Pathophysiology Unit 2 | Chapter 3 (Porth 5th Edition) Flashcards
Atrophy
Decrease in cell size due to reduced workload, adverse conditions, or nutrient deprivation. Causes include disuse, denervation, loss of endocrine stimulation, inadequate nutrition, or ischemia. Reversible with stimulus removal.
Hypertrophy
Increase in cell size and functional components (e.g., actin/myosin in muscle) due to increased workload. Examples: physiologic (exercise) or pathologic (left ventricular hypertrophy from hypertension).
Hyperplasia
Increase in cell number in tissues capable of mitosis (e.g., epidermis, liver). Types: hormonal (uterine enlargement during pregnancy) or compensatory (liver regeneration).
Metaplasia
Reversible replacement of one adult cell type with another (e.g., stratified squamous replacing ciliated columnar in smokers’ trachea). Adaptive response to chronic irritation.
Dysplasia
Abnormal cell growth with variation in size, shape, and organization. Often precursor to cancer (e.g., cervical dysplasia detected via Pap smear). Potentially reversible.
Intracellular Accumulations
Buildup of substances (lipids, proteins, pigments) due to metabolic errors, excess production, or exogenous agents. Examples: fatty liver, Tay-Sachs disease, lipofuscin.
Dystrophic Calcification
Calcium deposition in dead/dying tissues (e.g., atherosclerotic plaques, damaged heart valves). Occurs despite normal serum calcium levels.
Metastatic Calcification
Calcium deposition in normal tissues due to hypercalcemia (e.g., renal failure, hyperparathyroidism, vitamin D toxicity). Affects lungs, kidneys, blood vessels.
Free Radical Injury
Cell damage via reactive oxygen species (ROS) with unpaired electrons. Causes lipid peroxidation, enzyme inactivation, DNA damage. Counteracted by antioxidants (vitamins A, C, E).
Hypoxic Cell Injury
ATP depletion from oxygen deficiency, leading to anaerobic metabolism, lactic acidosis, Na+/K+ pump failure, cellular swelling. Irreversible if prolonged (e.g., brain cells after 4-6 minutes).
Impaired Calcium Homeostasis
Excess intracellular Ca²+ activates destructive enzymes (proteases, phospholipases). Linked to ischemia, toxins, and mitochondrial damage.
Reversible Cell Injury
Cellular swelling or fatty change due to ATP depletion. Fatty liver is an example. Reversible if cause is addressed.
Apoptosis
Programmed cell death via caspase activation. Features: cell shrinkage, chromatin condensation, apoptotic bodies. Roles: embryogenesis, immune regulation, tumor suppression.
Necrosis
Unprogrammed cell death with membrane rupture and inflammation. Types: coagulative (ischemic infarcts), liquefactive (abscesses), caseous (tuberculosis).
Gangrene
Necrosis with tissue decay. Dry gangrene (coagulative, arterial obstruction) vs. wet gangrene (liquefactive, bacterial infection) vs. gas gangrene (Clostridium infection).
Ionizing Radiation Injury
Damages DNA via free radicals or direct ionization. Targets rapidly dividing cells (bone marrow, gut). Causes mutations, cancer, tissue fibrosis.
Nonionizing Radiation
UV radiation causes DNA pyrimidine dimers (e.g., xeroderma pigmentosum). Infrared/microwaves induce thermal injury.
Lead Toxicity
Affects nervous system (neurobehavioral deficits), blood (anemia), kidneys. Sources: paint, soil. Chelation therapy for high blood levels (>45 µg/dL).
Oxidative Stress
Imbalance between ROS production and antioxidant defenses. Linked to aging, cancer, cardiovascular diseases, and neurodegenerative disorders.
Telomere Shortening
Progressive loss of chromosome-end DNA with cell division. Limits replicative capacity (Hayflick limit). Telomerase in cancer cells prevents senescence.
Coagulative Necrosis
Tissue death with preserved architecture (e.g., myocardial infarction). Acidosis denatures proteins, maintaining cell outlines.
Liquefactive Necrosis
Tissue liquefaction by enzymatic digestion (e.g., brain infarcts, abscesses).
Caseous Necrosis
Cheesy, granular debris in granulomas (e.g., tuberculosis). Combines coagulation and liquefaction.
Angiogenesis
Formation of new blood vessels stimulated by hypoxia-inducible factors (HIFs). Critical in wound healing and tumor growth.
Metaplasia Example
Squamous metaplasia in smokers’ trachea replaces ciliated epithelium, reducing mucus clearance. Reversible if smoking ceases.
Hyperplasia vs. Hypertrophy
Hyperplasia increases cell number; hypertrophy increases cell size. Both may coexist (e.g., pregnant uterus).
Programmed Cell Death
Includes apoptosis (controlled) and autophagy. Contrasts with necrosis (inflammatory).
Caloric Restriction
Extends lifespan by reducing mitochondrial free radical production. Linked to insulin/IGF-1 signaling pathways.
Xeroderma Pigmentosum
Genetic defect in DNA repair enzymes. Causes UV sensitivity, skin cancer. Demonstrates importance of DNA repair mechanisms.
Endothelial Dysfunction
Caused by oxidative stress, contributing to atherosclerosis. Impaired vasodilation and increased inflammation.
Lipofuscin
Wear-and-tear’ pigment from lysosomal digestion of organelles. Accumulates with age in heart, liver, nerve cells.
Metastatic Calcification Cause
Hypercalcemia from hyperparathyroidism, bone metastases, or vitamin D excess. Deposits in lungs, kidneys, gastric mucosa.
Free Radical Sources
Endogenous (mitochondrial respiration, phagocytosis) or exogenous (radiation, toxins). ROS include superoxide, hydroxyl radical, H₂O₂.
Hypoxia-Inducible Factors (HIFs)
Activate genes for erythropoiesis, glycolysis, angiogenesis. Critical in adapting to low oxygen conditions.
Apoptosis Pathways
Extrinsic (death receptors like Fas) and intrinsic (mitochondrial cytochrome c release). Both activate caspases for cell dismantling.
Necrosis vs. Apoptosis
Necrosis: accidental, inflammatory, cell swelling. Apoptosis: regulated, non-inflammatory, cell shrinkage.
Disuse Atrophy Example
Muscle wasting after cast immobilization. Reversed with resumed activity via IGF-1 and insulin signaling.
Neurohumoral Factors in Hypertrophy
Biomechanical stress (e.g., hypertension) and hormones (e.g., IGF-1) drive cardiac hypertrophy via gene activation.
Chemotherapy Injury
Antineoplastic drugs cause direct cell damage (e.g., liver necrosis from acetaminophen overdose due to glutathione depletion).
Mercury Toxicity
Affects CNS (neurodegeneration) and kidneys. Forms: vapor, inorganic, methyl/ethyl. Sources: fish (methyl), vaccines (thimerosal, rare).
Reperfusion Injury
Oxidative damage after restoring blood flow (e.g., post-heart attack). Free radicals overwhelm antioxidant defenses.
Ubiquitin-Proteasome System
Degrades cytosolic proteins (e.g., in atrophy). Tagged proteins are broken down in proteasomes.
Denervation Atrophy
Muscle wasting from loss of nerve supply (e.g., paralysis). Irreversible if prolonged.
Endometrial Hyperplasia
Excessive estrogen stimulation causes thickened endometrium, increasing cancer risk. Treated with progestins or surgery.
Papanicolaou (Pap) Smear
Detects cervical dysplasia (pre-cancerous changes). Early intervention prevents progression to invasive cancer.
IGF-1 Role
Stimulates muscle growth, inhibits protein degradation. Low levels contribute to atrophy (e.g., aging, malnutrition).
Antioxidant Enzymes
Include catalase, superoxide dismutase, glutathione peroxidase. Neutralize ROS to prevent oxidative damage.
Line of Demarcation
In dry gangrene, separates necrotic tissue from viable tissue. Indicates inflammatory response to dead cells.
Clostridium perfringens
Anaerobic bacterium causing gas gangrene via toxin production. Treatment includes debridement, antibiotics, hyperbaric oxygen.
Senescence
Aging-related cell cycle arrest due to telomere shortening or DNA damage. Evaded in cancer via telomerase activation.
Wet Gangrene Features
Swollen, foul-smelling tissue with bacterial infection. No clear demarcation. Requires urgent intervention to prevent sepsis.
FAS Receptor
Death receptor in apoptosis extrinsic pathway. Binding triggers caspase cascade (e.g., cytotoxic T cell-induced apoptosis).
Hypoxia in ATP Depletion
Loss of oxidative phosphorylation reduces ATP. Anaerobic glycolysis causes lactic acidosis, worsening cell injury.
Rubin’s Pathology Reference
Key textbook cited for mechanisms of cellular adaptation, injury, and death (e.g., metaplasia, necrosis).
