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- 2 outcomes of abscess
- encapsulation or rupture
- abscess rupture to peritoneum
- peritonitis
- abscess rupture to blood vessel
- systemic circulation of septic material (usually death)
- fever - purpose
- kill bacteria - human cells survive
- critical temps for fevers
- 105 degrees - protein denatures, 107 degrees - multiple organ failure and death.
- 4 agents or chronic inflammation
- microorganisms, foreign bodies, toxins, auto-immune reactions
- chronic inflam main events
- cellular infiltrate, tissue destruction, repair by scar
- granuloma
- chronic infection, macrophages differentiate - epitheloid cells, cluster
- 2 cell types assoc w granuloma
- multinucleated giant cell, langhans cell
- 4 disorders assoc w granulomatous inflam
- tuberculosis, syphilis, leprosy, crohns
- langhans cell characteristics
- nuclei around periphery, horseshoe shape
- granuloma significance
- storage facility for infectious agents body can’t destroy?
- another name for antibodies
- immunoglobulins
- antibody purpose
- form complex with antigen - complex marked for destruction
- 2 modes of destruction AbAg complex
- direct lysis, complement activation
- cells with FC receptors
- macrophages, NK cells, eosinophils, neutrophils
- direct lysis of AgAb complexes how
- cell with FC receptor engages FC fragment, releases lysosomes - destroys complex
- 2 basics of complement system
- hydrolytic enzymes directly lyse infectious agents or chemical mediators initiate acute inflammation, attract neutrophils to phagocytose
- intruder mediation by antibodies
- HUMOURAL immunity
- immunity conferred by Tcells etc
- CELLULAR immunity
- 2 main classes Tlymphocytes
- CD4s assist others, CD8s kill directly
- 3 types of antigen presenting cells
- dendritic(skin), macrophages, langerhans
- to activate Tcells, antigen must be
- cell-bound
- distinguish self from non-self
- major histocompatibility protein (MHP)
- two types of MHP & locations
- Class I - all cells, Class II - ONLY antigen presenting cells
- MHC protein recognition
- CD4s recognize class II, CD8s only class I
- cytokine, source activates Bcells
- interleukin produced by Type2 CD4s
- cytokine source - activates macrophages
- Interferon Gamma, produced by Type1 CD4s
- macrophage activation results
- increased size, lysosomal enzymes, ability to digest/kill, secretion of growth factors(endothelial cells, fibroblasts), hydrolytic enzymes
- macrophages kill what and how
- tuberculosis, parasites, fungi, tumour cells, organ transplants - via direct lysis or phagocytosis
- CD8s kill antigens how
- proteolytic enzymes -- osmotic lysis
- CD8s mostly kill
- virus infected cells, tumour cells, organ trans (non-self)
- viral destruction in liver problem
- CD8s kill HepB infected liver cell, destroy liver tissue
- stimulates scar repair in chronic inflam
- activated macrophages secrete growth factors
- scar tissue repair- what two celltypes prolif?
- fibroblasts(collagen) endothelial cells (angiogenesis)
- young vs. old scar tiss.
- collagen incr. over time, incr. density. vessels, fibroblasts decrease over time
- purpose of vessel dev. - scar tissue
- bring nutrients to dev. tissue
- Type I hypersensitivity mediated by Ig?
- IgE
- What is Type I hypersensitivity?
- allergy - rapid immune reaction w/in minutes
- 2 cell types central to Type I hypersensitivity
- mast cells and basophils
- mast cells - what and where
- from marrow, wide dist. in body, esp. around nerves, vessels, subepithelial where Type I reacts occur
- Mast cells/basophils activated how?
- crosslinking IgE receptors
- diff btwn mast cells and basophils
- basophils in blood, small numbers
- type of helper cell assoc. w Type I hypersens
- Type 2 CD4s
- What is produced by Type 2 CD4s
- Interleukins 4 and 5
- genetic predisposition to type 1 hypersensitivity called
- atopic disease (allergy) IgE diseases
- hay fever also known as
- allergic rhinitis
- other IgE mediated diseases
- asthma, dermatitis, gastrointestinal food allergy
- released upon exposure to allergen?
- histamines, leukotrines
- SRS-A
- slow-reacting substance of anaphylaxis
- ECF-A
- eosinophil chemotactic factor of anaphylaxis
- type 1 mediators act on what?
- vessels, sm. musc, secretory glands
- Type 1 mediators cause what?
- edema, cellular infiltrate, clinical features of allergy
- common in blood/nasal secretions during attack
- eosinophils
- IL4 is what
- IgE switch factor, produced by Th2, activates Bcells
- HDN is what
- hemolytic disease of newborn - Rh incompatibility
- HDN example of what type hypersensitivity
- Type II
- Antigen for Rh also called what
- D
- produced in mother in HDN following second child?
- IgG antibodies, which cross placenta
- problem with IgG crossing placenta?
- attack fetal erythrocytes
- result of IgG placental crossing
- hemolytic anemia of fetus
- natural antibodies reactive with AB blood groups
- IgM - can’t cross placenta
- 2 examples of Type II hypersensitivity
- organ rejection, myasthenia gravis
- define RA (rheumatoid arthritis)
- chronic systemic inflammatory autoimmune disease of the joints
- what histocompatibility complex assoc. with rheum arth
- HLA-D4, and HLA- DR4
- etiology of RA
- unknown
- what are rheumatoid factors
- immunoglobulins specific for FC fragment of IgG - an antibody against ones own antibody Immunoglobulin
- 2 examples Type III hypersensitivity
- serum sickness, arthus phenomenon
- inflammatory factors associated with rheumatoid arthritis
- histamine release, cytokine production (neutrophils, monocytes), white cells to synovial space
- problem with inflammation of joints
- tissue destruction, more lysosomes released
- define pannus
- vascular mass of lymphocytes around area of necrosis where bone and cartilage have degraded
- progression of rheum arth causes
- fusion of articular surfaces, dehabilitation, fibrous granulomar replacement of bone and cartilage
- cause of tuberculosis
- mycobacterium tuberculosis (or mycobac.T.bovine)
- TB is what type of hypersensitivity disease
- Type IV
- most common site of TB infection
- lungs, but can be anywhere
- TB inflammation type
- focal granulomatous with central caseous necrosis
- what helped prevent widespread TB during orig outbreak
- invention of pasteurization, milk pasteurizing
- tuberculosis vaccine
- BCG - bacille Camette Geurin
- Test for TB
- PPD purified protein derivative
- type of hypersensitivity reaction in TB
- delayed 24 - 72 hr Type IV reaction
- contact sensitivity
- delayed hypersensitivity to chloride or nickel salts, also type IV
- exogenous infection
- from exterior
- endogenous infection
- from interior - ones own flora attacking system
- 3 methods of infection
- direct contact, ingestion, innoculation
- how well an organism can produce symptoms
- pathogenicity
- how severe symptoms are that are prod. by organism
- virulence
- poisons secreted by bacteria
- exotoxins
- examples of 3 exotoxins
- diptheria, tetanus, enterotoxin
- diptheria pathology
- sore throat - death. destroys epithelium and mucous memb, leaving fibrous necrotic tissue, esp. in throat.
- tetanus pathology
- neurotoxin, interrupts motor nerve signals, causes spasm
- enterotoxin
- food poisoning - staphylococcus
- endotoxins released when
- when bacteria destroyed
- 3 bacterial metabolic examples - contrib. to disease
- hyaluronidase, streptokinase, coagulase
- metabolite - dissolves conn. tissue
- hyaluronidase
- metabolite - demineralizes tooth enamel
- plaque acid
- metabolite - breaks down fibrin
- streptokinase
- metabolite, breaks down DNA
- streptoadornase
- 3 examples where foreign organisms multiply - prod. inflammation
- shigellosis(dysentry), Salmonella Typhi (Typhoid Fever), Spirochete(necrotizing ulcerative gingivitis)
- organism in bloodstream from infection called
- bacteremia
- another name for blood poisoning
- sepsis
- 3 main factors - infection resistance
- patient factors(immunity, nutrition, biochem, secretions), organism virulence, site of infection, level of blood supp.
- atrophy caused by plasma protein deposition in tissue
- amyloidosis
- rhesis prophylaxis
- Anti-D given to mother after birth, leaves her desensitized for subsequent childbirth
- autoimmune disease where antibodies clog acetylcholine receptors
- myasthenia gravis - causes generalized muscular weakness
- chronic inflammatory disease of bowel
- crohns disease - alternating ulcers of GI tract
- How to identify granuloma
- multinucleated giant cells
- chronic rheumatic fever can lead to risk of
- infective endocarditis - heart valve deformity, incompetency
- asthma
- mast cell histamine release-mucous hypersecretion-more goblet cells - bsmt. memb. thickening-sm. vessel constriction
- 5 HIV related infections
- fungus in meninges, cytomegalovirus - gigantic langhans cell, lung yeast infection, carposis sarcoma, lymphoma
- 2 processes in wound healing
- regeneration or replacement
- cell entry to tissue via
- regeneration
- proteins that regulate cell cycle
- cyclins
- 3 types proliferative potential states in cells
- labile, stable, or permanent
- continuously regenerating cells
- labile, from stem cells, eg: marrow, epithelia
- cells which can but don’t normally divide
- stable- divide if injured, eg: liver, fibroblasts, sm. musc
- cells which can’t divide
- permanent - skeletal musc, cardiac, neurons
- cycle stage cells at
- G0 - resting(quiescent)
- matrix btwn cells - origin, composition
- interstitial matrix:fibroblasts-amorphous gel, collagen, elastin, proteoglycan, glycoproteins
- bsmt membrane composition
- platelike mesh, type IV collagen, glycoproteins
- extracellular matrix active in tissue repair how
- mech support, determine orientation, control regulate growth and differentiation, pres: regulatory molecules
- collagen - describe
- fibrous structure proteins from fibroblasts Xlink by VitC in triple helix
- source of cell growth factors
- activated macrophages
- 3 examples growth factors
- epidermal, fibroblast, cytokines
- 4 steps in scarring
- angiogenesis, fibroblast mig., prolif, deposition of matrix, maturation, reorganization of fibrous tiss.
- basic substrate extracell. matrix forms on and timing
- granulation tissue at abt. 3 days
- mature scars are?
- avascular
- char. of first intention healing
- more epithelial regen than fibrosis
- 1st intention - process
- neutrophils, mitosis; epithelial migration, new bsmt memb.; macrophages, granulation tissue, collagen fibres; epidermis - collagen fibre bridge
- char. of 2nd intention healing
- fibrosis rather than epithelial regen
- example 2nd intention
- ulcer (eg Diabetes)
- process 2nd intention
- big inflamm. reaction, lots of granulation tissue, wound CONTRACTS
- 3RD intention
- delayed closure to allow some natural disinfection
- exuberant collagen production in 1st intention wound
- keloid
- types of factors effecting healing
- local(infection, foreign body, blood supp, temp.) Systemic(immunosup.,vasc.disease, nutrition, alcohol)