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Pathology > Haematology Part 1 (p8-21- Blood film, anaemias, bleeding disorders + VTEs) > Flashcards

Haematology Part 1 (p8-21- Blood film, anaemias, bleeding disorders + VTEs) Flashcards

1
Q

In what conditions are acanthocytes found?

A

Abetalipoproteinaemia, liver disease, hyposplenism

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2
Q

In what conditions are basophilic RBC stippling found?

A

Lead poisoning, megaloblastic anaemia, myelodysplasia, liver disease, haemoglobinopathy

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3
Q

In what conditions are Burr cells found?

A

Uraemia, GI bleeding, stomach carcinoma

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4
Q

In what conditions are Heinz bodies found?

A

Glucose-6-phosphate dehydrogenase deficiency, chronic liver disease

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5
Q

In what conditions are Howell Jolly bodies found?

A

Post-splenectomy, hyposplenism (e.g. sickle cell disease), megaloblastic anaemia and hereditary spherocytosis

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6
Q

In what conditions are leucoerythroblastic anaemias found?

A

Marrow infiltration e.g. myelofibrosis

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7
Q

In what conditions are Pelger Huet cells found?

A

Congenital

Acquired (myelogenous leukaemia and myelodysplastic syndromes)

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8
Q

When is polychromasia found?

A

Premature/inappropriate release from BM

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9
Q

In what conditions are increased reticulocytes found?

A

Haemolytic anaemias

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10
Q

In what conditions are decreased reticulocytes found?

A

Aplastic anaemia

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11
Q

In what conditions is there right shift (hypermature white cells)?

A

Megaloblastic anaemia, uraemia, liver disease

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12
Q

When are rouleaux formations found?

A

Chronic inflammation, paraproteinaemia and myeloma

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13
Q

When are schistocytes found?

A

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

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14
Q

When are spherocytes found?

A

Hereditary spherocytosis, autoimmune haemolytic anaemia

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15
Q

When are stomatocytes found?

A

Hereditary stomatocytosis, high alcohol intake and liver disease

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16
Q

When are target cells found?

A

Liver disease, hyposplenism, thalassaemia and IDA

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17
Q

Clinical levels of anaemia in men and women?

A

Hb:
Men <135g/L
Women <115g/L

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18
Q

What are the general causes of anaemia?

A

Reduced production of RBCs
Increased loss of RBCs (haemolytic anaemia)
Increased plasma volume (pregnancy)

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19
Q

What are the symptoms and signs of anaemia?

A

Symptoms- fatigue, dyspnoea, faintness, palpitations, headache, tinnitus, anorexia
Signs- Pallor, Severe anaemia- hyperdynamic circulation e.g. tachycardia, flow murmurs

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20
Q

What are the causes of microcytic anaemia? (FAST)

A

Fe deficiency
Anaemia of chronic disease
Sideroblastic anaemia
Thalassaemia

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21
Q

What are the causes of normocytic anaemia?

A 
Acute blood loss
Anaemia of chronic disease
Bone marrow failure
Renal failure
Hypothyroidism
Haemolysis
Pregnancy
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22
Q

What are the causes of macrocytic anaemia? (FATRBC)

A 
Fetus (pregnancy)
Antifolates (phenytoin)
Thyroid (hypo)
Reticulocytosis 
B12 or folate deficiency
Cirrhosis (alcohol excess and liver disease)
Myelodysplastic syndrome
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23
Q

What are the signs of Fe deficiency anaemia?

A

Koilonychia, atrophic glossitis, angular cheliosis (inflammation of corners of the mouth), post-cricoid webs (Plummer Vinson). brittle hair and nails

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24
Q

What do you see on the blood film for Fe deficiency anaemia?

A

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

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25
Q

NICE guidelines for Fe deficiency anaemia with no obvious cause?

A

OGD + colonoscopy, urine dip and coeliac investigations

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26
Q

How do you treat Fe deficiency anaemia?

A

Treat the cause
Oral iron (SE- nausea, abdo discomfort, diarrhea/constipation, black stools)
IV if severe

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27
Q

Why is there anaemia of chronic disease?

A

Cytokine driven inhibition of red cell production

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28
Q

How do you diagnose sideroblastic anaemia?

A

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

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29
Q

What are the causes of sideroblastic anaemia?

A

Myelodysplastic disorders, following chemotherapy, irradiation, alcohol excess, lead excess, anti-TB drugs

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30
Q

How do you treat sideroblastic anaemia?

A

Remove the cause and give pyroxidine (Vit B6 promotes RBC production)

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31
Q

Plasma Iron Studies (Iron, TIBC + Ferritin):

What results would you see in iron deficiency?

A

Low iron, high TIBC + low ferritin

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32
Q

Plasma Iron Studies (Iron, TIBC + Ferritin):

What results would you see in ACD?

A

Low iron, low TIBC + high ferritin

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33
Q

Plasma Iron Studies (Iron, TIBC + Ferritin):

What results would you see in chronic haemolysis?

A

High iron, low TIBC, high ferritin

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34
Q

Plasma Iron Studies (Iron, TIBC + Ferritin):

What results would you see in haemochromatosis?

A

High iron, low or normal TIBC and high ferritin

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35
Q

Plasma Iron Studies (Iron, TIBC + Ferritin):

What results would you see in pregnancy?

A

High iron, high TIBC and normal ferritin

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36
Q

Plasma Iron Studies (Iron, TIBC + Ferritin):

What results would you see in sideroblastic anaemia?

A

High iron, normal TIBC and high ferritin

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37
Q

What are the sources of Vit B12 in human diet?

A

Meat and dairy products

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38
Q

What are the clinical features of Vit B12 deficiency?

A

Mouth- glossitis, angular cheilosis
Neuropsychiatric- irritability, depression, psychosis, dementia
Neurological- paraesthesia, peripheral neuropathy

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39
Q

What is the pathophysiology of pernicious anaemia?

A

Autoimmune atrophic gastritis -> achlorhydria and lack of intrinsic factor

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40
Q

What is most common cause of macrocytic anaemia in Western countries?

A

Pernicious anaemia (malabsorption leads to B12 deficiency)

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41
Q

Treatment of pernicious anaemia?

A

Replenish stores with IM hydroxocobalamin (B12)

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42
Q

What are the sources of Folate in human diet?

A

Green veg, nuts, yeast + liver

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43
Q

What are the causes of folate deficiency?

A

Poor diet
Increased demand (pregnancy or increased cell turnover e.g. haemolysis, malignancy, inflammatory disease and renal dialysis)
Malabsorption (coeliac disease)
Drugs (alcohol, anti-epileptics, methotrexate and trimethoprim)

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44
Q

What is the treatment for folate deficiency?

A

Oral folic acid

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45
Q

What would you see in haemolytic anaemia? (all, intravascular and extravascular)

A 
All:
Raised bilirubin (unconjugated), urobilinogen + LDH and reticulocytosis

Intravascular:
Increased free plasma Hb, low haptoglobin, haemoglobinuria (dark red urine)

Extravascular:
Splenomegaly

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46
Q

What are the inherited causes of haemolytic anaemia?

A

Membrane defects:
Hereditary spherocytosis
Hereditary eliptocytosis

Enzyme defects:
G6PD deficiency
Pyruvate kinase deficiency

Haemoglobinopathies:
SCD
Thalassaemias

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47
Q

What are the acquired causes of haemolytic anaemia?

A 
Autoimmune- warm or cold
Alloimmune- haemolytic transfusion reactions
Mechanical- metal valves or trauma
PNH, MAHA
Infections
Drugs
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48
Q

What is hereditary spherocytosis?

A

Autosomal dominant deficiency of spectrin or ankyrin (membrane proteins) leading to spherocyte formation

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49
Q

What are people with hereditary spherocytosis susceptible to?

A

Parvovirus B19 + often develop gallstones

Extravascular haemolysis also leads to splenomegaly

50
Q

How do you treat hereditary spherocytosis?

A

Splenectomy and folic acid

51
Q

What is hereditary elliptocytosis?

A

Autosomal dominant spectrin mutations (can lead to hydrops foetalis)

52
Q

What is the commonest RBC enzyme defect?

A

G6PD deficiency

53
Q

What is the inheritance route of G6PD deficiency?

A

X linked

54
Q

In what areas is G6PD deficiency common?

A

Areas of malarial endemicity e.g. Africa, middle east etc

55
Q

How does G6PD deficiency present?

A

Attacks- rapid anaemia and jaundice, with bite cells and Heinz bodies

56
Q

Why do drugs, broad beans, acute stressors, moth balls and acute infection lead predispose G6PD deficiency attacks?

A

These things are oxidants as G6PD helps RBCs make glutathione which protects them from oxidant damage

57
Q

How do you diagnose G6PD deficiency?

A

Enzyme assay ~2-3 months after a crisis

58
Q

How do you treat G6PD deficiency?

A

Avoid precipitants, transfuse if severe

59
Q

What is the inheritance route of pyruvate kinase deficiency?

A

Autosomal recessive

60
Q

What are the symptoms of pyruvate kinase deficiency?

A

Severe neonatal jaundice, splenomegaly and haemolytic anaemia

61
Q

What is the inheritance route for Sickle Cell Disease?

A

Autosomal recessive

62
Q

What is the mutation in sickle cell disease?

A

Single base mutation- GAG -> GTG, Glu -> Val at codon 6 of beta chain -> HbS instead of HbA

63
Q

What is the difference between Sickle cell disease, sickle cell anaemia and sickle cell trait?

A

Sickle cell disease- Umbrella term
Sickle cell anaemia- HbSS Severe
Sickle cell trait- HbAS (asymptomatic except under stress)

64
Q

When does sickle cell anaemia manifest and why?

A

At 3-6 months as it coincides with decreasing fetal Hb (HbF)

65
Q

What are the vaso-occlusive and infarction features of sickle cell anaemia (SICKLED)?

A 
Stroke
Infections (hyposplenism, CKD)
Crises (spenic, chest and pain)
Kidney (papillary necrosis, nephrotic)
Liver (gallstones)
Eyes (retinopathy)
Dactilitis (impaired growth)
Mesenteric ischaemia
Priapism
66
Q

How is sickle cell disease diagnosed?

A

Sickle cells and target cells on blood film
Sickle solubility test
Hb electrophoresis
Guthrie test (birth) to aid prompt pneumococcal prophylaxis

67
Q

How do you treat sickle cell disease?

A

Acute:
Opioid analgesia for painful crises
Exchange transfusion in severe crises

Chronic:
All should be on penicillin V, pneumovax, HIB vaccine

68
Q

What happens in beta thalassaemia?

A

Point mutations lead to reduced beta chain synthesis and excess alpha chains, which increases HbA2 and HbF

69
Q

What signs are there in beta thalassaemia?

A

Skull bossing, maxillary hypertrophy, hairs on end skull X-ray + hepatosplenomegaly

70
Q

How is beta thalassaemia diagnosed?

A

Hb electrophoresis (Guthrie test at birth)

71
Q

How is beta thalassaemia treated?

A

Minor and some intermedia don’t need regular treatment

Blood transfusions with desferrioxamine to stop iron overload, plus folic acid

72
Q

What happens in alpha thalassaemia?

A

Deletions- reduced alpha chain synthesis, excess beta chains

73
Q

What is hydrops foetalis?

A

Form of alpha thalassaemia where all 4 chains are deleted- incompatible with life

74
Q

What result for the Direct antiglobulin Test (DAT) or Coombs test would you get in an autoimmune acquired haemolytic anaemia?

A

Positive

75
Q

What result for the Direct antiglobulin Test (DAT) or Coombs test would you get in a non-immune acquired haemolytic anaemia?

A

Negative

76
Q

What are the differences between warm autoimmune haemolytic anaemia and cold agglutinin disease (features, causes and management)?

A

Warm:
Features- 37’C, IgG + Spherocytes
Causes- Idiopathic, Lymphoma, CLL, SLE, methyldopa
Management- Steroids, splenectomy and immunosuppression

Cold agglutinin disease:
Features- <37’, IgM, Raynaud’s
Causes- Idiopathic, lymphoma, infections, EBV, mycoplasma
Management- Treat, avoid cold and chlorambucil (chemo)

77
Q

What haemolytic anaemias would have a negative coombs test?

A

Non-immune (simplified term)

78
Q

Name some examples of MAHA?

A

Thrombotic thrombocytopenic purpura (TTP)

Haemolytic uraemic syndrome (HUS)

79
Q

What happens in a microangiopathic haemolytic anaemia?

A

Mechanical RBC destruction (forced through fibrin/pit mesh in damaged vessels) -> schistocytes

80
Q

What are the causes of MAHA?

A

HUS, TTP, DIC, Pre-eclampsia

81
Q

How is MAHA treated?

A

Usually plasma exchange

82
Q

What causes thrombotic thrombocytopenic purpura?

A

Autoimmune- antibodies against ADAMTS13 lead to long strands of VWF which act like cheese wire in the blood vessels, cutting up RBCs

83
Q

What is the pentad of symptoms for TTP?

A 
MAHA
Fever
Renal impairment
Neuro abnormalities
Thrombocytopenia
84
Q

What causes haemolytic uraemic syndrome?

A

E.Coli leads to toxin damaging endothelial cells, which leads to fibrin mesh and RBC damage, subsequently causing impaired renal function and MAHA

85
Q

What test is there to assess the intrinsic pathway?

A

Activated partial thromboplastin time (APTT)- to monitor heparin therapy
Starts with factor TWELVE

86
Q

What test is there to assess the extrinsic pathway?

A

Prothrombin time (PT)- to monitor warfarin therapy (INR). Factor SEVEN

87
Q

What test is there to assess the common pathway?

A

Thrombin time (TT)

88
Q

What sort of bleeding is there in vascular defects or platelet disorders?

A

Superficial bleeding into skin, mucosal membranes

Bleeding immediate after injury

89
Q

What sort of bleeding is there in coagulation disorders?

A

Bleeding into deep tissues, muscles and joints
Delayed but severe bleeding after injury
Bleeding often prolonged

90
Q

Name some congenital vascular defects

A

Osler-Weber-Rendu syndrome

CTD (Ehlers-Danlos)

91
Q

Name some acquired vascular defects

A

Senile purpura
Infection (meningococcal, measles, dengue)
Steroids
Scurvy

92
Q

Name some features of acute idiopathic thrombocytopenia?

A

Children
Commonly preceded by infection
Lasts 2-6w
Commonly spontaneous remission

93
Q

Name some features of chronic idiopathic thrombocytopenia?

A 
Adults
More common in F
Rarely preceded by infection
Long term
Treated with IVIg, steroids and splenectomy
94
Q

What is haemophilia A and what is its inheritance pattern?

A

Factor VIII deficiency (severity depends on level of factor VIII)
X-linked recessive

95
Q

How is haemophilia A diagnosed?

A

Increased APTT, normal PT and decreased factor VIII assay

96
Q

How is haemophilia A managed?

A

Avoid NSAIDs and IM injections, desmopressin, factor VIII concentrates as replacement

97
Q

What is haemophilia B and how is it inherited?

A

Factor IX deficiency

X-linked recessive

98
Q

How is haemophilia B treated?

A

Factor IX concentrates

99
Q

Types of Von Willebrand Disease

A

VWD 1- Quantitative
VWD 2- Qualitative
VWD 3- Both (most severe)

100
Q

What happens in VWD?

A

Decreased platelet function and factor VIII (as vWF carries factor VIII in circulation)

101
Q

What is the presentation of VWD?

A

Often bleeding of a platelet disorder but also coagulation disorders

102
Q

How is VWD diagnosed?

A

Increased APTT and bleeding time, decreased factor VIII and vWF Ag, normal INR

103
Q

How is VWD managed?

A

Desmopressin, VWF and Factor VIII concentrates

104
Q

What happens in disseminated intravascular coagulation?

A

Widespread activation of coagulation where clotting factors and platelets are consumed, leading to increased risk of bleeding

105
Q

Causes of DIC

A 
Malignancy
Sepsis
Trauma
Obstetric complications
Toxins
106
Q

Treatment for DIC

A

Cause and give transfusions, FFP, platelets, cryo etc

107
Q

How does liver disease lead to coagulation problems?

A

Decreased synthesis of II, V, VII, IX, X, XI and fibrinogen

Decreased absorption of vit K

108
Q

How does vit K deficiency lead to coagulation problems?

A

Vit K is needed for synthesis of Factors II, VII, IX and X and protein C/S

109
Q

What are the causes of vit K deficiency?

A

Warfarin, vit K malabsorption/malnutrition, Abx therapy, biliary obstruction

110
Q

What is the treatment of vit k deficiency?

A

IV Vit K or FFP for acute haemorrhage

111
Q

What is Virchow’s triad?

A

Three factors leading to venous thrombosis:
Vessel wall
Blood
Flow

112
Q

Name some inherited coagulopathies?

A 
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden
Prothrombin G20210A
Lupus anticoagulant
113
Q

What are the RFs for VTE?

A 
Age, Obesity
Previous DVT or PE
Immobilisation
Major surgery- esp ortho, >30 mins, plaster cast immobilisation
Long distance travel
Malignancy- esp pancreas
Pregnancy, COCP, HRT
Antiphospholipid syndrome
Polycythaemia
Thrombocythaemia
114
Q

What is the treatment for a DVT or PE?

A

LMWH (treatment dose SC) followed by warfarin or apixaban/rivaroxaban (DOACs)

115
Q

Why do you continue LMWH after starting warfarin when treating a DVT/PE?

A

Warfarin affects protein C/S and often leads to a procoagulant state in first few days before anticoagulant effect

116
Q

How does heparin work?

A

Potentiates antithrombin III which inactivates thrombin and factors 9, 10 and 11

117
Q

What is the antidote for heparin?

A

Protamine sulphate

118
Q

Side effects of heparin?

A

Bleeding and heparin induced thrombocytopenia (HIT) -> Osteoporosis with long term use

119
Q

How does warfarin work?

A

Inhibits the reductase enzyme responsible for regenerating the active form of vit K and therefore inhibits synthesis of factors 2, 7, 9, 10 and proteins C, S and Z

120
Q

How is the effect of warfarin reversed?

A

IV vit K/factor concentrates

121
Q

What is the target INR for someone following a 1st DVT or PE?

A

2.5

122
Q

What is the target INR for someone following a recurrent DVT or PE?

A

3.5

Pathology (13 decks)

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