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Phase 2a Lecture Notes > Urology > Flashcards

Urology Flashcards

1
Q

Function of the Urinary Tract

A

To collect urine produced continuously by the kidneys
To store collected urine safely
To expel urine when socially acceptable

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2
Q

Anatomy of kidney

A

Retroperitoneal organs
Lie between T11 – L3
Blood supply from renal artery direct from aorta at L1 level

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3
Q

How many nephrons does each kidney contain

A

1 million nephrons

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4
Q

How much urine does each kidney produce a day

A

1-1.5L of urine per day

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5
Q

Ureters- Anatomy

A

25cm – 30cm
Retroperitoneal organs
Run over psoas muscle, cross the iliac vessels at the pelvic brim and insert into trigone of bladder

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6
Q

Ureters function

A

Transport urine from the kidney to the bladder via peristalsis

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7
Q

What is preventing the reflex of urine

A

a valvular mechanism at the vesicoureteric junction

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8
Q

Nervous Control of the Bladder and Sphincter- 4 nerve

A

Parasympathetic Nerve (pelvic nerve)
Sympathetic Nerves (hypogastric plexus)
Somatic Nerve (pudendal nerve)
Afferent pelvic nerve

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9
Q

Nervous Control of the Bladder and Sphincter- Parasympathetic Nerve (pelvic nerve)

A
  • S2-S4
  • acetylcholine neurotransmitter
  • involuntary control
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10
Q

Nervous Control of the Bladder and Sphincter- Sympathetic Nerves (hypogastric plexus)

A

T11 – L2
noradrenaline neurotransmitter
involuntary control

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11
Q

Nervous Control of the Bladder and Sphincter- Somatic Nerve (pudendal nerve)

A

S2-S4
“Onuf’s nucleus”
acetylcholine neurotransmitter

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12
Q

Nervous Control of the Bladder and Sphincter- Afferent pelvic nerve

A

Sensory nerve
signals from detrusor muscle

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13
Q

Neural Control- Onuf’s Nucleus

A

Responsible for guarding reflex

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14
Q

Neural Control- Pontine Micturition Centre/Periaqueductal Grey

A

Responsible for Co-ordination of voiding

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15
Q

Neural Control- Cortex

A

Responsible for voluntary control

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16
Q

Neural Control- Sacral Micturition Centre

A

Responsible for Micturition reflex

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17
Q

Storage Phase

A

Bladder fills continuously
As the volume in the bladder increases the pressure remains low due to “receptive relaxation” and detrusor muscle compliance

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18
Q

Filling Phase

A

At lower volumes the afferent pelvic nerve sends slow firing signals to the pons via the spinal cord

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19
Q

Filling phase- nerves

A

-Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation
-Somatic (Pudendal) nerve stimulation maintains urethral contraction

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20
Q

Voiding Phase – Micturition Reflex

A

Autonomic spinal reflex
Higher volumes stimulate the afferent pelvic nerve to send fast signals to the sacral micturition centre in the sacral spinal cord

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21
Q

Voiding Phase – Micturition Reflex- nerves

A

Pelvic parasympathetic nerve is stimulated and the detrusor muscle contracts
Pudendal nerve is inhibited and the external sphincter relaxes

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22
Q

Guarding Reflex

A

Voluntary control of micturition

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23
Q

Guarding Reflex

A

Afferent signals from the pelvic nerve are received by the PMC/PAG and transmitted to higher cortical centres
If voiding is inappropriate the guarding reflex occurs
Sympathetic (hypogastric) nerve stimulation results in detrusor relaxation
Pudendal nerve stimulation results in contraction of the external urethral sphincter

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24
Q

Storage summary

A

Receptive Relaxation
Detrusor relaxation (sympathetic stimulation T11-L2)
External Urethral Sphincter contracted (pudendal stimulation S2-4)

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25
Q

Micturition

A

Voluntary control from cortex and PMC
Detrusor contraction (parasympathetic stimulation S2-4)
External Urethral Sphincter relaxation (pudendal inhibition S2-4)

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26
Q

Penile cancer epidemiology

A

Rare in UK, more common in far east and Africa
Very rare in circumcised
Related to smegma, chronic inflammation and viruses

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27
Q

Penile cancer presentation

A

Chronic fungating ulcer, bloody/purulent discharge
50% spread to lymph at presentation

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28
Q

Penile cancer treatment

A

Radiotherapy and iridium wires (protons instead of x-ray radiation) if early
Amputation and lymph node dissection if late

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29
Q

Benign diseases of the penis

A

Balanitis, Phimosis, Paraphimosis

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30
Q

Balanitis

A

Acute inflammation of the foreskin and glans
Association with strep and strap infections
More common in diabetes and young children with tight foreskins

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31
Q

Balanitis- treatment

A

Antibiotics, circumcision, hygiene advice

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32
Q

Phimosis

A

Foreskin occludes the meatus (hole where fluids leave body)
Young boys- recurrent balanitis + ballooning, may heal with time or require circumcision
Adult- presents with painful intercourse, infection, ulceration

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33
Q

Paraphimosis treatment

A

Ask patient to squeeze glans
Try applying 50% glucose-soaked swab (oedema may follow osmotic gradient), ice packs and lidocaine gel may help
May require aspiration, dorsal slit, circumcision

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34
Q

Paraphimosis

A

Occurs when tight foreskin is retracted and becomes irreplaceable, preventing to venous return leading to oedema and even ischemia of the glans
Can occur if the foreskin is not replaced after catheterization

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35
Q

Impotence

A

Erectile dysfunction
Common in over 50s
Physiological facet is common

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36
Q

Normal erection function

A

Results from neuronal release of NO which, via cGMP and Ca2+, hyperpolarizes and thus relaxes vascular and trabecular smooth muscle cells, allowing engorgement

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37
Q

Impotence causes

A

Physiological
Organic- Big 3- smoking, alcohol + diabetes
- Endocrine, neurological, pelvic surgery, radiotherapy, atheroma, renal/ hepatic failure, prostatic hyperplasia, penile abnormalities, drugs

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38
Q

Impotence investigations

A

Full sexual and physiological work up
Bloods- U+E, LFTs, glucose, TFT, LH, FSH, lipids, testosterone, prolactin
Doppler test (US to see how blood flows in the penis during and after an erection)

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39
Q

Impotence treatment

A

Treat underlying causes
Counselling
Oral phosphodiesterase inhibitors (increase cGMP)

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40
Q

Bladder tumours

A

In the UK >90% are transitional cell carcinomas
Adenocarcinomas and squamous cell carcinomas are rare in west
More common in men then women

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41
Q

Bladder tumours- grading

A

Grade 1- differentiated
Grade 2- intermediate
Grade 3- poorly differentiated

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42
Q

Bladder tumours- location

A

80% confined to bladder mucosa
20% penetrate muscle (worse prognosis)

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43
Q

Bladder tumour- presentation

A

Painless haematuria (blood in urine), recurrent UTIs, voiding irritability

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44
Q

Bladder tumour- associations

A

Smoking, aromatic amines (rubber industry), chronic cystitis schistosomiasis, pelvic irradiation

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45
Q

Bladder tumour- investigations

A

Cystoscopy with biopsy is diagnostic
CT urogram is diagnostic (provides staging)
Urine- microscopy/cytology
MRI/ lymphangiography may show involved nodes

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46
Q

Bladder tumour- staging Tis

A

Carcinoma in situ

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47
Q

Bladder tumour- staging Ta

A

Tumour confined to epithelium

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48
Q

Bladder tumour- staging T2

A

Invades muscle

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49
Q

Bladder tumour- staging T1

A

Tumour in submucosa or lamina propira

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50
Q

Bladder tumour- staging T3

A

Extends to perivesical fat

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51
Q

Bladder tumour- staging T4

A

Invades adjacent organs

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52
Q

Bladder tumour- staging N0-N4

A

N0- no lymph node involvement
N1-N4 progressive lymph node involvement

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53
Q

Bladder tumour- staging M0/M1

A

M0- no mets
M1- distant mets

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54
Q

Treatment of transitional cell carcinomas (TCC) of the bladder- Tis/Ta/T1

A

80% of all patients
Diathermy (deep heating) via transurethral cystoscopy or TURBT (transurethral resection of bladder tumour)
Consider intravesical BCG (stimulates a non specific immune response)

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55
Q

Treatment of transitional cell carcinomas (TCC) of the bladder- T2-3

A

Radical cystectomy (removal of bladder) is gold standard
Radiotherapy gives worse survival rates but preserves the bladder
Post-op chemo toxic but effective
Trying other surgical methods to preserve the bladder, but none are effective yet

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56
Q

Treatment of transitional cell carcinomas (TCC) of the bladder- T4

A

Usually palliative chemo/radiotherapy
Chronic catheterization and urinary diversions may help relive pain

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57
Q

What to use to measure chronic disease

A

eGFR and ACR (albumin to creatinine ratio)

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58
Q

Chronic kidney disease- prevalence in UK

A

4.19%, large differences in areas due to difference in age, health inequality

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59
Q

Most common cause of end stage kidney disease in the UK

A

Diabetes (diabetic neuropathy)
Other common causes- hypertension, glomerulonephritis, secondary to pre-eclampsia

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60
Q

Blood pressure control in CKD

A

High protein in urine= lower BP threshold for hypertension intervention
ACEi/ARBs are first line

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61
Q

Diabetic Nephropathy in CKD

A

Hyperglycaemia leads to increase in growth factors, RAAS activation and oxidative stress. This causes increase in glomerular capillary pressure, podocyte damage and endothelial dysfunction.
Albuminuria is 1st clinical sign, later scarring (glomerulosclerosis), nodule formation, and fibrosis with progressive loss of renal function ie CKD

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62
Q

Anaemia in CKD

A

Common as EPO is produced in peritubular cells of the kidney, when kidneys are damaged, EPO production reduces
Less EPO, less RBC production, less O2

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63
Q

Fluid overload in CKD

A

Progressive loss of renal function causes reduced sodium filtration and inappropriate suppression of tubular reabsorption that ultimately lead to volume expansion

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64
Q

Sodium in CKD

A

Sodium accumulation is one of the consequences of renal failure, resulting in increased water intake, increases in the extracellular volume, and accompanying rise in blood pressure

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65
Q

Most common cause of death with CKD

A

Cardiovascular events

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66
Q

Glomerulonephritis in CKD

A

inflammation of the glomeruli. Severe or prolonged inflammation associated with glomerulonephritis can damage the kidneys causing CKD

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67
Q

SGLT2 inhibitors in CKD

A

effective at slowing the progression of kidney disease, reducing heart failure, and lowering the risk of kidney failure and death in people with CKD and type 2 diabetes

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68
Q

Bone mineral disorders in CKD

A

Damaged kidneys stop
-turning vitamin D into calcitriol, creating an imbalance of Ca2+ in your blood
-removing excess phosphorus from your blood, triggering your blood to pull Ca2+ out of your bones and causing them to weaken
-release extra PTH, Ca2+ from your bones to restore your blood calcium levels

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69
Q

Who gets renal cancer?

A

Hypertension, obesity, smoking- (oxidative stress)

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70
Q

Other renal cancer RF

A

family history (5%- VHL usually)
ESRF
Tuberous sclerosis

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71
Q

Renal cancer investigation

A

Flank pain, palpable mass, blood in urine- classic trifecta
Imaging- CT, MRI

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72
Q

Horse shoe kidney

A

a condition in which the kidneys are fused together at the lower end or base

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73
Q

Haematuria and 2 week wait guidance

A

Visible Haematuria, over 45%, 30% risk of cancer
Non-visible haematuria, over 60, 5% risk of cancer

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74
Q

Cannonball metastases

A

Classic feature of metastatic renal cell carcinoma, appears as clearly defined circular opacites scattered throughout the lung

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75
Q

Most common renal cancer type

A

Clear cell renal carcinoma
Others- papillary and chromophobe carcinomas

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76
Q

Treatment options for renal cancer- surgical

A

Radical/partial nephrectomy, to remove tumour is first line

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77
Q

Treatment options for renal cancer- non invasive

A

Arterial embolisation- cutting off the blood supply to the affected kidney
Percutaneous cryotherapy- injecting liquid nitrogen to freeze and kill the tumour cells
Radiofrequency ablation- putting a needle in the tumour and using an electrical current to kill the tumour cells

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78
Q

GFR influenced by

A

Net Filtration Pressure (NFP)- Hydrostatic pressures + Colloid osmotic pressures
Renal Blood Flow (RBF)- Autoregulation
Filtration coefficient

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79
Q

4 starling forces effecting net fluid movement

A

Glomerular hydrostatic pressure- fluid out
Bowman’s Capsule fluid pressure- fluid in
Glomerular colloid osmotic pressure
(pi*G; protein)- fluid in
Bowman’s Capsule colloid osmotic pressure- should be negligible as albumen is filtered out

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80
Q

Net Filtration Pressure (NFP) =

A

Glomerular hydrostatic pressure - (Bowman’s Capsule fluid pressure + Glomerular colloid osmotic pressure)

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81
Q

Renal Auto-regulation

A

Intrinsic feedback mechanisms
-Afferent and efferent arterioles
-Tubuloglomerular Feedback

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82
Q

Why is creatine used to measure eGFR

A

Production rate is roughly similar to clearance rate in the body

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83
Q

GFR equation

A

urine flow rate * [creatine] urine] / [creatine] plasma

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84
Q

Problems with eGFR

A

Doesn’t consider creatinine tubular secretion
Significant decrease GFR small [Cr] plasma- Need several time points
Creatinine metabolism reflection on lean body mass
Not valid in pregnancy

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85
Q

DAMN drugs

A

Induce, exacerbate or complicate AKI: acidosis, hypovolaemia or hypertension

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86
Q

DAMN drugs- acronym meaning

A

Diuretics
ACEis/ARB
Metformin
NSAIDs

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87
Q

Factors that Decrease GFR

A

Increase Afferent artery resistance- NSAIDs
Decrease efferent artery resistance, decrease angiotensin II (ACEi/ARB)
Increase Glomerular colloid osmotic pressure- decrease renal BF, increase plasma proteins
Increase bowmens c

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88
Q

Factors that Decrease GFR- increase Afferent artery resistance

A

NSAIDs

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89
Q

Factors that Decrease GFR- decrease Efferent artery resistance

A

Due to decrease Angiotensin II ie ACEi/ARB

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90
Q

Factors that Decrease GFR- increase Glomerular colloid osmotic pressure

A

Decrease in renal BF, increase in plasma protein

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91
Q

Factors that Decrease GFR- increase Bowmen capsule fluid pressure

A

Urinary tract obstruction (kidney stones)

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92
Q

Factors that Decrease GFR- decrease kidney function

A

Renal disease Diabetes mellitus Hypertension

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93
Q

Factors that Decrease GFR- decrease Glomerular hydrostatic pressure

A

Decrease Arterial pressure (small effect)

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94
Q

Which ion has a key role in determining plasma volume and osmolality?

A

Na+

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95
Q

Expansion of Fluid Volume - A Simple System

A

Increase Blood volume
Increase BP
Increase renal excretion
Normal vol restored

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96
Q

Regulation of Blood Pressure and Volume

A

Baroreceptor reflexes (medulla)- measure BP
Osmoreceptor Reflexes (hypothalamus)- measure Na+

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97
Q

Pressure Natriuresis and Atrial Natriuretic Peptide (ANP)

A

ANP generally antagonises Angiotensin-II actions
- inhibits renin secretion
-afferent arteriole dilation

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98
Q

Benign prostatic hyperplasia- epidemiology

A

Very common
24% for 40-64
40% for 64+

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99
Q

Benign prostatic hyperplasia- pathology

A

Benign nodular or diffuse proliferation of musculofibrous and glandular layers
Inner (transitional) zone enlarges

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100
Q

Benign prostatic hyperplasia vs prostate carcinoma- pathology

A

Benign prostatic hyperplasia- Inner (transitional) zone enlarges
Prostate carcinoma- enlargement of peripheral layers of the prostate

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101
Q

Benign prostatic hyperplasia- presentation

A

LUTS (lower urinary tract symptoms)

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102
Q

LUTS (lower urinary tract symptoms)

A

Nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria, bladder stones, UTIs

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103
Q

Benign prostatic hyperplasia- tests

A

MSU (Midstream Specimen of Urine), U+Es, Ultrasound, PSA (prostate-specific antigen), transrectal ultrasound +/- biopsy

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104
Q

PSA (prostate-specific antigen)

A

A protein produced by both cancerous and noncancerous tissue in the prostate

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105
Q

Benign prostatic hyperplasia- lifestyle management

A

Avoid alcohol, caffeine
Relax when voiding, void twice to aid emptying
Train bladder by practising distraction methods and holding on

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106
Q

Benign prostatic hyperplasia- drug management

A

Alpha-blockers are 1st line (decrease smooth muscle tone)
5 alpha-reductase inhibitors- shrink the prostate gland if it’s enlarged, can be used alone or in combination

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107
Q

Benign prostatic hyperplasia- surgical indications

A

Have complications attributed to BPH, such as acute and/or chronic renal insufficiency, recurrent bladder stones, gross recurrent haematuria, recurrent UTIs
Have refractory responses to medication

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108
Q

Benign prostatic hyperplasia- surgical management

A

Transurethral resection of the prostate (TURP)- historical standard
Other options- Simple prostatectomy, Transurethral vaporisation of the prostate (TUVP)

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109
Q

Glomerulonephritis

A

Group of diseases that cause inflammation and damage to glomeruli
May be acute or chronic

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110
Q

Glomerulonephritis Signs/symptoms

A

Declining renal function
Hypertension
Leaky glomerulus- haematuria, proteinuria

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111
Q

Glomerulonephritis Progression

A

Causes 25% of ESKF

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112
Q

Glomerulonephritis Pathophysiology

A

Glomerulonephritis is usually immunologically mediated:
-Immunoglobulin deposits
-Inflammatory cells
-Response to immunosuppressive therapy

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113
Q

Acute Nephritic syndrome- characteristics

A

Acute kidney injury, active dipstick (haematuria and proteinuria), Oliguria, hypertension and fluid overload

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114
Q

Acute Nephritic syndrome- immune mediated examples

A

ANCA associated vasculitis
Goodpasture’s disease, SLE (systemic lupus erythematosus), systemic sclerosis, post-streptococcal infection, Crescentic IgA nephropathy, Henoch Schonlein purpura (HSP)

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115
Q

Acute Nephritic syndrome - Urine

A

Haematuria key feature- red ell casts on urine microscopy characteristic of glomerular bleeding
Proteinuria is variable but usually sub-nephrotic levels

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116
Q

Acute Nephritic syndrome - Hypertension

A

Hypertension common
Can be severe and present as hypertensive emergency
Risk of stroke, retinopathy, MI

117
Q

Acute Nephritic syndrome - Fluid

A

Fluid retention often seen
Signs/symptoms
- Hypertension
- Pulmonary oedema/effusions
- Peripheral oedema
- Raised JVP
-Orthopnea and Shortness of Breath
-Increasing weight

118
Q

ANCA-Associated Vasculitis

A

ANCA = antineutrophil cytoplasmic antibodies
Multisystem small vessel vasculitis

119
Q

Vasculitis

A

Inflammation of blood vessels

120
Q

ANCA-Associated Vasculitis- treatment

A

Immunosuppression: steroids, cyclophosphamide, rituximab, (plasma exchange)

121
Q

ANCA-Associated Vasculitis (ANCA-AAV) Features

A

systemic inflammatory features
Features of other organ system involvement.
Greater incidence in white and 50-79

122
Q

ANCA-Associated Vasculitis (ANCA-AAV)- investigation

A

Serum ANCA
Changes in ANCA titre correlate with disease activity
Biopsy of glomerulus

123
Q

ANCA-Associated Vasculitis (ANCA-AAV)- biopsy

A

Segmental glomerular necrosis with crescent formation. Degree of active lesions, fibrosis and tubular atrophy are important prognostic markers.

124
Q

IgA Nephropathy

A

Abnormality in IgA glycosylation leads to deposition in mesangium (close proximity to glomerulus)
May run a benign, insidious or aggressive course
Overlap with HSP (Systemic form)
Commonest cause of glomerulonephritis world wide

125
Q

Systemic Lupus Erythematosus (SLE)

A

autoimmune disease in which the immune system attacks its own tissues, causing widespread inflammation and tissue damage

126
Q

Systemic Lupus Erythematosus (SLE)- signs and symptoms

A

Rash, arthralgia, kidney failure, neurological symptoms, pericarditis, pneomonitis

127
Q

Systemic Lupus Erythematosus (SLE) - Treatment

A

Immunosuppression – steroids, cyclophosphamide, mycophenolate mofetil, rituximab

128
Q

Systemic Sclerosis

A

rare chronic disease of unknown cause characterized by diffuse fibrosis and vascular abnormalities in the skin, joints, and internal organs

129
Q

Anti- glomerular Basement Membrane disease (Goodpasture syndrome)

A

Autoimmune destruction of own collagen, affects alveoli and glomerulus primary

130
Q

Anti- glomerular Basement Membrane disease (Goodpasture syndrome)- clinicals signs

A

Rapidly progressive kidney failure, active dipstick. Haemoptysis

131
Q

Anti- glomerular Basement Membrane disease (Goodpasture syndrome)- treatment

A

remove antibody
-plasma exchange, immunosuppression -steroids/ cyclophosphamide

132
Q

Henoch Schonlein purpura (HSP)

A

Systemic form of IgA Nephropathy
More commonly children, often provoked by URTI

133
Q

Henoch Schonlein purpura (HSP)- clinical signs

A

Triad of: Purpuric rash, abdominal pain, acute kidney injury (IgA deposition on kidney biopsy)

134
Q

Nephrotic syndrome- clinical signs

A

Triad of heavy proteinuria, hypoalbuminemia, oedema
Other feature- Hypercholesterolaemia
- Haematuria usually absent or mild

135
Q

Common causes of nephrotic syndrome- primary

A

Minimal change – children+ adults
Membranous – caucasian adults
Focal Segmental Glomerulosclerosis – adults

136
Q

Common causes of nephrotic syndrome- secondary

A

Diabetes
Amyloid (usually AL)
Infections
SLE
Drugs – gold, penicillamine
Malignancy

137
Q

Management Nephrotic Syndrome

A

Establish Cause – renal biopsy usually required
Treat complications – manage fluid state
Treat underlying cause

138
Q

Nephrotic Syndrome- Investigations

A

Serum albumin, creatinine (+eGFR), lipids and glucose, urinalysis
Urine protein creatinine ratio – to quantify proteinuria

139
Q

Nephrotic Syndrome- supportive treatment

A

Control fluid state – diuretics, ACEi/ARBs, spironolactone
Statins
Anticoagulation
Prevent infections – prophylactic antibiotics in children

140
Q

Membranous Nephropathy

A

Thickening of glomerular capillary wall. IgG, complement deposit in sub epithelial surface causing leaky glomerulus

141
Q

Membranous Nephropathy- clinical features

A

nephrotic syndrome (Nephrotic range proteinuria, hypoalbuminemia and oedema)

142
Q

Membranous Nephropathy- diagnosis

A

serum PLA2R Ab, look for secondary causes, renal biopsy

143
Q

Membranous Nephropathy- natural history

A

10yr renal survival of 100% in those who achieve complete remission, 90% with partial remission and only 45% with no remission
30% spontaneous remission

144
Q

Membranous Nephropathy- treatment

A

Depends on risk
Wait and see for low risk
Steroid therapy for higher risk

145
Q

Minimal Change Disease

A

biopsy appears normal on light microscopy but fused podocytes on electron microscopy
Often in children or younger patients, does have spike in incidence at older ages

146
Q

Minimal Change disease- treatment

A

Steroids is first line

147
Q

Asymptomatic urinary abnormalities

A

Incidental finding of dipstick haematuria +/- proteinuria
Kidney function and blood pressure normal

148
Q

Asymptomatic urinary abnormalities common causes

A

IgA, Thin membrane disease

149
Q

Asymptomatic urinary abnormalities- diagnosis

A

usually clinical – don’t biopsy unless kidney function abnormal or significant proteinuria

150
Q

Thin membrane disease

A

Often inherited – may affect 1% of population
Probable benign and indolent natural history
Often genetic cause: Type IV collagen variants

151
Q

Glomerulonephritis- CKD causes

A

IgA nephropathy, membranous, diabetes, mesangiocapillary GN, HIV associated nephropathy, Alports

152
Q

Alports syndrome

A

genetic condition characterized by kidney disease, loss of hearing, and eye abnormalities caused by mutation in Type IV collagen
X-linked inheritance

153
Q

Alports Syndrome- features

A

-Renal: Progressive CKD, Haematuria, proteinuria
-Sensorineural Hearing loss
-Can develop nephrotic syndrome

154
Q

Prostate cancer

A

Commonest male malignancy
Incidence increase with age, 80% in men over 80

155
Q

Prostate cancer- pathophysiology

A

Most are adenocarcinomas arsing in peripheral
Spread may be local (seminal vesicles, bladder, rectum), via lymph or haematogenously (sclerotic bone lesions)

156
Q

Prostate cancer- symptoms

A

Asymptomatic or urinary retention, poor stream, frequency, and nocturia
Weight loss +/- bone pain suggest mets

157
Q

Prostate cancer- investigations

A

Prostate exam- hard, irregular prostate
High PSA
Transrectal US and biopsy (required for diagnosis), CT, MRI (for staging)

158
Q

Prostate cancer- treatment approach

A

Treatment decision depends on risk group, life expectancy and patient preference
Ranges from wait and see to androgen deprivation therapy (ADT), external beam radiotherapy (EBRT), brachytherapy to radical prostatectomy

159
Q

Prostate cancer- Androgen deprivation therapy (ADT)

A

Androgen deprivation may be achieved medically, with a luteinising hormone-releasing hormone (LHRH) agonist or antagonist, or by surgical castration (bilateral orchiectomy)

160
Q

Prostate cancer- Radical prostatectomy

A

Option when when the tumour is confined to the prostate and life expectancy is ≥10 years,

161
Q

Prostate cancer- Observation

A

Monitoring progression of symptoms, PSA levels and biopsies (active surveillance)

162
Q

PSA (prostate-specific antigen)

A

Serum PSA levels may be increased in patients with prostate cancer; however, other non-malignant conditions (e.g., prostatitis and benign prostatic hyperplasia) may increase PSA levels.
PSA levels may also vary according to race

163
Q

Acute kidney injury

A

Syndrome of decreased renal function, measured by serum creatine or urine output, occurring over hours-days

164
Q

Acute kidney injury- definition

A

Rise in creatine > 26 micromol/L within 48 hours
Rise in creatine >1.5x the baseline over a week
Urine output <0.5 mL/kg/h for 6 consecutive hours

165
Q

Acute kidney injury- pre renal

A

Decrease in blood volume and blood flow –> decrease in effective arterial blood volume

166
Q

Acute kidney injury- pre renal causes

A

hypovolemia of any cause
heart, liver, kidney failure
sepsis
emboli
RAS
Drugs NSAIDs, Tacrolimus, ACE I
Hyper Ca

167
Q

Acute kidney injury- pre renal causes- low cardiac output

A

Low CO> decrease in mean arterial pressure > increase in art renal resistance > decrease in eGFR > rise in serum Cr

168
Q

Acute kidney injury- pre renal causes- low albumin states

A

Low albumin states > low oncotic pressure > fluid in 3rd space > low mean arterial pressure > decrease in eGFR > rise in serum Cr

169
Q

Acute kidney injury- pre renal causes- increased permeability of vessels

A

Systemic vasodilation > fluid in 3rd space > decrease mean arterial pressure > decrease in eGFR > rise in serum Cr

170
Q

Acute kidney injury- intra renal

A

a disease process causes damage to the kidney itself resulting in AKI

171
Q

Acute kidney injury- intra renal causes

A

Acute tubular necrosis, Acute interstitial nephritis, Glomerulonephritis, Hypertension, thrombotic microangiopathies

172
Q

Acute kidney injury- intra renal- acute tubular necrosis causes

A

Low blood pressure
Drugs: aminoglycoside, vancomycin, acyclovir
Contrast
Hemolysis, rhabdomyolysis, tumor lysis

173
Q

Acute kidney injury- intra renal- Acute interstitial nephritis causes

A

Drugs: abx, PPI
infections
SLE, sarcoidosis

174
Q

Acute kidney injury- intra renal-thrombotic microangiopathies

A

thrombotic thrombocytopenic purpura (TTP), haemolytic uremic syndrome (HUS) and Disseminated intravascular coagulation (DIC)

175
Q

Acute kidney injury- post renal- pathology causes

A

Within renal tract or extrinsic compression

176
Q

Acute kidney injury- post renal- within renal tract causes

A

Stone, renal tract malignancy, stricture, clot

177
Q

Acute kidney injury- post renal- extrinsic compression causes

A

Pelvic malignancy, prostatic hypertrophy, retroperitoneal fibrosis

178
Q

Acute kidney injury- diagnosis investigations

A

Urine Cr, urine dip, urine osmolality, urine Na, Ultrasound of the Kidneys, Ureters & Bladder (KUB)

179
Q

Acute kidney injury- signs

A

Azotaemia, hyperkalaemia, decrease urine output, fluid overload, accumulation of drugs

180
Q

Azotaemia

A

biochemical abnormality- elevation, or build up of nitrogenous products, creatinine in the blood, and other secondary waste products within the body

181
Q

Acute tubular necrosis- urine dip

A

Muddy brown casts
Eosinophils

182
Q

Urinary casts

A

Tiny tube-shaped particles that can be found when urine is examined under the microscope during a test called urinalysis

183
Q

Acute kidney injury- management principles

A

Supportive therapy with close ongoing monitoring
Identification and management of the underlying cause (sepsis, nephrotoxic medication, urinary tract obstruction)
Recognition and correction of life-threatening complications (hyperkalaemia, acidosis, volume overload)

184
Q

Acute kidney injury-indications for dialysis

A

HyperK
Uraemia
Acidosis
Intoxication
Fluid overload

185
Q

Acute kidney injury- complications

A

Hyperkalaemia, Acidosis, Pulmonary oedema

186
Q

Acute kidney injury- Fluids principles

A

Resuscitation, replacement, maintenance

187
Q

Acute kidney injury- STOP AKI

A

Sepsis, Toxins, Optimise volume status/BP, Prevent harm

188
Q

UTI

A

Combination of clinical features and the presence of bacteria in the urine

189
Q

Lower tract UTI

A

Bladder (cystitis), prostate (prostatitis)

190
Q

Lower tract UTI

A

Pyelonephritis= infection of kidney/ renal pelvis

191
Q

UTI classifications

A

Complicated, Uncomplicated, Asymptomatic bacteriuria

192
Q

Complicated UTI

A

Structural/functional abnormalities of the GU tract ie obstruction, catheter, stones, neurogenic bladder, renal transplant
Common in pregnant, men, catheterised, children, immunocompromised

193
Q

Uncomplicated UTI

A

Normal renal tract structure and function
Non-pregnant women

194
Q

Most common cause of UTI

A

E. coli

195
Q

UTI organisms

A

Usually anaerobes and gram-negative bacteria from bowel and vaginal flora

196
Q

UTI organism examples

A

E. coli, Staph. saprophyticus, Proteus and Klebsiella

197
Q

UTI causes- ureters

A

Stasis during pregnancy, Ureteric stones, Proteus (produces urease, increase pH, stone formation

198
Q

UTI causes- bladder

A

Ureteric reflex, low urinary vol, bladder stones/tumour, E. coli fimbriae for bladder colonisation, obstruction from prostatic hypertrophy

199
Q

UTI causes- urethra

A

Bowel flora -> female shot urethra
Catheterisation allowing colonisation

200
Q

UTI symptoms- Cystitis

A

Frequency, dysuria, urgency, suprapubic pain, polyuria, haematuria

201
Q

UTI symptoms- Acute pyelonephritis

A

Classic triad- loin pain, fever, pyuria
Others- rigor, vomiting, costovertebral pain, associated cystitis symptoms, septic shock

202
Q

UTI symptoms- Prostatitis

A

Pain in periunem, scrotum, penis, bladder, lower back
Fever, malaise, nausea, urinary symptoms, swollen or tender prostate on DRE

203
Q

UTI clinical signs

A

Fever, abdominal or loin pain
Check for distended bladder, enlarged prostate

204
Q

Differential for vaginal discharge

A

Pelvic inflammatory disease

205
Q

Pelvic inflammatory disease

A

infection of the female reproductive system which includes the womb, fallopian tubes and ovaries.

206
Q

UTI first order investigations

A

Urine dipstick, Urine culture and sensitivity (MSU)

207
Q

UTI- urine dipstick test

A

Useful in unpregnant women <65
Positive for nitrite and leukocytes
Can be negative and still be a UTI

208
Q

UTI- Urine culture and sensitivity (MSU)

A

Use in pregnant women, men, children, not responding to empirical antibiotic

209
Q

UTI key diagnostic symptoms

A

dysuria, new nocturia, or cloudy-looking urine

210
Q

UTI- further investigations

A

Bloods- FBC, U+E, CRP and blood culture (if systemically unwell)
Imaging- USS and cystoscopy/ urodynamics/ CT

211
Q

UTI asymptomatic bacteriuria management

A

Do not use antibiotics for non pregnant women, men and adults with catheters
Treat pregnant women immediately with antibiotics

212
Q

Lower UTI management- Non pregnant women

A

3 day course of empirical antibiotics
Supportive care- fluids, paracetamol or ibuprofen for pain relief
Culture urine and pathogen-targeted antibiotic if empirical treatment fails

213
Q

Empirical antibiotics for lower UTI treatment

A

Trimethoprim
Nitrofurantoin if eGFR ≥45 mL/minute

214
Q

Upper UTI management- Non pregnant women

A

Urine culture
Treat initially with broad spectrum antibiotics
Consider hospitalisation if antibiotic resistant

215
Q

Empirical antibiotics for Upper UTI treatment

A

Amoxicillin/clavulanate (if culture results are available due to high resistance rates)
Cefuroxime
Ceftriaxone
Ciprofloxacin
Gentamicin or amikacin

216
Q

UTI- management in pregnant women

A

Culture rather than dipstick
Prescribe an immediate antibiotic, after sending urine for culture, for all pregnant women with symptoms of a UTI

217
Q

UTI- complicated management

A

Always send for culture
Longer antibiotic require- 7 days

218
Q

UTI- catheter management

A

All catharized patients are bacteriuric
Only send MSU for symptomatic- use narrow range antibiotic according to culture
Change long term catheter before antibiotic use

219
Q

UTI- catheter symptoms

A

May be non specific/ atypical for UTI
Fever, flank/suprapubic pain, change in voiding pattern, vomiting, confusion, sepsis

220
Q

UTI- investigation pyelonephritis

A

Abd exam- tenderloin, renal angle tenderness, rule out tubal/ ovarian/ appendix pathology
Bloods, USS (to rule out obstruction), MSU

221
Q

UTI- treatment pyelonephritis

A

Fluid replace, IV ABx (broad spectrum) for 7-14 days
Catheter
Analgesia

222
Q

Kidney stones epidemiology

A

More common in males
Commonest age 30-50 but decreasing
10-15% lifetime risk

223
Q

Kidney stones location

A

Anywhere from Collecting duct to External Urethral Meatus
Upper UT- Renal stones, Ureteric stones
Lower UT- Bladder stones, Prostatic stones, Urethral stones

224
Q

Kidney stones (Calculi)

A

Consist of crystal aggregates
Deposit anywhere from Collecting duct to External Urethral Meatus

225
Q

Kidney stones RFs

A

Anatomical factors
Urinary factors
Infection

226
Q

Kidney stones RFs- Anatomical factors

A

Congenital (horseshoe, duplex, PUJO, spina bifida)
Acquired (obstruction, trauma, reflux)

227
Q

Kidney stones RFs- Urinary factors

A

Metastable urine, promoters and inhibitors
Calcium, Oxalate, Urate, Cystine
Dehydration

228
Q

Mechanism of stone formation

A

“Nucleation theory” suggest that stones form from crystals in supersaturated urine

229
Q

Types of kidney stones

A

80% Ca2+ based – oxalate, phosphate
10% uric acid – usually lucent on KUB XR
5-10% struvite – infection stones
1% cystine – congenital

230
Q

Prevention of kidney stones

A

Overhydration, low Na diet, healthy Ca/ protein / diary intake
Reduce BMI, active lifestlye

231
Q

Prevention of kidney stones- uric acid stones

A

Only form in acid urine
Deacidification of urine to pH7-7.5 preventative

232
Q

Prevention of kidney stones- cystine stones

A

Excessive overhydration
Urine alkalinisation
Cysteine binders (eg Captopril, Penicillamine)
+/- genetic counselling

233
Q

Kidney stones presentation

A

Asymptomatic or pain (renal colic- lion to groin)
UTI- symptoms/ recurrent
Haematuria, proteinuria, sterile pyuria, anuria

234
Q

Renal colic pain

A

Unilateral loin pain
Rapid onset
Unable to get comfortable – writhing
Radiates to groin and ipsilateral testis/labia
Associated nausea / vomiting
Spasmodic / colicky, worse with fluid loading
Classically severe

235
Q

Investigations for kidney stones

A

ABC and give analgesia/antiemetic
Urinalysis, MSU if +ve
FBC, U+E, Calcium, Uric acid
Pregnancy test
Imaging- Non contrast CT- KUB scan for any nonpregnant adult patient with suspected renal colic

236
Q

Uretic colitis- Differential Diagnosis

A

Kidney stones
Vascular accident – ruptured AAA (>50yo) until proven otherwise
Bowel pathology – diverticulitis, appendicitis
Gynae – ectopic pregnancy, ovarian (cyst) torsion
Testicular torsion
Musculoskeletal

237
Q

How to interpret NCCT- KUB

A

1) Count the kidneys
2) Condition of kidneys:
- Perinephric tissues
- Cortical thickness
- Hydronephrosis +/- hydroureter
- Stones
3) Other pathology?

238
Q

Hydronephrosis

A

condition where one or both kidneys become stretched and swollen as a result of a build-up of urine inside them

239
Q

Management of Uretic colic

A

Analgesia- NSAID suppository/ Opiates
Antiemetic/s
+/- Admit
+/- IV fluids- May make pain worse as diuresis ensues
Observe for SEPSIS

240
Q

Pyonephrosis

A

Combination of infection and obstruction, can kill, sometimes very quickly
Can lose renal function in 24 hrs, systemic sepsis leading to septic shock

241
Q

Management of Uretic colic- Pyonephrosis

A

-IV Antibiotics. IVI. Oxygen. Escalate
-Drainage- nephrostomy, ureteric stent

242
Q

Kidney stone- treatment

A

Depend largely on site and size of stone, patient factors and complications / risks
Options include- conservative, medical, lithotripsy, surgical

243
Q

Kidney stone- treatment- renal stone: no evidence of obstruction, non-pregnant

A

1st line hydration + analgesia
Consider antibiotic therapy, watchful waiting
Consider ureteroscopy or ESWL if stone fails to pass after conservative treatment and PCNL for larger stones (>10mm)

244
Q

Kidney stone- treatment- ureteric stone: no evidence of obstruction, non-pregnant

A

1st line hydration + analgesia
Consider antibiotic therapy, medical expulsive therapy (alpha-blockers)
Consider ureteroscopy or ESWL if stone fails to pass after conservative treatment and PCNL for larger stones (>10mm)

245
Q

Kidney stone- treatment- alpha-blockers

A

Tamsulosin or alfuzosin
Cause ureteric relaxation of smooth muscle and antispasmodic activity of the ureter leading to stone passage

246
Q

Kidney stone- treatment- ureteroscopy

A

Tiny wire basket inserted into the lower ureter via the bladder, grabs the stone and pulls the stone free

247
Q

Kidney stone- treatment- ESWL (Extracorporeal shock wave lithotripsy)

A

series of shock waves generated by a machine called a lithotripter to break up stones
Can causes problems with fragment passage and clearance

248
Q

Kidney stone- treatment- PCNL (Percutaneous nephrolithotomy)

A

Key hole surgery to remove stones when large, multiple or complicated

249
Q

Kidney stone- treatment- indications for urgent intervention

A

Presence of infection and obstruction- Pyonephrosis (PCNL/ ureteric stent to remove stone)
Urosepsis, intractable pain or vomiting, impending AKI, bilateral obstructing stones

250
Q

Kidney stone- treatment- bladder stones

A

Conservative
Endoscopic- when obstructing
Open / Laparoscopic surgery- ideal for larger stones or if other open procedures required

251
Q

Gold standard for kidney stone diagnosis

A

NCCT KUB

252
Q

Hydronephrosis

A

Dilation of the renal pelvis or calyces

253
Q

Obstructive uropathy

A

functional or anatomic obstruction of urine flow at any level of the urinary tract

254
Q

Supravesical obstruction

A

Obstruction above the level of bladder

255
Q

Infravesical obstruction

A

Obstruction below the level of bladder

256
Q

Causes of UT obstructions

A

Luminal- stones, clots, sloughed papilla, tumours
Mural- congenital or acquired strictures, neuromuscular dysfunction, schistosomiasis- parasitic disease)
Extra-mural- abdominal or pelvic tumour/mass, retroperitoneal fibrosis

257
Q

Hemodynamic Changes with Unilateral Ureteral Occlusion

A

Triphasic pattern of renal blood flow and ureteral pressure changes
1-2 hrs after obstruction- RBF + ureteral pressure increase
3-4 hours later- ureteral pressure remain elevated, RBF decreases
5 hrs after obstruction- further decline in RBF and decrease in ureteral pressure

258
Q

Hemodynamic Changes with Bilateral Ureteral Occlusion

A

Only a modest increase in RBF lasting 90 minutes followed by a prolonged and profound decrease in RBF (>UUO)
Intrarenal distribution of blood flow changes from the inner to the outer cortex (opposite from UUO)

259
Q

Hemodynamic Changes with Bilateral Ureteral Occlusion after obstruction is released

A

Accumulation of vasoactive substances (ANP) cause to preglomerular vasodilation and post glomerular vasoconstriction
When obstruction is released, GFR and RBF remain depressed due to persistent vasoconstriction of the afferent arteriole
Results in post obstructive diuresis

260
Q

Effects of Obstruction on Tubular Function

A

Dysregulation of aquaporin water channels in the proximal tubule, thin descending loop, and collecting tubule- polyuria and impaired conc capacity
Na+, K+ and phosphate great excretions during post obstructive diuresis for BUO

261
Q

UT obstruction investigations

A

Blood tests – FBC, U&E, Coagulation profile, ABG
Urine – Dipstick / M,C&S
Imaging- Xray, Renal USG, CT Scan

262
Q

Upper UT obstruction treatment

A

Nephrostomy or ureteric stent (cause sig discomfort, alpha-blockers need to reduce pain)
Pyeloplasty to widen the PUJ for idiopathic PUJ obstruction
Treat underlying cause if possible

263
Q

Lower UT obstruction treatment

A

Ureteral/ suprapubic catheter to relive acute retention
Chronic obstruction only catharize if there is pain, UTI or renal impairment
Treat underlying cause if possible

264
Q

Nephrotic vs Nephritic syndromes

A

Nephrotic Syndrome is defined by severe proteinuria, pronounced oedema, and usually normal blood pressure
Nephritic Syndrome showcases haematuria, hypertension, and moderate glomerular damage

265
Q

Varicocele

A

Dilated veins of pampiniform plexus- feel like ‘bag of worms’
Left side more commonly effected
May cause dull pain

266
Q

Varicocele- associations

A

Subfertility but repair (surgery/ embolization) have little effect on subsequent pregnancy rates

267
Q

Testicular torsion

A

Spermatic cord rotates and becomes twisted. The twisting cuts off the testicle’s blood supply and causes sudden pain and swelling
Requires surgery

268
Q

Testicular torsion- symptoms

A

Sudden onset pain of one of the testis, which makes walking more uncomfortable
Pain in the abdomen, nausea and vomiting are common

269
Q

Testicular torsion- signs

A

Inflammation of one of the testis- vry tender, hot + swollen
Testis may lie high or transversely

270
Q

Testicular torsion- management

A

Doppler US may demonstrate lack of BF to testis if unsure
Do not delay on surgery, orchiectomy (full removal) versus orchidopexy (bilateral fixation) is based on the extent of damage to testicular tissue after exposing and untwisting testis

271
Q

Epididymal cyst

A

Usually develop in adulthood
Contain clear or milky fluid (spermatocele) fluid, usually lie/above behind the testis
Remove if symptomatic

272
Q

Hydroceles

A

Fluid in the tunic vaginalis (investing serosal covering of the testis)

273
Q

Hydroceles- primary

A

Associated with a patent processus vaginalis, typically resolves in 1st year of life
More common, larger and usually in younger men

274
Q

Hydroceles- secondary

A

Secondary to infection/ tumour/ trauma

275
Q

Hydroceles- management

A

Can resolve spontaneously
Aspiration (may be needed) or surgery: plicating the

276
Q

Acute epididymitis

A

Inflammation of the epididymis causing pain and swelling that develops over the course of a few days and lasts <6 weeks. It is usually unilateral

277
Q

Acute epididymitis- common causes in sexually active men

A

sexually transmitted organisms including Chlamydia trachomatis, Neisseria gonorrhoeae, and Mycoplasma genitalium

278
Q

Acute epididymitis- common causes in older men

A

causative organisms are often enteric pathogens, and epididymitis may be associated with bladder outlet obstruction, recent instrumentation of the urinary tract, or systemic illness

279
Q

Acute epididymitis- diagnostic tests

A

Gram stain of urethral secretions
Urine specimens for nucleic acid amplification tests for C trachomatis, N gonorrhoeae, and M genitalium
Urine microscopy and culture is also indicated if urinary pathogens are suspected

280
Q

Acute epididymitis- treatment

A

Supportive measures- bed rest, scrotal elevation, and analgesics
Empirical antibiotic therapy- antibiotics can be adjusted to target the causative organism

281
Q

Polycystic kidney disease (PKD)

A

Inherited renal cystic disease characterised by renal cysts and numerous systemic and extrarenal manifestations
2 types of PKD- dominant (more common) and recessive

282
Q

Polycystic kidney disease (PKD)- symptoms

A

Flank/abdominal pain, renal colic, and gross haematuria, and, less commonly, headaches
UTIs occur in 30-50% of pts with PKD

283
Q

Polycystic kidney disease (PKD)- key diagnostic factors

A

Renal cysts, hypertension, abdominal/flank pain, haematuria, palpable kidneys/abdominal mass, headaches, dysuria, suprapubic pain, fever

284
Q

Polycystic kidney disease (PKD)- risk factors

A

family history of autosomal-dominant PKD (ADPKD) or cerebrovascular event

285
Q

Polycystic kidney disease (PKD)- investigations

A

Renal ultrasound usually (CT+MRI can be used for smaller cysts)
Genetic testing for PKD1 or PKD2 although 10-15% of pts have no mutations

286
Q

Autosomal-dominant Polycystic kidney disease (PKD)- renal ultrasound diagnostic criteria

A

15 to 39 years of age - at least 3 (unilateral or bilateral) renal cysts;
40 to 59 years of age - at least 2 cysts in each kidney;
>60 years of age - at least 4 cysts in each kidney

287
Q

Autosomal-dominant Polycystic kidney disease (PKD)- treatment

A

Renoprotective lifestyle measures
Water intake 3-4L- to supress cyst growth
Hypertensive if HTN
Treat infections with antibiotics
Persistent/ severe pain- may need cyst decompression

288
Q
A

Phase 2a Lecture Notes (14 decks)

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