GU Flashcards
1
Q
What anatomical structures make up the lower urinary tract?
A
Bladder -> bladder neck -> prostate gland -> urethra and urethral sphincter.
2
Q
Give 4 functions of the lower urinary tract.
A
- Storage of urine.
- Converts the continuous process of excretion to an intermittent, controlled and volitional process.
- Prevents leakage of stored urine.
- Allows rapid, low pressure voiding.
3
Q
Is the detrusor muscle relaxed or contracted during storage?
A
Relaxed.
4
Q
Is the detrusor muscle relaxed or contracted during voiding?
A
Contracted.
5
Q
Is the urethral sphincter relaxed or contracted during storage?
A
Contracted.
6
Q
Is the urethral sphincter relaxed or contracted during voiding?
A
Relaxed.
7
Q
What type of epithelium lines the bladder?
A
Urothelium (transitional epithelium) - pseudo-stratified.
8
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.
9
Q
What are lower urinary tract symptoms (LUTS) in men > 50 likely to be due to?
A
Benign prostatic enlargement.
10
Q
LUTS: give 3 symptoms of storage problems.
A
- Frequency.
- Urgency.
- Nocturia.
11
Q
LUTS: give 4 symptoms of voiding problems.
A
- Straining.
- Hesitancy.
- Incomplete emptying.
- Poor flow.
12
Q
What might dysuria suggest?
A
Inflammation.
13
Q
What investigations might you do on someone who presents with LUTS.
A
- Urinary tests e.g. dipstick.
- Urinary flow: maximum flow rate and residual volume are important.
- Symptom assessment: international prostate scoring system.
- Blood tests e.g. PSA, U+E.
14
Q
Give 3 causes of nocturnal polyuria.
A
- Habitual.
- Congestive cardiac failure.
- Sleep apnea.
15
Q
Describe the treatment for someone who presents with mild LUTS.
A
Reassurance, watch and wait.
16
Q
Describe the treatment for someone who presents with moderate LUTS.
A
- Fluid management, avoid caffeine.
2. Bladder drill.
17
Q
Give 2 pharmacological therapies used in the treatment of moderate to severe LUTS.
A
- Alpha-1-blockers e.g. tamulosin.
2. 5-alpha-reductase-inhibitors.
18
Q
How do alpha-1-blockers work in the management of LUTS?
A
They cause vasodilation and so reduced resistance to bladder outflow.
19
Q
Give 2 potential side effects of tamulosin.
A
Tamulosin is an alpha-1-blocker used in the treatment of LUTS. 2 side effects include hypotension and retrograde ejaculation.
20
Q
How do 5-alpha-reductase-inhibitors work in the management of LUTS?
A
They inhibit the conversion of testosterone to dihydrotestosterone and so reduce prostate size.
21
Q
Give a surgical treatment for BPE.
A
TURP.
22
Q
Give 5 potential consequences of untreated LUTS.
A
- Bladder calculi (stones).
- UTI.
- Urinary incontinence.
- Reduced QOL.
- Acute urinary retention.
23
Q
Give 3 symptoms of acute urinary retention.
A
- PAINFUL!
- Sudden onset.
- > 500ml of urine in bladder.
24
Q
Name a rare but serious cause of acute urinary retention.
A
Spinal cord compression.
25
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.
26
Describe the treatment for someone with acute urinary retention.
Reassurance, catheterise, pain relief.
27
What nerve fibres do cavernous nerves carry?
Parasympathetic: S2-4.
Sympathetic: T11-L2.
28
Describe the physiology of an erection.
1. Parasympathetic stimulation.
2. Arteriolar dilation.
3. Smooth muscle relaxation.
4. Testosterone.
29
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.
30
What are the 2 main causes of erectile dysfunction?
1. Organic e.g. vasculogenic, neurogenic, hormonal, anatomical.
2. Psychogenic.
31
Give 3 characteristics of psychogenic erectile dysfunction.
1. Sudden.
2. Situational.
3. Younger males affected.
32
Give 4 risk factors for erectile dysfunction.
1. Obesity.
2. Lack of exercise.
3. Smoking.
4. Diabetes mellitus.
33
What is the non-pharmacological management of erectile dysfunction?
1. Lose weight, stop smoking.
| 2. Education and counselling of patient and partner.
34
What is the first line pharmacological management of erectile dysfunction?
Phosphodiesterase inhibitors e.g. viagra, cialis. They cause vasodilation and so increase arterial blood flow to the penis.
35
What is the second line pharmacological management of erectile dysfunction?
1. Intracavernous injections.
| 2. Vacuum devices.
36
What is the third line pharmacological management of erectile dysfunction?
Penile prosthesis implantation.
37
What is priapism?
Prolonged erection, lasting for >4 hours.
38
What is a potential consequence of priapism?
Permanent ischaemic damage.
39
Where might a transitional cell carcinoma arise?
1. Bladder (50%).
2. Ureter.
3. Renal pelvis.
40
Describe the epidemiology of transitional cell carcinoma.
1. M:F = 3:1.
| 2. Age > 40 y/o.
41
Give 5 risk factors for transitional cell carcinoma.
1. SMOKING.
2. Occupational exposure e.g. working in rubber factories (aromatic amines).
3. Increasing age.
4. Male gender.
5. Family history.
42
Give 5 symptoms of transitional cell carcinoma.
1. PAINLESS HAEMATURIA.
2. Frequency.
3. Urgency.
4. Dysuria.
5. Urinary tract obstruction.
43
Give 5 investigations that you might do in someone who you suspect has transitional cell carcinoma.
1. Urine dipstick.
2. Blood tests.
3. Flexible cystoscopy = diagnostic.
4. Imaging of upper urinary tract e.g. CT IVU.
5. TURBT.
44
Give 2 potential risks of flexible cystoscopy.
1. UTI's.
| 2. Problems passing urine.
45
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.
CT IVU, USS and XR can be used.
46
Why might you do a trans-urethral resection of bladder tumour (TURBT) in someone with TCC?
For histological and staging analysis.
47
What staging system is used for TCC?
TNM staging.
48
Describe the treatment for non-muscle invasive bladder cancer (CIS, Ta, T1).
1. TURBT.
| 2. Chemotherapy to reduce the risk of recurrence and progression to muscle invasion.
49
Describe the treatment for muscle invasive bladder cancer (T2, T3).
1. Radical cystectomy = gold standard.
2. +/- neo-adjuvant chemotherapy.
3. Radical radiotherapy if not fit/unwilling to undergo cystectomy.
50
Describe the treatment for T4 TCC (invasion beyond the bladder).
1. Palliative chemo/radiotherapy.
| 2. Chronic catheterisation for pain.
51
Name a helminth that can cause squamous cell carcinoma of the bladder.
Schistosomiasis.
52
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.
53
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.
54
What would you expect a typical GFR to be?
120ml/min.
55
Give an example of a marker substance used for estimating GFR.
Creatinine.
56
Estimating GFR: Give 3 essential features of a marker substance.
1. Not metabolised.
2. Freely filtered.
3. Not reabsorbed/secreted.
57
Name a drug that can inhibit creatinine secretion. What is the affect of this on GFR?
Trimethoprim.
| Serum creatinine rises and so kidney function (GFR) appears worse.
58
What is the affect on GFR of afferent arteriole vasoconstriction?
Decreased GFR.
59
What is the affect on GFR of efferent arteriole vasoconstriction?
Increased GFR.
60
Where in the nephron does the bulk of reabsorption occur?
At the proximal convoluted tubule.
61
What 7 things are reabsorbed at the PCT?
1. Sodium.
2. Chlorine.
3. Potassium.
4. Glucose.
5. Water.
6. Amino acids.
7. Bicarbonate.
62
What is Fanconi syndrome?
Failure of the nephron to reabsorb essential ions. Sugar, amino acids and bicarbonate are therefore present in the urine.
63
Give 2 signs of Fanconi syndrome.
1. Sugar in the urine.
2. Acidotic due to bicarbonate in the urine.
3. Rickets/osteomalacia.
64
Give 2 causes of Fanconi syndrome.
1. Myeloma.
| 2. Cystinosis.
65
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.
66
Which part of the loop of henle is permeable to H2O?
The descending limb is permeable to H2O.
67
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.
68
Macula densa cells detect a raised NaCl. What is the response?
AA constriction.
69
Macula densa cells detect a reduced NaCl. What is the response?
Renin secretion.
70
What 2 cell types are found in the nephron collecting duct?
Principal and intercalated cells.
71
What hormone is responsible for regulating sodium reabsorption?
Aldosterone.
72
Why might aldosterone secretion lead to hypokalaemia?
Aldosterone secretion leads to increased sodium reabsorption. Sodium reabsorption leads to increased potassium secretion and therefore hypokalaemia.
73
What is the affect of NSAIDs on the afferent arteriole of glomeruli?
NSAIDs inhibit prostaglandins and so lead to AA vasoconstriction = reduced GFR.
74
NSAIDs lead to a reduced GFR. Why?
NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction -> reduced GFR.
75
What is the affect of ACEi on the efferent arteriole of glomeruli?
ACEi cause EA vasodilation = reduced GFR.
76
Name 2 factors that govern renal potassium.
1. Na+.
| 2. Aldosterone.
77
What ion is responsible for volume control?
Sodium!
78
Name 2 hormones that increase sodium reabsorption.
1. Aldosterone.
| 2. Angiotensin 2.
79
Name a hormone that decreases sodium reabsorption.
ANP.
80
What is the function of EPO?
It stimulates the bone marrow -> RBC maturation.
81
Give 2 functions of calcitriol.
1. Increased calcium and phosphate absorption from the gut.
| 2. Suppression of PTH.
82
Why might someone with advanced CKD also have hyperparathyroidism?
Advanced CKD = calcitriol deficiency. Calcitriol suppresses PTH therefore deficiency -> hyperparathyroidism.
83
What triggers PTH secretion?
Low serum calcium.
84
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.
85
Name 2 hormones secreted from the posterior pituitary gland.
1. ADH.
| 2. Oxytocin.
86
Describe the function of ADH.
ADH acts on the collecting ducts. It increases insertion of aquaporin 2 channels leading to H2O retention.
87
Give 3 factors that stimulate renin release.
1. Sympathetic stimulation.
2. Decreased BP.
3. Decreased Na detected by macula densa.
88
Give 3 functions of ANP.
1. Renal vasodilator.
2. Inhibits aldosterone.
3. Closes ENaC (decreased reabsorption of Na+).
89
Where on the nephron does aldosterone act?
On the collecting ducts.
90
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.
91
Define urinary tract infection.
Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriruria and pyuria.
92
Name 3 UTI causative organisms.
1. Uropathogenic strains of E.coli (UPEC) - 82%.
2. CNS e.g. s.saprophyticus.
3. Proteus mirabilis.
4. Enterococci.
5. Klebsiella pneumonia.
93
Briefly describe the epidemiology of UTI's.
More common in women due to short urethra and its proximity to the anus.
94
Describe the pathophysiology of UTI's.
Organisms colonise the urethral meatus and ascend via the transurethral route.
95
What can facilitate bacteria ascent into the urinary tract via the urethra?
1. Sexual intercourse.
| 2. Catheterisation.
96
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.
97
What do type 1 pili bind to?
Uroplakin.
98
What do type P pili bind to?
Glycolipids on urothelium.
99
What type of pili would you associate with a lower UTI?
Type 1.
100
What type of pili would you associate with an upper UTI?
Type P.
101
The vagina is heavily colonised with lactobacilli. What is the function of this?
Helps maintain a low pH = host defence mechanism.
102
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.
103
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.
104
What is pyuria?
The presence of leukocytes in urine.
105
Name 4 lower urinary tract infections.
1. Cystitis.
2. Prostatitis.
3. Epididymitis.
4. Urethritis.
106
Name 1 upper urinary tract infection.
Pyelonephritis.
107
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.
108
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.
109
What is the first line treatment for an uncomplicated UTI?
- Trimethoprim or nitrofurantoin for 3 days.
| - Increased fluid intake and regular voiding.
110
How does trimethoprim work?
It affects folic acid metabolism.
111
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.
112
Give 3 causes of recurrent UTI's.
1. Re-infection.
2. Bacterial persistence.
3. Unresolved infection.
113
Define recurrent UTI.
> 2 episodes in 6 months of > 3 in 12 months.
114
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.
115
What is cystitis?
Inflammation of the bladder secondary to infection.
116
Give 4 risk factors for cystitis.
1. Obstruction.
2. Previous damage to bladder epithelium.
3. Bladder stones.
4. Poor bladder emptying.
117
Give 3 symptoms of cystitis.
1. Dysuria.
2. Frequency.
3. Urgency.
118
Describe the NIDDK classification for prostatitis.
- Type 1: acute bacterial prostatitis.
- Type 2: chronic bacterial prostatitis.
- Type 3a: Inflammatory chronic pelvic pain syndrome.
- Type 3b: non-inflammatory chronic pelvic pain syndrome.
- Type 4: asymptomatic inflammatory prostatitis.
119
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.
120
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.
121
Give a symptom of type 3 prostatitis.
Chronic pelvic pain.
122
What investigations might you do in someone with prostatitis?
1. Urinalysis and MSU.
2. Semen cultures.
3. STI screen.
4. Bloods including MCS.
123
Describe the treatment for type 1 prostatitis.
Type 1 = acute bacterial prostatitis.
| - IV Abx e.g. gentamicin, co-amoxiclav for 2-4 weeks.
124
Describe the treatment for type 2 prostatitis.
Type 2 = chronic bacterial prostatitis.
| - 4-6 weeks quinolone e.g. ciprofloxacin.
125
What can cause urethritis?
STI's e.g. gonorrhoea, chlamydia.
126
Give a symptom of urethritis.
Urethral pain/dysuria.
127
What is epididymo-orchitis?
Inflammation of the epididymis and testicle.
128
Give 3 symptoms of epididymo-orchitis.
1. Sudden onset tender swelling.
2. Dysuria.
3. Sweats/fever.
129
Describe the aetiology of epididymo-orchitis.
1. If <35 y/o = STI e.g. chlamydia.
| 2. If >35 y/o = UTI.
130
What investigations might you do on someone who you suspect has epididymo-orchitis?
1. Void urine.
2. Urehtral swab.
3. MSU.
Rule out testicular torsion!
131
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).
132
Define pyelonephritis.
Inflammation secondary to infection of the renal parenchyma and soft tissues of the renal pelvis.
133
What can cause pyelonephritis?
UPEC. Typically P pili.
| Infection is usually from the bladder.
134
Give 3 symptoms of pyelonephritis.
1. Loin pain.
2. Fever.
3. Pyuria.
May also have a severe headache and be fluid deplete.
135
What investigations might you do in someone with pyelonephritis?
1. Urinalysis.
2. MCS MSU.
3. Bloods - raised WCC, ESR and CRP.
136
Describe the treatment for pyelonephritis.
IV fluids and antibiotics e.g. gentamicin/co-amoxiclav.
- Drain obstructed kidney.
- Catheterise if necessary.
- Analgesics.
137
What is the likely cause of pyelonephritis in children?
Reflux or structural/functional abnormalities.
138
What is the function of the prostate?
The prostate secretes proteolytic enzymes into the semen which break down clotting factors in the ejaculate.
139
Which anatomical zone of the prostate does prostate cancer commonly affect?
The peripheral zone.
140
Where can prostate cancer commonly metastasise to?
Lymph nodes and bone.
141
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.
- History of LUTS.
- Trans-rectal USS.
- Prostate biopsy.
142
Other than prostate cancer. What can cause an elevated PSA?
1. Benign prostate enlargement.
2. UTI.
3. Prostatitis.
143
What grading system is used in prostate cancer?
Gleason grading.
The higher the score the more aggressive the cancer.
144
What is the treatment for localised prostate cancer?
- Observation.
- Surgery - radical prostatectomy.
- Radiotherapy (external beam).
- Adjuvant hormones.
145
What is the treatment for metastatic prostate cancer?
Palliative treatment e.g. hormone therapy - androgen deprivation.
146
Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer.
- Curative.
- Reduced patient anxiety.
- Can have adverse effects.
147
Give 2 advantages and 2 disadvantages of screening in prostate cancer.
- Screening can lead to early diagnosis/early treatment and so cure or effective palliation.
- Uncertain natural history.
- Screening leads to over diagnosis and treatment.
148
Name 2 groups of people that you would treat for bacteriuria?
- Pregnant ladies.
| - Children.
149
What is septic shock?
Severe sepsis with persistent hypotension.
150
Describe the pathophysiology of urosepsis.
```
A symptomatic UTI combined with >1 of:
1. Microbial resistance.
2. Immunosuppression.
3. Pressure.
= UROSEPSIS!
```
151
What can cause raised urinary tract pressure?
1. Stone in lumen of UUT.
2. Tumour in the wall.
3. LUT outflow obstruction: BPH, tumour, stone.
4. Bladder dysfunction.
152
Give 4 causes of urinary tract colonisation.
1. Diseases that require steroids or chemo e.g. diabetes, immunodeficiency.
2. Stones or tumour in the lumen of the urinary tract.
3. Poor bladder emptying.
4. Catheterisation.
153
Describe the treatment for sepsis.
The sepsis 6:
1. Give high flow oxygen.
2. Take blood cultures.
3. Give IV abx.
4. Give IV fluids.
5. Check lactate.
6. Monitor hourly urine output.
Also drainage to relieve pressure!
154
Describe the epidemiology of renal cell carcinoma.
1. Incidence increases in those > 60 y/o.
| 2. Males > females.
155
Give 3 risk factors for renal cell carcinoma.
1. Smoking.
2. Obesity.
3. Hypertension.
156
Name an inherited renal disease that can cause renal cell carcinoma.
Von Hippel Lindau disease.
Autosomal dominant. 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.
157
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.
158
What are the 3 classic signs of renal cell carcinoma?
1. Haematuria.
2. Flank mass.
3. Loin pain.
159
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.
160
Name 3 places that renal cell carcinoma might metastasise to.
1. Lymph nodes.
2. Lungs.
3. Bones.
161
What is varicocele?
An abnormal enlargement of the pampiniform venous plexus in the scrotum.
162
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.
163
Name the classification that helps differentiate between benign cystic lesions and cancerous cystic lesions.
The Bozniak classification.
164
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.
165
What is the treatment for localised renal cell carcinoma?
Surgical excision - partial nephrectomy.
166
What is the treatment for metastatic renal cell carcinoma?
- Palliative nephrectomy.
| - Radiotherapy.
167
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.
168
What information can you get from a bladder diary?
1. Frequency.
2. Volume.
3. Functional capacity.
4. Incontinence/day.
169
Name 3 types of incontinence.
1. Stress - associated with coughing or sneezing.
2. Urgency.
3. Mixed - stress and urgency.
4. Continuous - due to fistula.
170
What is the main cause of stress incontinence in women?
Stress incontinence is usually secondary to birth trauma.
171
Describe the treatment for stress incontinence in females.
1. Pelvic floor physio.
2. Duloxetine (concerns over SE's).
3. Surgery.
172
What is the main cause of stress incontinence in men?
Neurogenic or iatrogenic (prostatectomy).
173
Describe the treatment for stress incontinence in males.
1. Artificial sphincter.
| 2. Sling.
174
What are the symptoms of an overactive bladder?
Urgency and frequency in the absence of local pathology that would account for these symptoms.
175
Describe the treatment for an overactive bladder.
1. Behavioural e.g. limit caffeine and alcohol, bladder drill, hypnotherapy.
2. Pelvic floor physio.
3. Muscarinic antagonists.
4. Beta 3 agonists.
5. Botox.
6. Cystoplasty.
176
What is the role of the cortex in micturition?
It has roles in sensation and voluntary initiation of voiding.
177
What is the role of PMC/PAG in micturition?
Co-ordination and completion of voiding.
178
A patient presents with haematuria. A MSU sample is taken and a blood film is done. The RBC's look dysmorphic. Where in the urinary tract is the problem likely to be?
Dysmoprhic RBC's signify a glomerular origin.
If the RBC's looked normal the problem is likely to be with the LUT.
179
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.
180
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.
181
Describe the fluid distribution in the body.
ICF: 28L.
ECF: 14L
- Interstitial: 11L.
- Plasma: 3L.
Total body water: 42L.
182
How much extra-vascular fluid is there in the body?
ICF + interstitial = 39L.
183
How much intra-vascular fluid is there in the body?
Plasma: 3L.
184
What happens to the heart rate in hypovolaemia?
Increases - tachycardia.
185
What happens to the blood pressure in hypovolaemia?
Decreases - hypotension.
186
What happens to the JVP in hypovolaemia?
JVP is low.
187
What happens to tissue turgor in hypovolaemia?
Tissue turgor is reduced.
188
What happens to urine output in hypovolaemia?
Urine output is reduced.
189
What happens to weight in hypovolaemia?
Weight is reduced.
190
Give 2 symptoms of hypovolaemia.
Thirst and dizziness.
191
What happens to creatinine, haemoglobin and haematocrit levels in hypovolaemia?
They are raised.
192
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.
193
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.
194
What happens to the heart rate in hypervolaemia?
HR is normal.
195
What happens to blood pressure in hypervolaemia?
Blood pressure is high or normal.
196
What happens to JVP in hypervolaemia?
JVP is high.
197
What happens to tissue turgor in hypervolaemia?
Tissue turgor is normal.
198
What happens to urine output in hypervolaemia?
Urine output is normal.
199
What happens to weight in hypervolaemia?
Weight is increased.
200
Give 2 symptoms of hypervolaemia.
1. Shortness of breath.
| 2. Peripheral oedema.
201
What happens to creatinine, haemoglobin and haematocrit levels in hypervolaemia?
They are reduced.
202
Where might fluid accumulate in someone with hypervolaemia?
- Pulmonary oedema.
- Pleural effusion.
- Ascites.
- Bowel obstruction.
- Intra-abdominal collection.
203
Describe the management for hypovolaemia.
1. Oral fluid.
2. IV fluid if very ill.
3. Treat reversible causes.
204
Describe the management for hypervolaemia.
1. Diuretics e.g. furosemide.
2. Fluid restriction.
3. Treat reversible causes.
205
Name 3 isotonic solutions.
1. 5% dextrose.
2. 0.9% NaCl.
3. Hartmann's solution.
206
What type of IV fluid moves from the intra-vascular to the extra-vascular space?
Crystalloid.
Small molecules pass through cell membranes and so move from the intra-vascular to extra-vascular space.
207
Give an example of a colloid IV fluid.
Gelofusine.
208
Give 3 potential causes of rising creatinine.
1. Too aggressive with diuretics.
2. Extravascular hypervolaemia but intravascular hypovolaemia.
3. Progression of CKD.
209
Why do advanced CKD patients need regular fluid assessment?
They may be oligouric or anuric.
210
What is PSA?
A glycoprotein secreted by the prostate into the blood stream.
211
Give 4 symptoms of BPH.
1. Increased frequency of micturition.
2. Nocturia.
3. Hesitancy.
4. Post-void dribbling.
212
Describe the treatment for BPH.
1. Mild symptoms: watchful waiting.
2. Alpha-1-antagonists e.g. tamulosin.
3. 5-alpha-reductase inhibitors.
213
How does tamulosin work in improving the symptoms of BPH?
Tamulosin is an alpha-1-antagonist. It works by relaxing the smooth muscle in the bladder neck and prostate and so increases urinary flow. This improves obstructive symptoms.
214
How do 5-alpha-reductase inhibitors work in improving the symptoms of BPH?
5-alpha-reductase inhibitors block the conversion of testosterone to dihydrotestosterone (the androgen responsible for prostatic growth).
215
Give 4 symptoms of prostate carcinoma.
1. Increased frequency of micturition.
2. Nocturia.
3. Hesitancy.
4. Post-void dribbling.
(Same as BPH).
216
What investigations might you do in someone to see whether they have prostate carcinoma?
1. Trans-rectal USS of prostate.
2. Serum PSA - will be elevated.
3. Trans-rectal prostate biopsy.
217
Describe the treatment for prostate carcinoma.
1. Radical prostatectomy or radiotherapy.
| 2. For metastatic disease, remove the androgenic drive e.g. bilateral orchidectomy.
218
Describe the epidemiology of stones in the urinary tract.
- 10-15% lifetime risk.
- Males > females - 2:1 ratio.
- Common among 30-50 y/o.
219
Give 5 potential causes of stones in the upper urinary tract.
1. Congenital abnormalities.
2. Metastable urine.
3. Hypercalciuria/ high urate/ high oxalate.
4. Dehydration!
5. Infection.
220
Describe the pathophysiology of stone formation in the upper urinary tract.
Stones form from crystals in supersaturated urine.
| - 80% are calcium based e.g. calcium oxalate.
221
Give 5 symptoms of upper urinary tract stones.
1. 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.
222
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.
223
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 MSU.
4. NCCT-KUB - gold standard!
224
Describe the treatment for renal colic.
1. Analgesia e.g. NSAIDs (diclofenac).
2. Anti-emetics.
3. Check for sepsis.
225
How would you treat someone who presents with large 'stag horn' ureteric stones.
1. Analgesia and anti-emetics.
2. Observe for sepsis.
3. PCNL.
226
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.
227
Describe the pathophysiology of acquired polycystic kidney disease.
Cysts develop over time.
Renal injury/ischaemia -> abnormal cell proliferation.
228
What classification can be used to help differentiate between benign cystic lesions and cancerous lesions?
Bozniak classification.
229
Give 4 congenital causes of renal cysts.
1. ADPKD.
2. ARPKD.
3. VHL.
4. OFD1 (oral-facial-digital syndrome 1).
230
What is ADPKD?
An autosomal dominant condition characterised by progressive cyst development. Cysts increase in size -> renal enlargement and loss of function -> kidney failure.
231
A mutation in which genes can cause ADPKD?
1. PKD1 (associated with more severe disease).
| 2. PKD2.
232
Give 4 signs of ADPKD.
1. Hypertension.
2. Haematuria.
3. Polyuria.
4. Abdominal/loin pain.
5. Palpable bilateral costo-vertebral masses.
233
Give 2 extra-renal manifestations of ADPKD.
1. Polycystic liver disease.
| 2. Intracranial aneurysms e.g. SAH.
234
How can ADPKD be diagnosed?
- Symptoms.
- Family history.
- High BP.
- Urinalysis.
- USS.
235
What value can be used as a prognostic marker for ADPKD?
TKV - total kidney volume.
236
A mutation in what gene can cause AD tubulo-interstitial kidney disease?
HNF1 beta.
237
A mutation in what gene can cause ARPKD?
PKHD1.
238
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.
239
What is the access point in haemodialysis?
AV fistula.
240
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.
241
Give examples of waste products that are removed from the blood in dialysis.
1. Urea.
2. Creatinine.
3. Potassium.
4. Phosphate.
242
How many times a week and for how long does someone have hospital haemodialysis for?
3-5 hours, 3 times a week.
243
How many times a week and for how long does someone have home haemodialysis for?
2-3 hours, 4-5 times a week.
244
Why can someone on home haemodialysis take fewer tablets and have less dietary restrictions compared to someone on hospital haemodialysis?
Patients doing home haemodialysis dialyse more frequently and so can have less restriction on their diet.
245
Give 5 potential complications of haemodialysis.
1. Hypotension.
2. Cramps.
3. Nausea.
4. Chest pain.
5. Fever.
6. Blocked or infected dialysis catheter.
246
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.
247
What is the access point in peritoneal dialysis?
A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel.
248
How often does someone have to do CAPD?
30-40 minute exchanges, 3-5 times a day.
249
How often does someone have to do APD?
One exchange overnight (8 hours).
250
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.
251
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.
252
Where in the abdomen does a transplanted kidney lie?
In the iliac fossa.
253
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.
254
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.
255
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.
256
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.
257
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.
258
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.
259
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.
260
What are the 2 major causes of allograft failure?
1. Chronic rejection.
| 2. Death with functioning graft.
261
What are the 2 major causes of death after kidney transplant?
1. CV disease.
| 2. Infection.
262
Name the 3 types of renal allograft rejection.
1. Hyper-acute.
2. Acute.
3. Chronic.
263
Describe hyper-acute renal allograft rejection.
Preformed antibodies against HLA antigens of donor organ.
264
Why might someone have pre-formed antibodies against HLA antigens?
Can be a consequence of blood transfusion, pregnancy, prior transplant, auto-immune disease.
265
What can cause immediate graft loss?
Fibrinoid necrosis.
266
Describe acute renal allograft rejection.
Activated T lymphocytes. Occurs within the first 6 months but is often reversible e.g. with steroids.
267
Describe chronic renal allograft rejection.
Slow and gradual decline in renal function, accompanied by proteinuria.
268
What criteria can be used to diagnose allograft rejection?
Banff criteria.
269
Give 3 consequences of chronic immunosuppression.
1. Malignancy.
2. Infection.
3. SE's of other drugs.
270
Give 5 causes of CKD.
1. Diabetes mellitus.
2. Hypertension.
3. Atherosclerotic renal vascular disease.
4. Congenital e.g. PKD.
5. Urinary tract obstruction.
271
Give 5 signs of CKD.
1. Proteinuria.
2. Haematuria.
3. Impaired eGFR <60ml/min.
4. Rise in serum urea/creatinine.
5. Anaemia (reduced EPO).
6. Bone disease.
7. Polyneuropathy.
8. CV disease.
9. Erectile dysfunction.
10. Raised PTH.
272
Describe the management for CKD.
1. Treat the underlying cause.
2. Slow deterioration of kidney function e.g. maintain BP.
3. Reduce CV risk e.g. statins, smoking cessation.
4. Treat complications e.g. anaemia.
5. ESRF -> dialysis or transplant.
273
Give 3 consequences of glomerulonephritis (glomerular disease).
1. Leaky glomeruli -> haematuria and proteinuria.
2. High BP.
3. Deteriorating kidney function.
274
Briefly describe the pathophysiology of glomerulonephritis (glomerular disease).
Immunologically mediated: immunoglobulin deposits and inflammatory cells.
275
Give 4 causes of acute nephritic syndrome.
1. ANCA.
2. Goodpastures.
3. SLE.
4. Post streptococcal infection (immune complex deposition in the kidney).
5. IgA nephropathy.
276
Give 5 signs of acute nephritic syndrome.
1. Inflammation of glomeruli.
2. HAEMATURIA and PROTEINURIA.
3. Hypertension.
4. Fluid overload.
5. Oliguria.
6. Red cell casts.
277
What 4 signs are needed in order to make a diagnosis of nephrotic syndrome.
1. Hypoalbuminaemia.
2. Oedema.
3. Heavy proteinuria!
4. Hypercholesterolaemia.
278
What can nephrotic syndrome be secondary to?
1. Diabetes.
2. Amyloid.
3. Infections.
4. SLE.
5. Drugs.
279
Describe the treatment for nephrotic syndrome.
1. Treat complications e.g. diuretics for oedema; ACEi for proteinuria.
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.
280
What would you notice on the electron microscopy taken from someone with minimal change disease?
Fused podocytes.
281
What is the treatment for minimal change disease?
Steroids.
282
Name a loop diuretic.
Furosemide - acts on Na+/K+/2Cl- transporter (NKCC2).
283
Give 3 potential side effects of furosemide.
1. Hypokalaemia.
2. Hypotension.
3. Dehydration.
284
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.
285
Name a potassium sparing diuretic.
Spironolactone.
286
On which part of the nephron do thiazides act?
The distal tubule.
| Act on NCC channels.
287
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.
288
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.
289
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.
- Normally people present around 50 y/o.
- Raised creatinine and urea indicate a kidney problem.
- The kidneys can be HUGE in ADPKD hence the palpable masses.
- Intracranial haemorrhages are an extra-renal manifestation of ADPKD.
290
At what age do people with ADPKD normally present?
Normally present around 50 y/o.
Cysts increase in size with advancing age.
291
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!
292
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.
293
Where in the nephron are urinary tract stones formed?
In the collecting ducts.
294
Give 3 places where urinary tract stones are likely to get stuck?
1. Ureteropelvic junction.
2. Pelvic brim.
3. Vesoureteric junction.
295
Give 3 causes of renal colic.
1. Urinary tract stones.
2. UTI.
3. Pyelonephritis.
296
What is the affect of AKI on creatinine and urine output?
- Creatinine is raised.
| - Urine output is reduced.
297
Give 5 risk factors for AKI.
1. Increasing age.
2. CKD.
3. HF.
4. Diabetes mellitus.
5. Nephrotoxic drugs e.g. NSAIDs and ACEi.
298
Give a pre-renal cause of AKI.
1. Hypertension.
2. Heart failure.
3. Nephrotoxic drugs.
299
Give 5 renal causes of AKI.
1. Nephrotoxic drugs.
2. Vasculitis.
3. Autoimmune.
4. Acute tubular necrosis.
5. Glomerulonephritis.
300
What is the major complication someone with AKI might develop?
Hyperkalaemia!
This can lead to arrhythmias.
301
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.
302
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.
303
Give a primary cause of nephrotic syndrome.
Minimal change disease.
This is the most common cause in children.
304
What investigations might you do to determine whether someone has nephrotic syndrome?
1. Renal biopsy.
2. Urine dipstick - +++ protein.
3. Bloods: low serum albumin.
4. Look for auto-antibodies.
305
Give 2 potential complications of nephrotic syndrome.
1. Sepsis.
| 2. Venous thromboembolism.
306
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.
307
How does the epidemiology differ between ADPKD and ARPKD?
People with ADPKD normally present in middle age whereas people with ARPKD present in infancy.
308
What is the most common renal cancer in children?
Wilms tumour.
309
A sudden rise in creatinine level and a decreased urine output would be indicative of what?
AKI.
310
What CCB can be used to treat renal stones?
Nifedipine.
311
Why is someone with nephrotic syndrome at risk of sepsis?
Because you lose immunoglobulins in the urine.
312
What drug must you not give to someone with renal artery stenosis?
ACE inhibitors e.g. ramipril.
313
Is focal segmental glomerulosclerosis a cause of nephritic or nephrotic syndrome?
Nephrotic syndrome.
