Flashcards in Deck 5 - GU Deck (31)
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1
Q. Name a primary, secondary and tertiary technique for the prevention of HIV transmission
A. Primary prevention: reducing risk of acquiring STI (condoms, STI awareness campaigns, one-one risk discussion, vaccination, pre/post exposure prophylaxis)
B. Secondary prevention: aims to find and treat undetected cases of infection, thereby removing from community pool (increasing access to STI/HIV tests and treatment (confidential, self-referral, drop in, short waiting lists), targeted screening, partner notification
C. Tertiary prevention: treatment - reducing morbidity / mortality (anti-retrovirals for HIV, prophylactic antibiotics for PCP, acyclovir for suppression of genital herpes)
2
Q. Describe three differences between chlamydia and gonorrhoea
A. Chlamydia: most common, asymptomatic carriage more common
B. Gonorrhoea: less common, clinical manifestations more florid, diagnosis
associated with recent partner change, more prone to Abx resistance
3
Q. Describe the symptoms of chlamydia and gonorrhoea, what complications mayoccur?
A. Male: dysuria and urethral discharge, asymptomatic
a. Complications: epididymo-orchitis, reactive arthritis
B. Female: non-specific discharge, menstrual irregularity, dysuria, asymptomatic
a. Complications: pelvic inflammatory disease, tubal factor infertility, sctopic pregnancy, chronic pelvic pain, neonatal transmission (ophthalmic neonatorum, atypical pneumonia with CT), Fitz Hugh Curtis syndrome
(peri-hepatitis)
4
Q. How is chlamydia diagnosed?
A. Nucleic Acid Amplification Tests (NAAT)
B. High specificity and sensitivity
C. Female
– Self collected vaginal swab
– Endocervical swab
– First void urine – lower sensitivity. Sometimes used in community based
asymptomatic screening
D. Male – First void urine
5
Q. Describe chlamydia treatment
A. Azithromycin 1gram stat or doxycycline 100mg bd for 7 days – low resistance risk
B. Erythromycin 500mg bd for 14 days for azithromycin 1 gram stat in pregnancy
C. Also: test for other STIs, partner management
6
Q. How is gonorrhoea diagnosed?
Near patient testing: swabs of genital secretions from: male – urethra, female –
endocervix, rectum
B. Microscopy looking for gram –ve diplococci within cytoplasm of polymorphs
C. Culture on selective medium to confirm diagnosis, sensitivity testing
D. Nucleic acid amplification test
7
Q. How should gonorrhoea be treated?
A. Ceftriaxone 500mg IMI with Azithromycin 1 gram orally stat
B. Others: test for other STIs, partner notification, single dose Tx preferred,
continuous surveillance of Abx resistance
8
Q. Who is at a higher risk of contracting syphilis?
A. Men who have sex with men – unprotected anal intercourse
B. Also highly transmissible through oral sex
9
Q. Describe the stages/phases associated with syphilis
A. Primary: incubation 9-90, usually 21-25 days – 95% genital skin, nipples, mouth
a. Dusky macule, regional nodes, untreated heals without scaring
B. Secondary: onset 6-8/52 after infection
a. 70% present with skin rash, others: mucous membrane lesions,
generalised lymphadenopathy, alopecia (moth-eaten), hoarseness, bone
pain, hepatitis, nephrotic syndrome, deafness, iritis, meningitis, cranial
nerve palsies, constitutional
C. Late syphilis: (if untreated) – late benign gummatous (2-40yrs), neurosyphilis, (2-
40yrs), General paresis (cerebral atrophy, 10-15yrs), tabes dorsalis (slow
degeneration of neural tracts in dorsal columns – gait, lightening pains and
urinary incontinence) 15-35yrs, cardio (20-30yrs)
10
Q. How is syphilis diagnosed?
A. Serology: usually +ve if ulcer present for 2+ weeks, if serology –ve repeat at 6 and
12 weeks to exclude diagnosis
B. Genital ulcer – primary, rash – secondary syphilis
C. Confirmatory test for screening +ve tests, TPPA – Treponema pallidum particle
agglutination test, (also VDRL or RPR)
11
Q. What occurs in AD Tubulointerstitial kidney disease?
A. Renal cysts and diabetes syndrome (50% lifetime risk)
B. Associated with: gout, hypomagnesaemia, deranged LFTs, abnormal genital tract
C. Abnormal renal development (not necessarily cysts: single/horseshoe kidney,
abnormal renal pelvis)
D. AD – mutation in HNF1 beta – ch17q12
12
Q. What occurs in renal cystic disease?
A. Autosomal recessive: rare (1/20000), mutation in PKHD1, diagnosed antenatal or neonatal
B. Enlarged poly cystic kidneys
C. Associated with: hepatobiliary problems – Cong. Hepatic fibrosis, cholangitis, portal HTN, Pulmonary hypoplasia – leads to mortality (30%)
D. 30% develop kidney failure – dialysis/combined liver-kidney transplantation
13
Q. What is medullary sponge kidney?
A. Cystic dilation of collecting tubule, mostly sporadic, usually diagnosed
incidentally in adult hood
B. May be uni/bilateral
C. Benign* but associated with other complications: UTI, renal stones, renal tubular
acidosis, rarely - CKD
14
Q. What occurs in nephronophthisis?
A. Disappearance of nephrons
B. Kidneys tend to be smaller, very rare condition, causes kidney failure in 7% of children (UK), >20 casual genes
C. Associated problems (10-15% of cases): retinal problems – rentinitis pigmentosa (early cause of blindness), Neurodevelopmental delay, Hepatic fibrosis (10-15%)
15
Q. What is the most common inherited kidney disease? What occurs?
A. AD polycystic kidney disease (ADPKD)
B. Gradual, progressive cysts development and growth, Wide variability in
progression, onset 56-80yrs dependent on genetic mutation
C. Causal genes: PKD1 (85%) and PKD2 (15%)
16
Q. How may ADPKD present?
A. Clinical features: HTN, haematuria, polyuria
B. Diagnosed 20-40yrs (mean – 35yrs)
C. Incidental: abdo, loin pain/hernia/nephrolithiasis
D. Screening: known family history – use BP in children
E. Extra-renal manifestations: polycystic liver disease (70%), intracranial
aneurysm (8-10%), AAA< mitral valve prolapse (25%)
17
Q. How is ADPKD investigated/diagnosed?
A. Age related diagnostic criteria: 15-39yrs > 3 cysts, 40-59 > 2 cysts, 60yrs >4 on
imaging
B. Family history, BP, urinalysis, renal U/S, liver, spleen, pancreas
18
Q. How should patients with ADPKD be treated?
A. First treatment – tolvaptan – delays progression in ADPKD
B. Vasopressin (ADH) 2 receptor antagonists
C. Outcome RCT: change in total kidney volume (TKV) 50% decrease, 30% slower
eGFR decline
D. Tx: indicated in pts with rapid disease progression
E. Side effects: polydipsia, polyuria, deranged LFTs (serious) – Monthly monitoring!
19
Q. Name 2 of the most common causes of kidney failure
A. Diabetes, HTN, unknown, ADPKD
20
Q. Name two other forms of genetic kidney disease
A. Tuberous sclerosis complex: AD, seizures, developmental delay, pathognomonic
skin changes, benign hamartomas
B. Von Hippel Lindau: AD, multisystem malignant tumour predisposition syndrome,
renal cysts (60%), Hemangioblastomas: tumours of CNS, may also be
retinal/spinal cord
C. Orofacial digital syndrome: X-linked (lethal in males), developmental disorder –
face, oral cavity, digits, poly cystic kidneys: tend to be small/normal
D. AD tubule-interstitial kidney disease: medullary cystic. Two types:
a. MCKD1: slowly progressive CKS, ESRF – 60yrs
b. MCKD2: assoc gout, ESRF – 30yrs
21
Q. How are cysts imaged? What classification is used?
A. Renal U/S, CT has a high sensitivity (prevalence is increased)
B. Bosniak renal cyst classification – based on CT
C. Simples cysts are rarely detrimental – may be associated with HTN, no associated
risk of declining kidney function
22
Q. Name two types of dialysis, how is native access achieved? Name 3 complications
A. Haemodialysis: hospital (3-5hrs, 3x a week), home (2-3hrs, 4-5x a week)
a. Synthetic graft or arteriovenous fistula
b. Hypotension/cramps, nausea/headaches, chest pain, fever/rigors, blocked/infected catheter, aneurysmal fistula
B. Peritoneal dialysis: dialysis occurs by diffusion of metabolic waste products through the peritoneal capillaries down a conc gradient into the dialysis fluid, water is removed by varying conc of osmotic agents (usually glucose) in dialysis fluid to draw water through capillary membranes
a. CAPD - continuous ambulatory peritoneal dialysis: PD can be done manually; drain in 2-3 L of fluid, cap off and drain out again 3-6hrs later; the filling and exchange processes takes around 30-40mins
b. Infection (PD peritonitis), catheter exit site infection, tunnel line infection, peri-catheter leak, outflow failure, abdo wall herniation, intestinal perforation
23
Q. Name 2 reasons for choosing HD or PD
A .HD: live alone/frail/elderly, fear of operating machines, unsuitable for PD due to
prev abdo surgery, abdo hernia, recurrent PD peritonitis, lack of space at home
B. PD: young, fulltime work, wanting control/responsibility for own care, lack of
suitable access for HD, severe HF
24
Q. Why do pts on dialysis have a high risk of death due to cardiovascular disease?
A. Uraemia may result in: hyperparathyroidism, hyperhomocysteinaemia, oxidant
stress, acidosis, “chronic inflammation”
B. Other conventional causes: high BP, DM, smoking, age, sex, hyperlipidaemia
25
Q. What is Glomerulonephritis? What can it cause?
A. Disease of the glomeruli – may be acute or chronic – usually immunologically
mediated
B. May cause: Leaky glomeruli – haematuria and proteinuria (used in clinical
investigations..), high BP, deteriorating kidney function
C. Cause of 25% of end stage kidney failure – often treatable and reversible
26
Q. How may glomerulonephritis present?
A. Number of ways:
a. Acute nephrotic syndrome,: AKI, rapid deterioration in kidney function,
active dipstick (haematuria, proteinuria), oliguria, HTN, fluid overload
i. Caused by: ANCA associated vasculitis, good pasture’s disease,
SLE, systemic sclerosis, post-strep infection (classically 2 weeks
after tonsillitis) etc
b. Nephrotic syndrome: as part of systemic disease – nail infarts, pulmonary
infiltrates, ANCA associated vasculitis, multisystem small vessel vasculitis
(Tx = immunosuppression, steroids, cyclophosphamide, rituximab, plasma
exchange)
c. Asymptomatic urinary abnormalities, CKD (i.e. progressive decline in
kidney function with abnormal dipstick)
27
Q. What is Goodpasture’s disease?
A. Serology: Anti-glomerular basement membrane antibodies (Linear deposits of
antibody along basement membrane)
B. Rapidly progressive kidney failure, active dipstick. Haemoptysis.
C. Treatment – remove antibody – plasma exchange, immunosuppression-
steroids/cyclophosphamide
28
Q. Name 3 features of nephrotic syndrome
A. Heavy proteinuria (>3.5g/24hrs)
B. Hypoalbuminaemia (<30g/L)
C. Oedema
D. Hypercholesterolaemia/hypercoaguable state
29
Q. Compare nephritic syndrome and nephrotic syndrome
Nephritic: inflammation of glomeruli, HTN, haematuria, oliguria (Berger’s disease
IgA neuropathy is most common cause)
B. Nephrotic: hypoalbuminemia, hyperlipidaemia, massive proteinuria, peripheral oedema
30
Q. What is the commonest cause of asymptomatic glomerulonephritis world wide?
A. IgA nephropathy: Abnormality in IgA glycosylation leads to deposition in
mesangium
B. May run a benign or aggressive course – can present as nephritic, nephrotic, asymptomatic or as progressive CKD
C. Often associated with tonsillitis and macroscopic haematuria
31
