BIO 202 –Anatomy & Physiology II: Review for Final Exam
Components of Blood:
Plasma- a clear ECF (55% of blood). Plasma is 92% water and also contains a mixture of
proteins, enzymes, nutrients, wastes, hormones, lipids, carbs, trace elements, and gases. Serum
is plasma minus the clotting proteins. Proteins are the most abundant solute in plasma that are
used for clotting, defense, and transport. There are 3 categories of plasma proteins: albumins
(most abundant which contribute to viscosity and osmolarity and influence BP, blood flow, and
fluid balance), fibrinogen (clotting), and globulins (immune system defenses).
Leukocytes (=granulocytes which has cytoplasmic granules consist of neutrophils,
eosinophils, & basophils; agranulocytes which have no cytoplasmic granules consist of
lymphocytes like T-cells and B-cells & monocytes and macrophages)
-Mean RBC count= 4.2-6.2 million/microliter
-Mean WBC count= 5k-10k/microliter
-Mean platelet count= 130k-360k/microliter
Functions of Blood:
-oxygen from lungs to organs/cells
-oxygen from cells to lungs
-nutrients from digestive system and storage
-wastes to liver and kidneys
Regulates: body temperature by transporting heat out of the skin
Immunity: white blood cells
Stabilizes: water balance
Stabilizes: pH via buffers for acids & bases
Viscosity and osmolarity:
Viscocity- resistance to flow- “thickness/stickyness”. Blood is 4.5-5.5x more viscous than
water; plasma alone is 2x more viscous than water; too many or too few RBCs changes the
viscocity of blood and puts a strain on the heart.
Osmolarity: Total molar concentration of dissolved particles in 1 L of solution due to transfer
of nutrients and wastes between the blood and tissue fluids. If too high: bloodstream absorbs
too much fluid from the tissues thus causing hypertension. If too low: bloodstream transfers
too much fluid to tissues, resulting in edema and hypotension.
Function of hemoglobin- consists of 2 alpha and 2 beta globin chains that are
conjugated with a heme group that binds oxygen to ferrous ion (Fe2+).
-can carry up to 4 oxygens
*CompatibleABO & Rh types for blood donation: (RBC antigen=agglutinogenA& B;
Plasma antibodies= agglutinins anti-A& anti-B)
-YourABO blood type is determined by the presence or absence of agglutinogens (antigens)
A& B on RBCS.
-Blood type is (Rh+) if agglutinogens are present on RBCs, blood type is (Rh-) if
agglutinogens are NOT present on RBCs.Anti-D agglutinins are not normally present in blood
and form only in those that are exposed to Rh+ blood. If Rh- mother and Rh+ mother this is 2
mother-fetus mismatch; if mother is exposed to Rh+ agglutinogens its okay in 1 pregnancy but
in second the mother’s anti-D antibodies will agglutinate fetal RBC causing hemolytic disease
of the newborn. RhoGAM is given to pregnant Rh- women to prevent antibody formation.
–blood type AhasAagglutinogens and anti-B agglutinins
– blood type B has B agglutinogens and anti-A agglutinins
–AB has both A& B agglutinogens and neither agglutinin
–blood type O has neither agglutinogen, but both agglutinins
–blood type O is the most common;AB the rarest
•TypeA(anti-B) will react with RBC types B &AB
•Type B (anti-A) will react with RBC types A&AB
•Type AB will not react with any other RBCs
•Type O (ant-A& anti-B) will react withA, B &AB
Diseases and disorders:
Polycythemia: an excess of RBCs.
-1° polycythemia is due to cancer of erythropoietic cell line in the red bone marrow.
-2° is RBC count up to 8 million/microliter-- dehydration from more RBCs due to less plasma,
high altitude from extended stay at high altitude → RBC count rises up to 7-8 million
RBCs/microliter, physical conditioning from endurance training where athletes have 6.5
million RBCs due to higher o2 requirements, and emphysema where there is less lung tissue
but RBCs cannot correct for this but erythopoietin continues to be releses thus causing excess
*Dangers of polycythemia include increased blood volume, pressure and viscosity which can
lead to poor circulation, heart strain, and clogged capillaries which in turn result in embolism, 3
stroke, or heart failure.
Anemia – iron deficiency and pernicious anemia
Iron-deficiencyAnemia: dietary iron deficient = less hemoglobin.
Pernicious Anemia: inadequate vitamin B12 from poor nutrition or the lack of intrinsic factor
which facilitates B12 absorption.
=is a hereditary Hb defect.
-recessive allele modifies Hb structure-- homozygous recessive for HbS have sickle-cell
disease; heterozygous have HbS have sickle-cell trait
-sickle-cell disease individual has shortened life-- death by age 2 with NO treatment though
some live to age 50 with proper treatment. HbS turns to gell in low o2 concentrations.
-HbS is indigestible to malaria parasites so gene perisists despite its harmful effects to
Hemophilia- coagulation disorder:
-genetic lack of any clotting factors affect coagulation
-sex-linked recessive in males (inherited from mother)
-hemophiliaAis missing clotting factor VIII (83%)
-hemophilia B is missing clotting factor IX (15%)
-physical exertion causes bleeding & excruciating pain-- transfusion of plasma or purified
clotting factors; factor VIII now produced by transgenic bacteria
DIC- coagulation disorder-- Disseminated Intravascular Coagulation
-widespread clotting of blood within unbroken vessels
-triggers by bacteria (septicemia) or if blood slows down or stops as in cardiac arrest
Prevention of inappropriate coagulation: platelet repulsion, thrombin dilution, or natural
Platelet repulsion: platelets do NOT adhere to prostacyclin-coating
Thrombin dilution: normally diluted by rapidly flowing blood-- heart slowing in shock can
result in clot formation
Natural anti-coagulants: Antithrombin produced by the liver which deactivates thrombin
before it can act on fibrinogen; Heparin is secreted by basophils and mast cells that interfere
with formation of prothrombin activator.
Gene: unit of information from sequence of DNAnucleotides that codes for a specific trait
Alleles: alternative forms of the same gene
In ABO genetics-- the alleles for blood type areA, B, and O:
2 A, or Aand O=typeA
2 B, or B and O=type B
2 O results in= type O
Aand B results= type AB “codominant”
In Rh bloodtype genetics-- the alleles for blood type are + and -
+ is dominant to -, so only one + is necessary to make a person Rh+
Two +, or + and - results in = type Rh+
Two - results in =type Rh-
1. You have all seen movies of people stranded in the ocean aboard lifeboats. The
people are surrounded by water yet they cannot drink the seawater. The seawater would: 4
Increase the blood osmolality, and the tissues would become more dehydrated.
2. If skin and sclera turn yellow, there is an excess of ____ in the blood.
3. Aleukocyte count above 10,000 cells/ml of blood would indicate
4. Someone with blood typeAB-positive could donate blood to which of the following
5. Someone with blood typeAB-positive could receive blood from which of the
following blood types?
A+/-, B+/-,AB+/-, O+/-
6. Aperson with blood typeA-negative, can donate blood to someone with which blood
AB-neg, AB+,A-neg, A+
7. Awoman with blood typeAB marries a man with blood type O. What blood types
may be seen in their offspring?
8. Awoman with blood typeAmarries a man with blood type O. What blood types
may be seen in their offspring?
9. Awoman who is Rh-negative marries a man with Rh-positive blood. What blood
types may be seen in their offspring?
Both Rh-neg and Rh+
Located in thoracic cavity, specifically in mediastinum- (area between lungs)
– superior to diaphragm
– posterior to sternum
– 2/3 of heart to the left of midsagittal plane due to the liver taking space on the right
• Double walled membranous sac
• Anchored to diaphragm at the bottom & connective tissue elsewhere
• Allows heart to beat without friction, room to expand and resists excessive expansion
– outer, tough, fibrous layer of connective tissue
– folds over to become the visceral pericardium
Visceral pericardium (a.k.a. epicardium of heart wall-outermost layer of heart)
– inner, thin, smooth, moist serous layer covers heart surface
Pericardial cavity– space between parietal & visceral
– filled with pericardial fluid to reduce friction 5
Flow of blood through the heart:
Superior/inferior vena cava (carrying deoxygenated blood from the body) →
Right atrium →
Right atrioventricular (AV) or tricuspid valve →
Right ventricle →
Pulmonary semilunar valve →
Pulmonary trunk (1 part of pulmonary artery) →
Lung (CO2 discharged, O2 absorbed) →
Pulmonary veins (only veins that carry oxygenated blood) →
Left atrium →
Left atrioventricular (AV), bicuspid or mitral valve →
Left ventricle →
Aortic semilunar valve →
AV valves hang open & SL valves are closed when the ventricles are relaxed →
Ventricles fill with blood and then contract →
Pressure & blood in the ventricles push the AV valves closed (chordae tendinae prevent cusps
from bulging into the atria) →
The same pressure and blood pushes SL valves open →
Ventricles relax →
Blood flows back down the pulmonary trunk and aorta; fills cusps to force SL valves closed
Flow through the cardiac conduction system:
“Explanation from textbook”: Action potentials originate in the SAnode and travel across
the wall of the atrium from the SAnode to theAV node.APs pass slowly thruAV node to give
the atria time to contract. They then pass rapidly along theAV bundle, which extends from the
AV node thru the fibrous skeleton into the IV septum. TheAV bundle divides into right and left
bundle branches, andAPs descend rapidly to the apex of each ventricle along the bundle
branches.APs are carried by the purkinje fibers from the bundle branches to the ventricular
walls. The rapid conduction from theAV bundle to the ends of the purkinje fibers allows the
ventricular muscle cells to contract in unison, providing a strong contraction.
Myogenic - heartbeat originates within heart, not brain
Autorhymthic - depolarize spontaneously regularly
– SAnode: pacemaker; initiates heartbeat; sets heart rate; signal spreads through both atria;
located in roof of right atrium
– AV node: electrical gateway to ventricles ; located in side wall of right atria; can take over
pacemaker role if SAnode fails
– AV bundle (Bundle of His): pathway for signals fromAV node
– Right and left bundle branches: divisions ofAV bundle that enter interventricular septum
and descend to apex
– Purkinje fibers: upward from apex spread throughout ventricular myocardium 6
Systole = contraction;
Sinus rhythm – normal rhythm set by SAnode
– adult at rest is 70 to 80 bpm
Ectopic Foci – region other than SAnode sets rhythm
– nodal rhythm - set byAV node; 40 to 50 bpm
– intrinsic ventricular rhythm – AV bundle; 20-40 bpm (not enough to sustain normal
functioning so artificial pacemaker is implanted)
Arrythmia - abnormal cardiac rhythm; On ECG would be conduction failure atAV node
– caused by number of things including bundle disease/degeneration
Ventricular fibrillation (V-Fib) – uncoordinated contraction
– ventricles spasm→ heart cannot pump→ cardiac arrest
– defibrillation – strong electrical shock to depolarize myocardium and restore normal
• Amount ejected by each ventricle in 1 MIN
• CO= HR X SV
• Resting values: CO = 75 beats/min x70 ml/beat = 5,250 ml/min, usually about 4 to 6L/min
– this means that all of the body’s blood is circulated in 1 minute (*a RBC leaving the
heart will return in 1 min)
• Vigorous exercise increases CO to 21 L/min for a fit person and up to 35 L/min for world
class athlete (*they have a lower heart rate, but a higher stroke volume)
• Cardiac reserve: difference between CO maximum (during exercise) and resting CO
– Heart disease = little or no cardiac reserve
Effects of exercise:
• Effect of proprioceptors:
– HR increases at beginning of exercise due to signals from joints, muscles
• Effect of venous return:
– muscular activity increases venous return causes increased stroke volume (SV) 7
• Increased HR and increased SV cause increased CO
• Effect of ventricular hypertrophy:
– caused by sustained program of exercise
– Increased SV allows heart to beat more slowly at rest, 40-60bpm
– Incresed cardiac reserve, can tolerate more exertion
Diseases & disorders:
– Inflammation of the pericardium
– Painful friction between the two membranes when the heart beats
– Abnormal accumulation of fluid in the pericardial cavity
– Compresses the heart
– Interferes with ventricular filling
• The chamber of the heart most affected by cardiac tamponade is the right
• Heart attack - sudden death of heart tissue
• Caused by interruption of blood flow from the narrowing or occlusion of an
artery supplying the heart with blood
• Usually fat deposits or blood clots are responsible
• Lack of O →2ischemia
• If O 2upply is not restored, necrosis (tissue death) of myocardium occurs
• Responsible for ~1/2 of all deaths in United States
* Anastomoses defend against interruption by providing alternate blood
• Heart pain due to temporary and REVERSIBLE myocardial ischemia
Myocardium undergoes anaerobic fermentation →
Lactic acid is produced →
Pain receptors are stimulated.
• Fatty deposits form in a coronary artery
• Due to abnormal uptake of plasma lipids (ie. cholesterol) by the cells of the
• Corrected by:
– by-pass surgery – a blood vessel from elsewhere in the body is used to
direct blood flow around the area of blockage
– balloon angioplasty – balloon is inflated in the artery to push the fatty
deposit up against the blood vessel wall
– laser angioplasty – laser used to destroy fatty deposit
Ventricular fibrillation(V-FIB) – uncoordinated contraction
– ventricles spasm → heart can’t pump → cardiac arrest
– defibrillation – strong electrical shock to depolarize myocardium and restore
• sound of blood flowing backward due to valvular insufficiency
-Valvcular stenosis-- cusps are stiffened
-Mitral valve prolapse-- mitral valve cusps culge into left atrium 8
– an incompetent valve can eventually lead to heart failure
– defective valves can be replaced: pig valve or artificial valve
Congestive heart failure-
• a weakness of the heart that leads to a buildup of fluid in the lungs and
surrounding body tissues.
1. Complete cessation of a heartbeat is called
2. Ablockage in the ___________ would cause the most damage to the heart.
Left coronary artery
3. The heart does not receive any signals from the nervous system.
4. Repolarization of the ventricles produces the ______ of the ECG.
5. Aheart rate of 45 bpm and no Pwave on an ECG indicates
6. In an angiogram, the blood vessels are injected with a dye so that they may be
visualized. The angiogram is used to detect
Most common route:
heart→ arteries → arterioles → capillaries → venules → veins 9
Portal system: blood flows thru 2 consectutive capillary networks before returning to the heart
Shunts and anastomoses:
Anastomoses= 2 arteries/veins merge
Arteriovenous shunt: artery directly to vein i.e. fingers, toes, and ears. This reduces heat loss,
blood bypasses cold exposed areas, areas are vulnerable to frostbite.
Venous anastomsis: 2 veins merge-- very common; alternate drainage of organs.
Arterial anastomosis: alternative routes of blood flow; common around joints where
movement can obstruct one pathway.
Contrast arteries and veins:
Arteries: more muscular than veins (smooth muscle) & thicker, can withstand great pressure
from ventricular systole, perforated elastic tissue for expanding and recoiling, distribute blood
Veins: very porous, little smooth muscle/elastic tissue, exchange fluid w/ tissues at a specific
site, thin walls, lower BP, expand easily, aid skeletal muscles in upward flow, collapse when
empty, carry 54% of blood
What tissues have few/no capillaries?
-cartilage, cornea and lens of the eye
Blood pressure: Highest in blood vessels closest to heart
Diastolic: minimum BP between heartbeats
Systolic: peak BP during ventricular systole
Normal values: 120/80
-peripheral resistance: blood viscosity by RBCS and albumin (decreased viscocity with
anemia, hypoproteinemia; increased viscosity with polycythemia, dehydration); vessel length
with pressure and flow decline with distance; vessel radius is very powerful influence over
flow-- radius is the most adjustable variable and controls resistance very quickly. Vasomotion is
the change in vessel radius i.e. vasoconstriction, vasodilation. 10
Angiogenesis- local control of regulating BP and flow
=growth of new vessels
-regrowth of uterine lining, around obstructions, exercise, and malignant tumors
-controlled by growth factors and inhibitors
Causes and consequences of edema:
-Increased capillary filtration: (increased capillary BP or permeability)
>Poor venous return-- CHF, insufficient muscular activity
>Kidney failure (water retention, hypertension)
>Histamine makes capillaries more permeable
>Increased age → increased capillary permeability
-Reduced capillary reabsorption: not enough protein in blood (hypoproteinemia) → reduced
osmosis from tissue
>Cirrhosis: liver does not produce enough albumin
>Famine: dietary protein deficiency
>Protein excreted in urine-- burns, radiation sickness, kidney disease
-Obstructed lymphatic drainage: lymphatic vessels usually absorb fluid from tissues & return it
to bloodstream. Caused by obstructed lymphatic vessels or removal of lymph nodes.
-Circulatory shock: excess fluid in tissue spaces causes low blood volume and low BP
-Tissue necrosis: oxygen delivery and waste remove become impaired
-Pulmonary edema: suffocation
-Cerebral edema: headaches, nausea, seizures, and coma
Diseases & disorders:
Hypertension: most common cardio problem
>chronic resting BP greater than > 140/90
>30% ofAmericans over 50 y.o
>50% ofAmericans over 74 y.o
>Major cause of heart failure, stroke, & kidney failure
>ventricles must work harder
> myocardium enlarges → stretches and becomes less efficient strains by → endothelium tears
>can weaken small arteries and cause aneurysms
>arterioles in kidneys thicken → blood flow declines
1° Hypertension: due to obesity (need more bv → increases heart workload); sedentary
(exercise controls weight, reduces emotional tension and stimulates vasodilation); diet (high
cholesterol/fat → atherosclerosis; potassium and magnesium can reduce BP; now saying salt is
unrelated maybe); nicotine (stimulant-- makes heart beat faster and harder thus promotes
vasoconstriction → MI); & genetics (some are predisposed to HTN; more common in men
from 18-54 y.o, but then becomes more common in women over 65 y.o.)
2° Hypertension: caused by another disease.
Hypotension: chronic low resting BP
>Causes: blood loss, dehydration, anemia
-weak point in blood vessel or heart wall 11
-bulging sac forms and pulsates with each heartbeat
-can cause pain or death by exerting pressure on brain, nerve, air passages, or esophagus
-can lead to neurological disorders, congestion of tissues, cough, difficulty breathing or
Caused by: hypertension, artherosclerosis, congenital weakness of blood vessels, trauma,
*Dissecting aneurysm- blood pools between tunics causing degeneration of the tunica media
Shock – all types: any state where cardiac output is insufficient to meet
-Cardiogenic shock: inadequate pumping of heart (MI)
-Low venous return (LVR) Shock:
1) Hypovolemic shock- loss of blood volume (most common); from hemorrhage, trauma, bleeding
ulcers, burns & dehydration
2) Obstructed venous return shock- tumor or aneurysm
3) Venous pooling (vascular) shock- long periods of standing, sitting or widespread
4) Neurogenic shock- loss of vasomotor tone; caused from emotional shock to brainstem injury
5) Septic shock- bacterial toxins trigger vasodilation and increased capillary permeability
6) Anaphylactic shock- severe immune reaction causes generalized vasodilation and increased
TIA- transient ischemic attack:
-dizziness, loss of vision, weakness, paralysis, headache
-lasts from a moment to a few hours
-often early warming of impending stroke
CVA- cerebral vascular accident
-brain infarction caused by ischemia-- atherosclerosis, thrombosis, ruptured aneurysm
-effects range from unnoticable to fatal-- blindness, paralysis, loss of sensation, loss of speech
1. In cold conditions, it is crucial to keep vital organs of the body warm. Acirculatory
adaptation to conserve body heat is
2. If all of the arteries of the body dilated at once, what would happen?
Blood pressure would decrease
3. How does drinking alcohol affect blood pressure?
It depends on when BP is measured
4. Which of the following should occur if you had hypertension?
ANF would be released
Conducting verses respiratory divisions:
Conducting division: passages serve only for airflow, nostrils to bronchioles
Respiratory division: alevoli and distal gas-exhchange region.
Upper verses lower respiratory tract: 12
Upper: is larynx and above- organs in head and neck; nose through larynx.
Lower is trachea and below- organs of the thorax, trachea through lungs.
Pleurae- 2 membrane layers - visceral and parietal layers
• Visceral pleura– inner moist serous membrane; folds over
• Parietal pleura – outer layer
– adheres to mediastinum, diaphragm, rib cage
– pulmonary ligament extends from base of each lung to diaphragm
• Pleural cavity– space between pleurae; contains pleural fluid
– reduction of friction
– creation of pressure gradient
• lower pressure assists in inflation of lungs
• prevents spread of infection
-Presence of air in pleural cavity. The loss of negative intrapleural pressure allows lungs to
recoil and collapse.
Resistance to airflow-The greater the resistance, the slower the air flow.
Pulmonary compliance is the distensibility of the lungs. Decreased in disease with pulmonary
Bronchiolar diameter is the primary control over resistance to airflow:
-Bronchoconstriction: triggered by airborne irritants, cold air, parasympathetic stimulation,
-Bronchodilation: sympathetic nerves, epinephrine
-air inhaled or exhaled in one quiet breath (500 ml)
-amount of air that can be exhaled with maximum effort after maximum inspiration; assess
strength of thoracic muscles and pulmonary function
Primary stimulus of respiration= pH of CSF
-Respiratory acidosis when pH is less than 7.35 caused by failure of pulmonary ventilation→
-Respiratory alkalosis when pH is greater than 7.35 → hypocapnia.
Hypercapnia/hypocapnia– what effects will they cause and how will the body
Hypercapnia- (PCO2) is greater than > 43 mmHg. “Too much oxygen.”
-CO2 easily crosses brain-blood barrier, in CSF the CO2 reacts with water and releases H+,
central chemoreceptors strongly stimulate inspiratory center.
-Corrected by hyperventilation. Pushes reaction to left by “blowing off” CO2
- CO2 (expired) + H2O ← H2CO3 ← HCO3- + H+
Hypocapnia- (PCO2) is less than < 37 mmHg. “Not enough oxygen.”
-Corrected by hypoventilation, pushes reaction to right.
- CO2 + H2O → H2CO3 → HCO3- + H+
-Increased H+ will lower pH back to normal
*pH imbalances can have metabolic causes-- DM: fat oxidation causes ketoacidosis, can be
compensated for by Kussmaul respiration (deep rapid breathing) 13
Apnea-temporary cessation of breathing
Hyperventillation- increase in excess of metabolic demands. CO2 expelled too fast, this
increases blood pH; often due to anxiety!
Diseases and disorders:
Ondine’s curse-automatic respiratory functions do not work so much remember
to take each and every breath. Need to use ventilator while sleeping. Results from damage to
brain stem i.e. tramua or poliomyelitis.
-alveolar walls break down, much less respiratory membrane for gas exchange, lungs fibrotic
and less elastic, air passages collapse and obstruct outflow of air, air becomes trapped in lungs.
- allergen triggers histamine release, intense bronchoconstriction
-alveoli filled with fluid
-caused by: stretococcus pneumoniae, other bacteria, viruses, fungi, and protozoa
-fibrosis of lungs
-Mycobacteria infect lungs → lung forms tubercles around the invaders
- “Bends” N2 bubbles in joints, bones, muscles, pulmonary capillaries
1) TheAdam’sApple is an area of the thyroid cartilage of the larynx that is usually
more prominent in men. What could be a logical cause of the size difference?
Testosterone stimulates the growth of the cartilage
2) Atracheostomy is the surgical creation of an opening in the trachea to bypass the
upper respiratory tract if it becomes obstructed. What could be a complication of this
Membranes of the respiratory tract dry out
3) The muscles used for respiration (inhalation & exhalation) are:
4) In pleurisy, the pleural membranes can become dry and inflamed. Each breath
results in painful friction between the parietal and visceral pleura. This is similar to :
5) When you inhale, does your chest expand because your lungs inflate, or do your
lungs inflate because your chest expands?
Chest expands first
6) Which of these values should be the highest?
Lymphatic & Immune Systems
-Protect body from infections and disease
-Maintain fluid balance
-- absorbs plasma protein and tissue fluid and returns it to the bloodstream, 2-4 L/per
-- interference with lymphatic drainage can lead to severe edema
Lymph-clear fluid; similar to plasma but contains much less protein. Flows at low pressure and
Lymphatic capillaries-closed at one end; tethered by protein filaments; endothelial cells
overlapped-- this allows bacteria and cells entry to lymphatic capillary; and creates valve-like
flaps that open when interstitial fluid pressure is high, and close when its low and valve open
up; closed down to prevent blackflow
Mechanisms of flow:
-Lymph flows at low pressure and speed.
-Valves prevents backward flow.
-Moved along primarily by rhythmic contractions of lymphatic vessels (stretching of vessels
-Flow is aided by skeletal muscle pump.
-Thoracic pump aids flow from abdominal to thoracic cavity.
-Rapidly flowing bloodstream in subclavian veins, draws lymph into it.
-Exercise significantly increases lymphatic return
Route of lymphatic flow: lymphatic capillaries→ collecting vessels→ lymphatic trunk→
collecting ducts (right lymphatic duct or thoracic duct) → subclavian vein.
Functions of: lymph nodes, tonsils, thymus & spleen
-only organ that filters lymph
-fewer efferent vessels, slows flow thru node: reticular cells, macrophages phagocytize foreign
-lymphocytes respond to antigens
-common sites for metastaic cancer
-covered by epitelium, pathogens get into crypts and encounter lymphocytes
-pharyngeal (on wall of pharynx); palatine (2 of them), can see them and can be removed;
lingual (2 of them), root of tongue
-contains developing t-lymphocytes
-secretes hormones (thymopoietin & thymosins)
-very large in fetus, after age 14 begings involution
-in elderly, mostly composed of fatty and fibrous tissue
-cortex gives off trabeculae, divide parenchyma into lobules of cortex and medulla
-blood production in fetus
-immune reactions: filters blood, quick to detect antigens
-broadly effective, no prior exposure
-inflammation, fever 15
-From Textbook: external barriers, leukocytes and macrophages, antimicrobial proteins,
immune surveillance, inflammation and fever; guard equally against a broad range of
pathogens and their effectiveness does not depend on prior exposure, present from birth.
Skin: toughness of keratin; dry and nutrient-poor; defensins: peptides, from neutrophils attack
microbes; lactic acid (acid mantle) is a component of perspiration
Mucous membrane: stickiness of mucus; lysozyme: enzyme destroys bacterial cell walls
Subepithelial areolar tissue: tissue gel-- viscous barrier of hyaluronic acid; hyaluronidase--
enzyme used by pathogens
-defensive response to tissue injury
-limits spread of pathogens, then destroys them; removes debris, initiates tissue repair
-erythemia (caused by hyperemia);
-edema (caused by increased capillary permeability and filtration);
-heat (caused by hyperemia);
-pain (caused by inflammatory chemicals i.e. bradykinin, prostaglandins which are secreted by
damaged cells, puts pressure on nerves
-defense mechanism: can do more good than harm
-promotes interferon activity
-accelerating metabolic rate and tissue repair
-inhibiting pathogen reproduction
-Pyrogen: secreted by macrophages, stimualtes anterior hypothalamus to secrete PGE which
resets body thermostat higher - 102° F. Fever greater than 105° may cause delirium, 111°-115°
lead to coma-death.
Stages of fever: onset, stadium, defervescence
Types of non-specific WBCs:
– phagocytize bacteria
– create a killing zone
• degranulation: lysosomes discharge into tissue flui.- triggers
• respiratory burst: toxic chemicals are created (O 2 H O2, 2ClO)
– phagocytize antigen-antibody complexes, allergens, inflammatory chemicals
– enzymes block excess inflammation, limit action of histamine
– antiparasitic effects: aggregate and release enzymes
– aid mobility and action of WBC’s by the release of:
• histamine (vasodilator) increases blood flow to infected tissue
• heparin (anticoagulant) prevents immobilization of phagocytes
– natural killer (NK) cells, nonspecific defense, large cells lyse host cells infected with viruses
– circulating precursors to macrophages
Interferons- antimicrobial proteins:
-Polypeptides secreted by cells invaded by viruses
-Antiviral effect: generalized protection, interferons diffuse to neighboring cells and stimulate
them to produce antiviral proteins; activates natural killer cells and macrophages which destroy
infected host cells
-Anticancer effect: stimulates destruction of cancer cells
Mechanisms of complement action: group of proteins in blood that must be activated by
pathogens to exert their effect.
• Pathways of complement activation
– classical pathway
– alternate pathway
• *Mechanisms of action:*
– Enhanced inflammation-stimulates release of inflammatory chemicals
– Opsonization- promotes phagocytosis
– Cytolysis- membrane attack complex (MAC)
• MembraneAttack Complex= Complement proteins form a ring in plasma membrane of
enemy cell causing cytolysis
-Specificity and memory
• Humoral immunity: antibody mediated. From book: employs antibodies that do not
directly estroy pathogen but tag them for destruction by mechanisms. Effective against
extracellular viruses, bacterias, yeasts, protozoans, and noncellular pathogens such as toxins,
venoms, and allergens. Only works against extracellular stages of infectious microorganisms.
• Cellular immunity: cell-mediated. From book: employs lymphocytes that directly attack
and destroy foreign cells or diseased host cells. Way to rid body of pathogens that reside in
human cells where they are inaccessible to antibodies i.e. intracellular viruses, bacteria, yeasts,
and protozoans.Also acts against parasitic worms, cancer cells, and cells of transplanted tissues
-Triggers an immune response
-Complex molecules i.e. proteins, polysaccharides, glycoproteins, glycolipids
Antibodies (you don’t need to know the 5 specific types):
• By amino acid sequences of C region of antibody
• IgA: monomer in plasma; dimer in mucus, saliva tears, milk, intestinal secretions, prevents
adherence to epithelia
• IgD: monomer; B cell membrane, antigen receptor
• IgE: monomer; tonsils, skin, mucous membranes; stimulates release of histamines, attracts
• IgG: monomer; 75-85% circulating, crosses placenta to fetus, secondary immune response,
• IgM: monomer; B cell membrane, antigen receptor; pentamer in plasma, 1° immune
Humoral verses cellular specific immunity. What types of WBCs in each? What types of 17
pathogens does each protect against?
>Humoral is antibody mediated.
• Recognition- B cells recognize antigen, divide repeatedly, differentiate into plasma cells,
produce antibodies specific to that antigen.
Capping and endocytosis: antigen binds to several receptor sites on membrane of B cell.
Receptor sites are drawn together into a cluster (looks like a worm).Antigen is taken into B
cell by receptor-mediated endocytosis.Antigen is fully internalized.
Display, clonal selection & plasma cell differentiation: 1) Immunocompetent B cells exposed
to antigen.Antigen binds only to B cells with complementary receptors. 2) B cell displays
processed antigen fragments. Helper T cell binds to B cell and secretes helper factor. 3) Helper
factor stimulates B cell to divide repeatedly and form a clone. 4) Some cells of the clone
become memory B cells. Most differentiate into plasma cells. 5) Plasma cells synthesize and
• Attack- plasma cells release antibodies, bind to antigen, render it harmless, ‘tag it’for
Neutralization: antibodies mask pathogenic region of antigen
Complement fixation: antigen binds to IgM or IgG, antibody changes shape, initiates
complement binding; primary defense against foreign cells & bacteria
Agglutination: Antibody has 2-10 binding sites, binds to multiple enemy cells immobilizing
Precipitation: similar process, antibody binds antigen molecules not cells; creates antigen-
antibody complex that precipitates, phagocytized by eosinophil
• Memory- some B cells differentiate into memory cells
>Cellular is cell-mediated.
• Lymphocytes attack and destroy foreign cells and diseased host cells
• Cytotoxic (CD8) T cells - carry out attack
• Helper (CD4) T cells - promote cytotoxic T cell action and coordinate other defenses
• Suppressor T cells - limit attack
• Delayed-hypersensitivity T cells – allergic reaction
• Memory T cells - descended from cytotoxic T cells
• Role of MHC-I proteins
– found on nearly all body cells
– display antigens produced by host cells
– stimulate attack by cytotoxic T cells
• Role of MHC-II proteins
– found only on antigen presenting cells
– stimulate helper T cells
• MHC restriction: T cells in thymus develop receptors for either MHC-I or MHC-II proteins
• T CellActivation: CD4 and CD8 proteins
– CAMs that bind T cell to target cell
– Linked to 2nd messenger system that triggers clonal selection: activated T cell enlarges,
multiples, forms clone of identical T cells
– Clonal selection requires costimulation
helper T cells binds to macrophage
macrophage releases interleukin-1
stimulates helper T cell to release and synthesize receptors for interleukin-2 18
causes large population of activated T cells
Attack phase: role of helper T cells which secrete lymphokines and coordinate humoral and
Memory: memory T cells- following clonal selection some, cells become memory cells. T cell
recall response-- upon reexposure to same pathogen, memory cells launch a quick attack
Primary verses secondary immune response:
– Complement fixation: antigen binds to IgM or IgG,Antibody changes shape, initiates
complement binding; primary defense against foreign cells, bacteria
– IgG: monomer; 75-85% circulating, crosses placenta to fetus, secondary immune response,
– Hypersensitivity (Allergy)
Excessive immune reaction against antigens that most people tolerate - allergens
Major histocompatibility complex: family of genes on chromosome 6 that code for MHC
proteins on theAPC surface that each as identification tags. When anAPC encounters an
antigen, it internalizes via endocytosis, digests it and displays epitopes in grooves of the MHC
proteins-- this is known as antigen processing.
-Allergies & asthma
2 types of hypersensitivity: allergy & autoimmunity
Allergy: excessive immune reaction against atnigens that most people tolerate-- allergens.
Type 1 (acute) hypersensitivity- anaphylaxis occurs in sensitized people, allergen caps IgE on
mast cells, basophils; release inflammatory chemicals, cause local edema, mucous
hypersectretion, congestion; hives, water eyes, runny nose are typical
Asthma (most common chronic illness in children)- inhaled allergens, histamines, bronchiole
Anaphylactic shock: bronchiolar constriction, dyspnea, vasodilation, shock, death;
Type III (immune complex) hypersensitivity:
widespread antigen-antibody complexing
complexes trigger intesnse inflammation, involved in acute glomerulonephritis and in systemic
What can cause a failure of self-tolerance?
Failure of self tolerance: 19
– Failure of cross-reactivity/antigenic mimicry
• foreign antigens may be similar to self-antigens
– abnormal exposure of self-antigens - barrier breach
• Blood-testis barrier
– changes in structure of self-antigens
• induction by viruses
– failure of clonal deletion in the thymus
Production of autoantibodies
SCID- severe combines immunodeficiency disease
– hereditary lack of T and B cells
– vulnerability to opportunistic infection
– Invades helper T cells, macrophages, neutrophils and brain cells by “tricking” them to
internalize the viruses by receptor mediated endocytosis
– Retrovirus - reverse transcriptase uses viral RNA as template to synthesize DNA:
• new DNAinserted into host cell DNA
• may be dormant for months to years
1) If the right lymphatic duct was blocked, where might you see lymphedema?
The right arm
2) Should tonsils routinely be removed if they become infected?
3) In what situation would we derive the most benefit from inflammation?
Alaceration to the arm
4) If parasitic worms infest the body, which type of white blood cells will be prevalent?
5) If you are vaccinated for polio, what type of immunity is produced?
Artificial active immunity
6) The humoral immune response would be most effective against which of the
7) Which type of cells help to control type I allergic reactions?
Posterior pituitary hormones and their general actions
Stores and releases OT andADH which are produced in hypothalamus, transported down to 20
posterior love by hypothalamo-hypophyseal tract and the posterior pituitary secretes them.
Nerve signals trigger release of these hormones.
OT- labor contractions and milk release (lactation-ejection); synthetic forms of OT are used to
induce labor in pregnant women.
ADH- promotes water retention by the kidneys in response to low blood pressure
Anterior pituitary hormones and their general actions
Tropic hormones target other endocrine glands.
Gonadotropins target gonads i.e. FSH & LH
TSH a.k.a. Thyrotropin
ACTH a.k.a. Corticotropin
GH a.k.a. Somatotropin
Pituitary-gonadal axis, pituitary-adrenal axis, and pituitary-thyroid axis: principle hormones
and target organs shown, most hormone production declines with age.
FSH- Ovaries—stimulates development of eggs and follicles
Testes—stimulates production of sperm
LH- Females—stimulates ovulation → progesterone secretion
Males—stimulates testosterone secretion
ACTH- regulates milk synthesis, effect on adrenal cortex of the adrenal glands and secretion
of glucocorticoids; regulates secretion of insulin from the pancreases
PRL- Female—milk synthesis in mammary glands
Male—increases LH sensitivity, thus increases testosterone secretion
ADH- targets kidneys to increase water retention, reduce urine—which prevents dehydration;
ADH also functions as a neurotransmitter.
OT- Female—labor contractions, lactation (OT stimulates ejection of milk while PRL
stimulates the production of milk)
Male—possible roles in sperm transport & emotional bonding
Both—surges during sexual arousal and orgasm by the propulsion of semen and uterine
GH- pituitary produces at least 1000x more GH than any other hormones. GH targets liver to
produce somatomedins (insulin-like growth factors) which increase mitosis and cellular
differentiation for tissue growth—protein synthesis, lipid metabolism, carbohydrate
metabolism, electrolyte balance via promotes Na+, K+, Cl- retention, Ca2+ absorption.
During childhood, GH involved with bone/cartilage/muscle growth.
During adulthood, GH involved with osteoblastic activity, appositional growth affecting bone
thickening and remodeling.
Levels of GH: HIGHER during first 2 hours of deep sleep, after high protein meals, after
vigorous exercise; LOWER after high carbohydrate meals. Declines with age→ less protein
synthesis =Aging. At age 30 there is 10% bone, 30% muscle, and 20% fat and at age 75 there
is 8% bone, 15% muscle, and 40% fat.
Increases target organ hormone levels inhibit release of tropic hormones.
-Pituitary dwarfism which is in childhood with DECREASED GH.
-Panhypo-pituitarism which is complete cessation of pituitary secretion, causes broad range
of disorders including infertility