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7/29/2019 Physio exam
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What are the 2 control systemsof the body?
nervous and endocrinesystems
2 stages of transport ofECF?
1. movement of blood incirculatory system
2. movement of fluid betweencapillaries and cells
Percentage of ICF and ECF inbody weight and total body
water?
ICF: 40% bw, 60% tbwECF:
plasma- 5% bw, 8% tbwinterstitial fluid- 15% bw, 30%
tbw
Biggest components of plasma(ions, pr)?
Sodium, chloride,some pr
Biggest componentsinterstitial? Sodium, chloride
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Biggest componentsintracellular?
Potassium, pr
Reason for chemical differencebetween ICF and ECF?
ICF separated by selectivelypermeable membrane, favors
diff ions
Permeability of lipidbilayer?
FA chains major barrier towater-soluble substances butallow fat- soluble substances
5 functions ofmembrane proteins?
Receptors, enzymes, ionchannels, membrane carriers,
antigens
5 ways substancescross membranes?
Endo/exocytosis, l ipid bilayer diffusion, protein
channel diffusion, facilitated diffusion, activetransport
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How does diffusionwork?
moving molec approaches station molec,transfer energy, new elastic collisions, evening
out of concentrations
5 factors affectdiffusion rate?
[ ] gradient solute, x-sectionalarea, temp (p)solute size,
viscosity of medium (i)
Movement throughprotein channels?
some molecs move thru membrane faster thansimple diffusion would explain, use protein
channels to cross
4 factors that affect rate throughpr channels?
size, charge, electrochemgradient, pressure gradient
Factors that affectosmosis?
membrane permeabilty, [ ]
gradient of solute, pressuregradient thru membrane
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Body fluid shift during waterload? Water loss?
load: decrease osmolality, increase in volumeprop to both compartmentsloss: increase
osmolality, decrease volume
Body fluid shift during soluteload? Solute loss?
load: increase osmolality, ICF expanded, ECFcontractedloss: decrease osmolality, ICF
expanded, ECF contracted
Affects chem and electricgradient on membrane
transport?
move to areas of lower [], move to areas of oppcharge, if in opp directions movement depends
on balance (electrochemical gradient)
Polarized transportepithelial cells?
Epithelial cells lining lumen and those liningbasolateral membrane have different transport
mechanisms, are energy efficient, allowunidirectional transport
What cells have rmp?All cells have rmp, only nerves
and muscles are excitable
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Equal Na & K; membranepermeable to only K, how does
membrane potential arise?
K moves down gradient, adds + to Na section,further addition prevented, electrical potential
across membrane K part more -
Equal Na & K; membranepermeable only Na, how does
mp arise?
Na moves down gradient, adds + to K section,further addition prevented, electrical potential
across membrane Na part more -
Forces acting on ions?Chemical and
electrical gradients
Eq potentials and rmp K, Na, Clin nerve?
K -94mv, Na +35mv, Cl-65mvRmp -70mv
2 functions Na/Kpump?
Maintain concentration gradient
for K and Na, stops cells fromswelling by osmosis of water
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What is the ratio of Na:K ions inthe pump? How many ions
move during 1 AP?
3 Na removed for every 2 Kpumped in.Very few (1 millionth
of available ions)
Duration of AP in nerves,skeletal m, cardiac m?
Nerve 1ms, cardiac 300ms,skeletal 1.5-2ms
Why AP does notreach Na eq potential?
Increased Na permeability lastsonly a short time & there is no
time when only Na is permeable
Add NaCl to ECF; effect onmagnitude of AP?
Increase [] gradient for Na, magnitude of AP notaffected because mp approaches Na eq in a
normal AP anyway
Mechanism thatreturns AP to rmp?
Continued increased
conductance of K when Napermeability back to normal
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How do local anesthetics block AP? Would ametabolic inhibitor affect the generation of
further APs?
Act on activation gates of Na channels bymaking it difficult to open, decreases
excitabilityAPs generated before ions breakdown enough to prevent generation
Describe voltagedependent Na
channels.
activation & inactivation gate, inactivation openat rmp, mp decreases Na rushes in, inactivation
closes slowly, open once cell at rmp
2 physiochemical disturbancesproduced by stimulationexcitable membranes?
Propagated APs and local,non-propagated potentials
(subthreshold)
Membrane disturbances causedby sub- threshold stimuli?
Local, decays, not refractory(can sum), depolarizing EPSP or
hyperpolarizing IPSP
Direction current flows and whatcarries it?
Positive tonegativeIons carry it
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Describe how APpropagates?
Inside cell + at peak of AP, outside - and +current flow inside results in depolarization ofadjacent area, Na gates open, AP generated,
continues to propagate
Describe saltatory conductionand its advantages.
Myelination except at nodes focuses outwardcurrent to nodes, membrane permeability
changes only at nodes, leaps from node tonodeFaster, conserves energy, less space
2 factors affect velocityof AP?
Axon diameter (larger faster),myelination (myelinated faster)
Determines directionconduction AP?
Orthodromic movement, mpbehind AP still refractory so
moves only forward
First 3 steps of AP atNMJ?
1. AP in presynaptic MN2. Depolarization of MNterminal knobs
3. Opening of voltage-gated Ca channels inknobs
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Steps 4-6 of AP atNMJ?
4. Influx Ca down [] gradient into cell5. Achvesicles fuse to MN terminus, release Ach
6. Diffusion of Ach into cell at endplate
Steps 7-9 of AP atNMJ?
7. Ach attaches to receptors at end plate8.Small cation channels open at end plate
9. Influx Na into muscle at end plate
Steps 10-12 of AP atNMJ?
10. Depolarization of membrane at end plate(EPP)11. Generation AP across membrane to
adjacent end plate12. APs propagated along membrane, spread in
all directions from end plate
Ionic mechanisms of end platepotential (EPP)?
Ach binding to ep receptor causesconformational change allowing ions to enter.Only Na enters bc mp is close to eq p of K so
stationary to keep gradient & Ca has lessmobility
Structural componentsskeletal muscle?
Bundles of multinucleated cells, bundles ofmyofilaments (myofibrils) along long axis,
sarcomeres make up myofibrils, 2 typesmyofilament: thick and thin
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4 functions ATP inmuscle contraction?
Position myosin head & increase binding affinityfor actin, powers crossbridge movement,
release myosin head from actin, brings Ca backto SR
Grading of muscle activityaccomplished?
Varying stimulation frequency,recruitment
Briefly describe the slidingfilament theory of muscle
contraction
1) Ach released, goes through the sarcolemma& into the muscle fiber
2) Sarcoplasmic reticulum releases Ca2+,coating all of the microfibrils
3) Ca2+ bind to actin filament, causing myosinfilament to stick to actin filament
4) Myosin heads pull actin filaments together (Hzone and i band disappear)
5) Sarcomere shorten, causing muscle fiber toshorten, causing muscle to shorten
3 types tissueinnervated by ANS?
Smooth, cardiac,glands
Distinctive features ofANS?
Controls internal environ, less voluntary, doesnot initiate function just supports & regulates,
dual innervation (e, i), organs in ANS do notatrophy
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2 anatomical divisionsof ANS?
Sympathetic nervous system(SNS), parasympathetic nervous
system (PNS)
Fibers of the 2divisions of the ANS?
PNS: craniosacral, shortpost-ganglionic
SNS: thoracolumbar, shortpre-ganglionic
How are nerve impulsestransmitted pre to post in ANS?
Ach secreted by pre,synapse post
How are nerve impulsestransmitted from post to
effector?
Post releases neurotransmitter (Ach in PNS, NEin SNS) synapses with cells of effector organs
Note: SNS sometimes secrete Ach, sweatglands vasculature of skeletal muscle
Neurotransmitters for eachsynapse in ANS?
SNS: pre Ach, post NEPNS: preAch, post Ach
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Describe the synthesis andbreak down of ACh.
Synthesis happens in the nerve terminal.Choline + AcetylCoA -----> (choline
acetyltransferase) Acetylcholine + CoA
Metabolism - Acetylcholine ----> (acetylcholineesterase) Choline + acetic acid
Describe the synthesis andsecretion of acetylcholine
1. choline is transported (cotransport with Na)into cell
2. choline + acetyl-CoA converted to AChthrough choline acetyltransferase (ChAT)
3. ACh enters vesicles4. With increase in Ca, the vesicles fuse and
ACh gets secreted into the synapse5. membrane bound AChE (both presynapticnad postsynaptic) rapidly degrades ACh into
choline and acetate
What is the duration ofaction of Ach?
Few seconds
Pathway forepinephrinesynthesis?
Tyrosine ---> (Tyrosine Hydroxylase) --DOPA--->(DOPA decarboxylase)---Dopamine
---->(Dopamine Beta-Hydroxylase)---NE--->(phenylethanolamine-N-methyl-
transferase(PNMT))---Epinephrine
Describe secretion of Epi & NEby adrenal medulla.
PNMT only in adrenal medulla so secretes both
Epi and NE, stored in secretory vesicles,secreted via exocytosis
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Termination of NE action can beaffected via three mechanism:
Re-uptake of NE by active transport(up to 70%), then breakdown bypresynaptic MAO.
1.
Diffusion of NE from the synaptic cleftinto capillaries (the cleft is larger thanat endplate of skeletal muscle).
2.
Extra-neuronal uptake of NE by
COMT with subsequent intracellularbreakdown by enzymes
3.
Receptors for Achaction mediation?
nicotinic, muscarinic
Receptors for NE and Epi actionmediation?
alpha 1 (viscera), beta 1 (cardiac) --> excitatoryalpha 2 (sympathetic postganglion),beta 2
(skeletal muscle) ---> inhibitory
Effects ofparasympathetic
stimulation?
narrows pupil, decrease heart activity, dilatesarteries, increases stomach activity, stimulates
secretion of various glands
Effects of sympatheticinnervation?
increases heart activity, widens pupil, constrictsblood vessels, inhibits secretion of various
glands
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What is the significance of 300mmoles/Kg H2O?
Isotonic solution, where blood isnormally at
What are the mechanisms thatoccur during water load? Loss?
loss: increase osmolality, decrease in volume ofboth compartments
load: decrease body fluid osmolality, increase involume of both compartments
What are the mechanisms thatoccur during solute load? Loss?
load: increase osmolaloty, expansion ECF,contraction ICF
loss: decrease osmolality, ICF expanded, ECFcontracted
Net fluid movementequation?
NFM= Kf [(Pc-Pt)-(πc-πt)]
Describe voltagedependent K channels.
Activation gate on inside, mpdecreases gate opens slowly,permeability at max when Na
inactivated
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Role of circulatory system astransport system?
Transport O2 and nutrients to tissues, CO2 andwaste from tissues, reg body temp, distribute
hormones
Components of cvtransport system?
Central pump (heart), closed sysbv, fluid medium (blood)
Where does the pulmonary veincarry blood to?
Oxygenated blood intoLA, flows into LV
What happens withcontraction of LV?
Blood expelled into aorta, goesto arteries, arterioles, then
capillaries
What are capillariesresponsible for?
Exchange vessels, O2 and
nutrients pass into tissues, CO2and waste taken by blood
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Where does venous blood goafter the capillaries?
Venues to veins to RA,flows into RV
What happens withcontraction of RV?
Ejects venous blood into pulmonary artery,oxygenated blood passes thru lungs, goes to
pulmonary capillaries
What happens in the pulmonarycapillaries?
CO2 diffuses into alveoli, O2 intoblood
Describe the series circuitarrangement of the heart.
Blood flow to individual beds canbe controlled separately byartery supplying the bed.
Describe the parallel circuitarrangement of the heart.
Found in lower body, contributes
to low resistance, low pressure,organs connected in parallel
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Normal total bloodvolume in dogs?
3 to 4 L
Where is the largest part of theblood volume found?
Venous system(capacitance vessels)
What are the resistance vesselsand how much blood do they
contain?
Aterial system, 10%total blood volume
What are the exchange vesselsand what percent of bloodvolume do they contain?
Capillaries, 5% totalblood volume
What is stroke volume and howmuch is it?
Volume of blood ejected from LVby 1 beat of the heart, 70mL
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How is arterialpressure calculated?
flow (HR & SV) x resistance(caliber of small aterial vessels)
What is homeostasisfor the heart?
Stroke volume
Order the vessels in the arterialsystem from largest to smallest
lumen diameter.
aorta, arteries, arterioles,capillaries
Order the vessels in the venoussystem from largest to smallest
lumen diameter.
vena cava, veins,venules, capillaries
How does velocity change with cross-sectional
area? Which vessels have the greatest cross-sectional area?
As cross-sectional area increases, velocity
decreases. Capillaries have the greatest cross-sectional area
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Average pressure in aorta?Range & what do those
numbers mean?
100 mmHg. 80-120 mmHg, 80mmHg is diastolic pressure and120 mmHg is systolic pressure
Pressure in the arterioles?Capillaries at the start and end?
55 mmHg, 30 mmHgand 10 mmHg
Relationship between systemiccirculation pressure and vascular
resistance?
High pressure = low resistance,as resistance increases
pressure falls
Most resistance vessels & what% of resistance of system?
Arterioles, 50% of resistance ofentire system
How does elasticity change withthe different vessels?
Aorta most elastic, elasticity decreases to
capillaries, starts to increase again up to venacava (most elastic on venous side)
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Formula for resistancein circulation?
R= ΔP/Q
R= resistance, P= pressuregradient, Q= blood flow
Compare systemic circulationwith pulmonary circulation.
Systemic resistance is about 17 mmHg/min/L.Pulmonary resistance is about 1.7 mmHg/min/L
(low pressure-low resistance)
Pressures in heart chambers ofresting adult?
RA: 9/4RV: 24/4-10LV: 110/5-12
LA: 12/5
Pressures in majorvessels?
Pulmonary artery:23/16Aorta: 110/75
What is pulsepressure?
Systolic pressure -diastolic pressure
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What is mean arterialpressure?
MAP= diastolic- 1/3 pulsepressure,(Average pressure
throughout cardiac cycle)
2 major factors that affect pulsepressure?
Stroke volume output,compliance of arterial system
Increased SV affects PP how?Increased arterial compliance?
Increased SV= increasedPPIncreased compliance=
decreased PP
What body areas have thehighest blood flow distribution?
Liver, kidneys, muscle,brain
Besides muscle, why do other
areas of high blood flow requiredistribution?
Liver has to support high metabolic activity,
brain needs nutrition & prevent CO2 from bloodkidneys need for excretion
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What happens if blood flow tohigh need areas stops?
Organ failure for liver,brain, kidneys
How does blood flow differbetween inactive and active
skeletal muscle?
Inactive uses about 15% while active individualmuscle flow can increase 20-fold, total
metabolic rate 50-fold
Valves in left side ofheart?
Mitral valve (bicuspid) betweenLA and LV, aortic valve between
aorta and LV
Function of valves in left side ofheart?
Mitral valve closes during systole preventingback flow to LA. Aortic valve closes during
diastole preventing back flow to LV
Valves of right side ofheart?
Tricuspid valve between RA and
RV, pulmonic valve betweenpulmonary artery and RV
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Functions of valves on right sideof heart?
Tricuspid valve closes during systole preventingback flow to RA. Pulmonic valve closes during
diastole preventing backflow to RV
What are the atrioventricularvalves? Semilunar valves?
AV valves= mitral andtricuspidSemilunar= aortic and
pulmonic
How long doesdiastole last? Systole?
0.53 s, 0.27 s
How is a cardiac cycleinitiated?
Spontaneous generation ofaction potential SA node
What path does the AP in thecardiac cycle take?
SA node thru RA, conducted in
AV node (0.11s delay), passesto ventricles
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What does the P wave on anECG represent?
Depolarization of atria followedby atrial contractions
What does the QRS complex ofan ECG signify?
Depolarization ofventricles
What does the T wave of anECG represent?
Repolarization of theventricles
What are the major pressureelevations of the atrial pressure
curve?
a wave - caused by atrial contractionc wave -ventricles begin to contract
v wave- end of ventricular contraction
What causes the cwave?
Bulging of AV valves, pulling ofatrial muscles
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What causes the vwave?
Slow build up of blood in atriawhen AV valves are closed
How does atrial contractioncontribute to ventricular filling?
Most of the blood coming to atria can draindirectly from ventricles during diastole, about
30% comes from atrial contraction
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