Disorders of Hemodynamics and Hemostasis MCQs

Septic infarcts occur when infected cardiac valve vegetations embolize, or when microbes seed necrotic tissue. In these cases, the infarct is converted into an abscess, with a correspondingly greater inflammatory response and healing by organization and fibrosis. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:115

Levels of fibrin degradation products, including crosslinked fibrin degradation products (D-dimer), are usually increased in the presence of acute venous thromboembolism. Absence of an elevated level of D-dimer in patients undergoing an evaluation for acute DVT or PE has an excellent negative predictive value for thrombosis. Reference : Wintrobe's 12th/pg 1437

Venous thrombi (phlebothrombosis) are almost invariably occlusive; they frequently propagate some distance toward the heart, forming a long cast within the vessel lumen that is prone to give rise to emboli. Because these thrombi form in the sluggish venous circulation, they tend to contain more enmeshed red cells, leading to stasis or thrombi. The veins of the lower extremities are most commonly affected (90% of venous thromboses); however, venous thrombi also can occur in the upper extremities, periprostatic plexus, or ovarian and periuterine veins, and under special circumstances they may be found in the dural sinuses, portal vein, or hepatic vein. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:110

Causes of splenic infarcts are as follow: Haematological disorders: sickle cell anemia, Polycythemia vera, Hypercoagulable state, CML, Leukemia, Lymphoma, Myelofibrosis, Erythropoietin therapy Embolic disorders: Arterial fibrillation, Endocarditis, HIV associated mycobacterial infections Collagen vascular disorders: SLE, Kawasaki disease, Wegner’s granulomatosis, PAN Infections: Infectious mononucleosis, Kala-azar, Meningococcemia, Clostridium perfringes, Salmonellosis, P. vivax, Falciparum, Leptospirosis Trauma Miscellaneous: Amyloidosis, sarcoidosis, ARDS, Splenic vein thrombosis, Liver transplant Reference : Robbins Basic Pathology, 8 th edition, page number -634

Erythema is redness of skin or mucous membrane caused by hyperemia (increased blood flow). Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:97

Red infarcts occur (1) as a result of venous occlusions (such as in ovarian torsion); (2) in loose tissues (e.g., lung) where blood can collect in infarcted zones;(3) in tissues with dual circulations such as lung and small intestine, where partial, albeit inadequate perfusion by collateral arterial supplies is typical; (4) in previously congested tissues (as a consequence of sluggish venous outflow); and (5) when flow is reestablished after infarction has occurred (e.g., after angioplasty of an arterial obstruction). Reference: Robbins Basic Pathology, 10th ed, Pg-114-115

Hyperaemia and congestion both refer to an increase in blood volume within a tissue, but have different underlying mechanisms. Hyperemia is due to increased blood flow, congestion is due to decreased outflow Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:97

Microglia are phagocytic macrophage-derived cells of the CNS, accounting for 5% of all glial cells. In response to necrosis, macroglia become phagocytic, accumulate lipids and other cellular debris, and are designated gitter cells. Some reactive microglia exhibit a prominent elongated nucleus, in which case they are referred to as rod cells. After microglial phagocytosis, astrocytosis (choice a) then leads to local scar formation, which persists as telltale evidence of a prior injury. Reference: Robbins & Cotran Pathologic Basis of Diseases 10 th edition, Chapter – 28 pg 1243