A&P test 1 Flashcards

1
Q

define homeostasis and summarize homeostasis

A

the conditions inside the body are maintained at near constant conditions by many different way

summary: body is constantly changing in order to maintain a constant internal environment regardless of the changes going on like metabolism, changes in food, or environment. changes in physiological systems can alter drugs (anesthesia) in unhealthy ppl. and drugs can alter physiological systems

for this class our healthy pt is 70kg, 30 year old male

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2
Q

internal environment

A

internal environment is everything under our skin. we have about 35 trillion cells and they have a constant condition in the fluid that surrounds it. in order for the cells to work the environment must be in homeostasis

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3
Q

snow storm example of homeostasis

A

our body wants to maintain the temperature around 37 C. so if you go out in a snow storm your internal body temp will start coming down and the body senses that and does mechanisms to bring it up aka shivering

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4
Q

homeostasis in anethesia

A

during anesthesia we take the homeostasis controls offline aka the sensors that regulate BP, blood gases, temperature, etc. so we have to do the work for the pt body in OR

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5
Q

cells in homeostasis and how they stay constant

describe input, output, and waste products

A

cells need energy compounds(sugar, oxygen, and fats) to buffer the pH and control the body’s constant condition

all in all homeostasis in cells involves many different processes and some are metabolic and some are more specialized

what goes in must come out

input(energy compounds)–> output(work or heat) and then waste products(CO2 is byproduct of metabolism, protons and water, urea)

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6
Q

role of kidneys, GI, lungs, heart in homeostasis

A

kidney- responsible for maintaining BP at normal level and extracellular buffering and electrolytes

GI- replaces nutrients in the blood consumed by cells

Lungs- regulate blood gases

Heart- 2 pumps separated by septum that are responsible for ensuring we get a decent amount of gas exchange at lungs and the peripheral part of CV system is supplied with proper nutrients

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7
Q

tissue example of homeostasis

A

the tissue is the controller responsible for the blood flow within the CV system. blood coming in through the artery into the tissue then that fluid is being brought in by the CV system is carrying nutrients that cells need to use and then the veins remove the metabolic byproducts. The AMOUNT OF BF that goes through a tissue is determined by the metabolic demands of the tissue.

so if cell actively burning through oxygen and glucose, the composition of the fluid surrounding will change causing a deficiency and the tissue senses increased metabolism and blood flow increases. so if increased rate of metabolism, environment will change, and CV system will respond by increasing perfusion and bringing that environment back to normal levels

tightly controlled so cannot increase blood flow easily if not increase in metabolism

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8
Q

simplify negative feedback

A

body keeps processes to maintain homeostasis in check through process called negative feedback. almost all systems are managed via NF. the more important of a function the more sensors and more counteracting mechanisms

sensor out in periphary detects changes such as ph changing, O2, CO2 levels changings, etc. and that info is fed to some kind of controller and that controller does things to counteract change
ex) BP drops–> sensors–> nervous system–> squeezes blood vessels–> BP increases

initial change–> sensors(periphary)–> controller(corrects/counteracts problem)–> solution is always NEGATIVE to original change. change is negative to stimuli.

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9
Q

example of negative feedback
thermostat, BP, CO2

A

1) thermostat
thermostat set to 70 and if environment goes above or below then the thermometer(sensor) senses this and signals to the thermostat to turn on AC or furnace to raise or lower temp and then it stops once temp back to normal

2) BP
DECREASED MAP–> INCREASED sympathetic outflow so releases norepi–> MAP back to normal

DECREASED MAP–> drop PARASYMPATHETIC outflow–> MAP back to normal

DECREASED MAP–> INCREASED AVP/ADH(vasopressin and antidiuretic hormone)–> increased MAP

DECREASED MAP–> DECREASED ANP-> increased MAP

3)CO2
if CO2 levels in the blood go up then brain cell going to increase ventilation to get it back to normal

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10
Q

explain/simplify positive feedback

explains oxytocin and blood clotting cascade example

A

sensors sees a change–> feeds back to controller–> controller amplifies the change it is seeing–> should stop at certain checkpoint

vicious cycles- when positive feedback has run completely out of control.the only thing thats going to stop it now is severe organ injury of death. normal positive feedback systems are not thought of as vicious cycles but when positive feedback system is ran out of control and its pathologic thats when its a vicious cycle.

oxytocin) during labor the uterus contracts and pushes fetus towards cervix and when the cervix is exposed to this pressure from the fetus from the contraction it STRETCHES. the cervical stretch tells the brain to release oxytocin and oxytocin acts on smooth muscle in uterus to cause even more contractions on top of the already there contractions which stretches the cervix more which releases more oxytocin. so BASICALLY, contractions get stronger and stronger closer to birth until finally BIRTH and that is the checkpoint that shuts down whole system. cervix back to normal and oxytocin levels back to normal

blood clotting pathway) when endothelial cells in the blood vessels are harmed it starts bleeding and the coagulation factors are exposed which promote platelet plug formation. SO BLEEDING PROBLEM BUT PROBLEM RELEASES THINGS TO FIX IT. as the plug forms more and more platelets aggregate and make a clot and TXA2 vasospams etc. so when bleeding stops that is the checkpoint. this can get out of hand if the clotting doesnt stop then you get clotted blood vessel

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11
Q

Bad pathological positive feedback examples

A

1) severe hemorrhage
if we lose a lot of blood our BP is going to go down and coronary blood blood flow will decrease also. If coronary blood flow is insufficient for metabolic demand of heart then heart will drop CARDIAC OUTPUT which drops BP even more so then vicious cycle
2) sepsis
sepsis is widespread infection and cells are dying at faster rate than body can manage. when cells die they release their toxins(metabolic by products, potassium) into the environment and they come in contact with neighboring cells. so then these cells are dying bc of toxins on top of body fighting sepsis
3) severe acidosis
a little bit of acidosis the brainstem figures out whats going on and increases breathing but when we have severe acidosis, the central nervous system can be affected so much that that reduces respiratory drive. if respiratory drive is reduced then that accelerated acidosis and makes us even more acidotic
4)kidney failure
as we get older our million nephrons start to die(around 45-50) and with less nephrons this increases the load of the still living nephrons putting a heavier burden on them so then they die at faster rate. as more die the rate increases and increases. older and older you get the faster the rate the nephrons die bc of the burden the ones remaining have placed on them as the others die. results in renal failure

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12
Q

describe losing 1 liter of blood (20%) versus 2 liters(40%)

A

compensated shock negative feedback works well(in healthy person) bc our body can usually handle it. 1) our pump effectiveness is initially reduced when we lose 20% and BP will go down bc system is less full and bc less output. and the system should be back up in couple of hours bc our blood vessels will tighten and the heart will try to pump harder and we have massive fluid shifts to help our cardiovascular system out

decompensated shock positive feedback leads to death bc negative feedback insufficient; gain insufficient. if we lose 40% of our blood and not next to hospital then despite our BP controllers they are inadequate to deal with this. so then pathologic feedback kicks in and that outweighs negative feedback systems that are usually in charge of this. LOOK AT HEMORRHAGIC POSITIVE FEEDBACK RESPONSE

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12
Q

describe the cell, tissue, organ

A

-smallest living unit of the body and our body has 35 trillion human cells and 25 trillion are RBCs
-cells can sustain own lives with stuff inside them
-equipped with enzymatic machinery to put ATP together for energy
-most cells specialized aka INTERNAL CONTENTS DEFINES FUNCTION. ex) lung cells thin and narrow for gas exchange
-shield us from outside environment
-tissues are collection of cells that are like minded and work together to form function
-organs are collection of different type of tissues. responsible for maintaining internal environment of body

cell can move
-flagella–> move a cell around its environment. moves actual cell
-cilia–> move stuff around inside of cell

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13
Q

cell replication and RBC replication

A

most cells are capable of replication bc have DNA and normal machinery able to divide and replicate when cells die. if cant replicate then close to progenitor cell that can do task
ex) RBC does not have nucleus or genetic material to create copies of themselves so close to bone marrow with progenitor stem cells. RBCs last 90-120 days

neurons have hard time replicating. dont do it fast

cardiac cells are very slow to replicate

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14
Q

what are phospholipids

A

when enough phospholipids they aggregate to form bilayer to make themselves happy

hydrophillic head behaves well in water and is charged. Glycerol(carboxyl) and phosphate part

hydrophobic- anything that is uncharged is usually a fat. hydrogen and carbons together

specialized phospholipids are when something special is attached to phosphate head: cholesterol

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15
Q

point out organelles in cell
ribosomes
smooth ER
rough ER
golgi appartus
nucleus

A

1) smooth ER
2) rough ER
3) mitochondria
4) lysososome
5) nucleus
6) gogli apparratus

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16
Q

inside of cell

A

70-85% water except for adipose cells bc they are fatty and dont have high internal water content

cystoplasm: fluid part of cell where lot of chemical reactions take place

nucleus: barrier to keep DNA packed up and secure and out of reach of viruses and bacteria. where genes are stores

genes: can be turned on and off. carries instructions on how to make lipids or proteins

nuclear wall: separation btw cytoplasm and nucleus; double phospholipid bilayer. allows in steroids(through pores)to affect gene transcription and turn on stress response proteins.

structure- internal support needed to give and keep shape. structural components like filaments or proteins produced inside cell to prop it open and give it certain shape

organelles to know
mitochondria
lysosomes
peroxisomes
golgi apparatus
endoplasmic reticulum

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17
Q

describe ribosomes

A

-take amino acids and stick them together and use that structure to build proteins.
-located on rough ER. some are free floating
-where PROTEIN TRANSLATION OCCURS

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18
Q

describe the making of a protein and how vesicles are used

A

proteins that are formed at the RER are concentrated in storage vesicles and sent for processing and modification in GA. after processing, the proteins are typically active and ready to use so the modified proteins go around cell in vesicles

vesicles: specialized organelle that are storage places for proteins until ready to need
transport: move proteins within the cells
secretory: move active proteins outside of cell

1)nucleus contains DNA and transcribed into RNA 2) RNA leaves nucleus and interacts with ribosomes3) ribosomes translate the tRNA into mRNA to form proteins by linking AA(95% of this occurs in RER and 5% occurs in free floating ribosomes in cytoplasm but those dont get packaged) 4)go to GA for processing and packaged into VESICLES

RNA has some nucleotides in a certain sequence and that sequence dictates which AA get stuck together and in what order. SO ribosome moves RNA along its center and grabs AA from cytosol and attaches them to form a chain and typically folds. sometimes its modified at GA to fold more and be manipulated. the shape we get consists of strings of AA that are contorted and folded in a way that provides functional protein

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19
Q

describe ER
smooth and rough

A

ER: extension of nuclear wall. where fats and proteins are produced. a compartment within the cell that can used to store things like CALCIUM

rough: rough bc ribosomes(protein synthesis). takes infomation and forms proteins from it

smooth: does not have ribosomes. specializes in lipid production(cells need lipids to complete their day to day tasks)

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20
Q

golgi apparatus

A

close in proximity to ER and processes proteins created by rough ER. POST TRANSLATIONAL PROCESSING.
post translation: sometimes proteins modified so may fold differently, parts cut off. we normally alter proteins after making them and happens in GA

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21
Q

water inside cell(cytoplasm)

A

-70-85% water except for fat cell
-affects acid/base balance, electrolytes, and energy compounds
-all the processes happening al the time in the body keep these conditions fairly constant and if conditions change significantly then the chemistry doesnt work as predicted

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22
Q

mitochondria

A

-help us efficiently produce ATP from energy compounds and oxygen
-mitochondrial DNA separate from host DNA
- inherit all mito DNA from mother
-dozen or 20 sets of mito DNA which gives us variability with our body’s ability to inherit energy producing organelles that are super efficient bc if only inherited one set then might not be enough to get job done

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23
Q

lysosomes

A

-digestive organelle good at recycling bc…
-acidic environment that destroyes proteins and then that releases AA to be resused in cytoplasm

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24
Q

peroxisomes

A

-oxidizes
-can destroy proteins but better at processing toxins like ethanol
-liver contains peroxisomes that degrade alc and use oxidative stress to destroy and use oxidation reaction to destroy
-oxidation is what happens to iron if you put it out in oxygen for too long
-the cell can use oxidation reactions to destroy things that need to be broken down
-CATALASE–> enzyme present in peroxisomes that are used to oxidize compounds

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25
Q

sugars within cells

A

GLYCO=sugar group attached to something
CARBOXYL= starch(sugar)–> carboxylhemoglobin is example of sugar getting stuck on hemoglobin in blood–> the more sugar stuck to it the less functional it will be
-floating around cytoplasm to be used for ATP/energy. started in cytosol with anaerobic metabolism. GLYCOLYSIS typically happens within fluid and that means glucose being consumed to create ATP
-GLYCOPROTEINS–> sugars stuck onto proteins and sticking out of cell wall for IDENTIFICATION PURPOSES(specific shape) aka humans and bacteria produce ID tags that are different so sugars help cell identify self from non self and help immune system attack
-sugars also have specific NEGATIVE charge that repels proteins floating around that may also have negative charge
-GLYCOPROTEINS STRUCTURAL FUNCTION–> used to enable cells to attach to each other and hold cells together bc STICKY
-STICKY can be bad thing–> think hemoglobin example
-although sticky can also repel bc of negative charge
-kidneys use sugars to make sure we dont filter as much protein as we would–> look at Glut 1?

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26
Q

cholesterol

A

-lipid soluble not water soluble
-used to general all sorts of signaling compounds
-OH part is exposed to water to grab onto things

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26
Q

fats in cells

A

-related to cell function also; lipid soluble compounds also
-cholesterol and arachidonic acid
-hang out in cell wall bc thats where comfy bc non charged

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27
Q

soluble vs insoluble

A

soluble= electrolytes, proteins somewhat soluble, carbs bc charged, and gasses EXCEPT NITROUS, buffers

insoluble= cholesterol aka fat, steroid hormones, lipids, and nitrous gas

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28
Q

Body fluid compartments

A

TOTAL BODY WATER= 60%

ICF= intracellular; water inside of cells; largest internal body compartment. TWO THIRDS

ECF=water outside of cells so includes plasma and interstitial fluid(if see intercellular then thats ECF). ONE THIRD
-plasma= 1/4-1/5 of the ONE THIRD; fluid thats found within entire CV system(does not include volume of blood cells)
-interstitial= 3/4-4/5 of ONE THIRD; outside of cells but outside of CV system. useful when we lose bunch of blood and out body shifts fluid from interstitial to compensate

ex) take 60% of 70kg male and that gives us 42 kg of overall body content and 1L of water=1 kg. 2/3 is ICF and 2/3 of 42kg is 28. and then what if i ask you what the plasma volume then 1/3 of 42 is 14. 1/4 of 14 is 3.5 which is answer

steady state is the conditions are kept fairly constant but the steady state of ICF and ECF are different. much different from equilibrium

29
Q

Barriers

A

cell membrane is barrier btw ICF and ECF and is fairly impermeable barrier that separates cell from their outside environment. does not let charge compounds through without some type of regulation

capillary membrane separates CV system from interstitial and is fairly permeable bc of endothelial cells allow small charged ions to move in btw plasma and interstitial fluid except in BRAIN where they are very tight. capillary membrane still tight enough for proteins not to leak out of the CV system and that is good bc if we lose proteins in CV system then we can lose all sorts of volume and difficult to manage BP

30
Q

body fluid compartment math

A

write it out

31
Q

electrolytes and ions ICF vs ECF

A

Left 2 columns plasma ECF and interstitial–> remember leaky barrier so not much difference
right column is ICF intracellular

32
Q

difference of protein concentration ICF vs ECF

A

ECF- usually does not have difference btw plasma and interstitial but proteins do have difference bc not a lot of proteins interstitial but lots in plasma to keep blood in right places. plasma has 5x amount of proteins than interstitial

ICF vs ECF
the ICF has more protein concentration bc proteins made and used inside cells more than outside. major plasma protein is albumin(about 80%)

Amino acids build proteins so their concentration will be higher inside cell than outside cell and also when proteins are replaced and broken down this releases AA into cell

33
Q

sodium ICF vs ECF

and chloride

A

cation, positively charged
can be used to quickly determine osmolarity by doubling ECF concentration and thats around osmolarity

ECF- most predominantly positively charged ion in our ECF. btw 140-142

ICF- much much lower; 1/10 of ECF concentration of Na

hint: blood is salty aka more sodium in blood than in cells

chloride- dont need to know number but know it follows distribution of sodium. primary anion in ECF

34
Q

potassium in ECF vs ICF

A

moves in opposite direction than Na; important in how heart is going to function

ECF- normal is 4

ICF- usually about 30x more than ECF so if ECF 4 then ICF 4x30 is 120.

35
Q

Calcium in ECF vs ICF

A

dont need to know exact calcium number.
neuro and muscle cells rely heavily on Ca influx bc Ca is what gives us muscular contraction.

ICF- HARDLY ANY CALCIUM FLOATING AROUND INSIDE TYPICAL CELL so gives us number 0. cells use Ca as signal to turn on so cant be turned on all the time. at rest Ca levels low and then nuerotransmitter hits and it spikes which turns cell on and then Ca is removed and cell shuts off quickly. when body needs Ca it is packed into secretory vesicles released from ER into cytoplasm and transported outside of cell. Ca movement within the cell occurs through pumps on cell wall and ER

ECF- Ca levels outside of cell much MUCH higher than inside of resting cell. relative concentration is 10000:1

36
Q

magnesium in ICF vs ECF

A

opposite of Calcium so high inside cell versus outside cell bc Mg good for helping us with chemical reactions used as a cofactor in the intracellular reactions.

dont need to know number

37
Q

Bicarb in ICF vs ECF

A

-secondary anion in ECF(after chloride)
-primary ECF buffer so makes since higher concentration outside than inside
-levels managed by the kidneys to help compensate acid base balances

38
Q

phosphate ICF vs ECF
and phosphorylation summary

A

-INTRACELLULAR BUFFER so found in higher concentrations inside vs outside
-can also attach or detach from proteins to regular activity level; when phosphate added to target can either turn it on or off depending on target–> phosphorylation
-ENERGY STORAGE SYSTEM bc–> our primary energy currency within cell is ATP and to create ATP we stick phosphates onto adenosine and as we consume ATP we pull phosphates off. each time we add phosphate to ATP it requires energy and each time we pull it off it releases energy
-also tend to toggle switches that turn things on and off within cell

phosphates three primary functions
1) ICF buffer
2) on and off switch
3) energy storage system

39
Q

creatinine in ICF vs ECF

A

-mainly found in muscle cells where plays role in muscle contraction. we use ATP for muscle contraction so when the muscle needs to contract the force is generated by pulling off phosphate from ATP which releases energy
-in skeletal muscle cells you can get phosphocreatine by sticking phosphate onto creatine and when doing strenuous activity the muscle cell drives contractons by pulling phosphate from creatine
-super creatinine is also good energy source behind ATP so if muscle doing lots of work than will pull phosphate off of creatinine before breaking down ATP
-only have small amount of creatinine so depleted quickly
-so more inside than outside

40
Q

Lactate ICF vs ECF

A

metabolism occurs inside cell so lactate(by product of metabolism) is produced inside cells so concentration higher in ICF vs ECF

41
Q

ATP ICF vs ECF

A

so valuable that it is not found outside of cells and only leaves if trio of phosphates gets pulled outside to do something that requires lots of energy. then ADENOSINE can exit the cell(probs bc lots smaller than ATP) to help increase blood flow to area thats highly metabolic activity. adenosine opens up blood vessels which helps perfuse active tissues and take care of metabolic requirements

42
Q

corrected osmolarity and total osmolarity ICF vs ECF

A

-consistent btw ECF and ICF
-total(predicted) osmolarity- tells use how much of the dissolved compounds total are in the fluid sample. so if we measured all the concentrations of every compound that found in the fluid and add them up that will give us the total osmolarity(chemical osmolarity plus predicted osmolarity). should be close to 300
-in biological solution not all these items will be freely dissociated with one another like Na and Cl
-biological osmolarity is lower than predicted osmolarity so the CORRECTED osmolarity is 280-283 bc some of those ions are bound and not free
-osmolarity is one things that remains consistent across different compartments bc water likes to move freely btw compartments
-water moves freely; ions can move freely across capillary membranes but not cell wall

-water movement corrects when there is a change of stuff thats dissolved so evens out osmolarity
-good example of fluid shifts bc of this water moving is the cranium bc worried about Na levels in blood with high ICP and not wanting it to move into cranium bc then pressure builds up.
-total osmotic pressure is over 5000. our blood is 100 usually(so very large). so the movement of water helps us not explode

dr schmidt answer to my question
all the compartments have the 5000 pressure but what is making us not explode is the diffusion of water. but when we have hyponatremia that can cause pressures to not consistent throughout body

43
Q

sugars in the cell wall

A

-cell wall is primarily phospholipids but got stuff adjacent to them like proteins
-sugars stuck to proteins are GLYCOPROTEINs
-sugars stuck to phospholipids are GLYCOLIPIDS
-glycoproteins and glycolipids together are called GLYCOCALYX(sum of all external sugar structures)
-glycocalyx is the root of all these external sugar structures that body uses for immune system aka sugar on outside of cell doesnt look right then immune system takes extra look
-if high blood sugar then sugars can get stuck on cell wall so ppl with high blood sugar usually have massive inflammatory response bc the glycocalyx doesnt look right on that cell

44
Q

cholesterol in cell wall

A

-precursor molecule for stuff we need to synthesize
-stuck into cell wall and very lipid soluble(the carbons and hydrogen) except for OH groups(polar part sticking out for body to grab onto)
-lipid that doesnt like to hangout in water bc fatty and uncharged so hangout in cell wall so if body needs it it just grabs onto it(from OH group) and metabolize it
-dont want to go overboard with amount of cholesterol bc cholesterol is flat and RIGID and if too much can affect CV system bc blood vessels less stretchy

-reduces cell wall fluidity: stiff
-cholesterol rigid in normal temps (37C) but if frozen or lower temp then make it smoother like ice cream bc increase membrane fluidity
-if endothelial cells become rigid then atherosclerosis then heart problems bc blood vessels stiff

45
Q

proteins in cell wall

A

1) GATEWAY of allowing stuff across cell wall
-channel, pumps, pores
2) SIGNALS to help COMMUNICATE to get stuff done
-usually receptors in cell wall can handle neurotransmission for message to get inside cell
3) ENZYMES
-catalyze reactions; sometimes apart of receptor and sometimes close
-G protein–> 7 transmembrane spanning receptor with outward portion and then inward portion in proximity to subunits. some kind of compound binds to receptor and that receptor changes a bit which will change the intracellular components and will turn something on or off

46
Q

stuff in cell wall picture and performance of cell wall

A

-barrier to separate what inside of cell versus whats outside
-adhesion
-ID tags for immune system to regulate activity
-storing stuff(lipids, carbs, proteins, enzymes, precursor molecules) especially fatty molecules bc dont like to hangout in water

47
Q

cholesterol metabolites

A

-usually used as primary feed compound to produce our sex hormones that look similar
-different enzymes to manipulate the compound and need each enzyme in order to produce it and if missing just one enzyme not able to make the metabolite

Stuff cholesterol can be turned into
1) sex hormones top of list
-estradiol and testosterone go through bunch of manipulation
-progesterone would be third most active sex hormone
-androstenedione is precursor to testosterone–> baseball players were using this

2) stress hormones
-made at adrenal gland which goes through a lot of cholesterol
-cortisol and aldosterone which look VERY similar just an OH group is different
CORTISOL- has OH group
-reason why matters? CROSS REACTIVITY–> look so similar there is no distinct activity aka activity isn’t regulated to just one receptor bc they can use each others. for example, if not enough cortisol around, aldosterone can be used to interact with receptors
-body needs regulation of this issue

48
Q

cholesterol floating around in body

A

-body has capability of making lots of cholesterol
-usually creates more than it needs
-exogenous cholesterol is 1/5 of total cholesterol in body, 20% by diet
-80% is produced by own body
-so if you plan on tackling cholesterol you need more than just diet–> you need statin to regulate cholesterol
-statins interfere with whole cholesterol synthesis pathway-> reduce amount of cholesterol thats being produced by endogenous system

49
Q

Acetyl-CoA

A

-generic big kind of sugary compounds that the body can take to use as substrates to build other things(cholesterol falls into this category)
-can be used to make more ATP from glucose and oxygen

50
Q

specialized phospholipids

A

-specialized phospholipids stuck in cell wall just like the basic phospholipid but have something special on the head.
-involved in
1) surfactant- break surface tension on the fluid thats on the inside of the lungs and if dont have normal surfactant then big problem. collection of all the specialized phospholipids mentioned below and lots of proteins play some role in assembly of surfactant
-phosphatidyl compound= phosphatidyl refers to phospholipid and then the specialized compound is attached to the end

and STORING THINGS
1) phosphatidyl inositol(PI)- used in smooth muscles that regulates contraction–> IP3 is triphosphate that makes smooth muscle contract and the parent compound if PI which is a storage compound stuck in the cell wall. when smooth muscle needs to turn on this liberates some inositol in the cell wall and we have enzymes that work on that inositol and eventually gives us that muscle contraction

2) phosphatidylcholine (pCh)- choline another storage compound in cell wall useful in signal transduction. used to assemble acetylcholine
-acetylcholine very important in cell signaling and signal transduction

3) phosphatidylethanolamine

4)phosphatidylserine(cytosolic)- immune marker and in healthy cells should only have them INSIDE cell. FACING INWARD. and if immune system see serine facing OUTWARD then we will destroy whatever it is attached to
-we keep serine facing inward with enzyme FLIPPASE. this enzyme stuck in cell wall and just flips serine when facing outward. requires ATP so will have supply
-dysfunctional flippase–> a cell thats unhealthy or going to die usually starts running out of ATP so dont have energy for flippase so more and more serine outward facing and immune response comes and kills cell which is good but when widespread can be bad bc all inside now littered into environment

51
Q

sphingomyelin

A

-not specialized phospholipid but stuck in cell wall
-fatty compound that body uses to construct myelin for nervous system

52
Q

prostaglandins and TXA2 derivatives in arachindonic acid

A

Really important derivatives that are made from arachindonic acid and produced the ENZYMES COX1 and COX2(cycleoxygenase)

Prostaglandins- PGE2, PGI2, PGD2
-ramp up pain signals in body; not pain signals though–> INCREASE PAIN SENSITIVITY
-so get us not to notice pain if stop the pathway

TXA2
-thromboxane which is good thing that mediates healing in blood vessel injury–> if you slice blood vessel then you activate coagulation cascade and this liberates TXA2 and works on vessels to tighten them up and squeeze them. this reduces the blood flow and allows it to repair. so initiates VASOSPASM which we want in this case so it heals

52
Q

arachindonic acid

A

-really really long fatty chain that hangs out in cell wall and our body manipulates it to accomplish different tasks and is parent compound to many different stuff
-just like cholesterol some parts are polar like the OH group and double O=O and thats probs the part that is sticking out of cell wall

prostaglandins, TXA2, leuokotrienes, HEETS and EETS

prostaglandins and leukotrienes happy hanging out with water so not just stuck in cell!!!!!!!!! bc dont look too much like arachindonic acid

53
Q

COX1 and COX2

A

1)COX1 and COX2 enzymes catalyze 2 chemical reactions back to back where arachidonic acid is turned into a precursor compound which is PGG2 and then PGH2. aka cyclooxygenase enzyme speeds up TWO REACTIONS in a row to get PGG2 and PGH2

2) from there you have specialized enzymes that direct these compounds into different pathways to make different prostaglandins or TXA2. so depending on what enzyme is around that dictates which prostaglandins are produced

COX1
-widespread throughout body
-less pain control but still useful
-aspirin works on both but irreversible blocker of COX1 so BLEEDING problems–> remember TXA2
-tylenol and NSAIDS; tylenol not anti inflammatory but tends to target neurons in our body useful for pain control and stays away from bleeding aspect bc doesn’t target much outside nervous system

COX2
-usually the one that gets turned on in response to pain; really strong pain medications
-more specific COX2 means better at treating pain; strongest you can buy OTC is naproxen bc mostly COX2
-COX2 inhibitors pulled off market 20 years ago bc not only good pain med but also COX2 involved in keeping KIDNEYS HEALTHY and helping HEART MAKE CORRECTIONS after periods of ischemia
-COX2 better at keeping things away from hemorrage and GI bleeding problems
-ex) vioox was COX2 drug and ppl taking it having cardiovascular events…. old people finally off couch bc not hurting and then doing something havent done in a while then bam heart event(caveat)

aspirin and NSAIDS work on both

54
Q

Leukotriene part of AA pathway

A

-important effect on our immune response
-LTC4, LTD4, LTE4
-involved in immune mediated inflammation
-inflammation usually bad process bc makes lungs swell up and glands act goofy–> so if we can manipulate this pathway we can stay away from these problems
-ex) singulair is leukotriene receptor antagonist and the enzyme that drives it is LIPOXYGENASE(LO)
-LO takes Arachadonic acid and turns it into leukotrienes

55
Q

HEETS and EETS pathway of arachodonic acid

A

-really large fatty compounds that dont exist for long periods of time
-short lived bc tend to be involved in acute renal failure and other important disease processes
-not a lot of drugs attack this pathway and bc difficult to manipulate bc these compounds dont live long in water and unstable and tend to stay in cell wall

56
Q

simple diffusion

A

-the process of something moving across the cell without any help at all
-straight shot without using energy
-movement dictated by concentration(chemical) gradient or for electrolytes concentration gradient and also electrical gradient–> electrochemical gradient-> potential to move down chemical gradient or electrical gradient

GASSES
-can move across cell membrane without any help bc tend to be lipid soluble and small

CHANNEL PROTEINS
-can be ion specific and good for electrolytes to sneak through
-smaller charged particles need to get through
-going to be specific for an electrolyte or charge
-as long as no binding, releasing, or conformation change then simple diffusion
-allow water to cross cell wall bc water is permeable

WATER SPECIFIC CHANNELS AKA AQUAPORINS(AQP)
-area in body that needs to regulate its water permeability will probs going to have few ion channels bc make it hard to regulate water permeability
-want to regulate it by controlling number of aquaporins

-water can get specifically or nonspecifically

57
Q

facilitated diffusion and examples

A

-down the net movement and does not need energy BUT CONFORMATION CHANGE
-binding of compound–> conformation change(flip)–> releasing of compound on other side
-go both ways not just one way–> determined by concentration gradient
-98% of glucose movement across cell happens this way

58
Q

Active Transport

A

-either want to make transport go faster or want to put compounds where they don’t want to be
-requires energy

ex)Sodium Potassium ATPase pump which is enzyme and Calcium pumps and proton pumps

-FIRST DEGREE–> directly using ATP; being metabolized by pump

-secondary active transport
-pump does NOT USE ATP DIRECTLY; relies on ATP but that isn’t directly happening at pump
-NCX transporter/sodium calcium exchanger
-Na and glucose pump

59
Q

Sodium Potassium ATPase pump

A

-enzyme that metabolizes ATP–> ATP harnessed or pulled from inside of cell and pump takes ONE ATP and RIPS OFF A PHOSPHATE–> ADP and PHOSPHATE FALLS OFF
-using the energy from when phosphate comes off the pump moves 5 IONS where they dont want to go
- 3 SODIUM OUT OF CELL AND 2 POTASSIUM INSIDE CELL
-SODIUM does not want to go to outside bc 1) it is positively charge 2) against its concentration gradient
-sets up almost all the electrical gradients in our body bc of the sodium and potassium movement–> most of the other gradients are related to this pump
-uses 60-70% of energy in a cell so most energy requiring process in body

LOPSIDED PUMPING–> bc losing 3Na and gaining 2K so LOSE ONE POSITIVE CHARGE AKA MAKING THE CELL EVEN MORE NEGATIVE

DIURETIC EFFECT
-cells have a way for water to move across cell wall
-keeps OSMOLARITY of cell in check bc as cleans out excess sodium the water follows it out of cell
-maintains INTRACELLULAR VOLUME of cells
-if shut pump off then Na builds up and cell SWELLS UP aka CELLULAR EDEMA
-unhealthy ppl with less ATP so less ATPase so cell swells up and hard to fix bc fluid inside cell-> only way to fix is to give more ATP

indirectly affects lots of other electrolyte gradients like calcium which dictate charge of cell

60
Q

Calcium channel pumps

A

Calcium pump first degree active transport
-sometimes we want to keep Ca concentrations inside low so cell is able to turn self off
-in order to make sure intracellular Ca levels are maintained really low we have pumps in our cell wall that directly take Ca and move it outside of cell
-so we have neuron that is turned on and during an action potential calcium comes to turn it on and the cell is going to have to have a way to get rid of the calcium and turn it back off
-one of the ways to do that is to have a pump specific for calcium and pump it outside
-this process of placing Ca to an area it does not want to go requires ENERGY aka ATP and use it directly

61
Q

Acid producing cell pumps(proton pumps)

A

-gastric pH very very low bc gastric cells good at secreting acid
-simple acid pump(proton pump) that uses ATP directly to take protons from inside of cell and pump them outside of the cell which acidifies the environment

62
Q

NCX transporter/sodium calcium exchanger

A

-when ATPase pumps not able to move the amount of Ca the body wants it to
-helps us get rid of Ca after action potential; the action of moving 1 Ca out is linked to moving 3Na in
-source for ATPase but also now pump has to deal with it
-takes one thing and exchanges it for another
-takes one Ca from inside and moves it to outside by exchanging for 3 SODIUMS into cell
1Ca:3NA bc takes 3 sodium for Ca to go AGAINST its gradient and charge
-energy this pump relies on is based on ELECTROCHEMICAL gradient of SODIUM which set up by ATPase pump
-takes the energy of the sodiums wanting to come down their gradient
-summary: the sodium gradient creates urge for sodium to come into cell and when it does that energy generated is used to flip calcium from inside to outside
-secondary active transport and this is the one our cell uses for bulk of calcium removal

-some sodium does sneak into the cell at rest but not a lot
-sodium also comes into the cell during an action potential

63
Q

Sodium Glucose COUPLED pump

A

-secondary active transport bc something moving down gradient and then that speeds up or makes something else happen aka glucose coming in faster
-glucose wants to come into cell already but if our body wants it to come faster then we can COUPLE movement with Na
-Na wants to come in and so does glucose–> to make glucose come in faster than we usually want then COUPLES sodium entry
-sodium allowed to flood in and when it does glucose gets dragged along with it
-not throughout body; in kidney bc we want to reabsorb glucose so its not lost in urine

63
Q

Glut transporter

A

-once glucose binds to this transporter then we have conformation change with protein which then glucose has orientation change and now is on inside of cell and then released
-catch and release mechanism but with conformational change so net movement of the compound
-cant just use normal ion channel to come in with bc glucose is 1)large 2) really charged 3) polar 4) hydrophillic
-not using energy

dependent on 1) how many of theses transporters in cell wall bc can only catch and release so fast and 2)whats the electrochemical gradient of the compound being moved. if really high outside and really low inside then would happen faster

GLUT 4 transporters
-insulin dependent in fat and muscle cells
-when insulin is around then should move more of the glut transporters to cell wall and the more you have the easier it is for glucose to move into cell–> increase rate glucose moving out of blood
-best for body management of blood sugar
-can impact rest of body if going too fast bc massive containers

GLUT 1
-noninsulin dependent
-important glucose transporter for RBCs
-RBCs need energy and get this from glucose but are not insulin dependent glucose transport system bc don’t have insulin receptors on our RBCs

64
Q

osmotic pressure

A

-the amount of force from the movement of water down its concentration gradient through semi permeable membrane
-can look at it 2 ways
1) column getting higher by so many mmHg
2) how much mmHg I would have to apply to Left side to prevent that side from rising
-5000 mmof Mercury is the result of all the osmotic activity in the fluid
-the high number is balanced out because it is on BOTH sides
-but if changes in blood makeup then that affects the containers which can result in massive amounts of pressure on organs especially the container of the central nervous system bc that is surrounded by closed container

65
Q

osmolarity vs osmolality

A

-we will use OSMOLARITY in this class
-small difference btw the two bc IL of solution is little bit less than 1L of pure water bc blood(solution) has more stuff than just water in it. about 1% difference of the two
-units of millimoles (mOsm)

Osmolality
-quantity of stuff dissolved in 1kg of water
-1kg of pure H2O=1L of H2O
-so if we take 1 mOsm in 1L of water then osmolality is 1 and then take that number and multiply it by constant 19.3 then get OSMOTIC PRESSURE that solution has potential to be
-IMPRACTICAL to use bc would have to pull out 1L of pure solution from the blood

osmolarity
-looking at quantity of stuff dissolved in 1L of solution
-mOsm and mEQ are units of quantity

66
Q

describe the normal test tube and then what happens when you had solute to it

A

-the U shape test tube is filled with just water separated by a semi permeable membrane–> restricts movement of the SOLUTE but not solvent so water is distributed evenly

WHEN YOU ADD THE SOLUTE to ONE SIDE
1) increases the saltiness or osmolarity of the left side
2) bc of this has also messed with the water concentration on the LEFT side bc adding the solute DECREASES water concentration of the LEFT side
3) RIGHT side still high water concentration bc did not add solutes to that side
4) water wants to move down its concentration gradient so water will go from RIGHT TO LEFT which will push the LEFT SIDE VOLUME high but will never completely even out both sides

-if measure the height at which we pushed the column up then we could quantify the osmotic pressure in units of mmHg(mercury is liquid at room temp)
-remember 1 mOsm is 19.3mmHg in 1L so if 1 mOsm of solute in L side then L side will move up 19.3 mm
-dissolving 280 mOsm will have enough osmotic pressure to push column up 5000 mmHg
-only thing keeping the column from going all the way up is gravity and when increase the weight of the left side and gravity pulling it down.
-SO as the column of mercury goes up and up the osmotic pressure is being OFFSETTED BY GRAVITY BC OF THE INCREASE IN WEIGHT
-done at sea level bc in space the water would just go up and up
-so in theory 1 little electrolyte would make the water keep going up and up bc no matter what will never even out concentration of water bc LEFT will always be lower than right

-can also quantify osmotic pressure via applied pressure aka can be defined as amount of pressure needed to keep the left side from not going up in height at all aka stopping osmosis

67
Q

explain kinetics

A

Vmax is maximum speed at which the conformational changes can occur(if not transporter dont have to deal with this)

facilitated diffusion
-conformation change so rate of diffusion increases with increased gradient BUT HAS Vmax when those transporters get saturated
-so speed dependent on concentration gradient AND speed of conformation change
-only way to speed up diffusion at this point is to increase number of transporters around

simple diffusion
-rate of diffusion increases LINEARLY with increase in gradient–> speed determined by concentration of substances
-does not have Vmax bc doesnt have transporter

68
Q

what all determines diffusion rate

A

1) concentration inside vs outside–>the bigger the difference the faster the something will be able to move in

2)lipid solubility–> more lipid soluble something is usually higher diffusion rate

3)size–> the smaller the faster

4) # of pores

5) kinetic movement–> the warmer the faster

6) physical pressure–> BP on capillaries

7) electrical charge–> charge of the cell drawing the compound in

8) chemical gradient aka concentraion

69
Q

membrane potential and NERNST and Goldman equation

A

-membrane potential IS CHARGE DIFFERENCE ACROSS CELL WALL
-excitable cells are electronegative at rest and then when cell turns on they briefly flip positive–> might want to flip it on for heartbeat or electrical impulse for short amount of time then go back to resting state
-at rest membrane potential is negative and then Vrm we are able to figure out what the membrane potential would be if normal electrolyte concentration gradient and if permeable. cell at rest is permeable to potassium(10xmore) and sodium(less) so potassium more dominant electrolyte determining resting membrane potential
-mV(millivolts) describes actual charge of cell
-go back to basics to determine membrane permeability and membrane potential–> what is concentration gradient? which direction does electrolyte want to move bc of the concentration gradient? what is charge of electrolyte? so how would this movement affect the polarity of the cell?

NaKATPase in membrane potential
-sets up electrical gradient and chemical/electrolyte gradient–> sets up electrical charge because net losing one positive ion and sets up electrolyte gradient more Na outside than in and more K in than outside

Vrm= resting membrane potential and is negative bc 1) proteins AA usually more negative than positive so long chain protein is more negative making cell even more negative 2) NaKATPase -losing a positive ion and the effects of the electrolyte gradient which is seen in the NERNST

NERNST POTENTIAL(or equilibrium potential) is the voltage(mV) that will prevent ions from diffusing across the membrane down their concentration gradient
-relate permeability of ions to concentration and tells us the charge of the cell if we allow an ion to move across the cell wall which could change the polarity of the cell
-EMF(force in mV)= +/- 61 log(concentration difference inside/outside)–> +/- decided by opposite charge of ion you are talking about
-NERNST relates to us bc at rest cell is permeable to 2 ions: K and Na
-summary: talk about ions going down their concentration gradient and how that affects the membrane potential
1) SODIUM in NERNST is 61 so cell would be more positive if cell let sodiums come in
2) POTASSIUM in NERNST(affects CV) is -91 because going out and K is positive

-so bc K more dominant electrolyte in this bc more permeable then -91 and 60 the cell’s resting membrane potential is around -80

GOLDMAN EQUATION(GHK): each ion gradient we are talking about only contributes as much as the membrane is permeable to. a combination of individual equilibrium potentials for each ion we are interested in–> TELLS US THE OVERALL MEMBRANE POTENTIAL OF THE CELL TAKING INTO ACCOUNT ALL THE IONS THAT THE CELL IS PERMEABLE TO. so the concentration gradient influences this and the cell is able to influence the overall membrane potential aka it can open ton of sodium channels so more positive membrane potential
-EMF= -61 x log(concentration and permeability of each ion inside/verses outside C and P)
-the more permeable the ion the bigger the factor

-when cell wants to be activated is it increases permeability to other stuff so Na and Ca to change the overall charge and results in new membrane potential and this is how cell governs whether things are turned on or off

-so the equilibrium potential or the NERNST potential is prediction based on one electrolyte and action potential is just cell opening up sodium channels that changes polarity that causes cell to fire or contract whatever

70
Q

carrier proteins

A

if drug lipid soluble then will need help floating around blood stream aka carrier proteins for propofol