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PHASE 2A > Renal and Urogenital > Flashcards

Renal and Urogenital Flashcards

1
Q

What anatomical structures make up the lower urinary tract?

A

Bladder
Bladder neck
Prostate gland
Urethra and urethral sphincter

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2
Q

Give 4 functions of the lower urinary tract

A
  1. Storage of urine
  2. Converts the continuous process of excretion to an intermittent, controlled and volitional process
  3. Prevents leakage of stored urine
  4. Allows rapid, low pressure voiding
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3
Q

Is the detrusor muscle relaxed or contracted during storage?

A

Relaxed

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4
Q

Is the detrusor muscle relaxed or contracted during voiding?

A

Contracted

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5
Q

Is the urethral sphincter relaxed or contracted during storage?

A

Contracted

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6
Q

Is the urethral sphincter relaxed or contracted during voiding?

A

Relaxed

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7
Q

Briefly describe the storage phase of micturition

A

As the volume in the bladder increases the pressure remains low due to receptive relaxation and inhibition of detrusor muscle contraction

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8
Q

What maintains the inhibition of detrusor muscle contraction (relaxation of detrusor)?

A

Sympathetic nerve = Hypogastric plexus
T11-L2
Noradrenergic

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9
Q

Briefly describe the filling phase of micturition

A 
At lower volume the afferent pelvic nerve (parasympathetic = S2-4) send slow firing signals to the pons via the spinal cord 
Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation
Somatic (pudendal = S2-4) nerve stimulation maintains urethral contraction
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10
Q

Briefly describe the voiding phase of micturition

A

Higher volumes stimulated the afferent pelvic nerve (parasympathetic) to send fast signals to the sacral micturition centre in the sacral spinal cord
Pelvic parasympathetic nerve is stimulated and detrusor muscle contracts
Pudendal nerve is inhibited and the external sphincter relaxes

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11
Q

What nerve causes the contraction of the detrusor muscle?

A

Pelvic parasympathetic nerve

S2-4

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12
Q

What nerve causes the contraction of the urethral sphincter?

A

Somatic pudendal nerve

S2-4

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13
Q

What kind of reflex is the micturition reflex?

A

Autonomic spinal reflex

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14
Q

What is the guarding reflex?

A

Reflex that occurs when voiding is inappropriate

Controlled by Onuf’s nucleus

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15
Q

What type of epithelium line the bladder?

A

Urothelium (transitional epithelium) - pseudo-stratified

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16
Q

Give 4 functions of the kidneys

A
  1. Filter or secrete waste excess substances
  2. Retain albumin and circulating cells
  3. Reabsorb glucose, amino acids and bicarbonates
  4. Control BP, fluid status and electrolytes
  5. Activates 25-hydroxy vitamin D
  6. Synthesis erythropoietin
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17
Q

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

A

Benign prostatic enlargement

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18
Q

LUTS: Give 3 symptoms of storage problems

A
  1. Frequency
  2. Urgency
  3. Nocturia
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19
Q

LUTS: Give 4 symptoms of voiding problems

A
  1. Hesitancy
  2. Straining
  3. Intermittent stream
  4. Incomplete emptying
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20
Q

LUTS: give 3 other symptoms other than storage or voiding problems

A
  1. Post-micturition voiding
  2. Haematuria
  3. Dysuria
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21
Q

What might dysuria suggest?

A

Inflammation

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22
Q

What investigations might you do on someone who presents with LUTS?

A

Urinary tests - dipstick
Urinary Flow - maximum flow rate and residual volume
Symptom assessment = international prostate scoring system
Blood tests - PSA, U+Es

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23
Q

Describe the treatment for someone who presents with mild LUTS

A

Reassurance

Watch and wait

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24
Q

Describe the treatment for someone who presents with moderate LUTS

A

Fluid management and avoid caffeine

Bladder drill

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25
Q

Give 2 pharmacological treatments for someone who presents with severe LUTS

A
  1. Alpha-1-blockers - tamsulosin

2. 5-alpha-reductase inhibitors

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26
Q

How do Alpha-1-blockers work?

A

Cause vasodilation and so rescue the resistance to bladder outflow
Decreases smooth muscle tone in bladder and prostate

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27
Q

Give 2 potential side effects of tamsulosin

A

Tamsulosin = Alpha-1-blocker
Hypotension
Retrograde ejaculation

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28
Q

How do 5-alpha-reductase inhibitors work?

A

Inhibit the conversion of testosterone to dihydrotestosterone –> reduce prostate size

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29
Q

Give 5 potential complications of untreated LUTS

A
  1. Bladder calculi
  2. UTI’s
  3. Urinary incontinence
  4. Reduced QOL
  5. Acute urinary retention
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30
Q

Define benign prostatic hyperplasia (BPH)

A

Increase in cell number and size in transitional/peri-urethral prostate area WITHOUT the presence of malignancy

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31
Q

Describe the pathophysiology of Benign prostatic hyperplasia

A

Epithelial and stomal cell increase

Increased A1 adrenoreceptros –> smooth muscle contraction and mass effect of prostate size = obstruction

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32
Q

Give 4 symptoms of BPH

A
  1. Increased frequency of micturition
  2. Nocturia
  3. Hesitancy
  4. Post-void dribbling
    LUTS
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33
Q

What investigations might you do in someone who you suspect has BPH?

A

Digital rectal examination = enlarged but smooth prostate
Urinalysis
PSA
Flexible cystoscopy

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34
Q

What are the aims of the management of BPH?

A

Improve urinary symptoms
Improve QOL
Reduce complications of bladder outflow obstruction

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35
Q

What lifestyle changes can be made to manage symptoms of BPH?

A

Redue caffeine and alcohol intake
Distraction methods
Bladder training

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36
Q

Describe the treatment for BPH

A
  1. Mild symptoms = watchful waiting.
  2. Alpha-1-antagonists e.g. tamulosin
  3. 5-alpha-reductase inhibitors
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37
Q

Give the surgical treatment for BPH

A

Transurethral resection of prostate (TURP)

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38
Q

What are the indications in someone with BPH to do a TURP?

A

RUSHES

  • Retention
  • UTI’s
  • Stones
  • Haematuria
  • Elevated creatinine
  • Symptom deterioration
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39
Q

Why is incontinence less common in men than it is in 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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40
Q

What is the role of pontine micturition centre and periaqueductal grey control in micturition?

A

Coordination and completion of voiding

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41
Q

Define incontinence

A

Involuntary loss of urine

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42
Q

Name 3 types of incontinence

A
  1. Stress = associaste with coughing/strianing
  2. Urgency
  3. Mixed = stress and urgency
  4. Continuous = due to fistula
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43
Q

What is the main cause of stress incontinence in women?

A

Usually secondary to birth trauma

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44
Q

Describe the treatment for stress incontinence in women

A
  1. Pelvic floor physio
  2. Duloxetine = increase contraction of urtheral sphincter
  3. Surgery –> sling, colposuspension, bulking agents, artificial sphincter
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45
Q

What can cause stress incontinence in men?

A

Neurogenic

Iatrogenic (prostatectomy)

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46
Q

Describe the treatment for stress incontinence in males

A

Artificial sphincter

Male sling

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47
Q

What information can you get from a bladder diary?

A
  1. Frequency
  2. Volume
  3. Functional capacity
  4. Incontinence/day
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48
Q

What is an overactive bladder?

A

Urgency with frequency, with or without nocturia, when appearing in the absence of local pathology

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49
Q

Describe the treatment for an overactive bladder

A
  1. Behavioural - limit caffeine and alcohol, bladder drill
  2. Pelvic floor physio
  3. Muscarinic antagonists
  4. Beta 3 agonists
  5. Botox
  6. Sacral neuromodulation
  7. Cystoplasty
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50
Q

How do muscarinic antagonists work in the treatment of an overactive bladder?

A

Decrease parasympathetic activity –> decrease bladder contraction

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51
Q

How do beta 3 agonists work in the treatment of an overactive bladder?

A

Increase sympathetic activity at B3 receptor in bladder

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52
Q

How does botox work in the treatment of an overactive bladder?

A

Blocks neuromuscular junction for Ach release

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53
Q

What is sacral neuromodulation?

A

Insertion of electrode to S3 nerve root to modulate afferent signals from bladder
Preliminary trial

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54
Q

What is a cystoplasty?

A

Bladder enlargement using bowel (small bowel, colon or stomach)

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55
Q

What is the role of the cortex in micturition?

A

Sensation and voluntary ignition of voiding

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56
Q

What is a spastic spinal cord injury?

A

Supra-conal lesion = conus lesion above the caudal equina

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57
Q

What functions are lost due to a spastic spinal cord injury?

A

Coordination and completion of voiding

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58
Q

Give 3 features of a spastic spinal cord lesion

A
  1. Reflex bladder contractions
  2. Detrusor sphincter dyssynergia
  3. Poorly sustained bladder contraction
  4. Potentially unsafe = puts the kidneys at risk
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59
Q

What is a flaccid spinal cord injury?

A

Conus lesion –> decentralised bladder

Damage to sacral micturition centre

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60
Q

What functions are lost due to a flaccid spinal cord injury?

A

Reflex bladder contraction
Guarding reflex
Receptive relaxation

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61
Q

Give 3 features of a flaccid spinal cord injury

A
  1. Areflexic bladder
  2. Stress incontinence (as urethral sphincter is denervated)
  3. Risks of poor compliance
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62
Q

What is an areflexic bladder?

A

Bladder not able to empty by a reflex
Bladder will fill until it cannot fill anymore but there is no contraction and pressure will start to rise as it can’t stretch anymore

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63
Q

What are the aims of the management of a neurogenic bladder?

A
  1. Maintain bladder safety
  2. Continence/symtom control
  3. Prevent autonomic dysreflexia
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64
Q

What is autonomic dysreflexia?

A

Overstimulation of the sympathetic nervous system below the level of the lesion in response to a noxious stimulus

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65
Q

Where does a lesion have to be for autonomic dysreflexia to occur?

A

Lesion above T6

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66
Q

What happens as a result of autonomic dysreflexia?

A

Everything blow the lesion will contract –> vasoconstriction –> overload –> BP increase
Headache, hypertension, flushing

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67
Q

How do you treat autonomic dysreflexia?

A

Remove the noxious stimuli

Change catheter to allow bladder to drain

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68
Q

What is an unsafe bladder?

A

A bladder that put the kidneys at risk damage

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69
Q

Give 3 risk factors of an unsafe bladder

A
  1. Raised bladder pressure
  2. Vesico-ureteric reflux
  3. Chronic infection
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70
Q

How can you manage micturition in a paraplegic patient?

A
  1. Suprapubic catheter
  2. Convene
  3. Suppress reflexes or poorly compliant bladder converting bladder to safe type and then emptying regularly using intermittent self catheterisation (ISC)
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71
Q

Give 3 complications of a suprapubic catheter

A
  1. Infections
  2. Stones
  3. Autonomic dysreflexia if blocked
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72
Q

What bladder problems can occur due to MS?

A

Overactive bladder syndorme
Urinary urgency and frequency
Incomplete bladder emptying

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73
Q

What is the function of the prostate?

A

Secretes proteolytic enzymes into the semen which breaks down clotting factors in the ejaculate

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74
Q

Define prostate cancer

A

Adenocarcinoma in the peripheral zone of the prostate gland

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75
Q

Where can prostate cancer metastasise to?

A

Lymph nodes and bone

Rarely = brain, liver, lung

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76
Q

Briefly describe the pathophysiology of prostate cancer

A

Spreads locally through prostate capsule
Enter the transitional or central zones
Androgen dependent cancer that is dependent on testosterone

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77
Q

By what routes can prostate cancer spread?

A
  1. Lymphatic - to external iliac and internal iliac and presacral node
  2. Haematogenous - to bone, lung. liver, kidneys
  3. Direct - within in the prostate capsule
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78
Q

What can cause prostate cancer?

A
  1. High testosterone levels

2. Family history - 2/3x increased risk if 1st degree relative is affected

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79
Q

Give 2 symptoms of prostate cancer

A
  1. LUTS
  2. Bone pain, weight loss, anaemia = mets
    Most picked up in asymptomatic stage
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80
Q

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

A 
DRE --> hard, irregular, craggy 
Serum --> PSA and postage specific membrane antigen 
Urine --> PCA3 and gene fusion produces 
History of LUTS
Trans-rectal USS
CT/MRI = staging
Prostate biopsy --> DIAGNOSTIC
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81
Q

What are the indications for a prostate biopsy?

A
  1. Palpably suspicious DRE regardless of PSA
  2. PSA >3.0 ng/ml
  3. Suspicious lesion on MRI
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82
Q

What grading system is used in prostate cancer?

A

Gleason grading = higher the score, the more aggressive the cancer

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83
Q

What is the treatment for localised prostate cancer?

A

Observation
Radical prostatectomy
Radiotherapy (external beam)
Adjuvant hormones

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84
Q

What is the treatment for metastatic prostate cancer?

A

Surgical castration
Androgen deprivation therapy - Orchidectomy, LH antagonists, peripheral androgen receptor antagonists
Palliative care

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85
Q

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

A 
Advantages:
 1. Curative 
 2. Reduced patient anxiety 
Disadvantages:
 1. Can have adverse effects
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86
Q

How do LH antagonists work in treating prostate cancer?

A

First stimulate and then inhibit pituitary gonadotrophin

E.g. Leuprolide

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87
Q

Is a raised PSA confirmatory of prostate cancer?

A

NO

Prostate cancer indication

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88
Q

Other than prostate cancer, what can cause an elevated PSA?

A
  1. Benign prostate enlargement
  2. UTI
  3. Prostatitis
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89
Q

Give 2 advantages and 2 disadvantages of screening in prostate cancer

A

Advantages:
1. Early diagnosis of localised disease (cure)
2. Early treatment of advanced disease (effective palliation)
Disadvantages:
1. Over diagnosis of insignificant disease
2. Harm caused by investigation/treatment

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90
Q

What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream

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91
Q

Give 5 risk factors for haematuria

A
  1. Smoking
  2. UTI’s
  3. Catheterisation
  4. Travel parasites
  5. Cyclophosphamide (chemo)
  6. Family history
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92
Q

Give 3 causes of haematuria

A
  1. Kidney tumour, trauma, stones, cysts
  2. Ureteric stones or tumour
  3. Bladder infection, stone or tumour
  4. BPH or prostatic cancer
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93
Q

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

A
  1. Urinalysis
  2. Urine cytology
  3. USS of abdomen
  4. CT of abdomen
  5. Cystoscopy
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94
Q

Where might a transitional cell carcinoma arise?

A
  1. Bladder (50%)
  2. Ureter
  3. Renal pelvis
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95
Q

Describe the epidemiology of transitional cell carcinoma

A
  1. M:F = 3:1

2. Age >40 years old

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96
Q

Give 5 risk factors for transitional cell carcinoma (bladder cancer)

A
  1. Smoking
  2. Occupational exposure - working in rubber factories (aromatic amines)
  3. Increasing age
  4. Male gender
  5. Family history
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97
Q

Give 5 symptoms of transitional cell carcinoma (bladder cancer)

A
  1. Painless haematuria
  2. Recurrent UTI’s
  3. Voiding problems - hesitancy, intermittent stream etc
  4. Flank pain
  5. Lower limb oedema
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98
Q

What investigations might you do in someone you you suspect has transitional cell carcinoma (bladder cancer)?

A
  1. Urine microscopy/cytology
  2. Flexible cystoscopy and bladder wall biopsy
  3. Urinary tumour markers
  4. CT urogram
  5. Imaging - CT, MRI, USS
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99
Q

Give 2 potential risks of flexible cystoscopy

A
  1. UTI’s

2. Problems passing urine

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100
Q

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

A

Confirm three is no other TCC elsewhere in the urinary tract

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101
Q

Why might you do a trans-urethral resection of bladder tumour (TURBT) in someone with TCC?

A

For histological and staging analysis

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102
Q

What staging system is used for transitional cell carcinoma (bladder cancer)?

A

TNM

T1 (submucosa) –> T2 (muscle) –> T3 (outer fat) –> T4 (other organs)

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103
Q

Describe the treatment for non-muscle invasive bladder cancer (T1)

A

Transurethral resection of the bladder (TURB)

Adjuvant chemotherapy

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104
Q

Describe the treatment for muscle invasive bladder cancer (T2/3)

A 
Radical cystectomy (bladder removal) 
Adjuvant radio/chemotherapy
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105
Q

Describe the treatment for T4 bladder cancer

A

Metastasis so:

  • Palliative chemo/radiotherapy
  • Chronic catheterisation for pain
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106
Q

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

A

Schistosomiasis

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107
Q

Name the 2 types of renal cancer

A
  1. Renal cell carcinoma (95%) = arises from renal tubule

2. Transitional cell carcinoma = arises from renal pelvis (less aggressive)

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108
Q

Where does renal cancer commonly metastasise to?

A

Lung, skin, lymphoma and breast

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109
Q

Give 3 risk factors for renal cell carcinoma

A
  1. Smoking
  2. Regular NSAID use
  3. Obesity
  4. Hypertension
  5. Family history
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110
Q

Describe the epidemiology of renal cell carcinoma

A

Incidence increase in those >60 years old

Males > females

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111
Q

Name an inherited renal disease that can cause renal cell carcinoma

A

Von Hippel Lindau disease

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112
Q

What is Von Hippel Lindau disease?

A
  • Autosomal dominant, loss of tumour suppressor gene BHL

- Lots of benign cysts grow - some may develop into cancer

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113
Q

What are the 3 classical signs of renal cell carcinoma?

A
  1. Haematuria
  2. Flank mass
  3. Loin pain
    Often detected incidentally through imaging for something else in asymptomatic stage
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114
Q

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

A 
USS 
Bloods - FBC, U+Es, LFT, Ca profile
Abdominal CT 
Renal biopsy
Bone scan - for bone mets
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115
Q

Name the classification that helps differential between benign cystic lesion and cancerous cystic lesions

A

Bozniak classification

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116
Q

What is the treatment for localised renal cell carcinoma?

A

Surgical excision - partial nephrectomy

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117
Q

What is the treatment for metastatic renal cell carcinoma?

A

Radical nephrectomy
Chemotherapy and radiotherapy
Palliative care

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118
Q

Name the 2 types of testicular cancers that arise from germ cells

A
  1. Seminoma = most common, slow growing

2. Non-seminoma = yolk sac carcinoma/teratoma, rapid growth

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119
Q

Where does testicular cancer spread?

A

Locally into epididymis, spermatic cord and scortal wall

Pelvic and inguinal Metastasises

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120
Q

Give 3 risk factors for testicular cancer

A
  1. Cryptorchidism (undescended testes)
  2. Family history
  3. Previous testicular tumour
  4. Infant hernia
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121
Q

Give 3 symptoms of testicular cancer

A
  1. Painless testis lump - hard and craggy
  2. Testicular or abdominal pain
  3. UG = blood in ejaculate, secondary hydrocele
  4. Abdominal mass
  5. Dyspnoea
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122
Q

What investigations might you do on someone you suspect to have testicular cancer?

A
  1. Tumour markers = Alpha-fetoprotein (a-FP) and Beta subunit of human chorionic gonadotrophin (B-hCG)
  2. Testicular biopsy
  3. Imaging = US, CT/MRI
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123
Q

How is testicular cancer staged?

A 
1 = no mets 
2 = nodes under diaphragm 
3 = above diaphragm 
4 = lungs
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124
Q

What is the treatment for testicular cancer?

A

Orchidectomy = testis and spermatic cord excised

Chemo and radiotherapy (more effective in seminomas)

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125
Q

What is epididymitis?

A

Inflammation of the epididymis

Occurs mainly in young males

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126
Q

Give 2 causes of epididymitis

A
  1. E. coli

2. Chlamydia

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127
Q

What is an epididymal cyst?

A

Smooth extra-testicular, spherical cyst in the head of the epididymus

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128
Q

What is hydrocele?

A

Scrotal swelling as a result of excessive fluid in the tunica vaginalis

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129
Q

When does primary hydrocele normally occur?

A

In absence of disease in testis
Large and tense testis
Young boys mainly effected

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130
Q

Name 3 causes of secondary hydrocele

A
  1. Testicular tumours
  2. Infection
  3. Torsion
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131
Q

What is varicocele?

A

An abnormal enlargement of the pampiniform venous plexus in the scrotum
Caused by venous reflux

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132
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

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133
Q

What is testicular torsion?

A

Twisting of the spermatic cord resulting in occlusion of testicular blood vessels
Leads to ischaemia and postnatal loss of testis

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134
Q

What nerve fibres do cavernous nerves carry?

A 
Parasympathetic = S2-4 (erection)
Sympathetic = T11-L2 (ejaculation)
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135
Q

Describe the physiology of an erection

A
  1. Parasympathetic stimulation
  2. Arteriolar dilation
  3. Trabecular smooth muscle relaxation
  4. Testosterone
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136
Q

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

A 
Nitric oxide (NO) 
Causes a increase in intracellular cyclic GMP --> fall in cytoplasmic calcium --> smooth muscle relaxation
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137
Q

Define erectile dysfunction

A

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

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138
Q

What are the 2 main causes of erectile dysfunction?

A
  1. Organic - vasculogenic, neurogenic, hormonal, anatomical, drug induced
  2. Psychogenic
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139
Q

Give 3 risk factors of erectile dysfunction

A
  1. Obesity
  2. Lack of exercise
  3. Smoking
  4. DM
  5. Liver disease and alcohol
  6. Iatrogenic - prostatectomy
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140
Q

Give 3 characteristics of psychogenic erectile dysfucntion

A
  1. Sudden
  2. Situational
  3. Good nocturnal and early morning erections
  4. Younger males effected
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141
Q

What is the non-pharmacological management of erectile dysfunction?

A
  1. Lose weight and stop smoking

2. Education and counselling for patient and partner

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142
Q

What is the first line pharmacological management of erectile dysfunction?

A

Phosphodiesterase inhibitors - Viagra
Inhibit smooth muscle relaxation
Cause vasodilation –> increase arterial blood flow to penis
SE = headache, flushing, dyspepsia

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143
Q

What is the second line pharmacological management of erectile dysfunction?

A
  1. Intracavernous injections
  2. Sublingual apomorphine
  3. Vacuum devices
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144
Q

What is the third line pharmacological management of erectile dysfunction?

A

Penile prothesis implantation

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145
Q

What is priapism?

A

Prolonged erection lasting >4 hours

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146
Q

What is a potential complication of priapism?

A

Permanent ischaemic damage so aspirate corpora

147
Q

Define glomerular disease

A

= Glomerulonephritis

Group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons

148
Q

Give 3 consequences of glomerulonephritis

A
  1. Damage to filtration mechanism –> haematuria and proteinuria
  2. Damage to glomerulus restricts blood flow –> hypertension
  3. Loss of usual filtration capacity –> AKI
149
Q

Briefly describe the pathophysiology of glomerulonephritis

A

Immunologically mediated –> immunoglobulin deposits and inflammatory cells

150
Q

How can glomerulonephritis present?

A
  1. Nephritic syndrome
  2. Nephrotic syndrome
  3. Asymptomatic haematuria
151
Q

Give 3 causes of nephritic syndrome

A
  1. IgA nephropathy
  2. Post streptococcal infection
  3. Thin BM disease
  4. Cresenteric/rapidly progressive GN
  5. SLE
  6. DM
  7. Infections (MRSA, Hep B/C, Typhoid)
152
Q

Give 5 signs of acute nephritic syndrome

A
  1. Inflammation of glomeruli
  2. HAEMATURIA and PROTEINURIA
  3. Hypertension
  4. Oedema
  5. Oliguria (low urine output)
  6. Red cell casts
153
Q

What investigations might you do in someone who has nephritic syndrome?

A

Urinalysis (dipstick) = haematuria and proteinuria
Blood tests = high creatinine and urea
Kidney biopsy = diagnostic

154
Q

How do you manage nephritic syndrome?

A

Symptom control = antihypertensive to decrease BP and proteinuria
Inflammation control = corticosteroids
Treat underlying cause

155
Q

Describe the pathophysiology behind nephritic syndrome

A

Kidney inflammation –> large podocytic pores –> RBC, WBC, protein leaks into urine

156
Q

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

A
  1. Hypoalbuminaemia
  2. Oedema
  3. Proteinuria (>3.5ng/day)
  4. Hyperlipidaemia
157
Q

Describe the pathophysiology of nephrotic syndrome

A

Podocytes or basement membrane aren’t working properly –> portion leaks into urine

158
Q

What can nephrotic syndrome be secondary to?

A
  1. DM
  2. SLE
  3. Amyloidosis
  4. Infection
  5. Drugs
159
Q

What does primary nephrotic syndrome present as?

A

Either:

  • Minimal change disease
  • Membranous nephropathy
  • Membranoproliferative GN
160
Q

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

A

Fused podocyte foot processes

161
Q

How is minimal change disease treated?

A

High dose corticosteroids = prednisolone

162
Q

What is membranous nephropathy?

A

Thickening of glomerular capillary wall

IgG, complement deposition in sub-epithelial surface –> leaky glomerulus

163
Q

How would you diagnose membranous nephropathy?

A

Serum PLA2R antibodies

Renal biopsy = subepithelial immune complex deposits

164
Q

What is the management of membranous nephropathy?

A

30% = spontaneous remission
Immunosuppression
Control of symptoms

165
Q

What is the main symptom of nephrotic syndrome?

A

Pitting oedema

166
Q

What investigations might be carried out in someone with nephrotic syndrome?

A

Urinalysis (dipstick) = proteinuria
Blood tests = hyperlipidaemia and hypoalbuminaemia
Renal biopsy

167
Q

Describe the treatment for nephrotic syndrome

A
  1. Treat complications - diuretics (furosemide) and fluid/salt restriction for oedema, ACEi for proteinuria
  2. Treat underlying cause
  3. Stains and anticoagulation
168
Q

Give 3 complications of nephrotic syndrome

A
  1. Infections (Ig loss, complement activity decrease)
  2. Thromboembolism (more clotting factor)
  3. Hyperlipidaemia
169
Q

Give 3 causes of asymptomatic haematuria

A
  1. IgA nephropathy
  2. Thin membranous disease
  3. Alport’s syndrome
170
Q

What is IgA nephropathy?

A

Abnormality in IgA glycosylation –> IgA deposition in Mesangium

171
Q

What is the treatment for IgA nephropathy?

A

BP control

Immunosuppression - steroids if renal function declines

172
Q

What is Thin membranous disease?

A

Thin basement membrane causes blood to leak into urine

Autosomal dominant

173
Q

Give 3 features of Alport’s syndrome

A
  1. Haematuria, proteinuria –> progressive renal failure
  2. Sensorineural deafness
  3. Lens dislocation and cataracts
  4. Retinal flecks
174
Q

Where can urinary tract stones be found?

A 
Upper = renal and ureteric 
Lower = bladder, prostatic and urethral
175
Q

What are urinary tract stones composed of?

A

Calcium based (oxalate and phosphate) = 80%
Uric acid
Cystine
Struvite

176
Q

Describe the pathophysiology of stone formation in the upper urinary tract?

A

Stones form from crystals in supersaturated urine

177
Q

Describe the epidemiology of stones in the urinary tract

A

10-15% lifetime risk
Males > females (2:1)
Increases with age

178
Q

Give 5 potential causes of urinary tract stones

A
  1. Congenital abnormalities - horseshoe kidney, spina bifida
  2. Hypercalcaemia/high urate/high oxalate
  3. Hyperuricaemia
  4. Infection
  5. Trauma
179
Q

Give 5 symptoms of urinary tract stones

A
  1. Loin pain –> groin pain
  2. Renal colic
  3. UTI symptoms = dysuria, urgency, frequency
  4. Recurrent UTI’s
  5. Haematuria and proteinuria
180
Q

Give 3 differential diagnosis of urinary tract stones

A
  1. AAA (until proven otherwise)
  2. Diverticulitis
  3. Appendicitis
  4. Ectopic pregnancy
  5. Testicular torsion
181
Q

What investigations might you do on some who you suspect has a urinary tract stone?

A

Midstream urine = haematuria
Blood tests - FBC, U+Es, Ca, Uric acid
Kidney ureter bladder (KUB) XR = first line imaging
Non-contrast CT-KUB = diagnostic

182
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. Urine alkalisation
183
Q

When are urinary tract stone removed?

A

<5mm = watch and wait
>5mm:
- Oral nifedipine (CCB) or alpha blocker (tamsulosin)
- Extracorporeal shock wave lithotripsy (ESWL)
- Ureteroscopy (laser/basket)

184
Q

What is urosepsis?

A

Obstruction and infection

Treat with antibiotics, oxygen and surgical drainage

185
Q

What is renal colic?

A

Pain due to obstruction in the urinary tract

186
Q

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

A
  1. Bloods - including calcium, phosphate, urate
  2. Urinalysis
  3. MCS MSU
  4. NCCT-KUB = gold standard
187
Q

Describe the treatment for renal colic

A
  1. Analgesia - NSAIDS (diclofenac)
  2. Anti-emetics
  3. Check for sepsis
188
Q

Give 3 causes of renal colic

A
  1. Urinary tract stones
  2. UTI
  3. Pyelonephritis
189
Q

Give 3 places where urinary tract stones are likely to get stuck

A
  1. Ureteropelvic junction
  2. Pelvic brim
  3. Vesoureteric junction
190
Q

Give 5 functions of the kidney

A
  1. Filters and secretes waste/excess substances
  2. Blood volume/fluid management (BP control)
  3. Synthesises Erythropoietin
  4. Acid base regulation (reabsorption go Na, Cl, K, glucose, H2O, AA’s)
  5. Converts 1-hydroxyvitamin D –> 1,25-dihydroxyvitamin D (active)
191
Q

What is the GFR?

A

Volume of fluid filtered from the glomeruli into Bowman’s space pre unit time

192
Q

What would you expect a typical GFR to be?

A

120 ml/min

193
Q

Write an equations for GFR

A

(Um X urine flow rate) / Pm
Um = conc of marker substance in urine
Pm = conc of marker substance in plasma

194
Q

Give an example of a marker substance for estimating GFR

A

Creatinine

195
Q

Give 3 essential features of a marker substance for estimating GFR

A
  1. Not metabolised
  2. Freely filtered
  3. Not reabsorbed/secreted
196
Q

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

A

Trimethoprim

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

197
Q

What is the affect on GFR of afferent arteriole vasoconstriction?

A

Decreased GFR

198
Q

What is the affect on GFR of efferent arteriole vasoconstriction?

A

Increased GFR

199
Q

What does the eGFR require to be calculated?

A

Steady state

200
Q

Where in the nephron does the bulk of reabsorption occur?

A

Proximal convoluted tubule

201
Q

What is reabsorbed at the PCT?

A
  1. Sodium
  2. Chlorine
  3. Potassium
  4. Glucose
  5. Water
  6. Amino acids
  7. Bicarbonate
202
Q

What is Fanconi syndrome?

A

Failure of nephron to reabsorb essential ions

proximal tubular insult

203
Q

Give 2 signs of Fanconi syndrome

A
  1. Glycosuria
  2. Acidosis with failure or urine acidification
  3. Phosphate wasting –> rickets/osteomalacia
  4. Aminoaciduria
204
Q

Give 2 causes of Fanconi syndrome

A
  1. Cystinosis
  2. Tenofovir
  3. Wilson’s disease
205
Q

What is the function of the counter current multiplication system?

A

It generate a hypertonic medullary interstitium for H2O reabsorption
Na+ moves out of the ascending limb which increases the medullary osmolality so H20 follows

206
Q

Describe the tubuloglomerular feedback

A

Macula densa cells of the DCT detect NaCl and use this as an indicator of GFR

207
Q

Macula dense cells detect a raised NaCl - what is the response?

A

Afferent arteriole constriction

208
Q

Macula densa cells detect a reduced NaCl - what is the response?

A

Renin secretion

209
Q

What hormone is responsible for regulating sodium reabsorption?

A

Aldosterone

210
Q

Which might aldosterone secretion lead to hypokalaemia?

A

Aldosterone secretion –> increase sodium reabsorption –> increased potassium secretion –> hypokalaemia

211
Q

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

A

NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction = reduced GFR

212
Q

What is the effect of AECi on the efferent arteriole of glomeruli?

A

ACEi cause efferent arteriole vasodilation = reduced GFR

213
Q

Name 2 factors that govern renal potassium

A
  1. Na+

2. Aldosterone

214
Q

What ion is responsible for volume control?

215
Q

Name 2 hormones that increase sodium reabsorption

A
  1. Aldosterone

2. Angiotensin II

216
Q

Name a hormone that decrease sodium reabsorption

217
Q

What is the function of EPO?

A

Stimulates bone marrow –> RBC maturation

218
Q

Give 2 functions of calcitriol

A
  1. Increases Ca and phosphate absorption form the gut

2. Suppresses PTH

219
Q

Why might someone with advanced CKD also have hyperparathyroidism?

A

Advanced CKD = calcitriol deficiency

Calcitriol suppresses PTH therefore in deficiency = hyperparathyroidism

220
Q

What triggers PTH secretion?

A

Low serum calcium

221
Q

Give 3 ways in which PTH increase serum calcium

A
  1. Increased bone resorption
  2. Increase reabsorption of calcium at the kidneys
  3. Stimulates 1-hydroxylase –> 1,25-dihydroxyvitamin D –> increase calcium absorption from the intestine
222
Q

Describe the function of ADH

A

Acts on the collecting ducts to increase insertion of aquaporin 2 channels –> H20 retention

223
Q

Give 3 factors that stimulate renin release

A
  1. Sympathetic stimulation
  2. Decreased BP
  3. Decreased Na detected by macula densa
224
Q

Give 3 functions of ANP

A
  1. Renal vasodilator
  2. Inhibits aldosterone
  3. Closes ENaC (decreased reabsorption of Na+)
225
Q

Where on the nephron does aldosterone act?

A

Collecting ducts

226
Q

Describe the action of aldosterone

A

Increase ENaC and H+/K+ pumps

Increases Na+ absorption and K+ secretion –> H20 retention –> increases BP

227
Q

Define chronic kidney disease

A

Long standing, usually progressive, impairment in renal function for more than 3 months

228
Q

How is CKD classified?

A 
Using eGFR 
G1 = >90 ml/min
G2 = 60-90 ml/min = only CKD if other signs of kidney damage
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
229
Q

How is kidney damage staged?

A

Using album/creatinine ratio
A1 = <30 mg/24h = normal/mild
A2 = 30-300 mg/24h = moderate increase
A3 = >300 mg/24h = severe increase

230
Q

Briefly describe the pathophysiology begins CKD

A

Hyper-filtration for nephrons that work –> glomerular hypertrophy and reduced arteriolar resistance –> raised intraglomerular capillary pressure and strain –> accelerates remnant nephron failure (progressive)

231
Q

Name 4 cause of CKD

A
  1. DM
  2. Hypertension
  3. Glomerulonephritis
  4. Congenital - polycystic kidney disease
  5. Urinary tract obstruction
  6. Amyloidosis
232
Q

Give 3 signs of CKD

A

Often asymptomatic until very low kidney function

  1. Anaemia = pallor, fatigue, lethargy
  2. Bone disease = osteomalacia, bone pain, hyperparathyroidism (due to reduced vitamin D)
  3. Haematuira, Proteinuria and nocturia
  4. High urea = malaise, anorexia, weight loss, insomnia
  5. CVD
  6. Polyneuropathy - confusion, seizures –> coma
233
Q

What investigations might be done in someone who has CKD?

A

FBC = anaemia
U+Es = raised phosphate, uric acid, urea, creatine and decreased Calcium
Urine dipstick = haematuria and proteinuria
GFR
Imaging - USS, CT KUB, ECG, Xrays

234
Q

Describe the management of CKD

A
  1. Treat the underlying cause
  2. Maintain BP = antihypertensives - follow treatment plan for hypertension (ACD pathway)
  3. Reduce CV risk - statins, smoking cessation
  4. Treat complications - anaemia (give EPO), bone disease (give bisphosphonates, vitamin D supplements)
  5. End stage renal failure = Renal replacement therapy
235
Q

What is renal replacement therapy?

A

Dialysis or renal transplantation

236
Q

Name 2 types of dialysis?

A
  1. Haemodialysis

2. Peritoneal dialysis

237
Q

What is the access point in haemodialysis?

A

AV fistula

238
Q

How does haemodialysis work?

A

Blood passes over semi-permeable membrane against dialysis fluid
Impurities, salt, excess fluid drawn into dialysis fluid

239
Q

Give 3 examples of waste products that are removed from the blood in dialysis

A
  1. Urea
  2. Creatinine
  3. Potassium
  4. Phosphate
240
Q

How many times a week and for how long does someone have haemodialysis for?

A

3/4 times a week for around 4 hours

Can be done at home or in hospital

241
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
242
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 peritoneal dialysis (abdominal surgery/hernia)
243
Q

What is the access point for peritoneal dialysis?

A

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

244
Q

How often does someone have to do continuous ambulatory peritoneal dialysis (CAPD)?

A

30-40 minute exchanges, 3-5 times a day

245
Q

How often does someone have to do automated peritoneal dialysis (APD)?

A

One exchange overnight (8 hours)

246
Q

Give 4 potential complications of peritoneal dialysis

A
  1. Infection (peritonitis/catheter exit site infection)
  2. Peri-catheter leak
  3. Abdominal wall herniation
  4. Intestinal perforation
247
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
248
Q

Where in the abdomen does a transplanted kidney lie?

A

In the iliac fossa

249
Q

What has to be assessed for a renal transplant to occur?

A

Virology status = CMV, hepatitis, EBV
CVD
TB
ABO and HLA haplotype

250
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
251
Q

Give 3 contraindications for renal transplant

A
  1. ABO incompatibility
  2. Active infection
  3. Recent malignancy
  4. Morbid obesity
  5. Age >70
  6. AIDS
252
Q

What are the 2 main causes of death after a kidney transplant?

A
  1. CV disease

2. Infection

253
Q

Name 4 potential complications of a kidney transplant

A
  1. Thrombosis
  2. Obstruction
  3. Infections - URTI, chest
  4. Rejection (12% in 1st year)
254
Q

Describe the fluid distribution in the body

A 
Total = 42L 
ICF = 28L
ECF = 14 L 
 - interstitial = 11L
 - plasma = 3L
255
Q

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

A

ICF + interstitial = 39L

256
Q

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

A

Plasma = 3L

257
Q

Name the determinants of fluid movement

A
  1. Hydrostatic pressure
  2. Osmotic pressure (salt and electrolytes )
  3. Oncotic pressure (protein)
258
Q

What happens to the heart rate in hypovolaemia?

A

Increases - tachycardia

259
Q

What happens to the BP in hypovolaemia?

A

Decreases - hypotension

260
Q

What happens to the JVP in hypovolaemia?

A

JVP is low

261
Q

What happens to tissue turgor in hypovolaemia?

262
Q

What happens to the urine output in hypovolaemia?

263
Q

What happens to weight in hypovolaemia?

264
Q

Give 2 symptoms of hypovolaemia

A
  1. Thirst

2. Dizziness

265
Q

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

266
Q

Name 3 groups of people at risk of hypovolaemia

A
  1. Elderly
  2. Those who have had a ileostomy
  3. Bowel obstruction
  4. People taking diuretics
  5. People with short bowel syndrome
267
Q

Describe the management for hypovolaemia

A
  1. Oral fluid
  2. IV fluid is very ill/elderly with difficulties
  3. Treat reversible causes - stop ACEi, ARBs, diuretics
268
Q

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

A

Crystalloid

Small molecules pass through cell membrane

269
Q

Give an example of crystalloid IV fluid

A

Isotonic solutions

  • 5% dextrose
  • 0.9% NaCl
270
Q

Give an example of a colloid IV fluid

A

Gelofusine

271
Q

What happens to the heart rate in hypervolaemia?

A

HR is normal

272
Q

What happens to BP in hypervolaemia?

A

BP is high or normal

273
Q

What happens to JVP in hypervolaemia?

274
Q

What happens to tissue turgor in hypervolaemia?

275
Q

What happens to urine output in hypervolaemia?

276
Q

What happens to weight in hypervolaemia?

277
Q

Give 2 symptoms of hypervolaemia

A
  1. SOB

2. Peripheral oedema

278
Q

Where might fluid accumulate in someone with hypervolaemia?

A
  1. Pulmonary oedema
  2. Pleural effusion
  3. Ascites
  4. Bowel obstruction
  5. Intra-abdominal collection
279
Q

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

280
Q

Name 3 groups of people who are at risk of hypervolaemia

A
  1. AKI patients
  2. CKD patients
  3. Heart failure patients
  4. Liver failure patients
281
Q

Describe the management of hypervolaemia

A
  1. Diuretics - furosemide (loop)
  2. Fluid and salt restriction
  3. Treat reversible causes
282
Q

Why do advanced CKD patients need regular fluid assessment?

A

They may be oliguric or anuric

283
Q

Name a loop diuretic

A

Furosemide - acts on NKCC2 transporter

284
Q

Give 3 potential side effect of furosemide

A
  1. Hypokalaemia
  2. Hypotension
  3. Dehydration
285
Q

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

A

A potassium sparing diuretic e.g. spironolactone

Work on RAAS not ion channels so help control potassium levels in the blood

286
Q

On which part of the nephron do thiazides act?

A

The distal tubule

Act on NCC channels

287
Q

On which part of the nephron do aldosterone antagonists act on?

A

Collecting ducts

288
Q

Define Acute Kidney Injury (AKI)

A

An abrupt (hours-days) sustained rise in serum urea and creatinine due to a rapid decline in GFR

289
Q

Name 3 types of AKI and briefly describe their pathophysiology

A
  1. Pre-renal = decreased blood flow to kidneys –> decreased GFR
  2. Renal = kidney damage
  3. Post-renal = Urinary tract obstruction
290
Q

Give 5 risk factors for AKI

A
  1. Increasing age
  2. CKD
  3. HF
  4. DM
  5. Nephrotoxic drugs - NSAIDs, ACEi
291
Q

Give 2 pre-renal causes of AKI

A
  1. Heart failure
  2. Sepsis
  3. Hypotension
  4. Hypovolaemia (dehydration/haemorrhage)
292
Q

Give 2 renal causes of AKI

A
  1. Glomerulonephritis
  2. Nephrotoxic drugs
  3. Tubular necrosis
  4. Vasculitis
293
Q

Give 2 post-renal causes of AKI

A
  1. BPE/BPH
  2. Urinary tract stones
  3. Malignancy
  4. Strictures
294
Q

How does AKI present?

A
  1. Uraemia (high urea) = fatigue, weakness, vomiting, seizures
  2. Acidosis
  3. Arrhythmias
  4. Oliguria
  5. Oedema
295
Q

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

A
  1. Check potassium
  2. Bloods - Creatinine, U+Es
  3. Urine output
  4. Auto-antibodies
  5. Distinguish whether pre-renal, renal or post renal using imaging
296
Q

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

A

Creatinine = raised

Urine output = reduced

297
Q

What is the diagnostic criteria for AKI?

A

1/3 = diagnostic

  1. Rise in CR >26 mmol/L in 48 hours
  2. Rise in Cr >50% in 48 hours
  3. Urine output < 0.5 ml/kg/h for 6 hours
298
Q

How do you treat AKI?

A
  1. IV fluids (beware in post-renal)
  2. Stop nephrotoxic drugs (NSAIDs, ACEi, gentamicin)
  3. Treat underlying cause
    • Pre-renal = fluids, HF drugs, Abs for sepsis
    • Renal = Biopsy –> specialist treatment
    • Post-renal = Stone removal
  4. Renal replacement therapy = dialysis
299
Q

What is the major complication someone with AKI might develop?

A

Hyperkalaemia
Can lead to arrhythmias
ECG = tall tented T waves, increase PR interval and wide QRS complex

300
Q

How can hyperkalaemia be prevented in someone with AKI?

A

Give calcium gluconate to protect myocardium

Give insulin and dextrose (insulins drives K+ into cells and dextrose is to rebalance the blood sugar)

301
Q

Define urinary tract infection

A

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

302
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
  • Pregnant lady
  • Children
  • Immunocompromised
  • If it is recurrent
303
Q

Describe the pathophysiology of UTI’s

A

Organisms colonise the urethral meatus –> bacterial sent –> bacteriuria

304
Q

Name 3 UTI causative organisms

A
  1. Uropathogenic strains of E. coli (UPEC) - 82%
  2. Coagulase negative staph (s. saprophyticus)
  3. Proteus mirabilis
  4. Enterococci
  5. Klebsiella pneumonia
305
Q

Describe the epidemiology of UTI’s

A

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

306
Q

Give 4 risk factors of UTI’s

A
  1. Catheter
  2. Female
  3. Prostatic hypertrophy (obstructs)
  4. Low urine volume
  5. Urinary tract stones
  6. Pregnancy
307
Q

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

A
  1. Fimbriae/pili that adhere to urothelium
  2. Acid polysaccharide coat resists phagocytes
  3. Toxins (e.g. UPEC releases cytotoxins)
  4. Enzyme production (e.g. urease)
308
Q

What type of pili would you associate with lower UTI?

A

Type 1

Bind to uroplakin

309
Q

What type of pili would you associate with upper UTI?

A

Type P

Bind to glycolipids on urothelium

310
Q

The vagina is heavily colonised with lactobacilli, what is the function of this?

A

Helps maintain a low pH = host defence mechanism

311
Q

Give 2 reasons why a post-menopausal women is more susceptible to a UTI

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

2. Reduced mucus secretion

312
Q

Give 3 host defence mechanisms against UTIs

A
  1. Antegrade flushing of urine
  2. Tamm-horsfall protein
  3. GAG layer
  4. Low urine pH
  5. Commensal flora
  6. Urinary IgA
313
Q

Define pyuria

A

Presence of pus in urine

314
Q

Name 4 lower urinary tract infections

A
  1. Cystitis
  2. Prostatitis
  3. Epididymo-orchitis
  4. Urethritis
315
Q

Name a upper urinary tract infection

A

Pyelonephritis

316
Q

Give 4 classic UTI symptoms

A
  1. Urgency
  2. Frequency
  3. Dysuria
  4. Haematuria
  5. Abdominal pain
  6. Malaise
  7. Confusion (old patients)
317
Q

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

A
  1. Take a good history
  2. Urinalysis –> haematuria, proteinuria, increased WCC, pH, nitrates, ketones
  3. Microscopy, culture and sensitivity of MSU
    4 In recurrent/complicated UTI = imaging (bladder scan, USS, XR)
318
Q

What is the first line treatment for an uncomplicated UTI?

A

Trimethoprim or nitrofurantoin for 3 days

Increase fluid intake and regular voiding

319
Q

How does trimethoprim work?

A

It affects folic acid metabolism

320
Q

Describe the management for a complicated UTI

A

Culture sample –> Abx for 7 days

321
Q

Define recurrent UTI

A

> 2 episodes in 6 months or >3 in 12 months

322
Q

Describe the management for someone who is having recurrent UTIs

A
  1. Increase fluid intake
  2. Regular voiding
  3. Void pre and post intercourse
  4. Abx prophylaxis
  5. Vaginal oestrogen replacement
323
Q

What is cystitis?

A

Inflammation of the bladder secondary to infection

324
Q

Give 3 risk factors for cystitis

A
  1. Urinary obstruction
  2. Previous damage to bladder epithelium
  3. Poor bladder emptying
325
Q

Give 4 symptoms of cystitis

A
  1. Dysuria
  2. Frequency and urgency
  3. Suprapubic pain
  4. Offensive smelling/cloudy urine
  5. Haematuria
326
Q

What is the treatment for cystitis?

A

Trimethoprim or Cefalexin

ciprofloxacin or Co-amoxiclav = 2nd line

327
Q

Name 3 causative organism of prostatitis

A
  1. E. coli
  2. Proteus
  3. Klebsiella
  4. UTI’s
328
Q

Give 4 symptoms of acute prostatitis

A
  1. Fever
  2. Rigors
  3. Malaise
  4. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow)
  5. Pelvic –> anal pain
329
Q

Give 3 symptoms of chronic prostatitis

A
  1. Recurrent UTI’s
  2. Pelvic –> anal pain
  3. Voiding LUTS
    Symptoms for > 3 months
330
Q

What investigations might you do in someone with prostatitis?

A
  1. Urinalysis and MSU
  2. DRE = boggy, tender and hot to touch
  3. STI screen
  4. Microbiology = uropathogens in urine
  5. Imaging - TRUSS +/- CT abdo/pelvis
331
Q

How would you treat prostatitis?

A

Quinolone (ciprofloxacin) or trimethoprim (if unable to take quinolones) for 4-6 weeks
Treat pain = paracetamol/ibuprofen

332
Q

What can cause urethritis?

A

STI’s = Chlamydia, Gonorrhoea

333
Q

Give 3 symptoms of urethritis

A
  1. Dysuria
  2. Hesitancy
  3. Urethral discharge
334
Q

How would you treat urethritis?

A

STI treatment = Abx - ceftriaxone and doxycycline

335
Q

What is epididymo-orchitis?

A

Inflammation of the epididymus and testes

336
Q

Describe the aetiology of epididymo-orchitis

A

If < 35 = STI = chlamydia or gonorrhoea

If >35 = UTI = E.coli, enterococci

337
Q

Give 3 symptoms of epididymo-orchitis

A
  1. Unilateral scrotal pain +/- swelling
  2. UTI symptoms
  3. Fever
  4. Urethral discharge
338
Q

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

A
  1. Urethral swab
  2. MSU
  3. STI screen
    Must rule out testicular torsion
339
Q

Describe the treatment for epididymo-orchitis

A

Pain relief, no sex
Abx for 14 days
- STI = ceftriaxone and doxycycline
- UTI = ofloxacin or ciprofloxacin

340
Q

Define pyelonephritis

A

Inflammation secondary to infection of the renal pelvis and upper ureter

341
Q

What can cause pyelonephritis?

A

UTI = E.coli, Klebsiella, proteus

Haematogenous spread = S. aureus, candida

342
Q

Give 3 symptoms of pyelonephritis

A
  1. Loin –> back pain
  2. Fever
  3. Pyuria (pus in urine)
  4. Malaise
  5. UTI symptoms
  6. Septic shock
343
Q

What investigations might you do in someone with pyelonephritis?

A
  1. Urinalysis
  2. MCS MSU
  3. Bloods - raised WCC, ESR and CRP
344
Q

Describe the treatment for pyelonephritis

A

Fluid replacement
IV Abs - Ciprofloxacin or co-amoxiclav
Analgesics

345
Q

What can a prolonged pyelonephritis infection cause?

A

Renal abscess

Treatment = drainage

346
Q

Name 2 groups of people that you would treat for bacteriuria

A
  1. Pregnant ladies

2. Children

347
Q

What is septic shock?

A

Severe sepsis with persistent hypotension

348
Q

Describe the treatment for sepsis

A 
The sepsis 6:
1. Give high flow oxygen
2. Take blood cultures
3. Give IV Abx
4. Give IV fluids 
5. Check lactate
6. Monitor hourly urine output 
Drainage to relieve pressure
349
Q

Describe the pathophysiology of urosepsis

A

A symptomatic UTI combined with >1 of:

  1. Microbial resistance
  2. Immunosuppression
  3. Pressure
350
Q

Describe the epidemiology of gonorrhoea

A

More common in men –> 25-30 years

351
Q

Give 3 symptoms of gonorrhoea

A

Very common asymptomatic stage

  1. Dysuria
  2. Discharge
  3. Menstrual irregularity (women)
352
Q

What investigations might you do in someone you suspect to have gonorrhoea?

A
  1. Microbiology = gram -ve diplococci with polymorph cytoplasm
    - genital secretion from urethra (M)/endocervix (F)
  2. Culture on selective medium = confirmation
  3. Sensitivity testing
  4. Nucleic Acid Amplification Test (NAAT)
353
Q

What is the management of gonorrhoea?

A

Partner notification and further STI testing

500mg ceftriaxone AND 1g oral azithromycin

354
Q

Describe the epidemiology of Chlamydia

A

More common in women –> 16-20 years

355
Q

Give 3 symptoms of Chlamydia

A
  1. Dysuria
  2. Discharge
  3. Menstrual irregularities (F)
356
Q

What investigations might you do in someone you suspect to have Chlamydia?

A

Nucleic acid application test (NAAT)

  • Vaginal/endocervix swab (F)
  • First void urine (M)
357
Q

What is the management of Chlamydia?

A

Partner notification and further STI testing
1g oral azithromycin stat or Doxycycline 100mg bd for 7days
OR 500mg erythromycin (14 days) in pregnancy
Community screening

358
Q

Give 3 possible complications of chlamydia

A
  1. Reactive arthritis
  2. Epididymo-orchitis (M)
  3. Pelvic inflammatory pain (F)
  4. Neonatal transmission –> ophthalmia neonatorum and atypical pneumonia
359
Q

Name 3 types of Syphilis

A
  1. Primary = <90 days after inoculation = highly infectious
  2. Secondary = dissemination 4-10 weeks after chancre
  3. Tertiary = 20-40 years after infection
360
Q

How does primary Syphilis present?

A
  1. Primary chancre = painless ulcer (Macule –> papule –> typically painless ulcer)
  2. Regional nodes
361
Q

How does secondary Syphilis present?

A
  1. Presents with a skin rash
  2. Mucous membrane lesions
  3. Generalised lymphadenopathy
  4. Myalgia
  5. Hepatitis
362
Q

How does Tertiary Syphilis present?

A

Neurosyphilis = aseptic meningitis, focal neurological deficits, seizures, psychiatric symptoms
Gummatous syphilis = destructive granulomata in skin, mucus membrane, bones and viscera
Cardiovascular = aortitis, aortic regurgitation/aneurysm

363
Q

What investigations would you do for someone who you suspect to have syphilis?

A

Serology - genital ulcer
- if negative, repeat 6-12 weeks to exclude diagnosis
Confirmatory tests = TPPA (Treponema pallidum particle agglutination test)
Non-treponemal test for disease activity

364
Q

What is the treatment for syphilis?

A

Penicillin injection

Partner notification

PHASE 2A (16 decks)

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