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Patho. Ch. 1
Cell Injury
| Question | Answer |
|---|---|
| The result of cell injury | Signs and symptoms of a disorder. |
| Causes of cell injury (3). | Deficiencies, toxins, trauma. |
| Types of deficiencies (4). | Oxygen deficiency, nutrient deficiency, genetic defects causing deficiencies in metabolic intermediates, and deficiencies caused by infection. |
| Example of cell injury due to oxygen delivery deficiency. | Myocardial infarction is injury or death of cardiac cells due to the blockage of coronary arteries, resulting in decrease in oxygen delivery, preventing cardiac cells from making the ATP required for many cellular reactions. |
| Explain cell injury and death due to hypoxia as related to aerobic metabolism. | Less oxygen means less ATP produced. The Na+/K+ pump cannot run fast enough and Na+ accumulates in the cell, causing the cell to swell up with water due to osmosis. |
| What type of metabolism makes the most ATP? | Aerobic (versus anaerobic) metabolism. |
| Explain cell injury and death due to hypoxia as related to anaerobic metabolism. | Less oxygen causes more ATP to be made by anaerobic metabolism which has lactic acid as a byproduct. The acid damages cell membranes, intracellular structures, and DNA. |
| What is a primary nutrient deficiency? Example? | Dietary deficiency. Ex: Beriberi Disorder. Thiamin (Vit. B1) is needed for glucose met. in cells. Neurons use glucose to make ATP, so thiamine deficiency results in neuron injury (causes muscle weakness, poor coordination, and paralysis). |
| What deficiency can alcoholism result in? | Alcoholism can damage GI tract, decreasing absorption of B1, resulting in deficiency. |
| What is a secondary nutrient deficiency? Example? | Inability to absorb adequate amts of a nutrient. Ex:Pernicious anemia. Damaged gastric mucosa cells = inability to produce intrinsic factor needed to absorb B12 from the intestines. B12 needed to produce RBCs or get anemic = less oxygen to cells. |
| How can genetic defects cause deficiencies? | Can interfere with metabolic pathways and production of important cell molecules. |
| Example of deficiency caused by genetic defect. | Alpha 1-antitrypsin deficiency (A1AD or Alpha-1) causes reduced levels of alpha 1-antitrypsin in the blood and lungs. Can cause cellular injury in lungs resulting in emphysema. |
| How can viral infection cause deficiencies? | They reproduce by invading cells and using the cells' genetic machinery to reproduce. This uses metabolites that the cell would normally use, overtime causing cell deficiencies (injury or death). |
| How do toxins cause cell injury (broadly)? | They bind to cell structures and disrupt their function. |
| Two major types of toxins. | Exogenous and endogenous. |
| Example of toxin produced by a living organism. Term? Most commonly produced by what? | Example of biological exogenous toxin (usually bacteria): Cholera toxin (produced by bacteria Vibrio cholerae) binds to cells lining the small intestine, causing them to secrete excess amt of fluid and electrolytes which results in diarrhea. . |
| What is term for a toxin produced inside cell? Common cause? Example? | Endogenous toxin, usually genetic disorder. Ex:Huntington's disease. Gene mutation results in production of abnormal protein (toxin) in certain brain neurons, causing S/S jerky muscle mvmt, decr. coordination, decr. mental abilities + personality change |
| Types of trauma(4). How does trauma cause cell injury? | Extreme temperature, ionizing radiation, mechanical pressure, and the immune system can cause physical injury to cell structures such as plasma membrane. |
| Extreme temperature conditions causing cell injury. | Hypothermia (formation of ice crystals in cytoplasm causes cell damage. Ex:Frostbite). Hyperthermia (proteins denature resulting in decreased or altered function. Ex: burns). |
| What is ionizing radiation and how does it cause cell trauma? | High-energy, associated with x-rays and radioactive materials. High exposure can cause incr. in temp. in tissues (burns). Lower level exposure may form free radicals, damaging cell structures and enzymes. |
| What are free radicals? Characteristics? How removed? | Molecules with an unpaired electron in the outer electron shell. Extremely unstable and reactive, reacting with normal cell components and causing damage. Normally removed from body by antioxidants (ex: Vitamins C, A, and E). |
| Examples of mechanical pressure trauma. | Expanding tumors (affect nearby tissue function). Pressure applied to body surface (injure tissues causing change in cell function or cell death). |
| How can immune system reactions cause cell injury? Example? | Cause damage to cell membrane. Ex: Acute renal disease following streptococcal infection. Antigen-antibody complexes deposited in glomeruli in capillary walls> inflammation >increased pore size > RBCs cross wall and enter urine >hemoturia |
| Blood in urine = | Hemoturia |
| How does decreased oxygen supply alter cell metabolism? | Switch from oxidative phophorylation (aerobic production of ATP) to glycolysis (anaerobic production of ATP), resulting in lactic acid. |
| 3 major ways cells may change in response to cell injury (give scientific terms). | Cell size (atrophy and hypertrophy), cell number (hyperplasia), and cell type (metaplasia). |
| 6 causes of cell atrophy (examples). | Disuse (cast), loss of trophic signals (denervation or decreased hormone secretion)(SC injury, uterus postnatal), malnutrition and decreased blood flow (heart w/anorexia), persistent cell injury(small intestine villi w/celiac disease), and aging (brain). |
| Term for increase in cell size. Common in what cells? | Hypertrophy is due to increased workload, common in cells that don't readily divide (cardiac and skeletal muscle cells). |
| Causes for increase in cell size. Examples. | Physiologic hypertrophy (normal). Ex:athletes' hearts. Pathologic hypertrophy (abnormal). Ex: Hypertension caused cardiac muscle cell size increase (not uniform). Increase in size of 1 kidney after other removed. |
| 3 causes of physiological hyperplasia and examples. | Increased hormone stimulation (uterus and breasts when pregnant), increased functional demand (parathyroid gland in response to low Ca+ w/kidney disease), and compensation following cell loss (fibroblasts and blood vessels during wound healing). |
| 2 causes of pathological hyperplasia and examples. | Excessive hormone stimulation (ex: prostate w/estrogen androgen interaction, endometrium w/estrogen) and growth factors (ex: skin (warts) w/viral growth factors) |
| Term for cell function changing in response to cell function. Cause? Example. Permanent? | Metaplasia is the replacement of one adult cell type by another, caused by chronic inflammation. Ex: Smokers- ciliated, columnar epithelium lining the lungs is replaced w/stratified squamous epithelium. Reversible if irritant is removed. If not, cancer. |
| Term for normal cell being replaced by cells of abnormal size, shape, and appearance. Cause? Example. Permanent? | Dysplasia caused by chronic inflammation or irritation. Ex: Cervical dysplasia due to inflammation caused by HPV. Reversible, but may be precancerous. |
| Relationship of metaplasia and dysplasia. | Can occur together. |
| What 4 things may injured cells fill up with? Give examples. | Lipids (in liver of alcoholics), glycogen (in genetic diseases that affect metabolism), abnormal proteins (Alzheimer's disease), pigments (bilirubin resulting in jaundice, coal dust resulting in black lung). |
| Type of calcification linked to cellular inflammation or injury. Example. | Dystrophic calcification: accumulation of calcium crystals from inflammation or injury. Ex: Atherosclerosis- Injury to endothelium lining blood vessels causes deposition of calcium crystals in endothelial lining. |
| Type of calcification that may cause cell injury. | Metastatic calcification: occurs in normal tissue as a result of high blood calcium levels, often in lung and kidney, and may possibly interfere with function. |
| How may calcification affect the aortic valve? | Dystrophic calcification of aortic valve causes aortic stenosis (a narrowing of the valve opening). |
| 2 types of cell death and characteristics. | 1)Apoptosis: programmed cell death, normal process, controlled, removes old and worn out cells, no inflammation. 2) Necrosis: unregulated, caused by cell injury, cells swell and rupture contents into interstitial space, inflammation. |
| 4 examples of programmed cell death. | Destruction of embryonic tissues, involution (shrinking) of endometrium during menstrual cycle, removal of immune cells after inflammation, mechanism by which T cells kill viruses and bacteria. |
| Just give names of 3 types of necrosis. | Liquefaction, coagulation, and caseous necrosis. |
| An abscess is a result of what? | Liquefaction necrosis: catalytic enzymes released from dead cells into interstitial space liquefy surrounding tissue and a yellow fluid is formed. |
| What causes an infarction? | Coagulation necrosis seen in area of infarction (cell death) when artery supplying tissue is blocked >Hypoxia >lactic acid >denatures cell enzymes and structural proteins>tissue is firm and gray (same as cooked egg). |
| What is associated with lesions of tuberculosis? | Caseous necrosis (type of liquefaction n.). Has a cheese-like center. |
| What is gangrene and what are the three types? | A large area of necrotic tissue. Dry, wet, or gas gangrene. |
| What characterizes gas gangrene? | "Clostridium" infection produces toxins and H2S bubbles. |
| What characterizes dry gangrene (cause, ROS, where, type of necrosis)? | Cause: interference of arterial blood supply to body part (not venous)(= coagulation necrosis), slow spreading, in extremities. Area dries, shrinks, skin wrinkles, color darkens to drk brown or black. Is a line of demarcation. |
| Describe wet gangrene (cause, ROS, where, type of necrosis). | Lack of venous return(fluid accumulation). Area moist, black, under tension. Fast spreading, bacterial infection, can spread to internal organs, no line of demarcation, tissue tends to liquefy (liquefaction necrosis). Eventual death. |
| What cells are most vulnerable to ischemia and why? | CNS neurons most vulnerable to ischemia (decreased blood supply) because they have a high metabolic rate and rely on glucose to make ATP. |
| What cells are vulnerable to toxins? | Liver cells are more susceptible to toxins and they breakdown toxins and are therefore exposed to toxic byproducts. |
| What cells are most affected by ionizing radiation? | Rapidly dividing cells such as epidermis, red bone marrow, and epithelial cells lining the GI tract are most affected because ionization radiation damages DNA. |
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