Pathology I Flashcards
What is the major cause of cellular damage
Free radicals
- radiation
- hypoxia/ ischmia
- Toxins
- Inflammatory mediators
- Iron propagated free radicals
- Degraded by catalase, superoxide dismutase, glutathione,
Reversible cell injury
Mild ATN
Toxic live injury
Severe exercise
irreversible cell injury
holes in cell membrane Long Ca++ influx Mitochondrial loss apoptosis necrosis Mixed
Apoptosis
energy requiring programmed cell death Often normal phenomenon No inflamation. happens in -normal embryology -normal cell turnover -viral infection -cell damage(DNA, unfolded proteins) -Immunologically mediated -hormone withdrawal
Bcl-2
stabilize mitochondria
Bax
destabilizes mitochondria
Caspase cascade
Caspase 8 and 9 leads to caspase 3 cleavage leading to apoptosis.
Too much apoptosis
neurodegenerative disease Ischemic diseases ( MI, stroke)
Too little apoptosis
Neoplasms (p53 mutations very common) (cascases) (cell that should have killed itself, did not) Viral infectins (immune induced apoptosis)
Necrosis
Uncoordinated cell death. cell membrane disrupition. ATP depletion cells often swollen(loss of ion pump) cell content leak causing acute inflammation.
Gangrene
Necrosis of whole anatomical area
Coagulative necrosis
schemia, makes infarct
Liquefactive necrosis
loss of substance in brain or abscess. empty space
Fat necrosis
necrosis in fat
caseous necrosis
necrotizing granulomas. combination of liq and coagulative
Gangrenous necrosis
Necrosis of whole anatomic area
Fatty liver
Alcohol, obesity, starvation, toxins
abnormal glycogen accumulation
In liver in diabetes.
glycogen storage disease
certain tumors
abonormal lipid storage
Lipid storage disease Fabry’s, Gaucher.
In vessels atherosclerosis.
lipofuscin
degraded lipid in lysosomes
Bilirubin
hemoglobin breakdown product.
color seen with hyperbilirubinemia
homosiderin
hereditary iron storage disease.
get more free radical damage from excessive iron storage.
abnormal protein storage, intracellular
alpha 1 antitrypsin deficiency; liver
Russell bodies in plasma cells
Russell bodies in plasma cells
large deposit of immunoglobulin in plasma cell cytoplasm..
blue due to ribosomal RNA
abnormal protein storage, extracellular
Amyloid
Anthracosis
Carbon pigment, mostly in lungs
Calcification
hydroxyapatite
Metastatic calcification
Into normal tissue, disordered calcium metabolism.
renal failure
hyperparathyrodism
malignancy
Acute inflammation
Begins almost immediately
PMS, vessels, mast cells
Chronic inflamation
Begins 1 or more days later
Lymphoxytes, macrophages, +- plasma cells
Fever
can have vasodilation of vasoconstriction
shivering and chills, sweating,
Exudate
fluid rich in proteins (Ig, clotting factors, complement)
high specific gravity
Leukocytosis with neutrophilia
acute inflammation
bacterial infection
leukocytosis with lymphocytosis
chronic inflamation
viral infection
Continually dividing/labile
Bone marrow, epidermis, GI tract
Quiscent/Stable
Liver, renal tubules, smooth muscle, fibroblasts
nondividing/permanent
neurons, cardiac muscle
pluripotent stem cells
can make any tissue
Multipotent stem cells
can make some tissues. (hemato
Collagen I
Most abundant in CT
Collagen II
cartilage
Collagen III
in soft tissue, early wound healing
Collagen IV
basement membranes
Collagen VII
anchoring fibrils to epidermis
Collagen stain
Trichrome stain
CAMS
Cell Adhesion Molecules
transmembrane molecules inducing adherence to other cells or matrix, also cell sig
Selectins
margination of leukocytes
Integrins
adhesion to cells and matrix
Cadherins
bind extracellular matrix to cytoskeleton. regulates proliferation.
Main cell types in tissue healing
Macrophages,
platelets,
lymphocytes, fibroblasts, endothelial cells, epithelial cells
