Physiology Flashcards
(176 cards)
Why is pulse pressure determined by SV?
Pulse pressure is the difference between the highest (systolic) and lowest (diastolic) arterial pressures. It reflects the volume ejected by the left ventricle (stroke volume). Pulse pressure increases when the capacitance of the arteries decreases, such as with aging.
What is aortic insufficiency?
In aortic insufficiency the loss of blood from the arterial system during each diastole is abnormally high, and, therefore, the aortic diastolic pressure is low, and the pulse pressure (= systolic pressure - diastolic pressure) is high. This increased diastolic runoff of pressure during each cycle is also seen when the heart rate, total systemic resistance, or arterial compliance is decreased.
Reduction in the permeability of the sodium ion will result in
hyperpolarization of the cell. The permeability of the cell membrane to Na and the “leakage” of Na into the cell contributes to the resting membrane potential, making it less negative than would be predicted on the basis of potassium concentration and permeability, alone. Reduction in potassium ion permeability, on the other hand would cause depolarization of the cell, as would influx of calcium ion to increased extracellular concentration of sodium or potassium ion.
The resting membrane potential is not exactly equal to the Nernst potential for potassium because:
the membrane has some permeability to species other than potassium. At the normal external potassium concentration the permeability of the membrane to other ions (Na, Cl, Ca) resulting in positive or negative charge transfer across the membrane also influences and contributes to the resting membrane potential. However, the dominant determinant of the resting potential is the K permeability.
Under a particular set of experimental conditions, a mammalian axon was found to be permeable to only one ion, K+. The equilibrium potential for K+ in this axon was -97mV. On the basis of these data, we expect to find a resting membrane potential of:
-97 mV. Because this membrane is permeable to only K+, its resting membrane potential will equal the K+ equilibrium potential (EK). EK is determined by the concentration gradient for K+ that exists between the extracellular and intracellular fluids, as described by the Nernst equation. The EK is the transmembrane potential difference necessary to perfectly balance, thermodynamically, a K+ concentration gradient of a given magnitude. At EK the flux or transport of K+ across the membrane, in both directions, is equivalent and therefore, net flux or transport of K+ is 0. We can estimate EK using the Nernst equation if the concentration gradient for K+, (K+OUT)/(K+IN), is known. As shown above, EK=61.5log (K+OUT)/(K+IN) = -97mV. If the concentration gradient for K+ were 0.1, it would mean that K+ was 10 times more concentrated inside the cell than outside the cell and the EK would equal -61.5 mV, because the log of 0.1 is -1. As shown above, EK equals -97 mV, therefore the concentration of K+ inside the cell must be more than 10 times the concentration outside the cell, and therefore, statements A and B must be incorrect. When the resting potential is -97 mV, there is a “microscopic” separation of charge across the immediate vicinity of the membrane, which does not measurably change the anion or cation concentration of the intracellular or extracellular solution. An increase in sodium conductance or channel-mediated Na transport across the membrane, will decrease the trans-membrane potential difference toward more positive values (depolarization) in a direction toward ENa, which is approximately +66 mV. This is due to the outward-to-inward direction of the Na gradient across the membrane resulting in net transfer of positive charge into the cell.
If the concentration gradient for K+ were 0.1, it would mean that
K+ was 10 times more concentrated inside the cell than outside the cell
Which autonomic receptor mediates secretion of epinephrine by the adrenal medulla?
Cholinergic nicotinic receptors. Preganglionic sympathetic fibers synapse on the chromaffin cells of the adrenal medulla at a nicotinic receptor. Epinephrine and, to a lesser extent, norepinephrine are released into the circulation.
Heart rate is increased by the stimulatory effect of norepinephrine acting on β1 adrenergic receptors in the:
sinoatrial (SA) node (positive chronotropic effect). There are also sympathetic β1 adrenergic receptors in the heart that regulate contractility (positive inotropic effect).
Which receptor mediates constriction of arteriolar smooth muscle?
alpa 1. The α1 receptors for norepinephrine are excitatory on vascular smooth muscle and cause vasoconstriction. There are also β2 receptors on the arterioles of skeletal muscle, but they produce vasodilation.
Which autonomic receptor is activated by low concentrations of epinephrine released from the adrenal medulla and causes vasodilation?
β2 receptors on vascular smooth muscle produce vasodilation. α receptors on vascular smooth muscle produce vasoconstriction. Because β2 receptors are more sensitive to epinephrine than are α receptors, low doses of epinephrine produce vasodilation, and high doses produce vasoconstriction.
A 45-year-old woman complains of pain in her fingertips and toes during cold exposure or emotional stress. This “Raynaud phenomenon” is caused by exaggerated sympathetic vasoconstriction in the extremities, producing ischemic pain. What receptors are involved in this activity? Would an ACh inhibitor be an appropriate treatment for her?
Vasoconstriction is mediated by norepinephrine release from sympathetic nerve terminals. Norepinephrine binds to α-adrenergic receptors on vascular smooth muscle cells, so the patient’s vasospasm may be relieved by an α-adrenergic inhibitor. Sympathetic ganglia are located close to the vertebral column, not peripherally, and postganglionic neurons are unmyelinated. Synaptic transmission within sympathetic ganglia is cholinergic, and, thus, an acetylcholinesterase inhibitor would augment sympathetic efferent activity thereby worsening the symptoms.
Which autonomic receptor is blocked by hexamethonium at the ganglia, but not at the neuromuscular junction?
Cholinergic nicotinic receptors (N2). Hexamethonium is a nicotinic blocker, but it acts only at ganglionic N2-type (not neuromuscular junction N1-type) nicotinic receptors. This pharmacologic distinction emphasizes that nicotinic receptors at these two locations, although similar, are not identical.
What is the dichrotic notch?
small change in pressure when the aortic valve closes (backfilling)
What is normal TPR value?
1.2 PRU (peripheral resistance unit)
What is systolic P?
The blood pressure when the heart is contracting. It is specifically the maximum arterial pressure during contraction of the left ventricle of the heart. The time at which ventricular contraction occurs is called systole.
What is diastolic P?
Referring to the time when the heart is in a period of relaxation and dilatation (expansion).
What is the mean aterial pressure?
avg P during entire cardiac cycle, = DP + 1/3(SP-DP)
What is pulse pressure?
PP = SP - DP = SV/compliance difference between SP and DP
What is the osmolarity of sweat?
100mOsm
What is a sweat gland innervated by?
ACh-secreting sympathetic nerve
What does ADH do in the brain in response to exercise?
Sweating results in volume depletion and an increase in ECF osmolarity, which drives water from ICF to the ECF. When this occurs in the brain, a decrease in cell volume induces the release of ADH (vasopressin) which stimulates thirst and triggers water retention by the kidneys.
What is important about the axon hillock?
Lots of voltage-sensitive sodium channels that contribute to the all or none response of the AP down the axon
What is the difference between large and small axon diameters?
Large axon diameters conduct impulses faster, internal electrical resistance reduced due to larger cross-sectional area
What is axoplasm?
Cytoplasm of the axon, axoplasmic transport renews the contents of synaptic terminals, contains arrays of microtubules and neurofilaments that provide structural stability to transport materials back and forth between cell body and presynaptic terminal
