Urology Flashcards
1
Q
What is the function of the urinary tract
A
Collect urine produced continuously by the kidneys
To store collected urine safely
To expel urine when socially acceptable
2
Q
Where are the kidneys located
A
Retroperitoneal between T11 and L3
3
Q
What is the blood supply of the kidneys
A
Renal artery direct from the aorta at L1 level
4
Q
How much urine does each kidney produce per day
A
1-1.5L of urine per day
5
Q
How long are the ureters
A
25-30cm
6
Q
Describe the course of the ureters
A
Run over the poses muscle, cross the iliac vessels at the pelvic brim and insert into the trigone of bladder
7
Q
What are the three points of narrowing in the ureter
A
Pelvo-uteric junction
Crossing iliac vessels
Crossing trigone of bladder
8
Q
How is reflux of urine prevented
A
Valvular mechanisms at the vesicoureteric junction
9
Q
Describe the nervous control of the bladder and sphincter
A
- Parasympathetic nerve (Pelvic nerve (S2-S4)
- ACH
- Involuntary control - Sympathetic nerves (Hypogastric plexus, T11-L2)
- Noradrenaline
- involuntary control - Somatic nerve (Pudendal nerve S2-S4)
- Onuf’s nucleus
- ACH - Afferent pelvic nerve
- Sensory nerve
- Signals from detrusor muscle
10
Q
Describe the neural control of micturition
A
Cortex = voluntary control
Pontine micturition centre/periaqueductal grey = coordination of voiding
Sacral micturition centre
Onuf’s nucleus = guarding reflex
11
Q
Is the detrusor muscle relaxed or contracted during storage?
A
Relaxed.
12
Q
Is the detrusor muscle relaxed or contracted during voiding?
A
Contracted.
13
Q
Is the urethral sphincter relaxed or contracted during storage?
A
Contracted.
14
Q
Is the urethral sphincter relaxed or contracted during voiding?
A
Relaxed.
15
Q
What type of epithelium lines the bladder?
A
Urothelium (transitional epithelium) - pseudo-stratified.
16
Q
Describe the physiology of micturition.
A
The bladder fills and stretch receptors are stimulated. Afferent impulses stimulate parasympathetic action of detrusor muscle; it contracts. The urethral sphincters relax; this is mediated by inhibition of the neurones to them. The PAG is stimulated.
17
Q
Describe the storage phase
A
- Bladder fills continuously as urine is produced by kidney and is passed through the ureters into the bladder
- Normal adult bladder capacity 400-500ml with first sensation at 100-200ml
- As the volume in the bladder increases the pressure remains low due to “receptive relaxation” and detrusor muscle compliance (Sympathetic mediated)
18
Q
Describe the filling phase
A
- At lower volumes the afferent pelvic nerve sends slow firing signals to the pons via the spinal cord
- Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation
- Somatic (Pudendal) nerve stimulation maintains urethral contraction
19
Q
Describe the micturition reflex
A
- Micturition reflex is an autonomic spinal reflex
- Higher volumes stimulate the afferent pelvic nerve to send fast signals to the sacral micturition centre in the sacral spinal cord
- Pelvic parasympathetic nerve is stimulated and the detrusor muscle contracts
- Pudendal nerve is inhibited and the external sphincter relaxes
20
Q
Describe the process of bladder emptying
A
- Coordinated detrusor contraction with external sphincter relaxation to expel urine from bladder
- A positive feedback loop is generated until all urine is expelled
- Detrusor relaxation and external sphincter contraction after complete emptying of bladder
21
Q
Describe the guarding reflex
A
- Voluntary control of micturition can occur in anatomically and functionally normal adults
- Afferent signals from the pelvic nerve are received by the PMC/PAG and transmitted to higher cortical centres
- If voiding is inappropriate the guarding reflex occurs
- Sympathetic (hypogastric) nerve stimulation results in detrusor relaxation
- Pudendal nerve stimulation results in contraction of the external urethral sphincter
22
Q
Detrusor relaxation is controlled by what nerve
A
Sympathetic stimulation T11-L2
23
Q
External urethral sphincter contraction is controlled by what nerve
A
Pudendal stimulation (S2-S4)
24
Q
Detrusor contraction is controlled by what nerve
A
Pelvic nerve -= Parasympathetic stimulation S2-S4
25
External urethral sphincter relaxation is controlled by what nerve
Pudendal inhibition S2-S4
26
What is the normal function of the lower urinary tract
- Convert a continuous process of excretion (Urine production) to an intermittent process of elimination
- Store urine insensibly
- Void urine when convenient
27
What does the detrusor muscle do during storage
Relaxes
28
What does the detrusor muscle due during voiding
Contracts
29
What does the distal sphincter do during storage
Contracts
30
What does the distal sphincter do during voiding
Relaxes
31
What is the role of the parasympathetic S2S4 nerve in neural control of LUT
Drives detrusor contraction
32
What is the role of the sympathetic (T10-L2) nerve in the neural control of LUT
Sphincter/urethral contraction
| Inhibits detrusor contraction
33
What are lower urinary tract symptoms (LUTS) in men > 50 likely to be due to?
Benign prostatic enlargement.
34
What are the storage symptoms of LUT
a. Frequency
b. Nocturia
c. Urgency
d. Urgency Incontinence
35
What are the voiding symptoms of LUT
1. Straining.
2. Hesitancy.
3. Incomplete emptying.
4. Poor flow/intermittent strain
5. Terminal dribble
6. Haematuria
7. Dysuria
36
What might dysuria suggest?
Inflammation.
37
What is BPH
Benign prostatic hyperplasia
38
What is BPE
Benign prostatic enlargement
39
What is BOO
Bladder outflow obstruction (Urodynamic proven obstruction)
40
What is LUTS
Lower urinary tract symptoms, constellation of symptoms, neither gender nor disease specific
41
What is benign prostate hyperplasia
Increase in epithelial and stromal cell number and size in the transitional/peri-urethral prostate area
42
What are the causes of BPH
Increase in cell number
Decrease in apoptosis
Combination of both
43
What is another cause of BPH
Obstruction due to increase A1 adrenoceptors with leads to SM contraction and thus increase in prostate size
44
What are the causes of BPH
Unknown but thought to be associated with androgen
- Castration or genetic disease that inhibits androgen action or production prevents BPH
- Androgen withdrawal leads to partial involution of established BPH
45
Describe the epidemiology of BPH
Only affects men and the incidence increases with age
46
LUTS: give 3 symptoms of storage problems.
1. Frequency.
2. Urgency.
3. Nocturia.
47
LUTS: give 4 symptoms of voiding problems.
1. Straining.
2. Hesitancy.
3. Incomplete emptying.
4. Poor flow.
48
What other symptoms are associated with LUTS
post-micturition voiding, haematuria, dysuria
49
Name a symptom scoring system for LUTS
International prostate symptom score (IPSS)
50
What investigations might you carry out in someone with suspected LUTS
1. Urinary tests e.g. dipstick.
2. Urinary flow: maximum flow rate and residual volume are important (Frequency volume chart)
3. Symptom assessment: international prostate scoring system.
4. Blood tests e.g. PSA, U+E.
5. Flexible cystoscopy
51
What might dysuria suggest
Inflammation
52
What is the normal flow rate for someone under 40
21ml/s
53
What is the normal flow rate for someone between 40 and 60
18ml/s
54
What is the normal flow rate for someone >60
13ml/s
55
What 2 things can cause a decline in Flow rate
Obstruction within the lower urinary tract
| Detrusor under activity
56
What are the complications of LUTS
1. Bladder calculi (Stones)
2. Infections (Due to stagnant urine in the residual volume in the bladder)
3. Symptom progression
4. Haematuria
5. Acute retention
6. Chronic rentention
7. Interactive obstructive uropathy
57
Give 3 symptoms of acute urinary retention.
1. PAINFUL!
2. Sudden onset.
3. >500ml of urine in bladder.
58
How is the pain from acute urinary retention relieved
Catheterisation
Pain relief
Reassurance
59
Name a rare but serious cause of acute urinary retention.
Spinal cord compression.
60
What are the issues with chronic urine retention
Incomplete bladder emptying leads to increased risk of infections and stones
61
What are the aims of treatment for LUTS
Improve urinary symptoms
Improve quality of life
reduce the complications of bladder outflow obstruction
62
What lifestyle modifications can be made to reduce LUTS
Reduce caffeine and alcohol intakee
distraction methods
Bladder training
63
Describe the treatment for someone who presents with mild LUTS.
Reassurance, watch and wait.
64
Describe the treatment for someone who presents with moderate LUTS.
1. Fluid management, avoid caffeine.
| 2. Bladder drill.
65
Give 2 pharmacological therapies used in the treatment of moderate to severe LUTS.
1. Alpha-1-blockers e.g. tamulosin.
2. 5-alpha-reductase-inhibitors.
(finasteride, dutasteride)
66
How do alpha-1-blockers work in the management of LUTS?
They cause vasodilation of the smooth muscle in the bladder neck and prostate and so reduced resistance to bladder outflow.
67
Give 2 potential side effects of tamulosin.
2 side effects include hypotension and retrograde ejaculation.
68
How do 5-alpha-reductase-inhibitors work in the management of LUTS?
They inhibit the conversion of testosterone to dihydrotestosterone and so reduce prostate size.
69
Give a surgical treatment for BPE.
Transurethral resection of prostate (TURP)
70
What investigations might you do in someone with acute urinary retention?
1. Clinical examination: palpable bladder?
2. MRI.
2. Bloods.
4. Neurological tests; could be a sign of spinal cord compression e.g. pain in back, loss of anal reflex, leg weakness.
71
Give 4 symptoms of BPH.
1. Increased frequency of micturition.
2. Nocturia.
3. Hesitancy.
4. Post-void dribbling.
72
What are the indications for surgical management of LUTS (RUSHES)
```
Retention
UTI's
Stones
Haematuria
Elevated creatinine due to BOO
Symptom deterioration
```
73
What are the complications of trans-urethral resection of the prostate
```
Immediate = sepsis, haemorrhage
Early = sepsis, haemorrhage and clot retention
Late = retrograde ejaculation, ED, urethral stricture, bladder neck stenosis, urinary incontinence
```
74
What is the function of the prostate?
The prostate secretes proteolytic enzymes into the semen which break down clotting factors in the ejaculate.
75
What type of cancer is prostate cancer
Adenocarcinoma
76
Which anatomical zone of the prostate does prostate cancer commonly affect?
The peripheral zone initially but can then spread locally to the transition zone and central zone
77
Where can prostate cancer commonly metastasise to?
Lymph nodes and bone, brain, liver and lung
78
What are the causes of prostate cancer
Family history
High testosterone
Ethnicity - 2-3x higher in afro-caribbean
Genetic (HOXb13 and BRAC2)
79
What is the epidemiology of prostate cancer
Most common male malignancy
| mean age at diagnosis at 72
80
By what routes does prostate cancer spread
Lymphatics -> To external iliac (Obturator) and internal iliac and presacral node
Haematogenous to bone, liver and kidneys
Direct spread to the bladder, seminal vesicle, urethra, pubic bone, rectum, sciatic nerve and iliac blood vessels, ureter
81
What are the symptoms of prostrate cancer
LUTS
- Nocturia, hesitancy, intermittent stream, slow stream, terminal dribbling, frequency, post micturition dribble
Metastasis = bone pain, wt loss, anaemia and loss of appetite
Majority are picked up at the asymptomatic stage
82
What investigations might you do in someone who you suspect has prostate cancer?
- Serum: PSA.
- Urine: PCA3 and gene fusion products.
- DRE - hard, irregular, craggy, asymmetrical with textural difference
- History of LUTS.
- Trans-rectal USS.
- Prostate biopsy.
- CT/MRI
- CT abdomen
83
On examination, what things might you see that indicate prostate cancer
External anal sphincter tone (detect spinal cord compression)
Overdistended bladder due to outlet obstruction
Bony tenderness
84
What is PSA
Semen liquefaction protease
85
What is the issue with the PSA test
High sensitivity but low low specificity = prostate specific but not cancer specific
86
Other than prostate cancer. What can cause an elevated PSA?
1. Benign prostate enlargement.
2. UTI.
3. Prostatitis.
87
What is a normal level of PSA
3ng/ml - elevated suggests prostate cancer
88
What are the indications for prostate biopsy
Palpably suspicious DRE regardless of PSA
PSA >3.0ng/ml
Suspicious lesions on MRI
89
What is the grading system used in prostate cancer
Gleason grading
| - higher the score the more aggressive the cancer
90
Describe the Gleason grading system for prostate cancer
Histological appearance - add 2 most common histological presentations on biopsy to get a score from 2-10
T1 (No palpable tumour)
T2 (Only prostate)
T3 (Out of prostate)
T4 (Tumour is fixed or invades adjacent structures)
91
What are the benefits of PSA test
Early diagnosis of localised disease
Early treatment of advanced disease
92
What are the risks of PSA test
Overdiagnosis of insignificant disease
Harm caused by investigation/treatment
93
What is the treatment for localised prostate cancer?
- Observation.
- Surgery - radical prostatectomy.
- Radiotherapy (external beam).
- Adjuvant hormones.
94
What are the complications of radical prostatectomy
Urinary incontinence and impotence
95
What is the treatment for metastatic prostate cancer?
Palliative treatment e.g. hormone therapy - androgen deprivation,
surgical castration,
androgen receptor antagonists
96
Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer.
- Curative.
- Reduced patient anxiety.
- Can have adverse effects.
97
What are the forms of hormone therapy used In local or advanced/metastatic disease
Orchiectomy - remove testes
Luteinising hormone releasing hormone agonists
Antiandrogens - block testosterone
98
Name a Luteinising hormone releasing hormone agonists
Leuporelin or goserelin
99
Name an antiandrogen
Flutamide
100
What are the side effects of hormone therapy
```
Impotence
Depression
Hot flushes
Lethargy
Osteoporosis
```
101
Name some other treatments for metastatic prostate cancer
```
Chemotherapy
Bisphosphonates
Radiotherapy for bone pain
TURP to relieve symptoms of bladder outflow obstruction
Nephrostomies for ureteric obstruction
```
102
What is PSA?
A glycoprotein secreted by the prostate into the blood stream.
103
What is the role of the cortex in neuro-urology
Sensation
| Voluntary initiation
104
What is the role of the pontine micturition centre and periaqueductal grey in euro-urology
Co-ordination
| Completion of voiding
105
Name the spinal reflexes of micturition
Reflex bladder contraction (Sacral micturition centre)
Guarding reflex (Onuf's nucleus)
Receptive relaxation (Sympathetic spinal reflex)
106
Parasympathetic (Cholinergic) S3-S5 controls what
Detrusor muscle contraction
Smooth muscle sphincter relaxation
107
Sympathetic (Noradrenergic) T10-L2 controls what
Smooth muscle sphincter contraction
Inhibition detrusor muscle contraction (Allows relaxation)
108
What do the somatic nerves control
Striated sphincter contraction/relaxation (External urethral sphincter)
Voluntary control
109
What happens in bladder storage
a. Sympathetic activation causes detrusor relaxation and sphincter contraction
b. Bladder fullness increases and messages to the pons and higher centres to consider voiding
c. Can be postponed until it is convenient
110
What happens in bladder voiding
a. PMC coordinates voiding via parasympathetic detrusor contraction and sphincter relaxation at the same time
111
LUTs: Storage symptoms
Frequency
Urgency
Nocturia
Incontinence
112
LUTS: Voiding symptoms
```
Slow stream
Splitting or spraying
Intermittency
Hesitancy
Straining
Terminal dribble
```
113
LUTS: Post micturition
Post micturition dribble
| Feeling of incomplete emptying
114
What parameters are measured in a bladder diary
```
Frequency per day
Frequency per night
Volume per day
Volume per night
Nocturnal volume/24hr
Functional capacity
Incontinence
```
115
How many times does a normal person urinate per day
2-8 times
116
How much urine does a normal 70kg male pass per day
2-2.7
| >2.7L = polyuria
117
How much urine on average is produced per wee
500ml
118
Define incontinence
involuntary loss of urine
119
Define urgency incontinence
Associated with an urgent desire to void which is difficult to defer
120
Name three types of incontinence
Stress = associated with coughing/straining
Continuous = due to fistula
Mixed = combination of stress and urgency
Urgency
Social = occurs in those with dementia
121
Give a reason why incontinence in men is less common than it is women.
Men have a bladder neck mechanism and a strong urethral sphincter whereas women have only a weak urethral sphincter.
122
What are the causes of stress incontinence in females
Usually second to birth trauma
Can be neurogenic
Congenital
123
Describe the treatment for stress incontinence in females.
1. Pelvic floor physio.
2. Duloxetine - increases contraction of urethral sphincter (concerns over psychiatric SE's).
3. Surgery.
- sling
- Colposuspension
- Bulking agents
- artificial sphincter
124
What is the main cause of stress incontinence in men?
Neurogenic or iatrogenic (prostatectomy - ablated sphincter during prostatectomy)
125
Describe the treatment for stress incontinence in males.
1. Artificial sphincter.
| 2. Sling.
126
What are the surgical options for stress incontinence surgery
- TVT (Tension free vaginal tape)
- TOT (Transobturator tape)
- Autologous sling procedure using the rectus sheath muscle to tighten the urethral sphincter
- Bladder elevation
- Bulking urethra in elderly who cant undergo surgery
- Artificial urinary sphincter for men and women
127
Define overactive bladder
Defined as urgency with frequency with or without nocturne when appearing in absence of local pathology
128
Describe the treatment for an overactive bladder.
1. Behavioural e.g. limit caffeine and alcohol, bladder drill, frequency volume chart
2. Pelvic floor physio.
3. Muscarinic antagonists.
4. Beta 3 agonists.
5. Botox.
6. Cystoplasty.
7. Sacral neuromodulaion surgery
129
How to muscarinic antagonists help an overactive bladder
Decrease parasympathetic activity by blocking M2/3 receptors so prevents the bladder contracting
130
How to B3 agonists help an overactive bladder
Increase sympathetic activity at B3 receptor in the bladder which inhibits the detrusor muscle contraction enabling relaxation
131
What are the risks associated with botox treatment of overactive bladder
Risk of urinary retention
132
How does sacral neuromodulation work in the treatment of overactive bladder
percutaneous approach in which the 3rd sacral root electrode is connected to pacemaker which tells S3 nerve to relax so doesn't contract and reduces detrusor activity
133
What is bladder augmentation
Cystoplasty using the stomach, colon or small bowel where the bladder gets attached to one of these which increases bladder capacity for urine
134
What are the obstructive causes of voiding issues
BPE
Urethral stricture
Prolapse/mass
135
What is the management for obstruction induced voiding issues
If BPE = alpha blockers +/- alpha 5 reductase inhibitors
or PDE5i for men with ED as it relaxes the bladder neck
I
If above fails - trans-urethral reaction of the prostate
136
What are the non obstructive causes of voiding problems
Detrusor underactivity - bladder loses ability to contract
137
What are the management approaches for non obstructive voiding issues
Long term catheterisation
| Sacral neuromodulation
138
What is the treatment for a BPO male with no ED
1. Alpha antagonist
2. 5 reductase inhibitor
3. TURP
139
What is the treatment for a BPO male with ED
1. PDE5 inhibitor
2. Alpha antagonist
3. TURP
140
What is the treatment for someone with OAB
1. Antimuscarinic
2. B3 antagonist
3. Botox
141
What is the treatment for a women with OAB
1. Antimuscarinic
2. B3 agonist
3. Botox
142
What is the treatment for a women with stress urinary incontinence
Physiotherapy
| Surgery
143
A conus spastic spinal cord lesion above the cauda equina leads to loss of what micturition processes
Coordination
| Completion of voiding
144
What are the features of a conus spinal lesion
Reflex bladder contractions
Detrusor sphincter dyssynergia
Poorly sustained bladder contraction
145
Describe the pathophysiology of conus spinal lesions
Bladder fills and the natural reflex is for the bladder to squeeze and send a signal to the pontine micturition centre but the spinal cord lesions means the signal cant reach the PMC so the bladder becomes autonomous and squeezes on its own. This causes the guarding reflex to come into effect causing the sphincter to contract causing incomplete emptying of the bladder as the pons cant inhibit the guarding reflex - can lead to reflux which damages the kidneys
146
A flaccid spinal cord injury leads to damage to the sacral micturition centre - what are the effects of this
Reflex bladder contraction
Guarding reflex
Receptive relaxation
147
What are the features of a flaccid spinal cord injury
Areflexic bladder
Stress incontinence
Risk of poor compliance
148
What is the pathophysiology of flaccid spinal cord lesion
Bladder will fill until it cant fill anymore and there won't be any contraction so the pressure will start to rise and once it cant stretch anymore = areflexic bladder
Urethral sphincter becomes denervated leading to stress incontinence
149
What are the aims of neurogenic bladder
Bladder safety
Continence and symptom control
Prevent autonomic dysreflexia
150
Describe the pathophysiology of autonomic dysreflexia
Occurs at lesions above T6
- Overstimulation of sympathetic NS below the level of the lesion in response to noxious stimuli
- Everything below the lesion will contract causing vasoconstriction = blood pressure increase
151
What are the signs of autonomic dysreflexia
Headache
Severe hypertension
Flushing
152
What is the management of autonomic dysreflexia
Need to remove the noxious stimuli - change catheter to allow bladder to drain or help them to empty their bowels
153
Define unsafe bladder
One that puts the kidneys at the risk of damage
154
What are the risk factors for unsafe bladder
```
Raised blood pressure
Vesico-ureteric reflux
Chronic infection
- residual urine
- Stones
```
155
What are the causes of raised bladder pressure
Prolonged detrusor contraction and loss of compliance
156
What is the result of raised bladder pressure
Problems with drainage of urine from the kidneys and ultimately hydronephrosis and renal failure
157
What are the two routes to reflex the bladder
1. Harness reflexes to empty bladder into incontinence device
2. Suppress reflexes converting bladder to flaccid type then empty regularly
158
What is the bladder management for a paraplegic
Suprapubic catheter
Conveen (Condom is connected to bag and urine drains straight in)
Suppress reflexes or poorly compliant bladder
159
What is convene drainage
Condom attached to bag
| No indwelling catheter
160
What is a suprapubic catheter
inserted under anaesthetic into the bladder from the abdomen
Risk of infections and stones
161
What are the approaches for suppressing reflex bladder contraction
```
Anti-cholinergics
Mirabegron
Intravesical botulinum toxin
Posterior rhizotomy
Cystoplasty
```
162
What are some examples of flaccid and low spinal lesions
```
Spina bifida
Sacral fracture
Transverse myelitis
Ischaemic injuries
Cauda equina
```
163
What sort of cancer is bladder cancer
Transitional cell carcinoma
164
Where might a transitional cell carcinoma arise
1. Bladder
2. Ureter
3. Renal pelvis
4. Urethra
Areas lined by transitional epithelium
165
Describe the epidemiology of transitional cell carcinoma.
1. M:F = 3:1.
2. Age > 40 y/o.
3. more common in industrialised areas
4. Schistosomiasis endemic areas
5. Incidence increases with age
166
Give 5 risk factors for transitional cell carcinoma.
1. SMOKING.
2. Occupational exposure e.g. working in rubber factories (aromatic amines, polycyclic aromatic hydrocarbon's).
3. Increasing age.
4. Male gender.
5. Family history.
6. Chronic cystitis
7. Long term catheter
8. Chronic HPV - immunocompromised
167
Give 5 symptoms of transitional cell carcinoma (Bladder carcinoma)
1. PAINLESS HAEMATURIA.
2. Recurrent UTIs
3. Voiding problems (LUTS)
- Frequency.
- Urgency.
- Dysuria.
- Urinary tract obstruction.
- intermittent stream
- hesitancy
4. Flank pain, lower limb oedema, pelvic masses, weight loss and bone pain are uncommon
168
Give 5 investigations that you might do in someone who you suspect has transitional cell carcinoma (Bladder cancer)
1. Urine microscopy/cytology
2. Cystoscopy + bladder wall biopsy
3. CT urogram
4. Urinary tumour markers
5. MRI/lymphangiography
169
Give 2 potential risks of flexible cystoscopy.
1. UTI's.
| 2. Problems passing urine.
170
Why would you want to image the upper urinary tract of someone with transitional cell carcinoma?
You image the UUT to confirm that there is no other TCC elsewhere in the urinary tract.
171
What staging system is used for TCC?
TNM staging.
172
Describe the TNM staging for bladder cancer
T1 (Submucosa)
T2 (Muscle - where it becomes invasive)
T3 (Outer fat)
T4 (Other organs)
173
Describe the treatment for non-muscle invasive bladder cancer (CIS, Ta, T1).
1. Trans urethral resection of the bladder (TURBT)
| 2. Chemotherapy to reduce the risk of recurrence and progression to muscle invasion.
174
Describe the treatment for muscle invasive bladder cancer (T2, T3).
1. Radical cystectomy = gold standard.
2. +/- neo-adjuvant chemotherapy (Cisplatin)
3. Radical radiotherapy if not fit/unwilling to undergo cystectomy.
4. Intravesical chemotherapy (MMC) - inhibits DNA synthesis
5. Intravesical immunotherapy (BCG) - immune stimulant that unregulates cytokines (IL-6 and 8)
175
Describe the treatment for T4 TCC (invasion beyond the bladder).
1. Palliative chemo/radiotherapy.
| 2. Chronic catheterisation for pain.
176
Name a helminth that can cause squamous cell carcinoma of the bladder.
Schistosomiasis.
177
What are the two forms of renal cancer
Renal cell carcinoma
| Transitional cell carcinoma
178
Where does renal cell carcinoma arise from
From the proximal convoluted tubular epithelium
179
Where does transitional cell carcinoma arise from
Renal pelvis
180
What are the three types of transitional cell carcinoma
Clear cell - more aggressive
Papillary
Chromophobe
181
How is renal cancer spread
Direct
Lymphatics
Haematogenous
182
Describe the epidemiology of renal cell carcinoma.
1. Incidence increases in those > 60 y/o.
| 2. Males > females.
183
Give 3 risk factors for renal cell carcinoma.
1. Smoking.
2. Obesity.
3. Hypertension.
4. Regular NSAID use
5. Family history
6. Von hippel Lindau disease
7. Environmental (Petroleum, phenacetin, cadmium
8. Leather industry workers
184
Name an inherited renal disease that can cause renal cell carcinoma.
Von Hippel Lindau disease.
185
What is Von Hippel Lindau disease?
An autosomal dominant disease. There is a loss of the tumour suppressor gene VHL which is encoded for on chromosome 3. Lots of benign cysts grow, some of which may develop into cancer.
186
What are the 3 classic signs of renal cell carcinoma?
1. Haematuria.
2. Flank mass.
3. Loin pain.
4. Abdominal mass
5. Paraneoplastic symptoms
6. General = lethargy, malaise, anorexia and wt loss
187
Why do people with renal cell carcinoma rarely present with symptoms of the disease?
The signs of renal cell carcinoma are now rare as people with the disease are detected incidentally through imaging for something else before they show any symptoms.
188
Name 3 places that renal cell carcinoma might metastasise to.
1. Lymph nodes.
2. Lungs.
3. Bones.
189
What investigations might you do in someone with renal cell carcinoma?
- Ultrasound.
- Bloods: FBC, U+E, LFT, Ca profile.
- Abdo CT scan with contrast.
- Bone scan for boney metastases.
- Renal biopsy
190
What is the staging criteria used in renal cell carcinoma
Bosniak classification
1-2 = discharge
2F = follow up
3-4 = treat
191
What is the treatment for localised renal cell carcinoma?
Surgical excision - partial nephrectomy.
192
What is the treatment for metastatic renal cell carcinoma?
- Palliative nephrectomy.
| - Radiotherapy.
193
What is the most common cancer in males aged 15-44
Testicular cancer
194
Where does testicular cancer arise from
germ cells
195
What are the two types of testicular cancer
Seminoma = most common type, slow growing
Non-seminoma = yolk Choriocarcinoma/teratoma, rapid growth
196
Where does the testicular cancer spread locally
epididymis
spermatic cord
Scrotal wall
Leads to pelvic and inguinal metastasis
197
Where does testicular cancer metastasise to distally
Lungs, liver and bones
198
What are the risk factors for testicular cancer
```
Cryptorchidism
Fx history
Previous testicular tumour
Infertility
Infant hernia
Testicular intraepithelial neoplasia
Maternal oestrogen exposure
```
199
What are the signs and symptoms of testicular cancer
Painless testis lump - hard and craggy
Testicular or abdominal pain
Cough and dyspnoea indicative of lung metastases
Blood in ejaculate
Systemic - abdominal mass, dyspnoea, secreted hormone effects
200
What are the investigations for someone with testicular cancer
```
Tumour markers
- AFP (Alpha-fetoprotein)
- B-hCG (Beta subunit of human chorionic gonadotrophin)
Testicular biopsy
Imaging (US (Diagnosis)
CT/MRI for staging
```
201
What is the staging criteria used in testicular cancer
```
1 = (No mets)
2= (nodes under diaphragm)
3 = (Nodes above the diaphragm
4 = (Mets in the lungs)
```
202
What is the management of testicular cancer
Orchidectomy
Chemo and radiotherapy (More effective in seminomas below diaphragm)
Widespread tumours are treated with chemo and teratomas treated with chemo
203
What is an epididymal cyst
Smooth extra-testicular, spherical cyst in the head of he epididymis that develops around the age of 40 and contains a clear and milky spermatocele fluid
204
What is hydrocele
Abnormal collection of fluid within the tunica vagnalis
205
What are the two forms of hydrocele
Primary = more common, larger and usually present in younger men
Secondary hydrocele is secondary to
- testis tumour
- Trauma
- TB
- Infection
- Testicular torsion
- Generalised oedema
206
What is varicocele
Abnormal dilatation of the testicular veins in the pampiniform venous plexus in the scrotum caused by venous reflux
207
Why might renal cell carcinoma cause left sided varicocele?
If the renal tumour obstructs where the gonadal vein drains into the renal vein blood can back up and so you may see left sided varicocele.
208
Name the classification that helps differentiate between benign cystic lesions and cancerous cystic lesions.
The Bozniak classification.
209
What are the symptoms of a varicocele
Patient complains for a dull ache or scrotal heaviness
Scrotum hangs lower on the side of the varicocele
210
What is the treatment for varicocele
surgery if there is pain, infertility or testicular atrophy
211
What is testicular torsion
Torsion is twisting of the spermatic cord resulting in the occlusion of testicular blood vessels leading to Ischaemia and infarct and potential loss of the testis
212
What is an erection
Neurovascular phenomenon under hormonal control
- arterial dilatation
- smooth muscle relaxation
- Activation of the corporeal veno-occlusive mechanism
213
What is the arterial supply of the penis
Internal iliac
- Internal pudendal artery
(i) Dorsal penile artery
(ii) Cavernosal artery/deep penile arteries
(iii) Bulbar artery
214
What is the venous drainage of the penis
Subtunical plexus
- to circumflex veins
- to deep dorsal veins
Corpora cavernosa
- cavernosa veins
Internal pudendal veins
215
What nerve fibres do cavernous nerves carry?
Parasympathetic: S2-4.
Sympathetic: T11-L2.
216
Describe the physiology of an erection.
1. Parasympathetic stimulation.
2. Arteriolar dilation.
3. Trabecular Smooth muscle relaxation.
4. Testosterone.
217
What is central control of erections
Higher stimuli
- Hypothalamus
- Oxytocin pro erectile pathways
Spinal reflex
218
What are the primary causes of low testosterone
Pituitary
| Hypothalamus
219
What are the secondary causes of low testosterone
Testes
| - Tumour, injury, drugs
220
What are the congenital syndromes associated with low testosterone
Kleinfelters
| Noonans
221
What chemical compound is responsible for the smooth muscle relaxation that is required for an erection?
Nitric oxide (NO). It causes a fall in cytoplasmic calcium -> smooth muscle relaxation.
222
Define erectile dysfunction
Persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance
223
What are the 2 main causes of erectile dysfunction?
1. Organic e.g. vasculogenic, neurogenic, hormonal, anatomical drug induced
2. Psychogenic.
224
What are the risk factors for erectile dysfunction
CVS disease
- Lack of exercise
- Obesity
- Smoking
- Hypercholesterolaemia
- Metabolic syndrome (DM)
Liver disease and alcohol
Renal failure
Trauma (Pelvic fracture)
Iatrogenic (Prostatectomy)
225
Give 3 characteristics of psychogenic erectile dysfunction.
1. Sudden onset
2. Situational.
3. Younger males affected.
4. Good nocturnal and early morning erections
226
What investigations might you do for someone with suspected ED
Fasting glucose
Lipid profile
Morning testosterone
- If low testosterone then perform prolactin, FSH and LH
227
What are the specialised tests for ED
Nocturnal penile tumescence and rigidity
Intracavernosal injection test
Duplex USS of penile arteries
Arteriography
228
What is the goal of ED treatment
treat the reversible factors
229
What is the non-pharmacological management of erectile dysfunction?
1. Lose weight, stop smoking.
| 2. Education and counselling of patient and partner.
230
What is the treatment for testosterone deficiency ED
Testosterone replacement
- contraindicated if history of prostate cancer
- psychosexual counselling
231
What is the first line pharmacological management of erectile dysfunction?
Phosphodiesterase (PDE5) inhibitors e.g. viagra, cialis. They cause vasodilation and so increase arterial blood flow to the penis through action on nitric oxide
232
Name three phosphodiesterase inhibitors
Slidenafil (Viagra)
- effective 30-60 mins after admin
- Reduced efficiency after fatty meal
Tadalafil (Cialis)
- Effective 30 mins after admin
- Efficiency maintained for 36 hours
Vardenafil
- Effective 30 mins after administration
- Reduced effect after fatty meal
233
What are the common side effects of phosphodiesterase inhibitors
```
Headache
Flushing
Dyspepsia
Visual disturbance
Back pain
Myalgia
```
234
What is the second line pharmacological management of erectile dysfunction?
1. Intracavernous injections.
2. Vacuum devices.
3. Apomorphine sublingual
- Central acting dopamine agonist
4. Intraurethral alprostadil
235
What are the complications of intracavernous injections
Penile pain
| Priapism
236
What are the side effects of intraurethral alprostadil
Pain
Dizziness
Urethral bleeding
237
How does a vacuum device work
Passive engorgment with constriction
238
What are the side effects of a vacuum device for ED
Pain
Inability to ejaculate
Petechiae
Bruises and numbness
239
When are vacuum devices contraindicated
Bleeding disorders and anti-coagulants
240
What is the third line pharmacological management of erectile dysfunction?
Penile prosthesis implantation.
(i) Malleable prosthesis
(ii) Inflatable
241
Define priapism
Prolonged erection lasting for >4 hours
242
What is a potential consequence of priapism
Permanent Ischaemic damage
243
Define glomerulonephritis
Broad term that refers to a group of parenchymal kidney disease that results in inflammation of glomeruli and nephrons
244
Give 3 consequences of glomerulonephritis (glomerular disease).
1. Damage to the filtration mechanism = Leaky glomeruli -> haematuria and proteinuria.
2. Damage to glomerulus restricts blood flow = High BP.
3. Deteriorating kidney function due to loss of filtration capacity
245
What are the 4 presentations of glomerulonephritis
1. Asymptomatic haematuria
2. Nephrotic syndrome
3. Nephritic syndrome
4. CKD
246
Briefly describe the pathophysiology of glomerulonephritis (glomerular disease).
Immunologically mediated: immunoglobulin deposits and inflammatory cells.
247
What are the causes of glomerulonephritis
```
Idiopathic
Immune: SLE, goodpastures, vasculitis
Infection: HBV, Strep, HIV
Drugs: Penicillamine, gold
Amyloid
```
248
What are the investigations for someone with suspected glomerulonephritis
```
FBC/U+E/ESR
Abs = ANA, dsDNA, ANCA
Urine dipstick for proteinuria and haematuria
Renal ultrasound and biopsy
CXR for infiltrates
```
249
Describe the pathophysiology of nephritic syndrome
Kidney inflammation and immune réponse triggered by infection with causes large podocytic pores allowing RBC into the urine
250
Give 4 causes of acute nephritic syndrome.
1. ANCA associated vasculitis
2. Goodpastures.
3. SLE.
4. Post streptococcal infection (immune complex deposition in the kidney).
5. IgA nephropathy.
6. DM
7. Systemic sclerosis
251
Give 5 signs of acute nephritic syndrome.
1. Inflammation of glomeruli.
2. HAEMATURIA
3. PROTEINURIA --> oedema
3. Hypertension.
4. Fluid overload.
5. Oliguria and progressive renal impairment
6. Red cell casts.
7. Uraemia (Anorexia, pruritis, lethargy and nausea)
252
What are the signs of IgA nephropathy
Haematuria, IgA deposition in mesangium of the kidney associated with tonsillitis
253
What investigations would you carry out in someone with suspected IgA nephropathy
Diffuse mesangial IgA deposits
| Subendothelial, sub epithelial deposits on electron microscopy
254
What is the treatment for IgA nephropathy
- Induction = steroids and cyclophosphamide
| - Remission = steroids and azathioprine
255
What 4 signs are needed in order to make a diagnosis of nephrotic syndrome.
1. Hypoalbuminaemia (<35g/L) - due to compensatory increase in liver function
2. Oedema (Periorbital, genital, ascites, peripheral) due to decrease in oncotic pressure due albumin loss and movement of fluid into the tissues
3. Heavy proteinuria >3g/24hr due to gaps in podocytes and increase in glomerular perm causing protein to leak out
4. Hypercholesterolaemia.
256
What can nephrotic syndrome be secondary to?
1. Diabetes.
2. Amyloid.
3. Infections.
4. SLE.
5. Drugs.
257
What are the complications of nephrotic syndrome
1. Venous Thromboembolism = hypercoagulable state due to increased clotting factor production in liver
2. Susceptibility to infection due to IgG loss
3. Hyperlipidaemia (increased triglycerides and cholesterol due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin)
258
What are the investigations for someone with suspected nephrotic syndrome
Check bloods for hyperlipidameia and hypoalbuminaemia
Renal biopsy
Urinanalysis (Dipstick) +++ protein
Look for auto-antibodies
259
What are the causes of nephrotic syndrome
1. Minimal change glomerulonephritis
2. Membranous nephropathy
3. Focal segmental glomerulosclerosis
4. Membranoproliferative/mesangiocapillary glomerulonephritis
260
Describe the pathophysiology of minimal change glomerulonephritis
Podocyte loss, vacuolation and microvilli appearance
Commonest cause of nephrotic syndrome in children
261
What is the treatment for minimal change glomerulonephritis
Corticosteroids
262
Describe the pathophysiology of membranous nephropathy
Asymptomatic proteinuria/nephrotic syndrome +/- microscopic haematuria, HTN and renal impairment
263
Membranous nephropathy is associated with what conditions
Lung, colon, breast and stomach cancer
Autoimmune SLE and thyroid disease
Infections = HBV, Hep B or C, Schistosomiasis
Drugs = penicillamine, gold, NSAIDs
264
What investigations would you do for someone with suspected membranous nephropathy
Biopsy showing sub epithelial immune complex deposits (IgG and C3) and thickened glomerular basement membrane
265
What is the treatment for membranous nephropathy
Immunosuppression if renal function declines
266
Membranoproliferative or mesangiocapillary glomerulonephritis is associated with what
HBV
HCV
Endocarditis
Autoimmune
267
What is the management of nephrotic syndrome
1. Treat complications e.g. diuretics (Furosemide or IV bendroflumethiazide) for oedema; ACEi for proteinuria, statin for increased lipids
2. Treat the underlying cause.
3. Statins and anti-coagluation e.g. warfarin.
4. In children give steroids as minimal change disease is the most likely cause.
268
What would you notice on the electron microscopy taken from someone with minimal change disease?
Fused podocytes.
269
What is the treatment for minimal change disease?
Steroids.
270
Describe the pathophysiology behind nephritic syndrome.
Immune complex deposition in glomerular capillary -> neutrophil recruitment -> inflammation and damage to glomerular capillary membrane -> RBC, WBC, protein etc leaks into bowman's capsule and is excreted in the urine.
271
Describe the pathophysiology behind nephrotic syndrome.
Podocytes or basement membrane aren't working properly and so huge amounts of protein leaks into the bowman's capsule and is excreted in the urine.
272
What is the most common renal cancer in children?
Wilms tumour.
273
Is focal segmental glomerulosclerosis a cause of nephritic or nephrotic syndrome?
Nephrotic syndrome.
274
Why is someone with nephrotic syndrome at risk of sepsis?
Because you lose immunoglobulins in the urine.
275
Give 5 functions of the kidney.
1. Filters and excretes waste products from the blood.
2. Regulates BP.
3. Retains albumin.
4. Reabsorption of Na, Cl, K, glucose, H2O, amino acids.
5. Synthesises EPO.
6. Converts 1-hydroxyvitaminD to 1,25-dihydroxyvitaminD.
276
Write an equation for GFR.
(Um X urine flow rate) / Pm.
- Um = concentration of marker substance in urine.
- Pm = concentration of marker substance in plasma.
277
What would you expect a typical GFR to be?
120ml/min.
| 20% of cardiac output
278
Give an example of a marker substance used for estimating GFR.
Creatinine.
279
Estimating GFR: Give 3 essential features of a marker substance.
1. Not metabolised.
2. Freely filtered.
3. Not reabsorbed/secreted.
280
Name a drug that can inhibit creatinine secretion. What is the affect of this on GFR?
Trimethoprim/ cimetidine and ritonavir
| Serum creatinine rises and so kidney function (GFR) appears worse.
281
What is the affect on GFR of afferent arteriole vasoconstriction?
Decreased GFR.
282
What is the affect on GFR of efferent arteriole vasoconstriction?
Increased GFR.
283
Where in the nephron does the bulk of reabsorption occur?
At the proximal convoluted tubule.
284
What 7 things are reabsorbed at the PCT?
1. Sodium.
2. Chlorine.
3. Potassium.
4. Glucose.
5. Water.
6. Amino acids.
7. Bicarbonate.
285
What is Fanconi syndrome?
Failure of the nephron to reabsorb essential ions. Sugar, amino acids and bicarbonate are therefore present in the urine.
286
Give 2 signs of Fanconi syndrome.
1. Sugar in the urine (Glycosuria)
2. Acidotic due to bicarbonate in the urine.
3. Rickets/osteomalacia.
287
Give 2 causes of Fanconi syndrome.
1. Myeloma.
2. Cystinosis.
3. Anti-retrovirals (Tenfovir)
288
What is the function of the counter current multiplication system?
It generates a hypertonic medullary interstitium for H2O reabsorption. Na+ moves out of the ascending limb which increases the medullary osmolality, H2O follows.
289
Which part of the loop of henle is permeable to H2O?
The descending limb is permeable to H2O.
290
Describe tubuloglomerular feedback.
Macula densa cells of the DCT lie between the AA and EA. They detect NaCl and use this as an indicator of GFR.
291
Macula densa cells detect a raised NaCl. What is the response?
AA constriction.
292
Macula densa cells detect a reduced NaCl. What is the response?
Renin secretion.
293
What 2 cell types are found in the nephron collecting duct?
Principal and intercalated cells.
294
What hormone is responsible for regulating sodium reabsorption?
Aldosterone.
295
Why might aldosterone secretion lead to hypokalaemia?
Aldosterone secretion leads to increased sodium reabsorption. Sodium reabsorption leads to increased potassium secretion and therefore hypokalaemia.
296
What is the affect of NSAIDs on the afferent arteriole of glomeruli?
NSAIDs inhibit prostaglandins and so lead to AA vasoconstriction = reduced GFR.
297
NSAIDs lead to a reduced GFR. Why?
NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction -> reduced GFR.
298
What is the affect of ACEi on the efferent arteriole of glomeruli?
ACEi cause EA vasodilation = reduced GFR.
299
Name 2 factors that govern renal potassium.
1. Na+.
| 2. Aldosterone.
300
What ion is responsible for volume control?
Sodium!
301
Name 2 hormones that increase sodium reabsorption.
1. Aldosterone.
| 2. Angiotensin 2.
302
Name a hormone that decreases sodium reabsorption.
ANP.
303
What is the function of EPO?
It stimulates the bone marrow -> RBC maturation.
304
Give 2 functions of calcitriol.
1. Increased calcium and phosphate absorption from the gut.
| 2. Suppression of PTH.
305
Why might someone with advanced CKD also have hyperparathyroidism?
Advanced CKD = calcitriol deficiency. Calcitriol suppresses PTH therefore deficiency -> hyperparathyroidism.
306
What triggers PTH secretion?
Low serum calcium.
307
Give 3 ways in which PTH increases serum calcium.
1. Increased bone resorption.
2. Increased reabsorption of calcium at the kidneys.
3. Stimulates 1-hydroxylase -> 1,25-dihydroxyvitaminD -> increased calcium absorption from the intestine.
308
Name 2 hormones secreted from the posterior pituitary gland.
1. ADH.
| 2. Oxytocin.
309
Describe the function of ADH.
ADH acts on the collecting ducts. It increases insertion of aquaporin 2 channels leading to H2O retention.
310
Give 3 factors that stimulate renin release.
1. Sympathetic stimulation.
2. Decreased BP.
3. Decreased Na detected by macula densa.
311
Give 3 functions of ANP.
1. Renal vasodilator.
2. Inhibits aldosterone.
3. Closes ENaC (decreased reabsorption of Na+).
312
Where on the nephron does aldosterone act?
On the collecting ducts.
313
Describe aldosterone action.
Aldosterone acts on the collecting ducts. It increases ENaC and H+/K+ pumps. There is increased Na+ absorption and K+ secretion -> H20 retention -> increased BP.
314
Blood pressure control is determined by what
1. blood volume
| 2. Vasoconstriction
315
Where do loop diuretics act
Loop of Henle
316
where do thiazide diuretics work
DCT
317
Where do aldosterone antagonists act
Collecting duct
318
How do we measure kidney function
Creatine - waste product of muscle metabolism
eGFR
Proteinuria/Albuminuria
319
What is the definition of chronic kidney disease
Chronic impairment of kidney function normally over 3 months
320
What is the classification of CKD
G1 - >90 ml/min – Kidney damage with normal or increased GFR
G2 – 60-90 ml/min = only CKD if other signs of kidney damage – Kidney damage with mild decrease in GFR
G3a – 45-60 ml/min = mild/moderate CKD
G3b – 30-45 ml/min = moderate/severe CKD
G4 – 15-30 ml/min = severe CKD
G5 - <15ml/min = renal failure
o Albuminuria:
A1 - <30 mg/24h
A2 – 30-300 mg/24h
A3 - >300 mg/24h
321
What are the causes of chronic kidney disease
1. Diabetes mellitus.
2. Hypertension.
3. Atherosclerotic renal vascular disease.
4. Congenital e.g. PKD.
5. Urinary tract obstruction.
6. Glomerulonephritis
7. Drugs
8. SLE
9. Myeloma and amyloidosis
322
Give 5 signs of CKD.
1. Proteinuria.
2. Haematuria and nocturia
3. Impaired eGFR <60ml/min.
4. Rise in serum urea/creatinine.
5. Anaemia (reduced EPO)
- Pallor, fatigue, lethargy
6. Bone disease (Decreased vitamin D = osteomalacia, bone pain)
7. Polyneuropathy.
8. CV disease.
9. Erectile dysfunction.
10. Raised PTH.
11. Confusion, seizures and coma
323
What investigations would you carry out in someone with suspected chronic kidney disease
```
• Blood tests:
o FBC – normochromic normocytic anaemia
o U/Es – raised phosphate and uric acid, decreased Ca and increased PTH
• Urine dipstick – proteinuria and haematuria
• GFR – assess severity
• Imaging – USS for macroscopic damage
Bone X-rays
CXR = cardiomegaly, pleural effusion
```
324
What are the complications of chronic kidney disease
Renal osteodystrophy - Osteoporosis due to decreased 1a-hydroxylase which decreases vitamin D activation leading to decreased Ca2+ and increased PTH. Increased PTH leads to activation of osteoclasts leading to bone resorption and osteoporosis
Anaemia due to reduced EPO production
Cardiovascular disease
325
Describe the management for CKD
1. Treat the underlying cause.
- Hypertension = ACEi/ARB
- Bones = Osteoporosis
- Diabete
Anaemia - give ferrous sulphate IV
2. Slow deterioration of kidney function e.g. maintain BP.
3. Reduce CV risk e.g. statins, smoking cessation, low dose aspirin
4. Treat complications e.g. anaemia.
5. ESRF -> dialysis or transplant.
6. Lifestyle
- Exercise
- Healthy weight
- Stop smoking
- Na, fluid and PO4 restriction
326
What are the three forms of dialysis
Peritoneal dialysis
Haemodialysis
Kidney transplant
327
How often does someone need to go for haemodialysis
3x a week for 4 hours
328
How does haemodialysis work
o Access to the blood supply through a surgically created fistulae (joining of an artery and a vein), thin the blood then pump it through a dialyser where the impurities, salt and excess fluid are drawn into the dialysis solution and the cleansed blood is returned
329
How does peritoneal dialysis work
o Involves infusing a sugary solution into the abdomen which draws off toxins
o Waste in the patients’ blood diffuses into the fluid in the abdomen and the sugary solution moves into the patients circulation which is then absorbed so more sugar can be absorbed and then water moves back
330
What is the access point in haemodialysis?
AV fistula.
331
Why might someone having haemodialysis have a PFTE graft as opposed to an AV fistula?
If the patient has atherosclerotic veins or has had previous fistulas they may have a PFTE graft or a catheter tunnelled into the RA.
332
Give examples of waste products that are removed from the blood in dialysis.
1. Urea.
2. Creatinine.
3. Potassium.
4. Phosphate.
333
Give 5 potential complications of haemodialysis.
1. Hypotension.
2. Cramps.
3. Nausea.
4. Chest pain.
5. Fever.
6. Blocked or infected dialysis catheter.
334
Give 3 groups of people who haemodialysis is good for.
1. People who live alone/frail/elderly.
2. People who fear operating machines.
3. People who are unsuitable for PD e.g. previous abdominal surgery, abdominal hernia etc.
335
What is the access point in peritoneal dialysis?
A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel.
336
Give 4 potential complications of peritoneal dialysis.
1. Infection e.g. peritonitis/catheter exit site infection.
2. Peri-catheter leak.
3. Abdominal wall herniation.
4. Intestinal perforation.
337
Give 3 groups of people who peritoneal dialysis is good for.
1. Young people/those in full time work.
2. People who want control/responsibility of their care.
3. People with severe HF.
338
Where in the abdomen does a transplanted kidney lie?
In the iliac fossa.
339
Describe the criteria for selection of a living donor for kidney transplant.
1. Blood relative.
2. ABO blood group compatible.
3. HLA identical.
4. Excellent medical condition and normal renal function.
340
Name 3 medical conditions that can exclude living kidney donation.
1. Renal parenchymal disease.
2. History of stones/frequent UTI/hypertension/DM.
3. Recent malignancy.
341
Describe the criteria for selection of a cadaver donor for kidney transplant.
1. Irreversible brain damage.
2. Normal renal function.
3. No evidence of pre-existing renal disease or transmissible disease.
4. ABO compatible and best HLA possible.
342
What tests can be done to evaluate kidney function in a potential kidney donor?
1. Serum creatinine.
2. Creatinine clearance.
3. Urinalysis.
4. Urine culture.
5. GFR.
343
Give 5 contraindications for renal transplant.
1. ABO incompatibility.
2. Cytotoxic Ab's against HLA antigens.
3. Recent malignancy.
4. Active infection.
5. AIDS.
6. Morbid obesity.
7. Age > 70 y/o.
344
Give 3 ways in which recipient and donor matching is assessed.
1. HLA tissue typing (important to match DR antigens).
2. Lymphocytotoxic cross matching; checks there are no preformed antibodies against HLA antigens.
3. ABO blood group compatibility.
345
What are 3 surgical complications of kidney transplant
Thrombosis
Obstruction
Infection
346
Give 4 factors that can influence the longevity of renal allograft.
1. Age.
2. HLA matching.
3. Ischaemia time.
4. Number of acute rejection episodes.
5. Ethnicity.
347
What are the 2 major causes of allograft failure?
1. Chronic rejection.
| 2. Death with functioning graft.
348
What are the 2 major causes of death after kidney transplant?
1. CV disease.
| 2. Infection.
349
Name the 3 types of renal allograft rejection.
1. Hyper-acute.
2. Acute.
3. Chronic.
350
Describe hyper-acute renal allograft rejection.
Preformed antibodies against HLA antigens of donor organ.
351
Why might someone have pre-formed antibodies against HLA antigens?
Can be a consequence of blood transfusion, pregnancy, prior transplant, auto-immune disease.
352
What can cause immediate graft loss?
Fibrinoid necrosis.
353
Describe acute renal allograft rejection.
Activated T lymphocytes. Occurs within the first 6 months but is often reversible e.g. with steroids.
354
Describe chronic renal allograft rejection.
Slow and gradual decline in renal function, accompanied by proteinuria and increased creatine
355
Give 3 consequences of chronic immunosuppression.
1. Malignancy.
2. Infection.
3. SE's of other drugs.
356
Name a loop diuretic.
Furosemide - acts on Na+/K+/2Cl- transporter (NKCC2).
357
Give 3 potential side effects of furosemide.
1. Hypokalaemia.
2. Hypotension.
3. Dehydration.
358
What other drug might you prescribe with furosemide in someone with poorly controlled potassium?
A potassium sparing diuretic e.g. spironolactone. These work on RAAS (hormonal systems) as opposed to ion channels and should help control potassium levels in the blood.
359
Name a potassium sparing diuretic.
Spironolactone.
360
On which part of the nephron do thiazides act?
The distal tubule.
| Act on NCC channels.
361
Describe the fluid distribution in the body.
ICF: 28L.
ECF: 14L
- Interstitial: 11L.
- Plasma: 3L.
362
How much extra-vascular fluid is there in the body?
ICF + interstitial = 39L.
363
Fluid Movement is determined by what?
* Hydrostatic pressure
* Osmotic pressure (Salt and electrolytes)
* Oncotic pressure (protein)
364
What is the normal daily fluid intake for an adult
is 1.5L-2L daily for relatively sedentary lifestyle
365
What happens to the heart rate in hypovolaemia?
Increases - tachycardia.
366
What happens to the blood pressure in hypovolaemia?
Decreases - hypotension.
367
What happens to the JVP in hypovolaemia?
JVP is low.
368
What happens to tissue turgor in hypovolaemia?
Tissue turgor is reduced.
369
What happens to urine output in hypovolaemia?
Urine output is reduced.
370
What happens to weight in hypovolaemia?
Weight is reduced.
371
Give 2 symptoms of hypovolaemia.
Thirst and dizziness.
372
What happens to creatinine, haemoglobin and haematocrit levels in hypovolaemia?
They are raised.
373
Name 5 groups of people who are at risk of hypovolaemia.
1. Elderly.
2. Those who have had an ileostomy.
3. People with short bowel syndrome.
4. Bowel obstruction.
5. People taking diuretics.
374
Name 5 groups of people who are at risk of hypervolaemia.
1. Acute kidney injury patients.
2. CKD patients.
3. Heart failure patients.
4. Liver failure patients.
375
What happens to the heart rate in hypervolaemia?
HR is normal.
376
What happens to blood pressure in hypervolaemia?
Blood pressure is high or normal.
377
What happens to JVP in hypervolaemia?
JVP is high.
378
What happens to tissue turgor in hypervolaemia?
Tissue turgor is normal.
379
What happens to urine output in hypervolaemia?
Urine output is normal.
380
What happens to weight in hypervolaemia?
Weight is increased.
381
Give 2 symptoms of hypervolaemia.
1. Shortness of breath.
| 2. Peripheral oedema.
382
What happens to creatinine, haemoglobin and haematocrit levels in hypervolaemia?
They are reduced.
383
Where might fluid accumulate in someone with hypervolaemia?
- Pulmonary oedema.
- Pleural effusion.
- Ascites.
- Bowel obstruction.
- Intra-abdominal collection.
384
Describe the management for hypovolaemia.
1. Oral fluid.
2. IV fluid if very ill.
3. Treat reversible causes.
4. Stop taking blood pressure medications
385
Describe the management for hypervolaemia.
1. Diuretics e.g. furosemide.
2. Fluid restriction 1-1.5L daily
3. Treat reversible causes.
386
Name 3 isotonic solutions.
1. 5% dextrose.
2. 0.9% NaCl.
3. Hartmann's solution.
387
What type of IV fluid moves from the intra-vascular to the extra-vascular space?
Crystalloid.
388
Give an example of a colloid IV fluid.
Gelofusine.
389
Why do advanced CKD patients need regular fluid assessment?
They may be oligouric or anuric.
390
Give 3 potential causes of rising creatinine.
1. Too aggressive with diuretics.
2. Extravascular hypervolaemia but intravascular hypovolaemia.
3. Progression of CKD.
391
Define urinary tract infection.
Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriruria and pyuria.
392
Name 3 UTI causative organisms.
1. Uropathogenic strains of E.coli (UPEC) - 82%.
2. CNS e.g. stapylococcus.saprophyticus.
3. Proteus mirabilis.
4. Enterococci.
5. Klebsiella pneumonia.
6. P.aeruginosa
7. STI's = C.trachomatis and N. Gonorrhoea
393
Briefly describe the epidemiology of UTI's.
More common in women due to short urethra and its proximity to the anus.
394
Describe the pathophysiology of UTI's.
Organisms colonise the urethral meatus and ascend via the transurethral route. leading to bacteriuria
395
What can facilitate bacteria ascent into the urinary tract via the urethra?
1. Sexual intercourse.
| 2. Catheterisation.
396
Give 3 bacterial virulence factors that aid their ability to cause UTI's.
1. Fimbriae/pili that adhere to urothelium.
2. Acid polysaccharid coat resists phagocytosis.
3. Toxins e.g. UPEC releases cytotoxins.
4. Enzyme production e.g. urease.
397
The vagina is heavily colonised with lactobacilli. What is the function of this?
Helps maintain a low pH = host defence mechanism.
398
Give 2 reasons why a post menopausal woman is more susceptible to a UTI.
1. pH rises -> increased colonisation by colonic flora.
| 2. Reduced mucus secretion.
399
Give 5 host defence mechanisms against urinary tract infection.
1. Antegrade flushing of urine.
2. Tamm-horsfall protein.
3. GAG layer.
4. Low urine pH.
5. Commensal flora.
6. Urinary IgA.
400
What is pyuria?
The presence of leukocytes in urine.
401
Name 4 lower urinary tract infections.
1. Cystitis.
2. Prostatitis.
3. Epididymitis.
4. Urethritis.
402
Name 1 upper urinary tract infection.
Pyelonephritis.
403
What investigations might you do on someone who you suspect has a UTI?
1. Take a good history.
2. Urinalysis - multistix SG.
3. Microscopy; culture and sensitivity of mid-stream urine.
4. In recurrent/complicated UTI renal imaging is important.
404
What determines if a UTI is complicated or uncomplicated?
A UTI is deemed complicated if it affects:
- Someone with an abnormal urinary tract.
- A man.
- A pregnant lady.
- Children.
- The immunocompromised.
- If it is recurrent.
405
What is the first line treatment for an uncomplicated UTI?
- Trimethoprim or nitrofurantoin for 3 days.
| - Increased fluid intake and regular voiding.
406
How does trimethoprim work?
It affects folic acid metabolism.
407
Describe the management for a complicated UTI.
Same as for an uncomplicated UTI but a MCS MSU is essential! The patient would normally take a longer Abx course tailored to sensitivity.
408
Give 3 causes of recurrent UTI's.
1. Re-infection.
2. Bacterial persistence.
3. Unresolved infection.
409
Define recurrent UTI.
> 2 episodes in 6 months of > 3 in 12 months.
410
Describe the management for someone who is having recurrent UTI's.
1. Increase fluid intake.
2. Regular voiding.
3. Void pre and post intercourse.
4. Abx prophylaxis.
5. Vaginal oestrogen replacement.
411
What are the risk factors for UTI development
```
Female
Sex
Pregnancy
Menopause
DM
Abnormal tract - stones, obstruction, catheter, malformation
```
412
What is cystitis?
Inflammation of the bladder secondary to infection.
413
Give 4 risk factors for cystitis.
1. Obstruction.
2. Previous damage to bladder epithelium.
3. Bladder stones.
4. Poor bladder emptying = urinary retention
414
Give 3 symptoms of cystitis.
1. Dysuria.
2. Frequency.
3. Urgency.
4. polyuria
5. Suprapubic tenderness and loin and abdominal pain
6. Foul smelling urine
415
What are the investigations for someone with cystitis
Microscopy and sensitivity of mid stream urine
| Dipstick urinalysis
416
What is the treatment for cystitis
First line = trimethoprim or cefalexin
| Second line = Ciprofloxacin or co-amoxiclav
417
Define prostate inflammation
Prostate inflammation
418
What is the causative agents for prostatitis
E.coli, proteus and klebsiella and chlamydia
419
Give 5 symptoms of acute bacterial prostatitis (type 1).
1. Systemically unwell, fever.
2. Rigors.
3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow).
4. Pelvic pain.
420
Give 4 symptoms of chronic bacterial prostatitis (type 1).
1. Recurrent UTI's.
2. Pelvic pain.
3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow).
4. Uropathogens in urine.
The patient should have had the symptoms for >3 months.
421
What investigations might you do in someone with prostatitis?
1. Urinalysis and MSU.
2. Semen cultures.
3. STI screen.
4. Bloods including MCS.
5. DRE
422
Describe the treatment for type 1 prostatitis = acute
- IV Abx e.g. gentamicin, co-amoxiclav for 2-4 weeks.
423
Describe the treatment for type 2 prostatitis = chronic
- 4-6 weeks quinolone e.g. ciprofloxacin or trimethoprim
424
Define urethritis
Inflammation of the urethra
425
What are the causative agents of urethritis
STI's e.g. gonorrhoea, chlamydia.
| Non STI causes = trauma, urethral stricture and urinary calculi
426
Give a symptom of urethritis.
dysuria, hesitancy, urethral discharge (gonorrhoea), urethral pain, penile discomfort
427
What are the investigations for someone with suspected urethritis
urethral smear, urinalysis, STI screening, Nucleic Acid Amplification Test (NAAT) Female = vaginal swab and male = first void volume
428
What is the treatment of urethritis
Treat the STI
Chlamydia = Azithromycin or erythromycin if preggers
Gonorrhoea = Ceftriaxone with azithromycin
429
What is epididymo-orchitis?
Inflammation of the epididymis and testicle.
430
What are the causative organisms of epididymo-orchiditis
o STI – N. gonorrhoea, C. trachomatis
| o Non-STI – E. coli, enterococci, mumps, TB
431
What are the risk factors for someone with epididymo-orchiditis
Previous infection, indwelling catheter, structural abnormality of urinary tract
432
Give 3 symptoms of epididymo-orchitis.
unilateral scrotal pain +/- swelling, UTI symptoms, fever, urethral discharge, on examination there is tenderness and palpable swelling of the epididymis and testicles
433
Describe the aetiology of epididymo-orchitis.
1. If <35 y/o = STI e.g. chlamydia.
| 2. If >35 y/o = UTI.
434
What investigations might you do on someone who you suspect has epididymo-orchitis?
1. Void urine.
2. Urethral swab.
3. MSU.
4. Dipstick
Rule out testicular torsion!
435
Describe the treatment for epididymo-orchitis.
1. If STI aetiology suspected; refer to GUM and maybe give doxycycline.
2. If UTI aetiology suspected give quinolone (ciprofloxacin).
Pain relief and abstinence from sex
436
Define pyelonephritis.
Inflammation secondary to infection of the renal parenchyma and soft tissues of the renal pelvis.
437
What can cause pyelonephritis?
UPEC. Typically P pili.
| Infection is usually from the bladder or patients own bowel flora
438
Give 3 symptoms of pyelonephritis.
1. Loin pain.
2. Fever.
3. Pyuria.
4. Malaise
5. Rigor
6. Vomiting
7. Septic shock
439
What investigations might you do in someone with pyelonephritis?
1. Urinalysis.
2. MCS MSU.
3. Bloods - raised WCC, ESR and CRP.
440
Describe the treatment for pyelonephritis.
IV fluids and antibiotics e.g. gentamicin/co-amoxiclav.
- Drain obstructed kidney.
- Catheterise if necessary.
- Analgesics.
441
What is the likely cause of pyelonephritis in children?
Reflux or structural/functional abnormalities.
442
Gonorrhoea is caused by what
Neisseria gonorrhoea gram negative diplococci
443
Describe the epidemiology of gonorrhoea
More common in men (25-30)
| Urethra is primary infection site
444
What are the symptoms of gonorrhoea
Dysuria
Discharge
Menstrual irregularity in women
445
What investigations would you carry out in someone with suspected gonorrhoea
1. Genital secretions from urethra (Male) and endocervix (Female)
2. Microbiology look for gram -ve diplococci with polymorph cytoplasm
3. Nucleic acid amplification test (NAAT)
446
What is the management of someone with gonorrhoea
Partner notification and further STI testing
| Ceftriaxone and azithromycin
447
What is the causative agent of chlamydia
Chlamydia trachomatis infection (Gram negative)
448
What is the epidemiology of chlamydia
More common in women between 16 and 20
449
What are the symptoms of chlamydia
Dysuria, discharge and menstrual irregularities
450
What are the investigations for someone with suspected chlamydia
o Vaginal/endocervical swab (F) or first void urine (M)
| o Nucleic Acid Amplification Test (NAAT)
451
What is the management of chlamydia
o Partner notification and further STI testing
| o Treatment – 1g oral azithromycin or doxycycline -> 500mg erythromycin 14 days in pregnancy
452
What are the complications of STI's
Reactive arthritis
Epididymo-orchitis
Pelvic inflammatory pain
453
Why is notification of partner important in STIs
Prevent reinfection of index patient
Prevent complications in asymptomatic contacts
454
What is the causative bacteria in syphilis
Treponema pallidus subspecies pallidum
455
What are the symptoms of primary syphilis infection
Any anogenital ulcer is syphilis until proven otherwise
Macule at the site of sexual contact which becomes very infectious, painless hard ulcer (Chancre)
456
What are the symptoms of secondary syphilis
Occurs 4-8wks after chancre there is fever, malaise, lymphadenopathy, rash (Trunk, face, palms and soles), alopecia, hepatitis, iritis
457
What are the symptoms of tertiary syphilis
Following 2 to 20 years of latency there are gummas (granulomas occurring in the skin, mucosa, bones, joints, viscera ie lung and testis)
458
What are the symptoms of quaternary syphilis
Cardiovascular = Aortic aneurysms and aortic regurgitation
Neurosyphilis = CN palsies, stroke, dementia, psychoses
Sensory ataxia
459
What tests would you do in someone with syphilis
```
Cardiolipin Antibody (Venereal disease research laboratory)
Treponeme specific antibody (T. pallidum haemagglutination test)
```
In primary syphilis, treponemes may be seen by dark ground microscopy of chancre fluid (Serology often -ve at this point)
In secondary syphilis, treponemes are seen in lesions and both types are of antibody are positive
460
What are the treatments for syphilis
Penicillin injection
| Partner notification and follow up
461
Describe the Anderson and May model for STI and HIV
R=BCD
R = Reproductive rate = rate at which organism reproduces itself
B = infectivity rate= chance of infection passing per potential exposure (Depends on behaviour ie. condom use, type of sex)
C = Partners over time = numbers of opportunities for transmission with concurrent partners effective at sustaining transmission
D = Duration of infection, reduced by access to services screening high risk populations, influenced by health awareness and health seeking behaviour
462
What is primary prevention of STIs and give some examples
Reduce the risk of acquiring an STI in the first place
- STI awareness public campaigns to reduce personal risk behaviour 'Sex worth talking about'
- One to one risk reduction discussion (Structured interventions based on behaviour change theory)
- Vaccinate ie. Hep B and HPV and pre and post exposure prophylaxis
463
Describe the pre and post exposure prophylaxis for STI
1. Post exposure prophylaxis (PEP/PEPSE) which are available A and E and sexual health services
2. Pre-exposure prophylaxis (PrEP)
3. Treatment as prevention (TasP)
464
What is secondary prevention for STIs
Find and treat undetected cases of infection thereby removing the community pool
- Early access to STI/HIV test/treatment
- Partner notification (Contact tracing)
- Targeted screening (Antenatal screening for HIV and syphilis, National chlamydia screening programme, HIV home tests)
465
What is the tertiary prevention for STIs
Reduce morbidity and mortality
- Anti retrovirals for HIV
- Prophylactic antibiotics for PCP
- Acyclovir for suppression of genital herpes
466
What is partner notification
A public health activity that aims to control infection by identifying key individuals and sexual networks, warn the unsuspecting and attempt to break the chain of infection
467
Why do we trace partners
(i) Break the chain of transmission
(ii) Prevent the re-infection of the index patient
(iii) Prevent complications of untreated infection
468
How are partners traced?
Patient referral
Provider referral (Phone, text, letter, internet sites)
Conditional or contract referral
Emphasis on patient choice and confidentiality
469
Where do urinary tract stones
Anywhere from the collecting duct of the kidneys to the external urethral meatus
470
What are the three locations that urinary stones are likely to get stuck
Uteropelvic junction
Pelvic rim
Vesourteric junction
471
Describe the epidemiology of stones in the urinary tract.
- 10-15% lifetime risk.
- Males > females - 2:1 ratio.
- Common among 30-50 y/o.
472
What are the components of urinary stones
– calcium based (oxalate and phosphate), uric acid, cystine, struvite
473
Give 5 potential causes of stones in the upper urinary tract.
1. Congenital abnormalities (Horseshoe kidney, spina bidifa)
2. Metastable urine
3. Hypercalciuria/ high urate/ high oxalate.
4. Dehydration!
5. Infection.
6. Acquired (Trauma, obstruction, reflux)
474
Give 5 symptoms of upper urinary tract stones.
1. Rapid onset unilateral Loin pain -> groin pain.
2. 'Renal colic' - pain caused by a blockage in the urinary tract.
3. UTI symptoms e.g. dysuria, urgency, frequency.
4. Recurrent UTI's.
5. Haematuria and proteinuria
6. Unable to get comfortable associated with nausea and vomiting
475
Give 5 ways in which urinary tract stones can be prevented.
1. Stay well hydrated.
2. Low salt diet.
3. Healthy protein intake.
4. Reduced BMI.
5. Active lifestyle.
6. Deacidifcation of urine can prevent uric acid stones.
476
What investigations might you do to find out what is causing someone's renal colic?
1. Bloods - inc. calcium, phosphate and urate.
2. Urinalysis.
3. MCS Mid Stream Urine.
4. Non Contrast CT-KUB (Kidneys, ureters and bladder) - gold standard!
5. KUB XR
6. Ultrasound for hydronephrosis
477
Describe the treatment for renal colic.
1. Analgesia e.g. NSAIDs (diclofenac).
2. Anti-emetics.
3. Check for sepsis.
4. IV fluids and antibiotics if infection present
478
If someone presents with pyelonephritis, what is the treatment option
Drainage
- Nephrostomy
- Ureteric stent
479
Describe the treatment options for urinary stones.
1. Conservative e.g. if stone is <5mm and in a safe location or if the patient is asymptomatic or co-morbid.
2. Medical e.g. nifedipine.
3. Lithotripsy - fragment stones which will then pass spontaneously.
4. Surgical e.g. ureteroscopic; PCNL for larger 'stag horn' stones; nephrectomy.
480
Where in the nephron are urinary tract stones formed?
In the collecting ducts.
481
What is the treatment for urosepsis
Treat with IV antibiotics, oxygen and surgical drainage
482
Describe the pathophysiology of congenital polycystic kidney disease.
Genetic mutation -> predisposition to cyst development -> cell proliferation and loss of planar polarity -> fluid secretion and cyst expansion.
483
Describe the pathophysiology of acquired polycystic kidney disease.
Cysts develop over time.
| Renal injury/ischaemia -> abnormal cell proliferation.
484
What classification can be used to help differentiate between benign cystic lesions and cancerous lesions?
Bozniak classification.
485
Give 4 congenital causes of renal cysts.
1. ADPKD.
2. ARPKD.
3. VHL.
4. OFD1 (oral-facial-digital syndrome 1).
486
What is ADPKD?
An autosomal dominant condition characterised by progressive cyst development. Cysts increase in size -> renal enlargement and loss of function -> kidney failure.
487
A mutation in which genes can cause ADPKD?
1. PKD1 (associated with more severe disease).
| 2. PKD2.
488
Give 4 signs of ADPKD.
1. Hypertension.
2. Haematuria.
3. Polyuria.
4. Abdominal/loin pain.
5. Palpable bilateral costo-vertebral masses.
489
Give 2 extra-renal manifestations of ADPKD.
1. Polycystic liver disease.
| 2. Intracranial aneurysms e.g. SAH.
490
How can ADPKD be diagnosed?
- Symptoms.
- Family history.
- High BP.
- Urinalysis.
- USS.
491
What value can be used as a prognostic marker for ADPKD?
TKV - total kidney volume.
492
A mutation in what gene can cause AD tubulo-interstitial kidney disease?
HNF1 beta.
493
A mutation in what gene can cause ARPKD?
PKHD1.
494
Give 4 features of acquired renal cystic disease.
1. No genetic mutation.
2. No family history.
3. Normal kidney size.
4. Risk factor for renal cell carcinoma.
495
A 50 y/o M presents with haematuria. On examination he has HTN, increased serum Cr and urea, proteinuria and bilateral palpable costo-vertebral angle masses. You take a family history and find out that his dad died of a sub-arachnoid haemorrhage. What is the most likely diagnosis?
ADPKD.
496
At what age do people with ADPKD normally present?
Normally present around 50 y/o.
497
Why might someone with ADPKD have bilateral palpable costovertebral masses?
Cysts increase in size and cause renal enlargement. Often the kidney's can be HUGE!
498
What is the affect of AKI on creatinine and urine output?
- Creatinine is raised.
| - Urine output is reduced.
499
Give 5 risk factors for AKI.
1. Increasing age.
2. CKD.
3. HF.
4. Diabetes mellitus.
5. Nephrotoxic drugs e.g. NSAIDs and ACEi.
500
Give a pre-renal cause of AKI.
1. Hypertension.
2. Heart failure.
3. Nephrotoxic drugs.
501
Give 5 renal causes of AKI.
1. Nephrotoxic drugs.
2. Vasculitis.
3. Autoimmune.
4. Acute tubular necrosis.
5. Glomerulonephritis.
502
What is the major complication someone with AKI might develop?
Hyperkalaemia!
| This can lead to arrhythmias
503
What investigations might you do to determine whether someone has AKI?
1. Check potassium!
2. Bloods: creatinine, U+E.
3. Urine output.
4. Auto-antibodies.
504
How can hyperkalaemia be prevented in someone with AKI?
1. Give calcium gluconate to protect the myocardium.
2. Give insulin and dextrose.
Insulin drives potassium into cells and dextrose is to rebalance the blood sugar
505
A patient presents complaining that they are hardly passing any urine and in the small amount of urine they do pass there is blood in it. On further questioning they tell you they have recently finished a course of antibiotics (amoxicillin) for a chest infection they had 2 weeks ago. Their BP is high. What is the likely cause?
Nephritic syndrome
506
How does the epidemiology differ between ADPKD and ARPKD?
People with ADPKD normally present in middle age whereas people with ARPKD present in infancy.
A sudden rise in creatinine level and a decreased urine output would be indicative of what?
AKI.
507
What drug must you not give to someone with renal artery stenosis?
ACE inhibitors e.g. ramipril.
508
Give 5 causes of haematuria.
1. Kidney tumour, trauma, stones, cysts.
2. Ureteric stones or tumour.
3. Bladder infection, stones or tumour.
4. BPH or prostate cancer.
509
What further investigations might you do in someone who presents with haematuria?
1. Urinalysis.
2. Urine cytology.
3. Abdomen US.
4. Abdomen CT.
5. Cystoscopy.
