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Foundational toolkit III - wk2 > circulatory disturbances > Flashcards

circulatory disturbances Flashcards

1
Q

what does an imbalance betwen intravascular & interstitial compartments leads to

A

fluid accumulation in the interstitium

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2
Q

what is edema

A

fluid accumulation in tissues

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3
Q

what is effusion

A

fluid accumulation in body cavities

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4
Q

how does edema work

A

excess fluid can move freely in the interstitium & often settles in dependent areas due to gravity

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5
Q

macroscopic morphology of edema

A

transparent, colorless to light yellow (serum-like) fluid expanding tissues

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6
Q

microscopic morphology of edema

A

excess clear space or pale eosinophilic material between cells

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7
Q

what are the two classifications of effusion

A

transudate & exudate

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8
Q

what does transudate mean

A

fluid with low protein & cell count

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9
Q

what are some examples of transudate effusion

A
  • hydrothorax
  • hydropericardium
  • hydroperitoneum or ascites
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10
Q

what does exudate mean

A

fluid with high protein +/- high cell count due to inflammation

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11
Q

what are the two types of exudate effusion

A
  • nonseptic - caused by irritants (bile, urine, etc)
  • septic - caused by microorganisms
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12
Q

what are the 4 causes of edema/effusion

A
  1. increased vascular permeability
  2. increased intravascular hydrostatic pressure
  3. decreased plasma colloid osmotic pressure
  4. decreased lymphatic drainage
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13
Q

increased vascular permeability is due to ____

A

inflammation

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14
Q

increased vascular permeability sequense:

A

inflammatory stimuli -> local release of inflammatory mediators (histamine, bradykinin, leukotrienes) -> increased vascular permeability

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15
Q

increase in intravascular hydrostatic pressure is due to:

A

increase in blood volume in microvasculature

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16
Q

an increase in intravascular hydrostatic pressure - where and what is is specifically due to?

A
  • localized or generalized
  • due to impaired venous outflow (passive congestion)
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17
Q

what happens when there is a focal venous obstruction

A

increase in blood volume in vasculature behind the obstruction -> increase hydrostatic pressure -> localized edema

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18
Q

what happens with congestive heart failure

A

increase blood volume in vasculature behind the failing chamber(s) -> increase hydrostatic pressure -> generalized edema

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19
Q

what happens when there is right-sided heart failure

A

increase in blood volume in systemic veins -> subcutaneous edema, hydroperitoneium (acites)

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20
Q

what happens when there is left sided heart failure

A

increase blood volume in pulmonary veins -> pulmonary edema

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21
Q

a decrease in plasma colloid osmotic pressue is due to ____

A

hypoproteinemia

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22
Q

decrease plasma colloid osmotic pressure location and due to what specifically

A
  • generalized
  • due to increase protein loss or decrease protein synthesis
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23
Q

what happens with glomerular amyloidosis

A

loss of albumin in urine -> decreased plasma colloid osmotic pressure -> edema

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24
Q

what happens with end-stage liver disease (cirrhosis)

A

decreased protein synthesis by liver -> decreased plasma colloid osmotic pressure -> edema

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25
Q

what happens with associated hepatic fibrosis

A

interferes with portal blood flow -> increase portal vein hydrostatic pressure -> ascites

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26
Q

decreased lymphatic drainage is due to:

A

lymphatic obstruction

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27
Q

decreased lymphatic drainage location and specific compression or blockage

A
  • localized
  • trauma, fibrosis, invasive neoplasms, infectious agents, or congenital malformation (rare)
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28
Q

what happens when there is an invasive mammary neoplasm

A

lymphatic vessel obstruction -> decreased lymphatic drainage -> edema

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29
Q

what happens when there is lymphatic vessel hypoplasia/aplasia

A

decreased lymphatic drainage -> edema

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30
Q

what does the clinical significance of edema/effusion depend on

A

location & severity

  • cerebral edema (severe)
  • pulmonary edema, thoracic or pericardial effusion (severe)
  • peritoneal effusion
  • subcutaneous edema
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31
Q

what is normal hemostasis

A

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

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32
Q

what is primary hemostasis mediated by

A

platelets

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33
Q

what is secondary hemostasis mediated by

A

clotting factors

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34
Q

what is hemostatic balance

A
  • precisely orchestrated process involving platelets, clotting factors & endothelium
  • balance between hemostatic, anticoagulant & fibrinolytic pathways
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35
Q

disruption of hemostatic balance causes:

A

excessive bleeding or clotting

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36
Q

what is a hemostatic bleeding imbalance

A

imbalance between hemostatic, anticoagulant & fibrinolytic pathways -> blood loss or inappropriate clotting

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37
Q

what is hemorrhage

A

blood loss from the circulatory system

38
Q

small foci

petechiae

A

small hemorrhages up to a few mm diameter

39
Q

small foci

ecchymoses

A

slightly larger hemorrhages up to a few cm diameter

40
Q

hematoma

A

hemorrhage in tissue large enough to cause a visible blood clot

41
Q

contusion (bruise)

A

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

42
Q

what are ex of hemorrhage in body cavities

A
  • hemothorax
  • hemopericardium
  • hemoabdomen (or hemoperitoneum)
43
Q

hemorrhage in joints

A

hemarthrosis

44
Q

what are the 3 causes of hemorrhage

A
  1. blood vessel injury
  2. decreased platelets
  3. decreased clotting factors
45
Q

blood vessel injury is due to:

A
  • trauma
  • inflammation
  • invasive neoplasms
  • infectious agents
  • endotoxemia
  • uremia toxins
  • immune complexes
  • collagen disorders
46
Q

what happens when there is a fungal infection in gutteral pouch

A

carotid artery injury -> hemorrhage

47
Q

what happens when there is a vitamin C deficiency (scurvy)

A

decreased collagen cross-linking -> fragile blood vessels prone to injury -> periarticular hemorrhage

48
Q

a decrease in platelets is due to:

A
  • decreased production
  • increased destruction/consumption
  • decreased function
49
Q

what happens when there is immune-mediated destruction of megakaryocytes in bone marrow

A

thrombocytopenia -> cutaneous hemorrhages

50
Q

decreased clotting factors is due to:

A
  • inherited deficiencies
  • decreased production
  • increased consumption
51
Q

what happens with anticoagulant rodenticide poisoning

A

inhibition of VK epoxide reductase in liver -> decreased production of VK-dependent clotting factors -> visceral & cavity hemorrhage

52
Q

what is the clinical significance of hemorrhage

A

depends on volume, rate and location

  • subdural or cerebral hemorrhage (severe)
  • pulmonary hemorrhage, thoracic or pericardial hemorrhage (severe)
  • peritoneal hemorrhage (severe)
  • subcutaneous hemorrhage
53
Q

what is clotting hemostatic imbalance

A

imbalance between hemostatic, anticoagulant, & fibrinolytic pathways -> blood loss or inappropriate clotting

54
Q

what is thrombosis

A
  • inappropriate clotting within the circulatory system
  • blood clot formation within the circulatory system of a live animal
55
Q

what is a thrombus

A

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

56
Q

if a thrombus (or fragment of a thrombus) breaks loose and enters the circulation, it becomes a ____

A

thromboembolus

57
Q

what is an 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 dysfunction or necrosis

58
Q

what is a thromboembolus

A
  • embolus composed specifically of clotted blood
  • not all emboli are thromboemboli
59
Q

what is the macroscopic morphology of thrombi/thromboemboli

A
  • 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
60
Q

what is the macroscopic morphology of postmortem blood clots

A
  • 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”
61
Q

what are the 3 causes of thrombosis

A

virchow’s triad

  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
62
Q

what happens with stronglyus vulgaris larval migration

endothelial injury

A

cranial mesenteric artery inflammation & endothelial injury -> thrombosis

63
Q

what happens with feline hypertrophic cardiomyopathy

abnormal blood flow

A

left atrial dilation -> blood statis/turbulence -> mural thrombosis

64
Q

what happens with glomerular amyloidosis

hypercoagulability

A

loss of antithrombin III -> hypercoagulability -> right atrial thrombosis -> pulmonary thromboembolism

65
Q

how to classify cardiac/arterial thrombi

A
  • 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
66
Q

how to classify venous thrombi

A
  • 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
67
Q

how to classify microvascular thrombi

A

usually due to DIC (disseminated intravascular coagulation)

68
Q

what is the clinical significance of thrombi/emboli

A

depends on location & ability to block blood flow

69
Q

blockage of blood flow can result in:

A

decreased tissue perfusion & subsequent necrosis

70
Q

if thrombosis is widespread (DIC), it can lead to:

A

consumptive coagulopathy & subsequent hemorrhage

71
Q

what is normal blood flow

A
  • blood distribution within the circulatory system is highly variable
  • systemic neural & hormonal influences help maintain adequate blood flow to the tissues
72
Q

alterations in blood flow

A

accumulation of blood in vascular bed can be active or passive

73
Q

hyperemia

A

active engorgement of a vascular bed due to vasodilation & increased inflow

74
Q

congestion

A

passive engorgement of a vascular bed due to decreased outflow

75
Q

what is the morphology of hyperemia (active)

A

tissues are warm & bright red due to increased delivery of oxygenated blood

76
Q

what is the morphology of congestion (passive)

A

tissues are cool & dark red-blue (cyanotic) due to accumulation of deoxygenated blood

77
Q

congestive heart failure

A

blood passively accumulates in vessels behind the failing chamber(s)

78
Q

right sided heart failure

A

hepatic congestion (nutmeg liver)

79
Q

left-sided heart failure

A

pulmonary congestion

80
Q

what is ischemia

A

inadequate tissue perfusion

81
Q

ischemia characteristics

A
  • 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)
82
Q

the clinical significance of ischemia depends on:

A
  • local vascular anatomy (anastomoses, collateral circulation)
  • extent of the decreased perfusion
  • rate at which the decreased perfusion occured
  • metabolic needs of the tissue
83
Q

how do tissues vary in their susceptibility to ischemia

A
  • 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)
84
Q

what are the consequences of inadequate tissue perfusion (ischemia)

A
  • reperfusion after bried ischemia -> compolete recovery possible
  • reperfusion after prolinged ischemia -> exacerbation of cell injury (“reperfusion injury”)
  • if not corrected, ischemia -> tissue necrosis
  • infarct
85
Q

what is an infarct

A

area of tissue necrosis due to ischemia

86
Q

what is the morphology of acute-subacute infarct

A
  • usually angular or wedge-shaped areas with occluded vessel at the apex
  • swollen & dark red (hemorrhagic) or tan (lack of blood)
87
Q

what is the morphology of chronic infarcts

A

depressed, tan & firm (fibrotic/scarred)

88
Q

what is ischemia-reperfusion injury

A

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
89
Q

circulatory failure

what is shock

A

state of general circulatory failure that impaires tissue perfusion -> cellular hypoxia +/- cell injury & death

90
Q

cardiogenic shock

A

decreased cardiac output due to heart (pump) failure

91
Q

hypovolemic shock

A

decreased circulating blood volume due to massive hemorrhage/fluid loss

92
Q

distributive shock

A

decreased peripheral vascular resistance with pooling of blood in peripheral tissues due to sepsis, anaphylaxis, etc

Foundational toolkit III - wk2 (1 decks)

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