Nurs 5315: Advanced Pathophysiology Exam 1 Study Guide with Verified Answers, Exams of Nursing

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Nurs 5315: Adv Patho Exam 1 with verified

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Atrophy - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ E: 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 - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ E: 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 - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ Na and H2O enter cell and cause swelling. Organ increases in weight, becomes distended and pale. Associated with high fever, hypocalcemia, certain infections Fatty Infiltration - ** VERIFIED ANSWERS ** ✔✔ intracellular accumulation of lipids in the liver liver fails to metabolize lipids. usually from ETOH or high fat diet. can lead to cirrhosis

dystrophic calcification - ** VERIFIED ANSWERS ** ✔✔ accumulation 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 - ** VERIFIED ANSWERS ** ✔✔ accumulation 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 - ** VERIFIED ANSWERS ** ✔✔ sodium urate crystals are deposited in tissues- group of disorders collectively called gout- acute arthritis, chronic gouty arthritis, tophus, nephritis Coagulative Necrosis - ** VERIFIED ANSWERS ** ✔✔ kidneys, heart, adrenals- secondary to hypoxia Liquefactive Necrosis - ** VERIFIED ANSWERS ** ✔✔ nerve cells- brain- accumulation of pus Caseous Necrosis - ** VERIFIED ANSWERS ** ✔✔ lung disease- usually TB- tissue looks like clumped cheese Fat Necrosis - ** VERIFIED ANSWERS ** ✔✔ breast, pancreas, abdominal structures- creates soaps Gangrenous Necrosis - ** VERIFIED ANSWERS ** ✔✔ Dry- dark shriveled skin Wet- internal organs- can lead to death Gas- from clostridium- antitoxins and hyperbaric therapy Gout - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ E. 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 - ** VERIFIED ANSWERS ** ✔✔ Liver and germ cell tumors Carcinoembryonic Antigen - ** VERIFIED ANSWERS ** ✔✔ GI, pancreas, lung, breast tumors Prostate Specific Antigen - ** VERIFIED ANSWERS ** ✔✔ prostate tumors Carcino- - ** VERIFIED ANSWERS ** ✔✔ from epithelial tissue- renal cell carcinoma Sarco- - ** VERIFIED ANSWERS ** ✔✔ from connective tissue- chondrosarcoma Carcinoma in situ - ** VERIFIED ANSWERS ** ✔✔ preinvasive epithelial malignant tumors of glandular or squamous cells- cervix Lung ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Multiple organs including brain Colorectal ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Liver, lungs

Testicular ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Liver, lungs, brain Prostate ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Bones (especially lumbar spine), liver Head and neck ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Liver, bones, lymphatics Ovarian ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Peritoneal surfaces, diaphragm, omentum, liver Sarcoma metastasis - ** VERIFIED ANSWERS ** ✔✔ Lungs Melanoma metastasis - ** VERIFIED ANSWERS ** ✔✔ In transit lymphatics, lung, liver, brain, GI tract Mechanisms of ca metastasis - ** VERIFIED ANSWERS ** ✔✔ Local 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 - ** VERIFIED ANSWERS ** ✔✔ T= tumor size >/= correlates with metastatic ability N= whether lymph nodes are involved M= extra nodal involvement (liver, lungs) Intravascular fluid compartment - ** VERIFIED ANSWERS ** ✔✔ In venous system- 20% Osmolality - ** VERIFIED ANSWERS ** ✔✔ The measure of solute concentration in a fluid. 280-295 mOsm

Interstitial fluid compartment - ** VERIFIED ANSWERS ** ✔✔ Surrounds the cells and bathes them in nutrients- 20% Intracellular fluid compartment - ** VERIFIED ANSWERS ** ✔✔ Within the cells- 40% uk Osmosis - ** VERIFIED ANSWERS ** ✔✔ Passive- the movement of water from an area of low concentration of solute to one of higher concentration Osmotic pressure - ** VERIFIED ANSWERS ** ✔✔ Pulling- the amount of pressure or force that is exerted by solute molecules of a given compartment Hydrostatic pressure - ** VERIFIED ANSWERS ** ✔✔ Blood 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 - ** VERIFIED ANSWERS ** ✔✔ Colloid pressure keeps water inside the compartment, attracts water from interstitial space back into the capillary- losses or diminished albumin Effective arterial blood volume - ** VERIFIED ANSWERS ** ✔✔ The amount of blood within the arterial space- ECF changes will cause changes in the EABV in the same direction Renin Angiotensin Aldosterone System - ** VERIFIED ANSWERS ** ✔✔ Activated 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 - ** VERIFIED ANSWERS ** ✔✔ ANP and BNP- released by heart- works opposite RAAS to decrease blood volume, promotes urinary excretion of Na and water

Fluid volume deficit - ** VERIFIED ANSWERS ** ✔✔ Dehydration- 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 - ** VERIFIED ANSWERS ** ✔✔ Fluid intake exceeds body's needs C.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD, restlessness or anxiety Edema - ** VERIFIED ANSWERS ** ✔✔ Accumulation 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 - ** VERIFIED ANSWERS ** ✔✔ total body water loss, usually from DI C.M. severe polyuria and mild hypernatremia, weight loss, weak pulses, tachycardia, postural hypotension, fever, restless hypovolemic hypernatremia - ** VERIFIED ANSWERS ** ✔✔ from GI losses or diuretics C.M. Volume depletion, orthostatic hypotension, tachycardia, lack of organ perfusion hypervolemic hypernatremia - ** VERIFIED ANSWERS ** ✔✔ administration of hypertonic saline C.M. volume overload, edema, chf, htn, pulmonary edema mild hyponatremia - ** VERIFIED ANSWERS ** ✔✔ Na 125- C.M. anorexia, apathy, restless, nausea, lethargy, muscle cramps

moderate hyponatremia - ** VERIFIED ANSWERS ** ✔✔ Na 120- C.M. agitation, disorientation, headache severe hyponatremia - ** VERIFIED ANSWERS ** ✔✔ Na < C.M. seizures, coma, areflexia, incontinence, death isotonic hyponatremia - ** VERIFIED ANSWERS ** ✔✔ mOsm 280-295- not true hypovolemia- from elevated triglycerides or serum proteins hypertonic hyponatremia - ** VERIFIED ANSWERS ** ✔✔ mOsm >295- from solutes other than Na- osmotic pressure leads to fluid shift from intracellular to extracellular hypotonic hyponatremia - ** VERIFIED ANSWERS ** ✔✔ mOsm <280 and urine Na

100- fluid excess r/t intake or renal impairment insulin effect on K+ - ** VERIFIED ANSWERS ** ✔✔ K+ enters cell with glucose transport. Monitor Type II DM for hypokalemia Adrenergic agents effect on K+ - ** VERIFIED ANSWERS ** ✔✔ albuterol, 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+ - ** VERIFIED ANSWERS ** ✔✔ hyperosmolality causes water to shift out of cell via osmosis. K+ will also shift out, causing hyperkalemia. Cell lysis effect on K+ - ** VERIFIED ANSWERS ** ✔✔ intracellular K+ is released

into bloodstream Exercise effect on K+ - ** VERIFIED ANSWERS ** ✔✔ cellular ATP is diminished, opening K+ channels and allowing K+ to leave cell

Kidneys effect on K+ - ** VERIFIED ANSWERS ** ✔✔ excretion and absorption of K+ is regulated by tubule system magnesium and potassium - ** VERIFIED ANSWERS ** ✔✔ mag inhibits the potassium channels, keeping balance. when mag is low, more K+ exits the call, and is excreted via the kidneys. metabolic acidosis - ** VERIFIED ANSWERS ** ✔✔ E. increased acid production, loss of bicarb, diminished renal excretion of hydrogen C.M hyperventilation (compensatory), h/a, n/v/d, dehydration, hypotension pH <7.4 HCO3 < metabolic alkalosis - ** VERIFIED ANSWERS ** ✔✔ E. GI loss, diuretic use C.M. slow, shallow respirations, irritability, twitching, s/s of hypokalemia pH >7.4 HCO3 > respiratory acidosis - ** VERIFIED ANSWERS ** ✔✔ E. cns depression, airway abnormalities C.M. restless, confused, seizures, tachycardia pH <7.4 PaCO2 > respiratory alkalosis - ** VERIFIED ANSWERS ** ✔✔ E. usually anxiety, PE, chf, salicylate OD, illegal drugs C.M. light-headed, confused, tetany pH >7.4 PaCO2 < Allele - ** VERIFIED ANSWERS ** ✔✔ Paired genes on autosomal chromosomes Locus - ** VERIFIED ANSWERS ** ✔✔ Position in which a gene occupies on a chromosome

Phenotype - ** VERIFIED ANSWERS ** ✔✔ Outward appearance of an individual Genotype - ** VERIFIED ANSWERS ** ✔✔ A map of ones specific genes Polymorphic - ** VERIFIED ANSWERS ** ✔✔ Two or more alleles which occur with an appreciable frequency in a population Homozygous - ** VERIFIED ANSWERS ** ✔✔ Two dominant or recessive alleles Heterozygous - ** VERIFIED ANSWERS ** ✔✔ When both a dominant and a recessive allele are present Dominant - ** VERIFIED ANSWERS ** ✔✔ Trait seen in phenotype Recessive - ** VERIFIED ANSWERS ** ✔✔ Trait not seen in phenotype Codominance - ** VERIFIED ANSWERS ** ✔✔ Both alleles exhibit (blood type AB) Carrier - ** VERIFIED ANSWERS ** ✔✔ Person who has a diseased gene but is phenotypically normal Autosomal chromosomes - ** VERIFIED ANSWERS ** ✔✔ first 22 of 23 chromosomes sex-linked chromosomes - ** VERIFIED ANSWERS ** ✔✔ 23rd pair of chromosomes Hypertrophy - ** VERIFIED ANSWERS ** ✔✔ E. Increase in cell size P. Caused by hormonal stimulation or increased functional demand, which increased the cellular protein in the plasma membrane, endoplasmic reticulum, myofilaments, and mitochondria (not cellular fluid)

Physiologic: skeletal muscle hypertrophy for persons doing heavy work/weight lifting. one kidney removed, the other kidney increases in size to accommodate for workload Pathologic: cardiomegaly from HTN/L ventricular hypertrophy Hypoxic Injury Clinical Manifestations - ** VERIFIED ANSWERS ** ✔✔ ischemia which progresses to hypoxia. Intracellular enzymes such as CK, LDH, AST, ALT, troponin Hypoxic Injury - ** VERIFIED ANSWERS ** ✔✔ decreased O2, loss of H/H, decreased RBC production, disease of heart/lungs, ischemia CK enzymes - ** VERIFIED ANSWERS ** ✔✔ -most muscle cells, including heart excrete what enzyme LDH - ** VERIFIED ANSWERS ** ✔✔ - muscle cells, liver cells, heart cells, RBCs, brain secrete what enzyme AST enzymes are found where? - ** VERIFIED ANSWERS ** ✔✔ - liver cells (s) ALT enzymes are found where? - ** VERIFIED ANSWERS ** ✔✔ - liver cells (L enzyme) Troponin enzymes are found where? - ** VERIFIED ANSWERS ** ✔✔ - cardiac cells Hypoxic Injury Pathophysiology - ** VERIFIED ANSWERS ** ✔✔ lack of O2 causes decrease in mitochondrial function, causing decrease ATP production and increases anaerobic metabolism (generating ATP from glycogen), eventually anaerobic metabolism will stop and the cell will die. Reduction of ATP impairs Na/K pump, leads to increased Na/Ca in cell, K is diffused out of cell, water diffuses into cell causing swelling, ribosomal dilation and malfunction occur. Ribosomes produces protein and when it malfunctions causes decrease in protein synthesis. Death will occur if injury is not stopped.

Free Radical Etiology - ** VERIFIED ANSWERS ** ✔✔ have unpaired electron in its outer shell, making molecule unstable and highly reactive. aka being oxidized Reactive Oxygen Species ROS Etiology - ** VERIFIED ANSWERS ** ✔✔ byproduct of ATP production in the mitochondria Free Radical and Clinical Manafestations - ** VERIFIED ANSWERS ** ✔✔ to stabilize self, it will steal an electron from another molecule or give up and electron. The free radical will often steal an electron from another molecule, making that molecule a free radical Reactive Oxygen Species (ROS) Clinical Manafestations - ** VERIFIED ANSWERS ** ✔✔ can overwhelm mitochondria and exhaust intracellular antioxidants, causing cell injury/disease Free Radical and Pathophysiology - ** VERIFIED ANSWERS ** ✔✔ may by initated with in cells by (1) absorption of extreme energy sources such as radiation or UV light; (2) the occurrence of endogenous reactions, such as redox reactions in which oxygen is reduced to water have role in development of Alzheimer's, Parkinson's, Amyotrophic Lateral Sclerosis. Antioxidants are our bodies' defense, reducing agents that provide missing electron that can stabilize the ________ Reactive Oxygen Species (ROS) Pathophysiology - ** VERIFIED ANSWERS ** ✔✔ cause lipid peroxidation, damage proteins which maintain ion pumps and cellular transport, fragment DNA and causes less protein synthesis, cause chromatin destruction, and damage mitochondria. Ethanol Etiology - ** VERIFIED ANSWERS ** ✔✔ ETOH is metabolized to acetaldehyde in the cytoplasm of the cell, enzyme alcohol dehydrogenase (ADH) helps with conversion Ethanol Clinical Manafestations - ** VERIFIED ANSWERS ** ✔✔ adverse effects on liver and causes nutritional disorders. acute effects in the liver include inflammation, fatty infiltration, hepatomegaly, acute liver necrosis and suppressed fatty acid oxidation. liver failure is irreversible effect of chronic abuse

Ethanol Pathophysiolody - ** VERIFIED ANSWERS ** ✔✔ Conversion oxidized niacin (NAD+) is reduced to NADH. In the mitochondrial acetaldehyde is further converted by ADH to acetate and further oxidized niacin (NAD+) is reduced to NADH. the increased NADH/NAD+ ratio in the liver causes the following 1.Pyruvate change to lactic acid causing lactic acidosis

2. Oxaloacetate converted to malate, preventing gluconeogenesis leading to fasting hypoglycemia
3. Glyceraldehyde to glycerol which combines with fatty acids and forms triglycerides, leads to triglycerides in the liver, aka hepatosteatosis
4. decreases citric acid cycle production of NADH which leads to utilization of Acetyl-CoA for ketogenesis (causing ketoacidosis) and lipogenesis (causing hepatosteatosis) Oncosis Effects and Clinical Implications - ** VERIFIED ANSWERS ** ✔✔ cellular swelling, cellular injury because with most injuries there is some amount of O deprivation causing hypoxic injury Fatty infiltration Effects and Clinical Implications - ** VERIFIED ANSWERS ** ✔✔ E- intracellular accumulation of lipids CI- most common site is liver, but can occur in heart and kidneys. Caused by ethanol abuse or high fat diet, fatty infiltration of liver d/t fail to metabolize lipids Dystrophic Calcification Effects and Clinical Implications - ** VERIFIED ANSWERS ** ✔✔ E- accumulation of calcium that occurs in dying and dead tissues CI- pulmonary TB, atherosclerosis and heart valve injury Metastatic Calcification Effects and Clinical Implications - ** VERIFIED ANSWERS ** ✔✔ E-deposition of calcium in undamaged, normal tissues CI- Result of hypercalcemia secondary to hyperparathyroidism, hyperthyroidism, or toxic levels of vitamin D Urate accumulation Effects and Clinical Implications - ** VERIFIED ANSWERS ** ✔✔ E-byproduct of purine degradation

CI-accumulation gets deposited into the tissues of the kidney, heart, earlobes, joints -liver can produce more uric acid than can be eliminated -diuretics can trigger kidneys to increase absorption of uric acid -over accumulation or under secretion of uric acid can result in gout Necrosis - ** VERIFIED ANSWERS ** ✔✔ spectrum of cell changes after the cell dies Infarct - ** VERIFIED ANSWERS ** ✔✔ necrosis which results from sudden insufficiency of arterial blood flow 5 Types of Necrosis - ** VERIFIED ANSWERS ** ✔✔ coagulative, liquefactive, caseous, fat, gangrenous Coagulative - ** VERIFIED ANSWERS ** ✔✔ occurs in the kidneys, heart, and adrenal glands most commonly secondary to hypoxia (caused by protein denaturation, tissue firm and slightly swollen) Liquefactive - ** VERIFIED ANSWERS ** ✔✔ nerve cell necrosis Caseous - ** VERIFIED ANSWERS ** ✔✔ necrosis specific to lung tissue and occurs in TB. Dead cells disintegrate, but the debris is not digested completely by hydrolyses, appearance resembles clumped cheese Fat - ** VERIFIED ANSWERS ** ✔✔ necrosis breast, pancreas and other abdominal structures wet gangrene - ** VERIFIED ANSWERS ** ✔✔ develops when neutrophils invade the site, causing liquefactive necrosis Gangrenous - ** VERIFIED ANSWERS ** ✔✔ tissue death resulting from severe tissue hypoxia

dry gangrene - ** VERIFIED ANSWERS ** ✔✔ result of coagulative necrosis Role of the hepatocytes - ** VERIFIED ANSWERS ** ✔✔ liver cell, ketogenesis occurs in the mitochondria of the hepatocyte result of unavailability of glucose Role of the mitochondria - ** VERIFIED ANSWERS ** ✔✔ Ketogenesis is the formation of ketone bodies and occurs mostly in the mitochondria of the hepatocytes (liver cells) Triggers for ketogenesis - ** VERIFIED ANSWERS ** ✔✔ lack of glucose -occur from the depletion of carbohydrate stores or may occur bc the cell is not able to use glucose but the individual is hyperglycemic (type 2 DM) Role of Acetyl-CoA - ** VERIFIED ANSWERS ** ✔✔ processed by hepatocytes and undergoes transformation to 3 ketone bodies: Acetoacetate, Acetone and B- hydroxybutyrate (basis of ketoacidosis) -States of starvation or uncontrolled DM, cells do not receive enough glucose to produce energy, resulting in acceleration of the B-oxidation cycle and increasing oxidation of fatty acids or energy. B-oxidation cycle results in formation of acetyl- CoA Effect on oxaloacetate - ** VERIFIED ANSWERS ** ✔✔ Oxaloacetate is also used in gluconeogenesis, during starvation & uncontrolled DM oxaloacetate levels are insufficient due to gluconeogenesis... this depletion furthers the amount of acetyl- CoA Gout Etiology - ** VERIFIED ANSWERS ** ✔✔ over accumulation or under secretion of uric acid Gout Clinical Manifestations - ** VERIFIED ANSWERS ** ✔✔ Use of diuretics bc they trigger kidneys to increase the absorption of uric acid. The liver may produce more huric acid if a diet high in red meat, cream sauces, or red wines bc they are high in purines.

Gout Pathophysiology - ** VERIFIED ANSWERS ** ✔✔ Increase in purine degradation which leads to increased amounts of uric acid. Uric acid is a byproduct of purine degradation, accumulation of uric not excreted by the kidneys lead to increased UA in the kidney, heart, earlobes and joints. Inflammation process is triggered and the right great toe is most commonly affected, but it can affect any joint. Rhabdomyolysis Pathophysiology - ** VERIFIED ANSWERS ** ✔✔ 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. Alpha Fetoprotein (AFP) - ** VERIFIED ANSWERS ** ✔✔ Liver and germ cell tumors Carcinoembryonic Antigen CEA - ** VERIFIED ANSWERS ** ✔✔ GI, pancreas, lung, breast, ect tumors Beta Human Chorionic gonadotropin B-hCG origin - ** VERIFIED ANSWERS ** ✔✔ Germ cell tumors Prostate Specific Antigen PSA - ** VERIFIED ANSWERS ** ✔✔ Prostate tumors Carcino- (prefix) - ** VERIFIED ANSWERS ** ✔✔ arise from epithelial tissue Sarco- (prefix) - ** VERIFIED ANSWERS ** ✔✔ connective tissue (muscle and bone tissue) malignant cancers of the skeletal muscle are known as rhabdomyosarcomas gilomas - ** VERIFIED ANSWERS ** ✔✔ tissue of the brain and spinal cord adeno (prefix) - ** VERIFIED ANSWERS ** ✔✔ arise from ductal or glandular structures

Carcinoma in Situ - ** VERIFIED ANSWERS ** ✔✔ -preinvasive epithelial malignant tumors of glandular or squamous cell origin -# of sites including cervix, skin, oral cavity, esophagus and bronchus in breast, ductal carcinoma in situ (DCIS) fills the mammary ducts but has not progressed to local tissue invasion anaplasia - ** VERIFIED ANSWERS ** ✔✔ absence of differentiation -blastoma (suffix) - ** VERIFIED ANSWERS ** ✔✔ originates from precursor cells or blasts (immature or embryonic tissue). Ex: children, neuroblastoma, retinoblastoma Lung Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ multiple organs, including brain Colorectal Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ liver, lungs Testicular Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ lungs, liver, brain Prostate Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ bones (especially lumbar spine), liver Head and Neck Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ lymphatics, liver, bones Ovarian Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ peritoneal surfaces, diaphragm, omentum, liver Sarcoma Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ lungs

Melanoma Sites of Metastasis - ** VERIFIED ANSWERS ** ✔✔ in transit lymphatics, lung, liver, brain, GI tract Local invasion: - ** VERIFIED ANSWERS ** ✔✔ Cancer cells invade nearby normal tissue. Intravasation: - ** VERIFIED ANSWERS ** ✔✔ Cancer cells invade and move through the walls of nearby lymph vessels or blood vessels. Circulation: - ** VERIFIED ANSWERS ** ✔✔ Cancer cells move through the lymphatic system and the bloodstream to other parts of the body. Arrest and extravasation: - ** VERIFIED ANSWERS ** ✔✔ Cancer cells stop moving, in small blood vessels called capillaries at a distant location. They then invade the walls of the capillaries and migrate into the surrounding tissue Proliferation: - ** VERIFIED ANSWERS ** ✔✔ Cancer cells multiply at the distant location to form small tumors known as micrometastases. Angiogenesis: - ** VERIFIED ANSWERS ** ✔✔ Micrometastases stimulate the growth of new blood vessels to obtain a blood supply. A blood supply is needed to obtain the oxygen and nutrients necessary for continued tumor growth. T: - ** VERIFIED ANSWERS ** ✔✔ size or direct extent of the primary tumor Tx: - ** VERIFIED ANSWERS ** ✔✔ tumor cannot be evaluated Tis: - ** VERIFIED ANSWERS ** ✔✔ carcinoma in situ T0: - ** VERIFIED ANSWERS ** ✔✔ no signs of tumor

T1, T2, T3, T4: - ** VERIFIED ANSWERS ** ✔✔ size and/or extension of the primary tumor N: - ** VERIFIED ANSWERS ** ✔✔ degree of spread to regional lymph nodes Nx: - ** VERIFIED ANSWERS ** ✔✔ lymph nodes cannot be evaluated N0: - ** VERIFIED ANSWERS ** ✔✔ tumor cells absent from regional lymph nodes N1: - ** VERIFIED ANSWERS ** ✔✔ regional lymph node metastasis present; (at some sites: tumor spread to closest or small number of regional lymph nodes) N2: - ** VERIFIED ANSWERS ** ✔✔ tumor spread to an extent between N1 and N (N2 is not used at all sites) N3: - ** VERIFIED ANSWERS ** ✔✔ tumor spread to more distant or numerous regional lymph nodes M: - ** VERIFIED ANSWERS ** ✔✔ presence of distant metastasis M0: - ** VERIFIED ANSWERS ** ✔✔ no distant metastasis M1: - ** VERIFIED ANSWERS ** ✔✔ metastasis to distant organs Resp acid s/s - ** VERIFIED ANSWERS ** ✔✔ Apprehension, confusion, decreased DTR, diaphoretsis, headache,n/v, restless,tachy, tremors, dyspnea-with rapid, shallow respiration Resp alk causes - ** VERIFIED ANSWERS ** ✔✔ Hyperventilation, fever, like vet failure, sepsis(especially gram-)

Respiratory alkalosis - ** VERIFIED ANSWERS ** ✔✔ Decreased LOC, seizure, coma, hyperreflexia, carpopedal spasm, tetany, arrhythmia, angina Resp alk s/s - ** VERIFIED ANSWERS ** ✔✔ Anxiety, diaphoresis, dyspraxia, ECG changes, hyper reflexes, parasthesias, restlessness, tachy, tetany Resp acid level Uncompensated - ** VERIFIED ANSWERS ** ✔✔ pH <7. Paco2 > Bicarbonate normal Resp acid compensated - ** VERIFIED ANSWERS ** ✔✔ pH normal Paco2 > BBicarb > Resp alk Uncompensated - ** VERIFIED ANSWERS ** ✔✔ pH >7. Paco2 < Bicarbonate normal Resp alk Compensated - ** VERIFIED ANSWERS ** ✔✔ pH normal Paco2 < Bicarbonate < Metabolic acid Uncompensated - ** VERIFIED ANSWERS ** ✔✔ pH <7. Paco2 normal Bicarb <

Metabolic acid Compensated - ** VERIFIED ANSWERS ** ✔✔ pH <7.35 Paco2<35 Bicarb <22 Metabolic alk Uncompensated - ** VERIFIED ANSWERS ** ✔✔ pH >7.45 Paco2 normal Bicarb >26 Metabolic alk Compensated - ** VERIFIED ANSWERS ** ✔✔ pH normal Paco2 >45 Bicarb >26 A pathological immune response to an antigen which causes tissue and cellular damage to the host - ** VERIFIED ANSWERS ** ✔✔ What is a hypersensitivity? It implies an intolerance of our immune system to our own (endogenous) antigens - ** VERIFIED ANSWERS ** ✔✔ What does autoimmunity imply? Implies the formation of antibodies to foreign antigens (exogenous antigens) - ** VERIFIED ANSWERS ** ✔✔ What does alloimmunity imply? The pathologic consequence of autoimmunity - ** VERIFIED ANSWERS ** ✔✔ What is an Autoimmune Disease? A pathogen which triggers the immune response - ** VERIFIED ANSWERS ** ✔✔ What often precipitates autoimmune disease?

It then turns against our own antigens - ** VERIFIED ANSWERS ** ✔✔ What happens to the immune response that was initiated against the pathogen? The pathologic consequence of alloimmunity - ** VERIFIED ANSWERS ** ✔✔ What is alloimmune disease? An immediate hypersensitivity response to an environmental allergen - ** VERIFIED ANSWERS ** ✔✔ What it Type I hypersensitivity? Allergies to food, medication, pollen, etc. - ** VERIFIED ANSWERS ** ✔✔ What are most Type I hypersensitivity reactions attributed to? Minutes to hours from time of exposure - ** VERIFIED ANSWERS ** ✔✔ How long do Type I hypersensitivity reactions occur after exposure to the allergen? Antibody IgE - ** VERIFIED ANSWERS ** ✔✔ What does the Type I hypersensitivity pathogenesis begin with? It binds with the allergen - ** VERIFIED ANSWERS ** ✔✔ What does IgE do upon initial exposure to the allergen? It primes the stage for a reaction to occur later - ** VERIFIED ANSWERS ** ✔✔ What does the binding of IgE to the allergen do? (dependent on route the allergen entered the body); include urticarial, rhinitis, conjunctivitis, and asthma - ** VERIFIED ANSWERS ** ✔✔ What are the clinical manifestations of Type I hypersensitivities? Environmental allergies, asthma exacerbation, food allergies, drug allergies, animal allergies, and insect venom allergies Angioedema which causes swelling of lips, eyes, and larynx. (Anaphylaxis is most severe reaction. Is treated with epinephrine).

Atopic Disorders include hay fever, asthma, eczema, and urticarial. They have strong genetic disposition. - ** VERIFIED ANSWERS ** ✔✔ What are some examples of Type I hypersensitivities? Type II Hypersensitivity - ** VERIFIED ANSWERS ** ✔✔ (Antibody mediated or Cytotoxic Hypersensitivity); a reaction which is mediated by antibodies directed against fixed antigens on the plasma membranes of the cells; it is an IgG and IgM antibody mediated reaction Binding of IgG and IgM to an antigen on the plasma membrane - ** VERIFIED ANSWERS ** ✔✔ What does Type II Hypersensitivity pathogenesis begin with? It activates complement and it forms the membrane attack complex (MAC) which causes cell lysis - ** VERIFIED ANSWERS ** ✔✔ What does the binding of IgG and IgM do? IgG and C3b may also bind to the antigen and the macrophages and trigger cell lysis through phagocytosis - ** VERIFIED ANSWERS ** ✔✔ What else may IgG bind to and what does this do? Neutrophils to the tissues - ** VERIFIED ANSWERS ** ✔✔ What do IgG and complement attract? Neutrophils perform phagocytosis and release granules which cause tissue damage

• ** VERIFIED ANSWERS ** ✔✔ What do the neutrophils do in Type II hypersensitivities? They recognize the target cell antigen and release a toxic substance to destroy the target cell - ** VERIFIED ANSWERS ** ✔✔ What do NK cells do in Type II hypersensitivities? They react with the target cell's receptors and prevent the cell from interacting with normal ligands, replaces the ligand, destroys the receptor or inappropriately

stimulates the receptor. - ** VERIFIED ANSWERS ** ✔✔ What do antibodies do in Type II hypersensitivities? ABO incompatibilty and Rh incompatibility - ** VERIFIED ANSWERS ** ✔✔ What are some examples of Type II hypersensitivities? A, B, AB, O - ** VERIFIED ANSWERS ** ✔✔ What are the 4 blood types? A antigen - ** VERIFIED ANSWERS ** ✔✔ A person with Type A blood has what antigen? B - ** VERIFIED ANSWERS ** ✔✔ A person with Type A blood has what antibodies? B antigen - ** VERIFIED ANSWERS ** ✔✔ A person with Type B blood has what antigen? A - ** VERIFIED ANSWERS ** ✔✔ A person with Type B blood has what antibodies? AB - ** VERIFIED ANSWERS ** ✔✔ A person with Type AB blood has what antigens? None - ** VERIFIED ANSWERS ** ✔✔ A person with Type AB blood has what antibodies? None - ** VERIFIED ANSWERS ** ✔✔ A person with Type O blood has what antigen? AB - ** VERIFIED ANSWERS ** ✔✔ A person with Type O blood has what antibodies? O negative - ** VERIFIED ANSWERS ** ✔✔ What blood type is considered a universal donor?

AB positive - ** VERIFIED ANSWERS ** ✔✔ What blood type is considered a universal recipient? Rh antigen - ** VERIFIED ANSWERS ** ✔✔ What antigen does a person who is Rh positive have? None - ** VERIFIED ANSWERS ** ✔✔ What antigen does a person who is Rh negative have? The recipient will develop antibodies against the Rh+ antigen at time of first exposure. If they receive Rh+ blood again, it will cause a transfusion reaction - ** VERIFIED ANSWERS ** ✔✔ What happens if Rh+ blood is given to an Rh- recipient? Hemolytic disease of newborn; will cause jaundice - ** VERIFIED ANSWERS ** ✔✔ What happens if an Rh- mother gives birth to a fetus that is Rh+ (the second birth)? Administer Rh immune globulin (Rhogam) within 72 hours of the initial birth - ** VERIFIED ANSWERS ** ✔✔ How do we prevent Rh incompatibility reactions? Graves' disease, Myasthenia Gravis, and Guillain-Barre' Syndrome - ** VERIFIED ANSWERS ** ✔✔ What are some autoimmune examples of Type II hypersensitivities? A type of hyperthyroidism; autoantibodies formed against thyroid cells. They bind to thyroid cells and mimic action of TSH which causes an increase in secretion of thyroxine. - ** VERIFIED ANSWERS ** ✔✔ What is Grave's disease? Disorder of the neuromuscular junction; autoantibodies against acetylcholine bind to the post synaptic receptors and inhibit synaptic transmission of acetylcholine, leading to muscle weakness and paralysis - ** VERIFIED ANSWERS ** ✔✔ What is Myasthenia Gravis? Disorder of the peripheral nervous system; antibodies bind with myelin sheath of peripheral nervous system and trigger immune response, causing demyelination of