Physiology Final

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

Physiology Final

Physiology 277 with Lepri/tomlin at University of North Carolina - Greensboro

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