Patho Flashcards
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
