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Cell and General
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Biological
Membranes, Solutes and Solutions CE 2. Describe the
composition of a cell membrane. Diagram
its cross section, and explain how the distribution of phospholipids and
proteins influences the membrane permeability of ions, hydrophilic and
hydrophobic compounds. CE 3. Using a cell
membrane as an example, define a reflection coefficient, and explain how the
relative permeability of a cell to water and solutes will generate an
osmotic pressure. Contrast the
osmotic pressure generated across a cell membrane by a solution of particles
that freely cross the membrane with that of a solution with the same
osmolality, but particles that cannot cross the cell membrane. CE 4. Contrast the
following units used to describe concentration: mM, mEq/l, mg/dl, mg%.
List the typical value and normal range for plasma Na+, K+,
H+ (pH), HCO3-, Cl-, Ca2+,
and glucose, and the typical intracellular pH and concentrations of Na+,
K+, Cl-, Ca2+, and HCO3-. CE 5. Differentiate between the terms osmole, osmolarity, osmolality and tonicity. List the typical value and normal range for plasma osmolality. CE 6. Understand that
the difference in free energy of a solute or solvent between two components
can have chemical, electrical and/or hydrostatic pressure components.
At equilibrium, for a given component, the free energy difference
between the two compartments is zero. CE 7.
Define the Donnan equilibrium and list the resulting characteristics. CE 8.
Describe the linear relationship between forces and flows (e.g.,
Ohm’s Law, Fick’s Law of diffusion, and the law of hydrodynamic flow). CE 9.
Write Fick’s Law of diffusion, and explain how changes in the
concentration gradient, surface area, time, and distance will influence the
diffusional movement of a compound. CE 10.
Based on the principle of ionic attraction, explain how a potential
difference across a membrane will influence the distribution of a cation and
an anion. CE 11.
Define the term “steady state,” and differentiate it from
“equilibrium.” Relate the
pump‑leak model of steady-state ion content to cell solute gradients
and cell volume maintenance. CE 12.
Write the Nernst equation, and indicate how this equation accounts
for both the chemical and electrical driving forces that act on an ion. CE 13.
Based on the Nernst equilibrium potential, predict the direction that
an ion will move when the membrane potential a) is at its equilibrium
potential, b) is higher than the equilibrium potential, or c) is less than
the equilibrium potential. List
values in a typical non-excitable cell for the membrane potential, for ENa,
EK, ECl, and ECa. CE 14.
Define the concepts of electrochemical equilibrium and equilibrium
potential, and give internal and external ion concentrations.
Be able to calculate an equilibrium potential for that ion using the
Nernst equation. Contrast the
difference in EK (the Nernst potential for K+) caused by a 5 mEq/l
increase in extracellular K+ with the change in ENa (the Nernst
potential for Na+) caused by a 5 mEq/l increase in extracellular
Na+. CE 15.
Explain how the resting membrane potential is generated and calculate
membrane potential by using either a) the Goldman-Hodgkin-Katz equation or
b) the chord conductance equation. Given
an increase or decrease in the permeability of K, Na, or Cl, predict how the
membrane potential would change. CE 16.
Differentiate the following terms based on the source of energy
driving the process and the molecular pathway for: diffusion, facilitated
diffusion, secondary active transport, and primary active transport. CE 17.
Describe how transport rates of certain molecules and ions are
accelerated by specific membrane transport proteins (“carrier” and
“channel” molecules). CE 18. Describe how
energy from ATP hydrolysis is used to transport ions such as Na+,
K+, Ca2+, and H+ against their
electrochemical differences (e.g., via the Na+ pump, sarcoplasmic
reticulum Ca2+ pump, and gastric H+ pump). CE 19. Understand the role of ATP-binding cassette transporters in, for example, multi-drug resistance and its significance for cancer chemotherapy. CE 20. Explain how
energy from the Na+ and K+ electrochemical gradients
across the plasma membrane can be used to drive the net “uphill”
(against a gradient) movement of other solutes (e.g., Na+/glucose
co-transport; Na+/Ca2+ exchange or counter-transport).
Apply this principle to predict possible therapies for secretory
diarrhea. CE 21. Describe the role
of water channels (aquaporins) in facilitating the movement of water across
biological membranes. Excitable
Cells CE 23.
State the cell properties that determine the rate of electronic
conduction. CE 24.
Differentiate between the properties of electrotonic conduction,
conduction of an action potential, and saltatory conduction.
Identify regions of a neuron where each type of electrical activity
may be found. CE 25.
Contrast the cell-to-cell spread of depolarization at a chemical
synapse with that at a gap junction based on speed and fidelity (success
rate). At the chemical synapse,
contrast the terms temporal summation and spatial summation. CE 26.
Understand the principle of the voltage clamp and how it is used to
identify the ionic selectivity of channels. CE 27.
Contrast the gating of ion-selective channels by extracellular
ligands, intracellular ligands, stretch, and voltage. CE 28.
Know the properties of voltage-gated Na+, K+,
and Ca2+ channels, and understand that voltage influences their
gating, activation, and inactivation. CE 29. Understand how
the activity of voltage-gated Na+, K+, and Ca2+
channels generates an action potential and the roles of those channels in
each phase (depolarization, overshoot, repolarization, hyperpolarization) of
the action potential. CE 30.
Contrast the mechanisms by which an action potential is propagated
along both nonmyelinated and myelinated axons.
Predict the consequence on action potential propagation in the early
and late stages of demyelinating diseases, such as multiple sclerosis. Cell
Volume Regulation; Intracellular pH, and Organelles CE 32. Understand how various transporters (e.g. Na+/H+ exchange, Cl/HCO3 exchange, Na+-HCO3 co-transport, etc.) contribute to the control of intracellular pH. CE 33.
Describe Ca2+accumulation in the sarcoplasmic and
endoplasmic reticulum, mediated by Ca2+ ATPase. Regulation
of Cell Function CE 35.
Provide examples of how phosphorylation/dephosphorylation of proteins
(e.g. channels and membrane receptors) can act as negative and positive
effectors of signal transduction. CE 36.
Define the terms agonist and antagonist as related to membrane
receptor ligands. CE 37.
Diagram the intracellular signaling pathways for cholinergic
nicotinic, cholinergic muscarinic, alpha-1 adrenergic, alpha-2 adrenergic,
beta-1 adrenergic, beta-2 adrenergic, and beta-3 adrenergic receptors. CE 38. Contrast the receptor location and signaling pathways of peptide and steroid hormones. For peptide hormone receptors, describe the process of activation, inactivation, up-regulation, down-regulation, sensitization, and desensitization. Epithelia CE 40. Explain the role of the “tight” junctions in leaky and tight epithelia. CE 41.
Explain the functional significance of polarized distribution of
various transport proteins to the apical or the basolateral cell membrane. CE 42. Understand solute-solvent coupling in transport.
Cell Motors CE 44. Explain how the mobilization of calcium initiates contractions in smooth, striated, and cardiac muscle. Explain the sliding filament model of muscle contraction and contrast the cellular and molecular basis of muscle contraction in smooth and striated muscle. Transcapillary Transport CE 46.
Predict the permeability of cardiovascular capillaries to small
ions/crystalloids (e.g., NaCl) and proteins (albumin) based on the capillary
reflection coefficient. CE 47. Based on the Starling hypothesis, explain how permeability, hydrostatic pressure and oncotic pressure influence transcapillary exchange of fluid.
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