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Physiology 1 > Fluid Compartments (1) > Flashcards

Fluid Compartments (1) Flashcards

1
Q

Total body water

A

60% of body weight
= 42 L

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2
Q

ECF

A

20% of body weight
= 14 L

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3
Q

ICF

A

40% of body weight
= 28 L

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4
Q

Interstitial fluid

A

3/4 of ECF
= 10.5 L

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5
Q

Plasma

A

1/4 of ECF
= 3.5 L

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6
Q

Measurement of volume of fluid compartments

A

Dilution method
Adding tracer, allow mixing, measure concentration
Volume = Mass / Conc.

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7
Q

Dye for Total fluid compartment

A

Deuterium
(Hydrogen isotope)

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8
Q

Dye for ECF

A

Inulin

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9
Q

Dye for Blood plasma

A

Evans-blue
(binds albumin)

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10
Q

Na+ E/ICF

A

ECF: 135 - 147 mM
ICF: 10 - 15 mM

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11
Q

K+ E/ICF

A

ECF: 3.5 - 5.0 mM
ICF: 120 - 150 mM

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12
Q

Ca2+ E/ICF
(Total)

A

ECF: 2.1 - 2.8 mM
ICF: 100nM

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13
Q

Ca2+ E/ICF
(Free)

A

ECF: 1.1 - 1.4 mM
ICF: 100 nM

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14
Q

Cl- E/ICF

A

ECF: 95 - 105 mM
ICF: 20 - 30 mM

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15
Q

HCO3- E/ICF

A

ECF: 22 - 28 mM
ICF: 12 - 16 mM

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16
Q

Oncotic Pressure

A

Osmotic pressure of proteins
- Proteins are superosmols

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17
Q

Hyposmotic / Hypotonic

A

Cell volume increases

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18
Q

Hyperosmotic / Hypertonic

A

Cell shrinks

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19
Q

Isosmotic urea solution

A

Eventually Hypotonic due to movement of Urea into cell (permeable) causing hypotonicity and cell to swell

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20
Q

Osmolarity of most human body fluids

A

290 mOsm/L

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21
Q

2 Types of Protein mediated transport

A
  • Carriers
  • Channels
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22
Q

Carriers

A
  • Slow
  • Can saturate
  • Active
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23
Q

Channels

A
  • Fast
  • Can’t saturate
  • Passive
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24
Q

Primary vs Secondary active T

A
  • Prim: Pump
  • Sec: Coupled Active + Passive
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25
Q

Electrogenic vs Electroneutral T

A

Electrogenic T creates net charge across membrane

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26
Q

Facilitated diffusion

A
  • Faster than free diffusion
  • Passive
  • Specific
  • Integral pm protein
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27
Q

Aquaporins

A

Water transport across membrane
- 11 isoforms
- Passive

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28
Q

Special about GLUT4

A

Insulin dependent
(activates it)

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29
Q

GLUT 5

A

Transport of Fructose along with glucose

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30
Q

GLUT2 mech

A

Regulates glucose levels based on plasma glucose concentration, unlike GLUT1 which works constantly

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31
Q

Anion exchanger

A

Cl- / HCO3-
- RBCs fro CO2 transport
- Passive
- Electroneutral
- Antiporter

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32
Q

Na+ / K+ ATPase

A
  • 3Na out, 2K in
  • Electrogenic
  • Inh: Ouabain
  • In all cells
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33
Q

3 Ways to regulate Transporters
(in order of speed)

A

1) Activity (phosphorylation)
2) Trafficking (vesicle storage)
3) Expression (gene exp.)

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34
Q

Calcium ATPase
(SERCA)

A

Responsible for low cytoplasmic Ca levels
- Electrogenic
- SR & SER
- 2 Ca2+

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35
Q

ABC Transporter

A

Active transport of Hydrophobic compounds (Cholesterol, Bile,…)
- Responsible for multi-drug resistance of cells
- CFTR

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36
Q

2 Types of Exocytosis

A
  • Constitutive: Non-regulated continuous
  • Regulated secretory pathway (intracellular signalling)
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37
Q

Second messenger-gated channels

A

Controlled by changes of intracellular signaling molecules (cAMP, IP3)
- Sensors on IC membrane

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38
Q

VG Ca channels a1 subunit

A

a1 subunit forms ion pore

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39
Q

5 Types of VG Ca channels

A
  • L-Type (long-lasting)
  • T-Type (transient)
  • N-Type (neuronal)
  • P-Type (purkinje)
  • R-Type (residual)
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40
Q

N-type VG Ca channel

A

For Synaptic NT release in Brain and PNS
- High activation voltage

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41
Q

T-type VG Ca channel

A
  • SA node
  • Pacemaker activity
  • Low activation Voltage
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42
Q

L-type VG Ca channel

A
  • Skeletal, SM, Myocytes Contraction
  • High activation Voltage
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43
Q

Neurons Em

A

-70 mV

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44
Q

Skeletal muscle Em

A

-90 mV

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45
Q

RBC Em

A

-10 mV

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46
Q

Diffusion potential

A

Potential difference generated across a membrane when an ion diffuses down its conc. gradient
- Magnitude depends on size of con. gradient

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47
Q

Equilibrium potential (Eion)

A

Membrane potential when the net ion flow through an open channel is 0

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48
Q

What can we use to calc Eion

A

If we know ion conc. on both sides of a membrane and there is no net flow of the ions across the membrane,
= Nernst Equation

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49
Q

Relative permeability of Na, K, Cl

A

K: 1.0
Na: 0.01
Cl: 0.1

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50
Q

What happens if the permeability of an ion changes

A

The membrane potential will change in the direction of the equilibrium potential of that ion

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51
Q

Eion of ions K, Na, Cl, Ca

A

K: -94 mV
Na: +65 mV
Cl: -88 mV
Ca: +130 mV

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52
Q

Donnan Potential

A

Electric potential when impermeable ions (large molecules) create charge imbalance bw 2 compartments leading to unequal distribution of permeable ions

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53
Q

Action Potential

A

A spreading wave of VG Na+ Channel activation (all-or-none)
Spreads without Decrement
Rapid, Transient, Self-propagating.

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54
Q

Electrotonic potential
+ Examples

A

A localized change in the membrane potential in response to a stimulus.
Spreads with Decrement
- EPSP
- IPSP
- Receptor pot.
(size and duration proportional to the stimulus)

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55
Q

Receptor Potential

A

Change in Voltage across a receptor membrane proportional to the Stimulus Strength resulting in Inward current flow
- Sensory receptor

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56
Q

Length/Space constant

A

The distance over which the change in potential decreases to a factor 1/e of its maximal value
Higher S.C = Faster conduction

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57
Q

What type of signal is an AP

A

Digital signal
(all-or-none)

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58
Q

What type of signal is a Graded Electrotonic Potential

A

Analog
(electric pulses of varying amplitude)

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59
Q

How does AP form in relation to Electrotonic potential

A

AP is a result of Electrotonic potential which reaches the threshold voltage and stimulates VG ion channels

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60
Q

What is normal threshold potential of a cell for AP

A

-50 mV

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61
Q

Absolute refractory period

A
  • Inactivation of VG Na channels
  • No AP can form no matter the strength of the stimulus
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62
Q

Relative refractory period

A
  • Hyperpolarization due to K+ channels
  • Very strong stimulus needed to overcome the negative charge
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63
Q

Inhibitor of VD Na channel

64
Q

AP conduction is dependent on 2 factors

A
  • Axon diameter (thicker = faster, R = V/A)
  • Myelination (saltatory conduction bw nodes of ranvier)
65
Q

Measure of Drug potency

A

EC50
Effective concentration of a drug required to reach 50% or the drug’s max effect

66
Q

Measure of Drug efficacy

A

Emax
Max effect which can be expected from the drug

67
Q

Constitutive activity

A

Receptors which are active even in the absence of a ligand
But can still change effect when ligand is present

68
Q

Signaling by GTP-binding protein

A
  • GEF (guanidine exchange factor) removes GDP from G-protein, allowing GTP to bind
  • GAP (GTPase activating protein) cleaves GTP to GDP, inactivating the G-protein
69
Q

G-Protein Coupled Receptors (GPCR)
Structure

A
  • 7 TM domains
  • Heterotrimeric (a, B, y)
70
Q

G-Protein Coupled Receptors (GPCR)
Mechanism of Action

A

1) Ligand binds causing binding of receptor to G-protein
2) GTP to GDP
3) a-GTP dissociates from By
4) Act on effectors

71
Q

Gs

A

Act. of Adenylyl cyclase increasing cAMP
1) ATP to cAMP
2) cAMP act. of PKA
(PDE breaks down cAMP)

72
Q

Gi/o

A

Inh. of Adenylyl cyclase decreasing cAMP
1) cAMP drops, PKA drops
2) K+ channel act. = hyperpol.
3) Ca2+ channel inh
4) PLA2 act.

73
Q

Gq/11

A

Increase in I.C Ca2+ conc.
1) Stim. of PLC
2) PIP2 to IP3 and DAG
3) DAG activates PKC
4) IP3 increases sarcoplasmic and ER Ca2+ release
5) MLCK - muscle contraction
6) Act. of cAMP phosphodiesterase
(cAMP, PKA, inhib. of MLCK)

74
Q

G12/13

A

Regulates guanine nucleotide exchange factors
1) Activation of Rho Kinase by Rho-GTP
2) Smooth muscle contraction

75
Q

Ca2+ channels in ER (RyR)

A

IP3 receptors
- RyR1: Skeletal muscle
- RyR2: Cardiac receptor
- Ryr3: Others

76
Q

B-arrestin on GPCR

A

1) GPCRK phosphorylates the activated receptor with Ligand
2) Receptor binds B-arrestin
3) B-arrestin uncouples the receptor from G-proteins (desensitization)

77
Q

a1- AR

A
  • NE > E
  • Gq/11
  • Increase: IP3, Ca
  • SM contraction
78
Q

a2 - AR

A
  • NE > E
  • Gi/o
  • dec: cAMP, Ca
  • Inc: K+
  • Presynaptic inhibition
79
Q

B1 - AR

A
  • NE = E
  • Gs
  • cAMP inc.
  • Heart
80
Q

B2 - AR

A
  • E > NE
  • Gs
  • cAMP inc.
  • Smooth m. Relaxation
81
Q

B3 - AR

A
  • NE > E
  • Gs
  • cAMP inc.
  • Adipocytes
    (Thermogenesis)
82
Q

Ion channels

A
  • Faster than GPCR
  • Uses paracrine signaling
  • Neurotransmitters
83
Q

Ach-R

A

Nicotinic: Na+ / K+
Inh. by Curare
(Excitatory)

84
Q

Glutamate-R

A
  • NMDA: Na+ / K+ / Ca2+
  • AMPA, Kinate: Na+ / K+
    (Excitatory)
85
Q

GABA-R

A

Type A&C: Cl-
(Inhibitory)

86
Q

Glycine-R

A

Cl-
(Inhibitory)

87
Q

2 types of Cholinergic-R

A
  • Muscarinic
  • Nicotinic
88
Q

Muscarinic Ach-R

A
  • Activate GPCR
  • Inh. by Atropine
  • M1, M3, M5: Gq/11
  • M2, M4: Gi/o
89
Q

Receptor Tyrosine Kinase (RTK)

A
  • GF, Insulin
  • E.C binding site, I.C tyrosine kinase domain
90
Q

RTK mechanism

A

1) Ligand binding causes dimerization
2) Autophosphorylation
3) SH2 domain of GRB2 recognizes phosphotyrosine
4) Signaling pathway

91
Q

RTK signaling pathway

A

1) GRB2 recruits SOS
2) SOS activates RAS by GDP to GTP
3) MAPK produced
4) Phosphorylation of transcription factors in Nucleus
5) Cell proliferation / Survival

92
Q

PIP3 Kinase Role

A

Inhibits Apoptosis pathway
1) PIP3 Kinase binds RTK with SH2 domain
2) PIP2 phosph. to PIP3
3) PIP3 recognized by PDK and PKB
4) PIP3-PDK activates PIP3-PKB
5) PKB phsophorylates “Bad” protein holding the death-inh. protein

93
Q

How does NO synth work?

A

In soluble guanylyl cyclase
1) Cytosolic Ca with Calmodulin
2) Activates NOsynth
3) NO binds sGC making cGMP
4) PKG increase
5) MLCP act, MLCK inh.

94
Q

Serine-Threonine Kinase-R

A

1) TGF-B (transf. growth f-B)
2) Binds type II subunit
3) Phosphorylated domain
4) Kinase activity on
5) Phosphorylation of target protein

95
Q

Enzyme activity Linked -R

A
  • GH receptor with no intrinsic TK activity
  • Signaling mediated by JAK to activate STAT
  • Gene regulation in Nucleus
  • Cytokines, Prolactin, GH
96
Q

Non-RTK associated-R
Steps

A

1) Ligand binding leads to JAK phosphorylation
2) Phosphorylation of receptor
3) Phosphorylation of STAT
4) Dimerized STAT enters nucleus to regulate gene expression

97
Q

I.C Receptors

A
  • For Hydrophobic molecules (Steroids, TH, VitD)
    1) Binds Hsp90
    2) NLS revealed
    3) Receptor goes to Nucleus for transcription regulation
98
Q

Thick muscle Filaments

A
  • Contains myosin
  • 1 pair of heavy chains
  • 2 pairs of light chains
  • Form 2 heads with ATPase
  • Cross bridge: 2 heads on 1 myosin arm
99
Q

Thin muscle Filaments
(Skeletal)

A
  • 3 Proteins
  • Actin, Tropomyosin, Troponin
100
Q

Tropomyosin

A
  • At rest blocks myosin binding sites on Actin
  • Needs to move in order for contraction to occur
101
Q

Troponin

A
  • TnT: Attaches troponin to tropomyosin
  • TnI: Inh. of actin-myosin interaction by blocking binding site
  • TnC: Ca2+ binds here to move tropomyosin out of way allowing Myosin to bind Actin (contraction)
102
Q

Electromechanical Coupling

A

Process where an electrical signal triggers Ca2+ release from SR initiating Muscle contraction

103
Q

Electromechanical Coupling
Steps

A

1) AP propagates in T-tubules
2) Membrane depol. causes DHP-R change (L-VGCC)
3) RyR activated via mechanical coupling
4) Ca2+ increase, TnC activates, Contraction

104
Q

What Decreases intracellular Ca2+

A
  • Na+ / Ca2+ Exchanger (out)
  • Ca2+ Pump (out)
  • SERCA (to SR)
  • PMCA
105
Q

What binds Ca2+ in SR?

A
  • Calreticulin
  • Calsequestrin
    Ca Storage and release from SR.
106
Q

Myosin Cross-Bridge Cycle
(Sliding Filament Theory)

A

1) Myosin head binds Actin filament
2) Myosin does Power Stroke pulling Actin to center of Sarcomere
3) ATP binds myosin releasing it from Actin
4) ATP hydrolyzed and E used to Recock head

107
Q

What happens when no ATP is in muscle

A

Rigor position
No ATP to dissociate Myosin head from actin filament causing a tight attachment and stiffness

108
Q

Isometric Contraction

A

Muscle contraction without change in length of muscle
- Tension/Tone/strength increases

109
Q

Isotonic Contraction

A

Muscle contraction without change in the force of contraction (tone)
- Length changes
- Constant level of force

110
Q

Name when Isotonic and Isometric work together

A

Auxotonic contraction

111
Q

Length-Tension relationship

A

Force of muscle contraction depends on the length of the sarcomere

112
Q

Temporal summation muscle

A

When multiple stimuli are applied to a muscle in quick succession and they sum up

113
Q

Slow Oxidative Motor units (I)

A
  • Sustained movements (standing, posture)
  • Less fatiguable
  • Red fibers (myoglobin)
114
Q

Fast Motor units (II)

A
  • During bursting movement (jump, sprint)
  • Glycolytic
  • More fatiguable
  • White fibers
115
Q

Types of Muscle growth

A
  • Lengthening
  • Hypertrophy: Doubling myofibril diameter
  • Hyperplasia: New fibers as a result of injury
116
Q

Muscle fatigue

A
  • Accumulation of Lactate in sarcoplasm, pH drop, Ca binding to TnC decreases
  • Accumulation of Pi in sarcoplasm, Ca released from SR decreases, Ca sens. decreases, less a-m binding
117
Q

Smooth Muscle

A
  • Spindle shaped
  • No sarcomeres
  • No T-tubules
118
Q

Thin muscle Filaments
(Smooth)

A
  • Actin
  • Tropomyosin
  • NO TROPONIN
119
Q

Single Unit SMC

A
  • Gap Junctions
  • Large regions contract in unison
  • Characterized by spontaneous pacemaker activity
120
Q

Multi-unit SMC

A
  • Each cell has its own innervation
  • Tightly regulated
121
Q

Tonic contractions of SMC

A

Depol. does not peak beyond the electrical threshold (basal activity)

122
Q

What channel is absent in SMC AP generation

A

T-type VGCC

123
Q

3 ways to increase I.C Ca2+

A
  • L-VGCC (primary)
  • Ligand gated CC
  • IP3 gated CC / RyR (SR)
124
Q

How does contraction occur in SMC

A

1) Calcium binds Calmodulin
2) Ca-Calmodulin activates MLCK
3) Phosphorylates MLC increasing ATPase activity
4) Cross-bridge cycling

125
Q

Ca2+ independent Contraction

A

1) G12/13 activates GEF
2) Activating Rho-GTP
3) Inh. of MLCP
4) MLCK phosphorylates

126
Q

cGMP effects in SMC

A
  • Activation of phosphatase
  • Phosphorylation of IP3R
  • Inh. Ca entry to cell
127
Q

B2-AR effects in SMC

A

1) more cAMP
2) more PKA
3) Phosphorylates/inactivates MLCK
4) no contraction

128
Q

Chemical Synapse

A
  • Diffusion of NT
  • Unidirectional
  • 1-5 ms delay (to release NT)
  • 20nm
  • CNS & PNS
129
Q

Electrical Synapse

A
  • Ion transfer
  • Bidirectional
  • No delay
  • 2nm
  • CNS, PNS, SMCs, Heart
130
Q

EPSPs

A
  • 0.1-5 mV Depol. for milliseconds
  • Ligand-gated non-selective cation channels
  • Glutamate
  • AMPA, NMDA, mGLU1-8
131
Q

Metabotropic Glutamate -R
mGLU

A
  • Mostly: Gi
  • 1&5: Gq
132
Q

IPSPs

A
  • 0.1-5 mV Hyperpol. for milliseconds
    OR - Stabilization of Em at Negative values
  • Ligand-gated Cl- or K+ channels
  • GABA (y-aminobutyric acid)
133
Q

GABA receptors

A
  • GABA-A: Ligand-gated Cl- channel (activated by Benzodiazepine)
  • GABA-B: Gi-Protein coupled-R (opening of K+ channels)
134
Q

Types of Summation of Postsynaptic Potentials

A
  • Temporal Summation
  • Spatial Summation
  • Cancellation
135
Q

Temporal Summation

A

2 potentials from the same origin occur together at the same time.
2 potentials add together to make a stronger one

136
Q

Spacial Summation

A

2 Synapses of different origin close to each other add together to have an effect on the postsynaptic potential

137
Q

Cancellation

A

EPSP and IPSP of the same magnitude added together, cancelling each other out

138
Q

Loading of NT into Vesicles

A
  • H+ ATPase pumps H+ into vesicle
  • H+/NT exchanger takes H+ out and NT into vesicle
    (Secondary Active Transport)
139
Q

Ach synthesis

A
  • Synthesized from Choline and Acetyl-coA by Choline Acetyl-transferase
  • Into vesicle using secondary active transport of NT/H+ exchanger
140
Q

Ach Recycling

A
  • Ach broken down to Choline and Acetate by Ach Esterase
  • Uptake of choline using Secondary active transport of Na+/Ach cotransporter
141
Q

Depolarizing Muscle Relaxant

A

Agonist of Ach-R binds and can not be broken down or breaks down much slower than Ach
Causes over-activation and inactivation of the Na Channels
(Succinylcholine, Carbachol)

142
Q

Non-Depolarizing Muscle Relaxant

A

Ach-R Antagonist
Binds Ach-R and blocks Na channel signal
(Curare, Turbocurarine, Pancuronium)

143
Q

Myesthenia Gravis

A

NM autoimmune disease leading to muscle weakness due to auto-antibodies against nAch-R

144
Q

Myesthenia Gravis Treatment

A

Neostigmine
Inhibits breakdown of Ach in NMJ so more Ach available for binding on Receptor

145
Q

Parasympathetic Nervous System

A
  • Long Preganglionic fiber
  • Short Postganglionic fiber
  • Ggl in organ
  • Postganglionic fiber goes to Muscarinic Ach receptor
    (CN, S2-S4)
146
Q

Postganglionic Parasymp. Axon transmitters

A
  • ACh
  • VIP
  • NO
147
Q

Sympathetic Nervous System

A
  • Short Preganglionic fiber
  • Long Postganglionic fiber
  • Postggl. use NE (usually)
  • Preggl. can go straight to adrenal gland causing E (NE) release
    (T1-L2)
148
Q

What do both Parasymp. & Symp. use for signaling from Preggl. to Ggl?

149
Q

What receptor promotes Renin secretion in the Kidney?

150
Q

Blood Volume

151
Q

Hematocrit

152
Q

Hemoglobin Conc.

A

120 - 160 g/L

153
Q

Blood H+ conc.

154
Q

I.C H+ conc.

155
Q

Blood plasma protein conc.

156
Q

Blood Oncotic Pressure

157
Q

Conduction speed of Nerves

A
  • A: up to 120 m/s
  • B: 3 - 15 m/s
  • C: 0.5 - 2 m/s (unmyelinated)

Physiology 1 (12 decks)

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