Exam 13: April 17-24 Flashcards
what is inside alveoli?
air that diffuses out into the circulatory system
what are alveoli?
alveoli are chambers within the lungs surrounded by the circulatory system capillaries to do exchange
what are the characteristics of alveoli?
they create lots of surface area and have very thin walls because of diffusion
what are the types of alveoli cells?
type I and type II
what are type I alveolar cells?
gas exchange
thin cells that reduce distance for diffusion and also have big surface area
what are type II alveolar cells?
surfactant
they look like regular cells, don’t have extra surface area or decreased distance
they keep alveoli open
why do we need type II alveolar cells?
water from your body is pushing on air so not much hydrostatic pressure is needed to take out Type I cells since they won’t be able to withstand water inside your body
so you somehow need to keep air bubbles from collapsing on themselves from push of water which is what Type II cells do
what do type II cells produce?
a blue film aka surfactant which allows air bubbles to withstand hydrostatic pressure
helps out the type I cells by decreasing surface tension
what is surfactant?
it’s a soapy solution secreted by type II cells to ensure that alveoli don’t collapse
it’s reduces surface tension and allows air bubbles to last
what cells in babies respiratory systems are not developed?
immature babies don’t have developed Type II cells so they would breath in air and their alveoli would collapse
so to help them, they gave them a soapy solution until their Type II cells develop to maximize surface area
what is the effect of having undeveloped type II cells?
reduced surface area of alveoli because they are collapsing
reduced surface area means not enough oxygen exchange so the body isn’t making enough ATP
what are the limits of the thoracic cavity?
ribs on the sides and the top
diaphragm on the bottom of the thoracic cavity
what are the contents of the thoracic cavity?
the lungs and heart
what controls the size of the thoracic cavity?
intercostal muscles and diaphragm
what do the intercostal muscles do?
they control the position of your ribs
they don’t move your lungs, they move your skeleton! aka the ribs
what does Bronson want to open when she retires?
an intercostal restaurant
when you’re eating ribs you’re actually eating intercostal muscle!
what type of muscle are the intercostal muscle and diaphragm?
skeletal!!
we have control over our breathing aka it’s under somatic control
how come we don’t have to think about breathing even though our intercostal and diaphragm aren’t under autonomic control?
we can control skeletal muscles with reflexed!
so we don’t always have to control these muscles through the motor cortex, we can do it through the spine
what is the pleural sac?
it’s a water-filled balloon around the lungs
it’s a super thin film
it has two walls: one associated with the thoracic cavity and another wall associated with the lungs
in between the two walls is fluid
what are the parts of the pleural sac?
the parietal pleura and the visceral pleura
in between the parietal and visceral pleura is pleural fluid that serves to prevent friction between the two layers
what is the parietal pleura?
it’s the outside wall of the pleural sac connected to the thoracic cavity
what is the visceral pleura?
it’s the inside wall of the pleural cavity connected to the lungs
what are the lungs attached to?
the visceral and parietal pleural are layers/lining around the lungs so the lungs themselves aren’t attached to the ribs
the lungs are indirectly attached to the bones since your bones are connected to the parietal pleural
what is the purpose of the pleural fluid?
water is polar so the hydrogen bonds make water cohesive and fluid which allows for movement transfer
when you move the parietal pleural (since it’s attached to your ribs) the pleural fluid transferred the movement and passed it along to the visceral pleura
if you put too much water or you put in the pleural cavity then the two walls will move separately
what happens to a cold bottle and coaster on a hot day?
to drink something cold in the nice weather, your drink probably sweated and stuck to the coaster so you pick up both the bottle and the coaster because you created a thin film of water and the cohesiveness of the water was strong enough to pick up the coaster
what happens if you rupture the pleural sac?
if one of the walls is damaged, you can get air coming in which means the two walls will move separately from each other
what is a pneumothorax?
it’s a collapsed lung
this means a disconnect from our ability to move both walls of the pleural cavity at the same time
someone with pneumothorax will have a ribcage that’s moving fine but there won’t be convection because lungs wont be moving with the rib cage
no convection
this is not the same as collapsed alveoli
what happens if there’s collapsed alveoli?
pneumothorax and collapsed alveoli are not the same
you can still have convection with collapsed alveoli because your lungs are still moving
collapsed alveoli just means lost surface area
what does air pressure depend on?
1) temperature
2) gases present
how does air pressure depend on temperature?
we change the temperature of the air and by the time it gets to alveoli, it’s down to body temperature
how does air pressure depend on the gases present?
“n” matters
air is a mixture of gases and it’s not just oxygen so we have to pay attention to which gases are present and at what level
we can add pressures of individual gases to get total pressure so each gas has a partial pressure
what gases are present in the air and at what partial pressures?
N2 = 79%
very little CO2 and H2O
P(O2) = 21% or 160 mmHg
P(CO2) = 0.3 mmHg
how do gases diffuse?
gases diffuse from high to low partial pressure
gases can also diffuse into and out of liquids
how do we do gas exchange between alveoli and the circulatory system?
exchange between alveoli and circulatory system is based on partial pressure of blood entering the lungs and the partial pressure of the air in the alveoli
what is the partial pressure of gases in the blood entering the lungs? how about the air in the alveoli? what will happen?
blood entering lungs:
PCO2 = 46 mmHg
PO2 = 40 mmHg
blood coming to the lungs is deoxygenated
air in alveoli:
PCO2 = 40 mmHg
PO2 = 105 mmHg
CO2 will diffuse out of the blood and into the lungs while the O2 will diffuse out of the alveoli and into the lungs due to the partial pressure gradients
is the partial pressure of gases in the alveoli the same as the composition of air?
no
when you squeeze air out of the lungs, we can never have zero air in the lungs
we take the air that we did the exchange with and pushed most of it out and then brought in fresh air so the numbers are an average
numbers will drop for oxygen and rise for CO2 because we’re mixing remnants of old air with new air
the only time the numbers will match is your very first breath
what is the source of the control of ventilation?
skeletal muscles so that we can control our breathing via our cerebral cortex
what part of your brain is devoted to breathing?
respiratory rhythm generator (RRG)
where is the respiratory rhythm generator located?
the medulla oblongata in your brainstem
your brainstem controls all the keys to life like setting up a base heart rate and breathing and digestion
what are the inputs to the respiratory rhythm generator?
1) pacemaker potentials
2) chemoreceptors
3) pulmonary stretch receptors
what input to the RRG do pacemaker potentials give?
if everything stayed as is, you would keep at a steady pace in breathing and the pacemaker potentials set this rate however, things usually change and you have to breath faster or slower sometimes
what input to the RRG do chemoreceptors give?
they register O2, CO2 and H+ levels that tell you if you need to breath more or less to get to the right levels in your blood
this is afferent input
what input to the RRG do pulmonary stretch receptors give?
further afferent input because you can’t overstretch your lungs or else they’ll pop because you can’t overinflate
what is the chain of events when you breath in?
stimulate –> contract –> expansion –> inspiration
Shortening of intercostals moves ribs to create more space
the diaphragm runs from one side of the rib cage to the other so the diaphragm drops down to make the thoracic cavity bigger
so now we’ve made lung volume bigger because your pleural sac changed the size of the lungs in the process of intercostal contraction
increased lung volume means the pressure inside your lungs drops compared to the outside of your body so air comes into your lungs = follows pressure gradient from high to low
what is the chain of events when you breath out?
no stimulation –> relax –> rebound –> expiration
you stop sending stimulation to muscles to contract so that they relax which causes rebound which gets space to become smaller
if volume goes down then pressure goes up relative to the outside of your body so air goes out and you exhale
how can you change the amount of air in your lungs?
we can change the amount of air coming in by changing pressure gradient by changing volumes that we create
we can inhale more by stimulating longer or we can exhale more by stopping stimulation
duration of stimulation or non stimulation sets size/amount of air
what is the limit of how much you can inhale?
if you try to inhale too much you’ll inhale then get a quick exhale
you’ve activated stretch receptors and they tell you to stop because you don’t want to blow out the lungs
the stretch receptors cause inhibition on motor neurons that control the diaphragm and intercostal muscles and cut the stimulation so your muscles relax and you get expiration
what happens if you raise the pressure outside your body so that your lungs get a lot of stimulation from outside rather than yourself?
pulmonary stretch receptors will go off if there’s a very large inhale and inhibit motor neurons that control intercostal/diaphragm usuallyyy
but if the pressure outside your body is so big that your lungs are being stimulated to expand from something other than your body….air will come in because it’s not ht lungs controlling it
the pulmonary stretch receptors will go off and tell you to exhale but the pressure outside is telling you to inhale
this is why in an explosion, the purpose of the bomb was to create high enough pressure area that it actually blew the people’s lungs out from the inside: you should close your nose and not breath in
another situation is using an adult bag on a little kid during CPR but you could blow out their lungs because you’ve created a pneumothorax
GO LISTEN TO LECTURE
what is the tidal volume?
how much air you move in one breath
analogous to stroke volume
tidal volume varies from resting to vital capacity
what are the limits of tidal volume?
minimum TV = resting (500 mL)
maximum TV = vital capacity (5 L)
what is the vital capacity?
maximum TV
this is the maximum that you can accomplish aerobically
if you need more than this you’re in trouble
what is the equation for vital capacity?
VC = IRV + TV + ERV
what is the expiratory reserve volume?
ERV
maximal volume of air, usually about 1000 milliliters, that can be expelled from the lungs after normal expiration
if we exhale more, we’re using the reserve
what happens as you increase your tidal volume?
as we increase TV towards our vital capacity, we’ll end up using one or more of our reserve; we either have to inhale or exhale more
what happens at the vital capacity?
IRV and ERV are being used and their size at their maximum
What happens if tidal volume = vital capacity?
then IRV and ERV are at zero because you’ve used them all up
what is the inspiratory reserve volume?
IRV
the maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration
can you change your vital capacity short term?
no
between today and tumor you can’t change it
can you change your vital capacity long term?
yes
how much you inhale/exhale depends on skeletal muscles
you can also stop training and decrease vital capacity by letting muscles atrophy
what is residual volume?
this is the minimum amount of air that we can never get out of the lungs
we can’t put all the air out of our lungs, we’ll always have air left in the lungs
why do always have air left in your lungs? aka why do you have a residual volume?
bronchioles that are part of conducting part of respiratory system that have low resistance to air flow and you can’t close your bronchioles so you have space there
your alveoli have paper thin walls but you don’t want walls to mush against each other because they’ll stick and rip so you can get alveoli smaller but not completely collapsed which is why you have air left in the lungs
can you change residual volume?
?
probably
is O2 dissolved in the blood?
dissolved, but poorly
oxygen is small and nonpolar but your blood is polar
the measurement that the doctor takes is only measuring the 1% of oxygen in your blood that is free, the 99% isn’t being detected
what oxygen level does your doctor measure?
the 1% free oxygen in your blood
99% isn’t being measured because it’s reversibly bound to Hb in RBC
this is the reason we can have a polar environment moving our key nonpolar gas because we effectively give it a plasma binding protein
what is the structure of hemoglobin?
4 identical subunits that all have heme which needs Fe to share electrons with oxygen and allow it to bind
how does Hb carry oxygen?
each Hb carries 4 oxygens
the oxygen reversibly binds with Fe and shares electrons
it doesn’t give up electrons because covalent bonds are a lot harder to break and we need oxygen to pop off Hb once it gets to tissues
how is cooperativity expressed in Hb?
oxygen is binding at each subunit and binding is dependent on shape and charge; each subunit has specificity for oxygen
once one oxygen binds, the affinity for oxygen increases at the other subunits
we bind and change the shape of one subunit, it will change the shape of all the other 3 subunits and increase affinity for oxygen and make it more likely for oxygen to bind
then once an oxygen binds to the second subunit, the affinity in the remaining two, again increases
then, if one oxygen comes off, it lowers the affinity in the other three spots and they’re more likely to come off so both loading and unloading happen quickly
how does hemoglobin increase the amount of O2 transferred to tissues?
Hb helps increase amount of O2 transferred by aiding diffusion by maintaining a large diffusion gradient
there’s 8 oxygens in the blood and the in the air so the gradient is gone; if we put Hb in the blood, 6 oxygen will be attached to Hb so now the gradient is reformed since we’re only looking at the free oxygen
there’s 8 oxygen in the lungs but 2 in the blood so we’ve recreated the gradient = oxygen will move into the blood and Hb will continue to grab oxygen due to cooperatively and you end up being able to move 14/16 oxygen into the blood!
what factors affect Hb affinity for O2?
1) CO2
2) H+
3) DPG
4) CO
5) temperature
how does CO2 affect Hb affinity for O2?
binding of CO2 causes decreased affinity for O2
changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site
how does H+ affect Hb affinity for O2?
binds and shape changes and decreases affinity for O2
changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site
how does temperature affect Hb affinity for O2?
T changes shape of proteins
heating Hb decreases O2 affinity
changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site
how does DPG affect Hb affinity for O2?
key component in glycolysis
if glycolysis is occurring, there’s DPG in the system
DPG binds to Hb and decreases O2 affinity
changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site
how does CO affect Hb affinity for O2?
this one does interfere at the actual site
it has the appropriate shape and size to bind at oxygen’s binding site so it’s a competitor
it’s an antagonist because it replaces oxygen
CO has a higher affinity than O2 which starts dropping 99% number
does CO or O2 have a higher affinity for Hb?
CO
it binds to Hb better
what is on the axis of the Hb saturation curve?
% saturation of Hb vs. P(O2)
direct relationship
what relationship is there between the % saturation of Hb and the partial pressure of O2?
direct relationship
increasing partial pressure of oxygen increases % saturation of Hb
what % saturation of Hb is there in the lungs?
the partial pressure is around 100 so we’ll have fully saturated in Hb since [O2] is so high
what % saturation of Hb is there coming back to our lungs?
partial pressure is around 40 mmHg so we’re at about 80% saturation since our tissues are taking oxygen
what is the venous reserve?
it’s the amount of oxygen associated with Hb returning to the heart and going to return to the lungs (it can be tapped into)
our pick up location is around 100% but drop off location is lower than 100% which means that oxygen got dropped off at tissues = partial pressure of free oxygen is lower
but nearly 80% of Hb is still loaded with oxygen from the last pass around!
there’s oxygen coming back to the heart and out to the pulmonary system that is from the last cycle = venous reserve
Lots of Hb take the whole loop and never offload their oxygen – this is referred to as the venous reserve
what’s the point of hands only CPR?
to tap into the venous reserve!
we just need to get convection going and we’ll get venous reserve activated and we don’t need any new oxygen to be transferred over, we just need the oxygen already on the Hb to get transferred to the tissues
can P(O2) = 0?
you cells can have a partial pressure of zero but your blood cannot
if our blood has zero free oxygen in it and your cells have any oxygen in them, then the oxygen will follow gradient and go from cells to the blood
so the only time your blood has a partial pressure of zero is if you cells have zero oxygen and if that’s true, you’re dead because neither your cells or blood have oxygen
so your blood can’t have zero P(O2) but your cells can have P(O2) of zero like during anaerobic conditions which run off of glycolysis
so the cells for a little while can have P(O2) =0 which will help us drive oxygen towards those cells because of the gradient
is CO2 soluble in the blood?
it’s a little more soluble than O2 because it’s not as non polar
how much free CO2 is there in the blood?
about 10%
compared to only 1% free O2 in the blood
how much CO2 is carried on Hb?
CO2 can bind to Hb so 30% of CO2 is carried on Hb
when CO2 binds it lowers Hb affinity for oxygen
where is the rest of the CO2 in the body?
we convert it to HCO3-!
CO2 is waste so we don’t care if we change it and we don’t need it to do anything so it’s okay if we do a chemical reaction with it
CO2 + H2O ←→ HCO3- + H+ (equation 3)
why do we want HCO3- in our blood?
we want bicarbonate in our blood because HCO3- is polar so it’s soluble in the plasma which can be transported a lot more easily
what kind of system is plasma?
plasma is a buffered system
buffered system means that if you pour acid or base into it and measure it’s pH, it doesn’t really change
if the blood wasn’t buffered we wouldn’t be able to have 60% transport of CO2
what help to make plasma a buffered system?
Hb and albumin help make plasma a buffered system by binding H+ so then the reaction will shift right towards bicarbonate
because we keep pulling out H+ we make high levels of HCO3- possible
do veins or arteries have higher pH?
venous pH < arterial pH
veins are more acidic than arteries
we’re still going to be having some H+ created when our tissues make CO2 waste from glycolysis so the blood associated with our venous side will decrease in pH as H+ increases
equation 3 happens in the tissues
so we’ll see a slightly more acidic pH in venous side than arterial side
why do arteries have a higher pH?
we’re offloading CO2 at the lungs
this means we need to run the equation towards the left
CO2 is moving out of our plasma and into lungs so it’ll shift the equilibrium to the left which turns more HCO3- into CO2
H+ levels decrease which increases pH
what factors influence the ventilation rate?
pacemakers and chemoreceptors
do oxygen levels impact ventilation rate?
there’s no change in ventilation rate regardless of oxygen levels as long as it’s above 60 mmHg = intensive above 60 mmHg
when O2 levels drop below 60 mmHg then you see increased ventilation rate
60 mmHg is where you start to see a significant drop in saturation on the Hb binding curve
what type of O2 do chemoreceptors measure?
they aren’t responsive to bound O2, they just measure free O2**
CO binds and replaces O2 so the free doesn’t change so the ventilation doesn’t change
HOW IS THIS POSSIBLE
what is the sensitivity of chemoreceptors to CO2?
they’re sensitive to small changes in CO2 levels in blood will have immediate changes in respiration rate
increased CO2 levels in blood = increased respiration rate
what happens to the respiratory rate at super super high levels of CO2?
you drop to zero respiration rate because the CO2 that is not really high in the blood has now impacted and killed our neurons of which some control our respiratory rhythm generators so we can no longer control our respiration and we stop breathing
no ventilation rate at very high levels of CO2 like killing mice in lab
what do chemoreceptors in the respiratory system respond to?
1) unbound O2
2) CO2
3) H+
what happens is there’s high levels of H+?
ventilation rate will increase
what happens during anaerobic conditions to ventilation rate?
under anaerobic conditions we only run glycolysis which makes lactic acid which moves out of muscles and into blood so we’re acidifying blood and raising H+ concentration when we’re doing anaerobic activity
this is why we breathe harder when we’re exercising hard
you get rid of CO2 so the equilibrium shifts left to get rid of H+
what is metabolic acidosis?
anaerobic exercise
the metabolism has created an acidity problem in our blood via anaerobic glycolysis (lactic acid build up in the blood)
we need to correct this by decreasing H+ by breathing off CO2 and increasing VR
what is metabolic acidosis? what causes it?
vomiting is bringing up stomach content
the stomach is acidic so we’re bringing out all the acid
we need to replace this acid after you vomit and this acid comes from the blood
so after you vomit, your blood pH increased = metabolic alkalosis
what happens if you anaerobically exercise too much?
if you stay anaerobic for a long time you’ll start to feel nauseous like during a super hard practice
your body is getting put into metabolic acidosis and telling the individual to slow down
the body’s only recourse is to vomit to try to get rid of acid since breathing harder isn’t doing enough to remove H+
what are ventilation rate issues attributed to?
CO2 issues make you have either too high or low of a rate a problem
what is hypoventilation? what condition does it lead to?
Individual isn’t breathing off enough CO2 so CO2 goes through the heart and back into the system so CO2 goes into arteries
now due to equilibrium shift you’ll have increased H+ and decreased pH
you’re sending your tissues a higher H+ concentration of blood
since it’s a respiratory cause for this acidosis problem it’s referred to as respiratory acidosis*
why is respiratory acidosis a problem?
arterial pH is lower since CO2 levels are high and shifting equilibrium to the right
decreased pH is a problem because proteins work best and physiological pH so low pH means they can’t do they’re job
Hb is impacted by H+ and will kick off O2 when it binds H+ which is bad because you’re trying to deliver O2 to tissues in the arteries
what is hyperventilation? what condition does it lead to?
too much CO2 is being taken out of the system
arterial P(CO2) is decreased so there’s an increase in pH
respiratory alkalosis
why is respiratory alkalosis a problem?
causes protein issues because again, you’re out of physiological pH range
increased O2 on Hb which can be bad because then delivery rate is lower since Hb is holding onto oxygen too well and won’t deliver it when it gets to the tissues
what is hypoxia?
O2 deficiency in tissues
every single person will die of some type of hypoxia essentially
what is hypoxic hypoxia?
insufficient O2 intake
you’re not getting enough O2 from in front of you into alveoli
could be that you’re in a low oxygen environment like high altitudes or it could be that you’re having a problem with convection (you have a pneumothorax or you’re choking
if you don’t get enough to alveoli, you don’t have enough O2 to arteries to our tissues
what is anemic hypoxia?
you get oxygen to blood just fine but there’s something wrong with your RBC
normal partial pressure of free O2 in the blood
all the anemia types you learned about contribute to anemic hypoxia because the O2 amount bound to Hb is not where it’s supposed to be so tissues aren’t getting enough O2
what is ischemic hypoxia?
insufficient blood flow to deliver O2
individuals that have heart attacks or strokes actually died because of ischemic hypoxia
what is histotoxic hypoxia?
cell toxic hypoxia
cells are unable to use O2
we get the oxygen to the tissues but there’s something wrong with the mitochondria that they can’t use the oxygen
what kind of hypoxia do spies in movies experience when they pop a cyanide pill?
if spies don’t want to give up information they take a cyanide pill and die of histotoxic hypoxia since cyanide actually prevents ETC from finishing the process and takes all mitochondria off line and your whole body can’t run on glycolysis alone
what is the primary function of the renal system?
regulate water and ions in the blood
what is the secondary function of the renal system?
1) get rid of wastes and toxins in the blood
2) endocrine and enzyme production (RBC, Ca, Na)
kidney makes EPO which helps with RBC production, kidney makes enzymes that help with Ca regulation etc.
what’s the problem with your kidneys filtering out toxins and wastes in the blood?
your kidney’s don’t recognize most drugs as something that should stay in your so your kidneys filter them right out and they end up in your urine
this is how drug tests works
what kind of filtration does your kidney do?
size filtration, period, there’s no other kind
it doesn’t matter what it is;
if it’s smaller than a protein, it will go out into the kidneys and get filtered out
uh this is a problem because water, AA, Na, K, Ca, glucose are all smaller than a protein
but not to fear the kidney has reabsorption techniques to bring them back into the body
urea is smaller than a protein but that’s fine, we usually don’t want it
what stuff gets reabsorbed into the kidney?
the “good” stuff is returned
what’s good depends on your current status
are you in a good range?
daily loss = daily intake
ex. if your BP is really high then you want to lose H20
ex. if Na levels are really high you want to get rid of Na
what does your kidney adjust for?
your kidney is the biggest player in making sure intake = loss!!
your kidney makes adjustments for diet, environment, activity to make sure you have a proper daily output
ex. if you bring in more water than you pee out, you’re overhydrated and vice versa if you lose more water than you bring in = dehydrated
what is the functional unit of the kidney?
nephron
what is the renal pelvis?
part of the kidney that collects urine so that it can be sent out via one vessel, the ureter
all the nephrons empty urine into the renal pelvis
what are the parts of the renal system?
1) kidney (2)
2) ureter (2)
3) bladder (1)
4) urethra (1)
5) sphincter muscles (2)
what are the components of the urethra?
1) internal urethral sphincter
2) external urethral sphincter
what is the internal urethral sphincter? what controls it?
part of the urethra
a ring of muscle that we can squeeze closed and cut off all flow from the vessel
under sympathetic control
the SNS is always keeping IUS closed because even though you’re kidney is making urine right now, you’re not peeing on the chair in class
you don’t have to think about not peeing because you’re under sympathetic control in the autonomic nervous system
what is the external urethral sphincter? what controls it?
part of the urethra
skeletal muscle (somatic control) because you have control to when you urinate aka you’re potty trained
you don’t go just because the autonomic tells you to go, it’s under somatic control
what happens in the bladder when you have to pee?
bladder fills because you’re constantly making urine but the sphincters are kept closed so you don’t leak urine at all times
you have stretch receptors (mechanoreceptors) that register a larger “n” so there’s also an increase P and an increased stretch on the muscle which tells you need to empty bladder and decrease V = empty bladder
mechanoreceptors provide this information
what happens in an unpotty trained individual?
the bladder starts contracting under PNS control
this means decreased volume and increased pressure and they just pee when their body tells them it’s time
they can’t hold it
what are the parts of the kidney?
cortex = outside; above the blood vessels
medulla = inside; below the blood vessels
what is the ureter?
each kidney has a ureter
each kidney has a renal pelvis which collects urine and send it out via the ureter vessel
the ureter then sends urine to the bladder
what is the bladder?
it’s smooth muscle controlled by the parasympathetic nervous system
receives urine from the ureter
are the sphincters in the urethra open or closed?
the sphincters are kept closed
sympathetic keeps internal closed
somatic keeps external closed
what is micturition?
urine exiting the body
what are the components of the nephron?
1) renal corpuscle
2) tubules
what does the renal corpuscle do?
it’s part of the nephron in the kidney where we actually do the filtering of the blood
what are the components of the renal corpuscle?
1) glomerulus
2) bowman’s capsule
what does the glomerulus do?
it’s part of the renal corpuscle in the nephron
it’s the part of the vascular system that is associated with the nephrons that allows for filtering of the blood to happen
how does the glomerulus filter flood?
via fenestration
spaces between endothelial cells that is size dependent*
it has openings/holes in the endothelial layer rather than tight connections
does everything that get filtered in the blood get excreted?
no
GFR = 180 L/day exiting your blood and going into your kidney
urine production = 1.8 L/day
aka the kidney’s bring back a lot of stuff that doesn’t go into the collecting duct
we need to reabsorb a lot of stuff
what is the bowman’s capsule?
part of the renal corpuscle in the nephron of the kidney
it’s the “catch” component that has tubules coming off of it that runs through the rest of the nephron
once you’ve left the blood, you’ve actually left the body: the original kidney was just the blood vessels on the surface but we realized it was better if we brought the kidney back in
so the tubule walls are actually made of epithelial cells because we can actually take a device and put it through your urethra all the way up without breaking a single cell
what are tubules?
a component of the nephron
what types of tubules are there in the nephron?
1) PCT
2) loop of henle
3) DCT
4) CD
what is the PCT?
proximal convoluted tubule in the nephron
it’s the first tubule after the Bowman’s capsule
whatever came out of the Bowman’s capsule was whatever was able to fit out via size filtration so we lost some good things
active transporters bring back glucose, AA, Na, and water
why don’t we urinate 180 L a day even though that’s how much the kidney is filtering each day?
the proximal convoluted tubule has active transporters that bring back glucose, AA, Na and other “good” stuff
as we create gradients by bringing things back, we also bring water with them and this is why we don’t urinate 180 L a day
where is the PCT located?
in the cortex of the kidney
what happens if the transporters in the PCT are saturated?
the PCT reabsorbs good things that were filtered out in the bowman’s capsule via active transporters
if the transporters are saturated aka we have too much sugar in our system, you see too sugar in the urine because it wasn’t pulled back in
where is the loop of henle located?
the medulla of the kidney
what are the parts of the loop of henle?
ascending and descending limb
what does the descending limb of the loop of henle do?
has aquaporins that allows water to move out of descending limb and come back into us
reabsorbs water via aquaporins
what does the ascending limb of the loop of henle do?
has transporters that allow Na to come back in and be kept
what is the DCT?
distal convoluted tubule of the nephron
it fine tunes what we have in the filtrate
don’t need to know anything else for this class
it comes up right next to the renal corpuscle, right next to the glomerulus side
what’s special about the collecting duct?
part of multiple nephrons because it collect from multiple nephrons
everything else we’ve seen is only part of one nephron
where is the collecting duct located?
both the medulla and the cortex
everything else has been only part of one
CD collects in the cortex and then moves through the medulla
what impacts the collecting duct?
ADH impacts kidney in the CD
if ADH is present, CD will allow water to be reabsorbed
if there’s no ADH then water will stay in collecting duct and we’ll produce more urine
under what conditions would be reabsorb urea?
sometimes we reabsorb urea in the CD sometimes because the only way we can get water to come back is to pull something else back so that it follows the osmolarity gradient
when do you get rid of H+?
in the collecting duct
another way to get rid of H+ other than the lungs is dumping it into the urine
but you don’t want to do it too early in the system because low pH can damage proteins like the transporters and aquaporins so you dump the H+ as late as possible to limit damage to the other tubules
what symptoms will a person with acidosis have?
they will breath more to get rid of CO2 and shift the equation left = decrease H+
they will also have more acidic urine
where can water exit the kidney?
the descending limb of the loop of henle
water cannot exit the ascending limb
where can Na exit the kidney?
in the ascending limb of the loop of henle
Na cannot exit in the descending limb
where is the countercurrent multiplier?
the loop of henle in the kidney
what happens in the countercurrent multiplier?
1) flow from the PCT comes down descending limb - osmolarity is 300 inside and outside the tubule so lumen osmolarity = IF osmolarity and there’s no driving force for diffusion
2) flow reaches ascending limb and NaCl is pumped into IF so IF increases in osmolarity and lumen osmolarity decreases
3) new flow enters descending limb at 300 osmolarity and water will move out of the tubule via aquaporins since you’ve created a gradient and IF has increased osmolarity
4) continual new flow allows the process to repeat so that the osmolarity in the IF in the medulla increases more and more
what is lumen osmolarity?
osmolarity inside the tubule
when do you first see changes in the osmolarity of the lumen?
the ascending limb
NaCl can be pumped out of the tubule into IF
when does the lumen osmolarity change?
lumen osmolarity:
increases in the descending limb
decreases in the ascending limb
where is the IF in reference to the loop of henle?
the IF is in the medulla
what would increase the osmotic gradient created by the loop of henle?
a longer loop of henle
how would you make more concentrated urine?
that means you’re trying to reabsorb more water into the IF
you would have to increase the osmolarity of the IF even more
what controls the movement of the collecting duct?
a gradient
what happens in the collecting duct if ADH is present?
if ADH present: aquaporins in CD will let water follow gradient so that the IF in the medulla and what’s in the CD will have the same osmolarity
what happens in the collecting duct if ADH isn not present?
with no ADH: the aquaporins will go away and water can’t exit so we will see a low concentration of urine; dilute urine with low osmolarity
what is the fast way to regulate Na+ and H2O levels?
changing GFR via smooth muscle
glomerulus is our vessel that has smooth muscle around it and can change size of vessel = change flow of blood
how do you decrease GFR quickly?
1) contract smooth muscle around afferent arteriole
2) dilate smooth muscle around efferent arteriole
result: increases Na+/H2O
to decrease GFR we want less to go through fenestrations so contract afferent smooth muscle that’s incoming –> so if less comes in, less will go through the holes aka contract the afferent
also if we dilate the efferent smooth muscle and make it easier to exit then less will go through the holes so we’ll also decrease GFR
if we get the kidney less to do, the kidney will be able to do its job better
decreasing GFR means we can reabsorb more sodium and water
how do we increase GFR quickly?
1) dilate afferent smooth muscle
2) contract efferent smooth muscle
result: decrease Na/H2O
to have a bigger GFR we want to dilate the afferent smooth muscle so more comes in means more goes in both directions
or we want to close off the exit by contracting efferent smooth muscle
bigger GFR means we overloaded kidney and we lose more sodium and water and don’t reabsorb as much because it’s harder for the kidney to do its job
how do you slowly regulate Na and water levels?
endocrines via reabsorption
what endocrines will slowly alter Na/H2O levels?
1) renin-angiotensin-aldersterone system (RAAS)
2) pulmonary capillaries
3) aldosterone
4) atrial natriuretic peptide (ANP)
what kicks the RAAS system into place?
what kicks this system into play is:
1) decreased NaCl
2) decreased BP
3) decreased ECF volume
how does the RAAS regulate Na and H2O levels? what does the RAAS system do?
RAAS helps us keep water on board by keeping NaCl on board aka increase BP
juxtaglomerular cells release renin if any indicators are registered by chemoreceptors
the cells right by the glomerulus on the afferent and efferent tubules will put renin into the system
when renin is in the system, it converts inactive angiotensinogen from the liver into angiotensin I
what does angiotensin I do?
once activated by renin, ATI will end up in the pulmonary capillaries
angiotensin-converting enzyme (ACE) in the pulmonary capillaries will finish the conversion of ATI to angiotensin II
ATII is a vasoconstrictor
what are ACE inhibitors?
ACE converts angiotensin I to angiotensin II which is a vasoconstrictor
people with high BP get put on ACE inhibitors so that they can’t make AT II which is a vasoconstrictor among other things
ACE inhibitors help lower BP
what does angiotensin II do?
- it’s a vasoconstrictor
- it makes sure we get more vasopressin into the system which is another vasoconstrictor
- helps hold water in collecting duct (increases BP)
- makes you more thirsty = brings in more water
- increases aldosterone levels
where does aldosterone come from?
adrenal cortex which is above the kidney releases aldosterone
what stimulates release of aldosterone?
angiotensin II binds adrenal cortex receptors to stimulate release of aldosterone
what does aldosterone do?
impacts kidney and increases Na transporters
transporters bring back Na which brings back water with it
however, transporters that bring Na back cause us to lose K
what causes atrial natriuretic peptide (ANP) to be released?
1) high NaCl
2) high BP
3) high ECF volume
what does ANP do?
it comes from the heart and decreases BP
inhibits secretion of other things to decrease water volume by decreasing osmolarity
inhibits release of renin, aldosterone, vasopressin
you want to be losing water, you want a diuretic
what is the effect of ANP on GFR?
ANP increases GFR by impacting the smooth muscle
increased GFR overwhelms the kidney so you lose more water and sodium
why does ANP come from the heart?
we don’t want to much volume in the heart because if EDV gets too big, we’ll get congestive heart failure
we don’t want our heart to get too big
ANP is analogous to pulmonary stretch receptors in the lungs in that it makes sure we don’t overinflated the heart
lowering levels of water and sodium
what’s the pathway of the reproductive system?
GnRH –> FSH and LH –> gonads
what are the gonads?
testis or ovary
what do gonads do?
1) release sex endocrines
2) create gametes
what are gametes?
egg and sperm
what is the creation of egg and sperm?
gametogenesis
creation of gametes
what type of cells are gametes?
haploid cells
aka they only have 1/2 of the DNA so that when you combine with another gamete you have a full set
haploid = 23 chromosomes
diploid = 46 chromosomes
via what process are gametes created?
meiosis
meiosis creates haploids via 2 divisions
how many gametes do males make?
males are always making gametes
constantly putting cells through meiosis
males have billions of true haploid cells
when do females make their gametes?
females make all of their gametes in utero
all eggs get stopped before the 1st meiotic division at birth
when does the first meiotic division of female gametes happen?
ovulation
when does the second meiotic division of female gametes happen?
fertilization
when egg meats sperm
how many true haploid cells do females have?
the number of true haploid cells in a girl is the number of times she’s pregnant
how long is the overian cycle?
28 days
what are the phases of the ovarian cycle?
folliclar phase (12-14 days)
luteal phase (about 14 days)
what happens during the follicular phase?
controlled by follicle
starts with loss of the uterine wall
estrogen released from follicle which causes a build up of the uterine wall
what controls the luteal phase?
controlled by the corpus luteum
what is the corpus luteum?
the remanence of the follicle after the egg is released from it
what is the luteal phase?
post ovulation
maintain the uterine wall: more blood supply and glucose
estrogen and progesterone secreted from corpus luteum
when does the corpus luteum die?
10 days after ovulation if there’s no intervention
it takes with it the estrogen and progesterone levels so they drop = signal to deteriorate wall because you don’t need it
if there’s a pregnancy the corpus luteum survives
what are the steps of the ovarian cycle?
1) loss of wall
2) follicular phase
3) ovulation
4) luteal phase
what is the GFR?
the amount exiting your blood and going into your kidney
how are ANP and RAAS related?
they do the opposite things
ANP decreases BP
RAAS increases BP
