First Aid-Pathology Flashcards
First Aid 2012
changes in the levels of anti and pro-apoptotic factors lead to
Bax (pro apoptotic), bcl-2 (anti apoptotic); increased mitochondrial permeability and release of cytochrome c in intrinsic pathway of apoptosis which leads to cytosolic caspases activation
apoptosis
activation of caspases mediate cellular breakdown; no sig inflammation
2 extrinsic pathways of apoptosis
ligand receptor interactions (fas ligand binding to Fas (cd95); immune cell (cytotoxic T cell release of perforin and granzyme B)
pyknosis
basophilia
karyorrhexis
pyknotic nuclear fragmentation
karyolysis
nuclear fading
necrosis is what kind of process as opposed to apoptosis?
inflammatory process
type of necrosis: coagulative
heart, liver, kidney
type of necrosis: liquefactive
brain bacterial abscess, pleural effusion
type of necrosis: caseous
TB, systemic fungi
type of necrosis: fatty
pancreas (saponification)
type of necrosis: fibrinoid
blood vessels
type of necrosis: gangrenous
dry (ischemic coagulative) or wet (with bacteria); common in limbs and GI tract
intrinsic pathway of apoptosis
occurs during embryogenesis, hormone induction, and atrophy
Bax
pro apoptotic; in intrinsic pathway
Bcl-2
anti-apoptotic; in intrinsic pathway
2 extrinsic apoptotic pathways
FasL and killer T cells
cell injury reversible with oxygen
CELL swelling, nuclear chromatin clumping, decreased glycogen, fatty change, ribosomal detachment
irreversible cell injury
nuclear pyknosis, karyolysis, calcium influx causing caspase activation, plasma membrane damage, lysosomal rupture, mitochondrial permeability
watershed areas
an area susceptible to hypoxia; located at splenic flexure; ACA/MCA
REd (hemorrhagic) infarcts
loose tissues lie liver, lungs, or intestine or following REperfusion
pale infarcts occurs
in solid tissues like single blood supply such as heart, kidney, and spleen
septic shock
decrease in TPR; dilated arterioles, high venous return, hot patient
hypovolemic/cardiogenic shock
low output failure, increase TPR, low cardiac output, cold clammy patient
granulation tissue
resolution of inflammation that results in highly vascularized and fibrotic tissue
granuloma
nodular collections of epitheliod macrophages and giant cells
chronic inflammation is mediated by
mononuclear cells
chronic inflammation is characterized by
persistent destruction and repair; associated with blood vessel proliferation, fibrosis
acute inflammation is mediated by
neutrophils, eosinophils and antibodies
steps in leukocyte extravasation
rolling (e-selectin and p-selectin), tight binding (ICAM), diapedesis (PECAM), and migration, phagocytosis
bacterial products in migration process of leukocyte extravasation
CILK: C5a, IL-8, LTB4, Kallikrein
how do free radicals damage cells?
membrane lipid peroxidation, protein modification and DNA breakage
pathologies of free radicals
retinopathy of prematurity, bronchopulmonary dysplasia, CCL4 leading to liver necrosis, acetaminophen, iron overload, reperfusion after anoxia
free radicals can be eliminated by
enzymes (catalase, SOD, glutathione peroxidase), spontaneous decay, or antioxidants (vit A, C, E.)
What induces and maintains granuloma formation?
cells secrete gamma interferon, activating macrophages; TNF-alpha from macrophages; therefore anti-TNF drugs can break down granulomas leading to disseminated disease
phases of wound healing
inflammatory (platelets, neutrophils, macrophages); Proliferative (fibroblasts, myofibroblasts, endothelial cells, keratinocytes); remodeling (1 week later, fibroblasts)
what occurs during proliferative phase of wound healing?
deposition of grnaulationt issue and collagen, angiogenesis, epitheljial cell proliferation, dissolution of clot and wound contration (mediated by myofibroblasts)
what happens during remodeling phase of wound healing?
type 3 collagen replaced by type 1 collagen; increased tensile strength of tissue
transudate
hypocellular, protein poor, SG of < 1.012
exudate
cellular, protein rich, sg of > 1.020
exudate is due to
lymphatic obstruction and inflammation
transudate is due to
increased hydrostatic pressure, decreased oncotic pressure, and na+ retention
increased in erythrocyte sedimentation rate indicates
infections, inflammation, cancer,pregnancy, SLE
decreased ESR indicates
sickle cell, polycythemia (too many), CHF
acute iron poisoning
gastric bleeding
chronic iron poisoning
metabolic acidosis, scarring leading to GI obstruction
amyloidosis stain
apple green birefringence of Congo red stain under polarized light
Bence jones amyloidosis
AL protein
secondary amyloidosis
AA protein
senile cardiac amyloidosis
transthyretin protein derived from AF