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!Final Year > Renal and Urology > Flashcards

Renal and Urology Flashcards

1
Q

What is acute kidney injury (AKI)?

A

An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output

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2
Q

What is the aetiology of acute kidney injury (AKI)?

A

Pre-renal, renal and post renal
AKI may be due to various insults such as:
- impaired kidney perfusion
- exposure to nephrotoxins
- outflow obstruction
- intrinsic kidney disease

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3
Q

What are the risk factors of acute kidney injury (AKI)?

A

Advanced age
Underlying kidney disease
DM
Sepsis: may result in ATN, pre-kidney AKI from hypotension
Nephrotoxins e.g. aminoglycosides, NSAIDs, vancomycin

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4
Q

What are the pre-renal causes of an AKI?

A

Reduced renal perfusion:
1. Shock (hypovolaemic, septic, cardiogenic)
2. Hepatorenal syndrome (liver failure)

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5
Q

What are the renal causes of an AKI?

A
  1. Acute tubular necrosis: ischaemia, drugs and toxins
  2. Acute glomerulonephritis
  3. Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides
  4. Vessel obstruction:
    - Renal artery/vein thrombosis
    - Cholesterol emboli
    - Vasculitis
  5. Other causes: myeloma, haemolysis, nephropathy
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6
Q

What are the post renal causes of an AKI?

A
  1. Stone
  2. Tumour (pelvic, prostate, bladder)
  3. Blood clots
  4. Retroperitoneal fibrosis
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7
Q

What are the presenting symptoms of AKI?

A

Usually asymptomatic
Lower urinary tract symptoms:
- Urgency
- Frequency
- Hesitancy
Low urine output (oliguria)
Malaise
Anorexia
Nausea and vomiting
Pruritus (itching)
Drowsiness
Convulsions, coma (caused by uraemia)

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8
Q

What are the signs of acute kidney injury (AKI) on physical examination?

A
  1. Reduced urine output
  2. Pulmonary and peripheral oedema
  3. Arrhythmias (secondary to changes in potassium and acid-base balance)
  4. Features of uraemia (e.g. pericarditis or encephalopathy)
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9
Q

What are the appropriate investigations for AKI?

A
  1. U&Es: serum creatinine (rise of 26 micro mol/L in 48 hours or >50% in 7 days), potassium, sodium and urea
  2. Urinalysis: all suspected AKI patients, cellular casts (glomerulonephritis)
  3. Renal ultrasound: if no identifiable cause of deterioration or risk of obstruction
  4. ECG: changes associated with hyperkalaemia (tented T waves) and CXR
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10
Q

How do you assess a patient’s fluid status in an AKI?

A

Pulse rate
Lying and standing BP
JVP
Skin turgor
Chest auscultation
Peripheral oedema
Central venous pressure
Fluid and weight charts
ECG monitoring (hyperkalaemia)

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11
Q

What is the management for a patient with an AKI?

A

Largely supportive
1.Assess hydration and fluid balance: hypovolaemic or hypervolaemic
2. Review patient’s medications
3. Assess hyperkalaemia

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12
Q

How do you manage an hypovolaemic patient with an AKI?

A
  1. Fluid resuscitation
  2. Review medications and stop nephrotoxins
  3. Identify and treat underlying cause
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13
Q

How do you manage an hypervolaemic patient with an AKI?

A
  1. :Loop diuretic (NOT ROUTINE -under specialist supervision) and sodium restriction
  2. Identify and treat underlying cause
  3. Consider: renal replacement therapy
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14
Q

Which medications should be stopped in patients with an AKI?

A
  1. NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
  2. Aminoglycosides
  3. ACE inhibitors
  4. Angiotensin II receptor antagonists
  5. Diuretics
    May have to stop: Metformin, lithium and digoxin
    ‘stop the DAMN drugs’: diuretics, ACEi, metformin and NSAIDs
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15
Q

What are some of the complications of an AKI and what would you switch to?

A

Hyperkalaemia
Pulmonary oedema
Acidosis or uraemia (e.g. pericarditis, encephalopathy)
Switch to renal replacement therapy e.g. haemodialysis

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16
Q

What is the management of hyperkalaemia?

A

Medical emergency!
1. Cardio protection: Intravenous calcium gluconate
2. Short term shift in potassium from extracellular to intracellular: Combined insulin/dextrose infusion and nebulised salbutamol
3. Removal of potassium from body: Calcium resonium (orally or enema), loop diuretics, finally dialysis

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17
Q

What is the treatment for acute pulmonary oedema?

A

P- positioning (sit up)
O- oxygen
D- diuretic (furosemide) and fluid restriction
M- (dia)morphine
A- anti-emetics
N- nitrates (GTN infusion if SBP >110, or 2 puffs GTN spray if SBP >90)

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18
Q

What is amyloidosis?

A

A (heterogenous) group of diseases characterised by extracellular deposition of insoluble amyloid fibrils

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19
Q

What are the two types of amyloidosis?

A
  1. AL amyloid = primary, immunoglobulin light chain amyloidosis, associated with Myeloma
  2. AA amyloid = secondary, non-familial and familial
    Non- familial AA = Inflammatory polyarthropathies account for 60% of cases, then chronic infections, IBD
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20
Q

What are the risk factors for amyloidosis?

A

PMH of inflammatory conditions (AA)
Chronic infections (AA)
Positive FH

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21
Q

What are the renal features of primary amyloidosis (AL)?

A

Glomerular lesions—proteinuria and nephrotic syndrome

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22
Q

What are the renal features of secondary non-familial amyloidosis (AA)?

A

PMH of chronic inflammation (e.g. RA/ IBD) or chronic infection (e.g. TB)
May present with proteinuria, nephrotic syndrome, or hepatosplenomegaly

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23
Q

What are the appropriate investigations for amyloidosis?

A

Diagnosis made with biopsy of affected tissue: positive Congo Red staining with apple-green birefringence under polarized light microscopy
The rectum or subcutaneous fat are relatively non-invasive sites for biopsy and are positive in 80%

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24
Q

What is the management of amyloidosis?

A

AL: optimize nutrition; PO melphalan + prednisolone extends survival
High-dose IV melphalan with autologous stem cell transplantation may be better
AA: manage the underlying condition optimally

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25
Q

What is the prognosis of patients with amyloidosis?

A

Median survival is 1–2 years
Patients with myeloma and amyloidosis have a shorter survival than those with myeloma alone

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26
Q

What is benign prostatic hyperplasia?

A

A common condition seen in older men that presents with lower urinary tract symptoms

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27
Q

What are the risk factors for benign prostatic hyperplasia?

A
  1. Age (50% of >50s, 80% of >80s)
  2. Ethnicity: Black> White> Asian
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28
Q

How can the symptoms of benign prostatic hyperplasia be categorised?

A

Lower urinary tract symptoms:
1. Voiding (obstructive) symptoms
2. Storage symptoms (irritative)
3. Post-micturition
4. Complications

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29
Q

What are the voiding symptoms seen in benign prostatic hyperplasia?

A
  1. Weak or intermittent urinary flow
  2. Straining
  3. Hesitancy
  4. Terminal dribbling
  5. Incomplete emptying
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30
Q

What are the storage symptoms of benign prostatic hyperplasia?

A
  1. Urinary urgency
  2. Increased frequency
  3. Urinary incontinence
  4. Nocturia
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31
Q

What is the post-micturition symptom of benign prostatic hyperplasia?

A

Dribbling

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32
Q

What are the complications of benign prostatic hyperplasia?

A
  1. Urinary tract infection
  2. Urinary retention
  3. Obstructive uropathy
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33
Q

How is benign prostatic hyperplasia investigated?

A
  1. Dipstick urine
  2. Bloods:
    a. U&Es if chronic retention is suspected
    b. PSA: if there are obstructive symptoms, exclude prostate cancer
  3. Urinary frequency-volume chart: for at least 3 days
  4. International prostate symptom score
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34
Q

What is the International Prostate Symptom Score in benign prostatic hyperplasia?

A

A tool for classifying the severity of lower urinary tract symptoms and assessing the impact on quality of life:
1. Score 0-7 = mildly symptomatic
2. Score 8-19 = moderately symptomatic
3. Score 20-35 = severely symptomatic

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35
Q

What are the management options for benign prostatic hyperplasia?

A
  1. Watchful waiting
  2. Alpha-1 antagonists e.g. tamsulosin
  3. 5-alpha reductase inhibitors e.g. finasteride
    (2 and 3 are often used in combination therapy)
  4. Antimuscarinic can be tried if an alpha blocker alone does not improve voiding or storage symptoms e.g. tolterodine
  5. Surgery = transurethral resection of prostate (TURP)
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36
Q

What is the mechanism of action of alpha-1 antagonists in benign prostatic hyperplasia?

A
  1. Decrease smooth muscle tone of the prostate and bladder
  2. Used as first line (improve symptoms in 70%) e.g. tamsulosin
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37
Q

What are some of the side effects of alpha-1 antagonists in benign prostatic hyperplasia?

A
  1. Dizziness
  2. Postural hypotension
  3. Dry mouth
  4. Depression
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38
Q

What are 5 alpha reductase inhibitors in benign prostatic hyperplasia?

A
  1. Block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH
  2. Indicated if the patient has a significantly enlarged prostate and is considered to be at high risk of progression
  3. E.g. finasteride
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39
Q

What is the benefit of 5 alpha reductase inhibitors over alpha-1 antagonists for benign prostatic hyperplasia?

A
  1. Causes a reduction in prostate volume therefore may slow disease progression
  2. May also decrease PSA concentrations by up to 50%
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40
Q

What are some of the side effects of 5 alpha reductase inhibitors in benign prostatic hyperplasia?

A
  1. Erectile dysfunction
  2. Reduced libido
  3. Ejaculation problems
  4. Gynaecomastia
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41
Q

What are some of the lifestyle measures in the management of benign prostatic hyperplasia?

A
  1. Avoid caffeine and alcohol (to reduce urgency/nocturia)
  2. Relax when voiding and void twice in a row to aid emptying
  3. Control urgency by practising distraction methods (e.g. breathing exercises)
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42
Q

What is the best way to differentiate between AKI and chronic kidney disease?

A
  1. Most patients with CKD will have bilateral small kidneys*
  2. Hypocalcaemia due to lack of vitamin D
    *Some exceptions:
    a. Autosomal dominant polycystic kidney disease
    b. Diabetic nephropathy (early stages)
    c. Amyloidosis
    d. HIV associated nephropathy
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43
Q

What is chronic kidney disease?

A

Defined by either:
1. A pathological abnormality of the kidney, such as haematuria and/or proteinuria or
2. A reduction in the glomerular filtration rate to <60 mL/min/1.73 m² for ≥3 months’ duration

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44
Q

What are the common causes of chronic kidney disease?

A
  1. Diabetic nephropathy
  2. Chronic glomerulonephritis
  3. Chronic pyelonephritis
  4. Hypertension
  5. Adult polycystic kidney disease
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45
Q

What are the most common causes of chronic kidney disease?

A
  1. Diabetes
  2. Hypertension
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46
Q

What are the features of chronic kidney disease?

A
  1. Usually asymptomatic- diagnosed following abnormal U&Es
  2. Some patients with undetected late-stage disease may become symptomatic
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47
Q

What are the late-stage disease features of chronic kidney disease?

A
  1. Oedema e.g. ankle swelling, weight gain
  2. Polyuria
  3. Lethargy
  4. Pruritus (secondary to uraemia)
  5. Anorexia, weight loss
  6. Insomnia
  7. Nausea and vomiting
  8. Hypertension
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48
Q

What are the investigations for chronic kidney disease?

A
  1. U&Es
  2. Serum creatinine to calculate the estimated glomerular filtration rate (eGFR)
  3. Urinalysis: presence of haematuria, proteinuria, microalbuminuria
  4. Renal ultrasound: bilaterally small kidneys, presence of obstruction
  5. Consider imaging for osteomalacia, hyperparathyroidism
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49
Q

What is a common complication of chronic kidney disease?

A

Secondary hyperparathyroidism:
1. Parathyroid gland hyperplasia as a result of low calcium
2. Biochemical findings: high PTH, low Calcium, high phosphate, low Vit D

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50
Q

What is the best diagnostic marker for chronic kidney disease?

A

eGFR

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51
Q

What are the different stages of chronic kidney disease?

A

Stage 1: > 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests are normal, there is no CKD)
Stage 2: 60-90 ml/min with some sign of kidney damage (if kidney tests are normal, there is no CKD)
Stage 3a: 45-59 ml/min
Stage 3b: 30-44 ml/min
Stage 4: 15-29 ml/min
Stage 5: < 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

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52
Q

What factors might affect the eGFR for chronic kidney disease?

A
  1. Pregnancy
  2. Muscle mass e.g. amputees, body builders
  3. Eating red meat 12 hours prior to sample taken
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53
Q

What are the variables used to calculate the eGFR?

A
  1. Serum creatinine
  2. Age
  3. Gender
  4. Ethnicity
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54
Q

What are the different areas of management for patients with chronic kidney disease?

A
  1. Mineral bone disease
  2. Bone disease
  3. Anaemia
  4. Hypertension
  5. Proteinuria
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55
Q

What is proteinuria?

A
  1. Presence of protein in the urine
  2. Important marker of CKD, especially in diabetic nephropathy
  3. Used as part of the albumin: creatinine ratio
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56
Q

How in an albumin: creatinine ratio (ACR) sample collected?

A
  1. ‘spot’ sample
  2. First-pass morning urine
  3. If the initial ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample
  4. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested
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57
Q

What is clinically important proteinuria?

A

Confirmed ACR of 3 mg/mmol or more

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58
Q

What ACR result is recommended for a referral to a nephrologist?

A
  1. Urinary ACR of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
  2. Urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a UTI
  3. Consider if: ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or CVD
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59
Q

What is the management of proteinuria in CKD?

A
  1. ACE inhibitors (or angiotensin II receptor blockers)
  2. Should be first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
  3. If ACR > 70 mg/mmol they are indicated regardless of the patient’s BP
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60
Q

What is the management of hypertension in CKD?

A
  1. Often will require more than two drugs
  2. First line = ACEi (particularly in patients with diabetes due to proteinuria)
  3. Furosemide (loop diuretic): useful when eGFR falls below 45ml/min, added benefit of lowering serum potassium
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61
Q

What is an important consideration of using ACEi in CKD?

A

Tend to reduce the filtration pressure: so there may be a small fall in the GFR or a rise in creatinine (up to 30% is acceptable)
*If it rises more than this, monitor and exclude other causes e.g. AKI

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62
Q

What is an important consideration of furosemide in the treatment of CKD?

A

If the patient becomes at risk of dehydration (e.g. gastroenteritis) then consideration should be given to temporarily stop the drug

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63
Q

Why do patients with CKD develop anaemia?

A
  1. Most important reason is reduced erythropoietin levels
  2. Normochromic normocytic anaemia
  3. Becomes apparent when the GFR < 35 ml/min
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64
Q

What are patients with anaemia in CKD at risk of developing?

A

Left ventricular hypertrophy

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65
Q

What are the causes of anaemia in chronic kidney disease?

A
  1. Reduced erythropoietin levels
  2. Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  3. Reduced absorprtion of iron
  4. Anorexia/ nausea due to uraemia
  5. Reduced red cell survival (especially if on haemodialysis)
  6. Blood loss due to capillary fragility and poor platelet function
  7. Stress ulceration = chronic blood loss
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66
Q

What is the management of anaemia in CKD?

A
  1. Aim for a target Hb of 10-12g/dl
  2. Determination and optimisation of iron status should be carrie out before giving erythropoiesis-stimulating agents (ESA) e.g. erythropoietin and darbepoetin
  3. Oral iron should be given to patients not on ESA or haemodialysis
    *ESA should be given to patients who will likely benefit in terms of QoL and physical function
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67
Q

Why do patients with chronic kidney disease develop mineral bone disease?

A
  1. 1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low Vit D levels
  2. Kidneys normally excrete phosphate → CKD leads to high phosphate
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68
Q

What is mineral bone disease in CKD patients?

A
  1. High phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
  2. Low calcium: due to lack of vitamin D, high phosphate
  3. Secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
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69
Q

What is the management of mineral bone disease in CKD patients?

A
  1. First-line: reduce dietary intake of phosphate
  2. Phosphate binders
  3. Vitamin D: alfacalcidol, calcitriol
  4. Parathyroidectomy may be needed in some cases
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70
Q

What are phosphate binders in the management of mineral bone disease in CKD?

A
  1. Bind to dietary phosphate and prevents its absorption
  2. Other benefits include reducing uric acid levels and improving the lipid profiles
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71
Q

What types of bone disease can develop in patients with CKD as a result of low calcium?

A
  1. Osteitis fibrosa cystica (hyperparathyroid bone disease)
  2. Adynamic (reduction in cellular activity: both osteoblasts and calsts, from over treatment of Vit D)
  3. Osteomalacia (from low Vit D)
  4. Osteosclerosis
  5. Osteoporosis
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72
Q

Which drugs should you avoid in renal failure?

A
  1. Antibiotics such as tetracyclines, nitrofurantoin
  2. NSAIDs
  3. Lithium
  4. Metformin
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73
Q

Which drugs are likely to accumulate in CKD and therefore require dose adjustment?

A
  1. Most Abx including penicillins, cephalosporins
  2. Digoxin
  3. Atenolol
  4. Methotrexate
  5. Sulphonylureas
  6. Furosemide
  7. Opioids
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74
Q

Which drugs are relativelt safe and can sometimes be given at normal doses in CKD?

A
  1. Antibiotics such as erythromycin, rifampicin
  2. Diazepam
  3. Warfarin
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75
Q

What is circumcision?

A

A religious or cultural procedure in which the foreskin is removed just behind the head of the penis

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76
Q

What are the medical indications for circumcision?

A
  1. Phimosis: inability to retract the foreskin
  2. Recurrent balanitis: skin irritation of the head of the penis
  3. Paraphimosis (MEDICAL EMERGENCY) : if the foreskin is very tight it can get stuck and cannot go back to it’s original position
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77
Q

What is important to exclude prior to circumcision?

A

Hypospadias: where the opening of the urethra is not located at the top of the penis (birth defect)

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78
Q

Are there any medical benefits of circumcision?

A

Remains controversial, some evidence suggests:
1. Reduces risk of penile cancer
2. Reduces risk of UTI
3. Reduces risk of acquiring STIs including HIV

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79
Q

What is renal failure?

A

When the GFR is less than 15ml/min

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80
Q

What is the epidemiology of CKD and renal failure?

A
  1. 1in 8 people have CKD
  2. 10% of those with CKD will go on to develop renal failure
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81
Q

What are the different types of renal replacement therapy?

A
  1. Haemodialysis
  2. Peritoneal dialysis
  3. Renal transplant
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82
Q

How is the decision about the type of renal transplant therapy made?

A
  1. Made jointly by the patient and the healthcare team
  2. Looks at predicted quality of life and life expectancy
  3. Patient preference
  4. Any co-existing medical conditions
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83
Q

What is Haemodialysis?

A
  1. Most common form of renal replacement therapy
  2. Involves regular filtration of the blood through a dialysis machine
  3. Most patients need dialysis 3 times per week, each session lasting 3-5 hours
  4. Some patients may be trained to perform home haemodialysis
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84
Q

What surgery is required before a patient can be started on haemodialysis?

A
  1. Creation of an arteriovenous fistula: site for haemodialysis
  2. Must be carried out at least 8 weeks before the start of dialysis
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85
Q

What are some of the complications of haemodialysis?

A
  1. Site infection
  2. Endocarditis
  3. Stenosis at site
  4. Hypotension
  5. Cardiac arrhythmia
  6. Air embolus
  7. Anaphylactic reaction to sterilising agents
  8. Disequilibration syndrome
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86
Q

What is Disequilibration syndrome?

A

Rare but serious complication of haemodialysis:
1. Neurological symptoms: disturbed consciousness, convulsions, coma
2. Nausea and vomiting
3. Tranisent and self-limiting
4. Can be fatal

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87
Q

What is peritoneal dialysis?

A
  1. Filtration occurs within the patient’s abdomen
  2. Dialysis solution is injected into the abdominal cavity through a permanent catheter
  3. The high dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum
  4. After several hours of ‘dwell’ time: the dialysis solution is drained and exchanged with a new dialysis solution
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88
Q

What are the two types of peritoneal dialysis?

A
  1. Continuous ambulatory peritoneal dialysis: standard therapy, each exchange lasting 30-40 minutes and each dwell time lasting 4-8 hours, the patient may go about their normal activities with the dialysis solution inside their abdomen
  2. Automated peritoneal dialysis: a dialysis machine fills and drains the abdomen while the patient is sleeping, performing 3-5 exchanges over 8-10 hours each night
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89
Q

What are the complications of peritoneal dialysis?

A
  1. Peritonitis
  2. Sclerosing peritonitis
  3. Catheter infection/ blockage
  4. Constipation
  5. Fluid retention
  6. Hyperglycaemia
  7. Hernias
  8. Back pain
  9. Malnutrition
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90
Q

What is renal transplantation?

A
  1. Involves the receipt of a kidney from either a live or deceased donor
  2. The average wait for a kidney in the UK is 3 years, though patients may also receive kidneys donated by cross-matched friends or family
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91
Q

What is the procedure of a renal transplant?

A
  1. The donor kidney is transplanted into the groin, with the renal vessels connected to the external iliac vessels
  2. The failing kidneys are not removed
  3. Following transplantation, the patient must take life-long immunosuppressants to prevent rejection of the new kidney
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92
Q

What is the average lifespan of a donor kidney?

A
  1. From deceased donors: 10-12 years
  2. From living donors: 12-15 years
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93
Q

What are the complications of renal transplant?

A
  1. DVT/ PE
  2. Opportunistic infections
  3. Malignancies: lymphoma, skin cancer
  4. Bone marrow suppression
  5. Recurrence of original disease
  6. Urinary tract obstruction
  7. CVD
  8. Graft rejection
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94
Q

What is the life expectancy of a patient with renal failure that does not receive renal replacement therapy?

A

6 months

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95
Q

What are some of the symptoms suggestive of a patient not being adequately managed with renal failure?

A
  1. Breathlessness
  2. Fatigue
  3. Insomnia
  4. Pruritus
  5. Poor appetite/ weight loss or gain
  6. Swelling
  7. Abdominal/ muscle cramps
  8. Nausea
  9. Headaches
  10. Cognitive impairment
  11. Anxiety/ depression
  12. Sexual dysfunction
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96
Q

What is involved in Continuous Ambulatory Peritoneal Dialysis?

A
  1. Dialysis solution is injected into the abdominal cavity through a permanent catheter
  2. The high dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum
  3. After several hours of ‘dwell’ time: the dialysis solution is drained with all the waste products and exchanged with a new dialysis solution
  4. Involves x4 2L exchanges a day
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97
Q

How is peritonitis managed as a complication of Continuous Ambulatory Peritoneal Dialysis?

A
  1. Antibiotics should cover both gram positive and negative organisms
  2. Coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause
  3. BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth
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98
Q

What is Epididymo-orchitis?

A

An infection of the epididymis +/- testes resulting in pain and swelling

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99
Q

What are the common causes of epididymo-orchitis?

A

Local spread of infections:
1. Genital tract e.g. Chlamydia trachomatis and Neisseria gonorrhoeae (younger patients)
2. Bladder e.g. E.coli (older patients/ low risk sexual Hx)

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100
Q

What are the features of epididymo-orchitis?

A
  1. Unilateral testicular pain and swelling
  2. Urethral discharge (but urethritis is often asymptomatic)
  3. Important to consider testicular torsion if < 20 years, severe pain and an acute onset
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101
Q

What is the most important differential diagnosis in epididymo-orchitis?

A

Testicular torsion!
1. Because the patient presents with unilateral testicular pain and swelling
2. Needs to be excluded to prevent ischaemia of the testicle

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102
Q

What is the most common cause of isolated orchitis?

A
  1. Rare
  2. Mumps infection (can be caused by other viral infections)
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103
Q

What are the signs of epididymo-orchitis on examination?

A
  1. Diffuse enlargement of the testis
  2. Erythema of the scrotal skin
  3. Swelling for < 6 weeks: otherwise indicates chronic inflammation
  4. Swelling may be tender and eased by elevating testis
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104
Q

What are the investigations for epididymo-orchitis?

A

Typically guided by age of the patient:
1. Younger adults: assess for STIs e.g. STI screen, urine dip and MCS, urethral swab
2. Older adults with low-risk sexual Hx: mid-stream urine (MSU) for MCS, urine dip

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105
Q

What is the management of epididymo-orchitis?

A
  1. If an STI is most likely cause: urgent referral to STI clinic
  2. If enteric cause is most likely: send MSU and start empiric antibiotics such as quinolone for 2 weeks
  3. Also analgesia, scrotal support, drainage for any abscess
  4. Consider further tests if needed to exclude structural abnormalities
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106
Q

What is the management of epididymo-orchitis if the cause is an STI but the organism is unknown?

A

Ceftriaxone 500mg intramuscularly single dose plus doxycycline 100mg by mouth twice daily for 10-14 days

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107
Q

What are the possible complications for epididymo-orchitis?

A
  1. Usually if it is more chronic (enteric organisms > STI)
  2. Chronic pain
  3. Reactive hydrocele
  4. Abscess formation
  5. Testicular torsion (if not excluded)
  6. Reduced fertility (rare from testicular atrophy)
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108
Q

What is glomerulonephritis?

A

Group of diseases that are generally classified by inflammatory changes in the glomerular capillaries and glomerular basement membrane (GBM)

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109
Q

What are the four main types of glomerulonephritis?

A
  1. Membranous glomerulonephritis
  2. Post-streptococcal glomerulonephritis
  3. Rapidly progressive glomerulonephritis
  4. Membranoproliferative glomerulonephritis
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110
Q

What is membranous glomerulonephritis?

A
  1. The commonest type of glomerulonephritis
  2. Third most common cause of end-stage renal failure
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111
Q

What is the usual presentation of membranous glomerulonephritis?

A

Nephrotic syndrome or proteinuria

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112
Q

What are the causes of membranous glomerulonephritis?

A
  1. Idiopathic: due to anti-phospholipase A2 antibodies
  2. Infections: Hep B, malaria, syphilis
  3. Malignancy: prostate, lung, lymphoma
  4. Drugs: gold, NSAIDs
  5. Autoimmune diseases: SLE, thyroiditis, rheumatoid arthritis
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113
Q

What are the findings of membranous glomerulonephritis on electron microscopy renal biopsy?

A
  1. Basement membrane is thickened with subepithelial electron dense deposits
  2. This creates a ‘spike and dome’ appearance
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114
Q

What is the management of membranous glomerulonephritis?

A
  1. First line: ACEi or ARB to reduce proteinuria
  2. Immunosuppression (only in severe or progressive disease): corticosteroids plus another agent e.g. cyclophosphamide
  3. Consider anticoagulation for high risk
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115
Q

What is the prognosis of membranous glomerulonephritis?

A
  1. 1/3rd = spontaneous remission
  2. 1/3rd = remain proteinuric
  3. 1/3rd = develop end-stage renal failure
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116
Q

What are good prognostic features in membranous glomerulonephritis?

A
  1. Female sex
  2. Young age at presentation
  3. Asymptomatic proteinuria of a modest degree at presentation
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117
Q

What is post-streptococcal glomerulonephritis?

A

Typically occurs 7-14 days following a Group A beta-haemolytic streptococcus infection (usually Streptococcus pyogenes)

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118
Q

What is post-streptococcal glomerulonephritis caused by?

A
  1. Group A beta-haemolytic streptococcus infection (usually Streptococcus pyogenes)
  2. This causes immune complex (IgG, IgM and C3) deposition in the glomeruli
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119
Q

Who is most commonly affected in post-streptococcal glomerulonephritis?

A

Young children

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120
Q

What are the features of post-streptococcal glomerulonephritis?

A
  1. Generally headache and malaise
  2. Visible haematuria
  3. Proteinuria: may result in oedema
  4. Hypertension
  5. Oliguria
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121
Q

What investigation is used to confirm post-streptococcal glomerulonephritis?

A

Raised anti-streptolysin O titre (plus low C3 levels on bloods- not as important)

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122
Q

What are the main differences between IgA nephropathy and post-streptococcal glomerulonephritis ?

A

Post-strep:
1. Develops 1-2 weeks after URTI
2. Proteinuria
3. Low C3
IgA:
1. Develops 1-2 days after URTI
2. Young males
Both:
1. Recent URTI
2. Visible haematuria

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123
Q

What are the renal biopsy features of post-streptococcal glomerulonephritis?

A
  1. Acute, diffuse proliferative glomerulonephritis
  2. Endothelial proliferation with neutrophils
  3. On electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
  4. On immunofluorescence: granular or ‘starry sky’ appearance
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124
Q

What is the management of post-streptococcal glomerulonephritis?

A
  1. Largely supportive: fluid restriction, anti-hypertensives if severe
  2. Carries a good prognosis
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125
Q

What is rapidly progressive glomerulonephritis?

A
  1. A term used to describe a rapid loss in renal function associated with the formation of epithelial crescents in the majority of glomeruli
  2. Associated with diseases e.g. Goodpastures, Wegeners
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126
Q

What are the causes of rapidly progressive glomerulonephritis?

A
  1. Goodpasture’s syndrome (anti-GBM)
  2. Wegener’s granulomatosis
  3. SLE
  4. Microscopic polyarteritis
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127
Q

What are the features of rapidly progressive glomerulonephritis?

A
  1. Nephritic syndrome
  2. features of underlying cause:
    a. Haemoptysis: Goodpasture’s
    b. Vasculitic rash or sinusitis with Wegener’s
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128
Q

What is nephritic syndrome (in context of rapidly progressive glomerulonephritis)?

A
  1. Haematuria with red cell casts
  2. Proteinuria
  3. Hypertension
  4. Oliguria
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129
Q

What is Anti-glomerular basement membrane (GBM) disease?

A
  1. Previously known as Goodpasture’s syndrome
  2. Rare type of small vessel vasculitis
  3. Associated with pulmonary haemorrhage and rapidly progressive glomerulonephritis
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130
Q

What is Anti-glomerular basement membrane (GBM) disease caused by?

A

Anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen

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131
Q

What is the epidemiology of Anti-glomerular basement membrane (anti-GBM) disease?

A
  1. More common in Men (2:1)
  2. Bimodal age distribution: peaks at 20-30 and 60-70
  3. Associated with HLA DR2
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132
Q

What are the features of Anti-glomerular basement membrane (GBM) disease?

A
  1. Pulmonary haemorrhage
  2. Rapidly progressive glomerulonephritis: rapid onset acute kidney injury plus nephritis (proteinuria and haematuria)
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133
Q

What are the investigations for Anti-glomerular basement membrane (GBM) disease?

A
  1. Renal biopsy: linear IgG deposits along basement membrane
  2. Raised transfer factor secondary to pulmonary haemorrhage
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134
Q

What is the management of Anti-glomerular basement membrane (GBM) disease?

A
  1. Plasma exchange: plasmapharesis
  2. Steroids
  3. Cyclophosphamide
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135
Q

What increases the likelihood of pulmonary haemorrhage in anti-glomerular basement membrane (GBM) disease?

A
  1. Smoking
  2. LRTI
  3. Pulmonary oedema
  4. Inhalation of hydrocarbons
  5. Young males
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136
Q

What is membranoproliferative glomerulonephritis?

A
  1. Also known as mesangiocapillary glomerulonephritis
  2. May present as nephrotic syndrome, haematuria or proteinuria
  3. Carries a poor prognosis
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137
Q

What are the different types of membranoproliferative glomerulonephritis?

A

Type 1: 90% of cases, caused by hepatitis C
Type 2: ‘dense deposit disease’, caused by partial lipodystrophy
Type 3: Caused by hepatitis B and C

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138
Q

What is the management of membranoproliferative glomerulonephritis?

A

Steroids may be effective

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139
Q

What is nephrotic syndrome?

A

Triad of:
1. Proteinuria (>3g/24 hours)
2. Hypoalbuminaemia (<30g/L)
3. Oedema
*proteinuria leads to hypoalbuminaemia and oedema

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140
Q

What diseases are associated with nephrotic syndrome?

A
  1. Minimal change disease
  2. Membranous glomerulonephritis (and the other 3 types of glomerulonephritis)
  3. Focal segmental glomerulosclerosis
  4. Amyloidosis
  5. Diabetic nephropathy
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141
Q

What is nephritic syndrome?

A
  1. Haematuria with red cell casts
  2. Proteinuria
  3. Hypertension
  4. Oliguria
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142
Q

What diseases are associated with nephritic syndrome?

A
  1. Rapidly progressive glomerulonephritis
  2. IgA nephropathy
  3. Alport syndrome
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143
Q

What is a hydrocele?

A

Accumulation of fluid within the tunica vaginalis (between the parietal and visceral layers of the membrane that surrounds the testes)

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144
Q

What can hydroceles be divided into?

A

Communicating and non-communicating

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145
Q

What is a communicating hydrocele?

A
  1. Caused by patency of the processus vaginalis
  2. Allows peritoneal fluid to drain down into the scrotum
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146
Q

In what group are communicating hydroceles common in?

A

Newborn males: usually resolve within the first few months of life

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147
Q

What is a non-communicating hydrocele?

A

Caused by excessive fluid production within the tunica vaginalis

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148
Q

What are the common causes of hydroceles?

A

Occur secondary to:
1. Epididymo-orchitis
2. Testicular torsion
3. Testicular tumours

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149
Q

What are the features of a hydrocele?

A
  1. Soft, non-tender swelling of the hemi-scrotum (anterior and below the testicle)
  2. Swelling in confined to the scrotum (examination can get ‘above’ the mass)
  3. Transilluminated with a pen torch*
  4. Testis may be difficult to palpate if the hydrocele is large
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150
Q

How is a hydrocele diagnosed?

A
  1. Clinically
  2. Ultrasound is required if there is any doubt in diagnosis or if underlying testis cannot be palpated
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151
Q

How are hydroceles managed?

A
  1. Infantile hydroceles: repaired if they do not resolve spontaneously by the age of 1-2 years
  2. Adults = conservative (scrotal ) approach (depends on severity of presentation and what it is secondary to e.g. testicular torsion)
    a. Further investigation (e.g. ultrasound) is warranted to exclude an underlying cause such as testicular tumour
    b. Hydrocele sac can be excised or plicated
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152
Q

What are the main considerations of a hydrocele?

A
  1. Non painful, soft fluctuant swelling
  2. Usually contain clear fluid
  3. Will often transilluminate
  4. May be the presenting feature of testicular cancer in young men
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153
Q

What are epididymal cysts?

A
  1. Single or multiple cysts
  2. May contain clear or opalescent fluid (spermatoceles)
  3. Usually occur over 40 years
  4. Painless
  5. Lie above and behind the testis
  6. Can be excised using a scrotal approach
154
Q

What is hydronephrosis?

A

Dilatation of the collecting system of the kidney above the level of the pelvic-ureteric junction

155
Q

What are the causes of unilateral hydronephrosis?

A
  1. Pelvic-ureteric obstruction (congenital or acquired)
  2. Aberrant (anatomical variant) renal vessels
  3. Calculi
  4. Tumours of the renal pelvis
    (PACT)
156
Q

What are the causes of bilateral hydronephrosis?

A
  1. Stenosis of the urethra
  2. Urethral valve
  3. Prostatic enlargement (BPH)
  4. Extensive bladder tumour
  5. Retro-peritoneal fibrosis
157
Q

What are the symptoms of hydronephrosis?

A
  1. Can be asymptomatic
  2. Flank pain
  3. Fever/ signs of sepsis: if urine has become infected
  4. Lower urinary tract symptoms: frequency, urgency, incomplete emptying
  5. Inability to urinate (plus abdominal distension = urinary retention)
158
Q

What are the investigations for hydronephrosis?

A
  1. First line = ultrasound: identifies the presence of hydronephrosis and can assess the kidneys
  2. U&Es: creatinine
  3. Intravenous urography: assess position of obstruction
  4. Non-contrast CT = investigation of choice for suspected renal colic
159
Q

What is the management of hydronephrosis?

A
  1. Remove obstruction and drainage of urine
  2. Acute upper urinary tract obstruction: nephrostomy tube (drains urine from kidney into collecting bag)
  3. Chronic upper urinary tract obstrcution: ureteric stent or a pyeloplasty (removes the blocked part of ureter)
160
Q

What is a nephrostomy?

A
  1. Opening between the kidney and skin
  2. When a small tube is inserted through the skin into the kidneys to allow urine to drain out into a collecting bag
  3. Function is to temporarily drain the urine that is blocked
161
Q

What are the indications for a nephrostomy?

A

Acute upper urinary obstruction

162
Q

What happens during a nephrostomy?

A
  1. Under sedation/ GA
  2. Radiological guidance: ultrasound ± x-rays
  3. Contrast is injected to ensure that the tube has been inserted into the collecting system and is draining the urine
163
Q

What are the complications of a nephrostomy?

A
  1. Severe bleeding (blood stained urine is okay, should clear in 1-2 days)
  2. Tube dislodgement
  3. Tube blockage
  4. Vascular injury requiring removal or affected kidney (emboli)
  5. Reaction to contrast (check kidney function and allergies)
164
Q

What is a ureteric stent?

A

Thin plastic tube which is inserted into the ureter to allow urine to pass easily from the kidney to the bladder

165
Q

What are the indications for a ureteric stent?

A

Chronic upper urinary obstruction:
1. Kidney stone (or part of one)
2. Narrowing of the ureter (stenosis)
3. Inflammation of ureter

166
Q

What are some of the side effects of a ureteric stent?

A
  1. Increased frequency of passing urine
  2. Increased urgency
  3. Blood stained urine
  4. Sensation of incomplete emptying
  5. Slight risk of episodes of incompetence
167
Q

What are some of the complications of a ureteric stent?

A
  1. Increased risk of UTI
  2. Dislodgement/ displacement
  3. Should be removed after a recommended period of time: not to stay in permanently (usually up to 6 months)
168
Q

What is the triad of nephrotic syndrome?

A
  1. Proteinuria (>3g/24hr) causing
  2. Hypoalbuminaemia (<30g/L)
  3. Odema
169
Q

What are patients with nephrotic syndrome at predisposition of?

A

Thrombosis: this is due to loss of antithrombin-3, protein C and S in the urine and an associated rise inn fibrinogen levels

170
Q

What is the commonest cause of nephrotic syndrome?

A

Minimal change glomerulonephritis in children (2-5 years)

171
Q

What is the most common cause of nephrotic syndrome in adults?

A
  1. Membranous glomerulonephritis
  2. Diabetes (in diabetic nephropathy)
172
Q

What are some of the other features of nephrotic syndrome?

A
  1. Triad (proteinuria, hypoalbuminaemia, oedema)
  2. Hyperlipidaemia
  3. Hyper coagulable state (from loss of antithrombin-3, Proteins C and S)
  4. Predisposition to infection (from loss of immunoglobulins)
173
Q

What are the complications of nephrotic syndrome?

A
  1. Increased risk of VTE from loss of antithrombin-3: DVT, PE, renal vein thrombosis
  2. Hyperlipidaemia: increased risk of ACS, stroke
  3. CKD: from membranous glomerulonephritis
  4. Increased risk of infection (loss of immunoglobulins)
  5. Hypocalcaemia (loss of vitamin D and binding protein in urine)
  6. In
174
Q

What is minimal change disease?

A
  1. Type of glomerulonephritis in children (mainly)
  2. T-cell and cytokine-mediated damage to the glomerular basement membrane which nearly always presents as nephrotic syndrome
175
Q

What is the epidemiology of minimal change disease?

A

75% of cases are in children

176
Q

What are the causes of minimal change disease?

A
  1. Majority of cases are idiopathic
  2. Drugs: NSAIDs. rifampicin
  3. Hodgkin’s lymphoma, thymoma
  4. Infectious mononucleosis
177
Q

What is the pathophysiology of minimal change disease?

A
  1. T-cell and cytokine-mediated damage to the glomerular basement membrane
  2. Reduction in electrostatic charge
  3. Therefore increased glomerular permeability to serum albumin (proteinuria)
178
Q

What are the features of minimal change disease?

A
  1. Nephrotic syndrome
  2. Normotensive (rare to be hypertensive)
  3. Highly selective proteinuria: only intermediate sized proteins can leak through the glomerular e.g. albumin
179
Q

What are the investigations for minimal change disease?

A
  1. Urine dip and analysis
  2. Renal biopsy:
    a. Normal glomeruli on light microscopy
    b. Electron microscopy: fusion of podocytes and effacement of foot processes
180
Q

What is the management of minimal change disease?

A
  1. First line = oral corticosteroids (80% of cases are steroid responsive)
  2. Cyclophosphamide are second line if steroid resistant
181
Q

What is the prognosis of minimal change disease?

A
  1. Generally carries a good prognosis due to oral corticosteroids
  2. Relapse is common:
    a. 1/3rd have just one episode
    b. 1/3rd have infrequent relapses
    c. 1/3rd have frequent relapses which stop before adulthood
182
Q

What is an orchidectomy?

A

Surgical procedure to remove a testicle

183
Q

What is an orchidectomy indicated for?

A

Testicular cancer

184
Q

What type of orchidectomy is used in the management of testicular cancer?

A

Orchidectomy via an inguinal approach: allows high ligation of the testicular vessels and avoids exposure of another lymphatic field to the tumour

185
Q

What can be offered to young males who are being managed for testicular cancer via an orchidectomy?

A

Prosthesis

186
Q

What are the risks of an orchidectomy?

A
  1. Swelling and bruising (some is expected)
  2. Change in body appearance - mental health impact
  3. Continued scrotal pain
  4. Need for further treatment
187
Q

What do patients who have had an orchidectomy need to avoid following surgery?

A

Strenuous activities: bicycle riding, jogging, weight lifting (only for 2-3 weeks)

188
Q

What is polycystic kidney disease?

A

Inherited disorder characterised by the development of multiple renal cysts that gradually expand and replace normal kidney tissue, as well as systemic and extrarenal manifestations

189
Q

What are the two types of polycystic kidney disease?

A
  1. Autosomal dominant (more common) PKD
  2. Autosomal recessive PKD
190
Q

What is autosomal dominant PKD?

A

The most common inherited cause of kidney disease: affects 1 in 1,000 Cuacasians

191
Q

What are the two different types of autosomal dominant PKD?

A

Type 1:
1. 85% of cases
2. Chromosome 16
3. Presents with renal failure earlier
Type 2:
1. 15% of cases
2. Chromosome 4

192
Q

What is the screening investigation for relatives with autosomal dominant PKD?

A

Abdominal ultrasound

193
Q

What is the abdominal ultrasound diagnostic criteria in patients with positive family history for autosomal dominant PKD?

A
  1. Two cysts, unilateral or bilateral, if aged < 30 years
  2. Two cysts in both kidneys if aged 30-59 years
  3. Four cysts in both kidneys if aged > 60 years
194
Q

What is Polycystic Kidney Disease characterised by?

A
  1. Renal cysts
  2. Hypertension
  3. Extrarenal cysts
  4. Haematuria
  5. Intracranial aneurysms
  6. Mitral valve prolapse
  7. Abdominal wall hernias
  8. Later: develop chronic kidney disease
195
Q

What is polycystic kidney disease associated with?

A

Intracranial berry’ aneurysms and may present with subarachnoid haemorrhage: sudden thunderclap ‘onset headache

196
Q

What is the management of autosomal dominant polycystic kidney disease?

A
  1. Tolvaptan: vasopressin receptor 2 antagonist
  2. An option to slow the progression of cyst development and renal insufficiency if:
    a. they have CKD stage 2 or 3 at the start of treatment
    b. there is evidence of rapidly progressing disease
    c. the company provides it with a discount
197
Q

What is autosomal recessive PKD?

A
  1. Much less common form of polycystic kidney disease
  2. Due to defect in a gene located on chromosome 6- encodes fibrocystin
  3. Fibrocystin is an important protein for normal renal tubule development
198
Q

How is autosomal recessive PKD diagnosed?

A
  1. On prenatal ultrasound
  2. In early infancy with abdominal masses and renal failure
199
Q

What are the features of autosomal recessive PKD?

A

Presents in newborns or childhood:
1. Newborns: Potter’s syndrome (lack of amniotic fluid and kidney failure in a fetus) secondary to oligohydramnios
2. Childhood:
a. abdominal masses
b. end-stage renal failure
c. liver involvement e.g. portal and interlobular fibrosis

200
Q

What is found on renal biopsy in patients with autosomal recessive PKD?

A

Multiple cylindrical lesions at right angles to the cortical surface

201
Q

What are the long-term complications of Polycystic Kidney Disease?

A
  1. Hypertension
  2. Increased cardiovascular morbidity and mortality
  3. Chronic kidney disease
  4. Aneurysms: intracranial, coronary, thoracic and abdominal
  5. Liver and pancreatic cysts
  6. End-stage renal disease
202
Q

What is Prostate cancer?

A
  1. A malignant tumour of glandular origin situated in the prostate
  2. The most common cancer in men (second common cause of death after lung)
203
Q

What are the risk factors for prostate cancer?

A
  1. Increasing age
  2. Obesity
  3. Afro-Carribean ethnicity
  4. Family history
204
Q

What are the early features of prostate cancer

A
  1. Localised prostate cancer is often asymptomatic
  2. This is because prostate cancers tend to originate in the periphery of the prostate
  3. Therefore obstructive symptoms do not develop until later (once the tumour has grown)
205
Q

What are the late features of prostate cancer?

A
  1. Bladder outlet obstruction: hesitancy, urinary retention
  2. Haematuria, haematospermia
  3. Pain: back, perineal or testicular
206
Q

What are the findings of prostate cancer on examination?

A

Digital rectal examination:
1. Asymmetrical
2. Hard
3. Nodular
4. Enlarged mass with loss of median sulcus

207
Q

What is considered as the first line investigation for prostate cancer?

A

Multiparametric MRI

208
Q

What used to be considered the first line investigation for prostate cancer?

A

Transrectal ultrasound-guided (TRUS) biopsy
Complications included:
1. Sepsis
2. Pain (lasting > 2 weeks)
3. Fever
4. Haematuria and rectal bleeding

209
Q

How is multiparametric MRI interpreted in the investigation of prostate cancer?

A

5-point Likert scale:
1. If ≥ 3 : multiparametric MRI-influenced prostate biopsy is offered
2. If 1 or 2: NICE recommend discussing with patients the pros and cons of having a biopsy

210
Q

What is PSA?

A

Prostate specific antigen: a protease enzyme produced by normal and malignant epithelial cells

211
Q

What can raise PSA levels?

A
  1. Prostate cancer
  2. Benign prostatic hyperplasia (BPH)
  3. Prostatitis and UTI
  4. Ejaculation
  5. Vigorous exercise
  6. Urinary retention
  7. Instrumentation of the urinary tract
212
Q

Why is the use of the PSA controversial in diagnosing prostate cancer?

A
  1. Can be raised from other causes e.g. BPH
  2. Poor specificity and sensitivity:
    a. 33% of men with a PSA of 4-10 ng/ml will be found to have prostate cancer
    b. around 20% with prostate cancer have a normal PSA
213
Q

What are the NICE recommendations regarding referral and PSA levels?

A

Men aged 50-69 years should be referred if the PSA is >= 3.0 ng/ml OR there is an abnormal DRE

214
Q

What investigation is important in prostate cancer staging?

A

MRI/CT and bone scan

215
Q

What is the pathophysiology of prostate cancer?

A
  1. 95% are adenocarcinoma
  2. Often multifocal
  3. 70% lie in the peripheral zone
  4. Graded using the Gleason grading scale
  5. Lymphatic spread occurs first to the obturator nodes and local extra prostatic spread to the seminal vesicles is associated with distant disease
216
Q

What is the general management of prostate cancer?

A
  1. Treatment depends on life expectancy and patient choice
  2. Conservative: active monitoring and watchful waiting (T1/2)
  3. Radical prostatectomy
  4. Radiotherapy: external beam and brachytherapy
  5. Hormonal therapy
217
Q

What is the preferred management option for prostate cancer in low risk men?

A

Active surveillance:
1. Must have had at least 10 biopsy cores taken
2. Have at least one re-biopsy

218
Q

What is a radical prostatectomy in the management of prostate cancer?

A
  1. Surgical removal of the prostate
  2. Standard treatment for localised disease
  3. The obturator lymph nodes are also removed to complement the staging process
219
Q

What is a common complication of a radical prostatectomy?

A

Erectile dysfunction

220
Q

What does radiotherapy for prostate cancer involve?

A
  1. External beam and brachytherapy
  2. Patients may develop proctitis
221
Q

What are patients who have had radiotherapy for prostate cancer at risk of developing?

A

Bladder, colon and rectal cancer

222
Q

When is hormonal therapy used in prostate cancer?

A
  1. In the management of metastatic prostate cancer
  2. Anti-androgen therapy
  3. Often a combination of medications: synthetic GnRH agonists or antagonist, androgen synthesis inhibitors
223
Q

What treatment is used to rapidly reduce testosterone levels in advanced prostate cancer?

A

Bilateral orchidectomy

224
Q

What is transurethral prostatectomy?

A

Common treatment for BPH

225
Q

What is involved in transurethral prostatectomy?

A
  1. Insertion of a resectoscope via the penile urethra
  2. The bladder and prostate are irrigated and strips of prostatic tissue removed using diathermy
226
Q

What are the complications of a transurethral prostatectomy?

A
  1. Haemorrhage
  2. Urosepsis
  3. Retrograde ejaculation
  4. Electrolyte disturbances from the irrigation fluids during the procedure
227
Q

What is renal artery stenosis?

A

Stenosis (narrowing) of the renal artery

228
Q

What is the most common cause of renal artery stenosis?

A

Atherosclerosis (90% of renal vascular disease)

229
Q

What is the other cause of renal artery stenosis?

A

Fibromuscular dysplasia:
1. May be associated with collagen disorders and Takayasu vasculitis
2. May be associated with micro-aneursyms in the mid and distal renal arteries

230
Q

What are the features of renal artery stenosis?

A
  1. Hypertension: accelerated or difficult to control
  2. Chronic kidney disease
  3. PMH of ‘flash pulmonary oedema’: sudden or unexplained
231
Q

What may be found on abdominal examination for renal artery stenosis?

A

Renal bruit

232
Q

What are the investigations for renal artery stenosis?

A
  1. Bloods:
    a. Serum creatinine
    b. Potassium (low if excessive activation of RAS)
    c. Aldosterone: renin ratio: if low exclude primary aldosteronism
  2. Duplex USS: assess severity of stenosis
  3. CT/MR angiography
233
Q

What is the management of renal artery stenosis?

A
  1. Conservative: control risk factors e.g. smoking cessation, glycaemic control
  2. Urinalysis and sediment evaluation
  3. Blood pressure control: may already be on multiple antihypertensives, add in aspirin and statin as secondary prevention
  4. Renal artery stenting
234
Q

What are the primary options for anti-hypertensives in patients with renal artery stenosis?

A
  1. Captopril (ACEi)
  2. Enalapril (ACEi)
  3. Valsartan (ARB)
  4. Losartan (ARB)
235
Q

What are the complications of renal artery stenosis?

A
  1. Progression of stenosis
  2. Progression of chronic kidney disease
236
Q

What is renal cell carcinoma?

A
  1. Malignancy arising from the renal parenchyma/ cortex
  2. Accounts for > 80% of primary renal malignancies
237
Q

What is the most common type of renal cell carcinoma?

A

Clear cell

238
Q

What are the associations of renal cell carcinoma?

A
  1. Smoking
  2. von Hippel-Lindau syndrome (rare inherited disorder- malignant tumour growth)
  3. Tuberous sclerosis (benign tumour growth)
  4. Autosomal dominant PKD (risk only slightly increased)
239
Q

What is the epidemiology of renal cell carcinoma?

A

More common in middle aged men

240
Q

What is the classical triad in renal cell carcinoma?

A
  1. Haematuria
  2. Loin pain
  3. Abdominal mass
241
Q

What are some of the endocrine effects of renal cell carcinoma?

A
  1. Erythropoetin production: lead to polycythaemia
  2. Parathyroid hormone-related protein: hypercalcaemia
  3. ACTH: skin pigmentation, cushings
242
Q

What are the features of renal cell carcinoma?

A

Can be asymptomatic
1. Classic triad: haematuria, loin pain, mass
2. Pyrexia of unknown irgin
3. Endocrine effects
4. 25% have metastases
5. Varicocele: caused by tumour compressing veins

243
Q

What is Stauffer syndrome in the context of renal cell carcinoma?

A
  1. Paraneoplastic disorder
  2. Typically presents as cholestasis/ hepatosplenomegaly
  3. Thought to be secondary to increased levels of IL-6
244
Q

What are the investigations for renal cell carcinoma?

A
  1. Bloods
  2. Urine
  3. Imaging
245
Q

What are the blood findings for renal cell carcinoma?

A
  1. FBC: polycythaemia from erythropoietin secretion
  2. Lactate dehydrogenase: elevated in advanced RCC
  3. Serum creatinine (U&E): indicative of chronic renal insufficiency if elevated with reduced creatinine clearance
  4. Calcium: advanced RCC: >2.5 mmol/L (>10 mg/dL)
  5. ALP (bony mets?)
246
Q

What are the urine findings for renal cell carcinoma?

A
  1. Haematuria and/or proteinuria
  2. RBC sediments: send for cytology
247
Q

What are the imaging findings for renal cell carcinoma?

A
  1. US: diagnosis is usually suggested by abnormal renal cyst/mass, lymphadenopathy
  2. CT/MRI: to assess renal mass, regional lymphadenopathy, and/or visceral/bone metastases
248
Q

What is a common site for metastases for renal cell carcinoma?

A

Lungs: ‘cannon ball’ pulmonary metastases

249
Q

How is renal cell carcinoma staged?

A

T1: Tumour ≤ 7 cm and confined to the kidney
T2: Tumour > 7 cm and confined to the kidney
T3: Tumour extends into major veins or perinephric tissues, but not into the ipsilateral adrenal gland and not beyond Gerota’s fascia
T4: Tumor invades beyond Gerota’s fascia (including contiguous extension into the ipsilateral adrenal gland)

250
Q

What is the management for renal cell carcinoma?

A
  1. Small mass/ T1 or T2: typically offered a partial or total nephrectomy, depends on size
  2. Patients with metastases: alpha-interferon and interleukin-2 have been used to reduce tumour size
251
Q

What medical management for renal cell carcinoma has been shown to have superior efficacy?

A

Receptor tyrosine kinase inhibitors e.g. sorafenib, sunitinib

252
Q

What is an allograft?

A

An organ is transplanted from one individual to another

253
Q

What are the main antigens that give rise to graft rejection?

A
  1. ABO blood group
  2. Human leucocyte antigens (HLA)
  3. Minor histocompatibility antigens
254
Q

What are the four most important HLA alleles?

A
  1. HLA A
  2. HLA B
  3. HLA C
  4. HLA DR
255
Q

What are the different types of organ rejection?

A
  1. Hyperacute: occurs immediately through presence of pre formed antigens (such as ABO incompatibility)
  2. Acute: occurs during the first 6 months and is usually T cell mediated, usually tissue infiltrates and vascular lesions
  3. Chronic: occurs after the first 6 months, vascular changes mainly
256
Q

What type of organ is at greatest risk for a hyperacute organ rejection?

A

Renal transplant

257
Q

What types of patients are considered for renal transplant?

A

Patients with end stage renal failure who are dialysis dependent or likely to become so in the immediate future

258
Q

What is the exclusion criteria for renal transplant?

A
  1. Active malignancy
  2. Old age (due to limited organ availability)
259
Q

Who are the preferred donor kidneys from in renal transplant?

A

Live related donors and close family: less HLA mismatches that general population

260
Q

What procedure is preferred for donors in renal transplant?

A

Laparoscopic donor nephrectomy

261
Q

What occurs once the donor kidney has been removed in renal transplant?

A
  1. Usually prepared on the bench in theatre by the transplant surgeon immediately prior to implantation
  2. Factors such as accessory renal arteries and vessel length are assessed and managed
262
Q

How is a renal transplant procedure performed?

A
  1. Under GA
  2. A Rutherford-Morrison incision is made on the preferred side
  3. The external iliac artery and vein are dissected out and following systemic heparinisation are cross clamped
  4. The vein and artery are anastamosed to the iliacs and the clamps removed
  5. The ureter is then implanted into the bladder and a stent is usually placed to maintain patency
  6. The wounds are then closed and the patient recovered from surgery
263
Q

What complication is encountered in renal transplant if using cadaveric kidneys (dead donor)?

A

Acute tubular necrosis, but this tends to resolve

264
Q

What is the prognosis of graft survival in renal transplants?

A
  1. Cadaveric transplants: 1 year = 90%, 10 years = 60%
  2. Living-donor transplants1 year = 95%, 10 years = 70%
265
Q

What are some of the post-operative complications of a renal transplant?

A
  1. ATN of graft
  2. Vascular thrombosis
  3. Urine leakage
  4. UTI
266
Q

What is a hyperacute rejection of a renal transplant?

A
  1. Occurs minutes to hours after surgery
  2. Due to pre-existing antibodies against ABO or HLA antigens
  3. Type II hypersensitivity reaction
  4. Leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
  5. No treatment is possible and the graft must be removed
267
Q

What is acute graft failure of a renal transplant?

A
  1. Occurs < 6 months
  2. Usually due to mismatched HLA
  3. Cell-mediated (cytotoxic T cells)
  4. Usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
  5. May be caused by cytomegalovirus infection
  6. May be reversible with steroids and immunosuppressants
268
Q

What is a regime of immunosuppressants for renal transplant?

A
  1. Initial: ciclosporin/tacrolimus with a monoclonal antibody
  2. Maintenance: ciclosporin/tacrolimus with MMF or sirolimus
  3. Add steroids if more than one steroid responsive acute rejection episode
269
Q

What is ciclosporin in immunosuppression following renal transplant?

A

Inhibits calcineurin, a phosphotase involved in T cell activation

270
Q

Why are the pros and cons of Tacrolimus in immunosuppression following renal transplant?

A
  1. Lowers incidence of acute rejection compared to ciclosporin
  2. Can cause hypertension and hyperlipidaemia
  3. High incidence of impaired glucose tolerance and diabetes
271
Q

What are the complications of long-term immunosuppression?

A
  1. CVD: from tacrolimus and ciclosporin which can cause hypertension, hyperlipidemia: accelerated CVD
  2. Renal failure: nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney
  3. Malignancy: patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinomas
272
Q

What is chronic graft failure in renal transplants?

A
  1. Occurs > 6 months
  2. Both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
    recurrence of original renal disease (Membranoproliferative GN > IgA > focal segmental glomerulosclerosis)
273
Q

What is Focal segmental glomerulosclerosis?

A
  1. A cause of nephrotic syndrome and chronic kidney disease
  2. It generally presents in young adults
274
Q

What are the causes of focal segmental glomerulosclerosis?

A
  1. Idiopathic
  2. Secondary to other renal pathology e.g. IgA nephropathy
  3. HIV
  4. Heroin
  5. Alport’s syndorme
  6. Sickle cell
275
Q

What is the prognosis of focal segmental glomerulosclerosis following a renal transplant?

A

High recurrence rates (chronic graft failure)

276
Q

What are the renal biopsy findings for focal segmental glomerulosclerosis?

A
  1. Focal and segmental sclerosis and hyalinosis on light microscopy
  2. Effacement of foot processes on electron microscopy
277
Q

What is the management of focal segmental glomerulosclerosis?

A

Steroids ± immunosuppressants

278
Q

What is the prognosis of untreated focal segmental gomerulosclerosis?

A

Untreated FSGS has a < 10% chance of spontaneous remission

279
Q

What is rhabdomyolysis?

A

The end result of any disease that causes muscle cell lysis (mycoyte death)

280
Q

What is a typical history of rhabdomyolysis?

A

A patient who has had a fall or prolonged epileptic seizure and is found to have an acute kidney injury on admission

281
Q

What are the causes of rhabdomyolysis?

A
  1. Seizure
  2. Collapse (fall)
  3. Ecstasy
  4. Crush injury
  5. Statins, especially if co-prescribed with clarithromycin
282
Q

What are the symptoms and signs of rhabdomyolysis?

A
  1. Muscular pain or discomfort (common)
  2. Can be none
283
Q

What are the main investigations for rhabdomyolysis?

A
  1. U&Es
  2. Urinalysis: myoglobinuria
  3. VBG/ABG: metabolic acidosis
284
Q

What are the U&Es findings of rhabdoymolysis?

A
  1. Acute kidney injury with disproportionately raised creatinine
  2. Elevated creatine kinase (CK)
  3. Hypocalcaemia (myoglobin binds calcium)
    4.Elevated phosphate (released from myocytes)
  4. Hyperkalaemia (may develop before renal failure)
285
Q

What is the key finding supporting rhabdomyolysis?

A

History: collapse/ fall plus an acute kidney injury with a disproportionately raised creatinine, confirmed with elevated CK

286
Q

What is the management of rhabdoymolysis?

A
  1. IV fluids to maintain good urine output (mainstay of treatment)
  2. Sometimes use urinary alkalinization (administration of IV sodium bicarbonate)
287
Q

What is McArdle’s disease?

A

Rare, metabolic muscle disorder that can cause rhabdomyolysis

288
Q

What is testicular cancer?

A
  1. Cancer that presents as a hard, painless nodule on one testis
  2. Most common malignancy in men aged 20-30 years
289
Q

What is the aetiology of testicular cancer?

A
  1. 95% of cases are germ-cell tumours:
    a. Seminomas
    b. Non-seminomas: embyronal, yolk sac, teratomas
  2. Non-germ cell tumours e.g. Leydig cell tumours, sarcomas
290
Q

What is the epidemiology of testicular cancer?

A
  1. Most common malignancy in men aged 20-30 years
  2. Peak incidence for seminomas = 35 years
  3. Peak incidence for teratomas (non-germ cell) = 25 years
291
Q

What are the risk factors for testicular cancer?

A
  1. Infertility (increases risk x3)
  2. Cryptorchidism (congenital undescended testis)
  3. FH
  4. Klinefelter’s syndrome (47,XXY)
  5. Mumps orchitis: causes testicular atrophy
292
Q

What are the features of Klinefelter’s syndrome?

A

47, XXY
1. Often taller than average
2. Lack of secondary characteristics
3. Small, firm testes
4. Infertile
5. Gynaecomastia (increased risk of breast cancer)

293
Q

What are the features of testicular cancer?

A
  1. Painless lump (most common PC)
  2. Pain in a minority of men
  3. Hydrocele
  4. Gynaecomastia
294
Q

Why do patients develop gynaecomastia in testicular cancer?

A
  1. Increased oestrogen: androgen ratio
  2. Germ cell tumours have increased hCG levels, increasing oestrogen levels
  3. Leydig cell tumours: directly secrete more oestradiol and convert additional androgen precursors to oestrogens
295
Q

What is the first line investigation for testicular cancer?

A

Ultrasound

296
Q

What are the other investigations for testicular cancer?

A
  1. Bloods: beta-hCG, AFP, LDH
  2. Other imaging: CT/ MRI/ CXR: staging tool, identify metastases
297
Q

What are the tumour markers for the different types of testicular cancer?

A

Tumour markers are mainly for germ cell tumours:
1. Seminoma: hCG (elevated in around 20%)
2. Non-seminomas: AFP and/or beta-hCG (elevated in 80-85%)
3. LDH elevated in 40%

298
Q

What is the management of testicular cancer?

A
  1. Dependent on whether it is a seminoma or non-seminoma
  2. Orchidectomy tends to be used for both, retroperitoneal lymph node dissection for no-seminomas
  3. Chemotherapy and radiotherapy may be given depending on staging and tumour type
299
Q

What is testicular torsion?

A

A twist of the spermatic cord resulting in testicular ischaemia and necrosis

300
Q

What is the epidemiology of testicular torsion?

A

Most common in males aged between 10 and 30 (peak incidence 13-15 years)

301
Q

What are the features of testicular torsion?

A

Pain is usually severe and of sudden onset - may be referred to the lower abdomen
Nausea and vomiting may be present

302
Q

What are the signs of testicular torsion on examination?

A
  1. Usually a swollen, tender testis retracted upwards
  2. The skin may be reddened
  3. Cremasteric reflex is lost
  4. Elevation of the testis does not ease the pain (Prehn’s sign)
303
Q

What is the management of testicular torsion?

A
  1. Urgent surgical exploration
  2. If a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral
304
Q

What condition can present as testicular torsion?

A

Epididymo-orchitis

305
Q

What is a Transurethral resection of the prostate (TURP)?

A
  1. Surgical procedure used in the treatment of an enlarged prostate (benign prostatic hyperplasia)
  2. Aims to relive pressure on the urethra by removing parts of the prostate tissue (gland) and improve the urinary symptoms
306
Q

What are the indications for a Transurethral resection of the prostate (TURP)?

A

Most common type of surgery for treating an enlarged prostate:
1. Benign prostatic enlargement (BPE)
2. Benign prostatic hyperplasia (BPH)

307
Q

What are the possible complications of a Transurethral resection of the prostate (TURP)?

A
  1. Retrograde ejaculation (ejaculate flows into your bladder)
  2. Degree of urinary incontinence
  3. Erectile dysfunction (10%)
  4. Narrowing of the urethra (urethral strictures) is estimated to develop in up to 4% of cases
  5. Bleeding- 3% need to have a blood transfusion
  6. Urinary retention- need a catheter
  7. Prostate becoming enlarged again- 10% will need another operation within 4-10 years
    UTI (5%) after the surgery
308
Q

What is the most common complication following a transurethral resection of the prostate (TURP)?

A

Retrograde ejaculation: 90% of cases

309
Q

What is TURP syndrome?

A

Rare and life-threatening complication following transurethral resection of the prostate

310
Q

What does TURP syndrome present with?

A

CNS, respiratory and systemic symptoms

311
Q

What is TURP syndrome caused by?

A
  1. Irrigation with large volumes of glycine
  2. Glycine is hypo-osmolar and is systemically absorbed when prostatic venous sinuses are opened up during prostate resection
  3. This results in hyponatremia, and when glycine is broken down by the liver into ammonia, hyper-ammonia and causes visual disturbances
312
Q

What are the risk factors for developing TURP syndrome?

A
  1. Surgical time > 1 hr
  2. Height of bag > 70cm
  3. Resected > 60g of prostate tissue
  4. Large blood loss
  5. Perforation
  6. Large amount of fluid used
  7. Poorly controlled CHF
313
Q

What is TURBT?

A

Transurethral resection of bladder tumour

314
Q

When is TURBT indicated?

A

Can be used as both diagnostic and therapeutic for bladder cancer (superficial lesions), 90% of cases are urothelial (transitional cell) carcinoma

315
Q

What is the procedure of a TURBT?

A
  1. Cystoscope into urethra to visualise the bladder
  2. Remove the non-muscle invasive bladder cancer and use diathermy to minimise blood loss
  3. Take samples to biopsy
  4. May insert a catheter at the end to directly insert chemotherapy into the bladder, this is drained an hour afterwards
316
Q

What are the complications of a TURBT?

A
  1. Urine infection
  2. Another TURBT due to insufficient removal/ resection
  3. DVT
  4. Bleeding: small amounts is acceptable, haematuria
317
Q

What is nephrolithiasis?

A
  1. Also known as kidney stones
  2. Refers to the presence of crystalline stones (calculi) within the urinary system
318
Q

What are the different types of kidney stone?

A
  1. Calcium oxalate = 85%
  2. Calcium phosphate = 10%
  3. Uric acid = 5-10%
  4. Struvite = 2-20%
  5. Cystine = 1%
319
Q

What are the most common type of kidney stone?

A
  1. Calcium oxalate
  2. Hypercalciuria is a major risk factor
  3. Stones are radio-opaque
320
Q

What are calcium phosphate kidney stones?

A
  1. 10% of renal stones
  2. May occur in renal tubular acidosis- increases risk of stone formation
  3. Can cause a rise in pH
  4. Radio-opaque: composition similar to bone
321
Q

What are uric acid kidney stones?

A
  1. Uric acid is a product of purine metabolism
  2. May precipitate if urine pH is low
  3. May be causes by diseases with extensive tissue breakdown e.g. malignancy
  4. Common in children with inborn errors of metabolism
  5. Radiolucent
322
Q

Which renal stones are radio-opaque?

A
  1. Calcium oxalate
  2. Mixed calcium oxalate/ phosphate
  3. Triple phosphate stones = stag horn calculi
  4. Calcium phosphate stones
323
Q

What are stag-horn calculi?

A
  1. Triple phosphate stones
  2. Develop in alkaline urine
  3. Composed of struvite: ammonium magnesium phosphate and triple phosphate
  4. Involve the renal pelvis and extend into at least 2 calyces
  5. Proteus infections predispose to the formation of them
324
Q

What are the risk factors for renal stones?

A
  1. Dehydration
  2. Hypercalciuria, hyperparathyroidism, hypercalcaemia
  3. Cystinuria
  4. Renal tubular acidosis
  5. Polycystic kidney disease
325
Q

What are the risk factors for urate renal stones?

A
  1. Gout
  2. Ileostomy: loss of bicarbonate and fluids → acidic urine
  3. Acidic urine predisposes to uric acid
326
Q

What drugs promote calcium renal stones?

A
  1. Loop diuretics
  2. Steroids
  3. Theophylline
327
Q

Which drugs can prevent calcium renal stones?

A

Thiazides: increase distal tubular calcium resorption

328
Q

What are the key features of renal stones in the history?

A
  1. Acute, severe flank pain that radiates to the ipsilateral groin (renal colic)
  2. Some patients may be asymptomatic and have no radiation
  3. PMH of renal stones
329
Q

What are the other features of renal stones?

A
  1. Renal colic
  2. Nausea and vomiting in an acute episode
  3. Urinary frequency or urgency
330
Q

What are the signs of renal stones on examination?

A
  1. Patients may in be extreme discomfort
  2. Tachycardia
  3. Hypotension
  4. Abdomen tender on palpation on the affected side
  5. Lack of peritoneal signs (guarding, rebound, rigidity)
331
Q

What is the preferred imaging modality for renal stones?

A

Non-contrast helical CT scan of kidneys, ureters and bladder (KUB)

332
Q

What are the initial investigations for renal stones?

A
  1. Urine dipstick and culture (microscopic haematuria)
  2. Bloods:
    a. Serum creatinine and electrolytes to check kidney function
    b. FBC/CRP for associated infection
    c. Blood cultures if pyrexial or other signs of sepsis
333
Q

What are the imaging investigations for renal stones?

A
  1. Non-contrast CT KUB: for all patients within 14 hours of admission
  2. Urgent non-contrast CTKUB if:
    a. fever
    b. solitary kidney
    c. uncertain diagnosis e.g. ruptured AAA
  3. CT > ultrasound
334
Q

What is the management of renal stones?

A

Depends on size and development of complications:
1. If stones < 5mm: will pass spontaneously within 4 weeks
2. More intensive and urgent treatment includes: nephrostomy tube placement, insertion of ureteric catheters and ureteric stent placement

335
Q

What are the complications renal stones?

A
  1. Ureteric obstruction
  2. Infection: sepsis
336
Q

What happens if there is ureteric obstruction from stones with infection?

A

Surgical emergency: must be decompressed

337
Q

What is shockwave lithotripsy in the management of renal stones?

A

A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone fragmentation

338
Q

What are the complications of shockwave lithotripsy in the management of renal stones?

A
  1. The passage of shock waves can result in the development of solid organ injury
  2. Fragmentation of larger stones may result in the development of ureteric obstruction
  3. The procedure is uncomfortable for patients and analgesia is required during the procedure and afterwards
339
Q

What is ureteroscopy in the management of renal stones?

A
  1. Indicated in patients where lithotripsy is contraindicated and in complex stone disease
  2. A ureteroscope is passed retrograde through the ureter and into the renal pelvis
  3. In most cases a stent is left in situ for 4 weeks after the procedure
340
Q

What is percutaneous nephrolithotomy in the management of renal stones?

A
  1. Access is gained into the renal collecting system
  2. Intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed
  3. For complex renal calculi and staghorn calculi
341
Q

How can calcium renal stones be prevented?

A
  1. High fluid intake
  2. Low animal protein, low salt diet
  3. Thiazide diuretics: increase distal tubular calcium resorption
342
Q

How can uric acid stones be prevented?

A
  1. Treatment of gout e.g. allopurinol
  2. Prevent acidic urine e.g. urinary alkalinization through oral bicarbonate
343
Q

What are the complications/prognosis of urinary tract calculi?

A
  1. Recurrent calculi
  2. Complications of surgery (bleeding, haematoma, infection)
  3. Nephrolithiasis is a lifelong disease process
344
Q

What is a urinary tract infection (UTI)?

A

An inflammatory reaction of the urinary tract epithelium in response to pathogenic micro-organisms, most commonly bacteria

345
Q

What are the classifications of UTIs?

A
  1. Uncomplicated (>80% of cases): infection in a healthy individual with anatomically and functionally normal urinary tract. More common in sexually active females
  2. Complicated: infection associated with factors that increase colonization and decrease the efficacy of therapy. More common with catheters, nursing home and hospitalised patients
346
Q

What are the commonly associated pathogens in uncomplicated UTIs?

A
  1. E.coli
  2. Proteus Mirabilis (kidney stones or contamination)
  3. Klebsiella pnuemoniae
  4. Staphylococcus Saprophyticus
  5. Enterococcus species
347
Q

What are the commonly associated pathogens in complicated UTIs?

A
  1. E.coli
  2. Pseudomonas aeruginosa
348
Q

What is the most common causative organism in UTIs?

A

E.coli

349
Q

What is the epidemiology of UTIs?

A
  1. The prevalence of bacteriuria in young, non-pregnant women is about 1% - 3%
  2. Up to 40% to 50% of the female population will experience a symptomatic urinary tract infection at some time during their life
350
Q

What are the different groups of patients who experience UTIs?

A
  1. Uncomplicated: generally women who are not pregnant
  2. Complicated: in general, infection in:
    a. Men
    b. Pregnant women
    c. Children
    d. Patients who are hospitalised or in health care- associated settings
351
Q

What are the risk factors for UTIs?

A
  1. Increased bacterial inoculation: e.g. sexual activity, urinary incontinence
  2. Increased binding of uropathogenic bacteria: e.g. reduced oestrogen/ menopause
  3. Reduced urine flow: e.g. dehydration, obstructed urinary tract
  4. Increased bacterial growth: e.g. DM, immunosuppression, stones, catheter, pregnancy
352
Q

What are the clinical features of UTIs?

A
  1. Dysuria
  2. Urinary frequency
  3. Urinary urgency
  4. Cloudy/offensive smelling urine
  5. Lower abdominal pain
  6. Fever: typically low-grade in lower UTI
  7. Malaise
353
Q

What is an additional feature to be aware of for elderly patients with a UTI?

A

Acute confusion/ delirium

354
Q

What is the initial investigation for an uncomplicated UTI?

A

Urine dipstick

355
Q

When should a urine microscopy, sensitivity and culture be sent off?

A
  1. Women aged over 65 years
  2. Recurrent UTIs: 2 episodes in 6 months, or 3 episodes in 12 months
  3. Pregnant women
  4. Men
  5. Visible or non-visible haematuria (on dipstick)
356
Q

What are the urine dipstick findings for the likelihood of UTIs?

A
  1. Negative for all nitrite, leukocyte and red blood cells = UTI less likely
  2. Negative for nitrite, positive for leukocyte = UTI is equally likely to other diagnoses
  3. Positive for nitrite or leukocyte AND red blood cells = UTI is likely
357
Q

When should a urine dipstick not be used to investigate UTIs?

A
  1. Women > 65 years (can be used to aid diagnosis if there are no risk factors for complicated UTI)
  2. Men
  3. Catheterised patients
358
Q

What is the management of UTIs in non-pregnant women?

A
  1. Follow local trust guidelines
  2. NICE recommend: trimethoprim or nitrofurantoin for 3 days
  3. Send a urine culture if over 65 or visible or non-visible haematuria
359
Q

What is the management of UTIs in pregnant women?

A
  1. Urine culture sent off in all cases
  2. First line: nitrofurantoin (avoid near term) for 7 days
  3. Second line: amoxicillin, cefalexin
  4. Treat regardless of symptoms/ asymptomatic due to risk of progression to acute pyelonephritis
360
Q

What medication should be avoided in the management of UTIs in pregnant women?

A

Trimethoprim: teratogenic in first trimester, should be avoided during pregnancy

361
Q

What should be performed in all pregnant women with a UTI following 7-day treatment?

A

Further urine culture as a test of cure (urine culture at first antenatal visit as well)

362
Q

What is the management of UTIs in men?

A
  1. Send urine culture
  2. Immediate antibiotic prescription of trimethoprim or nitrofurantoin for 7 days
  3. Referral to urology is not routinely required if this is their first uncomplicated UTI
363
Q

What is the management of UTIs in catheterised patients?

A
  1. Do not need to treat asymptomatic patients
  2. If they have symptoms, treat with antibiotics (trust guidelines) for 7 days
  3. Consider removing or changing the catheter as soon as possible if longer than 7 days old
364
Q

What is acute pyelonephritis?

A
  1. Upper UTI
  2. Most commonly caused by an ascending lower UTI (usually E.coli)
  3. Can be caused by a bloodstream spread of infection e.g. sepsis
365
Q

What are the clinical features of acute pyelonephritis?

A
  1. Fever, rigors
  2. Loin pain
  3. Nausea and vomiting
  4. Symptoms of cystitis: dysuria, urinary frequency
366
Q

What are the differentiating features of a UTI and pyelonephritis?

A

Fever and loin pain (plus nausea and vomiting)

367
Q

What is the investigation of choice for acute pyelonephritis?

A

Mid-stream urine (MSU): before starting antibiotics

368
Q

What is the management of acute pyelonephritis?

A
  1. Consider hospital admission
  2. Local antibiotic guidelines
  3. BNF: broad spectrum cephalosporin or quinolone (for non-pregnant women) for 7-10 days
369
Q

What is a varicocele?

A

The abnormal enlargement of the testicular veins

370
Q

What are the causes of a varicocele?

A
  1. Increased hydrostatic pressure in the left renal vein
  2. Incompetent or congenitally absent valves
371
Q

What are the features of varicocele?

A
  1. Usually asymptomatic
  2. Classic: ‘bag of worms’
  3. Subfertility: fertility problems
372
Q

Which side are varicoceles more common on?

A

Left side (>80%)
Due to increased pressure in left renal vein

373
Q

What is an important complication of varicoceles?

A

Subfertility

374
Q

What are the investigations for a varicocele?

A
  1. Usually clinical diagnosis
  2. Scrotal ultrasound with colour flow doppler imaging: identification of varicocele
  3. Semen analysis: for infertile men with a varicocele (2 or 3 semen analyses are recommended)
375
Q

What is the management of a varicocele?

A
  1. Usually conservative
  2. Occasionally surgery is required if the patient has a lot of pain
376
Q

What is a vasectomy?

A
  1. A surgical procedure to seal the spermatic cords to permanently prevent pregnancy
  2. Also known as male sterilisation
377
Q

What form of sterilisation is more effective?

A

Male sterilisation: 99% effective for pregnancy prevention

378
Q

What type of anaesthetic can be used during a vasectomy?

A

Local

379
Q

What advice should couples receive regarding a vasectomy?

A
  1. Does not work immediately: should use a back-up contraception until 12 weeks post-op
  2. At 12 weeks, men should have a semen analysis to confirm success of operation
  3. Reversal is not routinely available
380
Q

What are the complications of a vasectomy?

A
  1. Bruising
  2. Haematoma
  3. Infection
  4. Sperm granuloma
  5. Chronic testicular pain (5-30%)
381
Q

What is the success rate of a vasectomy reversal?

A
  1. If done within 10 years = up to 55%
  2. If done after more than 10 years = 25%

!Final Year (26 decks)

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