Review Sheet -- Exam 2 Bio 212 Dr. Adams
INTEGUMENTARY SYSTEM (Skin); know hypodermis (superficial fascia -- adipose)
Epidermis: avascular, innervated from underneath
Cells -- Keratinocytes, Melanocytes and Merkel=s cells (s. basale), Langerhans cells (s.
spinosum) -- know functions of each cell type
Strata -- basale, spinosum, granulosum, (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
Skin Color: melanin (phagocytized from melanocytes by keratinocytes), carotene, hemoglobin
Skin Appendages: all are epidermal derivatives
I. Glands: sweat (sudoriferous) and oil (sebaceous) glands
A. Sweat: Eccrine and "Apocrine"; simple coiled tubular glands; located everywhere
except nipples and parts of external genitalia; functionally merocrine
1. Eccrine: widely distributed; "typical' acidic sweat; salts, Ab=s, nitrogenous wastes
2. Apocrine: Axillary and perineal areas; contains fats/proteins as well. Function may
be pheromonal. Not true apocrine glands; these are also functionally merocrine
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)
II. Hairs: keratinocytes with hard keratin; cuticle, cortex, medulla; hair shaft
Follicles: hair root, hair bulb, root hair plexus, 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
III. Nails: hard keratin
free edge, body, root; nail bed, nail matrix, nail folds, eponychium (cutilcle)
Skin Functions: Protection (physical/chemical/biological), Tb regulation (blood
sensation, metabolic functions (e.g., vitamin D synthesis), excretion, blood reservoir
SKELETAL TISSUES (Skeletal Cartilages and growth)
Cartilages -- already covered (structure and location) in tissues chapter; quick review
Bones -- Functions: support, movement, protection, mineral storage, hematopoiesis
Classification: types of boney tissue -- compact/spongy bone
Types of bones (shapes): Long, short, flat (diploe), irregular
Structure: for long bones -- diaphysis, epiphysis (with plate/line)
Periosteum w/ Sharpey=s fibers, endosteum; osteoblasts/osteoclasts; marrow
Microscopic structure: osteon w/ lamellae, interstitial/circumferential lamellae,
Haversian/Volkmann=s canals, osteocyctes in lacunae, canaliculi
Chemical Composition: Cells/Osteoid (organic portion of matrix: collagen, etc.); inorganic
components: mineral salts, mostly calcium phosphates
Hematopoietic tissue: red bone marrow; distribution becomes more restricted as you mature.
Know location of active hematopoietic tissue in an adult.
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.
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.
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:
I. Fluid (synovial) filled cavity within synovial membrane, which itself is inside . . .
II. 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)
III. May have intra-/extracapsular ligaments, menisci
IV. Bursae and Tendon sheaths: synovial sacs placed to reduce friction between bone
processes and bones and tendons
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)
b. abduction/adduction Circumduction (combines a & b)
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 (beginning of Chapter 10): 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 posture, stabilizing joints, thermogenesis
Functional characteristics: Excitability (irritability), contractility, extensibility, elasticity
Gross Anatomy of skeletal muscles:
1. Wrappings: 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 9.3
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 regulated Na+ gates.
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.
Know what the concept of "refractory period" means.
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
Whole Muscle Contraction:
Involves motor units -- single motor neurons and all muscle cells they stimulate
Latent period, period of contraction/relaxation different for different motor units
Graded 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
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
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 9.22)
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)
1. White fast twitch (fast glycolytic [anaerobic]): fast myosin ATPase, little
myoglobin, high glycogen content, few mitochondria/capillaries, fatigable
2. Red slow twitch (slow oxidative): slow myosin ATPase, lots of myoglobin, low
glycogen content, many mitochondria/capillaries, fatigue-resistant
3. Red intermediate (fast oxidative): fast myosin ATPase, lots of myoglobin,
intermediate glycogen content, many mitochondria/capillaries, moderately
Different muscles have different muscle fiber content, and muscle fiber content is
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,