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Week 227 - Acute Renal Injury Flashcards

1
Q

Week 227 - Acute Renal Injury: What are the pre-renal causes of Acute Renal Failure?

A

• Due to disturbance in renal blood supply.

- E.g. Hypotension/Hypovolaemia, Cirrhosis, renal artery stenosis.

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2
Q

Week 227 - Acute Renal Injury: What are the renal/intrinsic causes of Acute Renal Failure?

A

• Damage to the parenchyma of the kidney itself.

- E.g. glomerulonephritis, acute tubular necrosis, acute interstitial nephritis.

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3
Q

Week 227 - Acute Renal Injury: What are the post-renal causes of Acute Renal Failure?

A

• Usually a consequence of urinary tract obstruction.

- E.g. BPH, renal stones, obstructed urinary catheter, bladder stones or malignancy.

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4
Q

Week 227 - Acute Renal Injury: What is Rhabdomyolysis?

A
  • Skeletal muscle breakdown secondary to injury.
  • For example following strenuous exercise, trauma or infection.
  • Leading to the leakage of potentially toxic intracellular contents into the blood stream,
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5
Q

Week 227 - Acute Renal Injury: What is the ‘triad’ of Rhabdomyolysis?

A

1) Myalgia
2) Generalized weakness
3) Tea-coloured urine.

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6
Q

Week 227 - Acute Renal Injury: How can rhabdomyolysis cause acute renal failure?

A
  • Obstruction with haem pigment casts.
  • Proximal tubular injury by haem iron.
  • Volume depletion (Damaged muscles can accumulate fluid over time, causing a reduction in circulating volume).
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7
Q

Week 227 - Acute Renal Injury: What are some of the non-traumatic causes of rhabdomyolysis?

A
  • Marathon runners
  • Hot weather
  • Hypokalaemia
  • Prolonged convulsions
  • Metabolic myopathy
  • Malignant hyperthermia
  • Hypothermia
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8
Q

Week 227 - Acute Renal Injury: Which drugs can cause rhabdomyolysis?

A

• Alcohol, opiates, statins, colchicine, cyclosporin.

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9
Q

Week 227 - Acute Renal Injury: How is rhabdomyolysis induced AKI diagnosed?

A
  • History
  • Red to brown urine
  • Elevated serum enzyme level - CK, LDH
  • Electrolyte abnormalities.
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10
Q

Week 227 - Acute Renal Injury: Which electrolyte abnormalities do you get with rhabdomyolysis induced AKI?

A
  • Hyperkalaemia
  • Hyperphosphatamia
  • Hyperuricaemia
  • Hypocalcaemia (However, you will get hypercalcaemia in the recovery phase)
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11
Q

Week 227 - Acute Renal Injury: What are the preventative options for stopping rhabdomyolysis causing AKI?

A
  • Fluid repletion - Improve renal perfusion, washout obstructing casts.
  • Forced alkaline diuresis - Using Sodium Bicarbonate - Reduces myoglobin precipitation.
  • Forced diuresis - Using Mannitol.
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12
Q

Week 227 - Acute Renal Injury: What is Mannitol used for and what are the complications of its use?

A
  • Osmotic diuretic - Forced diuresis - Free radical scavenger.
  • Can cause hypernatraemia.
  • And can cause increased plasma osmolality and volume expansion in those with poor renal function.
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13
Q

Week 227 - Acute Renal Injury: What are urinary casts?

A
  • They are cylindrical structures formed in the distal convoluted tubules.
  • They are primarily made from tubular mucoprotein (Tamm-Horsfall protein).
  • The presence of the them in urine microscopy can signify a number of disease states.
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14
Q

Week 227 - Acute Renal Injury: The presence of a red blood cell cast can indicate which disease state?

A

• Patients with glomerular haematuria.

- E.g. glomerulonephritis.

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15
Q

Week 227 - Acute Renal Injury: The presence of a white blood cell cast indicates which disease state?

A

• Acute pyelonephritis or interstitial nephritis.

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16
Q

Week 227 - Acute Renal Injury: The presence of a fatty cast indicates the presence of which disease state?

A

• Lipiduria

- E.g. nephrotic syndrome.

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17
Q

Week 227 - Acute Renal Injury: What is nephrotic syndrome?

A

• This is where the permeability of the walls of the glomerulus is increased resulting in proteinuria.

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18
Q

Week 227 - Acute Renal Injury: The presence of a pigmented cast indicates the presence of which disease states?

A
  • Haemoglobinuria

* Myoglobinuria

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19
Q

Week 227 - Acute Renal Injury: What is the shape of calcium oxalate crystals?

A

Square, enveloped shapes.

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20
Q

Week 227 - Acute Renal Injury: What is the shape of a triple phosphate crystal? What does it indicate?

A
  • Coffin lid shape.
  • Alkaline urine
  • Proteus UTI
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21
Q

Week 227 - Acute Renal Injury: What shape are uric acid crystals? What does their presence indicate?

A
  • Diamond shaped.

* Hyperuricaemia.

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22
Q

Week 227 - Acute Renal Injury: What is the definition of clearance (In terms of measuring renal function)?

A
  • Volume of plasma cleared of substance in unit time.

* Measured as the volume of indicator removed from plasma divided by average plasma concentration during a given time.

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23
Q

Week 227 - Acute Renal Injury: What are the limitations of using creatinine clearance to measure renal function?

A
  • Difficult, time consuming.
  • Inaccurate urine collections.
  • Diurnal and day-to-day variations in creatinine clearance.
  • Not adjusted for age,gender,race etc.
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24
Q

Week 227 - Acute Renal Injury: What is the eGFR, clinical findings and treatment of stage one of CKD?

A
  • Normal kidney function but urine findings or structural abnormalities point to kidney disease.
  • eGFR 90+
  • Observation, control of BP.
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25
Q

Week 227 - Acute Renal Injury: What is the eGFR, clinical findings and treatment of stage two of CKD?

A
  • Mildly reduced kidney function and urine/structural/genetic findings point to kidney disease.
  • eGFR 60-89
  • Observation, control of BP, Control of risk factors.
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26
Q

Week 227 - Acute Renal Injury: What is the eGFR, clinical findings and treatment of stage three of CKD?

A
  • Moderately reduced kidney functions.
  • eGFR 30-59
  • Observation, control of BP, Control of risk factors.
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27
Q

Week 227 - Acute Renal Injury: What is the eGFR, clinical findings and treatment of stage four of CKD?

A
  • Severely reduced kidney function.
  • eGFR 15-29
  • Planning for end stage renal failure.
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28
Q

Week 227 - Acute Renal Injury: What is the eGFR, clinical findings and treatment of stage five of CKD?

A
  • Very severe, or end stage renal failure.

* eGFR

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29
Q

Week 227 - Acute Renal Injury: What is the RIFLE criteria?

A

• Categorizes the degree of renal failure into,

  • Risk
  • Injury
  • Failure
  • Loss
  • End stage kidney disease
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30
Q

Week 227 - Acute Renal Injury: What are the pulmonary complications of acute kidney injury?

A
  • Fluid overload > Pulmonary oedema
  • Increased pulmonary vascular permeability.
  • Leucocyte migration
  • Pulmonary haemorrhage
  • Infection
  • ARDS
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31
Q

Week 227 - Acute Renal Injury: What are the CNS complications of acute kidney injury?

A
  • Inflammatory reaction
  • Acidosis
  • Electrolyte imbalance
  • Confusion
  • Convulsions
  • Altered conscious levels
  • Coma
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32
Q

Week 227 - Acute Renal Injury: What are the cardiac complications of acute kidney injury?

A
  • Acidosis
  • Sympathetic overactivity
  • Hypertension
  • Pericarditis
  • Arrhythmia
  • Cardiac hypertrophy
  • Heart Failure
  • MI
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33
Q

Week 227 - Acute Renal Injury: What characterises pre-renal acute renal failure?

A 
• Intravascular volume depletion.
• Decreased effective blood volume.
• Altered intrarenal haemodynamics 
- Afferent vasoconstriction
- Efferent vasodilation
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34
Q

Week 227 - Acute Renal Injury: What are the characteristics of intrinsic acute renal failure?

A
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Acute glomerulonephritis
  • Acute vascular syndromes
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35
Q

Week 227 - Acute Renal Injury: What is third space sequestration?

A
  • Accumulation of fluid in the third space - i.e. the transcellular compartment.
  • Can be a result of bowel obstruction, peritonitis, pancreatitis, ascites.
  • Can result in hypovolaemia resulting in acute renal injury.
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36
Q

Week 227 - Acute Renal Injury: How can third space sequestration clinically manifest?

A
  • Respiratory compromise.
  • Decreased cardiac output.
  • Intestinal ischaemia.
  • Hepatic dysfunction.
  • Oliguric renal failure - Oliguria occurs when intra-abdominal pressure exceeds 15mmHg, with anuria developing when the pressure exceeds >30mmHg.
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37
Q

Week 227 - Acute Renal Injury: How is third space sequestration treated?

A

• Abdominal decompression.

  • Paracentesis
  • Surgical decompression
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38
Q

Week 227 - Acute Renal Injury: What is the normal GFR?

A

120 ml/min, >7L/hr

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39
Q

Week 227 - Acute Renal Injury: In cases of partial post-renal obstruction, what dysfunction does the distal tubule experience in terms of concentration and acid/base balance?

A
  • Reduced concentration - Polyuria

* Loss of acidification resulting in a metabolic acidosis.

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40
Q

Week 227 - Acute Renal Injury: In terms of history and examination, what may indicate post-renal failure?

A
  • History - Colic, stone disease, polyuria, nocturia, Haematuria, DM, Neurological condition.
  • Examination - Palpable bladder, bladder scan, post-micturition residual urine, KUB ultrasound scan.
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41
Q

Week 227 - Acute Renal Injury: What type of acute kidney injury is acute tubular necrosis?

A

Intrinsic

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42
Q

Week 227 - Acute Renal Injury: What are some of the causes of acute tubular necrosis?

A

• Ischaemic - e.g. Hypotension, Sepsis.

• Nephrotoxic - Drug-induced e.g. Aminoglycosides, cisplatinum, paracetamol.
- Pigment nephropathy - Intravascular haemolysis, rhabdomyolysis.

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43
Q

Week 227 - Acute Renal Injury: What is the most common form of intrinsic acute renal failure?

A

• Acute Tubular Necrosis (ATN)

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44
Q

Week 227 - Acute Renal Injury: What is the mortality rate of uncomplicated ATN?

A

7%-23%

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45
Q

Week 227 - Acute Renal Injury: 50% of radiocontrast nephropathies develop after which procedures?

A

• Cardiac diagnostic and interventional procedures.

46
Q

Week 227 - Acute Renal Injury: What are the risk factors for developing radiocontrast nephropathy?

A
  • Pre-existing renal disease.
  • DM
  • Hypertension
  • ACEI, NSAIDs
  • Volume depletion
  • Large volume of contrast
47
Q

Week 227 - Acute Renal Injury: How can the risk of developing radiocontrast nephropathy be reduced?

A
  • Low-osmolality contrast media.
  • IV fluid

(Antioxidants, N acetyl cysteine, diuretics, IV sodium bicarbonate)

48
Q

Week 227 - Acute Renal Injury: What are the causes of Acute tubulo-interstitial nephritis?

A
  • Drug-induced - Penicillins, cephalosporins, sulfonamides, rifampicin, frusemide, NSAIDs.
  • Infection - Bacterial, viral, rickettsial disease, tuberculosis.
49
Q

Week 227 - Acute Renal Injury: What (from history, signs, examination, investigations) would lead you to consider acute tubulo-interstitial necrosis?

A
  • History - Exposure, drug/infection.
  • Fever
  • Rash
  • Arthralgia
  • Oesinophilia
  • Biopsy - cellular infiltrate.
50
Q

Week 227 - Acute Renal Injury: How do you treat acute tubulo-interstitial necrosis?

A
  • Withdraw the offending agent/ treat infection.
  • Steroids.

• Has a very good outcome.

51
Q

Week 227 - Acute Renal Injury: What are the three life-threatening complications of acute kidney injury?

A
  • Metabolic Acidosis
  • Hyperkalaemia
  • Acute pulmonary oedema
52
Q

Week 227 - Acute Renal Injury: How is the serum anion gap calculated?

A 
AG = Cations - Anions
AG= Na + K - Cl - HCO3
53
Q

Week 227 - Acute Renal Injury: What occurs during normal anion gap metabolic acidosis? What causes it?

A
  • Acidosis is due to loss of bicarbonate, this is replaced by chloride resulting in a normal anion gap.
  • Can be caused by diarrhoea, renal tubular acidosis.
54
Q

Week 227 - Acute Renal Injury: What occurs to give an increased anion gap metabolic acidosis? What can cause it?

A
  • Increased acid production with anion other than Cl.

* Can be caused by lactic acidosis, DKA, Renal failure, Methanol, Ethylene Glycol.

55
Q

Week 227 - Acute Renal Injury: What is the clinical effect of a metabolic acidosis?

A
  • Muscle weakness
  • Altered mental state
  • Kussmaul breathing
  • Hyperkalaemia
  • Hypotension
56
Q

Week 227 - Acute Renal Injury: What is Kussmaul breathing?

A
  • Deep and labored breathing.

* Associated with severe metabolic acidosis.

57
Q

Week 227 - Acute Renal Injury: What is the treatment of metabolic acidosis?

A
  • Treat the cause!
  • Volume expansion
  • IV sodium bicarbonate (Only in severe acidosis
58
Q

Week 227 - Acute Renal Injury: What are the effects of hyperkalaemia?

A
  • Muscle weakness
  • Constipation
  • Cardiac effects
  • ECG changes - loss of P wave, AV block, bradycardia, V tachycardia, asystole.
59
Q

Week 227 - Acute Renal Injury: What are the ECG changes associated with hyperkalaemia?

A
  • Loss of p waves.
  • AV block
  • Bradycardia
  • V tachycardia
  • Asystole
60
Q

Week 227 - Acute Renal Injury: What are the treatment options for hyperkalaemia?

A
  • Treatment of the cause!
  • IV fluid
  • Bicarbonate therapy
  • IV dextrose insulin - shifts K into intracellular.
61
Q

Week 227 - Acute Renal Injury: What are the four main mechanisms for maintaining blood pressure?

A

1) Sympathetic stimulation.
2) Stimulation of renin-angiotensin system.
3) Mechanisms to retain fluid - Thirst + ADH
4) Retaining sodium

62
Q

Week 227 - Acute Renal Injury: How does sympathetic activation maintain blood pressure?

A

1) Tachycardia and increased cardiac contractility

2) Peripheral vasoconstriction > Diverting blood to vital organs.

63
Q

Week 227 - Acute Renal Injury: What are the key steps in the renin-angiotensin pathway? Pro-Renin > Aldosterone

A

Pro-renin > Renin converts Angiotensinogen > Angiotensin I > Angiotensin II (Angiotensin II has a number of effects)

64
Q

Week 227 - Acute Renal Injury: ACE is responsible for what step in the renin-angiotensin system?

A

Conversion of angiotensin I into angiotensin II.

65
Q

Week 227 - Acute Renal Injury: What are the 5 effects of angiotensin II?

A

1) Increases sympathetic activity.
2) Tubular Na, Cl reabsorption and K excretion, H20 retention.
3) Stimulates adrenal cortex to release aldosterone.
4) Arteriolar constriction.
5) Stimulates posterior pituitary gland to increase ADH secretion.

66
Q

Week 227 - Acute Renal Injury: Where are the juxtaglomerular cells?

A

Afferent arterioles.

67
Q

Week 227 - Acute Renal Injury: Where is the macula densa?

A

Distal tubular cells.

68
Q

Week 227 - Acute Renal Injury: What occurs in the kidney in response to a low GFR?

A
  • You will get decreased tubular flow rate. Results in,
  • Decreased Cl delivery to macular densa. The Macula densa then,
  • Decreases afferent arteriolar resistance, which,
  • Increases renal blood flow, which
  • Increases glomerular pressure, causing an
  • Increase in tubular flow.
69
Q

Week 227 - Acute Renal Injury: How does the kidney respond to high BP?

A

Afferent arteriolar constriction in order to protect the glomeruli.

70
Q

Week 227 - Acute Renal Injury: How does the kidney respond to low BP?

A

• Barostretch receptors are triggered causing afferent dilation and an increase in angiotensin II causing efferent constriction and an increase in glomerular pressure.

71
Q

Week 227 - Acute Renal Injury: How does a high GFR affect the kidney?

A

• Rise in tubular flow, causing an increased delivery of Na and Cl to the macula densa, there is then afferent constriction to reduce glomerular pressure.

72
Q

Week 227 - Acute Renal Injury: What effect does angiotensin II have on the afferent/efferent arterioles?

A

Constricts both. However efferent is already narrower, so has the net effect of increasing glomerular pressure.

73
Q

Week 227 - Acute Renal Injury: What can cause the dilation of the afferent arterioles?

A
  • Prostaglandins
  • Ca channel blockers
  • Decreased tubular flow rate.
74
Q

Week 227 - Acute Renal Injury: What can cause constriction of the afferent arterioles?

A
  • Increased barostretch
  • Increased tubular flow rate
  • Increased sympathertic activity
  • NSAIDs
  • Angiotensin II
75
Q

Week 227 - Acute Renal Injury: What is the effect of volume depletion in the kidney?

A
  • Decreased barostretch > Afferent dilation.
  • Increased sympathetic tone > Increased renin.
  • Increase in Renin and ATII > Rise in GFR
  • Increase of Na absorption in proximal convoluted tubules due to ATII.
  • Decreased delivery of NaCl to macula densa which also decreases afferent resistance.
76
Q

Week 227 - Acute Renal Injury: What does losartan do?

A

• Angiotensin receptor blocker.

77
Q

Week 227 - Acute Renal Injury: What blood flow is required for effective dialysis?

A

200ml/min

78
Q

Week 227 - Acute Renal Injury: What is a Scribner shunt?

A

An external AV shunt used to dialysis. Goes from the radial artery into a vein in the arm (Ulna side). Or ankle.

79
Q

Week 227 - Acute Renal Injury: What is hyponatraemia?

A

• Low sodium (

80
Q

Week 227 - Acute Renal Injury: What can cause the pituitary to release more ADH?

A
  • Angiotensin II
  • Sympathetic stimulation
  • Hyperosmolarity
  • Hypovolaemia
  • Hypotension
81
Q

Week 227 - Acute Renal Injury: How does Vasopressin/ADH increase arterial pressure?

A
  • V1 receptors - Causes vasoconstriction

* V2 receptors - Renal fluid reabsorption

82
Q

Week 227 - Acute Renal Injury: What are the causes of high plasma osmolality, than can in turn cause hyponatraemia?

A
  • Hyperglycaemia, DKA
  • Mannitol
  • Hyperlipidaemia
  • Glycine solutions
83
Q

Week 227 - Acute Renal Injury: How is serum osmolality calculated?

A

(2x serum Na) + serum glucose + plasma urea

84
Q

Week 227 - Acute Renal Injury: What are the causes of hyponatraemia with a normal/high serum osmolality?

A
  • Renal failure - Uraemic solutes compensate for low osmolality.
  • Marked hypoglycaemia, DKA
  • Mannitol therapy - Osmotic diuresis.
85
Q

Week 227 - Acute Renal Injury: What is pseudohyponatraemia?

A

Hyponatraemia caused by severe hyperlipidaemia or hyperproteinaemia.

86
Q

Week 227 - Acute Renal Injury: Hyponatraemia can result from which three main mechanisms?

A
  • High ADH
  • Low ADH
  • high plasma osmolality.
87
Q

Week 227 - Acute Renal Injury: How can excessive exercise cause hyponatraemia?

A
  • Increased water intake

* Exercise stimulates ADH secretion

88
Q

Week 227 - Acute Renal Injury: How does MDMA cause life threatening hyponatraemia?

A
  • Increased CNS level of serotonin, norepinephrine and dopamine.
  • Increased plasma level of ADH, prolactin, cortisol, ACTH.
  • Have a direct effect on water retention and thirst centre.
89
Q

Week 227 - Acute Renal Injury: How does hyponatraemia occur when there is appropriate suppression of ADH?

A
  • Renal failure - Impairment in water excretion.

* Primary polydipsia (thirst) - May be due to antipsychotic drugs, hypothalamic lesions, beer drinkers.

90
Q

Week 227 - Acute Renal Injury: How does hyponatraemia clinically manifest?

A

• The severity of the symptoms reflect the severity of cerebral oedema.

  • Nausea, confusion.
  • Headache, lethargy.
  • Convulsions, coma.
91
Q

Week 227 - Acute Renal Injury: What investigations should be performed for suspected hyponatraemia?

A
  • Serum osmolality
  • Urine osmolality
  • Urinary Na concentration
92
Q

Week 227 - Acute Renal Injury: What investigation results would suggest SIADH?

A
  • Low serum osmolality
  • Low serum Na
  • Low blood urea
  • High urine osmolality
  • High urinary Na
  • Normal acid/base balance
  • Normal adrenal and thyroid function.
93
Q

Week 227 - Acute Renal Injury: What is the management of hyponatraemia?

A
  • Treat underlying cause!
  • Fluid restriction
  • Salt replacement
  • Loop diuretics
  • ADH receptor antagonist
94
Q

Week 227 - Acute Renal Injury: What should the rate of correction be in both acute and chronic hyponatraemia?

A
  • Acute - safe to correct rapidly.
  • Chronic - Risk of osmotic demyelination
  • Increase by 10 in 1st 24hrs
  • Increase by 18 in next 24 hrs.
95
Q

Week 227 - Acute Renal Injury: Which drugs can cause hypokalaemia?

A
  • Thiazide diuretics

* Loop diuretics

96
Q

Week 227 - Acute Renal Injury: Which drugs can cause hyperkalaemia?

A
  • ACE inhibitors
  • Angiotensin receptor blockers
  • Spironolactone
97
Q

Week 227 - Acute Renal Injury: The long term use of which drugs may cause irreversible renal damage?

A
  • Aminoglycosides (gentamicin)

* NSAIDs

98
Q

Week 227 - Acute Renal Injury: Which drugs can cause rhabdomyolysis / High CK?

A
  • Statins

* Calcineuin inhibitors : Cyclosporin / tacrolimus

99
Q

Week 227 - Acute Renal Injury: What is the most appropriate investigation? A patient presented with ARF, chest symptoms, urine dipstock showed blood +++ and protein +++.

A

Renal Biopsy

100
Q

Week 227 - Acute Renal Injury: What is the most appropriate investigation? Patient presented with ARF, fever, night sweats, dysuria and loin pain.

A

Urine microscopy looking for cell casts, urine culture.

101
Q

Week 227 - Acute Renal Injury: What is the most appropriate investigation? An elderly patient developing ARF 4 days after knee replacement.

A

Urinary Na

102
Q

Week 227 - Acute Renal Injury: What is the most appropriate investigation? Patient with symptoms of poor stream, dribbling hesitancy and nocturia developing a gradual rise of serum urea and creatinine.

A

Physical examination and bladder scan.

103
Q

Week 227 - Acute Renal Injury: Choose the electrolyte abnormality. ARF after a marathon run.

A

Hypocalcaemia

104
Q

Week 227 - Acute Renal Injury: Choose the electrolyte abnormality. Recovery phase of ARF due to rhabdomyolysis.

A

Hypercalcaemia

105
Q

Week 227 - Acute Renal Injury: Choose the electrolyte abnormality. ARF after introduction of ACE inhibitor in a patient with chronic heart failure.

A

Hyperkalaemia

106
Q

Week 227 - Acute Renal Injury: Choose the electrolyte abnormality. Chronic use of thiazide diuretics.

A

Hypokalaemia

107
Q

Week 227 - Acute Renal Injury: Match the following urinary casts to the pathological conditions. RBC cast.

A

Glomerulonephritis

108
Q

Week 227 - Acute Renal Injury: Match the following urinary casts to the pathological conditions. WBC cast.

A

Pyelonephritis

109
Q

Week 227 - Acute Renal Injury: Match the following urinary casts to the pathological conditions. Fatty casts.

A

Nephrotic syndrome

110
Q

Week 227 - Acute Renal Injury: Match the following urinary casts to the pathological conditions. Pigmented casts.

A

Rhabdomyolysis

Revision Cards (61 decks)

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