1
Q
List six functions of the kidneys.
A
metabolic waste excretion endocrine functions drug metabolism/excretion control of solutes and fluid status blood pressure control acid/base balance
2
Q
What is the normal amount of protein excreted from the kidneys over 24 hours?
A
150mg
3
Q
Name the three ways that urinary protein excretion is measured.
A
- 24hr urine collection (g/24h)
- protein:creatinine ratio on morning spot sample
- albumin:creatinine ratio
4
Q
Differentiate between non-visible haematuria and visible haematuria.
A
- non: can be blood detectable on dipstick only
- visible: can come from anywhere in the urinary tract
5
Q
List causes of visible haematuria.
A
kidney stones, infection, malignancy, cysts, inflammation
6
Q
Define renal clearance (GFR) and how it is calculated.
A
= volume of plasma which would be cleared of the substance per unit of time
(urine conc of substance x urine volume) / plasma conc of substance
7
Q
The MDRD*4 formula for estimation of GFR from plasma creatinine concentration is based on which 4 factors?
A
plasma creatinine conc.
age
gender
race
8
Q
Describe the staging of chronic kidney disease using eGFR.
A
1: eGFR > 90 ml/min normal
2. 60-89 normal unless evidence of kidney disease
3. 30-59 moderate impairment
4. 15-29 severe impairment
5. < 15 advanced renal failure
9
Q
List some of the secondary causes of GN.
A
- diabetes
- haem: myeloma, CLL, PRV
- bacterial endocarditis
- resp: bronchiectasis, lung cancer, TB
- gastro: ALD, IBD, coeliac
- drugs: NSAIDs, bisphosphonates, heroin
- rhemu: RA, lupus, amyloid
- ID: hepatitis, HIV, antibiotics, malaria
10
Q
Following presentation and history, what is required to make a diagnosis of GN?
A
kidney biopsy
11
Q
What are the three ways in which the kidney cortex biopsy is examined?
A
- light microscopy (glomerular and tubular structure)
- immunofluorescence (looking for Ig and complement)
- electron microscopy (BM and deposits)
12
Q
Describe how different types of GN present including RPGN, nephritic and nephrotic.
A
- RPGN: rapid rise in serum creatinine, crescentic damage, vasculitis, lupus, IgA
- nephritic: blood and protein in urine, high BP, rising sCr, proliferative/acute inflammation, IgA, lupus, post-infectious
- nephrotic: >3,5mg proteinuria, low sAlb, oedema, non-proliferative, podocyte damage, minimal change/FSGS/membranous
13
Q
List the four criteria used to define nephrotic syndrome.
A
- 3.5g proteinuria per 24hr
- Serum albumin <30
- Oedema
- Hyperlipidaemia
14
Q
What are the two main risks associated with nephrotic syndrome?
A
risk of venous thromboembolism
increased risk of infection
15
Q
What are the possible therapeutic strategies of GN in relation to the stage:
- insult precipitant e.g. infection, antibody
- injury
- response to injury
- outcome
A
- control infection
- remove AB/IC
- steroids, cytotoxics, anti-hypertensives
- dialysis, transplantation, slow progression, resolution
16
Q
Describe the four stage spectrum of IgA nephropathy.
A
1 minor urinary abnormalities
2 hypertension
3 renal impairment and heavy proteinuria
4 rapidly progressive GN
17
Q
What is the most common primary glomerular disease?
A
IgA nephropathy causing mesangial disease
18
Q
What causes IgA nephropathy?
A
precipitated by infection - Occurring intercurrently with an episode of pharyngitis (synpharyngitic)
secondary = HSP, cirrhosis, coeliac
19
Q
Describe the brief pathophysiology of IgA nephropathy and how it presents.
A
abnormal/over-production of IgA1 leading to mesangial deposition and subsequent proliferation
haematuria, hypertension, proteinuria
20
Q
What treatment is available for IgA nephropathy?
A
no specific therapy
antihypertensive Rx - ACEi
21
Q
How does membranous GN present?
A
nephrotic syndrome
22
Q
Which antibody is seen in 70% of cases of membranous GN?
A
anti-phospholipase A2 receptor antibody
23
Q
Which type of GN is secondarily caused by malignancy, connective tissue diseases and drugs?
A
membranous
24
Q
In membranous GN, where are immune complexes located?
A
in basement membrane and sub-epithelial space
25
Describe the variable natural history of membrane GN.
```
1/3 = spontaneously remit
1/3 = progress to ESRF over 1-2 years
1/3 = persistent proteinuria, maintain GFR
```
26
What are the three stages in treating membranous GN?
1 underlying cause if secondary
2 supportive non-immunological e.g. ACEi, statins, diuretics, salt restriction
3 immunotherapy e.g. steroids, alkylating agents, cyclosporin, rituximab (anti-CD20 MAB)
27
What is the commonest form of GN in children?
minimal change
28
What are the main pathological features seen in minimal change GN?
podocyte foot process fusion
T cell cytokine mediated - target glom. epithelial cell
causes nephrotic syndrome
29
How might minimal change GN present?
acute - may follow URTI
| GFR normal or reduced due to intravascular depletion
30
Describe the treatment for minimal change GN.
high dose steroids - prednisolone 1mg/kg for up to 8 weeks
31
List the five commonest causes of crescentic/rapidly progressive GN.
```
ANCA vasculitis
Goodpasture's syndrome (anti-GBM disease)
Lupus nephritis
infection associated
HSP nephritis
```
32
What is RPGN?
group of conditions which demonstrate glomerular crescents on kidney biopsy
33
Discuss the approach to the patient in suspected glomerulonephritis.
- full medical and drug history
- basics: UEs, dip urine for blood, quantify proteinuria, check albumin, check USS
- glomerulonephritis screen
34
In a glomerulonephritis screen, many diseases may be detected. What are these and what substance are they associated with?
- diabetic nephropathy: HbA1c
- ANCA/anti-GBM: vasculitis
- ANA/PLA2R/virology: membranous
- complement/ANA/dsDNA: lupus
- complement/virology(hep B, C, HIV)/Igs/RF: MPGN, FSGS
35
Discuss the different types of glomerulonephritis including proliferative and non-proliferative.
```
proliferative = nephritic syndrome e.g. IgA nephropathy, post-infectious, RPGN
non-proliferative = nephrotic syndrome e.g. minimal change disease, focal segmental GN, membranous GN
```
36
What is the triad of nephritic syndrome?
1 haematuria
2 decreased urine production
3 hypertension
leading to end-stage kidney failure
37
List four of the main systemic diseases associated with renal dysfunction.
diabetes mellitus
atheromatous vascular disease
amyloidosis
SLE
38
Briefly describe how diabetes leads to renal failure.
hyperglycaemia, volume expansion, intra-glomerular hypertension, hyperfiltration, proteinuria, hypertension and renal failure
39
Describe the structural changes seen in diabetic kidney disease.
thickening of glomerular BM
fusion of foot processes
loss of podocytes with denuding of the glomerular BM
mesangial matrix expansion
40
How might the risk of diabetic nephropathy be reduced?
tight glycaemic control
good BP control
SGLT2 inhibitors e.g. empagliflozin
41
Describe how SGLT2 inhibition leads to cardiac and renal protection.
- glycosuria and natriuresis
| - weight loss, lower HbA1c, lower BP, decreased intraglomerular hypertension, decreased atherosclerosis
42
List three causes of non-proteinuric AKI.
- obstruction
- renovascular disease - renal artery stenosis
- interstitial nephritis
43
Discuss the pathogenesis of renovascular disease.
1 progressive narrowing of renal arteries with atheroma
2 perfusion falls, GFR falls but tissue oxygenation of cortex and medulla maintained
3 RA stenosis 70%, cortical hypoxia causes microvascular damage and activation of inflammatory pathways
4 parenchymal inflammation and fibrosis irreversible
44
Describe the 3 point management of renal artery stenosis.
1. Medical - BP control (not ACEi/ARB), statin
2. Lifestyle - smoking cessation, exercise
3. Angioplasty - in rapidly deteriorating renal failure, uncontrolled hypertension, flash pulmonary oedema
45
What is amyloidosis and what organs does it affect?
deposition of highly stable insoluble proteineous material in extracellular space
kidney, heart, liver, gut
46
Describe the specific ultrastructural features of amyloid.
8nm linear aggregated fibrils of variable length forming a felt-like structure made of beta-pleated sheets
47
What type of amyloid is seen from previous TB and familial Mediterranean fever?
AA amyloid
48
How is amyloidosis detected using microscopy?
light microscopy: congo red stain = apple green birefringence
electron microscopy: amyloid fibrils 8nm cause mesangial expansion
49
Differentiate between the two classes of amyloidosis, AA and AL and how they are treated.
```
AA = systemic amyloidosis (inflammation/infection). Treat underlying infection source.
AL = Ig fragments from haematological conditions e.g. myeloma. Treat underlying haematological condition.
```
50
What is systemic lupus erythematosis?
auto-immune disease, immune complex mediated glomerular disease
51
What are the autoantibodies present in SLE directed against?
DNA, histones, snRNPs, transcription/translation factors
52
Describe the pathophysiology of lupus nephritis.
- autoantibodies produced against dsDNA or nucleosomes (anti-dsDNA, anti-histone)
- form intravascular immune complexes or attach to GBM
- activate complement
- renal damage
53
How is SLE treated?
immunosuppression - steroids, MMF, cyclophosphamide, rituximab
54
Describe the presenting features of urinary tract infections to include both cystitis and pyelonephritis.
- cystitis: dysuria, frequency, urgency, suprapubic pain, haematuria
- pyelonephritis: the above PLUS fever, chills/rigors, flank pain, costo-vertebral angle tenderness, N+V
55
What are the risk factors to developing a UTI?
- infancy
- abnormal urinary tract
- female
- bladder dysfunction
- 'foreign' body e.g. catheter
- diabetes mellitus
- renal transplant
- immunosuppression
56
How is the diagnosis of UTI made?
- multistix: leucocytes + nitrites
- microscopy/flow cytometry: pus cells + bacteria
- urine culture - in all children <3 years if clinical suspicion
57
Which organism is the most likely cause of UTI?
E. coli
58
What criteria must be reached from the urine culture to define UTI?
single organism > 10^5 CFU/ml
59
Discuss the antibiotic treatment for UTI.
oral unless vomiting, severely unwell, infant <3 months = trimethoprim, co-amoxiclav, nitrofurantoin, cephalosporin
IV = 3rd gen cephalosporin e.g. ceftriaxone, gentamicin
60
What is the importance of investigation and management of UTI in childhood?
- imaging: US, micturating cystourethrogram (gold standard for VUR and PUV), nuclear medicine imaging e.g. DMSA (scarring)
- antibiotic prophylaxis: not in simple UTI, consider for CAKUT, trimethoprim, nitrofurantoin
61
What is vesico-ureteric reflux?
a condition in which urine flows retrograde, or backward, from the bladder into the ureters/kidneys
62
Give examples of two congenital abnormalities of kidney and urinary tract.
- vesico-ureteric reflux
| - obstruction of urinary drainage tracts
63
What is oligohydramnios and what does it suggest?
deficiency of amniotic fluid
| significant renal impairment
64
Describe the medical and surgical management of VUR and UTI.
- medical: antibiotic prophylaxis for high grade VUR until toilet trained
- surgical: if recurrent, proven febrile UTI and/or new scarring on meds, 'STING' procedure - narrows ureteric orifice
65
List common causes of bladder outlet obstruction.
- prostatic hypertrophy
- functional obstruction: neurogenic bladder (spina bifida, trauma etc), prune belly syndrome
- posterior urethral valve
66
What is Prune Belly Syndrome?
triad of:
1. Megacystis/megaureters
2. Absent abdominal wall muscles
3. Bilateral cryptochidism
67
How does a posterior urethral valve present?
antenatal hydronephrosis
urinary tract infection
poor urinary stream
renal dysfunction
68
How is a posterior urethral valve managed?
valve resection
antibiotic prophylaxis
CKD care
69
What is the commonest cause of hydronephrosis in children?
pelvi-ureteric junction obstruction
70
What are the complications associated with PUJO?
abdominal mass, pain, haematuria, UTI
71
What does VUJO stand for?
vesico-ureteric junction obstruction
72
Describe the management of ureteric obstruction.
1. PUJO
- observant: USS, DMSA, MAG3 diuresis renogram
- surgical: pyeloplasty
2. VUJO
- observant: most resolve, USS, DMSA, MAG3 diuresis renogram
- surgical: for symptoms or increasing dilatation, stent insertion, resection or re-implantation
73
What is a kidney cyst and what problems can they cause?
- sac-like structure containing fluid arising from the tubules
- compressing other structures, replacing useful tissues, becoming infected, bleeding, pain
74
Is adult polycystic kidney disease AD or AR?
autosomal dominant
75
What gene mutations are associated with APKD and what do they code for?
- PKD1 on c16 - polycystin 1
- PKD2 on c4 - polycystin 2
- 25% no FHx
76
How do the PKD gene mutations lead to APKD?
- polycystins are located in renal tubular epithelium
- overexpressed in cyst cells
- membrane proteins involved in intracellular calcium regulation
77
How is APKD diagnosed?
US: If FHx US at age 21:
- age 15-30: 2 unilateral or bilateral cysts
- age 30-59: 2 cysts in each kidney
- over age 60: 4 cysts in each kidney
No FHx: 10 or more cysts in both kidneys, renal enlargement, liver cysts
78
What are the clinical consequences of APKD?
- renal complications - ESRD
- hypertension
- intracranial aneurysms
- mitral valve prolapse
- aortic incompetence
- diverticular disease
- liver/pancreas cysts
79
Discuss the management of APKD.
- supportive management
- early detection and BP management
- treat complications
- renal replacement therapy
- ?tolvaptan - vasopressin V2 receptor antagonist
80
What are the potential implications of using tolvaptan as a drug therapy for APKD?
- delay onset of RRT by around 4-5 years
- heavy monitoring
- SE: hepatotoxicity, hypernatraemia
- very expensive
81
List four other rare kidney cystic diseases.
Von Hippel Lindau
tuberous sclerosis
AR PKD
medullary cystic disease
82
What is Von Hippel Lindau disease?
visceral cysts and benign tumours with potential for subsequent malignant transformation
AD
83
What is tuberous sclerosis?
multiple benign tumours - brain, eyes, heart, kidney, skin
epilepsy and LD
AD
84
What is AR PKD?
rare inherited childhood condition, where the development of the kidneys and liver is abnormal - hepatic fibrosis
85
What is medullary cystic disease?
AD
cysts in medulla not cortex
small to normal sized kidney
gout
86
What gene mutations are associated with Alport's syndrome?
```
usually X-linked
collagen 4 abnormalities
- alpha 3
- alpha 4 (COL3A4)
- alpha 5 (COL3A5)
```
87
What are the clinical consequences of Alport's syndrome?
deafness (sensorineural hearing loss)
renal failure (microscopic haematuria and proteinuria)
50% on dialysis by 25y
88
Describe the changes seen in the basement membrane in Alport's.
defect in collagen 4 = abnormally split and laminated GBM
89
What is Fabry's disease?
X-linked storage disorder
| alpha-galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3)
90
How does Fabry's disease lead to renal failure?
Gb3 accumulated in glomeruli, particularly podocytes causing proteinuria and ESRF
91
What extra-renal features are associated with Fabry's syndrome?
neuropathy
cardiac
skin - angiokeratoma
92
How is Fabry's disease diagnosed and managed?
diagnosis:
- measure alpha-Gal A activity in leucocytes
- renal biopsy - inclusion bodies of Gb3
management: enzyme replacement therapy
93
Define AKI according to UKRA guidelines.
decline of renal excretory function over hours or days.. recognised by the rise in serum urea and creatinine
94
What are the three stages of AKI severity according the KDIGO?
1. Serum creatinine 1.5-2x AKI baseline
2. 2-3x AKI baseline
3. >3x AKI baseline
95
Can you give examples of causes of:
1. pre-renal AKI
2. intrinsic AKI
3. post-renal AKI?
1. hypovolaemia + hypotension, reduced circulatory volume, drugs, renal artery stenosis
2. glomerulonephritis, tubular dysfunction, myeloma, sarcoid, acute tubular necrosis
3. renal papillary necrosis, kidney stones, cervix carcinoma, prostatic hypertrophy, urethral strictures
96
ATN is always due to under perfusion of the tubules and/or direct toxicity. What are the three main causes of this?
hypotension, sepsis, toxins
97
What happens to glomerular filtration as pressure falls?
prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80mmHg
98
Describe the effects of NSAIDs and ACEis on the glomerulus.
- NSAIDs: block dilatation of afferent arterioles
| - ACEi: block constriction of efferent arterioles
99
Describe the treatment of AKI.
- restore renal perfusion (hyperkalaemia and pulmonary oedema)
- remove causes (drugs and sepsis)
- exclude obstruction and consider 'renal' causes
100
Discuss the diagnostic process of AKI.
- need for urgent action may take precedence over making final diagnosis
- history and exam
- drugs
- urinalysis
- renal US
- 'GN' screen
101
What features of a clinical exam would make you suspect AKI?
sepsis, rashes, haemoptysis, rhabomyolysis
102
What level of serum potassium is classified as a medical emergency?
>6.5
103
How would you treat hyperkalaemia?
- reduce absorption from gut - calcium resonium
- insulin - moves K+ into cells
- calcium gluconate - cardiac membrane stabiliser
104
Raised potassium levels can lead to acidosis. How is this treated?
IV NaBicarc 1.26%
105
What is the definition of CKD?
kidney damage or GFR<60ml/min per 1.73m2 for 3 months or more
106
What is the criteria for albuminuria?
ACR > 30
107
List some causes of CKD.
- diabetic nephropathy
- renovascular disease/ischaemic nephropathy
- chronic glomerulonephritis
- chronic pyelonephritis
- ADPKD
- obstructive uropathy
108
What are the symptoms of advanced CKD?
pruritus, nausea, anorexia, weight loss, fatigue, leg swelling, breathlessness, nocturia, joint/bone pain, confusion
109
What are the signs of advanced CKD?
peripheral and pulmonary oedema, pericardial rub, rash/excoriation, hypertension, tachypnoea, cachexia, pallor and/or lemon yellow tinge
110
What methods of management are available to slow down progression of CKD?
- BP control: ACEi/ARB
- diabetic control
- diet
- smoking cessation
- lowering cholesterol
- treat acidosis
111
Anaemia is common in CKD, especially as eGFR falls below 30. Describe its management.
- replace iron, B12, folate
| - darbopoietin
112
CKD leads to increased levels of PTH leading to secondary hyperparathyroidism and metabolic bone disease. How can this be treated?
- vit D supplements
- Mg supplements
- phosphate binders
- calcimimetic
- parathyroidectomy
113
What are the indications for starting renal replacement therapy?
1. medically resistant hyperkalaemia
2. medically resistant pulmonary oedema
3. medically resistant acidosis
4. uraemic pericarditis
5. uraemic encephalopathy
6. GFR between 5-10 ml/min/1.73m2
114
Name the main RRT modalities.
- haemodialysis
- peritoneal dialysis
- renal transplant
115
What are the two main points of access for haemodialysis?
- TCVC Tunneled Central Venous Catheter
| - AVF arteriovenous fistula
116
What is the standard amount of times that a patient requires HD a week?
4 hours 3 times a week
117
What are some of the complications associated with haemodialysis?
- 'crash' - acute hypotension
- access problems
- cramps, fatigue
- hypokalaemia
- blood loss
- dialysis disequilibrium
- air embolism
118
List the complications associated with PD.
- peritonitis
- glucose load: development or worsening control of diabetes
- mechanical: hernia, diaphragmatic leak, dislodged catheter
- peritoneal membrane failure
- hypoalbuminaemia
119
What patients are not suitable for peritoneal dialysis?
- grossly obese
- intra-abdominal adhesions
- frail
- home not suitable
120
What issues associated with kidney disease are not helped by dialysis?
- anaemia
- renal bone disease
- neuropathy
- endocrine disturbances
121
Discuss the pros and cons of renal transplantation.
- pros: no dialysis, better level of renal function, independence, better life expectancy
- cons: immunosuppression, increased CV and infection risk, skin malignancies
122
Name three immunosuppressive medications typically used in renal transplantation.
cyclosporin
tacrolimus
MPA
123
What is the most effective form of RRT?
transplant
124
What is urosepsis?
complicated UTI
- temp > 38
- HR > 90
- RR > 20
- WBC > 12 or < 4
125
What are the common organisms that cause UTI?
1. Gram -ve bacilli e.g. E. coli, Klebsiella sp, Proteus sp., Pseudomonas sp.
2. Gram +ve e.g. staph, strep
3. Anaerobes
4. Candida sp.
126
UTI during pregnancy is common and is usually treated with amoxicillin or cephalexin. Which antibiotics should be avoided?
trimethoprim in 1st trimester
| nitrofurantoin near term
127
What is the definition of recurrent UTI?
>2 episodes in 6 months
128
What advice should be given to women who suffer from recurrent UTI?
hydration, urge-initiated and post-coital voiding, intravaginal/oral oestrogen
129
What antibiotic therapy is available from recurrent UTI?
- self-administered single dose/short course therapy
- single dose post coital abx
- prophylactic antibiotics
130
What are some of the complications associated with catheters?
- CAUTI
- obstruction-hydronephrosis
- chronic renal inflammation
- urinary tract stones
- long term risk of bladder cancer
131
What measures can be taken to prevent catheter infections?
- only if necessary
- remove when no longer needed
- remove/replace if causing infection
- hand hygiene
132
How would you treat catheter related UTI?
- check recent/previous microbiology
- start empirical antibiotics
- remove catheter if not needed
- antibiotics: broad spectrum, historically gent/cipro
133
What is the standard treatment for community acute pyelonephritis?
co-amoxiclav/ciprofloxacin/trimethoprim
134
What are the complications associated with pyelonephritis?
renal and perinephric abscess
135
What are the risk factors for developing a perinephric abscess?
- untreated LUTI, anatomical abnormalities
- renal calculi
- bacteraemia, haematogenous spread
136
How is a perinephric abscess treated?
treat empirically as complicated UTI - poor response -> surgical management
137
Which antibiotics are effective against uncomplicated UTI?
PO amoxicillin, trimethoprim, nitrofurantoin
138
What antibiotics should be used in complicated UTI?
IV
- amoxicillin/vancomycin
- gentamicin/aztreonam/temocillin
139
What are the signs of acute bacterial prostatitis?
fever, perineal/back pain, UTI, urinary retention, diffuse oedema
140
What are the likely organisms to have caused acute bacterial prostatitis?
- gram -ve bacilli
- S. aureus
- N. gonorrhoea
141
List the complications associated with acute bacterial prostatitis.
- prostatic abscess
- spontaneous rupture
- epididymitis
- pyelonephritis
- systemic sepsis
142
Describe the antibiotic management of acute bacterial prostatitis.
ciprofloxacin - no strep cover
143
Chlamydia urethritis is associated with which chronic condition?
chronic prostatitis
144
What is epididymitis and describe its aetiology?
- inflammatory reaction of the epididymis
- ascending infection from urethra
- urethral instrumentation
145
Describe the symptoms associated with epididymitis.
pain, fever, swelling, penile discharge - symptoms of UTI/urethritis
146
What are the organisms commonly associated with epididymitis?
- GNB, enterococci, staphylococci
- TB in high risk areas
- chlamydia, gonorrhoea
147
Orchitis is inflammation of one or both testicles. What would the symptoms of this be?
testicular pain and swelling, dysuria, fever, penile discharge
148
What are the complications of bacterial orchitis?
testicular infarction and abscess formation
149
What is Fournier's gangrene?
a type of necrotizing fasciitis or gangrene affecting the external genitalia and/or perineum
150
What are the risk factors to developing Fournier's gangrene?
- > 50
- UTI
- complications of IBD
- trauma
- recent surgery
151
Describe the management of Fourier's gangrene.
- blood cultures, urine, tissue/pus
- surgical debridement
- broad spectrum Abx initially
152
Describe the range of drugs which must be avoided or dose reduced in renal disease.
- avoid: metformin, NSAIDs
| - reduce dose: antibiotics, LMWH, digoxin, phenytoin
153
What changes should be made to dose and dosage interval in:
1. Renal disease
2. Hepatic disease
1. Dose = none. Dosage interval = increase
| 2. Dose = decrease. Dosage interval = increase
154
Why do kidney stones form?
abnormal urine, urinary obstruction, urinary infection
155
Describe the composition of urine that leads to stone formation.
- low volume, low pH, low citrate, low Mg
| - high uric acid, high calcium, high oxalate
156
What are the congenital and acquired urinary obstructions that lead to stone formation?
congenital: medullary sponge kidney, PUJO, mega-ureter, ureterocele
acquired: ureteric stricture, anastamotic stricture
157
Which organisms can increase the possibility of kidney stone formation?
- urease producing organisms
| - proteus mirablis: splits urea to form ammonia, raises urine pH, struvite
158
List the different types of kidney stones.
- calcium: calcium oxalate monohydrate or dihydrate, calcium phosphate
- infection stones: struvite
- uric acid stone - metabolic syndromes
- cystine - genetic
159
Describe the presentation of a patient with kidney stones.
- pain: colic, radiates from loin to groin, cannot settle, unable to stay still
- haematuria
- UTI or sepsis
- often incidental
160
How are kidney stones managed non-surgically?
- small/asymptomatic = observation
- medical = dissolution therapy (urate)
- pain: analgesia, NSAIDs
161
What are the surgical treatments available for kidney stones?
- extracorporeal shockwave lithotripsy
- ureteroscopy
- percutaneous nephrolithotomy
- emergency stent and nephrostomy
162
What are the risk factors for development of prostate cancer?
- elderly men
- genetics: HPC1, BRCA2, PTEN, TP53?
- westernised nations
163
What are the symptoms of prostate cancer?
- often asymptomatic
- painful or slow micturition
- UTI
- haematuria
- urinary retention
- lympdoedema
- metastatic: bone pain, renal failure
164
Name three processes of diagnosing and screening for prostate cancer.
- digital rectal exam
- prostate-specific antigen
- TRUS guided needle biopsy
165
Describe the pathology of prostatic cancer.
- primary adenocarcinoma
| - usually arises in peripheral zone of prostate
166
What are the treatment options available for prostate cancer?
- active surveillance
- RTx
- radical prostatectomy
- cryotherapy
- TURP if symptomatic
- androgen ablation therapy in advanced
167
What are the metastatic complications of prostatic cancer?
- spinal cord compression: urological emergency, severe pain, retention, constipation, urgent MRI
- ureteric obstruction: anorexia, weight loss, raised creatinine
168
Name 3 risk factors for the development of bladder cancer.
smoking, old age, caucasian, environmental carcinogens, stones, long term catheters, drugs e.g. cyclophosphamide, pelvis RTx
169
Describe the presentation of bladder cancer and subsequent investigation.
- classically painless frank haematuria
| - cystoscopy and renal USS
170
Describe the pathology of bladder cancers.
- 90% transitional cell carcinoma
- 5% squamous carcinoma
- 2% adenocarcinoma
171
How are bladder cancers treated?
- urgent TURBT
| - intravesical mitomycin reduces risk of recurrence
172
What are the risk factors to developing renal cancer?
smoking, obesity, hypertension, acquired renal cystic disease, haemodialysis, genetics (VHL)
173
How does renal cancer present?
- 80% incidental
- <25% systemic = night sweats, fever, fatigue, weight loss, haemoptysis
- 10% triad of mass, pain, haematuria
- varicocele
- lower limb oedema
174
What are the paraneoplastic syndromes associated with kidney cancer?
polycythaemia, hypercalcaemua, hypertension, deranged LFTs, Cushing's
175
What are the risk factors to developing testicular cancer?
- men 20-45 y/o
- cryptorchidism
- HIV
- caucasian
176
What is the main clinical presentation of testicular cancer and how it this investigated?
- painless lump
| - investigations: scrotal US, tumour markers = AFP, beta-hCG, LDH
177
Describe the treatment available for testicular cancer.
- radical orchidectomy
- chemotherapy
- para-aortic nodal RTx
- retroperitoneal lymph node dissection
178
What infection is associated with penile cancer?
HPV 16 + 18
179
What is the treatment available for penile cancer?
circumcision, topical treatment, penectomy +/- reconstruction
Phase 3
flashcards
Decks in class (10)
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