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Human Physiology I > Chapter Eight > Flashcards

Chapter Eight Flashcards

1
Q

Muscle fiber is covered by

A

A plasma membrane called, sarcolemma

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2
Q

Singular skeletal muscle is a

A

Muscle fiber

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3
Q

T-tubules

A

Bring AP into center of the muscle fibers

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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

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5
Q

Glycogen reserves breaks down to create

A

Glucose

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6
Q

Sarcoplasmic reticulum acts similar to the

A

Smooth endoplasmic reticulum
-as it stores Ca in terminal cisternae

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7
Q

Calcium is very important for…?

A

Contractions

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8
Q

Striated muscle fiber

A

Unique self organized proteins, creating light and dark areas -due to sacromere
-contractile protein

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9
Q

Sarcolemma

A

Plasma membrane of the muscle cell

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10
Q

Sarcomere

A

Basic contractile unit of a muscle fiber

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11
Q

Contractile proteins

A

-form filaments
-myosin and actin

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12
Q

Myosin

A

-thick filament
-2 identical monomers
head needs ATP and then binds to actin

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13
Q

Actin

A

-thin filament
-globular molecule

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14
Q

Cross bridge

A

Myosin binding to actin

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15
Q

Regulatory proteins

A

-tropomyosin
-troponin

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16
Q

Tropomyosin

A

Covers actins binding site until calcium is released

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17
Q

Troponin

A

Binds to Calcium to expose active site of actin
-moves the tropomyosin off of the actin

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18
Q

Accessory proteins

A

Nebulin and titin

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19
Q

nebulin

A

Runs through thin filaments to stabilize
-largest chain

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20
Q

Titin

A

Runs through thick filaments to stabilize

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21
Q

Dystrophin

A

Attaches entire sarcolemma

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22
Q

Muscular dystrophy

A

Missing the protein dystrophin

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23
Q

Contraction

A

Muscle shortening
-Z line closer to the middle

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24
Q

Where does contraction begin

A

At neuromuscular junction
-excited by ACH
-graded
-AP

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25
Q

Contraction: SER and T tubules release

A

CALCIUM

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26
Q

SER and t tubule receptors

A

Both has four “button like” receptors that match up

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27
Q

SER receptors

A

Ryanodinic receptors
-foot receptors

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28
Q

T tubule receptors

A

Dihydropyridine receptor (DHP)

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29
Q

Ryanodinic receptors function

A

Calcium release channels
-zip together with DHP receptors

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30
Q

DHP stands for

A

Dihydropyridine receptor

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31
Q

DHP receptor

A

Voltage gated sensors
-releases calcium into cytosol

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32
Q

Released calcium during contraction allows

A

Troponin to bind to the calcium, and then move the tropomyosin to reveal the actin

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33
Q

After tromopyosin is removed….

A

A cross bridge is formed (myosin binds to actin)

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34
Q

Power stroke

A

Myosin pulling the actin inward

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35
Q

What is released during a power stroke

A

Pi

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36
Q

What is released after a power stroke

A

ADP

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37
Q

Role of ATP in contraction

A

ATP binds to myosin cross bridge, breaking linkage between actin and myosin

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38
Q

Formation

A

ADP and Pi

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39
Q

Deformation

A

ATp—-> Pi
-released

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40
Q

Sliding filament

A

Increase of calcium allows thin filaments together

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41
Q

Sliding filament pulls what bands together

A

-I band
-Z lines
-H band

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42
Q

Sliding filament parts that doesn’t change

A

-m line
-A band

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43
Q

Process of relaxation: acetylcholinersterae does what?

A

Breaks down ACH @ neurotransmitter

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44
Q

Relaxation process: once acetylcholinesterae breaks down ACH…

A

Muscle fiber AP stops

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45
Q

Relaxation process: muscle fiber AP stops then….

A

Calcium moves back into SER by ATP
Through calcium ATPase pump

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46
Q

Relaxation process: after calcium stops….

A

Tropomyosin turns “off”
-covers actin site

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47
Q

Relaxation process: once tropomyosin covers actin site

A

Cross bridge stops

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48
Q

Rigor mortis

A

Stiffens upon death, locking of muscles in place
-there is no ATP as metabolism stops

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49
Q

If calcium cannot be released it causes

A

Stiffening

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50
Q

Twitch summation

A

Sustained elevation of cystolic calcium
-form of temporal summation

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51
Q

Twitch summation and tetanus

A

Muscle fiber sustained temporal summation
-continous contraction

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52
Q

Tetanus

A

Force/tension
-a continous contraction

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53
Q

“Bad” tetanus infection

A

Infects body and disables neuron function, blocks GABA
Symptoms: spasms due to lack of relaxation

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54
Q

Muscle length

A

Creates force for muscle movement

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55
Q

Optimal length

A

The best cross bridge formation
-lots of power strokes
-L zero

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56
Q

Isotonic contractions

A

-equal stretch
-same lengthening, same shortening
-force and movement

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57
Q

Two types of isotonic

A

-concentric and esecentric

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58
Q

Concentric-isotonic contractions

A

Muscle flexion, towards center

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59
Q

Escentric-isotonic contractions

A

Away from, lengthening/extension
-most common move for injury

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60
Q

Isometric contractions

A

-equal measurement
-force, no movement
Example- yoga, plank or Pilates

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61
Q

Types of muscle fibers

A

-slow oxidative
-fast oxidative
-fast glycolytic

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62
Q

Liver breaks down glycogen turning it into

A

Glucose

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63
Q

What is the main source of energy

A

Glucose

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64
Q

Creatine phosphate mobilizes

A

energystores as creatine kinase

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65
Q

Energystores are

A

-creatine
-releases phosphate to create ATP

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66
Q

When is creatine phosphate formed

A

When muscle is at rest

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67
Q

Moving muscle and creatine phosphate

A

First few minutes is breaking phosphate to release ATP

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68
Q

What are examples in which energystores are mobilized

A

Sprint and speed

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69
Q

Creatine supplement

A

affects the GI and dehydrates
-weight gain

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70
Q

Glycolysis

A

First step of glucose breakdown
2 ATP are produced

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71
Q

Aerobic -glycolysis

A

Oxygen used!
-creates pyruvic acid
-into the kreb cycle

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72
Q

Oxidative phosphorylation

A

-citric acid cycle
-electron transport

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73
Q

Anaerobic

A

-no use of oxygen
-back into body
Lactic acid production

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74
Q

Citric acid cycle

A

Needs oxygen

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75
Q

Electron transport

A

Needs oxygen!!

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76
Q

Fatty acids…

A

Enter straight into the kreb cycle

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77
Q

Myoglobin

A

Creates red colour
White fiber vs red fiber

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78
Q

Slow oxidative (type 1 fiber)

A

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

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79
Q

Fast-oxidative (type11a fiber)

A

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

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80
Q

Fast-glycolytic (type 11x)

A

Fast: twitches, contractile cycle, calcium release, ATP usage
-occasionally used
-oxygen or not
-few: mitochondria, blood vessels, O2, myoglobin
-fatigue more (less ATP produced)

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81
Q

Example of slow-oxidative

A

Posture, walking, standing

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82
Q

Muscles require

A

ATP

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83
Q

Muscle fatigue

A

No longer responds to stimulations with some degree of contractile

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84
Q

Central fatigue

A

-CNS
-psychological (mind/matter)
-abnormality in CNS due to monotomy
-something wrong with somatic motor neuron

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85
Q

Monotomy

A

Same over and over
-not necessarily strenuous
-assembly line

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86
Q

Peripheral fatigue

A

-NMJ is vulnerable
-at the SR and T tubules
-build up of lactic acid or lack of ATP
-depleted glucose

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87
Q

Optimal muscle length

A

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

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88
Q

EPOC stands for

A

Excess post-exercise oxygen consumption

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89
Q

EPOC function

A

Breath heavily to bring in O2
-removes lactic acid
-creates more ATP by inc of glycolysis

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90
Q

Muscular dystrophy

A

Males>females
-genetic (carried in X chromosome)
Symptom: cannot walk, deformities, fatal

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91
Q

Muscular dystrophy reason

A

Lacking protein gene as distrophin
-attaches sacromere to sarcolemma
-move/shorten will cause deformation

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92
Q

Treatment for muscular dystrophy

A

Genetic therapy

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93
Q

Basal nuclei

A
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94
Q

Cerebellum

A

Skilled, fine movements

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95
Q

Thalamus

A
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96
Q

Brain stem

A
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97
Q

Spinal cord

A
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98
Q

Muscle spindle

A

-skeletal muscle receptors
-controls stretch/overdoing any action

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99
Q

Gamma motor

A

From CNS
-wraps around middle portion

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100
Q

Intrafusal

A

-CNS
-gamma motor neuron sends to intrafusual
-determining how much stretch

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101
Q

Extrafusul

A

-from CNS
-to alpha motor neuron
-extra fusul Myofibrils
-to NMJ

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102
Q

Golgi tendon organ

A

-monitors tension/force
-excessively heavy loads —>eg dropping as protection for muscles

103
Q

Golgi tendon organ is made up of

A

Collagen and sensory neuron afterent

104
Q

Contractile area of muscle spindle

A

The end

105
Q

Noncontractile region of muscle spindle

A

Middle area

106
Q

Smooth muscle is found in

A

Hollow organs, has no striation

107
Q

Myosin and actin in smooth muscle

A

YES
-forms cross bridges

108
Q

Intermediate in smooth muscle

A

YES
-not involved in contractions

109
Q

Troponin in smooth muscle

A

NO
-no binding to CA
-instead binding to Calmodulin

110
Q

Tropomyosin in smooth muscle

A

YES
-present

111
Q

SR and T tubules in smooth muscle

A

-very few SR
-T tubules completely absent

112
Q

Calcium storage in smooth muscle

A

-stored in few SR
-mostly in ECF

113
Q

Smooth muscle Z-lines

A

ABSENT
-dense body has the myosin and actin held together by proteins

114
Q

Mechanism of action for smooth muscle

A

Shortens more globular due to no structure
-scrunches up

115
Q

Calmodulin binds to

A

Calcium

116
Q

Calcium comes from

A

SR and ECF

117
Q

Calcium and Calmodulin form..

A

Ca2+-Calmodulin complex

118
Q

____ _____ activates the myosin light chain kinase

A

Inactive myosin (MLK enzyme)

119
Q

ATP activates myosin to form

A

Phosphorylated myosin cross bridge
-activates myosin head
-CROSS BRIDGE

120
Q

Multiunit (subtypes of smooth muscles)

A

Must be separately stimulated + neurogenic
-multiple units of makeup

121
Q

Single unit (subtypes of smooth muscle)

A

Contract as one single unit
-self excitable
-syncytium (one cel)

122
Q

Single unit contains

A

Gap junctions
-electrical passing along

123
Q

Benefit of single unit smooth muscles

A

Slow and energy efficient

124
Q

Example of single unit

A

Hollow organs found in the GI tract

125
Q

Electrical activity of smooth muscle

A

Slow wave potential and pacemaker potential

126
Q

Slow wave potential

A

When threshold reached, then potential is released

127
Q

Pacemaker potential

A

Sets own pace
-gradual depolarization regular periodic basis
-self induced

128
Q

Advantages of electrical activity of smooth muscle

A

-contractile response is much slower
-very energy efficient
-relaxes slower
-cross bridge stays longer

129
Q

Cardiac muscle

A

Striated and contains sarcomere structure
-just much smaller

130
Q

Branches of cardiac muscle held together by

A

Intercalated discs
-gap junctions and desmosomes

131
Q

Cardiac muscle contains

A

Actin, myosin, troponin and tropomyosin

132
Q

Cardiac muscle does not contains

A

Intermediate discs

133
Q

SR and T tubules in cardiac muscle

A

-fairly well developed SR
-much larger T tubules

134
Q

Calcium comes from cardiac muscle

A

SR and ECF

135
Q

Cardiac muscle- blood vessels

A

Bound to myoglobin
-bring in high amounts of oxygen

136
Q

mitochondria in cardiac muscle

A

Flooded with mitochondria
-energy is highly needed

137
Q

Pulmonary circulation

A

Deoxygenated
-to the lungs

138
Q

Systemic circulation

A

Oxygenated

139
Q

Valves

A

Right atrial ventricle valve
Left atrial ventricle valve
Aortic valve
Pulmonary valve

140
Q

Right AV

A

Tricuspid, found in right atrium/ventricle

141
Q

Left AV

A

Bicuspid valve
-left atrium/ventricle

142
Q

Aortic/pulmonary valve

A

Semilumar valves

143
Q

Endothelium/endocardium

A

Inner layer

144
Q

Myocardium

A

Middle layer, cardiac muscle

145
Q

Epicardium

A

Outer layer

146
Q

Pericardium

A

Double layer serous membrane
-sac enclosed entire heart

147
Q

Fibrous pericardium

A

Outer, tough layer

148
Q

Pericardial fluid

A

Releases friction

149
Q

Autorhymthmicity

A

Sets its own rhythm
-heart contracts rythmictly due to AP generated by it self

150
Q

Contractile cell

A

Do the work of pumping, cardiac muscle fibers

151
Q

Autorhythmic cell

A

Generates AP and sets the pace

152
Q

Endocarditis

A

Infection

153
Q

SA node

A

Right atrial wall
70-80 BPM
-normal pacemaker

154
Q

AV node

A

Near septum
40-60 BPM
-latent pacemaker

155
Q

Bundle of his

A

Running either side of heart
-latent pacemaker
20-40 BPM

156
Q

Purkinjie fibers

A

Entire ventricular muscle
6x faster

157
Q

Inter-nodal pathway

A

Connects SA and NA
-delay of 100m/s

158
Q

Av nodal delay

A

Ensure ventricles fill

159
Q

Interatrial pathway

A

Excite left atria 30ms

160
Q

total contraction

A

160ms

161
Q

Pacemaker activity

A

Rhythm set by a healthy SA node

162
Q

I-f

A

I- current f-funny
-first pacemaker current to be identified
-activated by hyperpolarization

163
Q

T-type calcium channel

A

Open at lower membrane potentials
-open during slow depolarization

164
Q

Pacemaker at rest

A

-60mv

165
Q

Threshold of pacemaker

A

-40mv

166
Q

Pacemaker threshold brought too by

A

I-f and I-t
-hyperpolarization

167
Q

I-f activates

A

Na and K

168
Q

I-t

A

I- current t-transium
Bring to threshold

169
Q

Cyclic nucleotide gated channels

A

Slow pace making

170
Q

Peak is….

A

0mv due to Ica and L

171
Q

L is

A

Long lasting channel

172
Q

Falling phase pacemaker

A

Increased opening of I-k channels
-bring to rest

173
Q

Normal pacemaker

A

75BPM

174
Q

SA node “derails”

A

Av node takes over
-55 BPM

175
Q

SA node functional, AV node “derail”

A

SA node is 75 BPM at atrial
-bundle of his/purkinjie is 35 BPM

176
Q

SA and NA node functional, but purkinjie is abnormal

A

140BPM (double)
-ectopic focus/out of focus —> eventually muscles die

177
Q

Electrical activity of contraction cell

A
  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
Q

Contractile cell electrical activity timing

A

250ms
-much longer `

179
Q

Protection of contractile cel

A

By producing refractory period (300ms)
-heart never tetanus or summation
-cannot have another AP
time for one AP till that AP is done

180
Q

Electrocardiogram or ECG

A

Non invasive - to see state of heart
-beats/min
-measurement of sum action potential

181
Q

Order of ECG

A

P,Q,R,S,T,P

182
Q

P wave

A

Atrial depolarization

183
Q

QRS complex

A

Ventricular repolarization

184
Q

ST segment

A

Time for heart to empty, blood ejected

185
Q

T wave

A

ventricular depolarization

186
Q

Rate of heart measured by ECG

A

P to P
Or
R to R

187
Q

Tachycardia

A

Higher than normal
>100BPM

188
Q

Brachychardia

A

Lower heart rate
<60BPM

189
Q

Arrhythmia

A

Variation from normal rhythm

190
Q

Atrial fibulation

A

Rapid and irregular
-no definite p wave
-QRS is sporadic
-atrial beating faster than ventricle

191
Q

Ventricular fibulation

A

Uncoordinated and chaotic
-reset SA node with paddles (reset ventricles)
-most dangerous
Danger: brain gets no blood/loss cognitive functions

192
Q

Heart block

A

Conduction pathway is blocked
Atrial:ventricle
-2:1
-3:1
-complete

193
Q

Events of a cardiac cycle -A

A

A- ventricular diastole, AV valve open
-passive filling (no pressure is applied)

194
Q

Events of a cardiac cycle -B

A

B- atrial contraction, P wave
-pushing rest of blood out so Av valve can close

195
Q

Events of a cardiac cycle -C

A

C- AV valves closed, volume is stable
-isovolumetric contraction

196
Q

Events of a cardiac cycle -D

A

D-ventricular polarization and ejection
-volume lowers
-systole

197
Q

endsystolic volume

A

65mL

198
Q

enddiastolic volume

A

135mL

199
Q

Events of a cardiac cycle -E

A

E- preparing and relaxing

200
Q

Max volume in the cardiac cycle

A

A and B

201
Q

Diastole

A

Filling and relaxing

202
Q

Systole

A

Contracting and emptying

203
Q

Sounds of cardiac cycle

A

Lub and dub

204
Q

Lub

A

First, low pitch and longer, softer
-filing the heart
-ending ventricular diastole

205
Q

Lub sound comes from

A

Closure of AV valve

206
Q

Dub

A

Second, high pitch and shorter, softer
-ending ventricular systole

207
Q

Dub sound is from

A

Closure of SL valves

208
Q

Laminar

A

No sound

209
Q

Turbulent

A

Has sound due to disruptence
-sign of murmurs

210
Q

Heart murmurs

A

Are valve malfunctions
-in the opening and closing
-mechanical

211
Q

Stenotic heart murmurs

A

Due to a stiff and narrow valve
-does not open completely and blood has to be forced resulting in turbulence

212
Q

Sound of stenotic murmur

A

Whistling sound

213
Q

Insufficient heart murmur

A

Due to a leaky valve
-valve edges do not close properly
-blood flows backwards creating turbulence

214
Q

Insufficient murmurs sound

A

Swishing sound

215
Q

Rheumatic fever

A

Infection by strep into heart causing infection of midtral valve
-chest pain, murmur and heart failure

216
Q

Systolic murmur timing

A

Happens between 2 sounds
-Lub MURMUR dub

217
Q

Diastole murmur timing

A

Happens between two cycles
-Lub dub MURMUR Lub dub

218
Q

Lub-whistle-dub

A

Systolic and stenotic
Valve: SL

219
Q

Lub-dub-whistle

A

Diastole and stenotic
Valve: AV

220
Q

Lub-swish-dub

A

Systolic and insufficient
Valve: AV

221
Q

Lub-dub-swish

A

Diastole and insufficient
Valve: SL

222
Q

Average cardiac output

A

5L/min

223
Q

What is cardiac output

A

-amount of blood leaving ventricles
-example: excersizing CO is high

224
Q

cardiac output is related to

A

Sympathetic or parasympathetic state of the heart

225
Q

parasympathetic cardiac output (SA, AV, ventricles)

A

Reducing and slowing the heart rate
SA- slow rate by increasing K (hyperpolarization)
AV- increasing a delay
Ventricles- no effect

226
Q

Sympathetic impact on CO (SA, AV, ventricles and atria)

A

Heart ramps up
SA- threshold much quicker
AV- delay reduced
Ventricles- push out blood quicker
Atria- contract faster

227
Q

Sympathetic CO pathway

A

From: thoraco-lumbar
Impacts: NE/E
Receptor: Adenergic B
increases: cAMP

228
Q

Parasympathetic CO pathway

A

Straight from cervical region
-vagus CN X
Releases: Ach
Binds: receptor and G protein (muscrinic receptor)
+cAMP messenger

229
Q

Intrinsic control (sympathetic activity)

A

Built in, increases venous return
EDV and SV increases

230
Q

Extrinsic sympathetic activity

A

Directly increases contractions
SV increases

231
Q

Frank startling law

A

What is brought in diastole, pumps out at systole
-Inc EDV will in SV
-force = stretch

232
Q

Heart failure

A

Cannot produce amount of SV needed to supply the bodies demands

233
Q

Compensatory measures: heart failure

A
  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
Q

Decompensated heart failure

A

Compensatory measures fail

235
Q

Three decompensated heart failures

A
  1. Forward failure (blood forward)
  2. Left side failure
  3. Backward failure (lungs fill with blood)
236
Q

Healthy heart

A

Fresh supply through aortic artery

237
Q

Coronary vessel

A

Supplies nutrients to itself (the heart)

238
Q

When does coronary ciruculation occur

A

During ventriculardiastole

239
Q

Why does coronary circulation occur at ventricular diastole

A

Systole compresses coronary vessels, which contracts
-closure of aorta causes disturbance
-pressure is released

240
Q

Adenosine

A

Triggers blood flow or vasodilation in the coronary arteries q

241
Q

CAD or coronary artery disease

A

Pathological change in coronary wall that diminishes blood flow
-block of coronary vessel

242
Q

Early stages of CAD

A

Vascular spasm
-reversible
-usually due to PAF (platelet , activating factor not bringing in enough O2 to heart)

243
Q

Altherosclerosis

A

Oxidized cholesterol creates vasoconstriction
-serious as no oxygen

244
Q

Altherosclerosis: oxidized cholesterol accumulates

A

Macrophages to eat up the cholesterol, and they enlarge

245
Q

Altherosclerosis: enlarged macrophages

A

Form a plaque, and bulge into the coronary vessel reducing the diameter

246
Q

Altherosclerosis: formed plaque of fatty macrophages

A

Are covered by smooth muscles called atheromas

247
Q

Altherosclerosis: atheromas

A

Smooth muscle that covers the plaque, bulges into lumen

248
Q

Altherosclerosis: atheromas attract

A

Fibroblast, which begins to form a cap

249
Q

Altherosclerosis: calcium ions…

A

Precipitate around the cap formation to create a solid plague
-hardening the coronary artery

250
Q

Thromboembolism

A

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
Q

Angina pectoris

A

Heart pain felt in shoulder
Treatment: nitroglyceron (vasodilator)

252
Q

Embolus

A

Risk of clogging smaller vessels
-cap floating around coronary vessels

253
Q

Acute myocardial infraction

A

The heart is too weak

Human Physiology I (10 decks)

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