Altered Cells and Tissue Biology Study Guide PDF

Summary

This document is a study guide on altered cells and tissue biology. It covers various topics such as pathogenesis, pathophysiology, diagnosis, and different types of cell injuries and necrosis. The guide provides a comprehensive overview of the subject matter.

Full Transcript

Altered Cells and Tissue Biology ​ Pathogenesis: beginning of suffering, steps in development of disease ○​ Ex: atherosclerosis to myocardial infarction ​ Pathophysiology: functional changes from syndrome/disease ○​ To understand that leads to the end result ​ Diagnosis: way...

Altered Cells and Tissue Biology ​ Pathogenesis: beginning of suffering, steps in development of disease ○​ Ex: atherosclerosis to myocardial infarction ​ Pathophysiology: functional changes from syndrome/disease ○​ To understand that leads to the end result ​ Diagnosis: way to label/pin disease to patient, sum of signs and symptoms ○​ Signs: objective ○​ Symptoms: subjective ​ Etiology: cause/origin of risk factors ○​ Risk factors: may or may not lead to disease occurring ​ Ex: smoking leading to hypertension ​ Idiopathic: unknown mechanism/cause of disease ​ Iatrogenic: unwanted event, human error causes the disease ○​ Ex: perforating bowel ​ Predisposing factors: tendency to promote disease ○​ Ex: having diabetes increasing likelihood of hypertension ​ Prophylaxis: prevention, to maintain/prevent health ​ Insidious: slow/gradual onset, vague symptoms ​ Subclinical: disease present, not showing signs/symptoms ​ Manifestation: evidence of disease ​ Lesion: specific local changes changes to tissue ​ Sequelae: unwanted outcome (adverse effect) ​ Cellular Responses ○​ Hemostasis: constant internal environment, equilibrium ​ When broken, diseases sets in ○​ Stressors lead to adaptations lead to return to hemostasis ○​ Stressors exceeds adaptive abilities leads to cell injury leads to cell death ​ Cellular Injury ○​ Unable to maintain homeostasis, reversible=cell recovers, irreversible=cell deaths ○​ Hypoxia: reduced oxygen in tissue cell ○​ Ischemia: insufficient blood flow to tissue ​ Most common cause of hypoxia ○​ Infarct: cell death from ischemia ○​ Necrosis: cell death from any cause, pathogenic ○​ Apoptosis: programmed cell death ○​ Other causes of cell injury ​ ATP depletion, ROS, calcium entry, mitochondrial damage, membrane damage, protein misfolding/DNA damage ​ Manifestations ○​ Intracellular accumulations ​ Can be systemic, sign of cell injury and can lead to cell death ​ Adaptations: reversible changes, response to a triggering mechanism ○​ Atrophy: lack growth, small cells ​ Lack of nutrition ​ Loss of intracellular substances/wasting away ​ Save energy, if not in use=no resources ​ Causes: Denervation, Loss of Function, Age, Lack of Growth Hormone ○​ Hypertrophy: increase in cellular size without increasing number of cells ​ Myometrium(uterus) ​ Cardiac Muscles ○​ Hyperplasia: Increase in the number of cells ​ Physiological: Endometrium(uterus), Mammary glands ​ Pathological: excess hormone, virus ○​ Metaplasia: reversible, replacing adult tissue type with another better suited for the changes, changes DNA=increase risk for mutation=increased risk of malignancy ​ GERD (gastroesophageal reflux disease) ​ Smoking ○​ Dysplasia: abnormal/not true adaptation, abnormal growth in size/shape/organization, leads to cancer ​ Low Grade: appearance still resembles parent cell ​ High Grade: cells look nothing like parent cells, carcinoma in situ/cancer on site ​ Necrosis: pathologic irreversible cell death, ruptures cell membrane, cellular content ruptures into interstitial space, causes inflammation and pain ○​ Coagulative Necrosis: denatures/breaks down proteins, becomes round and creates barriers, prevents further cell deaths ​ Occurs in most organs, especially those in the circulatory system (heart, spleen) ○​ Liquefactive Necrosis: in the brain, no connective tissue so it enzymes liquify tissue ​ Occurs in the brain and spinal cord ○​ Caseous Necrosis: cheese like, both coagulative and liquefactive, TUBERCULOSIS ○​ Fat Necrosis: PANCREAS injury, release of pancreatic lipase leads to breakdown of fat, opaque/chalky white ○​ Gangrenous Necrosis: necrosis superimposed by CLOSTRIDIUM PERFRINGIS ​ Apoptosis: active process, programmed cell death, no inflammation occurs, con be physiological or pathological, intrinsic or extrinsic

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