Accumulation of fluid in the pleural cavity

Conditions leading to inadequate synthesis or increased loss of ___ from the circulation are common causes of reduced plasma oncotic pressure.

Non-inflammatory edema and effusions are protein-poor fluids called __.

Microscopically, it is appreciated as clearing and separation of the extracellular matrix and subtle cell swelling; most commonly in subcutaneous tissues, lungs, and brain.

Effusions involving the pleural cavity

Effusions involving the pericardial cavity

Effusions involving the pericardial cavity

An active process in which arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow; affected tissues turn red (erythema)

A passive process resulting from reduced outflow of blood from a tissue.

Chronically congested tissues will produce capillary rupture and small hemorrhagic foci; subsequent catabolism of extravasated red cells can leave residual telltale clusters of hemosiderin-laden macrophages called __.

Microscopic finding of the lung: thickened or fibrotic alveolar septa, numerous hemosiderin-laden macrophages (heart-failure cells) in the alveoli.

Diagnosis of a liver condition where macroscopically cut section of the liver looks like a cut nutmeg.

Disc-shaped anucleate cell fragments that are shed from megakaryocytes in the bone marrow in the bloodstream.

A constituent of subendothelial connective tissue that acts as a bridge between the platelet surface receptor glycoprotein Ib (GpIb) and exposed collagen; mediator of platelet adhesion.

<br />Activated platelets also produce the prostaglandin ___, a potent inducer of platelet aggregation.<br />a. Plasmin<br />

This substance inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TxA2 synthesis.

The conformational change in glycoprotein IIb/IIIa that occurs with platelet activation allows binding of ___, a large bivalent plasma polypeptide that forms bridge BETWEEN adjacent platelets, leading to their aggregation

Inherited deficiency of GpIIb-IIIa results in a bleeding disorder called __.

A precisely orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury and culminates in the formation of a blood clot, which serves to prevent or limit the extent of bleeding.

Occurs immediately and markedly reduces blood flow to the injured area

A potent endothelium-derived vasoconstrictor.

Tissue factor activates factor ___ until it culminates in thrombin generation.

Play a critical role in hemostasis by forming the primary plug that initially seals vascular defects and by providing a surface that binds and concentrates activated coagulation factors.

Laboratory test that assesses the function of the proteins in the extrinsic pathway (factors VII, X, V, II, and fibrinogen).

Laboratory test that assesses the function of the proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen).

Deficiency of coagulation factor __ does not cause bleeding but instead may cause thrombosis.

The most important coagulation factor that has various enzymatic activities that control diverse aspects of hemostasis and link clotting to inflammation and repair.

Converts fibrinogen into crosslinked fibrin.

Fibrinolysis is largely accomplished through the enzymatic activity of ___, which breaks down fibrin and interferes with its polymerization.

Breakdown products of fibrinogen (often called fibrin split products), useful clinical markers of several thrombotic states.

The most important plasminogen activator is ___; synthesized principally by endothelium.

Activated protein C/ protein S complex is a potent inhibitor of coagulation factors __ and __.

Mechanism of action of heparin drugs

Bleeding into joints called __ following minor trauma that is particularly characteristic of hemophilia.

Hemorrhages sometimes simply called bruises are 1 to 2 cm in size.

Extravasated Blood

Contributes to arterial and cardiac thrombosis by causing endothelial injury or dysfunction, as well as by forming countercurrents that contribute to local pockets of stasis.

Hypercoagulability is also called as ____.

Included in Virchow triad, Except ___

What is the most important factor in the Virchow triad?

Inherited hypercoagulability state where the Arg to Glu substitution in amino acid residue 506 leading to resistance to activated protein C.

Cystathione β-synthetase inherited deficiency leads to elevated___; contributor of arterial and venous thrombosis.

Unfractionated heparin induces the appearance of antibodies that recognize complexes of heparin and platelet factor 4 on the surface of platelets. Binding of these antibodies to platelets results in activation, aggregation, and consumption (hence the name in the syndrome).

This syndrome has protean clinical manifestations, including recurrent thromboses, repeated miscarriages, cardiac valve vegetations, and thrombocytopenia.

Arterial or cardiac thrombi usually begin at sites of turbulence or endothelial injury; tend to grow ____.

Laminations of pale platelet and fibrin deposits alternating with darker red cell-rich layers.

Thrombi occurring in heart chambers or in the aortic lumen are designated as __.

Thrombi on heart valves are called ___.

DVTs are asymptomatic in approximately 50% of affected individuals; due to opening of venous collateral channels.

A venous embolus that pass through an interatrial or interventricular defect and gains access to the systemic arterial circulation.

Condition where gas bubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow and cause distal ischemic injury.

A more chronic from of decompression sickness; the persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis, the more common sites are the femoral heads, tibia, and humeri.

Classic findings in autopsy include the presence of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or GI tract in the maternal pulmonary microvasculature.

Type of infarct in tissues with dual circulations (e.g., lung and small intestine) that allow blood to flow from an unobstructed parallel supply into a necrotic zone.

Type of infarct that occur with arterial occlusions in solid organs with end-arterial circulation (e.g., heart, spleen, and kidney), and when tissue density limits the seepage of blood from adjoining capillary beds into the necrotic area.

Occurs when infected cardiac valve vegetations embolize or when microbes seed necrotic tissues.

A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia.

Shock that results from low cardiac output due to myocardial pump failure.

Shock that result from low cardiac output due to low blood volume (e.g., massive haemorrhage or severe burns).<br />

Shock that result from bacterial, viral or fungal infections; it is a systemic inflammatory condition characterized by endothelial cell activation, tissue edema, DIC, and metabolic derangements that often lead to organ failure and death.

Shock that results from an anesthetic accident or a spinal cord injury.

Shock that result from an IgE-mediated hypersensitivity reaction.

Cellular changes in the kidneys induced by cardiogenic or hypovolemic shock.

Septic shock is most frequently triggered by 3 microorganisms (descending order):

Cellular changes in the lungs caused by sepsis or trauma; so called shock lung.

<br />Cellular changes in septic shock leading to DIC, except:<br />

Shock characterized by warm and flushed skin because of peripheral vasodilation.

Shock characterized by hypotension; weak, rapid pulse; tachypnea; and cool, clammy, cyanotic skin.