Review Sheet B Test #2 Biology 2213 Dr. James Adams
Chapter 20 B Lymphatic System
and Lymphoid Organs/Tissues
Two functions: Circulatory, Immune
Circulatory function: Lymphatic Vessels
3 liters of fluid lost from (fenestrated) capillaries daily, returned to circulatory system
via lymph vessels.
Lymphatic capillaries: dead ended in tissues.
Cells of simple squam. E act like minivalves;
allow in fluid, bacteria, etc. Distal ends of cells anchored by collagen
fibers.
Lymphatic trunks (veins): like circulatory veins;
the same factors that aid venous return
aid lymph transport (a pumpless system)
Know: Lumbar, intestinal, bronchomediastinal, subclavian, jugular
trunks; cisterna
chyli,
thoracic duct, right lymphatic duct (these dump lymph into circ. system at juncture of
internal jugular vein and subclavian vein);
also know lacteals
Immune Function: Lymphoid Tissues -- framework of
reticular CT
Lymphoid Cells B Lymphocytes/macrophages/dendritic
cells (See immune system,
below); reticular cells (secrete reticular fibers of stroma of lymphoid organs)
Diffuse Lymphatic Tissue -- found throughout walls of most
mucosal membranes
Lymphoid Organs -- primary: where B & T cells mature -- bone marrow,
thymus
secondary: where lymphocytes encounter antigens and are activated.
I. Lymph nodes -- cortex (with lymphocytes [follicles, w/germinal centers]), medulla
(with macrophages), capsule with trabeculae, stroma (reticular network)
Found where many smaller (afferent) vessels come together; fewer efferent vessels
(exit at hilus) causes lymph to slowly percolate through sinuses of nodes,
which gives time for lymph to be cleaned. ONLY lymph organs to
clean lymph.
Concentration where
"appendages" attach to trunk (inguinal, axillary, cervical
regions)
"Buboes": Infected -- swollen and painful; Cancerous B
swollen, with little pain initially
Other lymphoid organs: all have supportive reticular networks, stored macrophages/
lymphocytes, efferent (but no afferent) lymphatic vessels
so cannot filter/clean lymph
II. Spleen -- left side beneath diaphragm;
hilum -- main entry/exit point for nerves/vessels
Functions: like lymph nodes, site of immune surveillance
(macs./lymphs.) Also blood
filter (includes removing old RBC=s/platelets), stores
(complexed) iron (from old
hemoglobin), stores platelets.
Produces RBC's in fetus.
Anat.: red pulp - processes
RBC's/platelets; white pulp - follicle "islands" in red pulp
III. Tonsils -- pharyngeal (adenoids), palatine, lingual, tubal
Obvious germinal centers for lymphocytes.
Not fully
encapsulated to allow entry of bacteria for activation of immune system;
however, crypts may be easily infected
IV. Peyer=s Patches --
lymphoid nodules, at end of ileum (small intestine)
V.
Appendix -- off of cecum (beginning of large intestine); many
lymphoid follicles
Tonsils, Peyer=s Patches, and
appendix, along with diffuse lymphatic tissue in the
mucosal
linings, make up the MALT (Mucosal Associated Lymphatic Tissue)
VI. Thymus -- functions early in life; activates T lymphocytes
Cortex/medulla, with epithelial tissue
(star-shaped thymocytes) framework -- these
thymocytes are the source of the lymphocyte activating hormones.
Chapter 21 B Immune System:
Innate and Adaptive Defenses
Functional System -- main components: lymphocytes (specific) and macrophages (non-
specific) functions: Direct cell attack,
antibody production against foreign antigens.
Innate defenses, though originally considered non-specific,
do respond to some very
specific
chemicals, many of which are the same that the adaptive respond to, and many
of which are released by both as well. Indeed, the innate is often responsible
for alerting
the adaptive
defenses. The adaptive defenses are very specific, but must be primed
(by exposure).
I. Non-specific (Innate) defenses
A. Surface membrane barriers:
cutaneous/mucus membranes -- First Line of defense
keratin of
stratified squamous epithelium of skin, mucus (sticky) of mucus membs.
Chemical protection (of membs.):
mucus, sebum, lysozyme (saliva, tears), acids,
defensins, etc.
B. Cellular/Chemical defenses (if surfaces breached)
-- Second Line of defense
1. phagocytosis (macrophages,
neutrophils, eosinophils)
2. natural killer cells (non-specific
"lymphocytes")
-- drop chemical "bombs" on
tumor/viral-infected cells
3. Inflammatory response
(initiated by chemicals [histamine, prostaglandins, kinins,
lymphokines, etc.] released by many different cells [basophils, etc.])
importance: prevents spread of "nasties" into nearby tisues, dilutes/loosens
cell debris/pathogens for disposal, alerts the immune sys., initiates repair
4. antimicrobial substances (interferons, complement)
5. fever
(pyrogens) -- How does fever help?
II. Specific Defenses -- The
Immune response -- Third Line of defense
(nice summary,
Focus Fig.
21.1, pgs. 808-809; Table 21.8, pg. 810)
Characteristics: Specific, memory, systemic
Immunity:
Humoral (antibodies [Ab=s], produced by B lymphoctyes)
Cell-mediated (T lymphocytes).
Immunocompetence (mature and able to recognize antigens) in R-bone
marrow and thymus respectively
Antigens activate certain pre-existing populations of B cells (free-floating
antigens
immunogenic and reactive)
and T cells (through antigen-presenting macrophages) to
divide, producing plasma cells,
for current usage (lots of rER in B cells for making
Ab=s [2000 per second]) and memory cells
(for secondary response). Antigens may
have > one antigenic determinant
(p. 791). Haptens (p.
791) and allergies (p. 811)
Self-Antigens: Major Histocompatibility complex (MHC) proteins (see * below)
Antigen receptor and Ab diversity: involves genetic
recombination -- Know basic idea
Other cells of
the immune response -- Macrophages, although non-specific, activate
helper T lymphocytes by
presenting antigens (APC's), which, in turn, activate more
lymphocytes (both B & T
cells) and macrophages, which also phagocytize Ab covered
antigens (rough foreign particles).
Dendritic cells and even B cells can also activate helper
T cells
by presenting antigens as well.
Humoral Response -- B-Cell Activation (free-floating antigens); B-cells release
Antibodies: structure
-- two heavy
(±400 A.A.) and two light (±200 A.A.) chains,
each with constant (between all Ab types) and variable (for attachment to Ag=s)
regions (Fig.
21.14, pg. 798). Some classes with multiple Ab units.
Activation pro-
duces plasma and
memory cells, which give you protection with a second and future
exposure. See primary and secondary humoral response (Fig. 21.12, pg.
797).
Active and Passive Humoral immunity;
natural/artificial acquisition
Antibody targets and functions: Complement fixation, neutralization, agglutination,
promote phagocytosis by opsonization
Cell-Mediated Response -- T-Cell Activation
Most T cells require antigen-presentation
-- recognition of combined self-antigens
(Major Histocompatibility Complex [MHC] proteins) and pieces of antigens
*MHC Classes I & II
-- Know where found (see Table 21.6, p.803)
Activation similar to B cells --
Both B and T cells require
costimulation from antigens and chemicals
-- helper T
cells are major releasers
of some of these costimulatory chemicals and are therefore
responsible for helping
activate both arms of the immune system. Explains why HIV
(which
targets helper T cells) and AIDS are so devastating.
T cell types: cytotoxic (CD8), helper (CD4) (understand the functions),
other classes
Transplants and rejection.
See summary Table 21.7, Table 21.8, and
Focus Figure
21.1.
Chapter 22 -- Respiratory System
Respiration -- exchange of O2 and CO2; system open to air
Steps: pulmonary ventilation, external
respiration, transport (blood), internal respiration
(external and internal
respiration [exchange] completely passive diffusion)
(Fifth step: Cellular
Respiration [chapter 24])
Anatomy:
I. Conducting Zone
A. Nose: humidifies & warms air, filters (air, mucus), olfaction
bridge/septum (hyaline cart, bones), nostrils (nares), nasal cavities
(surrounded by
bones
[maxillae/palatine on floor]) with conchae/meati (for turbulence)
Epithelium: P.C.C.E. with goblet cells
(why?); sneezing
Paranasal Sinuses
B. Pharynx: naso- (with openings for auditory tubes), oro-, laryngopharynx
oro- and laryngopharynx shared with digestive system
uvula/epiglottis (elastic cartilage, with taste buds) close off
nasopharynx/larynx
respectively, when swallowing
know appropriate epithelial linings; tonsils here (which in which part?)
C. Larynx (Voice box, Adam=s apple): framework of hyaline cartilage (know thyroid,
cricoid, arytenoid cartilages), cricothyroid ligament, laryngeal muscles; support
and stretch vocal cords (elastic conn. tissue)
Vocal cords avascular; vibrate to produce sound. Higher frequency vibration
(pulled
tight) = higher pitch; forceful expiration = louder. Sound involves pharynx,
tongue,
nasal cavities, sinuses, etc.
Glottis = opening between vocal cords;
Stratified Squamous above (including epiglottis),
P.C.C.E. below
glottis
Valsalva maneuver, involves epiglottis
D. Trachea: C-rings of hyaline cart., trachealis muscles
(involved in coughing)
Submucosa, with seromucous glands, P.C.C.E.: cilia move mucus up
E. Major Bronchi, lobar bronchi, smaller bronchi, bronchioles
(including terminal)
Trends as tubes get smaller:
1. cartilage rings replaced by irregular plates, and, in smallest, no cartilage
2. epith. thins to simple cuboidal (non-ciliated) in terminal bronchioles
3. relative amount of smooth muscle in wall increases (important in bronchioles for
controlling air flow)
II. Respiratory Zone -- Gas exchange occurs here
(diffusion) across moist membrane
F. Respiratory bronchioles and Alveoli --
@140m2 of surface area
Respiratory membrane = simple
squamous layer (type I cells) of alveolus + simple
squamous endothelium of
capillaries + sparse basement membrane between
Respiratory Surface.: Type II
alveolar (H2O + surfactant secreting) cells, keeps
membrane moist;
alveolar macrophages scour surfaces for pathogens
Gross Anatomy of Lung- Stroma (elastic conn. tissue), apex, base (on diaphragm),
hilus, cardiac notch (left), bronchial arteries/veins
Pleurae (visceral/parietal)
Physiology
Breathing (inspiration [inhalation], active; expiration [exhalation], passive
Intrapleural pressure (due to
adhesiveness of serous fluid [water] between pleurae)
must always be less than intrapulmonary
pressure; holds pleurae together (i.e., holds
lungs to chest wall/diaphragm) during inspiration
and allows for stretching of stroma
I. Pulmonary Ventilation: Boyle=s Law
P1V1 = P2V2
Inspiration: diaphragm and external intercostal muscles; generates
negative pressure,
increases volume 0.5 liters (during normal,
at rest breath)
Expiration: largely passive relaxation and elastic recoil of lungs; forced
expiration
involves more muscles
(and is therefore active, requiring energy)
Energy used in inspiration needed to overcome: resistance (see
pgs. 838-839), lung
compliance/elasticity, alveolar surface tension (reason for surfactants)
Respiratory Volumes/Capacities and dead space: tidal,
inspiratory/expiratory reserve,
residual (volume);
vital, total lung (capacity)
Dead Space -- basically air in
conducting zone (not involved in exchange)
Measurements: Minute respiratory volume, alveolar ventilation rate
(AVR which is
more precise
measure of actual ventilation)
II. Gas Exchanges in the Body
Need to Know: Dalton=s Law of Partial Pressures, Henry=s Law
Partial Pressures (Po2 and Pco2 directly proportional to concentrations;
need to know
typical partial pressures of gases in lungs (alveoli) and at tissues
Gases (O2 and CO2) diffuse based on partial pressure gradients, and
solubilities in
water
(respiratory membrane/plasma) or attachment to Hb
Blood usually completely
oxygenated in .25s (blood in caps. for .75s at rest; fig. 22.21)
Gas flow in bronchioles coupled to blood flow in
alveolar capillaries
(perfusion)
(nervous/chemical control of smooth muscles in both tubes; Fig. 22.23, p. 846)
External and internal respiration: partial pressure gradients opposite, but exchange
mechanisms the same
III. Gas Transport in the Blood -- Handout and
page 833.
A. O2 -- 1.5% in plasma, 98.5% to heme;
know oxy-(HbO2) and deoxy- (or reduced;
HHb) hemoglobin (Hb)
Hb can hold four O2 molecules; when one molecule attaches, easier for others to
attach, due to a conformational change. Same is true for O2 release.
Factors influencing Hb - O2 affinity:
SEE curves, fig. 22.24, p. 850
1. Po2: saturation curves; venous blood usually only about 30% deoxygenated
2. Temperature: As TB 8, Hb - O2 affinity 9 (why important?)
3. pH: As pH 9, Hb - O2 affinity 9 (why important?) ; called the Bohr effect.
typically, HHb can carry less O2 than Hb.
4. NO -- also carried attached to Hb, unloaded when O2 unloaded
B. CO2
-- > 20% bound to globin of Hb (carbaminohemoglobin), 7-10% dissolved
directly in plasma, < 70% dissolved as HCO3- in plasma (catalyzed by carbonic
anhydrase inside RBC=s) (remember, H2O + CO2 ø H2CO3 ø H+ + HCO3-).
HCO3- diffuses out of RBC=s once made; Cl- moves in to offset negative ion
loss --
called the chloride shift. CO2 doesn=t directly interfere with Hb - O2
affinity, but
pH goes down, which does interfere with O2 carrying capacity.
SEE fig. 22.23.
Haldane effect
-- tied to Bohr effect; reflects increased ability of reduced Hb to carry
more CO2, which means that CO2 increases the ability
of blood to carry CO2.
Everything
that happens at the tissues happens in reverse at the lungs -- we blow off
CO2 which drags the above chemical equation to the left, which
reduces the acidity,
which allows more O2 to load into the RBC's; in other words,
everything happens
precisely in the manner we want it to! (Chloride shift reverses as well).
Control of Respiration
-- relatively complex
Neural mechanisms: Medullary respiratory centers
Ventral respiratory group (VRG)
-- the apparent pace-setter
(eupnea).
involves phrenic and intercostal nerves, both of which contain neurons that fire
during
inspiration and others during expiration, with mutual inhibition working between
them,
with feedback from stretch receptors in the lungs as well (see DRG)
Dorsal respiratory group
(DRG) -- not well understood; appears to be involved in
integrating stretch and chemoreceptor inputs and communicating this info to VRG
Pontine respiratory center -- also
not well understood; appear to smooth out the transition
from inspiration to expiration and back; also appears to modify the normal VRG
generated rate during activities such as talking, exercise, etc.
Generation of normal ventilation --
requires interconnections (as describe above) between
neuronal networks, with two basic sets to generate the rhythm (see under VRG)
-->
one for inspiration and one for expiration that inhibit each other
Factors influencing rate & depth of
breathing:
1. Chemical influences: most important in immediate air intake adjustments.
connected to nervous system controls -- work through chemoreceptors in carotid
arteries; in the final analysis, adjustments during rest are aimed primarily at
regulating
the H+ concentration in the brain.
CO2 levels most important
(why?); O2 and arterial pH influence air intake, too.
2. Stretch receptors
Influence of Higher brain centers
Hypothalamus (involuntary alterations
in ventilation)
emotional/pain responses; body temperature responses
Cortical controls (voluntary)
Reflexes altering/controlling ventilation
a. pulmonary irritant
reflexes
b. Hering-Breur
(over inflation) reflex
Respiratory Adjustments during Exercise and at High Altitude
(pg. 857-858)
Understand basic changes that happen at beginning and during
exercise
Understand basic changes that happen over the course of a few
weeks at high altitude