General Path Flashcards
Disolution of Chromatin
Karyolysis
in apoptosis
nuclear fragmentation
karyohexis
Nuclear shrinkage
pyknosis
Initiation of Intrinsic apoptosis pathway
Growth factor withdrawl
exposure to injurious stimuli
Initiation of Extrinsic apoptosis path
Fas (CD95)
Cytotoxic T cell release perforin and granzyme B
Reperfusion type of necrosis
Red coagulative
Rolling receptors for Neutrophils and vascular tissue
Vascular–E and P selectin
leukocyte–Sialyl-Lewis
Tight bonding receptors for leukocyte
Vascular–ICAM-1
leukocyte–LFA-1 (integrin)
Diapedisis receptors for leukocytes
PECAM-1 for leukocytes and vascular tissue
Migration chemotactic signals for leukocytes
C5a
IL-8
LTB4
Kallikrein
“CILK”
Inflammatory phase of wound healing cells
plts., neutrophils, macrophages
Proliferative Phase of wound healing cells
fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages
Remodeling phase of wound healing cells
fibroblasts
Inflammatory phase of wound healing
clot formation
vessel permeability and neutrophil migration
Macs clear debris in 2 days
Proliferative Phase (2-3 days post injury)
Deposition of granulation tissue and collagen (type III) angiogenesis epithelial cell proliferation dissolution of clot wound retraction due to myofibroblasts
Remodeling phase (1 week post injury)
Type III collagen replaced by Type I
increased tensile strength of tissue
Granuloma formation mechanism
INF-gamma from TH1 cells activate macrophages
macrophages secrete TNF-alpha –> induce and maintain granuloma
Fluid with:
Hypocellular
Protein poor
Specific gravity < 1.012
Transudate
Due to increased hydrostatic pressure
decreased π
Na retention
Fluid with:
Hypercellular
Protein Rich
Specific Gravity > 1.020
Exudate
Due to :
Lymphatic obst.
Inflammation
increased permeability
Mechanism of cell death with Fe poisoning
Sx
Peroxidation of lipid membrane
Sx: GI bleed (acute)
Metabolic acidosis, scarring –> GI obstruction (Chronic)
ß pleated sheet structures deposition leading to cell death and apoptosis
Amyloidosis
Congo Red
Apple Green Birefringence
AL Amyloidosis (1º)
Ig Light Chains
plasma cell disorder associated with multiple myeloma
AA Amyloidosis (2º)
Fibrils composed of Amyloid A
RA
IBD
TB
Dialysis related Amyloidosis
ß2-microglobin
Carpal tunnel Syndrome, joint pain
Heritable Amyloidosis
Transthyretin (TTR or prealbumin) gene mutation
ATTR–neurologic/cardiac amyloidosis
Age Related Amyloidosis
Depostion of normal TTR in myocardium (other sites too)
Slower progression than AL
Organ Specific Amyloidosis
Deposition in specific organ
Most important–Alzheimer’s Disease
ß-amyloid protein
Neoplastic progression
Normal –> Hyperplasia –> CA in situ –> Invasion –> Metastasis
how do tumors invade basement membrane
collegenases and hydrolases
Loss of size, shape, orientation of cell
dysplasia
Increase in # of cells
hyperplasia
Increase in size of cells
hypertrophy
One adult cell type replaced by another
metaplasia
abnormal cells lacking differentiation
anaplasia
clonal proliferation fo cells taht is uncontrolled and excessive
neoplasia
Fibrous tissue formation in response to neoplasm
desmoplasia
Prognostic predictor of tumor
stage
degree of localization/spread
Degreee of cellular differentiation
Tumor Grade
Benign tumor of epithelium
Adenoma
Papilloma
Malignant tumor of Epithelium
adenocarcinoma
papillary carcinoma