116 infection 1

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87 Terms

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physical barriers

skin (keratin) and mucous membranes (nose, GI tract)

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body defenses

phagocytosis, inflammatory mediators, interferons and interleukins, specific (memory) response, fever

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interferons and IL

immunogenic proteins (cytokines) secreted by WBCs, stimulate immune responses

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WBCs

eosinophil, basophil, monocyte, neutrophils, T, B and NK cells

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secrete ILs

naive t cells and Th2 cells

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th2

aid in immune response, communicates via IL

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allergy first responders

T reg, cytotoxic, Th2 -secrete IL

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neutrophils

up to 70% of WBCs -1st to site of damage -live up to 1 week -immature = band

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lymphocytes

innate and adaptive (memory) -NK, B cells, T cells

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monocytes

in blood, and macrophages in tissues -specific to tissues

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eosinophils

allergy response -release enzymes/ chem mediators to destroy allergens and parasites

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basophils

allergy response -pro inflammatory and anti-coagulating

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boosters

boost memory, promoting active immunity

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passive immunity

transferred from one person to another -fetus, meds

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B cells

antigen presents itself and b cells clone (millions of copies, aka plasma cells) -antibodies secreted which circulate: immunoglobulins

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immunoglobulins

most common IgG, secreted from B cells

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antibodies fx

neutralize or mark for destruction (by phagocytic cells)

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the next exposure

memory b cells always remember antigen and response is immediate and very fast during

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t cell types

helper, cytotoxic, memory

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t cells

t helper activates B cells, secrete cytokines -t memory cells develop post exposure and recognize antigen next time to respond fast

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cytokines

interleukins, interferon, tumor necrosis factor, perforin

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causes of decreased WBC

autoimmune disease, drug therapy, chronic infection/inflammation, immunodeficiencies, cancer

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autoimmune disease

like IBD -systemic inflammation decreases synthesis and proliferation -depletion due to chronic inflammatory requirements

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drug therapy

glucocorticoids (lower inflammatory process) -immunosuppressant drugs (biologics)

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chronic infection/inflammation

mononucleosis, HIV -longterm infections = depletion due to chronic requirements

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immunodeficiencies

look up during patient research -inborn errors

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cancer

lymphomas, leukemias -destruction of production organs -interference with maturation of normal WBCs

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causes an infection

host susceptibility, pathogenicity, port of entry

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pathogenicity

organisms ability evade or overcome body defenses

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pathogens

bacteria, viruses, fungi, parasites

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virulence

the power to produce disease (covid 19 has high virulence)(potency) -even low numbers of pathogen are able to produce disease

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port of entry

into the body past endogenous defenses

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mechanisms of infection

strength in numbers and toxin production (raises ability to live in host environment)

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prevention by decreasing numbers

80% of infections spread by hands (WASH) -streptococcus septicemia common in early 1990s

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microflora

microorganisms present on/in human body -commensalism, mutualism (intestinal flora), parasitic relationship

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intestinal flora

vitamin K and B formation -balance of good and bad

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infectious disease

pathogens -host is negatively affected -parasitic relationship

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opportunistic

affects one person but not another -any microorganism causing disease -eg. intestinal infection in an immuno suppressed host -common in high risk patients: chronic illness, elderly, newborn, drug tx, malnutrition

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parasites

animals -3 main groups: protozoa (malaria), helmiths (tapeworm), arthropods (lice, ticks, mites, fleas) -not high numbers, not often in hospitals

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fungi

eukaryotic (organized nucleus), freely reproduce -yeast and mold (candida albicans) -like dark, moist environments -severe disease is rare in a non compromised host

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fungi disease

superficial: superficial mycoses (athletes foot, thrush, ringworm) -systemic: (lung, GI) rare serious and difficult to treat -prevention is key

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viruses

no cell structure: protein coat and nuleic acid only (DNA or RNA) -retroviruses like HIV

-host needs to survive and replicate -more common and contagious than other pathogens

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retroviruses

RNA only, requires reverse transcription into DNA (enzyme reverse trascriptase) -HIV (cause of aids)

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virus host

must replicate and survive -must access host cell -may lyse host cell -eg HIV lyses host cell during replication -HPV alters host cell = oncogenic

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common viral infections

covid 19, influenza, common cold, laryngitis

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virus tx

symptom management: antivirals -immune system support: IVIG (boost immune response like interferons) -prevention: immunizations

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bacteria

prokaryotes -no organized nucleus -contain DNA (small DNA bodies: plasmids) and RNA -reproduce autonomously -colonize affected areas: biofilms -like specific conditions -less contagious than viruses -commonly secrete toxin (exogenous pyrogens) = contribute to inflammation and disease process -gram negative or positive

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bacteria tx

antibiotics -resistance is increasing

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port of entry examples

direct content, inhalation, ingestion

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direct contact

with the infected host -STIs, diseases causing a wound/rash (chickenpox)

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inhalation

of airborne pathogens -resp diseases, colds, pathogens causing meningitis, childhood disease -chicken pox

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ingestion

of contaminated foods -food poisoning -parasites (eggs) -food borne viruses (Hep A)

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source of infection

nosocomial: acquired in hospital -community acquired: outside of hospital

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emia suffix

for pathogen presence in blood -bacter____ = bacteria in blood

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incubation

pathogen present and replicating -no symptoms -can infect others

<p>pathogen present and replicating -no symptoms -can infect others</p>
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prodromal stage

initial symptoms: malaise, mild fever, headache, myalgia -generic in nature (hard to differentiate)

<p>initial symptoms: malaise, mild fever, headache, myalgia -generic in nature (hard to differentiate)</p>
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acute stage

maximum presence of pathogen, maximum response by host -maximum impact of infection -more specific and consistent symptoms

<p>maximum presence of pathogen, maximum response by host -maximum impact of infection -more specific and consistent symptoms</p>
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convalescent period

pathogen decreasing in numbers -progressive host repair of damages -recovery

<p>pathogen decreasing in numbers -progressive host repair of damages -recovery</p>
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resolution

no signs of disease

<p>no signs of disease </p>
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1st step

where is the illness -based on health hx, and focused health assessment

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immunization sched canada

part of assessing for something rare, should they already be protected against this?

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common imunizations

DTaP, IPV, HPV

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DTaP immunization

diptheria, tetanus, pertussis

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IPV

polio virus immunization

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HPV

human papillomavirus vaccine

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botulism

less common due to prevention -gram + and anaerobic, neurotoxin (Ach block) -prevention with preservatives (potassium nitrate)

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antitoxin HBAT

botulism tx -lowers binding of neurotoxin to ach receptors -need to treat in time

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neurotoxin

Ach block -botulism does this -need for para, symp, and somatic NS fx -muscle paralysis

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potassium nitrate salt

a way to prevent botulism -its a preservative

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2nd step

identify what is causing illness -bacterial vs viral? CBC & diff, s&s, hx, culture from source

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cbc

wbc, rbc, hemoglobin (HGB), hematocrit (HCT), PLT

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diff

neutrophils, band neuts, lymphocytes

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cbc and diff

to determine if bacterial or viral -part of identifying whats causing illness -24hrs

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neutrophils

highest in bacterial infection -band _____ high in severe overwhelming infection

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lymphocytes

T, B, NK? usually higher in viruses

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culture tests

up to 72hrs -want to identify infection -blood culture, swaps, etc -on wounds -also sensitivity

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sensitivity test

is it sensitive to this antibiotic or not

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gram negative

thinner peptidoglycan, and has an outer membrane -ecoli, klebsiella, pseudomonas, salmonella, hib, cholera, syphillis, gonorrhea, nisseria M.

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gram positive

thick peptidoglycan layer -staphylococci, streptococci (pneumococci), enterococci, listeria, c dif

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tuberculosis

neither gram positive or negative

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3rd step

antibacterial tx process -empiric or focal

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abx empiric tx

based on suspected bacteria -evidence decision -broad spectrum may be used -starts ASAP -drug must reach target (ADME, patient compliance)

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broad spectrum abx

effective at killing anything -both G + and -

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abx focal tx

culture and sensitivity results used -tx initiated once results known -empiric tx maybe switched to focal -narrow spectrum abx better choice for that pathogen

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streptococcus pyogenes

group A strep -bacterial pathogen -pharyngitis (sore throat) -incubation 2-4 days; highly infectious -post strep disease risk: glomerulonephritis, endocarditis (caused rheumatic fever)

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streptococcus pyogenes symptoms

fever, sore throat, headache, malaise

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variety of pathogens

an illness can be caused by