Review Sheet -- Exam 2 Bio 212 Dr. Adams
INTEGUMENTARY SYSTEM (Skin); know hypodermis (superficial fascia -- adipose)
Epidermis: avascular, nourished by blood vessels in dermis; innervated from underneath
Continuous cell production from underneath produces a new epidermis every 25 -
45
days,
depending on location. The vast majority of cells here are keratinocytes.
Cells -- Keratinocytes: contain keratin;
lots of desmosomes; tough and water resistant
Melanocytes and tactile (Merkel)
cells in the s. basale: melanin transferred to
keratinocytes for U.V. protection; tacticle cells detect pressure (and temp.)
Dendritic (Langerhans) cells (s. spinosum): branches extend between virtually
all cells-- function as in house protection
Strata -- basale (with melanocytes and tactile cells); spinosum
(with dendritic cells);
granulosum
-- last living cells towards surface (know keratohyaline and lamellar
granules and what they do); (lucidum), corneum
Know where new cells are produced, and what happens as they migrate toward surface
Dermis: vascularized and innervated
Papillary (loose [areolar]) and Reticular (dense irregular) layers;
why papillae?
Dermal (and epidermal) ridges -- friction ridges,
cleavage/tension lines, flexure lines
Hypodermis (superficial fascia): adipose tissue -- energy storage, cushion, insulator
Skin Color: melanin (phagocytized from melanocytes by keratinocytes), carotene, hemoglobin
Skin Appendages: all are epidermal derivatives
I. Hairs: keratinocytes with hard keratin;
structure: cuticle (shingled), cortex, medulla
Cross sectional shape determines quality: flat -- kinky; oval -- wavy;
round -- straight
hair shaft
-- keratinization is complete; hair root (in folllicle) -- keratinization
ongoing
Follicles: hair root, hair bulb (with
melanocytes, much like s. basale), hair papilla; root hair
plexus
(sensation), root sheaths (epithelial and connective
tissue)
arrector pili muscles and
sebaceous glands associated with follicles (see below)
Types: terminal, vellus
Growth: influenced most by hormones and nutrition; rate of growth varies, and there are
growth cycles
of differing lengths for different follicles, so different hairs will stop
growing and fall after reaching different lengths
II. Nails: hard keratin
free edge, body, root; nail bed, nail matrix, nail folds, eponychium
(cutilcle)
III. Glands: sweat (sudoriferous) and oil (sebaceous) glands
A. Sweat: Eccrine
(merocrine) and "Apocrine"; simple coiled tubular glands; located
everywhere except nipples and parts of external genitalia
1. Eccrine: widely distributed; "typical'
acidic sweat; mostly water, with salts, Ab=s,
nitrogenous wastes, dermicidin. Sympathetically controlled.
2. Apocrine: Axillary and perineal areas; contains fats/proteins as well. Function
may
be pheromonal. Not true apocrine glands; these are also functionally merocrine
Sympathetic stimulation increases activity of these during pain and stress.
Specialized types: Ceruminous, mammary
B. Sebaceous: Simple alveolar glands (holocrine); everywhere except palms/soles.
Sebum consists of lipids, membrane fragments (oils), typically secreted onto hair
follicles. Has bactericidal qualities, and keeps hair supple. (Whiteheads/blackheads)
Skin Functions: Protection (physical/chemical/biological), Tb regulation (blood
flow/sweat)
sensation, metabolic functions (e.g., vitamin D synthesis), excretion, blood reservoir
Know a bit about burns.
SKELETAL TISSUES (Skeletal Cartilages and growth)
Cartilages -- already covered (structure and location) in
tissues chapter; quick review
Chondrocytes/chondroblasts; appositional and interstitial growth
Bones -- Functions: support, movement, protection, mineral storage, hematopoiesis
Classification: types of boney tissue -- compact/spongy bone
KNOW details of the structure of both types; spongy with trabeculae; compact
with osteons -- lamellae, osteocytes in lacunae, canaliculi, central canals
(below)
Types of bones (shapes): Long, short, flat (diploe),
irregular
Structure: for long bones -- diaphysis, epiphysis (with
epiphyseal plate/line)
Periosteum w/
perforating
fibers, endosteum (Fig. 6.5); osteoblasts/osteoclasts;
medullary cavity with yellow (fat) or red (hematopoietic) marrow
Microscopic structure: osteon w/ lamellae, interstitial/circumferential lamellae,
Central (Haversian)/perforating canals (Figs. 6.8, 6.9)
Chemical Composition: Cells/Osteoid (organic portion of matrix: collagen, etc.);
inorganic
components: mineral salts, mostly calcium phosphates
Bone Formation: Intramembranous (typical of flat bones), endochondral (typical of long
bones) ossification -- know the basics.
Bone Growth: In length: much like endochondral ossification; epiphyseal plates (hyaline
cartilage) produce new chondrocytes, thickening the epiphyseal plates. As cells move in
toward the bone cavity, the matrix calcifies, chondrocytes die, and osteoblasts take over
the ossification.
Some of this new spongy bone is eventually destroyed by osteoclasts,
enlarging the
medullary (marrow) cavity. The epiphyses and the diaphysis nearby must be
continually remodeled* during growth in
length. In diameter (appositional growth):
osteoblasts (periosteal) form new osteons on the
external bone surface, increasing the
amount of compact bone. To prevent overdense
(heavy) bones, this is offset by lower
levels of osteoclast (endosteal) activity, enlarging
the medullary cavity.
Hormonal Regulation during youth: involves growth hormone, thyroid hormone, and is
influenced by increase in sex hormones during puberty which initially enhance growth,
but also close (ossify)
the epiphyseal plates; estrogen MORE powerful in stimulating
growth than testosterone, but also ossifies the plates more rapidly.
Bone Remodeling*: Osteoblasts (bone deposit) and osteoclasts (bone resorption) are
the remodeling units. Presence of constant thickness osteoid seam and calcification front
suggests that tissue must Amature@ before calcification.
I. Hormonal Effects: Parathyroid hormone, released when blood calcium levels are below
homeostatic levels, stimulate osteoclasts, as well as activating vitamin D in the epithelial
cells of the small intestine to enhance calcium absorption from food. Calcitonin, released
from the thyroid gland in response to above normal blood calcium levels, stimulate
osteoblasts. Note: these hormones involved in blood, not bone, homeostasis. Calcium,
needed for other things in the body, may be removed from already depleted bones.
II. Mechanical factors: stressed bone becomes thicker; probably in response compression
and tension on opposite sides of the bone, which generates opposite electrical charges
(and therefore current from one side to the other). Hormonal and mechanical factors work
together to determine which bones and where bones are remodeled.
Repair of fractures: Know the basics.
ARTICULATIONS (JOINTS)
Classification of joints:
I. Functional: synarthroses, amphiarthroses, and diarthroses
II. Structural: (see figures 8.1 & 8.2) Know structures/functions/locations for the following
A. Fibrous joints: sutures, syndesmoses, gomphoses
B. Cartilaginous joints: Synchondroses (hyaline), symphyses (fibrocartilaginous pads)
C.
Synovial joints
Synovial joints -- parts (Fig. 8.3):
I.
Articular cartilages
II. Joint cavity -- surounded
by . . .
III. Articular Capsule (continuous with periostea);
articular (hyaline) cartilages
Synovial fluid
"stored" in cartilages, enters cavity with compression (exercise);
becomes
more fluid (better lubricant) when warmed (during exercise)
IV. Fluid (synovial) filled cavity within synovial membrane, which itself is inside
. . .
V. Reinforcing intra-/extracapsular ligaments, menisci
VI. Nerves and blood vessels
May be additional bursae and tendon sheaths: synovial sacs placed to reduce friction between
bone processes and bones and tendons,
not directly in the joint. (Fig. 8.4)
Factors Stabilizing Joints: Fit of articular surfaces, supporting ligaments, muscle tone
Movements of Joints: Know generally which joints allow which movements
1. Gliding (non-axial movement, typical of plane joints)
2. Angular:
a. flexion/(hyper)extension
b.
abduction/adduction
Circumduction (combines a & b)
3. Rotation
Special movements: Dorsi-/plantar flexion of the foot, lateral flexion of the neck,
pronation/supination, inversion/eversion, protraction/retraction,
depression/elevation
Types of synovial joints (and planes of motion):
1. Plane (non-axial and gliding [see above])
2. Hinge (uniaxial allowing flexion/extension)
3. Pivot (uniaxial allowing rotation)
4. Condyloid (biaxial allowing flexion/extension and abduction/adduction
[circumduction])
Bicondyloid (like knee) are functionally hinge joints, allowing flexion/extension mainly
5. Saddle (two "saddle" shaped surfaces) -- functionally like condyloid but greater flexibility
6. Ball-and-Socket (multiaxial allowing flexion/extension, abduction/adduction, and rotation)
You will be held responsible for the Homeostatic Imbalances section of this chapter.
Lever Systems (Chap. 10, pgs. 327-329): Fulcrum, load, effort. Joints act as levers
Those with a mechanical advantage
(load closer to fulcrum than load) have great power
Those with a mechanical disadvantage
(effort closer to fulcrum) sacrifice power but gain
speed and range of motion
Types: First-class (fulcrum in middle), second-class (load in middle), third-class (effort in middle)
MUSCLES AND MUSCLE TISSUES -- Will concentrate mainly on skeletal muscle
Types: Skeletal, cardiac and smooth (know main differences covered in tissues chapter)
Cells long and thin, therefore called muscle fibers
Basic functions: movement, maintaining body posture and stabilizing joints
(tone), thermogenesis
Functional characteristics: Excitability (irritability), contractility, extensibility, elasticity
Gross Anatomy of skeletal muscles: (Fig. 9.1)
1. Wrappings (sheaths): endo-(single cell)/peri-(fascicles)/epimysium
(whole muscles)
epimysium
blends together around some muscle groups -- deep fascia
2. Nerve supply (each muscle cell with own axon
terminals)
3. Blood supply (capillaries long and winding to accommodate changes in muscle length)
4. Attachments: Know the meaning of point of origin/insertion
Direct (uncommon) and indirect (much more common) through a tendon/aponeurosis
Microscopic Anatomy: Muscle fibers (syncytia)
Sarcolemma, sarcoplasm -- contains
myoglobin, glycogen
Myofibrils (account for 80% of cell volume) -- these are the contractile elements of the
cell,
and are separated into single contractile units called sarcomeres (Z-line to Z-line)
Thick filaments (made of myosin) and thin filaments (made of actin)
-- for arrangement,
see figure 9.2;
will be discussed in detail in class
Molecular composition of myofilaments:
Thick: numerous myosin molecules with heads sticking out
Thin: microfilaments (actin), with tropomyosin wrapped around the filament blocking the
binding sites for myosin heads on the actin, and three part troponin molecules, used to
roll the tropomyosin out of the way during contraction.
Sarcoplasmic reticulum (SR) and (Transverse) T tubules
SR holds calcium necessary for contraction; spans each sarcomere in distinctive pattern
(Figure 9.5);
T tubules are extensions of the sarcolemma into the cell, and wrap each
myofibril near ends of sarcomeres, with SR on either side of the T tubule. T tubule
necessary for passing electrical impulses, as well as nutrients, deep inside the cell.
Muscle Cell Contraction: sliding filament mechanism
Action potentials (AP; electrical impulse, described in detail in Chapter
11) carried by excitable
[neuron, muscle]
cell membs.) Stimulus received, causing sodium to flood in, which depolarizes
the membrane, opens more (electrically regulated) Na+ gates, depolarizing membrane further.
Wave
of depolarization flows down membrane (including T tubules). This is followed by
wave
of
repolarization, as K+ gates open in response to depolarization. AP responsible (as
stated above), for release of Ca+2 from SR. Neuron release of ACh at neuromuscular junction
(synapse) due to AP flowing down
motor neuron, allowing Ca+2 to enter axon end, which
stimulates release of ACh. ACh binds to receptors on muscle cell membrane (at motor end
plate), opening chemically gated Na+ channels.
Contraction: The sodium flowing in initiates an electrical impulse (action potential),
which travels
down T tubules; change in polarity (resting membrane potential) of membrane as sodium ions
rush in opens calcium gates in nearby SR; calcium ions flood sarcoplasm and bind to part of
troponin; cause conformational change (bend) in troponin, which rolls the tropomyosin out of
the way of myosin binding sites on the actin; myosin heads, already in high
energy (binding)
configuration, bing to actin and "pull"
(power stroke); new ATP detaches myosin head and
infuses new energy into the head, preparing it for another
power stroke. Single power strokes
shorten muscle cells 1% -- contracting muscles
shorten 30+%, indicating each myosin head
pulls several times during single contraction.
Contraction continues only as Ca+2 is available --
when membrane repolarizes, Ca+2 is
pumped back into SR, troponin no longer bent, myosin
therefore no longer can bind.
Contraction is all-or-none (as AP is all-or-none) -- cells contract fully or not at all.
ACh must be removed or contraction will continue; destroyed by AChesterase in motor
end
plate membrane.
Whole Muscle Contraction:
Involves motor units -- single motor neurons and all muscle cells they stimulate
Muscle twitch -- allows for visualization of latent period, period of contraction/relaxation
which are different for different motor units
Graded whole muscle responses -- accomplished by multiple motor unit (spatial) summation,
or recruitment, or wave (temporal) summation (maximal results in tetanus). Both typically
involved in any partial muscle contraction, and motor units often recruited
asynchronously.
Allows individual motor units to rest during contraction. Know the concept of muscle tone
Isotonic contractions -- muscle changes length (concentric/eccentric)
Isometric contractions -- muscle generates tension but maintains length
Understand the above and be able to give examples
Muscle metabolism:
First few seconds -- stored ATP; next several seconds -- conversion of creatine
phosphate to ATP; after about 15 seconds -- new ATP generated by cellular respiration.
Cellular respiration may be aerobic (with lots of ATP made) or anaerobic (with less ATP
made), which also will build up lactic acid in muscle cells (can lead to burning sensation)
Muscle fatigue -- physiological inability to contract (due to deficit of ATP); total lack of
ATP
results in cramps/ contractures (myosin heads unable to detach, Ca+2 not pumped
back into
SR, Na+-K+ pumps not working); also explains rigor mortis. Deficit of ATP
of course tied
to O2 debt.
Force/Velocity/Duration of Muscle Contraction:
Force influenced by: number of motor units stimulated, whole muscle size, series elastic
elements, and degree of muscle stretch (you must understand Figure
9.19)
Velocity and Duration influenced by: Load, Muscle Fiber type
Muscle fiber types: differ in speed of contraction (myosin
ATPase activity), and ATP
forming pathways (see Table 9.2,
pg. 308)
1. Red slow twitch (slow oxidative): slow myosin ATPase,
lots of myoglobin, low
glycogen content,
many mitochondria/capillaries, fatigue-resistant
2. Red intermediate (fast oxidative): fast myosin
ATPase, lots of myoglobin,
intermediate glycogen content, many mitochondria/capillaries, moderately
fatigue-resistant
3. White fast twitch (fast
glycolytic [anaerobic]): fast myosin ATPase, little
myoglobin, high glycogen content, few mitochondria/capillaries, fatigable
Different muscles have different muscle fiber content, and muscle fiber content is
genetically
influenced -- which means there
are born sprinters/runners to a point.
Effects of Exercise/Disuse on Muscles: understand discussion in class
Fascicle Arrangement: (from beginning of chapter 10)
parallel, pennate (uni-/bi-/multi-), circular, convergent -- know examples
parallel provides for great range of motion, but are often less powerful than pennate
Interactions of Skeletal muscles: understand the terms prime mover (agonist), antagonist,
synergist, fixator