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Finals > Nephrology and Urology > Flashcards

Nephrology and Urology Flashcards

1
Q

What is creatinine?

A

A waste product from muscle and protein metabolism.

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2
Q

Serum creatinine is a good marker of what?

A

Kidney function.

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3
Q

Why is serum creatinine a good marker of kidney function?

A

Creatinine is excreted by the kidneys. If filtration in the kidney is deficient serum creatinine concentrations rise.

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4
Q

Define acute kidney injury (AKI).

A

Reduction in renal function following an insult to the kidneys.

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5
Q

What are four clinical features of acute kidney injury?

A

Reduced urine output, pulmonary oedema, peripheral oedema and arrhythmias.

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6
Q

What are the three categories of causes of acute kidney injury?

A

Prerenal (ischaemic).
Intrinsic.
Postrenal (obstructive).

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7
Q

What are two pre-renal causes of AKI?

A

Hypovolaemia (secondary to diarrhoea and vomiting).

Renal artery stenosis.

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8
Q

What are five intrinsic causes of AKI?

A 
Glomerulonephritis. 
Acute tubular necrosis. 
Acute interstitial nephritis. 
Rhabdomyolysis. 
Tumour lysis syndrome.
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9
Q

What are three post-renal causes of AKI?

A

Kidney stone in ureter or bladder.
Benign prostatic hyperplasia.
External compression of the ureter.

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10
Q

What two measurements are used to stage the severity of AKI?

A

Serum creatinine.

Urine output.

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11
Q

How is stage 1 AKI defined?

A

1.5x rise in serum creatinine from baseline (in the past 7 days).
Urine output < 0.5ml/kg/hour for six hours.

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12
Q

How is stage 2 AKI defined?

A

2-3x rise in serum creatinine from baseline (in the past 7 days).
Urine output < 0.5ml/kg/hour for at least twelve hours.

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13
Q

How is stage 3 AKI defined?

A

More than 3x rise in serum creatinine from baseline (in the past seven days).
Urine output < 0.3ml/kg/hour for 24 hours // Anuria for twelve hours.

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14
Q

How is AKI managed?

A

Supportive therapy. Fluid balance (ensure kidneys perfused without causing fluid overload).

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15
Q

Give examples of four classes of drug that should be stopped in AKI as they will worsen renal function.

A

NSAIDs, ACE inhibitors, ARBs and diuretics.

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16
Q

Give examples of three drugs that should be stopped in AKI as they may become toxic.

A

Metformin, lithium and digoxin.

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17
Q

What is renal artery stenosis?

A

Narrowing of the lumen of the renal artery (suppling the kidney).

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18
Q

What is main feature of renal artery stenosis?

A

Refractory hypertension.

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19
Q

Why does renal artery stenosis result in hypertension?

A

Reduced blood flow to the kidneys leads to activation on the RAAS… leading to an increase in blood pressure.

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20
Q

How does renal artery stenosis result in kidney damage?

A

Reduced blood flow to the kidneys leads to reduced glomerular filtration rate… leading to atrophy and fibrosis.

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21
Q

What investigations may be ordered in the diagnosis of renal artery stenosis?

A

Serum creatinine.
Duplex ultrasonography.
CT/MR angiography.

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22
Q

What does serum creatinine reveal in patients with renal artery stenosis?

A

Raised creatinine.

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23
Q

What is the pharmacological management of renal artery stenosis?

A

Captopril (ACEi).
Furosemide (thiazide diuretic).
Statin.

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24
Q

What is the long term (surgical) management option of renal artery stenosis?

A

Renal artery stenting.

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25
Q

What is glomerulonephritis?

A

The umbrella term for pathology affecting the glomerulus of the kidney. Spectrum of nephrosis to nephritis.

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26
Q

What is the characteristic triad of nephrotic syndrome?

A

Proteinuria, hypoalbuminaemia and oedema.

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27
Q

Other than the characteristic triad, what other features can be found on investigation in people with nephrotic syndrome?

A

Hyperlipidaemia.

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28
Q

Why do patients with nephrotic syndrome have hyperlipidaemia?

A

Low albumin = low oncotic pressure which prompts increased hepatic protein synthesis (including of lipoproteins).

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29
Q

What are complications of nephrotic syndrome?

A

Thrombosis, infections, cardiovascular complications, anaemia, acute renal failure, hypovolaemic crisis.

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30
Q

Why does nephrotic syndrome predispose to thrombosis?

A

Loss of antithrombin-III, proteins C and S.

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31
Q

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

A

Minimal change disease.

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32
Q

How does minimal change disease present?

A

Periorbital/genital oedema, ascites and shortness of breath.

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33
Q

What is the pathophysiological process behind minimal change disease?

A

T-cell and cytokine-mediated damage to glomerular basement membrane. Polyanion loss and reduction in electrostatic charge. Increased glomerular permeability to serum albumin.

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34
Q

What investigation is indicated in patients suspected of minimal change disease?

A

Biopsy with electron microscopy.

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35
Q

What does biopsy with electron microscopy reveal in patients with minimal change disease?

A

Effacement of podocyte foot processes.

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36
Q

Where does minimal change disease get its name from?

A

Investigation with light microscopy appears normal.

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37
Q

What is the management of minimal change disease?

A

Corticosteroids.

In steroid-resistant cases give cyclophosphamide.

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38
Q

How should predisposition to thrombosis in nephrotic syndrome be treated?

A

Low molecular weight heparin (dalteparin).

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39
Q

What is focal segmental glomerulosclerosis?

A

A non-proliferative glomerulonephritis that causes nephrotic syndrome. Characterised by sclerosis of segments of some glomeruli and fusion of podocyte foot processes.

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40
Q

Focal segmental glomerulosclerosis (FSG) can be primary (idiopathic) or secondary. What are two causes of secondary FSG?

A

HIV and heroin use.

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41
Q

What investigation is indicated in patients suspected of focal segmental glomerulosclerosis?

A

Biopsy and light microscopy.

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42
Q

What does biopsy with light microscopy reveal in patients with focal segmental glomerulosclerosis?

A

Focal and segmental sclerosis and hyalinosis.

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43
Q

What is the management of focal segmental glomerulosclerosis?

A

Restricted salt intake, blood pressure control (w/ ACEi, ARB), loop diuretic (furosemide) and corticosteroids (in idiopathic disease).

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44
Q

What is membranous glomerulonephritis?

A

Slow progressive form of glomerulonephritis that causes nephrotic syndrome.

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45
Q

Membranous glomerulonephritis (MG) can be primary (idiopathic) or secondary. What are four secondary causes of MG?

A

Malignancy, infection, immunological disease, drugs.

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46
Q

What investigation is indicated in patients suspected of membranous glomerulonephritis?

A

Biopsy.

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47
Q

What does biopsy reveal in patients with membranous glomerulonephritis?

A

Spikes on silver staining.

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48
Q

What is the management of membranous glomerulonephritis?

A

Restrict salt intake, control blood pressure (w/ ACEi, ARB), loop diuretic (furosemide). In those at high risk of progression give corticosteroids and cyclophosphamide.

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49
Q

What are the four characteristic features of nephritic syndrome?

A

Haematuria, proteinuria, oliguria and hypertension.

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50
Q

What is nephritic syndrome?

A

Proliferative form of glomerulonephritis marked by an increased number of cells in the glomerulus.

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51
Q

What are three causes of nephritic syndrome?

A

IgA nephropathy.
Post-Strep glomerulonephritis.
Membranoproliferative glomerulonephritis.

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52
Q

What are three causes of nephrotic syndrome?

A

Minimal change disease.
Focal segmental glomerulonephritis.
Membranous glomerulonephritis.

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53
Q

What is IgA nephropathy glomerulonephritis?

A

The commonest form of primary glomerulonephritis in high-income countries.

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54
Q

Describe the pathophysiology of IgA nephropathy glomerulonephritis.

A

Develops several days after an upper respiratory tract infection because of IgA deposits in the space between glomerular capillaries.

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55
Q

How does IgA nephropathy glomerulonephritis present?

A

Features include visible haematuria, low grade proteinuria and hypertension.

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56
Q

How is IgA Nephropathy glomerulonephritis managed?

A

Conservatively in most cases though some will require antihypertensives (ACEi, ARB).

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57
Q

What is post-Strep glomerulonephritis?

A

Glomerulonephritis that develops three weeks after an upper respiratory tract infection.

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58
Q

How does post-Strep glomerulonephritis present?

A

Gross haematuria, oliguria, oedema.

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59
Q

How is post-Strep glomerulonephritis managed?

A

Supportively.

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60
Q

What is membranoproliferative glomerulonephritis associated with?

A

Hepatitis C and autoimmune conditions like SLE.

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61
Q

What does biopsy and light microscopy reveal in a patient with membranoproliferative glomerulonephritis?

A

Thickened glomerular basement membrane and tram-track appearance.

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62
Q

How is membranoproliferative glomerulonephritis managed?

A

Managed blood pressure (w/ ACEi, ARB).

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63
Q

What is the most common intrinsic cause of AKI?

A

Acute tubular necrosis.

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64
Q

What is acute tubular necrosis?

A

Damage to tubular cells from prolonged ischaemia or the presence of toxins.

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65
Q

What investigations are performed in patients with suspected acute tubular necrosis?

A

Urinary sodium.

Urine osmolality.

66
Q

What do urinary sodium and urine osmolality reveal in a patient with acute tubular necrosis?

A

High urinary sodium and low urine osmolality.

67
Q

What investigation finding is pathognomic for acute tubular necrosis?

A

Muddy brown casts.

68
Q

What are three ischaemic causes of acute tubular necrosis?

A

Shock, sepsis, dehydration.

69
Q

What are three toxic causes of acute tubular necrosis?

A

Radiology contrast dye, gentamicin, NSAIDs.

70
Q

How is acute tubular necrosis managed?

A

Provide intravenous fluid and stop nephrotoxic medications.

71
Q

What is the prognosis for acute tubular necrosis?

A

Epithelial cells have the ability to regenerate therefore ATN is reversible. Usually takes 7-21 days to recover.

72
Q

What is acute interstitial nephritis?

A

A condition of inflammation of the space between cells and tubules (the interstitium) of the kidney.

73
Q

What are the most common causes of acute interstitial nephritis?

A

Penicillin, rifampicin, NSAIDs, allopurinol and furosemide.

74
Q

How does acute interstitial nephritis present clinically?

A

Fever, rash and arthralgia.

75
Q

What investigations are performed on a patient suspected of acute interstitial nephritis?

A

Full blood count.
Urea and electrolytes.
Blood pressure.
Urinalysis.

76
Q

What are the findings on investigation of acute interstitial nephritis?

A

Eosinophilia.
Renal impairment.
Hypertension.
White cells on urinalysis.

77
Q

How is acute interstitial nephritis managed?

A

Treat underlying cause and consider giving steroids.

78
Q

What is haemolytic uraemic syndrome?

A

A condition that occurs as a result of thrombosis in small blood vessels throughout the body.

79
Q

Describe the pathophysiology of haemolytic uraemic syndrome.

A

Thrombosis consumes platelets (thrombocytopenia). Clots damage red blood cells causing haemolysis (anaemia). Blood supply to kidneys disrupted (AKI).

80
Q

What is rhabdomyolysis?

A

Condition of skeletal muscle breakdown.

81
Q

What causes rhabdomyolysis?

A

Underuse (prolonged immobilisation for many hours following a fall).
Overuse (prolonged epileptic seizure).
Trauma.

82
Q

Rhabdomyolysis: what four things are released from myocytes when they undergo apoptosis?

A

Myoglobin.
Potassium.
Phosphate.
Creatine kinase.

83
Q

What are the clinical features of rhabdomyolysis?

A

Muscle swelling and tenderness, fatigue, urine discolouration.

84
Q

What investigations are performed in a patient suspected of rhabdomyolysis?

A 
Creatinine (kidney function). 
Creatine kinase. 
Urinalysis. 
Serum phosphate. 
Serum potassium.
85
Q

What does creatinine reveal in a patient with rhabdomyolysis?

A

Raised (acute kidney injury).

86
Q

What does creatine kinase reveal in a patient with rhabdomyolysis?

A

Raised 10-100 times normal.

87
Q

What does serum phosphate/potassium reveal in a patient with rhabdomyolysis?

A

Elevated phosphate.

Hyperkalaemia.

88
Q

How is rhabdomyolysis managed?

A

Intravenous fluid.

Consider giving sodium bicarbonate to alkalinise urine.

89
Q

What are the majority of renal stones made of?

A

Calcium oxalate.

90
Q

What are the three main sites of renal stone deposition in the urinary tract?

A

Pelviureteric junction.
Pelvic brim.
Vesicoureteric junction.

91
Q

Where do renal stones form?

A

Collecting ducts of the kidney.

92
Q

How do renal stones present clinically?

A

Majority asymptomatic. Renal colic (loin to groin pain), nausea + vomiting, infection, haematuria, sterile pyuria, anuria.

93
Q

What is the imaging investigation of choice for renal stones?

A

Non-contrast CT.

94
Q

What pain relief is given for the management of renal stones?

A

Diclofenac.

95
Q

What factor determines management of renal stones?

A

Size (< 5 mm likely to pass spontaneously).

96
Q

When should renal stones be managed pharmacologically?

A

Size > 5 mm or if pain not resolving.

97
Q

What pharmacological therapies can be used in the management of renal stones?

A

Nifedipine (CCB) or tamsulosin (alpha-blocker).

98
Q

What is the next step in management if pharmacological intervention fails to resolve renal stones?

A

Extracorporeal shockwave lithotripsy… or later percutaneous nephrolithotomy.

99
Q

What steps can be taken to reduce the risk of developing renal stones?

A

Lifestyle changes (high fluid intake, low animal protein, low salt diet). Thiazide diuretic use.

100
Q

What are the three categories of urinary tract obstruction?

A

Luminal.
Mural.
Extra-mural.

101
Q

Give examples of luminal lesions of urinary tract obstruction.

A

Stones, blood clot, sloughed papilla, tumour (renal, ureteric, bladder).

102
Q

Give examples of mural lesions of urinary tract obstruction.

A

Congenital/acquired stricuture, neuromuscular dysfunction, schistosomiasis.

103
Q

Give examples of extra-mural lesions of urinary tract obstruction.

A

Abdominal or pelvic mass/tumour, retroperitoneal fibrosis, iatrogenic.

104
Q

What is the difference between the presentation of unilateral and bilateral urinary tract obstruction?

A

Unilateral obstruction may be clinically silent.

105
Q

What is the clinical presentation of acute upper urinary tract obstruction?

A

Loin pain radiating to groin, possible superimposed infection with or without loin tenderness.

106
Q

What is the clinical presentation of chronic upper urinary tract obstruction?

A

Flank pain, renal failure, superimposed infection, polyuria.

107
Q

What is the clinical presentation of acute lower urinary tract obstruction?

A

Suprapubic pain, confusion, distended and palpable bladder.

108
Q

What is the clinical presentation of chronic lower urinary tract obstruction?

A

Urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence with distended palpable bladder.

109
Q

What is the imaging modality of choice for urinary tract obstruction?

A

Ultrasound.

110
Q

If ultrasound confirms distension (urinary tract obstruction) what should be next step of investigation?

A

CT to determine level of obstruction.

111
Q

Define hydronephrosis.

A

Dilatation of the renal pelvis and calyces.

112
Q

Define pelviectasis.

A

Dilatation of the renal pelvis.

113
Q

Define caliectasis.

A

Dilatation of the renal calyces.

114
Q

Define hydroureter.

A

Dilatation of the ureter.

115
Q

What is the management of upper urinary tract obstruction?

A

Nephrostomy or ureteric stent. Give tamsulosin to reduce stent-related pain.

116
Q

What is the management of lower urinary tract obstruction?

A

Urethral or suprapubic catheters. Give tamsulosin if prostatic obstruction.

117
Q

What % of men over 50 and 80 years old, respectively, have benign prostatic hyperplasia?

A

50% of men over 50.

80% of men over 80.

118
Q

What is benign prostatic hyperplasia?

A

Noncancerous increase in size of the prostate gland.

119
Q

What are the three groups of lower urinary tract symptoms?

A 
Voiding symptoms (obstructive). 
Storage symptoms (irritative). 
Post-micturition symptoms.
120
Q

Give examples of voiding symptoms of BPH?

A

Weak/intermittent urinary flow, straining, hesitancy, terminal dribbling, incomplete emptying.

121
Q

Give examples of storage symptoms of BPH?

A

Urgency, frequency, urgency incontinence, nocturia.

122
Q

Give an example of a post-micturition symptoms of BPH?

A

Dribbling.

123
Q

What are two possible complications of benign prostatic hyperplasia?

A

Urinary tract infection.

Retention.

124
Q

What pharmacological therapies can be used in the treatment of BPH?

A

Tamsulosin (alpha-blocker).

Finasteride (5 alpha-reductase inhibitor).

125
Q

What is the mechanism of action of tamsulosin in the treatment of BPH?

A

Alpha-1 antagonist. Causes relaxation of smooth muscle of the bladder neck, prostate, ureter and urethra.

126
Q

What is the mechanism of action of finasteride in the treatment of BPH?

A

5-alpha reductase inhibitor blocks conversion of testosterone to dihydrotestosterone, which is known to induce BPH.

127
Q

What is the definitive management option for BPH?

A

Transurethral resection of prostate (TURP).

128
Q

What is autosomal dominant polycystic kidney disease (ADPKD)?

A

The most common inherited cause of kidney disease. Characterised by the development of cysts which grow and compress the normal architecture and vasculature of the kidney.

129
Q

What are the features of ADPKD?

A

Abdominal pain, abdominal masses, headaches, haematuria, hypertension, recurrent UTIs and renal stones.

130
Q

Give examples of extra-renal manifestations of ADPKD?

A

Liver cysts, berry aneurysms, valvular heart disease, pancreatic cysts, splenic cysts.

131
Q

How is ADPKD diagnosed?

A

Renal ultrasound along with CT KUB.

132
Q

How is ADPKD managed?

A

Tolvaptan (decreases cell proliferation). Long term management is renal transplant.

133
Q

Define chronic kidney disease (CKD).

A

Reduction in kidney function or structural damage present for at least three months, with associated health implications.

134
Q

Over what period of time does CKD typically develop?

A

Months to years.

135
Q

What are late signs of CKD?

A

Peripheral oedema, lethargy, nausea, loss of appetite, pruritus, muscle cramps and confusion.

136
Q

What are four complications of CKD?

A

Cardiovascular disease.
Bone disease.
Anaemia.

137
Q

Give five potential causes of CKD?

A 
Diabetes mellitus. 
Hypertension. 
Glomerulonephritis. 
Polycystic kidney disease. 
Nephrotoxic drugs.
138
Q

How is CKD diagnosed?

A

Calculation of estimated glomerular filtration rate (eGFR) and presence of albumin in the urine (proteinuria) on urinalysis.

139
Q

What eGFR corresponds to severe reduction in kidney function?

A

< 30 ml/min.

140
Q

What eGFR corresponds to established kidney failure?

A

< 15 ml/min.

141
Q

How is CKD managed?

A

Blood pressure control with ACEi or ARBs. Further treatment with furosemide (loop diuretic) particularly if eGFR < 45.

142
Q

What are side effects of furosemide?

A

Ototoxicity, hypokalaemia, dehydration, allergy, nephritis and gout.

143
Q

How is phosphate excretion affected in chronic kidney disease?

A

Phosphate excretion is impaired and phosphate accumulates in the blood.

144
Q

What is the affect of high serum phosphate levels on bone?

A

Phosphate drags calcium from the bones causing osteomalacia.

145
Q

What investigation can be used to monitor bone health?

A

DEXA scans (measures bone mineral density).

146
Q

What role do the kidneys have in the balance of vitamin D?

A

1-alpha hydroxylation (the process of converting calcifediol to calcitriol) occurs in the tubules of the kidneys.

147
Q

How is vitamin D affected in chronic kidney disease?

A

Less active vitamin D is produced.

148
Q

In CKD: how does low vitamin D affect calcium levels and why?

A

Vitamin D helps to increase absorption of calcium from the diet… therefore low serum calcium.

149
Q

In CKD: low serum calcium can lead to the development of what two conditions?

A

Osteoporosis.

Secondary hyperparathyroidism.

150
Q

What is the management of bone disease in CKD?

A

Reducing dietary intake of phosphate (avoid excessive meat, fish, dairy). Consider providing phosphate binders (aluminium salts, calcium carbonate) and vitamin D supplements. Give bisphosphonates (alendrotnic acid) to reduce the rate of bone turnover.

151
Q

Why does CKD result in anaemia?

A

Erythropoietin is secreted by the kidneys that stimulates red blood cell production in the bone marrow. In CKD erythropoietin production release is impaired causing anaemia. In addition, uraemia has a toxic effect on the bone marrow which further reduces erythropoiesis.

152
Q

What stimulates erythropoietin secretion by the kidneys?

A

Cellular hypoxia.

153
Q

What is the management of anaemia in CKD?

A

If iron stores are insufficient give intravenous iron infusion. Ir iron stores are sufficient give erythropoietin/

154
Q

What are the clinical features of renal failure?

A

Breathlessness, fatigue, insomnia, pruritus, poor appetite, oedema, weakness, abdominal cramps, anxiety and cognitive impairment.

155
Q

What are the two management pathways for a patient with renal failure?

A

Palliative care or renal replacement therapy.

156
Q

What are three types of renal replacement therapy?

A

Haemodialysis.
Peritoneal dialysis.
Renal transplantation.

157
Q

Describe the process of haemodialysis.

A

Filtration of the blood through a dialysis machine in hospital, typically requires three sessions per week (each lasting three to five hours).

158
Q

Describe the process of peritoneal dialysis.

A

Filtration occurs within the patient’s abdomen. Dialysis solution is injected into the abdominal cavity via a permanent catheter. The solution draws waste products from the blood across the peritoneum. After several hours of dwell time the solution is exchanged for a new solution.

159
Q

In renal transplantation: what site is the donor kidney transplanted to?

A

The groin, renal vessels are connected to the external iliac vessels.

160
Q

Following renal transplantation patients have an increased risk of what cancer and why?

A

Squamous cell carcinoma of the skin due to effects of long-term immunosuppressants.

Finals (11 decks)

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