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 hyperplasia
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.
- DRE
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 (finasteride)
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 - transurethral resection of the prostate
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 4 symptoms of transitional cell carcinoma.
1. PAINLESS HAEMATURIA.
2. Dysuria
3. Urgency.
4. Frequency
43
Give 4 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.
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?
what imaging?
You image the UUT to confirm that there is no other TCC elsewhere in the urinary tract.
CT, ultrasound 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.
non-muscle-invasice bladder cancer
invasive bladder cancer
48
Describe the treatment for non-muscle invasive bladder cancer (CIS, Ta, T1).
1. TURBT (trans urethral resection of bladder tumour)
| 2. intravesical 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 - antibiotic to treat bacterial infections (UTI)
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 and distal tubule
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. Klebsiella pneumonia.
3. Candida albicans
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
The vagina is heavily colonised with lactobacilli. What is the function of this?
Helps maintain a low pH = host defence mechanism.
98
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.
99
Give 4 host defence mechanisms against urinary tract infection.
1. Antegrade flushing of urine.
2. Low urine pH.
3. Commensal flora.
4. Urinary IgA.
100
What is pyuria?
The presence of leukocytes in urine.
101
Name 4 lower urinary tract infections.
1. Cystitis.
2. Prostatitis.
3. Epididymitis.
4. Urethritis.
102
Name 1 upper urinary tract infection.
Pyelonephritis.
103
What investigations might you do on someone who you suspect has a UTI?
1. Take a good history.
2. Urinalysis - leukocytes, nitrites
3. Microscopy; culture and sensitivity of mid-stream urine.
4. In recurrent/complicated UTI renal imaging is important.
104
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.
105
What is the first line treatment for an uncomplicated UTI?
- 3 days antibiotics (nitrofurantoin)
| - Increased fluid intake and regular voiding.
106
How does trimethoprim work?
It affects folic acid metabolism.
| so avoid in first trimester of pregnancy
107
Describe the management for a complicated UTI.
- MSU sample is essential
- Immunocompromised women: 5-10 days Abx (nitrofurantoin)
- Men, pregnant women, chatter: 7 days Abx (Nitrofurantoin)
108
Give 3 causes of recurrent UTI's.
1. Re-infection.
2. Bacterial persistence.
3. Unresolved infection.
109
Define recurrent UTI.
> 2 episodes in 6 months of > 3 in 12 months.
110
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.
111
What is cystitis?
Inflammation of the bladder secondary to infection.
112
Give 4 risk factors for cystitis.
1. Obstruction.
2. Previous damage to bladder epithelium.
3. Bladder stones.
4. Poor bladder emptying.
113
Give 3 symptoms of cystitis.
1. Dysuria.
2. Frequency.
3. Urgency.
114
what is acute prostatitis ?
Painful inflammation with the prostate usually with recent or ongoing infection
115
who does acute prostatitis usually affect?
Most frequent urological diagnosis in men <50
116
Give 4 symptoms of acute prostatitis
- Acute LUTS (dysuria, urinary frequency, perineal discomfort)
- Systemic signs (fever, chills, malaise)
- Tender prosate
- lower abdo + ejaculatory pain
117
complication of acute prostatitis
development to chronic prostatitis, sepsis, urinary retention
118
What investigations (4) might you do in someone with prostatitis?
```
1. Urinalysis and MSU (leukocytes, bacteria)
+ urine cultures
2. Semen cultures (bacteria)
3. STI screen.
4. Bloods cultures
```
119
Describe the treatment prostatitis.
- Treat with Abx (quinolone)
- Prolonged course often required if chronic prostatitis follows
- Analgesia (NSAID)
120
What can cause urethritis?
STI's e.g. gonorrhoea, chlamydia.
121
Give a symptom of urethritis.
- Dysuria.
- Urethral discharge
- Pruritus at end of urethra
122
What is epididymo-orchitis?
Inflammation of the epididymis and testicle.
123
Give 3 symptoms of epididymo-orchitis.
1. Sudden onset tender swelling (usually unilateral)
2. Dysuria.
3. urethral discharge
4. Systemic symptoms: Sweats/fever.
124
Describe the aetiology of epididymo-orchitis.
1. If <35 y/o = STI e.g. chlamydia, gonorrhoea
2. If >35 y/o = enteric E.coli
Mumps
125
What investigations might you do on someone who you suspect has epididymo-orchitis?
1. Urehtral swab.
2. MSU: urine microscopy, culture + sensitivity
3. Saliva swap (PCR testing for mumps)
Rule out testicular torsion! (ultrasound)
126
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).
-Analgesia (paracetamol), supportive underwear, decrease physical activity, abstain from sex
127
Define pyelonephritis.
Inflammation secondary to infection of the renal parenchyma and soft tissues of the renal pelvis.
128
What can cause pyelonephritis?
- bacterial ascent (urethra colonised with bacteria (intercourse can force bacteria into female bladder), E.coli
- haematogenous (s.aureus/ candida)
129
Give 3 symptoms of pyelonephritis.
1. Loin pain.
2. Fever.
3. Pyuria.
4. LUTS
aymtomattic (30%)
130
What investigations might you do in someone with pyelonephritis?
1. Urinalysis (leukocytes, nitrates, non-visible Haematuria, WBC casts
2. urine culture (microscopy + Abx susceptibility)
3. Bloods - raised WCC, ESR and CRP.
131
Describe the treatment for pyelonephritis.
IV fluids and antibiotics e.g. gentamicin/co-amoxiclav.
- Drain obstructed kidney.
- Catheterise if necessary.
- Analgesics.
132
What is the likely cause of pyelonephritis in children?
Reflux or structural/functional abnormalities.
133
What is the function of the prostate?
produce the fluid that nourishes and transports sperm (seminal fluid).
134
Which anatomical zone of the prostate does prostate cancer commonly affect?
The peripheral zone.
135
Where can prostate cancer commonly metastasise to?
Lymph nodes and bone.
136
What investigations might you do in someone who you suspect has prostate cancer?
- Serum: PSA.
- DRE - hard, irregular, craggy.
- History of LUTS.
- Trans-rectal USS.
- Prostate biopsy.
137
Other than prostate cancer. What can cause an elevated PSA?
1. Benign prostate enlargement.
2. UTI.
3. Prostatitis.
4. exercise - cycling
138
What grading system is used in prostate cancer?
Gleason grading.
The higher the score the more aggressive the cancer.
139
What is the treatment for localised prostate cancer?
- Observation.
- Surgery - radical prostatectomy.
- Radiotherapy (external beam).
- Adjuvant hormones.
140
What is the treatment for metastatic prostate cancer?
Palliative treatment e.g. hormone therapy - androgen deprivation.
141
Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer.
- Curative.
- Reduced patient anxiety.
- Can have adverse effects.
142
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.
143
Name 2 groups of people that you would treat for bacteriuria?
- Pregnant ladies.
| - Children.
144
What is septic shock?
life-threatening condition that happens when your blood pressure drops to a dangerously low level after an infection
145
Describe the pathophysiology of urosepsis.
```
A symptomatic UTI combined with >1 of:
1. Microbial resistance.
2. Immunosuppression.
3. Pressure.
= UROSEPSIS!
```
146
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.
147
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.
148
Describe the treatment for sepsis.
The sepsis 6: give 3, take 3
1. Give IV fluids
2. Give IV Abx
3. Give high flow oxygen
4. Take blood cultures
5. Check lactate
6. monitor hourly uric output
Also drainage to relieve pressure!
149
Describe the epidemiology of renal cell carcinoma.
1. Incidence increases in those > 60 y/o.
| 2. Males > females.
150
Give 3 risk factors for renal cell carcinoma.
1. Smoking.
2. Obesity.
3. Hypertension.
151
What are the 3 classic signs of renal cell carcinoma?
1. Haematuria.
2. Flank mass.
3. Loin pain.
152
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.
153
Name 3 places that renal cell carcinoma might metastasise to.
1. Lymph nodes.
2. Lungs.
3. Bones.
154
What is varicocele?
An abnormal enlargement of the pampiniform venous plexus in the scrotum.
155
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.
156
Name the classification that helps differentiate between benign cystic lesions and cancerous cystic lesions.
The Bozniak classification.
157
What investigations might you do in someone with renal cell carcinoma?
- Ultrasound.
- Bloods: FBC, U+E, LFT, Ca profile.
- urine dipstick (Haematuria)
- Abdo CT scan with contrast.
- Bone scan for boney metastases.
158
What is the treatment for localised renal cell carcinoma?
Surgical excision - partial nephrectomy.
159
What is the treatment for metastatic renal cell carcinoma?
- Palliative nephrectomy.
| - Radiotherapy.
160
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.
161
What information can you get from a bladder diary?
1. Frequency.
2. Volume.
3. Functional capacity.
4. Incontinence/day.
162
Name 3 types of incontinence.
1. Stress - associated with coughing or sneezing.
2. Urgency.
3. Mixed - stress and urgency.
4. Continuous - due to fistula.
163
What is the main cause of stress incontinence in women?
Stress incontinence is usually secondary to birth trauma.
164
Describe the treatment for stress incontinence in females.
1. Pelvic floor physio.
2. Duloxetine (concerns over SE's).
3. Surgery.
165
What is the main cause of stress incontinence in men?
Neurogenic or iatrogenic (prostatectomy).
166
Describe the treatment for stress incontinence in males.
1. Artificial sphincter.
| 2. Sling.
167
What are the symptoms of an overactive bladder?
Urgency and frequency in the absence of local pathology that would account for these symptoms.
168
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.
169
What is the role of the cortex in micturition?
It has roles in sensation and voluntary initiation of voiding.
170
What is the role of PMC/PAG in micturition?
Co-ordination and completion of voiding.
171
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.
172
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.
stones, infection, cancer
173
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.
174
Describe the fluid distribution in the body.
ICF: 28L.
ECF: 14L
- Interstitial: 11L.
- Plasma: 3L.
Total body water: 42L.
175
How much extra-vascular fluid is there in the body?
ICF + interstitial = 39L.
176
How much intra-vascular fluid is there in the body?
Plasma: 3L.
177
What happens to the heart rate in hypovolaemia?
Increases - tachycardia.
178
What happens to the blood pressure in hypovolaemia?
Decreases - hypotension.
179
What happens to the JVP in hypovolaemia?
JVP is low.
180
What happens to tissue turgor in hypovolaemia?
Tissue turgor is reduced.
181
What happens to urine output in hypovolaemia?
Urine output is reduced.
182
What happens to weight in hypovolaemia?
Weight is reduced.
183
Give 2 symptoms of hypovolaemia.
Thirst and dizziness.
184
What happens to creatinine, haemoglobin and haematocrit levels in hypovolaemia?
They are raised.
185
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.
186
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.
187
What happens to the heart rate in hypervolaemia?
HR is normal.
188
What happens to blood pressure in hypervolaemia?
Blood pressure is high or normal.
189
What happens to JVP in hypervolaemia?
JVP is high.
190
What happens to tissue turgor in hypervolaemia?
Tissue turgor is normal.
191
What happens to urine output in hypervolaemia?
Urine output is normal.
192
What happens to weight in hypervolaemia?
Weight is increased.
193
Give 2 symptoms of hypervolaemia.
1. Shortness of breath.
| 2. Peripheral oedema.
194
What happens to creatinine, haemoglobin and haematocrit levels in hypervolaemia?
They are reduced.
195
Where might fluid accumulate in someone with hypervolaemia?
- Pulmonary oedema.
- Pleural effusion.
- Ascites.
- Bowel obstruction.
- Intra-abdominal collection.
196
Describe the management for hypovolaemia.
1. Oral fluid.
2. IV fluid if very ill.
3. Treat reversible causes.
197
Describe the management for hypervolaemia.
1. Diuretics e.g. furosemide.
2. Fluid restriction.
3. Treat reversible causes.
198
Name 3 isotonic solutions.
1. 5% dextrose.
2. 0.9% NaCl.
3. Hartmann's solution.
199
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.
200
Give an example of a colloid IV fluid.
Gelofusine.
201
Give 3 potential causes of rising creatinine.
1. Too aggressive with diuretics.
2. Extravascular hypervolaemia but intravascular hypovolaemia.
3. Progression of CKD.
202
Why do advanced CKD patients need regular fluid assessment?
They may be oligouric or anuric.
203
What is PSA?
A glycoprotein secreted by the prostate into the blood stream.
204
Give 4 symptoms of BPH.
1. Increased frequency of micturition.
2. Nocturia.
3. Hesitancy.
4. Post-void dribbling.
205
Describe the treatment for BPH.
1. Mild symptoms: watchful waiting.
2. Alpha-1-antagonists e.g. tamulosin.
3. 5-alpha-reductase inhibitors (finasteride)
4. surgical option: TURP
206
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.
207
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).
208
Give 4 symptoms of prostate carcinoma.
1. Increased frequency of micturition.
2. Nocturia.
3. Hesitancy.
4. Post-void dribbling.
(Same as BPH).
209
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.
210
Describe the treatment for prostate carcinoma.
1. Radical prostatectomy or radiotherapy.
| 2. For metastatic disease, remove the androgenic drive e.g. bilateral orchidectomy.
211
Describe the epidemiology of stones in the urinary tract.
- 10-15% lifetime risk.
- Males > females - 2:1 ratio.
- Common among 30-50 y/o.
212
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.
213
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.
214
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.
215
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.
216
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!
(non contrast CT (Kidneys, ureter, bladder)
217
Describe the treatment for renal colic.
1. Analgesia e.g. NSAIDs
2. Anti-emetics.
3. Check for sepsis.
218
How would you treat someone who presents with large 'stag horn' ureteric stones.
1. Analgesia and anti-emetics.
2. Observe for sepsis.
3. PCNL (removal of stone)
219
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.
220
Describe the pathophysiology of acquired polycystic kidney disease.
Cysts develop over time.
Renal injury/ischaemia -> abnormal cell proliferation.
221
What classification can be used to help differentiate between benign cystic lesions and cancerous lesions?
Bozniak classification.
222
Give 4 congenital causes of renal cysts.
1. ADPKD.
2. ARPKD.
3. VHL.
4. OFD1 (oral-facial-digital syndrome 1).
223
What is ADPKD?
An autosomal dominant condition characterised by progressive cyst development. Cysts increase in size -> renal enlargement and loss of function -> kidney failure.
224
A mutation in which genes can cause ADPKD?
1. PKD1 (associated with more severe disease).
| 2. PKD2.
225
Give 4 signs of ADPKD.
1. Hypertension.
2. Haematuria.
3. Polyuria.
4. Abdominal/loin pain.
5. Palpable bilateral costo-vertebral masses.
226
Give 2 extra-renal manifestations of ADPKD.
1. Polycystic liver disease.
| 2. Intracranial aneurysms e.g. SAH.
227
How can ADPKD be diagnosed?
- clinical diagnosis + family history
- Urinalysis.
- Kidney USS.
- genetic testing
228
What value can be used as a prognostic marker for ADPKD?
TKV - total kidney volume.
229
A mutation in what gene can cause AD tubulo-interstitial kidney disease?
HNF1 beta.
230
A mutation in what gene can cause ARPKD?
PKHD1.
231
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.
232
What is the access point in haemodialysis?
AV fistula.
233
Give examples of waste products that are removed from the blood in dialysis.
1. Urea.
2. Creatinine.
3. Potassium.
4. Phosphate.
234
How many times a week and for how long does someone have hospital haemodialysis for?
3-5 hours, 3 times a week.
235
How many times a week and for how long does someone have home haemodialysis for?
2-3 hours, 4-5 times a week.
236
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.
237
Give 5 potential complications of haemodialysis.
1. Hypotension.
2. Cramps.
3. Nausea.
4. Chest pain.
5. Fever.
6. Blocked or infected dialysis catheter.
238
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.
239
What is the access point in peritoneal dialysis?
A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel.
240
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.
241
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.
242
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.
243
What are the 2 major causes of death after kidney transplant?
1. CV disease.
| 2. Infection.
244
Give 3 consequences of chronic immunosuppression.
1. Malignancy.
2. Infection.
3. SE's of other drugs.
245
Give 5 causes of CKD.
1. Diabetes mellitus.
2. Hypertension.
3. Atherosclerotic renal vascular disease.
4. Congenital e.g. PKD.
5. Urinary tract obstruction.
6. AKI
246
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.
247
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.
248
Give 3 consequences of glomerulonephritis (glomerular disease).
1. Leaky glomeruli -> haematuria and proteinuria.
2. High BP.
3. Deteriorating kidney function.
249
Briefly describe the pathophysiology of glomerulonephritis (glomerular disease).
generic term that means inflammation in kidney => reduction in kidney function => haematuria, proteinuria, oliguria (reduced urine output), fluid retention
250
Give 4 causes of acute nephritic syndrome.
1. Goodpastures.
2. SLE.
3. Post streptococcal infection (immune complex deposition in the kidney).
4. IgA nephropathy.
251
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.
252
What 4 signs are needed in order to make a diagnosis of nephrotic syndrome.
1. Hypoalbuminaemia.
2. Oedema.
3. Heavy proteinuria!
4. Hypercholesterolaemia.
253
What can nephrotic syndrome be secondary to?
1. Diabetes.
2. Amyloid.
3. Infections.
4. SLE.
5. Drugs.
254
Describe the treatment for nephrotic syndrome.
children ?
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.
255
What would you notice on the electron microscopy taken from someone with minimal change disease?
Fused podocytes.
256
What is the treatment for minimal change disease?
- High dose Steroids (prednisolone)
- low salt diet
- diuretic (for oedema)
- albumin infusions (if sever hypoalbuminaemia)
257
Name a loop diuretic.
Furosemide - acts on Na+/K+/2Cl- transporter (NKCC2).
258
Give 3 potential side effects of furosemide.
1. Hypokalaemia.
2. Hypotension.
3. Dehydration.
259
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.
260
Name a potassium sparing diuretic.
Spironolactone.
261
On which part of the nephron do thiazides act?
The distal tubule.
| Act on NCC channels.
262
Describe the pathophysiology behind IgA nephropathy
autoimmune
IgA gets glycosylated (sugar sticks to it) => when moves through kidney, gets deposited => inflammation and scarring (nephritis)
263
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.
264
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.
265
At what age do people with ADPKD normally present?
Normally present around 50 y/o.
Cysts increase in size with advancing age.
266
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!
267
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.
268
Where in the nephron are urinary tract stones formed?
In the collecting ducts.
269
Give 3 places where urinary tract stones are likely to get stuck?
1. Ureteropelvic junction.
2. Pelvic brim.
3. Vesoureteric junction.
270
Give 3 causes of renal colic.
1. Urinary tract stones.
2. UTI.
3. Pyelonephritis.
271
What is the affect of AKI on creatinine and urine output?
- Creatinine is raised.
| - Urine output is reduced.
272
Give 5 risk factors for AKI.
1. Increasing age.
2. underlying KD
3. HF.
4. Diabetes mellitus.
5. Nephrotoxic drugs (NSAIDs and ACEi)
273
Give a pre-renal cause of AKI.
decreased renal perfusion
1. hypovolaemia
2. haemorrhage
3. sepsis
4. overdiuresis
5. HF
274
Give 5 renal causes of AKI.
Disease in kidney
1. Nephrotoxic drugs (NSAIDS, ACEI, cancer therapy)
2. interstitial nephritis
3. Acute tubular necrosis.
4. Glomerulonephritis.
275
What is the major complication someone with AKI might develop?
Hyperkalaemia!
This can lead to arrhythmias.
276
What investigations might you do to determine whether someone has AKI?
1. Check potassium!
2. Bloods: creatinine (raised)
3. Urine output (low)
4. urinalysis
5. imaging (ultrasound), look for stones
277
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.
278
Give a primary cause of nephrotic syndrome.
Minimal change disease.
This is the most common cause in children.
279
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.
280
Give 2 potential complications of nephrotic syndrome.
1. Sepsis.
| 2. Venous thromboembolism.
281
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.
282
How does the epidemiology differ between ADPKD and ARPKD?
People with ADPKD normally present in middle age whereas people with ARPKD present in infancy.
283
What is the most common renal cancer in children?
Wilms tumour.
284
A sudden rise in creatinine level and a decreased urine output would be indicative of what?
AKI.
285
What CCB can be used to treat renal stones?
Nifedipine.
286
Why is someone with nephrotic syndrome at risk of sepsis?
Because you lose immunoglobulins in the urine.
287
What drug must you not give to someone with renal artery stenosis?
ACE inhibitors e.g. ramipril.
288
Is focal segmental glomerulosclerosis a cause of nephritic or nephrotic syndrome?
Nephrotic syndrome.
