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Urinary Flashcards

1
Q

Definition of a UTI?

A

WCC >105 per ml of fresh MSU

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2
Q

Investigations in UTI?

A

Dipstick urine:

  • If positive: Treat and send for MSU for specificity
  • If negative: Send for MSU, to confirm absence of infection.

Send MSU regardless if male, child, immunosuppressed, pregnant or unwell.

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3
Q

Management of lower UTI in females?

A

Non-pregnant adult females

  • Nitrofurantoin 50mg QDS 3 days or Trimethoprim 200mg BD 3 days.
  • If vaginal itch/change in discharge consider gynae cause: thrush, chlamydia (swabs)
  • Encourage fluids and frequent voiding

Pregnant females

  • Urine dip and culture at every antenatal visit
  • Treat both symptomatic and asymptomatic bacteriuria with abx
  • Consult local guidelines
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4
Q

Management of lower UTI in males?

A

Usually due to structural or functional abnormality

  • Trimethoprim 200mg BD 7 days or Nitrofurantoin 50mg QDS 7 days
    • Refer urology if upper UTI or prostatitis
    • May require 2 week course of quinolone e.g. levofloxacin
    • Do not treat asymptomatic bacteriuria in men >65 with abx
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5
Q

Prevention of UTIs?

A

General

  • Drink more water
  • Abx prophylaxis if recurrent - self-treatment with single abx dose when symptoms first present
  • Cranberry juice/tablets

Men with prostatism

  • Finasteride/dutastride and doxasozin decreases UTI incidence

HRT

  • Topical oestrogen decreases incidence in menopausal women
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6
Q

Causes of lower UTI?

A

E.coli (75-90%)

Others

  • Klebsiella pneumoniae
  • Proteus mirabilis
  • Staphylococcus saprophyticus
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7
Q

Causes of pyelo?

A

E.col = 80%

Others

  • Proteus, staphylococcus, streptococcus, klebsiella, pseudomonas
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8
Q

Aetiology of pyelo?

A

Secondary to lower UTI

  • More common if ureteric reflux or stasis (e.g. obstruction)

Pathology in kidney

  • Renal stones, pelvi-uteric obstruction

Haematogenous infection

  • Complication of sepsis (usually gram –Ve bacillius)
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9
Q

Complications of pyelo?

A

Urosepsis

Perinephric abscess

Necrotising papillitis (usually in diabetics)

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10
Q

Investigations in pyelo?

A

Bedside

  • Urine - dip and MC&S (negative MSU does not exclude)

Bloods

  • FBC, U+E, CRP, LFTs, clotting, amylase
  • Blood cultures

Imaging

  • AXR - may show stone
  • USS KUB - may show dilated collecting system
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11
Q

Indications for admission with pyelo?

A
  • Dehydration/unable to take oral fluids/meds
  • Sepsis
  • Pregnant
  • Frail/elderly with recurrent UTIs/recent admission
  • No improvement after 24 hours of abx
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12
Q

Management of pyelo (primary and secondary care)?

A

Empirial Abx

  • Ciprofloxacin 500mg BD 7 days OR
  • Co-amoxiclav 625mg TDS 7 days
    • Once sensitivity confirmed –> trimethoprim 200mg BD 14 days

If Admitted

  • Broad spec abx - IV initially (Co-amox)
  • Analgesia (opiates)
  • Monitor fluid balance - fluids if reduced intake

Surgical

  • Percutaneous nephrostomy if obstructed
  • Surgery if abscess develops
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13
Q

Causes of acute retention?

A

82% caused by prostatic obstruction (BPH, Malignancy)

Others

  • Constipation, alcohol, drugs (anticholinergics, diuretics), UTI, hernia repair,

Rare

  • Urethral stricture, clot retention, spinal cord compression, bladder stone
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14
Q

Presentation of acute urinary retention?

A

Symptoms

  • Inability to pass urine with sensation of needing to go, suprapubic abdominal pain, oliguria, delirium.

Signs

  • Palpable bladder (tender and dull to percussion)
  • Suprapubic tenderness
  • DRE: enlarged +/- irregular prostate
  • Check perianal sensation, if decreased ?neuro cause
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15
Q

Management of acute retention?

A

Investigations

  • Bladder scan/Pass a catheter
    • Urine dip/MSU of sample
  • Urgent MRI spine if neurological cause suspected
  • Fluid balance and U+E monitoring

Management

  • Urgent catheterisation
  • Treat causes (infection/constipation)
  • TWOC - monitor for recurrence of retention
    • Treat as chronic retention if recurs
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16
Q

Complication of retention management?

A

Post-obstructive diuresis

  • Polyuric response –> loss of water and electrolytes
  • Monitor these
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17
Q

What are the functions of the kidney?

A
  1. Excretory
  2. Homeostasis
    • Fluid, BP, acid base
  3. Endocrine
    • EPO, bone metabolism (Ca2+)
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18
Q

Definition of chronic kidney disease?

A

Abnormality of kidney structure or function present for more than 3 months

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19
Q

Causes of CKD?

A
  • Diabetic nephropathy
  • Hypertension
  • Glomerulonephritis
  • Systemic disease (e.g. SLE, vasculitis, amyloid, myeloma)
  • Renal Artery Stenosis
  • Hereditary (e.g. polycystic kidney disease)
  • Chronic pyelonephritis/vesicoureteric reflux
  • Urinary tract obstruction (e.g. prostatic disease)
  • Heart failure
  • Drugs (e.g. NSAIDs)
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20
Q

Signs and symptoms of CKD?

A

Signs

  • Hypertension, pulmonary oedema, peripheral vascular disease, pigmentation

Symptoms (if symptomatic)

  • Fluid retention, polyuria, nocturia
  • Anorexia, nausea, vomiting, malnutrition
  • Peripheral neuropathy, restless legs
  • Pruritis
  • Bone pain, fractures, arthropathy
  • Erectile dysfunction, oligomenorrhoea, reduced fertility
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21
Q

Complications of CKD?

A
  1. Anaemia
  2. Bone mineral disorder (reduced vitamin D absorption and secondary hyperparathyroidism)
  3. Metabolic acidosis
  4. Hyperkalaemia
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22
Q

Classification of CKD?

A
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23
Q

Investigations in CKD?

A

Urine

  • Urine dip, microscopy (Casts indicate glom damage)
  • ACR - prognostic importance (<3 = normal, 3-70 needs retesting with EM sample, >70 no need)

Bloods

  • FBC, U+E, LFTs, Clotting
  • Immunology screen - SLE, vaculitis, myeloma

Imaging

  • Renal USS
    • Normal, obstruction, cystic disease, scarring, renovascular abnormality +/- renal biopsy, angiography
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24
Q

Management of CKD?

A

Conservative

  • Stop smoking, healthy BMI, avoid nephrotoxins, avoid dehydration
  • Salt/phosphate/potassium restriction
  • Fluid requirements vary between patients - diuretics for fluid retention. Risk of dehydration is poor intake/increased loss.

Medical

  • HTN - aim <140/90 (if diabetic <130/90). ACEi/ARB unless RA stenosis
  • Statin as primary/secondary prevention
  • Antiplatelets for secondary prevention only
  • Be wary of nephrotoxics/drugs renally excreted (opioids, digoxin etc)

Long-Term

  • RRT/palliation
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25
Q

Management of complications of CKD?

A

Bone Metabolism/Osteoporosis/Secondary Hyperparathyroidism

  • Measure serum calcium, phosphate and PTH if GFR less than 30
  • Bisphosphonates if indicated in people with a GFR of 30 or more
  • Colecalciferol or ergocalciferol to treat vitamin D deficiency
  • Dietary restriction of phosphate, phosphate binder medications

Anaemia

  • Recombinant human EPO

Metabolic Acidosis

  • Consider oral bicarbonate if GFR less than 30 and a serum bicarbonate concentration of less than 20 mmol/litre (advice from renal)
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26
Q

Dialysis?

A
  1. Haemodialysis
    • 4 hours 3x per week
    • Access via AV fistula
  2. Peritoneal Dialysis
    • CAPD (continuous ambulatory PD) - 4x 2-3 litre exchanges per day
    • APD (automated PD) - exchanges whilst asleep at night
  3. Kidney Transplantation
    • Best rehabiliation and patient survival
    • Requires life-long immunosuppression, may fail after a time
    • Some may not be suitable
    • Donor = deceased, live (related, altruistic)
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27
Q

Risk factors for stress incontinence?

A
  • Age (menopause)
  • Vaginal delivery
  • Prolapse
  • Previous bladder neck surgery

Caused by weakness of pelvic floor muscles

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28
Q

Investigations in stress incontinence?

A
  • Urine dipstick +/- MSU
  • Frequency/volume chart
  • Urodynamics
    • Urine leaks with no change in pressure in the bladder, provoked by increased pressure in the abdomen
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29
Q

Management of stress incontinence?

A

Conservative

  • Physio (pelvic floor exercises)
  • Vaginal cones
  • Electrical stimulation
  • Optimise BMI

Medical

  • Duloxetine (SE = hesitancy when initiating)

Surgical

  • TVT
  • Colposuspension
  • Injectables (collagen, botulinum etc)
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30
Q

Triad of nephrotic syndrome?

A
  1. Proteinuria (ACR >200mg/mmol)
  2. Hypoalbuminaemia (<25 g/L)
  3. Oedema (particularly periorbital)

Commonly with hyperlipidaemia

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31
Q

Causes of nephrotic syndrome?

A
  • Minimal Change Disease
    • 80% cause in children, 25% in adults
    • Relapse common (75%)
  • Minimal change glomerulonephritis
  • Membranoproliferative glomerulonephritis
  • Membranous glomerulonephritis
  • Focal segmental glomerulonephritis

Rare = SLE, HSP, amyloidosis, drug reactions

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32
Q

Presentation of nephrotic syndrome?

A

Signs

  • Periorbital, genital, dependent oedema (worse in the face in morning, swelling descends with gravity later in the day), ascites, pleural effusions

Symptoms

  • Abdominal discomfort (hypovolaemia, ascites, peritonitis), diarrhoea and/or vomiting. Frothy urine
  • In children: upper resp. tract infection with oedema, lethargy, irritability and decreased appetite
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33
Q

Complications of nephrotic syndrome?

A
  • Thromboembolism (loss of anti-thrombotic proteins)
  • Infection (loss of Ig - pneumococcal, offer vaccination)
  • Hypovolemia and renal failure
  • Hyper-cholesterolaemia
  • Loss of specific proteins
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34
Q

Investigations in nephrotic syndrome?

Differentials to exclude?

A
  • Urine dip: 3+ or 4+ protein
  • Urine PCR: >200mg/mmol
  • Microscopy of urine: red cells, casts
  • Bloods
    • U&Es, creatinine, eGFR,
    • LFTs (albumin <25g/L),
    • Cholesterol
    • ESR, FBC

Must exclude primary cardiac failure, with raised JVP, pulmonary oedema and mild proteinuria. Exclude liver disease (possible cause of hypoalbuminaemia).

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35
Q

Management of nephrotic syndrome?

A

Conservative

  • Low sodium diet

Medical

  • Diuretics (furosemide 80-160mg PO)
  • ACEi or ARB for BP reduction
  • LMWH for VTE prophylaxis or warfarin if symptomatic of VTE
  • Penicillin prophylactically
  • Oral prednisolone for 12-16 weeks (tapered down - if minimal change disease)
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36
Q

Risk factors for detrusor instability (urge incontinence)?

A

Age, high caffeine intake, smoking

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37
Q

Indications for 2WW referral if urinary incontinence?

A
  • Miscroscopic haematuria (if age >50)
  • Visible haematuria
  • Recurrent or persistant UTI with haematuria (>40 yrs)
  • Suspected malignant mass rising from urinary tract
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38
Q

Urodynamics in urge incontinence?

A

Involuntary bladder muscle activity causes increase in pressure and leads to leakage of urine

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39
Q

Management of detrusor instability?

A

Conservative

  • Reduce tea/coffee intake
  • Stop smoking
  • Bladder retraining

Medical

  • Anticholinergics (oxybutinin)
  • TCA/desmopressin

Surgical

  • Intra-vesical botox
  • Sacral nerve stimulation
  • Other more complex things - clam cystoplasty, neuromodulator implant, detrusor myomectomy.
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40
Q

STOP AKI?

A
  1. Sepsis - treat with BUFALO
  2. Toxins - stop nephrotoxic drugs
  3. Optimise BP
    • IV access and fluids if hypovolaemic
    • Volume status assessment
    • Consider holding anti-hypertensives
    • Consider vasopressors
  4. Prevent Harm
    • Treat complications (hyperkalaemia, pulmonary oedema, acidosis)
    • Identify cause
    • Review medication and doses
    • Refer for RRT if necessary

Monitor

  • Daily volume assessment
  • Fluid balance
  • U+Es, bicarbonate
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41
Q

Types of bladder cancer?

A

90% = transitional cell carcinoma

5-8% = SCC

1-2% = adenocarcinoma

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42
Q

Risk factors for bladder cancer?

A
  • Male
  • Smoking
  • Aromatic amine exposure (textiles)
  • Schistosomiasis (for SCC)
  • Chronic UTI
  • Stasis of urine
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43
Q

Presentation of bladder cancer?

A

Signs

  • Microscopic haemautria
  • Sterile pyuria
  • Palpable suprapubic mass

Symptoms

  • Painless haematuria
  • Uterine colic due to clots from upper tract lesion
  • Malignant cystitis (frequency, dysuria, infection)
  • UTI in men or recurrent UTI in women
  • Loin pain
    • General FAWR symptoms - fever, weight loss, anorexia/anaemia, reduced energy
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44
Q

Complications of bladder cancer?

A

Outflow obstruction

Ureteric obstruction

Enlarged pelvic lymph nodes

Metastasis (liver, bone)

45
Q

Investigations in bladder cancer?

A

Urine

  • Urine dip and MC&S
  • Cytology for malignant cells

Bloods

  • FBC, U+E

Imaging

  • USS KUB
  • Cystoscopy to visualise tumour
  • CXR
46
Q

Management of bladder cancer?

A

T1 - transurethral resection of tumour (TURBT) and single dose of intra- vesical chemo. Follow up with regular cystoscopy.

T2 - TURBT and radiotherapy. Follow up with regular cystoscopy.

T3 - Radical cystectomy +/- radiotherapy.

T4 - TURBT for local symptoms. Palliative radiotherapy +/- chemo. Palliative care involvement.

47
Q

Risk factors for prostate cancer?

A
  • Age (85% >65)
  • First degree relative affected
  • Black afro-carribean population
  • Dietary (low fruit, high fat and meat diet)
48
Q

Spread of prostate ca?

A

LNs, seminal vesicles

Bone, liver, brain

49
Q

Presentation of prostate ca?

A

Symptoms

  • Early: symptomless, usually detected on PSA
  • Local : protastism, urinary retention, haematuria, lower extremity oedema
  • Metastatic: Malaise, weight loss, bone pain, pathological fractures, spinal cord compression, ureteric obstruction leading to renal failure

Signs

  • On DRE
    • Local: hard nodule in prostate
    • Local advanced: prostate hard, non-tender, loss of sulci
    • Metastatic signs
50
Q

Investigations in prostate cancer?

A

DRE

Bloods

  • PSA - >40 = high chance of nodal spread, >100 = metastatic spread very likely.

Imaging

  • Transrectal ultrasound and biopsy
  • MRI, CT, X-ray, bone scan
51
Q

Management of prostate cancer?

A

Early Disease

  • Active surveillance - PSA and regular DRE
  • Radical prostatectomy
  • Radiotherapy/Brachytherapy
  • Hormone treatment not beneficial in early disease

Symptomatic Disease

  • LHRH Analgoues
    • e.g. Goserulin, SC injection every 4-12 weeks. Decreases testosterone levels to levels of castration in <2 months.
    • SE: impotence, hot flushes, gynaecomastia, local bruising/infection
  • Anti-androgens
    • Flutamide, bicalutamide
    • Prevent side effects of testosterone flare when giving LHRH analogues
  • Surgical castration
    • Rarely used

Metastatic Disease

  • Local radiotherapy and corticosteroids
52
Q

Where do renal cell carcinomas arise/invade?

A

From epithelium of the proximal convoluted tubule. Known as clear cell carcinomas.

Invasion of renal vein is common.

53
Q

Risk factors for renal cell carcinoma?

A

Smoking, high BMI, HTN

Other

  • Occupational exposure (asbestos, trichloroethylene)
  • Polycystic kidney disease
  • Chronic hep C infection
  • Genetics: 2-3% hereditary e.g von Hippel-Lindau, 2.5x higher with a first degree relative
54
Q

Presentation of renal cell carcinoma?

A

Symptoms

  • Triad of haematuria, flank pain, palpable flank mass (in order of how common)

Signs

  • Local extension into IVC = bilateral leg oedema and collateral venous circulation

Metastasis

  • Bone pain, persistent cough, upper GI bleed, neuro deficits
  • Varicocele if extends into left renal vein
55
Q

Complications of renal cell carcinoma? (paraneoplastic syndromes)

A
  • Polcythaemia due to EPO secretion
  • Hypercalcaemia due to PTH related peptide
  • Hypertension due to renin secretion
  • Neuromyopathy
56
Q

Investigations in renal cell carcinoma?

A

Urine

  • Urine dip + Microscopy (haematuria)

Bloods

  • FBC, U+E, LFTs

Imaging

  • Renal USS
  • Plain abdo Xray, CXR (cannonball mets)
  • Abdo CT - function of contralateral kidney, primary tumour extension, venous involvement
57
Q

Management of renal cell carcinoma?

A

Local Disease

  • Partial nephrectomy - tumours <7cm, if limited renal funciton or 1 kidney
  • Radical nephrectomy
  • Ablative - Radiofrequency ablation for small masses in frail patients/poor renal function

Metastatic Disease

  • Cytoreductive nephrectomy and chemotherapy
  • Largely resistant to chemo, radio and hormonal therapy
  • Aim to relieve symptoms and maintain function with IFN alpha or interleukin 2 immunotherapy
58
Q

Definition of hydronephrosis?

A

Aseptic distention of renal pelvic and calyces of the kidney with urine due to obstruction of urine outflow

59
Q

Causes of hydronephrosis?

A

Unilateral

  • Lumen - calculi
  • Wall - ureterocoele, stricture, malignancy
  • External - blood vessel, lymphadenopathy

Bilateral

  • Congenital - strictures, valves
  • Acquired - bladder neck hypertrophy, prostatic hypertrophy or malignancy, urethral stricture, phimosis
60
Q

Presentation of hydronephrosis?

A

Symptoms

  • Pain in back or side, may be acute or gradual onset.
  • Haematuria, oliguria
  • UTI symptoms (inc. rigors, nausea, vomiting)

Signs

  • Temperature, rigors, may have visibly swollen kidneys
61
Q

Complication of hydronephrosis?

A

Atrophy of the kidney parenchyma, leading to decrease in renal function

62
Q

Investigations in hydronephrosis?

A

Urine

  • Urine dip and microscopy

Bloods

  • FBC, U&Es, LFTs, CRP

Imaging

  • USS KUB/CT KUB
63
Q

Management of hydronephrosis

A

Drain urine from bladder using catheter - if unable to obtain large volume of urine, blockage may be in ureter or bladder.

If blocked ureter…

  • Urethral stent
  • Nephrostomy tube (drain urine through back)
  • Abx to control infection

May require surgery if caused by scar/clot

Endoscopic surgery if caused by stone

64
Q

Types of urethritis?

A
  • Gonococcal urethritis
  • Non-gonococcal urethritis (Reiter’s)
  • Persistent/recurrent urethritis
    • 30-90 days after treatment of acute NGU
    • Most likely to be multifactorial, mycoplasma genitalium, t. vaginalis
65
Q

Causes of urinary stones?

A

Most idiopathic

Hypercalciuria, hyperoxaluria, hyperuricaemia, cystinuria, schistosomiasis

Risk Factors

  • Hyperparathyroidism, gout, chemo for leukaemia, enlarged prostate, hydronephrosis, UTI, catheter
66
Q

Presentation of urinary stones?

A

Symptoms

  • Acute onset severe unilateral colickly pain from loin to groin (testicle pain)
  • N+V, sweating
  • Haematuria, dysuria
  • Frequent painful passage of small volumes of urine with feeling of incomplete emptying

Signs

  • High HR, sweating, restlessness
  • Some tenderness over affected loin
67
Q

Investigations in renal colic?

A

Urine

  • Urine dip (blood) - nitrites = UTI
  • PT if female

Bloods

  • U+E, FBC, calcium, urate

Imaging

  • CT KUB (99% of stones), KUB X-ray (60%)
68
Q

Differentials in renal colic?

A

Always exclude other causes of abdominal pain such as AAA rupture, especially if no prior renal disease.

Male

  • Testicular tumour, epididymitis or prostatitis

Female

  • Gynae cause inc. torsion, cyst and ectopic pregnancy.
69
Q

Management of urinary stones?

A

Conservative

  • Analgeisa (NSAIDs, then opioids)
  • Antiemetic
  • Fluid replacement
  • Watch urine for stone

Surgical

  • Endoscopic rather than open/Shockwave lithotripsy
  • Indications
    • Large stones (>5mm), infection above site of obstruction, failure of conservative treatment, evidence of renal impairment, anatomical abnormality

Prevention

  • Drink plenty of fluids, treat cause of stone
70
Q

What is adult polycystic disease?

A

Autosomal dominant condition, cause of renal failure. Always bilateral, growth of cysts in the tubules throughout the nephrons

71
Q
A
72
Q

Presentation of adult polycystic disease?

A

Function usually preserved until 40-50yrs.

In adults:

  • Acute loin pain +/- haematuria
  • Vague abdominal/loin discomfort due to increasing size of kidneys
  • Hypertension
  • Features of uraemia
73
Q

What is a urethral stricture

A

Fixed, abnormal narrowing of the urethra that causes obstruction to outflow and back pressure on the bladder, ureters and kidneys.

Most commonly iatrogenic in origin, ask about trauma, infection or urethral instrumentation.

74
Q

Presentation of urethral stricture?

A

Progressive diminution in urine flow, with other features of bladder outflow obstruction.

  • Spraying or forking of urinary stream may be experienced.
  • Must examine external meatus and palpate urethra for areas of fibrosis in corpus spongiosum.
75
Q

What is vesico-ureteric reflux?

A
  • Abnormal backflow of urine from the bladder into ureter and kidney.
  • Very common anatomical abnormality of renal tract
  • Predisposes to infection
  • Can lead to scarring and destruction of the kidney.
76
Q

Presentation of vesico-ureteric reflux?

A

Urinary tract infection (raise concerns after 1 UTI in boys, 2 in girls)

Incontinence, frequency, dysuria, abdominal pain

77
Q

Summary of glomerulonephritis?

A
78
Q

Definition of glomerulonephritis?

A

Glomerular injury by

  • Immunological component
  • Completement activation, platelet aggregation, neutrophil infiltration, activation of the kinin system.

May occur in isolation or secondary to disease e.g. polyarteritis nodosa and SLE.

79
Q

Difference between nephrotic and nephritic syndromes?

A

Nephrotic syndrome = proteinuria, low albumin, oedema

Nephritic syndrome = haematuria, uraemia, facial oedema

80
Q

Presentation of glomerulonephritis?

A

Categorised by haematuria with red cell casts in the urine.

May present clinically as:

  • Nephrotic syndrome (proteinuria, low albumin, oedema)
  • Nephritic syndrome (haematuria, uraemia, facial oedema)
  • Acute or chronic renal failure
  • Asymptomatic haematuria and/or proteinuria
81
Q

What is orthostatic proteinuria?

A
  • Proteinuria in the day which is absent from early morning urine samples.
  • Prognosis normal up to 40 years following diagnosis.
  • Common in young males.

Significant renal abnormality more likely if haematuria and proteinuria are detected

82
Q

Who is susceptible to AKI?

A
  • Dehydration
  • Advanced age
  • CKD
  • Cardiac disease
  • Diabetes
  • Myeloma
  • Nephrotoxic drugs
83
Q

Renal causes of AKI/

A
  • Acute glomerulonephritis
  • Vasculitis, SLE
  • Myeloma (paraproteins can be toxic)
  • Rhabdomyolysis
  • Hepatorenal (haemodynamic changes in context of chronic liver disease)
  • Toxins – drugs, radiocontrast, chemicals
  • Tumour lysis
  • Thrombotic microangiopathy (HUS, TTP)
  • Pregnancy related
  • Accelerated hypertension
84
Q

What is acute tubular necrosis?

A
  • Tubular damage – from pre-renal ischaemic/toxic insult
  • Manifests as AKI not immediately reversed by resuscitation – i.e. oliguria no longer a physiological response
  • Period of established reduced kidney function, followed by recovery/polyuric phase
  • Kidney function recovery may be incomplete
85
Q

Assessment of a patient with AKI/

A

ABCDE

  • Assessment of hydration/haemodynamic status
  • Previous measure of kidney function
  • Evidence of sepsis
  • Any nephrotoxins?
86
Q

Investigaitons in AKI?

A
  • Urinalysis
    • Blood and protein = glomerulonephritis/vasculitis (RBC casts)
  • FBC, biochemistry, CRP
  • Sepsis screen
  • CK if rhabdo
  • Immune screen
    • (ANCA, ANA, Anti-GBM, ASO titres, C3, C4)
  • Myeloma screen
    • Serum electrophoresis and free light chains, urine electrophoresis (Bence Jones protein)
  • USS
  • Renal biopsy
    • If unexplained, no obstruction
87
Q

Biochemistry in AKI?

A
  • Urea increases
  • Creatinine increases (can be in normal range)
    • Increased urea/creatinine ration = pre-renal
    • eGFR not meaningful if rapid change creatinine
  • Hyperkalaemia
  • Metabolic acidosis
  • Calcium tends to fall but PO4 tends to rise
  • High Ca - can cause AKI, suspect myeloma
88
Q

Clinical features of AKI/

A
  • Renal
    • Oligrua (can be polyuria)
  • CVS/Resp
    • Fluid overload, pericarditis
  • GI
    • Anorexia, nausea, vomiting, peptic ulceration
  • CNS
    • Drowsiness, encephalopathy, fits
  • Haem
    • Bleeding tendency, drop in Hb (< compared to CKD)
89
Q

Management of AKI?

A
  • Fluid Management
    • Resus - then careful assessment/monitoring and fluid input according to need
    • Diuretics and fluid restriction for fluid overload
  • Vasopressors/Inotropes
  • Restrict potassium intake - only give if potassium is low
  • Avoid nephrotoxins
  • Nutrition - because they are catabolic
  • Consider ulcer prophylaxis - at risk of GI bleeding
  • Monitoring renal function (bloods, urine output)
  • Treat underlying cause
90
Q

How does ACEi worsen AKI?

A

Because it dilates the efferent arteriole –> less back pressure leads to less glomerular pressure –> the pressure is what creates flow of urine –> worsens AKI

91
Q

Sick day rules for ACEi?

A

DONT TAKE - can precipitate AKI

92
Q

Types of RRT?

A
  1. Acute intermittent haemodialysis (quite intensive changes in hydration and chemistry over short periods of time)
  2. Continuous haemofiltration - unstable patients requiring inotropes
  3. Peritoneal diaylsis - not usually in AKI
93
Q

Management of rhabdo?

A
  • Fluid status assessment and resuscitation
  • Bloods - U+Es
  • Assessment for compartment syndrome
    • Pressure of body weight and hard floor below may exceed perfusion pressure

Causes = crush injury, long lie, drugs (MDMA, statins, phenothiazines), arterial ischaemia, myositis (infection, autoimmune)

94
Q

Definition of rhabdo? Presentation and bloods?

A

Muscle damae with release of intracellular contents including myoglobin - toxic to tubules

Urine dark in colour, positive haematuria (myoglobin)

Bloods

  • V.high CK (tens of thousands)
  • Hyperkalaemia
  • High PO4, low Ca
95
Q

Post-renal AKI management?

A

Confirm diagnosis - examination, bladder scan or formal USS

Catheter

Fluid replacement - monitor hydration, fluid balance and electrolytes (post-obstructive diuresis)

96
Q

Management of renal AKI?

A

Investigations

  • Haematoproteinuria - suggests glomerular disease - red cell cast (RBCs stuck together - glomerular)
  • Immunology screen
  • CRP or plasma viscosity
  • Renal USS and biopsy
97
Q
A
98
Q

Indications for monitoring patients at risk of developing CKD?

A
  • DM
  • HTN
  • CVD
  • Structural renal disease
  • Mutlisystem illness (SLE)
  • Nephrotoxic drugs
99
Q

Biochemical abnormalities in CKD?

A

Raised urea and creatinine in blood

Hyperkalaemia

Metabolic acidosis (reduced serum bicarb)

Bone biochemistry

Raised serum urate (renally excreted –> gout)

100
Q

Features of CKD?

A

Renal

  • Fluid retention, inability to concentrate urine (polyuria, nocturia)

Cardiovascular

  • HTN, pulmonary oedema
  • LVF, vascular disease, dyslipidaemia, vascular calcification, pericarditis

GI

  • Anorexia, nausea, vomiting, malnutrition, peptic ulceration

Neuro, derm, endocrine features too.

101
Q

Risk factors for CKD progression?

A
  • More advanced CKD (lower GFR)
  • BP control
  • Proteinura/albuminuria
    • Race, gender
    • Smoking
    • Hyperglycaemia, hyperlipidaemia
    • Obesity
    • CVS disease
    • Nephrotoxic drugs
102
Q
A
103
Q

Why are ACEi/ARBs good in CKD? Things to remember about ACEi in CKD?

A

Renoprotective Effect (even if normal BP) –> need to be on the maximum tolerated dose, may cause further decrease in proteinuria.

  • May cause transient decrease in GFR (<20% is fine)
  • Profound drop in GFR in RA stenosis
  • Risk of hyperkalaemia
  • Monitoring U+Es baseline and at 1 week
104
Q

Why is high phosphate bad in secondary hyperparathyroidism?

A

Phosphate is thought to increase vascular calcification –> development of CV disease

105
Q
A
106
Q

Things to check in diabetic kidney check?

A

BP

U+E

Urine dipstick

Urine albumin/creatinine ratio

107
Q

What is microalbuminuria?

A
  • Increased urinary albumin excretion, but below the level that registers on protein dipstick
  • Normally small amount of protein (small molecules) in urine, but very little albumin (large protein) - increase suggests ‘glomerular leakiness’
  • In diabetes, the risk of progression to established diabetic nephropathy (persistent proteinuria) - CVS risk and increased diabetes complications

Way of picking them up early

108
Q

Diabetes management in CKD?

A

Stop metformin when eGFR <30 (lactic acidosis)

Drug dose alterations for oral drugs

Reducing insulin requirements/hypoglycaemia with worsening kidney function (low appetite, intake etc).

- FINALS (24 decks)

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