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2a high tier > Renal/ Genitourinary > Flashcards

Renal/ Genitourinary Flashcards

1
Q

What is the aetiology of renal colic?

A

Upper urinary tract obstruction e.g. from clots

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2
Q

What is the clinical presentation of renal colic?

A
  • Rapid onset pain – woken from sleep
  • Excruciating ureteric spasms
  • Pain from loin to groin that comes and goes in waves
  • Associated with nausea and vomiting
  • Worse with fluid loading
  • Radiates to groin and ipsilateral testis/ labia
  • Often cannot lie still
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3
Q

What is the differential diagnosis of renal colic?

A

Peritonitis

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4
Q

How is renal colic managed?

A

Strong analgesic e.g. IV diclofenac

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5
Q

What is the aetiology of AKI?

pre-renal, intrinsic renal and post-renal

A
  • Rapid decline in GFR
  • Ischaemia, sepsis, nephrotoxins
  • PRE-RENAL = renal hypoperfusion, hypovolaemia (dehydration), low cardiac output (cardiac failure), renal hypoperfusion (NSAIDs)
  • INTRINSIC RENAL = renal parenchyma damage, acute tubular necrosis, vascular (renal artery/vein thrombosis, vasculitis, malignant hypertension), glomerular (glomerulonephritis, autoimmune), interstitial (drugs)
  • POST-RENAL = urinary tract obstruction, stones, clots, malignancy, BPH, strictures, extrinsic compression from malignancy
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6
Q

What is the pathophysiology of AKI?

A

Sustained rise in serum urea and creatinine leading to a failure to maintain fluid, electrolyte and acid-base homeostasis

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7
Q

What are the risk factors of AKI?

A
  • Age > 75y
  • Heart failure
  • Peripheral vascular disease
  • Chronic liver disease
  • Sepsis
  • Poor fluid intake/ increased losses
  • History of urinary symptoms
  • Chronic kidney disease
  • Past history of AKI
  • Hypovolaemia
  • Diabetes
  • Prostate cancer
  • Nephrotoxic drugs
  • Repeated use of radiological contrast
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8
Q

What is the clinical presentation of AKI?

A
  • May be palpable bladder, palpable kidneys, abdominal/pelvic masses and rashes
  • Oliguria (small amount of urine) in early stages
  • Irregular heartbeats
  • Symptoms of uraemia (fatigue, anorexia, nausea, vomiting then confusion, seizures and coma)
  • Breathlessness
  • Pericarditis
  • Impaired platelet function causes bruising
  • Infection
  • Postural hypertension
  • Oedema
  • Thirst
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9
Q

What are the differential diagnoses of AKI?

A
  • Abdominal aortic aneurysm
  • Alcohol toxicity
  • Alcohol and diabetic ketoacidosis
  • Chronic renal failure
  • Dehydration
  • GI bleed
  • Heart failure
  • Metabolic acidosis
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10
Q

How is AKI diagnosed?

A
  • Rising serum urea and creatinine
  • Urine dipstick (can suggest infection and glomerular disease)
  • Blood count (anaemia and high ESR = myeloma or vasculitis)
  • Mid-stream urine specimen
  • Renal USS (assessment of kidney size and distinguish obstruction, look for abnormalities)
  • CT of kidneys, ureters and bladder (CT-KUB) (see if obstruction causing no urine – relieved by catheter)
  • ECG – for hyperkalaemia changes
  • CXR – for pulmonary oedema)
  • Renal biopsy
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11
Q

How is AKI managed?

A
  • Treat underlying cause – pre-renal (fluids, antibiotics), intrinsic renal (refer early to nephrology), post-renal (catheterise and CT renal tract)
  • Stop nephrotoxic drugs (NSIADs, ACEi, gentamicin)
  • Optimise fluid balance
  • For hyperkalaemia give calcium gluconate and insulin and glucose
  • Treat acidosis with sodium bicarbonate
  • Treat pulmonary oedema with diuretics
  • Diet – Na+, K+ restriction, vitamin D supplement
  • Renal replacement therapy (hemofiltration, haemodialysis, transplant)
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12
Q

What is the aetiology of kidney cancer?

A
  • Smoking
  • Obesity
  • Hypertension
  • Renal failure and haemodialysis
  • Polycystic kidneys
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13
Q

What is the pathophysiology of kidney cancer?

A
  • Malignant cancer of proximal convoluted tubular epithelium

- Spread can be direct (renal vein), by lymph nodes or haematogenous (bone, liver, lung)

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14
Q

What are the risk factors of kidney cancer?

A
  • Smoking
  • Obesity
  • Hypertension
  • Renal failure and haemodialysis
  • Polycystic kidneys
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15
Q

What is the clinical presentation of kidney cancer?

A
  • Often asymptomatic and found incidentally
  • Haematuria, flank pain, abdominal mass
  • Anorexia, malaise, weight loss
  • Sometimes invasion of left renal vein causing a varicocele
  • Polycythaemia
  • Hypertension
  • Anaemia
  • Fever
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16
Q

What are the differential diagnoses of kidney cancer?

A
  • Transitional cell carcinoma
  • Wilms’ tumour
  • Renal oncocytoma
  • Leiomyosarcoma
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17
Q

How is kidney cancer diagnosed?

A
  • Renal USS (distinguish cyst from tumour)
  • CT chest and abdomen with contrast (detect renal mass – contrast demonstrates kidney function)
  • MRI (tumour staging)
  • BP (increased from renin secretion)
  • FBC (polycythaemia, anaemia from EPO decrease)
  • ESR (raised)
  • LFT may be abnormal
  • Renal biopsy
  • Bone scan
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18
Q

How is kidney cancer managed?

A
  • Localised = surgery (nephrectomy or partial)
  • Ablative techniques e.g. cryoablation and radiotherapy (if lots of comorbidities so can’t have surgery)
  • Metastatic or locally advanced = interleukin-2 and interferon alpha first line
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19
Q

What is the carcinoma type of bladder cancer?

A

Transitional cell carcinoma (most common type of TCC)

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20
Q

What is the pathophysiology of bladder cancer?

A

Tumour spread:

  • Local → pelvic structures
  • Lymphatic → iliac and para-aortic nodes
  • Haematogenous → liver and lungs
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21
Q

What are the risk factors of bladder cancer?

A
  • Smoking
  • Occupational exposure to carcinogens (esp. petroleum, chemical, cable and rubber industries)
  • Exposure to drugs (cyclophosphamide)
  • Chronic inflammation of urinary tract (e.g. from Schistomiasis)
  • > 40y
  • Male
  • Family history
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22
Q

What is the clinical presentation of bladder cancer?

A
  • Painless haematuria (maybe pain from clot retention)
  • Recurrent UTIs
  • Voiding irritability
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23
Q

What are the differential diagnoses of bladder cancer?

A
  • Haemorrhagic cystitis
  • Renal cancer
  • UTI
  • Urethral trauma
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24
Q

How is bladder cancer diagnosed?

A
  • Cystoscopy with biopsy (diagnostic)
  • Urine microscopy/ cytology
  • CT urogram – staging
  • Urinary tumour markers
  • MRI to see involved pelvic nodes
  • CT/ MRI of pelvis
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25
Q

How is bladder cancer managed?

Non-muscle invasive, localised muscle invasive and metastatic

A

NON-MUSCLE INVASIVE: surgical resection ± chemotherapy (mitomycin, doxorubicin and cisplatin)

LOCALISED MUSCLE INVASIVE: radical cystectomy, post-op chemo, radical radiotherapy (if not fit for surgery), chemo

METASTATIC: palliative chemotherapy and radiotherapy

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26
Q

What is the aetiology of prostate cancer?

A

Hormonal factors e.g. increased testosterone

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27
Q

What is the pathophysiology of prostate cancer?

A
  • Most are adenocarcinomas in the peripheral prostate
  • Androgen receptors on the prostate are responsible for cancerous growth

Tumour spread:

  • Local → seminal vesicles, bladder, rectum
  • Lymph
  • Haematogenous → bone, brain, liver lung
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28
Q

What are the risk factors of prostate cancer?

A
  • Family history (3+ affected relatives or 2 with early onset)
  • Genetic (HOXB13)
  • Increasing age
  • Black ethnicity
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29
Q

What is the clinical presentation of prostate cancer?

A
  • LUTS if local disease (nocturia, hesitancy, poor stream, terminal dribbling, obstruction)
  • Weight loss, bone pain and anaemia suggest metastasis
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30
Q

What are the differential diagnoses of prostate cancer?

A
  • BPH
  • Prostatitis
  • Bladder tumours
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31
Q

How is prostate cancer diagnosed?

A
  • DRE – hard, irregular prostate
  • Raised PSA
  • Trans-rectal ultrasound (TRUS) and biopsy – diagnostic
  • Urine biomarkers (PCA3 or gene fusion protein)
  • Endorectal coil MRI to locally stage
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32
Q

How is prostate cancer managed?

A
  • LOCAL: radical proctectomy, radiotherapy + hormone therapy, brachytherapy (implantation of radioactive material targeted at tumour), hormone therapy temporarily, active surveillance (if >70y and low risk)
  • METASTATIC: endocrine therapy (androgen deprivation) – orchidectomy (testes removal), LHRH agonists, androgen receptor blockers)
  • Analgesia
  • Treat hypercalcaemia
  • Radiotherapy for bone metastases/ spinal cord progression
33
Q

What cells do testicular cancers arise from?

A
  • 96% arise from germ cells

- 4% arise from non-germ cells

34
Q

What are the risk factors of testicular cancer?

A
  • Undescended testes
  • Infant hernia
  • Infertility
  • Family history
35
Q

What is the clinical presentation of testicular cancer?

A
  • Painless lump in testicle, testicular pain and/or abdominal pain
  • Hydrocele
  • Cough and dyspnoea (indicative of lung metastases)
  • Back pain
  • Abdominal mass
36
Q

What are the differential diagnoses of testicular cancer?

A
  • Testicular torsion
  • Lymphoma
  • Hydrocele
  • Epididymal cysts
37
Q

How is testicular cancer diagnosed?

A
  • USS to differentiated between masses in the body of the testes and other intrascrotal swellings
  • Biopsy and histology
  • Serum tumour markers
  • CXR and CT for staging
38
Q

How is testicular cancer managed?

A
  • Radical orchidectomy via inguinal approach
  • Radiotherapy for seminomas with metastases below diaphragm
  • Chemotherapy for more widespread tumours and teratomas
  • Sperm storage offered
39
Q

What is the aetiology of CKD?

A
  • Diabetes mellitus (2>1)
  • Hypertension
  • Atherosclerotic renal vascular disease
  • Polycystic kidney disease
  • Tuberous sclerosis
  • Primary glomerulonephritides (e.g. IgA nephropathy)
  • SLE
  • Amyloidosis
  • Hypertensive nephrosclerosis
  • Small/medium vessel vasculitis
  • Family history of stage 5 CKD or hereditary kidney disease
  • Hypercalcaemia
  • Neoplasma
  • Myeloma
  • Idiopathic
40
Q

What is the pathophysiology of CKD?

A
  • Many nephrons have failed and scarred so the burden of filtration falls to fewer functioning nephrons
  • Increased flow per nephron raises intraglomerular capillary pressure which accelerates nephron failure
  • Increased strain can be detected as new/ increasing proteinuria
41
Q

What are the risk factors of CKD?

A
  • Diabetes mellitus
  • Hypertension
  • Old age
  • CVD
  • Renal stones or BPH
  • Recurrent UTIs
  • SLE
  • Proteinuria
  • AKI
  • Smoking
  • African, afro-Caribbean or Asian origin
  • Chronic NSAID use
42
Q

What is the clinical presentation of CKD?

A
  • Early stages are often asymptomatic
  • Malaise
  • Anorexia and weight loss
  • Insomnia
  • Nocturia and polyuria
  • Itching
  • Nausea, vomiting and diarrhoea
  • Peripheral/ pulmonary oedema
  • Amenorrhea in women
  • Erectile dysfunction in men
  • Increased risk of peptic ulceration, acute pancreatitis, hyperuricaemia and incidence of malignancy
43
Q

What is the differential diagnosis of CKD?

44
Q

How is CKD diagnosed?

A
  • ECG for high potassium
  • URINALYSIS: haematuria, proteinuria, mid-stream urine sample, albumin to creatinine ratio
  • URINE MICROSCOPY: white cells = UTI; eosinophilia = allergic tubulointerstitial nephritis;, granular cells = active renal disease; red cells = glomerulonephritis
  • SERUM BIOCHEMISTRY: U&E raised, low eGFR, raised alk phos, raised PTH (if CKD > stage 3)
  • BLOODS: raised phosphate, low Ca2+, low Hb
  • IMMUNOLOGY: auto-antibody screening for SLE, Hep B, C and HIV antigen tests
  • IMAGING: USS to check renal size, CT to detect stones, retroperitoneal fibrosis and other causes of urinary obstruction
45
Q

How is CKD managed?

limiting progression, symptom control and renal replacement therapy

A
  • Aims to slow deterioration of kidney function, reduce cardiovascular risk and treat complications
  • Identify and treat reversible causes (relieve obstruction, stop nephrotoxic drugs, stop smoking, tight glucose control in diabetes)
  • LIMIT PROGRESSION AND COMPLICATIONS: BP (ACEi, ARB, diuretic, CCB), bone disease (treat raised PTH, restrict diet, vitamin D, phosphate binders), CVD (statins and aspirin)
  • SYMPTOM CONTROL: anaemia (iron/ folate/ folic acid), acidosis (sodium bicarbonate), oedema (furosemide)
  • RENAL REPLACEMENT THERAPY: hemofiltration, haemodialysis, peritoneal dialysis, transplant
46
Q

What is the aetiology of benign prostate hyperplasia?

A

Increased in size of prostate without a malignancy

47
Q

What is the pathophysiology of benign prostate hyperplasia?

A
  • Benign nodular or diffuse proliferation of musculofibrous and glandular layers of the prostate
  • Inner (transitional) zone enlarges in contrast to peripheral layer expansion
  • As prostate gets bigger, it may squeeze or partly block the urethra
48
Q

What are the risk factors of benign prostate hyperplasia?

A
  • Increasing age

- Castration is protective (testosterone is a requirement for BPH)

49
Q

What is the clinical presentation of benign prostate hyperplasia?

A
  • LUTS (nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria, bladder stones, delay in initiation of micturition, incomplete emptying of bladder)
  • Enlarged bladder on abdominal exam
  • Acute urinary retention
  • Can cause anuria (no urination) if BPH causes bladder to become occluded
  • NO erection problems
50
Q

What are the differential diagnoses of benign prostate hyperplasia?

A
  • Bladder tumour
  • Bladder stones
  • Trauma
  • Prostate cancer/ chronic prostatitis
  • UTI
51
Q

How is benign prostate hyperplasia diagnosed?

A
  • DRE – enlarged but smooth prostate
  • Serum electrolytes and renal USS to exclude renal damage from obstruction
  • TRUS – prostate size
  • PSA may be raised in large BPH
  • Biopsy and endoscopy
  • Mid-stream urine sample to exclude infection
  • Flow rates and residual volume
  • Frequency volume chart
52
Q

How is benign prostate hyperplasia managed?

A
  • Watchful waiting if minimal symptoms
  • Lifestyle advice: no caffeine or alcohol, relax when voiding, void twice in a row
  • Drugs in mild disease or pre-surgery: alpha-1 antagonists e.g. oral tamsulosin (first line), 5-alpha-reductase inhibitor e.g. oral finasteride
  • Surgery for large prostate or no response to other treatments: transurethral resection of prostate (TURP) or transurethral incision of prostate (TUIP)
53
Q

What is the aetiology of pyelonephritis?

A
  • Infection of renal parenchyma and soft tissues of renal pelvis and upper ureter
  • Majority caused by uropathogenic E.coli
  • Others = klebsiella, enterococcus, proteus, staphylococcus
54
Q

What is the pathophysiology of pyelonephritis?

A
  • Infection due to bacteria from patient’s bowel flora

- More common via ascending transurethral route (can also be via bloodstream or lymphatics)

55
Q

What are the risk factors of pyelonephritis?

A
  • Structural renal abnormalities
  • Calculi (stones)
  • Catheterisation
  • Pregnancy
  • Diabetes
  • Immunocompromised
56
Q

What is the clinical presentation of pyelonephritis?

A
  • Loin pain, fever, pyuria
  • May have a severe headache
  • Rigors
  • Significant bacteriuria
  • Malaise, nausea, vomiting
  • Oliguria if causes AKI
57
Q

What are the differential diagnoses of pyelonephritis?

A
  • Diverticulitis
  • Abdominal aortic aneurysm
  • Kidney stones
  • Cystitis
  • Prostatitis
58
Q

How is pyelonephritis diagnosed?

A
  • Tender loin on examination
  • Urine dipstick: nitrates, leucocyte elastase, foul-smelling, protein
  • Midstream urine microscopy, culture and sensitivity
  • FBC – elevated WCC
  • CRP and ESR raised in acute infection
  • Urgent USS for calculi, obstruction, abnormal anatomy
59
Q

How is pyelonephritis managed?

A
  • Rest
  • Cranberry juice and lots of water
  • Analgesia
  • Antibiotics (oral ciprofloxacillin or oral co-amoxiclav) – is severe then IV gentamicin or IV co-amoxiclav
  • Surgery to drain abscesses or relieve calculi that are causing infection
60
Q

What is the aetiology of cystitis?

A
  • Urinary infection of the bladder

- Most commonly caused by E. coli

61
Q

What are the risk factors of cystitis?

A
  • Urinary obstruction resulting in urinary stasis
  • Previous damage to bladder epithelium
  • Bladder stones
  • Poor bladder emptying
62
Q

What is the clinical presentation of cystitis?

A
  • Dysuria
  • Frequency
  • Urgency
  • Suprapubic pain
  • Haematuria
  • Offensive smelling/ cloudy urine
  • Abdominal/ loin tenderness
63
Q

How is cystitis diagnosed?

A
  • Microscopy and sensitivity of sterile mid-stream urine

- Dipstick urinalysis (positive blood, nitrates and leucocytes)

64
Q

How is cystitis managed?

A

Antibiotics

  • First line: trimethoprim or cefalexin
  • Second line: ciprofloxacin or co-amoxiclav
65
Q

What is the aetiology of acute prostatitis?

A
  • Streptococcus faecalis
  • E.coli
  • Chlamydia
66
Q

What is the aetiology of chronic prostatitis?

bacterial and non-bacterial

A

BACTERIAL (e.g. streptococcus faecalis, E.coli, chlamydia)

NON-BACTERIAL (e.g. elevated prostatic pressure, pelvic floor myalgia)

67
Q

What are the risk factors of prostatitis?

A
  • STI
  • UTI
  • Indwelling catheter
  • Post-biopsy
  • Increasing age
68
Q

What is the clinical presentation of acute prostatitis?

A
  • Systemically unwell
  • Fever
  • Rigors
  • Malaise
  • Pain on ejaculation
  • Significant voiding LUTS
  • Pelvic pain
69
Q

What is the clinical presentation of chronic prostatitis?

A
  • Acute symptoms for >3m
  • Recurrent UTIs
  • Pelvic pain
70
Q

What are the differential diagnoses of prostatitis?

A
  • Cystitis
  • BPH
  • Calculi
  • Bladder neoplasia
  • Prostatic abscess
71
Q

How is prostatitis diagnosed?

A
  • DRE – tender, hot, tough prostate, hard from calcification
  • Urine dipstick (positive for leucocytes and nitrates)
  • Mid-stream urine microscopy and sensitivity
  • Blood cultures
  • STI screen
  • TRUSS
72
Q

How is acute prostatitis managed?

A

IV gentamicin + IV co-amoxiclav or IV tazocin or IV carbapenem

2-4w on a quinolone once well (2nd line trimethorpin)

TRUSS guided abscess drainage if necessary

73
Q

How is chronic prostatitis managed?

A

4-6w quinolone e.g. ciprofloxacin ± alpha blocker

NSAIDs

74
Q

What is the aetiology of urethritis?

A
  • Primarily a sexually acquired disease
  • Chlamydia trachomatis (most common)
  • Neisseria gonorrhoea
  • Trauma, urethral stricture, irritation, urinary calculi
75
Q

What are the risk factors of urethritis?

A
  • Sexually active
  • Unprotected sex
  • Male-with-male sex
  • Male
76
Q

What is the clinical presentation of urethritis?

A
  • May be asymptomatic
  • Dysuria ± discharge, blood or pus
  • Urethral pain
  • Penile discomfort
  • Skin lesions
  • Systemic symptoms
77
Q

What are the differential diagnoses of urethritis?

A
  • Candida balanitis
  • Epididymitis
  • Cystitis
  • Acute prostatitis
  • Urethra; malignancy
78
Q

How is urethritis diagnosed?

A
  • Nucleic acid amplification test (NAAT) – female = self-collected vaginal swab; male = first void volume
  • Microscopy of gram-stained smears of genital secretions
  • Blood cultures
  • Urine dipstick to exclude UTI
  • Urethral smear
79
Q

How is urethritis managed?

A
  • Patient education
  • Contact tracing

CHLAMYDIA:

  • Oral azithromycin state or 1w oral doxycycline
  • Test for other STIs

GONORRHOEA:

  • IM ceftriaxone with oral azithromycin
  • Partner notification

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