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Divisions of pathology:
General pathology reactions of cells and tissues to abnormal stimuli and to
inherited defects
Systemic pathology alterations in specialized organs and tissues that are
responsible for disorders involving the organ
Four Aspects of a disease
1. Etiology
a. Genetic
b. Acquired
c. Idiopathic
d. Iatrogenic unintended or unwanted medical treatment
2. Pathogenesis
3. Molecular and morphological changes
4. Clinical manifestations
a. Signs observed manifestations
b. Symptoms subjective feelings of abnormality
c. Sequelae disease produces a subsequent pathologic condition
d. Complication new or separate process that may arise
History
Hippocrates father of medicine; first to deal with the anatomy and
pathology of the human spine
Benivieni pioneered autopsy
Leeuwenhoek father of microscopy
Virchow father of modern pathology
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ADAPTATIO
Atrophy
Ubiquitin-proteosome pathway
Hypertrophy
Myocardial hypertrophy
Athletes heart mechanical stimuli IGF-1 (IGF1R)
PI3K hypertrophy
Diseased myocardium wall stress Ang II, ET-1
transcription of hypertrophic gene
Hyperplasia
Precursor for malignancies
Metaplasia
Reprogramming of stem cells or of undifferentiated
mesenchymal stem cells
Precursor for malignancies
Intracellular accumulation of various substances
Normal cellular constituents fat, water, protein
Abnormal substances exogenous or endogenous by-products
DESCRIPTION
PHYSIOLOGIC
PATHOLOGIC
Atrophy
Reduction of cell
size and number
Involution
related
irreversible
Hypertrophy
Hyperplasia
Increase
number
Metaplasia
Replacement of one
cell type by another
INTRACELLUL
DESCRIPTION
IDENTIFICATION
Disuse, denervation,
lack
of
trophic
hormones, ischemia,
malnutrition
Cardiac
hypertrophy
(box-shaped nucleus),
chronic alcoholism
endometrial
hyperplasia,
HPVinduced
lesions,
adenomatous
hyperplasia
in
pulmonary epithelium
Squamous metaplasia
Respiratory
epithelium, cervix
Barretts metaplasia
squamous
to
columnar w/ goblet
cells
SEEN IN
Accumulation of
Oil-Red O or Sudan IV
in
cell
ageand
AR
ACCUMULATI
ONS
Steatosis
Cholesterol
and
cholesterol
esters
Proteins
Keratin
(Mallory
body)
Neurofilame
nts
Hyaline
change
Glycogen
Exogenous
pigments
Endogenous
pigments
triglycerides
Accumulation of
cholesterol laden
macrophages
(orange red)
Foam cells
Defect in protein
folding or transport
Eosinophilic
vacuoles,
aggregates
Accumulation of
keratin inside
hepatocytes
Thickened coarse
filaments
resembling braids
which is a sign of
cytoskeletal lesion
Intracellular:
Russel bodies in
plasma cells
indicative of
myeloma or chronic
inflammatory state
Extracellular
Diabetic
glomerulosclerosis
Lack of enzyme
Tattoo
Coal dust/carbon
anthracosis
Dental amalgam
Hematogenous
Hemosiderin
Hematoma
Tyrosine derived
melanin
Lipofuscin - Cells
undergoing slow,
regressive changes
droplets,
or
Cholesterolosis,
chronic cholecystitis,
skin xanthoma,
atherosclerosis
Severe proteinuria,
emphysema
Alcoholic liver disease
H&E:
homogenous
glassy pink
Plasma cells
Kidney
Hemosiderin pigment
iron-rich brown
Lipid-rich
pigment
brown
Nuclear changes
Pyknosis condensation of chromatin
Karyolysis lysis of chromatin
Karyorrhexis fragmentation of nuclear material
o Mitochondria
rupture of double membrane
fragmentation
myelin figures concentric whorls of membranes derived from
damaged cytoplasmic organelles. Prominent in Tay-Sachs and
other inborn errors of metabolism damaging the cytoplasmic
membranes
calcifications
Dx signs
o Release of cytoplasmic enzymes into the blood
CK cardiac or skeletal muscle injury
AST and ALT liver cells
LDH ruptured RBC and other cells
o
Cell death
Apoptosis
Cell death based on sequential activation of death genes and suicide pathway
enzymes
Aka programmed cell death
How is it initiated?
o Extrinsic pathway
Via death receptors such as TNF or Fas ligand
o Intrinsic mitochondrial pathway
Initiated by an increased permeability of mitochondria release
proaptotic molecules such as cytochrome act on initiator
caspases
o Initial signal from membrane or mitochondria initiator caspases
activated execution caspase activated act on enzymes leading to
fragmentation into membrane bound apoptotic bodies phagocytized
by neighboring cells or macrophages
Morphologic and biochemical changes
o Cell shrinkage (vs swelling in necrosis)
o Does not illicit inflammatory reaction
Example:
o Parkinsons disease
o Apoptosis of limb bud to form hands
Cellular aging
Progressive decline in cellular function and viability caused by genetic
abnormalities and accumulation of cellular and molecular damage due to the
effects of exposure to exogenous influences
Mechanisms of cell aging
o Telomere shortening
o Environmental insults
o DNA repair defects
o Abnormal growth