week 1-6 theory Flashcards
Identify the Causes of Disease
Genetic: Diseases that are caused entirely by inherited or prenatally acquired genetic defects.
Multifactorial: Diseases that result from the interaction of both genetic and environmental factors.
Environmental: Diseases caused entirely by environmental factors, such as infections, toxins, and physical injury
Describe the Various Forms of Cellular Injury
- Chemical Injury:
Direct injury: Toxins directly interact with cellular components (e.g., mercuric chloride).
Indirect injury: Chemicals are converted to toxic metabolites that damage the cell (e.g., free radicals causing membrane damage). - Physical Injury:
Kinetic force: Trauma or injury caused by mechanical forces.
Thermal injury: Damage due to extreme heat (burns) or cold (frostbite). - Infective Injury: Caused by microorganisms such as bacteria, viruses, fungi, and parasites
Describe the Physiological and Pathological Role of Apoptosis
Physiological Role: Apoptosis is a form of programmed cell death that helps regulate tissue homeostasis. It eliminates damaged or unwanted cells without triggering an inflammatory response.
Pathological Role: When apoptosis is deregulated, it can contribute to various diseases, including cancer (failure to undergo apoptosis) or neurodegenerative diseases (excessive apoptosis). Apoptosis can be triggered by external factors such as radiation, toxins, and free radicals
Identify and Describe the Types of Necrosis
- Coagulative Necrosis:
Preserves the underlying tissue architecture. Common in hypoxic injuries to solid organs (e.g., heart, kidneys). - Liquefactive Necrosis:
Characterized by enzymatic digestion of dead cells, often seen in bacterial infections or ischemic infarcts in the brain. - Caseous Necrosis:
Creates a “cheesy” appearance and is most characteristic of tuberculosis.
Fat Necrosis:
Seen in acute pancreatitis, where pancreatic lipases digest fat, leading to the release of fatty acids and chalky white areas of fat saponification. - Gangrenous Necrosis:
A form of tissue death due to ischemia, often affecting soft tissues. It can be classified as dry or wet depending on the presence of infection
Define Ischemia and Infarction
Ischemia: A condition where there is impaired vascular perfusion, leading to a lack of oxygen and nutrients in tissues. This can result from conditions like thrombosis, embolism, or atherosclerosis
Infarction: Refers to tissue death (necrosis) caused by ischemia. This results when the blood supply to a part of the body is completely cut off, leading to irreversible cell death
Causes of Ischemia
Thrombosis: The formation of a solid mass of blood constituents in vessels, which can obstruct blood flow.
Embolism: A mass traveling in the bloodstream that can lodge in vessels and block blood flow.
Atheroma: Plaque formation in arteries, commonly due to atherosclerosis.
Vasculitis: Inflammation of blood vessels.
Vascular Spasm: Sudden contraction of blood vessel muscles.
Compression: External pressure on blood vessels (commonly in veins).
Hyperviscosity: Thickened blood impairing its flow, commonly due to blood disorders
Thrombosis occurs when…
Thrombosis occurs when blood clots form abnormally within a blood vessel. It can lead to infarction, embolism, or edema.
what is
Virchow’s Triad
Virchow’s Triad: Three factors that contribute to thrombus formation:
Endothelial injury.
Abnormal blood flow (stasis or turbulence).
Hypercoagulability
Signs of inflammation
Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
Process of Inflammation
Vascular Phase: Increased blood flow and permeability of blood vessels.
Cellular Phase: Movement of immune cells, like neutrophils, from the blood to the tissue(
Vascular Mediators of Inflammation
Vascular mediators: Histamine, prostaglandins, and nitric oxide cause vasodilation and increased vascular permeability.
cellular Mediators of Inflammation
Cellular mediators: Neutrophils, macrophages, and lymphocytes respond to injury by migrating to the site of damage.
chemical Mediators of Inflammation
Chemical mediators: Cytokines, bradykinin, and complement proteins act to stimulate the inflammatory response
Acute inflammation
A short-term, immediate response to injury with the main goal of removing the causative agent and repairing tissue. Characterized by fluid accumulation, immune cell infiltration, and swelling.
Chronic inflammation
Prolonged inflammation resulting from persistent stimuli. It involves ongoing tissue destruction and repair processes, often leading to scarring or fibrosis. Chronic inflammation can be associated with diseases like rheumatoid arthritis or tuberculosis