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Yr3 Medicine- Renal > Acute Tubular Necrosis > Flashcards

Acute Tubular Necrosis Flashcards

1
Q

What is acute tubular necrosis?

A

Damage and necrosis of epithelial cells of renal tubules. Damage to kidney cells occurs due to ischaemia or toxins.

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2
Q

What is the most common cause of AKI?

A

Acute tubular necrosis

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3
Q

Discuss whether acute tubular necrosis is reversible

A

Epithelial cells have ability to regenerate so ATN is reversible; takes about 7-21 days

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4
Q

We have said ATN can occur due to ischaemia or toxins; state some ischaemic causes and state some toxin causes

A

Ischaemia can occur secondary to hypoperfusion in:

  • Shock
  • Sepsis
  • Dehydration

Direct damage from toxins such as:

  • Radiology contrast dye
  • Gentamycin
  • NSAIDs
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5
Q

What investigation finding is pathognomonic for acute tubular necrosis?

A

Muddy brown casts on urinalysis

May also be tubular epithelial cells in urine

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6
Q

Discuss the mangement of ATN

A

REMEMBER, ATN is most common cause of AKI hence most of our management is same as for AKI:

  • Supportive management
  • IV fluids
  • Stop nephrotoxic medications
  • Treat complications
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7
Q

Define interstitial nephritis

A

Inflammation of space between cells and tubules (interstitium) within kidney. Different to glomerulonephritis in which there is inflammation around the glomerulus.

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8
Q

State the two types of interstitial nephritis

A
  • Acute interstitial nephritis
  • Chronic interstitial nephritis
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9
Q

For acute interstitial nephritis, discuss:

  • How it presents
  • Causes
  • Management
A
  • Presents with AKI and hypertension. May also present with feaatures of generalised hypersensitivity e.g. rash, fever, eosinophilia
  • Usually caused by hypersensitivity reaction e.g. to drugs (NSAIDs, abx e.g. beta lactams) or infection
  • Management:
    • Treat underlying cause/withdraw causative agent
    • Steroids to reduce inflammation
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10
Q

For chronic interstitial nephritis, discuss:

  • How it presents
  • Causes
  • Management
A
  • Presents with CKD
  • Causes: autoimmune, infectious, iatrogenic, granulomatous disease
  • Management:
    • Treat underlying cuase
    • Steroids (specialist involvement)
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11
Q

What is rhabdomyolysis?

State some possible causes

A

Skeletal muscle tissue breaks down and releases products into blood.

Triggerd by event that causes muscle breakdwon e.g. extreme underuse or overuse, crush injury, seizure, prologned immobility etc…

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12
Q

When mycotyes undergo apoptosis in rhabdomyolysis, what 4 things are released into blood

A
  • Myoglobin
  • Potassium
  • Phosphate
  • Creatine kinase
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13
Q

Of the products released by myocytes when they undergo apoptosis, which is most dangerous and why?

A
  • Potassium
  • Cardiac arrhythmias which can result in cardiac arrest
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14
Q

Discuss the impact of rhabdomyolysis on kidneys

A
  • Breakdown products are filtered by kidney
  • Myoglobin is toxic to kidney in high concentrations and can cause AKI
  • AKI cuases breakdown products to further accumulate in blood
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15
Q

State some signs & symptoms of rhabdomyolysis

A
  • Muscle aches & pains
  • Oedema
  • Fatigue
  • Confusion
  • Red-brown urine
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16
Q

Discuss what investigations are required if you suspect rhabodmyolysis, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • ECG: assess for hyperkalaemic changes
  • Urine dipstick:will test +ve for blood if there is myoglobinurea
  • VBG: get electrolytes quicker

Bloods

  • U&Es: AKI and hyperkalaemia
  • Creatine kinase: raised (in thousands to hundreds of thousands of units/L)
  • Calcium: low
  • Phosphate: high
17
Q

Discuss the management of rhabdomyolysis

A
  • IV fluids (to rehydrate pt and encourage filtration of breakdown products)
  • Treat complications e.g hyperkalaemia
  • Consider IV sodium bicarbonate (makes urine more alkaline reducing toxicity of myoglobin on kidneys. Evidence not clear so some debate as to whether to use)
  • Consider IV mannitol (aims to increase GFR to help remove breakdown products and reduce oedema surrounding muscles & nerves. Must correct hypovolaemia first. Evidence not clear so some debate whether to use)
18
Q

For haemoltyic uraemic syndrome (HUS), discuss

  • What it is
  • Who it usually affects
  • Most common cause
  • Triad
A
  • Haemolytic uraemic syndrome occurs when there is thrombosis throughout small blood vessels in body
  • Children
  • Often related to gastroenteritis caused by E-coli 0157:H7 which produces verotoxins such as shiga-like toxin
  • Triad:
    • Haemolytic anaemia
    • AKI
    • Thrombocytopenia
19
Q

Explain how E-coli 0157:H7 can cause HUS

A

E-coli 0157:H7 produces verotoxins such as shiga-like toxins. Toxins bind to receptors on endothelial cells of microvasculature; causes endothelial cells to break down. This results in platelet activation due to exposure to tissue factor. Leads to intravascular thrombosis which uses up platelets leading to thrombocytopenia. Blood clots in small vessels cause fragmentation of RBCs as they pass leading to haemolytic anaemia. Blood clots and damaged RBCs decrease blood flow through kidney and lead to AKI.

20
Q

Discuss the typical presenation of HUS

A

Typically start displaying symptoms around 5 days after start of gastroenteritis:

  • Reduced urine output
  • Haematuria or dark brown urine
  • Abdo pain
  • Lethargy
  • Irritability
  • Cofusion
  • Hypertension (due to renal failure)
  • Bruising (due to thrombocytopenia)
  • Pallor (anaemia)
21
Q

What investigations would you do if you suspect haemolytic uraemic syndrome, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • Stool culture:identify causative organism
  • Urine dip: haematuria

Bloods​

  • FBC: anaemia, thrombocytopenia
  • Blood smear: schistiocytes
  • U&Es: AKI
  • Haptoglobin: decreased
  • LDH: increased (released by RBC when damaged)
22
Q

Discuss the management of HUS

A

Medical emergency managed mainly by supportive treatment:

  • Antihypertensives
  • Blood transfusions
  • Dialysis

Yr3 Medicine- Renal (8 decks)

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