Cell Bio Flashcards
periosteum vs endosteum
covers cortex; dense layer of vasc connective tissue vs covers medulla; gives nutrients to osteocytes via capillaries
Outer layer/cortex/compact bone vs Inner layer/medulla = spongy/cancellous/trabecular bone, marrow
Haversian systems, lamellae, canaliculi, osteocytes vs no Haversian systems; lamellae, canaliculi, osteocytes
RankL vs OPG vs glucocorticoid vs PTH vs vit D
pre to osteoclast, promote clast activity vs from osteoblastic and stromal cells, soluble member of TNF receptor fam; dec RankL –> prevents it from activating clast activity –> protect bone from clast activity vs inc RankL and dec OPG –> clast activity vs low circ Ca2+ –> PTH binds to osteoblasts –> osteoblasts secrete RankL –> inc clast activity; protects from hypocalcemia by bone resorption vs says circ Ca2+ = nml –> make CaSR to bind Ca2+ –> no PTH, no RankL; protects from hypocalcemia by inc Ca2+ reuptake by GI
Osteomalacia & rickets vs osteopetrosis vs Osteoporosis vs scurvy
vit D defic –> not enough of Ca2+ to mineralize bone matrix –> bone malformation vs mutation or loss of RankL –> Dec osteoclast activity/bone resorption –> too much bone vs loss of OPG. Type 1 = postmenopausal women; no estrogen –> inc in osteoclast activity (estrogen inc blast activity & dec clast activity; blasts/cytes/clasts have estrogen receptors). Type 2 = elderly; dec in osteoblast activity vs vit C defic –> osteoblasts can’t make bone matrix/collagen b/c no adding hydroxyl groups –> bleeding in joints, hematomas, purpuras
AP channel blockers: I, III, IV
Class I: Na+ channel blockers –> slower rate of depolarization
Class III: K+ channel blockers –> slower rate of repolarization
Class IV: Ca2+ channel blockers –> block Ca2+ entry into cell –> dec ctx
pos current vs neg current
pos charge out/neg charge in vs pos charge in/neg charge out
where are Na+, Ca2+, K+ near cell? Nernst potential for each?
Na+ and Ca2+ = more outside; K+ = more inside. Na+ and Ca2+ = pos Nernst potential (Ca2+ = more pos than Na+); K+ = neg Nernst potential
AP for nerves & skel muscle vs heart
Na+ enters cell –> depolarization –> K+ exits cell –> repolarization vs Na+ enters cell –> Ca2+ enters cell to stay pos longer => plateau phase –> gives heart more time to contract to make sure all blood ejected into circ –> K+ exits cell –> repolarization
Epimysium vs Perimysium vs Endomysium vs Basement membrane vs Sarcolemma vs Transverse tubules vs Sarcoplasmic reticulum vs sarcomere vs Myofibrils
surrounds entire muscle vs surrounds fascicle vs surrounds muscle fibers vs just below endomysium vs muscle cell membrane vs b/w sarcolemma and SR vs Ca2+ storage sites vs fxnal unit of muscle vs actin and myosin
actin vs myosin
Actin monomers –> long linear actin filaments –> 2 coiled actin filaments => thin filaments; 2 tropomyosin filaments wrap around actin filaments –> control muscle ctx; contain regulatory proteins, troponins T/I/C vs 2 myosin monomers = globular head + hydrophobic tail –> myosin dimer; contains myosin regulatory chain, alkali chain; Tug on actin –> control muscle ctx; convert chemical energy to mechanical energy
Sliding Filament Model aka Swinging Lever-Arm Model
Reduction in distance b/w Z disk of sarcomere during muscle ctx
Cross bridges b/w actin and myosin
Myosin DOES NOT MOVE, only pulls/slides actin
NMJ of skel muscle
Jxn b/w motor neuron and muscle fiber; involves motor end plate (pocket around motor neuron near sarcolemma), neuromuscular cleft (gap b/w neuron and muscle fiber); Ach released from presynaptic jxn to AchR in postsynaptic jxn —> end plate potential —> depolarization of muscle fiber
Innervation of smooth muscle: autonomic nerve fibers vs varicosities
Innervate smooth muscle vs release neurotransmitters into a wide synaptic cleft (diffuse jxn)
Multi unit vs unitary smooth muscle + examples
Each smooth muscle cell = innervated; ex: eye, pilorector muscles vs some muscle cells = innervated —> communicate via gap jxns; ex: visceral organs. both have spikes in AP graphs like skel muscle and plateaus like cardiac muscle
Excitation-Contraction Coupling in skel muscle
AP in sarcolemma —> depolarization of T tubules -> open L-type Ca2+ channels/DHP receptors –> direct physical contact w/ SR Ca2+ channels/Ryanodine receptors —>open SR Ca2+ channels/Ryanodine receptors –> Ca2+ released from SR to sarcoplasm of muscle fiber —> Ca2+ binds to troponin C —> conformational change of C, T & I —> tropomyosin moves to unblock myosin binding site on actin —> myosin acts on actin —> ctx —> Ca2+ go back to SR —> relaxation
Excitation-Contraction in cardiac muscle
Aka calcium-induced calcium release (CICR); AP on sarcolemma —> depolarization of T-tubule —> EXTRACELLULAR Ca2+ influx thru L type Ca2+voltage gated channel (no physical contact) => plateau phase —> Ca2+ released from SR thru SR Ca2+ channel —> ctx; extracellular Ca2+ = key role in cardiac (not seen in skel); also no physical contact b/w T-tubule Ca2+ voltage gated/L type channel w/ SR Ca2+ channel (seen in skel)
Excitation-Contraction in smooth muscle
No T-tubules but got caveoli; Ca2+ go thru Cav channels in caveoli —> CICR; or PLC —> IP3 —> PI3R —> more Ca2+ released from Sr; ctx can be slow or intense
Thin vs thick filament mediated excitation
In striated muscle; Ca2+ released from SR —> interacts w/ troponin C —> troponin I/T undergo conformational change —> tropomyosin undergoes conformational change —> myosin acts on actin vs aka cross bridging cycle of smooth muscle; Ca2+ binds to calmodulin —> Ca2+CaM —> Ca2+CaM activates myosin light chain kinase (MLCK) —> phosphorylate myosin regulatory light chain —> activates myosin. Myosin light chain phosphatase deP RLC —> dec myosin activity —> smooth muscle relaxes; smooth muscle tone = balance b/w de/phosphorylation of RLC
how do ions cause depolarization vs hyperpolarization?
pos ions move in cell –> cell = more pos vs out of cell –> cell = more neg
Vm = voltage of membrane. Why is resting Vm for a cell around -80 mV?
b/c K+ can equilibrate across the membrane almost to their Nernst potential –> K+ has greatest influence on resting voltage; Na+ and Ca2+ ions can NOT equilibrate across the membrane and their Nernst potentials = FAR from -80mV
how do Nernst potentials affect driving force?
K+ has a very low driving force since Vm is near its Nernst potential; Na+ and Ca2+ experience a large driving force since their Nernst potentials are far from the resting Vm
how are cardiac muscles interconnected?
intercollated discs containing desmosomes and fascia adherens –> link adjacent cardiocytes for strength; containing gap jxns –> link adjacent cardiocytes electrically –> concerted ctx and directional blood flow
pacemaker cells of cardiac muscle
SA node makes AP –> atria –> AV node –> septum –> ventricles; this allows ctx of atria to squeeze all blood down to ventricles –> ctx ventricles to squeeze blood up and out of heart
activity of heart = modded by what?
sympathetic nerves (stimulatory) and parasympathetic nerves (relaxing) act on SA and AV nodes to ctrl AP generation on cardiac contractile cells –> inc performance prn
AP trends in skel vs cardiac muscle
fast twitch –> fastest AP, slow twitch –> slower AP; both release Ca2+ from SR; both allow for twitch summation and tetani vs similar to skel muscle but have plateau phase –> more time for CICR; inc absolute refractory period –> more time for ventricles to fully ctx/relax
What determines contractile force of skel muscle?
Amount of [Ca2+] in myoplasm
cross bridging cycle of skel and cardiac muscle
attached: myosin touches actin –> catalytically active; ATP binds to myosin –> myosin lets go of actin => released –> ATP = hydrolyzed => cocked –> myosin attaches to new actin => cross bridge –> Pi = released => power stroke –> ADP = released from myosin –> rpt
muscle relaxation in skel vs cardiac muscle
no AP, L type Ca2+ channel closed, SR Ca2+ channel closed. SR Ca2+ pump/SERCA (ATP dependent active transport protein) transports all Ca2+ to SR vs SERCA regulated by phospholamban (PLB) transports 2/3 of Ca2+ to SR, sarcolemmal sodium-calcium exchanger/NCX transports 1/3 of Ca2+ to SR via antiport –> 3 Na+ in cell, 1 Ca2+ out of cell
what happens if there are defects in SERCA or NCX?
incomplete relaxation of muscle b/c Ca2+ will not return to resting level
calrecticulin and calsequestrin
low affinity Ca2+ binding protein that keeps free Ca2+ manageable
fast twitch vs slow twitch muscles
bursts of high activity, bigger diameter –> bigger force, fast ATPase rate, faster to fatigue, high Ca2+ pumping. type IIA = fast oxidative fibers, red muscle (b/c more mito –> moderate to fatigue); type IIB = fast glycolytic fibers, white muscle (b/c anaerobic ATP prod: pyru to lactate) vs light activity, smaller diameter, slow ATPase rate, slower to fatigue, moderate Ca2+ pumping. type I = slow oxidative fibers, red muscle
fast twitch muscles vs slow twitch muscles use which kinds of energy fuel?
avail ATP first, ATP from phosphocreatine, glycogen for glycolysis vs FA, ketone bodies, glu for cell resp
what can happen if fast twitch muscles does glycolysis?
byprod = lactic acid –> dec intracellular pH –> lactic acidosis –> Ca2+ can’t bind to troponin –> can’t make muscle ctx –> fatigue
epi vs muscular glycogen phosphorylase vs adipose hormone sensitive lipase
inc muscle performance and metab of stores to meet energy needs during exer vs break down glycogen in muscle –> G6P –> glycolysis vs break down stored TG –> exported to blood via albumin –> energy for type I and mixed fibers
what is a motor unit? how to inc intensity of ctx?
single motor nerve + all muscle fibers it innervates => fxnal unit of muscle ctx –> neuron firing –> all muscle fibers ctx simul. inc freq of motor neuron firing –> faster ctx (but risk tetany) or inc # of motor units –> more force
small precision ctrl muscles vs large muscles
have few muscle fibers per motor unit –> fingers playing piano/surgery/typing vs have hundreds of muscle fibers per unit –> locomotion and posture
size principle
at start of muscle ctx, small motor units = activated/recruited first, then bigger units prn
low excitatory input vs high excitatory input
recruit smaller motor units and slow twitch/type I fibers first –> less force but energy efficient for low vel vs recruit larger motor units and fast twitch/type II fibers –> more power for high vel
relationship b/w vel and muscle power
low load –> high vel and vice versa. as load inc –> vel dec => concentric ctx –> need to recruit more units/fibers to keep up. if load exceeds vel or muscle ctx –> power declines –> end point = no load displacement => isometric ctx
series vs parallel muscle growth/development
adding sarcomeres at ends of muscle fibers –> inc vel, inc shortening capacity; faster to form vs hypertrophy of muscle cells –> inc force –> bulk
aerobic/endurance exer vs anaerobic/resistance exer
inc muscle capillaries, # of mito, myoglobin synthesis –> fast glycolytic fibers convert to fast oxidative fibers –> inc endurance, strength, resist to fatigue vs muscle hypertrophy; inc myofilaments, glycogen stores, connective tissue
how does twitch summation lead to tetany?
AP de/repolarizes really fast => twitch; if 2nd AP activates before 1st AP calms –> ctx force inc –> intracellular Ca2+ inc and stays in myoplasm –> force exceeds twitch –> tetany (reversible, physiological). slow twitch muscles tetanize at lower stimulation freq
muscle spindles vs Golgi tendon
both = proprioceptors; for intrinsic muscle control; have afferent neurons to relay info about ctx vs tension. senses muscle length and rate of change in muscle length –> prevent hyperelongation of muscle and tissue development; intrafusal muscle fibers enclosed in sheaths running parallel to extrafusal muscle fibers; compressed when ctx, stretched when relaxed vs senses tendon tension and rate change of tension –> prevent excess tension in muscle and tissue dmg; wrapped around collagen/connective tissue
isotonic vs isometric ctx
force = constant, muscle length = measured; wght stretches muscles => preload –> resting tension –> PEC resists stretch/compress to store PE, SEC stretches to dec thin/thick filaments; afterload –> active tension –> ctx; concentric = shortening of muscle when exerting force (bicep curl), eccentric = lengthening of muscle when exerting force (uncurl bicep in ctrlled fashion) vs muscle length = constant (ie. no muscle shortening/lengthening), no load displacement, force = measured (pushing on wall, doing planks)
PEC vs SEC
compressed during ctx; provided by muscle membrane, ECM, connective tissue vs stretched during ctx; provided by tendons, connective tissue
what leads to muscle fatigue?
substrates: dec glycogen –> dec glycolysis –> dec ATP (IIB); dec creatine phosphate –> dec ATP; dec O2 to tissue –> dec ATP (IIA, I). metabolites: lactic acidosis –> dec pH (IIB); inc K+ from rpted AP
Can cardiac vs smooth muscle have oxidative fibers?
yes. ctx quickly & powerfully vs ctx slowly & powerfully
muscle cramps/spasms vs muscle guarding vs muscle soreness
painful involuntary ctx, dehydration/electrolyte imbalance, can cause muscle/tendon injuries vs involuntary ctx to splint area and minimize pain via limited motion vs overexertion in strenuous exer –> muscle pain; acute onset = w/ fatigue, occurs immediately after exer. delayed onset = w/ microtrauma to muscle and/or connective tissue, occurs 24-48h after exer, subsides in 2-3d
muscle strain
tension exceeds weakest structural element of muscle d/t failure of muscle spindle and golgi tendon
1st degree/mild vs 2nd degree/moderate vs 3rd degree/severe muscle strain vs tendon rupture
strain muscle; minimal dmg and hemorrhage –> tenderness and pain w/ active ROM vs pulled muscle; partial muscle tear –> hemorrhage vs torn muscle; complete muscle tear –> complete loss of fxn, extensive hemorrhage –> dec or total loss of active ROM, nerve dmg vs need surgical repair
tendon vs ligament
muscle to bone, TYPE I COLLAGEN + elastin –> strong ropelike connective tissue –> flexible and absorb impact energy, wrap around joint for muscle movement and joint articulation vs bone to bone, type I collagen + ELASTIN –> short band tough flexible fiber –> motion of connected structures and prevent their separation
tendon & ligament composition
fibroblast cells surrounded by ECM of type I collagen (ropelike, main component of tendon + elastin –> stretchy), elastin (stretchy protein, main component of ligament + collagen –> strength), and proteoglycans
lysyl oxidase
crosslinks tropo/procollagen –> collagen’s tensile strength
Ehlers-Danlos syndrome
defect in collagen synthesis –> loose flexible collagen –> no tensile strength or rigidity –> vulnerable to trauma; affects skin, ligaments, joints
Osteogenesis Imperfecta/brittle bone dz
defect in type I collagen synthesis d/t mutations in alpha1 & alpha2 chains of collagen molec –> no 3x helix; auto dom
osteoblasts vs cytes vs clasts
make bone vs from osteoblasts, maintain bone: transfer minerals from interior to growth surfaces, in lacunae of bony matrix vs break bone, multinucleated, found on growth surfaces of bone
ECM = for and made of?
strength, stability, stretching, twisting. organic osteoid: proteoglycans, glycoproteins, collagen; inorganic hydroxyapatite: Ca2+ and PO43-
what is an osteon/Haversian system?
structural unit of compact bone, each represent wt-bearing pillar –> group of concentric rings around a canal
collagen rings run in what direction in each lamellae?
opposite direction
intramembranous vs endochondral ossification
bone formed from mesenchymal tissue w/o cartilage model; flat bones, skull bones x/ some at base of skull, clavicle vs bone formed from hyaline cartilage model –> primary then secondary oss center –> articular cartilage and epiphyseal plate; long bones, all other bones not from intramembranous
jxnal vs longitudinal SR
primary site for SR Ca2+ release –> ctx vs primary site for SR Ca2+ reuptake –> relax
how to get more skel vs cardiac vs smooth muscle power?
activate more motor units vs inc freq or force of contractility vs more phosphorylation of myosin RLC
where is epiphyseal plate? stages?
b/w diaphysis and epiphysis after bone growth.
Reserve zone: resting chondrocytes ready to build bone
Zone of prolif: dividing chondrocytes secrete bone and collagen
Zone of hypertrophy: maturing chondrocytes
Zone of mineralization: bring calcium and phosphate
Primary spongiosa: get inside to where bone marrow is
appositional growth
Other form of growth of bones where diameter is increased by adding new bony tissue on the surface via osteoblasts
