vert phys exam 1 Flashcards

1
Q

acclimatization example

A

at high altitude with low pO2, more BPG and RBCs to carry oxygen

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2
Q

positive feedback ex

A

blood clotting;
blood vessel injury releases chemicals that activate platelets and cause coagulation
activated platelets release more chemicals and attract more platelets to injury site

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3
Q

autocrine regulation

A

chem. regulators affect same cells as produce them

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4
Q

physiology

A

study of functioning organisms and how organisms function
structure determines function, following laws of chem and phys

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5
Q

EC fluid - interstitial =

A

plasma volume

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6
Q

plasma vol + EC fluid =

A

interstitial fluid volume

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7
Q

plasma vol + EC fluid =

A

interstitial fluid vol

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8
Q

homeostatic mechanisms EX

A

shivering

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9
Q

epithelial cell function

A
  1. form boundary between compartments
  2. selectively permeable to ions and organic molecules
    - basolateral surf rests on basement membrane
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10
Q

steady state value that body maintains

A

set point

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11
Q

set point

A

steady state value that body maintains

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12
Q

location of internal pacemaker that sets biological rhythms

A

suprachiasmatic nucleus of the brain

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13
Q

suprachiasmatic nucleus of the brain

A

location of internal pacemaker that sets biological rhythms

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14
Q

endocrine control EX

A

heart rate increases from epinephrine release by adrenal medulla into bloodstream

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15
Q

4 cell types

A

epithelial, nerve, muscle, connective-tissue

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16
Q

homeostatic variable

A

in steady state of DYNAMIC CONSTANCY that is regulated to remain near a stable set point value

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17
Q

feed forward regulation

A

smell of bad food triggers the gag reflex
Smell/odor receptors trigger response in digestive sys
prepare stomach for arrival of food before it comes
saliva, churning, produce acid

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18
Q

steady state EX

A

upon entering a hot room, begins sweating
continued sweating keeps body temp stable

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19
Q

ID the EFFECTORS -
eating salt-rich meal increases blood volume and pressure, stretching vessel walls
nerve signals sent to brainstem stimulate Changes in hormonal/neural signaling.
heart rate slowed, blood vessel walls relax, kidneys increase salt exerted in urine
BP returns to normal

A

heart, blood vessels, kidney

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20
Q

ligand

A

molecule/ion that binds protein

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21
Q

A solution containing proteins of a particular type is exposed to the same concentrations of ligands X and Y, but the percent saturation of molecule X is greater than the percent saturation of molecule Y. why?

A

soon protein has a higher affinity for ligand X

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22
Q

increase temp of chem rxn

A

increase forward and reverse run rate

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23
Q

products of glycolysis under anaerobic conds

A

2 ATP, 2 H2O, 2 lactate

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24
Q

krebs cycle

A

generates ATP directly by substrate level phosphorylation

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25
Q

RDS in metabolic path

A

slowest reaction, subject to end-product inhibition

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26
Q

true of fatty acid synthesis

A

begins with acetyl coenzyme A (coA)
occurs in cytosol
requires more energy than is produced by catabolism of same fatty acid
results in even # of carbon atoms only
\enzymes that synthesize fatty acids are found separately from enzymes that catabolize

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27
Q

muscle cell types

A

skeletal, cardiac, smooth

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28
Q

connective tissue cells

A

form ECM (fibers and collagen)

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29
Q

tissues

A

aggregates of differentiated cells with same type

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30
Q

body fluid compartments

A

intracellular fluid 67%
plasma: part of blood which cells are suspended
interstitial

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31
Q

EC fluid

A

interstitial fluid and plasma

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32
Q

why is there homogeneous solute composition in EC fluid?

A

EC fluid = interstitial + plasma
Because of exchanges, concentrations of dissolved substances are identical in the plasma and interstitial fluid, EXCEPT for protein concentration (higher in plasma)

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33
Q

Compartmentalization

A

achieved by barriers
- plasma membranes surround each cell, separate the intracellular from the extracellular fluid
- 2 components of extracellular fluid— interstitial fluid and plasma—are separated by blood vessel walls.

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34
Q

homeostasis

A
  1. state of dynamic constancy
  2. stability of variable achieved by balancing input and output (not magnitudes)
  3. Traits fluctuate within a predictable and often narrow range. 4. When disturbed out of normal range, restored to normal.
  4. dynamic process regulates adaptive responses of body to changes in environ
    - require sensor to detect environ change
    - require compensatory mechs
    - achieved by expenditure of energy
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35
Q

compensatory mechanisms

A

restore homeostasis/set point

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36
Q

body temp as control sys EX

A
  1. person at norm temp into cold
  2. person loses heat to ext. enviro bc cold outside
  3. compensation: chem rxns produce heat at rate = rate heat loss
  4. blood vessel narrow and restricted, reducing blood flowing thru skin, decreasing heat loss from warm blood across skin into environ
  5. body undergoes no net change and remains about constant;
    steady state
    - control sys operates around set point; maintainence
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37
Q

steady state

A

system where a variable is not changing but in which heat/energy must be added continuously to maintain stable, homeostatic condition
NOT equilibrium (no input of energy req’d to maintain constant)
ALL homeostatic control sys operate around a set point

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38
Q

negative feedback

A

thermoregulation
a change in variable being regulated brings response that moves opposite the initial change towards the original point.
corrective resp. after steady state perturbed

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39
Q

Negative feedback EX

A

product formed from substrate –> product reaction by an enzyme negatively feeds back to inhibit further action by enzyme (ATCase; ATP)
as ATP accumulates, it inhibits the activity of enzyme and production slows down

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40
Q

resetting set points

A

FEVER;
set point for body temp has been set higher and body responds by shivering to generate heat

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41
Q

feedforward regulation

A

improves the speed of body homeostatic response and minimizes fluctuations of regulated variable (reduces variation from set point) using environmental detectors/learning
CHANGES IN REGULATED VARIABLES ARE ANTICIPATED/PREPARED FOR BEFORE THEY OCCUR

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42
Q

changes in regulated variable are anticipated/prepared for before they can occur
improves speed of homeostatic response

A

feedforward regulation

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43
Q

feedforward regulation of temp

A

temp-sens neurons in skin monitor temp outside
when its cold out, neurons detect change and relay info to brain which signals blood vessels/muscles resulting n heat conservation and increased heat production
COMPENSATORY thermoregulation is ACTIVATED BEFORE colder outside temps can cause a decrease in internal boy temp

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44
Q

reflexes (control sys)

A

specific involuntary built-in response to stimulus
can be automatic or learned/acquired from practice

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45
Q

specific involuntary built-in response to stimulus
can be automatic or learned/acquired from practice

A

reflex

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46
Q

reflex arc mediation

A

stimulus acts on receptor and produces signal to be relayed to integrating center. signal travels along AFFERENT pathway to integrating center
output is sent to EFFECTOR which acts along efferent pathway
- if effector response causes decrease in stimulus trigger, then reflex leads to negative feedback and typical homeostatic control

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47
Q

stimulus

A

detectable change in environ

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48
Q

local homeostatic responses

A

initiated by change in environment/stimulUs, induce alteration of activity with NET EFFECT OF COUNTERACTING STIMULUS

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49
Q

stimulus/change in environment causes change in activity met by response with net effect of counteracting the stimulus

A

local homeostatic response
- result from stimulus
- local area resp.
- nor nerves/hormones directly involved

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50
Q

hormones

A

chem. messenger that communicate and use the blood as a delivery sys for target

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51
Q

NTs

A

chem messengers released from neurons ending on other cells and diffuse thru EC FLUID separating neuron from its target
NOT released into blood like hormone

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52
Q

paracrine

A

local communication between neighbor cells
- NTS

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53
Q

adaptation

A

characteristic that favors survival in specific environments
- homeostatic control systems are inherited and allow individuals to adapt to environ changes

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54
Q

acclimatization

A

prolonged exposure to environmental change = improved functioning of already existing homeostatic system
reversible

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55
Q

adaptation/acclimatization EX

A

sweating in heat
day 1: expose to 30 mins of heat and make exercise. body temp increases, sweating begins
sweating is mechanism for increasing heat loss from body so body temp doesn’t rise
vol sweat measured
day7 - subject begins to sweat sooner and much more profusely than day1.
as consequence, body temp does NOT increase as much. subject ACCLIMATIZED to heat - undergone BENEFICIAL CHANGE INDUCED BY REPEATED EXPOSURE AND NOW BETTER ABLE TO RESPOND
- reversible: if exposure stops, subject reverts to preacclimatized values

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56
Q

sweating

A

adaptation allows heat loss from body to minimize an increase in body temp in hot environments

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57
Q

cause of acclimatization

A

increase in number, size or sensitivity of 1+ cell types in homeostatic control system for response to exposure

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58
Q

biological rhythms

A

add an anticipatory comp. to homeostatic control
like feedforward mechanism without detectors
allow homeostatic mechanisms to be utilized automatically by activating when a challenge is likely to occur but before it does occur

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59
Q

an anticipatory comp. for homeostatic control like feedforward mechanism without detectors

A

biological rhythm

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60
Q

EX of biological rhythms

A
  1. body temp increase prior to waking up so metabolic pathways can operate more efficiently
  2. during sleep, metabolism slower than awake so body temp decreases
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61
Q

cause of biological rhythm

A

environ factors do NOT drive rhythm but provide timing cues for entrainment (set the rhythm)

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62
Q

total body balance

A

depends on relative rates of net gain/loss to body
pool concentration depends on total amount of substance in the body and exchanges of substance within the body

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63
Q

total body balance depends on

A
  1. relative rates of net gain/loss
  2. pool concentration/total amount of substance in the body
  3. exchanges of substance within the body
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64
Q

3 states of total body balance

A
  1. loss exceeds gain: total amount substance is decreasing = negative balance
  2. gain exceeds loss: total amount of substance in body is increasing = Positive balance
  3. gain equals loss = stable balance
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65
Q

body balance EX

A

Calcium ions
conc [Ca] in EC fluid
the control system for balancing Ca targets the intestines and kidneys so amount of Ca absorbed from diet is balances with excretion
during childhood, net balance Ca is + and deposited in growing bone
later, Ca released from bones and lost in urine (rate of Ca loss exceeds intake so balance is negative)

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66
Q

homeostasis requires

A

energy to expend
compensatory mechs
sensor to detect environ change

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67
Q

Case study: A hot day

A

body temp increase, heat production decrease and heat loss increases
sweating caused EC fluid levels to decrease
eventually, fluid levels decrease so much that blood available to be pumped from heart decreased.
IF EC FLUID DECREASES, BP DECREASES.
sweat from EC fluid. more sweating and losing water (sweat is dilute EC fluid), more concentrated EC fluid is

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68
Q

sweat

A

from the EC fluid
more dilute than EC fluid bc more H2O than ions is secreted
more sweating = more concentrated EC fluid (saltier
decrease EC fluid, BP decrease

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69
Q

prokaryotes

A

bacteria,
lack membranous organelles

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70
Q

plasma membrane

A

limiting barrier, regulate passage, link adjacent cells by junctions and anchor cells to ECM
double layer of lipid molecules with embedded proteins

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71
Q

largest intracellular fluid comp

A

cytoplasm/cytosol

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72
Q

phospholipid bilayer

A

plasma membrane
amphipathic
random lateral movement of lipids and proteins bc lack of bonds
characteristic flex and fluidity

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73
Q

cholesterol

A

slightly amphipathic bc polar hydroxyl
close association limits the ordered packing of fatty acids
no cholesterol = tightly packed, less fluid
MAINTAIN IM FLUIDITY

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74
Q

Integral proteins

A

amphipathic, move laterally, associated w membrane
most are TRANSMEMBRANE
form channels

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75
Q

Transmembrane proteins

A

integral proteins
form channels

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76
Q

peripheral proteins

A

NOT amphipathic
at membrane surface, cytosolic surface and bind polar regions
assoc. w CYTOSKELETAL shape and mobility

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77
Q

fluid mosaic model

A

plasma membrane is lipid bilayer mosaic of membrane proteins that are free to move in a sea of lipids

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78
Q

junctions

A

provide barrier to movement of molecules
between cells
form tissues

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79
Q

integrins

A

transmembrane protein organizes cells into tissues by binding to ECM proteins and linking adjacent cell membranes

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80
Q

transmembrane protein organizes cells into tissues by binding to ECM proteins and linking adjacent cell membranes

A

integrin

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81
Q

desmosome

A

between 2 adj. cells
structural support and integrity
- characterized by accumulation of protein dense plaques along cytoplasmic surf of membrane
- anchoring proteins to bind cadherins of adj. cell
- bind to IM filaments
- connect w integrins
- adhesive junctions, hold adj. cells firmly together
- in areas of mechanical stress, give stability
- contains cadherins
- keratin filaments anchor

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82
Q

feature between 2 adj cells that provides structural support/integrity
accumulation of protein dense plaques on cytoplasmic surf

A

desmosome

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83
Q

desmosome dense plaques

A

anchoring proteins for cadherins
extend from 1 cell into EC space to bind w/ cadherins of adj. cell
- disk shape membrane.

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84
Q

in areas of mechanical stress, provide support by adhering 2 cells together in disk shape with cadherins

A

desmosome

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85
Q

tight junction everything

A

forms when EC surf of 2 adj. plasma membranes join together so not EC space remains between them
- adhering junctions (desmosome) must form 1st
- occurs in band around circumference of cell
- joined at apical surf
- limits movement thru EC space
- limits paracellular diffusion
- forces passage thru cells and NOT between (NO LEAKS)
- Claudin composition
- prevent epithelial mesenchymal transition
- encircle epithelial cell by connecting to actin microfilaments
- ZO-1 acts to tether cytoskeleton to transmembrane barrier protein

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86
Q

occurs in band around circumference of cell after an adherins/desmosome leaving so EC space between the cells

A

tight junctions
of epithelial cells
- at apical surf

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87
Q

composition includes claudin

A

TJ

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88
Q

limits movement through EC space,
limits paracellular diffusion,
prevents Epithelial mesenchymal transition

A

TJ force passage thru cells and not leaking between

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89
Q

connect to actin MFs

A

TJs

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90
Q

gap junction

A

protein channels linking cytosol of adjacent cells
- connexins proteins
small diam. of channel limits passage thru to small ions

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91
Q

protein channels linking cytosol of adjacent cells

A

gap junction

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92
Q

nucleus

A

Nuclear envelope contains 2 membranes with nuclear pores. RNA moves thru pores.
DNA forms w histones into chromatin (dense)
chromatin becomes chromosomes

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93
Q

free ribosomes

A

release proteins into cytosol

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94
Q

rough ER

A

proteins synthesized here pass into lumen of ER and then Golgi and secreted out

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95
Q

smooth ER

A

lipid molecules synthesized.
stores Ca2+ for muscle contractions

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96
Q

golgi

A

prots arrive from rough er and undergo mods and sorting with transport vesicles

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97
Q

mitochondria organelle

A

chem process transfer energy from bonds to ATP
most ATP formed in mitochondria BY CELLULAR RESPIRATION
- inner and outer membrane
- inner membrane folded has crustal into the matrix

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98
Q

cellular respiration

A

produces most ATP in mitochondria
consumes O2 and produces, CO2, heat water

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99
Q

mitochondria membranes

A

inner and outer
inner folds into crustal, extends into matrix

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100
Q

lysosomes

A

have acidic fluid w digestive enzymes
defense
break down

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101
Q

peroxisomes

A

consume molecular oxygen
NOT used in transfer of energy to ATP
removes H from organic molecules prods H2O2
toxic in high conc.
break down fatty acids in 2C sources which can be used for ATP

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102
Q

cytoskeleton

A

formed by protein filaments
determines cell shape, movements and contractions
- actin filaments = microfilaments (thin)
- IM
- microtubules (tubulin units)

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103
Q

IM filaments

A

assoc w desmosomes to provide support/stability

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104
Q

microtubules

A

hollow tubulin protein subunits
rigid, in neurons
radiate from centrosome
cilia core

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105
Q

cilia

A

core of microtubules
motile on epithelial cells (move mucus)

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106
Q

no signal sequence

A

synthesis continues on free ribosome and then released into cytosol, destined for function in cell/enzyme

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107
Q

proteome

A

the specific proteins expressed in a cell

108
Q

protein degradation

A

some have high affinity for proteolytic enzymes
unfolded plots more easily digested
targeted for degradation by attachment of ubiquitin which directs the protein to a proteasome

109
Q

proteasome

A

protein complex that unfolds and breaks down a protein

110
Q

ubiquitin

A

regulatory protein that targets proteins for degradation by proteasome
- covalent attachment to lysine

111
Q

specificity

A

depends on shape of binding site
ability of protein to bind active site

112
Q

affinity

A

strength of ligand-protein binding
depends on strength and attraction between protein-ligand
with high affinity, very little ligand is required to bind

113
Q

saturation

A

fraction of total binding sites that are occupied
% saturation depends on [unbound ligand] and affinity of binding site for the ligand
- if binding site had high affinity, low [ligand] conc. will result in high saturation bc once bound to site, ligand not easily dislodged

114
Q

competition

A

the ability and presence of 1+ ligands to bind to same binding site affects the % of occupation
- cooperation

115
Q

allosteric modulation

A

as shape of binding site changes, cooperation changes shape of other regions of the protein
non covalent binding of ligand to 1 site can alter the shape and binding characteristics (affinity)
active site for binding and regulatory binding site
modulators bind regulatory site

116
Q

Hb EX

A

4 subunits for O2. when 1 O binds, affinity of other sites for O2 increase

117
Q

covalent mods

A

often phosphate group (-) added
charge alters distribution of electrical forces and changes conformation
protein kinase mediates phosphorylation

118
Q

kinase

A

proteins modulates phosphorylation
catalyze transfer of Pi from ATP to OH on side chain

119
Q

phosphatase

A

dephosphorylation

120
Q

metabolism

A

cells cannot use heat energy
synthesis and breakdown of organic molecules req’d for structure and function
generates water

121
Q

reaction rate is influenced by

A

reactant conc.
activation energy
temperature
catalysts

122
Q

active site

A

region of enzyme that binds substrate

123
Q

cofactors

A

trace metals bind and work with the enzyme
can alter enzyme conformation

124
Q

coenzyme

A

cofactor that directly participates as a substrate in a reaction. the coenzyme remains in original form throughout
derived from vitamins, NAD+, FAD

125
Q

oxidized

A

lose electrons

126
Q

loss of electrons

A

oxidation

127
Q

gain electron

A

reduced

128
Q

reduced

A

gain electrons

129
Q

ATP

A

primary molecule that stores energy transferred from breakdown

130
Q

glycolysis

A

carbs (glucose) only
sugar breakdown/catalysis
10 enzymatic reactions
NO Oxygen
Occur in cytosol
break down 6C glucose into 2 3C pyruvate (ionized pyruvic acid)
Net GAIN of 2 ATP, 4 H (2 released), 2 transferred NAD+
All IMs between glucose and pyruvate end prod contain ionized phosphate groups (remain trapped in cells since cannot penetrate plasma membrane)
most pyruvate is reduced to lactate

131
Q

where is glycolysis

A

in cytoplasm, NO oxygen

132
Q

1st step of (an)aerobic respiration

A

glycolysis in cytoplasm

133
Q

glycolysis process

A

glucose broken down into 2 3C pyruvates. then, either lactate or to krebs cycle

134
Q

pyruvate

A

2 3C pyruvate formed by glycolysis
mostly reduced to lactate
otherwise onto kreb’s cycle

135
Q

pyruvate reduced to lactate

A

2 3C pyruvate of glycolysis reduced to lactate
1. 2 H atoms from NADH+ and H+ transferred to pyruvates molecules to form lactate and NAD+ is regenerated
2. remainder of pyruvate is not converted to lactate but enters kreb’s to be broken down to CO2
lactate released into blood, liver (precursor to glucose)
converted back into pyruvate, used as energy source

136
Q

Kreb’s cycle

A

citric acid cycle forms CO2, some ATP in the inner mitochondrial matrix
pyruvate enters mitochondria from cytosol metabolized into 2C acetyl coA (release CO2)
1. primary molecule: acetyl coenzyme A coA transfers acetyl group to 4C oxaloacetate to form 6C citrate
- acetyl-CoA reacts –> generation of reduced cofactors NADH and FADH2, production of ATP thru substrate-level phosphorylation.
directly prods 1 high E NTP

137
Q

Krebs cycle conditions

A

ONLY AEROBIC
oxidative phosphorylation is necessary for regeneration of H-free form of coenzymes
used in oxidative phosphorylation to form lots of ATP

138
Q

reduced cofactors

A

NADH, FADH2

139
Q

oxidative phosphorylation

A

most important mechanism for energy derivation
energy for ATP derived from energy
- mitochondria
- aerobic
E released when H ions combine with molecular O2 to form H2O
H comes from NADH, H+, FADH2 coenzymes of Kreb’s cycle, by metabolism of fatty acids
-embedded in mitochondrial membrane is ATP synthase - forms channels

140
Q

coenzymes of krebs cycle

A

soluble in mitochondrial matrix

141
Q

cytochromes

A

proteins contain iron heme and copper cofactors
form components of electron transport chain and transfer electrons:
- 2 e- from H are transferred … eventually to O2 to form water

142
Q

potential energy of oxidative phosphorylation

A

hydrogen ion conc. gradient
energy of gradient converted into chemical bond by ATP synthase (catalyzes formation of ATP from ADP)

143
Q

ATP synthase

A

embedded in mitochondrial membrane
forms channels

144
Q

step forming the most ATP

A

oxidative phosphorylation in inner mitochondrial membrane, aerobic

145
Q

occurs at inner mitochondrial membrane

A

krebs (cofactors) and oxidative phosphorylation (most ATP)

146
Q

glycogen storage

A

muscles and liver
synthesis from glucose

147
Q

synthesis of glycogen

A

add phosphate group to glucose, form glucose 6 phosphate to be broken down to pyruvate to to form glycogen

148
Q

gluconeogenesis

A

major substrate is pyruvate formed from lactate
liver and kidneys

149
Q

essential amino acids

A

9/20

150
Q

vitamins

A

diff solubility
water soluble vitamins form parts of coenzymes like NAD+, FAD+, coA

151
Q

hypoxia

A

lack of O2

152
Q

Tylenol case study

A

cause of death was hypoxia (low O2) despite blood oxygen levels elevated
cell death and mitochondrial damage
BC
oxygen not delivered to tissues, accumulated in blood
O is final electron acceptor

153
Q

stripping electrons

A

carbons become more oxidized for ETC

154
Q

NAD+

A

oxidized acceptor

155
Q

NADH

A

reduced donor

156
Q

reduced

A

has the H

157
Q

why are ppl so vulnerable to protein deficiency

A

no essential amino acids can be synthesized by the body, must be consumed

158
Q

required for binding

A

concentration, orientation, and affinity
binding is random

159
Q

cytochrome C oxidase

A

enzyme; complex 4 of ETC
transfers electrons to molecular O2 (substrate), reducing it to water

160
Q

higher respiration

A

more water produced

161
Q

law of mass action

A

drive rxn forward by increasing substrate. increase prods = drive backwards

162
Q

when available ATP is exhausted

A

catabolism ensues

163
Q

Km

A

measure of affinity
strength/tightness of ligand-protein binding

164
Q

simple diffusion

A

no energy input besides movement from heat, NO ATP; passive

165
Q

graded potentials

A

magnitude is related to intensity of stimulus that elicits them

166
Q

magnitude is related to intensity of stimulus that elicits them

A

graded potential

167
Q

neuronal time constant

A

proportional to product of membrane resistance and capacitance

168
Q

proportional to product of membrane resistance and capacitance

A

neuronal time constant

169
Q

speed of conduction of nerve impulse can be determined by

A

temperature and diameter of axon

170
Q

If apply Na channel agonist to squid axon that is voltage clamped to -100mV…

A

large inward sodium current
AND
voltage gated K+ channels remain closed

171
Q

EX of synaptic plasticity

A
  1. increasing amount of NT released from AP
  2. Increasing number of receptors on postsynaptic membrane
  3. altering amount of Ca entering the cell at presynaptic terminus
172
Q

stimulus intensity/strength is encoded in

A

freq. of Pas with stronger stimuli eliciting higher frequencies

173
Q

Serotonin

A

excitatory NT

174
Q

Effect of fluoxetine in post-synaptic neuron

A

acts on serotonin - excitatory NT
= graded potentials of longer duration in post-synaptic neuron

175
Q

oxidative phosphorylation

A
  1. ETC
  2. chemiosmosis
    ATP synthase complex uses E released from ETC proton gradient to make ATP
176
Q

electron transport chain

A

proteins bound to inner mitochondrial membrane; electrons pass through series of redox reactions, release energy

transfers e- from reduced molecules onto O2 to become H2O (most reduced)
as e- passed, E released and used to pump protons, create proton gradient (PE)

177
Q

cellular respiration

A
  1. glycolysis in cytosol
    AEROBIC, Mitochondria
  2. krebs
  3. oxidative phosphorylation & ETC
178
Q

net products of glycolysis

A

2 ATP (net), 2 H+, 2 H2O, 2 NADH, 2 pyruvate (–> lactate)

179
Q

glycolysis reaction

A

glucose + 2 ATP + 2 NAD+ –> 2 pyruvate, 4 ATP, 2 NADH, 2 H+, 2 H2O

180
Q

all IMs contain ionized phosphate group so cant permeate membrane and leave

A

glycolysis in cytosol
- body pH

181
Q

step 4 glycolysis

A

fructose 1,6 - diphosphate splits into 2 molecules.
isomerase converts 1 into the other so 2 of same molecule
UNSTABLE bc 2 phosphate groups

182
Q

step 1 glycolysis

A

glucose phosphorylated by kinase
USE 1 ATP
Mg2+ cofactor lowers Ea

183
Q

step 2 glycolysis

A

becomes fructose

184
Q

step 3 glycolysis

A

USE 2nd ATP w/ cofactor Mg to phosphorylate

185
Q

step 5

A

split apart into 2. DHAP converts by isomerase into glyceraldehyde

186
Q

step 6 glycolysis

A

2 NADH is reduced to 2 NAD+ and 2 H+
exergonic rxn releases energy to be used to phosphorylate again

187
Q

step 7 glycolysis

A

ATP Is formed x2 from each molecule
SUBSTRATE LEVEL PHOSPHORYLATION: Pi transferred from IM substrate onto an ADP

188
Q

glycolysis step 8/9

A

isomerize and LOOSE WATER =
PEP is unstable and looses phosphate group x2

189
Q

step 10 glycolysis

A

unstable PEP x2 donates it phosphate group to ADP = 2 ATP
and becomes 2 pyruvate (end prod)
- go on to krebs and make CO2 or
- into lactate

190
Q

end of glycolysis

A

if oxygen is available,
krebs and ETC breaks down pyruvate all the way into ATP

191
Q

what does glycolysis NEED

A

2 ATP energy
carbohydrate
2 NAD+

192
Q

NADH/NAD+ cycling

A

Oxygen:
NADH can pass its electrons into the electron transport chain, regenerating
NAD+ glycolysis.
Anaerobic: fermentation

193
Q

erythrocytes

A

RBCs have enzymes for glycolysis but NO MITOCHONDRIA so no other pathways

194
Q

lactate

A

prod during muscle activity
released into blood
- can be converted back into pyruvate (oxidized)
- used as precursor in liver to form glucose

195
Q

use of lactate

A

released into bloodstream
- converted back into pyruvate
- or stored in liver as precursor to glucose

196
Q

critic acid cycle facts

A

uses carbs, fats, and proteins to prod CO2, H atoms (half bound to coenzymes), some ATP

197
Q

step 1 krebs

A
  1. Acetyl coA forms citrate
    (transfer acetyl group from coA onto oxaloacetate)
    pyruvate enters mitochondria from cytosol after glycolysis
    metabolized into acetyl coA and CO2
    NAD+ –> NADH
198
Q

acetyl coA

A

enzyme derived from vitamin B transfer acetyl group w/ pyruvate or fatty acid breakdown
1st step of krebs
produced from OXIDATION OF PYRUVATE

199
Q

krebs step 2

A

citrate isomerized with loss/addition of water molecule

200
Q

krebs step 3

A

isocitrate is oxidized and releases CO2
NAD+ is reduced to NADH

201
Q

krebs production of ATP

A

directly prods 1 high E GTP –> ATP
uses substrate level phosphorylation

202
Q

How kreb’s creates ATP

A

substrate level phosphorylation: Pi onto GDP = GTP
GTP + ADP = ATP + GDP
creates ATP from GTP

203
Q

Krebs cycle most important

A

H atoms transferred to reduce coenzymes and free H generated are used in oxidative phosphorylation to gen. ATP

204
Q

reaction of krebs

A

Acetyl CoA + 3 NAD+ + FAD + GDP + Pi + 2 H2O –> 2 CO2, CoA, 3 NADH, 3H+, FADH2, GTP

205
Q

why must oxidative phosphorylation/krebs be aerobic

A

nec. for regeneration of oxidized, H-free form of coenzymes
mitochondria CANNOT remove H from coenzymes under anaerobic conds

206
Q

step 4 krebs

A

reduced NAD+ to NADH
release CO2
forms succinyl coA

207
Q

step 5 krebs

A

CoA group of succinylcholine CoA is replaced by phosphate, then transferred to ADP to make ATP
= succinate

208
Q

step 6 krebs

A

succinate oxidized.
2 H atoms are transferred to FAD = FADH2

209
Q

7/8 krebs

A

water added, converts molecule
and malate regenerates into starting oxaloacetate
NAD+ is reduced to NADH

210
Q

products of citric acid cycle

A

2 C enter on acetyl CoA
2 CO2 released
3 NADH
1 FADH2
1 ATP
per acetyl coA

211
Q

why krebs cant operate without O2

A

when ET cant oxidize NADH to NAD+, there is no NAD+ available for krebs (finite)

212
Q

krebs regulation

A

by oxygen and availability of NAD+

213
Q

oxidative phosphorylation ENERGY

A

E transferred to ATP is derived from E released when H ions combine w/ molecular O2 to form H2O
H comes from NADH + H+ and FADH2 coenzymes generated in krebs (metabolism of fatty acids (and glycolysis))

as e= are transferred from 1 protein to another, some E released is used by cytochromes to PUMP H ions from matrix to intermemb. space = CREATES SOURCE OF PE AS H+ ION CONC. GRADIENT

214
Q

oxidative phosphorylation EQ

A

1/2 O2 + NADH + H+ –> H2O + NAD + E

215
Q

Krebs cycle enzymes

A

soluble in mitochondrial matrix

216
Q

proteins of oxiphospho

A

embedded in mitochondrial membrane
1. transfer H onto molecular O2
2. couple E released to synthesis of ATP

217
Q

ETC components

A

cytochromes (Fe and Cu cofactors) transfer H down to O2 with proteins

218
Q

general ETC

A

2 H e- are transferred from NADH + H+ or FADH thru the chain w/ cofactor until reach O2 and form H2O
- use free H ions and coenzyme H ions

219
Q

oxidized H-free coenzymes

A

regenerated in ETC so available to accept 2 more H from other paths

ETC regenerates H-free oxidized coenzymes NAD+ and FAD by transferring the H onto O2
rxns prod. conc gradient
flow of H+ back across membrane provides E for ATP synthase

220
Q

coenzymes of krebs

A

oxidized in ETC so now available to accept 2 more H

221
Q

H ion conc gradient

A

PE source of ETC
e- are transferred from 1 protein to another, releasing E to be used by cytochromes to pump the ions from the matrix into intermembrane space

222
Q

ATP synthase

A

embedded in mitochondrial membrane enzyme that forms a channel in membrane allowing H ions to flow to matrix side

223
Q

reason for channel/conc gradient in ETC

A

lipid bilayer blocks diffusion of ions

ATP synthase creates channel for H ions to flow to matrix side
= chemiosmosis

224
Q

conc gradient of ETC Energy

A

E converted to chemical BOND E by ATP synthase,
catalyzes form of ATP from ADP

225
Q

chemiosmosis

A

ATP synthase embedded in mitochondrial membrane that forms channel in membrane allowing H ions to flow to matrix side

226
Q

most ATP is formed

A

oxidaphosphorylation from H atoms of Krebs cycle (breakdown macromolecules)

227
Q

mitochondria

A

prods most ATP, consumes most O2, releases most CO2

228
Q

entering substrate of ETC

A

H atoms of NADH + H+ and FADH2;
O2 formed during glycolysis and krebs

229
Q

products of ETC

A

2-3 ATP for each NADH + H+
1-2 ATP for each FADH2

230
Q

carb catabolism

A

breakdown carb to pyruvate or lactate by glycolysis
metabolize pyruvate to CO2 and H2O by krebs and ox phosphorylation

231
Q

substrate level phosphorylation

A

glycolysis and krebs
net gain of 2 ATP from glycolysis
2 more ATP from krebs GTP
- 1 ATP for each of 2 pyruvate molecules entering cycle

232
Q

max ATP

A

34 ATP

233
Q

ATP production of krebs

A

glucose –> 2 pyruvate molecules –> 2 GTP –> 2 ATP (substrate level phosphorylation)

234
Q

Anaerobic ATP production

A

only 2 ATP from substrate level phosphorylation in glycolysis -> lactate

235
Q

energy in Anaerobic conditions

A

2 ATP from glycolysis
lots of glucose break down into lactate

236
Q

glycogen

A

small amounts of glucose can be stored as reserve as polysaccharide glycogen, in liver and muscles

237
Q

glycogen synthesis

A

from glucose
enzymes in cytosol
1. transfer phosphate from ATP to glucose
SAME 1st step as glycolysis
So, IM can be broken down to pyruvate or glycogen

238
Q

glucose storage

A

as glycogen in liver/muscles (polysaccharides)

239
Q

glycogen synthesis pathways

A
  1. catabolized to provide energy for ATP formation
  2. in liver cells, converted to free glucose by removal of phosphate group, then glucose can enter blood
240
Q

glucose synthesis

A
  1. in liver, breakdown glycogen
    gluconeogenesis
241
Q

gluconeogenesis

A

generate new glucose from noncarbohydrate precursors
major substrate is pyruvate, formed from lactate

242
Q

what determines if glucose is broken down to pyruvate or if pyruvate is used to synthesize glucose?

A

concentrations of glucose and pyruvate and hormones that alter/change expression

243
Q

adipocyte function

A

synthesize and store triglycerides, release as needed for E and ATP formation

244
Q

beta oxidation

A

coA derivative of fatty acid goes thru process which splits off acetyl coA and transfer 2 pairs of H atoms to enzymes ( 1 to FAD and 1 to NAD+)
H atoms from co enzymes then enter oxidative phosphorylation path to form ATP

245
Q

ATP formed from fatty acid catabolism

A

18 C saturated = 146 ATP
1 glucose yields max 38 ATP
catabolism of 1g fat is 2.5x greater than 1g carb

246
Q

fatty acid synthesis

A
  1. cytoplasmic acetyl coA transfers acetyl group to another and start forming chain, repetition builds up by 2C at a time
    all fatty acids synthesized have even #
247
Q

acetyl coA enzyme

A

starting material for fatty acid synthesis, Krebs cycle, formed from pyruvate

248
Q

acetal coA derived from fatty acid breakdown

A

CANNOT be used to synth new glucose
1. pyruvate broken down into acetyl coA and CO2 is irreversible
2. the 2 C atoms in acetyl coA are used to form 2 molecules of CO2 during krebs

249
Q

glucose and fatty acids

A

glucose can readily be metabolized to synthesize fat
fatty acids can NOT be used to synth glucose

250
Q

proteases

A

protein catabolism break peptide bonds

251
Q

macromolecules

A

all can enter the Krebs cycle thru some IM
all can be used as source of E for synthesis of ATP

252
Q

keto acids

A

formed by removal of amino groups from AAs

253
Q

ammonia

A

used to form urea in liver; excreted in urine

254
Q

essential nutrients

A

water
(body looses more than oxphospho prods)
HILK MF TVW

255
Q

water soluble vitamins

A

form coenzymes NAD+, FAD, coA
excreted in urine
- accumulation in body is limited

256
Q

fat soluble vitamins

A

ADEK are not coenzymes
A - retinol

257
Q

what structure contains enzyme required for oxidative phosphorylation

A

inner membrane of mitochondria
NOT matrix

258
Q

ligand-protein binding reaction

A

allosteric modulation can alter affinity of protein for ligand
phosphorylation of protein is a covalent mod
if 2 ligands can bind same binding site of protein, = competition
binding reactions are electrical or hydrophobic

259
Q

what can be used to synthesize glucose by glujconeogeneis in liver?

A

glycerol (?)

260
Q

catabolism of fatty acids

A

2 steps

261
Q

strength of ligand protein binding of binding site is

A

affinity

262
Q

membrane structures that form channel linking together the cytosol of 2 cells and permitting movements of substances between cells

A

gap junction

263
Q

fluid inside cells but NOT within organelles

A

cytosol
liquid portion of the cytoplasm, excluding the organelles

264
Q

significance of folds on inner mitochondrial membrane

A

increases total SA
enzymes required to generate ATP are here
structure –> function

265
Q

proteins and ligands relationship

A

protein function can be altered by allosteric changes in structure
charge attraction

266
Q

energy for homeostasis

A

ATP provides E required for homeostatic processes
generation of ATP is under NEGATIVE feedback control.