Exam 3 Flashcards
1
Q
2 major components of blood
A
1) Formed elements: cells and parts of cells
2) Matrix (binding element): Plasma
2
Q
During clotting, what becomes visible?
A
No fibers present normally, dissolved strands of fibrin become visible during clotting
3
Q
Function of blood: Transporter
A
Of important substance within body
Substances delivered to organ system
Oxygen - from lungs to tissue
Metabolic waste - urea delivered to kidneys to be excreted
Various hormones - from thyroid or adrenals to target tissue
4
Q
Function of blood: Body temperature
A
Blood acts as large sink - absorbs and distributes heat
Working in combination with the heart and blood vessels system
5
Q
Function of blood: Body pH
A
Blood contains proteins and solutes which prevent abrupt changes in acidity
Blood acts as buffer (anything that lessens changes in pH)
6
Q
Function of blood: volume
A
Blood proteins can osmotically “pull” fluid from tissue space into circulation
7
Q
Function of blood: protection
A
Protein from environmental factors which can disrupt homeostasis
8
Q
Function of blood: hemorrhage
A
Hemorrhage: formed elements (platelets) initiate blood clot formation
Prevents blood loss in damaged vessels
9
Q
Function of blood: infection
A
Blood plasma contains antibodies and immune cells (leukocytes)
Work together to defend against foreign substances
10
Q
mixed blood is considered a…
A
suspension: large solute particles (formed elements) which fall to the bottom of plasma when not mixed
To rapidly separate the formed elements from plasma - centrifuge blood sample
11
Q
Normal levels of components of blood
A
55 % plasma - fluid portion/less dense
45% red blood cells - hematocrit/most dense
<1% WBCs and platelets - buffy coat
12
Q
Total blood volume
A
5-6 L in males
4-5 L in females
Account for 8 % of total body weight
13
Q
What is in the highest quantity in the blood?
A
Electrolytes are the most abundant dissolved component in the blood, followed by proteins
14
Q
Mixture type of plasma
A
colloid - scatters light but dissolved components stay dissolved
92 % water
15
Q
Electrolytes in the blood
A
other electrolytes such as chloride, calcium, magnesium, phosphate, and bicarbonate
Help to maintain plasma pH - slightly alkaline (7.35-7.45)
16
Q
Other plasma components: proteins
A
carrier molecules made by the liver to transport substances through blood,
such as glucose, fatty acids, etc.
osmotically maintain fluid balance
17
Q
Most abundant plasma protein
A
Albumin (60%)
large: not permeable through capillary wall
Causes water to stay in blood vessel via osmotic pressure
counter-balance blood pressure pushing water out of vessel
18
Q
What happens when plasma protein is too low?
A
Low plasma protein results in edema
Fluid accumulation in interstitial space, joint cavities, lungs
Healthy liver will make more if needed
19
Q
Other plasma proteins are…
A
Globulins (36%) and Fibrinogen (4%)
20
Q
Globulins
A
maintain fluid balance
- transport lipid soluble nutrients (Vitamins D, E, K)
- contribute to immune response (antibodies)
21
Q
Fibrinogen
A
Largest protein in blood
contributes to blood coagulation (clotting) - strands of fibrin
22
Q
major plasma components: Non-protein Nitrogenous Substances (NPNs)
A
Molecules that contain nitrogen, but are not proteins
Urea: product of protein catabolism; about 50 % of NPNs
Amino acids: product of protein digestion
creatinine: product of creatine metabolism in muscle
23
Q
Creatinine in blood
A
Kidney should almost completely remove from blood to be excreted in urine
Creatine supplement causes strain on kidneys
24
Q
What contributes to BUN level?
A
NPNs, particularly urea contribute to blood urea nitrogen (BUN) level
25
BUN levels and what they indicate
Indicator of kidney health: Normal 7-21 mg/dl
High BUN: kidney is not excreting urea in normal quantity causing urea to accumulate in blood
Low BUN: impaired liver function - not breaking down proteins
26
Other factors that can effect BUN
burns, dehydration, malnutrition
other tests usually needed to investigate kidney/liver function
27
major plasma components: gases and nutrients
Blood gases: oxygen, carbon dioxide - small amount dissolved in plasma (most is bound to hemoglobin in RBCs)
Plasma nutrients: amino acids, sugars (glucose), nucleotides, lipids: fats (triglycerides), phospholipids, cholesterol
28
Why are platelets and erythrocytes not considered true cells?
Platelets: cell fragments
Erythrocytes have no nuclei or organelles - without mitochondria, they can only produce ATP via glycolysis
Most blood cells do not divide - blood stem cells in red bone marrow divide to replace them
29
Erythrocytes structure
Small doughnut shaped cells (bi-concave disk) - most abundant of all formed elements in blood
Very simple structure but highly functional
30
Erythrocytes function in relation to Hb
carry oxygen bound to hemoglobin
Hb: RBC protein that binds to oxygen - greatly increases amount of O2 that can be carried by non-Hb containing cells
Discounting water, RBC is 97% Hb
31
Why are RBCs efficient?
they do not have organelles - only use anaerobic metabolism for ATP - glycolysis, can never consume the O2 it is carrying
Doughnut shape = 30 % more surface area for absorbing dissolved O2 from plasma - cytoplasm within RBC is never far from cell surface
Good for O2 delivery to tissues
32
What gives RBCs its doughnut shape?
RBCs contain a structural protein called spectrin - attached to the inner surface of plasma membrane
Forms of network of structural proteins just under cell surface which maintains its irregular shape
33
Spectrin
highly flexible
Allows RBCs to bend and contort to squeeze through capillaries smaller than diameter of cell
34
what do changes in RBC count indicate?
changes in blood's oxygen-carrying capacity
35
Anemia
O2 carrying capacity of blood is reduced, due to low RBCs or hemoglobin
- Bone marrow deficiency damaged by radiation
- iron/B12 deficiency
36
Sickle cell disease
Oddly shaped RBCs occlude small vessels
rupture very easily - releases iron which clogs kidneys
37
Carbon Monoxide Poisoning
CO binds strongly to hemoglobin
Less room for O2 to bind
Less willing to release O2 to tissues
RBCs and Hb levels remain normal - O2 content of blood is reduced
38
Polycythemia (and causes)
Too many RBCs which causes the blood to be thick and viscous
Increased strain on the heart
Causes: dehydration, blood doping (artificial erythropoietin)
39
Erythropoiesis (the process)
Occurs in red bone marrow - axial skeleton in adults
Begin as blood stem cells = hematopoietic stem cell
- aka hemocytoblast
- does have a nucleus
Matures over a 15 day period
- commit to becoming RBC
- produce ribosomes and Hb
- eject nucleus
40
Stimulus for erythropoiesis
Low blood O2 causes kidney and liver to release EPO (erythropoietin), which stimulates RBC production
Negative feedback loop
41
Dietary factors related to RBCs
Vitamin B12 and folic acid: required for DNA synthesis; necessary for the growth and division of all cells
Iron: required for hemoglobin synthesis
42
Destruction of RBC
RBC cells live 120 days, circulate 75,000 times, become fragile with age
Damaged cells rupture when passing through liver or spleen
White blood cells phagocytize damaged RBCs
Some iron from hemoglobin recycled to make new heme and RBCs
remaining iron is turned into bilirubin - yellow pigment - picked up by liver for concentration (liver damage- jaundice)
43
General Functions of White Blood cells
least numerous of formed elements
Protect against disease - can leave bloodstream to fight infection
Chemical signal released by damaged or infected tissue
44
Diapedesis
(WBCs) cross through capillary wall by squeezing between endothelial cells and can leave blood vessel; can migrate toward infection site
45
Chemotaxis
Attract WBC to area of infection by chemicals released by damaged cells
Stimulate production of more WBCs
46
5 types of WBCs
Granulocytes (granular cytoplasm):
Neutrophils, Eosinophils, Basophils
Agranulocytes (no noticeable granules):
Lymphocytes, Monocytes
47
Neutrophil apperance
More numerous of WBC: 50 - 70% of all WBCs - 2x size of RBCs
Small, light purple granules in acid-base strain type
Lobed nucleus; 3-6 sections
48
Neutrophils function
Bacteria slayers - first to arrive at infection site
- strong phagocytes - engulf bacteria, fungus
After phagocytosis, kill bacteria in 2 ways
- produce oxygen free radicals - "respiratory burst"
- granules in cytoplasm make protein "spears" to puncture cell wall
49
Eosinophils appearance
2 - 4% of WBCs
Coarse granules - color varies by strain type
Bi - lobed nucleus connected by wide bridge
50
Eosinophils function
Defend against parasite infestations
- Flatworms/roundworms from food/contact
- Burrow into intestinal or respiratory mucosae along with eosinophils
Most parasite too large to phagocytize
- eosinophil granules release digestive enzymes directly onto parasite
51
Basophils function
Increased during allergic reaction
granules release histamine and heparin
- histamine - attracts more WBCs, increases vessel permeability
- Heparin - vasodilator, increases blood flow
52
Basophils appearance
rarest of all WBCs, less than 1% of WBCs
Large granules with obscure view of multi-lobed nucleus
53
Monocytes appearance
Largest of WBCs (3 - 8% of WBCs)
No granules in cytoplasm
Single nucleus in kidney or U-shaped with some cytoplasm visible
54
Monocytes function
Main function: defense against viral infection
Also attack some bacterial parasites and chronic infections - leave bloodstream and enter tissue to become macrophages
HIGHLY proficient phagocyte
Also activate lymphocytes to mount a stronger immune response
55
Lymphocytes appearance
Most are only slightly larger than RBCs; smallest WBC (25-33 % of all WBCs)
Large spherical nucleus surrounded by thin rim of cytoplasm
56
Lymphocytes function
2 major types of lymphocytes:
- T cells: attack virus infected cells and tumor cells
- B cells: produce antibodies - tag foreign cells or molecules
57
Where are lymphocytes found?
Do not reside in blood, mainly found in lymphoid tissue (spleen, lymph node)
58
Leukocytosis
High WBC count (> 10,800 / microliter)
Acute infections, vigorous exercise, great loss of bodily fluids
59
Leukopenia
Low WBC count (< 4,800 / microliter)
Measles, mumps, chicken pox, AIDS, polio, anemia
60
Most mobile and active phagocytes
Neutrophils and Monocytes
61
Inflammatory response by WBCs
Reaction that restricts spread of infection; promoted by basophils, by secretion of heparin and histamine; involves swelling and increased capillary permeability
62
Thrombocytes
Fragments of megakaryocytes: a type of stem cell in red bone marrow
63
What regulates formation of platelets?
Thrombopoietin regulates formation of platelets
Megakaryocytes send extensions out of bone marrow into blood vessel within bone
- extension breaks off to form a platelet
64
Platelets (and what they contain)
Has membrane, lacks a nucleus - less than half of a RBC in size
Platelet count: 150,000 - 350,000 / microliter of blood
Contain granules that release Ca2+, serotonin (5-HT), and factors which assist in clot formation - all contribute to hemostasis
65
What is hemostasis and what the 3 steps?
Hemostasis refers to the stoppage of bleeding - limit blood loss
3 steps that limit or prevent blood loss include:
- Blood vessel spasm - decrease blood flow
- Platelet plug formation - plug hole in injured vessel
- Blood coagulation - thicken blood near clot
66
Hemostasis: Vascular Spasm
When blood vessel is ruptured, smooth muscle in blood vessel contracts rapidly
- slows blood loss very quickly
- end of vessel may close completely
67
What is the vascular spasm triggered by?
Triggered by:
- stimulation of the blood vessel wall
- Local pain receptor reflexes
- Chemical released by damaged endothelial cells
Effect continues for 20 - 30 minutes
- allows time for other 2 homeostasis mechanisms to take effect
68
Hemostasis: Platelet plug formation
triggered by exposure of platelets to collagen
- activates platelets causing them to become sticky
--- activated platelets also release 5-HT, Ca2+, and thromboxane A2
- increases platelet clumping and vascular spasm
- acts as positive feedback loop
69
Hemostasis: Blood coagulation
- most effective mechanism of chemostasis: happens very fast
- form blood clot in a complex series of reactions which reinforce platelet plug with fibrin threads
--- acts as a molecular glue to trap blood cells
- effective in sealing larger openings
- involves numerous clotting factors (several require Vitamin K for production)
70
What are blood clotting mechanisms caused by overall?
By release of chemical from damaged cells
By contact with foreign surface without tissue damage
71
What happens to blood clots? (Fate of Blood Clots)
After a blood clot forms, it contracts and pulls the edges of a broken blood vessel together
- Platelets contain actin and myosin
Platelet-derived growth factor (PDGF) stimulates smooth wall muscle cells and fibroblasts to repair damaged blood vessel walls
Fibrynolysis: Plasmin (clot buster) digests fibrin threads and dissolved the blood clot
72
Thrombosis
Blood clot in a vessel supplying a vital organ (brain, heart)
leads to infarction: death of tissues which have blocked blood vessels
73
Artherosclerosis
Accumulation of fat in arterial linings
- fat can rupture and cause clot formation
74
Deep vein thrombosis
Clot formation due to pooling of stagnant blood, mainly in femoral or popliteal veins
Can lead to pulmonary embolism
75
Antigen
Molecule located on cell which identifies it
76
Antibody
Free floating protein that will act against foreign antigens
77
Agglutination
When RBCs come in contact with antibodies against them, they will agglutinate (clump together):
severe immune response (fever, seizures, heart attack)
78
Autorhythmic cells
A small fraction (1%) of cardiac muscle cells are autorhythmic cells
aka pacemaker cells
determine the heart rate
79
Contractile cells
Remaining 99% are contractile cells
determine the stroke volume
80
Location of heart
Within mediastinum posterior to sternum
Angled down left
Medial to lungs
Anterior to the vertebral column
81
Inferior/Superior location of heart
The base lies beneath the 3rd rib
Base: Broad flat posterior surface
The apex lies at the 5th intercostal space
Between 5th and 6th rib: "Apical Heartbeat"
82
pericardium
Heart is covered with tough double layered sac called pericardium
83
Fibrous pericardium
Outer cover, toughest, dense irregular connective tissue
protects heart
anchors heart to surrounding tissue
prevents overfilling (does not occur in healthy individuals)
84
Serous pericardium
Also has 2 layers
Forms fluid filled sac around heart
parietal pericardium
visceral pericardium (also called epicardium)
Between 2 serous layers --> pericardial cavity: filled with fluid
85
pericardial cavity
contains serous fluid which lubricates 2 membranes
- allows heart to work in friction free environment
86
pericarditis
inflammation of pericardium - roughing of serous membranes
- deep chest pain
- can be heart on stethoscope
87
Cardiac tamponade/ cardiac effusion
extreme inflammation fluid buildup in pericardial cavity
88
Layers of heart
epicardium (outer layer)
Myocardium
endocardium
89
Epicardium
Also called visceral pericardium
Thin layer of fat, thicker in elderly
Simple squamous epithelium
- contains coronary vessels
90
Myocardium
Middle layer, thickest layer
Composed of cardiac muscle tissue
arranged in spiral pattern
91
Endocardium
inner layer
forms thin continuous inner lining
epithelial and connective tissue
In all chambers, valves and vessels
92
Atria: ridges of muscle
Pectinate muscles
Increase volume/contraction strength
More prominent in RA
93
Features of ventricles
forms bulk of muscle tissue
trabeculae carne: increases strength of contraction, also ridges
Papillary muscles and chordae tendineae
Reinforce atrial valves during contraction
94
Heart valves 2 concepts
All 4 heart valves only allow blood flow in one direction
Valves open and close in response to pressure difference (not due to papillary muscle contraction)
95
SA node
Pacemaker; located in the right atrium
Initiates cardiac cycle
Starts with depolarization (contraction) of atria
96
AV node
Delays impulse
Allows atria to finish contracting and filling the ventricles with blood
Secondary pacemaker
97
Bundle of His
Allows depolarization to travel from atria to ventricles
Only electrical connection between atria and ventricles
98
Left and Right Bundle Branches
Located in septum of heart
Guide depolarization to apex
99
Purkinje fibers
Large fibers: conduct impulses to ventricular myocardium
Tertiary pacemaker
100
Abnormal EKGs: Atrial Fibrillation
Uncoordinated atrial depolarization
seldom reaches AV node
Causes: damaged Atrial Myocardium (ectopic depolarization)
101
Abnormal EKGs: Junctional Rhythm
SA node is non-functional: no p-waves
AV node sets pace 40 - 60 bpm
Causes: damaged SA node
102
2nd degree AV block
P-wave occasionally does not trigger QRS complex
- damaged AV node
Cause: Ischemia from blockade of coronary artery
103
Prolonged QRS complex
Damage to Bundle of His
cause: ischemia from blockade of coronary artery
104
Abnormal EKGs: Ventricular Fibrillation
Uncoordinated ventricular depolarization
cause: blocked coronary artery, toxic drugs, electrical activity, physical damage
105
Coronary circulation drains into...
The coronary sinus
- large vein on posterior side of heart
- returns deoxygenated blood to right atrium
Great, Middle, and Small cardiac veins drain deoxygenated blood from myocardium
106
Parasympathetic innervation of the heart
Muscarinic receptors:
- decreases excitability of SA node
- decreases HR
107
Sympathetic innervation of the heart
Beta Adrenergic receptors:
- increases excitability of SA node/ventricles
- increases HR and SV
108
What drives blood flow?
Pressure differences
body does not actually sense CO/blood flow, it only senses pressure
109
Baroreceptors monitor...
They are sensors that monitor stretch (pressure) in the aortic arch and carotid sinuses
110
MAP
mean arterial pressure (MAP)
weighted average of systolic and diastolic
MAP = CO * TPR
111
What occurs if a decrease in stretch is sensed?
Activates sympathetic nervous system to restore pressure
112
TPR
Total peripheral resistance
Sum of resistance in all vessels of body
113
Vascular System Functions
- Provide a conduit for blood to go from heart to organs
- Regulation of both blood pressure and blood flow:
--- maintain enough resistance to ensure adequate BP in entire system
--- Match blood flow to metabolic demand of each organ system
114
What occurs if BP is too low?
Vessel constricts to increase TPR
This will increase MAP to increase blood flow
115
What generates initial pressure difference to drive blood flow?
The heart
116
Tunica Intima
Inner layer of blood vessel
Contain endothelium; direct contact with blood
Simple squamous cells = low friction
117
Tunica Media
Middle layer of blood vessel
Contain smooth muscle
Innervated by sympathetic nerve fibers --> controls diameter of blood vessels
Responds to circulating hormones, also effects diameter
Increase blood flow = vasodilate
Decrease blood flow = vasoconstrict
118
Tunica Externa
Outer layer of blood vessel
Contains collagen fibers
Structural reinforcement/anchoring to surrounding tissues
large vessels = vasa vasorum
119
2 major properties of arteries
Elasticity: elastic tissue in T. interna and Media can withstand high pressure
Contractility: smooth muscle in T.media (direct blood flow and limit bleeding - vascular spasm)
120
2 types of arteries
Elastic arteries (conducting arteries) - act as a pressure reservoir
Muscular arteries (distributing arteries) - contribute to blood flow regulation
121
Elastic Arteries
Thick wall of smooth muscle
Also contain elastin
Stretchiness acts as pressure reservoir
- maintains blood flow during diastole
Arteries distend during systole
- recoil during diastole
Recoil propels blood through artery
122
Muscular Arteries
Most common type of artery
Thickest T.media (smooth muscle)
- good capacity for vasodilation/vasoconstriction
- plays a minor role in regulating blood flow to tissue
- most blood flow regulation is accomplished by arterioles
123
Arterioles
Large arterioles contain all 3 tunics
Small = mainly smooth muscle surrounding endothelium
Contain loops of smooth muscle = precapillary sphincters
124
Precapillary sphincters
Main determinant of vascular resistance (TPR)
contraction/relaxation of precapillary sphincters - adjust resistance to flow
125
Extrinsic Flow Control
Activated by baroreceptors in response to decrease in MAP
- released epinephrine and norepinephrine
- non-specific - all organ systems are affected
Response determined by which the receptors the organ has
126
Types of receptors of organs for extrinsic flow control
Alpha-adrenergic receptors = vasoconstriction
Beta-adrenergic receptors = vasodilation
Most non-essential organs have mainly alpha-adrenergic receptors
127
Extrinsic flow control: sympathetic activation leads to...
Sympathetic activation increases vasoconstriction
increase TPR --> increases MAP
Problem: need to get blood into tissue that has a high metabolic rate
128
Local (Intrinsic) Flow Control mechanisms
Control mechanisms at the site of the vessels themselves
Active hyperemia and flow autoregulation
- different cause but same effect = vasodilation
129
Active hyperemia
Up Metabolic activity of Organ ->
Down O2, Up metabolites in organ interstitial fluid ->
Arteriolar dilation in organ ->
Blood flow to organ
130
Flow autoregulation
Down arterial pressure in organ ->
Down blood flow to organ ->
Down O2, Up metabolites, Down vessel-wall stretch in organ ->
Arteriolar dilation in organ ->
Restoration of blood flow toward normal in organ
131
Problem caused by intrinsic flow control
overall decrease in TPR
Blood flows out of arterioles faster than it is replaced in arteries
Drop in MAP = all organs get less blood
132
How does body protect itself from decreases in pressure?
Baroreceptors activate the sympathetic nervous system -> Increases CO -> Vasoconstriction in non-essential organs (extrinsic flow control)
133
Capillary
Smallest of all vessels
Huge surface area for nutrient delivery
Lack outer 2 tunic
- Thin T.lamina - single endothelial cell in thickness
Primary point of exchange between the blood and tissues
134
Anatomy of capillary network through organ
Flow is regulated by arteriole precapillary sphincters
Nutrients/waste exchanged in capillary bed
Spent blood drains through venules
135
How to get through capillary wall?
Diffusion occurs via 2 pathways
Transcellular - through endothelial cell
and Paracellular - around cells
Both pathways require concentration gradient
136
Transcellular
Through endothelial cell
From apical to basolateral side
Aided by thin walls
137
Paracellular
Around cells
Cells joined by tight junctions
Incomplete in capillaries
Gap = intercellular cleft
138
Continuous capillaries
Intercellular clefts are gaps between neighboring cells
Skeletal and smooth, connective tissue and lungs
139
Fenestrated capillaries
Plasma membranes have many holes
Kidneys, small intestine, choroid plexuses, ciliary process, endocrine glands
140
Sinusoids
Very large fenestrations
Incomplete basement membrane
Liver, bone marrow, spleen, anterior pituitary, and parathyroid gland
141
Major Functions of Venules and Veins
Low pressure/resistance path to return blood to heart:
- due to very large vessel lumen
Large blood reservoir
- sympathetic venoconstriction = increase venous return to the heart
142
How much of blood volume is in veins?
60 % of total blood volume is in the veins
143
Venule and Vein structure
Thinner walls than arteries - do have all 3 tunics
but very small venules = lack outer 2 (like capillaries)
Highly porous endothelium - allows for movement of WBC and other phagocytes
Tunica media less developed
- still vasodilate or constrict
Function as blood reservoir - highly distensible
Very large vessel lumen
144
Venous valve systen
One way valves - only allows blood to flow back to heart
blood pressure in veins is very low
Lower body = pressure almost cannot overcome gravity - need to MOVE
145
What is venous flow assisted by?
By the skeletal muscle pump mechanism working in combination with one-way valves
146
Anastomoses
Union of 2 or more arteries supplying the same body region
Blockage of only one pathway has no effect
- Circle of Willis underneath brain
- coronary circulation of heart
147
Collateral circulation
Alternate route of blood flow through an anastomosis is known as collateral circulation
- can occur in veins and venules as well
148
End arteries
Arteries that do not anastomose
- occlusion of an end artery interrupts the blood supply to a whole segment of an organ, producing necrosis of that segment
Alternate route to a region can also be supplied by nonanastomosing vessels
149
Minor roles of lymphatic system
Returning leaked proteins from interstitial fluid to plasma
Transporting dietary fats (intestinal villi)
150
Major roles of lymphatic system
Return excess fluid from interstitial space back to plasma
Protection against infection
- House B- and T- lymphocytes in lymph nodes
151
How does excess fluid get into interstitial space?
Fluid comes from capillaries in our tissue
Nutrient diffusion occurs via 2 pathways
- transcellular or paracellular
Fluid can exit capillaries via same pathways
- driven by Starling Forces
---- pressure gradient
152
Hydrostatic pressure
Physical pressure pushing water through capillary wall
153
Colloid Osmotic pressure
Non-penetrating proteins (colloids) that osmotically draws in fluid
154
What happens to fluid that doesn't get absorbed?
Enter lymphatic capillaries
Now called lymph
returned to venous circulation
155
Structure of lymphatic capillaries
Very thin walled and permeable
contains overlapping flaps which form mini-valves to let fluid in
Flaps have anchoring filaments
- attaches them to surrounding tissue
- when fluid levels increase= flaps pull up to let more fluid in
156
Where are lymphatic capillaries located?
Located everywhere except:
CNS, cornea, cartilage, and epidermis
157
Lymphatic capillaries drain into...
Larger collecting vessels
- Have 3 main tunic but thin-like veins
- also have one way valves - like veins
158
Collecting vessels drain into...
Collecting vessels unite and drain into lymphatic trunks named by body region
159
Right Lymphatic Duct
Drains lymph from upper right torso, right arm, and right side of head
Returns lymph to circulation at junction of right subclavian and jugular vein
160
Thoracic Duct
Drains lymph from rest of body including both veins
Return lymph to circulation at junction of left subclavian and jugular vein
161
Cisternae chyli
In some individuals, the thoracic duct starts as an enlarged sac called the cisternae chyli
162
What is lymph transport assisted by?
Like venous blood - assisted by skeletal muscle movement
One- way valves to prevent backflow
Pulsations from arteries and smooth muscle in lymph vessels assist lymph movement
163
T-lymphocytes (T-cells)
When activated, coordinate immune response and directly attack infected cells
164
B-lymphocytes (B-cells)
When activated, produce plasma cells which secrete antibodies
Antibodies mark foreign cells for destruction
165
Macrophages
Phagocytize foreign objects and activate T-cells
166
Dendritic cells (Antigen Presenting cell)
Capture foreign antigen and brings them to lymph nodes to alert other immune cells
167
Primary lymphoid organs
Where B and T cells mature, but don't encounter pathogens (immunocompetence and self-tolerance)
Thymus (between sternum and heart):
T-cell maturation
Red Bone marrow: B-cell maturation
168
Secondary lymphoid organs
Where mature lymphocytes come in contact with and are activated by pathogens
- lymph nodes
- spleen
- mucosa associated lymphoid tissue
169
MALT
mucosa-associated lymphoid tissue
- tonsils, peyer's patches, appendix
170
Lymph nodes
Small capsules located close to lymph vessels
Most dense in areas of body likely to encounter pathogens
171
2 main functions of lymph nodes
Cleanse lymph: contain macrophages to phagocytize pathogens and debris
Activate the immune system: Antigen Presenting cells will bring antigens to lymph nodes to activate B and T lymphocytes
172
Lymph Node Structure
Capsule: outer fibrous covering
Trabeculae: connective tissue extensions
- divides nodes into separate chambers
Outer layer: cortex
Inner chamber: medulla
173
The flow of lymph in the nodes
Lymph enters via afferent vessels
- enters bag-like subscapular sinuses in cortex
---> contain macrophages attached to connective tissue fibers to filter lymph
Some lymph leaks into lymph follucle and germinal center
- activate rapidly dividing B-cells
Lymph move toward center (medulla) of node
- enters medullary sinus
- contains macrophages
- comes in contact with medullary cords
- contains both B and T cells waiting for activation
Cleansed lymph moves toward hilum (indentation) of node
Exits via efferent vessels
174
Spleen
Site of lymphocyte proliferation and blood cleansing
Largest lymphatic organ
2 main components: red pulp and white pulp
175
Red Pulp
Breaks down damaged RBCs and stores released iron
Stores platelets and monocytes for later use
176
White Pulp
Where lymphocyte proliferation occurs
177
MALT function
strategically located lymphoid tissue
Main function: gathers pathogens which enter body through air or diet
used for activation and creation of B/T memory cells before a severe infection ever occurs
178
Locations of MALT
Tonsils - located throughout pharynx
peyer's patches - clusters of lymph tissue in small intestine
Appendix
179
Elephantiasis: clinical application
Parasitic worms infest lymphatic system - block fluid drainage.
Results in blocked lymph drainage, edema - accumulation (abnormal) of fluid beneath the skin
180
Innate Immunity
Present at birth: responds to any foreign pathogen which has not been identified
Always vigilant and responds with minutes of invasion
Less effective than adaptive immunity
181
Adaptive immunity
Only attacks identified pathogens
Extremely effective by takes longer to respond than innate immunity
182
2 branches of Innate Immune
Surface Barriers - 1st line of defense
- skin and mucous membranes
Internal Defenses - 2nd line of defense
- only needed if surface barriers are breached
- phagocytes, NK cells, inflammation, antimicrobial proteins (complement), fever
183
Skin as a Surface Barrier
Skin and mucous membrane are physically tough and have chemical defenses
Skin: outer keratinized layer is very durable and acidic
- acid (acid mantle) inhibits bacterial growth
184
Mucous membranes as a Surface Barrier
Not as durable as skin but can have several types of defenses
- acid (stomach, eye, vagina, bladder/urine)...destroys microorganisms
- Enzymes - usually lysozymes which destroy microorganisms
- Mucin - mucous traps microorganisms
- filtering mechanisms (cilia or hairs) trap and physically remove pathogens
185
Highly adapted mucous membrane: trachea
Trachea has most of the defense mechanisms associated with mucous membranes
- goblet cells create mucous: trap pathogens and contain lysozymes
- elongated cells are physically durable
- cilia (filter) - removes pathogens trapped in mucous
186
When tissue is damaged, what occurs?
2 things-
Damaged tissue releases inflammatory chemicals
Immune cells are recruited to the area of damage
187
How are immune cells recruited?
Attracted directly to inflammatory chemicals
Called by chemicals from cells with pattern recognition receptors
188
TLRs
Major class of recognition receptors: toll-like receptors (TLRs)
These receptors generally identify foreign objects
If a pathogen is present, TLR containing cells release chemicals to attract more immune cells to the area
189
How do immune cells get to site of infection/injury? (list)
1) Leukocytosis
2) Marginalization
3) Diapedesis
4) Chemotaxis
190
How do immune cells get to site of infection/injury? : Leukocytosis
Neutrophils are released from bone marrow and enter bloodstream
- WBC count can increase 4-5x
191
How do immune cells get to site of infection/injury? : Marginalization
Inflammatory chemicals cause endothelial cells in blood vessels and immune cells to sprout cell adhesion molecules (CAMs)
- causes passing immune cells to stick
192
Cells recruited in an innate immune response
Neutrophils (WBC) 1st and Macrophages (2nd)
Macrophages are derived from monocytes which leave the bloodstream
Both are phagocytes
193
Phagocytosis (the process)
1) Phagocyte must adhere to carbohydrate signature (glycocalyx) on pathogen!
2) Pathogen is engulfed to form a membrane enclosed phagosome
3) Phagosome fuses with lysosome to form phagolysosome
4) Enzymes from lysosome destroys pathogen
194
How can phagocytosis fail?
Some pathogens can conceal their carbohydrate signature to avoid phagocytosis
Our defense: opsonization
195
Opsonization
Free floating immune proteins called opsonins - a type of complement protein - can recognize foreign objects
--- Usually an antibody - attaches to foreign objects and provides "handles" which phagocytes can grab onto
196
Respiratory burst
Some pathogens are resistant to lysosome enzymes
Our defense: respiratory burst
197
Certain lymphocytes can activate macrophages....
Certain lymphocytes can activate macrophages to produce additional enzymes
- Free radicals and oxidizing chemicals
break chemical bonds in bacterial cell wall
Increases acidity of macrophage
198
NK cell
Natural killer cell - defense against virus infected and cancerous cells
NK cells scan for abnormalities in our cells
(example - lack of a self cell maker called a major histocompatibility (MHC) protein)
NK cell then functions like a friendly "hacker" - comes into contact with infected cell and triggers apoptosis
199
While immune cells are being recruited to the area...
Inflammatory chemicals released from infected/damaged cells are doing the following:
- limiting the spread of the infection
- calling more immune cells
- clearing cell debris
- promoting healing
200
Acute Inflammation
Cardinal signs: heat, redness, swelling, pain
Several major inflammatory chemicals - histamine, kinins, prostaglandins, complement proteins, cytokines
All have same general function: increase blood flow and increase capillary permeability
201
How acute inflammation helps fight infection?
Increased blood flow (hyperemia) via arteriolar dilation increases delivery of immune cells and chemicals
- accounts for heat and redness
Increased capillary permeability helps deliver a fluid called exudate to site of infection
- accounts for swelling and pain
--- excess fluid presses on nerve ending, prostaglandins cause pain
202
Exudate
Excess fluid helps sweep foreign particles into the lymphatic system for destruction
Also contains:
- clotting factors - walls off infection and provides scaffolding for healing
- complement proteins - free floating proteins which "complement" innate and adaptive immune response
203
Complement Proteins
Recognize and bind to carbohydrate layer on foreign cells
Opsonizes foreign cell - enhance phagocytosis
Forms a Membrane Attack Complex (MAC)
-- it's just a hole: punctured cell wall takes on water and cell is lysed
204
Interferons
Protection against virus infection
Small proteins released by certain virus infected cells
- viruses must invade host cells because they lack their own replication machinery
Interferons trigger viral defense mechanisms in nearby cells which have not yet been infected by the virus
--- halts protein production and degrades viral RNA - prevents replication of virus
205
Fever (in relation to immunity)
Triggered by release of pathogens from immune cells when pathogens are encountered
Increases body temperature by acting on hypothalamus
Unclear how fever fights infection - higher temp may damage pathogens, increased metabolic rate of normal tissue may clear infection faster
206
The adaptive immune response...
Takes longer to initiate
Utilizes T and B cells
Is specific: only attacked identified pathogens
Is systemic: not limited to the site of infection
Has memory: once it has encountered a pathogen, then next time it appears, it will be eliminated with much greater efficiency
207
The 2 branches of Adaptive Immune System
Humoral (antibody mediated)
- utilizes free floating antibodies secreted by B-lymphocytes
- targets: extracellular (toxins, bacteria, free viruses)
Cellular
- utilizes T-lymphocytes to directly attack pathogens
- targets: cellular (virus/parasite infected cells, cancerous cells)
- T-cells can also indirectly attack by releasing inflammation enhancing chemicals
208
Adaptive Immune System trigger
Antigens
- a marker used to identify a particle or cell
Some antigens encountered will be identified as foreign, which will initiate the immune response
2 types of antigen: complete and haptens
209
Complete Antigen
2 requirement:
- reacts with activated lymphocytes and the antibodies they release
- must be immunogenic
--- stimulates the production of more lymphocytes (examples - pollen, bacteria, fungi)
210
Antigenic determinants
Only certain parts of the antigen are immunogenic, called antigen determinants
Located on antigen surface
these are what antibodies and lymphocytes bind to
Large antigen particles can have many determinants
Each one can bind a different lymphocyte/antibody
211
Incomplete Antigens or haptens
Includes many types of very small molecules, peptides, and nucleotides
can be reactive, but not immunogenic on their own
212
how do haptens antigens work?
Haptens bind to a friendly protein
Makes a combination the immune system marks as foreign
example - poison ivy toxin
213
MHC proteins
Certain immune cells can only bind to antigens contained on Major histocompatibility complex (MHC) proteins
MHC proteins are located on the cell surface with a "pocket" for an antigen
- protein in the pocket can be a self-antigen or foreign antigen
214
Adaptive IS: B-lymphocytes (B-cells)
Oversee humoral immunity
215
Adaptive IS: T-lymphocytes (T cells)
Oversee cellular immunity
216
Antigen presenting cells
assist T-cells in recognizing pathogens
- these cells will contain MHC proteins
217
5 steps of B/T cell development
1) B/T cells originate in red bone marrow
2) migration to primary lymphoid tissue for maturation (B-cells to red bone marrow and T-cells to thymus)
3) Release of primary lymph tissue and seeding of secondary lymph tissue
- here they likely encounter pathogens
4) antigen encounter and activation
- lymphocytes which have never seen a pathogen = naive
- pathogen binding activates the lymphocyte
5) once activated, B/T cells proliferate and differentiate (proliferation helps fight more of the same pathogens)
218
B/T cells can differentiate into 2 main types:
Effector cells: fighting force
Memory cells: respond quickly to same pathogen
219
2 Important abilities granted by maturation phase (B/T cell development)
Immunocompetence - develops receptors which can bind to one specific antigen
- all receptors on the same lymphocyte are the same
- each lymphocyte is committed to recognizing only one type of pathogen
Self-tolerance - must be unresponsive to self-antigens
220
Test of lymphocytes
Tested for the 2 properties, those which fail the test are destroyed
- only about 2 % of lymphocytes survive
221
How APCs work
1) Ingest foreign antigen
2) Embed a fragment of the antigen within their MHC protein
3) present the fragment to a naive T-cell to activate its cell which can act as APCs: dendritic cells, macrophages, B cells
222
Humoral Immunity
Occurs when a B cell encounters an antigen that can bind its unique receptors
Causes that B-cell to proliferate or create clones of itself - called clonal selection
223
clone differentiation
Some will become effector cells called plasma cells
- Plasma cells secrete 2000 antibodies/sec which bind to the encountered antigen
- marks the antigen for destruction by both innate and adaptive immune cells
The other will become memory cells
- survive for years and can mount an immediate immune response if the same antigen shows up again
224
Memory cells causing immunological memory
When a B-cell first encounters the antigen, the proliferation and differentiation which occurs is called the primary immune response
- 3-4 day lag before antibody production ramps up
If the same antigen appears the second time, the memory cells immediately mount a secondary immune response
- little to no lag period
- more rapid antibody production
225
Active humoral immunity
Antigens activate B-cells via natural infection or from a vaccine
- memory cells maintain the immunity
226
Passive humoral immunity
Pre made antibodies are directly introduced into body
- can be naturally passed from mother to fetus or administered (snake anti-venom)
- these antibodies are degraded, providing only short-term immunity
227
How do antibodies work?
When antibody binds with its recognized antigen, it forms an immune complex
- formation of the complex inactivate the pathogen in several ways
---neutralization
---precipitation
---agglutination
all 3 enhance phagocytosis
228
Neutralization
binding sites on viruses and bacterial toxins are blocked
229
Precipitation
like agglutination for small soluble molecules, not cells
230
Cellular immunity
Mainly provides defense against virus/bacteria infected cells and foreign or cancerous cells
Involves activation of T-lymphocytes rather than B-cells
231
Differences between B and T cells
All T-cells are activated only by antigens presented to them on MHC proteins, not free floating antigens
2 types of naive effector T-cells: CD4 and CD8 cells
232
CD4 and CD8 cells
When activated by APCs, CD4 and CD8 cells differentiate into different effector cells
233
Activated CD4 cells can becomes 2 possible effector cells
T-helper cell: activate B cells, other T cells, macrophages, and APCs
T-regulatory cell: moderates immune response
- dampens the immune response to prevent auto-immune conditions
234
Activated CD8 cells become...
cytotoxic T cells: these cells directly destroy anything harboring a foreign antigen
- bind to and give infected cells a "death hug"
- release perforins and granzymes
- granzymes enter perforin pore and activate apoptosis
235
Role of MHC proteins in antigen presentation
Antigens embedded within MHC proteins are "read" by T-cells to determine if that cells is healthy or infected, foreign or friendly
236
MHC I proteins
found in almost all "self" cells
In its pocket, it has an antigen made of proteins from inside that cell (endogenous antigen)
if a self-cell becomes infected or cancerous, the antigen on its MHC I protein changes
- activate specifically naive CD8 cells
- signals cytotoxic T cells to destroy it
237
MHC II proteins
Other type of MHC proteins
Found mainly on APCs - specifically activate CD4 cells
MHC II proteins can only contain in their pocket an antigen made from proteins engulfed by the APC
- these are exogenous antigens
238
Dendritic cells
Unique type of APC
Contains both MHC I and MHC II proteins which are used to activate both CD4 and CD8 cells
- after it engulfs a foreign antigen, a piece of it gets embedded in both its MHC I and II proteins
239
what do only dendritic cells do?
Only type of immune cell which can display an exogenous antigen in its MHC I complex
- allows them to activate both CD4 and CD8 cells
