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FTK III- Gen Path > Circulatory Disturbances > Flashcards

Circulatory Disturbances Flashcards

(54 cards)

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1
Q

normal fluid distribution

A

2/3 of total body water is intracellular
1/3 of total body water is extracellular

of the 1/3, 80% is interstitial (space between the cells) and 20% is intravascular (in the blood)

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2
Q

normal fluid homeostasis

A

hydrostatic pressure: drives fluid out of vasculature
osmotic pressure: suspended plasma proteins appy pressure to push fluid into vasculature

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3
Q

fluid imbalance

A

imbalance betwen intravascular and interstitial compartments leads to fluid accumulation in the interstitium

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4
Q

edema

A

fluid accumulation in tissues

works based on gravity- animals= limbs and ventral aspect of body

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5
Q

effusion

A

fluid accumulation in body cavities

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6
Q

morphology of edema

A

macroscopically: transparent, colorless to light yellow (serum-like) fluid expanding tissues, wet, gelatinous, shiny looking tissue

microscopic: excess clear space or pale eosinophilic material between cells

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7
Q

classification of effusion

A

transudate: fluid with low protein and cell count; water or serum-like
ex- hydrothorax, hydropericardium, hydroperitoneum (Ascites)

exudate: fluid with high protein and high cell count due to inflammation
ex- septic (caused by microorganisms) or nonseptic (caused by irritants- bile, urine etc.)

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8
Q

causes of edema/effusion

A

increase in vascular permeability

increase in hydrostatic pressure

decrease in plasma colloid osmotic pressure

decreased lymphatic drainage

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9
Q

increase in vascular permeability

A

inflammatory stimuli leads to local release of inflammatory mediators which increases vascular permeability

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10
Q

increase in hydrostatic pressure

A

due to increased blood volume in microvasculature, usually due to impaired venous outflow (passive congestion- something obstructing vein or compressing it)

can be local or generalized

can happed with hypervolemia due to fluid therapy but less common

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11
Q

congestive heart failure

A

congestive heart failure leads to increased blood volume in vasculature behind the failing chamber(s) leading to increased hydrostatic pressure and generalized edema

L side failure–> pulmonary edema

R side failure–> subcutaneous edema or hydroperitoneum (ascites)

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12
Q

decrease in plasma colloid osmotic pressure

A

due to hypoproteinemia (typically hypoalbumenia)

usually generalized

due to increased protein loss (GI dx) or decreased protein synthesis (malnourished or liver dx)

ex: glomerular amyloidosis–> loss of albumin in urine–> decreased osmotic pressure –> edema

ex: end-stage liver disease (cirrhosis) –> decreased protein synthesis by liver–> decreased osmotic pressure –> edema

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13
Q

decreased lymphatic drainage

A

due to lymphatic obstruction

usually localized

compression blockage due to trauma, fibrosis, invasive neoplasm, infectious agents, or congenital malformations

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14
Q

clinical significance of edema/effusion

A

severe= cerebral, pulmonary, thoracic or pericardial

less severe= peritoneal and subcutaneous

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15
Q

normal hemostasis

A

physiologic response at site of blood vessel injury to seal the injured vessel and prevent blood loss

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16
Q

primary hemostasis

A

mediated by platelets

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17
Q

secondary hemostasis

A

mediated by clotting factors

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18
Q

hemorrhage

A

blood loss from the circulatory system

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19
Q

petechiae

A

small hemorrhages up to a few mm diameter
tend to be on surfaces (skin, serosal surface)

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20
Q

ecchymoses

A

slightly larger hemorrhages up to a few cm in diameter

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21
Q

hematoma

A

hemorrhage in tissue large enough to cause a visible blood clot

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22
Q

contusion

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A

blood leakage from injured vessel into surrounding tissue; associated with blunt trauma

23
Q

hemorrhage in body cavities

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A

hemothorax
hemopericardium
hemoabdomen

24
Q

hemorrhage in joints

25
causes of hemorrhage
blood vessel injury decreased platelets decreased clotting factors
26
blood vessel injury
due to: trauma, inflammation, invasive neoplasms, infectious agents, endotoxemia, uremic toxins, immune complexes, collagen disorders, etc
27
decreased platelets
due to: decreased production increased destruction/consumption decreased function
28
decreased clotting factors
due to: inherited deficiencies decreased production increased consumption
29
clinical significance of hemorrhage
severe= subdural, cerebral, pulmonary, thoracic, pericardial, or peritoneal not severe= subcutaneous
30
thrombosis
inappropriate clotting within the circulatory system blood clot formation within the circulatory system of a live animal
31
thrombus
aggregate of platelets, fibrin, and other blood elements formed on a vessel or heart wall
32
thromboembolus
a thrombus that breaks loose and enters the circulation
33
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 dysfuntion or necrosis
34
morphology of thrombi/thromboemboli
macroscopic: -if mostly platelets and fibrin= pale red-tan, firm, dull, friable, often laminated -if many erythrocytes= dark red, soft, shiny, gelatinous
35
morphology of postmortem blood clots
macroscopic: usually shiny and gelatinous not attached to vessel/heart wall components may separate making the clot two toned--> yellow (serum rich) portion and dark red (RBC rich) portion
36
causes of thrombosis
endothelial injury abnormal blood flow (blood stasis/pooling or turbulent flow) hypercoagulability
37
cardiac/arterial thrombi
usually initiated by endothelial injury rapid blood flow limits passive incorporation of RBCs--> pale red-tan thrombi may or may not occlude the lumen
38
venous thrombi
often occurs at areas of stasis (venous outflow obstructed--> pooling) leads to increased activation of coagulation elements and decreased clearance rate of activated clotting factors stasis leads to incorporation of RBCs--> dark red thrombi almost always occlude the lumen
39
microvascular thrombi
usually due to disseminated intravascular coagulation (DIC)
40
clinical significance of thrombi/emboli
blockage of blood flow can result in decreased tissue perfusion and subsequent necrosis if thrombosis if widespread (DIC), it can lead to consumptive coagulopathy and subsequent hemorrhage
41
alterations in blood flow
accumulation of blood in a vascular bed can be active or passive
42
hyperemia
active engorgement of a vascular bed due to vasodilation and increased inflow leads to redness tissues are warm and bright due to increased delivery of oxygenated blood
43
congestion
passive engorgement of a vascular bed due to decreased outflow tissues are cool and dark red-blue (cyanotic) due to accumulation of deoxygenated blood
44
congestive heart failure (revisited)
blood passively accumulates in vessels behind the failing chambers R side--> hepatic congestion (nutmeg liver) L side--> pulmonary congestion ** then the increase in hydrostatic pressure leads to pulmonary edema
45
ischemia
inadequate tissue perfusion due to vascular obstruction, congestion, or decreased cardiac output metabolic needs of tissue are not met: - decreased O2 delivery --> hypoxia - decreased nutrient delivery - decreased waste removal
46
clinical significance of ischemia
depends on local vascular anatomy, extent of the decreased perfusion, rate at which the decreased perfusion occurred, metabolic needs of the tissue brain and heart= most susceptible lungs, GI tract, kidneys, skin= more resistant (already receive more blood than they need) skeletal muscle= receives blood based on immediate needs
47
consequences of ischemia
reperfusion after brief ischemia --> complete recovery possible reperfusion after prolonged ischemia --> exacerbation of cell injury (reperfusion injury) if not corrected --> tissue necrosis
48
infarct
are of tissue necrosis due to ischemia
49
morphology of infarcts
acute/subacute= angular or wedge-shaped areas with occluded vessel at apex; swollen and dark red or tan chronic= depressed tan and firm (fibrotic/scarred)
50
ischemia-reperfusion injury
restoration 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 tha restore blood flow attributed to oxidative stress, inflammation, and intracellular calcium overload
51
circulatory failure shock
state of general circulatory failure that impairs tissue perfusion--> cellular hypoxia +/- cell injury and death
52
cardiogenic shock
decreased cardiac output due to heart failure
53
hypovolemic shock
decreased circulating blood volume due to massive hemorrhage /fluid loss
54
distributive shock
decreased peripheral vasculature resistance with pooling of blood in peripheral tissues due to sepsis, anaphylaxis, etc.

FTK III- Gen Path (5 decks)

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