Pathology Flashcards
eosinophilic cytoplasm and basophilic nucleus
apoptotic cell
DNA laddering
fragments in multiples of 180 base pairs
signals apoptosis
karyorrhexis
fragmentation of internucleosomal regions
signals apoptosis
types of apoptosis
intrinsic (mt) and extrinsic
BAX/BAK and Bcl-2
intrinsic proapoptotic and antiapoptotic
APAF-1 pathway
cytochrome C - caspase 9 - cascade to apoptosis
Bcl-2 binds
cytochrome C
Fas is
CD95 causing extrinsic apoptosis
increased cytoplasmic binding of acidophilic dyes
coagulation necrosis
when do you see coagulation necrosis?
ischemia
when do you see liquefactive necrosis?
bacterial abscess, brain infarct
when do you see caseous necrosis?
TB, fungi
fragmented cells and debris surrounded by lymphocytes and mpgs
caseous necrosis
when do you see fat necrosis?
acute pancreatitis, trauma
dark blue H&E staining cells, outlines of cells
fat necrosis
when do you see fibrinoid necrosis?
vessel immune reactions
what are the types of gangrene? and the types of necrosis?
dry - ischemia - coagulative
wet - superinfection - liquefaction superimposed on coagulative
where in the colon is vulnerable to ischemia?
splenic flexure, rectum
where in the kidney is vulnerable to ischemia?
straight segment of proximal tubule, thick ascending limb
both in the medulla
what cells in the brain are most vulnerable to ischemia?
purkinje cells in cerebellum
pyramidal cells of hippocampus and neocortex
what do red infarcts suggest?
reperfusion injury from free radicals
chromatolysis
neuronal cell body reaction to axonal injury
increased protein synthesis
dystrophic calcification
Ca deposits in abnormal tissues from injury/necrosis
metastatic calcification
widespread Ca deposits in normal tissue secondary to hypercalcemia
What are the factors released in extravasation?
selections, Gly-CAM, CD34 ICAM, VCAM PECAM C5a, IL-8, LTB4, kallikrein, PAF selection GIVs People chances
scar strength
70-80% of original, after 3 months
hypertrophic scarring
parallel collagen, on original boarders of wound
vascular remodeling, smooth muscle migration, fibroblast stimulation
PDGF
angiogenesis
FGF, VEGF, TGF-B
cell growth via tyrosine kinase
EGF
angiogenesis, fibrosis, cell cycle arrest
TGF-B
tissue remodelling
metalloproteinases
wound healing collagen
wound remodelling collagen
type III
then replaced by type I
what is found in granulomatous disease?
IFN-gamma from Th1 cells, TNF-a from mpgs
bacteria causing granulomas
mycobacteria, bartonella, listeria, treponema
fluid SpG >1.020
exudate (thick, infective)
decreased ESR
sickle cell, polycythemia, HF, microcytosis, hypofibrinogenemia
amyloidosis
abnormal aggregation of proteins into B pleated sheets
congo red stain
apple green birefringence with polarised light
amyloid
AL - primary due to
Ig light chain deposition
AA - secondary due to
chronic inflammatory conditions - fibrils have serum amyloid A
B2-microglobulin fibrils
dialysis-related amyloidosis
transthyretin gene mutation
heritable amyloidosis