study aid 3 Flashcards
(154 cards)
1
Q
skeletal m. - shape
A
long cylinder striations
2
Q
cardiac m. - shape
A
branched striations
3
Q
smooth m. - shape
A
spindle
no striations
4
Q
skeletal m. - nuclei
A
multiple/cell
5
Q
cardiac m. - nuclei
A
1-2/cell
6
Q
smooth m. - nuclei
A
1/cell
7
Q
skeletal m. - myofibrils
A
yes
8
Q
cardiac m. - myofibrils
A
yes
9
Q
smooth m. - myofibrils
A
no
10
Q
skeletal m. - gap junctions
A
no
11
Q
cardiac m. - gap junctions
A
yes - allow ions to pass from cell to cell, allows whole heart to contract, anaerobic resp generates H+ which blocks GJ
12
Q
smooth m. - gap junctions
A
yes: unitary m.
no: multi-unit m.
13
Q
skeletal m. - T-tubules
A
yes
14
Q
cardiac m. - T-tubules
A
yes
15
Q
smooth m. - T-tubules
A
no
16
Q
skeletal m. - control
A
voluntary (somatic) excitation
17
Q
cardiac m. - control
A
involuntary intrinsic (autonomic) excitation or inhibition
stretch, hormones
18
Q
smooth m. - control
A
involuntary intrinsic (autonomic) excitation or inhibition
stretch, hormones
19
Q
skeletal m. - receptors
A
cholinergic
20
Q
cardiac m. -receptors
A
cholinergic & adrenergic
21
Q
smooth m. - receptors
A
cholinergic & adrenergic
22
Q
skeletal m. - individual neuromuscular junctions
A
yes
23
Q
cardiac m. - individual neuromuscular junctions
A
no
24
Q
smooth m. - individual neuromuscular junctions
A
no: unitary m.
yes: multi-unit m.
25
sarcolemma
skeletal muscle fiber plasma membrane
26
sarcoplasm
skeletal muscle cytoplasm but also has glycosomes (granules of stored glycogen) and myoglobin (1 subunit O2 storage)
27
t-tubules
deep invaginations of sarcolemma filled with ECF, AP propagates from sarcolemma to t-tubules
28
sarcoplasmic reticulum
SER that stores and releases calcium ions for muscle contraction and relaxation
contains Ca2+ ATPase actively pumping Ca2+ back into the SR after contraction
29
Ionotropic receptors - ligand-gated channels
Accepts ions and NTs
binding of an NT opens pore
responses are immediate/brief
30
metabotropic
NOT an ion channel
Hydrophilic NT binds to a GPCR
Activated G proteins controls 2nd messenger production (cAMP, cGMP, Ca2+)
responses are indirect, slow, and often prolonged
31
metabotropic receptors - 2nd messenger functions
cAMP, cGMP, Ca2+ activate/inhibit other things
open/close ion channels, activate kinase enzymes/genes & induce protein synthesis
32
acetylcholine receptors
ALL are cholinergic
1. nicotinic ACh receptors
2. muscarinic ACh receptors
33
nicotinic ACh receptors - nAChR
ionotropic - excitatory
- Somatic nerves
- Skeletal m.s: found at neuromuscular junctions
- ANS – autonomic ganglia (sympathetic/parasympathetic)
- Some CNS pathways
Always lead to excitation or depolarization of the cell
- Fast, short-lived responses
34
muscarinic ACh receptors
metabotropic - GPCR, excitatory or inhibitory
- Parasympathetic effects
- Open K+ channels – slow HR
- Close K+, open Na+/Ca2+ - smooth m. contraction
- Glands
- P & CNS
Can lead to both excitement or inhibition
- Slower, longer-lasting responses
35
adrenergic receptors - metabotropic
GPCR - EP/NE (catecholamines)
- sympathetic functions
- released from sympathetic nerve endings and adrenal medulla
36
cholinesterase - purpose, what happens if it is inactivated
Is a group of enzymes that breaks down ACh (a NT), promotes m. contraction
If inhibited, ACh accumulates in the synaptic cleft, leading to overstimulation of nicotinic and muscarinic ACh
37
actin
filamentous actin (consists of globular/g protein actin subunits), twisted double strands, G actin subunits bear binding sites for myosin heads. Tropomyosin and troponin are regulatory proteins
38
myosin (heads -4, tails - 1)
heads contain
1. 2 smaller, light polypeptide chains that act as cross bridges during contraction
2. binding sites for actin of thin filaments
3. binding sites for ATP
4. ATPase enzymes
tails contain
1. interwoven, heavy polypeptide chains
39
titin
a protein, acts as a molecular spring, stabilize the thick filaments to the z disk
40
troponin
promotes muscle contraction, made up of three subunits
41
tropomyosin
blocks muscle contraction, rod-shaped protein that wraps around the actin
42
dystrophin
protein that bound actin through the PM proteins to the ECM
43
myoglobin
one heme group, stores O2 in muscle tissue
44
creatine kinase
takes one phosphate from ATP and gives it to the creatine. Reverses this reaction when muscles are resting: CP + ADP -> Creatine + ATP
45
no dystrophin
still electrical, chemical signaling & mechanical sliding no generation of tension to move it
Duchenne muscular dystrophy - dystrophin genetic mutation - m. weakness, m. atrophy, death
46
what stores does skeletal muscle have
glycogen
47
myofibrils
rodlike elements per m. fiber with actin & myosin - 80% volume
sarcomeres are the smallest functional unit of myofibrils
48
how is myosin arranged in respect to actin bundles
myosin overlaps with the actin filaments
49
a-band
myosin runs the entire length, with actin partway at the end
50
i-band
only contains actin
51
h-zone
contains only myosin, filaments do not overlap, around the m-line
52
z-disk
sheet of protein that anchors the thin filaments & connects myofibrils to each other
53
m-line
line of protein myomesin that holds adjacent thick filaments together
54
what is the difference between myofibers, myofibrils, and myofilaments?
myofiber - muscle cell that contains myofibrils
myofibril - rod-like structure f multiple myofibers
myofilaments - thick and thin that make up the myofibrils
55
end plate potential
nAChR generates this graded potential when ACh binds to ligand-gated channels, Na+ influx, K+ efflux - EPP depolarizes membrane
56
what branches of the NS control skeletal and cardiac myocytes?
skeletal: controlled by the somatic NS
cardiac: controlled by the ANS - sympathetic and parasympathetic
57
what NTs/hormones trigger skeletal/cardiac m.
Skeletal: ACh (NT) to trigger contraction at the neuromuscular junction
Cardiac: ACh (NT) from parasympathetic decreases HR, NE/EP (hormones) from sympathetic increases HR and contractility
58
skeletal muscle AP
activation of ACh receptors leads to membrane depolarization, V-G Na+ channels open, AP is propagated: depol wave along sarcolemma & t-tubules. K+ channels open - repolarization. resting potential = -80mV
- encoded strength of contraction directly proportionately to AP frequency
59
what continues m. contraction
muscle APs only start contraction, depolarization open Ca2+ channels on SR, during contraction, Ca2+ stays elevated, the motor neuron keeps releasing NTs and firing APs
60
excitation-coupling contraction steps
1. APs on T-tubules
2. Stimulate V-activated Ca2+ channels on T-tubules (most dont open)
3. V-CaC activate a Ca2+ release channel by shifting own shape & tugging open the channel on SR allowing receptions/passages
4. SR releases Ca2+ into the cytosol
61
Ca2+ interaction with troponin/tropomyosin
Under resting conditions, intra Ca2+ is low, myosin binding sites on actin are blocked by tropomyosin. depol unleashes Ca2+ from SR to cytosol, Ca2+ binds to regulatory sites on troponin which changes shape of tropomyosin, moving it. Myosin binds sites now available.
62
skeletal muscle: ATP storage and generation
only stores a small amount of ATP directly, around 4-6 sec worth of ATP b/c if a lot of ATP is available, all ATPases are running fast.
ATP is regenerated by creatine phosphate, anaerobic, and aerobic respiration.
63
3 uses for ATP
1. Contraction - cross-bridge, re-energize myosin motor
2. remove Ca2+ from cytosol (active transport)
3. Na+/K+ restoration across sarcolemma & t-tubules
64
creatine phosphate
Reaction: CP + ADP <-> Creatine + ATP
<- = inactive, -> = use
CP is stored & can donate its P to ADP & convert it quickly to ATP during exercise
m. cells store 5 CP per 1 ATP, stores will last 15 sec
65
Anaerobic glycolysis
glucose -> pyruvic acid + 2 ATP
- pyruvic acid -> lactate -> glucose in liver
lots of glucose yields little ATP - 1 min duration
lactate promotes m. fatigue
anaerobic workouts burn more kcal due to the inefficient ATP generation
66
the cori cycle
lactate recycling, prevent acidosis
1. 2 Lactate from skeletal m. released into blood and taken into liver.
2. 2 lactate converted to 2 pyruvate
3. 2 pyruvate + 6 ATP = glucose
4. released into blood
5. glucose into skeletal m. yeilding 2 ATP & 2 pyruvate
6. 2 pyruvate converted to 2 lactate
begins again
67
aerobic respiration
glucose + O2 -> CO2 + H2O + 36ATP
much slower process - hours
68
C-B cycle: binding
high-energy myosin strongly attracted to exposed myosin binding sites on actin
69
C-B cycle: power stroke
myosin head binds & pivots: changes from high-energy state to bend, low-energy state
think filament slides towards center of sarcomere/M-line
ADP & Pi released - bond btw myosin & actin becomes stronger
70
C-B cycle: cross bridge detachment
ATP molecule binds to myosin head, causing detachment
71
C-B cycle: resetting/repowering of myosin
ATP hydrolysis -> ADP + Pi
- provides energy needed to return myosin head to cocked position
72
rigor mortis
cytosolic ATP in a dead cell, no more production, cannot pump any Ca2+ into the SR
high cytosolic Ca2+ (myosin binds) but no more ATP so it stays contracted
73
what happens to the i-band, a-band, h-zone, and z-disks during sarcomere shortening or lengthening?
Shortening - i-band shortens, a-band stays the same length, h-band shortens, z-disks get closer.
74
how is the overlap of actin and myosin heads related to tension generation
more overlap leads to more cross-bridges which leads to greater force production
75
what is muscle twitch
response of a muscle to a single, brief threshold stimulus
76
muscle twitch - latency period
first few ms post stimulation
no muscle response detected/no tension generated even though AP is spreading
77
muscle twitch - contraction period
10-100ms
cross-bridge cycle, Ca2+ floods the cytosol, onset of shortening/contraction to peak tension development
78
muscle twitch - relaxation period
10-100 ms
initiated by re-entry of Ca2+ into SR: tension gradually reduces to 0 b/c Ca2+ must diffuse & get pumped in by Ca2+ ATPase pump
79
what is treppe
muscle not used for a long time, not ready to contract/generate maximum potential
80
what is wave summation
m. depolarized then Ca2+ drops. Stimulated again before potential reaches resting: more channels open, Ca2+ released on existing Ca2+. Tension is proportional to cytosolic Ca2+ concetrations
81
unfused/incomplete tetanus
*a more extreme wave summation*
m. contractions are not sustained, partial relaxations between twitches
82
fused/complete tetanus
continuous & sustained contraction, only need cell depolarized for a small amount of time for Ca2+ to keep elevated
83
7 simplified steps of skeletal m. contraction
1. Motor neuron AP
2. Exocytosis of ACh
3. Skeletal m. end plate potential
4. Skeletal m. AP on PM & T-tubule
5. Ca2+ channel on t-tubule pulls open channel on SR
6. Ca2+ increase in cytosol
7. Removal of troponin
84
myofiber relationship to somatic motor neurons, ACh, cholinergic or adrenergic receptors? ionotropic of metabotropic receptors? nicotinic or muscarinic receptors?
skeletal m. contraction is controlled by somatic motor neurons which released ACh onto nAChRs (*all ACh receptors are cholinergic)
receptors found at neuromuscular junction & excitatory = ionotropic
85
endomyosium
areolar CT between individual m. fibers
86
fasicle
several m. fibers surrounded by perimysium
87
perimysium
fibrous CT btw fascicles
88
epimysium
dense irregular CT wraps m. (several fascicles)
89
compartment syndrome
excess pressure in m.s that pinches BVs/n.s causing pain & cramping
90
what are motor units and how are they associated with recruitment?
motor units are the fundamental unit of motor control; one motor neuron & all the m. fibers it stimulates.
The NS increases the # of motor units activated to generate a stronger m. contraction. Small generated first, then large.
91
small motor units
fine movement m.s - fingers, eyes
- 1 neuron - few myofibers
92
large motor units
large, weight-bearing m.s - thighs, hips
- 1 neuron - many myofibers
93
isotonic contraction
muscle length changes & tension overcomes the load & moves the load during shortening, muscle is still tense as it lengthens again
- lifting a weight
94
isometric contraction
tension increases but load is not moved (m.s = same length)
- doing a plank
95
isotonic - concentric
tension during shortening
- more cross bridges form, generating force
96
isotonic - eccentric
tension during elongation
- less cross bridges form, controlling force
97
What is happening to the cross-bridge cycle during tension generation when the sarcomere is shortening? lengthening? not changing length
shortening - cross bridges formed - power stroke
lengthening - cross bridge detachment
isometric - maintaining tension with a constant # of cross-bridges
98
What does an electromyogram show and how is it different from an EKG?
EMG shows the electrical activity of muscles, EKG shows the electrical activity of the heart
99
how are muscle fiber types classified
1. speed of contraction
- speed of ATP hydrolysis
- type I (slow) or type II (fast)
- speed of removing Ca2+ from the cytosol
2. pathway of ATP formation
- oxidative (aerobic) fibers - type I
- glycolytic (anaerobic) fibers -- type II
100
slow oxidative fibers - TYPE I (contraction time, respiration, mitochondria, myoglobin, BVs, color, example)
relatively slow contraction w/ little power
aerobic respiration
large # of mitochondria (ox phos)
many myoglobin for O2 delivery
rich blood supply
color - red
aids in posture maintenance, running long distance
101
fast glycolytic fibers - TYPE II (contraction time, respiration, mitochondria, myoglobin, BVs, color, example)
contracts quickly, short-term, fatigues rapidly
anaerobic respiration
fewer mitochondria
little myoglobin
little blood supply
color - white
burn kcal the quickest, sprints, intense moves
102
fast oxidative fibers (contraction time, respiration, myoglobin, BVs, color, example)
less common intermediate fiber structured like a fast twitch m. (can be converted to slow)
aerobic respiration
rich supply of myoglobin & capillaries
color - dark
middle distance running, repeated lifts below max weight
103
CICR
calcium induced calcium release
104
what are the difference between APs of contractile cardiac myocytes and skeletal muscle cells?
cardiac APs are significantly longer and initiated by pacemaker cells. All cardiomyocytes contract as a unit, or none do. Cells are electrically coupled via gap junctions
skeletal m. are shorter and initiated by motor neurons
105
what are the difference between AP duration of depolarization of contractile cardiac myocytes and skeletal muscle cells?
cardiac - 200-400 ms
skeletal - 2-5 ms
106
what are the difference between AP role of plasma membrane Ca2+ channels of contractile cardiac myocytes and skeletal muscle cells?
cardiac - PM Ca2+ channels prolong the AP and trigger CICR, leading to contraction
skeletal - act as voltage sensors for initiating Ca2+ release from the SR
107
how do cardiomyocytes increase or decrease their strength of contraction
modulating intracellular calcium levels as well as strength of contraction and stretch. More stretch/overlap - stronger contraction
symp - NE binding to beta-adrenergic receptors increases contractility
para - ACh binding to muscarinic cholinergic receptors decreases contractility
108
intrinsic cardiac conduction system
The SA node generated impulses
- connected via internodal pathway
The AV node receives signaling to depolarize
- 100 ms delay
AV bundle connects the atria to the vents
- R/L bundle branches conduct impulse through interventricular septum towards apex
the subendocardial conducting network depolarizes the contractile cells of both vents
109
pacemaker potential - 1. slow depolarization
opening of slow Na+ permeable channels
closing of K+ channels
110
pacemaker potential - 2. fast depolarization
Calcium threshold reached (~40 mV), Ca2+ V-G Ca2+ channels open
Ca2+ influx produces the rapid rising phase of AP
111
pacemaker potential - 3. repolarization
inactivation of V-G Ca2+ channels
opening of slow V-G K+ channels
112
pacemaker potential - 4. hyperpolarization
reactivates slow opening of Na+ permeable channels
MP has to hit this in order for another electrical trigger
113
What modifies the speed of pacemaker potentials (heart rate), acetylcholine. Are these receptors cholinergic or adrenergic? Ionotropic or metabotropic? Nicotinic or muscarinic?
ACh decreases HR by slowing depolarization at SA node.
Receptors - muscarinic (cholinergic) receptors. Receptors are metabotropic.
114
What modifies the speed of pacemaker potentials (heart rate norepinephrine, Are these receptors cholinergic or adrenergic? Ionotropic or metabotropic? Nicotinic or muscarinic?
NE increase HR by increasing SA depolar using cAMP & protein kinase
Receptors - beta-adrenergic (metabotropic)
115
What modifies the speed of pacemaker potentials (heart rate), epinephrine, Are these receptors cholinergic or adrenergic? Ionotropic or metabotropic? Nicotinic or muscarinic?
EP increase HR by increasing SA depolar using cAMP & protein kinase
Receptors - beta-adrenergic (metabotropic)
116
What modifies the speed of pacemaker potentials (heart rate) atropine, Are these receptors cholinergic or adrenergic? Ionotropic or metabotropic? Nicotinic or muscarinic?
Atropine increases HR by blocking ACh effects
receptors - muscarinic cholinergic receptors (metabotropic)
117
what regions of the heart does the SA node, AV node, AV bundle, bundle branches, and purkinje fibers cause contraction
SA node - atria to contract
AV node - delays and transmits the signal to the vents through the AV bundle, bundle branches, and purkinje fibers leading to ventricular contraction
118
cardioacceleratory center
sympathetic/adrenal medulla stimulation
NE/EP bind to beta-adrenergic receptors and act on SA, AV, & ventricular myocytes to increase HR & increase force of contraction
119
cardioinhibitory center
parasympathetic stimulation
ACh binds to cholinergic (muscarinic) receptors and acts on SA & AV nodes to slow HR
- atropine blocks this
120
blood flow
SVC - RA - tricuspid valve - RV - pulmonary SL valve - pulmonary trunk - L. pulmonary a. - L pulmonary v.s - LA - bicuspid valve - LV - aortic SL valve - Aorta
121
electrical and mechanical events during P wave
e: depolarization of SA node & atria
m: atrial contraction
122
electrical and mechanical events during P-R interval
e: impulse delay btw atria & vents, atria depolarization to ventricular depolarization
m: atrial contraction, ventricular diastole
123
electrical and mechanical events during QRS complex
e: depolarization of vents and atrial repolarization
m: beginning of ventricular contraction, AV valves close
124
electrical and mechanical events during S-T interval
e: ventricular myocytes are all depolarized
m: ventricular contraction
125
electrical and mechanical events during Q-T interval
e: beginning of vent depol to end of vent repol
m: vent contract and relax
126
electrical and mechanical events during T-wave
e: ventricular repolarization begins at apex
m: vents relax
127
what is the electrical axis of the heart and how can it be determined with 3 electrical leads?
the electrical axis represents the overall direction of electrical activity during ventricular depolarization
lead I & II positive deflections, lead III slightly pos, equal, or neg.
128
where are the 3 electrical leads connected
Lead I: R - L arm - measuring depolarization of atria R - L
Lead II: RA - LL - measuring depolarization from base to apex
Lead III: LA - LL
129
What is the relationship between the opening and closing of the AV and SL valves with ventricular pressures
AV: open when ventricular pressure is less than atrial during ventricular diastole. closed when vent pressure is greater than atrial during vent systole
SL: open when vent pressure is greater than aorta & pulm a. during vent systole. closed when vent pressure is less than aorta & pulm a. during vent diastole
130
What is the relationship between the opening and closing of the AV and SL valves with atrial pressures
AV: open when atrial pressure exceeds vents, close when atrial pressure is lower than vents
SL: open when atrial pressure is less than vents, closed when atrial pressure exceeds vents
131
What is the relationship between the opening and closing of the AV and SL valves with pressures in the pulmonary trunk and ascending aorta/aortic arch
AV: open arterial pressure is greater than vent and atrial pressure
SL: open when vent pressure exceeds pressure in large a.s
132
What is the relationship between the opening and closing of the AV and SL valves with heart sounds
AV: 1st as AV valves close; beginning of vent systole
SL: 2nd as SL valves close; beginning fo vent diastole
133
cardiac cycle: ventricular filling (systole/diastole, valves, LV volume, pressure, EKG, major events)
occurs mid-to-late vent diastole
AV valves open: vent pressure less than atria
LV volume - increases
LV pressure - relatively low till the end of diastole
EKG - P-wave - atrial contraction
Atrial systole delivers remaining blood volume
reaching EDV
134
end diastolic volume (EDV)
volume of blood in each vent at end of ventricular diastole - peak volume
135
cardiac cycle: isovolumetric contraction (systole/diastole, valves, LV volume, pressure, EKG, major events)
atria repolarize & relax; vents begin to contract (systole)
AV valves are now closed, SL already closed
LV volume - stays the same (EDV)
LV pressure - rises to 80 mmHg
EKG - QRS complex
136
cardiac cycle: ventricular emptying (systole/diastole, valves, LV volume, pressure, EKG, major events)
early ventricular systole, vent pressure exceeds pressure in large a.s, vent blood drains (not all)
SL valves open
LV volume - falling
LV pressure - rises to around 120 mmHg
EKG - S-T segment
reaches ESV
137
end systolic volume & high BP problem
volume of blood remaining after systole
high systemic BP - causes aortic SL valve to close sooner leaving more blood in LV
138
cardiac cycle: isovolumetric relaxation (systole/diastole, valves, LV volume, pressure, EKG)
early diastole - vents relax, atria already relaxed & filling, back pressure of blood in aorta & pulm trunk
SL valves close, AV valves already closed
LV volume - stays the same, ESV
LV pressure - falling
EKG - T-wave
139
Heart/AV block 1, 2, and 3 degree
1st: P-R interval longer than 200 ms (should be 100) - delay from atria to vents
2nd: some P waves are not conducted through AV node, more P waves that QRS
3rd: SA & AV nodes do not communication, P waves all over
140
missing SA depolarization problem
AV node takes over, slower (40-60 bpm)
141
missing AV depolarization problem
may cause heart block
few or no impulses reach vents (beat at own intrinsic rate)
142
ectopic focus
can lead to arrhythmias because a location outside SA node is generating electrical signals causing heart to beat out of sync - uncoordinated atrial & ventricular contractions
143
extrasystole (premature contraction)
heart palpitations: missing beat followed by a rapid beat, occurring after vent or atrial repol
Atrial - after QRS complex
Vent - after T-wave
144
incompetent valves
blood backflows so heart works harder to re-pump the same blood
145
valvular stenosis
stiff, thickened, or fused valves
constrict opening - heart generates more pressure/force to pump blood
can be replaced w/ mechanical, animal or cadaver valves
146
pericarditis
inflammation of the pericardium caused by little fluid - friction - inflammation - swelling - hardened heart tissue - pericardial friction rub
147
cardiac tamponade
excess fluid/blood buildup btw heart & pericardium
compress the heart, limited pumping ability, and ventricle works harder, decreasing ventricular volume, increases EDV
148
what happens to APs w/ natural toxins?
1) Na+ channel blockade - inhibits depolarization (tetrodotoxin), can also inhibit sensory (lidocaine, Novocain)
2) K+ channel blockade - cause hyperexcitability/constant contraction (charybtoxin, apamin, iberiotoxin)
3) Ca2+ channel blockade - prevent exocytosis/inhibits Ca2+ influx in axon terminal - no NT release (w-conotoxin)
149
natural toxin that hydrolyze secretory proteins
botulinum toxins hydrolyze proteins required for NT exocytosis, can cause respiratory failure, is extremely toxic for humans, used for cosmetic surgery
botulism - made under anaerobic conditions
tetanus toxins - hydrolyze proteins required for NT exocytosis from inhibitory neurons
150
nAChR disturbing agents
channel inhibitors block these receptors inhibiting skeletal m. contract (bungarotoxin, curare)
cholinesterase inhibitors are hydrophobic, can be used on skin that promote m. contact (sarin, physostigmine, and VX nerve agent)
151
AA NT excitatory
glutamate (mostly ionotropic and inhibitory only in vision)
MSG (some metabotropic)
152
AA NT inhibitory
GABA (ionotropic (for Cl-) or metabotropic)
glycine (ionotropic for Cl-)
153
during the QRS complex, what is maximized in the ventricle
pressure
154
what is the atrial kick
most blood drains/is passive into the vent, the kick gets the rest of it
