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Renal Flashcards

1
Q

What is AKI?

A

a sudden decline in renal function over hours or days that leads to an inability to maintain fluid, electrolyte, and acid base balance. Diagnosed by measuring serum creatinine.

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2
Q

What is the criteria for the diagnosis of an AKI?

A
  • Rise in creatinine of ≥26 micromol/L in 48 hrs
  • Rise in creatinine of ≥50% in 7 days
  • Urine output of <0.5 ml/kg/hour for >6 hours
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3
Q

Risk factors for AKI

A
  • CKD
  • History of AKI / urological hx e.g., stones
  • Heart failure
  • Diabetes
  • Liver disease
  • > 65 yo
  • Cognitive impairment
  • Nephrotoxic medications – NSAIDs, ACEi, aminoglycosides, ARBs, diuretics
  • Contrast medium in CT scans (iodinated)
  • Sepsis
  • Hypovolemia
  • Emergency surgery
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4
Q

What are the 3 categories of causes of AKI?

A
  1. Pre-renal: most common, due to inadequate blood supply to kidneys
  2. Intrinsic disease: due to reduced filtration of blood
  3. Post-renal: obstruction to outflow of urine from kidney, and the back pressure causes reduced kidney function
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5
Q

Pre-renal causes of AKI?

A
  • Dehydration- haemorrhage, burns, vomiting, diarrhoea
  • Hypotension (shock)
  • Heart failure
  • Renal artery stenosis / thrombosis
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6
Q

Intrinsic causes of AKI?

A

• Glomerulonephritis
• Interstitial nephritis (caused by penicillin, rifampicin, NSAIDs, allopurinol & furosemide – fever and rash)
• Acute tubular necrosis – brown granular casts in urine
* Rhabdomyolysis
* Tumour lysis syndrome

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7
Q

Post-renal causes of AKI?

A
  • Kidney stones (in ureter or bladder)
  • Masses – Ca in abdomen or pelvis
  • Ureter / urethral strictures
  • BPH / Prostate Ca
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8
Q

signs of AKI

A
  • Hypotension
  • Kidney insults
  • Reduced urine production
  • Lower urinary tract symptoms if there is obstruction
  • Symptoms of volume overload if there is HF
  • Vomiting / nausea
  • Haematuria if there are kidney stones, infection, tumour or acute glomerulonephritis
  • Pulmonary and peripheral oedema
  • Arrhythmias - secondary to changes in K and acid-base balance
  • Features of uraemia - pericarditis or encephalopathy
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9
Q

Ix for AKI

A
  1. U&Es
  2. LFTs
  3. Serum potassium
  4. FBC
  5. Bicarbonate
  6. CRP
  7. Blood culture
  8. Urinalysis
    a. Leukocytes + nitrates = infection
    b. Protein + blood = acute nephritis
    c. Glucose = diabetes
  9. Urine culture
  10. Urine output monitoring
  11. Fluid challenge
  12. US urinary tract – to look for obstruction
  13. VBG
  14. CXR – for signs of overload
  15. ECG
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10
Q

Mx of AKI

A
  • Continual monitoring of fluid balance
  • Fluid rehydration – IV fluids / if patient is hypervolemic, fluid restriction +/- diuretics
  • Stop nephrotoxic medications
  • Relieve obstructions
  • Specialist input for severe (stage 3) AKI
  • If there is hyperkalaemia:
    o 10 ml 10% calcium carbonate (to protect the myocardium)
    o Insulin + dextrose and salbutamol (to move potassium from extracellular to intracellular compartment)
  • Calcium resonium, loop diuretics and dialysis (to remove K from body )
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11
Q

Medications safe to continue in AKI

A 
Paracetamol
Warfarin
Statins
Aspirin (at 75mg)
Clopidogrel
B blockers
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12
Q

Medications that should be stopped in AKI as they worsen renal function

A 
NSAIDs
Aminoglycosides - genatmicin, neomycin
ACEi
ARBs
Diuretics
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13
Q

Medications to stop during AKI due to increased risk of toxicity (not because of worsening kidney function)

A

Methotrexate
Lithium
Digoxin

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14
Q

Pneumonic for remembering assessment and management of AKI

A

RENAL DRS 26

  • R = Record baseline creatinine (+ do regular U&Es)
  • E = Exclude obstruction
  • N = Nephrotoxic drugs stopped
  • A = Assess fluid status
  • L = Losses +/- catheterisation
  • D = Dipstick (blood +/- protein)
  • R = Review medications
  • S = Screen (consider acute renal screen)
  • 26 = creatinine rise for AKI diagnosis
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15
Q

Complications of AKI

A
  • Hyperkalaemia
  • Fluid overload, heart failure and pulmonary oedema
  • Metabolic acidosis
  • Uraemia (high urea) – can lead to encephalopathy or paricarditis
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16
Q

When is haemodialysis required in AKI?

A

When the patient doesn’t respond to medical treatments

Complications e.g., hyperkalaemia, pulmonary oedema, acidosis or uraemia

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17
Q

How can AKI be staged?

A

stage 1, 2 or 3

Using The kidney disease: improving global outcomes (KDIGO) criteria

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18
Q

What is a stage 1 AKI?

A

Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

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19
Q

What is a stage 2 AKI?

A

Increase in creatinine to 2.0 to 2.9 times baseline, or

Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours

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20
Q

what is a stage 3 AKI?

A

Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

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21
Q

What is benign prostatic hyperplasia?

A

common condition affecting older men causing hyperplasia of the stromal and epithelial cells of the prostate. Usually presents with LUTs.

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22
Q

Pathology of BPH

A

BPH is a hormone dependent process involving testosterone and dihydrotestosterone production. There’s failure of normal apoptosis and abnormal epithelial & stromal proliferation.
Proliferation occurs primarily in the transition zone = restriction of the prostatic urethra and urinary flow.

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23
Q

Symptoms of benign prostatic hyperplasia

A
  1. Hesitancy
  2. Weak flow
  3. Urgency
  4. Frequency
  5. Intermittency
  6. Straining to pass urine
  7. Terminal dribbling
  8. Incomplete emptying
  9. Nocturia
  10. Retention = acute or chronic
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24
Q

What scoring system is used to assess the severity of LUTS?

A

International prostate symptom score (IPSS) = scoring system that can be used to assess the severity of LUTS.

  • 0-7 mild
  • 8-19 moderate
  • 20-35 severe
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25
Q

Ix for BPH?

A
  • DRE: irregular enlargement think cancer. Benign prostate = smooth, symmetrical, soft with maintained central sulcus
  • Abdominal examination
  • Urinary frequency volume chart
  • Urine dipstick – to check for infection
  • FBC, U&E, LFT
  • US – abdominal or transrectal to evaluate the size of the prostate
  • MRI prostate – to diagnose malignancy
  • Prostate specific antigen: Unreliable test with high rate of false positives and false negatives
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26
Q

common causes of raised PSA

A 
	Prostate cancer
	BPH
	Prostatitis
	UTI
	Vigorous exercise e.g., cycling 
	Recent ejaculation / prostate stimulation
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27
Q

Mx for BPH

A
  1. Exclude malignancy
  2. Conservative watchful waiting
  3. Medical management - alpha blockers (tamsulosin) and 5-alpha reductase inhibitors (finasteride)
  4. Surgical -
    - Transurethral resection of prostate (TURP)
    - Transurethral incision of prostate (TUIP)
    - Prostatic urethral lift
    - folium laser enucleation of the prostate (HoLEP)
    - Open prostatectomy
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28
Q

Mechanism of action of tamsulosin in BPH & side effects

A

Alpha blocker
Inhibit the action of moradrenaline on smooth muscle in the prostate = reduces tone

SE:

  • Postural hypotension
  • Ejaculatory dysfunction
  • Intra-operative floppy iris syndrome
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29
Q

Mechanism of action of finasteride in BPH & side effects

A

5-Alpha reductase inhibitor
Reduce the production of dihydrotestosterone which mediates androgen effects on the prostate
gradually reduces size of the prostate - 6 months to reduce size

Used if patient has significantly enlarged prostate & is at high risk of progression

SEs:

  • Reduced libido
  • Erectile dysfunction
  • Ejaculatory dysfunction
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30
Q

Complications of transurethral resection of prostate

A 
retrograde ejaculation 
urinary infection 
urinary catheter
clot retention
urinary incontinence
urethral stricture
 erectile dysfunction

TURP syndrome - caused by irrigation with glycine during procedure (hyponatraemia, hyper ammonia, visual disturbances)

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31
Q

Complications of BPH

A

Urinary retention

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32
Q

What is interstitial nephritis and what are the 2 types?

A

inflammation of the space between cells and tubules (the interstitium) in the kidney

Two types: acute interstitial nephritis and chronic tubulointerstitial nephritis

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33
Q

Histology of acute interstitial nephritis

A

marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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34
Q

Causes of acute interstitial nephritis

A 
-	Drugs :
o	Penicillin 
o	Rifampicin
o	NSAIDs
o	Allopurinol
o	Furosemide
  • Infection
    o Hanta virus
    o Staphylococci
  • Systemic disease
    o SLE
    o Sarcoidosis
    o Sjogrens syndrome
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35
Q

Presentation of acute interstitial nephritis

A
  • AKI
  • Hypertension
  • Symptoms of generalised hypersensitivity reaction:
    o Rash
    o Fever
    o Eosinophilia
    o Arthralgia
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36
Q

What are urinalysis results for acute interstitial nephritis?

A 
Stile pyuria (^WCC in urine)
White cell casts
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37
Q

Mx for acute interstitial nephritis

A
  • Treat underlying cause
  • Steroids to reduce inflammation
  • Stop causative medication
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38
Q

What is bladder cancer?

A

cancer of the epithelial lining of the bladder (urothelium) and most are non-invasive of the muscle (superficial) at presentation.

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39
Q

What is the typical exam hx for a bladder cancer patient?

A

retired dye factory worker with painless haematuria

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40
Q

Risk factors for bladder cancer

A
  • Smoking
  • Increased age
  • Aromatic amines – in dye and rubber industry
  • Schistosomiasis = squamous cell carcinoma of the bladder (in countries with high prevalence of the infection)
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41
Q

what is the type of cancer seen in bladder cancer?

A
  • Transitional cell carcinoma (90%)
  • Squamous cell carcinoma (5%)
  • Rarer causes = adenocarcinoma, sarcoma and small cell carcinoma
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42
Q

What is the presentation for bladder cancer?

A
  1. Painless macroscopic haematuria

2. Some may present with incidental microscopic haematuria

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43
Q

when to do a two week wait referral for bladder cancer

A
  1. <45 yo + unexplained visible haematuria (without UTI or persisting after tx for UTI)
  2. > 60 yo + microscopic haematuria + dysuria/raised WCC
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44
Q

Ix for bladder cancer

A

Cystoscopy (rigid or flexible) + biopsy

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45
Q

Staging for bladder cancer

A

TNM staging (tumour, lymph node, metastasis)
- Clear distinction required between: non-muscle invasive bladder cancer and muscle invasive bladder cancer
- Non-muscle invasive bladder cancer =
o Tis / carcinoma in situ = cancer affecting urothelium and flat
o Ta = cancer affecting urothelium and projecting into bladder
o T1 = cancer invading connective tissue but not muscle
- Invasive bladder cancer: T2-T4 & any lymph node or metastatic spread

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46
Q

Mx for bladder cancer

A
  • Transurethral resection of bladder tumour (TURBT) – remove tumour during cystoscopy
  • Intravesical chemotherapy – chemotherapy given into bladder through a catheter
  • Intravesical bacillus Calmette-Guerin (BCG) – BCG vaccine given into bladder to stimulate immune system
  • Radical cystectomy with urostomy and ileal conduit
  • Chemotherapy
  • Radiotherapy
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47
Q

What is chronic kidney disease?

A

chronic reduction in kidney function. Is permanent and progressive.

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48
Q

Causes of CKD

A
  • Diabetes – diabetic nephropathy
  • HTN
  • Age related decline
  • Glomerulonephritis
  • Polycystic kidney disease
  • Medications = NSAIDs, PPIs and lithium
  • Chronic pyelonephritis
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49
Q

Risk factors for CKD

A
  • Older age
  • HTN
  • DM
  • Smoking
  • Use of medications that affect the kidneys
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50
Q

Presentation of CKD

A
  • Asymptomatic and diagnosed on routine testing
  • Loss of appetite
  • Nausea +/- vomiting
  • Oedema
  • Muscle cramps
  • Peripheral neuropathy
  • Pallor
  • HTN
  • Uraemia symptoms: restless legs, pruritis
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51
Q

Ix for CKD

A
  1. Estimate glomerular filtration rate (eGFR)
    a. On a U&E
    b. Need 2 tests, 3 months apart to diagnose CKD
  2. Urine albumin:creatinine ratio
    a. Proteinuria >/= 3mg/mmol
  3. Urine dipstick
    a. Haematuria
    b. If haematuria, ix for bladder cancer
  4. Renal USS
    a. Do if theres:
    i. Accelerated CKD
    ii. Haematuria
    iii. Family hx of polycystic kidney disease
    iv. Evidence of obstruction
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52
Q

How do you stage CKD?

A

according to GFR AND Albumin:creatinine ratio (for proteinuria)

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53
Q

What is CKD stage 1?

A

eGFR >90 ml/min

With some sign of kidney damage on other tests – U&Es and proteinuria (if all the kidney tests are normal/score A1 = no CKD)

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54
Q

What is CKD stage 2?

A

eGFR = 60-98 ml/min

With some sign of kidney damage on other tests – U&Es and proteinuria (if all the kidney tests are normal/score A1 = no CKD)

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55
Q

what is CKD stage 3a?

A

eGFR - 45-59 ml/min

A moderate reduction in kidney function

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56
Q

what is CKD stage 3b?

A

eGFR = 30-44 ml/min

A moderate reduction in kidney function

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57
Q

What is CKD stage 4?

A

eGFR - 15-29 ml/min

A severe reduction in kidney function

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58
Q

what is CKD stage 5?

A

eGFR Less than 15 ml/min

Established kidney failure – dialysis or kidney transplant may be needed

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59
Q

What is the A score used in the classification of CKD?

A

A score is based on albumin:creatinine ratio and shows whether there’s proteinuria

A1 <3 mg/mmol
A2 3-30 mg/mmol
A3 >30 mg/mmol

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60
Q

When should you refer a patient with CKD to a specialist?

A
  • eGFR <30
  • ACR >/= 70 mg/mmol
  • Accelerated disease progression
  • Uncontrolled HTN despite >/= 4 antihypertensives
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61
Q

Management of CKD

A
  1. Slow the progression of CKD
    a. Optimise diabetic control
    b. Optimise HTN control
    c. Treat glomerulonephritis
  2. Reduce the risk of complications
    a. Exercise, maintain healthy weight and stop smoking
    b. Special dietary advice about phosphate, sodium, potassium and water intake
    c. Offer atorvastatin 20mg for primary prevention of CVD
  3. Treat complications
    a. Sodium bicarbonate for metabolic acidosis
    b. Iron supplementation and erythropoietin for anaemia
    c. Vitamin D for renal bone disease
    d. ACEi/ARB to treat proteinuria (if ACR >30 + HTN or if just ACR >70)
    e. Dialysis in end stage renal failure
    f. Renal transplant in end stage renal failure
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62
Q

Complications of CKD

A 
Anaemia (normocytic)
Renal bone disease
CVD
Peripheral neuropathy
Dialysis related problems
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63
Q

Why do patients with CKD get anaemia and how is it managed?

A

o Normochromic, normocytic anaemia
o Kidney cells produce erythropoietin (hormone that stimulates RBC production).
o Give exogenous erythropoietin in anaemia after treating any iron deficiency anaemia

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64
Q

What are the symptoms of renal bone disease?

A

osteomalacia, osteoporosis, osteosclerosis

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65
Q

What sign is seen on an x-ray of the spine in patients with renal bone disease?

A

sclerosis of ends of the vertebra & osteomalacia in centre of vertebra = rugger jersey spine

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66
Q

Why do patients with CKD get renal bone disease?

A

 High phosphate (kidneys usually excrete phosphate)
 Low vitamin D (kidneys usually metabolise vitamin D into active form)
 Low calcium (vitamin D needed for calcium absorption)
 Secondary hyperparathyroidism from low calcium, high phosphate and low vitamin D = increased osteoclast activity
 Get osteomalacia from low calcium
 Get osteosclerosis as osteoblasts increase activity in response to high osteoclast activity
 Get osteoporosis due to increased age and steroid use

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67
Q

How is renal bone disease managed?

A

calcitriol (vitamin D),
low phosphate diet,
bisphosphonates for osteoporosis

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68
Q

Symptoms of dehydration

A
  • Dry mucous membranes
  • Loss of skin turgor
  • Sunken eyes
  • Tachycardia
  • Hypotension
  • Delirium
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69
Q

What is diabetic nephropathy?

A

kidney damage caused by type I and type II diabetes mellitus

Diabetic nephropathy is the most common cause of glomerular pathology and CKD in the UK.

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70
Q

What is the pathology behind diabetic nephropathy?

A

chronic high level of glucose passing through the glomerulus causes scarring = glomerulosclerosis

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71
Q

Risk factors for diabetic nephropathy

A
  • Family hx
  • Poor control of diabetes
  • Long duration of diabetes
  • Poor control of hypertension
  • Obesity
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72
Q

Symptoms of diabetic nephropathy

A

Asymptomatic

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73
Q

Ix for diabetic nephropathy

A

Proteinuria + progressive reduction in GFR in the setting of a long duration of diabetes (>10 years)

  • Screen annually with urinary albumin:creatinine ratio (ACR)
  • Early morning specimen
  • ACR > 2.5 = microalbuminuria
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74
Q

Mx of diabetic nephropathy

A
  • Control hyperglycaemia
  • Dietary protein restriction
  • BP control
  • Statins
  • ACEi / ARB = reduce constriction of efferent arteriole = lower pressure in glomerulus (give ACEi even if they have a normal BP in diabetic nephropathy)
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75
Q

what is epididymitis? and what’s the function of the epididymis?

A

Inflammation of the epididymis

Epididymis are found posterior to each testicle, sperm are released from the testicle into the head of the epididymis and travel through the head, body then tail of the epididymis. Sperm mature & are stored in the epididymis then drain into the vas deferens

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76
Q

What is orchitis?

A

Inflammation of the testicles

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77
Q

what is epididymo-orchitis?

A

usually result of infection that spreads from the genital tract or the bladder in the epididymis and testicle on one side

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78
Q

Causes of epididymo-orchitis

A
  • Escherichia coli
  • Chlamydia trachomatis
  • Neisseria gonorrhoea
  • Mumps
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79
Q

Mumps symptoms

A

parotid gland swelling and unilateral orchitis, can also cause pancreatitis

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80
Q

Presentation of epididymo-orchitis

A
  • Acute onset over minutes to hours
  • Testicular pain
  • Dragging or heavy sensation
  • Swelling of testicle and epididymis
  • Tenderness on palpation, especially over epididymis
  • Urethral discharge if chlamydia/gonorrhoea
  • Systemic symptoms = fever / sepsis
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81
Q

Key differential diagnosis of epididymo-orchitis

A

testicular torsion (<20 yo, severe pain and acute onset)

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82
Q

Ix for epididymo-orchitis

A
  • Urine MC&S
  • Chlamydia and gonorrhoea NAAT testing on first pass urine
  • Charcoal swab for gonorrhoea culture & sensitivity
  • Salvia swab for PCR testing of mumps
  • Serum antibodies for mumps (IgM = acute infection, IgG = previous infection/vaccine)
  • US – for testicular torsion or tumours
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83
Q

Mx for epididymo-orchitis that is suspected to be caused by an STI

A

GUM referral

Unknown organism but STI likely = ceftriaxone 500mg IM stat dose + doxycycline 100mg PO BD 10-14 days

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84
Q

Mx for epididymo-orchitis that is not suspected to be caused by an STI

A

ofloxacin 14 days

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85
Q

What is nephrotic syndrome?

A

the basement membrane in the glomerulus becomes highly permeable to protein, allowing proteins to leak from the blood into the urine.

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86
Q

Classic triad seen in nephrotic syndrome

A
  1. Low serum albumin
  2. High urine protein content (>3+ protein on urine dipstick)
  3. Oedema
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87
Q

Who is nephrotic syndrome common in?

A

Most common in 2–5-year-olds.

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88
Q

Presentation of nephrotic syndrome

A
  • Frothy urine
  • Generalised oedema
  • Pallor
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89
Q

Signs of nephrotic syndrome

A
  • Low serum albumin: <30g/L
  • High urine protein content: >3g in 24 hours
  • Oedema
  • Deranged lipid profile – high levels of cholesterol, triglycerides and low density lipoproteins
  • High blood pressure
  • Hypercoagulability – loss of antithrombin II
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90
Q

Causes of nephrotic syndrome

A
  1. Minimal change disease (most common – 90% of cases in children under 10)
  2. Secondary causes:
    a. Focal segmental glomerulosclerosis
    b. Membranoproliferative glomerulonephritis
    c. Henoch schonlein purpura
    d. Diabetes
    e. HIV
    f. Hepatitis
    g. Malaria
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91
Q

What does minimal change disease cause?

A
  • Most common cause of nephrotic syndrome in children
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92
Q

Presentation of minimal change disease

A

oedema, proteinuria and low albumin

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93
Q

Ix for minimal change disease

A

urinalysis shows small molecular weight proteins and hyaline casts

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94
Q

Mx of minimal change disease

A

corticosteroids (prednisolone)

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95
Q

Prognosis of minimal change disease

A

most children make full recovery but it can

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96
Q

Management of nephrotic syndrome

A
  • High dose steroids e.g. prednisolone
  • Low salt diet
  • Diuretics to treat oedema
  • Albumin infusions in severe hypoalbuminaemia
  • Abx prophylaxis
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97
Q

complications of nephrotic syndrome

A
  • Hypovolaemia
    o Due to oedema
    o Causes low BP
  • Thrombosis
    o Proteins to prevent clotting lost in kidneys: antithrombin II and plasminogen
    o Pro-thrombotic proteins produced by liver in response to low albumin
  • Infection
    o Kidney leaks Ig, weakening immune system response
    o Steroids weaken immune system
  • Acute / chronic kidney failure
  • Relapse
  • Hyperlipidaemia = increased CVD risk
  • Hypocalcaemia – vitamin D and binding protein lost in urine
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98
Q

what is prostate specific antigen?

A

Is a glycoprotein produced by epithelial cells of the prostate. Its secreted into the semen, with a small amount entering the blood. It thins the semen so its has a liquid consistency after ejaculation.
Is specific to the prostate.

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99
Q

What type of cancer is prostate cancer usually?

A

Adenocarcinoma

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100
Q

Where does prostate cancer typically happen?

A

In the peripheral zone of the prostate

101
Q

Where does advanced prostate cancer typically spread to?

102
Q

Risk factors for prostate cancer

A
  • Increasing age
  • Family history
  • Black
  • Tall stature
  • Anabolic steroids
103
Q

Presentation of prostate cancer

A
  1. Asymptomatic
  2. LUTS
    a. Hesitancy
    b. Frequency
    c. Weak flow
    d. Terminal dribbling
    e. Nocturia
  3. Haematuria
  4. Erectile dysfunction
  5. Symptoms of advanced disease/metastases e.g., weight loss, bone pain or cauda equina syndrome
104
Q

Ix for prostate cancer

A
  1. PSA – high rates of false positive and false negatives
  2. Prostate examination on DRE –
    a. Benign prostate = smooth, symmetrical, and slightly soft with a maintained central sulcus. Enlarged in BPH.
    b. Infected/inflamed prostate (prostatitis) = enlarged, tender, warm
    c. Cancerous prostate = firm, hard, asymmetrical, craggy, irregular, loss of central sulcus.
  3. Multiparametric MRI, results reported on a scale:
    a. 1 = very low suspicion
    b. 2 = low suspicion
    c. 3 = equivocal
    d. 4 = probable cancer
    e. 5 = definite cancer
  4. Prostate biopsy
    a. Done if scoring 3 or above on multiparametric MRI
    b. Risk of false negative if non-cancerous area is biopsied
    c. Can be a transrectal US guided biopsy (TRUS) or transperineal biopsy
  5. Isotope bone scan for metastases
105
Q

Risks of prostate biopsy

A

i. Pain
ii. Bleeding
iii. Infection
iv. Urinary retention
v. Erectile dysfunction (rare)

106
Q

Grading of prostate cancer

A

Grading of prostate cancer = GLEASON GRADING SYSTEM

  • Based on the histology from prostate biopsies
  • Is used to determine what treatment is most appropriate
  • The greater the gleason score, the more poorly differentiated the tumour cells are and the worse the prognosis
  • Graded from 1 (closest to normal prostate cells) to 5 (most abnormal)
  • Gleason score is made up of the SUM of 2 numbers: 1st number is the grade of the most prevalent pattern in the biopsy, 2nd number is the grade of the second most prevalent pattern in the biopsy
107
Q

What do the total scores of the Gleason grade mean?

A

o 6 = low risk
o 7 = intermediate risk
o 8+ - high risk
prostate cancer

108
Q

How is prostate cancer staged?

A

TMN (tumour, lymph nodes, metastases)

109
Q

What is the management for prostate cancer?

A
  • Surveillance / watchful waiting in early prostate Ca
  • External beam radiotherapy
  • Brachytherapy
    o Implantation of radioactive metal seeds into prostate to deliver continuous, targeted radiotherapy
  • Hormone therapy
  • Surgery
    o Radical prostatectomy
110
Q

What is the main complication of external beam radiotherapy used in the treatment of prostate cancer?

A

proctitis (inflammation in rectum)

111
Q

What are the complications of brachytherapy used in the treatment of prostate cancer?

A

inflammation of bladder and rectum, erectile dysfunction, incontinence and increased risk of bladder or rectal cancer

112
Q

What hormone therapy is used in prostate cancer?

A

o Androgen receptor blockers e.g., bicalutamide
o GnRH agonists e.g., goserelin
o Bilateral orchidectomy – rarely testicles removed

113
Q

SEs of hormone therapy used in prostate cancer

A

hot flushes, sexual dysfunction, gynaecomastia, fatigue, osteoporosis

114
Q

SEs of radial prostatectomy for prostate cancer?

A

erectile dysfunction, urinary incontinence

115
Q

What type of cancer is testicular cancer?

A

testicular cancer arises from the germ cells in the testes (cells that produce gametes). There are other rarer types of testicular tumours: non-germ cell tumours and secondary metastases.

1) Germ cell testicular tumours can be divided into 2 types:
•	Seminomas 
•	Non-seminomas  
o	Teratomas (mostly)
o	Embryonal
o	Yolk sac
o	Choriocarcinoma

2) Non-germ cells testicular tumours include:
• Leydig cell tumours
• Sarcomas

3) Secondary metastases

116
Q

Who gets testicular cancer?

A

Mostly affects men aged 20-30 years old.

117
Q

Risk factors for testicular cancer

A
  • Infertility (increased risk by 3 times)
  • Cryptorchidism: when one or more of the testes doesn’t descend into the scrotum
  • Family history
  • Klinefelter’s syndrome
  • Mumps orchitis
118
Q

Presentation of testicular cancer

A
  1. Painless lump on testicle
  2. Lump is:
    a. Non tender
    b. Arising from testicle
    c. Hard
    d. Irregular
    e. Not fluctuant
    f. No transillumination
  3. Gynaecomastia in Leydig cell tumours
119
Q

Ix for testicular cancer and what tumour markers are used?

A
  • Scrotal USS
  • Tumour markers for testicular cancer =
    o Alpha-fetoprotein: teratoma
    o Beta-hCG: teratoma and seminoma
    o Lactate dehydrogenase (LDH): germ cell tumours
  • Staging CT
120
Q

How is testicular cancer staged?

A

Staging = ROYAL MARSDEN STAGING SYSTEM
• Stage 1 = isolated to testicle
• Stage 2 = spread to the retroperitoneal lymph nodes
• Stage 3 = spread to the lymph nodes above the diaphragm
• Stage 4 = metastasised to other organs

121
Q

Where does testicular cancer commonly metastasise to?

A
  • Lymphatics
  • Lungs
  • Liver
  • Brain
122
Q

Mx of testicular cancer

A
  • Surgery to remove testicle = radial orchidectomy & insert prosthesis
  • Chemotherapy
  • Radiotherapy
  • Sperm banking
123
Q

Long term side effects of patients treated for testicular cancer

A
  • Infertility
  • Hypogonadism – may require testosterone replacement
  • Peripheral neuropathy
  • Hearing loss
  • Lasting kidney, liver or heart damage
  • Increased risk of cancer in the future
124
Q

Prognosis of testicular cancer

A
  • 90% cure rate

- Follow up with tumour markers, CT scans and CXRs

125
Q

What is testicular torsion?

A

twisting of the spermatic cord with rotation of the testicle, is a urological emergency.

Urological emergency = without intervention there is ischaemia and loss of the testis, leading to subfertility or infertility.

126
Q

who gets testicular torsion?

A

10 to 30 yo men

127
Q

Possible cause of testicular torsion

A
  • Bell-clapper deformity
    o Normally the testicle is fixed posteriorly to the tunica vaginalis
    o In bell clapper deformity, the fixation between the testicle and tunica vaginalis is absent
    o The testicle hangs in a horizontal position and can rotate within the tunica vaginalis, twisting at the spermatic cord
128
Q

Differential diagnoses for testicular torsion

A
  • Trauma
  • Epididymo-orchitis
  • Torsion of the epididymal appendage
  • Hydrocele
  • Inguinal hernia
  • Systemic disease – Henoch-Schonlein purpura, Mumps
129
Q

Symptoms of testicular torsion

A
  • Testicular pain, quick onset
  • Is often triggered by activity e.g., playing sports
  • Swelling, redness
  • Nausea and vomiting
  • Lifting of testicle increases pain
  • Abdominal pain
  • Horizontal lie
  • Prehn’s sign
  • Cremasteric reflex – stroking inner thigh leads to cremasteric contraction and elevation of the scrotum on the same side. Absent in torsion.
130
Q

What is Prehn’s sign?

A

– elevation of the affected testicle relives the pain of epididymitis but not of testicular torsion

131
Q

What do you find on examination of testicular torsion

A
  • Firm swollen testicle
  • Elevated (retracted) testicle
  • Absent cremasteric reflex
  • Abnormal testicular lie – often horizontal
  • Rotation so that the epididymis is not in normal posterior position
132
Q

What are the investigations for testicular torsion?

A

clinical diagnosis, do surgical exploration.

- Can do scrotal USS if it doesn’t delay tx = whirlpool sign (spiral appearance to spermatic cord and blood vessels)

133
Q

What is the management for testicular torsion?

A

surgical exploration within 4-6 hours
NBM, analgesia, urgent senior urology assessment
- Orchidoplexy = fixation of the testicle with sutures (fix contralateral testicle due to increased risk of further torsion)
- Orchiectomy if non-viable testicle is found

134
Q

What is erectile dysfunction?

A

the persistent inability to attain and maintain and erection sufficient to permit satisfactory sexual performance
- Organic or psychogenic cause

135
Q

Factors favouring organic cause of erectile dysfunction

A

o Gradual onset of symptoms
o Lack of tumescence
o Normal libido

136
Q

Factors favouring psychogenic cause of erectile dysfunction

A 
o	Sudden onset of symptoms
o	Decreased libido
o	Good quality spontaneous or self stimulated erections 
o	Major life event
o	Problems/changes in a relationship 
o	Previous psychological problems 
o	Hx of premature ejaculation
137
Q

Risk factors for erectile dysfunction

A 
o	CVD
o	DM
o	Obesity
o	HTN
o	Smoking
o	Alcohol
o	SSRIs
o	Beta blockers
138
Q

Ix for erectile dysfunction

A

o Calculate 10 year cardiovascular risk
o Measure free testosterone between 9-11am
 If low = measure FSH, LH and prolactin
 If theyre abnormal = refer to endocrinology

139
Q

Mx for erectile dysfunction

A

o PDE-5 inhibitors (sildenafil)
o Vacuum erection devices
o Refer to urology if young man who has always had difficulty in achieving an erection

140
Q

Organic causes of erectile dysfunction

A

o Vascular – inadequate blood supply e.g., atherosclerosis, HTN and DM
o Penile trauma
o Hormonal derangement

141
Q

What is acute tubular necrosis?

A

damage and necrosis of the epithelial cells of the renal tubules. Most common cause of AKI. Damage to the kidney cells occurs due to ischaemic or toxins. The epithelial cells can regenerate making acute tubular necrosis reversible – takes 7-21 days to recover.

142
Q

What’s the difference between acute tubular necrosis and acute interstitial nephritis?

A

Acute tubular necrosis is damage to the epithelial cells lining the renal tubules while acute interstitial nephritis is damage to the interstitium in the kidneys.

get white cell casts in acute interstitial nephritis and muddy brown casts in acute tubular necrosis

143
Q

causes of acute tubular necrosis?

A
  • Ischaemia secondary to:
    o Shock
    o Sepsis
    o Dehydration
-	Direct damage from toxins:
o	Radiology contrast dye
o	Gentamycin
o	NSAIDs
o	Myoglobin secondary to rhabdomyolysis
o	Lead
144
Q

Presentation of acute tubular necrosis

A
  • Oligouric phase
  • Polyuric phase
  • Recovery phase
145
Q

Ix for acute tubular necrosis

A
  • Urinalysis = MUDDY BROWN CASTS

- Features of AKI = raised urea, creatinine and potassium

146
Q

Mx of acute tubular necrosis

A
  • Supportive management
  • IV fluids
  • Stop nephrotoxic medications
  • Treat complications
147
Q

How does someone with acute interstitial nephritis present?

A

Causes an allergic type picture – raised urinary WCC, IgE and eosinophils, with impaired renal function, rash and fever. Arthralgia a common symptom. Usually after taking a penicillin.

148
Q

What is a hydrocele?

A

a collection of fluid within the tunica vaginalis ( a sealed pouch of membrane that surround the testes).

149
Q

What are the types of hydrocele?

A

simple infantile hydrocele
Communicating hydrocele
Non-communicating hydrocele

150
Q

What is a simple infantile hydrocele?

A
  • common in newborn males
  • Occur when fluid is trapped in the tunica vaginalis.
  • Usually the fluid get reabsorbed over time and the hydrocele disappears = resolve within first few months of life
  • If not resolved spontaneously by 1-2 years old = surgically repaired
151
Q

What is a communicating hydrocele?

A
  • Patency of the processus vaginalis allows peritoneal fluid to drain into the scrotum
  • Allows the hydrocele to fluctuate in size
152
Q

What is a non-communicating hydrocele?

A
  • Excessive fluid production in the tunica vaginalis
153
Q

What is found on examination of a hydrocele?

A
  • Soft
  • Non tender
  • Swelling around 1 testicle
  • Swelling usually anterior to and below the testicle, confined to the scrotum
  • Can get above the mass and the testicles can be difficult to palpate if the hydrocele is large
  • Simple hydroceles = remain one size
  • Communicating hydroceles = can communicate in size
  • Transilluminate with light
154
Q

What can hydroceles develop secondary to?

A
  • Epididymo-orchitis
  • Testicular torsion
  • Testicular tumours
155
Q

Ix for hydrocele

A

Clinical diagnosis can do scrotal USS

156
Q

Mx for hydrocele

A
  • Simple hydroceles = resolve within 2 years with no lasting negative effects
  • Communicating hydroceles = can have surgery to ligate the processus vaginalis
157
Q

What are the symptoms of urinary storage problems in men?

A
  • Urgency
  • Frequency
  • Nocturia
  • Urinary incontinence
158
Q

Ix for incontinence in men

A
  • Urinalysis to exclude infection
  • DRE to examine prostate
  • PSA
  • Urinary frequency-volume chart – to differentiate between urinary frequency, polyuria, nocturia and nocturnal polyuria
  • IPSS (international prostate symptom score) – to assess impact of LUTS on patients life
159
Q

Management for voiding symptoms in men

A

a. Pelvic floor muscle training
b. Bladder training
c. Prudent fluid intake
d. Alpha blocker e.g., doxazosin
e. 5-alpha reductase inhibitor e.g., finasteride for enlarged prostate

160
Q

Mx for overactive bladder in men

A

a. Moderate fluid intake
b. Bladder retraining
c. Antimuscarinic drugs: oxybutynin, tolterodine, darifenacin
d. If all else fails = mirabegron

161
Q

Mx for nocturia in men

A

a. Moderate fluid intake at night
b. Furosemide 40mg late afternoon
c. Desmopressin (manmade vasopressin)

162
Q

What is a urinary tract infection?

A

Lower urinary tract infections = infection in the bladder, causing cystitis (inflammation of the bladder).
LUTIs can spread up to the kidneys = pyelonephritis

163
Q

Causes of LUTIs

A
  • E. coli [gram -ve anaerobic rod]
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans (fungal)
164
Q

What is e.coli?

A

gram -ve anaerobic rod]

165
Q

Risk factors for UTI

A
  • Female
  • Sexual activity
  • Incontinence
  • Poor hygiene
  • Urinary catheters
166
Q

Presentation for UTI

A
  • Dysuria – pain, stinging or burning on passing urine
  • Suprapubic pain or discomfort
  • Frequency
  • Urgency
  • Incontinence
  • Haematuria
  • Cloudy or foul smelling urine
  • Confusion in elderly
167
Q

symptoms for pyelonephritis

A
  • Fever
  • Loin/back pain
  • Nausea/vomiting
  • Renal angle tenderness on examination
168
Q

Ix for LUTIs

A

Urine dipstick: nitrites/leukocytes + RBCs

Midstream urine sample for MC&S

169
Q

who needs a urine sample when a UTI is suspected?

A

a. Pregnant patients
b. Patients with recurrent UTIs
c. Atypical symptoms
d. When symptoms don’t improve with antibiotics
e. >65 yo
f. Visible or non-visible haematuria in women

170
Q

Antibiotics for UTIs

A 
o	Trimethoprim
o	Nitrofurantoin (avoid if eGFR <45)
o	Pivmecillinam 
o	Amoxicillin 
o	Cefalexin
171
Q

How long do patients need abx for if they have a UTI?

A

o 3 days = simple LUTIs in women
o 5-10 days = immunosuppressed women, abnormal anatomy, impaired kidney function
o 7 days = men, pregnant women or catheter associated UTIs

172
Q

Should men be referred to urology if they have a UTI

A

o Don’t routinely refer to urology if one uncomplicated UTI

173
Q

When should you treat a patient with a catheter associated UTI?

A

Only if they have symptoms

174
Q

What are pregnant women with UTIs at risk of?

A

o Pyelonephritis
o Premature rupture of membranes
o Pre-term labour

175
Q

What is the management for pregnant women with UTI?

A

o 7 days of nitrofurantoin (avoid in 3rd trimester – risk of neonatal haemolysis), amoxicillin (after sensitivities known) or cefalexin
o Treatment for asymptomatic pregnant women (urine culture sent at first antenatal visit) – to prevent progression to pyelonephritis
o Do MC&S of urine sample
o Do a second urine culture to check cure in pregnant women
o DON’T GIVE TRIMETHOPRIM (especially in 1st trimester) = folate antagonist = neural tube defects

176
Q

When can’t you use nitrofurantoin to treat a UTI?

A

3rd trimester of pregnancy

If eGFR <45

177
Q

When can’t you use trimethoprim to treat a UTI?

A

Pregnancy (especially 1st trimester) = folate antagonist = neural tube defect
With methotrexate

178
Q

What is obstructive uropathy?

A

flow of urine is blocked, causing the urine to flow back up into one or both kidneys and causing kidney injury

179
Q

causes of obstructive uropathy

A
  • Enlarged prostate: BPH, prostate ca
  • Kidney stones
  • Urethral stricture
  • Cancers: renal cell, transitional cell carcinoma of the ureter, bladder cancer, prostate cancer, malignancy of urethra
  • Extrinsic compression of ureter
  • Ureterocele (ballooning of most distal part of the ureter, congenital usually)
  • Neurogenic bladder
180
Q

What is a neurogenic bladder?

A
  • Abnormal function of the nerves that innervate the bladder and urethra
  • Results in over or under activity in the detrusor muscle of the bladder and the sphincter muscles of the urethra
181
Q

Causes of neurogenic bladder

A 
o	MS
o	Diabetes
o	Stroke
o	Parkinson’s disease
o	Brain/spinal cord injury 
o	Spina bifida
182
Q

Problems caused by a neurogenic bladder

A

o Urge incontinence
o Increased bladder pressure
o Obstructive uropathy

183
Q

Complications of obstructive uropathy

A
  • Hydronephrosis – swelling of renal pelvis and calyces in kidney
  • Post renal AKI
  • Pain
  • CKD
  • Infection due to stagnant urine
  • Urinary retention
  • Overflow incontinence of urine
184
Q

symptoms of obstructive uropathy

A 
Upper urinary tract obstruction =
-	Loin to groin or flank pain 
-	Reduced/no urine output
-	Vomiting 
-	Impaired renal function e.g., raised creatinine
Lower urinary tract obstruction =
-	Difficulty / inability to pass urine 
-	Urinary retention 
-	Impaired renal function e.g., raised creatinine
185
Q

Ix for obstructive uropathy

A
  • USS kidneys, ureter, bladder
186
Q

Mx obstructive uropathy

A
  • Remove or bypass the obstruction
  • Nephrostomy if obstruction in upper urinary tract
  • Urethral or suprapubic catheter if obstruction in lower urinary tract
187
Q

What is hydronephrosis

A

swelling of the renal pelvis and calyces in the kidney

188
Q

Causes of hydronephrosis

A
  • Obstruction of urinary tract

- Idiopathic hydronephrosis – due to narrowing at pelviureteric junction (congenital or develops later)

189
Q

Presentation of hydronephrosis

A
  • Renal angle tenderness

- Mass in kidney area

190
Q

Ix for hydronephrosis

A
  • USS
  • CT
  • Intravenous urogram (x-ray with IV contrast collecting in the urinary tract)
191
Q

Mx for hydronephrosis

A
  • Treat underlying cause
    o E.g., pyeloplasty to correct the narrowing and restructure the pelvis in idiopathic hydronephritis
  • Percutaneous nephrostomy
  • Antegrade ureteric stent
192
Q

What is prostatitis?

A

inflammation of the prostate usually caused by a gram-negative bacterium entering the prostate via the urethra.

193
Q

Causative organism of acute bacterial prostatitis?

194
Q

risk factors for acute bacterial prostatitis

A
  • Recent UTI
  • Urogenital instrumentation
  • Intermittent bladder catheterisation
  • Recent prostate biopsy
195
Q

symptoms of acute bacterial prostatitis

A
  • Referred pain to perineum, penis, rectum and back
  • Obstructive voiding symptoms
  • Fever
  • Rigors
  • Sexual dysfunction – ED, pain on ejaculation and haemtospermia
  • DRE = tender, boggy prostate
196
Q

Ix for acute bacterial prostatitis

A
  • Urine dipstick – for infection
  • Urine MC&S
  • Chlamydia and gonorrhoea testing NAAT
197
Q

Mx for acute bacterial prostatitis

A
  • 14 days of ciprofloxacin/ofloxacin or trimethoprim

- Screen for STIs

198
Q

Complications of acute bacterial prostatitis

A
  • Sepsis
  • Prostate abscess
  • Acute urinary retention
  • Chronic prostatitis
199
Q

what is pyelonephritis?

A

inflammation of the kidneys resulting from bacterial infection. Affects renal pelvis and parenchyma.

200
Q

risk factors for pyelonephritis

A
  • Female
  • Structural urological abnormalities
  • Vesico-ureteric reflux
  • Diabetes
201
Q

most common cause of pyelonephritis

A

most common = e.coli (gram -ve anaerobic rod shaped bacteria)

202
Q

presentation of pyelonephritis

A
  • Fever
  • Loin or back pain
  • Nausea and vomiting
  • Loss of appetite
  • Haematuria
  • Renal angle tenderness
  • White cell casts in urine
203
Q

ix for pyelonephritis

A
  • Urine dipstick – nitrites, leukocytes and blood
  • Midstream urine sample for MC&S
  • CRP and WCC raised
  • USS / CT kidneys
204
Q

mx for pyelonephritis

A 
-	Treat any sepsis
o	Blood lactate level
o	Blood cultures
o	Urine output 
o	Oxygen 
o	Empirical broad spectrum abx IV
o	IV fluid
-	7-10 days of cefalexin / co-amoxiclav / trimethoprim
205
Q

what are kidney stones also called?

A

renal calculi, urolithiasis and nephrolithiasis

206
Q

what are kidney stones?

A

Are hard stones that form in the renal pelvis.

207
Q

what are the types of kidney stones?

A
  1. Calcium based stones (80%)
    a. Calcium oxalate (more common)
    b. Calcium phosphate
  2. Uric acid (not visible on x-ray)
  3. Struvite (made of magnesium ammonium phosphate, produced by bacteria so associated with infection)
  4. Cystine (associated with cystinuria, autosomal recessive disease)
208
Q

which type of kidney stone isn’t visible on X-ray?

209
Q

what is the most common type of kidney stone?

A

calcium oxalate

210
Q

what type of kidney stone is associated with infection?

211
Q

What are stag horn calculus?

A

the stone forms in the shape of the renal pelvis, giving it a similar appearance to antlers of a deer stag. It sits in the renal pelvis with horns extending into the renal calyces – can be seen on x-ray. Most commonly these are struvite stones.

212
Q

What increases the risk of calcium based kidney stones?

A

increased risk with hypercalcaemia and low urine output

213
Q

causes of kidney stones

A
  1. Hypercalcaemia
  2. Calcium oxalate – high concentrations of oxalate in urine, loss of natural stone inhibitors e.g., citrate, magnesium, high urinary pH
  3. Struvite – proteus and klebsiella (urease producing microorganisms)
  4. Uric acid – hyperuricaemia
  5. Cystine – cystinuria (genetic disorder)
214
Q

what are the symptoms of Hypercalcaemia?

A

Renal stones, painful bones, abdominal groans and psychiatric moans

215
Q

risk factors for kidney stones

A
  • Dehydration
  • High salt intake
  • Increased BMI
  • High meat intake
  • Male
  • Family hx
  • Infection
  • Metabolic disorders
  • Crohn’s disease
  • Anatomical abnormalities
216
Q

Presentation of kidney stones

A
  • Asymptomatic
  • Renal colic:
    o Unilateral loin to groin pain – worse than childbirth
    o Colicky – fluctuating in severity
  • Restlessness with pain
  • Haematuria
  • Nausea / vomiting
  • Reduced urine output
  • Symptoms of sepsis if infection is present
217
Q

Ix for kidney stones

A
  • Urine dipstick – haematuria
  • FBC, U&E and serum calcium
  • Abdominal x-ray (shows calcium based stones but not uric acid stones)
  • CT KUB – diagnostic (non-contrast scan)
  • US KUB – doesn’t rule out kidney stones if clear but good in pregnant women and children
218
Q

Mx of kidney stones

A
  1. Renal colic management:
    a. IM diclofenac
  2. Anti-emetics for vomiting
  3. Stones <5mm = pass spontaneously
  4. Shockwave lithotripsy
  5. Ureteroscopy
  6. Percutaneous nephrolithotomy
219
Q

prevention of kidney stones

A
  • Avoid excess salt
  • Good hydration + add lemon juice to drinking water
  • Avoid carbonated drinks
  • A balanced diet
  • Healthy weight loss
  • Potassium citrate for those with recurrent calcium oxalate stones
  • Thiazides for recurrent stones that are calcium oxalate and still have hypercalciuria after restricting salt intake to 6g/day
220
Q

What is glomerulonephritis?

A

= a number of conditions where there is damage to the glomerular apparatus, causing the appearance of blood and protein in the urine. There’s inflammation of or around the glomerulus and nephron.

221
Q

What is nephritic syndrome?

A

haematuria, oliguria, proteinuria (<3g/24hrs), fluid retention

222
Q

What is nephrotic syndrome?

A

peripheral oedema, proteinuria (>3g/24hrs), hypoalbuminaemia (serum albumin less than 25g/L), hypercholesterolaemia

223
Q

What is minimal change disease?

A

Causes nephrotic syndrome
Most common in children
Steroids

224
Q

What is focal segmental glomerulonephritis?

A

Causes nephrotic syndrome
Most common cause of nephrotic syndrome in adults
Idiopathic or associated with HIV / heroin abuse
Poor response to steroids

225
Q

What is membranous Glomerulonephritis

A

Cause of nephrotic syndrome
Most common cause of glomerulonephritis overall
Bimodal age peak in 20s and 60s
Histology shows IgG and complement deposits on the basement membrane
Often mild
Majority idiopathic, but can be secondary to malignancy, rheumatoid disorders and drugs e.g., NSAIDs

226
Q

What is IgA nephropathy (Berger’s disease)?

A

Most common cause of primary glomerulonephritis
Causes nephritic syndrome
Peak presentation in 20s
Presentation = macroscopic haematuria in young people following URTI
Associated with: alcoholic cirrhosis, coeliac disease, dermatitis herpetiformis, HSP
Histology shows IgA deposits and glomerular mesangial proliferation
Mx: no treatment if isolated haematuria, ACEi if persistent haematuria, immunosuppression with corticosteroids if active disease & failure to respond to ACEi

227
Q

What is post streptococcal glomerulonephritis?

A

Under 30’s
1-3 weeks after a streptococcal infection (tonsillitis or impetigo)
Develop nephritic syndrome
Usually there’s a full recovery
Presentation = proteinuria and interval between URTI and onset of renal problems

228
Q

What is rapidly progressive glomerulonephritis?

A

Severely oliguric
Develop renal failure in weeks/months – patients respond well to treatment
Immune mediated in many cases
Glomeruli show crescent shaped masses of proliferating cells and leukocytes within the glomerular tuft
Often secondary to Goodpasture syndrome

229
Q

What is Goodpastures syndrome?

A

Anti-GBM (glomerular basement membrane) antibodies attack the glomerulus and pulmonary basement membranes.
Causes glomerulonephritis and pulmonary haemorrhage (AKI + haemoptysis)

230
Q

What is a varicocele?

A

abnormal enlargement of testicular veins. Usually asymptomatic but may be important as they are associated with infertility.

231
Q

Presentation of varicocele

A
  • Much more common on L side
  • Bag of worms on palpation
  • Subfertility
232
Q

Diagnosis of varicocele

A
  • USS with doppler studies
233
Q

Mx of varicocele

A
  • Conservative

- Surgery if pain

234
Q

What type of cancer is renal cell carcinoma?

A

adenocarcinoma that arises from proximal renal tubular epithelium. Most common type is clear cell.

235
Q

Risk factors for renal cell carcinoma

A
  • Middle aged man
  • Smoking
  • Obesity
  • HTN
  • End stage renal failure
  • Von Hippel-Lindau syndrome
  • Tuberous sclerosis
  • Autosomal dominant polycystic kidney disease
236
Q

Presentation of renal cell carcinoma

A
  1. Haematuria
  2. Loin pain
  3. Abdominal mass
    • Pyrexia
    • Endocrine effects:
    o Erythropoietin = polycythaemia
    o PTH = hypercalcaemia
    o Renin = HTN
    • Paraneoplastic hepatic dysfunction syndrome
    • Varicocele
    o Left sided
    o Tumour compresses veins
    • Stauffer syndrome
    o Abnormal LFTs without liver mets
237
Q

When to refer on two week wait for renal cell carcinoma

A

2 week wait referral for >45 yo with unexplained visible haematuria (without UTI or persisting after UTI treatment)

238
Q

Spread of renal cell carcinoma

A
  • Spreads to tissues around the kidney within Gerota’s fascia: renal vein + IVC
  • Cannonball metastases = in lungs. Clear defined circular opacities scattered through the lung fields on CXR
239
Q

Staging for renal cell carcinoma

A
  • TNM staging
  • OR number staging specific to renal cell carcinoma
    o Stage 1 = less than 7cm and confined to kidney
    o Stage 2 = bigger than 7cm and confined to kidney
    o Stage 3 = local spread to nearby tissues or veins but not beyond Gerota’s fascia
    o Stage 4 = spread beyond Gerota’s fascia including mets
240
Q

Mx of renal cell carcinoma

A
  • Nephrectomy (partial or radical)
  • Alpha-interferon and IL-2 to reduce tumour size
  • Chemotherapy and radiotherapy
241
Q

Why transplant a kidney?

A

Transplant kidney into a patient with end stage renal failure, add around 10 years to life compared to just dialysis and significantly improves QoL.

242
Q

How is donor matching done for a kidney transplant?

A
  • HLA type A, B, C on chromosome 6
243
Q

Procedure for kidney transplant

A
  • Patients kidneys left in place
  • Donor kidney blood vessels anastomosed with pelvic vessels (usually external iliac vessels), ureter anastomosed with bladder
  • Donor kidney placed in abdomen in iliac fossa
  • Hockey stick scar
244
Q

Immunosuppression for kidney transplant

A

Immunosuppression after transplant (lifelong)

  • Tacrolimus (tremor)
  • Mycophenolate
  • Prednisolone (Cushing’s syndrome)
245
Q

Complications with kidney transplant

A 
-	With transplant 
o	Transplant rejection
o	Transplant failure
o	Electrolyte disturbances
-	With immunosuppression
o	IHD
o	T2DM
o	Infections 
o	Non-Hodgkin’s lymphoma 
o	Skin cancer (SSC)
246
Q

How do epipdymal cysts feel on examination?

A
  • On examination = separate from body of testicle, posterior to testicle
247
Q

What is alports syndrome?

A
  • X-linked dominant inheritance
  • Defect in gene coding for type IV collagen = abnormal glomerular basement membrane
  • More severe in males
248
Q

How does alports syndrome present?

A 
-	Presents in childhood:
o	Microscopic haematuria
o	Progressive renal failure
o	Bilateral sensorineural deafness
o	Lenticonus – protrusion of lens into surface of anterior chamber 
o	Retinitis pigmentosa
249
Q

Ix for alports syndrome

A
  • Renal biopsy = splitting of lamina densa on electron microscopy = basket weave appearance
  • Also do molecular genetic testing

Finals Revision (18 decks)

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