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PH2501- pharmacology > Lec 22- anaemia > Flashcards

Lec 22- anaemia Flashcards

1
Q

What is anaemia

A

-anaemia is a decrease in the number of red blood cells RBC/ Hb in the blood
Epidemiology
-World-50% pregnant women; 40% of infants
-UK-14% women 55-64; 3% of men 35-64

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2
Q

Symptoms of anaemia

A
  • Tiredness and lethargy
  • Inhibition of physical exercise
  • Reduced mental performance
  • The available blood will be fully oxygenated in the lungs
  • May get a compensatory increase in cardiac output
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3
Q

Clinical assessment/ investigation of a patient with suspected anaemia

A
  • Investigations- it is essential to find the underlying cause. There is no place for blind treatment
  • Full blood count is an essential screening test
  • 1st step look at MCV(mean cap volume) (rem diam 2-2.5)
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4
Q

The full blood count- Why; when; how

A

Why- full blood counts are commonly requested as part of a general screen in a patient who is unwell to screen for a variety of disorders- anaemia; infection; inflammation; nutritional status; bleeding

  • When- as determined by the clinician, there are many illnesses which will affect the full blood count and the result may help to make a diagnosis
  • How- A blood sample take from a vein in the arm or finger-prick or heel prick (new borns)
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5
Q

Fe in Hb- structure of Hb

A

-4 sub units- 2a and 2b
-Fe
Haem
Binds 4 O2 molecules

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6
Q

Production of red blood cells (normal erythropoiesis)

A
  • Pluripotent stem cell –>
  • Erythyroid burst forming unit (EPO target) –>
  • Erythroid colony forming unit>
  • Erythroblast –>
  • Reticulocyte –>
  • Erythrocyte –>
  • MADE IN BONE MARROW
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7
Q

Underlying causes of anaemia

A

1) RBC loos without RBC destruction (Haemorrhage)
2) Deficient RBC production
3) Increased RBC destruction- haemolytic anaemias

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8
Q

1) RBC loss without RBC distraction

A
  • Haemorrhage- due to trauma; due to disorders- cancer, ulcer, TB, IBS
  • Menstrual flow
  • Gynaecological disorders (endometriosis; fibroids)
  • Pregnancy-especially at gestation
  • Parasitism- hookworm
  • 100mls blood= 40 days Fe intake, in a western diet
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9
Q

2) Deficient effective RBC production

This is the MAIN ONE

A

A)Regulation of erythropoiesis
B)Fe deficiency anaemia
C)Sideroblastic anaemia- cannot incorporate Fe into Hb
D)Megaloblastic anaemia: pernicious anaemia(cannot absorb B12); B12 deficiency; folate deficiency

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10
Q

A) regulation of erythropoiesis

A
  • Kidneys monitor blood O2 (hypoxaemia)
  • If renal tissue is hypoxic, erythropoietin is produced by renal peritubular interstitial cells
  • Athletes- altitude training
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11
Q

Factors necessary for erythropoiesis

A
  • Erythropoietin
  • Fe
  • B12
  • Folic acid
  • Ascorbic acid
  • Pyridoxine (B6)
  • Amino acids
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12
Q

Recombinant Erythropoietin (RhuEPO) is used to treat anaemia in:

A
  • CKD- prior to dialysis (there is always destruction of RBC in dialysis as the blood goes through the dialysis pump)
  • AIDS
  • Transplants
  • Cancer- for patient who have undergone Chemotherapy that destroyed some fo the bone marrow
  • Premature children
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13
Q

Haemocrit

A
  • Plasma 55%
  • Buffy coat- leukocytes and platelets <1%
  • Erythrocytes 45%
  • EPO- abused primarily by professional cyclists
  • Causes increased blood viscosity; increase BP; increased Heart workload; can lead to HF
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14
Q

B) Fe deficiency anaemia

A
  • Fe deficiency is the most common cause of anaemia

- Results in microcytic hypo chromic anaemia (small RBC)

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15
Q

Normocytic

A
  • Normal RBC’s.They have a zone of central pallor about 1/3 the size of the RBC.
  • A few small fuzzy blue platelets are seen
  • In the centre of the Field are a band of neutrophil on the left and a segmented neutrophil on the right
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16
Q

Microcytic

A
  • The RBC here are smaller than normal and have an increase zone of pallor
  • This is indicative of a hypo chromic (less Hb in each RBC) microcytic (smaller size) anaemia
  • The most common cause of this is Fe deficiency
17
Q

Fe deficiency anaemia- common causes

A
  • Lack of Fe in diet
  • Partial gastrectomy due to ulcers (gut removed so can’t absorb)
  • Blood loss due to: bleeding peptic ulcers; malignancy
  • Malabsorption syndromes: CF; coeliac disease
18
Q

Fe - absorption’s

A
  • Absorbed from the duodenum (where most drugs are absorbed) and upper jejunum
  • Vit C taken with the Fe increases absorption by reducing dietary ferric (Fe3+) to ferrous (Fe2+) Fe
  • Caffeine and other xanthines decrease absorption
  • Usually 1-2mg dd
  • Macrophages when they break down RBC they recycle Fe
19
Q

Fe therapy

A
  • Lots of Fe
  • Normal levels 12g/dL of blood
  • Takes 40 days to obtain Fe in 100mls of blood
  • Therapy ferrous sulphate 200mg TDS
  • Will take 1-2 weeks to raise by 1g/dL
20
Q

Fe therapy- side effects of oral preparations

A

-Only absorbed well in the ferrous form
-Ferrous sulfate; ferrous gluconate; ferrous fumarate
Side effects: nausea; gastric discomfort; constipation; cramps; diarrhoea; dark stools

21
Q

C) sideroblastic anaemia’s

A
  • A group of conditions diagnosed by finding ring sideroblasts in bone marrow
  • Both hereditary (rare) and acquired forms
  • 30% of alcoholics admitted to hospital having sideroblastic anaemia
  • Main defect- reduced activity of enzyme 5-aminolevulinate synthase (ALAS)- involved in haem synthesis
  • ALAS= involved in the 1st step of the synthesis of haem- and requires pyridoxal phosphate (Vit B6) (precursor pyridoxine) as co-factor
22
Q

sideroblastic anaemia

A
  • Erythroblasts have Fe granules surrounding the cell nucleus
  • Rings are known as ring sideroblasts
  • Fe is concentrated in mitochondria suggesting cell is unable to bind haem and Fe due to deficient enzymes
23
Q

Causes of acquired sideroblastic anaemia

A 
-Associated with other disorders 
\+Myeloid Leukaemia 
\+Myeloma 
\+Collagen disease 
-Drugs and toxins 
\+Alcohol (metabolite +acetaldehyde lowers levels of ALAS and pyridoxal) 
\+Isoniazid 
\+Chloramphenicol 
\+Lead poisoning
24
Q

Treatment of sideroblastic anaemia

A
  • The main medication-pyridoxine- may take months to see the benefit
  • If reversible (drugs and toxins)- remove the offending agents
  • Severe cases- blood transfusions- however, there is a problem with Fe overload- so a chelating agent e.g. desferrioxamine is required
25
Q

D) Megaloblastic (microcytic) anaemia

A
  • Due to lack of folic acid or Vit B12
  • Folate (folic acid) interacts with Vit B12: essential for normal blood and nerve function
  • Lack of either prevents the formation of DNA so RBC production doesn’t occur or occur abnormally
  • Macrocytic cells (large cells) which may have enough Hb, but are not concave and are fewer in number
  • Therefore cannot take up or transport O2 normally
  • The cells are more easily damaged- also contributing to the anaemia
26
Q

Macrocytic anaemia

A
  • The hypersegmented neutrophil and also that the RBC are almost as large as the lymphocyte
  • Finally, not that there are fewer RBC’s
27
Q

Pernicious anaemia: Vit B12

A
  • Also called the extrinsic factor
  • Must combine with intrinsic factor IF produced by the parietal glands of the stomach
  • The combination enables binding to receptor and phagocytosis of the complex by the distal ileum cells
  • Lack of Vit B12 is called pernicious anaemia
  • It is usually a result of an autoimmune disease, that destroys the parietal cells of the stomach
28
Q

Vit B12 treatments

A
  • Normal patients= oral

- Pernicious anaemia- B12 can be given via IM or IV

29
Q

Folic acid therapy

A

Sources

  • Green veg; nuts; cereal; fruit; yeast
  • Folate therapeutics- usually in multivitamin preparations; also as folic acid 5mg tablets
30
Q

Pregnancy

A
  • Pregnant female needs 3.5mg folic acid per day compared with 0.9mg for adult male
  • Partially suppled by increase absorption (and pica- craving)
  • Also a much greater need for folate for developing foetus
31
Q

3) Increased RBC destruction (haemolytic anaemias)

A

Intrinsic abnormalities
-Thalassaemia (deficient a or b protein)
-Sickle cell anaemia
-Glucose-6-phosphate dehydrogenase deficiency
Extrinsic abnormalities
-Infection- malaria
-Drugs- sulfasalazine

32
Q

Haemolytic anaemia

A

Thalassaemias
-Autosomal recessive condition
-Many types of mutation in a and b subunit. affects O2 carrying capacity
Sickle cell anaemia
-Inherited condition genetically. Autosomal recessive gene
-Another from Hb s produced. Also makes RBC membranes inflexible, problems in microcirculation
-Symptoms- feel ill, ab pain, jaundice; dark urine

33
Q

Haemolytic anaemia- treatment

A
  • Increase the RBC production, therefore, folate may help in sickle cell anaemia; EPO is very severe cases
  • No effective treatment for thalassaemia, severe sufferers may need blood transfusion from an early age
34
Q

G6PD- anaemia-

Glucose-6-phosphate dehydrogenase deficiency

A
  • Autosomal recessive hereditary condition
  • Affects 400 million people worldwide
  • 300 different forms of deficiency- only some cause anaemia
  • The most common form found in 15% of Afro-Caribbean origin- anaemia caused when the individual is exposed to a trigger factor
  • A more severe form is the Mediterranean variant- patients may have chronic haemolytic anaemia without a trigger
  • G6PD- is an enzyme that indirectly involved in the production of reduced glutathione
  • Glutathione produced in response to oxidising agents and protects RBC
35
Q

G6PD- investigation/treatment

A

Investigation
-clinical history (family) and any findings- may be used to differentially diagnose suspected cases
-Confirmation- by measuring G6PD activity
Treatment
-Avoid trigger factors or food (broad beans) often called favism due to eating fava beans
-No specific drug treatments
-Patients can be given a list of drugs to avoid but since these are POM, it is important the patient informs HPC of their conditions

36
Q

Malaria

A
  • Plasmodium …
  • Parasite infects RBC and replicates
  • They then break out and kill that RBC
37
Q

Anaemia diagnosis

A

-Important to know which type of anaemia especially for microcytic, since folate treatment will not treat B12 deficiency induced neuropathy
-Blood tests- examine RBC morphology
-Measure blood folate levels
0Use a B12 radio-ligand to test absorptions, test for antibodies to instrinsic factor

38
Q

Differential diagnosis using MCV

A
  • Macrocytic anaemia- larger than normal cells (MCV=150fl)
  • Normocytic (MCV=80-96fl)- cells are normal in volume
  • Microcytic anaemia (MCV=50 fl)- cells are smaller than normal
39
Q

Algorithm for the assessment of anaemia

A

LOOK AT BB SLIDE

PH2501- pharmacology (47 decks)

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