Exam 2

Components of Blood and Proportions

formed elements = 45%

• RBCs/erythrocytes

• WBCs/leukocytes

• platelets/thrombocytes

plasma = 55%

• mainly water

Functions of Blood

1. transportation

2. protection

3. homeostasis

Transportation

O2, CO2, nutrients, wastes, hormones

supply must meet bodily demands

RBCs transport O2, CO2, H+

Protection

immune responses, blood clotting

protect from pathogens

WBCs

Homeostasis

thermoregulation

pH control

maintaining fluid volume

Components of Plasma

water = 90%

proteins = 8%

respiratory gases

nutrients

waste products… nitrogenous waste, pollutants

electrolytes

hormones

Structure and Function of Erythrocytes

shape and why it is advantageous

• biconcave discs… circular + flat with indentation on each side

• good b/c increased surface area to carry more

structure (not a true cell)

• no nucleus, no mitochondria

why it can generate ATP anaerobically, why advantageous

• good b/c the cell won’t eat its own cargo/O2

• ex: if a ice cream truck driver ate all of the ice cream, there would be none to give out to customers

Hemoglobin

4 globin chains

• hold CO2 waste

• made of proteins

4 heme groups

• made of iron

• hold O2

different names based on what is attached:

• oxyhemoglobin = holds O2, in arteries, ruby red

• deoxyhemoglobin = holds H+, dark red

• carbaminohemoglobin = holds CO2

Oxyhemoglobin

holds O2

found in arteries… oxygenated blood

ruby red blood

Carbaminohemoglobin

holds CO2

found in veins… deoxygenated blood

Deoxyhemoglobin

holds H+

found in veins… deoxygenated blood

Erythropoiesis

begins as stem cell → becomes reticulocyte after 15 days → matures into erythrocyte within 2 days of release

Reticulocyte Count

1-2% of all RBC in blood sample

important b/c demonstrates proper production of RBCs and function of bone marrow

Homeostatic Control of Erythropoiesis

stimulus = hypoxia… due to low RBC, low hemoglobin, low O2 availability

kidney released ERYTHROPOIETIN or EPO

erythropoietin stimulates red bone marrow to produce RBCs

more RBCs released into bloodstream

body can carry more O2

back to homeostasis

Causes of Hypoxia

low O2 availability… living at high altitudes

low hemoglobin to carry O2… anemia

low RBC count

Production Process of RBCs

low O2 levels in blood

kidneys produce erythropoietin/EPO

EPO in blood triggers erythropoiesis in bone marrow

new erythrocytes enter bloodstream after 120 days

Destruction Process of RBCs

hemoglobin scrapped by spleen/liver and bone marrow

broken into heme and globin units

heme breakdown creates bilirubin by-product, iron is stored in liver

globin is turned into amino acids back into blood

Red Blood Cell Count

4-6 million RBC/mm3

Reticulocyte Count

1-2% of all RBC in blood sample

indicate proper function of bone marrow and production of RBCs

Hematocrit

female = 42 ± 5%

male = 47 ± 5%

measures how much of blood volume is made up of RBCs

Hemoglobin Concentration

female = 12-16 grams/100mL

male = 13-18 grams/100mL

Differential White Blood Cell Count

4,800-10,800/uL

test allows doctor to see how many of each specific WBC is in blood

reveals immunocompromization or specific infection

Leukocyte Types + Percentages

most prevalent

neutrophils = 50-70%

lymphocytes = 25-45%

monocytes = 3=85

eosinophils = 2-4%

basophils = 0.5-1%

least prevalent

NEUTROPHIL LYMPHOCYTE MONOCYTE EOSINOPHIL BASOPHIL

NEVER LET MONKEYS EAT BANANAS

Neutrophils

50-70% of WBCs

specialized to kill bacteria by PHAGOCYTOSIS

1st soldier on the battlefield

numbers increase with bacterial infection

MAIN FUNCTION = eat/engulf bacteria invaders

Lymphocytes

25-45% of WBCs

can carry out immune response via cell attack or antibody production

mostly in spleen and lymph nodes

T and B cells

MAIN FUNCTION = direct cell attack (T cells) and antibody production (B cells)

Monocytes/Macrophages

3-8% of WBCs

in blood = monocyte

outside of blood = macrophage

PHAGOCYTIZE INVADING PATHOGENS AND DEBRIS

MAIN FUNCTION = leave blood + eat invaders/debris

Eosinophils

2-4% of WBCs

use digestive enzymes to kill parasitic worms

numbers increase w/ allergic reaction or parasitic infection

MAIN FUNCTION = secrete digestive enzyme to kill parasitic worms

Basophils

0.5-1% of WBCs

release histamine → dilates vessels → increased blood flow to tissue → allows WBCs to get to and fight infection + inflammation

MAIN FUNCTION = secrete histamine to dilate vessels + allow for more WBCs to enter and fight infection

Antigen Receptor

“looks” of cell

protein bumps on surface of cell membrane

used for identification

Antibody

WBC that detects if antigen/cell belongs in body

matches antigen = identification that cell belongs

no match = sign to destroy, foreign

Type A Antigens + Antibodies

antigens = A

antibodies = B

Type B Antigens + Antibodies

antigens = B

antibodies = A

Type AB Antigens + Antibodies

antigens = A + B

antibodies = none

Type O Antigens + Antibodies

antigens = none

antibodies = A + B

Blood Types Compatible with A+

A+

A-

O+

O-

Blood Types Compatible with A-

A-

O-

Blood Types Compatible with B+

B+

B-

O+

O-

Blood Types Compatible with B-

B-

O-

Blood Types Compatible with AB+

AB+

AB-

A+

A-

B+

B-

O+

O-

Blood Types Compatible with AB-

AB-

A-

B-

O-

Blood Types Compatible with O+

O+

O-

Blood Types Compatible with O-

O-

Universal Donor

O-

can be donated to all because it has no antigens

no antigens = no antibodies will kill it

Universal Recipient

AB+

has all of the antigens so it has no antibodies against antigens

all antigens = can accept any blood without it being a harm

Rh Factor and Positive or Negative Classification

Rh+ = has the antigen

Rh- = does not have the antigen… only will have antibodies if exposed before to Rh+

Rh- Woman Pregnant with Rh+ Children

Rh- mother has no antibodies against Rh factor because no previous exposure

Rh- mother gets pregnant and baby has Rh+ blood

during delivery, Rh- mother is exposed to Rh+ blood

Rh- mother develops antibodies

without rhogam:

Rh- mother gets pregnant with second baby with Rh+ blood

mother now has antibodies which attach baby’s blood… hemolytic anemia

with rhogam:

Rh- mother gets pregnant with second baby with Rh+ blood

mother takes rhogam

rhogam weakens immune system (B cells)

baby’s blood is not attacked + healthy pregnancy occurs

Steps of Hemostasis

process by which the body stops leakage of blood from a damaged blood vessel

1. vascular spasm

2. platelet plug formation

3. coagulation

Vascular Spasm

smooth muscle contracts

immediate response to slow leakage

vessel walls tighten to try to line up ripped edges together

Platelet Plug Formation

platelets adhere to rip and become sticky

more platelets aggregate + stick on… positive feedback loop

platelets glue together edges of ripped vessels

Coagulation

mesh is created using fibrin

mesh stabilizes plug + creates a clot

clot seals off blood vessel

glue dries ripped vessel walls together

Three Phases of Coagulation

1. two pathways to prothrombin activator

2. common pathway to thrombin

3. common pathway to fibrin mesh

Two Pathways to Prothrombin Activator

intrinsic = within blood vessel

extrinsic = in tissue around blood vessel

Common Pathway to Thrombin

prothrombin activator converts prothrombin to thrombin

Common Pathway to Fibrin Mesh

thrombin converts fibrinogen into fibrin

fibrin can now be used to form mesh + plug blood vessel

Clot Retraction

30-60 mins after injury

actin and myosin within platelets contract

pulls torn edges of vessel closer together

Fibrinolysis

breaks down clot once healing has occurred

plasmin digests fibrin

about 2 days after clot formation

Fibrin-Digesting Enzyme or “Clot Buster”

PLASMIN

Why Patients with Advanced Kidney Disease are often Anemic

poor kidney function → low EPO production → low creation of RBCs in bone marrow → ANEMIA

Hemophilia and why Aspirin Should Not be Taken

hemophilia = thin blood, low clotting

should not take aspirin because it inhibits platelet plug formation

simple: hemophiliacs already have thin blood, they don’t need it even thinner and unable to clot

Anemia

blood’s O2 carry capacity is too low

broad categories:

• blood loss

• low RBC production

• rapid RBC destruction

Anemia due to Blood Loss

hemorrhagic anemia

can be acute (bleed from wound) or chronic (bleed from ulcers)

once bleed is resolved, erythropoiesis should restore RBC count

Anemia due to Low RBC Production

potential causes:

• lack of raw materials… low amino acids or iron

• red bone marrow failure

examples:

• iron-deficiency anemia… diet is insufficient or cannot absorb

• renal anemia… kidneys do not produce enough EPO

• aplastic anemia… red marrow destroyed or inhibited

Anemia due to Destruction of RBCs

hemolytic anemia… RBCs rupture prematurely

potential causes:

• abnormal hemoglobin

• mismatched blood transfusion

• infection

examples:

• sickle-cell anemia

• thalassemia… one of globin chains is absent/faulty… thin Hb deficient RBCs made

Sickle Cell Anemia

deformed RBCs that can rupture easily and get stuck in smaller vessels

O2 deficiency causes pain, gasping for air

NEED TRANSFUSION IN CRISIS

s/s = pain, fatigue, gasping for air

Effects of Leukemia on Production of WBCs, RBCs, and Platelets

overproduction of cancerous WBCs → reduced production of RBCs + platelets

• fewer platelets → poor clotting → hemorrhage

• WBCs produced are ineffective → immunocompromised

• fewer RBCs → anemia

Lymphatic System Functions

return interstitial fluid and leaked plasma proteins back to blood

provide structural basis of immune system

Lymph Vessels vs Blood Vessels

capillaries

• lymph capillaries are more permeable

• lymph capillaries have one-way minivalves

collecting vessels

• collecting vessels in skin travel with superficial veins

• collecting vessels deep travel with arteries

• nutrients are supplied from branching vasa vasorum

Lymphatic Vessels

direction of flow

• one direction from TISSUE TO HEART

presence of nodes + collecting vessels

• capillaries → collecting vessels → trunks and ducts

Flow of Lymph from Interstitial Fluid to Subclavian Veins

5 different trunks

2 main ducts

veins that empty the lymph

5 Lymphatic Trunks

paired lumbar = drains lower back + legs

paired bronchomediastinal = drains respiratory + thoracic

paired subclavian = drains arms

paired jugular trunks = drains head + neck

single intestinal trunk = drains abdomen

2 Main Lymphatic Ducts

right lymphatic duct

thoracic duct

empties lymph into venous circulation at junction of internal jugular and subclavian veins on own side of body

Mechanisms Helping Flow of Lymph

pulsation of nearby arteries propels lymph

skeletal muscle pump

respiratory pump

valves in vessels

NO SYMPATHETIC CONSTRICTION… NO MUSCLES IN WALLS

T Cells

kill viruses + bacteria

manage immune response

destroy + attack foreign cells by chemical injection + lysis

B Cells

produce antibodies

produce plasma cells which secrete antibodies

Macrophages

phagocytize foreign substances and help activate T cells

Structure and Function of Lymph Nodes

function = FILTER LYMPH

• macrophages destroy microorganisms + debris

• immune function = lymphocytes are activated + mount an attack

remove viruses/bacteria/invaders b4 they reach the heart

embedded in connective tissue, in clusters along lymphatic vessels

near body surface in inguinal, axillary, and cervical body regions

Afferent and Efferent Lymph Node Vessels

few efferent vessels, more afferent vessels → creates slow flow of lymph for better filtration + consumption of pathogens

lymph enters, travels through sinuses, exits node

Inflamed Lymph Nodes

have to filter many pathogens → inflamed and tender → swollen glands

PAIN IS A GOOD SIGN… means inflammation is present

Cancerous Lymph Nodes

nonpainful, swollen is a sign of cancerous

lymphoma

Spleen

largest lymphoid organ

functions:

• site of lymphocyte proliferation and immune response

• cleanses blood of aged cells + debris

• stores breakdown products of RBC for reuse

• stores blood platelets

• contains lymphocytes, macrophages, and erythrocytes

structure:

• white pulp = lymphocytes

• red pulp = blood vessels

JUNKYARD SALVAGING DEAD CELLS FOR PARTS

Thymus

increases in size with age → stops growing during adolescence → atrophies

most active during childhood

contains lymphocytes and macrophages

site of T-cell maturation

Tonsils

ring of lymphatic tissue around the pharynx

first line of defense against pathogens

crypts in tissue trap and destroy bacteria

Innate Defenses

BORN WITH THESE DEFENSES

surface barriers (skin and mucosa)

internal defenses (cells + chemicals)

Adaptative Defenses

NOT BORN WITH, ADAPT/PICK UP AS YOU GROW + ARE EXPOSED

humoral immunity

cellular immunity

First Line of Defense: Non-Specific Surface Membrane Barriers

SERVE AS A PHYSICAL BARRIER AGAINST MICROORGANISMS

role of skin

• skin is tough and resistant to many toxins and enzymes

• hairs can trap and filter particles

role of mucous membranes

• mucous can trap microorganisms and sweep upward

other

• various chemicals within body can kill bacteria

• enzymes in stomachs kill different microorganisms

Second Line of Defense: Non-Specific Internal Defenses

different types of phagocytes + mechanism

• neutrophils + macrophages

• phagocyte adheres to pathogen → forms capsule and engulfs → enzymes digest the particles → exocytosis removes the residual material

natural killer cells

• specialized T cels

• nonspecific

• secrete enzymes + chemicals to kill cells

• perforin chemical makes holes in cell membrane → cytotoxin enters… “need to make holes in wall before you throw grenade in”

inflammatory response → process + signs

• basophils release histamine → vasodilation of local vessels → increased capillary permeability → plasma and WBC leak out

• benefits = sets stage for repair, disposes of pathogens

• s/s = warmth, pain, redness, swelling

antimicrobial proteins

• complements = emergency response activator… label cell for phagocytosis and attract phagocytic cells, forms damaging holes in plasma membrane

• interferons = invaded cell produces interferons → go to neighbor cell → warns it that an invader is coming → neighbor cell goes into lockdown

fever

• abnormally high body temperature

• WBCs release pyrogens that reset hypothalamus thermostat

• increased temp inhibits bacterial growth + enhances repair

• s/s = discomfort, fatigue, dehydration

• NEED A FEVER TO SPEED UP IMMUNE PROCESS

Third Line of Defense: Adaptive Defenses

specific: target and kill only virus

systemic: protect whole body

memory: do not need to make new ones in response to repeat exposure

B Cells

contact extracellular antigen → create plasma cells → release antibodies → prepare antigen for destruction

Antigen-Presenting Cell

comes around when it discovers a threat

attaches to antigen receptors on infected cells → collects intel → migrates to lymph node → tells B cells to make antibodies to match viral antigen

dendritic cells, macrophages, and B cells

Graph of Antibody Concentration in Response to Primary and Secondary Exposure

secondary immune response is quicker, stronger, and longer lasting

Lymphocyte Maturation

immunocompetence = able to recognize a specific antigen by binding to it

self-tolerant = unresponsive to self-antigens… doesn’t attack own body cells

B cell maturation in BONE MARROW

T cell maturation in THYMUS

1. origin = B and T cells originate in bone marrow from stem cells

2. maturation = T cells go to thymus, B cells stay in bone marrow + mature

3. seeding = mature lymphocytes seed lymphoid organs and circulate through blood + lymph… still naive

4. antigen encounter + activation = activated after encountering an antigen

5. proliferation/differentiation = multiply and can become plasma or memory cells, then circulate body

Differences Between Primary and Secondary Immune Responses

secondary response is FASTER, LARGER, AND PROLONGED

• already has memory cells that can quickly react → do not need to identify and then produce plasma cells

Humoral Immunity

B-lymphocytes

antibody-mediated, protect against extracellular antigens

B lymphocyte is activated after encountering matching antigen → B cells clone themselves into plasma cells (release antibodies) and memory cells (increase response rate during next exposure)

Active Naturally Acquired

active = you are making antibodies

infection + contact with pathogen → body becomes infected and eventually builds protection

ex: chicken pox parties

HIGH RISK

Active Artificially Acquired

active = you are making antibodies

vaccine; dead or weakened pathogens activate T + B cells

ex: COVID vaccine

LOW RISK

Passive Naturally Acquired

passive = someone else makes antibodies for you

antibodies passed from mother to fetus via placenta, antibodies passed from mother to infant via breastmilk

Passive Artificially Acquired

passive = someone else makes antibodies for you

injection of exogenous antibodies

ex: antivenom, rabies, tetanus shot

Vaccines

exposure to dead or weakened pathogen → body builds immune response → if exposed to active pathogen, body has secondary response

Cellular Immunity

T-lymphocytes

• activated by antigen encounter

• kill directly or release chemicals that regulate other components of immune system

protect against intracellular antigens

Helper T Cells

help activate T and B cells

activate macrophages

recruit other immune cells