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Anatomy > Anatomy 2 Midterm 1 > Flashcards

Anatomy 2 Midterm 1 Flashcards

1
Q

What is blood composed of?

A
  • Formed elements: Erythrocytes (RBC), Leukocytes (WBC), platelets
  • Plasma
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2
Q

What is the main type of plasma protein?

A

Albumin

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3
Q

What is the structure of an RBC?

A

-Biconcave disc with large surface area
-Composed of mostly hemoglobin

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4
Q

What are the functions of erythrocytes?

A

Transport respiratory gases around the body. (Gas exchange and transportation)

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5
Q

What is the structure of hemoglobin?

A
  • 4 polypeptide chains (2 alpha, 2 beta)
  • 1 heme group per polypeptide
  • iron in the center of heme group (oxygen reversibly binds to iron)
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6
Q

What is the function of hemoglobin?

A

Reversibly binds oxygen to iron in the heme group. When oxygen is attached it’s called oxyhemoglobin. When oxygen is released it’s called deoxyhemoglobin. CO2 attaches to the amino acids of hemoglobin and when that occurs it’s called carbaminohemoglobin.

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7
Q

What is the process of creating erythrocytes?

A

Erythropoiesis
1. starts as hemocytoblast (hematopoietic stem cell)
2. enters the committed cell phase (proerythroblast)
3. ribosome synthesis
4. hemoglobin accumulation
5. ejection of nucleus
6. reticulocyte
7. erythrocyte

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8
Q

What is erythropoietin?

A

Erythropoietin is a glycoprotein hormone that stimulates the rate of production of erythrocytes in cases where there’s excess RBC destruction, high altitude, or increased demand

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9
Q

Where is erythropoietin produced?

A

Primarily in the kidneys but also some from liver. Gets sent to red bone marrow to stimulate rate of production

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10
Q

Why do men have higher EPO than women?

A
  1. Menstruation
  2. Testosterone causes an increase in EPO
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11
Q

What is the lifespan of an erythrocyte (when it’s useful)?

A

100-120 days

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12
Q

What is the mechanism of control in erythrocytes?

A
  1. Stimulus presents issue
  2. Stimulates kidneys and kind of liver to release EPO
  3. This stimulates red bone marrow
  4. The RBC count increases
  5. Oxygen levels increase
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13
Q

What happens to an erythrocyte when it becomes old?

A

It becomes rigid as spectrin deteriorates. It also loses hemoglobin and due to it’s lack of flexibility most likely gets trapped in the spleen. Macrophages engulf them and the heme group splits off from globin. The iron is saved and bound to protein for later use. Heme group becomes bilirubin and metabolizes in the intestine; becoming urobilinogen. most of this pigment leaves the body as stercobilin in feces. the globin is broken down into amino acids and released into circulation.

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14
Q

What are the steps of hemostasis?

A
  1. Vascular spasm
  2. Platelet plug formation
  3. Coagulation
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15
Q

What is the first step of hemostasis?

A

Vascular spasm:
- damaged blood vessels respond to injury by contracting (vasoconstriction)

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16
Q

What causes vascular spasm to occur?

A
  • Direct injury to smooth muscle
  • Chemicals released by damaged endothelial cells and activated platelets
  • reflexes initiated by local pain receptors
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17
Q

What is the second step of hemostasis?

A

Platelet Plug Formation:
- Activated platelets stick together to temporarily form a plug in the wall to seal the blood vessel

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18
Q

Why do platelets normally not stick to each other or endothelial linings?

A

Intact endothelial cells release nitric oxide and prostacyclin to prevent platelets from clumping

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19
Q

How do platelets activate (become sticky)?

A

Damaged endothelial cells expose collagen and the platelets adhere to the collagen fibers in the basement membrane. A large protein called the Von Willebrand factor stabilizes the platelets by forming bridges between the collagen and platelets. This causes platelets to release chemicals called adenosine phosphate (ADP), serotonin, and thromboxane (A2). More and more platelets come and release their chemicals activating the platelets in a positive feedback cycle.

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20
Q

What is the 3rd step of hemostasis?

A

Coagulation:
- Platelet plug is converted to a sturdier structure with fibrin threads
- Liquid blood becomes gel when these proteins (fibrins) are added

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21
Q

What are the 3 phases in coagulation?

A

1) Formation of prothrombin activator
2) Prothrombin converts to thrombin
3) Fibrinogen molecules become fibrin mesh

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22
Q

What are the 2 pathways in phase 1 of coagulation?

A

1) Intrinsic Pathway
- Activates when collagen is exposed
- Clotting of blood outside body or in a slightly damaged vessel

2) Extrinsic Pathway
- Activates due to exposed blood to tissue factor
- Clotting of blood in response to damage
- Faster than intrinsic; quick way to factor X and PA.

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23
Q

What is phase 2 of coagulation

A

Prothrombin converts to thrombin

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24
Q

What is phase 3 of coagulation?

A
  • Thrombin catalyzes the formation of soluble fibrinogen to insoluble fibrin
  • Also when present with calcium, thrombin activates the XIII factor (fibrin stabilizing factor) that causes fibrin to link firmly together forming a fibrin mesh.
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25
Q

What is clot retraction?

A
  • platelets contract; pulling on surrounding fibrin strands
  • serum squeezed from clot
  • ruptured ends of blood vessels pulled closer together
  • PDGF (Platelet derived growth factor) stimulates smooth muscles and fibroblasts to divide and rebuild a wall.
  • VEGF (Vascular endothelial growth factor) causes endothelial cells to multiply and fill gap in lining
  • Clot covers area of lining while healing begins
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26
Q

What is fibrinolysis and what are the steps?

A
  • Removes the clot when no longer needed
    1. tPA (tissue plasminogen activator) is released by endothelial cells
    2. tPA activates plasminogen to become plasmin
    3. Plasmin breaks down the clot
    4. tPA and plasmin are both inhibited after clot is removed

tPA inhibited by PAI and plasmin inhibited by plasmin inhibitor

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27
Q

What are the factors that limit clot growth and formation?

A

Either swift removal of coagulation factor or inhibition of activated clotting factors

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28
Q

How does swift removal of coagulation factors work?

A

Normally blood washes away procoagulants

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29
Q

How does inhibition of activated clotting factors work?

A
  • when thrombin forms it’s absorbed onto fibrin threads
  • antithrombin III inactivates escaping thrombin
  • antithrombin III and protein C inactivate many intrinsic pathway procoagulants
  • heparin enhances activity of antithrombin III and inhibits intrinsic pathway
  • smooth endothelial lining of undamaged blood vessels prevents undesirable clotting (also since nitric oxide and prostacyclin form and prevent activation of platelets)
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30
Q

What is a thrombus?

A
  • A clot that is present in an unbroken blood vessel
  • Can block critical blood circulation to those tissues
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31
Q

What might cause thrombus to form?

A

Hypertension, unmoving blood, exposure of collagen

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32
Q

What is an embolus?

A
  • A thrombus that broke free and can get stuck in smaller vessels
  • They can cause heart attacks or strokes
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33
Q

How to treat an embolus or thrombus?

A

tPA or streptokinase to dissolve clots through plasmin

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34
Q

What are the different blood types?

A

A, B, AB, and O

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35
Q

What is the universal donor and why?

A

Type O is the universal donor because it has no antigens present so it won’t attack the immune system of the recipient.

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36
Q

What is the universal recipient and why?

A

Type AB is the universal recipient because it has both A and B antigens present so nothing would cause the to produce antigens they don’t have so they won’t have the possibility of clumping.

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37
Q

Why is knowing blood type important in transfusions?

A

To ensure that the person has the correct antigens because antigens promote agglutination (clumping) especially if combined with incompatible blood.

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38
Q

What are Rh factors?

A

They determine whether or not the blood type of 2 people will be compatible when mixed.

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39
Q

Why is it important for people who want to have a baby to have the same Rh factor?

A

If an Rh- woman is pregnant with an Rh+ baby as their first child, the mother will be sensitized upon exposure to the Rh antigens. The antibodies will attack the mother’s RBCs. RH- mothers carrying a second RH+ child should be reated with RhoGAM (anti-Rh serum) to prevent erythroblastosis fetalis as the mothers antibodies will attack the fetus’s RBC’s.

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40
Q

What are the possible problems with transfusions?

A

If there are incompatible antigens it could lead to agglutination or clumped RBC’s can rupture. Overall this would cause blocked flow to tissues, reduced O2 carrying abilities and Hb clogging kidney tubules

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41
Q

What is the heart?

A

A transport system pump

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42
Q

What is the internal and external anatomy of the heart?

A

External:
- Enclosed within the mediastinum of the thorax
- right side of heart lies on diaphragm
- 2/3 mass on left side of heart (left is thicker)
- coronary sulcus
- anterior-posterior interventricular sulcus

Internal:
- 2 Atria
- 2 Ventricles
- interatrial and interventricular septa
- pectinate muscles
- fossa ovalis
- foramen ovale
- trabeculae carneae
- papillary muscles
- 4 Heart valves:
- Atrioventricular valves
- tricuspid valve (right
atrium to right ventricle)
- mitral (bicuspid) valve (left
atrium to left ventricle)
- Semilunar valves:
- pulmonary valve (right
ventricle to pulmonary
trunk)
- aortic valve (left ventricle
to the aorta)

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43
Q

What are the 3 layers to the heart?

A

1) Pericardium
- outer covering of the heart
- has 2 layers
-fibrous pericardium: prevents overfilling of heart. Protects and anchors heart.
- serous pericardium: Allows the heart to fill and empty. Filled with fluid.

2) Myocardium
- cardiac muscles makes up most of the heart
- Strengthens the walls of the heart with connective tissue
- Protects+anchors cardiac muscle fibers
- Direct spread of action potentials across the heart

3) Endocardium
- Has direct contact to blood as its continuous with endothelium of vessels leaving and entering the heart

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44
Q

What is the pathway for the pulmonary circuit?

A
  1. Blood enters the right atrium through the SVC (superior vena cava), IVC (inferior vena cava), and the coronary sinus
  2. Blood enters the right ventricle through the tricuspid valve
  3. Blood goes into the pulmonary trunk through the pulmonary valve
  4. Blood goes to lungs through pulmonary capillaries
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45
Q

What is the pathway for the systemic circuit?

A
  1. Oxygenated blood enters the left atrium through the 4 pulmonary veins
  2. Blood enters the left ventricle through the mitral (bicuspid) valve
  3. Blood goes to the aorta through the aortic valve
  4. Blood goes through systemic capillaries and back to the right atrium
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46
Q

Describe the organization of the coronary circulation

A
  • shortest but one of the most important circulations in the body
  • Right and left coronary arteries branch from the base of the aorta around the heart in the coronary sulcus.
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47
Q

What are the key physiological properties of cardiac muscle?

A
  • striated
  • 1 or 2 nuclei per cell
  • contract as a unit
  • few wide T tubules
  • Less elaborate sarcoplasmic reticulum with no terminal cisterns
  • Ca+ for contraction comes from SR and ECF
  • Pacemaker cells
  • Ca2+ binds to troponin
  • Aerobic only for ATP
  • 2 types of cell junctions:
    -gap junctions: direct
    communication between cells
    -desmosomes: strong cell-cell
    adhesion during contraction
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48
Q

What is the difference between autorhythmic and contractile cardiac muscle cells?

A

Autorhythmic: Sets the rate of your heart beat
Contractile- Responsible for contractions that pump blood throughout the body

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49
Q

What is the action potential of contractile cardiac muscle cells?

A

1) Depolarization- due to sodium influx through fast voltage-gated sodium channels
2) Plateau Phase- Calcium influx through slow calcium channels. Keeps cell depolarized because few potassium channels are open
3) Repolarization- Calcium channels inactivate and potassium channels open, resulting in K+ efflux which returns membrane potential to normal

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50
Q

Why is the absolute refractory period important?

A

It allows the heart to fill again

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51
Q

What determines heart rate?

A

Sinus rhythm

52
Q

What is the action potential of autorhythmic cells?

A

1) Pacemaker potential- Na+channels open and K+ channels close

2) Depolarization- Calcium influx through calcium channels

3) Repolarization- Calcium channels inactivate and potassium channels open, resulting in K+ efflux

53
Q

What do autorhythmic cells have that contractile cells do not

A

unstable resting membrane potentials

54
Q

How does the intrinsic conduction system allow the heart to function as a pump?

A
  1. Sinoatrial node generates an action potential
  2. AP passed to the atrioventricular node
  3. Then passed to atrioventricular bundles
  4. then right and left bundle branches
  5. Finally the subendocardial conducting network
55
Q

Why is the sinoatrial node the pacemaker?

A

It continuously generates electrical impulses

56
Q

What are the influences of the PNS and SNS on cardiac function?

A

Rate of the sinoatrial (SA) node depolarization is regulated by the ANS

Parasympathetic: decreases depolarization rate

Sympathetic increases depolarization and repolarization rates

57
Q

What is bradycardia, tachycardia, and sinus rhythm

A

Bradycardia- slower than normal heart rate
Tachycardia- faster than normal heart rate
Sinus rhythm- normal heart rate

58
Q

What is ECG tracing?

A

Records electrical changes during heart activity (autorhythmic)

59
Q

What are the different stages of ECG tracing?

A
  1. P-wave (atrial depolarization)
  2. QRS complex (ventricular depolarization)
  3. T-wave (ventricular repolarization)
60
Q

Where is atrial repolarization in an ECG tracing?

A

Hidden behind the QRS complex

61
Q

What are the phases of the cardiac cycle?

A

Systole- contraction of hear
Diastole- filling of heart

there’s both atrial systole + diastole and ventricular systole + diastole

62
Q

What is the first event of the cardiac cycle?

A

Ventricular Filling:
- mid-late diastole
- AV valves are open; SL valves are closed
- After 70% filled, AV valves begin to close -> P wave and atrial systole; atrial pressure increases and final 30% enters ventricles
- atrial diastole for rest of cycle

63
Q

What is the second event of the cardiac cycle?

A

Ventricular Systole (QRS + T waves):
- ventricles begin to contract
- increased pressured closes the AV valves
- period of isovolumetric contraction (volume constant; closed system)
- increased pressure opens the SV valves
- ventricular ejection phase

64
Q

What is the third event of the cardiac cycle?

A

Isovolumetric relaxation:
- early diastole (ventricles relax)
- pressure decreases rapidly
- backflow of aortic/pulmonary blood closes the SL valves
- ventricles a closed system

And to restart the AV valves open as the atria continued in diastole the entire time

65
Q

What are the 2 features that drive the cardiac cycle?

A

1) pressure changes
2) goes from higher to lower pressure through any opening

66
Q

What are the 2 heart sounds that can be heard from a stethoscope?

A

1) First heart sound: closure of AV valves (beginning of systole)
2) Second sound: closure of SL valves (end of systole)

Heart sounds due to vibrations of heart/chest due to valve closure

67
Q

What is cardiac output?

A

The volume of blood that’s pumped from each ventricle per minute

68
Q

How do you calculate cardiac output?

A

CO= HR (heart rate) x SV (stroke volume)

SV can be calculated by subtracting EDV (end-diastolic volume) - ESV (end-systolic volume)

69
Q

What is heart rate determined by?

A
  • rate of spontaneous depolarization of the SA node
  • autonomic fibers innervating the SA node
  • circulating hormones
  • plasma electrolyte concentrations
  • body temperature
  • Norepinephrine increases rate of spontaneous depolarization
  • ACh decreases rate of spontaneous depolarization

Resting conditions: parasympathetic ns is dominant (vagal tone)

70
Q

Why does extreme tachycardia lead to a decreased CO?

A

The heart doesn’t have enough time to fill during diastole and contracts too quickly so there’s not a lot of volume of blood in the ventricle.

71
Q

What factors influence stroke volume?

A
  • increase in preload (the heart will pump whatever volume of blood it receives) causes an increase in stroke volume
  • increased afterload (pressure that needs to be overcome to force open valves and eject blood) reduces the ability of ventricles to eject blood leading to increased ESV and decreased SV.
72
Q

What factors influence heart rate?

A
  • changes in autonomic CNS output (eg. fear, anxiety, etc)
  • increased sympathetic activity
  • reduced parasympathetic activity

All increase heart rate.

73
Q

What are 2 extrinsic influences on stroke volume?

A
  • change in strength of contraction due to increased calcium influx
    1. sympathetic stimulation: increases strength and rate of contraction and relaxation
    2. drugs: i.e. digoxin- increases heart contractility
74
Q

What are the differences and similarities between the walls of capillaries, arteries, and veins?

A

Capillaries:
- Basement membrane
- Endothelial cells
- thin tunica intima

Arteries:
- 3 tunics (tunica media, tunica intima, tunica externa)
- Has external elastic membrane
- Vasa vasorum

Veins:
- 3 tunics (tunica media, tunica intima, tunica externa)
- Vasa vasorum

75
Q

What are the 3 types of arterial vessels?

A
  1. Elastic Arteries
  2. Muscular Arteries
  3. Arterioles
76
Q

What are elastic arteries?

A
  • large diameter arteries near the heart
  • contain lots of elastin
  • smooths out fluctuations in pressure
  • recoil helps maintain pressure and flow of blood
77
Q

What are muscular arteries?

A
  • Delivers blood to specific organs
  • More smooth muscle than elastin
78
Q

Why is it good that there is more smooth muscle than elastin in muscular arteries?

A
  • This allows arteries to change in diameter and fine-tune where blood is being sent
79
Q

What are arterioles?

A
  • smallest arteries
  • Determine which capillary beds get flushed
  • large arterioles have 3 tunica but the smallest ones leading to the capillary bed on have a single layer of smooth muscle cells.
  • tunica media is primarily smooth muscle
80
Q

What are the 3 types of capillaries?

A

1) Continuous
2) Fenestrated
3) Sinusoidal

81
Q

What is the function of capillaries?

A

To exchange materials between blood and tissue cells

82
Q

What is a continuous capillary?

A
  • Endothelial cells linked by tight junctions to provide an uninterrupted lining
  • In major regions of the body (skin, muscle, brain
  • Continuous everywhere except CNS where there are intercellular clefts for limited passage of small solutes and fluids
83
Q

What is a fenestrated capillary?

A
  • A capillary with a lot of tiny pores
  • Has increased permeability to small solutes/fluids
  • Found in small intestine, kidney, and endocrine organs
84
Q

What is a sinusoidal capillary?

A
  • Leaky capillaries
  • Have large irregular lumen
  • Found in liver, bone marrow, lymphoid tissues and endocrine organs
  • Is typically fenestrated and has fewer tight junctions and large intercellular clefts for the passage of RBC’s and proteins
85
Q

What is microcirculation?

A

Microcirculation is the flow of blood from an arteriole to a venule through a capillary bed

86
Q

What determines the rate of flow of blood through the capillaries?

A

The diameter of the terminal arteriole

87
Q

What are true capillaries?

A

Actual exchange vessels

88
Q

What is the structure and function of a venule?

A

Structure:
- Large venules: thin tunica adventitia and a couple layers of smooth muscle cells
- post capillary venules: endothelium and a few fibroblasts

Function:
- Receives blood from capillaries and channels them into larger veins

89
Q

What is the structure and function of a vein?

A

Structure:
- 3 tunics
- Large lumen
- tunica adventitia is the heaviest layer

Function:
- Blood reservoirs

90
Q

Define blood flow and blood pressure

A

Blood Flow:
- measured in mL/min
- can be regulated independently for various tissues and organs
- FLOW ONLY OCCURS IN A PRESSURE GRADIENT

Blood Pressure:
- force that’s exerted on the wall of a blood vessel by its contained blood
- usually refers to systemic arterial blood pressure in large arteries near the heart

91
Q

What is resistance?

A
  • Major determinant of blood flow
  • Measures the totals of frictional forces that impede flow
92
Q

What influences resistance?

A
  • Blood viscosity (n)
  • Length of blood vessel (L)
  • Radius of blood vessel (r)

R has a relationship with (nL)/(r^4)

93
Q

Why are arterioles important in peripheral resistance?

A

Arterioles change in diameter quite quickly which when increasing in diameter causes a decrease in resistance.

94
Q

Define systolic and diastolic pressure

A
95
Q

What is pulse pressure?

A

Can be calculated by subtracting systolic bp- diastolic bp

  • indicates strength of contraction of ventricle
  • provides info on elasticity of aorta
  • decreases with distance from heart
96
Q

What is mean arterial pressure (MAP)?

A

Can be calculated by adding diastolic pressure + 1/3 pulse pressure

  • The pressure that propels blood to tissues during the cardiac cycle
  • Decreases with distance from heart
97
Q

What and why is the value of mean capillary blood pressure the way it is?

A
  • low pressure: 35 mmHg
  • high pressure: 17 mmHg
  • Because capillaries are fragile and can rupture if the pressure is too high
  • most capillaries are extremely permeable and there’s a lot of exchange at low blood pressure
98
Q

What is venous blood pressure?

A
  • very steady
  • hardly changes (only around 15 mmHg change)
  • there is a gradient and veins will provide more pathways so blood will flow forward
99
Q

What aids venous return?

A

1) Venous valves + muscular pump
2) Respiratory pump
3) Sympathetic vasoconstriction

100
Q

What is a pulse?

A

Pressure wave due to alternating recoil and expansion of elastic arteries

101
Q

What is blood pressure?

A
  • Measured in the brachial artery
  • Pressure of circulating blood on walls of blood vessels
102
Q

What is the normal blood pressure of a healthy individual?

A

120/80

103
Q

How do you regulate blood pressure in the short term and the long term?

A

Short term:
- Blood vessel diameter (peripheral resistance)
- Cardiac output

Long term:
- blood volume
- adjustments made at kidneys

104
Q

What does short-term regulation of blood pressure normally involve?

A
  • Baroreceptors
  • Vasomotor Centre of Medulla
  • Vascular Smooth Muscle
105
Q

What does the cardiovascular center respond to input from for blood pressure?

A
  • Baroreceptors
  • Chemoreceptors
  • Higher brain centres or hormones
106
Q

What are the steps from the vasomotor centre when the baroreceptors are initiated?

A
  1. Increased MAP stretches receptors and causes arterioles to dilate
  2. Venodilation occurs to have blood flow to venous reservoirs
  3. Afferents to cardiac centres to decrease heart rate and contractile force

Decreasing MAP does the opposite

107
Q

Where are baroreceptors located?

A

In the carotid sinus and the aortic arch as well as arteries in the neck and thorax

108
Q

How are chemoreceptors activated and what happens?

A
  • drop in O2, ph or rise in CO2
  • reflex vasoconstriction
  • rise in blood pressure that speeds return of blood to heart and lungs
109
Q

How do hormones play a role?

A

Vasoconstrictors:
- Angiotensin II
- Adrenal medulla hormones (NE/E) (increases CO)
- Antidiuretic hormone (ADH) (primarily long term regulation)

Vasodilators:
- Atrial natriuretic peptide (ANP)

110
Q

How do kidneys play a role in long-term regulation?

A
  • Kidneys can alter blood volume
  • If blood levels are increased, kidneys unload salt and water
111
Q

What is direct action and indirect action of kidneys in blood volume regulation?

A

Direct action:
- If blood volume is high then the rate of filtrate formation increases and there isn’t enough time to reclaim water so more urine is formed

Indirect action:
- If MAP decreases then kidney cells release renin
- reactions occur to produce angiotensin II (vasoconstrictor)
- angiotensin II stimulates the secretion of aldosterone which stimulates increased renal absorption of sodium
- Angiotensin II increases release of ADH which promotes water reabsorption

112
Q

What are the mechanisms of autoregulation with local blood flow?

A
  • Organs regulate blood flow by varying resistance of arterioles
  • Myogenic controls
  • Metabolic controls
113
Q

What are metabolic controls?

A
  • When blood flow is too low to meet a tissues metabolic needs it drops in oxygen and accumulates metabolic products
  • The metabolic products are typically hydrogen, potassium, adenosine and prostaglandins
  • These work together which release nitric oxide, a vasodilator, which dilates the arterioles.
  • Therefore sending blood to needy tissues
114
Q

What are myogenic controls?

A
  • Controls when there’s fluctuations in systemic blood pressure
  • vascular smooth muscle responds to passive stretched by increased tone which resists the stretch and causes vasoconstriction
  • vascular smooth muscle responds to reduced stretch in vasodilation
115
Q

What is longterm autoregulation?

A

When the number of blood vessels increase (angiogenesis) and existing vessels enlarge. This can only take place in a matter of a few weeks so they can develop.

116
Q

What are the forces that influence capillary exchange?

A
  1. Diffusional
  2. Osmotic
  3. Hydrostatic
117
Q

What are the capillary exchange mechanisms and what do they do?

A

1) Vesicle Transport
- Shuttles from blood to interstitial fluid through endocytosis, then exocytosis
- Transports large, lipid insoluble molecules
- Also transports antibodies from mother to fetus

2) Diffusion
- Mechanisms for dissolved solutes and gases (O2, CO2, glucose)
- Goes through water-filled pores, fenestrations, or through the bilayer

3) Bulk flow
- important for fluid movement
- carries nutrients and wastes in appropriate directions

118
Q

How do you calculate net filtration pressure?

A

Outward pressure-inward pressure
(HC+Oif) - (Hif+OC)

119
Q

What are the 2 main divisions of the lymphatic system?

A
  1. Lymphatic vessels
  2. Lymphatic organs/tissues
120
Q

What is leukocytosis?

A

The body’s response to a bacterial invasion where the number of leukocytes can double within hours

121
Q

What are the 2 main divisions of leukocytes?

A
  1. Granulocytes
  2. Agranulocytes
122
Q

What are the types of granulocytes and how do they differ?

A

Neutrophils:
- Most common leukocyte
- Contain granules that are hydrolytic enzymes and anti-biotic like proteins (defensins)= polymorphic leukocytes
- phagocytes: ingest and destroys bacteria

Eosinophils:
- 2-4% of leukocytes
- red-blue nucleus + course red granules
- 2 lobes
- controls/influences immune response to allergies and asthma

Basophils:
- Rarest leukocyte (0.5% of WBC’s)
- cytoplasmic granules contain histamine (vasodilator and attracts WBC’s )
- Dark purple nucleus often S-shaped or U-shaped

123
Q

What are the types of agranulocytes and how do they differ?

A

Lymphocytes:
- 2nd most common leukocyte
- Dark purple nucleus with light blue rim of cytoplasm
- found in lymphoid tissue i.e. lymph nodes, spleen, etc.
- 2 different types:
- T lymphocytes: acts against virus-infected cells (Terminates tumor cells)
- B lymphocytes: gives rise to plasma cells that produce antibodies

Monocytes:
- Largest leukocyte
- Gray blue cytoplasm
- U shaped nucleus
- Differentiate into macrophages
- phagocytic in chronic infections, viruses, and some bacteria

124
Q

What are the steps in leukopoiesis?

A
  1. All begin as hemocytoblast
  2. Splits into myeloid stem cell and lymphoid stem cell

Myeloid stem cell:
a. splits into myeloblast and monoblast
b. myeloblast splits into neutrophils, eosinophils, and basophils
c. monoblast becomes monocyte

Lymphoid stem cell:
a. become lymphoblast
b. becomes lymphocyte

125
Q
A

Anatomy (3 decks)

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