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Pathogenesis
Mechanism of development:
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Morphologic Changes
Structural changes induced in the cells and organs of the body
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Clinical Significance
Functional consequences of the morphological changes
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Gross/Histologic
Macroscopic/Microscopic
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Prognosis
Expected outcome
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Necropsy
study of cadavers
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Surgical Pathology
examination of tissues from living patients
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Cytopathology
study of individual cells
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Clinical Pathology
analysis of various specimens
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Forensic Pathology
medicolegal investigation into death
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Closed Biopsy
needle inserted into mass to obtain a bit of tissue
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Open Biopsy
incision made to obtain a larger mass of tissue
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Excisional Biopsy
mass or entire organ removed
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FNAC
- fine needle aspiration cytology
- - thin bore needle used to obtain a few cells
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Frozen Sections
done to get a rapid diagnosis while the patient is on the operating table
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Routine stains - Hematoxylin/Eosin
- hematoxylin - nuclei
- eosin - cytoplasm
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Fontanna-Mason Stain
melanin
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Prussion Blue
iron/hemosidrin
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Trichrome Stain/Reticulin
connective tissue
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Warthin Starry Silver
spirochetes (syphylis, Lyme disease)
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Acid Fast
-Zeihl Neelsen
-Fite Stain
- -mycobacterium tuberculosis
- -M leprae
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Gomori Methenamine Silver
fungi/pneumocystis carinii
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Periodic Acid Schiff (PAS)
- glycogen/mucin/fungi
- -for outlining tissue structures, basement membrane, capsules etc
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Wright Giemsa Stain
peripheral smears
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Leukocyte Alkaline Phosphatase Stain
differentiate CML from leukemoid rxn
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Tartarate Resistant Acid Phosphatase Stain
hairy cell leukemia
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Myeloperoxidase
myeloblasts
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Immunoperoxidase Stain
cytokeratin, vimentin, desmin, PSA
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Cytopathologic Stains
- May-Grunwald-Giemsa
- Papanicolaou (PAP)
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Hyperplasia
- increase in # of cells
- potential for developing cancer if not treated
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Hypertrophy
- increase in size of cells
- usually occurs w/hyperplasia
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Atrophy
decrease in size/function of cells
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Metaplasia
replacement of 1 cell type by another
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Dysplasia
disorderly growth
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Ex of Physiologic Hyperplasia/Hypertrophy
breast/uterus during pregnancy
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Ex of Pathologic Hyperplasia
high unopposed estrogen = endometrial hyperplasia***
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Labile cells
undergo hyperplasia
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Stable Cells
undergo hyperplasia/hypertrophy
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Permanent Cells
undergo hypertrophy only
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Causes of Atrophy (8)
disuse, denervation, reduced blood supply, indadequate nutrition, decreased hormonal stimulation, aging, occlusion of secretory ducts, pressure
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Lipofuscin
- indigestible yellow-brown material left behind after cell autophagy
- "wear and tear" pigment
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Agenesis
abscence of an organ due to failure to develop
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Aplasia
primordium is present but no further development
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Hypoplasia
incomplete or partial development
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Metaplasia
replacement of 1 adult cell type by another
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Squamous Metaplasia
- columnar cells in lung replaced by squamous in order to tolerate chronic cigarette smoke
- OFTEN REVERSIBLE***
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Glandular Metaplasia
- replacement of squamous by glandular epithelium
- ex - Barrett's esophagus
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Connective Tissue Metaplasia
- connective tissue in abnormal places
- ex - sesamoid bone in muscle
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Myeloid Metaplasia
- blood formation outside of bone marrow
- ex - spleen or liver
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Dysplasia
- disorderly growth/proliferation of cells
- change in size/shape/number
- loss of organization
- may progress to cancer if irritant is not removed
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Hypoxic Cell Injury
inadequate oxygenation of tissue
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Ischemia
decreased arterial flow to tissue
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Hypoxemia
decreased amt of O2 dissolved in plasma
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Anemia/CO Poisoning leads to...
decreased O2 carrying capacity of blood
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Consequences of Hypoxia
- decreased ATP production
- impaired Na-K ATPase = cellular swelling
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Consequences of ATP Depletion in Hypoxia
- switch to anaerobic glycolysis for ATP
- then depletion of glycogen
- then accumulation of lactic acid
- increased pH, denaturation of proteins, denatured enzymes, decreased protein synthesis, accumulation of lipid
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In Irreversible Cell Damage, Mt Damage Can Lead to...
- release of cytochrome C into cytosol
- (trigger for apoptosis)
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Ca2+ Role in Irreversible Cell Injury
enzyme activation - ATPase, phopholipase, proteased, endoculeases
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Pyknosis
shrinkage and darkening of the nucleus
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Karyorrhexis
fragmentation and breakdown of the nucleus
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Karyolysis
dissolution of the nucleus into "purple haze"
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Ischemia-Reperfusion Injury
- cessation of blood flow followed by its restoration
- may cause death of some cells via apoptosis
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How does reperfusion injury occur?
- increased generation of free radicals
- influx of Ca2+
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Free Radical Pathogenesis
- 1. lipid peroxidation of membranes = increased permeability
- 2. oxidative modification of proteins = protein fragmentation/degradation
- 3. rxns w/thymine, thymine dimers = single stranded breaks in DNA
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How is Tylenol converted to a free radical?
- cytochrome P-450 system in the liver
- this free radical then neutralized by glutathione leading to damage to hepatocyte
- FR damages hepatocyte cell membrane
- MCC OF FULMINANT HEPATIC NECROSIS DUE TO A DRUG
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Infarction
death of tissue due to blockage in blood supply
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atherosclerotic plaque - cholesterol crystals
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