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Y3 Renal and Uro > Epididymitis and orchitis - Renal cell carcinoma > Flashcards

Epididymitis and orchitis - Renal cell carcinoma Flashcards

1
Q

Define epididymitis and orchitis

A

• Inflammation of the epididymis (epididymitis) or testes (orchitis)
o 60% of epididymitis is associated with orchitis
o Most cases of orchitis are associated with epididymitis

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2
Q

Infective causes of epidymitis/orchitis (viral, bacterial 6 and age, fungal) and what proportion are idiopathic

A 
•	Most cases are INFECTIVE in origin
•	Bacterial
o	If < 35 yrs: Chlamydia and Gonococcus
o	If > 35 yrs: mainly coliforms (e.g. Enterobacter, Klebsiella)
o	RARE: TB, syphilis 
•	Viral
o	Mumps 
•	Fungal
o	Candida if immunocompromised 
•	1/3 are IDIOPATHIC
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3
Q

RF of epididymitis and orchitis (3)

A

Vasculitis
Unprotected sex
Bladder outflow obstruction

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4
Q

Epidemiology of epididymitis and orchitis

A
  • COMMON
  • Affects all age groups
  • Most commonly: 20-30 yrs
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5
Q

S/s of epididymitis and orchitis (9)

A
  • Painful, swollen and tender testis or epididymis
  • NOTE: sudden onset but less acute onset than testicular torsion
  • Penile discharge – found on primary catch urine sample
  • Dysuria
  • Sweats/fever
  • Swollen and tender epididymis or testis
  • Scrotum may be erythematous and oedematous
  • Pyrexia
  • Walking will be painful
  • Eliciting a cremasteric reflex may be painful
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6
Q

Ix for epididymitis and orchitis (6)

A 
•	Urine
o	Dipstick
o	Early morning urine collections for MC&amp;S
•	Bloods
o	FBC - high WCC
o	High CRP 
o	U&amp;Es
•	Imaging
o	Increased blood flow on duplex examination
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7
Q

Mx of epididymitis and orchitis (medical for different ages, surgical)

A

• Medical
o Antibiotics
If <35 yrs, doxycycline (covers chlamydia). If gonorrhoea suspected, add ceftriaxone. Treat sexual partners!
If >35 yrs (mostly non-STI), associated UTI is common so try ciprofloxacin or ofloxacin
Should use antibiotics for 2-4 weeks
o Also, analgesia + scrotal support
• Surgical
o Exploration of testicles if testicular torsion cannot be excluded clinically
o Required if an abscess develops – abscess drainage

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8
Q

Complications of epididymitis and orchitis (4)

A
  • Pain
  • Abscess
  • Fournier’s gangrene (if the infection is left untreated and spreads)
  • Mumps orchitis could cause testicular atrophy and fertility issues
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9
Q

Prognosis of epididymitis and orchitis

A
  • GOOD if treated

* May take up to 2 months for the swelling to resolve

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10
Q

Define glomerulonephritis

A

• An immunological mediated inflammation of the renal glomeruli and nephrons

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11
Q

Consequences of inflammation in glomerulonephritis

A

• The consequences of inflammation are:
 Damage to glomerulus restricts blood flow compensatory increase in BP
 Damage to filtration mechanism  allows protein and blood to enter urine
 Loss of filtration capacity  acute kidney injury

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12
Q

What 6 general things are glomerulonephritis caused by with and specific examples

A
  • Bacteria (e.g. Streptococcus viridans, Staphylococci)
  • Viruses (e.g. HBV, HCB, measles, mumps, EBV)
  • Protozoal (e.g. Plasmodium malariae, schistosomiasis)
  • Inflammatory/Systemic diseases (e.g. SLE, vasculitis, cryoglobulinaemia)
  • Drugs (e.g. gold, penicillinamine)
  • Tumour (lung cancer, colorectal cancer, leukaemia)
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13
Q

Main complication of glomerulonephritis

A

Accounts for 25% of the cases of chronic renal failure

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14
Q

Difference between nephrotic and nephritic syndrome

A

o Nephrotic syndrome: increased permeability of the glomerulus leading to loss of proteins into the tubules – LOSS OF A LOT OF PROTEIN
o Nephritic syndrome: thin glomerular basement membrane with pores that allow protein and blood into the tubule – LOSS OF A LOT OF BLOOD

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15
Q

S/s of glomerulonephritis

A
  • Haematuria
  • Subcutaneous oedema
  • Polyuria or oliguria
  • History of recent infection
  • Symptoms of uraemia or renal failure (acute and chronic)

• Hypertension
• Proteinuria
• Haematuria (especially in IgA nephropathy)
• Renal failure
• Nephrotic syndrome - consists of a TRIAD of:
o Proteinuria > 3.5 g/24 hrs
o Low serum albumin < 24 g/L
o Oedema
o NOTE: due to the hypoalbuminaema, the liver tries to compensate and increases production of lipids, causing hyperlipidaemia
• Nephritic syndrome (TRIAD: hypertension + proteinuria + haematuria)
o Syndrome comprising of signs of nephritis
o Pores in the podocytes are large enough to allow protein AND red blood cells to pass into the urine
o MAIN FEATURE: Haematuria
• This contrasts with nephrotic syndrome, which is mainly concerned with proteinuria
o There may also be red cell casts in the urine - indicative of glomerular damage
o Other features:
• Proteinuria
• Hypertension
• Low urine output (due to decreased renal function)
o NOTE: in nephrotic syndrome, only PROTEINS are moving into the urine

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16
Q

What are the main s/s of nephrotic syndrome

A

• Nephrotic syndrome - consists of a TRIAD of:
o Proteinuria > 3.5 g/24 hrs
o Low serum albumin < 24 g/L
o Oedema
o NOTE: due to the hypoalbuminaema, the liver tries to compensate and increases production of lipids, causing hyperlipidaemia

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17
Q

What are the main s/s of nephritic syndrome

A

• Nephritic syndrome (TRIAD: hypertension + proteinuria + haematuria)
o Syndrome comprising of signs of nephritis
o Pores in the podocytes are large enough to allow protein AND red blood cells to pass into the urine
o MAIN FEATURE: Haematuria
• This contrasts with nephrotic syndrome, which is mainly concerned with proteinuria
o There may also be red cell casts in the urine - indicative of glomerular damage
o Other features:
• Proteinuria
• Hypertension
• Low urine output (due to decreased renal function)

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18
Q

Which antibodies can be involved in glomerulonephritis (4)

A
  • ANA
  • Anti-dsDNA
  • ANCA
  • Anti-GBM antibody
  • Cryoglobulins
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19
Q

Ix for glomerulonephritis (14)

A 
•	To look for degree of damage and potential cause
•	Bloods
o	FBC
o	U&amp;Es + creatinine 
o	LFTs (check albumin) 
o	Lipid profile 
o	Complement studies
o	Antibodies:
•	ANA
•	Anti-dsDNA 
•	ANCA
•	Anti-GBM antibody
•	Cryoglobulins
•	Urine
o	Microscopy - check for red cell casts 
o	24 hr collection: creatinine clearance and protein 
•	Imaging
o	Renal tract ultrasound to exclude other pathology (e.g. obstruction)
•	Renal Biopsy
o	For microscopy
o	Gives most information and helps decide which sub-set
•	Investigations for associated conditions (e.g. HBV, HCV and HIV serology)
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20
Q

What is a hydrocoele

A

The excessive collection of serous fluid within the tunica vaginalis

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21
Q

What type of fluid accumulates in a hydrocoele

A

Serous

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22
Q

Causes of hydrocoele (6)

A
  • Trauma
  • Infection
  • Testicular torsion
  • Epididymitis
  • Varicocele operation
  • Testicular tumour
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23
Q

RF of hydrocoele (7)

A
  • Male
  • Prematurity and Low Birth Weight
  • Infants < 6 months
  • Increased intraperitoneal fluid or Pressure
  • Inflammation or injury within scrotum
  • Testicular cancer
  • Connective tissue disorders (increased risk communicating hydrocoele)
  • Filariasis (in countries of high prevalence)
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24
Q

Epidemiology of hydrocoele

A
  • Very common in children in the first year of life
  • Incidence in adult men is UNKNOWN (20% develop hydrocoele post varicocelectomy)
  • NOTE: they can occur in females
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25
Q

S/s of hydrocoele

A

o Variation in scrotal mass during the day
o Enlargement in scrotal mass following activity such as coughing, straining
- Usually ASYMPTOMATIC
- Patients may complain of pain or urinary symptoms due to the underlying cause

Scrotal swelling

  • If communication is large it will be SOFT
  • If communication is small it will be TENSE
  • May be restricted to scrotum or extend into the inguinal canal
  • It is possible to get above the swelling
  • Difficult to separate the swelling from the testicle

Transilluminate (due to the fluid).

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26
Q

Ix for hydrocoele

A 
•	Ultrasound: exclude tumour (indicated due to inability to palpate testis or suggestion of underlying pathology i.e. fever, GI symptoms, shadow on transillumination)
•	Urine: dipstick and MSU for infection 
•	Blood: markers of testicular tumours:
o	α-fetoprotein 
o	β-HCG
o	Lactate dehydrogenase
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27
Q

What should you check for if you suspect a hydrocoele

A

Testicular tumours
o α-fetoprotein
o β-HCG
o Lactate dehydrogenase

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28
Q

Markers of testicular tumors (3)

A

o α-fetoprotein
o β-HCG
o Lactate dehydrogenase

29
Q

Mx for hydrocoele

A
  • Observation (< 1 years old and/or no discomfort and/or no infection)
  • Surgery
  • Aspiration
30
Q

Complications of a hydrocoele

A
  • Haematoma
  • Inguinal hernia
  • Testicular injury after surgery
  • Pain in inguinal area radiating to abdomen
  • Lower extremity oedema
  • Testicular atrophy
  • Hydronephrosis
  • Infertility
31
Q

Prognosis of a hydrocoele

A
  • MOST non-communicating hydrocoele cases resolve within the first 2 years of life
  • Low recurrence
32
Q

Nephrotic syndrome is characterised by… (3)

A
  1. Proteinuria (> 3 g/24 hour)
  2. Hypoalbuminaemia (< 30 g/L)
  3. Oedema (hypercholesterolaemia is also a common feature due to liver compensation)
33
Q

Causes of nephrotic syndrome (9)

A 
-	Most common cause in children: minimal change glomerulonephritis 
All forms of glomerulonephritis
-	Diabetes mellitus 
-	Sickle cell disease
-	Amyloidosis 
-	Malignancies (lung and GI adenocarcinomas)
-	Drugs (e.g. NSAIDs)
-	Alport's syndrome
-	HIV
34
Q

Injury to what cell is the main cause of nephrotic syndrome

A

Podocytes

35
Q

Most common causes of nephrotic syndrome in adults (2)

A

o Diabetes mellitus

o Membranous glomerulonephritis

36
Q

S/s of glomerulonephritis (10)

A
  • Family history of atopy (in those with minimal change glomerulonephritis)
  • Family history of renal disease

Swelling (due to hypalbuminaemia) of the:

  • Face – often 1st sign in children
  • Abdomen
  • Limbs
  • Genitalia

Other symptoms:

  • Weight gain
  • Symptoms of underlying cause (i.e. SLE)
  • Symptoms of complications (i.e. loin pain, haematuria)
  • Oedema: periorbital, peripheral, genital
  • Ascites: fluid thrill, shifting dullness
  • Tachycardia
  • Muehrcke’s line: white banding of nails (due to hypalbuminaemia)
  • Xanthelasma
37
Q

Ix for nephrotic syndrome (22)

A 
Bloods
•	FBC 
•	U&amp;Es
•	LFTs (low albumin)
•	ESR/CRP
•	Glucose
•	Lipid profile (check for secondary hyperlipidaemia) 
•	Immunoglobulins 
•	Complement

Tests to identify the cause
• SLE: ANA, anti-dsDNA antibodies
• Infections:
o Group A β-haemolytic streptococcal infection (ASO titre)
o HBV infection (serology)
o Plasmodium malariae (blood film)
• Goodpasture’s Syndrome: anti-glomerular basement antibodies
• Vasculitides: polyangiitis with granulomatosis, microscopic polyarteritis (check ANCA)

Urine
• Urinalysis (check protein and blood)
• MC&S
• 24-hour collection (calculate creatinine clearance and 24 hour protein excretion)

Other
• Renal Ultrasound: Exclude other causes (e.g. reflux nephropathy)
• Renal Biopsy
• Other imaging: Doppler ultrasound, renal angiogram, CT or MRI (if renal vein thrombosis suspected)

38
Q

RF of prostate cancer (5)

A
  • Age > 50
  • Afro-Caribbean
  • Family history
  • Increased dietary fat intake
  • Occupational exposure to cadmium
39
Q

Where do prostate cancers spread usually (4)

A

• Spread may be local (seminal vesicles, bladder, rectum) or via lymph or haematogenously (sclerotic bony lesions)

40
Q

Epidemiology of prostate cancer

A
  • COMMON – commonest cancer in males

* 2nd most common cause of male cancer deaths

41
Q

S/s of prostate cancer (5 then 6 for metastatic disease)

A 
•	Often ASYMPTOMATIC
•	Lower Urinary Tract Obstruction
o	Frequency 
o	Hesitancy 
o	Poor stream
o	Terminal dribbling 
o	Nocturia
•	Metastatic Spread
o	Bone pain 
o	Cord compression
o	Systemic symptoms: malaise, anorexia, weight loss 
o	Paraneoplastic syndromes (e.g. hypercalcaemia)
  • Asymmetrical hard nodular prostate – DRE exam
  • Loss of midline sulcus
42
Q

Signs of prostate cancer in DRE

A
  • Asymmetrical hard nodular prostate – DRE exam

* Loss of midline sulcus

43
Q

Ix for prostate cancer (4)

A
  • First line: PSA (not very specific)
  • Then, DRE
  • Then, transrectal ultrasound-guided biopsy (GOLD STANDARD)
  • Then, isotope bone scan to check for bone metastases
44
Q

What is renal artery stenosis AKA

A

Renovascular disease

45
Q

What is renovascular disease AKA

A

Renal artery stenosis

46
Q

2 causes of renal artery stenosis

A

o Atherosclerosis 85% (older patients) - widespread aortic disease involving the renal artery ostia, often co-exists with IHD, stroke or PVD
o Fibromuscular Dysplasia 10% (younger patients)
• Unknown aetiology
• May be associated with collagen disorders, neurofibromatosis and Takayasu’s arteritis
• May be associated with micro-aneurysms in the mid and distal renal arteries (resembling a string of beads on angiography)

47
Q

• Pathogenesis/Pathophysiology of renal artery stenosis

A

o Renal hypoperfusion (due to the stenosis) stimulates the renin-angiotensin system leading to increased angiotensin II and increased aldosterone
o This leads to increased blood pressure
o The high blood pressure leads to fibrosis, glomerulosclerosis and renal failure

48
Q

Epidemiology of renal artery stenosis

A
  • Prevalence unknown
  • Accounts for 1-5% of all hypertension
  • Fibromuscular dysplasia occurs mainly in women with hypertension < 45 yrs
49
Q

What is contraindicated in renal artery stenosis

A

ACEi

50
Q

S/s of renal artery stenosis (8)

A
  • Hypertension – resistant to treatment
  • Signs of renal failure in advanced bilateral disease
  • Renal artery bruits
  • Abdominal +/- carotid or femoral bruits
  • Weak leg pulses
  • History of hypertension in < 50 yrs
  • Accelerated hypertension and renal deterioration on starting ACE inhibitors – in bilateral RAS
  • History of flash pulmonary oedema
51
Q

Ix for renal artery stenosis (9)

A

• Serum creatinine, potassium, urinanalysis
• Non-Invasive
o Duplex ultrasound
o Ultrasound measurement of kidney size
• CT Angiogram or MR Angiography: risk of contrast nephrotoxicity
• Digital Subtraction renal Angiography = GOLD STANDARD (image) – but done after CT/MR as it is invasive
• Renal Scintigraphy
o Uses radio-agent that is either excreted by glomerular filtration or by the tubules
o Addition of an ACE inhibitor causes delayed clearance by the affected kidney (may not be useful in bilateral renal artery stenosis)

52
Q

Gold standard Ix for renal artery stenosis

A

• Digital Subtraction renal Angiography (but done after CT/MRI due to being invasive)

53
Q

Why are NSAIDs harmful to the kidneys

A

PGs are a major determinant of afferent arteriole vasodilation. PGs can cause afferent arteriole vasoconstriction and reduce GFR.

54
Q

Types of renal cell carcinoma (3)

A

• Renal clear cell carcinoma (80%) - UNKNOWN CAUSE
• Papillary carcinoma (10%) - UNKNOWN CAUSE
• Transitional cell carcinoma (10%)
o NOTE: these occur at the renal pelvis

55
Q

RF of renal cell carcinoma (9)

A
  • Smoking (most established modifiable risk factor)
  • Family history of renal cell cancer
  • Polycystic Kidney Disease
  • Chronic Dialysis
  • Male Sex
  • Hypertension
  • Obesity

Associated with certain inherited conditions:

  • von Hippel-Lindau disease (headaches, dizziness, limb weakness, increased BP)
  • Tuberous sclerosis (rare genetic condition causing growth of benign tumours)
56
Q

Associated conditions of renal cell carcinoma (2)

A
  • von Hippel-Lindau disease (headaches, dizziness, limb weakness, increased BP)
  • Tuberous sclerosis (rare genetic condition causing growth of benign tumours)
57
Q

Age of renal cell carcinoma

A

40-60

58
Q

S/s of renal cell carcinoma (12 with a triad)

A 
o	Asymptomatic in 90%
o	Triad of Symptoms:
•	Haematuria
•	Flank pain
•	Abdominal mass
•	25% have metastases at presentation
•	Transitional Cell Carcinoma
o	Presents EARLIER with haematuria
•	Systemic Signs of Malignancy
o	Weight loss
o	Malaise 
o	Paraneoplastic syndromes (e.g. fever, hypercalcaemia, polycythaemia)
  • Palpable renal mass
  • Hypertension
  • Plethora
  • Anaemia
  • A left-sided tumour can obstruct the left testicular vein as it joins the left renal vein, and cause a left-sided varicocoele
59
Q

How can a varicocele be caused be renal cell carcinoma

A

• A left-sided tumour can obstruct the left testicular vein as it joins the left renal vein, and cause a left-sided varicocoele

60
Q

Ix for renal cell carcinoma (10)

A 
•	Urinalysis
o	Haematuria
o	Cytology
•	Bloods
o	FBC – polycythaemia from EPO secretion
o	U&amp;Es
o	ALP – bony mets
o	Calcium
o	LFTs
o	High ESR (in 75%)
•	Abdominal Ultrasound
o	Best first-line investigation 
o	Can distinguish between solid masses and cystic structures 
•	CT/MRI
o	Useful for staging
•	Staging system: Robson Staging
•	CXR: cannon ball metastases
61
Q

DDx of renal cell carcinoma (3)

A
  1. Benign Renal Cyst
  2. Ureteric Cancer
  3. Bladder Cancer
62
Q

Define PCKD

A
  • Autosomal dominant inherited disorder characterised by the development of multiple renal cysts that gradually expand and replace normal kidney substance, variably associated with extrarenal (liver and cardiovascular) abnormalities
  • You can also get autosomal recessive polycystic kidney disease – very rare
63
Q

Which genes and chromosomes are involved in PCKD (2)

A
  • 85% caused by mutations in PKD1 on chromosome 16 (membrane-bound multidomain protein involved in cell-cell and cell-matrix interactions)
  • 15% caused by mutations of PKD2 on chromosome 4
64
Q

Pathophysiology of PCKD

A
  • Proliferative/hyperplastic abnormality of the tubular epithelium
  • Early on, the cysts are connected to the tubules from which they arise and the fluid content is glomerular filtrate
  • When cyst diameter > 2 mm, they detach from the tubule and the fluid content is derived from secretion of the lining epithelium
  • With time, the cysts enlarge and cause progressive damage to adjacent functioning nephrons
65
Q

Extrarenal manifestations of PCKD (6)

A

liver cysts, intra-cranial aneurysm  SAH, mitral valve prolapse, ovarian cysts, diverticular disease

66
Q

RF of PCKD (2)

A
  • Family history of autosomal-dominant PKD

- Family history of cerebrovascular event

67
Q

Epidemiology of PCKD

A
  • MOST COMMON inherited kidney disorder (20% have no family history)
  • Responsible for 10% of end-stage renal failure in adults
    30-40 years old
68
Q

S/s of PCKD (9)

A
  • May be asymptomatic
  • Flank Pain - may result from cyst enlargement/bleeding, stone, blood clot migration, infection
  • Haematuria
  • Hypertension
  • Associated with berry aneurysms and may present with subarachnoid haemorrhage
  • Abdominal distension
  • Enlarged cystic kidneys
  • Palpable liver
  • Signs of chronic renal failure (at late stage)
  • Signs of associated AAA or aortic valve disease (MURMURS)
69
Q

Ix for PCKD (4)

A

• US – first line
o Will show multiple cysts bilaterally in enlarged kidneys
o Liver cysts may also be seen
o If US unclear  CT
• Genetic testing for PKD1 is difficult
• Genetic testing for some PKD2 mutations is available
• MRI for SAH

Y3 Renal and Uro (3 decks)

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