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Physiology P-215 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Major Functions of the Circulatory System

A
  • transportation-nutrients, oxygen, hormones, waste products
  • wound care-protect body from losing blood
  • immune function
  • heat regulation
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2
Q

AV Valves

A

-one way; pressure in atria causes change; will shut when pressure builds up in ventricle (tricuspid and mitral-left)

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3
Q

Chordae Tendinae and Papillary Muslces

A
  • chordae tendinae: attached to AV valves
  • papillary muscles: continuous with wall contract when muscle contracts
  • chordae and papillary tug on AV valve to keep flaps on ventricular side so no flopping back when ventricle builds up lots of pressure-never open valve
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4
Q

Semilunar Valve

A
  • toward top of valve
  • pulmonary: deoxygenated to lungs
  • aortic: oxygenated to body; thicker/rigid stronger on their own
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5
Q

Septum

A
  • divides left side from right side
  • prevents blood from mixing
  • conductive: electrical signals/AP’s will pass through
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6
Q

Fibrous Skeleton

A
  • divides atria from ventricles
  • all valves embedded in this
  • not conductive: absorbs AP’s and electrically insulated atria from ventricles
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7
Q

Pericardium

A
  • outer two layers
  • protective
  • doesn’t touch heart but lines outside
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8
Q

Epicardium

A
  • outer layer of heart that touches heart
  • protective
  • coronary blood vessels that supply blood to heart
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9
Q

Pericardial Space

A
  • fluid filled

- heart moves a lot and this allows lubrication to stop friction and provides a space to move in

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10
Q

Myocardium

A
  • muscular layer after epicardium

- force generating; think in Atria, thick in ventricle

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11
Q

Endocardium

A

-innermost layer that smoothly transitions from the inside of the heart to the blood vessels to try to keep smooth blood flow and prevent turbulation that would slow blood flow

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12
Q

Cardiac Muscle Structure

A
  • branching and connected more strongly
  • provides support because great force is generated
  • muscle fibers share AP’s because of gap junctions-don’t rely on external signal
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13
Q

Cardiac Muscle Function

A

-generates force-when they contract space gets smaller and develops pressure to move blood through body

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14
Q

AP’s in Cardiac Muscle

A
  • uses calcium ions in addition to sodium and potassium
  • calcium increases the length of the action potential
  • age is the only thing that can change this which will increase it more
  • contract simultaneously and summation of this like in skeletal muscle would destroy the heart-too much force than the structure could maintain so this is solved by longer AP’s (long absolute refractory period-no new AP)
  • have a maximum beat per minute because of this long AP which sets the maximum heart rate
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15
Q

Path of Electrical Activity in Heart

A
  • SA Node
  • AV Node
  • AV Bundle
  • Left and Right Bundle Branches
  • Purkinje Fibers
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16
Q

SA Node

A
  • in right atrium
  • AP starts here spontaneously and is released through gap junctions and both sides beat simultaneously because the septum is conductive but not to ventricles
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17
Q

AV Node

A
  • embedded in fibrous skeleton
  • only point where AP not absorbed by fibrous skeleton
  • tunnel between atrium and ventricle and starts AP on pathway to AV bundle
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18
Q

AV Bundle

A
  • axon/insulated wire
  • transitions AP down pathway to L&R bundle branches
  • working way toward apex of heart
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19
Q

Purkinje Fibers

A
  • raw nerve endings that release AP out into ventricular muscle that start at apex
  • want contraction to start at apex because SL valves are at the top and want contraction to start at bottom and create wave of pressure toward SL valve. Builds up pressure to area with valves so it’s most efficient way to maximally use pressure
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20
Q

SA Node Depolarization Mechanism

A
  • funny channels are always open but the rate of flow chan change; resting heart rate is different from exercising because of how open these channels are
  • funny current: spontaneous leakage; ungated and always open to some extent; depolarize muscle fiber by allowing Na+ to continually leak in
  • voltage gated calcium channel waiting for a certain voltage (threshold) to open and then an influx of calcium ions will rush in; combo of these two events makes AP (Na+ and Ca2+)
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21
Q

Regulation of Cardiac Rate

A
  • autonomic innervation of SA node is primary modifier of heart rate
  • sympathetic nerve endings in the atria and ventricles can increase strength of cardiac contraction
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22
Q

Sympathetic Effect

A
  • SA node: increases funny current and thus heart rate
  • AV node: increases conduction rate; receives AP and passes to ventricles/AV bundle a little faster; goal is to make sure atria and ventricles are in synchrony with each other; AV node keeps up to make sure ventricles contract at same rate
  • atrial and ventricular muscle: increase in contraction strength
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23
Q

Parasympathetic Effect

A
  • SA node: decrease funny current and thus heart rate
  • AV node: decrease conduction rate
  • no effect on atrial and ventricular muscle because you have a baseline of contraction you don’t want to go below
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24
Q

Bradycardia

A
  • slow heart rate at rest below 60 bpm
  • not necessarily bad
  • fewer number of AP’s per time
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25
Q

Tachycardia

A
  • fast heart rate at rest above 100 bpm
  • clinically unhealthy
  • less time between AP’s so more per unit time
  • what’s changing is the time taken to get to threshold is shortening
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26
Q

Fibrillation

A

-heart contracting not in synchrony; not cohesive; all pressures cancel out, space doesn’t get smaller; no pressure generated to open valve

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27
Q

Atrial Fibrillation

A
  • missing a little extra blood in ventricles so not as much is pumped out but still enough to be alive
  • would typically notice during exercise but ventricles can still function normally
  • only real problem is turbulence which can cause blood clots
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28
Q

Ventricular Fibrillation

A
  • can’t open semilunar valves which means can’t move blood around body so it’s fatal
  • why we have defibrillators: generates AP and forces fibers to all act at same time like they should
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29
Q

How can electrical signals from the heart be accurately measured from the skin?

A

-simultaneous contraction of a strong muscle generates large enough electrical signal sent out into the contractile water to be measured on the surface of the skin

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30
Q

P-wave

A

-represents atrial contraction-electrical signal has been sent out; can’t tell how strong just that there was one

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31
Q

QRS Complex

A

-represents ventricular contraction

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32
Q

T-wave

A
  • represents ventricular repolarization

- moving ions back where they came from is strong enough signal that we can see

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33
Q

Electrical Signal Traveling

A
  • SA node generates impulse; atrial excitation begins
  • impulse delayed at AV node: pause for conduction between atria and ventricle allows atria to top off ventricle; no pause there would be simultaneous contraction down bundle branches and would nullify atrial effect
  • impulse pass to apex and ventricular excitation begins
  • ventricular excitation complete
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34
Q

Order of Events During Cardiac Cycle

A
  • atria begin filling passively because there is nowhere else for blood to go
  • ventricles begin filling because of the increased pressure in the atria opens the AV valve and blood passively flows in 85-90%
  • atria contract to push last 15-10% into ventricles because funny channels are leaky enough to send out the AP-spontaneous and set amount of time to fill
  • ventricles contract and AV valves shut because AV node sends out impulse down to purkinje fibers at apex to push contraction and generate pressure
  • atria relax (happens at same time ventricles contract)
  • ventricles relax
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35
Q

End Systolic Volume

A
  • minimum volume of blood in heart

- after contraction (systole)

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36
Q

End Diastolic Volume

A
  • refilling during relaxation (diastole)

- maximum volume for this cardiac cycle

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37
Q

Stroke Volume

A
  • amount of blood successfully pumped out of ventricle in a single beat
  • calculated by subtracting ESV from EDV
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38
Q

Why is the local blood pressure in and around the heart important?

A
  • need pressure gradient to open valves

- without pressure nothing moves

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39
Q

What would happen if cardiac blood pressure was constant? Does this ever happen?

A
  • wouldn’t be any blood flow

- happens in ventricular fibrillation

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40
Q

What is the pressure of blood entering the atria? Why?

A
  • close to 0

- veins are thin and flexible and expand when blood enters them-no push back so don’t pressurize blood

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41
Q

What is the pressure of blood in the aorta? Why?

A
  • 120/80; highest because arteries are pressurized, narrow and more rigid so they push against blood and cause a pressure
  • blood flows into the aorta and ventricle is contracting and aorta stretches out but blood is being pushed into a space that already has a high pressure so it snaps back when the pressure in the ventricle is lower than that in the aorta
  • this elastic recoil sends blood in both directions which is what shuts the SL valve and we depend on it to push blood out into body
  • cardiac cycles overlap and as the next is happening you have to fight against previous stroke volume in aorta and the high pressure needed to open SL valve
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42
Q

Ventricular Pressure-Volume Loop

A
  • A: ESV, lowest volume and pressure
  • B: EDV, maximum volume; end of relaxation
  • B-C: isovolumetric contraction phase; ventricular contraction; huge increase in pressure with no change in volume because valves aren’t open yet-have to equalize and exceed pressure in aorta before they open
  • C: semilunar valves open; pressure in ventricle exceeds pressure in aorta; volume starts to decrease
  • C-D: blood flow out of ventricle into aorta-ejection of blood; stroke volume
  • D: semilunar valve closes because of elastic recoil of aorta creating a back pressure or afterload; aortic pressure exceeds ventricular pressure; no more volume change
  • D-A: isovolumetric relaxation phase; ventricular relaxation; huge decrease in pressure
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43
Q

Pressure and Volume

A
  • not directly related to each other
  • pressure due to muscle contraction not volume
  • volume change means a valve is open
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44
Q

Ventricular Ejection Fraction

A
  • SV/EDV
  • 80/120 so 57%
  • how much we successfully moved compared to; how much we could move
  • don’t need that much blood flow at rest so it’s as efficient as it needs to be
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45
Q

Flow of Blood in Heart

A

-vena cava–>RA–>RV–>pulmonary artery (deoxygenated)–>lungs–>pulmonary vein–>LA–>LV–>aorta–>body

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46
Q

Cardiac Output

A
  • amount of blood pumped out of one ventricle in a minute
  • CO=heart rate x stroke volume
  • heart rate and stroke volume are independent of each other
  • average cardiac output is 5.5 liters per minute
  • average total blood volume a person has is 5.5 liters
  • takes about 1 minute for a red blood cell to travel through the body at rest
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47
Q

Three Factors That Effect Stroke Volume

A
  • EDV/preload (stretch on muscle fibers before contraction)
  • TPR
  • Contractility
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48
Q

TPR

A
  • total peripheral resistance
  • impedes blood flow outside of heart
  • combined value of all resistance in body impeding blood flow out of the arteries
  • indirectly effects SV
  • resistance backs up toward SLV in aorta which makes already high pressure in aorta rise; pressure in ventricle must rise even higher to open SLV which will then mean less pressure is available to actually move blood out thus decreasing SV
  • increase in TPR means increase in afterload which is the physical force against the SLV keeping it closed or back pressure
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49
Q

Contractility

A
  • how much pressure you will potentially be able to generate based on certain circumstances
  • influenced by extrinsic and intrinsic factors
  • extrinsic: ANS-sympathetic drive increases contraction strength in the atria and ventricles
  • intrinsic: The Law of the Heart=length tension relationship: EDV increases, contractility increases because of optimum overlap of actin and myosin give greatest force
  • the longer the sarcomere, the stronger the force it can generate which means more pressure so more SV
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50
Q

High Blood Pressure Effect on Ventricular Pressure Volume Loop

A
  • no reason to change EDV-atria not affected; same venous return
  • change in TPR which means that point C or the point where the SLV opens is affected; will take more pressure to overcome increased pressure in aorta which means there will be a change in D
  • stroke volume decreases: aorta changed pressure but ventricle hasn’t so you need more pressure to open SLV; have certain amount of force we can use and once we do that’s it and valve closes
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51
Q

Heart Attack Effect on Ventricular Pressure Volume Loop

A
  • hypoxia of heart muscle and it dies; decrease in contractility because decrease in pressure able to be generated
  • no change in EDV because atria not affected
  • no change in point C SLV opening because no TPR increase so aortic pressure hasn’t changed
  • decreases length of C to D or stroke volume because you no longer have 100% muscle force to use; less pressure total and used normal amount to open SLV
  • decrease in contractility, decrease in pressure, decrease in stroke volume
52
Q

Mitral Valve Stenosis Effect on Ventricular Pressure Volume Loop

A
  • change in EDV-slowing down of passive filling in the limited amount of time normally have
  • no change in opening of SLV because no change in aortic pressure
  • decrease in SV because decrease in pressure and contractility; decrease maximum amount of blood that could be moved
53
Q

Systemic vs. Pulmonary Circuts

A
  • systemic=path from LV to body and back to heart
  • pulmonary=path from RV through lungs and back to heart
  • more blood in systemic because there are more vessels
  • systemic circulation rate is equal to flow rate through pulmonary circuit because if it wasn’t blood would build up in places
  • peripheral resistance is systemic circut is 5-7 x’s greater than pulmonary because the sheer length of tubing providing more friction
  • so the amount of work done by the LV is 5-7 x’s harder than the RV and as a result it is thicker and more muscular
54
Q

Structure of Blood Vessels

A
  • tunica externa: connective tissue and elastic
  • tunica media: smooth muscle
  • tunica interna: little bit more connective tissue and elastic
  • endothelial: single layer of cells
  • as you decrease size of vessels you strip away layers
  • capillaries are only endothelial layer and arterioles have last little bit of tunica media for their sphincters
55
Q

Major Characteristics of Arteries

A
  • lots of muscular layer
  • narrow lumen that won’t stretch far
  • relatively rigid and resist change to generate pressure
56
Q

Major Characteristics of Arterioles

A

-the resistance vessels because of precapillary sphincters that can be dilated or constricted to cause impedence

57
Q

Major Characteristics of Capillaries

A
  • exist for transport
  • only place because everything else is too thick
  • extensive surface area
  • create some resistance
58
Q

Continuous Capillaries

A
  • single endothelial cell layer with tight junctions between cells
  • only very small things can leak through
  • not very permeable-majority of our capillaries are these
59
Q

Fenestrated Capillaries

A
  • have pores that make them 200-300 x’s more permeable than continuous
  • only very small molecules go through easily
  • found in kidney; good for filtration
60
Q

Discontinuous Capillaries

A
  • very loose connections between cells
  • larger molecules can get through
  • specialized seen only in a few places like the liver and bone marrow
61
Q

Major Characteristics of Veins and Venules

A
  • capacitance vessels
  • huge lumen compared to arteries
  • valves inside
  • thinner layers compared to arteries; less structural integrity
  • low pressure environment
  • nothing driving blood out-need external help so usually run through skeletal muscle and get pushed up and valves keep backflow from happening
  • no movement you get sores because blood has pooled
62
Q

Blood Flow

A
  • continuous movement of blood through the circulatory system
  • continuous blood flow requires a pressure gradient
  • the stronger the gradient, the more blood flow
  • central venous pressure is 0 mmHg and aortic pressure is 93 mmHg so pressure gradient is 93-0=93
  • overall drive of strong pressure in aorta and weak in vena cava establishes continuous movement of blood through the circuit making sure we are sending blood back to the heart=venous return
  • combination of difference between two segments and the resistance of arterioles and capillaries between them
  • pressure difference/resistance=blood flow
63
Q

Hypertension Effects on Continuous Blood Flow

A
  • increased TPR so increased pressure in aorta
  • will increase the pressure gradient which means blood will return to the heart faster
  • important to separate the arteries from the veins-the blood is returning from the veins not the arteries and this is happening slightly faster in this case
64
Q

Pressure Gradient at Rest

A
  • pressure gradient from arteries to veins remains relatively constant so the body uses changes in resistance to regulate blood flow to satisfy needs of organs
  • vascular resistance determines ease of blood flow
65
Q

Active Changes to Resistance by Circulatory System

A
  • vasodilation: tunica media dilates; increase in diameter of vessel, decrease in resistance, increase in blood flow
  • vasoconstriction: smooth muscle layer contracts, decrease diameter of vessel, increase resistance, slows blood flow
  • resistance will also change if volume and or viscosity of the blood changes (dehydration, blood doping, hemorrhage)
66
Q

Local Resistance vs. Total Resistance

A
  • somewhat related
  • resistance surrounding one area/muscle/organ=local
  • local balances can counteract each other thus not changing total resistance
  • total resistance: all locals added up to see net balance
  • increasing total resistance will increase venous return to heart because overall gradient is allowing more blood to leave the veins a little bit faster
67
Q

Systolic Pressure

A
  • contraction phase (1/3 of the time)
  • point where artery is at its fullest stretch
  • highest pressure seen
  • aorta maximally filled prior to snapping
  • 120
68
Q

Diastolic Pressure

A
  • 2 x’s as often so twice as long (2/3 of the time)
  • low point after all the blood that is going to leave the artery has left
  • most relaxed point
  • 80
69
Q

Pulse Pressure

A
  • systolic BP minus diastolic BP
  • shows range of arterial pressures
  • need a decent range between the two
  • as pulse pressure starts to drop, not a lot of pressure gradient something wrong with heart contraction-less dynamic action
  • not generating enough blood to be usefully and move it around
  • don’t really have a clinical correlation; can vary for person to person
70
Q

Mean Arterial Pressure (MAP)

A
  • 1/3 pulse pressure + diastolic BP = MAP
  • gives you weighted average of arterial pressure
  • most commonly around 93 mmHg
  • must be >60 mmHg or organs die; pressure has dropped a lot at capillary level which could result in 0 at capillary level which means blood is pooling
  • need high pressure to drive blood throughout the body cause resistance starts to happen
  • too high BP would cause increased workload on the heart
71
Q

3 Main Factors That Determine Arterial BP

A
  • TPR: increase TPR, more blood backs up to aorta, pressure rises
  • increase in cardiac output: increase BP-more blood being pushed into arteries than is leaving and arteries start to pressurize
  • total blood volume: more blood into vessels, more stretched out-more pressure-largely affected by dehydration (decrease in blood volume)
72
Q

Intrinsic Control of BP

A
  • baroreceptors

- hormones

73
Q

Baroreceptors

A
  • pressure sensors connected to nervous system that sense pressure through now stretched out vessels
  • rapidly communicate with CNS to some integrating center that will send out effector response
  • usually cause vasoconstriction to increase TPR and make pressure increase to normal
  • short term, acute changes
  • located near carotid and aorta
  • carotid measures blood flow to brain and aortic arch is where it all starts so if BP drops, there nothing will get better anywhere else; uses a baseline measurement
74
Q

Hormones

A

-regulate blood volume (ADH, aldosterone) when these increase in bloodstream we will retain more water which modulates our blood volume and affects BP (seen at kidney)

75
Q

Extrinsic Control of BP

A
  • stress: increase because increase in cortisol creating sympathetic response
  • smoking: increases BP because nicotine causes vasoconstriction throughout body (short term) and hardens arteries (long term) and become more resistant-constant increase in TPR
  • diet: unsaturated fats can remove cholesterol and decrease BP; diet high in fat will increase BP
  • exercise: long term will decrease BP, during exercise BP increases
76
Q

Hypertension

A
  • silent disease: asymptomatic
  • heart works harder for a long time without you knowing which results in a stretch on arteries causing damage over time (atherosclerosis)
  • stimulate heart to make more muscle: pathological LV hypertrophy which decreases the volume of the chamber and limits EDV so it’s never relaxed to repair and add new muscle. Fibers laid down haphazardly and not cohesive so there’s no increase in contractility
  • athletes have a good environment to build muscle and fibers are placed properly which increases contractility because muscle is built outward
77
Q

Orthostatic Hypotension

A
  • drop in blood pressure caused when you stand up
  • blood drops into the veins and they expand ~600 mL drop toward lower extremities
  • blood volume relocates to lower body so decrease in the top and pressure drops
  • some people faint because neurons get hypoxic because not enough blood is getting to brain
  • characteristics that make it less likely: cardiac output-hypertension would make it less likely, increase in TPR, larger blood volumes
  • baroreceptors will vasoconstrict lower extremity vessels to send ~600 ml back to where it’s supposed to be in the body
  • negative feedback/homeostasis
78
Q

Total Blood Volume

A
  • 5-6 liters
  • whole blood=formed elements suspended and carried in plasma
  • formed elements are erythrocytes, leukocytes, and platelets
79
Q

Erythrocytes

A
  • hemoglobin to carry oxygen and carbon dioxide; no mitochondira because we want them to carry oxygen and not use it because mitochondria use oxygen as an electron acceptor
  • hematocrit is the percentage of RBC’s in the blood
  • normal hematocrit level is around 45%
80
Q

Platelets

A
  • smallest formed elements
  • very helpful for clot formation cause vasoconstriction in area of damage which increases resistance and less blood is able to flow through quickly so it limits blood loss
  • help heal/damage blood vessels
  • not necessarily required
  • these and leukocytes make up less than 1% of blood
81
Q

Plasma

A
  • 90% water with many dissolved solutes (electrolytes, hormones, etc)
  • used as transport
  • normal is about 55%
82
Q

Anemia

A
  • hematocrit level of 30%
  • lose more cells than you can make so hematocrit dropped
  • results in fatigue because you’ve lost cells that transport oxygen so less ATP is made
  • blood volume stays the same; RBC’s decrease so something else has to make up so more water from the body is taken into the plasma
83
Q

Polycythemia

A
  • hematocrit rises-70%
  • make RBC’s faster than you’re losing them
  • plasma decreases to maintain same total blood volume
  • lots of oxygen being transported through system-fatigue resistant
  • results in thicker blood which starts to stick and back up in the vasculature and pressure builds in the aorta which can result in heart damage
84
Q

Dehydration

A
  • water loss and not being replaced so total blood volume drops
  • decrease in TBV means decrease in pressure
  • only takes slight change in volume to see performance changes
  • will change viscosity but doesn’t really factor in too much
85
Q

Hematopoiesis

A
  • formation of blood cells from stem cells in bone marrow and lymph nodes
  • erythropoiesis is formation of RBC’s: stimulated by erythropoietin (EPO) which is released by kidney; production occurs in bone marrow
  • leukopoiesis is formation of WBC’s: stimulated by immune system-can be made in more than one location
86
Q

Hemostasis in Cessation of Bleeding

A
  • promoted by reactions initiated by vessel injury
  • vasoconstriction: increases resistance, diverts blood elsewhere when there’s not damage
  • formation of a platelet plug: can release chemical that can help; platelets stimulated by signal from endothelial layer and are sticky and have a positive feedback in which one becomes active then more become active and stick together to plug up the hole
  • fibrin web completes the clot and is being woven through the area due to this cascade
87
Q

Fluid Volume Review

A
  • 2/3 water in bodies is intracellular
  • 1/3 is extracellular
  • 75% of ECF is interstitial (not inside blood stream; fluid washing around cells
  • 25% of ECF is blood plasma
  • movement of water between compartments is a result of a pressure gradient
  • movement of water among ICF, plasma, ISF is in a state of dynamic equilibrium: follows gradient
88
Q

Sweating

A
  • increase in concentration of sodium in ISF
  • water in two other compartments wants to enter and dilute and try to equalize pressure across all three compartments
  • plasma water will most quickly enter ISF because if ICF water drops too much, cells don’t function as well
  • exercise in hot weather: ISF osmolarity increases, water donated to plasma to dilute so plasma osmolarity increases and then ICF moves to try to dilute and its osmolarity increases
89
Q

Filtration vs. Absorption

A

dynamic equilibrium between ISF and plasma is result of filtration-water leaving the capillary (plasma–>ICF)
-absorption-water moving into capillary (ICF–>plasma)

90
Q

Pressures Involved in Net Fluid Movement

A
  • hydrostatic pressure (P)

- Colloid osmotic (oncotic) pressure (pi)

91
Q

Hydrostatic Pressure

A
  • physical pressure of water pushing against capillary wall
  • capillary hydrostatic pressure: filtration force; water trying to get out of capillary; 38 mmHg at arterial end and 16 mmHg at venous end because friction has slowed down the particles and energy decreased and force decreased; 38 mmHg is related to blood pressure and can change
  • interstitial fluid hydrostatic pressure: absorption force; water trying to get into capillary; 1 mmHg normally but can change with injury or swelling to increase
92
Q

Colloid Osmotic (Oncotic) Pressure

A
  • osmotic force
  • pulling solutes toward water to dilute them
  • due to concentration of plasma proteins-water wants to dilute these and pulls them closer
  • capillary oncotic pressure: 25 mmHg; constant under normal circumstances because plasma proteins are too larger to leave the capillaries
  • interstitial fluid oncotic pressure: 0 mmHg outside capillaries so no plasma proteins should be out there: can change with damage to capillary
93
Q

Net Fluid Movement

A
  • sum of pressures driving water out + sum of pressures driving water in
  • (Pcap+πIF)-(PIF+πcap)
  • helps determine which way water is moving
  • Pcap and πIF are both outward forces and PIF and πcap are both inward forces
  • positive number means net filtration and a negative number means net absorption in which inward forces are greater than the outward forces
94
Q

Filtration

A
  • stronger of the two forces and we do this more than we absorb
  • water in ISF rises when we filter more than we bring in and if this goes unchecked we get swelling
  • to combat imbalance we use extra filtration via the lymphatic system
  • lymphatic capillaries interwoven with pulmonary and systemic ones and vacuum out the excess fluid and pass it through lymph nodes to detect pathogens and return it to venous system
95
Q

Lymphatic System

A
  • lymphatic vessels, lymph nodes, tonsils, spleen, and thymus
  • functions: pick up excess fluid filtered out in capillary beds and returns it to veins-prevents build up of ISF water by vacuuming it out; helps provide immunological defense: pathogens most likely to be found in ISF so WBC’s in bloodstream and lymph nodes: none in ISF so need some mechanism to get this fluid to lymph nodes to wash it and return ISF (early warning network for pathogen invasion); transports absorbed fat from the SI to the liver
96
Q

Immune System Function

A
  • defense: protection and prevention; very important and not very expensive
  • offense: actively fight off invasion; energy and materials consuming-expensive
97
Q

Sources That Stimulate Immune Response

A
  • pathogens
  • cell damage
  • genetic mutation
  • autoimmunity
98
Q

Pathogens

A
  • recognized by WBC’s because all cells have different antigens and the ones in our body are distinguished by these surface shapes
  • if cell comes in with unfamiliar antigen an offensive attack is launched
  • common pathogens: bacteria; most common life form ~3% are harmful to us and viruses that bypass defenses and use our cells to reproduce (HIV, flu, herpes)
99
Q

Cell Damage

A
  • a normal cell is recognized by immune system as being smooth
  • damaged cell has roughness and WBC’s recognize and trigger immune response
  • cell releases chemical signals it’s not supposed to that surrounding cells pick up on and send out signals that attract WBC’s to clean up damaged cell and leave healthy cell that can divide and replace damaged cell
100
Q

Genetic Mutation

A
  • internal cell damage
  • DNA damaged: vital proteins may not be made so cell doesn’t function and may die on its own or it can become cancerous which is characterized by rapid replication and proliferation
  • cancer cells look like our other cells and immune system can’t identify them from abnormal cells
101
Q

Auto-Immunity

A
  • WBC attacks perfectly normal healthy cell of our own-usually very specific one
  • type 1 diabetes targets insulin producing cells, MS targets myelin sheath, myasthenia gravis targets ACh receptors at neuromuscular junction
  • to treat sometimes use immunosuppressant which makes it much easier to get sick by other means
102
Q

Types of White Blood Cells

A
  • neutrophils: majority of WBC’s non-specific 4-72 hr lifespan because very active and wear out fast
  • eosinophils and basophils very small portion 4-72 hr lifespan; nonspecific
  • monocytes/macrophages: nonspecific; 100-300 day lifespan
  • lymphocytes: more common than monocytes; specific responder-only attack one kind of pathogen
103
Q

Post Infection Timeline for Most Common Leukocytes

A
  • neutrophils come first and have short life and as they die monocytes come into play
  • monocytes have a little longer life and when they die off T-lymphocytes activate
  • T-lymphocytes activity plateaus and they live for longer
104
Q

Central Tissues of Lymphatic System

A
  • where WBC’s come from or are specialized
  • bone marrow: first WBC’s made here and they they can go to lymph nodes and replicate
  • thymus gland: specialization of lymphocytes; some undifferentiated WBC’s released from bone marrow go here to go through rigorous process to be specialized into T-lymphocytes
105
Q

Peripheral Tissues

A
  • adenoids and tonsils, spleen, lymph nodes (make up most of these peripheral tissues)
  • see lymphnodes in places where external fluid comes in contact with internal fluid
106
Q

Non-Specific Barriers

A
  • skin: physical barrier and bacteria that are mostly beneficial
  • GI tract: HCl, digestive enzymes, and bacteria; HCl denatures and destroys food and bad things ingested with it
  • respiratory: mucous, cilia, coughing sneezing; pathogens get stuck in mucous and cilia bring them up to be coughed out
  • other protective secretions: tears and sweat contain lysozyme which is an all purpose microbial that works as an enzyme to break down pathogens on skin or in eyes
  • lymph nodes
107
Q

Lymph Nodes

A
  • close to places where external fluid is potentially close to internal fluid–>ISF close to outside fluid system
  • have lots of long lasting WBC’s: monocytes and lymphocytes
  • works like a kidney to filter lymph and ISF
  • increase probability of WBC’s finding a pathogen by sending ISF through small area filled with WBC’s
  • increase in proximity increases the probability
108
Q

Interferons

A
  • chemical signal secreted by infected cell
  • surrounding cells sense this and lock down DNA and slow down protein synthesis
  • when they become infected they have a delay against the virus using its protein synthesis pathway
  • signal is released into ISF then gets into bloodstream and creates a gradient for WBC’s to detect and follow
109
Q

Cytokines

A
  • any chemical signal that draws WBC’s to area
  • ex: interferons, damaged cell and neighboring cell signals, endogenous pyrogens
  • these all increase the probability of WBC finding the pathogen
110
Q

Chemotaxis

A
  • movement of WBC toward cytokine

- takes a while for WBC to follow and catch pathogen so need another mechanism

111
Q

Diapedesis/Extravasation

A
  • getting WBC out of blood
  • neutrophil is in capillary and pathogen is sending out cytokine in ISF
  • neutrophil senses signal and gets sticky and adheres to capillary wall
  • sends out signal to make gaps in capillary larger so it can squeeze out and follow cytokine
112
Q

Endogenous Pyrogens

A
  • secreted by WBC when they attack a pathogen
  • affects hypothalamus; tells it to increase core body temperature which is why you get chills, body reacts as if it’s hypothermic
  • causes you to shiver to increase to new temperature
  • fever is important because pathogens aren’t able to function best at high temperatures; affects replication and enzyme activity but our WBC’s thrive at high temperatures; gives them a chance to attack pathogen
113
Q

Immune System Point of View of Infection

A
  • increase leukopoiesis to counter infection; try to keep up with pathogen division
  • there’s a limit to how many WBC’s can make at a time so can’t keep up with pathogen’s exponential division
114
Q

Antigen Presenting Cells

A
  • neutrophil takes antigen from destroyed pathogen and inserts into own membrane and presents it to lymphocyte
  • now this lymphocyte has become specified to attack this kind of pathogen
  • intial killing happens in ISF so that’s where APC is made and is then swept into lymphatics and into lymph nodes where lymphocytes are waiting to be specified-good place for this specification because it’s where the two WBC’s come into contact
115
Q

Cell-Mediated Immunity

A
  • one of the two fundamental adaptive mechanisms that interact that the immune system has to better attack invading pathogen
  • uses T-cells
  • starts with a non-specific immunity and generally follows three steps
    1. APC
    1. APC sensitizes T-lymphocytes
    1. T-cells divide and differentiate into 4 different types (cytotoxic or killer T, helper T, suppressor T, memory T)
  • overall result of this is you get a specific cell made to go out and kill a specific pathogen
  • weakness: can’t keep up with exponential rate of division of pathogens
116
Q

Cytotoxic or Killer T

A
  • cell itself is killing pathogen; kills only the specific pathogen
  • directly attacks a specific antigen
  • attack membrane and DNA
  • used in bacterial and viral infections
117
Q

Helper T

A
  • work like APC’s so you have more than one to amplify the response and sensitize more T-cells more efficiently
  • also activates B cells
  • targeted by AIDS virus: virus prevents amplification so virus can replicate faster
  • crossover step
118
Q

Suppressor T

A
  • come into play once pathogen has been fought off
  • decrease activation of cytotoxic killer T cells and B cells
  • loss can lead to autoimmunity: killer T-cells go out and find cell with antigen close enough to a pathogen and kill it (misidentification)
  • gearing down step
119
Q

Memory T

A
  • store antigen pattern and after infection is fought off these last a long time (sometimes a lifetime) and wait for antigen to show up again
  • recognize return of pathogen so APC’s not needed next time
120
Q

Humoral Immunity

A
  • how B cells respond
  • same general 3 steps as cell-mediated
    1. APC
    1. APC sensitizes B-lymphocyte
    1. B-lymphocyte divides and differentiates into two different B cells (Memory B and Plasma (Active) B)
  • memory B do the same as memory T
121
Q

Plasma (Active) B

A
  • actually does the fighting but indirectly
  • secretes antibodies-small proteins
  • secrete at about 2,000 antibodies per second-need something to keep up with exponential division of pathogen-replicates faster than any pathogen can
122
Q

Antibody (Immunoglobulin)

A
  • have specific antigen binding sites

- fight off infection by neutralization, enhanced phagocytosis, and activation of compliment system

123
Q

Neutralization

A
  • pathogen surrounded by bound antibodies so it can’t affect target tissues because it can’t bind/touch tissues
  • aggregation of pathogens because antibody can bind to two different pathogens at once; easier for WBC to get to it because it’s bigger and all pathogens fight against each other so it’s static
124
Q

Enhanced Phagocytosis

A

-antibodies make pathogen more easily eaten/more at once and faster because they’re all stuck together

125
Q

Activation of Compliment System

A
  • antibody is bound to antigen and starts a process
  • when they bind they bring in solute proteins to use to build compliment protein
  • compliment protein has different parts to do different things
  • one part is soluble and acts as a cytokine to send out signal to ICF
  • insoluble part inserted into membrane of pathogen in a circular pattern-creates membrane attack complex that punches hole in pathogen membrane
  • osmosis happens so water rushes in and lyses pathogen
  • this decreases reliance on WBC by doing the killing
  • antibodies themselves do the killing but still need WBC’s to clean up dead pathogens-weakness

Physiology P-215 (4 decks)

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