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Phase 2a LIAM > GU > Flashcards

GU Flashcards

1
Q

What anatomical structures make up the lower urinary tract?

A

Bladder -> bladder neck -> prostate gland -> urethra and urethral sphincter.

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2
Q

Give 4 functions of the lower urinary tract.

A
  1. Storage of urine.
  2. Converts the continuous process of excretion to an intermittent, controlled and volitional process.
  3. Prevents leakage of stored urine.
  4. Allows rapid, low pressure voiding.
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3
Q

Is the detrusor muscle relaxed or contracted during storage?

A

Relaxed.

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4
Q

Is the detrusor muscle relaxed or contracted during voiding?

A

Contracted.

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5
Q

Is the urethral sphincter relaxed or contracted during storage?

A

Contracted.

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6
Q

Is the urethral sphincter relaxed or contracted during voiding?

A

Relaxed.

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7
Q

What type of epithelium lines the bladder?

A

Urothelium (transitional epithelium) - pseudo-stratified.

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8
Q

Describe the physiology of micturition.

A

The bladder fills and stretch receptors are stimulated. Afferent impulses stimulate parasympathetic action of detrusor muscle; it contracts. The urethral sphincters relax; this is mediated by inhibition of the neurones to them. The PAG is stimulated.

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9
Q

What are lower urinary tract symptoms (LUTS) in men > 50 likely to be due to?

A

Benign prostatic enlargement.

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10
Q

LUTS: give 3 symptoms of storage problems.

A
  1. Frequency.
  2. Urgency.
  3. Nocturia.
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11
Q

LUTS: give 4 symptoms of voiding problems.

A
  1. Straining.
  2. Hesitancy.
  3. Incomplete emptying.
  4. Poor flow.
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12
Q

What might dysuria suggest?

A

Inflammation.

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13
Q

What investigations might you do on someone who presents with LUTS.

A
  1. Urinary tests e.g. dipstick.
  2. Urinary flow: maximum flow rate and residual volume are important.
  3. Symptom assessment: international prostate scoring system.
  4. Blood tests e.g. PSA, U+E.
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14
Q

Give 3 causes of nocturnal polyuria.

A
  1. Habitual.
  2. Congestive cardiac failure.
  3. Sleep apnea.
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15
Q

Describe the treatment for someone who presents with mild LUTS.

A

Reassurance, watch and wait.

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16
Q

Describe the treatment for someone who presents with moderate LUTS.

A
  1. Fluid management, avoid caffeine.
  2. Bladder drill.
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17
Q

Give 2 pharmacological therapies used in the treatment of moderate to severe LUTS.

A
  1. Alpha-1-blockers e.g. tamulosin.
  2. 5-alpha-reductase-inhibitors.
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18
Q

How do alpha-1-blockers work in the management of LUTS?

A

They cause vasodilation and so reduced resistance to bladder outflow.

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19
Q

Give 2 potential side effects of tamulosin.

A

Tamulosin is an alpha-1-blocker used in the treatment of LUTS. 2 side effects include hypotension and retrograde ejaculation.

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20
Q

How do 5-alpha-reductase-inhibitors work in the management of LUTS?

A

They inhibit the conversion of testosterone to dihydrotestosterone and so reduce prostate size.

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21
Q

Give a surgical treatment for BPE.

A

TURP.

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22
Q

Give 5 potential consequences of untreated LUTS.

A
  1. Bladder calculi (stones).
  2. UTI.
  3. Urinary incontinence.
  4. Reduced QOL.
  5. Acute urinary retention.
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23
Q

Give 3 symptoms of acute urinary retention.

A
  1. PAINFUL!
  2. Sudden onset.
  3. > 500ml of urine in bladder.
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24
Q

Name a rare but serious cause of acute urinary retention.

A

Spinal cord compression.

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25
Q

What investigations might you do in someone with acute urinary retention?

A
  1. Clinical examination: palpable bladder?
  2. MRI.
  3. Bloods.
  4. Neurological tests; could be a sign of spinal cord compression e.g. pain in back, loss of anal reflex, leg weakness.
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26
Q

Describe the treatment for someone with acute urinary retention.

A

Reassurance, catheterise, pain relief.

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27
Q

What nerve fibres do cavernous nerves carry?

A

Parasympathetic: S2-4.
Sympathetic: T11-L2.

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28
Q

Describe the physiology of an erection.

A
  1. Parasympathetic stimulation.
  2. Arteriolar dilation.
  3. Smooth muscle relaxation.
  4. Testosterone.
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29
Q

What chemical compound is responsible for the smooth muscle relaxation that is required for an erection?

A

Nitric oxide (NO). It causes a fall in cytoplasmic calcium -> smooth muscle relaxation.

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30
Q

What are the 2 main causes of erectile dysfunction?

A
  1. Organic e.g. vasculogenic, neurogenic, hormonal, anatomical.
  2. Psychogenic.
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31
Q

Give 3 characteristics of psychogenic erectile dysfunction.

A
  1. Sudden.
  2. Situational.
  3. Younger males affected.
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32
Q

Give 4 risk factors for erectile dysfunction.

A
  1. Obesity.
  2. Lack of exercise.
  3. Smoking.
  4. Diabetes mellitus.
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33
Q

What is the non-pharmacological management of erectile dysfunction?

A
  1. Lose weight, stop smoking.
  2. Education and counselling of patient and partner.
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34
Q

What is the first line pharmacological management of erectile dysfunction?

A

Phosphodiesterase inhibitors e.g. viagra, cialis. They cause vasodilation and so increase arterial blood flow to the penis.

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35
Q

What is the second line pharmacological management of erectile dysfunction?

A
  1. Intracavernous injections.
  2. Vacuum devices.
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36
Q

What is the third line pharmacological management of erectile dysfunction?

A

Penile prosthesis implantation.

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37
Q

What is priapism?

A

Prolonged erection, lasting for >4 hours.

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38
Q

What is a potential consequence of priapism?

A

Permanent ischaemic damage.

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39
Q

Where might a transitional cell carcinoma arise?

A
  1. Bladder (50%).
  2. Ureter.
  3. Renal pelvis.
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40
Q

Describe the epidemiology of transitional cell carcinoma.

A
  1. M:F = 3:1.
  2. Age > 40 y/o.
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41
Q

Give 5 risk factors for transitional cell carcinoma.

A
  1. SMOKING.
  2. Occupational exposure e.g. working in rubber factories (aromatic amines).
  3. Increasing age.
  4. Male gender.
  5. Family history.
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42
Q

Give 5 symptoms of transitional cell carcinoma.

A
  1. PAINLESS HAEMATURIA.
  2. Frequency.
  3. Urgency.
  4. Dysuria.
  5. Urinary tract obstruction.
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43
Q

Give 5 investigations that you might do in someone who you suspect has transitional cell carcinoma.

A
  1. Urine dipstick.
  2. Blood tests.
  3. Flexible cystoscopy = diagnostic.
  4. Imaging of upper urinary tract e.g. CT IVU.
  5. TURBT.
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44
Q

Give 2 potential risks of flexible cystoscopy.

A
  1. UTI’s.
  2. Problems passing urine.
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45
Q

Why would you want to image the upper urinary tract of someone with transitional cell carcinoma?

A

You image the UUT to confirm that there is no other TCC elsewhere in the urinary tract.

CT IVU, USS and XR can be used.

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46
Q

Why might you do a trans-urethral resection of bladder tumour (TURBT) in someone with TCC?

A

For histological and staging analysis.

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47
Q

What staging system is used for TCC?

A

TNM staging.

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48
Q

Describe the treatment for non-muscle invasive bladder cancer (CIS, Ta, T1).

A
  1. TURBT.
  2. Chemotherapy to reduce the risk of recurrence and progression to muscle invasion.
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49
Q

Describe the treatment for muscle invasive bladder cancer (T2, T3).

A
  1. Radical cystectomy = gold standard.
  2. +/- neo-adjuvant chemotherapy.
  3. Radical radiotherapy if not fit/unwilling to undergo cystectomy.
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50
Q

Describe the treatment for T4 TCC (invasion beyond the bladder).

A
  1. Palliative chemo/radiotherapy.
  2. Chronic catheterisation for pain.
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51
Q

Name a helminth that can cause squamous cell carcinoma of the bladder.

A

Schistosomiasis.

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52
Q

Give 5 functions of the kidney.

A
  1. Filters and excretes waste products from the blood.
  2. Regulates BP.
  3. Retains albumin.
  4. Reabsorption of Na, Cl, K, glucose, H2O, amino acids.
  5. Synthesises EPO.
  6. Converts 1-hydroxyvitaminD to 1,25-dihydroxyvitaminD.
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53
Q

Write an equation for GFR.

A

(Um X urine flow rate) / Pm.

  • Um = concentration of marker substance in urine.
  • Pm = concentration of marker substance in plasma.
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54
Q

What would you expect a typical GFR to be?

A

120ml/min.

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55
Q

Give an example of a marker substance used for estimating GFR.

A

Creatinine.

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56
Q

Estimating GFR: Give 3 essential features of a marker substance.

A
  1. Not metabolised.
  2. Freely filtered.
  3. Not reabsorbed/secreted.
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57
Q

Name a drug that can inhibit creatinine secretion. What is the affect of this on GFR?

A

Trimethoprim.
Serum creatinine rises and so kidney function (GFR) appears worse.

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58
Q

What is the affect on GFR of afferent arteriole vasoconstriction?

A

Decreased GFR.

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59
Q

What is the affect on GFR of efferent arteriole vasoconstriction?

A

Increased GFR.

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60
Q

Where in the nephron does the bulk of reabsorption occur?

A

At the proximal convoluted tubule.

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61
Q

What 7 things are reabsorbed at the PCT?

A
  1. Sodium.
  2. Chlorine.
  3. Potassium.
  4. Glucose.
  5. Water.
  6. Amino acids.
  7. Bicarbonate.
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62
Q

What is Fanconi syndrome?

A

Failure of the nephron to reabsorb essential ions. Sugar, amino acids and bicarbonate are therefore present in the urine.

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63
Q

Give 2 signs of Fanconi syndrome.

A
  1. Sugar in the urine.
  2. Acidotic due to bicarbonate in the urine.
  3. Rickets/osteomalacia.
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64
Q

Give 2 causes of Fanconi syndrome.

A
  1. Myeloma.
  2. Cystinosis.
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65
Q

What is the function of the counter current multiplication system?

A

It generates a hypertonic medullary interstitium for H2O reabsorption. Na+ moves out of the ascending limb which increases the medullary osmolality, H2O follows.

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66
Q

Which part of the loop of henle is permeable to H2O?

A

The descending limb is permeable to H2O.

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67
Q

Describe tubuloglomerular feedback.

A

Macula densa cells of the DCT lie between the AA and EA. They detect NaCl and use this as an indicator of GFR.

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68
Q

Macula densa cells detect a raised NaCl. What is the response?

A

AA constriction.

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69
Q

Macula densa cells detect a reduced NaCl. What is the response?

A

Renin secretion.

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70
Q

What 2 cell types are found in the nephron collecting duct?

A

Principal and intercalated cells.

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71
Q

What hormone is responsible for regulating sodium reabsorption?

A

Aldosterone.

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72
Q

Why might aldosterone secretion lead to hypokalaemia?

A

Aldosterone secretion leads to increased sodium reabsorption. Sodium reabsorption leads to increased potassium secretion and therefore hypokalaemia.

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73
Q

What is the affect of NSAIDs on the afferent arteriole of glomeruli?

A

NSAIDs inhibit prostaglandins and so lead to AA vasoconstriction = reduced GFR.

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74
Q

NSAIDs lead to a reduced GFR. Why?

A

NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction -> reduced GFR.

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75
Q

What is the affect of ACEi on the efferent arteriole of glomeruli?

A

ACEi cause EA vasodilation = reduced GFR.

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76
Q

Name 2 factors that govern renal potassium.

A
  1. Na+.
  2. Aldosterone.
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77
Q

What ion is responsible for volume control?

A

Sodium!

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78
Q

Name 2 hormones that increase sodium reabsorption.

A
  1. Aldosterone.
  2. Angiotensin 2.
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79
Q

Name a hormone that decreases sodium reabsorption.

A

ANP.

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80
Q

What is the function of EPO?

A

It stimulates the bone marrow -> RBC maturation.

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81
Q

Give 2 functions of calcitriol.

A
  1. Increased calcium and phosphate absorption from the gut.
  2. Suppression of PTH.
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82
Q

Why might someone with advanced CKD also have hyperparathyroidism?

A

Advanced CKD = calcitriol deficiency. Calcitriol suppresses PTH therefore deficiency -> hyperparathyroidism.

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83
Q

What triggers PTH secretion?

A

Low serum calcium.

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84
Q

Give 3 ways in which PTH increases serum calcium.

A
  1. Increased bone resorption.
  2. Increased reabsorption of calcium at the kidneys.
  3. Stimulates 1-hydroxylase -> 1,25-dihydroxyvitaminD -> increased calcium absorption from the intestine.
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85
Q

Name 2 hormones secreted from the posterior pituitary gland.

A
  1. ADH.
  2. Oxytocin.
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86
Q

Describe the function of ADH.

A

ADH acts on the collecting ducts. It increases insertion of aquaporin 2 channels leading to H2O retention.

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87
Q

Give 3 factors that stimulate renin release.

A
  1. Sympathetic stimulation.
  2. Decreased BP.
  3. Decreased Na detected by macula densa.
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88
Q

Give 3 functions of ANP.

A
  1. Renal vasodilator.
  2. Inhibits aldosterone.
  3. Closes ENaC (decreased reabsorption of Na+).
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89
Q

Where on the nephron does aldosterone act?

A

On the collecting ducts.

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90
Q

Describe aldosterone action.

A

Aldosterone acts on the collecting ducts. It increases ENaC and H+/K+ pumps. There is increased Na+ absorption and K+ secretion -> H20 retention -> increased BP.

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91
Q

Define urinary tract infection.

A

Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriruria and pyuria.

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92
Q

Name 3 UTI causative organisms.

A
  1. Uropathogenic strains of E.coli (UPEC) - 82%.
  2. CNS e.g. s.saprophyticus.
  3. Proteus mirabilis.
  4. Enterococci.
  5. Klebsiella pneumonia.
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93
Q

Briefly describe the epidemiology of UTI’s.

A

More common in women due to short urethra and its proximity to the anus.

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94
Q

Describe the pathophysiology of UTI’s.

A

Organisms colonise the urethral meatus and ascend via the transurethral route.

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95
Q

What can facilitate bacteria ascent into the urinary tract via the urethra?

A
  1. Sexual intercourse.
  2. Catheterisation.
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96
Q

Give 3 bacterial virulence factors that aid their ability to cause UTI’s.

A
  1. Fimbriae/pili that adhere to urothelium.
  2. Acid polysaccharid coat resists phagocytosis.
  3. Toxins e.g. UPEC releases cytotoxins.
  4. Enzyme production e.g. urease.
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97
Q

What do type 1 pili bind to?

A

Uroplakin.

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98
Q

What do type P pili bind to?

A

Glycolipids on urothelium.

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99
Q

What type of pili would you associate with a lower UTI?

A

Type 1.

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100
Q

What type of pili would you associate with an upper UTI?

A

Type P.

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101
Q

The vagina is heavily colonised with lactobacilli. What is the function of this?

A

Helps maintain a low pH = host defence mechanism.

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102
Q

Give 2 reasons why a post menopausal woman is more susceptible to a UTI.

A
  1. pH rises -> increased colonisation by colonic flora.
  2. Reduced mucus secretion.
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103
Q

Give 5 host defence mechanisms against urinary tract infection.

A
  1. Antegrade flushing of urine.
  2. Tamm-horsfall protein.
  3. GAG layer.
  4. Low urine pH.
  5. Commensal flora.
  6. Urinary IgA.
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104
Q

What is pyuria?

A

The presence of leukocytes in urine.

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105
Q

Name 4 lower urinary tract infections.

A
  1. Cystitis.
  2. Prostatitis.
  3. Epididymitis.
  4. Urethritis.
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106
Q

Name 1 upper urinary tract infection.

A

Pyelonephritis.

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107
Q

What investigations might you do on someone who you suspect has a UTI?

A
  1. Take a good history.
  2. Urinalysis - multistix SG.
  3. Microscopy; culture and sensitivity of mid-stream urine.
  4. In recurrent/complicated UTI renal imaging is important.
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108
Q

What determines if a UTI is complicated or uncomplicated?

A

A UTI is deemed complicated if it affects:
- Someone with an abnormal urinary tract.
- A man.
- A pregnant lady.
- Children.
- The immunocompromised.
- If it is recurrent.

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109
Q

What is the first line treatment for an uncomplicated UTI?

A
  • Trimethoprim or nitrofurantoin for 3 days.
  • Increased fluid intake and regular voiding.
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110
Q

How does trimethoprim work?

A

It affects folic acid metabolism.

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111
Q

Describe the management for a complicated UTI.

A

Same as for an uncomplicated UTI but a MCS MSU is essential! The patient would normally take a longer Abx course tailored to sensitivity.

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112
Q

Give 3 causes of recurrent UTI’s.

A
  1. Re-infection.
  2. Bacterial persistence.
  3. Unresolved infection.
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113
Q

Define recurrent UTI.

A

> 2 episodes in 6 months of > 3 in 12 months.

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114
Q

Describe the management for someone who is having recurrent UTI’s.

A
  1. Increase fluid intake.
  2. Regular voiding.
  3. Void pre and post intercourse.
  4. Abx prophylaxis.
  5. Vaginal oestrogen replacement.
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115
Q

What is cystitis?

A

Inflammation of the bladder secondary to infection.

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116
Q

Give 4 risk factors for cystitis.

A
  1. Obstruction.
  2. Previous damage to bladder epithelium.
  3. Bladder stones.
  4. Poor bladder emptying.
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117
Q

Give 3 symptoms of cystitis.

A
  1. Dysuria.
  2. Frequency.
  3. Urgency.
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118
Q

Describe the NIDDK classification for prostatitis.

A
  • Type 1: acute bacterial prostatitis.
  • Type 2: chronic bacterial prostatitis.
  • Type 3a: Inflammatory chronic pelvic pain syndrome.
  • Type 3b: non-inflammatory chronic pelvic pain syndrome.
  • Type 4: asymptomatic inflammatory prostatitis.
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119
Q

Give 5 symptoms of acute bacterial prostatitis (type 1).

A
  1. Systemically unwell, fever.
  2. Rigors.
  3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow).
  4. Pelvic pain.
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120
Q

Give 4 symptoms of chronic bacterial prostatitis (type 1).

A
  1. Recurrent UTI’s.
  2. Pelvic pain.
  3. Voiding LUTS (straining, hesitancy, incomplete emptying, poor flow).
  4. Uropathogens in urine.

The patient should have had the symptoms for >3 months.

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121
Q

Give a symptom of type 3 prostatitis.

A

Chronic pelvic pain.

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122
Q

What investigations might you do in someone with prostatitis?

A
  1. Urinalysis and MSU.
  2. Semen cultures.
  3. STI screen.
  4. Bloods including MCS.
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123
Q

Describe the treatment for type 1 prostatitis.

A

Type 1 = acute bacterial prostatitis.
- IV Abx e.g. gentamicin, co-amoxiclav for 2-4 weeks.

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124
Q

Describe the treatment for type 2 prostatitis.

A

Type 2 = chronic bacterial prostatitis.
- 4-6 weeks quinolone e.g. ciprofloxacin.

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125
Q

What can cause urethritis?

A

STI’s e.g. gonorrhoea, chlamydia.

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126
Q

Give a symptom of urethritis.

A

Urethral pain/dysuria.

127
Q

What is epididymo-orchitis?

A

Inflammation of the epididymis and testicle.

128
Q

Give 3 symptoms of epididymo-orchitis.

A
  1. Sudden onset tender swelling.
  2. Dysuria.
  3. Sweats/fever.
129
Q

Describe the aetiology of epididymo-orchitis.

A
  1. If <35 y/o = STI e.g. chlamydia.
  2. If >35 y/o = UTI.
130
Q

What investigations might you do on someone who you suspect has epididymo-orchitis?

A
  1. Void urine.
  2. Urehtral swab.
  3. MSU.

Rule out testicular torsion!

131
Q

Describe the treatment for epididymo-orchitis.

A
  1. If STI aetiology suspected; refer to GUM and maybe give doxycycline.
  2. If UTI aetiology suspected give quinolone (ciprofloxacin).
132
Q

Define pyelonephritis.

A

Inflammation secondary to infection of the renal parenchyma and soft tissues of the renal pelvis.

133
Q

What can cause pyelonephritis?

A

UPEC. Typically P pili.
Infection is usually from the bladder.

134
Q

Give 3 symptoms of pyelonephritis.

A
  1. Loin pain.
  2. Fever.
  3. Pyuria.

May also have a severe headache and be fluid deplete.

135
Q

What investigations might you do in someone with pyelonephritis?

A
  1. Urinalysis.
  2. MCS MSU.
  3. Bloods - raised WCC, ESR and CRP.
136
Q

Describe the treatment for pyelonephritis.

A

IV fluids and antibiotics e.g. gentamicin/co-amoxiclav.

  • Drain obstructed kidney.
  • Catheterise if necessary.
  • Analgesics.
137
Q

What is the likely cause of pyelonephritis in children?

A

Reflux or structural/functional abnormalities.

138
Q

What is the function of the prostate?

A

The prostate secretes proteolytic enzymes into the semen which break down clotting factors in the ejaculate.

139
Q

Which anatomical zone of the prostate does prostate cancer commonly affect?

A

The peripheral zone.

140
Q

Where can prostate cancer commonly metastasise to?

A

Lymph nodes and bone.

141
Q

What investigations might you do in someone who you suspect has prostate cancer?

A
  • Serum: PSA.
  • Urine: PCA3 and gene fusion products.
  • DRE - hard, irregular, craggy.
  • History of LUTS.
  • Trans-rectal USS.
  • Prostate biopsy.
142
Q

Other than prostate cancer. What can cause an elevated PSA?

A
  1. Benign prostate enlargement.
  2. UTI.
  3. Prostatitis.
143
Q

What grading system is used in prostate cancer?

A

Gleason grading.

The higher the score the more aggressive the cancer.

144
Q

What is the treatment for localised prostate cancer?

A
  • Observation.
  • Surgery - radical prostatectomy.
  • Radiotherapy (external beam).
  • Adjuvant hormones.
145
Q

What is the treatment for metastatic prostate cancer?

A

Palliative treatment e.g. hormone therapy - androgen deprivation.

146
Q

Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer.

A
  • Curative.
  • Reduced patient anxiety.
  • Can have adverse effects.
147
Q

Give 2 advantages and 2 disadvantages of screening in prostate cancer.

A
  • Screening can lead to early diagnosis/early treatment and so cure or effective palliation.
  • Uncertain natural history.
  • Screening leads to over diagnosis and treatment.
148
Q

Name 2 groups of people that you would treat for bacteriuria?

A
  • Pregnant ladies.
  • Children.
149
Q

What is septic shock?

A

Severe sepsis with persistent hypotension.

150
Q

Describe the pathophysiology of urosepsis.

A

A symptomatic UTI combined with >1 of:
1. Microbial resistance.
2. Immunosuppression.
3. Pressure.
= UROSEPSIS!

151
Q

What can cause raised urinary tract pressure?

A
  1. Stone in lumen of UUT.
  2. Tumour in the wall.
  3. LUT outflow obstruction: BPH, tumour, stone.
  4. Bladder dysfunction.
152
Q

Give 4 causes of urinary tract colonisation.

A
  1. Diseases that require steroids or chemo e.g. diabetes, immunodeficiency.
  2. Stones or tumour in the lumen of the urinary tract.
  3. Poor bladder emptying.
  4. Catheterisation.
153
Q

Describe the treatment for sepsis.

A

The sepsis 6:
1. Give high flow oxygen.
2. Take blood cultures.
3. Give IV abx.
4. Give IV fluids.
5. Check lactate.
6. Monitor hourly urine output.

Also drainage to relieve pressure!

154
Q

Describe the epidemiology of renal cell carcinoma.

A
  1. Incidence increases in those > 60 y/o.
  2. Males > females.
155
Q

Give 3 risk factors for renal cell carcinoma.

A
  1. Smoking.
  2. Obesity.
  3. Hypertension.
156
Q

Name an inherited renal disease that can cause renal cell carcinoma.

A

Von Hippel Lindau disease.

Autosomal dominant. There is a loss of the tumour suppressor gene VHL which is encoded for on chromosome 3. Lots of benign cysts grow, some of which may develop into cancer.

157
Q

What is Von Hippel Lindau disease?

A

An autosomal dominant disease. There is a loss of the tumour suppressor gene VHL which is encoded for on chromosome 3. Lots of benign cysts grow, some of which may develop into cancer.

158
Q

What are the 3 classic signs of renal cell carcinoma?

A
  1. Haematuria.
  2. Flank mass.
  3. Loin pain.
159
Q

Why do people with renal cell carcinoma rarely present with symptoms of the disease?

A

The signs of renal cell carcinoma are now rare as people with the disease are detected incidentally through imaging for something else before they show any symptoms.

160
Q

Name 3 places that renal cell carcinoma might metastasise to.

A
  1. Lymph nodes.
  2. Lungs.
  3. Bones.
161
Q

What is varicocele?

A

An abnormal enlargement of the pampiniform venous plexus in the scrotum.

162
Q

Why might renal cell carcinoma cause left sided varicocele?

A

If the renal tumour obstructs where the gonadal vein drains into the renal vein blood can back up and so you may see left sided varicocele.

163
Q

Name the classification that helps differentiate between benign cystic lesions and cancerous cystic lesions.

A

The Bozniak classification.

164
Q

What investigations might you do in someone with renal cell carcinoma?

A
  • Ultrasound.
  • Bloods: FBC, U+E, LFT, Ca profile.
  • Abdo CT scan with contrast.
  • Bone scan for boney metastases.
165
Q

What is the treatment for localised renal cell carcinoma?

A

Surgical excision - partial nephrectomy.

166
Q

What is the treatment for metastatic renal cell carcinoma?

A
  • Palliative nephrectomy.
  • Radiotherapy.
167
Q

Give a reason why incontinence in men is less common than it is women.

A

Men have a bladder neck mechanism and a strong urethral sphincter whereas women have only a weak urethral sphincter.

168
Q

What information can you get from a bladder diary?

A
  1. Frequency.
  2. Volume.
  3. Functional capacity.
  4. Incontinence/day.
169
Q

Name 3 types of incontinence.

A
  1. Stress - associated with coughing or sneezing.
  2. Urgency.
  3. Mixed - stress and urgency.
  4. Continuous - due to fistula.
170
Q

What is the main cause of stress incontinence in women?

A

Stress incontinence is usually secondary to birth trauma.

171
Q

Describe the treatment for stress incontinence in females.

A
  1. Pelvic floor physio.
  2. Duloxetine (concerns over SE’s).
  3. Surgery.
172
Q

What is the main cause of stress incontinence in men?

A

Neurogenic or iatrogenic (prostatectomy).

173
Q

Describe the treatment for stress incontinence in males.

A
  1. Artificial sphincter.
  2. Sling.
174
Q

What are the symptoms of an overactive bladder?

A

Urgency and frequency in the absence of local pathology that would account for these symptoms.

175
Q

Describe the treatment for an overactive bladder.

A
  1. Behavioural e.g. limit caffeine and alcohol, bladder drill, hypnotherapy.
  2. Pelvic floor physio.
  3. Muscarinic antagonists.
  4. Beta 3 agonists.
  5. Botox.
  6. Cystoplasty.
176
Q

What is the role of the cortex in micturition?

A

It has roles in sensation and voluntary initiation of voiding.

177
Q

What is the role of PMC/PAG in micturition?

A

Co-ordination and completion of voiding.

178
Q

A patient presents with haematuria. A MSU sample is taken and a blood film is done. The RBC’s look dysmorphic. Where in the urinary tract is the problem likely to be?

A

Dysmoprhic RBC’s signify a glomerular origin.

If the RBC’s looked normal the problem is likely to be with the LUT.

179
Q

Give 5 causes of haematuria.

A
  1. Kidney tumour, trauma, stones, cysts.
  2. Ureteric stones or tumour.
  3. Bladder infection, stones or tumour.
  4. BPH or prostate cancer.
180
Q

What further investigations might you do in someone who presents with haematuria?

A
  1. Urinalysis.
  2. Urine cytology.
  3. Abdomen US.
  4. Abdomen CT.
  5. Cystoscopy.
181
Q

Describe the fluid distribution in the body.

A

ICF: 28L.
ECF: 14L
- Interstitial: 11L.
- Plasma: 3L.

Total body water: 42L.

182
Q

How much extra-vascular fluid is there in the body?

A

ICF + interstitial = 39L.

183
Q

How much intra-vascular fluid is there in the body?

A

Plasma: 3L.

184
Q

What happens to the heart rate in hypovolaemia?

A

Increases - tachycardia.

185
Q

What happens to the blood pressure in hypovolaemia?

A

Decreases - hypotension.

186
Q

What happens to the JVP in hypovolaemia?

A

JVP is low.

187
Q

What happens to tissue turgor in hypovolaemia?

A

Tissue turgor is reduced.

188
Q

What happens to urine output in hypovolaemia?

A

Urine output is reduced.

189
Q

What happens to weight in hypovolaemia?

A

Weight is reduced.

190
Q

Give 2 symptoms of hypovolaemia.

A

Thirst and dizziness.

191
Q

What happens to creatinine, haemoglobin and haematocrit levels in hypovolaemia?

A

They are raised.

192
Q

Name 5 groups of people who are at risk of hypovolaemia.

A
  1. Elderly.
  2. Those who have had an ileostomy.
  3. People with short bowel syndrome.
  4. Bowel obstruction.
  5. People taking diuretics.
193
Q

Name 5 groups of people who are at risk of hypervolaemia.

A
  1. Acute kidney injury patients.
  2. CKD patients.
  3. Heart failure patients.
  4. Liver failure patients.
194
Q

What happens to the heart rate in hypervolaemia?

A

HR is normal.

195
Q

What happens to blood pressure in hypervolaemia?

A

Blood pressure is high or normal.

196
Q

What happens to JVP in hypervolaemia?

A

JVP is high.

197
Q

What happens to tissue turgor in hypervolaemia?

A

Tissue turgor is normal.

198
Q

What happens to urine output in hypervolaemia?

A

Urine output is normal.

199
Q

What happens to weight in hypervolaemia?

A

Weight is increased.

200
Q

Give 2 symptoms of hypervolaemia.

A
  1. Shortness of breath.
  2. Peripheral oedema.
201
Q

What happens to creatinine, haemoglobin and haematocrit levels in hypervolaemia?

A

They are reduced.

202
Q

Where might fluid accumulate in someone with hypervolaemia?

A
  • Pulmonary oedema.
  • Pleural effusion.
  • Ascites.
  • Bowel obstruction.
  • Intra-abdominal collection.
203
Q

Describe the management for hypovolaemia.

A
  1. Oral fluid.
  2. IV fluid if very ill.
  3. Treat reversible causes.
204
Q

Describe the management for hypervolaemia.

A
  1. Diuretics e.g. furosemide.
  2. Fluid restriction.
  3. Treat reversible causes.
205
Q

Name 3 isotonic solutions.

A
  1. 5% dextrose.
  2. 0.9% NaCl.
  3. Hartmann’s solution.
206
Q

What type of IV fluid moves from the intra-vascular to the extra-vascular space?

A

Crystalloid.

Small molecules pass through cell membranes and so move from the intra-vascular to extra-vascular space.

207
Q

Give an example of a colloid IV fluid.

A

Gelofusine.

208
Q

Give 3 potential causes of rising creatinine.

A
  1. Too aggressive with diuretics.
  2. Extravascular hypervolaemia but intravascular hypovolaemia.
  3. Progression of CKD.
209
Q

Why do advanced CKD patients need regular fluid assessment?

A

They may be oligouric or anuric.

210
Q

What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream.

211
Q

Give 4 symptoms of BPH.

A
  1. Increased frequency of micturition.
  2. Nocturia.
  3. Hesitancy.
  4. Post-void dribbling.
212
Q

Describe the treatment for BPH.

A
  1. Mild symptoms: watchful waiting.
  2. Alpha-1-antagonists e.g. tamulosin.
  3. 5-alpha-reductase inhibitors.
213
Q

How does tamulosin work in improving the symptoms of BPH?

A

Tamulosin is an alpha-1-antagonist. It works by relaxing the smooth muscle in the bladder neck and prostate and so increases urinary flow. This improves obstructive symptoms.

214
Q

How do 5-alpha-reductase inhibitors work in improving the symptoms of BPH?

A

5-alpha-reductase inhibitors block the conversion of testosterone to dihydrotestosterone (the androgen responsible for prostatic growth).

215
Q

Give 4 symptoms of prostate carcinoma.

A
  1. Increased frequency of micturition.
  2. Nocturia.
  3. Hesitancy.
  4. Post-void dribbling.

(Same as BPH).

216
Q

What investigations might you do in someone to see whether they have prostate carcinoma?

A
  1. Trans-rectal USS of prostate.
  2. Serum PSA - will be elevated.
  3. Trans-rectal prostate biopsy.
217
Q

Describe the treatment for prostate carcinoma.

A
  1. Radical prostatectomy or radiotherapy.
  2. For metastatic disease, remove the androgenic drive e.g. bilateral orchidectomy.
218
Q

Describe the epidemiology of stones in the urinary tract.

A
  • 10-15% lifetime risk.
  • Males > females - 2:1 ratio.
  • Common among 30-50 y/o.
219
Q

Give 5 potential causes of stones in the upper urinary tract.

A
  1. Congenital abnormalities.
  2. Metastable urine.
  3. Hypercalciuria/ high urate/ high oxalate.
  4. Dehydration!
  5. Infection.
220
Q

Describe the pathophysiology of stone formation in the upper urinary tract.

A

Stones form from crystals in supersaturated urine.
- 80% are calcium based e.g. calcium oxalate.

221
Q

Give 5 symptoms of upper urinary tract stones.

A
  1. Loin pain -> groin pain.
  2. ‘Renal colic’ - pain caused by a blockage in the urinary tract.
  3. UTI symptoms e.g. dysuria, urgency, frequency.
  4. Recurrent UTI’s.
  5. Haematuria.
222
Q

Give 5 ways in which urinary tract stones can be prevented.

A
  1. Stay well hydrated.
  2. Low salt diet.
  3. Healthy protein intake.
  4. Reduced BMI.
  5. Active lifestyle.
  6. Deacidifcation of urine can prevent uric acid stones.
223
Q

What investigations might you do to find out what is causing someone’s renal colic?

A
  1. Bloods - inc. calcium, phosphate and urate.
  2. Urinalysis.
  3. MCS MSU.
  4. NCCT-KUB - gold standard!
224
Q

Describe the treatment for renal colic.

A
  1. Analgesia e.g. NSAIDs (diclofenac).
  2. Anti-emetics.
  3. Check for sepsis.
225
Q

How would you treat someone who presents with large ‘stag horn’ ureteric stones.

A
  1. Analgesia and anti-emetics.
  2. Observe for sepsis.
  3. PCNL.
226
Q

Describe the pathophysiology of congenital polycystic kidney disease.

A

Genetic mutation -> predisposition to cyst development -> cell proliferation and loss of planar polarity -> fluid secretion and cyst expansion.

227
Q

Describe the pathophysiology of acquired polycystic kidney disease.

A

Cysts develop over time.

Renal injury/ischaemia -> abnormal cell proliferation.

228
Q

What classification can be used to help differentiate between benign cystic lesions and cancerous lesions?

A

Bozniak classification.

229
Q

Give 4 congenital causes of renal cysts.

A
  1. ADPKD.
  2. ARPKD.
  3. VHL.
  4. OFD1 (oral-facial-digital syndrome 1).
230
Q

What is ADPKD?

A

An autosomal dominant condition characterised by progressive cyst development. Cysts increase in size -> renal enlargement and loss of function -> kidney failure.

231
Q

A mutation in which genes can cause ADPKD?

A
  1. PKD1 (associated with more severe disease).
  2. PKD2.
232
Q

Give 4 signs of ADPKD.

A
  1. Hypertension.
  2. Haematuria.
  3. Polyuria.
  4. Abdominal/loin pain.
  5. Palpable bilateral costo-vertebral masses.
233
Q

Give 2 extra-renal manifestations of ADPKD.

A
  1. Polycystic liver disease.
  2. Intracranial aneurysms e.g. SAH.
234
Q

How can ADPKD be diagnosed?

A
  • Symptoms.
  • Family history.
  • High BP.
  • Urinalysis.
  • USS.
235
Q

What value can be used as a prognostic marker for ADPKD?

A

TKV - total kidney volume.

236
Q

A mutation in what gene can cause AD tubulo-interstitial kidney disease?

A

HNF1 beta.

237
Q

A mutation in what gene can cause ARPKD?

A

PKHD1.

238
Q

Give 4 features of acquired renal cystic disease.

A
  1. No genetic mutation.
  2. No family history.
  3. Normal kidney size.
  4. Risk factor for renal cell carcinoma.
239
Q

What is the access point in haemodialysis?

A

AV fistula.

240
Q

Why might someone having haemodialysis have a PFTE graft as opposed to an AV fistula?

A

If the patient has atherosclerotic veins or has had previous fistulas they may have a PFTE graft or a catheter tunnelled into the RA.

241
Q

Give examples of waste products that are removed from the blood in dialysis.

A
  1. Urea.
  2. Creatinine.
  3. Potassium.
  4. Phosphate.
242
Q

How many times a week and for how long does someone have hospital haemodialysis for?

A

3-5 hours, 3 times a week.

243
Q

How many times a week and for how long does someone have home haemodialysis for?

A

2-3 hours, 4-5 times a week.

244
Q

Why can someone on home haemodialysis take fewer tablets and have less dietary restrictions compared to someone on hospital haemodialysis?

A

Patients doing home haemodialysis dialyse more frequently and so can have less restriction on their diet.

245
Q

Give 5 potential complications of haemodialysis.

A
  1. Hypotension.
  2. Cramps.
  3. Nausea.
  4. Chest pain.
  5. Fever.
  6. Blocked or infected dialysis catheter.
246
Q

Give 3 groups of people who haemodialysis is good for.

A
  1. People who live alone/frail/elderly.
  2. People who fear operating machines.
  3. People who are unsuitable for PD e.g. previous abdominal surgery, abdominal hernia etc.
247
Q

What is the access point in peritoneal dialysis?

A

A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel.

248
Q

How often does someone have to do CAPD?

A

30-40 minute exchanges, 3-5 times a day.

249
Q

How often does someone have to do APD?

A

One exchange overnight (8 hours).

250
Q

Give 4 potential complications of peritoneal dialysis.

A
  1. Infection e.g. peritonitis/catheter exit site infection.
  2. Peri-catheter leak.
  3. Abdominal wall herniation.
  4. Intestinal perforation.
251
Q

Give 3 groups of people who peritoneal dialysis is good for.

A
  1. Young people/those in full time work.
  2. People who want control/responsibility of their care.
  3. People with severe HF.
252
Q

Where in the abdomen does a transplanted kidney lie?

A

In the iliac fossa.

253
Q

Describe the criteria for selection of a living donor for kidney transplant.

A
  1. Blood relative.
  2. ABO blood group compatible.
  3. HLA identical.
  4. Excellent medical condition and normal renal function.
254
Q

Name 3 medical conditions that can exclude living kidney donation.

A
  1. Renal parenchymal disease.
  2. History of stones/frequent UTI/hypertension/DM.
  3. Recent malignancy.
255
Q

Describe the criteria for selection of a cadaver donor for kidney transplant.

A
  1. Irreversible brain damage.
  2. Normal renal function.
  3. No evidence of pre-existing renal disease or transmissible disease.
  4. ABO compatible and best HLA possible.
256
Q

What tests can be done to evaluate kidney function in a potential kidney donor?

A
  1. Serum creatinine.
  2. Creatinine clearance.
  3. Urinalysis.
  4. Urine culture.
  5. GFR.
257
Q

Give 5 contraindications for renal transplant.

A
  1. ABO incompatibility.
  2. Cytotoxic Ab’s against HLA antigens.
  3. Recent malignancy.
  4. Active infection.
  5. AIDS.
  6. Morbid obesity.
  7. Age > 70 y/o.
258
Q

Give 3 ways in which recipient and donor matching is assessed.

A
  1. HLA tissue typing (important to match DR antigens).
  2. Lymphocytotoxic cross matching; checks there are no preformed antibodies against HLA antigens.
  3. ABO blood group compatibility.
259
Q

Give 4 factors that can influence the longevity of renal allograft.

A
  1. Age.
  2. HLA matching.
  3. Ischaemia time.
  4. Number of acute rejection episodes.
  5. Ethnicity.
260
Q

What are the 2 major causes of allograft failure?

A
  1. Chronic rejection.
  2. Death with functioning graft.
261
Q

What are the 2 major causes of death after kidney transplant?

A
  1. CV disease.
  2. Infection.
262
Q

Name the 3 types of renal allograft rejection.

A
  1. Hyper-acute.
  2. Acute.
  3. Chronic.
263
Q

Describe hyper-acute renal allograft rejection.

A

Preformed antibodies against HLA antigens of donor organ.

264
Q

Why might someone have pre-formed antibodies against HLA antigens?

A

Can be a consequence of blood transfusion, pregnancy, prior transplant, auto-immune disease.

265
Q

What can cause immediate graft loss?

A

Fibrinoid necrosis.

266
Q

Describe acute renal allograft rejection.

A

Activated T lymphocytes. Occurs within the first 6 months but is often reversible e.g. with steroids.

267
Q

Describe chronic renal allograft rejection.

A

Slow and gradual decline in renal function, accompanied by proteinuria.

268
Q

What criteria can be used to diagnose allograft rejection?

A

Banff criteria.

269
Q

Give 3 consequences of chronic immunosuppression.

A
  1. Malignancy.
  2. Infection.
  3. SE’s of other drugs.
270
Q

Give 5 causes of CKD.

A
  1. Diabetes mellitus.
  2. Hypertension.
  3. Atherosclerotic renal vascular disease.
  4. Congenital e.g. PKD.
  5. Urinary tract obstruction.
271
Q

Give 5 signs of CKD.

A
  1. Proteinuria.
  2. Haematuria.
  3. Impaired eGFR <60ml/min.
  4. Rise in serum urea/creatinine.
  5. Anaemia (reduced EPO).
  6. Bone disease.
  7. Polyneuropathy.
  8. CV disease.
  9. Erectile dysfunction.
  10. Raised PTH.
272
Q

Describe the management for CKD.

A
  1. Treat the underlying cause.
  2. Slow deterioration of kidney function e.g. maintain BP.
  3. Reduce CV risk e.g. statins, smoking cessation.
  4. Treat complications e.g. anaemia.
  5. ESRF -> dialysis or transplant.
273
Q

Give 3 consequences of glomerulonephritis (glomerular disease).

A
  1. Leaky glomeruli -> haematuria and proteinuria.
  2. High BP.
  3. Deteriorating kidney function.
274
Q

Briefly describe the pathophysiology of glomerulonephritis (glomerular disease).

A

Immunologically mediated: immunoglobulin deposits and inflammatory cells.

275
Q

Give 4 causes of acute nephritic syndrome.

A
  1. ANCA.
  2. Goodpastures.
  3. SLE.
  4. Post streptococcal infection (immune complex deposition in the kidney).
  5. IgA nephropathy.
276
Q

Give 5 signs of acute nephritic syndrome.

A
  1. Inflammation of glomeruli.
  2. HAEMATURIA and PROTEINURIA.
  3. Hypertension.
  4. Fluid overload.
  5. Oliguria.
  6. Red cell casts.
277
Q

What 4 signs are needed in order to make a diagnosis of nephrotic syndrome.

A
  1. Hypoalbuminaemia.
  2. Oedema.
  3. Heavy proteinuria!
  4. Hypercholesterolaemia.
278
Q

What can nephrotic syndrome be secondary to?

A
  1. Diabetes.
  2. Amyloid.
  3. Infections.
  4. SLE.
  5. Drugs.
279
Q

Describe the treatment for nephrotic syndrome.

A
  1. Treat complications e.g. diuretics for oedema; ACEi for proteinuria.
  2. Treat the underlying cause.
  3. Statins and anti-coagluation e.g. warfarin.
  4. In children give steroids as minimal change disease is the most likely cause.
280
Q

What would you notice on the electron microscopy taken from someone with minimal change disease?

A

Fused podocytes.

281
Q

What is the treatment for minimal change disease?

A

Steroids.

282
Q

Name a loop diuretic.

A

Furosemide - acts on Na+/K+/2Cl- transporter (NKCC2).

283
Q

Give 3 potential side effects of furosemide.

A
  1. Hypokalaemia.
  2. Hypotension.
  3. Dehydration.
284
Q

What other drug might you prescribe with furosemide in someone with poorly controlled potassium?

A

A potassium sparing diuretic e.g. spironolactone. These work on RAAS (hormonal systems) as opposed to ion channels and should help control potassium levels in the blood.

285
Q

Name a potassium sparing diuretic.

A

Spironolactone.

286
Q

On which part of the nephron do thiazides act?

A

The distal tubule.
Act on NCC channels.

287
Q

Describe the pathophysiology behind nephritic syndrome.

A

Immune complex deposition in glomerular capillary -> neutrophil recruitment -> inflammation and damage to glomerular capillary membrane -> RBC, WBC, protein etc leaks into bowman’s capsule and is excreted in the urine.

288
Q

Describe the pathophysiology behind nephrotic syndrome.

A

Podocytes or basement membrane aren’t working properly and so huge amounts of protein leaks into the bowman’s capsule and is excreted in the urine.

289
Q

A 50 y/o M presents with haematuria. On examination he has HTN, increased serum Cr and urea, proteinuria and bilateral palpable costo-vertebral angle masses. You take a family history and find out that his dad died of a sub-arachnoid haemorrhage. What is the most likely diagnosis?

A

ADPKD.

  • Normally people present around 50 y/o.
  • Raised creatinine and urea indicate a kidney problem.
  • The kidneys can be HUGE in ADPKD hence the palpable masses.
  • Intracranial haemorrhages are an extra-renal manifestation of ADPKD.
290
Q

At what age do people with ADPKD normally present?

A

Normally present around 50 y/o.

Cysts increase in size with advancing age.

291
Q

Why might someone with ADPKD have bilateral palpable costovertebral masses?

A

Cysts increase in size and cause renal enlargement. Often the kidney’s can be HUGE!

292
Q

Describe the treatment options for urinary stones.

A
  1. Conservative e.g. if stone is <5mm and in a safe location or if the patient is asymptomatic or co-morbid.
  2. Medical e.g. nifedipine.
  3. Lithotripsy - fragment stones which will then pass spontaneously.
  4. Surgical e.g. ureteroscopic; PCNL for larger ‘stag horn’ stones; nephrectomy.
293
Q

Where in the nephron are urinary tract stones formed?

A

In the collecting ducts.

294
Q

Give 3 places where urinary tract stones are likely to get stuck?

A
  1. Ureteropelvic junction.
  2. Pelvic brim.
  3. Vesoureteric junction.
295
Q

Give 3 causes of renal colic.

A
  1. Urinary tract stones.
  2. UTI.
  3. Pyelonephritis.
296
Q

What is the affect of AKI on creatinine and urine output?

A
  • Creatinine is raised.
  • Urine output is reduced.
297
Q

Give 5 risk factors for AKI.

A
  1. Increasing age.
  2. CKD.
  3. HF.
  4. Diabetes mellitus.
  5. Nephrotoxic drugs e.g. NSAIDs and ACEi.
298
Q

Give a pre-renal cause of AKI.

A
  1. Hypertension.
  2. Heart failure.
  3. Nephrotoxic drugs.
299
Q

Give 5 renal causes of AKI.

A
  1. Nephrotoxic drugs.
  2. Vasculitis.
  3. Autoimmune.
  4. Acute tubular necrosis.
  5. Glomerulonephritis.
300
Q

What is the major complication someone with AKI might develop?

A

Hyperkalaemia!

This can lead to arrhythmias.

301
Q

What investigations might you do to determine whether someone has AKI?

A
  1. Check potassium!
  2. Bloods: creatinine, U+E.
  3. Urine output.
  4. Auto-antibodies.
302
Q

How can hyperkalaemia be prevented in someone with AKI?

A
  1. Give calcium gluconate to protect the myocardium.
  2. Give insulin and dextrose.

Insulin drives potassium into cells and dextrose is to rebalance the blood sugar.

303
Q

Give a primary cause of nephrotic syndrome.

A

Minimal change disease.

This is the most common cause in children.

304
Q

What investigations might you do to determine whether someone has nephrotic syndrome?

A
  1. Renal biopsy.
  2. Urine dipstick - +++ protein.
  3. Bloods: low serum albumin.
  4. Look for auto-antibodies.
305
Q

Give 2 potential complications of nephrotic syndrome.

A
  1. Sepsis.
  2. Venous thromboembolism.
306
Q

A patient presents complaining that they are hardly passing any urine and in the small amount of urine they do pass there is blood in it. On further questioning they tell you they have recently finished a course of antibiotics (amoxicillin) for a chest infection they had 2 weeks ago. Their BP is high. What is the likely cause?

A

Nephritic syndrome.

307
Q

How does the epidemiology differ between ADPKD and ARPKD?

A

People with ADPKD normally present in middle age whereas people with ARPKD present in infancy.

308
Q

What is the most common renal cancer in children?

A

Wilms tumour.

309
Q

A sudden rise in creatinine level and a decreased urine output would be indicative of what?

A

AKI.

310
Q

What CCB can be used to treat renal stones?

A

Nifedipine.

311
Q

Why is someone with nephrotic syndrome at risk of sepsis?

A

Because you lose immunoglobulins in the urine.

312
Q

What drug must you not give to someone with renal artery stenosis?

A

ACE inhibitors e.g. ramipril.

313
Q

Is focal segmental glomerulosclerosis a cause of nephritic or nephrotic syndrome?

A

Nephrotic syndrome.

Phase 2a LIAM (11 decks)

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