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PHASE 2A (Mine) > Renal > Flashcards

Renal Flashcards

1
Q

What are the functions of the kidneys?

A

Water and electrolyte balance
Filter and secrete excess/ waste substances
Reabsorb glucose, amino acids and bicarbonates
Activates 25-hydroxy vitamin D
Synthesise erythropoietin

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2
Q

What is GFR?

A

Glomerular filtration rate–> How much blood is filtered through the glomeruli into Bowman’s space per minute

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3
Q

What is a normal GFR?

A

120ml/min (7.2L/h, 170L/day)

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4
Q

What is the eGFR and how is it calculated?

A

The estimated glomerular filtration rate–> Best estimation of kidney function. Calculated from blood creatinine tests, age, body size and gender

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5
Q

What is creatinine and what happens to it?

A

A chemical compound left over from energy producing processes in the muscles that is filtered out of the blood by the kidneys and excreted in urine.

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6
Q

What does elevated creatinine levels indicate?

A

impaired kidney function or kidney disease

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7
Q

What are the different parts of the nephron?

A

Glomerulus, Bowman’s capsule, proximal convoluted tubule, Loop of Henle, Distal convoluted tubule, collecting duct.

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8
Q

What is the afferent arteriole?

A

Blood vessel that supplies the nephron (ARRIVES)

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9
Q

What is the efferent arteriole?

A

Blood vessels that carry blood away from the glomerulus (EXITS)

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10
Q

What is the glomerulus and what happens here?

A

Loop of capillaries, where ultrafiltration occurs

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11
Q

What makes up the filtration barrier at Bowman’s capsule?

A

Endothelial cells
Glomerular basement membrane
Podocytes

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12
Q

How is a pressure gradient created in the glomerulus to allow filtration?

A

The afferent arteriole dilates at the proximal glomerulus and the efferent arteriole constricts at the distal glomerulus.

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13
Q

What is the PCT lined with?

A

Simple cuboidal epithelial cels with brush borders and filled with large amount of mitochondria.

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14
Q

What is reabsorbed at the PCT?

A

65% of sodium, potassium and chloride, followed by water
100% of glucose
100% of amino acids
90% of bicarbonate.

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15
Q

What is the action of the loop of Henle?

A

Reabsorbs 25% of sodium and water

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16
Q

Which limb of the loop of Henle is impermeable to water?

A

The thick ascending limb.

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17
Q

Where do loop diuretics usually target?

A

The loop of Henle as this is where the most sodium filtration takes place.

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18
Q

What is the macula densa?

A

Area of specialised cells lining the proximal distal tubule. Play key sensory and regulatory functions in the maintenance of body fluid, electrolyte homeostasis and blood pressure. (sense salt levels and generate chemical signals to control kidney functions)

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19
Q

What happens at the distal convoluted tubule?

A

Fine tunes salt and water reabsorption and plays a major role in acid-base balance

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20
Q

What diuretics tend to target the distal convoluted tubule?

A

Thiazide diuretics

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21
Q

What is the main role of the collecting duct and how?

A

Reabsorption of water under the influence of ADH and aquaporins.

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22
Q

What is the juxtaglomerular apparaturs?

A

The location of renin-secreting cells and macula densa between the loop of Henle and distal nephorn which regulates blood pressure and GFR.

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23
Q

Where is water concentration detected?

A

Through osmoreception in the hypothalamus

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24
Q

When is erythropoietin produced by the kidney and why?

A

Produced in response to tissue hypoxia as it produced haemoglobin.

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25
Q

What is calcitrol and what are its actions?

A

Acitve form of vitamin D produced by the kidney:

Increases gut absorption of Ca2+ and phosphate, suppresses PTH.

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26
Q

Why is there a drop in Ca2+ in kidney failure?

A

Due to decreased renal production of ,25 (OH)2 vitamin D. (and increased serum phosphorus)

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27
Q

When/ why do kidney stones form?

A

When the urine contains more crystal-forming substances (calcium, ocalate and uric acid) than the fluid can dilute. The urine may also lack substances that prevent crystals from sticking together.

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28
Q

What forms 80% of renal stones? What else may form them?

A

Calcium oxalate most common

Can also be calcium phosphate, uric acid or struvite

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29
Q

What are staghorn calculi?

A

Renal calculi (stones) that are usually composed of struvite have a characteristic staghorn shape.

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30
Q

Where do staghorn calculi tend to sit?

A

Body in renal pelvis with horns extending into renal calyxes.

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31
Q

When do staghorn calculi tend to form?

A

In recurrent urinary tract infections: the bacteria can hydrolyse urea in urine to ammonia, creating the solid struvite.

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32
Q

How do renal stones present?

A 
May be asymptomatic/ never cause issue
Renal colic
Excruciating loin to groin pain
Colicky pain as the stone moves
Haematuria, nausea, vomiting, oliguria
May have symptoms of sepsis if infected (e.g. fever)
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33
Q

What is renal colic?

A

Type of abdominal pain caused by the obstruction of the ureter due to a dislodged kidney stones.

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34
Q

How are renal stones diagnosed?

A

CT KUB (non-contrast scan of kidney, ureters and bladder)
(Urine dipstick
Bloods for infection and kidney function
X-ray (may not be visible)

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35
Q

How are renal stones managed?

A
  • NSAIDs
  • Antiemetic if nausea/ vomiting
  • Fluids
  • Antibiotics if necessary
  • Wait for stone to pass: Tamsulosin can help spontaneous passage
  • Surgical interventions in large stones/ stones that do not pass
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36
Q

What is the usual outcome of renal stones?

A

Stones <6mm have > 50% of passing without intervention.

Spontaneous passage can take several weeks

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37
Q

What surgical interventions can be used for large renal stones?

A

Extracorporeal shock wave lithotripsy
Ureteroscopy and laser lithotripsy
Percutaneous nephrolithotomy
Open surgery

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38
Q

What is Extracorporeal shock wave lithotripsy?

A

External machine generates shock waves and directs them at the stone under X-ray guidance, breaking it into smaller parts and therefore they are easier to pass.

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39
Q

What is a Ureteroscopy with laser lithotripsy?

A

When a camera is inserted via the urethra, bladder and ureter, the stone is identified and broken up by targeted lasers making it easier to pass.

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40
Q

What is percutaneous nephrolithotomy?

A

When a nephroscope (small camera) is inserted via a small incision at the patient’s back, and is inserted through the kidney to assess the ureter. The stones can either be removed or broken up. (Performed in theatre under anaestehetic) .

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41
Q

What advice is given to prevent recurrent stones?

A
  • Increase oral fluids
  • Reduce dietary salt intake
  • Reduce intake of oxalate-rich foods for calcium stones
  • Reduce intake of urate-rich foods for uric acid stones
  • Limit dietary protein.
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42
Q

What is nephrolithiasis?

A

Kidney stones

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43
Q

What is AKI and how is it diagnosed?

A

Acute kidney injury–> diagnosed by measuring the serum creatinine.

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44
Q

What is the criteria for diagnosing an AKI?

A
  • Rise in creatinine of > 25 micromol/L in 48 hours
  • Rise in creatine of >50% in 7 days
  • Urine output of < 0.5ml/kg/hour for >6 hours
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45
Q

What are the key risk factors of acute kidney injury?

A 
Chronic kidney disease
Heart failure
Diabetes
Liver disease
Older age
Cognitive impairment
Nephrotoxic medications
Use of contrast medium (e.g. CT scan)
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46
Q

What are the causes of renal impairment?

A

Pre-renal
Renal
Post-renal?

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47
Q

What is pre-renal AKI?

A

Acute kidney injury caused by inadequate blood supply to the kidneys reducing the filtration of blood.

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48
Q

What are the causes of pre-renal AKI?

A

Dehydration
Hypotension
Heart failure

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49
Q

What is renal AKI?

A

When intrinsic disease leads to reduced filtration of the blood and AKI.

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50
Q

What are the causes of renal AKI?

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

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51
Q

What is post-renal AKI?

A

AKI caused by obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. (obstructive uropathy).

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52
Q

What causes post-renal AKI?

A

Kidney stones
Masses (e.g. cancer) in the abdomen or pelvis
Ureter or uretral strictures (narrowing)
Enlarged prostate or prostate cancer

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53
Q

What investigations are done to look into the cause of AKI?

A

Urinalysis for:

  • Protein and blood (suggest acute nephritis)
  • Leucocytes and nitrites (suggest infection)
  • Glucose (suggests diabetes)

Ultrasound to look for obstruction.

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54
Q

How is the first step in AKI management?

A

Correct underlying cause:

  • Fluid rehydration with IV fluids in pre-renal AKI
  • Stop nephrotoxic medications (e.g. NSAIDS and antihypertensives)
  • Relieve obstruction in post-renal (e.g. insert catheter)
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55
Q

What are the main complications of AKI?

A

Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (can lead to encephalopathy or pericarditis)

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56
Q

What is nephritis?

A

Inflammation of the kidneys

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57
Q

What is nephritic syndrome?

A

A group of symptoms that indicates inflammation of the kidney. (but not the underlying cause)

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58
Q

What are the features of nephritic syndrome?

A

Haematuria (blood in urine)
Oliguria (reduced urinary output)
Proteinuria (<3g in 24 hours)
Fluid retention

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59
Q

What is nephrotic syndrome and how is it classified?

A 
Group of symptoms that indicate the presence of an underlying disease (but not what the disease is):
Peripheral oedema
Proteinuria (>3g in 24 hours) 
Serum albumin (<25g/L)
Hypercholesterolaemia
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60
Q

How much protein must there be in urine to differentiate between nephritic and nephrotic syndrome?

A

Nephrotic syndrome >3g in 24 hours

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61
Q

What is glomerulonephritis?

A

A range of conditions that cause inflammation of/ around the glomerulus and nephron.

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62
Q

What is interstitial nephritis?

A

When there is inflammation of the interstitium (space between cells and tubules) in the kidney.

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63
Q

What are the two key forms of interstitial nephritis?

A

Acute interstitial nephritis

Chronic tubulointerstitial nephritis

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64
Q

What is glomerulosclerosis?

A

Pathological scarring of the glomerular tissue caused by other diagnoses.

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65
Q

What can cause glomerulosclerosis?

A

Glomerulonephritis, obstructive uropathy (urine outflow blockage) or focal segmental glomerulosclerosis (specific disease)

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66
Q

What are some examples of glomerulonephritis?

A 
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
IgA nephropathy (Berger's disease)
Post-streptococcal glomerulonephritis
Goodpasture sydrome 
Rapidly progressive glomerulonephritis
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67
Q

How are most types of glomerulonephritis treated?

A

Immunosuppression (e.g. steroids)

Blood pressure control ( ACE inhibitors, Angiotensin-II receptor blockers)

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68
Q

How does nephrotic syndrome usually present?

A

Oedema
Frothy urine (proteinurea)
Pallor

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69
Q

What does nephrotic syndrome predispose patients to?

A

Thrombodis, hypertension and high cholesterol

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70
Q

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

A

Minimal change disease

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71
Q

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

A

Focal segmental glomerulosclerosis

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72
Q

When does nephrotic syndrome occur?

A

When the glomerular basement membrane becomes highly permeable to proteins, allowing them to leak from the blood to the urine. (usually due to podocyte injury)

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73
Q

In what group is nephrotic syndrome most common?

A

2-5 year olds

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74
Q

What is the classic triad in nephrotic syndrome?

A

Low serum albumin
High urine protein content (>3)
Oedema

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75
Q

What other features occur in patients with nephrotic syndrome?

A

Deranged lipid profile (high cholesterol, triglyceride and LDL levels)
High blood pressure
Hyper-coagulability

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76
Q

What is minimal change disease?

A

The most common cause of nephrotic syndrome in children which occurs in isolation without any clear underlying condition of pathology.

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77
Q

What are the secondary causes of nephrotic syndrome?

A

Secondary to intrinsic kidney disease–> Focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis
Secondary to systemic illness–> HSP, diabetes, infection

78
Q

How is minimal change disease diagnosed?

A

Urinanalysis shows small molecular weight proteins and hyaline casts
(Renal biopsy usually doesn’t show abnormality)

79
Q

How is nephrotic syndrome usually managed?

A

High dose steroids (prednisolone)
Low salt diet
Diuretics

80
Q

What percentage of children treated for nephrotic syndrome are steroid sensitive and what happens to those that are resistant?

A

80% are steroid sensitive
80% are steroid sensitive (will relapse and need further steroids)
Steroid resistant children are treated with ACE inhibitors and immunosuppressants

81
Q

What are the complications of nephrotic syndrome

A

Hypovolaemia (causes oedema and low BP)
Thrombosis (clotting proteins are lost in the kidneys)
Infection (kidneys leak immunoglobulins)
Acute/ chronic renal failure
Relapse

82
Q

What is focal segmental glomerulosclerosis?

A

Scleroisis that occurs in small sections of limited glomeruli

83
Q

What is IgA nephropathy?

A

Berger’s disease–> type of primary glomerulonephritis

where IgA deposits in the nephrons cause inflammation

84
Q

How is IgA nephropathy diagnosed?

A

Renal biopsy shows IgA deposits and glomerular mesangial proliferation (mesangium is kidney structure)

85
Q

How is IgA nephropathy treated?

A

Supportive treatment of renal failure and immunosuppression (e.g. steroids)

86
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy

87
Q

What is membranous glomerulonephritis?

A

Glomerulonephritis that shows IgG and complement deposits on the basement membrane.

88
Q

What are the causes of membranous glomerulonephritis?

A

70% idiopathic

Secondary to malignancy, rheumatoid disorders or drugs

89
Q

What is the most common glomerulonephritis?

A

Membranous nephropathy

90
Q

What is post streptococcal glomerulonephritis?

A

(Diffuse proliferative glomerulonephritis) Glomerulonephritis caused by streptococcus infection (e.g. tonsillitis)

91
Q

How soon after B-haemolytic streptococcus infection does post-streptococcal glomerulonephritis occur?

A

1-3 weeks

92
Q

How does streptococcus cause glomerulonephritis?

A

Immune complexes of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation, leading to acute deterioration in renal function.

93
Q

When should post-streptococcal glomerulonephritis be considered?

A

Where there is nephritis with evidence of recent tonsillitis caused by streptococcus

94
Q

How is post-streptococcal glomerulonephritis managed?

A

Supportive- 80% make full recovery

Some may need treatment with antihypertensives and diuretics

95
Q

What is goodpastures syndrome?

A

When anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement mamranes, causing glomerulonephritis and pulmonary haemorrhage)

96
Q

How does Goodpastures syndrome usually present?

A

With AKI and haemoptysis (coughing up blood)

97
Q

What two syndromes should you consider in a patient presenting with acute renal failure and haemoptysis and how would you differentiate them?

A

Goodpastures syndrome and Wegener’s granulmatosis.

Goodpastures is associated with anti-GBM antibodies whereas Wegener’s is a type of vasculitis associated with ANCA antibodies (may also have a wheeze, sinusitis, or saddle shaped nose)

98
Q

What is rapidly progressive glomerulonephritis?

A

Glomerulonephritis that presents with very acute illness and whose histology shows crescentic glomerulonephritis (often secondary to goodpastures syndrome)

99
Q

What is chronic kidney disease?

A

Chronic reduction in kidney function that is usually permanent and progressive (> 3 months)

100
Q

What are the causes of chronic kidney disease?

A 
Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications (NSAIDs, PPIs, lithium)
101
Q

What are the main risk factors for chronic kidney disease?

A 
Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys
102
Q

How does chronic kidney disease usually present?

A 
Usually asymptomatic and diagnosed on routine testing. 
Pruritus
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
103
Q

What investigations can be done to test for chronic kidney disease?

A

eGFR (using U&E blood test)
Proteinuria (using urine albumin:creatinine ratio
Haematuria (using urine dipstick)
Renal ultrasound

104
Q

What are the G scores of chronic kidney disease?

A 
Based on eGFR:
G1= >90
G2= 60-89
G3a= 45-59
G3b= 30-44
G4= 15-29
G5= <15 --> End stage renal failure
105
Q

What is the A score that is used in chronic kidney disease?

A

Albumin: creatinine ratio:
A1= <3mg/mmol
A2= 3-30
A3= >30

(>3 is a significant result)

106
Q

What are the key complications in chronic kidney disease?

A 
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
107
Q

What must a patient have for a CKD diagnosis?

A

eGFR of at least < 60 or proteinuria

108
Q

Under what conditions would a CKD diagnosis need to be referred to a specialist?

A

eGFR <30
ACR > 70
Accelerated progression: Decrease in eGFR of 15-25%/ 15ml/min in one years
Uncontrolled hypertension despite >4 antihypertensives

109
Q

What are the main aims of CKD management?

A

Slow the progression
Reduce risk of cardiovascular disease
Reduce risk of complications
Treat complications

110
Q

How is CKD progression slowed?

A

Optimise diabetic control
Optimise hypertensive control
Treat glomerulonephritis

111
Q

How can patients with CKD reduce the risk of complications?

A

Exercise, maintain healthy weight and stop smoking
Special dietary advice (phosphate, sodium, potassium and water intake)
Atorvastatin (20mg) for primary prevention of CV disease

112
Q

How are complications of CKD treated?

A

Metabolic acidosis–> Oral sodium bicarbonate
Anaemia–> Iron supplementation and erythropoietin
Renal bone disease–> vitamin D
End stage renal failure–> Dialysis and renal transplant

113
Q

How can hypertension cause CKD?

A

Over time, it puts a strain on the small blood vessels in the kidneys and stops them working properly

114
Q

How can diabetes cause CKD?

A

Too much glucose in the blood can damage the tiny filters in the kidneys

115
Q

How can high cholesterol levels cause CKD?

A

Cause a build up of fatty deposits in the blood vessels supplying the kidneys

116
Q

What is the first line treatment in patients with chronic kidney disease and who is it offered to?

A

ACE inhibitors to treat hypertension. Offered to patients with:
Diabetes + ACR >3
Hypertension + ACR >30
All patients with ACR >70

117
Q

What needs monitoring in chronic kidney disease treatment and why?

A

Serum potassium–> CKD and ACE inhibitors cause hyperkalamia

118
Q

Why does CKD cause anaemia?

A

The kidney produces erythropoietin, the hormone which stimulates RBC production. Damaged kidney cells in CKD cause a drop in erythropoietin and therefore a drop in RBC production and anaemia.

119
Q

How can anaemia due to CKD be treated?

A 
Treat any iron deficiency first (IV iron) 
Exogenous erythropoietin
Blood transfusion ( should be limited as can sensitive immune system)
120
Q

What is renal bone disease (+its new name)?

A

When the kidneys fail to maintain the proper levels of calcium, phosphate, vitamin D and parathyroid hormone (PTH) in the blood.
Also known as chronic kidney disease-mineral and bone disorder (CKD-MBD)

121
Q

What are the key features of renal bone disease?

A

Osteomalacia (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis (bone hardening)

122
Q

What does an X-ray show in renal bone disease?

A

Sclerosis (denser white) of both ends of vertebrae
Osteomalacia in centre of vertebra (less white).

*Known as ‘rugger jersey’ spine after the stripes on a rugby shirt

123
Q

Why is there high serum phosphate in renal bone disease?

A

Due to reduced phosphate excretion

124
Q

Why is there low active vitamin D in renal bone disease and what does this cause?

A

The kidney is essential in metabolising vit. D to its active form. The active form is essential in calcium absorption from the intestines and kidneys and also regulates bone turnover.

125
Q

Why does secondary hyperparathyroidism occur in renal bone disease?

A

The parathyroid glands react to low serum calcium and high serum phosphate by excreting more PTH. This leads to increased osteoclast activity which leads to the absorption of calcium from bone.

126
Q

Why does osteomalacia occur in renal bone disease?

A

Due to increased turnover of bones without adequate calcium supply

127
Q

Why does osteosclerosis occur in renal bone disease?

A

When osteoblasts respond by increasing their activity to match that of osteoclasts by creating new tissue in bone, however low calcium levels mean that the new tissue is not properly mineralised

128
Q

How is renal bone disease caused by CKD managed?

A

Active forms of vitamin D (Alfacalcidol and calcitrol)
Low phosphate diet
Bisphosphonates (to treat osteoporosis)

129
Q

What is dialysis?

A

Method for performing the filtration tasks of the kidneys in patients with end stage renal failure or its complications

130
Q

What are the indications for acute dialysis?

A

AEIOU:
Acidosis (severe/ not responding to treatment
Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
Intoxication (Medication overdose)
Oedema
Uraemia symptoms (seizures/ reduced consciousness)

131
Q

What is uraemia?

A

When the toxins/ waste products that should normally end up in the urine end up in the bloodstream due to kidney failure.

132
Q

What are the indications for long term dialysis?

A

End stage renal failure

Any of the acute indications continuing long term

133
Q

What are the options fo maintenance dialysis?

A

Continuous ambulatory peritoneal dialysis
Automated peritoneal dialysis
Haemodialysis

134
Q

What is peritoneal dialysis?

A

When the peritoneal membrane is used as the filtration membrane

135
Q

What happens in peritoneal dialysis?

A

A dialysis solution containing dextrose is added to peritoneal cavity. Ultrafiltration occurs from the blood across the peritoneal membrane into the dialysis solution. The dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution.

136
Q

How is the dialysis solution added and waste solution taken away in peritoneal dialysis?

A

Using a Tenckhoff catheter–> Plastic tube inserted into the peritoneal cavity with one end on the outside, allowing access.

137
Q

What are the two types of peritoneal dialysis?

A

Continuous ambulatory peritoneal dialysis and Automated dialysis

138
Q

What is continuous ambulatory peritoneal dialysis?

A

Where the dialysis solution is in the peritoneum at all times. (Various regimes for changing the solution e.g. 4 times a day)

139
Q

What is automated dialysis?

A

When peritoneal dialysis occurs overnight. A machine continuously replaces dialysis fluid in the abdomen overnight to optimise ultrafiltration.

140
Q

What are the complications of peritoneal dialysis?

A 
Bacterial peritonitis (bacteria thrive in the glucose solution) 
Peritoneal sclerosis 
Ultrafiltration failure 
Weight gain
Psychosial effects
141
Q

What is ultrafiltration failure?

A

When the patient starts to absorb the dextrose in the filtration solution (causing weight gain), reducing the filtration gradient and making ultrafiltration more prominent over time.

142
Q

What is haemodialysis?

A

When patients have their blood filtered by a haemodialysis machine

143
Q

What is a typical regime for haemodialysis?

A

4 hours a day for 3 days a week

144
Q

What are the options for good blood supply access in haemodialysis?

A

Tunnelled cuffed catheter

Arterio-venous fistula

145
Q

What is a tunnelled cuffed catheter?

A

A tube inserted into the subclavian or jugular vein with a tip that sits in the superior vena cava or right atrium. Has two lumens- one where blood exits the body (red) and one where it enters the body (blue)

146
Q

What is a Dacron cuff?

A

Cuff that surrounds the catheter to promote healing and adhesion of tissue to the cuff, making the catheter more permanent and providing a barrier to bacterial infection.

147
Q

What is an A-V fistula?

A

An artificial connection between an artery to a vein, allowing blood to flow under high pressure from an artery directly to a vein (bypassing the capillary system), and therefore providing a large easy access blood vessel with high pressure arterial blood flow.

148
Q

What vessels are usually used to form a fistula?

A

Radio-cephalic
Brachio-cephalic
Brachio-basilic

149
Q

What are the complications of AV fistula?

A 
Aneurysm 
Infection
Thrombosis
STEAL syndrome
High output heart failure
150
Q

What is STEAL syndrome?

A

Where there is inadequate blood flow to the limb distal to the AV fistula due to the fistula diverting it away from where its supposed to flow.

151
Q

What is high output heart failure?

A

Blood flows very quickly from the arterial to the venous system through the fistula, meaning there is more rapid return of blood to the heart. This increases the pre-load and can cause hypertrophy of the heart and heart failure.

152
Q

How many extra years of life does a renal transplant add to a patient with end stage renal failure?

A

10 years

153
Q

How are patients and donors matched for a renal transplant?

A

Matched based on the human leukocyte antigen (HLA) type A,B and C on chromosone 6.

154
Q

What are the complications of a renal transplant?

A

Transplant rejection
Transplant failure
Electrolyte imbalances

155
Q

What is polycystic kidney disease?

A

Condition where the kidneys develop fluid-filled cysts and kidney function is significantly impaired

156
Q

What causes polycystic kidney disease?

A

genetic condition

157
Q

What are the extra-renal manifestations of polycystic kidney disease?

A

Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cerebral aneurysms
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilation

158
Q

What are the two types of polycystic kidney disease and which is more common?

A

Autosomal dominant (most common) and autosomal recessive

159
Q

How is polycystic kidney diseasediagnosed?

A

Ultrasound

Genetic testing

160
Q

What genes are associated with the autosomal dominant type of polycystic kidney disease?

A

PKD-1: chromosome 16 (85% cases)

PKD-2: chromosome 4 (15%)

161
Q

What are the key complications of polycystic kidney disease?

A 
Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria (with cyst rupture) 
Renal stones
End-stage renal failure
162
Q

When does the autosomal recessive type of polycystic kidney disease usually present and with what?

A

Often presents in pregnancy with oligohydramnios (low levels of amniotic fluid) as the fetus does not produce enough urine.

163
Q

What does oligohydramnios lead to?

A

Underdevelopment of the lungs resulting in respiratory failure shortly after birth.

164
Q

What does the baby usually present with in autosomal recessive polycystic kidney disease?

A

Respiratory failure
Dysmorphic features (underdeveloped ear cartilage, low set ears and flat nasal bridge)
Will have end-stage renal failure by adulthood

165
Q

How is polycystic kidney disease managed?

A

Tolvaptan (vasopressin receptor agonist) can slow the development of cysts and the progression of renal failure.
Supportive of complications (e.g. antihypertensives, analgesia, antibiotics, dialysis, renal transplant)

166
Q

What is the most common cause of glomerular pathology and chronic kidney disease in the UK?

A

Diabetic nephropathy

167
Q

What causes diabetic nephropathy?

A

The chronic high level of glucose passing through the glomerulus causes glomerulosclerosis (scarring)

168
Q

What is the key finding in diabetic nephropathy and why?

A

Proteinuria, due to damage to the glomerulus allowing protein to be filtered from blood to urine

169
Q

What is interstitial nephritis?

A

When there if inflammation of the space between cells and tubules (the interstitium) of the kidney

170
Q

What are the two types of interstitial nephritis?

A

Acute interstitial nephritis and chronic tubulointerstitial nephritis

171
Q

How does acute interstitial nephritis present?

A

With AKI and hypertension

May present with other features of generalised hypersensitivity reaction (rash, fever, eosinophilia)

172
Q

What causes acute interstitial nephritis?

A

Drugs (NSAIDS, antibiotics)

Infection

173
Q

What is chronic tubulointerstitial nephritis and how does it present?

A

Chronic inflammation of the tubules and interstitium, presenting with chronic kidney disease

174
Q

What is the most common cause of AKI?

A

Acute tubular necrosis

175
Q

What is acute tubular necrosis?

A

Damage and death of the epithelial cells of the renal tubules

176
Q

What causes acute tubular necrosis?

A

Ischaemia–> due to shock, sepsis or dehydration

Toxins–> Radiology contrast dye, NSAIDs, Gentamycin

177
Q

What is the recovery period for acute tubular necrosis and why?

A

7-21 days.

The epithelial cells have the ability to regenerate making it reversible.

178
Q

How can acute tubular necrosis be diagnosed?

A

‘Muddy brown casts’ (tube-shaped particles) found on urinalysis
Renal tubular epithelial cells in urine

179
Q

How is acute tubular necrosis managed?

A 
With same as other causes of AKI: 
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
180
Q

What are the causes of hyperkalaemia?

A

Acute kidney injury
Chronic kidney disease
Rhabdomyolysis (when skeletal muscle breaks down, releasing its products into the blood)
Adrenal insufficiency
Tumour lysis syndrome
Medications (Aldosterone antagonists, ACE inhibitors, Angiotensin II receptor blocker, NSAIDs, potassium supplements)

181
Q

What is the role of potassium in the body?

A

An electrolyte involved in fluid balance, nerve signals and muscle contraction.

182
Q

How is hyperkalaemia diagnosed?

A

U&E blood test.

183
Q

What are the ECG signs of hyperkalaemia?

A

Tall, peaked T waves
Flat/ absent P waves
Broad QRS complex

184
Q

How is hyperkalaemia treated?

A

Insulin and dextrose infusion + IV calcium gluconate.

185
Q

What is the action of insulin and dextrose in hyperkalaemia treatment?

A

Insuling drives glucose into cells, taking potassium with it. Dextrose must be given to counteract the hypoglycaemia caused by insulin.

186
Q

What is haemolytic uraemic syndrome?

A

Syndrome that occurs when there is thrombosis in small blood vessels throughout the body,

187
Q

What triggers haemolytic uraemic syndrome?

A

Shiga toxin produced by e.coli 0157 and shigella.

188
Q

What triad does haemolytic uraemic syndrome lead to?

A

Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)

189
Q

What happens in haemolytic uraemic syndrome?

A

Blood clots form in the small vessels, consuming platelets (thrombocytopenia). The clots break up the red blood cells as they pass by (haemolysis), causing anaemia. The blood flow through the kidney is affected by the clots and damaged red blood cells, leading to AKI.

190
Q

How does haemolytic uraemic syndrome present?

A 
E. coli causes gastroenteritis with bloody diarrhoea. 
Around 5 days after this, symtpoms of HUS present:
Reduced urine output
Haematuria
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising
191
Q

How is haemolytic uraemic syndrome managed?

A

Self limiting but needs supportive treatment (Antihypertensives, blood transfusions, dialysis)

192
Q

What is the percentage mortality of HUS?

A

10%

PHASE 2A (Mine) (15 decks)

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