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A set of vocabulary-style flashcards covering the major terms related to cell injury, death, and adaptations from the lecture notes.
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Etiology
Origin of a disease (causes and modifying factors).
Pathogenesis
How a disease develops: from initial trigger to cellular/molecular changes causing problems.
Homeostasis
Cells adjusting to maintain a stable internal state (e.g., structure, function).
Cell injury
Damage to cells when adaptation fails or stress is too much; basis of disease, can be reversible or irreversible.
Hypoxia
Lack of oxygen (most common cause of cell injury).
Ischemia
Reduced blood flow, cutting off oxygen and nutrients.
Toxins
Substances like pollution, drugs, or chemicals that harm cells.
Infectious agents
Germs (viruses, bacteria, fungi, parasites) that harm cells via toxins or immune reactions.
Immunologic reactions
Immune system attacks (autoimmune/allergic) causing inflammation and damage.
Genetic abnormalities
DNA errors (mutations, birth defects) that injure cells; key in cancer.
Nutritional imbalances
Too much or too little nutrition (e.g., vitamin deficiency, protein-calorie lack) harming cells.
Physical agents
Physical forces (trauma, heat, cold, radiation, shock) that cause cell injury.
Reversible cell injury
Cell damage that can be fixed if the cause is removed; cells often swell (hydropic change).
Hydropic change
Cell swelling from water absorption during reversible injury.
Fatty change (steatosis)
Fat buildup (lipids) inside cells, common in the liver.
Cytoplasmic eosinophilia
Injured cell cytoplasm turns red/pink when stained (due to protein changes).
Mitochondrial changes (reversible injury)
Mitochondria swell, ER expands, ribosomes detach, and chromatin changes during reversible cell injury.
Myelin figures
Phospholipid clumps from damaged cell membranes, seen in injured cells.
Necrosis
Uncontrolled, messy cell death: membranes burst, causing inflammation.
Coagulative necrosis
Tissue death where structure is kept (like a ghost outline), common in heart attacks (infarcts).
Liquefactive necrosis
Tissue turns to liquid (digested by enzymes); common in brain injury or pus-filled abscesses.
Caseous necrosis
Cheesy, lumpy cell death, typical in TB and other granulomas.
Fat necrosis
Fat tissue death, creates chalky white spots (e.g., from trauma or pancreatitis).
Fibrinoid necrosis
Bright pink, shapeless deposits in blood vessel walls, caused by immune system attacks (vasculitis).
Pyknosis
Nucleus shrinks and darkens (chromatin condenses).
Karyorrhexis
Shrunken nucleus breaks into fragments.
Karyolysis
Nucleus fades away as DNA is broken down by DNase.
Apoptosis
Planned, orderly cell suicide, no inflammation; removes unwanted/damaged cells.
Physiologic apoptosis
Normal, helpful apoptosis (e.g., during development, hormone changes, removing bad immune cells).
Pathologic apoptosis
Harmful apoptosis: when cells are too damaged to repair themselves.
Metaplasia
One cell type changes into another better able to handle stress.
Hypertrophy
Cells (and often organs) get bigger, usually from more work or hormones.
Hyperplasia
Increase in the number of cells (via more cell division).
Atrophy
Organ/tissue shrinks (cells get smaller or fewer) due to less use, poor supply, or aging.
Autophagy
Cell 'self-eats' its own parts (organelles) using special sacs (autophagic vacuoles).
Intracellular accumulations
Stuff building up inside cells abnormally (due to removal issues, overproduction, or outside sources).
Lipofuscin
Brown 'aging pigment' (wear-and-tear) seen in old or shrinking cells.
Cholesterol and cholesteryl esters
Fatty substances (lipids) that build up; key in cell membranes and artery hardening (atherosclerosis).
Glycogen
Stored sugar (glucose chains) that can build up, like in diabetes or specific organs (kidneys, heart, pancreas).
Pigments: Carbon
Black 'soot pigment' (anthracosis) from inhaled carbon, building up in lungs/tissues.
Pigments: Melanin
Natural brown/black pigment (from melanocytes) that protects skin from sun (UV).
Pigments: Hemosiderin
Yellow-brown pigment from iron buildup, found in iron-rich organs (e.g., bone marrow, spleen, liver).
Dystrophic calcification
Calcium buildup in damaged tissue, even with normal blood calcium levels.
Metastatic calcification
Calcium buildup in normal tissues due to high blood calcium (e.g., from too much PTH, Vit D issues).
Pus
Thick, yellowish liquid (dead cells, fluid) formed during bacterial infection, often in abscesses (liquefactive necrosis).
Gangrenous necrosis
Limb/tissue death (coagulative necrosis) with secondary infection, often turning mushy (wet gangrene).
Lysosomes
Cell 'recycling centers': sacs with enzymes to break down proteins, fats, sugars, and DNA.