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Clinical Pathology Exam 1: Circulatory
Terms in this set (89)
What is normal fluid homeostasis?
Unbroken delivery of oxygen and nutrients to maintain health of cells
Maintenance of vessel wall integrity, intravascular hydrostatic pressure, and osmotic pressure (protein)
What is thrombosis and things to consider?
Formation of blood clot
Blood needs to be in liquid form until injury occurs
Have to form a clot then stop the clotting process at the appropriate time
Have to keep fluid, cells, and clotting components circulating within the vascular system
What happens if you have more anti-coagulation signals than pro?
What happens if you have more pro-coag signals than anti?
Hemorrhage, shock, death
Thrombosis, embolism, infarcation
In normal blood flow, what changes occur at the capillaries?
Drop in velocity of flow
Large increase in cross sectional area
Drop in mean pressure of blood
High hydrostatic pressure pushed blood out at arterial end
High osmotic pressure pulls blood in at venous end
What are the roles of endothelial cells in the circulatory system?
Prevent adhesion of cells and platelets
Prevent leukocyte migration from vessel
Circulating clotting factors stay in circulation
Smooth muscle contraction is regulated
How does the endothelial cell of a blood vessel prevent coagulation or cause it?
Secrete Prostacyclin (PGI2):
formed from arachidonic acid in cell wall
prevents adhesion of platelets to endothelium
Release Tissue Factor (TF):
Binds to factor VIIa of clotting cascade
What other important secretions do endothelial cells provide?
smooth muscle relaxation
smooth muscle contraction
How do endothelial cells promote luekocyte migration and angiogenesis?
Leukocyte transendothelial migration:
Inflammatory stimulus causes endothelial cells to express "selectins" to "grip" leukocyte as it passes through
normal wound healing (and vascularization of tumors)
endothelial cell proliferation and migration via angiogenic factors
What is edema?
What are the 4 main causes
Abnormal accumulation of excess fluid in interstitial tissues spaces or body cavities
>Changes in vascular volume, pressue, protein content, or endothelial cell function affect net movement of water
1.Increased intravascular hydrostatic pressure
2. Decreased intravascular osmotic pressure
3. Impaired lymphatic drainage
4. Increased vascular permebility
Increased intravascular hydrostatic pressure
Congestion or hyperemia
Localized: venous obstruction (torsion, volvulus, bandage too tight)
Generalized: fluid overload (*congestive heart failure, iatrogenic, renal disease with sodium retention)
*Transudate (only fluid)
Reduced plasma osmotic pressure
Excessive loss or reduced synthesis of albumin: Hypoproteinemia
Albumin is synthesized in the liver
Liver disease (lack of production)
Kidney disease (Protein-losing nephropathy)
GI disease (Protein-losing enteropathy)
Impaired lymphatic drainage
Obstruction of lymphatic vessels causes fluid to accumulate in interstitial space
Surgery, neoplasms, lymphangitis, intravascular parasites, congenital malformation of lymphatic vessels
If drain fluid accumulation and its milky white: lymph
What is lymphangiectasia?
dilation of lymphatic vessels
Increased vascular permeability
Edema associated with vasculitis or inflammation
Interendothelial gaps become large enough to let fluid, proteins, and leukocytes
*Exudate: fluid AND proteins/cells
Burns, trauma, surgery, bacterial and viral infections
What are the definitions:
Effusion: fluid in body cavity
Ascites: Intraperitoneal accumulation serous fluid (abdominal effusion)
Anasarca: Generalized edema, can contain severe subcutaneous edema as well as thoracic and abdominal cavity
ex. severe right heart failure, hypoproteinemia, liver cirrhosis
Pitting edema: When you can push a finger into the skin and dent remains due to displacement of subcutaneous edema
What is "stocking up" in horses?
stagnation edema common in stabled horses or horses placed in a stall after exercise
Movement is needed to drive lymph circulation, lack of movement causes decreased lymph drainage
What will you see grossly with edema?
Clear fluid within tissues or body cavities
Tissues are wet, shiny, glistening, heavy
Froth in airways
What composes a non-inflammatory fluid?
Transudate: low protein (<2.5 g/dl) and few cells (<1500 cells/ul)
Increased hydrostatic pressure
Decreased osmotic pressure
Decreased lymphatic drainage
Heart failure, severe liver disease, malnutrition, renal disease, gastroenteritis
What composes inflammatory fluid?
Exudate: high protein (>3.0 g/dl), contains leukocytes (>5000 cells/ul)
Endothelial permeability during inflammation
Increased capillary permeability due to endothelial damage
What is modified transudate?
Fluid which has either more cells or more protein than a transudate, but not as much as an exudate
What is hyperemia?
*Active process: blood is pushed in
Arteriolar dilation is responsible for increased inflow of blood into the tissue
Common during inflammation
Tissue is bright red and warm
Must be alive
What is congestion?
*Passive process: blood is backed up
Impaired or decreased venular outflow of blood in tissue
Common cause: heart disease
Tissue is dark red and swollen, and cooler than normal
Acute and chronic varieties
What is chronic passive congestion?
Common with heart disease
Left sided = congestion in lungs (see heart failure cells: alveolar macrophages with hemosiderin from ingesting RBCs)
Right sided = all venous return (lesion in liver = nutmeg liver, jugular distension, abdominal effusion)
What is acute passive congestion?
splenic engorgement following barbiturate administration (euthanasia)
What occurs in congestive heart failure?
Clinical syndrome, CO is unable to keep pace with venous return
Water and sodium retained, blood volume increases, venous capillary beds are distended (increased hydrostatic pressure > edema)
Fluid accumulates in tissues:
Liver (right side failure) > hepatomegaly and centrilobular degeneration
Lung (left side failure) > congestion and heart failure cells
Subcutis (right side failure)
What are clinical signs and gross lesions that occur with left sided heart failure?
Upstream organ: lung
Dyspnea, coughing, exercise intolerance
Congestion and edema of lungs, left atrial dilation, left ventricle dilated or thickened
What are clinical signs and gross lesions that occur with right sided heart failure?
What is cor pulmonale?
Upstream organ: liver, spleen
Exercise intolerance, peripheral edema
Hepatomegaly and splenomegaly
Ascites, edema, distended veins
Cor Pulmonale: right sided heart failure that occurs secondary to pulmonary disease: dirofilariasis, COPD, pulmonary thromboembolism
What are the clinical signs and physical exam findings of canine heartworm disease?
Where are Dirofilaria immitis (worms) found?
What is the pathogenesis?
Exercise intolerance and coughing
Moist cough, respiratory crackles, normal rectal temperature
Pulmonary arteries: arteritis, pulmonary hypertension, thrombosis
Caused by dirofilaria immitis
1. pulmonary artery
2. right ventricle
3. right atrium if large numbers
4. vena cava, if large number, rare
Infection > arteritis/pulmonary hypertension/thrombosis > right ventricle pressure overload > right ventricular concentric hypertrophy > right heart failure aka cor pulmonale
What is hemorrhage?
What are names for different locations of hemorrhage?
The extravasation of blood into the extravascular space
Large accumulations of blood can occur in body cavities:
Hemothorax: blood in thorax
Hemoabdomen/Hemoperitoneum: blood in abdomen
Hemarthritis: blood in joints
Hemopericardium: blood in pericardium
What is exsaguination?
Bleeding to death
Decreased blood volume at least 20%
When does a small amount of hemorrhage cause a huge problem?
Stroke: hemorrhage in brain causes sudden death of brain cells due to impaired flow
Hemopericardium can cause cardiac tamponade= cardiac failure
What is *petechia?
Tiny 1-2mm foci of hemorrhage, often in skin, mucous membranes and serosal surfaces
causes: thrombocytopenia (decreased platelets), thrombocytopathy (abnormal platelet function), and vasculitis (inflammation of blood vessel)
Slightly larger (3mm)
Large hemorrhages (up to 2-3cm in diameter)
What is a hematoma?
when blood remains within a confined space
Capillaries are damaged and bleeding occurs in tissue, not in body cavity or potential space
Large coalescing hemorrhage
Escape of hemorrhage into a body cavity
What is hemostasis?
Arrest of bleeding
Complex interaction between vasculature, platelets, coagulation cascade, and the fibrinolytic system
These systems contain numerous checks and balances
What occurs during primary hemostasis?
1. Vasoconstriction, activation of platelets, formation of platelet plug
2. Formation of fibrin clot via clotting cascade
Removal of fibrin clot following adequate healing
What are the 4 teams involved in hemostasis?
activated platelet, Tissue factor III, Factor Xa, Factors V and VIII - coenzymes, and Thrombin
Prostacyclin, NO, Heparin, Protein C/S-Thrombomodulin, Antithrombin, Tissue Factor, Pathway inhibitor
Plasminogen + tPA +uPA = activated Plasmin
PAI-1 = plasminogen activator inhibitor
What maintains homeostatic anticoagulation?
Endothelial cells secrete prostacyclin (PGI2), NO, and Heparin to prevent blood clots from forming within vessels normally
What is present in an inactivated platelet?
TxA2 (Thromboxane) = procoagulant and vasoconstrictive
ADP granule = contains signal between platelets to active
What is present in an activated platelet?
Secretes ADP to activate other platelets
Adhesions and shape change
TxA2 causes aggregation among platelets and vasoconstriction
Expresses Gp1b: binds vonWillenbrand in collagen
Expresses GpIIb-IIIa: binds fibrinogen
What is the coagulation cascade? (during secondary hemostasis)
A series of enzymatic conversions that convert inactive proenzymes into active enzymes, and culminate in formation of thrombin
Thrombin converts fibrinogen (plasma protein) into fibrin (insoluble fibrous protein) incorporated into a clot at injury site to arrest bleeding
How are coagulation factors identified?
Where are they produced and what do they do?
What cofactors are dependent on Vit K?
Roman numeral and a name
Most coagulation factors are proteins produced by liver
Factors II, VII, IX, X, XI, XII, XIII are enzymes
Factors I, III, V, and VIII are non-enzymatic co-factors
The only non-protein cofactor is IV = Ionized calcium necessary for most steps in cascade
a = indicates activation
*Vitamin K dependent factors: II, VII, IX, X
What is the intrinsic pathway of the coagulation cascade?
12 > 11 > 9 +8 > 10
Common cascade: 10 +5 > 2 Thrombin becomes Prothrombin > 1 Fibrinogen becomes Fibrin > 13 forms crosslinks to strengthen
What is the extrinsic pathway of the coagulation cascade?
3 (TF) > 7 > 10
Common cascade: 10 +5 > 2 Thrombin becomes Prothrombin > 1 Fibrinogen becomes Fibrin > 13 forms crosslinks to strengthen
What does fibrinolysis do?
Limits the size of the final clot by inducing fibrinolytic cascade:
Plasminogen converted to Plasmin (activated)
-Factor XIIa generates plasmin
-T-PA from endothelial cells
-U-PA from plasma and tissue
Plasmin breaks down fibrinogen, fibrin, and cross-linked fibrin
Why must the clotting cascade be restricted to a local site of vascular injury?
Otherwise the entire vascular tree would clot
How does the damaged endothelial cell prevent fibrinolysis?
Releases Plasminogen Activator Inhibitor (PAI-1), this inhibits plasminogen from becoming plasmin to prevent the fibrinolysis of the local clot
What are the Anticoagulatory aspects of healthy endothelium?
Protein C- Protein S- Thrombomodulin:
Form a complex on the endothelial cell to inhibit Factors VIIIa and Va
-Proteins C and S are Vit K dependent
Neutralizes thrombin and Xa, localizes heparin sulfate to the injury site
Tissue Factor Pathway Inhibitor:
Inhibits the *Extrinsic pathway of coagulation cascade, its a protein that inactivates the Tissue Factor-Protein VIIa complex
What do test for in tests that measure platelet status and function?
buccal mucosal bleeding time: measures for platelet plug formation
What do you test for to measure soluble coagulation factors?
PTT (activated partial thromboplastin time): measures intrinsic and common pathways
PT (prothrombin time): measures extrinsic and common pathways
ACT (activated clotting time): measures intrinsic and common pathways, can be prolonged in thrombocytopenia or platelet dysfuction
What tests indicate increased fibrinolysis (usually secondary to increased clot production):
FDP (fibrin degredation products): breakdown products of fibrinogen, fibrin, or cross-linked fibrin
D-dimers: more specific for cross-liked fibrin
Fibrinogen: increases with inflammation, decreases with consumption
What are primary hemostasis disorders?
What are secondary hemostasis disorders?
Hemophilia A: Factor VIII deficiency
Hemophilia B: Factor IX deficiency
Vitamin K deficiency (Factors II, VII, IX, and X rely on this)
What are multifactorial hemostasis disorders?
Disseminated intravascular coagulation
What occurs in Thrombocytopenia?
What causes this disorder?
Decreased circulating platelets
Spontaneous bleeding disorders may occur with platelet counts < 20,000/mL of blood
Deficient formation of megakaryocytes in bone marrow
Excessive consuption of platelets, ex. widespread endothelial damage (DIC, septicemia)
Premature destruction of platelets (ITP)
Sequestration of platelets. Rare, due to splenic disease
What occurs in Thrombocytopathy?
What are the causes?
Defective platelet function, usually associated with an inability for the platelet to adhere during primary hemostasis
Can be inherited:
-von Willebrands disease: dysfunction or lack of vWF
-Chediak-Higashi Syndrome: storage disease, no ADP
-Glanzmann's thrombasthenia: defective GPIIbIIIa
-Bernard-Soulier syndrome: defective GPIb
Can be acquired:
Therapy with aspirin, phenylbutazone (NSAIDs), liver disease, uremia
What are clinical manifestations of thrombocytopathy?
Inability to adhere or aggregate platelets at the site of vascular injury
May see petechiae, ecchymosis, epistaxis, or more severe hemorrhage
What are the features of Von Willebrand's disease?
Absence or decreased von Willebrands factor
Platelet cannot bind to collagen in area of injury
Modes of inheretance: autosomal recessive and autosomal incomplete dominant
Clinical manifestations: in puppies see gingival bleeding when teeth erupt, prolonged estrus bleeding, increased bleeding following venipuncture
Platelet count: normal
*Buccal mucosal bleeding time: prolonged
What occurs in hemophilia?
Inherited lack of procoagulant proteins in plasma
Hemophilia A: Factor 8
Hemophilia B: Factor 9
Sex-linked, recessive inheritance: males affected, female carriers
Clincial manifestations: in puppies gingival bleeding when teeth erupt, hemarthrosis, subcutaneous hematomas, or increased bleeding following venipuncture
Platelet count: normal
Buccal mucosal bleeding time: normal
PTT: prolonged (intrinsic pathway being affected)
What occurs in these disorders of coagulation?
Vit K deficiency/Antagonism:
Disseminated IV coagulation:
Infections-Viral, Rickettsial, etc:
Decreased production of coagulation factors, decreased recycling of Vit K
Antagonism of recycling by toxins, decreased absorption from gut
Massive increase in systemic coagulation, then depletion of coagulation ingredients = hemorrhage
Can infect megakaryocytes or precursor cells: less production of platelets
What are Vit K dependent coagulation factors?
II, VII, IX, X
Also protein C/S
Animals poisoned following ingestion of Vit K antagonist = deficiency of Vit K
-dicumarol in moldy sweet clover (cattle)
-warfarin and anticoagulent rodenticides (dogs)
Platelet mucosal bleeding time: normal
Buccal mucosal bleeding time: normal
PT: prolonged (common pathway)
PTT: prolonged (intrinsic and common pathway)
What is Virvhow's triad of thrombosis? (blood clot)
Hypercoagulability: coagulation factors and platelet factors
Abnormal blood flow: stasis or turbulence
Can independently cause thrombosis or influence each other to cause thrombosis
What causes hypercoagulability of blood?
Any alteration in the coagulation pathway that predisposes to thrombosis
Genetic: mutation in coagulation factor genes
Inflammtion: most common, TNF induces procoagulant state
Protein-losing nephropathy: loss of antithrombin III
Enhanced platelet activity: diabetes mellitus, nephrotic syndrome, heartworm disease, uremia
Cancer: tumor cells can secrete procoagulant factors
What can cause endothelial cell injury that leads to thrombosis?
Thrombosis forms in arteries where flow rates are high
Any perturbation in the pro and antithrombotic functions of endothelial cells
Can be due to loss of cells or abnormal function
What alterations in normal blood flow can lead to thrombosis?
Turbulence: causes cell injury and pockets where stasis of blood occurs
-disrupts laminar flow of blood
-prevents dilution of activated clotting factors
-Retards the inflow of clotting factor inhibitors from blood and permits thrombi to build up
Stasis: veins have slower rate and reduced blood flow
-promotes activation of endothelial cells
-allows platelets to contact endothelial cells
What do you see with Arterial thrombosis? (arteriothrombosis)
Pale gray-tan mass with concentric layers of fibrin and platelets intermixed with blood
Begins at site of endothelial injury, forms in area of high blood flow
Growth of thrombus is
, resulting in tail that is not attached to the vessel wall, portions of the tail can break off and form thromboemboli
What occurs in venous thrombus? (phlebothrombosis)
Found in deep veins where blood flow is slower
Dark red, gelatinous, soft, shiny
Molded to shape of lumen of the vein and grow
from site of initiation
Large number of RBCs are loosely incorporated into thrombus because of slow blood flow
Most are occlusive
What is a postmortem clot?
"chicken fat clot" or "currant jelly clot"
*NO point of attachment to vessel wall
Off-white to yellow areas: chicken fat clot
Shiny red: currant jelly clot
Conforms to shape of lumen
What are the 4 fates of a thrombus?
1. Dissolution: removed by fibrinolytic activity
2. Incorporation into vessel: thrombus undergoes fibrosis and endothelium regrows over the defect, soluble fibrin is replaced with collagen
3. Recanalization: thrombus undergoes fibrosis with ingrowth of endothelial cells, smooth muscle cells and fibroblasts are present, new capillary channels are formed
4. Embolus: detached intravascular solid, liquid, or gaseous mass carried by blood to a site distant from its origin
Embolism: process of forming an embolus, sudden blocking of an artery by a clot of material (embolus0
What microscoptic features will you see if a thrombus or embolus decreased tissue perfusion?
Infarct that leads to
In tissues: coagulative necrosis
In CNS: liquefactive necrosis
What are factors that influence the rate of development of an infarct? (4)
1. Nature of vascular supply of that organ
-dual blood supply (liver, lung): infarcts are rare
-end-arterial blood supply (kidney): infarcts are common
2. Rate of development of occlusion:
-if slow: collateral circulation may prevent infarction
3. Vulnerability of affected tissue to hypoxia
-neurons and myocardial cells are highly metabolic and sensitive to hypoxia
4. Oxygen content of blood
-pre-existing anemia or congestive heart failure aids in development of infarction
What is Disseminated intravascular coagulation (DIC)?
Pathological activation of the clotting system that leads to generalized intravascular clotting
*Microthrombosis: occurs over extensive surface area (capillary beds)
*Consuption and depletion of platelets and clotting factors = widespread hemorrhage
Always secondary condition:
-Induced by agents that damage endothelium and/or activate the clotting cascade
-Seen with shock, some viral diseases, bacterial septicemias, heatstroke, severe burns, etc
What kind of disorder is Disseminated Intravascular coagulation (DIC)?
What is occurring in the coagulation cascade?
Thrombo-hemorrhagic disorder: there is too much thrombin being generated, which leads to widespread coagulation and depletion of circulating clotting factors
Potential complication of any disorder that causes increased expression of TF or activation of proteases that active clotting systemically
Hemorrhage is terminal manifestation, may occur at many sites: organ failure
*Extrinsic pathway activation: lots of TF3 released leading to excessive thrombin systemically
Deplete clotting factors and platelets in capillaries
Also, massive production of plasmin > proteolysis of clotting factors and fibrinolysis
Any new damage = hemorrhage
What would be the blood values in DIC?
Platelet count: decreased
Buccal mucosal bleeding time: decreased
PT: prolonged (extrinsic pathway*)
PTT: +/- prolonged
Fibrinogen: decreased (being consumed)
D-dimer: Increased (plasmin massively activated)
What is shock? aka cardiovascular collapse
Circulatory dyshomeostasis associated with loss of circulating blood, reduced CO, and/or inappropriate peripheral vascular resistance
Impaired tissue perfusion > Cellular hypoxia > cell death
What are the 3 causes of shock?
Cardiogenic: myocardial pump failure = reduced CO and stroke volume (heart diseases)
Major compensatory mechanism: sympatheitc stimulation
Hypovolemic: reduced circulating blood volume (hemorrhage, severe fluid loss)
Blood maldistribution: vasodilation, peripheral blood pooling (sepsis*= peripheral vasodilation is caused by bacteria or fungi ex. LPS of gram-, anaphylactic shock= histamine causes vasodilation, neurogenic shock)
What are the 3 stages of shock?
1. Non-progressive stage: reflex compensatory mechanisms are activated and perfusion of vital organs is maintained
2. Progressive stage: tissue hypoperfusion and acidosis occur
3. Irreversible stage: syndrome of multiple organ failure occurs, cellular and tissue injury is so severe that survival is not possible
What are clinical signs of shock?
hypotension, weak/rapid pulse, tachypnea (breath faster), cool/clammy/cyanotic extremities, hyperemic/cyanotic membranes
Second phase: organ insufficiency
What are morphologic lesions of shock?
Adrenal glands: necrosis and hemorrhage
Kidney: acute tubular necrosis, renal cortical necrosis
Lung: diffuse alveolar damage, fibrin thrombi
Hemorrhages on serosal surfaces and skin (DIC)
What is anemia?
How is it measured?
What are clinical features
A reduction below the normal limits of the total circulating red blood cell mass
Measured by packed cell volume and hemoglobin level in blood, species dependent
Clinical features: pale mucous membranes, muscle weakness, exercise intolerance, rapid respiratory rate
How do we classify anemia? What are common forms of each type?
Lack of production: non-regenerative
ex. chronic hemorrhage (Iron deficiency gradually develops)
chronic inflammation (hepcidin from liver inhibits iron transfer from enterocyte to plasma and iron release from macrophages)
renal disease (lack of erythropoietin)
Bone marrow stem cell diseases: (aplastic anemias)
Blood loss: regenerative
ex. acute hemorrhage (trauma, splenic hemangiosarcoma)
Increased destruction = Hemolytic anemia: regenerative
ex. immune mediated: antibody-mediated transfusion reaction or autoimmune disease
clinical signs: icterus and splenomegaly, mainly extravascular hemolysis
Hemoparasites (babesia and and anaplasma)
Copper toxicity in sheep (intravascular hemolysis)
What do we see with hemolytic anemia from copper toxicity in sheep?
Pathogenesis: diets high in Cu, stored in hepatocytes, the functional reserve of hepatocytes exceeded > hepatic necrosis and Cu release to blood
Cu is toxic to blood, Cu in circulation kills circulated RBCs and releases hemoglobin into the blood > hemoglobinuric nephrosis (hemoglobin is toxic to kidney)
= Intravascular hemolysis
What is one of the most common causes of anemia in juvenile animals?
ex. Haemonchus contortus in lambs/kids are blood eaters (RBC an protein) > anemia and hypoproteinemia
Ancylostoma caninum in puppies
What is cardiomyopathy?
What are the 3 forms?
Primary myocardial disease with unknown etiology
What is concentric hypertrophy in the heart?
myocardial cells become thicker, increased myofibrils
Secondary response to pressure overload
Ventricular wall is noticeably thicker
What is eccentric hypertrophy?
Myocardial cells and myofibrils elongate
Secondary response to volume overload
Ventricular wall looks stretched out
What do you see with dilated cardiomyopathy?
All heart chamber volumes are enlarged
Atria and ventricles may be dilated and flabby
Dysfunction in systolic phase of cardiac cycle
Common in large breed dogs, genetic basis
What do you see in hypertrophic cardiomyopathy?
Both ventricles undergo symmetric, concentric hypertrophy
Ventricle is abnormally stiff, resulted in impaired ventricular filling = *diastolic phase dysfunction
clinical presentation: unexpected death
Inherited disease: cats (maine coon and ragdoll)
What do you see in restrictive cardiomyopathy?
Reduced ventricular filling due to decreased compliance of ventricles
Fibrosis of endocardium and/or myocardium
Dysfunction of diastolic phase
Where does fluid accumulate with only left ventricular failure?
Left: pulmonary edema, hemosiderophages (heart failure cells) in alveoli of lungs
Right: passive congestion in liver (centrilobular), ascites, jugular distension
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