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Human Physiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Break down the muscle starting from the muscle as a whole describe each if necessary

A

Muscle, Muscle fascicle, muscle fibers, myofibril, sarcomere (Z-disk to Z-disk), thick (m-line) and thin (Z-disk) filaments
Thick- myosin (myosin head, hinge region, myosin tail), titin (anchors)
Thin-actin (structure), troponin (calcium binding protein), tropomyosin (regulates interaction between actin and myosin)

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2
Q

Sliding Filament Theory

A

myosin binds to actin and it slides it, pulling the Z-lines closer together, and reducing the width of the I-bands

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3
Q

Molecular steps to muscle contraction

A
  1. ATPase activity of myosin hydrolyzes the ATP, ADP and P inorganic remain bound to myosin (Energized resting state)
  2. Myosin head binds weakly to a new actin molecule (cross-bridge formation)
  3. Release of inorganic phosphate initiates the power stroke, myosin head rotates on its hinge, pushing actin past it
  4. After power stroke the myosin head released ADP and resumes the rigor state
  5. Tight binding in the rigor state
  6. ATP binds at site on myosin head. Myosin dissociates from actin.
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4
Q

Cross bridge formation

A

binding of myosin head to think filament, ADP and inorganic phosphate are still bound

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5
Q

Power stroke

A

triggering process, the release of inorganic phosphate flexes the hinge region, pulling filament and shortening the muscle

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6
Q

Rigor state

A

After ADP is released, muscle stuck in contraction until ATP binds releasing it

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7
Q

Energized resting state

A

Energized- myosin heads have a molecule of ADP and inorganic phosphate bound from broken down ATP
Resting state- no binding of myosin to thin filament, muscle is at rest

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8
Q

Steps of tropomyosin and troponin regulation

A
  1. Calcium levels increase
  2. Calcium binds to troponin
  3. Complex pulls tropomyosin out of the way
  4. Myosin binds to actin, completing the power stroke
  5. Actin moves
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9
Q

Neuromuscular Junction

A

synapse between motor neuron and muscle fiber used to trigger muscle contraction

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10
Q

Excitation-contraction Coupling steps

A
  1. Somatic motor neuron releases Acetylcholine at neuromuscular junction
  2. Net entry of Sodium through the Acetylcholine receptor channel initiates a muscle action potential
  3. Action potential in t-tubule alters conformation of the DHP receptor
  4. DHP receptor opens calcium release channels in the sarcoplasmic reticulum and Calcium (important signaling molecule) enters cytoplasm
  5. Calcium binds to troponin, allowing strong actin-myosin binding
  6. Myosin heads execute power strokes
  7. Actin filament slides towards center of sarcomere (shortening muscle)
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11
Q

Transverse Tubules (t-tubules)

A

bring action potentials into the interior of the skeletal muscle fibers so depolarization can stimulate calcium release

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12
Q

DHP receptor

A

voltage sensitive receptor that changes shape due to a change in voltage opening a gate on the sarcoplasmic reticulum so calcium can enter

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13
Q

How are muscles relaxed?

A

Acetylcholinesterase removes ACh from synapse
Depolarization stops
Calcium is pumped back into sarcoplasmic reticulum by Calcium- ATPase
Tropomyosin shifts back blocking sites
Filaments slide back into resting position

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14
Q

Muscle fatigue

A

Inability to generate or maintain muscle contraction
Central- tried psychological feeling, lactic acid
Peripheral- glycogen depletion, ion imbalance (calcium, phosphate, potassium) Acetylcholine depletion

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15
Q

What determines the total tension developed by a muscle?

A

Amount of tension developed by each fiber
The number of active fibers

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16
Q

Temporal Summation

A

The increase in muscle tension from successive action potentials

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17
Q

Tetanic Contraction and types

A

sustained contraction, does not allow for complete relaxation
Unfused- some degree of relaxation
Fused- prevents any degree of relaxation

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18
Q

Why does tetanus produce more tension/force than a twitch contraction?

A
  1. Tetanus has persistent elevation of calcium leading to more cross bridging
  2. Initial twitch overcomes elastic elements of skeletal muscles allowing all the force to go into contraction
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19
Q

Series of elastic elements

A

absorb tension and must be over-come to shorten the muscle (Isometric)
Once it is overcome the entire muscle can shorten (Isotonic)

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20
Q

Describe the length-tension relationship

A

Position of Sarcomeres
Optimal muscle length- ideal degree of overlap and ability to shorten. The peak
As you shorten- lots of overlap but no additional room for shortening
As you lengthen- lots of room for sliding but little to no overlap

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21
Q

What are the types of skeletal muscle fibers and their characteristics?

A

Fast glycolytic Fibers (Type IIB)- white fibers, rapid contraction, susceptible to fatigue, fast uptake of calcium, faster ATP splitting (running, lifting)
Slow-oxidative Fibers (Type 1)- red fibers, resistance to fatigue, long term activity, high amounts of myoglobin, dense capillaries
Fast-oxidative-glycolytic fibers (Type IIA)-pink fibers, can adapt to be red or white, intermediate speed

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22
Q

Irisin

A

hormone produced during exercise that changes the behavior of white fat cells, increasing their activity so they act like brown fat cells

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23
Q

Brown adipose tissue

A

High rate of metabolism, assists with thermo-regulation by causing non-shivering thermogenesis producing heat without the contraction of skeletal muscles

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24
Q

Uncoupling protein 1

A

uncouples electron transport and chemiosmosis and result in greater heat production without ATP production in the mitochondria
hydrogen atoms move across gradient to produce heat

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25
Q

Motor Unit recruitment

A

the activation of additional motor units to increase the strength of contraction, fine motor control requires smaller motor units

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26
Q

What are the “Z-disks” called in smooth muscle that anchor the thin filaments?

A

Dense Bodies

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27
Q

What are the types of smooth muscle and describe?

A

Single unit- connected by gap junctions allowing the spread of depolarization and action potentials, work together, strong contraction.
Multi-unit- not electrically linked, each cell must be stimulated independently, allows for more fine control.

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28
Q

How does smooth muscle contraction differ from skeletal muscle?

A
  1. The initial source of calcium is extracellular and could later trigger the release of calcium form sarcoplasmic reticulum. NO tubules, no DHP
  2. Different calcium binding protein- CaM (calmodulin)
  3. The calcium CaM complex activates MLCK
  4. Myosin must be Phosphorylated before it will bind to actin.
  5. To relax myosin must be dephosphorylated
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29
Q

How are smooth muscles activated compared to skeletal muscles?

A

Skeletal is only by the nervous system (NT)
Smooth- nervous system (NT) (involuntary=autonomic), Hormones, change in local chemistry, stretch, autorhythmic depolarization (own AP causing depolarization)

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30
Q

Intercalated disks

A

how adjacent cardiac cells are connected together, tight connection containing gap junctions

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31
Q

What is the purpose for gap junctions in between cardiac cells?

A

Allows for rapid spread of electrical impulses creating a forceful and unified contraction

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32
Q

What causes striations on skeletal and cardiac cells?

A

Overlap of thick and thin filaments

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33
Q

What is the difference between cardiac muscle contraction and skeletal muscle contraction?

A
  1. Different source of initial calcium- extracellular, lead to more release for sarcoplasmic reticulum
  2. L-type Calcium channel allowing calcium to enter- long lasting, open for a long period of time
  3. Difference in electrical activity-long-lasting action potential creating a long refractory period preventing tetanic contraction and allowing time for relaxation and filling of the heart
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34
Q

What is the purpose of valves in the heart?
What are the four valves and where are they?

A

Valves keep blood form flowing backwards into atria or into ventricles
Right AV valve (tricuspid) and Left AV valve (bicuspid)- atria and ventricles
Aortic Semilunar and Pulmonary Semilunar- arteries and ventricles

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35
Q

What separates the two sides of the heart and describe the oxygenation of each side?

A

Interventricular septum
Right- low oxygen to lungs
Left- high oxygen to body tissues

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36
Q

Myogenic

A

Heart initiates its own depolarization in the absence of nervous system input

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37
Q

Describe the spread of electrical activity generated by the heart

A

Depolarization of cells in the SA node that spread using gap junctions. (at same time)
the Atrioventricular node moves the electrical activity to the ventricles by depolarizing the bundle of hiss that carries it down the septum and branching at the apex
these branches are purkinje fibers that depolarize the pumping cells in the ventricle (at same time) using gap junctions

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38
Q

What does a ECG/EKG do and what are the waves that make it up?
Up vs down waves

A

Record electrical activity
1. P-waves- depolarization of the atria (small)
2. QRS- complex- depolarization of ventricles (large)
3. T-wave- repolarization of ventricles (small)
Up is towards
Down is away

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39
Q

What is the AV delay and what is its purpose?

A

Slowing of the conduction velocity in AV node
This allows for time between atrial contraction and contraction of ventricles so the atrium can fully empty and the ventricle can fully fill

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40
Q

Describe the ion channels involved with an action potential in the myocardial pumping cell

A

Has a resting membrane potential
1. Depolarize opening voltage gates sodium channels that open when threshold is reached
2. voltage gated l-type calcium channels open causing a plateau of depolarization due to long lasting
3. Sodium and calcium channels close and voltage gated potassium channels open causing repolarization

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41
Q

Describe the ion channels involved with the action potential in the SA node

A

No resting membrane potential, myogenic part
1. Sodium ions leak in through F-type sodium channels and calcium move in through T-type Calcium channels causing a threshold graded potential
2. Opening of voltage gated (L-type) calcium channels causes repaid depolarization
3. Reopening of voltage gates potassium channels and the closing of the calcium channels is responsible for repolarization

42
Q

Systole

A

Contraction

43
Q

Steps of the mechanical events of the heart, describe and the pressure involved

A
  1. Late diastole- both chambers relaxed, ventricles fill
  2. Atrial systole- atrial contractions forces small amounts of additional blood into ventricles (Atrial P> Ventricular P= AV valves open)
    3.Isovolumic- ventricular contraction- no blood ejected, AV valves closed but semilunar not open (Ventricular P< Atrial P=AV closed)
  3. Ventricular ejection- blood is ejected due to high ventricular pressure (ventricular P> Arterial P= semilunar open)
  4. Isovolumic Ventricular relaxation- ventricles relax blood is not refilling ventricles (Ventricular P< Arterial P= semi-lunar closed) ( Atrial P< Ventricular P= AV valve closed)
44
Q

Diastole

A

Relaxation

45
Q

Cardiac Output definition and how it is calculated

A

Volume of blood pumped by one ventricle in a given period of time
CO=Heart Rate X Stroke volume

46
Q

How do you speed up Heart rate to increase cardiac output?

A

Deliver sympathetic hormone (epinephrine), release more sympathetic neuron
Parasympathetic does the opposite

47
Q

What is Starling’s Law of the heart and how stroke volume effects cardiac output
Is it near optimal?

A

By increasing end diastolic volume you increase Stroke volume, the more blood in ventricle increasing SV causing a better alignment of the sarcomere.
This is not near optimal so there is room for improvement when it is needed (exercise)

48
Q

How does adding sympathetic signals effect Stroke volume?

A

It increases contractibility by triggering the release of Calcium and shifts the curve so any end-diastolic volume will get a greater SV

49
Q

What is the endothelium layer and what is its purpose?

A

single cell layer that lines all vessels, only layer in capillaries
Allows for exchange: O2, CO2, glucose, and waste

50
Q

Where is blood pressure the highest? The lowest?

A

Arteries
Venules

51
Q

How do you measure BP

A

Inflate cuff stopping blood flow, slowly release pressure until sputtering of blood through is heard (systolic pressure), continue to release until no sound is heard and the artery is no longer compressed (diastolic pressure)

52
Q

Mean Arterial pressure

A

function of cardiac output and resistance in the arterioles, takes into account length of time (closer to diastolic because it is longer) proportional to Cardiac output and TPR

53
Q

What is the function of the arterioles? and how do they do this?

A

Control blood pressure and regulate blood flow to capillaries
Smooth muscle so: hormones, nervous system, local conditions

54
Q

Metarteriole

A

Allows blood to flow form arteriole to venule by bypassing capillaries

55
Q

What regulates bulk flow in capillaries and describe

A

Hydrostatic pressure (blood pressure)- outward force, declines as it moves due to friction
Triggers filtration-arterial end, fluid moving out of blood, high rate in day and excess is recollected by lymphatic system

Osmotic pressure- protein in blood causing force, more protein in blood than in tissue drawing water into capillary (inward directing force)
Triggers Absorption- venous end, fluid into capillaries

56
Q

Bulk flow

A

Mass movement as a result of hydrostatic or osmotic pressure gradients
In capillaries its water

57
Q

What is the job of Veins and Venules?

A

Carry blood back to the heart and serve as a reservoir for blood volume

58
Q

What are all types of blood vessel structures?

A

Arteries, arterioles, capillaries, venules, veins

59
Q

What is the role of skeletal muscles and the respiratory pump in venous return?

A

To assist blood in its movement against gravity
Contraction- pushes open the one way valves that prevent backflow and blood pooling, moving it upward
Respiratory pump- using pressure differences caused by the movement of the thoracic cavity

60
Q

What are the primary sensors of arterial blood pressure?

A

Baroreceptor neurons in the aorta and wall of carotid arteries
tonically active, detect outward force/pressure

61
Q

Steps of Baroreceptor reflex

A
  1. Change in blood pressure
  2. sensed by the carotid and aortic baroreceptors
  3. Sent to the integrating center in the brain stem called the medulla oblongata
  4. sent to effectors: Parasympathetic- slows HR
    Sympathetic-increases HR, and effects stroke volume (increases CO and MAP) and vasoconstriction and dilation of veins and arterioles(TPR)
    Influencing cardiac output and TPR to regulate blood pressure
62
Q

What is TPR

A

resistance from blood vessels on blood flow, proportional to MAP
It is dependent on vasodilation and vasoconstriction.

63
Q

What are the components of the blood?

A

Matrix: Plasma- made of water and dissolved solutes that draws in water from tissues
Formed elements: Red blood cells (transport oxygen to cells) White blood cells, platelets (fragments of larger cells essential to blood clotting, fighting infections, and recovery, cause strokes and heart attacks)

64
Q

How is O2 transported?

A

(99%) Hemoglobin in red blood cells are oxygen binding proteins made of two alpha and two beta protein chains that each have an iron ring in the middle where oxygen binds.
(1%) through the plasma

65
Q

Name of hemoglobin before and after oxygen binding

A

Oxygen bound: Oxyhemoglobin
Oxygen not bound: Deoxyhemoglobin

66
Q

How is CO2 transported?

A

(23%) CO2 binds to hemoglobin forming a carbaminohemoglobin complex
(10%) Transported as free CO2
(66%) Transported as bicarbonate in red blood cells
CO2 binds to water because of carbonic anhydrase forming carbonic acid which is then broken down into bicarbonate ion (equilibrium tissues form bicarbonate, lungs form CO2)

67
Q

Describe Red blood cell formation/break down

A

Produced in the red bone marrow controlled by erythropoietin produced by the kidneys when there are low levels of O2 in the blood
Broken down in the liver and spleen forming Bilirubin giving Bile the yellow green color

68
Q

Describe each blood type in the ABO system, including their antigens, antibodies, and what blood they can recieve

A

Type A- H and A antigens (N-acetylgalactosamine), Anti-B antibodies, can receive A and O blood
Type B- H and B antigens (galatose), Anti-A antibodies, can receive B and O blood
Type AB- H, A, B, antigens, No antibodies (universal receiver), can receive all blood types
Type O- Just H antigen, anti-A and anti-B antibodies (universal donor), can receive only type O blood

69
Q

How do you classify Rh blood types

A

Positive- have D antigen
Negative- no D antigen
Those with positive can only receive positive blood, and vice versa

70
Q

Hemolytic Disease of the newborn

A

Baby is positive and mom is negative.
During birth fetal blood is recognized by the mothers and the immune system creates memory cells
If the next pregnancy is the same the memory cells will be activated and target the fetus
Can administer a vaccine that suppresses the immune system of the mother during the first pregnancy to prevent the formation of memory cells

71
Q

What causes Hemophilia A and B?

A

A: Absence of factor VIII
B: Absence of factor IX

72
Q

Structure of the respiratory tree

A

Trachea, left primary bronchus, Secondary Bronchus, bronchiole, alveoli

73
Q

Conducting Zone

A

Trachea, primary bronchus, secondary bronchus
Transmission and delivery
Low resistance pathway getting air to the respiratory zone, defense, warms and moistens the air, and phonates (talking)

74
Q

Respiratory Zone

A

Bronchiole, Alveoli
Gas exchange (air here is completely saturated)

75
Q

What are the two types of alveolar cells and describe

A

Type 1- gas exchange, thin and flat (close to the capillary)
Type 2- Produce surfactant which lowers the surface tension of water, preventing the walls from sticking together during contraction, typical cell shape, no gas exchange

76
Q

Atrial Systole

A

First step
Started by p-wave (atrium depolarization)
Atrial contraction builds up pressure opening AV valves, blood into ventricle increasing volume, QRS complex begins (ventricular depolarization)

77
Q

Isovolumic Ventricular contraction

A

Second Step
Ventricle starts to contract.
Ventricular pressure rises above atrial (AV valves close SN1), semi-lunar valves are closed, blood is not ejected so ventricular volume is unchanged.

78
Q

Ventricular Systole

A

Third Step
Ventricular pressure rises higher then Aortic pressure causing semi-lunar valves to open
Blood is ejected out of ventricles decreasing volume
Ventricles begin to repolarize (T-wave) causing ventricular pressure to decrease

79
Q

Early Ventricular Diastole

A

Fourth Step
Ventricular pressure drops below aortic pressure causing the semi-lunar valves to close (SN2)
Volume remains constant
Ventricular relax causing a pressure decrease
Atrium fills with blood building up pressure, AV valves open when atrial pressure passes ventricular pressure

80
Q

Ventricular Diastole

A

Fifth Step
Blood flows passively into ventricles
Ventricular blood volume increases
Process repeats

81
Q

Ventilation and how it relates to Boyles Law

A

Air enters when Pressure alveoli is less than pressure atmosphere
Air exists when Pressure Alveoli is greater than pressure atmosphere
Under Boyle’s law pressure and volume are inversely related so changing the volume of the lungs changes the internal pressure

82
Q

What occurs during inspiration?

A

Active process where the diaphragm (move down) and the external intercostals (move up and out) contract increasing volume and therefore decreasing the internal pressure, allowing air to flow in

83
Q

What occurs during expiration?

A

Passive process where there is no contraction with reduced volume meaning increased pressure allowing air to flow out
Can be made active when you contract the abdominal muscles and internal intercostals further decreasing the volume

84
Q

What is the typical partial pressures of oxygen in the alveoli, arterial blood, and tissues?

A

Alveoli- 100 mmHg
Arterial blood- 100 mmHg
Tissues- Less than our equal to 40 mmHg
Pulmonary- 40 mmHg

85
Q

What is the typical partial pressure of carbon dioxide in the alveoli, arterial blood, and tissues?

A

Alveoli- 40 mmHg
Arterial- 40 mmHg
Tissues- Greater than or equal to 46 mmHg
Pulmonary- 46 mmHg

86
Q

How is oxygen transported in blood?

A

Plasma and Hemoglobin
The partial pressure of oxygen in the tissues change, dictating the amount of oxygen leaving the hemoglobin
Supply and demand

87
Q

How is CO2 transported in the blood?

A

Plasma, Hemoglobin, Bicarbonate
Bicarbonate is formed in the RBC and sent into the plasma to act as a buffer, when it leaves it causes Cl- to flux in (chloride shift)
Opposite effect occurs in the lungs

88
Q

What does the oxygen-hemoglobin dissociation curve tell you?

A

The effect of partial pressure of oxygen on hemoglobin saturation. At higher oxygen concentrations the percentage of hemoglobin saturated with bound oxygen increases until all of the oxygen binding sites are occupied (100% saturation)
Hemoglobin Affinity

89
Q

What are the factors that influence the loading/unloading of oxygen?

A

pH, temperature, Carbon Dioxide concentration, and 2,3-DHP
A right shift means that there is a less affinity for oxygen.
A reduced pH, increase in temperature, an increase in Carbon dioxide concentration, and an increase in 2,3-DHP will cause a decrease in affinity

90
Q

What is the difference with fetal hemoglobin?

A

Has a left shift in the partial pressure graph to promote hemoglobin’s affinity for oxygen. This promotes the oxygen transfer from mother to fetus because it cannot ventilate its own oxygen

91
Q

How is Breathing controlled/monitored?

A

Chemoreceptors monitor oxygen, carbon dioxide, and acidity of the blood using Carotid Bodies, Aortic Bodies, and central chemoreceptors
Send signals to the integrating center- respiratory control center (medulla oblongata)
Sent to effectors (diaphragm, intercostals) to induce breathing

92
Q

What is the most and least important stimulus to stimulate ventilation?

A

Oxygen is the least important, it requires a drastic change in oxygen levels to stimulate
CO2 and therefore acidity are the most important molecules in breathing rate. The slightest increase in CO2 concentrations dramatically changes the ventilation by the body in attempt to get rid of this waste product, when bicarbonate is produced during Co2 transport it increases the H+ concentration also increasing the rate of breathing

93
Q

What is the challenge our bodies face when going up high altitudes (physiologically)?

A

Going up in elevation deceases Partial pressure of the atmosphere, reducing the gradient PO2 travels to fill and empty the lungs

94
Q

AMS

A

Acute mountain sickness
least “dangerous”
dizziness, headache, nausea, weakness
Symptoms can terminate as elevation is decreased.
Variable from person to person and from time to time

95
Q

HACE

A

High altitude cerebral edema
medical emergency
Swelling in and around the brain due to leaking blood vessels working to supply the brain with more oxygen
Chang in mental state, coordination
Symptoms can come on quickly

96
Q

HAPE

A

High altitude pulmonary edema
Can occur after days or weeks at high elevation
Difficulty breathing, coughing, congestion, weakness
Coughing up blood due to the leaking blood vessels working to supply more oxygen to compensate for lack of it

97
Q

How does the body acclimate to high altitude?

A

More ventilation
Erythrocyte synthesis (produce more RBC)
Increase in DPG (shifts curve to the right, but may cause less oxygen to be unloaded in the lungs)
Increase in capillaries (increase oxygen transfer)
Reduce plasma volume (increases the density of RBC to transport more oxygen)

98
Q

Hypoxia

A

Deficiency in the amount of oxygen reaching the tissues

99
Q

HIF-1

A

Monitors oxygen levels in cells and it is activated when low oxygen levels are detected
Alpha subunit binds to Beta subunit to make a working protein that operates as a transcription factor:
Glycolytic enzymes
Angiogenesis
Erythropoietin
Stress porteins

100
Q

Carbon Dioxide bound to hemoglobin

A

Carbaminohemoglobin

101
Q

Difference in refractory period of Skeletal muscle vs Cardiac muscle

A

Skeletal- can do tetanic contractions, has a short AP and short refractory period
Cardiac- can NOT do tetanic contractions, has long AP, long refractory period to ensure that the ventricle is fully contracted and able to refill before another stimulus.

Human Physiology (4 decks)

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