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UKMLA Prep > Renal System 🫘 > Flashcards

Renal System 🫘 Flashcards

1
Q

What is metabolic acidosis commonly classified according to?

A

Anion gap

Metabolic acidosis is categorized into normal anion gap and raised anion gap.

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2
Q

What are some causes of normal anion gap metabolic acidosis? (4)

A
  • Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
  • Renal tubular acidosis
  • Drugs: e.g. acetazolamide, ammonium chloride injection
  • Addison’s disease
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3
Q

What conditions are associated with raised anion gap metabolic acidosis? (4)

A
  • Lactate: shock, hypoxia
  • Ketones: diabetic ketoacidosis, alcohol
  • Urate: renal failure
  • Acid poisoning: salicylates, methanol
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4
Q

What causes metabolic alkalosis?

A
  • Loss of hydrogen ions
  • Gain of bicarbonate

It is mainly due to problems of the kidney or gastrointestinal tract.

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5
Q

List some causes of metabolic alkalosis.

A
  • Vomiting / aspiration
  • Diuretics
  • Liquorice, carbenoxolone
  • Hypokalaemia
  • Primary hyperaldosteronism
  • Cushing’s syndrome
  • Bartter’s syndrome
  • Congenital adrenal hyperplasia
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6
Q

What conditions may lead to respiratory acidosis?

A
  • COPD
  • Decompensation in respiratory conditions (e.g. life-threatening asthma, pulmonary oedema)
  • Sedative drugs: benzodiazepines, opiate overdose
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7
Q

What are common causes of respiratory alkalosis? (6)

A
  • Anxiety leading to hyperventilation
  • Pulmonary embolism
  • Salicylate poisoning
  • CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
  • Altitude
  • Pregnancy
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8
Q

What is the most commonly isolated pathogen in acute bacterial prostatitis?

A

Escherichia coli

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9
Q

What are risk factors for acute bacterial prostatitis?

A
  • Recent urinary tract infection
  • Urogenital instrumentation
  • Intermittent bladder catheterisation
  • Recent prostate biopsy
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10
Q

What are the features of acute bacterial prostatitis?

A
  • Pain referred to perineum, penis, rectum, or back
  • Obstructive voiding symptoms
  • Fever and rigors
  • Tender, boggy prostate gland on digital rectal examination
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11
Q

What accounts for 25% of drug-induced acute kidney injury?

A

Acute interstitial nephritis

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12
Q

List some common causes of acute interstitial nephritis.

A
  • Drugs: particularly antibiotics (e.g. penicillin, rifampicin, NSAIDs, allopurinol, furosemide)
  • Systemic disease: SLE, sarcoidosis, Sjogren’s syndrome
  • Infection: Hanta virus, staphylococci
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13
Q

What are the histological features of acute interstitial nephritis?

A

Marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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14
Q

What are common symptoms of tubulointerstitial nephritis with uveitis (TINU)?

A
  • Fever
  • Weight loss
  • Painful, red eyes
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15
Q

How is acute kidney injury (AKI) characterized?

A

Reduction in renal function following an insult to the kidneys

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16
Q

What percentage of hospitalized patients develop acute kidney injury (AKI)?

A

Approximately 15%

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17
Q

What are the traditional categories of causes of AKI?

A
  • Prerenal
  • Intrinsic
  • Postrenal
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18
Q

What are examples of prerenal causes of AKI?

A
  • Hypovolaemia secondary to diarrhoea/vomiting
  • Renal artery stenosis
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19
Q

What intrinsic causes may lead to AKI?

A
  • Glomerulonephritis
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis (AIN)
  • Rhabdomyolysis
  • Tumour lysis syndrome
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20
Q

What are examples of postrenal causes of AKI?

A
  • Kidney stone in ureter or bladder
  • Benign prostatic hyperplasia
  • External compression of the ureter
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21
Q

What are risk factors for acute kidney injury (AKI)?

A
  • Chronic kidney disease
  • Other organ failure/chronic disease
  • History of acute kidney injury
  • Use of nephrotoxic drugs
  • Age 65 years or over
  • Oliguria
  • Neurological or cognitive impairment
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22
Q

What are two key ways AKI may be detected?

A
  • Reduced urine output (oliguria)
  • Fluid overload
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23
Q

What blood tests are commonly used to detect AKI?

A
  • Sodium
  • Potassium
  • Urea
  • Creatinine
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24
Q

What criteria can be used to diagnose acute kidney injury (AKI)?

A
  • Rise in serum creatinine of 26 micromol/litre or greater within 48 hours
  • 50% or greater rise in serum creatinine within the past 7 days
  • Fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours
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25
Q

What is the management approach for AKI?

A

Supportive management focusing on careful fluid balance and reviewing medications

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26
Q

Which drugs should be stopped in AKI as they may worsen renal function? (8)

A
  • NSAIDs
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
  • Metformin
  • Lithium
  • Digoxin
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27
Q

What is the role of renal replacement therapy in AKI?

A

Used when a patient is not responding to medical treatment of complications

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28
Q

What are the phases of acute tubular necrosis (ATN)?

A
  • Oliguric phase
  • Polyuric phase
  • Recovery phase
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29
Q

What is the most common inherited cause of kidney disease?

A

Autosomal dominant polycystic kidney disease (ADPKD)

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30
Q

What are the two disease loci identified in ADPKD?

A
  • PKD1
  • PKD2
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31
Q

What are the ultrasound diagnostic criteria for ADPKD in patients with a positive family history?

A
  • Two cysts, unilateral or bilateral, if aged < 30 years
  • Two cysts in both kidneys if aged 30-59 years
  • Four cysts in both kidneys if aged > 60 years
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32
Q

What is a common acute phase protein measured in acutely unwell patients?

A

CRP

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33
Q

What are some examples of acute phase proteins?

A
  • CRP
  • Procalcitonin
  • Ferritin
  • Fibrinogen
  • Alpha-1 antitrypsin
  • Caeruloplasmin
  • Serum amyloid A
  • Serum amyloid P component
  • Haptoglobin
  • Complement
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34
Q

What are the two types of Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

A

ADPKD type 1 and ADPKD type 2

ADPKD type 1 accounts for 85% of cases, while type 2 accounts for 15%.

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35
Q

What chromosome is associated with ADPKD type 1?

A

Chromosome 16

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36
Q

What chromosome is associated with ADPKD type 2?

A

Chromosome 4

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37
Q

What is the screening investigation for relatives of ADPKD patients?

A

Abdominal ultrasound

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38
Q

What are the ultrasound diagnostic criteria for ADPKD in patients with a positive family history aged < 30 years?

A

Two cysts, unilateral or bilateral

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39
Q

What are the ultrasound diagnostic criteria for ADPKD in patients aged 30-59 years?

A

Two cysts in both kidneys

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40
Q

What are the ultrasound diagnostic criteria for ADPKD in patients aged > 60 years?

A

Four cysts in both kidneys

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41
Q

What medication may be used for select patients with ADPKD?

A

Tolvaptan

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42
Q

What are the features of ADPKD?

A
  • Hypertension
  • Recurrent UTIs
  • Flank pain
  • Haematuria
  • Palpable kidneys
  • Renal impairment
  • Renal stones
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43
Q

What is the most common extra-renal manifestation of ADPKD?

A

Liver cysts

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44
Q

What percentage of ADPKD patients develop liver cysts?

A

70%

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45
Q

What is Alport’s syndrome usually inherited as?

A

X-linked dominant pattern

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46
Q

What defect causes Alport’s syndrome?

A

Defect in the gene coding for type IV collagen

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47
Q

What are common features of Alport’s syndrome?

A
  • Microscopic haematuria
  • Progressive renal failure
  • Bilateral sensorineural deafness
  • Lenticonus
  • Retinitis pigmentosa
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48
Q

What is the characteristic finding in renal biopsy for Alport’s syndrome?

A

Longitudinal splitting of the lamina densa of the glomerular basement membrane

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49
Q

What is amyloidosis?

A

Extracellular deposition of an insoluble fibrillar protein termed amyloid

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50
Q

What is the most common form of amyloidosis?

A

AL amyloidosis

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51
Q

What precursor protein is associated with AL amyloidosis?

A

Immunoglobulin Light chain fragments

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52
Q

What diagnostic test shows apple-green birefringence in amyloidosis?

A

Congo red staining

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53
Q

What is the normal range for anion gap?

A

8-14 mmol/L

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54
Q

What are causes of normal anion gap metabolic acidosis?

A
  • Gastrointestinal bicarbonate loss
  • Renal tubular acidosis
  • Drugs (e.g. acetazolamide)
  • Addison’s disease
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55
Q

What is Anti-glomerular basement membrane (GBM) disease commonly known as?

A

Goodpasture’s syndrome

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56
Q

What are the main features of Anti-GBM disease?

A
  • Pulmonary haemorrhage
  • Rapidly progressive glomerulonephritis
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57
Q

What is the main complication of Anti-GBM disease?

A

Pulmonary haemorrhage

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58
Q

What is the cause of Autosomal Recessive Polycystic Kidney Disease (ARPKD)?

A

Defect in a gene located on chromosome 6 which encodes fibrocystin

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59
Q

What are the risk factors for Benign Prostatic Hyperplasia (BPH)?

A
  • Age
  • Ethnicity (black > white > Asian)
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60
Q

What are the storage symptoms associated with BPH?

A
  • Urgency
  • Frequency
  • Nocturia
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61
Q

What is the International Prostate Symptom Score (IPSS) range for severely symptomatic patients?

A

20-35

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62
Q

What is the most common type of bladder cancer?

A

Urothelial (transitional cell) carcinoma

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63
Q

What is the primary risk factor for urothelial carcinoma of the bladder?

A

Smoking

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64
Q

What is the staging classification for bladder cancer associated with no evidence of tumor?

A

T0

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65
Q

What percentage of patients with T2 bladder cancer are expected to have a good prognosis?

A

60%

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66
Q

What condition is characterized by recurrent renal stones due to a defect in membrane transport?

A

Cystinuria

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67
Q

What test is used to diagnose cystinuria?

A

Cyanide-nitroprusside test

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68
Q

What is a key feature of chronic pyelonephritis?

A

Scarring of the renal parenchyma

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69
Q

What is the genetic basis for cystinuria?

A

Defect in the SLC3A1 gene on chromosome 2 and SLC7A9 on chromosome 19

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70
Q

What are the common symptoms of diabetes insipidus?

A

Decreased secretion of antidiuretic hormone (ADH)

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71
Q

What is the mnemonic for arginine?

A

COLA

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72
Q

Which chromosomes contain the SLC3A1 and SLC7A9 genes?

A

Chromosome 2 (SLC3A1), Chromosome 19 (SLC7A9)

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73
Q

What is a classic feature of recurrent renal stones?

A

They are classically yellow and crystalline, appearing semi-opaque on x-ray

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74
Q

Which test is used for the diagnosis of renal stones?

A

Cyanide-nitroprusside test

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75
Q

What is the management for renal stones?

A
  • Hydration
  • D-penicillamine
  • Urinary alkalinization
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76
Q

What characterizes diabetes insipidus (DI)?

A

Decreased secretion of antidiuretic hormone (ADH) or insensitivity to ADH

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77
Q

What are the causes of cranial diabetes insipidus?

A
  • Idiopathic
  • Post head injury
  • Pituitary surgery
  • Craniopharyngiomas
  • Infiltrative diseases (e.g., histiocytosis X, sarcoidosis)
  • DIDMOAD syndrome
  • Haemochromatosis
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78
Q

What are the causes of nephrogenic diabetes insipidus?

A
  • Genetic mutations affecting ADH receptors or aquaporin 2 channel
  • Electrolyte imbalances (e.g., hypercalcaemia, hypokalaemia)
  • Lithium
  • Demeclocycline
  • Tubulo-interstitial disease
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79
Q

What are the main features of diabetes insipidus?

A
  • Polyuria
  • Polydipsia
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80
Q

What findings would you expect in the investigation of diabetes insipidus?

A

High plasma osmolality, low urine osmolality

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81
Q

What is the urine osmolality threshold that excludes diabetes insipidus?

A

> 700 mOsm/kg

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82
Q

What is a management option for nephrogenic diabetes insipidus?

A
  • Thiazides
  • Low salt/protein diet
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83
Q

What is the most common cause of end-stage renal disease (ESRD) in the western world?

A

Diabetic nephropathy

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84
Q

What percentage of patients with type 1 diabetes mellitus develop diabetic nephropathy by age 40?

A

33%

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85
Q

What histological changes are associated with diabetic nephropathy?

A
  • Basement membrane thickening
  • Capillary obliteration
  • Mesangial widening
  • Kimmelstiel-Wilson nodules
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86
Q

What are the modifiable risk factors for developing diabetic nephropathy?

A
  • Hypertension
  • Hyperlipidaemia
  • Smoking
  • Poor glycaemic control
  • Raised dietary protein
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87
Q

What are the non-modifiable risk factors for developing diabetic nephropathy?

A
  • Male sex
  • Duration of diabetes
  • Genetic predisposition
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88
Q

What effect do thiazide diuretics have on serum potassium levels?

A

They decrease serum potassium levels

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89
Q

What is the mechanism of action of ezetimibe?

A

Inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption

90
Q

What is familial hypercholesterolaemia (FH)?

A

An autosomal dominant condition resulting in high levels of LDL-cholesterol

91
Q

What are the Simon Broome criteria for diagnosing definite FH?

A
  • Total cholesterol (TC) > 7.5 mmol/l and LDL-C > 4.9 mmol/l
  • Tendon xanthoma or DNA-based evidence of FH
92
Q

What is Fanconi syndrome?

A

A generalized reabsorptive disorder of renal tubular transport in the proximal convoluted tubule

93
Q

What are the features of Fanconi syndrome?

A
  • Type 2 renal tubular acidosis
  • Polyuria
  • Aminoaciduria
  • Glycosuria
  • Phosphaturia
  • Osteomalacia
94
Q

What is the primary use of fibrates?

A

Management of hyperlipidaemia, particularly raised triglycerides

95
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

A cause of nephrotic syndrome and chronic kidney disease, presenting in young adults

96
Q

What are the common causes of focal segmental glomerulosclerosis?

A
  • Idiopathic
  • Secondary to other renal pathology (e.g., IgA nephropathy)
  • HIV
  • Heroin
  • Alport’s syndrome
  • Sickle-cell
97
Q

What is the triad of symptoms in haemolytic uraemic syndrome?

A
  • Acute kidney injury
  • Microangiopathic haemolytic anaemia (MAHA)
  • Thrombocytopenia
98
Q

What is the most common cause of typical haemolytic uraemic syndrome in children?

A

Shiga toxin-producing Escherichia coli (STEC) 0157:H7

99
Q

What is Henoch-Schonlein purpura (HSP)?

A

An IgA mediated small vessel vasculitis usually seen in children following an infection

100
Q

What are the common features of Henoch-Schonlein purpura?

A
  • Palpable purpuric rash
  • Abdominal pain
  • Polyarthritis
101
Q

What is the management for hypercalcaemia?

A
  • Rehydration with normal saline
  • Bisphosphonates
  • Calcitonin
  • Steroids in sarcoidosis
102
Q

What is the management for hyperkalaemia?

A

Management may include stabilization of cardiac membrane, short-term potassium shift, and removal of potassium from the body

103
Q

What ECG changes are associated with hyperkalaemia?

A
  • Tall-tented T waves
  • Loss of P waves
  • Broad QRS complexes
  • Sinusoidal wave pattern
104
Q

What characterizes hungry bone syndrome?

A

Occurs after parathyroidectomy with rapid bone remineralization and systemic hypocalcaemia

105
Q

Fill in the blank: Familial hypercholesterolaemia affects about 1 in _____ people.

106
Q

What are the initial management steps for hyperkalaemia?

A
  • Address precipitating factors
  • Stop aggravating drugs
107
Q

What is the frequency of horseshoe kidney in the general population?

108
Q

What is the frequency of horseshoe kidney in Turner’s syndrome?

109
Q

What is the initial treatment for severe hyperkalaemia (≥ 6.5 mmol/L)?

A

Emergency treatment is required, including IV calcium gluconate, insulin/dextrose infusion, and possibly nebulised salbutamol

IV calcium gluconate stabilizes the myocardium. Insulin/dextrose infusion helps shift potassium from extracellular to intracellular fluid.

110
Q

What is the Fredrickson classification used for?

A

It classifies types of hyperlipidaemia based on genetic factors

The classification includes types I to V, each with specific genetic abnormalities.

111
Q

What is the cause of type I hyperlipidaemia in the Fredrickson classification?

A

Lipoprotein lipase deficiency and apolipoprotein C-II deficiency

These deficiencies lead to impaired lipid metabolism.

112
Q

List the causes of hypocalcaemia.

A
  • Vitamin D deficiency (osteomalacia)
  • Chronic kidney disease
  • Hypoparathyroidism
  • Pseudohypoparathyroidism
  • Rhabdomyolysis
  • Magnesium deficiency
  • Massive blood transfusion
  • Acute pancreatitis

Contamination with EDTA can falsely lower calcium levels.

113
Q

What are the clinical features of hypocalcaemia?

A
  • Tetany
  • Perioral paraesthesia
  • Depression (chronic)
  • Cataracts (chronic)
  • Prolonged QT interval on ECG

Neuromuscular excitability is a significant feature due to low extracellular calcium.

114
Q

What is Trousseau’s sign?

A

Carpal spasm induced by inflating a blood pressure cuff above systolic pressure

It is seen in around 95% of patients with hypocalcaemia.

115
Q

What conditions can cause hypokalaemia with hypertension?

A
  • Cushing’s syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
  • Liddle’s syndrome
  • 11-beta hydroxylase deficiency

Carbenoxolone and excess liquorice can also lead to hypokalaemia associated with hypertension.

116
Q

What is the management for acute severe hyponatraemia?

A

Administer hypertonic saline (typically 3% NaCl) and monitor closely

Patients should preferably be monitored in a high-dependency unit or above.

117
Q

What can cause osmotic demyelination syndrome?

A

Over-correction of severe hyponatraemia

Symptoms may include dysarthria, dysphagia, and ‘locked-in syndrome’.

118
Q

What are the consequences of hypophosphataemia?

A
  • Red blood cell haemolysis
  • White blood cell and platelet dysfunction
  • Muscle weakness and rhabdomyolysis
  • Central nervous system dysfunction

Hypophosphataemia can result from conditions like alcohol excess and diabetic ketoacidosis.

119
Q

What is IgA nephropathy also known as?

A

Berger’s disease

It is the most common cause of glomerulonephritis worldwide.

120
Q

What is the main symptom of post-streptococcal glomerulonephritis?

A

Proteinuria

This condition is often associated with low complement levels.

121
Q

What is the typical presentation of lower genitourinary tract trauma?

A

Most bladder injuries occur due to blunt trauma, often associated with pelvic fractures

Up to 10% of male pelvic fractures can result in urethral or bladder injuries.

122
Q

What is the recommended investigation for urethral injury?

A

Ascending urethrogram

This helps to assess the extent of the injury.

123
Q

What is the most common cause of hypopituitarism?

A

Compression of the pituitary gland by non-secretory pituitary macroadenoma

Other causes include pituitary apoplexy and Sheehan’s syndrome.

124
Q

What is an ascending urethrogram?

A

An investigation technique used to visualize the urethra.

125
Q

What management is indicated for suprapubic catheter placement?

A

Surgical placement, not percutaneously.

126
Q

What are common causes of external genitalia injuries?

A
  • Penetration
  • Blunt trauma
  • Continence- or sexual pleasure-enhancing devices
  • Mutilation
127
Q

What are the two types of bladder rupture?

A
  • Intra-peritoneal
  • Extra-peritoneal
128
Q

What symptoms suggest a bladder or urethral injury?

A

History of pelvic fracture and inability to void.

129
Q

What investigation is used to confirm bladder injury?

A

IVU or cystogram.

130
Q

What is the management for intraperitoneal bladder injury?

A

Laparotomy.

131
Q

What is Medullary cystic disease?

A

An autosomal dominant condition leading to progressive tubulointerstitial fibrosis and renal failure.

132
Q

What are the characteristic features of Medullary cystic disease?

A
  • Renal failure
  • Small kidneys
133
Q

What is another name for Membranoproliferative glomerulonephritis?

A

Mesangiocapillary glomerulonephritis.

134
Q

What is the most common cause of Type 1 Membranoproliferative glomerulonephritis?

A

Cryoglobulinaemia, hepatitis C.

135
Q

What is the hallmark appearance of Type 1 Membranoproliferative glomerulonephritis on renal biopsy?

A

‘Tram-track’ appearance due to immune deposits.

136
Q

What is Type 2 Membranoproliferative glomerulonephritis also known as?

A

‘Dense deposit disease.’

137
Q

What are common causes of Type 2 Membranoproliferative glomerulonephritis?

A
  • Partial lipodystrophy
  • Factor H deficiency
138
Q

What is the recommended management for Membranous glomerulonephritis?

A
  • ACE inhibitor or ARB
  • Immunosuppression if severe
139
Q

What is the prognosis for Membranous glomerulonephritis?

A

One-third spontaneous remission, one-third remain proteinuric, one-third develop ESRF.

140
Q

What is metabolic acidosis classified by?

A

Anion gap.

141
Q

What is the normal range for anion gap?

A

10-18 mmol/L.

142
Q

What causes normal anion gap metabolic acidosis?

A
  • Gastrointestinal bicarbonate loss
  • Renal tubular acidosis
  • Addison’s disease
143
Q

What are common causes of raised anion gap metabolic acidosis?

A
  • Lactate
  • Ketones
  • Urate
  • Acid poisoning
144
Q

What is the typical presentation of Minimal change disease?

A

Nephrotic syndrome.

145
Q

What is a common cause of Minimal change disease?

A

Idiopathic.

146
Q

What is the treatment for Minimal change disease?

A

Oral corticosteroids.

147
Q

What is Nephroblastoma also known as?

A

Wilm’s tumours.

148
Q

At what age does Nephroblastoma usually present?

A

In the first 4 years of life.

149
Q

What are the three components of Nephrotic syndrome?

A
  • Proteinuria (> 3g/24hr)
  • Hypoalbuminaemia (< 30g/L)
  • Oedema
150
Q

What are primary causes of Nephrotic syndrome?

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
151
Q

What is the pathophysiology of Nephrotic syndrome?

A

Damage to the glomerular basement membrane leads to increased permeability to proteins.

152
Q

What are common complications of Nephrotic syndrome?

A
  • Increased risk of thromboembolism
  • Hyperlipidaemia
  • Increased risk of infection
153
Q

What defines contrast media nephrotoxicity?

A

A 25% increase in creatinine within 3 days of contrast media administration.

154
Q

What are risk factors for contrast-induced nephropathy?

A
  • Known renal impairment
  • Age > 70 years
  • Dehydration
  • Cardiac failure
155
Q

What preventive measure is recommended for high-risk patients before contrast procedures?

A

Intravenous 0.9% sodium chloride.

156
Q

What is Oxalate nephropathy caused by?

A
  • Ethylene glycol ingestion
  • Vitamin C overdose
157
Q

What are common causes of polyuria?

A
  • Diuretics, caffeine & alcohol
  • Diabetes mellitus
  • Lithium
  • Heart failure
158
Q

What is Post-streptococcal glomerulonephritis associated with?

A

Recent group A beta-haemolytic Streptococcus infection.

159
Q

What laboratory finding confirms recent streptococcal infection in Post-streptococcal glomerulonephritis?

A

Raised anti-streptolysin O titre.

160
Q

What is the most common cause of infravesical outflow obstruction in males?

A

Posterior urethral valves.

161
Q

What is the primary treatment for prostate cancer?

A

Radical prostatectomy.

162
Q

What is the normal upper limit for PSA?

163
Q

What grading system is used for prostate cancer?

A

Gleason grading system.

164
Q

What is the management for early prostate cancer?

A

Watch and wait.

165
Q

What percentage of testosterone is derived from the testis?

166
Q

What is the preferred option for low-risk men with prostate cancer according to NICE?

A

Active surveillance

167
Q

What clinical criteria suggest a candidate for active surveillance in prostate cancer?

A
  • Clinical stage T1c
  • Gleason score 3+3
  • PSA density < 0.15 ng/ml/ml
  • Cancer in < 50% of biopsy cores
  • < 10 mm of any core involved
168
Q

What are the treatment options for localized prostate cancer?

A
  • Active monitoring
  • Watchful waiting
  • Radical prostatectomy
  • Radiotherapy (external beam and brachytherapy)
169
Q

What complications are associated with radical prostatectomy for localized advanced prostate cancer?

A

Erectile dysfunction

170
Q

What is the aim of hormonal therapy in metastatic prostate cancer?

A

Reducing androgen levels

171
Q

What is the initial effect of GnRH agonists on testosterone levels?

A

Testosterone level will rise initially for 2-3 weeks before falling to castration levels

172
Q

What is a common anti-androgen medication used in prostate cancer treatment?

A

Bicalutamide

173
Q

What is the classical triad of symptoms for renal cell cancer?

A
  • Haematuria
  • Loin pain
  • Abdominal mass
174
Q

What are the management options for renal cell cancer confined to the kidney?

A
  • Partial nephrectomy
  • Total nephrectomy
175
Q

What is pseudohyperkalaemia?

A

A rise in serum potassium due to excessive leakage during or after blood collection

176
Q

What is rapidly progressive glomerulonephritis characterized by?

A

Rapid loss of renal function with formation of epithelial crescents

177
Q

What causes renal papillary necrosis?

A
  • Severe acute pyelonephritis
  • Diabetic nephropathy
  • Obstructive nephropathy
  • Analgesic nephropathy
178
Q

What percentage of renal stones are calcium oxalate stones?

179
Q

What urinary pH conditions favor the formation of calcium phosphate stones?

A

Normal to alkaline urine (>5.5)

180
Q

What is the recommended analgesia for renal colic according to NICE?

181
Q

What is the risk of over-diagnosis associated with PSA testing in prostate cancer?

182
Q

What is the PSA threshold for men aged 50-59 years?

A

> 3.5 ng/ml

183
Q

True or False: PSA testing should be postponed for at least 6 weeks after treatment for prostatitis.

184
Q

What is the significance of a PSA level of 4-10 ng/ml?

A

Around 33% of men will be found to have prostate cancer

185
Q

What is a common feature of nephroblastoma?

A

It accounts for 80% of all genitourinary malignancies in those under 15 years

186
Q

What is Stauffer syndrome associated with?

A

Renal cell cancer

187
Q

How does analgesic nephropathy contribute to renal papillary necrosis?

A

It is one of the causes of coagulative necrosis of the renal papillae

188
Q

What analgesia is recommended by both BAUS and NICE for renal colic?

A

NSAID

Non-steroidal anti-inflammatory drugs are the first-line treatment for managing pain in renal colic.

189
Q

Which NSAID has traditionally been used for renal colic but carries increased cardiovascular risks?

A

Diclofenac

Diclofenac and ibuprofen are noted for their increased risk of cardiovascular events.

190
Q

What is recommended by NICE if NSAIDs are contraindicated or ineffective for pain relief?

A

IV paracetamol

Intravenous paracetamol is suggested for patients who need effective pain management.

191
Q

What type of medication do alpha blockers represent in the management of renal colic?

A

Smooth muscle relaxants

Alpha blockers help dilate the ureter and may facilitate stone passage.

192
Q

For distal ureteric stones less than what size do NICE recommend the use of alpha blockers?

A

< 10 mm

Alpha blockers are particularly considered for smaller distal ureteric stones.

193
Q

What initial investigations are recommended for renal colic?

A

Urine dipstick and culture, serum creatinine and electrolytes, FBC/CRP, calcium/urate

These tests help assess renal function and identify underlying causes.

194
Q

What imaging technique should be performed on all patients with renal colic within 24 hours of admission?

A

Non-contrast CT KUB

This imaging modality is essential for diagnosing ureteric stones.

195
Q

What is the sensitivity and specificity of CT KUB for ureteric stones?

A

Sensitivity: 97%, Specificity: 95%

These high rates make CT KUB a reliable diagnostic tool.

196
Q

What is the first-line management for renal stones < 5 mm according to NICE?

A

Watchful waiting

Stones smaller than 5 mm are likely to pass spontaneously.

197
Q

What procedure is recommended for renal stones measuring 10-20 mm?

A

Shockwave lithotripsy or ureteroscopy

Both options are viable for managing stones of this size.

198
Q

What is shockwave lithotripsy?

A

A procedure that generates shock waves to fragment stones

It is an external method used to treat renal stones.

199
Q

What is a potential complication of shockwave lithotripsy?

A

Solid organ injury

The procedure can lead to injury due to the passage of shock waves.

200
Q

What is the role of ureteroscopy in the management of renal stones?

A

Used for complex stone disease and when lithotripsy is contraindicated

Ureteroscopy allows direct access to stones via the ureter.

201
Q

What is percutaneous nephrolithotomy?

A

A procedure to access the renal collecting system for stone removal

This method is used for larger stones that cannot be managed with other techniques.

202
Q

What dietary recommendations can help prevent calcium stones?

A
  • High fluid intake
  • Add lemon juice to drinking water
  • Avoid carbonated drinks
  • Limit salt intake

These lifestyle changes can reduce the risk of stone formation.

203
Q

What is a risk factor for urate stones?

A

Gout

Gout can lead to elevated uric acid levels, increasing the risk of urate stones.

204
Q

What is the appearance of calcium oxalate stones on X-ray?

A

Opaque

Calcium oxalate stones are the most common type and can be easily identified on radiographs.

205
Q

What is the major histocompatibility complex (MHC) in humans known as?

A

HLA system

The HLA system plays a crucial role in immune response and organ transplantation.

206
Q

What is the relative importance of HLA antigens when matching for a renal transplant?

A

DR > B > A

DR antigen compatibility is prioritized over B and A antigens.

207
Q

What is the 1-year graft survival rate for cadaveric transplants?

A

90%

This statistic reflects the success of cadaveric renal transplants at the one-year mark.

208
Q

What type of urinary cast is associated with glomerulonephritis?

A

Red blood cell casts

These casts indicate damage to the glomeruli.

209
Q

What is hyperacute rejection in the context of renal transplantation?

A

Rejection occurring minutes to hours due to pre-existing antibodies

This is a severe form of rejection that necessitates immediate graft removal.

210
Q

What are the common causes of acute graft failure?

A
  • Mismatched HLA
  • Cytomegalovirus infection

Acute graft failure typically occurs within the first six months following transplantation.

211
Q

What can cause chronic graft failure after renal transplantation?

A

Fibrosis from both antibody and cell-mediated mechanisms

Chronic allograft nephropathy is a common cause of long-term graft failure.

212
Q

What is Wilms’ nephroblastoma?

A

One of the most common childhood malignancies

Typically presents in children under 5 years of age, with a median age of 3 years old.

213
Q

What syndrome is associated with Wilms’ tumour?

A

Beckwith-Wiedemann syndrome

Also associated as part of WAGR syndrome with Aniridia, Genitourinary malformations, and mental Retardation.

214
Q

What is a common genetic mutation found in Wilms’ tumour cases?

A

Loss-of-function mutation in the WT1 gene on chromosome 11

Around one-third of cases are associated with this mutation.

215
Q

What is the most common presenting feature of Wilms’ tumour?

A

Abdominal mass

216
Q

What are some other features of Wilms’ tumour?

A
  • Painless haematuria
  • Flank pain
  • Anorexia
  • Fever
217
Q

What percentage of Wilms’ tumour cases are unilateral?

218
Q

In what percentage of patients are metastases found in Wilms’ tumour?

A

20%

Most commonly to the lung.

219
Q

What should be done for children with an unexplained enlarged abdominal mass?

A

Arrange paediatric review within 48 hours

220
Q

What is the primary management for Wilms’ tumour?

A
  • Nephrectomy
  • Chemotherapy
  • Radiotherapy if advanced disease
221
Q

What is the prognosis for Wilms’ tumour?

A

Good, with an 80% cure rate

222
Q

What are the histological features of Wilms’ tumour?

A
  • Epithelial tubules
  • Areas of necrosis
  • Immature glomerular structures
  • Stroma with spindle cells
  • Small cell blastomatous tissues resembling the metanephric blastema

UKMLA Prep (48 decks)

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