L38 Dysuria: Urethritis, Cervicitis and testicular pain Flashcards

1
Q

What other symptoms are asked about when male presents with Dysuria (5)

A
  1. bladder dysfunction: cystitis?
  2. Any discharge: urethritis: what type and when
  3. Where is pain: (generally at meatus, but can be anywhere along the shaft)
  4. Any other: testicular pain, pain with ejaculation (epididymo orchitis), deep pain , radiation to back (prostate)
  5. Anal symptoms (MSM)
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2
Q

What are the steps of investigating dysuria after history

A
  1. Examine genitals carefully:
    - check for discharge on underwear
    - skin, glans, shaft, foreskin retracted, testicles, epididymis,
    - inguinal lymph nodes.
    - skin around anus and PR exam if indicated (prostate)
  2. If discharge: strongly suggest urethritis.
    Do a urethral swab for culture and maybe #3 too.
  3. If no discharge: do a first pass urine Nucleic acid amplification test for detection of N. gonorrhoae or C. trachomatis.
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3
Q

Why is it important to do culture and NAAT for UTI. What does gonorrhoea and chlamyidia look like on microscopy

  • chlaymidia more common, gon more severe
A

Culture allows susceptibility testing to help population health surveillance to make appropriate changes to antibiotic policy if needed.

You can’t cultivate gonorrhoea or chlaymidia from urine.
On microscopy they both have only neutrophils stained showing inflammation
- Gonorrhoea is gram - diplococci.
-chlamydia doesn’t show up

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4
Q

What are is likely cause of 3 types of discharge : purulent, muco-purulent (cloudy, mucoid) and watery/clear

A

Urethritis

  1. Purulent: 75% Gonococcal (esp if coupled with severe symptoms
  2. muco-purulent: 50% Non gonoccocal (Chlamydia), 25% Gon.
  3. watery/clear: 25-50% Non Gon, 4% gon.
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5
Q

Describe the structure and how Neisseria gonorrhoeae infects and causes dysuria

A

N. gon lacks an outer capsule (unlike mengitidis) so exposes LPS which is potent driver of immune system –> rare potential for bad sepsis

1, NG pili allow binding to carcinoembryonic antigen related cell adhesion molecules or Heparin sulphate proteoglycan on cell surface of columnar/cuboidal epithelium in GU tract

  1. It is internalised and kills the cell via toxins (endotoxin, lipo-oligosaccharide)
  2. Damaged cells permit bacteria to invade to deeper tissues
  3. Cytokines released by damaged cells recruit macrophages and neutrophils and initiate inflammation/immune response
  4. Immune proteins irritate nociceptors in the area causing dysuria
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6
Q

What are the epidemiological risks of Gonorrhea infection in NZ

A
  • Poverty - lack of access to healthcare
  • Rural areas - lack of clinics, sexual education
  • Urban area- MSM due to less condom use bc of no need for birth control
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7
Q

What diseases does N. gonorrhoeae/chlamydia cause in women- how does it present and how is it investigated

A

Cervicitis&raquo_space;>pelvic inflammatory disease (up fallopian) > urethritis

Presents with

  • mucopurulent discharge from cervix, cervix inflamed on speculum exam
  • deep pain , dyspareunia, abnormal bleeding
  • many asymptomatic (esp chlamyidia)
  • vulva and vagina often normal

Investigate
1. speculum exam of cervix, also external genitalia exam
2. Endocervical swab for culture and Nucleic acid amplification test
or 3. Self collected high vaginal swab for NAAT. but not culture.

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8
Q

Describe the structure and how Chlamydia infects

A
  1. Infective form : Elementary bodies
    - don’t have peptidoglycan cell wall, but have cell wall
    - have DNA and stored ATP but no machinery to replicate/make ATP
  2. They bind to columnar epithelial cells via ATP mediated process and are then endocytosed.
  3. Change to become non-infectious form: Reticulate bodies. (immature).
  4. It uses host cells energy for replication and after 24 hrs the cell is destroyed due to pile up of EB - 100-1000 which are released to keep infecting
  5. Damaged epithelial cell releases cytokines to trigger an inflammatory response
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9
Q

Compare the treatment for Chlamydia and Gon + when its given

A

Chlamydia

  • Penicillin/cephalosporins have no target. Need to get high intracellular conc
  • So use Doxycycline 100mg for 7 days (good for rectal chlaymidia
  • Or Azithromycin 1g stat - targets ribosome to stop new proteins/enzymes.

Gonorrhoea
- Ceftriaxone 500mg IM injection stat + azithromycin to prevent resistant gonorrhoea and get rid of any undiagnosed chlamydia.

Best practice is to give treatment when patient presents to clinic so can be documented even before culture results. just based on other info.

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10
Q

What is the mechanism of quinolone antibiotics, what do they treat now vs before and why

eg. Ciprofloxacin, moxifloxacin

A
  1. Inhibit DNA gyrase: which usually untwists DNA supercoils formed by rapid unzipping + copying of bacterial DNA by DNA polymerase. Without it Supercoils stop DNA polymerase from replicating DNA
  2. Inhibits Topoisomerase 4 which unlinks and separates the two chromosomes before cell division of bacteria.

Therefore stops bacterial cell replication and secondary systems cause the cell to die - quick, broad spectrum and safe with IV dose= oral.

Used to treat gonorrhoea/chlamydia but rapid resistance developed due to only a point mutation needed to reduce binding to DNA gyrase, even while on treatment can gain it. Now sometimes used to treat drug resistant TB

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