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FINALS > Renal & uro-genital > Flashcards

Renal & uro-genital Flashcards

1
Q

CKD

How is chronic kidney disease (CKD) scored using the G system?

A
  • G1 = GFR>90 but needs kidney damage (protein or haematuria) for Dx
  • G2 = GFR 60–90 but needs kidney damage (above incl. raised urine ACR) for Dx
  • G3a = GFR 45–59
  • G3b = GFR 30–44
  • G4 = 15–29
  • G5 = <15 end stage renal failure (ESRF)
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2
Q

CKD

What variables does the Modification of Diet in Renal Disease equation use to calculate GFR?

A

CAGE –

  • Creatinine
  • Age
  • Gender
  • Ethnicity
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3
Q

CKD

How is CKD scored using the A system?

A
  • A1 = <3mg/mmol
  • A2 = 3–30mg/mmol
  • A3 = >30mg/mmol
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4
Q

CKD

What are the causes of CKD?

A
  • Systemic (v common) = DM, HTN
  • Glomerular = primary (IgA nephropathy) or secondary (SLE)
  • Vascular = vasculitis + renal artery stenosis
  • Tubulointerstitial = amyloidosis + myeloma
  • Congenital = PKD + Alport syndrome
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5
Q

CKD

What is the clinical presentation of CKD?

A
  • Non-specific = nausea, HTN, anaemia, loss of appetite, pruritus, pallor
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6
Q

CKD

What initial investigations would you do in someone for CKD?

A
  • FBC = normocytic anaemia of chronic disease, check iron studies
  • U&E, Ca2+ (low), phos (high), PTH (high) = secondary hyperparathyroid
  • Albumin creatinine ratio (ACR) from first void urine ≥3mg/mmol = significant
  • Renal USS
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7
Q

CKD

When would you refer someone with CKD to a nephrologist?

A
  • eGFR <30
  • ACR ≥70mg/mmol
  • Uncontrolled HTN despite ≥4 antihypertensives
  • Accelerated progression = decrease in eGFR of 15 or 25% in 12m
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8
Q

CKD

What are the various complications of CKD and why they occur?

A
  • CVD = #1 cause of death
  • Inadequate waste excretion = uraemia (encephalopathy, pericarditis), high phosphate + potassium
  • Poor fluid balance regulation = HTN, oedema
  • Acid-base imbalance = metabolic acidosis
  • Reduced EPO = anaemia
  • Lack of vitamin D activation for calcium + waste excretion of phosphate = renal bone disease (osteomalacia, osteoporosis + osteosclerosis)
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9
Q

CKD
In CKD how do you manage…

i) CVD risk?
ii) oedema?
iii) anaemia?
iv) ESRF?

A

i) Atorvastatin
ii) Fluid + salt restriction or if not furosemide
iii) Correct iron deficiency first, then monthly s/c EPO
iv) Renal replacement therapy (haemodialysis, peritoneal dialysis or renal transplant)

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10
Q

CKD

What is the management of mineral bone disease in CKD?

A
  • Renal diet (avoid high K+ & phosphate foods) = first-line
  • Phosphate binders like calcium carbonate/acetate = second-line
  • Alfacalcidol for vitamin D deficiency or parathyroidectomy last-line
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11
Q

CKD

What is a side effect of using calcium based phosphate binders?

A
  • Hypercalcaemia

- Vascular calcification

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12
Q 
CKD
What is the management of proteinuria and HTN in CKD?
What's the criteria for starting?
How might this affect renal function?
What are your targets?
A
  • ACEi/ARB are first-line
  • DM + ACR >3, HTN + ACR >30, all with ACR >70
  • Decrease in eGFR of ≤25% or creatinine rise of ≤30% is acceptable
  • <140/90 or <130/80 if ACR >70
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13
Q

CKD

What is the process of haemodialysis?

A
  • AV fistula (brachiocephalic, radiocephalic) created by vascular surgeons 8w before treatment or can use tunnelled cuffed catheter so they can be dialysed 3x/week in hospital via machine with counter-current flow of blood/dialysate, haemofiltration via decreased dialysate hydrostatic pressure.
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14
Q

CKD

When examining a fistula, what should you notice?

A
  • Palpable thrill

- Machinery murmur on auscultation

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15
Q

CKD

What is the process of peritoneal dialysis?

A
  • Dialysate is injected into abdominal cavity via a permanent catheter + filtration occurs using the peritoneal membrane as the dextrose concentration of the solution draws waste products from the blood
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16
Q

CKD

What are the 2 types of peritoneal dialysis?

A
  • Continuous ambulatory peritoneal dialysis (CAPD) = dialysate in peritoneum all day + changed about QDS, pts continue normal activities
  • Automated peritoneal dialysis (APD) = machine continuously replaces dialysate in abdomen overnight to optimise ultrafiltration over 8–10h
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17
Q

CKD
What are the 2 types of renal transplants?
What is the ongoing management?
What might you find on examination?

A
  • Living donor (lasts 12–15y) or deceased donor (lasts 10–12y)
  • Lifelong immunosuppression = tacrolimus, mycophenolate
  • Hockey-stick scar and palpable kidney
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18
Q

CKD

What are the main complications with haemodialysis?

A
  • Infection
  • Aneurysm
  • Thrombosis
  • Stenosis
  • STEAL syndrome = inadequate blood flow to limb distal of AV fistula leading to ischaemia
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19
Q

CKD
What is the key complication of peritoneal dialysis?
How does it present?
How do you manage it?

A
  • Peritonitis from coagulase-negative staphylococcus epidermidis
  • Abdo pain, pyrexia, cloudy PD fluid
  • Vancomycin in dialysate + PO ciprofloxacin
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20
Q

CKD

What are some other complications of peritoneal dialysis?

A
  • Peritoneal sclerosis > failure
  • Constipation can make ineffective
  • Weight gain
  • Ultrafiltration failure overtime as dextrose absorbed
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21
Q

CKD

What are some complications of renal transplant?

A
  • Malignancy
  • Infection (incl unusual PCP, CMV, TB)
  • Graft rejection (hyperacute in mins, acute <6m or chronic >6m)
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22
Q

CKD

What is the difference between hyperacute and acute graft rejection?

A
  • Hyperacute = pre-existing Ab against ABO/HLA antigens leading to T2HR needing GRAFT REMOVAL
  • Acute = mismatched HLA, ?reversible with steroids + immunosuppressants
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23
Q

AKI

What is acute kidney injury (AKI) defined by?

A

Abrupt deterioration in renal function leading to…

  • Increase of serum creatinine of 26.5umol/L <48h
  • Increase in serum creatinine ≥1.5x baseline within 1w OR
  • Urine output <0.5ml/kg/h for 6h
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24
Q

AKI

What are the three stages of AKI?

A
  • Stage 1 = creatinine 1.5–1.9x baseline, UO <0.5ml/kg/h for 6h, creatinine rise ≥26 in 48h
  • Stage 2 = creatinine 2–2.9x baseline, UO <0.5ml/kg/h for 12h
  • Stage 3 = creatinine ≥3x baseline, UO <0.3ml/kg/h for ≥4h or creatinine >354
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25
Q

AKI

How is the aetiology of AKI divided?

A
  • Pre-renal = impaired perfusion of the kidneys
  • Renal = instrinsic kidney damage
  • Post-renal = obstructive uropathy causing urine backflow affecting renal function
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26
Q

AKI

What are some pre-renal causes of AKI?

A
  • Shock = hypovolaemia, cardiogenic, sepsis

- Atherosclerosis = renal artery stenosis

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27
Q

AKI

What are some renal causes of AKI?

A
  • Glomerular = glomerulonephritis
  • Tubules = acute tubular necrosis
  • Interstitium = acute interstitial nephritis (can be caused by penicillins)
  • Vessels = HUS, vasculitis
  • Tumour lysis syndrome + rhabdomyolysis
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28
Q

AKI

What are some post-renal causes of AKI?

A
  • Stones
  • Renal/urinary tract malignancy
  • BPH
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29
Q

AKI

What are some risk factors for developing an AKI?

A
  • Age ≥75
  • CKD + renal transplant
  • Heart failure + hypovolaemia
  • DM
  • Nephrotoxic drugs = NSAIDs, aminoglycosides, ACEi/ARBs, diuretics, contrast
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30
Q

AKI

What are the complications and so clinical presentation of AKI?

A
  • Hyperkalaemia = arrhythmias = cardiac arrest
  • Fluid overload = pulmonary + peripheral oedema
  • Metabolic acidosis
  • Oliguria
  • Uraemia > encephalopathy, pericarditis
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31
Q

AKI
What investigations would you do in AKI?
What result would make you think of dehydration as a cause?

A
  • FBC, U&E, LFT, glucose, clotting, calcium, ABG
  • Urinalysis, bladder scan, ECG, CXR
  • Renal USS <24h if ?cause + risk of urinary tract obstruction
  • Urea proportionally higher than rise in creatinine
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32
Q

AKI

What is the management of a pre-renal AKI?

A
  • IV fluids if hypovolaemia
  • IV Abx if septic
  • Stop DAMN drugs (Diuretics, ACEi, Metformin, NSAIDs) also gent
  • Suspend renally excreted drugs = lithium, digoxin
  • Adjust renally excreted drugs = opioids (oxycodone preferred)
  • Monitor fluid balance input/output
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33
Q

AKI

What is the mechanism of NSAIDs and ACEi causing AKI?

A
  • Prostaglandins cause DILATION of AFFERENT arterioles so NSAIDs cause CONSTRICTION + so reduced perfusion/GFR
  • Angiotensin-II causes CONSTRICTION of EFFERENT arterioles so ACEi cause DILATION + so reduced pressure/GFR
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34
Q

AKI
What is the management of…

i) renal AKI?
ii) post-renal AKI?

A

i) Nephrology review to identify the less common causes

ii) Catheterisation + urology r/v

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35
Q

AKI

What are the indications for acute dialysis?

A

AEIOU –

  • Acidosis (severe metabolic pH <7.2)
  • Electrolyte imbalance (persistent refractory hyperkalaemia >7)
  • Intoxication (poisoning)
  • Oedema (refractory pulmonary oedema)
  • Uraemia (encephalopathy or pericarditis)
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36
Q

HYPERKALAEMIA

What are the causes of hyperkalaemia?

A
  • Impaired excretion = AKI/CKD, ACEi, K+ sparing diuretics, LMWH, Addison’s
  • Increased release = rhabdo, tumour lysis, lactic acidosis
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37
Q

HYPERKALAEMIA

What investigations would you do in hyperkalaemia?

A
  • U&Es > mild 5.5–5.9, moderate 6.0–6.4, severe ≥6.5
  • ECG (tall-tented T waves, small P waves + widened QRS)
  • Can eventually lead to sinusoidal pattern + asystole or VF
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38
Q

HYPERKALAEMIA
When would hyperkalaemia require emergency treatment?
What first-line treatment would you give?
How does it work?

A
  • Severe ≥6.5 or ≥6 WITH ECG changes
  • IV calcium gluconate 10ml of 10%
  • Stabilises the myocardium, does NOT impact potassium levels
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39
Q

HYPERKALAEMIA
What other acute treatment is given in emergent hyperkalaemia?
What does this do to potassium levels?

A
  • Combined insulin/dextrose infusion (actrapid 10 units/dex 50ml of 50%)
  • Nebulised salbutamol
  • Short-term shift of K+ from ECF > ICF
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40
Q

HYPERKALAEMIA

What treatments for hyperkalaemia actually removes the potassium from the body?

A
  • Calcium resonium (PO or enema which is more effective as K+ secreted from rectum)
  • Loop diuretics (furosemide)
  • Dialysis if refractory hyperkalaemia >7mmol/L
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41
Q

RENAL STONES

What are the different types of renal stones that you can get?

A
  • Calcium oxalate = #1, radiopaque
  • Calcium phosphate = RTA types 1 + 3
  • Struvite = staghorn calculi, associated with Proteus mirabilis + recurrent UTI
  • Cysteine = semi-opaque, ground glass appearance, seen in AR cystinuria
  • Xanthine + uric acid stones = radiolucent
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42
Q

RENAL STONES

What are some risk factors for the development of renal stones?

A
  • Dehydration
  • Hypercalciuria + hypercalcaemia
  • Hyperparathyroidism
  • Drugs (calcium stones) = loop diuretics, steroids, acetazolamide
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43
Q

RENAL STONES

What is the clinical presentation of renal stones?

A
  • Renal colic = unilateral loin>groin, fluctuates in onset and severity
  • Haematuria
  • N+V
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44
Q

RENAL STONES

What initial investigations would you do in renal stones?

A
  • Urine dipstick = haematuria and send urine MC&S
  • FBC, CRP (infection), U&E to monitor electrolytes
  • Calcium + urate levels
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45
Q

RENAL STONES
What is the first-line and gold standard imaging? What might it show?
What other imaging would you consider and why?

A
  • Non-contrast CT KUB = peri-ureteric stranding ?recent stone passage
  • XR for Mx as need visible stone for extracorporeal shockwave lithotripsy
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46
Q

RENAL STONES

What is a key complication of renal stones?

A
  • Obstruction, commonly at ureteropelvic junction, pelvic brim or vesicoureteric junction leading to AKI or infection with obstructive pyelonephritis
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47
Q

RENAL STONES

How can you prevent calcium stone formation?

A

Decrease hypercalciuria –

  • High fluid intake, low animal protein + low salt diet
  • Thiazide diuretics to increase distal tubular calcium resorption
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48
Q

RENAL STONES

How can you prevent oxalate stones?

A
  • Cholestyramine + pyridoxine to reduce urinary oxalate secretion
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49
Q

RENAL STONES

How can you prevent uric acid stones

A
  • Allopurinol ± urinary alkalinisation (e.g., PO bicarb)
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50
Q

RENAL STONES
When would renal stones need emergency management?
How would you manage it?

A
  • Ureteric obstruction with infection

- Decompression via nephrostomy tube, ureteric catheter or stent

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51
Q

RENAL STONES

What is the management for renal stones?

A
  • NSAID analgesia = IM diclofenac 75mg
  • Ureteric calculi <5mm = expectant
  • Stone burden <2cm = extracorporeal shockwave lithotripsy
  • Stone burden <2cm in pregnancy = ureteroscopy
  • Complex renal calculi + staghorn = percutaneous nephrolithotomy
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52
Q

URINARY TRACT INFECTION
What is the pathophysiology of urinary tract infections (UTI)?
What is the most common cause?
What are some other causes?

A
  • Trans-urethral ascent of colonic commensals
  • E.coli (gram -ve anaerobic rod)
  • Klebsiella, Proteus, pseudomonas
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53
Q

URINARY TRACT INFECTION

What are some risk factors for UTIs?

A
  • Women (shorter urethra than men)
  • Pregnancy
  • Catheters
  • Renal stones
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54
Q

URINARY TRACT INFECTION

What is the clinical presentation of lower UTIs?

A
  • LUTS = dysuria, increased frequency, urgency, offensive urine, haematuria
  • Suprapubic tenderness
  • Low-grade fever
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55
Q

URINARY TRACT INFECTION
What is the clinical presentation of upper UTIs?
What are some complications of this?

A
  • Loin/back pain with renal angle tenderness on examination
  • Fever, N+V
  • Renal abscess, chronic pyelonephritis + sepsis
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56
Q

URINARY TRACT INFECTION
What first-line investigations would you do in suspected UTI?
What results would confirm the diagnosis?

A
  • Urine dipstick + send off MSU for MC&S
  • Nitrites + leukocytes (nitrites suggest bacteria, isolated leukocytes not UTI)
  • Haematuria may be present
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57
Q

URINARY TRACT INFECTION

What additional investigations would you consider in pyelonephritis?

A
  • Routine bloods show raised inflammatory markers (WCC, CRP)

- Renal USS to look for hydronephrosis if severe infection + ?post-renal AKI

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58
Q

URINARY TRACT INFECTION
What is the management of UTI in…

i) not pregnant women?
ii) symptomatic pregnant women?
iii) men?
iv) catheterised not-pregnant?
v) catheterised pregnant?

A

i) Nitrofurantoin or trimethoprim for 3d
ii) Nitrofurantoin (avoid 3rd trimester), 2nd line = amoxicillin or cefalexin
iii) Nitrofurantoin or trimethoprim for 7d
iv) ONLY if symptomatic give nitrofurantoin or trimethoprim for 7d
v) Cefalexin for 7d

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59
Q

URINARY TRACT INFECTION
How would you detect asymptomatic bacteriuria in pregnant women?
How and why is it managed?

A
  • Sample sent at first antenatal visit

- Immediate nitro if not amox/cefalexin with follow-up test of cure due to risk of progression to pyelonephritis

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60
Q

URINARY TRACT INFECTION

What antibiotic should absolutely not be given to pregnant women and why?

A
  • Trimethoprim, folate antagonist + teratogenic in first trimester
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61
Q

URINARY TRACT INFECTION
How do you manage pyelonephritis in the community?
How do you manage someone severely unwell with pyelonephritis?

A
  • PO cefalexin (7–10d) or PO ciprofloxacin (7d)

- Admission, broad-spectrum IV Abx (e.g., cipro, gent)

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62
Q

RENAL CELL CARCINOMA
What is a renal cell carcinoma (RCC)?
What is the most common histological subtype?

A
  • Adenocarcinoma of renal cortex arising from PCT epithelium

- Clear cell

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63
Q

RENAL CELL CARCINOMA

What are some associations of RCC?

A
  • Male aged >55
  • Smoking, obesity, HTN
  • Von-Hippel-Lindau syndrome + tuberous sclerosis
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64
Q

RENAL CELL CARCINOMA
What is the classic clinical presentation of RCC?
What other complications may arise form it?

A
  • Triad of haematuria, loin pain and palpable abdominal mass
  • Endo = may secrete EPO (polycythaemia), PTH (hypercalcaemia), renin + ACTH (HTN)
  • LEFT varicocele > occlusion of L testicular vein which drains into L renal vein
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65
Q

RENAL CELL CARCINOMA
What is the 2ww criteria for suspected RCC?
What investigations would you consider?

A
  • ≥45 with unexplained visible haematuria without UTI/after treatment
  • Urinalysis = haematuria
  • USS renal ?mass, CT/MRI abdomen for Dx
  • CXR may show classic cannonball metastases in the lung
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66
Q

RENAL CELL CARCINOMA

What is the management of RCC?

A
  • Confined disease = partial (T1 lesions) or radical nephrectomy (T2 + above)
  • Often resistant to chemo and radiotherapy
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67
Q

BLADDER CANCER

What are the types of bladder cancer?

A
  • Most common = transitional cell carcinoma

- Regions affected by schistosomiasis = squamous cell carcinoma

68
Q

BLADDER CANCER

What are the risk factors for the two main types of bladder cancer?

A
  • Smoking (TCC + SCC)
  • Exposure to aromatic amines (rubber, dyes, chemical industry) for TCC
  • Schistosomiasis (SCC)
69
Q

BLADDER CANCER

What is the clinical presentation of bladder cancer?

A
  • Classically painless, macroscopic haematuria
  • May present with UTIs and hydronephrosis
  • Systemic = weight loss, night sweats
70
Q

BLADDER CANCER

What is the 2ww criteria for bladder cancer?

A
  • ≥45 + unexplained visible haematuria without UTI/after treatment
  • ≥60 + unexplained non-visible haematuria WITH dysuria or raised WCC
71
Q

BLADDER CANCER

What is the diagnostic investigation for bladder cancer?

A
  • Flexible/rigid cystoscopy with biopsy

- CT/MRI CAP for staging

72
Q

BLADDER CANCER
What counts as muscle non-invasive bladder cancer?
What is the management?

A
  • Carcinoma in situ, Ta + T1

- Transurethral resection of the bladder tumour (TURBT) ± intravesical chemotherapy ± BCG immunotherapy

73
Q

BLADDER CANCER
What is the management of muscle invasive bladder cancer?
What happens afterwards?

A
  • Radical cystectomy with urinary diversion
  • Urostomy formation e.g., ileal conduit, neo-bladder
  • Radio/chemotherapy may be offered in either curative or palliative capacity
74
Q

PROSTATE CANCER
What is the histology of prostate cancers?
What are some risk factors?

A
  • Majority adenocarcinoma affecting peripheral zone
  • Non-modifiable = African ethnicity, FHx, increasing age
  • Modifiable = obesity, smoking
75
Q

PROSTATE CANCER

What is the clinical presentation of prostate cancer?

A
  • LUTS = urgency, hesitancy + retention
  • Erectile dysfunction
  • Metastatic = bone pain
  • Asymmetrical, hard, nodular prostate with loss of central sulcus on DRE
76
Q

PROSTATE CANCER
What blood test would you consider in prostate cancer?
How would you act on it?

A
  • Prostate specific antigen (PSA)

- Men 50–69 2ww if PSA ≥3.0ng/ml OR abnormal DRE

77
Q

PROSTATE CANCER
What are the drawbacks of the PSA test?
What contributes to this?

A
  • Poor sensitivity + specificity with high rate of false +ve/-ve so need counselling prior but >50 can request
  • False +ve = prostatitis, UTI, BPH, vigorous DRE/exercise, ejaculation
78
Q

PROSTATE CANCER
What is the first line investigation for prostate cancer?
What other investigations would you do?

A
  • Multiparametric MRI reported using Likert scale (≥3 go on for transrectal ultrasound guided biopsy)
  • CT CAP + isotope bone scan for staging, graded using Gleason grading system
79
Q

PROSTATE CANCER

What is the management of localised prostate cancer (T1/2)?

A
  • Conservative = active monitoring + watchful waiting
  • Radical prostatectomy
  • Radiotherapy = external beam + brachytherapy
80
Q

PROSTATE CANCER

What is the management of localised advanced prostate cancer (T3/4)?

A
  • Hormonal therapy with synthetic GnRH agonists (Goserelin) and anti-androgens (Bicalutamide)
  • Radical prostatectomy
  • Radiotherapy as previous
81
Q

PROSTATE CANCER

What is the mechanism of action of synthetic GnRH agonists in prostate cancer management?

A
  • Paradoxically blockades LH/FSH at pituitary causing overstimulation which disrupts feedback systems
  • Leads to transient testosterone increase for 2–3w before falling to castration levels so need anti-androgen cover to prevent tumour flair
82
Q

PROSTATE CANCER
What are the complications of…

i) hormonal therapy?
ii) radical prostatectomy?
iii) radiotherapy?

A

i) Libido loss, gynaecomastia, osteoporosis, weight gain, infertility
ii) Erectile dysfunction
iii) Increased risk of bladder + colorectal cancer, proctitis

83
Q

PROSTATE CANCER

What is the management of metastatic prostate cancer?

A
  • Hormonal therapy (Goserelin and bicalutamide)
84
Q

TESTICULAR CANCER

What are the two main types of testicular cancers?

A
  • 95% germ-cell tumours (seminoma #1, non-seminomatous e.g., embryonal, teratoma, yolk sac, choriocarcinoma)
  • Non-germ cell tumours (Leydig cell tumours + sarcomas)
85
Q

TESTICULAR CANCER

What are some risk factors for developing testicular cancer?

A
  • Cryptorchidism
  • Infertility
  • FHx
  • Klinefelter’s syndrome
  • Mumps orchitis
86
Q

TESTICULAR CANCER

What is the clinical presentation of testicular cancer?

A
  • Painless lump (hard, irregular, non-fluctuant)
  • Hydrocele
  • Men aged 20–30
  • Gynaecomastia
87
Q

TESTICULAR CANCER

Why does gynaecomastia occur in testicular cancer?

A
  • Increased oestrogen:androgen ratio as germ-cell tumours release hCG leading to Leydig cell dysfunction so rise in oestradiol >testosterone
88
Q

TESTICULAR CANCER

What investigations would you do for testicular cancer?

A
  • Tumour markers non-seminomas = AFP ± beta-hCG, seminomas = LDH (few have beta-hCG)
  • First-line = USS scrotum
  • CT CAP for staging (Royal Marsden)
89
Q

TESTICULAR CANCER

What is the management of testicular cancer?

A
  • Radical orchidectomy with prosthesis + sperm banking

- Chemo/radiotherapy may be given depending on staging

90
Q

BPH
What is the pathology of benign prostatic hyperplasia (BPH)?
What are some risk factors?

A
  • Hyperplasia of the stromal + epithelial cells of the prostate in the transition zone
  • Age + ethnicity (black > white > Asian)
91
Q

BPH

What is the clinical presentation of BPH?

A
  • Voiding = straining, hesitancy, weak/intermittent flow, incomplete emptying
  • Storage = urgency, frequency, incontinence, nocturia
  • Post-micturition = terminal dribbling
  • DRE = smooth, symmetrical with maintained central sulcus
92
Q

BPH

What are some investigations for BPH?

A
  • Urinalysis, U&E, PSA (if obstructive Sx)
  • Urinary frequency-volume chart for at least 3d
  • International prostate symptom score assesses impact of LUTS on QOL
93
Q

BPH

What are some complications of BPH?

A
  • UTI
  • Urinary retention (acute or chronic)
  • Obstructive uropathy > AKI
94
Q

BPH
What is the first line management of BPH?
How does it work?
Side effects?

A
  • Alpha-1 antagonists (tamsulosin)
  • Decreases smooth muscle tone of prostate + bladder, helps voiding Sx
  • Postural hypotension, dizziness, dry mouth
95
Q

BPH
What is the second line management of BPH?
How does it work?

A
  • 5 alpha-reductase inhibitors (finasteride)
  • Blocks testosterone > dihydrotestosterone conversion causing reduction in prostate volume + can slow disease progression (can take 6m)
96
Q

BPH
When are 5 alpha-reductase inhibitors indicated?
What are some side effects?

A
  • Significantly enlarged prostate + high risk of progression

- Erectile dysfunction, reduced libido, ejaculation problems

97
Q

BPH

When would you consider combining both tamsulosin and finasteride?

A
  • Mod-severe voiding Sx and prostatic enlargement
98
Q

BPH
Other than medical management, what other management may be considered for BPH?
What are the potential complications?

A
  • Transurethral resection of prostate

- Bleeding, infection, erectile dysfunction, urethral strictures

99
Q

NEPHROTIC SYNDROME
What is the pathology of nephrotic syndrome?
What are the classic findings?

A
  • Increased permeability of serum protein through a damaged basement membrane
  • Triad of:
    – Proteinuria >3g/24h (>1g/m^2/24h or +++ in paeds) = frothy urine
    – Hypoalbuminaemia <30g/L (<25g/L in paeds)
    – Oedema
100
Q

NEPHROTIC SYNDROME

What are the three main conditions which make up nephrotic syndromes and what’s the epidemiology?

A
  • Minimal change disease = #1 in paeds 2–5y/o
  • Membranous glomerulonephritis = commonest overall, bimodal peak in 20s + 60s
  • Focal segmental glomerulosclerosis = #1 in adults, more common in Afro-Carribbean
101
Q

NEPHROTIC SYNDROME
What are the causes of…

i) minimal change disease?
ii) membranous glomerulonephritis?
iii) focal segmental glomerulosclerosis?

A

i) #1 idiopathic, drugs (NSAIDs, rifampicin), Hodgkin’s lymphoma
ii) #1 idiopathic, cancers, infections (hep B), SLE
iii) Idiopathic, HIV, Alport’s

102
Q

NEPHROTIC SYNDROME
What does renal biopsy/histology show in…

i) minimal change disease?
ii) membranous glomerulonephritis?
iii) focal segmental glomerulosclerosis?

A

i) Normal light microscopy, podocyte fusion + foot process effacement on electron
ii) IgG + complement deposits on basement membrane
iii) Focal + segmental sclerosis

103
Q

NEPHROTIC SYNDROME
What is the management of…

i) minimal change disease?
ii) membranous glomerulonephritis?
iii) focal segmental glomerulosclerosis?

A

i) Majority steroid responsive, if not cyclophosphamide, relapse likely
ii) BP control with ACEi/ARB, steroids
iii) Steroids/cyclophosphamide, may progress to ESRF

104
Q

NEPHROTIC SYNDROME

What investigations would you do in suspected nephrotic syndrome?

A
  • Urinalysis (proteinuria) + urinary ACR (raised)
  • FBC, CRP/ESR, complement C3/4 levels, autoimmune screen
  • Renal biopsy in ALL adults but ONLY in children if atypical presentation
105
Q

NEPHROTIC SYNDROME

What are some complications from nephrotic syndrome?

A
  • VTE risk due to loss of antithrombin III
  • Hyperlipidaemia
  • Infection due to urinary immunoglobulin loss
  • Loss of thyroxine-binding globulin lowers total but not free thyroxine levels
106
Q

NEPHRITIC SYNDROME
What is nephritic syndrome?
How does it present?

A
  • Immune complexes trigger an inflammatory response
  • Haematuria (micro or macroscopic)
  • Fluid retention > HTN
  • Proteinuria but not nephrotic range (<3g/L)
107
Q

NEPHRITIC SYNDROME

What are the 4 main types of nephritic syndrome?

A
  • IgA nephropathy (Berger’s disease) = commonest primary glomerulonephritis
  • Post-streptococcal glomerulonephritis
  • Membranoproliferative glomerulonephritis
  • Rapidly progressive glomerulonephritis
108
Q

NEPHRITIC SYNDROME
How does IgA nephropathy present?
What is the histology of IgA nephropathy?

A
  • Macroscopic haematuria in young people ONE TO TWO DAYS post URTI
  • IgA deposits + glomerular mesangial proliferation
109
Q

NEPHRITIC SYNDROME

How is IgA nephropathy managed?

A
  • Follow-up
  • ACEi if proteinuria
  • Active disease = steroids
110
Q

NEPHRITIC SYNDROME
What causes post-streptococcal glomerulonephritis?
What pertinent investigations would you see?

A
  • Proteinuria ONE TO TWO WEEKS post Strep pyogenes tonsillitis/impetigo
  • Low complement levels + raised ASO titre
111
Q

NEPHRITIC SYNDROME
What is membranoproliferative glomerulonephritis?
How does it present?

A
  • Capillary basement membrane thickening associated with hepatitis
  • Nephritic or nephrotic
112
Q

NEPHRITIC SYNDROME
What are the causes of rapidly progressive glomerulonephritis?
What is it classically associated with?

A
  • Goodpasture’s syndrome, granulomatosis with polyangiitis

- Associated with formation of epithelial crescents in majority of glomeruli

113
Q

TESTICULAR TORSION
What is testicular torsion?
What is the epidemiology?

A
  • Twisting of testis + spermatic cord > testicular ischaemia

- Teenagers

114
Q

TESTICULAR TORSION

What are some causes of testicular torsion?

A
  • Trauma

- Bell-clapper deformity = tunica vaginalis has abnormally high attachment to the spermatic cord

115
Q

TESTICULAR TORSION

What is the clinical presentation of testicular torsion?

A
  • Tender, red testicle which may be swollen + retracted upwards
  • Acute abdo pain (lower abdo/scrotal)
  • N+V
  • Loss of cremasteric reflex
  • Elevation of testis does NOT ease pain (Prehn’s sign differentiates from epididymitis)
116
Q

TESTICULAR TORSION
What is a key differential of testicular torsion?
How does it present?

A
  • Torsion of testicular appendage (hydatid) = remnant of Mullerian duct
  • Can rapidly enlarge prior to puberty due to gonadotropins = blue dot sign
117
Q

TESTICULAR TORSION

What investigations would you do in testicular torsion?

A
  • Doppler USS = decreased blood flow (testicular ischaemia) but do NOT delay surgical exploration until torsion excluded
118
Q

TESTICULAR TORSION

What is the management of testicular torsion?

A
  • Urgent surgical exploration = untort <6h, fixate both testes (orchidopexy)
  • Orchidectomy if testicle dead
119
Q

EPIDIDYMO-ORCHITIS
What is epididymo-orchitis?
What is a key DDx?

A
  • Infection of the epididymis + testes due to local spread of genital tract infections
  • Testicular torsion
120
Q

EPIDIDYMO-ORCHITIS

What are the causes of epididymo-orchitis?

A
  • <35, new sexual partners in past 12m + urethral discharge = STI (#1 = chlamydia trachomatis, neisseria gonorrhoea)
  • > 35 more likely E. coli
  • Can be mumps
121
Q

EPIDIDYMO-ORCHITIS

What is the clinical presentation of epididymo-orchitis?

A
  • Unilateral testicular pain + swelling
  • ?Urethral discharge
  • Prehn’s sign positive
122
Q

EPIDIDYMO-ORCHITIS

What are the investigations and management of epididymo-orchitis?

A
  • Urine MC&S, chlamydia + gonorrhoea NAAT on first pass urine, USS scrotum
  • Organism unknown = IM ceftriaxone 500mg STAT + doxycycline 100mg PO BD 10–14d
123
Q

HYDROCELE
What is a hydrocele?
What are the two types?
What are the causes?

A
  • Accumulation of fluid within the tunica vaginalis
  • Communicating + non-communicating
  • Idiopathic or secondary to testicular cancer, torsion, epididymo-orchitis + trauma
124
Q

HYDROCELE

What is the difference between communicating + non-communicating hydroceles?

A
  • Communicating = patency of processus vaginalis > peritoneal fluid drains into scrotum (newborn males, usually resolve within first few months)
  • Non-communicating = excess fluid production within tunica vaginalis
125
Q

HYDROCELE

What is the clinical presentation of hydrocele?

A
  • Soft, non-tender swelling of hemi-scrotum
  • Swelling confined to scrotum + can get ABOVE mass on examination
  • Transilluminates with pen torch
126
Q

HYDROCELE

What are the investigations and management for hydrocele?

A
  • USS to confirm Dx esp. in adults to exclude tumour
  • Paeds = repair if not resolved by 1-2y
  • Adults = conservative if not severe
127
Q

VARICOCELE
What is a varicocele?
Where does it normally affect?

A
  • Abnormal dilatation of the testicular veins (pampiniform plexus)
  • L due to angle of L testicular vein entering the L renal vein
128
Q

VARICOCELE

What is the clinical presentation of varicocele?

A
  • ‘Bag of worms’
  • Heavy dragging sensation
  • More prominent on standing
  • Subfertility
129
Q

VARICOCELE

What are the investigations + management of varicocele?

A
  • USS with doppler studies

- Conservative unless pain then embolisation or surgery

130
Q

EPIDIDYMAL CYST

What are some associations with epididymal cysts?

A
  • Polycystic kidney disease
  • Cystic fibrosis
  • Von Hippel-Lindau syndrome
131
Q

EPIDIDYMAL CYST

What is the clinical presentation of an epididymal cyst?

A
  • Separate from the body of the testicle

- Found posterior to testicle

132
Q

EPIDIDYMAL CYST

What is the investigations + management of epididymal cysts?

A
  • Diagnosis = USS

- Conservative but surgical removal or sclerotherapy if larger or symptomatic

133
Q

PROSTATITIS
What is the most common cause for prostatitis?
What are some risk factors?

A
  • E. coli

- Recent UTI, catheter, recent prostate biopsy, epididymitis

134
Q

PROSTATITIS

What is the clinical presentation of prostatitis?

A
  • Pain can be referred to perineum or prostate
  • LUTS = dysuria, frequency, urgency
  • Systemic = fever + rigors
135
Q

PROSTATITIS

What investigations would you do in prostatitis?

A
  • DRE = tender, warm, swollen prostate gland
  • MSU for MC&S
  • Screen for STIs with NAAT testing on first pass urine
136
Q

PROSTATITIS

What is the management of prostatitis?

A
  • Analgesia

- 14d course of quinolone e.g., ciprofloxacin

137
Q

POLYCYSTIC KIDNEY DISEASE

What are the two types of polycystic kidney diseases (PKD) and what are the genetics behind it?

A

Autosomal dominant –
- PKD1 polycystin 1 = chromosome 16 in 85%, renal failure earlier
- PKD2 polycystin 2 = chromosome 4 in 15%, renal failure later
Autosomal recessive –
- Fibrocystin gene on chromosome 6

138
Q

POLYCYSTIC KIDNEY DISEASE

What is the pathophysiology of autosomal dominant PKD?

A
  • Cystic dilation of renal tubular epithelium leading to destruction of renal parenchyma
  • Can be clear, turbid or bloody fluid
139
Q

POLYCYSTIC KIDNEY DISEASE

What is the pathophysiology of autosomal recessive PKD?

A
  • Fibrocystin responsible for renal tubulogenesis so often presents in pregnancy with oligohydramnios leading to pulmonary hypoplasia + potentially Potter syndrome requiring early dialysis
140
Q

POLYCYSTIC KIDNEY DISEASE

What is the clinical presentation of PKD?

A
  • Renal = flank pain, HTN, haematuria, palpable costovertebral masses
  • Extra-renal = cysts (liver, pancreas, spleen), SAH (berry aneurysms), mitral valve prolapse (regurg), diverticular disease
141
Q

POLYCYSTIC KIDNEY DISEASE

What are the investigations for PKD?

A
  • Diagnosis by renal USS + genetic testing
  • Screening for relatives = abdominal USS
  • Monitoring = U&E, regular USS
142
Q

POLYCYSTIC KIDNEY DISEASE

What medical management would you consider in PKD and why?

A
  • Tolvaptan = vasopressin receptor 2 antagonist

- Can slow development of cysts + progression of renal failure

143
Q

POLYCYSTIC KIDNEY DISEASE

What conservative management is there in PKD?

A
  • Treat complications (HTN)
  • Genetic counselling
  • Avoid contact sports due to risk of cyst rupture
  • Avoid anti-inflammatory meds + anticoagulants
144
Q

ERECTILE DYSFUNCTION
What is erectile dysfunction?
What are some risk factors?

A
  • Persistent inability to attain + maintain an erection sufficient to permit satisfactory sexual performance
  • CVD risk factors, alcohol, drugs (SSRIs, beta-blockers)
145
Q

ERECTILE DYSFUNCTION

What are some causes of erectile dysfunction?

A
  • Vascular = atherosclerosis
  • Autonomic neuropathy (DM)
  • Psychogenic (sudden onset, decrease libido)
  • Pelvic surgery = bladder, prostate
  • Peyronie’s disease = fibrous scar tissue on penis (bent, painful erections)
146
Q

ERECTILE DYSFUNCTION

How would you investigate erectile dysfunction?

A
  • Young man always had difficulties = urology
  • Free testosterone measured 9–11am
  • If low/borderline then repeat with FSH/LH + prolactin and if abnormal = endo referral
147
Q

ERECTILE DYSFUNCTION
What is the first-line management of erectile dysfunction?
What is offered if that isn’t acceptable?

A
  • Phosphodiesterase-5 inhibitors e.g., sildenafil

- Vacuum erection devices

148
Q

ERECTILE DYSFUNCTION

What are some contraindications and side effects of phosphodiesterase-5 inhibitors?

A
  • Recent stroke/MI, nitrates, hypotension, arrhythmias

- Nasal congestion, flushing, blue visual disturbances, priapsim

149
Q

ERECTILE DYSFUNCTION

What conservative advice is given in erectile dysfunction?

A
  • Cycle >3h/w then stop
150
Q

ACUTE INTERSTITIAL NEPHRITIS

What is the histology of acute interstitial nephritis?

A
  • Marked interstitial oedema + interstitial infiltrate in the connective tissue between renal tubules
151
Q

ACUTE INTERSTITIAL NEPHRITIS

What causes acute interstitial nephritis?

A
  • Hypersensitivity reaction to drugs #1 = Abx (penicillin, rifampicin), NSAIDs, allopurinol, furosemide
  • Or systemic disease = SLE, sarcoidosis, Sjogren’s
152
Q

ACUTE INTERSTITIAL NEPHRITIS

How does acute interstitial nephritis present?

A
  • Fever, rash + arthralgia
  • Eosinophilia, sterile pyuria + white cell casts
  • Renal impairment + HTN
153
Q

RENAL TUBULAR ACIDOSIS

What is the pathophysiology of renal tubular acidosis (RTA)?

A
  • Normal anion gap hyperchloraemic metabolic acidosis due to impaired acid excretion leading to activation of RAAS > potassium wasting
154
Q 
RENAL TUBULAR ACIDOSIS
What is type 1 RTA?
What are the causes?
What are the features?
How is it managed?
A
  • Inability to secrete H+ in DISTAL tubule > hypoK+
  • SLE, Sjogren’s, RA
  • Rickets/osteomalacia, renal stones, nephrocalcinosis > ESRF, high urinary pH >6
  • PO bicarb
155
Q 
RENAL TUBULAR ACIDOSIS
What is type 2 RTA?
What are the causes?
What are the features?
How is it managed?
A
  • Decreased HCO3- reabsorption in PROXIMAL tubule > hypoK+
  • Fanconi syndrome, idiopathic
  • High urinary pH >6
  • PO bicarb
156
Q

RENAL TUBULAR ACIDOSIS

What is type 3 RTA?

A
  • Very rare

- Carbonic anhydrase II deficiency > hypoK+

157
Q 
RENAL TUBULAR ACIDOSIS
What is type 4 RTA?
What are the causes?
What are the features?
How is it managed?
A
  • Reduced aldosterone > reduced PROXIMAL tubular ammonium excretion = HIGH K+
  • Adrenal insufficiency, SLE, HIV, diabetes
  • Low urinary pH
  • Fludrocortisone, PO bicarb
158
Q

ACUTE TUBULAR NECROSIS

What is acute tubular necrosis?

A
  • Necrosis of renal tubular epithelial cells leading to intrinsic AKI (#1 cause)
159
Q

ACUTE TUBULAR NECROSIS

How is the aetiology of acute tubular necrosis split?

A
  • Ischaemic = shock, sepsis

- Nephrotoxins = NSAIDs, aminoglycosides, myoglobin (rhabdo), contrast agents

160
Q

ACUTE TUBULAR NECROSIS
What are the clinical features of acute tubular necrosis?
How is it managed?

A
  • AKI = raised urea, creatinine + potassium, oliguria
  • Muddy brown casts on urinalysis = pathognomonic
  • Manage as per AKI (IV fluids, stop DAMN drugs)
161
Q

ACID-BASE DISORDERS
How do you calculate the anion gap?
What picture does a normal anion gap show?

A
  • (Na + K) – (HCO3 + Cl)

- Hyperchloraemic metabolic acidosis

162
Q

ACID-BASE DISORDERS

What are some causes of a normal anion gap metabolic acidosis?

A
  • GI bicarb loss = diarrhoea
  • Renal tubular acidosis
  • Addison’s disease
163
Q

ACID-BASE DISORDERS

What are some causes of a high anion gap metabolic acidosis?

A

MUDPILES –

  • Methanol
  • Uraemia (renal failure)
  • DKA
  • Paracetamol
  • Isoniazid/iron
  • Lactic acidosis
  • Ethanol
  • Salicylates
164
Q

ACID-BASE DISORDERS
What causes a metabolic alkalosis?
What are some causes?

A
  • Loss of H+ or gain of HCO3-
  • Vomiting + hypokalaemia
  • Diuretics
  • Primary hyperaldosteronism + Cushing’s syndrome
  • Congenital adrenal hyperplasia
165
Q

ACID-BASE DISORDERS
What causes a respiratory acidosis?
What are some causes?

A
  • Inadequate ventilation
  • Obstruction = COPD
  • Resp depression = opiates
  • Neuromuscular disease = GBS, MND, MG
  • Pulmonary disease = fibrosis, pneumonia
166
Q

ACID-BASE DISORDERS
What causes a respiratory alkalosis?
What are some causes?

A
  • Hyperventilation
  • Pulmonary embolism + hypoxia
  • Anxiety
  • Increased respiratory drive (salicylate poisoning)

FINALS (20 decks)

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