Concise summary of Blood and Nutrition

Chapter 9 – Blood and Nutrition



o Nitrofurantoin
Chapter 9 – Blood and o Primaquine (30mg weekly for 8 weeks is
Nutrition found to be without undue harmful effects
in African and Asian people)
ANAEMIAS o Quinolones (nalidixic acid – not UK market)
o Rasburicase
 Before starting Tx, determine anaemia type o Sulfonamides – incl. co-trimoxazole
Sickle-cell anaemia Drugs with possible risk of haemolysis in some
 Sickle cell disease – caused by structural G6PD-deficient individuals:
abnormality of haemoglobin resulting in o Aspirin – acceptable up to a dose of at least
deformed, less flexible RBCs. 1g in most deficient Pts
 Sickle cell crisis requires hospitalisation, IV o Chloroquine – acceptable in acute malaria
fluids, analgesia and Tx of any infection o Menadione – water-soluble derivatives
 Risk of infection can be reduced by the o Quinidine – not on UK market
pneumococcal, haemophilus influenzae o Quinine – acceptable in acute malaria
type B and annual influenza vaccines and
o Sulfonylureas
prophylactic penicillin
o Hydroxycarbamide – reduces frequency of Hypoplastic, haemolytic and renal anaemias
crisis and need for blood transfusions in SCD o Tx options = anabolic steroids, pyridoxine,
antilymphocyte immunoglobulin, rituximab
G6PD deficiency
 Glucose 6-phosphate dehydrogenase (G6PD) Antilymphocyte immunoglobulin – given via IV
 Highly prevalent in those from Africa, Asia, over 12-18hrs daily for 5 days
Oceania and Southern Europe
Pyridoxine – indicated in idiopathic acquired
 More common in males
and hereditary sideroblastic anaemia. Also
 If deficient, Pts are susceptible to acute
consider in reversible sideroblastic anaemia
haemolytic anaemia when taken with
caused by pregnancy, haemolytic anaemia,
certain drugs and fava beans (broad beans)
alcohol dependence or during isoniazid Tx
When prescribing drugs in a deficient Pt:
Epoetins – used to treat anaemia linked with
1. G6PD deficiency is genetically heterogenous
erythropoietin deficiency in chronic renal failure
hence if a drug is safe in some Pts, it may
and to shorten the period of symptomatic
not be equally safe in others
anaemia in chemo Pts
2. Manufacturers do NOT routinely test drugs
for their effects in G6PD-deficient Pts Iron deficiency anaemia
3. Risk and severity of haemolysis is almost  Tx with an iron prep is justified only if an
dose-related iron-deficiency state is present
 Before starting Tx, exclude underlying
Drugs with definite risk of haemolysis in most
causes like gastric erosion, GI cancer
G6PD-deficient individuals:
 Prophylaxis may be appropriate in
o Dapsone – higher doses for dermatitis likely
malabsorption, menorrhagia, pregnancy,
to cause problems
following gastrectomy, in haemodialysis Pts
o Fluoroquinolones – incl. ciprofloxacin,
and to manage low birth-weight infants
moxifloxacin, norfloxacin, ofloxacin
o Methylthioninium chloride Oral dose of elemental iron for iron-deficiency
o Niridazole, Pamaquine (not in UK market) anaemia = 100-200mg daily

, Chapter 9 – Blood and Nutrition


Ferrous Fe  Ascorbic acid – enhances iron excretion
Fe salt/amount
content induced by desferrioxamine
Ferrous fumarate 200mg
65mg NEUTROPENIA
Ferrous sulfate, dried 200mg
Ferrous sulfate 300mg 60mg Management
Ferrous gluconate 300mg 35mg  Recombinant human granulocyte-colony
stimulating factor – stimulates production
 Preps containing folic acid and iron are used of neutrophils and reduces duration of
in pregnant women at high risk of deficiency chemo-induced neutropenia hence reducing
the risk of sepsis
 Ascorbic acid – may aid absorption of iron  Alternatives = filgrastim, lenograstin

 M/R preps are licensed for OD dose. This PLATELET DISORDERS
allows low incidence of SEs Idiopathic thrombocytopenic purpura
Parenteral iron = iron dextran, iron sucrose,  Tx = corticosteroid e.g. prednisolone and
ferric carboxymaltose, iron isomaltoside. immunoglobulin preps
 It’s usually reserved when oral therapy fails
FLUID AND ELECTROLYTE IMBALANCES
as Pt cannot tolerate oral iron, cannot take
it reliably or if there’s continuing blood loss Oral Potassium

 Other purposes = chemo-induced anaemia, Compensation for K+ loss is esp. necessary:
haemodialysis with chronic renal failure 1. In Pts taking digoxin or anti-arrhythmics
(due to risk of arrythmias)
Megaloblastic Anaemia (MA) 2. In Pts with secondary hyperaldosteronism
 Usually results from a lack of B12 or folate occurs (e.g. cirrhosis, nephrotic syndrome,
 Pernicious anaemia – lack of gastric severe heart failure)
intrinsic factor due to an autoimmune 3. In Pts with excessive losses of K+ in faeces
gastritis causes B12 malabsorption (e.g. chronic diarrhoea linked with
 Hydroxocobalamin – preferred B12 form. malabsorption or laxative abuse)
It’s retained in the body for longer than
cyanocobalamin hence maintenance therapy Management of HYPER-kalaemia
can be given at intervals of up 3 months Acute, severe (>6.5mmol/L or ECG changes)
 Folic acid – avoid alone in undiagnosed MA 1. Calcium gluconate 10% via slow IV
unless B12 is given too (neuropathy risk) 2. Soluble insulin (5-10 units) with 50ml
 Folate deficient megaloblastic anaemia – glucose 50%
due to poor nutrition, pregnancy or AEDs 3. Salbutamol via nebulisation or slow IV
requires daily folic acid for 4 months 4. Sodium bicarbonate – to correct acidosis
Iron Overload Oral Sodium and Water
 May occur in aplastic and other refractory
anaemia due to repeated blood transfusions Sodium chloride – indicated in sodium depletion
 Venesection – used to treat iron overload Oral rehydration therapy (ORT)
associated with haemochromatosis
 Desferrioxamine mesylate – alternate Tx. It  Intestinal absorption of sodium and water is
must not be given through the same line as enhanced by glucose (and other carbs)
the blood or added to the blood hence by giving solutions containing Na, K