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52 Cards in this Set
- Front
- Back
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Hyperemia vs Congestion |
Hyperemia: active process. Vasodilation of small muscular arteries and arterioles to fill increased physiological need. Congestion: Passive process. Venous obstruction past area of congestion resulting in decreased outflow of blood and increase in deoxygenated blood to tissue. Pathological |
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Effects of vascular congestion |
Edema Hemorrhage Long term - parenchymal loss and replacement by fibrosis (parenchyma die first because have high metabolic need) |
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Two most common types of vascular congestion |
Pulmonary congestion Hepatic congestion |
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Pulmonary congestion |
Increased lung capillary pressure due to heart failure leads to pulmonary edema and small hemorrhages. Chronic changes are: 1. Thickened, fibrotic lobular septa with loss of lung parenchyma 2. Hemosiderin macrophages ("heart failure cells") in alveoli. Hemosiderin is a heme breakdown product following hemorrhage that is taken up by macrophages. |
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Chronic liver congestion |
Gross appearance is "nutmeg liver" Punctate areas of necrosis surrounding viable liver. Liver has arterial and portal blood supply which enter hepatic lobule via portal tract. Both flow through hepatic sinusoids drain to central vein. Zone furthest from portal tract and closest to central vein (Zone 3) is nutrient and oxygen poor, and most susceptible to ischemic injury. In chronic liver congestion, slowed flow due to congestion = ischemic injury, necrosis of hepatocytes, and fibrosis leading to cirrhosis. |
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Edema |
Increased extracellular fluid (transudate) that is low in plasma proteins. Collects in interstitium (called tissue edema) and serosal cavities (effusion) Can be localized (due to venous obstruction) or systemic (due to increased osmotic pressure) |
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Ascites |
Effusion in peritoneal cavity |
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Systemic edema |
Anasarca |
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Types of edema |
Cutaneous, localized Dependent - most common in elderly, secondary to heart failure Pulmonary - secondary to heart failure Cerebral Ascites - liver failure Pleural/pericardial effusions |
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Starling equation |
Jv = Kf [(Pc-Pi)-(PIc-PIi)] Fluid movement is equal to different in hydrostatic pressure minus difference in osmotic pressure. Osmotic pressure increases over capillary bed, hydrostatic pressure decreases. |
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Is osmotic pressure ever dominant over hydrostatic pressure? |
No - requires lymphatic system to get unresorbed ECF back into circulation. |
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Causes of edema |
Physical/chemical (most common) - Increased hydrostatic pressure due to venous obstruction (heart failure) or lymphatic obstruction (lymphedema) - Decreased plasma osmotic pressure due to protein wasting conditions or liver dysfunction (low production of plasma proteins Primary damage to capillaries (endothelial activation = leaky capillaries) - Heat, inflammation, shock, angiogenesis |
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Dependent edema |
Due to defects in systemic circulation, most commonly heart failure but also protein wasting conditions (nephrotic syndromes or GI) Tissue edema where gravity pulls fluid down Also called "pitting edema" because does not rebound. |
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Pulmonary edema |
Commonly caused by acute or chronic heart failure due to increased hydrostatic pressure. Also caused by infections, toxins, and non-inflammatory endothelial damage (or altitude sickness) Alveolar spaces fill with thin fluid. Results in dyspnea, low O2 sat. |
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Ascites |
Increased hydrostatic pressure, usually due to liver scarring/cirrhosis (central vein obstruction). Due to either intrinsic liver disease or right heart failure causing chronic passive congestion of liver. Liver failure can cause hypoproteinemia, leading to more edema. Associated with splenomegaly due to congestion - splenic vein feeds into portal vein. |
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Pleural effusion |
Caused by decrease in outflow from lungs (pulmonary venous congestion) due to heart failure or, less commonly, infections or tumors. |
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Anasarca |
Systemic edema Usually caused by decreased osmotic pressure due to decreased plasma protein. Septisemia -> vascular changes, decreased osmotic component due to liver hypoperfusion -> edema |
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Lymphedema |
Lymphatic obstruction. Can be due to radiation, surgery, or neoplasms commonly. Or parasitic infections, cellulitis, or obstruction of thoracic duct. Morphologically similar to localized edema. Extremely thickened, tree bark-like dermis is a sequelae |
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Thrombosis |
Inappropriate blood clot formation that may obstruct blood flow resulting in hypoperfusion/infarction. |
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Sequence of thrombotic events |
1. Endothelial injury 2. Vasoconstriction 3. Platelet adherence and aggregation 4. Coagulation cascade leading to fibrin clot 5. Fibrinolysis/thrombosis equilibrium where clot forming and dissolved at same rate. |
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Virchow's Triad |
Summarized prothrombotic factors Endothelial injury, abnormal blood flow, hypercoaguability |
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Endothelial injury in thrombosis |
Typically due to trauma. Inappropriately activated in diabetes, hypertension, and atherosclerosis causing thrombi. |
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Abnormal blood flow in thrombosis |
May be due to: Varicosities (dysfunctional venous valves) Venous stasis (i.e. immobility) Arterial aneurysms Dilated heart chambers which causes areas of reduced blood flow a. In atria, atrial fibrillation or mitral valve disease b. In ventricles, aneurysms from healed infarcts or dilated cardiomyopathy |
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Causes of dilated heart chambers leading to thrombosis |
In atria - atrial fibrillation or mitral valve disease In ventricles - dilated cardiomyopathy or healed infarcts (infarct resolves fibrotically, fibrosis allows outpouching of cardiac muscles) |
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Causes of hypercoaguability leading to thrombosis |
Primary - due to defects in coagulation cascade Acquired - more common, can be due to immobilization, carcinomas, antiphospholipid syndrome, HIT, and low-risk behaviors (smoking, OCPs, nephrotic syndrome) |
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Trousseau Syndrome |
Mucin secreting adenocarcinomas cause migratory thrombosis (both arterial and venous) once access vascular system. Very uncommon to have migatory thrombosis in arteries but mucin is highly procoagulative. |
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Why should women on OCPs not smoke? |
Both smoking and OCP use are risk factors for prothrombotic states. |
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Venous thrombosis syndromes |
Deep Venous Thrombosis (thrombosis forms in legs and may lead to PE) Pulmonary embolism IVC thrombosis Hepatic vein thrombosis (Budd-Chiari Syndrome) Portal vein thrombosis |
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Pulmonary Embolism |
3-5% of hospital deaths. Usually from leg veins. Risk factors include: DVT, trauma, obesity (due to immobility), malignancy, chronic heart disease (due to venous stasis) and genetic diseases involving hypercoaguability. |
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Thrombosis of the IVC |
Usually caused by tumors infiltrating the lumen rather than thrombus formation as a result of hypercoaguability. Results in lower extremity edema, proteinuria due to renal dysfunction if involving renal vein. |
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Renal cell carcinoma spread |
Tend to spread through venous circulation rather than lymphatics. Can spread to IVC and cause thrombosis. |
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Budd-Chiari syndrome |
Thrombosis of hepatic vein, resulting in occlusion of mesenteric and hepatic circulation. Liver failure (most significant), hepatosplenomegaly, massive ascites, ischemia of mesentery. Usually idiopathic, but can also be caused by tumors or hypercoaguable state. |
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Hemorrhage |
Extravasation of blood from vessels, often from trauma. May be external or accumulate within a tissue as a hematoma. |
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Common hemorrhagic/antithrombotic states |
Iatrogenic: due to anticoagulation therapy Genetic: defects in coagulation factor and platelets Acquired: Liver failure - clotting factor deficiency Uremia - metabolites cause dysfunction of coagulation factors Infections Leukemia Vitamin K deficiency |
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Manifestations of bleeding diatheses |
Petechiae (1-2 mm) Purpura (larger) Hematoma Hematochezia - blood in stool Bleeding gums Nosebleed Hemarthrosis - can cause joint compression because closed spaces Retinal hemorrhages Cerebral hemorrhages |
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Petechiae vs erythema |
If push down on petechiae, do not blanch - stay red. |
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Embolism |
Movement of physiologic or foreign material within artery or vein that lodges elsewhere. Emboli can be: - Thrombus (sterile or septic) - Fat (marrow, lipid) - Amniotic fluid - Tumors - Air - Foreign materials (iatrogenic) - either therapeutic or unintentional |
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Infectious endocarditis embolism |
Septic - clot consists of fibrin and bacteria that can break off and circulate systemically. |
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Therapeutic emboli |
Interventional radiologist can put vascular catheter in vascular supply of tumor to inject embolism material to clot off blood supply or to inject chemotherapy |
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Types of embolism by where it travels |
Systemic - Start in left heart (heart valves or ventricle) and float into systemic circulation, or can be iatrogenic from therapeutic tumor embolization. Pulmonary - Usually from systemic venous return (leg veins) Paradoxical - Originates in systemic venous circulation, goes to right heart, and crosses foramen ovale to reach systemic arterial circulation. This is common cause of stroke in patients with patent FO. |
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Pulmonary thromboembolism |
Predisposing factors include: immobilization, post-surgical, or coagulation disorders. Usual source is DVT Diagnosed by CT angiogram, used to be diagnosed by VQ scan. Treat with anticoagulant - give heparin in acute steting and warfarin in chronic setting. May perform thrombolysis via catheter also. |
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Saddle pulmonary embolus |
Embolus gets caught in major bifurcation of pulmonary artery, causing serious defect in VQ status of lung. |
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Fat embolism |
Usually from bone marrow from broken bone during resuscitation from trauma. Typically incidental. Or... Post surgical changes - introduced by incision. Non-surgical - pancreatitis and bone marrow infarct can release fat into blood supply. |
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Amniotic fluid embolism |
Occurs during late pregnancy or delivery. Increased risk with C-section or uterine trauma. Rare, but accounts for 10% of obstetric deaths. Results in diffuse alveolar damage and coagulopathy because amniotic fluid contains keratin and other prothrombotic factors, and factors are used up responding to these factors. |
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Embolization of medical devices |
IVC filter used to catch thrombi from embolizing. If not properly secured, can float up IVC into right atrium resulting in death. |
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Infarction |
Irreversible ischemic injury secondary to hypoxia resulting in coagulative necrosis. Usually result of occlusion of blood supply due to thrombus or embolus. Can be red (hemorrhagic) or white (non-hemorrhagic) |
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Ischemia vs infarction |
Ischemia is irreversible, infarction is irreversible. |
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Red vs white infarction |
Red (hemorrhagic) - in organs with reperfusion, blood continues flowing during infarction/tissue damage causing hemorrhage into that tissue. Occurs in bowel, lung, heart. Or can occur if lyse clot interventionally causing reperfusion. White (non-hemorrhagic) - in organs without reperfusion such as heart, kidney, liver, or spleen. Coagulative necrosis is replaced with white-colored fibrosis. |
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Factors influencing likelihood of infarct |
Nature of blood supply - are there collaterals or a dual blood supply? Rate of occlusion - if slow, tissue will compensate by recruiting collaterals and reducing chance of infarct. Vulnerability of tissue to hypoxia - Neurons die within minutes, myocytes die in minutes to hours, and fibroblasts can live without blood supply for hours to days. Oxygen content of blood - If hypoxic blood, larger chance of infarct. |
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Shock |
Systemic hypotension resulting in tissue hypoperfusion and hypoxia/ischemia Can be due to decreased cardiac contractility, decreased intravascular volume (hemorrhage or dehydration), or vasodilation |
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Three kinds of shock - cause, cardiac output, and TPR |
Hypovolemic due to trauma - normal cardiac output because HR is raised to compensate for reduced stroke volume. TPR is increased to compensate. Septic due to bacteria - Increased cardiac output. Decreased TPR due to systemic inflammatory response syndrome Cardiogenic shock due to heart failure - decreased cardiac output and increased vascular resistance to compensate. |
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Systemic inflammatory response syndrome |
In sepsis, peripheral vessels dilate |
