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A&P2 > Test 2: Blood Vessels & Lymphatic System COPY > Flashcards

Test 2: Blood Vessels & Lymphatic System COPY Flashcards

1
Q

Lymphatic System Functions

A
  1. Fluid Recovery
  2. Immunity
  3. Lipid Reabsorbtion
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2
Q

3 Vessel Layers

A
  1. Tunica Interna
  2. Tunica Media
  3. Tunica Externa
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3
Q

Tunica Interna: Structure & Function

A

Structure:

Lines inside of the vessel

Consists of simple squamous epithelium (endothilium)

Function

Lining is selectively permeable barrier

Secretes chemicals to influence vasodialation and vasoconstriction

Endothelium: Smooth lining prevents blood cells and platelets from congregating/ sticking to walls. Also, when tissue around vessel is inflammed, endothelium cells produce cell-adhesion molecules that induce leukocytes to adhere to surface. Congreare where their defense mechanisms are needed.

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4
Q

Tunica Media: Structure & Function

A

Structure:

Middle layer of blood vessel

Consists of smooth muscles, collagen, and elastic tissue

Smooth muscle & elastic tissue vary between vessels

Function:

Tunica Media strengthens vessels and prevents blood pressume from rupturing the vessel

Also regulates the diameter of the vessel

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5
Q

Tunica Externa: Structure & Function

A

Structure:

Outermost layer

Consists of loose connective tissue that merges with other blood vessels, nerves, or other ogans

Function:

Anchors vessels to adjacent tissues and provides passage for small nerves, lymphatic vessels, and smaller blood vessels

Vaso Vasorum: small vessels that supply blood to outer part of the larger vessels

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6
Q

Why are arteries called resistance vessels ?

A

Have strong, resilient tissue structure that can withstand heavy loads of blood and pressure

They are more muscular than veins and can retain their shape when empty

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7
Q

3 Types of Arteries

A
  1. Conducting (elastic or large) arteries:
  2. Distributing (muscular or medium) arteries
  3. Resistance (small) arteries
  4. Metaraterioles
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8
Q

Conducting (elastic or large) Arteries: Structure & Function

A

Arteries are sometimes called resistance vessels because of their strong, resilient tissue structure

Structure:

The largest

Has tons of elastic tissue, internal elastic lamina, at the border between interna and media

Function:

They expand when they recieve blood during ventricular systole and recoil during diastole. Expansion takes pressure of smaller downstream vessels. Recoil maintains pressure during relaxation and keeps blood moving.

Examples: aorta, common caratid, subclavian, pulmonary trunk, common iliac

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9
Q

Arteriosclerosis

A

Stiffening of arteries (usually with age)

Protective effect of arteries weaken and downstream vessels are subjected with greaer stress and risks of aneurysm and hemorrhage rise

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10
Q

Distributing (muscular or medium) Arteries: Structure & Function

A

Smaller branches of arteries that supply blood to specific organs

Structure:
Compared to exit ramps where as conducting arteries are interstate highways

These arteries have a ton of muscle (more than elastic tissue- about 3/4 of wall thickness)

Function:

Supply blood to specific organs

Example: femoral, brachial, renal, and splenic

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11
Q

Resistance (Small) Arteries: Structure & Function

A

–Resistance (small) arteries

Structure:

  • Arterioles: smallest arteries
  • Thicker tunica media in proportion to their lumen than large arteries and very little tunica externa

Function:

–Control amount of blood to various organs

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12
Q

Metaarteriales

A

Link arterioles directly to venules

Provide shortcuts through which blood could bypass capillaries

•Muscle cells form a precapillary sphincter around entrance to capillary

–Constriction of these sphincters reduces blood flow through their capillaries

–Diverts blood to other tissues

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13
Q

Types of Blood Vessels

A
  • Arteries carry blood away from heart
  • Veins carry blood back to heart
  • Capillaries connect smallest arteries to smallest veins
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14
Q

Aneurysm

A

•Aneurysm—weak point in artery or heart wall

Mechanism

–Forms a thin-walled, bulging sac that pulsates with each heartbeat and may rupture at any time

–Dissecting aneurysm: blood accumulates between tunics of artery and separates them, usually because of degeneration of the tunica media

–Most common sites: abdominal aorta, renal arteries, and arterial circle at base of brain

Causes

–Result from congenital weakness of blood vessels, trauma, or bacterial infections

Most common cause is atherosclerosis and hypertension

Symptoms

–Can cause pain by putting pressure on other structures

–Can rupture causing hemorrhage

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15
Q

Arterial Sense Organs

A

•Sensory structures in walls of major vessels that monitor blood pressure and chemistry

–Transmit information to brainstem to regulate heart rate, blood vessel diameter, and respiration

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16
Q

Arterial Sense Organs: Types

A
  • Carotide Bodies: Baroreceptors
  • Carotid Bodies: Chemoreceptors
  • Aortic Bodies: Chemoreceptors
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17
Q

Carotid sinuses: baroreceptors

A
  • In walls of internal carotid artery
  • Monitor blood pressure

–Transmit signals through glossopharyngeal nerve

–Allow for baroreflex

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18
Q

Carotid Bodies: Chemoreceptors

A
  • Oval bodies near branch of common carotids
  • Monitor blood chemistry
  • Transmit signals through glossopharyngeal nerve to brainstem respiratory centers

Adjust respiratory rate to stabilize pH, CO_2, and O_2

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19
Q

Aaortic Bodies: Chemoreceptors

A
  • One to three bodies in walls of aortic arch
  • Same structure and function as carotid bodies, but innervation is by vagus nerve
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20
Q

Capillaries

A

•exchange vessels: site where gasses, nutrients, wastes, and hormones pass between the blood and tissue fluid

–The “business end” of the cardiovascular system

–Composed of endothelium and basal lamina

–Absent or scarce in tendons, ligaments, epithelia, cornea, and lens of the eye

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21
Q

Capillary Types

A

–Three capillary types distinguished by ease with which substances pass through their walls (permeability):

  1. continuous capillaries
  2. fenestrated capillaries
  3. sinusoids
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22
Q

Continuous Capillaries

A

–Continuous capillaries:

Location: occur in most tissues

Structure:

  • Endothelial cells have tight junctions forming a continuous tube with intercellular clefts
  • Allow passage of solutes such as glucose
  • Pericytes wrap around the capillaries and contain the same contractile protein as muscle

Function:

–Contract and regulate blood flow

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23
Q

Fenestrated Capillaries

A

Location: kidneys, small intestine

Structure:

  • Organs that require rapid absorption or filtration
  • Endothelial cells riddled with holes called filtration pores (fenestrations)

–Spanned by very thin glycoprotein layer

Allow passage of only small molecules

Function:

  • Allow for rapid absorbtion/ filtation
  • Allow passage of only small molecules
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24
Q

Sinusoid Capillaries

A

–Sinusoids (discontinuous capillaries):

Location: liver, bone marrow, spleen

Structure:

•Irregular blood-filled spaces with large fenestrations

Function:

•Allow proteins (albumin), clotting factors, and new blood cells to enter the circulation

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25
Q

Capillary Beds: Structure

A

•Capillary beds are networks of 10-100 capillaries

–Usually supplied by a single arteriole or metarteriole

–At distal end, capillaries transition to venules or drain into a throroughfare channel (continuation of metarteriole)

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26
Q

Capillary Beds: Function

A

–At any given time, three-fourths of body’s capillaries are shut down

  • Most control of flow involves constriction of arterioles that are upstream from the capillaries
  • Within the capillary bed, precapillary shincters control flow

–When sphincters are relaxed, capillaries are well perfused with blood

–When sphincters contract, they constrict the entry to the capillary and blood bypasses the capillary

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27
Q

Veins: Struture & Function

A

Structure:

  • Greater capacity for blood containment than arteries
  • Thinner walls, flaccid, less muscular and elastic tissue

Function:

  • Collapse when empty, expand easily
  • Have steady blood flow
  • Merge to form larger veins
  • Subjected to relatively low blood pressure

–Averages 10 mm Hg with little fluctuation

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28
Q

Vein Types

A
  1. Post Capillary Venules- smallest veins
  2. Muscular Venules- up to 1 mm in diameter
  3. Medium Veins- up to 10 mm in diameter
  4. Venuous Sinuses
  5. Large Veins- > 10 mm in diameter
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29
Q

Post Capillary Veins; Structure/ Function

A

–Smallest Veins

Structure/ Function:

–Even more porous than capillaries so also exchange fluid with surrounding tissues

–Tunica interna with a few fibroblasts and no muscle fibers

–Most leukocytes emigrate from the bloodstream through venule walls

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30
Q

Muscular Veins: Structure/ Function

A

Structure/ Function:

-Up to 1 mm in diameter

–One or 2 layers of smooth muscle in tunica media

–Have a thin tunica externa

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31
Q

Medium Veins: Structure/ Function

A

Structure/ Function:

•up to 10 mm in diameter

–Thin tunica media and thick tunica externa

–Tunica interna forms venous valves

–Varicose veins result in part from the failure of these valves

–Skeletal muscle pump propels venous blood back toward the heart

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32
Q

Venous Sinuses: Structure/ Function

A

–Veins with especially thin walls, large lumens, and no smooth muscle

–Dural venous sinus and coronary sinus of the heart

–Not capable of vasomotor responses

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33
Q

Large Veins: Structure/ Function

A

–Some smooth muscle in all three tunics

–Thin tunica media with moderate amount of smooth muscle

–Tunica externa is thickest layer

•Contains longitudinal bundles of smooth muscle

–Venae cavae, pulmonary veins, internal jugular veins, and renal veins

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34
Q

Varicose Veins

A

•Blood pools in the lower legs of people who stand for long periods stretching the veins

–Cusps of the valves pull apart in enlarged superficial veins, further weakening vessels

–Blood backflows and further distends the vessels, their walls grow weak and develop into varicose veins

  • Hereditary weakness, obesity, and pregnancy also promote problems
  • Hemorrhoids are varicose veins of the anal canal
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35
Q

Circulatory Routes: Simplest

A

•Simplest and most common route for blood

– Heart > arteries > arterioles > capillaries > venules > veins

–Passes through only one network of capillaries from the time it leaves the heart until the time it returns

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36
Q

Capillary Exhange

A
  • The most important blood in the body is in the capillaries
  • Only through capillary walls are exchanges made between the blood and surrounding tissues
  • Capillary exchange—two-way movement of fluid across capillary walls

–Water, oxygen, glucose, amino acids, lipids, minerals, antibodies, hormones, wastes, carbon dioxide, ammonia

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37
Q

Capillary Exchange: Three Routes

A

•Chemicals pass through the capillary wall by three routes

  1. Through endothelial cell cytoplasm
  2. Intercellular clefts between endothelial cells
  3. Filtration pores (fenestrations) of the fenestrated capillaries
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38
Q

Capillary Exchange: Mechanisms Involved

A

–Diffusion, transcytosis, filtration, and reabsorption

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39
Q

Capillary Exchange Mechanism: Diffusion

A

•Diffusion is the most important form of capillary exchange

–Glucose and oxygen, being more concentrated in blood, diffuse out of the blood

–Carbon dioxide and other waste, being more concentrated in tissue fluid, diffuse into the blood

•Capillary diffusion can only occur if:

–The solute can permeate the plasma membranes of the endothelial cell, or

–Find passages large enough to pass through

•Filtration pores and intracellular clefts

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40
Q

Difussion: molecules & passivity

A

1.Lipid-soluble substances

–Steroid hormones, O_2, and CO_2 diffuse easily through plasma membranes

2.Water-soluble substances

–Glucose and electrolytes must pass through filtration pores and intercellular clefts

3.Large particles such as proteins held back

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41
Q

Capillary Exchange Mechanism: Transcytosis

A
  • endothelial cells pick up material on one side of their membrane by pinocytosis or receptor-mediated endocytosis, transport vesicles across cell, and discharge material on other side by exocytosis
  • Important for fatty acids, albumin, and some hormones (insulin)
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42
Q

Capillary Exchange Mechanism: Filtration & Reabsorbtion

A
  • Fluid filters out of the arterial end of the capillary and osmotically reenters at the venous end
  • Delivers materials to the cell and removes metabolic wastes
  • Opposing forces:

–Blood hydrostatic pressure drives fluid out of capillary

•High on arterial end of capillary, low on venous end

–Colloid osmotic pressure (COP) draws fluid into capillary

  • Results from plasma proteins (albumin)—more in blood
  • Oncotic pressure = net COP (blood COP − tissue COP)
  • Hydrostatic pressure

–Physical force exerted against a surface by a liquid

  • Blood pressure in vessels is hydrostatic pressure
  • Capillaries reabsorb about 85% of the fluid they filter
  • Other 15% is absorbed by the lymphatic system and returned to the blood
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43
Q

The Forces of Capillary Filtration and Reabsorbtion

A
  • Capillary filtration at arterial end
  • Capillary reabsorption at venous end
  • Variations

–Location

  • Glomeruli—devoted to filtration
  • Alveolar capillary—devoted to absorption

–Activity or trauma increases filtration

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44
Q

Variations in Capillary Filtration and Reabsorbtion

A
  1. Capillaries usually reabsorb most of the fluid they filter with certain exceptions

–Kidney capillaries in glomeruli do not reabsorb

–Alveolar capillaries in lung absorb completely to keep fluid out of air spaces

  1. Capillary activity varies from moment to moment

–Collapsed in resting tissue, reabsorption predominates since BP is low

–Metabolically active tissue has increase in capillary flow and BP

•Increase in muscular bulk by 25% due to accumulation of fluid

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45
Q

Edema

A

•accumulation of excess fluid in a tissue

–Occurs when fluid filters into a tissue faster than it is absorbed

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46
Q

Venous Return

A

•the flow of blood back to the heart; relies on: pressure gradient, gravity, skeletal muscle pump, thoracic pump, and cardiac suction

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47
Q

Venous Return: Mechanisms

A

1.Pressure gradient

  • Blood pressure is the most important force in venous return
  • 7 to 13 mm Hg venous pressure toward heart
  • Venules (12 to 18 mm Hg) to central venous pressure: point where the venae cavae enter the heart (~5 mm Hg)

2.Gravity drains blood from head and neck

3.Skeletal muscle pump in the limbs

•Contracting muscle squeezes blood out of the compressed part of the vein

4.Thoracic (respiratory) pump

•Inhalation—thoracic cavity expands and thoracic pressure decreases, abdominal pressure increases, forcing blood upward

–Central venous pressure fluctuates

  • 2 mm Hg—inhalation, 6 mm Hg—exhalation
  • Blood flows faster with inhalation

5.Cardiac suction of expanding atrial space

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48
Q

Circulatory Shock

A

•any state in which cardiac output is insufficient to meet the body’s metabolic needs

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49
Q

Brain Blood Flow

A

•Total blood flow to the brain fluctuates less than that of any other organ (700 mL/min.)

–Seconds of deprivation causes loss of consciousness

–Four to 5 minutes causes irreversible brain damage

–Though total flow is constant, blood is shifted to active brain areas from moment to moment

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50
Q

Brain Blood Flow 2

A

•Brain regulates its own blood flow to match changes in BP and chemistry

–Cerebral arteries dilate as systemic BP drops, constrict as BP rises

–Main chemical stimulus: pH

  • CO_2+ H_2 O →H_2 CO_3® H^++〖(HCO_3)〗^-
  • Hypercapnia—CO_2 levels increase in brain, pH decreases, triggers vasodilation
  • Hypocapnia—raises pH, stimulates vasoconstriction

–Occurs with hyperventilation, may lead to ischemia, dizziness, and sometimes syncope

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51
Q

Skeletal Muscle Blood Flow

A
  • Variable blood flow depending on state of exertion
  • At rest

–Arterioles constrict, most capillary beds shut down

–Total flow about 1 L/min.

•During exercise

–Arterioles dilate in response to muscle metabolites such as lactate, CO_2, and H^+

–Blood flow can increase 20-fold

  • Blood is diverted from digestive and urinary organs
  • Muscular contraction impedes flow

–Isometric contraction causes fatigue faster than intermittent isotonic contractions

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52
Q

Lung Blood Flow

A
  • Low pulmonary blood pressure
  • Flow slower, more time for gas exchange

–Oncotic pressure overrides blood (hydrostatic) pressure

  • Pulmonary capillaries absorb fluid (almost no filtration)
  • Prevents fluid accumulation in alveolar walls and lumens
  • Unique response to hypoxia

–Pulmonary arteries constrict in diseased area

–Redirects flow to better ventilated region

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53
Q

Lymphatic System Function: Fluid Recovery

A

–Fluid continually filters from the blood capillaries into the tissue spaces

  • Blood capillaries reabsorb 85%
  • 15% (2 to 4 L/day) of the water and about half of the plasma proteins enter the lymphatic system and then are returned to the blood
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54
Q

Lymphatic System Function: Immunity

A

–Excess filtered fluid picks up foreign cells and chemicals from the tissues

  • Passes through lymph nodes where immune cells stand guard against foreign matter
  • Activates a protective immune response
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55
Q

Lympathic System Function: Lipid Absorbtion

A

–Lacteals in small intestine absorb dietary lipids that are not absorbed by the blood capillaries

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56
Q

Lymphatic System: Parts

A
    1. Lymph: the recovered fluid
    1. Lymphatic vessels: Transport the lymph
    1. Lymphatic tissues: composed of aggregates of lymphocytes and macrophages that popoulate many organgs in the body
    1. Lymphatic organs: defense cells are especaially concentrated in these organs. They are seperated from surrounding organs by connective tissue capsules
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57
Q

Lymph: Structure/ Function

A

–Clear, colorless fluid, similar to plasma, but much less protein

–Originates as extracellular fluid drawn into lymphatic capillaries

–Chemical composition varies in different places (in intestines, after lymph nodes)

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58
Q

Lymphatic Vessels- Capillaries: Structure/ Function

A

-Also called terminal lymphatics

–Penetrate nearly every tissue of the body

•Absent from cartilage, cornea, bone, and bone marrow

–Capillary wall is endothelial cells overlapping each other like roof shingles

–Closed at one end

–Cells tethered to surrounding tissue by protein filaments

•Gaps between cells are large enough to allow bacteria and cells to enter lymphatic capillary

–Endothelium creates valve-like flaps that open when interstitial fluid pressure is high, and close when it is low

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59
Q

Lymphatic Vessels- Larger Ones: Structure/ Function

A

•Larger ones composed of three layers

–Tunica interna: endothelium and valves

–Tunica media: elastic fibers, smooth muscle

–Tunica externa: thin outer layer

  • Converge into larger and larger vessels
  • Collecting vessels course through many lymph nodes
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60
Q

Lymphatic Vessels: Six Lymphatic Trunks

A
  • Jugular
  • Subclavian
  • Bronchomediastinal
  • Intercostal
  • Intestinal (unpaired)
  • Lumbar
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61
Q

Lymphatic Vessels: Two Collecting Ducts

A
  1. Right Lymphatic Duct: receives lymph from right arm, right side of head and thorax; empties into right subclavian vein
  2. Thoracic Duct: –larger and longer, begins as a prominent sac in abdomen called the cisterna chyli; receives lymph from below diaphragm, left arm, left side of head, neck, and thorax; empties into left subclavian vein
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62
Q

Lymphatic Vessels: Subclavian Veins

A

collect from thoracic duct

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63
Q

Flow of lymph

A
  • Lymph flows under forces similar to those that govern venous return, except no pump (heart)
  • Lymph flows at low pressure and slower speed than venous blood
  • Moved along by rhythmic contractions of lymphatic vessels

–Stretching of vessels stimulates contraction

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64
Q

Flow of Lymph: Mechanisms

A
  • Flow aided by skeletal muscle pump (Exercise significantly increases lymphatic return)
  • Arterial pulsation rhythmically squeezes lymphatic vessels
  • Thoracic pump aids flow from abdominal to thoracic cavity
  • Lymph Mechanisms: Smooth muscle layer AND Valves prevent backward flow
  • Rapidly flowing blood in subclavian veins, draws lymph into it
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65
Q

Lymphatic Cell Types

A
  1. Natural killer (NK) cells
  2. T lymphocytes (T cells)
  3. B lymphocytes (B cells)
  4. Macrophages
  5. Dendritic Cells
  6. Reticular Cells
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66
Q

Lymphatic Cell: Natural Killer Cells

A

–Large lymphocytes that attack and destroy bacteria, transplanted tissue, host cells infected with viruses or that have turned cancerous

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67
Q

Lymphatic Cell: T Cells

A

Mature in thymus

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68
Q

Lymphatic Cells: B Cells

A

–Activation causes proliferation and differentiation into plasma cells that produce antibodies

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69
Q

Lymphatic Cells: Macrophages

A

–Large, avidly phagocytic cells of connective tissue

–Develop from monocytes

–Phagocytize tissue debris, dead neutrophils, bacteria, and other foreign matter

–Process foreign matter and display antigenic fragments to certain T cells alerting immune system to the presence of the enemy

–Antigen-presenting cells (APCs)

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70
Q

Lymphatic Cells: Dendritic Cells

A

–Branched, mobile APCs found in epidermis, mucous membranes, and lymphatic organs

–Alert immune system to pathogens that have breached the body surface

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71
Q

Lymphatic Cells: Reticular Cells

A

–Branched stationary cells that contribute to the stroma of a lymphatic organ

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72
Q

Lymphatic Tissue: Types

A
  1. Lymphatic (Lymphoid) Tissue
  2. Diffuse Lymphatic Tissue
  3. Lymphatic Nodules (follicles))
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73
Q

Lymphatic Tissue: Lymphoid

A

•aggregations of lymphocytes in the connective tissues of mucous membranes and various organs

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74
Q

Lymphatic Tissue: Diffuse Lymphatic Tissue

A

•simplest form

–Lymphocytes are scattered (not clustered)

–Prevalent in body passages open to the exterior

  • Respiratory, digestive, urinary, and reproductive tracts
  • Mucosa-associated lymphatic tissue (MALT)
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75
Q

Lymphatic Tissue: Lymphatic Nodules (follicle)

A

–Dense masses of lymphocytes and macrophages that congregate in response to pathogens

–Constant feature of the lymph nodes, tonsils, and appendix

–Aggregated lymphoid nodules: dense clusters in the ileum, the distal portion of the small intestine

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76
Q

Lymphatic Organs: Primary/ Secondary Types

A

•Lymphatic organs are anatomically well-defined

–Have connective tissue capsule that separates lymphatic tissue from neighboring tissues

Primary:

–Red bone marrow and thymus

–Site where T and B cells become immunocompetent: able to recognize and respond to antigens

Secondary:

–Lymph nodes, tonsils, and spleen

–Immunocompetent cells populate these tissues

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77
Q

Lymphatic Organ: Red Bone Marrow

A

•Red bone marrow is involved in hemopoiesis (blood formation) and immunity

–Soft, loosely organized, highly vascular material

–Separated from osseous tissue by endosteum of bone

–As blood cells mature, they push their way through the reticular and endothelial cells to enter the sinus and flow away in the bloodstream

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78
Q

Lymphatic Organs: Thymus

A

•Thymus—member of the endocrine, lymphatic, and immune systems

–Houses developing lymphocytes

–Secretes hormones regulating their activity

–Bilobed organ located in superior mediastinum between sternum and aortic arch

–Degeneration (involution) with age

•Fibrous capsule gives off trabeculae (septa) that divide the gland into several lobes

–Lobes have cortex and medulla populated by T lymphocytes

•Epithelial cells seal off cortex from medulla forming blood–thymus barrier

–Produce signaling molecules thymosin, thymopoietin, thymulin, interleukins, and interferon

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79
Q

Lymphatic Vessels: Lymph Nodes

A

•Lymph nodes—most numerous lymphatic organs

–About 450 in typical young adult

–Serve two functions

  • Cleanse the lymph
  • Act as a site of T and B cell activation
  • Elongated, bean-shaped structure with hilum
  • Enclosed with fibrous capsule with trabeculae that divide interior into compartments

–Stroma of reticular fibers and reticular cells

•Parenchyma divided into cortex and medulla

–Germinal centers where B cells multiply and differentiate into plasma cells

  • Several afferent lymphatic vessels lead into the node along its convex surface
  • Lymph leaves the node through one to three efferent lymphatic vessels that leave the hilum
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80
Q

***Lymph Node: 7 Types

A
  1. Cervical Lymph Node
  2. Axillary Lymph Node
  3. Thoracic Lymph Node
  4. Abdominal Lymph Node
  5. Intestinal/ Mesentric Lymph Node
  6. Inguinal Lymph Nodes
  7. Popiteal Lymph Nodes
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81
Q

Lymph Node: Cervical

A

Structure/ Location: Deep and superficial group in the neck

Function: Monitor lymph coming from head and neck

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82
Q

Lymph Node: Axillary

A

Structure/ Location: Concentrated in armpit

Function: Recieve lymph from upper limb and female breast

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83
Q

Lymph Node: Thoracic

A

Structure/ Location: –In thoracic cavity, especially embedded in mediastinum

Function:–Receive lymph from mediastinum, lungs, and airway

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84
Q

Lymph Node: Abdominal

A

Structure/ Location: –Occur in posterior abdominopelvic wall

Function: –Monitor lymph from the urinary and reproductive systems

85
Q

Lymph Node: Intestinal and Mesentric Lymph

A

Structure/ Location: –Found in the mesenteries, adjacent to the appendix and intestines

Function: –Monitor lymph from the digestive tract

86
Q

Lymph Node: Inguinal Lymph Nodes

A

Strucure/ Location/ Function: –In the groin and receive lymph from the entire lower limb

87
Q

Lymph Node: Popiteal Lymph Node

A

Structure/ Location: –Occur on the back of the knee

Function: –Receive lymph from the leg proper

88
Q

Lymphadenitis vs Lymphadenopathy

A

When a lymph node is under challenge by an antigen..

–Lymphadenitis: swollen, painful node responding to foreign antigen

–Lymphadenopathy: collective term for all lymph node diseases

89
Q

Metastais & Lymph Nodes

A

•Metastasis—cancerous cells break free from original tumor, travel to other sites in the body, and establish new tumors

–Metastasizing cells easily enter lymphatic vessels

–Tend to lodge in the first lymph node they encounter

–Multiply there and eventually destroy the node

•Swollen, firm, and usually painless

–Tend to spread to the next node downstream

–Treatment of breast cancer is lumpectomy, mastectomy, along with removal of nearby axillary nodes

90
Q

Tonsils: Structure/ Function

A

•patches of lymphatic tissue located at the entrance to the pharynx

–Guard against ingested or inhaled pathogens

–Covered with epithelium

–Have deep pits: tonsillar crypts lined with lymphatic nodules

–Tonsillitis and tonsillectomy

91
Q

*** Tonsil Types

A

–Palatine tonsils

  • Pair at posterior margin of oral cavity
  • Most often infected

–Lingual tonsils

•Pair at root of tongue

–Pharyngeal tonsil (adenoids)

•Single tonsil on wall of nasopharynx

92
Q

Spleen: Structure/ Function

A
  • Spleen—the body’s largest lymphatic organ
  • Parenchyma exhibits two types of tissue

–Red pulp: sinuses filled with erythrocytes

–White pulp: lymphocytes, macrophages surrounding small branches of splenic artery

•Spleen is highly vascular and vulnerable to trauma and infection

–Ruptured spleen requires splenectomy, but this leaves person susceptible to future infections, premature death

Function:

–Healthy red blood cells (RBCs) come and go

–For old, fragile RBCs, spleen is “erythrocyte graveyard”

–Blood cell production in fetus (and very anemic adults)

–White pulp monitors blood for foreign antigens and keeps an army of monocytes for release when needed

–Stabilizes blood volume through plasma transfers to lymphatic system

93
Q

***Pathogens

A

•agents capable of producing disease

–Include viruses, bacteria, and fungi

94
Q

***Three Lines of Defense against pathogens

A

–First line of defense: skin and mucous membranes

–Second line of defense: several innate defense mechanisms

•Leukocytes and macrophages, antimicrobial proteins, natural killer cells, inflammation, and fever

–Third line of defense: adaptive immunity

•Defeats a pathogen, and leaves the body with a “memory” of it so it can defeat it faster in the future

95
Q

***Innate Defenses

A

•guard equally against a broad range of pathogens

–They lack capacity to remember pathogens

–Local, nonspecific, lacks memory

96
Q

Innate Defenses: 3 Types

A

–Three kinds of innate defenses:

  • Protective proteins
  • Protective cells
  • Protective processes
97
Q

***Adaptive Immunity

A

•body must develop separate immunity to each pathogen

–Body adapts to a pathogen and wards it off more easily upon future exposure (memory)

98
Q

External Barriers: Types

A
  1. Skin
  2. Mucous Membranes
  3. Subepitheial Areolar Tissue
99
Q

External Barrier: Skin

A

–Makes it mechanically difficult for microorganisms to enter the body

–Toughness of keratin

–Too dry and nutrient-poor for microbial growth

–Acid mantle: thin film of lactic and fatty acids from sweat and sebum that inhibits bacterial growth

–Dermicidin, defensins, and cathelicidins: peptides in the skin that kill microbes

100
Q

External Barrier: Subepithelial Arelor Tissue

A

–Viscous barrier of hyaluronic acid

•Hyaluronidase—enzyme used by pathogens to make hyaluronic acid less viscous

101
Q

External Barrier: Mucous Membrane

A

–Digestive, respiratory, urinary, and reproductive tracts are open to the exterior and protected by mucous membranes

–Mucus physically traps microbes

–Lysozyme: enzyme destroys bacterial cell walls

102
Q

Leukocyte Types

A

–Neutrophils

–Eosinophils

–Basophils

–Monocytes

–Lymphocytes

103
Q

***Phagocytes

A

cells that engulf foreign matter

104
Q

Neutrophils

A

–Wander in connective tissue killing bacteria

–Can kill using phagocytosis and digestion

–Can kill by producing a cloud of bactericidal chemicals

  • Lysosomes degranulate—discharge enzymes into tissue fluid causing a respiratory burst
  • Creates a killing zone around neutrophil, destroying several bacteria
105
Q

Eosinophils

A

–Found especially in mucous membranes

–Guard against parasites, allergens (allergy-causing agents), and other pathogens

–Kill tapeworms and roundworms by producing superoxide, hydrogen peroxide, and toxic proteins

–Promote action of basophils and mast cells

–Phagocytize antigen–antibody complexes

–Limit action of histamine and other inflammatory chemicals

106
Q

Basophils

A

–Secrete chemicals that aid mobility and action of other leukocytes

–Leukotrienes: activate and attract neutrophils and eosinophils

–Histamine: a vasodilator, which increases blood flow

•Speeds delivery of leukocytes to the area

–Heparin: inhibits clot formation

  • Clots would impede leukocyte mobility
  • Mast cells also secrete these substances

–Type of connective tissue cell very similar to basophils

107
Q

Lymphocytes: Types & %

A

T- 80%

B-15%

NK cells- 5%

108
Q

Innate Immunity Lymphocyte Cell Type

A

NK Cells and T-Helper Cells

109
Q

Adaptive Immunity & Cell Type

A

T (and T Helper) and B Cells

110
Q

Monocytes

A

emigrate from the blood into connective tissues and transform into macrophages

111
Q

Macrophage System

A

•all the body’s avidly phagocytic cells, except leukocytes

–Wandering macrophages: actively seek pathogens

•Widely distributed in loose connective tissue

–Fixed macrophages: phagocytize only pathogens that come to them

  • Microglia—in central nervous system
  • Alveolar macrophages—in lungs
  • Hepatic macrophages—in liver
112
Q

Antimicrobiaal Proteins & Types

A
  • Proteins that inhibit microbial reproduction and provide short-term, Innate Immunity to pathogenic bacteria and viruses
  • Two families of antimicrobial proteins

–Interferons

–Complement system

113
Q

Interferons: Structure & Function

A

•Interferons—secreted by certain cells infected by viruses

–Of no benefit to the cell that secretes them

–Alert neighboring cells and protect them from becoming infected

–Bind to surface receptors on neighboring cells

•Activate second-messenger systems within

–The alerted cell synthesizes various proteins that defend it from infection

•Breaks down viral genes or prevents replication

–Also activates NK cells and macrophages

•Destroy infected cell before they can liberate a swarm of newly replicated viruses

–Activated NK cells destroy malignant cells

114
Q

***Complement System

A

•a group of 30 or more globular proteins that make powerful contributions to both innate immunity and adaptive immunity

–Synthesized mainly by liver

–Circulate in the blood in inactive form

–Activated by presence of a pathogen

115
Q

***Complement System: Pathogen Destruction Methods & Activation

A

–Activated complement brings about four methods of pathogen destruction

  • Inflammation
  • Immune clearance
  • Phagocytosis
  • Cytolysis

–Three routes of complement activation

  • Classical pathway
  • Alternative pathway
  • Lectin pathway
116
Q

***Complement System: Classical Pathway

A

–Requires antibody molecule

•Thus part of adaptive immunity

–Antibody binds to antigen on surface of the pathogenic organism

•Forms antigen–antibody (Ag–Ab) complex

–Changes the antibody’s shape

  • Exposing a pair of complement-binding sites
  • Binding of the first complement (C1) sets off a reaction cascade called complement fixation

–Results in a chain of complement proteins attaching to the antibody

117
Q

***Complement System: Alternative Pathway

A

–Nonspecific, does not require antibody

–C3 breaks down in the blood to C3a and C3b

  • C3b binds directly to targets such as human tumor cells, viruses, bacteria, and yeasts
  • Triggers cascade reaction with autocatalytic effect where more C3 is formed
118
Q

***Complement System: Lectin Pathway

A

–Lectins: plasma proteins that bind to carbohydrates

  • Bind to certain sugars of a microbial cell surface
  • Sets off another cascade of C3 production
119
Q

Complement System Mechanisms of Proteins: Inflammation

A
  • C3a stimulates mast cells and basophils to secrete histamine and other inflammatory chemicals
  • Activates and attracts neutrophils and macrophages
  • Speeds pathogen destruction in inflammation
120
Q

Complement System Mechanism: Immune Clearance

A
  • C3b binds with antigen–antibody (Ag-Ab) complexes to red blood cells
  • These RBCs circulate through liver and spleen
  • Macrophages of those organs strip off and destroy the Ag–Ab complexes leaving RBCs unharmed
  • Principal means of clearing foreign antigens from the bloodstream
121
Q

Complement System Mechanism: Phagocytosis

A
  • Neutrophils and macrophages cannot phagocytize “naked” bacteria, viruses, or other pathogens
  • C3b assists them by opsonization

–Coats microbial cells and serves as binding sites for phagocyte attachment

–Makes the foreign cell more appetizing

122
Q

Complement System Mechanism: Cytolysis

A
  • C3b splits complement protein C5 into C5a and C5b
  • C5b binds to enemy cell
  • Attracts more complement proteins—membrane attack complex forms

–Forms a hole in the target cell

–Electrolytes leak out, water flows in rapidly, cell ruptures

123
Q

Natural Killer Cells: Structure/ Function

A
  • Natural killer (NK) cells continually patrol body looking for pathogens and diseased host cells
  • NK cells attack and destroy bacteria, transplanted cells, cells infected with viruses, and cancer cells
  • Recognize enemy cell and bind to it
  • Release proteins called perforins

–Polymerize a ring and create a hole in its plasma membrane

•Secrete a group of protein-degrading enzymes—granzymes

–Enter through pore and degrade cellular enzymes and induce apoptosis (programmed cell death)

124
Q

Fever

A

•an abnormal elevation of body temperature

–Synonym: pyrexia; febrile—pertaining to fever

–Results from trauma, infections, drug reactions, brain tumors, and other causes

125
Q

Fever Mechanisms

A

•Fever is an adaptive defense mechanism that, in moderation, does more good than harm

–Promotes interferon activity

–Elevates metabolic rate and accelerates tissue repair

–Inhibits reproduction of bacteria and viruses

126
Q

Antipyretics

A

•fever-reducing medications

–Include aspirin and ibuprofen that inhibit Prostaglandin E_2 synthesis

127
Q

Exogenous pyrogens & Fever

A

•Fever usually triggered by exogenous pyrogens—fever-producing agents

–Glycolipids on bacterial and viral surfaces

128
Q

Endogenous pyrogens and Fever

A

•Endogenous pyrogens include polypeptides secreted by neutrophils and macrophages

–These raise hypothalamic set point for body temperature

–Neurons in the anterior hypothalamus secrete prostaglandin E_2 which also raises set point

129
Q

Stages of Fever

A
  1. Onset
  2. stadium,
  3. defervescence
130
Q

Inflammation

A

•local defensive response to tissue injury, including trauma and infection

131
Q

Inflammation: General Purposes

A

–Limits spread of pathogens, then destroys them

–Removes debris from damaged tissue

–Initiates tissue repair

132
Q

Signs of Inflammation

A

–Redness, swelling, heat, pain

133
Q

-itis meaning

A

•Suffix -itis denotes inflammation of specific organs: arthritis, pancreatitis, dermatitis

134
Q

Cytokines: Structure/ Function

A

•small proteins that regulate inflammation and immunity

–Secreted mainly by leukocytes

–Alter physiology of receiving cell

–Act at short range, neighboring cells (paracrines) or the same cell that secretes them (autocrines)

–Include interferon, interleukins, tumor necrosis factor, chemotactic factors, and others

135
Q

Inflammation: 3 Major Processes

A

–Mobilization of body defenses

–Containment and destruction of pathogens

–Tissue cleanup and repair

136
Q

Inflammation: Mobilization of Defenses

A
  • Most immediate requirement after tissue injury is to get defensive leukocytes to the site quickly
  • Achieved by local hyperemia—increasing blood flow

–Local vasodilation due to vasoactive chemicals

  • Histamine, leukotrienes, and other cytokines
  • Secreted by basophils, mast cells, cells damaged by trauma, toxins, or organisms triggering inflammation
  • Hyperemia also washes toxins and metabolic waste from the site more rapidly
  • Vasoactive chemicals also stimulate endothelial cells to contract, thereby widening gaps between them

–This increases capillary permeability

–Fluid, leukocytes, and plasma proteins leave bloodstream

  • Including complement, antibodies, and clotting proteins
  • Selectins: cell-adhesion molecules made by endothelial cells that aid in the recruitment of leukocytes

–Make membranes sticky, so leukocytes adhere to vessel wall (margination)

–Diapedesis or emigration: leukocytes crawl through gaps in the endothelial cells and enter tissue fluid

•Extravasated: cells and chemicals that have left the bloodstream

137
Q

Inflammation: Mobilization of Defenses SIGNS

A

•Basis for the four cardinal signs of inflammation

–Heat: results from hyperemia

–Redness: due to hyperemia, and extravasated RBCs in the tissue

–Swelling (edema): due to increased fluid filtration from the capillaries

–Pain: from direct injury to the nerves, pressure on the nerves from edema, stimulation of pain receptors by prostaglandins, bacterial toxins, and bradykinin

138
Q

Mobilization of Defenses: Neutrophil Behaviors

A

–Margination

•Selectins cause leukocytes to adhere to blood vessel walls

–Diapedesis (emigration)

•Leukocytes squeeze between endothelial cells into tissue space

139
Q

Inflammation: Containment and Destruction of Pathogens

A

•Priority of inflammation is to prevent pathogens from spreading throughout body

–Fibrinogen that filters into tissue fluid clots

•Forms a sticky mesh that walls off microbes

–Heparin prevents clotting at site of injury

  • Pathogens are in a fluid pocket surrounded by clot
  • Attacked by antibodies, phagocytes, and other defenses
  • Neutrophils, the chief enemy of bacteria, accumulate at the injury site within an hour

–After leaving the bloodstream, they exhibit chemotaxis

140
Q

Chemotaxis

A

•Chemotaxis—attraction to chemicals such as bradykinin and leukotrienes that guide them to the injury site

”‘-Taxis”- movement

141
Q

Containment and Destruction of Pathogens: Neutrophils

A

•Neutrophils quickly respond to and kill bacteria

–Phagocytosis

–Respiratory burst

–Secrete cytokines for recruitment of macrophages and additional neutrophils

–Macrophages and T cells secrete colony-stimulating factor to stimulate leukopoiesis (production of more leukocytes) thereby raising WBC counts in blood

  • Neutrophilia—5,000 cells/μL to 25,000 cells/μL in bacterial infection
  • Eosinophilia—elevated eosinophil count in allergy or parasitic infection
142
Q

Tissue Cleanup and Repair: Monocytes

A

•Monocytes—the primary agents of tissue cleanup and repair

–Arrive in 8 to 12 hours and become macrophages

–Engulf and destroy bacteria, damaged host cells, and dead and dying neutrophils

143
Q

Tissue Cleanup & Repair: Edema

A

•Edema contributes to tissue cleanup

–Swelling compresses veins and reduces venous drainage

–Forces open valves of lymphatic capillaries, promoting lymphatic drainage

–Lymphatics collect and remove bacteria, dead cells, proteins, and tissue debris better than blood capillaries

144
Q

Tissue Cleanup & Repair: Pus

A

•Pus—yellow accumulation of dead neutrophils, bacteria, cellular debris, and tissue fluid

–Abscess: accumulation of pus in a tissue cavity

145
Q

Tissue Cleanup & Repair: Platelets

A

•Platelet-derived growth factor is secreted by blood platelets and endothelial cells in injured area

–Stimulates fibroblasts to multiply

–Synthesizes collagen

146
Q

Tissue Cleanup & Repair: Hyperemia

A

•Hyperemia delivers oxygen, amino acids, and other necessities for protein synthesis

147
Q

Tissue Cleanup & Repair: heat, fibrin, pain

A
  • Increased heat increases metabolic rate, speeds mitosis, and tissue repair
  • Fibrin clot forms a scaffold for tissue reconstruction
  • Pain makes us limit the use of a body part so it has a chance to rest and heal
148
Q

Immune System

A

•a large population of widely distributed cells that recognize foreign substances and act to neutralize or destroy them

149
Q

•Three characteristics distinguish immunity from innate immunity

A

–Systemic effect: throughout the body

–Specificity: immunity directed against a particular pathogen

–Memory: when reexposed to the same pathogen, the body reacts so quickly that there is no noticeable illness

150
Q

Two Types of Immunity

A
  1. Cellular
  2. Humoral
151
Q

Cellular (Cell-Mediated) Immunity

A
  • Lymphocytes directly attack and destroy foreign cells or diseased host cells
  • Rids the body of pathogens that reside inside human cells, where they are inaccessible to antibodies
  • Kills cells that harbor them
152
Q

Humoral (anti-body mediated) Immunity

A
  • Mediated by antibodies that do not directly destroy a pathogen but tag it for destruction
  • Many antibodies are dissolved in body fluids (“humors”)
  • Can only work against the extracellular stages of infections by microorganisms
153
Q

Natural vs Artificial Active Immunity

A

•Natural active immunity

–Production of one’s own antibodies or T cells as a result of infection or natural exposure to antigen

•Artificial active immunity

–Production of one’s own antibodies or T cells as a result of vaccination against disease

–Vaccine: consists of dead or attenuated (weakened) pathogens that stimulate the immune response without causing the disease

–Booster shots: periodic immunizations to stimulate immune memory to maintain a high level of protection

154
Q

Natutral vs Artifical Passive Immunity

A

•Natural passive immunity

–Temporary immunity that results from antibodies produced by another person

  • Fetus acquires antibodies from mother through placenta, milk
  • Artificial passive immunity

–Temporary immunity that results from the injection of immune serum (antibodies) from another person or animal

•Treatment for snakebite, botulism, rabies, tetanus, and other diseases

155
Q

Antigens

A

•any molecule that triggers an immune response

–Large molecular weights of over 10,000 amu

–Complex molecules with structures unique to the individual

–Proteins, polysaccharides, glycoproteins, glycolipids

–Characteristics enable body to distinguish “self” molecules from foreign ones

156
Q

Epitopes

A

-Also known as Antigenic Determinants

certain regions of an antigen molecule that stimulate immune responses

157
Q

Haptens

A

•too small to be antigenic in themselves

–Can trigger an immune response by combining with a host macromolecule and creating a complex that the body recognizes as foreign

–Subsequently, haptens alone may trigger response

–Cosmetics, detergents, industrial chemicals, poison ivy, and animal dander

–Penicillin binds to host proteins in allergic individuals

158
Q

Antibody is also called a _______

A

Immunoglobulin (Ig)

159
Q

Where are antibodies found ?

A

found in blood plasma, tissue fluids, body secretions, and some leukocyte membranes

160
Q

Name these structures & function

A

A= Disulfide Bridges

B=Antigen Binding Sites: Antigen-binding site: formed from the V regions of the heavy and light chain on each arm

•Attaches to the epitope of an antigen molecule

C=Light Chain= –Two light chains about half as long

D=Hinge Region

E=Heavy Chain

F=Constant Regions= has the same amino acid sequence within one person and determines mechanism of antibody action

G= Variable Regions= Variable (V) region in all four chains

•Gives the antibody its uniqueness

161
Q

Antibody Classes: types

A

Named for their structure of the C region

  1. IGA
  2. IgD
  3. IgE
  4. IgG
  5. IgM
162
Q

IgA

A

–monomer in plasma; dimer in mucus, saliva, tears, milk, and intestinal secretions

  • Prevents pathogen adherence to epithelia and penetrating underlying tissues
  • Provides passive immunity to newborns
163
Q

IgD

A

–monomer; B cell transmembrane antigen receptor

•Thought to function in B cell activation by antigens

164
Q

IgE

A

–: monomer; transmembrane protein on basophils and mast cells

•Stimulates release of histamine and other chemical mediators of inflammation and allergy

–Attracts eosinophils to parasitic infections

–Produces immediate hypersensitivity reactions

165
Q

IgG

A

–monomer; constitutes 80% of circulating antibodies

•Crosses placenta to fetus, secreted in secondary immune response, complement fixation

166
Q

IGM

A

–pentamer in plasma and lymph

•Secreted in primary immune response, agglutination, complement fixation

167
Q

Antibody Diversity: How many different antibodies, & How are variety of proteins accomplished?

A

•Human immune system capable of as many as 1 trillion different antibodies BUT there are as few as 20,000 genes in the human genome, so the variety of proteins must be accomplished by:

  1. Somatic recombination: DNA segments shuffled and form new combinations of base sequences to produce antibody genes
  2. Somatic hypermutation: B cells in lymph nodules rapidly mutate creating new sequences
168
Q

Lymphocyte Types

A

–Natural killer (NK) cells: immune surveillance

–T lymphocytes (T cells)

–B lymphocytes (B cells)

169
Q

Major cells in the immune system?

A

•Major cells of the immune system

–Lymphocytes

–Macrophages

–Dendritic cells

170
Q

Where are the major cells of the immune system concentrated ?

A

•Especially concentrated in strategic places such as lymphatic organs, skin, and mucous membranes

171
Q

Lymphocyte T Cells: Life Stages

A

–Born in bone barrow

–Educated in thymus

–Deployed to carry out immune function

172
Q

T Cells within the Thymus

A

–Cortical epithelial cells release chemicals that stimulate maturing T cells to develop surface antigen receptors

–With receptors, the T cells are now immunocompetent: capable of recognizing antigens presented to them

–Positive selection

–Medullary epithelial cells test T cells by presenting self-antigens to them; T cells can fail by:

  • Being reacting to the epithelial cell
  • Reacting to the self-antigen

–Would attack one’s own tissues

–T cells that fail are eliminated by negative selection

  • Clonal deletion—self-reactive T cells die and macrophages phagocytize them
  • Anergy—self-reactive T cells remain alive but unresponsive
173
Q

T cells that fail are eliminated by ____

A

–eliminated by negative selection

  • Clonal deletion—self-reactive T cells die and macrophages phagocytize them
  • Anergy—self-reactive T cells remain alive but unresponsive
174
Q

T Cells & Negative Selection

A

•Negative selection leaves the body in a state of self-tolerance—the surviving T cells respond only to suspicious antigens (ignoring the body’s own proteins)

–Only 2% of T cells pass the test

175
Q

Naive Lymphocyte Pool

A

•immunocompetent T cells that have not yet encountered foreign antigens

176
Q

T Cells & Deployment

A

–Naive T cells leave thymus and colonize lymphatic tissues and organs everywhere in the body

177
Q

Lymphocyte B Cells Development

A

•B cells develop in bone

–Some fetal stem cells remain in bone marrow and differentiate into B cells

  • B cells that react to self-antigens undergo either anergy or clonal deletion, same as T cell selection
  • Self-tolerant B cells synthesize antigen surface receptors, divide rapidly, produce immunocompetent clones
  • Leave bone marrow and colonize same lymphatic tissues and organs as T cells
178
Q

T Cells & APCs

A

•T cells cannot recognize antigens on their own. Antigen-presenting cells (APCs) are required

–Dendritic cells, macrophages, reticular cells, and B cells function as APCs

•Function of APCs depends on major histocompatibility (MHC) complex proteins

–Act as cell “identification tags” that label every cell of your body as belonging to you

–Structurally unique for each individual, except for identical twins

179
Q

APCs stands for ____

A

Antigen Presenting Cells

180
Q

Antigen Processing

A

–APC encounters antigen

–Internalizes it by endocytosis

–Digests it into molecular fragments

–Displays relevant fragments (epitopes) in the grooves of the MHC protein

181
Q

Antigen Presenting

A

–Wandering T cells inspect APCs for displayed antigens

–If APC only displays a self-antigen, the T cell disregards it

–If APC displays a nonself-antigen, the T cell initiates an immune attack

–APCs alert the immune system to presence of foreign antigen

–Key to successful defense is to quickly mobilize immune cells against the antigen

–With so many cell types involved in immunity, they require chemical messengers to coordinate their activities—interleukins

182
Q

Cellular (cell-mediated) immunity

A

–A form of specific defense in which the T lymphocytes directly attack and destroy diseased or foreign cells

–The immune system remembers the antigens and prevents them from causing disease in the future

–Uses 4 classes of T-cells: cytotoxic, helper, regulatory, and memory

183
Q

Cellular (cell-mediated) immunity: T Cell Classes

A
  1. cytotoxic
  2. helper
  3. regulatory
  4. memory
184
Q

Cytotoxic Cells

A

•killer T cells (T8, CD8, or CD8+)

–“Effectors” of cellular immunity; carry out attack on enemy cells

185
Q

Helper T (Th) cells

A

–Help promote T_C cell and B cell action and innate immunity

186
Q

Regulatory T Cells (Tr)

A

–Inhibit multiplication and cytokine secretion by other T cells; limit immune response

–Like T_H cells, T_R cells can be called T4, CD4, CD4+

187
Q

Memory T Cells (Tm)

A

–Descend from the cytotoxic T cells

–Responsible for memory in cellular immunity

188
Q

Cellular & Humoral Immunity: 3 Stages

A

–Recognition

–Attack

–Memory

or the 3 Rs

–Recognize

–React

–Remember

189
Q

Cellular Immunity: Recognition

A
  • Aspects of recognition in cellular immunity: antigen presentation and T cell activation
  • Antigen presentation

–APC encounters and processes an antigen

–Migrates to nearest lymph node

–Displays it to the T cells

–When T cells encounter a displayed antigen on the MHC protein, they initiate the immune response

•T cells respond to two classes of MHC proteins: MHC-1 and MHC-II

–MHC-I proteins

  • Constantly produced by nucleated cells, transported to, and inserted on plasma membrane
  • If they are normal self-antigens, they do not elicit a T cell response
  • If they are viral proteins or abnormal cancer antigens, they do elicit a T cell response

–Infected or malignant cells are then destroyed before they can do further harm to the body

–MHC-II proteins (human leukocyte antigens, HLAs)

  • Occur only on APCs and display only foreign antigens
  • T_C cells respond only to MHC-I proteins

T_H cells respond only to MHC-II proteins

190
Q

Cellular Immunity: T Cell Activation

A

–Begins when T_C or T_H cell binds to a MHC protein displaying an epitope that the T cell is programmed to recognize

–T cell must then bind to another APC protein related to the interleukins

–T cell must check twice to see if it is really bound to a foreign antigen—costimulation

  • Helps ensure the immune system does not launch an attack in the absence of an enemy
  • Would turn against one’s own body and injure our tissues
  • Successful costimulation will trigger clonal selection

–Activated T cell undergoes repeated mitosis

–Gives rise to a clone of identical T cells programmed against the same epitope

–Some cells of the clone become effector cells and carry out the attack

Other cells become memory T cells

191
Q

Cellular Immunity: Attack

A
  • Helper and cytotoxic T cells play different roles in the attack phase of cellular immunity
  • Helper T cells play central role in coordinating both cellular and humoral immunity
  • When helper T cell recognizes the Ag-MHC Protein complex:

–Secretes interleukins that exert three effects

  • Attract neutrophils and NK cells
  • Attract macrophages, stimulate their phagocytic activity, and inhibit them from leaving the area

Stimulate T and B cell mitosis and maturation

192
Q

Only T Cell that directly attacks other cells

A
  • Cytotoxic T (T_C) cells are the only T cells that directly attack other cells
  • When T_C cell recognizes a complex of antigen and MHC-I protein on a diseased or foreign cell, it “docks” on that cell
193
Q

Tc Cells Chemicals for cellular attack

A

–Perforin and granzymes—kill cells in the same manner as NK cells

–Interferons—inhibit viral replication

•Recruit and activate macrophages

–Tumor necrosis factor (TNF)—aids in macrophage activation and kills cancer cells

•After releasing chemicals, T_C cell goes off in search

of another enemy cell while chemical do their work

194
Q

Cellular Immunity: Memory

A
  • Immune memory follows primary response in cellular immunity
  • Following clonal selection, some T_C and T_H cells become memory cells

–Long-lived

–More numerous than naive T cells

–Fewer steps to be activated, so they respond more rapidly

195
Q

Cellular Immunity: Memory- T Cell Recall Response

A

–Upon re-exposure to same pathogen later in life, memory cells launch a quick attack so that no noticeable illness occurs

–The person is immune to the disease

196
Q

Humoral Identity

A
  • Humoral immunity is a more indirect method of defense than cellular immunity
  • B lymphocytes of humoral immunity produce antibodies that bind to antigens and tag them for destruction by other means

–Cellular immunity attacks the enemy cells directly

197
Q

Humoral Identity 3 Stages

A

•Works in three stages like cellular immunity

–Recognition

–Attack

–Memory

198
Q

Humoral Identity: Recognition

A

–Immunocompetent B cell has thousands of surface receptors for one antigen

–Activation begins when an antigen binds to several of these receptors, links them together and is taken into the cell by receptor-mediated endocytosis

•Small molecules are not antigenic because they cannot link multiple receptors together

–B cell processes (digests) the antigen

•Links some of the epitopes to its MHC-II proteins

–Displays these on the cell surface

–Usually B cell response goes no further unless a helper T cell binds to this Ag–MHC protein complex

•Bound T_H cell secretes interleukins that activate B cell

–Triggers clonal selection

  • B cell mitosis gives rise to a battalion of identical B cells programmed against the same antigen
  • Most differentiate into plasma cells

–Larger than B cells and contain an abundance of rough ER

•Plasma cells secrete antibodies at a rate of 2,000 molecules per second during their life span of 4 to 5 days

–First exposure to antigen triggers production of IgM antibodies, later exposures to the same antigen, IgG

–Antibodies travel through body in blood, other body fluids

199
Q

Humoral Identity: Attack

A

–Antibodies bind to antigen, render it harmless, “tag it” for destruction

200
Q

Humoral Identity: Memory

A

–Some B cells differentiate into memory cells

201
Q

Humoral Attack: Mechanisms

A

neutralization, complement fixation, agglutination, and precipitation

202
Q

Humoral Attack: Neutrolization

A

–Antibodies mask pathogenic region of antigen

203
Q

Humoral Attack: Complement Fixation

A

–IgM or IgG bind to antigen, change shape and initiate complement binding which leads to inflammation, phagocytosis, immune clearance, or cytolysis

–Primary defense against foreign cells, bacteria, and mismatched RBCs

204
Q

Humoral Attack: Aggulination

A

–Antibody has 2 to 10 binding sites; binds to multiple enemy cells, immobilizing them from spreading

–Enhances phagocytosis by creating “bigger bites”

205
Q

Humoral Attack: Preciptation

A

–Antibody binds antigen molecules (not cells); creates antigen–antibody complex that precipitates, allowing them to be removed by immune clearance or phagocytized by eosinophils

206
Q

Humoral Memory

A
  1. Primary: immune reaction brought about by the first exposure to an antigen
  2. Secondary: if reexposed to the same antigen
207
Q

Humoral Memory: Primary Response

A

•Primary response leaves one with an immune memory of the antigen

–During clonal selection, some of the cells becomes memory B cells

–Found mainly in germinal centers of the lymph nodes

–Mount a very quick secondary response

208
Q

Humoral Memory: Secondary Response

A

•—if reexposed to the same antigen

–Plasma cells form within hours

–IgG titer rises sharply and peaks in a few days

–Response is so rapid that the antigen has little chance to exert a noticeable effect on the body

–No illness results

–Low levels of IgM also secreted (then quickly decline)

–IgG remain elevated for weeks to years

  • Conferring long-lasting protection
  • Memory does not last as long in humoral immunity as in cellular immunity
209
Q

Explain this graph

A

A&P2 (13 decks)

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