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168 Terms
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Presentation of urinary tract infections
* dysuria (pain on micturition) * frequency * smelly urine * cloudy or dark urine * unwell, failure to thrive in the very young * incontinence, off their feet in the very old
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Investigations for urinary tract infections
mid-stream specimen of urine (MSSU)
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Causative micro-organisms of UTIs
* mostly bacteria, especially E.coli * viral infection rare
What MSSU culture result is indicative of infection?
10⁵
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Risk factors for UTIs
* sex * pregnancy * kidney stones * urinary catheters
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Management of UTIs
* analgesia * short course of antibiotics
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What is glomerulonephritis?
conditions that cause inflammation of or around the glomerulus and nephron
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What is interstitial nephritis?
inflammation of the space between cells and tubules (the interstitial) within the kidney
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What is glomerulosclerosis?
the pathological process of scarring of the tissue in the glomerulus
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What are most types of glomerulonephritis treated with?
* immunosuppression e.g. steroids * blood pressure control by blocking the renin-angiotensin system (ACE inhibitors or angiotensin-II receptor blockers)
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Presentation of nephrotic syndrome
* oedema * frothy urine (proteinuria)
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Management of nephrotic syndrome
* treat oedema * salt and fluid restrictions * loop diuretics * hypertension * Renin-Angiotensin-Aldosterone-blockade * reduce risk of thrombosis * heparin * warfarin * treat dyslipidemia * statins
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Complications of nephrotic syndrome
* thrombosis * hypertension * high cholesterol
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What is the most common cause of nephrotic syndrome in children?
minimal change disease
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Management of minimal change disease
* prednisolone - 1mg/kg for up to 16 weeks * initial relapse treated with further steroid course
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What is the most common cause of nephrotic syndrome in adults?
focal segmental glomerulosclerosis
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What is the most common cause of primary glomerulonephritis?
IgA nephropathy
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What does histology of IgA nephropathy (Berger’s Disease) show?
IgA deposits and glomerular mesangial proliferation
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What is the most common type of glomerulonephritis?
membranous glomerulonephritis
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What does histology of membranous glomerulonephritis show?
IgG and complement deposits on the basement membrane
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What can membranous glomerulonephritis be secondary to?
* malignancy * rheumatoid disorders * drugs e.g. NSAIDs
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Presentation of post streptococcal glomerulonephritis (diffuse proliferation glomerulonephritis)
* 1-3 weeks after a streptococcal infection * nephritic syndrome * under 30 years of age
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Treatment of post-streptococcal glomerulonephritis
* antibiotics for infection? * loop diuretics for oedema - frusemide * anti-hypertensive - vasodilator drugs
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What are the 4 common presentations of glomerulonephritis?
* pain * pyrexia * haematuria * proteinuria * pyuria * mass on palpation * renal failure
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What is the definition of proteinuria?
urinary protein excretion > 150mg/day
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What is the definition of microscopic haematuria?
≥3 red blood cells per high power field
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Presentation of chronic renal failure
* Asymptomatic (found on blood and urine testing) * Tiredness * Anaemia * Oedema * High blood pressure * Bone pain due to renal bone disease * Pruritus (in advanced renal failure) * Nausea/vomiting (in advanced renal failure) * Dyspnoea (in advanced renal failure) * Pericarditis (in advanced renal failure) * Neuropathy (in advanced renal failure) * Coma (untreated advanced renal failure)
* give boluses of fluid as per intravenous fluid prescription guidelines * continue to reassess until volume replete * then treat as per euvolaemia
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How to manage euvolaemia in acute kidney injury
* give only maintenance fluid * fluid can be given oral or IV depending on patient intake and clinical condition * ensure you have daily fluid balance targets
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How to manage hypervolaemia in acute kidney injury
if fluid overloaded and also oliguric, the patient will need a senior review
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Indications for renal referral in acute kidney injury
* persistent oliguria or ongoing deterioration * persistent hyperkalaemia * persistent pulmonary oedema * severe metabolic acidosis * suspicion of intrinsic renal disease * AKI with low platelets * AKI stage 3
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What should be checked at AKI review?
BUMP
* Bloods: * consider daily bloods * consider more frequent review for hyperkalaemia * Ultrasound: * consider renal ultrasound * Medicines: * ensure appropriate dose adjustment of drugs * Plan for fluid maintenance * review fluid balance and adjust fluid prescription based on volume status * continuation of fluid balance chart * daily weights
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What should be done at AKI follow-up?
RRT
* Record * document the AKI happened, why and how bad, what investigations showed * this will help avoidance of further episodes * Repeat Bloods * check that renal function has returned to patient’s baseline - plan when and who to repeat * if renal function has not returned to patient’s baseline, may need review for other diagnosis * Treatment and Medicines Review * ensure that medicines are now optimised or there is a plan in place to optimise * does the patient need to restart diuretics, antihypertensives or other medications - when? * who needs to assess and when?
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What ECG changes can be seen in hyperkalaemia?
* peaked T waves * tall tented T waves * P wave widens and flattens * PR segment lengthens * P waves eventually disappear
* lymph nodes * iatrogenic * abdominal / pelvic mass
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Causes of obstruction at the vesico-ureteric junction
Intrinsic
* stone * bladder tumour * ureteric tumour
Extrinsic
* cervical tumour * prostate cancer
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Prevention of upper tract obstruction
* pain * frank / microscopic haematuria * symptoms of complications * palpable mass
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Complications of upper urinary tract obstruction
* infection and sepsis * renal failure
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Presentation of lower urinary tract obstruction?
* lower urinary tract symptoms * acute / chronic urinary retention * recurrent UTIs and sepsis * frank haematuria * formation of bladder stones * renal failure
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In retention, when should you catheterise?
immediately
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What is tenesmus?
the feeling that you need to pass stools, even though your bowels are already empty
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Risk factors for prostate cancer
* age * race / ethnicity * African or Afro-Caribbean men have higher risk * White men have moderate risk * East Asian men have lowest risk * geography * family history * first degree relative (2x risk) * HPC1, BRCA1 + 2 (5x) * Lynch syndrome (HNPCC) (2-5x) * obesity * diet