Urology Flashcards
(160 cards)
1
Q
At what spinal level are the kidneys?
A
Usually T12 - L3
right kidney is generally lower than the left due to the liver
2
Q
What are the two main regions of kidney parenchyma ?
A
- inner medulla
2. outer cortex
3
Q
Role of the renal corpuscle
A
= site of initial filtration
Consists of Bowman’s Capsule and Glomerulus
4
Q
Role of proximal convoluted tubule
A
Brush border to increase luminal surface area for reabsorption of ions and solutes.
Also important for regulating pH by secreting bicarbonate
5
Q
Loop of Henle - permeability of descending thin limb
A
impermeable to ions, but high permeability to water
6
Q
Loop of Henle - permeability of ascending thin and thick limb
A
mostly impermeable to water, permeable to ions (passive diffusion in thin part and active transport in thick part).
7
Q
What is the aim of the loop of henle
A
Aims to create a strong osmotic gradient for absorption of large amounts of water from the descending limb
8
Q
Role of distal convoluted tubule
A
Regulation of potassium, sodium, calcium and pH.
Macula Densa cells involved in paracrine function (detect Na+ levels and initiate RAAS).
9
Q
Role of collecting duct
A
Filtrate is concentrated to form urine, which feeds into the renal pelvis and then the ureters.
Electrolyte and fluid balance, regulated by aldosterone and ADH
10
Q
What is the role of the kidney?
A
Regulating volume and composition of bodily fluids.
Regulating acid-base balance.
Excretion of metabolic breakdown products
=> Ammonia, urea, uric acid, creatinine, drugs, toxins.
Hormonal functions
=> Produces EPO
=> Vitamin D metabolism (converts to active form)
=> Secretes renin in response to reduced afferent pressure.
11
Q
Renin-Angiotensin-Aldosterone System
A
The juxtaglomerular cells of the kidneys are stretch-receptors
Reduced stretch from a decrease in blood volume will lead to the release of renin.
Renin is involved in the cleavage of angiotensinogen to AI. AI is cleaved to AII by ACE.
12
Q
What is the role of angiotensin II?
A
- Vasoconstriction (of afferent arteriole)
- Increase release of aldosterone
=> Enhances reabsorption of sodium and water
13
Q
What is AKI?
A
= a rapid decline in kidney function occurring over hours or days, as measured by serum urea and creatinine.
This results in a failure to maintain fluid, electrolyte and acid-base homeostasis
Causes can be pre-renal, intrinsic or post-renal
14
Q
When is AKI common?
A
very common in acute illness
(>15% of emergency admissions and 25% of septic patients).
15
Q
Risk factors for AKI
A
- Age >65 years.
- Pre-existing CKD
- Male
- Cardiac failure
- Chronic liver disease
- Diabetes
- Sepsis
- Hypovolaemia
16
Q
Pre-renal AKI
A
Reduced renal perfusion leads to a reduction in GFR
Main causes:
- Shock – hypovolaemic, cardiogenic, distributive.
- Renovascular obstruction – AAA, renal artery stenosis (and ACEis given in bilateral renal artery stenosis), renal vein thrombosis.
- Fluid overload – cardiac failure, cirrhosis, nephrotic syndrome.
If interruption in the blood supply is prolonged, there will be acute tubular necrosis (ATN).
17
Q
Acute tubular necrosis in pre-renal AKI
A
Ischaemia leads to necrosis of the cells lining the renal tubules.
Leads to porous tubular membranes (leading to loss of concentrating power) and also blockage of the tubules by necrosed cells
18
Q
Causes of hypovolaemia
A
Hypovolaemia can be caused by:
- haemorrhage,
- dehydration,
- third space losses (e.g. due to bowel obstruction/pancreatitis),
- burns and GI losses (vomiting and diarrhoea).
19
Q
Post-renal AKI
A
Occurs when there is obstruction of the urinary tract
=> Leads to a backflow of urine, damage to the kidney architecture and resultant organ failure
e.g. blockage of ureter (stones, strictures, clots, malignancy) or bladder outlet obstruction
20
Q
Intrinsic AKI
A
= Injury or damage to the renal parenchyma, by 3 potential mechanisms
- Acute tubular necrosis
- Interstitial nephritis
- Glomerular disease
21
Q
Renal causes of Acute tubular necrosis
A
due to drugs/toxins damaging the tubular cells (rather than ischaemia, which is pre-renal).
- Drugs – aminoglycosides, cephalosporins, radiological contrast mediums, NSAIDs.
- Toxins – heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome (HUS).
22
Q
Interstitial nephritis
A
Damage is not limited to tubular cells (as in ATN) and bypasses the basement membrane to cause damage to the interstitium
Most commonly caused by drugs (especially antibiotics, but also diuretics, NSAIDs allopurinol and PPIs).
Can be caused by infection, auto-immune mechanism or lymphoma.
Normally responds to withdrawal of the drugs and a short course of oral steroids
23
Q
Myoglobinuria
A
Follows an episode of rhabdomyolysis (muscle breakdown from trauma, strenuous exercise or medications), releasing myoglobin which is readily filtered by the glomerulus.
Gives the classical dark urine, but in high quantities will precipitate out within the tubules to cause damage
24
Q
haemolytic uraemic syndrome (HUS)
A
Occurs in children following diarrhoeal illness caused by verotoxin-producing E. coli O157, or following a URTI in adults.
Thrombocytopaenia, haemolysis and ATN.
Children recover within a few weeks, prognosis for adults is poor.
Treatment is supportive, including dialysis
25
Signs and Symptoms of AKI
```
Reduced urine output
Nausea and vomiting
Dehydration
Confusion
Fatigue
```
Signs depend on cause - look for:
- Fluid overload
- Hypotension
- Palpable abdominal mass
- Associated features of vasculitis – petechiae, skin changes, bruising, etc.
26
NICE criteria for diagnosis of AKI
1. A rise of serum creatinine >26 micromol/L in 48 hours
2. A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
3. A fall in urine output <0.5mL/kg/hour for more than 6 consecutive hours
27
AKI Stage 1
Serum Creatinine
150-200% increase OR
>25 micromol/L increase in 48h
Urine Output
<0.5 mL/kg/hour for 6h
28
AKI Stage 2
Serum Creatinine
200-300% increase
Urine Output
<0.5 mL/kg/hour for 12h
29
AKI Stage 3
Serum creatinine
>300% increase OR
>350 micromol/L increase in 48h
Urine output
<0.3 mL/kg/h for 24h OR
Anuria for 12h
30
AKI - Bedside tests
```
Urine dip
Urine cultures
Observations – BP, RR, HR
Glucose
ECG
```
31
AKI - Bloods
```
FBC
U&E
LFTs
Coag
CRP
```
ABG – ?acid-base imbalance
Creatine Kinase if indicated
Immunology if indicated
32
AKI - imaging
USS KUB
CXR if pulmonary oedema
CT KUB if obstruction
33
When would test for creatinine kinase be indicated in AKI?
Creatine kinase can show rhabdomyolysis, but this would only be done if indicated in the history and symptoms/signs
34
Management of AKI
Treat the underlying cause
Fluid management (input and output)
Medication review
=> hold/change dose?
Seek renal specialist input if indicated
35
What might indicate the need for renal specialist input in AKI?
No improvement
| Complicated cases
36
Complications of AKI
```
Hyperkalaemia
Other electrolyte imbalances
Metabolic acidosis
Volume overload
Uraemia
CKD and ESRD
```
37
What electrolyte imbalances are associated with AKI?
Hyperkalaemia
Hyperphosphataemia
Hypermagnesaemia
Hyponatraemia
Hypocalcaemia
38
Indications for renal replacement therapy
Refractory pulmonary oedema
Persistent hyperkalaemia (>7)
Severe metabolic acidosis
Ureamic complications (encephalopathy, pericardial rub)
Drug overdose
39
What is the biggest cause of CKD?
Diabetes mellitus
40
Causes of CKD:
Diabetes mellitus
Interstitial diseases
Glomerular diseases
Obstructive uropathy
Hypertension
Renovascular disease
Drugs (long-term NSAIDs)
Congenital/inherited
Unknown causes
41
Symptoms of CKD
Often asymptomatic until very advanced
```
Polyuria/nocturia
Restless leg syndrome
Sexual dysfunction
Nausea & Pruritis (early uraemia)
Yellow pigmentation, encephalopathy and pericarditis (severe uraemia)
Pedal oedema & pulmonary oedema.
```
42
Signs of CKD
```
Pallor – due to anaemia
Excoriations – due to pruritis
Hypertension/fluid overload signs
Pericardial rub (rare)
Proteinuria
```
43
What are some very late features of CKD?
```
Hiccups
Kussmaul’s respiration (due to metabolic acidosis)
Muscle twitching
Drowsiness
Coma
Fits
```
44
Assessment of CKD
```
Bloods - anaemia? hyperkalaemia?
Urinalysis
ECG - hyperkalaemia?
Renal USS
Renal biopsy - if cause unclear
24-hour CrCl - for staging
```
45
What would small kidneys on USS indicate?
Chronicity of disease (not acute presentation)
46
What would asymmetry of kidneys on USS indicate?
renovascular or developmental disease
47
How is CKD diagnosed?
when any two tests three months apart show reduced eGFR and can be stages 1-5 depending on the level of reduction
48
CKD Stage 1
eGFR >90 but urine findings/structural abnormalities/ genetic traits suggest CKD
Pt will be asymptomatic
49
CKD Stage 2
eGFR 60-89
Mildly reduced eGFR and other findings (as for stage 1) point to CKD
Pt will be asymptomatic
50
CKD Stage 3A
"Moderate CKD"
eGFR 45-59
usually asymptomatic
51
CKD Stage 3B
"Moderate-severe CKD"
eGFR 30-44
Pt might be anaemic
52
CKD Stage 4
"Severe CKD"
eGFR 15-29
Symptoms often at eGFR <20
Electrolyte disturbances
53
CKD Stage 5
"End-stage renal failure (ESRF)"
eGFR <15 / dialysis
Significant complications and symptoms
Dialysis usually at eGFR <10
54
Management of CKD
Treat reversible causes – e.g. obstruction, nephrotoxic drugs
1st line = BP control/diabetic control
2nd line = control of complications
=> recombinant EPO
=> calcium/vitD supplementation
=> K+ restriction for hyperkalaemia
RRT in ESRD
55
What are the complications of CKD?
Renal anaemia
Renal bone disease
Electrolyte disturbances
Myopathy
Peripheral neuropathy
Increased risk of infection
GI – Anorexia, N+V, peptic ulcer disease.
CV – pericarditis, atherosclerosis, HTN, hyperlipidaemia.
Depression – particularly in later stages/dialysis
56
Renal anaemia
Lack of secretion of EPO in response to hypoxia
Severity of anaemia correlate with severity of CKD
Recombinant EPO can be given to correct it
BUT treating anaemia may not affect mortality and returning Hb to normal may carry additional risks (hypertension, thrombosis).
57
Renal bone disease
Kidneys normally hydroxylate vitamin D to its active form.
Low VitD levels in CKD cause:
- reduced intestinal Ca2+ absorption
- reduced renal reabsorption of Ca2+
- reduced bone protective activities
thus lead to osteoporosis, osteosclerosis and osteomalacia
hyperparathyroid bone disease can occur (due to low Ca2+)
58
What are the indications for renal replacement therapy?
```
A intractable acidosis
E electrolyte disturbance (hyperkalaemia, hyponatraemia, hypercalcaemia)
I intoxitants
O intractable fluid overload
U uraemia symptoms
```
59
Is the risk of renal disease higher in T1DM or T2DM?
Risk is equivalent
60
How does diabetes mellitus affect the kidneys?
1. Direct glomerular damage
2. Ischaemia due to arterial disease
3. Ascending infection (more common in DM)
61
What factors of DM contribute to renal disease?
Multifactorial
the most important factors:
1. extent and duration of hyperglycaemia
2. hypertension.
Other:
Smoking, obesity, physical inactivity, dyslipidaemia, proteinuria, dietary factors
62
What are the principles of management for diabetic nephropathy?
the same as for CKD, but with additional tight glycaemic control
63
What are the types of polycystic kidney disease?
1. Autosomal dominant (ADPKD) – more common
| 2. Autosomal recessive (ARPKD)
64
What does polycystic kidney disease consist of?
Renal and extra-renal cysts (e.g. liver)
Intracranial aneurysms
Dolichoectasias (elongated and distended arteries)
Aortic root dilatation and aneurysms
Mitral valve prolapse
Abdominal wall herniae
65
How do patients with polycystic kidney disease present?
= most common cause of ballotable kidneys.
systemic hypertension,
CKD
abdominal swelling due to very large kidneys bilaterally.
Cysts in the liver lead to portal hypertension and fibrosis
66
Management of polycystic kidney disease?
the same as for CKD, but consider screening for berry aneurysms
67
Chronic pyelonephritis
chronic tubulointerstitial inflammation and deep segmental cortical renal scarring
clubbing of the pelvic calyces as the papillae retract into scars
Most commonly caused by chronic vesico-ureteric reflux.
68
What are the 3 layers of the glomerulus?
| What is the purpose of this structure?
1. Fenestrated capillary endothelium
2. Basement membrane
3. Visceral layer – formed by podocytes.
to allow small, charged ions through, but not transport of proteins or blood
69
pathophysiology of Glomerulonephritis/glomerular disease
involves an immunological attack by an antibody or T cell, attacking a primary/secondary antigen in the glomerulus
The immune attack leads to pathological responses in the glomerulus:
=> thickened basement membrane
=> deposition of cells in bowman's space
=> endothelial cell proliferation, capillary wall necrosis and sclerosis
70
What can cause deposition of a secondary antigen in the glomerulus?
Neoplasm, SLE, amyloid, infection, diabetes, Henoch Schonlein Purpura
71
Global glomerular pathology
when the whole glomerulus is diseased
72
Segmental glomerular pathology
Small patches of one glomerulus are damaged in a “patchy” fashion
73
Diffuse glomerular pathology
Affecting >50% of glomeruli
74
Focal glomerular pathology
Affecting <50% of glomeruli
75
How can glomerular damage manifest?
```
AKI
CKD
Asymptomatic haematuria
Nephrotic Syndrome
Nephritic Syndrome
```
Rapidly progressive glomerulonephritis (acute version of nephritic syndrome).
76
What is the triad of nephrotic syndrome?
1. Proteinuria - >3.5 g in 24h
2. Hypoalbuminaemia - <30g/L
=> due to protein loss in the urine.
=> In response, liver will produce albumin (but also cholesterol, resulting in hypercholesterolaemia)
3. Oedema
=> due to decreased capillary oncotic pressure
a NON-PROLIFERATIVE condition
77
Symptoms/signs of nephrotic syndrome
```
Fatigue – hypoalbuminaemia.
Leukonychia – hypoalbuminaemia.
Xanthelasma and xanthomata – dyslipidaemia.
Oedema
Breathlessness – pulmonary oedema
Urine “frothy” in appearance - protein
```
78
Causes of nephrotic syndrome
Minimal change nephropathy
Membranous glomerulonephritis
Focal Segmental Glomerulosclerosis
Bacterial/viral infection
Diabetic nephropathy
Drugs
Neoplasm
79
Nephrotic Syndrome - investigations
Urine Dipstick, MSU
FBC, U&E, LFT, Ca2+, CRP, glucose
Serum and urine immunoglobulins
Autoimmune screen, Hep B&C, HIV
CXR – pleural effusion/oedema
USS kidneys (+ renal biopsy?)
80
Minimal change nephropathy
= most common cause of nephrotic syndrome in childhood
Characterised by minimal change on light microscopy of renal biopsy
81
Nephrotic Syndrome - management
Treat the cause.
Diuretics, salt/water restriction and ACEis to reduce proteinuria.
Anticoagulation if immobile due to risk of thrombosis
82
Nephritic Syndrome
Presents as a tetrad of:
1. Haematuria and red cell casts (can be microscopic)
2. Oliguria
3. Proteinuria (can be <3.5 g/day)
4. Hypertension
It is proliferative, with increased cell numbers as well as damage to the basement membrane
83
Causes of nephritic syndrome
IgA nephropathy
Goodpasture’s disease
SLE
Henoch Schonlein Purpura (HSP)
84
What is the main risk factor for UTI?
BEING FEMALE
- shorter urethra (closer to anal and genital regions).
- Pregnancy - hormonal changes lead to urinary stasis and thereby vesicoureteric reflux
- Post-menopause - low oestrogen levels cause decreased amounts of lactobacilli, which leads to increased pH (better conditions for E. coli colonisation)
85
Risk factors for UTI in males
```
Lack of circumcision
Urologic Surgery
Catheterisation
Neurogenic bladder
Urinary Tract obstruction (incl. caliculi)
Renal Transplant
Immunosuppression
Penetrative anal intercourse
Functional/mental impairment.
Prostatic enlargement
Convene
```
86
Risk factors for UTI in females
```
Previous UTI
Urologic Surgery
Catheterisation
Neurogenic Bladder
Urinary Tract obstruction (incl. calculi)
Renal Transplant
Immunosuppression
Sexual intercourse
Lack of urination after sex
Spermicides
Pregnancy
Diaphragm Use
Diabetes
Functional/mental impairment
Oestrogen deficiency
Bladder prolapse
```
87
What are the two most common pathogens causing UTI?
What are some rarer causes?
1. E. coli (most common - ~80%)
2. Staph. saprophyticus (common in young, sexually active females)
Rarer:
3. Enterococci
4. Proteus
5. Klebsiella
6. Pseudomonas (more likely from catheterisation)
88
Upper UTI
Above the Vesico-ureteric junction (VUJ)
=pyelonephritis
89
Lower UTI
below the Vesico-ureteric junction (VUJ)
= Cystitis
90
Clinical Features of Lower UTI
Increased frequency, urgency and nocturia
Dysuria (typically “burning” pain).
Suprapubic pain/tenderness
Foul smelling/cloudy urine.
Strangury – painful, frequent urination of small volume, expelled only by straining despite a severe sense of urgency.
Haematuria
Eventually confusion, lethargy and fatigue – signs of urosepsis.
91
Lower UTI - investigations
Urine dipstick – double positive nitrites and leucocytes.
Midstream urine culture and sensitivity – confirms diagnosis if >10^5 pathogenic organisms per mL.
--
Symptomatic women - empirical treatment is started if nitrites and leucocytes are positive on dipstick.
Women should have MCS sent in certain situations, and men should have MCS sent in all suspected UTI.
92
What should be ruled out before starting empirical UTI treatment?
Check for vaginal discharge to rule out STI
93
When is renal tract imaging needed in lower UTI?
```
in children,
persistent symptoms,
recurrent UTIs,
if ?pyelonephritis,
if an unusual organism is grown
```
94
What is the difference between persistent UTI symptoms and recurrent UTI?
Persistent symptoms – symptoms after more than 48-72 hours of antibiotic treatment.
Recurrent UTI – within a few weeks of appropriate treatment.
95
What is sterile pyuria and what are the causes?
= raised WBCs in urine, but no organism grown
* Recently treated UTI
* Appendicitis
* TB
* Chlamydia
* Bladder cancer
96
Lower UTI - treatment
Lifestyle advice – personal hygiene, drinking plenty of fluids, urinating often.
Simple uncomplicated UTIs are treated with antibiotics:
Most commonly Trimethoprim or Nitrofurantoin (though resistance is increasing)
• 3-day course for women (100mg b.d.)
• 7-day course for men (100mg b.d.)
Symptomatic control (for pain) - NSAIDs/paracetamol
If problems with recurrent UTIs, sometimes put on prophylactic Abx but might need further investigations.
97
Clinical features of upper UTI
```
Dysuria (typically “burning” pain).
Frequency
Flank pain > suprapubic pain
Haematuria
High grade fever
Nausea and vomiting
```
Usually acute onset and systemically unwell.
98
Upper UTI - investigations
Urine dip and MCS still key but additional investigations needed
Bloods -
=> FBC – raised WCC and CRP
=> U&E – renal function maintained? AKI?
Blood cultures?
Imaging
=> USS KUB - 1st line, can help identify obstruction, inflammatory changes and hydronephrosis.
=> CT
=> DMSA scan
99
when is CT generally avoided in investigating upper UTI?
in children or pregnant women due to radiation
100
What does a DMSA scan do?
allows for detailed imaging of the renal cortices and helps clarify areas of poor renal function and scarring
101
Upper UTI - Treatment
If severe symptoms, patients will need to be admitted to hospital and have a 7-day course of IV antibiotics (cefuroxime or ciprofloxacin).
If not severely unwell, patients can have oral Abx for 7 days (ciprofloxacin, trimethoprim or co-amoxiclav).
Drink lots of fluid to prevent dehydration.
May need imaging (USS KUB) to look for structural damage or changes
102
Complications of upper UTI
Sepsis
AKI > CKD
Perinephric abscess
Renal papillary necrosis
103
What are the possible causes of ureteric obstruction?
```
Stones
Clots
Severe constipation (more common in children)
Enlargement of prostate
Strictures
Malignancy
Pregnancy
```
Congenital abnormalities
=> Duplicated ureters, ureterocoele, connection abnormalities
104
What is the most common cause of ureteric obstruction?
Ureteric Stones
105
When can ureteric clots occur?
can form when large amounts of blood are passing into the urine (e.g. in renal malignancy)
106
When can ureteric strictures occur?
following previous injury (e.g. previous stone)
following infections (particularly recurrent).
107
Acute ureteric obstructions
Stones
Clots
Severe constipation
108
Chronic ureteric obstructions
```
Enlarged prostate
Strictures
Malignancy
Pregnancy
Congenital abnormalities
```
109
Luminal ureteric obstruction
Stones
Clots
TCC of renal pelvis
Bladder tumour
110
Mural ureteric obstruction
Ureteric stricture
Congenital pelviureteric neuromuscular dysfunction
Congenital mega-ureter
111
Extra-mural ureteric obstruction
```
Pelviureteric compression
(due to external tumours, diverticulitis, AAA, retroperitoneal fibrosis)
```
112
Clinical features of ureteric obstruction
```
Symptoms:
• Pain – “ureteric colic”
• N+V
• Frank haematuria
• Difficulty passing urine
• Recurrent UTIs
```
```
Signs:
• Frequency
• Oliguria
• Haematuria
• Hypertension
• Pyrexia
• Rigors
```
113
Where are the 3 sites of ureteric constriction?
What is the clinical relevance of these points?
1. Pelviureteric Junction
2. Pelvic Brim
3. Vesicoureteric Junction
= the 3 common sites where stones can get lodged
114
Risk factors for urolithiasis
More common in males (3:1)
More common in affluent areas
Anatomical abnormalities
=> E.g. horseshoe kidney, ureteral stricture
```
HTN
Gout
Hyperparathyroidism
Immobilisation
Dehydration
Metabolic disorders
```
115
What can renal/ureteric stones consist of (most to least common)?
1. Calcium
2. Urate
3. Struvite - magnesium, ammonium, phosphate
4. Cysteine
116
What are the risk factors for calcium stones?
Low urine volume
| Hypercalciuria (e.g. primary parahyperthyroidism).
117
What are the risk factors for urate stones?
high levels of blood purines from diet (increased red meat) or haematological disorders
118
Which ureteric/renal stones are radiolucent?
urate stones
119
Staghorn calculi
where the the renal pelvis and calices are filled with stone to give a "stag horn" appearance
120
What are the risk factors for cysteine stones?
associated with familial disorders of cysteine metabolism
121
What is the cause of ureteric colic?
occurs due to increased peristalsis around the site of the obstruction.
the pain radiates down to the testis, scrotum, labia or anterior thigh
122
Investigation of Ureteric Obstruction
BLOODS – FBC, U&Es, CRP, LFTs, coag, calcium, phosphate, glucose, bicarbonate and urate levels
Urine dip - blood? infection?
(including bHCG)
Urine MCS
Abdominal exam
Imaging - AXR, renal tract USS, Non-contrast CT KUB
123
what is the gold-standard imaging modality for ureteric obstruction?
Non-contrast CT KUB
124
Causes of true frank haematuria
```
Malignancy of renal tract
Stones
Infection
Nephritis
Bleeding disorders (incl. over-coagulation)
Trauma
```
125
Causes of apparent (i.e. not true) frank hematuria
Menstruation
Dyes
Some drugs (e.g. rifampicin)
126
Spontaneous passing of renal stones
~ 80% pass spontaneously (esp if <5mm or in lower ureter)
can take 1-3 weeks
Fluid resuscitation + analgesia (buscopan as antispasmodic?)
Abx if infection
127
Management of large renal stone (>5mm)
ESWL - sonic waves are used to break up the stone
```
Percutaneous nephrolithotomy (PCNL)
=> for complex renal calculi and staghorn calculi.
```
Endoscopic removal
Open surgery
128
When should hospital admission be considered in renal stones?
1. Post-renal AKI
2. Uncontrollable pain from simple analgesics
3. Evidence of infection or shock.
4. Stone >5mm
129
Complications of renal stones?
Acute obstruction – infection, post-renal AKI.
| Recurrent/chronic obstruction – CKD, renal scarring
130
what temporary measures can be done to relieve obstruction and avoid renal damage?
1. Retrograde stent insertion:
=> Placement of a stent within the ureter, allows the ureter to be kept patent and temporarily relieve the obstruction.
2. Nephrostomy
=> A tube placed directly through the skin on the back, into the renal pelvis and collecting system, relieving the obstruction proximally.
131
Renal cell carcinoma - presentation
60% of patients have haematuria
Other symptoms include mild loin discomfort and a loin mass.
132
Renal cell carcinoma - pathophysiology
Invades along the renal vein to the IVC and spreads via haematological route.
Forms PTH-related protein, so patients may get pathological fractures.
133
Renal cell carcinoma - diagnosis
Typically forms a solid mass on USS; also seen on CT scan
Bloods commonly show anaemia and may show a raised ALP and/or ESR
134
Renal cell carcinoma - treatment
Radical nephrectomy
No role for chemo/radiotherapy (ineffective)
Tyrosine Kinase inhibitors can be useful; as can renal artery embolisation
135
Renal cell carcinoma - prognosis
Classically causes cannonball lung metastases.
Even T1 disease has only 70% 5-year survival prognosis.
Average survival with mets is <2 years.
136
What are common causes of bladder outlet obstruction?
```
Benign Prostatic Hypertrophy (BPH)
Bladder stones
Urethral strictures
Prostate cancer
Tumours of the rectum, uterus, or cervix.
```
137
What are risk factors for bladder stones?
due to stasis of urine
=> such as in chronic retention, infection, obstructive uropathy of other aetiology, and catheters.
138
Bladder stones - presentation
Lower Urinary Tract Symptoms
Chronic irritation of bladder epithelium increases transitional cell carcinoma risk
139
Bladder stones - investigation
As for renal stones
140
Bladder stones - management
Cystoscopy
Stone drainage
Lithotripsy
141
Bladder cancer - presentation
Typically painless haematuria (+/- clots)
Recurrent UTI
Voiding symptoms
Pain from invasion of local structures.
142
Risk factors for bladder cancer
Male, smoker, age >50, aromatic amines, schistosomiasis
143
Bladder cancer - pathophysiology
= transitional cell carcinoma
Commonly due to prolonged carcinogen contact
Initially forms carcinoma in situ
144
Bladder cancer - diagnosis
Screening undertaken of those who work in at-risk industries.
Usually diagnosed visually (with biopsies) on flexi-cystoscopy.
145
Which industries are considered "at risk" of bladder cancer?
Rubber/plastic/dye industry workers
146
Bladder cancer - treatment and prognosis
Cystoscopic removal of the tumour +/- intravesical BCG
In extensive cases – radical cystectomy
Need to look for parallel primaries in the entire urinary tract. 50% change of recurrence so follow-up is life-long
147
Benign Prostatic Hyperplasia
Benign nodular/diffuse proliferation of the glandular layers of the prostate, leading to enlargement of the inner transitional zone
Common in middle-aged men
148
BPH - symptoms
Symptoms occur due to urethral compression:
```
Hesitancy
Poor flow
Terminal dribbling
Frequency and nocturia
UTI
Retention (less common)
```
149
BPH - Complications
```
UTI
Overflow incontinence
Bladder calculi
Bladder diverticulae
Bilateral hydronephrosis and renal failure
```
150
BPH - treatment
Acute retention – attempt urethral catheter drainage
If symptoms are mild – “watch and wait”
Medical management with alpha-blockers or 5alpha-reductase inhibitors
If medical management fails, then Trans-urethral resection of the prostate
151
Prostate cancer - presentation
Most commonly raised PSA (but 20% have normal PSA)
Often asymptomatic
PR exam – hard and craggy prostate
152
Where does prostate cancer commonly metastasise to?
bone
iliac/para-aortic nodes.
153
Prostate cancer - treatment
T1/2 = active surveillance.
| T 3/4 = radiotherapy or surgery
154
Apart from prostate cancer, what else can affect PSA levels ?
mountain biking, infection, recent intercourse (48h), cystoscopy
155
Gleason Grade of prostate cancer
Two areas of tissue are graded out of 5 to give a combined score out of 10.
Vital for prognosis
```
<7 = low risk;
>7 = high risk.
```
156
what might an enlarged prostate with a deep sulcus suggest?
benign prostatic hyperplasia
157
what might an enlarged and very tender prostate suggest?
(acute/chronic) prostatitis
158
what might an enlarged prostate with a rough nodule suggest?
unilateral prostate cancer
159
what might a hard, asymmetrical and irregular prostate with an impalpable sulcus suggest?
prostate cancer
160
what are some things to comment on when examining the prostate in a PR exam?
```
Size – normal size?
Sulcus – normal central sulcus?
Symmetry – are the lobes symmetrical?
Consistency – smooth/irregular?
Any pain on palpation?
```
