Liver Apoptosis and Injury Quiz

<p>Massive apoptosis (C)</p> Signup and view all the answers

<p>Death receptor activation (C)</p> Signup and view all the answers

<p>They are involved in apoptosis induction. (C)</p> Signup and view all the answers

<p>Inflammatory liver diseases (C)</p> Signup and view all the answers

<p>Normal hepatocytes can effectively undergo apoptosis. (B)</p> Signup and view all the answers

<p>Hepatic stellate cell activation (A)</p> Signup and view all the answers

<p>Intrinsic is primarily triggered by internal signals. (D)</p> Signup and view all the answers

<p>Inflammation and fibrogenesis (B)</p> Signup and view all the answers

<p>Extent of ATP depletion (B)</p> Signup and view all the answers

<p>Mallory-Denk Bodies (B)</p> Signup and view all the answers

<p>Regeneration of mature liver cells (B)</p> Signup and view all the answers

<p>Apoptosis is a specific cascade; necrosis is unregulated cell death. (C)</p> Signup and view all the answers

<p>HELLP syndrome (B)</p> Signup and view all the answers

<p>Increased oxidative stress (D)</p> Signup and view all the answers

<p>Phagocytosis of apoptotic bodies. (D)</p> Signup and view all the answers

<p>Increasing intracellular calcium levels (A)</p> Signup and view all the answers

<p>Extrinsic pathway (A)</p> Signup and view all the answers

<p>Optimal portal blood flow (D)</p> Signup and view all the answers

<p>Membrane volume control derangement (C)</p> Signup and view all the answers

<p>Necroptosis (C)</p> Signup and view all the answers

<p>Necrosis involves intracellular ATP depletion. (D)</p> Signup and view all the answers

<p>To signal that they cannot regenerate (D)</p> Signup and view all the answers

<p>Interferes with normal lobular arrangement (A)</p> Signup and view all the answers

<p>Type IX (A)</p> Signup and view all the answers

<p>Active stem/progenitor cell processes (D)</p> Signup and view all the answers

<p>Laminin (D)</p> Signup and view all the answers

<p>Microvascular rearrangement (C)</p> Signup and view all the answers

<p>CK 7 (A)</p> Signup and view all the answers

<p>Presence of fibrogenesis (C)</p> Signup and view all the answers

<p>Cytokines secreted by Kupfer cells (C)</p> Signup and view all the answers

<p>Kupfer cells (D)</p> Signup and view all the answers

<p>Proliferation of hepatic progenitor cells (C)</p> Signup and view all the answers

<p>It represents a stable state from which they can re-enter the cell cycle (D)</p> Signup and view all the answers

<p>Interleukin-6 (D)</p> Signup and view all the answers

<p>Inhibition of hepatocyte proliferation (C)</p> Signup and view all the answers

<p>Proliferation of stem cells (D)</p> Signup and view all the answers

<p>Engulfment of dead cells (D)</p> Signup and view all the answers

<p>Obstruction of endothelial pores (C)</p> Signup and view all the answers

<p>Formation of porto-central shunts (A)</p> Signup and view all the answers

<p>It is associated with a decrease in endothelial permeability (C)</p> Signup and view all the answers

<p>They bypass normal portal circulation (C)</p> Signup and view all the answers

<p>Decreased parenchymal loss lesions (C)</p> Signup and view all the answers

<p>It promotes the accumulation of HIF-1 in endothelial cells (B)</p> Signup and view all the answers

<p>Chronic viral hepatitis (C)</p> Signup and view all the answers

<p>Development of pre-sinusoidal vascular resistance (C)</p> Signup and view all the answers

<p>It activates HSC and myofibroblast proliferation (A)</p> Signup and view all the answers

<p>Vascular changes increase risk of focal ischemic injury (C)</p> Signup and view all the answers

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.