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GBA Physiology > Cell Physiology - Theoretical Questions > Flashcards

Cell Physiology - Theoretical Questions Flashcards

1
Q

1,1) What are the two factors determining the net movement of water across the body compartments?

A

Hydrostatic Pressure - from Heart pump force + gravity

Osmotic Pressure - from solute but mostly plasma proteins (Oncotic)

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2
Q

1,1) Ion concentration difference is kept by?

What kind of transport?

A

Na+/K+ ATPase (3 Na out and 2 K In)

Primary Active Transport

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3
Q

1,1) What is the name of the process which uses the Sodium concentration gradient to increase the cells amount of other nutrients?

A

Secondary active transport

With Co-transports like SGLT for Na+Glucose (or Amino Acids Co-transporters)

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4
Q

1,1) How is plasma concentration of ions different from general ECF ion concentration?
Why?

A

Plasma is slightly more positive, containing more - Cations.

Due to higher Protein content(-) attracts more positive ions, Gibs Donham Equilibrium

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5
Q

1,1) What are the examples of transcellular fluids?

A

Ocular, Synovial, CSF, Pleural, Peritoneal Fluids

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6
Q

1,1)Effect of Liver disease on body fluid distribution? (Among many others.. from Oral exam)

A

No Production of Albumin, Oncotic Pressure decreases, Less fluid gets reabsorbed back to capillaries, Edema in the Limbs.

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7
Q

1,1) What is the Reflection coefficient?

Possible values and their meaning?

A

Reflection Coefficient (Sigma) - describes how easily the ion can pass through the membrane (Ranges from 0 to 1)
1 - Impermeable (Albumin) = Not Diffusible.
0 - Permeable (Urea) = Diffusible

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8
Q

1,1) would we calculate the amount volume of a body compartment using a solute? The general formula and application. (from oral exam)

A

CV=CV (=Moles)
After the fluid was obtained (blood/urine/csf..) using lab specific technics concentration and volume measurements - indirect indication of body compartment volume.

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9
Q

1,1) What solute do we use to measure Blood plasma volume? Why?

A

Evans blue
It is bound to Plasma proteins therefore it will not penetrate the endothelial layer and go to the Interstitial fluid compartment or ICF.

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10
Q

1,1) What solute do we use to measure ECF volume? Why?

A

Inulin. It is a small carbohydrate molecule that can travel to Interstitial fluid and back (from plasma), Secreted in urine. No transporter to get to ICF.

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11
Q

1,1) How should we measure Interstitial fluid volume?

A

ECF - Blood plasma = Interstitial Fluid.

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12
Q

1,1) How should we measure ICF volume?

A

Total Body water - ECF = ICF.

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13
Q

1,1) What solute do we use to measure TBW volume? Why?

A

TBW - Total body water is measured by Deuterium, an Isotope of Hydrogen - “Heavy water” formes.
This is a substance that goes through all the body compartments.

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14
Q

1,2) Membrane Structure - General Features:

A

According to Fluid Mosaic Model : Primarily phospholipid Bilayer, also cholesterol, proteins and Glycoproteins.

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15
Q

1,2) Give examples for substances that the phospholipid membrane is permeable to:

A

Non-Polar/Hydrophobic Substances:

Oxygen, Carbon Dioxide, Fatty Acids, Steroids

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16
Q

1,2) Give examples for substances that the phospholipid membrane is Impermeable to:

A

Polar/Hydrophilic Substances:

Ions, Glucose, Amino Acids

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17
Q

1,2) Give examples for Amphipathic phospholipids:

A

Most abundant are Lecithin and Sphingomyelin

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18
Q

1,2) Give an example for membrane lipid that participates in signaling process ? what is the mechanism? What is the result?

A

Gq activated PLC cleaves Phosphatidylinositol Bisphosphate to form the Signaling molecule IP3.
DAG is also released. General Ca+ and PKC activation.

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19
Q

1,2) What is the job of cholesterol in the phospholipid membrane?

A

Responsible for Membrane fluidity and Adaptations to different temperatures.
Creates lipid rafts, Separates the phospholipids from one another in specific areas.

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20
Q

1,1) Gibbs-Donnan Ratio:

A

Plasma concentration relative to Interstitial fluid concentration.
Expressed for specific Ions

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21
Q

1,2) What are the Integral Proteins?

What are their jobs?

A

Integral Protein - Embedded into the Membrane.

Some are Transmembrane -Connecting ICM to ECM, Cross it several times,

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22
Q

1,2) What are the Integral Proteins?

What are their jobs?

A

Integral Protein - Embedded into the Membrane by Hydrophobic Interactions.
Some are Transmembrane -Connecting ICM to ECM, Cross it several times, Examples are Ion channels, Na/K ATPase, GPCRS.

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23
Q

1,2) What are the Peripheral Membrane Proteins?

What are their jobs?

A

Peripheral Membrane Proteins - Attached to ECM or ICM side by Electrostatic interactions with Integral Proteins. Ankyrin is an Example.

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24
Q

1,2) What are the Glycoproteins?

What are their jobs?

A

Glycoproteins - Carbohydrates chains attached to the surface and continuous with Integral membrane proteins. Examples are MHC units that function in Immunity and cell cell interactions.

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25
Q

1,2) Simple diffusion:

A

Passive; Concentration gradient dependent solute movement. Not mediated by a carrier. Doesn’t require any metabolic energy.
According to Fick’s 1st law: J=-DxAx C/X.

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26
Q

1,2) Facilitated Diffusion :

A

Passive; Concentration gradient dependent solute movement. Mediated by a carrier. Doesn’t require any metabolic energy. Like GLUT4 or Aquaporins.

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27
Q

1,2) Primary Active Transport :

A

Active; Movement of solute against the Concentration gradient. Mediated by a carrier. Uses Direct metabolic energy in the form of ATP.Like ATPases - Na/K, H/K…

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28
Q

1,2) Cotransport:

A

Cotransport - Secondary Active transport; Uses the Na+ Concentration gradient as a indirect source of energy to move the solute INSIDE the cell. Like SGLT.

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29
Q

1,2) Countertransport:

A

Countertransport - Secondary Active transport; Uses the Na+ Concentration gradient as an indirect source of energy to move the solute OUTSIDE the cell. Like Na+/H+ exchanger.

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30
Q

1,2) Vesicular Transport: Give examples.

A

Endocytosis example - Clathrin coated Cholesterol uptake or Phagocytosis in Macrophages.
Exocytosis - Could be Constitutive or Regulated: For example Insulin secretion in beta cells is regulated by calcium signal.

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31
Q

1,2) Paracellular: Give examples.

A

Across tight junctions:
In small intestines - Leaky, water movement.
In Kidney collecting Ducts - Regulated by Aldosterone

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32
Q

1,3) What is Saturation in regard to Transport processes?

A

When all of the solute binding sites on the transport proteins are occupied. Can be calculated by Michaelis Menten equations. Tm is the Abbreviation (Like Vmax).

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33
Q

1,3) What is is the difference between the Saturation of Ion channels and Carrier proteins?

A

Ion channels do not bind the solute but simply make it energetically favorable for it to move across them - therefore their Saturation is diffusion limited while Carrier proteins are saturated faster.

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34
Q

1,3) What are the 6 Ion channel basic characteristics?

A

1)Passive transport 2)Charge and Size Selectivity 3)Transmembrane Proteins 4)Gated - Conformation change by Ligand or Voltage 5)Diffusion Limited - No saturation in physio conditions. 6) 10^8 Ions/Sec - FAST

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35
Q

1,3) What are the 4 Ion channel basic roles?

A

1)Development of Resting Em (K channels) 2)AP Formation 3)Secretion 4)Cell Volume - Osmosis

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36
Q

1,3) Na+ Voltage gated channels:

A

Na VGC: Activated by Depolarization. Cyclic Action Modes: Closed-Inactivable, Closed-Activable, Open. Fact activation, Slow inactivation. Acts in AP formation.

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37
Q

1,3) K+ Voltage gated channels:

A

K-VGC: Responsible for Repolarization stage of AP.

Movement of K outside.

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38
Q

1,3) Inwardly rectifying K channels:

A

IRK: Active when Membrane is Hyperpolarized letting Potassium into the cell, Closes when Membrane is Depolarized not letting K out.

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39
Q

1,3) Classification of Ion channels:

A

By Ion Charge/By Solute selectivity/ By Gating Mechanism

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40
Q

1,3) Examples for Second Messenger activated Ion channels:

A

IP3R - ER membrane Calcium channel.
RYR- Calcium induced Calcium Release from ER.
ATP Sensitive K channel - CLOSES when ATP attaches OPENS when ADP attaches.

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41
Q

1,3) Examples Ligand gated Ion channels:

A

Ligand Gated Na+ : AMPA Glutamate receptor.

Ligand Gated Cl- : GABA A receptor

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42
Q

1,3) Mechanosensitive Channels Examples:

A

Muscle spindles have Mechanosensitive

channels that respond in unitary manner, where stretch directly correlates to amplitude.

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43
Q

1,3) Heat sensitive Channels Examples:

A

TRPV family - Capsaicin from Chilli peppers is an Agonist but this is mainly a Heat sensitive channel.

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44
Q

1,3) Heat sensitive Channels an Example:

A

TRPV family - Capsaicin from Chilli peppers is an Agonist but this is mainly a Heat sensitive channel. These are Non selective channels.

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45
Q

1,3) General Roles of Voltage Gated Calcium Channels:

A
  • Ca+ Sensitive K Channel
  • Muscle Contraction
  • Hormone and Neurotransmitter release from Synaptic Terminal.
  • Gene Expression Regulation
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46
Q

1,3) Why is Calcium such an Efficient intracellular Signal?

A

Its Intracellular Concentration is 100nM which is very low in comparison to the mM range in EC or ER - Peaks FAST. PMCA and SERCA are able to restore normal concentrations quickly as well. Many proteins are activated by calcium.

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47
Q

1,3) L-Type Voltage Gated Calcium Channels:

A

“Long lasting” - Aids in Muscle contraction (NMJ), Cardiac AP Plateau, High activation range - (-25mV)

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48
Q

1,3) T-Type Voltage Gated Calcium Channels:

A

“Transient” - SA Node, Pacemaker activity, Low activation range - (-40mV)

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49
Q

1,3) N-Type, P-Type, R-type Voltage Gated Calcium Channels:

A

N - CNS and PNS, Release of Synaptic Vesicles
P - Purkinje Cells
R- Neuronal

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50
Q

1,4) Defenition of Resting Membrane Potential: What is it dependent on?

A

Relatively static Potential, for the Membrane of cell which is not active. It is the Potential Difference between EC and IC. Dependent on the large Potassium permeability and the Action of Na/K ATPases.

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51
Q

1,4) Defenition of Diffusion Potential:

A

Caused by Transmembrane movement of a Ion.
Could occur only if the Membrane is permeable to this Ion (Via Channels) . Measured in mV, It’s sign depends on the charge of the Ion.

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52
Q

1,4) Defenition of Equilibrium Potential:

A

This is an extension of the concept of Diffusion potential. It is the Potential where no net movement of the Ion of interest. It is an Electrochemical Equilibrium.

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53
Q

1,4) What is the Nernst Equation:

A

E= (-2.3RT/zF)xLog(Ci/Ce) (-2.3RT/F is -60 at STP)

Converts the concentration difference of an Ion into voltage. z is the Ion charge.

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54
Q

1,4) What is a Driving Force (In relevance to Em and Eq):

A

A Driving force is the difference between the actual Membrane Resting Potential and the Equilibrium potential for an Ion of Interest. This will determine the Ion Current Direction and Magnitude.

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55
Q

1,4) What are the values that the resting membrane potential is close to? why?

A

Em is close to the equilibrium potentials of Cl- and K+.

Because the permeability to these Ions is the Highest.

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56
Q

1,4) What are the values that the resting membrane potential is far from ? why?

A

Em is far from the equilibrium potentials of Na+ and Ca+.

Because the permeability to these Ions is the lowest.

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57
Q

1,4) How can we calculate the Resting Membrane Potential of the Cell?

A

Goldman-Hodgkins-Katz Equation- “Extended Nernst”:

-60 times Log of Summing all the Ions EC and IC concentrations while multiplied by their specific permeability values.

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58
Q

1,4) How Does Na/K Atpases contribute to the Membrane potential value?

A

1) Electrogenic - 3Na out and 2K in. (Minor effect ~5mV)

2) Indirect - Establishing the K gradient (Greater effect)

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59
Q

1,4) What is the Physical cause of Permeability for an Ion?

A

Amount of “Leaky” channels for the specific Ion will determine its Permeability.
For example Inwardly rectifying K channels in ventricular Myocytes increase its K permeability.

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60
Q

1,4) What is Different for the equilibrium potential of Chloride?

A

It is Inverted- negative because of the Negative charge of the Chloride Ion. Meaning that in HGK Equation it will be noted as Ce/Ci .

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61
Q

1,5)Depolarization:

A

Depolarization: the process of making the membrane potential less negative. Meaning more positive Ions travel into the cell.

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62
Q

1,5)Hyperpolarization:

A

Hyperpolarization: the process of making the membrane potential more negative.

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63
Q

1,5)Threshold Potential:

A

Threshold Potential: The potential value from which the occurrence of an Action potential is Inevitable. The beginning of the AP Upstroke.

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64
Q

1,5)Refractory Period:

A

Refractory Period: a period during which another normal action potential cannot be elicited in an excitable cell. Refractory periods can be absolute or relative. Relative = Hard to form another AP, Absolute = Impossible.

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65
Q

1,5)Properties of Action Potentials:

A

1) Stereotypical size and shape - Identical Normally.
2) Propagation - Nondecremental.
3) All-or-None Response - Threshold Dependent, Enough graded potential will cause an AP formation (Temporal and Spatial Summation).

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66
Q

1,5) Cause of Absolute Refractory Period:

A

Absolute refractory Period happens when Na VDC close and Inactive for a while - “Cooling off Period”. (1 sec)

67
Q

1,5) Cause of Relative Refractory Period:

A

Relative Refractory Period happens due to K VDC opening; High K+ outflow will make it very hard to reach the threshold potential again in 1-2 sec.

68
Q

1,5) AP Conduction favoring factors:

A

1) Nerve Diameter - More room for Ions.
2) Myelination - causes insulation that forces the current to flow in the low resistance path.
3) Nodes of Ranvier - Unmyelinated intervals with high Na VDC amount: Saltatory conduction.

69
Q

1,5) Cardiac (Ventricular) Myocytes AP Formation:

1) Upstroke - Na VDC from -90mV to +20mV
2) Initial Repolarization - Na VDC Inactivation, Transient Outwards K+ Channels open.
3) ________________________
4) Repolarization Ca current drops and K current rises (Delayed rectifiers opens) Em is back -85mV

A

3) Plateau - Inwardly rectifying K+ channels decrease K+ permeability by closing (at -50mV ) and L-Type (DHP) is activated causing ultimately Calcium Induced Calcium release on RYR of ER.
K Current out and Ca Current In are balanced .

70
Q

1,5) SA Node AP Formation:

1) Pre-Potential/Pacemaker Potential:__________
2) Upstroke- VDCC Opened: -40mv T-Type , -25mV L-type.
3) Repolarization - K Delayed rectifier channels to -65mV.

A

SA Node Prepotential:
If (Funny Current): Caused by HCN, Hyperpolarization Cyclic Nucleotide Activated - nonselective cation channels open at -65mV threshold lowered by cAMP.

71
Q

1,5) Formation of AP in Neurons:

1) From -70mV, AchR Nicotinic receptors cause Na Inflow
2) at -50mV, Na+ VDC Opens
3) P-Na>P-K = Overshoot to 40mV
4) _______________

A

Repolarization of Neuronal AP:
A)Slow inactivation of closed Na+ VDC
B)K VDC Opens and Creates an K outward current

72
Q

1,5) What is the difference between the neuronal AP and Skeletal Muscle AP?

A

Although both are similar in shape Neuronal AP takes 1-2 seconds while Skeletal Muscle AP takes 5 Seconds

73
Q

1,5) What are the differences between the neuronal AP and Smooth Muscle cell AP ? (3)

A

Compared with Neuronal, SMC AP are:

1) Lower in Amplitude
2) Longer Duration
3) Uses different Ion currents - Calcium dependent

74
Q

1,5) What are the special features Smooth Muscle cell Excitation ? (5)

A

1) They have no constant Em; Slow waves between -40 to -80 mV. Initiated by Interstitial Cajal cells in GI.
2) Slow waves are enough to cause a Contraction!
3) But AP cause Stronger Contractions.
4) Depol. By L-Type VDCC and Repol. By K VDC.
5) Plateau is caused by Ca activated K channels

75
Q

1,5) Membrane Capacitance:

A

Membrane Capacitance: The ability of the cell membrane to store charge.

76
Q

1,5) Membrane Resistance:

A

Membrane Resistance: When High, current cannot cross the membrane easily.

77
Q

1,5) Time constant (Was asked):

A

Time constant: Equals to Membrane Capacitance times Membrane Resistance. The amount of time it takes for a current injected to change the potential to 63% of the final value.

78
Q

1,5) Space constant (Was asked):

A

Space constant: Proportional to root of Internal Resistance times Membrane Resistance. The distance from current injected point where the potential fallen by 63% from the original value.

79
Q

1,6) What are the General types of Communication between cells (6):

A

1) Gap Junction - Ions move between neighboring cells.
2) Autocrine - Mediators for own kind receptors
3) Paracrine - Local mediators
4) Contact dependent - Integrins or MHC
5) Synaptic - NT activated Channels
6) Endocrine - Blood carried Hormones

80
Q

1,6) Membrane Receptors General Properties:

A

1) Reversible Binding
2) Could Saturate
3) Specific Ligand Binding
4) High Affinity Marked by Low Kd

81
Q

1,6) Kd Defenition:

A

Inversely proportional to the Affinity of the Receptor to the Ligand.
At 50% Bounded Ligands - the Kd value = Ligand Conc.

82
Q

1,6) Give an Example for a receptor with constitutive activity. What does it mean?

A

AT1 receptor can create vasoconstriction without ligand binding.

83
Q

1,6) Full agonist

A

100% of a Response could be formed by it binding to the Receptor as a Ligand.

84
Q

1,6) Partial agonist

A

Not 100% of a Response could be formed by it binding to the Receptor as a Ligand.

85
Q

1,6) Antagonist

A

Blocks the Binding site for potential Ligands, thus creating a zero overall effect.
NOT INVERSE EFFECT.

86
Q

1,6) Inverse agonist

A

Causes the Opposite response to that of an Agonist.

87
Q

1,6) What are the two molecular switches:

A

1) ATP, Phosphorylation of Proteins

2) GTP, Binding to Proteins

88
Q

1,6) What does GEF and GAP do?

A

GEF - Removal of GDP and Addition of GTP to Proteins.
GAP - Dephosphorylation of Bound GTP, forming
GDP-Protein complex.
GEF is activating while GAP is inactivating.

89
Q

1,6) First Messengers are:

A

Ligands that bind to Receptors Extracellularly.

90
Q

1,6) Second Messengers are:

A

Molecules formed in the cell due to the Receptor’s ligand binding. Examples are : IP3, Ca, DAG, cAMP and cGMP.

91
Q

1,6) What are GPCRs?

A

G-Protein Coupled Receptors: (Ligand Activated).
Inactive state when GDP is bound to Alpha subunit.
Active state when Alpha is bound by GTP and the
Beta-Gamma complex dissociated. Each has an effect.

92
Q

1,6) Gs Pathway?

A

Gs causes activation of Adenylyl Cyclase, elevation in cAMP causes activation of PKA.

93
Q

1,6) Gq Pathway?

A

Gq causes activation of PLC that produces IP3 and DAG.

IP3R Releases calcium and DAG activates PKC with it .

94
Q

1,6) Gi Pathway?

A

Gi causes inhibition of Adenylyl Cyclase, Less PKA active. Also activates PLA2 which promotes Eicosanoids formation and Can activate GIRK in Heart and cause Hyperpolarization.

95
Q

1,6 GPCRs Examples:

A

Adrenergic Receptors - QISS (KISS) :
Alpha-1 - Gq, Alpha-2 - Gi, Beta receptors - Gs.
Acetylcholine Muscarinic Receptors - QIQ (kick):
M1,M3,M5 - Gq, M2,M4 - Gi .

96
Q

1,6) Ion channels Receptors Examples:

A

Excitatory (Na or K): Nicotinic AchR, Glutamate-NMDA, Glutamate-AMPA, 5HT3R.
Inhibitory (Cl) : GABA-A

97
Q

1,6) Receptors with enzyme activity- Tyrosine Kinase Pathways:

A

Tyr-Kinase Binding of GF or Insulin - Autophospho. , Dimerization and SH2 Domain activated proteins (3):

1) GRBS - SOS - RAS+GTP - Raf - MAPK -Growth
2) PI3K - PIP3 - PH Domain: PDK+PKB - BAD inactivation.
3) PLCgamma- PKC activated TFs and Cyclins from Ca

98
Q

1,6) Receptors with enzyme activity- other than Tyrosine Kinase give 2 other examples:

A

1) Guanylyl Cyclase -PKG -Vasodilation (NO to soluble GC).

2) Serine/Threonine:TGF-beta - Autophosphorylation and Dimerization - SMAD-CO-SMAD-TFs for Differentiation or Apoptosis.

99
Q

1,6) Receptors with enzyme linked activity Pathway Examples:

A

GH , Prolactine, Cytokines Receptors (No intrinsic TyrK)

JAK - STAT activation - T.F.

100
Q

1,6)Intracellular Receptors Pathway Examples:

A

Hydrophobic ligands: Receptors acts as T.F.

Steroids, Thyroids, VitD3, Retinoic Acid, Eicosanoids.

101
Q

1,7) General Pathway of Skeletal Muscle contraction:
AchR is activated on the Postsynaptic Muscle - End plate potential is achieved - VDC Na opens as well. where will AP propagate when formed? What will it cause?

A

AP Propagates to T-Tubules.
DHP activated by Depol. on T-Tubules will cause electromechanical Coupling and activate the RYR on the SR. High Calcium ion release into the cytosol.

102
Q

1,7) General Pathway of Skeletal Muscle contraction:

Why is Calcium essential for Skeletal Muscle contraction?

A

Activation of Cross Bridge Cycle -Ca binds Troponin C which allows Tropomyosin to be displaced from Myosin and Myosin free to Bind Actin. Contraction Possible.

103
Q

1,7) General Pathway of Skeletal Muscle contraction:

How is calcium removed from the Cytoplasm? What does this cause in regard to muscle contraction?

A 
SERCA mostly (PMCA as well).
Relaxation relaxation.
104
Q

1,7) Skeletal muscle cell general features:

A

1) Multinucleated cell - Fusion of embryonic Myoblasts
2) Myofibrils are surrounded by Sarcoplasmic Reticulum and Invaginated by Transverse tubules (T-tubules).
3) Myofibrils are divided to Sarcomeres by the Z-lines of T-Tubules - Striations shown.

105
Q

1,7) Sarcomeres

Thick filament - General Features:

A

Thick filament - Myosin: 6 polypeptide chains protein.
One pair of Heavy chains - 2 tails
Two pair of Light chains - 2 heads with ATPase Action.
(Head = Cross-Bridge Head)

106
Q

1,7) Sarcomeres

Thin filament - General Features:

A

Thin filament: 1) Actin- to bind Myosin in contraction.

2) Tropomyosin-Blocks Actin Myosin interaction noramly.
3) Troponin - Several Types (Another Card).

107
Q

1,7) Sarcomeres

Troponin - Different types:

A

Troponin T - Binds tropomyosin
Troponin I - Acts with Tropomyosin to Inhibit the Actin-Myosin Binding.
Troponin C - Binds Calcium - Causing Tropomyosin to move and Actin and Myosin to bind.

108
Q

1,7) What are the T-Tubules?

A

Muscle cell membrane extensions that are carrying depolarization into the L-tubules of Sarcoplasmic Reticulum.

109
Q

1,7) Cross Bridge cycle Steps:

A

1) Cross Bridge Heads Hydrolyze ATP and Extend towards Actin.
2) Ca binds Troponin-Tropomyosin, Conformation changes moves complex - Actin binding sites are free.
3) Actin-Myosin Head are bound - Power stroke occurs from Myosin head - Pulling Actin. (ATPs Energy).
4) Release of ADP+Pi - New cycle.

110
Q

1,7) What is Rigor Mortis?

A

Stiff position of Myosin Head when no New ATP could be Hydrolyzed. Step 1 of Cross bridge cycle “Freeze”.

111
Q

1,7) Force-Length Relationship, Explain the Limitation of Each Extremity:

A

Force of contraction is dependent on the Length, but:
1)If sarcomere is too short, Filaments are too meshed together and cannot interact properly.
2)If Sarcomere is too long Filaments do not Reach each other.
There is a Certain Optimum for the Length-Force Curve.

112
Q

1,7) What kinds of contractions are there?

A

Isotonic - Constant Tension, Varying Length.
Isometric - Varying Tension, Constant Length.
Auxotonic - Varying Tension and Length.

113
Q

1,7) Voluntary Movement is formed by two components of Tension:

A

Active Tension - From the Cross-Bridge cycle.

Passive Tension - From the Elasticity (Titin) of a muscle stretched passed the optimum of Contraction.

114
Q

1,7) Muscle Fatigue Reasons:

A

Ach/Creatin-P/ATP depletion.

Lactate inactivating by Low pH.

115
Q

1,7) What is Preload?

A

The present length of

116
Q

1,8) Smooth Muscle cells General Features:

A

1) Uninucleated cells with no Striations - No Sarcomeres
2) Thick+Thin filaments present but no Z-lines.
3) No T-Tubules, but SR present
4) Found around lumen containing organs (Tubes)
5) Dense Bodies are connection points for Actin.

117
Q

1,8) Classes of Smooth Muscle cells:

A

1) Unitary SMC - Linked by Gap Junctions, Propelling its Slow waves to Others (GI, Bladder, Uterus, Ureters)
2) Multi-Unit SMC - No Gap junction, Contractions occur separately. Ciliary Muscles, Iris.

118
Q

1,8) What are the sources of Calcium for the SMC contractions?

A

1) VDCC
2) RYR - Calcium induced calcium release
3) Hormone/NT Controlled Channel
4) IP3R

119
Q

1,8) Contraction mechanism of SMCs:

A

Calcium rise causes a Calcium-Calmodulin complex formation - Active MLCK - MLC-P formed - Myosin ATPase Active - Cross Bridge Cycle Active - SERCA Restores Ca to SR.

120
Q

1,8) SMC In contrast to Sk-MC: What are the differences in the Light and Heavy chains of the Thick filaments? What is different in the Thin filament?

A
  • Thin filament : No Troponin!

- Myosin : 2 Light chains and 2 Heavy chains.

121
Q

1,8) Since there is no Troponin in SMC, How is the cross bridge cycle stopped in time when no contraction happens?

A

Calponin and Caldesmin - Inhibit Myosin ATPase at low Calcium concentrations.
MLCK - Phosphorylates and Inactivates them.

122
Q

1,8) What are the Basic properties of SMC Contraction?

A

1) Long Lasting Ca signal
2) Less ATP needed
3) Slow Cross Bridge cycle

123
Q

1,8) What are the effects of cGMP on SMC contraction?

A

SMC Relaxation is caused by cGMP - PKG :

1) Activating Phosphatase to remove P from MLC
2) Phosphorylating IP3R, therefore inactivating it.

124
Q

1,8) What are the effects of cAMP on SMC contraction?

A

SMC Relaxation is caused by cAMP - PKA :

Phosphorylation of MLCK, therefore causing it to deactivate.

125
Q

1,8) What are the effects of Rho-GTP on SMC contraction?

Monomeric G-Protein

A

SMC Contraction is caused by Rho-GTP.
Rho-GTP activates Rho-Kinase which in turn:
1)Activates and Phosphorylates MLC
2)Inactivates and Phosphorylates Phosphatase

126
Q

1,9) What are electrical Electrical Synapses?

What are their properties?

A

Electrical synapses are actually Gap junctions:

1) Fast conduction 2)Present in Cardiac and Unitary SMC
3) Bidirectional Transmission 4)No Delay

127
Q

1,9) What is a Chemical Synapse?

What are their properties?

A

Chemical Synapse - Synaptic Cleft between two or more cells that pushes forward the AP stimulation with a chemical mediator a Neurotransmitter.
1)Unidirectional 2)1-5 mSec Delay

128
Q

1,9) Steps of Synaptic transmission:

A

1) AP in Presynaptic terminal causes VDCC activation
2) Calcium signal allows Vesicular Exocytosis of NT
3) NT binds the postsynaptic membrane receptors
4) EPSP or IPSP occurs depending on Receptor and NT
5) NT is recycled back/Diffused away/Degraded

129
Q

1,9)EPSP Properties:

A

EPSP:Excitatory Postsynaptic Potential - Depol.

  • Opening of a Non-Selective Cation channel like AMPA or NMDA by Glutamate (Usually).
  • Lasts 0.1-5 mSec
130
Q

1,9)IPSP Properties:

A

IPSP:Inhibitory Postsynaptic Potential - Hyperpol.

  • Opening of a Cl-channel like GABA A receptor.
  • Lasts 0.1-5 mSec
131
Q

1,9) Give 6 Examples for Neurotransmitters, their location and action:

A

1) Ach -In brain for memory, In ANS for Parasym - Excitatory.
2) Dopamine - In CNS for Reward - Inhibitory
3) GABA, Major Inhibitory for CNS
4) Glutamate, Major Excitatory for CNS
5) NE - ANS Sym - Excitatory / Inhibitory per receptor
6) Serotonin - Inhibitory in Pain pathway

132
Q

1,9) Where are synaptic vesicles synthesized? How are they transported in the cell?

A

Synaptic vesicles are synthesized in the cell body.

Transported to Axon terminal by Kinesin and back by Dynin.

133
Q

1,9) How are NT taken into the Synaptic vesicles?

A

NT-H+ Antiporter uses the H+ gradient formed in the Vesicles ,by H+ V-ATPase, to use secondary active transport of NT to the Vesicle.

134
Q

1,9) How are the multiple signals summed in the postsynaptic neuron? What is the consequence?

A

EPSPs and IPSPs are Spatially and Temporally summed.
If the summed potential is strong enough in the area of the Axon hillock the Na VDCs gets activated by it - Threshold potential for the Next AP.

135
Q

1,10)NMJ - what is the main NT used? Who is releasing it? what does it activates on the postsynaptic side?

A

Acetylcholine is released by A-Alpha motor Neuron travels down the synaptic cleft to activate a Nicotinic AchR which lets Na In and K out.

136
Q

1,10) What is an End plate potential?

A

Caused by adequate AchR stimulation, turning the Skeletal muscle membrane potential from -90mV to -50mV. 1 EPP = 1 Muscular AP = Contraction.
AP could reach +40mV.

137
Q

1,10) How is Ach degraded? Products? Fates?

A

Ach is degraded by Acetylcholinesterase (Sarcolemma bound), it is forming Acetate which diffuses away and Choline which is retaken up to the Presynaptic vesicle along in Na cotransport.

138
Q

1,10) By understanding that Ach are released all at once in order to form the EPP of Skeletal Muscle contraction We can quantize the Ach into a MicroEPP. What is the calculation? each Ach vesicle gives 0.4mV change.

A

From -90mV to -50mV there is a 40mV difference made by Ach vesicles. If one vesicle gives 0.4mV change than the total quanta needed is 100 vesicles.
100 MEPP are needed for EPP formation.

139
Q

1,10) Botulinum toxin - Action in NMJ:

A

Botulinum toxin - Blocks Ach release from Axon terminal.

Causes respiratory Paralysis and Death.

140
Q

1,10) Curare - Action in NMJ:

A

Curare - Competitive inhibitor of AchR, no depolarization no EPP. Paralysis and death.

141
Q

1,10) A-Bungarotoxin- Action in NMJ:

A

A-Bungarotoxin - Causes Depolarization in an inappropriate way via AchR

142
Q

1,10) Neostigmine- Action in NMJ:

A

Neostigmine - Inhibits the action of Ach-Estrase thus prolonging the effect of Ach in the muscle. Twitches and spasms, Desensitization happens eventually - Paralysis and death.

143
Q

1,10) Hemichilineum- Action in NMJ:

A

Hemichilineum Blocks the Na dependent reuptake of Choline. Less Formation of Ach (No Intrinsic Choline synthesis in Neurons)

144
Q

1,11) Parasympathetic First order neurons?

For what pathways?

A

1) Dorsal Vagal Nucleus - Internal organs activity
2) Edinger Westphal - Pupil and Lens diameter
3) Inf+Sup Salivatory - Salivary, Lacrimal, Nasal glands
4) Sacral Plexus - Internal organs activity

145
Q

1,11) Parasympathetic ANS: Location of the Ganglia? Pre and Post ganglionic fibers length? NT and transmission used for both?

A
  • Ganglia are inside or near the target organ.
    -Fibers: Preganglionic Long, Postganglionic Short.
    -Ganglionic cells take Ach-Nicotinic transmission
    -Target organs take Ach-Muscarinic transmission.
    (NO or VIP could be used as well)
146
Q

1,11) Parasympathetic ANS: Heart regulation.

A

Right vagus Nerve - SA Node - Decreases chronotropy
(GIRK Activation by Gi)
Left Vagus Nerve - AV - Decrease Dromotropy

147
Q

1,11) Which are the Parasympathetic Ganglia?

A
  • Ciliary
  • Pterygopalatine
  • Submandibular
  • Otic
  • Intramural ganglia for Vagal and Sacral nerves
148
Q

1,11) What is the Muscarinic Ach receptor antagonist? How is it used?

A

Atropine, Blocks the Parasympathetic signal for the heart thus creating an Increased heart rate.

149
Q

1,11) In which specific tissue the Parasympathetic NS doesn’t have any effect?( although Sympathetic NS has)

A

Tissues that are NOT controlled by Parasympathetic NS:

  • Skeletal and Smooth muscle cells
  • Skin:Sweat glands and Thermoregulation
  • Liver, Adipose and Kidney
150
Q

1,12) Sympathetic First order neurons?

For what pathways?

A

Thoracic to L2-L3 Spinal cord neurons

Pathways travel through Superior cervical ganglion/ Sympathetic chain. Generally follows great vessels plexuses.

151
Q

1,12)Sympathetic ANS: Location of the Ganglia? Pre and Post ganglionic fibers length? NT and transmission used for both?

A
  • Ganglia are located near the spinal cord as a chain
  • Preganglionic Short, Postganglionic Long
  • Postganglionic: NE, Epi, Neuropeptide Y, SST, Ach for Sweat glands
  • All Preganglionic NTs are Ach.
152
Q

1,12)Sympathetic ANS: Receptors type?

A

-Adrenergic receptors for all except sudomotor, Sweat glands(Ach) and Skin vessels(VIP)
(Some Neuropeptide Y and ATP receptors as well)

153
Q

1,12)Sympathetic ANS - Role of Adrenal Medulla:

A

-By release of Ach to Chromaffin cells there will be an Hormonal release of 20% NE and 80% (Produced) Epi.
General Blood mediated sympathetic effect.

154
Q

1,12)Sympathetic ANS - Alpha-1 Agonists Affinity and effect location:

A

Alpha-1: More sensitive to NE than Epi.

by Gq mechanism increases contraction in Vessels, GI and Skin.

155
Q

1,12)Sympathetic ANS - Alpha-2 Agonists Affinity and effect location:

A

Alpha-2: More sensitive to NE than Epi.

by Gi mechanism decreases contraction in vessels and GI.

156
Q

1,12)Sympathetic ANS - Beta-1 Agonists Affinity and effect location:

A

Beta-1: Sensitive equally to NE and Epi.

By Gs mechanism Increases Hear contraction force and Renin secretion from Juxtamedullary cells.

157
Q

1,12)Sympathetic ANS - Beta-2 Agonists Affinity and effect location:

A

Beta-2: More sensitive to Epi than NE.

By Gs mechanism causes Lungs, GI and Vessels vasodilation (and bronchodilation)

158
Q

1,12)Sympathetic ANS - Beta-3 Agonists Affinity and effect location:

A

Beta-3:More sensitive to NE than Epi.

By Gs mechanism causes increased Lipolysis

159
Q

1,12)Give an example of the reciprocal relationship between the Para and Sym NS? Exception to this idea?

A
  • Effecting opposing organs: Dilator/Sphincter Pupillae

- Liver/Kidney/Adipose/Skin : More Sym/Less Sym

160
Q

1,12) Where are Parasympathetic and Sympathetic Nervous systems Complementary?

A
  • Erection -Para + Ejaculation - Sym

- Salivary glands: Sym-Mucous , Para-Serous

161
Q

Efficacy:

A

The maximum response of a receptor by a ligand

162
Q

Potency

A

The rate at which the receptor reaches its maximum response by a ligand

163
Q

Gibbs-Donnan effect:

A

High Extracellular Protein amount leading to attraction of Cations and Repling Anions from and to the Intracellular (Respectively)

GBA Physiology (12 decks)

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