Anaemias Flashcards

1
Q

Sickle-cell anaemia is caused by

A

structural abnormality of haemoglobin resulting in deformed, less flexible red blood cells.
- Varying degrees of haemolytic anaemia are present with increased erythropoiesis. This increases folate requirements

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2
Q

… can reduce the frequency of sickle cell crises

A
  • Hydroxycarbamide can reduce the frequency of sickle cell crises and the need for blood transfusions in sickle-cell disease… however the beneficial effects may not be evident for several months.
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3
Q

G6PD deficiency

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is common in individuals from Africa, Asia, Oceania and Southern Europe – it is more common in males.
• Individuals with G6PD deficiency are at risk of developing haemolytic anaemia when given some common drugs. The risk is almost ALWAYS dose-related.

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4
Q

• Drugs with definite risk of haemolysis in most G6PD deficient patients

A

o Dapsone + other sulfones, Fluroquinolones (inc. Ciprofloxacin, Moxifloxacin, Norfloxacin + Ofloxacin), Methylthioninium chloride, Nitrofurantoin, Primaquine, Quinolones, Rasburicase, Sulfonamides (Co-trimoxazole)

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5
Q

• Drugs with possible risk of haemolysis in some G6PD deficient patients

A

o Aspirin, Chloroquine, Menadione, Quinine, SU (Gliclazide)

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6
Q

Hypoplastic, haemolytic and renal anaemia

A

Anabolic steroids, pyridoxine, antilymphocyte immunoglobulin and various corticosteroids are used in hypoplastic + haemolytic anaemias.

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7
Q

Erythropoietin’s

A

 Epoetin’s are used to treat anaemia associated with erythropoietin deficiency in in chronic renal failure
 Epoetin beta prevents anaemia in pre-term neonates of low birth weight
 Darbopoetin alpha is a hyperglycosylated derivative of epoetin, longer half-life and less frequent administration than epoetin
 Methoxy polyethylene glycol-epoetin beta is licensed to treat symptomatic anaemia associated with chronic kidney disease. It has a longer duration of action than epoetin.

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8
Q

Epoetin MHRA…

A

o Severe cutaneous adverse reactions including SJS + toxic epidermal necrolysis. Stop if such reactions occur
o Overcorrection of haemoglobin conc. (should be within range 10-12g/100ml) in patients with chronic kidney disease may increase the risk of death + serious cardiovascular events. In patients with cancer may increase risk of thrombosis
o Tumour progression

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9
Q

Epoetin - SE

A

Hypertensive crisis, headache, Pure red cell aplasia

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10
Q

Epoetin - monitor

A

BP (interrupt treatment if uncontrolled), Reticulocyte counts, Haemoglobin, Electrolytes, Iron

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11
Q

Iron deficiency anaemia symptoms

A

Tiredness, pallor, SOB + palpitations

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12
Q

Prophylaxis with an iron preparation may be appropriate in

A

malabsorption, menorrhagia, pregnancy, after subtotal or total gastrectomy, in haemodialysis patients, and in the management of low birth-weight infants such as preterm neonates.

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13
Q

Oral iron

A
  • Iron should be given by mouth unless there are good reasons for using another route.
  • There is little difference between the iron salts, choice is based on side-effects and cost
  • The oral dose of elemental iron for iron-deficiency anaemia should be 100mg-200mg daily. Ferrous sulphate is usually used, but ferrous fumarate or gluconate can be used.
  • Oral irons can cause gastrointestinal irritation, this includes: nausea, pain and diarrhoea or constipation.
  • They are best absorbed on an empty stomach but can be taken after food to reduce GI side effects. Oral irons can discolour the stools.
  • Take with glass of orange juice (vitamin C aids absorption of iron)
  • Compound preparation: Folic acid + iron  only for pregnant women at high risk of developing iron + folic acid deficiency
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14
Q

iron treatment duration

A

Patients in a deficient state are usually given Iron for a month to reach the required levels and continued for another 3 months to replenish the iron stores in the body

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15
Q

formulations of iron

A
  • There is no benefit to giving Modified-release formulations
  • Iron can be given parenterally if oral therapy is unsuccessful because the patient cannot tolerate oral iron or does not take it reliably, if there is continuing blood loss or in malabsorption.
  • Parenteral iron does not produce a faster haemoglobin response than oral iron except in patients with severe renal failure receiving dialysis.
  • Serious hypersensitivity reactions have been reported in patients receiving I.V. iron, thus it should only be administered when appropriately trained staff and resuscitation facilities are immediately available.
  • Patients should be monitored for signs of hypersensitivity during and for 30 minutes after each administration. The risk of hypersensitivity is increased in those with allergies, immune or inflammatory conditions (asthma, eczema, etc.)  only use if benefits outweigh the risks.
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16
Q

IV iron in pregnancy

A

• I.V. iron should be avoided in the 1st trimester, and only used in 2nd and 3rd trimester if benefits > risks.

17
Q

Megaloblastic anaemia

A

Megaloblastic anaemia’s (larger red blood cells but less of them) result from a lack of either Vitamin B12 or Folate

 Symptoms: numbness, tingling hands/feet, muscle weakness, depression
 One cause of megaloblastic anaemia is pernicious anaemia in which lack of gastric intrinsic factor resulting from an autoimmune gastritis causes malabsorption of vitamin B12.
 Vitamin B12 is also needed to treat megaloblastosis caused by prolonged nitrous oxide anaesthesia, which inactivates the vitamin + in rare syndrome of congenital transcobalamin II deficiency.
 Treatment should not be initiated until the results of the tests are available.

  • Vitamin B12 deficiencies are more common in vegetarians and people who’ve had a total or partial gastrectomy. Thus, vitamin B12 should be given prophylactically after total/partial gastrectomy.
  • Apart from dietary deficiency, all other causes of Vitamin B12 deficiency are due to malabsorption
  • Hydroxocobalamin is the form of Vitamin B12 of choice for therapy. Treatment is generally initiated with frequent administration of I.M. injections to replenish depleted body stores. Thereafter maintenance treatment (usually for life) is initiated
18
Q

In folate-deficient megaloblastic anaemia

A
  • (because of poor nutrition, pregnancy or antiepileptic drugs) daily folic acid supplementation for 4 months replenishes body stores.
  • Do not use alone in undiagnosed megaloblastic anaemia unless vitamin B12 is administered concurrently as neuropathy of spinal cord may occur.
  • Broccoli is a good dietary source of folic acid