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Phase 2A > Genitourinary tract > Flashcards

Genitourinary tract Flashcards

1
Q

what are the functions of the kidney?

A
  • filter or secrete waste/excess substances
  • maintains acid-base balance
  • retains albumin and circulating cells
  • reabsorbs glucose, amino acids and bicarbonates
  • controls BP, fluid status and electrolytes
  • activates 25-hydroxy vitamin D (by hydroxylating it to form 1,25 dihydroxy vitamin D)
  • synthesises erythropoietin
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2
Q

what is the GFR?

A

glomerular filtration rate

  • the volume of fluid filtered from the glomeruli into Bowman’s space per unit time (minutes)
  • 120ml/min = 7.2L/h = 170L/day
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3
Q

what is the creatinine clearance rate?

A
  • volume of blood plasma that is cleared of creatinine per unit time
  • useful measure for approximating the GFR
  • creatinine clearance exceeds GFR due to creatinine secretion, which can be blocked by cimetidine
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4
Q

what is reabsorbed in the proximal tubule?

A
  • 2/3rds of salt and water (via Na/K ATPase pump)
  • 100% of organic solutes (glucose, amino acids, inorganic phosphate)
  • 65% of potassium
  • 50% of urea
  • 80% of phosphate
  • 70-90% of citrate
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5
Q

what is Fanconi syndrome? what does it lead to?

A
  • syndrome of inadequate reabsorption in the proximal renal tubules
  • affects the PCT and proximal straight tubule
  • glycosuria
  • acidosis with failure of urine acidification
  • phosphate wasting resulting in rickets/osteomalacia
  • aminoaciduria
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6
Q

what are some causes of Fanconi syndrome?

A
  • cytinosis
  • Wilson’s
  • tenofovir
  • congenital or acquired diseases
  • toxicity
  • ADRs
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7
Q

what is reabsorbed in the loop of Henle?

A
  • thin descending limb has low permeability to ions and urea, and is highly permeable to water
  • thin ascending limb is impermeable to water but permeable to ions
  • ascending limb reabsorbs sodium, potassium and chloride via NKCC2, and magnesium and calcium
  • cortical thick ascending limb drains urine into the DCT
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8
Q

what is reabsorbed in the DCT?

A
  • regulates pH by absorbing bicarbonate and secreting protons, or by absorbing protons and secreting bicarbonate
  • secretes potassium and absorbs sodium (mediated by aldosterone and WNK kinases)
  • reabsorbs calcium (mediated by PTH)
  • expresses arginine vasopressin receptor 2
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9
Q

what is the function of the collecting duct?

A
  • does salt handling; by this point, most of the salt has been reabsorbed
  • tightly regulated by aldosterone (aldosterone increases the transcription of eNac channels which absorb Na+ in exchange for K+)
  • secrete K+ and H+ into the urine
  • water handling is also done here and water is absorbed via aquaporin 2 channels (regulated by vasopressin)
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10
Q

what are features of renal potassium control?

A
  • K+ is freely filtered and mostly reabsorbed in the proximal tubule/loop of Henle
  • distal tubule secretion determines renal excretion
  • insulin and catecholamines drive cellular K+ uptake, buffering acute changes
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11
Q

what renal medication causes hypokalaemia?

A
  • loop diuretics

- thiazide diuretics

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12
Q

what renal medication causes hyperkalaemia?

A
  • spironolactone (aldosterone antagonist)
  • amiloride (acts on eNac channels)
  • ACE inhibitors
  • angiotensin receptor blockers (ARB)
  • trimethoprim (acts on eNac channels but milder)
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13
Q

how can diuretics affect kidney disease?

A
  • diuretics are not nephrotoxic but hypovolaemia is (which they can cause)
  • in advanced kidney disease you require huge amounts of diuretics to do the work
  • thiazide and loop diuretics are extremely powerful and effective together resulting in profound diuresis
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14
Q

what happens if plasma is too concentrated?

A

if things are too concentrated then ADH is released resulting in increased aquaporins in the collecting duct and thus more water is absorbed, thereby diluting plasma

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15
Q

what are features of erythropoietin in the kidney? when is anaemia seen?

A
  • the renal cortex acts as an oxygen sensor; blood flow and oxygen requirement (GFR) are matched
  • anaemia is mainly seen after eGFR < 30
  • erythropoietin is hormone that produces haemoglobin, it is produced in response to tissue hypoxia
  • in advanced kidney disease and anaemia, erythropoietin will be given to help increase O2 transport
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16
Q

what is the process of vitamin D hydroxylation in the kidneys?

A

it takes 25-hydroxy vitamin D and hydroxylates it to form 1,25-dihydroxy vitamin D (calcitriol) by the enzyme 1alpha hydroxylase - this is the active form of vitamin D

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17
Q

what are the actions of calcitriol?

A
  • increases Ca2+ and phosphate absorption from the gut
  • increases phosphate absorption to a lesser extent
  • suppresses parathyroid hormone (PTH)
  • deficiency results in secondary hyperparathyroidism
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18
Q

how does deficiency of calcitriol result in secondary hyperparathyroidism?

A
  • low vitamin D results in low Ca2+ and phosphate resulting in increased PTH which causes Ca2+ and phosphate leeching out of the bones
  • PTH also acts on osteoclasts by increasing their activity and thus increasing their turnover resulting in reduced bone quality
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19
Q

what is the function of the lower urinary tract?

A

to convert the continuous process of excretion (urine production) to an intermittent, controlled volitional process (micturition)

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20
Q

what are the essential features of the lower urinary tract?

A
  • low pressure and insensible storage of urine of adequate capacity
  • prevents leakage of the urine stored
  • allows rapid, low-pressure voiding at an appropriate time and place
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21
Q

what is the pressure like in the kidney?

A
  • mean arterial pressure 60-70mmHg drives filtration in the Bowman’s capsule
  • there is progressive reduction in pressure along the nephron due to reabsorption, until at the collecting system pressure is 3-10mmHg
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22
Q

what is the neural control of voiding?

A
  • pontine micturition centre stimulates excitatory control to detrusor nucleus and inhibits Onuf’s nucleus
  • signal is transmitted from spinal root S3,4,5 via the parasympathetic nervous system and this results in contraction of detrusor muscles and relaxation of the urethra
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23
Q

what is the neural control of storage?

A
  • pontine storage centre stimulates and sends inhibitory signals to detrusor muscles and excitatory signals to Onuf’s nucleus
  • signal is transmitted from spinal root T10, L1 and L2 via the sympathetic nervous system and this results in the relaxation of the bladder and contraction of the urethral sphincter
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24
Q

what is the function of the sacral micturition centre?

A

at the sacral micturition centre there is a reflex that, when bladder is full it initiates voiding - this is inhibited by conscious parts of the brain:
• if the cord is cut above S2,3,4 then will only urinate when the bladder is full, but the descending pathway will not be able to inhibit this with the brain as descending pathway will be destroyed

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25
Q

what occurs in voiding? is it parasympathetic or sympathetic?

A
  • detrusor muscle contraction of bladder

- parasympathetic (cholinergic) - S3, S4, S5

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26
Q

what occurs in storage? is it parasympathetic or sympathetic?

A
  • urethral contraction
  • inhibition of detrusor muscle contraction of bladder
  • sympathetic (noradrenergic) - T10, L1, L2
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27
Q

what is the histology of the bladder?

A

has urothelium (transitional epithelium):
• highly specialised stratified, 3-7 cells thick
• umbrella structure that is completely impermeable so cannot resorb urine
• able to fold and unfold to increase volume

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28
Q

what is the difference between women and men in urethras? what does this mean?

A
  • men have a greater voiding pressure due to them having a longer urethra; more likely to develop retention
  • women have a shorter urethra with lower resistance and thus higher flow rates; more likely to develop incontinence
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29
Q

what are renal stones?

A
  • nephrolithiasis/urolithiasis
  • renal stones (calculi) consist of crystal aggregates; stones form in collecting ducts and may be deposited anywhere from the renal pelvis to the urethra
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30
Q

where do renal stones classically occur?

A

occur classically at these 3 narrowings:

  • pelviureteric junction
  • pelvic brim
  • vesicoureteric junction
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31
Q

what is the epidemiology of renal stones?

A
  • incidence is increasing
  • 10-15% lifetime risk
  • peak age is between 20-40 yrs
  • more common in males than females
  • unusual in children
  • more than 50% lifetime risk of recurrence once you’ve had them
  • most stones are composed of calcium oxalate and phosphate
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32
Q

what are risk factors and aetiology of renal stones?

A
  • anatomical abnormalities that predispose to stone formation e.g. obstruction or trauma
  • chemical composition of urine that favours stone crystallisation
  • dehydration resulting in a concentrated urine
  • infection
  • hypercalcaemia, hyperoxaluria, hypercalciuria, hyperuricaemia
  • primary renal disease e.g. polycystic kidneys or renal tubular acidosis
  • drugs e.g. diuretics, antacids, acetazolamide, corticosteroids, aspirin, allopurinol, vitamin C and D
  • diet e.g. chocolate, tea, strawberries, rhubarb all increase oxalate levels
  • gout
  • family history
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33
Q

what are types of renal stones?

A

renal stone/calculi form from crystals in supersaturated urine:
• calcium oxalate are the most common stones (60-65%)
• calcium phosphate stones are uncommon (10%)

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34
Q

what are causes of hypercalcuria?

A
  • hyperparathyroidism resulting in hypercalcaemia
  • excessive dietary intake of Ca2+
  • idiopathic hypercalciuria - increased absorption in gut
  • primary renal disease such as polycystic kidneys or medullary sponge kidney
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35
Q

what are causes of hyperoxaluria?

A
  • high dietary intake of oxalate rich food e.g. spinach, rhubarb, chocolate and tea
  • low dietary Ca2+ resulting in decreased binding of oxalate (by Ca2+) so increased oxalate absorption and urinary excretion
  • increased intestinal resorption due to GI disease e.g. Crohn’s
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36
Q

what are causes of uric acid stones?

A
  • associated with hyperuricaemia with/without gout
  • dehydration
  • patients with ileostomies are at particular risk, both from dehydration and from bicarbonate loss from GI secretion resulting in the production of an acidic urine (uric acid is more soluble in alkaline than acidic) thereby stimulating stone formation
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37
Q

what causes infection-induced kidney stones?

A
  • mixed infective stones are composed of magnesium ammonium phosphate as well as calcium
  • these are often large
  • usually due to UTI with an organism such as Proteus mirabilis that hydrolyses urea forming ammonium hydroxide
  • the increased ammonium ions and the alkalinity both favour stone formation
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38
Q

what are cystine stones caused by?

A
  • caused by cystinuria

* this results in excessive urinary excretion and formation of cysteine stones

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39
Q

what is clinical presentation of kidney stones?

A
  • most are asymptomatic
  • renal colic
  • loin pain
  • if urinary tract is obstructed then fluid/diuretics make the pain worse as peristaltic flow increases
  • bowel sounds may be reduced
  • BP may be low
  • dysuria, strangury, frequency
  • recurrent UTI’s
  • haematuria
  • acute pyelonephritis
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40
Q

what is the clinical presentation of renal colic?

A
  • rapid onset - woken from sleep
  • pain that results from upper urinary tract obstruction
  • excruciating ureteric spasms
  • pain is from loin to groin and comes and goes in waves as the ureters peristalise
  • associated with nausea and vomiting
  • worse with fluid loading
  • radiates to groin and ipsilateral testis/labia
  • often cannot lie still (differentiates from peritonitis)
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41
Q

what are differential diagnoses of kidney stones?

A
  • vascular accident e.g. ruptured AAA if over 50 yrs until proven otherwise
  • bowel pathology e.g. diverticulitis or appendicitis
  • ectopic pregnancy or ovarian cyst torsion
  • testicular torsion can present with loin pain and nothing else
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42
Q

what is used to diagnose kidney stones?

A
  • history and examination
  • urine dipstick
  • mid-stream specimen of urine sent for microbiology culture and sensitivity
  • bloods
  • KUBXR
  • NCCT-KUB
  • ultrasound
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43
Q

how is a urine dipstick used to diagnose kidney stones?

A
  • usually positive for blood - haematuria

* also looks for red cells, protein and glucose

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44
Q

how is KUBXR used to diagnose kidney stones?

A

Kidney Ureter Bladder X-ray
• first line investigation
• 80% sensitive
• see stone in line of renal tract

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45
Q

how is NCCT-KUB used to diagnose kidney stones?

A

non-contrast CT kidney ureter bladder
• gold standard
• very rapid
• 99% sensitive for stones - diagnostic
• no contrast so no renal damage or allergy
• but no functional info and gives radiation dose equivalent to 18 months background radiation

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46
Q

how is ultrasound used to diagnose kidney stones?

A
  • shows kidney stones and renal pelvis dilatation well but ureteric stones can be missed
  • sensitive for hydronephrosis
  • very poor at visualising stones in ureter
  • useful in pregnant and younger recurrent stone-formers
  • rarely used acutely
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47
Q

what is the treatment of kidney stones?

A
  • strong analgesic
  • antibiotics if infection e.g. IV cefuroxime or IV gentamicin
  • antiemetics to prevent vomiting
  • observe for sepsis
  • stones less than 5mm in lower ureter 90% pass spontaneously
  • medical expulsive therapy (oral nifedipine or alpha blocker)
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48
Q

what is the treatment if kidney stones are still not passing?

A
  • extracorporeal shockwave lithotripsy; ultrasound fragments stone
  • endoscopy with YAG - laser for larger stones
  • percutaneous nephrolithotomy; keyhole surgery to remove stones that are large, multiple or complex
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49
Q

how can kidney stones be prevented from recurring?

A
  • overhydration
  • normal/low Ca2+ dietary intake
  • low salt diet
  • normal daIry intake
  • reduce BMI
  • reduction in animal proteins
  • active lifestyle
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50
Q

how can uric acid stones be prevented from recurring?

A
  • can be caused by long term allopurinol use
  • only form in acid urine
  • deacidification of urine e.g. oral sodium bicarbonate to alkalinise urine
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51
Q

how can cysteine stones be prevented from recurring?

A
  • overhydration
  • urine alkalisation
  • cysteine binders e.g. captopril
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52
Q

what is the definition of acute kidney injury/acute renal failure?

A

an abrupt (over hours to days) sustained rise in serum urea and creatinine due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis - it is usually but not always reversible or self-limiting

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53
Q

what is the RIFLE classification?

A
  • old system that was used to define AKI
  • uses either an increase in serum creatinine (SCr) or a decrease in urine output
  • RIFLE describes three levels of renal dysfunction (RIF) and two outcome measures (LE) - these criteria indicate an increasing degree of renal damage and have a predictive value for mortality
  • risk, injury, failure, loss, end-stage renal disease
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54
Q

what is the GFR and urine output criteria for the Risk category of RIFLE for AKI?

A

GFR criteria: 1.5 fold increase in creatinine or GFR decrease >25%

urine output criteria: UO <0.5 ml kg^-1 h^-1 x6h

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55
Q

what is the GFR and urine output criteria for the Injury category of RIFLE for AKI?

A

GFR criteria: 2 fold increase in creatinine or GFR decrease >50%

urine output criteria: UO <0.5 ml kg^-1 h^-1 x12h

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56
Q

what is the GFR and urine output criteria for the Failure category of RIFLE for AKI?

A

GFR criteria: 3 fold increase of GFR decrease >75% or creatinine >4mg per 100ml (acute rise of >0.5mg per 100ml dl)

urine output criteria: UO <0.3 ml kg^-1 h^-1 x24h or anuria x12h

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57
Q

what is the criteria for the Loss category of RIFLE for AKI?

A

persistent ARF = complete loss of kidney function >4hrs

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58
Q

what is the criteria for the ESKD category of RIFLE for AKI?

A

end-stage kidney disease (>3 months)

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59
Q

what is the KDIGO classification for AKI?

A
  • staging system for AKI used currently

- also uses serum creatinine and urine output to assess severity

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60
Q

what is the serum creatinine (sCr) criteria for AKI in the KDIGO classification?

A
  1. increase >26umol/L in 48hrs OR increase >1.5 x baseline
  2. increase 2-2.9 x baseline
  3. increase >3 x baseline OR >354umol/L OR commenced on RRT irrespective of stage
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61
Q

what is the urine output criteria for AKI in the KDIGO classification?

A
  1. <0.5mL/kg/h for >6 consecutive hours
  2. <0.5mL/kg/h for >12hrs
  3. <0.3mL/kg/h for >24hrs or anuria for 12hrs
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62
Q

what is the epidemiology of AKI?

A
  • AKI is common, occurring in 18% of hospital patients
  • about 25% of patients with sepsis and 50% of patients with septic shock will have AKI
  • severe AKI (creatinine > 500μmol/L, often requiring dialysis) affects about 130-140 per million population per year
  • common in the elderly
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63
Q

what is AKI associated with?

A
  • diarrhoea
  • haematuria
  • haemoptysis
  • hypotension
  • urine retention
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64
Q

what are the causes of AKI?

A
  • commonest are ischaemia, sepsis and nephrotoxins
  • pre-renal (40-70%)
  • intrinsic renal (10-50%); required renal biopsy for diagnosis
  • post-renal (10-25%)
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65
Q

what are causes of pre-renal (40-70%) AKI?

A
  • renal hypoperfusion e.g. hypotension (due to hypovolaemia or sepsis) resulting in a drop in GFR
  • hypovolaemia of any cause - dehydration or haemorrhage
  • hypotension without hypovolaemia - cirrhosis or septic shock
  • low cardiac output - cardiac failure or cardiogenic shock
  • renal hypoperfusion - NSAIDs, ACE inhibitors
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66
Q

what are the causes of intrinsic renal AKI (10-50%)?

A
  • renal parenchyma damage
  • acute tubular necrosis - commonest renal cause of AKI, caused by pre-renal damage or nephrotoxins e.g. NSAIDs, radiological contrast, uric acid crystals, myeloma and increased Ca2+
  • vascular
  • glomerular
  • interstitial
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67
Q

what are vascular causes of intrinsic renal AKI?

A
  • renal artery/vein thrombosis
  • cholesterol/thrombus emboli from angiography
  • vasculitis e.g. in SLE
  • haemolytic uraemic syndrome - thrombotic microangiopathy; haemolytic anaemia and reduced platelets
  • malignant hypertension
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68
Q

what are glomerular causes of intrinsic renal AKI?

A
  • glomerulonephritis or nephrotic syndrome

- autoimmune (SLE), drugs, infections

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69
Q

what are interstitial causes of intrinsic renal AKI?

A

drugs, infiltration with e.g lymphoma, infection, tumour lysis syndrome following chemo

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70
Q

what are causes of post-renal (10-25%) AKI?

A
  • urinary tract obstruction at ureter, bladder or prostate
  • luminal: stones, clots or sloughed papillae
  • mural (wall)
  • extrinsic compression from malignancy especially from pelvis or due to retroperitoneal fibrosis
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71
Q

what are causes of mural post-renal AKI?

A
  • malignancy e.g. ureteric, bladder or prostate
  • benign prostate hyperplasia (BPH)
  • strictures
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72
Q

what are risk factors for AKI?

A
  • age > 75 yrs
  • heart failure
  • peripheral vascular disease
  • chronic liver disease
  • sepsis
  • poor fluid intake/increased losses
  • history or urinary symptoms
  • chronic kidney disease (CKD) especially if GFR < 60
  • past history of AKI
  • hypovolaemia
  • haematological malignancy
  • diabetes
  • prostate cancer
  • nephrotoxic drugs
  • repeated use of radiological contrast
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73
Q

what is the clinical presentation of AKI?

A
  • depends on underlying cause or severity
  • on examination there may be palpable bladder, palpable kidneys, abdominal/pelvic masses, rashes
  • oliguria occurs in early sages
  • arrhythmias due to hyperkalemia
  • breathlessness occurs from a combination of anaemia and pulmonary oedema secondary to volume overload
  • pericarditis occurs with severe untreated uraemia and may be complicated by a pericardial effusion, tamponade or pericardial rub
  • impaired platelet function causes bruising and GI bleeding
  • infection due to immune suppression
  • postural hypotension
  • oedema
  • thirst - indicated fluid depletion and dehydration (possible cause of AKI)
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74
Q

what are differential diagnoses of AKI?

A

abdominal aortic aneurysm, alcohol toxicity, alcoholic and diabetic ketoacidosis, chronic renal failure, dehydration, GI bleed, heart failure, metabolic acidosis

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75
Q

when should you suspect chronic kidney disease?

A

small kidneys on ultrasound, anaemia, low Ca2+, high phosphate or high creatinine/low GFR

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76
Q

how is a urine dipstick used to diagnose AKI?

A

can suggest infection (leucocytes + nitrites) and glomerular disease (blood + protein)

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77
Q

how is blood count used to diagnose AKI?

A

anaemia and very high ESR suggests myeloma or vasculitis as underlying cause

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78
Q

what is used to exclude infection in AKI?

A
  • urine and blood cultures to exclude infection

- mid-stream-specimen of urine sent for microbiology culture and sensitivity

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79
Q

how is ultrasound used to diagnose AKI?

A
  • give assessment of renal size (very small indicates CKD)
  • can be used to distinguish obstruction and hydronephrosis and look for cysts, small kidneys (CKD), masses and corticomedullary differentiation (reduced in CKD)
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80
Q

how is CT-KUB used to diagnose AKI?

A
  • complete anuria is rare but if present it suggests obstructive cause
  • in elderly men this should be considered prostatic e.g BPH and can be relieved by catheterisation
  • if catheterisation does not relieve anuria then suspect obstruction above prostate
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81
Q

what is done when catheterisation does not relieve anuria? what does this suggest? what is looked for?

A
  • suspect obstruction above prostate
  • get an urgent ultrasound to look for hydronephrosis
  • get an urgent CT-KUB which can look for obstructing masses or calculi as well as retroperitoneal fibrosis
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82
Q

how is ECG used to diagnose AKI?

A

to look for hyperkalaemic changes

  • tall tented T waves
  • prolonged PR interval
  • widening QRS complex
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83
Q

how is CXR used to diagnose AKI?

A

to look for pulmonary oedema

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84
Q

how is renal biopsy used to diagnose AKI?

A
  • intrarenal causes of AKI

* perform for every patient with unexplained AKI and normal kidneys

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85
Q

what is the treatment of pre-renal AKI?

A
  • correct volume depletion with fluids

- treat sepsis with antibiotics

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86
Q

what is the treatment of intrinsic renal AKI?

A

refer early to nephrology if concern over tubulointerstitial or glomerular pathology

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87
Q

what is the treatment of post-renal AKI?

A
  • catheterise and consider CT of renal tract (CTKUB)
  • if signs of obstruction and hydronephrosis then do cystoscopy and retrograde stents or nephrostomy insertion; this buys time to allows treatment of cause of obstruction
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88
Q

what are some nephrotoxic drugs?

A
  • NSAIDs
  • ACE-inhibitor
  • gentamicin
  • amphotericin
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89
Q

what is the treatment of hyperkalaemia in AKI?

A
  • calcium gluconate; cardioprotective
  • insulin to drive K+ into cells with glucose and dextrose to prevent hypoglycaemia
  • use dialysis or haemofiltration
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90
Q

what is the treatment of AKI?

A
  • hyperkalaemia treatment
  • diuretics or dialysis/haemofiltration for pulmonary oedema
  • sodium and potassium restriction and vitamin D supplied
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91
Q

what are indications for dialysis in AKI?

A
  • symptomatic uraemia including pericarditis or tamponade
  • hyperkalaemia not controlled by conservative measures
  • pulmonary oedema thats unresponsive to diuretics
  • severe acids
  • high potassium
  • tall T waves, low flat p waves, broad QRS or arrhythmias on ECG
  • metabolic acidosis
  • fluid overload that is resistant to diuretics
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92
Q

what are components of renal replacement therapy?

A

haemofiltration and haemodialysis

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93
Q

what are complications of RRT?

A
  • cardiovascular disease due to combination of hypertension and calcium/phosphate dysregulation
  • infection
  • amyloid accumulates in long-term dialysis and may cause carpal tunnel syndrome, arthralgia and fractures
  • malignancy is commoner in dialysis patients; may be due to causes of end-stage renal failure e.g. urothelial tumours
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94
Q

what is glomerulonephritis?

A

glomerulonephritis is a broad term that refers to a group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons

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95
Q

what does glomerulonephritis cause?

A
  • damage to the filtration mechanism resulting in haematuria and proteinuria
  • damage to the glomerulus restricts blood flow, leading to compensatory hypertension
  • loss of the usual filtration capacity leads to AKI
  • causes 25% of end stage kidney failure
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96
Q

how can glomerulonephritis present itself?

A
  • acute nephritic syndrome (acute glomerulonephritis)
  • nephrotic syndrome
  • asymptomatic urinary abnormalities; haematuria, proteinuria or both
  • chronic kidney disease (CKD)
  • haematuria; visible or non-visible (red cell casts seen on microscopy)
  • proteinuria (usually < 2g in 24hrs)
  • hypertension and oedema (periorbital, leg, or sacral)
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97
Q

what is acute nephritic syndrome often caused by?

A

often caused by an immune response triggered by an infection of other disease

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98
Q

what is the commonest primary cause of acute nephritic syndrome?

A

IgA nephropathy

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99
Q

what is the aetiology of acute nephritic syndrome?

A
  • bacterial infection e.g. MRSA, typhoid or secondary syphilis
  • Hepatitis B and C
  • schistomiasis
  • malaria
  • post-streptococcal infection e.g. Strep. pyogenes
  • infective endocarditis
  • SLE
  • systemic sclerosis
  • ANCA associated vasculitis
  • Goodpastures disease
  • IgA nephropathy
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100
Q

what are features of post-streptococcal infection as a cause of acute nephritic syndrome?

A
  • occurs classically 2 weeks after tonsillitis

* bacterial antigen becomes trapped in the glomerulus leading to diffuse proliferative glomerulonephritis

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101
Q

how can SLE cause acute nephritic syndrome? what is the clinical presentation of it?

A
  • rash, arthralgia, kidney failure, neurological symptoms, pericarditis and pneumonitis
  • anti-nuclear antibody (ANA) positive and double stranded DNA positive
  • low complement C3 and C4
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102
Q

what is the treatment of SLE as a cause of acute nephritic syndrome?

A

immunosuppression; steroids, cyclophosphamide, rituximab

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103
Q

how does systemic sclerosis cause acute nephritic syndrome? what is the clinical presentation?

A
  • ANA positive, Anti-Ro and Anti-La positive
  • severe hypertension
  • ‘onion skin’ changes on renal biopsy, raynauds phenomenon, fibrotic skin, oesophageal dysmotility
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104
Q

what is the treatment of ANCA associated vasculitis as a cause of acute nephritic syndrome?

A

immunosuppression, steroids, cyclophosphamide, rituximab, plasma exchange

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105
Q

what is Goodpastures disease?

A
  • anti-glomerular basement membrane disease
  • rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs and kidney failure
  • attacks alpha-3 subunit of type IV collagen
  • the co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage and the presence of circulating antibodies directed against an intrinsic antigen to the basement membrane of both kidney and lung
  • antibodies against glomerular basement membrane
  • rapidly progressive kidney failure
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106
Q

what is the treatment of Goodpastures disease?

A
  • remove antibody via plasma exchange
  • immunosuppression
  • steroids/cyclophosphamide
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107
Q

what is the commonest cause of nephritic syndrome in the developed world?

A

IgA nephropathy

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108
Q

how does IgA nephropathy cause acute nephritic syndrome?

A
  • form of glomerulonephritis
  • deposition of IgA antibody in the glomerulus
  • haematuria, IgA deposition in kidney mesangium (provides structural support to glomerulus) and kidney gets attacked
  • associated with tonsillitis and results in haematuria
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109
Q

what is the treatment of IgA nephropathy?

A

BP control: ACEi/ARBs

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110
Q

what is the clinical presentation of acute nephritic syndrome?

A
  • haematuria (mild macrocytic)
  • proteinuria; usually less than 2g in 24 hours
  • hypertension (moderate-severe increase) and oedema (periorbital (around eyes), leg or sacral) caused by salt and water retention
  • oliguria (little urine)
  • uraemia and symptoms of it
  • deteriorating kidney function
  • moderate-severe decrease in GFR
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111
Q

what are symptoms of uraemia?

A
  • anorexia
  • pruritus i.e rash
  • lethargy and nausea
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112
Q

how is acute nephritic syndrome diagnosed?

A
  • take history to determine cause
  • measure eGFR, proteinuria, serum urea and electrolytes and albumin to determine current status and monitor progress
  • culture; swab from throat or infected skin
  • urine dipstick to detect proteinuria and haematuria
  • renal biopsy if necessary
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113
Q

how is hypertension treated in acute nephritic syndrome?

A

salt restriction, loop diuretics, calcium channel blockers

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114
Q

what is the triad of nephrotic syndrome?

A
  • proteinuria > 3.5g/24 hours
  • hypoalbuminaemia
  • oedema
  • severe hyperlipidaemia is often present
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115
Q

why is severe hyperlipidaemia often present in nephrotic syndrome?

A

liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol

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116
Q

what is nephrotic syndrome? what is it caused by? what is kidney function like?

A
  • collection of symptoms due to kidney damage; includes protein in urine, low blood albumin levels, high blood lipids and significant swelling - don’t develop kidney failure but are leaking huge amounts of protein but kidney function remains the same
  • caused by structural and functional abnormalities of podocytes
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117
Q

what is the epidemiology of nephrotic syndrome?

A
  • relatively rare
  • diabetes is most common secondary cause
  • minimal change disease accounts for 10-25% of nephrotic syndrome in adults and is the commonest cause of nephrotic syndrome in children
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118
Q

what are the primary causes of nephrotic syndrome?

A
  • minimal change disease - seen in children and adults
  • membranous glomerulonephritis - adults
  • focal segmental glomerulosclerosis
  • membranoproliferative glomerulonephritis
  • rapidly progressive glomerulonephritis
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119
Q

what is the most common cause of nephrotic syndrome in adults?

A

focal segmental glomerulosclerosis

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120
Q

what is membranous nephropathy?

A
  • asymptomatic proteinuria/nephrotic syndrome +/- microscopic haematuria, hypertension and renal impairment
  • deposition of IgG and C3 along outer aspect of glomerular basement membrane
  • treated with immunosuppression
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121
Q

what are causes of membraneous nephropathy?

A
  • drugs e.g. penicillamine, gold or NSAIDs
  • autoimmune - SLE, thyroiditis
  • infection e.g. hepatitis B or C, schistomiasis
  • neoplasia e.g. lung, colon, stomach and breast
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122
Q

what is focal segmental glomerulosclerosis?

A
  • unknown aetiology
  • scarring that is focal and only some glomeruli involved and segmental (only part of glomerulus affected)
  • CD80 deposited in podocytes resulting in increased permeability in glomeruli and thus proteinuria and haematuria
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123
Q

what is clinical presentation of focal segmental glomerulosclerosis?

A

secondary hypertension and renal impairment

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124
Q

what is treatment of focal segmental glomerulosclerosis?

A

corticosteroids and immunosuppressants

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125
Q

what are secondary causes of nephrotic syndrome?

A
  • diabetes mellitus - most common secondary cause
  • amyloid
  • infections e.g. Hep B or C and HIV
  • SLE, RA
  • drugs e.g. gold, penicillamine, NSAIDs and ACE-inhibitors
  • malignancy
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126
Q

what is the most common secondary cause of nephrotic syndrome?

A

diabetes mellitus

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127
Q

what are risk factors for nephrotic syndrome?

A

diabetes mellitus

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128
Q

what is the pathophysiology of nephrotic syndrome?

A
  • injury to podocyte appears to be the main cause of proteinuria
  • podocytes wrap around the glomerular capillaries and maintain the filtration barrier, preventing large molecular weight proteins from entering the urine
  • damage to podocyte foot processes or loss of podocytes can cause heavy protein loss
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129
Q

what is the clinical presentation of nephrotic syndrome?

A
  • normal-mild increase in BP
  • proteinuria > 3.5g/day
  • normal-mild decrease in GFR
  • hypoalbuniaemia
  • pitting oedema of ankles, genital, abdominal wall and sometimes face (periorbital)
  • frothy urine
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130
Q

what are differential diagnoses of nephrotic syndrome?

A
  • congestive heart failure

- cirrhosis

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131
Q

how can congestive heart failure be distinguished from nephrotic syndrome?

A
  • where there is oedema and raised JVP

* in nephrotic syndrome there is normal or low JVP (unless there is renal failure and oliguria)

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132
Q

how can cirrhosis be distinguished from nephrotic syndrome?

A
  • where there is hypoalbuminaemia and oedema

* but there are signs of chronic liver failure e.g. jaundice, fever and loss of body hair

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133
Q

how is nephrotic syndrome diagnosed?

A
  • establish cause - usually via renal biopsy
  • urine dipstick shows very high protein
  • CXR or ultrasound for pleural effusion or ascites
  • serum albumin is low
  • BP is usually normal or mildly increased
  • renal function is usually normal or mildly impaired
  • serum creatinine, eGFR, lipids and glucose
  • ANA, double-stranded DNA antibody, C3 and C4 indicates SLE
  • antiphospholipase A2 receptor antibody indicated membranous nephropathy
  • HepB surface antigen, HepC antibody or HIV
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134
Q

what are metabolic/immunologic levels like in nephrotic syndrome?

A
  • serum creatinine, eGFR, lipids and glucose
  • ANA, double-stranded DNA antibody, C3 and C4 indicates SLE
  • antiphospholipase A2 receptor antibody indicates membranous nephropathy
  • HepB surface antigen, HepC antibody or HIV
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135
Q

what are complications of nephrotic syndrome?

A
  • susceptibility to infection
  • thromboembolism
  • hyperlipidaemia
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136
Q

what infections does nephrotic syndrome increase susceptibility to?

A

cellulitis, Streptococcus infections and spontaneous bacterial peritonitis

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137
Q

why does nephrotic syndrome cause increased susceptibility to infections?

A

due to low serum IgG, decreased complement activity and reduced T-cell function due in part to loss of immunoglobulin in urine and also to immunosuppressive treatment

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138
Q

how does nephrotic syndrome increase risk of thromboembolism?

A

hypercoaguable state due to increased clotting factors (produced by liver due to low albumin since liver goes into overdrive) and platelet abnormalities

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139
Q

how does nephrotic syndrome increase risk of hyperlipidaemia?

A

increased cholesterol and triglycerides due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin

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140
Q

what is the treatment of nephrotic syndrome?

A
  • reduce oedema
  • reduce proteinuria
  • reduce risk of complications
  • treat underlying cause
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141
Q

how is oedema reduced in nephrotic syndrome?

A
  • loop diuretics e.g. IV furosemide - IV since gut oedema may prevent oral absorption
  • thiazide diuretics e.g. IV bendroflumethiazide
  • fluid and salt restriction while giving diuretics
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142
Q

how is proteinuria reduced in nephrotic syndrome?

A
  • ACE inhibitor e.g. ramipril
  • angiotensin receptor blocker e.g. candesartan
  • eat normal rather than high protein diet
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143
Q

how is risk of complications reduced in nephrotic syndrome?

A
  • prophylactic anticoagulation with warfarin, especially when albumin is low (<20g/l)
  • reduce cholesterol with statins e.g. simvastatin
  • treat infections promptly and vaccinate
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144
Q

what is the most common cause of nephrotic syndrome in children?

A

minimal change disease

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145
Q

what is minimal change disease?

A

disease affecting the kidneys which causes nephrotic syndrome

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146
Q

what is the epidemiology of minimal change disease?

A
  • commonest cause of nephrotic syndrome in children
  • occurs most commonly in boys under the age of 5
  • accounts for 20% of adult nephritic syndrome
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147
Q

what are risk factors and causes of minimal change disease?

A
  • can be idiopathic
  • atopy is present in 30% of cases and allergic reactions can trigger nephrotic syndrome
  • drugs
  • Hep C, HIV and TB are rare causes
  • associated with Hodgkins lymphoma
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148
Q

what are drugs that can cause minimal change disease?

A
  • NSAIDs
  • lithium
  • antibiotics e.g. cephalosporins, rifampicin and ampicillin
  • bisphosphonates
  • sulfasalazine
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149
Q

what is the pathophysiology of minimal change disease?

A
  • glomeruli appear normal on light microscopy, but on electron microscopy, fusion of the foot processes of the podocytes is seen, consistent with a disrupted podocyte actin cytoskeleton
  • immature differentiating CD35 stem cells appear to be responsible for pathogenesis
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150
Q

what is the clinical presentation of minimal change disease?

A
  • proteinuria
  • oedema, predominantly around the face
  • fatigue
  • frothy urine
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151
Q

how is minimal change disease diagnosed?

A

biopsy
• normal under light microscopy
• electron microscopy shows fused podocyte foot processes

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152
Q

what is the treatment of minimal change disease?

A
  • high dose corticosteroids can reverse proteinuria in 95% cases, however the majority relapse
  • frequent relapse or steroid-dependent disease is treated with cyclophosphamide or ciclosporin/tacrolimus
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153
Q

what are asymptomatic urinary abnormalities? how is it diagnosed?

A
  • incidental finding of dipstick haematuria +/- proteinuria
  • kidney function and blood pressure are normal
  • diagnosis is usually clinical, don’t biopsy unless kidney function abnormal or significant proteinuria
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154
Q

what are causes of asymptomatic urinary abnormalities?

A
  • IgA nephropathy

- thin membrane disease

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155
Q

how does IgA nephropathy cause asymptomatic urinary abnormalities? what can it present as?

A
  • abnormality in IgA glycosylation leads to deposition in mesangium (provides structural support for glomerulus)
  • can present as nephritic, nephrotic, asymptomatic or as progressive chronic kidney disease
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156
Q

what is the commonest cause of glomerulonephritis worldwide?

A

IgA nephropathy

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157
Q

what is IgA nephropathy associated with?

A

tonsillitis and macroscopic haematuria

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158
Q

what is the treatment of IgA nephropathy?

A

treated with BP control and immunosuppression in aggressive disease

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159
Q

how does thin membrane disease cause asymptomatic urinary abnormalities?

A

thin basement membrane so more likely to leak blood into urine

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160
Q

what is chronic kidney disease? what is it defined as?

A
  • CKD is longstanding, usually progressive impairment in renal function (haematuria, proteinuria or anatomical abnormality) for more than 3 months
  • defined as a GFR < 60mL/min/1.73 m2 for more than 3 months with/without evidence of kidney damage (haematuria, proteinuria or anatomical abnormality)
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161
Q

what is the epidemiology of chronic kidney disease?

A
  • between 6% - 11% of people can be defined as having CKD
  • risk of CKD increases with age; incidence rising as we are living longer
  • more common in females than males
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162
Q

what is stage 1 CKD?

A
  • GFR >90mL/min

- normal or raised GFR with other evidence of renal damage

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163
Q

what is stage 2 CKD?

A
  • GFR 60-89mL/min

- slight decreased GFR with other evidence of renal damage

164
Q

what is stage 3 CKD?

A
  • 3A GFR: 45-59mL/min
  • 3B GFR: 30-44mL/min
  • moderate decreased GFR with or without evidence of other renal damage
165
Q

what is stage 4 CKD?

A
  • GFR 15-29mL/min

- severe decreased GFR with or without evidence of other renal damage

166
Q

what is stage 5 CKD?

A
  • GFR <15mL/min

- established renal failure

167
Q

what are signs of renal damage?

A

proteinuria, haematuria or evidence of abnormal anatomy or systemic disease

168
Q

what is the aetiology of CKD?

A
  • diabetes mellitus - Type II > Type 1
  • hypertension
  • atherosclerotic renal vascular disease
  • polycystic kidney disease
  • tuberous sclerosis
  • primary glomerulonephritides e.g. IgA nephropathy
  • SLE
  • amyloidosis
  • hypertensive nephrosclerosis (common in black africans)
  • small and medium-sized vessel vasculitis
  • family history of stage 5 CKD or hereditary kidney disease e.g. polycystic kidney disease
  • hypercalcaemia
  • neoplasma
  • myeloma
  • idiopathic - 20% cases
169
Q

what are risk factors for CKD?

A
  • diabetes mellitus
  • hypertension
  • old age
  • CVD
  • renal stones or benign prostatic hyperplasia (BPH)
  • recurrent UTI’s
  • SLE
  • proteinuria
  • AKI
  • smoking
  • African, Afro-Caribbean or Asian origin
  • chronic use of NSAIDs
170
Q

what is the pathophysiology of CKD?

A
  • in CKD, where many nephrons have failed, and scarred, the burden of filtration falls to fewer functioning nephrons
  • functioning (remnant) nephrons experience increased flow per nephron (hyperfiltration), as blood flow has not changed, and adapt with glomerular hypertrophy and reduced arteriolar resistance
  • increased flow, increased pressure and increased shear stress set in motion a vicious cycle of raised intraglomerular capillary pressure and strain, which accelerates remnant nephron failure
  • this increased flow and strain may be detected as new/increasing proteinuria
171
Q

what is the effect of reduced renal perfusion?

A

reduced renal perfusion

  • > decreased transglomerular pressure
  • > decreased GFR
172
Q

what is the response to reduced renal perfusion?

A

intrarenal activation of RAAS

  • > efferent arteriolar vasoconstriction
  • > increases transglomerular pressure
  • > restores GFR
173
Q

what are the effects of angiotensin II in CKD?

A

• produced locally, modulates intraglomerular capillary pressure and GFR, causing vasoconstriction of postglomerular arterioles, and increasing the glomerular hydraulic pressure and
filtration fraction
• by its effect on mesangial cells and podocytes, it increases the pore sizes and impairs the size-selective function of the basement membrane for macromolecules, resulting in increased proteinuria
• also modulates cell growth by upregulating TGF-beta, increasing collagen synthesis and epithelial cell
transdifferentiation to myofibroblasts, leading to excessive matrix formation
• also up regulates plasminogen activator inhibitor-1, which inhibits matrix proteolysis by plasmin, resulting in the accumulation of excessive matrix and scarring in the glomeruli and interstitium

174
Q

what does the prognosis of CKD correlate with?

A
  • hypertension - particularly if poorly controlled
  • proteinuria
  • degree of scarring in the interstitium on histology
175
Q

what is therapy for CKD aimed at?

A

aimed at inhibiting angiotensin II and reducing proteinuria mainly with ACE inhibitors or angiotensin receptor antagonists

176
Q

what is the clinical presentation of CKD?

A
  • malaise
  • anorexia and weight loss
  • Insomnia
  • nocturia and polyuria (>40ml/kg/24hours) due to impaired concentrating ability
  • itching
  • nausea, vomiting and diarrhoea
  • symptoms due to salt and water retention; peripheral or pulmonary oedema
  • amenorrhea in women and erectile dysfunction in men
  • increased risk of peptic ulceration, acute pancreatitis, hyperuricaemia and incidence of malignancy
177
Q

what is used as surrogates of accumulating metabolites in CKD? why?

A

serum urea and creatinine are used as surrogates of accumulating metabolites (uraemic toxins) since their measurement is easy and there is a rough correlation between toxins and them

178
Q

when are symptoms of CKD common?

A

symptoms are common when the serum urea concentration exceeds 40mmol/L but many patients develop uraemic symptoms at lower levels of serum urea

179
Q

what does CKD increase the risk of?

A

peptic ulceration, acute pancreatitis, hyperuricaemia and incidence of malignancy

180
Q

what are blood complications of CKD?

A

normochromic normocytic anaemia:

• due to reduced erythropoietin production by diseased kidney

181
Q

what are bone complications of CKD?

A

• bone pain
• renal osteodystrophy; osteomalacia, osteoporosis,
hyperparathyroidism
• renal phosphate retention and impaired 1,25-dihydroxy vitamin D production lead to a fall in serum Ca2+ and thus a compensatory increase in PTH which can result in skeletal decalcification leading to bone disease

182
Q

what are neurological complications of CKD?

A
  • occurs in almost all patients with severe CKD
  • autonomic dysfunction presents as postural hypotension and disturbed GI motility
  • polyneuropathy resulting in peripheral paraesthesiae and weakness
  • in advanced uraemia there is depressed cerebral function, myoclonic twitching and seizures
183
Q

what are cardiovascular complications of CKD? why do they occur?

A
  • highest mortality is from CVD particularly MI, cardiac failure, sudden cardiac death and stroke
  • occurs due to an increased frequency of hypertension, hyperlipidaemia and vascular calcification
  • pericarditis and pericardial effusion occurs in severe anaemia
  • pericardial friction rub
  • flow murmurs
184
Q

what are skin complications of CKD?

A
  • pruritus due to nitrogenous waste products of urea; may be scratch marks
  • brown discolouration of nails
185
Q

what are differential diagnoses of CKD?

A

AKI

186
Q

how can CKD be differentiated from AKI?

A
  • to differentiate it depends on history, duration of symptoms and previous urinalysis or measurement of serum creatinine
  • a normochromic anaemia, small kidneys on ultrasound and the presence of renal osteodystrophy favour CKD
187
Q

how is CKD diagnosed?

A
  • ECG for high potassium signs
  • urinalysis
  • urine microscopy
  • serum biochemistry
  • bloods
  • immunology
  • imaging
  • biopsy and histology to diagnose condition causing renal failure
188
Q

what is seen in urinalysis in CKD?

A
  • haematuria - indicates glomerulonephritis
  • proteinuria - if heavy suggestive of glomerular disease, can also be caused by infection
  • mid-stream urine sample sent for microscopy and sensitivity
  • albumin to creatinine ratio or protein to creatine ratio
189
Q

what is seen on urine microscopy in CKD?

A
  • white cells - bacterial UTI
  • eosinophilia - allergic tubulointerstitial nephritis/cholesterol emboli
  • granular casts - active renal disease
  • red cells - glomerulonephritis
190
Q

what is seen on serum biochemistry in CKD?

A
  • urea, electrolytes, bicarbonate and creatine - high urea and creatinine
  • low eGFR
  • raised alkaline phosphatase (renal osteodystrophy)
  • raised PTH if CKD stage 3 or more
191
Q

what is seen in bloods in CKD?

A
  • raised phosphate
  • low Ca2+
  • Hb low - normochromic normocytic anaemia
  • raised viscosity - myeloma or vasculitis
  • fragmented red cells indicate intravascular haemolysis
192
Q

what is seen on immunology in CKD?

A
  • auto-antibody screening for SLE, scleroderma and Goodpastures
  • Hep B, C, HIV and streptococcal antigen tests
193
Q

how is ultrasound used in diagnosis of CKD? what is seen?

A

ultrasound to check renal size and exclude hydronephrosis:

  • in CKD kidneys tend to be small
  • can be large in infiltrative disorders e.g. amyloidosis
194
Q

how is CT used to diagnose CKD?

A

detect stones, retroperitoneal fibrosis and other causes of urinary obstruction and maybe cortical scarring

195
Q

what are the aims of treatment of CKD?

A
  • therapy aimed at the underlying cause of renal disease
  • slow the deterioration of kidney function
  • reduce cardiovascular risk
  • identify and treat reversible causes
  • limit progression and complications
196
Q

how does CKD treatment identify and treat reversible causes?

A
  • relieve obstruction
  • stop nephrotoxic drugs
  • stop smoking and achieve healthy weight to deal with cardiovascular risk
  • tight glucose control in diabetes
197
Q

what is the target BP in CKD?

A

< 130/80mmHg

198
Q

what is the treatment of BP in CKD?

A
  • ACE-inhibitor
  • angiotensin receptor blocker
  • in diabetes start with ARB
  • diuretic to prevent hyperkalaemia and help reduce BP
  • calcium channel blocker if goals not met
199
Q

what is the treatment of bone disease in CKD?

A
  • check PTH and treat if raised
  • restrict diet
  • give phosphate binders to decrease gut absorption and avoidance of phosphate-rich food e.g. milk, cheese, eggs
  • vitamin D e.g. calcitriol and Ca2+ supplements
200
Q

what is the treatment of CVD in CKD?

A

statins and aspirin

201
Q

what is the treatment of anaemia in CKD?

A

iron/folate/folic acid

202
Q

what is the treatment of acidosis in CKD?

A
  • systemic acidosis accompanies the decline in kidney function and may contribute to increased serum potassium levels as well as dyspnea and lethargy
  • treat with sodium bicarbonate
203
Q

what is the best form of renal replacement therapy? what is another form?

A
  • the ‘best’ form of renal replacement therapy is transplantation, since it can restore 100% renal function, but this involves surgery and it is not always successful
  • dialysis can maintain stability but has complications
204
Q

what are indications for dialysis?

A
  • symptomatic uraemia including pericarditis or tamponade
  • hyperkalaemia not controlled by conservative measures
  • pulmonary oedema unresponsive to diuretics
  • severe acids
  • high potassium
  • tall T waves, low flat p waves, broad QRS or arrhythmias on ECG
  • metabolic acidosis
  • fluid overload that is resistant to diuretics
205
Q

what is haemofiltration? how is it done?

A
  • most commonly used
  • achieves blood flow using a blood pump to draw and return blood from the lumen of a dual-lumen catheter placed in the jugular, subclavian or femoral vein
  • ultrafiltrate is continuously removed from patient combined with simultaneous infusion of replacement solution
  • has less haemodynamic instability than haemodialysis
206
Q

what is haemodialysis? how is it done?

A
  • blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction, thus blood is always meeting a less-concentrated solution and diffusion of small solutes occurs down the concentration gradient
  • larger solutes do not clear as effectively
  • blood is taken from artery the and returned into a vein at an atrioventricular fistula (not suitable for atherosclerotic patients or those who have many fistulas)
  • allows good clearance of solutes in short periods but requires patient to be haemodynamically stable
  • time-consuming
207
Q

what are complications of haemodialysis?

A
  • hypotension/cramps
  • nausea/headache
  • chest pain
  • fever/rigors
  • infected dialysis catheter
208
Q

what is peritoneal dialysis? how is it done?

A
  • mainly used for CKD, rare in AKI
  • process uses patient’s peritoneum in the abdomen as a membrane across which fluid and solutes are exchanged with blood
  • all peritoneal dialysis is done at home, at night
209
Q

what are complications of peritoneal dialysis?

A
  • infection e.g. peritonitis
  • abdominal wall herniation
  • intestinal perforation
  • loss of membrane function over time
210
Q

what are complications of RRT?

A
  • cardiovascular disease due to combination of hypertension and calcium/phosphate dysregulation
  • infection
  • amyloid accumulates in long-term dialysis and may cause carpal tunnel syndrome, arthralgia and fractures
  • malignancy is commoner in dialysis patients - may be due to the cause of end-stage renal failure
211
Q

what is a renal cyst? when can they occur? what can they cause?

A
  • a renal cyst is a fluid collection in or on the kidney
  • solitary or multiple renal cysts are common, especially with advancing age; 50% of those over 50 have one or more such cysts
  • these cysts are often asymptomatic and are found
    incidentally on ultrasound examination
  • occasionally they may cause pain and/or haematuria if large, or bleeding may occur into the cyst
212
Q

what are the different types of kidney cysts?

A
  • simple cysts - most common form; benign
  • polycystic; recessive or dominant
  • hydronephrosis is when ureter is blocked and kidney dilates and gets bigger
  • dysplasia – when not formed properly
  • medullary sponge – dilation of collecting ducts
  • acquired cystic disease – medullary uraemic, dialysis cystic
213
Q

what are features of congenital renal cysts?

A
  • present at birth
  • uni/bilateral
  • isolated or multisystem disorder
  • inherited; autosomal or recessive
214
Q

how do congenital renal cysts develop?

A
  • genetic mutation leads to predisposition for cyst formation
  • increased abnormal cell hyperproliferation → loss of planar polarity → cyst initiation → fluid secretion by epithelial cells → cyst
215
Q

what are features of acquired renal cysts?

A
  • develop over time
  • no genetic mutation
  • bilateral/unilateral
  • isolated to kidneys
  • normal/small kidney size
  • associated with chronic kidney disease
  • route of development not clear
216
Q

what are causes of renal cysts?

A
  • simple cysts develop over time
  • acquired cysts e.g. CKD
  • drugs e.g. lithium
  • autosomal dominant/recessive polycystic kidney disease
  • syndromic disease; tuberous sclerosis
217
Q

what is autosomal dominant polycystic disease?

A
  • genetic disorder in which the renal tubules become structurally abnormal, resulting in the development and growth of multiple cysts within the kidney
  • cysts may begin in utero, infancy, childhood or adulthood
  • multiple cysts develop, gradually and progressively, throughout the kidney eventually resulting in renal enlargement and kidney tissue destruction
218
Q

what is the epidemiology of ADPKD?

A
  • commonest inherited kidney disease
  • autosomal dominant inheritance with high penetrance
  • usually presents in adulthood (20-30)
  • more common in males than females
  • if one parent affected then 50% chance of transmission
  • if both parents affected then 50% chance being affected, 25% normal, 25% being homozygous for disease (these babies die in the womb)
219
Q

what is the aetiology/genetics of ADPKD?

A
  • mutations in PKD1 (85%) gene on chromosome 16

- mutations in PKD2 (15%) gene on chromosome 4

220
Q

what are risk factors for ADPKD?

A

family history of ADPKD, ESRF or hypertension

221
Q

what does PKD1 do?

A

PKD1 encodes polycystin 1 which is involved in cell-cell and/or cell-matrix interactions; regulates tubular and vascular development in the kidneys

222
Q

what does PKD2 do?

A

PKD2 encodes polycystin 2 which functions as a calcium ion channel

223
Q

what does disruption of the polycystin pathway due to genetic mutations lead to?

A

disruption of the polycystin pathway results in reduced cytoplasmic Ca2+, which, in principal cells of the collecting duct, causes defective ciliary signalling and disorientated cell division resulting in cyst formation

224
Q

what causes progressive loss of renal function in ADPKD?

A
  • mechanical compression, apoptosis of healthy tissue and reactive fibrosis
  • rate of renal function decline is dependent on the growth and size of cysts; patients with rapidly growing cysts on MRI lose renal function more rapidly
225
Q

what is the clinical presentation of ADPKD?

A
  • can be clinically silent for many years, so family screening is essential
  • symptoms tend to start to present from 20 yrs onwards
  • loin pain and/or haematuria from haemorrhage into a cyst, cyst infection or urinary tract stone formation
  • loin or abdominal discomfort as size of kidneys increase
  • excessive water and salt loss
  • nocturia
  • bilateral kidney enlargement
  • renal colic due to clots
  • hypertension
  • renal stones, mainly uric acid stones
  • progressive renal failure
226
Q

what is extrarenal clinical presentation of ADPKD?

A
  • subarachnoid haemorrhage associated with berry aneurysm rupture
  • polycystic liver disease (70%)
  • pancreatitis
  • male infertility (rare)
  • mitral valve prolapse
  • ovarian cysts
  • diverticular disease
227
Q

what are differential diagnoses of ADPKD?

A
  • acquired and simple cysts of the kidneys
  • autosomal recessive PKD
  • medullary sponge kidney
  • tuberous sclerosis
228
Q

how is ADPKD diagnosed?

A
  • personal history
  • family history of ADPKD, ESRF, hypertension
  • BP may be raised
  • ultrasound
  • genetic testing for PKD1 and PKD2
229
Q

when is ultrasound diagnostic for at risk individuals?

A
  • 15-39yrs ≥ 3 cysts (uni/bilateral)
  • 40-59yrs ≥ 2 cysts (each kidney)
  • 60yrs+ and ≥ 4 cysts (each kidney)
230
Q

when can ultrasound be used to exclude ADPKD?

A

≥ 40yrs with < 2 cysts

231
Q

when can ultrasound not be used to exclude ADPKD?

A

if <30yrs

232
Q

what is the treatment of ADPKD?

A
  • no treatment shown to slow disease progression
  • blood pressure control with ACE-inhibitor
  • treat stones and give analgesia
  • laparoscopic removal of cysts to help with pain/nephrectomy
  • disease progression monitored by serial progression of serum creatinine
  • renal replacement therapy for ESRF
  • children and siblings of patients with the disease should be offered screening by renal ultrasound in their 20s
  • counselling and support
233
Q

what are indications for genetic testing?

A
  • individual older case with no family history
  • atypical cystic disease
  • very early onset (<2 yrs)
  • prenatal/pre-implantation genetic diagnosis
  • to facilitate life choices/reproduction decisions
  • potential living related kidney donor (<40yrs with positive imaging)
234
Q

what is autosomal recessive polycystic kidney disease?

A
  • recessive form of polycystic kidney disease
  • associated with a group of congenital fibrocystic syndromes
  • mutations in PKHD1 causes ARPKD
  • PKHD1 mutation on long arm (q) of chromosome 6
235
Q

what is the epidemiology of ARPKD?

A
  • rarer than ADPKD with prevalence at 1 in 40,000
  • autosomal recessive inheritance
  • disease of infancy
236
Q

what is the clinical presentation of ARPKD?

A
  • variable
  • many present in infancy with multiple renal cysts and congenital hepatic fibrosis
  • enlarged polycystic kidneys
  • 30% develop kidney failure
237
Q

what are differential diagnoses of ARPKD?

A
  • ADPKD
  • multicystic dysplasia
  • hydronephrosis
  • renal vein thrombosis
238
Q

how is ARPKD diagnosed?

A
  • diagnosed antenatally or neonatally
  • ultrasound to see cysts
  • CT and MRI to monitor liver disease
  • genetic testing
239
Q

what is the treatment of ARPKD?

A
  • currently no treatment available
  • genetic counselling for family members
  • laparoscopic removal of cysts to help with pain/nephrectomy
  • blood pressure control with ACE-inhibitor
  • treat stones and give analgesia
  • renal replacement therapy for ESRF
  • counselling and support
240
Q

what are different types of scrotal masses? how are they diagnosed?

A

• cannot get above - inguinoscrotal hernia or
proximally extending hydrocele
• separate and cystic - epididymal cyst
• separate and solid - epididymitis or varicocele
• testicular and cystic - hydrocele
• testicular and solid - tumour, haematocele
- orchitis

241
Q

what is an epididymal cyst?

A

smooth, extratesticular, spherical collection of fluid in the head of the epididymis

242
Q

what is the epidemiology of epididymal cysts?

A
  • usually develop around the age of 40
  • not uncommon
  • rare in children
243
Q

what is the clinical presentation of epididymal cysts?

A
  • contain clear and milky fluid
  • lie above and behind the testis
  • normally present having noticed a lump
  • often are multiple and may be bilateral
  • small cysts may remain undetected and asymptomatic
  • once they get large then may be painful
  • well defined and will transluminate since fluid-filled
  • testis is palpable quite separately from the cyst (unlike hydrocele where the testis is palpable within the fluid filled swelling)
244
Q

what are differential diagnoses of epididymal cysts?

A
  • spermatocele
  • hydrocele
  • varicocele
245
Q

what is a spermatocele? how is it differentiated from an epididymal cyst?

A
  • retention cyst of a tubule of the rete testes or the head of the epididymis, distended with barely watery fluid that contains spermatozoa
  • fluid and sperm filled cyst in the epididymis
  • no way clinically to differentiate between a cyst of the epididymis and spermatocele
  • can be differentiated as sperm are present in the milky fluid aspirate of a spermatocele
246
Q

what is a hydrocele?

A
  • accumulation of serous fluid in a body cavity
  • hydrocele testis is the accumulation of fluids around a testicle, within the tunica vaginalis
  • often caused by fluid secreted from a remnant piece of peritoneum wrapped around the testicle (tunica vaginalis)
247
Q

what is a varicocele?

A

an abnormal dilation of the testicular veins in the pampiniform venous plexus in the scrotum, caused by venous reflux

248
Q

how is an epididymal cyst diagnosed?

A

scrotal ultrasound

249
Q

how is an epididymal cyst treated?

A
  • usually not necessary

- if painful and symptomatic then surgical excision

250
Q

what is the epidemiology of hydrocele?

A
  • clinically apparent scrotal hydrocele are evident in 6% of term males beyond the newborn period
  • most paediatric hydroceles are congenital
251
Q

what is the aetiology of primary hydrocele?

A
  • more common and larger
  • usually in younger men
  • associated with a patent processus vaginalis, which typically resolves during the 1st year of life
252
Q

what is the aetiology of secondary hydrocele?

A

rarer and present in older boys and men

253
Q

what is secondary hydrocele secondary to?

A
  • testis tumour
  • trauma
  • infection
  • TB
  • testicular torsion
  • generalised oedema
254
Q

what is a simple hydrocele?

A

overproduction of fluid in the tunica vaginalis

255
Q

what is a communicating hydrocele?

A

processus vaginalis fails to close, allowing peritoneal fluid to communicate freely within the scrotal portion

256
Q

what is the clinical presentation of a hydrocele?

A
  • scrotal enlargement with a non-tender, smooth, cystic swelling
  • pain is not a feature unless the hydrocele is infected
  • testis are usually palpable but may be difficult to palpate in large hydrocele
  • lies anterior to and below the testis and will transluminate
257
Q

what are differential diagnoses of hydrocele?

A

must differentiate from testicular torsion and strangulated hernia

258
Q

what is used to diagnose hydrocele?

A
  • ultrasound
  • serum alpha-fetoprotein and human chorionic gonadotrophin to help exclude malignant teratomas or other germ cell tumours
259
Q

what is the treatment of hydrocele?

A
  • resolve spontaneously
  • many of infancy resolve by 2 yrs
  • therapeutic aspiration or surgical removal
260
Q

what is the epidemiology of varicocele?

A
  • left side more commonly affected
  • unusual in boys under 10yrs
  • incidence increases after puberty
  • associated with sub fertility
261
Q

what is the aetiology of varicocele?

A
  • more common on the left
  • angle at which the left testicular vein enters the left renal vein
  • increased reflux from compression of the renal vein
  • lack of effective valves between the testicular and renal veins
262
Q

what is the clinical presentation of varicocele?

A
  • often visible as distended scrotal blood vessels that feel like ‘a bag of worms’
  • patient may complain of a dull ache or scrotal heaviness
  • scrotum hangs lower on the side of the varicocele
263
Q

what are differential diagnoses of varicocele?

A

secondary to other pathological processes blocking the testicular vein e.g. kidney tumours and other retroperitoneal tumours

264
Q

what is used to diagnose varicocele?

A
  • venography

- colour doppler ultrasound (to see blood flow)

265
Q

what is treatment of varicocele?

A

surgery if there is pain, infertility or testicular atrophy

266
Q

what is testicular torsion?

A

torsion (twisting) of the spermatic cord resulting in occlusion of the testicular blood vessels which can rapidly lead to ischaemia and infarct and thus there is potential loss of the testis (germ cells are the most susceptible cell line to ischaemia)

267
Q

what is the aim of treatment of testicular torsion?

A
  • aim is to recognise this condition before the cardinal symptoms fully manifest, as prompt surgery saves testes
  • if surgery is performed in < 6hrs the salvage rate is 90-100%; if > 24hrs it is 0-10%
268
Q

what is the epidemiology of testicular torsion?

A
  • common urological emergency among adolescent boys and young men
  • typically occurs in neonates or post-pubertal boys but can occur in males of all ages, most common at 11-30yrs
  • left side is more commonly affected than right
269
Q

what is the aetiology of testicular torsion?

A

underlying congenital malformation (belt-clapper deformity) where the testis is not fixed to the scrotum completely, allowing for free movement leading to twisting

270
Q

what is the clinical presentation of testicular torsion?

A
  • in any boy presenting with abdominal pain, the testes should be checked
  • sudden onset of pain in one testis, makes walking uncomfortable
  • pain often comes on during sport or physical activity
  • pain in abdomen, nausea and vomiting are common
  • inflammation of one testis; it is very tender, hot and swollen
  • testis may lie high and transversely
  • with intermittent torsion the pain may have passed on presentation, but if it was severe then prophylactic fixing may be wise
271
Q

what are differential diagnoses of testicular torsion?

A
  • epididymo-orchitis (main one)
  • tumour, trauma and an acute hydrocele
  • torsion of testicular or epididymal appendage (remnant of Mullerian duct)
  • idiopathic scrotal oedema
272
Q

what are features of tosion of testicular or epididymal appendage as a differential diagnosis of testicular torsion?

A
  • usually occurs in boys between 7-12yrs and causes less pain
  • small blue nodule under scrotum
  • due to the surge in gonadotrophins that signal the onset of puberty
273
Q

what are features of idiopathic scrotal oedema as a differential diagnosis of testicular torsion?

A

benign condition usually occurs between 2-10yrs and is differentiated from torsion by the absence of pain and tenderness

274
Q

what is used to diagnose testicular torsion?

A
  • doppler ultrasound may demonstrate lack of blood flow to testis
  • urinalysis to exclude infection and epididymis
  • do not delay surgical exploration
275
Q

what is the treatment of testicular torsion?

A
  • surgery: expose and untwist testis; 6 hour window to save testis
  • orchidectomy (removal of testis) and bilateral fixation
276
Q

what is BOO?

A

bladder outflow obstruction (urodynamic diagnosis)

  • urine is unable to flow from the kidneys through the ureters and out of the bladder through the urethra
  • decreased flow of urine leads to hydronephrosis
277
Q

what is hydronephrosis?

A

dilation of the renal pelvis and calyces as a result of obstruction to urine flow

278
Q

what is obstructive uropathy?

A

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

279
Q

what is the normal function of the lower urinary tract?

A
  • convert a continuous process of excretion (urine production) to an intermittent process of elimination
  • store urine insensibly
  • void urine when convenient
280
Q

what is the action of the detrusor muscles? what is the neural supply? is it parasympathetic or sympathetic?

A

• relaxes during storage (compliant)
• contracts during voiding
• parasympathetic cholinergic control via S3,S4 and S5:
- drives detrusor contraction

281
Q

what is the distal sphincter mechansim? what is the neural supply? is parasympathetic or sympathetic?

A 
• contracts during storage
• relaxes during voiding
• sympathetic noradrenergic control via T10,L1 and L2:
- sphincter/urethral contraction
- inhibits detrusor contraction
282
Q

what are storage symptoms in LUTS?

A
  • urgency
  • nocturia (> 30% voided volume at night)
  • frequency
  • overflow incontinence (leaking urine during day/wetting bed)
283
Q

what are voiding symptoms in LUTS?

A
  • poor intermittent stream
  • hesitancy
  • incomplete emptying
  • post micturition dribbling
  • straining
  • haematuria
  • dysuria
284
Q

what are red flags of LUTS?

A

haematuria and dysuria - warning symptoms of infection, stones or cancer

285
Q

what is PSA?

A

Prostate Specific Antigen

  • glycoprotein that is expressed by normal and neoplastic prostate tissue
  • small amounts in bloodstream normally
286
Q

when is PSA raised?

A
  • BPH
  • prostate cancer
  • perianal trauma and mechanical manipulation of the prostate e.g. in cytoscopy (endoscopy of bladder), prostate biopsy or surgery
  • BMI < 25
  • taller men
  • recent ejaculation
  • black africans
  • prostatitis
  • UTI
287
Q

what level of PSA confers an increased risk of LUTS progression?

A

PSA >1.4ng/ml

288
Q

what are flow rates and residual volume of the urine?

A
  • how much urine being passed, how long for and flow rate
  • maximum flow rate is useful if more than 150ml voided
  • max flow rate < 10ml per second is suggestive of bladder outflow obstruction due to BPH
289
Q

what flow rate suggests BOO due to BPH?

A

max flow rate < 10ml per second is suggestive of bladder outflow obstruction due to BPH

290
Q

what are features of the frequency volume chart used in LUTS?

A
  • measure volumes voided and time over minimum of 3 days
  • calculates whether polyuric (>40ml/kg/24hrs)
  • calculates whether nocturic (>30% voided volume at night)
291
Q

what characterises polyuria?

A

> 40ml/kg/24hrs

292
Q

what characterises nocturia?

A

> 30% voided volume at night

293
Q

what is acute urinary retention?

A
  • sudden onset of painful inability to pass urine usually with over 500ml in the bladder
  • bladder is usually tender
294
Q

what are causes of acute urinary retention?

A
  • prostatic obstruction e.g. due to BPH or prostate cancer
  • urethral strictures
  • anticholinergics
  • alcohol
  • constipation
  • post-op (pain/inflammation/anaesthetics)
  • infection
  • neurological (spinal compression - cauda equina syndrome)
295
Q

what is the examination of acute urinary retention?

A

abdomen, prostate (DRE), perineal sensation (to check for cauda equina syndrome)

296
Q

what is used to diagnose acute urinary retention?

A
  • normal renal biochemistry, since not affected usually
  • renal ultrasound if abnormal biochemistry
  • PSA test to look for BPH/prostate cancer
297
Q

what is the treatment of acute urinary retention?

A
  • catheter relieves pain
  • alpha-1 blocker which relaxes smooth muscle in bladder neck to aid voiding
  • prevent by giving 5-alpha-reductase inhibitor which reduces testosterone conversion to dihydrotestosterone and thus reduces prostate size
298
Q

what are features of chronic urinary retention?

A
  • more insidious and may be painless
  • more difficult to define
  • incomplete bladder emptying
  • results in a increased risk of infection
  • can be low pressure with detrusor failure
  • can be high pressure with risk of interactive obstructive uropathy
299
Q

what can the pressures be like in chronic urinary retention?

A
  • can be low pressure with detrusor failure

* can be high pressure with risk of interactive obstructive uropathy

300
Q

what are causes of chronic urinary retention?

A
  • prostatic enlargement due to BPH/prostate cancer
  • pelvic malignancy or rectal surgery
  • diabetes
301
Q

what is the clinical presentation of chronic urinary retention?

A
  • overflow incontinence; leaking urine during the day/wetting bed
  • loss of appetite
  • constipation
  • distended abdomen
  • UTI
302
Q

what is the management of chronic urinary retention?

A

only catheterise if there is pain, urinary infection or renal impairment

303
Q

what are features and types of urinary tract obstruction?

A
  • common and should be considered in anyone with renal impairment
  • damage can be permanent if the obstruction is not treated properly
  • can be partial, complete, unilateral or bilateral
304
Q

what are causes of luminal urinary tract obstruction?

A

stones, blood, clot, sloughed papilla, tumour

305
Q

what are causes of mural urinary tract obstruction?

A

congenital or acquired stricture, neuromuscular dysfunction or schistomiasis

306
Q

what are causes of extra-mural urinary tract obstruction?

A
  • abdominal or pelvic mass/tumour, retroperitoneal fibrosis, BPH, prostate cancer
  • pregnancy
  • inflammation e.g. peritonitis or diverticulitis
307
Q

what is the clinical presentation of urinary tract obstruction?

A
  • acute upper tract (kidney and ureter) obstruction
  • chronic upper tract (kidney and ureter) obstruction
  • acute lower tract (bladder to urethra) obstruction
  • chronic lower tract (bladder to urethra) obstruction
308
Q

what is the clinical presentation of acute upper urinary tract (kidney and ureter) obstruction?

A

loin pain radiating to groin

309
Q

what is the clinical presentation of chronic upper urinary tract (kidney and ureter) obstruction?

A

flank pain, renal failure, infection and polyuria may occur due to impaired urinary concentration

310
Q

what is the clinical presentation of acute lower tract (bladder to urethra) obstruction?

A
  • acute urinary retention with severe suprapubic pain, often preceded by symptoms of bladder outflow obstruction
  • distended, palpable bladder that’s dull to percussion
311
Q

what is the clinical presentation of chronic lower tract (bladder to urethra) obstruction?

A
  • urinary frequency, hesitancy, poor stream, terminal dribbling and overflow incontinence
  • distended, palpable bladder +/- large prostate on rectal exam
  • complications are UTI and urinary retention
312
Q

what is used to diagnose urinary tract obstruction?

A
  • bloods: U+Es and monitor creatinine; this will be raised
  • mid-stream urinary sample; culture and sensitivity
  • ultrasound: if there is hydronephrosis then arrange CT
313
Q

what is the treatment of upper urinary tract obstruction?

A
  • nephrostomy: artificial opening created between the kidney and the skin which allows for the urinary diversion directly from the upper tract
  • alpha-1 antagonist (bladder neck smooth muscle relaxer) improves flow
  • 5-alpha reductase inhibitor inhibits conversion of testosterone to active form and thus reduces prostate size
314
Q

what is the treatment of lower urinary tract obstruction? what should be monitored?

A
  • urethral catheter
  • suprapubic catheter
  • beware of large diuresis after obstruction relief as can result in a temporary salt losing nephropathy resulting in weight loss; monitor weight and maintain fluid balance
315
Q

what are advantages/disadvantages of suprapubic catheters for lower urinary tract obstruction?

A
  • less risk of urethral damage and thus UTI
  • requires general anaesthetic for insertion
  • small risk of bowel injury during insertion
  • less likely to be colonised by bacteria than with a long term urethral catheter
  • long term urethral catheter can lead to urethral erosion and damage to the urethral sphincter
316
Q

how is surgery used to treat urinary tract obstruction?

A

transurethral resection of the prostate

• less than 14% impotent, 1% incontinent and 10% erectile dysfunction

317
Q

what are indications for surgery for LUTS? (RUSHES)

A

RUSHES

  • Retention
  • UTI’s
  • Stones
  • Haematuria
  • Elevated creatinine due to bladder outflow obstruction
  • Symptoms deterioration
318
Q

what is benign prostatic enlargement/hyperplasia?

A
  • increase in the size of the prostate without the presence of malignancy
  • prostate secretes 70% of the volume of seminal fluid and is hormone dependent
  • the prostate gland surrounds the urethra, the tube that carries urine from the bladder out of the body
319
Q

what is the epidemiology of benign prostatic enlargement/hyperplasia?

A
  • common - 24% of men 40-64 and 40% of men over 60
  • more common over 60
  • unusual before the age of 45
  • affects Afro-Caribbean’s more severely than white men, probably due to the high levels of testosterone
320
Q

what are the risk factors for benign prostatic enlargement/hyperplasia?

A
  • increases with age

- castration (removal of testicles) is protective

321
Q

why is castration protective against benign prostatic enlargement/hyperplasia?

A
  • androgens do not cause BPH but are a requirement for BPH
  • BPH is not seen in those with castration prior to puberty, or those with genetic diseases that inhibit androgen action or production
322
Q

what is the pathophysiology of benign prostatic enlargement/hyperplasia?

A
  • benign nodular or diffuse proliferation of musculofibrous and glandular layers of the prostate
  • inner (transitional) zone enlarges in contrast to the peripheral layer expansion that is seen in prostate carcinoma
  • as the prostate gets bigger, it may squeeze or partly block the urethra
  • this often causes problems with urinating
323
Q

what is the clinical presentation of benign prostatic enlargement/hyperplasia?

A
  • LUTS
  • abdominal exam reveals enlarged bladder
  • acute urinary retention
  • in a small number of cases, BPH may cause the bladder to become occluded leading to anuria, resulting in acute urinary retention leading to UTI’s, bladder stones or kidney damage
  • BPH does not affect ability to father children
  • BPH does not cause prostate cancer or erection problems
324
Q

what are some LUTS that occur in benign prostatic enlargement/hyperplasia?

A
  • nocturia (>30% voided volume at night)
  • frequency
  • urgency
  • post-micturition dribbling
  • poor stream/flow
  • hesitancy
  • overflow incontinence
  • haematuria
  • bladder stones
  • delay in initiation of micturition
  • incomplete emptying of bladder
325
Q

what are differential diagnoses of BPH?

A
  • bladder tumour
  • bladder stones
  • trauma
  • prostate cancer
  • chronic prostatitis
  • UTI
326
Q

what is used to diagnose BPH?

A
  • digital rectal exam; prostate would feel enlarged but smooth
  • serum electrolytes and renal ultrasound to exclude renal damage caused by obstruction
  • transrectal ultrasound to see size of prostate
  • serum PSA
  • biopsy and endoscopy
  • mid-stream urine sample to exclude infection
  • flow rates and residual volume (max flow rate < 10ml per second is suggestive of BOO due to BPH)
  • frequency volume chart (measure over 3 days)
327
Q

what lifestyle changes are made to treat BPH?

A
  • avoid caffeine and alcohol to reduce urgency and nocturia
  • relax when voiding
  • void twice in a row to aid emptying
  • watchful waiting if minimal symptoms
328
Q

what first line drugs are used to treat BPH?

A

alpha1 antagonists e.g. oral tamsulosin

329
Q

what is the action of alpha 1 antagonists? give an example

A
  • oral tamsulosin
  • relax smooth muscle in the bladder neck and prostate thereby producing increase in urinary flow rate and improvement in obstructive symptoms
330
Q

what are some side effects of alpha1 antagonists?

A

drowsiness, dizziness, depression, ejaculatory

failure, extra-pyramidal signs, weight increase and nasal congestion

331
Q

when should alpha1 antagonists be avoided?

A

postural hypertension

332
Q

what is second line treatment of BPH?

A

5-alpha-reductase inhibitor e.g. oral finasteride

333
Q

what is the action of 5-alpha-reductase inhibitor? give an example

A
  • e.g. finasteride
  • blocks the conversion of testosterone to dihydrotestosterone (responsible for prostatic growth)
  • alternative to alpha-antagonist especially in men with very large prostate
334
Q

what are side effects of 5-alpha-reductase inhibitors?

A

impotence, decreased libido

335
Q

when is surgery used to treat BPH?

A
  • usually reserved for those with a large prostate or failure to respond to an adequate trial of medical therapy
  • surgery is required if there is acute urinary retention, failed voiding trials, recurrent gross haematuria, renal insufficiency due to obstruction or failure of medical treatment
336
Q

what are types of surgery used to treat BPH?

A

transurethral resection of prostate (TURP):
• gold standard
• less than 14% impotent, 1% incontinent and 10% erectile dysfunction

transurethral incision of prostate (TUIP):
• less destruction than TURP and less risk to sexual function, best for smaller prostate

337
Q

what are complications of BPH if untreated?

A
  • bladder calculi
  • UTI
  • haematuria
  • acute retention
338
Q

where does renal cell carcinoma arise from?

A
  • also known as hypernephroma and Grawitz tumour
  • malignant
  • arises from PCT epithelium
339
Q

what is the epidemiology of renal cell carcinoma?

A
  • most common renal tumour in adults
  • accounts for 2-3% of all malignancies
  • more common in males than females
  • usually present after 50 yrs of age
  • rare before 40 yrs
  • average age at presentation is 55 yrs
  • highest incidence is in the Czech republic
340
Q

what is the most common renal tumour in adults?

A

renal cell carcinoma

341
Q

what are risk factors and aetiology of renal cell carcinoma?

A
  • smoking
  • obesity
  • hypertension
  • renal failure and haemodialysis (15% develop RCC)
  • polycystic kidneys
  • Von Hippel Lindau (VHL) syndrome
342
Q

how is VHL inherited? what are its effects? what can it predispose to?

A
  • autosomal dominant
  • mutation of chromosome 3 on the short arm
  • loss of both copies or tumour suppressor gene
  • 50% develop RCC that is often bilateral and multifocal
  • renal and pancreatic cysts as well as cerebellar malignancy also arise
343
Q

what is the pathophysiology of renal cell carcinoma?

A
  • malignant cancer of the proximal convoluted tubular epithelium
  • spread may be direct (renal vein), via lymph or haematogenous (bone, liver, lung)
  • 25% have metastases at presentation
344
Q

what is the clinical presentation of renal cell carcinoma?

A
  • often asymptomatic and discovered incidentally
  • haematuria, loin/flank pain and abdominal mass
  • anorexia, malaise and weight loss
  • rarely, invasion of the left renal vein results in the compression of the left testicular vein causing a varicocele
  • polycythaemia in 5%
  • hypertension in 30% due to renin secretion by tumour
  • anaemia due to depression of erythropoietin
  • fever in around 20%
345
Q

what are differential diagnoses of renal cell carcinoma?

A
  • transitional cell carcinoma
  • Wilms’ tumour
  • renal oncocytoma
  • leiomyosarcoma
346
Q

what is used to diagnose a renal cell carcinoma?

A
  • ultrasound (to distinguish cysts from tumour)
  • CT chest and abdomen with contrast
  • MRI (for tumour staging)
  • blood pressure (may be raised due to renin)
  • bloods
  • renal biopsy
  • bone scan (only if there are signs or serum Ca2+ raised)
347
Q

how is CT chest and abdomen with contrast used to diagnose renal cell carcinoma?

A
  • more sensitive than ultrasound in detecting a renal mass and will show involvement of the renal vein of inferior vena cava, if present
  • using contrast demonstrates kidney function since in normal kidney should see it being taken up and excreted well
348
Q

what is seen in bloods in renal cell carcinoma?

A
  • FBC to detect polycythaemia and anaemia due to EPO decrease
  • ESR may be raised
  • liver biochemistry may be abnormal
349
Q

how is localised renal cell carcinoma treated with surgery?

A
  • nephrectomy, unless tumours are bilateral

* if bilateral involvement then partial nephrectomy

350
Q

what are ablative techniques used to treat renal cell carcinoma?

A
  • cryoablation and radiotherapy are used in patients with significant comorbidities who would not tolerate surgery
  • can harm kidney function
351
Q

what is the treatment of malignant or locally advanced renal cell carcinoma?

A
  • interleukin-2 and interferon alpha produce remission in 20%
  • biological angio-genesis targeted therapy: sunitinib, bevacizumab and sorafenib
  • temsirolimus (mTOR inhibitor) found to improve survival more than interferon
  • last 2 options given if patients do not respond to 1st
352
Q

what is Wilms’ tumour?

A
  • childhood tumour of the primitive renal tubules and mesenchymal cells
  • seen within the first 3 years of life; it is the chief abdominal malignancy in children
353
Q

what is the presentation of Wilms’ tumour?

A

presents as an abdominal mass and less commonly with haematuria

354
Q

what is the diagnosis and treatment of Wilms’ tumour?

A
  • diagnosis is established by ultrasound, CT and MRI

* treated with a combination of nephrectomy, radiotherapy and chemotherapy

355
Q

what is bladder cancer? what is affected?

A
  • type of transitional cell carcinoma (TCC)
  • TCCs are responsible for 3% of deaths from all forms of malignancy
  • the calyces, renal pelvis, ureter, bladder and urethra are all lined by transitional epithelium and are all susceptible to transitional cell carcinoma
  • bladder tumours are the most common TCC
356
Q

what is the epidemiology of bladder cancer?

A
  • bladder tumours account for 50% of TCC’s
  • 4th most common cancer in men
  • 8th most common cancer in women
  • more common in males than females
  • incidence peaks in the 8th decade
  • most commonly occurs after the age of 40 yrs
357
Q

what are risk factors for bladder cancer?

A
  • smoking
  • occupational exposure to carcinogens
  • exposure to drugs e.g. phenacetin and cyclophosphamide
  • chronic inflammation of urinary tract e.g. schistomiasis (usually associated with squamous carcinoma) or indwelling catheter
  • > 40 yrs
  • male
  • family history
358
Q

what carcinogens can cause bladder cancer?

A
  • beta-napthylamine, benzidine, azo dyes

* workers in the petroleum, chemical, cable and rubber industries are at risk

359
Q

what is the tumour spread of bladder cancer?

A
  • local → to pelvic structures
  • lymphatic → to iliac and para-aortic nodes
  • haematogenous → to liver and lungs
360
Q

what is the clinical presentation of bladder cancer?

A
  • painless haematuria; most common symptom however, pain may result due to clot retention
  • any patient over 40 presenting with haematuria should be assumed to have a urothelial tumour until proven otherwise
  • recurrent UTI’s
  • voiding irritabiliity
361
Q

what are differential diagnoses of bladder cancer?

A
  • haemorrhagic cystitis
  • renal cancer
  • UTI
  • urethral trauma
362
Q

what is used to diagnose bladder cancer?

A
  • cytoscopy with biopsy; diagnostic
  • urine microscopy/cytology; cancers may cause sterile pyruria
  • CT urogram; provides staging and is diagnostic
  • urinary tumour markers
  • MRI/lymphangiography may show involved pelvic nodes
  • CT/MRI of pelvis
363
Q

what is the treatment of non-muscle invasive bladder cancer? what chemotherapy is used?

A
  • surgical resection

- and/or chemotherapy: mitomycin, doxorubicin, cisplatin, to reduce recurrence

364
Q

what is the treatment of localised muscle invasive disease? what chemotherapy is used?

A
  • radical cystectomy; gold standard
  • post-op chemotherapy: m-vac; methotrexate, vinblastine, adriamycin and cisplatin
  • radical radiotherapy if not fit for surgery
  • chemotherapy: CMV; cisplatin, methotrexate, vinblastine
365
Q

what is m-vac chemotherapy?

A

methotrexate, vinblastine, adriamycin and cisplatin

366
Q

what is CMV chemotherapy?

A

cisplatin, methotrexate, vinblastine

367
Q

what is the treatment of metastatic bladder cancer?

A

palliative chemotherapy and radiotherapy

368
Q

what are features of prostatic carcinomas?

A
  • commonest male malignancy
  • the majority of prostate cancers are adenocarcinomas arising in the peripheral zone of the prostate gland
  • most are slow growing but some can be aggressive
  • most common site of metastases is the bone and lymph nodes
  • malignant change becomes more common with age
369
Q

what is the most common cancer in men?

A

prostatic carcinoma

370
Q

what is the epidemiology of prostatic carcinoma?

A
  • accounts for 7% of all cancers in men and is the 6th most common in the world
  • incidence increases with age
  • by the age of 80 yrs, 80% of men have malignant foci within the gland but most of these appear to lie dormant
  • more common in black people due to higher testosterone
371
Q

what are risk factors for prostatic carcinoma?

A
  • family history
  • genetics
  • increasing age
  • black
  • hormonal factors
  • if one first-degree relative has prostate cancer then risk is doubled (3 or more affected relatives or 2 relatives who have developed early onset)
372
Q

how does genetics act as a risk factor for prostatic carcinoma?

A
  • HOXB13 is a predisposition gene

* BRCA2 confers a 5-7 times higher risk

373
Q

what is the spread of prostate cancer?

A

spread may be:
• local → seminal vesicles, bladder and rectum
• lymph
• haematogenously; bone (sclerotic bony lesions) or less commonly brain, liver and lung

374
Q

what is the clinical presentation of prostate cancer? which ones suggest metastasis?

A
  • LUTS if there is local disease:
    • nocturia
    • hesitancy
    • poor stream
    • terminal dribbling
    • obstruction - bladder outflow problems similar to BPH e.g. urinary retention
  • weight loss, bone pain and anaemia suggest metastasis
375
Q

what are differential diagnoses of prostate cancer?

A

BPH, prostatitis, bladder tumours

376
Q

what is used to diagnose prostate cancer?

A
  • DRE (hard, irregular prostate)
  • raised PSA (can be normal in 30% cancers) - if metastatic then will be >16ng/ml
  • trans-rectal ultrasound and biopsy (diagnostic; uses Gleason score)
  • urine biomarkers e.g. PCA3 or gene fusion protein
  • endorectal coil MRI to locally stage tumour
377
Q

what is treatment of prostate cancer that’s confined to the prostate?

A
  • radical prostatectomy if <70yrs; excellent disease free survival
  • radiotherapy + hormone therapy; alternative to surgery
  • brachytherapy; implantation of radioactive material targeted at tumour
  • hormone therapy temporarily delays tumour progression
  • active surveillance if >70yrs and low risk
378
Q

what endocrine therapy is used to treat prostate cancer?

A
  • prostate cancer is the most hormone-sensitive malignancy
  • binding at the androgen receptor stimulates tumour growth
  • androgen deprivation
379
Q

what are types of androgen deprivation treatments used for prostate cancer?

A
  • orchidectomy (removal of testes)
  • LHRH agonists
  • androgen receptor blockers
380
Q

what are examples of LHRH agonists?

A

SC goserelin or SC leuprorelin

381
Q

what are features of LHRH agonists?

A
  • they first stimulate and then inhibit the pituitary gonadotrophin, testosterone
  • due to this they can lead to an initial surge in testosterone which can lead to a tumour ‘flare’ and short worsening of symptoms and an anti-androgen e.g. oral cyproterone acetate is used
382
Q

what is an example of androgen receptor blocker?

A

bicalutamide

383
Q

what are the side effects of androgen receptor blockers?

A

weakness, nausea, hot flushes, weight changes

384
Q

what is the treatment of symptomatic prostate cancer?

A
  • analgesia
  • treat hypercalcaemia
  • radiotherapy for bone metastases/spinal cord compression
385
Q

what is the epidemiology of testicular tumours?

A
  • most common cancer in males aged 15-44 yrs
  • 10% occur in undescended testes
  • more than 96% arise from germ cells
  • 4% arise from non-germ cells
386
Q

what are testicular tumours that arise from germ cells?

A
  • seminomas - 25-40 yrs and 60 yrs

* teratomas - infancy

387
Q

what are testicular tumours that arise from non-germ cells?

A
  • leydig cell tumours
  • sertoli cell tumours
  • sarcomas
388
Q

what are risk factors for testicular tumours?

A
  • undescended testis
  • infant hernia
  • infertility
  • family history
389
Q

what is the clinical presentation of testicular tumours?

A
  • painless lump in testicle
  • testicular pain and/or abdominal pain
  • hydrocele
  • cough and dyspnoea is indicative of lung metastases
  • back pain is indicative of para-aortic lymph node metastasis
  • abdominal mass
390
Q

what are differential diagnoses of testicular tumours?

A

testicular torsion, lymphoma, hydrocele, epididymal cyst

391
Q

what is used to diagnose testicular tumours?

A
  • ultrasound (differentiates between masses and swellings and tumours)
  • biopsy and histology
  • serum tumour markers (alpha-fetoprotein and/or beta-hCG)
  • CXR and CT to assess tumour staging
392
Q

what levels of serum tumour markers are seen in different testicular tumours?

A
  • raised AFP and B-hCG in teratomas
  • B-hCG in minority of those with seminomas
  • AFP is not elevated in those with pure seminomas
393
Q

what is treatment of testicular tumours?

A
  • radical orchidectomy via inguinal approach
  • seminomas with metastases below diaphragm are only treated with radiotherapy
  • more widespread tumours are treated with chemotherapy
  • teratomas treated with chemotherapy
  • sperm storage offered
394
Q

what is a urinary tract infection? what is it defined as?

A
  • the inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria
  • defined as > 10^5 organisms/ml or fresh mid-stream urine
395
Q

what 5 pathogens account for nearly all isolate from primary care for UTI? (KEEPS)

A

KEEPS:

  • Klebsiella spp.
  • E.coli (most common)
  • Entercocci
  • Proteus spp.
  • Staphylococcus spp
396
Q

how are UTIs classified?

A
  • lower urinary tract vs upper
  • uncomplicated vs complicated
  • single/isolated vs unresolved
  • acute vs chronic
397
Q

what surface attachment molecules do UPECs have?

A
  • fimbriae/pilli
  • afimbrial attachments e.g. glycocalix
  • acid polysaccharide coat that resists phagocytosis
398
Q

what do bacteria adhere to in UTIs?

A
  • urothelium
  • vaginal epithelium
  • vaginal mucus
399
Q

when are there higher rates of adhesion of bacteria to cause UTIs?

A
  • oestrogen depletion due to the loss of lactobacilli and pH change (seen post-menopause where pH rises and there is increased colonisation by colonic flora and reduction in vaginal mucus secretion)
  • those with HLA-A3 blood group antigen tend to have recurrent UTIs
400
Q

how do bacteria avoid host defences?

A
  • capsule to resist phagocytosis, toxins (E.coli) and enzyme production (Proteus secretes urease)
  • adhere to urothelium, vaginal epithelium and vaginal mucus
401
Q

what are some Gram negative bacteria that secrete urease?

A

Proteus, Klebsiella and Pseudomonas

402
Q

what are some Gram positive bacteria that secrete urease?

A

Staphylococci and Mycoplasma

403
Q

what are host defence mechanism against UTIs?

A
  • antegrade flushing of urine
  • Tamm-Horsfall protein has antimicrobial properties
  • low urine pH and high osmolarity
  • urinary IgA
404
Q

what are types of UTI?

A
  • pyelonephritis
  • cystitis (bladder)
  • prostatitis
  • epididymo-orchitis
  • urethritis
405
Q

what is secreted by the proximal tubules?

A
  • medications

- ammonium (via breakdown of glutamine to alpha-ketoglutarate, generating ammonium and bicarbonate ions)

Phase 2A (28 decks)

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