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202 Cards in this Set

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normal pH in blood
7.35-7.45
if a person is acidotic chronically, how does the body compensate
make more ammonia, which binds the acid and removes in urine
how does an acidotic coma work
extra H bumps Ca off of plasma proteins, extra Ca around shields the Na channels, no Na can enter, leads to depression of nervous system
kidney failure results in this problem
acidosis - dont excrete the acid via kidneys
what effect does aldosterone have on Na and K
increases reabsorption of Na
increases release of K
explain addison's disease
hypoadrenalism
low aldosterone
higher levels of K
leads to cardiac arrest and fibrillation
explain hypocalcemic tetany
ex. PTHectomy
Ca normally shields Na channels, lack of Calcium leads to rapid firing of channels, spontaneous action potentials
death by laryngospasm
PTHectomy results in less PTH and thus less calcium in the blood
how can colloid pressure affect the brain
lack of proteins in the blood leads to a low colloid pressure
low blood volume
osmotic force thus not sufficient
not enough blood to brain or coronary vessels
how does addisons lead to circulatory shock
hypoadrenalism, lack of aldosterone, less Na retained, not enough blood volume so less blood to tissues
given for anuresis, ADH overdose can cause
water intoxication
this increases blood calcium levels
PTH
causes massive diarrhea and hypovolumic shock
cholera
anaphylactic shock
vasodilation
increased permeability of capillaries thanks to histamine
fluid leaks into tissues
drops blood pressure and venous return
explain intermittent claudication
pain in legs upon walking
drinks coffee, smokes, no water
nicotine causes vasoconstriction
low blood volume
average temp
98.2
core temperature kept fairly constant
homeotherms
what kills in hypothermia
death by ventricular fibrillation from hypoxic heart muscle
2 causes of hyperthermia
exercising without adequate fluid
no temp regulation - infants and elderly
2 outcomes of positive feedback
death or new steady state
examples of limited positive feedback
learning, nerve growth causing limb growth, action potential in that Na enters and more follows, ovarian cycle in that increased estrogen leads to increased LH secretion leads to ovulation
loose carbohydrate coat of outside surface of cell
glycocalyx
ficks law of diffusion
flux = diffusion coefficient D x area A x Cin - Cout / thickness

or PA(C1-C2) p = permeability and a = area
type of diffusion with saturation kinetics
facilitated because eventually all of the carriers are occupied so the graph levels out
addisons blood is ______tonic to regular blood
hypotonic, no aldosterone so no Na reabsorption, more K in the cell
van't hoff equation
osmotic pressure = concentration of particle x universal gas constant x temperature
osmotic pressure is a ______ property
colligative
explain diabetes osmotic diuresis
hyperglycemia, so high glucose in urine, water follows glucose
osmotic pressure produced by plasma proteins
colloid osmotic/oncotic pressure
colloid pressure is counteracted by
hydrostatic pressure
which is greater, colloid pressure or hydrostatic pressure
hydrostatic, bulk flow is usually out of capillary at arterial end
edema causes a __crease in colloid oncotic pressure
decrease
filtration is a _____ process
passive
resting potential due to
K
explain no reflow phenomenon
following anoxic event, after heart stops, when heart restarts, endothelial linings of blood vessels are too swollen to allow reflow, brain cells die even as blood is being pumped again
secondary active transport uses this for energy
energy stored in Na concentration gradient
sodium glucose is ____port
symport
sodium amino acid is ____port
symport
sodium calcium is _____port
antiport
digitalis and dijoxin are cardiac glycosides that..
block Na/K pump (ATPase)
less Na out
less Na back in
less Ca pushed out
more calcium inside
increased force of contraction
cardiac muscles get calcium from
outside the cell
states that for every positive in, a negative must come out
law of electroneutrality
explain equilibrium/nernst potential
potential energy just necessary to stop the ion's movement
nernst equation
Eion = -RT/nF x 1n (Cin/Cout)

Eion = -60/n(valence) x log Cin/Cout
cholesterol does what to melting pt
depresses melting point
ohms law
Iion= Gion x Vm - Eioin
Vm - E ion is
electrochemical gradient AKA driving force
chord conductance equation
Vm = Gion/Gion + Gother ion x E ion
do that for each ion and add them
membrane potential depends only on the
equilibrium potentials and relative conductances for each ion that can permeate the membrane
same class as digitalis and dijoxin, blocks the Na/K pump
ouabain, a poisonous cardiac glycoside
conductance is highest at steady state for
K
Mg levels higher....
in the cell
HCO3 levels higher....
outside the cell
HPO4 levels higher...
inside the cell
proteins, AA, urea higher.....
inside the cell
H higher...
inside the cell
level of depolarization above which an action potential results
threshold
all or none response is
nondecrementing - it will travel entire length of nerve
electrotonic conduction is
decrementing - it will eventually die out, so it is a local response
two reasons for absolute refractory period
Na channels already opening as fast as possible
Na inactivation already occuring at the peak and downward swing of the action potential
Tetrodotoxin
blocks voltage sensitive Na channel
TEA tetraethyl ammonium ion
blocks voltage sensitive K channel
local anesthetics block
voltage sensitive Na channel, so no signals to brain
what is faster with internodal distance
larger internodal distance is faster
normal direction of an impulse propagation
orthodromic
opposite direction of an impulse propagation
antidromic
EPP, endplate potential is
chemically graded
blocks Ca release from SR
dihydropyridine
continually allows Ca to be released from SR
ryanodine
genetically abnormal ryanodine receptor
under anesthetic can trigger these channels to open and not close, induces malignant hyperthermia because muscles keep contracting
in skeletal muscle, this binds to troponin C
calcium binds to troponin C, freeing actin from tropomyosin
Ca released from SR via
voltage change
calcium removed from cell via
secondary active transport, antiport with Na
botulinum toxin does this to neurotransmitters
inhibits all neurotransmitters
tetanus toxin does this to neurotransmitters
interferes with transmission of inhibitory neurons - causes lockjaw
black widow spider venom does this to neurotransmitters
causes release of all transmitters
endplate potential responds how so
graded, proportional to amount of ACh that binds to receptor
curare
reversible inhibition of ACh receptor, flaccid

at EPP
alpha-bungarotoxin
irreversible inhibitor of EPP
succinyl choline
nACHR agonist, opens the channel - depolarizing, can lead to excess Ca release and thus malignant hyperthermia
AChE inhibitors
DFP, parathion (insecticide), chemical warfare use others
myasthenia gravis
muscle weakness
autoantibodies destroy AChR
AChE inhibitors help because more ACh is available for the few AChR available
energy for rephosphorylation of ATP in skeletal muscle contraction comes from
phosphocreatine
carbs, fat, protein
95% from oxphos
causes of fatigue
glycogen depletion in muscle
fatigue at NMJ - not enough transmitter released
interruption of blood flow through contracting muscle
acidosis on brain
3 ways to vary force generated by muscle
strength of stimulus
length of muscle
frequency of stimulation
increase in strength off electrical stimulation causes
increase in isometric force by activating more muscle fibers (spatial summation)
heart afterload =
arterial pressure
optimum sarcomere length falls on which graph
active tension curve
many twitches over time in same number of fibers
temporal summation
more muscle area and fibers recruited
spatial summation
temporal summation with no relaxation
tetanus
can you have tetanus in the heart
no, absolute refractory period
optimal sarcomere length has to do with
max number of cross bridges
increase in force of contraction due to repetitive stimulation
temporal summation
tetanus/tetanic contraction is
when the summation is sufficient to result in a smooth sustained contraction
spatial summation
activating more motor units
composed of the elements that stretch when a muscle contraction is going on
series elastic component
increasing the afterload increases the
duration of isometric portion of the contraction
velocity of shortening decreases with
increasing afterload
extent of shortening decreases with
increasing afterload because at increased load the sarcomere is stretched
describe fast muscle
size of fibers and nerves
SR
sugar
blood supply
mito
large fibers, large nerves
extensive SR for Ca
glycolytic enzymes
less blood supply
fewer mito
gastrocnemius is this kind of muscle
mixed fast and slow twitch
characteristics of slow muscle (red)
smaller, smaller nerve
more vascularization
more mito
myoblogin
muscle tone
sustained partial contraction of muscle, helps with posture
contractile force given by size
strength
amount of work / time
power
depends on amount of glycogen stored in a muscle
endurance
does carbs or fat give more energy
hi carb - 240 minutes
mixed - 120 minutes
hi fat - 85 minutes - less endurance
does slow or fast twitch have more nerves
fast stitch has less muscle per nerve so better control, like the eye
after long period of rest, initial strength of contraction is weak
treppe or staircase effect
full or tetanic contracture
cramps
causes of cramps
low blood Ca - increased Na permability - nerves/muscles have spontaneous action potential
damage - nerves in area become hyperexcitable
damage causes lysis - more k into ECF, can briefly cause APs
damage - spinal cord reflex - increases muscle contraction
low Mg
Mg given for
preeclampsia - relaxes smooth muscle, prevents hypertension
in muscle atrophy, these can occur
denervation, and renervation
if 3 months, full
if 2 years, little function, muscle replaced by fat
can muscle cells regenerate
yes, with satellite cells
what is destroyed in mysasthenia gravis
ACh receptors, nicotinic, at skeletal NMJ
muscles affected first in myasthenia gravis?
muscles of the face, small number of receptors
removal of thymus in myasthenia gravis patient is helpful because
thumus makes antibodies that destroy receptors, by knocking out antibodies you can help
whole motor unit contracts as a ripple on the skin
fasciculation
denervated muscles begin to have spontaneous impulses
fibrillation
high cortisol leads to hyperglycemia and increased insulin. what should happen?
downregulation of insulin receptors
type of smooth muscle innervated by a single nerve ending; control exerted mainly by nerve signals from ANS
multiunit smooth muscle
type of smooth muscle where sheets function as a single unit; cells arranged in sheets or bundles with gap junctions forming electrical synapses, fibers from functional syncitium that contracts as large area at a time
visceral smooth muscle (single-unit)
similarities of smooth muscle with skeletal
actin and myosin in both
process activated by Ca, ATP ->ADP
cAMP can affect both (regulates passage of Ca through ion channels)
same strength, smooth muscle may be stronger
differences of smooth muscle from skeletal
irregularly arranged, few myosin, may be stronger
slower contraction time
chemical reactions slower - cross bridges have very slow ATPase activity
very little energy required to maintain tension
Ca binds to calmodulin, activated myosin light chain kinase, activates ATPase of myosin head
two kinds of action potentials in smooth muscle
plateaus - long periods of contraction in some types of smooth muscle, Ca channels open much more slowly
spike potentials - look like skeletal muscle but are slower
controls rhythmic contractions in smooth muscle, intrinsic to smooth muscle, a local depolarization can initiate APs
spontaneous slow waves - pacemaker waves
causes depolarization in smooth muscle
stretching
describe diffusion of calcium in smooth muscle
diffusion is slow, much of the long latent period (time between excitation and contraction) is due to the diffusion of calcium
in smooth muscle, what determines whether transmitters are excitatory or inhibitory
the receptor
smooth muscle can stay contracted for very long times with little energy
latch mechanism of smooth muscle
how does latch mechanism work
actin and myosin fail to detach because it requires an enzyme to release
how does lactic acid cause vasodilation
lactic acid means lower Oxygen and ATP, so increased K from decrease in Na/K pump, causing decrease in Calcium, leading to lack of contraction of smooth muscle, thus vasodilation
hormones that cause vasoconstriction
norepi, epi, angiotensin, vasopressin
hormones that cause vasodilation
histamine
hormone that causes uterine contractions
oxytocin
smooth vs skeletal muscle contraction
smooth to 1/2 to 1/4 its original length
skeletal to 3/4 original length
explain stress-relaxation of smooth muscle
muscle stretches increasing tension, muscle rearranges, decrease toward original tension
this allows hollow organs to accommodate their contents
stress relaxation and reverse stress relaxation
in cardiac muscle, these release Ca in addition to SR
T Tubules
how long is refractory period in heart
refractory period lasts almost full AP and almost same length of time as contraction, so contraction does not sum; no tetany
valve between R atrium and R ventricle
Tricuspid
valve between L atrium and L ventricle
Mitral
valve at end of R ventricle
pulmonary
valve at end of L ventricle
aortic valve
incisura seen on which curve
aortic pressure curve
ECG wave - spread of depolarization through atria
P wave
ECG wave - spread of depolarization through ventricles
QRS
ECG wave - repolarization of ventricles
T wave
first 1/3 of ventricle diastole
period of rapid filling
second 1/3 of ventricle diastole
diastasis - only blood coming back from heart goes from atria to ventricles
how does atrial fib occur and pt is not injured quickly
atrial contraction only gives last 1/3 of blood that isnt really needed
how do ventricles eject blood, like how fast?
1st 1/3 ejects 70%
2nd 2/3 ejects 30%
cardiac output =
SV x HR
average end diastolic volume
average stroke volume output
averated end systolic volume
120-130 mL
70 mL
50-60 mL
ejection fraction =
SV/EDV
are SV and HR changed in an athelete
SV higher
HR lower
what happens to ejection fraction in heart failure
decreases from about 60% to less than 55%
A-V valves
tricuspid and mitral
attach AV valves by chordae tendinae, prevent buldging too far back toward artia during vent. systole
papillary muscles
semilunar valves
aortic and pulmonary
name the four heart sounds
1. closing of AV
2. closing of semilunar
3. sloshing in
4. a stiff wall
blocks ACh in muscarinic repceptors, thus accelerating heart beat
atropine
what causes an inversion of T wave
ischemia, occlusion of coronary artery
more H, which is antiported with Na, depolarizing the membrane and repolarizing it in the opposite way
significant Q wave means
Q wave is wider and deeper because it represents additionally the vector of Right ventricle depolarizaiton in infarction
ST segment elevation is from
area between healthy and injured tissue
tissue here is injured
what part of change in ECG lasts forever
significant Q wave
case 5 how to reduce preload?
give nitro which diminishes venous return
case 5 how to reduce afterload?
phenotolamine was given, which blocks epi and norepi on alpha-adrenergic receptors in arteriolar smooth muscle
case 5 how to increase cardiac output?
dobutamine makes left centricle pump more forcefully, increasing contractility
what is pulse pressure
difference between systolic and diastolic blood pressure
PAWP is
pulmonary artery wedge pressure, a good estimate of left ventricular filling pressure
increase in ventricle contraction strength is
positive inotropic effect
ability to stretch/change volume without a large change in pressure
compliance
atrial pressure waves are
a c v
a is atrial systole
c is bulging of tricuspid into atrium during isovolumetric vent. contraction
v wave is rise in atrial pressure before the tricuspid opens during diastole
two means of regulating the volume that is pumped to adapt to such extremes in blood pumping required
intrinsic regulation of pumping in response to changes in volume flowing into heart
reflex control by the autonomic nervous system
intrinsic regulation of heart pumping
frank starling law - heart pumps any amount that comes into it
sympathetic is positively/negatively inotropic and chronotropic
positively chronotropic (increases HR)
positively inotropic (increases force)
parasympathetic is positively/negatively inotropic and chronotropic
negatively chronotropic (decreases HR)
increase in atrial pressure results in an increase in HR
bainbridge reflex
thyroxine does this to metabolic rate
increases metabolic rate, possibly leading to damage to heart
impulse in heart is delayed here before moving on
A-V node
pacemaker of the heart
SA node
this causes delay in A-V node
low resting potential, so it takes longer to depolarize
small fibers are slow conducting
fewer gap junctions
size of purkinje fibers
very large so transmission is very fast
why does SA depolarize so easily
membrane potential is very close to threshhold - easily depolarized, easily excitable
how does parasympathetic work in the heart
ACh causes increase in K permeability leading to hyperpolarization. this decreases the heart rate by decreasing the SA node rate and also decreasing the AV node excitability
how does sympathetic work in the heart
norepinephrine - increases Na permability and Ca permeability so it is easier to get to threshold and have stronger contractions
this causes synchronous ventricular contraction
purkinje system
norepinephrine's effect on:
ventricular function curve
max pressure per time
ESV
EDV
SV
positive inotropic agent
shifts vent function curve up and to left
increases pressure per time
decreases ESV
decreases EDV
increases SV
5 causes of abnormal heart rhythms
abnormal rhytmicity of pacemaker itself
shift of pacemaker from SA to other parts of heart
blocks at different points in transmission of impulse
abnormal pathways of impulse transmission through the heart
spontaneous generation of abnormal impulses in almost any part of the heart
heart block which slows impulses but all make it past the block
1st degree
heart block which some impulses make it past the block
2nd degree
complete heart block
3rd degree
difference between 2nd and 3rd degree heart blocks
3rd has p wave and QRS independent of each other on ECG
2nd degree block has the 2:1 or 3:1 ratio of p waves for each QRS
rhythm in which impulse travels around the heart without stopping
circus movement
two types of reentry
flutter
atrial fib
rapid but coordinated rentry
flutter
reentry in which erratic, high frequency but uncoordinated so no parts contract in unison
A fib
most common cause of clots
A fib, which can cause ventricular tachycardia
types of medicines to take if you are in A fib
blood thinners
rate control drugs
antiarrhythmic drugs
when contraction is premature and comes from somewhere other than SA node
ectopic foci
one form of tachycardia
ectopic focus becomes so irritable that it causes rhythmical contraction at rate faster than SA node and becomes pacemaker