Test 1 Flashcards

1
Q

what is the study of all the processes that make life happen

A

physiology

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2
Q

what is meant by form fits function

A

anatomy

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3
Q

what is the constant conditions inside the “internal environment”

A

homeostasis

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4
Q

what is meant by “internal environment”

A

ECF

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5
Q

what percentage of fluid is ECF

A

1/3

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6
Q

what is ECF comprised of

A

plasma and interstitial fluid

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7
Q

what percentage of fluid is intracellular fluid

A

2/3

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8
Q

who coined the term homeostasis

A

Walter Cannon

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9
Q

what do cells need

A

constant conditions and supply of energy

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10
Q

in order to maintain homeostasis

A

input must equal output

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11
Q

what is considered input (homeostasis)

A

food, energy, O2

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12
Q

what is considered output (homeostasis)

A

work, heat, potential energy, CO2, H+ (protons), H2O, urea, poop

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13
Q

what does anesthesia do to homeostasis

A

disrupts, takes “control systems offline”

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14
Q

arterioles deliver _________ to meet ____________, and venules ____________

A

only enough nutrients/fluid
tissue demands
remove all metabolic byproduct

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15
Q

what happens in the peripheral circulatory beds if tissue/metabolic demand increases

A

changes in ECF are detected (lowering of O2/glucose), the body increases perfusion to meet demands

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16
Q

in relation to homeostasis: how is blood flow determined

A

by the metabolic demands of the tissue

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17
Q

how do the R/L heart participate in homeostasis

A

gas exchange and delivery of nutrients to the periphery

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18
Q

how do the lungs participate in homeostasis

A

maintenance of blood gas levels

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19
Q

how does the GI system participate in homeostasis

A

replaces nutrients in the blood

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20
Q

how do the kidneys participate in homeostasis

A

maintain BP, help ECF buffer via PH

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21
Q

how does the liver participate in homeostasis

A

filters toxins

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22
Q

how do peripheral vascular beds participate in homeostasis

A

increase perfusion to meet tissue demands

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23
Q

process: changes in homeostasis are sense by the body, which reacts to counteract the change, and return the body to homeostasis

A

negative feedback

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24
Q

explain how a thermostat is negative feedback

A

sense temperature increase/decrease, turns on heater/AC, temperature returns back to set point

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25
Q

“change is negative to the stimuli”

A

negative feedback loop

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26
Q

explain how breathing is a negative feedback loop

A

body senses increased CO2, increases RR, causes CO2 to decrease

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27
Q

explain how blood pressure maintenance is a negative feedback loop (4)

A

body senses a decreased MAP, increases sympathetic activity, MAP increases
body senses a decreased MAP, decreases parasympathetic activity, MAP increases
body senses a decreased MAP, increases AVP/ADH (vasopressin/ADH), MAP increases
body senses a decreased MAP, decreases ANP (atrial naturitic peptide), MAP increases

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28
Q

why are the multiple negative feedback loops involved in BP maintenance

A

more “sensors” are involved in systems that are vital for life, multiple mechanisms occur at once

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29
Q

process: changes in homeostasis are detected and the body responds by amplifying the change

A

positive feedback

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30
Q

what is it called when a positive feedback loop operates unchecked

A

vicious cycle/pathologic positive feedback

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31
Q

explain how labor is a positive feedback loop

A

uterus contracts, fetal head stretches cervix, oxytocin is released, oxytocin increases uterine contractions

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32
Q

what is the checkpoint for the positive feedback loop that is labor

A

birth

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33
Q

explain how the clotting cascade is a positive feedback loop

A

endothelial injury occurs, txa2 is released, vessels vasoconstrict, increasing platelet aggregation, which causes additional txa2 release

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34
Q

what is the checkpoint for the positive feedback loop in the clotting cascade

A

bleeding stops

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35
Q

in what instance is the positive feedback loop of the clotting cascade harmful

A

if it occurs in the coronary vessels, it can lead to MI

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36
Q

explain how sepsis/necrosis is a pathologic positive feedback loop

A

cells die and release toxins, this causes additional cells to die

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37
Q

explain how severe acidosis is a pathologic positive feedback loop

A

decreased CNS activity, decreases respiratory drive, which increases CO2, which further drives acidosis

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38
Q

explain how diabetic renal inflammation is a pathologic positive feedback loop

A

nephrons die, other nephrons have to work harder, causing them to tire out and also die

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39
Q

how are pathologic positive feedback loops maintained

A

speed up exponentially with time

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40
Q

explain how severe hemorrhage is a pathologic positive feedback loop

A

MAP decreases, which decreases coronary blood flow, which decreases cardiac output, which further decreases MAP

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41
Q

is compensated shock a negative or positive feedback loop

A

negative

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42
Q

is decompensated shock a negative or positive feedback loop

A

positive

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43
Q

if the body loses ______% of blood volume, the body enters a negative feedback loop

A

<20%

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44
Q

if the body loses ____% of blood volume, the body enters a pathologic positive feedback loop

A

> 40%

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45
Q

why does severe hemorrhage cause decompensated shock

A

the negative feedback loops present cannot overcome the injury, so the body enters a positive feedback loop

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46
Q

explain the negative feedback loop associated with compensated hemorrhagic shock

A

blood pressure and cardiac output drop, to compensate the body shifts fluid, increases heart rate and contractility, and vasoconstricts, blood pressure and cardiac output return to baseline until body can replenish lost volume

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47
Q

explain the positive feedback loop associated with decompensated hemorrhagic shock

A

blood pressure and cardiac output drop, deficit cannot be overcome by compensatory processes, tissue hypoxia occurs, which leads to acidosis, which further decreases blood pressure and cardiac output, which causes additional tissue hypoxia

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48
Q

exceptions to statement “cells are capable of replication”

A

RBCs

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49
Q

how are new RBCs regenerated

A

in bone marrow by progenerator cells, replaced every 90-120 days

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50
Q

what types of cells have an extremely low rate of regeneration

A

cardiac cells and neurons

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51
Q

how many cells are in the body

A

35 trillion

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52
Q

how many RBCs are in the body

A

25 trillion

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53
Q

what determines the function of a cell

A

the internal contents

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54
Q

what are the walls of the nucleus made of

A

double phospholipid bilayer

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55
Q

why are the walls of the nucleus made of a double phospholipid bilayer

A

to keep DNA secure

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56
Q

how do substance enter the nucleus

A

through pores

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57
Q

how do steroids work

A

enter the nucleus through pores and effect gene transcription (turn on stress response proteins)

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58
Q

how do cells accomplish different tasks

A

genes in nucleus are turned off/on

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59
Q

the recycling plant of the cell

A

lysosome

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60
Q

what organelle uses acidic conditions to pull apart individual amino acids from proteins and then releases them into the cytoplasm to be reused

A

lysosome

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61
Q

how does the lysosome break down proteins

A

acidic conditions

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62
Q

what percent water is the cytoplasm

A

70-85%

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63
Q

where do chemical reactions take place in the cell

A

cytoplasm

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64
Q

what organelle uses oxidative stress to destroy waste (toxins)

A

peroxisome

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65
Q

what kind of cell is not 70-85% water

A

adipose

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66
Q

how do peroxisomes destroy waste

A

oxidative stress

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67
Q

where are the majority of peroxisomes located

A

liver

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68
Q

when you think peroxisome think…..

A

ethanol

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69
Q

what organelle uses enzymatic material to help produce ATP from energy compounds and oxygen

A

mitochondria

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70
Q

what is the cell membrane made of

A

phospholipid bilayer

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71
Q

where is the endoplasmic reticulum located

A

an extension of the nuclear wall

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72
Q

what are the functions of the endoplasmic reticulum (3)

A

produce lipids, produce proteins, store calcium (in muscles)

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73
Q

where are lipids produced in the cell

A

smooth ER

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74
Q

where are proteins produced in the cell

A

rough ER (by ribosomes)

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75
Q

where are ribosomes located

A

on rough ER (95%), in cytoplasm (5%)

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76
Q

what is the function of the ribosome

A

translate instructions from RNA to form “unmodified” proteins

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77
Q

how do ribosomes make (translate) protein

A

moves along RNA and “grabs” amino acids from cytosol to form protein

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78
Q

what is the function of the golgi apparatus

A

post-translation modification of proteins

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79
Q

what is the function of vesicles

A

transport concentrated modified protein

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80
Q

what are proteins

A

strings of amino acids put together to accomplish some specialized task

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81
Q

what helps charged molecules move across the cell membrane (past phospholipid bilayer)

A

specialized proteins

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82
Q

explain the process of protein production

A

nucleus transcribes DNA to RNA, RNA is translated into protein in the rough ER by the ribosomes, protein is the modified to be functional by the golgi apparatus

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83
Q

what determines what amino acids get put together and in what order

A

RNA nucleotide sequence

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84
Q

water makes up what percentage of the cell

A

70-85%

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85
Q

what does water assist with in the cell (4)

A

acid/base balance, electrolytes, proton concentration, energy compounds

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86
Q

list cell components (13)

A

water, electrolytes, membranes, organelles, enzymes, sugars, structural components, fats, motility structures, genetic material, protein, secretory granules, membrane components

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87
Q

what are enzymes

A

a type of protein

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88
Q

what is the function of enzymes

A

help catalyze chemical reactions

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89
Q

suffix for enzymes

A

-ase

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90
Q

what is the function of Na/K ATPase

A

metabolizes ATP to pump electrolytes across the cell wall

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91
Q

what is the function of muscle ATPase

A

helps produce force when muscle contracts

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92
Q

what is the function of catalase

A

enzyme in peroxisomes to oxidize compounds

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93
Q

prefixes for sugars

A

glyco-, carboxy-, carb-

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94
Q

where are sugars located

A

free floating in cytoplasm or in/on cell wall

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95
Q

what are the functions of sugars (6)

A

energy, protein formation, structure, identification, anchoring, repel negatively charged proteins in the kidneys

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96
Q

how do sugars function as “ID tags”

A

glycoproteins on cell wall help cell identify self vs nonself

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97
Q

what kind of sugars help cells anchor to one another

A

glycoprotein

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98
Q

how do cells maintain shape

A

filaments and proteins formed inside cell

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99
Q

what kind of charge do sugars have

A

negative

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100
Q

why do sugars repel negatively charged proteins in the kidneys

A

to make sure we don’t filter our too much protein

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101
Q

how do sugars help with energy production

A

creates ATP through glycolysis in the cytosol (anaerobic process)

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102
Q

charge of fats/lipids in the cell

A

uncharged

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103
Q

where do fats/lipids exist in a cell

A

“oily space” of cell wall

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104
Q

motility structure used to move the cell itself

A

flagella

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105
Q

motility structure used to move things around outside of the cell

A

cilia

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106
Q

where is genetic material in the cell

A

nucleus and mitochondria

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107
Q

how many sets of mitochondrial DNA exist and where do they come from

A

12-20 sets, inherited from mother

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108
Q

what determines the specialized role of a cell

A

what genes are expressed which reflects what proteins are found in the cell

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109
Q

protein can be (3)

A

structural, functional, or enzymatic

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110
Q

what dictates how drugs work

A

the chemistry of the ICF

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111
Q

hydrophilic compounds found in ICF

A

charged ions, substances that dissociate in water

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112
Q

hydrophobic compounds found in ICF

A

fats/lipids, uncharged molecules

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113
Q

list things that are soluble in ICF (6)

A

ions, most proteins, carbohydrates, some gases, buffers, some drugs

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114
Q

why are carbohydrates soluble in ICF

A

they are charged

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115
Q

example of soluble gas in ICF

A

CO2

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116
Q

list things that are insoluble in ICF (5)

A

cholesterol, steroids, lipids, some gases, some drugs

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117
Q

example of gas insoluble in ICF

A

nitrous

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118
Q

if propofol is insoluble, how does it enter the plasma

A

must be combined with carrier

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119
Q

what is the ECF comprised of

A

plasma and interstitial fluid

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120
Q

what is the barrier between plasma and interstitial fluid

A

capillary membrane

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121
Q

what is the barrier between interstitial fluid and ICF called

A

cell membrane

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122
Q

what percent mass is the TBW

A

60%

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123
Q

what is the TBW

A

total body water- mass amount that ECF + ICF comprises

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124
Q

how to calculate mass/volume amount of ICF

A

60% of total mass, then 2/3 of that

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125
Q

how to calculate mass/volume amount of ECF

A

60% of total mass, then 1/3 of that

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126
Q

how to calculate mass/volume amount of plasma

A

60% of total mass, 1/3 of that, then 1/4 of that

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127
Q

how to calculate mass/volume amount of interstitial fluid

A

60% of total mass, 1/3 of that, then 3/4 of that

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128
Q

normal fluid distribution in a 70kg adult

A

TBW: 42L
ICF: 28L
PLASMA: 3L
INTERSTITAL: 11L

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129
Q

volume of all fluid in the cardiovascular system, not including the weight/volume of RBCs

A

plasma

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130
Q

what are capillary membranes permeable/impermeable to

A

permeable: water, charged ions (electrolytes)
impermeable: plasma proteins (stay in plasma)

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131
Q

what happens if the is a massive blood loss (fluid shifts)

A

fluid shifts from interstitial to plasma to compensate

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132
Q

where are the capillary membranes not permeable

A

in the brain

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133
Q

what is fluid surrounding the cells

A

interstitial fluid

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134
Q

what is the cell membrane permeable/impermeable to

A

permeable to water
impermeable to ions (charged molecules)

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135
Q

what happens to correct changes in osmolarity

A

fluid shifts between compartments (ICF, interstitial, and plasmaa)

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136
Q

what does steady state mean

A

concentrations of ICF are different than concentrations of ECF but are kept at constant levels

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137
Q

is fluid concentration (ECF v ICF) in equilibrium

A

no- its a steady state

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138
Q

what are ions/electrolytes measured by

A

mOsm/L

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139
Q

primary cation in the ECF

A

Na+

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140
Q

concentration of Na+ in ECF

A

140-142

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141
Q

concentration of Na+ in ICF

A

14

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142
Q

ECF:ICF ratio of Na+

A

10:1

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143
Q

how do you estimate total osmolarity if only given Na+

A

2 x Na+ = good estimate of osmolarity

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144
Q

electrolyte that is important for the electrical system of the heart

A

K+

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145
Q

concentration of K+ in the ECF

A

4

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146
Q

concentration of K+ in the ICF

A

120

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147
Q

ECF:ICF ratio of K+

A

1:30

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148
Q

electrolyte that is important for action potential in neuro and muscles

A

Ca+2

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149
Q

electrolyte that “surges to turn things on, the returns back to zero”

A

Ca+2

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150
Q

ICF concentration of Ca+2

A

zero

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151
Q

ECF:ICF ratio of Ca+2

A

10,000:1

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152
Q

electrolyte that stabilizes the heart

A

Mg+2

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153
Q

electrolyte that acts as a cofactor for chemical reactions inside the cell

A

Mg+2

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154
Q

where is Mg+2 in greater concentration

A

ICF

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155
Q

what electrolyte is the primary anion

A

Cl-

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156
Q

where is Cl- in greater concentration

A

ECF

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157
Q

what electrolyte does Cl- follow the distribution of

A

Na+

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158
Q

what is the secondary anion

A

HCO3-

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159
Q

what is the primary buffer in the ECF

A

HCO3-

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160
Q

what organ manages HCOs-

A

kidneys

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161
Q

what is the concentration of HCO3- in the ECF

A

25

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162
Q

where is HCO3- in greater concentration

A

ECF

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163
Q

what is the primary buffer in the ICF

A

HPO4-2

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164
Q

what are the 3 functions of HPO4-2

A

phosphorylation, turning processes on/off, energy creation/storage

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165
Q

where is HPO4-2 in greater concentration

A

ICF

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166
Q

where does phosphocreatine exisit

A

skeletal muscles

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167
Q

what is one way energy is generated in a muscle cell

A

breaking a phosphate off phosphocreatine to form creatine

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168
Q

short term energy reserve in muscle cells, used before breaking down ATP

A

phosphocreatine

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169
Q

where is phosphocreatine in greater concentration

A

only in ICF

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170
Q

the building blocks of protein

A

amino acids

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171
Q

why is there a greater concentration of amino acids in the ICF

A

proteins are built in the cell

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172
Q

where are amino acids in greater concentration

A

ICF

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173
Q

where is creatine found

A

skeletal muscle cells

174
Q

where is creatine in greater concentration

A

ICF

175
Q

metabolic byproduct of anaerobic metabolism inside the cell

A

lactate

176
Q

where is lactate in higher concentration

A

ICF

177
Q

where is ATP in higher concentration

A

only in ICF, cannot exit cell

178
Q

what is a byproduct of ATP that can leak outside the cell

A

adenosine

179
Q

when does adenosine leak outside the cell

A

if it is utilizing a lot of ATP

180
Q

what effect does adenosine have

A

increases blood flow

181
Q

where is glucose in higher concentration

A

ECF

182
Q

intersitital:plasma ratio of protein

A

1:5

183
Q

where is protein in higher concentration

A

ICF

184
Q

the total osmolarity can also be called

A

predicted osmolarity

185
Q

total osmolarity can be defined as

A

the total of all dissolved compounds

186
Q

what is the total osmolarity in ICF, plasma, and intersitital

A

300

187
Q

the corrected osmolarity can also be called

A

biologic osmolarity

188
Q

which osmolarity measurement accounts for dissociated ions

A

corrected

189
Q

what is the corrected osmolarity in ICF, plasma, and interstitial

A

280-283

190
Q

how does osmolarity correct itself

A

fluid (water) shifts

191
Q

what is the osmotic pressure in ICF, plasma, and interstitial

A

all almost =, all >5000mmHg

192
Q

what does the cell membrane contain

A

phospholipids, glycolipids, cholesterol, precursor molecules, protein, glycoproteins, and the glycocalyx

193
Q

what happens if there are too many lipids in the cell wall

A

effects the shape of the cell membrane, which negatively effects the CV system

194
Q

the sum of all external sugar structures

A

glycocalyx

195
Q

what structure serves as the “ID tag”

A

glycocalyx

196
Q

what happens to the glycocalyx with diabetes

A

increases sugars on glycocalyx, making the “ID tag” look foreign, so the body begins to attack it

197
Q

describe the head of a phospholipid

A

hydrophilic, charged, phosphate head

198
Q

describe the tail of a phospholipid

A

hydrophobic, uncharged, lipid, oily, only made of C + H

199
Q

what makes up the bulk of the cell wall

A

phospholipid tails

200
Q

what prevents charged molecules from entering the cell wall

A

phospholipid tails

201
Q

what dictates the orientation of phospholipids

A

environment

202
Q

where does the majority of cholesterol exist

A

lipid tail section of phospholipid bilayer

203
Q

how does cholesterol and arachadonic acid exit the cell wall

A

OH head (polar) is exposed and is used help “pull” it out of cell wall

204
Q

why does the -OH head of cholesterol and arachadonic acid hand out of the phospholipid bilayer

A

because it is uncharged

205
Q

describe the shape of cholesterol

A

planar, only made up of C + H, either single of double bonded to one another

206
Q

what is the fluidity of cholesterol @ 37C and above

A

rigid, reduces cell wall fluidity, increases the stiffness of blood vessels

207
Q

large sugars involved in cholesterol formation (synthesis)

A

substrates

208
Q

2 important substates for cholesterol synthesis

A

Acetyl-CoA and HMG-CoA

209
Q

byproduct of cellular metabolism, helps produce ATP from glucose and O2

A

Acetyl-CoA

210
Q

statins target to interfere with endogenous cholesterol synthesis

A

HMG-CoA

211
Q

what percent of cholesterol is exogenous (comes from diet)

A

20%

212
Q

what percent of cholesterol is endogenous

A

80%

213
Q

what breaks down cholesterol to be able to form metabolites

A

enzymes

214
Q

what happens with each enzymatic action in the production of cholesterol metabolites

A

structure and function changes

215
Q

most important metabolites of cholesterol (6)

A

estradiol (E2), testosterone, progesterone, andosterdione, cortisol, aldosterone

216
Q

precursor to testosterone

A

andosterdione

217
Q

what was used by baseball players 20 years ago to improve performance

A

andosterdione

218
Q

stress hormones

A

cortisol and aldosterone

219
Q

where are cortisol and aldosterone produced

A

adrenal glands

220
Q

describe the cross reactivity with cortisol and aldosterone

A

structures are so similar that they can be used interchangeably if deficient in 1

221
Q

what are precursor molecules

A

specialized phospholipids with an extra compound stuck to their polar head

222
Q

examples of precursor molecules (5)

A

polyunsaturated fats, arachadonic acid, phosphatidyl- compounds, sphingomyelin, cholesterol

223
Q

what makes up arachidonic acid

A

a polyunsaturated fat

224
Q

what plays a role in surfactant production in the lungs

A

phosphatidyl- compounds

225
Q

what breaks the surface tension of fluid in the lungs

A

surfactant

226
Q

besides surfactant, what is another role of phsophatidyl- compounds

A

play a role in signal transduction processes

227
Q

phospholipid that is used as a storage compound for a chemical that is a precursor to IP3

A

phosphatidylinositol (PI)

228
Q

what is the precursor to IP3

A

ionsitol

229
Q

what is IP3 used for

A

smooth muscle contraction

230
Q

the storage compound for an immune marker

A

phosphatidylserine

231
Q

an immune marker that always faces inwards (towards ICF) in healthy cells

A

serine

232
Q

which way does serine face in healthy cells

A

inwards (towards ICF)

233
Q

what happens if the immune system identifies serine

A

it destroys it

234
Q

an enzyme in the cell wall that assures that all serine is facing the right way and reorients it if it is not facing the right way

A

flipase

235
Q

does flipase require ATP

A

yes

236
Q

what happens if there is not enough ATP for flipase to perform its function

A

more serines get disoriented so the immune system destroys the entire cell

237
Q

what causes cell destruction in energy deficient situations (such as ischemia)

A

serine buildup d/t flipase not being able to perform function d/t lack of ATP

238
Q

what is a phosphatidyl- compound that we discussed but did not elaborate

A

phosphatidylethanolamine (PE)

239
Q

what is a storage compound for a precursor to acetylcholine (Ach)

A

phosphatidylcholine

240
Q

what is acetylcholine used for

A

signal transduction

240
Q

what is a precursor to acetylcholine (Ach)

A

choline

241
Q

is sphingomyelin a phospholipid

A

no, but it is found in cell wall

242
Q

what is a fatty compound used to produce myelin

A

shingomyelin

243
Q

what kind of lipids make up arachadonic acid

A

saturated and unsaturated

244
Q

what are the 3 main pathways of arachadoninc acid metabolism

A

HETE/EET, prostaglandins, and leukotrines

245
Q

large, short living fat, involved in AKF and other harmful conditions

A

HETE/EET

246
Q

what enzyme breaks arachadonic acid to make HETE/EET

A

cytochrome p450

247
Q

describe arachadonic acid metabolism in relation to prostaglandins

A

AA -> COX1/2 -> PGG2 -> COX1/2 -> PGH2 -> specific synthases -> prostaglandins (PGE2, PGI2, PGF2a) and TXA2

248
Q

what is PGI2 also known as

A

prostacyclin

249
Q

what is the name of TXA2

A

thromboxane A2

250
Q

what role do prostaglandins serve

A

pain sensitivity

251
Q

what role does TXA2 serve

A

mediates the healing of vessel injury, causes blood vessels to vasospasm which decreases BF to an area so healing can occur

252
Q

what is the name of COX1/2

A

cyclooxygenase

253
Q

what is the role of COX1/2

A

catalyzes AA to form PGG2 then PGG2 to form PGH2

254
Q

where is COX1 found

A

all over the body

255
Q

which is more specific to TXA2- COX1 or COX2

A

COX1

256
Q

an isoform of cyclooxygenase turned on by painful stimuli

A

COX2

257
Q

more “inducable” form of cyclooxygenase

A

COX2

258
Q

which COX enzyme is more specific to pain

A

COX2

259
Q

strong irreversible blocker of COX1 (some COX2 activity) has the side effect of bleeding due to blocking TXA2 synthesis

A

aspirin

260
Q

strongest OTC COX2 blocker (has some COX1 effects)

A

naproxen

261
Q

NSAIDS block

A

both COX1 and COX2

262
Q

drug specific to COX1/2 found on neurons, no anti-inflammatory effects, decreases bleeding side effects

A

Tylenol

263
Q

an extremely specific COX2 blocker which is no longer available due to cardiovascular events occurred in patients due to preventing remodeling from happening after ischemia

A

Vioxx

264
Q

describe to pathway from arachadonic acid to leukotrienes

A

AA -> lipoxygenase (LO) -> leukotrines

265
Q

name the leukotrines

A

LTA4, LTB4, LTC4, LTD4, LTE4

266
Q

what is responsible for immune-mediated inflammation

A

leukotrines

267
Q

drug that is a leukotrine antagonist

A

singular

268
Q

purpose of enzymes

A

catalyze reactions

269
Q

what receptor is important in heart rate pacing

A

GPCR

270
Q

any signal from outside the cell must interact with ________ to enter the cell

A

protein

271
Q

no energy is required, and it moves ions in and out of the cell based on chemical concentration or electrical gradient

A

diffusion

272
Q

types of diffusion

A

simple or facilitated

273
Q

the movement that occurs with diffusion is based on

A

electrochemical gradient

274
Q

type of movement utilized by dissolved gases and electrolytes

A

simple diffusion

275
Q

as far as electrical gradients, cells move in what direction

A

more positive to less positive

276
Q

do gases need channels to enter the cell

A

no

277
Q

do electrolytes need channels to enter the cell

A

yes

278
Q

facilitated diffusion process

A

binding, conformational change, releasing

279
Q

does facilitated diffusion require energy (ATP)

A

no

280
Q

does facilitated diffusion require a carrier protein

A

yes

281
Q

pumps that go against concentration gradients

A

active transporters

282
Q

what do active transporters need (2)

A

energy (possibly ATP) and a carrier protein

283
Q

when is ATP required for in active transport

A

if exchange is going to happen quickly or going against an electrochemical gradient

284
Q

what drives the movement of an active transporter

A

the concentration gradient

285
Q

the speed of an active transporter is dependent on (2)

A

number of transporters and concentration gradient

286
Q

does facilitated diffusion require energy

A

no

287
Q

how does 95% of glucose enter cell

A

GLUT transporters

288
Q

describe the mechanism of a GLUT transporter

A

“catch and release”

289
Q

GLUT transporters primarily move glucose in what direction (but are capable of either direction)

A

outside of cell to inside of cell

290
Q

non-insulin dependent GLUT

A

GLUT-1

291
Q

where are GLUT-1 found

A

RBCs

292
Q

insulin-dependent GLUT

A

GLUT-4

293
Q

where are GLUT-4 found

A

skeletal muscles, liver, and fat

294
Q

what does insulin do to GLUT

A

increases the number of receptors on the cell surface therefore increasing the rate of glucose removal from the blood

295
Q

can H2O travel through ion channels

A

yes

296
Q

specific H2O channels used in passive diffusion

A

aquaporins (AQP)

297
Q

if a cell has many AQPs what happens to the ion channels

A

less ion channels

298
Q

examples of 1st degree active transport

A

Ca+2 pump, proton pump, sodium/potassium ATPase pump

299
Q

how does Ca+2 exit the cell after a neuronal action potential

A

Ca+2 pump (1st degree active transport)

300
Q

does a Ca+2 pump require ATP

A

yes

301
Q

used in cells in the lining of the stomach to produce an acidic environment

A

proton pump

302
Q

which direction is Ca+2 going with a Ca+2 pump

A

outside the cell (against concentration gradient)

303
Q

which direction is H+ going in a proton pump

A

outside the cell (against the concentration gradient)

304
Q

does a proton pump require ATP

A

yes

305
Q

what percentage of the bodies energy goes towards the maintenance of Na/K ATPase pumpes

A

60-70% (majority)

306
Q

what are all action potentials reliant on

A

Na/K ATPase

307
Q

per 1 ATP what is the exchange of ions in a Na/K ATPase

A

2 K+ in, 3 Na+ out

308
Q

1st degree active transporters directly require

A

ATP

309
Q

2nd degree active transporters DO NOT directly require

A

ATP

310
Q

where do 2nd degree active transporters receive their energy

A

the electrochemical gradient or performing coupled movements

311
Q

examples (2) of 2nd degree active transporters

A

NCX (sodium/calcium exchanger) and SGLT (Na+/glucose transporter)

312
Q

where does an NCX receive its energy

A

electrochemical gradient maintained by Na+/K+ ATPase

313
Q

what is used for the bulk removal of Ca+2 from muscle cells

A

NCX (sodium/calcium exchanger)

314
Q

movement of ions in an NCX (sodium/calcium exchanger)

A

3 Na+ in, 1 Ca+2 out

315
Q

speeds up glucose movement into the cell by coupling it with sodium movement

A

SGLT (Na+/glucose transporter)

316
Q

purpose of SGLT (Na+/glucose transporter)

A

reabsorb glucose into the kidney cell so glucose is not lost in the urine

317
Q

where is SGLT (Na+/glucose transporter) found

A

kidneys

318
Q

how would you describe the movement of an SGLT (Na+/glucose transporter)

A

coupled (Na and glucose- both moving with chemical gradient, but Na serves to speed up movement of glucose)

319
Q

quantity of stuff dissolved in 1L of solution

A

osmolarity

320
Q

is 1L of solution equal to 1kg of water

A

no- there are things (cells, proteins, electrolytes) dissolved in solution

321
Q

in weight: 1L H2O in solution ____ 1L H2O

A

less than

322
Q

what is the % difference in osmolarity vs osmolality

A

1%

323
Q

quantity of stuff dissolved in 1kg H2O

A

osmolality

324
Q

which one is used due to practicality

A

osmolarity

324
Q

which is more technically correct: osmolarity or osmolality

A

osmolality

325
Q

the hydraulic (physical) pressure that can be generated via osmosis

A

osmotic pressure

326
Q

what happens if osmotic pressures become unbalanced and where is this particularly dangerous

A

organ damage
CNS

327
Q

formula for osmotic pressure

A

19.3 x corrected osomlarity

328
Q

____ mOsm can exert ______ mmHg of pressure on _______ kg/L of H2O

A

1
19.3
1

329
Q

mEq and mOsm are units of

A

quantity

330
Q

simple diffusion increase __________ with increases in concentration gradient

A

linearly

331
Q

facilitated diffusion increases with increased concentration gradient until ______________________

A

all transporters are being used and going as fast as possible

332
Q

VMax =

A

max speed at which conformational changes can occur

333
Q

Na/K ATPase: for everytime the pump cycles ________ is lost which contributes to the inside of the cell being negative

A

1 positive ion (Na+)

334
Q

how does the cell keep its osmolarity/intracellular volume in check

A

Na/K ATPase, there is a loss of one electrolyte per cycle which water follows

335
Q

functions of Na/K ATPase (2)

A

keeps membrane potential/electrochemical gradient and osmolarity/intracellular volume in check

336
Q

how does sodium enter the cell (3)

A

NCX, leaky cell wall, during action potential

337
Q

what happens if the Na/K ATPase pump ceased to work

A

intracellular edema- Na+ would build up in the cell, allowing H2O to build up in the cell as well

338
Q

what causes intracellular edema

A

conditions where not enough ATP is present for the Na/K ATPase pump to work properly

339
Q

diffusion rate: concentration inside vs outside

A

bigger difference = faster

340
Q

diffusion rate: membrane (lipid) solubility

A

more lipid soluble = faster

341
Q

diffusion rate: size of particle

A

smaller = faster

342
Q

diffusion rate: size of pore

A

larger = faster

343
Q

diffusion rate: kinetic movement (heat)

A

increased temp = faster

344
Q

diffusion rate: physical pressure

A

increased pressure = faster

345
Q

diffusion rate: electrical charge

A

the more negative the inside of the cell, the faster positive ions will enter

346
Q

osmosis: H2O wants to flow

A

down its concentration gradient (high conc to low conc)

347
Q

can solutes cross the semipermeable membrane

A

no

348
Q

if there is an increase in solute concentration, what happens to H2O concentration

A

decreases

349
Q

will water every be able to equalize its concentration difference

A

no- due to the force of gravity

350
Q

what would happen with the u shaped tube in space

A

all the water would go to the side with more solute

351
Q

the amount of force that is generated from H2O moving down its concentration gradient through a semipermeable membrane

A

osmotic pressure

352
Q

____ mOsm of solute can move a column of mercury _______

A

1
19.3mm

353
Q

_____ of pressure is required to prevent movement from ____ mOsm of solute

A

19.3mmHg
1

354
Q

what hormone regulates osmotic pressure

A

vasopressin (ADH)

355
Q

resting membrane potential acronym

A

Vrm

356
Q

what is the main contributor to the resting membrane potential

A

Na/K ATPase

357
Q

what helps facilitate all other electrochemical gradients

A

Na/K ATPase

358
Q

at rest excitable cells are ________ compared to the outside of the cell

A

electronegative

359
Q

____________ cells are capable of firing

A

resting

360
Q

when a cell is “turned on” it has a brief moment of

A

positive charge

361
Q

how is voltage/charge measured

A

mV

362
Q

the potential difference between 2 places

A

voltage

363
Q

concentration of protein inside the cell (especially right at the cell wall) is ______ compared to protein concentration outside the cell

A

greater than

364
Q

proteins carry a _________ charge

A

negative

365
Q

Nernst potential equation

A

EMF = +/- 61 x log ([inside]/[outside])

366
Q

in the nernst equation, cations have what charge

A

negative

367
Q

in the nernst equation, anions have what charge

A

positive

368
Q

tells us what the charge of a cell would be if 1 type of ion was allowed across the cell wall

A

nernst equation

369
Q

nernst potential for Na+

A

+61 mV

370
Q

nernst potential for K+

A

-91 mV

371
Q

if a cell was only permeable to one ion, the overall charge of the cell would be

A

the nernst #

372
Q

goldman equation

A

EMF = -61 x log (([A inside]/[A outside]x relative permeability of A) + ([B inside]/[B outside]x relative permeability of B) + ……. etc)

373
Q

at rest the cell is almost exclusively permeable to what ions (2)

A

Na+ and K+

374
Q

the cell is ______ times as permeable to _____ as it is to ______

A

10
K+
Na+

375
Q

overall resting membrane potential in a cell at rest

A

-80 mV

376
Q

what is the dominant electrolyte defining membrane potential

A

K+

377
Q

what is a reflection of concentration gradients AND relative permeability

A

Goldman equation

378
Q

cells can change membrane potential by

A

adjusting permeability

379
Q

concentration of what electrolyte effects neurons

A

chloride

380
Q

word to describe Na/K ATPase pump

A

electrogenic

381
Q

contributors to resting membrane potential (4)

A
  1. protein concentration
  2. Na/K ATPase
  3. concentration of individual electrolytes
  4. permeability of individual electrolytes
382
Q

the charge required inside the cell to prevent an electrolyte from moving down its concentration gradient

A

nernst potential/equilibrium potential

383
Q

what is polarization

A

a difference in electrical charge between the inside and the outside of the cell

384
Q

charge difference

A

polarization

385
Q

resting cells are considered to be (depolarized/repolarized/polarized)

A

polarized

386
Q

what is depolarization

A

to become less polar (more positive) usually means stimulated/turned on

387
Q

membrane potential becomes more positive, increases, greater than

A

depolarization

388
Q

aka excitation

A

depolarization

389
Q

what is hyperpolarization

A

overshoot after repolarization, more polar, more negatively charged

390
Q

what happens when a cell is hyperpolarized

A

more difficult to excite

391
Q

what causes hyperpolarization

A

result of K+ channels being open due to their slow closure

392
Q

what is repolarization

A

return to resting membrane potential from a depolarized state (after action potential)

393
Q

what would happen if there was no repolarization

A

no reset of the fast sodium channels meaning no future action potentials could occur

394
Q

what causes repolarization

A

fast Na+ channels closing and K+ channels opening

395
Q

do action potential curves always look the same

A

no

396
Q

what kind of channels are fast Na+ and K+ channels

A

voltage gated

397
Q

how are neural messages translated

A

fast Na+ channels

398
Q

how does an action potential work

A

depolarization occurs in a local area, causing a full-action potential

399
Q

how do -caine drugs work

A

affect the resetting of fast Na+ channels (on ECF side-activation/m gate)

400
Q

steps of fast sodium channels

A

resting: activation/m-gated closed (ECF side) and inactivation/h-gate open (ICF side)

activation: activation/m-gate open (ECF side), sodium floods into the cell
for a very short period, both gates are opened

inactivated: inactivation/h-gate (ICF side) closes
resetting occurs- activation/m-gate closed (ECF side), inactivation/h-gate (ICF side) opens

401
Q

is there a period during the fast sodium channel opening/closing that both gates are closed

A

yes

402
Q

“resetting” of the fast Na+ channel is dependent on

A

repolarization

403
Q

where is the gate located in a voltage gated K+ channel

A

ICF side

404
Q

steps of activation of a voltage gated K+ channel

A

resting: gate closed

slow activation: opens during repolarization and slowly closes once at Vrm

405
Q

what causes hyperpolarization

A

slow closure of the voltage gated K+ channel

406
Q

what does the plateau period of a cardiac action potential signify

A

the length of the plateau correlates with how strong the heartbeat is (how long it is “in action potential”)

407
Q

if Vrm is increased (closer to 0) due to electrolyte abnormalities what would happen

A

the cell might not be able to reset sodium channels fast enough, leading to a slower response (due to the decreased # of fast Na+ channels), the cell doesn’t have time to rest/repolarize

408
Q

what causes v. fib. with hyperkalemia

A

High potassium causes a higher Vrm, so the cell doesn’t have time to rest

409
Q

what happens if Vrm becomes more negative

A

cell is harder to excite (especially neurons), require a stronger stimulus to fire

410
Q

what determines resting membrane potential

A

“leaky channels”

411
Q

do cells actually have to have a current

A

no, just the potential to based on concentration gradients and permeability

412
Q

what is driving force

A

how fast ions want to enter/exit the cell

413
Q

what does driving force depend on (3)

A
  1. charge of ion
  2. concentration gradient
  3. charge on the inside of the cell
414
Q

what is conductance

A

inverse of resistance, the ease at which an ion can cross the cell wall

415
Q

at rest is there a lot of K movement outside the cell

A

no! despite there being the potential for movement based on concentration gradient, the Vrm makes potassium want to stay in the cell

416
Q

peroxisomes __________ drugs/toxins

A

neutralizes

417
Q

generation of nerve action potential is an example of a ___________ feedback loop

A

positive

418
Q

what is the second most abundant component in the cell (water is 1)

A

protein

419
Q

what is the majority of the cell wall made of, and what is the 2nd most abundant component

A
  1. protein
  2. phospholipid
420
Q

the resting membrane potential of a cell is closest to the _________________ of the ion with the highest _______________

A

equilibrium potential
conductance (permeability)

421
Q

the difference in mv between the membrane potential and the equilibrium potential

A

driving force

422
Q

the __________________ is greatest at the point when resting membrane potential is furthest from _____________

A

driving force
equilibrium potential

423
Q

resting membrane potential of most cells is due to

A

K+

424
Q

fast Na+/slow K+ are examples of

A

diffusion

424
Q
  • (neg) ion with + equilibrium potential will have greater concentration where
A

ICF

425
Q
  • (neg) ion with - equilibrium potential will have greater concentration where
A

ECF

426
Q

+ ion with + equilibrium potential will have greater concentration where

A

ECF

427
Q

+ ion with - equilibrium potential will have greater concentration where

A

ICF

428
Q

a normal healthy male has a hematocrit of

A

40