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131 Cards in this Set

  • Front
  • Back
chemoreceptors in blood
sensitive to pH levels of the blood
how does exercise activate chemoreceptors? (4)
1) skeletal muscles contracting directly activates the chemoreceptors

2) the increase in epi sensitizes the chemoreceptors

3) the buildup of lactic acid lowers pH and activates chemoreceptors

4) metabolic acidosis that occurs due to exercise also activates.
how does venous blood gas concentrations change throughout the body?
depends on how much a certain part of body is used. i.e. during exercise, the PCO2 of skeletal veins will rise due to the high need for O2...
how does arterial blood gas concentrations change throughout the body?
DOESN'T!! think about it!
how does oxygen dissolve in the body?
by itself, it dissolves very poorly. use hemoglobin!
hemoglobin
heme: 4 groups of atoms with 4 Fe in the middle. They are globular proteins (as opposed to fibrous).

The heme (Fe) binds to Oxygen so each hemoglobin can carry 4 oxygen.

Globulin can bind other things but not oxygen.
why is there a sigmoidal curve when you add oxygen to blood in the PO2 vs hemoglobin saturation curve?
because of cooperative binding. When the first subunit binds oxygen, there is a conformational change. This makes the other subunits more receptive to oxygen!

Subunits cooperate so that binding to one O makes it easier to get more O. so harder at first but then gets easier.

this is important because even low PO2 levels have a high saturation %.
hemoglobin + oxygen reaction?

which direction is favored?
Hb + O2 --> HbO2

the direction depends on the amount of reactants and products present. if there is lots of O2 then the reaction proceeds forward. if there is little O2, then it proceeds in reverse (and O2 is released for use).

so basically, hemoglobin acts like a natural reservoir of oxygen using the law of mass action.
why are chemoreceptors not very sensitive to oxygen?
The fact that the curve flattens out at high levels of Po2 explains why the chemoreceptors are not sensitive to o2. because even at lower po2 levels, you still get good saturation.
why is the plateau part of the sigmoidal curve important?

why is the steep part of the curve important?
plateau is important because a large change in po2 will still keep a relativly constant saturation level of hemoglobin.

steep part is important because at critical levels, a very small change in po2 can result in a very big change in saturation and unloading of o2 from hemoglobin.
how does the addition of hemoglobin change oxygen distribution between two compartments?
the hemoglobin absorbs some of the oxygen in one compartment resulting in a new equilibirum so that the po2 levels of the 2 compartments are equal.
how does oxygen move from the air to the blood?
o2 enters alveolus through inspiration. since po2 in alveolus > po2 in puolmonary capillary it diffuses through.

once in capillary, the po2 capillary > po2 erythrocyte so o2 enters the RBC. once o2 levels increase, the hemoglobin/o2 reaction proceeds forward and binds to keep the po2 RBC < po2 capillary so that more o2 diffuses in.
how does the oxygen move from the blood to the cells?
when o2 is consumed by cells, the po2 cell < po2 interstitial fluid so more o2 enters the cell. eventually the po2 interstitial fluid becomes < po2 capilary so the o2 diffuses out of the capillary to the interstitial fluid.

eventually po2 capillary < po2 RBC so o2 diffuses out of the RBC to the blood. and now since the o2 levels are dropping in the RBC, the hemoglobin/o2 reaction goes in reverse to free bound o2.
what can alter the sigmoidal curve in po2 vs % saturation?
DPG, pco2, temp, h+.

when any of these factors are elevated (which occurs in active tissue), the sigmoidal curve shifts to the right.

this means that the hemoglobin has less affinity for the oxygen and dumps it more readily. this helps the more active tissues get more oxygen.
how does heat, co2, and h+ alter hemoglobin association with o2?
heat: decreases the strength of association b/w o2 and hb.

co2 and h+: bind allosterically to decrease affinity for o2.
what is the main similarity between local arteriolar resistance controls and hemoglobin affinity controls?
they are the same molecules! (co2, h+, and heat)

so an active tissue elevates these factors causing both an increase in blood flow AND an increase in o2 dumpage!

so spectacular!
fetal hemoglobin
higher affinity for o2 than normal hemoglobin (different gene).

this is necessary so that the fetus can successfully steal o2 from the mother! the mother compensates by elevating progesterone which increases breathing.

since the fetal hb has higher affinity for o2, the sigmoidal curve shifts to the left! this means that less o2 is needed for complete saturation.
how is co2 carried in the blood?
1/3 is carried in hb (hb + co2 --> hbco2)

2/3 is made into bicarbonate
how is bicarbonate made?
co2 + h20 --> carbonic anhydrase --> h2co3 --> hco3 + h+
main difference between co2 and o2 transport in blood?
o2 is mostly carried by hb.

also, co2 needs an enzyme (carbonic anhydrase)
chloride shift
situation where the co2 in RBC gets converted to hco3. the hco3 moves out of the RBC in an antitransport system bringing in Cl. so hco3 leaves and Cl enters the RBC
functions of the kidneys
1) regulate H2O, ion and h+ balance

2) remove waste from blood and excrete

3) remove foregin chemicals from blood and excrete

4) gluconeogensis

5) produce epo (RBC production), renin (controls AII and thus vasoconstriction), and vitamin D (ca balance)
examples of metabolic waste:
urea (from catabolism of protein)
uric acid (from nucleic acids)
creatinine (from muscle creatine)
urinary system anatomy
2 kidneys create urine and send down 2 ureters that meet at the bladder. the bladder (storage) then sends down through the urethra to urinate.
why do you need a bladder?
evolutionary... so the predators dont find you?!?!
renal cortex and renal medulla
cortex is outer part: this is where filtration occurs

medulla is inner part: this is where urine gets concentrated (water is removed).

Fine-tuning of composition of urine occurs here as well.
flow of urine in the kidneys
starts in the renal corpuscle in the bowmans capsule. travels down the proximal tubule, loop of henle, distol tubule, and into the collecting duct system. finally all the urine from all the nephrons collect at the renal pelvis and travel down the ureter.
flow of blood in the kidneys
afferent arteriole enters the glomerulus and the glomerular capillaries.

the blood then leaves the glomerulus in the efferent arteriole and then travels along the nephron in the peritubular capillaries. they then empty into the veins and travel back to the heart.
bowmans space
where the glomerular capillaries are located. fluid and solutes are filtered out into the space which marks the beginning of urine formation
proximal tubule
location where the vast majority of UNREGULATED reabsorption and secretion occurs.

huge surface area with microvilli.

organic molecules are cotransported with Na.

Na leaves the basolateral end via the PUMP.

K enters and leaves the basolateral end via leaky channels.

water follows the net movement of solutes by osmosis
distal tubule
location where fine tuning of reabsoprtion/secretion of na,h20, and k are controlled by aldosterone.

aldosterone causes more Na/K pumps to come up and thus excrete more K and reabsorb more Na and H2O
collecting tubule
location where final regulation of water is allowed by ADH.

ADH stimulates the release of aquaporins into the membrane of the epithelial cells which allows more water to be reabsorbed in the cortical collecting ducts.
how much blood is filtered in the glomerulus
20%
renal corpuscle anatomy
this is the glomerias where intitial filtration occurs.

there are podocytes which wrap around and prevent proteins and RBC and large molecules from passing through.

the membrane is also negatively charged to help prevent proteins from passing.
starling forces during filtration
there is the glomerular capillary pressure from the blood which pushes the fluid into the bowmans space.

countering that, is the fluid pressure in the bowmans space AND the osmotic pressure due to the proteins being in the plasma but not the bowmans space!
proteinuria
protein in the urine (should not happen)

this is indicative of kidney disease!
GFR
glomerular filtration rate. the volume of fluid that is filtered from the glmoeruli into the bowmans space in a period of time (usually L/day).

it is not constant...can change from vasoconstriction and vasodilation in the afferent and efferent arteries.

if you constrict afferent (via A II), than Pgc drops and filtration decreases

if you constrict efferent, than Pgc elevates due to backflow of blood.
transport maximum
the limit to the amount of solute that can be reabsorbed in the proximal tubule. this limit is based on the amount of mediated transporters and their effriciency.
filtered load
the amount of a solute in the filtrate.

filtered load = GFR x Plasma concentration of solute
excretion rate
the rate at which a solute is excreted from the body.

excretion rate = urine solute concentration x urine flow rate
what is the problem if there is glucosuria?
the extra glucose in the urine keeps water (by osmosis) and so you lose more water from diuresis.
osmotic diuresis
diuresis caused by osmotic movement of water (clinically called polyuria)
polydipsia
drinking heavily to compensate for diuresis caused by polyuria
dipsogen
something that makes you thirsty
GFP
net glomerular filtration pressure

GFP = Pgc - Pbs - osmotic pressure
clearance
how well a compound is cleared from the blood by the kidneys

Cs = UsV/Ps

Us: urine concentration of S
Ps: plasma concentration of S
inulin
small polysacharride in fiber in plants that gets completely ignored by the kidneys. Meaning, whatever gets filtered, gets excreted. in other words, GPR = Ci!

so this is a wonderful way to calculate the gpr of the body for clinical tests.
creatinine
waste product of the muscles. almost completely ignored by kidneys. it is secreted slightly but the Ccreatinine is almost equal to the GFR.

a good screening test of renal function, remmeber to overcompensate since there is some secretion!
how can you tell how a certain molecule is handled by the kidneys?
compare the clearance of the molecule to the GFR of the individual.

if C = GFR, then kidneys do nothing
if C > GFR, then kidneys secrete
if C < GFR, then kidneys reabsorb
how to figure out what doses of a drug to give?
check the clearance of the drug.

if clearance is high, then you need a big dose

if clearance is low, then you need a small dose
what happens to GFR when dehydrated?
less water means less blood pressure. this means that the GFR decreases.

so water reabsorption is increased by ADH!
where are microvilli found?
anywhere that a REALLY high surface area is needed. i.e. the gut and the proximal tubule
diabetes insipidus
a diabetes where the person cannot reabsorb water and thus excretes ALOT.

this is caused by the lack of ADH i.e. damage to Posterior pituitary

or the inabilitiy of the kidney to respond to ADH!
what activates aldosterone?
hyperkalemia.

also indirect pathway where it is activated by a drop in BP/blood volume.

the baroreceptors activate the SNS which synapses on juxtagolmerular cells to release renin. Renin activates A II which is a vasoconstrictor AND an activator of aldosterone!

also a low GFR (from low BP) also contributes to activation since the macula densa can sense this and also activate the renin pathway.
renin
turns angiotensigoen into A I. then A I gets activated into A II by ACE which lines the capillaries!
how can GFR be altered by diarhea?
lower venous pressure activates SNS which constricts afferent arterioles and decreases GFR.

also, the atrial pressure drops which also activates SNS.

lastly, arteriol bp drops which both activates SNS and directly lowers GFR by decreasing the amount of blood that enters the glomeruli.
the point where distal tubule folds over next to the glomeruli
the macula densa are the cells of the distal tubule that come in contact with afferent arterioles.

the wall cells of the afferant arterioles that come in contact with the macula densa are the JG cells.

the SNS directly innervates the JG cells
what can stimulate the release of ADH? (3)
nausea (feedforward mechanism)

stress

pregnancy (need higher blood volume)
what can inhibit ADH release
ethanol! that is why you pee
sources of H gain
from Co2
loss of bicarbonate
production of acids
hypoventilation
sources of H loss
use H in metabolism
vomit
urine
hyperventilation
where does digestive system start?
in the mouth --> pharynx --> esophagus --> stomach --> small instestine --> large intestine --> rectum --> anus
esophagus
pathway from pharynx to stomach.

highly lubricated: secretes mucus
stomach
sac-like organ where food dissolves and is partially digested (proteins by pepsin)

highly acidic: secretes HCl, pepsins, and mucus
mouth and pharynx
initial digestion of carbs with amylase.

secretes mucus and amylase.
pancreas
secretes enzymes and bicarbonate.

exocrine enzymes: lipase, protease, nuclease, carbase

endocrine enzymes: insulin

bicarb: to neturalize the Hcl from the stomach
gall bladder
stores bile
saliva contains? (4)

under control of?
contains amylase to break down starch

also contains antibodies to attack bacteria

also contains bicarbonate to neutralize the acid that any remaining bacteria may secrete

also contains mucus to lubricate the food and make it easier to swallow

under control from pSNS
cephalic phase
phase of digestion that initiates the feedforward mechanisms that will get body ready to ingest food
esophageal sphinctor
both upper and lower. upper is inconsequential

lower is important in keeping stomach acids out of the esophagus or else it will cause alot of damage to the lining.
why is esophagus more susceptible to acid then stomach?
stomach is big, thick, and well coated and esophagus is not!
GERD
gastroesophogeal reflux disease.

disease (chronic) where the lower sphinctor is faulty and stomach acid can leak back into the esophagus and burn away the lining. can lead to an ulcer
why does fatty diets lead to heartburn?
because fats take longer to digest and so food stays in the stomach longer. and the longer it is in the stomach, the more of a chance it has to leak out.
chyme
the solution of food and stomach acids that gets injected into the small intestine for further digestion
pyloric sphinctor
separates stomach from small intestine.

communicates with the small intestine so that it knows when to allow a squirt of chyme into the small intestine for digestion

as intestine enlarges, sends a signal to inhibit the sphinctor.

as intestine shrinks, sends a signal to activate the sphinctor
enteric nervous system
part of ans.

controls: strength of contraction of stomach, mucus secretion, and allows communication from one organ to another.
small intestine
huge surface area: almost all absorption occurs here.

100% fat
98% carb
80% protein
liver in digestion
produces bile!
bile
a mixture of substances

it has some waste products but also has: bile salts, phospholipids for fat digestion
bile salts
help lipases digest fats by preventing them from clumping adn thus increasing the available surface area.
how is bile secreted/released?
secreted from the liver down the hepatic bile duct into the gallbladder.

from gallbladder down the common bile duct through the sphinctor of oddi into the small intestine

gallbladder has no neural inputs only hormonal.

CCK gets released by intestine when it senses fat and CCK causes the gallbladder to constrict
how does the intestine time things perfectly with the gallbladder when to release bile?
when it senses fat, it releases CCK which caues the activation of the gallbladder
what part of digestive system can you live without and what cant you live without?
can live without stomach or gallbladder

NEED pancreas!
how does pancreas know when to release enzymes?
neural: PSNS feedforward mechanism when you smell food and when the intestines expand

hormonal: when intestine expands, releases secretin and cck to stimulate the pancreas
cck
released by the intestine to stimulate the pancreas to release enzymes. also opens the sphinctor of oddi. also causes the gallbladder to squeeze.

can also inhibit appetite
anatomy of gi tract
serosa is the bottom of the wall (closest to the abdominal cavity)

mucosa is the top layer with mucus

between the two layers are the submucosa and muscularis externa which are muscles, neurons and blood
different kinds of muscle in gi tract
circular and longitudnal muscles allow for churning of the stomach
how is gi motility regulated?
cck and secretin: inhibits
distention: inhibits (sends signal to stomach to stop!
short reflex
only the enteric system no CNS
long reflex
uses the CNS
2 regions of increased surface area in the gut
folding of epithelial into villi and each villi have microvilli
Celiac sprue disease
a disease that is triggered by autoimmune reaction to proteins that are found in grains. Those proteins are called "gluten" this is not an allergic reaction, it is an autoimmune genetic disease triggered by the presence of these antigens.

They erode the microvilli so you have nutrient deficiencies.

less surface area means that less is absorbed.
anatomy of microvilli
there are blood vessels for absorption and lacteals.

the lacteals (lymph) absorb most of the fat since it is usually too big for the capillaries
3 major classes of carbs
starch (plants)
cellulose (plants)
glycogen (animals)
why cant we absorb disacharides?
beacuse we dont have the transporters. they may also be too big but the main reason is because of the transporters!
how to break down from disachride to monosacharide?
there are lactase/sucrase... on the microvilli and they find disacharides and slice them!
how are nutrients absorbed from gi into circulation?
same as the kidneys (Na cotransporters)
why are the gluts in the gi insulin independent?
because the glucose needs to be in the body to activate the GIP to activate the pancreas to secrete insulin! it would be a catch 22
what makes insulin secreted?
glucose in the SI activates GIP which enters the endocrine system and targets the endocrine glands of the pancreas to secrete insulin! (feedforward)
how can you get fat on a carb diet?
because the liver and adipose tissue converts excess glucose into fatty acids and triglyceride
how are fats digested?
fat is emulsified into droplets by bile salts and phospholipids. triglyceride is broken down into monoglyceride and 2 fatty acids by lipase.

monoglyceride can be absrobed
sequence of events of fat digestion
chyme enters SI. it directly and indirectly (through distention) activates cck and secretin.

the distended SI activates the PSNS and SI motility.

the PSNS potentiates the cck and secretin

cck/secretin both inhibit the stomach, contract the gallbladder, stimulate hco3 release, relaxes the sphinctor of oddi and may inhibit appetite
co-lipase
sticks out of the fat molecule with bile salt and phospholipids to recruit the lipase
micelle
small fat droplets which help in fat absorption.

polar ends stick out and nonpolar ends are in the middle.

the products of fat digestion by lipase are held in the micellar state so that they do not reaggregate into larger fat droplets.

as micelle break apart when fat gets absrobed, more broken down fats reform the micelle
what happens to fat after it is absorbed?
it is put back together into triglyceride in the SI cells. this helps maintain a diffusion gradeint so that fat keeps coming in.

the triglycerides are packaged into chylomicrons to lessen the osmotic load.

then coat chylomicrons with apopproteins to solubilize it and secrete into the lacteal
chylomicrons
small droplets of fat that has been absorbed. this lessens the osmotic load (i.e. 1 milecule instead of hundreds)
apoproteins
proteins that coat the chylomicrons so that they solubilize and can be secreted
lipoprotein lipase
breaks down chylomicron so that it can get into the adipose cells for storage. the triglyceride is broken down and then resynthesized in the adipose cell
what is constant about fat digestion
triglycerides are broken down for transport and then reassembled in the new compartment
hdl and ldl
lipoprotein lipases to break down chylomicrons
insulin and lipase
insulin stimulates lipase activity so that the fats can get absorbed into the adipose cells.

when insulin goes down, so does lipase activity so fat can now be utilized for energy

insulin also inhibits the hormone sensitive lipase in the adipose cells since it wants the energy to be stored.
hormone senstive lipase
breaks down triglycerides IN adipose cells
where is fat not used for energy?
the brain!
a hallmark of diabetes mellitus
peeing alot.
high glucose levels
the presence of fat int he blood (since no brake on the HSL)
protein digestion
pepsinogen is inactive and made in the stomach.

HCl converts it into pepsin (active)

pepsin and HCl work together to make proteins more accesible for degradation in the SI.
chief cell (stomach)
secretes pepsinogen
parietal cell (stomach)
secretes HCl and intrinsic factor
mucous cells (stomach)
release mucus to neutralize the acid so it doesnt burn through!
gastric pit
contains mucus cells, gastric gland,parietal cells, chief cells, ECL cells, and D cells
ECL cells (stomach)
release histamine
D cells (stomach)
release somatostatin
gastric gland
releases gastrin into circulation (if it released into the stomach it would be digeted!)
parietal cell regulation
gastrin is released when senses peptides.

gastrin stimulates the release of histamine

the distention of the stomach activates PSNS mACh receptors.

also, when hungry PSNS is activated to activate mAch receptors

when activated, proton pumps get sent to the plasma surface and start pumping H into the stomach to activate pepsin

the acid activates somatostatin release which inhibits gastrin and ACh and histamine and stops acid release
how do you get the parietal cells to release H for extended period of time?
need to ignore the negative feedback of H on somatostatin.

proteins in the stomach soak up the H so now somatostatin stops inhibiting and more H gets produced!
PPI
proton pump inhibitors. they are used to treat too much acid in the stomach. by limiting the amount of acid that can be released.
prilosec, nexium, protonix (anything with a Pr...)
these are examples of PPI's
h2 histamine receptor blockers
these work to stop the potentiating effects of histamine on the parietal cells and limit stomach acid
pepcid, zantac...
examples of hs histamine blockers
muscarinic ACh blocker
atropine! can also help limit stomach acid production
proteases in SI
trypsin, chymotrypsin, carboxpeptidase, elastase
protein digestion in SI
the proteins are digeted by proteases and then clipped into single amino acids by emzymes on the microvilli and then absorbed in capillaries and sent into cells by INSULIN