circulatory disturbances Flashcards
what does an imbalance betwen intravascular & interstitial compartments leads to
fluid accumulation in the interstitium
what is edema
fluid accumulation in tissues
what is effusion
fluid accumulation in body cavities
how does edema work
excess fluid can move freely in the interstitium & often settles in dependent areas due to gravity
macroscopic morphology of edema
transparent, colorless to light yellow (serum-like) fluid expanding tissues
microscopic morphology of edema
excess clear space or pale eosinophilic material between cells
what are the two classifications of effusion
transudate & exudate
what does transudate mean
fluid with low protein & cell count
what are some examples of transudate effusion
- hydrothorax
- hydropericardium
- hydroperitoneum or ascites
what does exudate mean
fluid with high protein +/- high cell count due to inflammation
what are the two types of exudate effusion
- nonseptic - caused by irritants (bile, urine, etc)
- septic - caused by microorganisms
what are the 4 causes of edema/effusion
- increased vascular permeability
- increased intravascular hydrostatic pressure
- decreased plasma colloid osmotic pressure
- decreased lymphatic drainage
increased vascular permeability is due to ____
inflammation
increased vascular permeability sequense:
inflammatory stimuli -> local release of inflammatory mediators (histamine, bradykinin, leukotrienes) -> increased vascular permeability
increase in intravascular hydrostatic pressure is due to:
increase in blood volume in microvasculature
an increase in intravascular hydrostatic pressure - where and what is is specifically due to?
- localized or generalized
- due to impaired venous outflow (passive congestion)
what happens when there is a focal venous obstruction
increase in blood volume in vasculature behind the obstruction -> increase hydrostatic pressure -> localized edema
what happens with congestive heart failure
increase blood volume in vasculature behind the failing chamber(s) -> increase hydrostatic pressure -> generalized edema
what happens when there is right-sided heart failure
increase in blood volume in systemic veins -> subcutaneous edema, hydroperitoneium (acites)
what happens when there is left sided heart failure
increase blood volume in pulmonary veins -> pulmonary edema
a decrease in plasma colloid osmotic pressue is due to ____
hypoproteinemia
decrease plasma colloid osmotic pressure location and due to what specifically
- generalized
- due to increase protein loss or decrease protein synthesis
what happens with glomerular amyloidosis
loss of albumin in urine -> decreased plasma colloid osmotic pressure -> edema
what happens with end-stage liver disease (cirrhosis)
decreased protein synthesis by liver -> decreased plasma colloid osmotic pressure -> edema
what happens with associated hepatic fibrosis
interferes with portal blood flow -> increase portal vein hydrostatic pressure -> ascites
decreased lymphatic drainage is due to:
lymphatic obstruction
decreased lymphatic drainage location and specific compression or blockage
- localized
- trauma, fibrosis, invasive neoplasms, infectious agents, or congenital malformation (rare)
what happens when there is an invasive mammary neoplasm
lymphatic vessel obstruction -> decreased lymphatic drainage -> edema
what happens when there is lymphatic vessel hypoplasia/aplasia
decreased lymphatic drainage -> edema
what does the clinical significance of edema/effusion depend on
location & severity
- cerebral edema (severe)
- pulmonary edema, thoracic or pericardial effusion (severe)
- peritoneal effusion
- subcutaneous edema
what is normal hemostasis
physiologic reponse at site of blood vessel injury to seal the injured vessel and prevent blood loss
what is primary hemostasis mediated by
platelets
what is secondary hemostasis mediated by
clotting factors
what is hemostatic balance
- precisely orchestrated process involving platelets, clotting factors & endothelium
- balance between hemostatic, anticoagulant & fibrinolytic pathways
disruption of hemostatic balance causes:
excessive bleeding or clotting
what is a hemostatic bleeding imbalance
imbalance between hemostatic, anticoagulant & fibrinolytic pathways -> blood loss or inappropriate clotting
what is hemorrhage
blood loss from the circulatory system
small foci
petechiae
small hemorrhages up to a few mm diameter
small foci
ecchymoses
slightly larger hemorrhages up to a few cm diameter
hematoma
hemorrhage in tissue large enough to cause a visible blood clot
contusion (bruise)
blood leakage from injured vessel into surrounding tissue; associated with blunt trauma
what are ex of hemorrhage in body cavities
- hemothorax
- hemopericardium
- hemoabdomen (or hemoperitoneum)
hemorrhage in joints
hemarthrosis
what are the 3 causes of hemorrhage
- blood vessel injury
- decreased platelets
- decreased clotting factors
blood vessel injury is due to:
- trauma
- inflammation
- invasive neoplasms
- infectious agents
- endotoxemia
- uremia toxins
- immune complexes
- collagen disorders
what happens when there is a fungal infection in gutteral pouch
carotid artery injury -> hemorrhage
what happens when there is a vitamin C deficiency (scurvy)
decreased collagen cross-linking -> fragile blood vessels prone to injury -> periarticular hemorrhage
a decrease in platelets is due to:
- decreased production
- increased destruction/consumption
- decreased function
what happens when there is immune-mediated destruction of megakaryocytes in bone marrow
thrombocytopenia -> cutaneous hemorrhages
decreased clotting factors is due to:
- inherited deficiencies
- decreased production
- increased consumption
what happens with anticoagulant rodenticide poisoning
inhibition of VK epoxide reductase in liver -> decreased production of VK-dependent clotting factors -> visceral & cavity hemorrhage
what is the clinical significance of hemorrhage
depends on volume, rate and location
- subdural or cerebral hemorrhage (severe)
- pulmonary hemorrhage, thoracic or pericardial hemorrhage (severe)
- peritoneal hemorrhage (severe)
- subcutaneous hemorrhage
what is clotting hemostatic imbalance
imbalance between hemostatic, anticoagulant, & fibrinolytic pathways -> blood loss or inappropriate clotting
what is thrombosis
- inappropriate clotting within the circulatory system
- blood clot formation within the circulatory system of a live animal
what is a thrombus
aggregate of platelets, fibrin and other blood elements formed on a vessel or heart wall
if a thrombus (or fragment of a thrombus) breaks loose and enters the circulation, it becomes a ____
thromboembolus
what is an embolus
any mass (solid, liquid, or gas) carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or necrosis
what is a thromboembolus
- embolus composed specifically of clotted blood
- not all emboli are thromboemboli
what is the macroscopic morphology of thrombi/thromboemboli
- depends on underlying cause, location, & composition (proportion of platelets, fibrin, & other blood cells)
- mostly platelets & fibrin = pale red-tan, firm, full, friable, often laminated
- many erythrocytes = dark red, soft, shiny, gelatenous
- can be occulsive or non-occlusive
what is the macroscopic morphology of postmortem blood clots
- usually shiny & gelatinous
- not attached to vessel/heart wall
- components may separate
- yellow (serum-rich) portion = “chicken fat clot”
- dark red (RBC-rich) portion = “currant jelly clot”
what are the 3 causes of thrombosis
virchow’s triad
- endothelial injury
- abnormal blood flow
- hypercoagulability
what happens with stronglyus vulgaris larval migration
endothelial injury
cranial mesenteric artery inflammation & endothelial injury -> thrombosis
what happens with feline hypertrophic cardiomyopathy
abnormal blood flow
left atrial dilation -> blood statis/turbulence -> mural thrombosis
what happens with glomerular amyloidosis
hypercoagulability
loss of antithrombin III -> hypercoagulability -> right atrial thrombosis -> pulmonary thromboembolism
how to classify cardiac/arterial thrombi
- usually initiated by endothelial injury -> site for firm platelet attachment & incorporation of fibrin
- rapid blood flow limits passive incorporation of RBCs -> pale red-tan thrombi
- may or may not occlude lumen
how to classify venous thrombi
- often occurs in areas of stasis -> increased activation of coagulation elements & decreased clearance rate of activated clotting factors
- blood stasis or decreased flow -> greater incorporation of RBCs -> dark red thrombi
- almost always occlude lumen
how to classify microvascular thrombi
usually due to DIC (disseminated intravascular coagulation)
what is the clinical significance of thrombi/emboli
depends on location & ability to block blood flow
blockage of blood flow can result in:
decreased tissue perfusion & subsequent necrosis
if thrombosis is widespread (DIC), it can lead to:
consumptive coagulopathy & subsequent hemorrhage
what is normal blood flow
- blood distribution within the circulatory system is highly variable
- systemic neural & hormonal influences help maintain adequate blood flow to the tissues
alterations in blood flow
accumulation of blood in vascular bed can be active or passive
hyperemia
active engorgement of a vascular bed due to vasodilation & increased inflow
congestion
passive engorgement of a vascular bed due to decreased outflow
what is the morphology of hyperemia (active)
tissues are warm & bright red due to increased delivery of oxygenated blood
what is the morphology of congestion (passive)
tissues are cool & dark red-blue (cyanotic) due to accumulation of deoxygenated blood
congestive heart failure
blood passively accumulates in vessels behind the failing chamber(s)
right sided heart failure
hepatic congestion (nutmeg liver)
left-sided heart failure
pulmonary congestion
what is ischemia
inadequate tissue perfusion
ischemia characteristics
- due to vascular obstruction, congestion, or decreased cardiac output
- metabolic needs of the tissue are not met:
- decreased O2 delivery -> hypoxia
- decreased nutrient delivery (e.g. glucose)
- decreased waste removal (e.g., CO2, lactic acid)
the clinical significance of ischemia depends on:
- local vascular anatomy (anastomoses, collateral circulation)
- extent of the decreased perfusion
- rate at which the decreased perfusion occured
- metabolic needs of the tissue
how do tissues vary in their susceptibility to ischemia
- brain & heart: most susceptible (hivh metabolic needs, poor collateral circulation)
- lungs, GI tract, kidneys, skin: more resistant (already receive more blood than they need)
- skeletal muscle: receives blood based on immediate needs (exercise)
what are the consequences of inadequate tissue perfusion (ischemia)
- reperfusion after bried ischemia -> compolete recovery possible
- reperfusion after prolinged ischemia -> exacerbation of cell injury (“reperfusion injury”)
- if not corrected, ischemia -> tissue necrosis
- infarct
what is an infarct
area of tissue necrosis due to ischemia
what is the morphology of acute-subacute infarct
- usually angular or wedge-shaped areas with occluded vessel at the apex
- swollen & dark red (hemorrhagic) or tan (lack of blood)
what is the morphology of chronic infarcts
depressed, tan & firm (fibrotic/scarred)
what is ischemia-reperfusion injury
restorartion of blood flow after prolonged ischemia can exacerbate cell injury -> cell death
- reperfused tissues may sustain loss of viable cells in addition to those irreversibly damaged by ischemia
- contributes to tissue damage following therapies that restore blood flow (correction of GI volvulus/torsion)
- attributed to oxidative stress, inflammation, & intracellular calcium overload
circulatory failure
what is shock
state of general circulatory failure that impaires tissue perfusion -> cellular hypoxia +/- cell injury & death
cardiogenic shock
decreased cardiac output due to heart (pump) failure
hypovolemic shock
decreased circulating blood volume due to massive hemorrhage/fluid loss
distributive shock
decreased peripheral vascular resistance with pooling of blood in peripheral tissues due to sepsis, anaphylaxis, etc
