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Phase 2 Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

Explain the formation process of a RBC

A

Erythropoiesis:
Haemapoietic stem cells -> pro erythroblasts -> early erythroblasts (stage of ribosome synthesis - synthesise Hb) -> late erythroblasts (Hb accumulation) -> normoblast (contains Hb)-> reticulocyte (loses nucleus)

The reticulocyte stays in the bone marrow for 3 days until it enters circulation and after 1-2 days matures into an erythrocyte (RBC).

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2
Q

What is the life span of an RBC?

A

120 days

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3
Q

Where do old erythrocytes go?

A

Macrophages in the spleen, liver and bone engulf and breaks them down. The Hb breaks down into haem and globin. This then further breaks down into Fe2+ and bilirubin, and AA all to be recycled.

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4
Q

How does iron renter circulation?

A

It obtains transferrin (a transporter) from the liver and then goes into circulation and bone marrow

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5
Q

What happens to bilirubin?

A

Goes back to liver and then secreted / excreted through the bile system into duodenum / SI and excreted in faeces or reabsorbed

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6
Q

How does hypoxia stimulate erythropoiesis?

A

It stimulates the kidneys to produce erythropoietin, hence kidney failure can cause anaemia

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7
Q

What are RBC?

A

Small, bison cave, anucleated cells with few organelles but many Hb. CO2 can bind and transport but aim to excrete CO2 as by product of inspiration.

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8
Q

What is 2,3 DPG?

A

2,3 DPG plays a large role in O2 detachment of iron and its affinity to O2

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9
Q

What is the structure of haemaglobin?

A

4 haem (a pigment) and 4 globin (protein) chains. 1 RBC has millions of Hb molecules. 2 globin chains are α and 2 are β.

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10
Q

What percentage of blood is plasma, erythrocytes and the buffy coat?

A

55% plasma, 45% erythrocytes, <17% buffy coat

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11
Q

What is the buffy coat?

A

Buffy coat is leukocytes and platelets.

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12
Q

Where do platelets originate from and what do they do?

A

Platelets originate from granular cell in bone marrow which differentiates into megakaryotes which rupture and release the platelets. Platelets help to clot blood

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13
Q

What are leukocytes and what do they do?

A

Leukocytes are granular or agranular and have a role in immune response.

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14
Q

What are the three types of granulocytes?

A

Granulocytes include neutrophils, eosinophils and basophils.
Neutrophils main function is phagocytosis however they are highly inflammatory as they blow up in the process.
Eosinophils are part of the allergic response and secrete chemicals that activate mast cells to promote the response. They also have a host defence role against bacteria, fungi and parasites. Big role in pathogenesis against asthma.
Basophils also secrete chemicals to promote the allergic response. They activate T-cells. In mice, basophils are APCs.

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15
Q

What are the 5 types of agranulocytes?

A

Mast cells, dendritic cells, monocytes, t lymphocytes and b lymphocytes.
Mast cells are granular but are classed as agranulocytes. They release histamine in response to pathogen or allergy and are big in allergic and inflammatory responses. They cause vasodilation and an increase in vascular permeability.
Dendritic cells are important in innate immunity (first line of defence) - they are phagocytes and the main APC so activate T cells.
Monocytes circulate in blood and are phagocytes. When they migrate from blood to tissue they become macrophages (APC and phagocytes)
T lymphocytes are CD4 (helper) or CD8 (cytotoxic). CD4 promote macrophage activity and activate B lymphocytes. CD8 kills infected, abnormal or tumour cells. T memory cells also exist.
B lymphocytes are plasma cells or memory cells. Plasma cells secrete antibodies to combat allergens and pathogens, memory B cells for specific memory to antigens.

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16
Q

What three places are used to make cells?

A

Spleen, liver and bone marrow

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17
Q

What do haematopoietic stem cells differentiate into?

A

Myeloid progenitor cells or common lymphoid progenitor cells

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18
Q

What do common lymphoid progenitor cells differentiate into?

A

Lymphoid cells which can then differentiate into lymphocytes, or dendritic cells.

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19
Q

What do common myeloid progenitor cells differentiate into?

A

Myeloblasts and eventually immature granulocytes which will mature in circulation. They can also differentiate into pro monocytes and mast cells precursors, which will eventually develop into monocytes / macrophages / dendritic cells and mast cells. With stimulation of thrombopoietin they can become megakaryocytes or erythropoietin stimulates erythroblasts

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20
Q

What is the difference between medullary and extramedullary haematopoiesis?

A

Extramedullary refers to haematopoiesis occurring outside the medulla of the bone (bone marrow) e.g. liver and spleen

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21
Q

When is EMH more likely to occur?

A

In infection or with a pathological cause. Also pre birth, until halfway through pregnancy. Lymph nodes have a very low constant input from this point onwards.

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22
Q

What is the Hb cutoff for anaemia?

A

Hb<120g/L for female

Hb<140g/L for men

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23
Q

What are the 3 different RBC sizes?

A

Microcytic, normocytic and macrocytic

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24
Q

What causes microcytic anaemia?

A

Iron deficiency , chronic inflammatory disease and thalassaemia

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25
Q

What causes normocytic anaemia?

A

If the reticulocyte count is high - haemolytic anaemia, blood loss or a bone marrow disorder

26
Q

What causes macrocytic anaemia?

A

Macrocytic will have a high MCV but low Hb and will require a blood film to determine whether it is megaloblastic or non megaloblastic.
Non megaloblastic macrocytic anaemia is caused by alcohol abuse, hypothyroidism or pregnancy
Megaloblastic (large immature RBC with hypersegmented neutrophils) is usually VB12 deficiency, folate deficiency or drug toxicity.

27
Q

Anaemia can also be categorised by mechanism. What is included in decreased production?

A

Bone marrow disorders, CKD (decreased erythropoietin), hyperthyroidism, Fe or Vit B12 deficiency, chronic inflammatory disease

28
Q

Anaemia can also be categorised by mechanism. What is included in blood loss?

A

Surgery, trauma, periods, GI etc

29
Q

Anaemia can also be categorised by mechanism. What is included in increased destruction (haemolysis)?

A

Intravascular - DIC (disseminated intravascular coagulopathy), TTP (thrombotic thrombocytopaenic purpura), HUS (haemolytic uraemic syndrome), mechanical heart valve
Extravascular - hypersplenism, inherited haemolytic anaemia - sickle cells or hereditary spherycytosis, acquired haemolytic anaemia

30
Q

What is DIC?

A

Disseminated intravascular coagulopathy - formation of small blood clots that block vessels

31
Q

What is TTP?

A

Thrombotic thrombocytopoenic purpura. Forms clots and uses up platelets

32
Q

What is HUS?

A

Haemolytic uraemic syndrome. There’s reduced RBC, acute kidney failure and decreased platelets

33
Q

Hat do RBC release when destroyed?

A

Lactate dehydrogenase, Hb, globin, unconjugated bilirubin and iron

34
Q

What clears up free haemoglobin?

A

Haptoglobins

35
Q

What are the symptoms of anaemia?

A

Fatigue, lethargy, pallor,

conjunctival pallor, sclerae icterus, bone tenderness, lymphadenopathy, dyspnoea, hepatosplenomegaly

36
Q

What is the platelet boundary for thrombocytopenia?

A

Platelets <150,000/mm3

37
Q

What are the 3 stages of haemostasis?

A

Vasoconstriction, plug formation and coagulation

38
Q

Why does vasoconstriction occur for haemostasis?

A

To reduce blood flow and loss. Platelets, RBC and clotting factors circulate in the blood.

39
Q

What happens in plug formation in haemostasis? What are the 3 As?

A

Platelets bind to exposed collagen in injured vessel, with help of vWF

  1. Adhesion - binding to exposed collagen and activate
  2. Activation - activated platelets release ADP and TXA2 to recruit more platelets
  3. Aggregation - the extra activation / aggregation forms a temporary plug
40
Q

What happens in coagulation stage of haemostasis?

A

Clotting factors activated after series of cascades including CF2 -> thrombin -> prothrombin. This activates fibrinogen to form fibrin for fibrin mesh.

41
Q

Why doesn’t haemostasis occur in healthy tissue?

A

Healthy tissue releases NO and prostacyclins

42
Q

What is a sialylated platelet?

A

Sialylated platelets contain sialylic acid on it surface. New platelets are sialylated.

43
Q

How are damaged platelets recognised?

A

Damaged platelets have a different morphology - they are desialylated. Normal platelets live for around 7 days but damaged ones will be cleared by the reticuloendothelial system

44
Q

In what ways can thrombocytopenia occur?

A

Reduced production (BM disorders, ITP)
Platelet consumption (DIC, TTP/HUS, heparin induced)
Splenomegaly (portal hypertension, feltys syndrome)
Dilutional(massive fluid resuscitation)
Platelet destruction (ITP)
Infection

45
Q

How does thrombocytopenia present clinically?

A 
Skin changes - purpura, petrichae, mucosal bleeding 
Lymphadenopathy 
Hepatomegaly 
Splenomegaly
Constitutional symptoms
46
Q

What is haemolytic anaemia?

A

Premature RBC destruction. Reticuloendothelial system works in overdrive so macrophages and monocytes destroy RBC excessively

47
Q

What stimulates erythropoiesis?

A

Erythropoietin, androgens and thyroid hormones

48
Q

What are the classic RBC changes seen on bloods with haemolytic anaemia?

A

Increased lactate dehydrogenase
Increased Hb
Increased free Hb, haem and globin (and therefore increased bilirubin and iron)
Decreased hepatoglobin (as used up clearing up Hb)

49
Q

Mechanical valve is one intravascular way haemolytic anaemia can form. Explain how.

A

RBC destruction from sheer stress trauma to RBC from valve

50
Q

Microangiopathic haemolysis is one intravascular way haemolytic anaemia can form. Explain how.

A

Prothrombotic / coagulation states can damage RBC as cell membranes get destroyed and they pass through clot - they burst and die (TTP/HUS/DIC)

51
Q

Immune mediated is one intravascular way haemolytic anaemia can form. Explain how.

A

Paroxysmal cold haemolytic anaemia and nocturnal haemoglobinuria both result in depletion through complement activation. CAHA has antibodies recognise antigens on RBC at temps below core body temperature and induce destruction, usually extravascular.

52
Q

Osmotic lysis is one intravascular way haemolytic anaemia can form. Explain how.

A

Hypotonic mean h2o enters RBC causing them to swell and burst

53
Q

Acute transfusion reaction is one intravascular way haemolytic anaemia can form. Explain how.

A

Incorrect matching of antigens means antibodies will bind and attack.

54
Q

Abnormal RBC is one extracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

Abnormal RBC means the RE will destroy it

55
Q

Warm autoimmune haemolytic anaemia is one extracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

Antibodies attack RBC membranes when there is an increase in body temperature

56
Q

Hypersplenism is one extracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

Usually due to the sequestration of cells and increased activity of macrophages

57
Q

Infections are one extracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

Malaria and bartenollosis invade RBC making them abnormal

58
Q

Haemaglobinopathies are one intracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

Sickle cell and thalassaemia have a faulty Hb structure so RBC are destroyed

59
Q

Cell membrane defects are one intracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

Hereditary spherocytosis, elliptocytosis and somatocytosis have an abnormal structure

60
Q

Enzyme deficiencies are one intracorpuscular extravascular way haemolytic anaemia can form. Explain how.

A

G6P deficiency: in RBC anaerobic glycolysis is the main pathway to energy in form of ATP during which free radicals are made. G6P helps decrease free radicals for,action keeping cells healthy, deficiency means cells are damaged

Phase 2 Revision (6 decks)

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