintain BP?

A
  • involves changes in blood volume
  • to maintain oxygen delivery at normal rates, blood volume changes must involve changes to both plasma and RBC levels
  • adjustment to blood volume are slow, but they can maintain BP throughout the circulatory system without constant energy input
84
Q

What is the response to long-term low blood pressure? (4 p)

A
  • is organized by 2 hormones secreted by the kidneys

Hormones:
-> renin: leads to increased plasma volume
-> erythropoietin (EPO): drives RBC production

  • low BP or blood volume leads to lower levels of perfusion through kidney tissue, stimulating the release of 2 hormones
85
Q

What is the long-term response to high blood pressure? (4p)
- ANP
- BNP

A
  • is organized by 2 hormones secreted by heart muscle
  • high BP ( or blood volume) leads to increased stretching in heart chamber walls, which leads to the release of natriuretic peptides (ANP and BNP)

ANP: atrial natriuretic peptide (released by the atria)

BNP: brain natriuretic peptide (released by the ventricles)

86
Q

What happens during the major loss of blood? (3p)

A
  • Blood volume changes through normal physiological mechanisms are usually slow
  • but, if blood vessels (especially large ones) are damaged, causing hemorrhage, blood volume can decrease rapidly
  • the body goes into survival mode
87
Q

What is the short-term response to blood loss?

A
  • involve natural reflexes and the physiological stress response
  • systemic veins can hold large volumes of blood
  • reducing the diameter of medium and large veins by vasoconstriction can return a large amount of blood from these ‘venous blood reservoirs’ without affecting perfusion
88
Q

what can epinephrin and other hormones lead to?

A

can also lead to vasoconstriction or dilation
-> Whether a hormone causes vasoconstriction or vasodilation in a particular blood vessel relates to the type of intracellular biochem triggered by its receptors

89
Q

What happens during active hyperemia?
(4p)
-Hyperemia: an excess of blood in the vessels supplying an organ or other part of the body.

A
  • in skeletal muscle during exercise, intrinsic mechanisms override extrinsic regulation, leading to active hyperemia
  • exercise/ active hyperemia: despite sympathetic activity increases during exercise promoting vasoconstriction (α1 receptors), blood flow is still greatly increased to skeletal muscles during exercise
  • this is due to direct metabolic autoregulation
  • Intrinsic regulation > Extrinsic regulation
90
Q

What happens during exercise hyperemia? (4p)

A
  • coronary arteries indirectly driven by intrinsic factors
  • Adenosine (paracrine factor release when ATP is used) - a key driver of vasodilation in coronary arterioles (ex: indirect metabolic autoregulation)
  • coronary blood vessels that supply heart muscle also exhibit vasodilation during exercise
91
Q

What happens during skin arterioles? (4p)

A
  • changes in constriction of skin arterioles change the proportion of blood flow through deep vs. superficial veins
  • superficial veins collect blood from skin
  • if there is superficial vasoconstriction, blood returns only through deep veins, maintaining core body heat (when body temp or blood volume are low)
92
Q

What regulates blood flow through blood vessels in the skin

A

CNS to help maintain thermal homeostasis

93
Q

How does blood flow help with getting rid of excess heat?

A
  • since the skin is not metabolically active during exercise, blood flow increases to the skin to help lose excess heat generated by skeletal muscle
94
Q

What happens during erectile tissue?

A
  • it undergoes vasodilation driven by activity in sacral parasympathetic fibres which release NO
  • Parasympathetic postganglionic neurons that innervate reactive tissue release NO (instead of or in addition to ACh)
  • NO leads to smooth muscle relaxation, allowing the large spaces within erectile tissue to fill with blood
95
Q
A