Fundamentals of Pathology Quiz

A reversible change in which one adult cell type is replaced by another adult cell type.

Disordered cellular growth, often precancerous cell proliferation.

A condition where the lining of the esophagus changes to a different type of cells.

Failure of cell production during embryonic development.

Reduced cell production during embryonic development, causing a smaller-than-normal organ.

Damage to cells when stress overwhelms their ability to adapt.

A type of metaplasia in the breast that does not increase cancer risk.

Connective tissue within muscle changes to bone during healing from trauma.

Insufficient oxygen delivery to tissues, leading to cellular injury. It's a common cause of cell damage.

Reduced blood flow to an organ, causing oxygen deprivation. Can be caused by blocked arteries or veins.

Low oxygen levels in the blood, specifically a decrease in partial pressure of oxygen (PaO2).

Inability of blood to carry sufficient oxygen, due to problems with hemoglobin.

Oxygen is the final electron acceptor in oxidative phosphorylation, a process that produces ATP, the cell's energy source.

Lack of ATP (energy) disrupts essential cellular functions, leading to damage and potentially cell death.

Examples include atherosclerosis (narrowed arteries), Budd-Chiari syndrome (blocked veins), and shock (poor blood flow throughout the body).

Causes include high altitude (low atmospheric pressure), hypoventilation (inefficient breathing), diffusion defects (thickened lung barrier), and ventilation/perfusion mismatch.

A type of necrosis where the dead tissue remains firm due to protein coagulation. Cell shape and organ structure are preserved, but the nucleus disappears.

Tissue death caused by a lack of blood supply, often seen in coagulative necrosis.

Coagulative necrosis often appears as a wedge-shaped area pointing to the point of blood vessel blockage (occlusion).

A type of infarction where blood re-enters a loosely organized tissue, causing the area to appear reddish.

A type of necrosis where the dead tissue is liquefied due to enzymatic breakdown of cells and proteins.

Liquefactive necrosis is often seen in the brain due to the high concentration of enzymes.

A protein released from damaged mitochondria, triggering apoptosis (programmed cell death).

Damage to the lysosome membrane releases enzymes into the cytosol, further contributing to cell death.

Chemical species with an unpaired electron in their outer orbit, highly reactive and can cause damage to cells.

Process in mitochondria where energy is produced from food, but also generates free radicals as a byproduct.

Excess production of free radicals can overwhelm the body's defense mechanisms, leading to cellular damage.

A form of energy that can directly damage cells by creating free radicals.

The body's response to injury, but it can generate free radicals as a defense mechanism.

Can generate free radicals through a reaction called the Fenton reaction.

Some medications or substances can be metabolized by the liver, producing free radicals as a byproduct.

The body has various mechanisms to neutralize free radicals and repair damage.

A disease caused by the abnormal buildup of amyloid protein in organs. Amyloid is a protein that normally exists in small amounts, but in amyloidosis it accumulates and forms deposits in tissues, interfering with normal function.

A type of amyloidosis where mutated transthyretin protein deposits in the heart, leading to restrictive cardiomyopathy, making it difficult for the heart to pump blood.

In type II diabetes, amylin, a protein related to insulin, can deposit in the pancreas, affecting insulin production and regulation.

Alzheimer's disease involves deposits of Aβ amyloid protein in the brain, forming plaques and tangles that disrupt brain function.

β2-microglobulin, a protein filtered by the kidneys, can build up in joints in people on dialysis, causing amyloidosis.

CCl3 free radical, generated by the P450 system in hepatocytes, causes cell injury. This injury manifests as swelling of the endoplasmic reticulum (RER), leading to detachment of ribosomes and impaired protein synthesis. Consequently, decreased apolipoproteins contribute to fatty change in the liver.

Reperfusion injury occurs when blood flow returns to ischemic tissue, leading to the production of oxygen-derived free radicals. These radicals further damage the already compromised tissue. This is particularly evident in myocardial infarction, where cardiac enzyme levels (e.g., troponin) continue to rise after reperfusion.

Amyloid is a misfolded protein that accumulates in the extracellular space, leading to tissue damage. These misfolded proteins have a shared β-pleated sheet configuration and exhibit Congo red staining with apple-green birefringence under polarized light.

Amyloid deposition can be systemic, affecting multiple organs, or localized, affecting specific areas. Systemic amyloid deposition is further categorized into primary and secondary amyloidosis.

Primary amyloidosis is characterized by systemic deposition of AL amyloid, derived from immunoglobulin light chains. It is often associated with plasma cell dyscrasias like multiple myeloma.

Secondary amyloidosis is characterized by systemic deposition of AA amyloid, derived from serum amyloid-associated protein (SAA). SAA is an acute phase reactant, elevated in chronic inflammatory states, malignancy, and Familial Mediterranean fever.

Serum amyloid-associated protein (SAA) is an acute-phase reactant, meaning its levels rise in response to inflammation and other conditions like malignancy and Familial Mediterranean fever. This increased SAA can contribute to the development of secondary amyloidosis.

Familial Mediterranean fever (FMF) is an inherited condition associated with recurrent episodes of inflammation. These episodes lead to increased production of SAA, which can further increase the risk of developing secondary amyloidosis.