This site is 100% ad supported. Please add an exception to adblock for this site.

psl 250 final comprehensive


undefined, object
copy deck
realtionship between molecules, cells, and tissues.
molecules are the assembly of atoms, cells are the basic unit of life made, and tissues are collections of similar cells with same local function
what is the internal environment?
interstitial fluid, liquid around cells
what's negative feedback?
event x causes a change away from set point and response y causes a return to set point ex: blood pressure
what is the function of ribosomes?
they make proteins for use in cytosol
difference between rough and smooth e.r.
rough- has ribosomes, site of protein synthesis, new proteins move through er to smooth er smooth- no ribosomes, fat/membrane synthesis, produces vesicles that carry new protein to golgi app.
contain digestive enzymes, digest molecules down to usable size, ex: proteins to amino acids
aerobic energy production..
citric acid cycle...
in mitochondrial matrix, 7 rxs, pyruvate/NAD/FAD go in, CO2/ATP/NADH/FADH2 comes out
mitochondrial inner membrane...
cytochromes form system on inner membrane
oxidative phosphorylation...
NADH donates electron to ETS, H+ follows, NAD recycled. As e- passes, ATP made at 3 cytochromes.
what are vaults?
octagonal barrel-shaped structures that may be involved in transport (of mRNA and ribosomes) from the nucleus to the cytoplasm
what do microtubles do?
cell stability/ transport along neurons, move vesicles, organelles and chromosomes
hydrophillic vs. hydrophobic
phillic- outer sides of membrane, don't cross by diffusion except H20 phobic- cross easily
prevents close packing of fatty acid chains, create membrane fluidity
difference between channels, carriers, and receptors
channels- holes, only ions go thru, open or closed carriers- "revolving" proteins (no ATPase), alternative open side, molecules move w/ gradient or co-trans. w/ ion receptors- on outside, bind to solute, some activated by a physical change, activate either channel or enzyme
difference between tight junctions, desmosomes, and gap junctions
tj- water can pass thru, block movement between cells, create tissue sidedness, allows selective transport, must go thru cells d- cellular rivets, hold moving cells together gj- channels between cells, electrical signal from one cell activates next
fick's law of diffusion
rate of diffusion = permiablitiy x area x concentration gradient / molecular weight
ion channels-
different types for different ions, allows ion to move by chemical/ electrical gradients
difference between facilitated diffusion, active transport, Na-K ATPase
fd- no ATP used, move down diffusion gradient, molecules bind to one side and leaves on the other, high->low conc. at- pumps low->high conc., uses ATP, ions move by this na-k- creates ion gradient that produces all electric, moves Na out of cells and K in, electrical signaling
secondary active transport
hydrophillic, carrier has 2 binding sites: agonist and Na energy, cotransport or countertransport
difference between concentration and permeability
c- determine size of membrane in potential cells, differences in MP reflect differences in intracellular concentration p- determined by number of open channels, number of each open K or Na channels determines the MP
diffence: depolarization & hyperpolarization
d- MP is less negative, causes by K channels closing and Na channels opening, moves MP toward Na equilibrium potential h- MP gets more negative, caused by K channels opening and Na channels closing, MP moves toward K equilibrium potential (brain prevents signals from being sent)
graded potentials...
carries signal short distances, triggered by agosnists/physical force,don't send signals to brain, needed to reach threshold of action potentials
voltage-gated channels...
open when membrane reaches particular voltage, all v-gated channels open together causing action potential, inactivated soon after opening making refractory period
ap spike
all identical, Na enters and rapid depolarization to +20mV occurs, doesn't reach Na equilibrium potential b/c some v-gated K channels also open
v-gated Na channels close after 1-2 msec, K channels still open and K leavs and membrane potential falls
recieve neurotransmitter from other neurons, many branches, no action potential only graded.
very long-carry AP away from cell body
accelerates rate at which axons are carried
difference between hydrophillic/phobic hormones in regard to activation
phillic- can't cross membrane, rely on membrane receptor activation phobic- diffuse past membrane into cell to activate genes
refractory period
after v-gated channels close they are unopenable for a time, no new APs during this time, AP only travel along axon in one direction (can't go back)
presynaptic neuron
end of axon, receive AP down axon, opens Ca channels
contain neurotransmitter,increase in Ca triggers merger with cell membrane
difference between EPSPs and IPSPs
e-NT bins and Na channels open, Na enters and causes depol., one isn't enough to reach threshold i- K/Cl channels opened by NT, MP more negative, less likely to reach threshold
difference between convergence and divergence
con- multiple synapses into single neuron div-each axon has many synaptic knobs to other neurons, an AP in one neuron delivers NT to all its div. neurons at the same time.
local hormone, released from one cell, affects cell next door, important in control of blood flow
backbone of membrane
what is the enzyme EVERYTHING has?
Na-K ATPase
what's the resting membrane potential?
voltage across cell membrane when cell is NOT activated, determined by open ion channels
second messengers
activated by hydrophillic hormones
activates kinases which cascades which amplifies signals
g proteins
regulate vesicle movement, cytoskeleton, growth, vision
afferent vs efferent
a- carry info into CNS e- carry info from CNS to body
glial cells
supports neural activity
control neural growth and blood vessel growth in brain
cancer potential
neural cells DON'T divide and can't form cancers but glial cells can
when you learn something you alter number of synapses you have
used for death determination.
basal nuclei
controls balance, postural control is non-conscious
receives sensory input from opposite side, directs and edits input to cerebral cortex
limbic system
detects emotions and memory formation
few connections to cortex-limited cortical control of emotion, can't make emotions just go away
difference between short term/long term/ and working memory
st-hippocampus, alter activity in existing neurons lt-temporal, creation of new synapses and memory traces, makes copies of important memories over years w-frontal lobe, comparing new experiences to old recalls to determine relevance
cerebellum (balance/coordination)
controls coordinated/learned movements -maintains balance and controls eye movement -afferent input gives current muscle positions, as practice occurs, motor cortex/parietal lobe/cerebellum take over
slow wave sleep vs. REM (paradoxical sleep)
slow wave before REM sw- 4 stages rem-new synaptic contacts made increase long term memory
reflex/ components of reflex arch
r-neural response w/o conscious input ra- effectors are muscles and glands
stretch reflex
fastest b/c afferent neuron synapses directly with efferent
difference between physical and chemical receptors
p-changes open ion channels, changes MP c- taste, smell, chemical binds receptors/opens channels/changes MP
dcreases AP # despite prolonged stimulus
difference: phasic/tonic receptors
p- adapt over time t- don't adapt (few tonic receptors)
difference: fast/slow pain
f- sharp, localized, passes quickly. myelinated affarents- glutamate NT s- diffuse, dull, long lasting. unmyelinated afferents- substance P NT
bind to opioid receptors, short time course, block pain pathways
taste receptors
salty- Na sweet- organic sturctures acid,sour- H bitter,bases-cations, poisons, most sensitive receptor umami- glutamate (MSG)
olfactory adaptation
in CNS- brain can overcome adaptation
lens-ciliary body
lens refracts light to focus on retina, ciliary body has muscles parallel to lens that focuses
aqueous humor
glaucoma: decrease drainage or excess production increases pressure causing retinal damage
rods- shades of grey cones- color receptors (fewer) both converge on bipolar cell
bipolar cells
activated by rods/cones, no APs-synapse w/ ganglion cells, edge effect
ganglion cells
reach threshold and fire APs that leave eye for CNS, carry visual info to lateral geniculate
hardening of lens, reduces rounding of lens for near vision
color vision
3 different opsins with retinene (yellow,green,blue)
ear bones
malleus (hammer), incus (anvil), stapes (stirrup), vaces waves to oval window
middle ear
amplifies sound 20x
eustachian tube
drains middle ear fluid
basilar membrane, hair cells, tectorial membrane
bm- vibrates to sound waves shape hc-rest on basilar mem. airs imbedded in tectorial mem. tm- when bm vibrates imbedded hairs pulled on, hair cells produce GP->NT to afferent neurons, APs to CNS by auditory nerve
timbre (pronounced tambur)
overtones that allow source distinction
rotational acceleration
as fluid lags in motion, fluid pulls on hair cells
semicircular canals
reequilibrates when hard rotation stops
fight or flight response
designed to remove danger, increase blood flow to skeletal muscle and heart
receptor types (alpha/beta/beta2)
a- cause increase in tissue activity (fast) b-increase Ca in heart and increase heart activity b2-bronchiole constriction
parasympathetic responses
decrease heart rate, increase GI contractions/secretions, increase pancreatic secretions, contracts urinary bladder, relaxes internal anal and urinary sphincters
acetylcholine release, endplate potential, AchE
ar-ach binds to receptors on muscle membrane ep- larger than EPSP AchE- removes Ach
functional unit of contraction
components of thick/thin filaments
thin- actin polymer backbone, tropomyosin, troponin thick- myosin polymer
troponin-Ca binding
Ca binds to troponin on thin filament
tropomyosin shift
how skeletal/cardiac muscle are activated
diff. between force generation and filament sliding
fg- caused by loss of P fs- minimizes energy
motor unit
motor neuron and muscle fibers it innervates, activates all fibers in a motor unit
twitch vs tetanus
tw- single muscle activation te-summation of twitches
force-velocity relation/inverse relation
fr-heavy loads moved slowly, light loads moved quickly ir-high force = low velocity, vice versa
times of phophocreatine, flycolysis, oxidative phosphorilation
p- supports 20 seconds of full activity g- 2 mins op- 2 hours
hypertrophy/ filament number
change as function of activity
nuclear bag fibers/dynamic response vs. nuclear chain fibers/static response
nbf-tells change in length dr-detect change in length ncf-tells length sr-detects fiber length
gamma motor fibers
contract muscle portions of intrafusal fibers
dense bodies
analogs of the z line and sarcomere
activation of smooth muscle with no stimulus
myosin light chain kinase
enzyme that activates smooth muscle
maintains force with little energy use
visceral SM vs. Multi-unit SM
v-one contracts, all contract/ gap junctions m-each cell individually active/ no gap junctions or APs
intercalated disks
desmosomes for strenght, gap junctions for electrical activation spread
SA node
where heartbeat is initiated
ventricular muscle
sodium dominated
sum of changes in cardiac APs
P wave/QRS complex/T wave
p- atrial depol. qrs-ventricular depol. t- ventricular repol.
ventricular systole and aortic pressures affect
vs- contraction of ventricles ap- determine load on on heart
heart rate dependence
if heart rate gets too high perfusion of coronary system goes down and heart doesn't deliver blood efficiently
cardiac output
product of stroke volume x heartrate, amount of blood pumped per minute
effect of neural influences
para-slow heart down symp-speed heart up
vessel radius
most important variable factor controlling flow thru vessel
determined by number of RBCs
coronary circulation
heart rate dependent
alcohol effect on atherosclerosis
dissolves fatty streak in stage one
capillary flud exchange and filtration/reabsorption
-balance of BP forcing fluid out and osmotic presure from plasma proteins drawing fluid in f-at high pressure end r-at vesous end with lower pressure
lymph flow and edema
lf-return of filtered fluid e- excess filtration causing swelling
venous valves
prevent backflow, help blood from lower body get back to heart
metabolic vasodilators
more active = more bloodflow
enothelial factors/ nitric oxide
ef- paracrines no- hormonal/neural activation
stretch receptors
control of vasoconstriction and dilation/ resetting
c-short-term control of BP r-body adjusts to own normal BP
cardiac effects
hurts heart if BP too high, hypertrophy
diuretics/ACE inhibitors
d-increase Na excretion/lowers blood volume/decreases BP a-boock conversion of angiotensin I to II
plasma proteins
albumin, globulins, fibringogen
RBCs, lose cholesterol and rupture in tightest capillaries after 120 days
4 protein chains can carry 4 O2 molecules, 1/chain
platelets/ activation
pinched off parts of megakaryocytes in bone marrow a-by collagen and other proteins in connective tissue of blood vessels
intrisic/extrinsic system
i- in plasma, collagen activates cascade e- thromboplastin starts cascade
clot removal
activation of plasmin
rapid response/ diapedesis
convert into macrophages by moving into tissue
produce acids that kill parasites and allergic response
complement system (activation/pore formation)
major bacteria killer a- by antibodies or protein properdin pf- c5-c9 forms pores in membrane
increases blood flows and capillary permeability
activates anti-viral defenses in cells near virus infected cells
antigen presentation
part of antigen linked to MHC protein and put into cell membrane
plasma cell vs. memory cell
p-limited lifetime (1 week), make antibodies m-few cells have long life, provide antigen immunity
primary response vs. secondary response
p- activation of b cells slow short and weak s- activation of memory cells is fast strong and long
antibody functions
major- activate complement system to kill bacteria, labels cells for ingestion by phagocytes, activate natural killer cells
cytoxic t cells vs. helper t cells
c- bind to cell and inject perforin to form pores and cause osmotic lysis h- release cytokines that activate all b and t lymphocytes
MHC class I/II
1- self-antigens on surface of cells/identify cells as self 2-ingest and present antigens/activate t cells
e-desmosomes and keratin fibers hold cells together, prevents evaporation d- regulates heat loss, increase touch sensitivity, absorbs UV h- insulates body from heat loss
type I/II cells
1-separate air from interstitial fluid 2- produce surfactant to decrease resistance to alveolar opening
boyle's law
pressure x volume = constant, controls breathing
caused by contractions of diaphragm
alveolar surface tension and how surfactant breaks it up
a- adherence of water molecules creates surface tension on inside of alveoli s- several phospholipids mix w/ water and decrease surface tension
anatomical dead space
normal tidal volume is 500 ml (150 of mouth, pharynx, trachea, bronchi, bronchioles. 350 is normal alveolar inflation)
composition of alveolar air
P02 = 100mmHg, PC02 = 40
diffusion acroos alveolar wall
oxygen moving into blood, carbon dioxide moving out
Oxygen transport (oxygen-hemoglobin binding)
ot- 1.5% carried by dissolved O2, 98.5% carried by binding to hemoglobin oh- sigmoidal curve- cooperativity between 4 Hb subunits
carbon monoxide affects
binds to Hb, shifts Hb-02 curve to left
carbon dioxide transport
10% dissolved, 30% bound to plasma protein and Hb, 60% converted to bicarbonate
medullary control centers
dorsal/ventral respiratory groups. initate normal breathing and increases inspiration/expiration
chemical control of respiration
CO2 controlled
emphysema (decreased alpha-antitrypsin, surface area)
e- cigarette smoke, coal tar are most common causes d-protects lung tissue from digestion sa- progressive decrease in sa, need pure O2 to fill Hb
cystic fibrosis
recessive gene, decreased Cl channel activity, loss of airway Na and water, mucus sticky and digestive enzymes increase
functional unit of kidney
vascular/tubular system
v- 2 capillary systems, 1 for filtering, 1 for reabsorption t- from bowmans capsule to ureter
glomerular filtration
from glomerulus into bowmans capsule,only cells and proteins not filtered
tubular reabsorption
must recover most filtrate (125 filtered, 124 ml/min reab. = 2 ml/min urine = 2.88 L/day)
if glucose in urine, blood must have 3x amount normal glucose
sodium reabsorption
controls reabsorption of many other molecules
renin-angiotensin system (production/effects)
r-maintain BP by increasing Na and water reabsorption p- already know e- powerful vasoconstrictor, releases aldosterone
tubular secretion
3 process in kidneys, extra removal from plasma, move material into filtrate
H secretion vs. K secretion
increase in secretion of one decreases secretion of the other
vasopressin/ aquaporins
v- causes insertion of aquaporins in CD membrane a- H2O channels, retain H2O
urine buffering
filtrate pH must be 4.5 or greater for H to enter filtrate, urine buffered by bicarbonate/phosphate/ammonia
increases number of active Na carriers on lumenal side of CD tubular cells
bladder sphincter
internal- smooth muscle, involuntary external- skeletal muscle, voluntary
i- 2/3 total body water, K dominated w/ protein e- 1/3, Na dominated, no protein
BP control/ salt intake
b- short term drop in pressure causes auto-transfusion, long term is balance of thirst/intake and kidney fluid action s- kidneys need .5g NaCl/day, pee out extra
ECF osmolarity control vs. tonicity
ecf- needed to prevent swelling/shrinking of cells t- behavior of cells in solution
-cells shrink in hypertonic solution
acidosis effects
causes neural problems
control of H (extra cellular buffer)
e-bicarbonate most important buffer
repiratory control of H
second line of H defense, works with non-respiratory source of H, reduces CO2 in blood, reducing H back toward normal
repiratory/metabolic acidosis
r- abnormal CO2 retention from hypoventilation, renal compensation by increased H secretion m- most common acid-base disorder, excess H production durin fat use in diabetics, exercise leading to lactic acid and H production
complex carbohydrates
must be broken down by enzymes to be absorbable monosaccharides
lactose intolerance
no lactose produced = no digestion of lactose
protein digestion (proenzymes)
pd- must be broken down into amino acids p- released in protective form as to not harm pancreas
infant protein absorption
absorb protein directly
micelles/absorption/portal vein
m- help absorption of fats, carry fats to brush border a- MG and FFA cross and reform into TG in mucosal cells pv- transports water soluble foods directly to liver
potassium absorption
most critical to not have any neural problems
vitamin travel
B and C- portal vein. A,D,E,K fat soluble-micelles-lymph
basic electrical rhythm
function of SI.
migrating motility complex
clears small intestine at end of meal
g- initiates mass movement in LI that triggers defecation s- neutralizes stomach acid in duodenum
mouth secretions
bicarbonate, H2O, amylase, lipase, mucus, lysosome anti-bacterial enzyme
incomplete closure of lower esophogeal sphincter, acid irritates esophagus
stomach secretions
pepsinogen, HCl, mucus, gastrin
stomach emptying
pyloric sphincter secretes chyme in small amounts
exocrine pancreas
produces bicarbonate solution and enzymes for digestion
alkaline secretion
high bicarbonate conc.
enzymatic secretions
different enzymes for digestion
bilirubin metabolism
major waste product in feces and urine, breakdown product of heme
gall bladder function
stores bile between meals and delivers it when CCK comes along
microvilli vs. villi
mv- folds of cell membrane v- folds of SI wall tissue
SI motility
segmentation of mixing contractions and circular smooth muscle
loss of H2O and K, usually from LI
gastroileal reflex
emptying from small to large intestine when new meal comes
almost identical to urination, gastrin triggers colonic contraction
Basal metabolic rate
2000 calories/day
hypothalamic control of intake
matching feeding to energy needs, balance of hunger and satiety
Neuropeptide Y/ melanocortins
released by HT, stimulate appetite m- realeased by HT, suppress appetite
increasing fat storage signals satiety by releasing leptins
heat exhange
radiation, conduction, convection
response to cold/heat
c- decreased skin bloodflow, human adaptation h- increased skin blood flow, increased sweating
diurnal/circadian secretion
day/night around a day rhythms- on a 24 hour cycle
down regulation/permissiveness/synergism/antagonism
d-desensitization p-one hormone enhances response of second s- two hormones increase each others activity a- one hormone reduces the effect of another
plasma calcium
99% Ca stored in bone
parathyroid hormone
increases reabsorption of Ca, necessary for life
low blood Ca, larynx and diaphragm spasms- no air

Deck Info