Chapter 2_2 flashcards
(32 cards)
Hypoxia: Detailed Definition & Common Cause [cite: 1, 2]
A deficiency of oxygen at the cellular level[cite: 1]. The most common cause of cellular hypoxia is ischemia (diminished circulation)[cite: 2], often due to obstruction of arterial blood flow.
Vulnerability of Brain Cells to Hypoxia [cite: 2]
Brain cells cannot withstand low oxygen delivery (hypoxia) for more than 6 minutes before irreversible damage or death occurs. [cite: 2]
Ischemia vs. Infarction: Detailed Definitions [cite: 3]
Ischemia: Lack of blood supply (diminished circulation) to tissue, leading to cellular hypoxia[cite: 3].
Infarction (Ischemic Necrosis): Death of tissue as a consequence of prolonged ischemia. [cite: 3]
Example of Infarction: Myocardial Infarction (Heart Attack) [cite: 4]
Death of cardiac muscle tissue due to prolonged ischemia, typically from a blocked coronary artery. [cite: 4] Lysosomal enzymes (CPKmb) and cardiac proteins (troponin) are released from dead cells into bloodstream.
Ischemic-Reperfusion Injury: Mechanism [cite: 5]
Occurs when oxygen/blood flow is restored to ischemic tissues[cite: 5]. New damaging forces (e.g., reactive free radicals from damaged mitochondria, inflammation) are activated during reperfusion, causing further death of cells that might have otherwise recovered. [cite: 5]
Apoptosis: Detailed Process & Characteristics [cite: 6]
Genetically programmed, step-by-step, involutional cell death[cite: 6]. Cell shrinks, DNA undergoes orderly fragmentation, organelles degenerate. Degenerated cells are phagocytosed by WBCs. Does NOT stimulate inflammation. [cite: 6] Can be physiological (e.g., embryonic development, menopause) or pathological (e.g., increased rates in neurodegenerative diseases, decreased rates in some cancers). [cite: 6]
Necrosis: Detailed Process & Characteristics [cite: 7]
Irreversible cell death due to overwhelming injury[cite: 7]. Cell swells, loses membrane integrity, chromatin fragments, lysosomes activate & release enzymes (autolysis). Stimulates an inflammatory reaction. [cite: 7]
Gangrene: Detailed Description & Common Bacterium [cite: 8, 9]
Necrotic tissue becomes a medium for bacterial infection[cite: 8]. Clostridium perfringens (anaerobic) often proliferates, emitting a foul gas/odor[cite: 8, 9]. Often seen in PAD of lower extremities. Requires surgical intervention. [cite: 9]
Hypertrophy: Definition & Cellular Change [cite: 10]
Increase in individual cell size, resulting in enlargement of functioning tissue mass. Increases cell’s functional components (e.g., actin/myosin, enzymes, mitochondria). [cite: 10]
Physiological Hypertrophy vs. Pathological Hypertrophy (Heart Example)
Physiological (e.g., athlete’s heart): Enlarged muscle is adequately perfused due to angiogenesis; proportional increase in cell size and coronary blood supply. Pathological (e.g., hypertensive LVH): Increase in cell size without corresponding increase in blood vessel growth; enlarged muscle outgrows blood supply, susceptible to ischemia.
Hyperplasia: Definition & Cellular Mechanism [cite: 11]
Increase in the number of cells in a tissue or organ, occurring in mitotically capable tissues (e.g., epithelium, glandular). Stimulated by hormonal or compensatory mechanisms. [cite: 11]
Physiological vs. Pathological/Maladaptive Hyperplasia Examples [cite: 11]
Physiological: Hormonal (e.g., breast gland cells in pregnancy, benign prostatic hyperplasia (BPH) in older males due to testosterone). Pathological/Maladaptive: Keloid (excessive accumulation of epithelial cells/connective tissue in wound healing). [cite: 11]
Atrophy: Definition & Causes [cite: 12]
Cellular adaptation where cells revert to a smaller size due to changes in metabolic requirements or environment[cite: 12]. Causes: Disuse, diminished workload, lack of nerve stimulation (paralysis), loss of hormonal stimulation, inadequate nutrition, decreased blood flow (ischemia), aging. [cite: 12]
Metaplasia: Definition, Mechanism & Example [cite: 13]
Replacement of one cell type by another, likely due to genetic reprogramming in response to chronic inflammation or environmental change, enabling tissue survival[cite: 13]. Example: Barrett’s esophagus in GERD (squamous epithelium in lower esophagus changes to columnar stomach-like cells). [cite: 13]
Dysplasia: Definition, Cellular Characteristics & Example [cite: 14]
Deranged cellular growth in a specific tissue, often from chronic inflammation or as a precancerous condition[cite: 14]. Histology: Cells vary in size, shape, and architectural organization. Example: Cervical dysplasia (precursor to cervical cancer). [cite: 14]
Neoplasia: Definition & Classification [cite: 15]
New, disorganized, uncoordinated, uncontrolled proliferative cell growth, usually cancerous[cite: 15]. Classified as benign (well-differentiated, non-metastasizing) or malignant (poorly differentiated, metastasizing) based on cellular differentiation. [cite: 15]
Significance of Poor Cell Differentiation in Cancer [cite: 15]
Poorly differentiated neoplastic cells do not resemble healthy cells of their tissue of origin and are a hallmark of malignant neoplasms, indicating a higher likelihood of aggressive behavior and metastasis. [cite: 15]
Pathologist Evaluation of Cancerous Potential [cite: 16]
Pathologists evaluate cell differentiation (how much cancer cells resemble normal cells) and tumor margins (extent of spread) to determine cancerous potential and guide treatment. [cite: 16]
Free Radical Injury: Mechanism & Counteraction
Free radicals (reactive oxygen species with unpaired electron) cause oxidative degradation of cell membranes, organelles, and DNA. Cells have enzymes (superoxide dismutases) to remove them. Antioxidants (vitamins A, E, C, beta-carotene) can counteract injury.
Pathological Calcification: Conditions & Examples (Box 2-2)
Deposition of calcium and minerals in tissues, often in areas of cell injury/death. Examples: Arteriosclerosis (calcified plaque), Aortic sclerosis (calcified aortic valve), Microcalcifications in breast malignancies.
Intracellular Accumulation: Fatty Liver (Steatosis)
Alcohol abuse -> toxic hepatocyte injury -> accumulation of intracellular fat -> liver enlarges and becomes dysfunctional.
Intracellular Accumulation: Xanthomas/Xanthelasma
Familial hypercholesterolemia -> defective cholesterol metabolism -> excess cholesterol accumulates within epithelial cells -> yellow, raised skin lesions (especially around eyelids for xanthelasma).
Intracellular Accumulation: Anthracosis (Coal Miner’s Lung)
Chronic inhalation of coal dust -> accumulation within respiratory tract epithelial cells -> blackening of lung tissues.
Intracellular Accumulation: Jaundice
Excess RBC breakdown or liver dysfunction -> bilirubin accumulation in bloodstream -> bilirubin (yellow pigment) has high affinity for elastin -> yellow hue in skin and sclera.
