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Path Guide > Haematology > Flashcards

Haematology Flashcards

1
Q

What is an acanthocyte

A

A spur/spike cell- RBCs show many spicules

Underlying conditions include Liver disease, hyposplenism, Abetalipoproteinaemia (fat absorption interference)

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2
Q

Basophilic RBC Stippling

A

Accelerated erythropoiesis or defective Hb synthesis, small dots at the periphery are seen (rRNA)

Lead poisoning, megaloblastic anaemia, myelodysplasia, liver disease, haemoglobinaopathy (e.g. thalassemia)

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3
Q

Burr Cells (Echinocyte)

A

Irregularly shaped cells

Uraemia, GI bleedng, stomach carcinoma

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4
Q

Heinz bodies

A

Inclusions within RBCs of denatured Hb

Glucose-6-phosphate dehydrogenase deficiency
Chronic Liver disease

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5
Q

Howell-Jolly Bodies

A

Basophilic (purple spot) nuclear remnants in RBCs

Post-splenectomy or hyposplenism (e.g. sickle cell disease), coeliac disease, congenital, UC/Crohn’s, myeloproliferative disease, amyloid)

Megaloblastic anaemia, hereditary spherocytosis.

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6
Q

Leucoerythroblastic (myelophthisic anaemia)

A

Marrow infiltration- nucleated RBCs and primitive WBCs into peripheral blood.

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7
Q

Pelger Huet Cells

A

Hyposegmented neutrophil

Congenital (lamin B receptor mutation)
Aquired (myelogenous leukaemia and myelodysplastic syndromes)

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8
Q

Polychromasia (sign of reticulocytes)

A

Red blood cells of multiple colours (particularly grey-blue), due to differing amounts of Hb in RBC

Premature/inappropriate release from BM

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9
Q

Reticulocytes

A

Immature RBCs (mesh like network of ribosomal RNA becomes visible with certain stains (i.e. methylene blue)

INCREASE in haemolytic anaemia
DECREASE in aplastic anaemia, chemo

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10
Q

Right Shift

A

Hypermature white cells- hypersegmented polymorphs (>5 lobes to nucleus)

Megaloblastic anaemia, uraemia, liver disease

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11
Q

Rouleaux formation

A

Red cells stacked on each other.

Chronic inflammation, paraproteinaemia, myeloma

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12
Q

Schistocytes

A

Fragmented parts of the RBCs- typically irregularly shaped, jagged and asymemetrical

Microangiopathic anaemia e.g. DIC, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, pre-eclampsia

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13
Q

Central pallor is straight or curved rod like shape. RBCs appear as “smiling faces” or “fish mouth”

A

Stomatocytes

Underlying conditions: hereditary stomatocytosis, high alcohol intake, liver disease

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14
Q

Bull’s-eye appearence in central pallor

A

Targel Cells (codocyte)

Underlying conditions: Liver disease, hyposplenism, thalassaemia, Iron Deficiency Anaemia

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15
Q

Anaemia in Men Hb level?

A

Hb <135 g/L (13.5g/dL)

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16
Q

Anaemia in Women Hb Level?

A

Hb < 115g/L (11.5g/dL)

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17
Q

3 causes of anaemia

A

1) Reduced PRODUCTION of RBCs
2) Increased LOSS of RBCs (haemolytic anaemias)
3) Increased PLASMA VOLUME (pregnancy)

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18
Q

Symptoms of anaemia

A

fatigue, dyspnoea, faintness, palpitations, headache, tinnitus, anorexia

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19
Q

Signs of anaemia

A

pallor

in severe anaemia (Hb <80g/L) hyperdynamic circulation e.g. tachycardia, flow murmers (ejection systolic loudest over apex)»» Heart failure

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20
Q

MCV in Iron defieciency anaemia

A

Low

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21
Q

MCV in Anaemia of chronic disease

A

Low/normal

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22
Q

MCV in acute blood loss

A

normal

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23
Q

MCV in fetus/pregnancy

A

high

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24
Q

MCV in antifolates (e.g. phenytoin)

A

high

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25
Q

MCV in sideroblastic anaemia

A

low

ringed cells (e.g. in myelodisplastic syndromes)

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26
Q

MCV in thalassaemia (in the absence of anaemia)

A

low

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27
Q

MCV in bone marrow failure

A

normal

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28
Q

MCV in renal failure

A

normal

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29
Q

MCV in hypothyroidism

A

normal/high

30
Q

MCV in haemolysis

A

normal

31
Q

MCV in pregnancy

A

normal

32
Q

MCV in reticulocytosis

A

high

release of larger immature cells e.g. with haemolysis)

33
Q

MCV in B12 or folate deficiency

A

high

34
Q

MCV in cirrhosis

A

high (alcohol excess or liver disease)

35
Q

MCV in myelodysplastic syndromes

A

high

36
Q

Signs of Iron Deficiency Anaemia (IDA)

A

Koilonychia, atrophic glossitis, angular cheilosis, post-cricoid webs, brittle nails and hair

37
Q

What is plummer-vinson syndrome

A

Rare disease characterised by difficulty swallowing, iron deficiency anaemia, atrophic glossitis and oesophageal webs.

pre malignant»> post cricoid carcinoma

38
Q

Blood film for IDA?

A

Microcytic, hypochromic, anisocytosis (varying size), poikilocytosis (abnormal shape), pencil cells

39
Q

What is the cause of IDA until proven otherwise?

A

Bleeding

40
Q

GI Blood loss causes of IDA

A
  • Meckel’s diverticulum (older children)
  • Peptic ulcers/Gastritis (chronic NSAID use)
  • Polyps/colorectal Ca (most common cause in adults >50 years)
  • Menorrhagia (women <50 years)
  • Hookworm infestation (developing countries)
41
Q

2 examples of increased utilisation of blood that leads to IDA

A

Pregnancy/lactation

Growth in infants and children

42
Q

2 examples of how you can have a decreased intake of Fe

A

1) Suboptimal diet

2) Prematurity- loss of Fe each day fetus is not in utero

43
Q

2 examples of causes of decreased absorption that lead to IDA

A

coeliac disease (absence in villous surface in duodenum)

post gastric surgery (rapid transit, decrease in acid which helps Fe absorption)

44
Q

3 Intravascular haemolysis that cause IDA

A
  • Microangiopathic (chronic loss of Hb in urine» Fe deficiency)
  • Haemolytic anaemia
  • PNH (Paroxysmal Nocturnal Haemoglobinuria) is a rare acquired, life-threatening disease of the blood. The disease is characterized by destruction of red blood cells (hemolytic anemia), blood clots (thrombosis), and impaired bone marrow function (not making enough of the three blood components).
45
Q

How to investigate cause of IDA?

A

2013 NICE guldelines for IDA suggest if no obvious cause then patients should have

  • OGD & colonoscopy
  • urine dip
  • coeliac investigations.
46
Q

Treatment for IDA

A

Treat the cause.

Oral iron or IV iron if severe

47
Q

Side effects of oral iron

A

nausea, abdo discomfort, diarrhea/constipation, black stools

48
Q

What is anaemia of chronic disease?

A

cytokine driven inhibition of red cell production

49
Q

Causes of anaemia of chronic disease?

A
  • chronic infection (e.g. TB, osteomyelitis)
  • vasculitis
  • rheumatoid arthritis
  • malignancy etc.
50
Q

What is high in anaemia of chronic disease?

A

Ferritin (intracellular protein, iron store) is high.

Iron is sequestrated (separated) in macrophage to deprive invading bacteria of Iron (unless the patient has co-existing IDA).

51
Q

What is the difference in Anaemia of Chronic Disease in renal failure?

A

It is not cytokine driven but due to EPO deficiency.

Erythropoietin (EPO) is a hormone produced by the kidney. Erythropoietin promotes the formation of red blood cells by the bone marrow.

52
Q

In anaemia of chronic disease, what do inflammatory markers like IFNs, TNF and IL1 reduce?

A

EPO receptor production (and thus EPO synthesis) by kidneys

53
Q

What do you know about iron metabolism in Anaemia of Chronic Disease?

A

Iron metabolism is dysregulated. IL6 and LPS stimulate the liver to make hepcidin, which decreased iron absorption from gut (by inhibiting transferrin) and also causes iron accumulation in macrophages.

In states in which the hepcidin level is abnormally high such as inflammation, serum iron falls due to iron trapping within macrophages and liver cells and decreased gut iron absorption. This typically leads to anemia due to an inadequate amount of serum iron being available for developing red cells.

54
Q

What is sideroblastic anaemia

A

Ineffective erythropoiesis» iron loading (BM) causing haemosiderosis (endocrine, liver and cardiac damage due to iron deposition).

In sideroblastic anemia, the body has iron available but cannot incorporate it into hemoglobin, which red blood cells need in order to transport oxygen efficiently. The disorder may be caused either by a genetic disorder or indirectly as part of myelodysplastic syndrome, which can develop into hematological malignancies (especially acute myeloid leukemia).

Sideroblasts are atypical, abnormal nucleated erythroblasts (precursors to mature red blood cells) with granules of iron accumulated in the mitochondria surrounding the nucleus

55
Q

Diagnosis of sideroblastic anaemia?

A

ring sideroblasts seen in the marrow (erythroid precursors with iron deposited in mitochondria in a ring around nucleus)

56
Q

Causes of sideroblastic anaemia?

A

myelodysplastic disorders, following chemotherapy, irradiation, alcohol excess, anti-TB drugs or myeloproliferative disease.

57
Q

Treatment of Sideroblastic anaemia?

A

remove the cause.

Pyridoxine (vitamin B6 promotes RBC production)

58
Q

Iron LOW
Total iron binding capacity HIGH
Ferritin LOW

A

Iron deficiency

59
Q

Iron LOW
Total iron binding capacity LOW
Ferritin HIGH

A

Anaemia of chronic disease

60
Q

Iron HIGH
Total iron binding capacity LOW
Ferritin HIGH

A

chronic haemolysis

61
Q

Iron HIGH
Total iron binding capacity LOW/NORMAL
Ferritin HIGH

A

Haemochromatosis

62
Q

Iron HIGH
Total iron binding capacity HIGH
Ferritin NORMAL

A

Pregnancy

63
Q

Iron HIGH
Total iron binding capacity NORMAL
Ferritin HIGH

A

Sideroblastic anaemia

64
Q

Why do you have to check CRP with every ferritin you send in clinical practice?

A

Ferritin is an acute phase protein and increases with inflammation e.g. infection, malignancy.

65
Q

3 genres of macroytosis

A

Megaloblastic, Non megaloblastic and Other

66
Q

What are megaloblastic causes of macrocytosis

A

B12 deficiency
Folate deficiency
cytotoxic drugs

67
Q

What are non- megaloblastic causes of macrocytosis

A
  • Alcohol (most common cause of macrocytosis WITHOUT anaemia)
  • Reticulocytosis (e.g. in haemolysis)
  • liver disease
  • hypothyroidism
  • pregnancy
68
Q

Other haematological diseases that cause macrocytosis

A

myelodysplasia, myeloma, myeloprofilerative disordrs, aplastic anaemia.

69
Q

What do you see on a megaloblastic blood film?

A

hypersegmented polymorphs, leucopenia, macrocytosis, anaemia, thromocytopenia

70
Q

Source of vit b12?

A

meat and dairy products (we have large body stores)

71
Q

Causes of b12 deficiency?

A

Dietary (e.g. vegans)

Malabsorption

  • Stomach (lack of intrinsic factor which is produced by gastric parietal cells)&raquo_space; Pernicious anaemia, post gastrectomy
  • Terminal ileum (absorption) due to ileal resection, Crohn’s disease, bacterial overgrowth, tropical sprue and tapeworms.

Path Guide (1 decks)

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