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