Patho Flash Cards
Increase in size of cells resulting in increased size of organ.
Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
Increase in number of cells.
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
Hypertrophy of hyperplasia?Uterus during pregnancy
Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
Hypertrophy or hyperplasia?Wound healing
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4
Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.
Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7
Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7
Type of cell death which results from a pathologic cell injury.
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9
Type of cell death associated with inflammation.
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.
Pyknosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
It is the destructive fragmentation of the nucleus of a dying cell.
Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
It is the complete dissolution of the chromatin of a dying cell.
Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
This is the first manifestation of almost all forms of injury to cells.
Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8
Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.
Hydropic change or Vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
Appearance of lipid vacuoles in the cytoplasm.
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.
Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.
Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
These are chemical species with a single unpaired electron in the outer orbital.
Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
Most common cause of cell injury in clinical medicine.
Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.
Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19
Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.
Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
Pathway of apoptosis trigerred by loss of survival signals, DNA damage and accumulation of misfolded proteins. Inhibited by Anti-apoptotic members of the Bcl family.
Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.
Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
Refers to any abnormal accumulation of triglycerides within parenchymal cells. Most often seen in the liver but can also occur in the heart, sk m., and kidneys.
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
Other name for macrophages in contact with lipid debris of necrotic cells or abnormal forms of lipoproteins. Filled with minute, membrane-bound vacuoles of lipid, imparting a foamy appearance to their cytoplasm.
Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons.
Xanthomas(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
Hypertrophy or hyperplasia?Cardiomegaly due to hypertension
Hypertrophy Due to increased workload(TOPNOTCH)
Most common exogenous pigment?
Carbon(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
“Wear and Tear pigment”?
Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Pigment produced by tyrosinase-catalyzed oxidation of tyrosine to dihydroxyphenylalanine.
Melanin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Hemoglobin-derived granular pigment that is golden-yellow to brown in color. Accumulates in excess of iron.
Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Histochemical reaction used to identify hemosiderin.
Prussian blue test(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Abnormal calcium deposition occuring in the absence of calcium metabolic derangements.
Dystrophic calcification.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Calcium deposition in normal tissues occuring in the presence of hypercalcemia.
Metastatic calcification (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Grossly seen as fine white granules or clumps, often felt as gritty deposits. Histologically, intra/extracellular basophilic deposits.
Calcium salts(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.27
A result of a progressive decline in the proliferative capacity and lifespan of cells.
Cellular aging(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.29
Appears as round or oval masses with intensely eosinophilic cytoplasm, nuclei with various stages of chromatin condensation and aggregation, karyorrhexis.
Apoptotic cell(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20
Membrane bound vesicles of cytosol and organelles quickly extruded and phagocytosed without eliciting inflammatory response.
Apoptotic bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20
Clear vacuoles within parenchymal cells, displacing the nucleus to the cell periphery.
Fatty change (TOPNOTCHRobbins Basic Pathology, 8th ed. p.24
Focal, intracellular fat deposits creating alternating bands of yellowed myocardium with alternating bands of darker red-brown uninvolved heart or “tigered effect”.
Fatty change of the heart(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
Rounded, eosinophilic accumulation of newly synthesized immunoglobulins in the rough ER of plasma cells.
Russel bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25
Eosinophilic cytoplasmic inclusion in liver cells composed of aggregated intermediate filaments which resist degradation. Seen in patients woth alcoholic liver disease.
Mallory body / “alcoholic hyalin”(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25
Aggregated protein inclusions that contain microtubule-associated proteins and neurofilaments, reflecting disrupted neuronal cytoskeleton.
Neurofibrillary tangles in Alzheimer’s disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
An insoluble brownish-yellow granular intracellular material that accumulates as a function of age and atrophy. Appears as perinuclear electron-dense granules on electron microscopy.
Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
Refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction.
Fat necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11
A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists.
Fibrinoid necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11
Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue.
Liquefactive necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.
Gangrenous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
It is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.31
Inflammation which is characterized by plasma protein exudation and a predominantly neutrophilic leukocyte accumulation.
Acute inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and fibrosis.
Chronic inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
Five cardinal signs of inflammation?
Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
Initial vascular response to injury?
Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33
An ultrafiltrate of blood which contains little protein. Results from arteriolar vasodilation and increased blood flow.
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
Results from increased vascular permeability, leading to leakage of protein into tissues.
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
Fluid accumulation in extravascular space.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Rolling
Selectins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
State the molecule in the lymphocyte responsible for this stage of vascular inflammatory response:Firm adhesion
Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Transmigration
PECAM-1/CD 31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion
ICAM -1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin
Sialyl-Lewis X modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin
Sialyl-Lewis X-Modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1
Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31
CD-31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
The process of luekocyte accumulation at the periphery of blood vessels is called ______.
Margination(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
Arrange the following steps in the inflammatory response:A. Recruitment of leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. Resolution
C, A, D, B, E(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35
Arrage the steps in leukocyte recruitment:A. TransmigrationB. Rolling C. MarginationD. Firm adhesion
C, B, D, A(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35
Process of coating microorganisms with proteins that facilitate phagocytosis.
Opsonization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.38
A lymphocyte with ingested microorganism fused with lysosome is called _______.
Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.39
The most important lysosomal enzyme involved in bacterial killing.
Elastase(TOPNOTCH)
Process of leukocyte migration toward sites of infection or injury along a chemical gradient.
Chemotaxis(TOPNOTCH)
The most important lysosomal enzyme involved in bacterial killing.
Elastase(TOPNOTCH)
A peptide Leukocyte granule constituent which kills microbes by creating holes in their membranes.
Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40
Predominant form of leukocyte during the first 6 - 24 hours of inflammation?
Neutrophils(TOPNOTCH)
Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?
Monocytes(TOPNOTCH)
Substances responsible for leukocyte-induced tissue injury?
Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)
Defective synthesis of CD 18 B-subunit of leukocyte integrins LFA-1 and Mac-1 leading to impaired leukocyte adhesion and migration through endothelium.
Leukocyte adhesion deficiency type 1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
Caused by a defect in fucose metabolism resulting in absence of sialyl-lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium.
Leukocyte adhesion deficiency type 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
Results from a defect in the protein involved in membrane docking and fusion.
Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
NADPH deficiency or defect resulting in decreased oxidative burst.
Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42
Type of acute inflammation characterized by the outpouring of watery, relatively protein-poor fluid derived from the serum or endothelial lining of peritoneal, pleural, and pericardial cavities.
Serous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
Fluid in a serous cavity is called ______.
Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
This type of inflammation is manifested by the presence of large amounts of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid.
Suppurative (purulent) inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
It is an excavation of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of inflammatory necrotic tissue.
Ulcer(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.
Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
Complement fragments which are anaphylotoxins.
C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
Complement fragment which aids in opsonization.
C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
Membrane attack complex
C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
It is the cytolytic endproduct of the complement cascade, which forms a transmembrane channel causing osmotic lysis of target cells.
Membrane attack complex (C5b,C6-9)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
Enzyme blocked by NSAIDS.
Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
Enzyme inhibited by glucocorticoids
Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
Polypeptide products of many cell types that function as mediators of inflammation and immune response.
Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.
Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
Major cytokines in acute inflmmation.
TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.
Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49
This component of the coagulation cascade initiates four systems involved in the inflammatory response, namely the kinin, clotting, fibrinolytic and complement systems.
Activated Hageman Factor / Factor XIIa(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.52
Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.
Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53
Macrophages in the liver
Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
Macrophages in the spleen and lymph nodes
Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
Macrophages in the CNS
Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
Macrophages in the lungs
Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
A focus of epiheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.
Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli
Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Acid-fast bacilli in macrophages, noncaseating granulomas
Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellulr outline
Gumma (Syphilis)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Rounded or stellate granuloma containing central granular debris and recognizable neutrophils, giant cells uncommon.
Cat-scratch Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Noncaseating granulomas with abundant activated macrophages
Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate
Chron disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Cells with pink, granular cytoplasm with indistinct boundaries.
Epitheloid cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
40-50 um in size, consisting of a large mass of cytoplasm and many nuclei.
Giant cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.
Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.
TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57
Cells of these tissues are continuously being lost and replaced by maturation from stem cells and by proliferation of mature cells. Can readily regenerate after injury as long as the pool of stem cells is preserved.
Labile tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Cells of theses tissues are quiescent and have only minimal replicative activity in their normal state. Capable of proliferating in response to injury or loss of tissue mass.
Stable tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Cells of these tissues are considered to be terminally differentiated and nonproliferatvie in postnatal life.
Permanent tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
Labile, stable or permanent tissues:Bone marrow
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Vaginal epithelium
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Salivary glands
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Liver parenchyma
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Endothelium
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Smooth muscle cells
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Neurons
Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
Labile, stable or permanent tissues:Cardiac muscle
Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
Type of collagen found in basement membrane
Type IV collagen(TOPNOTCH)
Type of collagen found in basement membrane
Type IV collagen(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.67
This is the most abundant glycoprotein in basement membrane.
Laminin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.68
The pink, soft, granular tissue seen beneath the scab of a skin wound.
Granulation tissue(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70
Maturation and reorganization of fibrous tissue
Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70
Healing of a clean, uninfected surgical incision approximated by surgical sutures
Healing by first intention / Primary Union(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.74
Type of healing wherein tissue is allowed to heal by itself before suturing. Used in large wounds, in the presence of abscess, or ulceration.
Healing by secondary intention / secondary union(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.76
Wound strength reaches 70 - 80 % of normal in ______ months.
3 months(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Single most important cause of delay in wound healing.
Infection(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
True or false: Complete restoration can occur only in tissues composed of stable and labile cells.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Refers to the restoration of tissue architecture and function after an injury.
Repair (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
True or false:Injury to tissues composed of permanent cells does not result to scarring.
False. Injury to tissues composed of permanent cells, inevitably results to scarring.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Process of replacing damaged components of a tissue, returning to a normal state.
Regeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Migration and proliferation of fibroblasts with deposition of ECM.
Scar formation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72
Maturation and reorganization of fibrous tissue
Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.73
The pink, soft, granular tissue seen beneath the scab of a skin wound.
Granulation tissue(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.73
Arrange the steps in cutaneous wound healing:A. Formation of granulation tissueB. ECM remodelingC. Inflammation
C, A, B(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72
It consists of a series of steps at which the cell checks for the accuracy of replication and mitosis and instructs itself to proceed to the next step.
Cell cycle(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
In the cell cycle, this is called the presynthetic growth phase.
G1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
In the cell cycle, this is also called the premitotic growth phase.
G2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
These steps in the cell cycle prevents DNA replication or mitosis of damaged cells and either transiently stop the cell cycle to allow repair, or eliminate irreversibly damaged cells by apoptosis.
Checkpoint control(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
These enzymes promote DNA replication and various aspects of mitosis. They are required for cell cycle progression. Forms complexes with cyclin.
Cyclin-deoendent kinases (CDK)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
This cytokine is released from activated macrophages, and is mitogenic for keratinocytes and fibroblasts. It also stimulates keratinocyte migration and granulation tissue formation.
Epidermal Growth Factor (EGF)(TOPNOTCH)
This cytokine increases vascular permeability and is mitogenic for endothelial cells.
Vascular Endothelial Growth Factor (VEGF)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.71
Pattern of extracellular signaling wherein the target cell is itself.
Autocrine(TOPNOTCH)
Pattern of extracellular signaling wherein the target cell is adjacent to the secretory cell.
Paracrine(TOPNOTCH)
Pattern of extracellular signaling wherein the target cell is distant to the secretory cell.
Endocrine(TOPNOTCH)
Synthesized by mesenchymal cells, present in the spaces between cells in connective tissue, between epithelium and supportive vascular and smooth muscle structures.
Interstitial Matrix(TOPNOTCH)
Component of ECM which confers tensile strength and recoil.
Fibrous proteins s.a. Collagen and elastin(TOPNOTCH)
Component of ECM that permits resilience and lubrication.
Proteoglycans, hyaluronan(TOPNOTCH)
Component of ECM that connect the elements to one another and to the cells.
Adhesive glycoproteins(TOPNOTCH)
Extravasation of fluid into interstitial spaces due to increases in vascular volume or pressure, decreases in plasma protein content or alterations in endothelial function.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
It is a severe and generalized edema with profound subcutaneous tissue swelling.
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
The edema fluid occuring with volume or pressure overload or under conditions of reduced plasma protein.
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
Edema secondary to increased vascular permeability and inflammation.
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
The serum protein most responsible for maintaining intravascular colloid osmotic pressure.
Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
In breast cancer, infiltration and obstruction of superficial lymphatics can cause edema of the overlying skin, called _______ appearance.
Peau d’ orange(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
Microscopically, it is reflected primarily as a clearing and separation of the extracellular matrix elements with subtle cell swelling.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Diffuse edema usually more prominent in certain body areas as a result of the effects of gravity.
Dependent edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
True or false:Dependent edema is a prominent feature of left-sided heart failure.
False.Dependent edema is a feature of right-sided HF, while pulmonary congestion is a feature of left-sided HF.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Edema due to renal dysfunction which manifests disproportionately in tissues with loose connective tissue matrix, e.g. Eyelids.
Periorbital edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Finger pressure over significantly edematous subcutaneous tissue displacing the interstitial fluid, leaving a finger-shaped depression on the skin.
Pitting edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Condition wherein the lungs weigh 2-3x the normal, and on sectioning reveals frothy, sometimes blood-tinged mixture of air, fluid and extravasated red cells.
Pulmonary edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Condition wherein the brain is grossly swollen, with narrowed sulci and distended gyri showing signs of flattening against the underlying skull.
Brain edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
It is an active process resulting from augmented blood flow due to arteriolar dilation.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
The affected tissue is redder than normal, because of engorgement with oxygenated blood.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
It is a passive process resulting from impaired venous rturn out of a tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Tissue has a blue-red color due to accumulation of hemoglobin in the affected tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage.
Acute pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.
Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Hemosiderin- laden macrophages
Heart- failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration. The periportal hepatocytes are better oxygenated.
Acute hepatic congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
The central regions of the hepatic lobules are grossly red-brown and slightly depressed and are accentuated against the surrounding zones of uncongested tan, sometimes fatty liver (nutmeg liver).
Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage and hemosirin-laden macrophages
CPC of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Extravasation of blood from vessels into the extravasclar space.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Accumulation of blood within a tissue.
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.
Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
1-2cm subcutaneous hematomas/bruises.
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
It is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.
Normal hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Pathologic form of hemostasis.
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
It occurs after an initial injury, as a result of reflex neurogenic mechanisms.
Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
A potent endothelium-derived vasocontrictor.
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Receptors responsible for platelet adhesion.
GpIb receptors- plateletVon Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of GpIIb-IIIa receptors.
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of Factor VIII.
Von Willebrand Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
It is a membrane-bound procoagulant glycoprotein synthesized by endothelium, which becomes exposed at the site of injury.
Thromboplastin/Factor III(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Formation of a hemostatic plug due to platelet aggregation
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Hemostasis characterized by activation of thrombin through the coagulation cascade.
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
True or false:The primary aggregation of platelets is irreversible.
FalseReversible(TOPNOTCH)
Two substances essential for the formation of a primary hemostatic plug.
ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87
True or false:Activation of the coagultion cascade and subsequent thrombin formation is reversible.
FalseIrreversible(TOPNOTCH)
Substance that activates the coagulation proteins.
Calcium(TOPNOTCH)
Substance that medites further platelet aggregation and degranulation.
ADP(TOPNOTCH)
Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.
TXA2(TOPNOTCH)
Most important initiator of the coagulation cascade.
Tissue factor(TOPNOTCH)
A protein found on endothelial cells involved in the breakdown of blood clots which catalyzes conversion of plasminogen to plasmin.
Tissue plasminogen activator (t-PA) and Urokinase(TOPNOTCH)
Components of Virchow’s triad?
Endothelial injuryStasisHypercoagulability(TOPNOTCH)
It is a major contributor to the development of VENOUS thrombi.
Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
Type of blood flow found in normal blood vessels, wherein platelets flow centrally in the vessel lumen, separated from the endothelium by a slow moving clear zone of plasma.
Laminar flow(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
This contirbutes to arterial and cardic thrombisis by causing endothelial injury or dysfunction as well as formation of countercurrents and local pockets of stasis.
Turbulence(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
Any alteration of the coagulation pathway that predisposes to thrombosis.
Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
A detached, intravascular solid, liquid or gaseous mass that is carried by the blood distal to its point of origin.
Embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
Apparent laminations seen in a thrombus, representing pale platelet and fibrin layers alternating with darker erythrocyte-rich layers.
Lines of Zahn(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Significance of Lines of Zahn?
Represents thrombosis in the setting of blood flow, seen in antemortem clots.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Thrombi occuring in heart chambers or aortic lumen
Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Gelatinous thrombi with a dark red dependent portion where red cells have settled by gravity with a yellow “chicken fat” supernatant. Usually unattached to underlying wall.
Postmortem thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Thrombi on heart valves.
Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Sterile, verrucous endocartidis occuring in patients with SLE.
Limban-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Thrombi occuring in heart chambers or in aortic lumen.
Mural thrombi(TOPNOTCH)
Vegetations occuring in the presence of non - infected valves in hypercoagulable states.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Fate of a thrombus wherein the thrombus accumulates additional platelets and fibrin, eventually causing vessel obstruction.
Propagation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Fate of a thrombus wherein it may dislodge or fragment and transported elsewhere in the vasculature.
Embolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Fate of a thrombus as a result of of fibrinolytic activity leading to rapid shrinkage and even total lysis of recent thrombi.
Dissolution(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Fate of a thrombus wherein it may induce inflammation and fibrosis and establish some degree of blood flow.
Organization and recanalization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
True or false:Therapeutic administration of fibrinolytic agents is generally effective only within a few hours of thrombus formation.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Most common site of venous thrombosis.
Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Most common sequelae of deep venous thrombosis.
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Tumor-associated procoagulant release largey responsible for the increased risk of thromboembolic phenomena seen in disseminated cancers.
Migrating thrombophlebitis or Trousseau’s syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
Hardening or thickening of the arteries as a result of the accumulation of fatty materials, macrophages, platelets and other inflammatory mediators.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
Fates of a thrombus (4)
PropagationResolution/DissolutionOrganization and recanalizationEmbolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
Embolus occluding a bifurcation in the pulmonary tree.
Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
True or false:A patient who has had one pulmonary embolus has a decreased risk of developing another embolus.
False.The patient is at risk of developing more pulmonary emboli.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.
Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Most common symptom of pulmonary embolism.
None/ Asymptomatic (60-80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Right Ventricular failure secondary to pulmonary hypertension.
Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Emboli in the arterial circulation.
Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Most common origin of systemic thrombi.
Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Major site of arteriolar embolization.
Lower extremities (75%)Brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma.
Fat embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Symptoms of pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia characterize what syndrome?
Fat embolism syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.
Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Amount of air in the circulation which produces clinical effects of air embolism.
> 100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
This occurs when individuals are exposed to sudden changes in atmospheric pressure (e.g. Deep sea divers, scuba divers).
Decompression sickness(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and around joints causing pain.
Bends(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.
Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
More chronic form of decompression sickness where persistence of gas emboli in the bones leads to multiple foci of ischemic necrosis.
Caisson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Treatment of choice for decompression sickness.
Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Underlying cause of amniotic fluid embolism.
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)
Underlying cause of amniotic fluid embolism.
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Presence of marked pulmonary edema, diffuse alveolar damage, and presence of squamous cells in the pulmonary circulation shed from fetal skin, lanugo hair, fat and mucin.
Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Venous occlusion
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Lung infarction
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Intestinal infarct
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Myocardial infarction
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarction?Splenic infact
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarction?Wedge infarct
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
The dominant histologic characteristic of infarction.
Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Histologic characteristic of brain infarcts.
Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
This occurs when bacterial vegetations from a heart valve embolize or when microbes seed an area of necrotic tissue.
Septic infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Most common sequalae of septic infarcts.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Major determinants of the eventual outcome of an infarct. (4)
Nature of vascular supplyRate of development of occlusionVulnerability to hypoxiaOxygen content of blood(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Neurons undergo irreversible damage when deprived of their blood supply for _______.
3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
Myocardial cells undergo irreversile damage after ______ minutes of ischemia.
20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
It is the final common pathway for severe hemorrhage, extensive trauma, burns, large MI, pulmonary embolism and sepsis.
Shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
End results of shock (3)
HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock results from failure of the cardic pump which maybe caused by MI, ventricular arrythmias, cardiac tamponade or outflow obstruction.
Cardiogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock results from loss blood or plasma volume.
Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock is caused by microbial infection, caused by gram negative and gram positive bacteria and fungi
Septic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
True or false:Systemic bacteremia must be present to induce septic shock.
FalseHost inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102
Type of shock which occurs in the setting of an anesthetic accident or spinal cord injury as a result of loss of vascular tone and peripheral pooling of blood.
Neurogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock represents systemic vasodilation and increased vascular permeability caused by IgE hypersensitivity reaction.
Anaphylactic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
Septic shock caused by gram negative bacilli.
Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
Criteria for SIRS.
Temp 38 CelciusHR >90 bpmRR >20 or PaCO2 12,000 cells/mm3 or 10% bands(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
Adrenal changes in shock.
Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
Kidney changes in shock.
Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
Gastrointestinal changes in shock.
Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
Lung changes in shock.
Diffuse alveolar damage if due to bacterial sepsi and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
These agents cause transmissible spongiform encephalopathies.
Prions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 321
Infected cells show distinct nuclear and ill-defined cytoplasmic inclusions.
CMV infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
Infected cells show glassy nuclear inclusions, frequently with a surrounding halo.
Herpesvirus infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
Infected hepatocytes show diffuse granular (ground-glass) cytoplasm.
Hepatitis B viral infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
Sexually transmitted protozoan that can colonize the vagina and male urethra.
Trichimonas vaginalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325
Protozoan acquired either by contact with oocyte-shedding kittens or by consumption of cyst-ridden undercooked meat.
Toxoplasma gondii(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325
Size of microorganisms for them to be inhaled directly into the alveoli.
5 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
These microorganisms grow in contaminated food and releases powerful enterotoxins that cause food poisoning symptoms without any bacterial multiplication in the gut.
Staphylococcal strains(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
Intestinal helminth that cause disease when present in large numbers or cause obstruction of the gut.
Ascaris lumbricoides(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 326
Helminth that causes iron deficiency anemia by chronic loss of blood.
Hookworms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
Helminth that depletes vitamin B12 giving rise to an illness resembling pernicious anemia.
Diphyllobotrium latum(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
Placentofetal route as a mode of transmission is also referred to as ________.
Vertical transmission(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 329
The ability of bacteria to cause disease.
Virulence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 331
Bacterial surface molecules that bind to host cells.
Adhesins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332
Filamentous proteins on gram negative bacteria which allow exchange of genes between bacteria, and also involved in adherence.
Fimbriae/pili(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332
Clostridium perfringens produces this toxin that disrupts plasma membranes resulting in digestion of host tissues and collagen.
Alpha toxin (lecithinase)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
Bacterial toxins with the capacity to stimulate large populations of T lymphocytes, functionally resulting in a “cytokine storm”.
Superantigens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
Examples of antigen presenting cells.
Dendritic cellsMacrophagesB-cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
A superantigen secreted by S. aureus which causes inflammation, fever and shock. Found in the vagina of menstruating women.
Toxic shock syndrome toxin (TSST-1)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
Collection of neutrophils which gives rise to localized liquefactive necrosis.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
High risk agents of bioterrorism which are easily disseminated and has high potential for mortality. An example is smallpox.
Category A(TOPNOTCH)
A distinctive form of mononuclear inflammation usually evoked by infectious agents that resist eradication, but are capable of stimulating strong T cell mediated immunity. Characterized by epitheloid cells which may fuse to form giant cells.
Granulomatous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 335
Agents that are relatively easy to disseminate and produces moderate morbidity and low mortality. An example is E.coli O157:H7 which can cause HUS.
Category B(TOPNOTCH)
Includes emerging pathogens that have the potential for mass dissemination with high morbidity and mortality. Examples are Nipah virus and Hanta virus.
Category C(TOPNOTCH)
This term refers to protection against infections.
Immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
It is the collection of cells and molecules that are responsible for defending against pathogenic microbes.
Immune system(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of immunity mediated by neutrophils, macrophages and natural killer cells and includes epithelial barriers of the skin, GIT and respiratory tract.
Innate immunity (natural/native)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of immunity mediated by lymphocytes and their products, and is normally silent and responds to the presence of microbes by becoming active, expanding and generating potent mechanisms for neutralizing and eliminating microbes.
Adaptive immunity (acquired/specific)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Type of adaptive immunity mediated by T lymphocytes.
Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Mediated by antibodies and is effective against extracellular microbes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Reaction of T-lymphocytes, designed to combat cell-associated microbes (e.g. Phagocytosed microbes and microbes in the cytoplasm of infected cells).
Cell-mediated immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Reaction of immune system against one’s own cells.
Autoimmunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.119
Results from activation of TH2 CD4+ helper T cells by environmental antigens, leading to the production of IgE antibodies, which become attached to mast cells.
Type I Hypersensitivity (immediate)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Caused by antibodies that bind to fixed tissue or cell surface antigens and promote phagocytosis and destruction of the coated cells or trigger pathologic inflammation in tissues.
Type II Hypersensitivity (Antibody-mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Caused by antibodies binding to antigens to form complexes that circulate and may deposit in vascular beds and stimulate inflammation, secondary to complement activation.
Type III Hypersensitivity (immune complex mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Cell-mediated immune responses in which T lymphocytes cause tissue injury, either by producing cytokines that induce inflammation and activate macrophages, or by directly killing cells.
Type IV Hypersensitivity (T-cell mediated/Delayed)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:SLE
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Multiple sclerosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Transplant rejection
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Anaphylaxis
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Goodpasture syndrome
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Serum sickness
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Arthus reaction
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Allergies
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Type I DM
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Bronchial asthma
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Polyarteritis nodosa
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Rheumatoid arthritis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Inflammatory bowel disease
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculin reaction
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Reactive arthritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Graves disease
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Myasthenia gravis
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Insulin resistant DM
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Pernicious anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
A special form of graft rejection occuring in the setting where preformed antidonor antibodies are present in the circulation of the host before transplant. Occurs within minutes to a few hours after transplantation.
Hyperacute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Rejection which occurs within days to weeks of transplantation in a nonimmunosuppressed host. Caused by both cellular and humoral immune mechanisms.
Acute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Acute rejection most commonly seen within the first months after transplantation, typically accompanied by signs of renal failure. Extensive CD4+ and CD8+ T-cell infiltration with edema and mild interstitial hemorrhage.
Acute cellular rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Acute rejection caused by antidonor antibodies. May take the form of necrotizing vasculitis with endothelial cell necrosis, neutrophilic infiltration, deposition of antibody, complement, and fibrin, and thrombosis.
Acute humoral rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Rejection which present clinically months to years after transplantation with a progressive rise in serum creatinine levels. Dominated by arteriosclerosis, interstitial fibrosis and loss of renal parenchyma.
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
A multisystem autoimmune disease which principally affects the skin, kidneys, serosal membranes, joints and heart. Associated with autoantibodies including ANAs.
Systemic Lupus Erythematosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.139
SOAP BRAIN MD mnemonic for SLE stands for?
SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
How many symptoms must be present in a patient for her/him to be diagnosed as having SLE?
4 out of 11 symptoms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
Most serious and most common form of renal lesion in SLE. “Wire-loop” appearance of glomerular capillary walls.
Diffuse proliferative glomerulonephritis (Class IV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.142
Cardiac manifestation of SLE, which occurs as nonspecific mononuclear infiltrates and the presence of irregular 1-3mm warty deposits on either surface of the leaflets.
Libman-Sacks Endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.144
A systemic, chronic inflammatory disease affecting many tissues but principally attacking the joints to produce a nonsuppurative proliferative synovitis that frequently progress to destroy articular cartilage and underlying bone with resulting disabling arthritis.
Rheumatoid arthritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.145
Characteristic lesion in RA, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue and fibrous connective tissue.
Pannus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
Cytokine which plays a central role in the pathogenesis of RA.
TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.
Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148
Characterized by progressive fibrosis involving the skin, GIT and other tissues. May be a result of activation of fibroblasts by cytokines produced by T cells.
Systemic sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.149
A vascular disorder characterized by reversible vasospasm of the arteries. Typically the hands turn white due to vasospasm, then blue due to cyanosis, then red due to reactive hyperemia.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.151
One of the more common forms of primary immune deficiency characterized by absent or markedly decreased numbers of B-cells in the circulation, with depressed serum levels of all classes if immunoglobulin.
X-linked agammaglobulinemia (Bruton disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.152
Most common of all the primary immune deficiencies characterized by recurrent sinopulmonary infections and diarrhea.
Isolated IgA deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
A constellation of genetically distinct syndromes with common feature of defects in both humoral and cell-mediated immune responses, making affected infants susceptible to severe recurrent infections by bacteria, viruses, fungi, protozoans, and opportunistic infections.
Severe Combined Immunodeficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
Autosomal recessive form of SCID is due to deficiency of what enzyme?
Adenosine deaminase (ADA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
An X-linked recessive disease characterized by thrombocytopenia, eczema, and marked vulnerability to recurrent infection ending in early death.
Wiskott-Aldrich Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.155
HIV viral surface proteins essential for viral entry into cells.
gp41 and gp120(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.157
A form of pneumonia in HIV patients caused by a yeast-like fungus.
Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)
Main cellular target of HIV.
CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.158
P.carinii pneumonia occurs in AIDS patients with CD4+ T cell count of ______.
Less than 200 cells/uL(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
Most common secondary infection of the CNS in patients with AIDS.
Toxoplasmosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
Most common neoplasm in AIDS patients, caused by HHV8. Characterized by cutaneous lesions with or without internal involvement.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.164
A disorder of protein misfolding, causing extracellular deposition of pink or red colored deposits stained with Congo red, with apple-green birefringence in polarized light.
Amyloidosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.166
This term literally means “new growth”.
Neoplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
An abnormal mass of tissue the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after the cessation of stimuli which evoked the change.
Neoplasm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Study of tumors.
Oncology(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Localized
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Amenable to surgical removal
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Invades and destroys adjacent tissues.
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
What are the two basic components of tumors?
Parenchyma and Stroma(TOPNOTCH)
Benign or malignant?Metastasis
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
This component of tumors largely determines its biologic behavior.
Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
This component of tumors determines the name of the growth.
Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
This component of tumors is crucial to the growth of neoplasms since it carries the blood supply and provides support to the growth of cells.
Stroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Fibroma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Chondroma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Adenoma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Hepatoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Papilloma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Malignant neoplasms arising in mesenchymal tissue or its derivatives.
Sarcomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
Benign tumor arising in fibrous tissue is called?
Fibroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
A benign cartilagenous tumor is called?
Chondroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
This is a benign epithelial neoplasm which produces glandular patterns or neoplasms derived from glands but not necessarily exhibit glandular patterns
Adenoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.
Papillomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
A mass that projects above a mucosal surface to form a macroscopically visible structure.
Polyps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
A cancer of fibrous tissue origin.
Fibrosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
Malignant neoplasms of epithelial cell origin.
Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
Carcinoma of squamous cell origin.
Squamous cell carcinoma(TOPNOTCH)
Carcinoma of squamous cell origin.
Squamous cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Lymphoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Seminoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
The extent to which neoplastic cells resemble their normal forebears morphologically and functionally.
Differentiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
This is considered a hallmark of malignancy, which literally means “to form backward”.
Anaplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177
These cells display marked pleomorphism, nuclei are variable and bizzare in size and shape. Chromatin is course and clumped. Mitoses are often numerous and distinctly atypical.
Anaplastic cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177
This term is defined by disorderly but non-neoplastic proliferation of cells, described as a loss in uniformity of individual cells and in their architectural orientation.
Dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
Defined as dysplactic changes which involve the entire thickness of the epithelium.
Carcinoma -in - situ(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
True or false?Dysplasia always progress to cancer.
False(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
True or false?Lack of capsule in a neoplastic growth indicates malignancy.
FalseSome benign tumors are not encapsulated.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
This term describes the development of secondary implants discontinuous with the primary tumor, in remote tissues.
Metastasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
Next to metastasis, this is the most reliable feature that distinguishes malignant from benign tumors.
Local invasiveness(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
Methods of dissemination of malignant neoplasms? (3)
SeedingLymphatic spreadHematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
This is the mode of dissemination of cancers of the ovary and CNS.
Spread by seeding(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
This is the mode of dissemination more typical of carcinomas.
Lymphatic spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
This is the mode of dissemination more typical of sarcomas.
Hematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
It is defined as the first lymph node in a regional lymphatic basin that receives lymph flow from a primary tumor.
Sentinel lymph node(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
What are the most common sites of metastasis involved in hematogenous dissemination of cancer?
Liver and lungs(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.181
This substance is a byproduct of metal smelting, a component of alloys, electrical and semiconductor devices which could cause cancer of the lungs and skin and hemangiosarcomas.
Arsenic and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance was formerly used for fire-resistant textiles and construction materials which could cause lung cancer and more prominently malignant mesothelioma
Asbestos(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is commonly used as a solvent in paint, rubber, dry cleaning, adhesives and detergents which could cause leukemias and Hodgkin lymphoma.
Benzene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is used as hardener for metal alloys used in aerospace applications and nuclear reactors which is commonly associated with cancer of the lung.
Beryllium and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is used in solders, batteries and metal alloys commonly associated with cancers of the prostate.
Cadmium and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is a refrigerant and used as adhesive for plastics, which causes hepatic angiosarcoma.
Vinyl chloride(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
Inherited gene : Cancer syndromeRB gene :__________
Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndromep53 : ______________
Li Fraumeni Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome__________ : Familial Adenomatous Polyposis / Colon CA
APC Gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome_________ : Breast on Ovarian Tumors
BRCA 1 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome_________ : Breast Cancer only
BRCA 2 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndromeRET gene : _________
Multiple Endocrine Neoplasia 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome__________ : Colon cancer
kras gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Normal cellular genes whose products promote cell proliferation.
Proto-oncogenes(TOPNOTCH)
Normal cellular genes whose products promote cell proliferation.
Proto-oncogenes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.188
It is a naturally occurring carcinogenic agent produced by some strains of Aspergillus, a mold that grows on improperly stored grains and nuts.
Aflatoxin B(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
There is a strong correlation between the dietary level of Aflatoxin and what type of cancer?
Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
These substances require metabolic conversion to be carcinogenic.
Indirect - acting carcinogens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
These substances stimulate proliferation of the mutated cells.
Promoters(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
How does ionizing radiation cause cancer?
Through chromosome breakage, translocations and point mutations leading to genetic damage and carcinogenesis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
What is the mechanism of action of UV rays in the formation of neoplastic cells?
UV rays induce formation of pyrimidine dimers within DNA leading to mutations.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
This is the only retrovirus that has been demonstrated to cause cancer in humans.
Human T-cell Leukemia Virus -1 (HTLV-1)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.211
HPV strains which has been implicated in the genesis of cervical and anorectal cancer.
HPV 16, 18(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.212
EBV has been implicated in the pathogenesis of the following cancers except:A. Burkitt lymphomaB. Lymphoma in HIV patientsC. Nasopharyngeal carcinomaD. Hodgkin lymphomaE. None of the above
E. none of the above(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.212
Which hepatitis virus leads to hepatocellular carcinoma?
HBV, HCV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213
This is the first bacterium to be classified as a carcinogen.
Helicobacter pylori(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213
What type of cancer can be caused by H.pylori?
Gastric adenocarcinoma Gastric MALT lymphomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.214
These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.
Papillomas(TOPNOTCH)
Tumor antigens are presented on the cell surface by MHC Class I molecules to which type of T lymphocytes?
CD8+ T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.215
These disorders are derived from one’s parents, transmitted through gametes through the generations, and are therefore familial.
Hereditary disorders(TOPNOTCH)
This term literally means “present at birth”.
Congenital(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This term refers to permanent changes in the DNA.
Mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This type of mutation results from the substitution of a single nucleotide base by a different base, resulting in the replacement of one amino acid by another.
Missense mutation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This type of mutation results in the replacement of one amino acid by a stop codon, resulting in chain termination.
Nonsense mutation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
Missense, nonsense and silent mutations are examples of ________ mutations, wherein only one base pair is replaced.
Point mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This type of mutation occur when the insertion or deletion of one or two bse pairs alters the reading frame of the DNA strand.
Frameshift mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
These mutations are characterized by amplification of a sequence of three nucleotides.
Trinucleotide repeat mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
Disease characterized by CGG trinucleotide repeats.
Fragile X Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This is a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems.
Huntington’s disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
Genetic mutation in Huntington’s disease?
CAG trinucleotide repeats(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
This disorder is a chronic, slowly progressing inherited genetic disorder characterized by muscle wasting, cataracts, heart conduction defects, endocrine changes and myotonia.
Myotonic Dystrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
Genetic mutation found in myotonic dystrophy?
CTG Trinucleotide repeats(TOPNOTCH)
A point mutation wherein a single base pair is replaced but codes for the same amino acid, therefore has no effect on the functioning of the protein.
Silent mutation(TOPNOTCH)
An example of point mutation wherein a purine base is replaced by another purine base or a pyrimidine base is replaced by another pyrimidine base.
Transition(TOPNOTCH)
A point mutation wherein a purine is replaced by a pyrimidine or vice versa.
Transversion(TOPNOTCH)
Diseases caused by single gene defects are called?
Mendelian Disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
A condition wherein both dominant and recessive alleles of a gene pair may be fully expressed in the heterozygote.
Codominance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
The presence of many allelic forms of a single gene is called _______.
Polymorphism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
This occurs when one gene influences or leads to multiple phenotypic traits.
Pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
A phenomenon wherein a single phenotype or genetic disorder may be caused by mutations of several genetic loci or allele.
Genetic heterogeneity Note: compare with pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
A transmission pattern of inheritance which is manifested in the heterozygous state, wherein at least one parent of an index case is usually affected, both males and females are affected and both can transmit the condition.
Autosomal dominant (AD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
This pattern of inheritance occur when BOTH of the alleles at a given gene locus are mutants, wherein the parents are not affected, but offspring have 1 in 4 chance (25%) of being affected.
Autosomal recessive(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
Pattern of inheritance wherein the disorder is transmitted by heterozygous female carriers only to 50% of the sons. An affected male does not transmit the disorder to sons but all daughters are carriers.
X-linked disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
An autosomal dominant disorder of connective tissues characterized by abnormally long legs, arms and fingers, joint hyperextensibility, pectus excavatum, lens subluxation and increased risk of aortic dissection.
Marfan Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
Integral component of elastic fibers defective in Marfan Syndrome.
Fibrillin 1(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
Fibrillin 1 is encoded by what gene?
FBN1 gene (chromosome 15q21)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
A collection of disorders caused by defects in collagen synthesis or structure, characterized by hyperextensible skin and joint hypermobility, rupture of internal organs and poor wound healing.
Ehlers-Danlos SyndromesThere are 6 variants to Ehlers-Danlos (nice to know)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.231
This autosomal recessive inborn error of metabolism is characterized by inability to convert phenylalanine to tyrosine, strong mousy or musty odor of urine and sweat, decreased pigmentation of hair and skin, eczema, seizures and mental retardation.
Phenylketonuria (PKU)(TOPNOTCH)
This autosomal dominant disorder is caused by a mutation in the gene that specifies the receptor for LDL, impairing the intracellular transport and catabolism of LDL.
Familial hypercholesterolemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.232
Enzyme deficient in classic PKU.
Phenylalanine hydroxylase (PAH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234
An autosomal recessive disorder of galactose metabolism characterized by jaundice, liver damage, cataracts, neural damage, vomiting and diarrhea.
Galactosemia(TOPNOTCH)
Deficiency of this enzyme can also cause symptoms of phenylketonuria due to decreased synthesis of a cofactor in the conversion of phenylalanine to tyrosine.
Dihydrobiopteridine reductase (DHPR)Enzyme responsible for the reduction of Dihydrobiopterin (BH2) to Tetrahydrobiopterin (BH4).(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234
Enzyme deficient in galactosemia.
Galactose-1-phosphate uridyltransferase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.235
Lysosomal storage disease due to deficiency of glucosylceramidase.
Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease due to deficiency of B-Hexosaminidase A.
Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease due to deficiency of a-Galactosidase A.
Fabry disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease due to deficiency of Sphingomyelinase.
Niemann-Pick disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease common among Ashkenazi Jews characterized by motor weakness, mental retardation, blindness, neurologic dysfunction and death.
Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease characterized by accumulation of glucosylceramide in mononuclear phagocytic cells, which enlarge, forming “wrinkled tissue paper” cytoplasmic appearance.
Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
What do you call the pathognomonic cell characterized by “wrinkled tissue paper” cytoplasmic appearance.
Gaucher cell(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
These disorders result from the accumulation of mucopolysaccharides in many tissues including the liver, spleen, heart, blood vessels, brain, cornea and joints. Affected patients have coarse facial features.
Mucopolysaccharidoses(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
Mucopolysaccharidosis characterized by corneal clouding, coronary arterial and valvular depositions, which occurs due to deficiency of a-L-iduronidase, leading to accumulation of dermatan and heparan sulfate.
Hurler syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239
An X-linked mucopolysaccharidosis which is due to a deficiency of L-iduronate sulfatase. Symptoms are similar to Hurler sundrome, but without corneal clouding.
Hunter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239
Glycogen storage disease characterized by hepatomegaly, renomegaly, hypoglycemia, hyperlipidemia and hyperuricemia, leading to gout and skin xanthomas.
von Gierke’s disease (Type I)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
von Gierke’s disease is due to a deficiency of what enzyme?
Glucose-6-phosphatase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
Glycogen storage disease characterized by accumulation of glycogen in skeletal muscles leading to painful cramps during strenuous exercise and myoglobinuria.
McArdle syndrome (type V)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
Glycogen storage disease characterized by mild hepatomegaly, cardiomegaly, muscle hypotonia, and may lead to cardiorespiratory failure.
Pompe disease (type II)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
Enzyme deficient in McArdle syndrome.
Muscle phosphorylase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.
Cytogenetic disorders(TOPNOTCH)
These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.
Cytogenetic disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.241
It is a term used to describe the presence of two or more populations of cells in the same individual.
Mosaicism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.242
This refers to a lack of one chromosome of the normal complement (e.g. XO).
Monosomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
This refers to the presence of three copies of a particular chromosome, instead of two.
Trisomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
This mechanism occurs due to the failure of chromosome pairs to separate properly during meiosis stage 1 or 2.
Nondisjunction(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
This mechanism implies transfer of a part of one chromosome to another chromosome.
Translocation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
This mechanism involves loss of a portion of a chromosome.
Deletion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
Patients with this syndrome have severe mental retardation, flat facial profile, epicanthic folds, cardiac malformations, increased risk of leukemia, and premature development of Alzheimer’s disease.
Down syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
Down syndrome is also called _________
Trisomy 21(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Trisomy 18 is also called ________ syndrome.
Edwards syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Trisomy 13 is also called _________ syndrome.
Patau syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
Syndrome characterized by a prominent occiput, low set ears, micrognathia, rocker-bottom feet, renal malformation, mental retardation and heart defects.
Edwards syndrome / trisomy 18(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Syndrome characterized by mental retardation, microcephaly, micropthalmia, polydactyly, cleft lip and palate, cardiac and renal defects, umbillical hernia and rocker-bottom feet.
Patau syndrome/Trisomy 13(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Syndrome characterized by thymic hypoplasia with diminished T-cell immunity and parathyroid hypoplasia with hypocalcemia.
DiGeorge syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Syndrome characterized by congenital heart disease affecting outflow tracts, facial dysmorphism and developmenta delay.
Velocardiofacial syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Deletion of genes from this chromosome gives rise to DiGeorge and velocardiofacial syndromes.
22q11.2Remember mnemonic CATCH22(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
The q from 22q11.2 refers to ________.
“Long arm” of chromosome 22.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Syndrome defined as male hypogonadism that develops when there are at least two X chromosomes and one or more Y chromosomes.
Klinefelter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Syndrome manifested by a eunochoid body habitus, reduced facial, body and pubic hair, gynecomastia, testicular atrophy, decreased serum testorerone and incresed urinary gonadotropin levels. It is the most common cause of hypogonadism in males.
Klinefelter syndrome (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Most common chromosomal derangement in Klinefelter syndrome.
47XXY(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Syndrome which results from the partial or complete monosomy of the short arm of the X chromosome.
Turner syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247
Inheritance associated with mitochondrial DNA.
Maternal inheritance(TOPNOTCH)
Neurodegenerative disease which manifests as progressive bilateral loss of central vision that leads to blindness. This is the prototypical disorder of mutations in mitochondrial genes.
Leber hereditary optic neuropathy(TOPNOTCH)
Inheritance associated with mitochondrial DNA.
Maternal inheritance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247
An epigenetic process wherein certain genes are differentially “inactivated” during paternal and maternal gametogenesis.
Genomic imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.252
This refers to transcriptional silencing of the maternal allele.
Maternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
Refers to the transcriptional silencing of the paternal allele.
Paternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
Syndrome characterized by mental retardation, short stature, hypotonia, obesity, small hands and feet, and hypogonadism. Paternal imprinting.
Prader-Willi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
Syndrome manifested as mental retardation, ataxic gait, seizures and inappropriate laughter. Also called the “happy puppet syndrome”. Maternal imprinting.
Angelman syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
These represent primary errors of morphogenesis due to an intrinsically abnormal developmental process.
Malformations(TOPNOTCH)
These represent primary errors of morphogenesis due to an intrinsically abnormal developmental process.
Malformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
These result from secondary destruction of an organ or body region that was previously normal in development, due to an extrinsic disturbance in morphogenesis.
Disruptions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
These are due to generalized compression of the growing fetus by abnormal biomechanical forces, for example uterine constraint.
Deformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
This refers to multiple congenital anomalies that result from secondary effects of a single localized aberration in organogenesis. The initiating event may be a malformation, deformation or disruption.
Sequence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
This refers to the presence of several defects that cannot be explained on the basis of a single localizing initiating error in morphogenesis.
Malformation syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253
Elements of the TORCH complex.
TOxoplasmaTreponema pallidumRubellaCytomeglovirusHerpesvirus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.256
Most common cause of neonatal mortality.
Congenital anomalies(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253
Second most common cause of neonatal mortality.
Prematurity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
Lungs of infants with this disease are normal size but are heavy and relatively airless. They have a mottled purple color, with poorly developed atelectatic alveoli.
Neonatal Respiratory Distress Syndrome / Hyaline Membrane Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
Characteristic eosinophilic membranes line the respiratory bronchioles, alveolar ducts and random alveoli, which contain necrotic epithelial cells admixed with extravasated plasma proteins.
Hyaline Membrane Disease / Neonatal RDS(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
Two well known complications of high concentration ventilator administered oxygen in infants suffering from RDS.
Retrolental fibroplasia / retinopathy of prematurityBronchopulmonary dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
Characteristic lesion in the retina of infants suffering from retrolental fibroplasia?
Neovascularization or retinal vessel proliferation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
Main component of pulmonary surfactant.
Dipalmitoylphosphatidylcholine (DPPC) ~40%
Characteristic abnormality in bronchopulmonary dysplasia?
Alveolar hypoplasia or a decrease in the number of mature alveoli.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
What is the fundamental abnormality in neonatal RDS?
Insufficient pulmonary surfactant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
This condition occurs more commonly in very-low-birth-weight infants, as a result of intestinal ischemia, bacterial colonization of gut and formula milk feeding.
Necrotizing enterocolitis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
Microscopic features of NEC.
Presence of submucosal gas bubbles, transmural coagulative necrosis, ulceration and bacterial colonization.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.259
Defined as the sudden death of an infant under 1 year of age which remains unexplained after a thorough investigation.
Sudden Infant Death Syndrome / SIDS(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.260
Multiple petechiae of the thymus, visceral and parietal pleura and epicardium, congested lungs with vascular engorgement with or without pulmonary edema.
Sudden Infant Death Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.260
Results from antibody-induced hemolytic disease in the nnewborn that is caused by blood group incompatibility between mother and fetus, leading to edema fluid accumulation.
Immune Hydrops(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
Erythroid precursors with large homogenous, intranuclear inclusions and a surrounding peripheral rim of residual chromatin can be seen in the bone marrow aspirate of an infant infected with this virus. This leads to development of non-immune hydrops.
Parvovirus B19(TOPNOTCH)
Isolated postnuchal fluid accumulation in fetuses with hydrops.
Cystic hygroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
A lethal condition characterized by generalized edema of the fetus.
Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
Increased hematopoietic activity leading to the presence of large number of immature red cells, including reticulocytes, normoblasts and erythroblasts. Characteristic finding in fetal anemia-associted hydrops.
Erythroblastosis fetalis(TOPNOTCH)
Primary gene defect in cystic fibrosis.
Abnormal CFTR (CF transmembrane conductance regulator) Chromosome 7q31.2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262
Lungs with extensive mucous plugging and dilated tracheobronchial tree. Pancreatic ducts dilated and plugged with eosinophilic mucin, atrophic parenchymal glands replaced by fibrous tissue. Hepatic steatosis, Azoospermia and infertility are some of the features of this disease.
Cystic fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262
Patients with cystic fibrosis are prone to developing infections caused by these three organisms.
S. aureusH. InfluenzaeP. aeruginosa(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.266
How is cystic fibrosis diagnosed?
Persistently elevated sweat chloride concentration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Most common tumors of infancy.
Hemangioma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Microscopically normal cells or tissues that are present in abnormal locations.
Heterotopia or choristoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Port wine stains are associted with these syndromes. (2)
von Hippel-Lindau Sturge-Weber syndromes(TOPNOTCH
This refers to an excessive but focal overgrowth of cells and tissues native to the organ in which it occurs.
Hamartoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Large, flat to elevated, irregular, red-blue masses in the skin.
Port wine stains(Large hemangiomas)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
These represent the lymphatic counterpart of hemangiomas characterized as cystic and cavernous spaces lined by endothelial cells and surrounded by lymphoid aggregates,usually containing pale fluid.
Lymphangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268
What do you call the rosettes found in neuroblastomas?
Homer-Wright pseudorosettes(TOPNOTCH)
Most common germ cell tumors of childhood,associated with meningocoele and spina bifida.
Sacrococcygeal teratomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268
Tumor of the adrenal medulla composed of small, primitive-appearing cells with dark nuclei, scant cytoplasm, and poorly defined cell borders growing in solid sheets within a finely fibrillar matrix. Rosettes can be found in which tumor cells are concentrically arranged about a CENTRAL SPACE FILLED with neuropil.
Neuroblastomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.269
This is used in the screening of patients with neuroblastoma.
Urinary vanillylmandelic acid and homovanillic acid (VMA/HVA)(TOPNOTCH)
Differentiated lesions containing more large cells with vesicular nuclei and abundant eoinophilic cytoplasm, in the absence of neuroblasts, usually accompanied by mature spindle shaped Schwann cells.
Ganglioneuroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270
Disseminated neuroblastoma with multiple cuteaneous metastases with deep blue discoloration to the skin.
“Blueberry muffin baby”(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270
This tumor is composed of small, round cells with large hyperchromatic nuclei and scant cytoplasm, with characteristic structures consisting of clusters of cuboidal or short columnar cells arranged around a CENTRAL LUMEN. The nuclei are displaced away from the lumen, which appears to have a limiting membrane.
Retinoblastoma(Differentiate with neuroblastoma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Rosettes in retinoblastoma are called _______.
Flexner-Wintersteiner rosettes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Clinicial findings include poor vision, strabismus, whitish hue to the pupils (“cat’s eye reflex”), pain and tenderness to the eye.
Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Most common primary tumor of the kidney in children.
Wilm’s tumor / Nephroblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Components of the WAGR syndrome.
Wilm’s tumorAniridiaGenital abnormalitiesMental retardation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Presents grossly as a large, solitary, well-circumscribed mass. On cut-section, tumor is soft, homogenous, and tan to gray, with occasional foci of hemorrhage, cystic degeneration and necrosis.
Wilm’s tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Microscopically, a combination of blastemal, stromal and epithelial cell types is observed. (Triphasic combination) Blastemal components described as sheets of small blue cells with few distinctive features. Stromal cells are fibrocytic or myxoid in nature. Epithelial cells take the form of abortive tubules or glomeruli.
Wilm’s tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Associated with inactivation of the WT1 gene of chromosome 11p13.
WAGR syndrome and Denys-Drash syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
A gas formed by sunlight-driven reactions involving nitrogen oxides. Together with oxides and fine particulate matter, it forms “smog”.
Ozone(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
A nonirritating , colorless, tasteless, odorless gas produced bu the imperfect oxidation of carbonaceous materials. Binds to hemoglobin with high affinity causing systemic asphyxiation and CNS depression.
Carbon monoxide(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
Carbon monoxide in the blood is called _______.
Carboxyhemoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
Acute poisoning of carbon monoxide produces this characteristic color of the skin and mucous membranes.
Cherry red color(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
Microcytic, hypochromic anemia, with basophilic stippling of erythrocytes, peripheral demyelinating neuropathy which manifests as footdrop and wristdrop, colic characterized by extremely severe, poorly localized abdominal pain, and chronic renal damage are the features of poisoning with this heavy metal.
Lead(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
Main source of exposure to this heavy metal are contamintaed fish and dental amalgams, causing tremor, gingivitis and bizarre behavior.
Mercury(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Consumption of fish contaminated with methyl mercury causing cerebral palsy, deafness, blindness, and major CNS defects in children exposed in utero.
Minamata disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Antidote for mercury poisoning.
Thimerosal(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Chronic exposure with this heavy metal results in hyperpigmentation and hyperkeratosis which may develop into basal or squamous cell carcinomas.
Arsenic(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
This heavy metal is used mainly in batteries and fertilizers, which can contaminate soil. Can cause obstructive lung disease and kidney damage.
Cadmium(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Disease caused by cadmium in Japan, presenting as a combination of osteoporosis and osteomalacia, associated with renal disease.
Itai-itai disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
May be released from combustion of fossil fuels, burning of coal and gas, and also present in tar and soot. Among the most potent carcinogens, implicated in lung and bladder cancer.
Polycyclic hydrocarbons(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
Synthetic products that resist degradation and are lipophilic, typically used as pesticides, with anti-estrogenic and anti-androgenic activity, and causes neurologic toxicity.
Organochlorines (e.g. DDT)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
These can cause skin disorders such as folliculitis and chloracne, consisting of acne, cyst formation, hyperpigmentation, and hyperkeratosis, around the face and behind the ears.
Dioxins and Polychlorinatedbiphenyls (PCB)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
It is the most preventable cause of human death.
Smoking(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
Components of cigarette smoke that are potent carcinogens in animals and are most likely involved in the causation of lung carcinomas in humans.
Polycyclic hydrocarbons and nitrosamines(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 288
A long acting tetracycline which can cause a diffuse blue-gray pigmentation of the skin.
Minocycline(TOPNOTCH)
Chronic alcoholics are at an increased risk of developing this type of cancer as a result of liver injury.
Hepatocellular carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 290
These refer to untoward effects of drugs that are given in conventional therapeutic settings.
Adverse drug reactions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 291
A long acting tetracycline which can cause a diffuse blue-gray pigmentation of the skin.
Minocycline(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 293
Oral contraceptives have a protective effect against these cancers.
Endometrial and ovarian CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Oral contraceptives may increase the risk of developing this type of cancer in women.
Cervical CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Prolonged use of oral contraceptives is associated with the development of this rare benign tumor especially in older women.
Hepatic adenoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Toxic metabolite of paracetamol or acetaminophen.
NAPQI (N-acetyl-p-benzoquinoneimine)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Toxic dose for acetaminophen.
15-25 grams/day(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Antidote for acetaminophen poisoning.
N-acetylcysteine(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 294
Manifested by headache, dizziness, tinnitus, difficulty of hearing, mental confusion, drowsiness, nausea, vomiting, and diarrhea, with CNS changes that can progress to convulsions and coma.
Salicylism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Adult toxic dose of aspirin.
10-30 grams(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Mixtures of aspirin and phenacetin, or its active metabolite acetaminophen, when taken over several years can cause tubulointerstitial nephritis and renal papillary necrosis called _______.
Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
This drug of abuse can precipitate lethal arrythmias, hyperpyrexia, seizures, amd respiratory arrest during acute overdose. Causes nasal septal perforation, decrease in lung diffusing capacity in those who inhale smoke and dilated cardiomyopathy during chronic use.
Cocaine or “crack” (cocaine derivative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 295
Addictive opiod derived from the poppy plant which can cause euphoria, hallucinations, somnolence, sedation, and increased risk of sudden death.
Heroin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 296
Drug made from the leaves of Cannabis sativa plant which can cause distortion of sensory perception and impairs motor coordination.
Marijuana(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 297
Psychoactive substance found in marijuana.
Delta 9- Tetrahydrocannabinol (THC)(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297
Mechanism of action of aspirin.
Irreversibly blocks the enzyme cyclooxygenase.(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297
A wound produced by scraping or rubbing resulting in removal of superficial layer of the skin.
Abrasion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A wound usually produced by a blunt object, characterized by damage to blood vessels and extravasation of blood into tissues.
Contusion (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A tear or disruptive stretching of tissue caused by the application of force by a blunt object, causing jagged and irregular edges to the skin.
Laceration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A wound inflicted by a sharp instrument, wherein bridging blood vessels are severed.
Incision(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A wound caused by a long, narrow instrument.
Puncture wound(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Burn classification which involves total destruction of the epidermis and dermis, with loss of thermal appendages.
Full thickness burn (3rd and 4th degree)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Burn classification wherein the thermal appendages are spared but involves at least the deeper portions of the skin.
Partial thickness burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Partial thickness burn that involves both the epidermis and superficial dermis.
Second degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Partial thickness burn that involves the epidermis only.
First degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Grossly, these burns are white or charred and anesthetic due to nerve ending destruction.
Full thickness burns(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
These burns are pink or mottled with blisters and are painful.
Second degree burn (partial thickness)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Histologic change in the skin during burns.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Leading cause of death in burn patients.
Organ system failure secondary to burn sepsis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Cramping of voluntary muscles in association with vigorous exercise as a result of electrolyte loss via sweating.
Heat cramps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Most common hyperthermic syndrome. A sudden onset of prostration and collapse, resulting from failure of the cardiovascular system to compensate for hypovolemia, secondary to water depletion.
Heat exhaustion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Associated with high ambient temperatures and high humidity. Thermoregulatory mechanisms fail, sweating ceases and core body temperature rises. Due to marked generalized peripheral vasodilation with peripheral pooling of blood and decreased effective circulating volume.
Heat stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Two types of injuries caused by electricity.
BurnsVFib or cardiac and respiratory center failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
This may injure cells directly or indirectly by generating free radicals from water or molecular oxygen, damages DNA and rapidly dividing cells. Exposure may predispose to neoplastic transformation, vascular damage, sclerosis and tissue fibrosis.
Ionizing radiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 300
Malnutrition caused by lack of nutrients from the diet.
Primary malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304
Malnutrition caused by malabsorption, impaired nutrient utilization or storage, excess losses or increased nutrient needs.
Secondary or conditioned malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304
Protein energy malnutrition which occurs when protein deprivation is relatively greater than reduction in total calories. Associated with generalized edema, flaky paint appearance of the skin, alternating bands of pale and dark hair, enlarged fatty liver, apathy, listlessness and loss of appetite.
Kwashiorkor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 305
Protein energy malnutrition caused by a decrease in both protein and calorie intake, and weight falls below 60% of normal for sex, height and age. Serum albumin is normal or slightly reduced.
Marasmus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 305
Self-induced starvation, resulting in marked weight loss.
Anorexia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306
A condition wherein a patient binges on food and then induces vomiting.
Bulimia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306
Deficiency of this vitamin causes night blindness, xerophthalmia, keratomalacia, Bitot spots and eventually corneal ulceration.
Vitamin A(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 307
Condition in children as result of vitamin D deficiency causing the following signs and symptoms: frontal bossing of the head, rachitic rosary, pigeon breast deformity, lumbar lordosis and bow legs.
Rickets (children)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 309
Deficieny of this vitamin causes impaired collagen formation, leading to gum bleeding, easy bruisability, and impaired wound healing.
Vitamin C (Scurvy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 312
Symptoms of cheilosis, stomatitis, glossitis, dermatitis and corneal vascularization results from deficiency of this vitamin.
Vitamin B2 (Riboflavin)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314
Symptoms of cheilosis, glossitis, dermatitis, and peripheral neuropathy.
Vitamin B6 (Pyridoxine)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314
In these arteries, elastic fibers alternate in layers with smooth muscle cells. Examples are the common carotid artery, iliac arteries and pulmonary arteries.
Large or elastic arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
In these arteries, tunica media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina. Examples are the coronaries and renal arteries.
Medium-sized or muscular arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These are the principal control points for regulation of physiologic resistance to blood flow.
Arterioles(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These vessels are approximately the diameter of an RBC, have an endothelial cell lining but no media.
Capillaries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Diameter of an RBC.
7-8 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are thin-walled, endothelium lined channels that drain excess interstitial tissue fluid, returning it to blood via the thoracic duct.
Lymphatics(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are small spherical dilatations, typically in the circle of Willis.
Developmental/berry aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries.
Arteriovenous fistulas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Focal, irregular thickening of the walls of medium and large muscular arteries. Segments of the vessel wall are focally thickened by combination of irregular medial and intimal hyperplasia and fibrosis, causing luminal stenosis.
Fibromuscular dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Literally means hardening of the arteries, term reflecting arterial wall thickening and loss of elasticity, affecting small arteries and arterioles.
Arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by calcific deposits in muscular arteries, typical in persons older than 50 yrs old. The radiographically visible, palpable calcifications do not encroach on the vessel lumen, and are not clinically significant.
Mockenberg medial calcific sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by intimal lesions called atheromas that protrude into vascular lumina.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Three principal components of an atheromatous plaque.
- Cells (SM cells, macrophages, T cells)2. Extracellular matrix (collagen, elastic fibers, proteoglycans)3. Intracellular and extracellular lipidFibrous cap, central lipid core, neovascularization(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Non-modifiable risk factors for atherosclerosis. (4)
Increasing ageMale genderFamily historyGenetic abnormalities(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
Arrange in descending order, based on which blood vessel is most extensively involved in development of atherosclerosis.Popliteal arteries, internal carotid arteries, circle of Willis, coronaries, abdominal aorta
Abdominal aorta > coronaries > popliteal arteries > internal carotid arteries > circle of Willis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 350
Fate of an atheromatous plaque wherein the luminal surface exposes the bloodstream to highly thrombogenic substances and induces thrombus formation.
Rupture, ulceration or erosion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque due to rupture of the overlying fibrous cap or the thin-walled vessels in the areas of neovascularization.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque causing discharge of debris into the bloodstream, producing microemboli composed of plaque contents.
Atheroembolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atherosclerotic plaque due to increased pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, leading to weakness of the vessel wall.
Aneurysm formation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Most common cause of hypertension.
Idiopathic (essential hypertension)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 355
This vascular lesion consists of a homogenous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. A major morphologic characteristic in benign nephrosclerosis.
Hyaline arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
Characteristic of malignant hypertension, associated with “onion-skin” concentric, laminated, thickening of the walls of arterioles with luminal narrowing. These laminations consist of smooth muscle cells and thickened duplicated basement membrane.
Hyperplastic arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysm which involves all three layers of the arterial wall, or the attenuated wall of the heart.
True aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
A breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space.
False aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Arises when blood enters the wall of an artery, as a hematoma dissecting between its layers. Often, but not always aneurysmal in origin.
Arterial dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which are spherical outpouchings, involving only a portion of the vessel wall, varying in size from 5-20cm in diameter and often contain thrombi.
Saccular aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which involve diffuse, circumferential dilation of a long vascular segment, varies in diameter and length, and can involve extensive portions of the aortic arch, abdominal aorta,and iliacs.
Fusiform aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Two most important causes of aortic aneurysms.
AtherosclerosisCystic medial degeneration of the arterial media(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Infection of a major artery that causes weakness to its wall.
Mycotic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
This disease can more commonly affects men >50 years old. Lesion usually positioned below the renal arteries and above the aortic bifurcation. Can be saccular or fusiform.
Abdominal aortic aneurysm (AAA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Abdominal aortic aneurysm characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic infiltrate with manybmacrophages and often giant cells.
Inflammatory AAA(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 358
Atherosclerotic lesions infected by lodging of circulating microorganisms in the wall, particularly in the setting of bacteremia from a Salmonella gastroenteritis. Suppuration further destroys the media, potentiating rapid dilation and rupture.
Mycotic abdominal aortic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Small blood vessels and vasa vasorum show luminal narrowing and obliteration (obliterative endarteritis), scarring of the vessel wall and a dense surrounding rim of lymphocytes and plasma cells that may extend into the media. Characteristic of the tertiary stage of syphilis.
Syphilitic aortitis(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 359
Most common point of origin of an aortic dissection.
Ascending aorta, 10 cms from the aortic valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 360
Most frequent pre-existing histologically detectable lesion in aortic dissection, characterized by elastic tissue fragmentation and separation of the elastic and smooth muscle cell elements of the media by cystic spaces filled with amorphous proteoglycan-rich extracellular matrix.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissection involving either them ascending aorta only or both the ascending and descending aorta.
Type A dissections (proximal) Type I DeBakey - ascending aorta only Type II DeBakey - ascending and descending aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissections involving the descending aorta only, usually distal to the subclavian artery.
Type B dissection / type III DeBakey(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Granulomatous inflammation frequently involving the temporal artery, occuring in patients >50 years old, associated with polymyalgia rheumatica.
Giant cell (Temporal) arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 363
Granulomatous inflammation usually occuring in patients younger than 50 years old. Classically involves the aortic arch, with intimal hyperplasia and irregular thickening of the vessel wall. Origin of great vessels are obliterated causing weakness of peripheral pulses.
Takayasu arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
Used to distinguish between giant cell arteritis and takayasu arteritis of the aorta.
Age of patient40 Giant cell arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
In this disease, affected blood vessels develop nodular intimal thickening, granulomatous inflammation within the inner media centered on the internal elastic membrane, and fragmentation of the internal elastic lamina. Typically involves temporal and ophthalmic arteries.
Giant - cell/Temporal arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
A systemic vasculitis causing transmural necrotizing inflammation of small to medium sized vessels, with mixed infiltvrate of neutrophils, eosinophils, and mononuclear cells, frequently accompanied by fibrinoid necrosis.Typically involves renal arteries but spares pulmonary vessels.
Polyarteritis Nodosa (PAN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365
Arteritis associated with mucocutaneous lymph node syndrome, which usually occurs in children. Coronary arteries can be involved with aneurysm formation or thrombosis. Fibrinoid necrosis usually less prominent.
Kawasaki disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 366
Granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels, including cresencteric glomerulonephritis. Associated with c-ANCA.
Wegener granulomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367
A necrotizing vasculitis that generally affects capillaries, arterioles and venules, with few or no immune deposits. Necrotizing glomerulonephritis and pulmonary capillaritis are common. Associated with p-ANCA.
Microscopic polyangiitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Eosinophil-rich and granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels. Associated with asthma and blood eosinophilia. Associated with p-ANCA.
Churg-Strauss syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Characterized by sharply segmental avute and chronic vasculitis of medium sized and small arteries, predominantly of the extremities. There is acute and chronic inflammation accompanied by luminal thrombosis, containing microabscess composed of neutrophils surrounded by granulomatous inflammation. Stromg relationship with cigarette smoking.
Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Results from an exaggerated vasoconstriction of digital arteries and arterioles, inducing paroxysmal pallor or cyanosis of the digits of the hands and feet.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
Reflects an exaggeration of central and local vasomotor responses to cold or emotion. Structural changes in the arterial walls are absent except late in course when intimal thickening can appear.
Primary Raynaud phenomenon (Raynaud disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
Reflects vascular insufficiency of the extremities in the context of arterial disease caused by other entities including SLE, Buerger disease, or atherosclerosis.
Secondary Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Abnormally dilated, tortous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. Veins show wall thinning at the points of maximal dilation with smooth muscle hypertrophy and intimal fibrosis. Focal thrombosis and venous valve deformities are common.
Varicose veins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Most common blood vessels involved in development of varicose veins.
Superficial veins of the upper and lower leg(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Three sites of varices produced in the presence of portal hypertension.
GEJ (Esophageal varices)Rectum (Hemorrhoids)Periumbillical veins (Caput medusae)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Common and serious complication of of deep vein thrombosis (DVT).
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
The acute inflammation elicited when bacterial infections spread into and through the lymphatics.
Lymphangitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
These are bright red to blue lesions, that vary from a few millimeters tomseveral centimeters in diameter. Unencapsulated aggregates of closely packed, thin-walled capillaries, usually blood-filled and lined by flattened endothelium. Vessels are separated by scant connective tissue stroma.
Capillary hemangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 372
Appears as red-blue, soft, spongy masses 1-2 cm in diameter, which can affect large subcutaneous areas of the face, extremities, and othe body regions. Mass is sharply defined but not encapsulated, composed of large, cavernous, blood-filled spaces.
Cavernous hemangioma(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 372
This form of capillar hemangioma is a rapidly growing peduncular red nodule on the skin, gingival, or oral mucosa, bleeds easily and is often ulcerated.
Pyogenic granuloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
These are round, slightly elevated, red-blue firm nodules, less than 1 cm diameter that can resemble a minute focus of hemorrhage UNDER THE NAIL. Histologically, these are aggregates, nests, and masses of tumor cells intimately associated with branching vascular channels.
Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
A specialized arteriovenous structure involved in thermoregulation.
Glomus body(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
This lesion is the ordinary “birthmark” and is the most common form of ectasia. Characteristically a flat lesion on the head or neck, ranging in color from light pink to deep purple.
Nevus flammeus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
This non-neoplastic vascular lesion grossly resembles a spider. There is radial, often pulsatile array of dilated subcutaneous arteries or arterioles about a central core, that blanches when pressure is applied to its center.
Spider telangiectasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
An opportunistic infection in immunocompromised persons that manifest as vascular proliferations involving skin, bone, brain and other organs. Characterized grossly by red papules and nodules, or rounded subcutaneous masses. Histologically, there is capillary proliferation with prominent epitheloid EC’s showing nuclear atypia and mitoses. Lesions contain stromal neutrophils, nuclear dust nd purplish granular material.
Bacillary angiomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
Common in patients with AIDS, caused by HHV 8, causing skin lesions ranging from patches, plaques to nodules.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375
These are malignant endothelial neoplasms, with varying histology from plump, anaplastic but recognizable endothelial cells producing vascular channels to widely undifferentiated tumors having solid, spindle cell appearance and producing nondefinite blood vessels.
Angiosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 376
The morphologic and clinical effects of this condition primarily result from progressive damming of blood within the pulmonary circulation. The left ventricle is hypertrophied and dilated, with secondary left atrial dilation. The lungs are heavy and boggy, with perivascular and interstitial transudate, alveolar septal edema, and intra-aleolar edema. Hemosiderin-laden macrophages are present.
Left sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hemosiderin laden macrophages are also called _______
Heart failure cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
This is usually the earliest and most significant compaint of patients in Left sided HF.
Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Most common cause of right sided HF.
Left sided HF(TOPNOTCH)
This is a particularly dramatic form of breathlessness, awakening patients from sleeo with attacks of extreme dyspnea bordering on suffocation.
Paroxysmal nocturnal dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.
Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.
Cardiac cirrhosis(TOPNOTCH)
The liver is increased in size and weight, a cut section reveals congested red centers of liver lobules surrounded bybpaler, sometimes fatty peripheral regions.
Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Right-sided HF produces a tense, enlarged spleen, achieving weights of 300-500 grams. Sinusoidal dilation present.
Congestive splenomegaly(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
This is a hallmark of right sided HF.
Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
Generalized, massive edema is called ______.
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
Most congenital heart disease arise from faulty embryogenesis during what AOG?
3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
An abnormal communication between chambers of the heart or blood vessels.
Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These a typically smooth-walled defects near the foramen ovale, usually without associated cardiac abnormalities. Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy and dilation of the pulmonary artery.
Ostium secundum ASD(TOPNOTCH)
Reversal of blood flow through a prolonged (left-to-right shunt) due to pulmonary hypertension, yielding right-sided pressures that exceed those on the left side. This causes unoxygenated blood to go into circulation, causing cyanosis.
Eisenmenger syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These occur at the lowest part of the atrial septum and can extend to the mitral and tricuspid valves. Abnormalities of the AV Valves are usually present, forming a cleft in the anterior leaflet of the mitral valve or septal leaflet of the tricuspid valve.
Ostium primum ASD(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384
Incomplete closure of the ventricular septum leading to left-to-right shunting. The right ventricle is hypertrophied and often dilated. Diameter of pulmonary artery is increased because of the increased volume by the right ventricle.
Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
In this condition, some of the oxygenated blood flowing from the left ventricle is shunted back to the lungs. Proximal pumonary arteries, left atrium and ventricle can become dilated.
Patent ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
The most common cause of cyanotic congenital heart disease. Heart is large and “boot shaped” as a result of right ventricular hypertrophy.
Tetralogy of Fallot(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
Components of Tetralogy of Fallot.
Pulmonary valve stenosisOverriding of aortaRight ventricular hypertrophyVentricular septal defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa. Right ventricular hypertrophy becomes prominent, while the left ventricle becomes somewhat atrophic.
Transposition of the Great Arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
Predominant manifestation of TGA?
Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Characterized by tubular narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus. DA is usually patent and is the main source of blood to the distal aorta. RV is hypertrophied and dilated, pulmonary trunk is also dilated.
Preductal “infantile” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Aorta is sharply constricted by a ridge of tissue at or just distal to the ligamentum arteriosum. Constricted segment is made of smooth muscle and elastic fibers that are continuous with the aortic media, and lined by thickened intima. Ductus arteriosus is closed. Proximally, the aortic arch and its vessels are dilated, LV is hypertrophic.
Postductal “adult” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
There is upper extremity hypertension, due to poor perfusion of the kidneys, but weak pulses and low blood pressure in the lower extremities. Claudication and coldness of the lower extremities also present. Enlarged intercostal and internal mammary arteries due to collateral circulation, seen as rib “notching” on xray.
Postductal coarctation of the aorta (without a PDA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Atrial septal defect
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?TOF
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?VSD
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Eisenmenger syndrome
Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Transposition of great arteries
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.
Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.
Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This can result from a lethal arrythmia following myocardial ischemia.
Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?
70-75% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest?
90%(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand. Pain described as crushing or squeezing substernal sensation which can radiate to left arm. Relieved by rest or vasodilators.
Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.
Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Angina occuring at rest due to coronary artery spasm.
Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Infarct involving >= 50% of the myocardial wall thickness.
Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391
Most common blood vessel involved in myocardial infarction?
Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392
Electron microscope findings 30 minutes after an ischemic event.
Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)
An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?
12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393
Coagulation necrosis ensues how many hours after MI?
4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.
Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.
Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
This cardiac enzyme is detectable in the blood within 2-4 hrs of MI, peaks at 24-48 hrs and returns to normal within approximately 72 hrs.
CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
Myocardial rupture may occur how many days after MI?
3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This occurs within 2-3 days of a transmural infarct and typically resolves within time. It is the epicardial manifestation of the underlying myocardial inflammation.
Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.
Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.
Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
In this disease the left ventricle may exceed 2.0cm in thickness and the heartvmay weigh >500 grams. Microscopically, myocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia (“box-car nuclei”), and increased interstitial fibrosis.
Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
It is the failure of a valve to open completely, obstructing forward flow.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This results from failure of a valve to close completely, thereby allowing reversed flow.
Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
The hallmark of this disease is heaped-up calcified masses on the outflow side of the cusps, which protrude intonthe sinuses of Valsalva and mechanically impede valve opening. Cusps may become secondarily fibrosed and thickened.
Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This is characterized by ballooning or hooding of the mitral leaflets. Affected leaflets are enlarged, redundant, thick and rubbery. The tendinous cords are elongated, thinned and occasionally ruptured. Histologically, there is thinning of the fibrosa layer of the valve, accompanied by expansion of the middle spongiosa layer with increased deposition of mucoid material.
Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.
Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Pathognomonic sign for rheumatic fever,consisting of of a cental zone of degenerating, hypereosinophilic ECM infiltrated by lymphocytes, ocassional plasma cells and plump, activated macrophages.
Aschoff bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
These cells have abundant cytoplasm and central nuclei with chromatin arrayed in a slender, wavy ribbon (caterpillar cells) which can be found in all three layers of the heart in rheumatic fever. A component of Aschoff bodies.
Anitschkow cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Characterized by organization and subsequent scarring, as a sequelae of rheumatic fever. The mitral (or tricuspid) valve is involved, with leaflet thickening, commisural fission and shortening, thickening and fusiong of the chordae tendinae. Fibrous bridging across valvular commisures create “fishmouth” or “ buttonhole” deformity.
Chronic Rheumatic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Most common valve involved in RHD.
Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405
Major components Jones Criteria for RF.
CarditisMigratory polyarthritisSubcutaneous nodulesErythema marginatumSyndenham chorea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Minor components Jones criteria for RF
FeverArthralgiaElevated acute phase reactants (e.g. CRP)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
How many major and/or minor manifestations are needed to diagnose RF?
Remember: 20122 major 0 minor or1 major 2 minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis of previously normal valves, the most common causative agent is S. aureus.
Acute bacterial endocarditis(TOPNOTCH)
Serious infection characterized by microbial invasion of heart valves or mural endocardium, often with destruction of the underlying cardiac tissues. The heart valves are friable, bulky and potentially destructive.
Infective endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.
Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Most consistent sign of infective endocarditis.
Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
Characterized by deposition of sterile, non-inflammatory, nondestructive and small (1mm) masses of fibrin, platelets and other blood components on cardiac valves, along the line of closure of leaflets or cusps.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
Sterile vegetations thatvcan develop on the valves of patients with SLE. These are small, granular, pinkish vegetations 1-4mm in diameter and can be located on the undersurface of AV valves, on the cords or endocardium.
Libman-Sacks endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
The lesions of this disease are distinctive, glistening white intimal plaquelike thickenings on the endocardial surfaces of the cardiac chambers and valve leaflets seen in patients with carcinoid tumors. The lesions are composed of muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix.
Carcinoid heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
Cardiomyopathy which is characterized by progressive cardiac dilation and contractile dysfunction. The heart is characteristically enlarged and flabby, with dilation of all chambers,the ventricular thickness may be less than, equal to or greater than normal.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Alcohol intake and infection with coxsackie B virus are some of the causes of this cardiomyopathy.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Characterized by myocardial hypertrophy, abnormal diastolic filling and ventricular outflow obstruction. The heart is thick-walled, heavy and hypercontracting. There is an assymetrical septal hypertrophy described as “banana-like”. Histologically, there is severe myocyte hypertrophy and disarray with interstitial fibrosis.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
Mechanism of heart failure in hypertrophic cardiomyopathy.
Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
A common cause of sudden death in young athlethes.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
The ventricles are of approximately normal size or slightly enlarged, the cavities not dilated, and the myocardium is firm. Biatrial dilation is common. Microscopically, there is interstitial fibrosis, varying from minimal to patchy to extensive and diffuse.
Restrictive cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Mechanism of heart failure in restrictive cardiomyopathy.
Diastolic dysfunction or impaired compliance(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Inflammation of the myocardium.
Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.
Lymphocytic myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils.
Hypersensitivity myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis characterized by widespread inflammatory infoltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis.
Giant-cell myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis distinctive by virtue of parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages and occasional eosinophils.
Chagas myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Viruses which account for most cases of myocarditis.
Coxsackie A and B(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Type of pericarditis found in patients with uremia or viral infection. The exudate imparts an irregular apperance to the pericardial surface (bread and butter pericarditis).
Fibrinous pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Bacterial pericarditis manifests with this type of exudate.
Fibrinopurulent (suppurative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.
Constrictive pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Normal amount of pericardial fluid in pericardial sac.
30 - 50 mL of thin, straw-colored fluid(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Serous pericardial effusion can be caused by _________
CHF, hypoalbuminemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Chylous pericardial fluid can be caused by _______
Mediastinal lymphatic obstruction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Rapidly developing collections of fluid within the pericardial sac can restrict diastolic cardiac filling producing this fatal sequelae.
Cardiac tamponade(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
The most common tumor of the heart.
Metastatic tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Most common primary tumor of the adult heart.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
The most frequent primary tumor of the heart in infants and children. These are generally small gray-white myocardial masses composed of a mixed population of cells, the most characteristic of which are large, rounded or polygonal cells containing numerous glycogen-laden vacuoles separated by strands of cytoplasm, so-called spider cells.
Rhabdomyomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
Serosanguinous pericardial effusion can be caused by ________
Blunt chest trauma, malignancy, ruptured MI, aortic dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
Average volume per cell, expressed in femtoliters.
Mean cell volume (MCV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
A reduction in the oxygen-transporting capacity of blood.
Anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 422
The average content of hemoglobin per red cell, expressed in picograms.
Mean cell hemoglobin (MCH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
The average concentration of hemoglobin in a given volume of packed red cells, expressed in g/dL.
Mean cell hemoglobin concentration (MCHC)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
The coefficient of variation of red cell volume.
Red cell distribution width (RDW)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
Anemia of acute blood loss is described as ______.
Normocytic, normochromic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
Life span of a normal red cell.
120 days(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Anemia characterized by an increased rate of cell destruction, a compensatory increase in erythropoeisis that results in reticulocytosis, and retention of products of cell destruction, including iron.
Hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
A circulating protein that binds and clears free hemoglobin.
Haptoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Hemolysis that can result from mechanical trauma, or biochemical or physical agents that damage the red cell membrane.
Intravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Hemolysis which takes place largely within phagocytic cells of the spleen and liver.
Extravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
This disorder is characterized by an intrinsic defect in the red cell membrane, that renders the cells spheroidal, less defomable and vulnerable to splenic sequestration and destruction.
Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Small, dark nuclear remnants seen within red cells in PBS of hereditary spherocytosis.
Howell-Jolly bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
On PBS, red cells are spherical which lack central pallor, and they show increased osmotic fragility when placed in hypotonic salt solutions.
Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
Structural proteins that are defective in hereditary spherocytosis.
Spectrin and ankyrin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
This results from substitution of valine for glutamic acid at the 6th position of the B-chain, producing HbS.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 426
Bizarre, elongated, spindled or boat-shaped cells on PBS.
Sickel cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427
Prominent cheekbones and changes in skull resembling a “crew-cut” skull x-ray.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427
Patients with sickle cell disease are predisposed to infections caused by these type of bacteria.
Encapsulated bacteria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Treatment for sickle cell disease by increasing levels of HbF.
Hydroxyurea(TOPNOTCH)
Treatment for sickle cell disease by increasing levels of HbF.
Hydroxyurea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Feared complication of sickle cell disease which can be trigerred by pulmonary infections or fat emboli from necrotic marrow that secondarily involve the lung.
Acute chest syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Major complication of sickle cell disease which occurs in the setting of acute chest syndrome, causing ischemic injury to the CNS.
CNS stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Represents a sudden but usually temporary cessation of erythropoeisis, usually trigerred by parvovirus B19 infections in patients with sickle cell disease.
Aplastic crises(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
In beta thalassemia, an individual who inherits one abnormal allele (out of 2) has this asymptomatic to mildly symptomatic condition.
B- Thalassemia minor/trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
Individuals with B-thalassemia who inherit two abnormal alleles, with severe anemia requiring regular blood tranfusions.
B- Thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
Red cells with a central, dark-red puddle due to collection of hemoglobin.
Target cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
Target cells are often seen in this condition.
B-thalassemia minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
In the PBS of this condition, nucleated red cells (normoblasts) are seen, which reflect underlying erythropoeisis.
B-thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
Anemia of beta thalassemia.
Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
Disease caused by deletion of 3 alpha globin genes.
Hemoglobin H disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
Condition caused by deletion of 1 alpha globin gene.
Silent carrier(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
Condition caused by deletion of 2 alpha globin genes.
Alpha thalassemia trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
Condition caused by deletion of all four alpha globin genes.
Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
Precipitates of denatured globin seen in RBC’s.
Heinz bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
