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78 Cards in this Set

  • Front
  • Back

What are the functions of the repiratory system

pH regulation-Co2 combines with water and forms carbonate to form acid


Exchange gas


Protection from pathogens


Conditions Air - warms air, adds water vapor, filtering out foreign material

Use of oxygen and what does it do with metabolites

Oxygen is used in every cell for final electron acceptor


Also the glucose metabolism produces a lot of Co2 so needs to get rid of

What is the difference between internal and external respiration

Internal is cellular respiration in the mitochondria


External is breathing

Cystic Fibrosis

when a Cl- channel doesnt function properly, and the mucous is too viscous

What happens to the velocity in the broncholes

The higher cross section area slows down which is good for diffusion but also means particles can diffuse and get stuck here

What makes alveoli good for exchange

huge surface area and filled with capillaries

Type 1 vs Type 2 cells

Type 1 are flat, good for gas exchange


Type 2 - yellow fluffy cells that produce surfactant

Frog lungs vs rat lungs (mammallian)

Frog is just a big sac and mammals have many different alvoli


Mammals - smaller distance, more SA

Pulmonary edema

has a small interstitum so it fills up fast, and ends up in aveoli which makes it hard to breath

Different Plueras

Visceral pleura close to lunch and parietal pleura touching thoracic cavity

Lungs are like spandex

When you exhale lungs expand and collapse back


Lungs like to collapse when left to their own devices because of the elastin and collagen fibers


Your thoracic likes to?

Natural it likes to expand, but because there is interstitial fluid it makes the lungs and the chest wall together so each pulls on that little space, and fluid isnt every expandable. Which generates a negative pressure in the interstitial space

Boyles Law

PV = P2V2


If volume increases there is less pressure


Pressure is inversely proportional to volume

Transpulmonary pressure

pressure difference between the lungs and the interstital space


As you drop pressure in the lungs air will come in until the pressure gradient is gone

Restrictive disease

low complience


(iron bands around your ribcage

Obstructive lung disease

high air way resistance, something obstructing

What is compliance

the change in pressure needed to inflate the lungs to a particular volume, the ability to stretch

High compliance

Emphasema Increasse compliance but also decrease recoil.

Low compliance

need more change in pressure to inflate


Fibrosis, you have a lot of scar tissue

Change in Transpulmonary pressure

Pressure across lunch tissue


Palv - Pip


First breath is hard because no volume in lungs


Low compliance is still doesnt like to stretch with scar tissue that cross stitch

Surface Tension

Allows water particles to stick together- like beading of water on a slick window



Aveoli - the beading leads to more water accumulating and low pressure which makes them collapse. Since they are connected to the same wall when once collaspe they all do. House of cards effect

The Law of LaPlace

If no surfactant the way water and air interact is the same, so they same surface tension of different radius of aveoli



Smaller bubbles collapse first, and they would blow up the bigger ones next to it


Surfactant

are amphiphilic so can associate with the air and water


it disrupts the hydrogen binding with each other, because it causes the water to have such high affinity for each other. Prevents the beading up and it splits out into a film which makes easier for transport



working hypothesis of why smaller aveoli less tension

in the smaller avoeli the surfactant are closer to each other more potent which lowers the surface tension more potent. Equalizes pressure easier

If u of obstructive

forceful exhalation is very hard, so folks with enphasema to breath gently to not increase resistance

If an alveoli has high resistance it will build up

Increasse Pco2 and decrease Po2


Pulmonary with decrease O2 constrict instead of dilate like systemic


Hypoxic vasoconstriction - if there is an alveoli that is not functioning properly, you want to use your resources better to other alveoli



If you have hypoxia everywhere then vasoconstrict everywhere and your left ventricle afterload would be very high.

%FEV1

Measure of resistance of the airways


You take your force exhalation in 1 seconds divided by your total capacity.



obstructive disease would change this but restrictive you would have a normall FEV1

Atmospheric pressure decreases as

you go higher because less pressure on top of you

Contents of atmosphere

PO2 is 20% at


PN is 70-90%

When in dead space the partial pressure is dropped by 10 because

it gets humidified, so adding water to O2 makes the pressure lower

Do oxygen levels fluxuate a lot?

no because you always have functional residual capacity in your lungs (alveoli) The PA02 (alveolar) is around 105 mmHG

You need to start at 160mmHg to get to a 3mmHg of oxygen in mitochondrion

pH is lower in venous blood because it produces bicarbonate

If you are not breathing enough for homeostasis and you are hypoventilation

your co2 goes up and O2 goes down you build H+ and your go through acidosis



Alkandosis for opposite

When O2 binds to hemoglobin it is no longer exerting a partial pressure so there can be more gradient

If we didnt have hemoglobin we would need a cardiac output of 67 L /min instead of 5

At low Po2 RBC changes shape and becomes a releasing molecule

Emphasema is both restrictive and obstructive

Oxy-Hemoglobin relationship

with more Po2 there is more Hb saturation

The Bohr effect

with a more acidic lower pH it has to work harder



it is sigmoid because cooperatotive binding, when more o2 bind the more it wants to bind.

23 DPG - glycolysis metabolite means there is a greater need for oxygen

which also causes a right shift



Right shift means more oxygen is needed

CO causes a left shift

holds on to the O2 even harder because full binding

How a glomus cell in coratid body works

When you have a low P02 the Kchannels close which depolarizes the cells and Ca2+ channels open



More Ca enter cells and neurotransmitters



Hydrogen in the capillary cannot to through blood blain barrier

Bronchoconstricion

when you breath something bad in you breaths become shallow so the bad thing doesnt get in

Amino acid determines the hemoglobin shape


oxygen modulates and changes the shape to make it release instead of bind

when there is a right shift the hemoglobin is being more generous with the oxygen because there is a local factor telling that you need more oxygen

hemoglobin bound to oxygen is red and blue if it is not

Co2 is lipid soluble can readily dissolve in RBC


Co2 goes in and binds to amino groups in hemoglobin (not where the oxygen binds)


As o2 is leaving the cell co2 has a higher affinity to hydrogen binding


Co2 doesnt saturate because we can continue to shift it to HCO2

At the alveoli we are promoting the carbonic anhydrase to shift to the left so we can blow off the Co2

if you have local hypoxia you will end up with global hypoxia and that is dire to the right side of your heart

What the hell is a hormone?

a chemical signaler secreted into the blood or intersistial fluid by on cell or group of cells and has physcioligcal control effect through a specific receptor



cytokines go intracellular so not considered a hormone, they can be called a paracrine agent

What are some important characteristics of hormones?

Potent of small concentrations - because they amplify


Regulate biological functions


Work through receptors that are specific

The gene is a lot bigger then the active peptide, you make a molecule that is much bigger and inactive, there has to be post translational modification until it is biologically active

done by cleaving some things off


adding some carb groups to make a glycoprotein

Activation of AE produces multiple cAMP

Tysosine Kinase doesn't need a g protein it phorylates already

Peptide hormones are fast acting but short lasting

What makes 2nd messenger so fast is because it turns on a protein that is waiting


when they unbind peripheral enzymes can get rid of them pretty fast



Gene transcription takes a hella long time

Steroids hormones interesting facts

they are lipid so simple diffusion, which means they need to bind to a protein to travel in the blood. They have a longer half life because these protects them from enzymes



Cytoplasmic and nuclear receptors


makes it easier for RNA transcrptase to find the promotor



Cortisol - can go the opposite thing, blocks promotor region so when you get a misquito bite you dont get inflammed.

Since steroid hormones are biochemically connected, if you have high testonerone you will also have high of everything else so if you take steriods take a aromatase or you grow

boobs

Upregulation


The number of the beta adrenoreceptors in response to T3 - it tells the heart to upregulate their beta receptors which increases the sensitivity to increase heart rate



Because it is saturated with ligands?



What is down regulation

Down regulation - decreased number of receptors


Decrease tissue sensitivity


Down regulation of GH receptors with chronic stress - when you are young and you are stress you can down regulate the Growth hormone to save your energy for survivial. It will make u a midget

If you dont have a lot of ligand a cell can upregulate to see if something is out there


A cell can also take in receptors if a cell is being bombared

Upregulation can occur before more hormone release.

Synergism

Combined effet is greater than the sum of indivial effects


Glucagon and epinephrine

Permissiveness (to give permission)

Need second hormone to get full effect


Hormone A does the job Hormone B doesnt do the job but it does something that makes Hormone A to do the job.


Cortisol is needed for glucagon to do its job correctly.


Kushings disease too much cortisol so though are hyperglycemic

Thyroid hormone is lipid soluble so it goes into cell and increase gene expression for upregulation of beta receptor to increase lipolysis

UPregulation is a major way that permissiveness occurs

Hypothalamus - talks to both anterior pit with portal system and post pit with an axon

Stimulus - level of hormone


Sensor - monitors hormone level


Input signal - sensor sends a signal to center


There are often times with endocrine cells plays more than one role


Parathyroids cell is the receptor integration center and 1 more

Feed forward mechanism is a varible that anticipates the thing by negative feedback



Ex. Stomach stretch but you blood glucose levels have yet to gone up yet. But it will eventually so it like warns them to get going

Negative feedback - normally it all starts in the negative thalamus

Pituitary looks like a ballsack and sits in a bony cavity.


Posterior pituitary - embyonic extension of the hypothalamus because it is where the axons from the hypo terminate


releases ADH


Oxytocin



Hypo can make hormones and pack in vesicles to put it into capillary

Axis refers to 3 systems to work together to produce something.



Hypothalmus produces releasing hormones that go through a portal system that goes to anterior pituitary



ANT Pit will produce the hormone in response to the hormone the hypo released



Then your peripheral glands will secrete the hormones

Typically the both the 2nd and 3rd hormone in the axis can give a negative feedback

IGF-1 (insulin like growth factor) its a mitogen tells cells to divide


before puberty is makes you grow after it just maintains your bones


Growth hormones before puberty - gigantism you be like 8 ft tall


after puberty - acromegaly - you dont get taller but bigger

Cortisol

Hypo - receives a stress and releases Cortisol releasing hormone


Ant pit - releases



Function of Cortisol


it makes sure you dont lose vasoconstriction or you die


inhibits inflammation so you can live before you deal with some inflammation..


The genitalia and internal tubing are all the same early stages of the embryro, the only time the male SRY gene is expressed in the embryonic stage which leads undifferentiated cells to turn male and female structures to disappear

Leydig cells produce testosterone which makes female structures die

Semineferous tubules then the epididymus (swim school)

Prostate gland acts as a donut around the urethra so growth in it can cause increase resistance

There is a valve that when semen is going through it permits urine from going in

Desending balls is important because temp


being outside decreases temp but also the heated blood from artery will transfer heat to the vein leaving the scrotum

Spermatogonium - stem cells that can undergo mitosis (reproducing themselves that is why they are called stem cells)

They are located at basal as they differenate they get closer to the lumen of the semiferous tubules until they turn into spermatozoa.


There is no blood in the semitub so sertoli cell take care of it. There is a blood-teste barrier


Leydig cell product testosterone which can simply diffuse

1 cell produced both FSH and LH in the ant pit, named this because endocrine studied females first

FSH has receptor on sertoli cells, helps sperm grow and tell them to make androgen binding protein(keep testonrone local), and they also create inhibin which inhibits FSH

LH binds to leydig which produces testosterone, also goes to rest of body to help you grow

At age 8 Kisspeptin makes your brain think you have less testosterone


First sign of puberty in boys bigger balls, then penis

Progesterone normally lead to differentiation


Endometrium is the inner layer of the uterus that is hormone sensitive

Endometrium gets sweeped off with menses

Oogonia - mitotic division and producted 2-4 million oocyte



Every girl born with a limited number of oocytes and then go through mitosis and stop until you hit puberty. At puberty they fully mature a few and ovulate them, when menupause no more

Primordial follicles - primary follicles

Theca cells produce androgen precursor used by granulosa cells and diffuse into granulosa cells which have aroma cells to make estrogen

During secondary follicle they develop fluid filled cavity called antrum it is good because it lowers diffusion distance for oxygen, and glucose to enter


The whole follicle is not going to be ovulated, only the oocyte with its crown of cells (corona radiada)

The left over follicle from ovulation gets worked on by LH to make corpus luteum

Menstrual phase - when endometrium gets sluffed off because no hormone to maintain it

Proliferative phase - FSH is stimulating the follicle to produce estrogen which makes the follicle grow


Also makes endometrium grow and it produces progesterone to make glycogen for the fetus

LH surge gives signal for ovulation

Secretory phase - when the uterus turns into a gland

Progesterone negatively feedbacks producing another egg

No ovulation with first mentuals because there isnt enough estrogen for positive feedback to cause LH spike for ovulation

Estrogen does not directly affect the hypothalamus


Estrogen affects kiss peptin

Estrogen low it increases GnRH


When estrogen is medium and increasing there is still negative feedback but it affects kiss peptin neuron to decrease GnRH


When estrogen is very high we set off positive feedback which increases GnRH because it activates another neuron that releases kiss peptin



Most of the follicular phase the system works on a negative feedback


1-2 days before ovulation it switches to positive feedback

Progesterone makes the uterine become a exocrine gland which excretes glycogen on top of the endothial so u get a build up (secretory phase)


also cases smooth muscle relaxation in case implantation occurs

progesterone inhibit ovulation and follicle formation



by introducing exogenous estrogen you dont produce enough estrogen endogenously to get a spike in GnRH activing that 2nd thing

Iodination make thes molecule more lipid soluable so T4 is more and has a higher half life

What does testosterone do on the body


increase muscle mass, deepens voice,

if you take a steroid you gotta take a enzyme inhibitor or else you grow boobs and such.

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