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Haematology > More Anaemia > Flashcards

More Anaemia Flashcards

1
Q

Serum ferritin

A

Small amount in serum derived from storage pool of body iron
If low it represents iron deficiency

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2
Q

Haemosiderin

A

Insoluble storage form - stained with perls stain

Can identify high or low iron stores

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3
Q

Transferrin significance

A

Iron transport
Each molecule can bind 2 iron atoms but usually only 1/3 saturated therefore increased or decreased saturation representative of iron levels

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4
Q

Where is iron absorbed?

A

In duodenum and upper jejunum

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5
Q

What is iron absorption controlled by?

A

Total iron stored and erythropoiesis rate
Eg. If iron stores okay can still get increased iron absorption due to increased erythropoiesis rate from red blood cell breakdown eg thalassemia

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6
Q

Causes of iron deficiency anaemia

A

Menstruation
GI bleeding
Malnutrition
Malabsorption

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7
Q

What type of anaemia is iron deficiency anaemia and why?

A

Microcytic and hypochromic
Because normally Hb inhibits normoblast division stopping mitosis at the usual 4
Therefore low iron means low haemoglobin therefore more mitosis occurs and so smaller erythrocytes are made

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8
Q

What do you find on blood film in iron deficiency?

A

Anisocytosis (variation in RBC size) and poikilocytosis (variation in RBC shape)
Cigar cells and pencil cells

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9
Q

What are platelets and leukocytes normally like in iron deficiency anaemia?

A

Platelets often high especially if GI bleeding chronically

Leukocytes typically normal

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10
Q

When will you get microcytic/hypochromic picture with normocytic cells?

A

Iron replacement or transfusion in iron deficiency anaemia

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11
Q

Transferrin saturation in iron deficiency anaemia

A

10%

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12
Q

Signs of iron deficiency anaemia x5

A 
Angular stomatitis 
Glossitis 
Koilonychia
Brittle nails 
Dysphagia due to oesophageal web - Paterson-Kelly or Plummer-Vinson syndrome
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13
Q

Another name for B12 and B9

A 
B12 = cobalamin 
B9 = folate/folic acid
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14
Q

What type of anaemia do b12 and folate cause? And why?

A

Macrocytic anaemia because both of them are needed for Dna synthesis and so you get less mitosis with deficiency which causes macrocytic erythrocytes

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15
Q

What else do you get with b12 and folate - other blood cells?

A

Pancytopenia because all DNA synthesis is affected

Multilobulated neutrophils

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16
Q

What biochemical findings do you get with b12 and folate deficiency?

A

Unconjugated hyperbilirubinaemia and increased lactic dehydrogenase because increased breakdown in marrow and premature removal of macrocytes

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17
Q

Where do you get b12 from?

A

Foods of animal origin - therefore can get deficiency problems in veganism

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18
Q

How does b12 get absorbed?

A

Bound to intrinsic factor which is produced by gastric parietal cells
Then it is absorbed in terminal ileum

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19
Q

How quickly does b12 deficiency develop?

A

Couple of years because only need 1ug a day for DNa synthesis and body stores are 2-3mg

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20
Q

Mechanisms of iron deficiency

A 
Pernicious anaemia - lack of intrinsic factor
Gastrectomy - lack of intrinsic factor 
Congenital lack of IF 
Ileal resection - lack of absorption
Crohn's - lack of absorption
Blind loop syndrome - bacteria competing for b12 
Tropical sprue 
Nutritional
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21
Q

What is pernicious anaemia

A

Autoimmune lack of IF
either autoimmune atrophy of gastric parietal cells
Or antibodies to IF
F>m and rarely before age 30

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22
Q

Systemic effects of pernicious anaemia

A 
Peripheral neuropathy 
Optic atrophy (less common) Psychiatric symptoms (less common)

Atrophic glossitis

Lethargy, breathlessness and heart failure due to hypoxia

Weight loss due to malabsorption

Bruising and mucosal haemorrhage due to thrombocytopenia

Replacement of parietal/chief cells following atrophy with mucus secreting goblet cells - leads to sore mouth and increased risk of stomach cancer

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23
Q

Why do you need to be careful giving a blood transfusion to someone with anaemia?

A

Hypoxia can cause heart failure

Can cause fluid overload giving blood to a heart failure patient

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24
Q

How do you treat b12 deficiency? What isn’t treated?

A

Giving b12 parenterally - not orally because problem with absorption - hydroxocobalamin

Neuropathy and gastric atrophy are not reversible

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25
Q

Effect of treatment on b12 deficiency anaemia

A

Reticulocytes go up in 2-3 days
WCC and platelet count recover over a few days
Hb increases by 10g/day
Erythropoiesis makes normal RBCs within 48hours

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26
Q

Where do you get folic acid from?

A

Most food sources but vegetables and fruit - are especially rich in folates

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27
Q

Where is folic acid absorbed?

A

In proximal jejunum

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28
Q

How quickly does folate deficiency develop?

A

Can develop in weeks/months because 200ug needed daily

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29
Q

When can folic acid deficiency develop?

A

Pregnancy (increased folate requirements) and in some disease states

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30
Q

Causes of folic acid deficiency?

A

Malnutrition
Malabsorption
Increased requirements (pregnancy, disease states)
Drugs (anticonvulsants eg phenytoin and phenobarbitone) which impair absorption
(Anti Cancer drugs eg methotrexate which is a folic acid antagonist)

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31
Q

When give folic acid supplements

A

Pregnancy (maternal folic acid deficiency causes neural tube defects)

People on methotrexate
People on phenytoin and phenobarbital

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32
Q

What sort of anaemia develops in chronic disease

A

Normocytic and normochromic

33
Q

What chronic disorders can cause anaemia

A

Chronic inflammatory diseases eg. connective tissue disprders

Malignancies eg. Carcinoma or lymphoma

Chronic infections eg. Osteomyelitis or TB

34
Q

How severe is the anaemia of chronic disorders (usually)?

A

Not that severe. Usually Hb still >80g/l

35
Q

What is possible mechanism behind anaemia of chronic disease?

A

Il-6 inhibits release from iron-exporting cells

TNF - induces RBC apoptosis

36
Q

Storage of iron in the body

A

60% in RBCs

30% stored in RE system eg.bone marrow as ferritin and haemosiderin

37
Q

Anaemia associated with acute blood loss

A

No anaemia at first as plasma is lost too but after 48hours it will become present

Normocytic and normochromic - increased number polychromatic erythrocytes & reticulocytes - due to increased haemopoeisis

38
Q

General signs of haemolytic anaemia

A

Raised serum unconjugated bilirubin - jaundice and pigment gallstones

Raised urine urobilinogen and faecal stereobilinogen
Raised serum LDH

Splenomegaly (hepatomegaly in chronic)

Reticulocytosis

Erythroid hyperplasia in bone marrow

39
Q

Two defects in red cell membrane causing haemolysis. how does it happen? Extra feature

A

Hereditary spherocytosis
Hereditary elliptocytosis

  • Altered structural protein - spherical shape therefore stuck in spleen - breakdown

More sensitive to lysis under osmotic stress (osmotic fragility tests)

40
Q

Management of membrane defects

A

All need folate

Splenectomy helps some

41
Q

2 defects of red cell enzymes

A

Glucose-6-phosphate dehydrogenase deficiency

Pyruvate kinase deficiency

42
Q

How is G6PD deficiency genetically transmitted

A

x-linked, increased prevalence in africans as some protection f.malaria
female heterozygotes usually asymptomatic

43
Q

Presentation of G6PD deficiency

A

Mainly asymptomatic
Haemolytic episode/oxidative crises triggered by reduction in glutathione production
Trigger eg. drugs (primaquine, sulfonamides, aspirin), fava bean
or illness/infection/surgery

Rapid anaemia and jaundice

44
Q

Signs of G6PD on blood film

A

Heinz bodies - bite and blister cells after heinz body has been removed by the spleen

45
Q

Management of G6PD

A

Avoid trigger - eg. henna

Transfuse if necessary

46
Q

How is pyruvate kinase deficiency linked?

A

Autosomal recessive

47
Q

What do you get in pyruvate kinase deficiency

A

less atp production therefore shorter survival of RBCs

Increased o2 delivery to tissues therefore not as symptomatic as expected

48
Q

Type of anaemia in thalassaemia

A

Microcytic and hypochromic

49
Q

XRAY appearance in thalassaemia

A

Hair-on-end appearance - due to gross erythroid hyperplasia

50
Q

Systemic signs of thalassaemia

A

Bone problems - fractures etc
Splenomegaly and hepatomegaly (due to haemolysis but also extramedullary haemopoeisis)

Iron overload - pituitary, hypogonadism, heart and liver failure, DM

Severe anaemai

51
Q

Treatment of thalassaemia

A

Transfusion and iron chelation therapy - deferiprone and deferasirox

52
Q

What happens with paroxysmal nocturnal haemoglobinuria? Rx?

A

Rare acquired stem cell disorder, haemolysis, thrombosis and marrow failure

Thrombosis of portal, hepatic, renal and CNS veins

Rx - anticoagulation and eculizumab (anti-complement monoclonal antibody)

53
Q

What happens in autoimmune haemolytic anaemia?

A

Antibodies to RBC cause complement binding and then this causes increased breakdown in the spleen

Partial breakdown first in reticuloendothelial cells creates a spherocyte

54
Q

Features of ‘warm antibody’ AHA

A

Usually IgG - bind at 37degrees
Can be triggered by drugs or associated with other disease
Jaundice, anaemia and splenomegaly
Rx - stop drug, immunosuppression/steroids and sometimes splenectomy

55
Q

Features of ‘cold antibody’ AHA

A

IgM - complement binding in periphery - up to 30degrees
Get agglutination of RBCs in slower areas
Anaemia worsened by cold - cyanosis
Rx - maintain warm environment - cholrambucil may help

56
Q

What is microangiopathic haemolytic anaemia?

A

Physical trauma to RBCs when pushed through damaged microvasculature

57
Q

Cells seen with microangiopathic haemolytic anaemia?

A

Schistocytes

58
Q

Other causes of haemolytic anaemia

A 
Burns
Snake/spider bites 
Chemicals
Malaria 
Hypersplenism
59
Q

Detection of autoimmune haemolytic anaemia

A

Coombs test - direct antiglobulin test

60
Q

What cells are found in hodgkins lymphoma?

A

Mirror image nuclei Reed-Sternberg cells

61
Q

When does hodgkin’s lymphoma present?

A

Young adults and elderly M:F = 2:1

62
Q

Symptoms and signs of hodgkin’s lymphoma?

A

Rubbery, non-tender, enlarged lymph nodes - typically cervical and also axillary/inguinal

25% have systemic features - weight loss, fever, night sweats, pruritus and lethargy

Alcohol induced lymph node pain

Mediastinal lymph nodes - mass effect (SVC/bronchial obstruction), direct extension (pleural effusions)

Hepatosplenomegaly

Cachexia and anaemia

63
Q

Staging for lymphoma

A 
Ann Arbor Staging 
1 - Single LN region 
2 - More than one - same side of diaphragm 
3 - Nodes of both sides of diaphragm 
4 - Beyond LN's - liver and bone marrow

A - no systemic symptoms other than pruritus
B – WL >10% in 6 months, unexplained >38degrees, night sweats

64
Q

Treatment for lymphoma

A

Chemotherapy (short course with radio if I-A or II-A)

More intensive if more than II-A or II-A with 3 or more regions = ABVD - Adriamycin, bleomycin, vinblastine, dacarbazine

65
Q

Risk of radiotherapy in lymphoma

A

Increased risk of malignancies in thorax areas, IHD, hypothyroid and lung fibrosis

66
Q

5 year survival of lymphoma, I-A and IV-B

A

IA (lymphocyte predominant) >95%

IV-B (lymphocyte depleted)

67
Q

What % of non-hodgkin’s lymphoma has nodal involvement at presentation?

A

75%

68
Q

Where do most NHL derive from?

A

B cells

69
Q

Types of NHL

A

T cell lymphoma = Sezary syndrome
Gastric MALT - h-pylori
non-MALT gastric - large cell B lymphoma
small bowel lymphoma

70
Q

Presentation of NHL

A

Systemic symptoms -WL, fever, night sweats

Pancytopenia if there is BM involvement

71
Q

What is the more curable NHL

A

More aggressive high grade eg. Burkitts lymphoma (jaw lymphadenopathy in children)

Low grade - more indolent and incurable

72
Q

Treatment of low grade lymphoma

A

Can do radio if localised

Cholrambucil if diffuse - alpha interferon or rituximab

73
Q

Treatment of high grade lymphoma

A

R-CHOP

Rituximab, cyclophosphamide, hydroxydaurubicin, vincristine, prednisolone

74
Q

Cause of absolute polycythaemia

A

Polycythaemia rubra vera

75
Q

PRV genetic mutation

A

JAK2 >90%

76
Q

Cell changes in PRV

A

RBCs, WBCs and platelets all increased - therefore hyperviscosity & thrombosis

77
Q

Signs of PRV

A

Headaches, dizziness, tinnitus and visual disturbances
Burning fingers and toes and itch after bath

Gout from increased urate from increased RBC turnover (also splenomegaly in 60%)

Arterial and venous thrombosis

78
Q

Treatment of PRV

A

Venesection if young
Elderly - higher risk hydroxycarbamide

Aspirin

79
Q

Two conditions of increased platelets

A

Essential thrombocytoaemia -proliferation of megakaryocytes therefore increased platelets - treat with aspirin or hydroxycarbamide

Myelofibrosis - hyperplasia of megakaryocytes - platelet derived growth factor - fibrosis of bone marrow & myeloid metaplasia - Therefore hepatosplenomegaly - Do marrow support and stem cell transplant

Haematology (6 decks)

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