Term
|
Definition
Pain
•PGD2
•Bradykinin
Vasodilation &
increase permeability
•Histamine
•Serotonin
•PGE2, F2
•C3a, C5a
•Bradykinin |
|
|
Term
|
Definition
Pain
•PGD2
•Bradykinin
Vasodilation &
increase permeability
•Histamine
•Serotonin
•PGE2, F2
•C3a, C5a
•Bradykinin |
|
|
Term
|
Definition
Vasodilation &
increase permeability
•Histamine
•Serotonin
•PGE2, F2
•C3a, C5a
•Bradykinin |
|
|
Term
|
Definition
Vasodilation &
increase permeability
•Histamine
•Serotonin
•PGE2, F2
•C3a, C5a
•Bradykinin
Leukocyte
adhesion
•C5a
•LTB4
Leukocyte
chemotaxis
•C5a
•C567
•LTB4
Opsinize
C3b |
|
|
Term
|
Definition
Leukocyte
chemotaxis
•C5a
•C567
•LTB4
Leukocyte
adhesion
•C5a
•LTB4 |
|
|
Term
|
Definition
series of plasma proteins with proteolytic activity
-Activated by contact with bacterial surface or by antibody bound to an antigen (immune complexes)
-Sequentially activate successive members of the cascade, yielding activated components |
|
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Term
|
Definition
| (anaphylatoxins) are the primary permeability-increasing components and act on mast cell/basophil degranualtion to produce vasoactive amines, proteases and chemotactic factors for neutrophils & eosinophils |
|
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Term
|
Definition
| is a powerful chemotactic to neutrophils and monocytes |
|
|
Term
|
Definition
| act as opsonin that recognizes neutrophil, macrophage and eosinophil receptors |
|
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Term
|
Definition
•Complement proteins are present in circulation and can be activated by a variety of mechanisms
•Complement cascade can generate active compounds such as C3b that functions as an opsonin, or C5a that attracts neutrophils
•C5-9 complex ("membrane attack complex")is generated, the cell to which the complex is attached can be lysed by perforation of its cell membrane
•Bacterial products can set off the "alternate pathway" as shown in the schema |
|
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Term
|
Definition
| is generated, the cell to which the complex is attached can be lysed by perforation of its cell membrane |
|
|
Term
| Complement activation, classic pathway |
|
Definition
•Attached immunoglobulins can set off the "classic pathway" as shown
•Complement cascade can generate C3b that functions as an opsonin, or C5a that attracts neutrophils
•C5-9 complex "membrane attack complex" enables the cell membrane be lysed by perforation |
|
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Term
|
Definition
•Synthesis of adhesion molecules on the vascular endothelium is stimulated by interleukin 1 and endotoxin
•Adhesion molecules on both leukocytes and the endothelium are stimulated by tumor necrosis factor
•Corticosteroids interfere with the adhesion molecules, which leads to an absolute neutrophilic leukocytosis (an increased total neutrophil count in the peripheral blood) and less chance for the leukocytes to emigrate into the area of injury (one reason why corticosteroids are anti-inflammatory) |
|
|
Term
| Inhibited by corticosteroids |
|
Definition
|
|
Term
| Inhibited by asprins and NSAIDS |
|
Definition
|
|
Term
| Acute Inflammation Mediators |
|
Definition
•Corticosteroids block both leukotriene and prostaglandin synthesis, while aspirin and nonsteroidals (NSAIDs) only block prostaglandins; this underscores powerful effect of steroidal anti-inflammatory agents
•At the standard dose of aspirin, platelet thromboxane A2 (TXA2) formation is inhibited, but the synthesis of prostacyclin (PGI2) continues in the endothelium
•LTC4, LTD4, and LTE4 constrict the bronchi as in bronchial asthma, constricts and increase vessel permeability
•Aspirin blocks prostaglandin synthesis, thus leaving the leukotriene pathway available for powerful vaso-& bronchoconstrictors |
|
|
Term
| Activated Hageman's factor XII |
|
Definition
| interacts with the coagulation, fibrinolytic, and kinin cascade systems and activates the intrinsic clotting system to produce a fibrin clot, the kinin system to produce bradykinin and the fibrinolytic system to produce plasmin |
|
|
Term
|
Definition
(a) Cyclooxygenase pathway: Thromboxane A2 induces platelet aggregation and vasoconstriction
•Prostacyclin (PGI2) produces vasodilation and inhibition of platelet aggregation
•Prostaglandins I9, PGE1,PGE2, and PGD2act as vasodilators and increase the chance of edema
•Prostaglandin E, may be responsible for some of the pain and fever seen in inflammation |
|
|
Term
|
Definition
•Leukotrienes C4, D4, E4increase vascular permeability (1000X more powerful than histamine), produce vasoconstriction and bronchospasm
•Leukotriene B4is a potent chemotactic agent for leukocytes and promotes adhesion of leucocytes to endothelium |
|
|
Term
|
Definition
•Polypeptide released by lymphocytes (lymphokines) and monocytes (monokines)
•IL-1 and tumor necrosis factor (TNF) are primarily secreted by macrophages and have an important role in both acute and chronic inflammation
•IL-8 produced by activated macrophages, acts as a powerful chemotactic agent and activator of neutrophils
•Enhance endothelial surface adhesion molecules and increase prostacyclin and PAF (Platelet Activating Factor)
•In acute phase, cytokines are associated with fever, release of leucocytes, septic shock (TNF may mediate endotoxicity) |
|
|
Term
|
Definition
•Stimulate bone marrow release of postmitotic neutrophil pool (metamyelocytes, bands, and neutrophils), producing an absolute neutrophilic leukocytosis and increase of band neutrophils and less mature cells "left shift“ infection
•Reduce the serum concentration of zinc and iron, enhancing bacterial reproduction
•Stimulate an increase in serum copper, a cofactor in enzymes that inactivate free radicals; copper also involved in hemoglobin synthesis
•Stimulate prostaglandin synthesis in the hypothalamus, which-in turn-stimulates the vasomotor center to increase sympathetic activation of peripheral vessels in the skin, thus reducing heat loss and producing fever |
|
|
Term
|
Definition
| catalase-positive, so endogenously-derived peroxide generated during its metabolism is quickly destroyed by its own catalase, thus evading destruction within the phagolysosome |
|
|
Term
|
Definition
| are catalase-negative, so they generate peroxide to form HOCI, and thus the organisms are destroyed |
|
|
Term
|
Definition
•Stimulate acute phase-reactant (APR) synthesis by the liver
•APRs include such proteins as lactoferrin, fibrinogen, coagulation factors, C-reactive protein, and SSA protein
•In order to have sufficient amino acids to generate APRs, the synthesis of binding proteins such as transferrin and albumin are decreased, and there is an increased catabolism of muscle tissue as well |
|
|
Term
|
Definition
•Dissolution of the basement enables the RBCs, basophils, and eosinophils to follow passively (diapedesis) through the defect out into the interstitial space
•Leukocytes possess microtubules and contractile microfilaments (actin and myosin) that enable them to move through the tissue
•Chediak Higashi syndrome is an autosomal recessive disease with a primary defect in the polymerization of microtubules in leukocytes, which interferes with their emigration through tissue in response to the chemotactic agents. Leukocytes contain giant lysosomes that are unable to release lysosomal enzymes into the phagosomes, thus impairing bactericidal function as well |
|
|
Term
|
Definition
•Associated with Nasopharyngeal carcinoma and Burkitt’slymphoma
-EBV infects B-Lymphocytes
-common in childhood and occurs in regions where malaria is endemic
-EBV is found in all Burkitt'sLymphoma's in Africa, and about 20% in USA
-Can be caused by a translocation
-EBV is found in about 50% of Hodgkin’s Disease
•Infectious Mononucleosis is caused by an acute EBV infection |
|
|
Term
|
Definition
•Both beingnand malignant tumors are composed of parenchyma consisting of prolifeartingcells and supporting stroma made up of connective tissue, blood vessels and sometimes lymphatics
•Parenchymal component determines its behavior and frequently the name of the tumor |
|
|
Term
|
Definition
•Usually encapsulated; exceptions: leiomyomasof the uterus; dermatofibroma
•Remain localized and do not penetrate adjacent tissue borders nor they do spread to distant sites
•Well differentiated than malignant tumors and resemble tissue of origin
•Exhibit normal mitotic spindles (not tetraploid)
•Composed of parenchymal cells that closely resemble the tissue of origin and frequently classified, with some exceptions, by adding the suffix-omato the cell type, e.g. lipoma |
|
|
Term
|
Definition
•Most frequent target sites are liver and lung
•Favored by sarcomas (not exclusively) with spread to the lungs and liver as a common finding
•Carcinomas with a propensity for hematogenousinvasion:
-Renal adenocarcinomasinvading the renal vein
-Hepatocellularcarcinomas invading the hepatic and portal veins
-Follicular carcinomas of the thyroid, which commonly bypass the cervical lymph nodes and metastasize to the lungs and bone |
|
|
Term
|
Definition
| A benign tumor that arises from germ cells and contain derivatives of different germ layers is labeled a teratoma |
|
|
Term
|
Definition
Teratomamay contain variety of structures, such as skin, neurons, and glial cells, thyroid, intestinal epithelium, and cartilage
-mesodermal---> cartilage, bone, etc.
-An ovarian cystic teratomafrequently demonstrates teeth and bone on x-ray
Teratomasare also germ cell tumors |
|
|
Term
|
Definition
Mixed tumors have two different morphologic patterns that are derived from the same germ layer
•Mixed tumor of the parotid gland is the most common overall salivary gland tumor
•Mixed tumors have two different morphologic patterns that are derived from the same germ layer |
|
|
Term
|
Definition
•Hamartomarefers to localized disordered differentiation during embryonic development
-not a true neoplasm that contain cartilages, ducts, connective tissue, blood vessels and lymphoid tissue
-An overgrowth of tissue that is normally present in the organ (e.g. a bronchial hamartomaof the lung composed of mature cartilage) |
|
|
Term
|
Definition
| •Choristomasare not true tumors that represent normal tissue in a foreign location (e.g. benign pancreatic tissue in the wall of the stomach) |
|
|
Term
|
Definition
•The guardian of the genome
•Located on chromosome 17
•Prevents a mutated cell from proliferating
•Induced in response to DNA damage
•Inhibits the cell from entering S-Phase, and ultimately making it undergo apoptosis
•Binds cyclin-dependent kinasesinduce cyclin-inhibitor WAF inhibit cyclinprevent cell division
•P53 mutations are the most common genetic defect found in cancers |
|
|
Term
|
Definition
•Systemic effects of cancers in the host that are not due primarily to tumor or its metastases
•FEVER: especially with Hodgkin's, Renal cell carcinomas, osteogenicsarcomas
•Anorexia and weight loss
•Endocrine syndromes
-Inappropriate antidiuresis
•Hypercalcemia-About ten percent of all patients. Usually attributed to secreted of a PTH-like peptide by an epithelial tumor |
|
|
Term
|
Definition
| About ten percent of all patients. Usually attributed to secreted of a PTH-like peptide by an epithelial tumor |
|
|
Term
|
Definition
•Anemia: Frequently cause is not understood, and sometimes from tumor bleeding
•Thrombocytosisoccurs in about one third of patients and the cause is unknown |
|
|
Term
|
Definition
| •Venous thrombosis is often found in mucin-secreting cancers (mucin in the cancerous cells displaces the nucleus to the periphery and gives the appearance of signet ring cells (e.g. pancreatic cancers) |
|
|
Term
| Ectopic Hormone Production |
|
Definition
the inappropriate secretion of hormones from a tumor, which can occur in any tumor regardless of its origin
-Cushing‘s syndrome can result from ectopic production of cortisol
-Gonadotropic Syndrome
-Hypoglycemia
•Neurologic Syndromes
-Spinal cord
-Peripheral
•Skeletal |
|
|
Term
|
Definition
| can result from ectopic production of cortisol |
|
|
Term
|
Definition
•Apoptosis is an orderly process of individual cell death
•Genetically determined programmed cell death involving, e.g. the turning off BCL-2 genes and turning on Bax genes)
•Enables surplus cells to be eliminated via Intracellular proteolytic enzymes called caspases
•Occurs as a physiologic and pathologic process |
|
|
Term
|
Definition
occurs as a result of
-Developmental morphogenesis ( implantation, organogenesis and developmental involution)
-Hormone-dependent involution (menstrual cycle, menopause & cessation of breast feeding)
-Deletion of a portion of proliferating cells (intestinal crypt epithelia)
-Selective death of immunocytes (T lymphocytes in thymus and B lymphocytes in lymph nodes) |
|
|
Term
|
Definition
occurs subsequent to
-Environmental hazards (radiation & viral infection)
-Cancers (neoplastic cells undergo apoptosisslows growth of malignant tumors)
-Viral diseases-associated with councilman bodies in viral hepatitis
-Pathologic atrophy-prostatic atrophy after castration
-Ductal obstruction-pancreas and parotid gland
-Immune rejection mediated cell death by cytotoxic lymphocytes
-Anticancer drugs, mild thermal injury and radiation |
|
|
Term
| Characteristics of Apoptosis |
|
Definition
•Shrinkage & detachment of the affected cell from their neighborsengulfment by macrophages
•Chromatin condensation-most common
•Formation of apoptotic bodies-condensed organelles with cytoplasm with or without nuclear fragments
•Phagocytosis of apoptotic bodies by intact parenchymal cells or macrophages
•Electron micrographic changes, such as nuclear condensation and fragmentation, segregation of cytoplasmic organelles, formation of membrane blebs & fragmentation of dead cells
•No inflammatory response occurs in apoptosis |
|
|
Term
|
Definition
•Shrinkage in the size of the cell by loss of structural components associated with the formation of autophagic vacuoles
•A response to injury by "downsizing" to conserve the cell
Etiologies
-Decreased work load e.g., hospitalization
-Lower motor neuron palsy
-Ischemia (e.g., atherosclerosis)
-Inadequate nutrition (e.g., protein-caloric deficiencies)
-Loss of hormonal stimulation (e.g., menopause)
-Aging |
|
|
Term
|
Definition
| In this image with trichrome stain, some of these skeletal muscle fibers show atrophy, compared to normal fibers |
|
|
Term
|
Definition
| The right image shows an atrophied testis and is much smaller than the normal testis to the left. |
|
|
Term
|
Definition
| Here is the centrilobular portion of liver adjacent to a central vein. The cells have reduced in size or been lost from hypoxia. The pale brown-yellow pigment is lipochrome that has accumulated as the atrophic and dying cells undergo autophagocytosis |
|
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Term
|
Definition
•Refers to the combined changes seen in coagulative and liquefactive necrosis
•Usually occurs when the tissue loses its blood supply and the necrotic tissue initially undergoes coagulative necrosis becomes secondarily infected with bacteria leading to liquefactive action of the bacteria and proteolytic enzymes released by leukocytes. Gastrointestinal tract, gallbladder and testis. May also be affected
•Wet gangrene -liquefactive process is the dominant pattern. |
|
|
Term
|
Definition
•Occurs as a result of inflammation, e.g. acute pancreatitis where enzymatic fat necrosis ensues and also in response to trauma (traumatic fat necrosis)
•Necrosis appears as an irregular, chalky-white area embedded in otherwise normal adipose tissue |
|
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Term
|
Definition
| liquefactive process is the dominant pattern |
|
|
Term
|
Definition
| Alcoholic hyaline in liver cells; aggregates of prekeartin intermediate filament |
|
|
Term
|
Definition
-Occurs in the walls of blood vessels especially in the kidney in long standing hypertension
-Forms homogeneous eosinophilic inclusions (Russell bodies) in plasma cells
-beta protein (coded by chromosome 21) Alzheimer's disease; also seen in Down's syndrome
Calcitoninmedullary carcinoma of the thyroid |
|
|
Term
|
Definition
| •Abnormal calcification is subdivided into dystrophic and metastatic calcification |
|
|
Term
|
Definition
•Refers to the calcification of previously damaged tissue due to extracellular/and or intracellular deposition of calcium in non viable or dying tissue
•Serum calcium and phosphorous remains normal |
|
|
Term
|
Definition
•Visible as sandy grains or rock-hard material in tuberculous caseous necrosis, mitral or aortic valve calcification associated with rheumatic fever, calcific mitral stenosis, calcified atherosclerotic plaques, periventricular calcification in congenital cytomegalovirus infections & calcified granulomas (histoplasmosis)
•Pineal gland shows calcium concretions in old age
•Psammoma bodies, formed by calcified lamellated concretions, are formed by papillary carcinoma of the thyroid and ovary, and also in meningioma |
|
|
Term
|
Definition
•This is a dystrophic calcification in the wall of the stomach
•Note an artery with calcification at the far left
•Note also irregular bluish-purple deposits of calcium in the submucosa
•Calcium is more likely to be deposited in tissues that are damaged. |
|
|
Term
|
Definition
•Hemoglobin-derived, iron-containing golden-yellow granular pigment that contains aggregates of ferritin micelles (storage form of iron)
•Considered as a byproduct of hemolysis (breakdown of RBC's) and release of the iron in heme
•Contained in small amount in fixed macrophages in the bone marrow and Kupffer cells, as part of iron recycling
•Prussian blue stain is used to identify hemosiderin in tissue
•Seen in common bruises
•Hemosiderin that resides in alveolar macrophages in chronic lung congestion are called "heart failure" cells; responsible for rusty colored sputum
•Hemosiderin shows up by the Prussian Blue Reaction, indicating the presence of iron inside granules |
|
|
Term
|
Definition
-a reduction in the amount of oxygen with reduced production of ATP secondary to Ischemia
--common cause: atherosclerosis, compression of vessels, heart failure (low cardiac output)
hypoxemia-a reduced amount of oxygen dissolved in blood
-occurs as a result of respiratory acidosis with retention of CO2
-PE (perfusion disorders) or interstitial fibrosis (diffusion disorders)
-hemoglobin (Hgb) disorders and loss of oxygen carrying capacity: anemia (reduction of Hgb concentration and RBC count), methoglobinemia (Hgb in the ferric (+3) state increased by oxidizing agents nitrites (well water, nitroprusside, nitroglycerine ) and sulfa drugs |
|
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Term
|
Definition
-CO poisoning (CO has much larger affinity to oxygen than Hgb), also blocks cytochrome oxidase in the electron transfer chain and decrease ATP
-Defective oxidative phosphorylation that reduces ATP as a result of uncoupling agents that damage the mitochondrial membrane and funnels off proton away that normally produces ATP, such as alcohol, aspirin in large doses, malignant hyperthermia predisposed by anesthetics , such as ether, methoxyflurane, halothane |
|
|
Term
|
Definition
•a component of the mitochondrial electron transport chain
•produced in the cytosol and mitochondria by enzymes such as, xanthine oxidase, and cytochrome P450Catabolized by superoxide dismutase |
|
|
Term
|
Definition
(H2O2(two electrons)
•reduced to water by catalase within the peroxisomes and glutathione peroxidase in cytosol and mitochondria |
|
|
Term
|
Definition
•Formed by the radiolysis of water (electromagnetic radiation) or by hydrogen peroxide reaction with ferrous iron (Fenton reaction)
•Produces cellular injury via Lipid peroxidation:
-Hydroxyl radical removes a hydrogen atom from the unsaturated fatty acids of the membrane phospholipids and produces a free lipid radical |
|
|
Term
| Etiology of Cellular Injury |
|
Definition
-Lipid radical reacts with molecular oxygen and forms a lipid peroxide radical that removes another hydrogen from a second unsaturated fatty acid and the chain reaction continues
-Loss of cell membrane integrity results from destruction of the unsaturated fatty acids of the membrane phospholipids (lipid peroxidation)
-Antioxidants, such as Vitamin E inhibits peroxidation and thus protect cell membrane
•Hydroxyl radicals can interact with DNA and inhibit replication of proliferating cells (excluding hepatocytes & neurons) and initiate apoptosis and cell death
•Hydroxyl radical can also cause cellular injury by causing cross-linking of cell membrane proteins through disulfide bond formation |
|
|
Term
|
Definition
1. Cytotoxic T cells display fas ligand binds & activates the fas receptor on the target cells 1) activation of endonuclease DNA fragmentation and chromatin condensation, (2) activation of caspases (cytoplasmic enzymes) proteolysis (protease cytoskeleton disruption and cell shrinkage) and , (3) generation of ceramides that damage the mitochondria
•Apoptosis is promoted by P53 (tumor suppressor gene) and Bax |
|
|
Term
| Free radicals are neutralized by cellular action which include |
|
Definition
•Superoxide undergoes a dismutation reaction with superoxide dismutase (SOD) peroxide (H202) and 02
•Peroxide is reduced to water by catalase and glutathione peroxidase via glutathione (generated in the hexose monophosphate shunt catalyzed by glucose 6 phosphate dehydrogenase)
•Antioxidants like vitamin E--> neutralize oxidized LDL, which is more atherogenic than native LDL |
|
|
Term
|
Definition
•Increase in the number of cells in an organ or tissue classified into physiologic and compensatory hyperplasia
•Physiologic (Hormonal) hyperplasia is seen in glandular epithelium of the female breast at puberty and uterine endometrium during pregnancy
•Compensatory hyperplasia -regeneration of an organ or tissue subsequent to partial hepatectomy
•Pathologic hyperplasia is due to excessive hormonal stimulation or the effects of growth factors on target cells as seen in the endometrium of a post-menopausal woman or subsequent to viral infections (e.g. papillomaviruses -condyloma) |
|
|
Term
|
Definition
| This is an example of prostatic hyperplasia. The normal adult male prostate is about 3 to 4 cm in diameter. The number of prostatic glands, as well as the stroma, has increased in this enlarged prostate seen in cross section. The pattern of increase here is not uniform, but nodular. This increase is in response to hormonal manipulation, but in this case is not a normal physiologic process |
|
|
Term
|
Definition
| Here is one of the nodules of hyperplastic prostate, with many glands along with some intervening stroma. The cells making up the glands are normal in appearance, but there are just too many of them. |
|
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Term
|
Definition
•Direct Acting Carcinogens
-Not metabolized in the liver
-generally electrophilicand thus attracted to the negatively charged substituentsin the nucleus
•Nitrogen Mustard: A chemotherapeutic agent that is ironically also carcinogenic
•Benzyl Chloride
•Nitrosylmethylurea |
|
|
Term
| Promotion of Chemical Carcinogenesis |
|
Definition
•is slow, reversible in the early stages -is non-additive and causes the initiated cells to replicate (growth promoter---> estrogen), so the mutational event can be passed on to future generations of cells
•repeated mitoses predispose to additional mutations, which ultimately transforms the cell
•most carcinogens are complete carcinogens meaning that they both initiate and promote a cell (e.g. asbestos is both an initiator and promoter) |
|
|
Term
| Initiation of Chemical carcinogenesis |
|
Definition
•Initiates (mutagenic) and promotes (proliferation)
•initiation is the first step in the transformation of a cell, where the proto-oncogene becomes activated into a c-onc(e.g. rasoncogenehas a point mutation and becomes c-ras)
•Initiation is rapid, prefers rapidly dividing cells, has memory, & produces a permanent mutational change in the cell’s DNA
e.g. vinyl chloride -angiosarcomaof the liver |
|
|
Term
|
Definition
(Papovavirusfamily) -benign squamous papillomasprogressing to squamous cell carcinoma. exv)
DNA oncogenicviruses |
|
|
Term
|
Definition
(Herpes family) -Burkitt'slymphoma and undifferentiated nasopharyngeal carcinoma
DNA oncogenicviruses |
|
|
Term
|
Definition
(Hepadenovirusfamily) -hepatocellularcarcinoma
DNA oncogenicviruses |
|
|
Term
|
Definition
associated herpesvirus(HHV8)
DNA oncogenicviruses |
|
|
Term
| Acute Transforming Viruses |
|
Definition
Rous sarcoma virus
RNA oncogenicviruses |
|
|
Term
| Slow Transforming Retroviruses |
|
Definition
chronic leukemia virus
RNA oncogenicviruses |
|
|
Term
| Human T-cell Leukemia Virus |
|
Definition
(HTLV-1) -adult T-cell leukemia/lymphoma
RNA oncogenicviruses |
|
|
Term
|
Definition
•A chronic, systemic infection that begins with a characteristic skin lesion and later manifests as cardiac, neurologic, or joint disturbances
•Lyme disease occurs in three distinctive stages |
|
|
Term
|
Definition
•Exhibits distinctive skin lesion, erythema chronicummigrans, which appears at the site of the tick bite
•Erythema chronicummigransis accompanied by fever, fatigue, headache, arthralgias, and regional lymphadenopathy
•Skin lesion begins as an erythematous maculeor papule, and then grows into erythematous patch 5 to 50 cm in diameter
•Treatment with tetracycline or erythromycin is effective in eliminating early Lyme disease |
|
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Term
|
Definition
| •Begins within several weeks to months of the skin lesion and is characterized by migratory musculoskeletal pains as well as cardiac and neurologic abnormalities |
|
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Term
|
Definition
•Begins months to years after the tick bite and is manifested by joint, skin, and neurologic abnormalities
•Joint abnormalities develop in more than half of infected persons and include severe arthritis of the large joints, especially the knee |
|
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Term
|
Definition
•Partial double-stranded, partial single-stranded DNA virus
•Associated with hepatocellularcarcinoma, particularly in Asia and Africa and the level of risk is synergistic with the carcinogenic effects of Aflatoxin-B1
•Hepatitis Virus codes for proteins that block Tumor Suppressor proteins |
|
|
Term
|
Definition
a protein encoded by HBV that blocks activation of P53
•Hepatitis-C Virusis also associated with increased hepatomarisk |
|
|
Term
| Human T-cell Leukemia Virus I and II (HTLV-I and II) |
|
Definition
-Only known oncogenicRetrovirus
-Associated with rare T-Cell Leukemiasin Japan and Carribean |
|
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Term
|
Definition
•Skip metastases not following the usual lymphatic drainage are seen with testicular tumors (seminoma), which commonly go to the paraaorticnodes first (follow the same route the testicles used in descending into the scrotum)
•Stomach cancers, which often involve Virchow's node in the left supraclavicular chain
•Cervical cancer, which can also spread to the left supraclavicular nodes |
|
|
Term
| Body’s defense against micro-organisms revolves around two interrelated systems |
|
Definition
•Natural (innate) immunity-non-specific and is mediated by cellular elements of inflammatory process; unaffected by previous exposure
•Acquired (adaptive) immunity-specific and requires previous sensitization |
|
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Term
|
Definition
-primary elements able to recognize and react with specific antigen
-originate from yolk sac stem cells and become either T cells (thymus-derived) or B cells (bone-marrow-derived), and null cells which include natural killer cells |
|
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Term
|
Definition
| formed by the sequential expression of genes on the stem cell precursors of lymphocytes after interacting with thymic epithelium-express specific surface markers, and cluster designation (CD) or differentiation numbers that distinguish between lymphocyte subsets-consist of cortical (early & late T cells) and medullary T cells -Both T-and B-lymphocytes re-circulate throughout the body and are activated in secondary lymphoid tissues, such as lymph nodes |
|
|
Term
| innate (rapid) immuneresponse |
|
Definition
| •Monocytes, macrophages, neutrophils and NK (natural killer) cells are the principal players in the |
|
|
Term
| adaptive (acquired) immune response |
|
Definition
•Lymphocytes (B cells and T cells) and their progenitors are the principal players in the adaptive (acquired) immune response which is slow
•Dendritic cells and macrophages link the innate (natural) with the adaptive (acquired) immune response |
|
|
Term
|
Definition
adds focus (specificity) and
power (clonal expansion, memory) to the
innate immune response
Unlike the innate immune system, the
adaptive immune system
1. Slower but more variable in scope
2. Exhibits numerous, highly selective
specificities
3. Improves during the response
4. Produces immunologic memory
Therefore, the adaptive immune system
is said to provide “acquired immunity” or
“protective immunity.” |
|
|
Term
| Systemic Lupus Erythematosis (SLE) |
|
Definition
| • Congenital deficiency of C2 and C4 complement promotes SLE development•• 10 females for every male affected--estrogen seems to accelerate SLE• Most common in child-bearing years; children and elderly adults only occasionally affected • Familial predisposition is evident, linked to certain HLA types, especially DR2 and DR3. |
|
|
Term
| Autoantibodies in Systemic Lupus |
|
Definition
• B lymphocytes are hyperactive and generate multiple autoantibodies in SLE
•Autoantibodies are unique enough to be useful for making a diagnosis |
|
|
Term
| Diagnostically important antibodies in Systemic Lupus |
|
Definition
• ANA (AntiNuclear Antibodies): Present in more than 95% of SLE patients • Anti-native DNA (anti-double stranded DNA) • Anti-Sm (Anti-Smith) • Other common autoantibodies in SLE: anti-rbc, anti-lymphocyte, antiphospholipid (anticardiolipin), etc
•Each autoantibodies adds additional signs and symptoms to the joint and connective tissue |
|
|
Term
| Lupus Erythematosus Therapy |
|
Definition
•Change behavior to reduce stress, and avoid sun
•Immunosuppressives as necessary to control renal, cutaneous, and other symptoms
•Corticosteroids
•Cytoxan
•6-mercaptopurine All have long and short-term side effects Five year survival is now ~ 80%.
•Imunosuppressive toxicity (BM aplasia, secondary neoplasms, infectious diseases) can cause death
•Renal failure
•Others are less common |
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Definition
• A lupus like syndrome caused by drugs which induce ANA formation
• (e.g. Procainamide, hydralazine, isoniazid, Penicillamine)
• Typically patients do not exhibit CNS or renal manifestations, unlike normal lupus
• Anti-DS-DNA antibody negative
• Anti-histone antibody positive
• Patients with HLA-DR4 are more susceptible follow hydralazine administration
• Symptoms subside with cessation of medication |
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Definition
| X-Linked Agamma-globulinemia [due to defective BTK =Bruton’s tyrosine kinase] |
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| X-linked hyper-IgM syndrome |
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Definition
| [due to CD40L deficiency on T cells] |
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Term
| Autoimmune (Hashimoto's) thyroiditis |
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Definition
Organ Specific Diseases Autoimmune (Hashimoto's) thyroiditis
•Immunopathologic mechanisms -Type II cytotoxicity and possibly Type IV cell-mediated cytotoxicity involved
•Autoantibodies to thyroid antigens (mainly thyroid peroxidase) are present in ~ 95% of patients
•Hypothyroidism develops slowly
•Patients will eventually require thyroid hormone
•Affects adult females (10-20X more common than males). Swollen neck due to variable enlargement of the thyroid gland
•Patient may be euthyroid, hyperthyroid or hypothyroid at different stages of disease
•Thyroid gland is infiltrated by both B and T lymphocytes; and slowly becomes hypotrophic as glandular epithelium is destroyed and replaced by fibrous tissue |
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Definition
| Express WeibelPalade bodies |
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Term
| Small cell carcinoma of the lung, neuroblastomasand carcinoid tumors |
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Definition
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Term
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Definition
| thick and thin myofilaments |
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Term
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Definition
| (malignant histiocytictumor) Birbeckgranules in Langerhan'scells (histiocytes) |
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Definition
-Cytokeratinseparates a carcinoma (positive) from a malignant lymphoma (negative) and a mesothelioma(positive) from an adenocarcinoma (negative)
-S 100 protein positive in malignant melanoma and neuroblastomas
-Factor VIII related antigen positive in vascular tumors
-Lineage-associated markers, such as prostate-specific antigen (PSA), carcino-embryonic antigen (CEA) in colon cancers
-Chromogranins, a family of proteins found in neurosecretory granules of neuroendocrine tumor
-Carcinoembryonic antigen (CEA) negative in mesothelioma and positive in adenocarcinoma
-Desminpositive in muscle sarcomas
•Southern blot assays involve the extraction of DNA from cells
•Northern blot assays involve the extraction of RNA from cells |
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Term
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Definition
•Human papillomaviruses (HPVs) are DNA viruses, which are members of the papovavirusgroup
•Cause proliferative lesions of the squamous epithelium
•Produce common warts, flat and plantar warts, anogenitalwarts (condyloma acuminatum), and laryngeal papillomatosis
•Infection with HPVs also contributes to the development of squamous cell dysplasiasand squamous cell carcinomas of the genital tract |
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Term
| Delayed and Granulomatous hypersensitivity |
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Definition
Delayed and Granulomatous hypersensitivity have a long time course
• Delayed hypersensitivity: Local erythema and induration appear after 8-12 hours. Reaction peaks after 2-7 days and slowly subsides.
• Granulomatous: Require weeks to months to develop and may resolve slowly or persist indefinitely.
• Rejection in Transplantation is Similar to TYPE IV reactions. (But, technically grafts are not self) |
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Term
| Pertussis(whooping cough) |
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Definition
•A prolonged upper respiratory tract infection characterized by debilitating coughing paroxysms followed by a long, high-pitched inspiration—the "whoop“
•Lasts from 4 to 5 weeks
•Caused by Bordetellapertussis, a small, Gram-negative coccobacillussimilar in appearance to Haemophilussp
•Produces an extensive tracheobronchitis
•Primarily a disease of children younger than 5 years, and many cases occur in children younger than 1 year
•Vaccination protects against B. pertussis |
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Term
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Definition
•Most commonly afflicts menstruating women
•Patients present with high fever, nausea, vomiting, diarrhea, myalgias, and eventually, shock
•Associated with use of hyperabsorbenttampons, which provide a site for S. aureus replication and toxin elaboration |
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