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Phase 2a > Urogenital > Flashcards

Urogenital Flashcards

1
Q

What is renal colic?

A

Pain due to renal calculi (kidney stones)

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2
Q

What are renal calculi/kidney stones also known as?

A

Nephrolithiasis

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3
Q

Describe the epidemiology of nephrolithiasis

A
  • 10% lifetime risk
  • More common in men (2:1)
  • Higher prevalence in Middle East
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4
Q

What are 6 causes of nephrolithiasis?

A
  1. Urinary (dehydration)
  2. Infection (proteus, Klebsiella, Pseudomonas)
  3. Hypercalciuria
  4. Hyperoxaluria
  5. Uric acid stones
  6. Cystine stone
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5
Q

What are 6 risk factors for nephrolithiasis?

A
  1. Chronic dehydration
  2. Obesity
  3. High protein/salt diet
  4. Recurrent UTIs
  5. Hyperparathyroidism
  6. Congenital abnormalities
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6
Q

Describe the pathophysiology of nephrolithiasis (nucleation theory)

A
  • Urine is composed of water (solvent) and particles (solute)
  • When solute becomes too concentrated –> supersaturated –> solute precipitates and forms crystals
  • Occurs due to an increase in solute or decrease in solvent
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7
Q

What commonly occurs in nephrolithiasis?

A

Stones cause obstructions leading to hydronephrosis (one/both kidneys become stretched/swollen due to the build-up of urine inside)

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8
Q

What are the 3 most common blockage sites in nephrolithiasis?

A
  1. Pelviureteric junction (PUJ) - most common
  2. Pelvic brim
  3. Vesicoureteric junction (VUJ)
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9
Q

What 7 things commonly make up the components of kidney stones/renal calculi?

A
  1. Calcium oxalate (forms in acidic urine)
  2. Calcium phosphate (forms in alkaline urine)
  3. Calcium carbonate
  4. Struvite (ammonium phosphate)
  5. Uric acid
  6. Cystine
  7. Drug precipitants
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10
Q

What is the main symptom of nephrolithiasis?

A

Renal colic:
- Severe unilateral abdominal pain
- Starts in loin and radiates to ipsilateral groin/testicle/labia
- Classically onset and early in the morning

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11
Q

What are 4 other symptoms of nephrolithiasis?

A
  1. Restlessness
  2. Nausea and vomiting
  3. Haematuria (blood in urine)
  4. Dysuria (painful urination)
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12
Q

What are 4 investigations for nephrolithiasis?

A
  1. Non contrast CT KUB (GOLD STANDARD)
  2. Ultrasound KUB in pregnancy
  3. Dipstick (haematuria, leucocytes, nitrites)
  4. Bloods (FBC, CRP, U&Es)
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13
Q

What is the treatment for nephrolithiasis?

A
  • Small enough stones (<5mm) pass on their own
  • ESWL (extracorporeal shock wave lithotripsy - breaks stones into smaller fragments using shockwaves)
  • Ureteroscopy PCNL (percutaneous nephrolithotomy - nephroscope used to remove stone)
  • Symptomatic relief (NSAIDs/opioids)
  • Decrease sodium/protein intake
  • Increased citrus fruit
  • Rehydration/adequate fluid intake
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14
Q

What are 3 complications of nephrolithiasis?

A
  1. Recurrence is common
  2. Irreversible renal damage
  3. Long term blockage can cause sepsis
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15
Q

What is acute kidney injury (AKI)?

A

Rapid deterioration of renal function

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16
Q

Describe the epidemiology of AKI

A
  • 15% of adults admitted to hospital develop AKI
  • More common in the elderly
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17
Q

What are 8 risk factors of AKI?

A
  1. HTN
  2. Volume depletion
  3. CKD
  4. Diabetes
  5. Cirrhosis
  6. Nephrotoxic medications
  7. Cancer
  8. Trauma
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18
Q

Describe the pathophysiology of pre-renal AKI

A

Decreased volume = decreased perfusion = decreased GFR and decreased creatinine clearance

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19
Q

What are 2 pre-renal causes of AKI?

A
  1. Low blood volume (bleeding/dehydration/shock/D&V)
  2. Low effective circulating volume (cirrhosis/congestive HF)
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20
Q

Describe the pathophysiology of glomerular intra-renal AKI

A

Barrier damage and protein leakage = decreased oncotic pressure = decreased GFR

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21
Q

What is a cause of glomerular intra-renal AKI?

A

Glomerulonephritis

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22
Q

Describe the pathophysiology of tubular intra-renal AKI

A

Complex blood supply –> cells infarct –> break away –> plug tubules –> decreased hydrostatic pressure = decreased GFR

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23
Q

What are 3 causes of tubular intra-renal AKI?

A

Necrosis:
1. Prolonged ischaemia
2. Infection
3. Nephrotoxins

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24
Q

Describe the pathophysiology of interstitial intra-renal AKI

A

Inflammation and immune cells = damage

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25
Q

What are 3 causes of interstitial intra-renal AKI?

A

Acute interstitial nephritis:
1. Infection
2. Ischaemia
3. Connective tissue disease

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26
Q

Describe the pathophysiology of vascular intra-renal AKI

A
  • Damaged vasculature = decreased O2 (necrosis)
  • Damaged endothelium = RBC breakdown
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27
Q

What are 4 causes of vascular intra-renal AKI?

A
  1. Vasculitis
  2. Microangiopathic haemolytic anaemia (MAHA)
  3. Thrombotic thrombocytopenic purpura (TTP)
  4. Haemolytic uremic syndrome (HUS)
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28
Q

Describe the pathophysiology of post-renal AKI

A

Back pressure into tubules = decreased hydrostatic pressure = decreased GFR

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29
Q

What are 3 causes of post-renal AKI?

A

Obstruction:
1. Stones
2. Prostate enlargement (e.g. due to cancer)
3. Infection

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30
Q

What are 3 general signs of AKI?

A
  1. High creatinine
  2. Arrythmia (due to hyperkalaemia)
  3. Pericarditis (due to uraemia)
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31
Q

What are 2 signs of pre-renal AKI?

A
  1. Hypotension
  2. Oedema
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32
Q

What are 2 signs of intra-renal AKI?

A
  1. Infection
  2. Signs of underlying disease (vasculitis, glomerulonephritis, DM)
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33
Q

What are 2 general symptoms of AKI?

A

Often asymptomatic
1. Oliguria/anuria (low/no urine output)
2. Muscle weakness (due to hyperkalaemia)

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34
Q

What are 3 symptoms of pre-renal AKI?

A
  1. Diarrhoea
  2. Nausea and vomiting
  3. Syncope/pre-syncope
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35
Q

What is a symptom of post-renal AKI?

A

Lower urinary tract symptoms

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36
Q

What are 3 investigations for AKI?

A
  1. Bloods - U&E (eGFR)
  2. Creatinine
  3. USS/CT KUB
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37
Q

What is the NICE guidelines for diagnosis of AKI?

A
  • Rise in serum creatinine of 25 umol/L within 48 hours
  • 50% rise in serum creatinine from baseline within 7 days
  • Fall in urine output to <0.5 mL/kg/hr for >6 hours
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38
Q

What is the treatment for AKI?

A
  • Treat underlying casue
  • Fluid balance
  • Stop nephrotoxic drugs e.g. NSAIDs, ACEi, metformin, lithium etc.
  • Dialysis (if severe)
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39
Q

What are 2 complications of AKI?

A
  1. Volume overload
  2. Metabolic acidosis
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40
Q

What is chronic kidney disease (CKD)?

A

Long-term, usually progressive impairment of kidney function (>3 months of abnormal kidney structure/function)

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41
Q

Describe the epidemiology of CKD

A
  • Between 6-11%
  • More common in females
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42
Q

What are 7 causes of CKD?

A
  1. Diabetes
  2. HTN
  3. Age-related decline
  4. Glomerulonephritis
  5. PKD
  6. Obstruction (e.g. kidney stones, enlarged prostate)
  7. Medications
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43
Q

What are the 4/5 most nephrotoxic types of drugs?

A
  1. Diuretics
  2. ACE inhibitors/angiotensin receptor blockers
  3. Metformin
  4. NSAIDs
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44
Q

What are 4 other common nephrotoxic types of drugs?

A
  1. PPIs
  2. Lithium
  3. Antidepressants
  4. Antibiotics
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45
Q

What are 6 risk factors for CKD?

A
  1. Diabetes
  2. HTN
  3. Female
  4. Increased age
  5. Smoking
  6. Nephrotoxic drugs
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46
Q

What are 5 signs of CKD?

A
  1. HTN
  2. Raised JVP
  3. Anaemia
  4. Osteomalacia
  5. Hyperparathyroidism
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47
Q

What are 8 symptoms of CKD?

A

Often asymptomatic until end-stage
1. Pruritus
2. Loss of appetite
3. Nausea
4. Oedema
5. Muscle cramps
6. Peripheral neuropathy
7. Palpitations
8. Pallor

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48
Q

What are 4 investigations for CKD?

A
  1. Bloods - U&E - estimated glomerular filtration rate (eGFR)
  2. Urine albumin:creatinine ratio (proteinuria)
  3. Urine dipstick (haematuria)
  4. Renal ultrasound
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49
Q

What is a G score in CKD?

A

Groupings for eGFR
G1 = >90
G2 = 60-89
G3a = 45-59
G3b = 30-44
G4 = 15-29
G5 <15 (end-stage)

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50
Q

What is an A score in CKD?

A

Groupings for albumin:creatinine ratio
A1 = <3mg/mmol
A2 = 3-30mg/mmol
A3 = >30mg/mmol

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51
Q

What is needed for a diagnosis of CKD?

A

eGFR of at least <60 or proteinuria

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52
Q

What is the treatment for CKD?

A
  • Exercise/maintain healthy weight
  • Stop smoking
  • Dietary restrictions regarding phosphate, sodium, potassium and water intake
  • Statins (for primary prevention of CVD)
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53
Q

What is the main treatment aim for CKD?

A

Slow progression

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54
Q

What are 6 complications of CKD?

A
  1. Anaemia
  2. Renal bone disease (osteodystrophy)
  3. Encephalopathy
  4. CVD
  5. Peripheral neuropathy
  6. Dialysis related problems
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55
Q

What is a urinary tract infection (UTI)?

A

Presence of microorganism in the urinary tract

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56
Q

Describe the epidemiology of UTIs

A

More common in women due to shorter urethras

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57
Q

What are the 5 most common causes of UTIs?

A

KEEPS
K - Klebsiella
E - E. Coli (50% of cases)
E - Enterococci
P - Proteus
S - Staphylococcus coagulase negative

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58
Q

What are 2 ways in which UTIs are commonly spread?

A
  1. Sexual activity
  2. Urinary catheter
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59
Q

What does an upper UTI often lead to?

A

Pyelonephritis (infection and inflammation of the kidney)

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60
Q

What 4 things can a lower UTI lead to?

A
  1. Cystitis (infection of urinary bladder)
  2. Urethritis (inflammation of urethra)
  3. Epididymo-orchitis (inflammation of epididymis and/or testis)
  4. Prostatitis (inflammation and swelling of prostate gland)
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61
Q

What is an uncomplicated UTI?

A
  • More common/less severe UTI
  • Infection in lower urinary tract/bladder/urethra
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62
Q

What is a complicated UTI?

A
  • Infection extends beyond bladder to the kidneys
  • Present with greater morbidity, carry a higher risk of treatment failure and typically require longer antibiotic courses
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63
Q

What are 5 examples of complicated UTIs?

A
  1. Males
  2. Pregnancy
  3. Result of obstruction
  4. Hydronephrosis
  5. Colovesical fistula
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64
Q

What are 7 clinical presentations of pyelonephritis (upper UTI)?

A
  1. Fever
  2. Loin/suprapubic/back pain
  3. Malaise
  4. Vomiting
  5. Loss of appetite
  6. Haematuria
  7. Renal angle tenderness
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65
Q

What are 5 clinical presentations of lower UTIs?

A
  1. Dysuria
  2. Suprapubic pain
  3. Frequency/urgency
  4. Incontinence
  5. Confusion
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66
Q

What is the investigation for patients with UTIs?

A

Urine dipstick:
- Nitrites present
- Leukocytes present

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67
Q

What is the treatment for UTIs?

A

Antibiotics:
- First choice = trimethoprim, nitrofurantoin
- Alternatives = pivmecillinam, amoxicillin, cefalexin

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68
Q

Which patients for UTIs are given a 3 day course of antibiotics?

A

Women with simple lower UTIs

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69
Q

Which patients for UTIs are given a 5-10 day course of antibiotics?

A
  • Women that are immunosuppressed
  • Women that have abnormal anatomy
  • Women that have impaired kidney function
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70
Q

Which patients for UTIs are given a 7 day course of antibiotics?

A
  • Men
  • Pregnant women
  • UTIs catheter related
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71
Q

What are 3 complications of UTIs?

A

In pregnancy, increased risk of:
1. Pyelonephritis
2. Premature rupture of membranes
3. Pre-term labour

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72
Q

What is nephritic syndrome?

A

Inflammation within the kidney defined by haematuria, oliguria, proteinuria and hypertension

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73
Q

What are 4 systemic causes of nephritic syndrome?

A
  1. Systemic lupus erythematosus
  2. Post-streptococcal glomerulonephritis
  3. Small vessel vasculitis (Henoch Schoenlein pupura)
  4. Goodpasture’s/anti GBM
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74
Q

What is a renal cause of nephritic syndrome?

A

IgA nephropathy (most common cause in UK/high income countries)

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75
Q

Describe the pathophysiology of nephritic syndrome

A
  • Inflammation cause podocytes to develop large pores
  • This allows blood flow into the urine
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76
Q

What are 3 investigations for patients with nephritic syndrome?

A
  1. Urine dipstick (haematuria)
  2. Bloods (elevated ESR and CRP)
  3. Kidney biopsy (to find cause)
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77
Q

What is the treatment for nephritic syndrome?

A
  • Treat underlying cause
  • ACE inhibitors/angiotensin receptor blockers (to reduce proteinuria and preserve renal function)
  • Corticosteroids (to reduce inflammation and damage)
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78
Q

What are 2 complications of nephritic syndrome?

A
  1. AKI
  2. Decreased resistance to infection
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79
Q

What is IgA nephropathy (a.k.a Berge Disease)?

A

Deposition of IgA into the mesangium of the kidney (component of glomerulus) causing inflammation and damage

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80
Q

How does IgA nephropathy present?

A

Asymptomatically with microscopic haematuria

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81
Q

How is IgA nephropathy diagnosed and treated?

A
  • Biopsy
  • Treatment the same as nephritic syndrome
  • Fish oil and steroids given if persistent proteinuria after 3-6 months
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82
Q

What is Goodpasture’s disease/anti GBM disease?

A

Autoimmune disease - autoantibodies (anti-glomerular basement membrane) to type IV collagen in glomerular and alveolar membrane

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83
Q

How does Goodpasture’s disease/anti GBM disease present?

A

SOB and oliguria

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84
Q

How is Goodpasture’s disease/anti GBM disease diagnosed and treated?

A
  • Anti-GBM antibodies in blood and biopsy
  • Plasma exchange, steroids and cyclophosphamide (immune suppression)
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85
Q

What is post-streptococcal glomerulonephritis?

A

Nephritic syndrome following an infection 3-6 weeks prior due to the deposition of strep antigens in glomeruli causing inflammation and damage

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86
Q

How does post-streptococcal glomerulonephritis present?

A

Haematuria and acute nephritis

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87
Q

How is post-streptococcal glomerulonephritis diagnosed and treated?

A
  • Find evidence of strep infection (e.g. positive throat swab results)
  • Antibiotics to clear strep and supportive care
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88
Q

What is Henoch Schoenlein purpura?

A

Small vessel vasculitis that affects the kidney and joints due to IgA deposition

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89
Q

How does Henoch Schoenlein purpura present?

A

Purpuric rash on legs, nephritis symptoms and joint pain

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90
Q

How is Henoch Schoenlein purpura diagnosed and treated?

A
  • Diagnosis confirmed with renal biopsy
  • Treated the same as nephritic syndrome = ACE inhibitors/angiotensin receptor blockers and corticosteroids
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91
Q

What is nephrotic syndrome?

A

Increased permeability of glomerular basement membrane to proteins

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92
Q

Describe the epidemiology of nephrotic syndrome

A
  • Most common in children aged 2-5
  • Twice as common in men
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93
Q

What are 3 primary causes of nephrotic syndrome?

A
  1. Minimal change disease (25% of adult causes and most common cause in children)
  2. Focal segmental glomerulosclerosis
  3. Membranous nephropathy (25% of adult cases)
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5
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94
Q

What are 5 secondary causes of nephrotic syndrome?

A

DDANI
D - Diabetes
D - Drugs
A - Autoimmune
N - Neoplasia
I - Infection

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95
Q

Describe the pathophysiology of nephrotic syndrome

A
  • Issue with filtration barrier
  • Podocytes are primarily implicated and develop gaps
  • Protein is able to leak into the urine
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96
Q

What are 5 clinical presentations of nephrotic syndrome?

A
  1. FROTHY URINE
  2. OEDEMA
  3. Pallor
  4. Hypoalbuminemia
  5. Hyperlipidaemia
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97
Q

What are 4 investigations for patients with nephrotic syndrome?

A
  1. Urine dipstick (proteinuria >3+ protein)
  2. Urine protein:creatinine ratio
  3. Bloods (renal function, elevated lipids, low serum albumin)
  4. Renal biopsy
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98
Q

What is the treatment for nephrotic syndrome?

A
  • Treat cause
  • Manage complications
  • Fluid and salt restriction
  • Loop diuretics
  • ACE inhibitors/ARB
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99
Q

What are 2 complications of nephrotic syndrome?

A
  1. Hyperlipidaemia (loss of albumin = increased cholesterol - managed with statins)
  2. Venous thromboembolism (increase clotting factors - manage with heparin)
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100
Q

How is minimal change disease diagnosed and treated?

A
  • Normal appearance upon microscopy but abnormal function
  • Biopsy
  • Treat with high dose steroids e.g. prednisolone
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101
Q

What are 4 causes of focal segmental glomerulosclerosis?

A
  1. Idiopathic
    Secondary to:
  2. HIV
  3. Heroin
  4. Lithium
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102
Q

How is focal segmental glomerulosclerosis diagnosed and treated?

A
  • Presence of scarring of glomeruli i.e. focal sclerosis
  • Blood pressure control = ACE inhibitors/ARB (all)
  • Steroids (idiopathic)
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103
Q

Describe membranous nephropathy

A

Immunologically mediated

104
Q

How is membranous nephropathy diagnosed and treated?

A
  • Renal biopsy (thickened glomerular basement membrane)
  • Anti-phospholipase A2 receptor antibody found in 70-80% of patients
  • ACE inhibitors/ARB (all)
  • Prednisolone and cyclophosphamide (in patients with a high risk of progression)
105
Q

What is diffuse proliferative glomerulonephritis?

A

Histological form of renal injury commonly seen in patients suffering from autoimmune disease

106
Q

How does diffuse proliferative glomerulonephritis present?

A

Can present as either nephritic or nephrotic syndrome

107
Q

What are the investigations for patients with diffuse proliferative glomerulonephritis?

A

Microscopy:
- Mesangial and endothelial cell proliferation
- Polymorphonuclear cell infiltrate
- Granular subepithelial deposits of C3 and immunoglobulins
- Swollen glomeruli

108
Q

What is membranoproliferative glomerulonephritis?

A

Kidney disorder involving inflammation and changes to kidney cells

109
Q

What is involved in all types of membranoproliferative glomerulonephritis?

A

Nephritic factor

110
Q

Describe the pathophysiology of type I membranoproliferative glomerulonephritis

A
  • Circulating immune complexes form due to antigen release from a chronic infection e.g. Hep B/C
  • Bound by antibodies in the blood
  • Travel to glomerulus and activates complement pathway
  • = deposition of immune complexes and complement
  • Basement membrane thickening
111
Q

Describe the pathophysiology of type II membranoproliferative glomerulonephritis

A
  • Complement deposits
  • No immune complexes
112
Q

Describe the pathophysiology of type III membranoproliferative glomerulonephritis

A

Immune complex and complement deposits in subendothelial and subepithelial spaces

113
Q

How does membranoproliferative glomerulonephritis present?

A

Can present as either nephritic or nephrotic syndrome

114
Q

What are 2 investigations for patients with membranoproliferative glomerulonephritis?

A
  1. Tram track on light microscopy
  2. Granular on immunofluorescence
115
Q

How is membranoproliferative glomerulonephritis treated?

A

Corticosteroids

116
Q

What is benign prostatic hyperplasia?

A

Hyperplasia of inner transitional zone of prostate gland without malignancy

117
Q

Describe the pathophysiology of benign prostatic hyperplasia

A
  • Glandular epithelial cells and stroma cells undergo hyperplasia
  • Median lobe usually affected
118
Q

What are 3 storage symptoms of benign prostatic hyperplasia?

A
  1. Frequency/urgency
  2. Nocturia
  3. Urgency incontinence
119
Q

What are 5 voiding symptoms of benign prostatic hyperplasia?

A
  1. Weak/intermittent stream
  2. Post-micturition dribbling
  3. Straining
  4. Incomplete emptying
  5. Hesitancy
120
Q

What are the 2 main investigations for patients with benign prostatic hyperplasia?

A
  1. Digital rectal examination (DRE) = smooth but enlarged prostate
  2. Prostate-specific antigen test (PSA) = raised
121
Q

Why are PSA tests unreliable?

A

High rate of false positives (75%) and negatives (15%)

122
Q

What are 6 things that may cause a patient’s PSA to be raised?

A
  1. Prostate cancer
  2. Benign prostatic hyperplasia
  3. Prostatitis
  4. Urinary tract infections
  5. Vigorous exercise (notably cycling)
  6. Recent ejaculation or prostate stimulation
123
Q

What are 2 other investigations that may be used for patients with benign prostatic hyperplasia?

A
  1. Bladder diaries
  2. Ultrasound
124
Q

What is the treatment for benign prostatic hyperplasia?

A
  • Reduce caffeine/alcohol intake
  • Alpha blockers e.g. doxazosin, tamsulosin
  • 5-alpha reductase inhibitor e.g. finasteride
  • Surgery - transurethral resection of prostate (TURP)
125
Q

What do alpha blockers do?

A

Relax the smooth muscle in the neck of the bladder and prostate - for patients with severe voiding problems

126
Q

What do 5-alpha reductase inhibitors do?

A

Block the conversion of testosterone to dihydrotestosterone and therefore decreases the size of the prostate

127
Q

Why may surgery be required in patients with benign prostatic hyperplasia?

A
  • If prostate fails to respond to treatment
  • If there is acute urinary retention
  • If there is gross haematuria
  • If it spreads to the kidneys
128
Q

What are 2 complications of benign prostatic hyperplasia?

A
  1. Recurrent UTI
  2. Bladder calculi
129
Q

Describe the epidemiology of prostate cancer

A

Most common cancer in men

130
Q

What are 5 risk factors for prostate cancer?

A
  1. Increasing age
  2. Family history
  3. Black African or Caribbean origin
  4. Tall stature
  5. Anabolic steroids
131
Q

Describe the pathophysiology of prostate cancer

A
  • Almost always androgen dependent
  • Majority are adenocarcinomas and grow in peripheral zone of prostate
  • Advanced prostate cancer commonly spreads to lymph nodes and bones
132
Q

What are 4 symptoms of prostate cancer?

A

Can be asymptomatic
1. LUTS e.g. hesitancy, frequency/urgency, weak flow, dribbling, nocturia
2. Haematuria
3. Erectile dysfunction
4. Symptoms of metastasis e.g. weight loss/bone pain

133
Q

What are 5 investigations for patients with prostate cancer?

A
  1. DRE
  2. PSA test
  3. Transrectal USS
  4. Biopsy
  5. Gleason grading system
134
Q

What are the result of a DRE in patient with prostate cancer?

A

Prostate feels firm/hard, asymmetrical and craggy with loss of a central sulcus

135
Q

What is the Gleason grading system?

A
  • Based on histology from prostate biopsies
  • Greater score (1-5) = worse prognosis
136
Q

What is the treatment for patients with prostate cancer?

A
  • Prostatectomy
  • Hormone therapy
  • Radiotherapy
  • Chemotherapy
137
Q

What are 3 types of hormone therapy used in patients with advanced prostate cancer?

A
  1. Goserelin (zoladex) or leuprorelin (prostap) = GnRH agonists
  2. Bicalutamide = androgen-receptor blocker
  3. Bilateral orchidectomy
138
Q

Describe the epidemiology of testicular cancer

A
  • More common in younger men (15-35)
  • 98% 5 year survival
139
Q

What are 6 risk factors for testicular cancer?

A
  1. Caucasian
  2. HIV
  3. Undescended testis (cryptorchidism)
  4. Male infertility
  5. Family history
  6. Increased height
140
Q

Describe the pathophysiology of testicular cancer

A
  • 90% arise from germ cells in the testes (seminomas, teratoma, choriocarcinoma)
  • Non-germ cell tumours (sertoli, leydig, lymphoma, mesenchymal)
  • Commonly metastasises to lymphatics, lungs, liver, brain
141
Q

What are 4 clinical presentations of testicular cancer?

A
  1. Painless lump on testicle
  2. Hydrocele (swollen scrotum)
  3. Gynaecomastia
  4. Haematospermia
142
Q

Describe a painless lump in patients with testicular cancer

A
  • Non tender
  • Hard
  • Irregular
  • Not fluctuant
  • No transillumination
143
Q

What are 2 investigations for patients with testicular cancer?

A
  1. Scrotal ultrasound
  2. Tumour markers = alpha-fetoprotein, beta-Hcg, lactate dehydrogenase (LDH)
144
Q

What is the treatment for testicular cancer?

A
  • Surgery (orchidectomy)
  • Chemotherapy
  • Radiotherapy
145
Q

What is a complication of testicular cancer?

A

Infertility (sperm banking often used to save sperm for future use)

146
Q

Describe the epidemiology of bladder cancer

A
  • Most common GU tract malignancy
  • 10th most common cancer
  • 3% of all cancer deaths
  • More common in men
147
Q

What are 6 risk factors for bladder cancer?

A
  1. Smoking
  2. Age over 55
  3. Male
  4. Caucasian
  5. Previous pelvic radiotherapy
  6. Exposure to aromatic amines (carcinogen in dye/rubber/cigarette smoke)
148
Q

Describe the pathophysiology of bladder cancer

A
  • Most common type is transitional cell carcinoma (90%)
  • Arise from transitional cells of mucosal urothelium
  • Most commonly metastasises to lymph nodes, bones, lungs, liver
149
Q

What are 4 other types of bladder cancer?

A
  1. Squamous cell carcinoma (5% - higher in areas of schistosomiasis)
  2. Adenocarcinoma (2%)
  3. Sarcoma (rare)
  4. Small cell carcinoma (rare)
150
Q

What are 4 symptoms of bladder cancer?

A
  1. PAINLESS HAEMATURIA
  2. Urgency
  3. Suprapubic pain
  4. Symptoms of systemic spread e.g. bone pain, weight loss
151
Q

What are 3 investigations for patients with bladder cancer?

A
  1. Cystoscopy and biopsy
  2. Urinalysis
  3. Bloods
152
Q

What is the treatment for bladder cancer?

A
  • Radiotherapy
  • Chemotherapy
  • Surgery = transurethral resection of bladder tumour (TURBT), cystodiathermy (excision of small lesions of bladder), cystectomy (removal of bladder)
153
Q

Describe the epidemiology of renal cancer

A
  • Mean age of diagnosis = 55
  • Twice as common in men
154
Q

What are 7 risk factors for renal cancer?

A
  1. Smoking
  2. Obesity
  3. Hypertension
  4. End-stage renal failure
  5. Von Hippel-Lindau disease
  6. Tuberous sclerosis
  7. Family history
155
Q

Describe the pathophysiology of renal cancer

A
  • Most common type is renal cell carcinoma (90%) (arises from proximal convoluted tubular epithelium)
  • Can secrete PTH, ACTH, EPO and renin
  • Also transitional cell carcinoma (arises from renal pelvis)
  • Both commonly metastasise to lymph system, lung, breast and skin
156
Q

What are 5 clinical presentations of renal cancer?

A

Renal cell carcinoma - often asymptomatic
Classic triad of presentation:
1. Vague loin pain
2. Haematuria
3. Abdominal mass

  1. Anorexia/weight loss
  2. Varicocele
157
Q

What are 6 investigations for patients with renal cancer?

A
  1. Ultrasound = 1st line
  2. CT chest/abdomen/pelvis
  3. Other imaging e.g. CT/MRI/CXR
  4. Renal biopsy
  5. Bloods (polycythaemia)
  6. Raised BP
158
Q

What is the treatment for renal cancer?

A

Total/partial nephrectomy

159
Q

What are 4 complications of renal cancer?

A

Paraneoplastic changes:
1. Polycythaemia
2. HTN
3. Hypercalcaemia
4. Cushing’s

160
Q

What is polycystic kidney disease (PKD)?

A

Inherited condition where clusters of fluid-filled cysts develop within the kidneys

161
Q

Describe the epidemiology of PKD

A
  • Autosomal dominant presents after 20s (any age) and is more common than autosomal recessive
  • Autosomal recessive typically presents at birth
162
Q

Describe the pathophysiology of PKD

A
  • Cysts develop (recessive - born with) and grow over time in tubular portion of kidney
  • Leads to compression of renal parenchyma and vasculature
  • Progressive impairment
163
Q

Which genes are affected in PKD?

A

Autosomal dominant:
- PKD-1 = chromosome 16 (85% of cases)
- PKD-2 = chromosome 4 (15% of cases)
Autosomal recessive:
- Chromosome 6

164
Q

What are 4 clinical presentations of PKD?

A

Asymptomatic
1. HTN
2. Bilateral flank/back/abdominal pain
3. Headache
4. LUTS

165
Q

What is a common presentation of autosomal recessive PKD?

A

Oligohydramnios (lack of amniotic fluid) which leads to underdevelopment of lungs resulting in resp failure shortly after birth

166
Q

What are 3 investigations for PKD?

A
  1. Kidney USS
  2. Renal biopsy
  3. Genetic testing
167
Q

What is the treatment for PKD?

A
  • Tolvaptan (vasopressin receptor antagonist - slows cyst development)
  • Antihypertensives
  • Analgesia
  • Renal replacement therapy for end-stage renal failure
168
Q

What are 7 complications of PKD?

A
  1. Berry aneurysms (intracranial aneurysms that present as sub arachnoid haemorrhages)
  2. Chronic back pain
  3. HTN
  4. CVD
  5. Haematuria
  6. Kidney stones
  7. End-stage renal failure
169
Q

What is chlamydia?

A

Bacterial infection caused by gram-negative bacteria chlamydia trachomatis

170
Q

Describe the epidemiology of chlamydia

A

Most common bacterial STI

171
Q

Describe the pathophysiology of chlamydia

A
  • Chlamydia trachomatis
  • Intracellular organism
  • Enters and replicates within cells before rupturing the cell and spreading to others
172
Q

How does chlamydia present in men?

A
  • 50% asymptomatic
  • Testicular pain
  • Dysuria
  • Urethral discharge/discomfort
173
Q

How does chlamydia present in women?

A
  • 70% asymptomatic
  • Vaginal discharge (white/yellow/green)
  • Dysuria
  • Abnormal vaginal bleeding
  • Dyspareunia (painful sex)
174
Q

What are the 2 swabs used to investigate patients with chlamydia?

A
  • Charcoal swab (allows for microscopy, culture and sensitivities)
  • Nucleic acid amplification testing (NAAT - checks directly for DNA/RNA of organism)
175
Q

How are swabs most commonly collected in patients with chlamydia?

A
  • Vulvovaginal swab (women)
  • Urethral swab (men)
  • First-catch urine sample (both)
176
Q

What are 4 things usually found on examination in patients with chlamydia?

A
  1. Pelvic/abdominal tenderness
  2. Cervical motion tenderness
  3. Inflamed cervix
  4. Purulent discharge
177
Q

What is the standard treatment and advice for chlamydia?

A
  • Doxycycline 100mg twice a day for 7 days
  • Avoid sex until treatment is complete
178
Q

When can doxycycline not be used to treat chlamydia?

A

Contraindicated in pregnancy and breastfeeding

179
Q

What are 3 alternative drugs used to treat chlamydia?

A
  • Azithromycin
  • Erythromycin
  • Amoxicillin
180
Q

What are 5 complications of both chlamydia and gonorrhoea?

A
  1. Infertility
  2. Pelvic inflammatory disease
  3. Chronic pelvic pain
  4. Epididymo-orchitis
  5. Conjunctivitis
181
Q

What are 2 other complications of chlamydia?

A
  1. Lymphogranuloma venerum
  2. Reactive arthritis
182
Q

What are 6 pregnancy-related complications of chlamydia?

A
  1. Pre-term delivery
  2. Premature rupture of membranes
  3. Low birth weight
  4. Postpartum endometritis
  5. Neonatal infection e.g. conjunctivitis, pneumonia
  6. Ectopic pregnancy
183
Q

What is gonorrhoea?

A

Bacterial infection caused by gram-negative diplococcus bacteria Neisseria gonorrhoea

184
Q

Describe the epidemiology of gonorrhoea

A

2nd most common STI in the UK

185
Q

Describe the pathophysiology of gonorrhoea

A
  • Infects mucous membranes with a columnar epithelium e.g. endocervix, urethra, rectum, conjunctiva and pharynx
  • Spread via contact with mucous secretions from infected areas
186
Q

How does gonorrhoea present in men?

A
  • 10% asymptomatic
  • Odourless purulent discharge (green/yellow)
  • Dysuria
  • Testicular pain/swelling (epididymo-orchitis)
187
Q

How does gonorrhoea present in women?

A
  • 50% asymptomatic
  • Odourless purulent discharge (green/yellow)
  • Dysuria
  • Pelvic pain
188
Q

What are 4 common presentations of gonorrhoea?

A
  1. Rectal infection (anal/rectal discomfort)
  2. Pharyngeal infection (sore throat)
  3. Prostatitis (perineal pain, urinary symptoms, prostate tenderness)
  4. Conjunctivitis (erythema, purulent discharge)
189
Q

What are the 2 swabs used to investigate patients with gonorrhoea?

A
  • Charcoal swab (allows for microscopy, culture and sensitivities)
  • Nucleic acid amplification testing (NAAT - checks directly for DNA/RNA of organism)
190
Q

How are swabs most commonly collected in patients with gonorrhoea?

A
  • Vulvovaginal swab (women)
  • Urethral swab (men)
  • First-catch urine sample (both)
  • Rectal and pharyngeal swabs (recommended in all men who have sex with men - MSM)
191
Q

What is the first line treatment for gonorrhoea?

A

Single dose of intramuscular ceftriaxone 1g

192
Q

Why can there be difficulty in treating gonorrhoea?

A

High levels of antibiotic resistance i.e. ciprofloxacin or azithromycin

193
Q

What are 7 other complications of gonorrhoea?

A
  1. Prostatitis
  2. Urethral stricture
  3. Disseminate gonococcal infection
  4. Skin lesions
  5. Fitz-Hugh-Curtis syndrome
  6. Septic arthritis
  7. Endocarditis
194
Q

What is syphilis?

A

Bacterial infection caused by spirochete Treponema pallidum

195
Q

Describe the pathophysiology of syphilis

A
  • Bacteria gets in through skin or mucous membranes
  • Replicates and disseminates throughout body
  • Incubation period between initial infection and symptoms = 21 days on average
196
Q

What are 4 methods of transmission for syphilis?

A
  1. Oral/vaginal/anal sex
  2. Vertical transmission
  3. IV drug use
  4. Blood transfusions/transplants
197
Q

How does primary syphilis present?

A
  • Painless ulcer (chancre) at original site of infection (tends to resolve over 3-8 weeks)
  • Local lymphadenopathy
198
Q

How does secondary syphilis present?

A
  • Maculopapular rash
  • Condylomata lata (grey wart-like lesions around genitals/anus)
  • Low-grade fever
  • Lymphadenopathy
  • Alopecia
  • Oral lesions
  • Symptoms resolve after 3-12 weeks
199
Q

What is latent syphilis?

A

Patient is asymptomatic but still infected

200
Q

How does tertiary syphilis present?

A
  • Occurs many years after initial infection
  • Development of gummas (granulomatous lesions)
  • Aortic aneurysms
  • Neurosyphilis
201
Q

How does neurosyphilis present?

A
  • Headache
  • Altered behaviour
  • Dementia
  • Tabes dorsalis
  • Ocular syphilis
  • Paralysis
  • Sensory impairment
202
Q

What are 3 investigations for patients with syphilis?

A
  1. Antibody testing (antibody to T. pallidum bacteria)
  2. Dark field microscopy (for T. pallidum bacteria)
  3. Polymerase chain reaction (PCR - for T. pallidum)
203
Q

What is the 1st line treatment for syphilis?

A

Single intramuscular dose of benzathine benzylpenicillin

204
Q

What are 3 alternative drugs used to treat syphilis?

A
  1. Ceftriaxone
  2. Amoxicillin
  3. Doxycycline
205
Q

What is a varicocele?

A

An abnormally dilated testicular vein in pampiniform venous plexus

206
Q

Describe the epidemiology of varicocele

A
  • Affects around 15% of men
  • 90% occur on the left side
  • Incidence increases after puberty
207
Q

What are 2 causes of varicocele?

A
  1. Venous reflux (due to incompetent valves)
  2. Left can indicate an obstruction due to renal cell carcinoma
208
Q

Describe the pathophysiology of varicocele

A
  • Impaired venous drainage leads to increased resistance and venous pressure
  • = vein dilatation
  • Increased resistance in the left testicular vein therefore is more commonly affected
209
Q

Describe the effects of varicocele on sperm

A
  • Pampiniform plexus is involved in regulating the blood temperature to ensure that it is the optimum temperature required to produce sperm
  • Varicoceles generate heat which can affect sperm quality by reducing the proteins required for healthy sperm
210
Q

What are 2 signs of varicocele?

A
  1. Scrotal mass that feels like ‘a bag of worms’
  2. Asymmetry in testicular size
211
Q

What are 2 symptoms of varicocele?

A
  1. Dragging/soreness/heaviness of scrotum
  2. Throbbing/dull pain/discomfort (worse on standing and usually disappears when lying down)
212
Q

What are 3 investigations for patients with varicocele?

A
  1. USS with Doppler imaging
  2. Semen analysis (if concerned about fertility)
  3. Hormonal tests e.g. FSH and testosterone (if concerned about function)
213
Q

What is the treatment for varicocele?

A
  • Conservative management for uncomplicated cases
  • Surgical repair if pain
214
Q

What are 2 complications of varicocele?

A
  1. Infertility
  2. Testicular atrophy
215
Q

What is a hydrocele?

A

Collection of fluid within the tunica vaginalis

216
Q

What are 5 causes of hydrocele?

A
  1. Idiopathic
  2. Testicular cancer
  3. Testicular torsion
  4. Epididymo-orchitis
  5. Trauma
217
Q

What is the difference between a simple, communicating and non-communicating hydrocele?

A

Simple = overproduction of fluid, common at birth (usually disappears within first 2 years of life)
Communicating = connection between scrotum and peritoneal fluid
Non-communicating = imbalance between secretion and reabsorption of fluid

218
Q

What are 4 signs of a hydrocele?

A
  1. Testicle is palpable within hydrocele
  2. Testicle is soft, fluctuant and may be swollen
  3. Irreducible and has no bowel sounds (distinguish from hernia)
  4. Transilluminated
219
Q

What is a symptom of a hydrocele?

A

Usually painless but may be some pain

220
Q

What are 2 investigations for hydrocele?

A
  1. Examination - palpate and transilluminate
  2. USS
    (Rule out testicular cancer)
221
Q

What is the treatment for hydrocele?

A
  • Most idiopathic hydroceles resolve spontaneously (manage conservatively)
  • Surgery/aspiration/sclerotherapy may be required for large/symptomatic cases
222
Q

What is a complication of hydrocele?

223
Q

What is testicular torsion?

A

Medical emergency! Torsion of spermatic cord

224
Q

Describe the epidemiology of testicular torsion

A

Most commonly affects teenage boys

225
Q

What is the cause of testicular torsion?

226
Q

Describe the pathophysiology of testicular torsion

A

Occlusion of testicular blood vessels

227
Q

How does a testicular appendage torsion differ from testicular torsion?

A
  • Twisting of vestigial appendage along testicle (has no function)
  • Only thing that needs to be managed is pain if any
228
Q

What are 5 signs of testicular torsion?

A
  1. Firm, swollen testicle
  2. Elevated/retracted testicle
  3. Absent cremasteric reflex
  4. Abnormal testicular lie (often horizontal)
  5. Prehn’s sign negative
229
Q

What is a cremasteric reflex?

A

Stroking of inner thigh causes cremaster muscle to contract and pull ipsilateral testicle up towards inguinal canal

230
Q

What is Prehn’s sign?

A

Lift the scrotum and observe if there is any change in pain
positive = pain eased
negative = no change

231
Q

What are 3 symptoms of testicular torsion?

A
  1. Acute rapid onset of unilateral testicular pain (often following sports/physical activity)
  2. May have abdominal pain
  3. May be vomiting
232
Q

What are 2 investigations for patients with testicular torsion?

A
  1. Examination
  2. Scrotal ultrasound (whirlpool sign - spiral appearance to spermatic cord and blood vessels)
233
Q

What is the treatment for testicular torsion?

A
  • De-torsion
  • Analgesia
  • Orchidectomy if necrosis
234
Q

What are 2 complications of testicular torsion?

A
  1. Ischaemia/atrophy and necrosis of testicle
  2. Infertility
235
Q

What is an epididymal cyst?

A

An extra-testicular spherical cyst in the head of the epididymis

236
Q

What is a spermatocele?

A

Epididymal cyst containing sperm (identical presentation/treatment to epididymal cyst)

237
Q

Describe the epidemiology of epididymal cysts

A
  • Occur in around 30% of men
  • Most common cause of scrotal swelling
238
Q

What are 3 signs of epididymal cysts?

A
  1. Smooth, round lump typically at top of testicle
  2. Cyst and testes can be palpated separately
  3. Transilluminates (contains clear and milky fluid)
239
Q

What are symptoms of epididymal cysts?

A

Usually asymptomatic

240
Q

What are 2 investigations for epididymal cysts?

A
  1. Examination
  2. May be found incidentally on ultrasound
241
Q

What is the treatment for epididymal cysts?

A

Usually none required - usually dissolve within 10 days

242
Q

What is a complication of epididymal cysts?

A

Torsion of cyst (extremely rare)

243
Q

What are 4 LUTS (storage)?

A
  1. Frequency
  2. Urgency
  3. Nocturia
  4. Incontinence
244
Q

What are 5 LUTS (voiding)?

A
  1. Straining
  2. Hesitancy
  3. Incomplete emptying
  4. Post-micturition dribbling
  5. Poor stream
245
Q

What are the two types of urinary incontinence?

A

Urge = overactivity of detrusor muscle of bladder
Stress = weakness of pelvic floor and sphincter muscles

246
Q

How do urge and stress incontinence differ in their presentation?

A

Urge = sudden urge to urinate (often urinate before reaching a bathroom)
Stress = urine leaks at times of increased pressure on bladder e.g. when laughing/coughing/surprised

247
Q

How is urge incontinence managed?

A
  • Bladder retraining
  • Anticholinergic medications e.g. oxybutynin
  • Mirabegron
  • Invasive procedures (if failure to respond to retraining/medication)
248
Q

What are 4 invasive procedures used to treat urge incontinence?

A
  1. Botulinum toxin type A injection into bladder wall
  2. Percutaneous sacral nerve stimulation
  3. Augmentation cystoplasty
  4. Urinary diversion
249
Q

How is stress incontinence managed?

A
  • Avoid caffeine/diuretics
  • Avoid excessive or restricted fluid intake
  • Weight loss if appropriate
  • Supervised pelvic floor exercises
  • Surgery
  • Duloxetine (if surgery less preferred)
250
Q

What are 4 surgical procedures used to treat stress incontinence?

A
  1. Tension-free vaginal tape (TVT)
  2. Autologous sling procedures
  3. Colposuspension
  4. Intramural urethral bulking
251
Q

What is mixed incontinence?

A

Combination of urge and stress incontinence

252
Q

What are 8 risk factors for urinary incontinence?

A
  1. Increased age
  2. Postmenopausal status
  3. Increased BMI
  4. Previous pregnancies/vaginal deliveries
  5. Pelvic organ prolapse
  6. Pelvic floor surgery
  7. Neurological conditions e.g. multiple sclerosis
  8. Cognitive impairment and dementia
253
Q

What is overflow incontinence?

A

Chronic urinary retention due to an obstruction to outflow of urine (unable to fully empty bladder so causes frequent leaking)

254
Q

Describe the epidemiology of overflow incontinence

A

More common in men

255
Q

What are 4 causes of overflow incontinence?

A
  1. Anticholinergic medications
  2. Fibroids
  3. Pelvic tumours
  4. Neurological conditions e.g. multiple sclerosis, diabetic neuropathy and spinal cord injuries
256
Q

What is urinary retention?

A

Inability to empty urine from bladder

257
Q

What are 5 causes of urinary retention?

A
  1. Lower urinary tract obstruction
  2. Benign prostatic hyperplasia
  3. Pelvic organ prolapse
  4. Urinary tract stones (calculi)
  5. Constipation

Phase 2a (29 decks)

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