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Flashcards in Deck 5 - GU Deck (31)
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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)


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


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



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


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


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


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


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


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)


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)


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


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


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


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%)


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%)


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%)


Q. How is ADPKD investigated/diagnosed?

A. Age related diagnostic criteria: 15-39yrs > 3 cysts, 40-59 > 2 cysts, 60yrs >4 on


B. Family history, BP, urinalysis, renal U/S, liver, spleen, pancreas


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!


Q. Name 2 of the most common causes of kidney failure

A. Diabetes, HTN, unknown, ADPKD


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


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


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


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


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


Q. What is Glomerulonephritis? What can it cause?

A. Disease of the glomeruli – may be acute or chronic – usually immunologically


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


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


c. Asymptomatic urinary abnormalities, CKD (i.e. progressive decline in

kidney function with abnormal dipstick)


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-



Q. Name 3 features of nephrotic syndrome

A. Heavy proteinuria (>3.5g/24hrs)

B. Hypoalbuminaemia (<30g/L)

C. Oedema

D. Hypercholesterolaemia/hypercoaguable state


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


Q. What is the commonest cause of asymptomatic glomerulonephritis world wide?

A. IgA nephropathy: Abnormality in IgA glycosylation leads to deposition in


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


Q. How is Glomerulonephritis diagnosed?

A. Kidney biopsy, serological tests (ANCA, IgA etc)