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Haematology Flashcards

1
Q

What is blood made up of?

A

Plasma (liquid of the blood) contains RBC, WBC and platelets ALSO contains clotting factors e.g. fibrinogen

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2
Q

Once clotting factors are removed from blood what is left?

A

Glucose

Electrolytes e.g. sodium and potassium

Proteins e.g. immunoglobulins and hormones

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3
Q

Where is bone marrow found?

A

Pelvis

Vertebrae

Ribs

Sternum

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4
Q

Label the following:

A
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5
Q

Name some pleuipotent haematopoietic stem cells?

A

Undifferentiated cells with potential to transform:

Myeloid stem cells

Lymphoid stem cells

Dendritic cells

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6
Q

What doe RBCs develop from? How long do they last?

A

Reticulocytes (myeloid stem cells)

Survive 3 months

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7
Q

What are platelets made from? How long do they last?

A

Megakaryocytes (live for 10 days) - clump together and plug gaps

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8
Q

What are the WBC?

A

Myeloid stem cells (become promyelocytes, then:)

  • Monocytes then macrophages
  • Neutrophils
  • Eosinophils
  • Mast cells
  • Basophils

Lymphoid stem cells (become lymphocytes)

  • B cells (mature in bone marrow to become plasma cells and memory B cells)
  • T cells (mature in thymus gland to become CD4 T helper cells, CD8 cytotoxic T cells, natural killer cells)
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9
Q

What are some key blood film findings and when are they seen?

A

Anisocytosis - variation in size of blood cells (myelodysplastic syndrome)

Target cells - iron deficiency anaemia, post-splenectomy

Heinz bodies - blobs of denatured globin seen in G6PD and alpha-thalassaemia

Howell-Jolly bodies blobs of DNA (post-splenectomy and severe anaemia - body is regenerating cells quickly)

Reticulocytes - immature RBC, slightly larger than RBC with RNA material in (reticular - mesh like appearance), 1% of reticulocytes is normal, increases in haemolytic anaemia

Schistocytes - fragments of RBC - indicate damaged RBC from networks of clots e.g. haemolytic uraemic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenia purpura, metallic heart valves and haemolytic anaemia

Sideroblasts - immature RBC with blobs of iron (bone marrow is unable to incorporate iron in to Hb molecules) - myelodysplastic syndrome

Smudge cells - ruptures WBC due to fragile cells during blood film - chronic lymphocytic leukaemia

Spherocytes - spherical RBCs without normal bi-concave disk space - autoimmune haemolytic anaemia or hereditary spherocytosis

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10
Q

What is anaemia?

A

Low level of Hb in the blood

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11
Q

What are the normal Hb ranges in men and woman?

A

Women = 120-165

Men = 130-180

MCV = 80-100

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12
Q

What are the causes of microcytic anaemia?

A

T – Thalassaemia

A – Anaemia of chronic disease

I – Iron deficiency anaemia

L – Lead poisoning

S – Sideroblastic anaemia

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13
Q

What are the causes of normocytic anaemia?

A

A – Acute blood loss

A – Anaemia of Chronic Disease

A – Aplastic Anaemia

H – Haemolytic Anaemia

H – Hypothyroidism

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14
Q

What are the two types of macrocytic anaemia?

A

Megaloblastic = impaired DNA synthesis - rather than dividing it keeps growing (caused by vitamin deficiency)

Normoblastic

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15
Q

Give examples of causes of megaloblastic and normoblastic macrocytic anaemia?

A

Megaloblastic = B12 deficiency, folate deficiency

Normoblastic macrocytic anaemia = alcohol, reticulocytosis (usually from haemolytic anaemia / blood loss), hypothyroidism, liver disease, drugs e.g. azathioprine

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16
Q

What are the symptoms of anaemia?

A

Tiredness

SoB

Headaches

Dizziness

Palpitations

Worsening of other conditions e.g. angina, HF, PVD

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17
Q

Which symptoms are specific to iron deficiency anaemia?

A

Pica - dietary cravings for abnormal things

Hair loss

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18
Q

What are some generic signs of anaemia?

A

Pale skin

Conjunctival pallor

Tachycardia

Raised RR

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19
Q

What are some signs of specific causes of anaemia?

A

Koilonychia is spoon shaped nails and can indicate iron deficiency

Angular chelitis can indicate iron deficiency

Atrophic glossitis is a smooth tongue due to atrophy of the papillae and can indicate iron deficiency

Brittle hair and nails can indicate iron deficiency

Jaundice occurs in haemolytic anaemia

Bone deformities occur in thalassaemia

Oedema, hypertension and excoriations on the skin can indicate chronic kidney disease

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20
Q

What are some inital investigations of anaemia?

A

Hb

MCV

B12

Folate

Ferritin

Blood film

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21
Q

What are some further investigations for anaemia?

A

Oesophago-gastroduodenoscopy (OGD) and colonoscopy to look for GI cause of iron deficiency - on urgent referral for GI cancer

Bone marrow biopsy - if cause is unclear

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22
Q

When can iron deficiency occur?

A

Insufficient dietary intake

Requirements increase (e.g. pregnancy)

Iron is lost (e.g. bleeding from colon cancer)

Inadequate absorption

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23
Q

Where is iron mainly absorbed?

A

Duodenum

Jejunum

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24
Q

What can cause problems with iron absorption?

A

Medications that reduce stomach acid e.g. proton pump inhibitors (lansoprazole and omeprazole) as acid is need to keep iron in soluble ferrous Fe2+ form

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25
Q

Which conditions can cause inadequate iron absorption?

A

Coeliacs

Crohns

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26
Q

What are some causes of iron deficiency anaemia?

A

Blood loss

Dietary insufficiency

Poor iron absorption

Increased requirements e.g. pregnancy

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27
Q

What can cause iron deficiency anaemia due to blood loss?

A

Women = menorrhagia (heavy periods)

Men = GI tract (oesophagitis, gastritis, IBD)

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28
Q

How does iron travel around the body?

A

Ferric ions (Fe3+) bound to carrier protein transferrin

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29
Q

What is total iron binding capacity?

A

Total space on the transferrin molecule for the iron to bind

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30
Q

What is the formula for proportion of transferrin molecules that are bound to iron?

A

Transferin saturation - serum iron / TIBC

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31
Q

What is ferritin?

A

Form iron takes with stored in cells

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32
Q

When is extra ferritin released? What if it’s low?

A

Inflammation (infection / cancer)

If low = iron deficiency

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33
Q

Can a patient with normal ferritin have iron deficiency?

A

Yes

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34
Q

Does serum iron vary? Is it a good measure?

A

Yes, rises after iron containing meals, not useful on its own

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35
Q

How do TIBC and transferrin levels change?

A

Increase in iron deficiency

Decrease in iron overload

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36
Q

What can give the impression of iron overload?

A

Supplementation

Acute liver damage

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37
Q

What are the investigations for iron deficiency anaemia?

A

Oesophago-gastroduodenoscopy (OGD) and colonoscopy look for cancer of GI tract (if no clear cause e.g. menorrhagia / pregnancy)

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38
Q

What are the management options for iron deficiency anaemia?

A

Blood transfusion

Iron infusion e.g. cosmofer (small risk of anaphylaxis, avoided in sepsis as iron ‘feeds’ bacteria)

Oral iron e.g. ferrous sulfate 200mg TDS (causes constipation and black coloured stools - unusable if malabsorption problems)

Expect rise of 10g/L per week

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39
Q

What is pernicious anaemia?

A

Cause of B12 deficiency anaemia

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40
Q

What is intrinsic factor and where is it made?

A

Needed for absorption of vitamin B12 in the ileum made in the parietal cells

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41
Q

What happens in pernicious anaemia?

A

Antibodies form against parietal cells or intrinsic factor

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42
Q

What results from vitamin B12 deficiency?

A

Neurological symptoms:

  • Peripheral neuropathy with numbness / paraesthesia
  • Loss of vibration sense or proprioception
  • Visual changes
  • Mood / cognitive changes
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43
Q

Which antibodies are tested for in pernicious anaemia?

A

Intrinsic factor antibody (first line)

Gastric parietal cell antibody (less helpful)

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44
Q

What is the management of dietary deficiency of B12/ pernicious anaemia?

A

Dietary deficiency = oral replacement with cyanocobalamin (unless deficiency is severe)

Pernicious anaemia = 1mg IM hydroxycobalamin 3 times weekly for 2 weeks then every 3 months

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45
Q

How to treat combined folate and B12 deficiency?

A

Treat B12 deficiency first before correcting folate deficiency (if giving folic acid first = subacute combined degeneration of the cord - combined UMN and LMN signs with sensory loss)

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46
Q

What is haemolytic anaemia?

A

Destruction of RBC leading to anaemia

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47
Q

List some inherited haemolytic anaemias?

A

Hereditary spherocytosis

Hereditary elliptocytosis

Thalassaemia

Sickle cell anaemia

G6PD deficiency

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48
Q

List some acquired haemolytic anaemias?

A

Autoimmune haemolytic anaemia

Alloimmune haemolytic anaemia (transfusions reactions and haemolytic disease of newborn)

Paroxysmal nocturnal haemoglobinuria

Microangiopathic haemolytic anaemia

Prosthetic valve related haemolysis

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49
Q

What are the features of haemolytic anaemia?

A

Anaemia - due to reduction in circulating RBCs

Splenomegaly - filled with destroyed RBCs

Jaundice - bilirubin is released during destruction of RBCs

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50
Q

What are the investigations of haemolytic anaemia?

A

FBC (normocytic anaemia)

Blood film (schistocytes - fragments of RBCs)

Direct coombs test (positive in autoimmune haemolytic anaemia)

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51
Q

What is the most common inherited haemolytic anaemia in northern europeans?

A

Hereditary spherocytosis (autosomal dominant)

Sphere shaped RBCs - fragile and easily break down

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52
Q

How does hereditary spherocytosis present?

A

Jaundice

Gallstones

Splenomegaly

Aplastic crisis (in presence of parvovirus)

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53
Q

How is hereditary spherocytosis diagnosed?

A

EMA binding assay

FH

Clinical features

Spherocytes on blood film

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54
Q

What does the FBC reveal for haemolytic anaemia?

A

MCHC (mean corpuscular haemoglobin concentration) is raised

Reticulocytes raised

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55
Q

What is the treatment of hereditary spherocytosis?

A

Folate supplementation

Splenectomy

Cholecystectomy (removal of gallbladder for gallstones)

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56
Q

What is hereditary elliptocytosis?

What is the pattern of inheritance?

Managment?

A

Same as hereditary spherocytosis except RBC are ellipse shaped

Autosomal dominant

Presentation and management the same

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57
Q

What is G6PD deficiency?

Who is it more common in?

What is the mode of inheritance?

A

Defect in the RBC enzyme G6PD

Common in mediterranean and african patients

X-linked recessive

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58
Q

What can trigger the crises in G6PD deficiency?

A

Infections

Medications

Fava beans (broad beans)

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59
Q

How does G6PD present?

A

Jaundice (neonatal period)

Gallstones

Anaemia

Splenomegaly

Heinz bodies on blood films

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60
Q

How can a diagnosis of G6PD deficiency be made?

A

G6PD enzyme assay

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61
Q

Which medications trigger haemolysis in G6PD deficiency?

A

Primaquine (an antimalarial)

Ciprofloxacin

Sulfonylureas

Sulfasalazine

Sulphonamide drugs

(Sulph-group)

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62
Q

What is autoimmune haemolytic anaemia?

What are the two types?

How can it be tested for?

A

Antibodies are created against the patient’s RBC

Warm type / cold type autoimmune haemolytic anaemia

Positive direct Coombs test

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63
Q

What is warm type autoimmune haemolytic anaemia?

What is it associated with?

A

More common, haemolysis occurs at normal or above normal temperatures (usually idiopathic) arising without a clear cause

CLL, lymphoma, SLE

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64
Q

What is cold type autoimmune haemolytic anaemia? What is it also known as?

What is it associated with?

A

Lower temps (< 10oC) = antibodies against RBC attach and cause them to clump together (agglutination) causing destruction of RBC as immune system is activated against them

Also known as cold agglutinin disease

Associated with lymphoma and presents with Raynaud’s phenomenon

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65
Q

What can cold type AIHA occur secondarily to?

A

Lymphoma

Leukaemia

Systemic lupus erythematosus

Infections = mycoplasma, EBV, CMV, HIV

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66
Q

What is the management of autoimmune haemolytic anaemia?

A

Blood transfusions

Prednisolone (steroids)

Rituximab (monoclonal antibody against B cells)

Splenectomy

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67
Q

What are the two scenarios where alloimmune haemolytic anaemia occurs?

A

Transfusion reactions

Haemolytic disease of the newborn

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68
Q

What happens in haemolytic transfusion reactions?

A

Immune system produces antibodies against antigens on foreign RBC

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69
Q

What is paroxysmal nocturnal haemoglobinuria?

A

Rare condition - genetic mutation in haematopoietic stem cells in bone marrow occurs during patients lifetime.

Loss of protein on the surface of RBC which usually inhibit the completment cascade - causes destruction of RBCs

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70
Q

How does paroxysmal nocturnal haemoglobinuria present?

A

Red urine in the morning containing haemoglobin and haemosiderin causing anaemia

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71
Q

What are patients with paroxysmal nocturnal haemoglobinuria predisposed to?

A

Thrombosis (e.g. DVT, PE and hepatic vein thrombosis)

Smooth muecle dystonia (e.g. oesophageal spasm and erectile dysfunction)

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72
Q

What is the management of paroxysmal nocturnal haemoglobinuria?

A

Eculizumab (monoclonal antibody that targets completment component 5, C5 - suppressing complement system) or bone marrow transplantation (can be curative)

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73
Q

What is microangiopathic haemolytic anaemia (MAHA)?

A

Small blood vessels have structural abnormalities causing haemolysis of blood cells

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74
Q

What can microangiopathic haemolytic anaemia usually secondary to?

A

Haemolytic uraemic syndrome (HUS)

Disseminated intravascular coagulation (DIC)

Thrombotic thrombocytopenia purpura (TTP)

Systemic lupus erythmatosus (SLE)

Cancer

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75
Q

What is a key complication of prosthetic heart valves? (both bioprosthetic and metallic)

A

Haemolytic anaemia - due to turbulence

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76
Q

What is the management of prosthetic valve haemolysis?

A

Monitoring

Oral iron

Blood transfusion if severe

Revision surgery in severe cases

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77
Q

What does normal haemoglobin consist of?

A

2 alpha and 2 beta-globin chains

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78
Q

What is thalassaemia?

A

Genetic defect in protein chains that make up Hb

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79
Q

What are the two types of thalassaemia?

What is the pattern of inheritance?

A

Alpha thalassaemia

Beta thalassaemia

Autosomal recessive

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80
Q

What are the features of thalassaemia?

A

RBC = fragile and break down

Splenomegaly

Bone marrow expands = susceptibility to fractures, pronounced forehead, malar eminences (cheekbones)

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81
Q

What are the potential signs and symptoms of thalassaemia

A

Microcytic anaemia (low mean corpuscular volume)

Fatigue

Pallor

Jaundice

Gallstones

Splenomegaly

Poor growth and development

Pronounced forehead and malar eminences

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82
Q

How is a diagnosis of thalassaemia made?

A

FBC showing microcytic anaemia

Haemoglobin electrophoresis to diagnose globin abnormalities

DNA testing to look for genetic abnormality

Pregnant women are offered screening at booking

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83
Q

How to monitor for iron overload in thalassaemia?

A

Monitor serum ferritin

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84
Q

How to manage iron overload in thalassaemia?

A

Limit transfusions

Iron chelation

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85
Q

What are the features of iron overload in thalassaemia?

A

Fatigue

Liver cirrhosis

Infertility and impotence

Heart failure

Arthritis

Diabetes

Osteoporosis and joint pain

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86
Q

On what chromosome is the defect in alpha-thalassaemia?

A

Chromosome 16 (codes for alpha-globin chains)

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87
Q

What is the management of alpha thalassaemia?

A

Monitor FBC

Monitor for complications

Blood transfusions

Splenectomy

Bone marrow transplant can be curative

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88
Q

On which chromosome is the defect in beta-thalassaemia?

A

Chromosome 11 (gene coding for beta-globin chains)

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89
Q

What are the three types of beta thalassaemia?

A

Thalassaemia minor

Thalassaemia intermedia

Thalassaemia major

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90
Q

What are the features and treatment of thalassaemia minor?

A

Carrier of an abnormally functioning beta globin gene (one abnormal and one normal)

Causes microcytic anaemia (require only monitoring and no active treatment)

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91
Q

What are the features and treatment of thalassaemia intermedia?

A

Two abnormal copies of the beta-globin gene (either two defective or one defective and one deletion)

Requires monitoring and occasional blood transfusions (may require iron chelation to prevent overload)

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92
Q

What are the features of thalassaemia major?

What is the treatment?

A

Homoxygous for the deletion gene (no functioning beta-globin genes at all)

Presents with severe anaemia and failure to thrive in early childhood

Causes:

  • Severe microcytic anaemia
  • Splenomegaly
  • Bone deformities

Management:

  • Regular transfusions
  • Iron chelation
  • Splenectomy
  • Bone marrow transplant can be curative
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93
Q

What is sickle cell anaemia?

A

Genetic condition causes sickle (crescent) shaped RBCs (making them fragile = haemolytic anaemia)

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94
Q

What happens in sickle cell disease?

A

Have abnormal variant called haemoglobin S (HbS) causing RBC to be sickle shaped

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95
Q

When is fetal haemoglobin (HbF) usually replaced by haemoglobin A (HbA)?

A

Around 6 weeks

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96
Q

What is the pattern of inheritance for sickle cell disease?

What are the 2 different kinds?

A

Autosomal recessive (abnomal gene for beta-globin on chromosome 11)

One copy = sickle cell trait

Two copies = sickle cell disease

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97
Q

Why is sickle cell disease more common in pts from areas affected by malaria (e.g. africa, india, middle east, and caribbean) ?

A

Being sickle cell trait reduces the severity of malaria

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98
Q

When is sickle cell disease routinely tested for?

A

Pregnant woman at risk of being carriers

Newborn screening heel prick test (5 days old)

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99
Q

What are some complications of sickle cell disease?

A

Anaemia

Increased risk of infection

Stroke

Avascular necrosis in large joints such as the hip

Pulmonary hypertension

Painful and persistent penile erection (priapism)

Chronic kidney disease

Sickle cell crises

Acute chest syndrome

100
Q

What is the management of sickle cell anaemia?

A

Avoid dehydration and other triggers

Ensure vaccinations up to date

Antibiotic prophylaxis to protect against infection with pen V

Hydroxycarbamide to stimulate production of HbF

Blood transfusion (for severe)

Bone marrow transplant can be curative

101
Q

What is a sickle cell crisis?

What causes them?

How to treat?

A

Spectrum of acute crises related to condition

Causes = infection, dehydration, cold / significatn life events

Supportive management = low threshold for admission, treat any infection, keep warm, keep well hydrated (IV fluids), simple analgesia e.g. paracetamol / ibuprofen, penile aspiration in priapism

NSAIDs avoided where there is renal impairment

102
Q

What is a vaso-occlusive crisis (aka painful crisis)?

A

Clogginf of capillaries causing distal ischaemia associated with dehydration and raised haematocrit

103
Q

What are the symptoms of a vaso-occlusive crisis?

A

Pain

Fever

Those of triggering infection

Priapism (blood trapping in penis - treated urgentky with aspiration)

104
Q

What is a splenic sequestration crisis?

What is the management?

A

RBCs blocing blood flow in the spleen = acutely enlarged and painful spleen causing severe anaemia and circulatory collapse (hypovolaemic shock)

Considered an emergency

Management = supportive with blood transfusions and fluid resus

Splenectomy prevents

105
Q

What is an aplastic crisis?

A

Temporary loss of creation of new blood cells (commonly triggered by infection with parvovirus B19) leading to significant anaemia - management is supportive (blood transfusions if necessary)

Usually resolve spontaneously in a week

106
Q

What is acute chest syndrome in sickle cell disease?

A

Diagnosis =

Fever / resp symptoms with

New infiltrates on CXR

107
Q

What causes acute chest syndrome?

A

Infection = pneumonia or bronchiolitis

Non-infective causes = pulmonary vaso-occlusion or fat emboli

108
Q

What is the treatment of acute chest syndrome (emergency)?

A

Abx or antivirals for infections

Blood transfusions for anaemia

Incentive spirometry using a machine to encourage effective and deep breathing

Artificial ventilation with NIV or intubation

109
Q

What is leukaemia?

A

Cancer of a particular line of the stem cells in the bone marrow (causing unregulated production of certain cells)

Can be chronic or acute and affect myeloid or lymphoid cell lineage

110
Q

What are the four main types of leukaemia?

A

Acute myeloid leukaemia

Acute lymphoblastic leukaemia

Chronic myeloid leukaemia

Chronic lymphocytic leukaemia

111
Q

Name another rarer leukaemia (unlikely to come up in exams)?

A

Acute promyelocytic leukaemia

112
Q

What can whe excessive production of a single type of cell lead to?

A

Pancytopaenia (anaemia, leukopaenia, thrombocytopaenia)

113
Q

What ages do the various leukaemias occur?

A

ALL CeLLmates have CoMmon AMbitions

Under 5 and over 45 = ALL

Over 55 = CLL

Over 65 = CML

Over 75 = AML

114
Q

How does leukaemia present?

A

Non-specific (get urgent FBC if leukaemia on differentials)

  • Fatigue
  • Fever
  • Failure to thrive (children)
  • Pallor due to anaemia
  • Petechiae and abnormal bruising due to thrombocytopaenia
  • Abnormal bleeding
  • Lymphadenopathy
  • Hepatosplenomegaly
115
Q

What are the differential diagnosis of petechiae?

A

Leukaemia

Meningococcal septicaemia

Vasculitis

Henoch-Schonlein Purpura

Idiopathic Thrombocytopenia Purpura (ITP)

Non-accidental injury

116
Q

How is leukaemia diagnosed?

A

FBC (within 48 hrs if suspected leukaemia, if petechiae / hepatosplenomegaly then referred immediately to hospital)

Blood film to look for abnormal cells / inclusions

LDH (can be raised in other cancers)

Bone marrow biopsy (main investigation for diagnosis)

CXR (infection / mediastinal lymphadenopathy)

Lymph node biopsy (assess lymph node involvement / investigate for lymphoma)

LP (CNS involvement)

CT, MRI, and PET scans for staging ans assessing for lymphoma / other tumours

117
Q

What are the different types of bone marrow biopsies?

A

Aspiration = liquid sample of cells from bone marrow

Trephine = solid core sample for better assessment of cells

Biopsy = from iliac crest, with local anaesthetic and specialist needle (examined straight away, trephine sample takes a few days of preparation)

118
Q

What is ALL?

A

Malignant change in a lymphocyte precursor cell causing proliferation of single type of lymphocyte (usually B-cells) leading to pancytopaenia

Peaks at 2-4 years old and most common cancer in children

Associated with Down’s syndrome

119
Q

What does a blood film show on ALL?

A

Blast cells

120
Q

What genetic defect is ALL associated with?

A

Philadelphia chromosome (t(9:22) translocation) in 30% of adults and 3-5% of children

121
Q

What is chronic lymphocytic leukaemia?

A

Chronic proliferation of single type of well differentiated lymphocyte (usually B-lymphocytes)

122
Q

How does CLL present?

A

Often asymptomatic but can present with infections e.g. anaemia, bleeding and weight loss

Can cause warm autoimmune haemolytic anaemia

123
Q

What can CLL transform into? What is this called?

A

High-grade lymphoma called Richter’s transformation

124
Q

What does a blood film show for CLL?

A

Smear or smudge cells (occur during process of preparing blood film where fragile WBC rupture)

125
Q

What are the three phases to chronic myeloid leukaemia?

A

Chronic phase = 5 years, asymptomatic, incidental diagnosis from raised WCC

Accelerated phase = abnormal blast cells take high proportion of cells in bone marrow and blood (10-20%), more symptomatic, anaemic, thrombocytopaenic, immunocompromised

Blast phase = high proportion of blast cells and blood (>30%) severe symptoms and pancytopaenia, often fatal

126
Q

What cytogenic change is characteristic of CML?

A

Philadelphia chromosome: translocation of genes between chromosome 9 and 22

t(9:22) translocation

127
Q

What is acute myeloid leukaemia?

A

Most common acute leukaemia in adults

Can result from myeloproliferative disorder e.g. polycythaemia ruby vera or myelofibrosis

Blood film shows high proportion of blast cells which have rods inside their cytoplasm and are named auer rods

128
Q

What are the causes of massive splenomegaly?

A

CML

Myelofibrosis

Malaria

Gaucher’s syndrome

129
Q

What is helpful in exams to remember for:

ALL

CLL

CML

AML?

A

ALL = children and downs

CLL = most common leukaemia in adults overall, associated with warm haemolytic anaemia, Richter’s transformation, smudge / smear cells

CML = three phases including 5 year asymptomatic chronic phase, philadelphia chromosome

AML = most common adult leukaemia, result of transformation from myeloproliferative disorder, associated with Auer rod

130
Q

What is the management of leukaemia?

A

MDT

Treatment mainly chemo and steroids

Other treatments = RT, bone marrow transplant, surgery

131
Q

What are some complications of chemo?

A

Failure

Stunted growth / development in children

Infections due to immunodeficiency

Neurotoxicity

Infertility

Secondary malignancy

Cardiotoxicity

Tumour lysis syndrome

132
Q

What is tumour lysis syndrome caused by?

A

Release of uric acid from cells being destroyed in chemo (potassium and phosphate is also released)

133
Q

What can result from high uric acid?

A

Forms crystals in the interstitial tissue and tubules of the kidneys causing AKI

134
Q

Which medications are used to reduce high uric acid levels?

A

Allopurinol or rasburicase

High phosphate can cause low calcium so this is also monitored

135
Q

What are lymphomas?

A

Cancers affecting lymphocytes inside the lymphatic system causing cancerous cells to proliferate in lymph nodes

136
Q

Where may the enlarged lymph nodes be found in lymphomas?

A

Cervical

Axillary

Inguinal

137
Q

What are the two main categories of lymphoma?

A

Hodgkin’s lymphoma

non-Hodgkin’s lymphoma

138
Q

What amount of lymphomas are Hodgkin’s?

What age do people get it?

A

1 in 5

20 and 75 years

139
Q

Whar are the risk factors for Hodgkin’s lymphoma?

A

HIV

EBV

Autoimmune conditions e.g. RA and sarcoidosis

FH

140
Q

How does Hodgkin’s lymphoma present?

A

Lymphadenopathy (non-tender and rubbery)

Sometimes pain in lymph nodes when drinking alcohol

B symptoms (fever, weight loss, night sweats)

Other symptoms = fatigue, itching, cough, SoB, abdo pain, recurrent infections

141
Q

What are the investigations for lymphomas?

A

LDH - often raised in Hodgkin’s lymphoma (not specific)

Lymph node biopsy (key diagnostic test - looking for Reed-Sternberg cell = abnormally large B cell with multiple nuclei and nucleoli inside)

CT, MRI and PET can be used for diagnosing and staging lymphoma

142
Q

What staging system is used for HL and NHL? What are the stages?

A

Ann Arbor

Stage 1: confined to one region of lymph nodes

Stage 2: more than one region but same side of diaphragm

Stage 3: above and below diaphragm

Stage 4: widespread involvement including non-lymphatic organs e.g. lungs or liver

143
Q

What is the management of lymphomas? What are the associated risks?

A

Chemotherapy = leukaemia and infertility

RT = cancer, damage to tissues, hypothyroidism

144
Q

What are a few notable non-Hodgkin’s lymphomas?

A

Burkitt lymphoma = associated with EBV, malaria and HIV

MALT lymphoma = affects the mucosa-associated lymphoid tissue usually around the stomach, associated with H. pylori infection

Diffuse large B cell lymphoma = rapidly growing painless mass in patients over 65 years

145
Q

What are some risk factors for non-Hodgkin’s lymphoma?

A

HIV

EBV

H. pylori (MALT lymphoma)

Hepatits B or C infection

Exposure to pesticides and specific chemical called trichloroethylene used in several industrial processes

FH

146
Q

How does NHL present?

A

Similarly to HL (only differentiated when lymph node is biopsied)

147
Q

What is the management of lymphoma?

A

Watchful waiting

Chemotherapy

Monoclonal antibodies e.g. rituximab

RT

Stem cell transplantation

148
Q

What is myeloma?

A

Cancer of the plasma cells (type of B lymphocyte that produce antibodies)

149
Q

What is multiple myeloma?

A

Myeloma affects multiple areas of the body

150
Q

What is monoclonal gammopathy of undetermined significance?

A

Excess of a single type of antibosy / antibody components without other features of myeloma (incidental finding in otherwise healthy person, significance is unclear, routinely followed up)

151
Q

What is smouldering myeloma?

A

Progression of MGUS with higher levels of antibodeies or antibody components

Premalignant and more likely to progress to myeloma than MGUS

152
Q

What is Waldenstrom’s macroglobulinemia?

A

Type of smouldering myeloma with excessive IgM specifically

153
Q

What are antibodies? What are they also called?

What happens to antibodies in myeloma?

A

Immunoglobulin - molecules made up from two heavy chains and two light chains arranged in a Y shape

There are 5 main types: A, G, M, D and E

In myeloma one of these will be significantly abudant (mostly IgG) - this single type of antibody is called a monoclonal paraprotein

154
Q

What is the Bence Jones protein?

A

Found in the urine of many patients with myeloma (part of a subunit of antibody called light chains)

155
Q

What happens when cancerous plasma cells invade the bone marrow? What is this also called?

A

Bone marrow infiltration (anaemia, neutropenia, thrombocytopenia)

156
Q

What is myeloma bone disease?

A

Result of increased osteoclast activity and suppressed osteoblast activity - more bone is reabsorbed then constructed

Caused by cytokines released from plasma cells and stromal cells (other bone cells) when incontace tiwh plasma cells

157
Q

Where does myeloma bone disease typically affect?

A

Skull

Spine

Long bones

Ribs

Thin bone described as osteolytic leading to pathological fractures e.g. vertebral body in spine may collapse

158
Q

What is another result of osteoclast activity?

A

Hypercalcaemia

159
Q

What tumours can patients with myeloma develop?

A

Plasmacytomas - individual tumours made up of cancerous plasma cells (occur in bones, replacing normal bone tissue)

160
Q

Why does myeloma renal disease occur?

A

High levels of immunoglobulins (antibodies) blocking flow through tubules

Hypercalcaemia impairs renal function

Dehydration

Medications used to treat myeloma e.g. bisphosphonates can be harmful to kidneys

161
Q

What happens to the viscosity of blood in myeloma?

A

Hyperviscous due to large amounts of immunoglobulins

162
Q

What can raised plasma viscosity cause?

A

Easy bruising

Easy bleeding

Reduced or loss of sight due to vascular disease in eye

Purple discolouration to extremities (purplish palmar erythma)

Heart failure

163
Q

What 4 features of myeloma to remember for exams?

A

CRAB

Calcium (elevated)

Renal failure

Anaemia (normocytic, normochromic) from replacement of bone marrow

Bone lesions / pain

164
Q

What are the risk factors for myeloma?

A

Older age

Male

Black African ethnicity

Family history

Obesity

165
Q

When should myeloma be suspected? What investigations to order?

A

FBC (low WBC count)

Calcium (raised)

ESR (raised)

Plasma viscosity (raised)

166
Q

What further tests if any initial results return positive for myeloma?

A

Urgent serum protein electrophoresis

Urgent Bence-Jones protein test

167
Q

What are some more specific tests for myeloma?

A

B - Bence-Jones protein (requent urine electrophoresis)

L - Serum-free Light-chain assay

I - Serum Immunoglobulins

P - Serum Protein electrophoresis

Bone marrow biopsy to confirm diagnosis of myeloma

Imaging (in order of preference) = whole body MRI, whole body CT, skeletal survey (x-ray images of full skeleton)

168
Q

What are the x-rays signs of myeloma?

A

Punched out lesions

Lytic lesiosn

“Raindrop skull” caused by many punched out (lytic) lesions through skull

169
Q

What is the management of myeloma?

A

MDT

  • Chemo = bortezomid, thalidomide, dexamethasone
  • Stem cell transplantation as part of clinical trial
  • VTE prophylaxis with aspirin / LMWH when on certain chemos e.g. thalidomide as higher risk of developing thrombus
170
Q

What is the management of myeloma bone disease?

A

Bisphosphonates (suppress osteoclast activity)

Radiotherapy to bone lesions for pain

Orthopaedic surgery to stabalise bones (e.g. inserting prophylactic intramedullary rod) or treating fractures

Cement augmentation - injecting cement into vertebral fractures or lesions to improve spine stability and pain

171
Q

What are some complications of myeloma?

A

Infection

Pain

Renal failure

Anaemia

Hypercalcaemia

Peripheral neuropathy

Spinal cord compression

Hyperviscosity

172
Q

When do myeloproliferative disorders occur? What are they considered as?

A

Uncontrolled proliferation of a single type of stem cell

Type of bone marrow cancer

173
Q

What myeloproliferative disorders are there to remember?

A

Primary myelofibrosis = proliferation of haematopoietic stem cells

Polycythaemia vera = proliferation of erythroid cell line

Essential thrombocytopaenia = proliferation of megakaryocytic cell line

174
Q

What can myeloproliferative disorders progress into?

A

Acute myeloid leukaemia

175
Q

What arhe the mutations associated with myeloproliferative disorders?

A

JAK2

MPL

CALR

176
Q

What can myelofibrosis result from?

A

Primary myelofibrosis, polycythaemia vera or essential thrombocythaemia

177
Q

What happens in myelofibrosis?

A

Proliferation of cell line leads to fibrosis of the bone marrow (replaced by scar tissue) in response to cytokines that are released from proliferating cells (important cytokine = fibroblast growth factor)

Affects production of blood cells and leads to anaemia and low white blood cells (leukopenia)

178
Q

Where else is haematopoiesis after myelofibrosis?

A

Haematopoiesis = liver and spleen (extramedullary haematopoiesis) - hepatomegaly and splenomegaly leading to portal hypertension

If occuring in spin = spinal cord compression

179
Q

How do myeloproliferative disorders present?

A

Systemic symptoms = fatigue, night sweats, weight loss, fever

Underlying condition signs = anaemia (except in polycythaemia), splenomegaly (abdo pain), low platelets (bleeding and petechiae), thrombosis is common in polycythaemia and thrombocythaemia, raised blood cells (thrombosis and red face), low white blood cells (infections)

180
Q

What are the three key signs on examination for polycythaemia vera?

A

Conjunctival plethora (redness in conjunctiva of eye)

Ruddy complexion

Splenomegaly

181
Q

What are the FBC findings for the various myeloproliferative disorders?

A

Polycythaemia vera = raised Hb

Primary thrombocythaemia = raised platelet count

Myelofibrosis (due to primary MF or secondary to PV or ET) can give variable findings - anaemia, leukocytosis or leukopenia (high or low white cell count), thrombocytosis or thrombocytopenia (high or low platelet counts)

182
Q

What will a blood film show in myelofibrosis?

A

Teardrop-shaped RBCs, varying sizes of RBC (poikilocytosis) and immature red and white cells (blasts)

183
Q

How are myeloproliferative disorders diagnosed?

A

Bone marrow biopsy (aspiration is normally ‘dry’ as bone marrow has turned to scar tissue)

184
Q

What can help guide management in myeloproliferative disorders?

A

JAK2

MPL

CALR genes

185
Q

What is the management of primary myelofibrosis?

A

If disease minimal then monitor with no active treatment

Allogenic stem call tranplantation (potentially curative but carries risk)

Chemo to control disease, improve symptoms and slow progression but not curative alone

Supportive management of anaemia, splenomegaly and portal hypertension.

186
Q

What is the management of polycythaemia vera?

A

Venesection - keeps Hb in normal range (first line treatment)

Aspirin - reduces risk of developing blood clots (thrombus formation)

Chemotherapy - controls disease

187
Q

What is the management of essential thrombocytopenia?

A

Aspirin reduces the risk of developing blood clots (thrombus formation)

Chemo to control disease

188
Q

What is myelodysplastic syndrome?

A

Caused by myeloid bone marrow cells not maturing properly and not producing healthy blood cells

Causing low levels of:

Anaemia

Neutropenia (low neutrophil count)

Thrombocytopenia (low platelets)

189
Q

When is myelodysplastic syndrome most common?

What is the risk associated?

A

Patients above 60 years old and previous treatment with chemo / radio

Risk it may turn into acute myeloid leukaemia

190
Q

How may patients with myelodysplastic syndrome present?

A

Symptoms of anaemia (fatigue, pallor, SoB)

neutropenia (severe / frequent infections)

thrombocytopenia (purpura / bleeding)

191
Q

How is myelodysplastic syndrome diagnosed?

A

FBC abnormal

Blasts on blood film

Diagnosis from bone marrow aspiration and biopsy

192
Q

What are the management options for myelodysplastic syndrome?

A

Watchful waiting

Supportive treatment with blood transfusions if severely anaemic

Chemotherapy

Stem cell transplantation

193
Q

What is thrombocytopenia? What is the normal range?

A

Low platelet count

Normal = between 150 and 450

194
Q

What can cause problems with production of platelets?

A

Sepsis

B12 or folic acid deficiency

Liver failure causing reduced thrombopoietin production in the liver

Leukaemia

Myelodysplastic syndrome

195
Q

What can cause problems with destruction of platelets?

A

Medications (sodium valporate, methotrexate, irotretinoin, antihistamines, proton pump inhibitors)

Alcohol

Immune thrombocytopenic purpura

Therombotic thrombocytopenic purpura

Heparin-induced threombocytopenia

Haemolytic-uraemic syndrome

196
Q

How does thrombocytopenia present on blood film?

A

Asymptomatic and found incidentally

Below 50 x 109/L = easy / spontaneous bruiding / prolonged bleeding (nose bleeds, bleeding gums, heavy periods, blood in urine / stools)

Below 10 x 109/L high risk of spontaneous bleeding (intracranial / GI)

197
Q

What are some differentials for abnormal / prolonged bleeding?

A

Thrombocytopenia (low platelets)

Haemophilia A and haemophilia B

Von Willebrand disease

Disseminated intravascular coagulation (usually secondary to sepsis)

198
Q

What are the other names for autoimmune thrombocytopenic purpura?

A

Idiopathic thrombocytopenic purpura

Primary thrombocytopenic purpura

199
Q

What is ITP?

A

Condition where antibodies are created against platelets

Causing immune response and destruction

200
Q

What are the management options for ITP?

A

Prednisolone (steroids)

IV immunoglobulins

Rituximab (a monoclonal antibody against B cells)

Splenectomy

201
Q

What are the extra management steps for ITP?

A

Platelet count monitored

Education on persistent headaches and melaena

Careful control of blood pressure and suppressing menstrual periods

202
Q

What is thrombotic thrombocytopenic purpura?

A

Tiny blood clots form in small vessels (microangiopathy) using up platelets and causing thrombocytopenia and bleeding under skin

203
Q

How does TTP present?

A

Fever

Neuro signs

Thrombocytopenia

Haemolytic anaemia

Renal failure

204
Q

Why does thrombotic thrombocytopenic purpura occur?

A

Problem with protein called ADAMTS13 (normally inactivates von Willebrand factor and reduces platelet adhesion to vessel walls and clot formation)

Blood clots that form break up causing haemolytic anaemia

205
Q

Why does a deficiency in ADAMTS13 protein occur?

A

Inherited genetic mutation

Autoimmune disease (antibodies created against protein)

206
Q

What is the treatment of TTP?

A

Plasma exchange

Steroids

Rituximab (monoclonal antibody against B cells)

207
Q

What is hepatin induced thrombocytopenia (HIT)?

A

Development of antibodies against platelets in response to exposure to heparin (specifically target protein on the platelets called platelet factor 4 (PF4)

These are anti-PF4 / heparin antibodies

208
Q

What is the action of the HIT antibodies?

A

Bind to platelets and acitvate clotting mechanisms causing hypercoagulable state leading to thrombus (also break down platelets and cause thrombocytopenia (patient on heparin with low platelets forms blood clots)

209
Q

How is a diagnosis of HIT made?

What is the management?

A

Testing for HIT antibodies

Stopping heparin and using alternative anticoagulant guided by specialist

210
Q

What is Von Willebrand disease (VWD)?

A

Most common inherited cause of abnormal bleeding (haemophilia) many different genetic causes most of which are autosomal dominant- causing deficiency / absence / malfunctioning glycoprotein called von Willebrand factor (VWF)

Three types based on underlying cause, type 3 = most severe

211
Q

How to patients with VWD present?

A

Bleeding gums with brusing

Nose bleeds (epistaxis)

Heavy menstrual bleeding (menorrhagia)

Heavy bleeding during surgical operations

Family history of VWD is very relevant

212
Q

How is a diagnosis of VWD made?

A

History of abnormal bleeding, family history, bleeding assessment tools and lab investigations

Due to all underlying causes = no easy test = diagnosis is challenging

213
Q

What is the management of VWD?

A

Usually no day to day treatment, management = for controlling major bleeding / prep for operations

Desmopressin can stimulate release of VWF

VWF can be infused

Factor VIII infused along with plasma-derived VWF

Control of heavy periods (tranexamic, mefanamic acid, norethisterone, COCP, mirena coil)

Hysterectomy in severe cases

214
Q

What are haemophilia A and haemophilia B?

A

Inherited severe bleeding disorders

Haemophilia A = deficiency in factor VIII

Haemophilia B (aka christmas disease) = deficiency in factor IX

215
Q

What is the pattern of inheritance of haemophilia A and B?

A

X linked recessive

men only require one abnormal copy as they only have one X chromosome, women require both (if one = carrier)

Haemophila A and B almost exclusively affect males

216
Q

What are the signs and symptoms of haemophilia A and B?

A

Severe bleeding disorders (bleed excessively in response to minor trauma and risk of spontaneous haemorrhage)

Presentation in neonates = intracranial haemorrhage, haematomas and cord bleeding

Spontaneous bleeding into joints (haemoathrosis) and muscles are a classic feature (untreated = joint damage and deformity)

217
Q

Where can abnormal bleeding occur in haemophilia?

A

Gums

GI tract

Urinary tract = haematuria

Retroperitoneal space

Intracranial

Following procedures

218
Q

How is haemophilia diagnosed?

A

Bleeding scores

Coagulation factor assays

Genetic testing

219
Q

What is the management of haemophilia?

A

Affected clotting factors (VIII or IX) replaced by IV infusion either prophylactically or in response to bleeding (complication = antibodies against the clotting factor - treatment will be unaffective)

Acute episodes of bleeding

  • Infusion of the affected factor (VIII or IX)
  • Desmopressin to stimulate the release of von Willebrand factor
  • Antifibrinolytics e.g. tranexamic acid
220
Q

How can a VTE cause a stroke?

A

Hole in heart (atrial septal defect)

221
Q

What are the risk factors for VTE?

A

Immobility

Recent surgery

Long haul flights

Pregnancy

Hormone therapy with oestrogen (COCP and HRT)

Malignancy

Polycythaemia

SLE

Thrombophilia

222
Q

What are thrombophilias? Give someexamples?

A

Conditions which predispose patients to blood clots

e.g:

Antiphospholipid syndrome

Antithrombin deficiency

Protein C or S deficiency

Factor V Leiden

Hyperhomocysteinaemia

Prothrombin gene variant

Activated protein C resistance

223
Q

What is the VTE prophylaxis if a patient is deemed at risk on admission?

What are some contraindications?

A

LMWH (e.g. enoxaparin)

Contraindications = active bleeding, existing anticoagulation with warfarin or a NOAC

Antiembolic compression stockings (unless peripheral arterial disease)

224
Q

How does DVT present?

A

Calf / leg swelling (measure circumference of cald 10cm below tibial tuberosity > 3cm difference is significant)

Dilated superficial veins

Tenderness to calf (particularly over site of deep veins)

Oedema

Colour changes to the leg

Ask questions incase of PE

225
Q

What is Wells score?

A

Risk of patient with symptoms actually having DVT or pulmonary embolism (takes into account recent surgery, clinical findings)

226
Q

What other conditions may cause a raised D-dimer?

A

Pneumonia

Malignancy

Heart failure

Surgery

Pregnancy

227
Q

How is a VTE diagnosed?

A

DVT = ultrasound doppler (repeat in 6-8 days if negative and positive D-dimer with Wells score suggesting DVT)

Pulmonary embolism = diagnosed with CT pulmonary angiogram or ventilation-perfusion (VQ) scan

228
Q

What is the initial management of VTE?

A

Treatment dose LMWH (started immediately) e.g. enoxaparin / dalteparin

229
Q

What is the long term anticoagulation in VTE?

A

Warfarin (target INR = 2-3, continue LMWH for 5 days when switching or INR is 2-3 for 24 hours, whichever longer)

NOAC / DOAC (oral anticoagulation that aren’t warfarin, require less monitoring, originally called ‘novel oral anticoagulants’ changed to ‘non-vitamin K oral anticoagulants’ because no longer novel - changing to direct acting oral anticoagulants e.g. apixaban, dapifatran and rivaroxaban

LMWH is first line in pregnancy / cancer

LMWH

230
Q

How long to continue anticoagulation for in VTE?

A

3 months = obvious reversible cause (then review)

Beyond 3 months = cause unclear, recurrent VTE, irreversible underlying cause e.g. thrombophilia (review at 6 months)

6 months in active cancer (then review)

231
Q

What are inferior vena cava filters?

A

Devices fitted into inferior vena cava to filter blood (used in recurrent PEs or those that are unsuitable for anticoagulation)

232
Q

How to investigate unprovoked DVT?

A

Investigate for possible cancer:

  • History and examination
  • CXR
  • Bloods (FBC, calcium and LFTs)
  • Urine dip
  • CT abdo and pelvis in patients over 40
  • Mammogram in women over 40

Investigate for antiphospholipid syndrome by checking for antiphospholipid antibodies

If family history then test for hereditary thrombophilias:

  • Factor V Leiden (most common hereditary thrombophilia)
  • Prothrombin G20210A
  • Protein C
  • Protein S
  • Antithrombin
233
Q

What is Budd-Chiari syndrome?

A

Where blood clot (thromobosis) develops in the hepatic veins blocking the outflow of blood (associated with hyper-coagulable state)

Causes acute hepatitis

Classic triad:

  • Abdo pain
  • Hepatomegaly
  • Ascites

Management = anticoagulation (heparin / warfarin) investigating for underlying cause of hyper-coagulation and treating hepatits

234
Q

What are irradiated blood products?

Who should recieve them?

A

Blood depleted of T-lymphocytes used to avoid transfusion associated graft versus host disease

  • Granulocyte transfusions
  • Intra-uterine transfusions
  • Neonates (up to 28 post expected dates of delivery)
  • Bone marrow / stem cell transplants
  • Immunocompromised
  • Hodgkin’s disease
235
Q

Name some transfusion complications?

A

Immunological = acute haemolytic, non-haemolytic febrile, allergic / anaphylaxis

Infective

TRALI (transfusion related acute lung injury)

TACO (transfusion related circulatory overload)

Other (hyperkalaemia, iron overload, clotting)

236
Q

What causes non-haemolytic febrile reaction?

How does it present?

How is it managed?

A

Antibodies react to WBC fragments and cytokines (often the result of sensitisation by previous pregnancies)

Presents as chills, fever

Manage by slowing / stop transfusion and paracetamol

237
Q

What causes minor allergic reaction?

How does it present?

What is the management?

A

Caused by foreign plasma proteins

Presents with pruritus and urticaria

Managed by temporarily stopping transfusion and antihistamine

238
Q

What can cause anaphylaxis during blood transfusion?

How does it present?

How is it managed?

A

Thought to be caused by patients with IgA deficiency and high anti-IgA antibodies

Presents with hypotension, dyspnoea, wheezing and angiooedema within minutes

Managed by stopping transfusion, IM adrenaline and ABC support (oxygen, fluids) also consider corticosteroids or bronchodilators

239
Q

Why does acute haemolytic reaction occur in blood transfusions?

How does it present?

How to manage?

What are some complications?

A

ABO incompatibility - IgM mediated (stop transfusion)

Presents as fever, abdo pain and hypotension within minutes

Manage by stopping transfusion, confirm pt ID, DCT, fluid (generous with saline) and resus

Complications = DIC and renal failure

240
Q

How does TACO (transfusion associated circulatory overload occur?

How does it present?

How is it managed?

A

Caused by excessive rate of transfusion and / pre-existing heart failure

Presents as pulmonary oedema and hypertension!!

Managed with slowing / stopping transfusion and IV loop diuretics e.g. furosemide and oxygen

241
Q

What causes TRALI (transfusion related acute lung injury)?

How does it present?

What is the management?

A

Non-cardiogenic pulmonary oedema (due to increased vascular permeability caused by host neutrophils)

Presents as hypoxia, pulmonary infiltrates on CXR, fever, hypotension within 6 hours

Managed by stopping the transfusion and oxygen and supportive care

242
Q

What is the MOA of dabigatran, rivaroxaban and apixaban?

A

Rivaroxaban and apixaban = Direct factor Xa inhibitor

Dabigatran = Direct thrombin inhibitor

243
Q

What class of drug is tranexamic acid?

When is it given?

A

Antifibrinolytic given for menorragia and trauma (within 3 hrs as IV bolus followed by slow infusion)

244
Q

What are some contraindications to platelet transfusions (even below 10)?

A

Chronic bone marrow failure

Autoimmune thrombocytopenia

Heparin-induced thrombocytopenia

Thrombotic thrombocytopenic purpura

245
Q

What factors carry a worse prognosis for Hodgkin’s lymphoma?

A

Male

>45

B symptoms

Hb <10.5 g/dL

Lymphocyte depleted

246
Q

What are the indications for NOACs?

A

Prevention of VTE following hip/knee surgery

Treatment of DVT and PE

Prevention of stroke in non-valvular AF

Cancer care (5 decks)

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