Renal and Urology Flashcards
(112 cards)
1
Q
Define Urinary Tract Infection
A
An infection of the kidneys (upper UTI), bladder, urethra or prostate (prostatitis) (lower UTI). Infectious cystitis (bacteral infection of bladder) is the most common type of UTI.
The presence of a pure growth of > 105 organisms per mL of fresh MSU
2
Q
What is pyelonephritis and which signs and symptoms are suggestive of this?
A
Infection of the kidney that often occurs via bacterial ascent
Costovertebral angle tenderness and fever
3
Q
What is the difference between complicated and uncomplicated UTI?
A
Uncomplicated UTI: normal renal tract and function
Complicated UTI: abnormal renal/genitourinary tract, voiding difficulty/obstruction, reduced renal function, impaired host defences, virulent organism (e.g. S. aureus)
4
Q
Describe the aetiology of urinary tract infection
A
Transurethral ascent of organisms following colonisation of the vagina.
Amplified by factors that promote the introduction of bacteria at the urethral meatus.
Stasis of bladder urine impairs the defence against infection provided by bladder emptying.
Uncomplicated UTI:
Escherichia coli is the most common cause of uncomplicated UTI (70-95% of cases)
Staphylococcus saprophyticus
Enterobacteriaceae eg Klebsiella, enterococci, group B streptococci, Pseudomonas aeruginosa
Atypical organisms that can cause UTI (in immunocompromised individuals):
Klebsiella
Candida albicans
Pseudomonas aeruginosa
5
Q
What are the risk factors of urinary tract infections?
A
Female Sexual activity Spermicide use Pregnancy Post-menopause Family history of UTIs History of recurrent UTIs Presence of a foreign body eg catheterisation Immunosuppression Urinary tract obstruction eg stone, stricture
Insulin-treated diabetes
Recent antibiotics
Poor bladder emptying
Increasing age
6
Q
Summarise the epidemiology of urinary tract infections
A
10% of women over 18 report at least one suspected UTI a year 20-40% of women develop recurrent UTIs VERY COMMON More common in women Rarely cause significant renal damage
7
Q
What are the presenting symptoms of a urinary tract infection?
A
Cystitis: Increased urinary frequency Increased urinary urgency Dysuria Suprapubic pain Haematuria Smelly cloudy urine
Prostatitis: Flu-like symptoms Fever Low back pain/perineal Few urinary symptoms Swollen or tender prostate on PR Urgency Hesitancy Intermittency Post-micturition dribbling Poor Stream
Acute Pyelonephritis: High fever Malaise Vomiting and rigors Back/Flank pain Loin pain and tenderness Oliguria (small amounts of urine - if AKI) Urinary symptoms similar to cystitis Costovertebral angle tenderness
Elderly: Malaise Nocturia Incontinence Confusion
8
Q
What are the signs on physical examination of urinary tract infections?
A
Cystitis: Fever Suprapubic tenderness Bladder distension Foul-smelling urine
Pyelonephritis:
Fever
Loin/flank tenderness
Prostatitis:
Tender, swollen prostate on DRE
9
Q
What are the appropriate investigations for urinary tract infections?
A
Urine dipstick - positive for nitrites and leukocyte esterase, blood, protein
Urine microscopy - confirm organism to allow antibiotic selection - bacteria, WBCs, RBCs
Urine culture and sensitivity - growth of >10⁵ CFU/mL
Ultrasound: Rule out obstruction
Renal USS – exclude structural abnormalities in women with recurrent UTIs, children, men
Bloods: FBC, U&Es (renal function), CRP, blood cultures (systemically unwell/urosepsis risk)
10
Q
What is the management of urinary tract infections?
A
Oral antibiotics: TRIMETHOPRIM or NITROFURANTOIN
Treat for 3-6 days
Men with UTI may need a longer course of antibiotics
Alternative antibiotics: Co-amoxiclav or Cefalexin
Co-trimoxazole
Amoxicillin
Ciprofloxacin
IV gentamicin, cefuroxime or ciprofloxacin in pyelonephritis plus paracetamol
Prevention: High fluid intake Regular micturition (esp. after sex) Cranberry juice Low dose prophylactic antibiotic therapy inrecurrent UTI in recurrent cystitis associated with intercourse
11
Q
What are the possible complications of urinary tract infections?
A
Sepsis Renal and peri-renal abscess Acute kidney injury Emphysematous pyelonephritis - acute necrotising renal infection commonly in immunocompromised older Xanthogranulomatous pyelonephritis Pyelonephritis Hydronephrosis or pyonephrosis Prostatic involvement (e.g. prostatitis)
12
Q
What is the prognosis of urinary tract infections?
A
Very good prognosis
Most resolve with treatment
With appropriate antimicrobial treatment and resolution of symptoms, there is unlikely to be long-term sequelae.
13
Q
Define benign prostatic hyperplasia
A
Slowly progressive nodular hyperplasia of the periurethral/transitional zone of the prostate gland, causing lower urinary tract symptoms due to bladder outlet obstruction (voiding/obstructive & storage symptoms).
14
Q
Summarise the aetiology of benign prostatic hyperplasia
A
Aetiology is unknown
Shifts in age-related hormones may cause androgen/oestrogen imbalances
Risk factors: Age >50 years old Family history Non-Asian race Cigarette smoking Metabolic syndromes
15
Q
Summarise the epidemiology of benign prostatic hyperplasia
A
Common
Affects 82% of men between 71-80 years old
50% of men with BPH will experience symptoms
Prevalence increases with age
More common in the West
More common in Afro-Carribeans
16
Q
What are the presenting symptoms of benign prostatic hyperplasia?
A
Storage symptoms:
Frequency
Urgency
Noturia
Voiding symptoms: Hesitancy Dysuria Weak stream Intermittency Incomplete emptying Post-void dribbling Straining
FUNDHIPS: Frequency Urgency Nocturia Dysuria Hesitancy Incomplete voiding Poor stream Smell/odour
17
Q
What are the symptoms of urinary retention?
A
Acute retention symptoms:
Sudden inability to pass urine
Severe pain
Chronic retention symptoms:
Painless
Frequency: with passage of small volumes of urine
Nocturia is a major feature
18
Q
What are the signs on physical examination of benign prostatic hyperplasia?
A
DRE: the prostate is usually smoothly enlarged with a palpable midline groove
Poor correlation between the size and the severity of the symptoms
Signs of Acute Retention: Suprapubic pain and a distended, palpable bladder
Signs of Chronic Retention: A large distended painless bladder (volume > 1 L) and signs of renal failure.
19
Q
What are the appropriate investigations for benign prostatic hyperplasia?
A
Urinalysis - look for signs of UTI (leukocytes, nitrites, blood)
PSA - may also be raised in prostate cancer and prostatitis
U+Es - check for impaired renal function
Volume charting to record frequency and volume of voiding
International Prostate Symptom Score - score from 0-35
Imaging:
USS - may show mass, urolithiasis or hydronephrosis
CT abdo/pelvis - may show mass, urolithiasis or hydronephrosis
Cystoscopy - may show mass, stone or stricture
Bladder scanning to measure pre- and post-voiding volumes
Transrectal ultrasound scan (TRUS): allows assessment of bladder size and volume
20
Q
What is the management of benign prostatic hyperplasia?
A
Emergency acute urinary retention: catheterisation
Conservative if mild - watchful waiting, limitation of fluids, bladder training focused on timed and complete voiding
Medical:
Alpha-blocker eg terazosin, tamsulosin - relax smooth muscle in prostate and internal urinary sphincter (effective in days)
5-alpha-reductase inhibitor eg finasteride - decrease conversation of testosterone to DHT which reduces prostate volume (effective in months)
PDE5 inhibitors
Anticholinergic therapy
Surgery: TURP or open prostatectomy
21
Q
What are the possible complications of benign prostate hyperplasia?
A
BPH progression UTI Renal insufficiency Bladder stones Haematuria Sexual dysfunction Acute urinary retention Overactive bladder
Complications of TURP
TURP syndrome: seizures or cardiovascular collapse caused by hypervolemia and hyponatraemia due to absorption of glycine irrigation fluid.
22
Q
What is the prognosis of benign prostatic hyperplasia?
A
Mild symptoms are usually well controlled medically
Majority of patients require ongoing therapy
Most patients get significant relief from surgery
2.5% of patients will develop acute urinary retention and another 6% will require invasive therapy over a 5-year period
23
Q
Define chronic kidney disease
A
Chronic renal failure characterised by the presence of kidney damage or decreased kidney function by a eGFR < 60 ml/min/1.73 m² and/or pathological abnormality of the kidney such as microalbuminuria, proteinuria, haematuria for three months or more.
24
Q
Explain the aetiology of chronic kidney disease
A
Most common cause in adults is diabetes - 1/3 of diabetics will develop it
Second most common cause is hypertension
Less frequent causes:
Cystic disorders of the kidney (polycystic kidney disease)
Obstructive uropathy
Glomerular nephrotic and nephritic syndromes
25
What are the risk factors for chronic kidney disease?
```
Diabetes
Hypertension
Age >50
Childhood kidney disease
Smoking
Obesity
Male
Family history of CKD
Autoimmune disease
Long term NSAID use
Black or hispanic ethnicity
```
26
Summarise the epidemiology of chronic kidney disease
Common - 11% of the adult population has CKD
Often not recognised until advanced
Incidence increasing
More common in Black and hispanic patients and those with family history
Those who have had previous AKI are at increased risk
27
What are the presenting symptoms of chronic kidney disease?
Often ASYMPTOMATIC and incidental finding of a routine blood or urine test.
```
Symptoms of Severe CKD:
Swelling in peripheries and/or around eyes (due to oedema)
Muscle cramps
Orthopnoea and/or Dyspnoea (due to pulmonary oedema)
Sexual dysfunction
Fatigue
Nausea and vomiting
Pruritis
Anorexia
```
28
What are the signs on physical examination of chronic kidney disease?
May show signs of underlying disease (e.g. SLE)
May show complications of CKD (e.g. anaemia)
```
Signs of CKD:
Skin pigmentation
Excoriation marks due to pruritis
Pallor
Hypertension
Peripheral oedema
Peripheral vascular disease
Retinopathy
```
29
What are the appropriate investigations for chronic kidney disease?
Serum Creatinine – elevated > 97micromol/L
May be falsely low in conditions of low muscle mass, older or malnourished people and patients with liver failure
Serum Urea: Varies massively depending on hydration status and diet
Urinalysis: Haematuria and/or proteinuria
Serum or urine protein electrophoresis: check for multiple myeloma
Urine microalbumin: microalbuminuria (30-300 mg/day)
Renal ultrasound: Small kidney, presence of obstruction/hydronephrosis
Abdominal x-ray/CT/MRI
Estimation of GFR (more accurate than serum creatinine alone) - <60 mL/minute/1.73 m²
ISOTOPIC GFR: gold standard but expensive
Renal Biopsy Biochemistry
Glucose: check for undiagnosed diabetes and diabetic control
Potassium: raised
Serology:
Antibodies: ANA (SLE), c-ANCA (granulomatosis with polyangiitis – Wegener's) and anti-GBM (Goodpasture's syndrome)
Hepatitis serology
HIV serology
30
Define epididymitis
Inflammation of the epididymis characterised by unilateral scrotal pain and swelling of less than 6 weeks' duration which may be associated with irritative lower urinary tract symptoms, urethral discharge, and fever.
31
Define orchitis
Inflammation of the testes.
60% of epididymitis is associated with orchitis
Most cases of orchitis are associated with epididymitis
32
Explain the aetiology of epididymitis and orchitis
Sexually active men:
Usually caused by sexually transmitted organisms
Chlamydia trachomatis
Neisseria gonorrhoeae
Mycoplasma genitalium
Insertive partner during anal intercourse may develop acute epididymitis from enteric E. coli organisms
Older men (>35 years):
Enteric causative pathogens
Associated with bladder outlet obstruction, recent instrumentation of the urinary tract, or systemic illness.
Enterobacter, Klebsiella
Rare: TB, syphilis
Viral: Mumps
Fungal: Candida if immunocompromised
33
What are the risk factors of epididymitis and orchitis?
```
Diabetes
Vasculitis
Unprotected sexual intercourse
Bladder outflow obstruction - BPH, urethral stricture
Instrumentation of urinary tract
Mumps
Exposure to TB
Amiodarone
```
34
Summarise the epidemiology of epididymitis and orchitis
Most common cause of acute scrotal pain
Can present at any age but most patients are 20-39 years old
Majority of cases in children occur around puberty in early adolescence
35
What are the presenting symptoms of epididymitis and orchitis?
```
Unilateral scrotal pain and swelling of gradual onset
Tender scrotum
Hot, erythematous, swollen hemiscrotum
Frequent and painful micturition
Purulent urethral discharge
```
36
What are the signs on physical examination of epididymitis and orchitis?
Swollen and tender epididymis or testis
Scrotum may be erythematous and oedematous
Pyrexia
Walking will be painful
Eliciting a cremasteric reflex may be painful
37
What are the appropriate investigations for epididymitis and orchitis?
Gram stain of urethral secretions - ≥5 WBC per oil immersion field; presence of intracellular gram-negative diplococci
Urine dip for first-void MC&S - early morning urine sample - ≥10 WBC per high-power field
Nucleic acid amplification test/urethral secretions/first-void urine - test for C. trachomatis, N. gonnorrhoeae and mycoplasma genitalium
Bloods: FBC (elevated WCC), elevated CRP and U&Es Imaging: Increased blood flow on duplex examination
38
What is the management of epididymitis and orchitis?
Due to bacterial infection:
Antibiotics - ceftriaxone + doxycycline (+azithromycin if due to gonnorrhoea), ceftriaxone + a fluoroquinolone if due to enteric organism
Supportive measures - bed rest, analgesia, scrotum elevation, NSAIDs, advice to avoid unprotected sex
If due to TB - anti-tuberculosis antibiotics
Surgical: Exploration of testicles if testicular torsion cannot be excluded clinically. Required if an abscess develops.
39
What are the possible complications of epididymitis and orchitis?
Abscess formation
Testicular ischaemia/infarction
Epididymal obstruction
Chronic pain
Fournier's gangrene (if the infection is left untreated and spreads)
Mumps orchitis could cause testicular atrophy and fertility issues
40
What is Fournier's gangrene?
A life-threatening form of necrotizing fasciitis that affects the genital, perineal, or perianal regions of the body.
41
What is the prognosis of epididymitis and orchitis?
Symptoms usually resolve rapidly following antibiotic therapy
May take up to two months for the swelling to resolve
Inadequately treated infectious epididymitis, particularly sexually transmitted infection, can in rare cases lead to epididymal obstruction or testicular atrophy and subsequent infertility problems.
42
Define glomerulonephritis
An immunologically mediated inflammation of the renal glomeruli. This causes glomerular injury. Inflammatory changes are often in the glomerular capillaries and the glomerular basement membrane (GBM).
It presents with proteinuria, haematuria or both and can cause CKD or progress to kidney failure.
43
Explain the aetiology of glomerulonephritis
Many different types of glomerulonephritis with differing aetiologies
Some types are caused by the deposition of antigen-antibody complexes in the glomeruli. The antibodies which are produced are UKNOWN but may be associated with:
Bacteria - Streptococcus viridans, Staphylococci
Viruses - HBV, HCB, measles, mumps, EBV
Protozoal - Plasmodium malariae, schistosomiasis
Inflammatory/Systemic diseases - SLE, vasculitis, cryoglobulinaemia
Drugs - gold, penicillinamine
Tumour - lung cancer, colorectal cancer, leukaemia
44
What are the risk factors of glomerulonephritis?
```
Group A β-haemolytic Streptococcus
Respiratory/GI infections
Hep B/C
Infective Endocarditis
HIV
SLE
Lung/Colorectal Cancer
Drugs
Systemic vasculitis
Leukaemia
```
45
Summarise the epidemiology of glomerulonephritis?
In the US and Europe, glomerulonephritis is the third commonest cause of end-stage renal disease, after diabetes and hypertension.
Worldwide, glomerulonephritis is the commonest cause of End-Stage Renal Disease.
Accounts for 25% of cases of chronic renal failure
46
What are the presenting symptoms of glomerulonephritis?
```
Haematuria
Oedema
Oliguria (producing abnormally small amounts of urine)
Anorexia
Malaise
Nausea
Weight loss
Fever
Skin rash
Arthralgia
Haemoptysis
Abdominal pain
Sore throat
```
47
What are the signs on physical examination of glomerulonephritis?
```
Hypertension
Skin rash
Oedema
Weight loss
Signs of nephrotic or nephritic syndrome
```
48
What are the appropriate investigations for glomerulonephritis?
Urinalysis: haematuria, proteinuria, dysmorphic RBCs, leukocytes, and RBC casts
Bloods:
FBC: normochromic normocytic anaemia
U&Es + creatinine: increased creatinine indicates severe/advanced disease
LFTs (check albumin): increased liver enzymes in Hep B/C, hypoalbuminaemia
ESR/CRP: elevated if due to vasculitis or normal
Lipid profile: hyperlipidaemia
GFR: normal or low
Urine ACR: If ACR is >220 mg/mmol, patients are classified as having nephrotic-range proteinuria
Urine MC&S, RBC casts
Complement studies: decreased or normal C3 in immune complex diseases
Antibodies: ANA, Anti-dsDNA, ANCA, Anti-GBM antibody, Cryoglobulins
Imaging: Renal tract ultrasound to exclude other pathology (e.g. obstruction)
Renal Biopsy: Cellular proliferation and the number of glomeruli involved. Necessary for diagnosis!!
Investigations for associated conditions (e.g. HBV, HCV and HIV serology)
49
What is nephrotic syndrome?
TRIAD of:
1. Proteinuria > 3.5 g/24 hours (main feature)
2. Low serum albumin < 24 g/L
3. Peripheral Oedema: due to the hypoalbuminaemia
Due to hypoalbuminaemia, the liver tries to compensate and increases production of lipids, causing hyperlipidaemia.
50
What is nephritic syndrome?
TRIAD of
1. Hypertension
2. Proteinuria
3. Haematuria (main feature)
Pores in the podocytes are large enough to allow protein AND red blood cells to pass into the urine.- There may be red cell casts in the urine: indicative of glomerular damage
There may also be low urine output (due to decreased renal function)
51
What are the main differences between nephrotic and nephritic syndrome?
In nephrotic syndrome only protein is passing into the urine, whereas in nephritic syndrome protein and blood are passing into the urine.
52
Define hydrocoele
A collection of serous fluid between the layers of the membrane (tunica vaginalis) that surrounds the testis or along the spermatic cord
53
What are the two types of hydrocoele and how do they differ?
1. Communicating hydrocoele - patent processus vaginalis connects the peritoneum with the tunica vaginalis, which allows peritoneal fluid to flow freely between both structures
2. Non-communicating hydrocoele - processus vaginalis is closed and more fluid is being produced by the tunica vaginalis than is being absorbed
54
Explain the aetiology of hydrocoele
Most paediatric hydrocoeles are congenital (due to patent processus vaginalis) and are resolved within a year of life.
Most adult hydrocoeles are acquired.
```
Non-communicating hydrocoele:
Minor trauma
Infection
Testicular torsion
Epididymitis
Varicocele operation
Testicular tumour
```
Communicating hydrocoele:
Following increased intra-abdominal fluid or pressure (due to shunts, peritoneal dialysis, or ascites) if there is a patent processus vaginalis.
Connective tissue disorders
55
What are the risk factors for hydrocoele?
```
Male
Prematurity
Low birth weight
Infant <6 months of age
Inflammation or injury to the scrotum
Testicular cancer
Connective tissue disorder
Increased intraperitoneal pressure or fluid
Varicocelectomy
Filariasis
```
56
Summarise the epidemiology of hydrocoele
Rare in females
Common in male infants and children
Processus vaginalis usually closes within first year of life so incidence decreases after this
Often associated with indirect inguinal hernia
1-3% of full term infants get a hydrocoele
More prevalent in premature infants and in infants whose testes descend relatively late
Up to 20% of patients develop hydrocoele following varicocelectomy
57
What are the presenting symptoms of hydrocoele?
Scrotal mass
Enlargement of scrotal mass following activity (coughing, straining, crying, raising the arms)
Variation in scrotal mass throughout the day - smaller in the morning and after lying down
Usually asymptomatic
May be pain or urinary symptoms due to the underlying cause
58
What are the signs on physical examination of hydrocoele?
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)
59
What are the appropriate investigations for hydrocoele?
Mainly clinical diagnosis
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 (α-fetoprotein, β-HCG, Lactate dehydrogenase)
60
Define nephrotic syndrome
A triad of proteinuria (>3.5g/24 hours), hypoalbuminaemia (<30g/L) and peripheral oedema.
It can also be associated with hyperlipidaemia and thrombotic disease.
Nephrotic syndrome is not a single disease but a constellation of several symptoms that can be caused by several renal diseases
61
Explain the aetiology of nephrotic syndrome
Nephrotic syndrome is a collection of symptoms that can be caused by various renal disease.
Most common cause in children: minimal change nephropathy which can be primary or secondary
Hodgkin's lymphoma is the most common type of secondary minimal change
Most common cause in adults is focal segmental glomerulosclerosis which is either primary or secondary.
Can be secondary to HIV infection, reflux nephropathy, morbid obesity, chronic glomerular hyperfiltration from a solitary kidney, any cause of extensive nephron loss or to certain drugs
ALL forms of glomerulonephritis can cause nephrotic syndrome
```
Other causes:
Diabetes mellitus (diabetic nephropathy is most common cause in diabetic adults)
Sickle cell disease
Amyloidosis
Malignancies (lung and GI adenocarcinomas)
Drugs (e.g. NSAIDs)
Alport's syndrome
HIV
```
62
What are the main risk factors for nephrotic syndrome?
Obesity
| Family history of renal disease
63
What are primary and secondary causes of nephrotic syndrome?
Primary: minimal change disease (abnormal podocyte function), membranous nephropathy (immune-mediated podocyte damage), focal segmental glomerulosclerosis (podocyte injury/death) and membranoproliferative glomerulonephritis (pathology in glomerular basement membrane)
Secondary: diabetes, lupus nephritis, myeloma, amyloid, pre-eclampsia
64
Summarise the epidemiology of nephrotic syndrome
90% of nephrotic syndrome in CHILDREN is due to minimal change glomerulonephritis
Most common cause of nephrotic syndrome in ADULTS:
Diabetes mellitus
Membranous glomerulonephritis
65
What are the presenting symptoms of nephrotic syndrome?
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
```
Foamy urine
Weight gain
Symptoms of underlying cause (i.e. SLE - rash, arthralgia, photosensitivity)
Symptoms of complications (i.e. loin pain, haematuria)
Systemic symptoms eg joints, skin involvement
66
What are the signs on physical examination of nephrotic syndrome?
Oedema: periorbital, peripheral, genital (generalised pitting oedema)
Ascites: fluid thrill, shifting dullness
Tachycardia
Muehrcke’s line: white banding of nails (due to hypalbuminaemia)
Xanthelasma
Raised JVP
67
What are the appropriate investigations for nephrotic syndrome?
24-hour urine collection (normal <150 mg/day, nephrotic range >3.5 g/day) OR spot urine protein-to-creatinine ratio on a random urine specimen (this closely correlates with a 24-hour urine protein).
Urinalysis with microscopy to check for the presence of cellular casts. Urine should also be sent for urine protein electrophoresis.
```
Serological studies:
Auto-immune screen (ANA, complement, cryoglobulins)
Serum free light chains
Syphilis serology
Hepatitis B and C serology
```
```
Bloods:
FBC
U&Es
LFTs (low albumin)
ESR/CRP
Glucose
Lipid profile (check for secondary hyperlipidaemia)
```
Renal ultrasound
Renal biopsy to determine the type of nephrotic syndrome
Tests to identify the cause:
SLE: ANA, anti-dsDNA antibodies
Infections: Group A β-haemolytic streptococcal infection (ASO titre), HBV infection (serology), Plasmodium malariae (blood film)
Goodpasture's Syndrome: anti-glomerular basement antibodies
Vasculitides: polyangiitis with granulomatosis, microscopic polyarteritis (check ANCA)
68
Define polycystic kidney disease
Part of a heterogeneous group of disorders characterised by renal cysts and numerous systemic and extrarenal manifestations.
There are 2 types: autosomal-dominant PKD and autosomal-recessive PKD.
69
Define autosomal dominant polycystic kidney disease
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.
70
Explain the aetiology of polycystic kidney disease
There are two genes affected in autosomal dominant polycystic kidney disease:
1. PKD1 on chromosome 16 in 85% of cases which codes for polycystin 1
2. PKD2 on chromosome 4 in 15% of cases which codes for polycystin 2
A wild-type copy of the gene causes an inactivating somatic mutation, leading to loss of polycystin function and clonal cyst development. Usually membrane-bound multidomain protein involved in cell-cell and cell-matrix interactions
71
What are the risk factors of polycystic kidney disease?
Family history of autosomal-dominant polycystic kidney disease
Family history of cerebrovascular event
72
Summarise the epidemiology of polycystic kidney disease
MOST COMMON inherited kidney disorder
Responsible for 10% of end-stage renal failure in adults
Occurs worldwide and in all races
End Stage Renal Disease due to Autosomal Dominant Polycystic Kidney Disease is less common among black people than white (due to higher incidence of ESRD from other causes in black people)
Disease more progressive in men than women
Autosomal dominant PKD more common than autosomal recessive
73
What are the presenting symptoms of polycystic kidney disease?
Presentation normally at 30-40 years old
```
Flank pain - due to cyst enlargement/bleeding, stone, clot migration or infection
Haematuria
Headaches
Fever
Chest pain
```
Urinary symptoms:
Dysuria
Urgency
Suprapubic pain
Polycystic kidney disease is associated with berry aneurysms which present as subarachnoid haemorrhage: SUDDEN ONSET, THUNDERCLAP HEADACHE
74
What are the signs on physical examination of polycystic kidney disease?
Hypertension
Palpable enlarged kidneys/abdominal mass
Cardiac murmur: mitral prolapse, mitral regurgitation, aortic regurgitation
Hepatomegaly due to liver cysts (more common in women)
Abdominal distension
Signs of chronic renal failure (at late stage)
Signs of associated AAA
75
What are the appropriate investigations for polycystic kidney disease?
Bloods:
U+Es - normal or elevated
Creatinine - normal or elevated
Fasting lipids - normal or elevated (linked to prognosis)
Urinalysis - bacteriuria if UTI, microscopic haematuria, proteinuria, increased urinary albumin excretion (increased albumin excretion linked to progression to CKD, LVH)
eGFR
Imaging:
Renal USS - sensitivity of detection lower in those <20
If inconclusive, CT abdo/pelvis or MRI abdo/pelvis
Multiple cysts bilaterally in enlarged kidneys
If no family history - 10 cysts needed in each kidney to be diagnostic
If family history:
<30y/o - at least 2 unilateral or bilateral cysts
30 to 59y/o - 2 cysts in each kidney
>60y/o - 4 cysts in each kidney
ECG - check for left ventricular hypertrophy
CT brain - if sudden onset thunderclap headache is presentation
76
Define renal artery stenosis
A narrowing of the renal artery lumen typically due to atherosclerotic disease or fibromuscular dysplasia. It is considered angiographically significant if there is more than a 50% reduction in vessel diameter.
77
Explain the aetiology of renal artery stenosis
1. Atherosclerosis (older patients):
Widespread aortic disease involving the renal artery ostia
2. Fibromuscular dysplasia (younger patients):
Unknown aetiology
Associated with collagen disorders, neurofibromatosis or Takayasu's arteritis
May be associated with micro-aneurysms in the mid and distal renal arteries (resembling a string of beads on angiography)
```
Others:
Post-transplant (site of vascular anastomosis)
Miscellaneous renal arterial disease
Renal artery aneurysm
Accessory renal artery
Takayasu's arteritis
Atheroemboli
Thromboemboli
Williams syndrome
Neurofibromatosis
Spontaneous renal artery dissection
Arteriovenous malformations
Arteriovenous fistulas
Trauma
Abdominal radiotherapy
Retroperitoneal fibrosis
```
78
What are the risk factors of renal artery stenosis?
```
Atherosclerosis
Diabetes mellitus
Dyslipidaemia
Smoking
Female
```
79
Explain the pathophysiology of renal artery stenosis
Renal hypoperfusion due to stenosis stimulates the renin-angiotensin system leading to increased angiotensin II and increased aldosterone.
This leads to increased blood pressure.
The high blood pressure leads to fibrosis, glomerulosclerosis and renal failure.
80
Summarise the epidemiology of renal artery stenosis
Prevalence of 0.2 to 5% in hypertensive patients
Atherosclerotic renal artery stenosis accounts for 90% of RAS
2% of End-Stage Renal Disease is due to ischaemic nephropathy
Fibromuscular dysplasia renal artery stenosis is 2 to 10 times more likely in females and onset is typically before 30.
81
What are the presenting symptoms of renal artery stenosis?
Presence of risk factors eg smoking, dyslipidaemia, diabetes
History of hypertension in individuals < 50 years with no family history of hypertension
Hypertension refractory to treatment
History of unexplained kidney dysfunction
History of multi-vessel coronary artery disease
Accelerated hypertension and renal deterioration on starting ACE inhibitors
History of flash pulmonary oedema
Refractory angina
82
What are the signs on physical examination of renal artery stenosis?
Hypertension
Signs of renal failure in advanced bilateral disease
Renal artery bruit
83
What are the appropriate investigations for renal artery stenosis?
Bloods:
Creatinine - useful to estimate GFR. Normal or high
Potassium - normal or low
Urinalysis - normal unless kidney dysfunction due to diabetic nephropathy or hypertensive glomerulosclerosis
Non-Invasive:
Duplex ultrasound - shows renal arteries and measures flow velocity (>50% reduction in vessel diameter)
Ultrasound measurement of kidney size
CT Angiogram or MR Angiography (risk of contrast nephrotoxicity)
Digital Subtraction Angiography = GOLD STANDARD!!
Renal Scintigraphy: uses radio-agent that is either excreted by glomerular filtration or by the tubules. Addition of an ACE inhibitor causes delayed clearance by the affected kidney (may not be useful in bilateral renal artery stenosis)
84
Why are ACE inhibitors contraindicated in bilateral renal artery stenosis?
Angiotensin II is the major determinant of efferent arteriole vasoconstriction.
Angiotensin II helps to maintain GFR when renal perfusion is low ie in bilateral renal artery stenosis
Blocking the effect of Ang II with ACEi and ARBs can cause acute kidney failure due to inability to maintain GFR.
85
Define testicular torsion
A urological emergency caused by the twisting of the testicle on the spermatic cord leading to constriction of the vascular supply and time-sensitive ischaemia and/or necrosis of testicular tissue.
Twisting or torsion of the spermatic cord results, initially, in venous outflow obstruction from the testicle, progressing to arterial occlusion and testicular infarction if not corrected.
86
Explain the aetiology of testicular torsion
Intra-vaginal testicular torsion:
SPERMATIC CORD TWISTS WITHIN THE TUNICA VAGINALIS
Bell-clapper anatomical deformity (tunica vaginalis joins high on the spermatic cord, leaving the testis free to rotate ie both attachments of tunica are superior to the testicle)
Trauma
Extra-vaginal testicular torsion:
Occurs in neonates
ENTIRE TESTIS AND TUNICA VAGINALIS TWIST IN VERTICAL AXIS ON SPERMATIC CORD
Due to incomplete fixation of the gubernaculum to the scrotal wall allowing free rotation
Unknown aetiology
No anatomical defects indicated
87
What are the risk factors for testicular torsion?
Age under 25 years - 12-18 at greatest risk
Neonate (extra-vaginal testicular torsion)
Bell clapper deformity
Trauma/exercise
Intermittent testicular pain (chronic intermittent torsion)
Undescended testicle
Cold weather
88
Summarise the epidemiology of testicular torsion
Bimodal distribution - extra-vaginal common in neonates, intra-vaginal common in adolescence
Intra-vaginal torsion can affect men of any age
Males <25y/o, incidence is 1 in 4000
Most common cause of acute scrotal pain in 10 to 18y/o
89
What are the presenting symptoms of testicular torsion?
Sudden-onset severe testicular pain/hemiscrotal pain
Nausea and vomiting
No pain relief upon elevation of scrotum
Scrotal swelling
Affected testicle may be higher than the unaffected
Abdominal pain
90
What are the signs on physical examination of testicular torsion?
Testicular tenderness
Scrotal oedema
Scrotal erythema
Reactive hydrocoele formation
Horizontal lie and higher lie of affected testicle
Absence of cremasteric reflex on affected side (stroking up inner thigh causes cremaster muscle contraction resulting in ipsilateral testicle being pulled up)
Fever
Thickened cord
Testicular Appendix: there may be a visible necrotic lesion on transillumination
91
What are the appropriate investigations for testicular torsion?
If history and examination are suggestive of torsion, no further diagnostic tests are needed - immediate treatment should occur to increase chance of testicle viability
Grey scale USS - shows presence of fluid and the whirlpool sign (the swirling appearance of the spermatic cord from torsion as the ultrasound probe scans downwards perpendicular to the spermatic cord)
Power or colour doppler ultrasound - allows visualisation of testicular blood flow (power doppler is more sensitive)
Scintigraphy - decreased uptake of radioactive technetium-99m to the affected testicle in patients with testicular torsion
Tests to rule out other diagnosis (epididymitis or orchitis):
Urinalysis - normal in torsion
FBC - normal in torsion
CRP - normal in torsion
Arterial inflow REDUCED in testicular torsion and INCREASED in epididymo-orchitis
92
What is the appropriate management of testicular torsion?
Immediate urological consultation for emergency scrotal exploration and operative repair within 6 hours of symptom onset
After the testicle is twisted back into place, a bilateral orchidopexy is performed - involves suturing the testicle to the scrotal tissue to prevent recurrence
If the testicle is necrotic, orchidectomy may be performed
Supportive care: analgesia and sedation (morphine sulfate), anti-emetics
If surgery not available within 6 hours, manual de-torsion is attempted
93
What are the possible complications of testicular torsion?
Infarction of testicle/permanent damage to testicle/loss of testicle
Infertility secondary to loss of testicle
Psychological effects following loss of testicle
Cosmetic deformity
Recurrent torsion
Impaired pubertal development
94
Summarise the prognosis of testicular torsion
The longer it takes for diagnosis and repair, greater likelihood of tissue necrosis, decreased tissue viability, decreased spermatogenesis, and possible infertility.
Prosthetic devices can be offered which are usually a saline-filled silicone implant
From the onset of torsion, a testicle may only survive 4-6 hours
Twisted for 10 to 12 hours, ischaemia and irreversible testicle damage are likely.
After 12 hours, necrosis most likely has occurred.
With prompt surgical intervention, most testicles are salvaged
95
Define urinary tract calculi
The presence of crystalline stones (calculi) within the urinary tract
Nephrolithiasis: in the kidney
Ureterolithiasis: in the ureter
Cystolithiasis: in the bladder
96
What are the types of urinary tract calculi?
```
Calcium oxalate: MOST COMMON (65%). Radio-opaque
Calcium phosphate (15%)
Magnesium ammonium phosphate (10-15%)
Urate (radiolucent, 2-5%)
Cysteine (semi-opaque, 1%)
```
97
Explain the aetiology of urinary tract calculi
Most common causes:
Idiopathic
Dehydration
UTI
Change in urinary pH:
Alkaline urine: calcium oxalate, calcium phosphate and Struvite stones
Acidic urine: Cystine and Uric acid stones
Metabolic Causes:
Hypercalciuria: idiopathic, drugs (lithium, thiazides)
Hypercalcaemia: Malignancy, Hyperparathyroidism, Sarcoidosis, Myeloma
Hyperuricaemia: Tumour Lysis Syndrome, High cell turnover states
Hypercystinuria: Autosomal recessive, Defect of renal tubular transport of cystine
Hyperoxaluria: increased intake, increased colonic absorption in patients with small bowel disease/resection
Anatomic abnormalities: Horse shoe kidney
98
What are the risk factors for urinary tract calculi?
```
High protein and/or salt intake
Male
Dehydration
Obesity
Crystalluria
Occupational exposure to dehydration
Warm climate
Family history
Precipitant drugs (i.e. antacids)
```
99
Summarise the epidemiology of urinary tract calculi
Very common
| Nephrolithiasis is 3 times more common in males
100
What are the presenting symptoms of urinary tract calculi?
May be ASYMPTOMATIC
Acute SEVERE loin to groin pain (ureteric stones)
Loin pain (kidney stones)
Dysuria, frequency & penile tip pain (bladder stones)
Urinary retention and bladder distension (urethral stones)
Nausea and vomiting
Haematuria
Testicular pain
Symptoms of UTI and obstruction: i.e. urgency and frequency
101
What are the signs on physical examination of urinary tract calculi?
Loin to lower abdominal tenderness (flank, groin)
NO signs of peritonism
Fever if associated with urinary obstruction: may be a sign of Struvite stones (commonly occur in association with infection)
Signs of systemic sepsis: Tachycardia and Hypotension
102
What are the appropriate investigations for urinary tract calculi?
```
Bloods:
FBC: high WCC if infection
U&Es: check renal function
Calcium: if elevated, may suggest hyperparathyroidism
Urate: if elevated, may suggest gout
TFTs, Albumin, PTH, Vitamin D
```
Urinalysis:
Dipstick: haematuria (COMMON), leucocytes, nitrates
MC&S: WBCs, RBCs or bacteria
24-hour collection: creatinine clearance, calcium, phosphate, oxalate and urate
X-Ray KUB:
Calcium Oxalate stones are radio-Opaque
Cystine Stones are semi-Opaque
Urate Stones are radio-lucent (white)
OTHER:
Intravenous Urography (IVU): Allows visualisation of the kidneys and ureters
Ultrasound: May show hydronephrosis and hydroureter
Non-enhanced Spiral CT: Can also be used to image stones
Isotope Radiography: Used to assess kidney function
103
What is the management of urinary tract calculi?
ACUTE PRESENTATION:
Analgesia (Opiates & NSAIDs )and anti-emetics (Ondansetron)
Ca2+ channel antagonist (i.e. nifedipine) and α-antagonist (i.e. tamsulosin) to decrease ureteric spasm
Rehydration (Oral/IV)
Urine collection to retrieve any stone that has passed (most <5mm pass spontaneously)
Treatment of cause i.e. infection
An obstructed and infected kidney is an EMERGENCY and should be removed ASAP.
REMOVAL OF CALCULI:
Urethroscopy
Extracorporeal Shock-Wave Lithotripsy (ESWL): non-invasive
Percutaneous Nephrolithotomy (PCNL): for large, complex stones
104
What are the possible complications of urinary tract calculi?
Stones:
Infection (PYELONEPHRITIS)
Septicaemia
Urinary retention
Ureteroscopy:
Perforation
False passage
Lithotripsy:
Pain
Haematuria
105
What is the prognosis of urinary tract calculi?
Approximately 20% of calculi will NOT pass spontaneously
However, infection of the calculus could lead to irreversible renal scarring
Recurrence of about 50% over 5 years
106
Define varicocoele
The abnormal dilation of the internal spermatic veins and pampiniform plexus that drain blood from the testis
107
Explain the aetiology of varicocoele
More common on the left (80-90%)
Results from a combination of anatomical factors and due to venous incompetence (similarly to varicose veins)
1. Increased hydrostatic pressure in the left renal vein
2. Incompetent or congenitally absent valves between the left internal spermatic vein and left renal vein
3. Increased reflux from compression of the renal vein between the superior mesenteric artery and the aorta
The left internal spermatic vein inserts into the left renal vein at a right angle and is 8-10cm longer than the right causing increased hydrostatic pressure.
The right internal spermatic vein joins the inferior vena cava at an oblique angle.
Rare: retroperitoneal or abdominal compressive mass.
108
What are the risk factors for varicocoele?
Tall/low BMI
| Family history of varicocoele
109
Summarise the epidemiology of varicocoele
10-15% of men and adolescent boys have a varicocoele
80% of adult varicocoeles are NOT associated with infertility
Increased prevalence in people with infertility
Very rare pre-puberty
90% are on the left side, 10% are bilateral
Isolated right sided varicocoele is VERY rare
110
What are the presenting symptoms of varicocoeles?
```
Painless scrotal mass
Left-sided signs and symptoms
Small testicle (large varicocoeles cause testicular growth arrest)
Scrotum feels like a bag of worms/heavy
Age over 12
Scrotal or groin pain
```
111
What are the signs on physical examination of varicocoeles?
Patient must be STANDING for examination
The side of the scrotum with the varicocele will hang lower
The swelling may reduce when lying down
Valsalva manoeuvre (close mouth, hold nose and try to blow out) whilst standing will increase dilatation
Cough impulse
112
What are the appropriate investigations for varicocoeles?
Mainly a clinical diagnosis from history and examination
Scrotal USS with colour flow Doppler imaging
Semen analysis for infertile men with varicocoele - reduced sperm count, impaired sperm motility
Serum FSH - may be elevated due to impaired spermatogenesis
Serum testosterone - may be low
CT or MRI abdomen/pelvis if varicocoele does not diminish in supine position - exclude abdominal, pelvic or retroperitoneal mass
