Pathophysiology - week 2

Plasma cells, which can then produce antibodies.

Cascade is the sequential activation of plasma protein systems.

They provide enzymes for digestion, usable metabolites, and antibacterial factors.

Antigens and lymphocytes.

They contain microbial properties that can kill or inhibit growth and identify and neutralize pathogens.

Continuation of cellular differentiation, scar tissue formation, and scar remodelling over time.

They are cell-mediated and do not involve antibodies, involving cytotoxic T lymphocytes or lymphokine-producing Th1 and Th17 cells.

T-Helper Lymphocytes help other cells by driving the maturation of B and T cells and facilitate the interaction between APCs and immunocompetent lymphocytes.

Immediate hypersensitivity reactions occur within minutes to a few hours after exposure to an antigen, often caused by antibodies, such as in anaphylaxis.

Memory T cells are formed during an immune response and help the immune system respond more rapidly upon subsequent exposures to the same antigen.

Antigens are substances that trigger an immune response, usually foreign substances that bind to antibodies or antigen receptors on B and T cells.

Clonal selection is the process by which lymphocytes with specific antigen receptors proliferate after antigen processing and presentation.

With the specificity of a key into a lock, maintained by noncovalent chemical interactions.

To prevent the mixing of blood, which could introduce Rh+ antigens to the Rh- mother and lead to an immune response in future pregnancies.

APCs show antigens to B cells with the help of T helper cells, leading B cells to mature into plasma cells that produce IgE.

Ability to survive inside the macrophage, toxins, chemicals, particulate matter, or physical irritants.

Wounds that heal under conditions of minimal tissue loss, often using glue or sutures, with a small gap to fill.

Secretions such as saliva, tears, earwax, sweat, and mucus derived from epithelial cells.

A systematic process that responds to cellular or tissue damage, whether the tissue is septic or sterile.

Serum sickness and Raynaud Phenomenon.

Fibrinous exudate is thick and clotted, indicating more advanced, active inflammation. It contains fibrin and can impair healing.

Immediate hypersensitivity occurs within minutes to a few hours and is usually caused by antibodies, while delayed hypersensitivity takes several hours to appear and is at maximal severity days after re-exposure, usually caused by cells.

Because the body may attack the donated erythrocytes due to different antigens expressed on different types of blood.

An array of microorganisms that colonize the body’s surfaces, unique to particular locations like the skin or GI tract.

Granulation (new tissue growth), epithelialization (epithelial growth), and requires fibroblast proliferation which produces collagen and creates wound contraction.

Redness, heat, swelling, pain, and loss of function due to increased blood flow and fluid accumulation.

Local manifestations result from vascular changes and corresponding leakages of circulating components into the tissue, including heating, swelling, redness, pain, and exudating fluids.

Superantigens are crucial for recognizing how some pathogens cause widespread interruption of the immune system. They bypass the normal antigen presenting site, binding the variable portion of the TCR and the MHC class II molecules outside of their antigen presentation sites, activating a large population of T-lymphocytes regardless of antigen specificity, leading to an overwhelming immune response.

The fibrinolytic system activates plasminogen in the blood to form the enzyme plasmin, which degrades fibrin and limits the size of the clot.

Granulocytes are cells packed with granules that contain histamine, cytokines, and chemotaxis factors.

Immune complexes.

The skin provides a tough shield that prevents microorganisms from entering the body.

Wounds that require a lot more tissue replacement, usually too large or complex for sutures, healing happens from the bottom up with granulation tissue and epithelial cells growing over it.

Ischemia, excessive bleeding, excessive fibrin deposition, and predisposing disorders such as diabetes and obesity.

IgA is the most dominant immunoglobulin in secretions, and it prevents adhesions.

Environmental antigens cause atypical immunological responses in genetically predisposed individuals, often involving allergens that are too big to be phagocytized or are protected by a nonallergenic coat.

T-regulatory cells regulate the immune response to avoid attacking 'self' and maintain tolerance to prevent autoimmune reactions.

It forms a fibrinous meshwork that localizes microorganisms and foreign bodies, preventing their spread.

The antigen that is recognized by an antibody.

As we age, the number of migrating T cells declines, impacting our ability to respond to new infections and manage a proper immune response. The thymus also shrinks, decreasing thymus hormones and impairing T cell maturation. The number of antibodies decreases, resulting in a weaker immune response.

When T and B cells interact with an antigen.

If a woman is Rh- and is going to have an Rh+ baby, the medical team must ensure that the blood does not mix during delivery to prevent the mother from developing an immune response to the Rh+ antigens.

Fibrin is an insoluble protein that facilitates healing.

Mast cells degranulate and release substances like histamine.

Antibodies bind to a cell/tissue and mark them for destruction, and complement proteins break them down.

Mast cells and basophils release histamine and other mediators that contribute to inflammation.

Sloughing off cells, coughing and sneezing, flushing (urine), vomiting, mucus, and cilia.

Inducible, specific, long-lived, and has memory.

It can alter the normal microbiome, decreasing its protective activity, and lead to an overgrowth of pathogenic microorganisms.

Lymphoid tissues that protect the external surfaces of the body include secretory glands that guard mucosal surfaces.

A keloid scar is a type of scar that results from excessive collagen synthesis.

Contracture is the impaired contraction of a wound.

Th1 cells help in developing cell-mediated immunity, while Th2 cells help in developing humoral immunity by activating B cells and producing cytokines for antibody production.

The body will develop a response to the Rh+ antigens, which can cause complications in subsequent pregnancies due to an immune response.

Specific cells or tissues.

Skin, lining of the GI, genitourinary, and respiratory tracts.

Microorganisms that can cause disease if there is a break in the individual’s defenses.

Complement system, clotting system, and kinin system.

Serous exudate is watery, clear or yellow, and indicates early inflammation.

Staphylococcus aureus.

Clonal diversity is the process by which all necessary receptor specificities are produced, resulting in naïve but immunocompetent T and B cells, primarily occurring in the fetus.

Histamines, cytokines, and chemotaxis factors.

To clear parasites and modulate the immune response.

Immunoglobulin M (IgM).

Four polypeptide chains: two light and two heavy chains, with a hinge region for flexibility.

Human to human via vectors and usually ingested.

Toxin damage or inflammatory/immune response.

C1 esterase inhibitor inhibits the complement system, clotting system, and kinin pathway components.

Innate immunity is the built-in immunity comprised of physical, mechanical, and biochemical barriers.

Inflammation phase, proliferative phase, and remodelling and maturation phase.

Occurs in tissues with a blood supply, activated rapidly, depends on both cellular and chemical components, and is non-specific.

Vasodilation increases the amount of blood flow to the affected area.

Humoral immunity involves antibodies circulating in the blood to defend against extracellular microbes and microbial toxins.

Superantigens induce an excessive production of cytokines, causing fever, low blood pressure, and potential shock.

T-Cytotoxic (Tc) Cells destroy cancer cells or cells infected with viruses by using perforin, granzymes, or direct receptor interactions to induce apoptosis.

The fetus has sufficient IgM but deficient IgG and IgA responses. Maternal antibodies provide protection within the fetal circulation and during the first months of life. Infants are immunologically immature at birth with deficiencies in antibody production, phagocytic activity, and complement activity, making them more vulnerable as their immune system develops.

Allergic rhinitis, gastrointestinal issues, and systemic anaphylaxis.

The kinin system activates and assists inflammatory cells.

1. Cell destruction by antibodies and complement, 2. Cell destruction through phagocytosis, 3. Soluble antigen deposits on tissues, 4. Antibody-dependent cell-mediated cytotoxicity, 5. Target cell malfunction.

They engulf and destroy targeted cells.

Mucus traps and facilitates the removal of pathogens.

Adaptive immunity destroys infectious microorganisms that are resistant to inflammation and provides long-term, highly effective protection against future exposure to the same microorganism.

By competing with pathogens for nutrients and blocking their attachment to the epithelium.

To prevent and limit infection, control the inflammatory process, initiate adaptive immune response, and initiate healing by removing dead cells and tissues.

Inadequate nutrients, medications, and tobacco.

Dehiscence is the separation of wound edges.

Forms a fibrinous meshwork at an injured or inflamed site to prevent the spread of infection, localize microorganisms and foreign bodies, form a clot that stops bleeding, and provide a framework for repair and healing.

Plasma proteins, formed in the liver, are integral to the inflammatory response and begin as inactive proenzymes that start a cascade, ensuring a rapid and effective reaction.

Autoimmune diseases originate from an initiating event in a genetically predisposed individual, characterized by the loss of self-tolerance to self-antigens, leading to widespread inflammation. Example: Systemic Lupus Erythematosus.

Fever is caused by exogenous and endogenous pyrogens that act directly on the hypothalamus, creating a less favorable environment for pathogens.

They cause local vasodilation and increase permeability.

Coagulation, infiltration of wound healing cells, and angiogenesis.

WBC adherence to the inner walls of the vessels and migration through the vessels, facilitated by increased vascular permeability.

Infection, tissue necrosis, ischemia, trauma, physical or chemical injury, foreign bodies, and immune reactions.

Cytotoxic T cells directly kill cells, while T helper cells recruit phagocytic cells.

Cell-mediated immunity involves effector T cells circulating in the blood and tissues to defend against intracellular pathogens and cancer cells.

Haemorrhagic exudate contains blood and indicates bleeding at the site of inflammation.

The primary immune response is the first exposure to an antigen, with a latent period or lag phase. After 5-7 days, an IgM antibody for a specific antigen is detected, followed by an IgG response that is equal or slightly less.

Immunogens are a subset of antigens that induce an immune response, including the production and activation of antibodies, T and B cells. All immunogens are antigens, but not all antigens are immunogens.

In the loose connective tissue close to blood vessels in the skin, digestive lining, and respiratory tract.

Basophils are found in blood and function similarly to mast cells.

In bodily secretions like tears, mucus, and breast milk, forming a protective barrier to prevent pathogen adherence.

Responsible for most of the biological functions of antibodies.

Through inhibitory and activating receptors.

Deleterious effects of hypersensitivity to environmental (exogenous) antigens.

Attachment, penetration, biosynthesis, and maturation.

Phagocytosis is a process by which a cell ingests and disposes of foreign materials, clearing out infection and maintaining healthy tissues.

Margination, or pavementing, is the adherence of leukocytes to endothelial cells, causing them to move to the edge of the vessel walls.

The primary kinin is bradykinin, which causes vasodilation, smooth muscle contractions (bronchoconstriction), induces pain, and increases vascular permeability.

Soluble antigens can stick to tissues, leading to their destruction by complement and neutrophil granules.

Dense infiltration of lymphocytes and macrophages, granuloma formation, epithelioid cell formation, giant cell formation (fusion of macrophages), and pertulient.

It can be commensal (each benefits without affecting one another) or mutualistic (benefits both organisms).

They are formed in the circulation and later deposited in vessel walls or extravascular tissues, leading to a large release of lysosomal enzymes.

Antibodies present in tears, sweat, saliva, mucus, and breast milk include IgA, IgG, and IgM.

Produces biologically activated fragments that recruit phagocytes, activate mast cells, and destroy pathogens through reactions.

Superantigens bind the variable portion of the TCR and the MHC class II molecules outside of their antigen presentation sites, activating a large population of T-lymphocytes regardless of antigen specificity.

By producing factors that can destroy pathogens directly or activate/increase the activity of other components of the inflammatory and adaptive immune response.

Alloimmune diseases occur when the immune system of one individual produces an immunological reaction against tissues of another individual. Example: Pregnant women and Rh blood groups, or incompatible blood transfusions.

The secondary immune response occurs upon subsequent exposures to an antigen. It is more rapid and produces larger amounts of antibodies due to memory cells that require less further differentiation. IgM may be transiently produced, but IgG is produced in considerably greater numbers.

Haptens are small molecules that become immunogenic after combining with larger molecules that function as carriers.

Chronic inflammation lasts two weeks or longer, often related to an unsuccessful acute inflammatory response, characterized by pus formation, suppuration, and incomplete wound healing.

IgG3.

Effector T cells (T helper or T cytotoxic), which can orchestrate and kill infected cells.

They recognize and eliminate cells infected with viruses and cancers.

The immune system responds to dead toxoids, remembering the antigen without actually getting the cells.

Purulent exudate is thick, opaque, green or yellow pus, indicating an active bacterial infection.

Passive immunity involves the transfer of antibodies, such as from mother to infant or through antibody transfer.

The antigen-binding site on the antibody.

Responding to polysaccharide antigens.

By limiting overreactions.

Combined deficiencies.

Adequate B and T cells but defective cooperation and inability to produce MHC class I and II.

Thymic aplasia or hypoplasia and diminished parathyroid development, resulting in T cell deficiency and calcium deficiency.

Macrophages.

Disturbance in the immunological tolerance of self-antigen.

Biological preparations of weakened (attenuated) or dead pathogens.

Inhibition of host cell DNA, RNA, or protein synthesis; disruption of lysosomal membranes; transformation to cancer cells; promotion of secondary bacterial infection; fusion of infected adjacent cells; alteration of antigenic properties.

The ability to spread from one individual to others and cause disease.

The ability of an agent to produce disease.

Diapedesis is the emigration of cells through endothelial junctions, allowing white blood cells to pass through endothelial cells.

The ability to produce soluble toxins or endotoxins.

Chemokines are synthesized by cells like macrophages, fibroblasts, and endothelial cells in response to proinflammatory cytokines, inducing chemotaxis to promote phagocytosis and wound healing.

Active immunity is the immunity gained after exposure to an antigen, either naturally or via immunization.

Different types of blood group antigens must be compatible to avoid immunological reactions during blood transfusions.

It can be caused by another illness and is more common than primary immunodeficiency.

They get to the site quickly and release mediators.

Functions as a B-cell antigen receptor and is involved in the initiation and regulation of B cell activation.

By phagocytes and T lymphocytes.

Immunoglobulin G (IgG), accounting for 80-85% of immunoglobulins.

IgE mediated, against environmental antigens, with IgE binding to Fc receptors on the surface of mast cells, leading to histamine release from mast cell degranulation.

Overprescribing, not finishing antibiotics, lack of compliance with therapeutic regimen, and overuse.

They adapt through wide temperature variation, digesting keratin, and surviving in low oxygen conditions.

Cytokines are intracellular signaling molecules that help activate the inflammatory response.

Systemic manifestations include fever, leucocytosis (increased numbers of circulating leukocytes), and increased plasma protein synthesis.

Fighting bacterial infections.

Macrophages, dendritic cells, and B cells.

Development of unusual or recurrent severe infections, T cell deficiencies (viral, fungal, yeast, and atypical microorganisms), B cell and phagocyte deficiencies (microorganisms requiring opsonization), and complement deficiencies.

Degranulation and synthesis.

Unicellular protozoa to large worms, including flukes, nematodes, and tapeworms.

Neutralization, agglutination, and precipitation.

Activating components of the innate immune response such as complement and phagocytes.

In peripheral organs and skin; they capture and process antigens and interact with T lymphocytes to generate an acquired immune response.

The ability to infect a host cell.

Failure of the immune mechanism of self-defense.

Phagocytosis promotes the inflammatory process by producing adhesion molecules, facilitating margination (adherence to leukocytes and endothelial cells), and enabling diapedesis (emigration of cells through endothelial junctions).

The route by which a pathogenic microorganism infects the host.

A phagosome is a vesicle that contains the ingested target, formed with its own membrane.

The actual growth and multiplication of bacteria in the blood, leading to severe complications.

Leucocytosis is an increased number of circulating leukocytes and occurs during systemic inflammation.

Acute-phase reactants are proteins synthesized by liver cells during inflammation, commonly measured by laboratory tests such as fibrinogen, erythrocyte sedimentation rate, and C-reactive protein.

They attract cells to the site of inflammation.

Mostly in the blood.

Two identical antigen-binding fragments (Fabs) and one crystallizable fragment (Fc).

Malaria, amoebae, and flagellates.

They engulf dead cells and release cytokines that promote tissue repair.

It provides passive immunity from the placenta.

A permissive host cell.

Dermatophytes are fungi that invade the skin, hair, or nails, causing diseases known as tineas (e.g., tinea capitis, tinea pedis, tinea cruris).

Communicability, infectivity, extent of tissue damage, and virulence.

The steps of phagocytosis are adherence, engulfment, phagosome formation, fusion with lysosomal granules, and destruction of the target.

The cell wall structure and what antibiotics the bacteria will respond to.

Failure of the body's defense mechanisms, often caused by Gram-negative bacteria.

It is important in mucosal immunity.

Few detectable lymphocytes, underdeveloped thymus, and absent or reduced IgM and IgA levels.

Depressed IgM production with bleeding and platelet disorders due to platelet formation.

Neutralization, agglutination, and precipitation.

Activation of components of the innate immune response such as complement and phagocytes.

Histamine release from mast cell degranulation leads to sneezing and itching through H1 and H2 receptors, and antihistamines work by blocking histamine from binding.

A genetic anomaly resulting from a single gene defect, generally not inherited, and may appear early or late in life.

Measles and pertussis.

By damaging tissue or disrupting bodily functions.

Interleukins (ILs) are produced primarily by macrophages and lymphocytes in response to stimulation.

Specialized glycoproteins produced by B cells.

It mediates many common allergic responses by causing allergy symptoms when binding to allergens.

Allergy, autoimmunity, and alloimmunity.

They provide long-lasting protective immune responses without causing disease in a healthy recipient.

Gradual changes in antigens responsible for protection against influenza, including antigenic drift (minor change) and antigenic shift (major change).

The capacity or severity of a pathogen to cause severe disease.

During engulfment, the cells extend a membrane around the target and ingest it.

The presence of bacteria in the blood without being pathogenic.

A particular set of immunoglobulins known to have specificity for a particular antigen.

Activated by tissue destruction and inflammation, they interact with the coagulation cascade to stop bleeding.

By initiating an inflammatory reaction to attract eosinophils.

Immune reaction to tissues of another individual, such as in organ transplants or blood transfusions.

Genetic mutation, inactivation of antibiotics, modification of target molecules, and increasing active efflux of antibiotics.

Attachment to cell surface, release of enzymes, escaping phagocytes, and spreading through lymph and blood to tissues.

During adherence, immune cells find the target and stick to its surface using receptors.

Toxins produced by Gram-negative bacteria that activate the inflammatory response and produce fevers.

Aerosol, infected blood, sexual contact, and vectors (e.g., birds, bugs).

Mycoses, which can be superficial, deep, or opportunistic.

Aerobic and anaerobic.

TNF-α is secreted by macrophages in response to PAMP and toll-like receptor recognition, inducing fever, increasing synthesis of inflammatory serum proteins, and causing muscle wasting and intravascular thrombosis at high levels.

Fungi are large microorganisms with thick, rigid cell walls without peptidoglycans. They reproduce by simple division or budding.

The ability of a pathogen to invade and multiply in the host.

A phagolysosome is formed by the fusion of a phagosome with lysosomal granules, containing enzymes that kill bacteria and digest debris.

Interferon (INF) protects against viral infections by being produced and released by virally infected host cells in response to viral double-stranded RNA, inducing an antiviral state in neighboring healthy cells.

Direct contact, inhalation, ingestion, and bites.

Enzymes that can damage the plasma membranes of host cells or inactivate enzymes critical to protein synthesis.

They activate the complement and clotting systems, leading to capillary permeability and potential cardiovascular shock.