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68 Cards in this Set

  • Front
  • Back
what are the fates of thrombi?
(1) resolved by fibrinolysis (2) organized & incoporated into vessel wall (3) organized and recanalized (4) embolization; either arterial or venous
define infarct?
a localized area of ischemic necrosis in an organ or tissue resulting from the occulusion of either its arterial supply or venous drainage
what are the causes of infarcts?
(1) thrombosis and thromboemboli (2) arterial spasm (3) ligation, external pressure, strangulation
what are the types of infarcts?
(1) color classfication: white infarct or red infarct (2) classified by presence or absence of contaminating bacteria: septic infarct (3) by morphology
define embolism?
an embolus is detached intravascular undissolved material that is carried by the blood to a site distant to its point of origin
what are the effects of embolism?
(1)metastasis, (2) infarction,(3) acute circulartory failure (4) abscessation
what is microsvasculature?
small arterioles, arterial capillaries, venous capillaries, small venules
what distrubances of the micrcirculation occur?
edema and yperemia/congestion
what is Starling's Law of Microvascular Equilibrium?
(1) microvasculature consists of small arterioles, capillaries and small venules (2) forces favoring outward movement of fluid (intravascular hydrostatic pressure - 30-17 & colloidal-osmotic pressure of interstitial fluid - 10) & forces favoring inward movement of fluid (tissue hydrostatic pressure - 8 & colloidal osmotic pressure of plasma - 23-25)
what is Starling's Equilibirum under normal conditions?
there is net movement of fluid out of the microvasculature
During inflammation how is Starling's Equilibrium affected?
increased movement of fluid (and cells) out of the microvasculature due to increased vascular permeability and increased tissue colloidal osmotic pressure
define edema?
abnormal accumulation of fluid in the intercellular tissue spaces or body cavities
name terms that describe edema?
anasarca, ascites, hydrothorax, hydropericardium, dependent edema
define anasarca?
generalized massive edema of most tissue and organs, especially subcutaneous
define ascites?
edema fluid in peritoneal cavity
define hydrothroax?
collectiof edema fluid anywhere in thorax
define hydropericardium?
collection of edema fluid in bpericardial sac
define debpendent edema?
edema of lower legs and ventral midline (gravitational influences)
what is transudate?
colorless to yellow, <1500 WBC/ul, <2.5 g/dl protein, SG <1.012 (ultrafiltrate of plasma across intact endothelium)
what is exudate?
cloudy, flocculent, >7000 WBC/ul, >3g/dl protein, SG 1.020 (inflammatory extravascular fluid high in protein and cell debris)
what is purulent exudate?
exudates high in neutrophils, degenerate neutrophils, and cell debris
what is another term for purulent exudate?
pus
what is another term for pus?
purulent exudate
what is the pathogenesis of edema?
decreased colloidal-osmotic pressure, increased intravascular hydrostatic pressure, increased vascular permeability, lymphatic obstruction
describe the pathogenesis of decreased colloidal-osmotic pressure?
always generalized (transudate), decreased protein synthesis( toxin, liver disease/cirrhosis), decreased protein intake or malabsorption (agroceriosis, EPI, GI disease), protein loss (parasites, renal failure = PLN, GI disease = PLE)
describe the pathogenesis of increased intravascular hydrostatic pressure?
inflammation causes local arteriolar dilation, local or general (transudate), CHF is right or left (portal cypertension from liver cirrhosis)
describe the pathogenesis of increased vascular permeability?
always localized and distribution depends on extent of inflammation (exudate), inflammatory edema
give a brief description of decreased plasma colloidal-osmotic pressure?
hypoproteinemia (albumin < 1.5g/dl)
give a brief description of increased intravascular hydrostatic pressure?
impeded venous drainage
give a brief description of increased vascular permeability?
proteins/plasma escape to tissue, water pulled out due to increased tissue colloid-oncotic pressure
describe the pathogenesis of lympatic obstruction?
localized, transudate
what pathogenesis of edema consist of transudate?
decreased colloidal-osmotic pressure, increased intravascular hydrostatic pressure, lymphatic obstruction
what pathogenesis of edema consist of exudate?
increased vascular paermeability
what are the clinical derangements causing generalized edema?
hypoproteinemia, congestive heart failure, liver cirrhosis
what does PLE stand for?
protein losing enteropathy
what does PLN stand for?
protein losing nephropathy
describe how hypoproteinemia causes generalized edema?
PLE/PLN, malabsorption, starvation, parasitism, liver disease
describe how congestive heart failure causes generalized edema?
right heart results in ascites, left hear results in pulmonary edema
describe how liver cirrhosis cause generalized edema?
impaired synthesis of albumin (portal hypertension resulting in ascites)
what are the clinical derangements causing localized edema?
impaired venous drainage, inflammation/allergy, lymphatic obstruction, pulmonary edema
describe how impaired venous drainage causes localized edema?
thrombosis, neoplastic obstruction, bandage
describe how inflammation/allergy causes localized edema?
results in increased vascular permeability
describe how lymphatic obstruction causes localized edema?
tumor metastasis, inflammation, congenital malformation
describe how pulmonary edema causes localized edema?
L heart failure, hypoproteinemia, infections, toxins, hypersensitivity reactions, inhaled hot gases cause damage to endothelial/epithelial linging cells of alveolar septa
what is the mophology of edema?
(1) CT heavy, sowllen, rounded, pale, wet, glistening (2) tissue has fluid/doughy consistency and 'pit' with finger pressing (pitting edema) (3) cut surface oozes clear straw-colored to colorless fluid (4) edematous lungs heavy and wet, fail to collapse completely when removed from thorax (5) lungs reddended if also hyperemia or congestion of vessels (6) airways will have white stable foam (pink if alveolar hemorrhage) with fluid in interlobular septa
what is the histology of edema?
(1) increased clear spaces, separation of tissues (especially in CT) (2) if lots of protein in edema so interstitium may stain pale smudgy pink (eosinophilic) (3) lymphatic dilatation (4) in lung fluid collects around bronchi and interlobular septa causing alveoli to be filled with pink fluid
what is the clinical significance of edema?
life treathening in critical locations (brain, heart, larynx, lungs), little functional significance in subcutaneous and other viscera, and pleural effusions (hydrothorax) can lead to compression atelectasis
what is the general definition of hyperemia/congestion?
an increase in the volume of blood in the microvasculature of the affected part
define hyperemia?
an active proces, arteriole and arteriolar dilatation results increased flow into capillary beds
define congestion?
a passive process, impaired venous drainage impedes blood flow out of capillaries and venules
define erythema?
a dermatology term for abnormal redness of skin due to capillary congestion, usually localized
what is the morphology of hyperemia?
redness, enlarged, rounded, mushy/turgor, cut surface oozes blood
what is the morphology of congestion?
initial redness turns to blue-red due to increased concentration of deoxygenated hemoglobin in blood, the intensification is called cyanosis
what is the morphology of systemic congestion?
increased deoxygenated hemoglobin resulting in cyanosis
what is the histology of hyperemia and congestion?
look similar becaues the capilaries and venules dilated, filled with blood
what are examples of clinically important hyperemia?
usually localized due to inflammation; physiologic hyperemia is a result of activities like exercise affecting skin and muscles or eating affecting GI tract or blushing affecting skin
what are examples of clinically important congestion?
chronic pulmonary congestion/edema (left heart failure), torsion, nasal congestion, chronic passive congestion of liver, hypostatic congestion, shock/circulatory collapse
what is the pathologenesis of chronic pulmonary congestion?
alveoli contain hemosiderin-laden alveolar MPs (heart failure cells) from microhemorrhages
what is the pathologenesis of torsion?
congestion (testicular, GI, liver lobe)
what is the pathogenesis of nasal congestion?
increased vascular permeability (inflammation), later results in pus
what is the pathogenesis of chronic passive congestion of liver?
results from R heart failure or caudal vena cava obstruction resulting in atrophy of centrilobular region (last hepatocytes to get blood) causing the pooling of blood
what is the morphology of chronic passive congestion of liver?
capsule of liver is uniformly textures, the cut surface has distinctive lobular mottling with dark red centrilobular regions surrounded by yellow-brown periportal regions known as a nutmeg liver
what is the histology of chronic passive congestion of liver?
centrilobular hepatic cords atrophic, sinusoids dilated and blood-filled
what may result from chrnoic passive congestion of liver?
centrilobular fibrosis (cardia cirrhosis)
what is the pathogenesis of hypostatic congestion?
pooling in lower (dependent) areas because of gravity and failing circulation
what is the morphology of hypostatic congestion?
lower lung and kidney darker than upper and lower lung edematous, predisposed to developing hypostatic pneumonia
what is the pathogenesis of shock/circulatory collapse?
widespread hypoperfusion due to reduction in blood volume/CO or redistribution of blood results in inadequate effective circulating blood volume, causing systemi hypoxia triggeringa shift to anaerobic metablism causing metabolic acidosis with is reversible in early phases by correction of hemodynamics and metabolic disturbanced, but failure leads to irreversible injury and death of cells
what does clinically important congestion depend on?
organ affected and acute or chronic affect