1. What causes the rapid change in the resting membrane potential to initiate an action potential?
a. Potassium gates open, and potassium rushes into the cell, changing the membrane potential from negative to positive.
b. Sodium gates open, and sodium rushes into the cell, changing the membrane potential from negative to positive.
c. Sodium gates close, allowing potassium into the cell to change the membrane potential from positive to negative.
d. Potassium gates close, allowing sodium into the cell to change the membrane potential from positive to negative.
2. What is a consequence of leakage of lysosomal enzymes during chemical injury?
a. Enzymatic digestion of the nucleus and nucleolus occurs, halting DNA synthesis.
b. Influx of potassium ions into the mitochondria occurs, halting the ATP production.
c. Edema of the Golgi body prevents the transport of proteins out of the cell.
d. Shift of calcium out of the plasma membrane occurs, destroying the cytoskeleton.
3. In hypoxic injury, sodium enters the cell and causes swelling because:
a. The cell membrane permeability increases for sodium during periods of hypoxia.
b. ATP is insufficient to maintain the pump that keeps sodium out of the cell.
c. The lactic acid produced by the hypoxia binds with sodium in the cell.
d. Sodium cannot be transported to the cell membrane during hypoxia.
4. What mechanisms occur in the liver cells as a result of lipid accumulation?
a. Accumulation of lipids that obstruct the common bile duct, preventing flow of bile from the liver to the gallbladder
b. Increased synthesis of triglycerides from fatty acids and decreased synthesis of apoproteins
c. Increased binding of lipids with apoproteins to form lipoproteins
d. Increased conversion of fatty acids to phospholipids
5. During an IgE-mediated hypersensitivity reaction, the degranulation of mast cells is a result of which receptor action?
a. Histamine bound to H2
b. Chemotactic factor binding to the receptor
c. Epinephrine bound to mast cells
d. Acetylcholine bound to mast cells