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Phase 2a Resits > Haematology > Flashcards

Haematology Flashcards

1
Q

How is anaemia defined?

A
  • lower than normal concentration of haemoglobin/RBCs
  • Hb <130 in men
  • Hb <120 in women
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2
Q

What are the different types of anaemia?

A
  • haemolytic = increased breakdown of RBCs
  • aplastic = decreased RBC, WBC, platelets
  • microcytic = reduced MCV
  • macrocytic = raised MCV
  • normocytic = normal MCV
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3
Q

What is MCV?

A

mean corpuscular volume

- average size of RBCs

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4
Q

General symptoms of anaemia

A
  • fatigue
  • headache
  • dizziness
  • dyspnoea esp on exertion
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5
Q

General signs of anaemia

A
  • tachycardia
  • skin pallor
  • conjunctiva pallor
  • intermittent claudication
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6
Q

What are signs of iron deficiency?

A
  • koilonychia = spoon-shaped nails

- angular stomatitis

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7
Q

What are signs of B12 deficiency?

A
  • angular stomatitis

- lemon-yellow skin

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8
Q

What are signs of haemolytic anaemia?

A
  • jaundice

- dark urine

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9
Q

What are the causes of microcytic anaemia?

A
  • iron deficiency
  • anaemia of chronic disease
  • sickle cell
  • thalassemia
  • sideroblastic anaemia
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10
Q

Investigations for iron deficiency microcytic anaemia

A

FBC → low Hb/MCV

Iron studies

  • low ferratin unless active inflammation
  • low serum iron
  • low transferrin saturation
  • raised transferrin

blood film → small, hypochromic cells

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11
Q

Causes of iron deficiency microcytic anaemia

A

reduced absorption

  • low intake
  • malabsorption
  • drugs eg PPIs and tetracyclines

increased utilisation → pregnancy

blood loss

  • stools
  • urine
  • trauma
  • surgery
  • menorrhagia
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12
Q

Investigations for chronic disease microcytic anaemia

A

FBC

  • low Hb
  • low/normal MCV
  • high ESR

Iron studies

  • normal/raised ferratin
  • low serum iron
  • low transferrin saturation/transferrin
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13
Q

Causes of chronic disease microcytic anaemia

A
  • chronic infection
  • chronic inflammation → connective tissue diseases
  • neoplasia
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14
Q

What is thalassemia?

A
  • inherited alpha or beta globin mutations
  • varied presentation
  • generally microcytic, hypochromic cells
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15
Q

What is sideroblastic anaemia?

A
  • iron levels normal
  • body cannot insert iron into Hb
  • microcytic
  • increased iron, transferrin, ferratin
  • ringed sideroblasts on blood film
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16
Q

Causes of normocytic anaemia

A
  • acute blood loss
  • bone marrow failure
  • pregnancy
  • haemolytic anaemia
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17
Q

Presentation of haemolytic anaemia

A
  • jaundice

- dark urine

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18
Q

Investigations for haemolytic anaemia

A
  • raised reticulocytes (chronic)
  • raised bilirubin
  • raised urobilinogen
  • schistocytes on blood film
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19
Q

Causes of haemolytic anaemia

A
  • autoimmune
  • sepsis
  • DIC
  • sickle cell
  • thalassemia
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20
Q

What is the main cause of macrocytic anaemia?

A

B12 deficiency

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21
Q

Causes of B12 deficiency in macrocytic anaemia

A
  • pernicious anaemia
  • malabsorption → coeliac, IBD, bowel resection, ileostomy
  • decreased dietary intake
  • chronic NO use
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22
Q

Investigations for B12 deficiency in macrocytic anaemia

A

bloods

  • raised MCV
  • low Hb, B12
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23
Q

Signs and symptoms of B12 deficiency in macrocytic anaemia

A
  • general anaemia presentation
  • range of neurological symptoms

presents as megaloblastic anaemia

  • cell changes on blood smear
  • oval shaped RBCs
  • hypersegmented neutrophils
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24
Q

Causes of macrocytic anaemia

A
  • B12 deficiency
  • diseases of the liver and spleen
  • haematological malignancy
  • alcohol → chronic consumption affects bone marrow
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25
Q

What is neutrophilia?

A

too many neutrophils

causes

  • infection
  • inflammation
  • CML
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26
Q

What is neutropenia?

A

not enough neutrophils

causes

  • Abs
  • chemo
  • marrow failure
  • liver disease
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27
Q

What is thrombocytosis?

A

too many platelets

causes

  • infection
  • inflammation
  • tissue injury
  • splenectomy
  • essential thrombocythemia
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28
Q

What is thrombocytopenia?

A

not enough platelets

causes

  • production failure → marrow failure, congenital
  • increased removal → ITP, TTP, DIC
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29
Q

What is lymphocytosis?

A

too many lymphocytes

causes

  • EBV
  • cytomegalovirus
  • hepatitis
  • malignancy → CLL, ALL, lymphoma
  • stress
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30
Q

What is lymphocytopenia?

A

not enough lymphocytes

causes

  • steroids
  • HIV
  • post viral
  • marrow failure
  • chemo
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31
Q

What is haemostasis?

A

process that stops bleeding

primary haemostasis

  • initiation and formation of platelet plug
  • platelet activation

secondary haemostasis

  • formation of fibrin clot
  • intrinsic and extrinsic coagulation cascade
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32
Q

What are the effects of platelet activation?

A
  • platelet shape change
  • dense granule release
  • alpha granule release
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33
Q

Inheritance of sickle cell

A
  • autosomal recessive

- gene on Cr11 → glutamic acid substitution with valine → B-globin polymerisation

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34
Q

What is sickle cell disease

A
  • sickled cells
  • endothelial damage
  • reduced O2 carrying capacity
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35
Q

Acute presentation of sickle cell (7)

A
  • bone and joint pain
  • infection
  • dyspnoea
  • cough
  • hypoxia
  • stroke
  • sequestrian crisis → blood outflow from spleen is blocked → blood accumulates → splenomegaly
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36
Q

Risk factors of sickle cell

A
  • low O2
  • cold weather
  • parvovirus B19
  • exertion
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37
Q

Chronic complications of sickle cell

A
  • avascular necrosis of joints
  • silent CNS infarcts
  • retinopathy
  • nephropathy
  • ED
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38
Q

Investigations for sickle cell

A
  • FBC → low MCV, Hb
  • blood smear → sickled erythrocytes
  • sickle solubility test → detects HbS → does not distinguish trait from disease
  • Hb electrophoresis → band of Hbs
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39
Q

Management of sickle cell

A

acute

  • morphine
  • O2
  • IV fluids
  • transfusion exchange

chronic
- hydroxycarbamide → decreases DNA synthesis

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40
Q

What is HIV?

A
  • human immunodeficiency virus
  • leads to AIDS
  • RNA retrovirus
  • virus enters and destroys CD4 T helper cells
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41
Q

How is HIV transmitted?

A
  • unprotected anal, vaginal, oral sex
  • mother to child during pregnancy or breastfeeding → vertical transmission
  • exposure to blood or bodily fluids
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42
Q

What are AIDS-defining illnesses?

A

occur when CD4 count drops to level that allows unusual infections and malignancies to appear

  • Kaposi’s sarcoma
  • PCP
  • cytomegalovirus
  • candidasis
  • lymphomas
  • TB
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43
Q

Who should be screened for HIV

A
  • everyone admitted to hospital with an infectious disease should be tested
  • patients with risk factors
  • test initially then 3 months after exposure
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44
Q

Investigations for HIV

A
  • antibody test
  • p24 antigen → quicker
  • PCR testing for HIV RNA gives viral load
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45
Q

Monitoring HIV

A
  • CD4 count

- viral load

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46
Q

Treatment for HIV

A
  • antiretroviral therapy ART

- aim is normal CD4 count and undetectable viral load

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47
Q

Natural progression of HIV

A
  1. acute primary infection → acute seroconversion illness
  2. asymptomatic phase
  3. early symptomatic HIV
  4. AIDS
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48
Q

Additional management of HIV

A
  • if AIDS, prophylactic septrin to protect against PCP
  • monitor and reduce CVD risk
  • annual cervical smears for women
  • up to date vaccines, but avoid live vaccines
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49
Q

What is HAART?

A
  • highly active ART
  • 2 nucleotide reverse transcriptase inhibitors and 1 non-nucloetide reverse transcriptase inhibitor
  • 2 NRTIs and 1 protease inhibitor
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50
Q

What is PEP?

A
  • post exposure prophylaxis
  • must be started within 72 hours
  • combination of ART therapy for 28 days
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51
Q

What is PrEP?

A
  • pre exposure prophylaxis
  • Take ART before exposure as prevention
  • highly effective
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52
Q

What is leukaemia?

A

cancer of the bone marrow

  1. immature blast cells uncontrollably proliferate
  2. take up space in bone marrow
  3. then infiltrate into other tissues

lack of space in bone marrow → fewer healthy cells can mature and be released into blood

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53
Q

What are the 4 types of leukaemia

A
  • acute lymphoblastic
  • acute myeloid
  • chronic lymphoblastic
  • chronic myeloid
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54
Q

Features of ALL

A
  • most common leukaemia in children → 0-4

- proliferation of immature lymphoblasts

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55
Q

Presentation of ALL

A
  • general anaemia symptoms
  • bleeding/bruising
  • infections
  • hepatosplenomegaly
  • lymphadenopathy
  • CNS infiltration → headaches, CN palsies
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56
Q

Diagnosis of ALL

A
  • FBC → anaemia, thrombocytopenia, neutropenia
  • blood film
  • bone marrow biopsy
  • CT/chest xray → lymphadenopathy

lumbar puncture in cases of CNS involvement

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57
Q

Management of ALL

A
  • blood/platelet transfusions
  • chemo → methotrexate
  • steroids
  • stem cell/bone marrow transplant
  • Abs
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58
Q

Features of AML

A
  • mostly elderly

- proliferation of immature myeloblasts

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59
Q

Presentation of AML

A
  • general anaemia symptoms
  • bleeding/bruising
  • infections
  • hepatosplenomegaly
  • gum hypertrophy
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60
Q

Diagnosis of AML

A
  • FBC → anaemia, thrombocytopnenia
  • blood film
  • bone marrow biopsy → auer rods
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61
Q

Management of AML

A
  • blood and platelet transfusions
  • chemo
  • stem cell/bone marrow transplant
  • Abs
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62
Q

Features of CLL

A
  • mostly 60+
  • most common type of leukaemia in adults
  • proliferation of B lymphocytes
63
Q

Presentation of CLL

A
  • often asymptomatic
  • lymphadenopathy
  • may have night sweats and weight loss
64
Q

Diagnosis of CLL

A
  • FBC → anaemia, thrombocytopenia, leukocytosis
  • blood film → smudge cells
  • bone marrow biopsy
65
Q

Management of CLL

A
  • watch and wait in early stages
  • chemo → rituximab
  • stem cell/bone marrow transplant
66
Q

Features of CML

A
  • most common in 40+
  • proliferation of myeloid blood cells
  • associated with philadelphia chromosome
67
Q

Presentation of CML

A
  • general anaemia symptoms
  • bleeding/bruising
  • infections
  • hepatosplenomegaly
  • weight loss, night sweats
  • gout
68
Q

Diagnosis of CML

A
  • FBC → anaemia, thrombocytopenia, leukocytosis
  • bone marrow biopsy
  • blood film
  • genetic testing
69
Q

Management of CML

A
  • chemo
  • stem cell/bone marrow transplant
  • tyrosine kinase inhibitors → imatinib
70
Q

Features of hodgkin lymphoma

A
  • proliferation of lymphocytes in lymph nodes
  • associated with EBV, immunosuppression
  • bimodal distribution → early 20s then 70s
71
Q

Presentation of hodgkin lymphoma

A
  • lymphadenopathy → painful upon drinking alcohol

- B symptoms → fever, night sweats, weight loss

72
Q

Diagnosis of hodgkin lymphoma

A
  • ESR raised
  • CT/chest xray for staging
  • lymph node biopsy → Reed Sternberg cells
73
Q

Management of hodgkin lymphoma

A
  • ABVD chemo
  • radiotherapy
  • steroids
  • stem cell/bone marrow transplant
74
Q

What is ABVD chemo?

A
  • adriamycin
  • belomycin
  • vinblastine
  • decarbazine
75
Q

Features of non-hodgkin lymphoma

A
  • predominantly adults 40+

- associated with EBV, immunosuppression

76
Q

Presentation of non-hodgkin lymphoma

A
  • painless lymphadenopathy
  • B symptoms
  • can get hepatosplenomegaly
77
Q

Diagnosis of non-hodgkin lymphoma

A
  • CT/chest xray for staging

- lymph node biopsy → no Reed sternberg

78
Q

Management of non-hodgkin lymphoma

A
  • RCHOP chemo

- radiotherapy

79
Q

What is RCHOP chemo?

A
  • rituximab
  • cyclophosphamide
  • hydroxy-danorubicin
  • oncovin
  • prednisolone
80
Q

What staging is used for lymphoma staging?

A

Ann Arbor staging

81
Q

What is Ann Arbor staging

A
  1. disease in only one area
  2. disease in 2 or more areas on same side of diaphragm
  3. disease in 2 or more areas on both sides of diaphragm
  4. disease spread beyond lymph nodes
82
Q

Features of multiple myeloma

A
  • predominantly 40+

- close link to MGUS

83
Q

What is MGUS

A
  • monoclonal gammopathy of undetermined significance
  • too much immunoglobulin released by abnormal plasma cells
  • 1% develop into myeloma
84
Q

Presentation of multiple myeloma

A

CRAB

  • calcium elevation → polydipsia
  • renal impairment
  • anaemia
  • bone lesions → bone pain
85
Q

Diagnosis of multiple myeloma

A
  • FBC → anaemia
  • ESR raised
  • blood film → Rouleaux formation
  • serum and urine electrophoresis → Bence Jones protein in urine
  • bone marrow biopsy
  • CT/xray → bone lesions
86
Q

Management of multiple myeloma

A
  • chemo
  • stem cell transplant
  • analgesia
  • bisphosphonates → zoledronic acid
  • blood transfusions
87
Q

Common chemo combinations for multiple myeloma

A
  • VCD
  • VTD
  • MTP
88
Q

What is polycythaemia

A
  • high concentration of erythrocytes in the blood

- 2 types → absolute and relative

89
Q

What is relative polycythaemia?

A
  • normal number of erythrocytes
  • reduction in plasma

causes

  • obesity
  • dehydration
  • excessive alcohol
90
Q

What is absolute polycythaemia?

A
  • increased number of erythrocytes

- 2 types → primary and secondary

91
Q

What is primary polycythaemia?

A
  • abnormality in the bone marrow

- AKA polycythaemia vera

92
Q

What is secondary polycythaemia?

A
  • disease outside bone marrow causing overstimulation of bone marrow

causes

  • COPD
  • sleep apnoea
  • PKD
  • renal artery stenosis
  • kidney cancer
93
Q

Features of polycythaemia vera

A
  • myeloproliferative neoplasm
  • most people have JAK2 mutation
  • affected bone marrow can also produce excessive platelets, WBCs
94
Q

Presentation of polycythaemia vera

A
  • headaches
  • dizziness
  • fatigue
  • blurred vision
  • red skin → hand, face, feet
  • HTN
  • itching esp after conact with warm water
  • hepatosplenomegaly
95
Q

Diagnosis of polycythaemia vera

A
  • FBC → raised Hb, haematocrit, WCC, platelets
  • genetic testing
  • serum erythropoietin → decreased (raised/normal in other polycythaemias)
96
Q

Management of polycythaemia vera

A
  • venesection
  • low dose aspirin daily
  • hydroxycarbamide → if high risk of thrombus
97
Q

What is pernicious anaemia?

A
  • lack of intrinsic factor
  • usually produced by parietal cells in stomach
  • allows B12 absorption in terminal ileum
  • low B12 = B12 deficiency macrocytic anaemia
98
Q

Pathophysiology of TTP

A
  1. dysfunctional vWF cleaving protease
  2. can’t break clumps of vWF into useful monomers
    3 microvascular clots form
  3. problem with primary haemostasis
99
Q

Presentation of TTP

A
  • fatigue
  • fever
  • jaundice
  • petechiae
  • purpura
  • neurological deficit
100
Q

Investigations for TTP

A

FBC

  • raised WCC
  • low Hb, platelets

blood smear → schistocytes

other → raised bilirubin, creatinine

normal clotting

101
Q

Treatment of TTP

A
  • plasma exchange
  • IV methylprednisolone
  • monoclonal Abs
102
Q

Pathophysiology of ITP

A
  • autoimmune
  • IgG destruction of GpIIb/IIIa
  • platelets cannot activate
  • problem with primary haemostasis
103
Q

Presentation of ITP

A

same as TPP

104
Q

Investigations for ITP

A
  • FBC → raised WCC, low Hb and platelets
  • clotting normal
  • blood smear normal
105
Q

Treatment of ITP

A
  • steroids

- IV IgG

106
Q

What is DIC

A
  • disorder of primary and secondary haemostasis

- widespread activation of coagulation cascade and platelet activation

107
Q

Presentation of DIC

A
  • bleeding

- ARDS

108
Q

Investigations for DIC

A

bloods

  • low platelets
  • low fibrinogen
  • high d-dimer
  • long PT
  • long APTT

blood smear → schistocytes

109
Q

Treatment for DIC

A
  • treat underlying cause
  • low fibrinogen → cryoprecipitate
  • low platelets → transfusion
110
Q

Causes of DIC

A
  • sepsis
  • crush injury
  • malignancy
111
Q

What is haemophilia

A

A

  • factor VIII deficiency (intrinsic)
  • secondary haemostasis
  • X linked recessive

B
- factor IX deficiency (intrinsic)

112
Q

Presentation of haemophilia

A

soft tissue bleeding pattern → into muscles, joints, haematoma formation

113
Q

Investigations for haemophilia

A
  • APTT long
  • PT may be normal
  • genetic testing
  • factor VIII/IX testing
114
Q

Treatment for haemophilia

A
  • recombinant factor VIII or IX

- depends on type

115
Q

What is Von Willebrand’s disease?

A
  • defect in quantity or quality of vWF
  • many subtypes
  • varied inheritance
  • primary haemostasis disorder
116
Q

What is the most common type of Von Willebrand’s disease?

A
  • type 1
  • autosomal dominant
  • quantitative disease
117
Q

Presentation of Von Willebrand’s disease

A

mucocutaneous bleeding

  • epistaxis
  • GI bleeds
  • menorrhagia
  • easy bruising
118
Q

Investigations for Von Willebrand’s disease

A
  • plasma vWF

- APTT can be prolonged if FVIII low

119
Q

How does Von Willebrand’s disease cause factor VIII deficiency?

A
  • vWF protects FVIII from liver protein C destruction

- FVIII deficiency occurs is vWF affected

120
Q

Treatment for Von Willebrand’s disease

A
  • type 1 responds to desmopressin

- tranexamic acid → reduces acute bleeding

121
Q

What is alpha thalassemia

A

gene deletion of one or both alpha chains

4 gene deletion

  • incompatible with life
  • infants often stillborn

3 gene deletion

  • moderate anaemia
  • splenomegaly
  • not transfusion dependent

2 gene deletion

  • microcytosis
  • carrier presentation
122
Q

Diagnosis of alpha thalassemia

A

FBC

  • microcytic anaemia
  • raised serum iron

Hb electrophoresis

123
Q

Treatment of alpha thalassemia

A
  • transfusion during crises
  • desferrioxamine → iron excretion
  • folic acid
124
Q

What is beta thalassemia?

A
  • decreased/absent beta chains
  • excess alpha chains
  • point mutations in gene
125
Q

Presentation of minor beta thalassemia

A
  • mild anaemia
  • hypochromic RBCs
  • often asymptomatic
126
Q

Presentation of intermedia beta thalassemia

A
  • infections
  • gallstones
  • recurrent leg ulcers
  • bone deformities
127
Q

Presentation of major beta thalassemia

A
  • failure to thrive
  • severe anaemia from 3-6 months
  • thalassemic faces
  • bone abnormalities
128
Q

Diagnosis of beta thalassemia

A

blood film

  • reticulocytosis
  • microcytic anaemia
  • nucleated RBCs in circulation
129
Q

Treatment of beta thalassemia

A

regular life long

  • transfusions
  • iron-chelating agents → deferipone
  • ascorbic acid
  • folic acid
130
Q

What is malaria?

A
  • parasitic infection Plasmodium
  • spread by female mosquito
  • most common in Africa
131
Q

What are the species of Plasmodium?

A
  • p.falciparum → most common
  • p.vivax
  • p.ovale
  • p.malariae → least common
132
Q

Signs and symptoms of malaria

A

non-specific symptoms

  • fever, chills
  • headache
  • cough
  • splenomegaly

severe disease in p.falciparum

  • SOB
  • fits and hypovolaemia
  • AKI and nephrotic syndrome
133
Q

Investigations for malaria

A
  • travel history
  • thick and thin blood smears → 3 over 48hrs
  • rapid diagnostic tests → detect parasitic antigens
  • PCR
  • bloods
  • chest xray
  • lumbar puncture
134
Q

Treatment for malaria

A

non-falciparum malaria
- chloroquine

falciparum malaria

  • oral quinine sulphate
  • IV quinine dihydrochloride for severe disease

do not treat those with G6PD deficiency

135
Q

What is tumour lysis syndrome?

A

collection of metabolic disturbances occurring with rapid destruction of neoplastic cells

136
Q

Signs of tumour lysis syndrome

A

following chemo, rapid development of:

  • hyperuricaemia, hyperkalaemia, hyperphosphatemia
  • hypocalcemia
  • AKI
137
Q

Risk factors of tumour lysis syndrome

A

occurs more frequently with aggressive treatment of

  • non-Hodgkin lymphoma
  • leukaemia
138
Q

Treatment for tumour lysis syndrome

A

allopurinol alongside chemo

139
Q

What is G6PD?

A
  • glucose-6-phosphate dehydrogenase
  • role in pentose sugar metabolism
  • protects RBCs from damage
140
Q

What is G6PD deficiency?

A

RBCs exposed to more oxidative stress → haemolysis

141
Q

Risk factors for G6PD deficiency

A
  • X linked

- west africa, middle east, asia

142
Q

Presentation of G6PD deficiency

A
  • haemolytic anaemia

- splenomegaly

143
Q

Investigations for G6PD deficiency

A

bloods

  • anaemia
  • increased LDH and reticulocytes → markers of haemolysis

blood smear → Heinz bodies

144
Q

Treatment for G6PD deficiency

A
  • blood transfusion

- stop exacerbating drugs

145
Q

What is antiphospholipid syndrome?

A
  • type of inherited thrombophilia

- AP antibodies bind to cell surfaces

146
Q

Risk factors for antiphospholipid syndrome

A
  • SLE
  • females
  • diabetes
  • HTN
  • obesity
147
Q

Presentation of antiphospholipid syndrome

A
  • unexplained thrombosis
  • recurrent miscarriage
  • Livedo reticularis

CLOT

148
Q

What is heparin-induced thrombocytopenia

A
  1. heparin administration
  2. antibodies bind to drug
  3. prothrombotic state

problem with primary haemostasis

149
Q

Presentation of heparin-induced thrombocytopenia

A
  • onset of emboli → PE, DVT, CSVT
  • suspect in any patient on heparin who’s platelets fall >50%
  • bloods → low platelets, high D-dimer
150
Q

Treatment of heparin-induced thrombocytopenia

A
  • stop heparin

- anticoagulate

151
Q

What is myelodysplasia

A
  • heterogenous group of conditions
  • defined by cell dysplasia
  • often manifests as anaemia and bone marrow failure
  • haemopoietic tissue is displaced by dysplastic cells
152
Q

Presentation of myelodysplasia

A
  • signs and symptoms of anaemia

- neutropenia → frequent infections

153
Q

Investigations for myelodysplasia

A
  • histological diagnosis

- wide variety of abnormalities

Phase 2a Resits (10 decks)

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