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NUR 2063 Essentials of Pathophysiology Final Exam Review Study Guide 1. Cirrhosis (end stage liver disease) - irreversible end-stage of many different hepatic injuries Alcoholism, acute hepatitis, toxic hepatitis (taking too much Tylenol), and liver is fi
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NUR 2063 Essentials of Pathophysiology
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NUR 2063 Essentials Of Pathophysiology
NUR 2063 Essentials of Pathophysiology Final Exam Review Study Guide 1. Cirrhosis (end stage liver disease) - irreversible end-stage of many different hepatic injuries Alcoholism, acute hepatitis, toxic hepatitis (taking too much Tylenol), and liver is fibrotic and scarred 2. What is another name f...
nur 2063 essentials of pathophysiology final exam review study guide 1 cirrhosis end stage liver disease irreversible end stage of many different hepatic injuries alcoholism
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NUR 2063 / NUR2063: Essentials of Pathophysiology
Final Exam Review Study Guide (Latest 2020)
Rasmussen
Pathophysiology Final Study Guide
Patho Section 1
Cell & Tissue Function/Dysfunction
Atrophy: decrease in size of cells.
Hypertrophy: increase in cell size.
Hyperplasia: increase in number of cells.
Metaplasia: mature cell type is replaced by a different mature cell type.
Dysplasia: cells vary in size & shape within a tissue.
Anaplasia: undifferentiated cells with variable nuclear & cell structure.
Neoplasm: tumor.
Cell Damage
Ischemia: oxygen deficit due to respiratory or circulatory problems.
Hypoxia: reduced oxygen in tissue.
Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular Na.
Temperature: inactivation of some enzymes, damages organelles, protein coagulation,
disruption of cell membrane.
Micro-organisms
Abnormal Metabolites: caused by genetic disorders or altered metabolism.
Nutritional Deficits
Cell Death
Apoptosis:programmed cell death controlled by genetics.
Necrosis:lysis of a cell, cell components leak into blood.
Liquification:dead cells liquefy due to release of enzymes.
Coagulation:cell proteins are altered or denatured causing coagulation.
Caseous:form of coagulation necrosis, thick, yellowish, cheesy.
Fat: fatty tissue is broken down into fatty acids.
Tissue Damage from Chemicals
Exogenous: from environment.
Endogenous: from inside the body,
Tissue Damage from Physical Agents
Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic shock ↓ blood
pressure.
Hyperthermia: causes general vasodilatation, decrease in circulating blood
volume.
Radiation: primarily affects actively dividing cells
Biological Agents
Insects/Animals: direct injection of toxin, transmission of infectious agent,
allergic reaction to insect proteins.
Food Poisoning
Normal Defenses of the Body
1st Line Defense
,NUR 2063 / NUR2063: Essentials of Pathophysiology
Final Exam Review Study Guide (Latest 2020)
Rasmussen
Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots.
Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat.
2nd Line Defense-non-specific
, NUR 2063 / NUR2063: Essentials of Pathophysiology
Final Exam Review Study Guide (Latest 2020)
Rasmussen
Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat.
Inflammation: automatic response to cell injury.
3rd Line Defense-specific defense produced by
Antibodies
Cell Mediated Immunity
Cellular Defenses
Mast Cells: located in tissue & release histamine & bradykinin.
Macrophages: monocytes that enter tissue & act as phagocytes.
Interferons: small proteins made by lymphocytes to prevent virus replication.
White Blood Cells
Granulocytes
Neutrophils: work by phagocytosis.
Basophils: release histamine leading to inflammation.
Eosinophils:combat the effects of histamine.
Agranulocytes
Monocytes:can enter tissue to become macrophages which
function as phagocyte.
Lymphocytes: B & T
Acute Inflammation
Vascular Response: vasodilatation & increased capillary permeability.
Cellular Response: migration of inflammatory cells through chemotaxis to injury site to
destroy ineffective organism, remove damaged cells, released inflammation mediators.
Exudate
Serous: watery, mostly fluids, some proteins and WBC’s.
Fibrinous: thick, sticky, high fibrin content.
Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms.
Abscess: Pocket of purulent exudates or pus in a solid tissue.
Local Effects of Inflammation-Cardinal Signs of Inflammation
Redness & Warmth: due to increased blood flow to area.
Swelling: shift of protein & fluid into interstitial space.
Pain: pressure on free nerve endings, chemical mediators irritate nerves.
Loss of Function: edema may restrict movement.
Systemic Effects of Inflammation
Mild Fever: due to resetting of hypothalamic thermoregulatory set point, release of
endogenous pyrogens.
Malaise
Fatigue
Headache
Anorexia
Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of
leukocytes & mast cells.
Types of Healing
, NUR 2063 / NUR2063: Essentials of Pathophysiology
Final Exam Review Study Guide (Latest 2020)
Rasmussen
Resolution: minimal tissue damage, cells can repair themselves.
Regeneration: damaged tissue is replaced by identical tissue.
Replacement: functional tissue replaced by scar or fibrous tissue.
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