Final Flashcards
Functions of LI
absorbs remaining water and water soluble vitamins
compaction of feces
how is water absorbed by LI
establish ion gradient using Na and then water moves by osmosis
what is the main component of feces?
indigestible starch components, we don’t have the enzymes to break down cellulose–fiber. Also some metabolic waste
role of bacteria in LI
LI is colonized by bacteria.
some breakdown of starch
produce vitamin K
produce gas through cellular respiration
defacation
2 anal sphincter. 1 smooth internal, one skeletal external
conscious urge is triggered by stretch of rectum
contract ab muscles to change pressure
valsalva maneuver
contraction of ab muscles and increased pressure in thorax assists in defecation. By holding breath you can create a change in pressure to help with defecation
But your heart rate will slow down
absorptive state
ingested nutrients are entering the vbloo from the GI tract (in the 4 hours after a meal)
-body wants to absorb more calores thana re required immediatle
some go to blood stream, the remainder are stored.
-total body storage is adequate for the average person to go weekks without food
post-absorptive state
GI tract is empt of nutrients fro stored nutrients must be used(in between meals)
the role of the liver
most ingested nutrients are carbs and proteins which are absorbed immediately into the blood and transported to the liver in hepatic portal vein
liver can filter/alter nutrients before then tracel to the heart and throughout the body
inactivates and removes toxins using liver enzymes
glucose is taken up
absorptive state events carbs
blood glucose levels rise.
is taken up by liver and skeletal muscle which stores it as glycogen
any excess is take up by the liver and converted to fatty acids and triglycerides for storage
gucose stoarge as lipids
synthesized lipids in liver are released into the bloodstream bound to protein transport molcules called lipoproteins: FDL, LDL and VLDL
What do newly made lipids from glucose travel on?
in blood on VLDLs. These are too big to cross out of capillart. gets to areas of adipose tissue which secrete lipoprotein lipase which seperates the lipid from the liporpotein allowing it to move into the adipose tissue.
fate of absorbed carbohydrates
- directly into blood to boost blood sugar levels
- stored as glycogen in liver or muscle
- stored as fat in adipose tissue
absorptive state events of lipids
go directly into lymph, then added to the blood in the vena cava.
Travel in aggregates
lipoprotein lipase breaks up aggregates and allows monomers to diffuse out of the bloodstrem to the adipose tissue
how are lipids stored?
as triglycerides
formation of triglycerides
glycerol head synthesized by glucose in the adipocyte: can be made by 3 sources, glucose from blood thats stored in adipocytes as fatty acids, glucoe from blood can be converted to stored fatty acids in the liver. ingested fatty acids from the blood
cholesterol
a type of lipid necessary for plasma membranes, bile salts, hormones.
can’t be used to cellular respiration
too much in circulation can contribute to atherosclerosis
changes in cholesterol levels
liver can make it
SI can transport some into blood
some passes as feces
liver can also remove colesterol from blood to make bile salts
cholesterol set point
liver is primary control
works by negative feedback (if blood cholesterol is to high, the liver cholesterol production will be inhibited and more will be transported to digestive system
set point can change based on diet etc
HDLs
remove cholesterol from blood and deliver it to liver or endocrine glands
LDLs
supply all cells with cholesterol for membranes
What non-diet factors impact HDLs?
smoking decreases HDLs
Exercise increases HDLs
circulating estrogen increases HDLs
absorptive state events of proteins
absorbed as AA, which are absorbed by cells for production of new proteins.
If needed for energy some amino acids can be converted to metabolic precursors in the liver– but the N group must be removed as urea–makes urine
Fate of ingested amino acids
- converted to metabolic precursors for energy
each cell stores the AA for protein synthesis
excess is converted to glycofen or lipids for protein storage
post absorptive state
no additional sources of enery
must maintain plasma glucose levels
where can glucose come from in the post absorptives tate?
liver glycogen–> glucose
adipose tissue: triglycerides–>glucose
muscle
protein breakdown and conversion to glucose
how long can you subside on liver glycogen?
~3 hours
using glucose and fats for energy
-can provide 720cal/day
organs go into glucose sparing mode where they preferentially use lipids for energy
ketones
form when the liver breaks down fats for energy, leads to ketosis
Control of nutrient use:
endocrine pancrease (insulin and glucagon)
epinepherine and cortisol
sympathetic innervation to liver and adipose
insulin
storage hormone
secreted by beta cells of pancreas
controls cell-expresion of glucose receptors
-promotes glycogen production in the liver and inhibits glucose secretion by the liver
glucose present, results in insulin release–binds to insulin receptors which results in expression of glucose receptor to bind glucose and transfer it into the cells
When does a cell membrane of neuron express glucose transporters?
-always expresses glucose transporters
they are insulin independent
if you had a mutation so you didn’t express lipoprotein lipase you would
- have very little body fat but high blood lipids
- decelop atherosclerosis
- have endocrine issues
more insulin–> what change in blood glucose production?
less glucose in blood
If you accidenly inject excess insulin, what happens?
blood flucose is absorbed by the cells, not enough is left for the brain
Which cells require insulin
skeletal and cardiac muscle, and adipose
NOR BRAIN and NS
incretins
secreted by enteroendocrin cells in GI tract increase insulin
ie sense candy bar in your stomach, so increase insulin to deal wiht it
Control over insulin
glucose level in blood
incretins
hormones that inhibit insulin
sympathetic neurons– fight or flight inhibts insulin secretion
diabetes mellitus
cells cannot take up glucose from the bloodstream
Cause of Type I
auto immune, beta cells are attacked
Type II cause
genetics and lifestyle
cells become insulin resistant, later beta cells slow insulin production
glucose receptors internalize after excessive stimulation.
gestational diabetes cause
idiopathic, probably genetic or tendency toward insulin insensitivity
are then more likely to develop type II
if mom has high glucose levels–baby gets high glucose, and baby doesn’t have diabetes so gets it all.
Type I Treatment
injected insulin at each meal for life
Type2 treatment
diet+ exercise, injectable insulin or incretins,
metformin-down reg liver gluconeogenesis, increases insulin sensitivity
gestational diabetes treatment
lifestyle, glucose monitoring
what would be one of the first signs of type Ii diabetes?
- high blood bressure, b/c excess sugar as a solute in the blood, will drive water in
- increased frequency of infections-high glucose levels in tissues too, feeds more bacteria/yeast to grow.
glucagon
- produced by alpha cells of pancreas
- increase glycogen breakdown and gluconeogenesis in the liver
- effected by some hormones and sympathetic innervations
gluconeogenesis
making of glucose from amino acids or fatty acids
what would the effect of the fight or flight response be on blood sugar?
blood sugar increases
what is energy used for in body?
protein synthesis, ion pumps, cellular transport, muscle contraction, heat
excess is stored
basal metabolic rate
amount of energy to fuel basic properties without exercise or other increase in metabolism
based on body size, typical caloric intake and age
BMR and Body size
losing weight slows down metabolism
- losing 10% body weight–>15% decrease in energy expenditure
- gaining 10% body weight–>15% increase in energy expenditure.
leptin
inhibits appetite. Mice withour leptin voaraciously eat and become obese
- made by adipocytes and released in proportion to the amount ot fat in adipose cells
- stimulates metabolism
- says that you have enough energy, don’t need to eat as much
ghrelin
made by somach lining cells
stimulates appetite
lack of stretch of stomach results in release (empty somach
signals to stop eating
leptin
insulin release
-increase in body temperature
-stretch receptors and hormones in stomach, SI, LI
corticotropin releasing hormone and appetite
decreases appetite
leptin source and impact on appetite
adipose tissue decrease,
insulinsource and impact on appetite
pancrease, decrease
ghrelin source and impact on appetite
stomach, increase
CCK source and impact on appetite
intestine decrease
peptide YY source and impact on appetite
intestine, increase
extreme biggest loser diet
ghrelin soar, leptin levels sink, body thinks you’re starving, these changes remain for 6 years
genetic influece in weightloss
hormone levels, BMR, food preference may be genetically driven, tendency to gain/lose weigjt
twin weight study
] increased calorie intake, decreased exercise
all twins gained the same amount of weight and in the same places, some sets of twins gained 10, some gained 30. l
psychological factors and hunger
stress adrenaline and cortisol-decrease appetite and GI motility
-serotonin is released by intestines in response to food- might change depression
thrifty gene
if poor nutrition at young age, your genome encourages the storage of more energy
adiponectin
produced by adipose
decreases inflammation, promites using energy stores
resistin
adipose hormone, leads to insulin resistace
visfatin
agonist to insulin receptor, increases glucose uptake from the blood, mimics insulin
adipose hormone
adipo-cytokines
promote inflammation and mitosis in local areas
adipose hormone
according to the thrifty gene hypothesis, poor nutrition in infancy would result in
obesity in adulthood
what kind of ghrulin levels would you expect in a person who recently lost weight?
high ghrelin levels
would inhibiting glucagon lower blood glucose levels?
yes,
hypoxia
lack of O2
hypercapnia
too much CO2
functions of the respiratory system
gas exchange, acid-base balance, vocalization, immunity, waterloss and heat loss
cellular respiration
intracellular reaction that uses O2 and glucose to make Co2, h20 and ATP
external respiration
movement of gases betwen the environment and th bodys cells
ventilation
air exchange between lungs and external air
steps of respiration
- ventilation
- exchange of O2 and CO2 between alveoli and capillary
- transport of O2 and CO2 in blood
- exchange of O2 and Co2 betwee blood and tissues
- cellular utilization of O2 and production of Co2
type 1 alceolar cells
small thin for gas exchange between alveoli and capillaries
type ii alveolar cells
synthesize surfactant
- lowers surface tension of alceolus, allowing the cells to inflate
- prevents alveli from collapising alveloi
premature babies and surfactant problems
get respiratory distress because type 2 alveolar cells ar one of the last cell types to develop
is there smooth muscle in lungs?
no
elastic fibers cause recoil so that lungs return to resting after the inhale
inflation of lungs
- work of muscles bbetween ribs and diaphram
- widen the thorax and pull the lungs with them by fluid surface tension.
F=
change in p/r
boyle’s law of gases
if temp is constant:
pressure in inversely proportional to volume
if you increase volume, you decrease pressure`
we must icrease the volume of our lungs (And thus decrease the pressure) to sufficienctly form a pressure gradient with atmospheric pressure and allow for flow
BOyles law applied
inhale, air moves in because pressure is lower inside
exhale- air moves out if pressure is greater outside
If you experience systemic vasodialation, what happens to BP?
decreases
pneumothorax
air gets between the peural layers and the lung is no longer held t othe thorax by surface tension
what happens to flow if you narrow a vessel?
flow decreases, due to increase of resistance
asthma
inflammation and swelling of bronchiole walles
decreased diameter of bronciole- bronchoconstriction
less O2 air to alveloi
CO2 build up in alveoli
increased resistance lowers air flow
pulmonary edem
increased blood pressure, increased pressure, fluid leaves lungs and increases diffusion distance.
emphysema
decreased alveoli surface area=less diffusion
-treatment is to increased PO2
Daltons Law
total pressure=sum of partial pressures
daltons law applied
chemoreceptors in the blood are sensitive to hypoxia– you can increase or decrease the conc. of O2 by changing partial pressure (administering O2) or changing total pressure (changes with altitude_
henry’s law
states that the partial pressure of a liquid will equilibrate to that of a gas— means the partial pressure of a liquid will equilibrate to that of a gas
PO2 in air=PO2 in alveoli=PO2 in blood
4 laws of respiration
boyle-pressure and volume
fick-diffusion
dalton-gasses and proportional pressure
Henry-liquids and gases
PO2 in alveoli=
PO2 in arterial blood
PO2 in tissues=
between the PO2 in alveoli and the PO2 in venous blood
PCO2 in alveoli=
PCO2 in arterial blood
PCO2 in tissues=
same as PCO2 in venous blood, or more
hypercapnia
elevated PCO2–causes acidosis
control of respiration
diaphragm and intercostal muscles
- dont need to think about it, but can change it if you want
-
what directs cyclic innate breathin?
respiratory center in the medulla oblongata–based on chemoreceptors
peripheral chemoreceptors
in aortic and carotid bodies, detect O2 and pH cahngse
central chemoreceptors
monitor pH changes in th CSF
When will PO2 trigger an increase in ventilation?
<60mmHg– the point where Hb dissociation changes
COPD
narrowing, hardening and mucus build up in the bronchioles.
leads to chronic hypoxia and hypercapniia (low O2, high CO2)
-over time the chemoreceptors adapt, which means that the stimulus for increasing ventilation switches from high PCO2 to low PO2,
what normally stimulates an increase in ventilation?
high CO2
what happens if you give a COPD patient O2?
they stop breathing, because they have adapted to low O2 being a trigger to breath, so now having excess O2 they are not prompted to breath
Functions of the Urinary System
- Regulate extracellular volume and BP
- Regulation of osmolarity
- Maintainance of ion balance
- Regulation of pH–kidneys selectively secrete H of HCO3
- Excretion of waste and foreign chemicals
- Priduction of hormones
How does the urinary section work, 4 steps
- Filter
- Reabsorb
- Secrete
- Excete
nephron
the functional unit of the kidney
-blood processing unit
-work with capillaries to monitor and filter plasma
has 2 functional sections: renal corpuscle, tubule
portal system
when 2 capillary beds meet without first going to the heart
Renal Corpuscle
a capillary nest and cup around it that filters the plasma–filtration
tubule
long pipes, secretes and reabsorbs- fine tunes what leaves the body and what stays
glomerulus
the capillary nest
-fenestrated- but doesn’t allow RBC or plasma proteins out
bowmans capsule
the surrounding capsule
catches filtrate and directs it through the tubules
Has 2 walls: parietal and visceral, with a lumen space between these 2 layers
carpuscle
bowmans capsule+glomerulus
capillary is fenestrated— leaky
nephron
corpuscle+ tubule
parietal layer
the outer layer of bowmans capsule
visceral layer
the inner layer of the bowmans capsule- has epithelial cells called podocytes that cover the glomerular surface
podocytes
part of vsceral wall
have branching pedicles that wrap around the capillary and intertwine with each other
-connect to the basement mmbrane of the capillary endothelium
filtration slits
spaces between pedicles- line up with fenestrae
filtration membrane
-endothelium+ podocyte with lined up slits/fenestrae
proximal convoluted tubule
the tubule as it leaves the glomerular capsule
-reabsorbs stuff that we filtered out of the plasma
loop of henle
concentrating/diluting urin
-has 3 parts: descending, hairpin turn, ascending
distal convoluted tubule
name of tubule as it neats the collecting duct
-mostly secretion
kidney vasculature
efferent arteriole–> peritubular capillaries
as materials are reabsorbed from the tubule they enter back into the blood flowing through the peritubular capillaries
peritubular capillaries
- arise from efferent arteriole and drain into venules to return blood to the heart
- supply glucose, O2 to the nephron
- reabsorbed materials return to the blood here
- secreted substances are moved from the blood to the tubule here
where does filtration happen?
glomerulus
where does reabsorption/secretion happen?
peritubular capillaries
filtration
the bulk flow of plasma out of capillaries into vowmans capillary- affected by osmotic pressure and hydrostatic pressure
hydrostatic pressure-
higher in capillary, drives fluid out of the capillary
osmotic pressure
is higher inside the capillary, draws fluid In to the capillary
What happens if you constrict the afferent arteriole?
decreased GFR
what happens if you dialate the efferet arteriole?
decreased GFR
what happens if you constrict the efferent arteriole?
increased GFR
what happens if you dialate the afferent arteriole?
increased GFR
when do you want to control GFR?
high/low BP, increase/decrease blood solutes, stress
afferent arteriole characteristics
has a larger diameter (to increase GFR)
has ha higher density of receptors for sympathetic innervation and hormones
efferent arteriole characteristics
smaller diameter
exits the glomerular capsule and brings blood to the peritubular capillaries
-blood here has low pressure and is very concentrated
glomerular filtrate
once it is out of the capillary
what 3 barriers does filtrate pass through before getting to the lumen of the tubule?
- glomerular capillary endothelium
- capillary basement membrane
- epithelium of podocyte- visceral layer of the bowwmans capsule
glomerular filtration rate
the volume filtered into bowmans capsule per unit of time
average GFR=
125ml/min
what 3 factors determine the GFR?
- hyrostatic pressure– higher in drives fluid out
- osmotic pressure-higher in, drives water IN
- hydrostatic pressure of the capsule– since it is an enclsed space, the pressure can drive fluid back into the capilary
how many times is the entire blood volume filtered each day
60 times
do normal changes in blood pressure alter GFR?
between 80-120 has no difference, because the afferent arteriole can change its diameter to maintain a constant GFR
myogenic control of GFR
when stretch receptors are activated in the affterent arteriole due to an increase in BP, smooth muscle cells constrict, decreasing flow into the glomerulus
increase in pressure–>decrease rate of flow–> maintained GR
juxtaglomerular apparatus
an anatomical site here the afferent arteriole and DCT are adjacent to each other.
juxtaglomerular cells
the smooth muscle cells of the afferent arteriole– these are mechanoreceptors that sense blood pressure in the afferent arteriole
sense stretch and then can contract or relax in response
secrete renin
macula densa
the enlarged epithelial cells in the DCT
these are osmoreceptors, chemoreceptors and mechanoreceptors. They detect solute concentration changes in the tubular lumen
juxtaglomerular apparatus and control of GFR
-when more solutes are detected in the DCT, the macula densa cells in the DCT send a paracrine message to the juxtaglomerular cells in the A.A. to constrict and decrease GFR
what does to many solutes at the end of the tubule indicate?
hat the filtration/reabsorption/secretin is going to fast and needs to slow down, will signal constrivtion of A.A.
renin
secreted by juxtaglomerular cells to increase solute reabsorption
is reabsorption or molecules uder physiological control?
Some yes. ie we can alter how much water we reabsorbed based on need
some no– ie we always reabsorb as much glucose as possible
How is reabsorption accomplished?
through active or passive transport—-NOT BY BULK FLOW
What 2 surfaces does reabsorption occur across?
luminal membrane of the tubular cells, the blood facing side of the tubular cells
transcellular transport
from inside the tubular lumen all the way to the capillary
what is reabsorbed by passice transport via simple diffusion?
anything small, non-polar, lipid soluble down its conc. gradient
what is rabsorbed cia facillitated diffusion?
anything eith a transporter protein down its conc. gradient
how are Na and glucose/AA transported into the proximal tubule celles from tubular lumen?
Na+/H+ counter transport
countertransport of Na/ glucose or AA
How are glucose/K/Na transported from the proximal tubule cells out into the intersticial fluid?
down their conc. with simple diffusion, or via active transport Na/K pump
how does the reabsorbed stuff get back into the blood?
peritubular capillaries are very low in pressure, so it flows in via bulk flow and diffusion
What is secreted?
organic ions, metabolic waste, drugs, some H_, J
Renal clearance:
how quickly we rid the plasma of a substace.
Mas od S excreted per unit time/ Plasma [S]
What are transporters ruled by?
competition, specificity, saturation
Diabetes and the kidneys:
increased plasma [glucose]
increased BP
Increase GFR
increased urine volume
since glucose transporters are sturated, the glucose remains in the rubule, which results i more water remaining in the tubule.
polyuria
more water excrete
polydipsea
excessive dehydration and thirts
what secretes vasopressin
hypothalamus/posterior pituitary
what influencesvasopressin secretion?
osmoreceptors in the hypothalamus and baroreceptors in the carotid and aorta
what is the action of vasopressin
opens aquaporins in collecting duct, water is free to leave followig osmotic gradient
what inhibits vasopressin?
alochol consumption
what happens if vasopressin is inhibited
water is not reabsorbed, increased urination
what does aldosterone do?
increases reabsorption of Na in DCT
-also controls K secretion because some Na transporters are Na/K pumps
IF VASOPRESSIN Is present– H20 follows the Na reabsorption via osmotic gradient
what secretes aldoseterone?
adrenal medulla
what triggers aldoseterone secretion?
decreased BP– JG cells secrete renin
angiotensinogen is converted to angiotensin I by renin
Angiotensin I is concerted to angiotensin II by ACE
Angiotensin II trigers release of aldosterone
angiotensinogen
is always present and inactive in the blood
is converted to angioteni I by renin (from JG cells in response to decreased BP
angiotensi I
made by angiotensinogen + renin
is converted to angioteni II by ACE
ACE
converts angiotensin I to angiotensin II
Angiotensin II
travels in blood to adrenal medulla and triggers the release of aldosterone
-increases BP
how does angiotensin II increase BP?
- increases vasopressin secretion
- increases thirst
- potent vasoconstrictor
- increases sympathetic output to the heart
what do ACE inhibitors do?
prohibits formation of angiotensin I– act as ablood pressure drug
atrial natriuretic peptide
produced in myocardial cells of the right atrium in response to stretch
increase GFR, decrease Na reabsorptoin
mechanisms for increasing BP
aldosterone, vasopressin, thirst
mechanisms for decreasing BP
atrial natiuretic peptide
skeletal muscle
long, multinucleated, myofibrils, striated, voluntary contraction
smooth muscle
no banding, not voluntary contraction, spindle shaped, contract as a sheet, can divide
smooth muscle contraction
-don’t have tropoin or sarcomere
thin filaments are anchored to membrane or dense bodies. Contraction pulls the ends of the cell closer together and widens the middle
Ca binds to Calmodulin, which activates a kinase that phosphorylates myosin, activating it and allowing for cross bridge cycling
Ca comes from sarcoplasmic reticulum and the extracellular flud
No Na
Cardiac Muscle
striated, troponin and tropomyosin, single nucleated, forked. Fused ends called intercalated disks
Cardiac muscle contraction
Na procivide intiail depolarization, which then opens the Ca channels
tropic hormone
stimulate other glands to make and release hormones
humoral stimulus
endocrine glands monitor the blood and release hormoes in response to a change in the blood
hypothalamus
influences hormone secretion from the anterior pituitary, produces hormones itself. Oversees hormone secreting by the adrenal medulla
posterior pituitary
stores hypotalamic hormones
anterior pituitary hormones:
thyroid stimulaing hormone, prolactin, adrenocorticotropic hormone, growth hormone, follicle stimulting hormone and luteinizing hormone
posterior pituitary hormones
oxytocin and vasopressin
oxytocin
cervical opening in labor, milk let down in lactatione, role in bonding with baby
vasopressin
constricts smooth muscles around blood vessels increasing blood pressure and decreasing urine output
calcitonin
encourages calcium deposition intot he brain from the blood “calcium to the bone”
parathyroid hormones
opposes calcionin, stimulates vit D formation,
growth hormone
stimulates maturation and mitosis of chondrocytes, triggers release of insulin like growth factors from the liver and osteoprogenitor cells
cortisol
stunts growth
interstitial/leydig cells
in seminiferous tubule– secrete testosteron
triggered by LH
sertoli cells
make up the seminiferous tubules, aid in spermatogenesis
filter nutrients for developing sperm, transport testosterone to the lumen.
Trigered by FSH
production of testosterone
endocrine cells in the testes
cholesterol–> androstenedione (also made in adrenal cortex)–>testosterone
testosterone is also converted to estradiol via aromatase
egg production
egg matures in follicle.
After ovulation the follicle remains in the ovary and is called the corpus luteum (this time after ovulation is the luteal phase
theca sells
stimilated by LH, make androgens
granulosa cells
stimulated by FSH, convert androgens to estrogen
progesterone
made by corpus luteum and placentaa, also by adrenal cortex.
Maintain uterine lining, water and ion balance, regulation of synaptic activity associated with mood, memory and immune functions
also in kidney.
ovarian cycle
estrogen peaks, triggeres LH secretion LH triggers ovulation (secretion of LH by anterior pituitary is controlled by estrongen
menstruation occur when progesterone levels fall (corpus luteum that had been secreting progesteron dies)
FSH
stimulates development of follicles
LH
trigger ovulation
estrogen
prepares uterine lining,
the surge in estrogen is what triggers LG secrection.
progesteron
maintains uterine lining (Secreted by corpus luteum) and inhibits secretion of FSH and LH– so you don’t keep ovulating while pregnane
Prostaglandin
increases with decrease of estrogen and progesterone, , this trigers vasoconstriction and uterine contractions
adrenal glands
-cortex-secretes aldosterone+ cortisol+androgens
medulla–> epinephrine
Salt, sugar and sex
epinephrine
increases breathing rate, increases heart rate, breaks down glycogen and fat for more glucose in the blood, decreased appetitei
cortisol
shifts blood flow to skeletal muscles
breakdown protien and fat for more glucose in the blood. decrease sex drive, decreased inflammtion and immunity, decrease bone growth etx increases need to eat to replenish glucose stores
what does cortisol do to blood pressure?
causes ssystemic blood presure which increases bloodpressure
what does stress do to ADH and vasopressing,
have decreased need to pee, so increases ADH and vasopressin
adreal insufficienct: hyposecretion
weakness, fatigue, decresed appetite, decreased BP, decreased glucose. caused by decreased cort.
hypersecretion/cushings sydrome
due to increased cort. leads to osteoporosis, hypertension, hyperglycemia, immunosuppression
albumin
in blood plasma– is an osmotic regulator to reduce edema and increase viscosity
tramsferrin
plasma protein tha inds iron
ferritin
liver protein what stores iron
RBC production
triggered by erythropoietin which is a hormone released by the kidneys when O2 delivery to the kidneys falls below a certain level
testosterone also triggers erythroopoitin
anemia
reduced O2 capacity
pernicious-lack of b12
iron deficiendy
polycythemia
too many RBCs
clot formation
platelets gather, exposed to collagen, leads to platelet activation.
prothrombin (plasma prot.) is cleaved into thrombin
thrombin cleaves fibrinogen to fibrin monomers
fibrin monomers polymerize into fibrin net
bacteria
single celled, reproduce on their own, can share DNA via proximity
virus
can’t reproduce on own, insert their DNA into ours, we reproduce them.
fungus
reproduce on their own, have nucleuys
parasites
must be transmitted from host to host, can reproduce on their own
b cells
antibody production
helper t cells
recruit other cells to sites of infection
killer t cells
kill infected cells
macrophages
clean up waste and extracellular pathogens– activate b and t cells
neutrophils
engulf and kill pathogen
eosinophils, basophils, mast cells
inflammation
• Ventricular muscle cell contracAon must be
Rapid
– have a long absolute refractory period
– Have a short relaAve refractory period to be ready
for next impulse
ventriculat muscle cell depolarization
-has leaky k to begin with
Na enters,
Ca enters, later than Na but for longer (long absolute fractory period
K exits (short relative refractory period)
nodal cell decpolarization
spontaneous (a few Na and Ca channels open when voltage is negative, more Ca open when threshold is reached
rapid
long absolute
short relative does not depolarize all the way to 30, stops at zero
How does the parasympathetic nervous system impact heart rate?
increases k permeability, decreases Ca permeability
how does sympathetic nervous system impact heart rate?
increases ca and na permeability
p wave
atria depolarizing
qrs
ventricle depolarizing
t wave
ventricle repolarizing
systole
contraction- blood is ejected
diastole
relaxation, blood filld
cardiac output
HR*stroke volume
portal systems
1. Hepa7c Portal Vein: delivers nutrients to liver
from intesAnes, low O2
2. Hypothalamus-Pituitary Portal system: brings tropichormones from hypothalamus to pituitary
3. Kidneys: delivers plasma to be filtered for
urinaAon, connects arterial capillary to arterial
capillary
angiogenesis
making new blood vessels
blood pressure in veins
pulmonary pump and skeltal muscle pump
pulse pressure
systolic-diastolic
Mean arterial pressure
avg blood pressure in the vessels over time. Diastole lasts longer than systole so the mean pressure is closer to diastollic
MAP
HRSVTPR
heart rate, stroke volume, total peripheral resistance
how tp change bblood flow?
change resistance or change pressure (voume or HR)
myogenic mechanism
increased blood flow, results in hincreased diameter and your body decreases diameter as a responese to limit blood flow
CCk
from SI, stimulates bile release, inhibits gastric emptying
secretein
from SI, inhibits acid and motility in stomach, stimulates HCO3 release
cephalic phase
sight smell taste etx
gastric phase
stretch, acidity, contents of stomach
