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smbj week 2
| Question | Answer |
|---|---|
| streptococcus | gram (+); catalase (-); occurs in pairs/chains; facultative anaerobes (grows aerobicially and anaerobically); makes lactic acid; requires complex nutrients |
| group A strep | strep. pyogenes; gram +, catalase -; facultative anaerobes; produce capsules, strongly B hemolytic; m protein as key virulence factor; bacitracin susceptible |
| M protein | present on group A strep; stops neutraphils from phagocytosing; can also act like a superantigen; we form antibodies against it and can be immune to a particular strain of strep (but there are many); these Ab can be autoreactive (rheumatic fever) |
| streptococcal pyrogenic exotoxins | virulence factor of group A strep; superantigens associated with scarlet fever rash, TSS, and necrotizing fascitis |
| GAS associated diseases | scarlet fever, pyoderma(impetigo), cellulitis, erysipelas, necrotizing fasciiitis, streptococcal toxic shock syndrom, etc. |
| cellulitis | deeper dermis and subQ fat; rapidly spreading edema, redness, heat; may see vesicles, bullae, cutaneous hemorrhage, fever, tachycardia, confusion, hypotension, leukocytosis; |
| cellulitis risk factors | obesity, previous cutaneous damage (trauma, ulcer, fissured toe webs from fungal infection), edema (venous insufficiency, lymphatic obstruction, saph vein excision for bypass surgery); chronic disease (atopic dermatitis) |
| cellulitis causative agents | group A strep most common; other Bhemolytic strep; staph aureus w/ increasing CA-MRSA |
| erysipelas | upper dermis; borders are elevated and sharply demarcated; more common in infants, young children, older adults; almost always group A strep |
| diabetic foot | acute wounds: s. aureous; B hemolytic strep; chronic wounds: enterocci, obligate anaerobes, p. aeruginosa, enterobacteriaceae; CA-MRSA increasingly |
| necrotizing fasciitis | deep infection of fascial and/or muscle compartments; results from initial break in skin (trauma or surgery); presents like cellulitis |
| Necrotizing fasciitis red flags | sever pain, bullae, skin necrosis, large purpura; hard subQ tissue; cutaneous anesthesia; systemic toxicity; rapid spread during antibiotic therapy |
| causative agents | monomicrobial: s. pyogenes, s. aureus, anaerobic strep (community acquired and in pts with DM or vascular insufficiency) polymicrobial: an/aerboic(bowel flora); associated w/ abdominal surgery, decubitis/perianal ulcer, artholin abscess, IVDU |
| GAS clinical manifestations | fever, toxicity, severe pain; 50% have defined portal of entry; tachycardia, hypotension, wbc left shift, low platelets, bullae, purpura; less common in children, mortality 30-60% |
| gas gangrene/myonecrosis | infection of area below fascia of the muscle resulting from penetrating trauma or crush injury that interrupts blood supply; |
| causative agents of gas gangrene | traumatic - c. perfringes, c. novyi, c. histolyticum; spontaneous (hematogeneous) - c. septicum in pts with GI malignancy or neutropenia |
| therapy for GAS gangrene | aggressive surgical debridement and penicillin and clindamycin |
| susurgical site infections | - most due to s.aureus, coag negative staph, enterococcus, e.coli; early infections (first 48 hrs) often due to strep. pyogenes and clostridium |
| clean wound | uninfected, uninflammed operative wound with no entry of respiratory, GI, genital, urinary tracts |
| clean, contaminated wound | entry of respiratory, GI, GU under controlled conditions w/o unusual contamination |
| contaminated wound | open trauma, major breaks in sterile technique, gross spillage GI, incisions w/ acute inflammation |
| dirty-infected wound | old trauma wounds w/ devitalized tissue and those with clinical infection or perforated viscera |
| B-lactam antibiotics | penicillins, cephalosporins, monobactams, carbapenems; 4-membered carbon ring=B-lactam nucleus; target penicillin binding proteins and inhibit the transpeptidase activity |
| penicillin binding protein | bacterial enzymes w/ transpeptidase and carboxypeptidase activity; cross-link peptidoglycan chains forming cell walls; regulate cell shape/size; different PBPs in a cell w/ different functions; numbered by size (1=largest); B-lactams target different PBPs |
| penicillin structure | house and garage; five membered ring adjacent to B-lactam nucleus; 1 R side chain |
| cephalosporin structure | 6 membered ring and B-lactam nucleus; 2 R side chains |
| monobactam structure | only B-lactam nucleus |
| carbapenem structure | 5 membered ring attached to B-lactam nucleus; 1 R side chain; 1 double bond and a sulfur atom |
| autolysin | responsible for cell wall turnover and permit cell growth; produce controlled weak points allowing for expansion of cell wall; stimulated by B-lactams causing breakdown of peptidoglycan, osmotic fragility -> cell lysis |
| major mechanisms of resistance to B-lactams | B-lactam hydrolysis by B-lactamases; altered PBPs, reduced membrane permeability |
| B-lactamases | bacterial enzyme that blocks B-lactam from binding transpeptidase by opening 4membered ring; plasmid mediated B-lactamases spread via conjugation; chromosomal B-lactamases are present in most bacteria & cause clinical resistance; now can jump to plasmids |
| penicillin pharmacology | - oral absorption varies; well distributed; enter CNS if meninges inflamed (5-10% -> enough to treat meningitis); short 1/2 life -> frequent dosing; renal excretion |
| penicillin G | active against gram + cocci (B-hemolytic strep; viridans strep); drug of choice for s. pneumoneiae, syphilis, N. meningitidis, many anaerobes, (not DOC for bacteroides); given IV or intramuscular (not orally usually) |
| benzathine PCN | IM use; used for syphilis, rheumatic fever prophylaxis, strep throat; low levels that last for 15-30 days |
| penicillin V | - orally, acid stable, better absorption than PCN G |
| methicillin | has bulky side chain that allows it to block B-lactamases but cant cross porin proteins so has no gram - activity; active against most streptococci; staph resistant b/c of altered PBP |
| nafcillin | has bulky side chain that allows it to block B-lactamases but cant cross porin proteins so has no gram - activity; active against most streptococci; used for MSSA; give dicloxacillin PO |
| aminopenicillins | ampicillin and amoxicillin; better than PCN for enterococcus, listeria, H.flu; limited against gram - bacilli b/c of B-lactamases; amoxicillin is preferred (better oral bioavailability, less frequent administration); DOC for strep throat, ear infection |
| extended spectrum pnicillins | increased affinity for PBPs and increased periplasmic space entry; piperacillin=protype drug; DOC for pseudomonas; in combo w/ B-lactamase inhibitor b/c very susceptible to B-lactamases |
| B-lactamase inhibitors | bind B-lactamases irreversibly (mostly plasmid encoded not chromosomal); combine with PCN; weakly antibiotic; better activity against MSSA, h.flu, e.coli, klebsiella, moraxella catarhalis, anaerobes, nosocomial gram - bacilli depending on PCN used |
| agumentin | amoxicillin/clavulanic acid; PO; useful for URI's sinusitis, otitis, DOC for bite wound prophylaxis; diarrhea common side effect |
| Unasyn | ampicillin/sulbactam; IV; use for odontogenic, diabetec foot infections, aspiration pneumonia (mixed infection); not good for nosocomial gram - bacilli |
| zosyn | piperacillin/tazobactam; mixed infections and nosocomial gram - bacilli (pseudomonas)and nosocomial mixed infections |
| SPACE | serratia, psuedomonas, acinetobacter, citrobacter, enterobacter; nosicomial gram - bacilli; can develop resistance to all PCN and cephalosporins; not blocked by B-lactamase inhibitors |
| cephalosporins | good safety profile, longer 1/2 life than PCN; renally eliminated; good oral bioavailability; wide spectrum activity; 3rd and 4th gen. have good CSF penetration; B-lactamase stability better than PCN; DONT cover enterococcus, MRSA, listeria |
| cefazolin (ancef) | 1st gen; cephalexin is similar in oral; active against strep and s. aureous; CA gram - bacilli (e.coli, proteus mirabilis, klebsiella); good for SSTI; preop prophylaxis |
| 3rd generation cephalosporins | more gram - and less gram + activity; some activity against s.aureus; active against s. pneumoniae; very active against e.coli, klebsiella, proteus, providencia, serratia; inactivated by chromosomal B-lactamases in nosocomial gram- bacilli; good CSF entry |
| ceftriaxone (rocephin) | 1/2 life=8hrs, given 1/day; treats complicated UTI's, CA pneumonia(pneumococcal) some nosocomial infections, meningitis |
| ceftazidime (fortaz) | very bad gram+ & anaerobic activity of 3rd gen; antipseudomonal - only used when pseudomonas is present or suspected; nosicomial infections, febrile neutropenia, DOC pseudomonas meningitis |
| cefipime (maxipime) | 4th gen; broad aerobic activity; resistant to chromosomal B-lactamases; active against enterobacter and citrobactor; antipseudomonal; gram+ activity includig MSSA; gram- nosocomial infections w/ resistance to other drugs |
| ceftaroline | increased binding affinity for PBP2a -> active against MRSA and PCN resistant S. pneumoniae; good gram - activity; SSTI, CApneumonia; new |
| monobactams | aztreonam(azactam); broad gram - activity (incl. pseudomonas aeruginosa); not active agst acinetobacter (makes aztreonam); doesn't bind PBPs of gram+ & anaerobes; no IgE cross rxn w/ PCN or cephalosporins (except ceftazidime)-> used in allergic pt |
| carbapenems | meropenem (merrem); widest spectrum B-lactam; cross outer cell membrane; B-lactamase stability; high affinity to PBPs; against most gram+ cocci (except MRSA, VRE, e. faecium), most anaerobes, most gram- bacilli; restricted use b/c resistance is a problem |
| appropriate uses for carbepenems | infections with antibiotic resistant gram - bacilli; empiric Rx of serious infections in pts previously treated with broad-specturm antibiotics; some polymicrobial infections instead of multidrug regime |
| carbapenemases | most versatile B-lactamase; were chromosomally encoded, now on plasmid and can be transferred to other bacteria |
| Klebsiella pneumonia carbapenemase (NDM-1) | hydrolyzes B-lactams of all classes; on transferable plasmid; often in multidrug resistant K.pneumoniae |
| IgE mediated allergy | type I; most serious; immediate <1 hr; urticaria, anaphylaxis, wheezing, laryngeal edema, hypotension; epitope=penicillin nucleus (highly cross reactive); should avoid cephalosporins if there is alternative |
| IgG, IgM mediated allergy | type II; occurs w/ long course of therapy; drug-induced nephritis; can attach to RBC and cause hemolytic anemia, thrombocytopenia, neutropenia |
| Immune complex mediated allergy | type III; 7-14 days into therapy; drug fever (fever goes away and comes back or persists w/ therapy); serum sickness |
| cell mediated allergy | type IV; contact dermatitis (not used topically) |
| idiopathic allergy | maculopapular rash, exfoliative dermatitis, SJS, eosinophilia, vasculitis; late rxn (days-weeks); cause unknown, common and most impt; can affect mucous membranes; can cause loss of skin and 2ndary infections |
| osteoperosis | skeletal disorder characterized by compromised bone strenght, predisposing a person to an increased risk of fracture; involves quality and density; T<-2.5 |
| bone density | grams of mineral per area or volume |
| bone quality | architecture, turnover, damage accumulation and mineralization |
| calcitrol | active form of vitamin D - binds vitamin D receptor which modulates gene expression involving ca absorption |
| too little/too brittle bone disorders | osteoporosis; osteomalacia, osteogenesis imperfecta, hypophosphatasia |
| too much/wrong place; slcerosing bone disorders | osteopetrosis, osteosclerosis; increased formation or decreased resorption; susceptible to fracture b/c of abnormal quality; mutations in osteoblast/clast differentiation or in remodeling |
| chaotic bone disorders | pagets, jevnile pagets, familial expansile osteolysis |
| osteopetrosis | autosomal recessive infantile malignant (more severe); autosomal dominant osteopetrosis type II; both are defective osteoclastic resorption |
| autosomal recessive infantile osteopetrosis (ARO) | dense, brittle bone that fractures; defect in Cl- pump b/c of ClCN7, TCIRG mutation (normal OC #s); or RANKL mutation (low OC#); bone replaces marrow reducing hematopoeitc function; cranial nerve compression; death <10 w/o treatment (marrow transplant) |
| autosomal dominant osteopetrosis | later childhood onset; spine slcerosis; fractures common, heterozygous ClCN17 mutation in Cl- pump (milder); skull sclerosis -> CN compression; osteomyelitis of mandible b/c of dental abscess; variable penetrance & severity; sandwich vertebra |
| pycnodysostosis | rare autosomal recessive; infancy/early childhood dx; short stature, clubbed fingers, large cranium, facial dysmorphism, small square hands, hypoplasia of fingernails; sunken chest, kyphoscoliosis, lumbar lordosis; fractures; mutation in cathepsin K of OC |
| cathepsin K | osteoclast protein; lysosomal cystein protease that breaks down bone and cartilage, specifically elastin, colalgen, gelatin |
| carbonic anhydrase II deficiency | autosomal recessive defect in CAII deficiency; affects other organs; renal tubular acidosis, cerebral calcifications; mental subnormality, dental malocclusion, optic nerve compressio; sclerosis diminishes w/ age |
| disorders with increased bone formation | progressive diaphyseal dysplasia, endosteal hyperostosis related disorders, fibrodysplasia ossificans progressiva; hereditary multiple exostoses |
| Progressive diaphyseal dysplasia (camurati-engelmann disease) | autosomal dominant; gradual symmetric bone growth on long bones; variable age of onset, severity; mutation in TGFB sequestering protein which normally inactivates bone growth factors BMP/TGFB, or TFGB itself; RANKL mutation in some has unclear pathophys |
| endosteal hyperostosis and related disorders | related to WNT signaling; van Buchem disease, sclerosteosis, endosteal hyperostosis (worth); |
| van buchem and sclerosteosis | loss of function mutations in SOST and DKK; which are normal inhibitors of WNT singlaing -> constitutively active wnt signaling -> constant bone formation; optic atrophy, facial nerve palsy, deafness; point pressure on long bones; serum alkphos high |
| endosteal hyperostosis (worth type) | dominant, benign; no fractures, bone remodels normally, very high bone densities; flattened forehead, elongated mandible, toras palatinus, mutation in binding wnt coreceptor to inhibitor of wnt signaling -> excessive bone formation |
| pachydermoperiostosis | autosomal dominant; adolescent disorder; big hands, feet, thick skin; joint pain; bone groth on tubular bones, clubbing; inactivation of HPGD causes loss of degradation and PGE-2 accumulation stimulating ostoeblasts |
| fibrodysplasia ossificans progressiva | child turns to bone; starts often at site of trauma; also have malformation of great toes; doesnt involve cardiac tissue diaphragm, tongue, extraocular muscles; live until ribs fuse; mutation makes BMP receptor hyperactive -> osteoblasts in wrong tissues |
| Paget's disease | dirsorder of bone remodeling; disorganized woven bone; deformity, fracture, metabolic derangement; likely due to osteoclast function; areas of sclerosis and resorption; age of onset 50s-70s; more common in males; genetic susceptibility; poly/mono-ostotic |
| symptoms of pagets disease | skeletal deformities (bowed leges); warm to touch b/c of hypermetabolism; moth-eaten bone appearance (sclerosis and resorption); skull problems; spine pain - picture frame vertebrae; |
| skull involvement in pagets disease | big head, heavier, hearing loss, sclerosis and lytic regions, platybasia [weak base can cause brain hernia], hydrocephalus[csf buildup]; pagetic steal syndrome[shunts blood to high metabolic areas, can cause stroke]; leontis ossea[large face/tooth probs] |
| leontiasis ossea | rare complication of paget's disease; enlarged facial bones, jaw involvement; malocclusion, loss of teeth, hemorrhagic complications of oral surgery, difficult tooth extraction |
| complications of pagets | pain, fracture, neurologic syndromes; osteosarcoma, giant cell tumors, hypercalcemia/hypercalciuria; gout, high output heart failure |
| indications for tx of pagets | advanced disease, symptomatic/active disease; asymptomatic pts w/ weight bearing bone or skull involvement; prolonged immobilization |
| tx options for pagets | analgesics, nsaids, cox2, PT, ortho/neurosurgery for pain; antiresorptive drugs (bisphosphonates and salmon calcitonin-analgesic and retracts osteoclasts) |
| piriformis fossa | area on the femur near the greater trochanter; entry point for intramedullary devices to fix a fracture |
| labrum | rim of the acetabulum, forms seal round joint and keeps synovial fluid in to minimize stress and provide stability |
| ligaments of the hip | iliofemoral, ischiofemoral, pubofemoral |
| weak spots of hip | anterior space between iliofemoral and pubofemoral; posterior space between iliofemoral and ischiofemoral |
| meralgia parasthetica | impingement on lateral femoral cutaneous nerve at its exit from pelvis under the inguinal ligament; loss of sensation to skin around pants pocket |
| mode of action for hip fracture - high energy | in younger people w/ good bone quality and healing potential, ex: MVA |
| mode of action for hip fracture- low energy | older people w/ poor bone quality and lower healing potential, ex: ground level fall |
| mode of action for hip fracture - pathologic | fracture secondary to underlying pathology (osteoporosis, tumor, etc); injury pattern not consistent with mechanism; hx of pain in the same location prior to injury |
| femoral neck fracture | 95% of all hip fractures; blood supply at risk; doesnt heal well b/c of synovial fluid; displaced and non displaced; low surface area for healing; sucapital, transcervical, basicervical |
| subtrochanteric fracture | rare, high energy trauma, usually in younger pts |
| femoral head fracture | reare, high energy trauma, usually causes dislocation |
| intertrochanteric fracture | along line between trochanters; high rate of healing b/c there isnt synovial fluid, blood supply isnt at risk and there is a larger surface area |
| internal fixation criteria | younger (<50); non-displaced, good bone quality, less vertical fracture; normal joint and cognitive function |
| arthroplasty criteria | elderly; displaced; bad bone quality; more vertical fracture; arthritic joint, compromised cognitive function |
| acute osteomyelitis | onset in days-wks |
| chronic osteomyeltis | onset in wks-months; necrotic bone is common; can persist for years |
| hematogenous osteomyelitis | bacterimic seeding of bone; occurs in children and older adults; involves long bones(humerus, femur, tibia) and vertebrae; |
| contiguous osteomyelitis | spread from infections, traumatic/penetrating injuries, post ortho surgery, diabetic and ischemic ulcers; in skull, mandible, hand,femur,tibia,foot; likely polymycrobial (s.aureus, strep, enterococci, enterobacter, pseudomonas, anaerobes; subtle symptoms) |
| hematogenous osteomyelitis in children | bacteria may be trapped in small vessels w/o immune cells (metaphysis of long bones); <1 and >puberty dont have grwoth plate, may spread to joint; 1-puberty, growth plate acts as barrier; staph.aureous; group B strep (newborns); other strep, coag- staph |
| hematogenous osteomyelitis in elderly | common in vertebral bodies (highly vascularized); may spread via batson's venous plexus; staph aureus, gram negatives |
| hematogenous osteomyelitis in IVDU | sternoclavicular, sacriliac and pubic bones; s.aureous, pseudomonas aergurinosa, serratia |
| staphylococcus aureus | hardiest,nonsporeforming organism; gram+cocci in clusters; catalase+; coagulase +(other staph are -); +mannitol fermentation; hemolytic; yellow colonies; highly virulent; carried in nasopharynx, skin, vagina |
| s. aureus infections | SSTI; bone,joint infections; post surgery/trauma; bloodstream (complications: bone/joint, meningitis, endocarditis, pericarditis, lung..); toxin mediated disease (food poisoning, scalded skin, TSS) |
| s. aureus virulence factors | catalase(interferes w/ phagocytic killing); clumping factor, techoic acid, proteins A/B(adherence); lipases (abscess formation); leukocidin(pore foramtion and lysis of phagocytic cells); toxins (superantigens: TSST-1, enterotoxin, exfoliative toxins) |
| imaging osteomyelitis | xray: takes 2-3weeks to be +, see motheaten, periostial elevation, later see sclerosis; ct: sensitive; bone scan: early disease but false+; MRI: preferred, early changes and defines soft tissue abnormalities clearer |
| diabetic foot osteomyelitis | if probe hits bone-dx is osteomyelits; polymicrobial(s.aureus/Bhemolytic strep for acute, enteroocci, anaerobes, pseudomonas, enterobacteriacea for chronic; CA-MRSA becoming common) |
| tx for MSSA osteomyelitis | nafcillin or oxacillin |
| tx for MRSA osteomyelitis | vancomycin or daptomycin |
| tx for streptococci osteomyelitis | penicillin G cefriaxone, cefazolin |
| tx for enteric gram negative osteomyelitis | ciprofloxacin, ceftriaxone |
| tx for serratia or pseudomonas aerguinosa osteomyelitis | ceftazidime, piperacillin-tazobactam, cefepime |
| tx for anaerobe osteomyelitis | clindamycin, metronidazole |
| surgical tx for osteomyelitis | debridement to remove necrotic bone(common with DM foot, rare for vertebral); revascularization for large vessel arterial disease |
| acute septic arthritis | hematogenous spread; staph.aureus, strep, gram - rods, n. gonorrhoeae (DGI); acute monoarticular arthiritis is considered septic until disproved; joint fluid: elevated WBC but not specific to infection; drain joint and give system antibiotcs for 2-4wks |
| disseminated gonococcal infection (DGI) | more common in females; asymptomatic mucosal infxn, gram - diplococci inside wbc; serum resistant, hard to culture so cultures blood, joint, and mucosa; bacteremic or localized |
| bactermic DGI | tenosynovitis, dermatitis, polyarthralgia/arthritis, fever, papules and pustular skin lesions (4-40) |
| localized joint DGI | prurulent arthritis (1-2 joints) |
| early prosthetic joint infection | acute; continguous infection, <3 mo post op, virulent organism (s. aureus); symptoms: overt pain, erethyma, fever |
| delayed prosthetic joint infection | chronic, contiguous infection, 3-24 mos post op; less virulent (coag negative staph); subtle symptoms: loosening/pain of joint |
| late prosthetic joint infection | hematogenous spread, >2 yrs post op; organisms depend on source of bacteremia; not from surgery but later infxn; symptoms: pain, erythema after long period of no symptoms |
| chronic septic arthrits | presents over wks-mos; mycobacteria (TB and non-TB), lyme disease, fungi(sporothrix, coccidiodes, cryptococcus, bastomyces, candida) |
| viral agents associated with arthritis | childhood viruses presenting in adults: rubella and parvovirus B19 in women and mumps in men |
| non surgical treatment options for knee OA | weight loss, strength/aerobic exercise, joint protection devices; acetaminophen, NSAIDS, COX II inhibitors, topical capsaicin, intraarticular steroid and hyaluronic acid injections |
Created by:
hwhitworth