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Bateman - Phase 2a COPY > Renal and Urogenital System > Flashcards

Renal and Urogenital System Flashcards

1
Q

What is the 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

What kind of organs are the kidneys?

A

Retroperitoneal.

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3
Q

Where are the kidneys located?

A

T11-L3.

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4
Q

Where is the blood supply to the kidneys from?

A

Blood supply from renal artery direct from aorta at L1 level

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5
Q

How many nephrons does each kidney contain and how much urine is produced each day?

A

Each kidney contains around 1 million nephrons and produces 1-1.5L of urine per day.

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6
Q

Where do they ureters run?

A

Run over psoas muscle, cross the iliac vessels at the pelvic brim and insert into trigone of bladder.

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7
Q

How is reflux of urine prevented?

A

valvular mechanism at the vesicoureteric junction.

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8
Q

What does the Bladder, Sphincter and Urethra look like?

A
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9
Q

What is the nervous control of the bladder and spincters?

A
  1. Parasympathetic Nerve (pelvic nerve)
    - S2-S4
    - acetylcholine neurotransmitter
    - involuntary control
  2. Sympathetic Nerves (hypogastric plexus)
    - T11 – L2
    - noradrenaline neurotransmitter
    - involuntary control
  3. Somatic Nerve (pudendal nerve)
    - S2-S4
    - “Onuf’s nucleus”
    - acetylcholine neurotransmitter
  4. Afferent pelvic nerve
    - Sensory nerve
    - signals from detrusor muscle
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10
Q

What is each of these doing in neural control?

Cortex

Pontine Micturition Centre

Sacral

Mictruition Centre

Onuf’s Nucleus

A
  • Cortex: voluntary control
  • Pontine Micturition Centre/Periaqueductal Grey: Co-ordination of voiding
  • Sacral Micturition Centre: Micturition reflex
  • Onuf’s Nucleus: Guarding reflex
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11
Q

What are the different phases of micturition?

A

Storage.

Guarding Reflex.

Micturition Reflex.

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12
Q

What happens in the storage phase of mictruition?

A
  • Bladder fills continuously as urine is produced by kidney and is passed through the ureters into the bladder
  • Normal adult bladder capacity 400-500ml with first sensation at 100-200ml
  • As the volume in the bladder increases the pressure remains low due to “receptive relaxation” and detrusor muscle compliance
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13
Q

What happens during the filling phase of mictruition?

A
  • At lower volumes the afferent pelvic nerve sends slow firing signals to the pons via the spinal cord.
  • Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation.
  • Somatic (Pudendal) nerve stimulation maintains urethral contraction.
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14
Q

What happens during the voiding phase?

A
  • Micturition reflex is an autonomic spinal reflex
  • Higher volumes stimulate the afferent pelvic nerve to send fast signals to the sacral micturition centre in the sacral spinal cord
  • Pelvic parasympathetic nerve is stimulated and the detrusor muscle contracts
  • Pudendal nerve is inhibited and the external sphincter relaxes
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15
Q

What happens during bladder emptying and what is needed?

A
  • Coordinated detrusor contraction with external sphincter relaxation to expel urine from bladder
  • A positive feedback loop is generated until all urine is expelled
  • Detrusor relaxation and external sphincter contraction after complete emptying of bladder
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16
Q

What happens during the guarding reflex?

A
  • Voluntary control of micturition can occur in anatomically and functionally normal adults
  • Afferent signals from the pelvic nerve are received by the PMC/PAG and transmitted to higher cortical centres
  • If voiding is inappropriate the guarding reflex occurs
  • Sympathetic (hypogastric) nerve stimulation results in detrusor relaxation
  • Pudendal nerve stimulation results in contraction of the external urethral sphincter
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17
Q

What does the urinary tract have to do?

A

Convert a continuous process of excretion (urine production) to an intermittent process of elimination.

Store urine insensibly.

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18
Q

What are some lower urinary tract symptoms?

A

Storage symptoms

Frequency

Nocturia

Urgency

Urgency incontinence.

Voiding symptoms

Hesitancy

Straining

Poor/intermittent stream

Incomplete emptying

Post mictruition dribbling

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19
Q

What are these definitions?

BPH?

BPE?

BOO?

LUTS?

A

Nenignm prostatic hyperplasia.

Benign prostatic enlargement

bladder outflow obstruction

Lower urinary tract symptoms

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20
Q

What is BPH?

A

Increase in epithelial and stromal cell numbers in the periurethral area of the prostate.

May be due to increase in cell number

Or due to decrease apoptosis

Or due to combination of the two.

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21
Q

What are the features of BPH?

A

Lower urinary tract symptoms (LUTS) = nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria, bladder stones, UTI.

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22
Q

What tests would you do for BPH?

A

MSU; U&E; ultrasound (large residual volume, hydronephrosis—fig 1). ‘Rule out’ cancer: PSA,1 transrectal USS ± biopsy. Then consider:

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23
Q

What are the management options for BPH?

A

Lifestyle: Avoid ca eine, alcohol (to urgency/nocturia). Relax when voiding. Void

twice in a row to aid emptying. Control urgency by practising distraction methods

(eg breathing exercises). Train the bladder by ‘holding on’ to time between voiding.

Drugs are useful in mild disease, and while awaiting surgery. • -blockers are 1st line (eg tamsulosin 400μg/d PO; also alfuzosin, doxazosin, terazosin). smooth muscle tone (prostate and bladder). SE: drowsiness; depression; dizziness; BP; dry mouth; ejaculatory failure; extra-pyramidal signs; nasal congestion; weight. •5-reductase inhibitors: can be added, or used alone, eg finasteride 5mg/d PO (testosterone’s conversion to dihydrotestosterone).2 Excreted in semen, so warn to use condoms; females should avoid handling. SE: impotence; libido. E ects on

prostate size are limited and slow. • There is no evidence for phytotherapy.237 • Surgery:

  • Transurethral resection of prostate (TURP) ≤14% become impotent (see BOX). Crossmatch 2U. Beware bleeding, clot retention and TUR syndrome: absorption of washout causing hyponatraemia and fits. ~20% need redoing within 10yrs.
  • Transurethral incision of the prostate (TUIP) involves less destruction than TURP,238 and less risk to sexual function, but gives similar benefit.239 It achieves this by relieving pressure on the urethra. It is perhaps the best surgical option for those with small glands <30g—ie ~50% of those operated on in some areas.

Retropubic prostatectomy is an open operation (if prostate very large).

Transurethral laser-induced prostatectomy (TULIP) may be as good as TURP.

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24
Q

Where can you get stones?

A

Anywehere from collecting duct to external urethral meatus (EUM).

Upper Urinary tract

Renal Stones

Ureteeric Stones

Lower urinary tract

Bladder stones

prostatic stones

urethral stones

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25
Q

Why do patients get stones?

A

Anatomical factors

  • Congenital (horseshoe, duplex)
  • Acquired (obstruction, surgery)

Urinary factors

  • metastable urinem promotors and inhibitors
  • calcium, oxalate, urate, cystine
  • dehydration

Infection

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26
Q

How are stones formed?

A

Nucleation theory suggest that stones form from crystals in supoersaturated urine.

Solubility point and formation point play factors

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27
Q

What are stones made of?

A

80% calcium - oxalate, phosphate.

10% uric acid.

5-10% struvite - infection stones.

1% cystine - congenital.

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28
Q

How can stones be prevented?

A

Overhydration.

Low salt

Normal dietary intake

Healthy protein intake

Reduce BMI

Active lifestyle

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29
Q

How can you prevent uric acid stones?

A

Only form in acid urine

Deacidification of urine to ph7-7.5 preventative

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30
Q

How do you prevent cystine stones?

A

Excessive overhydration

Urine alkalinisation

Cysteine binders

+/- genetic counselling

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31
Q

What symtpoms can a kidney stone cause?

A

Asymptomatic

Loin pain

Renal colic

UTI symtpoms

-dysuria, stangury, urgency, frequency

Recurrent UTIs

Haematuria

-visible and non-visible (85%)

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32
Q

What is renal colic?

A

Pain resulting from upper urinary tract obstruction.

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33
Q

What are the symtpoms of renal colic?

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 12/10, worse than labour

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34
Q

How do you investigate a ureteric colic?

A

ABC and give analgesia/antiemetic

Focused history and examination

Urinalysis, MSU if positive

FBC, UandE, Calcium, Uric acid

Imaging NCCT-KUB (Non-contrast computerised tomography)

KUBXR

(USS)

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35
Q

What are the differential diagnosis of renal colic?

A

Vascular accident - ruptured AAA, until proven otherwise

Bowel pathology - diverticulitis, appendicitis

Gynae - ectopic pregnancy, ovarian (cyst) torsion

Testicular torsion

Musculoskeletal

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36
Q

How do you manage ureteric colic?

A

Analgesia

  • NSAID suppository
  • Opiates

Antimetic/s

Admit

IV fluids

OBserve for SEPSIS

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37
Q

Why does infection matter?

A

Pyonephrosis

Can lose renal function in 24hrs

Systemic sepsis leading to septic shock

IV antibiotics.

Drainage

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38
Q

How can you manage drainage?

A

Nephrostomy

Ureteric Stent

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39
Q

What are the treatment options for renal stones?

A

Site and size of stone, pateint factors dependent

Conservative

Medical

Lithotripsy

Surgical

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40
Q

What is the management of renal stones?

A

Conservative - small, safe location, asymptomatic, static size.

ESWL - up to 1-2cm

Uretericscopic - flexible, laser only <2cm

PCNL - ideal for larger stones

Nephrectomy - if split function <10-15%

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41
Q

What is the management of ureteric stones?

A

Conservative - allow 2/52 to pass - majority <4mm will pass

Drainage if sepsis

Medical expulsive therapy

ESWL - stones <1cm

Ureteroscopy - suitable for any stone, laser, basket extraction

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42
Q

What is ESWL?

A

Energy source

Focusing

Coupling

Targeting

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43
Q

What are the general symtpoms of cancer?

A

·Systemic or Constitutional

–Non-specific

–Specific

–Paraneoplastic syndromes

·Local

–e.g. Haematuria in Bladder Cancer

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44
Q

What are the constitutional non-specific symtpoms of cancer?

A

·Non-specific

–Weight Loss

–Anorexia

–Fever

–Anaemia (normocytic)

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45
Q

What are the specific constitutional symptoms of cancer?

A

·Hypercalcaemia

  • Anorexia
  • Thirst
  • Confusion
  • Collapse

·Marrow replacement

  • Purpura
  • Anaemia
  • Immune suppression
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46
Q

What type of cancer is prostate cancer? Where does it occur in the prostate?

A
  • Adenocarcinoma
  • Occurs in peripheral zone of prostate
  • 85% of tumours are multifocal
  • Spreads locally through prostate capsule
  • Metastasises to lymph nodes and bone (sclerotic) and occasionally to lung, liver and brain
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47
Q

What are the biomarkers for prostate cancer?

A

·Tissue

·Serum

–Prostate-specific Antigen (PSA)

–Prostate-specific membrane antigen (PSMA)

·Urine

–PCA3

–Gene fusion products (TMPRSS2-ERG)

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48
Q

What is PSA?

A

·Serine protease responsible for liquefaction of semen

·Small amount of retrograde leakage

·Detected in small quantities in the blood

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49
Q

How is PSA involved in prostate cancer?

A

·PROSTATE SPECIFIC not CANCER SPECIFIC

·Elevated in benign prostate enlargement, urinary tract infection, prostatitis

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

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

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50
Q

How can you diagnose prostate cancer?

A
  • Lower urinary tract symptoms (LUTS)
  • Prostate specific antigen (PSA)
  • Transrectal ultrasound scan (TRUSS)
  • Prostate biopsy
  • Prostate cancer grading (Gleason grading)
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51
Q

What different procedures can you do at each stage?

A

•T stage T1 - no palpable tumour on DRE
T2 - palpable tumour, confined to prostate
T3 - palpable tumour extending beyond prostate

  • N stage MRI scan, CT scan, (laparoscopy)
  • M stage Bone scan
  • Partin’s nomograms predict pathological T and N stage by combining clinical T stage, PSA and biopsy Gleason score
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52
Q

What are the different stages of prostate cancer?

A

Localised

Locally advanced

Metastatic

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53
Q

How is localised prostate cancer diagnosed?

A

·PSA detected disease

·Occasionally detected during surgery for benign prostatic obstruction

·Transrectal ultrasound and biopsy of prostate gland

·No clinical evidence of metastatic disease

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54
Q

What is the treatment for localised prostate cancer?

A

•Surgery - radical prostatectomy
open, laparoscopic, robotic

•Radiotherapy - external beam
- brachytherapy

•Observation - watchful waiting
- active monitoring/ surveillance

•Focal Therapy e.g. High intensity ultrasound (HIFU), photodynamic therapy (TOOKAD)

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55
Q

What is the treatment for locally advanced prostate cancer?

A

Surgery

Radiotherapy and neoadjuvant hormone therapy.

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56
Q

What is the treatment for metastatic prostate cancer?

A

Hormone therapy.

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57
Q

What is the differential diagnosis of renal, bladder and testis cancer?

A

Infection: UTI, pyelonephritis, TB.

Malignancy: anywhere in tract

Stones: bladder, kidneym ureteric

Trauma: penetrating Vs Blunt

Nephrological: diabetes, nephropathy

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58
Q

What investigations can you do for GU cancers?

A

Bloods: FBC, UandE, PSA, glucose

MSU/Dip: microscopy, culture, sensitivity

Cytology: if available

Imaging (USS/CTU)

Flexible cytoscopy

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59
Q

How can bladder cancer present?

A

85% painless VH

Irritative voiding / recurrent UTI’s (CIS)

Go through haematuria clinic

24% VH have malignancy, 9.4% NVH

15% present metastasis

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60
Q

How can you diagnose a bladder tumour?

A

Via tissue with transurethral resection of bladder tumour (TURBT) Specimenm must include muscle to stage

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61
Q

What are the different types of bladder cancer are there?

A

>90% Transitional cell carcinoma

5% squamous cell carcinoma

<1% adenocarcinoma

Rare: sarcoma, lymphoma, melanoma and secondaries

CIS: poorly differentiated, but confined epithelium, 50% become MI.

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62
Q

What are the different stages of bladder cacner?

A

Ta surface

T1 lamina propria, not hit the muscle

T2 hit the muscle

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63
Q

How cna you treat a bladder tumour with MI?

A

Cystectomy

Radiotherapy

+ / - chemotherapy

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64
Q

How can you grade bladder tumours of NMIBC?

A

G1 - well differentiated

G2 - moderate

G3 - poorly differentiated

G4 - carcinoma in situ

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65
Q

What are some risk factors of developing bladder cancer?

A

Paraplegia

Smoking

Occupational

Drugs

Bladder stones

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66
Q

How is renal cancer diagnosed?

A

Haematuria pathway.

66% picked up incidentally

30% will have mets on presentation: haematuria, flank pain, mass, weight loss, nodes

Usual risk factors (smoking, obesity, hypertension)

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67
Q

What tumours are majority of renal tumours?

A

Renal cell carcinoma, TCC

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68
Q

what is stage 1 of reanl canceer? What are the management options?

A

Under 7cm big.

Limited to the kidney.

5-year survival rate of 95%

Partial nephrectomy.

Radical nephrectomy.

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69
Q

What is stage 2 of renal cancer? What are the management options?

A

More than 7cm.

Limited to the kidney.

85% survival 5 years.

Radical nephrectomy.

Partial nephrectomy in selected patients.

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70
Q

What is stage 3 of renal cancer? What are the management of options?

A

Tumour in the major veins or adrenal gland with an intact Gerota’s fascia.

Or regional lymph nodes involved.

59% survival.

Radical nephrectomy plus adrenalectomy, tumour thrombus excision (if appropriate) and/or lymph node dissection.

Systemic treatment if inoperable. or owing to poor performance status.

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71
Q

What is stage 4 of renal cancer? What are the management options?

A

Tumour beyond Gerota’s fascia.

Distant metastases.

5-year survival of 20%.

Systemic treatment

Elective cytoreductive nephrectomy

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72
Q

How do you diagnose testicular cancer?

A

Look, feel, move.

Sign of a true scotal mass is this it is possbile to get above it.
Cystic masses can be transilluminated. Solid masses do not.

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73
Q

What is the differential diagnosis for testicular cancer?

A

Inguinal hernias.

Epididymitis

Infection.

Torsion.

Catheters, UTI.

Hydrocele.

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74
Q

What is the diffrerence between having varicoceles in the left and right vein?

A

Left drains into the left renal vein at 90 degrees, possibl kidney tumour.

Right into right VC

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75
Q

What are hydrocele?

A

Result of excessive fluid in tunica vaginalis (serous space surrounding testes).

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76
Q

Why do you remove the testicle out through the groin?

A

Damage testicle, release tumour cells into skin.

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77
Q

What are some risk factors for testicular tumours?

A

Cryptochidism - undecended testicle.

Fhx - family history.

Previous testicular tumour.

Poorly understood.

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78
Q

How do testicle tumours present?

A

80% painless lump in testis (hard/craggy, lies within testis, can be felt above).

Often found incidentally.

Other preseting symptoms include.

HYDROCOELE

PAIN

METASTASES

79
Q

What are some investigations for testicular tumour?

A

USS same day

Tumour markers:

AFP alpha feta protein (1/2 life 5 days) - also liver cancer, secreted by placenta

B-hcg (24-48)

LDH - lactacte dehydrogenase - shows turnover of cells.

CXR if respiratory symtpoms

Staging CT.

80
Q

What operations do you do for testicular tumour?

A

Early inguinal orchidectomy if malignant.

Types of tumour -

SEMINOMAS are very radiosensitive.

NON-SEMINOMAS (TERATOMAS) - cytotoxic chemotherapy.

81
Q

What is the staging of testicular cancer?

A

Stage 1 - COnfined to testicle

Stage 2 - Spread but below diaphragm

Stage 3 - Above diaphragm or in solid organs.

82
Q

What are the funtions of the kidney?

A

Homeostasis

Filtration and reabsorption

Blood pressure

Potassium.

Vitamin D and bone disease

Erythropoeitin.

83
Q

What happens with homeostasis?

A

Filtration - Blood minus cells and large negatively charged molecules.

Reasborption and secretion.

84
Q

What is there a net excretion of?

A

Sodium.

Phosphate.

Potassium.

Acid.

Uraemic toxins.

85
Q

What is the glomerular filtration rate? What percentage of cardiac output does it take?

A

120ml/min = 170L/day.

20% of cardiac output.

86
Q

What happens when you progressively worse CKD?

A

Anaemia.

Bone disease.

87
Q

At what eGFR is dialysis end stage disease needed?

A

7-10.

88
Q

How do you calculate eGFR?

A

Predict creatinine generation from age, gender, race.

Require steady state.

Extremes of muscle mass may be misleading.

89
Q

What can make serum creatinine look worse?

A

Creatinine is secreted as well as filtered:

Creatinine clearnace > GFR

More porminant at low GFR

Inhibitors of this secretion will make serum Cr rise and function look worse

Inhibitors of secretion: trimethoprim.

90
Q

How can you measure how leaky the glomerulus is?

A

Look at the levels of Albumin.

>30mg Normal.

30-300mg Microalbuminuria

>300mg macro albuminuria

>1g Heavy’ glomerular pathology likely

>3g Nephrotic range

91
Q

How can you work out how much Albumin a person produces in one day?

A

Get the proportion of creatinine and use this in Albumin.

92
Q

What happens at the proximal tubule?

A

70% filtered sodium.

Phosphate.

Glucose

Amino acids.

93
Q

What happens with acute tunular necrosis?

A

Proximal tubules don’t get an adequte blood supply and subsequently die.

94
Q

What is Fanconi syndome?

A

Proximal tubular insult.

Glycosuria

Acidosis with failure of urine acid secretion

Phosphate wasting; rickets/osteomalacia

Aminoaciduria.

Various causes: Cystinosis, tenofovir, paraprotein disease.,

95
Q

How do the kidneys control blood pressure?

A

Volume

Vascocontriction.

96
Q

How is volume control done?

A

All about sodium.

70% in proximal tubule

25% loop of Henle

5% distal tubule

2% collecting duct.

97
Q

What happens at the loop of Henle? What is the disease assocaited with this?

A

Concentration gradient,

Dilute at top of loop

Concentrated at bottom of loop

Used at collecting ducts, passive transport of water.

Diabetes insipidus.

98
Q

When do you get extra water retention? How can you treat this?

A

Kidney failure

Heart failure

Liver failure

Loop diuretics.

Thiazides (distal tubule)

Aldosterone antagnosit (collecitng duct) - Spiraloactone - pottasium sparing diuretic.

Aquaporins - vasopressin antagnoist.

99
Q

What happens at the juxtaglomerular apparatus?

A

Macula densor cells next to the afferent arterioles.

Sense amount of sodium in the distal convoluted tuble.

More blood = more filtered, more delivered to distal tubule.

Drop in delivery secretes renin and then opens up afferent arteriole.

100
Q

What is the renin-angiotensin pathway?

A

Angiotensinogen + Renin->

Angiotensin + ACE ->

Anginotensin 2->

Vasoconstriciton (increase blood pressure) and Aldosterone (affects reabsorption of sodium).

101
Q

What happens in renal artery stenosis?

A

Kidneys are getting less blood,

Renin gets reduced.

Retain more sodium.

More vasoconstriction.

Blood pressure goes higher until adequete flow.

102
Q

What do NSAIDs do to the kidneys?

A

Lower the amount of prostaglandin, prostaglandin preferentially dilates the afferent arteriole and therefore gets constricted.

Angiotensin 2 preferentially constricts the efferent arteriole, block this and it will dilate.

Therefore little blood flow in + more coming out = no filtration.

103
Q

What can Albumin do to the kidneys if it is filtered?

A

Damages the kidneys on the way through.

104
Q

What can treat proteinuric CKD?

A

ACE inhibitors and ARB.

A small drop in eGFR is okay.

105
Q

Where is potassium control done?

A

K freely filtered and mostly absorbed in proximal tubule/loop of Henle.

Distal secretion determines renal excretion.

106
Q

What is potassium control governed by?

A

Distal delivery of Na.

Aldosterone. (help pumps working)

Distal tubule - sodium reabsorption and potassium secretion. 1 for 1.

107
Q

How is buffereing of acute changes controlled?

A

Insulin and catecholamines drive cellular potassium uptake.

108
Q

Why do ACE inhibtors, aldosterone inhibitors give hyperkalemia?

A

Block aldosterone, end up with low sodium and high potassium and high hydrogen.

109
Q

How is vitamin D activated?

A

7-dehydrocholesterol to cholecalciferol (vitamin D3) using UV light.

Cholecalciferol to 25-hydroxyvitamin D.

25 to 1-25 in kidney

calcitriol = active vitamin D.

110
Q

What does calcitriol do?

A

Increases calcium and phosphate absorption from the gut.

Suppresses parathyroid hormone.

Deficiency causes secondary hyperparathyroidism.

PTH has effects on bone health.

111
Q

What does renal anaema do?

A

Erythropoetin deficiency in advanced kdiney disease leads to reduced haemopoesis and anaemia.

Exacerbated by functiuonal iron deficiency in renal disease.

Seldom seen until eGFR below 30.

112
Q

How do you diagnose acute kidney injury?

A

Rise in creatine > 26 micromol/L in 48 hrs (above baseline).

Rise in creatinine > 50% (best figure in last 6 months).

Urine output < 0.5 ml/kg/hr for > 6 consecutive hours.

113
Q

How many of the diagnosis do you need to diagnose a AKI?

A

1 out of the 3.

114
Q

What are the risk factors for acute kidney injury?

A
  • Age >75
  • Chronic kidney disease
  • Cardiac failure
  • Peripheral vascular disease • Chronic liver disease
  • Diabetes
  • Drugs (esp newly started)
  • Sepsis
  • Poor fluid intake/increased losses • History of urinary symptoms
115
Q

What are the most common causes of AKI?

A

Commonest are ischaemia, sepsis and nephrotoxins, although prostatic dis- ease causes up to 25% in some studies and has the best prognosis.

116
Q

What are the pre-renal causes of AKI?

A

Pre-renal (40–70%) due to renal hypoperfusion, eg hypotension (any cause, in- cluding hypovolaemia, sepsis), renal artery stenosis ± ACE-i.

117
Q

What are the Intrinsic renal causes of AKI?

A

ntrinsic renal (10–50%) may require a renal biopsy for diagnosis:

Tubular—acute tubular necrosis (ATN) is the commonest renal cause of AKI, of- ten a result of pre-renal damage or nephrotoxins such as drugs (eg aminoglyco- sides), radiological contrast (see p293), and myoglobinuria in rhabdomyolysis.

Also crystal damage (eg ethylene glycol poisoning, uric acid), myeloma, Ca2+

Glomerular—autoimmune such as SLE, HSP, drugs, infections, primary glomeru-

lonephritides are important not to miss (see p300)

Interstitial—drugs, infiltration with, eg lymphoma, infection, tumour lysis syn-

drome following chemotherapy

Vascular—vasculitis, malignant BP, thrombus or cholesterol emboli from angi-

ography, HUS/TTP (p308), large vessel occlusion, eg dissection or thrombus

118
Q

What are the post renal causes of AKI?

A

ost-renal (10–25%) caused by urinary tract obstruction:

  • Luminal—stones, clots, sloughed papillae
  • Mural—malignancy (eg ureteric, bladder, prostate), BPH, strictures
  • Extrinsic compression—malignancy (esp pelvic), retroperitoneal fibrosis.
119
Q

How can you assess AKI?

A
  • Assess volume status—check BP, JVP, skin turgor, capillary refill (<2s), urine output (catheterize).
  • Check an urgent K+ on a venous blood specimen and an ECG to check for life- threatening hyperkalaemia (see p293).

History: check for risk factors (see BOX), comorbidities, ask about previous renal disease, recent fluid intake and losses, new drugs including chemotherapy, sys- temic features such as rash, joint pain, fevers. Other systems—productive cough, haemoptysis, GU or GI symptoms, etc.

Examination: Full systemic examination. Specific features to look for include a palpable bladder, palpable kidneys (polycystic disease), abdominal/pelvic masses, renal bruits (signs of renovascular disease), rashes.

Bedside tests: Always, always dip the urine. See p236. Dipstick can suggest infec- tion (leucocytes + nitrites), glomerular disease (blood + protein). Microscopy for casts, crystals and cells. Culture for infection. Consider Bence Jones protein.

Blood tests: U&E, FBC, LFT, clotting, CK, ESR, CRP. Consider ABG for acid base assess- ment. Culture blood if signs of infection. Consider blood film and renal immunology if systemic cause suspected: immunoglobulins and paraprotein electrophoresis, complement (C3/C4), autoantibodies (ANCA, ANA, anti-GBM, esp if haemoptysis, see p300, p555) and ASOT.

Imaging: A renal USS can help to distinguish obstruction and hydronephrosis, and look for abnormalities such as cysts, small kidneys, masses, as well as assess corti- comedullary di erentiation (reduced in chronic kidney disease). Complete anuria is unusual in AKI and if present suggests an obstructive cause. In elderly men this should be considered prostatic and can often be relieved by catheterization. If catheterization does not resolve anuria and you suspect obstruction above the prostate, get an urgent USS to check for hydronephrosis and consider an urgent CTKUB (does not require contrast), which can show obstructing masses or calculi. Consider CXR if signs of fluid overload.

120
Q

What is the management for AKI?

A

General measures
Assess volume status
Aim for euvolaemia
Stop nephrotoxic drugs
Monitoring
Nutrition

Manage complications

Renal replacement therapy

121
Q

How can you treat pre-renal AKI?

A

Pre-renal: Correct volume depletion with appropriate fluids, treat sepsis with an- tibiotics, consider referral to ICU for inotropic support if signs of shock (see p804).

122
Q

How can you treat post-renal AKI?

A

Post-renal: Catheterize and consider CT of renal tract (CTKUB) and urology refer- ral if obstruction likely cause. If signs of obstruction and hydronephrosis on CT/ USS then discuss with urology regarding cystoscopy and retrograde stents or ne-

phrostomy insertion; this buys time to allow treatment of cause of obstruction, eg

stone, mass.

123
Q

How can you treat intrinsic renal?

A

Intrinsic renal: Refer early to nephrology if concern over tubulointerstitial or

glomerular pathology, any signs of systemic disease, multi-organ involvement (eg pulmonary-renal, hepatorenal syndromes) or indications for dialysis (see p291).

124
Q

What would you see on a hyperkalemic ECG?

A

Peaked T waves.

Small or indiscernible P waves.

125
Q

How can you manage hyperkalaemia?

A

Insulin and Dextrose. ( insulin drive potasssium into cell).

Calcium gluconate. (to protect heart)

IV fluid.

Salbutamol.

Calcium resonium.

126
Q

What do you do before referral?

A
  • Proper history and examination
  • Blood tests & Imaging
  • IV fluid
  • Urine dip sticks
  • Review of drugs
  • Fluid balance ( intake /output )
  • Current volume status
127
Q

When do you refer to a Nephrologist?

A
  • Treat the urgent causes first !
  • Hyperkalaemia or fluid overload unresponsive to medical treatment
  • Urea > 40mmol/L +/- signs of uraemia
  • No obvious cause
  • Creatinine > 300 or rising > 50micromol/L per day
128
Q

When will you start dialysis?

A
  • Refractory pulmonary oedema
  • Persistent hyperkalaemia
  • Severe metabolic acidosis
  • Uraemic encephalopathy or pericarditis
  • Drug overdose – BLAST ( Barbiturate, Lithium, Alcohol-ethylene glycol, Salicylate, Theophylline)
129
Q

What is glomerulonephritis?

A

Inflammation in the glomerulus.

130
Q

What are the consequences of glomerulonephritis?

A

Damage to the glomerulus restricts blood flow, leading to compensatory BP
• Damage to the filtration mechanism allows protein and blood to enter the urine
• Loss of the usual filtration capacity leads to acute kidney injury

131
Q

What is the spectrum of glomerulonephritis disease?

A

1 Blood pressure: normal to malignant hypertension

2 Urine dipstick: proteinuria mildnephrotic; haematuria mildmacroscopic

3 Renal function: normal to severe impairment

132
Q

What do pateints normally present with?

A

Syndrome BP Urine GFR

Nephrotic (p302) Normal–mild  Proteinuria >3.5g/day Normal–mild 

Nephritic Moderate–severe  Haematuria (mild–macro) Moderate–severe 

133
Q

What are the causes of glomerulonephritis?

A

Syndrome Common primary causes Common secondary causes

Nephrotic Membranous Minimal change

FSGS (p303) Mesangiocapillary GN

Diabetes
SLE (class V nephritis) Amyloid
Hepatitis B/C

Nephritic IgA nephropathy

Post streptococcal Mesangiocapillary GN Vasculitis

SLE (other classes of nephritis) Anti-GBM disease (Figs 1 & 2) Cryoglobulinaemia

134
Q

What tests can you do for glomerulonephritis?

A

looking for degree of damage and potential cause. Blood: FBC, U&E, LFT, ESR, CRP; immunoglobulins, electrophoresis, complement (C3, C4); autoantibodies (p555): ANA, ANCA, anti-dsDNA, anti-GBM; blood culture, ASOT, HBsAg, anti-HCV (p406). Urine: RBC casts, MC&S, Bence Jones protein, ACR (see p286). Imaging: CXR, renal ultrasound.

Renal biopsy (p297) will give the most information and is where many of the com- plex names arise. Generally it is reported as follows: what is a ected (mesangial cells, capillaries, basement membrane, endothelium), how much of the kidney is involved (focal vs di use), how much of the glomerulus is involved (segemental vs global), and what is seen on immunofluorescence (deposition of Igs, complement, immune complexes or pauci immune) and electron microscopy.

135
Q

What is vasculitis?

A

Inflammation of the blood vessel wall.

Large, Medium or Small.

ANCA - Anti neutrophil cytoplastic antibody.

ANCA makes an antibody against structures within the cell.

Protinase 3 antigen and perinuclear antigen (mpo).

136
Q

What are the features of vasculitis?

A

Purpuric rash on extensor surfaces (typically on the legs), flitting polyarthritis, abdominal pain (GI bleeding) and nephritis.

137
Q

What is the diagnosis of vasculitis?

A

Urine dipstick for ANCA

changes in ANCA titre correlate with disease activity.

Biopsy: segmental glomerular necrosis with cresent formation.

138
Q

How do you treat vasculitis?

A

Immunosuppresion.

Steroids, Cyclophosphamide.

139
Q

What is IgA nephropathy?

A

Mesangial proliferative GN with diffuse mesangial IgA deposits.

HSP is differentiated from IgA with extra renal manifestations.

Visible haematuria with mucosal infection.

IgA nephropathy is the most prevalent pattern of glomerular disease

140
Q

What are the clinical features of IgA nephropathy?

A

Episodic macroscopic haematuria (synpharyngitic haematuria) in 40-50% of cases in second or thris of life

A symptomatic urine testing identifies 30-40% of cases.

Nephrotic syndrome occurs in only 5% of all cases.

AKI at presentation could be due to ATN or crescentic GN.

141
Q

How can you diagnose IgA nephropathy?

A

Biopsy” diffuse mesangial igA deposits, subendothelial and sub epithelial depositis on EM is not uncommon.

142
Q

What is the management of IgA nephropathy?

A

Supportive care: BP control with RAAS inhibitors, Diet, Lower Cholesterol.

Immunosuppression: Induction: Steroids, Cyclophosphamide.

Remission: Steroids, Azathioprine.

143
Q

What is nephrotic syndrome?

A

Metabloic consequences are hyalbuminaemia, hypercoagulability, loss of binding proteins needing drug dose adjusments and risk of infecitons.

144
Q

What is membranous GN?

A

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

Secondary MN: Associated with autoimmune conditions, virsues, drugs and tumours.

`Primary MN: Glomerular podocyte membrane PLA2R antigen is the target antigen in 70-80% cases of primary MN.

145
Q

What are the clinical features of MN?

A

Nephrotic syndrome, benign urinary sediment.

146
Q

What is the diagnosis for MN?

A

Serum PLA2R Ab, renal biopsy.

147
Q

What is the treatment for MN?

A

Immunosuppresents.

Control of oedema, hypertensiom, hyperlipdidemia and proteinuria.

148
Q

What does the female lower urinary tract anatomy look like?

A
149
Q

What does the male lower urinary tract anatomy look like?

A
150
Q

What does the cortex do in neuro-urology?

A

Cortex

–Sensation

–Voluntary initiation

151
Q

What does the PMC(Pontine micturition center)/PAG(Periaqueductal gray) do in neuro-urology?

A

PMC/PAG

–Co-ordination

–Completion of voiding

152
Q

What do the spinal reflexes do in neuro-urology?

A

Spinal Reflexes

–Reflex bladder contraction

Sacral micturition centre

–Guarding reflex

Onuf’s nucleus

–Receptive relaxation

Sympathetic

153
Q

What is the neural control of the LUT?

A

uParasympathetic (Cholinergic) S3-5

Detrusor contraction

Smooth muscle sphincter relaxation

uSympathetic (Noradrenergic) T10-L2

Smooth muscle sphincter contraction

Inhibit detrusor contraction (allows bladder relaxation)

uSomatic

Striated sphincter contraction/ relaxation

uCentral co-ordination from pontine micturition centre

154
Q

What does normal bladder function consist of?

A

Storage (99%)

Sympathetic causes detrusor relaxation and sphincter contraction

Bladder fullness increases, messages to the pons and higher

centres to consider voiding

Can be postponed until it is convenient

uVoiding (1%)

PMC co-ordinates voiding via Parasympathetic causes detrusor

contraction and sphincter relaxation at same time

155
Q

What LUTS can you get with storage?

A
  • Frequency
  • Urgency
  • Nocturia
  • Incontinence
156
Q

What LUTS can you get with voiding?

A
  • Slow stream
  • Splitting or

spraying

  • Intermittency
  • Hesitancy
  • Straining
  • Terminal dribble
157
Q

What LUTS can you get with post-micturition?

A
  • Post-micturition dribble
  • Feeling of incomplete emptying
158
Q

What is overactive bladder defined as?

A

OAB is defined as urgency with frequency, with or without nocturia, when appearing in the absence of local pathology.

Wet and Dry

159
Q

What are the management options for an OAB?

A

Behavioural therapy

Frequency volume chart

Caffeine, alcohol Bladder drill

Anti-muscarinic agents

Decrease parasympathetic activity by blocking M2/3 receptors but have S/E- dry mouth

B3 agnosits

Increase sympathetic activity at B3 receptor in bladder

Botox

Blocks neuromuscular junction for Ach release

S/E Incomplete bladder emptying and need to catheterise in 15%

Sacral neuromodulation

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

Surgery

Augmentation cystoplasty Involves major surgery

160
Q

What is stress incontinence in females?

A

Usually secondary to birth trauma

–Denervation of pelvic floor and urethral sphincter

–Weakening of fascial support of bladder and urethra

Neurogenic

Congenital

161
Q

What are the management options for stress urinary incontinence?

A

Pelvic floor Physiotherapy

Duloxetine

Surgery

–Sling (TVT, TOT, autologous sling)

–Colposuspension

–Bulking agents

–Artificial sphincter

162
Q

What is stress incontinence in males?

A

Neurogenic

Iatrogenic (prostatectomy)

163
Q

How can you treat male stress incontinence?

A

Treat with artificial sphincter or male sling

164
Q

How can you treat uObstructive- BPE, urethral stricture, prolapse/mass?

A

If BPE then give alpha blockers +/- 5alpha reductase inhibitor

Another option is PDE5i in men with erectile dysfunction

If above fails then TURP

165
Q

How can you treat Non obstructive- detrusor underactivity?

A

Long term catheterisation to empty- ISC/LTC/SPC

Sacral neuromodulation in trial phase-works in Fowlers syndrome

166
Q

Management summary for urinary incontinence?

A
167
Q

What happens in spastic spinal cord injury?

A

Lost

–Co-ordination

–Completion of voiding

Features

–Reflex bladder contractions

–Detrusor sphincter

dyssynergia

–Poorly sustained bladder contraction

Effect

–Potentially unsafe

–DSD, poorly sustained bladder contraction

168
Q

What happens in flaccid spinal cord injury?

A

Lost

–Reflex bladder contraction

–Guarding reflex

–Receptive relaxation

Features

–Areflexic bladder

–Stress incontinence

–Risk of poor compliance

Effect

–Potentially unsafe

–DLPP, poor compliance

169
Q

What are the aims of management of Neurogenic bladder?

A

Bladder safety

Continence\Symptom control

Prevent autonomic dysreflexia

170
Q

What is autonomic dysreflexia? What symptoms do you get?

A

Occurs lesions above T6

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

Headache, severe hypertension, flushing

171
Q

What is an unsafe bladder?

A

–One that puts the kidneys at risk of damage

172
Q

What are the risk factors for an unsafe bladder?

A

–Raised bladder pressure

–Vesico-ureteric reflux

–Chronic infection

uResidual urine

uStones

173
Q

What causes a raised bladder pressure?

A

prolonged detrusor contraction loss of compliance

174
Q

What results from a raised bladder pressure?

A

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

175
Q

How can you control a reflex bladder?

A

1.Harness reflexes to empty bladder into incontinence device (may not keep bladder safe!!)

2.Suppress reflexes converting bladder to flaccid type and then empty regularly

176
Q

What symptoms does a paraplegic have?

A

Paralysed from waist down

Normal upper body function

Can do ISC, transfers

Spasm

Reflex Bladder

177
Q

How can a paraplegic manage their bladder?

A
  • Suprapubic catheter
  • Conveen

OR

•Suppress reflexes or poorly compliant bladder converting bladder to safe type and then empty regularly using ISC

178
Q

What is convene drainage?

A

No indwelling catheter

Needs monitoring

Develop incomplete bladder emptying long term

Options for making sphincter safe includes sphincterotomy

179
Q

What is SPC and what are the risks?

A

Suprapubic catheter

uInserted under anaesthetic

uInfections

uStones

uAutonomic Dysreflexia if blocked

uUse Clip and Release if possible

180
Q

How can you supress reflex bladder contractions?

A

uAnticholinergics

uMirabegron

uIntravesical botulinum toxin

uPosterior rhizotomy

uCystoplasty

181
Q

What bladder problems are there in MS?

A

Overactive bladder syndrome

urinary urgency and frequency, caused by neurogenic detrusor overactivity

Incomplete bladder emptying

182
Q

What is the progression of MS and the risks on urinary tract with time?

A
183
Q

How is erectile function controlled?

A

•Erection is a neurovascular phenomenon under hormonal control

–Arterial dilatation, smooth muscle relaxation, activation of the corporeal veno occlusive mechanism

184
Q

What is erectile dysfunction?

A

•The persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance

185
Q

What is the aeitology of erectile dysfunction?

A

•Organic

–Vasculogenic

–Neurogenic

–Hormonal

–Anatomical

–Drug induced

•Psychogenic

186
Q

What are some common risk factors for erectile dysfunction?

A

•In common with CVS disease

–Lack of exercise

–Obesity

–Smoking

–Hypercholesterolaemia

–Metabolic syndrome

•Diabetes x 3 risk of ED

187
Q

What diseases are associated with erectile dysfunction?

A
  • Diabetes mellitus
  • Cardiovascular disease

–MI, hypertension

  • Liver disease and alcohol
  • Renal failure
  • Trauma

–Pelvic fracture

•Iatrogenic

–Prostatectomy

188
Q

How can you diagnose ED?

A

•Indicators of psychological aetiology

–Sudden onset of ED

–Good nocturnal and early morning erections

–Situational ED

–Younger patient

•IIEF (International index for Erectile Function)

•Erectile function, orgasmic function, sexual desire, ejaculation, intercourse and overall satisfaction

Physcial examination

  • BP and heart rate
  • Hepatosplenomegaly
  • Genitalia

–Peyronie’s disease

  • Prostatic enlargement or cancer
  • Hypogonadism

–Small testes, secondary sexual characteristics

189
Q

What is Peyronies disease?

A
190
Q

What labratory tests can you do?

A

•Fasting glucose

•Lipid profile

•Morning testosterone

–If low testosterone perform prolactin, FSH, LH

•Nocturnal penile tumescence and rigidity

•Intracavernosal injection test

•Duplex USS of penile arteries

•Arteriography

191
Q

What are the treatment options for ED?

A

•Goal is to treat underlying condition

–ie treat reversible factors

  • Identify and treat reversible causes of ED
  • Lifestyle and risk factor modification
  • Patient and partner involvement in education and counselling
192
Q

What are some curable causes of ED?

A

•Hormonal causes

–Testosterone deficiency

  • Primary testicular failure
  • Pituitary/hypothalamic failure

–Testosterone replacement

–Contraindicated if history of prostate cancer

–Check DRE and PSA beforehand

–Monitor for hepatic or prostatic disease

•Psychosexual counselling

–Variable results

193
Q

What is each line of treatment for ED?

A

•First Line

–Phosphodiesterase (PDE5) inhibitors

•Second Line

–Apomorphine SL

–Intracavernous injections

–Intraurethral alprostadil

–Vacuum devices

•Third Line

–Consider penile prosthesis implantation

194
Q

What do PDE5 inhibitors do?

A

–PDE5 inhibitors result in increased arterial blood flow, vasodilatation, and erection

–Action on Nitric oxide

–3 PDE5 inhibitors have been approved. Not initiators of erections – require sexual stimulation

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