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Sirpi's Phase 2A Medicine > Nephrology + Genitourinary Disease > Flashcards

Nephrology + Genitourinary Disease Flashcards

1
Q

What is the effect of parasympathetic innervation on the lower urinary tract?

A

Causes detrusor muscle contraction and smooth muscle urethral sphincter relaxation to allow for urine voiding.

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2
Q

What nerve and roots are responsble for the parasympathetic innervation of the lower urinary tract?

A

Pelvic nerve, roots S2-S4

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3
Q

What is the effect of sympathetic innervation on the lower urinary tract

A

Detrusor muscle relaxation
Contraction of internal urethral sphincter

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4
Q

What nerve and roots are responsble for the sympathetic innervation of the lower urinary tract?

A

Hypogastric nerve, T12-L2

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5
Q

What are the 3 types of urinary incontinence?

A

Stress incontinence
Urge incontinence
Overflow incontinence

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6
Q

Aetiology of stress incontinence

A

Weakened pelvic floor muscles or urethral sphincters

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7
Q

Pathophysiology of stress incontinence

A

Coughing or sneezing can cause increased intra-abdominal pressure causing leakage of urine.

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8
Q

Who can be especially affected by stress incontinene?

A

Postpartum women
Post-prostatectomy men

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9
Q

Management of stress incontinence

A

Females:
Pelvic floor exercises
Urethral slings

Males:
Artificial urethral sphincter

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10
Q

Aetiology of urge incontinence

A

Detrusor muscle and bladder overactivity

Can be primary, due to UTIs or neural factors like parkinson’s.

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11
Q

Pathophysiology of urge incontinence

A

Rise in detrusor pressure upon bladder filling causes urgency and leakage.

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12
Q

Management of overactive/reflex bladder and urge incontinence

A

Bladder exercise therapy

Anti-muscarinics - e.g oxybutynin to reduce detrusor contraction.

B3 agonists - increase sympathetic detrusor relaxation.

Botox - blocks neuromuscular junction

Sacral neuromodulation - insertion of electrode in S3 to modulate afferent impulses.

Intermittent self-catheterization.

Surgery - cystoplasty

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13
Q

What is the effect of somatic innervation on the lower urinary tract?

A

Voluntary contraction/relaxation of the external urethral sphincter.

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14
Q

What nerve and nerve roots are responsbible for the somatic innervation of the lower urinary tract?

A

Pudendal nerve, S2-4

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15
Q

Side effect of urinary botox use?

A

Urinary retention

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16
Q

What are the spinal urinary reflexes?

A

Reflex blader contraction
Guarding reflex
Bladder receptive relaxation

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17
Q

What is reflex bladder contraction?

A

When bladder fills it automatically triggers contraction.

Pelvic nerve mediated.

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18
Q

What is the urinary guarding reflex?

A

Urine in proximal urethra causes impulse to spinal cord to tell Onuf’s nucleus to close proximal urethreal sphincter to store urine.

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19
Q

What is receptive relaxation of the bladder?

A

The detrusor muscle relaxes as the bladder fills with urine in order to maintain constant bladder pressure.

Hypogastric nerve mediated.

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20
Q

What is the role of the pontine micturition center?

A

Coordinates the central and peripheral neuromodulation of voiding.

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21
Q

What is the role of the cortical micturition center?

A

Mediates voluntary micturition.

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22
Q

Pathophysiology of urinary effects of spastic (supra-conal) spinal cord injury

A

Loss of pontine co-ordination of voiding.

Can result in detrusor-sphincter dyssenergia.

Poorly sustained and involuntary bladder/bowel contraction

Can potentially result in unsafe bladder if both contract.

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23
Q

Pathophysiology of urinary effects of flaccid (conal) spinal cord injury

A

Loss of reflexes (bladder contraction, guarding, RR)

Arreflexic bladder and bowel.

Bladder filling without detrusor compliance can lead to an unsafe bladder.

Can result in stress incontinence.

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24
Q

What can cause a conal spinal cord injury?

A

Ischaemia such as transversus myelitis or diabetic neuropathy

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25
Q

Aetiology of autonomic dysreflexia

A

Requires almost complete spinal injury.

Occurs in lesions at or above T6.

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26
Q

Pathophysiology of autonomic dysreflexia

A

Overstimulation of sympathetic nervous system below level of lesion in response to a noxious stimulus (stimulus causing pain/discomfort) such as full blader.

Due to lack of sensation due to lesion.

Can cause constriction of splanchnic vessels (T6) causing significant hypertension.

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27
Q

Clinical presentation of autonomic dysreflexia

A

Patient will feel dizzy, headache, body below lesion is white and above will be red (flushing).

Bradycardia in response to hypertension.

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28
Q

What is an unsafe bladder?

A

A bladder with high pressure that is at risk of damaging the kidneys.

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29
Q

Aetiology of an unsafe bladder

A

Decreased detrusor compliance
Vesico-ureteric reflux
Bladder obstruction - stones, residual urine, etc.

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30
Q

Complications of an unsafe bladder

A

Renal failure

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31
Q

What type of urinary obstructions (obstructive uropathy) are there?

A

Luminal
Mural
Extraluminal

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32
Q

Aetiology of luminal urinary obstruction

A

Renal calculi
Thrombus
Tumour of renal pelvis, ureter, bladder

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33
Q

Aetiology of mural urinary obstruction

A

Ureteric stricture
Neuropathic bladder
Congenital bladder neck obstruction

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34
Q

Aetiology of extraluminal urinary obstruction

A

Retroperitoneal tumours
Benign prostatic hyperplasia
Phimosis

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35
Q

Clinical presentation of upper urinary tract obstruction

A

Renal colic
Loin pain
Complete anuria - complete bilateral obstruction/that of a single kidney

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36
Q

Clinical presentation of lower urinary tract obstruction

A

LUTS:

Issues with storage:

Frequency
Urgency
Nocturia (> 30% voided volume @ night)
Overflow incontinence (leaking urine during day/wetting bed)

Issues with voiding:

Straining
Hesitancy
Incomplete emptying
Poor intermittent stream
Post micturition dribbling

Haematuria
Dysuria (painful urination)

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37
Q

Pathophysiology of urinary obstruction (obstructive uropathy)

A

Buildup of urine can lead to increased pressure in bladders, ureters and kidneys leading to renal pelvis dilation (hydronephrosis) which can lead to renal failure.

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38
Q

What is urinary retention?

A

Inability to pass urine with over 500ml left in the bladder.

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39
Q

What is the most common form of bladder cancer?

A

Transitional cell/urothelial carcinoma

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40
Q

Aetiology/risk factors for bladder cancer

A

Smoking
Age > 55
Male
Occupational exposure to chemicals e.g napthylamine
Drugs like cyclophosphamide
Schistosomiasis

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41
Q

Clinical presentation of bladder cancer

A

Weight loss
Painless haematuria
LUTS
Recurrent UTIs
Hydronephrosis if obstruction

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42
Q

Investigation of bladder cancer

A

Urinalysis - can show pyuria
GS - Flexible cystoscopy (bladder endoscopy) + biopsy
CT urogram - can stage and is also diagnostic

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43
Q

Management of bladder cancer

A

Non-muscle invasive:
Transurethral tumour resection
With chemotherapy - mitomycin and BCG

Muscle invasive:
Radical cystoprostatectomy
With radiotherapy

CAN METASTASIZE TO LUNGS, LIVER, BONE.

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44
Q

What are the different types of renal cancer?

A

Clear cell carcinomas (most common)
Papillary carcinoma
Chromophobe carcinoma
Collecting duct carcinoma

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45
Q

Aetiology/risk factors for renal cancer

A

Smoking
Hypertension
Haemodialysis
Male
Obesity

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46
Q

What type and location is most common for renal cancer?

A

Clear cell carcinoma, proximal convoluted tubule.

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47
Q

Clinical presentation of renal cancer

A

Haematuria
Loin pain
Palpable Abdominal Mass
Varicocele

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48
Q

Investigation of renal cancer

A

First line - Abdominal ultrasound

GS - CT kidney with renal mass protocol

Staging - CT CAP

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49
Q

What are some paraneoplastic effects of renal cell carcinomas?

A

FBC - polycythaemia due to increased erythropoetin secretion

Raised BP due to renin secretion

Hypercalcaemia due to increased Vit.D activation

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50
Q

Management of renal cell carcinoma

A

If less than 4cm - ablation/crytherapy

GS - partial nephrectomy

Can also do nephrectomy

Then immunotherapy such as tyrosine kinase inhibitors

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51
Q

Aetiology/Risk Factors of Testicular Cancer

A

Cryptorchidism - abnormal descending of testicle
Family history
HIV
Caucasian males
Common in younger patients
Klinefelter’s syndrome

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52
Q

Types of Testicular Tumours

A

Germ Cell - Seminoma, Teratoma, Yolk Sac tumour, Choriocarcinoma

Non-Germ Cell - Leydig, Sertoli, testicular lymphoma

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53
Q

Clinical Presentation of Testicular cancer

A

Painless testicular mass

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54
Q

Investigation of Testicular cancer

A

Same day testicular ultrasound - GS

Serum alpha fetoprotein, Beta-hCG, lactate dehydrogenase - tumour markers.

CXR if respiratory symptoms

Staging - CT CAP

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55
Q

Management of testicular cancer

A

Radical inguinal orchidectomy with chemotherapy

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56
Q

What are areas that renal cancers can metastasize to?

A

Liver, lungs, bones.

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57
Q

What is Glomerulonephritis?

A

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

Common cause of end stage renal failure.

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58
Q

What conditions are under Nephritic Syndrome (Acute Glomerulonephritis)?

A

IgA Nephropathy - most common
SLE, systemic sclerosis
Post strep GN
Small vessel vasculitis
Goodpasture’s/anti-GMB disease
Henoch Schonlein purpura

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59
Q

Pathophysiology of Nephritic Syndrome

A

Damage to glomerular basement membrane causing RBCs to not be filtered and pass into urine.

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60
Q

Clinical Presentation of of Nephritic Syndrome

A

Haematuria
Proteinuria (mild)
Oliguria - low urine output
Hypertension

Nosebleeds
Haemoptysis

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61
Q

Investigation of Nephritic Syndrome

A

Urinalysis - haematuria, albuminuria
Blood pressure - hypertension
Oliguria due to decreased GFR

Diagnostic is kidney biopsy

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62
Q

Aetiology of IgA Nephropathy

A

Associated with respiratory and GI conditions such as tonsilitis.

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63
Q

Pathophysiology of IgA Nephropathy

A

Abnormal IgA glycosylation causes deposition of IgA into the mesangium of the kidney.

This results in inflammation and damage

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64
Q

Clinical Presentation of IgA Nephropathy

A

Presents asymptomatically with episodic visible haematuria.

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65
Q

Investigation of IgA Nephropathy & Henoch Schonlein Purpura

A

Renal biopsy - mesangial IgA deposits.

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66
Q

Management of IgA Nephropathy & Henoch Schonlein purpura

A

Steroids (e.g prednisolone) + immunosuppression
BP control - ACE inhibitors/ARBs

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67
Q

Pathophysiology of Goodpasture’s Disease

A

Type II Hypersensitivity reaction

Caused by autoantibodies to Type IV collagen (anti-BM antibodies) in glomerular and alveolar membrane.

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68
Q

Clinical Presentation of Goodpasture’s Disease

A

Normal nephritic syndrome symoptoms, but can present with resp symptoms like dyspnoea, haemoptysis.

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69
Q

Investigation of Goodpasture’s Disease

A

Serology - anti-GBM antibodies

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70
Q

Management of Goodpasture’s Disease

A

Remove antibody through plasma exchange
Steroids e.g prednisolone + immune suppression e.g cyclophosphamide

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71
Q

Investigation of SLE

A

Anti-nuclear antibody (ANA) positive and Double stranded DNA positive
Low complement C3 & C4 levels

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72
Q

Pathophysiology of Henoch Schonlein Purpura

A

This is a small vessel vasculitis that affects the kidney and joints due to IgA deposition

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73
Q

Clinical Presentation of Henoch Schonlein Purpura

A

Presents with a purpuric rash on legs, nephritic symptoms, and abdominal/joint pain due to IgA deposition.

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74
Q

Pathophysiology of ANCA Associated Vasculitis:

A

Multisystem small vessel vasculitis attack small vessels in the kidney and eye

ANCA = anti-neutrophil cytoplasmic antibodies

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75
Q

Clinical Presentation of ANCA Associated Vasculitis

A

Systemic inflammatory features.

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76
Q

Investigation of ANCA Associated Vasculitis

A

Serology - raised ANCA

Raised ESR, CRP

Renal biopsy - macrophages and lymphocyte infiltration of glomerulus

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77
Q

Management of ANCA Associated Vasculitis

A

Steroids e.g prednisolone + immunosuppression e.g cyclophosphamide

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78
Q

Investigation of Systemic Sclerosis

A

Serology: Anti nuclear antibody positive

Renal biopsy: Onion skin’ changes on renal biopsy, raynauds phenomenon, fibrotic skin, oesophageal dysmotility

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79
Q

Management of Systemic Sclerosis

A

ACE inhibitors

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80
Q

Aetiology of Nephrotic Syndrome

A

Primary:
Membraneous nephropathy
Focal segmental glomerulosclerosis
Minimal change disease

Secondary:
Amyloidosis
Diabetic nephropathy

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81
Q

What is the most common cause of Nephrotic Syndrome in children?

A

Minimal change disease

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82
Q

Pathophysiology of Nephrotic Syndrome

A

Issue with the filtration barrier and podocytes results in leaking of protein into the urine.

Loss of plasma proteins causes increased activation of the liver which can result in increased hepatic lipogenesis.

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83
Q

Clinical Presentation of Nephrotic Syndrome

A

Proteinuria - frothy urine
Hypoalbuminemia
Oedema
Dyslipidaemia

Mild/absent haematuria

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84
Q

Investigation of Nephrotic Syndrome

A

Protein:creatinine ratio

Urinalysis - Proteinuria

LFT - Hypoalbuminemia

Renal biopsy - diagnostic

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85
Q

General Management of Nephrotic Syndromee

A

Fluid management - diuretics, ACEi/ARBs to reduce BP

Dyslipidaemia - Statins

Loss of anticoagulant factors - anticoagulants

Loss of immunoglobulins - Antibiotics

Treatment of underlying cause

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86
Q

Investigation of Minimal Change Disease

A

Light microscopy of renal biopsy - No change

Electron microcroscopy of renal biopsy - Fusion and effacement of podocyte foot processes.

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87
Q

Management of Minimal Change Disease

A

Steroids e.g prednisolone + immunosuppression e.g cyclophosphamide

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88
Q

Aetiology/risk factors for Membraenous Nephropathy

A

NSAIDs
Autoimmune conditions such as SLE
Infections - schistosomiasis
Malignancy - lung

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89
Q

Pathophysiology of Membraneous Nephropathy

A

Thickening of glomerular capillary wall

Immunoglobulin (IgG) and complement deposition in sub-epithelial surface.

Results in leaky glomerulus.

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90
Q

Investigation of Membraneous Nephropathy

A

Serology - PLA2 receptor antibody

Renal biopsy - Thickened glomerular basement membrane.

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91
Q

Management of Membraneous Nephropathy

A

ACE Inhibitors e.g ramipril

Steroids e.g Prednisolone + immunosuppression e,g Cyclophosphamide

Anti CD-20 antibodies e.g Rituximab

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92
Q

Aetiology/Risk Factors of Focal Segmental Glomerulosclerosis

A

Can be idiopathic or secondary to HIV, heroin, lithium

Higher prevalence in Black people

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93
Q

Investigation of Focal Segmental Glomerulosclerosis

A

Renal biopsy - Segmental scarring of glomeruli

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94
Q

Management of Focal Segmental Glomerulosclerosis

A

Steroids e.g prednisolone + Immunosuprresion e.g cyclophosphamide

ACE inhibitors

95
Q

What is Erectile Dysfunction?

A

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

96
Q

What corpus surrounds the urethra?

A

Corpus spongiosum

97
Q

What corupus fills with blood during an erection?

A

Corpus spongiosum

98
Q

What corpus surrounds the corpus spongiosum?

A

Corpus cavernosum

99
Q

What is the name of the fibrous membrane that surrounds both the corpus cavernosum and spongiosum?

A

Tunica albuginea

100
Q

What is the effect of parasympathetic stimulation on the penis?

A

Causes an erection.

101
Q

What nerve and nerve roots are responsible for parasympathetic stimulation of the penis?

A

Cavernous nerve, S2-S4

102
Q

What is the effect of sympathetic stimulation on the penis?

A

Causes ejaculation.

103
Q

What nerve and nerve roots are responsible for sympathetic stimulation of the penis?

A

Dorsal nerve, S2-S4

104
Q

Physiology of an erection

A

Parasympathetic stimulation causes arteriolar dilation.

Nitric oxide release from endothelium causes intracellular cyclic GMP rise

This which decreases cytoplasmic calcium allowing for smooth muscle relaxation.

105
Q

What androgen is needed for erectile function?

A

Testosterone

106
Q

Aetiology of Erectile Dysfunction

A

Neurogenic issues - failure to initiate
Arteriogenic issues - failure to fill
Venogenic issues - failure to store

Psychogenic issues - anxiety, depression

107
Q

Risk Factors for Erectile Dysfunction

A

Smoking
Obesity
Old age
Diabetes
Trauma - pelvic fracture, prostatectomy

108
Q

First Line Management of Erectile Dysfunction

A

Phosphodiesterase 5 (PDE5) inhibitors
Eg. sildenafil (viagra), tadalafil, vardenafil

109
Q

Pharmacodynamics of PDE5 inhibitors

A

Phosphodiesterase is the enzyme that degrades cyclic GMP so inhibition causes prolonged smooth muscle relaxation allowing for erections to last longer.

110
Q

Side Effects of PDE5 Inhibitors

A

Headache
Dyspepsia

111
Q

Second Line Management of Erectile Dysfunction

A

Sublingual apomorphine

Vacuum constriction devices - can cause inability to ejaculate, petechiae

Intracavernous injections

112
Q

Surgical Management of Erectile Dysfunction

A

Prosthetic Penile Implant

113
Q

What is Prostate Specific Antigen (PSA)?

A

Protease responsible for the liquefaction of semen.

114
Q

Causes of Raised PSA Levels

A

BPH
Prostate cancer
UTI
Prostatitis
Exercise
Recent ejaculation/prostate stimulation.

115
Q

Aetiology/Risk Factors of Prostate Cancer

A

Family history
BRCA2 confers a 5-7 times higher risk
Increasing age
Black ethnicity
Smoking
High animal fat diet

116
Q

Pathophysiology of Prostate Cancer

A

Usually originates in the periphery of the prostate
Mostly adenocarcinomas

117
Q

Clinical Presentation of Prostate Cancer

A

LUTS

Frequency
Urgency
Nocturia
Incomplete Voiding

Straining
Hesitancy
Intermittency
Post-micturition dribbling

Weight loss, bone pain, anaemia suggest metastasis.

118
Q

Investigation of Prostate Cancer

A

FL - Digital rectal exam - Hard, irregular prostate, or multi-parametric prostate MRI

Raised PSA

GS - Trans-rectal ultrasound + biopsy

Biopsy goes through gleason staging

119
Q

TNM Staging of Prostate Cancer

A

T1- no palpable tumour on DRE

T2 - palpable tumour, confined to prostate

T3 - palpable tumour extending beyond prostate capsule

T4 – invading local structures (sphincter/ rectum

120
Q

Management of Localised Prostate Cancer

A

Radical prostatectomy if <70yrs - excellent disease free survival

Radiotherapy = brachytherapy (implantation of radioactive material targeted at tumour)

Active surveillance if >70yrs and low risk

121
Q

Management of Metastatic Prostate Cancer

A

Surgical castration - takes away testosterone

If castration resistant - Androgen deprivation therapy

122
Q

What Drugs can be used in Androgen Deprivation Therapy for Prostate Cancer?

A

Androgen receptor antagonists such as abiraterone, enzalutamide

GnRH agonists such as goserelin which inhibit androgen circulation through negative feedback loops.

123
Q

What is an uncomplicated urinary tract infection?

A

When a non-pregnant, under 65 y/o woman gets inefected.

124
Q

What is a complicated urinary tract infection?

A

When there is potential for a structural abnormality in the urinary tract such as:

Male gender
Pregnancy
Catheterized patients
Immunocompromised patients
Children

125
Q

What organisms most commonly cause UTIs?

A

KEEPS

Klebsiella pneumoniae
Eschericha coli (uropathogenic e.coli so UPEC)
Enterococci
Proteus mirabilis
Staphylococcus saprophyticus

Staphylococcus aureus
Pseudomonas aeruginosa

126
Q

Aetilogy/Risk Factors for UTIs

A

Pregnancy
Female gender
Catherization
Urinary tract stones
Sexual activity

127
Q

Virulence Factors of UPEC

A

Fimbriae for surface adherence
Flagellum for motility
Haemolysin for pore formation
Aerobactin for iron acquisition

128
Q

Pathophysiology of UTIs

A

Catherisation allows direct bacterial entry and formation of biofilm on catheter.

Urinary obstruction from stones, BPH, etc can cause stasis of urine flow resulting in bacterial proliferation.

Low urinary volume (e.g not drinking enough) causes less urine through the bladder to flush out any bacteria.

Pregnancy can cause stasis of urine.

129
Q

Clinical Presentation of Lower UTI (Urethritis, Cystitis)

A

Suprapubic pain
Frequency
Urgency
Dysuria - burning sensation when peeing

Fever

130
Q

Clinical Presentation of Upper UTI (Pylonephritis)

A

Loin Pain
Haematuria
Swinging Fever
Cloudy urine (pyuria)
Confusion
Chils

More systemic effects.

131
Q

Investigation of UTIs

A

First line: Urine dipstick - nitrates, leukocyte, haematuria positive

Gold standard: Mid stream urine microscopy, culture and sensitivity

132
Q

Why does the urine sample for testing UTIs have to be mid stream?

A

Cannot be first void because it includes peroneal bacteria which can contaminate sample.

133
Q

How can a urine sample be obtained for kids?

A

Clean catch

134
Q

What can be deduced from urine microscopy for UTIs?

A

Pyuria - >10^4 leukocytes/mil

Bacteriuria - >10^5 colony forming units/mil

135
Q

Investigation of Catheter Associated UTI

A

Direct mid stream urine culture, no dipstick or microscopy.

136
Q

Why is urine microscopy not performed on catheter associated UTIs?

A

A urinary catheter will produce a urethral inflammatory response even in the absence of infection so microscopic pyuria will not be a specific result.

137
Q

Investigation of asymptomatic/symptomatic pregnant women with UTI

A

Urine dipstick + mid stream urine culture

If positive results on culture, confirm with second sample.

138
Q

Why are all pregnant women screened with urine dipsticks and mid stream urine cultures?

A

Dipstick - To check for pre-eclampsia

MSUC - To check for asymptomatic bacteraemia which could potentially lead to a UTI

139
Q

Management of a lower UTI (Cystitis)

A

First line is nitrofurantoin (if renal function is good or if non-pregnant)/trimethoprim

Uncomplicated: Nitrofurantoin/trimethoprim for 3 days

Complicated: Nitrofurantoin/trimethoprim for 7 days.

140
Q

Side effects of nitrofurantoin

A

Nausea/Vomiting
Headaches
Syncope
Neuropathy risk

141
Q

Contraindications of nitrofurantoin

A

Cannot be used in third trimester of pregnancy due to increaed risk of infantile jaundince and HDFN

Should not be used in renal impairment (eGFR/creatinine clearance <45ml/min)

142
Q

Contraindications of trimethoprim

A

Cannot be used in first trimester of pregnancy

143
Q

Pathophysiology of Pylonephritis

A

Infection of the renal parenchyma and soft tissues of renal pelvis /upper ureter

Can be ascending spread - urethra colonised with bacteria.
Massage of the urethra during intercourse can force bacteria into the female bladder

Can be haematogenous spread - S.aureus

Lymphatic spread (rare)

144
Q

Examination of Pylonephritis

A

Renal angle and loin tenderness

145
Q

Investigation of Pylonephritis

A

Urine dipstick - leukocyte, nitrates, haematuria positive

Midstream urine microscopy, culture and sensitivity

FBC - leukocytosis

ESR, CRP - elevated

Renal Ultrasound - rule out obstruction

Renal CT - wedge shaped areas of inflammation

146
Q

Management of Pylonephritis

A

Fluid resuscitation

Oral ciprofloxacin + co-amoxiclav for 7-14 days

If non-responsive then IV co-amoxiclav + gentamicin for 7-14 days

147
Q

Complications of Pyelonephritis

A

Renal abscess formation
Emphysematous pyelonephritis

148
Q

What regions are urinary stones usually found in?

A

Pelviureteric junction
Pelvic brim
Vesicoureteric junction

149
Q

Aetiology/Risk Factors for Urinary Stones

A

Dehydration
Hypercalcaemia - calcium based stones
Hyperuricaemia - uric acid stones
Recurrent UTIs - struvite stones
Diuretics

150
Q

What is the composition of urinary stones?

A

80% Ca based - calcium oxalate/calcium phosphate - radioopaque.

10% uric acid - cannot be seen on on KUB XR (radiolucent) but can be seen on CT

5-10% struvite (magnesium ammonium phosphate) - infection stones, usually in kidney

1% cystine - congenital defect in cystein transporter system.

151
Q

Pathophysiology of urinary stone formation

A

Nucleation theory - stones form crystals in supersaturated urine.

Proteus mirabilis UTI - secretes urease causing increasing urinary pH which can result in increased likelihood of stone formation.

152
Q

Clinical presentation of nephrolithiasis

A

Renal colic - severe loin to groin pain that comes in waves.

Worse with fluid intake

Visble haematuria

Can have UTI symptoms susch as dysuria, frequency

Recurrent UTIs

153
Q

Investigation of nephrolithiasis

A

Urinalysis - haematuria
KUB XR
Pregnant women and children - FL is renal ultrasound

GS: Non contrast CT KUB (NCCT-KUB)

154
Q

Lifestyle management of urinary stones

A

Proper hydration
Low Na diet
Increased exercise
Reduce BMI

155
Q

Medical management of urinary stones

A

FL - Fluid hydration and strong analgesics e.g IV diclofenac

If UTI symptoms, antibiotis e.g oral cefalexin + co-amoxiclav or IV gentamicin + co-amoxiclav for pyelonephritis.

For uric acid stones: sodium bicarbonate tablets for urine deacidifcation

156
Q

Interventional management of nephrolithiasis

A

If < 5mm, exrete it during urine passing.

If large stone (<4mm will pass normally), consider

Endoscopic sound wave lithotripsy (ESWL)

Ureteroscopy

Percutaneous nephrolithectomy (PCNL)

157
Q

Differential diagnoses for renal colic/loin pain

A

Abdominal aortic aneurysm
Appendicitis
Ectopic pregnancy, ovarian torsion
Testicular torsion

158
Q

Complications of urinary stones

A

Pyelonephritis/cystitis
Sepsis

159
Q

Aetiology/Risk Factors for BPH

A

Increasing age
Afro-carribean ethnicity

160
Q

Pathophysiology of BPH

A

Enlargement of inner (transitional) zone of the prostate gland.
Can compress on the prostatic urethra to cause obstruction.

161
Q

Clinical Presentation of BPH

A

LUTS
Frequency
Urgency
Nocturia
Incomplete voiding

Straining
Hesitancy
Intermittency
Post-micturition dribbling

162
Q

Investigation of BPH

A

FL: Digital rectal exam - smooth, diffuse enlargement.

PSA - prostate specific antigen (elevated)

163
Q

Management of BPH

A

Reduce caffeine intake

FL: Alpha 1 receptor antagonists e.g tamsulosin

5-alpha-reductase inhibitors such as finasteride

164
Q

Side effects of tamsulosin

A

Side effects: retrograde ejaculation, postural hypotension, syncope.

165
Q

What is AKI?

A

Sudden decline in kidney function over a period of hours or days.

166
Q

KDIGO Classification of AKI

A

Uses serum creatinine and urine output to assess severity

Level 1:
Increase of >26micromols/L or 1/5x baseline level over 48 hours.

<0.5/kg/ml urine output for >6 consecutive hours

167
Q

Pre-renal Aetiology of AKI

A

Hypovolaemia

Dehydration
Haemhorrage
Diuretic usage

168
Q

Intra-Renal Aetiology of AKI

A

Parenchymal damage

Acute tubular necrosis
Glomerulonephritis
PKD
Trauma

169
Q

Post-Renal Aetiology of AKi

A

Urinary tract obstruction

Urolithiases
BPH
Bladder tumour

170
Q

Pathophysiology of AKI

A

Can cause accumulation of excreted substances like electrolytes.

Can cause uraemia which can lead to pericarditis/cardiac tamponade.

171
Q

Clinical Presentation of AKI

A

Oliguria (low urine output)

Can have cola colored urine (rhabdomyolysis) if traumatic cause.

Fatigue, dizziness, vomiting - uraemia

Dyspnoea - pulmonary oedema due to salt and fluid retention.

Palpitations - arrhythmias due to hyperkalaemia

Palpable/enlarged bladder if obstructed

172
Q

Investigation of AKI

A

U & E - can show hyperkalaemia,
FBC & ESR/CRP - check for infection]

ABG - metabolic acidosis

Renal biopsy for intrarenal causes.

Renal ultrasound/NCCT-KB for obstruction and post renal causes.

173
Q

Management of AKI

A

Manage underlying disease

Sodium and potassium restriction

Hyperkalaemia: IV calcium gluconate or IV insulin/dextrose infusion with nebulised salbutamol if no ECG changes.

IV fluids if hypovolemic

May need renal replacement therapy.

174
Q

What are the 2 types of PKD?

A

Autosomal dominant PKD - most commonly inherited kidney disorder.

Autosomal recessive PKD - less common.

175
Q

Aetiology of PKD

A

ADPKD:
Mutation in PKD1 gene on chromosome 16 - most common
Mutation in PKD2 gene on chromosome 4

ARPKD:
Mutation in PKHD1 gene on chromosome 6

176
Q

Pathophysiology of ADPKD

A

Disruption of the polycystin pathway results in reduced cytoplasmic Ca2+.

In principal cells of the collecting duct this causes defective ciliary signalling and disorientated cell division.

Results in cyst formation

177
Q

Pathophysiology of ARPKD

A

Mutation in PKHD1 which encodes for fibrocystin causes cystic dilation of collecting ducts.

Cyst formation can also cause obstruction of urine flow and UTI.

178
Q

Clinical Presentation of PKD

A

BETWEEN AGES OF 30-40

Hypertension
Bilateral flank loin pain.
Painless Haematuria - bursting of cyst
Polyuria

Subarachnoid haemhorrage due to berry aneurysm rupture

Can also have UTI presentations.

179
Q

Investigation of PKD

A

GS: Renal ultrasound - enlarged kidneys with cysts.

U + E

Genetic testing for PKD gene mutations

180
Q

Management of PKD

A

Medical:

Vasopressin receptor antagonists e.g tolvaptan
Somatostain analogues e.g ocreotide

These reduce cAMP in principal cells to reduce cyst growth.

ACE inhibitors e.g ramipril for hypertension.

Surgical:

Laparoscopic cyst removal
RRT
Nephrectomy

181
Q

Conditions associated with PKD

A

SAH
Liver abscesses
Mitral valve prolapse

182
Q

Aetiology of Prostatitis

A

Streptococcus faecalis
Chlamydia trachomatis
UPEC

183
Q

Clinical Presentation of Prostatitis

A

Fever
Chills
Malaise
Pain upon ejaculation
Pelvic pain
Voiding LUTS

184
Q

Investigation of Prostatitis

A

DRE: tender and hot prostate.

Elevated PSA

Trans-rectal ultrasound

Urine dipstick: positive for leukocytes, nitrates, haematuria

Mid stream urine culture microscopy sensitivity

185
Q

Management of Prostatitis

A

IV ciprofloxacin

186
Q

Aetiology of Urethritis

A

Primarily a STI

Non gonoccocal - chlamydia, trichomonas vaginalis
Chlamydia is most common.#

Gonoccocal - neisseria gonorrhoeae

Male to male sex
Unprotected sex

187
Q

Clinical Presentation of Urethritis

A

Dysuria
Urethral discharge - blood, pus.

188
Q

Investigation of Urethritis

A

Culturing of genital secretions (black swab)

Nucleic acid amplification test (NAAT)

If suspected UTI, urine dipstick + mid stream urine microscopy culture sensitivity.

189
Q

Management of Urethritis

A

Gonorrhoea: IM ceftriaxone + oral azithromycin

Chlamydia: Oral doxycycline + oral azithromycin

190
Q

Clinical Presentation of Epididymal Cyst

A

Palpable lump(s) in the posterior aspect of the testicle.

Are transilluminate (will allow light to pass through) since fluid-filled.

If sperm filled - spermatocele.

191
Q

Investigation of Epididymal Cyst

A

Scrotal ultrasound

192
Q

What is a hydrocele?

A

Accumulation of fluid within the tunica vaginalis.

193
Q

Aetiology of Hydroceles

A

Primary - Patent processus vaginalis during testicular descent.

Secondary - testicular cancer, testicular torsion
oedema

194
Q

Pathophysiology of Hydrocele

A

Overproduction of fluid in the tune vaginalis (non-communitcating hydrocele)

Processus vaginalis fails to close, allowing peritoneal fluid to drain into the scrotum (communicating hydrocele)

195
Q

Clinical Presentation of Hydrocele

A

Enlargement of scrotum with non-tender, smooth cystic swelling.

Testes should be palpable

Swelling will normally be antero-inferior and will be transilluminate.

196
Q

Investigation of Hydrocele

A

Scrotal ultrasound

197
Q

What is a Varicocele

A

Abnormal dilation of the testicular veins in the pampiniform venomous plexus, caused by venous reflux

198
Q

Aetiology of Varicocele

A

Testicular/renal vein thrombosis/compression.
Pelvic tumour

199
Q

Pathophysiology of Varicocele

A

More common in left testes because testicular vein drains into left renal vein at a perpendicular angle before entering IVC.

Right testicular vein enters directly into IVC

Compression causes increased backpressure and swelling.

200
Q

Clinical Presentation of Varicocele

A

Swollen and distended scrotal blood vessels - looks and feels like a bag of worms around the testes.

Typically painless

201
Q

What is testicular torsion?

A

Twisting (torsion) of the spermatic cord

202
Q

Aetiology of Testicular Torsion

A

Can be due to congenital deformities such as belt-clapper deformity.

Cryptorchidism

Rough sexual activity

Trauma

203
Q

Pathophysiology of Testicular Torsion

A

Can cause occlusion of testicular blood vessels leading to ischaemic infarction.
Left testicle more commonly affected

204
Q

Clinical Presentation of Testicular Torsion

A

Sudden severe unilateral testicular pain

Unilateral testicular inflammation

Nausea/vomiting

205
Q

Examination of Testicular Torsion

A

Negative cremasteric reflex - no proximal movement of testicle upon stroking of inner thigh.

Negative Prehn’s sign - no pain relief upon elevation of scrotum.

206
Q

Investigation of Testicular Torsion

A

Doppler ultrasound to check testicular blood-flow

207
Q

Management of Testicular Torsion

A

FL: Surgical exploration & orchidoplexy

Orchidectomy

If within 6 hours, 90-100% chance of saving the testicle.

208
Q

What is chronic kidney disease?

A

CKD is longstanding, usually progressive, impairment in renal function
(haematuria, proteinuria or anatomical abnormality) for more than 3 months

Defined as a GFR < 60mL/min/1.73 m for more than 3 months with/without
evidence of kidney damage (haematuria, proteinuria or anatomical abnormality)

209
Q

What are the stages of chronic kidney disease?

A

Stage 1: eGFR >90 ml/min
Stage 2: eGFR 60-89 ml/min
Stage 3a: eGFR 45-59 ml/min
Stage 3b: eGFR 30-44 ml/min
Stage 4: eGFR >15-29 ml/min
Stage 5: eGFR < 15 ml/min

210
Q

Pathophysiology of chronic kidney disease

A

In CKD filtration is performed by fewer functioning nephrons.

These experience hyperfiltration which can lead to accelerated nephronic decline.

In order to compensate for decreased GFR the RAAS system is activated, but this increases the effect of hyperfiltration and increases glomerular basement membrane permeability.

211
Q

Investigation of CKD

A

Urinalysis - haematuria, proteinuria

U + E - high urea, creatinine, potassium, low calcium

FBC - normochromic normocytic anaemia (ACD)

212
Q

Management of CKD

A

Symptomatic management.
Diuretics

If in end stage, renal replacement therapy

213
Q

What are the different types of renal replacement therapy available?

A

Haemoialisis
Haemofiltration
Peritoneal dialysis

214
Q

What is haemodialysis?

A

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction, thus blood is always meeting a less-concentrated solution and diffusion small solutes occurs down the concentration gradient.

Taken from artery and returned to vein through AV fistula.

215
Q

Pros and cons of haemodialysis

A

Pros
Can be commenced quickly, used during emergencies.
Patient doesn’t need training.

Cons
Cannot be performed at home - must be in hospital.
Risk of issues with vascular access.
Does not work for haemodynamically unstable patients.

216
Q

What is peritoneal dialysis?

A

Process insert catheter into patient’s abdomen and use peritoneum in the abdomen as a membrane across which fluid and solutes are exchanged with blood

217
Q

Pros and cons of peritoneal dialysis

A

Pros
Can be done at home - more convenient.
Lesser risk of hypotension

Cons
Requires training
Increased infection risk - peritonitis.
Does not work for ;arge patients or those with poor residual function

218
Q

What is haemofiltration?

A

Most commonly used

Achieves blood flow using a blood pump to draw and return blood from the lumen of a dual-lumen catheter placed in the jugular, subclavian or femoral vein.

Ultrafiltrate is continuously removed from patient combined with simultaneous infusion of replacement solution

219
Q

Pros and cons of haemofiltration

A

Pros
Is more hemodynamically stable compared to other methods.
Allows for larger range of uraemic solute removal.

Cons
Shorter circuit life
More expensive

220
Q

Aetiology/Risk factors of haemolytic uraemic syndrome

A

Post-EHEC infenction.

221
Q

Pathophysiology of haemolytic uraemic syndrome

A

Shiga toxin released by EHEC causes small vessel thrombosis, leading to platelet depletion (thrombocytopaenia), haemolysis and pre-renal AKI.

222
Q

Clinical presentation of haemolytic uraemic syndrome

A

Haemolytic anaemia - pallor, dyspnoea
Thrombocytopaenia - easy bleeding, bruising
Acute Kidney Injury - oliguria

223
Q

Investigation of haemolytic uraemic syndrome

A

Blood film - schistiocytes and helmet cells.

224
Q

Management of haemolytic uraemic syndrome

A

Supportive management.

Antihypertensives
Diuretics
Blood transfusions

225
Q

Aetiology/risk factors for CKD

A

Polycystic kidney disease
Hypertension
Diabetes mellitus
Chronic pyelonephritis

226
Q

Aetiology of epidiymo-orchitis

A

UTI - KEEPS
STI - chlamydia

227
Q

Clinical Presentation of epidiymo-orchitis

A

Unilateral testicular pain and swelling.

228
Q

Investigation of epidiymo-orchitis

A

If <35, STI test

If >35, mid stream urine microscopy and culture.

229
Q

Mangement of epidiymo-orchitis

A

If STI - IM ceftriaxone + oral doxycycline

If UTI - ciprofloxacin

230
Q

Pharmacodynamics of 5-alpha-reductase inhibitors

A

E.g finasteride.

Reducess size of prostate through
inhibits conversion of testosterone to dihydrotestosterone which is the active form needed for prostatic growth.

231
Q

Pharmacodynamics of alpha-1-antagonists

A

E.g tamsulosin

Causes smooth muscle relaxation in the bladder neck to reduce obstruction and improve urinary flow.

232
Q

Antimicrobial managment of chlamydia

A

Oral doxycycline + oral azithromycin

233
Q

Antimicrobial management of gonorrhoea

A

IV ceftriaxone + oral azithromycin

Sirpi's Phase 2A Medicine (13 decks)

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