Path

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Pathology

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is the study of the cause of disease relating to structural and functional abnormalities that occur in diseases of organs and systems.

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Cell injury

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occurs when the cells ability to adapt and maintain homeostasis is beyond what the cell can handle.

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Causes of cell injury

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oxygen deprivation, chemical changes, infectious agents, immune reactions, genetic defects, nutritional imbalance, physical agents, aging

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Hyperplasia

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the number of cells in a certain tissue or organ increases

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Hypertrophy

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an increase in the size of cells and consequently an increase in the size of an organ.

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Atrophy

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the size of an existing cell reduces in an organ or tissue

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Metaplasia

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a reversible change in which one adult cell type is replaced by another adult cell type.

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Dysplasia

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a loss of uniformity in individual cells and a loss in their architectural orientation. Size, shape and/or organization of the cells within a tissue could all be factors in this abnormal presentation.

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Apoptosis

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programmed cell death or cellular suicide. It prevents the accumulation of unneeded cells, regulates the number of cells in a tissue, and prevents damaged cells from accumulating and proliferating when cellular suicide is triggered.

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Antioxidant Example

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Vitamin C, Vitamin A, Vitamin E, Glutathione, superoxide dismutase and various peroxidases

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Antioxidant

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An agent that prevents or inhibits oxidation. Antioxidants are substances that may protect cells from the damaging effects of oxygen radicals, highly reactive chemicals that play a part in atherosclerosis, some forms of cancer, and reperfusion injuries. "free radical scavengers" and hence prevent and repair damage done by these free radicals.

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mitotic stabile cells

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Queiscent cells are adult cells which do not divide, but under certain stimulation when it is needed, it can undergo cell division. One example are hepatocytes (liver cells).

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Mitotic labile cells

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are actively dividing cells

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mitotic permanent

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cells that do not divide at all and have no such capabilities. No matter what happens, it could only undergo hypertrophy. Examples are neurons, and skeletal and cardiac muscle cells

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Necrosis

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pathological cell death that can be indicative of disease or injury to tissues and cells or cellular homicide. It is unregulated so it can be pathogenic in the sense that it could lead to embolisms in the blood stream if the dead tissues and cells are not digested or phagocytized properly.

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Inflammation

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is a protective response to eliminate the cause of cell injury.

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Inflammation process:

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initial vasoconstriction results in less blood flow, followed by vasodilatation and capillary swelling bringing O2, nutrients and immune cells to the injured area (dilatation causes change in capillary permeability – allowing the immune cells to leach out of the vascular walls – edema), neutrophils move in and phagocytosis occurs with inflammatory mediator release occurs, chemotaxis occurs, margination and adhesion occurs, more chemotaxis which leads to emigration of macrophages and lymphocytes and possibly more RBC’s, eventually healing of tissue including scarring.

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The cardinal effects of inflammation

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rubor (redness), calor (heat), dolor (pain), tumor (swelling) and loss of function.

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Chemical mediators of inflammation

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, Serotonin, Serotonin, Substance P, Hageman factor, Plasminogen activator, Kinin Polypeptides, Bradykinin, Prostaglandins, Leukotrienes, Lipoxins, Thromboxane A2, Platelet activating factor, Cytokines, Nitric oxide, Reactive oxygen species (ROS), Proteases

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Histamine

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– released from mast cells during type I hypersensitivity reactions. Causes vasodilation, smooth muscle constriction, tissue swelling, itching, mucus production

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Serotonin

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– found in blood platelets, released during platelet aggregation

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Substance P

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vasodilator; neurotransmitter

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Hageman factor

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– deficiency of Hageman factor = blood takes longer than normal to clot in a test tube. Also known as plasma protein factor XII.

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Plasminogen activator

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– prevents fibrin clot formation

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Kinin Polypeptides

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– that induce local vasodilation and contraction of smooth muscle

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Bradykinin

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– (PAIN!) Similar to histamine

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Prostaglandins

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– vasodilation, fever, pain

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Leukotrienes

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– released by mast cells, cause vasoconstriction. Most spasmogenic substance known to man!

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Lipoxins

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– promote the resolution phase of inflammation

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Thromboxane A2

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– substance made by platelets that causes blood clotting

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Platelet activating factor

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– a compound that reduces inflammation by increasing permeability of blood vessels and contracting various involuntary muscles

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Cytokines

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– vasoconstrictors (interleukins, interferons, erythropoietin, tumor necrosis factors) that are produced primarily by WBC’s.

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Nitric oxide

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– vasodilator, inhibits aggregation of platelets and the inflammatory process. Also decreases lymphocyte recruitment in the inflammatory process

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Reactive oxygen species (ROS)

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– vasoconstrictor

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Proteases

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– enzymes that break down peptide bonds that join the amino acids in a protein

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Transudate

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The fluid that passes through a membrane, esp. that which passes through capillary walls.  Compared with an exudate, a transudate has fewer cellular elements and is of a lower specific gravity

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exudate

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Any fluid released from the body with a high concentration of protein, cells, or solid debris.  Exudates may be classified as fibrinous, hemorrhagic, diphtheritic, purulent, and serous. A fibrinous exudate may wall off a cavity, resulting e.g.,in adhesions following surgery, or in restrictive lung disease, following an empyema, Sanguineous= Bloody, Purulent= puss, catarrhal= mucus membranes.

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Chronic inflammation

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: prolonged inflammation with simultaneous active inflammation, tissue injury and tissue repair. When macrophages move in to clean up they trigger fibroblasts to proliferate and increase synthesis of collagen. The macrophages continue to destroy tissue in an effort to repair the damaged area and then fibroblast proliferation causes fibrosis, an accumulation of extracellular matrix. Together they don’t know how to turn each other off, perpetuating the cycle of inflammation.

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Fibrosis

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The repair and replacement of inflamed tissues or organs by connective tissues. The process results in the replacement of normal cells by fibroblasts (and eventually, the replacement of normal organ tissue by scar tissue

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fibrosis cells types

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Lung, uterus, arteriole, macula, liver, skin, heart

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ExtraCellular Matrix

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connective tissue in animals Interstitial matrix is present between various animal cells (i.e., in the intercellular spaces). Gels of polysaccharides and fibrous proteins fill the interstitial space and act as a compression buffer against the stress placed on the ECM.[2] Basement membranes are sheet-like depositions of ECM on which various epithelial cells rest. This lays down the framework for wound healing. Proteoglycans (attract water), Heparan sulfate(vessels), Chondroitin sulfate(cartillage strength), Hyaluronic acid (regulates cell growth), collagen. elastin, Fibronectin (proteins connecting to collagen), laminens (web like) All started to be laid down by fibroblast

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The four components of the tissue repair process are:

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formation of new blood vessels, proliferation of fibroblasts, depositions of extra cellular matrix, reorganization of fibrous tissue into a scar

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Healing by second intention

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If reinjury occurs, poor nutriion (Vit C def),infection, glucocorticoids (antinflammatory), poor perfusion (diabetes), Foreign bodies: granulation tissue grows into the exudate, and a fibrous scar ultimately forms.

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Edema

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increased/excess fluid in the interstitial tissue

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Causes of Edema

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Increased hydrostatic pressure(increase in intravascular pressure)Due to impaired venous return, Congestive heart failure, Constrictive pericarditis, Ascites (liver cirrhosis), Venous obstruction or compression, Thrombosis, External pressure, Reduced plasma osmotic pressure (Hypoproteinemia), Nephrotic syndrome-excess loss of synthesis of albumin, Albumin=serum protein responsible for maintaining Osmotic pressure, Liver cirrhosis (ascots) - reduced synthesis of albumin, Malnutrition-also causes reduced albumin synthesis, Lymphatic obstruction (impaired lymphatic drainage causing Lymphedema) Usually localized and arising from: Inflammatory obstruction, Neoplastic obstruction, Sodium retention (where salt goes so does water), May be a sign of acute renal failure, Inflammation, Acute inflammation, Chronic inflammation, Angiogenesis (the development of new blood vessels),

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Hemorrhage

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– extravasation of blood due to rupture of blood vessels

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Thrombosis

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– the pathologic converse of hemostasis, it is the formation of a blood clot in uninjured vessels or a thrombotic occlusion of a vessel after a minor injury.

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Embolus

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– a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin, where it lodges in a vessel too Small to permit passage resulting in partial or complete vascular occlusion.

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Infarction

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– ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.

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Shock

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– aka ‘cardiovascular collapse’ constitutes an acute fall in blood pressure causing systemic Cardiogenic, Hypovolemic, Sepsishypoperfusion (inadequate blood flow). This loss of blood flow is due to a reduction in either cardiac output or circulating blood volume. This can be caused by blood loss, acute trauma, severe burns, bacterial infection, allergic reaction, DIC, or sudden emotional stress. It presents with cold pallid skin, irregular breathing, rapid pulse and dilated pupils. Secondary Renal Failure, acidosis. Treat by calling 911, Airway, breathing, manage blood loss, o2, transfusion, IV

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Hemostasis (blood clot formation)

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Vasoconstriction – neuro-mediated and brief in duration, Platelet aggregation – occurs when platelets are exposed to foreign substance (ie. Air, extra cellular matrix, etc). They change shape and adhere to each other. Platelets also release secretory granules. These granules are part of a coagulation cascade. Formation of fibrin – an activated form of fibrinogen, that is activated by thrombin Cementing of Fibrin and Platelets into a clot

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Virchow's Triad 3-main influences that predispose to thrombus formation

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Endothelial injury (pg90) – endo integrity is the single most important factor – This does not have to be from acute trauma, can also be caused by things such as chronic hypertension, bacterial endotoxins, etc. Alterations in normal blood flow – Turbulence contributes to arterial and cardiac Thrombosis by causing endothelial injury or dysfunction. Stasis is a major factor in venous thrombi. Stasis and turbulence: disrupt laminar flow and bring platelets in contact with endothelium, prevent dilution of activated clotting factors by fresh-flow blood, retard the inflow of clotting factor inhibitors and allow thrombi build-up, promote endothelial activation, predisposing to local thrombosis, Leukocyte adhesion, etc. Hypercoagulability – generally contributes less to thrombus formation (def.: an alteration in the coagulation pathways that predisposes to thrombosis), 2 types – primary (genetic) – secondary (acquired)

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Humoral immunity

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B lymphocytes – Derived from bone marrow, Source of antibodies (proteins). Antibodies participate in immunity by directly neutralizing extra cellular microbes or by activating complement and neutrophils and macrophages to kill microorganisms

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Cellular immunity

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T lymphocytes - Derived from the Thymus gland, Can either directly lyse targets or can orchestrate the antimicrobial immune response of other cells by producing cytokines

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CD4 lymphocytes

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Receptor on Tcell helper activates cell after antigen presenting cell. CD4 binds to class II MHC molecules, CD4+ helper T cells recognize class II-associated peptides, which are usually derived from ingested proteins. cytokine IL-2 and expression of high-affinity receptors for IL-2. IL-2 is a growth factor that acts on these T lymphocytes and stimulates their proliferation, leading to an increase in the number of antigen-specific lymphocytes. Some of the progeny of the expanded pool of T cells differentiate into effector cells that can secrete different sets of cytokines and thus perform different functions.

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CD8 lymphocyte

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antigens in the cytoplasm are displayed by class I MHC molecules and are recognized by CD8+ cytotoxic T cells, because CD8 binds to class I MHC. Activated CD8+ lymphocytes differentiate into CTLs that kill cells harboring microbes in the cytoplasm. This segregation of different antigens is key to the specialized functions of CD4+ and CD8+ T cells; as we discuss below, the two classes of T cells are designed to combat microbes that are located in different cellular compartments.

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HLA

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"human leukocyte antigen major histocompatibility complex (MHC) in humans. The superlocus contains a large number of genes related to immune system function in humans. This group of genes reside on chromosome 6, and encode cell-surface antigen-presenting proteins and many other genes. The HLA genes are the human versions of the MHC genes that are found in most vertebrates (and thus are the most studied of the MHC genes). The proteins encoded by certain genes are also known as antigens, as a result of their historic discovery as factors in organ transplantations. The major HLA antigens are essential elements for immune function. Different classes have different functions:HLA class I antigens (A, B & C) present peptides from inside the cell (including viral peptides if present). These peptides are produced from digested proteins that are broken down in the proteasomes. The peptides are generally small polymers, about 9 amino acids in length. Foreign antigens attract killer T-cells (also called CD8 positive- or cytotoxic T-cells) that destroy cells.

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Cytokines effects

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Cytokine effect Leukocytes are attraction to a dammaged area, Fibroblast proliferation, endothelium dysfunction poor adherence to eachother basement layer.

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Immediate Hypersensitivity reactions

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1)Immediate: Also called allergic reactions, or allergiesInduced by environmental antigens (allergens) that stimulate strong TH2 responses and IgE production in genetically susceptible individualsIgE coats mast cells by binding to Fcε receptors; re-exposure to the allergen leads to cross-linking of the IgE and FcεRI, activation of mast cells, and release of mediators.Principal mediators are histamine, proteases and other granule contents; prostaglandins and leukotrienes; cytokines.Mediators are responsible for the immediate vascular and smooth muscle reactions and the late-phase reaction (inflammation).The clinical manifestations may be local or systemic, and range from mildly annoying rhinitis to fatal anaphylaxis

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Antibody-mediated Hypersensitivity

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Antibodies can coat (opsonize) cells, with or without complement proteins, and target these cells for phagocytosis by phagocytes (macrophages), which express receptors for the Fc tails of lgG and for complement proteins. The result is depletion of the opsonized cells.Antibodies and immune complexes may deposit in tissues or blood vessels, and elicit an acute inflammatory reaction by activating complement, with release of breakdown products, or by engaging Fc receptors of leukocytes. The inflammatory reaction causes tissue injury.Antibodies can bind to cell surface receptors or essential molecules, and cause functional derangements (either inhibition or unregulated activation) without cell injury.

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Immune complex-mediated Hypersensitivity response:

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The morphologic appearance of immune complex injury is dominated by acute necrotizing vasculitis, microthrombi, and superimposed ischemic necrosis accompanied by acute inflammation of the affected organs. The necrotic vessel wall takes on a smudgy eosinophilic appearance calledfibrinoid necrosis, caused by protein deposition (see Fig. 1-14, Chapter 1). Immune complexes can be visualized in the tissues, usually in the vascular wall; examples of such deposits in the kidney lupus are shown in Figure 5-21E. In due course the lesions tend to resolve, especially when they were brought about by a single exposure to antigen (e.g., acute serum sickness and acute poststreptococcal glomerulonephritis [Chapter 14]). However, chronic immune complex disease develops when there is persistent antigenemia or repeated exposure to an antigen. This occurs in some human diseases, such as systemic lupus erythematosus (SLE). Most often, even though the morphologic changes and other findings strongly implicate immune complex disease, the inciting antigens are unknown.

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T-cell-mediated

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Delayed-type hypersensitivity (DTH): CD4+ T cells are activated by exposure to a protein antigen and differentiate into TH1 effector cells. Subsequent exposure to the antigen results in the secretion of cytokines. IFN-γ activates macrophages to produce substances that cause tissue damage and promote fibrosis, and TNF promotes inflammation.T-cell-mediated cytotoxicity: CD8+ cytotoxic T lymphocytes (CTLs) specific for an antigen recognize cells expressing the target antigen and kill these cells. CD8+ T cells also secrete IFN-γ.

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SLE definition

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Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease of protean manifestations and variable behavior 1. Malar rash Fixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds, 2. Discoid rash Erythematous raised patches with adherent keratotic scaling and follicular plugging; atrophic scarring may occur in older lesions, 3. Photosensitivity Rash as a result of unusual reaction to sunlight, by patient history or physician observation, 4. Oral ulcers Oral or nasopharyngeal ulceration, usually painless, observed by a physician, 5. Arthritis Nonerosive arthritis involving two or more peripheral joints, characterized by tenderness, swelling, or effusion,6. Serositis Pleuritis-convincing history of pleuritic pain or rub heard by a physician or evidence of pleural effusion, or Pericarditis-documented by electrocardiogram or rub or evidence of pericardial effusion, 7. Renal disorder Persistent proteinuria >0.5gm/dL or >3+if quantitation not performed or Cellular casts-may be red blood cell, hemoglobin, granular, tubular, or mixed, 8. Neurologic disorder Seizures: in the absence of offending drugs or known metabolic derangements (e.g., uremia, ketoacidosis, orelectrolyte imbalance), or Psychosis: in the absence of offending drugs or known metabolic derangements (e.g., uremia, ketoacidosis, or electrolyte imbalance), 9. Hematologic disorder Hemolytic anemia: with reticulocytosis, or Leukopenia: <4.0 ×109 cells per liter (4000 cells per mm3) total on two or more occasions or Lymphopenia: <1.5 ×109 cells per liter (1500 cells per mm3) on two or more occasions or Thrombocytopenia: <100 ×109 cells per liter (100 ×103 cells per mm3) in the absence of offending drugs, 10. Immunologic disorder Anti-DNA antibody to native DNA in abnormal titer, or Anti-Sm: presence of antibody to Sm nuclear antigen or Positive finding of antiphospholipid antibodies based on (1) an abnormal serum level of IgG or IgM anticardiolipin antibodies, (2) a positive test for lupus anticoagulant using a standard test, or (3) a false-positive serologic test for syphilis known to be positive for at least 6 months and confirmed by negative Treponema pallidum immobilization or fluorescent treponemal antibody absorption test, 11. Antinuclear antibody: An abnormal titer of antinuclear antibody by immunofluorescence or an equivalent assay at any point in time and in the absence of drugs known to be associated with drug-induced lupus syndrome

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more SLE

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"Morphology

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RA

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RA is a chronic inflammatory disease that affects mainly the joints, especially small joints, but can affect multiple tissues.The disease is caused by an autoimmune response against an unknown self antigen(s), which leads to T-cell reactions in the joint with production of cytokines that activate phagocytes that damage tissues and stimulate proliferation of synovial cells (synovitis). The cytokine TNF plays a central role, and antagonists against TNF are of great benefit. Antibodies may also contribute to the disease.

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SLE vs RA

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RA The natural history of the disease has been one of progressive joint destruction leading to disability after 10-15 years ulnar deviation. SLE usually affects younger girls and is systemic

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RF

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RF is often evaluated in patients suspected of having any form of arthritis even though positive results can be due to other causes, and negative results do not rule out disease. But, in combination with signs and symptoms, it can play a role in both diagnosis and disease prognosis. It is part of the usual disease criteria of rheumatoid arthritis. The presence of rheumatoid factor in serum can also indicate the occurrence of suspected autoimmune activity unrelated to rheumatoid arthritis, such as that associated with tissue or organ rejection. In such instances, RF may serve as one of several serological markers for autoimmunity.

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ANA

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antinuclear antibody isnt very specific to a single disease levels can indicate any autoimmune Systemic lupus erythematosus, drug-induced lupus erythematosus, Collagen vascular disease, Myositis (inflammatory muscle disease), Sjogren syndrome, Chronic liver disease, Rheumatoid arthritis, Increased ANA levels may sometime be seen in people with: Systemic sclerosis (scleroderma), Thyroid disease

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Sjögren Syndrome

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characterized by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia

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Scleroderma

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systemic sclerosis (SS), because it is characterized by excessive fibrosis throughout the body and not just the skin. Cutaneous involvement is the usual presenting symptom and eventually appears in approximately 95% of cases, but it is the visceral involvement-of the gastrointestinal tract, lungs, kidneys, heart, and skeletal muscles-that produces the major morbidity and mortality. Diffuse scleroderma, characterized by initial widespread skin involvement, with rapid progression and early visceral involvementLimited scleroderma, with relatively mild skin involvement, often confined to the fingers and face. Involvement of the viscera occurs late, and hence the disease in these patients generally has a fairly benign course. This is also called the CREST syndrome because of its frequent features of calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia.

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Secondary Immune Deficiencies

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Immune deficiencies secondary to other diseases or therapies are much more common than the primary (inherited) disorders. Secondary immune deficiencies may be encountered in patients with malnutrition, infection, cancer, renal disease, or sarcoidosis. However, the most common cases of immune deficiency are therapy-induced suppression of the bone marrow and of lymphocyte function

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Complications of immunodeficiency

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Clinically, patients with immune deficiency present with increased susceptibility to infections as well as to certain forms of cancer. The type of infections in a given patient depends largely on the component of the immune system that is affected. Patients with defects in Ig, complement, or phagocytic cells typically suffer from recurrent infections with pyogenic bacteria, whereas those with defects in cell-mediated immunity are prone to infections caused by viruses, fungi, and intracellular bacteria. Here we describe some of the more important primary immune deficiencies, followed by a detailed description of the acquired immunodeficiency syndrome (AIDS), the most devastating example of secondary immune deficiency.

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HIV reverse transcriptase

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makes DNA from RNA,

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HIV Integrase

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Inserts the Viral DNA into the host's DNA

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HIV Transmission

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the major routes of HIV infection are sexual contact, parenteral inoculation, and passage of the virus from infected mothers to their newborns

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HIV prevention

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Condom, universal precautions

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HIV cellular receptor target

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binding to CD4 is not sufficient for infection; the HIV envelope gp120 must also bind to other cell surface molecules (coreceptors) to facilitate cell entry. Two cell surface chemokine receptors, CCR5 and CXCR4, serve this role. HIV envelope gp120 (noncovalently attached to transmembrane gp41) binds initially to CD4 molecules (see Fig. 5-31). This binding leads to a conformational change that exposes a new recognition site on gp120 for the CXCR4 (mostly on T cells) or CCR5 (mostly on macrophages) coreceptors. The gp41 then undergoes a conformational change that allows it to insert into the target membrane, and this process facilitates fusion of the virus with the cell. After fusion, the virus core containing the HIV genome enters the cytoplasm of the cell.

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HIV Clinical Expression

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The clinical manifestations of HIV infection range from a mild acute illness to severe disease. Because the salient clinical features of the acute, early and chronic, middle phases of HIV infection were described earlier, only the clinical manifestations of the terminal phase, full-blown AIDS, are summarized here. In the United States the typical adult patient with AIDS presents with fever, weight loss, diarrhea, generalized lymphadenopathy, multiple opportunistic infections, neurologic disease, and (in many cases) secondary neoplasms. The infections and neoplasms listed in Table 5-11 are included in the surveillance definition of AIDS. The anatomic changes in the tissues (with the exception of lesions in the brain) are neither specific nor diagnostic. In general, the pathologic features of AIDS are those of widespread opportunistic infections, KS, and lymphoid tumors. Most of these lesions are discussed elsewhere, because they also occur in patients who do not have HIV infection. To appreciate the distinctive nature of lesions in the CNS, they are discussed in the context of other disorders affecting the brain (Chapter 23). Here the focus is on changes in the lymphoid organs. Biopsy specimens from enlarged lymph nodes in the early stages of HIV infection reveal a marked follicular hyperplasia (Chapter 12). The medulla contains abundant plasma cells. These changes, affecting primarily the B-cell areas of the node, are the morphologic counterparts of the polyclonal B-cell activation and hypergammaglobulinemia seen in AIDS patients. In addition to changes in the follicles, the sinuses show increased cellularity, due primarily to increased numbers of macrophages but also contributed to by B-cell lymphoblasts and plasma cells. HIV particles can be demonstrated within the germinal centers, concentrated on the villous processes of the follicular DCs. Viral DNA can also be detected in macrophages and CD4+ T cells. With disease progression, the frenzy of B-cell proliferation gives way to a pattern of severe follicular involution and generalized lymphocyte depletion. The organized network of follicular DCs is disrupted, and the follicles may even become hyalinized. These "burnt-out" lymph nodes are atrophic and small and may harbor numerous opportunistic pathogens. Because of profound immunosuppression, the inflammatory response to infections both in the lymph nodes and at extranodal sites may be sparse or atypical. For example, with severe immunosuppression, mycobacteria do not evoke granuloma formation, because CD4+ T cells are lacking. In the empty-looking lymph nodes and in other organs, the presence of infectious agents may not be readily apparent without the application of special stains. As might be expected, lymphoid depletion is not confined to the nodes; in the later stages of AIDS, the spleen and thymus also appear to be "wastelands." Non-Hodgkin lymphomas, involving the nodes as well as extranodal sites such as liver, gastrointestinal tract, and bone marrow, are primarily high-grade diffuse B-cell neoplasms

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Benign Neoplasic Cells

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"Well-defined margins, Good differentiatin, Slow growth, few mitoses, Normal nucleus/cytoplasm ratio

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Malignant Neoplastic Cells

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Malignant Neoplastic Cells: Poorly defined margins, Poor Differentiation, Invasion into surrounding tissue, many mitoses, High nucleus-to-cytoplasm ratio

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Mutation

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Change in the DNA sequence of the gene

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teratogen

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Any agent that can disturb the development of an embryo or fetus. Teratogens may cause a birth defect in the child. Or a teratogen may halt the pregnancy outright. The classes of teratogens include radiation, maternal infections, chemicals, and drugs.

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Carcinoma in situ

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Cancer that involves only the place in which it began and that has not spread. Carcinoma in situ is an early-stage tumor.

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Tumor grade:

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The degree of abnormality of cancer cells, a measure of differentiation, the extent to which cancer cells are similar in appearance and function to healthy cells of the same tissue type. The degree of differentiation often relates to the clinical behavior of the particular tumor. Based on the microscopic appearance of cancer cells, pathologists commonly describe tumor grade by four degrees of severity: Grades 1, 2, 3, and 4. The cells of Grade 1 tumors are often well-differentiated or low-grade tumors, and are generally considered the least aggressive in behavior. Conversely, the cells of Grade 3 or Grade 4 tumors are usually poorly differentiated or undifferentiated high-grade tumors, and are generally the most aggressive in behavior

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Cancer Staging

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a descriptor (usually numbers I to IV) of how much the cancer has spread. The stage often takes into account the size of a tumor, how deeply it has penetrated, whether it has invaded adjacent organs, how many lymph nodes it has metastasized to (if any), and whether it has spread to distant organs. Staging of cancer is important because the stage at diagnosis is the most powerful predictor of survival, and treatments are often changed based on the stage.

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Viral Carcinogen

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Hepatitis B (Lr CA) , HPV (cervical CA)

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First-degree burns

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Epidermis involvement Erythema, significant pain, lack of blisters: Superficial

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Second-degree burns

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Superficial (papillary) dermis Blisters, clear fluid, and pain Partial thickness

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Third-degree burns

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Deep (reticular) dermis Whiter appearance or fixed red staining (no blanching), reduced sensation: Full thikness, Deep (reticular) dermis, Whiter appearance or fixed red staining (no blanching), reduced sensation

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Heat exhaustion

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most common hyperthermic syndrome. Its onset is sudden, with prostration and collapse, and it results from a failure of the cardiovascular system to compensate for hypovolemia, secondary to water depletion. After a period of collapse, which is usually brief, equilibrium is spontaneously re-established.

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Heat Stroke

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associated with high ambient temperatures and high humidity. Thermoregulatory mechanisms fail, sweating ceases, and core body temperature rises. Body temperatures of 112° to 113°F have been recorded in some terminal cases. Clinically, a rectal temperature of 106°F or higher is considered a grave prognostic sign, and the mortality rate for such patients exceeds 50%. The underlying mechanism is marked generalized peripheral vasodilation with peripheral pooling of blood and a decreased effective circulating blood volume. Necrosis of the muscles and myocardium may occur. Arrhythmias, disseminated intravascular coagulation, and other systemic effects are common. Elderly persons, individuals undergoing intense physical stress (including young athletes and military recruits), and persons with cardiovascular disease are prime candidates for heat stroke.

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Marasmus and kwashiorkor

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Ends of the spectrum for Protein Energy Malnutrition: Protein intake isnt able to meet the body's needs, there are two compartments Somatic (skeletal muscle catabolism, evidence of immunodef.: Marasmus affects this) and visceral ( LR is enlarged and fatty, small bowel mucosal changes are reversible: Kwashiorkor). Malnourishment is when the body is below 60% of normal.

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Obesity Complications

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It increases the risk for a number of important conditions such as insulin resistance, type 2 diabetes, hypertension, and hypertriglyceridemia, which are associated with the development of coronary artery disease. Obesity contributes to the development of nonalcoholic fatty liver disease, which may progress to fibrosis and cirrhosis, and increases the formation of cholesterol gallstones.Obesity is associated with increased risk of endometrial and breast cancers, perhaps as a result of hormonal changes.

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Prions

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Protein that causes other proteins to take on a folded state that is not conducive to normal function and causes other proteins to take this on

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Virus

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Viruses possess specific cell surface proteins that bind to selected host cell surface proteins. Many viruses use normal cellular receptors of the host to enter cells. Viral replication interferes with normal cellular functions and may lead to cell death. For example, viral replication and release is the mechanism by which influenza virus kills respiratory epithelial cells, yellow fever virus kills hepatocytes, and poliovirus and rabies destroy neurons.Immune cell-mediated killing. Viral proteins expressed on host cell surfaces are recognized as foreign by the immune system and induce attack by cytotoxic T lymphocytes. Although this is a normal response to eliminate virally infected cells, it can clearly lead to significant host injury. Thus, liver cell injury during HBV infection is largely driven by cytotoxic T lymphocytes

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Bacterial injury

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disease (virulence) depends on their ability to (1) adhere to host cells, (2) invade cells and tissues, and/or (3) deliver toxins that damage cells and tissues. Pathogenic bacteria have virulence genes that encode proteins that confer these properties.

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Bacterial endotoxin

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lipopolysaccharide (LPS) that is a major component of the outer cell wall of gram-negative bacteria

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bacterial exotoxin

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Exotoxins are secreted proteins that directly cause cellular injury and frequently underlie disease manifestations. Some exotoxins are bacterial enzymes (proteases, hyaluronidases, coagulases, fibrinolysins) that act on target substrates and contribute to normal bacterial housekeeping and survival. Nevertheless, they can contribute significantly to pathologic manifestations of an infection

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Bacterial Shape

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Coccus: Spherical StreptoCocci: String of cocci Coccobacillus: Elliptoid Bacillus: capsule shaped Budding or appendaged, Spirals and with flagella

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MMR vaccine

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measles, mumps and rubella (also called German measles)

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Vaccine immunity

Back 101

Vaccines contain the same antigens or parts of antigens that cause diseases, but the antigens in vaccines are either killed or greatly weakened. When they are injected into fatty tissue or muscle, vaccine antigens are not strong enough to produce the symptoms and signs of the disease but are strong enough for the immune system to produce antibodies against them (Tortora and Anagnostakos, 1981). The memory cells that remain prevent re-infection when they encounter that disease in the future.

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The natural barriers to infection and the characteristics of the barriers are:

Back 102

Skin - PH balance, Mucous membranes of the respiratory GI and GU tracts - IgA, the principal immunoglobulin in exocine secretions, which prevents pathogens from invading the body through mucosal lining of the pulmonary, GI and genitourinary tracts. The cilia of the respiratory tract – threadlike projections from epithelial cells that sweep materials, such as mucus or dust, across the surface of the respiratory tract. GI tract - Bowel bacterial flora GU tract - Vaginal bacterial flora

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Atheroma

Back 103

Pathogenesis of plaque formation: Endothelial injury, Accumulation of lipid proteins in the vessel wall (LDLs), Smooth muscle cell proliferation which leads to accumulation of collagen and proteoglycans which help to thicken the endothelial tissue of the vessels, Oxidation of lipids which increased the amount of free radicals present and the chance of attracting inflammatory responses.Dangers of plaque formation: Myocardial infarction (MI), cerebral infarction (Stroke), aortic aneurysm, peripheral vascular disease (like gangrene).

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Plaque composition

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Lipids: Cholesterol and Cholesterol esters. Smooth Muscle cells, ECM, Macrophages become foam cells, cytokines and growth factors.

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Blood Pressure

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Systolic: Heart contraction Diastolic: Heart at rest

Front 106

Increased cardiac output

Back 106

increased oxygen demand, increased venous return, needed for increased exercise

Front 107

Valvular stenosis vs regurgitation

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Stenosis is the failure of a valve to open completely, obstructing forward flow. Valvular stenosis is almost always a chronic process caused by a primary cuspal abnormality (e.g., calcification or valve scarring). .Insufficiency results from failure of a valve to close completely, thereby allowing reversed flow. Valvular insufficiency may result from either intrinsic disease of the valve cusps (e.g., valve destruction) or distortion of the supporting structures

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Renin-Angiotensin

Back 108

Decreased kidney blood flow causes secretion of renin in the kidney, Renin converts angiotensinogen into angiotensin I, Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE), Angiotensin II causes vasoconstriction and promotes sodium and water retention

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Hypertension

Back 109

Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic kidney failure. Dammage of the vessel walls and dammage of tissues at the end of the arterioles. 140–159/90-99

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Aneurism, Varicosity, vasculitis

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An aneurysm is a localized abnormal dilation of a blood vessel or the heart (Fig. 10-17). When an aneurysm involves all three layers of the arterial wall (intima, media, and adventitia) or the attenuated wall of the heart, it is called a "true" aneurysm. Vasculitis, or inflammation of vessel walls, occurs in diverse clinical settings. Depending on the vascular bed affected (e.g., central nervous system vs. heart vs. small bowel), the manifestations can be protean. Besides the findings referable to the specific tissue(s) involved, clinical manifestations common to these entities typically include constitutional signs and symptoms such as fever, myalgia, arthralgias, and malaise. Varicose veins are abnormally dilated, tortuous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support.Varicose dilation renders the venous valves incompetent and leads to stasis, congestion, edema, pain, and thrombosis

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Heart Failure and compensatory mechanisms

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develops when the heart cannot maintain the circulation due to extra work demand or damaged heart muscle. Congestive Heart failure is chronic, Increased heart rate, Ventricular hypertrophy, dilation of the heart chambers and activation of the renin-angiotensin system

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Left heart failure

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Results in: pulmonary hypertension due to blood backing up into the pulmonary circulation and poor perfusion of tissues in the body due to inadequate cardiac output

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Right Heart failure

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Results in: enlarged liver, peripheral edema and jugular vein engorgement due to blood backing up into the superior and inferior vena cava

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Angina and ischemic Heart Dz

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Angina pectoris (literally chest pain), wherein the ischemia causes pain but is insufficient to lead to death of myocardium; as we will discuss, angina may be stable (occurring reliably after certain levels of exertion), may be due to vessel spasm (variant angina or Prinzmetal angina), or may be unstable (occurring with progressively less exertion or even at rest) Acute myocardial infarction (MI), wherein the severity or duration of ischemia is enough to cause cardiac muscle deathChronic IHD refers to progressive cardiac decompensation (heart failure) following MI.Sudden cardiac death (SCD), can result from a lethal arrhythmia following myocardial ischemia. 2 Risk factors for ischemic heart disease (atherosclerosis): Hyperlipidemia – high cholesterol (esp. low density lipoprptein cholesterol) and triglyceride levels, Hypertension, Smoking, Diabetes, Genetics

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Rheumatic fever

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Rheumatic fever (RF) is an acute, immunologically mediated, multisystem inflammatory disease that occurs a few weeks after an episode of group A β-hemolytic streptococcal pharyngitis; it can also rarely occur with streptococcal infections at other sites (e.g., skin). Acute rheumatic heart disease (RHD) is the cardiac manifestation of RF and is associated with inflammation of the valves, myocardium, or pericardium. Chronic valvular deformities are the most important consequences of RHD; these are characterized by diffuse and dense scarring of valves resulting in permanent dysfunction (mitral stenosis being most common). Decreased incidence

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Subacute Bacterial Endocarditis

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Subacute endocarditis refers to infections by organisms of low virulence colonizing a previously abnormal heart, especially when there are deformed valves. The disease typically appears insidiously and follows a protracted course of weeks to months with most patients recovering after appropriate antibiotic therapy. Subacute endocarditis is typically associated with less valvular destruction than is acute endocarditis. Microscopically, in subacute IE vegetations often have granulation tissue at their bases, suggesting chronicity. As time passes, fibrosis, calcification, and a chronic inflammatory infiltrate may develop. Fever is the most consistent sign of IE. However, in subacute disease (particularly in the elderly) fever may be absent, and the only manifestations may be nonspecific fatigue, weight loss, and a flulike syndrome. Splenomegaly is common in subacute IE. In contrast, acute endocarditis has a stormy onset with rapidly developing fever, chills, weakness, and lassitude. Murmurs are present in 90% of patients with left-sided lesions, but these may merely relate to the pre-existing cardiac abnormality predisposing to IE. Diagnosis is largely made on the basis of positive blood cultures, echocardiographic findings, and other clinical and laboratory findings.

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Anemia and causes

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"is a reduction in the oxygen-transporting capacity of blood, which usually stems from a reduction of the total circulating red cell mass to below-normal amounts. Results from excessive bleeding, increased red cell destruction, or decreased red cell production Anemia is the reduction in oxygen carrying capacity of the blood usually due to decreased red blood cells from blood loss, increased destruction of red blood cells, decreased production of red blood cells. Anemia d/t:

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Aplastic anemia vs. hemolytic

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Aplastic anemia is a condition where bone marrow does not produce sufficient new cells to replenish blood cells. The condition, per its name, involves both aplasia and anemia. Hemolytic. Bone marrow cant keep up with destruction

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leukocytosis

Back 119

raised leukocyte level WBC general

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lekopenia

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lowered leukocyte count

Front 121

neutrophilia

Back 121

increased number of neutrophils means a bacterial infection

Front 122

eosinophilia

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increased number of eosinophils means allergy or worms

Front 123

lymphocytosis

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increased number of lymphocytes means viral infection

Front 124

splenomegaly

Back 124

enlarged spleen infection CA

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hepatomegaly

Back 125

enlarged liver: Alcohol CHF

Front 126

thrombocytopenia

Back 126

Low production of platelets in the bone marrow, Increased breakdown of platelets in the bloodstream (called intravascular), increased breakdown of platelets in the spleen or liver (called extravascular

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common childhood leukemia, course & complication

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acute lymphoblastic leukemia (ALL) rapidly growing tumors, normal bone marrow progenitors grow at an even more rapid rate. The principal pathogenetic problem in acute leukemia is a block in differentiation. This leads to the accumulation of immature leukemic blasts in the bone marrow, which suppress the function of normal hematopoietic stem cells by physical displacement and other poorly understood mechanisms. Eventually bone marrow failure results, which accounts for the major clinical manifestations of acute leukemia. Thus, the therapeutic goal is to reduce the leukemic clone sufficiently to allow normal hematopoiesis to resume. These include fatigue (due mainly to anemia), fever (reflecting infections resulting from the absence of mature leukocytes), and bleeding (petechiae, ecchymoses, epistaxis, gum bleeding) secondary to thrombocytopenia.Bone pain and tenderness. These result from marrow expansion and infiltration of the subperiosteum.Generalized lymphadenopathy, splenomegaly, and hepatomegaly. These reflect dissemination of the leukemic cells, and are more pronounced in ALL than in AML.Central nervous system manifestations. These include headache, vomiting, and nerve palsies resulting from meningeal spread; these features are more common in children than in adults and are more common in ALL than AML. Children 2 to 10 years of age have the best prognosis; most can be cured. Other groups of patients do less well. Variables correlated with worse outcomes include male gender, age younger than 2 or older than 10 years, and a high leukocyte count at diagnosis

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Clinical Signs of Lymphoma

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CLL/SLL is often asymptomatic at presentation. The most common symptoms are nonspecific and include easy fatigability, weight loss, and anorexia. Generalized lymphadenopathy and hepatosplenomegaly are present in 50% to 60% of cases. The total leukocyte count may be increased only slightly (in SLL) or may exceed 200,000 cells/μL. Hypogammaglobulinemia

Front 129

Hodgkins Lymphoma

Back 129

in a single lymph node or chain of lymph nodes and spread characteristically in a stepwise fashion to the anatomically contiguous nodes. it is characterized morphologically by the presence of distinctive neoplastic giant cells called Reed-Sternberg (RS) cells, which are admixed with reactive, nonmalignant inflammatory cells. Second, it is often associated with somewhat distinctive clinical features, including systemic manifestations such as fever. Third, its stereotypical pattern of spread allows it to be treated differently than most other lymphoid neoplasms. Despite these distinguishing features, molecular studies have shown that it is a tumor of B-cell origin. Clinical Course Hodgkin lymphomas, like NHLs, usually present as a painless enlargement of the lymph nodes. Although a definitive distinction from NHL can be made only by examination of a lymph node biopsy specimen, several clinical features favor the diagnosis of Hodgkin lymphoma (Table 12-10). Younger patients with the more favorable histologic types tend to present in clinical stages I or II and are usually free of systemic manifestations. Patients with disseminated disease (stages III and IV) are more likely to have systemic complaints such as fever, unexplained weight loss, pruritus, and anemia. As mentioned earlier, these patients generally have the histologically less favorable variants. The outlook after aggressive radiotherapy and chemotherapy for patients with this disease, including those with disseminated disease, is generally very good. With current modalities of therapy, the clinical stage is the most important prognostic indicator. The 5-year survival rate of patients with stage I-A or II-A disease is close to 100%. Even with advanced disease (stage IV-A or IV-B), the overall 5-year disease-free survival rate is around 50%.

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Non Hodgkins Lymphoma

Back 130

"Hodgkin Lymphoma More often localized to a single axial group of nodes (cervical, mediastinal, para-aortic) Orderly spread by contiguity, Mesenteric nodes and Waldeyer ring rarely involved, Extranodal involvement uncommon. Non-Hodgkin Lymphoma More frequent involvement of multiple peripheral node, Noncontiguous spread, Mesenteric nodes and Waldeyer ring commonly involved, Extranodal involvement common

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Reed-sternberg Cells

Back 131

distinctive neoplastic giant cells in hodgkins lymphoma. Particularly characteristic are cells with two mirror-image nuclei or nuclear lobes, each containing a large (inclusion-like) acidophilic nucleolus surrounded by a distinctive clear zone; together they impart an owl-eye appearance. The nuclear membrane is distinct.

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differentiation between myologenous and chronic lymphocytic leukemia

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"affects older persons, with the peak incidence being between the sixth and seventh decades. Most clinical symptoms of this disease can be traced to the presence of large amounts of IgM (macroglobulin). Because of their size, the macroglobulins greatly increase blood viscosity. This gives rise to the hyperviscosity syndrome known as Waldenström macroglobulinemia, which is characterized by the following features:

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multiple myeloma clinical presentation and its cells

Back 133

50 and 60 yo,most common of the malignant plasma cell dyscrasias, is a clonal proliferation of neoplastic plasma cells in the bone marrow that is usually associated with multifocal lytic lesions throughout the skeletal system. The proliferation of neoplastic plasma cells, also called myeloma cells, is supported by the cytokine interleukin 6 (IL-6), which is produced by fibroblasts and macrophages in the bone marrow stroma. Although any bone can be affected, the following distribution was found in a large series of cases: vertebral column, 66%; ribs, 44%; skull, 41%; pelvis, 28%; femur, 24%; clavicle, 10%; and scapula, 10%. These focal lesions generally begin in the medullary cavity, erode the cancellous bone, and progressively destroy the cortical bone. The bone resorption results from the secretion of certain cytokines (e.g., IL-1β, tumor necrosis factor, IL-6) by myeloma cells. These cytokines stimulate production of another cytokine called RANK-ligand, which promotes the differentiation and activation of osteoclasts (Chapter 21). Plasma cell lesions often lead to pathologic fractures, which occur most frequently in the vertebral column. The bone lesions usually appear radiographically as punched-out defects of 1 to 4 cm in diameter (Fig. 12-19A), but in some cases diffuse skeletal demineralization is evident. Bone pain, resulting from infiltration by neoplastic plasma cells, is extremely common. Pathologic fractures and hypercalcemia occur, with focal bone destruction and diffuse resorption. Hypercalcemia can cause neurologic manifestations such as confusion and lethargy; it also contributes to renal disease. Anemia results from marrow replacement as well as from inhibition of hematopoiesis by tumor cells.

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polycythemia vera and clinical course

Back 134

excessive neoplastic proliferation and maturation of erythroid, granulocytic, and megakaryocytic elements, producing a panmyelosis. Although platelet and granulocyte numbers are increased, the most obvious clinical signs and symptoms are related to the absolute increase in red cell mass. low levels of erythropoietin in the serum, which is a reflection of the hypersensitivity of the neoplastic clone to erythropoietin and other growth factors. PCV appears insidiously, usually in late middle age. Patients are plethoric and often somewhat cyanotic. Histamine release from the neoplastic basophils may contribute to pruritus, which can be intense. Excessive histamine release may also account for the peptic ulceration seen in these individuals. Other complaints are referable to the thrombotic and hemorrhagic tendencies and to hypertension. Headache, dizziness, gastrointestinal symptoms, hematemesis, and melena are common. Because of the high rate of cell turnover, symptomatic gout is seen in 5% to 10% of cases, and many more patients have asymptomatic hyperuricemia. The diagnosis is usually made in the laboratory. Red cell counts range from 6 to 10 million per microliter, and the hematocrit often approaches 60%. The other myeloid lineages are also hyperproliferative: the granulocyte count can be as high as 50,000 cells/mm3, and the platelet count is often greater than 400,000 cells/mm3. The basophil count is also frequently elevated. The platelets are functionally abnormal in most cases, and giant forms and megakaryocyte fragments are seen in the blood. About 30% of patients develop thrombotic complications, usually affecting the brain or heart. Hepatic vein thrombosis, giving rise to the Budd-Chiari syndrome (Chapter 16), is an uncommon but grave complication. Minor hemorrhages (e.g., epistaxis and bleeding from gums) are common, and life-threatening hemorrhages occur in 5% to 10% of patients. In those receiving no treatment, death occurs from vascular complications within months after diagnosis; however, if the red cell mass is maintained at near normal levels by phlebotomies, the median survival is around 10 years. Prolonged survival with treatment has revealed that PCV tends to evolve to a "spent phase," during which the clinical and anatomic features of primary myelofibrosis develop. After an average interval of 10 years, 15% to 20% of tumors undergo such a transformation. This transition is marked by creeping fibrosis in the bone marrow and a shift of hematopoiesis to the spleen, which enlarges markedly. Transformation to a "blast crisis" identical to AML also occurs but much less frequently than in CML

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Thrombocytopenia risks of and for

Back 135

characterized by spontaneous bleeding, a prolonged bleeding time, and a normal PT and PTT . Drug-induced: alcohol, thiazides, cytotoxic drugs. Infections: measles, HIV infection

Front 136

Atelectasis –

Back 136

1. incomplete expansion of the lung or a portion of the lung. 2. airlessness or collapse of a lung that had once been expanded. 3. absence of air in a normally air-filled space such as the middle ear.

Front 137

Dyspnea

Back 137

– breathlessness or shortness of breath; difficult and labored respiration.

Front 138

Hemoptysis

Back 138

– expectoration of blood or of blood-stained sputum.

Front 139

Asthma

Back 139

– bronchospasm and airway inflammation and edema; inflammation can be triggered by hypersensitivity response to antigen or inflammatory response to irritants, exertion, cold air, and infections.

Front 140

Pleurisy

Back 140

– inflammation of the pleura; symptom is stabbing chest pain with coughing or breathing.

Front 141

COPD

Back 141

– chronic obstruction pulmonary disease; a mixture of asthma, chronic bronchitis and emphysema.

Front 142

Chronic bronchitis

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– mucosal inflammation with mucous gland hyperplasia and mucus hypersecretion; daily productive cough for 3 months in two consecutive years; common in cigarette smokers.

Front 143

Obstructive lung disease

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– decreased expiratory flow due to increased airway resistance (airway narrowing) and/or decreased outflow pressure due to loss of lung elastic recoil.

Front 144

Emphysema

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– due to increased production of proteases that destroy the elastin in the alveolar walls causing decreased elastic recoil of the lung and loss of alveolar surface area; common in cigarette smokers

Front 145

Chronic Restrictive Pulmonary Dz

Back 145

gradual onset of a nonproductive cough and progressive dyspnea. On physical examination, most individuals with IPF have characteristic "dry" or "Velcro"-like crackles during inspiration. Cyanosis, cor pulmonale, and peripheral edema may develop in the later stages of the disease. Surgical lung biopsy remains the gold standard for diagnosing IPF and for excluding other causes of pulmonary fibrosis. Unfortunately, the progress of IPF is relentless despite therapy, and the mean survival is 3 years or less. Lung transplantation is the only definitive therapy available. Loss of Lung Volume due to inhalation of Fibrosing agents the lung loses elasticity

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Cystic Fibrosis

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Two processes are crucial and intertwined in the pathogenesis of bronchiectasis: obstruction and chronic persistent infection. Either of these two processes may come first. Normal clearance mechanisms are hampered by obstruction, so secondary infection soon follows; conversely, chronic infection in time causes damage to bronchial walls, leading to weakening and dilation. This is caused by the abnormally viscid mucus

Front 147

cor pulmonale

Back 147

or pulmonary heart disease is enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs. There are several mechanisms leading to pulmonary hypertension and cor pulmonale: Pulmonary, vasoconstriction, Anatomic changes in vascularization, Increased blood viscosity, Idiopathic or primary pulmonary hypertension

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Pulmonary Embolus

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is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). Usually this is due to embolism of a thrombus (blood clot) from the deep veins in the legs, a process termed venous thromboembolism. A small proportion is due to the embolization of air, fat or amniotic fluid.

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Pneumonia and Consolidation

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Consolidation is a clinical term for solidification into a firm, dense mass. It is more specifically used in reference to a region of lung tissue that, normally compressible, has filled with liquid,[1] a condition marked by induration[2] (swelling or hardening of normally soft tissue) of a normally aerated lung. Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that contains liquid instead of gas. This consolidation is patchy in bronchopneumonia involving multiple lobes and Lobar it fills generally from the bottom up.

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Lung cancer number 1 killer

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Carcinoma of the lung: Carcinomas of the lung are silent, insidious lesions that more often than not have spread so as to be unresectable before they produce symptoms. In some instances, chronic cough and expectoration call attention to still localized, resectable disease. By the time hoarseness, chest pain, superior vena caval syndrome, pericardial or pleural effusion, or persistent segmental atelectasis or pneumonitis makes its appearance, the prognosis is grim. Too often, the tumor presents with symptoms emanating from metastatic spread to the brain (mental or neurologic changes), liver (hepatomegaly), or bones (pain). Although the adrenals may be nearly obliterated by metastatic disease, adrenal insufficiency (Addison disease) is uncommon because islands of cortical cells sufficient to maintain adrenal function usually persist.

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Aphthous Ulcers (Canker Sores)

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These lesions are extremely common, small (usually <5 mm in diameter), painful, shallow ulcers. Characteristically, they take the form of rounded, superficial erosions, often covered with a gray-white exudate and having an erythematous rim. The lesions appear singly or in groups on the nonkeratinized oral mucosa, particularly the soft palate, buccolabial mucosa, floor of the mouth, and lateral borders of the tongue. They are more common in the first 2 decades of life and are often triggered by stress, fever, ingestion of certain foods, and activation of inflammatory bowel disease. In patients who are not immunosuppressed or do not have known viral infection such as with herpesvirus, an autoimmune basis is suspected. The canker sores are self-limited and usually resolve within a few weeks, but they may recur in the same or a different location in the oral cavity. Herpesvirus Infection, Herpetic stomatitis is an extremely common infection caused by herpes simplex virus (HSV) type 1. The pathogen is transmitted from person to person, most often by kissing; by middle life over three-fourths of the population have been infected. In most adults the primary infection is asymptomatic, but the virus persists in a dormant state within ganglia about the mouth (e.g., trigeminal ganglia). With reactivation of the virus (which may be caused by fever, sun or cold exposure, respiratory tract infection, trauma), solitary or multiple small (<5 mm in diameter) vesicles containing clear fluid appear. They occur most often on the lips or about the nasal orifices and are well known as cold sores or fever blisters. They soon rupture, leaving shallow, painful ulcers that heal within a few weeks, but recurrences are common.

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leukoplakia

Back 152

refers to a whitish, well-defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis. The lesions are of unknown cause except that there is a strong association with the use of tobacco, particularly pipe smoking and smokeless tobacco Oral leukoplakia is an important finding because 3% to 25% (depending somewhat on location) undergo transformation to squamous cell carcinoma (see Fig. 15-3A). It is impossible to distinguish the innocent lesion from the ominous one on visual inspection. The transformation rate is greatest with lip and tongue lesions and lowest with those on the floor of the mouth. Those lesions that display significant dysplasia on microscopic examination have a greater probability of cancerous transformation.

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Acute otitis externa and otitis media

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"acute otitis externa is predominantly a microbial infection, occurs rather suddenly, rapidly worsens, and becomes very painful and alarming. The ear canal has an abundant nerve supply, so the pain is often severe enough to interfere with sleep. Wax in the ear can combine with the swelling of the canal skin and any associated pus to block the canal and dampen hearing to varying degrees, creating a temporary conductive hearing loss. In more severe or untreated cases, the infection can spread to the soft tissues of the face that surround the adjacent parotid gland and the jaw joint, making chewing painful. Acute otitis media (AOM) is most often purely viral and self-limited, as is its usual accompanying viral URI (upper respiratory infection). There is congestion of the ears and perhaps mild discomfort and popping, but the symptoms resolve with the underlying URI. 1st phase - exudative inflammation lasting 1-2 days, fever, rigors, meningism (occasionally in children), severe pain (worse at night), muffled noise in ear, deafness, sensitive mastoid process. 2nd phase - resistance and demarcation lasting 3-8 days. Pus and middle ear exudate discharge spontaneously and afterwards pain and fever begin to decrease. This phase can be shortened with topical therapy. 3rd phase - healing phase lasting 2-4 weeks. Aural discharge dries up and hearing becomes normal.

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Serous Otitis Media

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Otitis media with effusion (OME), also called serous or secretory otitis media (SOM), is simply a collection of fluid that occurs within the middle ear space as a result of the negative pressure produced by altered Eustachian tube function. This can occur purely from a viral URI, with no pain or bacterial infection, or it can precede and/or follow acute bacterial otitis media. Fluid in the middle ear sometimes causes conductive hearing impairment, but only when it interferes with the normal vibration of the eardrum by sound waves.

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Meniere's Dz

Back 155

Ménière's often begins with one symptom, and gradually progresses. However, not all symptoms must be present for a doctor to make a diagnosis of the disease.[5] Several symptoms at once is more conclusive than different symptoms at separate times.[6] is a disorder of the inner ear that can affect hearing and balance to a varying degree. It is characterized by episodes of vertigo and tinnitus and progressive hearing loss, usually in one ear.

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Otitis Externa

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– is infection of the ear canal, typically by bacteria. Symptoms include itching, pain, and discharge.

Front 157

Acute Otitis Media

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– is a bacterial or viral infection of the middle ear, usually accompanying a URI. Symptoms include otalgia (earache), often with systemic symptoms (fever, nausea, vomiting, diarrhea), especially in the very young.

Front 158

Serous Otitis Media

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– is an effusion in the middle ear resulting from incomplete resolution of acute otitis media or obstruction of the eustachian tube without infection. Symptoms include hearing loss and a sense of fullness or pressure in the ear.

Front 159

Tinnitus

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– is a noise in the ears; it is experienced by 10 to 15% of the population. Subjective tinnitus is perception of sound in the absence of an acoustic stimulus and is heard only by the patient. Objective tinnitus results from noise generated by vascular tissue near the ear and, in some cases, is heard by the examiner.

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Rhinitis

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– is inflammation of the nasal mucous membrane, with resultant nasal congestion, rhinorrhea, and variable associated symptoms depending on etiology (eg, itching, sneezing, purulence, anosmia, ozena).

Front 161

Sinusitis

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– is inflammation of the paranasal sinuses due to viral, bacterial, or fungal infections or allergic reactions. Symptoms include nasal obstruction and congestion, purulent rhinorrhea, cough, facial pain, malaise, and sometimes fever.

Front 162

Pharyngitis

Back 162

– is pain in the posterior pharynx, with or without swallowing. Pain can be severe; many patients refuse oral intake.

Front 163

Epiglottitis

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– is a rapidly progressive bacterial infection of the epiglottis and surrounding tissues that may lead to sudden respiratory obstruction and death. Symptoms include severe sore throat, dysphagia, high fever, drooling, and inspiratory stridor.

Front 164

Laryngitis

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– is inflammation of the larynx, usually due to a virus or overuse. The result is acute change in the voice, with decreased volume and hoarseness.

Front 165

Meniere’s Disease

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is characterized by severe vertigo, hearing loss and tinnitus.

Front 166

Polyuria

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– is increased urination due to increased intake, osmotic diuresis (concentrated excessive urine output, decreased renal tubular response to ADH (anti-diuretic hormone)

Front 167

Oliguria

Back 167

– is decreased urination due to decreased renal perfusion, obstruction or renal disease. Oliguria can result in renal failure if not treated.

Front 168

Anuria

Back 168

– is a lack of urination due to renal failure or complete obstruction.

Front 169

Nocturia

Back 169

– is increased night urination due to urine retention from obstruction, renal disease, or heart failure.

Front 170

Dysuria

Back 170

– is painful urination due to irritation or inflammation of the bladder or urethra

Front 171

Hematuria

Back 171

– is blood in the urine due to renal or bladder disease, tumor, calculi (stones) or bladder infection.

Front 172

Proteinuria

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– is protein in the urine due to glomerular basement membrane damage

Front 173

Azotemia

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Azotemia refers to an elevation of blood urea nitrogen and creatinine levels and is largely related to a decreased glomerular filtration rate (GFR). Azotemia is produced by many renal disorders, but it also arises from extrarenal disorders. Prerenal azotemia is encountered when there is hypoperfusion of the kidneys, which decreases GFR in the absence of parenchymal damage. Postrenal azotemia can result when urine flow is obstructed below the level of the kidney. Relief of the obstruction is followed by correction of the azotemia

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Chronic and Acute renal failure

Back 174

"Acute renal failure is dominated by oliguria or anuria (no urine flow), with recent onset of azotemia. It can result from glomerular injury (such as crescentic glomerulonephritis), interstitial injury, vascular injury (such as thrombotic microangiopathy), or acute tubular necrosis.

Front 175

nephrotic syndrome

Back 175

The __________ refers to a clinical complex that includes the following: (1) massive proteinuria, with daily protein loss in the urine of 3.5 gm or more in adults; (2) hypoalbuminemia, with plasma albumin levels less than 3 gm/dL; (3) generalized edema, the most obvious clinical manifestation; and (4) hyperlipidemia and lipiduria. At the onset there is little or no azotemia, hematuria, or hypertension. Kidneys affected by nephrotic syndrome have small pores in the podocytes, large enough to permit proteinuria (and subsequently hypoalbuminemia, because some of the protein albumin has gone from the blood to the urine) but not large enough to allow cells through (hence no hematuria). By contrast, in nephritic syndrome, RBCs pass through the pores, causing hematuria.

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Chronic Glomerular vs Acute Pyelonephritis

Back 176

"By the time chronic GN is discovered, the glomerular changes are so far advanced that it is difficult to discern the nature of the original lesion. It probably represents the end stage of a variety of entities, prominent among which are the CrGNs, FSGS, MN, IgA nephropathy, and MPGN. It has been estimated that perhaps 20% of cases arise with no history of symptomatic renal disease. Although chronic GN may develop at any age, it is usually first noted in young and middle-aged adults. Acute pyelonehritis Urinary obstruction, either congenital or acquiredInstrumentation of the urinary tract, most commonly catheterizationVesicoureteral reflux. Increased VUR contributes to the risk of developing pyelonephritis.Pregnancy. 4% to 6% of pregnant women develop bacteriuria sometime during pregnancy, and 20% to 40% of these eventually develop symptomatic urinary infection if not treated.Patient's sex and age. After the first year of life (when congenital anomalies in males commonly become evident) and as far as around age 40 years, infections are much more frequent in females. With increasing age, the incidence in males rises as a result of the development of prostatic hyperplasia and frequent instrumentation.Preexisting renal lesions, causing intrarenal scarring and obstructionDiabetes mellitus, in which acute pyelonephritis is caused by increased susceptibility to infection and neurogenic bladder dysfunctionImmunosuppression and immunodeficiency.

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Strep and kidney dz

Back 177

Streptococcal tonsillitis is important to recognize and treat early, because of its potential to develop peritonsillar abscesses ("quinsy") or result in post-streptococcal glomerulonephritis and acute rheumatic fever.

Front 178

Kidney Dz and diabetes

Back 178

Benign nephrosclerosis, the term used for the renal changes in benign hypertension, is always associated with hyaline arteriolosclerosis. Some degree of benign nephrosclerosis, albeit mild, is present at autopsy in many persons older than 60 years of age. The frequency and severity of the lesions are increased at any age, This renal lesion alone rarely causes severe damage to the kidney except in susceptible populations, such as African Americans, where it may lead to uremia and death. However, all persons with this lesion usually show some functional impairment, such as loss of concentrating ability or a variably diminished GFR. A mild degree of proteinuria is a frequent finding.

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renal artery stenosis

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This renal lesion alone rarely causes severe damage to the kidney except in susceptible populations, such as African Americans, where it may lead to uremia and death. However, all persons with this lesion usually show some functional impairment, such as loss of concentrating ability or a variably diminished GFR. A mild degree of proteinuria is a frequent finding

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renal stones

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Stones may be present without producing either symptoms or significant renal damage. This is particularly true with large stones lodged in the renal pelvis. Smaller stones may pass into the ureter, producing a typical intense pain known as renal or ureteral colic, characterized by paroxysms of flank pain radiating toward the groin. Often at this time there is gross hematuria. The clinical significance of stones lies in their capacity to obstruct urine flow or to produce sufficient trauma to cause ulceration and bleeding. In either case, they predispose the sufferer to bacterial infection. Fortunately, in most cases the diagnosis is readily made radiologically.

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BPH

Back 181

"benign enlargement (hyperplasia) of the prostate gland 1. sx of bladder outlet obstruction, 2. urinary frequency and urgency, 3. nocturia, 4. hesitancy and intermittency with decreased force and size of stream of urine, 5. terminal dribbling, sense of incomplete emptying, 6. overflow incontinence, 7. possible complete urinary retention, 8. enlarged, rubbery prostate, a. if tender - prostatitis, b. if hard and/or nodular - carcinoma

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Prostatis

Back 182

inflammation of the prostate gland 1. urinary frequency and urgency, 2. dysuria - burning pain on urination, 3. hesitancy, dribbling, 4. nocturia, 5. high fever, chills, 6. perineal and low back pain, 7. possibly hematuria, 8. tender, boggy prostate, 9. may become chronic,10. chronic nonbacterial prostatitis is common, Acute prostatitis is characterized by the presence of an acute, neutrophilic inflammatory infiltrate, congestion, and stromal edema. Neutrophils are initially most conspicuous within the prostatic glands. As the infection progresses, the inflammatory infiltrate destroys glandular epithelium and extends into the surrounding stroma, resulting in the formation of microabscesses. Grossly visible abscesses are uncommon but can develop with extensive tissue destruction, e.g. in diabetic patients. The histologic features of chronic prostatitis are nonspecific in most cases and include a variable amount of lymphoid infiltrate, evidence of glandular injury, and, frequently, concomitant acute inflammatory changes. Evidence of tissue destruction and fibroblastic proliferation, along with the presence of other inflammatory cells, such as neutrophils,

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varicocele

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an abnormal enlargement of the veinthat is in the scrotum draining the testicles. The testicular blood vessels originate in the abdomen and course down through the inguinal canal as part of the spermatic cord on their way to the testis. Upward flow of blood in the veins is ensured by small one-way valves that prevent backflow. Defective valves, or compression of the vein by a nearby structure, can cause dilatation of the veins near the testis

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testicular cancer

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Testicular tumors are the most common cause of painless testicular enlargement. They occur with increased frequency in undescended testis and in males with gonadal dysgenesis.Germ cells are the source of 95% of testicular tumors, and the remainder arise from Sertoli or Leydig cells. Germ cell tumors may be composed of one histologic pattern (60% of cases) or mixed patterns (40%).They are often preceded by in situ lesions.The most common single histologic patterns of testicular tumors are seminoma, embryonal carcinoma, yolk sac tumors, choriocarcinoma, and teratoma. Mixed tumors conatain more than one element, most commonly embryonal carcinoma, teratoma, and yolk sac tumors.Clinically testicular tumors can be divided into two groups: seminomas and nonseminomatous tumors. Seminomas remain confined to the testis for a long time and spread mainly to para-aortic nodes-rarely to distant sites. Nonseminomatous tumors tend to spread earlier both by lymphatics and blood vessels.hCG is produced by syncytiotrophoblasts and is always elevated in choriocarcinomas and in those seminomas that have syncytiotrophoblasts. AFP is made by yolk sac cells and is elevated in yolk sac tumors. Most nonseminomatous tumors have mixed patterns and hence elevation of both hCG and AFP.

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testicular torsion

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In ___________ the spermatic cord that provides the blood supply to a testicle is twisted, cutting off the blood supply, often causing orchialgia. Prolonged testicular torsion will result in the death of the testicle and surrounding tissues. It is also believed that torsion occurring during fetal development can lead to the so-called neonatal torsion or vanishing testis, and is one of the causes of an infant being born with monorchism (one testicle).

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Hiatal Hernia

Back 186

separation of the diaphragmatic crura and widening of the space between the muscular crura and the esophageal wall permits a dilated segment of the stomach to protrude above the diaphragm.

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GERD

Back 187

"65. Gastroesophageal reflux disease (GERD) occurs when the esophageal-gastric sphincter is incompetent leading to reflux of the gastric contents into the esophagus. It can lead to:

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Peptic ulcer

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"Chronic gastritis and peptic ulcers are mostly caused by helicobacter pylori infection that: induces an inflammatory and immune response, secretes enzymes and toxins, enhances acid secretion, impairs bicarbonate, Ulcers are also caused by NSAIDS that inhibit prostaglandin secretion resulting in increased acid secretion and decreased bicarbonate and mucin (a glycoprotein found in mucus) production and inhibition of healing.

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Hemorrhoids

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are varicosities of the anal and perianal sub mucosal venous plexuses.

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diarrhea:

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"Types of __________. Watery diarrhea 3 times a day. Secretory – occurs when small and large intestines secrete more electrolytes and water than they absorb. Usually caused by infectious organisms or enterotoxins (rotavirus, E. coli). Osmotic – unabsorbable, water-soluble solutes (i.e., antacids, lactulose, lactose) retain water in the intestinal lumen. Exudative or inflammatory – mucosal inflammation resulting in output of plasma, serum proteins, blood and mucus. Usually caused by infectious organisms that damage intestinal mucosa and transmitted person-to-person or through contaminated water or food.

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Constipation

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Chronic ________ can be due to hypothyroid, hypercalcemia, IBS, neurological disorders, tumors, low fiber diet, lack of exercise, lack of fluids and laxative abuse.

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Bowel infarct

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Risks gangrene, bowel perforation, peritonitis, sepsis and death Ischemic bowel injury is most common in the later years of life. With the transmural lesions, there is the sudden onset of abdominal pain, often out of proportion to the physical signs. Sometimes the pain is accompanied by bloody diarrhea. The onset of pain tends to be more sudden with mesenteric embolism than with arterial or venous thrombosis. Because this condition may progress to shock and vascular collapse within hours, the diagnosis must be made promptly

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Crohn’s Disease

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_______ is an inflammatory bowel disease marked by patchy areas of full-thickness inflammation anywhere in the gastrointestinal track, from the mouth to the anus. It frequently involves the terminal ileum of the small intestine or the proximal large intestine and may be responsible for abdominal pain, diarrhea, malabsorption, fistula formation between the intestines and other organs and bloody stools. It is characterized by mucosal damage of the bowel, fissures of the bowel with formation of fistulae (an abnormal tube-like passage from a normal cavity/tube to a free surface or another cavity) and abscesses due to exaggerated and destructive mucosal immune response. It is most common in the second and third decades of life.

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Ulcerative Colitis

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________ is an inflammatory bowel disease marked pathologically by continuous inflammation of the intestinal mucosa, which typically involves the anus, rectum, and distal colon, and sometimes affects the entire large intestine. It is characterized by edema, bleeding and ulceration of the colon mucosa. The disease is associated with an increased incidence of colorectal carcinoma.

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Diverticulosis

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The treatment of this condition merits brief mention, because it bears on its pathogenesis. A high-fiber diet is recommended on the theory that the increased stool bulk reduces the exaggerated peristalsis. Whether a high-fiber diet prevents disease progression or protects against superimposed diverticulitis is unclear, but the diet itself is a source of discomfort

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Colorectal Carcinoma: Risk Factors

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(1) a low content of unabsorbable vegetable fiber, (2) a corresponding high content of refined carbohydrates, (3) a high fat content (as from meat), and (4) decreased intake of protective micronutrients such as vitamins A, C, and E. It is theorized that reduced fiber content leads to decreased stool bulk, increased fecal retention in the bowel, and an altered bacterial flora of the intestine. When colorectal cancer is found in a young person, preexisting ulcerative colitis or one of the polyposis syndromes must be suspected. In addition, individuals with hereditary nonpolyposis colorectal cancer syndrome (HNPCC, also known as Lynch syndrome), caused by germ-line mutations of DNA mismatch repair genes, are at a high risk of developing colorectal cancers.

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Colorectal Carcinoma: Clinical presentation

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Colorectal cancers remain asymptomatic for years; symptoms develop insidiously and frequently have been present for months, sometimes years, before diagnosis. Cecal and right colonic cancers most often are called to clinical attention by the appearance of fatigue, weakness, and iron deficiency anemia. Left-sided lesions may produce occult bleeding, changes in bowel habit, or crampy left lower quadrant discomfort. Although anemia in females may arise from gynecologic causes, it is a clinical maxim that iron deficiency anemia in an older man means gastrointestinal cancer until proved otherwise. All colorectal tumors spread by direct extension into adjacent structures and by metastasis through the lymphatics and blood vessels. In order of preference, the favored sites for metastasis are the regional lymph nodes, liver, lungs, and bones, followed by many other sites including the serosal membrane of the peritoneal cavity. In general, the disease spreads beyond the range of curative surgery in 25% to 30% of patients. Carcinomas of the anal region are locally invasive and metastasize to regional lymph nodes and distant sites. Almost 80% of malignant tumors of the anal canal are squamous cell carcinomas.Tumors in the proximal colon tend to grow as polypoid, exophytic masses that extend along one wall of the capacious cecum and ascending colon (Fig. 15-41). Obstruction is uncommon. When carcinomas in the distal colon are discovered, they tend to be annular, encircling lesions that produce so-called napkin-ring constrictions of the bowel and narrowing of the lumen (Fig. 15-42); the margins of the napkin ring are classically heaped up. Both forms of neoplasm directly

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Colorectal Carcinoma: US CA Morbidity

Back 198

15% of all cancer-related deaths in the United States.

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Baseline Colonoscopy

Back 199

the general recommendation for a baseline colonoscopy is beginning at age 50 and thereafter every three to five years. Or with a family history 10 years prior to the youngest diagnosed family member.

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IBS: Clinical Presentation and Pathophysiology

Back 200

Irritable Bowel Syndrome is a condition marked by abdominal pain, disturbances of evacuation, bloating and abdominal distention and the passage of mucus in stools. It can be diarrhea predominate, constipation predominate or mixed diarrhea and constipation. It occurs when the bowel muscle is hyper reactive or hypo reactive and presents with hypersensitivity to intraluminal distention of the bowel. Women to men ratio is 3:1.

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Jaundice (icteric)

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"Jaundice is the retention of bilirubin (end product of heme degradation) resulting in yellow skin and sclerae. It is caused by increased bilirubin production, impaired uptake or conjugation or decreased excretion of bilirubin (orange or yellow pigment in bile derived from the hemoglobin of red blood cells that have completed their life span).

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jaundice (icteric)

Back 202

Spleen Lysis the RBC(Hemoglobin and bilivirden) which is converted into indirect bilirubin and released into the bloodstream bound to albumin. The liver takes up the bilirubin but not the albumin converted it into conjugated bilirubin which is released with the bile into the Duodenum.

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Hepatic Failure Clinical Presentation

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characterized by jaundice, low albumin, high blood ammonia & estrogen levels, bleeding due to decreased production of clotting factors and encephalopathy. the clinical signs of hepatic failure occurring in individuals with chronic liver disease are much the same. Jaundice is an almost invariable finding. Impaired hepatic synthesis and secretion of albumin leads to hypoalbuminemia, which predisposes to peripheral edema.

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cirrhosis

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is scarring of the liver and poor liver function as a result of chronic liver disease. is a disruption of liver structure by chronic hepatocellular death, ineffective hepatocellular regeneration and fibrosis. Clinical symptoms of the disease result from loss of functioning liver cells and increased resistance to blood flow through the liver (portal hypertension) Portal hypertension is increased resistance to portal blood flow (caused by an obstruction of the flow of blood through the liver) with ascites (collection of fluid in the abdomen), hemorrhoids, esophageal varices (twisted or tortuous enlargements of veins) and splenomegaly.

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Cirrhosis from Alcohol and fatty Liver disease

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Chronic alcohol consumption has a variety of adverse effects (Chapter 8). Of great impact, however, are the three distinctive, albeit overlapping, forms of alcoholic liver disease: (1) hepatic steatosis (fatty liver), (2) alcoholic hepatitis, and (3) cirrhosis, collectively referred to as alcoholic liver disease (Fig. 16-14). Ninety to 100% of heavy drinkers develop fatty liver (steatosis), and of those, 10% to 35% develop alcoholic hepatitis. However, only 8% to 20% of chronic alcoholics develop cirrhosis. Steatosis and alcoholic hepatitis may develop independently, and thus, they do not necessarily represent a continuum of changes.

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Hepatitis and Hepatocellular carcinoma

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HCC is highest 85% in areas with high levels of hep B HEPATITIS Lleads to DNA dammage Heptocellular carcinoma is linked with hepatitis B & C infections and alcoholic liver disease. A malignant growth made up of liver epithelial cells that tend to infiltrate the surrounding tissues and give rise to metastases. Liver cancer.

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Cholelithiasis

Back 207

Gallstones: Cholesterol, bilirubin and Calcium salts. Can block the common bile duct and be painful

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Hep A

Back 208

Hepatitis A is transmitted by a fecal-oral route and is benign and self-limited (it does not produce a carrier state).

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Hep B

Back 209

"is transmitted by blood, sexual contact and birth. It can be acute or chronic. It has a carrier state and predisposes a person to hepatocellular carcinoma. It can be diagnosed with antibody titers.

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Hep c

Back 210

is transmitted mainly by blood. It has a high rate of persistent chronic infection and has a carrier state.

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Cholecystitis Pathophysiology

Back 211

From gall stones Pain is in the Right Upper Quadrant and can radiate to the right shoulder due to diaphragmatic irritation.

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Pancreatitis

Back 212

Acute pancreatitis occurs due to pancreatic duct obstruction or direct injury to pancreatic acinar cells (group of secretory cells surrounding a cavity) and results in autodigestion of the pancreas.

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Insulin

Back 213

Insulin promotes glucose formation into glycogen and into fatty acids in the liver, and inhibits liver gluconeogenesis. Glycogen – the storage form of glucose found in the liver and muscles. Glycogen plays a role in controlling blood sugar levels. Gluconeogenesis – is the process of making glucose (sugar) from its own breakdown products or from the breakdown products of lipids (fats) or proteins. Gluconeogenesis occurs mainly in cells of the liver or kidney. Fatty acids – lipids, (organic compounds with limited solubility in water), that can be directly utilized as a source of energy by most body cells. Promotes glucose uptake in Muscle cells. Insulin promotes glucose transport into fat cells and the formation of triglycerides. Triglycerides – lipids carried through the bloodstream to tissues. Most of the body’s fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. Insulin promotes uptake of amino acids into cells and promotes the formation of DNA, RNA, and the transcription of RNA to form proteins. Amino acids – the building blocks of proteins. DNA – the material inside the nucleus of cells that carries genetic information. The scientific name for DNA is deoxyribonucleic acid. RNA – a molecule similar to DNA, which helps in the process of decoding the genetic information carried by DNA. RNA Transcription – is the process through which a DNA sequence is enzymatically copied by an RNA polymerase to produce a complementary RNA. In the case of protein-encoding DNA, transcription is the beginning of the process that ultimately leads to the translation of the genetic code (via the mRNA intermediate) into a functional peptide or protein. Insulin secretion is stimulated by an increase in blood glucose levels and is stopped when blood glucose levels return to normal fasting levels.

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Hyperthyroid

Back 214

Graves everything is sped up and warm, enlarged thyroid eye protrusion, insomnia weight loss tremor, increased sweating, SOB. Increased thyroxin.

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Hypothyroid

Back 215

Poor muscle tone (muscle hypotonia), Fatigue, Cold intolerance, increased sensitivity to cold, Depression, Muscle cramps and joint pain, Carpal Tunnel Syndrome, Goitre, Thin, brittle fingernails, Thin, brittle hair, Paleness, Osteoporosis, Decreased sweating, Dry, itchy skin, Weight gain and water retention, Bradycardia

Front 216

Goiter

Back 216

enlargement of thyroid with improper function. Goiter is enlargement of the thyroid gland and can be caused by hyperplasia, thyroid tumors, Hashimoto thyroiditis or dietary iodine deficiency.

Front 217

Addisons Dz and Cushings Syndrome

Back 217

"Addison’s Disease is deficiency of adrenocortical hormones (cortisol and aldosterone), is due to atrophy of the adrenal cortex, and is characterized by weakness, fatigue, increased skin pigmentation, diarrhea, cold intolerance, dizziness, weight loss, and hypoglycemia. Adrenal crisis is triggered by stress or trauma with adrenocortical hormone deficiency, and can lead to vascular collapse and death, and can be precipitated by abrupt withdrawal of corticosteroids.

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Diabetes mellitus

Back 218

is a syndrome of disordered metabolism and inappropriate hyperglycemia (high blood sugar).

Front 219

DM1 and DM2

Back 219

"Type 1 diabetes mellitus is due to immune destruction of pancreatic islet beta cells resulting in deficiency of insulin secretion.

Front 220

Tissue effects of DM

Back 220

92. Peripheral tissue insulin resistance is made worse by high levels of fatty acids, obesity, inactivity, sustained hyperglycemia (higher than normal blood glucose level), and hyperinsulinemia (excess insulin levels). 93. Complications of diabetes mellitus are caused by glycosylation of proteins and collagen, and by the damage to cells by hyperglycemia with sorbitol accumulation of the cell. Glycosylation – the process of adding sugar units such as in the addition of glycan chains to proteins. Sorbitol – a sugar used to sweeten foods. 94. Macrovascular complications of diabetes mellitus include coronary artery disease, peripherial vascular disease, and cerebrovascular disease.Macrovascular – referring to the large blood vessels, Coronary artery disease – a build-up of fatty material in the wall of the coronary artery that causes narrowing of the artery. Peripherial vascular disease – diseases of blood vessels outside the heart and brain. It is often a narrowing of vessels that carry blood to leg and arm muscles, which may cause pain in exercising or walking. Cerebrovascular disease – disease involving the blood vessels supplying the brain, including cerebrovascular accident (CVA), also known as a stroke. 95. Microvascular complications of diabetes mellitus include damage to capillaries in the retina, kidney, and nerves causing retinopathy, nephropathy and peripheral neuropathy. Microvascular – referring to the small blood vessels. Retinopathy – non-inflammatory degenerative disease of the retina. Nephropathy – abnormal functioning of the kidney, Peripheral neuropathy – nerve damage (usually affecting the feet and legs) that causes pain, numbness, or a tingling feeling. 96. Diabetics have decreased immune function and decreased wound healing. 97. Tight control of blood glucose levels in diabetics can delay and slow complications.

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Metabolic syndrome

Back 221

Metabolic syndrome is characterized by hyperglycemia, hyperinsulinemia, dyslipidemia, hypertension, and truncal obesity.

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Dyslipidemia

Back 222

Dyslipidemia – excess levels of blood lipids such as cholesterol, high-density lipoproteins, triglycerides, etc.

Front 223

Hyperinsulinemia

Back 223

excess insulin levels, if chronic usually the result of insulin resistance.

Front 224

Hemoglobin A1c

Back 224

The HbA1c level is proportional to average blood glucose concentration over the previous four weeks to three months. is a form of hemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time. It is formed in a non-enzymatic pathway by hemoglobin's normal exposure to high plasma levels of glucose. Glycation of hemoglobin has been associated with cardiovascular disease, nephropathy, and retinopathy in diabetes mellitus. Monitoring the HbA1c in type-1 diabetic patients may improve treatment.

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Diabetes Insipidus

Back 225

is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine, with reduction of fluid intake having no effect on the latter. There are several different types of DI, each with a different cause. The most common type in humans is central DI, caused by a deficiency of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). The second common type of DI is nephrogenic diabetes insipidus, which is caused by an insensitivity of the kidneys to ADH. It can also be an iatrogenic artifact of drug use.

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Estrogen/Progesterone in Fibrocystic breast Dz

Back 226

Classified as nonproliferative cystic lesions or proliferative lesionsProliferative lesions include epithelial proliferations of ducts and lobules, with or without features of atypia, and adenosis, the proliferation of terminal ducts, sometimes associated with fibrosis (sclerosing adenosis).Atypical hyperplasia of ductular or lobular epithelium is associated with a five-fold increase in the risk of developing carcinoma; when associated with a family history of breast carcinoma, the risk is 10-fold. Excess estrogen makes the breast worse, Progesterone improves.

Front 227

PCOS

Back 227

Polycystic ovarian syndrome is characterized by insulin resistance and hyperinsulinemia causing increased production of testosterone and estrogen by the ovary resulting in anovulation, hirsutism, and obesity. a. Anovulation: The absence of ovulation. b. Hirsutism: Development of male-pattern hair growth in women. Caused chiefly by increased production of male sex hormones (androgens). Ovarian Cysts Follicle and luteal cysts in the ovaries are so commonplace as almost to constitute physiologic variants. These innocuous lesions originate in unruptured graafian follicles or in follicles that have ruptured and immediately sealed. Such cysts are often multiple and develop immediately subjacent to the serosal covering of the ovary. Usually, they are small (1-1.5 cm in diameter) and are filled with clear serous fluid. Occasionally, they achieve diameters of 4 to 5 cm and may thus become palpable masses and produce pelvic pain. When small they are lined by granulosa lining cells or luteal cells, but as the fluid accumulates, pressure may cause atrophy of these cells. Sometimes these cysts rupture, producing intraperitoneal bleeding and acute abdominal symptoms.

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Ovarian Carcinoma

Back 228

"Estimates indicate that 1 in 70 women will develop ovarian cancer in her lifetime. The ovaries are the ninth most common site of cancer in women, accounting for approximately 3% of all new cases, but ovarian cancer causes 5% of cancer deaths—more than any other cancer of the female reproductive system. Symptoms: Abdominal pressure, fullness, swelling or bloating,Urinary urgency, Pelvic discomfort or pain, Persistent indigestion, gas or nausea

Front 229

Ectopic Pregnancy

Back 229

"Abnormal vaginal bleeding, Amenorrhea, Breast tenderness

Front 230

Preeclampsia

Back 230

development of hypertension, accompanied by proteinuria and edema in the third trimester of pregnancy, is referred to as preeclampsia. This syndrome occurs in 5% to 10% of pregnancies, particularly with first pregnancies in women older than age 35 years. In those severely affected, convulsive seizures may appear, and the symptom complex is then termed eclampsia. By long historical precedent, preeclampsia and eclampsia have been referred to as toxemia of pregnancy.

Front 231

Spontaneous abortion

Back 231

miscarriage with bleeding

Front 232

Hyperemesis Gravidarum

Back 232

extreme morning sickness

Front 233

pituitary adenoma

Back 233

Prolactinomas: amenorrhea, galactorrhea, loss of libido, and infertilityGrowth hormone (somatotroph cell) adenomas: gigantism (children), acromegaly (adults), impaired glucose tolerance, and diabetes mellitusCorticotroph cell adenomas: Cushing syndrome, hyperpigmentationAll pituitary adenomas, particularly nonfunctioning adenomas, may be associated with mass effects and hypopituitarism. Pituitary adenomas can cause visual disturbances or increased intracranial pressure due to enlargement of the pituitary.

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carcinoma of the breast

Back 234

Risk factors include delayed child bearing, long duration between menarche and menopause, atypical proliferative lesions, and family history of breast cancer in a first-degree relative, particularly if the disease was multifocal or premenopausal.Only 5% to 10% of all breast cancers are related to inherited mutations; the majority are in the BRCA1 and BRCA2 genes, less commonly in p53, PTEN or ATM genes.Ductal carcinoma in situ (DCIS) is a precursor to invasive ductal carcinoma and is typically found on mammographic examination as calcifications or as a mass.

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Acute mastitis

Back 235

develops when bacteria gain access to the breast tissue through the ducts; when there is inspissation of secretions; through fissures in the nipples, which usually develop during the early weeks of nursing; or from various forms of dermatitis involving the nipple. pain and tenderness in the involved areas

Front 236

gynecomastia

Back 236

enlargement of the male breast

Front 237

Cervical Intraepithelial Neoplasia (CIN) and Squamous Cell Carcinoma

Back 237

The cervical epithelial changes included within the term CIN begin with mild dysplasia, called CIN I or flat condyloma. This lesion is characterized by koilocytotic changes mostly in the superficial layers of the epithelium. Koilocytosis, as you will recall from the earlier discussion of condylomata acuminata, is composed of nuclear hyperchromasia and angulation with perinuclear vacuolization produced by cytopathic effect of HPV

Front 238

endometriosis

Back 238

endometrial glands and stroma in a location outside the endomyometrium. clinical manifestations of endometriosis depend on the distribution of the lesions. Extensive scarring of the oviducts and ovaries often produces discomfort in the lower abdominal quadrants and eventually causes sterility. Pain on defecation reflects rectal wall involvement, and dyspareunia (painful intercourse) and dysuria reflect involvement of the uterine and bladder serosa, respectively. In almost all cases, there is severe dysmenorrhea and pelvic pain as a result of intrapelvic bleeding and periuterine adhesions.

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uterine leiomyoma

Back 239

Benign tumors that arise from the smooth muscle cells in the myometrium. Leiomyosarcomas typically arise de novo from the mesenchymal cells of the myometrium, not from preexisting leiomyomas. They are almost always solitary tumors, in contradistinction to the frequently multiple leiomyomas. Leiomyoma, or uterine fibroid tumors are benign tumors of the myometrium (smooth muscle of the uterine wall) that can cause dysmenorrhea, excessive menstrual bleeding, and pressure symptoms.

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Chlamydia

Back 240

Chlamydia is a common sexually transmitted disease (STD) caused by the bacterium, Chlamydia trachomatis, which can damage a woman's reproductive organs. Even though symptoms of chlamydia are usually mild or absent, serious complications that cause irreversible damage, including infertility, can occur "silently" before a woman ever recognizes a problem. Chlamydia also can cause discharge from the penis of an infected man. In women, the bacteria initially infect the cervix and the urethra (urine canal). Women who have symptoms might have an abnormal vaginal discharge or a burning sensation when urinating. If the infection spreads from the cervix to the fallopian tubes (tubes that carry fertilized eggs from the ovaries to the uterus), some women still have no signs or symptoms; others have lower abdominal pain, low back pain, nausea, fever, pain during intercourse, or bleeding between menstrual periods. Chlamydial infection of the cervix can spread to the rectum. Men with signs or symptoms might have a discharge from their penis or a burning sensation when urinating. Men might also have burning and itching around the opening of the penis. Pain and swelling in the testicles are uncommon.

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Bacterial vaginosis

Back 241

Bacterial vaginosis is vaginal condition that can produce vaginal discharge and results from an overgrowth of normal bacteria in the vagina. The symptoms of bacterial vaginosis are vaginal discharge and odor. Usually, there are no other symptoms.

Front 242

endometritis

Back 242

Inflammation of the endometrium is seen as part of the wider spectrum of pelvic inflammatory disease, a condition with consequences for the integrity of the fallopian tubes and subsequent fertility, as discussed below. Endometritis may be associated with retained products of conception subsequent to miscarriage or delivery, or a foreign body such as an intrauterine device. Retained tissue or foreign bodies act as a nidus for infection, frequently by flora ascending from the vaginal and intestinal tract, and removal of the offending tissue or foreign body typically results in resolution. Endometritis is classified as acute or chronic based on whether there is a predominant neutrophilic or lymphoplasmacytic response; however, components of both may be present in a given uterus. Generally the diagnosis of chronic endometritis requires the presence of plasma cells. Acute endometritis is frequently due to N. gonorrhoeae or C. trachomatis. Histologically, neutrophilic infiltrate in the superficial endometrium and glands coexists with a stromal lymphoplasmacytic infiltrate. Prominent lymphoid follicles are more commonly seen in chlamydial infection. By contrast, Mycoplasma infection has a subtle lymphocytic stromal infiltrate. All forms of endometritis may present with fever, abdominal pain, menstrual abnormalities, infertility and ectopic pregnancy due to damage to the fallopian tubes. Salpingitis may be acute and clinically evident, as with gonorrhea, or chronic and subclinical, as with Mycoplasma or Chlamydia.Salpingitis results in scarring of the fallopian tube lining, increasing the risk of tubal ectopic pregnancy. Extension beyond the fallopian tube gives rise to pelvic inflammatory disease

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Menopause

Back 243

is the point at which a female of menopausal age goes 12 months without her menses.

Front 244

Perimenopause

Back 244

can start in the late 30’s and early 40’s, and is characterized by an increase in estrogen and a decrease in progesterone. It may also result in menstrual changes, hot flashes, night sweats, anxiety and mood swings, insomnia, and palpitations.

Front 245

Postmenopause

Back 245

begins at menopause and can continue into older age. It is characterized by low estrogen and no progesterone levels, hot flashes, vaginal atrophy and bone loss.

Front 246

Cervical intraepithelial neoplasia (CIN)

Back 246

is a precancerous lesion of the cervix that is strongly associated with HPV infections and can progress to invasive cervical carcinoma. The screening test is a PAP smear (cell collection from the outer cervix and also the endocervix which is placed in a smear and screen for abnormal cells).

Front 247

Endometritis

Back 247

is an infection of the endometrium (lining of the uterus).

Front 248

Endometriosis

Back 248

is proliferation of endometrial tissue outside the uterus wheich causes severe dysmenorrhea, pelvic pain, and infertility.

Front 249

Menorrhagia

Back 249

is profuse and or prolonged bleeding during menses.

Front 250

Metrohorragia

Back 250

is irregular bleeding between menses.

Front 251

Dysfunctional uterine bleeding (DUB)

Back 251

often occurs due to excess estrogen and inadequate progesterone stimulation of the endometrium; common in puberty and perimenopause.

Front 252

Endometrial hyperplasia

Back 252

occurs due to excessive estrogen stimulation of the endometrium, and can lead to endometrial carcinoma.

Front 253

Endometrial cancer

Back 253

should be suspected in a postmenopausal women with bleeding.

Front 254

Dysmenorrhea

Back 254

is painful menstruation, and the primary form is caused by increased levels of the inflammatory prostaglandins.

Front 255

Carcinoma of the breast

Back 255

Carcinoma of the breast is the come common cause of cancer in US women. Risk factors include: older age, longer menstrual life, no pregnancies, family history, BRCA1 and BRCA2 (tumor suppressor genes) genetic mutations, exogenous estrogen exposure. Invasive ductal carcinoma is the most common type of breast cancer, and presents as a hard, palpable, fixed mass. Inflammatory carcinoma of the breast presents with swollen red breast without a mass.

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Cerebral Infarct

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cerebral infarction is the ischemic kind of stroke due to a disturbance in the blood vessels supplying blood to the brain. It can be atherothrombotic or embolic. Risk factors: atherosclerosis: Diabetes, Tobacco smoking, Hypercholesterolemia, hyperlipoproteinemia, High blood pressure, Obesity.

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CNS Tumors

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Tumors of the nervous system may arise from the cells of the coverings (meningiomas), from cells intrinsic to the brain (gliomas, neuronal tumors, choroid plexus tumors), or other cell populations within the skull (primary CNS lymphoma, germ-cell tumors), or they may spread from elsewhere in the body (metastases).Even low-grade or benign tumors can have a poor clinical outcome depending on where in the brain they occur.Glial tumors are broadly classified into astrocytomas, oligodendrogliomas, and ependymomas. Increasing tumor malignancy is associated with more cytologic anaplasia, increased cell density, necrosis, and mitotic activity. The most aggressive and poorly differentiated glial tumor is glioblastoma; it contains anaplastic astrocytes and shows striking vascular abnormalities.Metastatic spread of brain tumors to other regions of the body is rare, but the brain is not comparably protected against spread of tumors from elsewhere. Carcinomas are more commonly metastatic to the nervous system than lymphoid malignancies; sarcomas infrequently metastasize to the brain.

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Increased cranial pressure

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"Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:

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Migraine

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Migranes – a vasospasm in the arterioles of the brain, causing both vasodilation and vasoconstriction and affecting the arterial blood flow to the brain and scalp, activates an inflammation response and increases capillary permeability. The inflammation response includes leukocyte and platelet activation. When the arterioles dilate, nerves become compressed and it causes facial neurologic deficits such as auras, blindness, photophobia, sensitivity to smells, nausea and vomiting. Pain will occur with some migraine sufferers because of the increase of inflammatory mediators. It is unclear what mechanism causes the arterioles to vasospasm but there are several known triggers including red wine, chocolate, tomato sauce, nuts, dairy products, stress, lack of sleep and changes in serotonin and adrenaline levels.

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Tension Headache –

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a headache that lasts 30 minutes to 7 days, is non-pulsating, mild to moderate, bilateral, not aggravated by exertion or associated with N/V, or sensitivity to light, The pain can radiate from the neck, back, eyes, or other muscle groups in the body. Tension-type headaches account for nearly 90% of all headaches.

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Seizures –

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“an abnormal, unregulated electrical discharge that occurs within the brains cortical gray matter and transiently interrupts normal brain function.” It typically causes “altered awareness, abnormal sensations, involuntary movements or convulsions” (Merck manual p.1822). They can be secondary to fever, head trauma, cerebral edema or hypoxia, infection, tumors, metabolic disturbances , toxic drugs. They can also be primary or epilepsy when seizures are not related to reversible stressors.

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Cluster Headache

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Sharp pain behind the eyes, Regular timing

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Sinus Headache –

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Inflammation of the sinuses

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Cervical HA

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originate from disorders of the neck, including the anatomical structures innervated by the cervical roots C1–C3. Cervical headache is often precipitated by neck movement and/or sustained awkward head positioning. It is often accompanied by restricted cervical range of motion, ipsilateral neck, shoulder, or arm pain of a rather vague non-radicular nature or, occasionally, arm pain of a radicular nature.

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Insomnia

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"Insomnia – difficulty falling asleep or staying asleep. Can be caused by emotional disturbance, pain, respiratory problems, stimulant drugs, withdrawal of medications, poor sleep schedule, other sleep disorders. Also depression, anxiety and perimenopause may prevent someone from staying asleep.

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Sleep Apnea –

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when breathing stops during sleep for > 10 seconds, occurs > 20 times per hour causing hypoxia. Usually caused by upper airway obstruction, Muscle weakness, tiredness, memory issues, aches and pains

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Restless Legs Syndrome

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uncomfortable sensations when lying down to sleep that are relieved by movement

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CVA

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Cerebrovascular Accidents (CVA) – or strokes are disorders involving “sudden, focal interruption of cerebral blood flow, causing neurologic deficit.” They can be ischemic (80%), resulting from thrombosis or embolism, or hemorrhagic (20%), resulting from vascular rupture. Cause of CVAs (strokes) – most strokes (CVA) are due to ischemia and infarction caused by atherosclerosis with thrombi or emboli occluding an artery in the brain

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TIA

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TIA – a transient ischemic attack is an episode of non-traumatic focal loss of cerebra or visual function for <24 hours; TIAs are considered a precursor to stroke.

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Multiple sclerosis (MS)

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Multiple sclerosis (MS) is immune mediated demyelination in the CNS leading to failure of axonal function and neurological dysfunction. Symptoms include muscular weakness, numbness, visual disturbances, loss of bowel or bladder control, loss of sexual functions. Women are twice as likely to get the disease as men.

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Alzheimers

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143. Alzheimer’s is characterized by dementia (progressive memory impairment and cognitive deficits) and brain findings include neurofibrillary tangles, senile plaques, amyloid deposits.

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Parkinsons

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144. Parkinsons disease is progressive degeneration of the pigmented neurons of the substantia nigra that produce dopamine causing disruption of the dopaminergic pathways from the substantia nigra to the basal ganglia. is The result of this degeneration is disruption of motor function characterized by progressive rigidity, pill-rolling tremors and loss of voluntary movement.

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Peripheral Neuropathy

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145. List 4 characteristics of Peripheral Neuropathy and 4 differential diagnoses that can lead to it: Characteristics – sensory loss, muscle weakness and atrophy, decreased deep tendon reflexes, autonomic changes. Differential diagnoses: Acquired metabolic disorder such as Diabetes, renal failure, chronic liver disease, Nutritional deficiencies (B12, B6 and Vitamin E deficiency), Toxic exposure (i.e. heavy metal exposure, alcohol and poisons), Inflammatory conditioned (autoimmune and trauma), Trauma cut off all or part of the nerve supply to an area, avulsion

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Dermatitis

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There are many specific inflammatory dermatoses; they may be mediated by IgE antibodies (urticaria), antigen-specific T cells (eczema, erythema multiforme, and psoriasis), and trauma (lichen simplex chronicus).The histologic features can be grouped into patterns of inflammation such as interface dermatitis (e.g. lichen planus and erythema multiforme), superficial perivascular dermatitis, and panniculitis (inflammation in subcutaneous fat) that provide insight into the mechanism and the ability to organize the diseases into pathogenic categories.Careful clinical correlation is needed to diagnose specific skin diseases, since the features overlap within histologic pattern groups. Acute Eczematous Dermatitis (Eczema) produces a red, papulovesicular, oozing, crusted lesion. Can be due to a Type IV Hypersensitivity response to contact with antigen (Allergic Contact Dermatitis) or genetic susceptibility to environmental triggers (Atopic Dermatitis).

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Skin cancer

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"Squamous cell carcinoma – carcinoma that develops primarily from squamous cells (eg. On the skin, mouth, lungs, brinchi, esophagus or cervix)

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Macule

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a pigmented dermatological lesion that is flat and cannot be felt. The color may be brown, blue, red or hypopigmented.

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Papule

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a small, solid, raised portion of skin that does not contain pus. They generally occur in clusters.

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Plaque

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– a broad, raised area of skin that is broader than it is high.

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Vesicle

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– a small blister that is less than 0.5 centimeters in diameter.

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Pustule

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– a small collection of pus that is either in the epidermis or dermis layer. The pus is from the accumulation of inflammatory cells and liquid.

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lipoma

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are benign tumors of fat, and are the most common soft tissue tumors of adulthood. Most lipomas are solitary lesions; multiple lipomas usually suggest the presence of rare autosomal dominant syndromes. are soft, yellow, well-encapsulated masses of mature adipocytes; they can vary considerably in size. Histologically, they consist of mature white fat cells with no pleomorphism.

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osteoporosis

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Osteoporosis is a disease characterized by increased porosity of the skeleton resulting from reduced bone mass. It is associated with an increase in bone fragility and susceptibility to fractures. The clinical outcome of osteoporosis depends on which bones are involved. Thoracic and lumbar vertebral fractures are extremely common, and produce loss of height and various deformities, including kyphoscoliosis that can compromise respiratory function. Pulmonary embolism and pneumonia are common complications of fractures of the femoral neck, pelvis, or spine, and result in as many as 50,000 deaths annually. prevention and treatment begins with adequate dietary calcium intake, vitamin D supplementation, and a regular exercise regimen-starting before the age of 30-to increase the peak bone density. Calcium and vitamin D supplements later in life can also modestly reduce bone loss. osteoclast resorption is faster than osteoblast remodeling. Leading to compression. Primary osteoporosis is due to increased bone resorption that occurs with aging or with decreased estrogen levels at menopause. Estrogen helps to inhibit osteoclast formation. DEXA is the test to assess bone density.

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RA

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Rheumatoid Arthritis (RA) is an autoimmune inflammation disease of the joints that destroys articular cartilage and bone. It is characterized by symmetric arthritis of small joints, and presents with fever, malaise and joint pain and stiffness.

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OA

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131. Osteoarthritis (OA) is degeneration of articular cartilage with aging and wear and tear, inflammation is secondary to cartilage loss. It is characterized by joint stiffness and pain that is aggravated by use and may affect one or several joints, especially larger joints.

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Rickets

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The major function of the fat-soluble vitamin D is the maintenance of normal plasma levels of calcium and phosphorus. In this capacity, it is required for the prevention of bone diseases known as rickets (in children whose epiphyses have not already closed), osteomalacia (in adults), and hypocalcemic tetany. With respect to tetany, vitamin D maintains the correct concentration of ionized calcium in the extracellular fluid compartment required for normal neural excitation and relaxation of muscle.

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osteomyelitis

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Staph formally designates inflammation of the bone and marrow cavity, Osteomyelitis classically manifests as an acute systemic illness with malaise, fever, leukocytosis, and throbbing pain over the affected region. Symptoms can also be subtle with only unexplained fever, particularly in infants, or only localized pain in the adult. Diagnosis is suggested by characteristic radiologic findings: a destructive lytic focus surrounded by a sclerotic rim. In many untreated cases, blood cultures are positive, but biopsy and bone cultures are usually required to identify the pathogen. A combination of antibiotics and surgical drainage is usually curative, but up to a quarter of cases do not resolve and persist as chronic infections. Chronicity may develop when there is delay in diagnosis, extensive bone necrosis, abbreviated antibiotic therapy, inadequate surgical debridement, and/or weakened host defenses. Besides occasional acute flare-ups, chronic osteomyelitis is also complicated by pathologic fracture, secondary amyloidosis, endocarditis, sepsis, development of squamous cell carcinoma in the sinus tract, and rarely osteosarcoma.

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infectious arthritis

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infectious arthritis is a joint infection that evolves over hours or days. The infection resides in synovial or periarticular tissues and is usually bacterial—in younger adults, frequently Neisseria gonorrhoeae. However, nongonococcal bacterial infections can also occur and can rapidly destroy joint structures. Symptoms include rapid onset of pain, effusion, and restriction of both active and passive range of motion, usually within a single joint. Diagnosis requires synovial fluid analysis and culture. Treatment is IV antibiotics and drainage of pus from joints.

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Osteosarcoma

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Osteosarcoma is a bone-producing malignant mesenchymal tumor. Outside of myeloma and lymphoma, osteosarcoma is the most common primary malignant tumor of bone, accounting for approximately 20% of primary bone cancers; a little over 2000 cases are diagnosed annually in the United States. Osteosarcomas occur in all age groups but some 75% of patients are younger than age 20, with a second peak occuring in the elderly, usually with other conditions, including Paget disease, bone infarcts, and prior irradiation. Men are more commonly affected than women (1.6 : 1)

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Gout

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Gout is caused by the accumulation of uric acid crystals in the joint tissue causing severe local pain in the affected joint.

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Myasthenia gravis

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is an autoimmune disorder of the neuromuscular junction characterized by muscle weakness. Typically, weakness is first noticed in the extraocular muscles; drooping eyelids (ptosis) and double vision (diplopia) cause the patient to seek medical attention. The generalized muscle weakness can fluctuate dramatically, with alterations occurring over the course of days, hours, or even minutes. Repetitive electrophysiologic stimulation typically elicits diminishing muscle strength, and patients show marked improvement after administration of anticholinesterase agents-the latter presumably by increasing the levels of ACh in the neuromuscular synapse; both maneuvers are diagnostically useful. Sensory and autonomic functions are not affected in myasthenia gravis. Respiratory compromise was a major cause of mortality in the past; 95% of patients now survive more than 5 years after diagnosis because of improved treatment (anticholinesterase drugs, prednisone, plasmapheresis, and thymic resection), as well as ventilatory support.

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Muscular Dystrophy

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The muscular dystrophies are a heterogeneous group of inherited disorders, often presenting in childhood, that are characterized by progressive degeneration of muscle fibers leading to muscle weakness and wasting. Histologically, in advanced cases muscle fibers are replaced by fibrofatty tissue. This histologic feature distinguishes dystrophies from myopathies (described later), which also present with muscle weakness.

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rhabdomyosarcoma

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Rhabdomyosarcoma is the most common soft tissue sarcoma of childhood and adolescence, usually appearing before age 20. Interestingly, they occur most commonly in the head and neck or genitourinary tract, usually at sites where there is little, if any, skeletal muscle as a normal constituent. aggressive neoplasms treated with a combination of surgery, chemotherapy, and radiation. Location and the histologic variant of the tumor influence survival; embryonal, pleomorphic, and alveolar variants have progressively worsening prognoses. The malignancy is curable in almost two-thirds of children, but adults do much more poorly.

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Muscle Atrophy

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loss of muscle innervation causes atrophy of the associated fibers. As discussed in detail below, neurogenic atrophy is characterized by involvement of both fiber types and by clustering of myofiers into small groups. Simple disuse (e.g., prolonged bed rest, immobilization to allow healing of a bone fracture, etc.) can also cause profound atrophy. Deprived of their normal enervation, skeletal fibers undergo progressive atrophy. It is important to recall that loss of a single neuron will affect all muscle fibers in a motor unit, so that the atrophy tends to be scattered over the field. However, following re-enervation, adjacent intact neurons send out sprouts to engage the neuromuscular junction of the previously de-enervated fibers. Once the new connection is established these fibers assume the type of the innervating neuron