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Core Conditions > Renal > Flashcards

Renal Flashcards

1
Q

UTI

A

inflammatory reaction of the urinary tract epithelium in response to pathogenic micro-organisms most commonly bacteria (e.g. E.coli)
• Infectious cystitis is the most common type of UTI which is caused by a bacterial infection of the bladder
• Complicated UTI: LUTI pts with tract abnormality or systemic disease involving the kidney (DM, sickle cell)

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2
Q

how common is UTI

A

Second most common infection among non-institutionalised patients

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3
Q

causes of UTI

A
  • UTI results from pathogenic organisms gaining access to the urinary tract and not being effectively eliminated
  • • The bacteria ascend the urethra and generally have an intestinal origin – e.coli cause most utis in men and women (70%) and proteus mirabilis (10%)
    • In hospitals it is usually klebsiella aerogenes and enteroccus faecalis
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4
Q

risk factors for UTI

A
  • MEN: BPH, urinary tract stones, urological surgery, urethral strictures, age>50, previous UTI, catheterisation
  • WOMEN: sexual activity, spermicide use, post-menopuase, positive Fx of UTIs, Hx of recurrent UTIs, presence of a foreign body
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5
Q

symptoms/ signs for UTI

A
  • MEN: presence of risk factors, dysuria, urinary frequency and urgency, suprapubic pain, hesistancy, nocturia, enlarged prostate
  • WOMEN: presence of risk factors, dysuria, urinary frequency, haematuria, back/flank pain, costovertebral angle tenderness
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6
Q

DDx for UTI

A
  • MEN: BPH, prostatitis, pyelonephritis, urinary tract stones, gonococcal urethritis, chlamydia urethritis, bladder or prostate or renal cancer, epididymitis
  • WOMEN: over-active bladder, urothelial carcinoma of the bladder or upper urinary tract non-infetious urethritis, foreign body in bladder, vaginitis due to candidia or trichomonas
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7
Q

investigations for UTI

A

• MEN:
• 1ST LINE:
o Urine dipstick  positive leukocyte esterase and/or nitrite
o Urine microscopy  leukocytes and/or bacteria
o Urine culture  >10^2 CFU/mL, do this when pt is over 65, pregnant or Abxs are ineffective
o Gram stain  bacteria
o US  if suspect obstruction
• WOMEN:
• 1ST LINE:
o Urine dipstick  positive leukocyte esterase and/or nitrite
o Urine microscopy  leukocytes and/or bacteria
o Urine culture and sensitivity  growth of >10^5 CFU/mL

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8
Q

management of UTI

A
  • MEN: tends to be complicated uti
  • 1ST LINE: ciprofloxacin
  • 2nd LINE: trimethoprim
•	WOMEN:
•	UNCOMPLICATED:
o	1ST LINE: oral abx therapy – nitrofurantoin (oral)
o	2nd LINE: trimethoprim
o	IF PREGNANT  amoxicillin
•	COMPLICATED:
o	1ST LINE: ciprofloxacin (oral)
o	IF PREGNANT  cephalexin (oral)
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9
Q

prognosis and complications for UTI

A

prognosis:
• MEN: younger men have better prognosis
• WOMEN: excellent prognosis with appropriate antimicrobial treatment

complications: sepsis, AKI, pyelonephritis, prostatitis (men)

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10
Q

Acute pyelonephritis definition

A

• Severe infectious inflammatory disease of the renal parenchyma, calicles and pelvis that can be acute, recurrent or chronic

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11
Q

how common is Acute pyelonephritis

A

• Estimated to account for at least 250,000 surgery consultations and 200,000 hospitalisations

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12
Q

risk factors for Acute pyelonephritis

A
  • Frequent sexual intercourse
  • UTI
  • Diabetes mellitus
  • Stress incontinence
  • Foreign body in urinary tract
  • Anatomical/functional urinary abnormality
  • Pregnancy
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13
Q

symptoms / signs for Acute pyelonephritis

A
  • Presence of risk factors
  • Fever
  • Nausea and vomiting
  • Dysuria, frequency or urgency
  • Flank pain or costovertebral angle tenderness
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14
Q

Ddx for Acute pyelonephritis

A
  • Chronic pyelonephritis
  • Pelvic inflammatory disease
  • Pelvic pain syndrome
  • Cystitis
  • Acute prostatitis
  • Lower lobe pnuemonia
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15
Q

Igx for Acute pyelonephritis

A
  • 1st LINE:
  • Urinalysis  WBC >10/HPF, RBCs >5/HPF
  • Gram stain  typically gram negative rods, less typically gram-positive cocci
  • Urine culture  bacteria > 100,000 colony-forming units (CFU)/mL
  • FBC  leucocytosis
  • ESR and CRP  elevated
  • Procalcitonin  elevated
  • Blood culture  any bacterial growth is considered abnormal
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16
Q

Management for Acute pyelonephritis

A
  • MILD-TO-MODERATE SYMTPOMS:
  • 1ST LINE: empiric oral abx therapy  cefixime or ciprofloxacin (oral)
  • 2nd LINE: levofloxacin or trimethoprim/sulfamethoxazole (oral)
  • SEVERE SYMPTOMS:
  • 1ST LINE: gentamicin IV
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17
Q

prognosis and complications of Acute pyelonephritis

A

good prognosis

complications - • Need for catheterisation, renal failure, abx failure, allergic reaction to abx, sepsis, renal abscess formation

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18
Q

causes of Acute pyelonephritis

A
  • Acute uncomplicated pyelonephtiritis most often develops as a result of an ascending urinary tract infection
  • Pathogenesis may involve haematogenous seeding of the kidneys in patients with bacteraemia
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19
Q

chronic pyelonephritis definition

A

• Chronic pyelonephritis is a complex renal disorder characterised by chronic tubulointerstitial inflammation and deep segmental cortical renal scarring and clubbing of the pelvic calyces as the papillae retract into the scars

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20
Q

how common is chronic pyelonephritis

A
  • More common in children
  • More common in caucasians than in people of African descent
  • More common in women
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21
Q

causes of chronic pyelonephritis

A
  • Renal damage occurs slowly over a long-period of time in responde to a chronic inflammatory process or infections
  • Results in thinning of the renal cortex along with deep, segmental, coarse cortical scarring
  • Obstruction predisposes the kidney to infection and chronic obstruction contributes to parenchymal atrophy
  • Obstruction can be bilateral, resulting in renal insufficiency or unilateral
  • Recurrent infections superimposed on diffuse or localised obstructive lesions lead to recurrent bouts of renal inflammation and scarring
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22
Q

risk factors for chronic pyelonephritis

A
  • Acute pyelonephritis
  • VUR
  • Obstruction
  • Renal calculi
  • Diabetes mellitus
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23
Q

symptoms/signs for chronic pyelonephritis

A
  • Hx of vesicoureteral reflux, acute pyelonephritis or renal obstruction
  • Female
  • Nausea
  • Elevated
  • Children and infants (risk of VUR)
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24
Q

DDx of chronic pyelonephritis

A
  • Acute pyelonephritis
  • Renal calculi
  • Renal cancer
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25
Q

Investigations for chronic pyelonephritis

A
  • 1st LINE:
  • Urinalysis  may be normal, dipstick positive for leukocytes, nitries, blood
  • Renal function  elevated creatinine and estimated GFRm reduced creatinine clearance
  • Urine culture  positive or may be sterile
  • Electrolyte panel  hyponatraemia, hyperkalaemia, acidosis
  • FBC  anaemia, leucocytosis
  • Renal USS  small, irregular, scarred kdineys with echogenic parenchyma
  • UB X-Ray  renal stones, small or large kidneys, air in renal collecting/parenchymal system
  • CT Abdomen
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26
Q

prognosis and complications of chronic pyelonephritis

A

prognosis varies on cause

complications- Acute renal failure, hyperparathyroidism, acute pyelonephritis, obstruction, CKD

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27
Q

Hydronephrosis (obstructive uropathy) definition

A
  • Blockage of urinary flow, which can affect one or both kidneys depending on the level of obstruction
  • If only one kidney is affected, urinary output may be unchanged and serum creatinine can be normal
  • When kidney function is affected this is termed obstructive nephropathy
  • Hydronephrosis refers to dilation of the renal pelvis and can be present with or without obstruction
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28
Q

How common is Hydronephrosis (obstructive uropathy)

A
  • Unilateral obstructive uropathy is most commonly due to ureteral stones
  • Stones are more common in hot and dry climates and obesity appears to increase the incidence
  • BPH is a common cause of acute and chronic bilateral obstruction
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29
Q

Causes of Hydronephrosis (obstructive uropathy)

A
  • Obstructive uropathy, regardless of the specific cause, can cause back pressure on the kidney by preventing urinary flow
  • Can result in decreased renal blood flow, decreased glomerular filtration rate and up-regulation of the RAAS system
  • This can in turn cause atrophy and apoptosis of the renal tubules and interstitial fibrosis with infiltration of the interstitial spaces by macrophages
  • These changes may lead to decreased re-absoprtion of solutes and water, inability to concentrate the urine and impaired excretion of hydrogen and potassium
  • If left untreated, obstructive nephropathy can cause irreversible renal damage, obstruction can ultimately cause tubulointerstitial fibrosis and tubular atrophy and interstitial inflammation
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30
Q

risk factors for Hydronephrosis (obstructive uropathy)

A
  • BPH
  • Constipation
  • Medication  anticholinergic agents, narcotic analgesia, alpha receptor antagonists
  • Urolithiasis (ureteric calculi)
  • Spinal cord injury, parkinson’s disease, or MS
  • Malignancy
  • Posterior urethral valves
  • Meatal stenosis
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31
Q

symptoms/signs for Hydronephrosis (obstructive uropathy)

A
  • Flank pain
  • Fever
  • Lower urinary tract symptoms
  • Distended abdomen/palpable bladder
  • Inability to urinate
  • Enlarged or hard nodular prostate on rectal examination
  • Costovertebral angle tenderness
  • Haematuria
  • Increasing age
  • Meatal narrowing
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32
Q

DDx for Hydronephrosis (obstructive uropathy)

A
  • Parapelvic cysts
  • Hydronephrosis of pregnancy
  • AAA
  • Appendicitis
  • Gynaecological disorders e.g. ovarian torsion, cyst
  • Ectopic pregnancy
  • Renal failure
  • Bowel obstruction
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33
Q

investigations for Hydronephrosis (obstructive uropathy)

A
  • 1st LINE:
  • Urinary dipstick  nomrla or positive nitrites, leukocyte esterase and/or blood in presence of infection, microscopic haematuria in renal colic
  • Renal ultrasound  hydronephorsis affecting the upper urinary tract
  • Urea and creatinine  normal or elevated
  • FBC  normal or elevated WBC if infection present, low haemoglobin and haematocrit if bleeding
  • CT pyelogram  stones in the urinary tract identified as causing obstruction
  • IV pyelohram (excretory urography)  delayed nephrogram and drainage if obstruction present
  • CONSIDER: PSA, tumour markers, CT scan abdomen and pelvis, bladder ultrasound, MRU (urography)
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34
Q

prognosis and complications for Hydronephrosis (obstructive uropathy)

A

prognosis - can result in permanent renal damage if left untreated but the majority of patient recover fully

complications - renal failure, severe sepsis, post-obstructive diuresis, septic shock

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35
Q

management of Hydronephrosis (obstructive uropathy)

A
  • SIGNS OF SEPSIS: 1ST LINE – analgesia and rehydration, nephrostomy or ureteric sten and abx - gentamicin
  • RENAL STONES:
  • SMALL: 1ST LINE – trial of passge with analgesia and rehydration – ketorolac IM, 2nd LINE – active stone removal
  • LARGE: 1ST LINE - trial of passge with analgesia and rehydration – ketorolac IM
  • NOT DUE TO STONES: 1ST LINE – ureteric stent + paracetamol + gentamicin (1st) or meropenem (2nd) both IV, 2nd LINE: nephrostomy
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36
Q

acute renal failure - pre renal (aka Pre-Renal Azotaemia) definition

A

• Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output

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37
Q

how common is acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A
  • Very common in acute illness
  • Stage 1 AKI is found in more than 15% of emergency hospital admissions
  • AKI with plasma creatinine >500micromol/L is diagnosed in 2 to 7.5 per 10,000 adult population per year in the UK
  • Injury counts when serum creatinine is 2X increased from the baseline
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38
Q

causes of acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A
  • Impaired perfusion of the kidneys with blood due to one or more of hypovolaemia, hypotension, impaired cardiac pump efficiency or vascular disease limiting renal blood flow
  • The kidneys can normally cope with a variety of blood pressure but they need to autoregulate
  • This is dependent on the intrarenal production of prostaflandins and angiotensin II
  • With severe or prolonged hypovolaemia there is eventually a drop in GFR (pre-renal failure)
  • Drugs that impair renal autoregulation such as ACEi and NSAIDs increase the tendency to develop prerenal uraemia
  • Is characterised in the early stages by lack of structural damage and rapid reversibility once normal renal perfusion has been restored
  • However, all causes of prerenal uraemia may, if sustained, lead to ischaemic tubule cell injury (ischaemic intrinsic AKI) form which recovery will be delayed
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39
Q

risk factors for acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A
  • General:
  • > 65 Hx of AKI
  • CKD (eGFR <60mL/min/1.73m2)
  • Symptoms or Hx of urological obstruction or conditions which may lead to obstruction
  • Chronic conditions such as HF, liver disease and diabetes mellitus
  • Neurological or cognitive impairment or disability (which may limit fluid intake)
  • Sepsis
  • Hypovolaemia
  • Oliguria (urine output <0.5mL/kg/hour)
  • Nephrotoxic drug use within the last week (e.g. ACEi and NSAID, ARBS, and diuretics)
  • Exposure to iodinated contrast agents within the last week
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40
Q

symptoms of acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A
  • Suspect AKI if presented with an acute illness and any of the risk factors above
  • Also new onset or significantly worsening urological symptoms
  • Symptoms or signs of a multi-sysem disease affecting the kidneys and other organ systems
  • Alteration of urine volume: oliguria usually occurs in the early stages, recovery of renal function typically occurs after 7-21 days and in the recovery phase which may last some weeks, often passage of large amounts of dilute urine
  • Biochemical abnormalities: hyperkalaemia, metabolic acidosis, hyponatraemia (due to water overload as a result of continued drinking), hypoglycaemia due to reduced production of Vit D and hyperphosphataemia due to phosphate reduction
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41
Q

signs of acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A
  • Symptoms are very non-specific  symptoms in AKI are usually related to the underlying causes rather than the AKI itself
  • N & V
  • Drowsiness
  • SOB – due to pulmonary oedema or metabolic acidosis
  • Arrhythmias
  • Orthopnea
  • Paroxysmal nocturnal dyspnoea
  • Peripheral odema
  • Hypotension
  • Tachycardia
  • Dizziness
  • All patients with AKI should be examined for evidenc of obstruction (enlarged palpable kidneys or bladder, large prostate on rectal exam, pelvic masses on vaginal exam in women)
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42
Q

DDx for acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A

• Intrinsic and post-renal AKI

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43
Q

Investigations for acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A
  • 1st LINE:
  • Basic metabolic profile (inc urea and creatinine) – acutely evelated serum creatinine, high serum potassium, metabolic acidosis
  • Ratio of serum urea and creatinine – serum urea to creatinine ratio >20:1 supports pre-renal azotaemia
  • Urinalysis – RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase (in cases iof infection)
  • Urine culture – bacterial or fungal growth may occur
  • FBC – anaemia, leucocytosis, thrombocytopenia
  • Fractional excretion of sodium - <1% supports pre-renal azotaemia
  • Fractional excretion of urea - <35% supports pre-renal azotaemia
  • Urinary eosinophil count - >5% to 7% supports a diagnosis of interstitial nephritis
  • VBG – diagnostic for metabolic acidosis and certain intoxications
  • Fluid challenge – renal function improves rapidly in pre-renal azotaemia
  • Bladder catheterisation – significant urine volume released after catheter placement (in cases of bladder outlet obstruction), minimal residual urine after catheter placement (in cases of impaired urine production or higher level obstruction)
  • Urine osmolality – high in pre-renal azotaemia, close to serum osmolality in acute tubular necrosis
  • Renal ultrasound – dikated renal calyces (suggesting obstruction)
  • CXR and ECG
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44
Q

Management for acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A

• 1st LINE:
• Volume expansion and/or RBC transfusion – crystalloid (normal saline or lactated Ringer’s), colloid might be used if there is significant hypoalbuminaemia
o + severe hy: potension  vasopresser e.g. dopamine IV
o + volume overload  diuretic e.g. furosemide

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45
Q

Prognosis and complications for acute renal failure - pre renal (aka Pre-Renal Azotaemia)

A

Prognosis is variable and depends on cause of injury and the severity and duration of AKI

Complications include hyperphosphatemia, volume overload, hyperkalaemia, metabolic acidosis

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46
Q

Acute Renal Failure – Intrinsic (Acute Tubular Necrosis) definition

A

• Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output

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47
Q

how common is Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A
  • Very common in acute illness
  • Stage 1 AKI is found in more than 15% of emergency hospital admissions
  • AKI with plasma creatinine >500micromol/L is diagnosed in 2 to 7.5 per 10,000 adult population per year in the UK
  • Injury counts when serum creatinine is 2X increased from the baseline
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48
Q

causes of Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A
  • Most commonly due to acute tubular necrosis as a result of renal ischaemia or direct renal toxins
  • Other causes include disease affecting the interstitium (drug hypersensitivities, infections) the renal vasculature (vasculitis, accelerate hypertension, cholesterol embolism, HUS, thrombotic thrombocytopenic purpura) and acute glomerulonephritis
  • CAUSES:
  • Haemorrhage, burns, diarrhoea, vomiting and fluid loss from fistula
  • Acute pancreatitis, diurectics, MI, CHF, endotoxic shock, snake bite
  • Myoglobinaemia, haemoglobinaemia, hepatorenal syndrome
  • Radiological contrast agents
  • Drugs  aminoglycosides, NSAIDs, ACEis, platinum derivatives
  • Abruptio placentae, pre-exlampsia and eclampsia
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49
Q

risk factors for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A
  • General:
  • > 65 Hx of AKI
  • CKD (eGFR <60mL/min/1.73m2)
  • Symptoms or Hx of urological obstruction or conditions which may lead to obstruction
  • Chronic conditions such as HF, liver disease and diabetes mellitus
  • Neurological or cognitive impairment or disability (which may limit fluid intake)
  • Sepsis
  • Hypovolaemia
  • Oliguria (urine output <0.5mL/kg/hour)
  • Nephrotoxic drug use within the last week (e.g. ACEi and NSAID, ARBS, and diuretics)
  • Exposure to iodinated contrast agents within the last week
50
Q

symptoms for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A
  • Suspect AKI if presented with an acute illness and any of the risk factors above
  • Also new onset or significantly worsening urological symptoms
  • Symptoms or signs of a multi-sysem disease affecting the kidneys and other organ systems
  • Alteration of urine volume: oliguria usually occurs in the early stages, recovery of renal function typically occurs after 7-21 days and in the recovery phase which may last some weeks, often passage of large amounts of dilute urine
  • Biochemical abnormalities: hyperkalaemia, metabolic acidosis, hyponatraemia (due to water overload as a result of continued drinking), hypoglycaemia due to reduced production of Vit D and hyperphosphataemia due to phosphate reduction
51
Q

signs for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A
  • Symptoms are very non-specific  symptoms in AKI are usually related to the underlying causes rather than the AKI itself
  • N & V
  • Drowsiness
  • SOB – due to pulmonary oedema or metabolic acidosis
  • Arrhythmias
  • Orthopnea
  • Paroxysmal nocturnal dyspnoea
  • Peripheral odema
  • Hypotension
  • Tachycardia
  • Dizziness
  • All patients with AKI should be examined for evidenc of obstruction (enlarged palpable kidneys or bladder, large prostate on rectal exam, pelvic masses on vaginal exam in women)
52
Q

DDx for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A

• Intrinsic and post-renal AKI

53
Q

Investigations for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A
  • 1st LINE:
  • Basic metabolic profile (inc urea and creatinine) – acutely evelated serum creatinine, high serum potassium, metabolic acidosis
  • Ratio of serum urea and creatinine – serum urea to creatinine ratio >20:1 supports pre-renal azotaemia
  • Urinalysis – RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase (in cases iof infection)
  • Urine culture – bacterial or fungal growth may occur
  • FBC – anaemia, leucocytosis, thrombocytopenia
  • Fractional excretion of sodium - <1% supports pre-renal azotaemia
  • Fractional excretion of urea - <35% supports pre-renal azotaemia
  • Urinary eosinophil count - >5% to 7% supports a diagnosis of interstitial nephritis
  • VBG – diagnostic for metabolic acidosis and certain intoxications
  • Fluid challenge – renal function improves rapidly in pre-renal azotaemia
  • Bladder catheterisation – significant urine volume released after catheter placement (in cases of bladder outlet obstruction), minimal residual urine after catheter placement (in cases of impaired urine production or higher level obstruction)
  • Urine osmolality – high in pre-renal azotaemia, close to serum osmolality in acute tubular necrosis
  • Renal ultrasound – dikated renal calyces (suggesting obstruction)
  • CXR and ECG
54
Q

Management for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A

• 1ST LINE:
• Tx of underlying condition – nephrotoxic agents should be ceased and management varies according to aetiology
o volume overload  diuretic e.g. furosemide
o pre-exisitng pre-renal azotaemia  volume expansion e.g. crystalloid

55
Q

Prognosis and complications for Acute Renal Failure – Intrinsic (Acute Tubular Necrosis)

A

prognosis is variable and depend on cause of injury and severity and duration of AKI

complications - hyperphosphataemia, volume overload, hyperkalaemia, metabolic acidosis

56
Q

Acute Renal Failure – Post-Renal definition

A

• Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output

57
Q

how common is Acute Renal Failure – Post-Renal

A
  • Very common in acute illness
  • Stage 1 AKI is found in more than 15% of emergency hospital admissions
  • AKI with plasma creatinine >500micromol/L is diagnosed in 2 to 7.5 per 10,000 adult population per year in the UK
  • Injury counts when serum creatinine is 2X increased from the baseline
58
Q

causes of Acute Renal Failure – Post-Renal

A
  • Occurs when both urinary outflow tracts are obstructed or when the tract is obstructed in a pt with a single functioning kidney
  • It is usually quickly reversed if the obstruction is relieved
59
Q

risk factors of Acute Renal Failure – Post-Renal

A
  • General:
  • > 65 Hx of AKI
  • CKD (eGFR <60mL/min/1.73m2)
  • Symptoms or Hx of urological obstruction or conditions which may lead to obstruction
  • Chronic conditions such as HF, liver disease and diabetes mellitus
  • Neurological or cognitive impairment or disability (which may limit fluid intake)
  • Sepsis
  • Hypovolaemia
  • Oliguria (urine output <0.5mL/kg/hour)
  • Nephrotoxic drug use within the last week (e.g. ACEi and NSAID, ARBS, and diuretics)
  • Exposure to iodinated contrast agents within the last week
60
Q

symptoms of Acute Renal Failure – Post-Renal

A
  • Suspect AKI if presented with an acute illness and any of the risk factors above
  • Also new onset or significantly worsening urological symptoms
  • Symptoms or signs of a multi-sysem disease affecting the kidneys and other organ systems
  • Alteration of urine volume: oliguria usually occurs in the early stages, recovery of renal function typically occurs after 7-21 days and in the recovery phase which may last some weeks, often passage of large amounts of dilute urine
  • Biochemical abnormalities: hyperkalaemia, metabolic acidosis, hyponatraemia (due to water overload as a result of continued drinking), hypoglycaemia due to reduced production of Vit D and hyperphosphataemia due to phosphate reduction
61
Q

DDx of Acute Renal Failure – Post-Renal

A

Intrinsic and post-renal AKI

62
Q

Investigations of Acute Renal Failure – Post-Renal

A
  • 1st LINE:
  • Basic metabolic profile (inc urea and creatinine) – acutely evelated serum creatinine, high serum potassium, metabolic acidosis
  • Ratio of serum urea and creatinine – serum urea to creatinine ratio >20:1 supports pre-renal azotaemia
  • Urinalysis – RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase (in cases iof infection)
  • Urine culture – bacterial or fungal growth may occur
  • FBC – anaemia, leucocytosis, thrombocytopenia
  • Fractional excretion of sodium - <1% supports pre-renal azotaemia
  • Fractional excretion of urea - <35% supports pre-renal azotaemia
  • Urinary eosinophil count - >5% to 7% supports a diagnosis of interstitial nephritis
  • VBG – diagnostic for metabolic acidosis and certain intoxications
  • Fluid challenge – renal function improves rapidly in pre-renal azotaemia
  • Bladder catheterisation – significant urine volume released after catheter placement (in cases of bladder outlet obstruction), minimal residual urine after catheter placement (in cases of impaired urine production or higher level obstruction)
  • Urine osmolality – high in pre-renal azotaemia, close to serum osmolality in acute tubular necrosis
  • Renal ultrasound – dikated renal calyces (suggesting obstruction)
  • CXR and ECG
63
Q

Management of Acute Renal Failure – Post-Renal

A
  • 1st LINE:
  • Bladder catheterisation: should be done in all cases of AKI if bladder outlet obstruction cannot be quickly ruled out by ultrasound
  • 2nd LINE:
  • Relief of obstruction above bladder neck: ureteral stenting or percutaneous nephrostomy
64
Q

Prognosis and complications of Acute Renal Failure – Post-Renal

A

variable and depends on cause of injury and the severity and duration

complications - hyperphosphataemia, volume overload, hyperkalaemia, metabolic acidosis

65
Q

signs of Acute renal failure - post renal

A
  • Symptoms are very non-specific  symptoms in AKI are usually related to the underlying causes rather than the AKI itself
  • N & V
  • Drowsiness
  • SOB – due to pulmonary oedema or metabolic acidosis
  • Arrhythmias
  • Orthopnea
  • Paroxysmal nocturnal dyspnoea
  • Peripheral odema
  • Hypotension
  • Tachycardia
  • Dizziness
  • All patients with AKI should be examined for evidenc of obstruction (enlarged palpable kidneys or bladder, large prostate on rectal exam, pelvic masses on vaginal exam in women)
66
Q

Chronic Renal Failure (CKD) definition

A

• Pathological abnormality of the kidney such as haematuria and/or proteinuria or a reduction in the GFR to <60mL/minute/1.73m2 for more than 3 months duration

67
Q

how common is Chronic Renal Failure (CKD)

A

• 11% of adult population worldwide has CKD

68
Q

causes of Chronic Renal Failure (CKD)

A
  • In response to renal injury, there is thought to be an increase in intra-glomerular pressure with glomerular hypertrophy as the kidney attempts to adapt to nephron loss to maintain constant GFR
  • An increase in glomerular permeability to macro-moleculres such as transforming growth factor-beta (TGF-beta), fatty acids, pro-inflammaotry markers of oxidant stress and protein may result in toicity to the mesangial matrix, causing mesangial cell expansion, inflammation, fibrosis and glomerular scarring
  • Additionally, renal injury results in an increase in angiotensin II production, causing an upregulation of TGF-beta, contributing to collagen synthesis and renal scarring within the glomerulus
  • Both the structural alterations and accompanying biochemical, cellular and molecular changes seem to account for progressive renal scarring and loss of kidney function
69
Q

risk factors for Chronic Renal Failure (CKD)

A
  • Diabetes mellitus  most common cause of CKD
  • Hypertension
  • Age >50yrs
  • Childhood kidney disease
  • WEAK: smoking, obesity, black or Hispanic ethnicity, Fx of CKD, autoimmune disorders, male, long-term use of NSAIDs
70
Q

symptoms for Chronic Renal Failure (CKD)

A
  • Presence of risk factors
  • Fatigue
  • Oedema
  • Nausea with/without vomiting
  • Pruritus
  • Anorexia
  • Arthralgia
  • Enlarged prostate gland
71
Q

signs for Chronic Renal Failure (CKD)

A
  • Foamy-appearing urine  indicative of proteinuria
  • Cola-coloured urine  indicative of haematuria
  • Rashes
  • Retinopathy
72
Q

DDx for Chronic Renal Failure (CKD)

A
  • Diabetic kidney disease
  • Hypertensive nephrosclerosis
  • Ischaemic nephropathy
  • Obstructive uropathy
  • Nephrotic syndrome
  • Glomerulonephritis
73
Q

Investigations for Chronic Renal Failure (CKD)

A
  • 1ST LINE:
  • Serum creatinine – elevated
  • Urinalysis – haematuria and/or proteinuria
  • Urine microalbumin – microaluminuria
  • Renal USS – small kidney size, presence of obstruction/hydronephrosis, kidney stones
  • eGFR - <60mL/minue/1.73m2
74
Q

Management for Chronic Renal Failure (CKD)

A
  • STAGES 1-4:
  • 1ST LINE: ACEi or AT2 antagonist e.g. lisinopril + statin e.g. simvastatin
  • 2nd LINE: non-dihydropyridine calcium-channel blocker e.g. diltiazem
  • STAGE 5 OR WITH URAEMIA:
  • 1ST LINE: dialysis
  • 2nd LINE: kidney transplant
75
Q

Prognosis and complications Chronic Renal Failure (CKD)

A

prognosis - progressive and will eventually lead to end-stage renal disease

complications - anaemia, renal osteodystrophy, CVD

76
Q

classification for CKD

A

CLASSIFICATION:
• Stage 1: kidney damage with normal or increased GFR, ≥90 mL/minute/1.73m²
• Stage 2: kidney damage with mild decrease in GFR, 60 to 89 mL/minute/1.73m²
• Stage 3a: kidney damage with moderate decrease in GFR, 45 to 59 mL/minute/1.73m²
• Stage 3b: kidney damage with moderate decrease in GFR, 30 to 44 mL/minute/1.73m²
• Stage 4: kidney damage with severe decrease in GFR, 15 to 29 mL/minute/1.73m²
• Stage 5: kidney failure (end-stage kidney disease), with GFR <15 mL/minute/1.73m²

77
Q

Benign Prostatic Hypertrophy

A

• Multi-factorial involving smooth muscle hyperplasia, prostatic enlargement and bladder dysfunction as well as input from the CNS

78
Q

how common is Benign Prostatic Hypertrophy

A

most common in elderly men

common presentation in infection and in malignancy

79
Q

causes of Benign Prostatic Hypertrophy

A
  • Hyperplasia of both epithelial and stromal prostatic components
  • Increased stromal:epithelial ratio
  • Over time, prostatic hyperplasia can result in bladder outlet obstruction
  • Obstruction has both a prostatic component due to increased epithelial tissue, particularly in a transition zone, and a dynamic component due to increases in stromal smooth muscle tone
  • A large number of alpha-adrenergic receptors are present in the prostate capsule, stroma, and the bladder neck
  • The predominant alpha-1 receptor in prostatic stromal tissue is the alpha-1A receptor
  • Treatment of symptomatic BPH is mainly accomplished via the reduction of the size of the glandular component following inhibition of the formation of dihydrotestosterone (DHT) by 5-alpha-reductase inhibitors and through relaxation of smooth muscle tone with alpha-blockers
80
Q

risk factors for Benign Prostatic Hypertrophy

A

Age over 50

81
Q

DDx for Benign Prostatic Hypertrophy

A
  • Overactive bladder
  • Prostatitis
  • Prostate cancer
  • Urinary tract infection (UTI)
  • Bladder cancer
  • Neurogenic bladder
  • Urethral stricture
82
Q

Investigations for Benign Prostatic Hypertrophy

A
  • 1st LINE:
  • Urinalysis – pyuria
  • PSA – elevation greater than age guideline
  • International prostate symptom score – score of 0 to 35 to define severity of symtpoms
  • Global bother score – score 0-6 dependent on degree of bother
  • Volume charting – diary of frequency and volume of vodiing
83
Q

Management for Benign Prostatic Hypertrophy

A
  • 1st LINE: alpha blocker e.g. terazosin/doxazosin OR 5a-reductase inhibitor e.g. finasteride
  • 2nd LINE: combo of alpha blocker and 5a-reductase inhibitor
84
Q

Prognosis and complications for Benign Prostatic Hypertrophy

A

prognosis - • Majority of pts can expect at least moderate improvemet of their symptoms with a decreased bother socre and improved QOL

85
Q

symptoms/signs of Benign Prostatic Hypertrophy

A
  • Over 50
  • Storage symtpoms – frequency, urgency and nocturia
  • Voiding symptoms – weak stream, hesitancy, intermittency, straining, incomplete emptying and post-void dribbling

• BPH progression, UTI, renal insufficiency, bladder stones

86
Q

prostate carcinoma definition

A

malignant tumour of glandular origin, situated in the prostate

87
Q

causes of prostate carcinoma

A
  • High-grade prostatic intra-epithelial neoplasia is the histological entity widely considered to be the most likely precursor of invasive prostate cancer
  • PIN is characterised by cellular proliferation within pre-existing ducts and glands with cytological changes that mimic neoplasm
  • Prostate cancer tends to spread along the capsular surface of the gland and may invade the seminal vesicles, peri-prostatic tissue and eventually the bladder neck
88
Q

risk factors for prostate carcinoma

A
  • Over 50
  • Black
  • North American or Northwest European descent
  • Fx of prostate cancer
  • High levels of dietary fat
89
Q

symptoms/signs of prostate carcinoma

A
  • Presence of risk factors
  • Elevated PSA
  • Nocturia
  • Urinary frequency and hesitancy
  • Dysuria
  • Abnormal digital rectal exam
  • Asymmetrical, nodular prostate
90
Q

DDx for Prostate carcinoma

A
  • BPH

* Chronic prostatitis

91
Q

Investigations for Prostate Carcinoma

A
  • 1ST LINE:
  • Serum PSA – elevated (>4micrograms/L)
  • Testosterone – normal
  • LFTs – normal
  • FBC – normal, except for advanced metastatic disease
  • Renal function – normal, except for locally advanced disease causing obstruction
  • Prostate biopsy – malignant cells detected in one or more biopsy specimens
92
Q

Management for prostate carcinoma

A
  • 1st LINE:
  • Active Surveillance – monitoring with the additional use of prosyate bopsies until symptoms or signs of disease become clinically evident with the expectation to treat with definitive treatment (e.g. external-beam radiotherapy, brachytherapy, or radical prostatectomy) if there is disease progression
93
Q

prognosis for prostate cancer

A

dependant on gleason score

94
Q

complications for prostate cancer

A

dependant radiation - induced dysuria and/or frequency, radiation induced rectal bleeding

95
Q

bladder carcinoma (in situ)

A
  • 90% of cancers of the urinary bladder are urothelial carcinoma (aka transitional cell carcinoma)
  • Non-muscle invasive tumours are most common
  • Low-grade tumours are papillary and generally easy to visualise
  • High-grade tumours are often flat or in-situ and can be difficult to visualise
96
Q

how common is Bladder carcinoma (in situ)

A

tanks ninth in worldwide cancer incidence

97
Q

causes of bladder carcinoma (in situ)

A
  • Smoking is the most important causative factor in bladder cancer increasing the risk two to fourfold and accounting for an estimate one half of the cases in men and one third in women
  • Second-hand smoke, occupational exposure to chemical carcinogens such as aromatic amines used in rubber and dye industries and polycyclic aromatic hydrocarbons used in the aluminium, coal and roofing industries and exposure to arsenic in drinking water account for one quarter or more of cases
98
Q

risk factors for bladder carcinoma (in situ)

A
  • Tobacco exposure
  • Exposure to chemical carcinogens
  • Over 55
  • Pelvic radiation
  • Systemic chemotherapy
  • Schistosoma infection
  • Male
  • Chronic bladder inflammation
  • Positive Fx
99
Q

symptoms/signs for bladder carcinoma (in situ)

A
  • Presence of risk factors
  • Haematuria (gross of microscopic) – present in over 80% of pts
  • Dysuria – typical of carcinoma in situ, but also seen in high-grade urothelial carcinoma
  • Urinary frequency – rearely the sole symptom of bladder cancer but does occur
100
Q

DDx for Bladder carcinoma (in situ)

A
  • BPH
  • Haemorrhagic cystitis
  • Prostatitis
  • UTI
  • Nephrolithiasis
  • Renal cell carcinoma
  • Renal urothelial carcinoma
101
Q

Investigation for Bladder carcinoma (in situ)

A
  • 1st LINE:
  • URINALYSIS: haematuria is typical but may be absent, pyuria may also be seen, resulting in confusion with urinary infection
  • RENAL AND BLADDER USS: bladder tumours and/or upper tract obstruction may be seen
102
Q

Management for Bladder carcinoma (in situ)

A
  • 1st LINE:
  • TRANSURETHRAL RESECTION
  • 2nd LINE:
  • RADICAL/PARTIAL CYSTECTOMY
103
Q

Prognosis and complications for Bladder carcinoma (IN SITU)

A

prognosis is dependant on cause

complications - prostatic urothelial carcinoma, upper tract TCC, hydrophrosis, urinary retention

104
Q

Renal Cell Carcinoma definition

A

Renal malignancy arising from the renal parenchyma/ Corte and accounts for about 85% of renal cancers

105
Q

how common is renal cell carcinoma

A

• Accounts for 85% of renal cancers

106
Q

causes of renal cell carcinoma

A
  • Smoling is the most-well established risk factor for RCC

* Obesity and hypertension are als known risk factors

107
Q

risk factors for renal cell carcinoma

A
  • Smoking
  • Male
  • Age 55-84 years
  • Residence in developed
  • Black/American-Indian ethnicity
  • Obesity
  • Hypertension
108
Q

symptoms/signs for renal cell carcinoma

A
  • Presence of risk factors
  • Asymptomatic (incidental finding)
  • Haematuria
  • Flank pain
  • Palpable abdominal mass
109
Q

DDx for renal cell carcinoma

A
  • Benign renal cyst
  • Ureteric cancer
  • Bladder cancer
  • Upper urinary tract urotherlial tumour
  • Angiomyolipoma
  • Oncocyoma
  • Secondary metastases
110
Q

Investigations for Renal Cell Carcinoma

A
  • 1ST LINE:
  • FBC: paraneoplastic syndrome: reduced Hb or elevated RBC
  • LDH: advanced RCC: >1.5 times the upper limit of normal
  • CORRECTED CALCIUM: advanced rcc: >2.5MMOL/l
  • LFTs: metastatic disease/paraneoplastic syndrome: abnormal
  • COAGULATION PROFILE: paraneoplastic syndrome: elevated PT
  • URINALYSIS: haematuria and/or proteinuria
  • ABDOMINAL/PELVIC ULTRASOUND: abnormal renal cyst/mass, lymphadenopathy, and/or other visceral metastatic lesions
  • CT ABDOOMEN/PELVIS: renal mass, regional lymphadenopathy and/or visceral/bone metastases
111
Q

management for Renal Cell Carcinoma

A

• 1st LINE:
• SURGERY: surgical resection
- ADJUNCT: targeted molecular therapy (sorafenib, sunitinib  target vascular endothelial growth factor receptors and inhibit them

112
Q

prognosis and complications for renal cell carcinoma

A

variable prognosis

complications - anaemia, hypercalcaemia, erythrocytosis

113
Q

definition of urinary tract stones

A
  • Nephrolithiasis refers to the presence of crystalline stones within the urinary system
  • Such renal stones are composed of varying amounts of crystalloid and organic matrix
  • Ureteric stones almost always originate in the kidney but then pass down into the ureter
114
Q

how common is urinary tract stones

A

• Common condition with a 7% to 10% lifetime risk for women and men

115
Q

causes of urinary tract stones

A
  • Renal colic from nephrolithiasis is secondary to obstruction of the collecting system by the stone
  • The stretching of the collecting system or ureter is due to an increase in intraluminal pressure
  • This causes nerve enndings to stretch and therefore the sensation of renal colic
  • Pain from urinary calculi can also be due to local inflammatory mediators, oedema, hyperperistalsis and mucosal irritation
116
Q

risk factors for urinary tract stones

A
  • High protein intake
  • High salt intake
  • White
  • Male
  • Dehydration
  • Obesity
  • Crystalluria
117
Q

symptoms/ signs of urinary tract stones

A
  • Acute, severe flank pain
  • Nausea and vomiting
  • Previous episodes
  • Haematuria
  • Testicular pain
  • Urinary frequency/urgency
118
Q

DDx for urinary tract stones

A
  • Acute appendicitis
  • Ectopic pregnancy
  • Ovarian cyst
  • Diverticular disease
  • Bowel obstruction
  • Testicular torsion
119
Q

investigations for urinary tract stones

A

• 1ST LINE:

  • URINALYSIS: may be normal, dipstick pos for leukocytes, nitrates, blood, microscopic analysis pos for WBCs, RBCs or bacteria
  • FBC: raised WBC may suggest infection
  • SERUM ELECTROLYTES, UREA AND CREATININE: variable
  • URINE PREGNANCY TEST: negative
  • NON-CONTRAST HELICAL CT SCAN: calcification seen in renal collecting system or ureter, hydronephrosis, perinephric stranding (indicative of inflammation or infection)
  • STONE ANALYSIS: stone composition
120
Q

management of urinary tract stones

A

• 1st LINE:

- HYDRATION, PAIN CONTROL AND ANTI-EMETICS: crystalloids, ketorolac and/or morphine sulfate, ondansetron

121
Q

prognosis and complications for urinary tract stones

A

prognosis - lifelong disease process

complications - PCNL bleeding, pneumothorax, ureteric stricture, visceral organ injury

Core Conditions (13 decks)

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