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202 Cards in this Set
- Front
- Back
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normal pH in blood
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7.35-7.45
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if a person is acidotic chronically, how does the body compensate
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make more ammonia, which binds the acid and removes in urine
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how does an acidotic coma work
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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
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kidney failure results in this problem
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acidosis - dont excrete the acid via kidneys
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what effect does aldosterone have on Na and K
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increases reabsorption of Na
increases release of K |
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explain addison's disease
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hypoadrenalism
low aldosterone higher levels of K leads to cardiac arrest and fibrillation |
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explain hypocalcemic tetany
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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 |
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how can colloid pressure affect the brain
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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 |
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how does addisons lead to circulatory shock
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hypoadrenalism, lack of aldosterone, less Na retained, not enough blood volume so less blood to tissues
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given for anuresis, ADH overdose can cause
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water intoxication
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this increases blood calcium levels
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PTH
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causes massive diarrhea and hypovolumic shock
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cholera
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anaphylactic shock
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vasodilation
increased permeability of capillaries thanks to histamine fluid leaks into tissues drops blood pressure and venous return |
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explain intermittent claudication
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pain in legs upon walking
drinks coffee, smokes, no water nicotine causes vasoconstriction low blood volume |
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average temp
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98.2
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core temperature kept fairly constant
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homeotherms
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what kills in hypothermia
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death by ventricular fibrillation from hypoxic heart muscle
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2 causes of hyperthermia
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exercising without adequate fluid
no temp regulation - infants and elderly |
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2 outcomes of positive feedback
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death or new steady state
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examples of limited positive feedback
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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
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loose carbohydrate coat of outside surface of cell
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glycocalyx
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ficks law of diffusion
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flux = diffusion coefficient D x area A x Cin - Cout / thickness
or PA(C1-C2) p = permeability and a = area |
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type of diffusion with saturation kinetics
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facilitated because eventually all of the carriers are occupied so the graph levels out
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addisons blood is ______tonic to regular blood
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hypotonic, no aldosterone so no Na reabsorption, more K in the cell
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van't hoff equation
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osmotic pressure = concentration of particle x universal gas constant x temperature
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osmotic pressure is a ______ property
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colligative
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explain diabetes osmotic diuresis
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hyperglycemia, so high glucose in urine, water follows glucose
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osmotic pressure produced by plasma proteins
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colloid osmotic/oncotic pressure
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colloid pressure is counteracted by
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hydrostatic pressure
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which is greater, colloid pressure or hydrostatic pressure
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hydrostatic, bulk flow is usually out of capillary at arterial end
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edema causes a __crease in colloid oncotic pressure
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decrease
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filtration is a _____ process
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passive
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resting potential due to
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K
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explain no reflow phenomenon
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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
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secondary active transport uses this for energy
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energy stored in Na concentration gradient
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sodium glucose is ____port
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symport
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sodium amino acid is ____port
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symport
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sodium calcium is _____port
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antiport
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digitalis and dijoxin are cardiac glycosides that..
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block Na/K pump (ATPase)
less Na out less Na back in less Ca pushed out more calcium inside increased force of contraction |
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cardiac muscles get calcium from
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outside the cell
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states that for every positive in, a negative must come out
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law of electroneutrality
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explain equilibrium/nernst potential
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potential energy just necessary to stop the ion's movement
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nernst equation
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Eion = -RT/nF x 1n (Cin/Cout)
Eion = -60/n(valence) x log Cin/Cout |
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cholesterol does what to melting pt
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depresses melting point
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ohms law
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Iion= Gion x Vm - Eioin
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Vm - E ion is
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electrochemical gradient AKA driving force
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chord conductance equation
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Vm = Gion/Gion + Gother ion x E ion
do that for each ion and add them |
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membrane potential depends only on the
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equilibrium potentials and relative conductances for each ion that can permeate the membrane
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same class as digitalis and dijoxin, blocks the Na/K pump
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ouabain, a poisonous cardiac glycoside
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conductance is highest at steady state for
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K
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Mg levels higher....
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in the cell
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HCO3 levels higher....
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outside the cell
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HPO4 levels higher...
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inside the cell
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proteins, AA, urea higher.....
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inside the cell
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H higher...
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inside the cell
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level of depolarization above which an action potential results
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threshold
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all or none response is
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nondecrementing - it will travel entire length of nerve
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electrotonic conduction is
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decrementing - it will eventually die out, so it is a local response
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two reasons for absolute refractory period
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Na channels already opening as fast as possible
Na inactivation already occuring at the peak and downward swing of the action potential |
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Tetrodotoxin
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blocks voltage sensitive Na channel
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TEA tetraethyl ammonium ion
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blocks voltage sensitive K channel
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local anesthetics block
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voltage sensitive Na channel, so no signals to brain
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what is faster with internodal distance
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larger internodal distance is faster
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normal direction of an impulse propagation
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orthodromic
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opposite direction of an impulse propagation
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antidromic
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EPP, endplate potential is
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chemically graded
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blocks Ca release from SR
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dihydropyridine
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continually allows Ca to be released from SR
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ryanodine
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genetically abnormal ryanodine receptor
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under anesthetic can trigger these channels to open and not close, induces malignant hyperthermia because muscles keep contracting
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in skeletal muscle, this binds to troponin C
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calcium binds to troponin C, freeing actin from tropomyosin
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Ca released from SR via
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voltage change
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calcium removed from cell via
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secondary active transport, antiport with Na
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botulinum toxin does this to neurotransmitters
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inhibits all neurotransmitters
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tetanus toxin does this to neurotransmitters
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interferes with transmission of inhibitory neurons - causes lockjaw
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black widow spider venom does this to neurotransmitters
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causes release of all transmitters
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endplate potential responds how so
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graded, proportional to amount of ACh that binds to receptor
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curare
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reversible inhibition of ACh receptor, flaccid
at EPP |
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alpha-bungarotoxin
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irreversible inhibitor of EPP
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succinyl choline
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nACHR agonist, opens the channel - depolarizing, can lead to excess Ca release and thus malignant hyperthermia
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AChE inhibitors
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DFP, parathion (insecticide), chemical warfare use others
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myasthenia gravis
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muscle weakness
autoantibodies destroy AChR AChE inhibitors help because more ACh is available for the few AChR available |
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energy for rephosphorylation of ATP in skeletal muscle contraction comes from
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phosphocreatine
carbs, fat, protein 95% from oxphos |
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causes of fatigue
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glycogen depletion in muscle
fatigue at NMJ - not enough transmitter released interruption of blood flow through contracting muscle acidosis on brain |
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3 ways to vary force generated by muscle
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strength of stimulus
length of muscle frequency of stimulation |
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increase in strength off electrical stimulation causes
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increase in isometric force by activating more muscle fibers (spatial summation)
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heart afterload =
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arterial pressure
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optimum sarcomere length falls on which graph
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active tension curve
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many twitches over time in same number of fibers
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temporal summation
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more muscle area and fibers recruited
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spatial summation
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temporal summation with no relaxation
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tetanus
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can you have tetanus in the heart
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no, absolute refractory period
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optimal sarcomere length has to do with
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max number of cross bridges
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increase in force of contraction due to repetitive stimulation
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temporal summation
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tetanus/tetanic contraction is
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when the summation is sufficient to result in a smooth sustained contraction
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spatial summation
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activating more motor units
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composed of the elements that stretch when a muscle contraction is going on
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series elastic component
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increasing the afterload increases the
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duration of isometric portion of the contraction
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velocity of shortening decreases with
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increasing afterload
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extent of shortening decreases with
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increasing afterload because at increased load the sarcomere is stretched
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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 |
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gastrocnemius is this kind of muscle
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mixed fast and slow twitch
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characteristics of slow muscle (red)
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smaller, smaller nerve
more vascularization more mito myoblogin |
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muscle tone
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sustained partial contraction of muscle, helps with posture
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contractile force given by size
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strength
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amount of work / time
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power
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depends on amount of glycogen stored in a muscle
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endurance
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does carbs or fat give more energy
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hi carb - 240 minutes
mixed - 120 minutes hi fat - 85 minutes - less endurance |
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does slow or fast twitch have more nerves
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fast stitch has less muscle per nerve so better control, like the eye
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after long period of rest, initial strength of contraction is weak
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treppe or staircase effect
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full or tetanic contracture
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cramps
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causes of cramps
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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 |
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Mg given for
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preeclampsia - relaxes smooth muscle, prevents hypertension
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in muscle atrophy, these can occur
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denervation, and renervation
if 3 months, full if 2 years, little function, muscle replaced by fat |
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can muscle cells regenerate
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yes, with satellite cells
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what is destroyed in mysasthenia gravis
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ACh receptors, nicotinic, at skeletal NMJ
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muscles affected first in myasthenia gravis?
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muscles of the face, small number of receptors
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removal of thymus in myasthenia gravis patient is helpful because
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thumus makes antibodies that destroy receptors, by knocking out antibodies you can help
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whole motor unit contracts as a ripple on the skin
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fasciculation
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denervated muscles begin to have spontaneous impulses
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fibrillation
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high cortisol leads to hyperglycemia and increased insulin. what should happen?
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downregulation of insulin receptors
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type of smooth muscle innervated by a single nerve ending; control exerted mainly by nerve signals from ANS
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multiunit smooth muscle
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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
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visceral smooth muscle (single-unit)
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similarities of smooth muscle with skeletal
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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 |
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differences of smooth muscle from skeletal
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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 |
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two kinds of action potentials in smooth muscle
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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 |
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controls rhythmic contractions in smooth muscle, intrinsic to smooth muscle, a local depolarization can initiate APs
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spontaneous slow waves - pacemaker waves
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causes depolarization in smooth muscle
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stretching
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describe diffusion of calcium in smooth muscle
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diffusion is slow, much of the long latent period (time between excitation and contraction) is due to the diffusion of calcium
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in smooth muscle, what determines whether transmitters are excitatory or inhibitory
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the receptor
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smooth muscle can stay contracted for very long times with little energy
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latch mechanism of smooth muscle
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how does latch mechanism work
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actin and myosin fail to detach because it requires an enzyme to release
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how does lactic acid cause vasodilation
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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
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hormones that cause vasoconstriction
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norepi, epi, angiotensin, vasopressin
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hormones that cause vasodilation
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histamine
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hormone that causes uterine contractions
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oxytocin
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smooth vs skeletal muscle contraction
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smooth to 1/2 to 1/4 its original length
skeletal to 3/4 original length |
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explain stress-relaxation of smooth muscle
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muscle stretches increasing tension, muscle rearranges, decrease toward original tension
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this allows hollow organs to accommodate their contents
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stress relaxation and reverse stress relaxation
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in cardiac muscle, these release Ca in addition to SR
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T Tubules
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how long is refractory period in heart
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refractory period lasts almost full AP and almost same length of time as contraction, so contraction does not sum; no tetany
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valve between R atrium and R ventricle
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Tricuspid
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valve between L atrium and L ventricle
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Mitral
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valve at end of R ventricle
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pulmonary
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valve at end of L ventricle
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aortic valve
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incisura seen on which curve
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aortic pressure curve
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ECG wave - spread of depolarization through atria
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P wave
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ECG wave - spread of depolarization through ventricles
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QRS
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ECG wave - repolarization of ventricles
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T wave
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first 1/3 of ventricle diastole
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period of rapid filling
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second 1/3 of ventricle diastole
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diastasis - only blood coming back from heart goes from atria to ventricles
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how does atrial fib occur and pt is not injured quickly
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atrial contraction only gives last 1/3 of blood that isnt really needed
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how do ventricles eject blood, like how fast?
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1st 1/3 ejects 70%
2nd 2/3 ejects 30% |
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cardiac output =
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SV x HR
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average end diastolic volume
average stroke volume output averated end systolic volume |
120-130 mL
70 mL 50-60 mL |
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ejection fraction =
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SV/EDV
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are SV and HR changed in an athelete
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SV higher
HR lower |
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what happens to ejection fraction in heart failure
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decreases from about 60% to less than 55%
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A-V valves
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tricuspid and mitral
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attach AV valves by chordae tendinae, prevent buldging too far back toward artia during vent. systole
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papillary muscles
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semilunar valves
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aortic and pulmonary
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name the four heart sounds
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1. closing of AV
2. closing of semilunar 3. sloshing in 4. a stiff wall |
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blocks ACh in muscarinic repceptors, thus accelerating heart beat
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atropine
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what causes an inversion of T wave
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ischemia, occlusion of coronary artery
more H, which is antiported with Na, depolarizing the membrane and repolarizing it in the opposite way |
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significant Q wave means
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Q wave is wider and deeper because it represents additionally the vector of Right ventricle depolarizaiton in infarction
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ST segment elevation is from
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area between healthy and injured tissue
tissue here is injured |
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what part of change in ECG lasts forever
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significant Q wave
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case 5 how to reduce preload?
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give nitro which diminishes venous return
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case 5 how to reduce afterload?
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phenotolamine was given, which blocks epi and norepi on alpha-adrenergic receptors in arteriolar smooth muscle
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case 5 how to increase cardiac output?
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dobutamine makes left centricle pump more forcefully, increasing contractility
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what is pulse pressure
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difference between systolic and diastolic blood pressure
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PAWP is
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pulmonary artery wedge pressure, a good estimate of left ventricular filling pressure
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increase in ventricle contraction strength is
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positive inotropic effect
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ability to stretch/change volume without a large change in pressure
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compliance
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atrial pressure waves are
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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 |
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two means of regulating the volume that is pumped to adapt to such extremes in blood pumping required
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intrinsic regulation of pumping in response to changes in volume flowing into heart
reflex control by the autonomic nervous system |
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intrinsic regulation of heart pumping
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frank starling law - heart pumps any amount that comes into it
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sympathetic is positively/negatively inotropic and chronotropic
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positively chronotropic (increases HR)
positively inotropic (increases force) |
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parasympathetic is positively/negatively inotropic and chronotropic
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negatively chronotropic (decreases HR)
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increase in atrial pressure results in an increase in HR
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bainbridge reflex
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thyroxine does this to metabolic rate
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increases metabolic rate, possibly leading to damage to heart
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impulse in heart is delayed here before moving on
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A-V node
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pacemaker of the heart
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SA node
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this causes delay in A-V node
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low resting potential, so it takes longer to depolarize
small fibers are slow conducting fewer gap junctions |
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size of purkinje fibers
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very large so transmission is very fast
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why does SA depolarize so easily
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membrane potential is very close to threshhold - easily depolarized, easily excitable
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how does parasympathetic work in the heart
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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
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how does sympathetic work in the heart
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norepinephrine - increases Na permability and Ca permeability so it is easier to get to threshold and have stronger contractions
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this causes synchronous ventricular contraction
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purkinje system
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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 |
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5 causes of abnormal heart rhythms
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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 |
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heart block which slows impulses but all make it past the block
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1st degree
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heart block which some impulses make it past the block
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2nd degree
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complete heart block
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3rd degree
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difference between 2nd and 3rd degree heart blocks
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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 |
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rhythm in which impulse travels around the heart without stopping
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circus movement
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two types of reentry
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flutter
atrial fib |
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rapid but coordinated rentry
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flutter
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reentry in which erratic, high frequency but uncoordinated so no parts contract in unison
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A fib
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most common cause of clots
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A fib, which can cause ventricular tachycardia
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types of medicines to take if you are in A fib
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blood thinners
rate control drugs antiarrhythmic drugs |
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when contraction is premature and comes from somewhere other than SA node
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ectopic foci
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one form of tachycardia
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ectopic focus becomes so irritable that it causes rhythmical contraction at rate faster than SA node and becomes pacemaker
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