Nurs 5315: Adv Patho Exam 1Questions & Answers

Atrophy - ANSWERSE. Cells decrease in size P. Still functional; imbalance between protein synthesis and degradation. Essentially there is an increase in the catabolism of intracellular organelles, reducing structural components of cell Physiologic: thymus gland in early childhood Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood supply, nutrition, hormonal stimulation, or nervous stimulation) Hyperplasia - ANSWERSE: cells increase in number, mitosis (cell division) must occur, size of cell does not change Phys: increased rate of division, increase in tissue mass after damage or partial resection; may be compensatory, hormonal, or pathologic Patho: abnormal proliferation of normal cells usually caused by increased hormonal stimulation (endometrial). increase of production of local growth factors Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or mammary gland enlargement during pregnancy Dysplasia - ANSWERSE. Not true adaptation; Cells abnormal change in size, shape, organization (classified as mild, moderate, severe) P. caused by cell injury/irritation, characterized by disordered cell growth. aka atypical hyperplasia or pre-cancer, a disorderly proliferation Physiologic: N/A Pathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breast cancer development; pap smears often show dysplastic cells of the cervix that must undergo laser/surgical tx Metaplasia - ANSWERSE: reversible change, one type of cell changes to another type for survival P: reversible; results from exposure of the cells to chronic stressors, injury, or irritation; Cancer can arise from this area, stimulus induces a reprogramming of stem cells under the influence of cytokines and growth factors Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or normal ciliated epithelial cells of the bronchial linings are replaced by stratified squamous epithelial cells.; Phys: Barrett Esophagus- normal squamous cells change to columnar epithelial cells in response to reflux, aka intestinal metaplasia Hypoxia injury - ANSWERSE. inadequate oxygenation of tissues P. decrease in mitochondrial function, decreased production of ATP increases anaerobic metabolism. eventual cell death. C.M. hypoxia, cyanosis, cognitive impairment, lethargy Free radical and ROS - ANSWERSE. normal byproduct of ATP production, will overwhelm the mitochondria- exhaust intracellular antioxidants P. lipid peroxidation, damage proteins, fragment DNA C.M. development in Alzheimer's, heart disease, Parkinson's disease, Amyotrophic Lateral Sclerosis Ethanol - ANSWERSE. mood altering drug, long term effects on liver and nutritional status P. metabolized by liver, generates free radicals C.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4, inflammation and fatty infiltration of liver, hepatomegaly, leads to liver failure irreversible Oncosis - ANSWERSNa and H2O enter cell and cause swelling. Organ increases in weight, becomes distended and pale. Associated with high fever, hypocalcemia, certain infections Fatty Infiltration - ANSWERSintracellular accumulation of lipids in the liver liver fails to metabolize lipids. usually from ETOH or high fat diet. can lead to cirrhosis dystrophic calcification - ANSWERSaccumulation of Ca in dead or dying tissues calcium salt clump and harden- interfere with cellular structure and function r/t pulmonary TB, atherosclerosis, injured heart valves, chronic pancreatitis metastatic calcification - ANSWERSaccumulation of Ca in normal tissue result of hypercalcemia r/t hyperparathyroidism, hyperthyroidism, toxic levels of Vit D. Can also r/t hyperphosphatemia in renal failure urate accumulation - ANSWERSsodium urate crystals are deposited in tissues- group of disorders collectively called gout- acute arthritis, chronic gouty arthritis, tophus, nephritis Coagulative Necrosis - ANSWERSkidneys, heart, adrenals- secondary to hypoxia Liquefactive Necrosis - ANSWERSnerve cells- brain- accumulation of pus Caseous Necrosis - ANSWERSlung disease- usually TB- tissue looks like clumped cheese Fat Necrosis - ANSWERSbreast, pancreas, abdominal structures- creates soaps Gangrenous Necrosis - ANSWERSDry- dark shriveled skin Wet- internal organs- can lead to death Gas- from clostridium- antitoxins and hyperbaric therapy Gout - ANSWERSE. disturbances in serum urate levels. uncommon for < 30 years old. P. uric acid is deposited in the tissues of kidney, heart, earlobes, and joints. C.M. inflammation, painful joints. result of diuretic use or diet high in cream sauces, red wine, or red meat Rhabdomyolysis - ANSWERSE. cell hypoxia caused by severe muscle trauma, hyperthermia, crush injuries, or severe dehydration P. hypoxia to cell causes failure of the Na-K pump, causing accumulation of intracellular sodium, oncosis, and eventual cell death. Cell death releases enzymes such as CK, uric acid, LDH, AST, etc. C.M. Causes: trauma, hyperthermia, crush injuries, severe dehydration; s/s: CK is 5x upper normal limit, muscle pain, weakness, dark, reddish-brown urine, hypercalcemia, renal failure Alpha Fetoprotein Origin - ANSWERSLiver and germ cell tumors Carcinoembryonic Antigen - ANSWERSGI, pancreas, lung, breast tumors Prostate Specific Antigen - ANSWERSprostate tumors Carcino- - ANSWERSfrom epithelial tissue- renal cell carcinoma Sarco- - ANSWERSfrom connective tissue- chondrosarcoma Carcinoma in situ - ANSWERSpreinvasive epithelial malignant tumors of glandular or squamous cells- cervix Lung ca metastasis - ANSWERSMultiple organs including brain Colorectal ca metastasis - ANSWERSLiver, lungs Testicular ca metastasis - ANSWERSLiver, lungs, brain Prostate ca metastasis - ANSWERSBones (especially lumbar spine), liver Head and neck ca metastasis - ANSWERSLiver, bones, lymphatics Ovarian ca metastasis - ANSWERSPeritoneal surfaces, diaphragm, omentum, liver Sarcoma metastasis - ANSWERSLungs Melanoma metastasis - ANSWERSIn transit lymphatics, lung, liver, brain, GI tract Mechanisms of ca metastasis - ANSWERSLocal invasion, followed by invasion of surrounding tissues. Cells then may invade blood and lymphatic vessels. They must survive in circulation, then enter and survive in a new location. Then the cells can multiply and form a new tumor. TNM staging system - ANSWERST= tumor size >/= correlates with metastatic ability N= whether lymph nodes are involved M= extra nodal involvement (liver, lungs) Intravascular fluid compartment - ANSWERSIn venous system- 20% Osmolality - ANSWERSThe measure of solute concentration in a fluid. 280-295 mOsm Interstitial fluid compartment - ANSWERSSurrounds the cells and bathes them in nutrients- 20% Intracellular fluid compartment - ANSWERSWithin the cells- 40% uk Osmosis - ANSWERSPassive- the movement of water from an area of low concentration of solute to one of higher concentration Osmotic pressure - ANSWERSPulling- the amount of pressure or force that is exerted by solute molecules of a given compartment Hydrostatic pressure - ANSWERSBlood pressure- pushes fluid outside of the vessels, the force of fluid against the walls of a compartment- venous obstruction, Na and water retention Oncotic pressure - ANSWERSColloid pressure keeps water inside the compartment, attracts water from interstitial space back into the capillary- losses or diminished albumin Effective arterial blood volume - ANSWERSThe amount of blood within the arterial space- ECF changes will cause changes in the EABV in the same direction Renin Angiotensin Aldosterone System - ANSWERSActivated by low blood volume, triggers release of renin which converts angiotensinogen to angiotensin 1. ACE converts angiotensin 1 to angiotensin which causes arterial vasoconstriction and stimulates release of aldosterone. Aldosterone stimulates renal Na reabsorption and K+ excretion. Water is retained, less urine is produced, blood volume increases. Natriuretic hormones - ANSWERSANP and BNP- released by heart- works opposite RAAS to decrease blood volume, promotes urinary excretion of Na and water Fluid volume deficit - ANSWERSDehydration- intake is not enough for body's needs C.M. Poor skin turgor, dry mucous membranes, sunken eyes, sunken fontanelles, decreased urine output, fatigue Fluid volume excess - ANSWERSFluid intake exceeds body's needs C.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD, restlessness or anxiety Edema - ANSWERSAccumulation of fluid within the interstitial space- venous obstruction, Na and water retention C.M. can be localized or dependent, tightness of skin, facial swelling, rales, decreased wound healing, increased risk of pressure sores, weight gain Euvolemic Hypernatremia - ANSWERStotal body water loss, usually from DI C.M. severe polyuria and mild hypernatremia, weight loss, weak pulses, tachycardia, postural hypotension, fever, restless hypovolemic hypernatremia - ANSWERSfrom GI losses or diuretics C.M. Volume depletion, orthostatic hypotension, tachycardia, lack of organ perfusion hypervolemic hypernatremia - ANSWERSadministration of hypertonic saline C.M. volume overload, edema, chf, htn, pulmonary edema mild hyponatremia - ANSWERSNa 125-135 C.M. anorexia, apathy, restless, nausea, lethargy, muscle cramps moderate hyponatremia - ANSWERSNa 120-125 C.M. agitation, disorientation, headache severe hyponatremia - ANSWERSNa <120 C.M. seizures, coma, areflexia, incontinence, death isotonic hyponatremia - ANSWERSmOsm 280-295- not true hypovolemia- from elevated triglycerides or serum proteins hypertonic hyponatremia - ANSWERSmOsm >295- from solutes other than Na- osmotic pressure leads to fluid shift from intracellular to extracellular hypotonic hyponatremia - ANSWERSmOsm <280 and urine Na >100- fluid excess r/t intake or renal impairment insulin effect on K+ - ANSWERSK+ enters cell with glucose transport. Monitor Type II DM for hypokalemia Adrenergic agents effect on K+ - ANSWERSalbuterol, beta blockers, and alpha adrenergic antagonists cause K+ movement into the cell. Alpha adrenergic receptors shift K+ out of the cell Osmolality effect on K+ - ANSWERShyperosmolality causes water to shift out of cell via osmosis. K+ will also shift out, causing hyperkalemia. Cell lysis effect on K+ - ANSWERSintracellular K+ is released into bloodstream Exercise effect on K+ - ANSWERScellular ATP is diminished, opening K+ channels and allowing K+ to leave cell