NSG 530 Ch. 4 Altered Cell & Tissue
UPDATED ACTUAL Exam Questions and
CORRECT Answers
When does a cell become irreversibly injured? - CORRECT ANSWER - 1. The exact
point of irreversible injury can vary based on a variety of factors, and the exact point of
irreversible damage is up for debate. However, structurally, when severe vacuolization of the
mitochondria occurs and calcium moves into the cell, irreversible injury is imminent.
Discuss the pathogenesis of hypoxic injury. - CORRECT ANSWER - Hypoxia leads to a
reduction in ATP levels which causes the plasma membrane's sodium-potassium (Na+-K+)
pump and sodium-calcium exchange mechanism to fail, leading to an intracellular accumulation
of sodium and calcium and diffusion of potassium out of the cell. Sodium and water then can
enter the cell freely. The entire cell becomes markedly swollen, with increased concentrations of
sodium, water, and chloride and decreased concentrations of potassium. Continued hypoxic
injury with accumulation of calcium subsequently activates multiple enzyme systems resulting in
membrane damage, cytoskeleton disruption, DNA and chromatin degradation, ATP depletion,
and eventual cell death.
What are the mechanisms of ischemia-reperfusion injury? - CORRECT ANSWER - 1.
Restoration of blood flow and oxygen to ischemic tissues can increase recovery of cells
reversibly injured, but paradoxically result in additional injury known as ischemia-reperfusion
injury.
Mechanisms of ischemia-reperfusion injury include:
a. Oxidative Stress: Reoxygenation induces oxidative stress by generating highly ROS and
nitrogen species. These include hydroxyl radical (OH-), superoxide radical (O.2) and hydrogen
peroxide (H202). Nitrogen based free radicals present mostly in the form of nitric oxide (NO)
and are generated by endothelial cells, macrophages, neurons and other cells. The radicals further
damage the already compromised membrane and facilitate calcium overload within the
mitochondria. Additionally, reperfusion injury promotes pro-inflammatory neutrophil adhesion
to the endothelium where they release toxic oxidants and harmful proteases. Antioxidants such as
Vitamin C & E reverse neutrophil adhesion and neutrophol-mediated reperfusion in cardiac
muscle.
b. Increased intracellular calcium concentration - Intracellular and mitochondrial calcium
accumulate within the cell during acute ischemia. Reperfusion results in more calcium influx
because of damaged cell membranes and ROS-mediated injury to the sarcoplasmic reticulum.
, The increased calcium enhances mitochondrial permeability; damaged mitochondria have
decreased or ceased production of ATP.
c. Inflammation: Ischemic injury promotes inflammation. Dead cells stimulate immune cells to
release cytokine-mediated danger signals, thus initiating inflammatory response.
d. Complement activation: May exacerbate damage which has occurred secondary to reperfusion
injury.
Why are children more susceptible to the toxic effects of lead exposure? - CORRECT
ANSWER - 1. Children have an increased hand-to-mouth behavior and thus prone to
putting objects found in their environment into their mouths.
2. The blood-brain barrier in children is immature during fetal development, contributing to
greater accumulation in the developing brain.
3.Infant absorption of lead is greater than adults. In adults, the body burden of lead is found in
bone. In children, growth results in a rapid turnover in skeletal bone causing a continuous
leaching of lead into the bone.
4. In cases of compromised nutrition, where dietary intake of iron and calcium is insufficient,
children are more likely to have elevated lead levels.
Discuss the nutritional implications in chronic alcoholism. - CORRECT ANSWER - 1.
Major nutritional deficiencies associated with alcohol abuse include those of magnesium,
vitamin B6, thiamine, folic acid and phosphorus.
2. Folic acid deficiency becomes especially serious when alcohol is consumed during pregnancy
and may contribute to fetal alcohol syndrome.
3. Thiamine deficiency results in major neurologic sequele.
4. Increased risk of head and neck cancers
Discuss mechanisms of cell injury related to chronic alcoholism - CORRECT ANSWER -
1. Protein transport malfunctions
2. Increased intracellular cellular water
3. Decreased mitochondrial fatty acid oxidation
4. Excessive membrane rigidity
5. Liver cell necrosis
UPDATED ACTUAL Exam Questions and
CORRECT Answers
When does a cell become irreversibly injured? - CORRECT ANSWER - 1. The exact
point of irreversible injury can vary based on a variety of factors, and the exact point of
irreversible damage is up for debate. However, structurally, when severe vacuolization of the
mitochondria occurs and calcium moves into the cell, irreversible injury is imminent.
Discuss the pathogenesis of hypoxic injury. - CORRECT ANSWER - Hypoxia leads to a
reduction in ATP levels which causes the plasma membrane's sodium-potassium (Na+-K+)
pump and sodium-calcium exchange mechanism to fail, leading to an intracellular accumulation
of sodium and calcium and diffusion of potassium out of the cell. Sodium and water then can
enter the cell freely. The entire cell becomes markedly swollen, with increased concentrations of
sodium, water, and chloride and decreased concentrations of potassium. Continued hypoxic
injury with accumulation of calcium subsequently activates multiple enzyme systems resulting in
membrane damage, cytoskeleton disruption, DNA and chromatin degradation, ATP depletion,
and eventual cell death.
What are the mechanisms of ischemia-reperfusion injury? - CORRECT ANSWER - 1.
Restoration of blood flow and oxygen to ischemic tissues can increase recovery of cells
reversibly injured, but paradoxically result in additional injury known as ischemia-reperfusion
injury.
Mechanisms of ischemia-reperfusion injury include:
a. Oxidative Stress: Reoxygenation induces oxidative stress by generating highly ROS and
nitrogen species. These include hydroxyl radical (OH-), superoxide radical (O.2) and hydrogen
peroxide (H202). Nitrogen based free radicals present mostly in the form of nitric oxide (NO)
and are generated by endothelial cells, macrophages, neurons and other cells. The radicals further
damage the already compromised membrane and facilitate calcium overload within the
mitochondria. Additionally, reperfusion injury promotes pro-inflammatory neutrophil adhesion
to the endothelium where they release toxic oxidants and harmful proteases. Antioxidants such as
Vitamin C & E reverse neutrophil adhesion and neutrophol-mediated reperfusion in cardiac
muscle.
b. Increased intracellular calcium concentration - Intracellular and mitochondrial calcium
accumulate within the cell during acute ischemia. Reperfusion results in more calcium influx
because of damaged cell membranes and ROS-mediated injury to the sarcoplasmic reticulum.
, The increased calcium enhances mitochondrial permeability; damaged mitochondria have
decreased or ceased production of ATP.
c. Inflammation: Ischemic injury promotes inflammation. Dead cells stimulate immune cells to
release cytokine-mediated danger signals, thus initiating inflammatory response.
d. Complement activation: May exacerbate damage which has occurred secondary to reperfusion
injury.
Why are children more susceptible to the toxic effects of lead exposure? - CORRECT
ANSWER - 1. Children have an increased hand-to-mouth behavior and thus prone to
putting objects found in their environment into their mouths.
2. The blood-brain barrier in children is immature during fetal development, contributing to
greater accumulation in the developing brain.
3.Infant absorption of lead is greater than adults. In adults, the body burden of lead is found in
bone. In children, growth results in a rapid turnover in skeletal bone causing a continuous
leaching of lead into the bone.
4. In cases of compromised nutrition, where dietary intake of iron and calcium is insufficient,
children are more likely to have elevated lead levels.
Discuss the nutritional implications in chronic alcoholism. - CORRECT ANSWER - 1.
Major nutritional deficiencies associated with alcohol abuse include those of magnesium,
vitamin B6, thiamine, folic acid and phosphorus.
2. Folic acid deficiency becomes especially serious when alcohol is consumed during pregnancy
and may contribute to fetal alcohol syndrome.
3. Thiamine deficiency results in major neurologic sequele.
4. Increased risk of head and neck cancers
Discuss mechanisms of cell injury related to chronic alcoholism - CORRECT ANSWER -
1. Protein transport malfunctions
2. Increased intracellular cellular water
3. Decreased mitochondrial fatty acid oxidation
4. Excessive membrane rigidity
5. Liver cell necrosis
