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69 Cards in this Set
- Front
- Back
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what % of females have >1 UTI?
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1. 40% of females have >1 UTI
2. 8% have bacteriuria at a given time |
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what pts are UTI m/c in?
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1. sexually active young women
2. elderly 3. posturethral catheter or instrumentation 4. rare in males (increased rish c/ prostate dz) |
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what bacteria are m/c for UTI?
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1. e. coli (80%)
2. staph saprophyticus (15%) 3. other Gram-negative rods (proteus, klebsiella, enterobacter, pseudomonas) |
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what are si/sx of UTI?
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1. burning during urination
2. urgency 3. sense of incomplete bladder emptying 4. hematuria 5. lower abd pain 6. nocuria |
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what are systemic sx of UTI?
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1. fever
2. chills 3. back pain suggests pyelonephritis!!! |
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Back pain with an UTI suggests what...?!
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Pyelonephritis!!!!!
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what is the dx for a UTI?
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1. UA (urinalysis!!) showing pyurias
2. positive bacteria on Gram stain 3. positive culture results |
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what is the tx for a lower UTI
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1. bactrim (first line)--trimethoprim/sulfonamide
2. fluoroquinolone (floxacin) for refractory dz |
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what is the tx for uncomplicated pyelonephritis?
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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 |
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what do you do for adolescents and men with pyelonephritis or recurrent UTI??
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1. renal Utz and
2. intravenous pyelogram (IVP) to r/o anatomic etiology |
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what is tx for UTI secondary to bacterial prostatitis?
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6-12 wks of antibiotics!!!
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define asymptomatic bacteriuria
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1. urine culture >100,000 colony-forming units (CFUs)/mL
2. NO SX!!! |
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how do you tx asymptomatic bacteriuria?
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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 |
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what is the m/c cause of genital ulcers?
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HSV=herpes simplex virus (casues 60-70% of cases)
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what are si/sx of HSV?
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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 |
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how do you dx HSV?
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1. dx confirmed c/ direct fluorescent antigen (DFA) staining
2. Tzanck prep!!!!!!!! 3. serology, HSV PCR or culture |
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how do you tx HSV?
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1. acyclovir
2. famciclovir, or 3. valacyclovir to decrease duration of viral shedding and shorten initial course |
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what are the primary pathogens of pelvic inflammatory disease (PID)?
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1. chlamydia trachomatis
2. neisseria gonorrhoeae 3. PID is polymicrobial involving both aerobic and anaerobic bacteria |
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what is included with PID?
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1. endometritis
2. salpingitis 3. tubo-ovarian abscess (TOA) 4. pelvic peritonitis |
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what can occur in 15% of pts after 1 epiosode of salpingitis and up to 75% after >3 episodes?
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infertility!!!
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what is increased 7-10x in women with hx of salpingitis?
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risk of ectopic pregnancy
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how do you tx pts c/ PID who are toxic, have decreased immunity and are noncompliant?
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tx as inpts with IV abx
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how you tx PID?
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1. fluorquinolone plus metronidazole, or
2. cephalosporin plus doxycycline |
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when should you start tx for PID?
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start abx As soon as PID is suspected, even before culture results are available
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what are si/sx of PID?
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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 |
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what HPV serotypes are m/c with cervical CA?
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16 and 18
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what is the incubation period for HPV and how is it spread?
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6 wk to 3 mon incubation period,
spread by direct skin-to-skin contact |
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what is the transmission rate of HPV after a single contat c/ an infected individual?
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65%!!!
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what are si/sx of HPV?
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1. condyloma acuminata (genital warts)=soft, fleshy growths on vulva, vagina, cervix, perineum, anus
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how do you dx HPV?
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clinical, confirmed c/ bx
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how do you tx HPV?
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1. topical podophyllin or trichloroacetic acid
2. if refractory, try cyrosurgery or excision |
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what % of cervical CA is causes by HPV types 16, 18, 31, and 45?
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80%
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what % of cervical CA is diagnosed in the US found in women who have never been screened?
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50%
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how many cervical CA diagnoses are found in women who have not been screened in the last 5 yrs?
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10%
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what factors limit the accuracy of Pap testing?
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1. aberrant tissue changes can prevent abnormal cells from being seen
2. pap test are only moderately sensitive for detecting high-grade cervical lesions |
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what does a vaccine's valency refer?
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the number of serotypes against which the vaccine provides protection
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which HPV type is not considered a high-risk HPV type?
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6
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the quadrivalent HPV vaccine is designed to provide protection against the following HPV types:
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6, 11, 16, 18
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what is recommended in a pregnant pt with HPV?
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c-section to avoid vaginal lesions
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what are si/sx of syphilis (treponema pallidum)?
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1. painless ulcer
2. B/L inguinal adenopathy 3. chancre heals in 3-9 wks |
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why is primary syphilis often missed (treponema pallidum)?
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because of lack of sx (painless ulcer)
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what are the si/sx of secondary syphilis (treponema pallidum)?
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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 |
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how do you dx syphilis (treponema pallidum)?
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1. serologies
2. VDRL/RPR for screening 3. FTA-ABS to confirm |
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how do you tx syphilis (treponema pallidum)?
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benzathine penicillin G!!!!!
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what is the m/c code worldwide of AIDS?
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hererosexual transmission
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what is the biology of HIV?
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retrovirus with gag, pol and env genes
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what is p24 of HIV?
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p24 is a core protein encoded by gag gene
*it can be used clinically to follow disease progression |
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what are gp120 and gp41 of HIV?
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gp120 and gp41 are envelope glycoproteins that are produced on cleavage of gp160 and coded by env
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how does HIV integrate into the host DNA?
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reverse transcriptase (coded by pol) converts viral RNA to DNA
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what is encoded on the pol gene of HIV?
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reverse transcriptase for converting viral RNA to DNA
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what cytokine receptors of HIV allow for cellular entry?
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1. cellular entry is by binding to both CD4 and an additional ligand (CXCR4, CCR5, and others)
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what cells does HIV primarily infect?
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1. CD4-pos T cells
2. macrophages 3. thymic cells 4. astrocytes 5. dendritic cells |
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what is the mechanism of T-cell destruction?
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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 |
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when does death occur after HIV infection
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1. within 10-15 yr, after progression to AIDS
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what is a "long-term survivor" of AIDS?
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up to 5% are LT survivors, meaning the disease does not progress even after 15-20 yrs without tx
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what factors may lead to a long-term survivor of AIDS?
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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 |
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does HIV have a latent phase in its life cycle?
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NO!!! clinical silence in pts who eventually progress is the result of daily, temporarily successful host repopulation of T cells
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what causes death in AIDS pts?
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1. opportunistic infxns typically onset after CD4 counts fall <200
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what bugs should you worry about when CD4 cts are <200 in AIDS pts?
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1. pneumocysits carinii pneumonia (PCP)
2. Toxoplasma encephalitis 3. put all pts permanentally on Bactrium prophylaxis |
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what bugs should you worry about when CD4 cts are <50 in AIDS pts?
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1. Mycobacterium avium-intracellulare complex (MAC)
2. put all pts on azithromycin prophylaxis!! |
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what is a common skin CA fround in HIV pts, thought to be caused by co-transmission of human herpes virus-8 (HHV-8)
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kaposi's sarcoma
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what is the standard of care for HIV/AIDS?
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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 |
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how do nucleoside reverse transcription inhibitors (AZT) work?
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they are COMPETITVE antagonists of reverse transcriptase that bind to the active site of the nz and cause viral DNA chain termination
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how do non-nucleoside reverse transcription inhibitors work?
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they are NON-COMPETITIVE antagonists of reverse transcriptase that bind away from the active site and shut down nz activity
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how do protease inhibitors work?
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they block the action of a viral protease involved in viral maturation
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how do fusion inhibitors work?
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they block the ability of HIV to fuse to the target WBC (eg. enfuvirtide)
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what do the HIV drug regimens typically include?
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2 nucleoside analogues PLUS either a protease inhibitor or non-nucleoside reverse transcriptase inhibitor
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what do current tx for HIC aim to do?
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1. suppress viral replication and viral load to below detectable limits
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what is the primary reason for failure in tx for HIV?
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nonadherence c/ the drugs--resistance invariably develops in people who do not take the drugs as scheduled
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