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69 Cards in this Set

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  • Back
what % of females have >1 UTI?
1. 40% of females have >1 UTI
2. 8% have bacteriuria at a given time
what pts are UTI m/c in?
1. sexually active young women
2. elderly
3. posturethral catheter or instrumentation
4. rare in males (increased rish c/ prostate dz)
what bacteria are m/c for UTI?
1. e. coli (80%)
2. staph saprophyticus (15%)
3. other Gram-negative rods (proteus, klebsiella, enterobacter, pseudomonas)
what are si/sx of UTI?
1. burning during urination
2. urgency
3. sense of incomplete bladder emptying
4. hematuria
5. lower abd pain
6. nocuria
what are systemic sx of UTI?
1. fever
2. chills
3. back pain suggests pyelonephritis!!!
Back pain with an UTI suggests what...?!
what is the dx for a UTI?
1. UA (urinalysis!!) showing pyurias
2. positive bacteria on Gram stain
3. positive culture results
what is the tx for a lower UTI
1. bactrim (first line)--trimethoprim/sulfonamide
2. fluoroquinolone (floxacin) for refractory dz
what is the tx for uncomplicated pyelonephritis?
same abx for UTI given IV or PO, depending on severity of ilness:
1. bactrim (first line)--trimethoprim/sulfonamide
2. fluoroquinolone (floxacin) for refractory dz
what do you do for adolescents and men with pyelonephritis or recurrent UTI??
1. renal Utz and
2. intravenous pyelogram (IVP) to r/o anatomic etiology
what is tx for UTI secondary to bacterial prostatitis?
6-12 wks of antibiotics!!!
define asymptomatic bacteriuria
1. urine culture >100,000 colony-forming units (CFUs)/mL
2. NO SX!!!
how do you tx asymptomatic bacteriuria?
only tx in:
1. pregnant pts--use penicillins or nitrofurantoin
2. renal transplant
3. pts about to undergo GU procedure
4. severe vesicular ureteral reflux
5. sturvite calculi
what is the m/c cause of genital ulcers?
HSV=herpes simplex virus (casues 60-70% of cases)
what are si/sx of HSV?
1. painful vesicular and ulcerated lesions
2. 1-3 mm diameter
3. onset 3-7 days after exposure
4. lesions generally resolve over 7 days
5. primary infxn a/c malaise, low-grade fever, and inguinal adenopathy in 40% of pts
6. recurrent lesions are simliar appearing, but milder in severity and shorter in duration, lasting app. 2-5 days
how do you dx HSV?
1. dx confirmed c/ direct fluorescent antigen (DFA) staining
2. Tzanck prep!!!!!!!!
3. serology, HSV PCR or culture
how do you tx HSV?
1. acyclovir
2. famciclovir, or
3. valacyclovir
to decrease duration of viral shedding and shorten initial course
what are the primary pathogens of pelvic inflammatory disease (PID)?
1. chlamydia trachomatis
2. neisseria gonorrhoeae
3. PID is polymicrobial involving both aerobic and anaerobic bacteria
what is included with PID?
1. endometritis
2. salpingitis
3. tubo-ovarian abscess (TOA)
4. pelvic peritonitis
what can occur in 15% of pts after 1 epiosode of salpingitis and up to 75% after >3 episodes?
what is increased 7-10x in women with hx of salpingitis?
risk of ectopic pregnancy
how do you tx pts c/ PID who are toxic, have decreased immunity and are noncompliant?
tx as inpts with IV abx
how you tx PID?
1. fluorquinolone plus metronidazole, or
2. cephalosporin plus doxycycline
when should you start tx for PID?
start abx As soon as PID is suspected, even before culture results are available
what are si/sx of PID?
1. abd, adnexal and cervical motion tenderness PLUS at least one of the following:
a. positive pram stain
b. temp >38C
c. WBC >10,000
d. pus on culdocentesis or laparoscopy
e. TOA on bimanual or Utz
what HPV serotypes are m/c with cervical CA?
16 and 18
what is the incubation period for HPV and how is it spread?
6 wk to 3 mon incubation period,
spread by direct skin-to-skin contact
what is the transmission rate of HPV after a single contat c/ an infected individual?
what are si/sx of HPV?
1. condyloma acuminata (genital warts)=soft, fleshy growths on vulva, vagina, cervix, perineum, anus
how do you dx HPV?
clinical, confirmed c/ bx
how do you tx HPV?
1. topical podophyllin or trichloroacetic acid
2. if refractory, try cyrosurgery or excision
what % of cervical CA is causes by HPV types 16, 18, 31, and 45?
what % of cervical CA is diagnosed in the US found in women who have never been screened?
how many cervical CA diagnoses are found in women who have not been screened in the last 5 yrs?
what factors limit the accuracy of Pap testing?
1. aberrant tissue changes can prevent abnormal cells from being seen
2. pap test are only moderately sensitive for detecting high-grade cervical lesions
what does a vaccine's valency refer?
the number of serotypes against which the vaccine provides protection
which HPV type is not considered a high-risk HPV type?
the quadrivalent HPV vaccine is designed to provide protection against the following HPV types:
6, 11, 16, 18
what is recommended in a pregnant pt with HPV?
c-section to avoid vaginal lesions
what are si/sx of syphilis (treponema pallidum)?
1. painless ulcer
2. B/L inguinal adenopathy
3. chancre heals in 3-9 wks
why is primary syphilis often missed (treponema pallidum)?
because of lack of sx (painless ulcer)
what are the si/sx of secondary syphilis (treponema pallidum)?
4-8 wk after appearance of painless ulcer:
1. fever
2. lymphadenopathy
3. maculopapular rash affecting palms and soles
4. condyloma lata in intertriginous areas
how do you dx syphilis (treponema pallidum)?
1. serologies
2. VDRL/RPR for screening
3. FTA-ABS to confirm
how do you tx syphilis (treponema pallidum)?
benzathine penicillin G!!!!!
what is the m/c code worldwide of AIDS?
hererosexual transmission
what is the biology of HIV?
retrovirus with gag, pol and env genes
what is p24 of HIV?
p24 is a core protein encoded by gag gene
*it can be used clinically to follow disease progression
what are gp120 and gp41 of HIV?
gp120 and gp41 are envelope glycoproteins that are produced on cleavage of gp160 and coded by env
how does HIV integrate into the host DNA?
reverse transcriptase (coded by pol) converts viral RNA to DNA
what is encoded on the pol gene of HIV?
reverse transcriptase for converting viral RNA to DNA
what cytokine receptors of HIV allow for cellular entry?
1. cellular entry is by binding to both CD4 and an additional ligand (CXCR4, CCR5, and others)
what cells does HIV primarily infect?
1. CD4-pos T cells
2. macrophages
3. thymic cells
4. astrocytes
5. dendritic cells
what is the mechanism of T-cell destruction?
1. diect cell lysis
2. induction of cytotoxic T lymphocyte responses against infected CD4 cells
3. exhaustion of bone marrow production (suppression of production of T cells)
4. the virus induces alterations in host cytokine patterns, rendering surviving lymphocytes ineffective
when does death occur after HIV infection
1. within 10-15 yr, after progression to AIDS
what is a "long-term survivor" of AIDS?
up to 5% are LT survivors, meaning the disease does not progress even after 15-20 yrs without tx
what factors may lead to a long-term survivor of AIDS?
1. infection c/ defective virus
2. potent host immune response
3. genetic resistance of the host
4. pts c/ homozygous deletions of CCR5 or other viral coreceptors are highly resistant to infxn c/ HIV, wherease heterozygotes are less resistant
does HIV have a latent phase in its life cycle?
NO!!! clinical silence in pts who eventually progress is the result of daily, temporarily successful host repopulation of T cells
what causes death in AIDS pts?
1. opportunistic infxns typically onset after CD4 counts fall <200
what bugs should you worry about when CD4 cts are <200 in AIDS pts?
1. pneumocysits carinii pneumonia (PCP)
2. Toxoplasma encephalitis
3. put all pts permanentally on Bactrium prophylaxis
what bugs should you worry about when CD4 cts are <50 in AIDS pts?
1. Mycobacterium avium-intracellulare complex (MAC)
2. put all pts on azithromycin prophylaxis!!
what is a common skin CA fround in HIV pts, thought to be caused by co-transmission of human herpes virus-8 (HHV-8)
kaposi's sarcoma
what is the standard of care for HIV/AIDS?
triple combination therapy c/ drugs chosen from the following classes:
1. nucleoside reverse transcription inhibitors (AZT)
2. non-nonucleoside reverse transcriptase inhibitors
3. protease inhibitors
4. fusion inhibitors
how do nucleoside reverse transcription inhibitors (AZT) work?
they are COMPETITVE antagonists of reverse transcriptase that bind to the active site of the nz and cause viral DNA chain termination
how do non-nucleoside reverse transcription inhibitors work?
they are NON-COMPETITIVE antagonists of reverse transcriptase that bind away from the active site and shut down nz activity
how do protease inhibitors work?
they block the action of a viral protease involved in viral maturation
how do fusion inhibitors work?
they block the ability of HIV to fuse to the target WBC (eg. enfuvirtide)
what do the HIV drug regimens typically include?
2 nucleoside analogues PLUS either a protease inhibitor or non-nucleoside reverse transcriptase inhibitor
what do current tx for HIC aim to do?
1. suppress viral replication and viral load to below detectable limits
what is the primary reason for failure in tx for HIV?
nonadherence c/ the drugs--resistance invariably develops in people who do not take the drugs as scheduled