Micro Atchley Block 12 – Flashcards
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what are two other names for hospital acquired infection |
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nosocomal infection iatrogenic infection |
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what are the qualifications of HAI |
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acquired in hospital >48h after admission |
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who is at high risk for HAI |
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IV, port, cath, intubation, ICU, post op, immune compormised |
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how can HAI be prevented |
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hand washing, infection control programs, prudent antibiotic use |
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sources of HAI |
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self, others, air, food, dust, IV, cath, washbowl, bedpan, endoscope, ventilator, water, disinfectants |
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#1 hospital acquired infection in adults |
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URI |
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3 top causes of UTI HAI and their gram stain |
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1. E. coli GNR 2. Candidia KOH 3. P. aeruginosa GNR |
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#2 hospital acquired infection in adults |
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surgical wounds or LRI |
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2 causes of surgical wound infection HAI and their gram stain |
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1. S. aureus GPC 2. P. aeruginosa GNR |
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what is the most likley introduction method of microbes in a HAI LRI |
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ventilator |
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3 top causes of LRI HAI and their gram stain |
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1. S. ayreys GPC 2. P. aerguinosa GNR 3. A. baymanni GNR |
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what is the most likley introduction method of microbes in a HAI bacteremia |
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IV |
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what is the #1 HAI in infants and kids |
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bacteremia |
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3 top causes of HAI bacteremia and their gram stain |
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1. S. aureus GPC 2. enterococci GNR |
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4 signs of pneumonia |
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fever purulent sputum leukocytosis decline in O2 |
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#1 cause of CA pneumonia |
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S. pneumonia |
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S. aureus aka |
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MRSA/MSSA |
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S. aureus: catalase, coagulase, hemolysis? |
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B hemolytic catalase positive coagulase negative |
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which HA pneumo are difficult to treat, why |
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S. aureus - resistance due to mecA gene mutating PBP2a P. aeruginosa - antibiotic resistance : two drug bug A. baumannii - B lactaminase, alters porins, efflux pumps |
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transmission of S. aureus |
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nares, skin |
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P. aeruginosa: oxidaze, lactose? |
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oxidase positive non-lactose fermentind |
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P. aeruginosa: color, smell |
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green grapes |
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P. aeruginosa: who does it invade |
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weak invader: compormised |
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P. aerguinosa: where does it live and transfer on |
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soil, water, plants, animals, intestinal flora, skin, medical devices, hands |
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P. aerguinosa: virulence factors (2) |
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endotoxin A: similar to diptheria toxin antiphagocytic and adhesive capsule |
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P. aerguinosa: 7 clinical signs / conditions |
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Burns endocarditis pneumonia sepsis external malignant otitis media UTI diabetic osteomyelitis |
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Acinetobacter baumannii: oxidase, catalase? |
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catalse positive oxidase negative |
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Acinetobacter baumannii: location/transmission |
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ubiquitous: present everywhere soil, water, skin, secretions, medical devices, hands |
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Acinetobacter baumannii: who does it infect |
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weak invader: compormised |
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Acinetobacter baumannii: 4 clinical signs / conditions |
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Burns E Pneumonia Sepsis E UTI D O |
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Clostridium difficile: gram stain, metabolism, reproduction |
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anaerobic GPR spore forming |
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C. difficule: clinical condition, its cause, its tx |
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pseudomembranous colitis cause: clindamycin (metronidazole, vancomycin) tx: metronidazole, vancomycin |
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cause of FUO Post Op 1-2 days |
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wind: atelectasis, pneumonia |
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cause of FUO Post Op 3 days |
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water: UTI |
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cause of FUO Post Op 5 days |
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walk: deep vein thrombosis |
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cause of FUO Post Op 7 days |
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wound: surgical wound infection |
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cause of FUO Post Op 1-10 days |
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weird: drug induced fever |
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cause of FUO Post Op 10 days |
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wonder where: abscess |
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what are the 7 steps of sepsis |
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infection bacteremia fungemia systemic inflammatory response syndrome sepsis severe sepsis septic shock multiple organ dysfunction syndrome |
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define infection |
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inflammatory response to microbe due to invasion of a sterile site |
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define bacteremia/fungemia, what are the potential causes |
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presence of microbe in blood causes: bacteria, fungi, virus, parasite does not mean septicemia |
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causes of systemic inflammatoy response syndrome |
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infection, organ failure, trauma, burns, shock |
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qualifications for SIRS |
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temp >38 or <35C HT >90 RR >20 pCO@ <32 WBC <1200, 10% band cells |
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qualifications for sepsis |
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SIRS with at least one organ dysfunction, hypoperfusion, HYPOTENSION evidence of or strong suspicion of infection ex symptoms: LACTIC ACIDOSIS oliguria altered mental status mottled skin DIC ARDS CHF |
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qualifications for septic shock |
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sepsis with hypotension despite fluid recussitation, requires vasopressors |
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what is a determinant of outcome of septic shock |
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>3 organs failing means 50% chance of living |
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qualifications for multiple organ dysfunction syndrome |
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progressive distand organ failure |
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causes of multiple organ dysfunction syndrome |
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infection, burns, shock, trauma, other |
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what causes 50% of septic shock |
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gram positive organisms S. aureus: LRT S. pneumo: pneumo enterococcus: UTI |
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what causes 30% of septic shock |
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Gram negative bacteria E. coli |
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top three sources of infection leading to sepsis |
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lung 40% abdomen 20% urine 15% |
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manifestation of end organ dysfunction: carduac |
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tachycardia, decreased contraction |
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what is the second most common end organ dysfunction at the time of sepsis DX |
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cardiac |
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manifestation of end organ dysfunction: pulmonary |
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tachypena, respiratory alkalosis/acidosis, ARDS |
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what is the most common end organ dysfunction at the time of sepsis DX |
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pulmonary |
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manifestation of end organ dysfunction: vascular |
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decreased tone, increased permeability, shock |
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manifestation of end organ dysfunction: hematologic |
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DIC, thrombocytopenia, prolonged PTT/PT |
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what are the limits on PTT/PT |
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PTT>60 sec PT > 1.5 |
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manifestation of end organ dysfunction: renal |
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pre-renal azotemia, acute failure, acute tubular necrosis, increased BUN/CR |
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manifestation of end organ dysfunction: hepatic |
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increased transaminases, bilirubiin, jaundice |
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manifestation of end organ dysfunction: CNS |
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confusion |
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manifestation of end organ dysfunction: metabolic |
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acidosis, shock |
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manifestation of end organ dysfunction: GI |
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malabsorption |
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what on gram negatives cause septis |
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LPS/endotoxins bacterial flagellin nucleic acids |
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what on gram positives cause sepsis |
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trichoic acid peptidoglycan superantigens (cause TSS) bacterial flagellin nucleic acids |
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what microbes dont have peptidoglycan |
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mycoplasma and ureaplasma mostly chalmydia even though all atypicals, NOT legionella |
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what do viruses have that can cause septis |
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nucleic acids |
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role of TLR |
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have PRR (pattern recognition receptors) that see pathogen associated molecules (PAMPS) on microbes trigger release of proinflammatory metiators |
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MOA of TNF/IL-1/INFy |
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pro inflammatory release ROS and lipid mediators from PMN/mono/esino which cause vasodilation, permeability of capillaries, fever, hypotension, coagulation |
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endothelial cells and macrophages causes release of these 4 things when stimulated by TNF/IL1 |
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NO PLA2 COX2 LOX |
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what does NO do |
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vasodilation increased pulmonary A pressure decreased CO |
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what does PLA2 do |
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activate PAF which causes hypotension |
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what does COX2 do |
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activate PGE2 which causes fever, pain,inflammation |
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what does LOX do |
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activate leukotrienes causing neutrophil chemotaxis |
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define passive immunity, what are the benifits and down sides |
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subject receives antibodies in form of Ig immunity is not long term but good when immunity is needed rapidly |
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what is an example of natural passive immunity |
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mother to child IgG through placenta IgA through breast milk |
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what is an example of artificial passive immunity |
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immunization with antibodies |
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define active immunity |
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subject is exposed to infection and produces antibodies |
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what is an example of natural active immunity |
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natural infection |
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what is an example of artificial active immunity |
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immunization with antigen administration |
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why do we combine active and passive immunity for rabies |
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when infected with rabies you give the antibodies to take care of initial antigen the antibodies are short lived so they outlive the initial infectin so give the vaccine too so it picks up when the antibodies run out |
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define Ro |
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basic reproductive number average number of people directly infected by one infected person when they enter a susceptible popultation |
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what factors affect Ro |
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duration of infection infectiousness of the organism number of susceptible people they come in contact with |
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what is the overall percent of people who need to be vaccinated to protect the population from an epidemic |
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85% |
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what are the live attenuated vaccines |
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rotavirus influenza MMR varicella/yellow fever |
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what vaccines are contraindicated in those with egg allergies |
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influenza |
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what vaccines are contraindicated in those with neomycin allergies |
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MMR and inactivated salk polio |
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what are the contraindications to live attenuated vaccines, why |
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immune compormised, pregnancy may revert to wild type and become virulent again |
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what is a live attenuated vaccine made of, how does it work |
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pathogen is active but has reduced virulence they colonize, infect, and replicate within pt but do not cause disease this generates the most robust immunological response without auctally getting the disease |
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when is the DTap administered, why |
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6wk to 6yo it is a pediatric vaccine, if given to adult it works fine but they have already had it so their arm will swell and be very painful because the vaccine is a higher concentration |
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when is the Tdap vaccine administered, why |
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when an adult it is less concentrated and kids who have not been vaccinated before will not respond to it |
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how do you get shingles |
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if you have HAD varicella zoster. NOT if you just had the vaccine |
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why are the rates of shingles increasing |
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kids are now vaccinated and are not exposing the active disease to their parents so they do not get a "booster" exposure and the immune system weigns allowing it to surface again |
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4 nose flora |
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S. aureus S. epidermitis diptheroids streo |
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7 skin flora |
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S. epi s. aureus diptheroids strep pseudomonas anaerobes candidia |
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3 SI flora |
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lactobacilli strep bacteroides |
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5 LI flora |
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99%... bacteroides, fusobacteroim, enterococcus fecalis then... E. coli, lactobacillus |
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6 vagina flora |
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lactobacillus E. coli GBS diptheroids candidia trichomonas |
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4 urethra flora |
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S. epi strep GNR diptheroids |
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1 lung flora |
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PJP |
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6 throat flora |
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S. viridans S. pyogenes S. pneumo neisseria H. influenza S. epi |
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5 gingiva flora |
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bacteroides actinomyces fusobacterium trichomonas entaoemba gingivalis |
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1 teeth flora |
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S. viridans |
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4 mouth flora |
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S. viridans Strep E. corrodenes candidia |
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4 common pathogens eye |
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S. aureus HIB N gonorrhea C trachomatus |
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3 common pathogens sinus |
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S. pneumo H. influenza M. cararrhalis |
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3 common pathogens URT |
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S. pyogenes H. ineluenza B. pertussus |
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1 common pathogens GI |
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H. pylori |
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8 causes of food poisoning |
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camplobacter E. coli salmonella shigella C. difficile becillus aeromonas listeria Yersinia |
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5 common pathogens UTI |
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E. coli P. mirabilis E. fecalis S. saphrophiticus P. aeruginosa |
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6 common pathogens STD |
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C. trachomatis N. gonorrheae T. pallidum M. genitalium U. urealyticum H. ducreyi |
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3 common pathogens skin |
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S. aureus S. pyogenes P. aeruginosa |
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3 common pathogens otitis media |
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S. pneumo H. influenza M. catarrhalis |
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5 common pathogens meningitis |
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S. pneumo N. meningitidis H. influenza GBS listeria |
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4 common pathogens HA pneumo |
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P. aeruginosa NRSA K. pneumo actineobacteri |
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3 common pathogens CA pneumo |
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S. pneumo atypical bacteria H. influenza |
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4 common pathogens for atypical pneumo |
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mycoplasma, chalmydophila, legionalla TB - not atypical, fungal, mentally grouped only |
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explain how to distinguish the staphs |
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all gram positive cocci all catalase positive S. aureus is coagulase positive S. epi is novobiocin susceptible S. saphrophiticus is novobiocin resistant |
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explain how to distinguish the streps |
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all gram positive cocci all catalase negative a hemolytic - optochin sensitive S. pneumo - optochin resistant S. viridans, S. mutans, S. sanguis B hemolytic -Bacitracin sensitive GAS (S. pyogenes) -Bacitracin resistant GBS (S. aglactiae) Y hemolysis -6.5%NaCl positive E. fecalis -6.5%NaCl negative S. gallolyticus (S. bovis) - grows on Bile azide esculin agar |
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explain how to distinguish the GPR |
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acid fast positive: mycobacterium acid fast negative -spores: clostridium, bacillus -none: corynebactrium, listeria |
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explain how to distinguish the GP filamentous |
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acid fast positive: nocatdia acid gast negative: actinomyces |
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what are the difficult to culture / atypical bacteria |
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chalmydia/chalmydophlia mycoplasma ureaplasma legionella |
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explain how to distinguish the GNDC |
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glucose fermenting negative: moraxella catarrhalis glucose fermenting positive - maltose ferment positive: N. meningitidis - maltose ferment negative: N. gonorrhea |
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what are the GN coccoid rods, how can one be distuinguished |
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haemophius: needs X and V factors pasturella brucella bordatella pertussus |
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what are the GN comma rods |
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camplobacter jejuni vibro chlera |
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explain how to distinguish the GNR |
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lactose ferment positive: Klebsiella, E. coli, enterobacter lactose fermentnegative - oxidase negative: acinetobacter, proteus, salmonella, shigella - oxidase positive: helicobacter camplobacter, vibrio, PSEUDOMONAS |
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what does moraxella cararrhalis ferment |
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nothing |
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what diseases does moraxella cararrhalis cause |
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otitis media UTI |
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what does N. lactamia ferment |
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glucose, maltose, LACTOSE |
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what does N. meningitidis ferment |
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glucose, MALTOSE |
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what does N. gonorrhea ferment |
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GLUCOSE only |
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what does E. coli ferment |
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lactose |
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what are the ways to identify P. aerguinosa |
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non lactose fermenting oxidase positive |
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what are the ways to identify S. saphrophyticus |
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Novobiocin resistant catalase positive coagulase negative Non-mannitol fermenting |
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what are the ways to identify S. epi |
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novobiocin sensitive catalase positive coagulase negative |
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how is syphilis identified |
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RPR/VDRL positive |
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what does herpes look like |
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cluster of painful blisters |
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what does ducrei look like |
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soft cancer very painful |
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what does chalmydia L1-3 cause, what are the symptoms |
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lymphogranuloma venerium: nodes swell, erupt, form open sore |
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what does chalmydia A-C cause |
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trachoma |
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what does chalmydia serotype D-K cause |
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STI PID urethritis ectopic pregnancy neonatal conjunctivitis/pneumo |
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how is chalmydia identified |
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non-infectious reticular bodies in cells (infectious elementary bodies are invisible) |
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how is gonorrhea diagnosed |
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GNDC intracellular - in male (lactobacillus in female is too similar) nucleic acids in female |
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symptoms of gonorrhea |
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burning urination cream colored purulent discharge |
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why wouldnt an antibiotic work for an STD |
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they have a secondary infection |
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what is a complication of gonorrhea |
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septic arthritis |
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cause of trichomonas |
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sexual transmission, ping pong |
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identification of trichomonas |
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possible positive whiff test frothy green/yellow discharge strawberry cervic (punctuate microhemorrhages) wet prep: swimming pears |
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identification of gardenerella vaginalis |
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high pH (bacterial imbalance) fishy odor on whiff test clue/glittr cells |
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identification of candidia |
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white thick cottage cheese discharge hyphe on KOH |
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locations of candidia |
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oral and vaginal thrush diaper rash between fingers body folds - red |
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identification of HSV |
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tzank cells: multinucleated giant cells on wright gemisa stain |
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cause of osteomyelitis in sickle cell, why |
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salmonella: capillary occlusion due to intravascular sickling may devitalize the gut and infarct allowing salmonella to escape into bone |
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4 causes newborn meningitis |
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listeria GBS rubella E. coli |
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5 causes adult meningitis |
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S. pneumo N. meningitis H. influenza GBS listeria |
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most likley cause of CAP |
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S. pneumo |
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most likley cause of HAP |
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S. aureus/MRSA acineobacter P. aeruginosa |
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most likley cause of BAP |
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S. aureus/MRSA acineobacter P. aeruginosa |
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HepB blood markers: vaccinated |
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+anti-HBs |
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HepB blood markers: resolved |
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+ anti-HBs + anti-HBc (IgG) |
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HepB blood markers: chronic carrier (infectious and not) |
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+ HBsAg +/- HBeAg + anti-HBc (IgG) |
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HepB blood markers: infected (acute resolving) |
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+ HBsAg + anti-HBs + anti-HBc (IgM) + anti-HBc (IgG) |
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HepB blood markers: acute (early) |
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+ HBsAg + HBeAg + anti-HBc (IgM) + anti-HBc (IgG) |