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NURS 5315: ADV PATHO EXAM LATEST UPDATE - 2026 - 100+
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Dysplasia 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 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 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 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 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 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 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 accumulation of Ca in dead or dying tissues calcium salt clump and harden- interfere with cellular structure and function
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 Fat Necrosis breast, pancreas, abdominal structures- creates soaps Gangrenous Necrosis Dry- dark shriveled skin Wet- internal organs- can lead to death Gas- from clostridium- antitoxins and hyperbaric therapy Gout 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 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 Liver and germ cell tumors Carcinoembryonic Antigen GI, pancreas, lung, breast tumors Prostate Specific Antigen prostate tumors Carcino- from epithelial tissue- renal cell carcinoma Sarco- from connective tissue- chondrosarcoma Carcinoma in situ preinvasive epithelial malignant tumors of glandular or squamous cells- cervix Lung ca metastasis Multiple organs including brain Colorectal ca metastasis Liver, lungs Testicular ca metastasis Liver, lungs, brain Prostate ca metastasis Bones (especially lumbar spine), liver Head and neck ca metastasis
Osmosis Passive- the movement of water from an area of low concentration of solute to one of higher concentration Osmotic pressure Pulling- the amount of pressure or force that is exerted by solute molecules of a given compartment Hydrostatic pressure 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 Colloid pressure keeps water inside the compartment, attracts water from interstitial space back into the capillary- losses or diminished albumin Effective arterial blood volume The amount of blood within the arterial space- ECF changes will cause changes in the EABV in the same direction Renin Angiotensin Aldosterone System 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 ANP and BNP- released by heart- works opposite RAAS to decrease blood volume, promotes urinary excretion of Na and water Fluid volume deficit 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 Fluid intake exceeds body's needs C.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD, restlessness or anxiety Edema 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 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 from GI losses or diuretics C.M. Volume depletion, orthostatic hypotension, tachycardia, lack of organ perfusion hypervolemic hypernatremia administration of hypertonic saline C.M. volume overload, edema, chf, htn, pulmonary edema mild hyponatremia Na 125- 135 C.M. anorexia, apathy, restless, nausea, lethargy, muscle cramps
Exercise effect on K+ cellular ATP is diminished, opening K+ channels and allowing K+ to leave cell Kidneys effect on K+ excretion and absorption of K+ is regulated by tubule system magnesium and potassium mag inhibits the potassium channels, keeping balance. when mag is low, more K+ exits the call, and is excreted via the kidneys. metabolic acidosis 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 E. GI loss, diuretic use C.M. slow, shallow respirations, irritability, twitching, s/s of hypokalemia pH >7.4 HCO3 > respiratory acidosis E. cns depression, airway abnormalities C.M. restless, confused, seizures, tachycardia pH <7.4 PaCO2 > respiratory alkalosis E. usually anxiety, PE, chf, salicylate OD, illegal drugs C.M. light-headed, confused, tetany pH >7.4 PaCO2 <
Allele Paired genes on autosomal chromosomes Locus Position in which a gene occupies on a chromosome Phenotype Outward appearance of an individual Genotype A map of ones specific genes Polymorphic Two or more alleles which occur with an appreciable frequency in a population Homozygous Two dominant or recessive alleles Heterozygous When both a dominant and a recessive allele are present Dominant Trait seen in phenotype Recessive Trait not seen in phenotype Codominance Both alleles exhibit (blood type AB) Carrier Person who has a diseased gene but is phenotypically normal Autosomal chromosomes
ALT enzymes are found where?
- liver cells (L enzyme) Troponin enzymes are found where?
- cardiac cells Hypoxic Injury Pathophysiology 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 have unpaired electron in its outer shell, making molecule unstable and highly reactive. aka being oxidized Reactive Oxygen Species ROS Etiology byproduct of ATP production in the mitochondria Free Radical and Clinical Manafestations 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 can overwhelm mitochondria and exhaust intracellular antioxidants, causing cell injury/disease Free Radical and Pathophysiology
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 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 ETOH is metabolized to acetaldehyde in the cytoplasm of the cell, enzyme alcohol dehydrogenase (ADH) helps with conversion Ethanol Clinical Manafestations 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 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
- 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
spectrum of cell changes after the cell dies Infarct necrosis which results from sudden insufficiency of arterial blood flow 5 Types of Necrosis coagulative, liquefactive, caseous, fat, gangrenous Coagulative occurs in the kidneys, heart, and adrenal glands most commonly secondary to hypoxia (caused by protein denaturation, tissue firm and slightly swollen) Liquefactive nerve cell necrosis Caseous 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 necrosis breast, pancreas and other abdominal structures wet gangrene develops when neutrophils invade the site, causing liquefactive necrosis Gangrenous tissue death resulting from severe tissue hypoxia dry gangrene result of coagulative necrosis Role of the hepatocytes liver cell, ketogenesis occurs in the mitochondria of the hepatocyte
result of unavailability of glucose Role of the mitochondria Ketogenesis is the formation of ketone bodies and occurs mostly in the mitochondria of the hepatocytes (liver cells) Triggers for ketogenesis 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 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 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 over accumulation or under secretion of uric acid Gout Clinical Manifestations 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
arise from ductal or glandular structures Carcinoma in Situ
- 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 absence of differentiation
- blastoma (suffix) originates from precursor cells or blasts (immature or embryonic tissue). Ex: children, neuroblastoma, retinoblastoma Lung Sites of Metastasis multiple organs, including brain Colorectal Sites of Metastasis liver, lungs Testicular Sites of Metastasis lungs, liver, brain Prostate Sites of Metastasis bones (especially lumbar spine), liver Head and Neck Sites of Metastasis lymphatics, liver, bones Ovarian Sites of Metastasis peritoneal surfaces, diaphragm, omentum, liver
Sarcoma Sites of Metastasis lungs Melanoma Sites of Metastasis in transit lymphatics, lung, liver, brain, GI tract 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 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: Cancer cells multiply at the distant location to form small tumors known as micrometastases. 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. T: size or direct extent of the primary tumor
