Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

55 Cards in this Set

  • Front
  • Back
Outline the normal distribution of body water indicating: body compartments, consequences of fluid shifts, and normal mechanisms of homeostasis
Sixty percent of lean body weight is water; 2/3 is intracellular with the remainder being located in the extracellular space, mostly as interstitial fluid (only about 5% of total body water is in blood plasma). The opposing effects of vascular hydrostatic pressure and plasma colloid osmotic pressure are the major factors that govern fluid movement between the vascular and interstitial spaces. Either increased capillary pressure or diminished colloid osmotic pressure can lead to increased interstitial fluid (aka edema). Edema may also be caused by lymphatic obstruction and primary retention of sodium in renal disease
Define edema
Increased fluid in the interstitial tissue spaces
What is hydrostatic pressure, and how does it cause edema
Local increases in hydrostatic pressure may result from impaired venous outflow. Generalized increases in venous pressure, resulting in systemic failure occur commonly in congestive heart failure. The mechanism is that, with heart failure, there is reduced CO and  renal perfusion. This triggers the RAA system, inducing Na and water retention by the kidneys in order to  CO by  intravascular volume. However, if the failing heart cannot  CO, then the extra fluid load results only in  venous pressure and eventually edema.
What is plasma osmotic pressure, and how does it cause edema
Results from excessive loss or reduced synthesis of albumin (serum protein most responsible for maintaining colloid osmotic pressure). Albumin loss is often is caused by nephritic syndrome-a leaky glomerular capillary wall and generalized edema while reduced albumin synthesis occurs in diffuse liver pathology or as a consequence of protein malnutrition. The mechanism is that reduced plasma osmotic pressure leads to a net movement of fluid into the interstitial tissues and a resultant plasma volume contraction (followed by secondary aldosteronism).
What is lymphatic obstruction, and how does it cause edema
Usually localized, can result from inflammatory or neoplastic obstruction. Filariasis often causes massive lymphatic and lymph node fibrosis in the inguinal region resulting in extreme edema in the genitalia and lower limbs-elephantiasis. Breast cancer treated by removal or irradiation can lead to resection of the lymphatic channels (and scarring) can result in severe edema of the arm. Superficial lymph node obstruction in breast cancer can cause edema of the overlying skin (peau d’ orange appearance).
What is sodium and water retention, and how does it cause edema
Increased salt, with the obligate accompanying water, causes both increased hydrostatic pressure (due to the expansion of the intravascular fluid volume) and diminished vascular colloid osmotic pressure. May occur in glomerulonephritis and acute renal failure
Define Hyperemia
An active process resulting form augmented tissue inflow because of arteriolar dilation, as in dkeletal muscle during exercies or at sites of inflammation
Define Congestion
Passive process resulting from impaired outflow from a tissue. May occur systemically, as in cardiac failure, or locally, as in isolated venouse obstruction
Define hemorrhage
Extravasation of blood due to vessel rupture. An accumulation of blood withing tissue is a hematoma; minute (1-2mm) hemorrhages into skin, mucous membranes, or serosal surfaces are called petechia; hemorrhages>3mm are called purpura; >1 cm are called ecchymoses
Define thrombosis
The opposite of hemostasis; inappropriate activation of normal hemostatic processes, formation of a blood clot in uninjured vasculature or thrombotic occlusion of a vessel after relatively minor injury
Define Infarction
An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Nearly 99% of all infarcts result from thrombotic or embolic events (almost all from arterial occlusion)
List the major features of arterial thrombosis
seen microscopically as a vessel totally filled w/ organized thrombus (may be punctuated by small recanalized channels). May be caused by atherosclerosis and associated abnormal vascular flow-leads to stasis which brings platelets in contact with the endothelium, prevent dilution of activated clotting factors, retards inflow of clotting factor inhibitors, and promotes endothelial cell activation-along with loss of endothelial integrity-which can lead to platelet adhesion and clot development. Arterial thromboses lead to local obstructive consequences (in the vessels or heart) and can also affect other tissues, especially the brain, kidneys, and spleen (b/c of large flow volume).
List the major features of venous thrombosis
Often seen in superficial or deep veins of the leg. Gross appearance is that of red thrombi b/c of enmeshed erythrocytes. Occur as a result of stasis of the blood (may be caused by cardiac failure), which causes increased contact of platelets w/ endothelium, preventing dilution of clotting factors and retarding the inflow of clotting factor inhibitors, as well as promoting endothelial cell activation; the result is clot formation. “Superficial” may cause local congestion, swelling, pain, and tenderness along the course of the involved vein, but rarely embolize. “Deep” may embolize and cause local pain and distal edema, although are offset by collateral bypass channels, therefore 50% of deep venous thromboses are asymptomatic. Risk factors are advanced age, bed rest, and immobilization.
List the major features of an anemic (white) infarct
Occurs with arterial occlusions in solid organs with end-arterial circulation (i.e.-heart, spleen, and kidney). The solidity of tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds.
List the major features of hemorrhagic (red) infarct
Occurs in a number of different ways: venous occlusions (ie-ovarian torsion); in loose tissues (lung) which allow blood to collect in the infracted zone; in tissues w/ dual circulation (lung & small intestine) allowing blood flow from unobstructed vessel into necrotic zone; in tissues that were previously congested b/c of sluggish venous outflow.
What do both white and red infarcts lead to
The development of an inflammatory response along the margins w/in a few hours. This is followed by a reparative response and will ultimately be replaced by scar tissue (except in the brain where the ultimate result is liquefactive necrosis).
Briefly describe the coagulation cascade and list the major characteristics of each coagulation factor involved
Important highlights include the separation into two pathways: intrinsic and extrinsic. The intrinstic pathway is initiated by vasoconstriction (the exposure of collagen) and leads to the activation of Factor XII, which catalyzes the activation of Factor XI, which in turn catalyzes the activation of Factor IX; this, along with activated Factor VIII in the presence of Calcium activates Factor X. The extrinsic pathway is initiated by tissue injury with the exposure of tissue factor activating Factor VII, which serves to activate Factor IX of the intrinsic pathway and, in the presence of Ca, activates Factor X. After this point the pathways have converged with Factor X, along with activated Factor V (and Calcium) catalyzing the activation of Prothrombin to Thrombin which catalyzes the conversion of fibrinogen to fibrin, as well as activating factor XIII (both rxns occur in the presence of Calcium). Finally, factor XIII catalyzes the cross-linking of fibrin. Thrombin is also important because it induces platelet aggregation and secretion (of thromboxane) along w/ activating endothelium to generation leukocyte adhesion molecules and a variety of fibrinolytic and vasoactive mediators
List the factors associated with increased risk of thrombosis
Three major factors are associated w/ increased risk of thrombosis-the Virchow triad. Endothelial injury may occur over ulcerated plaques in atherosclerotic arteries, or at sites of traumatic or inflammatory vascular injury. Alterations in normal blood flow-turbulence and stasis-may be caused by ulcerated atherosclerotic plaques, abnormal aortic and arterial dilations (aneurysms), myocardial infarction, as well as sickle cell anemia. Hypercoagulability contributes less, but is important in some syndromes(ie- HIT & APS).
What is Heparin-induced thrombocytopenia syndrome (HIT)
occurs when administration of unfractionated heparin (as therapeutic anticoagulation) induces formation of antibodies that bind to molecular complexes of heparin and platelet factor 4 membrane protein. The result is platelet activation, endothelial injury, and a prothrombotic state
What is antiphospholipid antibody syndrome (APS)
Associated with high titers of circulating antibodies directed against anionic phospholipids creating a state of hypercoagulability. The mechanism is unclear, however, it may be due to direct platelet activation, inhibition of PGI2 production by endothelial cells, or interference w/ protein C synthesis or activity. Clinical manifestations: recurrent venous or arterial thrombi, repeated miscarriages, cardiac valvular vegetations, or thrombocytopenia (along w/ the consequences of these manifestations and their locations).
Discuss DIC, itis etiology, pathogenesis, and complications
Disseminated intravascular coagulation-sudden or insidious onset of widespread fibrin thrombi in the microcirculation-can cause diffuse circulatory insufficiency, particularly in the brain, lungs, heart and kidneys. The development of multiple thrombi leads to rapid concurrent consumption of platelets and coagulation proteins, but at the same time, fibrinolytic mechanisms are activated and, as a result, the initially thrombotic disorder can evolve into a serious bleeding disorder
What is the etiology and consequence of pulmonary thromboembolism
originate from deep leg vein thrombi above the knee and are carried through the circulation into the pulmonary vasculature. Sudden death, right heart failure, or CV collapse occurs when 60% or more of the pulmonary circulation is obstructed with emboli. Embolic obstruction of medium arteries may result in pulmonary hemorrhage, but not infarction b/c of dual flow from bronchial circulation. Multiple emboli over time may cause pulmonary hypertension w/ right heart failure
What is the etiology and consequence of systemic thromboembolism
most (80%) arise from intracardiac mural thrombi, two thirds are associated w/ left ventricular wall infarcts and another quarter w/ dilated and fibrillating left atria. The rest originate from aortic aneurysms, thrombi on ulcerated atherosclerotic plaques, or fragmentation of valvular vegetation. The consequence is mainly infarction of tissues downstream of the obstructed vessel
What is the etiology and consequence of fat embolism
microscopic fat globules found in circulation following fractures of long bones (have fatty marrow) or, in the setting of soft tissue trauma and burns. Symptoms manifest 1-3 days after injury. Fat embolism syndrome is characterized by pulmonary insufficiency, neurologic symptoms (irritability, restlessness, delirium, or coma), anemia, and thrombocytopenia.
What is the etiology and consequence of air embolism
gas bubbles obstruct vascular flow (causing distal ischemic injury). Air may enter circulation during obstetric procedures or as a consequence of chest wall injury. One form, decompression sickness, occurs when individuals are exposed to sudden changes in atmospheric pressure; consequences include the bends, the chokes, and caisson disease.
What is the etiology and consequence of amniotic fluid embolism
caused by infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of the uterine veins. Characterized by sudden sever dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma. Pulmonary edema, along w/ DIC may also develop
What is the sequence of events in hemostatis after injury
•Neurogenic arteriolar vasoconstriction. Augmented by endothelin (endothelium derived vasoconstrictor)
•Primary Hemostasis. Exposed subendothelial ECM allows platelet adhesion and activation. Activation – platelets undergo shape change and release secretory granules (ADP, TXA2) which recruit other platelets. Temporary hemostatic plug is formed
•Secondary Hemostasis. Injury exposes tissue factor, a membrance bound procoagulant factor made by endothelium. Activates the coagulation cascade, which results in thrombin generation>>converts fibrinogen to fibrin + increases platelet recruitment + granule release. A permanent plug is formed by polymerized fibrin + platelet aggregates
•Counter regulatory mechanisms (eg., t-Pa) are set in motion
What is a thrombus
A mass of platelets, fibrin, RBCs, and WBCs that attach to vascualr endothelia and pertially obstruct the vessel
What are the possible fates of a thrombus
1. Propagation-complete vessel obstruction
2. Embolization-particularly lungs with venous emboli
3. Dissolution- by finrinolytic activity
4. Organization and recanalization- reestablishing vascular flow with thrombus as part of the vessel
What is the morphology of deep venous thrombi
Ling red-blue cast of the vein lumen; thrombus contains enmeshed erythrocytes among fibrin strands; fibrin and attachment to the vessel distinguish stasis thrombi from postmortem clots
What is the morphology of arterial thrombosis
Gray-red and tend to have gross microscopic lamination (lines of Zahn) produced by pale layers of platelets and fibrin alternating with darker red cell-rich layers
What is the most serious venous thrombotic embolus
Saddle embolus, which impacts the bifurcation of the pulmonary arteries
What is a paradoxical embolus
Embolus may pass through an interatrial or interventricular defect to gain access to the systemic circulation
What are the major determinants of the consequences of a vascular occlusion
1. The nature of the vascular supply
2. The rate of development of the occlusion
3. The vulmerability of a given tissue to hypoxia
4. The blood oxygen content
What are the stages of shock
Nonprogressive phase (reflex compensatory mechanisms are activated and perfusion of vital organs is maintained); Progressive stage (characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including acidosis); Irreversible stage (sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible)
What is neurogenic shock
may occur in the setting of anesthetic accident or spinal cord injury; owing to loss of vascular tone and peripheral pooling of blood
What is hypovolemic shock
- results from loss of blood or plasma volume. This may be caused by hemorrhage, fluid loss from severe burns, or trauma
What is septic shock
Peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades. With a 25% to 50% mortality rate, ranks first among the causes of mortality in intensive care units and is estimated to account for over 200,000 deaths annually in the United States. Most cases of septic shock (approximately 70%) are caused by endotoxin-producing gram-negative bacilli. Endotoxins are bacterial wall lipopolysaccharides (LPSs) that are released when the cell walls are degraded (e.g., in an inflammatory response)
What is cardiogenic shock
results from myocardial pump failure. This may be caused by intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade) or outflow obstruction (e.g., pulmonary embolism)
What is anaphylactic shock
initiated by a generalized IgE-mediated hypersensitivity response, is associated with systemic vasodilation and increased vascular permeability. Widespread vasodilation causes a sudden increase in the vascular bed capacitance, which is not adequately filled by the normal circulating blood volume. Thus, hypotension, tissue hypoperfusion, and cellular anoxia result.
How does shock affect the brain
may develop so-called ischemic encephalopathy
How does shock affect the heart
may undergo focal or widespread coagulation necrosis or may exhibit subendocardial hemorrhage and/or contraction band necrosis
How does shock affect the kidneys
typically exhibit extensive tubular ischemic injury (acute tubular necrosis). Oliguria, anuria, and electrolyte disturbances constitute major clinical problems
How does shock affect the lungs
• lungs are seldom affected in pure hypovolemic shock because they are resistant to hypoxic injury. When shock is caused by bacterial sepsis or trauma, however, changes of diffuse alveolar damage may appear, the so-called shock lung
What are the adrenal changes seen in shock
• adrenal changes in shock are those seen in all forms of stress; essentially, there is cortical cell lipid depletion. This does not reflect adrenal exhaustion but rather conversion of the relatively inactive vacuolated cells to metabolically active cells that utilize stored lipids for the synthesis of steroids
How does shock affect the gastrointestinal tract
• gastrointestinal tract may suffer patchy mucosal hemorrhages and necroses, referred to as hemorrhagic enteropathy
How does shock affect the liver
• liver may develop fatty change and, with severe perfusion deficits, central hemorrhagic necrosis
What is hyperemia
an active process resulting from augmented tissue inflow because of arteriolar dilation, as in skeletal muscle during exercise or at sites of inflammation. The affected tissue is redder because of the engorgement of vessels with oxygenated blood
What is congestion
a passive process resulting from impaired outflow from a tissue. It may occur systemically, as in cardiac failure, or it may be local, resulting from an isolated venous obstruction. The tissue has a blue-red color (cyanosis), particularly as worsening congestion leads to accumulation of deoxygenated hemoglobin in the affected tissues. Congestion and edema commonly occur together, primarily since capillary bed congestion can result in edema due to increased fluid transudation. In long-standing congestion, called chronic passive congestion, the stasis of poorly oxygenated blood also causes chronic hypoxia, which can result in parenchymal cell degeneration or death, sometimes with microscopic scarring. Capillary rupture at these sites of chronic congestion may also cause small foci of hemorrhage; breakdown and phagocytosis of the red cell debris can eventually result in small clusters of hemosiderin-laden macrophages.
Describe chronic passive congestion of the lungs
• In chronic pulmonary congestion, the septa are thickened and fibrotic, and the alveolar spaces may contain numerous hemosiderin-laden macrophages (heart failure cells)
Describe chronic passive congestion of the liver
the central regions of the hepatic lobules are grossly red-brown and slightly depressed (owing to a loss of cells) and are accentuated against the surrounding zones of uncongested tan liver (nutmeg liver). In severe, long-standing hepatic congestion (most commonly associated with heart failure), there may even be grossly evident hepatic fibrosis (cardiac cirrhosis)
Describe subcutaneous edema
• Subcutaneous edema may have different distributions depending on the cause. It can be diffuse, or it may be relatively more conspicuous at the sites of highest hydrostatic pressures. In the latter case, the edema distribution is typically influenced by gravity and is termed dependent. Edema of the dependent parts of the body (e.g., the legs when standing, the sacrum when recumbent) is a prominent feature of congestive heart failure, particularly of the right ventricle
Describe edema as a result of renal dysfunction or nephrotic syndrome
generally more severe than cardiac edema and affects all parts of the body equally. It may, however, initially manifest itself in tissues with a loose connective tissue matrix, such as the eyelids; thus, periorbital edema is a characteristic finding in severe renal disease. Finger pressure over substantially edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression, so-called pitting edema
Describe pulmonary edema
is a common clinical problem most typically seen in the setting of left ventricular failure but also occurring in renal failure, acute respiratory distress syndrome, pulmonary infections, and hypersensitivity reactions. The lungs are two to three times their normal weight, and sectioning reveals frothy, blood-tinged fluid representing a mixture of air, edema fluid, and extravasated red blood cells
Describe edema of the brain
may be localized (e.g., owing to abscess or neoplasm) or may be generalized, as in encephalitis, hypertensive crises, or obstruction to the brain’s venous outflow. Trauma may result in local or generalized edema depending on the nature and extent of the injury. With generalized edema, the brain is grossly swollen, with narrowed sulci and distended gyri, showing signs of flattening against the unyielding skull