Hemodynamic Pathology Lecture 5 PDF

Hemodynamic Pathology Part 1 Dr. Floyd Adlaon  Objectives Describe the normal process of capillary exchange and the role of plasma proteins in retaining fluid within the vasculature. Explain the different pathophysiology of edema. Differentiate hyperemia and congestion. De...

Hemodynamic Pathology Part 1 Dr. Floyd Adlaon  Objectives Describe the normal process of capillary exchange and the role of plasma proteins in retaining fluid within the vasculature. Explain the different pathophysiology of edema. Differentiate hyperemia and congestion. Define hemostasis and explain its role in preventing excessive bleeding after vascular injury. Overview - Important Terms Edema- increased fluid in the extracellular matrix Hyperemia - increased blood flow Congestion - increased accumulation Hemorrhage - extravasation Hemostasis - stop blood flow Thrombosis - clotting of blood in the circulatory system Infarction - local death of tissue due to obstruction of blood supply Shock - circulatory failure/collapse Overview The health of cells and tissues depends on the circulation of blood, which delivers oxygen and nutrients and removes wastes generated by cellular metabolism. What will happen if there is accumulation of fluid? Pathophysiologic Categories of Edema Starling Forces at Play - Definitions Hydrostatic pressure -push fluid out (Arterial) Oncotic pressure -pull fluid in (Venous) Lymphatic circulation -higher hydrostatic ALBUMIN pressure->remove excess fluid EDEMA & EFFUSIONS EDEMA - accumulation of fluid in the tissues EFFUSIONS - accumulation of fluid in body cavities 2 Types of Fluid: Inflammatory or Non-inflammatory Inflammatory - protein-rich exudates due to increased vascular permeability Non-inflammatory - protein-poor transudates - due to heart failure, liver failure, renal disease, malnutrition  These are various causes of edema Normal hydrostatic pressure - arteriolar end 1. INCREASED HYDROSTATIC PRESSURE - 28-35mmHg, venular end 15-17mmHg (red square) mainly caused by disorders that impair Local increase in Hydrostatic pressure - impaired venous return (e.g., DVT & congestive venous outflow (DVT of limbs) heart failure) Generalized increase in venous pressure - result to systemic edema (Congestive heart failure) Normal pressures in Arterial and Venous End Mechanism of Reduced Cardiac EDEMA Output Heart failure -> reduced cardiac output-> reduced Renal blood flow  These are various causes of edema 2. REDUCED PLASMA OSMOTIC PRESSURE - decreased total protein (inadequate synthesis in liver disease or malnutrition) or increased loss of albumin (in nephrotic syndrome)  These are various causes of edema 3. SODIUM AND WATER RETENTION - Sodium retention is associated with obligate water retention - causes inc hydrostatic pressure (due to intravascular fluid volume expansion) and diminished vascular colloid osmotic pressure (due to dilution)  These are various causes of edema 4. LYMPHATIC OBSTRUCTION - trauma, fibrosis, invasive tumors, infectious agents, surgery Lymphatic Obstruction Filariasis - parasitic infection affecting inguinal lymphatics resulting in elephantiasis  These are various causes of edema Lymphatic obstruction - Neoplastic Resection and/or Radiation to axillary lymphatics -> arm edema Carcinoma of breast with obstruction of superficial lymphatics -> edema of breast skin “peau d’orange” (orange peel)  These are various causes of edema 5. Inflammatory edema - increased vascular permeability Too much fluids not drained to the lymphatics -> edema Types of Edema I. Localized or generalized II. Pitting or Non-pitting III. Transudate or exudate I. Localized or Generalized Localized: a. Inflammatory edema b. Lymphatic edema due to lymphatic obstruction c. Edema due to localized venous congestion d. Pulmonary edema Generalized: a. Cardiac edema b. Nutritional edema: Due to hypoprotenemia in malnutrition, malabsorption, liver disease c. Renal edema: starts at the eyelids then becomes generalized II. Pitting or Non-pitting Pitting edema: occurs when venous pressure is increased (righ sided heart failure) or osmotic pressure is decreased (hypoproteinemia) -More marked in dependent parts -Forms a pit when pressed by the thumb Non-pitting edema: No pitting takes place 1. Lymphatic edema 2. Sometimes inflammatory edema III. Transudate or exudate The edema fluid occuring in hydrodynamic derangements is typically protein-poor transudate. Conversely, because of increased vascular permeability, inflammatory edema is protein rich exudate Morphology of Edema Gross features: swelling, heaviness and pallor of the affected tissue Microscopically: clearing and separation of the extracellular matrix (ECM) and subtle cell swelling Subcutaneous Edema - diffuse or region with high hydrostatic pressure; distribution often influenced by gravity (appears on the legs with prolonged standing); pitting edema - finger pressure leaves a depression Morphology of Edema Edema due to renal dysfunction - appears first containing loose connective tissue. Periorbital edema is a finding of severe renal disease. Pulmonary edema - often two to three times their normal weight, and sectioning yields frothy, blood-tinged fluid—a mixture of air, edema, and extravasated red cells. Brain edema - narrowed sulci and distended, flattened gyri Clinical Correlation Pleural Cavity (Hydrothorax) Pericardial Cavity (Hydropericardium) Peritoneal Cavity (Hydroperitoneum or ascites) Anasarca - severe and generalized edema with SQ tissue swelling t HYPEREMIA AND CONGESTION HYPEREMIA AND CONGESTION Both stem from increased blood volumes within tissues with different causes HYPEREMIA - active arteriolar dilation (inflammation or exercise) -> increased blood flow ERYTHEMA - to increase delivery of oxygenated blood HYPEREMIA AND CONGESTION CONGESTION - passive from reduced venous outflow; systemic (cardiac failure) or localized (venous obstruction) CYANOSIS - accumulation of deoxygenated hemoglobin Chronic passive congestion - chronic hypoxia -> tissue injury and scarring; will show capillary rupture & hemosiderin-laden macrophages MORPHOLOGY of Hyperemia and Congestion Normal Congested Lung: Acute pulmonary congestion Marked by blood-engorged alveolar capillaries and viable degrees of alveolar septal edema and intra-alveolar hemorrhage The typical picture of acute pulmonary edema is congestad alveolar vessels with transudate inside of the alveoli. MORPHOLOGY of Hyperemia and Congestion Lung: Chronic pulmonary congestion GROSS: hard, with brown spots scattered - brown induration; soggy and frothy on cut section LM: septa thickened and fibrosis Alveolar spaces containing ‘heart failure cells’ - hemosiderin-laden macrophages (commonly seen in left sided heart failure) Manifestation: Rusty sputum, dyspnea Acute Passive Congestion, Liver The central vein and sinusoids are distended with blood, and there may even be central hepatocyte dropout due to necrosis The periportal hepatocytes, better oxygenated because of their proximity to hepatic arterioles, experience less severe hypoxia and may develop only reversible fatty change. Acute Passive Congestion, Liver The red “dots” are congested central veins. Chronic Passive congestion Liver with chronic passive congestion and hemorrhagic necrosis  CONGESTION LIVER: Chronic hepatic congestion “Nutmeg Liver” GROSS: red-brown zones accentuated against the yellow surrounding zones LM: centrilobular necrosis and congestions, and perilobular fatty changes; fibrosis Long-standing, severe hepatic congestions: hepatic fibrosis (cardiac cirrhosis) END OF PART 1