Renal and Urology Flashcards

1
Q

Define acute kidney injury

A

Acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output. Can range from mild renal impairment to severe renal failure.

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2
Q

Explain the aetiology/risk factors of acute kidney injury

A

Pre-renal - reduced renal perfusion due to:
hypovolaemia (haemorrhage, severe vomiting)
Hypotension (sepsis, shock, anaphylaxis)
hypo-perfusion (renal stenosis, NSAIDs, ACEi, ARBs)
heart failure
third spacing of fluid (severe pancreatitis)
Renal - problems can occur in the tubules, glomerulus or interstitium:
acute tubular necrosis
glomerulonephritis
interstitial nephritis
Post renal - due to obstruction of urinary outflow tract: retroperitoneal fibrosis,
tumour
BPH
ascending urinary infection (pyelonephritis)
urinary retention

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3
Q

Summarise the epidemiology of acute kidney injury

A

Incidences of hospitalised patients range from 13-22%
Acute tubular necrosis (renal cause of AKI) accounts for 45-75% of AKI
ATN in ICU patients is cause by sepsis (pre-renal cause of AKI) in 35-55% of cases

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4
Q

Recognise the presenting symptoms of acute kidney

A
Presence of risk factors (advanced age, underlying kidney disease, malignant HTN, T2DM and exposure to nephrotoxins)
oligourea (reduced urine output)
Nausea and vomiting 
Dizziness
confusion 
Orthopnoea 
Paroxysmal nocturnal dyspnoea
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5
Q

Recognise the signs of acute kidney injury on a physical examination

A

Hypertension
Dehydration leading to postural hypotension
Distended bladder
Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
Tachycardia
Orthostatic hypotension

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6
Q

Identify appropriate investigations for acute kidney injury and interpret the results

A

Basic metabolic profile (incl. urea and creatinine): elevated serum creatinine (this may be the only sign of a decline in renal function)
high serum potassium
metabolic acidosis

Ratio of serum urea to creatinine:
20:1 or higher supports pre-renal azotaemia

Urinalysis (MSU or clean catch specimen):
RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase (in cases of infection)

Urine culture:
bacterial or fungal growth may occur

FBC:
anaemia, leukocytosis, thrombocytopenia

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7
Q

Generate a management plan for acute kidney injury (pre-renal)

A
  1. volume expansion and/or RBC transfusion

with severe hypotension
2. vasopressor: dopamine 1mg/kg/min IV OR adrenaline 1mg/min IV

with fluid overload
3. diuretic: furosemide 20-40mg IV

with uraemia, metabolic acidosis, hyperkalaemia
4. renal replacement therapy

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8
Q

Generate a management plan for acute kidney injury (renal)

A
  1. treat underlying condition

with volume overload
2. diuretic: furosemide 20-40mg IV

with pre-existing pre-renal azotaemia
3. volume expansion: normal saline

  1. renal replacement therapy
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9
Q

Generate a management plan for acute kidney injury (post-renal)

A
  1. bladder catheterisation
  2. relief of obstruction above bladder neck

with volume overload
3. diuretic: furosemide 20-40mg IV

  1. renal replacement therapy
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10
Q

Identify the possible complications of acute kidney injury and its management

A
AKI:
hyperphosphataemia
uraemia
volume overload (pulmonary oedema, peripheral oedema)
hyperkalaemia
metabolic acidosis
end-stage renal disease
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11
Q

Summarise the prognosis for patients with acute kidney injury

A
In-hospital mortality rates associated with AKI vary from 6% to 80%
Indicators of poor prognosis: 
Age  
Multiple organ failure  
Oliguria 
Hypotension  
CKD  
Patients who develop AKI are at increased risk of developing CKD
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12
Q

Define benign prostatic hyperplasia

A

slowly progressive nodular hyperplasia of the periurethral (transitional) zone of the prostate gland. This leads to prostatic enlargement and bladder dysfunction

It is the most frequent cause of LUTS in adult males

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13
Q

Explain the aetiology / risk factors of benign prostatic hyperplasia

A

Aetiology
age-related hormonal problems creating androgen/oestrogen imbalances.
Increases in prostatic stem cells.
Progression to pathological BPH to clinical BPH (when symptoms present) may require additional factors such as prostatitis, vascular effects and changes to the glandular corpuscle.
Risk factors
Age above 50 years and a positive family history
reduced risk with soya/vegetable based diets and negative association with cirrhosis

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14
Q

Summarise the epidemiology of benign prostatic hyperplasia

A

COMMON

70% of men > 70 yrs have histological BPH (50% of them will experience symptoms)

More common in the west than the east
More common in Afro-Caribbeans

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15
Q

Recognise the presenting symptoms of benign prostatic hyperplasia

A

Storage/Irritative symptoms:
frequency, urgency and nocturia

Voiding/Obstructive symptoms:
weak stream, hesitancy, intermittency, straining, incomplete emptying and post-void dribbling

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16
Q

Recognise the presenting symptoms of benign prostatic hyperplasia. Pneumonic for obstructive and irritative symptoms?

A
FUND HIPS
Frequency 
Urgency 
Nocturia 
Dysuria 

Hesitancy
Incomplete voiding
Poor stream
Straining

17
Q

Recognise the signs of benign prostatic hyperplasia on physical examination

A

Fever with dysuria = perhaps complicated UTI

DRE - the prostate is usually smoothly enlarged with a palpable midline groove

NOTE: there is poor correlation between the size and the severity of the symptoms

Signs of Acute Retention
Suprapubic pain
Distended, palpable bladder

Signs of Chronic Retention
A large distended painless bladder (volume > 1 L)
Signs of renal failure

18
Q

Identify appropriate investigations for benign prostatic hyperplasia and interpret the results

A
  1. urinalysis
    pyuria (pus in the urine) suggests a complicated UTI
  2. PSA
    elevation greater than age guideline
  3. International prostate symptom score
    Self-administered patient questionnaire containing 7 questions covering both irritative and obstructive voiding symptoms.
    moderate score: 8-19
    severe score: 20-35
    There’s a further QOL question scored from 0-6
  4. volume charting
    diary of frequency and volume of voiding

May also consider transrectal US (TRUS) or CT abdo/pelvis (hydronephrosis, masses and urolithiasis) or flexible cystoscopy (mass, stone, stricture)

19
Q

Generate a management plan for benign prostatic hyperplasia

A

non-bothersome symptoms:
1. watchful waiting
2. behavioural management programme
limiting fluids, bladder training focused on timed and complete voiding

Bothersome symptoms with no indications of surgery

  1. alpha blocker (terazosin 1mg oral daily can increase dose to 20mg/day in 2 doses) + behavioural management programme
  2. 5 alpha reductase inhibitor (finasteride 5mg/day oral) + behavioural management programme
  3. Phosphodiesterase 5 (PDE-5) inhibitor (sildenafil 25-100mg/day oral) + behavioural management programme
  4. anticholinergic agent (tolterodine 2mg twice daily oral) + behavioural management programme
  5. 1 +2/3

Bothersome symptoms with indications for surgery

  1. transurethral microtherapy (TUMT), transurethral needle ablation (TUNA), and prostatic urethral lift (PUL).
  2. Trans urethral resection of the prostate (TURP)
  3. open prostatectomy
20
Q

Identify the possible complications of benign prostatic hyperplasia

A
recurrent UTIs
acute or chronic urinary retention 
urinary stasis 
bladder diverticula
stone development 
obstructive renal faillure 
post-obstructive diuresis
21
Q

Identify the possible complications of BPH’s management (TURP)

A

Complications of TURP

Retrograde ejaculation (you ejaculate up into your bladder because the internal urinary sphincter is relaxed)

Haemorrhage

Incontinence

TURP syndrome

DEFINITION: seizures or cardiovascular collapse caused by hypervolaemia and hyponatraemia due to absorption of glycine irrigation fluid

Urinary infection

Erectile dysfunction

Urethral stricture

22
Q

Summarise the prognosis for patients with benign prostatic hyperplasia

A

Mild symptoms are usually well controlled medically

Most patients get significant relief from surgery