Physiology Final
Physiology 277 with Lepri/tomlin at University of North Carolina - Greensboro
About this deck
By: Kaitlin Duncan
Created: 2011-04-26
Size: 227 flashcards
Views: 200
Created: 2011-04-26
Size: 227 flashcards
Views: 200
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Homeostasis
the body's dynamic mantenance of optimal physical condition - keeping optimal condition through chemicals and temperature
4 types of chemical bonds
Covalent, Ionic, H bond, Van der Waals forces (in order from greatest to weakest
Acids and Bases
Acids - low pH, Lots of H+
Bases - high pH, sparse H+
Law of Mass Action
adding substrate increases product formation
Parkinsonism
inadequate dopamine formation by midbrain leads to decrease stimulation of motor cortex
Glucose
low glucose - hungry
high glucose - full, satisfied, lots of urine
High Sugar - thirst, hungry, headache, pee, blurred vision, dry skin, drowsy, feeling sick
Glucose cont.
glycogen is a polymer of glucose
when it's abundant, glycogenesis in the liver and muscle store excess fuel
breaking of glucose molecules liberates energy that is use to synthesize ATP
ATP
7Kcal/mol
breaking of ATP provides small amount of chemical energy
substrate phosphorylation and O2 phosphorylation - reduces ATP in mitochondria
glycolysis - pyruvate conversion - citric acid cycle
Glycolysis
10 steps yields 4 ATP via sub phosphrylation and 2 NADH. citric acid cycle needs O2. No O2 = lactic acid - occurs with exercise happens
citric acid cycle
8 steps. 1 spin of cycle = 3 NADH, 1 FADH2, and 1 ATP
NADH and FADH2 are the power for the electron transport chain
NADH = 3 ATP. FADH2 = 2 ATP. H+ moving back into matrix = 1 ATP
Hydrolysis of ATP
phosphate bond is easy to break and requires energy
breaking the bond releases energy
breaking bonds requires ATP but making bonds releases energy
breaking apart glucose provides energy that is use to synthesize ATP, NADH and FADH2
Rate of diffusion
= available surface area * concentration gradient/resistance of membrane * thickness of membrane
Diffusional equilibrium
same amount of glucose inside as out - doesn't happen in living cell
glucose moves down concentration gradient
unlikely in living cells - true for O2 because it becomes H20
Primary Active Transport
uses ATP directly, solute moves UP in the concentration gradient - Na/K+ pump - 3 Na, 2K+
Secondary Active Transport
uses energy of a primary AT to pull something else in with it Ex: sodium coupled with glucose as a 20
saturation
when the cell has reached the maximum amount it can take in or out - limited # of glucose transporters restricts the transport rate
transport rate is proportional to substrate conc. until all carriers are saturated
Concentration of Na/K+
low concentration of sodium in cell and high on the outside
high concentration of potassium in cell and low on the outside
facilitated diffusion
needs a carrier protein but not ATP
transcytosis
come in one side of the cell and goes through the other side via a vesicle
Leaky junctions
lots of traffic, big spaces between then, ling the blood vessels in the liver, very active in detox and very active in protiens making albumin
Tight Junctions
very close, don't allow much traffic, prevents anything from passing through
important at brain endothelium - blood brain barrier
Desmosome
very strong connection between cells, have interlocking proteins, strong
used to connect cardiac muscles. very strong because it pumps and moves a lot
Gap junctions
connects two cells together, if something happens to one cell then it also happend to the other because the cytosol is connected, coordinated excitation
important are artery smooth muscle, vein smooth muscle, GI smooth muscle, heart pumping
autocrine signal
self regulating function
paracrine signals
signaling by neighbors/ other cells - only through interstitial fluid
Endocrine signals
has to pass through blood to get to other cells
lipophilic signals
can get into the cell easily - slow but sustained
ex: Steroids: estrogen, estradiol, androgens, testosterone, dihydrotestosterone, AR, Progestin. Mineralcorticoids: aldosterone, glucocorticoids, cortisol, thyroids, and Vitamin D
Ligand receptor
transcription factors that laters hormone regulated gene expression
lypophobic
non steroid - dramatic but brief, recpetor for compound that is capable for getting a response fast. receptors outside of the cell
Androgynous
males make a lot of testosterone but the androgen is broken down so they look like females
Agonist
primary ligan activated a receptor, an agonist also activated the receptor - both elicit a response
Antagonist
blocks receptor activity - no response
Ion channel change
Signals can alter ion movements across membranes, this is how some signals cause change in the activity of the excitable cells
G-proteins
one signal at the surface can result in the activation of millions of effectors proteins
Epinephrine
same signal but different responses at different targets - some have alpha receptors - makes blood vessels squeeze down small
beta recptors - make blood vessels expand
Adrenergic
epinephrine receptors
Difference in Alpha and Beta receptors
Alpha - avert blood away
Beta - bring blood here
Examples of Autocrine, Paracrine, and Endocrine
autocrine (works on self) - leydig cells
paracrine (next door neighbors) - sertoli cells
endocrine - skeletal muscles
Steroids vs. Non-Steroids
roids - slower response/longer lasting
non-roids - rapid response/short lived
Parasympathetic system
"rest and digest"
parasymp neuron - Achtylcholine - decrease heart rate
Sympathetic system
"fight or flight"
symp neuron - epinephrine - increases heart rate
Nicotinic receptors
respond to Ach
also respond to Nicotine
slow heart rate/muscular contraction
ligand gated
Muscarinic receptors
G-protein coupled receptors
responds to Ach
slow heart rate/muscular contraction
Nicotinic vs. Muscarinic
Nicotinic receptors are at the ganglion
Muscarinic receptors are at the target
Autonomic effectors
smooth and cardiac muscles, some endocrine and exocrine glands, some adipose tissue
Adrenal pathway
CNS - adrenal cortex - adrenal medulla - Ach - blood vessel to B2 receptors
A & B receptors
A and B1 receptors move through neurotransmitters
B2 receptors mostly move through blood
Ach pathway
HT - CRH - anterior pituitary - ACTH - adrenal cortex - cortisol - target tissue = response causes released of glucose from liver
Location of nuclear receptors
in: HT, Adrenal Cortex, target tissue and APG
stress effects
long term negative effects of stress are mediated by the immune system
Circadian Rhythm
daily pattern of fluctuation of cortisol
Cortisol
fat soluble so you can't store it
most active around the time you wake up
cushings disease - hyper cortiolism
Tripartite axis
CRH^ ACTH^ Cortisol^ - hypothalmus problem
CRHv ACTH^ Cortisol^ - anterior pituitary problem
CRHv ACTHv Cortisol^ - adrenal cortex problem
Depolarization
when the cell is becoming less negative allowing for influx of Na+
Repolarization
when the cells is returning to resting membrane potential
Hyperpolarization
when the cell is more negative than the membrane potential and is further away from the resting membrane potential
Ca2+
stored in smooth endoplasmic reticulum
huge concentration in SER
Dendrite
lots of endings to receive info from other cells
Axon hillock
transition from the reciever of the stimuli to the processing
delivery membrane
myelin sheath
proteins along the axon that speed the transmitting of neural impulses
the more myelination the faster those impulses can move
Axonal region
delivers info from axon terminal
graded potentials
change in ion permeability but not enough to fire and action potential
action potentials
all or none sequence of changes in membrane potential
firing results in depolarization and changing of ions
threshold depolarization
operates VGNa+ channels
opening of these channels rapidly means that membrane potential is moving toward 60 mV
slower opening of VGK+ moves membrane potential towards -90mV
Refractory period
time at which another AP cannot be fired
APs in neurons are non-summable and propogate without decay
Summation vs. No Summation
no sum - two subthreshold graded potentials will no initiate an AP if that are far apart enough in time
summation - if two subthreshold potentials arrive at the trigger zone without a short period of time they make sum and initiate an AP
Trigger zone for AP
decision point where the size of the graded depolarization determines whether or not an AP fires
threshold concept only apploes to vg ion channels and refers to the min depolarization required to initiate the cycle
Neurons
axon terminal is making contact with next dendrite so it can pass on the message
VG-Ca2+ channel open due to AP on axon terminal
Ca2+ is trigger
receptors is closed unless specific thing it need triggers then an AP will move to next cell
Graded depolariztion
caused by Na+ influx
transmitter and receptor complex allows Na+ into the post-synaptic cell
Ligand gated ion channels
Ach is a ligand that binds to an ion channel - Ach gated Na+ channel
Voltage gated ion channel
opn or close in response to changing ions - rapid depolarization - responsible for repolarization after hyperpolarization phase of AP
lateral inhibition
helps the sensor figure out where the sense is
stimulus - primary neuron response proportional to stimulus strength - pathway closest to the stimulus inhibit neighbor - inhibition enhances perception of stimulus
Senses
simple neural receptor - pain, olfaction
complex neural receptor - tactile (has mylienated axons)
special senses receptor - vision, audition, gustation
5 tastes
sour, sweet, salty, bitter, and umami (savory)
papillae
bumps on your tounge - each one had up to 150 taste buds
gustatory
first neuron only goes through graded potentials
second neurons have receptors
first neuron releases neurotransmitters all the time
first neuron has receptors for glucose and send out ATP
Bitter compounds
most people who dislike bitter things have lots of bitter sensory neurons
olfactory
primitive sense - doesn't get involved with higher order thinking
olfactory neurons span between nasal cavity and the brain
when you smell something, it has gotten into the mucus and been dissolved and the dendrite receives the smell
olfactory (2)
very quickly replaced
have to go through the skull - go through thinnest part at the cribiform plate
100,000 olfactory genomes
goes through limbic system - very primitive and ancient part of brain
olfactory (3)
trigeminal chemorecpetion mediates responses to noxious stimuli, such as CO2, capsaicin and NH3
monosodium glutamate - binds as a ligan to initate umami perceptions
visual
shape of lens can be altered - flat or round
elasticity reduces as you get older - lense gets stuck in one position
ciliary contracted - fibers slack - lens rounded - close vision
ciliary relaxed - fibers taught - lens flatish - far vision
visual (2)
rohdopsin - opsin and retinal - close Na+ channels
less glutamate - cause grade potential - neurotransmitter secrete onto ganglion cells - causing APs
Rods and Cones
primary sensory neuron in eyes - bipolar is secondary
light causes rods to hyperpolarize
light inhibits rod cells
Audition
sounds waves converted to physical motion in tympanic membrane
pinna - ear canal - tympanic membrane - rocking of malleus - ripples in cochlea - cohclear fluid - rippling bends cells and opens ion channels - transduction to brain
tectorial membrane
flap drags across hair cells causing open or closing of ion channels and that changes the amount of neurotransmitter that releases to cochlear neuron/brain
different wave lengths across this flap cause the different pitches
auditory neurotransmitter
go into brain stem from cochler neuron
this is how you tell which ear its from
mechanoreceptor
tactile sense
bent membrane of tactile neuron aalters the shape of ion channel and changes potential
spinal cord - somatosensory cortex through thalmus
very sensitive - focuses on touch and where located
Cerebrospinal fluid
filrate of the blood - choroid plexus forms a cushion in the brain
tight junctions make it difficult to get in and out and it only will transport certain things
constant renewal and circulation fluid
Parasympathetic pathway
ganglia near targets
pre gang release Ach - post gang have Ach-Rs - post gang release Ach - Targets have Ach-Rs
Sympathetic pathway
ganglia near spinal cord
pre gang relase Ach - post gang have Ach-Rs - Post gang release Ne/Epi - targets have NE/Epi-R's
skeletal muscle fibers
multimucleated conglomerations/ can only develop during a particular time as an embryo - can't be replaced
smooth muscle cells
actual cells
only have one nucleus and do regrow and regenerate
Myocardial cells
heart muscle
connected by intercolated disks
have adherens and gap junctions
Flexion and Extension
Flexion - biceps contracts/ triceps relax
Extension - biceps relax/ triceps relax
Sarcomere
organization of actin and myosin fibers
all contained in the sarcolemma
Titin
hold myosin and actin together
Actin and Myosin
in actin - troponin and tropomyosin holds it together
in myosin, nebulin hold things together
myosin heads have actin binding sites
Z disks are reduced when there is a contraction
T-Tubules
penetrate into muscle - when AP moves along the sarcolemma it will also spread down the tubes in between the cells to start the change
Actin and Myosin movement
Ca2+ pulls tropomyosin (blocker) away allowing myosin to bind with actin
Ca2+ causes exocytosis of Ach - binds to Ach Na channels - causes graded potentials usually enough to cause AP
Crossbridges
200-400 crossbridges for each myosin
myosin grabs actin and pulls it in
anchor for actin is nebulin and myosin is titin
ATP in muscle contraction
used in muscle to put Ca2+ back into the sarcoplasmic reticulum and used to break actin and myosin - NaK+ uses lots of ATP
Ca2+ and tropomyosin don't have a ligand receptor pair
Muscle contraction
first contraction that happens is "taking up the slack" - isometric - no change in length/ tension changin
when it's moving and the tension is the same - isotonic
Ratcheting
the actin myosin cycle repeats rapidly as you move any body part so the heads are almost ratcheting onto the actin sites
ATP in Muscle contraction
ATP binds then breaks apart with a partial hydrolysis causing it to cock the crossbridge and then binds to actin and moves actin
Crossbridges (2)
troponin has Ca2+ ligands on it
crossbridge has 2 binding sites: ATP binding site and Actin binding site
Muscle movement
motor unit - different fiber types
muscles are elastic
controlled by activation of neuromuscular junction
Maximum tension
tetanus - when the muscle give way to fatigure
heavier moves slower than lighter loads
length tension relationship
as you shorten a muscle and contract actin and myosin components, it can't put anymore tension on it and vice versa, when the muscle is too long, actin and myosin don't overlap
optimal resting length
where the muscle has the most potential to contract and have tension
Myoglobin
O2 binding characteristics
restoring O2 on myoglobin rebuilds phosphocreatine and cleans up metabolic acids
Working muscle
= Phosphocreatine + ADP --> creatine + ATP
Excess post exercise O2 consumption
cell energy use exceeds O2 uptake (O2 deficit)
Smooth Muscle
vascular, reproductive, digestive system
regulated by Ca2+
true cells - not multi-nucleated - able to undergo mitosis
slower than skeletal muscle - contracts and realxes slowly
both GP and AP's can alter tension
active over a wider range of stretch
Tension development
fastest in skeletal muscle and slowest in smooth
Ca2+ binding
regulated skeletal, smooth, and cardiac muscle and the exocytosis of neurotransmitters
Sodium leak
can repeatedly depolarize to thershold yielding rhythmic contractions
Pharmacomechamical coupling
hormones, neurotransmitters and drugs that work inside the smooth muscle can alter tension without any effect on membrane potentials
Electromechanical coupling
membrane potential changes
types of smooth muscle
single unit - can start AP at one end and it will spread to other smooth muscle cells
multi-unit - each of the smooth muscle cells has to recieve its own signal and generate its own AP
contraction of CSM
around blood vessel it contracts or releases causing vasoconstriction or vasodialation.
Left pump
left atria and ventricle - main driving force for blood movement in the systemic circuit
Right pump
right atria and ventricle - only pumps blood to the pulmonary system
both sides pump the same amount - if they didn't then it would cause a fluid buildup causing congestive heart failure
Blood pressure
the farther away from the heart, the lower the BP
Intercalated disks
include desmosomes for strength and gap junctions for integrated pumping action
Myocardial Muscle cells
branched
have a single nucleus
Types of myocardial cells
1% of the cells set the pace and conducting - pacemaker and conducting cells
99% of the cells are the ones doing the work - working/pumping cells
theses two determine cardiac output
Hormone control in heart
Minus and Plus controls that slow (ach) or increase (Epi/NE) heart rate
pumping cells on have plus controls
Cardiac output
= heart rate x stroke volume - how much blood is pumped
Autorythmic cells and Contractile cells
Autorythmic cells - determine heart rate
contractile cells - determine stroke volume
contractile cells have a longer depolarization which allows the chamber to fill up
pacemaker potential
gradually becomes less negative until it reaches threshold triggering an AP
has a sodium leak til it reaches threshold - graded depolarization
Myocardial AP's
instead of Na+ channels, the heart has Ca2+ channels that let in and K+ channels that lef out
Ca2+ influx is the depolarization phase of AP, K+ efflux is re-polarization/hyperpolarization of AP
EPI effects on heart
if given a little bit of EPI then graded depolarizations would happen faster but would also not allow for it to come back to a complete rest
Ach effects on heart
its drops into a deeper hyperpolarization and takes longer to reach threshold causing a slower heart rate
Cell connection in heart
almost all cells of the heart are connected by gap junctions, except for the atria which has none between atria and ventricles
atria goes through a specialized conduction system
Contraction cycle
start with fastest depolarizing autorythmic cells - SA node - to the septum and Purkinje fibers to ventricles
Heart crossbridges
heart actins don't all get a myosin unless the heart is at max production - only the amount it needs gets Ca2+ to pull off tropomyosin
Heart cell contraction
some Ca2+ comes in and opens SAR (has Ca2+Ca2+ channel) to release more Ca2+ to go the the actin and myosin
not saturated in resting person
if cardiac troponin is released in blood - means you had a heart attack
Actin and Myosin geometry
simply adding more blood to heart allows it to beat more forcefully - increased tension development, which increases stroke volume
length tension relationship in heart
increase volume of blood in heart, stroke volume gets bigger - if you had NE
stretch ventricles pump blood, stretfch and sympathetic stimulated ventricles to pump wayyy more blood
respiratory pump
alternating series of pressure change in thoracic cavity which helps return blood
Vegas nerve
has post ganglionic parasympathetic nerves
your body is always working to reduce heart rate because vegas nerve is always at work unless you are exercising
Diastole vs. Systole
Diastole - relaxing and let the heart rest
Systole - filling the heart with blood
late diastole - both sets of chamber are relazed and ventricles fill passively
atrial systole - atrial contraction forces a small amount additional blood into ventricle
isovolumic ventricular contract
pushes AC valves closed but doesn't create opening
ventricular ejection - as ventricular pressure rise and ecxceeds
isovolumic ventricular relaxation
opens AC valves and blood rushes out into systemic circuit
AV node
only point of electrical contact between atrium and ventricles
important becuase it delays AP's moving to ventricles until the atria finishes contracting
Sequence of excitation
SA node - atria = AV node - node ventricles
Electrical conduction
SA node - R/L atrium - AV node - bundle of HIS - purkinje fibers - R/L ventricle
Atrial fibrillation
ablation of the AV node
requires a pacemaker so that the heart doesn't beat too fast without having the AV node to delay AP's
Refractory Period
short compared with the amount of time required for the development of tension
MUST have a refractory period - heart cannot tetanize otherwise you will die
Sympathomimetic drugs
inotropic agents
inotropic means strength
Pressure in heart
in aorta: during conraction of ventricular emptying
ventricles: start with low pressure then jump when emptying
right heart pressure lower because only deliver to pulmonary system
Ventricle contraction
ventricles contract - semilunar valves open - aorta and arteries expand and sotre pressure in elastic walls
Ventricular Relaxation
semilunar valve shut preventing flow back into ventricle
Systolic/Diastolic pressure
ventricular systole (phase of contraction) endures about half as long as diastole
MAP
= Diastolic + 1/3(systolic - diastolic)
Hypertension
damages blood vessels and organs - main goal is to reduce MAP
B Adrenergic receptors in heart
can be blocked - use an antagonist causes a reduction in cardiac output
Ca2+ channel blockers
dihydropyridines
reduce HR
Reducing HR
filter some fluid out of blood and get rid of filtrate
diuretics
Cardiac control center
medulla oblongata
controls sympathetic and parasympathetic
MAP
determined by: Blood volume, effectiveness of heart, resistance of the system, relative distribution
Heart Rate & Stroke Volume
HR modulated by: ANS, Sympathetic, and Parasympathetic
SV modulated by: ANS and Sympathetic - direct effect
Radius of blood vessels
alteration occurs because of the changing state of Vascular Circular Smooth Muscle
Blood flow to a tissue
will increase of CO2 levels increase
contration state of Vascular circular smooth muscle in arterioles determine radius and resistance - how much blood with will flow downstream to capillaries
Blood Vessels
if you change the radius in one the other vessels will dilate to compensate
big radius - relaxed circular muscle
little radius - contracted circular muscle
8 factors that favor vasodilation
1- waste increases(CO2, H+) 2- decrease of good stuff(O2) 3- increase of NE/EPI at B receptors 4- Increase of ANP 5- Increase of NO, injury, genital vasodialation 6-Histamine from injury 7- Adenosine-vasodialation 8- K+ from injury
3 factors for vasoconstriction
1- NE/EPI at A receptors 2- ADH - antidiuretic hormone - reduces BP and conserves water 3- Ang II - RAAS - decreases renal BP - Ace inhibitors
Filtration in systemic capillaries
beginning side of capillary - the pressure is high and as you move the pressure gets lower
water is drawn in from an aqueous are into the protein rich capillary - capillaries and interstitial fluid exchange
hydrostatic pressure
Hydrostatic pressure from heart - arteriole - osmotic pressure - net absorption - venule
Lymphatic function
cell migration and fat absorption
if its blocked: causes elephantiasis
thoracic duct is where lymphatic circulatory system rejoins blood system
Blood return
smooth muscle in vein walls, one way valves, and sketetal muscle squeeze all help boost venous pressure for blood return
Histamine
local vasodilator - when mosquito bites you, local itch. benedryl focuses on target spot
Anaphylatic shock - occurs when histamine spreads systemically - reduces MAP
Edema
when you have excess fluid that isn't being pulled back in
caused by increased hydrostatic pressure
Hypotension
suboptimal BP
danger of irreparable damage to heart/brain
first priority to keep pressure in heart/brain loop: blood blood from periphery, get pump working harder, cut losses - water conservation
Hormones effecting MAP
cardiac output effectors - B blockers, Ca2+ blockers, diuretics
Peripheral resistance - Ace inhibitors, ANG II receptor blockers, A receptors, Ca2+ channel blockers, other vasodilators
RBCs vs. WBCs
RBC - no nucleus, bags of hemoglobin, carry O2, 4 month life cycle
WBC - true nucleus, less than 1 percent, short lived or long lived, several types
Plasma
includes water, ions, proteins, dissolved gases, nutrients, hormones, wastes, etc
hematocrit
way to measure the amount of RBC's and plasma % - rapid assessment of blood composition
Hypertonic vs. Hypotonic
hyper - saltier than RBC - would shrivel
hypo - less salty than RBC - would lyse
hemoglobin composition
normally composed of 2 alpha and 2 beta protein chains
in sickle cell anemia, a single amino acid error in one chain causes change in structure
Erythropoiesis
synthesis of RBCs - occurs in bone marrow
RBC formation pathway
O2 receptors in kidney - increase EPO secretion - EPO receptors in bone marrow - increase RBC in blood - O2 in blood - negative feedback loop starts again
Jaundice
common in infants
due to liver's inability to process bilirubin pigment metabolites of hemoglobin
Platelets
normally just flow around, but when there is an injury they go to wound site and become sticky and spiky
at uninjured site - PGI2 and NO inhibit platelet aggregation
myocardial cell death
if a cell dies then the gap junction close, the EKG shows that the electrical pattern has been disrupted, causes ven fib, or uncoordinated heart rhythm
Lungs
condition the gas content of the heart
Trachea
has lots of cartilage which holds the airway open
Gas Exchange
capillaries are close in proximity to alveoli which makes gas exchange easier
Surfactant
secreted by type 2 cells
lines alveolar space
cortisol enhances activity in neonates
Inhalation
Pip < Palv <Path
volume of thoracic cavity up and Palv down
diaphragm contracts - moves downward and flattens
intercoastals and scalenes pull ribcage outward and upward during more vigorous breathing
Expiration
Palv > Path Pip < Palv Pip < Path
thoracic down and Palv up
Diaphragm relaxes and moves upward and is dome shaped
Abs and internal intercostals contract
Hemlich
pushes diaphragm up and realxes it enough to hopefully push object out
Resistance to Airflow
main determinant for air to flow through the airway is diameter
Bronchodilation
increased airflow
EPI via beta Rs
Co2 in alveolar
decreased Ca2+
Bronchoconstriction
decreased airflow
parasympathetic stimulation
Ecosanoids/Histamines
increased Ca2+
Ventilation
alveoli is matched to perfusion through pulmonary capillaries, so no adjustments are needed
ventilation and blood flow are matched to maximize diffusion of O2
Diameter of bronchioles
mainly determined by Co2 in bronchioles during expiration
increased CO2 = dilation to get rid of the waste
Diameter of pulmonary arterioles
mainly controlled by O2
only send blood where the good stuff is
decreased O2 = vasoconstriction
Diameter of systemic arterioles
controlled by CO2 and O2
need to bring more good stuff in to get rid of the bad stuff
Partial pressure
resting - 40
saturated - 100
metabolic activity
working tissues - higher levels of CO2 - unloading
near lungs - lower levels of CO2 - loading
Heat in lungs
increased heat favors of unloading of O2
decreases heat favors loading of O2
Hemoglobin binding affinity
is 200 times greater for CO2 than for O2
Ph and Gas exchange
decreased Ph/ increased CO2 - increased respiration
increased Ph/ decreased CO2 - decreased respiration
Kidneys
condition the volume and ionic composition
to maintain fluid volumes: you have to keep input and output equal
we have physiological mechanisms to retain or excrete fluid or ions
Blood flow to kidneys
altered with EPI/NE bind with A adrenergic receptors
Nephrons
functional unit of kidney, epithelial cells
Renal function
homeostasis control of extracellular fluid volume and ionic composition-including pH
excretion of dietary and metabolic wastes - urea from protein metabolism - bilirubin makes it yellow
endocrine gland
gluconeogenesis
filtration
under pressure from blood to the nephron of the kidney - reabsorption of solutes and water from the nephron to the blood
water follows Na+ and other solutes when it can
filtration is non-specific
GFR increase
vasodialators - gets rid of excess fluid
increased atrial stretch - increased anp - vasodialtion - increased GFR - increased urine output
GFR reduction
vasocontrictors - conserve fluid
sympathetic output
increased ADH
Ang II
Renal autoregulation
MAP fluctuated between 80-100 mmHg result in constant GFR
Tubular Golmerular Feedback
increased DCT flow - macula densa - paracrine signal - contraction of afferent arteriole
decreased DCT - macula densa - paracrine - dilation of afferent arteriole
Urine
filtrate of blood
includes lymphatic fluid, sweat, saliva, digestive fluids, respiratory tract secretions, reproductive tract secretions
reabsorption in kidneys
70% of filtered Na+, 100% of filtered glucose already reabsorbed
Normal range of plasma glucose
between 100-200mg/ 100ml plasma
if you exceed 300, it will be lost in urine
Isomotic fluid
leaves PCT becomes progressively more concentrated in descending limb - removal of the solute in the thick ascending loop creating hyposmotic fluid - hromones control permeability - urine OsM depends on reabsorption in the collecting duct
acidosis
immediate - binding of H+ ions with buffers
short term - increased ventilation
long term - kidneys can add bicarbonate to your blood of excrete H+
alkalosis
short term - decreased ventilation
long term - kidneys can reduce H+ from filtrate
K+ regulation - increase
increase of K+ in plasma = hyperkalemia - resting membrane potential less negative/ cells depolarize more easily / can cause heart arrhythmias
K+ regulation - decrease
K+ decrease = hypokalemia - resting membrane potential more negative = cells less excitable/ failure of sketetal and cardiac muscle/ requires external inputs of K+
Ca2+ regulation
decrease: increase parathyroid
increase: reabsorption of DCT
increase activity of osteoclast
increase calcitol
Digestion
3 basic processes: ingestion of food, digestion of food, absorption mechanisms, the movement of material through the digestive tract is regulated
appetite regulation
ingestion of food - 60,000 lbs over a lifetime
low glucose - increased activity in the feeding center
high glucose - increased activity in the satiety center
Gastric stretch
decreased - increased Ghrelin - increased appetite
increased - decreased Ghrelin - decreased appetite
Phases
cephalic - anticipation of food
gastric - increasde gastric motility and secretions
intestinal - hromones reduce gastric motility and secretions
About this deck
By: Kaitlin Duncan
Created: 2011-04-26
Size: 227 flashcards
Views: 200
Created: 2011-04-26
Size: 227 flashcards
Views: 200
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