cell injury MCQs

Question 8 1 / 1 pts A 71-year-old woman with a history of hypercholesterolemia develops progressive loss of motor function in her left leg over 6 hours. Magnetic resonance angiography shows occlusion of a right middle cerebral arterial branch. A thrombolytic agent is administered. A repeat cerebral imaging study shows that the area of cerebral tissue injury has increased. The increased tissue damage is most likely mediated through which of the following? Misfolded proteins Ketone bodies Immunoglobulins Glutamate Free radicals

Free radicals are the correct answer. She has developed a reperfusion injury further to exacerbate the "stroke" from cerebral arterial occlusion. Early reperfusion via thrombolysis to limit the ischemic area is balanced against the potential for further injury when leukocytes release free radicals (and complement components attracting leukocytes), and reactive oxygen species enter the damaged tissues, expanding the zone of ischemic necrosis. The risk for reperfusion injury increases with the passage of time. Astroglial glutamine synthetase recycles glutamate to reduce neurotoxicity from the neural transmission; gliosis is a feature of remote cerebral injury, not acute. Immunoglobulins are not a significant part of ischemic injuries. The brain can adapt over days to use ketone bodies as fuel when glucose is limited, but there is no inflammation. More subtle, long-term cell stress may route misfolded proteins through the ubiquitin-proteasome pathway, but there is no inflammation.

Question 4 1 / 1 pts In an experiment, a large amount of a drug is administered to experimental organisms and is converted by cytochrome P-450 to a toxic metabolite. The accumulation of this metabolite leads to the formation of free radicals with increased intracellular lipid peroxidation. Depletion of which of the following intracellular substances within the cytosol exacerbates this form of cellular injury by this mechanism? Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase Glutathione Nitric oxide synthase Adenosine diphosphate (ADP) Sodium mRNA

Glutathione is the correct answer. The drug acetaminophen can be converted to toxic metabolites in this manner. Glutathione in the cytosol helps to reduce cellular injury from many toxic metabolites and free radicals. ADP is converted to adenosine triphosphate (ATP) by oxidative and glycolytic cellular pathways to provide energy that drives cellular functions, and a reduction in ATP leaves the cell vulnerable to injury. NADPH oxidase generates superoxide, which is used by neutrophils to kill bacteria. Nitric oxide synthase in macrophages produces nitric oxide, which aids in destroying organisms undergoing phagocytosis. Protein synthesis in cells depends on mRNA for longer survival and recovery from damage caused by free radicals. Failure of the sodium pump leads to increased cytosolic sodium and cell swelling with injury.

Question 7 1 / 1 pts A study is conducted involving the metabolism of a new pharmacologic agent. This drug is metabolized via the cytochrome P-450 system. It is observed that H2O2, along with OH and (H) radicals, are generated during biotransformation of this drug. At higher doses, there is cellular membrane damage. Which of the following is an intracellular substance that is most likely to be protective against these metabolites at a lower dose of this drug? Glutathione peroxidase Proteoglycan Ubiquitin BCL2 protein Cytochrome c oxidase

Glutathione peroxidase is the correct answer. Reactive oxygen species (ROS) can lead to cellular damage. They can modify nitrogenous bases of DNA, leading to DNA strand breakage. They play a significant role in lipid peroxidation and membrane destabilization. They can also react with nitric oxide (NO), forming peroxynitrite ion (ONOO −), and exert deleterious effects on DNA, protein, and lipid molecules. Glutathione peroxidases can protect against low-level generation of ROS. The BCL2 family of proteins is antiapoptotic. Cytochrome c oxidase is the last enzyme in the respiratory electron transport chain of mitochondria. Proteoglycans form a component of the extracellular matrix. Damaged, misfolded proteins can be recycled via the ubiquitin-proteasome pathway after the damage has occurred.

Question 5 1 / 1 pts In an experiment, metabolically active cells are subjected to radiant energy in the form of X-rays. This results in cell injury caused by the hydrolysis of water. Which of the following intracellular enzymes helps to protect the cells from this type of injury? Endonuclease Protease Lactate dehydrogenase Glutathione peroxidase Phospholipase

Glutathione peroxidase is the correct answer. The body has intracellular mechanisms that prevent damage from free radicals generated by exposure to X-rays. Glutathione peroxidase reduces such injury by catalyzing the breakdown of hydrogen peroxide. Endonucleases damage DNA in nuclear chromatin. Lactate dehydrogenase is present in a variety of cells, and its elevation in the serum is an indicator of cell injury and death. Phospholipases decrease cellular phospholipids and promote cell membrane injury. Proteases can damage cell membranes and cytoskeletal proteins.

Question 6 1 / 1 pts A 5-year-old child ingests 50 iron tablets, each with 27 mg of iron. Within 6 hours, the child develops abdominal pain and lethargy. On physical examination, he is hypotensive. Laboratory studies show metabolic acidosis. Through the formation of which of the following compounds is the cell injury in this child most likely mediated? Hemosiderin Ascorbic acid Nitric oxide Hydroxyl radical Superoxide dismutase

Hydroxyl radical is the correct answer. Excessive iron ingestion, particularly by a child, can overwhelm the body's ability to bind the absorbed free iron with the transport protein transferrin. The free iron contributes to the generation of cellular free radicals via the Fenton reaction. Ascorbic acid (vitamin C) and vitamin E both act as antioxidants to protect against free radical injury, albeit over a long time frame. Hemosiderin is a storage form of iron from an excess local or systemic accumulation of ferritin and by itself does not cause cell injury until large amounts are present, as with hemochromatosis. Nitric oxide generated within macrophages can be used to kill microbes. It can be converted to a highly reactive peroxynitrite anion. Superoxide dismutase helps to break down superoxide anion to hydrogen peroxide, thus scavenging free radicals.

Question 9 1 / 1 pts A 35-year-old woman with a history of familial hypercholesterolemia is brought to the emergency department with crushing retrosternal chest pain of one-hour duration. Laboratory evaluations reveal elevated serum levels of CK-MB and troponins. Coronary angiography reveals an occlusive thrombus in the right coronary artery. A stent is placed in the right coronary artery with restoration of normal coronary blood flow. The patient's condition is not improved, and his serum levels of CK-MB and troponins are found to have increased. Which of the following best explains the pathogenesis of this phenomenon? Release of cytokines Release of lysosomal enzymes Spasm of surrounding coronary arteries Increased calcium influx Hypertrophy of adjacent myocardial cells

Increased calcium influx

Question 2 1 / 1 pts A 47-year-old woman has poorly controlled diabetes mellitus and develops coronary artery disease. She has decreased cardiac output with blood pressure of 80/40 mmHg and an ejection fraction of 18%. An increase in which of the following substances in her blood is most indicative of reversible cell injury from decreased systemic arterial perfusion of multiple organs and tissues? Lactic acid Glucose Carbon dioxide Creatinine Troponin I

Lactic acid is the correct answer. Decreased tissue perfusion from hypotensive shock leads to hypoxemia and depletion of adenosine triphosphate when cell metabolism shifts from aerobic to anaerobic glycolysis. This shift causes depletion of glycogen stores and increased production and accumulation of lactic acid, reducing intracellular pH. Creatinine would increase with reduced renal function from decreased renal perfusion, but this would not explain the changes in other tissues. An increased glucose level would be indicative of poorly controlled diabetes mellitus, not decreased perfusion. Carbon dioxide is likely to be cleared via normal lungs, which are still sufficiently perfused by a failing heart. An increase in troponin I suggest irreversible myocardial injury.

Question 10 1 / 1 pts During a study of the response of cardiomyocytes to the ischemic injury, the coronary arteries in experimental animals are ligated for variable lengths of time. The myocardium is then examined by light and electron microscopy. Which of the following features would definitively indicate irreversible injury to the cardiomyocytes? (multiple correct answers) Multiple ruptures of cytomembrane Production of large amorphous densities in mitochondria Accumulation of water in the cytosol Production of small amorphous densities in mitochondria Formation of cytoplasmic blebs

Multiple ruptures of cytomembrane Production of large amorphous densities in mitochondria

An experimental drug administered to a tissue preparation is found to inhibit cellular oxidative phosphorylation when given in high doses, and adenosine triphosphate (ATP) production drops to 5% of normal. Cell membrane function is diminished. Which of the following substances is most likely to be present at an increased concentration in culture fluid bathing the tissue? Calcium Sodium Ketones Potassium Glucose

Potassium is the correct answer. Reduction in oxidative phosphorylation leads to a reduction in the synthesis of ATP and diminished activity of the plasma membrane sodium pump, which maintains high intracellular potassium concentration. Loss of ATP leads to the efflux of intracellular potassium, and the net influx of sodium and water promotes cell swelling. A marked rise in plasma potassium can indicate significant cell damage or death (e.g., skeletal muscle crush injury or hemolysis). When cells are not consuming glucose via oxidative metabolism, the glucose is metabolized via other pathways, and glucose is maintained within normal ranges. Although cell membranes are composed of lipids, dysfunction or disruption of those membranes does not significantly alter plasma lipid concentrations.

Question 3 1 / 1 pts A 54-year-old man experienced severe substernal chest pain for 3 hours. An ECG showed changes consistent with an acute myocardial infarction. After thrombolytic therapy with tissue plasminogen activator (t-PA), his serum troponin I level increased. Which of the following tissue events most likely occurred in the myocardium after t-PA therapy? Drug toxicity Cellular regeneration Myofiber atrophy Reperfusion injury Increased protein synthesis

Reperfusion injury is the correct answer. If existing cell damage is not great after myocardial infarction, the restoration of blood flow can help to prevent further cellular damage. However, the reperfusion of damaged cells results in the generation of oxygen-derived free radicals, causing a reperfusion injury. The elevation in the troponin level is indicative of myocardial cell necrosis because this intracellular enzyme does not leak in large quantities from intact myocardial cells, and cell injury diminishes cellular protein synthesis. Myocardial fibers do not regenerate to a significant degree, and atrophic fibers would have less CK to release. t-PA does not produce a toxic chemical injury; it induces thrombolysis to restore blood flow in occluded coronary arteries.