7 - Hemodynamics (1st Half) Flashcards by G V

Normal Homeostasis of Blood (4)

Integrity of vessel, hydrostatic pressure, colloidal osmotic presure, blood as a fluid

Fluid exits vessel because of hydrostatic pressure (e.g. blood pressure) pushing it out

Fluid returns to vessel because of oncotic (osmotic) pressure pulling it back in

At the capillary level, the pushing forces are about equal to the pulling forces

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Events due to failure of homeostasis (6)

Interstitial water accumulation (edema)

Clotting at inappropriate sites (thrombosis)

Migration of clots (embolism)

Blood flow obstruction to tissues –> cell death (infarction)

Inability to clot after vascular injury (hemorrhage)

Extensive hemorrhage –> hypotension (shock)

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Edema (2)

Increased accumulation of fluid in interstitial space

Generalized edema is known as anasarca

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Edema: Transudate (4)

Noninflammatory

Low protein

Low SG: <1.020

E.g. CHF, renal disorder, malnutrition

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Edema: Exudate (Pus) (4)

Inflammatory

High protein

High SG: >1.020

E.g. DIC

Inflammatory edema by acute inflammation caused with help of: histamine, PAF, C3a and C5a, and leukotrienes

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Possibilities of Edema (4)

Increased hydrostatic pressure

Reduced oncotic pressure

Lymphatic obstruction

Sodium/Water Retention (where sodium goes, fluid goes)

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Increased hydrostatic pressure problems (5)

CHF
Ascites
Pericarditis
Venous Thrombosis
Lower limb inactivity

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Problems with reduced plasma oncotic pressure (4)

Nephrotic syndrome
Protein losing enteropathy
Malnutrition
Liver cirrhosis

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Lymphatic obstruction

Inflammatory
Neoplastic
Postsurgical
Irradiation

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Sodium retention (3)

High salt intake

Increased renin-angiotensin mechanism

Reduced renal perfusion

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Term for cardiac edema and cause

Pulmonary edema

Cause: L/R heart failure due to various reasons

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Term for renal edema and cause

Associated with Nephrotic syndrome

Cause: trauma, infections, anasarca

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Term for brain edema and cause

Cerebral edema

Cause: Trauma, infections, tumors

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Features of lymphatic obstruction and cause

Peu-d’-orange appearance of breast in breast carcinoma

Cause: Filiariasis, any surgical procedures that impede the lymphatic channels, including radiation

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Hyperemia and Congestion

Increased blood volumes within tissues, but have DIFFERENT underlying MECHANISMS and CONSEQUENCES

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Hyperemia (5)

Def: Increased blood volume within tissue

Active process

Arteriolar dilatation

Red in color

E.g. skeletal muscle exercise or inflammation

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Congestion (5)

Increased blood volume within tissue

Passive process

Reduced outflow from tissue

Dusky red in color

E.g. chronic venous congestion of lung, liver

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Venous congestion of Lung: Chronic (3)

Septa are thickened and fibrotic

Lumen contains hemosidern laden macrophages called ‘heart failure cells’

Changes in chronic venous congestion of lung also known as brown induration of the lungs

Venous Congestion of Liver: Chronic (2)

Red brown, slightly depressed area with accentuated uncongested area - ‘nutmeg area’

Hepatocyte necrosis

CHF

Hemostasis

An orchestrated process involving platelets, clotting factors, and endothelium

Occurs at the site of vascular injury and culminates in the formation of a clot to prevent or limit the bleeding

Blood is always in a homeostasis between, and just like bone always is?

Hemostasis and thrombosis. Just like bone always is between ossification and resorption.

Hemostatic sequence at the injured vessel: Primary hemostasis (steps) (5)

Arteriolar vasoconstriction: Neurogenic, endothelin
Primary hemostasis: formation of platelet plug
von Willebrand fact (vWF) and collagen binds to subendothelial collagen
- vWf is glue between platelets and exposed ECM
Activation of platelets + release of secretory granules
Platelet aggregation to form a primary hemostatic plug

Hemostatic sequence at the injured vessel: Secondary Hemostasis (steps) (4)

Tissue factor binds and activates factor VII
Activation of coagulation cascade
Formation of fibrin meshwork
Clot stabilization and resolution

Role of endothelial cells: Antithrombotic Properties (4)

Antiplatelet effects: prostacyclin (PGI2) and nitric oxide, adenosine, diphosphatase

Thrombomodulin is tissue factor pathway inhibitor

Protein C and protein S inhibit factors Va and VIIIa

Fibrinolytic effects: t-PA

Role of endothelial cells: Pro-thrombotic properties (3)

Platelet effects: von Willebrand factor (vWF) Procoagulant effects: tissue factor Antifibrinolytic effects: inhibitors of plasminogen activator (PAIs)

Platelet release (4)

Thromboxane A2 ADP vWF and other clotting factors Platelet derived growth factor

Platelet aggregation (4)

Thromboxane A2 and ADP set up autocatalytic reaction ADP causes platelet aggregation and change in GpIIb-IIIa configuration for fibrinogen bridging GP1B deficiency = bernard soulier GP2B deficiency --> Glanzmann's thrombasthenia

Thrombin Functions: Conversion of fibrinogen to fibrin

Activates factors V, VII, XI, XIII

Thrombin Functions: Platelet activation

By activating platelet activating receptor (PAR)

Thrombin Functions: Pro-inflammatory effects

PAR's expressed on neutrophils and lymphocytes that helps in tissue repair and angiogenesis

Thrombin Functions: Anticoagulant effects

Thrombin stimulates production of tissue repair and angiogenesis

Lab: Prothrombin Time (PT)

Measures extrinsic pathway (7) 10-15 seconds

Lab: Partial Thromboplastin Time (PTT)

Measures only intrinsic pathway 25-30 seconds

Fibrinolytic Cascade (3)

Moderates the size of the ultimate clot Accomplished through the enzymatic activity of plasmin Plasmin breaks down fibrin

Fibrinolytic Substances (3)

Tissue plasminogen activator - most important plasminogen activator. Plasminogen becomes plasmin and than induces FIBRINOLYSIS Urokinase-like PA (u-PA) Streptokinase

Fibrinolytic Substances: Regulation of plasmin activity (2)

alpha 2 - plasmin inhibitor Plasminogen activator inhibitor (PAI)

Hemorrhagic Disorders: Hemostasis (assoicated with bleeding) (3)

Defect in vessel wall Platelets Coagulation factors

Hemorrhagic Disorders: Sudden massive bleeding disorders

Aortic dissection in Marfan's syndrome

Hemorrhagic Disorders: Mild bleeding disorders (2)

von Willebrand's Disease: epistaxis, surgical bleedings, menstruation Coagulation factor deficiencies

Defects of primary hemostasis (8)

1. Platelet of VWD 2. Small bleeds in skin and mucous membranes 3. Petechiae (1-3 mm) - pinpoint hemorrhages under skin 4. Purpura (3 mm) 5. Bleeding in mucus membranes 6. Menorrhagia 7. Epistaxis 8. Intracranial and GI bleeding

Defects of secondary hemostasis (4)

Coagulation factor deficiencies Bleeding into soft tissues and joints Hemarthrosis - bleeding into soft tissues and joints Intracranial hemorrhage

Generalized defects involve blood vessels (4)

Ecchymosis --> large palpable masses (> 3 mm) Palpable purpura Hematoma Vasculitidis

Thombosis: 3 parts

Endothelial injury: can lead to abnormal blood flow Stasis of turbulent blood flow Hypercoagulability of the blood