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FTK III- Gen Path > Circulatory Disturbances > Flashcards

Circulatory Disturbances Flashcards

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

A

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

23
Q

hemorrhage in body cavities

A

hemothorax
hemopericardium
hemoabdomen

24
Q

hemorrhage in joints

A

hemarthrosis

25
Q

causes of hemorrhage

A

blood vessel injury
decreased platelets
decreased clotting factors

26
Q

blood vessel injury

A

due to:
trauma, inflammation, invasive neoplasms, infectious agents, endotoxemia, uremic toxins, immune complexes, collagen disorders, etc

27
Q

decreased platelets

A

due to:
decreased production
increased destruction/consumption
decreased function

28
Q

decreased clotting factors

A

due to:
inherited deficiencies
decreased production
increased consumption

29
Q

clinical significance of hemorrhage

A

severe= subdural, cerebral, pulmonary, thoracic, pericardial, or peritoneal

not severe= subcutaneous

30
Q

thrombosis

A

inappropriate clotting within the circulatory system
blood clot formation within the circulatory system of a live animal

31
Q

thrombus

A

aggregate of platelets, fibrin, and other blood elements formed on a vessel or heart wall

32
Q

thromboembolus

A

a thrombus that breaks loose and enters the circulation

33
Q

embolus

A

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
Q

morphology of thrombi/thromboemboli

A

macroscopic:
-if mostly platelets and fibrin= pale red-tan, firm, dull, friable, often laminated
-if many erythrocytes= dark red, soft, shiny, gelatinous

35
Q

morphology of postmortem blood clots

A

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
Q

causes of thrombosis

A

endothelial injury
abnormal blood flow (blood stasis/pooling or turbulent flow)
hypercoagulability

37
Q

cardiac/arterial thrombi

A

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
Q

venous thrombi

A

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
Q

microvascular thrombi

A

usually due to disseminated intravascular coagulation (DIC)

40
Q

clinical significance of thrombi/emboli

A

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
Q

alterations in blood flow

A

accumulation of blood in a vascular bed can be active or passive

42
Q

hyperemia

A

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
Q

congestion

A

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
Q

congestive heart failure (revisited)

A

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
Q

ischemia

A

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
Q

clinical significance of ischemia

A

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
Q

consequences of ischemia

A

reperfusion after brief ischemia –> complete recovery possible

reperfusion after prolonged ischemia –> exacerbation of cell injury (reperfusion injury)

if not corrected –> tissue necrosis

48
Q

infarct

A

are of tissue necrosis due to ischemia

49
Q

morphology of infarcts

A

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
Q

ischemia-reperfusion injury

A

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
Q

circulatory failure
shock

A

state of general circulatory failure that impairs tissue perfusion–> cellular hypoxia +/- cell injury and death

52
Q

cardiogenic shock

A

decreased cardiac output due to heart failure

53
Q

hypovolemic shock

A

decreased circulating blood volume due to massive hemorrhage /fluid loss

54
Q

distributive shock

A

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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