Liver Apoptosis and Injury Quiz

A reversible form of liver cell injury characterized by swelling of hepatocytes.

Cellular inclusions (damaged proteins) in hepatocytes associated with liver injury, often seen in alcoholic liver disease.

Pathological cell death in liver cells, occurring due to severe injury.

Programmed cell death, a controlled process of cell destruction.

Pathological cell death characterized by uncontrolled cell breakdown.

Liver cell damage that can be repaired.

Accumulation of fat in liver cells.

Two main pathways (intrinsic and extrinsic) involved in programmed cell death within the cell.

Programmed cell death in liver cells, a response to acute or chronic liver injury.

Sudden liver damage, often caused by ischemia (low blood flow) or hypoperfusion.

Long-term liver damage, which may include acute exacerbations (worsening).

Cell death pathway triggered by external signals.

Cell death pathway triggered by cellular stress or abnormalities within the cell.

A problem with mitochondria, the 'powerhouses' of the cells, leading to apoptosis.

Programmed cell death in the liver, triggered by various factors like inflammation, toxins, and infections.

Uncontrolled cell death in the liver due to severe damage, causing cellular swelling and leakage.

Mature liver cells (hepatocytes) typically live for 200-300 days.

The liver's ability to repair itself by either stimulating mature liver cells to multiply or recruiting stem cells to produce new cells.

Chronic liver diseases are often triggered by infections, inflammation, toxic compounds, and autoimmune responses which lead to a chronic inflammatory response.

Liver damage caused by harmful substances, either from drugs or toxins.

The formation of scar tissue in the liver due to chronic inflammation or injury, often triggered by the release of profibrogenic cytokines.

Stellate cells (HSC) play a key role in liver damage by releasing profibrogenic cytokines (TGFβ) which trigger inflammation and fibrosis.

The liver's ability to regrow after injury, primarily using mature hepatocytes stimulated by Kupffer cells.

Immune cells in the liver that engulf and clear apoptotic cells.

The process of triggering hepatocytes (liver cells) to divide and reproduce following an injury.

A cytokine (signaling molecule) secreted by Kupffer cells, which stimulates more Kupffer cells.

A cytokine secreted by Kupffer cells that signals hepatocytes to enter the cell cycle.

Regeneration of the liver following acute injury, primarily due to mature hepatocytes.

Liver regeneration after chronic damage, mainly from progenitor and stem cells.

Stable state of hepatocytes (liver cells) when not actively dividing.

Progenitor cells are stem-like cells that can differentiate into specialized liver cells, contributing to regeneration when hepatocytes are unable to do so.

Excess collagen buildup (fibrosis) impairs the liver's ability to regenerate, as the fibrous tissue disrupts normal structure and prevents hepatocytes from performing their functions.

Extracellular Matrix (ECM) is a complex network of proteins and other molecules that provide structural support, organization, and communication within the liver.

Components of the ECM include fibrillary (collagen, elastin) and non-fibrillary (laminin, fibronectin) components that contribute to the liver's structural integrity.

ECM plays a crucial role in liver function by providing structural support, influencing cell behavior, and regulating communication within the liver.

In liver disease, ECM composition and arrangement change, often resulting in fibrosis, which can lead to impaired liver function.

Hepatic Fibrogenesis is the process of excessive ECM production and deposition in the liver, leading to fibrosis and scarring

Formation of a basal membrane-like structure in the Disse space, hindering nutrient and oxygen delivery to hepatocytes due to collagen accumulation.

Increased pressure within the sinusoids caused by collagen buildup, leading to vascular thrombosis and impaired blood flow.

Abnormal connections between blood vessels, such as porto-central shunts, bypassing the sinusoids due to high pressure and impaired blood flow.

Increased pressure in the portal vein due to obstruction of blood flow through the liver, leading to abnormal blood flow patterns.

Hepatic stellate cells (HSCs) transform into myofibroblasts, increasing contractility and contributing to sinusoidal resistance.

Formation of new blood vessels in the liver, triggered by chronic inflammation and hypoxia, leading to abnormal blood flow patterns and contributing to portal hypertension.

Areas of liver cell death caused by insufficient oxygen delivery, contributing to liver dysfunction.

Formation of small clusters of regenerating liver cells in the damaged liver, contributing to changes in liver structure.

Advanced liver disease characterized by fibrosis, nodulation, and vascular rearrangement, leading to impaired liver function and potential liver failure.