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Osha 3a > Haematology (paeds + GP) > Flashcards

Haematology (paeds + GP) Flashcards

1
Q

What is sickle cell anaemia?

A
  • mutation in β global gene > HbS
  • Autosomal recessive
  • HbS polymerises when deoxygenated
  • Blocks blood vessels > ischaemia, sequestration (away from organs)
  • chronic haemolysis > low baseline Hb
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2
Q

How is sickle cell anaemia diagnosed?

A
  • 1st line: sickle solubility test: cloudy looking
  • Gold: HPLC, capillary electrophoresis (Hb separated based on size and charge)
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3
Q

What are some complications of sickle cell disease?

A
  • sequestration in liver/spleen
  • thrombosis (DVT, PE)
  • acute chest syndrome
  • aplastic crisis
  • vaso-occlusive crisis
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4
Q

What is lymphoproliferative disease?

A
  • Cancer of the white blood cells
  • 2 categories: Hodgkin’s and non-Hodgkin’s (aggressive or indolent)
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5
Q

How does lymphoma present?

A
  • lymphadenopathy > neck, armpit, groin
  • non-tender, rubbery nodes
  • b symptoms: fever, night sweats, weight loss
  • pain after drinking alcohol (Hodgkin’s)
  • recurrent infection
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6
Q

How is lymphoma investigated?

A
  • lymph node biopsy: core needle or excision node
  • raised LDH
  • Reed-Stenberg test: abnormally large B cells with multiple nuclei: Hodgkin’s (owl eyes)
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7
Q

How is lymphoma treated?

A
  • Hodgkin’s: DBVD: doxorubicin, bleomycin, vinblastine, dacarbazine
  • NH: R-CHOP: rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone
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8
Q

What is pernicious anaemia and the pathophysiology?

A
  • B12 deficiency
  • parietal cells produce intrinsic factor for B12 absorption in ileum
  • antibodies form against parietal cells or intrinsic factor
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9
Q

How does pernicious anaemia present?

A
  • peripheral neuropathy, paraesthesia
  • loss of proprioception
  • visual changes
  • mood/cognitive changes
  • lemon yellow skin
  • angular chelitis and glossitis
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10
Q

How is pernicious anaemia diagnosed?

A
  • testing for auto-antibodies
  • 1st line: intrinsic factor antibody
  • can also test for gastric parietal cell antibodies
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11
Q

How is pernicious anaemia treated?

A
  • dietary: oral replacement with cyanocobalamin
  • 1mg of IM hydroxycobalamin every other day/3x week for 2 weeks then 3 monthly
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12
Q

What is mean corpuscular volume (mcv) and what are the reference ranges?

A
  • microcytic: <80
  • normocytic: 80-95
  • macrocytic: >95
  • normal range: 120-165g/l in women or 130-180g/l in men
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13
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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14
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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15
Q

What is megaloblastic anaemia?

A
  • megaloblastic: results from impaired DNA synthesis. Rather than dividing, the cell continues to grow becoming abnormally large.
  • B12 deficiency
  • folate deficiency
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16
Q

What are the causes of normoblastic macrocytic anaemia?

A
  • hypothyroidism
  • alcohol excess
  • liver disease
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17
Q

What are the causes of iron deficiency anaemia?

A
  • blood loss: menorrhagia, IBD, GI bleeding
  • dietary insufficiency in children
  • poor iron absorption
  • increased requirements during pregnancy
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18
Q

How is iron absorbed in the GI tract?

A
  • mainly absorbed in duodenum and jejunum
  • stomach acid needed to keep iron in soluble Fe2+ form
  • changes to Fe3+ when acid drops so PPIs interfere
  • travels around the blood as Fe3+ bound to transferrin
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19
Q

What is seen on investigation of iron deficiency anaemia?

A
  • low transferrin saturation and ferritin
  • high total iron binding capacity: space for transferrin molecules to bind
  • FBC
  • blood film: Howell Jolly bodies
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20
Q

How is iron deficiency anaemia managed?

A
  • OGD/colonoscopy if no clear cause
  • blood/iron infusion
  • oral iron (ferrous sulphate): take for 3 months after corrected for replenishment
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21
Q

How does iron deficiency anaemia present?

A
  • koilonychia (spoon shaped nails)
  • angular chelitis
  • atrophic glossitis
  • brittle hair and nails
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22
Q

What is thalassaemia?

A
  • genetic defect in protein chains making up Hb
  • autosomal recessive
  • defects in α chains > α thalassaemia
  • defects in β chains > β thalassaemia
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23
Q

What is the presentation of thalassaemia?

A
  • fatigue
  • pallor
  • jaundice
  • gallstones
  • splenomegaly: RBC fragile so more damaged collected by spleen
  • pronounced forehead and cheekbones: bone marrow expands
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24
Q

How is thalassaemia diagnosed?

A
  • FBC
  • Hb electrophoresis
  • DNA testing
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25
Q

How is α thalassaemia managed?

A
  • monitoring FBC
  • blood transfusions
  • splenectomy
  • bone marrow transplant
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26
Q

How is β thalassaemia managed?

A
  • monitoring
  • transfusions
  • iron chelation to prevent overload
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27
Q

What is haemolytic anaemia and how does it present?

A
  • destruction of RBC leading to anaemia
  • splenomegaly
  • jaundice: bilirubin released during destruction
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28
Q

How is haemolytic anaemia investigated?

A
  • FBC: normocytic anaemia
  • blood film shows schistocytes (fragments)
  • direct Coombs test: +ve in autoimmune haemolysis
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29
Q

What are the complications of sickle cell anaemia?

A
  • infection
  • avascular necrosis
  • pulmonary hypertension
  • CKD
  • acute chest syndrome
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30
Q

How is sickle cell anaemia managed?

A
  • Abx prophylaxis for infection
  • hydroxycarbamide stimulates HbF
  • blood transfusion
  • bone marrow transplant
31
Q

What are the different types of sickle cell crises?

A
  • vaso-occlusive: sickle shaped cell clogs capillaries
  • aplastic: temporary loss of creation of new RBC
  • splenic sequestration: RBC block flow into spleen > splenomegaly > hypovolaemic shock
32
Q

What is acute chest syndrome?

A
  • results from sickle cell anaemia
  • fever/resp symptoms + new infiltrates on X-Ray
  • can be due to infection or emboli
  • may need antibiotics, transfusion, ventilation
33
Q

What is leukaemia?

A
  • cancer of stem cells in bone marrow
  • classified as acute or chronic
  • myeloid or lymphoid depending on cell line affected
34
Q

What is the pathophysiology behind leukaemia?

A
  • genetic mutation in precursor cells leads to excessive production of single type of abnormal WBC
  • leads to suppression of other cell lines
35
Q

What is the epidemiology of leukaemia?

A
  • ALL: 2-5 years
  • AML: <2 years
36
Q

How does leukaemia present?

A
  • fatigue
  • fever
  • failure to thrive (kids)
  • lymphadenopathy
  • abnormal bleeding/bruising
37
Q

How is leukaemia diagnosed?

A
  • FBC
  • blood film >20% blast cells
  • LDH
  • GOLD: bone marrow biopsy
38
Q

How is leukaemia managed?

A
  • chemotherapy and steroids
  • radiotherapy
39
Q

Describe acute lymphoblastic leukaemia

A
  • acute proliferation of B-lymphocytes
  • associated with Downs
  • blood film shows blast cells
40
Q

How does ALL present?

A
  • anaemia: lethargy and pallor
  • thrombocytopenia: easy bruising
  • neutropenia: frequent infection
  • bone pain
  • hepato/splenomegaly
41
Q

Describe acute myeloid leukaemia

A
  • blood film: high proportion of blast cells
  • may have Auer rods in cytoplasm
42
Q

What is PT?

A
  • prothrombin time: the time taken for blood to clot via the extrinsic pathway
  • factor VII is the only factor in this pathway and rarely deficient so this measures overall clothing factor synthesis
  • affected by liver disease, vit K deficiency, warfarin levels
43
Q

What is INR?

A
  • international normalised ratio
  • calculated from PT: 1.0 represents the global average
  • used to monitor patients on warfarin
  • higher - takes longer to clot
44
Q

What is APTT?

A
  • activated partial thromboplastin time
  • time taken for blood to clot via intrinsic pathway
  • can indicate issues with factor VIII, vWF, IX and XI
  • heparin can cause prolonged APTT
45
Q

What is Ann Arbor staging for lymphoma?

A
  • if affected nodes are above or below diaphragm
  • Stage 1: confined to one region
  • Stage 2: in more than one region on same side of diaphragm
  • Stage 3: affects nodes above and below diaphragm
  • Stage 4: widespread involvement inc non-lymphatic organs
46
Q

What are some types of Non-Hodgkin’s lymphoma?

A
  • Burkitt: associated w EBV, malaria, HIV
  • MALT: affects mucosa-associated lymphoid tissue (H. pylori)
  • Diffuse large B cell
47
Q

What are risk factors for Non-Hodgkin’s lymphoma?

A
  • HIV, EBV, malaria, H. pylori
  • Hep B/C infection
  • exposure to pesticides and trichloroethylene
  • family history
48
Q

What is von Willebrand’s disease?

A
  • type 1: reduced amount of vWF
  • type 2: defective vWF
  • type 3: little/no vWF
  • important in platelet adhesion and binds to factor VIII
  • autosomal dominant
49
Q

How does von Willebrand disease present?

A
  • bleeding gums with brushing
  • epistaxis (nose bleeds)
  • menorrhagia
  • heavy bleeding
  • family history
50
Q

How is von Willebrand disease investigated?

A
  • APTT prolonged
  • Low factor VIII
  • immunoassay of vWF
51
Q

How is von Willebrand disease managed?

A
  • desmopressin: stimulates release of vWF
  • infused vWF and factor VIII
  • tranexamic acid
52
Q

What is the presentation of haemophilia?

A
  • spontaneous haemorrhage, bleeding into joints and muscles
  • intracranial haemorrhage and cord bleeding in newborns
  • bleeding: gums, GI, urinary tract, retroperitoneal space
53
Q

How is haemophilia diagnosed?

A
  • bleeding scores: prolonged APTT
  • coagulation factor assays (factor VIII/IX)
  • genetic testing
54
Q

How is haemophilia managed?

A
  • prophylaxis: infusions of factor VIII/IX
  • avoid NSAIDs and contact sport
  • desmopressin and tranexamic acid (antifibrinolytic)
55
Q

What is haemophilia?

A
  • X linked recessive inherited bleeding disorders
  • almost exclusively affect males, women would need 2 affected X copies
  • A: deficiency in factor VIII
  • B: deficiency in factor IX
56
Q

What are the normal reference ranges for neutrophils?

A
  • neutrophilia: high - acute bacterial infection
  • neutropenia: low - myeloma, lymphoma
57
Q

What are the normal reference ranges for platelets?

A
  • thrombocytosis: high - myeloproliferative disorders
  • thrombopenia: low - 150x10^9 - ITP
58
Q

What are the normal reference ranges for lymphocytes?

A
  • lymphocytosis: high - leukaemia
  • lymphocytopenia: low - infection
59
Q

What is immune thrombocytopenic purpura (ITP) and who does it affect?

A
  • autoimmune platelet destruction
  • in children 2-6 (post viral infection)
60
Q

How does ITP present, how is it diagnosed and how is it treated?

A
  • symptoms: purpuric rash, easy bleeds
  • diagnosis: thrombocytopenia, inc megakaryoblasts
  • prednisolone and IV immunoglobulins
61
Q

What is thrombotic thryombcytopenic purpura and how does it present?

A
  • inherited
  • deficiency in enzyme clearing vWF so aggregation at endothelial injury sites
  • causes platelets to clump in vessels
62
Q

How does TTP present?

A
  • purpuric rash
  • menorrhagia
  • AKI
  • anaemia
  • neuro symptoms
63
Q

How is TTP diagnosed and treated?

A
  • diagnosis: thrombocytopenia, schistocytes, dec ADAMTS13
  • treatment: plasmapheresis, prednisolone, rituximab
64
Q

How does malaria present and how is it diagnosed and treated?

A
  • anaemia, blackwater fever, hepatosplenomegaly
  • blood film
  • treatment: quinine and doxycycline
65
Q

What is aplastic anaemia?

A
  • pancytopenia where the bone marrow fails
  • deficiency in red cells, white cells and platelets
66
Q

What is sideroblastic anaemia?

A
  • ineffective erythropoesis due to defective Hb synthesis
  • leads to inc iron absorption, iron loading in bone marrow
  • cardiac, endocrine and liver damage due to iron deposition
67
Q

What is tumour lysis syndrome?

A
  • rapid cell death when starting chemo for rapidly proliferating blood cancers
  • causes rise in urate, K, PO4 > renal failure
  • low calcium
  • prevention with hydration and allopurinol
68
Q

What is disseminated intravascular coagulopathy?

A
  • widespread activation of coagulation due to release of procoagulant agents
  • clotting factors and platelets consumed > inc risk of bleeding
69
Q

What is hereditary spherocytosis?

A
  • sphere shaped RBC
  • easily destroyed
70
Q

What is the epidemiology and inheritance of hereditary spherocytosis?

A
  • MC inherited haemolytic anaemia in northern Europeans
  • autosomal dominant
71
Q

How does hereditary spherocytosis present?

A
  • jaundice
  • anaemia
  • gallstones
  • splenomegaly
  • crises
72
Q

What is aplastic crisis?

A
  • increased anaemia, haemolysis and jaundice
  • BM doesn’t create new reticulocytes
  • triggered by parvovirus
73
Q

How is hereditary spherocytosis diagnosed?

A
  • family history and clinical
  • spherocytes on film
  • mean corpuscular haemoglobin conc is raised
  • reticulocytes raised
74
Q

How is hereditary spherocytosis managed?

A
  • folate supplementation
  • splenectomy
  • transfusion in crises

Osha 3a (15 decks)

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