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IMS > Nerve and Muscle > Flashcards

Nerve and Muscle Flashcards

1
Q 
what do each of the cells do 
multipolar 
unipolar 
bipolar
neurogllia 
astrocytes 
oligodendrocytes 
microglia 
ependyma
A

motor neurones, can be pyramidal or stellate
PNS - in sensory ganglia cell body attached at the side
retinal - found in sensory structures
glial cells - considered supporting cells for neurones
involved in metabolic exchange between neurones and blood
militate the axon
less common immune defence
lining cells for ventricles have cilia on lumen

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2
Q

difference between dendrites axons and neuritis

A

neuritis are dendrites and axons
dendrites are shorter and thicker giving rise to small spins
axons are long and thin usually only one axon

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3
Q

difference between nerves and ganglia

A

nerves are axons and ganglia are cell bodies

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4
Q

what are nerves made up of

A

bundles (fascicles) of myelinated and non-myelinated axons plus blood vessels and shwwan cells

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5
Q

what are the two types of ganglia

A

sensory and autonomic (efferent neurones from ANS)

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6
Q

what is the structure of a peripheral nerve

A

epineurim - covers whole nerve
perineurium - covers whole fascicle
endoneruim covers individual nerve axons

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7
Q

what do satellite and schwaan cells do

A

satellite - surround nerve body and may aid in controlling chemical envirmoent of neurones
schwaan cells for myelin sheath around large nerve fibres and are phagocytic

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8
Q

what is the difference between oligodendrocytes and schwaan cells

A

oligo - myelin sheath in CNS (around several axons)

Schwaan cells - myelin sheath in PNS (one single axon)

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9
Q

difference between somatic and autonomic

A

somatic - voluntary

auto - involuntary - heart beat, lungs, BP etc

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10
Q

autonomic is split into what

A

sympathetic and parasympathetic

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11
Q

what is the difference in structure and neurotransmitter between pre ganglionic and postganlionic

A

Preganglionic fibres  long, myelinated (p.)  short, myelinated (s.)
Postganglionic fibres  short, few branches (p.)  long, many branches (s.)
Location of ganglia  near/in target tissue (p.)  close to spinal cord (s.)
Preganglionic transmitter  Ach (p.)  Ach (s.)
Postganglionic transmitter  Ach (p.)  Noradrenaline (s.)
When active  rest, sleep (p.)  stress, exercise (s.)
Physiological effect  slow things down (p.)  speed things up (s.)

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12
Q

what are the classifications of nerve fibres

A 
it is based on nerve fibre diameter and conductance 
1st class is A (fastest) B and C - motor fibres and some non-muscle sensory 
2nd class = I (fastest), II, III, IV
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13
Q

what are non myelinated sensory fibres referred to as

A

C fibres

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14
Q

what do proprioreceptors do

A

concerned with position of muscles tendons and joints

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15
Q

what are the 4 receptors endings

A

free endings - connective tissues/ muscle/ skin - slow or fats adapting - pain, touch, light, pressure
Pacinian corpuscle = deep dermis/tendons/joints/genitalia, vibration/deep pressure, fast adapting
Meissner’s or krause’s bulbs = oral mucosa/lips/genitalia/fingertips, touch/vibration/light pressure, rapid adapting
Ruffini organs = deep dermis/ligaments/joint capsules, stretch/deep pressure, very slow adapting

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16
Q

what is a simple spinal reflex pathway

A
  1. Sensory receptor = site of stimulus action
  2. Sensory neurone = transmits afferent info to the CNS
  3. Integration centre = one or more synapses within CNS (may also signal up to brain)
  4. Motor neurone = conducts efferent impulses to effector organ
  5. Effector = muscle fibre (or gland) that responds to impulses
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17
Q

what is the role of proteins on the resting potential

A

large negatively charged proteins can’t exit the cell and help maintain a -65 mV resting potential

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18
Q

what is the definition of the nerviest equation and what is it used for

A

cell resting membrane potential close to but not equal to K+ equilibrium potential, also small leak for Na+, equation determining equilibrium potential for any ion, determined using conc. of ion inside/outside and cell temp.

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19
Q

what are the 4 phases of an action potential

A

Phase 1 = Na+ channels open, Na+ enters nerve cell, membrane potential rises towards 0
Phase 2 = if threshold potential reached, voltage gated Na+ channels open, cell depolarises, Na+ ions flow into cell, action potential spike results
Phase 3 = Na+ channels close when Na+ equilibrium potential reached, voltage gated K+ channels open and K+ ions flow out of cell, membrane potential reverses
Phase 4 = K+ ions continue to flow out of cell while Na+ channels closed, hyperpolarisation results for brief period before normal resting potential restored, during this period (refractory period) another action potential cannot be generated, so action potentials only travel one way

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20
Q

what are the benefits of the refectory period

A

no further action potentials can be elicited, ensures action potential propagation is unidirectional, action potential can only travel along axon from cell body to terminal, during relative refractory period, larger stimulus can result in action potential

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21
Q

what is sensory transduction

A

conversion of environmental or internal signals into electrochemical energy

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22
Q

receptors in muscles are varied what are they

A

sensory, proprioceptors and mechanoreceptors

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23
Q

how and where are muscle spindle fibres stimulated

A

located within muscle and stimulated when muscle passively stretched, bundle of modified skeletal muscle fibres enclosed in connective tissue capsule

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24
Q

what is the golgi tendon organ

A

located in tendon and responds to tension (stimulated when associated muscle contracts), small bundles of tendon (collagen) fibres enclosed in layered capsule with terminal branches of large diameter afferent fibre intertwined with collagen bundles, active during passive stretch and active contraction, tension director that protects muscle against excess load

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25
Q

how does the spindle protect the muscle

A

When muscle is stretched passively the spindle is activated and initiates a reflex, when muscle contracts and shortens it is switched off, protects muscle being overstretched

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26
Q

describe the knee jerk pathway

A

monosynaptic stretch reflex, stretching of muscle stretches spindle resulting in increased discharge of sensory nerves, results in increased firing of motoneuron, muscle contracts, no spinal interneuron is involved, effect is to dampen stretch of the muscle, specific for muscle stretched

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27
Q

what are the differences in chemical vs electrical transmission

A 
Electrical = more common in invertebrate nervous system, do occur in human brain and involved in epileptiform activity, formed by interlocking connexon channels of adjacent neurones, connexons comprise connexin proteins, present at points of contact between neurones with no synaptic cleft, only very narrow gap, direct, very fast electrical transmission, unidirectional in mammalian CNS but bidirectional in invertebrates
Chemical = interface for chemical communication between neurones, release of transmitter from synaptic vesicles on arrival of an action potential in the terminal bouton of neuronal axon
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28
Q

what are the structural differences between ionotrophic and metabotrophic

A

ionotrophic receptor = cluster of similar subunits forming ion channels, that depolarise or hyperpolarise the postsynaptic cell (fast responses),
metabotrophic receptors = 7-transmembrane molecule coupled to intracellular proteins that transduce a signal to cell interior (slow responses)

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29
Q

what is a neuromuscular junction

A

synapse between a motor neurone and skeletal muscle fibres

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30
Q

where are neurotransmitter receptors concentrated

A

in post junctional folds

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31
Q

what neurotransmitter is released at NMJ

A

ACh

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32
Q

in a NMJ which receptors does ACh bind to

A

nicotinic receptors

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33
Q

where is AChE found

A

in the cleft and attached to the basal lamina

34
Q

what happens to ACh after it is broken down

A

into acetate and choline
choline reabsorbed to pre synapse
acetate binds with CoA to for acetyl c A which then reacts with choline to make more ACh

35
Q

what causes the concentrated vesicles full of ACh in the cell

A

Antiporter H+ / ACh - into vesicle

36
Q

how are vesicles reserved and blocked

A

Reserve vesicles anchored near active zone by synapsin that tethers them to actin filaments
Docking of vesicles, v-snare protein on vesicle binds to t-snare on membrane at active zone

37
Q

how is choline taken up

A

Na + co transporter

38
Q

what are synaptic vesicle pools

A

multiple, readily releasable, undergo exocytosis in response to single action potential as have been primed by docking at active zone, recycled synaptic vesicle pool, reserve pool ensures neurotransmitter is available even for highest physiological demands

39
Q

what does Curare do

A

comes from plants found in s. America, tribes used it to hunt and kill animals, causes muscle paralysis, so animals die from asphyxiation, If create artificial respiration for around 2 hours can recover

40
Q

what does tubocurarine do

A

non-depolarising competitive nAChR antagonist, competes with ACh for nicotinic receptor binding sites, muscle paralysis occurs gradually, reversed by AChE inhibitors, as ACh is around for longer so eventually outcompetes, hydrolysed by circulating esterases, therapeutic use in surgery, adverse effects are decreased DP and bronchospasm

41
Q

what does succinylcholine do

A

depolarising nAChR agonist, persistent depolarisation of NMJ, phase 1 = membrane depolarised causing brief period of muscle twitching as fibres firing off all of a sudden, phase 2 = end plate eventually repolarises, but as drug not metabolised as rapidly as ACh it continues to occupy receptor, causes flaccid paralysis, hydrolysed by circulating esterases, therapeutic use in surgery given continuously, adverse effects in halothane susceptible people experience malignant hyperthermia

42
Q

what does neostigtme/edrophonium do

A

cholinesterase inhibitors, therapeutic use as antidote for non-polarising blockers e.g. tubocurarine, treatment for and diagnosis of myasthenia gravis, adverse effects are generalised cholinergic activation (muscarinic and nicotinic), abdominal cramping, diarrhoea, salivation, incontinence, other uses nerve gas as weapon of war

43
Q

what does sarin do

A

liquid and gas, inhibits AChE, highly toxic and volatile agent, can linger on clothes so spread easily, causes muscle convulsive contractions, nose and eyes watering, drooling, nausea, vomiting, constriction of pupils to pinpoints, loss of control of bladder and bowel, chest pain, shortness of breath, collapse, seizures, death end result due to asphyxia

44
Q

what are tetanus and botulin toxins

A

reduce probability of neurotransmitter release by preventing vesicles binding to pre-synaptic membrane

45
Q

what does tetrodoxin do

A

binds to Na+ channel to block activation

46
Q

what is lambert-eaton syndrome

A

Reduced ACh release as autoantibodies stop Ca influx
associated with lung cancer
cancer symptoms, abnormal reflexes, lack of saliva
doesn’t usually affect respiratory/face/eyes
diagnosed with electromyography and test for antibodies
treatment - immunosuppressants or amifampridine - blocks K so action potential duration is bigger

47
Q 
what does these types of muscle mean 
pennate 
fusiform 
parallel 
convergent 
circular 
skeletal
cardiac 
smooth
A

feather like arrangement, unipennate (hands), bipennate (legs/thighs), multipennate (shoulders)
spindle shaped
fascicles lie parallel to axis of muscle, flat muscles (often have aponeuroses)
broad attachment from which fascicles converge to a single tendon
surround body opening/orifice, constricting when contracted
striated, multinucleated, voluntary, non-branching, attached to skeleton
striated, single nucleus, involuntary, branched, heart muscle
non-striated, single nucleus, involuntary (stimulus), tapered, forms walls of organs

48
Q

what is the basic muscle structure

A

sarcolemma inside of is sarcoplasm, which surrounds myofibril, which contains filaments made up of actin and myosin

49
Q

what is the difference between actin and myosin

A 
Actin = major component of I-band, extend into A-band
Myosin = bipolar, extend throughout A-band, major component of H-zone, crosslinked at centre by M-band
50
Q 
what do these refer to 
Z line 
I band 
A band 
H zone 
M line 
Titin
A

disc between I-bands appears as series of dark lines
Surrounds Z line zone of thin filaments not superimposed bu thick filaments - ie only actin present
a band - section contain whole of myosin
H zone - within A band, paler region, zone of thick filaments (myosin only)
M line - inside H zone middle of sarcomere - formed of cross connecting elements
connecting protein extends from Z line which binds to actin and M band which interacts with myosin

51
Q

what is the mechanism of muscle contraction

A

Troponin complex moves tropomyosin
This exposes myosin-binding sites on actin
Unblocking the binding sites
1. Action potential arrives at NMJ
2. ACh is released, binds to receptors, opens Na+ channels leading to action potential in sarcolemma
3. Action potential travels along T-tubule
4. Ca2+ released from sarcoplasmic reticulum
5. Ca2+ binds to TnC region of troponin
6. Troponin changes shape, moves tropomyosin, exposing binding site on actin filament
7. Myosin head with ADP + Pi binds actin and attaches
8. Myosin head bends, pulling along actin filament, ADP + Pi released during power stroke

52
Q

what happens to the bands in contraction of muscle

A

ATP and Ca2+, A-band remains unchanged, H-zone gets shorter, distance between Z-lines gets shorter

53
Q

what are isotonic contractions

A

causes muscle to change length as it contracts

54
Q

what is the differences between
concentric
eccentric
isometric

A

muscle shortens
muscle lengthens as it contracts such as a slow relation rep at the end of a set
no change in length as the muscle contracts

55
Q

what are the stages of a muscle twitch

A 
1 = latent period, delay of a few milliseconds between action potential and start of contraction, reflects time for excitation-contraction coupling
2 = contraction phase, starts at end of latent period and ends when muscle tension peaks, cytosolic calcium levels increasing as released calcium exceeds uptake
3 = relaxation phase, time between peak tension and end of contraction, when tension returns to 0, cytosolic calcium is decreasing as reuptake exceeds release
56
Q

what is the difference between fast twitch and slow twitch

A

fast twitch - type II fibres, white, lots of mitochondria, myoglobin less dense, contract quickly and powerfully, fatigues easily
slow twitch
red as lots of myoglobin, dense capillaries, contract slowly but little force, very resistant to fatigue, large amounts mitochondria, produces low amount of power, used in aerobic activities e.g. long distance running

57
Q

difference between type IIb and IIa

A

Type IIa = red as lots of myoglobin, resistant to fatigue, contains large amounts mitochondria, contracts relatively quickly, produces moderate amount of power when contracted, used in long-term anaerobic activities e.g. swimming, fast twitch A fibres
Type IIb = white as low myoglobin, fatigue very easily, contains low amounts mitochondria, contracts very quickly, produces high amount of power when contracted, used in short-term anaerobic activities e.g. sprinting and heavy lifting, fast twitch B fibres

58
Q

what does the force of muscle contraction rely on

A

the number of action potentials per second

59
Q

what happens when the muscle is stretched beyond the amount normal

A

number of cross bridges decreases as overlap between filaments decreases

60
Q

what are some examples of injury or oversuse of muscles

A

sprain/cramps/strain/tendinitis

61
Q

what is a genetic muscular disease

A

muscular dystrophy, more difficult to treat and diagnose, testing will happen and family history taken

62
Q

what are some neurological muscular disorders

A

multiple sclerosis/myasthenia gravis/Parkinson’s disease, as muscles require action potentials, can cause many issues

63
Q

what is myositis/polymyalgia rheumatica

A

short/long term condition, consequence of autoimmune condition (myositis), self-limiting treated with medication

64
Q

describe the structure of cardiac muscle

A

Striated with characteristic A and I bands, contains actin and myosin filaments in myofibrils
Branched, interconnected, small
Rich in myoglobin and mitochondria
Forms thick layer in the heart called myocardium
Each cell contains 1-2 centrally located nuclei
Mitochondria comprise 30% of volume of cell, require lots of energy

65
Q

what do intercalated discs do

A

specialised cell-cell contacts, cell membranes interlock, function for mechanical coupling (desmosomes – macula adherens – which hold cells together to stop separation during contraction) (and fascia adherens – actin anchoring sites connect to closest sarcomere) and electrical coupling (gap junctions allow action potentials to spread quickly to adjoining cells, permit passage of ions between cells allowing depolarisation

66
Q

what are the phases of ventricular action potential

A

Phase 0 = cell depolarisation, greatly increased membrane permeability to Na+ ions, rush in through fast channels, down conc. gradient reversing cell polarity
Phase 1 = partial repolarisation, loss of Na+ conductance and decrease in K+ conductance
Phase 2 = plateau, due to slow inward flow of Ca2+ ions through slow channels, also some inward movement of Na+ through slow channels and a decrease in membrane K+ conductance
Phase 3 = repolarisation, decreased Ca2+ conductance and increased K+ conductance, inside of cell again becomes negative relative to outside, Na+/K+ pump re-establishes distribution of ions
Phase 4 = interval between action potentials when the ventricular muscles are at their stable resting membrane potential
Long refractory period, no summation as refractory period lasts as long as twitch, so prevents tetanus

67
Q

what happens during complete heart block

A

no transmission through AV node, Purkinje fibres take over pacemaker, slower pacemaker activity in distal parts of conducting system allow heart to continue breating if SA node fails, patients have bradycardia and reduced cardiac output

68
Q

what is wolf parkinson white

A

disorder of conduction of the heart, pre-excitation syndrome, caused by presence of abnormal accessory electrical conduction pathway between atria and ventricles, electrical signals travel down abnormal pathway (bundle of Kent) may stimulate ventricles to contract prematurely, resulting in unique type of supraventricular tachycardia referred to as AV reciprocating tachycardia

69
Q

what are the 4 classes of anti arrhythmic agents and give examples

A

Class 1 = sodium channel blockers, treat ventricular ectopics
Class 2 = beta blockers (block effects of catecholamines in beta1-adrenergic receptors, decreasing sympathetic activity on the heart), slow conduction in the SA and AV nodes
Class 3 = potassium channel blockers, treat ventricular tachycardia and atrial fibrillation
Class 4 = calcium channel blockers, slow conduction in the SA and AV nodes, shorten plateau of action potential but allow body to retain adrenergic control of heart rate and contractility

70
Q

what does digoxin do

A

foxglove plant digitalis, inhibits Na+/K+ ATPase pump, increases intracellular Na+ causing less Ca2+ to be secreted, so intracellular Ca2+ conc. remains high, used to treat heart failure, causes decrease in heart rate, increased force of contraction as there is more release of Ca2+ from the SR so another increase in release of Ca2+ during each action potential

71
Q

describe the process of excitation contraction curling in the heart

A

Ca2+ enters through voltage-gated L-type Ca2+ channels in T-tubule membrane
Triggers further Ca2+ release from adjacent sarcoplasmic reticulum
Each L-type channel controls only one SR release channel, so tight local control
Ca2+ binds to troponin-C and contraction proceeds
After contraction, relaxation occurs when Ca2+ unbinds from troponin
Ca2+ pumped back into SR for storage
Ca2+ exchanged with Na+ at the membrane
Na+ gradient maintained by Na+/K+ ATPase

72
Q

how does noradrenaline affect excitation contraction coupling in the heart

A

Noradrenaline increases contractile force of the heart, acts through beta-type adrenergic receptor to increase cAMP, to activate PKA which phosphorylates L-type channel increasing passive Ca2+ influx
Amplifies Ca2+ (calcium-induced calcium release)

73
Q

what regulates heart and force of contraction

A

ACh from parasympathetic acts on SA from vagus nerve and decreases HR
NA from symp nerves increases rate of pacemaker cells

74
Q

what is the structure of smooth muscle

A 
2 sheets - one circular and one longitudinal 
more actin than myosin 
no troponin 
no sarcomeres
no striations 
no t tubules or SR 
have caveolae - act like T tubules 
actin attached to dense bodies
75
Q

what is the mechanism of action of contraction of smooth muscle

A

Ca2+ binds to calmodulin, interacts with enzyme myosin kinase to phosphorylate myosin
Once phosphorylated generates tension
Cytoplasmic Ca2+ falls, Ca2+ calmodulin complex dissociates, inactivating myosin kinase
Cross bridges dephosphorylated by enzyme myosin phosphatase

76
Q

which type of muscle can stay contracted for longer

A

smooth muscle
Reduced ATP consumption, so takes long time for each cross bridge to detach from actin
Rate of Ca2+ removal from cytoplasm is slow, so prolonging duration of contraction

77
Q

what is the difference between single unit and multi unit smooth muscle

A

Single unit = most common, gap junctions, located in GI, respiratory, urinary and reproductive tracts, in walls of small arteries, electrical activity may arise spontaneously due to presence of pacemaker cells, action potentials developed, nervous regulation via ANS, contract in response to stretch

lack gap junctions so cells innervated individually, allows fine control, examples include ciliary muscle of the eye, controlling size of pupil and piloerector muscles of hair follicles, not spontaneously active, innervation autonomic, no inherent response to stretch, contractions slow and sustained

78
Q

what is dilated cardiomyopathy

A

enlarged heart - sudden death poor function
weak muscles, short breath, heart failure
can be due to viral infection, autoimmune, exposure t toxic compound

79
Q

what is hypertrophic cardiomyopathy

A

thickening of muscle due to athetoid performance
myocardial disarray
can have genetic causes
common in young adults

80
Q

what is leiomyoma

A

fibroids of smooth muscle
heavy uterine bleeding
unknown genetic cause more common in afro-carribean race

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