GU Flashcards
1
Q
Kidney function?
A
Filter or secrete waste/excess substances
- Retain albumin and circulating cells
- Reabsorb glucose, amino acids and bicarbonates
- Control BP, fluid status and electrolytes
- Activates 25-hydroxy vitamin D (by hydroxylating it to form 1,25 dihydroxy
vitamin D)
- Synthesis erythropoietin
2
Q
GFR and eGFR??
A
The volume of fluid filtered from the glomeruli into Bowman’s space per unit
time (minutes)
- Normally this is 120ml/min = 7.2L/h, 170L/day
- Each kidney receives 20% of cardiac output
- eGFR predicts creatinine generation (produced by muscles and ONLY
ELIMINATED by the kidneys) from age, gender and race - Requires a steady state
3
Q
what happens in proximal convoluted tubule?
A
Sugars, amino acid, POTASSIUM and bicarbonate get reabsorbed here
- Also absorbs the MAIN PORTION (70%) of Na+ and water follows
Vulnerable to ischaemic injury resulting in acute tubular necrosis
4
Q
fanconi syndrome?
A
Rare
• Proximal tubular insult resulting in:
- Glycosuria (glucose in urine)
Acidosis with failure of urine acidification
- Phosphate wasting resulting in rickets/osteomalacia
- Aminoaciduria (amino acid in urine)
or can be caused by Wilsons and TENOFOVIR
5
Q
what happens in loop on henle?
A
Reabsorbs 25% Na+ here and water follows
- Sodium potassium chloride (Na2KCl) transporters are more active in the
ascending loop
- Loop diuretics work here most, since 25% Na+ filtered here, so water
follows if can block here then can have a large effect
6
Q
distal convoluted tubule, what happens here?
A
5% Na+ reabsorbed here and water follows
- Thiazide diuretics work here
7
Q
what happens at collecting duct?
A
Does salt handling - by this point, most of the salt has been reabsorbed
- Tightly regulated by aldosterone (aldosterone increase the transcription of
eNac channels which absorb Na+ in exchange for K+)
- Secrete K+ and H+ into the urine
- Water handling is also done here and water is absorbed via aquaporin 2
channels (regulated by vasopressin)
8
Q
renal potassium control?
A
- K+ is freely filtered and mostly reabsorbed in the proximal tubule/loop of
henle - Distal tubule secretion determines renal excretion
- Governed by:
• Distal delivery of Na+
• Aldosterone - Insulin and catecholamines drive cellular K+ uptake, buffering acute
changes
9
Q
k+ modifying renal medications
A
K+ modifying renal medication:
• Cause hypokalaemia:
- Loop diuretics
- Thiazide diuretics
• Cause hyperkalaemia:
- Spironolactone (aldosterone antagonist)
- Amiloride (acts on eNac channels)
- ACE inhibitors
- Angiotensin receptor blockers (ARB)
- Trimethoprim (acts on eNac channels but milder)
10
Q
diuretics?
A
Diuretics are NOT NEPHROTOXIC but hypovolaemia (which they can cause
e.g. loop & thiazide diuretics) IS
- In advanced kidney disease you require huge amounts of diuretics to do the
work
- Thiazide and loop diuretics are EXTREMELY POWERFUL & EFFECTIVE
TOGETHER resulting in profound diuresis
11
Q
EPO?
A
Erythropoietin is hormone that produces haemoglobin, it is produced in
response to tissue hypoxia
- In advanced kidney disease and anaemia, erythropoietin will be given to
help increase O2 transport
12
Q
vit d in kidnye?
A
Kidneys do vitamin D hydroxylation:
• It takes 25-hydroxy vitamin D and hydroxylates it to form 1,25-dihydroxy
vitamin D (calcitriol) - this is the active form of vitamin D
- In kidney failure the kidney cannot hydroxylate and thus there is a drop in
Ca2+
13
Q
calictriol actions
A
Increases Ca2+ and phosphate absorption from the gut
• Increases phosphate absorption to a lesser extent
• Suppresses parathyroid hormone (PTH)
• Deficiency results in secondary hyperparathyroidism:
Low vitamin D results in low Ca2+ and phosphate resulting in
increased PTH which causes Ca2+ and phosphate leeching out of
the bones
- PTH also acts on osteoclasts by increasing their activity and thus
increasing their turnover resulting in reduced bone quality
14
Q
upper urinary tract and lower urinarytract?
A
upper; kidney and ureters
lower; bladder, prostate gland, urethra
15
Q
what happens during voiding?
A
Pontine micturition centre stimulates excitatory control to detrusor
nucleus and inhibits Onuf’s nucleus
• Signal is transmitted from spinal root S3,4,5 via the parasympathetic
nervous system and this results in contraction of detrusor muscles and
relaxation of the urethra
16
Q
what happens during storage phase of urination?
A
Pontine storage centre stimulates and sends inhibitory signals to
detrusor muscles and excitatory signals to Onuf’s nucleus
• Signal is transmitted from spinal root T10, L1 & 2 via the sympathetic
nervous system and this results in the relaxation of the bladder and
contraction of the urethral sphincter
17
Q
men v women bladder?
A
Men have a greater voiding pressure due to them having a longer urethra
• More likely to develop retention
- Women have a shorter urethra with lower resistance and thus higher flow
rates
• More likely to develop incontinence
18
Q
renal stones?
A
• Renal stones (calculi) consist of crystal aggregates, stones form in collecting
ducts and may be deposited anywhere from the renal pelvis to the urethra
19
Q
renal stones epidemiology?
A
Peak age is between 20-40 yrs
M>F
Most stones are composed of calcium oxalate and phosphate
20
Q
risk factors and aetiology of renal stone?
A
Anatomical abnormalities that predispose to stone formation e.g. duplex,
obstruction or trauma
- Chemical composition of urine that favours stone crystallisation
- Dehydration resulting in a concentrated urine - seen particularly in those
working in hot climate
- Infection
- Hypercalcaemia, hyperoxaluria, hypercalciuria, hyperuricaemia
- Primary renal disease e.g. polycystic kidneys or renal tubular acidosis
- Drugs e.g. diuretics, antacids, acetazolamide, corticosteroids, aspirin,
allopurinol, vitamin C & D
- Diet e.g. chocolate, tea, strawberries, rhubarb - all increase oxalate levels
- Gout
- Family history
21
Q
renal sones pathophysiology - crystals?
A
Stones form because solute concentrations exceed saturation, often in the
context of a trigger that starts crystallisation
- Renal stone/calculi form from crystals in SUPERSATURATED URINE:
• Calcium oxalate are the most common stones (60-65%)
• Calcium phosphate stones are uncommon (10%)
- Stones vary in size and may be single or multiple
- They may be located within the renal parenchyma or within the collecting
system
- Stones regularly cause obstruction, leading to hydronephrosis; a
combination of obstruction and dilation of renal pelvis that often causes
lasting damage to the kidney
22
Q
renal stones pathophysiology - calcium stones?
A
Hypercalciuria (increased Ca2+ in urine) - causes:
- Hyperparathyroidism resulting in hypercalcaemia
- Excessive dietary intake of Ca2+
- Idiopathic hypercalciuria - increased absorption in gut
- Primary renal disease such as polycystic kidneys or medullary
sponge kidney
• Hyperoxaluria (increased oxalate in urine) - causes:
- High dietary intake of oxalate rich food e.g. spinach, rhubarb,
chocolate and tea
- Low dietary Ca2+ resulting in decreased binding of oxalate (by
Ca2+) so increase oxalate absorption and urinary excretion
- Increased intestinal resorption due to GI disease e.g. Crohn’s
23
Q
renal stones pathophysiology, uric acid?
A
Associated with hyperuricaemia with/without gout
• Dehydration
• Patients with ileostomies are at particular risk, both from dehydration
and from bicarbonate loss from GI secretion resulting in the production of an acidic urine (uric acid is more soluble in alkaline than acidic) thereby
stimulating stone formation
24
Q
renal stones pathophysiology infection?
A
Mixed infective stones are composed of magnesium ammonium
phosphate as well as calcium
• These are often large
• Usually due to UTI with organism such as Proteus mirabilis that
hydrolyse urea forming ammonium hydroxide
• The increased ammonium ions and the alkalinity both favour stone
formation
25
clinical presentation of renal stones?
- most are asymptomatic
- renal colic - pain from loin to groin
- dysuria
- recurrent UTI
- haematuria
26
investigations for renal stones?
KUBXR - Kidney Ureter Bladder X-ray:
• FIRST LINE INVESTIGATION
NCCT-KUB - Non-contrast Computerised Tomography:
• GOLD STANDARD
27
treatment for renal stones?
- Strong analgesic for renal colic e.g. IV DICLOFENAC
- Antibiotics if infection e.g. IV CEFUROXIME or IV GENTAMICIN:
- antiemetics
- Medical expulsive therapy:
• Stones larger than 5mm with pain and not resolving
• ORAL NIFEDIPINE or alpha blocker e.g. ORAL TAMSULOSIN can
promote expulsion and reduce analgesia requirements
- If still not passing then:
• Extracorporeal shockwave lithotripsy (ESWL) - ultrasound fragments
stone
• Endoscopy (uteroscopy) with YAG - laser for larger stones
• Percutaneous nephrolithotomy (PCNL) - keyhole surgery to remove
stones that are large, multiple or complex
28
AKI?
An abrupt (over hours to days) sustained rise in serum urea and creatinine
due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte
and acid-base homeostasis - it is usually but not always reversible or self-
limiting
29
criteria for diagnosing AKI?
- Rise in creatinine > 26μmol/L in 48hrs
• Rise in creatinine > 1.5 x baseline (best figure in last 3 months)
• Urine output < 0.5mL/kg/h for more than 6 consecutive hours
30
epidemiology of AKI?
- common in elderly
| - people with hypotension, diarrhoea, urinary retention, sepsis, heart failure
31
causes of AKI?
```
pre renal (most common)
- hypo perfusion due to hypovolemia or sepsis or medications
```
intrinsic renal
- renal parenchyma damage due to acute tubular necrosis (NSAIDs, uric acid crystals) or vascular issues (SLE, thrombosis) or glomerular or intersistial (cancer)
post renal
- obstruction at ureter, bladder or prostate due to clots, malignancy, BPH
32
clinical presentation of AKI?
- palpable bladder and kidney
- oliguria
- arrthymia
- high urea
- SOB
- oedema
- thirst
33
investigations of AKI?
- urine dipstick
- FBC
- midstream specimen of urine
- ultrasound
- CT-KUB
- ECG
- renal biopsy
34
AKI treatment
Treat underlying cause:
• Pre-renal:
- Correct volume depletion with fluids
- Treat sepsis with antibiotics
• Intrinsic renal:
- Refer early to nephrology if concern over tubulointerstitial or
glomerular pathology
• Post-renal:
- Catheterise and consider CT of renal tract (CTKUB)
- If signs of obstruction and hydronephrosis then think cystoscopy
and retrograde stents or nephrostomy insertion - this buys time to
allows treatment of cause of obstruction e.g. stone or mass
- stop nephrotoxic drugs
- CALCIUM GLUTONATE or INSULIN for hyperkalaemia
- acidosis with SODIUM BICARB
35
indications for dialysis?
- Symptomatic uraemia including pericarditis or tamponade
- Hyperkalaemia not controlled by conservative measures
- Pulmonary oedema thats unresponsive to diuretics
- Severe acids
- High potassium
- Tall T waves, low flat p waves, broad QRS or arrhythmias on ECG
- Metabolic acidosis
- Fluid overload that is resistant to diuretics
36
glomerular diseases?
Glomerulonephritis is a broad term that refers to a group of parenchymal kidney
diseases that all result in the inflammation of the glomeruli and nephrons
37
acute nephritic syndrome; acute glomerulonephritis?
Haematuria - visible or non-visible (red cell casts seen on microscopy)
- Proteinuria (usually < 2g in 24hrs)
- Hypertension and oedema (periorbital, leg, or sacral)-
38
causes of acute glomerulonephritis?
IgA nephropathy:
• COMMONEST CAUSE of nephritic syndrome in the developed world
- treatment -> BP control
Post-streptococcal infection e.g. STREPTOCOCCUS PYOGENES:
- 2 weeks after tonsillitis
- treatment ANTIBIOTICS
- infective endocarditis
- SLE
- systemic sclerosis
- ANCA vasculitis
- good pastures disease; Antibodies against glomerular basement membrane
39
clinical presentation of glomerulonephritis?
- haematuria
- proteinuria
- hypertension
40
investigations of glomerulonephritis?
- Measure eGFR, proteinuria, serum urea & electrolytes and albumin - to
determine current status and monitor progress
- Culture - swab from throat or infected skin
- Urine dipstick to detect proteinuria and haematuria
- Renal biopsy if necessary
41
nephrotic syndorme?
Proteinuria > 3.5g/24 hours
- Hypoalbuniaemia
- Oedema
- Severe hyperlipidaemia is often present:
- Liver goes into overdrive due to albumin loss and other protein loss which
increases risk of blood clots and produces raised cholesterol
42
epidemiology of nephrotic syndrome?
- diabetes secondary cause
| - minimal change disease primary cause
43
aetiology of nephrotic syndrome?
PRIMARY
- minimal change disease is most common n children
- membranous neuropathy where there is asymptomatic proteinuria caused by drugs, autoimmune or infection is common in adults
SECONDARY
- diabetes
- amyloid
- SLE
44
pathophysiology of nephrotic syndrome?
Injury to podocyte appears to be the main cause of proteinuria
- Podocytes wrap around the glomerular capillaries and maintain the
filtration barrier - preventing large molecular weight proteins from entering
the urine
- Damage to podocyte foot processes or loss of podocytes can cause heavy
protein loss
45
clinical presentation of nephrotic syndrome?
```
Normal-mild increase in BP
- Proteinuria > 3.5g/day
- Normal-mild decrease in GFR
- Hypoalbuniaemia
- Pitting oedema of ankles, genital, abdominal wall and sometimes face
(periorbital)
- Frothy urine
```
46
investigations of nephrotic syndrome?
Establish cause - usually via renal biopsy
- Urine dipstick shows very high protein
- Serum albumin is low
- BP is usually normal or mildly increased
- Renal function is usually normal or mildly impaired
47
complications of nephrotic syndome/
Susceptibility to infection:
• Such as cellulitis, Streptococcus infections and spontaneous bacterial
peritonitis
• Due to low serum IgG, decreased complement activity and reduced T
cell function due in part to loss of immunoglobulin in urine and also to
immunosuppressive treatment
Thromboembolism:
• E.g. DVT, PE, renal vein thrombosis
• Hypercoaguable state due to increased clotting factors (produced by
liver due to low albumin since liver goes into overdrive) and platelets
abnormalities
Hyperlipidaemia:
• Increased cholesterol and triglycerides due to hepatic lipoprotein
synthesis in response to low oncotic pressure due to low albumin
48
treatment for nephrotic syndrome?
Reduce oedema:
• Loop diuretics e.g. IV FUROSEMIDE - IV since gut oedema may prevent
oral absorption
• Thiazide diuretics e.g. IV BENDROFLUMETHIAZIDE
• Fluid and salt restriction while giving diuretics
Reduce proteinuria:
• ACE inhibitor e.g. RAMIPRIL
• Angiotensin receptor blocker e.g. CANDESARTAN
• Eat normal rather than high protein diet
- Reduce risk of complications:
• Prophylactic anticoagulation with WARFARIN, especially when albumin
is low (<20g/l)
• Reduce cholesterol with statins e.g. SIMVASTATIN
• Treat infections promptly and vaccinate
49
minimal change disease?
Disease of the kidney that can cause nephrotic syndrome
50
epidemiology of minimal change disease?
Commonest cause of nephrotic syndrome in children
| - Occurs most commonly in BOYS under the age of 5
51
risk factors and aetiology of minimal change syndrome?
```
Can be idiopathic
- Atopy is present in 30% of cases and allergic reactions can trigger nephrotic
syndrome
- Drugs: NSAIDs, lithium
- Hodgkin's
```
52
pathophysiology of minimal change syndrome?
- Glomeruli appear normal on light microscopy, but on electron microscopy,
FUSION of the FOOT PROCESSES of the PODOCYTES is seen, consistent
with a disrupted podocyte actin cytoskeleton
- Immature differentiating CD35 stem cells appear to be responsible for the
pathogenesis
53
clinical presentation of minimal change disease?
Proteinuria
- Oedema, predominantly around the face
- Fatigue
- Frothy urine
54
minimal change syndrome investigations and treatment?
Biopsy:
• Normal under light microscopy
• Electron microscopy shows FUSED PODOCYTE FOOT PROCESSES
treatment
High dose corticosteroids e.g. PREDNISOLONE - can reverse proteinuria in
95% cases - however the majority relapse
55
CKD?
CKD is longstanding, usually progressive, impairment in renal function
(haematuria, proteinuria or anatomical abnormality) for more than 3 months
• Defined as a GFR < 60mL/min/1.73 m2 for more than 3 months with/without
evidence of kidney damage (haematuria, proteinuria or anatomical abnormality)
56
epidemiology of CKD?
- increasing age
| - F>M
57
aetiology of CKD?
Diabetes mellitus - Type II > Type 1
- Hypertension
- Atherosclerotic renal vascular disease
- Polycystic kidney disease
- Tuberous sclerosis
- Primary glomerulonephritides e.g. IgA nephropathy
- SLE
- Amyloidosis
- Hypertensive nephrosclerosis (common in black africans)
- Small and medium-sized vessel vasculitis
- Family history of stage 5 CKD or hereditary kidney disease e.g. polycystic
kidney disease
- Hypercalcaemia
- Neoplasma
- Myeloma
58
pathophysiology of CKD?
CKD tends to progress to end-stage kidney disease (ESRF), although the
rate of progression may be slow
- Speed of decline tends to depend on the underlying nephropathy and on
blood pressure control
- Each kidney has roughly a million nephrons
- In CKD, where many nephrons have failed, and scarred, the burden of
filtration falls to fewer functioning nephrons
- Functioning (remnant) nephrons experience increased flow per nephron
(hyperfiltration), as blood flow has not changed, and adapt with glomerular
hypertrophy and reduced arteriolar resistance
- Increased flow, increased pressure and increased shear stress set in
motion a VICIOUS CYCLE of raised intraglomerular capillary pressure and
strain, which accelerates remnant nephron failure
- This increased flow and strain may be detected as new/increasing
proteinuria
59
clinical presentation of CKD?
- early stages asymptomatic as kidney has a lot of reserves
- malaise
- anorexia
- itching
- polyuria
- pulmonary oedema
60
complications of CKD?
Anaemia - normochromic normocytic anaemia:
• Due to reduced erythropoietin production by diseased kidney
- Bone disease:
• Bone pain
- Renal osteodystrophy - osteomalacia, osteoporosis,
hyperparathyroidism
Neurological:
• Occurs in almost all patients with severe CKD
• Autonomic dysfunction presents as postural hypotension and
disturbed GI motility
Cardiovascular disease:
• Highest mortality in CKD is from CVD particularly MI, cardiac failure,
sudden cardiac death and stroke
Skin disease:
• Pruritus due to nitrogenous waste products of urea - may be scratch
marks
61
investigations for CKD?
ECG for high potassium signs
- Urinalysis:
• Haematuria - indicates glomerulonephritis
- urine microscopy
Bloods:
• Raised phosphate
• Low Ca2+
• Hb low - normochromic normocytic anaemia
Immunology:
• Auto-antibody screening for SLE, scleroderma and Goodpastures
• Hep B, C, HIV and streptococcal antigen tests
- Imaging:
• Ultrasound to check renal size and exclude hydronephrosis
(obstruction & dilation of renal pelvis):
- In CKD kidneys tend to be small
62
treatment of CKD?
```
- Identify & treat reversible causes:
• Relieve obstruction
• Stop nephrotoxic drugs
• Stop smoking and achieve healthy weight to deal with cardiovascular
risk
• Tight glucose control in diabetes
```
BP
- target <130/80 -> RAMIPRIL
bone disease
- CALCITRIOL
CVD
- SIMVASTATIN
- ASPIRIN
63
renal cystic disease?
Solitary or multiple renal cysts are common,
especially with advancing age; 50% of those over 50
have one or more such cysts
• These cysts are often asymptomatic and are found
incidentally on ultrasound examination
64
types of kidney cysts?
Simple cysts - most common form - benign
- Polycystic when lot of them can be bad -
- Hydronephrosis is when ureter blocked
and kidney dilates and gets bigger
- Dysplasia – when not formed properly
- Medullary sponge – dilation of collecting ducts
65
ADPKD?
Multiple cysts develop, gradually and progressively, throughout the kidney
eventually resulting in renal enlargement and kidney tissue destruction
66
epidemiology of ADPKD?
COMMONEST INHERITED KIDNEY DISEASE
- Autosomal dominant inheritance with high penetrance
- Usually presents in adulthood (20-30)
- M>F
67
aetiology of ADPKD?
- Mutations in PKD1 (85%) gene on chromosome 16
| - Mutations in PKD2 (15%) gene on chromosome 4
68
pathophysiology of ADPKD?
PKD1 encodes polycystin 1 which is involved in cell-cell and/or cell-matrix
interactions - regulates tubular and vascular development in kidneys
- PKD2 encodes polycystin 2 which functions as a calcium ion channel
- The polycystin complex occurs in cilia that are responsible for sensing flow
in the tubule
- Disruption of the polycystin pathway results in reduced cytoplasmic Ca2+,
which, in principal cells of the collecting duct, causes defective ciliary
signalling and disorientated cell division resulting in cyst formation
- Progressive loss of renal function is usually attributed to mechanical
compression, apoptosis of the healthy tissue and reactive fibrosis
- Rate of renal function decline is dependent on the growth and size of cysts;
patients with rapidly growing cysts on MRI lose renal function more rapidly
69
clinical presentation of ADPDK?
Can be clinically silent for many years, so family screening is essential
- loin pain
- haematurnia
- renal colic
70
investigations of ADPKD?
Family history of ADPKD, ESRF, hypertension
- BP may be raised
- Ultrasound
* exclude ADPKD if >40 <2 cysts
71
treatment of ADPKD?
No treatment shown to slow disease progression
- Blood pressure control with ACE-inhibitor e.g. RAMIPRIL
- Treat stones and give analgesia
- Laparoscopic removal of cysts to help with pain/nephrectomy (remove
entire kidney)
- renal replacement therapy
72
ARPKD, epidemiology?
- rarer
- recessive
- infants
73
aetiology of ARPKD?
PKHD1 mutation on long arm (q) of chromosome 6
74
clinical presentation of ARPKD?
```
Variable
- Many present in infancy with multiple renal cysts and congenital hepatic
fibrosis
- Enlarged polycystic kidneys
- 30% develop kidney failure
```
75
investigations of ARPKD?
Diagnosed antenatally or neonatally
- Ultrasound - to see cysts
- CT & MRI to monitor liver disease
- Genetic testing
76
treatment of ARPKD?
Currently no treatment available
- Genetic counselling for family members
- Laparoscopic removal of cysts to help with pain/nephrectomy (remove
entire kidney)
- Blood pressure control with ACE-inhibitor e.g. RAMIPRIL
- Treat stones and give analgesia
- Renal replacement therapy for ESRF
77
epididymal cyst?
Smooth, extratesticular, spherical cyst in the head of the epididymis
78
epididymal cyst, epidemiology
Usually develop around the age of 40
79
pathophysiology of epididymal cysts?
Contain clear and milky (spermatocele) fluid
| - Lie above and behind the testis
80
clinical presentation of epididymal cysts?
Normally present having noticed a lump
- Often are multiple and may be bilateral
- Small cysts may remain undetected and asymptomatic
- Once they get large then may be painful
- Well defined and will transluminate since fluid-filled
- Testis is palpable quite separately from the cyst (unlike hydrocele where the
testis is palpable within the fluid filled swelling)
81
investigations and treatment of epididymal cyst?
```
Diagnosis:
- Scrotal ultrasound
• Treatment:
- Usually not necessary
- If painful and symptomatic then surgical excision
```
82
hydrocele?
Abnormal collection of fluid within the tunica vaginalis
83
aetiology of hydrocele?
Primary hydrocele:
• More common and larger
• Usually in younger men
• Associated with a patent processus vaginalis,
which typically resolves during the 1st year of
life
```
- Secondary hydrocele:
• Rarer and present in older boys and men
• Secondary to:
- Testis tumour
- Trauma
- Infection
- TB
- Testicular torsion
- Generalised oedema
```
84
pathophysiology of hydrocele ?
Overproduction of fluid in the tune vaginalis (simple hydrocele)
- Processus vaginalis fails to close, allowing peritoneal fluid to communicate
freely with the scrotal portion (communicating hydrocele)
85
clinical presentation of hydrocele?
Scrotal enlargement with a non-tender, smooth, cystic swelling
Pain is not a feature unless the hydrocele is infected
- Testis are usually palpable but may be difficult to palpate in large hydrocele
- Lied anterior to and below the testis and will transluminate
86
investigations of hydrocele?
Ultrasound
- Serum alpha-fetoprotein and human chorionic gonadotrophin to help
exclude malignant teratomas or other germ cell tumours
87
treatment of hydrocele?
- Resolve spontaneously
- Many of infancy resolve by 2 yrs
- Therapeutic aspiration or surgical removal
88
varicocele?
Abnormal dilation of the testicular veins in the pampiniform venomous
plexus, caused by venous reflux
89
aetiology of varicocele?
```
More common on the left
- Angle at which the left testicular vein
enters the left renal vein
- Increased reflux from compression of
renal vein
- incidence with increasing age
```
90
clinical presentation, varicocele?
Often visible as distended scrtoal blood vessels that feel like ‘a bag of
worms’
- Patient may complain of a dull ache or scrotal heaviness
- Scrotum hangs lower on the side of the varicocele
91
investigations and treatment of varicocele?
Diagnosis:
- Venography
- Colour doppler ultrasound (see blood flow)
• Treatment:
- Surgery if there is pain, infertility or testicular atrophy
92
testicular torsion?
Torsion (twisting) of the spermatic cord resulting in occlusion of the testicular
blood vessels - which can rapidly lead to ischaemia and infarct and thus the
potential loss of the testis (GERM CELLS are the MOST SUSCEPTIBLE CELL
LINE TO ISCHAEMIA)
93
epidemiology of testicular torsion?
Common UROLOGICAL EMERGENCY among
adolescent boys and young men
- Typically occurs in neonates or post-pubertal
boys but can occur in males of all ages - most
common at 11-30yrs
- LEFT SIDE is more commonly affected than
right
94
aetiology of testicular torsion?
Underlying congenital malformation - belt-clapper deformity - where the
testis is not fixed to the scrotum completely, allowing for free movement
leading to twisting
95
clinical presentation of testicular torsion
Any boy presenting with abdominal pain - the testes should be checked
- SUDDEN onset of pain in one testis - makes walking uncomfortable
- Pain often comes on during sport or physical activity
- Pain in abdomen, nausea and vomiting are common
- Inflammation of one testis - it is very tender, hot and swollen
- Testis may lie high and transversely
- With intermittent torsion the pain may have passed on presentation - but if it
was severe and the lie is horizontal then prophylactic fixing may be wise
96
investigations of testicualr torsion?
Doppler ultrasound may demonstrate lack of blood flow to testis
- Urinalysis to exclude infection and epididymis
- DO NOT DELAY SURGICAL EXPLORATION
97
treatment for testicualr torsion?
Surgery - expose and untwist testis - 6 hour window to save testis
- Orchidectomy (removal of testis) and bilateral fixation
98
```
BPE
BPH
BOO
hydronephrosis
obstructive uropathy
supravesical obstruction
intravesical obstruction
```
BPE:
• Benign prostatic enlargement - this is a CLINICAL DIAGNOSIS
- BPH:
• Benign prostatic hyperplasia - this is a HISTOLOGICAL DIAGNOSIS
- BOO:
• Bladder outflow obstruction - this is a URODYNAMIC DIAGNOSIS
- Hydronephrosis:
• Dilation of the renal pelvis of the kidney - leading to damage
- Obstructive uropathy:
• Functional or anatomical obstruction of urine flow at any level of the
urinary tract
- Supravesical obstruction:
• Above the level of bladder
- Infravesical obstruction:
• Below the level of bladder
99
PSA?
PSA is a glycoprotein that is expressed by normal and neoplastic prostate
tissue
- Produced by the prostate in semen
- Small amounts in bloodstream normally
100
acute urinary retention?
• Sudden onset of painful inability to pass urine usually with over 500ml in the
bladder
• Bladder is usually tender
101
aetiology of acute urinary retention?
Prostatic obstruction e.g. due to BPH or prostate cancer
- Urethral strictures
- Anticholinergics
- Alcohol
- Constipation
- Post-op (pain/inflammation/anaesthetics)
- Infection
- Neurological (spinal compression - cauda equina syndrome)
102
investigations of acute urinary retention?
- EXAMINATION
Abdomen, prostate (DRE), perineal sensation (to check for cauda equina
syndrome
• Diagnosis:
- Normal renal biochemistry - since not affected usually
- Renal ultrasound if abnormal biochemistry
- PSA test - to look for BPH/prostate cancer
103
treatment of acute urinary retention?
Catheter relieves pain
- Alpha-1 blocker e.g. TAMSULOSIN which relaxes smooth muscle in bladder
neck to aid voiding
- Prevent by giving 5-alpha-reductase inhibitor e.g. FINASTERIDE which
reduces testosterones conversion to dihydrotestosterone and thus reduces
prostate size
104
chronic urine retention?
Incomplete bladder emptying
| • Results in a increased risk of infection
105
causes of chronic urinary retention
Prostatic enlargement due to BPH/prostate cancer
- Pelvic malignancy or rectal surgery
- Diabetes
106
clinical presentation and management of chronic urinary retention
Clinical presentation:
- Overflow incontinence - leaking urine during the day/wetting bed
- Loss of appetite, constipation, distended abdomen, UTI
• Management:
- Only catheterise if there is pain, urinary infection or renal impairment
107
urinary obstruction?
Can be partial, complete, unilateral or bilateral
| - can be luminal (stones, clots), mural (stricture) or extra mural (fibrosis, BPH and cancer)
108
clinical presentation of urinary obstruction?
Acute upper tract (kidney & ureter) obstruction
• Loin pain radiating to groin
- Chronic upper tract (kidney & ureter) obstruction:
• Flank pain, renal failure, infection and polyuria may occur due to
impaired urinary concentration
- Acute lower tract (bladder to urethra) obstruction:
• Acute urinary retention with severe suprapubic pain, often preceded by
symptoms of bladder outflow obstruction
• There is a distended, palpable bladder thats dull to percussion
- Chronic lower tract (bladder to urethra) obstruction:
• Urinary frequency, hesitancy, poor stream, terminal dribbling and
overflow incontinence
• Distended, palpable bladder +/- large prostate on rectal exam
• Complications are UTI and urinary retention
109
investigation for urinary obstruction?
Bloods:
- U & Es and monitor creatinine - will be raised
• Mid-stream urinary sample - culture & sensitivity
• Ultrasound:
- If there is hydronephrosis then arrange CT
110
treatment for upper tract urinay obstruction?
Nephrostomy - artificial opening created between the kidney and
the skin which allows for the urinary diversion directly from the
upper tract i.e. renal pelvis
- Alpha-1 antagonist e.g. TAMSULOSIN (bladder neck smooth
muscle relaxer) - improves flow
- 5-alpha reductase inhibitor e.g. FINASTERIDE - inhibits
conversion of testosterone to active form and thus reduces
prostate size
111
treatment for lower tract obstruction?
Urethral catheter
- Suprapubic catheter:
• Less risk of urethral damage and thus UTI
• Requires general anaesthetic for insertion
• Small risk of bowel injury during insertion
• Less likely to be colonised by bacteria than a long term
urethral catheter
• Long term urethral catheter can leaf to urethral erosion and
damage to the urethral sphincter
112
BPH?
Increase in the size of the prostate WITHOUT the presence of malignancy
113
epidemiology of BPH
Common - 24% of men 40-64 and 40% of men over 60
- More common over 60
- Unusual before the age of 45
114
risk factors for BPH?
Age - increases with age
- Castration (removal of testicles) is PROTECTIVE:
• Androgens e.g. testosterone DO NOT CAUSE BPH but are a requirement
for BPH
115
pathophysiology of BPH?
Benign nodular or diffuse proliferation of musculofibrous and glandular
layers of the prostate
- Inner (transitional) zone enlarges in contrast to peripheral layer expansion
seen in prostate carcinoma
- As the prostate gets bigger, it may squeeze or partly block the urethra
(narrows the urethra)
116
clinical presentation BPH
```
• Nocturia (>30% voided volume at night)
• Frequency
• Urgency
• Post-micturition dribbling
• Poor stream/flow
• Hesitancy
- enlarged baller
```
117
investigations for BPH?
Digital rectal exam - feel prostate and would feel enlarged but SMOOTH
- Serum electrolytes and renal ultrasound - to exclude renal damage caused
by obstruction
- Transrectal ultrasound - to see size of prostate
- Serum prostate specific antigen (PSA):
• May be raised in large BPH
- Biopsy and endoscopy
- Mid-stream urine sample - to exclude infection
118
treatment for BPH?
- Lifestyle:
• Avoid caffeine and alcohol to reduce urgency and nocturia
• Relax when voiding
• Void twice in a row to aid emptying
- Drugs:
• Useful in mild disease or those awaiting surgery
• FIRST LINE:
- Alpha 1 antagonists e.g. ORAL TAMSULOSIN: relaxes smooth muscle (s/e ejaculatory failure, drowsiness)
5-alpha-reductase inhibitor e.g. ORAL FINASTERIDE:
- Blocks the conversion of testosterone to dihydrotestosterone
(active form) - the androgen responsible for prostatic growth (s/e decreased libido)
surgery; Transurethral resection of prostate (TURP):
• GOLD STANDARD
119
renal cell carcinoma?
Also known as Hypernephroma and Grawitz tumour
| • Arises from the PROXIMAL CONVOLUTED TUBULAR EPITHELIUM
120
renal cell carcinoma epidemiology
- most common renal tumour
- >50 yrs
- M>F
121
risk factor for renal cell carcinoma
- smoking
- obesity
- PCKD
- Von Hippel Lindau (VHL) syndrome:
• Autosomal dominant
• Mutation of chromosome 3 on the short arm
122
pathophysiology of renal cell carcinoma?
Malignant cancer of the proximal convoluted tubular epithelium
- Spread may be direct (renal vein), via lymph or haematogenous (bone, liver,
lung)
- 25% have metastases at presentation
123
clinical presentation of renal cell carcinoma?
Often asymptomatic and discovered incidentally
- Haematuria, loin/flank pain and abdominal mass
- Anorexia, malaise and weight loss
124
investigations of renal cell carcinoma?
Ultrasound:
• To distinguish simple cyst from complex cyst or tumour
- CT chest and abdomen with contrast:
• More sensitive than ultrasound in detecting a renal mass and will show
involvement of the renal vein of inferior vena cava, if present
- MRI - staging
- Bloods:
• FBC - detect polycythaemia and anaemia due to EPO decrease
• ESR may be raised
• Liver biochemistry may be abnormal
- Renal biopsy:
• Get histology to identify tumour
125
treatment of renal cell carcinoma?
SURGERY
- Nephrectomy (remove kidney) unless tumours are bilateral (present on
both kidneys)
ABLATIVE
Such as cryoablation and radiotherapy are used in patients with
significant comorbidities who would not tolerate surgery
MEDS
- Interleukin-2 & Interferon alpha - produce remission in 20%
• Biological angio-genesis targeted therapy:
- SUNITINIB, BEVACIZUMAB and SORAFENIB
• TEMSIROLIMUS (mTOR inhibitor) - found to improve survival more than
interferon
126
wilms tumour?
(NEPHROBLASTOMA):
• Childhood tumour of the primitive renal tubules and mesenchymal cells
• Seen within the first 3 years of life - it is the chief abdominal malignancy in
children
* Presents as an abdominal mass and less commonly with haematuria
* Diagnosis is established by ultrasound, CT and MRI
* Treated with a combination of nephrectomy, radiotherapy and chemotherapy
127
bladder cancer?
Type of transitional cell carcinoma (TCC)
| - most common TCC
128
epidemiology of bladder cancer?
M>F
| >40 yrs
129
risk factors for bladder cancer?
- Smoking
- Occupational exposure to carcinogens:
- chronic inflammation of urinary tract
130
pathophysiology of bladder cancer?
Tumour spread:
• Local → to pelvic structures
• Lymphatic → to iliac and para-aortic nodes
• Haematogenous → to liver and lungs
131
clinical presentation of bladder cancer?
- Painless haematuria - MOST COMMON SYMPTOM, however, pain may result
due to clot retention
- - Recurrent UTI’s
- Voiding irritabiliity
132
investigations for bladder cancer?
- Cytoscopy (bladder endoscopy) with biopsy - DIAGNOSTIC
- Urine microscopy/cytology - cancers may cause STERILE PYURIA (pus in
urine)
- CT urogram - provides staging and is DIAGNOSTIC
- Urinary tumour markers
- MRI/lymphangiography may show involved pelvic nodes
- CT/MRI of pelvis
133
treatment of bladder cancer?
Radical cystectomy (bladder removal) - GOLD STANDARD:
- Post-op chemotherapy: M-VAC; METHOTREXATE, VINBLASTINE,
ADRIAMYCIN and CISPLATIN
134
prostate cancer?
Commonest male malignancy
• The majority of prostate cancers are adenocarcinomas arising in the peripheral
zone of the prostate gland
135
risk factors of prostate cancer?
- Family history:
• 3 or more affected relatives or
• 2 relatives who have developed early onset
```
- Genetic:
• HOXB13 is a predisposition gene
• BRCA2 confers a 5-7 times higher risk
- Increasing age
- Black
```
136
pathophysiology of prostate cancer?
Most are adenocarcinomas arising in the peripheral prostate
- Spread may be:
• Local → seminal vesicles, bladder and rectum
• Via lymph
• Haematogenously - bone (sclerotic bony lesions) or less common; brain,
liver and lung
137
prostate cancer clinical presentation?
Nocturia
• Hesitancy
• Poor stream
• Terminal dribbling
• Obstruction - bladder outflow problems similar to BPH e.g. urinary
retention
- Weight loss, bone pain and anaemia suggest metastasis
138
investigations of prostate cancer?
Digital rectal exam (DRE):
• Hard, irregular prostate
- Raised PSA (can be normal in 30% cancers) - if metastases then will be
>16ng/ml
- Trans-rectal ultrasound (TRUS) & biopsy - DIAGNOSTIC:
• Histological diagnosis is essential before treatment
• Gleason score used
139
treatment for prostate cancer?
• Radical prostatectomy if <70yrs - excellent disease free survival
• Radiotherapy + hormone therapy - alternative to surgery
• Brachytherapy - implantation of radioactive material targeted at tumour
- endocrine therapy - • LHRH (luteinising hormone receptor hormone) agonists e.g. SC
GOSERELIN or SC LEUPRORELIN
140
testicular tumours, epidemiology?
Most common cancer in males aged 15-44 yrs
| - most from germ cells
141
risk factors testicular tumours?
Undescended testis
- Infant hernia
- Infertility
- Family history
142
clinical presentation for testicular tumours?
Painless lump in testicle
- Testicular pain and/or abdominal pain
- Hydrocele
- Cough and dyspnoea - indicative of lung metastases
- Back pain - indicative of para-aortic lymph node metastasis
- Abdominal mass
143
investigations for testicular tumours?
Ultrasound:
• To differentiate between masses in the body of the testes and other
intrascrotal swellings
- Biopsy and histology
- Serum tumour markers:
• Alpha-fetoprotein (AFP) and/or Beta subunit of human chorionic
gonadotrophin (B-hCG):
144
treatment of testicular tumours?
```
Radical orchidectomy (removal of testes) via inguinal approach
- chemotherapy
```
145
UTI; 5 main pathogens
KEEPS
```
klebsiella
E.coli
enterocci
proteus spp.
staph. spp
```
146
classification of UTI?
```
Location:
• Lower urinary tract vs. Upper
- Clinical risk:
• Uncomplicated vs. Complicated
- Timing:
• Single/isolated vs. Unresolved (persistent infection or re-infection)
• Acute vs. Chronic
```
147
what do uropathogenic strains of e-coli adhere to>
Urothelium
• Vaginal epithelium
• Vaginal mucus
148
upper tract UTI?
Pyelonephritis
149
lower tract UTI?
Cystitis (bladder)
• Prostatitis
• Epididymo-orchitis
• Urethritis
150
uncomplicated UTI?
UTI in healthy non-pregnant woman with normally functioning urinary tract
151
complicated UTI?
Infection in patients with abnormal urinary tract e.g. stones, obstruction or
systemic disease involving the kidney e.g. diabetes mellitus, sickle-cell, or
virulent organism e.g. Staphylococcus Aureus
- Treatment failure is more likely
Majority of UTI’s in MEN are considered complicated - associated with
urological abnormalities such as bladder outlet obstruction
152
risk factor of UTI?
Female
- Sex
- Pregnancy
- Menopause
- Decrease in host defence
- Urinary tract obstruction resulting in urine stasis
- Catheter
153
pyelonephritis?
Infection of the renal parenchyma and soft tissues of renal pelvis and upper
ureter
• Majority caused by UPEC - Uropathogenic E.coli
154
epidemiology of pyelonephritis
Predominantly affects FEMALES under 35 yrs
| - Associated with significant sepsis and systemic upset
155
risk factors of pyelonephritis
Structural renal abnormalities
- Calculi (stones)
- Catheterisation
- Pregnancy
- Diabetes
- Immunocompromised patient
156
pathophysiology of pyelonephritis
Infection is mostly due to bacteria (primarily E.coli) from own patients bowel
flora
- Most common via the ascending transurethral route but can be via the
bloodstream or lymphatics
157
clinical presentation of pyelonephritis
```
Triad of:
• Loin pain, fever and pyuria
- May have severe headache
- Rigors
- Significant bacteriuria
- Malaise, nausea, vomiting
- Oliguria (small amounts of urine) if causes AKI
```
158
investigations of pyelonephritis
Urine dipstick:
• Detects nitrites - bacteria breakdown nitrates to release nitrites
• Detect leucocyte elastase
• Foul-smelling urine
Midstream urine microscopy, culture and sensitivity - GOLD STANDARD for
diagnosis
- Bloods:
• FBC - shows elevated white cell count
• CRP & ESR may be raised in acute infection
- USS
159
pyelonephritis - treatment?
Rest
- Cranberry juice and lots of water
- Analgesia
- Antibiotics:
• ORAL CIPROFLOXACILLIN or ORAL CO-AMOXICLAV
• If severe then IV GENTAMICIN or IV CO-AMOXICLAV
160
cystitis?
Urinary infection of the bladder
161
epidemiology of cystitis?
Much more common in women
- Can occur in children
- Most common cause is E.coli
162
risk factors for cystitis?
Urinary obstruction resulting in urinary stasis
- Previous damage to bladder epithelium
- Bladder stones
- Poor bladder emptying
163
clinical presentation of cystitis?
Dysuria
- Frequency
- Urgency
- Suprapubic pain
- Haematuria
164
investigation of cystitis?
GOLD STANDARD is microscopy and sensitivity of sterile MID-STREAM
URINE
- Dipstick urinalysis:
165
treatment for cystitis?
```
- Antibiotics:
• First-line:
- TRIMETHOPRIM or CEFALEXIN
• Second-line:
- CIPROFLOXACIN or CO-AMOXICLAV
```
166
prostatitis?
Infection and inflammation of the prostate gland
| • Can be acute or chronic
167
epidemiology of prostatitis
Common in men of all ages
- Most common UTI in men < 50
- Usually presents > 35 yrs
- Associated with LUTs
168
aetiology of prostatitis?
Acute prostatitis:
• Streptococcus faecalis
• E.coli
• Chlamydia
Chronic prostatitis:
• Bacterial e.g. Streptococcus faecalis, E.coli or Chlamydia
169
risk factors for prostatitis?
- STI
- UTI
- Indwelling catheter
- Post-biopsy
- Increasing age
170
clinical presentations for prostatitis?
Acute prostatitis:
• Systemically unwell
• Fever, rigors, malaise
• Pain on ejaculation
• Significant voiding LUTs e.g. poor intermittent stream, hesitancy,
incomplete emptying, post micturition dribbling, straining, dysuria
• Pelvic pain
- Chronic prostatitis:
• Acute symptoms (above) > 3 months
• Recurrent UTIs
• Pelvic pain
171
investigations for prostatitis?
- DRE
- Urine dipstick - positive for leucocytes and nitrites
- Mid-stream urine microscopy and sensitivity
- Blood cultures
- Sexually transmitted infection screen - for chlamydia in particular
- Trans-urethral ultrasound scan (TRUSS)
172
treatment for prostatitis?
Acute prostatitis:
• IV GENTAMICIN + IV CO-AMOXICLAV or IV TAZOCIN or IV
CARBAPENEM
Chronic prostatitis:
• 4-6 week course of quinolone e.g. CIPROFLOXACIN (antibiotic)
- • +/- Alpha-blocker e.g. TAMSULOSIN
• NSAIDs e.g. IBUPROFEN
173
urethritis?
Urethral inflammation due to infectious of non-infectious causes
174
epidemiology of urethritis?
Most common condition diagnosed and treated in men at GUM clinics
- Non-gonococcal urethritis is the MORE COMMON than gonococcal
urethritis
- Chlamydia is the MOST COMMON STI in young people aged 15-24 yrs
175
AETIOLOGY of urethritis?
STI
Gonococcal:
- Neisseria gonorrhoea
• Non-gonococcal:
- Chlamydia trachomatis - MOST COMMON CAUSE
- Mycoplasma genitalium
- Ureaplasma urealyticum
- Trichomonas vaginalis
• Non-infective:
- Trauma
- Urethral stricture
- Irritation
- Urinary calculi
176
risk factors for urethritis?
Sexually active
- Unprotected sex
- Male to male sex
- Male
177
clinical presentation of urethritis?
May be asymptomatic (90-95% with gonorrhoea, 50% of patients with
chlamydia)
- Dysuria (painful urination) +/- discharge; blood or pus
- Urethral pain
- Penile discomfort
178
investigations for urethritis?
Nucleic acid amplification test (NAAT):
• Female - self collected vaginal swab (best), endocervical swab, first void
urine
• Male - first void volume
- Microscopy of gram-stained smears of genital secretions
- Blood cultures
- Urine dipstick - to exclude UTI
179
treatment of urethritis?
Chlamydia:
| • ORAL AZITHROMYCIN STAT or 1 WEEK ORAL DOXYCYCLINE
180
epididymo-orchitis
Acute epididymo-orchitis is a clinical syndrome of pain, swelling and
inflammation of the epididymis that can extend into the testis
181
epidemiology of epidiymo-orchitis
- 15-30 and >60
182
aetiology of epidiymo-orchitis
Under 35 yrs:
• Chlamydia trachomatis
• Neisseria gonorrhoea
- Over 35 years:
• UTI - KEEPS:
183
risk factors for epidymo-orhitis?
Previous infection
- Indwelling catheter
- Structural/functional abnormality of urinary tract
- Anal intercourse
184
clinical presentation of epidiymo-orchitis
Subacute onset of unilateral scrotal pain and swelling
- in STD, may be discharge
- headache, fever, sweats
185
investigations of epidiymo-orchitis
Nucleic acid amplification test (NAAT):
• Female - self collected vaginal swab (best), endocervical swab, first void
urine
• Male - first void volume
- midstream for uTI
- USS
186
treatment for epidymo-orchitis?
Chlamydia:
• ORAL DOXYCYCLINE 7 DAYS or STAT AZITHROMYCIN
- Gonorrhoea:
• IM CEFTRIAXONE + STAT ORAL AZITHROMYCIN
187
STI epidemiology?
Chlamydia is the MOST COMMON STI
* Chlamydia is more common in WOMEN and 15-25yr olds
* Gonorrhoea is more common in MEN and is LESS COMMON than chlamydia
188
stress incontience?
Caused by sphincter weakness
- Small leak of urine when intra-abdominal pressure rises e.g. when
coughing, laughing and standing up
treatment; pelvic floor exercises
189
urge incontinence?
Strong desire to void and unable to hold urine
- Cause: Detrusor overactivity - rise in detrusor pressure on filling associated
with urgency - MOST OFTEN IN WOMEN
treatment; bladder exercises and drugs (anticholinergic drugs, beta 3 agonists, botox)
190
function Pontine-micturition centre/periaqueductal grey:
Co-ordination
| - Completion of voiding
191
spastic spinal cord injury?
reflexes work but not controlled by brain:
Loss of co-ordination and completion of voiding
• Features:
- Reflex bladder contractions
- Detrusor sphincter dyssynergia - loss of completion of voiding
- Poorly sustained bladder contraction
192
flaccid spinal cord injury?
- Conus destroyed or non-functional
- Areflexic bladder - fills until it overflows
• Features:
- Areflexic bladder
- Stress incontinence
- Risk of poor compliance
