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formative 3b > Renal/GU > Flashcards

Renal/GU Flashcards

1
Q

describe the neural control of the lower urinary tract

A

Parasympathetic (cholinergic) S2-4 drives detrusor contraction Sympathetic (noradrenergic) T10-L2 contracts the sphincter and inhibits detrusor contraction

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2
Q

list 4 storage LUTS

A

frequency nocturia urgency urgency incontinence

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3
Q

list 7 voiding LUTS

A

hesitancy straining poor/intermittent stream incomplete emptying post micturition dribbling haematuria dysuria

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4
Q

what is the difference between BPH and BPE

A

benign prostatic hyperplasia is a histological finding whereas benign prostatic enlargement is found on DRE

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5
Q

what is BPH

A

increase in epithelial and stromal cell numbers in the periurethral area of the prostate. can be due to increase in cell number, decrease in apoptosis or combination of the two. it’s common - most men over 60 have some

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6
Q

what is BPO and what causes it

A

benign prostatic obstruction has a dynamic component which is the alpha 1 adrenoreceptor mediated contraction of the prostatic smooth muscle and a static component due to the volume effect of BPE

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7
Q

how are prostate symptoms assessed and what are the 8 points

A

the international prostate symptom score

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8
Q

what investigations for LUTS

A
  • flow rates and residual volume
  • frequency volume chart
  • renal biochemistry
  • imaging
  • PSA????
  • TRUSS (trans rectal ultrasound scan)
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9
Q

two reasons that flow rate might be reduced

A

due to obstruction in the lower urinary tract

due to detrusor underactivity

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10
Q

what is PVR

A

post void residual

100% of normal men have a PVR of <12ml

high PVR is a risk for hydronephrosis and elevated creatinine

consider detrusor underactivity as a cause of high PVR

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11
Q

name some complications of BPE

A

symptom progression

infections

stones

haematuria

acute retention

chronic retention

interactive obstructive uropathy

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12
Q

acute retention of urine presentation

A

extreme pain

600ml - 1L residual urine

normal U&E

pain is relieved by catheterisation

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13
Q

chronic retention of urine

A

more difficult to define

is basically incomplete bladder emptying

increased risk of infection and stones

can be low pressure: detrussor failure

can be high pressure if there’s obstruction

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14
Q

obstructive uropathy

A

nocturnal enuresis should alert to the risk of interactive obstructive uropathy

residual volume can be up to 4L

check U&Es and monitor daily if creatinine is raised

observe for a diuresis

check lying/standing blood pressures

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15
Q

treatment for prostate symptoms

A

watchful waiting for men with mild symptoms

the medical treatments are aimed at reducing the tone of prostatic smooth muscl or reducing the size of the prostate

alpha-adrenergic agonists (e.g. tamsulosin) improve flow

5-alpha-reductase inhibitors (e.g. finasteride) inhibit conversion of testoserone to the more active dihydrotestosterone (androgens are necessary for hyperplasia) this reduced prostate size

combination of the above are better than either singly

anti-cholinergics for overactivity

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16
Q

indications for prostate surgery

A

RUSHES

Retention

UTI

Stones

Haematuria that is refractory to 5-ARIs

Elevated creatinine due to BOO

Stmptom deterioration

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17
Q

what is BOO

A

Bladder Outflow obstruction

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18
Q

name a type of prostate surgery and some complications of it

A

TURP (trans urethral resection of prostate)

Immediate complications: sepsis, haemorrhage

Early: sepsis, haemorrhage and clot retention

Late: retrograde ejaculation, erectile dysfunction, urethral stricture, bladder neck stenosis and urinary incontinence

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19
Q

diagnosing AKI

A

you need one of the following:

rise in creatinine >26micromol/L in 48hrs

rise in creatinine >1.5x baseline within 7 days

urine output <0.5mL/kg/h for >6 consecutive hours

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20
Q

three types of causes of AKI

A

pre-renal (decreased perfusion to the kidney)

renal (intrinsic renal disease)

post renal (obstruction to urine)

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21
Q

four causes of pre-renal pathology with an example of each

A

decreased vascular volume (e.g. haemorrhage, burns or D&V)

decreased cardiac output (e.g. cardiogenic shock)

systemic vasodilation (e.g. sepsis)

renal vasoconstriction (e.g. NSAIDs, ACEi, ARB)

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22
Q

three examples of renal pathology and an example of each

A

glomerular problems (e.g. glomerulonephritis)

interstitial problems (e.g. infection, sarcoidosis)

vessel problems (e.g. vasculitis)

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23
Q

4 risk factors for AKI

A

pre-existing CKD

age

male sex

comorbidity (DM, CVD, malignancy etc)

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24
Q

5 most common causes of AKI

A
  1. sepsis
  2. major surgery
  3. cardiogenic shock
  4. other hypovolaemia
  5. drugs
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25
Q

management of hyperkalaemia

A

insulin + dextrose

calcium gluconate

IV fluid

salbutamol

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26
Q

investigation of AKI

A

Bloods: identify and treat hyperkalaemia

monitor fluid balance

do daily creatinine

urine dipstick to look for proteinuria and/or casts

imaging

assess current volume status

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27
Q

AKI management

A

Identify and treat cause

refer to renal for dialysis if necessary

treat sepsis

stop nephrotoxic medication

give IV fluid

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28
Q

what are the indications for dialysis

A

refractory pulmonary oedema

persistent hyperkalaemia

severe metabolic acidosis

uraemic encephalopathy or pericarditis

drug overdose

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29
Q

prognosis of AKI

A

dependent on cause it changes:

burns: 80% mortality

medical illness: 30% mortality

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30
Q

what is the nerve that controls the external sphincter of the bladder

A

pudendal nerve

S2-S4

uses acetylcholine neurotransmitter

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31
Q

which nerve tells us that the baldder is filling

A

the afferent pelvic nerve senses stretch in the detrussor muscle

it is a sensory nerve

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32
Q

describe the neural control of the bladder

A

the cortex mediates voluntary control

the pontine micturation centre and the periaqueductal grey coordinate voiding

the sacral micturation centre coordinates the micturation reflex

  • if there’s no coordination between this and the pontine M centre then you will void safely when the bladder is full but you will have no conscious control over when this happens
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33
Q

describe what is happening during the storage phase of bladder filling

A
  • normal adult bladder capacity is 400-500ml with first sensation at 100-200ml (mediated by pelvic nerve)
  • as the volime in the bladder increases the pressure remains low due to receptive relaxation
  • sympathetic stimulation (T11-L2) causes detrusor muscle relaxation
  • pudendal stimulation (S2-4) causes external urethral sphincter contraction
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34
Q

describe what happens during the voiding phase

A
  • voluntary control from the cortex and the PMC
  • PMC sends a signal to the sacral MC and mediates:
    • detrusor contraction via parasympathetic stimulation (S2-4)
    • external urethral sphincter relaxation via pudendal inhibition S2-4
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35
Q

What is OAB

A

overactive bladder is defined as urgency with frequency with or without nocturia when appearing in the absence of local pathology

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36
Q

what is the management of OAB

A
  • behavioural
    • reduce caffeine/alcohol intake
    • frequency volume chart
  • anti-muscarinic agents
    • decrease parasympathetic activity by blocking M2/3 receptors but give dise effects of dry mouth
  • botox
    • blocks nmj for ach release - se: incomplete bladder emptying and need to catheterise in 15%
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37
Q

stress incontinence in females

A

is usually secondary to birth trauma due to denervation of pelvic floor and urethral sphincter or weakening of fascial support of bladder or urethra

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38
Q

management on stress urinary incontinence

A

pelvic floor physiotherapy

surgery

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39
Q

stress incontinence in males: two causes and how to treat

A

iatrogenic following prostatectomy

neurogenic

treat with artificial sphincter or a male sling

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40
Q

what is the commonest cancer in men?

A

prostate cancer

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41
Q

what is the mean age at diagnosis for prostate cancer

A

72

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42
Q

what percentage of men die of prostate cancer

A

3%

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43
Q

what type of cancer is prostate cancer

A

adenocarcenoma

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44
Q

where does prostate cancer occur

A

it occurs in the peripheral zone of the prostate and spreads locally through the capsule

mets are to lymph nodes and bone and occasionally lung liver and brain

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45
Q

what is PSA

A

Prostate specific antigen is a serine protease thats responsible for the liquefaction of semen

it is commonly detected in small quantities in the blood

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46
Q

name some occasions when PSA is raised

A

in benign prostate enlargement, urinary tract infection and prostatitis as well as prostate cancer

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47
Q

how well does PSA work

A

70% of men with elevated PSA will not have prostate cancer

6% of men with prostate cancer will have a ‘normal’ PSA

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48
Q

prostate cancer diagnosis

A

LUTS
PSA

TRUSS

prostate biopsy is definitive diagnosis

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49
Q

how is prostate cancer graded

A

gleason grading based on histological appearance - a higher score has a worse prognosis

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50
Q

treatment of prostate cancer

A

based on how advanced the cancer is:

localised: watch and wait or curative surgery, radiotherapy

locally advanced: surgery, radiotherapy with neoadjuvant hormone therapy

metastatic: palliative care with hormone therapy

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51
Q

arguments against treatment for localised prostate cancer

A

it is a disease of the elderly

there may be competing causes of death

only 30% of men with prostate cancer die of prostate cancer

there are adverse effects of treatment

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52
Q

prognosis of advanced prostate cancer

A

median survival is 2.5 years but significant number of patients in long-term remission from androgen deprivation therapy

80% of tumours are androgen sensitive

castration leads to remission of advanced disease

there is far better palliation than in most metastatic solid tumourss

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53
Q

reasons for screening prostate cancer

A

commonest cancer in men

responsible for 10,000 deaths pa in UK

4th most common cause of cancer deaths

3% men will die of prostate cancer

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54
Q

reasons not to screen for prostate cancer

A

uncertain natural history

overtreatment

morbidity of treatment

anxiety associated with false positives

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55
Q

what is CKD

A

chronic kidney disease is abnormal kidney structure or function presnt for more than 3 months with implications for health

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56
Q

what is the lifetime risk of renal stones

A

10-15%

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57
Q

name 5 functions of the kidney

A

blood volume/fluid

generates erythropoietin for red cell production

waste/toxin/drug excretion

vitamin D metabolism

acid base regulation (excretes H+ iond and reabsorbs HCO3- ions)

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58
Q

what is creatinine

A

it is a waste product of muscle metabolism

it is purely excreted by the kidneys

there is a relationship between serum creatinine and GFR

this means that serum creatinine can be used to come up with eGFR

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59
Q

CKD risk factors

A

diabetes

dyslipidemia

left ventricular hypertrophy

age

smoking

male sex

hypertension

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60
Q

how is CKD classified

A

based on GFR category, the presence of albuminuria as a marker of kidney damage and the cause of the kidney disease

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61
Q

why might CKD cause anaemia

A

due to reduced production of erythropoietin

treat with EPO and IV iron supplements

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62
Q

how many people in the UK get haemodialysis and how often for how long

A

24,000 patients in the UK

vast majority do it 3 times a week for 4hrs a time

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63
Q

what is RRT

A

renal replacement therapy includes peritoneal dialysis, haemodialysis and kidney transplants

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64
Q

how many patients in the UK recieve peritoneal dialysis

A

6000

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65
Q

early complications of kidney transplantation

A

surgical complications

  • thrombosis
  • obstruction

infection

  • urinary tract
  • chest

rejection

  • can be easily treated
  • does affect long term survival of graft
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66
Q

what are the three most common causes of CKD in the UK

A

diabetes

glomerulonephritis

hypertension/renovascular disease

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67
Q

CKD is associated with

A

all cause mortality

superimposed AKI

progressing renal symptoms

cardiovascular disease

CKD patients are more likely to die of CVD than to need RRT

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68
Q

monitoring of renal function in CKD

A

GFR and albuminuria should be monitored at least annually, every 6 months if high risk and every 3 months if very high risk (based on heat map)

small fluctuations common but decrease in GFR of >25% is significant

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69
Q

what are the risk factors for decline of GFR

A

hypertension

diabetes mellitus

volume depletion

infection

NSAIDs

smoking

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70
Q

investigation of CKD

A

Blood

  • U&E - compare with previous
  • Hb - there may be normocytic anaemia
  • glucose - to check for DM
  • if there is renal bone disease there will be low Ca2+ and high PO43- with high PTH

Dipstick

  • check for proteinurea and casts

Ultrasound

  • check size and corticomedullary differentiation
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71
Q

what does glomerulonephritis mean

A

it is a term that encompasses a number of conditions that

  • are caused by pathology in the glomerulus
  • present with proteinuria, haematuria or both
  • are diagnosed on renal biopsy
  • cause CKD
  • can progress to kidney failure
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72
Q

what is the difference between nephrotic and nephritic syndromes

A

glomerulonephritis presents on a spectrum ranging from nephrosis (proteinuria due to podicyte pathology) to nephritis (haematuria due to inflammatory damage

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73
Q

5 types of nephritic glomerulonephritis

A

IgA nephropathy

Henoch-Schonlen purpura

post-streptococcal GN

anti-glomerular basement membrane (Anti-GBM) disease

rapidly progressive GN

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74
Q

what is the commonest primary GN

A

IgA nephropathy

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75
Q

IgA nephropathy

A
  • asymptomatic or presents with episodic haematuria 12-72hrs after non-specific URTI
  • high BP
  • proteinuria
  • 20-50% progress to renal failure over 30yrs
  • diagnosis is by renal biopsy showing IgA deposition
  • Treatment is with ACE-i/ARBs
  • corticosteroids if persistent disease
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76
Q

if there is oedema you should always

A

dipstick the urine to avoid missing renal disease

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77
Q

definition of nephrotic syndrome

A

triad of:

  • proteinuria
  • hypoalbuminaemia
  • oedema
78
Q

aetiology of nephrotic syndrome

A

primary renal disease or secondary to a disorder

  • primary renal disease
    • minimal change disease
    • membranous nephropathy
    • focal segmental glomerulosclerosis
  • secondary causes
    • DM
    • Lupus nephritis
    • myeloma
    • amyloid
    • pre-eclampsia
79
Q

pathophysiology of nephrotic syndrome

A

filtration barrier of kidneys, made of podicytes, the GBM and endothelieal cells is damaged and proteinuria results from podicyte pathology

  • minimal change disease - abnormally functioning podicytes
  • membranous nephropathy - immune mediated damage
  • FSGS - podicyte injury/death
80
Q

presentation of nephrotic syndrome

A

generalised pitting oedema - can be rapid and severe

81
Q

4 prinicples of management of nephrotic syndrome

A

reduce oedema

treat underlyign cause

reduce proteinuria

treat complications

82
Q

reducing oedema in nephrotic syndrome

A

fluid and salt restriction

diuresis with loop diuretics like furosemide

add thiazide diuretics if oedema persists

83
Q

Treating the underlying cause of nephrotic syndrome

A

biopsy is needed in adults to understand and treat cause

in children minimal change disease is the most common cause so treat with corticosteroids which induce remission in most. biopsy only needed if there’s no response to steroids

84
Q

reducing proteinuria in nephrotic syndrome

A

ACEi/ARBs reduce proteinuria but may not be needed in minimal change disease

85
Q

treating complications of nephrotic syndrome

A

thromboembolism - treat with heparin

infection - urine loss of Ig and immune mediators means they’ve increased risk of urinary, respiratory and CNS conditions. ensure pneumococcal vaccination is given

hyperlipidaemia - increased cholesterol, LDLs and triglycerides due to hepatic synthesis in response to decreased oncotic pressure

86
Q

3 types of glomerulonephritis

A

minimal change disease

focal segmental glomerulosclerosis (FSGS)

membranous nephropathy

87
Q

minimal change disease

A

~25% of adult nephrotic syndrome

most is idiopathic or due to drugs like NSAIDs

does not cause renal failure

diagnosis: light microscopy is normal but electron microscopy shows podicyte displacement

treatment is with prednisolone which normally causes remission - relapses managed longer term, stronger immunosupression (e.g. with cyclophosphamide)

88
Q

focal segmental glomerulosclerosis

A

this is the commonest glomerulonephritis seen on renal biopsy

primary is idiopathic but can be secondary to HIV, heroin, lithium, lymphoma

all are at risk of progressive CKD and kidney failure

disease recurs in 30-50% of kidney transplants

diagnosis: histology shows glomeruli scarring in spots (hence focal)

treatment is ACEi/ARBs and BP control. Corticosteroids in primary disease only

89
Q

membranous nephropathy

A

~25% of adult nephrotic syndromes

primarily idiopathic but can be secondary to: malignancy, infection (schistosomiasis, malaria, hep B/C), drugs and immunological disease (SLE, RA)

spontaneous remission in 25%

auto-antibodies present in most. there is a thickened GBM due to subepithelial immune deposits

treatment: ACEi/ARB and blood pressure control

90
Q

describe the nerve supply to the penis

A

parasympathetic

  • erectlie S2-4
  • mediates arteriolar dilatation

Sympathetic

  • ejaculation T11-12
  • in the flaccid state the sympathetic tome constricts arterioles

Cavernous nerve carries both of these fibres and passes posterolateral to the prostate so there is risk of damage in prostatectomy

91
Q

causes of low testosterone

A

Testosterone is required for normal erectile function

Primary

  • pituitary or the hypothalamus

Secondary

  • testes
    • tumour, injury etc

Congenital syndromes

  • kleinfelters
92
Q

role of nitric oxide in erection

A

released by cavernous nerves and endothelium

it causes smooth muscle relaxation and dilatation of the arterioles

93
Q

role of phosphodiesterase in erection

A

returns the penis to a flaccid state by degrading the cGMP produced by the nitric oxide in the smooth muscle cell

phosphodiesterase inhibitors stop the degradation of cGMP

sildenafil (viagra) is a phosphodiesterase inhibitor

94
Q

what is the definition of erectile dysfunction

A

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

95
Q

causes of ED

A

Organic

  • vasculogenic
  • neurogenic
  • hormonal
  • anatomical
  • drug induced

Psychogenic

96
Q

give 4 indicators that ED might be psychogenic

A

sudden onset

good nocturnal and early morning erections

situational ED

younger patients

97
Q

risk factors for ED

A

Lots are in common with CVS disease

  • lack of exercise
  • obesity
  • smoking
  • hypercholesterolaemia
  • metabolic syndrome
    • diabetes gives 3x risk of ED

others

  • renal fialure
  • trauma i.e. pelvic fracture
  • iatrogenic - prostatectomy
  • liver disease and alcohol overuse
98
Q

Physical examination of a patients with ED

A

BP and heart rate

prostatic enlargement (PR)

hypogonadism (small testes and secondary sexual characteristics)

check penile sensation to rule out CNS problem

in majority of patients the examination will be normal

99
Q

lab testing of an ED patient

A

morning testosterone - if low then look at prolactin, FSH and LH

in majority of patients blood tests will be normal

100
Q

treatment for ED

A

identify and treat the reversible causes of ED

advise on lifestyle and risk factor modification

patient partner involvement and counselling

oral phosphodiesterase inhibitors

101
Q

how do oral phosphodiesterase inhibitors work and name one

A

they increase intracellular CGMP (which N20 creates) in smooth muscle cells of the arterioles

sildenafil (viagra)

102
Q

what is the efficacy of sildenafil and what are some common adverse events

A

2/3 improved errections and 2/3 sumularly successful intercourse

common adverse events:

  • headache
  • flushing
  • dyspepsia
103
Q

what is a prolonged erection and what should you do

A

if it lasts more than 4 hours there’s risk of permanent ischaemic damage to the corpora

aspirate the corpora

if that fails then inject phenylephrenine

104
Q

three classifications of UTI

A

asymptomaric bacteruria

uncomplicated

complicated

105
Q

what is pyuria

A

it is the presence of leukocytes in the urine

it is associated with infection

but there can be sterile pyuria

106
Q

what is an uncomplicated UTI

A

this is when it occurs in non-pregnant women

107
Q

when is a UTI ‘complicated’

A

when there is some structural or functional abnormality of the urinary tract so when it is in:

pregnant

men

catheterised patients

children

the immunocompromised

when it’s recurrent

etc

108
Q
A
109
Q

what percentage of women experience a UTI in their lifetime

A

10-20%

there’s much higher incidences of UTI in hospitalised patients

110
Q

name a UTI causing pathogen associated with:

renal stones

hospital catheterisation

deep seated infection

A

renal stones: Proteus

  • they produce urea which boosts the pH and contributes to stone formation

hospital catheterisation: Klebsiella

deep seated infection: S.aureus

111
Q

what is by far the most likely pathogen to cause a UTI

A

E.coli causes >50% of UTIs

112
Q

what are the two types of lower urinary tract infection

A

cystitis (bladder) and prostatitis (prostate)

113
Q

what is an upper urinary tract infection

A

pylonephritis = an infection of the kidney and the renal pelvis

114
Q

what is the incidence of pylonephritis

A

3 per 1000 patients per year

115
Q

4 risk factors of a UTI

A

increased bacterial inoculation: e.g. sexual activity, urinary or faecal incontinence

increased binding of bacteria e.g. spermicide use, lowered oestrogen

decreased urine flow: e.g. dehydration

increased bacterial growth: e.g. immunosuppression, stones etc

116
Q

6 cystitis symptoms

A

frequency

dysuria

urgency

suprapubic pain

polyuria

haematuria

117
Q

7 symptoms of pylonephritis

A

fever

rigor

vomiting

loin-groin tenderness

associated systitis symptoms

septic shock

118
Q

prostatitis

A

pain in the perineum, rectum, scrotum, penis, bladder, lower back

fever

malaise

nausea

urinary symptoms

swollen or tender prostate on PR

119
Q

UTI investigation

A
  • in a non-pregnant woman with >3 symptoms or one severe symptom of cystitis then treat empiracally without further tests
  • otherwise:
    • dipstick
    • msu culture if >105 CFU/ml then indicative of infection
    • blood tests (U&E, FBC and CRP) if systemically unwell
120
Q

UTI treatment in non-pregnant women

A

if three or more symptoms (or one severe) of cystitis then treat with a three day course of nitrofurantoin or trimethoprim

if this first line treatment fails then culture MSU and treat according to abx sensitivity

in pylonephritis treat initially with broad spectrum like co-amoxiclav until you can treat according to antibiotic sensitivity

121
Q

treatment for prostatitis

A

ciprofloxacin cause it can penetrate the prostatic fluid

122
Q

what are casts and what does it indicate if they are found in the urine?

A

they are microscopic cylindrical structures formed in the distal convoluted tubule and collecting ducts of nephrons, then dislodge and pass into the urine in disease states

they are indicative of damage to the kidney epithelium i.e. glomerulonephritis

123
Q

catheter associated UTI pathogenesis

A

at risk of infection up to 24hrs post removal

forms biofilms

change and remove catheter when starting treatment

send a fresh sample, not from the bag

don’t dipstick bag as all catheters get colonised

124
Q

treatment of asymptomatic bacteriuria in >65

A

do not treat as very common and rarely causes problems

125
Q

UTI in pregnancy

A

this is a complicated UTI

asymptomatic bacteruria is common but should be treated as often turns into symptomatic pyelonephritis if untreated

culture rather than dipstick

sh

126
Q

what is pyelonephritis

A

it is the infection of the renal parenchyma and soft tissues of the rena pelvis/upper ureter

associated with sepsis and systemic upset and rigors

patients are often fluid depleted and require prompt fluid resuscitation

it predominantly affects women over 35

127
Q

classical triad of pyelonephritis symptoms

A

loin pain

fever

pyuria

128
Q

investigation of pyelonephritis

A

abdo exam

  • tender loins
  • renal angle tenderness
  • do a PV to rule out tubal/ovarian/appendix pathology

Bloods including cultures

US scan to rule out obstruction of upper tract

MSU

129
Q

Treatment for pyelonephritis

A

fluid replacement - increased losses

IB Abx - broad spectrum like co-amoxiclav or gentamicin

drain the obstructed kidney

catheter

analgesia

130
Q

are men or women more affected by urolithiasis

A

M:F is 2:1

131
Q

what is the commonest age to have urolithiasis

A

30-50

132
Q

what is the lifetime risk of recurrence of urolithiasis

A

>50%

133
Q

where can you get stones - split into upper and lower urinary tract

A

you can get them anywhere from the collecting duct to the external urethral meatus

  • upper urinary tract
    • renal stones
    • uretic stones
  • lower urinary tract
    • bladder stones
    • prostatic and urethral stones are much rarer
134
Q

why might patients get renal stones

A
  • anatomical factors
    • congenital (e.g. horseshoe kidney. spina bifida)
    • acquired (obstruction, trauma, reflux)
  • Urinary factors
    • calcium, oxalate, urate imbalance
    • dehydration
  • infection
135
Q

what is the nucleation theory of stone formation

A

stones form from crystals (Ca2+, oxalate etc) in supersaturated urine

136
Q
A
137
Q

what are the constituents of renal stones

A

most are made of normal urinary constituents

  • 80% are calciumbased with oxalate and phosphate
  • 10% are uric acid
  • 10% are struvite and these are infection stones

rarely they are formed of drugs

138
Q

how to prevent stones

A

overhydration

low salt diet

normal dairy intake

healthy protein intake

reduce BMI

active lifestyle

139
Q

what are the symptoms of renal stones

A

asymptomatic

loin pain

renal colic

UTI symptoms like urgency frequency and dysuria

recurrent UTIs

haematuria (visible and non-visible)

140
Q

what is renal colic

A

pain that results from upper urinary tract obstruction.

  • using socrates it presents like this:
    • 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 it’s very severe “worse than childbirth” “12/10”
141
Q

how to investigate renal colic

A
  • ABC and give analgesia/antiemetic
  • BE WARY OF SEPSIS - urolithiasis can cause pyonephrosis
  • focussed history and examination
  • urinalysis and MSU if +ve
  • Bloods
    • FBC
    • U&E
    • Calcium
    • Uric acid
  • Imaging
    • NCCT KUB
    • KUBXR
    • USS
142
Q

differential diagnoses for renal colic

A

vascular accident - it’s a ruptured AAA in >50 until proven otherwise

bowel pathology (diverticulitis/appendicitis)

Gynae (ectopic pregnancy, ovarian (cyst) torsion)

testicular torsion

MSK

143
Q

what is the gold standard diagnostic investigation for urolithiasis

A

NCCT-KUB

no contrast in case of allergies or impaired renal function

it’s 99% sensitive for stones and very specific

however: it doesn’t give any functional info and there’s a bit of radiation

144
Q

why would you do a USS for ureteric colic?

A

it’s more sensitive for hydronephrosis than CT as not all acute obstructions dilate

but it is very poor at detecting stones in the ureter

useful in the pregnant an the young as there is no radiation risk

145
Q

what is metabolic syndrome?

A

a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes. These conditions include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels

146
Q

what is the management of ureteric colic

A
  • analgesia
    • NSAID suppository
    • opiates
  • antiemetics
  • admit them
  • give IV fluid
    • be aware that this may make the pain worse
  • Observe them closely for sepsis
147
Q

what is pyonephrosis

A

it is where there is an infection of the kidney’s collecting system and the renal pelvis fills with pus causing obstruction

this can lead to sepsis and they can lose renal function in 24hrs

they need IV abx, IV oxygen and they need drainage with a nephrostomy or a uretic stent

this is serious and can kill a patient rapidly

148
Q

what are the 4 types of treatment for renal stones and what do they depend on

A

conservative

medical

surgical

lithotripsy

the treatment chosen depends on the site and site of the stone as well as patient factors and risks of complications

149
Q

which stones are dangerous and why/

A

big stones - they can occlude calyces and/or the PUJ

they can acutely obstruct and cause chronic renal damage including abscesses, fistulae and xanthogranulomatous pyelonephritis (XPN)

small stones <1cm can be observed and only 1/3 will progress

150
Q

treatment of renal stones

A
  • conservative treatment if they’re small, in a safe location and asymptomatic or if the patient’s very comorbid
  • drainage if there is sepsis
  • lithotomy by size
    • <2cm ureteroscopy
    • 1-2cm ESWL
    • for larger stones: PCNL
151
Q

ureteric stones treatment

A
  • conservative for 2 weeks
    • the majority <4mm will pass and only 10% >7mm will pass
  • drainage if there’s sepsis
  • ESWL for stones <1cm
  • laser ureteroscopy is suitable for any stone
152
Q

what does urolithiasis mean and what is the lifetime risk

A

the formation of stony concretions in the bladder or urinary tract

10-15%

153
Q

bladder stone treatment

A

conservative if they’re asymptomatic or unfit

endoscopic (can be accompanied by treatment of BOO)

Open/laperoscopic surgery (ideal for larger stones)

154
Q

what is the ECG appearance of hyperkalaemia

A

Tall tented T-waves

Flattening of P-waves

Broad QRS complexes

155
Q

what two types of PKD are there? and which is more common

A
  • autosomal recessive polycycstic kidney disease (ARPKD)
  • autosomal dominant polycystic kidney disease (ADPKD)
    • by far the more common
156
Q

what is the prevalence of ADPKD

A

1 in 400-1000 (7 million patients worldwide)

157
Q

what is ADPKD mostly caused by and how does this affect disease course

A

85% is caused by a mutation in PKD1 on chromosome 16 and these patients reach ESRF by their 50s

can also be caused by mutation in PKD2 on chromosome 4 and this has a slower disease course

10% of these mutations are de-novo

158
Q

presentation of ADPKD

try and think of 5 things

A

may be asymptomatic until increased size/haemorrhage of cysts

loin pain

visible haematuria

cyst infection

renal calculi

high blood pressure

progressive renal failure

159
Q

extrarenal features of ADPKD

A

propensity to sub arachnoid hemorrhage

  • so MRI screening for intracranial aneurysms is recommended if there is a family history of SAH/aneurysms

diverticular disease

ovarian cysts

160
Q

diagnosis of PKD generally

A

generally by USS

since renal cysts are common and prevalence increases with age the diagostic criteria reflect this

  • <39 years >3cysts
  • 40-59 >2 cysts in each kidney

liver and pancreatic cysts are supportive of diagnosis

genetic testing is available but there are ~1500 possible mutations so is limited to diagnostic uncertainty, potentia donors

161
Q

treatment for ADPKD

A
  • water intake of 3-4L per day can limit cyst growth if their GFR is good enough
  • blood pressure control
    • 1st line: ACEi/ARB
    • 2nd line: thiazide like diuretics
      • (e.g.chlorothiazide/hydrochlorothiazide)
    • 3rd line: Beta blockers
    • CCBs are contraindicated
  • 2/3 will need RRT which can include transplantation
162
Q

what is the prevalence of ARPKD

A

1 in 20,000

163
Q

what chromosom is the mutation for ARPKD

A

chromosome 6

164
Q

presentation of ARPKD

A

presents ante-perinatally with renal cysts (salt and pepper appearance on USS)

there’s congenital hepatic fibrosis as well which causes portal hypertension

there’s very poor prognosis if neonatal respiratory distress

no specific therapy

165
Q

two very important things to think about testicle examination

A

a testicular lump is cancer until proven otherwise

acute tender enlargement of testis is torsion until proven otherwise

166
Q

what is an epididymal cyst?

A

it usually develops in adulthood and comntains milky spermatocele fluid. they often lie above and behind the testis

only remove if symptomatic

167
Q

what is a hydrocele

A
  • this is fluid in the tunica vaginalis
  • can be primary or secondary
    • primary (more common)
      • resolve during 1st year of life typically
    • secondary
      • due to trauma, tumour or infection
  • may need aspiration but many resolve on their own
168
Q

varicocele

A

dilated veins

left side more commonly affected (lack of valves between testicular vein and the renal vein on left side whereas on right side testicular vein goes straight into the IVC)

scrotal blood vessels feel like a bag of worms

may be associated with a dull ache

169
Q

90% of renal cancers are what type

A

renal cell carcinoma

170
Q

what is the mean age at which people get RCC and are men or women affected more

A

mean age 55

M:F is 2:1

171
Q

what are the clinical features of RCC

A

haematuria

loin pain

abdominal mass

anorexia

malaise

weight loss

PUO

rarely presents with varicocele when if invasion compresses left testicular vein

50% are found incidentally

172
Q

what percentage of RCCs have mets at presentation?

A

25% have mets at presentation

173
Q

investigation of suspected RCC

A
  • increased BP from renin secretion
  • RBC (there may be polycythaemia from increased EPO secretion)
  • imaging
    • CT and MRI are best and you may see ‘cannonball’ mets
174
Q

treatment for RCC

A
  • it is generally chemo and radio resistant
  • radical nephrectomy can be curative
  • for unresectable/metastatic disease then options include:
    • high dose IL-2 to activate T-cells
    • anti-angiogenesis agents e.g. pazopanib
175
Q

the mayo prognostic risk score of RCCand what it means for prognosis

A
  • SSIGN uses info on
    • Stage
    • Size
    • Grade
    • Necrosis
  • 10yr survival:
    • 96% in scores 0-1
    • 19% in scores >10
176
Q

Where do you get transitional cell carcinoma

A

TCC can occur in the bladder (50%) ureter or renal pelvis

177
Q

who gets TCC

age sex and risk factords

A

age >40

M:F is 4:1

smokers

those with chronic cystitis

those with schistosomiasis

178
Q

presentation of TCC

A

painless haematuria

frequency

urgency

dysuria

urinary tract obstruction

179
Q

diagnosis of TCC

A

CT/MRI KUB

urine cytology (tumours can call sterile pyuria)

cystoscopy and biopsy

180
Q

what percentage of bladder cancers are TCCs

A

90%

181
Q

what is the UK incidence of bladder cancer

A

1:6000

182
Q

what is M:F for bladder cancer

A

5:2

183
Q

risk factors for bladder cancer

A

smoking

aromatic amines (so working in the rubber industry)

chronic cystitis

schistosomiasis infection

pelvic irradiation

184
Q

treatment of TCC Tis, Ta and T1

and what is the 5 yr survival

A
  • Tis, Ta and T1 are grades where the cancer has not yet invaded the muscle and has remained in or within the lamina propria
    • this is 80% of TCCs
    • trans urethral resection of bladder tumour (TURBT)
    • consider regimen of intravesical BCG which produces a non-specific immune response
  • 95% 5yr survival
185
Q

Treating TCC T2-4

A
  • palliative care for T4
  • T2-T3
    • radical cystectomy is the gold standard
    • post op chemotherapy like methotrexate or doxorubicin
    • they will need a urostoma
186
Q

what is phimosis

A

when the foreskin occludes the meatus

187
Q

what is paraphimosis

A

occurs when a tight foreskin is retracted and becomes irreplaceable preventing venous return and leading to oedema and even ischaemia of the glans

188
Q

which bacteria commonly cause prostatitis

A

chlamydia, e.coli and s.faecalis

189
Q

what is the commonest male malignancy

A

prostate cancer

190
Q

what are the associations of prostate cancer

A

age (80% of men >80%)

+ve family history

high testosterone

191
Q

treatment of prostate cancer

A

depends on prognosis

radical prostatectomy if <70yrs has excellent survival

radical radiotherapy ± hormone therapy can also be curative

hormone therapy alone can delay tumour progression but eventually leads to refractory disease

active surveillance if old and low risk

formative 3b (18 decks)

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