NURS5315 Pathophysiology Practice Exam With Answers (186 Solved Questions)

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Nurs 5315: Adv Patho Exam 1E. Cells decrease in sizeP. Still functional; imbalance between protein synthesis and degradation. Essentiallythere is an increase in the catabolism of intracellular organelles, reducing structuralcomponents of cellPhysiologic: thymus gland in early childhoodPathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood supply,nutrition, hormonal stimulation, or nervous stimulation)-AtrophyE: cells increase in number, mitosis (cell division) must occur, size of cell does notchangePhys: increased rate ofdivision, increase in tissue mass after damage or partialresection; may be compensatory, hormonal, or pathologicPatho: abnormal proliferation of normal cells usually caused by increased hormonalstimulation (endometrial). increase of production of localgrowth factorsEx: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or mammarygland enlargement during pregnancy-HyperplasiaE. Not true adaptation; Cells abnormal change in size, shape, organization (classified asmild, moderate, severe)P. caused by cell injury/irritation, characterized by disordered cell growth. aka atypicalhyperplasia or pre-cancer, a disorderly proliferationPhysiologic: N/APathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breastcancer development; pap smears often show dysplastic cells of the cervix that mustundergo laser/surgical tx-DysplasiaE: reversible change, one type of cell changes to another type for survivalP: 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 underthe influence of cytokines and growth factorsEx: Patho: Columnar cells change to squamous cells in lungs of smoker or normalciliated epithelial cells of the bronchial linings are replaced by stratified squamousepithelial cells.; Phys: Barrett Esophagus-normal squamous cells change to columnarepithelial cells in response to reflux, aka intestinal metaplasia-MetaplasiaE. inadequate oxygenation of tissuesP. decrease in mitochondrial function, decreased production of ATP increases anaerobicmetabolism. eventual cell death.C.M. hypoxia, cyanosis, cognitive impairment, lethargy-Hypoxia injuryE. normal byproduct of ATP production, will overwhelm the mitochondria-exhaustintracellular antioxidantsP. lipid peroxidation, damage proteins, fragment DNA

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C.M. development in Alzheimer's, heart disease, Parkinson's disease, AmyotrophicLateral Sclerosis-Free radical and ROSE. mood altering drug, long term effects on liver and nutritional statusP. metabolized by liver, generates free radicalsC.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4, inflammationand fatty infiltration of liver, hepatomegaly, leads to liver failure irreversible-EthanolNa and H2O enter cell and cause swelling. Organ increases in weight, becomesdistended and pale. Associated with high fever, hypocalcemia, certain infections-OncosisLiver and germ cell tumors-Alpha Fetoprotein OriginGI, pancreas, lung, breast tumors-Carcinoembryonic Antigenprostate tumors-Prostate Specific Antigenfrom epithelial tissue-renal cell carcinoma-Carcino-from connective tissue-chondrosarcoma-Sarco-preinvasive epithelial malignant tumors of glandular or squamous cells-cervix-Carcinoma in situMultiple organs including brain-Lung ca metastasisLiver, lungs-Colorectal ca metastasisLiver, lungs, brain-Testicular ca metastasisBones (especially lumbar spine), liver-Prostate ca metastasisLiver, bones, lymphatics-Head and neck ca metastasisPeritoneal surfaces, diaphragm, omentum, liver-Ovarian ca metastasisLungs-Sarcoma metastasisIn transit lymphatics, lung, liver, brain, GI tract-Melanoma metastasisLocal invasion, followed by invasion of surrounding tissues. Cells then may invade bloodand lymphatic vessels. They must survive in circulation, then enter and survive in a newlocation. Then the cells can multiply and form a new tumor.-Mechanisms of cametastasisT= tumor size >/= correlates with metastatic ability

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N= whether lymph nodes are involvedM= extra nodal involvement (liver, lungs)-TNM staging systemIn venous system-20%-Intravascular fluid compartmentThe measure of solute concentration in a fluid.280-295 mOsm-OsmolalitySurrounds the cells and bathes themin nutrients-20%-Interstitial fluid compartmentWithin the cells-40% uk-Intracellular fluid compartmentPassive-the movement of water from an area of low concentration of solute to one ofhigher concentration-OsmosisPulling-the amount of pressure or force that is exerted by solute molecules of a givencompartment-Osmotic pressureBlood pressure-pushes fluid outside of the vessels, the force of fluid against the walls ofa compartment-venous obstruction, Na and water retention-Hydrostatic pressureColloid pressure keeps water inside the compartment, attracts water from interstitialspace back into the capillary-losses or diminished albumin-Oncotic pressureThe amount of blood within the arterial space-ECF changes will cause changes in theEABVin the same direction-Effective arterial blood volumeActivated by low blood volume, triggers release of renin which converts angiotensinogento angiotensin 1. ACE converts angiotensin 1 to angiotensin which causes arterialvasoconstriction and stimulates release of aldosterone. Aldosterone stimulates renal Nareabsorption and K+ excretion. Water is retained, less urine is produced, blood volumeincreases.-Renin Angiotensin Aldosterone SystemANP and BNP-released by heart-works opposite RAAS to decrease blood volume,promotes urinary excretion of Na and water-Natriuretic hormonesDehydration-intake is not enough for body's needsC.M. Poor skin turgor, dry mucous membranes, sunken eyes, sunken fontanelles,decreased urine output, fatigue-Fluid volume deficitFluid intake exceeds body's needsC.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD,restlessness or anxiety-Fluid volume excessAccumulation of fluid within the interstitial space-venous obstruction, Na and waterretention

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C.M. can be localized or dependent, tightness of skin, facial swelling, rales, decreasedwound healing, increased risk of pressure sores, weight gain-EdemaK+ enters cell with glucose transport. Monitor Type II DM for hypokalemia-insulineffect on K+albuterol, beta blockers, and alpha adrenergic antagonists cause K+ movement into thecell. Alpha adrenergic receptors shift K+ out of the cell-Adrenergic agents effect on K+hyperosmolality causes water to shift out of cell via osmosis. K+will also shift out,causing hyperkalemia.-Osmolality effect on K+intracellular K+ is released into bloodstream-Cell lysis effect on K+cellular ATP is diminished, opening K+ channels and allowing K+ to leave cell-Exerciseeffect on K+excretionand absorption of K+ is regulated by tubule system-Kidneys effect on K+mag inhibits the potassium channels, keeping balance. when mag is low, more K+ exitsthe call, and is excreted via the kidneys.-magnesium and potassiumE. increased acid production, loss of bicarb, diminished renal excretion of hydrogenC.M hyperventilation (compensatory), h/a, n/v/d, dehydration, hypotensionpH <7.4 HCO3 <22-metabolic acidosisE. GI loss, diuretic useC.M. slow, shallow respirations, irritability, twitching, s/s of hypokalemiapH >7.4 HCO3 >26-metabolic alkalosisE. cns depression, airway abnormalitiesC.M. restless, confused, seizures, tachycardiapH <7.4 PaCO2 >44-respiratory acidosisE. usually anxiety, PE, chf, salicylate OD, illegal drugsC.M. light-headed, confused, tetanypH >7.4 PaCO2 <38-respiratory alkalosisPairedgenes on autosomal chromosomes-AlleleOutward appearance of an individual-PhenotypeA map of ones specific genes-GenotypeTwo or more alleles which occur with an appreciable frequency in a population-Polymorphic

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Two dominant or recessive alleles-HomozygousWhen both a dominant and a recessive allele are present-HeterozygousTrait seen in phenotype-DominantTrait not seen in phenotype-Recessivefirst 22 of 23 chromosomes-Autosomal chromosomes23rd pair of chromosomes-sex-linked chromosomesE. Increase in cell sizeP. Caused by hormonal stimulation or increased functional demand, which increasedthe 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 workloadPathologic: cardiomegaly from HTN/L ventricular hypertrophy-Hypertrophyischemia which progresses to hypoxia.Intracellular enzymes such as CK, LDH, AST, ALT, troponin-Hypoxic InjuryClinical Manifestationsdecreased O2, loss of H/H, decreased RBC production, disease of heart/lungs, ischemia-Hypoxic Injury-most muscle cells, including heart excrete what enzyme-CK enzymes-muscle cells, liver cells, heart cells, RBCs, brain secrete what enzyme-LDH-liver cells (s)-AST enzymes are found where?-liver cells (L enzyme)-ALT enzymes are found where?-cardiac cells-Troponin enzymes are found where?lack of O2 causes decrease in mitochondrial function, causing decrease ATP productionand increases anaerobic metabolism (generating ATP from glycogen), eventuallyanaerobic metabolism will stop and the cell will die. Reduction of ATP impairs Na/Kpump, leads to increased Na/Ca in cell, K is diffused out of cell, water diffuses into cellcausing swelling, ribosomal dilation and malfunction occur. Ribosomes producesprotein and when it malfunctions causes decrease in protein synthesis. Death will occurif injury is not stopped.-Hypoxic Injury Pathophysiologyhave unpaired electron in its outer shell, making molecule unstable and highly reactive.aka being oxidized-Free Radical Etiology

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byproduct of ATP production in the mitochondria-Reactive Oxygen Species ROSEtiologyto 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 thatmolecule a free radical-Free Radical and Clinical Manafestationscan overwhelm mitochondria and exhaust intracellular antioxidants, causing cellinjury/disease-Reactive Oxygen Species (ROS) Clinical Manafestationsmay by initated with in cells by (1) absorption of extreme energy sources such asradiation or UV light; (2) the occurrence of endogenous reactions, such as redoxreactions 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 ________-FreeRadical and Pathophysiologycause lipid peroxidation, damage proteins which maintain ion pumps and cellulartransport, fragment DNA and causes less protein synthesis, cause chromatindestruction, and damage mitochondria.-Reactive Oxygen Species (ROS)PathophysiologyETOH is metabolized to acetaldehyde in the cytoplasm of the cell, enzyme alcoholdehydrogenase (ADH) helps with conversion-Ethanol Etiologyadverse effects on liver and causesnutritional disorders. acute effects in the liver includeinflammation, fatty infiltration, hepatomegaly, acute liver necrosis and suppressed fattyacid oxidation. liver failure is irreversible effect of chronic abuse-Ethanol ClinicalManafestationsConversion oxidized niacin (NAD+) is reduced to NADH. In the mitochondrialacetaldehyde 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 following1.Pyruvate change to lactic acid causing lactic acidosis2. Oxaloacetate converted to malate, preventing gluconeogenesis leading to fastinghypoglycemia3. Glyceraldehyde to glycerol which combines with fatty acids and forms triglycerides,leads to triglycerides in theliver, aka hepatosteatosis4. decreases citric acid cycle production of NADH which leads to utilization of Acetyl-CoA for ketogenesis (causing ketoacidosis) and lipogenesis (causing hepatosteatosis)-Ethanol Pathophysiolodycellular swelling, cellular injury because with most injuries there is some amount of O2deprivation causing hypoxic injury-Oncosis Effects and Clinical Implicationsspectrum of cell changes after the cell dies-Necrosis

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necrosis which results from sudden insufficiency of arterial blood flow-Infarctliver cell, ketogenesis occurs in the mitochondria of the hepatocyteresult of unavailability of glucose-Role of the hepatocytesKetogenesis is the formation of ketone bodies and occurs mostly in the mitochondria ofthe hepatocytes (liver cells)-Role of the mitochondrialack of glucose-occur from the depletion of carbohydrate stores or may occur bc the cell is not able touse glucose but the individual is hyperglycemic(type 2 DM)-Triggers for ketogenesisprocessed 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 produceenergy, resulting in acceleration of the B-oxidation cycle and increasing oxidation offatty acids or energy. B-oxidation cycle results in formation of acetyl-CoA-Role ofAcetyl-CoAOxaloacetate is also used in gluconeogenesis, during starvation & uncontrolled DMoxaloacetate levels are insufficient due to gluconeogenesis... this depletion furthers theamount of acetyl-CoA-Effect on oxaloacetateLiver and germ cell tumors-Alpha Fetoprotein (AFP)GI, pancreas, lung, breast, ect tumors-Carcinoembryonic Antigen CEAGerm cell tumors-Beta Human Chorionic gonadotropin B-hCG originProstate tumors-Prostate Specific Antigen PSAarise from epithelial tissue-Carcino-(prefix)connective tissue (muscle and bone tissue)malignant cancers of the skeletal muscle are known as rhabdomyosarcomas-Sarco-(prefix)arise from ductal or glandular structures-adeno (prefix)-preinvasive epithelial malignant tumors of glandular or squamous cell origin-# of sites including cervix, skin, oral cavity, esophagus and bronchusin breast, ductal carcinoma in situ (DCIS) fills the mammary ducts but has notprogressed to local tissueinvasion-Carcinoma in Situoriginates from precursor cells or blasts (immature or embryonic tissue).Ex: children, neuroblastoma, retinoblastoma--blastoma (suffix)

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