Chp 4 Flashcards
edema
too much interstitial fluid in tissues and outside individual cells
intracellular edema
cloudy swelling win injured cells
anasarca
generalized, sever dedema
effusion
liquid in the pericardial, pleural, peritoneal, or joint cavities
ascites
effusion in the peritoneal cavity
hydrothorax
watery fluid in the pleural space
empyema
pus/purulent effusion in the pleural vavity
hydropericardium
watery fluid in the pericardial cavity
hydrocephalus
too much CSF
hydrocele
extra fluid within the membrane around the testis
hydrosalpinx
too much fluid in the fallopian tube following gonorrheal or other salpingitis
ileus
too much fluid in the small bowel
seroma
non-infected fluid in the surgical incision
loculated effusion
more than one compartment, due to scarring, harder to drain
blister
fluid in the epidermis or between dermis and epidermis
bulla vs vesicles
big vs little blisters
mechanisms in with edema can form (5)
1) excess total body fluid
2) increased pressure in the small veins of the body
3) decreased total plasma protein/albumin content
4) lymphatic vessel obstruction
5) leaky vessels from inflammation
examples of causes of edema
1) excess total body water- iatrogenic fluid overloading, kidney failure
2) increased venous pressure - CHF, pericardial disease, pregnancy, thrombus
3) decreased blood protein content - malnourishment, malabsorption, liver failure
4) lymphatic obstruction - filariasis, surgery, radiation, cancer
5) other - trauma, lead poisoning
chylous effusion
result from damaged lymphatics, thoracic duct, and produce turbid, lipid rich fluid
transudate
salt water, vessels keep protein in the bloodstream
exudate
leaky vessels produce protein rich edema
cardiac edema
edema first appearing in the feet after standing
from CHF
renal edema
edema first appearing around the eyes
total-body water overload/low blood albumin
liver disease
edema first appearing as excess fluid in the abdomen
low blood albumin plus increased resistance to portal venous flow
angioedema
syndrome in which blood vessels suddenly become extra-permeable
hereditary C1-esterase deficiency
side effect of captorpril
hyperemia
increased blood flow to an organ
red and throbs
congestion
decreased blood flow from organ
purple and doesn’t throb
watershed infarct
a
irreversible shock
a
progressve/decompensated shock
a
compensated shock
a
causes of shock
a
hemostasis events (4)
1) Vasoconstriction
2) Primary hemostasis
3) Secondary hemostasis
4) Clot stabilization and resorption
vasoconstriction event
function - reduce blood flow modulator - endothelin
primary hemostasis event
function - formation of platelet plug mechanism - von Willebrand factor and collagen exposed promotes platelet activation. platelets grow and release secretory granules to aggregate and recruit more platelets
secondary hemostasis event
function - deposit fibrin mechanism - tissue factor bind sand activates factor VII, cascades into thrombin formation. thrombin cleaves fibrinogen to fibrin. fibrin creates meshwork and activates more platelets
clot stabilization event
function - create permanent plug and repair mechanism - fibrin contracts. counterregulatory mechanisms activate to limit clotting
prothrombin time (PT)
assess function of extrinsic pathway
factors VII X V II, fibrinogen
how? tissue factor and calcium are added to plasma and timed
partial thromboplastin time (PTT)
assess function of intrinsic pathway
factors XII XI IX VIII X V II
how? ground glass activates XII phospholipids and calcium
fibrinolysis
accomplished via plasmin, from plasminogen catabolism via XII pathway or t-PA
