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2a - SBCS > Renal and genitourinary > Flashcards

Renal and genitourinary Flashcards

1
Q

What is benign prostatic hyperplasia (BPH)

A

Non malignant hyperplasia of stromal (CT) and glandular epithelial cells of the prostate

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2
Q

What are the RFs of BPH

A
  • Increasing age (over 50)
  • FHx
  • Non-Asian race - Asian men have smaller prostates at any given age
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3
Q

Describe the pathophysiology of BPH

A
  • Inner transitional zone of the prostate (muscular, gland) proliferate and narrows the urethra
  • More difficult to pass urine
  • Accumulation of urine causes bladder to dilate
  • Results in bladder hypertrophy and promotes bacterial growth (UTI)
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4
Q

Describe the presentation of BPH

A

Usually presents with lower urinary tract Sx (LUTS)
* Storage: frequency, urgency, nocturia, incontinence
* Voiding: Weak stream, terminal dribbling, incomplete emptying, straining, dysuria

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5
Q

4 investigations of BPH

A
  • DRE - smooth, symmetrical & enlarged
  • Prostate-specific antigen (PSA) - raised but not specific
  • Urine dipstick - assess for infection and haematuria
  • CT/MRI pelvis - prostate size and shape
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6
Q

Why is PSA testing an unreliable investigation

A
  • Can be raised for several conditions: prostate cancer, BPH, Prostatitis, UTI, vigorous exercise
  • High rate of false positives (75%)
  • Prostate specific not cancer specific
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7
Q

Describe the management of BPH (not including surgery)

A
  • May not require intervention if mild & manageable Sx = watchful waiting
    Medical:
  • Alpha blockers (Tamsulosin) - relax bladder neck
  • 5-alpha reductase inhibitors (finasteride) - gradually reduce size of prostate
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8
Q

When should caution be taken prescribing alpha blockers

A

Patients with postural hypotension or micturition syncope

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9
Q

Describe the MOA of 5-ARI in BPH

A

5-ARI blocks the synthesis of dihydrotestosterone and reduce levels of DHT in the prostate leading to a reduction in size
* Takes up to 6 months for effects to result in improved symptoms

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10
Q

What is a common side effect of 5-ARI

A

Sexual dysfunction due to reduced testosterone
* e.g. erectile dysfunction, low libido

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11
Q

Give 3 complications of TURP

A
  • Retrograde ejaculation (mc) - semen goes backwards
  • Urethral stricture
  • Bleeding
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12
Q

Describe the surgical management of BPH

A

<30g:
*Transurethral incision of prostate

30-80g:
* Transurethral resection of prostate (TURP)
* Holmium laser enucleation of prostate (HoLEP)

> 80g:
* Open prostatectomy
* Transurethral electrovaporisation of prostate (TUVP)

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13
Q

Define nephrolithiasis

A
  • A.k.a renal stones or calculi or urolithiasis
  • Hard stones found within urinary tract
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14
Q

Give 3 RFs of kidney stones

A
  • Dehydration
  • HyperPTH/ HyperCa
  • Previous kidney stones
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15
Q

Explain the pathophysiology of kidney stones

A
  • Urine is a combo of water and solutes
  • Excess solutes cause supersaturated urine
  • Solutes precipitate
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16
Q

Describe 5 types of kidney stone

A
  • Calcium oxalate (mc) - black/dark brown, radiopaque, envelope shaped
  • Ca phosphate - dirty white, radiopaque, wedge shaped
  • Uric acid - red/brown, radiolucent, diamond
  • Struvite (ammonium Mg phosphate) - infection stones, coffin-lid shaped
  • Cystine - yellow/light pink stone, radiolucent, hexagonal
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17
Q

RF of struvite stones

A

UTI

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18
Q

2 RFs of Ca oxalate stones

A
  • HyperCa
  • Chron’s
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19
Q

Describe the presentation of renal stones

A
  • Renal colic:
    unilateral loin to groin pain
    colicky = fluctuates as stone moves and settles
  • Moving restlessly
  • Haematuria
  • N+V
  • Fever - sepsis
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20
Q

Describe the investigation of kidney stones

A
  • GS: Urgent Non-contrast CT kidney ureter, bladder (CT KUB) - calcifications
  • Urinalysis - microhaematuria
  • Renal US: pregnancy and under 16 - calcifications and dilation
  • Urine pregnancy test - exclude pregnancy and ectopic pregnancy
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21
Q

Describe the acute management of nephrolithiasis

A
  • IV fluids
  • Analgesia: NSAIDS
    Ibuprofen/ rectal diclofenac
    IV paracetamol if NSAIDs CI
  • Ab if infection
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22
Q

Describe the management of nephrolithiasis <10mm

A
  • If stones are <5mm they should pass spontaneously
  • Alpha blocker (Tamsulosin) may be given to help passage of ureteric stones between 5-10mm
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23
Q

Describe the surgical management of nephrolithiasis

A
  • 2nd - Ureteroscopy - retrieve through urethra (higher stone free rate)
  • 1st - Shock wave lithotripsy (SWL) - sound waves to break stone into fragments (least invasive)
  • 3rd (1st if >20mm): Percutaneous nephrolithotomy (PCNL) - remove stone through incision in back (very invasive)
  • Open surgery
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24
Q

What are the guidelines on preventing recurrent stones

A
  • Increase fluid intake (2.5-3L)
  • Add fresh lemon to water
  • Maintain normal Ca
  • Reduce dietary salt intake
  • Limit dietary protein
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25
Q

What food should be avoided in calcium stones

A

Oxalate-rich foods
* Spinach
* Rhubarb
* Nuts
* Black tea

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26
Q

Which food should be avoided in uric acid stones

A

Purine-rich food
* Kidney
* Liver
* Sardines

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27
Q

Give 2 complications of nephrolithiasis

A
  • Obstruction and hydronephrosis (swollen) - AKI + RF
  • Urosepsis - infected obstructed stone
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28
Q

Define acute kidney injury (AKI)

A

Sudden decline in renal function over hours or days.

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29
Q

Describe the classification of AKI (KDIGO)

A

Kidney Disease: Improving Global Outcomes’ (KDIGO) criteria defines AKI based on one of the following:
- increase in serum creatinine by ≥ 26 micromol/L within 48 hours
- increase in serum creatinine to ≥ 1.5 times baseline within 7 days
- Urine output < 0.5 ml/kg/hr for six hours

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30
Q

Prerenal causes of AKI

A

Due to inadequate blood supply to kidneys (Hypoperfusion):
* HF
* Haemorrhage
* Sepsis
* Hypovolaemia
*Secondary to NSAIDs and ACEi use

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31
Q

Intrinsic causes of AKI

A

Nephron and parenchyma damage:
* Tubular necrosis - mc
* Interstitial nephritis
* Glomerulonephritis

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32
Q

Post-renal causes of AKI

A

Obstruction to outflow:
* Urinary stones
* BPH
* Strictures
* Malignancy - pelvis, abdo

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33
Q

6 RFs of AKI

A
  • Over 65
  • CKD/ previous AKI
  • DM
  • HF
  • Nephrotoxic drugs - NSAIDs & ACEi
  • Multiple myeloma
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34
Q

Describe the presentation of AKI

A

• Pre-renal: Thirst (hypovolaemia) and Hypotension
• Oliguria and haematuria
• LUTS Sx - urgency, frequency
• N+V
• Intrinsic - fever, rash +/- arthralgia
• Post-renal - Palpable bladder
• Fluid overload - swollen ankles, orthopnoea

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35
Q

Complications of AKI and how they present

A
  • Hyperkalaemia - arrhythmia
  • Hyperuraemia - encephalopathy, bruising, pericarditis
  • Fluid overload - oedema
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36
Q

Describe the investigation of AKI

A
  • FBC - anaemia, leukocytosis
  • U+E - Elevated serum K+
  • Urinalysis - nitrates, RBCs, WBCs, proteinuria
  • Raised CRP - infection/ vasculitis
  • Raised creatinine
  • ECG - hyperkalaemia changes
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37
Q

Describe management of AKI

A
  • Hypovolaemia - IV fluid
  • Hypervolemia - loop diuretics (furosemide)
  • Metabolic acidosis - Na bicarbonate
  • Hyperkalaemia (>6.5mmol/l) - IV Ca gluconate
  • Obstruction - catheter to relieve
  • Dialysis for severe cases
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38
Q

4 groups of people most affect by UTIs

A
  • Women
  • Children
  • Elderly
  • Hospitalised patients
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39
Q

What are the 5 common bacteria that cause UTIs

A

KEEPS:
* Klebsiella - catheter
* E.coli - mc
* Enterococci
* Proteus mirabilis - renal stones
* Staph. saprophyticus - young women

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40
Q

Why are females more susceptible to UTIs than males

A

Shorter urethra that is closer to the anus so it is easier for bacteria to colonise

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41
Q

What investigations are done for all UTIs

A
  • GS: Midstream urine (MSU) sample to send for culture, microscopy and susceptibility testing
  • Urine dipstick
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42
Q

Name an upper UTI

A

Pyelonephritis

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43
Q

What is pyelonephritis

A

Infection of renal parenchyma and renal pelvis/ upper ureter

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44
Q

Describe the epidemiology of pyelonephritis

A
  • Females <35
  • Associated with significant sepsis and systemic upset
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45
Q

What are the routes of infection in pyelonephritis

A
  • Ascending - urethra colonised with bacteria during intercourse
  • Haematogenous - s.aureus
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46
Q

RFs of pyelonephritis

A
  • Frequent sexual intercourse
  • Renal stones
  • Catheters
  • PKD
  • DM
  • Hx of UTIs
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47
Q

Describe the presentation of pyelonephritis

A
  • Flank/ loin pain
  • Fever & myalgia
  • Costovertebral angle tenderness
  • Pyuria (pus + wbc in urine)
  • N+V
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48
Q

How is pyelonephritis investigated

A
  • Urine dipstick: leukocytes, nitrates, non-visible haematuria
  • Blood culture - bacterial growth
  • US - rule out obstruction in upper tract
  • Raised ESR and CRP
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49
Q

Treatment of pyelonephritis

A
  • Broad spectrum Ab - e.g. co-amoxiclav
  • Pregnancy: cefalexin or, if severe, IV cefuroxime
  • Drain obstructed kidney
  • Analgesia - paracetamol
  • Fluid replacement
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50
Q

Complication of pyelonephritis

A

Renal abscess - mc in diabetics

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51
Q

Define cystitis

A

Inflammation of the bladder
* Lower UTI

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52
Q

Causes and RFs of cystitis

A

Cause: E.coli - mc
RFs:
* Urinary catheters
* DM
* Frequent sex
* Hx of UTI
* Post menopause
* Female

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53
Q

Presentation of cystitis

A
  • Suprapubic tenderness
  • LUTS: Dysuria, frequency, urgency
  • Haematuria
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54
Q

Investigation of cystitis

A

MSU sample:
* Urinalysis - +ve nitrates, leukocyte esterase and Hb
* Microscopy - RBC, WBC, bacteria
* Culture + sensitivity - identify infecting organism

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55
Q

Treatment of cystitis

A

Non-pregnant women
* oral nitrofurantoin or trimethoprim for 3 days
Complicated, non-pregnant:
* Ciprofloxacin
Pregnant:
* Amoxicillin or cefalexin

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56
Q

Define urethritis

A

Urethral inflammation
* Can be with or without infectious causes
* mc a sexually acquired disease

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57
Q

What are the causes of infectious urethritis

A
  • Gonococcal - Neisseria gonorrhoea (N.G)
  • Non-gonococcal (mc) - chlamydia trachomatis (C.T)
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58
Q

What causes non-infectious urethritis

A

trauma
Irritation
Urethral stricture

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59
Q

5 RFs of urethritis

A
  • Male to male sex
  • Unprotected sex
  • multiple sex partners
  • Age 15-24
  • Female sex
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60
Q

Signs and symptoms of urethritis

A
  • Can be asymptomatic
  • Dysuria
  • Urethral itching and pain
  • Urethral discharge
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61
Q

Investigation of urethritis

A
  • Nucleic acid amplification test (NAAT) - diagnose N.G or C.T
  • Culture of urethral discharge
  • Gram stain of urethral discharge: gram -ve diplococcus = gonorrhoea
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62
Q

Describe results of a culture of urethral discharge of someone with N.G urethritis

A

Chocolate agar positive
* grey/ white

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63
Q

Treatment of urethritis

A
  • NG - IM ceftriaxone with oral azithromycin
  • CT - doxycycline 100 mg twice a day for 7 days (or azithromycin in pregnancy)
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64
Q

Complication of urethritis

A

Reactive arthritis

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65
Q

What is acute bacterial prostatitis

A

Acute infection in the prostate presenting with rapid onset of symptoms

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66
Q

RFs and causes of acute bacterial prostatitis

A

E.coli - mc cause

  • UTI ++
  • mc in men <50
  • Benign prostatic enlargement
  • Catheters
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67
Q

Presentation of acute bacterial prostatitis

A
  • Fever, chills, malaise
  • Tender prostate
  • LUTS - dysuria, frequency, weak stream
  • Warm/ soft boggy gland
  • Perineal pain
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68
Q

Investigation of acute bacterial prostatitis

A
  • Urine dipstick - leukocytes and bacteria
  • Blood and urine cultures - identify organism
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69
Q

Treatment of acute bacterial prostatitis

A
  • Oral ciprofloxacin, levofloxacin
  • Sepsis: IV piperacillin, IV cefotaxime
  • NSAIDs to relieve pain
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70
Q

Define chronic prostatitis

A

Over 3 months of urogenital pain with or without infection

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71
Q

Presentation of chronic prostatitis

A
  • Urogenital pain - may affect perineum, genitalia, rectum
  • LUTS - dysuria, hesitancy, frequency
  • Sexual dysfunction - Erectile dysfunction, pain on ejaculation
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72
Q

Treatment of chronic prostatitis

A
  • Analgesia
  • Laxatives
  • Alpha blockers (Tamsulosin)
  • Ab if infection
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73
Q

Complications of acute bacterial prostatitis

A
  • Sepsis
  • Prostate abscess
  • Acute urinary retention
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74
Q

Define epididymo-orchitis

A
  • Epididymitis - inflammation of epididymis
  • Orchitis - inflammation of the testes
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75
Q

Function of epididymis

A

Coiled tube that stores sperm and transports it from the testes

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76
Q

Causes of E-O

A
  • E.coli
  • STIs - N.g, C.t
  • Mumps
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77
Q

Presentation of E-O

A
  • Unilateral scrotal pain and swelling
  • Phren’s sign: pain relieved with elevating scrotam
  • Cremaster reflex intact
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78
Q

Investigation of E-O

A
  • Urinalysis - first void sample
  • NAAT (Nucleic acid amplification test)
  • Culture of urethral secretions
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79
Q

Differential diagnosis of E-O

A

Testicular torsion

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80
Q

How is E-O managed

A
  • Ab depending on organism
  • Ceftriaxone and doxycycline
  • Analgesia
  • Supportive underwear
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81
Q

Complications of E-O

A
  • Sub-fertility or infertility
  • Abscess
  • Reactive arthritis
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82
Q

What is complicated vs Non-complicated UTI

A
  • complicated- males, pregnant, children, catheterised, immunocompromised
  • uncomplicated - non pregnant women
83
Q

What is polycystic kidney disease

A
  • Genetic disorder where the kidneys develop multiple fluid filled cysts
  • Can be autosomal dominant or recessive
84
Q

Which type of PKD is more common

A

Autosomal dominant PKD

85
Q

What causes ADPKD

A
  • PKD1 (mc and severe) and PKD2 mutations
    Type 1 is mc a mutation in chromosome 16
    Type 2 = chromosome 4
86
Q

Who is most commonly affected by ADPKD

A

Males aged 20-30

87
Q

Explain the pathophys of ADPKD

A
  • PKD 1 + 2 code for protein polycystin
  • In nephron, urinary filtrate flows by and causes cilia to bend
  • Polycystin 1 + 2 allow Ca2+ influx which inhibits cell proliferation
  • PKD mutation = no inhibition = cell proliferation = cysts
88
Q

Presentation of ADPKD

A
  • Bilateral flank/back/abdo pain
  • Painless haematuria - ruptured cysts
  • HTN
  • Palpable kidneys
  • Headaches associated with stroke
89
Q

Investigation of PKD

A
  • Kidney US - enlarged kidney with cysts
  • CT/MRI abdo/pelvis - cystic disease, kidney volume
  • CT brain - ruptured aneurysm
  • Genetic testing - if other tests are inconclusive
90
Q

Management of PKD

A
  • Vasopressin receptor antagonist (Tolvaptan) - slow development of cysts and progression of renal failure
  • HTN - ACEi (Ramipril)
  • UTIs and infection- Ab (ciprofloxacin)
  • Abdo pain and infected cysts - analgesia (avoid NSAIDs)
  • Transplant/ dialysis at end stage RF
91
Q

Complications of PKD

A
  • Ruptured cyst
  • Renal stones
  • Cerebral aneurysm
  • End-stage renal failure
92
Q

Describe autosomal recessive PKD

A
  • Less common than ADPKD but more severe
  • Disease of infancy
93
Q

Causes of ARPKD

A
  • PKHD1 mutation of chromosome 6
  • makes protein called fibrocystin
94
Q

Presentation of ARPKD

A
  • Oligohydramnios - too little amniotic fluid as foetus doesn’t produce enough urine
  • Potter syndrome (uterine wall compresses foetus) - underdeveloped ear cartilage, low set ears, flat nasal bridge, far set eyes, limb deformities
95
Q

Investigation of ARPKD

A

• Pre/neonatal US - bilaterally large kidneys with cysts and oligohydramnios
• Kidneys later decrease in size as amount of fibrosis increases

96
Q

Define chronic kidney disease (CKD)

A
  • progressive deterioration in renal function
  • Issues develop over at least 3 months
97
Q

Describe the G score for classification of CKD

A

Based on eGFR
* G1: 90+
* G2: 60-89
* G3a: 45-59
* G3b: 30-44
* G4: 15-29
* G5: <15 (ESRF)

98
Q

Which G scores are not classified as CKD unless accompanied with renal damage

A

G1 and G2

99
Q

Describe the A score

A

Based on albumin: creatinine ratio (ACR)
* A1 = <3mg/mmol (normal)
* A2 = 3-30mg/mmol
* A3 = >30mg/mmol

100
Q

RFs of CKD

A
  • HTN (2nd mc)
  • DM (mc)
  • > 50
  • Childhood kidney disease
  • Glomerulonephritis
  • Nephrotoxic drugs (NSAIDs)
  • Smoking
101
Q

Pathophysiology of CKD

A

Many nephrons are damaged in CKD which results in low GFR
* Increase in intra-glomerular pressure with glomerular hypertrophy in response to renal injury
* Increased glomerular permeability to macro-molecules
* These result in toxicity to the mesangial matrix, causing mesangial cell expansion, inflammation, fibrosis, and glomerular scarring
* Increased angiotensin 2 causes upregulation of transforming growth factor beta (TGF-beta) which contributes to mesangial (supportive tissue) scarring

102
Q

Presentation of CKD

A
  • Restless legs
  • Pruritus (itching) - accumulation of toxic waste
  • Oedema
  • Fatigue
  • Anorexia
  • Nausea +/- vomiting
103
Q

Investigation of CKD

A
  • eGFR - <60mL/min1.73m²
  • ACR - >3mg/mmol = significant proteinuria
  • Urine dip - proteinuria and haematuria
  • Renal ultrasound - bilateral kidney atrophy , evidence of obstruction
104
Q

Management of stage 5 CKD

A
  • Dialysis
  • Renal transplant
105
Q

Cx of CKD and how each are managed

A
  • Anaemia - erythropoietin and Fe
  • CVD - ACEi (e.g. Ramipril) and statins
  • Renal bone disease - calcitriol and reduce dietary phosphate (fish, nuts etc)
  • Metabolic acidosis - oral sodium bicarbonate
106
Q

Define nephritic syndrome and give identifying characteristics

A

Caused by inflammation (T3 hypersensitivity) that damages the glomerular basement membrane leading to:
* Haematuria (+ little proteinuria)
* Oliguria (reduced urine output)
* HTN
* Oedema

107
Q

Give 4 disorders that could cause nephritic syndrome

A
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy (mc)
  • SLE nephropathy
  • Goodpasture’s syndrome
108
Q

Presentation of IgA nephropathy (3)

A
  • Visible haematuria - ribena/coke colour
  • typically presents 1-2 days after upper respiratory tract infection or gastroenteritis
  • typically a young male
109
Q

Investigation of IgA nephropathy

A
  • Kidney biopsy:
  • immunofluorescence = IgA deposits in mesangial cells
  • Light microscopy = glomerular mesangial proliferation
  • electron microscopy: immune complexes are seen in the mesangium
110
Q

How is IgA nephropathy managed

A
  • ACEi - BP control
  • corticosteroids
111
Q

State the main DDx of IgA nephropathy and how they can be distinguished

A
  • IgA vasculitis (Henoch-Schonlein purpura)
  • IgA nephropathy only affects kidneys whereas IgA vasculitis has systemic effects
112
Q

What is post-streptococcal glomerulonephritis (PSGN)

A

usually an immunologically-mediated (T3 hypersensitivity) delayed consequence of pharyngitis or skin infections caused by streptococcus pyogenes

113
Q

Investigation of PSGN

A
  • Immunofluorescence - IgG, IgM and C3 deposits along glomerular BM and mesangium (starry sky)
  • Light microscope - hypercellular and enlarged glomeruli
  • Electron microscope - subepithelial deposits (humps)
114
Q

Presentation of PSGN

A
  • Visible haematuria occurs 1 to 3 weeks after the onset of strep infection
  • Proteinuria
  • headache and malaise
115
Q

Treatment of PSGN

A
  • Self limiting but can progress depending on age
  • Proteinuria - Furosemide
  • HTN - Ramipril
  • Ab
116
Q

Complication of PSGN

A

Rapidly progressing glomerulonephritis (RPGN)

117
Q

What is Goodpasture’s syndrome

A

Pulmonary haemorrhage and glomerulonephritis caused by anti-GBM (glomerular BM)

118
Q

Presentation of Goodpasture’s

A
  • Haemoptysis (cough up blood), SOB, cough
  • haematuria, proteinuria, HTN
  • Reduced urine output, lethargy, weight loss
119
Q

Treatment of Goodpasture’s

A
  • Prednisolone
  • Plasma exchange
120
Q

What is SLE nephropathy

A

Lupus nephritis secondary to systemic lupus erythematosus

121
Q

Diagnosis of Lupus nephritis

A
  • anti-nuclear antibodies
  • anti-double stranded DNA Ab
122
Q

How is lupus nephritis treated

A
  • Corticosteroids
  • Immunosuppressants
123
Q

What is the characteristic triad of haemolytic uremic syndrome

A
  • Microangiopathic haemolytic anaemia - physical damage to RBC
  • thrombocytopenia
  • AKI
124
Q

Causes of HUS

A

Shiga toxin producing E.coli

125
Q

Tx of HUS

A
  • IV fluids
  • Ab with non-E.coli HUS
126
Q

Give identifying characteristics of Nephrotic syndrome

A
  • proteinuria (>3.5g/24h)
  • hypoalbuminaemia (<30g/L)
  • Peripheral oedema
  • Hyperlipidaemia
127
Q

Primary causes of nephrotic syndrome

A

Due to direct sclerosis of podocytes on the glomerulus
* minimal change disease
* Focal segmental glomerulosclerosis (FSGS)
* Membranous nephropathy

128
Q

Main secondary cause of nephrotic syndrome

A

Diabetes

129
Q

What is the most common cause of nephrotic syndrome in children

A

Minimal change disease

130
Q

Investigation of MCD

A
  • Light microscopy - normal glomeruli
  • Electron microscopy - Effacement and fusion of podocyte foot processes
131
Q

Causes of Focal segmental glomerulosclerosis

A

1) Idiopathic
2) Heroin or HIV infection

132
Q

Investigation of Focal segmental glomerulosclerosis

A
  • Light - segmental sclerosis
  • Only parts of glomeruli are affected (<50%)
133
Q

Give 3 condition associated with Membranous nephropathy

A
  • infection - HBV, HCV, malaria
  • antiphospholipase A2 Ab
  • malignancy
134
Q

Investigation of membranous nephropathy

A
  • Light microscopy - thickened GBM caused by subepithelial electron dense deposits
  • Electron - Spike and dome appearance - new growth surrounding subpodocytes immune complex deposition
135
Q

How are primary causes of nephrotic syndrome treated

A

Corticosteroids
* MCD - very responsive
* FSGS - Often resistant, ciclosporin may be used
* MN - corticosteroid + immunosuppressant

136
Q

What is Rapidly progressive glomerulonephritis

A

50% decline in GFR within 3 months

137
Q

Diagnosis of RPGN

A
  • Light - crescent moon shape in bowman’s space
138
Q

What causes RPGN

A
  • Goodpasture’s
  • Wegener’s granulomatosis (GPA)
  • Microscopic polyangiitis
139
Q

What 2 conditions can present as both nephrotic and nephritic

A
  • Diffuse proliferative GN
  • Membranoproliferative GN
140
Q

What are all testicular lumps assumed to be

A

Cancer until proven otherwise

141
Q

What is an epididymal cyst

A

Smooth, extra-testicular sac of fluid above or behind testicle
* Usually harmless

142
Q

Investigation of epididymal cyst

A

Scrotal ultrasound

143
Q

Signs and Sx of epipidymal cyst

A
  • Palpable lump that will transluminate
  • May cause pain if large
  • Separate from testicle
144
Q

What is a hydrocele

A

Painless swelling caused by fluid collection in tunica vaginalis (membrane covering testes)

145
Q

Presentation of a hydrocele

A
  • Irreducible
  • Transillumination
  • Smooth and within testicle
146
Q

Investigation of a hydrocele

A

Testicular US

147
Q

What is a varicocele

A

Abnormal dilated veins within the pampiniform venous plexus
* most occur of the left side

148
Q

Explain the pathophys of a varicocele

A
  • Pampiniform plexus drain into the testicular veins
  • Increased resistance and incompetent valves in testicular veins = backflow to pampiniform plexus
  • Left testicular vein is longer and joins left renal vein at a right angle
149
Q

Presentation of a varicocele

A
  • Palpable veins (bag of worms)
  • Testicular atrophy on affected side
  • Painless swelling
150
Q

Investigation of a varicocele

A
  • Mainly clinical
  • Scrotal US - done if physical exam is difficult
151
Q

Treatment of a varicocele

A
  • Conservative - reassurance and observation
  • If painful/testicular atrophy - surgery
152
Q

Complication of a varicocele

A
  • Infertility
  • Testicular atrophy
153
Q

What is testicular torsion

A
  • Twisting of spermatic cord with rotation of the testicle
  • Urological emergency
154
Q

Consequence of delayed treatment for testicular torsion

A

6 hour window after onset before irreversible ischaemia and necrosis

155
Q

Presentation of testicular torsion

A
  • -ve Phren’s sign - not relieved on lifting ipsilateral testicle
  • N+V
  • Firm swollen and tender testicle
  • Lower abdo pain
  • Testicular pain - unilateral, sudden onset
  • Absent cremasteric reflex
156
Q

Describe the cremasteric reflex

A
  • Swipe upper inner thigh
  • Normal reflex contract cremaster muscle, pulling up ipsilateral testis
157
Q

RF of testicular torsion

A
  • Bell clapper deformity - when testicle lies horizontal
  • <25y/o (mc 12-18)
  • Neonate
158
Q

Investigation of testicular torsion

A
  • Immediate surgical exploration
  • US to check testicular blood flow, whirlpool sign
159
Q

Treatment of testicular torsion

A
  • Viable testicle: bilateral orchiopexy - untwisted and fixed to scrotal sac
  • Non-viable testicle: ipsilateral orchiectomy (removal) and contralateral orchiopexy
160
Q

Complications of testicular torsion

A
  • Infertility/ subfertility
  • Pubertal delay
161
Q

Storage LUTS

A

Occurs when bladder should be storing urine
* Frequency
* Urgency
* Nocturia
* Incontinence

162
Q

Voiding LUTS

A

bladder outlet obstructed
* Poor stream
* Terminal dribbling
* Hesitancy
* Intermittency
* Straining

163
Q

What could cause difficulty voiding

A
  • BPH
  • Urethral stricture
  • Masses
164
Q

What are the types of incontinence

A
  • Urge: detrusor muscle overactivity e.g. frequent urination
  • Stress: Urinary leakage with increased intraabdo pressure
  • Mixed
165
Q

Investigation of incontinence

A
  • Bladder diary
  • Post void bladder scan
  • U&E
  • Cough stress test
166
Q

What is urinary incontinence

A

Micturition happens involuntarily

167
Q

Tx of stress incontinence

A
  • Pelvic floor exercises
  • Lifestyle: reduce caffeine, weight loss
  • pseudoephedrine
168
Q

Tx for urge incontinence

A
  • Bladder training
  • Lifestyle changes - weight loss, reduce caffeine
  • Anticholinergics - e.g. oxybutynin
169
Q

What is retention

A

Unable to fully empty bladder:
* Typically seen in males
* AKA overflow incontinence

170
Q

What causes retention

A
  • Obstruction
  • BPH
  • Stones
171
Q

Treatment for urinary retention

A

Catheter to drain urine

172
Q

What is a renal cell carcinoma (RCC)

A

adenocarcinoma most commonly arising from the proximal convoluted tubule epithelium

173
Q

RFs of RCC

A
  • Smoking
  • Genetic
  • Obesity
  • Haemodialysis
  • HTN
174
Q

State 2 genetic syndromes that are a RF of RCC

A
  • Von Hippel Lindau - loss of tumour suppression gene
  • Tuberculosis sclerosis
175
Q

Presentation of RCC

A

Early RCC is asymptomatic

  • Varicocele
    Classic triad:
  • haematuria
  • flank pain,
  • abdo mass
176
Q

Investigations of RCC

A
  • 1st: kidney ultrasound
  • Gold: CT chest/abdo/pelvis
  • Biopsy
177
Q

What was previously used as the main staging of RCC

A

Robson staging

178
Q

Management of RCC

A
  • Radiofrequency ablation or cryotherapy
  • Partial/radical nephrectomy
  • Palliative - embolisation
179
Q

Give 3 types of RCC

A
  • Clear cell - mc
  • Papillary
  • Chromophobe
180
Q

Describe the types of bladder cancer

A
  • transitional cell (urothelium) carcinomas - 90%
  • Squamous cell carcinoma - associated with schistosomiasis and stones
  • Adenocarcinoma - rare with poor prognosis
181
Q

RFs of bladder cancer

A
  • Smoking
  • Aromatic hydrocarbons
  • Dyes
  • Rubber
  • Drugs - cyclophosphamide, Thiazolidinediones
182
Q

Presentation of bladder cancer

A
  • Painless haematuria
  • LUTS
  • Recurrent UTIs
183
Q

Investigation of bladder cancer

A
  • Flexible cystoscopy - quick, direct visualisation
  • Urinalysis - haematuria
184
Q

Management of bladder cancer

A
  • Transurethral resection of bladder
  • Intravesical chemo (directly into bladder) - mitomycin and Bacillus Calmette-Guérin (reduce progression and recurrence)
  • Cystectomy - muscle invasive
185
Q

Describe non-invasive and invasive bladder cancer

A
  • Non-muscle-invasive bladder cancer - superficial, not invading the muscle layer of the bladder
  • Muscle-invasive bladder cancer - invading the muscle and beyond
186
Q

Types of testicular cancer

A

Germ cell - 90%
non-germ cell

187
Q

2 types of germ cell tumours

A
  • Seminoma - mc, made of germ cells that multiply with no differentiation
  • Non-seminoma (Teratoma) - contain several types of tissue
188
Q

2 types of non-germ cell tumours

A
  • Leydig cell tumours
  • Sertoli
189
Q

RFs of testicular cancer

A
  • FHx
  • Infertility
  • Caucasian male
  • Cryptorchidism - testis don’t descend
  • Age - mc 20-40
190
Q

Presentation of testicular cancer

A
  • Firm non-tender testicular lump
  • Doesn’t transilluminate
191
Q

Investigation of testicular cancer

A
  • Urgent doppler ultrasound
  • raised Beta-human chorionic gonadotrophin
  • raised LDH (non-specific)
  • raised alpha-fetoprotein
  • CXR is respiratory Sx
192
Q

Treatment of testicular cancer

A
  • Radical inguinal orchidectomy
  • Sperm banking
  • Neoadjuvant chemotherapy
193
Q

DDx of scrotal mass

A
  • Testicular torsion
  • Hydrocele
  • Varicocele
  • Epididymal cysts
194
Q

What investigations are essential for visible haematuria

A
  • Upper tract imaging
  • Flexible cytoscopy
195
Q

What type of cancer are majority of prostate cancers

A

Adenocarcinomas growing in the peripheral (outermost) zone of the prostate

196
Q

RFs of prostate cancer

A
  • Age - 50+
  • Afro-Caribbean
  • FHx
  • Genetic - BRCA1 and BRCA2
  • Anabolic steroids
197
Q

Presentation of prostate cancers

A
  • LUTS
  • Systemic cancer Sx - weight loss, fatigue
  • Asymmetrical,, hard, nodular prostate with loss of median sulcus
  • Bone pain
198
Q

Where does prostate cancer typically metastasise to

A

Bone (sclerotic lesions) and lymph nodes

199
Q

Investigation of prostate cancer

A
  • PSA and DRE
  • MRI
  • Transrectal US and biopsy
  • Grading using biopsy - Gleason score (>8)
200
Q

Treatment for localised prostate cancer

A
  • Observation
  • Radical prostatectomy
201
Q

Treatment of locally advanced prostate cancer

A

*Radical prostatectomy
* Radiotherapy with anti-androgen therapy

202
Q

Treatment of metastatic prostate cancer

A

Hormone therapy:
* androgen deprivation therapy + docetaxel chemo
* GnRH agonists - e.g goserelin
* Bilateral orchidectomy

203
Q

mc type of colorectal cancer

A

Adenocarcinoma

2a - SBCS (9 decks)

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