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CP3 > Haematology > Flashcards

Haematology Flashcards

1
Q

ANAEMIA: List the typical symptoms of patients with anaemia

A
  • Fatigue
  • Lethargy
  • Pallor
  • Dyspnoea
  • Palpitations
  • Chest pain
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2
Q

ANAEMIA: Classify anaemia in terms of red cell indices and list common causes of each type of anaemia.

A
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3
Q

ANAEMIA: Discuss the common causes of confirm iron deficiency anaemia.

A
  • Dietary
  • Blood loss (menstruation)
  • Duodenum or proximal jejunum pathology that reduced absorption
  • Pregnancy
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4
Q

ANAEMIA: Outline the clinical features and laboratory diagnosis of sickle cell anaemia

A

Clinical features:

  • Sickle cell crisis1: Severe pain lasting up to 7/7
  • Recurrent infections
  • Anaemia (normocytic)
  • Failure to thrive

Laboratory findings:

  • High rectiulocyte count
  • Howell-Jolly bodies (a nucleated cell which provide evidence of functional asplenia, due to the sickled cells becoming stuck in the spleen) and target cells on blood smear
  • Iron levels are normal
  • Abnormal haemoglobin forms on electrophoresis - HgS and HgSC
  • Pathological basis: Defect in the beta chain of haemoglobin. Autosomal recessive condition

1: Symptoms arise due to the abnormally shaped cells blocking small blood vessels, reducing perfusion to distal sites which can in turn cause organ damage and increased vulnerabilty to infections (due to splenic damage)

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5
Q

ANAEMIA: Outline the clinical management of sickle cell crisis and the importance of sickle cell

A

Management of sickle cell crisis

  • Analgesia: Paracetamol, NSAIDS or opioids as appropriate for pain level
  • Supportive care and correction of cause:
    • Oxygen if hypoxic, fluids and antibiotics if required
    • Correct cause e.g. warming if hypothermic
  • Blood transfusion for life-threatening vaso-occlusive events
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6
Q

ANAEMIA: Describe the laboratory features of haemolysis. Outline the causes of haemolytic anaemia and their treatment.

A

Laboratory findings:

  • Normocytic anaemia
  • MCHC elevated (due to lysed RBCs releasing haemoglobin)
  • Increased reticulocyte count (as the body tries to increase RBC number)
  • Abnormal forms on peripheral smear (schistocytes)
  • Elevated LDH and unconjugated bilirubin due to increased RBC breakdown
  • Low haptoglobin (becomes depleted in the presence of high concentrations of haemoglobin, as acts to bind free haem)
  • Coomb’s test: Positive suggests an immune mediated cause (tests for IgG bound to the surface of RBCs)

Causes of haemolytic anaemia:

  • Rhesus incompatibility
  • ABO incompatibility
  • Hereditary causes:
    • RBC defects, enzymatic deficiencies, abnormal Hb (sickle cell), thalassaemia
  • Acquired haemolytic anaemia:
    • Immune mediated:
      • Autoimmune antibodies in conditions such as SLE, RA and scleroderma
      • Haemolytic disease of the newborn
    • Non-immune mediated:
      • ​Medication induced
      • Infection
      • HUS, DIC, TTP, HELLP syndrome

​​​Management of haemolytic anaemia

Coomb’s positive (immune mediated)

  • Treat causes plus steroids
  • Splenectomy1 plus rituximab (Monoclonal Ig against B cells)
  • Whole obody plasmaphoresis

Coomb’s negative (not immune mediated) e.g. prosthetic valve haemlysis, TPP, hypersplenism

Congenital

1: Splenectomy is helpful as the spleen is the major site of RBC destruction

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7
Q

ANAEMIA: Outline the laboratory features of microangiopathic anaemia and list the common causes.

A

Microangiopathic haemolytic anaemia (MAHA) is where the small blood vessels have structural abnormalities that cause haemolysis of the blood cells travelling through them. Imagine a mesh inside the small blood vessels shredding the red blood cells. This is usually secondary to an underlying condition:

  • Haemolytic Uraemic Syndrome (HUS)
  • Disseminated Intravascular Coagulation (DIC)
  • Thrombotic Thrombocytopenia Purpura (TTP)
  • Systemic Lupus Erythematosus (SLE)
  • Cancer

​Laboratory findings:

  • Schistocytes (products of RBC breakdown)
  • ?Thrombocytopenia (platelet aggregation in vessels leads to haemolysis of RBCs)
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8
Q

ANAEMIA: Outline the features and causes of inherited red cell membrane defects and of red cell enzymopathies.

A

Features:

  • Anaemia (haemolytic)
  • Jaundice
  • Gallstones (pigmented - due to the increased production of bilirubin)
  • Splenomegaly (due to the increased breakdown of RBCs)

Causes:

  • Hereditary Spherocytosis: Autosomal dominant. Sphere shaped, fragile RBCs which break easily when passing through the spleen.
  • Hereditary Elliptocytosis: As above but oval shaped RBCs
  • Thalassaemia: Defect in the alpha or beta chain of haemoglobin
  • Sickle Cell Anaemia
  • G6PD Deficiency: X-linked recessive. It causes crises that are triggered by infection, medications (antimalarials) or broad beans. Heinz bodies on blood film (can see bits of damaged haem attached to the sides of the RBCs)
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9
Q

ANAEMIA: Outline the clinical features and laboratory diagnosis of thalassaemia

A

Clinical features

  • Microcytic anaemia
  • Fatigue
  • Pallor
  • Jaundice
  • Gallstones
  • Splenomegaly
  • Poor growth and development
  • Pronounced forehead and prominent cheekbones

Laboratory diagnosis

  • FBC - microcytic anaemia
  • Haemoglobin electrophoresis reveals abnormal globin structure
  • Elevated ferritin (iron overload can be seen in patients with thalassaemia)
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10
Q

THE WHITE CELL: Interpret a blood count showing a leucocytosis and list common causes for neutrophilia and neutropaenia, lymphocytosis and lymphopaenia.

A
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11
Q

THE WHITE CELL: Describe the clinical features of acute leukaemia and discuss the laboratory diagnosis.

A
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12
Q

THE WHITE CELL: Outline the general principles of treatment of acute leukaemias

A

Primarily treated with chemotherapy and steroids.

Bone marrow transplant if prognosis is poor or relapse. Bone marrow transplant is necessary for those with the philadelphia chromosome in ALL.

Supportive care:

  • Hickman line for venous access
  • High calorie diet
  • Allopurinol to prevent chemo induced tumour lysis syndrome (reduces urate acid levels)
  • Monitor potassium and phosphate levels
  • Monitoring for neutropenic sepsis - temperature >38 degrees on 2 occasions more than an hour apart → start abx (cephalosporin plus gentamicin)
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13
Q

THE WHITE CELL: Describe the clinical features and laboratory diagnosis of chronic leukaemias and outline the principles of management.

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14
Q

THE WHITE CELL: Outline the clinical presentation of leukaemias and key ddx

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15
Q

THE WHITE CELL: Describe the clinical features and laboratory diagnosis of multiple myeloma. Outline the associated laboratory abnormalities

A

Clinical features: C.R.A.B.

  • Calcium: Hypercalcaemia
  • Renal: Impaired renal function due to light chain deposition
  • Anaemia: Due to bone marrow failure. Other consequences of bone marrow failure include recurrent infections and increased bleeding/bruising
  • Bone: Osteolytic bone lesions due to osteoclast activation (backache, pathological fractures)
  • Increased viscosity of blood

Laboratory diagnosis:

  • Monoclonal band/paraprotein (representative of excessive production of a single Ig)
  • Urine Bence-Jones protein postive
  • FBC: Normocytic normochromic anaemia, leukopenia
  • Blood film: Rouleaux formation (stacks of RBCs)
  • Raised ESR and calcium
  • Deranged U&Es
  • ‘Pepper pot’ skull on skeletal XR
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16
Q

THE WHITE CELL: Describe the clinical features of lymphoma. Classify lymphomas into Hodgkin’s and Non-Hodgkin’s disease and to high- and low- grade groups. Outline the principles of treatment.

A

Clinical features: (typically the same for Hodgkin’s and Non-Hodgkin’s)

  • Lymphadenopathy
    • Non-tender and rubbery
    • Classically in the neck, axilla or inguinal region
    • Pain after alcohol ingestion
  • B symptoms: Weight loss, night sweats, fever
  • Fatigue
  • Cough
  • Dyspnoea
  • Recurrent infections
  • Mediastinal lymph nodes can have mass effects (SVC/bronchial obstruction)
  • Hepatosplenomegaly

​Hodgkin’s lymphoma

  • Characterised by Reed-Sternburg cells (Owl eyes)
  • ~ 15% of cases
  • Slow growing, localised and rarely fatal
  • Consider risk factors (EBV, SLE, obesity, FHx)

Non-Hodgkin’s lymphoma

  • Includes all lymphomas without Reed-Sternburg cells
  • Can be classified into:
    • ​High grade: Divide rapidly, rapid onset. More aggressive but have better prognosis if identified and treated
    • Low grade: Divide slowly with a more insidious onset. Tend to be widely disseminated at presentation and incurable.
  • Can present with symptoms of extra-nodal disease (in 25%): Oropharynx, skin, CNS, gut or lung
    • ​Burkitt’s - associated with EBV, malaria and HIV
    • MALT lymphoma - associated with H.Pylori infection (?Hx of dyspepsia)

Investigations

  • FBC, U&Es, ESR, LFT, calcium
  • LDH - elevated
  • Lymph node biopsy is diagnostic
  • CT, MRI and PET for diagnosing and staging tumours

​Principles of treatment

  • Ann Arbor staging is use for staging
  • Chemotherapy, radiotherapy or chemo-radiotherapy
17
Q

THE PLATELET: Discuss the role of platelets in the pathophysiology of vascular disease including vascular thrombosis and platelet emboli

A

Role of the platelet:

Endothelial damage → exposure of collagen and vWF → platelet adhesion → synthesis of TXA2 by platelets to cause vasoconstriction and further aggregration → activation of the coagulation cascade to allow for the formation of fibrin

Role of pathophysiology:

Involved in the formation of thrombi, such as those causing MI, cerebrovascualar events and acute limb ischaemia

18
Q

THE PLATELET: Describe the mechanism of action of aspirin and outline its role in cardiovascular disease prevention.

A

Aspirin MoA:

Inhibits COX-1, preventing the synthesis of pro-thombotic prostaglandins (activate the coagulation cascade)

Role in CVD:

  • Reduces the risk of thrombus formation

Indications for aspirin:

  • Prophylaxis of CVD
  • Secondary prevention following MI: DAPT with aspirin and clopidogrel for 1 year, with aspirin continued
  • Acute stroke (300mg), with switch to clopidogrel +/- anticoagulant after 2/52
  • PVD
19
Q

THE PLATELET: Outline the clinical features, investigation and treatment of immune thrombocytopaenia.

A

Clinical features:

  • Purpuric rash
  • Bruising
  • Bleeding - epistaxis, menorrhagia, melaena
  • Splenic
  • In children: Usually follows viral infection. Tends to be acute and self limiting
  • In adults: Less acute. Normally in women with other autoimmune diseases

Investigation:

  • FBC: Thrombocytopenia
  • Platelet autoantibodies

Treatment:

  • Corticosteroids (prednisolone)
  • IV immunoglobulin
  • Rituximab (targets B cells)
  • 2nd line: Splenectomy
20
Q

HAEMOSTASIS: Describe the laboratory tests to assess the clotting system and recognise and interpret patterns of abnormality.

A
  • aPTT - intrinsic pathway
    • ​Used to monitor heparin therapy
  • aPT - extrinsic pathway
    • ​Increased by hepatic disease or warfarin use
    • Used as INR
  • Thrombin time (addition of thrombin to pts blood)
    • ​Prolonged in fibrinogen deficiency/dysfunction
21
Q

HAEMOSTASIS: Outline a plan of investigation for a patient complaining of easy bruising.

A
  • FBC: Platelet count, panctopenia suggestive of leukaemia
  • PT, PTT, thrombin time
  • Look for infective cause: CRP, ESR, WCs
  • Check for haemophilia with PTT
22
Q

HAEMOSTASIS: Describe the role of the liver in normal clotting, including the role of vitamin K in the synthesis of some clotting factors

A

Liver produces clotting factors

Vitamin K is required for the production of clotting factors II, VII, IX and X.

  • Deficiencies in vitamin K can arise from malabsorptive conditions (fat soluble), cholestatic jaundice (no bile salts) or antibiotics (gut flora disturbances)

​Inhibitors of coagulation

  • Anti-thrombin III: Potentiated by heparin
  • Activated protein C and protein S: Induce fibrinolysis by destruction of factors V and VIII

Fibrinolysis

  • Tissue plasminogen activator (t-PA) converts plasminogen to plasmin.
    • Plasmin breaks down fibrinogen and fibrin, producing degradation products such as D-dimer
  • Mediators, such as thrombin and protein C, stimulate the release of t-PA
23
Q

HAEMOSTASIS: Discuss the clinical features, diagnosis and management of inherited bleeding disorder including haemophilia and von Willebrands disease.

A

Haemophilia

Haemophilia A - factor VIII deficiency and Haemophilia B - factor IX deficiency

  • X-linked recessive
  • Raised aPTT and low clotting factor

Clinical features:

  • ​Major bleeds after minor trauma
  • Recurrent haemarthroses, leading to crippling arthropathies

​Management

  • Avoids NSAIDs and IM injections
  • Minor bleeding:
    • ​Compression and elevation
    • Desmopressin to raise factor VIII may be sufficient
  • Major bleeding:
    • ​Recombinant factor VIII/IX to raise factor level to 50% of normal

Von Willebrands Disease

May be autosomal recessive or dominant.

Diagnosis:

  • aPTT increased
  • INR and platelets normal

Clinical features:

  • Features of a platelet type disorder - epistaxis, menorrhagia

Management:

  • Transexamic acid for mild bleeding
  • Desmopressin and recombinant factor VIII1 for more severe bleeds

1: As vWF has a secondary role of binding factor VIII to prevent degradation. So low factor VIII levels co-exist

24
Q

HAEMOSTASIS: Discuss the pharmacokinetics and clinical use of warfarin including laboratory tests used to monitor clinical effect.

A

Pharmacokinetics of warfarin

  • Requires bridging treatment with heparin until INR is within the therapeutic range as takes up to 5/7 to have an effect on clotting factors
  • INR measured on alternate days

​Monitoring

  • INR
25
Q

HAEMOSTASIS: Outline the clinical management of over-anticoagulation with warfarin.

26
Q

HAEMOSTASIS: Discuss the pharmacokinetics and clinical use of heparin including laboratory tests used in monitoring heparin therapy. Outline the clinical management of over-anticoagulation with heparin

A

Pharmacokinetics of heparin:

  • Given IV or SC
  • Can be used in severe CKD (where LMWH is contraindicated)
  • Potentiates anti-thrombin III, increasing its ability to inhibit thrombin, Xa and IXa
  • S/E: Bleeding, HIT, hyperkalaemia
  • LMWH: Inactivates Xa (activates thrombin)

Laboratory tests for monitoring:

  • aPTT - should be checked at 6 hours, aiming for aPTT of 1.5-2.5

Clinical management of over-anticoagulation with heparin

  • Protamine sulphate
27
Q

HAEMOSTASIS: Discuss the clinical use of thrombolysis, including monitoring and complications.

A

Clinical use:

  • DVT
  • Ischaemic stroke
  • MI (if PPCI cannot be provided within 2 hours)
28
Q

HAEMOSTASIS: Outline the clinical indications for screening for thrombophilia and how this is done.

A

Thrombophilia: Inherited/acquired coagulopathy predisposing to thrombosis, usually venous.

Inherited causes: APC resistance/factor V Leiden mutation, antithrombin III deficiency, prothrombin gene mutation

Acquired causes: APL syndrome

Clinical indications:

  • Arterial thrombosis aged < 50
  • Venous thrombosis aged < 40, with no risk factors
  • Familial VTE
  • Recurrent unexplained VTE
  • Unusual site of thrombosis
  • Recurrent foetal loss (>3)

Screening tests:

  • FBC
  • Clotting
  • Fibrinogen concentration +/- APC (activated protein C) resistance test
  • Lupus anticoagulant/anti cardio-lipin antibodies
  • Antithrombin and protein C/S assays for deficiency
  • Factor V Leiden mutation PCR if APC resistance test is positive
  • PCR for prothrombin gene mutation
29
Q

HAEMOSTASIS: Outline the clinical features of disseminated intravascular coagulation including laboratory tests used in diagnosis

A

DIC: Sees systemic activation of coagulation pathways, leading to extensive intravascular coagulation and fibrin clot development. There is sequential thrombotic occlusion of arterial microvasculature and eventual organ failure.

Eventually, there is depletion of clotting factors and platelets, leading to bleeding.

Clinical features

  • Bruising
  • Excessive bleeding e.g. from venepuncture sites
  • Renal failure

Investigations

  • Thrombocytopenia (low plts)
  • Low fibrinogen
  • Raised PT and aPTT
  • Raised D-dimer
  • Blood films sees broken RBCs (schistocytes)

Causes:

  • Infection
  • Trauma
  • Malignancy
  • Obstetric complications e.g. amniotic fluid embolism, pre-eclampsia
  • Severe liver failure
  • Tissue destruction e.g. pancreatitis, burns
  • Toxic/immunogenic stimuli
30
Q

HAEMOSTASIS: Describe the principles of cross matching blood.

A

ABO, RhD group and check for atypical Igs.

If atypical Igs are present then crossmatching is performed.

  • Indirect agglutination test: Donor RBCs add to patients serum and then Coomb’s reagent added. Agglutination indicates that the pt has Igs for the donors RBCs. Always performed pre-transfusion
  • Direct agglutination: Pts washed RBCs added to Coomb’s reagent. Testing for autoimmune haemolysis.
31
Q

HAEMOSTASIS: Outline the principles of treatment of massive blood loss

A
  • Activate major haemorrhage protocol (signs of hypovolaemic shock)
  • 2 units of O negative blood are made available immediately
  • Blood of the same ABO and Rhesus status is available in 15 minutes
  • Fully cross-matched blood is available in 45 minutes
32
Q

HAEMOSTASIS: List the blood products available for transfusion and outline the rationale for using fresh frozen plasma, cryoprecipitate and platelets

A

Blood products available:

  • Packed red cells: Given with crystalloids/colloids in acute blood loss
  • FFP: Contains all coagulation factors
  • Cryoprecipitate: FFP minus supernatant
  • Albumin: For very fluid overloaded patients, resistant to diuretics
  • Immunoglobulin (IVIG): To prevent infections in hypogammaglobulinaemia or to dampen immune mediated destruction e.g. ITP, GBS

FFP: Coagulation factor replacement in acquired deficiencies e.g. liver disease, TTP, warfarin overdose where vitamin K would be too slow (takes several hours to work)

Cryoprecipitate: Conditions in which fibrinogen is very low e.g. DIC

Platelets: To treat severe thrombocytopenia or prophylactically in pts with bone marrow failure

33
Q

HAEMOSTASIS: Outline the management of a transfusion reaction.

A
  • Monitor every 30 minutes during a transfusion

Types of transfusion reaction and their management

  • Acute haemolytic reaction
    • Features: Increased temp, low BP, agitation, signs of DIC, abdo/chest pain
    • Managment: Stop the transfusion, keep IV line patient with 0.9% saline
  • Allergy/anaphylaxis
    • Simple allergy → slow transfusion, give chlorphenamine with close monitoring
    • Anaphylaxis → stop transfusion, treat
  • Bacterial contamination
    • Features: Rapid onset signs of sepsis and rigors
    • Managment: Stop transfusion, start sepsis 6
  • Tranfusion-related acute lung injury
    • Features: Dyspnoea, white out (bascially ARDs)
    • Management: Stop the transfusion, treat
  • Non-haemolytic febrile transfusion reaction
    • Features: Shivering and fever 0.5-1 hour after starting transfusion
    • Management: Slow transfusion, give antipyretic, monitor closely
  • Fluid overload
    • Features:
    • Managment: Slow or stop transfusion, oxygen and diuretic
34
Q

MISCELLANEOUS HAEMATOLOGY: Outline the clinical features and differential diagnoses of myelofibrosis, polycythaemia rubra vera and essential thrombocythaemia

A

Types of myeloproliferative disorders in which clones of haemopoetic stem cells proliferate in the bone marrow yet retain the ability to differentiate.

Uncontrolled proliferation of a single type fo stem cell. A type of bone marrow cancer. Each has the potential to transform in to AML.

PC: Fatigue, weight loss, nigth sweats, fever

Leads to ‘dry’ bone marrow, due to fibrosis, with subseqeunt boen marrow failure.

Associated with mutations e.g. JAK2

Primary Myelofibrosis

  • Proliferation of haemopoeietic stem cells

Polycythaemia rubra vera

  • Proliferation of erythoid cells
  • Gives a ruddy complexion, splenomgealy and conjunctival plethora
  • Raised Hb of FBC

Essential thrombocythaemia

  • Proliferation of megalokaryocyte cell line
35
Q

MISCELLANEOUS HAEMATOLOGY: Outline the clinical features of aplastic anaemia and describe the laboratory diagnosis and principles of treatment.

A

Aplastic anaemia arises due to failure of the bone marrow, without abnormal infiltrate or bone marrow fibrosis.

Features:

  • Pancytopenia
  • Hypocellular bone marrow

Diagnosis requires at least 2 of the following:

  • Haemoglobin concentration below 100 g/L.
  • Platelet count below 50 x 109/L.
  • Neutrophil count below 1.5 x 109/L.

​Treatment

  • Treatment is based around the degree of cytopenia. Asymptomatic pts do not require treatment
  • Stem cell transplant
  • Immunosuppresive therapy

CP3 (14 decks)

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