Unit 2 Study Guide: Pathophysiology Overview

Innate immunity

defense mechanisms that are present at birth and provide the initial response to invasion and injury

Innate barriers

first line of defense at the body's surfaces; physical, mechanical, and biochemical barriers

Inflammatory response

second line of defense; activated to protect the body from further injury, fight infection, and promote healing

Adaptive immunity

third line of defense; induced through a slower and more specific process and targets particular invaders and diseased tissues for the purpose of eradicating them

Lysozyme

enzyme which attacks the cell walls of gram-positive bacteria

Antimicrobial peptides

substances that kill or inhibit the growth of disease-causing bacteria, fungi, and viruses

Normal microbiome

previously normal flora; array of microorganisms that colonize the body's surfaces; combination of bacteria and fungi unique to body location and individual

Opportunistic pathogens

harmless under normal circumstances but can cause disease in immunocompromised individuals

Phagocytes

cells capable of ingesting other things like bacteria; neutrophils and macrophages

Plasma protein systems

multiple proteins and enzymes present in the blood in inactive forms, that may be activated in cascade and lead to a protective biologic function

Opsonization

phagocytosis using opsonins that adhere the phagocyte to the target

Opsonins

coat the surface of bacteria increasing their susceptibility to phagocytosis

Pattern recognition receptors (PRRs)

receptors on innate immune cells that allow them to recognize infectious microorganisms and cellular damage

Pathogen-associated molecular patterns (PAMPs)

molecules expressed by infections agents

Damage-associated molecular patterns (DAMPs)

products of cellular damage

Cytokines

small signaling proteins

Chemokines

cytokines that are chemotactic

Interleukins

cytokines released by lymphocytes and macrophages to alter behavior of other cells

Interferons

cytokine that protect against viral infections and modulate the immune response

Leukotrienes

lipids that induce smooth muscle contraction and increased vascular permeability

Exudates

fluid that leaks out of blood vessels into nearby tissues; can be serous, fibrinous, purulent, or hemorrhagic

Resolution

wound healing with regeneration of original tissue; damage is minor enough to heal without a scar

Repair

wound healing with replacement of original tissue with fibrous tissue; scar replaces damaged tissue

Primary intention

healing with minimal tissue loss, wound edges are closely approximated, clean edges, and can be directly sutured or closed

Secondary intention

healing with more extensive tissue loss, wound edges are not approximated and the wound heals from the bottom up

Scar tissue

composed primarily of collagen, restores tissue integrity and strength

Humoral immunity

antibodies circulating in the blood and defending against extracellular antigens

Cellular immunity

effector T cells circulating in the blood and tissues to defend against intracellular pathogens and abnormal cells

Antigen (Ag)

molecule that can bind with antibodies or antigen receptors on B and T cells; may be CD marker or other chemical tag that is seen as self or foreign

Antigenicity

foreignness, size, chemical complexity, quantity

Immunogen

molecule that binds to receptors and will induce an immune response

Clonal selection

the processing of antigen for a specific immune response; refers to the activation and proliferation of a particular lymphocyte

Active natural immunity

exposure leads to immunity

Active acquired immunity

vaccination with prepared Ag

Passive natural immunity

maternal Abs protecting the fetus

Passive acquired immunity

injection/transplant of exogenous Ab

B-cells

Antibody production, MHC II molecules, mature into plasma cells; BCR

Major Histocompatibility Complex (MHC) molecules

Coded for by HLA (human leukocyte antigen) genes

MHC I

All nucleated cells, present endogenous antigens; react with CD8 cells only

MHC II

Macrophages and B-cells, present exogenous antigens; react with CD4 cells only

Antibodies (Abs)

B-cell proteins, aka Igs; highly specific for antigen; neutralize, opsonize, agglutinate, precipitate, activate complement

IgG

Most predominant, crosses placenta, main memory Ig

IgM

Pentamer, main Ig in initial exposure/rxn

IgA

Dimer, main secretory Ab

IgE

Mast cell activator in allergies and parasite infections

IgD

Ag receptor for B-cells

Antigen presenting cell (APC)

In this case a macrophage, presents Ag on an MHC II protein to the generic CD4 T-cell (or T-helper cell) that is specific for that Ag.

IL-1

Secreted by the APC to activate the T-helper cell which turns it into a precursor T-helper cell (Thp cell).

Thp cell

Secretes IL-2 to stimulate its own proliferation into many identical Thp cells (this is the process of clonal selection).

Th1 cell

Formed when the predominant local cytokine is IL-12, stimulates CMI.

Th2 cell

Formed when the predominant cytokine is IL-4, stimulates humoral immunity.

Th17 cell

Formed when the predominant cytokine is IL-6, stimulates inflammation.

Treg cell

Formed when the predominant cytokine is IL-2, down-regulates the immune system.

Allergy

hypersensitivity reaction against noninfectious environmental substance

Autoimmune

hypersensitivity reaction misdirected against the body's own cells

Alloimmune

hypersensitivity reaction directed against beneficial foreign tissues

Immune deficiency

failure of the immune system or inflammatory response; insufficient to protect the host against pathogens and abnormal or foreign cells

Anaphylaxis

most rapid and severe immediate hypersensitivity; generalized, rapidly evolving, multi-systemic allergic reaction

Type I (IgE-mediated)

Mast cells, IgE; allergies, asthma

Type II (Tissue-specific)

Macrophages, IgM, IgG, C*/ADCC; Graves, ABO/HDN

Type III (Immune complex)

Neutrophils, IgM, IgG, C*; SLE, serum/arthus

Type IV (Cell-mediated)

Macrophages, T-cells; poison ivy, graft rejection (HVGD & GVHD)

Primary (Congenital) Immune Deficiency

defects affect development of both B and T lymphocytes

Severe combined immunodeficiencies (SCID)

Few detectable lymphocytes; all types of infections are potentially fatal ('bubble boy'); new treatment for some forms of SCID, genetic engineering/CRISPR

Bare lymphocyte

Lack of MHC-I and MHC-II molecules, thus no Ag presentation; all types of infections are potentially fatal

Predominantly Antibody Deficiencies

defects in B-cell maturation or function; low levels of circulating antibodies to no circulating antibodies

IgA deficiency

Selective deficiency of IgA; most asymptomatic but can have history of recurrent GI/respiratory infections

Bruton agammaglobulinemia

No mature B-cells thus little or no Abs; recurrent bacterial infections

Phagocyte Defects

range from inadequate numbers of phagocytes to defects in phagocyte function

Chronic granulomatous disease (CGD)

defective phagocytes that cannot destroy bacteria; leads to recurrent bacterial infections

Complement Deficiencies

defects in the components of the complement system

C3 deficiency

Lack of C3/C3b impairing complement response; leads to recurrent bacterial infections

Secondary (Acquired) Immune Deficiency

develops in response to HIV infection; infects Th-cells (CD4), leads to combined B and T-cell immune failure

Acquired immunodeficiency syndrome (AIDS)

transmitted through blood products, IVDU, sexual intercourse, Mother to fetus (placenta/canal/milk); HIV is an RNA retrovirus that hijacks T-cells to make more viruses

Endogenous microorganisms

already present in the body and part of the normal microbiome

Exogenous microorganisms

transmitted from an external source

Transmission

how pathogens are passed from host to another individual

Direct transmission

direct contact with infected individual, body fluids, or animals

Indirect transmission

contact with infected materials, inhalation of droplets, ingestion of contaminated products, inoculation

Colonization

ability of a pathogenic microorganism to survive and multiply on or within the human environment

Invasion

ability of pathogens to cross surface barriers

Communicability

ability to spread from one individual to others and cause disease

Immunogenicity

ability to induce an immune response

Infectivity

ability to invade and multiply in the host

Mechanism of action (MOA)

how the microorganism damages tissue

Pathogenicity

ability to produce disease—success depends on communicability, infectivity, extent of tissue damage, and virulence

Portal of entry (POE)

route by which a microorganism infects the host

Toxigenicity

ability to produce soluble toxins or endotoxins, factors that greatly influence the degree of virulence

Virulence

capacity to cause severe disease

Tumor

mass of non-structured new cells, which have no known purpose in the physiological function of the body

Neoplasm

new growth of body's own cells

Cancer

diseases in which abnormal cells divide without control and can invade nearby tissues

Benign

non-cancerous

Malignant

cancerous

Metastasis

cells from the tumor seed out to other parts of the body and then grow into tumors themselves

Carcinoma

Epithelial cancer

Adenocarcinoma

Cancer of ductal or glandular epithelium

Squamous cell carcinoma

Malignant cancer of the skin, mouth, cervix, other

Carcinoma in situ

Malignant epithelial cancer that hasn't yet invaded adjacent tissues

Sarcoma

Connective tissue cancer