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Y3 Medicine: Renal > Haemolytic Uraemic Syndrome > Flashcards

Haemolytic Uraemic Syndrome Flashcards

1
Q

What is haemolytic uraemic syndrome (HUS)?

A

Haemolytic uraemic syndrome (HUS) occurs when there is thrombosis in small blood vessels throughout the body.

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2
Q

What is the classic triad of HUS?

A

Haemolytic uraemic syndrome (HUS) is characterised by:

  1. Microangiopathic haemolytic anaemia,
  2. Thrombocytopenia (low platelet)
  3. Acute kidney injury
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3
Q

What can cause HUS?

A

The most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin and can cause HUS

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4
Q

Briefly describe the pathophysiology of HUS

A

The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood clots within the small vessels chop 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 acute kidney injury.

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5
Q

With regards to gastroenteritis, the use of what medication can increase the risk of HUS?

A

The use of antibiotics and anti-motility medications such as loperamide to treat the gastroenteritis increase the risk of developing HUS.

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6
Q

Briefly describe the presentation of gastroenteritis with Escherichia coli infection

A

Diarrhoea precedes the diagnosis of Shiga toxin-producing Escherichia coli (STEC) HUS in 91% of cases, and bloody diarrhoea is seen in 57% of cases.

HUS is diagnosed in approximately 15% of children with STEC infections, approximately 5 to 10 days after the onset of diarrhoea.

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7
Q

What are the signs of HUS?

A
  • Pallor
  • Hypertension
  • Bruising
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8
Q

What are symptoms of HUS?

A
  • Oliguria or anuria
  • Haematuria or dark brown urine
  • Abdominal pain
  • Lethargy and irritability
  • Confusion
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9
Q

What investigations should be ordered for HUS?

A
  • FBC
  • Peripheral blood smear
  • Renal function and creatinine
  • Serum electrolytes
  • PT and PTT
  • LDH
  • Haptoglobin
  • Stool culture to detect Shiga toxin
  • PCR to detect Shiga toxin
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10
Q

Why investigate FBC?

A

In Shiga toxin-producing Escherichia coli HUS, thrombocytopenia is common, with median platelet counts of 30 x 10³/microlitre, but normal or near-normal platelet counts are seen in up to 30% of cases.

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11
Q

Why investigate peripheral blood smear?

A

This is the critical step in establishing the diagnosis of a thrombotic microangiopathy. Review of the peripheral smear is necessary not only to detect the presence of schistocytes but also to obtain an accurate estimate of the platelet count.

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12
Q

Why investigate renal function and creatinine?

A

Renal endothelial cells are damaged in HUS. In Shiga toxin-producing Escherichia coli HUS, a rise in creatinine generally follows the development of thrombocytopenia and a fall in haemoglobin. In sporadic HUS, an elevated creatinine is present at diagnosis.

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13
Q

Why investigate serum electrolytes?

A

Electrolyte abnormalities may be present due to diarrhoea and acute kidney injury.

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14
Q

Why investigate PT and PTT?

A

Useful in ruling out other causes of thrombocytopenia, such as disseminated intravascular coagulation.

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15
Q

Why investigate LDH?

A

LDH is released from the red blood cells when they are destroyed. It is a non-specific sign in haemolytic anaemia.

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16
Q

Why investigate haptoglobin?

A

Haptoglobin binds free haemoglobin released by the haemolysed red blood cells. The haptoglobin-haemoglobin complex is then removed by the liver and spleen, resulting in low levels of serum haptoglobin.

17
Q

Why investigate using stool culture?

A

May be negative if not done early in the course of the diarrhoeal illness.

Shiga toxin-producing E coli cannot ferment sorbitol and appears as white colonies.

18
Q

Why investigate using PCR?

A

PCR assays can detect Shiga toxin 1 and Shiga toxin 2 genes from stool samples.

Confirms Shiga toxin-producing Escherichia coli infection.

19
Q

Briefly describe the treatment of HUS

A

HUS is a medical emergency and has up to 10% mortality. The condition is self limiting and supportive management is the mainstay of treatment:

  • Antihypertensives
  • Blood transfusions (for anaemia)
  • Dialysis (for AKI)
20
Q

When is dialysis used to treat HUS?

A

Dialysis is performed if clinically indicated: volume overload, oligoanuria, signs and symptoms of uraemia, hyperkalaemia, persistent severe acidosis (bicarbonate <10), hypertension secondary to volume overload that cannot be controlled with medical therapy, and necessity for transfusion in patients with volume overload and/or oliguria.

21
Q

When is blood trasnfusion used to treat HUS?

A

Red cell transfusions should be given to ameliorate cardiovascular or respiratory symptoms or for severe anaemia (haematocrit <18%).

22
Q

What % of patients make a full recovery from HUS?

A

70-80%.

23
Q

What are the complications of HUS?

A
  • Neurological complications
  • Cardiac dysfunction
  • Intestinal and pancreatic complications
24
Q

What differentials should be considered for HUS?

A
  1. Thrombotic thrombocytopenic purpura (TPP)
  2. Malignant hypertension
  3. Systemic lupus erythematous (SLE)
25
Q

How does HUS and thrombotic thrombocytopenic purpura (TPP) differ?

A

Differentiating signs and symptoms:

  • Low levels of the von Willebrand cleaving enzyme, ADAMTS13, in many patients with presentations typical of TTP but not those typical of HUS, suggests that there are distinct pathophysiological mechanisms involved

Differentiating investigations:

  • Levels of the von Willebrand cleaving enzyme, ADAMTS13, whose deficiency is implicated in the pathogenesis of TTP, are more consistently low in TTP than in HUS
26
Q

How does HUS and malignant hypertension differ?

A

Differentiating signs and symptoms:

  • Distinguishing feature is significantly elevated blood pressure

Differentiating investigations:

  • Platelet counts are generally normal in malignant hypertension
27
Q

How does HUS and systemic lupus erythematosus (SLE) differ?

A

Differentiating signs and symptoms:

  • There are many overlapping features between SLE and TTP/HUS, and because the two can co-exist, a distinction between them is generally not possible

Differentiating investigations:

  • Serological tests of underlying condition may be positive, but there are no tests to differentiate the cause of HUS

Y3 Medicine: Renal (13 decks)

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