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4th Year Surgery Block > Urology > Flashcards

Urology Flashcards

1
Q

Abdominal pain with blood and leucocytes on dipstick?

A

look for renal stones

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2
Q

Define recurrent urinary tract infections?

A
  • Defined as two proven episodes within six months or three within a year
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3
Q

Approach in clinic when patient with recurrent urinary tract infections?

A
  • Ask about risk factors for UTI
  • Check for haematuria
  • Check no systemic symptoms
  • Physical examination – general exam to rule out systemic conditions, abdominal exam to check for any palpable masses or palpable bladder, pelvic exam to look for atrophic vaginitis, vaginal prolapse and cystocele
  • Urine dipstick for leucocytes, nitrites and haematuria
  • Should do an ultrasound of the urinary tract to check no abnormalities
  • Flexible cystoscopy should be done to check for stenosis, bladder stones and tumours
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4
Q

Management of patient with recurrent urinary tract infections?

A
  • If underlying cause obviously treat this
  • Post-menopausal women to try vaginal oestrogens first
  • Then long term, low dose, prophylactic antibiotics
  • 4 antibiotics that are used are trimethoprim, nitrofurantoin, amoxicillin and cefalexin, these are used one at a time for 3 months and you rotate every 3 months to stop resistance
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5
Q

4 antibiotics that can be used for prophylaxis of recurrent urinary tract infections?

A

trimethoprim, nitrofurantoin, amoxicillin, cefalexin

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6
Q

Pathology of bladder cancer?

A

90% are transitional cell carcinoma, 9% squamous, 1% everything else
technically transitional cell can occur anywhere in the tract but bladder most common

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7
Q

Risk factors for bladder cancer?

A
  • Risk increases with age
  • Strong association with cigarette smoking
  • Exposure to industrial carcinogens e.g. beta-naphthylamine and benzidine
  • Exposure to certain drugs e.g. cyclophosphamide (used in some cancer and auto-immune disease treatment)
  • Squamous cell carcinomas arise from metaplastic change due to chronic inflammation e.g. recurrent UTIs and renal stones or schistosomiasis
  • In areas where schistosomiasis is endemic there is high incidence of squamous cell carcinoma of the bladder because the parasites lay eggs in the bladder causing inflammation
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8
Q

Presentation of bladder cancer?

A
  • Most common presentation is painless haematuria
  • Pain however can occur however if clot retention
  • Symptoms may be suggestive of a UTI i.e. urinary frequency, dysuria, nocturia but significant bacteruria is absent
  • Presenting symptoms may be pain from local nerve involvement or metastases
  • Flank pain if lesion causes ureteric obstruction
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9
Q

Investigations for bladder cancer?

A
  • Urine cytology for malignant cells
  • Cystoscopy (camera lens into urethra)
  • Urinary tumour markers
  • CT or MRI of pelvis
  • Excretory urography
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10
Q

Management of bladder cancer?

A

Depends on staging and grading:

  • In superficial disease - transurethral resection or local diathermy
  • If muscle invaded – radical cystectomy or radiotherapy, may do chemo
  • In metastatic disease – chemo
  • If reason to preserve bladder but invaded muscle – can do systemic chemo and then resection of tumour
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11
Q

What is multiple myeloma?

A
  • Malignant disease of bone marrow plasma cells
  • The cancer isn’t circulating but in the bone marrow (not sure it’s true but it’s helpful for me to think that there is this abnormal signal coming from somewhere causing all the bone marrow to become abnormally full of these monoclonal cells)
  • There is clonal expansion of abnormal, proliferating plasma cells producing a monoclonal paraprotein mainly IgG (55%) or IgA (20%)
  • Note: it’s called multiple myeloma because very occasionally you can get a solitary plasma cell tumour
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12
Q

Who tends to get multiple myeloma?

A
  • Disease of the elderly – median age at presentation is over 60, it is rare in under 40s
  • More common in males
  • More common in Black Africans but less common in Asians
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13
Q

Clinical features of multiple myeloma? Direct tumour cells effects and paraprotein mediated effects?

A

Direct Tumour Cell Effects
- Bone lesions (lytic)
- Hypercalcaemia
- Bone pain
- Replacement of normal marrow causing marrow failure

Paraprotein Mediated Effects:
- Renal failure
- Immunosuppression (reduction in normal antibodies)
- Hyperviscosity (due to increase in the amount of protein in the serum)
- Amyloid

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14
Q

Explain lytic bone disease in myeloma?

A
  • This involves a vicious cycle
  • Malignant plasma cells produce cytokines that interact with osteoblasts and osteoclasts
  • These cytokines cause an upregulation of osteoclasts but a down regulation of osteoblasts (so more bone is being destroyed but there are less osteoblasts to rebuild it)
  • Activated osteoclasts in turn produce other cytokines that in turn encourage myeloma cells to divide and multiply
  • Cause bone pain and commonly backache due to vertebral involvement
  • Can get spinal cord compression if lesions cause compression fractures
  • Skull XR may show many punched out lesions, sometimes referred to as pepper pot skull
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15
Q

Explain hypercalcaemia in multiple myeloma and symptoms?

A

Bone destruction causes hypercalcaemia
Symptoms:
- Bones > pain, osteoporosis and pathological fractures
- Stones > renal colic from stones, polydipsia, polyuria
- Abdominal groans > abdominal pain
- Psychiatric moans > chronic hypercalcaemia can cause depression but acute hypercalcaemia can cause confusion

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16
Q

Explain what happens in myeloma kidney?

A
  • Light chain cast nephropathy – due to low molecular weight, light chains can pass through glomerular filtrate and cause damage to the epithelial cells as the protein precipitates as casts
  • Hypercalcaemia can also damage the kidneys
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17
Q

Hypercalcaemia, back pain and AKI?

A

multiple myeloma

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18
Q

Investigations for myeloma?

A
  • FBC – Hb, WBC and platelet count are normal or low
  • ESR is often high
  • U and E – evidence of kidney injury
  • Serum calcium may be raised
  • Serum electrophoresis and immunofixation
  • Skeletal survey showing lytic lesions
  • Check urine for Bence Jones protein (light chains)
  • Rouleaux formation can be seen on blood film this is when there are stacks or aggregations of RBCs that form (although rouleaux formation can also be seen in other conditions)
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19
Q

Management of myeloma?

A
  • Myeloma is incurable and relapses are inevitable, survival is now 5-10 years for younger patients

Combination chemotherapy is the mainstay:
- Corticosteroids – dexamethasone
- Alkylating agents – cyclophosphamide, melphalan
- Novel agents – thalidomide, bortezomib and lenalidomide
- Monoclonal antibodies – daratumumab
- High dose chemo and autologous stem cell transplant can be done in fit patients where stem cells are taken out before chemo and put back in after chemo (so the patient isn’t at such high risk of infection and anaemia complications after chemo)

Symptom control:
- Treat kidney disease supportively
- Opiates for pain (avoid NSAIDs because they are not as good for the kidneys)
- Local radiotherapy – good for pain relief or spinal cord compression
- Bisphosphonates – correct hypercalcaemia and bone pain
- Vertebroplasty – inject sterile cement into fractured bone to stabalise it

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20
Q

Most LUTS in men are _____

A
  • Most of these are going to be due to benign prostatic hyperplasia, storage symptoms by themselves are generally not caused by BPH, but if part of a mixed picture will be
  • Storage symptoms by themselves more likely to be overactive bladder, carcinoma, stones or UTI so needs investigation
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21
Q

LUTS initial history?

A
  • Establish if symptoms are mainly voiding symptoms, storage symptoms or mixed
  • Voiding symptoms (outflow obstruction) and storage symptoms (frequency and urgency)
  • Voiding symptoms involve poor flow, intermittent stream, hesitancy and post void dribbling
  • Storage symptoms involve frequency, urgency, nocturia and incontinence
  • Rule out red flags: visible haematuria, sudden onset LUTS in absence of UTI, persistent dipstick haematuria, abnormal DRE, suspected retention of urine, non resolving storage symptoms
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22
Q

Investigations for LUTS?

A
  • Urine dipstick
  • Renal function tests
  • PSA
  • Post void bladder scan to check for retention
  • IPSS questionnaire
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23
Q

Management of voiding or mixed symptoms?

A
  • If mild symptoms simply give lifestyle advice (this should be given to everyone)
  • If moderate also try an alpha blocker e.g. tamsulosin (alpha blocker relaxes prostate and bladder smooth muscle) , review in 6 weeks if not settled add finasteride (reduces size of prostate)
  • If severe symptoms may consider surgery
  • In those with severe symptoms from the beginning e.g. long term chronic high pressure retention then may need to go straight to surgical intervention, if this is not suitable long term or intermittent self catheterisation
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24
Q

Management of storage symptoms?

A
  • Anticholinergics – however need to rule out chronic retention in these people
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25
Q

Describe prostate cancer?

A
  • Most common malignancy affecting men in the UK
  • There is a long natural history with an indolent course, many patients die with their cancer not of it
  • The majority of cancers are multifocal adenocarcinomas
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26
Q

Risk factors for prostate cancer?

A
  • Increasing age (by 80, 80% of men have malignant foci)
  • Family history
  • Hormonal factors
  • Race: Common in the black population in the USA but rare in China and Japan
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27
Q

Presentation of prostate cancer?

A
  • Majority are asymptomatic and picked up by PSA tests or abnormal DRE findings
  • The patient may have lower urinary tract symptoms similar to those of BPH e.g. nocturia, hesitancy, reduced stream, post void dribbling
  • May also present with haematuria or haematospermia
  • If the cancer has metastasized the patient may have bone, pain, anorexia and/ or weight loss
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28
Q

Describe DRE in prostate cancer?

A
  • 75-80% of prostate cancers arise in the peripheral zone which is at the back of the prostate
  • This is why DRE is helpful as it is the peripheral zone that will be felt when performing this exam
  • On DRE a doctor would be looking for asymmetry, nodules or a fixed craggy (uneven) mass
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29
Q

Describe sensitivity and specificity of PSA testing?

A
  • Sensitivity of PSA in detecting prostate cancer is very high at 90% (the test correctly identifies those with prostate cancer)
  • However, specificity of the test is very low at 40% (the test picks up a lot of people who don’t have prostate cancer)
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30
Q

What things other than prostate cancer can elevate PSA?

A
  • There are other conditions that can elevate PSA: benign prostatic hyperplasia, prostatitis, UTIs, retention, catheterisation and having a DRE recently performed, ejaculation in last 48 hrs, vigorous exercise
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31
Q

Indications for trans-rectal USS guided prostate biopsy?

A
  • Indications: men with abnormal DRE, elevated PSA, previous biopsies showing PIN (prostatic intraepithelial neoplasia) and ASAP (atypical small acinar proliferation), rising PSA trend despite previous normal biopsies
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32
Q

Pathology of prostate cancer?

A
  • Most are adenocarcinomas
  • The cancers can extend locally through the prostatic capsule to the urethra, bladder and seminal vesicles with perineural invasion along autonomic nerves
  • The most common sites for metastatic deposits= pelvic lymph nodes and skeleton (sclerotic lesions)
  • Gleason system is used and has grades 2-10 and indicates degree of differentiation from grade 2 which is well differentiation to grade 10 which is an aggressive cancer with poor prognosis
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33
Q

Prostate cancer management organ confined disease?

A
  • Watchful waiting – conservative approach, when tumour progresses can do palliative care
  • Active surveillance – close surveillance until at thresholds, designed to be curative
  • Radical surgery – radical prostatectomy, this would hopefully be curative however there is the risk of complications such as erectile dysfunction, incontinence and bladder neck stenosis
  • Radical radiotherapy – this can also be curative but come with the side effects of radiotherapy
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34
Q

Prostate cancer management locally advanced disease?

A
  • Radiotherapy with neo adjuvant hormonal therapy
  • Watchful waiting – done in those with well differentiated tumours and life expectancy < 10 years or patients who do not accept the treatment related complications
  • Hormonal therapy – done in symptomatic patients who need palliation of symptoms but are unfit for curative surgery
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35
Q

Prostate cancer management metastatic disease?

A

Androgen deprivation therapy: growth of prostate cancer cells is under influence of testosterone, if prostate cells are deprived of androgenic stimulation they undergo apoptosis
- Hormonal therapy with LHRH analogues or anti-androgens
- Bilateral subcapsular orchidectomy (removing the testis removes testosterone)
- Maximal androgen blockade

Hormonal therapy will come with expected side effects e.g. loss of libido, hot flushes and sweats, weight gain, gynaecomastia, osteoporosis, anaemia, cognitive changes

  • Diethylstibesterol which blocks testosterone synthesis is another treatment option (this is a synthetic oestrogen so will also cause hormonal side effects)
  • Cytotoxic chemotherapy can also be used
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36
Q

What is the most common type of testicular cancer?

A

germ cell tumours - seminomas or teratomas

  • Seminomas arise from the germinal epithelium of the seminiferous tubules
  • Teratomas arise from totipotent germ cells capable of differentiating into derivatives of ectoderm, endoderm and mesoderm
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37
Q

Risk factors/ who gets testicular cancer?

A
  • Largely a disease of young and middle aged men (most common malignancy in young men)
  • Cryptorchidism (undescended testes)
  • Previous testicular malignancy
  • Family history
  • Congenital abnormalities e.g. hypospadias, inguinal hernias
  • Infections e.g. mumps causing orchitis
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38
Q

Classic presentation of a testicular cancer

A
  • Testicular cancers usually present as a painless, insensitive testicular swelling – a hard stony mass
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39
Q

Investigations for a testicular cancer?

A
  • 95% sensitivity and specificity on ultrasound
  • If a patient has a hard testicular lump they should receive an ultrasound that day
  • Tumour markers: AFP, HCG and LDH
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40
Q

Management of testicular cancer?

A
  • Radical orchidectomy is usually performed for treatment
  • Orchidectomy is usually done as first step in all testicular cancers, may then do radiotherapy, chemotherapy etc.
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41
Q

Where do renal stones most commonly form?

A
  • Most commonly form in the kidneys themselves but can form in ureters, bladder or urethra
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42
Q

Most common type of kidney stone?

A

calcium oxalate stones

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43
Q

Why is hydration important in preventing renal stones?

A

low urine volume predisposes to stones

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44
Q

Risk factors for calcium oxalate stones?

A
  • Risk factors include hypercalcaemia (hyperparathyroidism etc), hypercalciuria (impaired renal tubular reabsorption) and hyperoxaluria (can be genetic defect, defect in liver metabolism or high dietary intake)
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45
Q

Give an example of an infection which can cause stones?

A

proteus

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46
Q

UTI stones are composed of?

A

ammonium, magnesium and phosphate

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47
Q

Presentation of renal stones?

A
  • Can be asymptomatic
  • May present with pain
  • May be a dull, achy flank pain or renal colic which is sharper flank pain that may radiate to the groin
  • Can also present with haematuria
  • UTI
  • Urinary tract obstruction (difficulty urinating, hydronephrosis, pain)
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48
Q

Diagnosis of renal stones?

A
  • Should offer urgent non contrast CTKUB for adults, ultrasound first for children
49
Q

Short term/ medium term management of stones?

A
  • Pain – NSAIDs, if NSAIDs plus paracetamol not giving adequate relief then offer an opioid
  • Small stones (less than 7mm) pass spontaneously usually and should just be sent home with medial expulsive therapy (alpha blockers), analgesics and followed up
  • If stones > 10mm patient needs booked in for surgery in next couple weeks
  • Shockwave lithotripsy can sometimes be used which is non-invasive and uses shock waves to help the stone pass
  • Surgical procedures include ureteroscopy and percutaneous nephrolithotomy

NICE guidelines
renal stones:
watchful waiting if stone < 5mm
stone < 10mm offer SWL
stone 10-20 mm offer PCNL first

ureteric stones:
< 10mm offer SWL
10 - 20 offer URS

50
Q

Long term management of stones?

A
  • Good fluid intake
  • Reduction in certain foods
  • In those with calcium oxalate stones can give cholestyramine
  • In those with uric acid stones can give allopurinol
  • can use thiazide diuretics to help in prevention of some calcium stones
51
Q

Define acute kidney injury

A
  • In adults, acute kidney injury can be detected by using any of the following criteria:
    o A rise in serum creatinine of 26 micromol/L or greater within 48 hours.
    o A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days.
    o A fall in urine output to less than 0.5mL/kg/hour for more than 6 hours.
52
Q

The most common cause of AKI is

A

pre-renal

53
Q

Some causes of pre renal AKI

A

Causes include:
1. Hypovolaemia e.g. haemorrhage, volume depletion in diarrhoea and vomiting or burns
2. Hypotension in shock e.g. cardiogenic, septic or anaphylactic shock
3. Renal hypoperfusion (i.e. problem not systemic) – NSAIDs, ACEi, hepatorenal syndrome

  • Often multifactorial e.g. an elderly person with already poor renal function gets a diarrhoeal illness and keeps taking their ACEi and NSAIDs
54
Q

Untreated pre-renal AKI will cause

A

acute tubular necrosis

55
Q

Management of pre-renal AKI involves

A
  • Patients with suspected pre-renal AKI should be fluid challenged with 0.9% NaCl or Colloid, give bolus of fluid, reassess repeat, if > 1000ml and no improvement seek help
56
Q

Causes of renal AKI?

A

include:
1. Tubule damage- acute tubular necrosis as a result of pre-renal AKI, nephrotoxins e.g. gentamicin, myoglobin (from muscle), ethylene glycol, contrast, uric acid (can occur in tumour lysis syndrome)
2. Glomerulus – all types of glomerulonephritis
3. Interstitium – acute interstitial nephritis – an adverse effect of some drugs

57
Q

Management of renal AKI involves?

A

If suspect renal AKI in a patient should fluid resuscitation, treat underlying cause e.g. stop nephrotoxic drugs, treat glomerulonephritis

58
Q

Causes of post-renal AKI?

A

AKI occurs when obstruction to urine flow leads to back pressure causing hydronephrosis (swelling of kidney), and thus loss of concentrating ability

Causes include:
1. Compression – caused by intra-abdominal tumours or BPH
2. Blockage inside the tract e.g. stones, strictures or tumours

59
Q

Management of post-renal AKI involves

A

relieving obstruction

60
Q

Approach to a patient with AKI?

A
  • Assess volume status – check fluid intake and losses, HR and BP, JVP, moistness of mucous membranes and skin turgor, changes in urination pattern, peripheral oedema and pulmonary crackles
  • Exclude hyperkalaemia
  • Ask about potential causes – unwell recently, symptoms of obstructions, history of CVS disease, symptoms of underlying inflammatory cause e.g. vasculitic rash, arthralgia, drug history, possibility of rhabdomyolysis e.g. skeletal muscle injury, exercise overexertion
  • Urine dipstick to check for blood, protein, leucocytes, nitrites and glucose
  • If blood or protein on dipstick request immunology – ANA, ANCA, Ig, C3/C4
  • Myeloma screen if over 50 with anaemia and hypercalcaemia
  • Blood tests to measure haemoglobin, bicarbonate, calcium, phosphate and if suspect sepsis CRP, lactate and cultures
  • Investigate for obstruction with CTKUB or US if suspect
  • Side note: AKI with negative urinalysis usually suggests a pre-renal cause but drugs should be considered
  • Stage AKI using NICE criteria
61
Q

Who needs to go to hospital with AKI for those not admitted what do you do?

A

Not everyone needs to go to hospital however should arrange urgent admission/ same day referral for:
* Stage 3
* Underlying cause that requires secondary care management e.g. obstruction, infection, GN
* Risk that the cause is obstruction
* Sepsis
* Need for fluid replacement as hypovolaemic
* Deterioration
* Complication of AKI
* No identifiable cause

For people who don’t need admitted give advice on hydration and think about stopping potentially nephrotoxic drugs e.g. ACEi
In hospital some patients may need haemodialysis

62
Q

Complications of AKI?

A
  • Uraemia
  • Metabolic acidosis
  • Hyperkalaemia
  • Spontaneous haemorrhage
  • Pulmonary oedema
63
Q

Ranges for hyperkalaemia?

A
  • Normal 3.5-5, hyper > 5.5, life threatening > 6.5
64
Q

Symptoms/ signs of hyperkalaemia?

A

intestinal cramping, weakness and paralysis, cardiac arrhythmias

65
Q

Classic ECG abnormality for hyperkalaemia?

A

tall tented t waves

66
Q

Management of hyperkalaemia?

A
  • Management: 10% calcium gluconate (stabalises the heart), insulin (and dextrose) and salbutamol (to move K+ back into cells), calcium resonium (prevents GI absorption of calcium)
  • If severe may need dialysis
67
Q

NICE definition of chronic kidney disease?

A

Chronic kidney disease has to be diagnosed on 2 tests 3 months apart.
eGFR < 60
or urinary albumin: creatinine ratio > 3

(kidney should be filtering creatinine into urine but not albumin so increased ratio suggest kidney is damaged and letting lots of protein into urine)

68
Q

Commonest causes of CKD? Some other causes?

A
  • Diabetes and hypertension are most common causes
  • Others examples include CVD, AKI, nephrotoxic drugs and obstructive uropathy
69
Q

Some signs and symptoms of CKD?

A
  • Uraemia: nausea, vomiting, anorexia, weight loss, fatigue, itch, altered taste, restless legs and muscle twitching, difficulties concentrating and confusion
  • In advanced uraemia can get lemon yellow skin, uraemic frost, twitching, encephalopathic flap, confusion, pericardial rub or effusion and Kussmaul breathing in metabolic acidosis
  • Anaemia: fatigue, muscle weakness, conjunctival and palmar pallor
  • Pain: bony, neuropathic, ischaemic and visceral pain
  • Hypercalcaemia symptoms (in tertiary hyperparathyroidism)
70
Q

Describe cardiovascular disease in CKD?

A
  • Includes CVD causing CKD and CKD causing CVD
  • In CKD pericarditis can occur due to high urea or phosphate or if severe hyperparathyroidism
  • Fluid overload and hypertension can cause LVH or a dilated cardiomyopathy
71
Q

Management of CVD in CKD?

A
  • Management: advice on smoking cessation, weight loss, aerobic exercise, limiting salt intake, control of hypertension and hyperlipidaemia
72
Q

Explain why you get mineral and bone disease in CKD?

A
  • Due to poorly functioning kidneys there is renal phosphate retention and inadequate renal vitamin D activation resulting in poor calcium absorption from the gut
  • There is therefore low serum calcium so PTH increases and there is secondary hyperparathyroidism
  • Eventually PTH secretion can become autonomous and fail to fall even when hypocalcaemia is treated – this is termed tertiary hyperparathyroidism
73
Q

Management of mineral and bone disease in CKD?

A
  • Management: need dietary advice and potentially supplements, in tertiary may need to remove parathyroids
74
Q

Why do you get anaemia in CKD?

A

kidneys are producing less EPO which is needed to make RBCs

75
Q

How is anaemia usually treated in CKD?

A

EPO injections

76
Q

General management points for people with CKD?

A
  • In people with CKD aim to keep the systolic BP below 140mmHg and diastolic below 90mmHg
  • In those with diabetic or with ACR 70mg/mmol aim 130 and 80
  • All people with CKD should be offered statin therapy and antiplatelet therapy for primary or secondary prevention of CVD
  • Ensure has influenza and pneumococcal vaccines
  • Use ACEi in some individuals
77
Q

Explain what is meant by epididymitis and orchitis?

A
  • The epididymis is a narrow tightly coiled tube that is attached to each of the testicles, sperm cells move from the testicles to the epididymis where they finish maturing and are stored
  • Epididymitis refers to inflammation of the epididymis and orchitis to inflammation of the testes
  • Orchitis is less common
78
Q

Causes of epididymitis?

A
  • In men under 35 it is often due to a STI e.g. chlamydia or gonorrhoea
  • In men over 35 may be due to gram negative enteric organism causing urinary tract infection e.g. E coli
  • However will be an overlap between these two groups, so history is important
79
Q

Causes of orchitis?

A
  • Can be viral, mumps orchitis is most common
  • Can be due to other types of infection e.g. bacterial, syphilis, TB
  • Trauma
  • Idiopathic
80
Q

Risk factors for epididymitis and orchitis?

A
  • STIs
  • Instrumentation and indwelling catheters
  • Structural or functional abnormalities of the urinary tract
  • Anal intercourse is a risk factor for infection with enteric pathogens
  • Reflux of infected urine can occur in valsava manoeuvre and strenuous exercise
81
Q

Presentation of epididymitis?

A
  • Gradual onset of usually unilateral scrotal pain, sometimes radiates to lower abdomen
  • Fever and chills
  • Frequency, urgency and dysuria
  • Less commonly urethral discharge, haematuria and haematospermia
  • Normal cremasteric reflex – stroking of the inner thigh causes the cremaster muscle to contract and pull up the ipsilateral testicle towards the inguinal canal
  • Prehn sign – elevating the scrotum relieves pain
  • Reactive hydrocele can be present
82
Q

Presentation of orchitis?

A
  • Unilateral or bilateral testicular tenderness, pain and scrotal swelling
  • Fever
  • Reactive hydrocele
  • Inguinal lymphadenopathy
  • Normal cremasteric reflex
83
Q

Explain what is the cremasteric reflex is and when it is absent?

A
  • Normal cremasteric reflex – stroking of the inner thigh causes the cremaster muscle to contract and pull up the ipsilateral testicle towards the inguinal canal
    absence of the reflex is considered to be diagnostic of testicular torsion
84
Q

Investigations for epididymitis and orchitis?

A
  • Ultrasound scrotum
  • Urine dipstick
  • Blood tests
  • STI or UTI testing
85
Q

Management of epididymitis and orchitis?

A
  • If infectious cause antimicrobial therapy
  • Rest
  • Analgesia
  • If can’t rule out testicular torsion surgery
86
Q

Define nephrotic syndrome?

A
  • Clinical syndrome of glomerulonephritis that consists of heavy proteinuria leading to hypoalbuminaemia and oedema
  • Defined as presence of proteinuria > 3g/24hr, hypoalbuminaemia and peripheral oedema
87
Q

How does nephrotic syndrome present?

A
  • First swelling of face, often periorbital oedema, then of entire body
  • Foamy urine will be present
  • May also complain of weight gain due to fluid retention, fatigue and loss of appetite
  • Often have hyperlipidaemia
88
Q

3 causes of nephrotic syndrome?

A
  • Minimal change disease
  • Focal Segmental Glomerulosclerosis
  • Membranous Glomerulonephritis
89
Q

What is the commonest cause of nephrotic syndrome in children?

A

minimal change disease

90
Q

Why is it called minimal change disease?

A
  • There are no abnormalities on light microscopy but electron microscopy reveals effacement of podocyte foot processes
91
Q

Prognosis of minimal change disease?

A
  • 94% show complete remission with oral steroids
  • Does not cause progressive renal failure
92
Q

FSGS is associated with what?

A

HIV, heroin use and congenital malformations

93
Q

Prognosis of FSGS?

A
  • Some will go into remission with steroids but 50% progress to renal failure
94
Q

Membranous glomerulonephritis is associated with?

A
  • Can be idiopathic or due to hep B, SLE, malignancies, penicillamine
95
Q

What may you see on microscopy and immunofluorescence with membranous glomerulonephritis?

A
  • It involves immune complex deposition and immunofluorescence shows IgG uptake
  • Spike and dome appearance on electron microscopy
96
Q

Approach and management of nephrotic syndrome?

A
  • History – what is cause
  • Management of oedema – low salt diet, fluid restrict, diuretic, check daily weights, patients with very low albumin may need IV albumin therapy
  • Treat renal pathology – corticosteroids are used as first line agents, immunosuppressive therapies may be used
  • Hyperlipidaemia – doesn’t initially need treatment only if prolonged
  • Hypertension – may use ACEi in adults with hypertension caused by renal disease as reduces proteinuria
97
Q

The principle feature of diabetic nephropathy is _______

A

proteinuria
starts off as intermittent microalbuminuria then progresses to constant proteinuria

98
Q

Pathology feature for diabetic nephropathy?

A

Kimmelsteil Wilson nodules

99
Q

Monitoring for kidney disease in those with diabetes?

A
  • Annual review measure urinary ACR or albumin concentration
  • Measure serum creatinine and eGFR
  • (note that microalbuminuria won’t be detectable on standard dipstick and need to use special dipstick)
100
Q

Management of those with diabetic nephropathy?

A
  • Generally, first people are offered an ACEi or ARB
  • Then may be offered SGLT 2 inhibitor
  • Other management similar to all CKD management
101
Q

Explain the 2 major forms of diabetes insipidus?

A

2 major forms:
1. Cranial – there is decreased secretion of ADH from the posterior pituitary, with less ADH, urine is less concentrated so patient develops polyuria and polydipsia
2. Nephrogenic – ADH is secreted normally but the kidney does not respond to ADH so again urine is dilute and in larger volumes

102
Q

Causes of cranial DI?

A
  • This is usually due disease of hypothalamus (disease of posterior pituitary tends not to cause problems unless it extends and puts pressure on hypothalamus because hypothalamus will continue to secrete)
  • Causes include idiopathic, tumours, intracranial surgery, head injury, sarcoidosis, infections, vascular disorders, some inherited forms
103
Q

Causes of nephrogenic DI?

A
  • This can be congenital/ genetic
  • Can also be caused by some electrolyte abnormalities (hypercalcaemia and hypokalaemia), CKD , obstructive disease and drugs
104
Q

Investigations for DI?

A
  • Water deprivation test – when dehydrated can the patient concentrate their urine – if not they have DI
  • Then test response to desmopressin (synthetic ADH) – cranial DI will respond and produce concentrate urine, nephrogenic will note
  • MRI of pituitary, hypothalamus and surrounding tissues
  • Renal tract US
105
Q

Management of DI?

A
  • Cranial DI can be managed with desmopressin tablets
  • Nephrogenic DI does not always need treated sometimes just ensure adequate hydration
  • For nephrogenic treat any underlying cause
  • For nephrogenic may do treatment with thiazide and NSAID
  • In extreme nephrogenic may need to catheterise intermittently to reduce urinary tract back pressure complications
106
Q

Sinusoidal ECG wave pattern?

A

a sign of severe hyperkalaemia

107
Q

Explain what enterovesical fistula is and what is can cause?

A

fistula between bowel and bladder
can make urine frothy and cause recurrent UTIs
may occur in colorectal malignancy

108
Q

What has replaced TRUS for diagnosis of prostate cancer?

A

multi parametric MRI

109
Q

Explain what a hydrocele is and causes?

A

collection of fluid in tunica vaginalis that surrounds the testes

Idiopathic or secondary to testicular cancer, torsion, epididymo-orchitis or trauma

110
Q

Presentation of a hydrocele?

A

painless soft scrotal swelling
testicle palpable within the hydrocele
soft fluctuant irreducible, transilluminable

111
Q

Management of hydrocele?

A

idiopathic are usually managed conservatively unless causing problems
other options = surgery, aspiration or sclerotherapy

112
Q

Explain what a varicocele is and what side it usually occurs on?

A

swollen veins in the pampiniform plexus

usually occurs on the left due to higher pressures, the left testicular vein drains into the left renal vein whereas right testicular vein drains directly into the IVC

113
Q

What is a worrying cause of varicocele? What makes this more likely?

A

varicocele can be a result of renal cell carcinoma - more worried about this if the varicocele does not disappear even on lying down

114
Q

What can varicoceles cause problems with?

A

fertility

115
Q

Presentation of varicocele?

A

asymptomatic
throbbing dull pain or discomfort
dragging sensation
feels like bag of worms
may disappear on lying down, more visible on standing

116
Q

What is an epididymal cyst, how may you differentiate it from a hydrocele?

A

these are cysts in the epididymis at the top of the testicle, they are very common, most are asymptomatic, the cyst is felt separately from the testicle where with hydroceles you feel the testicle within

117
Q

Indications for dialysis in AKI?

A

if someone has pre renal and has been fluid resuscitation but still anuric consider dialysis if one of:
metabolic acidosis
urea > 50
potassium > 6
pulmonary oedema

118
Q

Classic appearance of renal bone disease on spine XR

A

spine xr shows sclerosis at both ends of the vertebra and osteomalacia in centre of the vertebra
> rugger jersey spine
thicker white lines running up side of XR

4th Year Surgery Block (11 decks)

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