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| Vasodilation & increase permeability |
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•Histamine
•Serotonin
•PGE2, F2
•C3a, C5a
•Bradykinin |
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| (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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| is a powerful chemotactic to neutrophils and monocytes |
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| ("membrane attack complex")is generated, the cell to which the complex is attached can be lysed by perforation of its cell membrane |
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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)
block both leukotriene and prostaglandin synthesis, while aspirin and nonsteroidals (NSAIDs) only block prostaglandins; this underscores powerful effect of steroidal anti-inflammatory agents |
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| Synthesis of adhesion molecules on the vascular endothelium is stimulated by interleukin 1 and endotoxin |
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Bradykinin increase
produce a fibrin clot, the kinin system to produce bradykinin and the fibrinolytic system to produce plasmin |
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| Inhibited by corticosteroids |
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| Inhibited by aspirin and NSAIDS |
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| Acute Inflammation Mediators |
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•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 |
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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 |
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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 |
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| IL-1 and tumor necrosis factor (TNF) |
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Definition
are primarily secreted by macrophages and have an important role in both acute and chronic inflammation
•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
•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 |
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| produced by activated macrophages, acts as a powerful chemotactic agent and activator of neutrophils |
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| Stimulate acute phase-reactant (APR) |
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| include such proteins as lactoferrin, fibrinogen, coagulation factors, C-reactive protein, and SSA protein |
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| Leukocytes possess microtubules and contractile microfilaments (actin and myosin) that enable them to move through the tissue |
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| 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 |
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•Associated with Nasopharyngeal carcinoma and Burkitt’slymphoma
-EBV infects B-Lymphocytes
-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 |
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•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) |
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•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 |
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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 |
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-An overgrowth of tissue that is normally present in the organ (e.g. a bronchial hamartomaof the lung composed of mature cartilage)
Hamartomarefers to localized disordered differentiation during embryonic development
-not a true neoplasm that contain cartilages (Calcified substances), ducts, connective tissue, blood vessels and lymphoid tissue |
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•The guardian of the genome
•Located on chromosome 17
•Prevents a mutated cell from proliferating |
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Definition
•FEVER: especially with Hodgkin's, Renal cell carcinomas, osteogenicsarcomas
•Anorexia and weight loss
•Hypercalcemia-About ten percent of all patients. Usually attributed to secreted of a PTH-like peptide by an epithelial tumor
Hypercoaguable State
•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)
(Systemic effects of cancers in the host that are not due primarily to tumor or its metastases) |
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| Ectopic Hormone Production |
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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 |
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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) |
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Definition
-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) |
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-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 |
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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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•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 |
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| Forms homogeneous eosinophilic inclusions (Russell bodies) in plasma cells |
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| medullary carcinoma of the thyroid |
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•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
•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) |
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| In this image with trichrome stain, some of these skeletal muscle fibers show atrophy, compared to normal fibers |
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| The right image shows an atrophied testis and is much smaller than the normal testis to the left. |
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| 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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| 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 |
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| 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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•Hemoglobin-derived, iron-containing golden-yellow granular pigment that contains aggregates of ferritin micelles (storage form of iron)
•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 |
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-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) |
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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
-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 |
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•Produces cellular injury via 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 |
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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 |
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| Physiologic (Hormonal) hyperplasia |
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Definition
| is seen in glandular epithelium of the female breast at puberty and uterine endometrium during pregnancy |
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Definition
| 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) |
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Definition
•Direct Acting Carcinogens
-Not metabolized in the liver
-generally electrophilicand thus attracted to the negatively charged substituentsin the nucleus |
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•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 |
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Papillomaviruses
Epstein-Barr virus
Hepatitis B virus
Kaposi's sarcoma |
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benign squamous papillomasprogressing to squamous cell carcinoma.
•Infection with HPVs also contributes to the development of squamous cell dysplasiasand squamous cell carcinomas of the genital tract |
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| Burkitt'slymphoma and undifferentiated nasopharyngeal carcinoma |
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hepatocellular carcinoma
•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 |
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Acute Transforming Viruses
Slow Transforming Retroviruses
Human T-cell Leukemia Virus |
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| Acute Transforming Viruses |
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Definition
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| Slow Transforming Retroviruses |
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Definition
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| Human T-cell Leukemia Virus |
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Definition
| adult T-cell leukemia/lymphoma |
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•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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| •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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•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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•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 |
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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.” |
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| Systemic Lupus Erythematosis (SLE) |
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Definition
| • Congenital deficiency of C2 and C4 complement promotes SLE development |
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| Diagnostically important antibodies SLE |
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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 |
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| Lupus Erythematosus Therapy |
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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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| Autoimmune (Hashimoto's) thyroiditis |
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Definition
Swollen neck due to variable enlargement of the thyroid gland
•Patients will eventually require thyroid hormone
Type II cytotoxicity
•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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Definition
| positive in malignant melanoma and neuroblastomas |
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Definition
| -Cytokeratinseparates a carcinoma (positive) from a malignant lymphoma (negative) and a mesothelioma(positive) from an adenocarcinoma (negative) |
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| Factor VIII related antigen |
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Definition
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 |
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| Delayed and Granulomatous hypersensitivity |
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Definition
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| 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
•Produces an extensive tracheobronchitis |
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Definition
| •Associated with use of hyperabsorbenttampons, which provide a site for S. aureus replication and toxin elaboration |
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