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Hamzah's GU pathology > Hamzah's GU pathology > Flashcards

Hamzah's GU pathology Flashcards

1
Q

Where do renal stones form?

A

in the collecting duct

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2
Q

What is the lining of renal tubules?

A

cuboidal epithelium

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3
Q

Common sites of renal stones

A
  • pelviureteric junction
  • pelvic brim
  • vesicoureteric junction
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4
Q

Types of renal stones

A
  • calcium oxalate - 75%
  • magnesium ammonium phosphate (triple phosphate) - 15%
  • urate - 5%
  • brushite, cysteine - 1%
  • mixed - 1%
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5
Q

Aetiology of renal stones

A
  • stone formation occurs when normally soluble material supersaturates the urine and begins to form crystals
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6
Q

Inhibitors of crystal formation

A

magnesium, citrate

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7
Q

Epidemiology of kidney stones

A
  • common - lifetime incidence = 15%
  • peak age = 20-40yrs
  • M:F = 3:1
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8
Q

Risk factors for kidney stones

A
  • high protein diet
  • dehydration
  • FH
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9
Q

Pathophysiology of calcium stones

A
  • hypercalciuria - increased urinary calcium excretion
  • hyperparathyroidism –> hypercalcaemia
  • excessive dietary calcium
  • excessive bone resorption
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10
Q

Pathophysiology of uric acid stones

A
  • hyperuricemia
  • people who have ileostomies are at risk because of the loss of bicarbonate from GI secretions –> acidic urine –> reduced solubility of uric acid
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11
Q

UTI and renal stones

A
  • proteus produces urease

- urea –> NH3 (via urease) –> precipitation of triple phosphate stones

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12
Q

Clinical presentation of renal stones

A
  • renal colic - excruciating pain in loin to groin, nausea and vomiting, cannot lie still
  • renal obstruction = felt in loin between 12th rib and lateral edge of lumbar muscles
  • obstruction of mid-ureter = mimics appendicitis/diverticulitis - iliac fossa pain, fever, nausea, pyrexia
  • obstruction in bladder or urethra = pelvic pain, dysuria, interrupted flow, strangury
  • UTI - pyelonephritis - loin to groin pain, fever, rigors, nausea and vomiting
  • haematuria, proteinuria, pyuria, anuria (failure of kidneys to produce urine)
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13
Q

Differential diagnosis of renal stones

A
  • bleeding in kidney (e.g. after renal biopsy) –> clots can obstruct ureter
  • ectopic pregnancy
  • leaking AAA
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14
Q

Diagnostic tests for renal stones

A
  • FBC - U&Es, calcium, phosphate, glucose, bicarbonate, urate
  • urine dipstick
  • MSU - MC&S
  • 24hr urine - calcium, oxalate, urate, citrate, sodium, creatinine, stone biochemistry
  • imaging - non-contrast CT, KUB XR, IV urogram
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15
Q

Treatment of renal stones

A
  • analgesics - diclofenac (NSAID)
  • IV fluids
  • abx if infection - cefuroxime/gentamicin
  • stones <5mm - pass spontaneously –> increase fluid intake
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16
Q

Treatment of >5mm renal stones

A
  • medical expulsion oral nifedipine (CCB) or alpha blockers (tamsulosin)
  • extracorporeal shockwave lithotripsy (ESWL) - US waves shatter stone (SE=renal injury)
  • Percutaneous nephrolithotomy (PCNL) - if stone is in kidney, keyhole surgery is done to remove large stones
  • ureteroscopy with basket
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17
Q

Prevention of renal stones

A
  • drink plenty of fluids
  • normal dietary calcium intake - low calcium levels lead to oxalate excretion
  • thiazide diuretics decrease calcium excretion
  • allopurinol - decreases urate stones
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18
Q

What is acute kidney injury?

A

significant deterioration in renal function occurring over hours or days, measured by serum creatinine or urine output.

can be reversible

serum urea rises due to reduced renal excretion of nitrogenous waste products

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19
Q

Diagnostic criteria for AKI

A
  • rise in creatinine >26micromol/litre in 48hrs
  • rise in creatinine >1.5x baseline
  • urine output <0.5ml/kg/hr for 6 continuous hours
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20
Q

Epidemiology of AKI

A

common - affects up to 18% of hospital patients and approximately 50% of ICU patients

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21
Q

Risk factors for AKI

A

> 75, male gender, pre-existing CKD, cardiac failure, sepsis, drugs, chronic liver disease, PVD

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22
Q

Common causes of kidney failure

A
  • sepsis
  • major surgery
  • cardiogenic shock
  • hypovolaemia
  • diuretics, ACEi, lithium, methotrexate, gentamicin
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23
Q

Aetiology of AKI

A

divided according to site

  • pre-renal
  • renal
  • post-renal
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24
Q

Pre-renal AKI causes

A
  • hypovolaemia –> hypoperfusion of kidneys
  • low cardiac output –> hypotension
  • renal artery stenosis (atherosclerosis)
  • renal vasoconstriction (NSAIDs, ARBs, ACEi)
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25
Q

Renal causes of AKI

A
  • tubular - acute tubular necrosis
  • glomerular - autoimmune - SLE, glomerulonephritis, drugs, infection
  • interstitial - drugs, infiltration-lymphoma
  • vascular - vasculitis, malignant hypertension, thrombus
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26
Q

Post-renal causes of AKI

A
  • within renal tract = stone, renal tract malignancy, stricture, clot
  • extrinsic compression = benign prostate hyperplasia, pelvic malignancy
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27
Q

Pathophysiology of AKI

A

sudden damage to kidneys causes an abrupt deterioration in renal function

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28
Q

Clinical presentation of AKI

A

Nausea, low urine output, shortness of breath, oedema, fatigue, chest pain (hyperkalaemia)

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29
Q

Diagnostic test for AKI

A
  • assess volume status - BP, JVP, skin turgor, capillary refill time, urine output
  • check plasma potassium levels and ECG (life threatening hyperkalemia = tall tented T waves, increased PR interval)
  • urine dipstick - send for MC&S, look for blood and protein
  • Bloods - FBC, U&Es, LFTs, ESR, CRP, renal immunology - autoantibodies (ANCA, ANA)
  • imaging - renal US, KUB CT
  • renal biopsy
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30
Q

Treatment of AKI

A
  • stop nephrotic drugs - NSAIDs, ACEi, gentamicin, amphotericin
  • treat underlying cause
  • pre-renal = fluids, abx for sepsis, ICU referral
  • intra-renal = refer to ICU if glomerular/tubulointerstitial pathology
  • post-renal = catheterise, treat obstruction - stents
  • renal replacement therapy - haemodialysis, haemofiltration
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31
Q

Management of complications in AKI

A
  • hyperkalemia - IV calcium gluconate, IV insulin and glucose
  • pulmonary oedema
  • uraemia
  • acidaemia
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32
Q

What is chronic kidney disease?

A
  • = progressive and irreversible decline in renal function for longer than 3 months, classified into 5 stages
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33
Q

Aetiology of CKD

A
  • T2 DM
  • glomerulonephritis - IgA nephropathy, systemic disorders - SLE, RA
  • hypertension –> arteries thicken –> stenosis –> ischaemia of nephrons
  • inherited - Polycystic kidney disease
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34
Q

Risk factors for CKD

A
  • diabetes
  • hypertension
  • heart disease
  • smoking
  • obesity
  • > 65
  • FH
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35
Q

Pathophysiology of CKD

A
  • glomerular hyperfiltration –> glomerular hypertension –> glomerular injury –> glomerulosclerosis –> tubulointerstitial fibrosis
  • transforming growth factor (TGF-beta) is a key mediator in stimulating renal scarring
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36
Q

Clinical presentation of CKD

A
  • generally asymptomatic until late
  • nausea and loss of appetite
  • anaemia - decreased Epo production
  • renal osteodystrophy - reduced vit D activation by 1,alpha hydroxylase
  • encephalopathy - uraemia –> asterixis, coma, death
  • pericarditis - uraemia
  • CVD - MI, stroke, HF
  • bleeding
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37
Q

Differential diagnosis of CKD

A

AKI

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38
Q

Diagnostic tests in CKD

A
  • bloods - low Hb, high urea and creatinine, low calcium, high phosphate, ESR
  • urine - dipstick, MC&S, albumin:creatinine ratio
  • imaging - US - kidneys=small in CKD
  • Biopsy
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39
Q

Treatment of CKD

A
  • treat underlying cause
  • stop smoking
  • limit progression and stop complications
  • target BP <130/80 - ACEi/ARBs
  • calcium supplements
  • statins and aspirin
  • potassium and phosphate binders

Symptom control

  • anaemia - iron/folate supplements, recombinant human Epo
  • acidosis - sodium-bicarbonate replacement
  • oedema - loop diuretics (furosemide), sodium restriction
  • cramps - gabapentin

Prepare for dialysis

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40
Q

Acute upper tract obstruction

A
  • loin to groin pain
  • loin tenderness
  • enlarged kidney
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41
Q

Chronic upper tract obstruction

A
  • flank pain
  • renal failure
  • superimposed infection
  • polyuria - due to impaired urinary concentration
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42
Q

Acute lower tract obstrcution

A
  • severe suprapublic pain
  • poor stram, hesitancy, terminal dribbling
  • distended palpable bladder, dull to percussion
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43
Q

Chronic lower tract obstruction

A
  • urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence
  • distended palpable bladder, may have enlarged prostate
  • complications = UTI, urinary retention
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44
Q

Treatment of upper tract obstruction

A
  • nephrostomy or ureteric stent - alpha blockers reduce stent-related pain
  • pyeloplasty to widen PUJ
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45
Q

Treatment of lower tract obstruction

A
  • urethral or suprapubic catheter

- treat underlying cause

46
Q

What is erectile dysfunction?

A

When an individual is unable to develop or maintain an erection

47
Q

Main organic causes of impotence

A

alcohol, smoking, diabetes

48
Q

Other causes of impotence

A
  • psychological - stress, depression, performance anxiety
  • drugs
  • endocrine - hypothyroidism, hypogonadism, high prolactin
  • atheroma
  • hypertension
  • pelvic surgery
49
Q

Drugs that cause impotence

A
  • digoxin, beta-blockers, diuretics, antidepressants, finasteride, narcotics
50
Q

Physiology of an erection

A

PNS –> Ach –> muscarinic receptors –> activates NO synthase –> NO produced –> corpus cavernosum expands

51
Q

Diagnosis of impotence

A
  • sexual experience of patient
  • careful questioning
  • bloods - testosterone, glucose, prolactin
  • Duplex US - evaluate blood flow and atherosclerosis
52
Q

Treatment of impotence

A
  • treat causes
  • counselling
  • oral phosphodiesterase (PDE5) inhibitors increase cGMP –> NO (sildenafil, SE=headaches, flushing, dyspepsia, stuffy nose)
  • vaccum aids
  • intracavernosal injections
  • prosthetic implants
53
Q

Most common renal cancer

A
  • renal cell carcinoma = malignant epithelial tumour arising from the PCT
54
Q

Risk factors for RCC

A

smoking, obesity, hypertension

55
Q

Pathogenesis of RCC

A
  • linked to chromosome 3 mutations
  • leads to a mutation in IGF-1 –> dysregulated cell growth and upregulation of VEGF –> angiogenesis and tumour formation
  • tumours can invade renal vein –> IVC –> high risk of metastasis to lungs and bone
56
Q

Clinical presentation of RCC

A
  • haematuria, loin pain, abdo mass
  • anorexia, fever, malaise, weight loss, PUO (pyrexia of unknown origin)
  • varicocele - tumour of left kidney can onstruct left renal vein –> impeded venous drainage of left testis
  • paraneoplastic syndrome - high Epo–>polycythaemia, high renin–>hypertension
57
Q

Diagnostic tests in RCC

A
  • high BP
  • polycythemia
  • urine - haematuria, cytology - look for malignant cells
  • imaging - US/CT/MRI/CXR
58
Q

Treatment of RCC

A
  • RCC is resistant to radiotherapy and chemotherapy
  • radical nephrectomy
  • biological therapies - angiogenesis-targeting agents –> sorafenib, sunitinib
59
Q

Mayo prognostic score (SSIGN) for RCC

A
  • stage
  • size
  • grade
  • necrosis
60
Q

Most common bladder cancer

A

transitional cell carcinomas - 80% are confined to bladder mucosa, 20% penetrate the detrusor muscle

61
Q

Grading of transitional cell carcinomas

A
  • grade 1 = differentiated
  • grade 2 = intermediate
  • grade 3 = poorly differentiated
62
Q

Risk factors for transitional cell carcinomas

A
  • smoking
  • aromatic amines - rubber industry
  • chronic cystitis
  • schistosomiasis
  • pelvic irradiation
63
Q

Epidemiology of transitional cell carcinomas

A

men are more at risk

64
Q

Clinical presentation of transitional cell carcinomas

A
  • painless haematuria
  • recurrent UTIs
  • voiding irritability
65
Q

Diagnostic tests for transitional cell carcinomas

A
  • cystoscopy and biopsy = gold standard for diagnosis
  • urine - MC&S and cytology
  • CT urogram –> staging
  • Bimanual EUA –> assess spread
  • MRI - may show involved lymph nodes
66
Q

Treatment of local transitional cell carcinomas

A
  • diathermy via transurethral cystoscopy
  • TURBT
  • intravesical chemotherapy
67
Q

Treatment of advanced transitional cell carcinomas (deep muscle involved)

A
  • radical cystectomy
  • radiotherapy can preserve bladder
  • post-op chemotherapy - cisplatin
68
Q

Treatment of transitional cell carcinomas that have invaded beyond the detrusor muscle

A
  • palliative chemotherapy/radiotherapy

- chronic catheterisation

69
Q

What is prostate cancer?

A

adenocarcinoma (malignant epithelial tumour) arising in the prostate

70
Q

Spread of prostate cancer

A
  • local - seminal vesicles, bladder, rectum
  • lymph
  • haematogenous - sclerotic bone lesions
71
Q

Risk factors for prostate cancer

A

FH, advancing age, high testosterone

72
Q

Prognosis and Gleason score in prostate cancer

A
  • histological grade = Gleason score

The 2 most prominent glandular patterns are graded from 1-5. The sum of these 2 grades will range from 2-10

  • 2 = most differentiated
  • 10 = least differentiated - worse outcome
73
Q

Clincal presentation of prostate cancer

A
  • asymptomatic
  • lower back pain
  • LUTS - urgency, frequency, nocturia, poor stream
  • weight loss and bone pain = metastasis
74
Q

Diagnostic tests for prostate cancer

A
  • Needle biopsy = diagnostic. transperineal is better as it can reach anterior lesions of prostate
  • DR exam - hard, irregular prostate
  • raised PSA
  • transrectal USS
  • bone scan - CT/MRI
75
Q

Treatment for prostate cancer

A
  • disease confined to prostate = radical prostatectomy if <70yrs, radical radiotherapy with adjuvant surgery, hormone therapy
  • metastatic disease = hormonal drugs. LHRH agonists - GOSERELIN - suppresses production of androgens. SE=hormone resistance can occur.
  • symptomatic - analgesia, treat hypercalcaemia
76
Q

LUTS storage symtoms

A

frequency, nocturia, urgency

77
Q

LUTS voiding symtoms

A

(mainly affect men)

  • hesitancy, straining, poor stream, incomplete emptying, post micturition dribbling
  • haematuria, dysuria
78
Q

Types of testicular tumours

A
  • seminoma
  • lymphoma
  • mixed germ cell tumour
79
Q

RIsk factors for testicular tumours

A
  • undescended testis
  • infant hernia
  • infertility
80
Q

Epidemiology of testicular tumours

A

most common cancer in young men

81
Q

Clinical presentation of testicular tumours

A
  • painless testis lump
  • found after trauma/infection with hematospermia
  • secondary hydrocele
  • pain
  • dyspnoea - lung mets
  • abdominal mass
82
Q

Staging of testicular tumours

A
  1. no evidence of metastasis
  2. infradiaphragmatic node involvement
  3. supradiaphragmatic node involvement
  4. lung involvement
83
Q

Differential diagnosis of testicular tumours

A
  • epididymal cyst
  • varicocele
  • hydrocele
  • haematocele
84
Q

Diagnostic tests in testicular tumours

A
  • CXR/CT
  • excision biopsy
  • alpha-FP and beta-hCG - markers, monitor treatment
85
Q

Treatment of testicular tumours

A
  • radical orchiectomy (removal of testicles)
  • seminomas - very radiosensitive
  • NSGCT = bleomycin + etoposide + cisplatin
86
Q

What is BPH?

A

enlargement of the prostate gland due to an increase in cell number

87
Q

Aetiology of BPH

A

unknown

88
Q

Largest zone of the prostate gland

A

peripheral zone

89
Q

What is in the central zone of the prostate?

A

ejaculatory ducts which join the prostatic urethra

90
Q

What do the luminal/columnar cells secrete in the prostate?

A

secrete substances into the prostatic fluid like alkaline, nutrients for sperm and PSA (helps liquify sperm after ejaculation)

91
Q

Sperm movement in ejaculation

A

testes –> vas deferens (combines with seminal vesicles) –> ejaculatory ducts –> prostatic urethra –> urethra

92
Q

What cells produce testosterone?

A

Leydig cells in the testicles

93
Q

Where is dihydrotestosterone produced and mechanism of formation?

A
  • produced in the prostate
  • testosterone is converted into dihydrotestosterone
  • enzyme = 5 ALPHA-REDUCTASE
  • 10x more potent than testosterone –> binds to androgen receptors for much longer
94
Q

Pathogenesis of BPH

A
  • 5 alpha reductase activity increases with age –> more dihydrotestosterone –> prostate cells multiply - hyperplasia
  • hyperplastic nodules can form at periurethral zone. This compresses the prostatic urethra –> difficult for urine to pass –> urine builds up in bladder causing bladder dilation –> bladder hypertrophy and stagnation of urine in bladder promotes bacterial growth - UTI
95
Q

Clinical presentation of BPH

A
  • LUTS - post-micturition dribbling, nocturia, frequency, urgency, poor stream, hesitancy, UIT, haematuria
96
Q

Differential diagnosis of BPH

A

prostate carcinoma

97
Q

Diagnostic tests in BPH

A
  • PR exam
  • MSU
  • US - transurethral and biopsy
  • PSA - prostate specific antigen
  • U&Es
98
Q

Lifestyle treatment in BPH

A
  • avoid caffeine and alcohol - controls urgency/nocturia
  • relax when voiding
  • bladder exercises
  • void twice in a row to avoid emptying
99
Q

Pharmacological treatment in BPH

A
  • alpha blockers - tamsulosin - relaxes smooth muscle (SE=depression, dizziness, hypotension)
  • 5alpha-reductase inhibitors - finasteride - decreases dihydrotestosterone production (SE=impotence, low libido)
100
Q

Surgical treatment in BPH

A
  • TURP (transurethral resection of prostate - remove part/all of prostate)
  • TUIP (transurethral incision of prostate)
101
Q

Lower UTIs can cause…

A
  • urethritis (urethra)
  • prostatitis (prostate)
  • cystitis (bladder)
102
Q

Upper UTIs can cause…

A

pyelonephritis

103
Q

Classification of UTIs

A
  • uncomplicated UTI - normal renal tract and function

- complicated UTI - abnormal renal/GU tract, voiding difficulty/obstruction, decreased renal function, virulent organism

104
Q

Epidemiology of UTIs

A
  • extremely common

- approximately 60% of women will have a UTI at some point in their life

105
Q

Pathogens that can cause UTIs

A
  • E.coli = most common

- others = proteus mirabilis, klebsiella pneumonia

106
Q

Pathophysiology of E.coli and UTIs

A
  • E. coli have pili which allows them to bind to galactose-containing receptors on the surface of urothelial cells
  • virulence factors = haemolysin affects the invasion of tissues, K antigen protects the microorganism from neutrophil phagocytosis
107
Q

Risk factors for UTIs

A

female gender, sexual intercourse, exposure to spermicide in females (condoms/diaphragm), pregnancy, menopause (dry vagina), immunosuppression, urinary stones, catheter

108
Q

Clinical presentation of UTIs

A
  • cystitis = frequency, dysuria, urgency, haematuria, suprapubic pain
  • prostatitis = lower backache, pain in rectum, scrotum or penis, swollen/tender prostate on DRE
  • pyelonephritis = classic triad-nausea/vomiting, fever, flank-loin pain. oliguria, rigors
109
Q

Diagnostic tests in UTIs

A
  • symptoms present (or pregnancy) = urine dipstick - >10,000 organisms/ml - diagnostic
  • treat with empirical abx whilst waiting for MC&S of MSU if dipstick shows nitrates or leukocytes
110
Q

Treatment of UTIs

A
  • drink plenty of water
  • abx - amoxicillin, trimethoprim
  • lower UTI = oral abx (3-7 days)
  • upper UTI = IV abx - co-amoxiclav (combination of amoxicillin and potassium clavulanate) then oral abx when fever subsides
111
Q

Prevention of UTIs

A
  • drink plenty of water
  • antibiotic prophylaxis
  • cranberry juice

Hamzah's GU pathology (1 decks)

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