NURS 5315: ADVANCED PATHOPHYSIOLOGY UTA EXAM 1 LATEST UPDATED 2025

NURS 5315: ADVANCED PATHOPHYSIOLOGY UTA EXAM 1 LATEST UPDATED 2025 "Metaplasia - CORRECT ANSWER 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 - CORRECT ANSWER 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 - CORRECT ANSWER 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" "Alpha Fetoprotein Origin - CORRECT ANSWER Liver and germ cell tumors" "Carcinoembryonic Antigen - CORRECT ANSWER GI, pancreas, lung, breast tumors" "Prostate Specific Antigen - CORRECT ANSWER prostate tumors" "Carcino- - CORRECT ANSWER from epithelial tissue- renal cell carcinoma" "Sarco- - CORRECT ANSWER from connective tissue- chondrosarcoma" "Carcinoma in situ - CORRECT ANSWER preinvasive epithelial malignant tumors of glandular or squamous cells- cervix" "Lung ca metastasis - CORRECT ANSWER Multiple organs including brain" "Colorectal ca metastasis - CORRECT ANSWER Liver, lungs" "Testicular ca metastasis - CORRECT ANSWER Liver, lungs, brain" "Prostate ca metastasis - CORRECT ANSWER Bones (especially lumbar spine), liver" "Head and neck ca metastasis - CORRECT ANSWER Liver, bones, lymphatics" "Ovarian ca metastasis - CORRECT ANSWER Peritoneal surfaces, diaphragm, omentum, liver" "Sarcoma metastasis - CORRECT ANSWER Lungs" "Melanoma metastasis - CORRECT ANSWER In transit lymphatics, lung, liver, brain, GI tract" "Mechanisms of ca metastasis - CORRECT ANSWER 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 - CORRECT ANSWER T= tumor size >/= correlates with metastatic ability N= whether lymph nodes are involved M= extra nodal involvement (liver, lungs)" "Intravascular fluid compartment - CORRECT ANSWER In venous system- 20%" "Osmolality - CORRECT ANSWER The measure of solute concentration in a fluid. 280-295 mOsm" "Interstitial fluid compartment - CORRECT ANSWER Surrounds the cells and bathes them in nutrients- 20%" "Intracellular fluid compartment - CORRECT ANSWER Within the cells- 40% uk" "Osmosis - CORRECT ANSWER Passive- the movement of water from an area of low concentration of solute to one of higher concentration" "Osmotic pressure - CORRECT ANSWER Pulling- the amount of pressure or force that is exerted by solute molecules of a given compartment" "Hydrostatic pressure - CORRECT ANSWER Blood pressure- pushes fluid outside of the vessels, the force of fluid against the walls of a compartment- venous obstruction, Na and water retention" "hypovolemic hypernatremia - CORRECT ANSWER from GI losses or diuretics C.M. Volume depletion, orthostatic hypotension, tachycardia, lack of organ perfusion" "hypervolemic hypernatremia - CORRECT ANSWER administration of hypertonic saline C.M. volume overload, edema, chf, htn, pulmonary edema" "mild hyponatremia - CORRECT ANSWER Na 125-135 C.M. anorexia, apathy, restless, nausea, lethargy, muscle cramps" "moderate hyponatremia - CORRECT ANSWER Na 120-125 C.M. agitation, disorientation, headache" "severe hyponatremia - CORRECT ANSWER Na <120 C.M. seizures, coma, areflexia, incontinence, death" "isotonic hyponatremia - CORRECT ANSWER mOsm 280-295- not true hypovolemia- from elevated triglycerides or serum proteins" "hypertonic hyponatremia - CORRECT ANSWER mOsm >295- from solutes other than Na- osmotic pressure leads to fluid shift from intracellular to extracellular" "hypotonic hyponatremia - CORRECT ANSWER mOsm <280 and urine Na >100- fluid excess r/t intake or renal impairment" "insulin effect on K+ - CORRECT ANSWER K+ enters cell with glucose transport. Monitor Type II DM for hypokalemia" "Adrenergic agents effect on K+ - CORRECT ANSWER 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+ - CORRECT ANSWER hyperosmolality causes water to shift out of cell via osmosis. K+ will also shift out, causing hyperkalemia." "Cell lysis effect on K+ - CORRECT ANSWER intracellular K+ is released into bloodstream" "Exercise effect on K+ - CORRECT ANSWER cellular ATP is diminished, opening K+ channels and allowing K+ to leave cell" "Kidneys effect on K+ - CORRECT ANSWER excretion and absorption of K+ is regulated by tubule system" "magnesium and potassium - CORRECT ANSWER mag inhibits the potassium channels, keeping balance. when mag is low, more K+ exits the call, and is excreted via the kidneys." "metabolic acidosis - CORRECT ANSWER 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 <22" "metabolic alkalosis - CORRECT ANSWER E. GI loss, diuretic use C.M. slow, shallow respirations, irritability, twitching, s/s of hypokalemia pH >7.4 HCO3 >26" "respiratory acidosis - CORRECT ANSWER E. cns depression, airway abnormalities C.M. restless, confused, seizures, tachycardia pH <7.4 PaCO2 >44" "respiratory alkalosis - CORRECT ANSWER E. usually anxiety, PE, chf, salicylate OD, illegal drugs C.M. light-headed, confused, tetany pH >7.4 PaCO2 <38" "Allele - CORRECT ANSWER Paired genes on autosomal chromosomes" "Locus - CORRECT ANSWER Position in which a gene occupies on a chromosome" "Phenotype - CORRECT ANSWER Outward appearance of an individual" "Genotype - CORRECT ANSWER A map of ones specific genes" "Polymorphic - CORRECT ANSWER Two or more alleles which occur with an appreciable frequency in a population" "Homozygous - CORRECT ANSWER Two dominant or recessive alleles" "Heterozygous - CORRECT ANSWER When both a dominant and a recessive allele are present" "Dominant - CORRECT ANSWER Trait seen in phenotype" "Recessive - CORRECT ANSWER Trait not seen in phenotype" "Codominance - CORRECT ANSWER Both alleles exhibit (blood type AB)" "Carrier - CORRECT ANSWER Person who has a diseased gene but is phenotypically normal" "Autosomal chromosomes - CORRECT ANSWER first 22 of 23 chromosomes" "sex-linked chromosomes - CORRECT ANSWER 23rd pair of chromosomes" "LDH - CORRECT ANSWER - muscle cells, liver cells, heart cells, RBCs, brain secrete what enzyme" "AST enzymes are found where? - CORRECT ANSWER - liver cells (s)" "ALT enzymes are found where? - CORRECT ANSWER - liver cells (L enzyme)" "Troponin enzymes are found where? - CORRECT ANSWER - cardiac cells" "Necrosis - CORRECT ANSWER spectrum of cell changes after the cell dies" "Infarct - CORRECT ANSWER necrosis which results from sudden insufficiency of arterial blood flow" "5 Types of Necrosis - CORRECT ANSWER coagulative, liquefactive, caseous, fat, gangrenous" "Coagulative - CORRECT ANSWER occurs in the kidneys, heart, and adrenal glands most commonly secondary to hypoxia (caused by protein denaturation, tissue firm and slightly swollen)" "Liquefactive - CORRECT ANSWER nerve cell necrosis" "Caseous - CORRECT ANSWER 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 - CORRECT ANSWER necrosis breast, pancreas and other abdominal structures" "wet gangrene - CORRECT ANSWER develops when neutrophils invade the site, causing liquefactive necrosis" "Gangrenous - CORRECT ANSWER tissue death resulting from severe tissue hypoxia" "dry gangrene - CORRECT ANSWER result of coagulative necrosis" "Role of the hepatocytes - CORRECT ANSWER liver cell, ketogenesis occurs in the mitochondria of the hepatocyte result of unavailability of glucose" "Role of the mitochondria - CORRECT ANSWER Ketogenesis is the formation of ketone bodies and occurs mostly in the mitochondria of the hepatocytes (liver cells)" "Triggers for ketogenesis - CORRECT ANSWER 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 - CORRECT ANSWER 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" "Alpha Fetoprotein (AFP) - CORRECT ANSWER Liver and germ cell tumors" "Carcinoembryonic Antigen CEA - CORRECT ANSWER GI, pancreas, lung, breast, ect tumors" "Beta Human Chorionic gonadotropin B-hCG origin - CORRECT ANSWER Germ cell tumors" "Prostate Specific Antigen PSA - CORRECT ANSWER Prostate tumors" "Carcino- (prefix) - CORRECT ANSWER arise from epithelial tissue" "Sarco- (prefix) - CORRECT ANSWER connective tissue (muscle and bone tissue) malignant cancers of the skeletal muscle are known as rhabdomyosarcomas" "gilomas - CORRECT ANSWER tissue of the brain and spinal cord" "adeno (prefix) - CORRECT ANSWER arise from ductal or glandular structures" "Carcinoma in Situ - CORRECT ANSWER -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 - CORRECT ANSWER absence of differentiation" "-blastoma (suffix) - CORRECT ANSWER originates from precursor cells or blasts (immature or embryonic tissue). Ex: children, neuroblastoma, retinoblastoma" "Lung Sites of Metastasis - CORRECT ANSWER multiple organs, including brain" "Colorectal Sites of Metastasis - CORRECT ANSWER liver, lungs" "Testicular Sites of Metastasis - CORRECT ANSWER lungs, liver, brain" "Prostate Sites of Metastasis - CORRECT ANSWER bones (especially lumbar spine), liver" "Head and Neck Sites of Metastasis - CORRECT ANSWER lymphatics, liver, bones" "Ovarian Sites of Metastasis - CORRECT ANSWER peritoneal surfaces, diaphragm, omentum, liver" "Sarcoma Sites of Metastasis - CORRECT ANSWER lungs" "Melanoma Sites of Metastasis - CORRECT ANSWER in transit lymphatics, lung, liver, brain, GI tract" "Local invasion: - CORRECT ANSWER Cancer cells invade nearby normal tissue." "Intravasation: - CORRECT ANSWER Cancer cells invade and move through the walls of nearby lymph vessels or blood vessels." "Circulation: - CORRECT ANSWER Cancer cells move through the lymphatic system and the bloodstream to other parts of the body." "Arrest and extravasation: - CORRECT ANSWER 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: - CORRECT ANSWER Cancer cells multiply at the distant location to form small tumors known as micrometastases." "Angiogenesis: - CORRECT ANSWER 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: - CORRECT ANSWER size or direct extent of the primary tumor" "Tx: - CORRECT ANSWER tumor cannot be evaluated" "Tis: - CORRECT ANSWER carcinoma in situ" "T0: - CORRECT ANSWER no signs of tumor" "T1, T2, T3, T4: - CORRECT ANSWER size and/or extension of the primary tumor" "N: - CORRECT ANSWER degree of spread to regional lymph nodes" "Nx: - CORRECT ANSWER lymph nodes cannot be evaluated" "N0: - CORRECT ANSWER tumor cells absent from regional lymph nodes" "N1: - CORRECT ANSWER regional lymph node metastasis present; (at some sites: tumor spread to closest or small number of regional lymph nodes)" "N2: - CORRECT ANSWER tumor spread to an extent between N1 and N3 (N2 is not used at all sites)" "N3: - CORRECT ANSWER tumor spread to more distant or numerous regional lymph nodes" "M: - CORRECT ANSWER presence of distant metastasis" "M0: - CORRECT ANSWER no distant metastasis" "M1: - CORRECT ANSWER metastasis to distant organs" "Resp acid s/s - CORRECT ANSWER Apprehension, confusion, decreased DTR, diaphoretsis, headache,n/v, restless,tachy, tremors, dyspnea-with rapid, shallow respiration" "Resp alk causes - CORRECT ANSWER Hyperventilation, fever, like vet failure, sepsis(especially gram-)" "Respiratory alkalosis - CORRECT ANSWER Decreased LOC, seizure, coma, hyperreflexia, carpopedal spasm, tetany, arrhythmia, angina" "Resp alk s/s - CORRECT ANSWER Anxiety, diaphoresis, dyspraxia, ECG changes, hyper reflexes, parasthesias, restlessness, tachy, tetany" "Resp acid level Uncompensated - CORRECT ANSWER pH <7.35 Paco2 >45 Bicarbonate normal" "Resp acid compensated - CORRECT ANSWER pH normal Paco2 >45 BBicarb >26" "Resp alk Uncompensated - CORRECT ANSWER pH >7.45 Paco2 <35 Bicarbonate normal" "Resp alk Compensated - CORRECT ANSWER pH normal Paco2 <35 Bicarbonate <22" "Metabolic acid Uncompensated - CORRECT ANSWER pH <7.35 Paco2 normal Bicarb <22" "Metabolic acid Compensated - CORRECT ANSWER pH <7.35 Paco2<35 Bicarb <22" "Metabolic alk Uncompensated - CORRECT ANSWER pH >7.45 Paco2 normal Bicarb >26" "Metabolic alk Compensated - CORRECT ANSWER pH normal Paco2 >45 Bicarb >26" "A pathological immune response to an antigen which causes tissue and cellular damage to the host - CORRECT ANSWER What is a hypersensitivity?" "It implies an intolerance of our immune system to our own (endogenous) antigens - CORRECT ANSWER What does autoimmunity imply?" "Implies the formation of antibodies to foreign antigens (exogenous antigens) - CORRECT ANSWER What does alloimmunity imply?" "The pathologic consequence of autoimmunity - CORRECT ANSWER What is an Autoimmune Disease?" "A pathogen which triggers the immune response - CORRECT ANSWER What often precipitates autoimmune disease?" "It then turns against our own antigens - CORRECT ANSWER What happens to the immune response that was initiated against the pathogen?" "The pathologic consequence of alloimmunity - CORRECT ANSWER What is alloimmune disease?" "An immediate hypersensitivity response to an environmental allergen - CORRECT ANSWER What it Type I hypersensitivity?" "Binding of IgG and IgM to an antigen on the plasma membrane - CORRECT ANSWER What does Type II Hypersensitivity pathogenesis begin with?" "It activates complement and it forms the membrane attack complex (MAC) which causes cell lysis - CORRECT ANSWER 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 - CORRECT ANSWER What else may IgG bind to and what does this do?" "Neutrophils to the tissues - CORRECT ANSWER What do IgG and complement attract?" "Neutrophils perform phagocytosis and release granules which cause tissue damage - CORRECT ANSWER 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 - CORRECT ANSWER 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. - CORRECT ANSWER What do antibodies do in Type II hypersensitivities?" "ABO incompatibilty and Rh incompatibility - CORRECT ANSWER What are some examples of Type II hypersensitivities?" "A, B, AB, O - CORRECT ANSWER What are the 4 blood types?" "A antigen - CORRECT ANSWER A person with Type A blood has what antigen?" "B - CORRECT ANSWER A person with Type A blood has what antibodies?" "B antigen - CORRECT ANSWER A person with Type B blood has what antigen?" "A - CORRECT ANSWER A person with Type B blood has what antibodies?" "AB - CORRECT ANSWER A person with Type AB blood has what antigens?" "None - CORRECT ANSWER A person with Type AB blood has what antibodies?" "None - CORRECT ANSWER A person with Type O blood has what antigen?" "AB - CORRECT ANSWER A person with Type O blood has what antibodies?" "O negative - CORRECT ANSWER What blood type is considered a universal donor?" "AB positive - CORRECT ANSWER What blood type is considered a universal recipient?" "Rh antigen - CORRECT ANSWER What antigen does a person who is Rh positive have?" "None - CORRECT ANSWER 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 - CORRECT ANSWER What happens if Rh+ blood is given to an Rh- recipient?" "Hemolytic disease of newborn; will cause jaundice - CORRECT ANSWER 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 - CORRECT ANSWER How do we prevent Rh incompatibility reactions?" "Graves' disease, Myasthenia Gravis, and Guillain-Barre' Syndrome - CORRECT ANSWER 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. - CORRECT ANSWER 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 - CORRECT ANSWER 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 the peripheral nerves and a rapidly progressive, ascending paralysis. - CORRECT ANSWER What is Guillain-Barre' Syndrome?" "Type III Hypersensitivity - CORRECT ANSWER Antibodies form against and bind to circulating antigens. This forms an antigen-antibody complex" "Once the complex is formed, they are deposited in vessel walls or extravascular tissue and trigger an immune and inflammatory response - CORRECT ANSWER What happens once the antigen-antibody complex is formed in Type III hypersensitivities?" "It causes cellular and tissue damage - CORRECT ANSWER What does the immune and inflammatory response of Type III hypersensitivities cause?" "They are both IgG and IgM mediated responses. - CORRECT ANSWER How is Type III hypersensitivity similar to Type II hypersensitivity?" "Type III is not specific to a cell or tissue. The antigen antibody complexes are spread via circulation throughout the body and generate a more diffuse reaction. - CORRECT ANSWER How is Type III hypersensitivity different from Type II hypersensitivity?" "It is a T-cell mediated reaction that occurs 11-14 days after first exposure and 5-6 days after the second exposure. This results in mononuclear infiltration, decreased circulation and tissue necrosis. - CORRECT ANSWER What is a solid organ transplant rejection?" "Fluid Compartments - CORRECT ANSWER Intravascular, interstitial, intracellular" "Intravascular - CORRECT ANSWER - Extracellular fluid (ECF) that is within the blood vessels - blood plasma - 5% of total body water" "Intravascular pattern of fluid shift - CORRECT ANSWER -Water moves between plasma and interstitial space by osmosis and hydrostatic pressure, occur across the capillary membrane -The major forces for filtration are within the capillary." "Interstitial - CORRECT ANSWER - ECF, Fluid surround the tissue cells - 15% of total body water" "Interstitial pattern of fluid shift - CORRECT ANSWER hydrostatic pressure promotes the movement of about 10% of fluid along with small amount of protein into lymphatics which eventually returns to the circulation" "- Intracellular fluid (ICF) - CORRECT ANSWER - Fluid inside the cell - 40% of total body water" "Intracellular pattern of fluid shift - CORRECT ANSWER Water moves between ICF and ECF compartment by osmosis" "Capillary hydrostatic pressure (BP) - CORRECT ANSWER facilitates the outward movement of water from the capillary to the interstitial space" "Capillary (plasma) oncotic pressure - CORRECT ANSWER osmotically attracts water from the interstitial space back into the capillary" "Interstitial hydrostatic pressure - CORRECT ANSWER facilitates the inward movement of water from the interstitial space into the capillary" "Interstitial oncotic pressure - CORRECT ANSWER osomotically attracts water from the capillary into the interstitial space" "Starling hypothesis - CORRECT ANSWER fluid shift through capillary wall is know as Net Filtration= forces favoring filtration- forces opposing filtration" "Osmolality - CORRECT ANSWER - The measure of solute concentration in a solution (basically the concentration of plasma) aka Tonicity" "Osmotic pressure - CORRECT ANSWER amount of pressure of force that is exerted by solute molecules of a given compartment -pulling passive force" "plasma osmolality - CORRECT ANSWER 280-295 mOsm/kg" "- Na - CORRECT ANSWER responsible for osmotic balance of ECF space" "- K - CORRECT ANSWER responsible for osmotic balance of ICF space" "Osmosis - CORRECT ANSWER Movement of water b/w compartments from an area of low concentration of solutes to an area of high" "Osmotic Pressure - CORRECT ANSWER Amount of pressure or force exerted by solute molecules of a given compartment" "Hydrostatic Pressure - CORRECT ANSWER It is a force within a fluid compartment (the mechanical force of fluid against the walls of the compartment, ex: BP)" "Hydrostatic Pressure - CORRECT ANSWER - a pushing force, pushes fluid outside the compartment" "Oncotic Pressure - CORRECT ANSWER The force which helps to keep fluid/water within a compartment aka (colloid osmotic pressure)" "Oncotic Pressure - CORRECT ANSWER - contributes to osmotic pressure and is exerted by plasma proteins, mainly albumin" "Oncotic Pressure - CORRECT ANSWER In conditions where plasma proteins are reduced, e.g. from being lost in the urine or from malnutrition, there will be a reduction in oncotic pressure resulting in excess fluid buildup in the tissues (edema)." "Effective Arterial Blood Volume (EABV) - CORRECT ANSWER Amount of blood within the arterial space which effectively perfuses the organs and tissues" "ECF, EABV - CORRECT ANSWER - volume changes in the ____ compartment will cause changes in the _____ in the same direction" "Decreased arterial pressure - CORRECT ANSWER Acts as a potent stimulus to ADH secretion even in the presence of hypo-osmolality." "ADH - CORRECT ANSWER It plays an important role in homeostasis by regulation of water, glucose and salt in the blood. It is released when body is dehydrated; secreted by the pituitary gland in response to a water deficit, Na excess or low BP; It causes the kidneys to reabsorb water, thus increasing plasma volume" "Aldosterone - CORRECT ANSWER hormone secreted from the adrenal cortex and increases renal Na resorption and K excretion" "Renin Angiotensin Aldosterone System (RAAS) - CORRECT ANSWER It is activated by low blood volume. It regulates blood pressure and fluid balance" "Renin - CORRECT ANSWER low blood volume triggers release" "RAAS - CORRECT ANSWER " "Natriuretic Hormones - CORRECT ANSWER Hormones released from the atria or ventricle of the heart." "Natriuretic Hormones - CORRECT ANSWER It decreases blood volume by promoting urine excretion of sodium and water (opposite of RAAS)" "Natriuretic peptides - CORRECT ANSWER Have been found to be useful markers in differentiating patients presenting with acute onset of breathlessness and also as prognostic markers in patients with congestive cardiac failure." "Fluid Volume Deficit Etiology - CORRECT ANSWER Trauma, dehydration, increased output, decreased intake, burn, sepsis, DKA, gastroenteritis, diabetes insipidus" "Fluid Volume Deficit S/S - CORRECT ANSWER Hypotension, decreased skin turgor, dry mucous membrane, sudden weight loss, weak, rapid pulse, change in mental status, decreased urine output, hypovolemic shock." "Fluid Volume Deficit Pathophysiology - CORRECT ANSWER Results from loss of body fluids from ICF and ECF" "Fluid Volume Excess - CORRECT ANSWER occurs when fluid intake of fluid retention exceeds the bodies fluid needs" "Fluid Volume Excess Etiology - CORRECT ANSWER CHF, Hepatic failure, renal failure, low protein sources, nephrotic syndrome, corticosteroids, liver cirrhosis" "Fluid Volume Excess Pathophysiology - CORRECT ANSWER It is due to shifts in fluid from interstium to plasma, reduce excretion of sodium and water, excessive retention of sodium and water from chronic renal stimuli." "Fluid Volume Excess - CORRECT ANSWER S/S edema, tightness of the skin, puffiness of eyes, rales" "Edema Etiology - CORRECT ANSWER Sitting or standing in one position, DVT, steroid drugs, CHF, Kidney disease, cirrhosis," "Edema - CORRECT ANSWER S/S Swelling or puffiness of tissue, shiny skin, increased abdominal size, dyspnea, SOB, chest pain" "Edema - CORRECT ANSWER Excessive accumulation of fluid within the interstitial space" "Hydrostatic Pressure - CORRECT ANSWER It facilitates the outward movement of water from the vascular space to the interstitial space. It is determined by blood pressure and blood volume - in Edema, hydrostatic pressure is increased due to a venous obstruction or retention of Na" "Oncotic Pressure - CORRECT ANSWER It osmotically attracts water from the interstitial space back into the capillary - in Edema, oncotic pressure is decreased due to a loss or diminished production of albumin" "renal tubular system - CORRECT ANSWER responsible for absorption and excretion of Na" "Sodium Disorders - CORRECT ANSWER - Regulated by ADH, hypothalamus, RAAS, Kidneys" "Euvolemic Hypernatremia - CORRECT ANSWER Typically caused by diabetes insipidus" "Euvolemic Hypernatremia Etiology - CORRECT ANSWER When total water loss is equal from all parts of the body, not just from the intravascular space" "Hypovolemic Hypernatremia - CORRECT ANSWER Result of sodium and water loss. Water loss is usually greater than the sodium loss Volume depletion" "Hypovolemic Hypernatremia - CORRECT ANSWER uncommon but occurs most commonly from the administration of hypertonic sodium salts" "Hypovolemic Hypernatremia - CORRECT ANSWER s/s overload, hypertension, edema, CHF, pulmonary edema. In infants this is due to erroneous preparation of dietary formula and in outpatient adults the ingestion of concentrated salt solutions" "Hypervolemic Hypernatremia - CORRECT ANSWER Uncommon, but may occur when hypertonic saline salts is administered" "Hyponatremia - CORRECT ANSWER most common electrolyte imbalance in hospital 3 types: isotonic, hypertonic, hypotonic (euvolemic, hypovolemic, hypervolemic) Mild (126-130): anorexia, apathy, restlessness, nausea, lethargy, muscle cramps Moderate (120-125): agitation, disorientation, headache Severe (<120): seizure, coma, a reflex is, incontinence, death" "Isotonic Hyponatremia - CORRECT ANSWER (not a true hyponatremia) - osmolality is normal between 280-295 Usually caused by elevated triglycerides or serum proteins" "Hypertonic Hyponatremia - CORRECT ANSWER Serum Osmolality > 295, Caused by high osmolality from solutes that are not sodium, osmotic pressure cause a shift from intracellular space to extracellular space causing hyponatremia" "Euvolemic (hypotonic hyponatremia) - CORRECT ANSWER skin, GI, lung losses" "Hypovolemic (hypotonic hyponatremia) - CORRECT ANSWER psychogenic, low sodium intake, renal disease, hypothyroidism, SIADH, hypocortisolism" "Hypervolemic (hypotonic hyponatremia) - CORRECT ANSWER CHF, cirrhosis, renal disease" "Insulin - CORRECT ANSWER Shifts potassium intracellularly, it functions by increasing the rate the sodium potassium pump moves these ions across the membrane. Mainly by dietary intake." "Acid Base Balance effect on K+ - CORRECT ANSWER Hydrogen enters cell and is exchanged for potassium, allowing potassium to escape during acidosis, vice versa for alkalosis, to maintain ionic balance. H+ moves ICF and K+ moves ECF to maintain ionic balance." "Adrenergic Agonists - CORRECT ANSWER Stimulants of beta 2 receptors by albuterol increase the activity of the sodium potassium pump and shift potassium into the cell resulting in hypokalemia. Alpha adrenergic receptors cause a shift out of the cell and may lead to hyperkalemia. Beta 2 antagonist cause shift into cell space as well." "K > 5.5 - CORRECT ANSWER Commonly caused by end stage renal failure, medications (ACE inhibitors, NSAIDS), tissue trauma (Rhabdomy.), adrenal insufficiency, hypoxia, digitalis overdose, insulin deficits." "Calcium and Phosphorus - CORRECT ANSWER - regulated by 3 hormones: parathyroid (PTH), vit D, and calcitonin - rigidly controlled. - inverse relationship: if one increases= other one decreases" "Hypercalcemia - - CORRECT ANSWER >10mg/dl E: Causes decreased cell permeability to Na+, causing the threshold potential to become more positive and further from the membrane potential, meaning more stimulus is required to initiate an action potential. Causes: hyperparathyroidism and at times cancer of the bone resulting from breast cancer, lymphoma or myeloma CM: polyuria, renal stones, nausea, vomiting, constipation, weakness, fatigue, confusion, coma, hyporeflexia, lethargy, encephalopathy, a shortened QT segment and depressed, widened T waves on EKG." "Osmolar gap - CORRECT ANSWER Measured should be slightly greater than calculated If >10, then other solutes present If >50, then fatal" "metabolic acidosis - CORRECT ANSWER ph < 7.4 and HCO3 < 21 E: Increased H+ load - Decreased H+ excretion - Uremia, distal renal tubule acidosis; Concentration of non-carbonic acids increases or bicarbonate is lost from ECF or cannot be regenerated by the kidneys. Causes: ketoacidosis (DM, starvation), Lactic acidosis (shock-hypoxemia), ingestions ((high osmolar gaps) (ammonium Cl-, ethylene glycol, methanol, salicylates, paraldehyde); HCO3 loss - Diarrhea, renal failure, proximal renal tubule acidosis CM: Decreased myocardial contractility, decreased cardiac output, catecholamine resistant hypotension, hyperkalemia; Oxyhemoglobin dissociation curve shifts right." "Ca++ bound to albumin decreases leading to an increase in ionized Ca++. - CORRECT ANSWER Review the anion gap - if high, it's most likely from lactic acidosis, ketoacidosis, or renal failure. Normal anion gap (hyperchloremic acidosis) usually from diarrhea, saline administration in large volumes, NSAIDS, ACE inhibitors, or trimethoprim." "Metabolic Alkalosis - CORRECT ANSWER ph > 7.4 and HCO3 >28 E: loss of hydrochloric acid, normally H+ serves as a trigger for the pancreas to produce HCO3 which it gets from the blood, if H+ is lost, the pancreas doesn't remove HCO3 from the blood, causing a build up of HCO3 and alkalosis; Occurs when bicarbonate concentration is increased, usually due to a decrease in acid. Causes: Diuretics (promote H+ loss leading to NA+ and HCO3 reabsorption, the build up leads to alkalosis). Can also be from diarrhea or laxative abuse or vomiting or gastric suctioning, hyperaldosteronism, diuretics, CM: Hypokalemia symptoms, hypocalcemia symptoms, cardiac arrhythmias, hypoventilation; Oxyhemoglobin dissociation curve shifts left." "Respiratory Acidosis - CORRECT ANSWER ph < 7.4 and Pco2 >45 E: Restoration of adequate alveolar ventilation removes excess CO2. Alveolar hypoventilation, CO2 is retained (hypercapnia)m increasing H+ and producing acidosis. Cyanosis does not occur unless there is hypoxemia, skin may be pink from vasodilation from the elevated CO2 level. Causes: Respiratory depression (brainstem trauma, over sedation), paralysis of respiratory muscles (Guillain-Barre, polio, ALS, MS), airway obstruction, disorders of lung parenchyma (ARDS, COPD, PE, pneumonia) CM: Headache, lethargy, blurred vision, tremors, convulsions, coma." "Respiratory Alkalosis - CORRECT ANSWER ph > 7.4 and Pco2 < 35 E: Alveolar hyperventilation and decreased concentration of plasma CO2 (hypocapnia) Must identify underlying disturbance Causes: Hypoxemia (PE, CHF, high altitude), fever, gram negative sepsis, severe anemia, hyperventilation, hepatic failure, salicylate OD, catecholamines, nicotine, progesterone, mechanical ventilation CM: Dizziness, confusion, paresthesias, seizures, coma." "Hypoxic Injury - CORRECT ANSWER Etiology:decreased O2,loss of Hgb or Hgb function, decreased RBC production, disease of heart/lungs, ischemia Clinical Manifestations: ischemia which progresses to hypoxia. Intracellular enzymes as follows: CK-most muscle cells, including heart,LDH- muscle cells, liver cells, heart cells, RBCs, brain,AST- liver cells,ALT- liver cells Troponin- cardiac cells Patho: 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 and Reactive Oxygen Species (ROS) - CORRECT ANSWER Etiology:Free Radical- have unpaired electron in its outer shell, making molecule unstable and highly reactive. aka being oxidized ROS-byproduct of ATP production in the mitochondria Clinical Manif: FR- to stabilize self, it will steal an electron from another molecule or give up an electron. The free radical will often steal an electron from another molecule, making that molecule a free radical ROS- can overwhelm mitochondria and exhaust intracellular antioxidants, causing cell injury/disease Patho: ROS are produced by absorption of high energy sources such as radiation or UV light, have role in development of Alzheimer's, Parkinson's, Amyotrophic Lateral Sclerosis (ALS). ROS 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. Antioxidants are our body's defense against ROS- reducing agents that provide missing electron, stabilizing the free radical" "Ethanol - CORRECT ANSWER Etiology: ETOH is metabolized to acetaldehyde in the cytoplasm of the cell, enzyme alcohol dehydrogenase (ADH) helps with conversion Clinical Manifestation: 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 Patho: 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 Pyruvate change to lactic acid causing lactic acidosis Oxaloacetate converted to malate, preventing gluconeogenesis leading to fasting hypoglycemia Glyceraldehyde to glycerol which combines with fatty acids and forms triglycerides, leads to triglycerides in the liver, aka hepatosteatosis decreases citric acid cycle production of NADH which leads to utilization of Acetyl-CoA for ketogenesis (causing ketoacidosis) and lipogenesis (causing hepatosteatosis)" "Apoptosis - CORRECT ANSWER Cellular Effect: programmed cell death, normal process Clinical Implications: Death by apoptosis causes loss of cells in many pathologic states including: Severe cell injury, Accumulation of misfolded proteins, Infections (part. viral), Obstruction in tissue ducts dysregulated apoptosis - excessive or insufficient apoptosis. ex: survival of mutated cells can increase cancer risk. Increased apoptosis is known to occur in ischemic injury (MI and stroke)- prevents cellular proliferation resulting in a gigantic body" "Coagulative Necrosis - CORRECT ANSWER - occurs in the kidneys, heart, and adrenal glands most commonly secondary to hypoxia - hypoxia by chemical injury (esp. mercuric chloride) or severe ischemia" "Liquefactive Necrosis - CORRECT ANSWER - results from ischemic injury to neurons & glial cells in the brain- nerve cell necrosis- can also result from bacterial infections: staphylococci, streptococci, E. Coli" "Caseous Necrosis - CORRECT ANSWER - necrosis specific to lung tissue and occurs in TB- combination of coagulative and liquefactive necrosis" "Fat Necrosis - CORRECT ANSWER - necrosis breast, pancreas and other abdominal structures- cellular dissolution caused by powerful enzymes called lipases" "Gangrenous Necrosis - CORRECT ANSWER - tissue death resulting from severe tissue hypoxia- commonly occurring b/c of arteriosclerosis, or blockage, of major arteries, esp. in the lower leg- dry gangrene: result of coagulative necrosis- wet gangrene: develops when neutrophils invade the site causing liquefactive necrosis- gas gangrene: caused by infection of injured tissue by Clostridium (can be deadly)" "Ethanol Metabolism Pathway - CORRECT ANSWER Most of the ethanol in the body is broken down in the liver by an enzyme called alcohol dehydrogenase (ADH), which transforms ethanol into a toxic compound called acetaldehyde (CH3CHO), a known carcinogen. However, acetaldehyde is generally short-lived; it is quickly broken down to a less toxic compound called acetate (CH3COO-) by another enzyme called aldehyde dehydrogenase (ALDH). Acetate then is broken down to carbon dioxide and water, mainly in tissues other than the liver. *The enzymes cytochrome P450 2E1 (CYP2E1) and catalase also break down alcohol to acetaldehyde. However, CYP2E1 only is active after a person has consumed large amounts of alcohol, and catalase metabolizes only a small fraction of alcohol in the body. Small amounts of alcohol also are removed by interacting with fatty acids to form compounds called fatty acid ethyl esters (FAEEs). These compounds have been shown to contribute to damage to the liver and pancreas." "Hepatocellular damage:Fatty Liver - CORRECT ANSWER Alcohol is metabolized by alcohol dehydrogenase (ADH) into acetaldehyde, then further metabolized by aldehyde dehydrogenase (ALDH) into acetic acid, which is finally oxidized into carbon dioxide (CO2) and water ( H2O).[6] This process generates NADH, and increases the NADH/NAD+ ratio. A higher NADH concentration induces fatty acid synthesis while a decreased NAD level results in decreased fatty acid oxidation. Subsequently, the higher levels of fatty acids signal the liver cells to compound it to glycerol to form triglycerides. These triglycerides accumulate, resulting in fatty liver." "Hepatocellular damage:Alcoholic Hepatitis - CORRECT ANSWER Alcoholic hepatitis is characterized by the inflammation of hepatocytes. Between 10% and 35% of heavy drinkers develop alcoholic hepatitis. This is called alcoholic steato necrosis and the inflammation appears to predispose to liver fibrosis. Inflammatory cytokines (TNF-alpha, IL6 and IL8) are thought to be essential in the initiation and perpetuation of liver injury by inducing apoptosis and necrosis. One possible mechanism for the increased activity of TNF-α is the increased intestinal permeability due to liver disease. This facilitates the absorption of the gut-produced endotoxin into the portal circulation. The Kupffer cells of the liver then phagocytose endotoxin, stimulating the release of TNF-α. TNF-α then triggers apoptotic pathways through the activation of caspases, resulting in cell death." "Hepatocellular damage:Cirrhosis - CORRECT ANSWER Cirrhosis is a late stage of serious liver disease marked by inflammation (swelling), fibrosis (cellular hardening) and damaged membranes preventing detoxification of chemicals in the body, ending in scarring and necrosis (cell death). Acetaldehyde may be responsible for alcohol-induced fibrosis by stimulating collagen deposition by hepatic stellate cells.[2] The production of oxidants derived from NADPH oxi- dase and/or cytochrome P-450 2E1 and the formation of acetaldehyde-protein adducts damage the cell membrane.[2] Symptoms include jaundice(yellowing), liver enlargement, and pain and tenderness from the structural changes in damaged liver architecture. Without total abstinence from alcohol use, cirrhosis will eventually lead to liver failure. Late complications of cirrhosis or liver failure include portal hypertension (high blood pressure in the portal vein due to the increased flow resistance through the damaged liver), coagulation disorders (due to impaired production of coagulation factors), ascites (heavy abdominal swelling due to buildup of fluids in the tissues) and other complications, including hepatic encephalopathy and the hepatorenal syndrome. Cirrhosis can also result from other causes than alcohol abuse, such as viral hepatitis and heavy exposure to toxins other than alcohol. The late stages of cirrhosis may look similar medically, regardless of cause. This phenomenon is termed the "final common pathway" for the disease. Fatty change and alcoholic hepatitis with abstinence can be reversible. The later stages of fibrosis and cirrhosis tend to be irreversible, but can usually be contained with abstinence for long periods of time." "Role of the hepatocytes - CORRECT ANSWER Role: liver cell, ketogenesis occurs in the mitochondria of the hepatocyte Clinical Implications: result of unavailability of glucose" "Role of the mitochondria - CORRECT ANSWER Role: Ketogenesis is the formation of ketone bodies and occurs mostly in the mitochondria of the hepatocytes (liver cells) Clinical Implications:- level of ketone bodies too high, pH drops = ketoacidosis (commonly seen in uncontrolled DM1 and alcoholics" "Triggers for ketogenesis - CORRECT ANSWER Role:lack of glucose Clinical Implications: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 - CORRECT ANSWER Role:processed by hepatocytes and undergoes transformation to 3 ketone bodies: Acetoacetate, Acetone and B-hydroxybutyrate (basis of ketoacidosis) Clinical Implications: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 - CORRECT ANSWER Role: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 which activates ketogenesis Clinical Implications:Oxaloacetate (an intermediate) is involved in: Citric acid cycle*gluconeogenesis*urea cycle*amino acid synthesis*fatty acid synthesis" "Gout - CORRECT ANSWER Etiology: over accumulation or under secretion of uric acid Clinical Manifestations:Use of diuretics bc they trigger kidneys to increase the absorption of uric acid. The liver may produce more uric acid if a diet high in red meat, cream sauces, or red wines bc they are high in purines. Pathophysiology:Increase in purine degradation which leads to increased amounts of uric acid. Uric acid is a byproduct of purine degradation, accumulation of uric acid not excreted by the kidneys lead to increased uric acid 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 - CORRECT ANSWER Etiology:acute, disease of skeletal muscles that results in muscle destruction Clinical Manifestations:trauma, hyperthermia, crush injuries, or severe dehydration. S/S dark, reddish brown urine, hypercalcemia, and renal failure Pathophysiology: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." "Tumor Marker:Alpha Fetoprotein - CORRECT ANSWER Origin:proteins secreted by liver and germ cell tumors" "Tumor Marker:Carcinoembryonic Antigen - CORRECT ANSWER Origin:GI, pancreas, lung, breast, ect" "Tumor Marker:Beta Human Chorionic gonadotropin - CORRECT ANSWER Origin:Germ cell" "Tumor Marker:Prostate Specific Antigen - CORRECT ANSWER Origin: Prostate" "Carcino- (prefix) - CORRECT ANSWER Definition:arise from epithelial tissue Ex:Adenocarcinoma: arising from ductal/glandular glands" "Sarco- (prefix) - CORRECT ANSWER Definition:connective tissue Ex:malignant cancers of the skeletal muscle are known as rhabdomyosarcomas" "-oma (suffix) - CORRECT ANSWER Benign tumors generally named according to the tissue from which they arise Ex:- benign tumor of fat cells is a lipoma- smooth muscle of uterus is leiomyoma" "Carcinoma in Situ - CORRECT ANSWER Definition:-preinvasive epithelial malignant tumors of glandular or squamous cell origin- localized to the epithelium- not yet malignant- 3 fates: can remain stable for long time, progress to invasive/met CA, or regress and disappear Ex:- # 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" "Lung - CORRECT ANSWER multiple organs, including brain- via portal vein, LV" "Colorectal - CORRECT ANSWER liver - via mesenteric lymphatics, portal venous system,lungs - via IVC, RV, PA" "Testicular - CORRECT ANSWER lungs, liver, brain- lymph to periaortic area to subclavian vein to RV" "Prostate - CORRECT ANSWER bones (especially lumbar spine), liver - regional lymph and veins which drain to batson plexus" "Breast Ca Metastasis sites - CORRECT ANSWER bones, lung, brain, liver- axillary, transpectoral and internal mammary lymph" "Head and Neck - CORRECT ANSWER lymphatics, liver, bones - direct extension" "Ovarian - CORRECT ANSWER peritoneal surfaces, diaphragm, omentum, liver- direct extension, peritoneal seeding, mesenteric veins" "Sarcoma - CORRECT ANSWER lungs- IVC, RV, PA" "Melanoma - CORRECT ANSWER in transit lymphatics, lung, liver, brain, GI tract- regional lymphatics" "Evaluate and describe the mechanisms of cancer metastasis and the implications for clinical practice. - CORRECT ANSWER Metastasis is the spread of cancer from the site of the original tumor to distant tissue. Metastasis contributes significantly to pain and suffering from cancer and is the major cause of death in cancer patients. Mechanisms important in local invasion include recruitment of macrophages and other cell types to the primary tumor, where they promote digestion of connective tissue capsules and other structural barriers by secreted proteases; changes in cell-to-cell adhesion, often by changes in the expression of cell adhesion molecules such as cadherins and integrins, making the cancer cell more slippery and mobile; and increased motility of individual tumor cells. The mechanism of capsular dissolution is unclear. To transition from local to distant metastasis, the cancer cell must also be able to invade local blood and lymphatic vessels, a task facilitated by stimulation of neoangiogenesis and lymphangiogenesis by factors such as VEGF. Finally, a successful metastatic cell must be able to survive in the circulation, attach in an appropriate new environment, and multiply to produce an entire new tumor." "Cancer cell metastasis usually involves the following 6 steps: - CORRECT ANSWER Local invasion: Cancer cells invade nearby normal tissue. Intravasation: Cancer cells invade and move through the walls of nearby lymph vessels or blood vessels. Circulation: Cancer cells move through the lymphatic system and the bloodstream to other parts of the body. Arrest and extravasation: Cancer cells arrest, or 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 (extravasation). Proliferation: Cancer cells multiply at the distant location to form small tumors known as micro metastases. Angiogenesis: 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." "Chemotactic Factors - CORRECT ANSWER released by mast cells; attract neutrophils, eosinophils and monocytes: all of which begin to perform phagocytosis" "Neutrophils - CORRECT ANSWER show up at site of injury in 6-8 hours" "Monocytes - CORRECT ANSWER show up at site of injury 1-7 days" "Complement - CORRECT ANSWER functions include bacterial lysis, vasodilation and increase vascular permeability, triggers mast cell degranulation, chemotaxis and opsonization" "Kinin - CORRECT ANSWER is turned into bradykinin which is responsible for pain, chemotaxis, and increases vascular permeability and vasodilation" "Coagulation Cascade - CORRECT ANSWER activates the kinin system. function of this system to to form a fibrin mesh to stop bleeding and trap microorganisms" "VII - CORRECT ANSWER Hageman factor, activates dinin system" "monocytes - CORRECT ANSWER become macrophages when they enter the tissue and are responsible for presenting antigens to the CD4 cell which triggers T cell immunity --> triggers B cell immunity" "cytokine IL1 - CORRECT ANSWER causes fever, activates phagocytes and lymphocytes and also increases release of IL 6" "cytokine IL6 - CORRECT ANSWER stimulates the production of acute phase reactants and promotes the growth and stimulation of blood cells" "TNF - CORRECT ANSWER can cause fever, increase the synthesis of proinflammatory proteins by the liver, causes muscle wasting and induces thrombosis" "growth factors - CORRECT ANSWER promote the production and maturation of neutrophils" "Type I - CORRECT ANSWER immediate hypersensitivity response to an environmental allergen" "Type I - CORRECT ANSWER allergies to food, medication, pollen, reaction time occurs in minutes to hours from exposure" "Type I - CORRECT ANSWER antibody IgE binds with allergen, then re-exposure to allergen causes mast cell to degranulate, release of histamine triggers inflammatory cascade" "Type I - CORRECT ANSWER hypersensitivity include environmental allergies, angioedema, and atopic disorders (genetic predisposition to hay fever, asthma)" "Type II - CORRECT ANSWER Antibody mediated cytotoxic hypersensitivity, mediated by antibodies directed against fixed antigens on the plasma membranes of the cells" "Type II - CORRECT ANSWER IgG & IgM activates compliment and forms the membrane attack complex (MAC) which causes cell lysis" "Graves - CORRECT ANSWER autoimmune type II hypersensitivity of thyroid, antibodies formed against the thyroid cells, causings increase secretion of thyroxine, hyperthyroidism" "Myasthenia Gravis - CORRECT ANSWER autoimmune type II hypersensitivity neuromuscular junction, inhibited acetylcholine, leads to muscle weakness and paralysis" "Guillain-Barre Syndrome - CORRECT ANSWER autoimmune type II hypersensitivity of peripheral nervous system, antibodies bind with myelin sheath of peripheral nervous system, demyelination with ascending paralysis" "Type II - CORRECT ANSWER blood transfusion and Rh incompatibility are examples of what type of hypersensitivities" "Type III - CORRECT ANSWER complex hypersensitivity, antigen-antibody complex formed and triggers immune and inflammatory response in vessel walls or tissue." "Type III - CORRECT ANSWER IgG & IgM immune and inflammatory response causes cellular and tissue damage, but is not specific to a cell or tissue, spread via circulation and generate more diffuse reaction" "Type III - CORRECT ANSWER autoimmune disease type hypersensitivity" "Rheurmatoid Arthritis - CORRECT ANSWER autoimmune disease that causes chronic inflammation of connective tissues" "Systemic Lupus Erythematosus - CORRECT ANSWER Type III chronic, multi-system, inflammatory disease, Primarily in women 20-40 Antibodies formed against DNA and nucleus Butterfly rash, photosensitivity" "Type IV - CORRECT ANSWER delayed hypersensitivity mediated by T-Cell Lymphocytes and does NOT require antibody participation, delayed reaction that occurs in 24-72 hours" "Influenza - CORRECT ANSWER Incubation 1-4 days, large particle droplet, RNA viruses of the family Orthomyxoviridae" "pneumocystis jiroveci pneumonia (PCP) - CORRECT ANSWER Infection in the lung starts with the multiplication of the organism in the alveoli. As infection progresses, alveoli fill with exudates, there is type 2 pneumocyte hyperplasia, and mononuclear cells infiltrate the lung. In patients with AIDS, there are larger numbers of Pneumocystis organisms in the lungs and fewer inflammatory cells than in patients with Pneumocystis pneumonia (PCP) who are HIV-negative." "mycobacterium avium complex (MAC) - CORRECT ANSWER -Acid fast bacteria, often found in the environment-soil, water, and animals -The cell wall contains long-chained glycolipids (that make the wall thick) protect these facultative intracellular bacteria from lysosomal attack -90% to 95% of diseases in AIDS patients" "cytomegalovirus (CMV) - CORRECT ANSWER infected cells are protected from both T-cells, and NK cell killing because it has down-regulated MHC expression Once the virus is in the cell -it can inhibit cellular DNA, RNA, or protein synthesis, disruption of lysosomal membranes, resulting in release of digestive lysosomal enzymes -Promotion of apoptosis -fuses infected cells to produce multinucleated giant cells -transformation of infected cells into cancerous cells causing unregulated growth. -alteration of the antigenic properties, causing the immune system to attack the cell as if it were foreign" "CD4 - CORRECT ANSWER main cell which recognizes antigens and triggers the immune response" "HIV - CORRECT ANSWER CD4 count= or >200 AND has not had an AIDS defining illness" "Bactrim - CORRECT ANSWER treatment for PCP pneumocystis Jiroveci pneumonia" "clarithromycin and ethambutol for 6-12 months - CORRECT ANSWER treatment for MAC disseminated mycobacterium avium complex" "no treatment - CORRECT ANSWER treatment for CMV retinitis, commonly CD4 <50" "COX1 - CORRECT ANSWER maintain gastric mucosa,fluid and electrolyte balance, and platelet aggregation" "COX2 - CORRECT ANSWER pathway function mainly in the inflammatory process and produce pain and fever" "Cations - CORRECT ANSWER Sodium Ammonium Hydrogen Magnesium Potassium Calcium" "Anion - CORRECT ANSWER Chloride Bicarbonate Proteins Phosphate" "inflammatory process - CORRECT ANSWER -foundational concept -target of inhibition for many medications and treatments -starts with cellular injury then triggers five initial steps" "First 5 steps of inflammatory process - CORRECT ANSWER -mast cell degranulation -activation of coagulation cascade -activation of kinin cascade -release of chemotactic factors -activation of complement cascade" "Complement Cascade Activated - CORRECT ANSWER -MAC-lysis of bacteria -C2b-increase vasodilation and vascular permeability -C3a/C5a/C4a-triggers mast cell degranulation -C5a-attracts neutrophils (chemotaxis) -C3b-enhances opsonization" "Kinin system activated - CORRECT ANSWER -turned in to bradykinin which is released and responsible for pain, chemotaxis, and increase vascular permeability and vasodilation" "Coagulation cascade activated - CORRECT ANSWER -has role in activating kinin and complement system -Factor XII (Hageman factor) activates kinin -ultimate function is to form fibrin mesh to stop bleeding and trap microorganisms" "Released chemotactic factors attract: - CORRECT ANSWER -neutrophils, eosinophils, and monocytes all of which begin to perform phagocytosis -will eventually die and rupture releasing their intracellular contents -triggers release of acute phase reactants" "When do neutrophils show at the injury site? - CORRECT ANSWER 6-8 hours" "When do monocytes show at the injury site? - CORRECT ANSWER 1-7 days" "Mast cell degranulation - CORRECT ANSWER -major step of inflammatory cascade and has effect on every other aspect -leads to activation of acute phase reactants -results in release of histamine, cytokines, leukotrienes, and prostaglandins" "acute phase reactants - CORRECT ANSWER -coagulation proteins -kinin -complement" "histamine - CORRECT ANSWER -responsible for vasodilation -increases vascular permeability -increases blood flow to injury causing erythema and swelling" "cytokines - CORRECT ANSWER -can react quickly or be delayed -IL4 released early -IL3 released later -TNF released early and late" "leukotrienes - CORRECT ANSWER -released when mast cell degranulates -known as slow reaction substances of anaphylaxis (SRS-A) -prolong inflammatory response -cause vasodilation -attract neutrophils, monocytes, and eosiniophils -target of inhibition for singulair" "prostaglandins - CORRECT ANSWER -released in mast cell degranulation -produced by arachidonic pathway -cause vasodilation, platelet aggregation at injury site, fever and pain" "monocytes additional functions - CORRECT ANSWER -become macrophages when they enter tissue -responsible for presenting antigens to CD4 cell which triggers T cell immunity -T cell immunity goes on the trigger B cell immunity" "monocytes release which cytokines - CORRECT ANSWER -IL1 -IL6 -TNF -growth factors" "IL1 - CORRECT ANSWER -causes fever -activates phagocytes and lymphocytes -increases release of IL6" "IL6 - CORRECT ANSWER -stimulates production of acute phase reactants -promotes growth and stimulation of blood cells" "TNF - CORRECT ANSWER -can cause fever -increases synthesis of proinflammatory proteins by the liver -causes muscle wasting -induces thrombosis" "growth factors - CORRECT ANSWER -promote the production and maturation of neutrophils" "Diseases with inflammation as pathophysiologic basis (not all inclusive) - CORRECT ANSWER -asthma -autoimmune diseases -lupus -rheumatoid arthritis -gout -atherosclerosis -cerebral edema -cirrhosis -hepatitis" "Inflammation - CORRECT ANSWER -can be acute or chronic -chronic more of pathological process than physiologic process -chronic causes permanent damage to