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Phase 2 > Urology > Flashcards

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

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2
Q

Where are the kidneys located

A

Retroperitoneal between T11 and L3

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3
Q

What is the blood supply of the kidneys

A

Renal artery direct from the aorta at L1 level

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4
Q

How much urine does each kidney produce per day

A

1-1.5L of urine per day

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5
Q

How long are the ureters

A

25-30cm

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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

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7
Q

What are the three points of narrowing in the ureter

A

Pelvo-uteric junction
Crossing iliac vessels
Crossing trigone of bladder

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8
Q

How is reflux of urine prevented

A

Valvular mechanisms at the vesicoureteric junction

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9
Q

Describe the nervous control of the bladder and sphincter

A
  1. Parasympathetic nerve (Pelvic nerve (S2-S4)
    - ACH
    - Involuntary control
  2. Sympathetic nerves (Hypogastric plexus, T11-L2)
    - Noradrenaline
    - involuntary control
  3. Somatic nerve (Pudendal nerve S2-S4)
    - Onuf’s nucleus
    - ACH
  4. Afferent pelvic nerve
    - Sensory nerve
    - Signals from detrusor muscle
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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

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11
Q

Is the detrusor muscle relaxed or contracted during storage?

A

Relaxed.

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12
Q

Is the detrusor muscle relaxed or contracted during voiding?

A

Contracted.

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13
Q

Is the urethral sphincter relaxed or contracted during storage?

A

Contracted.

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14
Q

Is the urethral sphincter relaxed or contracted during voiding?

A

Relaxed.

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15
Q

What type of epithelium lines the bladder?

A

Urothelium (transitional epithelium) - pseudo-stratified.

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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.

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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)
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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
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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
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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
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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
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22
Q

Detrusor relaxation is controlled by what nerve

A

Sympathetic stimulation T11-L2

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23
Q

External urethral sphincter contraction is controlled by what nerve

A

Pudendal stimulation (S2-S4)

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24
Q

Detrusor contraction is controlled by what nerve

A

Pelvic nerve -= Parasympathetic stimulation S2-S4

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25
Q

External urethral sphincter relaxation is controlled by what nerve

A

Pudendal inhibition S2-S4

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26
Q

What is the normal function of the lower urinary tract

A
  • Convert a continuous process of excretion (Urine production) to an intermittent process of elimination
  • Store urine insensibly
  • Void urine when convenient
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27
Q

What does the detrusor muscle do during storage

A

Relaxes

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28
Q

What does the detrusor muscle due during voiding

A

Contracts

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29
Q

What does the distal sphincter do during storage

A

Contracts

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30
Q

What does the distal sphincter do during voiding

A

Relaxes

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31
Q

What is the role of the parasympathetic S2S4 nerve in neural control of LUT

A

Drives detrusor contraction

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32
Q

What is the role of the sympathetic (T10-L2) nerve in the neural control of LUT

A

Sphincter/urethral contraction

Inhibits detrusor contraction

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33
Q

What are lower urinary tract symptoms (LUTS) in men > 50 likely to be due to?

A

Benign prostatic enlargement.

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34
Q

What are the storage symptoms of LUT

A

a. Frequency
b. Nocturia
c. Urgency
d. Urgency Incontinence

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35
Q

What are the voiding symptoms of LUT

A
  1. Straining.
  2. Hesitancy.
  3. Incomplete emptying.
  4. Poor flow/intermittent strain
  5. Terminal dribble
  6. Haematuria
  7. Dysuria
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36
Q

What might dysuria suggest?

A

Inflammation.

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37
Q

What is BPH

A

Benign prostatic hyperplasia

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38
Q

What is BPE

A

Benign prostatic enlargement

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39
Q

What is BOO

A

Bladder outflow obstruction (Urodynamic proven obstruction)

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40
Q

What is LUTS

A

Lower urinary tract symptoms, constellation of symptoms, neither gender nor disease specific

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41
Q

What is benign prostate hyperplasia

A

Increase in epithelial and stromal cell number and size in the transitional/peri-urethral prostate area

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42
Q

What are the causes of BPH

A

Increase in cell number
Decrease in apoptosis
Combination of both

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43
Q

What is another cause of BPH

A

Obstruction due to increase A1 adrenoceptors with leads to SM contraction and thus increase in prostate size

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44
Q

What are the causes of BPH

A

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
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45
Q

Describe the epidemiology of BPH

A

Only affects men and the incidence increases with age

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46
Q

LUTS: give 3 symptoms of storage problems.

A
  1. Frequency.
  2. Urgency.
  3. Nocturia.
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47
Q

LUTS: give 4 symptoms of voiding problems.

A
  1. Straining.
  2. Hesitancy.
  3. Incomplete emptying.
  4. Poor flow.
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48
Q

What other symptoms are associated with LUTS

A

post-micturition voiding, haematuria, dysuria

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49
Q

Name a symptom scoring system for LUTS

A

International prostate symptom score (IPSS)

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50
Q

What investigations might you carry out in someone with suspected LUTS

A
  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
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51
Q

What might dysuria suggest

A

Inflammation

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52
Q

What is the normal flow rate for someone under 40

A

21ml/s

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53
Q

What is the normal flow rate for someone between 40 and 60

A

18ml/s

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54
Q

What is the normal flow rate for someone >60

A

13ml/s

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55
Q

What 2 things can cause a decline in Flow rate

A

Obstruction within the lower urinary tract

Detrusor under activity

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56
Q

What are the complications of LUTS

A
  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
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57
Q

Give 3 symptoms of acute urinary retention.

A
  1. PAINFUL!
  2. Sudden onset.
  3. > 500ml of urine in bladder.
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58
Q

How is the pain from acute urinary retention relieved

A

Catheterisation
Pain relief
Reassurance

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59
Q

Name a rare but serious cause of acute urinary retention.

A

Spinal cord compression.

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60
Q

What are the issues with chronic urine retention

A

Incomplete bladder emptying leads to increased risk of infections and stones

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61
Q

What are the aims of treatment for LUTS

A

Improve urinary symptoms
Improve quality of life
reduce the complications of bladder outflow obstruction

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62
Q

What lifestyle modifications can be made to reduce LUTS

A

Reduce caffeine and alcohol intakee
distraction methods
Bladder training

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63
Q

Describe the treatment for someone who presents with mild LUTS.

A

Reassurance, watch and wait.

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64
Q

Describe the treatment for someone who presents with moderate LUTS.

A
  1. Fluid management, avoid caffeine.

2. Bladder drill.

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65
Q

Give 2 pharmacological therapies used in the treatment of moderate to severe LUTS.

A
  1. Alpha-1-blockers e.g. tamulosin.
  2. 5-alpha-reductase-inhibitors.
    (finasteride, dutasteride)
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66
Q

How do alpha-1-blockers work in the management of LUTS?

A

They cause vasodilation of the smooth muscle in the bladder neck and prostate and so reduced resistance to bladder outflow.

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67
Q

Give 2 potential side effects of tamulosin.

A

2 side effects include hypotension and retrograde ejaculation.

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68
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.

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69
Q

Give a surgical treatment for BPE.

A

Transurethral resection of prostate (TURP)

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70
Q

What investigations might you do in someone with acute urinary retention?

A
  1. Clinical examination: palpable bladder?
  2. MRI.
  3. Bloods.
  4. Neurological tests; could be a sign of spinal cord compression e.g. pain in back, loss of anal reflex, leg weakness.
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71
Q

Give 4 symptoms of BPH.

A
  1. Increased frequency of micturition.
  2. Nocturia.
  3. Hesitancy.
  4. Post-void dribbling.
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72
Q

What are the indications for surgical management of LUTS (RUSHES)

A 
Retention 
UTI's 
Stones 
Haematuria 
Elevated creatinine due to BOO 
Symptom deterioration
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73
Q

What are the complications of trans-urethral resection of the prostate

A 
Immediate = sepsis, haemorrhage 
Early  = sepsis, haemorrhage and clot retention 
Late = retrograde ejaculation, ED, urethral stricture, bladder neck stenosis, urinary incontinence
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74
Q

What is the function of the prostate?

A

The prostate secretes proteolytic enzymes into the semen which break down clotting factors in the ejaculate.

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75
Q

What type of cancer is prostate cancer

A

Adenocarcinoma

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76
Q

Which anatomical zone of the prostate does prostate cancer commonly affect?

A

The peripheral zone initially but can then spread locally to the transition zone and central zone

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77
Q

Where can prostate cancer commonly metastasise to?

A

Lymph nodes and bone, brain, liver and lung

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78
Q

What are the causes of prostate cancer

A

Family history
High testosterone
Ethnicity - 2-3x higher in afro-caribbean
Genetic (HOXb13 and BRAC2)

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79
Q

What is the epidemiology of prostate cancer

A

Most common male malignancy

mean age at diagnosis at 72

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80
Q

By what routes does prostate cancer spread

A

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

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81
Q

What are the symptoms of prostrate cancer

A

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

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82
Q

What investigations might you do in someone who you suspect has prostate cancer?

A
  • 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
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83
Q

On examination, what things might you see that indicate prostate cancer

A

External anal sphincter tone (detect spinal cord compression)

Overdistended bladder due to outlet obstruction

Bony tenderness

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84
Q

What is PSA

A

Semen liquefaction protease

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85
Q

What is the issue with the PSA test

A

High sensitivity but low low specificity = prostate specific but not cancer specific

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86
Q

Other than prostate cancer. What can cause an elevated PSA?

A
  1. Benign prostate enlargement.
  2. UTI.
  3. Prostatitis.
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87
Q

What is a normal level of PSA

A

3ng/ml - elevated suggests prostate cancer

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88
Q

What are the indications for prostate biopsy

A

Palpably suspicious DRE regardless of PSA

PSA >3.0ng/ml

Suspicious lesions on MRI

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89
Q

What is the grading system used in prostate cancer

A

Gleason grading

- higher the score the more aggressive the cancer

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90
Q

Describe the Gleason grading system for prostate cancer

A

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)

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91
Q

What are the benefits of PSA test

A

Early diagnosis of localised disease

Early treatment of advanced disease

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92
Q

What are the risks of PSA test

A

Overdiagnosis of insignificant disease

Harm caused by investigation/treatment

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93
Q

What is the treatment for localised prostate cancer?

A
  • Observation.
  • Surgery - radical prostatectomy.
  • Radiotherapy (external beam).
  • Adjuvant hormones.
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94
Q

What are the complications of radical prostatectomy

A

Urinary incontinence and impotence

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95
Q

What is the treatment for metastatic prostate cancer?

A

Palliative treatment e.g. hormone therapy - androgen deprivation,
surgical castration,
androgen receptor antagonists

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96
Q

Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer.

A
  • Curative.
  • Reduced patient anxiety.
  • Can have adverse effects.
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97
Q

What are the forms of hormone therapy used In local or advanced/metastatic disease

A

Orchiectomy - remove testes

Luteinising hormone releasing hormone agonists

Antiandrogens - block testosterone

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98
Q

Name a Luteinising hormone releasing hormone agonists

A

Leuporelin or goserelin

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99
Q

Name an antiandrogen

A

Flutamide

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100
Q

What are the side effects of hormone therapy

A 
Impotence 
Depression 
Hot flushes 
Lethargy
Osteoporosis
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101
Q

Name some other treatments for metastatic prostate cancer

A 
Chemotherapy 
Bisphosphonates 
Radiotherapy for bone pain 
TURP to relieve symptoms of bladder outflow obstruction 
Nephrostomies for ureteric obstruction
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102
Q

What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream.

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103
Q

What is the role of the cortex in neuro-urology

A

Sensation

Voluntary initiation

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104
Q

What is the role of the pontine micturition centre and periaqueductal grey in euro-urology

A

Co-ordination

Completion of voiding

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105
Q

Name the spinal reflexes of micturition

A

Reflex bladder contraction (Sacral micturition centre)

Guarding reflex (Onuf’s nucleus)

Receptive relaxation (Sympathetic spinal reflex)

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106
Q

Parasympathetic (Cholinergic) S3-S5 controls what

A

Detrusor muscle contraction

Smooth muscle sphincter relaxation

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107
Q

Sympathetic (Noradrenergic) T10-L2 controls what

A

Smooth muscle sphincter contraction

Inhibition detrusor muscle contraction (Allows relaxation)

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108
Q

What do the somatic nerves control

A

Striated sphincter contraction/relaxation (External urethral sphincter)
Voluntary control

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109
Q

What happens in bladder storage

A

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

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110
Q

What happens in bladder voiding

A

a. PMC coordinates voiding via parasympathetic detrusor contraction and sphincter relaxation at the same time

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111
Q

LUTs: Storage symptoms

A

Frequency
Urgency
Nocturia
Incontinence

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112
Q

LUTS: Voiding symptoms

A 
Slow stream 
Splitting or spraying 
Intermittency 
Hesitancy 
Straining 
Terminal dribble
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113
Q

LUTS: Post micturition

A

Post micturition dribble

Feeling of incomplete emptying

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114
Q

What parameters are measured in a bladder diary

A 
Frequency per day 
Frequency per night 
Volume per day 
Volume per night 
Nocturnal volume/24hr 
Functional capacity 
Incontinence
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115
Q

How many times does a normal person urinate per day

A

2-8 times

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116
Q

How much urine does a normal 70kg male pass per day

A

2-2.7

>2.7L = polyuria

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117
Q

How much urine on average is produced per wee

A

500ml

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118
Q

Define incontinence

A

involuntary loss of urine

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119
Q

Define urgency incontinence

A

Associated with an urgent desire to void which is difficult to defer

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120
Q

Name three types of incontinence

A

Stress = associated with coughing/straining

Continuous = due to fistula

Mixed = combination of stress and urgency

Urgency

Social = occurs in those with dementia

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121
Q

Give a reason why incontinence in men is less common than it is women.

A

Men have a bladder neck mechanism and a strong urethral sphincter whereas women have only a weak urethral sphincter.

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122
Q

What are the causes of stress incontinence in females

A

Usually second to birth trauma
Can be neurogenic
Congenital

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123
Q

Describe the treatment for stress incontinence in females.

A
  1. Pelvic floor physio.
  2. Duloxetine - increases contraction of urethral sphincter (concerns over psychiatric SE’s).
  3. Surgery.
    - sling
    - Colposuspension
    - Bulking agents
    - artificial sphincter
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124
Q

What is the main cause of stress incontinence in men?

A

Neurogenic or iatrogenic (prostatectomy - ablated sphincter during prostatectomy)

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125
Q

Describe the treatment for stress incontinence in males.

A
  1. Artificial sphincter.

2. Sling.

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126
Q

What are the surgical options for stress incontinence surgery

A
  • 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
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127
Q

Define overactive bladder

A

Defined as urgency with frequency with or without nocturne when appearing in absence of local pathology

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128
Q

Describe the treatment for an overactive bladder.

A
  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
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129
Q

How to muscarinic antagonists help an overactive bladder

A

Decrease parasympathetic activity by blocking M2/3 receptors so prevents the bladder contracting

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130
Q

How to B3 agonists help an overactive bladder

A

Increase sympathetic activity at B3 receptor in the bladder which inhibits the detrusor muscle contraction enabling relaxation

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131
Q

What are the risks associated with botox treatment of overactive bladder

A

Risk of urinary retention

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132
Q

How does sacral neuromodulation work in the treatment of overactive bladder

A

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

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133
Q

What is bladder augmentation

A

Cystoplasty using the stomach, colon or small bowel where the bladder gets attached to one of these which increases bladder capacity for urine

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134
Q

What are the obstructive causes of voiding issues

A

BPE
Urethral stricture
Prolapse/mass

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135
Q

What is the management for obstruction induced voiding issues

A

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

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136
Q

What are the non obstructive causes of voiding problems

A

Detrusor underactivity - bladder loses ability to contract

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137
Q

What are the management approaches for non obstructive voiding issues

A

Long term catheterisation

Sacral neuromodulation

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138
Q

What is the treatment for a BPO male with no ED

A
  1. Alpha antagonist
  2. 5 reductase inhibitor
  3. TURP
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139
Q

What is the treatment for a BPO male with ED

A
  1. PDE5 inhibitor
  2. Alpha antagonist
  3. TURP
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140
Q

What is the treatment for someone with OAB

A
  1. Antimuscarinic
  2. B3 antagonist
  3. Botox
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141
Q

What is the treatment for a women with OAB

A
  1. Antimuscarinic
  2. B3 agonist
  3. Botox
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142
Q

What is the treatment for a women with stress urinary incontinence

A

Physiotherapy

Surgery

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143
Q

A conus spastic spinal cord lesion above the cauda equina leads to loss of what micturition processes

A

Coordination

Completion of voiding

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144
Q

What are the features of a conus spinal lesion

A

Reflex bladder contractions
Detrusor sphincter dyssynergia
Poorly sustained bladder contraction

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145
Q

Describe the pathophysiology of conus spinal lesions

A

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

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146
Q

A flaccid spinal cord injury leads to damage to the sacral micturition centre - what are the effects of this

A

Reflex bladder contraction
Guarding reflex
Receptive relaxation

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147
Q

What are the features of a flaccid spinal cord injury

A

Areflexic bladder
Stress incontinence
Risk of poor compliance

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148
Q

What is the pathophysiology of flaccid spinal cord lesion

A

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

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149
Q

What are the aims of neurogenic bladder

A

Bladder safety
Continence and symptom control
Prevent autonomic dysreflexia

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150
Q

Describe the pathophysiology of autonomic dysreflexia

A

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
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151
Q

What are the signs of autonomic dysreflexia

A

Headache
Severe hypertension
Flushing

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152
Q

What is the management of autonomic dysreflexia

A

Need to remove the noxious stimuli - change catheter to allow bladder to drain or help them to empty their bowels

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153
Q

Define unsafe bladder

A

One that puts the kidneys at the risk of damage

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154
Q

What are the risk factors for unsafe bladder

A 
Raised blood pressure 
Vesico-ureteric reflux 
Chronic infection 
 - residual urine 
 - Stones
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155
Q

What are the causes of raised bladder pressure

A

Prolonged detrusor contraction and loss of compliance

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156
Q

What is the result of raised bladder pressure

A

Problems with drainage of urine from the kidneys and ultimately hydronephrosis and renal failure

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157
Q

What are the two routes to reflex the bladder

A
  1. Harness reflexes to empty bladder into incontinence device
  2. Suppress reflexes converting bladder to flaccid type then empty regularly
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158
Q

What is the bladder management for a paraplegic

A

Suprapubic catheter
Conveen (Condom is connected to bag and urine drains straight in)
Suppress reflexes or poorly compliant bladder

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159
Q

What is convene drainage

A

Condom attached to bag

No indwelling catheter

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160
Q

What is a suprapubic catheter

A

inserted under anaesthetic into the bladder from the abdomen
Risk of infections and stones

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161
Q

What are the approaches for suppressing reflex bladder contraction

A 
Anti-cholinergics 
Mirabegron 
Intravesical botulinum toxin 
Posterior rhizotomy 
Cystoplasty
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162
Q

What are some examples of flaccid and low spinal lesions

A 
Spina bifida 
Sacral fracture 
Transverse myelitis 
Ischaemic injuries 
Cauda equina
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163
Q

What sort of cancer is bladder cancer

A

Transitional cell carcinoma

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164
Q

Where might a transitional cell carcinoma arise

A
  1. Bladder
  2. Ureter
  3. Renal pelvis
  4. Urethra

Areas lined by transitional epithelium

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165
Q

Describe the epidemiology of transitional cell carcinoma.

A
  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
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166
Q

Give 5 risk factors for transitional cell carcinoma.

A
  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
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167
Q

Give 5 symptoms of transitional cell carcinoma (Bladder carcinoma)

A
  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
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168
Q

Give 5 investigations that you might do in someone who you suspect has transitional cell carcinoma (Bladder cancer)

A
  1. Urine microscopy/cytology
  2. Cystoscopy + bladder wall biopsy
  3. CT urogram
  4. Urinary tumour markers
  5. MRI/lymphangiography
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169
Q

Give 2 potential risks of flexible cystoscopy.

A
  1. UTI’s.

2. Problems passing urine.

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170
Q

Why would you want to image the upper urinary tract of someone with transitional cell carcinoma?

A

You image the UUT to confirm that there is no other TCC elsewhere in the urinary tract.

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171
Q

What staging system is used for TCC?

A

TNM staging.

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172
Q

Describe the TNM staging for bladder cancer

A

T1 (Submucosa)
T2 (Muscle - where it becomes invasive)
T3 (Outer fat)
T4 (Other organs)

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173
Q

Describe the treatment for non-muscle invasive bladder cancer (CIS, Ta, T1).

A
  1. Trans urethral resection of the bladder (TURBT)

2. Chemotherapy to reduce the risk of recurrence and progression to muscle invasion.

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174
Q

Describe the treatment for muscle invasive bladder cancer (T2, T3).

A
  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)
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175
Q

Describe the treatment for T4 TCC (invasion beyond the bladder).

A
  1. Palliative chemo/radiotherapy.

2. Chronic catheterisation for pain.

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176
Q

Name a helminth that can cause squamous cell carcinoma of the bladder.

A

Schistosomiasis.

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177
Q

What are the two forms of renal cancer

A

Renal cell carcinoma

Transitional cell carcinoma

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178
Q

Where does renal cell carcinoma arise from

A

From the proximal convoluted tubular epithelium

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179
Q

Where does transitional cell carcinoma arise from

A

Renal pelvis

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180
Q

What are the three types of transitional cell carcinoma

A

Clear cell - more aggressive
Papillary
Chromophobe

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181
Q

How is renal cancer spread

A

Direct
Lymphatics
Haematogenous

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182
Q

Describe the epidemiology of renal cell carcinoma.

A
  1. Incidence increases in those > 60 y/o.

2. Males > females.

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183
Q

Give 3 risk factors for renal cell carcinoma.

A
  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
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184
Q

Name an inherited renal disease that can cause renal cell carcinoma.

A

Von Hippel Lindau disease.

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185
Q

What is Von Hippel Lindau disease?

A

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.

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186
Q

What are the 3 classic signs of renal cell carcinoma?

A
  1. Haematuria.
  2. Flank mass.
  3. Loin pain.
  4. Abdominal mass
  5. Paraneoplastic symptoms
  6. General = lethargy, malaise, anorexia and wt loss
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187
Q

Why do people with renal cell carcinoma rarely present with symptoms of the disease?

A

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.

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188
Q

Name 3 places that renal cell carcinoma might metastasise to.

A
  1. Lymph nodes.
  2. Lungs.
  3. Bones.
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189
Q

What investigations might you do in someone with renal cell carcinoma?

A
  • Ultrasound.
  • Bloods: FBC, U+E, LFT, Ca profile.
  • Abdo CT scan with contrast.
  • Bone scan for boney metastases.
  • Renal biopsy
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190
Q

What is the staging criteria used in renal cell carcinoma

A

Bosniak classification
1-2 = discharge
2F = follow up
3-4 = treat

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191
Q

What is the treatment for localised renal cell carcinoma?

A

Surgical excision - partial nephrectomy.

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192
Q

What is the treatment for metastatic renal cell carcinoma?

A
  • Palliative nephrectomy.

- Radiotherapy.

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193
Q

What is the most common cancer in males aged 15-44

A

Testicular cancer

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194
Q

Where does testicular cancer arise from

A

germ cells

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195
Q

What are the two types of testicular cancer

A

Seminoma = most common type, slow growing

Non-seminoma = yolk Choriocarcinoma/teratoma, rapid growth

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196
Q

Where does the testicular cancer spread locally

A

epididymis
spermatic cord
Scrotal wall
Leads to pelvic and inguinal metastasis

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197
Q

Where does testicular cancer metastasise to distally

A

Lungs, liver and bones

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198
Q

What are the risk factors for testicular cancer

A 
Cryptorchidism 
Fx history 
Previous testicular tumour 
Infertility 
Infant hernia 
Testicular intraepithelial neoplasia 
Maternal oestrogen exposure
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199
Q

What are the signs and symptoms of testicular cancer

A

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

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200
Q

What are the investigations for someone with testicular cancer

A 
Tumour markers 
 - AFP (Alpha-fetoprotein) 
 - B-hCG (Beta subunit of human chorionic gonadotrophin) 
Testicular biopsy 
Imaging (US (Diagnosis)
CT/MRI for staging
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201
Q

What is the staging criteria used in testicular cancer

A 
1 = (No mets)
2= (nodes under diaphragm)
3 = (Nodes above the diaphragm 
4 = (Mets in the lungs)
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202
Q

What is the management of testicular cancer

A

Orchidectomy
Chemo and radiotherapy (More effective in seminomas below diaphragm)
Widespread tumours are treated with chemo and teratomas treated with chemo

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203
Q

What is an epididymal cyst

A

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

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204
Q

What is hydrocele

A

Abnormal collection of fluid within the tunica vagnalis

205
Q

What are the two forms of hydrocele

A

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
Q

What is varicocele

A

Abnormal dilatation of the testicular veins in the pampiniform venous plexus in the scrotum caused by venous reflux

207
Q

Why might renal cell carcinoma cause left sided varicocele?

A

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
Q

Name the classification that helps differentiate between benign cystic lesions and cancerous cystic lesions.

A

The Bozniak classification.

209
Q

What are the symptoms of a varicocele

A

Patient complains for a dull ache or scrotal heaviness

Scrotum hangs lower on the side of the varicocele

210
Q

What is the treatment for varicocele

A

surgery if there is pain, infertility or testicular atrophy

211
Q

What is testicular torsion

A

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
Q

What is an erection

A

Neurovascular phenomenon under hormonal control

  • arterial dilatation
  • smooth muscle relaxation
  • Activation of the corporeal veno-occlusive mechanism
213
Q

What is the arterial supply of the penis

A

Internal iliac

  • Internal pudendal artery
    (i) Dorsal penile artery
    (ii) Cavernosal artery/deep penile arteries
    (iii) Bulbar artery
214
Q

What is the venous drainage of the penis

A

Subtunical plexus

  • to circumflex veins
  • to deep dorsal veins

Corpora cavernosa
- cavernosa veins

Internal pudendal veins

215
Q

What nerve fibres do cavernous nerves carry?

A

Parasympathetic: S2-4.
Sympathetic: T11-L2.

216
Q

Describe the physiology of an erection.

A
  1. Parasympathetic stimulation.
  2. Arteriolar dilation.
  3. Trabecular Smooth muscle relaxation.
  4. Testosterone.
217
Q

What is central control of erections

A

Higher stimuli

  • Hypothalamus
  • Oxytocin pro erectile pathways

Spinal reflex

218
Q

What are the primary causes of low testosterone

A

Pituitary

Hypothalamus

219
Q

What are the secondary causes of low testosterone

A

Testes

- Tumour, injury, drugs

220
Q

What are the congenital syndromes associated with low testosterone

A

Kleinfelters

Noonans

221
Q

What chemical compound is responsible for the smooth muscle relaxation that is required for an erection?

A

Nitric oxide (NO). It causes a fall in cytoplasmic calcium -> smooth muscle relaxation.

222
Q

Define erectile dysfunction

A

Persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance

223
Q

What are the 2 main causes of erectile dysfunction?

A
  1. Organic e.g. vasculogenic, neurogenic, hormonal, anatomical drug induced
  2. Psychogenic.
224
Q

What are the risk factors for erectile dysfunction

A

CVS disease

  • Lack of exercise
  • Obesity
  • Smoking
  • Hypercholesterolaemia
  • Metabolic syndrome (DM)

Liver disease and alcohol
Renal failure
Trauma (Pelvic fracture)
Iatrogenic (Prostatectomy)

225
Q

Give 3 characteristics of psychogenic erectile dysfunction.

A
  1. Sudden onset
  2. Situational.
  3. Younger males affected.
  4. Good nocturnal and early morning erections
226
Q

What investigations might you do for someone with suspected ED

A

Fasting glucose
Lipid profile
Morning testosterone
- If low testosterone then perform prolactin, FSH and LH

227
Q

What are the specialised tests for ED

A

Nocturnal penile tumescence and rigidity
Intracavernosal injection test
Duplex USS of penile arteries
Arteriography

228
Q

What is the goal of ED treatment

A

treat the reversible factors

229
Q

What is the non-pharmacological management of erectile dysfunction?

A
  1. Lose weight, stop smoking.

2. Education and counselling of patient and partner.

230
Q

What is the treatment for testosterone deficiency ED

A

Testosterone replacement

  • contraindicated if history of prostate cancer
  • psychosexual counselling
231
Q

What is the first line pharmacological management of erectile dysfunction?

A

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
Q

Name three phosphodiesterase inhibitors

A

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
Q

What are the common side effects of phosphodiesterase inhibitors

A 
Headache 
Flushing 
Dyspepsia 
Visual disturbance 
Back pain 
Myalgia
234
Q

What is the second line pharmacological management of erectile dysfunction?

A
  1. Intracavernous injections.
  2. Vacuum devices.
  3. Apomorphine sublingual
    - Central acting dopamine agonist
  4. Intraurethral alprostadil
235
Q

What are the complications of intracavernous injections

A

Penile pain

Priapism

236
Q

What are the side effects of intraurethral alprostadil

A

Pain
Dizziness
Urethral bleeding

237
Q

How does a vacuum device work

A

Passive engorgment with constriction

238
Q

What are the side effects of a vacuum device for ED

A

Pain
Inability to ejaculate
Petechiae
Bruises and numbness

239
Q

When are vacuum devices contraindicated

A

Bleeding disorders and anti-coagulants

240
Q

What is the third line pharmacological management of erectile dysfunction?

A

Penile prosthesis implantation.

(i) Malleable prosthesis
(ii) Inflatable

241
Q

Define priapism

A

Prolonged erection lasting for >4 hours

242
Q

What is a potential consequence of priapism

A

Permanent Ischaemic damage

243
Q

Define glomerulonephritis

A

Broad term that refers to a group of parenchymal kidney disease that results in inflammation of glomeruli and nephrons

244
Q

Give 3 consequences of glomerulonephritis (glomerular disease).

A
  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
Q

What are the 4 presentations of glomerulonephritis

A
  1. Asymptomatic haematuria
  2. Nephrotic syndrome
  3. Nephritic syndrome
  4. CKD
246
Q

Briefly describe the pathophysiology of glomerulonephritis (glomerular disease).

A

Immunologically mediated: immunoglobulin deposits and inflammatory cells.

247
Q

What are the causes of glomerulonephritis

A 
Idiopathic 
Immune: SLE, goodpastures, vasculitis 
Infection: HBV, Strep, HIV
Drugs: Penicillamine, gold 
Amyloid
248
Q

What are the investigations for someone with suspected glomerulonephritis

A 
FBC/U+E/ESR
Abs = ANA, dsDNA, ANCA
Urine dipstick for proteinuria and haematuria 
Renal ultrasound and biopsy 
CXR for infiltrates
249
Q

Describe the pathophysiology of nephritic syndrome

A

Kidney inflammation and immune réponse triggered by infection with causes large podocytic pores allowing RBC into the urine

250
Q

Give 4 causes of acute nephritic syndrome.

A
  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
Q

Give 5 signs of acute nephritic syndrome.

A
  1. Inflammation of glomeruli.
  2. HAEMATURIA
  3. PROTEINURIA –> oedema
  4. Hypertension.
  5. Fluid overload.
  6. Oliguria and progressive renal impairment
  7. Red cell casts.
  8. Uraemia (Anorexia, pruritis, lethargy and nausea)
252
Q

What are the signs of IgA nephropathy

A

Haematuria, IgA deposition in mesangium of the kidney associated with tonsillitis

253
Q

What investigations would you carry out in someone with suspected IgA nephropathy

A

Diffuse mesangial IgA deposits

Subendothelial, sub epithelial deposits on electron microscopy

254
Q

What is the treatment for IgA nephropathy

A
  • Induction = steroids and cyclophosphamide

- Remission = steroids and azathioprine

255
Q

What 4 signs are needed in order to make a diagnosis of nephrotic syndrome.

A
  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
Q

What can nephrotic syndrome be secondary to?

A
  1. Diabetes.
  2. Amyloid.
  3. Infections.
  4. SLE.
  5. Drugs.
257
Q

What are the complications of nephrotic syndrome

A
  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
Q

What are the investigations for someone with suspected nephrotic syndrome

A

Check bloods for hyperlipidameia and hypoalbuminaemia

Renal biopsy

Urinanalysis (Dipstick) +++ protein

Look for auto-antibodies

259
Q

What are the causes of nephrotic syndrome

A
  1. Minimal change glomerulonephritis
  2. Membranous nephropathy
  3. Focal segmental glomerulosclerosis
  4. Membranoproliferative/mesangiocapillary glomerulonephritis
260
Q

Describe the pathophysiology of minimal change glomerulonephritis

A

Podocyte loss, vacuolation and microvilli appearance

Commonest cause of nephrotic syndrome in children

261
Q

What is the treatment for minimal change glomerulonephritis

A

Corticosteroids

262
Q

Describe the pathophysiology of membranous nephropathy

A

Asymptomatic proteinuria/nephrotic syndrome +/- microscopic haematuria, HTN and renal impairment

263
Q

Membranous nephropathy is associated with what conditions

A

Lung, colon, breast and stomach cancer

Autoimmune SLE and thyroid disease

Infections = HBV, Hep B or C, Schistosomiasis

Drugs = penicillamine, gold, NSAIDs

264
Q

What investigations would you do for someone with suspected membranous nephropathy

A

Biopsy showing sub epithelial immune complex deposits (IgG and C3) and thickened glomerular basement membrane

265
Q

What is the treatment for membranous nephropathy

A

Immunosuppression if renal function declines

266
Q

Membranoproliferative or mesangiocapillary glomerulonephritis is associated with what

A

HBV
HCV
Endocarditis
Autoimmune

267
Q

What is the management of nephrotic syndrome

A
  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
Q

What would you notice on the electron microscopy taken from someone with minimal change disease?

A

Fused podocytes.

269
Q

What is the treatment for minimal change disease?

A

Steroids.

270
Q

Describe the pathophysiology behind nephritic syndrome.

A

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
Q

Describe the pathophysiology behind nephrotic syndrome.

A

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
Q

What is the most common renal cancer in children?

A

Wilms tumour.

273
Q

Is focal segmental glomerulosclerosis a cause of nephritic or nephrotic syndrome?

A

Nephrotic syndrome.

274
Q

Why is someone with nephrotic syndrome at risk of sepsis?

A

Because you lose immunoglobulins in the urine.

275
Q

Give 5 functions of the kidney.

A
  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
Q

Write an equation for GFR.

A

(Um X urine flow rate) / Pm.

  • Um = concentration of marker substance in urine.
  • Pm = concentration of marker substance in plasma.
277
Q

What would you expect a typical GFR to be?

A

120ml/min.

20% of cardiac output

278
Q

Give an example of a marker substance used for estimating GFR.

A

Creatinine.

279
Q

Estimating GFR: Give 3 essential features of a marker substance.

A
  1. Not metabolised.
  2. Freely filtered.
  3. Not reabsorbed/secreted.
280
Q

Name a drug that can inhibit creatinine secretion. What is the affect of this on GFR?

A

Trimethoprim/ cimetidine and ritonavir

Serum creatinine rises and so kidney function (GFR) appears worse.

281
Q

What is the affect on GFR of afferent arteriole vasoconstriction?

A

Decreased GFR.

282
Q

What is the affect on GFR of efferent arteriole vasoconstriction?

A

Increased GFR.

283
Q

Where in the nephron does the bulk of reabsorption occur?

A

At the proximal convoluted tubule.

284
Q

What 7 things are reabsorbed at the PCT?

A
  1. Sodium.
  2. Chlorine.
  3. Potassium.
  4. Glucose.
  5. Water.
  6. Amino acids.
  7. Bicarbonate.
285
Q

What is Fanconi syndrome?

A

Failure of the nephron to reabsorb essential ions. Sugar, amino acids and bicarbonate are therefore present in the urine.

286
Q

Give 2 signs of Fanconi syndrome.

A
  1. Sugar in the urine (Glycosuria)
  2. Acidotic due to bicarbonate in the urine.
  3. Rickets/osteomalacia.
287
Q

Give 2 causes of Fanconi syndrome.

A
  1. Myeloma.
  2. Cystinosis.
  3. Anti-retrovirals (Tenfovir)
288
Q

What is the function of the counter current multiplication system?

A

It generates a hypertonic medullary interstitium for H2O reabsorption. Na+ moves out of the ascending limb which increases the medullary osmolality, H2O follows.

289
Q

Which part of the loop of henle is permeable to H2O?

A

The descending limb is permeable to H2O.

290
Q

Describe tubuloglomerular feedback.

A

Macula densa cells of the DCT lie between the AA and EA. They detect NaCl and use this as an indicator of GFR.

291
Q

Macula densa cells detect a raised NaCl. What is the response?

A

AA constriction.

292
Q

Macula densa cells detect a reduced NaCl. What is the response?

A

Renin secretion.

293
Q

What 2 cell types are found in the nephron collecting duct?

A

Principal and intercalated cells.

294
Q

What hormone is responsible for regulating sodium reabsorption?

A

Aldosterone.

295
Q

Why might aldosterone secretion lead to hypokalaemia?

A

Aldosterone secretion leads to increased sodium reabsorption. Sodium reabsorption leads to increased potassium secretion and therefore hypokalaemia.

296
Q

What is the affect of NSAIDs on the afferent arteriole of glomeruli?

A

NSAIDs inhibit prostaglandins and so lead to AA vasoconstriction = reduced GFR.

297
Q

NSAIDs lead to a reduced GFR. Why?

A

NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction -> reduced GFR.

298
Q

What is the affect of ACEi on the efferent arteriole of glomeruli?

A

ACEi cause EA vasodilation = reduced GFR.

299
Q

Name 2 factors that govern renal potassium.

A
  1. Na+.

2. Aldosterone.

300
Q

What ion is responsible for volume control?

A

Sodium!

301
Q

Name 2 hormones that increase sodium reabsorption.

A
  1. Aldosterone.

2. Angiotensin 2.

302
Q

Name a hormone that decreases sodium reabsorption.

A

ANP.

303
Q

What is the function of EPO?

A

It stimulates the bone marrow -> RBC maturation.

304
Q

Give 2 functions of calcitriol.

A
  1. Increased calcium and phosphate absorption from the gut.

2. Suppression of PTH.

305
Q

Why might someone with advanced CKD also have hyperparathyroidism?

A

Advanced CKD = calcitriol deficiency. Calcitriol suppresses PTH therefore deficiency -> hyperparathyroidism.

306
Q

What triggers PTH secretion?

A

Low serum calcium.

307
Q

Give 3 ways in which PTH increases serum calcium.

A
  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
Q

Name 2 hormones secreted from the posterior pituitary gland.

A
  1. ADH.

2. Oxytocin.

309
Q

Describe the function of ADH.

A

ADH acts on the collecting ducts. It increases insertion of aquaporin 2 channels leading to H2O retention.

310
Q

Give 3 factors that stimulate renin release.

A
  1. Sympathetic stimulation.
  2. Decreased BP.
  3. Decreased Na detected by macula densa.
311
Q

Give 3 functions of ANP.

A
  1. Renal vasodilator.
  2. Inhibits aldosterone.
  3. Closes ENaC (decreased reabsorption of Na+).
312
Q

Where on the nephron does aldosterone act?

A

On the collecting ducts.

313
Q

Describe aldosterone action.

A

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
Q

Blood pressure control is determined by what

A
  1. blood volume

2. Vasoconstriction

315
Q

Where do loop diuretics act

A

Loop of Henle

316
Q

where do thiazide diuretics work

A

DCT

317
Q

Where do aldosterone antagonists act

A

Collecting duct

318
Q

How do we measure kidney function

A

Creatine - waste product of muscle metabolism
eGFR
Proteinuria/Albuminuria

319
Q

What is the definition of chronic kidney disease

A

Chronic impairment of kidney function normally over 3 months

320
Q

What is the classification of CKD

A

 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
Q

What are the causes of chronic kidney disease

A
  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
Q

Give 5 signs of CKD.

A
  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
Q

What investigations would you carry out in someone with suspected chronic kidney disease

A 
•	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
Q

What are the complications of chronic kidney disease

A

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
Q

Describe the management for CKD

A
  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
Q

What are the three forms of dialysis

A

Peritoneal dialysis
Haemodialysis
Kidney transplant

327
Q

How often does someone need to go for haemodialysis

A

3x a week for 4 hours

328
Q

How does haemodialysis work

A

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
Q

How does peritoneal dialysis work

A

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
Q

What is the access point in haemodialysis?

A

AV fistula.

331
Q

Why might someone having haemodialysis have a PFTE graft as opposed to an AV fistula?

A

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
Q

Give examples of waste products that are removed from the blood in dialysis.

A
  1. Urea.
  2. Creatinine.
  3. Potassium.
  4. Phosphate.
333
Q

Give 5 potential complications of haemodialysis.

A
  1. Hypotension.
  2. Cramps.
  3. Nausea.
  4. Chest pain.
  5. Fever.
  6. Blocked or infected dialysis catheter.
334
Q

Give 3 groups of people who haemodialysis is good for.

A
  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
Q

What is the access point in peritoneal dialysis?

A

A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel.

336
Q

Give 4 potential complications of peritoneal dialysis.

A
  1. Infection e.g. peritonitis/catheter exit site infection.
  2. Peri-catheter leak.
  3. Abdominal wall herniation.
  4. Intestinal perforation.
337
Q

Give 3 groups of people who peritoneal dialysis is good for.

A
  1. Young people/those in full time work.
  2. People who want control/responsibility of their care.
  3. People with severe HF.
338
Q

Where in the abdomen does a transplanted kidney lie?

A

In the iliac fossa.

339
Q

Describe the criteria for selection of a living donor for kidney transplant.

A
  1. Blood relative.
  2. ABO blood group compatible.
  3. HLA identical.
  4. Excellent medical condition and normal renal function.
340
Q

Name 3 medical conditions that can exclude living kidney donation.

A
  1. Renal parenchymal disease.
  2. History of stones/frequent UTI/hypertension/DM.
  3. Recent malignancy.
341
Q

Describe the criteria for selection of a cadaver donor for kidney transplant.

A
  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
Q

What tests can be done to evaluate kidney function in a potential kidney donor?

A
  1. Serum creatinine.
  2. Creatinine clearance.
  3. Urinalysis.
  4. Urine culture.
  5. GFR.
343
Q

Give 5 contraindications for renal transplant.

A
  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
Q

Give 3 ways in which recipient and donor matching is assessed.

A
  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
Q

What are 3 surgical complications of kidney transplant

A

Thrombosis
Obstruction
Infection

346
Q

Give 4 factors that can influence the longevity of renal allograft.

A
  1. Age.
  2. HLA matching.
  3. Ischaemia time.
  4. Number of acute rejection episodes.
  5. Ethnicity.
347
Q

What are the 2 major causes of allograft failure?

A
  1. Chronic rejection.

2. Death with functioning graft.

348
Q

What are the 2 major causes of death after kidney transplant?

A
  1. CV disease.

2. Infection.

349
Q

Name the 3 types of renal allograft rejection.

A
  1. Hyper-acute.
  2. Acute.
  3. Chronic.
350
Q

Describe hyper-acute renal allograft rejection.

A

Preformed antibodies against HLA antigens of donor organ.

351
Q

Why might someone have pre-formed antibodies against HLA antigens?

A

Can be a consequence of blood transfusion, pregnancy, prior transplant, auto-immune disease.

352
Q

What can cause immediate graft loss?

A

Fibrinoid necrosis.

353
Q

Describe acute renal allograft rejection.

A

Activated T lymphocytes. Occurs within the first 6 months but is often reversible e.g. with steroids.

354
Q

Describe chronic renal allograft rejection.

A

Slow and gradual decline in renal function, accompanied by proteinuria and increased creatine

355
Q

Give 3 consequences of chronic immunosuppression.

A
  1. Malignancy.
  2. Infection.
  3. SE’s of other drugs.
356
Q

Name a loop diuretic.

A

Furosemide - acts on Na+/K+/2Cl- transporter (NKCC2).

357
Q

Give 3 potential side effects of furosemide.

A
  1. Hypokalaemia.
  2. Hypotension.
  3. Dehydration.
358
Q

What other drug might you prescribe with furosemide in someone with poorly controlled potassium?

A

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
Q

Name a potassium sparing diuretic.

A

Spironolactone.

360
Q

On which part of the nephron do thiazides act?

A

The distal tubule.

Act on NCC channels.

361
Q

Describe the fluid distribution in the body.

A

ICF: 28L.
ECF: 14L
- Interstitial: 11L.
- Plasma: 3L.

362
Q

How much extra-vascular fluid is there in the body?

A

ICF + interstitial = 39L.

363
Q

Fluid Movement is determined by what?

A
  • Hydrostatic pressure
  • Osmotic pressure (Salt and electrolytes)
  • Oncotic pressure (protein)
364
Q

What is the normal daily fluid intake for an adult

A

is 1.5L-2L daily for relatively sedentary lifestyle

365
Q

What happens to the heart rate in hypovolaemia?

A

Increases - tachycardia.

366
Q

What happens to the blood pressure in hypovolaemia?

A

Decreases - hypotension.

367
Q

What happens to the JVP in hypovolaemia?

A

JVP is low.

368
Q

What happens to tissue turgor in hypovolaemia?

A

Tissue turgor is reduced.

369
Q

What happens to urine output in hypovolaemia?

A

Urine output is reduced.

370
Q

What happens to weight in hypovolaemia?

A

Weight is reduced.

371
Q

Give 2 symptoms of hypovolaemia.

A

Thirst and dizziness.

372
Q

What happens to creatinine, haemoglobin and haematocrit levels in hypovolaemia?

A

They are raised.

373
Q

Name 5 groups of people who are at risk of hypovolaemia.

A
  1. Elderly.
  2. Those who have had an ileostomy.
  3. People with short bowel syndrome.
  4. Bowel obstruction.
  5. People taking diuretics.
374
Q

Name 5 groups of people who are at risk of hypervolaemia.

A
  1. Acute kidney injury patients.
  2. CKD patients.
  3. Heart failure patients.
  4. Liver failure patients.
375
Q

What happens to the heart rate in hypervolaemia?

A

HR is normal.

376
Q

What happens to blood pressure in hypervolaemia?

A

Blood pressure is high or normal.

377
Q

What happens to JVP in hypervolaemia?

A

JVP is high.

378
Q

What happens to tissue turgor in hypervolaemia?

A

Tissue turgor is normal.

379
Q

What happens to urine output in hypervolaemia?

A

Urine output is normal.

380
Q

What happens to weight in hypervolaemia?

A

Weight is increased.

381
Q

Give 2 symptoms of hypervolaemia.

A
  1. Shortness of breath.

2. Peripheral oedema.

382
Q

What happens to creatinine, haemoglobin and haematocrit levels in hypervolaemia?

A

They are reduced.

383
Q

Where might fluid accumulate in someone with hypervolaemia?

A
  • Pulmonary oedema.
  • Pleural effusion.
  • Ascites.
  • Bowel obstruction.
  • Intra-abdominal collection.
384
Q

Describe the management for hypovolaemia.

A
  1. Oral fluid.
  2. IV fluid if very ill.
  3. Treat reversible causes.
  4. Stop taking blood pressure medications
385
Q

Describe the management for hypervolaemia.

A
  1. Diuretics e.g. furosemide.
  2. Fluid restriction 1-1.5L daily
  3. Treat reversible causes.
386
Q

Name 3 isotonic solutions.

A
  1. 5% dextrose.
  2. 0.9% NaCl.
  3. Hartmann’s solution.
387
Q

What type of IV fluid moves from the intra-vascular to the extra-vascular space?

A

Crystalloid.

388
Q

Give an example of a colloid IV fluid.

A

Gelofusine.

389
Q

Why do advanced CKD patients need regular fluid assessment?

A

They may be oligouric or anuric.

390
Q

Give 3 potential causes of rising creatinine.

A
  1. Too aggressive with diuretics.
  2. Extravascular hypervolaemia but intravascular hypovolaemia.
  3. Progression of CKD.
391
Q

Define urinary tract infection.

A

Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriruria and pyuria.

392
Q

Name 3 UTI causative organisms.

A
  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
Q

Briefly describe the epidemiology of UTI’s.

A

More common in women due to short urethra and its proximity to the anus.

394
Q

Describe the pathophysiology of UTI’s.

A

Organisms colonise the urethral meatus and ascend via the transurethral route. leading to bacteriuria

395
Q

What can facilitate bacteria ascent into the urinary tract via the urethra?

A
  1. Sexual intercourse.

2. Catheterisation.

396
Q

Give 3 bacterial virulence factors that aid their ability to cause UTI’s.

A
  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
Q

The vagina is heavily colonised with lactobacilli. What is the function of this?

A

Helps maintain a low pH = host defence mechanism.

398
Q

Give 2 reasons why a post menopausal woman is more susceptible to a UTI.

A
  1. pH rises -> increased colonisation by colonic flora.

2. Reduced mucus secretion.

399
Q

Give 5 host defence mechanisms against urinary tract infection.

A
  1. Antegrade flushing of urine.
  2. Tamm-horsfall protein.
  3. GAG layer.
  4. Low urine pH.
  5. Commensal flora.
  6. Urinary IgA.
400
Q

What is pyuria?

A

The presence of leukocytes in urine.

401
Q

Name 4 lower urinary tract infections.

A
  1. Cystitis.
  2. Prostatitis.
  3. Epididymitis.
  4. Urethritis.
402
Q

Name 1 upper urinary tract infection.

A

Pyelonephritis.

403
Q

What investigations might you do on someone who you suspect has a UTI?

A
  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
Q

What determines if a UTI is complicated or uncomplicated?

A

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
Q

What is the first line treatment for an uncomplicated UTI?

A
  • Trimethoprim or nitrofurantoin for 3 days.

- Increased fluid intake and regular voiding.

406
Q

How does trimethoprim work?

A

It affects folic acid metabolism.

407
Q

Describe the management for a complicated UTI.

A

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
Q

Give 3 causes of recurrent UTI’s.

A
  1. Re-infection.
  2. Bacterial persistence.
  3. Unresolved infection.
409
Q

Define recurrent UTI.

A

> 2 episodes in 6 months of > 3 in 12 months.

410
Q

Describe the management for someone who is having recurrent UTI’s.

A
  1. Increase fluid intake.
  2. Regular voiding.
  3. Void pre and post intercourse.
  4. Abx prophylaxis.
  5. Vaginal oestrogen replacement.
411
Q

What are the risk factors for UTI development

A 
Female
Sex
Pregnancy 
Menopause 
DM 
Abnormal tract - stones, obstruction, catheter, malformation
412
Q

What is cystitis?

A

Inflammation of the bladder secondary to infection.

413
Q

Give 4 risk factors for cystitis.

A
  1. Obstruction.
  2. Previous damage to bladder epithelium.
  3. Bladder stones.
  4. Poor bladder emptying = urinary retention
414
Q

Give 3 symptoms of cystitis.

A
  1. Dysuria.
  2. Frequency.
  3. Urgency.
  4. polyuria
  5. Suprapubic tenderness and loin and abdominal pain
  6. Foul smelling urine
415
Q

What are the investigations for someone with cystitis

A

Microscopy and sensitivity of mid stream urine

Dipstick urinalysis

416
Q

What is the treatment for cystitis

A

First line = trimethoprim or cefalexin

Second line = Ciprofloxacin or co-amoxiclav

417
Q

Define prostate inflammation

A

Prostate inflammation

418
Q

What is the causative agents for prostatitis

A

E.coli, proteus and klebsiella and chlamydia

419
Q

Give 5 symptoms of acute bacterial prostatitis (type 1).

A
  1. Systemically unwell, fever.
  2. Rigors.
  3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow).
  4. Pelvic pain.
420
Q

Give 4 symptoms of chronic bacterial prostatitis (type 1).

A
  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
Q

What investigations might you do in someone with prostatitis?

A
  1. Urinalysis and MSU.
  2. Semen cultures.
  3. STI screen.
  4. Bloods including MCS.
  5. DRE
422
Q

Describe the treatment for type 1 prostatitis = acute

A
  • IV Abx e.g. gentamicin, co-amoxiclav for 2-4 weeks.
423
Q

Describe the treatment for type 2 prostatitis = chronic

A
  • 4-6 weeks quinolone e.g. ciprofloxacin or trimethoprim
424
Q

Define urethritis

A

Inflammation of the urethra

425
Q

What are the causative agents of urethritis

A

STI’s e.g. gonorrhoea, chlamydia.

Non STI causes = trauma, urethral stricture and urinary calculi

426
Q

Give a symptom of urethritis.

A

dysuria, hesitancy, urethral discharge (gonorrhoea), urethral pain, penile discomfort

427
Q

What are the investigations for someone with suspected urethritis

A

urethral smear, urinalysis, STI screening, Nucleic Acid Amplification Test (NAAT)  Female = vaginal swab and male = first void volume

428
Q

What is the treatment of urethritis

A

Treat the STI
Chlamydia = Azithromycin or erythromycin if preggers
Gonorrhoea = Ceftriaxone with azithromycin

429
Q

What is epididymo-orchitis?

A

Inflammation of the epididymis and testicle.

430
Q

What are the causative organisms of epididymo-orchiditis

A

o STI – N. gonorrhoea, C. trachomatis

o Non-STI – E. coli, enterococci, mumps, TB

431
Q

What are the risk factors for someone with epididymo-orchiditis

A

Previous infection, indwelling catheter, structural abnormality of urinary tract

432
Q

Give 3 symptoms of epididymo-orchitis.

A

unilateral scrotal pain +/- swelling, UTI symptoms, fever, urethral discharge, on examination there is tenderness and palpable swelling of the epididymis and testicles

433
Q

Describe the aetiology of epididymo-orchitis.

A
  1. If <35 y/o = STI e.g. chlamydia.

2. If >35 y/o = UTI.

434
Q

What investigations might you do on someone who you suspect has epididymo-orchitis?

A
  1. Void urine.
  2. Urethral swab.
  3. MSU.
  4. Dipstick

Rule out testicular torsion!

435
Q

Describe the treatment for epididymo-orchitis.

A
  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
Q

Define pyelonephritis.

A

Inflammation secondary to infection of the renal parenchyma and soft tissues of the renal pelvis.

437
Q

What can cause pyelonephritis?

A

UPEC. Typically P pili.

Infection is usually from the bladder or patients own bowel flora

438
Q

Give 3 symptoms of pyelonephritis.

A
  1. Loin pain.
  2. Fever.
  3. Pyuria.
  4. Malaise
  5. Rigor
  6. Vomiting
  7. Septic shock
439
Q

What investigations might you do in someone with pyelonephritis?

A
  1. Urinalysis.
  2. MCS MSU.
  3. Bloods - raised WCC, ESR and CRP.
440
Q

Describe the treatment for pyelonephritis.

A

IV fluids and antibiotics e.g. gentamicin/co-amoxiclav.

  • Drain obstructed kidney.
  • Catheterise if necessary.
  • Analgesics.
441
Q

What is the likely cause of pyelonephritis in children?

A

Reflux or structural/functional abnormalities.

442
Q

Gonorrhoea is caused by what

A

Neisseria gonorrhoea gram negative diplococci

443
Q

Describe the epidemiology of gonorrhoea

A

More common in men (25-30)

Urethra is primary infection site

444
Q

What are the symptoms of gonorrhoea

A

Dysuria
Discharge
Menstrual irregularity in women

445
Q

What investigations would you carry out in someone with suspected gonorrhoea

A
  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
Q

What is the management of someone with gonorrhoea

A

Partner notification and further STI testing

Ceftriaxone and azithromycin

447
Q

What is the causative agent of chlamydia

A

Chlamydia trachomatis infection (Gram negative)

448
Q

What is the epidemiology of chlamydia

A

More common in women between 16 and 20

449
Q

What are the symptoms of chlamydia

A

Dysuria, discharge and menstrual irregularities

450
Q

What are the investigations for someone with suspected chlamydia

A

o Vaginal/endocervical swab (F) or first void urine (M)

o Nucleic Acid Amplification Test (NAAT)

451
Q

What is the management of chlamydia

A

o Partner notification and further STI testing

o Treatment – 1g oral azithromycin or doxycycline -> 500mg erythromycin 14 days in pregnancy

452
Q

What are the complications of STI’s

A

Reactive arthritis
Epididymo-orchitis
Pelvic inflammatory pain

453
Q

Why is notification of partner important in STIs

A

Prevent reinfection of index patient

Prevent complications in asymptomatic contacts

454
Q

What is the causative bacteria in syphilis

A

Treponema pallidus subspecies pallidum

455
Q

What are the symptoms of primary syphilis infection

A

Any anogenital ulcer is syphilis until proven otherwise

Macule at the site of sexual contact which becomes very infectious, painless hard ulcer (Chancre)

456
Q

What are the symptoms of secondary syphilis

A

Occurs 4-8wks after chancre there is fever, malaise, lymphadenopathy, rash (Trunk, face, palms and soles), alopecia, hepatitis, iritis

457
Q

What are the symptoms of tertiary syphilis

A

Following 2 to 20 years of latency there are gummas (granulomas occurring in the skin, mucosa, bones, joints, viscera ie lung and testis)

458
Q

What are the symptoms of quaternary syphilis

A

Cardiovascular = Aortic aneurysms and aortic regurgitation

Neurosyphilis = CN palsies, stroke, dementia, psychoses

Sensory ataxia

459
Q

What tests would you do in someone with syphilis

A 
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
Q

What are the treatments for syphilis

A

Penicillin injection

Partner notification and follow up

461
Q

Describe the Anderson and May model for STI and HIV

A

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
Q

What is primary prevention of STIs and give some examples

A

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
Q

Describe the pre and post exposure prophylaxis for STI

A
  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
Q

What is secondary prevention for STIs

A

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
Q

What is the tertiary prevention for STIs

A

Reduce morbidity and mortality

  • Anti retrovirals for HIV
  • Prophylactic antibiotics for PCP
  • Acyclovir for suppression of genital herpes
466
Q

What is partner notification

A

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
Q

Why do we trace partners

A

(i) Break the chain of transmission
(ii) Prevent the re-infection of the index patient
(iii) Prevent complications of untreated infection

468
Q

How are partners traced?

A

Patient referral
Provider referral (Phone, text, letter, internet sites)
Conditional or contract referral
Emphasis on patient choice and confidentiality

469
Q

Where do urinary tract stones

A

Anywhere from the collecting duct of the kidneys to the external urethral meatus

470
Q

What are the three locations that urinary stones are likely to get stuck

A

Uteropelvic junction
Pelvic rim
Vesourteric junction

471
Q

Describe the epidemiology of stones in the urinary tract.

A
  • 10-15% lifetime risk.
  • Males > females - 2:1 ratio.
  • Common among 30-50 y/o.
472
Q

What are the components of urinary stones

A

– calcium based (oxalate and phosphate), uric acid, cystine, struvite

473
Q

Give 5 potential causes of stones in the upper urinary tract.

A
  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
Q

Give 5 symptoms of upper urinary tract stones.

A
  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
Q

Give 5 ways in which urinary tract stones can be prevented.

A
  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
Q

What investigations might you do to find out what is causing someone’s renal colic?

A
  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
Q

Describe the treatment for renal colic.

A
  1. Analgesia e.g. NSAIDs (diclofenac).
  2. Anti-emetics.
  3. Check for sepsis.
  4. IV fluids and antibiotics if infection present
478
Q

If someone presents with pyelonephritis, what is the treatment option

A

Drainage

  • Nephrostomy
  • Ureteric stent
479
Q

Describe the treatment options for urinary stones.

A
  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
Q

Where in the nephron are urinary tract stones formed?

A

In the collecting ducts.

481
Q

What is the treatment for urosepsis

A

Treat with IV antibiotics, oxygen and surgical drainage

482
Q

Describe the pathophysiology of congenital polycystic kidney disease.

A

Genetic mutation -> predisposition to cyst development -> cell proliferation and loss of planar polarity -> fluid secretion and cyst expansion.

483
Q

Describe the pathophysiology of acquired polycystic kidney disease.

A

Cysts develop over time.

Renal injury/ischaemia -> abnormal cell proliferation.

484
Q

What classification can be used to help differentiate between benign cystic lesions and cancerous lesions?

A

Bozniak classification.

485
Q

Give 4 congenital causes of renal cysts.

A
  1. ADPKD.
  2. ARPKD.
  3. VHL.
  4. OFD1 (oral-facial-digital syndrome 1).
486
Q

What is ADPKD?

A

An autosomal dominant condition characterised by progressive cyst development. Cysts increase in size -> renal enlargement and loss of function -> kidney failure.

487
Q

A mutation in which genes can cause ADPKD?

A
  1. PKD1 (associated with more severe disease).

2. PKD2.

488
Q

Give 4 signs of ADPKD.

A
  1. Hypertension.
  2. Haematuria.
  3. Polyuria.
  4. Abdominal/loin pain.
  5. Palpable bilateral costo-vertebral masses.
489
Q

Give 2 extra-renal manifestations of ADPKD.

A
  1. Polycystic liver disease.

2. Intracranial aneurysms e.g. SAH.

490
Q

How can ADPKD be diagnosed?

A
  • Symptoms.
  • Family history.
  • High BP.
  • Urinalysis.
  • USS.
491
Q

What value can be used as a prognostic marker for ADPKD?

A

TKV - total kidney volume.

492
Q

A mutation in what gene can cause AD tubulo-interstitial kidney disease?

A

HNF1 beta.

493
Q

A mutation in what gene can cause ARPKD?

A

PKHD1.

494
Q

Give 4 features of acquired renal cystic disease.

A
  1. No genetic mutation.
  2. No family history.
  3. Normal kidney size.
  4. Risk factor for renal cell carcinoma.
495
Q

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?

A

ADPKD.

496
Q

At what age do people with ADPKD normally present?

A

Normally present around 50 y/o.

497
Q

Why might someone with ADPKD have bilateral palpable costovertebral masses?

A

Cysts increase in size and cause renal enlargement. Often the kidney’s can be HUGE!

498
Q

What is the affect of AKI on creatinine and urine output?

A
  • Creatinine is raised.

- Urine output is reduced.

499
Q

Give 5 risk factors for AKI.

A
  1. Increasing age.
  2. CKD.
  3. HF.
  4. Diabetes mellitus.
  5. Nephrotoxic drugs e.g. NSAIDs and ACEi.
500
Q

Give a pre-renal cause of AKI.

A
  1. Hypertension.
  2. Heart failure.
  3. Nephrotoxic drugs.
501
Q

Give 5 renal causes of AKI.

A
  1. Nephrotoxic drugs.
  2. Vasculitis.
  3. Autoimmune.
  4. Acute tubular necrosis.
  5. Glomerulonephritis.
502
Q

What is the major complication someone with AKI might develop?

A

Hyperkalaemia!

This can lead to arrhythmias

503
Q

What investigations might you do to determine whether someone has AKI?

A
  1. Check potassium!
  2. Bloods: creatinine, U+E.
  3. Urine output.
  4. Auto-antibodies.
504
Q

How can hyperkalaemia be prevented in someone with AKI?

A
  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
Q

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?

A

Nephritic syndrome

506
Q

How does the epidemiology differ between ADPKD and ARPKD?

A

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
Q

What drug must you not give to someone with renal artery stenosis?

A

ACE inhibitors e.g. ramipril.

508
Q

Give 5 causes of haematuria.

A
  1. Kidney tumour, trauma, stones, cysts.
  2. Ureteric stones or tumour.
  3. Bladder infection, stones or tumour.
  4. BPH or prostate cancer.
509
Q

What further investigations might you do in someone who presents with haematuria?

A
  1. Urinalysis.
  2. Urine cytology.
  3. Abdomen US.
  4. Abdomen CT.
  5. Cystoscopy.

Phase 2 (16 decks)

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