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Sharon's Phase 2a Medicine Revision > Renal and Genitourinary > Flashcards

Renal and Genitourinary Flashcards

1
Q

What are the different classifications of Lower Urinary Tract Symptoms (LUTS)?

A

Storage:

  • Frequency
  • Urgency
  • Norturia
  • Incontinence

Voiding:

  • Slow stream
  • Splitting or spraying
  • Hesitancy
  • Terminal dribble

Post-micturition:

  • Post-micturition
    dribble
  • Feeling of
    incomplete emptying
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2
Q

Name the different types of incontinence

A

1) Urge incontinence - caused by overactivity of the detrusor muscle of the bladder (overactive bladder)

2) Stress incontinence - caused by weakness of the pelvic floor and sphincter muscles. This allows urine to leak at times of increased pressure on the bladder e.g. laughing

3) Mixed (urge and stress)

4) Overflow incontinence - occurs when there is chronic urinary retention due to an obstruction to the outflow of urine

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3
Q

Define nephrothialisis

A

Renal stones or calculi in the urinary tract. The majority are composed of calcium oxalate

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4
Q

What are the risk factors for developing renal stones?

A
  • Male sex - twice as likely
  • Dehydration
  • Previous kidney stone
  • Stone-forming foods: chocolate, nuts, teas are high in oxalate
  • Systemic disease: Crohn’s disease (calcium oxalate stones)
  • Kidney disease-related: AD polycystic kidney disease
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5
Q

What is the pathophysiology of renal stones?

A

Renal stones in the urinary tract cause characteristic loin to groin pain.

The renal colic pain is caused by the peristaltic action of the collecting system in the renal pelvis (where urine collects before going to ureters) against the stone.

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6
Q

What are the different types of renal stones?

A
  • Calcium oxalate (more common)
  • Calcium phosphate
  • Uric acid – these are not visible on x-ray
  • Struvite – produced by bacteria, therefore, associated with infection
  • Cystine – associated with cystinuria, an autosomal recessive disease
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7
Q

What symptoms might a patient with renal stones present with?

A
  • Classic loin to groin pain. Patients are usually in severe pain, writhing around and unable to find a comfortable position.
  • Pain occurs in spasms (periods with no pain or dull aches) and lasts mins to hours
  • Nausea and vomiting
  • Urinary urgency or frequency
  • Haematuria: microscopic or macroscopic
  • Fever: suggests a septic stone or pyelonephritis
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8
Q

What signs might a patient with renal stones present with?

A
  • Flank or renal-angle tenderness
  • Hypotension and tachycardia: may indicate urosepsis / a septic stone
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9
Q

What investigations/tests are used to diagnose renal stones?

A
  • Gold standard is non-contrast CT kidney, ureter, bladder (CT KUB): shows renal calcification
  • Urinalysis (dipstick): microscopic haematuria +/- pyuria (pus) + elevated WBCs and CRP suggest pyelonephritis
  • U&Es: raised creatinine suggests AKI due to obstruction
  • Hypercalcaemia - underlying cause
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10
Q

What is an important DDx for new-onset severe flank pain?

A

Ruptured abdominal aortic aneurysm, particularly in elderly males with new-onset flank pain and no history of stones.

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11
Q

What is the acute management plan for renal stones?

A
  • IV fluids and anti-emetics
  • Analgesia: an NSAID by any route is considered first-line
  • PR diclofenac commonly used in clinical practice but increased risk of CV events
  • IV paracetamol is used if NSAIDs are contraindicated or ineffective.
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12
Q

What are the conservative and medical management for renal stones?

A

Conservative or medical management:

  • Analgesia: intramuscular diclofenac
  • Watchful waiting: stones <5mm should pass spontaneously and followed up in clinic
  • Alpha-blockers, e.g. tamsulosin to help spontaneous passage of stones
  • Surgery - stones > 10mm
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13
Q

What are the surgical treatment options for renal stones?

A

Surgical management is used when pain is ongoing, or the stone is unlikely to pass on its own.

Ureteroscopy (URS): a ureteroscope is passed through the urethra and bladder up to the ureter (retrograde) and retrieves the stone or fragments it with intracorporeal lithotripsy.

Extracorporeal shock wave lithotripsy (ESWL): high energy sound waves break the stone into tiny fragments. Contraindicated in pregnancy, use URS instead.

Percutaneous nephrolithotomy (PCNL): surgical incision to access the renal collecting system in the back for intracorporeal lithotripsy or stone fragmentation

Ureteral stenting: insertion of a plastic tube to assist drainage, left in for ~ 4 weeks

Percutaneous nephrostomy: insertion of a rubber tube into the kidney via the skin to drain urine and decompress the urinary tract (usually under local anaesthetic)

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14
Q

Define acute kidney injury (AKI)

A

Acute kidney injury (AKI) describes an acute reduction in renal function following an insult to the kidneys.

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15
Q

What is the pathophysiology of AKI?

A

The damage from an AKI occurs due to the inability to remove toxins and regulate bodily functions (such as acid-base balance).

Therefore, hyperkalemia, accumulation of fluid (causing pulmonary +/- peripheral oedema), H+ ions (causing acidosis) and urea (causing uraemia).

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16
Q

What is the aetiology of AKI?

A

Causes are divided into:

  • Pre-renal
  • Renal
  • Post-renal
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17
Q

What are some pre-renal causes of AKI?

A
  • Hypovolaemia (e.g. cannot maintain oral intake, haemorrhage, gastrointestinal losses, renal losses, burns)
  • Reduced cardiac output (e.g. organ failure (cardiac/liver failure), sepsis, drugs)
  • Drugs that reduce blood pressure, circulating volume, or renal blood flow
  • Sepsis
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18
Q

What are some renal causes of AKI?

A
  • Toxins and drugs (e.g. antibiotics - aminoglycosides, contrast, chemotherapy - cisplatin)
  • Vascular causes (e.g. vasculitis, thromboembolism)
  • Glomerulonephritis
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19
Q

What are some post-renal causes of AKI?

A

Obstruction to the urinary tract from:

Renal stones

Blocked urinary catheter

Enlarged prostate

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20
Q

What are the risk factors for developing AKI?

A
  • Increasing age: >65 years old
  • Chronic kidney disease (CKD): underlying CKD
  • Sepsis: leading to reduced kidney perfusion and pre-renal AKI
  • Organ failure: e.g. heart failure and liver failure
  • Diabetes mellitus
  • Nephrotoxic drugs: NSAIDs, ACE inhibitors, angiotensin II receptor antagonists (ARBs) - should be stopped
  • Iodine-based contrast media: if used within the last week
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21
Q

What medications should be stopped in a patient with AKI?

A

Nephrotoxic drugs: DAMN

D - Diuretic (potassium-sparing e.g. spironolactone)
A - angiotensin-converting enzyme (ACE) inhibitors + Angiotensin II receptor antagonists (ARBs)
M - aMinoglycosides (e.g. gentamicin)
N - NSAIDs

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22
Q

What signs and symptoms might a patient with AKI present with?

A

Presentation depends on the underlying cause:

Symptoms:

  • Reduced urine output
  • Cola-coloured urine (rhabdomyolysis)
  • Confusion or drowsiness
  • Dyspnoea +/- swollen legs
  • Suprapubic pain: e.g. if caused by urinary retention
  • Haematuria: e.g. if caused by glomerulonephritis

Signs:

  • Hypovolaemia
  • Uraemic skin changes: e.g. uraemic frost if severe (urea crystals on skin)
  • Volume overload (due to obstructive AKI):
    bibasal crackles (sound at lung base), raised JVP and peripheral oedema
  • Palpable bladder
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23
Q

What is the Kidney Disease: Improving Global Outcomes (KDIGO) definition of AKI?

A

Classification system for AKI:

  • Increase in serum creatinine by ≥26 micromol/L within 48 hours

OR

  • Increase in serum creatinine ≥ x 1.5 baseline within last 7 days
  • Urine volume <0.5 mL/kg/hour for 6 hours
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24
Q

KDIGO severity criteria: what is stage 1 AKI?

A
  • Rise in creatinine to 1.5-1.9 times baseline, or
  • Rise in creatinine by ≥26.5 µmol/L, or
  • Fall in urine output to <0.5 mL/kg/hour for ≥ 6 hours
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25
Q

KDIGO severity criteria: what is stage 2 AKI?

A
  • Rise in creatinine to 2.0 to 2.9 times baseline, or
  • Fall in urine output to <0.5 mL/kg/hour for ≥12 hours
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26
Q

KDIGO severity criteria: what is stage 3 AKI?

A
  • Rise in creatinine to ≥ 3.0 times baseline, or
  • Rise in creatinine to ≥353.6 µmol/L or
  • Fall in urine output to <0.3 mL/kg/hour for ≥24 hours
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27
Q

What investigations/tests are used to diagnose AKI?

A

Investigations aim to establish underlying cause.

Primary investigations:

  • Urea and electrolytes: to confirm the diagnosis and check serum potassium (hyperkalemia)
  • Full blood count and CRP: establishes infection
  • Venous blood gas: particularly to assess for metabolic acidosis
  • Chest X-ray: to investigate for pulmonary oedema
  • Ultrasound urinary tract: to investigate for obstruction or hydronephrosis
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28
Q

What is the first-line treatment for AKI?

A

Mainly supportive, depends on the underlying cause.

  • Treat complications: such as hyperkalemia
  • IV fluids: to rehydrate the patient
  • Abx if infection/sepsis, stop offending drug, remove the obstruction.
  • Loop diuretics not recommended, only when the patient is significantly overloaded
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29
Q

What is the second-line treatment for AKI?

A

Renal-replacement therapy (dialysis or transplant): when medical treatment fails, indicated in the following events:

  • Hyperkalaemia refractory to medical management
  • Severe metabolic acidosis refractory to medical management
  • Volume overload refractory to diuretic agents
  • Uraemic manifestations such as encephalopathy or pericarditis
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30
Q

When would a patient with AKI need to be referred to a nephrologist?

A
  • Severe AKI requiring renal-replacement therapy
  • AKI due to severe underlying processes such as vasculitis, glomerulonephritis, myeloma
  • Patients who already have CKD stage 4 or 5
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31
Q

Define chronic kidney disease (CKD)

A

Chronic kidney disease (CKD) describes a progressive deterioration in renal function.

NICE defines CKD as abnormalities of kidney function or structure present for more than 3 months:

  • Markers of kidney damage
  • GFR <60 on at least 2 separate occasions at least 90 days apart (+/- markers of kidney damage)
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32
Q

What is the aetiology of CKD?

A
  • Diabetes (most common)
  • Hypertension (second most common)
  • Medications such as NSAIDS, proton pump inhibitors and lithium
  • Age-related decline
  • Glomerulonephritis
  • Polycystic kidney disease
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33
Q

What are the different stages of CKD?

A

Stage and eGFR (ml/min/1.73m2 )

Stage 1: ≥ 90: not considered CKD unless evidence of renal damage* = Normal and high

Stage 2: 60 - 89: not considered CKD unless evidence of renal damage*

3A: 45 - 59: Mild to moderate reduction

3B: 30 - 44: Moderate to severe reduction

4: 15 - 29: Severe reduction

5: < 15: dialysis or renal transplantation may be required: End-stage kidney failure

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34
Q

What are the risk factors for developing CKD?

A
  • Increasing age: Natural decline in kidney function > 50
  • Afro-Caribbean
  • Diabetes mellitus
  • Hypertension
  • Autoimmune conditions: e.g. SLE
  • Glomerulonephritis
  • Nephrotoxic drugs: e.g. NSAIDs
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35
Q

What signs and symptoms might a patient with CKD present with?

A

Non-specific and usually as a result of toxic waste product build-up.

Symptoms:

  • Lethargy
  • Pruritus
  • Frothy urine
  • Swollen ankles

Signs:

  • Hypertension
  • Fluid overload
  • Uraemic sallow: a yellow or pale brown colour to the skin
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36
Q

How is CKD classified?

A

Stages 1 -5, based on estimated glomerular filtration rate (eGFR - ml/min/1.73m2)

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37
Q

Why are eGFR and serum creatinine used as markers of renal function?

A

Serum creatinine is a waste product of muscles, removed by the kidneys with little or no tubular reabsorption, therefore, raised levels in patients with deranged kidney function.

However, not reliable on its own, as it can be affected by age, the difference in muscle mass etc.

So the Modification of Diet in Renal Disease (MDRD) formula incorporates:

  • Serum creatinine
  • Age
  • Gender
  • Ethnicity

to calculate the eGFR

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38
Q

What investigations/tests are used to diagnose CKD?

A

Primary investigations:

  • Urine dip: screen for proteinuria and haematuria
  • Urine albumin: creatinine ratio (ACR): >3 mg/mmol is clinically significant proteinuria
  • U&Es: serum creatinine (elevated) and eGFR (<60) - 2 tests 90 days apart to confirm the diagnosis
  • FBC: anaemia of chronic disease
  • Renal ultrasound: bilateral kidney atrophy in CKD
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39
Q

What is the management plan for CKD regarding lifestyle changes?

A
  • Smoking cessation, exercise, drinking alcohol in moderation
  • Avoid nephrotoxic medications, e.g. NSAIDs
  • Diet: low salt and potassium diets, with fluid restriction if there is evidence of overload
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40
Q

What is the management plan for CKD?

A

Treat complications:

  • CKD-mineral bone disease - CKD causes hypocalcemia, so aim to reduce serum phosphate and PTH levels.
  • 1st line: dietary reduction of phosphate (e.g. meat)
  • Vitamin D replacement (early stage)

CVD:

  • Hypertension - 1st line is ACEi e.g. ramipril
  • Hypercholestrolimia - statins (atorvastatin)
  • Antiplatelet - for secondary prevention

Anaemia:

  • 1st line is Iron replacement: oral or IV

Renal replacement therapy:

  • When eGFR indicates CKD stage 5
  • Dialysis then kidney transplant if patient eligible
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41
Q

What complications can arise from CKD?

A

Cardiovascular disease - leading cause of death in CKD

  • Heart failure: due to fluid overload and anaemia

MSK:

  • CKD-metabolic bone disease

Endocrine:

  • Secondary hyperparathyroidism > tertiary hyperparathyroidism
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42
Q

Define pyelonephritis

A

Infectious inflammation of the kidneys, affecting the renal pelvis (joint between kidney and ureter) and renal parenchyma (tissues).

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43
Q

What microorganisms most commonly cause pyelonephritis?

A

Gram-negative bacteria

  • E.coli accounts for 60 - 80% of uncomplicated infections
  • Klebsiella species (20%)
  • Proteus mirabilis (15%)

The infection typically spreads to the kidney via the ascending lower urinary tract infection, can be haematogenous spread in septic patients

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44
Q

What is the difference between uncomplicated and complicated pyelonephritis?

A

Pyelonephritis is considered uncomplicated if the patient is:

  • non-pregnant, pre-menopausal women with no known relevant urological abnormalities or comorbidities

Pyelonephritis is considered complicated if the patient is/has:

  • Pregnant
  • Uncontrolled diabetes
  • Kidney transplants
  • Acute or chronic kidney failure
  • Immunocompromised
  • Hospital-acquired bacterial infections
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45
Q

What are the risk factors for developing pyelonephritis?

A
  • Women 6x more likely to develop pyelonephritis
  • Urinary tract infection
  • Uncontrolled diabetes mellitus: glucosuria provides bacteria with a source of energy
  • Urinary tract outlet obstruction
  • Immunocompromised patients
  • Pregnancy: increased chance of urinary tract infection
  • End-stage renal failure (ESRF)
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46
Q

What signs and symptoms might a patient with pyelonephritis present with?

A

Symptoms:

  • Flank pain
  • Myalgia
  • Dysuria (painful urination)
  • Haematuria
  • Confusion

Signs:

  • Renal angle tenderness
  • Fever
  • Tachycardia
  • Hypotension
  • Altered mental state
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47
Q

What investigations/tests are used to diagnose pyelonephritis?

A

1st line: urine dipstick - shows signs of infection, including nitrites, leukocytes and blood.

Gold standard: midstream urine (MSU) - microscopy, culture and sensitivity testing to establish the causative organism. Before abx.

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48
Q

What is the management plan for pyelonephritis?

A

Oral antibiotics (mild disease not requiring hospitalisation):

  • Cefalexin: 7-10 days
  • Ciprofloxacin: 7 days

Intravenous antibiotics (severe disease/sepsis):

  • Gentamicin
  • Ciprofloxacin

Adjuvant therapy:

  • Hydration: oral or IV
  • Analgesia: diclofenac PR effective for renal angle tenderness
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49
Q

What is the management plan if a patient with pyeloneprontis presents with sepsis?

A

For septic patients, follow the sepsis six pathway!

Three tests and three treatments.

Three tests:

  • Blood lactate level
  • Blood cultures
  • Urine output

Three treatments:

  • Oxygen - 94-98% (or 88-92% in COPD)
  • Empirical broad-spectrum IV antibiotics
  • IV fluids
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50
Q

What complications can arise from pyelonephritis?

A
  • Sepsis
  • Parenchymal renal scarring from frequent infections (normally in chronic pyelonephritis)
  • Recurrent urinary tract infections
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51
Q

What is chronic pyelonephritis?

A

Chronic pyelonephritis presents with recurrent kidney infection > scarring of the renal parenchyma > CKD > end-stage renal failure

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52
Q

Define lower urinary tract infection (cystitis)

A

Infection of the bladder, usually caused by bacteria from the gastrointestinal tract ascending through the urethra into the bladder (retrograde).

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53
Q

What is the aetiology of cystitis?

A

The 5 most common pathogens can be remembered with KEEPS:

  • Klebsiella
  • E coli- most common causing 70 - 95% of cases
  • Enterococci
  • Proteus
  • Staphylococcus coagulase negative
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54
Q

What are the risk factors for developing cystitis?

A
  • Female sex: the urethra is much shorter and closer to the anus
  • Post-menopause: the absence of oestrogen is a risk factor for UTIs

Recurrent UTI:

In young and pre-menopausal women:

  • Sexual intercourse
  • A mother with a history of UTI
  • History of UTI in childhood

In elderly and post-menopausal women:

  • History of UTI before menopause
  • Urinary incontinence
  • Catheterisation
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55
Q

What signs and symptoms might a patient with cystitis present with?

A

Symptoms:

  • Dysuria: painful or uncomfortable urination
  • Frequency: passing urine more often than usual
  • Urgency: a strong desire to urinate, which may result in urinary incontinence

Changes in urine appearance/consistency:

  • A cloudy or pungent odour
  • Haematuria

Suprapubic discomfort

Signs:

Suprapubic tenderness

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56
Q

The typical symptoms and signs of cystitis might not be present in elderly women with underlying cognitive impairment. What signs and symptoms might these patients have?

A
  • Delirium, lethargy, reduced appetite
  • Delirium or confusion once other sources of infection have been excluded (e.g. lower respiratory tract infection)
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57
Q

What investigations/tests are used to diagnose cystitis?

A

1st line: urine dipstick: positive nitrite OR leukocyte, AND positive RBCs: UTI is likely

Negative nitrite AND positive leukocyte: UTI is equally likely to other diagnoses

Gold standard: urine microscopy, culture and sensitivity (MC&S)

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58
Q

What is the management plan for non-pregnant women patients with cystitis?

A

1st line: nitrofurantoin (if eGFR ≥45ml/minute), or trimethoprim

3 days course

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59
Q

What is the management plan for pregnant patients with cystitis?

A

1st line: nitrofurantoin (if eGFR ≥45ml/minute; avoid near term)

2nd line: if no improvement within 48 hours or if first-line is unsuitable

Amoxicillin (only if culture results are available and susceptible), or Cefalexin

7 day course

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60
Q

What is the management plan for pregnant patients with cystitis?

A

1st line: nitrofurantoin (if eGFR ≥45ml/minute; avoid near term)

2nd line: if no improvement within 48 hours or if first-line is unsuitable

Amoxicillin (only if culture results are available and susceptible), or Cefalexin

7-day course

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61
Q

What is the management plan for men with cystitis?

A

Be aware that cystitis in men is more likely due to an underlying cause.

1st line: trimethoprim, or nitrofurantoin (if eGFR ≥45ml/minute)

7-day course

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62
Q

Define urethritis

A

Urethritis is inflammation of the urethra with/without infection.

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63
Q

What are the 2 categories of urethritis?

A
  • Gonococcal - caused by Neisseria gonorrhoeae
  • Non-gonococcal (NGU) - commonly caused by Chlamydia trachomatis and Mycoplasma genitalium
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64
Q

What are the risk factors for developing urethritis?

A
  • Age 15 to 24 years
  • Female sex
  • Men who have sex with men
  • Low socio-economic status
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65
Q

What signs and symptoms might a patient with urethritis present with?

A
  • Dysuria +/- urethral discharge (blood/pus)
  • Urethral pain
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66
Q

What investigations/tests are used to diagnose urethritis?

A
  • 1st line: nucleic acid amplification test (NAAT) - most sensitive test to detect gonorrhoea. Also recommended for chlamydial infection and mycoplasma genitalium
  • Gram stain of urethral discharge: to check for the presence of gonorrhoeal infection (gram-negative)
  • Culture of urethral discharge - positive for the causative organism
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67
Q

What is the management plan for urethritis?

A

NG - IM ceftriaxone/IM gentamicin + azithromycin

CT - azithromycin or doxycycline

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68
Q

What condition is urethritis commonly present in?

A

Reactive arthritis

  • Can’t see - conjuctivitis
  • Cant pee - urethritis
  • Can’t climb a tree - arthritis
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69
Q

Define epididymo-orchitis

A

Inflammation of the epididymis is referred to as epididymitis, whilst orchitis is inflammation of the testicle. The two may co-exist, and this is referred to as epididymo-orchitis.

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70
Q

What is the aetiology of epididymo-orchitis?

A

Sexually active males - STI microorganisms most common cause

  • Chlamydia trachomatis, Neisseria gonorrhoeae, and Mycoplasma genitalium
  • In older males, enteric pathogens most commonly cause epididymo-orchitis e.g. E.coli
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71
Q

What are the risk factors for developing epididymo-orchitis?

A
  • STI-related: young, multiple partners, unprotected sex
  • Enteric-related: elderly, bladder outflow obstruction, catherisation
  • Tuberculosis: can cause epididymo-orchitis
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72
Q

What signs and symptoms might a patient with epididymo-orchitis present with?

A

Symptoms:

  • Unilateral tender, red, and swollen testicle
  • Pain develops over a few days, torsion must always be ruled out
  • Lower urinary tract symptoms e.g. dysuria
  • Pyrexia +/-

Signs:

  • Cremasteric reflex (scrotum shrinks when the inner thigh is stroked due to contraction of cremasteric muscle) preserved (unlike torsion)
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73
Q

What DDx could cause the patient to have unilateral tender, red, and swollen testicles?

A

Testicular torsion

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74
Q

What investigations/tests are used to diagnose epididymo-orchitis?

A
  • Urinalysis using gram-staining: first void sample is most useful and should be sent for microscopy and culture. Detects presence/absence of gonococcal infection
  • Nucleic Acid Amplification Test (NAAT): first void urine sample for NAAT to detect the DNA/RNA of the causative organism
  • A swab of urethral secretions: less sensitive than NAAT but must also be performed in symptomatic men
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75
Q

What is the management plan for epididymo-orchitis?

A

Patients should be treated empirically without waiting for test results.

First-line for STI:

  • Empirical: ceftriaxone 500 mg IM single dose
    and doxycycline for 10-14 days
  • Additional management: no sex until review and partner notification to confirm STI causing epididymo-orchitis

First-line for enteric organisms:

  • Empirical: fluoroquinolone e.g. Ofloxacin or ciprofloxacin for 10-14 days

.

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76
Q

Define prostatitis

A

Prostatitis refers to inflammation of the prostate. It can be classed as:

  • Acute bacterial prostatitis – presents with a more rapid onset of symptoms
  • Chronic prostatitis – symptoms lasting for at least 3 months
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77
Q

How is chronic prostatitis further subdivided?

A
  • Chronic prostatitis or chronic pelvic pain syndrome (no infection)
  • Chronic bacterial prostatitis (infection)
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78
Q

What signs and symptoms might a patient with acute prostatitis present with?

A
  • Pelvic pain
  • Lower urinary tract symptoms, such as dysuria, hesitancy, frequency and retention
  • Sexual dysfunction, such as erectile dysfunction, pain on ejaculation and haematospermia
  • Systemic symptoms of infection: fever, myalgia, fatigue

Signs

  • Tender and enlarged prostate on examination (although examination may be normal)
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79
Q

What signs and symptoms might a patient with chronic prostatitis present with?

A

Symptoms present for at least 3 months:

  • Pelvic pain
  • Lower urinary tract symptoms, such as dysuria, hesitancy, frequency and retention
  • Sexual dysfunction, such as erectile dysfunction, pain on ejaculation and haematospermia (blood in the semen)
  • Pain with bowel movements
  • Systemic symptoms: fever, myalgia
  • Tender and enlarged prostate on examination (although examination may be normal)
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80
Q

What investigations/tests are used to diagnose prostatitis?

A
  • Urine dipstick testing can confirm evidence of infection.
  • Urine microscopy, culture and sensitivities (MC&S) can identify the causative organism and the antibiotic sensitivities.
  • Chlamydia and gonorrhoea NAAT testing on first pass urine, if STI
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81
Q

What is the management plan for acute prostatitis?

A
  • Hospital admission for systemically unwell or septic patients (for bloods, blood cultures and IV antibiotics)
  • Oral antibiotics, typically for 2-4 weeks (e.g., ciprofloxacin, ofloxacin or trimethoprim)
  • Analgesia (paracetamol or NSAIDs)
  • Laxatives for pain during bowel movements
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82
Q

What is the management plan for chronic prostatitis?

A
  • Alpha-blockers (e.g., tamsulosin) relax smooth muscle
  • Analgesia (paracetamol or NSAIDs)
  • Psychological treatment, where indicated (e.g., CBT and/or antidepressants)
  • Antibiotics if a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
  • Laxatives for pain during bowel movements
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83
Q

What is an uncomplicated UTI (lower urinary tract)?

A

UTI caused by typical pathogens in people with a normal urinary tract and kidney function and no predisposing co-morbidities.

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84
Q

What is a complicated UTI (lower urinary tract)?

A

UTI with an increased likelihood of complications such as persistent infection, treatment failure and recurrent infection.

Risk factors:

  • Structural abnormalities of the urinary tract
  • Urinary catheters
  • Virulent or atypical infecting organisms
  • Co-morbidities such as poorly controlled diabetes mellitus or immunosuppression
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85
Q

Define nephritic syndrome

A

This is a syndrome fitting a clinical picture of inflammation within the kidney.

Characterised by:

  • Haematuria- reflects inflammation of the kidney. Nephritic syndrome is dominated by haematuria
  • Oliguria (urine output < 400ml a day)- due to reduced GFR
  • Hypertension – due to fluid overload
86
Q

What are some causes of nephritic syndrome?

A

Systemic causes:

  • Systemic lupus erythematosus
  • Post strep glomerulonephritis
  • Goodpasture’s/anti-GBM (glomerular basement membrane) disease

Renal causes:

  • IgA nephropathy
87
Q

What are the general investigations/tests used to diagnose nephritic syndrome?

A

The diagnostic test for the cause of nephritic syndrome is a kidney biopsy

Urinalysis- shows haematuria in nephritic syndrome

Bloods- elevated ESR and CRP in inflammation. Anaemia might be present to reflect systemic disease

88
Q

What is the general management plan for nephritic syndrome?

A
  • Treat underlying cause
  • Blood pressure control- ACE-I/ARB - anti-hypertensive and anti-proteinuric
  • This reduces proteinuria and preserves renal function
  • Corticosteroids- this is to reduce the inflammation causing damage to the kidney
89
Q

Define IgA nephropathy (Berger’s disease)

A

Most common primary glomerulonephritis worldwide.

Characterised by the presence of IgA immune complexes in the mesangium of the glomerulus, resulting in nephritic syndrome and progressing to end-stage renal disease (ESRD) over many decades if untreated.

90
Q

What is the pathophysiology of IgA nephropathy?

A

Type 3 hypersensitivity reaction.

The deposition of IgA immune complexes in the mesangium causes glomerulonephritis.

Activation of complement pathway > glomerular injury

Episodes usually occur after an infection of the mucosal lining e.g. upper respiratory tract infection (URTI).

Likely due to increased IgA >
subsequent IgG recognition and deposition in the kidneys

91
Q

What signs and symptoms might a patient with IgA nephropathy present with?

A

Symptoms:

  • Pink, red or “coke” tinged urine (haematuria)
  • Foamy urine (proteinuria)
  • Sore throat: suggests a URTI as a recent trigger (common)

Signs:

  • Haematuria
  • Oedema: due to proteinuria
  • Cervical lymphadenopathy: suggests an URTI as a recent trigger
  • Hypertension
92
Q

What investigations/tests are used to diagnose IgA nephropathy?

A
  • Urine dipstick: blood and protein would be expected
  • U&Es: allows the assessment of baseline renal function, as well as monitoring for deterioration
  • C3 and C4 complement levels - normal (excludes other immune complex nephropathies)
  • Renal biopsy: definitive diagnostic investigation; demonstrates mesangial hypercellularity with positive immunofluorescence for IgA
93
Q

What is the management plan for IgA nephropathy?

A

Aim to prevent further deterioration of renal function:

  • 1st line: ACE-inhibitor/ARB (anti-hypertensive and anti-proteinuric)
  • Statins: control of high cholesterol has been shown to slow kidney damage
94
Q

Define lupus nephritis (SLE nephropathy)

A

A severe manifestation of SLE, which is a type 3 hypersensitivity reaction.

Deposition of antibody-antigen complexes in the kidneys can lead to lupus nephritis. This can result in end-stage kidney disease.

Diffuse proliferative glomerulonephritis is the most common form of lupus nephritis.

95
Q

What are the risk factors for developing lupus nephritis?

A

It will share risk factors with SLE as it develops secondary to SLE

  • Middle-aged: peak onset: 15 and 45 years old
  • Female gender: SLE is 12 times more common in females
  • African and Afro-Caribbean: SLE is more common and more severe in these patients
  • Family history
96
Q

What signs and symptoms might a patient with lupus nephritis present with?

A
  • Diffuse proliferative glomerulonephritis presents with nephritic syndrome:
  • Haematuria
  • Hypertension
  • Oedema.

Non-specific symptoms of renal impairment include:

  • Lethargy
  • Features of SLE - MSK pain, “butterfly” rash
97
Q

How is lupus nephritis classified?

A

It is classified and sub-divided by renal biopsy findings:

Class I = minimal mesangial = normal renal function. Mild or incidental

Class II = Mesangial proliferative = usually presents with microscopic haematuria +/- proteinuria > steroids.

Class III = focal segmental = usually presents with nephrotic syndrome > high-dose steroids

Class IV = diffuse proliferative = the most common and severe form > nephritic syndrome > steroids and immunosuppressants.

Class V = diffuse membranous > presents with nephrotic syndrome: extreme oedema
and +/- hypertension

Class VI = sclerosing = slowly progressive renal failure with proteinuria.

98
Q

What is the investigations/tests carried out for patients with suspected lupus nephritis?

A
  • Urinalysis: haematuria and proteinuria
  • U&Es: reduced eGFR as renal failure progresses
  • Renal USS: exclude structural pathology
  • Renal biopsy: gold-standard investigation shows hypercellular glomerulus, thickened basement membrane, “wired-loop” thickened capillary walls in severe disease
99
Q

What is the treatment/management plan for lupus nephritis?

A

Lifestyle: stop smoking, exercise

Medical management:

  • Corticosteroids
  • Immunosuppressive agents: such as cyclophosphamide or azathioprine
  • Hydroxychloroquine
  • Dialysis then kidney transplant: if eGFR continues to deteriorate
  • ACE inhibitor: preferred for patients with hypertension
100
Q

Define post-streptococcal glomerulonephritis (PSGN)

A

PSGN is the inflammation of the glomeruli (where filtering occurs in the kidneys) after infection by streptococcal bacteria - usually arises ~2 weeks after infection.

101
Q

Which type of streptococcal bacteria cause PSGN?

A

Group A beta-haemolytic streptococci - the specific antigen on the bacteria classifies it into “group A”.

Beta-haemolytic because the bacteria produce an enzyme called streptolysin break down (lysis) RBCs on a petri dish

102
Q

What. is the pathophysiology of PSGN?

A

Strep infection triggers type III hypersensitivity reaction

  • Immune complexes composed of antigens and antibodies (usually IgG or IgM) > travels in the bloodstream to the glomerulus > deposits end up in the glomerular basement membrane (GBM)

or

  • Bacterial antigens are first trapped in the glomeruli, and then antibodies there
  • Activation of C3 complement, inflammatory cytokines, oxidants, and proteases > podocyte damage
  • Kidney injury > allows larger molecules into urine e.g. RBCs, proteins > haematuria and proteinuria
  • Haematuria = cola/dark-coloured urine
103
Q

What signs and symptoms might a patient with PSGN present with?

A

General nephritic syndrome symptoms:

  • Haematuria
  • Oliguria
  • Oedema
  • Hypertension

Other symptoms:

  • Fever
  • Malaise
  • Anorexia
  • Headach
104
Q

What investigations/tests are used to diagnose PSGN?

A

Kidney biopsy - glomerulus looks enlarged and hypercellular under light microscopy, subepithelial deposits “humps” under EM

Urinanalysis - proteinurina and haemotauria

Immunofluorescence - immune complexes give a starry sky granular appearance along GBM

FBC - normochromic, normocytic anaemia associated with systemic disease

eGFR - normal or reduced

Blood tests - show antibodies against group A streptococcus—called anti-DNase B, and decreased complement levels (C3 and CH50)

105
Q

What is the management plan for PSGN?

A
  • Usually affects children and self-limiting so supportive management
  • Sometimes oral antibiotics are given
106
Q

What complications can arise from PSGN?

A

Rare, but some children might develop renal failure

25% of adults might develop rapidly-progressing glomerulonephritis > renal failure

107
Q

Define Goodpasture’s disease

A

Goodpasture’s disease, also known as anti-glomerular basement membrane antibody (anti-GBM) disease, is caused by an autoantibody to the alpha-3 chain of type IV collagen. Usually found in basement membranes of alveoli and glomeruli.

Goodpature’s disease is an important cause of pulmonary-renal syndrome, which consists of glomerulonephritis and pulmonary haemorrhage.

A nephritic syndrome

108
Q

What is the aetiology of Goodpasture’s disease?

A

Autoimmune disease caused by autoantibodies against the alpha-3 chain of type IV collagen - causing glomerular injury.

109
Q

What signs and symptoms might a patient with Goodpasture’s disease present with?

A
  • Reduced urine output (renal damage)
  • Haemoptysis (coughing up blood) (respiratory damage)
  • Oedema (renal damage)
  • SOB (respiratory damage)
  • Cough and fever might also be present
110
Q

What investigations/tests are used to diagnose Goodpasture’s disease?

A
  • Definitive diagnostic test - anti-GBM antibodies in bloods and biopsy
  • Renal biopsy - when viewed with immunofluorescence, characteristic linear IgG staining seen
111
Q

What is the management plan for Goodpasture’s disease?

A
  • Plasma exchange - removes pathogenic anti-GBM antibodies
  • Corticosteroids (i.e. steriods)
  • Cyclophosphamide (for immune suppression)
112
Q

What is a complication that can arise from Goodpasture’s disease?

A

Rare, but Goodpasture’s disease can lead to rapidly progressing glomerulonephritis, which can cause renal failure within days/weeks

113
Q

Define nephrotic syndrome

A

Nephrotic syndrome occurs when the glomerular basement membrane becomes highly permeable to protein, allowing protein to leak from the blood to urine.

This results in the triad characterising nephrotic syndrome:

  • Proteinuria (>3.5 g/24 hours) - nephrotic syndrome is dominated by proteinuria
  • Hypoalbuminaemia (<30 g/L) - due to loss of albumin in the urine
  • Peripheral oedema - loss of oncotic pressure. This can be rapid and severe
114
Q

Apart from the classic triad of proteinuria, hypoalbuminaemia and oedema, what other signs might be present in nephrotic syndrome?

A
  • Hyperlipidaemia - the liver increases the synthesis of lipids in response to low albumin
  • Hypogammaglobulinemia: due to loss of immunoglobulin in the urine
  • Hypercoagulability: due to loss of anticoagulation factors in the urine
115
Q

What is the aetiology of nephrotic syndrome?

A

It is caused by a number of primary and secondary diseases, including:

  • Minimal change disease - most common in children
  • Focal segmental glomerulosclerosis (FSGS) - most common in adults
  • Membranous nephropathy - most common in the elderly
116
Q

What general signs and symptoms might a patient with nephrotic syndrome present with?

A

The signs and symptoms depend on the exact underlying cause but some general signs and symptoms include:

Symptoms:

  • Frothy urine
  • Facial and peripheral oedema
  • Proteinuria
  • Recurrent infections: due to hypogammaglobulinemia (low Ig levels)

Signs:

Limited or absent haematuria (differentiates it from nephritic syndrome in which haematuria dominates)

117
Q

What investigations/tests are used to diagnose nephrotic syndrome?

A

Primary investigations:

  • Urinalysis: proteinuria predominates over haematuria; lipid casts
  • 24-hour urine protein collection: > 3.5 g protein
  • Urine albumin-creatinine ratio (ACR): raised due to proteinuria
  • U&Es: monitor eGFR and creatinine to assess for renal failure
  • LFTs: hypoalbuminemia < 25 g/L
  • Lipid profile: hypercholesterolaemia
118
Q

What investigations/tests are used to diagnose nephrotic syndrome?

A

Primary investigations:

Urinalysis: proteinuria predominates over haematuria; lipid casts
24-hour urine protein collection: > 3.5 g protein

  • Urine albumin-creatinine ratio (ACR): raised due to proteinuria
  • U&Es: monitor eGFR and creatinine to assess for renal failure
  • LFTs: hypoalbuminemia < 25 g/L
  • Lipid profile: hypercholesterolaemia and hypertriglyceridemia
  • Renal ultrasound: exclude structural pathology
119
Q

What are the basic principles when managing nephrotic syndrome?

A

The management varies between different causes of nephrotic syndrome. Below are the basic principles:

Lifestyle

  • Low salt, protein and fat diet
  • Improve cardiovascular risk factors

Corticosteroids and immunosuppressants:

  • Minimal change disease: very responsive to steroids
  • FSGS: response to steroids is variable
  • Ciclosporin may be used in steroid-resistant case
  • Membranous nephropathy: corticosteroids are combined with an immunosuppressant; cyclophosphamide first-line

Adjunctive therapies

  • Diuretics: symptomatic relief of fluid overload
  • ACE inhibitor: used to reduce proteinuria
120
Q

Nephrotic syndrome: what would be the biopsy findings in minimal change disease?

A

Light microscopy: normal glomeruli on light microscopy

Electron microscopy (EM): effacement of podocyte foot processes (flattened out due to damage)

121
Q

Nephrotic syndrome: what would be the biopsy findings in focal segmental glomerulosclerosis (FSGS)?

A
  • Light microscopy: focal and segmental glomerular sclerosis (scar tissue)
  • EM: effacement of foot processes
122
Q

Nephrotic syndrome: what would be the biopsy findings in membranous nephropathy?

A
  • Light microscopy: thick glomerular basement membrane
  • EM: subepithelial immune complex deposition (spike and dome pattern)
123
Q

What diseases are minimal change disease associated with?

A
  • My be preceded by upper respiratory tract infection
  • Associated with Hodgkin lymphoma
124
Q

What conditions are focal segmental glomerulosclerosis associated with?

A
  • HIV
  • Heroin use
  • Sickle cell disease
  • SLE
125
Q

What conditions are membranous nephropathy associated with?

A
  • Malignancy
  • Hepatitis B
  • NSAIDs
  • SLE
126
Q

What conditions are membranous nephropathy associated with?

A
  • Malignancy
  • Hepatitis B
  • NSAIDs
  • SLE
127
Q

What is the treatment for minimal change disease?

A
  • Lifestyle: low salt diet + fluid restriction
  • 1st line is corticosteroids: very responsive to steroids, with a 90% response rate
  • Corticosteroids + Immunosuppressant (e.g. cyclophosphamide) for frequent relapses
  • Adjuvant therapies: diuretics (furosemide) for symptomatic relief of fluid overload
128
Q

What is the treatment for focal segmental glomerulosclerosis?

A

Lifestyle

  • Low salt and fat diet - as sodium can block the effects of ACEi or ARB, and patients can have hyperlipidemia
  • Weight loss can decrease proteinuria in obese patients
  • 1st line: ACE inhibitors (preferred) or ARB as they are anti-hypertensive and reduce proteinuria
  • Treat underlying cause if secondary FSGS
  • Diretics e.g. furosemide for oedema
  • The response variable,~50% achieving remission.
129
Q

What is the treatment for membranous nephropathy?

A
  • 1st line: low salt and protein diet - low sodium reduce oedema, and low protein reduces proteinuria.
  • Corticosteroids + immunosuppressant (1st line is cyclophosphamide)
  • ACEi or ARB for hypertension
  • Diuretics e.g. furosemide for oedema
130
Q

Define Benign prostatic hyperplasia (BPH)

A

Benign prostatic hyperplasia is a very common condition affecting men in older age (usually over 50 years).

It is caused by hyperplasia of the stromal and epithelial cells of the prostate.

It usually presents with lower urinary tract symptoms (LUTS) - such as post-void dribbling, hesitancy and urgency.

131
Q

What are the aetiology/risk factors of BPH?

A
  • In men aged 51-60, 50% have BPH.
  • In men over 80, 80% have BPH.
  • Increasing age: particularly >50 years old
  • Family history
  • Ethnicity: more common in Afro-Caribbean men; black > white > Asian
  • Diabetes
  • Obesity: due to increased circulating oestrogens
132
Q

What is the pathophysiology of BPH?

A

Characterised by an increased stromal: epithelial ratio.

BPH = hyperplasia of glandular epithelial cells and stromal (connective tissue) cells.

Increasing age = increased activity of the enzyme 5-alpha reductase.

This increases dihydrotestosterone (DHT) and oestrogen > DHT causes hyperplasia within the prostate by acting on androgen receptors.

Mainly affects the peri-urethral region of the prostate, called the transition zone, resulting in compression of the prostatic urethra.

133
Q

What signs and symptoms might a patient with BPH present with?

A

Symptoms:
Lower urinary tract symptoms (LUTS)

  • Voiding: hesitancy, weak stream, straining, incomplete emptying, terminal dribbling
  • Storage: urgency, frequency, nocturia, urgency incontinence
  • Lower abdominal pain and inability to urinate - urinary retention

Signs

  • Digital rectal examination findings:
    Smooth, enlarged, and non-tender
    Not accurate for predicting prostate volume
  • Lower abdominal tenderness and palpable bladder:
  • Indicates acute urinary retention which require a bladder scan and urgent catheterisation
134
Q

What investigations/tests are used to diagnose BPH?

A

Primary investigations:

  • Urinalysis: the presence of pyuria suggests infection
  • Prostate-specific antigen (PSA): predicts prostate volume, progression and may suggest cancer if significantly raised; remember BPH can also raise PSA
  • U&Es: renal failure if there is significant obstruction
  • International Prostate Symptom Score (I-PSS): a 7-symptom questionnaire with an additional bother score (QOL) to predict progression and outcome
135
Q

What is the management plan for BPH for patients with non-bothersome symptoms?

A

1st line: lifestyle advice and modification if the patient has mild (non-bothersome) symptoms: treat constipation, reduce caffeine and fluid intake, medication review, bladder retraining.

136
Q

What is the management plan for BPH for patients with bothersome symptoms but no indication for surgery?

A

Bothersome symptoms but no indications for surgery:

  • 1st line: α-1 adrenergic antagonists: relaxes the smooth muscle in the prostate and bladder neck, e.g. tamsulosin
  • 5-α reductase inhibitors: inhibits DHT (dihydrotestosterone) formation to reduce prostate size, thus slowing progression (unlike α-blockers); e.g. finasteride.
  • Phosphodiesterase-5 inhibitor: used for severe LUTS, e.g. sildenafil
137
Q

What is the MOA of sildenafil?

A

Enhances the effect of nitric oxide (NO - vasdilation) by inhibiting phosphodiesterase-5 in the penile corpus cavernosum.

138
Q

Name 3 side effects of doxazosin.

A

Arrhythmias; asthenia (weakness, lack of energy) ; chest pain;

139
Q

BPH: What are the side effects of α-1 antagonists (tamsulosin or doxazosin)?

A

1) Postural hypertension due to vasodilation

2) Retrograde ejaculation (30%) due to over-relaxation of the bladder muscles allowing retrograde leakage of semen into the bladder

140
Q

BPH: what are the main side effects of 5-α reductase inhibitors (e.g. finasteride)?

A
  • Reduced libido
  • Erectile dysfunction,
  • Reduced ejaculate volume
  • Gynaecomastia
141
Q

BPH: what are the main side effects of Phosphodiesterase-5 inhibitors (e.g. sildenafil)?

A
  • Alopecia
  • Anaemia
  • Anxiety
  • Cough
  • Diarrhoea
  • Dizziness
142
Q

Why is the PSA (prostate-specific antigen) test not reliable?

A

PSA is usually used to screen for prostate cancer. However, many things can also raise PSA levels, such as benign prostate hyperplasia, prostatitis or UTI.

Therefore, it is not a specific test for prostate cancer as it can be raised even if the patient does not have prostate cancer.

143
Q

What is the management plan for BPH for patients with bothersome symptoms with indication for surgery?

A

Bothersome symptoms and indications for surgery:

Indications for surgery (RUSHES)

R - Recurrent or refractory urinary retention

U - Recurrent UTIs

S - Bladder stone

H - Haematuria refractory to medical therapy

E - Elevated creatinine due to bladder outflow obstruction

S - Symptom deterioration despite maximal medical therapy

  • Prostate <30 g: transurethral incision of the prostate (TUIP)
  • Prostate 30-80 g: transurethral resection of the prostate (TURP)
  • Prostate >80 g: open prostatectomy

Laser enucleation (HoLEP) is an alternative - a laser is used to remove tissue blocking urine flow

144
Q

What complications can arise from surgery for BPH?

A
  • Retrograde ejaculation
  • TUIP and TURP - 70% patients
  • Open prostatectomy - 80 - 90% patients
145
Q

Define prostate cancer

A

Prostate cancer is the most common cancer in males in the UK.

Adenocarcinomas are the most common type of prostate cancer, which most commonly arise from the peripheral zone of the prostate.

146
Q

What are the aetiology/risk factors for prostate cancer?

A

Thought to be associated with BRCA1 and BRCA2.

Risk factors:

  • Increasing age: men > 75 years ols
  • Family history: 5-10%
  • Afro-Caribbean ethnicity
  • Obesity and high-fat diet
  • Cadmium exposure: found in cigarettes, batteries and those working in the welding industry
147
Q

What is the pathophysiology of prostate cancer?

A
  • Adenocarcinomas - most common type, usually arise from the peripheral zone of the prostate.
  • High-grade prostatic intraepithelial neoplasia is considered the histological precursor of invasive prostate cancer.
  • Spread normally occurs along the capsular surface of the prostate, metastasising via the lymphatics and blood.
148
Q

What symptoms might a patient with prostate cancer present with?

A

Initially, it might not cause symptoms as it starts in the peripheral zones. Later it causes LUTS as it compresses the urethra.

Symptoms:

  • Common LUTS:
  • Frequency
  • Hesitancy
  • Terminal dribbling
  • Nocturia
  • Bone pain: e.g. lumbar back pain > suggests metastatic disease
  • Constitutional symptoms: e.g. weight loss
149
Q

What signs might a patient with prostate cancer present with?

A
  • Asymmetrical, hard, nodular prostate on digital rectal examination
  • Palpable lymphadenopathy - indicates metastatic disease
  • Urinary retention - presents with lower abdominal pain and tenderness, inability to urinate and a palpable bladder
150
Q

What investigations/tests are used to diagnose prostate cancer?

A

Primary investigations:

Prostate-specific antigen (PSA) - often increased in patients with prostate cancer.

1st line: multiparametric MRI identifies candidates for biopsy and differentiates clinically significant and non-significant tumours (≥3 points = biopsy, < 3 = discuss pros and cons)

Gold standard: prostate biopsy needed to confirm the diagnosis

151
Q

What is the management plan for CPG (Cambridge Prognostic Group) 1 (previously ‘low-risk’) localised prostate cancer?

A

Option 1: Active surveillance or observation (higher risk of progression but lower risk of complications)

Active surveillance is preferred in low-risk disease.

Option 2: Radical prostatectomy

Using robots, removing the prostate, seminal vesicles, ampulla, and vas deferens, +/- pelvic lymph node dissection. Commonly performed.

152
Q

What is the management plan for CPG 2, 3, 4 and 5 (‘intermediate or high-risk’) localised prostate cancer?

A

Option 1: Radical prostatectomy

Pelvic lymph node dissection is more frequently considered.

Option 2: Radical radiotherapy with anti-androgen therapy OR

Option 3: Radical radiotherapy with brachytherapy i.e. internal radiotherapy direct to prostate (can also be used in intermediate-risk cases)

153
Q

What is the management plan for metastatic prostate cancer?

A
  • Treated with docetaxel chemotherapy and antiandrogen therapy
  • Bilateral orchiectomy should be offered as an alternative to LHRH (luteinizing hormone-releasing hormone) agonists
154
Q

Define testicular cancer

A

Testicular cancer is the most common malignancy in young males and usually presents with a firm, painless testicular lump.

Divided into:

  • Germ cell tumours (95% of cases)
  • Non-germ cell tumours (sex-cord stromal tumours)
  • Lymphomas
155
Q

Testicular cancer: what is the pathophysiology of germ cell tumours?

A

Germ cell tumours arise from haploid germ cells which partake in spermatogenesis.

Divided into:

  • Seminoma - most common and best prognosis
  • Embryonal carcinoma - aggressive and metastasises early
  • Teratoma - composed of tissue from different germinal layers e.g. teeth. Common in children
156
Q

Testicular cancer: what is the pathophysiology of non-germ cell tumours?

A

Non-germ cell tumours arise from diploid sex-cord stroma cells, and are divided into:

  • Leydig cell tumour: androgen secreting causing precocious puberty
  • Sertoli cell tumour: usually clinically silent
157
Q

Testicular cancer: what is the pathophysiology of lymphoma?

A
  • Non-Hodgkin lymphoma is the most common and it is rare.
  • Most common in elderly
158
Q

What are the risk factors for testicular cancer?

A
  • Young males: seminoma > 35 years; non-seminoma < 35 years
  • Caucasian
  • Family history
  • Infertility: 3x
  • Cryptorchidism (absence of one or more testicles)
  • Mumps orchitis (testicle swelling after mumps)
  • Testicular atrophy: often following trauma
159
Q

What signs and symptoms might a patient with testicular cancer present with?

A

Symptoms:

  • Painless testicular lump: most common presenting complaint
  • Symptoms related to raised β-hCG (human chorionic gonadotropin)
  • Hyperthyroidism as β-hCG mimics TSH.
  • Gynaecomastia (breast tissue swelling in males)
  • Bone pain: indicates skeletal metastasis.
  • Breathlessness: indicates lung metastasis.

Signs:

  • Firm, non-tender testicular mass
  • Does not transilluminate (shining light does not go through)
  • Supraclavicular lymphadenopathy (swelling of lymph nodes above clavicles)
160
Q

What investigations/tests are used to diagnose testicular cancer?

A
  • 1st line and diagnostic: in over 90% of cases: ultrasound testicular doppler
  • Tumour markers: β-hCG, AFP (alpha-fetoprotein) and LDH must be measured prior to surgery. LDH is raised non-specifically in most testicular cancers

Germ cell tumour: Tumour marker

Seminoma: Occasionally β-hCG (20%)

Embryonal carcinoma: AFP

Teratoma: AFP

161
Q

What is the management plan for testicular cancer?

A

1st line: orchiectomy.

  • Seminomas are radiosensitive = adjuvant radiotherapy
  • Non-seminomas undergo chemotherapy.

Post orchiectomy:

Seminoma:

  • active surveillance for low-risk disease
  • radiotherapy for locally-invasive disease.

Non-seminoma: localised

  • active surveillance for low-risk disease
  • Adjuvant chemotherapy for high-risk disease

Advanced or metastatic disease:

  • Seminoma: adjuvant combination chemotherapy or radiotherapy
  • Non-seminoma: combination chemotherapy
162
Q

Define bladder cancer

A
  • > 90% transitional cell carcinoma (TCC) aka urothelial carcinoma
  • Transitional epithelium lines the renal pelvis, ureter, bladder, and urethra.
  • Squamous cell carcinoma (rare, 1-7% in the UK) associated with chronic cystitis secondary to schistosoma haematobium infection (most commonly seen in Egypt).
  • Adenocarcinoma occurs in 2% of patients.
163
Q

What are the different types of TCC?

A
  • Papillary: the majority of cases, usually superficial with finger-like projections, often non-invasive
  • Flat: lie flat against the bladder tissue and are more prone to invasion
164
Q

What are the aetiology and pathophysiology of TCC?

A

TCC is associated with loss of function of tumour suppressor genes p53 and retinoblastoma (Rb) gene.

TCCs may occur as solitary or multifocal lesions.

165
Q

What are the risk factors for developing bladder cancer?

A

Risk factors for urothelial carcinoma:

  • Increasing age: most common at 50 to 80 years old
  • Male
  • Family history
  • Smoking

Occupational exposure

  • Aromatic amines: rubber, dye and textile industries
  • Painters and hairdressers

Risk factors for squamous cell carcinoma:

  • Schistosoma haematobium: causes chronic bladder inflammation, most common in Egypt
166
Q

What signs and symptoms might a patient with bladder cancer present with?

A

The classic history of bladder cancer is an elderly patient with a history of smoking presenting with painless, macroscopic haematuria.

Symptoms

  • ‘Painless’ haematuria: microscopic or macroscopic
  • Dysuria - mostly ‘painless’, occasionally can cause dysuria
  • Frequency
  • Constitutional symptoms e.g. weight loss

Signs

  • Anaemia e.g. pallor, if chronic bleeding present
  • Palpable suprapubic mass in advanced cases
167
Q

When should you refer a patient with suspected bladder cancer for a 2-week wait specialist appointment?

A

NICE recommends:

Aged 45 and over and have:

  • Unexplained visible haematuria without UTI OR
  • Visible haematuria that persists after successful treatment of UTI
  • Aged 60 and over and have: unexplained microscopic haematuria and either dysuria or a raised WCC
  • Non-urgent referral - aged 60 and over with recurrent or persistent unexplained UTI
168
Q

What investigations/tests are used to diagnose bladder cancer?

A

Primary investigations :

  • Gold standard: flexible cystoscopy: under local anaesthetic to confirm the presence of a bladder tumour
  • Urinalysis: haematuria
  • CT urogram - allows staging

Bloods:

  • FBC: assess Hb in patients with chronic haematuria
  • U&Es: renal failure if significant bladder outflow obstruction
  • Bone profile: hypercalcaemia and raised ALP with bone metastasis
  • LFTs and coagulation screen: deranged in liver metastasis and to rule out coagulopathy
169
Q

What is the management plan for bladder cancer?

A

Superficial / non-muscle invasive (T1):

  • Trans-urethral resection of bladder tumour (TURBT).

Muscle-invasive (T2) or locally-advanced (T3):

  • Radical cystectomy with neoadjuvant chemotherapy; patients will require an ileal conduit (urostomy)
  • Radical radiotherapy with neoadjuvant chemotherapy is an alternative to surgery.

Metastatic (T4):

  • Palliative chemotherapy: cisplatin-based chemotherapy or radiotherapy for symptoms
170
Q

Define polycystic kidney disease

A

PKD is part of a heterogeneous group of disorders characterised by renal cysts and numerous systemic and extrarenal manifestations.

There are two types:

  • Autosomal-dominant PKD (ADPKD) Autosomal-recessive PKD (ARPKD)
171
Q

What is the aetiology of ARPKD?

A

Autosomal recessive polycystic kidney disease (ARPKD) presents in neonates and is usually picked up on antenatal ultrasound scans.

It results from a mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6.

This gene codes for the fibrocystin/polyductin protein complex (FPC), which is responsible for maintaining healthy epithelial tissue in the kidneys, liver and pancreas.

172
Q

What is the aetiology of ADPKD?

A

The most commonly affected genes are PKD1 or PKD2 in autosomal dominant polycystic kidney disease.

Patients with ADPKD often carry germline mutation in one allele of either PKD1 or PKD2, which causes pathogenic changes in tissue and organ development.

173
Q

What is the pathophysiology of ARPKD?

A

The underlying pathology causes:

  • Cystic enlargement of the renal collecting ducts
  • Oligohydramnios (too little amniotic fluid), pulmonary hypoplasia and Potter syndrome (syndrome associated with oligohydramnios and kidney failure)
  • Congenital liver fibrosis
174
Q

What is the pathophysiology of ADPKD?

A

The underlying pathology causes renal cysts to develop, which compresses the kidneys and intrarenal vessels > obstruction and apoptosis occur > increased kidney size, fibrosis and progressive renal impairment.

The kidneys progressively enlarge and become distorted with little recognisable parenchyma (tissue) on imaging

175
Q

What signs and symptoms might a patient with ARPKD present with?

A

Often present in neonates and picked up on antenatal screening (ultrasound scan):

  • Oligohydramnios (lack of amniotic fluid due to low urine production from fetus) and polycystic kidneys
  • Oligohydramnios > Potter syndrome and underdeveloped fetal lungs (pulmonary hypoplasia) > respiratory failure shortly after birth.
  • Patients need renal dialysis shortly after birth and develop end-stage renal failure before adulthood
176
Q

What complications do patients with ARPKD experience throughout their life due to PKD?

A
  • Liver failure due to liver fibrosis
  • Portal hypertension leading to oesophageal varices
  • Progressive renal failure
  • Hypertension due to renal failure
  • Chronic lung disease
177
Q

What signs and symptoms might a patient with ADPKD present with?

A
  • Family history of autosomal-dominant PKD (ADPKD) or end-stage renal disease
  • Family history of cerebrovascular events (strong association between ADPKD and intracranial aneurysm or subarachnoid haemorrhage)

Symptoms:

  • Abdominal/flank pain
  • Haematuria
  • Headaches
  • Dysuria

Signs

  • Renal cysts
  • Extrarenal cysts (e.g. berry aneurysms particularly in the circle of Willis)
  • Hypertension
  • Palpable kidneys/abdominal mass
178
Q

What investigations/tests are used to diagnose ADPKD?

A

Kidney ultrasound - bilateral kidney enlargement with multiple cysts can be seen

  • Genetic testing for PKD1 or PKD2 mutation if imagining inconclusive
179
Q

What is the management plan for ADPKD?

A

Renoprotective lifestyle changes -

  • Weight loss (or maintaining a healthy weight)
  • Regular cardiovascular exercise
  • Avoid smoke

Medical management:

Tolvaptan - vasopressin antagonist used to treat hyponatremia.

ACEi or AN-II antagonist for hypertension

Antibiotic therapy for UTI or infected renal cysts

Analgesia (paracetamol or opioids) for renal pain

End-stage kidney disease:
- 1st line: renal transplant
- 2nd line: dialysis

180
Q

Define varicoceles.

A

Varicoceles occurs when there is abnormal dilation of the internal spermatic veins and pampiniform plexus that drain blood from the testis

They can cause impaired fertility, probably due to disrupting the temperature in the affected testicle.

They may result in testicular atrophy, reducing the size and function of the testicle.

181
Q

What signs and symptoms might a patient with varicoceles present with?

A

Symptoms:

  • Painless scrotal mass
  • Scrotal or groin pain
  • Left-sided signs and symptoms (90% of varicoceles left-sided)
  • Dragging sensation
  • Infertility

Signs:

  • A scrotal mass that feels like a “bag of worms”
  • More prominent on standing
  • Disappears when lying down
  • Asymmetry in testicular size if the varicocele has affected the growth of the testicle
182
Q

What investigations and tests are used to diagnose varicoceles?

A
  • Mostly diagnosed through clinical presentation, but below are some investigations to consider:
  • Ultrasound with Doppler imaging can be used to confirm the diagnosis
  • Semen analysis if there are concerns about fertility
183
Q

What investigations and tests are used to diagnose varicoceles?

A
  • Mostly diagnosed through clinical presentation, but below are some investigations to consider:

Ultrasound with Doppler imaging can be used to confirm the diagnosis.

  • Semen analysis if there are concerns about fertility
  • Hormonal tests (e.g., FSH and testosterone) if there are concerns about function
184
Q

What is the management plan for varicoceles?

A
  • Uncomplicated cases can be managed conservatively.
  • Surgery such as open repair, laparoscopic repair or percutaneous embolisation may be indicated for pain, testicular atrophy or infertility.
185
Q

Define testicular torsion

A

Testicular torsion is a urological emergency caused by the twisting of the testicle on its spermatic cord, leading to ischaemia and eventually necrosis.

186
Q

What condition can often mimic testicular torsion?

A

Testicular appendage torsion, mimics testicular torsion.

The Hydatid of Morgagni is an embryonic remnant of the Mullerian duct.

Torsion of this small tissue can cause intense pain and characteristically causes a ‘blue-dot’ sign at the centre of the testicles but is often managed conservatively.

187
Q

What are the risk factors for developing testicular torsion?

A
  • Key risk factor = “bell clapper” abnormality: high riding testicle with a horizontal lie
  • Young age: peaks in the neonatal period and around puberty
  • Cryptorchidism: undescended testis
  • Trauma: trauma-induced torsion (>10% cases)
188
Q

What is a “bell clapper” abnormality?

A

This is when the tunica vaginalis - peritoneum covering the testicles does not attach to the scrotum properly, allowing the testicles to lie horizontally and hang and swing freely like a clapper in a bell

189
Q

What signs and symptoms might a patient with testicular torsion present with?

A

Symptoms:

  • Testicular pain - usually unilateral, sudden onset and excruciatingly painful.
  • Nausea and vomiting secondary to pain is common
  • Lower abdominal pain: referred pain

Signs:

  • Swollen, high-riding and tender testicle
  • Prehn’s sign negative: pain is not relieved on lifting the ipsilateral testicle, unlike in epididymitis
  • Absent cremasteric reflex
190
Q

What is an important differential diagnosis for acute, unilateral scrotal pain?

A

Epididymo-orchitis

191
Q

What investigations/tests are used to diagnose testicular torsion?

A

NICE recommends imagining studies NOT to be performed in patients where the history and physical examination suggests torsion because the treatment might be delayed.

  • Diagnosis is usually clinical - physical examination
  • Testicular ultrasound: ‘whirl-pool’ sign suggests torsion, as does decreased blood flow in the affected testicle on colour doppler
  • Surgical exploration: diagnostic and performed within 6 hours to prevent irreversible damage
  • Urinalysis: an abnormal result such as the presence of leukocytes and nitrites may suggest an alternative diagnosis, e.g. epididymo-orchitis
192
Q

What is the mangement plan for testicular torsion?

A

Viable testicle:

  • Bilateral orchiopexy: the affected testicle is untwisted and fixed to the scrotal sac. The contralateral testicle should always be fixed to prevent contralateral torsion.

Non-viable testicle (e.g. necrotic):

  • Ipsilateral orchiectomy and contralateral orchiopexy

In cases of surgical delay:

  • Manual detorsion: a temporary measure that should only be performed if surgery is not available within 6 hours.
193
Q

Define epididymal cysts

A

Epididymal cysts occur at the head of the epididymis (at the top of the testicle). A cyst is a fluid-filled sac. An epididymal cyst that contains sperm is called a spermatocele.

Transilluminates when light shines through.

194
Q

What signs and symptoms might a patient with epididymal cysts present with?

A

Most cases are asymptomatic.

  • Patients may present having felt a lump,
  • Or found incidentally on ultrasound

Examination findings are (i.e. signs):

  • Soft, round lump
  • Typically at the top of the testicle
  • Associated with the epididymis
  • Separate from the testicle
  • May be able to transilluminate large cysts
    (appearing separate from the testicle)
195
Q

How are epididymal cysts diagnosed?

A

Clinical diagnosis usually:

Examination findings are:

  • Soft, round lump
  • Typically at the top of the testicle
  • Associated with the epididymis
  • Separate from the testicle
  • May be able to transilluminate large cysts
    (appearing separate from the testicle)
  • Sometimes ultrasound of scrotum if clinical examinations not definitive.
196
Q

What is the management plan for epididymal cysts?

A

Usually, they are harmless and not associated with infertility or cancer.

Occasionally, they may cause pain or discomfort. Exceptionally rarely, there may be torsion of the cyst, causing acute pain and swelling.

In these cases, removal will be considered

197
Q

What are the lower urinary tract symptoms?

A

Lower urinary tract symptoms (LUTS)

  • Storage symptoms: occurs when bladder should be storing urine - need to pee

FUNI
Frequency, Urgency, Nocturia, (urgency) Incontinence

  • Voiding symptoms - occurs when the bladder outlet obstructed

SHID
- Voiding: (poor) Stream, Hesitancy, Incomplete emptying, Dribbling

198
Q

Define hydrocele

A

A hydrocele is a collection of serous fluid between the layers of the membrane (tunica vaginalis) that surrounds the testis or along the spermatic cord.

The tunica vaginalis is a sealed pouch of membrane that surrounds the testes.

199
Q

What are the two types of hydrocele

A
  • Simple - fluid is trapped in the tunica vaginalis. Reabsorbed over time and the hydrocele disappears. Common in newborn males.
  • Communicating - the tunica vaginalis around the testicle is connected with the peritoneal cavity via a pathway (processus vaginalis).

This allows fluid to travel from the peritoneal cavity into the hydrocele, allowing the hydrocele to fluctuate in size.

200
Q

What signs and symptoms might a patient with a hydrocele present with?

A
  • Soft, smooth, non-tender swelling around one of the testes.
  • In front and below the affected testicle
  • Simple hydroceles - one size
  • Communicating hydroceles - size fluctuation
  • Transilluminate - hold the pen torch flat against the skin, and it will light up like a bulb
201
Q

What investigations/tests are used to diagnose hydroceles?

A

Ultrasound is a useful investigation for confirming the diagnosis and excluding other causes.

202
Q

What are some main DDx for scrotal and inguinal swelling?

A

The key differential diagnoses of scrotal or inguinal swelling:

  • Hydrocele
  • Partially descended testes (neonates)
  • Inguinal hernia
  • Testicular torsion
  • Haematoma
  • Tumours (rare)
203
Q

What is the management plan for hydroceles?

A

Simple hydroceles will usually resolve within 2 years.

Parents can be reassured and followed up routinely. They may be offered surgery if it persists beyond two years of age, or if associated with other problems, such as a hernia.

Communicating hydroceles can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele (the processus vaginalis).

204
Q

What is cola-coloured urine as a result of?

A

Rhabdomyolysis

  • Damaged muscle tissue releases its proteins and electrolytes into the blood. These substances can damage the heart and kidneys and cause permanent disability or even death.
205
Q

Bendroflumethiazide

1) Use
2) MOA
3) Side effects

A

1) Thiazide diuretic - oedemia, hypertension

2) Thiazide diuretics act primarily by inhibiting the Na+-Cl− cotransporter in the distal tubule, promoting sodium excretion.

3) Postural hypotension; risk of hypokalaemia; dizziness

206
Q

Oxybutynin

1) Use
2) MOA
3) Side effects

A

1) Urinary frequency, Urinary urgency, Urinary incontinence, neurogenic bladder instability

2) Antimuscarinic (anticholinergic) that relaxes the smooth muscle of the bladder wall

3) Diahoerra

Oral: dry eye
Transdermal: GI discomfort

207
Q

Define renal cell carcinoma (RCC)

A

Renal cell carcinoma (RCC) is an adenocarcinoma most commonly arising from the epithelium of the proximal convoluted tubule.

RCC is the most common type of kidney cancer in adults

208
Q

What signs and symptoms might a patient with RCC present with?

A

Symptoms:

  • 50% asymptomatic
  • Classic triad: haematuria, flank pain, abdominal mass
  • Weight loss, fatigue, fever

Signs:

  • Flank mass
  • Left-sided varicocele (left testicular vein drains into left renal vein = back pressure, right testicular vein > directly to IVC)
  • Hypertension (risk factor)
  • Evidence of metastatic disease: SOB, Chronic liver disease, Bone pain
209
Q

What investigations/tests are used to diagnose RCC?

A
  • CT abdomen/pelvis with contrast: the definitive test for diagnosis
  • Urinalysis: microscopic haematuria or proteinuria

Bloods:

  • FBC: anaemia of chronic disease or polycythaemia
  • U&Es: assess for renal dysfunction
  • LFTs and coagulation profile: deranged = liver mets
  • Bone profile: hypercalcaemia = bone mets

LDH: elevated LDH non-specifically in cancer

210
Q

What is the management plan for RCC?

A

Localised disease:

Partial nephrectomy: T1 tumours (i.e. ≤ 7cm)

Radical nephrectomy: standard for T2-T3 tumours (i.e. > 7cm).

Minimally-invasive procedures: reserved for patients unfit for surgery, e.g. radiofrequency ablation

Metastatic disease:

Immunotherapy: 1st line are Sunitinib and Pazopanib (receptor tyrosine kinase inhibitors)

Radiotherapy

211
Q

What are DDx for RCC?

A
  • Benign renal cyst
  • Ureteric cancer
  • Bladder cancer
212
Q

What hereditary syndrome is a risk factor for developing RCC?

A

Von Hippel-Lindau syndrome

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