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IHD Part 2 306 > Renal and Genito-urinary system > Flashcards

Renal and Genito-urinary system Flashcards

1
Q

kidney and renal tract: What are the functions of the kidney?

A

Filter 180L fluid daily
Clear waste
Balance acid/base

Produce hormones:
Control blood pressure (renin)

Help to make blood (erythropoietin)

Regulate bone health (Ca, P) (vit. D)

selectivity barrier

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2
Q

kidney and renal tract: What is creatine?

A

End product of skeletal muscle catabolism

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3
Q

kidney and renal tract:

A
  1. glomerulus filtration - h2o and solutes move from blood into nephron
  2. tubular reabsorption - useful substances move from the filtrate in the to the blood
  3. tubular secretion - waste and excess substances move from blood into filtrate
  4. water reabsorption - h20 moves from filtrate into blood
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4
Q

kidney and renal tract: What 3 hormones does the kidney make?

A

Vitamin D - kidney hydroxylates to activate

makes erythropoietin - stimulates bone marrow to make red blood cells

makes renin - part of renin/angiotensin system

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5
Q

kidney and renal tract: What are 3 ways the kidney may dysfunction?

A

Salt and water homeostasis
Changes in total body water
Changes in blood pressure
Changes in urine volume or concentration

Excretion of waste products
Uraemia
Acidosis eg lactic acid, ketoacids
Others: Potassium, Phosphate, Uric acid
Clearance of drugs

Humoral disturbance
Anaemia
Renal bone disease - bones go soft
Hypertension

Barrier failure

  • haematuria
  • proteinuria - froth in the test-tube, ben’s Jone’s proteins come out of solution
  • lipiduria
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6
Q

kidney and renal tract: What investigations are done to investigate kidney disease?

A

Blood tests
- measured glomerular filtration rate GFR (between 60 and 100 may have signs of early kidney disease, below 60 is abnormal, below 15 as kidney failure)

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7
Q

kidney and renal tract: What is the classification of chronic kidney disease?

A

1 Kidney damage (structural/urinary/other)
and Normal GFR >90

2 Mildly reduced renal function 60-89

3 Moderately reduced renal function 30-59

4 Severely reduced renal function 15-29

5 Very severe to End-stage Kidney Failure <15
May require dialysis/transplantation

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8
Q

kidney and renal tract:What are the problems with kidney disease?

A

high blood pressure - beta blockers, ACE inhibitors, calcium channel blockers

anaemia -

bone problems - osteoporosis, renal bone disease, rickets

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9
Q

kidney and renal tract: What is nephrotic syndrome?

A

3 things

Heavy proteinuria
(>3.5g/24hrs or >350mg/mmol uPCR)
Low albumin (<30g/L) (normal 35-50g/L)
Peripheral Oedema

possibly…
Thrombosis – DVT, PTE
Hyperlipidaemia

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10
Q

kidney and renal tract: How is mild/moderate chronic kidney disease treated?

A

Diet/Fluid balance
Supplements- Alkali, Vitamin D, Iron
Drugs – Phosphate, Hypertension, Anaemia

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11
Q

kidney and renal tract: how is severe chronic kidney disease treated?

A

Dialysis

Transplantation

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12
Q

kidney and renal tract: how does dialysis work?

A

take blood from the patient, pass it through a dialysis machine to purify and put it back through again

catheter into the jugular or subclavian vein
risk of infection/sepsis, fistula is made

dialysis membrane is semi permeable and fluid sent in a counter current way

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13
Q

kidney and renal tract: What are the top 5 causes of kidney disease in the UK 2005?

A 
Glomerulonephritis - glomerular disease
pyelonephritis - tubular disease
diabetes 
polycystic kidney disease
hypertension/renovascular disease (problem of atherosclerosis)
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14
Q

kidney and renal tract: What are the complications of people with end stage renal failure?

A

CVD - hypertension, K related arrhythmias, cardiac valvular calcifications

infections
malnutrition
immunocompromised
renal osteodystrophy

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15
Q

kidney and renal tract: What are the complications of kidney transplant?

A

Immunosuppression but leads to:

  • Infection (atypicals) - oral thrush is common, gingival overgrowth (cyclosporin, calcium channel blockers - amylodopine etc)
  • Cancer (skin, post Tx lymphoproliferative (EBV))
  • Hypertension, Diabetes,

Cardiovascular disease
Recurrent disease

at 5 years - 70% of kidneys still working

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16
Q

Pathology of renal disease: How much fluid do your kidneys filter and reabsorbs per day?

A

180 litres per day

reabsorbs 178 litres per day

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17
Q

Pathology of renal disease: Why may there not be enough filtration?

A

Not enough blood flow - acute

Blocked filter (minimal change, membraneous blockage (proteins blocking), cells blocking (proliferative) - acute

lack of glomeruli - over years and can lead to chronic hypertension

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18
Q

Pathology of renal disease: Why may there be too much filtration?

A

Leaky membranes - pores are bigger than they should be so bigger molecules like albumin can get through e.g. proteinuria - acute

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19
Q

Pathology of renal disease: Why may there be too little reabsorption?

A

faulty tubules - pass too much urine

causes of tubule dysfunction - lack of blood supply so g et acute tubular necrosis - too much urine produced, cannot reabsorb, but tubules can regenerate

and because of toxins, myoglobin, ethylene glycol

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20
Q

Pathology of renal disease: why may you get blocked/inflamed tubules?

A

neutrophil casts?
crystals/calcification blocking
blood clots

bacteria, neutrophils, macrophages?

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21
Q

Pathology of renal disease: Why may tubules die off?

A

Pyelonephritis
papillary necrosis
tumours can develop - renal cell carcinoma (pain in loin, or blood in urine)

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22
Q

Pathology of renal disease: What are the risk factors for renal cell carcinoma?

A

obesity
cigarette
von hippel Lindau syndrome
acquired renal cystic disease (dialysis)

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23
Q

Pathology of renal disease: what is the treatment of RCC?

A

Surgical resection, radiotherapy

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24
Q

Pathology of renal disease: Where does RCC spread?

A

Direct, lymphatic, peritoneum, blood/bone

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25
Q

Pathology of renal disease: What are the risk factors for transitional cell carcinoma of the renal pelvis?

A

cigarette smoking
industrial dyes e.g. aniline
long term painkillers

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26
Q

Human herpesviruses: What is the structure of the herpes virus?

A

Small virus
120-200 nm
Icosahedral (viral shape) capsid surrounding ds (double stranded)DNA
80 genes coding for ~ 100 proteins

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27
Q

Human herpesviruses: how do you classify human herpes viruses classification?

A

α-herpesviruses - epidermal/neuronal viruses with a wide host range
Type 1 Herpes Simplex Virus Type 2 Herpes Simplex Virus Varicella-Zoster Virus (VZV)
HHV-1 HHV-2 HHV-3

β-herpesviruses - slow growth, primarily in T-cells and leukocytes
Cytomegalovirus (HCMV) Human Herpesvirus 6
Human Herpesvirus 7

γ-herpesviruses - primarily B-lymphocytes Epstein-Barr virus (EBV)
Human Herpesvirus 8
HHV-5 HHV-6 HHV-7
HHV-4 HHV-8

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28
Q

Human herpesviruses: What diseases are caused by herpes virus?

A

check slides

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29
Q

Human herpesviruses: How does the herpes virus infect and replicate?

A

virus binds to host receptor - binds to glycoproteins, then receptor

taken inside cell

dna released from virus particle - (uncoated)

translocates to the nucleus

viral dna in the nucleus interacts with host polymerases

Transcription occurs - mrna of viral protein, gets translated then,

viral proteins produced

viral protein binds to host polymerase - makes it more efficient

machinery replicates viral dna - lots of copies

everything is assembled - translocates to nucleus to get packaged to make new viral particles

host cell membrane bursts and releases viral particles to infect other cells

lots of cell damage occurs

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30
Q

Human herpesviruses: Where does HSV1 and HSV2 infect?

A

HSV 1
n Mainly Oral Infections
HSV 2
n Mainly Genital Infections

1° Herpes Simplex (infection) n also called Herpetic Gingivostomatitis
2° Herpes Simplex (reactivation) n Herpes Labialis (cold sores)

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31
Q

Human herpesviruses: Where does hSV1virus enter?

A

Virus enters trigeminal sensory neurones
Migrates to trigeminal ganglion
Becomes Latent in the Trigeminal Ganglion
In 50% of cases it remains dormant in the trigeminal ganglion

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32
Q

Human herpesviruses: How does hsv1 get reactivated - becomes secondary infection?

A

In 50% of cases it becomes reactivated
Migrates to peripheral nerve endings
Where active viral particles are shed

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33
Q

Human herpesviruses: What is secondary herpes infection caused by?

A 
Reactivation
caused by:
n  UV light 
Stress
n  Illness
n  Immuno-suppression

also causes herpes labialise - cold sores - Lesion resolves
Virus lays dormant again in trigeminal ganglion until reactivated

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34
Q

Human herpesviruses: What are the clinical features of primary hsv infection?

A

Incubation period around 5 days

Drinking and eating painful, often bad breath (halitosis)

Multiple oral vesicles - rupture to form extensive sloughing ulcers

Gingivitis with erythema (increased redness of the gums)

Malaise, pyrexia (temperature), lymphadenopathy (enlarged lymph nodes)

Duration 5-14 days

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35
Q

Human herpesviruses: How do you diagnose a primary hsv infection?

A

Typical clinical appearance

Main diagnostic difficulty with erythema multiforme

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36
Q

Human herpesviruses: How do you investigate a primary hsv infection?

A

Not normally done
Rising antibody titre / presence of IgM antibodies
Viral culture or now mainly PCR

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37
Q

Human herpesviruses: How is PCR carried out?

A

Denature DNA to single strands - 95 degrees
Annealing of specific primers to DNA Extension by polymerase - 55 degrees, then 72 degrees
Repeat 30-35 times

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38
Q

Human herpesviruses: What is the management for hsv 1?

A

Acyclovir (200mg 5 x daily for 5 days) if found early or in immunocompromised - must apply when tingling lips
Fluids and soft diet
Analgesics / antipyretics (paracetamol) Local antiseptics e.g. chlorhexidine Topical analgesics e.g. Difflam X-infection control

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39
Q

Human herpesviruses: How does acyclovir work?

A

HSV thymidine kinase (TK) is more effective at phosphorylating nucleotides than human TK. TK used to make bases for DNA ie viral DNA replication

ACV is a false nucleotide. Human cells cannot phosphorylate ACV very well

In HSV-infected cells, ACV is phosphorylated by the viral TK enzyme to ACV- P

ACV- P then inhibits virus replication –

i) Get incorporated into replicating viral DNA but further bases cannot be added as ACV- P lack a terminal hydroxyl group. It is a chain terminator.
ii) ACV- P acts on the virus DNA complex and inhibits the activity of DNA polymerase, so virus DNA manufacture is markedly inhibited.

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40
Q

Human herpesviruses: What are the clinical features of HSV 2?

A

Prodromal irritation
Vesicles at or near mucocutaneous junction of lips
Crusting lesions lasting 7-10 days
Usually re-occurs at the same sites
Rarely:
- may occur, intra-orally, in nose or elsewhere on ski

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41
Q

Human herpesviruses: What is the management for hSV2?

A

Management:
Acyclovir cream 5% if used very early OTC drying and antibacterial agents

Prophylactic treatment:
Rarely justified
Prophylactic acyclovir will prevent lesions in the immunocompromised or those susceptible to erythema multiforme

42
Q

Human herpesviruses: What is herpetic whitlow?

A

Herpetic infection of the fingers from handling the oral tissues of someone with active 1° or 2° Herpes simplex lesions (mainly dentists)
Very painful
Very difficult to treat Prevention better than cure - wear gloves

43
Q

Human herpesviruses: What is herpetic encephalitis?

A

Mainly affects frontal lobes of the brain
70% - 80% mortality if untreated
Of survivors, only 3% return to normal
Usually only people >50 years (HSV-1) and neonates (HSV-2) affected.

44
Q

Human herpesviruses: What are the symptoms of HSV encephalitis in adults?

A

Adults (HSV-1)
• Headache and behavioural changes over several days
• Fever
• only 11% of cases have a history of recurrent HSV infection

45
Q

Human herpesviruses: What are the symptoms of HSV 2 encephalitis in neonates?

A

Neonates (HSV-2)
• Skin rash, lesions and CNS symptoms
• Virus present in liver, lung and adrenal glands
• Respiratory distress
• Fits and convulsions
• Raised intracranial pressure
• Incidence is approximately one case per 300,000 live births in the UK

46
Q

Human herpesviruses: What Is the primary and secondary infection of HHV-3?

A

Chicken pox - varicella zoster virus

secondary - herpes zoster (shingles)

47
Q

Human herpesviruses: Where does varicella lay dormant?

A

In the dorsal root/ trigeminal ganglia

48
Q

Human herpesviruses: Why does HHV3/varicella reactivate?

A

Age (70% >50yrs)
• Stress
• Illness
• Immunosuppression

leads to secondary hsv - shingles, but seldom reoccurs

49
Q

Human herpesviruses: Where does a shingles rash classically appear?

A

chest and back

belt like rash - zoster

50
Q

Human herpesviruses: What are the 3 phases of the herpes zoster virus?

A

Pre-herpetic neuralgia
Rash
Post-herpetic neuralgia

51
Q

Human herpesviruses: What are the features of the pre-herpatic neuralgia phase?

A

Pain in the distribution of the affected division of the trigeminal nerve
Prior to the development of the rash
May mimic dental pain

52
Q

Human herpesviruses: What are the features of the rash phase?

A 
Unilateral vesicles in the
distribution of a branch of the
trigeminal nerve 
n  Ophthalmic
n  Maxillary
n  Mandibular

Vesicles break down to form n Ulcers (mucosa)
n Crusting lesions (skin)
Last 2-3 weeks

53
Q

Human herpesviruses: What optical problems can be caused by Zoster?

A

glaucoma, cataract, double vision and scaring of the cornea

54
Q

Human herpesviruses: How is herpes zoster managed?

A

Acyclovir 800mg 5 x daily for 7 days if seen soon after lesions develop
Analgesics
Ophthalmic referral if eye involved
Avoid contact with children

55
Q

Human herpesviruses: What are the new alternatives to acyclovir?

A

Valaciclovir 1g 3 x daily for 7 days

Famiciclovir 250mg 3 x daily for 7 days

bit more specific

56
Q

Human herpesviruses: What are the features of the post-herpatic neuralgia phase?

A

10% of patients go on to get extremely unpleasant intractable burning pain in the distribution of the affected nerve

More common in the elderly

Effective early treatment of zoster may ↓ risk of neuralgia

Treat pain with tricyclic anti-depressants and neuropathic pain drugs

57
Q

Human herpesviruses: What is EBV associated with?

A

Infectious Mononucleosis (Glandular Fever) – acute 1o infection with EBV

Burkitt’s Lymphoma – a B-cell malignancy

Nasopharyngeal Carcinoma – an epithelial cell malignancy

Oral Hairy Leukoplakia – seen i

58
Q

Human herpesviruses: Where does primary EBV replicate?

A

oro- pharyngeal epithelial cells but then establishes latency in B-lymphocytes

59
Q

Human herpesviruses: What are the symptoms of ebV?

A

Symptoms include sore throat, swollen cervical lymph nodes and mild fever

Petechiae on soft palate
Creamy exudates on fauces Cervical lymphadenopathy

Infections in the western world are usually seen in young adults

60
Q

Human herpesviruses: What is Burkitt’s lymphoma?

A

EBV gets into B cells - causes malignant B cell lymphoma

treatment - cyclophosphamide (chemo)

61
Q

Human herpesviruses: What happens to immunocompromised people that are infected with hHV-5?

A

Large ragged oral mucosal ulcers
Salivary gland swelling
Retinitis

62
Q

Human herpesviruses: What is Kaposi’s sarcoma?

A

lesions all over the body driven by HSV in aids patients

63
Q

Genito-urinary infections: What is the main defence to a UTI?

A

urination

64
Q

Genito-urinary infections: Where does the infection usually ascend from?

A

External site up the UT continuum which can lead to involvement of the kidneys

65
Q

Genito-urinary infections: What is a common route of infection of a UTI?

A

catheterisation

66
Q

Genito-urinary infections: Why are females more likely to get UTI’s?

A

Shorter ureter and nearer to anus

pregnancy - pressure on bladde reduces ability to empty bladder and some immunosuppression so higher chance of UTI

67
Q

Genito-urinary infections: What is dysuria and pyuria?

A

Painful urination

urine that contains pus

68
Q

Genito-urinary infections: What is pyelonephritis?

A

kidney infection, characterised by fever and back pain

69
Q

Genito-urinary infections: What is urethritis and cystitis?

A

Urethra infection

bladder infection

70
Q

Genito-urinary infections:What host factors contribute to getting a UTI?

A 
Renal calculi
ureteric reflux 
tumours
bladder stones
pregnancy
neurologic problems 
prostatic hypertrophy 
short urethra
catherisation
71
Q

Genito-urinary infections: What bacterial factors contribute to getting a UTI?

A 
capsular antigens
hemolysins
urease - raises pH so it can grow 
adhesion to uroepithelium 
introital colonisation
72
Q

Genito-urinary infections:What are the steps to diagnose a UTI?

A

Sampling of midstream Urine (with care)

  • cloudy or clear
  • haematuria? (urine might be pink)

culture on agar plates > 2x105 cells/ml *around 500 on a plate)

  • traces of protein, leukocytes >10/ml
  • Raised nitrites (NO3- > NO2-)- from bacterial metabolism

Pure or mixed growth?
- Gram Stain of isolated bacteria or direct staining from urine sample

73
Q

Genito-urinary infections:What is the main organism to cause a UTI?

A

E coli - gram negative rod

Proteus mirabilis- Gram negative pleomorphic rod- swarming motility

Staphylococcus saprophyticus- Gram positive coccus

74
Q

Genito-urinary infections: What media do you use to culture UTI bacteria?

A

Cysteine-lactose-electrolyte-deficient (CLED) media (turquoise coloured)

rich media containing lactose and lacking electrolytes (salt) to repress swarming

Subsequent plating on Macconkey agar if E.coli suspected (although Gram stain informative). - produces pink colonies

then strain designation by PCR and sequencing

75
Q

Genito-urinary infections:What are the features of E coli (UPEC)?

A

Gram-negative motile bacillus

  • Also causes GI-infections, but UTIs commonly caused by specific strains of E.coli known as UPEC
  • These differ at the genome level from enteric strains by having up to 1000 extra genes
  • Possesses potent adhesins for attachment to epithelium - pili
76
Q

Genito-urinary infections: What two types of pili do UPEC have?

A

Type 1 pili - Binds mannose receptors, common on glycoproteins in uroepithelium

P-fimbriae: (often found in pyelonephritis strains)
Binds to globobiose (aD-Gal-(1,4)-aD-Gal)
made up of linked ceramide host lipids

77
Q

Genito-urinary infections: Why do you need to track strains of UPEC?

A

for antibiotic resistance

78
Q

Genito-urinary infections: What does swarming mean?

A

ability to move over a surface

79
Q

Genito-urinary infections: Which organism can swarm over catheter surfaces?

A

Proteus?

80
Q

Genito-urinary infections: What are the viruelence factors for proteus?

A

Urease: urea» ammonia + CO2, raises pH of urine»> can cause precipitation of minerals to form kidney and bladder stones

IgA protease- reduces flushing…

Many pili adhesins

81
Q

Genito-urinary infections: What are the features of staphylococcus saprophyticus?

A

Gram positive- cocci
Haemagglutinin key to attachment to cells
common cause of UTIs in young women
Coagulase negative
Novobiocin resistant - used in diagnosis
Most common in young women

82
Q

Genito-urinary infections: What are the treatments for community UTI?

A

New guidelines do NOT indicate antibiotic use for uncomplicated lower UTI in Non-Pregnant women

Fever, pain in kidney area- antibiotics recommended, in men and pregnant women always indicated

> 3-day course in women, 7-day in men (infection is less common, can be more serious by the time detected)

Common antibiotics: Nitrofurantoin (1st-line) Ciprofloxacin, penicillins and trimethoprim

Resistance a growing issue, esp. for E. coli (>30% are Tm resistant)

83
Q

Genito-urinary infections: How can catheterisation leads to UTI’s

A

Usually skin commensals like S. aureus and epidermidis or Pseudomonas spp. (Strict aerobe), Klebsiella and Enterococcus

become opportunistic

and a lot of them are resistant

ESKAPE pathogens

84
Q

Genito-urinary infections: What are the ESKAPE pathogens?

A 
Enterococcus faecium
Staphylococcus aureus 
Klebsiella pneumoniae
Acinetobacter baumannii
Pseudomonas aruginosa
Enterobacter species
85
Q

Genito-urinary infections: What is the treatment for UTI in hospitals?

A

Similar to community but may require IV antibiotics: nitrofurantoin, cefalexin, Penicillins- depends on microbiological data, resistance profiles

Immediate removal and changing of catheter and bag

Super-resistant E.coli infections now treated with Plazomicin in USA_ expected to come to UK soon.

86
Q

Genito-urinary infections: How are STD’s transferred?

A

Any form of sexual activity in which no barrier is used and exchange of fluid or contact with mucosal epithelium occurs

87
Q

Genito-urinary infections: What are the main organisms causing STI’s?

A

Neisseria gonnorhoea &raquo_space;> Gonnnorhoea

Chlamydia trachomatis &raquo_space;> chlamydia

Treponema pallidum&raquo_space;> Syphilis

88
Q

Genito-urinary infections: What are the features of N.gonorrhoeae?

A

Exclusively a fully virulent human pathogen;
- never found as a commensal

Asymptomatic carrier state: mainly females

  • Acute urethritis
    in 95% males
  • only ~ 50% women show discharge, dysuria

Ascend to Fallopian tubes

  • acute salpingitis (infection of the Fallopian tubes), pelvic inflammatory disease
  • sterility

Ophthalmia neonatorum – infant blindness

Oral gonnorhea (bacteria prefers columnar epithelium instead of squamous)– very rare, but can result from oral sex with infected man

89
Q

Genito-urinary infections: What is the pathogenicity of N.gonorrhoeae?

A

Surface pili- pil proteins- attachment

Opa proteins- aid attachment

Lipo-ologosaccharide: sialylated (sialic acid is a host sugar)- complement resistance- host mimicry

Por proteins- nucleate actin aiding cell invasion

Possesses IgA protease- aids survival inside host cells

Release into bloodstream disseminates infection to other sites fever, arthiritis (1-3% women, much lower in men), endocarditis

90
Q

Genito-urinary infections: What does infection of N.gonorrhoeae increase the chance of?

A

Hiv x5

Co-infection of HIV and N. gonorrhoeae increases transmission of HIV by 500% (WHO)

91
Q

Genito-urinary infections: how is gonorrhoea diagnosed?

A

Urethral swab

  • Susceptible to dessication, so transport medium used
  • Sub-culture on chocolate agar
  • Sugar fermentation tests–glucose +ve
  • Oxidase test positive
92
Q

Genito-urinary infections:How is gonorrhoea treated?

A

Contact tracing- antibiotic prophylaxis of contacts

Historically penicillin and tetracyclines were drugs of choice

Ceftriaxone (IM) and azithromycin - most common (1g orally) recommended first line choice (also kills chlamydia).

Many 3rd world strains are Penicillin and Tetracycline resistant, susceptibility tests must be performed

93
Q

Genito-urinary infections: How does syphilis progress?

A

Initial incubation period (2- 10 weeks)
Primary lesion: chancre at site of infection
- Resolves spontaneously

Secondary syphilis :

  • 6-8 weeks post-infection, Bacteria disseminate around body
  • Flu-like illness: myalgia, headache, fever, rashes.

Latent syphilis: 3-30 years- no symptoms

Tertiary Syphilis:

  • Neurosyphilis- CNS
  • CV sequelae- aortic lesions, heart failure
  • skin and bone deformity

Treponema sensitive to long-acting penicillin- easily treatable
- slow-growth means long-acting course required.

94
Q

Genito-urinary infections: What organisms causes syphilis?

A

Treponema pallidum

TRANSMISSION:
Sexual contact via minute skin abrasions
Vertical transmission- cross placental: Congenital syphilis

95
Q

Genito-urinary infections: How does syphilis progress?

A

check slide 52

96
Q

Genito-urinary infections: how does congenital syphilis occur and how does it present?

A

Crosses placenta

  • Can lead to still-birth
  • Congenital infection
  • Birth deformities, silent infection – presents as facial and tooth deformities at 2 years of age
97
Q

Genito-urinary infections: What are the features of chlamydia trachoma’s?

A

Often asymptomatic in females
50% symptomatic in males
Re-infection common as immunity weak
Incubation period 7 – 14 days
Disease due to direct damage to cells and immunopathology causing fibrosis and scarring
Can also cause conjunctivitis- common co-occurence.

98
Q

Genito-urinary infections: What are the consequences of chlamydia in women?

A

Asymptomatic infection = 70 %
Mucopurulent cervicitis
Urethral infection

Pelvic inflammatory disease in up to 40% - ascending infection involving uterus, fallopian tubes, and other pelvic structures

Complications include chronic pelvic pain, ectopic pregnancy and infertility

99
Q

Genito-urinary infections: What is proctitis?

A

Inflammation of rectum

100
Q

Genito-urinary infections: What are the features of chlamydia bacteria?

A

Very small obligate intracellular parasite
Small genome
Enters through minute abrasions
Specialised life-cycle

Seems to avoid and not stimulate immune responses (privileged site?)

Prefers to infect non-ciliated columnar and cubiodal epithelium: genital tract from urethra up to fallopian tubes and rectum
Also respiratory and conjunctival cells

101
Q

Genito-urinary infections: How to diagnose and treat chlamydia?

A

Tests are available on NHS (and free in Gyms etc):
Culture in cells
Direct immunofluorescence and ELISA
PCR tests (known as NAAT)

TREATMENT:
Azithromycin (single dose).
Doxycycline (longer course).

IHD Part 2 306 (23 decks)

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