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Gen Path Intro

Gen Path Intro

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Published by: julo_05 on Jun 11, 2010
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Introduction to

Ma. Minda Luz M. Manuguid, M.D.

definition of Terms

‡Pathology ² pathos ± suffering; disease
logos ± study; knowledge - branch of medicine concerned with determining the nature & course of diseases by analyzing body tissues & fluids - study of diseases

‡ General vs. Systemic/Special: Systemic/Special:  General Pathology ² disease mechanisms ± may be common to several diseases  Systemic/Special Pathology ² genetic, cellular, molecular manifestations of specific diseases ‡ Anatomic/Surgical vs. Clinical  Anatomic/Surgical Pathology ² Autopsy; Biopsy; Cytopathology  Clinical Pathology ² Hematology & Blood Banking; Clinical Chemistry; Clinical Microscopy; Serology; Microbiology 

Forensic Pathology ² medicolegal investigations Cardiovascular Pathology

‡ Autopsy/Necropsy ² medical examination of a
dead human body, to determine cause of death, diagnosis, or disease progression ‡ Biopsy ² bio - µlife¶ ; opsis - µa viewing¶ ± the removal of a sample of tissue from a living person for laboratory examination; primarily for the detection of Cancer 
Excision biopsy Incision biopsy Fine needle aspiration biopsy (FNAB) Frozen section biopsy

‡Exfoliative Cytopathology ² microscopic
examination of cells in body tissues or body fluids primarily to determine if they are cancerous; uses the Papanicolaou method of staining, hence the term µPap¶ smear µPap¶

‡Clinical Microscopy ‡Hematology & Blood Banking ‡Serology & Immunology ‡Microbiology/Bacteriology ‡Clinical Chemistry

Four Aspects of a Disease 
Etiology ² cause /causes of the disease Pathogenesis ² development of the disease; chronologic progression of pathologic changes Morphologic changes - ´ signs µ ² anatomic / histologic changes; objective; can be seen or measured Functional derangements/Clinical significance ´symptomsµ ² subjective; what a patient feels; limitations on patients· normal activities; prognosis

Cellular Pathology: Cellular Adaptation Cellular Injury & Cell Death

Ma. Minda Luz M. Manuguid, M.D.

Cellular Adaptation; Cellular Injury; Cell Death
Normal Cell
Cellular--------------------Reversible---------------Cell Cellular--------------------Reversible---------------Cell Death Adaptation Injury 

Atrophy Hypertrophy Hyperplasia Metaplasia

Fatty Change Cloudy swelling

Necrosis Apoptosis

The Cell Cycle 
Labile cells ² cells that  
never leave the cell cycle; retain their mitotic ability Permanent cells ² cells that leave the cell cycle permanently; no mitotic ability Stable cells ² cells that have temporarily left the cell cycle; mitotic ability is retained but quiescent, may occur when needed




Cellular Adaptation 
Hyperplasia ² increase in number of cells through
cell division 

Hypertrophy ² increase in cell size due to
increase in cellular components Atrophy ² decrease in cell size due to reduction in cell components; associated with increased autophagic vacuoles & lipofuscin pigment Metaplasia ² change from one adult cell type to another due to chronic irritation; always pathologic

Cellular Adaptation
(cystic) hyperplasia


(squamous) metaplasia


Cellular Injury: Injury: General Considerations 
The structural & biochemical elements of the cell are so closely inter-related that whatever the precise point interof initial attack, injury at one locus leads to widewideranging secondary effects  Morphologic changes become apparent only when some critical biochemical system has been deranged  Reactions of the cell to injurious stimuli depend on the type, duration, & severity of injury, as well as on the type, state, & adaptability of the cell

Causes of Cellular Injury

Cellular Components/Processes most vulnerable to Injury 
Cell membrane ² Selective permeability  Mitochondria ² Aerobic respiration /
Oxidative phosphorylation  Ribosomes / Rough Endoplasmic reticulum ² Protein synthesis 

Nuclear chromatin ² Genetic material /
DNA ± control of cellular activities

Common Biochemical themes in Cellular Injury 
ATP depletion & defects in Membrane permeability  intracellular Calcium & loss of Calcium homeostasis  Oxygen & production of OxygenOxygenderived free radicals

Free Radicals  


definition ± chemical species that have a single unpaired electron in an outer orbital; extremely reactive & unstable, can react with organic or inorganic chemicals, esp. cell membranes & nucleic acids Hydroxyl OH¯; Hydrogen peroxide H2O2; Superoxide OH¯; O2¯; Nitric oxide NO actions ± lipid peroxidation of cell membranes; denaturation of proteins; DNA mutation neutralized by Anti-oxidants (vit E, vit C, sulfhydrilAnti(vit sulfhydrilcontaining compounds Cysteine, Glutathione-GSH, GlutathioneAlbumin, Ceruloplasmin, Transferrin, Superoxide dismutase, GSH peroxidase) peroxidase)

Reversible Cellular Injury 
Fatty change ²
replacement of parenchymal cells by lipid dropletsdroplets- most commonly seen in the liver 

Cloudy swelling ²
accumulation of water within cells - most commonly seen in renal ³ground tubular cells: glass´ glass´ or ³cloudy´ cloudy´ histologic appearance

Irreversible Cellular Injury / Cell Death 
changes that occur in the irreversibly injured cell denaturation of proteins & subsequent enzymatic digestion; digestion; always pathologic; involves a group of cells; accompanied by inflammation 

³falling off´off´ chromatin condensation & subsequent fragmentation of the dead cell into ³apoptotic bodies´; bodies´; physiologic or pathologic; may occur in a single cell; no inflammation

Patterns of Necrosis 
Coagulative/Coagulation ± cell shape is
preserved; denaturation of cellular proteins; cells´ ³tombstone cells´ Liquefactive/Liquefaction ± amorphous necrotic debris due to hydrolytic enzymatic dissolution; typical of brain injury; abscess Caseous/ Caseation ± coagulation, then incomplete dissolution; typical of TB Gangrenous/Gangrene ± coagulation + bacterial contamination (varying degrees of liquefaction): wet or dry - diabetic wounds Fat Necrosis : Traumatic ± breast; subcutaneous fat; Enzymatic ± pancreatitis

Coagulative Necrosis /Liquefactive Necrosis

Caseation Necrosis

Gangrenous Necrosis

Traumatic & Enzymatic Fat Necrosis

Physiologic :   

programmed destruction of cells during embryogenesis & organogenesis; ³developmental involution´; ³programmed cell death´ in adults, hormone-dependent involution e.g. menopause, hormonepostpost-partum, thymic involution cell deletion in proliferating cell populations e.g. epithelial renewal cell death in tumors; cell death in viral injury death of immune cells; cytotoxic T-cell action Tpathologic atrophy of hormone-dependent tissues hormonein parenchymal organs due to duct obstruction 

Pathologic : 


Councilman bodies in Hepatitis

Pathologic Calcification : deposition of

Calcium salts + smaller amounts of Fe, Mg, & other mineral salts 

Dystrophic ² in dead or  Metastatic ² in vital or viable dying tissues, regardless of tissues when there is Ca levels, in the absence of hypercalcemia, almost always abnormal Ca metabolism with some derangement of Ca metabolism  atheromas  


aging/damaged heart valves myocardial infarcts tuberculomas psammoma bodies  

usually in interstitial tissues of blood vessels, kidneys, lungs, gastric mucosa hyperCa: hyperparathyroidism hyperthyroidism, systemic sarcoidosis, vit D intoxication Addison¶s dse, metastatic tumors, bone tumors, MM

Pathologic Calcification 
gross: fine white granules or clumps felt as gritty gross: deposits; ´crumbled chalkµ appearance  microscopic: H & E : basophilic amorphous granular microscopic: or clumped deposits, intra- or extra- cellular; intra- extrapsammoma bodies ² lamellated circular Ca deposits ² seen in papillary tumors

Pathologic Calcification 
Dystrophic calcification ²
deposition of Calcium in dead or dying tissues 

Metastatic calcification ²
deposition of Calcium in viable tissues - due to hypercalcemia

Intracellular Accumulations 
intranuclear or cytoplasmic  normal cellular constituent or abnormal substance  endogenous or exogenous abnormal substance  may be a pigment (endogenous or exogenous)  may be an infectious product  accumulation may be due to overproduction, inadequate metabolism & excretion, or both

Intracellular Accumulations 
Lipids ² accumulation of Triglycerides within parenchymal cells 

Fatty Liver of Alcoholism, Kwashiorkor, DM, Obesity, Anoxia & Toxins may also occur in the Heart, Muscles, Kidneys 

Proteins ² usually as rounded eosinophilic droplets, vacuoles, masses 

Hyaline droplets in kidneys(PCT) in dses with proteinuria Russell bodies ± excess Igs in plasma cells Glycogen storage disorders Lipofuscin, Hematin, Melanin, homogentisic acid, 




Heterophagy ± ingestion of outside material by endocytosis Autophagy ± intracellular material (e.g. senescent organelles) is sequestered into autophagic vacuoles Residual bodies ± lysosomes with undigested debris Lipofuscin ± yellow-brown pigment granules that represent yellowundigested material from intracellular lipid peroxidation Barbiturates, Steroids, Carcinogenic hydrocarbons, insecticides, Alcohol, CCl4 

Smooth ER induction (Hypertrophy) ² for detoxification fn 

Mitochondria : alterations in size, shape, number 

Megamitochondria ± very large due to increased metabolic demands e.g. in alcoholic hepatitis, nutritional deficiencies Mitochondrial myopathies - in number, + abnormal cristae & crystalloids seen in skeletal muscle disorders increase in size & number ± in Oncocytomas of the salivary glands, thyroids, parathyroids, kidneys defects in cell locomotion & intracellular organelle movements e.g. Chediak-Hegashi syndrome; immotile cilia Chediaksyndrome accumulation of microtubules & intermediate filaments e.g. neurofibrillary tangles in Alzheimer¶s disease 


Thank you & Good Day !

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