Infarction & Necrosis Flashcards
explain the meaning of apoptosis
Programmed cell death is a natural and essential process in the growth and development of organisms. Apoptosis, which is derived from the Greek words “apo” (away) and “ptosis” (falling), is a specific type of programmed cell death. This process is crucial for maintaining the balance of cell populations, eliminating damaged or unnecessary cells, and shaping tissues during development.
During apoptosis, cells undergo a series of tightly regulated events that lead to their orderly and controlled self-destruction. This process is characterized by distinct morphological changes, such as cell shrinkage, chromatin condensation, nuclear fragmentation, and the formation of apoptotic bodies. Apoptosis plays a critical role in various physiological processes, including embryonic development, tissue homeostasis, and the immune response.
On the other hand, necrosis is another form of cell death, but it is typically associated with pathological conditions and is characterized by swelling of the cell and its organelles, leading to uncontrolled cell rupture. Unlike apoptosis, necrosis is generally considered a more inflammatory process.
explain apoptosis
Highly Regulated Process of Self-Degradation:
Apoptosis is indeed a tightly regulated process involving a series of molecular events that are carefully orchestrated to ensure controlled self-degradation. The regulation of apoptosis involves a complex interplay of signaling pathways and molecular mechanisms, including the activation of specific enzymes known as caspases.
Eliminates Unwanted Cells:
One of the primary functions of apoptosis is to eliminate cells that are no longer needed or are potentially harmful. This can include cells during embryonic development that serve a temporary function or cells that have undergone damage beyond repair.
Eliminates Dysfunctional Cells:
Apoptosis is crucial for removing dysfunctional or damaged cells, preventing them from becoming a source of potential harm or contributing to diseases like cancer. By eliminating cells with genetic mutations or other abnormalities, apoptosis helps maintain the overall health and integrity of tissues and organs.
Genome Fracture, Cell Shrinkage, and Apoptotic Bodies:
During apoptosis, the cell undergoes characteristic changes. The nucleus, or genome, fragments, leading to the formation of smaller apoptotic bodies. The cell also undergoes shrinkage, and these apoptotic bodies contain the cell’s remnants in a form that can be efficiently engulfed and cleared by neighboring cells or phagocytes.
Control of Cell Proliferation in Adults:
In adults, apoptosis continues to play a crucial role in maintaining tissue homeostasis by balancing cell proliferation. The controlled elimination of old or damaged cells allows for the controlled generation of new cells. This balance is essential for tissue renewal and repair, and disruptions in apoptosis regulation can contribute to various diseases, including cancer.
examples of various stimuli or conditions that can influence or trigger apoptosis in cells
TNF (Tumor Necrosis Factor):
TNF is a cytokine involved in systemic inflammation and is produced by immune cells. It plays a dual role in cell fate, as it can promote both cell survival and apoptosis depending on the context. In certain situations, TNF can activate apoptotic pathways, contributing to the regulation of immune responses and tissue development.
Reduction of Growth Factors:
Cells rely on growth factors for survival and proliferation. A reduction in the availability of these growth factors can trigger apoptosis. Cells receive signals from their environment, and if these signals indicate that growth conditions are unfavorable, apoptosis may be initiated as a mechanism to eliminate cells that cannot thrive under those conditions.
Oncogenes:
Oncogenes are genes that, when mutated or overexpressed, can contribute to the development of cancer. Some oncogenes can interfere with the normal regulation of cell growth and survival, tipping the balance in favor of cell proliferation. In some cases, the overactivation of oncogenes can also sensitize cells to apoptosis as a protective mechanism against the development of cancer.
Nutrient Deprivation:
Cells require nutrients for energy production and various cellular processes. If cells experience prolonged nutrient deprivation or conditions where essential nutrients are scarce, it can trigger apoptosis. This is a way for the body to eliminate cells that are not able to survive under nutrient-poor conditions.
Toxins:
Exposure to certain toxins or chemicals can induce cellular stress and damage, leading to the activation of apoptosis. This is a protective mechanism to eliminate cells that may be compromised due to toxin exposure.
UV and Gamma Radiation:
Exposure to ionizing radiation, such as UV and gamma radiation, can cause DNA damage. Cells with severe DNA damage may undergo apoptosis to prevent the propagation of genetic errors. This is a crucial mechanism to prevent the development of cancer, as uncontrolled cell growth with damaged DNA can lead to the formation of tumors.
explain the consequences of excessive apoptosis and deficient apoptosis
Excessive Apoptosis:
Neurodegenerative Diseases:
Neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s disease, are characterized by the progressive loss of neurons. Excessive apoptosis of neurons can contribute to the pathogenesis of these diseases. In some cases, the apoptotic machinery may be overactivated, leading to the premature death of neurons and the subsequent decline in cognitive or motor function.
Deficient Apoptosis:
Cancer:
One hallmark of cancer is the uncontrolled proliferation of cells. Deficient apoptosis, where cells evade the normal apoptotic pathways, can contribute to the development and progression of cancer. In cancer cells, the balance between pro-survival and pro-apoptotic signals is often disrupted, allowing the cells to resist apoptosis and continue growing uncontrollably.
Autoimmunity:
Autoimmune diseases occur when the immune system mistakenly targets and attacks the body’s own cells. Deficient apoptosis can contribute to autoimmunity by allowing the survival of autoreactive immune cells that should normally undergo apoptosis during development. These surviving cells can then contribute to the autoimmune response by attacking healthy tissues.
explain necrosis
Necrosis is a form of cell death that occurs due to external factors or pathological conditions, such as injury, exposure to toxic substances, radiation, or insufficient oxygen supply (hypoxia or anoxia). Unlike apoptosis, which is a programmed and orderly form of cell death, necrosis is typically unplanned and often associated with inflammation.
Key characteristics of necrosis include:
External Factors:
Necrosis is usually triggered by external factors that cause severe damage to the cell or its environment. This can include physical trauma, exposure to harmful chemicals, extreme temperature changes, or infections.
Unplanned and Disorderly:
Unlike apoptosis, necrosis is not a regulated and orderly process. It is often characterized by swelling of the cell and its organelles, leading to the rupture of the cell membrane. This can result in the release of cellular contents into the surrounding tissue, which may elicit an inflammatory response.
Inflammation:
Necrosis is associated with inflammation because the release of cellular contents into the extracellular space can attract immune cells and provoke an inflammatory reaction. This inflammatory response can contribute to further tissue damage.
Permanent Cell Damage:
Necrosis typically leads to irreversible damage, and the affected cells cannot recover. This is in contrast to apoptosis, where the process is carefully controlled, and the cell’s components are dismantled without causing inflammation or damage to surrounding tissues.
compare apoptosis & necrosis
Nature of Cell Death:
Apoptosis: Functional and planned.
Necrosis: Accidental and caused by external factors.
Physiological vs. Pathological:
Apoptosis: Can be physiological (normal part of development) or pathological (due to disease or injury).
Necrosis: Generally considered pathological, often resulting from injury or disease.
Energy Requirement:
Apoptosis: ATP-dependent (requires energy).
Necrosis: Does not require energy; it is often a passive, uncontrolled process.
Cell Changes:
Apoptosis: Cell shrinks and pulls away from neighboring cells.
Necrosis: Cell swells.
Nuclear Changes:
Apoptosis: Nucleus shrinks.
Necrosis: Entire cell balloons, eventually leading to cell rupture.
explain ischaemia
Ischemia refers to the inadequate supply of blood to a particular area of tissue, leading to a reduction in oxygen delivery and nutrient supply. This can result in hypoxia (oxygen deprivation), malnutrition, and the accumulation of waste products in the affected tissue. Ischemia is often caused by the interruption of arterial blood supply to the tissue, although it can also occur in conditions where blood flow is compromised.
Key points about ischemia include:
Hypoxia:
Ischemia leads to a decrease in oxygen supply to the affected tissue, resulting in hypoxia. Oxygen is crucial for cellular respiration, and a lack of oxygen can impair cellular function and energy production.
Malnutrition:
The inadequate blood supply associated with ischemia also means a reduced supply of nutrients to the affected tissue. This can lead to cellular dysfunction and, if severe or prolonged, cell death.
Waste Accumulation:
Proper blood flow is essential for removing waste products generated by cellular metabolism. In the absence of adequate blood supply, the accumulation of waste products can further contribute to cellular damage.
Arterial Supply Interruption:
Ischemia is typically caused by the interruption of arterial blood flow. This interruption can result from various conditions, such as atherosclerosis (narrowing of arteries due to plaque buildup), thrombosis (formation of blood clots), embolism (blockage of blood vessels by traveling clots), or other vascular disorders.
explain infarction
Infarction refers to an area of tissue that undergoes necrosis (cell death) due to a lack of blood supply, typically caused by arterial or venous ischemia. The interruption of blood flow can result from various factors, and you’ve mentioned several common causes:
Thrombus: Formation of a blood clot (thrombus) within a blood vessel can obstruct blood flow, leading to ischemia and subsequent infarction.
Embolism: An embolus, a detached clot or other material, can travel through the bloodstream and lodge in a vessel, causing a blockage and infarction.
Hypovolemia: Low blood volume, as seen in conditions like severe dehydration or blood loss, can reduce blood flow to tissues and contribute to infarction.
Hypotension: Low blood pressure can result in inadequate perfusion of tissues, leading to ischemia and infarction.
Vasospasm: Constriction of blood vessels, often due to abnormal and prolonged contraction of the vessel walls, can reduce blood flow and cause infarction.
Torsion: Twisting of blood vessels can compromise blood supply, leading to ischemia and infarction.
Occlusion by Pressure: Blood vessels can be compressed or occluded by external factors such as tumors or hematomas, reducing blood flow and causing infarction.
explain Subclavian steal syndrome (SSS)
Subclavian steal syndrome (SSS) is a vascular condition characterized by the occlusion or significant stenosis of the subclavian artery (SA) or innominate artery (IA). This obstruction hinders normal blood flow through the affected subclavian artery. As a compensatory mechanism, blood flow is “stolen” or diverted from the contralateral vertebral artery (VA) and basilar artery (BA) to supply the affected arm.
Here’s a breakdown of the key components:
Vascular Obstruction:
Subclavian steal syndrome involves an obstruction, such as atherosclerosis or significant stenosis, in the subclavian artery or innominate artery.
Retrograde Flow in the Ipsilateral Vertebral Artery:
Due to the obstruction in the subclavian or innominate artery, blood flow is redirected in a retrograde (backward) fashion through the ipsilateral vertebral artery. This is a compensatory mechanism to ensure sufficient blood supply to the arm.
Collateral Pathway:
The retrograde blood flow in the ipsilateral vertebral artery creates a collateral pathway. This collateral circulation helps provide an alternative route for blood to reach the arm.
Stealing Blood Supply from Contralateral Vertebral Artery and Basilar Artery:
The term “steal” in subclavian steal syndrome refers to the diversion of blood from the contralateral (opposite side) vertebral artery and the basilar artery to supply the arm on the affected side.
Subclavian steal syndrome can lead to symptoms such as arm pain, weakness, or dizziness, especially during activities that increase demand for blood flow to the affected arm. Diagnosis often involves imaging studies to assess blood flow patterns and the degree of arterial obstruction.
explain the important factors that influence the consequences of ischemia and infarction
Speed of Onset:
As mentioned earlier, a sudden onset of ischemia provides less time for collateral circulation to develop and compensate for reduced blood flow. Collateral circulation is a natural adaptive response that involves the development of alternative blood vessels to maintain perfusion to the affected area. The speed at which ischemia occurs influences the effectiveness of this compensatory mechanism.
Extent of Obstruction (Complete vs. Partial Occlusion):
The extent of vascular obstruction is a critical factor in determining the severity of ischemia. Complete occlusion, where the blood vessel is entirely blocked, can lead to more rapid and severe consequences compared to partial occlusion, where some blood flow may still be present.
Anatomy and Dual Blood Supply:
The anatomy of the vascular network, including the presence of dual blood supply or watershed areas, can influence the impact of ischemia. Tissues with dual blood supply or located in watershed areas may be more vulnerable to ischemia because they receive blood from multiple sources, making them sensitive to changes in perfusion.
Vulnerability to Hypoxia:
Different cell types have varying sensitivities to hypoxia (oxygen deprivation). Neurons are highly vulnerable and can sustain irreversible damage within 2-3 minutes of oxygen deprivation. Myocardial cells can tolerate a shorter duration of hypoxia compared to fibroblasts, which are more resilient and can survive for a few hours under hypoxic conditions.
Oxygenation Before Event:
The oxygenation status of tissues before the onset of an ischemic event is crucial. Well-oxygenated tissues are better equipped to endure temporary reductions in blood flow, while tissues already experiencing compromised oxygenation may be more susceptible to damage.
Duration:
The duration of ischemia significantly influences the extent of tissue damage. Prolonged ischemia can lead to irreversible cell injury and infarction. Quick restoration of blood flow is essential for minimizing tissue damage and preventing long-term consequences.
