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Flashcards in Classes 3-4 Deck (76):
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When does acute inflammation usually stop?

When injurious stimulus is removed, walled off, or broken down.

Outcomes: resolution, abscess formation, chronic inflammation.

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What are the possible outcomes of chronic inflammation?

Tissue destruction, fibrosis

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What are the 7 morphotypes of inflammation?

Serous
Fibrinous
Purulent
Ulcerative
Pseudo membranous
Chronic
Granulomatous

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Serous inflammation

Mildest form of inflammation
Characterized by clear fluid
Occurs in early stage; typical in viral infections, burns, arthritis

Exudate mostly albumin and immunoglobulin

Self limiting

Generally resolves easily.

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Fibrinous inflammation

Exudate rich in fibrin

Bacterial infections (strep throat, bacterial pneumonia, bacterial pericarditis).

Does not resolve easily. Often requires antibiotics.

Leads to growth of fibrous tissue (scarring) in parenchyma --> loss of function.

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Purulent inflammation

Typically formed by pus-forming bacteria. (Staph and strep)can accumulate on mucosa or in internal organs. May form abscess.

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Abscess

Localized collection of pus within an organ or tissue

Does not heal spontaneously; must be surgically excised.

May lead to fistula or sinus.

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Sinus

Cavity, usually occupied previously by an abscess that has ruptured, that drains through a tract to the surface of the body.

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Fistula

A channel between preexisting cavities and/or hollow organs and/or surface of the body.

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Empyema

Accumulation of pus in a preformed cavity (ex. gallbladder)

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Ulcerative Inflammation

Inflammation do body surfaces or mucosa.

Leads to ulceration or necrosis of epithelial lining.

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Ulcer

Defect involving the epithelium, which can also extend into connective tissue.

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Pseudomembranous inflammation

Combination of ulcerative, fibrinous and purulent inflammation.

Ulcerative with fibronopurulent exudate (with mucus and cellular debris) which forms a pseudomembrane on surface of ulcer.

Diphtheria (pseudomembranes form on throat); C. Difficile in large intestines (secondary to antibiotic use)

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Chronic inflammation

Because of length of inflammation, produces more tissue destruction, heals less readily and associated with more serious functional deficiencies.

Exudate contains monocytes, lymphocytes, macrophages, plasma cells.

Secretory products stimulate proliferation of fibroblasts (--> scarring --> loss of function) and recruit new inflammatory cells (perpetuating inflammation)

Sm

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Granulomatous inflammation

Not preceded by acute inflammation.

Not neutrophil driven.

T-lymphocytes and macrophages accumulate at site of injury.

Lymphocytes release cytokines, which transform macrophages into epithelioid cells.

Epithelial cells fuse with each other and form multinucleated giant cells.

Multinucleated giant cells, epithelium cells and lymphocytes form granulomas, which destroy cells and last long time.

Caseous and non caseous

TB, fungal infections, syphillis.

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Clinical correlations of inflammation

Fever 37 degrees +
Leukocytosis
Constitutional symptoms (fatigue, weakness, depression)

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What causes fever?

Pyrogenes cytokines (Tumour Necrosis Factor -- TNF -- and IL-1)
-- stimulate production of prostaglandins in hypothalamus

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Cell categories based on ability to proliferate

1. Continuously dividing/labile/mitotic
2. Quiescent/facultative mitotic/stable
3. Non-dividing/post-mitotic/permanent

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Continuously Dividing Cell

Labile, mitotic, stem cells

Typically found in basal layer of skin or mucosa of internal organs.

Outcome: minimal tissue damage, short recovery time

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Quiescent Cells

Facultative mitotic, stable

Do not divide regularly but can be stimulated to divide if necessary.

Form the parenchymal organs. (Eg liver, kidneys).

Outcome: regeneration, although may be limited.

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Non-dividing Cells

Post-mitotic, permanent.

No capacity to divide period. Ex: neurons.

Outcome: replacement of parenchymal tissue with connective tissue leads to loss of function.

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Healing by First Intention.

When wound is clean, free of foreign material and necrotic tissue, and edge are close together.

Scab
PMNs scavenge debris
2-4 days later granulation tissue develops.
3-6 weeks scar develops

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Healing by Second Intention

Large break in tissue, inflammation, longer healing and more scarring.

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Granulation tissue

Vascularized connective tissue rich in macrophages, myofibroblasts and angioblasts.

Part of wound healing. Develops in 2-4 days.

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PMN's role in wound healing

Scavenge briefly at injury site

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The role of connective tissue cells in wound healing

Produce scar tissue.

Include myofibroblasts, angioblasts, fibroblasts

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Epithelial cells and wound healing

Undergo mitosis and extend across wound.

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Macrophages and wound healing

Stay at site and produce cytokines and growth factors.

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Myofibroblasts and wound healing

Hybrids -- have properties of smooth muscle and fibroblasts.

In first few days, contract reduces defect and holds margins together.

Secrete matrix substances like fibroblasts.

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Angioblasts and wound healing

Precursors of blood vessels

Appear 2-3 days after incision and new blood vessels permeate site by 5-6th day.
New vessels provide route for scavenger cells to remove scab and debris and allow influx of nutrients and O2

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Fibroblasts and wound healing

Produce most of ECM
Fibronectin- forms scaffold
Collagens -- form fibrils in interstitial spaces

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Healing Process

1. Blood clot formation
2. Inflammation develops
3. Cellular debris removed by phagocytes, monocytes and macrophages
4. Granulation tissue develops in gap
5. Epithelial cells insert mitosis and extend across wound
6. Fibroblasts produce collagen
7. Fibroblasts and macrophages produce cytokines which attract more fibroblasts.
8. Fibroblasts stimulate epithelial cell proliferation and migration and angiogenesis.
9. Cross linking and shortening of collagen fibres
10. Capillaries decease.

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Contracture

Fixation and deformity of the joint

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Adhesion

Bands of scar tissue that join two normally separated surfaces b

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Immunity

Protection from disease, especially infectious disease.

Natural and acquired.

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Natural immunity

Primitive, nonspecific, inherited.

Include mechanical factors like skin and cilia, and phagocytic and NK cells.

Also includes protective proteins.

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Natural immunity includes what protective proteins?

1. Complement
2. Properdin (plasma protein that activates alternative complement pathway)
3. Lysozome (bactericidal protein found in tears, and in nasal and intestinal secretions)

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Acquired immunity

Based on body's ability to:
1. Distinguish self from non-self
2. Generate an immunologic memory
3. Mount an integrated reaction of various cells

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Immune competence

The body's ability to mint and appropriate immune response

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Cells of the immune system

1. Lymphocytes
-- T lymphocytes (T helper and T suppressor/cytotoxic cells)
-- B lymphocytes
2. Plasma cells

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Primary lymphoid organs

Thymus
Bone marrow

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Secondary lymphoid organs

Most notably lymph nodes and spleens.
Also GI tract and bronchial mucosa

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MALT

Mucosa associated lymphoid tissue.
Formed by lymphocytes. Unencapsulated, integrated in mucosa.

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T lymphocytes

Lymphocytes that have matured in thymus.

Account for 2/3 lymphocytes in blood. Also found in lymph nodes and spleen.

Include T helper (CD4) and T suppressor/cytotoxic cells (CD8)

All T cells have a membrane T cell receptor (TCR) linked to CD3 protein. Used for recognition of antigens.

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Natural Killer (NK) cells

T cells that do not express TCR-CD3 complex
Mediate innate immune reactions; not involved in T & B cell mediated reactions.

React against virus infected cells, and foreign and cancer cells

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T Helper Cells

Help B cells produce antibodies

Express CD4 on their surface.

Secrete cytokines. Classified as Th1 or 2 depending on which cytokines produced

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TH1 Cells

T helper cells that produce interleukin 2 (IL-2) and interferon gamma (IFN-gamma).

Stimulate macrophages to become phagocytic
Mediate formation of granulomas

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TH-2 cells

T helper cells that make IL-4, IL-5 and IL-13
Important for secretion if IgE and other immunoglobulins and activation of eisinophils

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T Suppressor/Cytotoxic cells

Express CD8 on their surface

Suppress unwanted antibody production
Mediate killing of virus-infected and tumour cells.

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Normal ratio of CD4:CD8 cells

2:1

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B lymphocytes

Cells that mature in the bone marrow.

When stimulated by antigens, differentiate into plasma cells

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Plasma cells

Fully differentiated descendants of B cells

Produce antibodies.

Cytoplasm contains an abundance of ribosomes and RER.

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Antibodies

Protiens of the immunoglobulin class secreted by plasma cells

Made up of about 110 amino acids

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IgM

Mega immunoglobulin (biggest)
Composed of five basic units

Functions to neutralize microorganisms.

First to appear after immunization.

Natural antibody against ABO antigens

Complement activator.

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IgG

Gnomish. (Smallest immunoglobulin)

Most abundant.

Produced in small amounts on initial immunization but production is boosted upon re-exposure.

Can cross placenta.

Acts as opsonin.

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IgA

Aw yucky

Found in mucosal secretions (tears, nasal secretions), milk and intestinal secretions.

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IgE

Evil (allergies)

Secreted by plasma cells in tissues

Locally attached to mast cells

Mediates allergic reactions (Type 1 hypersensitivity reaction)

Present in trace amounts in serum.

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IgD

Doh!

Cell-membrane bound; on B cells

Participates in antigenic activation of B cells; not released into serum or body fluids.

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Antibody production

Foreign antigen attaches to B-lymphocyte antigen receptor complex.

B cells internalize antigen and function as Antigen Presenting Cells

Present antigen to T cells. T helper cell produces cytokines, which transform B cell into plasma cell, which produces antibodies.

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Major histocompatability complex

Proteins present on surface of cell that identify cell as self/other.

The "identity" of pathogen that allows for specific immunity to be developed.

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Ag-Ab reaction

Ab and Ag bind to form complexes.

If large enough, may be phagocytosed in spleen/liver by fixed macrophages.

If small, may bind on RBCs or endothelial cells, or filter through capillary walls.

AbAg complexes on RBCs can cause agglutination --> hemolysis

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Hypersensitivity Reaction

An abnormal immune response to exogenous antigen or endogenous auto-antigen

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Types of hypersensitivity

I. Anaphylactic type reaction
II. Cytotoxic Ab-mediated type reaction
III. Immune complex mediated reaction
IV. Cell-mediated, delayed type reactions.

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Type I Hypersensitivity

Anaphylactic type
IgE mediated.
AgAb complex on mast cells trigger release of histamines

Hay fever (allergic rhinitis)
Eczema (atopic dermatitis)
Bronchial asthma
Anaphylactic shock.

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Type II Hypersensitivity

Mediated by IgM or IgG

Cytotoxic Abs react with Ags in cells or tissues.

Activates complement system (MAC) then cell lysis, or attracts cytotoxic T cells

Re exposure may lead to autoimmune disorders: Goodpastures, hemolytic anemia, Graves Disease, or Myasthenia gravies

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Goodpasture's Syndrome

Type II hypersensitivity disorder

Autoimmune reaction against Coolagen Type IV

Leads to renal and pulmonary damage

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Hemolytic Anemia

Type II hypersensitivity disorder

Can occur as a result of acute hemolytic reaction (transfusion of mismatched blood) or SLE (systemic lupus erythematosus)

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Epitope

Part of antigen that is recognized by immune system.

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Graves Disease

Type II hypersensitivity disorder

Form of hyperthyroidism in which antibodies to thyroid stimulating hormone receptors cause overproduction of thyroid hormones.

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Myasthenia Gravis

Type II hypersensitivity disorder

Antibodies to ACh receptors in NM junction prevent binding.

Results in severe weakness and paralysis.

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Type III Hypersensitivity Disorder

Mediated by AgAb complexes.

Complexes get trapped in semipermeable membranes, and active complement system, triggering inflammation characterized by fibrotic necrosis.

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Systemic Lupus Erythrematosus (SLE)

Lupus

Involves Type III hypersensitivity

Circulating AgAb complexes deposit on tissues and cause kidney disease, arthritis, skin disease, Eric.

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Post streptococcal Glomerulonephritis

Type III hypersensitivity disorder

Acute renal disease following URT strep infection.

AgAb complex gets stuck in glomerular basement membrane, evoking complement mediated inflammation.

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Polyarteritis Nodosa

Type III hypersensitivity disorder

AgAb mediated
Involves small to medium sized arteries.

Acute: fibroid necrosis and acute inflammation
Chronic: destruction of vessel wall; thrombosis and occlusion --> ischemia and infarcts

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Type IV Hypersensitivity Reaction

Cell mediated or Delayed Type Immune Reaction

Involves T cells and macrophages, which aggregate and form granulomas.

Accounts for granulomas developing in response to tumours, and idiopathic granulomatous diseases.

Response to M tuberculosis, mycobacterium Leprae, and fungi.

Contact dermatitis most common clinical form.

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Types of transplantation

Autograft -- self to self
Isograft -- identical twin to twin
Homografts: human to human
Xenografts: nonhuman to human