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 tactile (Merkel=s) cells (s. basale),
            Dendritic (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 flow/sweat)
            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.

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:
    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)
    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 (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 end 
plate membrane.

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

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 9.22)

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 
                 fatigue-resistant

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