circulatory disturbances Flashcards
(92 cards)
1
Q
what does an imbalance betwen intravascular & interstitial compartments leads to
A
fluid accumulation in the interstitium
2
Q
what is edema
A
fluid accumulation in tissues
3
Q
what is effusion
A
fluid accumulation in body cavities
4
Q
how does edema work
A
excess fluid can move freely in the interstitium & often settles in dependent areas due to gravity
5
Q
macroscopic morphology of edema
A
transparent, colorless to light yellow (serum-like) fluid expanding tissues
6
Q
microscopic morphology of edema
A
excess clear space or pale eosinophilic material between cells
7
Q
what are the two classifications of effusion
A
transudate & exudate
8
Q
what does transudate mean
A
fluid with low protein & cell count
9
Q
what are some examples of transudate effusion
A
- hydrothorax
- hydropericardium
- hydroperitoneum or ascites
10
Q
what does exudate mean
A
fluid with high protein +/- high cell count due to inflammation
11
Q
what are the two types of exudate effusion
A
- nonseptic - caused by irritants (bile, urine, etc)
- septic - caused by microorganisms
12
Q
what are the 4 causes of edema/effusion
A
- increased vascular permeability
- increased intravascular hydrostatic pressure
- decreased plasma colloid osmotic pressure
- decreased lymphatic drainage
13
Q
increased vascular permeability is due to ____
A
inflammation
14
Q
increased vascular permeability sequense:
A
inflammatory stimuli -> local release of inflammatory mediators (histamine, bradykinin, leukotrienes) -> increased vascular permeability
15
Q
increase in intravascular hydrostatic pressure is due to:
A
increase in blood volume in microvasculature
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)
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
18
Q
what happens with congestive heart failure
A
increase blood volume in vasculature behind the failing chamber(s) -> increase hydrostatic pressure -> generalized edema
19
Q
what happens when there is right-sided heart failure
A
increase in blood volume in systemic veins -> subcutaneous edema, hydroperitoneium (acites)
20
Q
what happens when there is left sided heart failure
A
increase blood volume in pulmonary veins -> pulmonary edema
21
Q
a decrease in plasma colloid osmotic pressue is due to ____
A
hypoproteinemia
22
Q
decrease plasma colloid osmotic pressure location and due to what specifically
A
- generalized
- due to increase protein loss or decrease protein synthesis
23
Q
what happens with glomerular amyloidosis
A
loss of albumin in urine -> decreased plasma colloid osmotic pressure -> edema
24
Q
what happens with end-stage liver disease (cirrhosis)
A
decreased protein synthesis by liver -> decreased plasma colloid osmotic pressure -> edema
25
what happens with associated hepatic fibrosis
interferes with portal blood flow -> increase portal vein hydrostatic pressure -> **ascites**
26
decreased lymphatic drainage is due to:
**lymphatic obstruction**
27
decreased lymphatic drainage location and specific compression or blockage
* **localized**
* **trauma, fibrosis, invasive neoplasms, infectious agents**, or congenital malformation (rare)
28
what happens when there is an invasive mammary neoplasm
lymphatic vessel obstruction -> decreased lymphatic drainage -> **edema**
29
what happens when there is lymphatic vessel hypoplasia/aplasia
decreased lymphatic drainage -> **edema**
30
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
31
what is normal hemostasis
physiologic reponse at site of blood vessel injury to seal the injured vessel and prevent blood loss
32
what is primary hemostasis mediated by
**platelets**
33
what is secondary hemostasis mediated by
**clotting factors**
34
what is hemostatic balance
* precisely orchestrated process involving platelets, clotting factors & endothelium
* balance between hemostatic, anticoagulant & fibrinolytic pathways
35
disruption of hemostatic balance causes:
**excessive bleeding or clotting**
36
what is a hemostatic bleeding imbalance
imbalance between hemostatic, anticoagulant & fibrinolytic pathways -> **blood loss or inappropriate clotting**
37
what is hemorrhage
**blood loss** from the circulatory system
38
# small foci
petechiae
small hemorrhages up to a few mm diameter
39
# small foci
ecchymoses
slightly larger hemorrhages up to a few cm diameter
40
hematoma
hemorrhage in tissue large enough to cause a visible blood clot
41
contusion (bruise)
blood leakage from injured vessel into surrounding tissue; associated with blunt trauma
42
what are ex of hemorrhage in body cavities
* hemothorax
* hemopericardium
* hemoabdomen (or hemoperitoneum)
43
hemorrhage in joints
hemarthrosis
44
what are the 3 causes of hemorrhage
1. blood vessel injury
2. decreased platelets
3. decreased clotting factors
45
blood vessel injury is due to:
* trauma
* inflammation
* invasive neoplasms
* infectious agents
* endotoxemia
* uremia toxins
* immune complexes
* collagen disorders
46
what happens when there is a fungal infection in gutteral pouch
carotid artery injury -> hemorrhage
47
what happens when there is a vitamin C deficiency (scurvy)
decreased collagen cross-linking -> fragile blood vessels prone to injury -> **periarticular hemorrhage**
48
a decrease in platelets is due to:
* decreased production
* increased destruction/consumption
* decreased function
49
what happens when there is immune-mediated destruction of megakaryocytes in bone marrow
thrombocytopenia -> **cutaneous hemorrhages**
50
decreased clotting factors is due to:
* inherited deficiencies
* decreased production
* increased consumption
51
what happens with anticoagulant rodenticide poisoning
inhibition of VK epoxide reductase in liver -> decreased production of VK-dependent clotting factors -> **visceral & cavity hemorrhage**
52
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
53
what is clotting hemostatic imbalance
imbalance between hemostatic, anticoagulant, & fibrinolytic pathways -> **blood loss or inappropriate clotting**
54
what is thrombosis
* **inappropriate clotting** within the circulatory system
* blood clot formation **within the circulatory system** of a live animal
55
what is a **thrombus**
aggregate of platelets, fibrin and other blood elements formed **on a vessel or heart wall**
56
if a thrombus (or fragment of a thrombus) **breaks loose and enters the circulation**, it becomes a ____
**thromboembolus**
57
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
58
what is a thromboembolus
* embolus composed specifically of clotted blood
* not all emboli are thromboemboli
59
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**
60
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"**
61
what are the 3 causes of thrombosis
**virchow's triad**
* endothelial injury
* abnormal blood flow
* hypercoagulability
62
what happens with stronglyus vulgaris larval migration
| endothelial injury
cranial mesenteric artery inflammation & endothelial injury -> **thrombosis**
63
what happens with feline hypertrophic cardiomyopathy
| abnormal blood flow
left atrial dilation -> blood statis/turbulence -> **mural thrombosis**
64
what happens with glomerular amyloidosis
| hypercoagulability
loss of antithrombin III -> hypercoagulability -> right atrial thrombosis -> **pulmonary thromboembolism**
65
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
66
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
67
how to classify microvascular thrombi
usually due to **DIC** (disseminated intravascular coagulation)
68
what is the clinical significance of thrombi/emboli
depends on **location & ability to block blood flow**
69
**blockage** of blood flow can result in:
**decreased tissue perfusion** & subsequent **necrosis**
70
if thrombosis is **widespread (DIC)**, it can lead to:
**consumptive coagulopathy** & subsequent **hemorrhage**
71
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
72
alterations in blood flow
accumulation of blood in vascular bed can be **active or passive**
73
hyperemia
**active** engorgement of a vascular bed due to **vasodilation & increased inflow**
74
congestion
**passive** engorgement of a vascular bed due to **decreased outflow**
75
what is the morphology of hyperemia (active)
tissues are **warm & bright red** due to increased delivery of oxygenated blood
76
what is the morphology of congestion (passive)
tissues are **cool & dark red-blue** (cyanotic) due to accumulation of deoxygenated blood
77
congestive heart failure
blood **passively accumulates** in vessels behind the failing chamber(s)
78
right sided heart failure
hepatic congestion (nutmeg liver)
79
left-sided heart failure
pulmonary congestion
80
what is ischemia
inadequate tissue perfusion
81
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)
82
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
83
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)
84
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**
85
what is an infarct
area of tissue necrosis due to **ischemia**
86
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)
87
what is the morphology of chronic infarcts
depressed, tan & firm (fibrotic/scarred)
88
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
89
# circulatory failure
what is shock
state of general circulatory failure that impaires tissue perfusion -> cellular hypoxia +/- cell injury & death
90
cardiogenic shock
decreased cardiac output due to heart (pump) failure
91
hypovolemic shock
decreased circulating blood volume due to massive hemorrhage/fluid loss
92
distributive shock
decreased peripheral vascular resistance with pooling of blood in peripheral tissues due to sepsis, anaphylaxis, etc
