Exam 3 Flashcards
Functions of Blood
-Transport – O2, nutrients, hormones, water Co2, waste -Prootection– WBC travel in blood and monitor for pathogens, Clotting factors protect us from blood loss -Temp. regulation- blood flows closer to surface when we are hot (cooling) and closer to core when cold (keep organs warm
How much blood in body?
5-5.5L
plasma
liquid part of blood -mostly water more viscous than water– has proteins is salty (0.9% NaCl) 3L of the 5-5.5L of blood is plasma
formed elements
“chunks” in blood: blood cells, fragments of cells (platelets
RBC
erythrocytes 4.5-5.5 million/mL Carry O2 also can carry Co2, H+, CO
WBC
leukocytes 5-10 thousand /mL immunity- protect from pathogens and cancers
Platelets
thrombocytes 200-400 thousand/mL help clot/ prevent blood loss
Most dense in blood
packed RBC, makes up 42% of volume
medium dense in blood,
white cells, <1%
least dense in blood
plasma, 58% includes clotting factors
serum
our plasma with clotting factors removed
What makes up plasma?
90% Water, 8% plasma proteins (from liver): albumin, gamma globulin, fibrinogen 2% small molecules, N, K, Ca, C, disolved gasses (O2, CO2, N2), nutrients such as glucose and AA
Albumin
most abundant, osmotic regulator (Reduces edema), and increases viscocity keeps water in the blood, as apposed to leaking out into tissues
Gamma globulin
antibodies, protect from pathogens
fibrinogen
part of clotting mechanism, during bleeding they become insoluble (precipitate out_ and form a fibrous network become a net when exposed to O2 to hold RBC in the body
Various protein carriers
carry hydrophobic molecuels that don’t dissolve in blood, and need to be carried by proteins that do ex. transferrin, LDL, HDL
transferrin
a protein carrier that carries iron
Red blood cell production
Are formed in the bone marrow and are released as fully mature and differentiated -incapable of mitosis- have no nucleus so always making new ones in the bone marrow
Red bone marrow
has hematopoetic stem cells that give rise to RBC, WBC, and platelets infants have red bone marrow in most of their vones, but adults only have it in a few.
RBC Development
No nucleus biconcave shape– more surface area for diffusion of O2 and CO2 flexible, can squeeze though tight spaces Gain Hb ER, mitochondria, shrink and disappear cytoplasm shrink mature RBC is 1/3 the size of immature
Whats inside RBC?
no mitochondria=no respiration, only glycolysis No ER- can’t repair themselves if hurt Hb- carries O2
Hemoglobin
iron containing protein undergoes shape change when it binds light red when bound to O2 dark red when not bound to O2
Hematocrit
measues %RBC of total blood volume, says how much O2 you can carry around your body
normal hematocrit for men
40-50%
normal hematocrit for women
38-46%
Anemia
less than a normal value for hematocrit don’t mka eenough or body is destroying them
blood doping
more RBC–> more o2 in blood
RBC lifespan
120 days - body replaces its entire blood volume every 120 days, or 1% a day -need enough energy and iron to maintain this production
WBC lifespan
variable 6 hrs- 80+ years
platelet lifespan
10 days
RBS breakdown and recycling
liver and spleen iron released into plasma, bound to transferrin and brought to bone marrow for new RBC to be made with it
ferritin
liver place for storage of excess iron
Too much iron
gets deposited in liver, can lead to liver issues
folic acid
dietary soure of precursor to the nucleic acid thymine
deficiency in folic acid
halts all cell division will not make all the eclls you need on a daily basis all mitosis haulted RBC are first indicator, within one week you’ll lose 7% of blood cell volume– leads to fatigue and weakness
B12
needed in order for folic acid to be used. Comes strictly from animal products, meas begans can get anemia
Erythropoietin
hormone released by the kidneys that triggers red blood cell division and maturation If O2 delivery to kitdey falls below a certain point it will release more erythropoietin, which will result in increased production of RBC testosterone can also trigger erythropoietin
When does O2 delivery to kidney’s decrease?
-prolonged high altitude exposure -insufficient pumping of heart -lung disease -anemia -prolonged exercise -problems with Hb
What decreases O2 carrying capacity (ie what causes anemia)?
-impaired RBC capacity -increased RBC destruction -blood loss– injury, menstruation -a combination
Pernacious anemia
a lack of B12
iron deficiency anemia
if not taking in enough iron–> can’t synthesize Hb can sometimes be used as a strategy for pathogen evasion– if we decrease our iron, the microbes can’t have it to live in us and will kill them off
Sickle cell anemia
irregularly shaped RBC, genetic disorder have enough, but they can’t carry O2 in the right way
Polycythemia
-too many RBCs -happens in doping, high altitude dwellers and in some forms of cancer -blood becomes too thick -causes a strain on the heart, decreased flow through vessels, can lead to death by blood clots
Co2 and O2 transport
-Co2 and o2 are small, non polar molecules can difuse through membrances and dissolve in liquids– but this is not sufficient (ex. diffusion from lung all the way to toes would take too long) -transport of both can be enhanced by Hb
O2 gas transport
-97% carried on RBC heme groups of hemoglobin bind O2 3% dissolved in plasma (this is the only portion that can be detected
CO2 gas transport
23% on RBC 7% dissolved in plasma 70% carried as bicarbonate
relationship between PO2 and Hb saturation
is not linear– bind more O2 if there is more of it around
hemoglobin
each have 4 heme groups. one Hb can pick up 4 O2 at a time ability to pick up and release O2 is influenced by environment: pH and CO2 levels in tissues surrounding the capillary bed Can also carry NO, CO2, H+ and CO When one heme group binds O2, the entire structure changes making it easier to bind another O2, making it easier for 3rd etc. (reverse is also true, with releasing O2
HB saturations when [O2] is high, ie PO2 is high (~100mmHg)
Hb is very saturated (98% of Hb is saturated)
HB saturations when [O2] is low, ie PO2 is below 60mmHg
Less Hb is saturated
Hb affinity and O2 conc.
When there is a high conc of O2, the affinity for O2 is high, when the Hb reaches an low O2 area, it will have less affinity and will release the O2 to that area
Fetal Hb
has a higher affinity for O2 than adult Hb. In pregnancy the uterine capillaries lose O2 to the placental apillaries due to the difference in affinity
In which environment would Hb have a higher affinity for O2? PO2 of 100mmHg or PO2 of 35mmHg?
PO2 of 100mmHg
What [NaCl] is isotonic to blood?
0.9% NaCl
Where is transferrin
It is plasma protein that moves iron from the spleeen to the bone marrow to recycle it and make new RBC
Can iron deficiciey anemia result from infection even if the diet is fine?
Yes– body decreases iron to kill off pathogens (who need it for survival)
Temperature effecy on Hb saturation
Hb has a lower affinity for O2 at higher temperatures -will have high temp. due to exercise, fever, and excess cell. resperation –helps to remove CO2 and bring O2 to areas that are doing more cellular respiration (which produces heat)
Hb affinity for CO
Hb has 250X the affinity for CO as O2, sobinds preferentually– and it can’t unbind this is why you become asphixiated when CO is in the air– takes RBC ‘s out of commision
What can Hb bind?
O2, CO2, CO, H+
Why does Hb bind H+?
more H+–> denaturation of proteins binds them and shuttles them out of the body to protect them
CO2 transport
7% of CO2 dissolves in plasma 70% is converted into bicarb 23% binds to Hb
Co2 –> bicarb equation
H20+CO2H2Co3H+ +HCO3 H2CO3=carbonic acid HCo3=bicarb H+ used in stomach HCO3– used to neutralize in SI
acid
any substance that can dissociate into H+
Why must we breathe out
otherwise we will become acidic inside
Nase
anything that reduces the H+ concentration in an environment
Bohr effect
decrease pH=more acid=more CO2–>Hb releases O2 makes Hb free to bind H+ and CO2 to get them out of the body
Hb and acidity
Hb O2 binding affinity is INVERSELY proportional to eh ACIDITY and concentration of CO2 in the blood. decrease in pH (or increase of CO2) Hb will release bound CO2
What happens if there is a decrease in pH
Hb will release bound O2 Hb will have a LOWER AFFINITY for O2
What happens if there is an increase in blood Co2
Hb will release bound O2 Hb will have a LOWER AFFINITY for O2
what happens if there is an increase in blood pH
Hb will retain bound O2 Hb will have a HIGHER AFFINITY for O2
What happens if there is a decrease in CO2 concentration
Hb will retain bound O2 Hb will have a HIGHER AFFINITY for O2
Thrombocytes
small fragments cells called megakaryocytes in bone marrow pinch off cytosplasm to make platelets no nucleus, small amount of ER so it can make chemicals involved clotting
megakaryocytes
large cell in bone marro that pinch off cytoplasm to make platelets
hemostasis
the stoppage of blood loss platelets gather and recruit fibrinogen
collagen
in connective tissue, binds platelets. When there is vessel damage the connective tissue is exposed
Platelet activation
platelets and collagen bind, activates platelets and releases secrectory vesicles that help clotting process –autocrine- platelets stick to each other –paracrine– make platelets contract and compress to form a plug
prothrombin
a plasma protein that is cleaved into thrombin
thrombin
enzyme acts to make fibrinogen into fibrin monomers which then polymerize into the fibrin net
fibrin net
made up of polymerized fibrin monomers– in the presence of oxygen.
fibrinogen
broken down into fibrin monomers by thrombin, used to make the fibrin net (in the presence of oxygen)
Leukocytes
Whate blood cells 5,000-10,000/ml but varies based on infection use blood as freeway system to get to body parts– but majority of their life is spent in tissues -act as immune defense -use inflammation
low WBC count
immunocompromised
High WBC count
actively fighting an infection
What does thrombin do?
acts as a enzyme to slices fibinogen into fibrin
Plug
compressed platelets with no protein net
At high pH what would Hb affinity be like for O2
high affinity for O2-holds on
Low CO2– what would Hb affinity be like for O2?
high affinity for O2
40C temp– what would affinity be like for O2
doing a lot of cellular respiration–so more O2 being used, so decreased affinity for O2
pathogen
a disease causing agent
antigen
a specific piece of the pathogen recognized by the immune system. Has an outer coating that our immune system recognizess
what is immune system
made up of skin (barrier immunity), mucus (barrier immunity), WBCs and lymph nodes -protects you from invasion of things that don’t belong (bacteria, viruses, and parasites) and cancer can be bad if it doesn’t work enough, or if it overreacts
lymphnodes
anatomical locations where immune cells can communicate and develop
bacteria
single celled reproduce on their own– binary fission can share DNA with other bacteria by proximity have no nucleus have a first and last name (ex. E. Coli) -most do no harm (only 1% are infectious)
how much bacteria in the body?
outnumber our own cells by 9-1
How quickly do bacteria reprouce
20-45 min
viruses
cann’t reproduce or unergo metabolism on their own -insert their DNA into ours and we reproduce them -usually 100s of copies of our virus cell -the host cell is destroyed -when not contained within a cell they go dormant for hours/years -mutate their own genome often have very small genome -we have no treatment for most viruses
Examples of viruses
Colds (coronaviruses and rhunoviruses), HIv, Hepatitis, Influenze
Funcus
-reproduce on own -have a nucleus -cause disease in the immunocompromised -must live in symbiosis in us -ex. yeast infection (Candida albicans) and athletes food
Parasites
multicellular pathogens must be transmiited from one host to another can reproduce on their own ex. tapeworms, malaria, flukes, fleas, elephentitis (worm in lymph system)
self v. non selg
you’r body learns during debelopment which proteins are “self”, eliminates enzymes that work against self proteins – then any thing else is treated as foreign and attacked by the immune system
How does the immune system work
3 lines of defense: 1. barriers 2. innate 3. Specific
first line of defense in immune system
barriers– mucus, skin
2nd line of defense
innate–inflammation when foreign invaders are found chemicals– cytokines to coordinate immune system and cause fever -macrophages and neutrophils engulf bacteria, clean up cellular debris, coordinate response
third line of defense
specific— specialized cells to kill off leukocytes-learn about pathogen, remmeber it and make a specific response: antibodies, cells to kill pathogen
inflammation
2nd line of defense -blood vessels dialate, WBC, chemicals and plasma to the area of infection, pain prevents further injury
macrophages and neutrophils
engulf bacteria, clean up cellular debris, coordinate response 2nd line of defense
leukocytes
3rd line of defense. learn about the pathogen, remember is and make a specific respose including: cells that kill the pathogen and any infected cells antibodies that can float in blood and disable pathogen
B Cells
make antibodies that are SPECIFIC to the pathogen can last for decades
Helper T cells
recruit other cells to sites of infection talk to macrophages to learn about pathogen, -coordinate entire adaptive immune responses including telling B cells when to make antibodies
killer t cells
kill infected cells or the pathogen - kil cells that are infected with intracellular pathogens
Macrophages
clean up waste and extracellular pathogens can activate B an T cells -collect cellular waste and pathogens throughout tissues -bring collected antigens back to lymph nodes to show and activate a specific line of defense -engulf bacteria, break down in lysosome and then release them to B and T cells
neutrophils
engulf and kill pathogen directly
eosinophils/basophils/mast cells
participate in inflammation and allergic responsees in US
example of imune response
-cut on finger infected with bacteria -immediate inflammatory response –vasodialation and vascular permeability-brings blood to infection, bring leukocytes to the wound, wound gets swollen and red –cytokine release by leukocytes–cause pain and sensitivity -Macrophages bring antigen to lymph nodes, talk to B cells and T cells -B and T cells become activated and reproduce -B and T cells migrate to the infection site, kill infected cells and secrete antibodies
phagocytes
macrophages and neutrophils big cell eaters -have receptors on surface to recognize things that are common to pathogens– bacteria outer cell wall -knows there is a bactera and englufs it, even if there is a variety of bacteria
lymphoid tissue– strategic placement
-located around boy to meet the most marcropahes -lymph nodes, appendix and tonsils are meeting places for immune cells -mouth, groin, armpits
lymphnodes
mouth, groin armpits macrophages and dendritic cells cary their antigens to the lymph nodes, find compatible T and B cells and activate them with cytokines. T and B cells then proliferate and go out to find the infection
cytokines
ommunicate between cells -all cells secrete them some secreted by non immune cells to signal damage to immue system some are released by immune cells to elicit fever, itching etc to help
homing
cytokines call to leukocytes to get them to infected tissues
how do leukocytes get to infected tissue
called by cytokines, bind to endothelial cells that line blood vessels, then squeeze between them to get out of blood vessel to the side of infection
why are leukocytes in veins not arteries?
lower force, rpessure and speed so their is better interactino between WBC and vessel walls
inflammattion
-endothelial cells become leky so leukocytes can get to infection, during this plasma gets out of blood vessels which leads to swelling –causes a drop in BP
what can chronic inflammation do/
lead to cancer do to icreased mitosis
antibodies
made by b cells can: -tag pathogen for destruction -bind to its parts and precent it from working -bind multiple pathogens and keep them from moving
no helper T cells
HIV– no coordinatino of immune response. Can be devestating
T and B cell education
develped during fetal development,
Primary T and B cell response
will test to see if they react with any of the pathogens antigens– if they are they multiply and kill off, as the infection dies the numbers decline, but some circulate in blood for years
Secondary “memory” response
if an infection occurs with the same pathogen the antigen specific T/B cells reproduce at the infection site, there is no innate cell recruitment in lymph nodes the infections resolce quickly, and are typically not symptomatic
when do leukocytes exit the blood stream?
in response to cytokines
what is an antigen?
a piece of a pathogen- that our immune system can recognize
active immunity
your immune system produces a response
passive imunity
someone elese immune system produces a respons anti venom transfer of antibodies from mom to fetus in pregnancy or through breast milk
vaccination
injected with the antigen of a specifinc pathogen includes chemicals that elicit an immune response this is your primary response, so the next time when you actualy see the pathogen you will have a secondary response— no symptoms! can bypass dengeroud primary resoonse -99% elimation of small poz, diptheria, tetanus, whooping cough, polio, measles, mumps, rubella –NOT LINKED TO AUTISM -mercury preservative is no longer in vaccines
Flu vaccine
mutates every year infections nov-april is an educated guess as to which strains to include
developing a strong immune system
requires exposure to antigens/pathogens regular activity promotes reactivity to pathogens and tolerance to non-pathogens -overly sterile environments may contribute to allergies and asthma
opportunistic infections
-when immune system is supplressed, bacteria that we normally live with seize the opportunity to infect us -can be suppressed by fatigue, stress, drugs, infections AIDS is a syndrome of pathofens we normally fight off
autoimmune disease
mistakes -self reactive cells survived immune cells react against a self protein
immuno diffeciency
SCID: infants die before age 1 AIDS: patients can’t fight opportunistic infections
cardiovascular system
heart, blood, vessels. function is to transport oxygen,glucose, nutrients, hormones, waste and other chemicals throughout the body
bulk flow
since all parts of the blood are equally subject to the pessure gradient, they all move togehter (lliquids and solids)
Pressure graduents
blood will only move through the cardiovascular system if a pressure gradient is established
systemic circulation
travels from heart all over the body and back (except lungs)
pulmonary circualtion
travels from heart to lungs and back to heart
the heart anatomy
4 chambers: top 2: atria— recieve blood from vessels bottom 2: ventricles: pump blood out of the heart Right: receives deoxygenated blood (70%O2) from body and pumps it to lungs Left: receives oxygenated blood from lungs (97% O2) and pumps it to the body
deoxygenated blood
70%O2
oxygenated blood
97% o2
right atrium
recieves deoxygenated blood from the vena cava
righ ventricle
receives deoxygenated blood from the right atrium via tricuspid(AV) valve
left atriumr
receives oxygenated blood from the pulmonary veins
left ventricle
receives oxxygenated blood and pumps it into the aorta
AV valves
between the atria and ventricles
Semilunar valves
are in the arteries leaving the heart (the aortic valve and pulmonary valve)
aorta
artery that pumps oxygenated blood from the left ventricle to the body
vena cava
veins taht return deoxygenated blood from the body to the heart (the right atrium)
coronary circulation
the circulation of blood in the blood vessels of the heart muscle
pulmonary artery
carries deoxygenated blood from the heart to the lungs (the only artery that caries deoxygenated blood)
pulmonary vein
carry oxygenated blood from the lungs to the left atrium of the heart
hydrostatic pressure
the force exerted by the fluid on its container
resistance
how difficult it is for the fluid to flow through a container (walls offer resistance, so you have to force to overcome resistance
flow=
change in pressure/resistance
when will flow increase?
if pressure increases and the pressure can over come resistance.
What happens if resistance increases
there will be a decrease in pressure and decrease in flow until you overcome resistance
factors that effect flow: distance
flow and pressyre decrease over distance because energy is lost due to friction
factors that effect flow: viscoscity
thicker fluids do not flow as well and require more pressure to move them
factors that effect flow: diameter of tube
larger diameter means that you need less pressure to create flow, smaller diameter more force required
what happens to resistance if you increase diameter
decrease in resistance
what happens to resistance if you increase length
increase resistance– requires more pressure to get through
what happens to resistance if increase viscocity
increase resistance, requires more pressure to get through
which organs need the most blood flow?
abdominal organs, kidneys, skeletal mustle, brain
atrial contractions
move blood to ventricles (can be done mostly by gravity)
ventriculat contractions
move blood to lungs and body (up and out of heart) needs strong contracion
Path of blood through system
- systemic veins (deoxygenated) 2. Vena cava ( 3. right atrium 4. throughright AV valve 5. reight ventricle 6. through semilunar valve 7. pulmonary trunk-pulmonary arteries GAS EXCHANGE IN LUNGS 8. pulmonary veins (oxygenated) 9.left atrium 10. left AV valve 11. left ventricle 12. aortic semilunar valve 13. aorta 14. systemic arteries 15. systemic veins back to begining`
valves
increased pressure during contraction closes the valve to prevent back flow low pressure between contractinos allows valves to open
If you have 2 hoses, one long one short with ater starting at the same pressure, will the water exit at the same pressure?
no, the shorter one wil have a greater pressure
if you are stressed and have vadoconstriction, is there more blood or less blood being delivered to the heart?
less blood to the heart.
you have stiffening of the right AV valve, which location would see less blood flow?
the lungs,
nodal cells and conducting fiber
parts of heart that conreol electrical impulses. pacemaker cells to make the heart beat
ventricular muscle contraction must be
rapid have long absolute refractory period have a short relative refractory period to be ready for the next impulse must relax and fill with blood before contracting again
ventriculat muscle cells at rest
leaky k chanels– so mostly hyperpolarized closed voltage gated Na+ channels closed coltage gated Ca ++
ventricular muscle cell depolarization
Na enters, ca enters (later than Na + but for longer– results in long absolute refractory period) K exits– to create the short relative refractory period
atrial cell depolarization
same as ventricular, but plateu is shorter less importance on atrial contraction because it can be accomplished by gravity
nodal cells must
spontaneously depolarize (pacemaker) rapid have a long absolute refractory period have a short relative refractory period to be ready for the next impulse
nodal cell depolarization
spontaneously depolarize by leaking ions, a few Na and Ca channels are open when voltage is ngrative below threshold, more Ca that open at threshold. (Steadyly depolarizes to threshold, then throws open the gates) don’t depolarize to 30, stop at zero ad then can repolarize much faster
SA Node
pacemaker– started the spontaneous depolarization of the heart spreads through walls of atrica, then hits AV node and spreads to ventrivles
p wave
depolarization of the atria
QRS
ddepolarization of the ventricles
t
repolarization of the ventricles
systole
contraction (blood is ejected)
diastole
relaxation (blood fills)
atril systole
atria contract- push blood down into ventricles this is the P wave
isovolumetric ventricular contraction
aka early ventricular contraction same volume, don’t eject blood, just squeeze it to snap AV valves closed begin to see QRS here this is the “lub” sound
ventricular ejection
aka late ventricular systole blood flows out of the ventricle into the pulmoary trunk or aorta opens up semilunar valve This is the highest portion of theQRS complex as ventricles relax it leads to the the snapping shut of the Semilunar valve makingthe dub sound
stroke volume
the amount of blood ejectedf rom one ventricle during systole (around 70ml)
end diastolic volume
volume of blood in the ventricle at the end of diastole (around 100-135ml)
end sytolic voluem
volume in ventricle at the end of systole
ejection fraction
the percent of the EDV that gets out
stroke volume=
EDV-ESV
what is the purpose of early ventricular systole?
close the AV valves
what is happening between the P wave and QRS complex?
blood is flowing between atria and ventricles
what is the depolarizing ion for nodal cells?
Na and Ca
ejection fraction=
SV/EDV usually around 50-75%
end diastolic volume
full ventricle
after systolve volume in aorta is
stroke volume
after systole the volume left in the ventricle is the
end systolic volume
ejection fraction
difference between original amount in ventricle and the amount in aota after systole
as blood vessels narrow, what happens to flow?
decreases
if flow goes down what happens to the ejection fraction?
decreases
frank starling laq
saromeres are able to contract more when stretched to a degree, then stretch inhibits sarcomere contraction in heart- ring of connective tissue that encircles the heard and prevents overfilling an increase in venous return, means an increase in stretch on muscle walls, so an increased amount of contraction possible– increases possible EJF
Cardiac output=
HR*SV during exercise CO can increse to 30-35L/min how much blood is leaving your heart in a minute
portal system
two capillary beds in series, link one organ to another without returning blood to the heart
hepatic portal vein
delivers nutrients to the liver from intestines, low o2
hypothalamus-pituitary portal system
brings tropic hormones from hypothalamus to pituitary
kidneys
portal system deliver plasma to be filtered for urination, connects arterial capillary to arterial capillary
angiogenesis
the growth of new blood vessels
when does angiogenesis happen?
in babies and children, after menstruation, in wound healing, in cancerous tumor development
blood pressure
generated by ventricular systole flow is proportional to change in P and inversely proportional to 1/R bigger
the ventricle needs to generate enough pressure to overcome…
-length of tubes leading back to the heart -decreasing diameter of those tubes -relative viscocity of blood
hypotension
abnormally low BP not enough force to overcome resistance, blood doesnt make it back to the heart (or brain) so dizziness ot fainting will occur bad short term
orthostatic hypotension
hypotension when changing position. Blood pools in lower extremities, more common in elderly
hypertesion
abnormally high BP puts stress on vessel walls fine short term– bad long term
systolic blood pressyre
during contraction -120
diastolic BP
during relaxation ~80
is there a difference between diastolic and systolic in the veins?
no, we lose that pressure as you get away from the heart
prehypertensve
120/80-139/89
hypertensive
140/90
pressure in pulmonary system
15/5 low pressure.. distance from heart to lung doesn’t need a lot of pressure
pressure i right atrium/vena cava
0 pressure, which encourages blood to return there
blood pressure in veins
low pressure, uses skeletal muscle pump and pulmonary pump also has vavles to prevent backflow
skeletal muscle pumps
sandwich veins between skeletal muscles so contraction of muscle will squeeze blood up
pulmonary pump
as you breathe in, your thoracic cage expands and diaphragm lowers towards abdomen this creastes a low pressure environment in the thorax this decreases the pressure in the inferior vena cava drawing venous blood up toward the heart
pulse pressure
systolc-diastolic
pulse
when the high pressure blood meets the low pressure blood, displacing it
mean arterial pressure
average blood pressure in the vessels over time diastole lastes longer than systole so mean pressure is closer to diastolic
mean arterial pressure=
HR*SV*TPR TPR=total periperal resistance
if you are feeling anxious and HR increases what happens to your MAP?
increases
you are under chronic stree and cortisol levels increase, what happens to MAP?
increases, would lead to vaso constriction, so more resistancce
you are stabbed and have lost a liter of blood, what happens to MAP?
decrease
what causes hypertension
increased peripheral resistance w/o change in cardiac output. Over time the vessels lose their elasticity idopathic can be caused by genetics, smoking and lack of cardiovascular exercisee
How can we change MAP?
total blood volune distribution of blood in circulation – moving food to stomach for digestion etx
if you want to change the rate of blood flow…
- change resisitance or change pressure
how can we change resistance
-vasoconstriction of dialation partition of blood flow– selectively change diameter to direct blood where you want it to go
capillart structure
one cell walls (endothelial cells)
capillary exchange
-diffusion of small molecules accross capillary endothelium -bulk flow of liquid00 plasma leaves the capillary and enters the extracellular fluid, this will help to maintain fluid and pressure on both sides -movement of fluid out of the capillary is usually greater than into the capillary -lose about 3L/day
plasma and extracellular fluid volumes
on average we have 3L of plasma and 11L of extracellular fluid
Dehydration
liquid from extracellular fluid into plasma to maintain blood volume
excess blood volume
more liquid into extracellular fluid
Starling forces
the ways that movement out of the capillaries is regulated -hydrostatic pressure -osmotic pressure
hydrostatic pressure–
greater pressure inseide the capillary than outside (P2-P1=deltaP), forces fluids out
osmotic pressure
there is a greater solute concentration in one place than another, which draws water into or out of the capillary (usually into)
how do we replace plasma water
lymphatic system drains tissues of excess water and then through capillary exchange replaces is in the capillaries
edema
swelling
edema causes
-lymph can’t drain properly (usually a blockage), can be cancer, parasite, surgery -capillary outflow greatly exceeds inflow from lymph. This can happen from an increase in hydrostatic pressure from cardia failure or a decrease in plasma protein production
how can you change blood flow?
-change resistance -change pressure– (change volume or heart rate)
hyperemia
an increase in blood flow accompanies an increase in metabolic activity
active hyperemia
exercise. muscles increase their metabolism and therefore their need for O2, blood flow to the miscles increases to meet the demand
reactive hyperemia
temporary– like foots asleep tissue uses its O2 stores and needs to replenish when flow is re established
what happens if blood volume changes?
blood pressure changes too, ex. increase in volume leads to increase of pressure ALWAYS, at least temporarily
dehydration
ex. the kidneys should compensate for changes in the diet or fluid intake but they cannot replace lost fluid, so a severe decrease in hydratoin will cause a decrease in blood volume.
vetricular performance
ventricles must have the same stroke volume
homeosatic control of MAP
MAP=SV*HR*TPR
heartrate control
-autorhythmicity-intrinsic sympathetic and parasympathetic innervation– from brain -hormones (epinepherine and norepinepherine increase, thyroid) -heat
Stroke Volume
frank starling– if venous return is high, frankstaarling increase sympathetic innervation/epinepherine hormone (amount of contractions in heart muscles) -afterload (pressure in aorta to overcome) (Decreases SV)
Total periferal resistance control
myogenic mechanism– arteriold controls its own diameter by responding to stretch or pressure exerted on the walls of the vessel (Response to stretch is to constrict– happens to protect capillaries ahead by decreasing flow. chemical mechanism– alters diameter of arteriole- vasodialators and vasocontrictors – ONLY sympathetic fibers that innervate the blood vessels
myogenic response
arteriold controls its own diameter by responding to stretch or pressure exerted on the walls of the vessel (Response to stretch is to constrict– happens to protect capillaries ahead by decreasing flow.
sympathetic tone
constantly maintained via signals from the brain. signal frequency increases or decreases to constrict or dialate the blood vessel
how is blood pressure monitored?
baro receptors in aorta and carotid artery
hypertension causes
90% idiopathic 10% secondary to a known disease, such as endocrine or renal disorders
hypertension
with chronic hypertension the baroreceptors become insensitive and fail to react to an increase in pressure -puts strain on heart, left ventricle has to work harder to overcome pressure gradient– left ventricle hypertrophy -cardiac failure
will contracting your calf muschles increase MAP?
yes
atherosclerosis
minor damage fro vesselwall patch with cholesterol until healed– too much can cause a build up overtime
aneurysm and stroke
narrowing o arteries cause blood build upp, the vessel can stroke resulting in a stroke
exercise and cardiovascular health
-increase diameter of vessels -increase elasticity of arteries -increase glycogen storage in cardiomyocytes -decreased risk for hypertension, atherosclerosis, heart attack, aneurism and stroke
entero-
pertaining to the GI tract
hydrolysis reactions
can depolyermize carbs and proteins sped up/ made possible by enzymes
will lipids be digested by water?
no hydrophobic
peristalisis
involuntary wavs of contraction and relaxation of smooth muscles in the organ walls through GI tract, move food
segmentation
contractions in the SI, segmental rings of contraction chop and mix the ingested food. slows down movement.
transport phases in digestion
-into intestinal epithelial cell -into interstitial fluid (and blood) from itestinal epithelial — almost always active
carbohydrates in diet
-1/2 of diet, mostly as large polysaccharides (starches) disaccharides (sugars) and rarely monosaccharides
lactose
glucose + galactose
how do we join monomers?
dehydration reaction, releases water bonds the monomers
sucrose
glucose+ fructose
maltose
glucose+glucose
fiber
cellulose and other complex plant polysaccharides can’t break them down partially metabolized by gut bacteria forms majority of feces
Carb digestion
begins in mouth-salivary amylase SI- pancreatic amylase -specific enzymes are required for some dissachharides, ex lactose, which are made by the intestinal epithelial cells makes monomers glucose, galactose and fructose which are then transported
Carb transport
glucose and fructose -some by primary active transport by glucose transporter proteins glucose and galactose undergo secondary active transport using Na graients SGLT then moves out of intestinal epithelial cell into interstitial fluid by facillitated diffusion
how is fructose transported?
GLUT secondary transport
how is glucose transported into intestinal epithelial cell??
GLUT and SGLT (na gradients)
how is galactose transported into intestinal epithelial cell???
SGLT Na gradient secondary active transport
how does carbs move out of the intestinal epithelial into intersticial fluid?
facillitated diffusion
carb ansorption
absorbed quickly broken down easily hydrophillic– travels in blood easily stored well in glycogen are the beggining reactant for cellular respiration
protein in diet
americans eat 2x’s more than we need 15% of calories rarely used for energy, just for building new proteins we add dietary proteins in the digestion process as in mucus and enzymes
how do we make proteins?>
AA come togeher via peptide bonds (using dehydration)
protein digestion
broken down in stomach and SI broken down by enzymes Stomach: pepsin (Released as inert precursor as pepsinogen, which is activated in low pH encironment) small protein fragments moce on to small intestine in small intestine, further breakdown by trypsin and chymotrypsin into individual AA or small chains
protein absorption
moved into intestinal epithelial by secondary active transport using H+ and Na+ gradients Some intact proteins can be moced through the intestinal epithelial by endocytosis and exocytosis
fat digestion
accomplished by lipase (some salivary, mostly pancreatic) which breaks fat down into a monoglyceride and 2 fatty acids fat molecules are hydrophobic and aggregate into fat globules– need bile to emulsify
bile salts
act as emulsifiers =, amking sure that monomers don’t re-aggregate back into alrge droplets. Big droplets are broken into small droplets called micelles, that further break down into monomers
where are bile slats made?
liver
colipase
a molecule that helps lipase adhere to the surface of the globules, is secreted with lipases
fat absorption
fatty acids and monoglycerides diffuse into the intestinal epithelial cells down the concentration gradient once inside the cell they are reassembled into triglycerides and are then exported out of the cell by exocytosis then travel into small lymph vessels called lacteals, into lymphatic circulation and then they are later dumped into the blood
why is fat allowed to reaggregate into micelles?
so that the transport of fat soluble vitamins is guaranteed
why does fat travel in lumph
capillary cells are too tightly adhered to each other and won’t allow fat dropets in -lymph vessels are overlapping flaps, they are not adhered and larger items can pass in
what is in each villus?
- an artery bringing oxygenated blood to the cells - a vein which drains to the hepatic portal vein– carbs and proteins are absorbed here -a lacteal– specialized lymphatic vessel that absorbs fats– contents are drained directly into venous circulation
lacteal
a specialized lymphatic vessel that absorbs fat, and is later drained directly into venous circulation (bypasses liver)
malabsorption
any interference of any nutrient– can lead to nutrient deficiencies
vitamin absorption
-fat soluble vitamins are absorbed in droplets with fatty acids and triglycerides -water soluble vitamines are absorbed by diffusion or mediated transport ***except B12– must be absorbed by a transport molecule called intrinsic factor
how much water must be reabsorbed each day?
8L
What % of water is absorbed by SI? LI?
SI- 80% LI-20%
how is water transported?
passive transport through aquaporins
what ion gradients are used to transport water?
Na- establised using the Na/K pump -Cl and HCO3 can be contransported with Na to create further osmotic preessure
Neural regulation of GI processes
has its own enteric nervous system -sensory stimuli– stretch in gut wall, chyme properties (pH, osmolarity etx) -are enteric sensory mechanoreceptors and chemoreceptors on the walls of the gut -motor output –can increase or decrease peristalsis or segmentation –contract around glands to influence secretion
Ascending tracts
neural regulation of GI Enterin NS communicates with brain to elicit behavior changes such as huunger, thirst
descending tracts
neural reg. of GI -sight, smell or thought of food can change secretion and movement within the GI tract
hormonal regulation of GI
-are receptors on enteroendocring cells that can trigger internal signalling the results in hormonal release -hormones are released through the non-lumenal side and absorbed into the blood
Gastron
-made in stomach -triggered by protein in stomach -stimulates acid secreting and SI and LI motility
CCK
-made in SI -triggered by proteins and fat in SI -stimulates bile release, inhibits gastric emptying
Secretin
made in SI -trigggered by acid in SI -inhibits acid and motility in stomach, stimulates HCO3, releases into small intestine
GIP
-made in SI -triggered by carb or fat in SI -triggers release of pancreatic enzymes.
what are the phases named for?
the location of the stimuli
cephalic phase
stimuli from head–sight smell, taste, chewing -parasympathetic fibers trigger neurons in enteric nervous system to initiate secretion, motility etc
gastric phase
stimuli from stomach (Stretching of wall, acidity amino acids or peptides in stomach) -enteric nervous system responds with changes in motility and secretion -gastrin is a component of gastric phase regulation
intestinal phase
stimuli from small intestine (Stretching of wall, acidity, osmolarity,) -enterin nervous system responds with changes in motility and secretion -secretin, CCK and GIP are componentes of this phase
mouth
-mechanical and chemical digestion -contains salivary amylase -
uses of saliva
-salivary amylase -solvent that allows taste buds to be stimulated -lubrication for food -bicarb to precent cavities and keep the mouth clean (keeps pH high) -kick starts digestion -has antibacterial properties and wound healing enzymes (histatins)
esophagus
transport tube down to stomach -bordered by sphincters -peristalsis
sphincters
rings of muscle that form one way valves -skeletal or smooth muscle -almost always contracted, relaxation opens and allows passage
Functions of stomach
-chemical digestion -mechanical digestion -protection from chemicals
pepsinogen
made in stomach an enzyme precursor that is converted to pepsin– an enzyme that digests proteins
HCl
released in stomach breaks H bonds mkes 2L a day
intrinsic factor
made by stomach binds B12 to allow it to be absorbed in SI
Gastrin
made in stomach hormone that stimulates the acid secretion and gastric motility
mucus
made in stomach basic and protective
mucus cells
secrete mucus
parietal cells
secrete Hcl and intrinsic factor
cheif cels
secrete pepsinogen
enteroendocrine cell
secretes gastrin
How is the stomach protected by itself?
-enzymes are released in inactive forms and then converted to active forms -acidic interior is seperated from cells by thick basic mucous cells -is bordered at the top and bottom by sphincters
Wat are the jobs of the SI?
continue digestion protect itself from chyme (acidic) -accomplish majority of absorption
Small intestine digestion
bile salts contributed by liver/gall bladder Pancreatic enzymes from pancreas
Trypsin
A pancreatic enzyme Breaks peptide bonds into amino acids
lipase
pancreatic enzyme breaks down triglycerides into individual fatty acids
amylase
pancreatic enzyme splits polysaccharides
ribo and deoxyribonuclease
pancreatic enzyme breaks down DNA and RNA
What are the pancreatic enzymes?
trypsin, lipase, amylase and Ribo and deoxyribonuclease
Small intestine protection
HCO3 is a secretion by the pancrease into the SI
Nodal Cell depolarization
vetricular cell depolarization
