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Block 2 > Cell Bio > Flashcards

Cell Bio Flashcards

1
Q

periosteum vs endosteum

A

covers cortex; dense layer of vasc connective tissue vs covers medulla; gives nutrients to osteocytes via capillaries

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2
Q

Outer layer/cortex/compact bone vs Inner layer/medulla = spongy/cancellous/trabecular bone, marrow

A

Haversian systems, lamellae, canaliculi, osteocytes vs no Haversian systems; lamellae, canaliculi, osteocytes

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3
Q

RankL vs OPG vs glucocorticoid vs PTH vs vit D

A

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

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4
Q

Osteomalacia & rickets vs osteopetrosis vs Osteoporosis vs scurvy

A

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

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5
Q

AP channel blockers: I, III, IV

A

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

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6
Q

pos current vs neg current

A

pos charge out/neg charge in vs pos charge in/neg charge out

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7
Q

where are Na+, Ca2+, K+ near cell? Nernst potential for each?

A

Na+ and Ca2+ = more outside; K+ = more inside. Na+ and Ca2+ = pos Nernst potential (Ca2+ = more pos than Na+); K+ = neg Nernst potential

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8
Q

AP for nerves & skel muscle vs heart

A

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

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9
Q

Epimysium vs Perimysium vs Endomysium vs Basement membrane vs Sarcolemma vs Transverse tubules vs Sarcoplasmic reticulum vs sarcomere vs Myofibrils

A

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

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10
Q

actin vs myosin

A

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

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11
Q

Sliding Filament Model aka Swinging Lever-Arm Model

A

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

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12
Q

NMJ of skel muscle

A

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

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13
Q

Innervation of smooth muscle: autonomic nerve fibers vs varicosities

A

Innervate smooth muscle vs release neurotransmitters into a wide synaptic cleft (diffuse jxn)

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14
Q

Multi unit vs unitary smooth muscle + examples

A

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

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15
Q

Excitation-Contraction Coupling in skel muscle

A

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

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16
Q

Excitation-Contraction in cardiac muscle

A

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)

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17
Q

Excitation-Contraction in smooth muscle

A

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

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18
Q

Thin vs thick filament mediated excitation

A

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

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19
Q

how do ions cause depolarization vs hyperpolarization?

A

pos ions move in cell –> cell = more pos vs out of cell –> cell = more neg

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20
Q

Vm = voltage of membrane. Why is resting Vm for a cell around -80 mV?

A

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

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21
Q

how do Nernst potentials affect driving force?

A

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

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22
Q

how are cardiac muscles interconnected?

A

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

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23
Q

pacemaker cells of cardiac muscle

A

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

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24
Q

activity of heart = modded by what?

A

sympathetic nerves (stimulatory) and parasympathetic nerves (relaxing) act on SA and AV nodes to ctrl AP generation on cardiac contractile cells –> inc performance prn

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25
Q

AP trends in skel vs cardiac muscle

A

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

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26
Q

What determines contractile force of skel muscle?

A

Amount of [Ca2+] in myoplasm

27
Q

cross bridging cycle of skel and cardiac muscle

A

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

28
Q

muscle relaxation in skel vs cardiac muscle

A

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

29
Q

what happens if there are defects in SERCA or NCX?

A

incomplete relaxation of muscle b/c Ca2+ will not return to resting level

30
Q

calrecticulin and calsequestrin

A

low affinity Ca2+ binding protein that keeps free Ca2+ manageable

31
Q

fast twitch vs slow twitch muscles

A

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

32
Q

fast twitch muscles vs slow twitch muscles use which kinds of energy fuel?

A

avail ATP first, ATP from phosphocreatine, glycogen for glycolysis vs FA, ketone bodies, glu for cell resp

33
Q

what can happen if fast twitch muscles does glycolysis?

A

byprod = lactic acid –> dec intracellular pH –> lactic acidosis –> Ca2+ can’t bind to troponin –> can’t make muscle ctx –> fatigue

34
Q

epi vs muscular glycogen phosphorylase vs adipose hormone sensitive lipase

A

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

35
Q

what is a motor unit? how to inc intensity of ctx?

A

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

36
Q

small precision ctrl muscles vs large muscles

A

have few muscle fibers per motor unit –> fingers playing piano/surgery/typing vs have hundreds of muscle fibers per unit –> locomotion and posture

37
Q

size principle

A

at start of muscle ctx, small motor units = activated/recruited first, then bigger units prn

38
Q

low excitatory input vs high excitatory input

A

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

39
Q

relationship b/w vel and muscle power

A

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

40
Q

series vs parallel muscle growth/development

A

adding sarcomeres at ends of muscle fibers –> inc vel, inc shortening capacity; faster to form vs hypertrophy of muscle cells –> inc force –> bulk

41
Q

aerobic/endurance exer vs anaerobic/resistance exer

A

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

42
Q

how does twitch summation lead to tetany?

A

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

43
Q

muscle spindles vs Golgi tendon

A

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

44
Q

isotonic vs isometric ctx

A

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)

45
Q

PEC vs SEC

A

compressed during ctx; provided by muscle membrane, ECM, connective tissue vs stretched during ctx; provided by tendons, connective tissue

46
Q

what leads to muscle fatigue?

A

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

47
Q

Can cardiac vs smooth muscle have oxidative fibers?

A

yes. ctx quickly & powerfully vs ctx slowly & powerfully

48
Q

muscle cramps/spasms vs muscle guarding vs muscle soreness

A

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

49
Q

muscle strain

A

tension exceeds weakest structural element of muscle d/t failure of muscle spindle and golgi tendon

50
Q

1st degree/mild vs 2nd degree/moderate vs 3rd degree/severe muscle strain vs tendon rupture

A

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

51
Q

tendon vs ligament

A

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

52
Q

tendon & ligament composition

A

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

53
Q

lysyl oxidase

A

crosslinks tropo/procollagen –> collagen’s tensile strength

54
Q

Ehlers-Danlos syndrome

A

defect in collagen synthesis –> loose flexible collagen –> no tensile strength or rigidity –> vulnerable to trauma; affects skin, ligaments, joints

55
Q

Osteogenesis Imperfecta/brittle bone dz

A

defect in type I collagen synthesis d/t mutations in alpha1 & alpha2 chains of collagen molec –> no 3x helix; auto dom

56
Q

osteoblasts vs cytes vs clasts

A

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

57
Q

ECM = for and made of?

A

strength, stability, stretching, twisting. organic osteoid: proteoglycans, glycoproteins, collagen; inorganic hydroxyapatite: Ca2+ and PO43-

58
Q

what is an osteon/Haversian system?

A

structural unit of compact bone, each represent wt-bearing pillar –> group of concentric rings around a canal

59
Q

collagen rings run in what direction in each lamellae?

A

opposite direction

60
Q

intramembranous vs endochondral ossification

A

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

61
Q

jxnal vs longitudinal SR

A

primary site for SR Ca2+ release –> ctx vs primary site for SR Ca2+ reuptake –> relax

62
Q

how to get more skel vs cardiac vs smooth muscle power?

A

activate more motor units vs inc freq or force of contractility vs more phosphorylation of myosin RLC

63
Q

where is epiphyseal plate? stages?

A

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

64
Q

appositional growth

A

Other form of growth of bones where diameter is increased by adding new bony tissue on the surface via osteoblasts

Block 2 (16 decks)

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