Circulatory Disturbances- Dr. Llanes Flashcards
Edema
Abnormal accumulation of excess extracellular water in interstitial spaces or in body cavities
or fluid outside of the vascular and cellular water compartments
Pathomechanisms of edema
- increased blood hydrostatic pressure
- decreased plasma colloidal osmotic pressure
- lymphatic obstruction
- increased vascular permeability
2 types of edema
Inflammatory & non-inflammatory
Inflammatory edema characteristics
referred to a exudate Increased vascular permeability Edema fluid is protein rich High specific gravity Less than 7000 nucleated cells per uL
Non-Inflammatory edema characteristics
Referred to as transudate
Edema fluid is protein poor
Low specific gravity
Less than 1500 nucleated cells per uL
Gross descriptors of edema
- wet
- gelatinous
- heavy
- swollen organs
- fluid weeps from cut surfaces
- may be yellow
histological appearance of edema
- Clear or pale eosinophilic staining depending on inflammatory or non
- spaces are distended
- blood vessels may be filled with RBC’s
- lymphatics are dilated
- collagen bundles are separated
pitting edema
When pressure is applied to an area of edema a depression or dent results as excessive interstitial fluid is forced to adjacent areas
Hydrothorax
fluid in the thoracic cavity
Pericardial effusion
- Mulberry heart disease
- type of inflammatory edema
- note fibrin strands and cloudy appearance of the pericardial fluid
Ascites or hydroperitoneum
fluid (transudate) in the peritoneal cavity
anasarca
generalized edema with profuse accumulation of fluid within the subcutaneous tissue
Submandibular edema- common name
Bottle jaw
Clinical significance of edema
- Depends on the extent, location and duration
- Tissue can become firm and distorted due to fibrous connective tissue buildup
Pulmonary edema
- Non-inflammatory is associated with left-side congestive heart failure
- Inflammatory due to damage to pulmonary capillary endothelium (such as pneumonia)
Chronic pulmonary edema
- associated with heart failure
- fibrosis can occur in alveolar walls
- accumulation of heart failure cells
Hyperemia
Local increase in blood volume and flow resulting in engorgement of vascular bed with oxygenated blood
Congestion
- passive engorgement of vascular bed
- similar to hyperemia, however due to decreased outflow instead of increased flow
Causes of physiological hyperemia
- digestion
- exercise
- heat dissipation
- neurovascular (blushing)
pathological hyperemia
- underlying pathological process (generally inflammation)
- arteriolar dilitation secondary to inflammatory stimulation
- reddening caused by inflammation and edema
Gastrointestinal congestion due to twisting which cuts off blood flow
-Gastric or intestinal volvulus
Pulmonary congestion is usually caused by
heart failure
Subacute to chronic hepatic congestion is usually the result of
Right-side congestive heart failure
Common name for chronic hepatic congestion
nutmeg liver
Hemorrhage
- the escape of blood from vasculature
- can be internal or external
Causes of Hemorrhage
-trauma
-sepsis
viremia, bacteremia, toxins
-abdominal neoplasia
-coagulation dysfunction
Clinical significance of hemorrhage is determined by
location and severity
largest concern in acute hemorrage
hypovolemic shock
Hemopericardium
blood in the pericardial cavity
Hemorrhage per rhexis
Hemorrhage caused by substantial tear in vascular or cardiac wall
Hemorrhage per diapedesis
- caused by a small defect in the vessel wall
- caused by RBC’s passing through vessel wall in cases of inflammation or congestion
Hemorrhagic diathesis
Increased tendency to hemorrhage from normally insignificant injuries
Hemothorax
blood in the thoracic cavity
Hemoarthrosis
blood within a join space
hemoptysis
- coughing up of blood
- blood-stained sputum from lungs or airways
Epistaxis
bleeding from nose
Petechia
small hemorrhagic foci on an organ
Ecchymosis
larger hemorrhagic foci
Agonal Hemorrhages
petechiae and ecchymoses associated with terminal hypoxia
Suffusive Hemorrhages
Larger than ecchymosis and contiguous
Methods of hemorrhage resolution
- reabsorption
- phagocytosis
- organizing hematoma
Stages of hematoma
- Hemoglobin (red-blue)
- Bilirubin (blue-green)
- Hemosiderin (yellow-brown)
Hemostasis
Arrest of hemorrhage by physiological or surgical means
Pathological hemostasis
thrombosis- unnecessary activation of physiological hemostatic agents forms a clot
Components necessary for normal hemostsis or thrombosis to occur
- vascular wall
- platelets
- coagulation cascade
Which vasoconstrictor is the first to be released when injury occurs?
endothelin
What causes platelets to adhere to von Willebrand factor and be activated?
glycoprotein lb (Gplb)
Activated platelets undergo a shape change from ______ to _________.
Small and rounded
Flat plates with increased surface area
During platelet activation _____ and _____ are releases which leads to platelet aggregation via ___________.
ADP, TXA2
Fibrinogen binding to Gplb-llla Receptors
At the end of primary hemostasis we are left with a _______ in the affected area.
Hemostatic plug
Pathogenesis of Thrombosis (Virchow triad)
- endothelial injury
- Alterations in blood flow
- Hypercoagulability
Verminous thrombosis
Thrombus in cranial mesenteric artery of horses with Strongylus vulgaris infection
Potential outcomes of thrombus
- lysis
- propagation
- embolization/recanalization
Embolism
Passage through the cardiovascular system of any material capable of lodging in the lumen of a vessel.
Thromboembolism
Embolism caused by pieces of a thrombus
Disseminated Intravascular Coagulation
Generalized activation of blood coagulation system
DIC can lead to________ and _________.
Consumptive coagulopathy, hemorrhagic diathesis
Infarction
Localized area of ischemic necrosis in a tissue or organ caused by occlusion of the cardiovascular system.
Types of Shock (Cardiovascular collapse)
- Cardiogenic
- Hypovolemic
- Anaphylactic
- Neurogenic
- Septic
Most common cause of septic shock
Endotoxin producing gram- bacilli
