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90 Cards in this Set
- Front
- Back
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MCC septic arthritis in kids
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Hib (H influ b)
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lymphogranuloma venereum
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=Chlamydia
-painless matted suppurative inguinal LN's |
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Reiter's syndrome
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(James)
=inflammatory arthritis of large joints in young men b/w 20 and 40 (James) -inflam of eyes: conjunctivitis/uveitis (james) -link to Chlamydia |
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lymphogranuloma venereum
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-d/t Chlamydia trachomatis
-starts with painless papule (bump) or ulcer on genitals that heals spontaneously -then migrates to regional LN, which enlarge over 2 months -LN's become tender and can break open and drain pus |
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Tx ricketssia
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doxycycline & chloramphenicol
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subacute meningitis with incr lymphocytes
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Treponema pallidum
M. tb |
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syphilis stages
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Primary:
(6 wk) *painless chancre Secondary: (6 wks after chancre healed, lasts 6 wks) Systemic Sx: *fever, weight loss, hair loss *generalized lymphadenopathy *maculopap rash on palms/soles *condylomata lata *can spread to CNS, eyes, bones, kidneys, joints Tertiary: (6+ years) *CNS (neurosyphilis) --subacute meningitis w/lots lymphocytes --tabes dorsalis *Ao aneurysms *gummas (granulomatous "gummy bears") of skin and bone "Rule of 6's": 6 axial filaments 6 week incubation period 6 weeks for chancre to resolve 6 weeks after chancre heals, secondary syphilis develops 6 weeks for secondary syphilis to resolve 6+ years for tertiary syph to develop 66% latent syphilis pts never develop tertiary syphilis |
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Dx syphilis
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1. First do Nonspecific Tests:
*VDRL *RPR (detect anti-cardiolipin Ig) 2. Confirm with Specific Test *FTA-ABS (indirect immuno"F"lourescent "T"reponemal "A"ntibody-"ABS"orption) (detect anti-Treponema pallidum Ig) |
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(-) VDRL/RPR & (+)FTA-ABS
suggests |
successfully treated syphilis
(successfully treated syphilis==>decr anti-cardiolipin I, but same levels of specific anti-treponemal Ig) |
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(+) VDRL/RPR & (-)FTA-ABS
suggests |
false positive for syphilis
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(+) VDRL/RPR & (+)FTA-ABS
suggests |
active treponemal infxn (syphilis)
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Tx syphilis
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Penicillin (can even cross placenta and cure congenital syphilis)
If allergic to penicillin, give: -erythromycin (can give to pregnant women to prevent congenital syphilis) -doxycycline (don't give to pregnant women b/c toxic to fetus) |
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Tx Lyme Dz
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penicillin family
or doxycycline |
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Relapsing fever
-etiology -transmission -Tx |
Borrelia recurrentis ("recurring" fever)
-transmitted by body louse Pediculus humanus -Tx with erythromycin or doxycycline (~Borrelia burgdorferi: Tx with penicillin family or doxycycline) |
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Tx Mycoplasma
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erythromycin + tetracycline
(penicillin and cephs don't work b/c Mycoplasma is tiny & only has simple sterol-packed cell membrane with no peptidoglycan cell wall) |
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beta-lactamase
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-secreted by G+ bacteria
-cleaves B-lactam's C-N bond (stops B-lactam before it even reaches the peptigoglycan cell wall) |
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penicillins that offer better coverage of G- bacteria
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AMpicillin & AMOxycillin kill G- bugs, like:
GI bugs: -E coli -Proteus -Shigella/Salmonella Amoxicillin Tx -bronchitis, sinusitis -UTI's caused by G- bug |
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transpeptidase
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AKA PBP's (Penicillin Binding Proteins)
-MRSA alters its transpeptidase (PCP)'s==>no drugs in penicillin family can bind |
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penicillinase-resistent penicillins
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AKA B-lactamase resistant penicillins; thus they can kill Staph aureus
Methicillin Nafcillin Oxacillin visualize pic and say "i MET a NAsty OX with a B-lactamase ring around its neck" (ridic p. 116) --------- ORALLY ACTIVE B-lactamase resistant drugs= CLOXacillin & diCLOXacillin "The CLOX were ticking: it was only a matter of time before they discovered the orally-active B-lactamase resistant drugs." -good against G+ B lactamase bacteria, but not G- i.e. person with skin wound==> most likely has SA or Strep B==>give CLOXacillin so you don't have to care for him around the CLOX ("clock") ------------------------ cephalosporins |
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Tx cellulitis, impetigo
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person with skin wound most likely has SA or Strep B
==>give CLOXacillin so you don't have to care for him around the CLOX ("clock") (CLOXacillin & diCLOXacillin are ORAL B-lactamse resistant penicillins) |
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broad G- coverage
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"Amp-gent" (Ampicillin & gentamicin, an aminoglycoside)
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Tx Pseudomonas
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gentamicin + one of these:
TICaricillin CARbenicillin PIPEracillin (ridic p. 117-8) -------------------------- cefTAZidime (3rd gen) ceFOPerazone (3rd gen) ceFEPime (4th gen) (imagine Kate (Pseudomonas) on FOP (~FEP) trip, when she gets attacked by TAZmanian devil) |
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B-lactamse inhibitors
-ex's -what Tx |
clavulanic acid
sulBACTAM tazoBACTAM (B-lACTAMase inhibitors) in order to Tx B-lactamse producing G+ (i.e. SA), G- (H flu), & anaerboes (B. fragilis), can give: penicillin that is not normally resistant to B-lactamase (ampicillin, amoxicillin, ticaricillin, piperacillin) with B-lactamase inhibitor (listed above) |
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how Tx B-lactamase producing G+ (i.e. SA), G- (H flu), or anaerboes (B. fragilis)
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can use a penicillin that is not normally resistant to B-lactamase (ampicillin, amoxicillin, ticaricillin, piperacillin)
COMBINED with B-lACTAMase inhibitor: clavulanic acid sulBACTAM tazoBACTAM |
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what bugs are resistant to cephalosporins
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MRSA & Enterococci
(b/c altered PCP's) [cephs are B-lactamase resistant, thus mech of resistance must be something else] |
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how Tx person with skin infxn who is allergic to penicillin
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1st generaton ceph
(1st generation= "PH=you must get a PH.D. in PHarmacology to learn the 1st gen ceph) cePHalothin cePHapirin cePHradrine cePHalexin exceptions=ceFAZolin, ceFADroxil (ceFAZolin/ceFADroxil don't have a PH. Don't let this FAZe/FADe your efforts!) |
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Tx E coli
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third generation ceph (higher generations are less effective against G+ and more effective against G-)
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general trend in 1st, 2nd, & 3rd generation cephalosporins
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(higher generations are less effective against G+ and more effective against G-)
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list the cephalosporins
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1st generaton ceph
(1st generation= "PH=you must get a PH.D. in PHarmacology to learn the 1st gen ceph) cePHalothin cePHapirin cePHradrine cePHalexin exceptions=ceFAZolin, ceFADroxil (ceFAZolin/ceFADroxil doesn't have a PH. Don't let this FAZe/FADe your efforts!) II. 2nd generation cephalosporins: "After you got your "PH."D., your FAMily, wearing FUR coats, MET to have some FUN (~FON). Your FOXy cousin, a PROfessional model, is drinking TEA in a toast to you. Your other cousin LORA arrives late to your party (honking her horn) in her shiny new car (LORACARbef)" ceFAMandole ceFAclor cefMETazole ceFONicid ceFURoxime ceFOXitin cefPROzil cefoTEtan ("pronounced cefo-TEA-tan) LORACARbef III. 3rd generation ceph: most have a "T" for Tri (3rd) in their name: cefTRIaxone cefTAZidime cefeTamet cefoTAXime cefTIzoxime cefTIbuten (exceptions: cefixime ceFOPerazone ceFPOdoxin) (note cefotetan (TEA) is a 2nd gen drug) (ridic p. 119-120) |
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Tx:
-intra-abdominal infxns -aspiration pneumonias -colorectal surgery prophylaxis |
all these involve conatmination from GI tract
==>thus anaerobic bacteria "A FOX (ceFOXitin) MET (ceMETazole) an anerobic bug for TEA (cefoTEtan)." (note these are all 2nd generationc cephalosporins) |
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Tx nosocomial pneumonia, meningitis, UTI, sepsis
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These are multi-drug resistant G- infxns.
Thus use 3rd gen ceph |
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Tx meningitis in neonates, children and adults
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cefTriaxone ("T"=Three=3rd gen ceph)
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Rx that kills G+, G-, and anaerobes
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Imipenem (broadest antibacterial coverage known to man!!; say "I'm a pen" and imagine myself crossing out all the hard-to-kill bugs)
-Give with cilastin to prevent kidney from breaking down imipenem. only bad thing: S/E=seizures *Meropenem is just as strong as Imipenem but don't need to give with cilastatin & doesn't cause seizures as much |
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Tx G- aerobic bacteria
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aztreonam
(good pic: ridic p. 121) MOA: binds PCP's of G- aerobic bacteria ONLY (not G+ or anaerobes) |
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DOC CAP
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erythromycin; b/c it covers:
-Strep pneumo -M tb -Chlamydia (TWAR strain) (pic: ridic p. 128) |
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Tx gonorrhea
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1. cefTriaxone (3rd gen ceph==>Tx G-) + doxycycline/azithromycin for chlamydia
2. quinolone antibiotics (ciprofloxacin, ofloxacin): "FLOCK OF SINners" 3. "Spectacular Spectinomycin" |
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what do these indicate:
-HBsAg -anti-HBsAg -anti-HBcAg -HBeAg -anti-HBeAg |
-HBsAg==>active infxn.
-anti-HBsAg==>immunity, no active infxn anti-HBcAg antibodies indicate infxn. These antibodies are not protective, but they tell how long the infxn has been going on: -IgM anti-HBcAg==>new infxn -IgG anti-HBcAg==>old infxn (chronic or resolving) -HBeAg==>active disease AND high infectivity. -anti-HBeAg==>active dz but low infectivity. |
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defective acute transforming virus
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Oncogenes are so long that most acute transforming viruses have lost their own viral RNA critical for viral replication. Thus, they are called "defective acute transforming viruses" and require a co-infecting virus to cause cancer.
-The Rous sarcoma virus is the only acute transforming virus AKA that is not defective. That means that in addition to the oncogene (src oncogene in Rous), it contains full RNA genome needed for replication. |
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erb B
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oncogene that looks like EGF receptor
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Rous sarcoma
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transmitted via virus.
-The Rous sarcoma virus is the only acute transforming virus AKA that is not defective. That means that in addition to the oncogene (src oncogene in Rous), it contains full RNA genome needed for replication. Oncogenes are so long that most acute transforming viruses have lost their own viral RNA critical for viral replication. Thus, they are called "defective acute transforming viruses" and require a co-infecting virus to cause cancer. Rous sarcoma is the only exception. |
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human retrovirus besides HIV
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HTLV (Human T-cell Leukemia Virus)
-causes tropical spastic paraparesis |
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acute transforming viruses
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retroviruses that carry intact oncogenes within their viral genome, which get integrate into host DNA and cuase malignant transformation. The integration is facilitated by "sticky" ends and an enzyme called integrase
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non-acute transforming viruses
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retroviruses that activate host proto-oncogenes by integrating viral DNA into a key regulatory region
(vs. acute transforming viruses which carry their own oncogene) |
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purpose of LTR's in HIV
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LTRs=Long Terminal Repeat sequences
2 purposes: 1. =Sticky Ends of the HIV virus (which are the part recognized by integrase, which then integrates HIV into host cell) 2. serve as promoter/enhancer |
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purpose of HIV gag
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gag (GAG="G"roup "Ag") codes for envelope proteins:
-nucleocapsid -capsid protein p24 -matrix proteins |
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purpose of HIV pol
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encodes viral protease, integrase, and reverse transcriptase enzymes
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p24
gp41 gp120 are located where in HIV virus? |
p24=caPsid protein
gp41 & gp120 = envelope proteins (gp=glycoprotein) |
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what are the regulatory genes of HIV
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1. tat
-encodes viral TransAcTivator protein (Trans=Transcription; thus tat=TranscriptionAcTivator) -activates transcription 2. rev -"REVs" up viral activity by the following MOA: HIV virus can be spliced into many pieces, or just a few pieces (gag, pol, env) which are the major things that produce virions -rev gene binds to the env gene to decrease splicing, so it REVs up teh reading of gag, pol, and env to produce virions! 3. nef -ppl with nef-deficient HIV do not develop AIDS or T cell destruction |
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what part of HIV binds to what part of CD4+ T cells & macrophages?
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HIV gp160 (composed of gp41 & gp120 envelope glycoproteins)
binds to: CD4+ T cells @ fusin surface protein CKR5 surface protein of macrophages |
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which opportunistic AIDS infxns occur at which CD4+ cell counts?
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CD4 < 400 ("pre-AIDS defining"):
-oral thrush (rubs off with tongue blade==>red bleeding base) -oral hairy leukoplakia (d/t EBV; on sides of tongue, does not rub off with tongue blade) -herpes zoster (shingles) -M. tb -systemic bact: ---S pneumo ---H flu ---Salmonella CD4 < 200 ("AIDS defining"): -PCP -Toxoplasmosis -Cryptococcal meningitis -Cryptosporidium & Isostora Belli Diarrhea -Coccidiomycosis (disseminated) CD4 < 50 ("AIDS defining"): -CMV retinitis -CMV esophagitis -CMV (disseminated) -Mycobacterium avium-intracellulare (disseminated) |
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effects of HIV on specific players in the immune system
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*T-cell death==>B cell dysfxn
*multinucleated giant cells --HIV gp160 binds CD4+ cell and then binds up to 500 adjacent CD4+ cells ==>This multinucleated giant cell allows virus can pass from CD4+ to CD4+ without being exposed to blood, so virus is shielded from circulating antibodies *Monocytes/Macrophages: -HIV virions replicate within macrophages but do not kill them ==>moncoytes/macs serve as reservoirs of HIV ==>monocytes/macs can migrate across BBB and infect the CNS |
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excluding opportunistic infxns, what illnesses does AIDS cause?
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1. Encephalopathy (HIV infected monocytes/macrophages cross BBB)
2. Malignancy: a. B-cell lymphoma, usu d/t EBV b. Kaposi's sarcoma |
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when is a Western blot considered positive?
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if it has bands (meaning the person has antibodies against) for 2 HIV gene products (p24, gp41, gp120)
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why is it difficult to develop HIV vaccine?
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1. rapidly mutating V3 (hypervariable) portion of gp120
2. HIV is transmitted from CD4+ to CD4+ in the multinucleated giant cell without contacting the blood ==>HIV protected from circulating antibodies |
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Tx Toxoplasmosis
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pyrimethamine/sulfa
(~Trim/sulfa: both TriMETHOprim & pyriMETHamine inhibit DHF-R) |
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Tx CMV retinitis
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ganciclovir or foscarnet
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Tx oral thrush/esophagitis
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Nystatin ("Nasty Nystatin")
fluconazole clomitrazole (all orally) |
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Tx systemic Candida in HIV
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amphotericin
fluconazole |
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Rx to prevent future Mycobacterium avium-intracellulare infxns in AIDS
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azithromycin or clarithromycin
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MCC viral encephalitis in US
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HSV-1
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herpes zoster
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shingles
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MC viral cause of MR
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CMV (it's a TORCHHS infxn that crosses placenta and causes MR in fetus)
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molluscum contagiosum
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-caused by poxvirus (which caused smallpox)
-usu in AIDS pts |
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Papovaviridae
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"PA-PO-vavirus" consists of:
I. "PA"pilloma virus II. "PO"lyomavirus I. "PA"pilloma virus a. warts b. cervical cancer II. "PO"lyomavirus a. BK Polyomavirus -"as ubiquitous as "B"urger "K"ing" -mild infxn in kids b. JC Polyomavirus ~BK in healthy ppl but in imm-s ppl, it causes PML (Progressive Multifocal Leukoencephalopathy): --damages the white matter of CNS ==>memory loss, poor speech, poor coordination |
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"slapped face" rash in kids
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=Erythema Infectiosum (Fifth disease)
d/t Parvovirus |
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Erythema Infectiosum
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(AKA Fifth disease)
-d/t Parvovirus -"slapped face" rash in kids |
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rubella belongs to what virus family
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togavirus
(togavirus also contains the Alpha viruses: WEE, EEE, VEE) |
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WEE, EEE, and VEE belong to what virus family
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these are Alpha viruses, which fall under Togavirus (rubella is also a togavirus)
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yellow fever
-belongs to what virus family -how spread -Sx |
-Flavivirus (Flavivirus consists of yellow virus, Dengue, and West Nile: mosquito says, "Mmm..good FLAVor")
-spread via mosquitoes -Sx: fever (duh), hepatitis with jaundice==>thus "yellow fever") |
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Dengue fever
-belongs to what virus family -how spread -Sx |
-Flavivirus (Flavivirus consists of yellow virus, Dengue, and West Nile: mosquito says, "Mmm..good FLAVor")
-spread via mosquitoes -Sx: painful backache, muscle and joint pain |
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West Nile virus
-belongs to what virus family -how spread -Sx |
Flavivirus (Flavivirus consists of yellow virus, Dengue, and West Nile; mosquitoes say, "Mmmm. Good FLAVor!")
-spread via mosquitoes, which feed on infected birds, or blood transfusion -Sx: usually mild flu-like illness, but can cause encephalitis & death in elderly |
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Hantavirus
-belongs to what virus family -how spread -Sx |
-Bunyavirus family
-spread via deer mouse (feces): imagine a deer mouse w/big bunyan on its toe -Sx: flu-like illness, followed by respiratory illness and death! |
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polio
-belongs to what virus family -how spread -pathogenesis |
-Picorna ("PEECORNA")
-fecal-oral spread -replicates in tonsils & intestinal Peyer's patches (thus fecal-oral spread) ==>hematogenous ==>CNS ant horn |
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Coxsackie virus
-what virus family -what does Coxsackie A vs. B cause |
-Picorna ("PEE Co Rn A")
Coxsackie A: -herpangina (mild; sore throat w/vesicles) Coxsackie B: -diabetes -MCC pericarditis & myocarditis |
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MCC myocarditis
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Coxsackie B is MCC of myocarditis & pericarditis
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MCC pericarditis
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Coxsackie B is MCC of myocarditis & pericarditis
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SARS belongs to what virus family
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Corona
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hydrophobia
-definition -Sx of what? |
=painful swallowing of liquids b/c pharyngeal muscles are contracting
-suggests rabies |
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Ebola belongs to what virus family
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filovirus
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marburg belongs to what virus family
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filovirus
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MOA of gangciclovir
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like acyclovir, gangciclovir is a guanosine analog
unlike acyclovir, gangciclovir does not need to be activated/phosphorylated by viral thymidine kinase; thus, it is active against ALL Herpesviridae including CMV (unlike acyclovir) |
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S/E of gangciclovir
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neutropenia
thrombocytopenia (pic in ridic p. 226) |
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foscarnet
-MOA -Tx |
-Tx CMV retinitis in AIDS pt (gangciclovir also Tx)
-Tx acyclovir-resistent herpes MOA: -pyrophosphate analog -inhibits DNA polymerase AND reverse transcriptase |
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MC opportunistic infxn in AIDS
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PCP
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silver-stain of alveolar lung secretion reveals fungus
Dx? |
PCP
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resistance to malaria
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-sickle cell trait (Hemoglobin AS) protects against Plasmodium falciparum (most aggressive)
-absence of Duffy coats A & B on RBC's (where P. vivax binds) protects against P. vivax |
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leishmaniasis
-how spread -pathogenesis |
-spread via sandfly (which had bitten a rodent/dog/fox)
-proMASTigotes (flagella==>motile) moves from sandfly's intestine to mouth (MAST~masticate~mouth) -sandfly bites human ==>Amastigates (A=without; without flagella==>non-motile) in human's: *blood *macs *organs Sx: ulcer that heals, then systemic invasion |
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African sleeping sickness
-name of the bug -how spread -pathogenesis -Sx |
(protozoa)
Trypanosoma gambiense Trypanosome rhodesiense -spread via bite of Tsetse fly 1. Trypomastigotes go to tsetse fly's midgut ==>convert to epimastigotes in midgut ==>convert back to trypomastigotes in salivary gland (MAST=masticate=mouth) 2. Tsetse fly bites human. ==>Amastigotes in human's: *blood *LN *CNS==>drowsiness, mental deterioration, coma death also: intermittent fevers d/t Variable Surface Glycoproteins (VSG): trypanosomes change their VSG's, so host keeps mounting new immune response (==>fevers) |
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Chagas Dz
-name of the bug -how spread -pathogenesis -Sx |
Trypanosoma cruzi
spread by reduvid (kissing) bug 1. Reduvid bug ingests trypomastigotes ==>converted to epimastigotes in bug's midgut ==>converted back to trypomastigotes in feces 2. Reduvid bug bites human and shits on their face. The feces contain trypomastigotes ==>Human develops trypomastigotes in *blood ==>Human develops amastigotes (A=without==>without flagella==>non-motile) in: *LN *heart==>dilated cardiomyopathy *colon==>megacolon (ridic pic p. 247) |
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what bugs cause elephantiasis
-what geographic regions? -Tx? |
*Wucheria bancrofti: Pacific islands, Africa (Luigi's sister: Pacific Islander married AfAm)
*Brugia malayi: Malaysia, SE Asia *Oncocerca volvulus (river blindness): Africa, Central & South Amer Tx w/Diethylcarbamazine (ridic p. 256) |
