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My Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

causes of microcytic anaemia

A
  • iron deficiency
  • thalassemias - alpha and beta
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2
Q

causes of normocytic anaemias

A
  • acute bleeding
  • chronic disease
  • renal disease
  • mixed picture = mix of big and small RBCs → normal mean size.
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3
Q

causes of Macrocytic anaemias

A
  • folate deficiency
  • B12 deficiency
  • haemolysis
  • bone marrow disorders
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4
Q

what are hypo chromic cells

A

pale RBCs due to reduced amounts of Hb - iron deficiency

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5
Q

what factors lead to decreased RBC production

A
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6
Q

what factors lead to increased increased RBC loss

A
  • Acute bleeding
  • Haemolysis
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7
Q

define anaemia

A
  • haemoglobin below lower limit of normal
    • (sex adjusted Female normal 110-147g/l, male 131 – 166g/l)
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8
Q

what other factors would you check in a pt with low Hb

A
  • platelet count
  • WBC level
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9
Q

define MCV

A
  • Mean Corpuscular [cell] Volume
  • average cell size of RBCs = 80-98fl
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10
Q

define MCH

A
  • Mean Cell Hb
  • amount of Hb in each cell
    • hypochromic, normochromic
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11
Q

T/F

reticulocyte count is part of a routine FBC

A

False

has to be requested specially

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12
Q

what is a reticulocyte count

A
  • count of the number of young RBCs
  • measures the rate of RBC production
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13
Q

causes of macrocytosis

A

NOTE: not necessarily always caused by anaemias.

  • Folate deficiency
  • B12 deficiency
  • Reticulocytosis
  • Raised immunoglobulins
  • Hypothyroidism
  • Alcohol
  • Bone marrow failure, especially myelodysplastic neoplasms
  • Drugs, e.g. methotrexate,
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14
Q

when is reticulocyte count a useful investigation

A
  • in pts with symptoms of anaemia with a normocytic MCV
    • increased of decreased reticulocyte count can help narrow down the cause of anaemia
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15
Q

what are the 2 main classes of normocytic anaemia

AND

what causes them

A
  • normocytic anaemia with increased reticulocyte count - therefore there is bone marrow response
    • acute bleed
    • haemolytic anaemias e.g. sickle cell. G6pd deficiency.
  • normocytic anaemia with decreased reticulocyte count - thus there is bone marrow failure
    • aplastic anaemia - bone marrow disorder
    • chronic diseases - esp. CKD
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16
Q

recommended iron/ day intake

amount of iron absorbed daily

function of iron

A
  • 15mg/ day
  • 1mg absorbed/day
  • used for Hb synthesis
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17
Q

causes of iron deficiency

A
  • blood loss - GI, menstrual
  • pregnancy - a quarter of iron is transferred to foetus
  • impaired absorption - gastrectomy, coeliac disease
  • dietary deficiency - elderly and vegans
  • hookworm - blood loss @ site of attachment
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18
Q

where is iron absorbed

A

SI: duodenum + jejunum

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19
Q

T/F ferritin is a good diagnostic tool for iron deficiency anaemia

A

True BUT:

  • Ferritin is used to store iron in the RBCs, so the amount of ferritin in the blood gives an indication of how much iron in the blood.
  • BUT ferritin is an acute phase protein so could go up in an infection even if the pt is anaemic
    • so normal or high ferritin doesn’t rule out Fe-deficient anaemia
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20
Q

what is transferrin and how is it used

A
  • A protein that binds iron.
  • transferrin saturation is used as a diagnostic tool: reduced saturation = Fe anaemia
    • transferrin synthesis is increased in Fe deficiency → reduced saturation as less is occupied by iron.
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21
Q

T/F

serum iron is a useful investigative tool for Fe anaemia

A

FALSE

serum iron is useless as there are day to day fluctuations and circadian variation

22
Q

management of Fe deficient anaemia

A
  • stop bleeding if there is bleeding
  • iron replacement - oral is preferred
    • Hb should rise 20mg every 3-4 weeks
    • oral and IV are equivalent so no benefit to IV
    • IV requires hospitalisation + there’s risk of extravasation → permanent skin discolouration
  • once Hb and MCV levels are normal continue replacement for a further 3 months to ensure bone marrow stores are replenished
23
Q

what are the results of iron studies in Fe deficient anaemia

A
  • ↓ ferritin
  • ↓ transferrin saturation
  • ↑total iron binding capacity
  • ↓ serum iron [not reliable]
24
Q

where is B12 absorbed in the gut

A

the terminal ileum

25
Q

what is the first stem cell for blood cells that → further cells

A

multipotent haematopoietic stem cell

26
Q

what cells are produced from the multipotent haematopoietic stem cell

A
  • myeloid stem cells
  • lymphoid stemcells
27
Q

what cells are derived from myeloblast cells

A
  • monocyte → macrophage
  • eosinophil
  • neutrophil
  • basophil
28
Q

what cells are derived from common myeloid progenitor cells

A
  • myeloblast
  • erythroblast
  • megakaryocytic
  • mast cells
29
Q

what cell are platelets derived from

A

megakaryocyte

30
Q

what cells are derived from lymphoid progenitor cells

A
  • B cells
  • T cells
  • Natural killer cells
31
Q

what is a reticulocyte

AND

what is it derived from

A
  • an immature RBC
  • derived from erythroblasts
32
Q

what cells are antigen presenting cells and which is the ‘professional’

A
  • professional = dendritic cell
  • APCs
    • macrophages, B cells + dendritic cells present using MHC2
    • all epithelial cells can present using MHC1.
33
Q

what is the most common inherited bleeding disorder

A

Von Willerbrand Disease

34
Q

what are the types of von willerbrand disease AND which is the most severe

A
  • type 1,2 and 3
  • type 3 is the most severe
35
Q

what is the cause of Von Willerbrand disease

A
  • an autosomal dominant genetic disease that → deficient, absent or malfunctioning Von Willerbrand Factor.
    • VWF = a glycoprotein needed for formation of the platelet plug
36
Q

what is Von Willerbrand Factor

A

a glycoprotein needed for platelet adhesion for the formation of the platelet plug.

37
Q

how does VWD present

A
  • pts present with unusually easy, heavy or prolonged bleeding:
    • Bleeding gums with brushing
    • Nose bleeds (epistaxis)
    • Heavy menstrual bleeding (menorrhagia)
    • Heavy bleeding during surgical operations
    • severe post-natal bleeding
38
Q

how is VWD diagnosed

A
  • no single diagnostic test, a combo of:
    • abnormal bleeding
    • family hx
    • bleeding assessment tools such as PT, APTT, FBC
39
Q

how is VWD managed

A
  • not managed on a day to day basis only in preparation for an operation or in response to major bleeding.
    • Desmopressin can be used to stimulates the release of VWF
    • VWF can be infused
    • Factor VIII is often infused along with plasma-derived VWF
40
Q

what are the main causes of bleeding disorders

A
  • over anticoagulation
    • heparin, aspirin, clopidogrel, heparins, thrombolytics
  • genetic conditions
    • VWD
    • haemophilia: A +B
  • DIC: Disseminated Intravascular Coagulopathy
41
Q

what causes haemophilia

  • A
  • B
A
  • haemophilia is an X-linked recessive disorder - men only need 1 and women need 2 X Genes.
  • haemophilia A is caused by a deficiency in factor 8
  • haemophilia B is caused by a deficiency in factor 9
42
Q

who is mostly affected by haemophilia

A
  • men as it is an X-Linked recessive condition.
  • women are rarely affected as 2 X-genes are needed
43
Q

symptoms of haemophilia

A
  • excessive bleeding in response to minor trauma
  • spontaneous haemorrhage without any trauma
  • easy bruising
  • epistaxis
44
Q

investigations for diagnosis of haemophilia

A
  • APTT: prolonged
  • plasma factor 8 + 9: decreased or absent = diagnostic
45
Q

signs of haemophilia

A
  • haemarthrosis: bleeding in joints: knees, ankles + elbows especially.
  • Prolonged bleeding following heel prick: common presentation in neonates
  • Cutaneous purpura: often first presentation of acquired haemophilia
46
Q

symptoms of haemophilia

A
  • spontaneous bleeding into joints
  • excessive bleeding
  • easy bruising
  • fatigue
47
Q

management of haemophilia

A
  • IV infusion factor 8 or 9 +
  • desmopressin
    • desmopressin stimulates release of VWF
  • tranexamic acid = antifibrinolytic
    • reduces bleeding
48
Q

what is disseminated intravascular coagulation

A
  • an acquired syndrome → over-activation of the coagulation cascade → formation of intravascular thrombi + depletion of clotting factors and platelets.
49
Q

what can trigger DIC

A
  • severe infection e.g. sepsis
  • major trauma
  • malignancy
  • major vascular disorder
  • immunological reactions
  • multiple organ failure
  • obstetric complication
50
Q

signs of DIC

A

in the context of severe systemic illness
- excessive bleeding
- petechiae
- bruising
- hypotension
- fever
- confusion
- coma

51
Q

investigations for DIC

A
  • PT: prolonged
  • platelet count: decreased
  • fibrinogen: decreased
  • imaging for sites of thrombosis

My Phase 2a (35 decks)

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