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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
S/s of hydrocoele
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).
26
Ix for hydrocoele
``` • 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 ```
27
What should you check for if you suspect a hydrocoele
Testicular tumours o α-fetoprotein o β-HCG o Lactate dehydrogenase
28
Markers of testicular tumors (3)
o α-fetoprotein o β-HCG o Lactate dehydrogenase
29
Mx for hydrocoele
- Observation (< 1 years old and/or no discomfort and/or no infection) - Surgery - Aspiration
30
Complications of a hydrocoele
* Haematoma * Inguinal hernia * Testicular injury after surgery * Pain in inguinal area radiating to abdomen * Lower extremity oedema * Testicular atrophy * Hydronephrosis * Infertility
31
Prognosis of a hydrocoele
- MOST non-communicating hydrocoele cases resolve within the first 2 years of life - Low recurrence
32
Nephrotic syndrome is characterised by... (3)
1. Proteinuria (> 3 g/24 hour) 2. Hypoalbuminaemia (< 30 g/L) 3. Oedema (hypercholesterolaemia is also a common feature due to liver compensation)
33
Causes of nephrotic syndrome (9)
``` - 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
Injury to what cell is the main cause of nephrotic syndrome
Podocytes
35
Most common causes of nephrotic syndrome in adults (2)
o Diabetes mellitus | o Membranous glomerulonephritis
36
S/s of glomerulonephritis (10)
- 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
Ix for nephrotic syndrome (22)
``` Bloods • FBC • U&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
RF of prostate cancer (5)
- Age > 50 - Afro-Caribbean - Family history - Increased dietary fat intake - Occupational exposure to cadmium
39
Where do prostate cancers spread usually (4)
• Spread may be local (seminal vesicles, bladder, rectum) or via lymph or haematogenously (sclerotic bony lesions)
40
Epidemiology of prostate cancer
* COMMON – commonest cancer in males | * 2nd most common cause of male cancer deaths
41
S/s of prostate cancer (5 then 6 for metastatic disease)
``` • 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
Signs of prostate cancer in DRE
* Asymmetrical hard nodular prostate – DRE exam | * Loss of midline sulcus
43
Ix for prostate cancer (4)
* 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
What is renal artery stenosis AKA
Renovascular disease
45
What is renovascular disease AKA
Renal artery stenosis
46
2 causes of renal artery stenosis
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
• Pathogenesis/Pathophysiology of renal artery stenosis
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
Epidemiology of renal artery stenosis
* Prevalence unknown * Accounts for 1-5% of all hypertension * Fibromuscular dysplasia occurs mainly in women with hypertension < 45 yrs
49
What is contraindicated in renal artery stenosis
ACEi
50
S/s of renal artery stenosis (8)
* 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
Ix for renal artery stenosis (9)
• 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
Gold standard Ix for renal artery stenosis
• Digital Subtraction renal Angiography (but done after CT/MRI due to being invasive)
53
Why are NSAIDs harmful to the kidneys
PGs are a major determinant of afferent arteriole vasodilation. PGs can cause afferent arteriole vasoconstriction and reduce GFR.
54
Types of renal cell carcinoma (3)
• 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
RF of renal cell carcinoma (9)
- 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
Associated conditions of renal cell carcinoma (2)
- von Hippel-Lindau disease (headaches, dizziness, limb weakness, increased BP) - Tuberous sclerosis (rare genetic condition causing growth of benign tumours)
57
Age of renal cell carcinoma
40-60
58
S/s of renal cell carcinoma (12 with a triad)
``` 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
How can a varicocele be caused be renal cell carcinoma
• A left-sided tumour can obstruct the left testicular vein as it joins the left renal vein, and cause a left-sided varicocoele
60
Ix for renal cell carcinoma (10)
``` • Urinalysis o Haematuria o Cytology • Bloods o FBC – polycythaemia from EPO secretion o U&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
DDx of renal cell carcinoma (3)
1. Benign Renal Cyst 2. Ureteric Cancer 3. Bladder Cancer
62
Define PCKD
* 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
Which genes and chromosomes are involved in PCKD (2)
- 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
Pathophysiology of PCKD
- 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
Extrarenal manifestations of PCKD (6)
liver cysts, intra-cranial aneurysm  SAH, mitral valve prolapse, ovarian cysts, diverticular disease
66
RF of PCKD (2)
- Family history of autosomal-dominant PKD | - Family history of cerebrovascular event
67
Epidemiology of PCKD
- 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
S/s of PCKD (9)
* 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
Ix for PCKD (4)
• 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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