First Aid Flashcards
hypoxic ischemic encephalopathy
affects pyramidal cells of hippocampus and Purkinje cells
areas of colon susceptible to ischemia
splenic flexure, rectum
leukocyte extravasation- protein mediators
Rolling– E and P selectin (vasculature), Sialyl-Lewis (leukocyte). Also GlyCAM-1, CD34 (vasculature) and L-selectin (leukocyte)
Tight binding - ICAM-1 /CD54(vasculature), CD11/18 integrins (LFA-1, Mac-1) (leukocyte). Also VCAM-1 (CD106) (vasculature) and VLA-4 integrin (leukocyte)
Diapedesis - PECAM-1 (CD31)
Migration- C5a, IL-8, LTB4, kallikrein, platelet activating factor
Apaf-1
Bcl-2 normally prevents cytochrome c release by binding to and inhibiting Apaf-1, which normally induces caspase activation
chromatolysis
involving cell body following axonal injury. increased protein synthesis–> swelling, nuclear displacement, Nissl substance dispersion
PDGF
secreted by activated PLTs and macrophages, induces vascular remodeling and smooth muscle cell migration. Stimulates fibroblast growth.
(wound healing)
FGF
angiogenesis stimulator
wound healing
TGF-beta
stimulates angiogenesis, fibrosis, cell cycle arrest.
wound healing
granuloma formation - mechanism
Th1 cells secrete gamma interferon, activates macrophages. TNF-alpha from macrophages induce and maintain granuloma formation. (anti-TNF drugs can cause granulomas to break down)
decreased ESR
RBCs fall at decreased rate in tube. see in sickle cell, polycythemia, CHF.
sx of iron poisoning
acute- gastric bleeding, N/V, lethargy
chronic- metabolic acidosis, scarring leading to GI obstruction
primary amyloidosis (AL)
deposition of proteins from Ig light chains. can be associated with MM. often affects renal, cardiac, hematologic, GI (hepatomegaly) and neurologic
secondary amyloidosis (AA)
seen with chronic conditions. Serum Amyloid A. multisystem.
Dialysis related amyloidosis
fibrils composed of beta-2 microglobulin. may present as carpal tunnel.
Heritable amyloidosis
eg ATTR neurologic/cardiac amyloidosis due to transthyretin (TTR or prealbumin) gene mutation
age-related amyloidosis
deposition of normal TTR in myocardium and other sites. slower progression of cardiac dysfunction.
organ specific amyloidosis
localized to single organ- eg in Alzheimer’s. also islet amyloid polypeptide (IAPP) commonly seen in DM type 2 and caused by deposition of amylin in pancreatic islets.
lipofuscin
yellow brown “wear and tear pigment” associated with aging. formed by oxidation and polymerization of autophagocytosed organellar membranes.
p-glycoprotein
(MDR1). expressed by some cancer cells to pump out toxins, including chemotherapeutic agents (one mechanism of resistance)