45 Medical terminologies you must know if you are medical student studying medical stuff. Study will be easier with this terms.
45 medical terminologies you must know
1. Membrane transport: The movement of substances across cell membranes through various mechanisms like diffusion, facilitated diffusion, active transport, or endocytosis and exocytosis, crucial for nutrient uptake and waste removal.
2. Cell signaling: The complex process where cells communicate and coordinate activities via signaling molecules, such as hormones or neurotransmitters, activating specific receptors and triggering cascades of biochemical reactions.
3. Lysosomal degradation: Intracellular digestion occurring in lysosomes, where enzymes break down proteins, lipids, carbohydrates, and other macromolecules, essential for cellular waste disposal and recycling.
4. Proteasomal degradation: The process by which unwanted or damaged proteins are marked for degradation by ubiquitin, then degraded in the proteasome, crucial for maintaining cellular protein homeostasis and regulating various cellular processes.
5. The cellular response to stress: Diverse physiological and biochemical reactions in cells facing external or internal stressors, enabling adaptation to adverse conditions, maintaining cellular balance, or leading to cell death under severe stress.
6. Causes of cell injury: Various factors, including physical agents, chemical substances, infectious agents, genetic abnormalities, immunological reactions, or nutritional imbalances, resulting in cellular dysfunction, leading to structural or functional damage.
7. Necrosis: A type of cell death characterized by swelling, rupture, and inflammation of the cell, often triggered by severe, acute, or prolonged injuries, disrupting cell membrane integrity and releasing cellular contents into the extracellular space.
8. Apoptosis: Controlled, programmed cell death crucial for normal development and homeostasis, involving cellular fragmentation, chromatin condensation, and membrane blebbing, without eliciting an inflammatory response.
9. Necroptosis: A regulated form of necrosis initiated by specific molecular pathways, sharing some features of apoptosis and necrosis, often triggered in response to pathogens, inflammation, or tissue damage.
10. Pyroptosis: An inflammatory form of programmed cell death activated by inflammasomes, resulting in cell swelling, membrane rupture, and release of pro-inflammatory intracellular contents, linked to the innate immune response against infections.
11. Ferroptosis: A regulated form of cell death characterized by iron-dependent lipid peroxidation, triggered by the accumulation of toxic lipid peroxides, and implicated in various pathological conditions, including neurodegeneration and cancer.
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12. Autophagy: A cellular recycling process where damaged organelles and proteins are sequestered into autophagosomes and delivered to lysosomes for degradation, promoting cellular survival during nutrient deprivation or stress.
13. Mitochondrial damage: Impairment or dysfunction of the mitochondria, resulting in compromised energy production, oxidative stress, and the release of pro-apoptotic factors, contributing to various diseases such as neurodegeneration and metabolic disorders.
14. Membrane damage: Disruption or impairment of cell membrane integrity due to physical, chemical, or biological factors, leading to altered cell permeability, ion imbalance, and the loss of essential cellular functions.
15. Damage to DNA: Alterations, mutations, or breaks in the DNA structure caused by environmental factors, radiation, chemicals, or errors in DNA replication, potentially leading to genomic instability and various diseases, including cancer.
16. Oxidative stress: Imbalance between the production of reactive oxygen species (ROS) and the cell’s ability to detoxify them, leading to cellular damage, impaired signaling, and the progression of various diseases, including neurodegenerative disorders and cardiovascular diseases.
17. Disturbance in calcium homeostasis: Disruption in the balance of intracellular and extracellular calcium levels, affecting various cellular functions, including muscle contraction, neurotransmission, and cell signaling, potentially leading to cellular damage or death.
18. Endoplasmic reticulum stress: Disruption of endoplasmic reticulum function, often caused by protein misfolding, nutrient deprivation, or oxidative stress, triggering the unfolded protein response and leading to cell dysfunction or apoptosis.
19. Mechanisms of ischemic cell injury: Cellular damage resulting from an inadequate blood supply, leading to oxygen and nutrient deprivation, impaired energy production, and the accumulation of toxic metabolites, causing cellular dysfunction and potentially irreversible damage.
20. Mechanisms of hypertrophy: Enlargement of cells or tissues in response to increased workload, hormonal stimulation, or pathological conditions, involving an increase in cell size, protein synthesis, and organelle numbers to accommodate greater functional demand.Certainly, here are concise explanations for each topic:
21. Mechanisms of hyperplasia: Increase in the number of cells in an organ or tissue due to cell division, often stimulated by growth factors or hormonal signals, crucial for tissue repair, regeneration, and compensatory responses to physiological demands.
22. Mechanisms of atrophy: Decrease in cell size or number due to reduced workload, hormonal changes, or nutrient deprivation, leading to a decrease in organ or tissue size and function, often seen in disuse, denervation, or aging.
23. Mechanisms of metaplasia: Reversible transformation of one mature cell type to another in response to chronic irritation or inflammation, enabling adaptation to environmental changes but increasing the risk of subsequent malignant transformation.
24. Vasodilation: Widening of blood vessels due to relaxation of smooth muscle cells, leading to increased blood flow, reduced blood pressure, and enhanced delivery of oxygen and nutrients to tissues, often triggered by various mediators, including nitric oxide and prostaglandins.
25. Stasis: Slowing or cessation of normal flow of bodily fluids, such as blood or lymph, through the vessels or channels, often leading to the accumulation of fluid, cells, or other components, contributing to thrombosis, edema, or impaired tissue perfusion.
These 45 Medical terminologies you should must know.
26. Leukocyte activation: Stimulation of white blood cells (leukocytes) by various inflammatory mediators, leading to their mobilization, adhesion to endothelium, and recruitment to sites of infection or tissue injury, crucial for the initiation of immune responses and inflammatory processes.
27. Phagocytosis: Process by which cells engulf and digest foreign particles, cellular debris, or pathogens, carried out primarily by specialized immune cells such as macrophages and neutrophils, essential for the clearance of pathogens and the resolution of inflammation.
28. Arachidonic acid metabolites: Bioactive compounds derived from the metabolism of arachidonic acid, such as prostaglandins, thromboxanes, and leukotrienes, playing critical roles in various physiological processes, including inflammation, immune responses, and vascular homeostasis.
29. Tumor necrosis factor and interleukin-1: Proinflammatory cytokines produced by immune cells in response to infection or tissue injury, regulating immune responses, inflammation, and apoptosis, implicated in the pathogenesis of various inflammatory and autoimmune diseases.
30. Complement system: A part of the immune system comprising a group of proteins that enhance the ability of antibodies and phagocytic cells to clear pathogens, crucial for immune surveillance, inflammation, and the removal of immune complexes and cellular debris.
31. Pathways of macrophage activation: Differentiation and activation of macrophages into distinct phenotypes, such as pro-inflammatory M1 or anti-inflammatory M2 macrophages, determined by specific cytokine signals, playing crucial roles in immune responses, tissue repair, and resolution of inflammation.
32. Repair of damaged tissues processes: Complex physiological processes involving inflammation, proliferation, and remodeling, enabling the restoration of tissue integrity after injury or damage, crucial for wound healing, regeneration, and maintaining tissue function and homeostasis.
33. Angiogenesis: Formation of new blood vessels from pre-existing vessels, often occurring in response to tissue damage, hypoxia, or during development, essential for wound healing, organ growth, and the progression of various pathological conditions, including cancer and ischemic diseases.
34. Mechanisms of systemic edema: Accumulation of fluid in the interstitial spaces or body cavities due to increased capillary permeability, impaired lymphatic drainage, or increased venous pressure, leading to tissue swelling, impaired organ function, and potential cardiovascular compromise.
35. Hyperemia: Increased blood flow to an organ or tissue, leading to localized redness, heat, and increased oxygen and nutrient delivery, often resulting from vasodilation in response to increased metabolic demands or tissue injury.
36. Hemostasis: The physiological process that stops bleeding, involving vasoconstriction, platelet adhesion, aggregation, and the coagulation cascade, crucial for maintaining vascular integrity and preventing excessive blood loss after injury.
37. Platelet adhesion and aggregation: Platelets adhering to exposed collagen at the site of vascular injury, leading to their activation, aggregation, and the formation of a platelet plug to prevent further bleeding, essential for primary hemostasis and wound healing.
38. The coagulation cascade: Complex sequential activation of clotting factors leading to the formation of a stable fibrin clot, crucial for secondary hemostasis, maintaining vascular integrity, and preventing excessive bleeding.
39. Thrombosis: Formation of a blood clot within a blood vessel, obstructing blood flow and potentially leading to tissue ischemia, infarction, or embolism, associated with various risk factors such as immobility, endothelial injury, or alterations in blood composition.
40. Endothelial injury: Damage to the endothelial cells lining blood vessels due to mechanical or chemical insults, inflammation, or oxidative stress, leading to alterations in vascular tone, platelet activation, and the initiation of thrombotic and inflammatory processes.
41. Heparin-induced thrombocytopenia syndrome: A potentially life-threatening immune reaction to heparin, characterized by a decrease in platelet count and an increased risk of thrombosis, mediated by antibodies against heparin-platelet factor 4 complexes, requiring immediate cessation of heparin therapy and alternative anticoagulation.
42. Antiphospholipid antibody syndrome: An autoimmune disorder characterized by the presence of antiphospholipid antibodies, leading to an increased risk of blood clots, pregnancy complications, and vascular pathologies, requiring long-term anticoagulation therapy and close monitoring.
43. Embolism: The obstruction of a blood vessel by an embolus, a detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its origin, potentially causing tissue ischemia, infarction, or organ dysfunction.
44. Shock: A life-threatening medical condition characterized by an inadequate supply of blood and oxygen to the body’s tissues and organs, leading to cellular and organ dysfunction, often caused by severe infections, trauma, or cardiovascular collapse, requiring prompt identification and aggressive management.
45. Pathogenesis of septic shock: A severe condition resulting from an overwhelming immune response to infection, leading to widespread inflammation, tissue damage, and multiple organ failure, involving complex interactions between pathogens, immune cells, and inflammatory mediators, requiring urgent antimicrobial therapy and hemodynamic support.
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