Term
| What determines whether regeneration or repair (fibrosis) will occur? |
|
Definition
| Cell type (Labile/stabile vs. permanent) and extracellular matrix damage (intact EM->regeneration, damaged EM->fibrosis). |
|
|
Term
| What is a permanent cell? |
|
Definition
| A cell that has lost the capacity to divide |
|
|
Term
|
Definition
| A cell that is constantly dividing and regenerating |
|
|
Term
|
Definition
| A cell that only divides when it is stimulated to do so |
|
|
Term
| What are multipotent Adult Progenitor Cells (MAPCs)? |
|
Definition
| Potential adult version of embryonic stem cells |
|
|
Term
| What cell type is the primary producer of extracellular matrix? |
|
Definition
|
|
Term
| Which cells are the first to migrate to the site of an injury? |
|
Definition
| Leukocytes (neutrophils and monocytes/macrophages) |
|
|
Term
| What is autocrine signalling? |
|
Definition
| A cell producing its own stimulus |
|
|
Term
| What is paracrine signalling? |
|
Definition
| A cell signalling a nearby cell |
|
|
Term
| What is endocrine signalling? |
|
Definition
| Signal molecules are dumped into the bloodstream and act on distant cells |
|
|
Term
| What is endocrine-like signalling? |
|
Definition
| Signals produced at the site of an injury find their way into the bloodstream and act on distant cells |
|
|
Term
| What is responsible for binding water in the extracellular matrix? |
|
Definition
|
|
Term
| What are the four main kinds of adaptation? |
|
Definition
| Hyperplasia, metaplasia, hypertrophy, atrophy |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What kinds of cells would use hyperplasia and which would use hypertrophy? |
|
Definition
| Permanent cells would use hypertrophy, and labile/stable cells would use hyperplasia |
|
|
Term
|
Definition
| Loss of cell size or reduction in cell number |
|
|
Term
|
Definition
| Substitution of one cell type for another |
|
|
Term
| What stimuli might induce hyperplasia? |
|
Definition
| Compensation/increased demand, chronic injury, or hormones (whether natural or pharmaceutical) |
|
|
Term
| What kind of responses might be expected in response to acid reflux disease? |
|
Definition
| A metaplastic shift to an acid-tolerant epithelial cell type |
|
|
Term
| What is the KEY to a metaplastic repsonse? |
|
Definition
| There MUST be pluripotent stem cells available |
|
|
Term
|
Definition
| A complete block of blood flow |
|
|
Term
| What is the amount (%) of ATP that must be maintained, below which injury results? |
|
Definition
| 10% of "normal" ATP amount |
|
|
Term
| What might one expect in cells suffering from an ischemia? |
|
Definition
| Build-up of lactic acid, low [ATP], low [glucose]/[O2], lowered pH, possible high [Na]/[Ca] |
|
|
Term
| What is the important reaction for making H2O2 damaging? |
|
Definition
| The fenton reaction (requires Fe), converting H2O2 to OH- |
|
|
Term
| What is the chemical used by neutrophils and macrophages to kill cells, and how is it formed? |
|
Definition
| OCl-, formed by MPO (Myeloperoxidase) |
|
|
Term
| How might the hydroxyl radical (OH-) damage DNA? |
|
Definition
| It introduces single-strand breaks and transversions |
|
|
Term
| How might the hydroxyl radical (OH-) damage protein? |
|
Definition
| It can attach itself to alophatic/aromatic amines, as well as abstracting Hydrogens |
|
|
Term
| What is the major target of ALL types of injury? |
|
Definition
|
|
Term
| If an individual has a non-functional alpha1-antitrypsin gene, what might we expect to be their pathological condition? |
|
Definition
| Premature/extended trypsin activation, autodigestive behavior, digestive system organ damage |
|
|
Term
| What are the two types of collagen used in fibrosis, and at which stage are they use? |
|
Definition
| Type III collagen used for provisional/"healing" extracellular matrix, type I collagen is used in a matured EM |
|
|
Term
| What are the primary types of cells in granulation tissue? |
|
Definition
| Fibroblasts and macrophages |
|
|
Term
| What is neovascularization? |
|
Definition
| Forming fully-fledged capillary beds in granulation tissue |
|
|
Term
| At best, a wound regains how much strength of the original tissue? |
|
Definition
|
|
Term
| What is the biggest factor that negatively affects healing? |
|
Definition
|
|
Term
|
Definition
| Overhealing/excessive repair components extending far beyond the original site of injury |
|
|
Term
| What kind of damage occurs from amyloid fibrils? (Mad cow disease) |
|
Definition
| Oxidative/nitrative damage |
|
|
Term
| What causes tatoos to last? |
|
Definition
| The ink is phagocytosed, and the residual macrophage bodies left behind has the ink incorporated into it |
|
|
Term
| What are the two kinds of cell death, and their overarching causes? |
|
Definition
| Apoptotic (physiological or pathological) and necrotic (pathological only) |
|
|
Term
| What happens to cell membranes in apoptotic and nectrotic cell death? |
|
Definition
| Necrotic death - cell enlargement and membrane ruptures; apoptotic death - cell reduction and intact membrane |
|
|
Term
| Which form of cell death causes inflammation and why? |
|
Definition
| Necrotic, since cell contents (which are natural inflammatory factors) are released |
|
|
Term
| What is the body's primary form of innate immunity? |
|
Definition
|
|
Term
| What are the major adaptive immunity cell types? |
|
Definition
| Lymphocytes (T, NK, and B cells) and plasma cells |
|
|
Term
| What immune cell types are inflammation-inducing? |
|
Definition
| Neutrophils, eosinophils, basophils, and mast cells |
|
|
Term
| What kind of a state are B cells in before they leave the bone marrow? |
|
Definition
|
|
Term
| All B cells start out expressing what immunoglobin molecule? |
|
Definition
|
|
Term
| Later on in their life, what kind of immunoglobin molecule(s) do B cells express? |
|
Definition
|
|
Term
| Which CD# cells bind which MHC# molecules? |
|
Definition
| CD4 bind MHC2, CD8 bind MHC1 |
|
|
Term
| The negative selection mediated by dendritic cells is for what purpose? |
|
Definition
| To get rid of a "too strong" self interaction |
|
|
Term
| What are the kind of professional antigen-presenting cells? |
|
Definition
| Monocytes, macrophages, dendritic cells, and B cells |
|
|
Term
| What is the result of a primary Ig deficiency? |
|
Definition
| The cell that is supposed to express it turns out non-functional |
|
|
Term
| What is the pathology of selective IgA deficiency? |
|
Definition
| IgA B cells produced, but no secreted IgA, mostly asymptomatic; high incidence of allergies |
|
|
Term
| What is the primary gene affected in SCID (Severe Combined Immunodeficiency)? |
|
Definition
| A mutation in a common gamma chain shared by many cytokine receptors |
|
|
Term
| What is the basic process of immune response? |
|
Definition
| 1) Dendritic cells present Ag to T cell in lymph node; 2) Activated T cells multiply, providing help to B cells or directly attacking; 3) Subset of activated T+B cells develop into memory cells |
|
|
Term
| What is the characteristic of IgE? |
|
Definition
|
|
Term
| What is the primary Ab used by the body? |
|
Definition
|
|
Term
| What type of Ab(s) are associated with Type I (allergic) hypersensitivity? |
|
Definition
|
|
Term
| What kind of cell is prominent in an acute infection? |
|
Definition
|
|
Term
| What kind of cell is prominent in a chronic infection? |
|
Definition
|
|
Term
| Higher-level organisms will not have this terminal sugar. |
|
Definition
|
|
Term
| What complement protein marks a microbe as foreign and needing destroyed by leukocytes/monocytes? |
|
Definition
|
|
Term
| What kinds of chemical eicosanoid signals are medically inhibited? |
|
Definition
| Phospholipases (by steroids), cyclooxygenase (aspirin), and leukotrienes (singulair), as well as other histamines |
|
|
Term
| The presence of immature B cells is indicative of what? |
|
Definition
| A severe inflammatory response |
|
|
Term
| In addition to causing various kinds of cell damage, ROS's can also function as what? |
|
Definition
| Signallers of inflammation |
|
|
Term
| What allows for local activation of leukocytes and what causes it? |
|
Definition
| "Rolling" - initial binding by P-selectin, slowing down by E-selectin, stopping and guiding by ICAM-1 and PECAM-1 |
|
|
Term
| What mediates neutrophil activation? |
|
Definition
| Cytokines, complement proteins, and pattern recognition |
|
|
Term
| What are some possible causes of chronic inflamation? |
|
Definition
| Viral infection, chronic bacterial infections, persistent injury, and autoimmune diseases |
|
|
Term
| What is a foreign body granuloma? |
|
Definition
| An attempt to isolate damaged areas within a tissue by phagocytosis of an indigestible particle |
|
|
Term
| A positive acid-fast stain is indicative of what? |
|
Definition
| Bacterial infection, very likely a mycobacterium. |
|
|
Term
| Inflammation works to do what? |
|
Definition
| Control and reverse damage to tissues |
|
|
Term
|
Definition
| Leakage into a body cavity |
|
|
Term
| What kinds of cells would be expected in pus? |
|
Definition
|
|
Term
| What is the cause of pus? |
|
Definition
| Increased vascular permeability and abundance of neutrophils |
|
|
Term
|
Definition
| Objective method of distinguishing disease |
|
|
Term
|
Definition
| A subjective method of distinguishing disease |
|
|
Term
| What is the diagnostic for cystic fibrosis (CF)? |
|
Definition
| 2 "abnormal" (>60mEq/L of chloride) sweat test results on 2 separate days |
|
|
Term
| What gene deletion accounts for ~70% of all CF cases? |
|
Definition
|
|
Term
| What is the etiology of CF? |
|
Definition
| Mucus dries out and cannot flow - provides a good environment for bacterial growth (error in cellular Ca excretion) |
|
|
Term
| What are the effects of chemokines? |
|
Definition
| Leukocyte chemotaxis and activation |
|
|
Term
| How can complement be activated? |
|
Definition
| Classical -> Ab-mediated, Lectin -> mannose-binding-lectin, Alternative -> C3b spontaneously binds antigen |
|
|
Term
| What are the outcomes of complement activation? |
|
Definition
| Formation of a membrane attack complex (MAC) in pathogen's membrane or phagocytosis of pathogen |
|
|
Term
| Explain phagocytosis and bacterial killing by neutrophils. |
|
Definition
| Phagocytosis by C3b recognition or Fc receptor (Ab constant region binding). Killing by ROS (OH- formed by fenton reaction) |
|
|
Term
| What is the etiology of a caseating granuloma? |
|
Definition
| Tuberculosis cells cannot be killed by neutrophils, so they are adsorbed by them and isolated until they "starve" to death - necrosis |
|
|
Term
| What are the two types of ECM and what are they composed of? |
|
Definition
| Basement membrane (type IV collagen, laminin as integrin ligand, PG structures, made for adherance); and interstitial (many kinds of collagen, strength and flexibility) |
|
|
Term
| What drives the difference between regeneration and scarring in the ECM? |
|
Definition
|
|
Term
| What cell types are recruited into sites and what is the general role of each? |
|
Definition
| Mast cells (acute inflammatory response), neutrophils/monocytes/macrophages (respond to complement, digest foreign particles), platelets (seal holes) and fibroblasts (begin fibrosis) |
|
|
Term
| What are the three main receptor types involved in repair? |
|
Definition
| Growth factor receptors, integrin receptors, and G-protein coupled receptors (chemokines) |
|
|
Term
| Explain how fibrosis occurs. |
|
Definition
| Activation of macrophages and lymphocytes, followed by cytokines, metalloproteinase activity, and growth factors; this would cause proliferation of fibrogenic cells, increased collagen synthesis, and decreased collagen degradation |
|
|
Term
| What kind of collagen would one expect to find in a keloid or hypertrophic scar and why? |
|
Definition
| Type III, since it is the immature collagen (excessive fibrosis = little collagen maturation) |
|
|
Term
| What is the function of IgA? |
|
Definition
| Secretory mucosal protection |
|
|
Term
| What is the function of IgD? |
|
Definition
|
|
Term
| What is the function of IgE? |
|
Definition
| Anti-protozoan activity, allergic response |
|
|
Term
| What is the function of IgG? |
|
Definition
| Bloodborne "protection" Ab - memory |
|
|
Term
| What is the function of IgM? |
|
Definition
| Antigen clearance - "workhorse" Ab |
|
|
Term
| What is the etiology of DiGeorge's disease? |
|
Definition
| No/little thymus (deletion on chromosome 22) |
|
|
Term
| What is the etiology of SCID? |
|
Definition
| Nonfunctional gamma chain of IL-2, no T cells, no functional B cells; both X-linked and autosomal |
|
|
Term
| What is hypersensitivity? |
|
Definition
| An immune response that results in injury to self cells/tissues |
|
|
Term
| What is type I hypersensitivity? |
|
Definition
| An allergic response to a presensitized antigen - B-cell/Ab mediated |
|
|
Term
| What is type II hypersensitivity? |
|
Definition
| Example of A-type blood to B-type recipient; usable cells, non-harmful, but reacted upon anyway - never had tolerance |
|
|
Term
| What is type III hypersensitivity? |
|
Definition
| Example of T1 diabetus - self cells seen as foreign and attacked - loss of tolerance |
|
|
Term
| What is type IV hypersensitivity? |
|
Definition
| Similar to type I, but T-cell mediated, resulting in a delayed reaction |
|
|
Term
|
Definition
| Systemic inflammatory response, culminating in shock as a result of the loss in blood pressure due to increased vasodilation because of histamine release |
|
|
Term
| What are the components of the disease process? |
|
Definition
| Etiology (why), pathogenesis (how), morphological changes (structural what), clinical significance (functional what) |
|
|
Term
| What are some etiological categories of cell stress? |
|
Definition
| Oxygen deprivation (ischemia), physical agents (ionizing radiation), chemical agents/drugs, infectious agents, immunological reactions, genetic alterations, and nutritional imbalance |
|
|
Term
| What are the outcomes of calcium flux? |
|
Definition
| Decreased ATP, membrane damage, nucleus chromatin damage |
|
|
Term
| What kinds of molecules do ROS target? |
|
Definition
| Lipids, DNA, alophatic/aromatic amine side chains, and amino acid backbones |
|
|
Term
| How might a decrease in cellular [O2] result in membrane damage? |
|
Definition
| Decreased phospholipid synthesis and repair, lipid breakdown, and protease activation (cytoskeletal damage) |
|
|
Term
| What is a hydropic change? |
|
Definition
| Swelling or shrinking of epithelial cells |
|
|
Term
| What is a lipofuscin granule? |
|
Definition
| Lipid-containing residue of lysosomal digestion |
|
|
Term
| What are the three kinds of apoptosis? |
|
Definition
| Ligand-induced, immunologic reactions, and mitochondrial permeability transition |
|
|
Term
| What kind of vascular changes occur with inflammation, and why? |
|
Definition
| At first vasoconstriction to isolate the site/allow accumulation of immune cells; then vasodilation and permeability to allow immune cells to move from the bloodstream to the interstitial fluid |
|
|
Term
| What kinds of chemical mediators induce vascular permeability? |
|
Definition
| Cell-derived (histamine, seratonin, prostaglandins, leukotrienes) and plasma-derived (Hageman factor, complement) |
|
|
Term
| How are prostaglandins and leukotrienes generated, and what do they do? |
|
Definition
| Generated by inflammatory/endothelial cells, prosta-fever, leuko-histamine response |
|
|
Term
| What are the effects of TNF and IL-1? |
|
Definition
| Master cytokines, activate the cytokine storm |
|
|
Term
| What is Hageman Factor and what does it do? |
|
Definition
| Clotting and kinin generation |
|
|
