Congestion, Edema, Hemmorrhage

Inflammatory Edema pathophysiology

ARteriolar dilation, capillary bed opening, increased capillary hydrostatic pressure, increased capillary membrane permeability causing plasma protein and leukocyte release and subsequent decrease in plasma osmotic pressure

Hyperemia

Also known as congestion, occurs when vascular spaces of tissue experience excess of of blood volume, increasing capillary hydrostatic pressure and often edema

Active hyperemia/congestion

Arteriolar dilation and recruitment of capillariles leading to increased blood flow into an organ, and reddening, as occurs during blushing, exercise, and inflammation

Edema in body cavities

Ascites, pulmonary effusion, anasarca (severe generalized edema, involves whole abdomen)

Cardiac tamponade

Blood fills pericardial sac, compressing heart, preventing heart filling, impairing cardiac output, death if not treated

Hypervolemia with Na+ and H20 retention

Cause of edema in CHF, nephrotic syndrome, cirrhosis; increases hydrostatic pressure, and decreases plasma osmotic pressure

Splenic Congestion

Cause: Back up in portal vein affecting splenic and superior mesenteric veins upstream Pathology: Loss of tissue architecture lobes and much of 'white' tissue, overly red

Liver Congestion

Cause: right heart failure causing backflow through inferior vena cava directly to portal vein and liver Pathology: Central vein and sinusoids overflowing with blood, centriolobular necrosis, periportal hepatocytes may remain viable

Lymphatic obstruction

Caused by tumors, fibrosis, radiation, surgery result: lymphedema, protein and fluid excess

Pulmonary edema

Causes: LHF, renal failure, lung infections Gross exam: wet, heavy, frothy Pathology: alveoli distended with pink homogenous fluid and air bubbles, impairing gas exchange and encouraging infection

Acute pulmonary congestion

Causes: acute failure of left ventricle, as due to MI Appearance of congested lung on gross exam: wet, heavy, hemorrhagic, congested, redder Histology/Pathology: Capillaries overflowing with blood, edema, and foci of intra-alveolar hemorrhage

Chronic passive pulmonary congestion

Causes: chronic heart failure Pathophysiology: increased blood pressure breaks capillaries, causing RBC release; macrophages consume rbcs, becoming hemosiderin laden (orange), indicative of heart failure

Cardiac hemorrhage

Causes: trauma, heart attack

Subcutaneous edema

Diffuse or dependent (on gravity, as in lower extremeties); can restrict blood flow, wound healing, encourage infection

Edema

Excess of fluid in interstitial tissue spaces and body cavities due to an increase in forces/factors which favor filtration, commonly occurs with increase in total body fluid

Passive hyperemia/congestion

Impaired ability of deoxygenated blood to leave tissues due to either a local issue such as a venous blockage or systemic issue such as heart failure; may cause cyanosis, degeneration, and eventual tissue death

Congestive heart failure pathophysiology

Impaired cardiac output overal, increased sodium and water retention by kidneys leading to hypervolemia, increasing venous pressure and edema

Cerebral edema

Interferes with blood supply, alters brain structure, may cause hernias

Hemorrhage

Loss of blood from vasculature, usually due to vessel rupture from pressure (capillaries) or injury (heart, artery, vein) such as trauma, inflammation, neoplasm, atherosclerosis

Edema causes

Non-inflammatory-- increased capillary hydrostatic pressure, dcreased plasma oncotic pressure, obstruction, hypervolemic Inflammatory -- tissue injury, infection

Edema and reduced plasma oncotic pressure

Pathophysiology: Decreased plasma protein due to excessive loss in nephrotic syndrome or decreased synthesis in cirrhosis of liver or protein malnutrition. Causes sodium and H20 retention, generalized edema, effusions, and in particular edema of eyes, eyelids, and other soft cts (periorbital edema)

Exudate

Protein rich fluid found in inflammatory edema

Hemorrhage contributing factors

Thrombocytopenia, platelet dysfunction, coagulation factor deficiency, capillary fragility

Metrorrhagia

bleeding outside of menses

hypotensive shock

blood vessels lose tone, vasodilation occurs (as in septic or anaphylactic shock)

Hemoptysis

coughing up blood

CHF signs and symptoms

dyspnea, distension of neck veins, chronic organ congestion (lungs, liver, spleen), peripheral and subcutaneous edema, rales and crackling breath sounds

Menorrhagia

excessive menstrual bleeding

Left sided heart failure

impaired blood flow causing backup upstream in pulmonary circulation, causing passive pulmonary congestion/edema

Right sided heart failure

impaired venous return causes passive congestion, typically in liver and spleen, and increased capillary pressure leading to subcutaneous edema in areas most affected by gravity, i.e. ascites, pleural effusions

Localized edema causes

inflammation, venous/lymphatic obstruction i.e. DVT

Skin hemorrhage

petechiae, ecchymosis, purpura

Transudate

protein poor fluid found in noninflammatory edema

Cardiogenic shock

shock caused by impaired heart function from trauma or heart attack

Hypovolemic shock

shock caused by low blood volume, as following hemorrhage or dehydration

Neurogenic shock

shock caused by nervous system damage, such as spinal injury

intracerebral hemorrhage

stroke

Generalized edema causes

systemic issues with fluid/electrolyte homeostasis such as congestive heart failure, nephrotic syndrome, cirrhosis

Hematemesis/hematochezia/melena

vomiting blood, bloody stool, black stool ; caused by bleeding in GI tract

Shock

when body lacks blood flow symptoms: hypotension, cold, clammy skin, tachycardia pathophysiology: lack of oxygen/nutrients causes cell injury in most sensitive organs, becomes irreversible if shock continues