Review for exam #1

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98 Terms

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formation of membrane attack complex

outcome of complement system

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alternative complement system

activated spontaneously by hydrolysis C3 and further triggered by structures on microorganisms and other foreign surfaces

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lymphadenitis/scrofula

caused my MTB and NTM, enlarged lyphnodes after bacteria from lungs travels to lymph nodes

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classical complement system

antibody-antigen complex binds C1 complex, most active in bacterial infections

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lectin complement system

Pattern recognition receptors, such as mannose-binding lectin (MBL) bind to carbohydrates on pathogens.

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toll like receptors

receptor that recognizes multiple targets

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TLR2

recognizes gram positive and some gram negative bacteria peptidoglycan

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TLR3

recognizes viral dsRNA

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TLR4

recognizes gram negative LPS

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TLR7 and TLR8

recognizes viral ssRNA

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NOD-like receptors

cytoplasmic and recognize mostly bacteerial pathogens

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RIG-like receptors

cytoplasmic sense viruses

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C-type lectin receptor

targets microbial carbohydrates in bacterial, viral, and fungal cell membranes

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TNF-a, IL-1, IL-6

major inflammatory cytokines

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activate engothelial cells and resident immune cells, stimulat phagocytosis and production of prostaglandins

local affects of major inflammatory cytokines

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act of hypothalamus as endogenous pyrogens (fever)

systeematic effects of major inflammatory cytokines

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hypotension, intravascular thrombosis, cachexia (wasting of muscle and fat cells)

systematic effects of TNFa

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IL-8 (CXCL8)

chemokines that recruites neutrophils

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monocyte chemoattractant protein (MCP-1, CCL2)

chemokine that recruites monocytes

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Dendritic cell, macrophage, mast cell

resident immune cells

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dendritic cell

antigen preseeenting cell that activates B and T cells

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mast cell

function in degranulation

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biogenic amines (histamines)

released from mast cell cause vasodilation and vascular leak

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cytokine (TNF)

released from mast cell cause inflammation

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enzymes

released from mast cell cause tissue damage

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neutrophils, monocytye/macrophage, natural killer cells, eosinophils, basophils


recruited inflammatory cells

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macrophage

phagocytosis, ROS and NO killing, repair damaged tissues by stimulating angiogenesis and fibrosis

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natural killer cells

kill infected cells and activate macrophages, perforin expression (holes in target membrane), and FcR expression (stimulate antibody-dependent cellular cytotoxicity (ADCC))

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eosinophils

specialized to fight parasitic infections, active in allergic responses

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basophils

infiltrate sites of allergic inflammation and release mediators and cytokines

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Fc region

portion of antibody that interacts with cell surface receptors, common to all antibodies

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fab region of antibody

what provides antibody specificity?

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VDJ recombination

what provides diversity of antibodies?

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IgM

pentameric or monomeric, first antibody secreted, activation of complement

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IgG

monomeric, highest concentration in blood, diffuse into extravascular sites/ cross placenta (passive immunity), activation of complement

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IgD

monomeric, least abundant, on B-cells

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IgE

monomeric, binds to mast cell receptors (histamine release), parasidic response and allergic reactions

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IgA

dimeric, passive immunity (breast milk), in mucous secretions, neutralization and agglutinating pathogens

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IgG, IgD, IgE

monomeric antibody isotypes

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IgM and IgG

which antibodies can activate complement

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MHC I

presents antigen to CD8 T cell

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MHC II

presents antigen to CD4 T cell

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antigen small peptide presented on MHC of antigen presenting cell (dentritic cell)

How are antigen recognized by TCR

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alloimune response

recipient T cells react to donor MHC molecules as foreign 

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Graft versus host disease (GVHD)

donor T cells react to  recipient MHC as foreign

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Oral GVHD

painful sores in mouth as result of donor T cells reacting to  recipient MHC as foreign

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streptococci are catalase negative

difference between streptococci and staphlococci

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streptococcus pyrogens (group a streptococcus)

beta-hemolytic streptococcus

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viridans (s. mutans)

alpha hemolytic streptococcus part of normal oral flora

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streptokinase

virulence factor of GAS dissolves blood clots to relaese additional bacteria

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hyluaronidase

virulence factor of GAS breaks down hyaluronic acid in connective tissue

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streptolysin

virulence factor of GAS toxic for neutrrophils, RBCs, and platelets

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streptodornase

virulence factor of GAS the digests DNA

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streeptococcal pyrogenic exotoxins (spe)

virulence factor of GAS, exotoxin, superantigen, causes scarlet fever

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M protein

virulence factor of GAS provides resistance to phagocytosis

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scarlet fever

caused by GAS exotoxin, circumoral pallor and strawberry tongue

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Necrotizing fasciitis

severe rapidly progressing connective tissue infection due to GAS exotoxin, toxin production can lead to toxic shock

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Streptococcal pharyngitis

GAS infection, symptoms include red swollen tonsils, fever, sore throat, red spots on roof of mouth

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Impetigo

superficial skin GAS infection, skin ulceration on face and lower extremities

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Post streptococcal glomerulonephritis (PSGN)

due to the immune response to infection following skin and pharyngeal infections (GAS infections ie. strep throat). characterized by DARK URINE

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Acute rheumatic Fever (ARF)

multi organ inflammatory syndrome as an immune response to untreated GAS pharryngitis, aschoff bodies in heart skins brain and joints

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S. aureus, streptococci, enterococci


most common causes of infective endicarrditis (IE)

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S. aureus

most deadly cause of infective endocarditis, associated with healthcare infections

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streptococcal

cause of infective endocarditis in oral cavity, poor dentition as risk factor, little pain or no symptoms

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Mycobacterium tuberculosis (MTB)

Aerosolized respiratory droplet nuclei, contagious, from other humans, primary pathogen, latentency common

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Nontuberculosis Mycobacterium (NTM)

Caused by M. avium complex, Non-contagois, Opportunistic pathogen, Found in water and soil, No latency

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latent tuberculosis

ccurs after immune response at granulomas kills most of MTB, bacteria latent in granulomas, asymptomatic, non contagious, no symptoms

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bacteroides, prevotella, fusobacterium, porphyromonas

Gram negative anerobes

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B. fragilis

opportunistic pathogen (friend to foe) , B lactimase confers penicillin resistance

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P. melanogenica

diagnostic marker for oral cancer

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F. nucleatum

common cause of acute necrotizing gingivitis

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Acute Necrotizing Ulcerative Gingivitis (ANUG)

associated with F. nucleatum, bleeding gingiva with abrupt onset, malaise/fever, excessive salivation and foul breath typically seen in people under 35

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gentle debridement, mouth rinses, antibiotics


treatment for acute necrotizing Ulcerative gingivitis

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C. perfingens

Which organism is mainly responsible for causing gas gangrene?

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C. tetani

causes lock jaw, blocks inhibitory neurotransmitters, can be neonatally transferred through umbilical cord, immunizations only treatment option

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C. botulinum

block release of acetylcholine, causes paralysis of muscles, associated with infant botulism

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actinomyces

part of normal flora in oral, urinogenital, and GI tract, pathogenic after trauma (ex: extraction)

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A. isralii

cause of cerevicofacial actinocmyces (pyogenic abceess “sulfur granules”)

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H. influenzae, Strep. pneumoniae, Neisseria meningitidis

bacteria that cause bacterial meningitis

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stiff calfs, can’t bend knees

kernigs sign of meningeal inflammation

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stiff neck, legs fold when neck bends

bruzinski’s signs of meningeal inflammation

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WBC increase


CSF cell count change with meningitis

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elevated protein


CSF protein change with meningitis

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low glucose


CSF glucose change with meningitis

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vaccination

main prevention method of meningitis

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IgA protease and polysaccharide capsule

N. meningitidis virulence factors

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Elimination, substitution, engineering controls, administering controls, PPE

five rungs of hierarrchy of controls from most to least effective

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befor and after touching patient, procedure, gloving/ungloving, body fluid exposure, touching surrounding

opportunities for hand washing

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C. difficle, catheder associated infections, central line infections, surgical site infections, MRSA, COVID

key healthcare associated infections

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increases patient suffering, lead to disability, increases healthcare cost, preventable

importance of healthcare-associated infections

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HIV, Hep B, Hep C

most common bloodborne pathogens

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Hep B

most infectious bloodborne pathogen

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treat all patient as infectious, vaccination, standard precautions, immediate action after exposure

prevention of bloodborne pathogens

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cleaning

removal of organic matter on soiled surfaces

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Disinfection

eliminates most pathogenesis microorganism, some microbial forms remain

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Sterilization

eliminates all forms of microbial life 

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high level heat sterilization

level of disinfection needed for Instruments that penetrate soft tissue or bone, instruments that contact mucous membranes, dental handpieces

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intermediate/ low level chemical disinfectant

level of disinfection needed for patient chair and room surfaces