L2 Pathology Circulatory Disturbance I (CVS) PDF

Level 2 Semester 3 ▪ Module CIBL309  Lecture Title Circulatory disturbance I (hyperemia, congestion , oedema, hemorrhage and shock )  Instructor information Dr/ Sarah Nabil Nasif MD Assistant professor of Pathology email: dr_sa...

Level 2 Semester 3 ▪ Module CIBL309  Lecture Title Circulatory disturbance I (hyperemia, congestion , oedema, hemorrhage and shock )  Instructor information Dr/ Sarah Nabil Nasif MD Assistant professor of Pathology email: [email protected] ILOs by the end of this lecture you will be able to: --define hyperemia &congestion , classify types of congestion -define oedema, understand its pathogenesis , classify its types -define hemorrhage , classify its types -define shock , classify its types Congestion and hyperemia HYPERAEMIA (Active hyperemia) Definition: Is an increase in the blood flow to an organ as a result of active dilation of its arterioles and capillaries. Active means change in the muscle tone of the vessels. Types: (1)Physiological: e.g. in muscular exercise. (2)Pathological: e.g. in acute inflammation. Congestion (Passive hyperemia) Definition: Increase venous blood in an organ as a result of obstruction to the venous outflow. The veins, venules and capillaries in the organ become passively dilated. Types: (1)General: which may be acute or chronic. (2) Local: which may be acute or chronic. I. GENERAL VENOUS CONGESTION (1)Acute General Venous Congestion Terminal condition in acute heart failure. All viscera show acute congestion. (2)Chronic General Venous Congestion Gradual venous congestion affecting the whole venous system. Chronic General Venous Congestion Causes: It is caused by right sided heart failure due to chronic obstructive lesions affecting : (1)The heart: As mitral stenosis and myocardial fibrosis caused by coronary atherosclerosis. (2) The pulmonary vessels: As congenital pulmonary stenosis and bilharziasis of the lung which cause narrowing of the pulmonary arterioles. (3)The lung: As emphysema and extensive fibrosis caused by tuberculosis and pneumoconiosis. Chronic General Venous Congestion Pathology: I-General effects: (1) Dyspnea. (2) Cyanosis: Caused by : (a) Stasis in the capillaries causes more hemoglobin reduction by the tissues. (b) Deficient oxygen saturation in the congested lung. (3) Cardiac oedema II-Local effects: Heart, lung, liver, spleen , kidney II. LOCAL VENOUS CONGESTION It is localized congestion in any part of the body whose venous outflow becomes obstructed. (1)Acute Local Venous Congestion Causes: Sudden complete venous obstruction due to thrombosis, ligature or twisting of the pedicle of a movable organ or strangulated hernia. Pathology: Rapid severe distention of the veins and capillaries which may rupture. Oedema occurs rapidly in the tissues. (2)Chronic Local Venous Congestion Causes: Gradual incomplete venous obstruction. It results from venous compression by a tumor, enlarged lymph node or pregnant uterus. Pathology (1) The veins, venules and capillaries below to the obstruction become dilated and congested resulting in oedema (2) Gradual opening of the collateral and anastomotic veins. Examples of chronic local venous congestion: (1) Compression of the femoral vein: Causes venous congestion, swelling, oedema and cyanosis of the lower limb. Oedema Oedema Definition: Oedema is accumulation of abnormal amounts of fluid in the intercellular tissue spaces and/or body cavities. Oedema fluid may be transudate (the normal tissue fluid but in amounts exceeding the normal), exudate (inflammatory fluid) or lymph. Pathogenesis of oedema 1-Increased Capillary Hydrostatic Pressure as in cases of venous congestion (localized or generalized) 2-Decreased Colloid Osmotic Pressure Of Plasma (hypoproteinemia) 3-Lymphatic Obstruction ( as filariasis and Surgical removal of lymphatics as in cases of radical mastectomy (surgical treatment of breast cancer by removal of breast and axillary lymphatics) Pathogenesis of oedema 4-Sodium and water retention: due to renal disease, Salt and water retention leads to increased capillary hydrostatic pressure. 5-Increased Capillary Permeability as in inflammation and hypersensitivity. Escape of proteins in the oedema fluid will lower the plasma osmotic pressure and raises the tissue osmotic pressure causing further oedema. 6-Increased Tissue Osmotic Pressure: It is usually secondary to increased capillary permeability (e.g in inflammation) TYPES OF OEDEMA 1-Localized Oedema: a) Inflammatory oedema (due to acute inflammation). Oedema fluid is exudate. b) Obstructive oedema: venous & lymphatic 2-Generalized Oedema(anasarca) a) Cardiac oedema b) Nutritional oedema c) Renal oedema: TYPES OF OEDEMA 1-Pitting Oedema: In all types of generalized oedema and in the congestive type of localized oedema, the fluid is transudate; which is poor in proteins and does not clot on standing 2-Non-pitting (hard) Oedema: It occurs in cases of lymphatic oedema and sometimes in inflammatory odema. PATHOLOGICAL ASPECTS OF OEDEMA 1-Extent: Oedema is most marked in serous membranes and extremely minimal in bone. 2-Gross Features: Oedema causes swelling, heaviness and pallor of the affected tissue. 3-Microscopic features: Oedema appears as homogenous pale eosinophilic substance. Eosinophilic staining is due to its protein content.Pale staining is due to fluid dilution. 4-Clinical effects depend on the site e.g dyspnea in cases of pulmonary oedema. Neurological manifestation in case of brain oedema due to increased intracranial tension. Hemorrhage Hemorrhage Definition :extravasation of blood from vessels or cardiac chambers into the extravascular spaces Causes : 1. Traumatic (eg. Accident or surgical) 2. Spontaneous Diseases of vascular wall: atheroma or aneurysm Inflammatory injury of vascular wall Destruction of vascular wall by TB, malignancy Hemorrhagic blood diseases as hemophilia and purpura Vitamin C or K deficiency Types of hemorrhage 1-External hemorrhage: escape of blood outside the body Epistaxis :bleeding from the nose Hematemesis : vomiting of blood (source from esophagus, stomach or duodenum ) Hemoptysis :coughing of blood Melena :presence of dark digested blood in stool Hematuria : blood in urine 2- internal hemorrhage :escape of blood inside body cavities Hemothorax :hemorrhage into pleura Hemoperitoneum: hemorrhage in peritoneum Hemopericardium : hemorrhage in pericardium 3- interstitial hemorrhage: escape of blood into interstitial spaces Prticheal hemorrhage, ecchymosis or heamatoma Effect of hemorrhage According to volume and rate of loss 1-small amount :no effect 2-repeated small amount :anemia 3-moderate amount (less than 750ml):anemia for sometimes 4-massive amount of blood: hemorrhagic shock SHOCK SHOCK Definition: a widespread hypoperfusion of the cells and the tissues, occurring due to inadequate effective circulating blood volume. Types: 1. Hypovolemic shock. 2. Cardiogenic shock. 3. Septic shock. 4. neurogenic and anaphylactic shock. The pathophysiology of shock: Shock is the final common pathway for a number of potentially lethal clinical events, including: severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis. Regardless of the underlying pathology, shock gives rise to systemic hypoperfusion; it can be caused either by reduced cardiac output or by reduced effective circulating blood volume.  The end results are hypotension, impaired tissue perfusion, and cellular hypoxia. Although the hypoxic and metabolic effects of hypoperfusion initially cause only reversible cellular injury, persistence of shock eventually causes irreversible tissue injury and can culminate in the death of the patient. HYPOVOLEMIC SHOCK Causes: Loss of blood or plasma volume. This may be caused by: (1)Severe hemorrhage: caused by trauma, surgical procedures, involvement of blood vessels in disease processes. (2)Severe burns: hypovolemia results from inflammatory exudation of plasma fluid from the damaged blood vessels in the vicinity of the extensive burns (3)Severe acute dehydration: due to vomiting and diarrhea in gastroenteritis and cholera. CARDIOGENIC SHOCK Cardiogenic shock results from failure of the cardiac pump and marked reduction in the cardiac output. This may be caused by: 1. Myocardial damage (infarction), 2. Ventricular arrhythmias. 3. Coronary artery occlusion. 4. Extrinsic compression (cardiac tamponade) 5. Outflow obstruction (e.g., pulmonary embolism) SEPTIC SHOCK Causes: Most cases of septic shock (approximately 70%) are caused by endotoxin producing gram-negative bacilli as E.coli (hence the term endotoxic shock)or gram positive bacteria as streptococci. * *Systemic vasodilation (hypotension) *Diminished myocardial contractility *Widespread endothelial injury and activation, causing systemic leukocyte adhesion and diffuse alveolar capillary damage in the lung *Activation of the coagulation system,. neurogenic and anaphylactic shock Neurogenic shock : result from a loss of vascular tone associated with anesthesia or secondary to a spinal cord injury Anaphylactic shock: result from systemic vasodilatation and increased vascular permeability that is triggered by an immunoglobulin E- mediated hypersensitivity reaction (eg.ceftriaxone )  Recommended references https://www.clinicalkey.com/student/content/book/3-s2.0- B9780323353175000041