Chapter Eight Flashcards
1
Q
Muscle fiber is covered by
A
A plasma membrane called, sarcolemma
2
Q
Singular skeletal muscle is a
A
Muscle fiber
3
Q
T-tubules
A
Bring AP into center of the muscle fibers
4
Q
Muscle fiber (five points)
A
-regenerates due to own nucleus
-contains a lot of mitochondria
-glycogen reserves
-sarcoplasmic reticulum
-protein structures make up contractile units
5
Q
Glycogen reserves breaks down to create
A
Glucose
6
Q
Sarcoplasmic reticulum acts similar to the
A
Smooth endoplasmic reticulum
-as it stores Ca in terminal cisternae
7
Q
Calcium is very important for…?
A
Contractions
8
Q
Striated muscle fiber
A
Unique self organized proteins, creating light and dark areas -due to sacromere
-contractile protein
9
Q
Sarcolemma
A
Plasma membrane of the muscle cell
10
Q
Sarcomere
A
Basic contractile unit of a muscle fiber
11
Q
Contractile proteins
A
-form filaments
-myosin and actin
12
Q
Myosin
A
-thick filament
-2 identical monomers
head needs ATP and then binds to actin
13
Q
Actin
A
-thin filament
-globular molecule
14
Q
Cross bridge
A
Myosin binding to actin
15
Q
Regulatory proteins
A
-tropomyosin
-troponin
16
Q
Tropomyosin
A
Covers actins binding site until calcium is released
17
Q
Troponin
A
Binds to Calcium to expose active site of actin
-moves the tropomyosin off of the actin
18
Q
Accessory proteins
A
Nebulin and titin
19
Q
nebulin
A
Runs through thin filaments to stabilize
-largest chain
20
Q
Titin
A
Runs through thick filaments to stabilize
21
Q
Dystrophin
A
Attaches entire sarcolemma
22
Q
Muscular dystrophy
A
Missing the protein dystrophin
23
Q
Contraction
A
Muscle shortening
-Z line closer to the middle
24
Q
Where does contraction begin
A
At neuromuscular junction
-excited by ACH
-graded
-AP
25
Contraction: SER and T tubules release
CALCIUM
26
SER and t tubule receptors
Both has four “button like” receptors that match up
27
SER receptors
Ryanodinic receptors
-foot receptors
28
T tubule receptors
Dihydropyridine receptor (DHP)
29
Ryanodinic receptors function
Calcium release channels
-zip together with DHP receptors
30
DHP stands for
Dihydropyridine receptor
31
DHP receptor
Voltage gated sensors
-releases calcium into cytosol
32
Released calcium during contraction allows
Troponin to bind to the calcium, and then move the tropomyosin to reveal the actin
33
After tromopyosin is removed….
A cross bridge is formed (myosin binds to actin)
34
Power stroke
Myosin pulling the actin inward
35
What is released during a power stroke
Pi
36
What is released after a power stroke
ADP
37
Role of ATP in contraction
ATP binds to myosin cross bridge, breaking linkage between actin and myosin
38
Formation
ADP and Pi
39
Deformation
ATp—-> Pi
-released
40
Sliding filament
Increase of calcium allows thin filaments together
41
Sliding filament pulls what bands together
-I band
-Z lines
-H band
42
Sliding filament parts that doesn’t change
-m line
-A band
43
Process of relaxation: acetylcholinersterae does what?
Breaks down ACH @ neurotransmitter
44
Relaxation process: once acetylcholinesterae breaks down ACH…
Muscle fiber AP stops
45
Relaxation process: muscle fiber AP stops then….
Calcium moves back into SER by ATP
Through calcium ATPase pump
46
Relaxation process: after calcium stops….
Tropomyosin turns “off”
-covers actin site
47
Relaxation process: once tropomyosin covers actin site
Cross bridge stops
48
Rigor mortis
Stiffens upon death, locking of muscles in place
-there is no ATP as metabolism stops
49
If calcium cannot be released it causes
Stiffening
50
Twitch summation
Sustained elevation of cystolic calcium
-form of temporal summation
51
Twitch summation and tetanus
Muscle fiber sustained temporal summation
-continous contraction
52
Tetanus
Force/tension
-a continous contraction
53
“Bad” tetanus infection
Infects body and disables neuron function, blocks GABA
Symptoms: spasms due to lack of relaxation
54
Muscle length
Creates force for muscle movement
55
Optimal length
The best cross bridge formation
-lots of power strokes
-L zero
56
Isotonic contractions
-equal stretch
-same lengthening, same shortening
-force and movement
57
Two types of isotonic
-concentric and esecentric
58
Concentric-isotonic contractions
Muscle flexion, towards center
59
Escentric-isotonic contractions
Away from, lengthening/extension
-most common move for injury
60
Isometric contractions
-equal measurement
-force, no movement
Example- yoga, plank or Pilates
61
Types of muscle fibers
-slow oxidative
-fast oxidative
-fast glycolytic
62
Liver breaks down glycogen turning it into
Glucose
63
What is the main source of energy
Glucose
64
Creatine phosphate mobilizes
energystores as creatine kinase
65
Energystores are
-creatine
-releases phosphate to create ATP
66
When is creatine phosphate formed
When muscle is at rest
67
Moving muscle and creatine phosphate
First few minutes is breaking phosphate to release ATP
68
What are examples in which energystores are mobilized
Sprint and speed
69
Creatine supplement
affects the GI and dehydrates
-weight gain
70
Glycolysis
First step of glucose breakdown
2 ATP are produced
71
Aerobic -glycolysis
Oxygen used!
-creates pyruvic acid
-into the kreb cycle
72
Oxidative phosphorylation
-citric acid cycle
-electron transport
73
Anaerobic
-no use of oxygen
-back into body
Lactic acid production
74
Citric acid cycle
Needs oxygen
75
Electron transport
Needs oxygen!!
76
Fatty acids…
Enter straight into the kreb cycle
77
Myoglobin
Creates red colour
White fiber vs red fiber
78
Slow oxidative (type 1 fiber)
Slow: twitches, contractile, ATP usage, Calcium release
-Used frequently
-all three cycles
-produces a lot of ATP
-alot of: mitochondria, blood vessels, O2, myoglobin
-less fatigue
79
Fast-oxidative (type11a fiber)
Fast: twitches, contractile cycle, calcium release
-fast usage of ATP
-occasionally used
-all three cycles
-produces a lot of ATP
-a lot of: mitochondria, blood vessels, oxygen, myoglobin
-less fatigue
80
Fast-glycolytic (type 11x)
Fast: twitches, contractile cycle, calcium release, ATP usage
-occasionally used
-oxygen or not
-few: mitochondria, blood vessels, O2, myoglobin
-fatigue more (less ATP produced)
81
Example of slow-oxidative
Posture, walking, standing
82
Muscles require
ATP
83
Muscle fatigue
No longer responds to stimulations with some degree of contractile
84
Central fatigue
-CNS
-psychological (mind/matter)
-abnormality in CNS due to monotomy
-something wrong with somatic motor neuron
85
Monotomy
Same over and over
-not necessarily strenuous
-assembly line
86
Peripheral fatigue
-NMJ is vulnerable
-at the SR and T tubules
-build up of lactic acid or lack of ATP
-depleted glucose
87
Optimal muscle length
Thin filaments optimally overlap regions of thick filament, giving maximal cross bridges to be formed
-Maximal force can be achieved on a contraction
-more tension can be achieved during tetanus
88
EPOC stands for
Excess post-exercise oxygen consumption
89
EPOC function
Breath heavily to bring in O2
-removes lactic acid
-creates more ATP by inc of glycolysis
90
Muscular dystrophy
Males>females
-genetic (carried in X chromosome)
Symptom: cannot walk, deformities, fatal
91
Muscular dystrophy reason
Lacking protein gene as distrophin
-attaches sacromere to sarcolemma
-move/shorten will cause deformation
92
Treatment for muscular dystrophy
Genetic therapy
93
Basal nuclei
94
Cerebellum
Skilled, fine movements
95
Thalamus
96
Brain stem
97
Spinal cord
98
Muscle spindle
-skeletal muscle receptors
-controls stretch/overdoing any action
99
Gamma motor
From CNS
-wraps around middle portion
100
Intrafusal
-CNS
-gamma motor neuron sends to intrafusual
-determining how much stretch
101
Extrafusul
-from CNS
-to alpha motor neuron
-extra fusul Myofibrils
-to NMJ
102
Golgi tendon organ
-monitors tension/force
-excessively heavy loads —>eg dropping as protection for muscles
103
Golgi tendon organ is made up of
Collagen and sensory neuron afterent
104
Contractile area of muscle spindle
The end
105
Noncontractile region of muscle spindle
Middle area
106
Smooth muscle is found in
Hollow organs, has no striation
107
Myosin and actin in smooth muscle
YES
-forms cross bridges
108
Intermediate in smooth muscle
YES
-not involved in contractions
109
Troponin in smooth muscle
NO
-no binding to CA
-instead binding to Calmodulin
110
Tropomyosin in smooth muscle
YES
-present
111
SR and T tubules in smooth muscle
-very few SR
-T tubules completely absent
112
Calcium storage in smooth muscle
-stored in few SR
-mostly in ECF
113
Smooth muscle Z-lines
ABSENT
-dense body has the myosin and actin held together by proteins
114
Mechanism of action for smooth muscle
Shortens more globular due to no structure
-scrunches up
115
Calmodulin binds to
Calcium
116
Calcium comes from
SR and ECF
117
Calcium and Calmodulin form..
Ca2+-Calmodulin complex
118
____ _____ activates the myosin light chain kinase
Inactive myosin (MLK enzyme)
119
ATP activates myosin to form
Phosphorylated myosin cross bridge
-activates myosin head
-CROSS BRIDGE
120
Multiunit (subtypes of smooth muscles)
Must be separately stimulated + neurogenic
-multiple units of makeup
121
Single unit (subtypes of smooth muscle)
Contract as one single unit
-self excitable
-syncytium (one cel)
122
Single unit contains
Gap junctions
-electrical passing along
123
Benefit of single unit smooth muscles
Slow and energy efficient
124
Example of single unit
Hollow organs found in the GI tract
125
Electrical activity of smooth muscle
Slow wave potential and pacemaker potential
126
Slow wave potential
When threshold reached, then potential is released
127
Pacemaker potential
Sets own pace
-gradual depolarization regular periodic basis
-self induced
128
Advantages of electrical activity of smooth muscle
-contractile response is much slower
-very energy efficient
-relaxes slower
-cross bridge stays longer
129
Cardiac muscle
Striated and contains sarcomere structure
-just much smaller
130
Branches of cardiac muscle held together by
Intercalated discs
-gap junctions and desmosomes
131
Cardiac muscle contains
Actin, myosin, troponin and tropomyosin
132
Cardiac muscle does not contains
Intermediate discs
133
SR and T tubules in cardiac muscle
-fairly well developed SR
-much larger T tubules
134
Calcium comes from cardiac muscle
SR and ECF
135
Cardiac muscle- blood vessels
Bound to myoglobin
-bring in high amounts of oxygen
136
mitochondria in cardiac muscle
Flooded with mitochondria
-energy is highly needed
137
Pulmonary circulation
Deoxygenated
-to the lungs
138
Systemic circulation
Oxygenated
139
Valves
Right atrial ventricle valve
Left atrial ventricle valve
Aortic valve
Pulmonary valve
140
Right AV
Tricuspid, found in right atrium/ventricle
141
Left AV
Bicuspid valve
-left atrium/ventricle
142
Aortic/pulmonary valve
Semilumar valves
143
Endothelium/endocardium
Inner layer
144
Myocardium
Middle layer, cardiac muscle
145
Epicardium
Outer layer
146
Pericardium
Double layer serous membrane
-sac enclosed entire heart
147
Fibrous pericardium
Outer, tough layer
148
Pericardial fluid
Releases friction
149
Autorhymthmicity
Sets its own rhythm
-heart contracts rythmictly due to AP generated by it self
150
Contractile cell
Do the work of pumping, cardiac muscle fibers
151
Autorhythmic cell
Generates AP and sets the pace
152
Endocarditis
Infection
153
SA node
Right atrial wall
70-80 BPM
-normal pacemaker
154
AV node
Near septum
40-60 BPM
-latent pacemaker
155
Bundle of his
Running either side of heart
-latent pacemaker
20-40 BPM
156
Purkinjie fibers
Entire ventricular muscle
6x faster
157
Inter-nodal pathway
Connects SA and NA
-delay of 100m/s
158
Av nodal delay
Ensure ventricles fill
159
Interatrial pathway
Excite left atria 30ms
160
total contraction
160ms
161
Pacemaker activity
Rhythm set by a healthy SA node
162
I-f
I- current f-funny
-first pacemaker current to be identified
-activated by hyperpolarization
163
T-type calcium channel
Open at lower membrane potentials
-open during slow depolarization
164
Pacemaker at rest
-60mv
165
Threshold of pacemaker
-40mv
166
Pacemaker threshold brought too by
I-f and I-t
-hyperpolarization
167
I-f activates
Na and K
168
I-t
I- current t-transium
Bring to threshold
169
Cyclic nucleotide gated channels
Slow pace making
170
Peak is….
0mv due to Ica and L
171
L is
Long lasting channel
172
Falling phase pacemaker
Increased opening of I-k channels
-bring to rest
173
Normal pacemaker
75BPM
174
SA node “derails”
Av node takes over
-55 BPM
175
SA node functional, AV node “derail”
SA node is 75 BPM at atrial
-bundle of his/purkinjie is 35 BPM
176
SA and NA node functional, but purkinjie is abnormal
140BPM (double)
-ectopic focus/out of focus —> eventually muscles die
177
Electrical activity of contraction cell
1. At rest: -80mv
2. Depolarization: massive 130mv P of NA is up
3. Peak: 50mv —> sodium inactivated
4. Sodium is down, K is up…. Plateau and nodal delay
5. Delayed rectifier K/complete repolarization
178
Contractile cell electrical activity timing
250ms
-much longer `
179
Protection of contractile cel
By producing refractory period (300ms)
-heart never tetanus or summation
-cannot have another AP
time for one AP till that AP is done
180
Electrocardiogram or ECG
Non invasive - to see state of heart
-beats/min
-measurement of sum action potential
181
Order of ECG
P,Q,R,S,T,P
182
P wave
Atrial depolarization
183
QRS complex
Ventricular repolarization
184
ST segment
Time for heart to empty, blood ejected
185
T wave
ventricular depolarization
186
Rate of heart measured by ECG
P to P
Or
R to R
187
Tachycardia
Higher than normal
>100BPM
188
Brachychardia
Lower heart rate
<60BPM
189
Arrhythmia
Variation from normal rhythm
190
Atrial fibulation
Rapid and irregular
-no definite p wave
-QRS is sporadic
-atrial beating faster than ventricle
191
Ventricular fibulation
Uncoordinated and chaotic
-reset SA node with paddles (reset ventricles)
-most dangerous
Danger: brain gets no blood/loss cognitive functions
192
Heart block
Conduction pathway is blocked
Atrial:ventricle
-2:1
-3:1
-complete
193
Events of a cardiac cycle -A
A- ventricular diastole, AV valve open
-passive filling (no pressure is applied)
194
Events of a cardiac cycle -B
B- atrial contraction, P wave
-pushing rest of blood out so Av valve can close
195
Events of a cardiac cycle -C
C- AV valves closed, volume is stable
-isovolumetric contraction
196
Events of a cardiac cycle -D
D-ventricular polarization and ejection
-volume lowers
-systole
197
endsystolic volume
65mL
198
enddiastolic volume
135mL
199
Events of a cardiac cycle -E
E- preparing and relaxing
200
Max volume in the cardiac cycle
A and B
201
Diastole
Filling and relaxing
202
Systole
Contracting and emptying
203
Sounds of cardiac cycle
Lub and dub
204
Lub
First, low pitch and longer, softer
-filing the heart
-ending ventricular diastole
205
Lub sound comes from
Closure of AV valve
206
Dub
Second, high pitch and shorter, softer
-ending ventricular systole
207
Dub sound is from
Closure of SL valves
208
Laminar
No sound
209
Turbulent
Has sound due to disruptence
-sign of murmurs
210
Heart murmurs
Are valve malfunctions
-in the opening and closing
-mechanical
211
Stenotic heart murmurs
Due to a stiff and narrow valve
-does not open completely and blood has to be forced resulting in turbulence
212
Sound of stenotic murmur
Whistling sound
213
Insufficient heart murmur
Due to a leaky valve
-valve edges do not close properly
-blood flows backwards creating turbulence
214
Insufficient murmurs sound
Swishing sound
215
Rheumatic fever
Infection by strep into heart causing infection of midtral valve
-chest pain, murmur and heart failure
216
Systolic murmur timing
Happens between 2 sounds
-Lub MURMUR dub
217
Diastole murmur timing
Happens between two cycles
-Lub dub MURMUR Lub dub
218
Lub-whistle-dub
Systolic and stenotic
Valve: SL
219
Lub-dub-whistle
Diastole and stenotic
Valve: AV
220
Lub-swish-dub
Systolic and insufficient
Valve: AV
221
Lub-dub-swish
Diastole and insufficient
Valve: SL
222
Average cardiac output
5L/min
223
What is cardiac output
-amount of blood leaving ventricles
-example: excersizing CO is high
224
cardiac output is related to
Sympathetic or parasympathetic state of the heart
225
parasympathetic cardiac output (SA, AV, ventricles)
Reducing and slowing the heart rate
SA- slow rate by increasing K (hyperpolarization)
AV- increasing a delay
Ventricles- no effect
226
Sympathetic impact on CO (SA, AV, ventricles and atria)
Heart ramps up
SA- threshold much quicker
AV- delay reduced
Ventricles- push out blood quicker
Atria- contract faster
227
Sympathetic CO pathway
From: thoraco-lumbar
Impacts: NE/E
Receptor: Adenergic B
increases: cAMP
228
Parasympathetic CO pathway
Straight from cervical region
-vagus CN X
Releases: Ach
Binds: receptor and G protein (muscrinic receptor)
+cAMP messenger
229
Intrinsic control (sympathetic activity)
Built in, increases venous return
EDV and SV increases
230
Extrinsic sympathetic activity
Directly increases contractions
SV increases
231
Frank startling law
What is brought in diastole, pumps out at systole
-Inc EDV will in SV
-force = stretch
232
Heart failure
Cannot produce amount of SV needed to supply the bodies demands
233
Compensatory measures: heart failure
1. Sympathetic reflect : revs up the heart, inc SV
2. Kidneys retain salt and water to inc plasma volume that inc SV and CO
234
Decompensated heart failure
Compensatory measures fail
235
Three decompensated heart failures
1. Forward failure (blood forward)
2. Left side failure
3. Backward failure (lungs fill with blood)
236
Healthy heart
Fresh supply through aortic artery
237
Coronary vessel
Supplies nutrients to itself (the heart)
238
When does coronary ciruculation occur
During ventriculardiastole
239
Why does coronary circulation occur at ventricular diastole
Systole compresses coronary vessels, which contracts
-closure of aorta causes disturbance
-pressure is released
240
Adenosine
Triggers blood flow or vasodilation in the coronary arteries q
241
CAD or coronary artery disease
Pathological change in coronary wall that diminishes blood flow
-block of coronary vessel
242
Early stages of CAD
Vascular spasm
-reversible
-usually due to PAF (platelet , activating factor not bringing in enough O2 to heart)
243
Altherosclerosis
Oxidized cholesterol creates vasoconstriction
-serious as no oxygen
244
Altherosclerosis: oxidized cholesterol accumulates
Macrophages to eat up the cholesterol, and they enlarge
245
Altherosclerosis: enlarged macrophages
Form a plaque, and bulge into the coronary vessel reducing the diameter
246
Altherosclerosis: formed plaque of fatty macrophages
Are covered by smooth muscles called atheromas
247
Altherosclerosis: atheromas
Smooth muscle that covers the plaque, bulges into lumen
248
Altherosclerosis: atheromas attract
Fibroblast, which begins to form a cap
249
Altherosclerosis: calcium ions…
Precipitate around the cap formation to create a solid plague
-hardening the coronary artery
250
Thromboembolism
The plaque keeps increasing and
1.reduces blood flow
2. or is lost and floating around
3. Or has blocked part of the heart and slowly is dying
251
Angina pectoris
Heart pain felt in shoulder
Treatment: nitroglyceron (vasodilator)
252
Embolus
Risk of clogging smaller vessels
-cap floating around coronary vessels
253
Acute myocardial infraction
The heart is too weak
