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CP1 > Urology > Flashcards

Urology Flashcards

1
Q

At what spinal level are the kidneys?

A

Usually T12 - L3

right kidney is generally lower than the left due to the liver

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2
Q

What are the two main regions of kidney parenchyma ?

A
  1. inner medulla

2. outer cortex

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3
Q

Role of the renal corpuscle

A

= site of initial filtration

Consists of Bowman’s Capsule and Glomerulus

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4
Q

Role of proximal convoluted tubule

A

Brush border to increase luminal surface area for reabsorption of ions and solutes.

Also important for regulating pH by secreting bicarbonate

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5
Q

Loop of Henle - permeability of descending thin limb

A

impermeable to ions, but high permeability to water

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6
Q

Loop of Henle - permeability of ascending thin and thick limb

A

mostly impermeable to water, permeable to ions (passive diffusion in thin part and active transport in thick part).

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7
Q

What is the aim of the loop of henle

A

Aims to create a strong osmotic gradient for absorption of large amounts of water from the descending limb

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8
Q

Role of distal convoluted tubule

A

Regulation of potassium, sodium, calcium and pH.

Macula Densa cells involved in paracrine function (detect Na+ levels and initiate RAAS).

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9
Q

Role of collecting duct

A

Filtrate is concentrated to form urine, which feeds into the renal pelvis and then the ureters.

Electrolyte and fluid balance, regulated by aldosterone and ADH

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10
Q

What is the role of the kidney?

A

Regulating volume and composition of bodily fluids.

Regulating acid-base balance.

Excretion of metabolic breakdown products
=> Ammonia, urea, uric acid, creatinine, drugs, toxins.

Hormonal functions
=> Produces EPO
=> Vitamin D metabolism (converts to active form)
=> Secretes renin in response to reduced afferent pressure.

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11
Q

Renin-Angiotensin-Aldosterone System

A

The juxtaglomerular cells of the kidneys are stretch-receptors

Reduced stretch from a decrease in blood volume will lead to the release of renin.

Renin is involved in the cleavage of angiotensinogen to AI. AI is cleaved to AII by ACE.

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12
Q

What is the role of angiotensin II?

A
  1. Vasoconstriction (of afferent arteriole)
  2. Increase release of aldosterone
    => Enhances reabsorption of sodium and water
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13
Q

What is AKI?

A

= a rapid decline in kidney function occurring over hours or days, as measured by serum urea and creatinine.

This results in a failure to maintain fluid, electrolyte and acid-base homeostasis

Causes can be pre-renal, intrinsic or post-renal

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14
Q

When is AKI common?

A

very common in acute illness

(>15% of emergency admissions and 25% of septic patients).

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15
Q

Risk factors for AKI

A
  • Age >65 years.
  • Pre-existing CKD
  • Male
  • Cardiac failure
  • Chronic liver disease
  • Diabetes
  • Sepsis
  • Hypovolaemia
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16
Q

Pre-renal AKI

A

Reduced renal perfusion leads to a reduction in GFR

Main causes:

  1. Shock – hypovolaemic, cardiogenic, distributive.
  2. Renovascular obstruction – AAA, renal artery stenosis (and ACEis given in bilateral renal artery stenosis), renal vein thrombosis.
  3. Fluid overload – cardiac failure, cirrhosis, nephrotic syndrome.

If interruption in the blood supply is prolonged, there will be acute tubular necrosis (ATN).

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17
Q

Acute tubular necrosis in pre-renal AKI

A

Ischaemia leads to necrosis of the cells lining the renal tubules.

Leads to porous tubular membranes (leading to loss of concentrating power) and also blockage of the tubules by necrosed cells

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18
Q

Causes of hypovolaemia

A

Hypovolaemia can be caused by:

  • haemorrhage,
  • dehydration,
  • third space losses (e.g. due to bowel obstruction/pancreatitis),
  • burns and GI losses (vomiting and diarrhoea).
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19
Q

Post-renal AKI

A

Occurs when there is obstruction of the urinary tract
=> Leads to a backflow of urine, damage to the kidney architecture and resultant organ failure

e.g. blockage of ureter (stones, strictures, clots, malignancy) or bladder outlet obstruction

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20
Q

Intrinsic AKI

A

= Injury or damage to the renal parenchyma, by 3 potential mechanisms

  1. Acute tubular necrosis
  2. Interstitial nephritis
  3. Glomerular disease
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21
Q

Renal causes of Acute tubular necrosis

A

due to drugs/toxins damaging the tubular cells (rather than ischaemia, which is pre-renal).

  • Drugs – aminoglycosides, cephalosporins, radiological contrast mediums, NSAIDs.
  • Toxins – heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome (HUS).
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22
Q

Interstitial nephritis

A

Damage is not limited to tubular cells (as in ATN) and bypasses the basement membrane to cause damage to the interstitium

Most commonly caused by drugs (especially antibiotics, but also diuretics, NSAIDs allopurinol and PPIs).

Can be caused by infection, auto-immune mechanism or lymphoma.

Normally responds to withdrawal of the drugs and a short course of oral steroids

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23
Q

Myoglobinuria

A

Follows an episode of rhabdomyolysis (muscle breakdown from trauma, strenuous exercise or medications), releasing myoglobin which is readily filtered by the glomerulus.

Gives the classical dark urine, but in high quantities will precipitate out within the tubules to cause damage

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24
Q

haemolytic uraemic syndrome (HUS)

A

Occurs in children following diarrhoeal illness caused by verotoxin-producing E. coli O157, or following a URTI in adults.

Thrombocytopaenia, haemolysis and ATN.

Children recover within a few weeks, prognosis for adults is poor.

Treatment is supportive, including dialysis

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25
Q

Signs and Symptoms of AKI

A 
Reduced urine output
Nausea and vomiting
Dehydration
Confusion 
Fatigue

Signs depend on cause - look for:

  • Fluid overload
  • Hypotension
  • Palpable abdominal mass
  • Associated features of vasculitis – petechiae, skin changes, bruising, etc.
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26
Q

NICE criteria for diagnosis of AKI

A
  1. A rise of serum creatinine >26 micromol/L in 48 hours
  2. A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  3. A fall in urine output <0.5mL/kg/hour for more than 6 consecutive hours
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27
Q

AKI Stage 1

A

Serum Creatinine
150-200% increase OR
>25 micromol/L increase in 48h

Urine Output
<0.5 mL/kg/hour for 6h

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28
Q

AKI Stage 2

A

Serum Creatinine
200-300% increase

Urine Output
<0.5 mL/kg/hour for 12h

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29
Q

AKI Stage 3

A

Serum creatinine
>300% increase OR
>350 micromol/L increase in 48h

Urine output
<0.3 mL/kg/h for 24h OR
Anuria for 12h

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30
Q

AKI - Bedside tests

A 
Urine dip
Urine cultures
Observations – BP, RR, HR
Glucose
ECG
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31
Q

AKI - Bloods

A 
FBC
U&E
LFTs 
Coag
CRP

ABG – ?acid-base imbalance

Creatine Kinase if indicated
Immunology if indicated

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32
Q

AKI - imaging

A

USS KUB

CXR if pulmonary oedema

CT KUB if obstruction

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33
Q

When would test for creatinine kinase be indicated in AKI?

A

Creatine kinase can show rhabdomyolysis, but this would only be done if indicated in the history and symptoms/signs

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34
Q

Management of AKI

A

Treat the underlying cause

Fluid management (input and output)

Medication review
=> hold/change dose?

Seek renal specialist input if indicated

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35
Q

What might indicate the need for renal specialist input in AKI?

A

No improvement

Complicated cases

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36
Q

Complications of AKI

A 
Hyperkalaemia
Other electrolyte imbalances
Metabolic acidosis
Volume overload
Uraemia
CKD and ESRD
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37
Q

What electrolyte imbalances are associated with AKI?

A

Hyperkalaemia
Hyperphosphataemia
Hypermagnesaemia

Hyponatraemia
Hypocalcaemia

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38
Q

Indications for renal replacement therapy

A

Refractory pulmonary oedema

Persistent hyperkalaemia (>7)

Severe metabolic acidosis

Ureamic complications (encephalopathy, pericardial rub)

Drug overdose

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39
Q

What is the biggest cause of CKD?

A

Diabetes mellitus

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40
Q

Causes of CKD:

A

Diabetes mellitus

Interstitial diseases
Glomerular diseases
Obstructive uropathy

Hypertension
Renovascular disease

Drugs (long-term NSAIDs)
Congenital/inherited
Unknown causes

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41
Q

Symptoms of CKD

A

Often asymptomatic until very advanced

Polyuria/nocturia
Restless leg syndrome
Sexual dysfunction
Nausea & Pruritis (early uraemia)
Yellow pigmentation, encephalopathy and pericarditis (severe uraemia)
Pedal oedema & pulmonary oedema.
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42
Q

Signs of CKD

A 
Pallor – due to anaemia
Excoriations – due to pruritis
Hypertension/fluid overload signs
Pericardial rub (rare)
Proteinuria
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43
Q

What are some very late features of CKD?

A 
Hiccups
Kussmaul’s respiration (due to metabolic acidosis)
Muscle twitching
Drowsiness
Coma
Fits
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44
Q

Assessment of CKD

A 
Bloods - anaemia? hyperkalaemia?
Urinalysis
ECG - hyperkalaemia?
Renal USS
Renal biopsy - if cause unclear 
24-hour CrCl - for staging
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45
Q

What would small kidneys on USS indicate?

A

Chronicity of disease (not acute presentation)

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46
Q

What would asymmetry of kidneys on USS indicate?

A

renovascular or developmental disease

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47
Q

How is CKD diagnosed?

A

when any two tests three months apart show reduced eGFR and can be stages 1-5 depending on the level of reduction

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48
Q

CKD Stage 1

A

eGFR >90 but urine findings/structural abnormalities/ genetic traits suggest CKD

Pt will be asymptomatic

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49
Q

CKD Stage 2

A

eGFR 60-89

Mildly reduced eGFR and other findings (as for stage 1) point to CKD

Pt will be asymptomatic

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50
Q

CKD Stage 3A

A

“Moderate CKD”

eGFR 45-59

usually asymptomatic

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51
Q

CKD Stage 3B

A

“Moderate-severe CKD”

eGFR 30-44

Pt might be anaemic

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52
Q

CKD Stage 4

A

“Severe CKD”

eGFR 15-29

Symptoms often at eGFR <20
Electrolyte disturbances

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53
Q

CKD Stage 5

A

“End-stage renal failure (ESRF)”

eGFR <15 / dialysis

Significant complications and symptoms
Dialysis usually at eGFR <10

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54
Q

Management of CKD

A

Treat reversible causes – e.g. obstruction, nephrotoxic drugs

1st line = BP control/diabetic control

2nd line = control of complications
=> recombinant EPO
=> calcium/vitD supplementation
=> K+ restriction for hyperkalaemia

RRT in ESRD

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55
Q

What are the complications of CKD?

A

Renal anaemia
Renal bone disease

Electrolyte disturbances
Myopathy
Peripheral neuropathy
Increased risk of infection
GI – Anorexia, N+V, peptic ulcer disease.
CV – pericarditis, atherosclerosis, HTN, hyperlipidaemia.

Depression – particularly in later stages/dialysis

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56
Q

Renal anaemia

A

Lack of secretion of EPO in response to hypoxia

Severity of anaemia correlate with severity of CKD

Recombinant EPO can be given to correct it
BUT treating anaemia may not affect mortality and returning Hb to normal may carry additional risks (hypertension, thrombosis).

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57
Q

Renal bone disease

A

Kidneys normally hydroxylate vitamin D to its active form.

Low VitD levels in CKD cause:

  • reduced intestinal Ca2+ absorption
  • reduced renal reabsorption of Ca2+
  • reduced bone protective activities

thus lead to osteoporosis, osteosclerosis and osteomalacia

hyperparathyroid bone disease can occur (due to low Ca2+)

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58
Q

What are the indications for renal replacement therapy?

A 
A	intractable acidosis
E	electrolyte disturbance (hyperkalaemia, hyponatraemia, hypercalcaemia)
I	intoxitants
O	intractable fluid overload
U	uraemia symptoms
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59
Q

Is the risk of renal disease higher in T1DM or T2DM?

A

Risk is equivalent

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60
Q

How does diabetes mellitus affect the kidneys?

A
  1. Direct glomerular damage
  2. Ischaemia due to arterial disease
  3. Ascending infection (more common in DM)
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61
Q

What factors of DM contribute to renal disease?

A

Multifactorial

the most important factors:

  1. extent and duration of hyperglycaemia
  2. hypertension.

Other:
Smoking, obesity, physical inactivity, dyslipidaemia, proteinuria, dietary factors

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62
Q

What are the principles of management for diabetic nephropathy?

A

the same as for CKD, but with additional tight glycaemic control

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63
Q

What are the types of polycystic kidney disease?

A
  1. Autosomal dominant (ADPKD) – more common

2. Autosomal recessive (ARPKD)

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64
Q

What does polycystic kidney disease consist of?

A

Renal and extra-renal cysts (e.g. liver)

Intracranial aneurysms

Dolichoectasias (elongated and distended arteries)

Aortic root dilatation and aneurysms

Mitral valve prolapse

Abdominal wall herniae

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65
Q

How do patients with polycystic kidney disease present?

A

= most common cause of ballotable kidneys.

systemic hypertension,
CKD
abdominal swelling due to very large kidneys bilaterally.

Cysts in the liver lead to portal hypertension and fibrosis

66
Q

Management of polycystic kidney disease?

A

the same as for CKD, but consider screening for berry aneurysms

67
Q

Chronic pyelonephritis

A

chronic tubulointerstitial inflammation and deep segmental cortical renal scarring

clubbing of the pelvic calyces as the papillae retract into scars

Most commonly caused by chronic vesico-ureteric reflux.

68
Q

What are the 3 layers of the glomerulus?

What is the purpose of this structure?

A
  1. Fenestrated capillary endothelium
  2. Basement membrane
  3. Visceral layer – formed by podocytes.

to allow small, charged ions through, but not transport of proteins or blood

69
Q

pathophysiology of Glomerulonephritis/glomerular disease

A

involves an immunological attack by an antibody or T cell, attacking a primary/secondary antigen in the glomerulus

The immune attack leads to pathological responses in the glomerulus:
=> thickened basement membrane
=> deposition of cells in bowman’s space
=> endothelial cell proliferation, capillary wall necrosis and sclerosis

70
Q

What can cause deposition of a secondary antigen in the glomerulus?

A

Neoplasm, SLE, amyloid, infection, diabetes, Henoch Schonlein Purpura

71
Q

Global glomerular pathology

A

when the whole glomerulus is diseased

72
Q

Segmental glomerular pathology

A

Small patches of one glomerulus are damaged in a “patchy” fashion

73
Q

Diffuse glomerular pathology

A

Affecting >50% of glomeruli

74
Q

Focal glomerular pathology

A

Affecting <50% of glomeruli

75
Q

How can glomerular damage manifest?

A 
AKI
CKD
Asymptomatic haematuria
Nephrotic Syndrome
Nephritic Syndrome

Rapidly progressive glomerulonephritis (acute version of nephritic syndrome).

76
Q

What is the triad of nephrotic syndrome?

A
  1. Proteinuria - >3.5 g in 24h
  2. Hypoalbuminaemia - <30g/L
    => due to protein loss in the urine.
    => In response, liver will produce albumin (but also cholesterol, resulting in hypercholesterolaemia)
  3. Oedema
    => due to decreased capillary oncotic pressure

a NON-PROLIFERATIVE condition

77
Q

Symptoms/signs of nephrotic syndrome

A 
Fatigue – hypoalbuminaemia.
Leukonychia – hypoalbuminaemia.
Xanthelasma and xanthomata – dyslipidaemia.
Oedema
Breathlessness – pulmonary oedema
Urine “frothy” in appearance - protein
78
Q

Causes of nephrotic syndrome

A

Minimal change nephropathy
Membranous glomerulonephritis
Focal Segmental Glomerulosclerosis

Bacterial/viral infection
Diabetic nephropathy
Drugs
Neoplasm

79
Q

Nephrotic Syndrome - investigations

A

Urine Dipstick, MSU

FBC, U&E, LFT, Ca2+, CRP, glucose

Serum and urine immunoglobulins

Autoimmune screen, Hep B&C, HIV

CXR – pleural effusion/oedema

USS kidneys (+ renal biopsy?)

80
Q

Minimal change nephropathy

A

= most common cause of nephrotic syndrome in childhood

Characterised by minimal change on light microscopy of renal biopsy

81
Q

Nephrotic Syndrome - management

A

Treat the cause.

Diuretics, salt/water restriction and ACEis to reduce proteinuria.

Anticoagulation if immobile due to risk of thrombosis

82
Q

Nephritic Syndrome

A

Presents as a tetrad of:

  1. Haematuria and red cell casts (can be microscopic)
  2. Oliguria
  3. Proteinuria (can be <3.5 g/day)
  4. Hypertension

It is proliferative, with increased cell numbers as well as damage to the basement membrane

83
Q

Causes of nephritic syndrome

A

IgA nephropathy
Goodpasture’s disease
SLE
Henoch Schonlein Purpura (HSP)

84
Q

What is the main risk factor for UTI?

A

BEING FEMALE

  • shorter urethra (closer to anal and genital regions).
  • Pregnancy - hormonal changes lead to urinary stasis and thereby vesicoureteric reflux
  • Post-menopause - low oestrogen levels cause decreased amounts of lactobacilli, which leads to increased pH (better conditions for E. coli colonisation)
85
Q

Risk factors for UTI in males

A 
Lack of circumcision
Urologic Surgery
Catheterisation
Neurogenic bladder
Urinary Tract obstruction (incl. caliculi)
Renal Transplant
Immunosuppression
Penetrative anal intercourse
Functional/mental impairment.
Prostatic enlargement
Convene
86
Q

Risk factors for UTI in females

A 
Previous UTI
Urologic Surgery
Catheterisation
Neurogenic Bladder
Urinary Tract obstruction (incl. calculi)
Renal Transplant
Immunosuppression
Sexual intercourse
Lack of urination after sex
Spermicides
Pregnancy 
Diaphragm Use
Diabetes
Functional/mental impairment
Oestrogen deficiency
Bladder prolapse
87
Q

What are the two most common pathogens causing UTI?

What are some rarer causes?

A
  1. E. coli (most common - ~80%)
  2. Staph. saprophyticus (common in young, sexually active females)

Rarer:

  1. Enterococci
  2. Proteus
  3. Klebsiella
  4. Pseudomonas (more likely from catheterisation)
88
Q

Upper UTI

A

Above the Vesico-ureteric junction (VUJ)

=pyelonephritis

89
Q

Lower UTI

A

below the Vesico-ureteric junction (VUJ)

= Cystitis

90
Q

Clinical Features of Lower UTI

A

Increased frequency, urgency and nocturia
Dysuria (typically “burning” pain).
Suprapubic pain/tenderness
Foul smelling/cloudy urine.

Strangury – painful, frequent urination of small volume, expelled only by straining despite a severe sense of urgency.

Haematuria
Eventually confusion, lethargy and fatigue – signs of urosepsis.

91
Q

Lower UTI - investigations

A

Urine dipstick – double positive nitrites and leucocytes.

Midstream urine culture and sensitivity – confirms diagnosis if >10^5 pathogenic organisms per mL.

–
Symptomatic women - empirical treatment is started if nitrites and leucocytes are positive on dipstick.

Women should have MCS sent in certain situations, and men should have MCS sent in all suspected UTI.

92
Q

What should be ruled out before starting empirical UTI treatment?

A

Check for vaginal discharge to rule out STI

93
Q

When is renal tract imaging needed in lower UTI?

A 
in children, 
persistent symptoms, 
recurrent UTIs, 
if ?pyelonephritis, 
if an unusual organism is grown
94
Q

What is the difference between persistent UTI symptoms and recurrent UTI?

A

Persistent symptoms – symptoms after more than 48-72 hours of antibiotic treatment.

Recurrent UTI – within a few weeks of appropriate treatment.

95
Q

What is sterile pyuria and what are the causes?

A

= raised WBCs in urine, but no organism grown

  • Recently treated UTI
  • Appendicitis
  • TB
  • Chlamydia
  • Bladder cancer
96
Q

Lower UTI - treatment

A

Lifestyle advice – personal hygiene, drinking plenty of fluids, urinating often.

Simple uncomplicated UTIs are treated with antibiotics:
Most commonly Trimethoprim or Nitrofurantoin (though resistance is increasing)
• 3-day course for women (100mg b.d.)
• 7-day course for men (100mg b.d.)

Symptomatic control (for pain) - NSAIDs/paracetamol

If problems with recurrent UTIs, sometimes put on prophylactic Abx but might need further investigations.

97
Q

Clinical features of upper UTI

A 
Dysuria (typically “burning” pain).
Frequency
Flank pain > suprapubic pain
Haematuria
High grade fever
Nausea and vomiting

Usually acute onset and systemically unwell.

98
Q

Upper UTI - investigations

A

Urine dip and MCS still key but additional investigations needed

Bloods -
=> FBC – raised WCC and CRP
=> U&E – renal function maintained? AKI?

Blood cultures?

Imaging
=> USS KUB - 1st line, can help identify obstruction, inflammatory changes and hydronephrosis.
=> CT
=> DMSA scan

99
Q

when is CT generally avoided in investigating upper UTI?

A

in children or pregnant women due to radiation

100
Q

What does a DMSA scan do?

A

allows for detailed imaging of the renal cortices and helps clarify areas of poor renal function and scarring

101
Q

Upper UTI - Treatment

A

If severe symptoms, patients will need to be admitted to hospital and have a 7-day course of IV antibiotics (cefuroxime or ciprofloxacin).

If not severely unwell, patients can have oral Abx for 7 days (ciprofloxacin, trimethoprim or co-amoxiclav).

Drink lots of fluid to prevent dehydration.

May need imaging (USS KUB) to look for structural damage or changes

102
Q

Complications of upper UTI

A

Sepsis
AKI > CKD
Perinephric abscess
Renal papillary necrosis

103
Q

What are the possible causes of ureteric obstruction?

A 
Stones 
Clots
Severe constipation (more common in children)
Enlargement of prostate
Strictures
Malignancy
Pregnancy

Congenital abnormalities
=> Duplicated ureters, ureterocoele, connection abnormalities

104
Q

What is the most common cause of ureteric obstruction?

A

Ureteric Stones

105
Q

When can ureteric clots occur?

A

can form when large amounts of blood are passing into the urine (e.g. in renal malignancy)

106
Q

When can ureteric strictures occur?

A

following previous injury (e.g. previous stone)

following infections (particularly recurrent).

107
Q

Acute ureteric obstructions

A

Stones
Clots
Severe constipation

108
Q

Chronic ureteric obstructions

A 
Enlarged prostate
Strictures
Malignancy
Pregnancy
Congenital abnormalities
109
Q

Luminal ureteric obstruction

A

Stones
Clots
TCC of renal pelvis
Bladder tumour

110
Q

Mural ureteric obstruction

A

Ureteric stricture
Congenital pelviureteric neuromuscular dysfunction
Congenital mega-ureter

111
Q

Extra-mural ureteric obstruction

A 
Pelviureteric compression
 (due to external tumours, diverticulitis, AAA, retroperitoneal fibrosis)
112
Q

Clinical features of ureteric obstruction

A 
Symptoms:
•	Pain – “ureteric colic”
•	N+V
•	Frank haematuria
•	Difficulty passing urine
•	Recurrent UTIs
Signs:
•	Frequency
•	Oliguria
•	Haematuria
•	Hypertension
•	Pyrexia
•	Rigors
113
Q

Where are the 3 sites of ureteric constriction?

What is the clinical relevance of these points?

A
  1. Pelviureteric Junction
  2. Pelvic Brim
  3. Vesicoureteric Junction

= the 3 common sites where stones can get lodged

114
Q

Risk factors for urolithiasis

A

More common in males (3:1)
More common in affluent areas

Anatomical abnormalities
=> E.g. horseshoe kidney, ureteral stricture

HTN
Gout
Hyperparathyroidism
Immobilisation
Dehydration
Metabolic disorders
115
Q

What can renal/ureteric stones consist of (most to least common)?

A
  1. Calcium
  2. Urate
  3. Struvite - magnesium, ammonium, phosphate
  4. Cysteine
116
Q

What are the risk factors for calcium stones?

A

Low urine volume

Hypercalciuria (e.g. primary parahyperthyroidism).

117
Q

What are the risk factors for urate stones?

A

high levels of blood purines from diet (increased red meat) or haematological disorders

118
Q

Which ureteric/renal stones are radiolucent?

A

urate stones

119
Q

Staghorn calculi

A

where the the renal pelvis and calices are filled with stone to give a “stag horn” appearance

120
Q

What are the risk factors for cysteine stones?

A

associated with familial disorders of cysteine metabolism

121
Q

What is the cause of ureteric colic?

A

occurs due to increased peristalsis around the site of the obstruction.

the pain radiates down to the testis, scrotum, labia or anterior thigh

122
Q

Investigation of Ureteric Obstruction

A

BLOODS – FBC, U&Es, CRP, LFTs, coag, calcium, phosphate, glucose, bicarbonate and urate levels

Urine dip - blood? infection?
(including bHCG)

Urine MCS

Abdominal exam

Imaging - AXR, renal tract USS, Non-contrast CT KUB

123
Q

what is the gold-standard imaging modality for ureteric obstruction?

A

Non-contrast CT KUB

124
Q

Causes of true frank haematuria

A 
Malignancy of renal tract
Stones
Infection
Nephritis
Bleeding disorders (incl. over-coagulation)
Trauma
125
Q

Causes of apparent (i.e. not true) frank hematuria

A

Menstruation
Dyes
Some drugs (e.g. rifampicin)

126
Q

Spontaneous passing of renal stones

A

~ 80% pass spontaneously (esp if <5mm or in lower ureter)

can take 1-3 weeks

Fluid resuscitation + analgesia (buscopan as antispasmodic?)

Abx if infection

127
Q

Management of large renal stone (>5mm)

A

ESWL - sonic waves are used to break up the stone

Percutaneous nephrolithotomy (PCNL) 
=> for complex renal calculi and staghorn calculi.

Endoscopic removal

Open surgery

128
Q

When should hospital admission be considered in renal stones?

A
  1. Post-renal AKI
  2. Uncontrollable pain from simple analgesics
  3. Evidence of infection or shock.
  4. Stone >5mm
129
Q

Complications of renal stones?

A

Acute obstruction – infection, post-renal AKI.

Recurrent/chronic obstruction – CKD, renal scarring

130
Q

what temporary measures can be done to relieve obstruction and avoid renal damage?

A
  1. Retrograde stent insertion:
    => Placement of a stent within the ureter, allows the ureter to be kept patent and temporarily relieve the obstruction.
  2. Nephrostomy
    => A tube placed directly through the skin on the back, into the renal pelvis and collecting system, relieving the obstruction proximally.
131
Q

Renal cell carcinoma - presentation

A

60% of patients have haematuria

Other symptoms include mild loin discomfort and a loin mass.

132
Q

Renal cell carcinoma - pathophysiology

A

Invades along the renal vein to the IVC and spreads via haematological route.

Forms PTH-related protein, so patients may get pathological fractures.

133
Q

Renal cell carcinoma - diagnosis

A

Typically forms a solid mass on USS; also seen on CT scan

Bloods commonly show anaemia and may show a raised ALP and/or ESR

134
Q

Renal cell carcinoma - treatment

A

Radical nephrectomy

No role for chemo/radiotherapy (ineffective)

Tyrosine Kinase inhibitors can be useful; as can renal artery embolisation

135
Q

Renal cell carcinoma - prognosis

A

Classically causes cannonball lung metastases.

Even T1 disease has only 70% 5-year survival prognosis.

Average survival with mets is <2 years.

136
Q

What are common causes of bladder outlet obstruction?

A 
Benign Prostatic Hypertrophy (BPH)
Bladder stones
Urethral strictures
Prostate cancer
Tumours of the rectum, uterus, or cervix.
137
Q

What are risk factors for bladder stones?

A

due to stasis of urine

=> such as in chronic retention, infection, obstructive uropathy of other aetiology, and catheters.

138
Q

Bladder stones - presentation

A

Lower Urinary Tract Symptoms

Chronic irritation of bladder epithelium increases transitional cell carcinoma risk

139
Q

Bladder stones - investigation

A

As for renal stones

140
Q

Bladder stones - management

A

Cystoscopy
Stone drainage
Lithotripsy

141
Q

Bladder cancer - presentation

A

Typically painless haematuria (+/- clots)
Recurrent UTI
Voiding symptoms
Pain from invasion of local structures.

142
Q

Risk factors for bladder cancer

A

Male, smoker, age >50, aromatic amines, schistosomiasis

143
Q

Bladder cancer - pathophysiology

A

= transitional cell carcinoma

Commonly due to prolonged carcinogen contact

Initially forms carcinoma in situ

144
Q

Bladder cancer - diagnosis

A

Screening undertaken of those who work in at-risk industries.

Usually diagnosed visually (with biopsies) on flexi-cystoscopy.

145
Q

Which industries are considered “at risk” of bladder cancer?

A

Rubber/plastic/dye industry workers

146
Q

Bladder cancer - treatment and prognosis

A

Cystoscopic removal of the tumour +/- intravesical BCG

In extensive cases – radical cystectomy

Need to look for parallel primaries in the entire urinary tract. 50% change of recurrence so follow-up is life-long

147
Q

Benign Prostatic Hyperplasia

A

Benign nodular/diffuse proliferation of the glandular layers of the prostate, leading to enlargement of the inner transitional zone

Common in middle-aged men

148
Q

BPH - symptoms

A

Symptoms occur due to urethral compression:

Hesitancy
Poor flow
Terminal dribbling
Frequency and nocturia
UTI
Retention (less common)
149
Q

BPH - Complications

A 
UTI
Overflow incontinence
Bladder calculi
Bladder diverticulae
Bilateral hydronephrosis and renal failure
150
Q

BPH - treatment

A

Acute retention – attempt urethral catheter drainage

If symptoms are mild – “watch and wait”

Medical management with alpha-blockers or 5alpha-reductase inhibitors

If medical management fails, then Trans-urethral resection of the prostate

151
Q

Prostate cancer - presentation

A

Most commonly raised PSA (but 20% have normal PSA)

Often asymptomatic
PR exam – hard and craggy prostate

152
Q

Where does prostate cancer commonly metastasise to?

A

bone

iliac/para-aortic nodes.

153
Q

Prostate cancer - treatment

A

T1/2 = active surveillance.

T 3/4 = radiotherapy or surgery

154
Q

Apart from prostate cancer, what else can affect PSA levels ?

A

mountain biking, infection, recent intercourse (48h), cystoscopy

155
Q

Gleason Grade of prostate cancer

A

Two areas of tissue are graded out of 5 to give a combined score out of 10.

Vital for prognosis

<7 = low risk; 
>7 = high risk.
156
Q

what might an enlarged prostate with a deep sulcus suggest?

A

benign prostatic hyperplasia

157
Q

what might an enlarged and very tender prostate suggest?

A

(acute/chronic) prostatitis

158
Q

what might an enlarged prostate with a rough nodule suggest?

A

unilateral prostate cancer

159
Q

what might a hard, asymmetrical and irregular prostate with an impalpable sulcus suggest?

A

prostate cancer

160
Q

what are some things to comment on when examining the prostate in a PR exam?

A 
Size – normal size? 
Sulcus – normal central sulcus? 
Symmetry – are the lobes symmetrical? 
Consistency – smooth/irregular? 
Any pain on palpation?

CP1 (12 decks)

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