Exam 3 Flashcards
autonomic nervous system
two branches- sympathetic and parasympathetic
involuntary control of organ function
organ contraction, HR/BP, stress response
ANS in relation to daily acitivity
sympathetic branch- associated with stress and physical activity, mental/emotional stress, exercise
parasympathetic- associated with rest and “slow” background activity, increased digestion, lower overall activity
ANS neuron configuration
2 neuron series- preganglionic neuron and postganglionic neuron
where is the cell body in a preganglionic neuron
cell body located within CNS
where is the cell body of a postganglionic neuron
cell body is located within autonomic ganglia
sympathetic: sympathetic chain ganglia parasympathetic: terminal ganglia, near or on surface of effector
2 neuron series sympathetic
start in spinal cord
preganglionic neuron goes to postganglionic neuron in sympathetic chain ganglia
postganglionic neuron goes to
effector
2 neuron series parasympathetic
start in brain stem
preganglionic neuron goes way down to postganglionic neuron at terminal ganglia
postganglionic neuron goes to effector
where are NTs released in 2 neuron series
at preganglionic to postganglionic and at postganglionic to effector
autonomic neurons and their NTs
different autonomic neurons secrete different NTs
neuron type based on the type of NT that is released
types of NTs released
cholinergic neuron
adrenergic neruon
cholinergic neuron releases
acetylcholine
adrenergic neuron releases
norepinehprine
receptors for specific NTs
cholinergic
adrengeric
cholinergic receptor
binds acetylcholine
2 types of cholinergic receptors
muscarinic
nicotinic
nicotinic receptor
on postganglionic neuron
both sympathetic and parasympathetic
muscarinic receptor
on surface of effector, mainly in parasympathetic
adrenergic receptor
binds norepinephrine and epinephrine
2 types of adrenergic receptors
alpha adrenergic receptor
beta adrenergic receptor
alpha adrenergic receptor
responds more to norepinephrine than epinephrine
beta adrenergic receptor
respond equally to norepinephrine and epinephrine
preganglionic neurons: NTs effects
preganglionic NTs secreted affects postganglionic neuron
in both sympathetic and parasympathetic
secretes acetylcholine
postganglionic neurons: NTs and effects
postganglionic NTs affect effector organs
in parasympathetic- cholinergic neurons- secrete acetylcholine in response to preganglionic stimulation
in sympathetic- adrenergic neurons- secrete norepinephrine in response to preganglionic stimulation
sympathetic prgn and pgn pathway
Prgn- cholinergic neuron secretes Ach binds to nicotinic receptor on pgn- adrenergic neuron secretes norepinephrine binds to alpha or beta adrenergic receptors on effector
parasympathetic prgn and pgn pathway
prgn- cholinergic neuron secretes Ach binds to nicotinic receptor on pgn- cholinergic neurons secretes Ach binds to muscarinic receptor on effector
regulation of ANS responses
many effector organs have input from sym and psym divisions
1 antagonistic effects
2 coordinated response
antagonistic effects
sympathetic and parasympathetic produce opposite effects
one may have a stronger effect than the other
coordinated response
1 one division can coordinate activity of multiple different structures
2 both divisions can coordinate activity of different structures for the same purpose
eyes sympathetic vs parasympathetic
sympathetic- pupil dilation
parasympathetic- pupil constriction
Bronchi sympathetic vs parasympathetic
sympathetic- bronchodilation
parasympathetic- bronchoconstriction
GI tract sympathetic vs parasympathetic
sympathetic- decrease digestion
parasympathetic- increase digestion
heart sympathetic vs parasympathetic
sympathetic- increase HR, BP, force of contraction
parasympathetic- decrease HR, BP, force of contraction
blood vessels sympathetic vs parasympathetic
sympathetic- mostly vasoconstriction (alpha adrenergic receptors), increase BP, some vasodilation (beta adrenergic receptors)
parasympathetic- vasodilation of some blood vessels, very little effect on systemic BP
response to stress
mass activity of sympathetic division- activates adaptations to escape stressor
increase BG, HR, blood flow to muscles, respiratory rate, inhibition of non-essential activities (digestion, reproduction)
fast acting response
system (whole body) effects
more noticeable with sympathetic stimulation
some preganglionic sympathetic neurons stimulate adrenal medulla
Ach goes to adrenal medulla, adrenal medulla secretes epinephrine, epinephrine enters circulation and affects functions of other organs
pharmacology
receptor agonists
receptor antagonists
receptor agonists
drugs that bind to receptor and mimics effects of endogenous NTs
sympathomimetic drugs
parasympathomimetic drugs
receptor antagonists
drugs that bind to receptor and block effect of endogenous NTs
innervation of vasculature
nervous stimulation- motor neurons
blood vessels- capillary beds around muscle fibers, supplied and drained by arteries and veins
delivery of oxygen rich blood
muscle fibers
composed of many myofibrils
myofibrils
composed of actin myofilaments (thin filament) and myosin myofilaments (thick filament), titan
sarcolemma
plasma membrane of muslce fiber
sarcoplasma
cytoplasm of muscle fiber
sarcomere
made up of action and myosin joined end to end
what is the smallest contractile structure
sarcomere
a band
length of myosin, some overlapping of myosin and actin
i band
contain actin and z disk
actin structure
F actin- 2 strands in a helix
G actin- has an active site for binding myosin heads
troponin
tropomyosin
troponin
3 subunits, 1 binds to g- actin, 1 binds to tropomyosin, 1 has binding site for Ca++
tropomyosin
sits within indention of helix
at rest- blocks active sites of g- actin
myosin
2 myosin heavy chains forming a rod
hinge region- allows bending of myosin heads
myosin heads- capable of binding to g-actin
4 myosin light chains- attached to myosin heads, regulatory function
myosin heads
cross bridge formation
binding of myosin head and actin molecule
facilitates contraction of muscle- hinge region, bending and straightening
heads have ATPase that does ATP hydrolysis that releases energy for bending of hinge
sliding filament model
actin myofilament sliding over the myosin myofilament shortening of sarcomere this translates to muscle contraction
sliding filament model
relaxation
lengthening of sarcomere
external forces- contraction of antagonist muscle or gravity
neuromuscular junction/ motor end plate
synapse of motor neuron on muscle fiber
Ach secretion by motor neuron
Ach binds to ligand gated ion channels on muscle fiber
Na+ rushes into muscle, depolarization of muscle fiber
excitation- contraction coupling
conversion of neural signals into physical process of contraction t-tubles sarcoplasmic reticulum (SR)
steps to muscle contraction
neuron action potential- muscle action potential- contraction
t-tubules
transverse tubules
infoldings of sarcolema
sarcoplasmic reticulum (SR) what is it what does it store and release
modified smooth ER, stores Ca++, release Ca++ into sarcoplasm in response to muscle AP
muscle fiber AP and conduction
AP of muscle fiber occurs at NMJ
AP propagates along sarcolemma and along t-tubules
this causes voltage gated Ca++ channels on SR to open
Ca++ flows out of SR, Ca++ binds to troponin
troponin molecules change conformation/position
this causes tropomyosin to move
active sites on G action exposed
myosin heads bind to G actin (cross bridge formation)
sliding filament and muscle contraction occurs
when complete Ca++ re enters SR, restoration of filaments to original position
cross bridge cycling
repeated interaction of myosin head and actin myofilament
cross bridge formation
energy stored in myosin heads facilitate sliding filaments
ATP binds to myosin heads, head is released
ATP hydrolyzed, energy stored for next round
happens many times in a single contraction
relaxation requires energy
muscle relaxation, Ach secretion at NMJ stops
stops APs along sarcolemma, stops Ca++ release from SR
movement of Ca++ back into SR, energy dependent process
Ca++ actively pumped back into SR (requires ATP)
restoration of membrane potential- Na+/K+ pump (requires ATP)
whole muscle physiology
motor unit
consists of single motor neuron and all muscle fibers it innervates
what does a motor unit respond to stimulation as
single unit
what does each muscle fiber have for a motor neuron
action potential
muscle twitch
single contraction of muscle in response to stimulus
AP in one or more of muscle fibers
phases of muscle twitch
lag
contraction
relaxation
force of contraction
all or none
graded muscle response
how to increase force of contraction- summation or recruitment
all or none
force of contraction
threshold must be reached for contraction to occur
graded muscle response-
force of contraction
different strength of contraction
to increase force of contraction
force of contraction
summation
increase force via more APs
to increase force of contraction
force of contraction
recruitment
increase number of muscle fibers/motor units that are contracting
frequency summation
stimuli applied in quick succession before muscle fully relaxed with each stimulus tension increasing
increased frequency of APs
complete tetnus
very rapid, high frequency continuous stimulation with no relaxation, causes sustained contraction of muscle
what does increased frequency of APs do
Ca++ accumulating in muscle fibers
results in increased force of contraction
types of muscle contractions
isometric
isotonic
isometric muscle contraction
no noticeable change in length of muscle, no movement of joint
increase in tension/force in muscle during contraction
example of isometric contraction
maintenance of posture
isotonic muscle contraction
tension produced by muscle is constant, change in length of muscle, movement occurs
example of isotonic muscle contraction
moving limbs or fingers
types of isotonic muscle contractions
concentric contraction
eccentric contraction
concentric contraction
working muscle shortens, tension in the muscle great enough to overcome the load
eccentric contraction
working muscle lengthens, tension being maintained against the load
fatigue
diminished ability to generate force
what causes fatigue
reduced neural stimulation
depletion of substrates (ATP or glycogen)
accumulation of metabolites (lactic acid, Mg++, ROS) may interfere with Ca++ release from SR
muscle fiber types and contraction
slow twitch
fast twitch
slow twitch muscle fibers/ type 1
slower contraction, slower response to nervous stimulation, smaller fiber diameter, extensive vasculature, higher mitochondria and myoglobin concentrations, dark appearance
slow ATPase activity on myosin heads, more resistant to fatigue
fast twitch muscle fiber/ type 2
faster response to nervous stimulation, fast ATPase activity on myosin heads, less vasculature, less myoglobin and mitochondria, lighter color, higher glycogen content, more susceptible to fatigue
what muscle fiber is for endurance
slow
what muscle fiber is for olympic lifting
fast
heat production
ATP metabolism
shivering thermogenesis
ATP metabolism
during muscle contraction- release of heat normal body temperature maintenance, increase with more contraction
shivering thermogenesis
uncoordinated involuntary contraction of skeletal muscle, initiated by hypothalamus in response to signals from skin and spinal cord, generation of heat in response to cold air temperature
blood cycle through heart
1 O2 poor blood carried in superior and inferior vena cava 2 enters RA 3 passes through tricuspid valve 4 enters RV 5 passes through pulmonary SL valve 6 carried through pulmonary arteries to lungs 7 O2 rich blood carried through pulmonary veins 8 enters LA 9 passes through bicuspid valve 10 enters LV 11 passes through aortic SL valve 12 carried to body by aorta
coronary circulatioin
carries oxygen rich blood to the heart itself and drains heart of oxygen poor blood
myocardial infraction
“heart attack”
necrosis of myocardium due to one or more coronary blockages
“widow maker”
blockage of left anterior descending artery
characteristics of cardiac muscle
cardiac myocytes
cardiac myocytes
striated, rich in mitochondria, elongated and branched, excitatory and conductive, conduction of AP
cardiac muscle functional unit
intercalated disk desmosomes gap junctions cardiac syncytium "all or none" principle synctia
intercalated disks
form close contact with adjacent cells
desmosomes
hold contact during contraction
gap junctions
free flow of cytoplasm for AP conduction
cardiac syncytium
when one cell becomes excited, all cells become excited and heart contracts as one unit
two syncytia of cardiac muscle
atrial syncytium
ventricular syncytium
types of cadiac myocytes
contractile
autorhythmic
autorhythmic myocytes
autonomic foci sinoatrial node atrioventricular node bundle of his (left and right bundle branches) purkinje fibers
autorhythmic foci
autorhythmic cells that fire at their own intrinsic rates
what does SA node do
spontaneously generates APs at regular intervals of 70 BPM
spread of excitation follows specific sequence
SA node fires- signal spreads across atria (.04s), atria contracts
signal delay (.11s) at AV node- allows atria to fully empty
signal reaches ventricles (.08s)
purkinje fibers stimulate ventricles to contract
force of ventricular contraction pushes blood through arteries
heart block
first degree
second degree
third degree
first degree heart block
impulses to ventricles slightly delayed
first degree heart block
impulses to ventricles slightly delayed
first degree heart block
impulses to ventricles slightly delayed
second degree heart block
impulses intermittently blocked
third degree heart block
no impulses from atria reach ventricles
atrial pacemaker- medical device that produces electrical signals
action potential in contractile myocytes
long refractory period compared to skeletal muscle
prevention of tetanus
what is the RMP for skeletal and contractile myocytes
-90 mV
fast Na+ channels
respond quickly to stimulation
L- type channels (long opening/slow)
respond slowly to stimulation
l- type Ca++ channels
AP in contractile myocyte graph
phase 0- depolarization, phase 1- early repolarization phase 2- plateau phase 3- regular repolarization phase 4- RMP
phase 0
AP in contractile myocytes
fast Na+ channels open, Na+ rushes in
at -40 mV l- type Ca++ channels open, small steady influx of Ca++
phase 1
early repolarization
AP in contractile myocytes
some K+ open briefly, K+ out
phase 2
plateau
AP in contractile myocytes
l- type Ca++ open, Ca++ in, K+ open, K+ efflux
counter balance with Ca++ and K+ at 0 mV
phase 3
regular repolarization
AP in contractile myocytes
Ca++ closed, K+ open, K+ out
action potential in autorhythmic myocytes
never at rest, SA node “pacemaker potential”, positive drift from -60 mV to -40 mV
allows for “readiness” to fire and spontaneous depolarization
three causes of pacemaker potential
1 increased influx of Na+- “funny channels” open in response to hyperpolarization, allows Na+ in, pushes up RMP
2 decrease efflux of K+- K+ channels close during hyperpolarization of AP, limiting K+ leaving cell (pushes up voltage)
3 differential influx of Ca++ ions- some Ca++ channels open before threshold, pushes voltage to threshold, once at threshold, l- type Ca++ channels open, producing AP
AP in autorhythmic myocytes
threshold- -40 mV
phase 1- pacemaker potential
phase 2- depolarization
phase 3- repolariztion
phase 1
pacemaker potential
AP in autorhythmic myocytes
in hyperpolarized state “funny” Na+ channels open, leads to Na+ coming into cell, closed K+ channels reduced K+ from leaving cell, as threshold approached some Ca++ channels open briefly, Ca++ moves into cell, threshold is reached
phase 2
depolarization
AP in autorhythmic myocytes
l- type Ca++ channels open, Ca++ in
phase 3
repolarization
AP in autorhythmic myocytes
Ca++ channels close, K+ channels open, K+ efflux
electrocardiogram (ECG)
record of electrical activity of heart
electrical events correlate with physical activity
p wave
atrial depolarization
onset of atrial contraction
QRS complex
ventricular depolarization
onset of ventricles contraction
t wave
ventricular repolarization
precedes ventricles relaxing
fibrillation “quiver”
atrial fibrillation
ventricular fibrillation
atrial fibrillation (A-fib)
irregular contraction of atria
compatible with life and full activity, irregular spacing of QRS complex and no p waves
treat with beta blockers (block beta-adrenergic receptors) to drop HR and reestablish SA node rhythm
ventricular fibrillation (V-fib)
emergency, results in “cardiac arrest”
ventricular twitches- not proper contractions
loss of consciousness within seconds
fatal unless immediate intervention (CPR and defibrillation)
defibrillator
applies strong electrical current that depolarizes most/entire heart at once, gives SA node time to re-establish normal sinus rhythm
cardiac cycle
pattern of contraction and relaxation of heart chambers initiated by spontaneous AP from SA node
atria- primer pumps- push blood into ventricles
ventricles- power pumps- force blood into pulmonary system and systemic circulation
diastole- relaxation- blood fills chambers
systole- contraction, blood pushed out of chambers
cardiac cycle
steps
1- passive ventricular filling- blood entering left and right ventricles through gravity
SA node
2 atrial systole- pushes rest of blood into ventricles
AV node to purkinje fibers
ventricular systole (early)- pressure increases in ventricles, causes AV valve to close, semilunar valves closed, no movement of blood
ventricular systole (late)- pressure strong enough to open SL valves, blood ejected into great arteries
ventricular diastole- ventricles relax
intrinsic regulation of heart
cardiac output- amount of blood pumped per minute
stroke volume- volume of blood pumped per beat
CO= HR*SV
changes in HR and SV leads to changes in CO
starling’s law of the heart
stroke volume of LV increases as volume of LV increases due to preload (stretch) of cardiac muscle
greater preload- greater force of contraction
scenario
starling’s law of the heart
vigorous exercise increases venous return of blood to heart
more blood filling chambers increases preload
increased preload increases stroke volume
healthy heart muscle is like a spring
extrinsic regulation of heart (autonomic ns)
PANS- vagus nerve, synpase a SA node and AV node
Ach binds to muscarinic receptors- inhibitory influences
SANS- project to heart as cardiac nerves, nerves synapse at SA node, AV node, and myocardium, NE binds to adrenergic receptors- excitatory influence,
also epinephrine from adrenal medulla binds to adrenergic receptors- excitatory influence