histopathology of syphilitic lesionat all stages classlcally demonstrate ☆proliferative endarteritis of small vessels with a surrounding plasma cell rich infiltrate
(eg. aortic aneurysm, condyloma lata)
reversible and irreversible cell injuryreversible
↓ATP →↓ activity of Ca2+ and Na+/K+ pumps→ ☆cellular swelling (earliest morphologic manifestation), ☆mitochondrial swelling, chromatin clumping, plasma membrane changes(eg bleb)
irreversible
Breakdown of plasma membrane→ cytosolic enzymes (eg, troponin) leak outside of cell, influx of Ca2+ → activation of degradative enzymes,
Mitochondrial damage/dysfunction→ loss of electron transport chain= ☆mitochondrial vacuolization→ ↓ATP, apoptosis, rupture of lysosomes→ autolysis pathologyUWorld HirotoShishido
histology of liposarcomacells with round clear cytoplasmic vaculoles scalloping the nuclear membrane
(lipoblasts)
the most common soft-tissue sarcoma in adults pathologydermatologyUWorld SIM2 HirotoShishido
HPV carcinogenesisHPV viral protein E6 binds to ☆p53, a tumor suppressor protein that normally inhibits the proliferation of cells with genetic abnormalities. Ubiquitination of the E6-p53 complex induces degradation of p53, leading to unregulated cellular growth.
HPV viral protein E7 binds to retinoblastoma(Rb) protein, which results in the displacement of E2F (a transcription factor that induces cell cycle activation), promoting unregulated DNA replication and cyclin-mediated cell cycling. microbiologypathologyfree120 HirotoShishido
lipofuscinA yellow-brown “wear and tear” pigment A associated with normal aging.
May be derived through ☆lipid peroxidation of polyunsaturated lipids of subcellular membranes.
PictureFollicular thyroid carcinomas (FTCs) are characterized by ☆invasion of the tumor capsule and/or surrounding blood vessels. endocrinologypathologyUWorld HirotoShishido
pathophysiology of aortic stenosisThere is subendothelial lipid deposition and infiltration of inflammatory cells (ie, macrophages, T lymphocytes) followed by the release of inflammatory mediators (eg,interleukin-1-beta, transforming growth factor beta-1).
Subsequently, there is increased production of proteins involved in tissue calcification (eg, osteopontin). ☆Fibroblasts differentiate into osteoblast-like cells, leading to aberrant bone matrix deposition with progressive valvular calcification and stenosis. cardiologypathologyUWorld HirotoShishido
p-glycoproteinAlso known as multidrug resistance protein 1 (MDR1).
Classically seen in adrenocortical carcinoma but also expressed by other cancer cells (eg, colon, liver).
Used to pump out toxins, including chemotherapeutic agents (one mechanism of responsiveness or resistance to chemotherapy over time).
+BBB(disruptions of tight junctions or ☆p-glycoprotein inhibition can improve drug delivery to the CNS),
+apical surface of enterocytes(can limit drug bioavailability by pumping the drug back) pathologyUWorld HirotoShishido
how does CpGs workThe methylation of cytosine residues in CpGs(cytosine-guanine dinucleotide repeats) prevents ☆transcription factors from binding to the promoter, effectively silencing transcription of genes not required by terminally differentiated somatic cells. pathologybiologyUWorld SIM1 HirotoShishido
hypertrophy and hyperplasiastructural proteins and organellesin size of cells (☆high rate of mRNA synthesis)
Example: cardiac hypertrophy.
controlled proliferation of stem cells and differentiated cells in number of cells (high rate of mitotic activity)
Excessive stimulation pathologic hyperplasia (eg, endometrial hyperplasia), which may progress to dysplasia and cancer.
Example: benign prostatic hyperplasia. pathologyUWorld SIM1 HirotoShishido
what cell junction does calcium dependent adhesion molecules form?Adherens junction (belt desmosome, zonula adherens),
desmosome (spot desmosome, macula adherens)
→removing calcium from extracellular fluid will cause dissociation of these cadherin-mediated junctions, leading to loss of cell-cell adhesion biologypathologyUWorld SIM1 HirotoShishido
