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Phase 2 v2 > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the clinical presentation of anaemia in general?

A

Anaemia:

  • Fatigue
  • Low energy
  • Pallor
  • Dyspnoea on exertion.
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2
Q

What are the specific clinical signs/symptoms of iron deficiency anaemia?

A

Signs:

  • Restless leg syndrome.
  • Glossitis
  • Angular stomatitis.
  • Nail spooning/flattening.

Symptoms:

  • Unusual cravings for non-food items.
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3
Q

What is the histological presentation of:

Iron deficiency anaemia?

Pernicious anaemia?

Folate-deficiency anaemia?

Haemolytic anaemia?

Sickle cell anaemia?

A

IDA - Microcytic, hypochromic.

PA - Macrocytic megaloblastic.

FDA - Macrocytic megaloblastic.

HbA - Normocytic, normochromic.

HbS - Sickled cells

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4
Q

What are the main risk factors for iron deficiency anaemia?

A
  • Pregnant.
  • Vegan/vegetarian.
  • Menorrhagia.
  • Coeliac.
  • Excessive NSAID use (causes peptic ulcers).
  • CKD (low erythropoietin).
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5
Q

What are the diagnostic tests for iron deficiency anaemia?

A
  • Low serum iron and low serum ferretin.
  • FBC: Low Hb
  • MCV: Low
  • MCHC: Low
  • Blood smear: Microcytic, hypochromic.
  • Low reticulocytes.
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6
Q

What is the treatment for iron deficiency anaemia?

A
  • 1st line: Ferrous sulfate (orally).
  • 2nd line: IV iron (used if ferrous sulfate is intolerated or the individual has IBD.)
  • RBC transfusion. Used if the individual begins to present with symptoms of CV compromise (chest pain, dyspnoea on rest).
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7
Q

What is pernicious anaemia?

A
  • Autoimmune disorder.
  • Destruction of the parietal cells of the stomach (that secrete IF) and production of intrinsic factor antibodies.
  • Causes malabsorption of B12, as If is required for the cotransportation process used for B12 absorption.
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8
Q

What are the specific signs/symptoms of pernicious anaemia?

A

B12 deficiency - Neurological problems:

Abnormal gait

Decreased vibration sense

Peripheral neuropathy

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9
Q

What are the risk factors for pernicious anaemia?

A
  • Vegan.
  • Over 65.
  • Metformin.
  • PPI (omeprazole) or H2 antagonist (famotidine).
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10
Q

What are the investigations used to confirm diagnosis of pernicious anaemia?

A

FBC - MCV increased.

Blood film - Shows macrocytic, megaloblastic RBCs with hypersegmented neutrophils. (SAME AS FOLATE-DEFFICIENCY ANAEMIA).

Intrinsic factor antibody test - Presence of these antibodies proves pernicious anaemia.

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11
Q

What is the treatment for pernicious anaemia?

A
  • Give hydroxocobalamin, a B12 analogue (1st line)
  • If there are neuro symptoms, refer to neurology/haematology.
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12
Q

What are the risk factors for folate-deficiency anaemia?

A
  • Pregnancy/lactation.
  • Old age.
  • Chronic alcohol abuse.
  • Low folate diet.
  • FH.
  • Coeliac disease.

Use of certain drugs:
- Trimethoprim.
- DMARDS (sulfasalazine, methotrexate).
- Anticonvulsants.
(therefore these drugs are contraindicated in pregnancy).

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13
Q

What are the signs/symptoms specific to haemolytic anaemia?

A

Limited specific signs.

Potentially there will be:

  • Jaundice (due to increased bilirubin from RBC breakdown).
  • Splenomegaly.
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14
Q

What are the investigations used to diagnose folate-deficiency anaemia?

A
  • FBC. Raised MCV and MCHC.
  • Blood film. Macrocytic, megaloblastic cells with hypersegmented neutrophils.
  • Serum folate: 1st line screening tool.
  • RBC folate: Gold standard. More sensitive than serum folate, but more expensive/complex.
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15
Q

What are the signs/symptoms specific to folate deficiency anaemia?

A
  • NO NEUROLOGICAL SYMPTOMS (would be seen in B12 deficiency anaemia).
  • Potentially glossitis, and angular stomatitis if severe.
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16
Q

What is the treatment for folate-deficiency anaemia?

A
  • Folic acid oral (1st line).
  • Consider RBC transfusion if severely anaemic.
  • Women planning/currently pregnant should be taking folic acid to reduce risk of neural tube defects.
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17
Q

What is haemolytic anaemia?

A

A number of conditions that occur due to increased destruction of RBCs.

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18
Q

What type of anaemia is haemolytic anaemia?

A
  • Normocytic usually.
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19
Q

What are the differentials for haemolytic anaemia?

A
  • Blood loss.
  • Transfusion reaction.
  • Underproduction anaemia. Caused by reduced production of RBCs rather than increased breakdown. Will therefore have a low reticulocyte count (would be high in haemolytic anaemia).
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20
Q

What are the risk factors for haemolytic anaemia?

A
  • FH.
  • Autoimmune disorders (especially SLE).
  • CLL
  • Cephalosporins.
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21
Q

What are the investigations used to diagnose haemolytic anaemia?

A

FBC - Reduced Hb

MCHC - Increased MCHC due to high amount of reticulocytes.

Reticulocyte count - raised

Blood film - Generally normocytic, but presence of abnormal RBC’s can help diagnose the specific type of haemolytic anaemia.

Coomb’s test - If positive indicates an autoimmune cause of haemolytic anaemia.

Consider ANA if SLE suspected.

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22
Q

What is the treatment for haemolytic anaemia?

A

Blood transfusions + folic acid.

  • If coomb’s test +ve, give prednisolone (reduces production of autoantibodies that drive RBC breakdown in autoimmune haemolytic anaemia).
  • If caused by a drug (commonly cephalosporins) give prednisolone and discontinue the drug.
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23
Q

What is sickle cell anaemia?

A
  • Hereditary deformation of RBC’s as a result of faulty Hb molecule formation.
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24
Q

What is the clinical presentation specific to sickle cell anaemia?

A
  • Vaso-occlusion. Early childhood acute pain in the hands and feet due to small vessel occlusion.
  • In adults, pain in the long bones, ribs, spine and pelvis too.
  • OFTEN SYMPTOMS OF ANAEMIA DO NOT APPEAR AS HbS HAS A LOW OXYGEN AFFINITY.
  • If they do appear, anaemic symptoms are:
  • Tiredness
  • Fatigue
  • Dyspnoea
  • Palpitations
  • Headache
  • Faintness
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25
Q

What is the pathophysiology of sickle-cell anaemia?

A
  • Changes in sequence of haemoglobin subunit causes faulty structure.
  • Distorts erythrocyte shape, making them sickle shaped.
  • Sickle cell RBC’s block vessels easily, and are easily destroyed.
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26
Q

What is the investigation used for sickle cell anaemia?

A
  • Usually identified in neonatal screening.
  • Otherwise, identified by presence of sickle cells on blood film.
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27
Q

What is the treatment for sickle cell anaemia?

A
  • Anaphylactic penicillin until 5 years old (children). Because they are at substantially increased risk of invasive pneumococcal infection.

- Hydroxycarbamide. Manages the pain.

  • Potentially blood transfusion.
  • Bone marrow stem cell transfusion if disease severe - still a very new treatment.
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28
Q

What is the alternative name for folic acid?

A

B9

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29
Q

What is a DVT?

A
  • Development of a blood clot in a major deep vein.
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30
Q

What is the clinical presentation of a DVT?

A
  • Calf swelling.
  • Localised pain and redness.
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31
Q

What are the risk factors for a DVT?

A
  • Bedridden.
  • Cancer.
  • Older age.
  • Recent long-haul travel.
  • Hypercoagulation disorder.
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32
Q

How is the likelihood of a DVT assessed and subsequently what tests are done?

A

Use Well’s score:

  • If Well’s <2: Do a D-dimer. If +ve, move on to venous ultrasound.
  • If Well’s ≥2: Straight to venous ultrasound.
33
Q

What is the treatment for a DVT?

A
  • Apixiban (anticoagulant) for at least 3 months.
34
Q

What is the main complication associated with DVT?

A

Pulmonary embolism (PE).

35
Q

What is polycythaemia vera?

A
  • A Philadelphia chromosome -ve myeloproliferative disorder.
  • Characterised by erythrocytosis.
  • Often also causes thrombocytosis, leukocytosis and splenomegaly.
36
Q

What genetic mutation is commonly linked to polycythaemia vera?

A
  • JAK2 mutation.
37
Q

When is polycythaemia vera considered?

A
  • Patient over 40 presenting with thrombosis/haemorrhage.
38
Q

What are the signs/symptoms of polycythaemia vera?

A

Signs:

  • Thrombosis (MI, stroke, DVT, PE)
  • Erythromelalgia (red fingers, palms and toes).
  • Splenomegaly.

Symptoms:

  • Headache.
  • Pruritus.
  • Fatigue.
39
Q

What are the investigations used for polycythaemia vera, and what are the usual findings?

What is the genetic test used?

A
  • FBC: Raised Hb, WCC, platelets.
  • Low erythropoietin (-ve feedback to erythrocytosis).
  • Genetic test for JAK2 mutation: +ve.
40
Q

What is the treatment for polycythaemia vera?

A
  • Low dose aspirin.
  • Phlebotomy (500ml of blood replaced with saline 2x per week).
    IF HIGH RISK: Hydroxycarbamide (cytoreductive therapy).
41
Q

What are the two main platelet disorders I need to be aware of?

A
  • Immune thrombocytopenic purpura (ITP)
  • Thrombotic thrombocytopenic purpura (TTP)
42
Q

What is immune thrombocytopenic purpura?

A
  • Haematological disorder characterised by an ISOLATED low platelet count (thrombocytopenia).
43
Q

What are the key signs/symptoms for immune thrombocytopenic purpura?

A

Symptoms: Fatigue.
Signs: Bleeding (esp. gums), bruising, petechiae (small purple/red spots on the skin).

44
Q

What are the investigations used and the findings in suspected ITP?

A
  • FBC. Isolated low platelets (thrombocytopenia).
    NOTE: If history involves heavy bleeding, Hb may also be slightly low. However, this is not a requirement for diagnosis.
  • Blood smear. No evidence of myelodysplasia.
45
Q

What is the treatment for ITP?

A
  • Corticosteroids (prednisolone).
46
Q

What is thrombotic thrombocytopenic purpura?

A
  • Thrombocytopenia AND haemolytic anaemia.
47
Q

What are is the diagnostic pentad for TTP?

A

Characteristic pentad:

  • Thrombocytopenic purpura.
  • Microangiopathic haemolytic anaemia.
  • Acute renal insufficiency.
  • Neurological abnormality.
  • Fever.
48
Q

What are the investigations/results for suspected TTP?

A

FBC: Low platelets (thrombocytopenia) and low haemoglobin (anaemia).

Blood smear: schistocytes present (red blood cell fragments due to the microangiopathic anaemia).

Raised urea/creatinine: Acute renal insufficiency.
Urine analysis: Proteinuria.

49
Q

What is the treatment for TTP?

A
  • Plasma exchange.
  • Prednisolone (corticosteroids).
50
Q

What are the 4 main types of leukaemia?

A
  • ALL. Acute lymphoblastic leukaemia.
  • CLL. Chronic myeloblastic leukaemia.
  • AML. Acute myeloid leukaemia.
  • CML. Chronic myeloid leukaemia.
51
Q

What are the key defining characteristics of ALL?

A
  • Childhood leukaemia. (Under 20).
  • Cancer of lymphoid progenitors.
52
Q

What are the key defining characteristics of CLL?

A
  • Smudge cells on blood film.
  • Cancer of B-cells (lymphoblastic lineage).
53
Q

What are the key defining characteristics of AML?

A
  • Auer rods inside myeloblasts on blood film.
  • Develops when CML progresses.
  • Cancer of myeloid progenitors.
54
Q

What are the key defining characteristics of CML?

A
  • Philadelphia chromosome strongly associated.
  • Eventually progresses to AML.
  • Cancer of myeloid progenitors.
55
Q

What are the key investigations used when leukaemia is suspected?

A
  • FBC + differential.
  • Blood smear.
  • Bone marrow biopsy.
56
Q

What are the generic symptoms for leukaemia?
What are the two symptoms that can differentiate leukaemia from other cancers?

A
  • Weight loss.
  • Fatigue.
  • Fever.
  • Pallor.

KEY SYMPTOMS SUGGESTIVE OF LEUKAEMIA RATHER THAN OTHER CANCER:

  • Petechiae.
  • Abnormal bleeding.
57
Q

What are the treatments used for leukaemia?

(2 specific named drugs)?

A
  • Rituximab (immunotherapy). CD20-targeting monoclonal antibody. Used for ALL, CLL.
  • Imatinib (tyrosine kinase inhibitor). Used for CML.
  • Stem cell transplant is an option for all leukaemia.
  • Chemotherapy and immunotherapy are mainstays of treatment.
58
Q

What is haemophillia?

A
  • Bleeding disorder that results from the deficiency of a coagulation factor.
59
Q

What is the difference between haemophilia A and B?

A

Haemophilia A - reduction/absence of factor VIII.
Haemophilia B - reduction/absence of factor IX.

60
Q

What is the inheritance pattern of haemophilia?

A
  • X linked recessive.
61
Q

What is the typical clinical presentation of haemophilia?

A
  • Male w/ family history
  • Recurrent and/or severe bleeding.
  • Epistaxis
  • Gum bleeding.
  • Easy bruising.
62
Q

What are the investigations used for haemophilia?

A
  • aPPT (intrinsic pathway measure). Will be raised.
  • Factor VIII/IX assay. Will show decrease/absence of one of the factors, and differentiate types A and B.
63
Q

What is the treatment for haemophilia?

A
  • Factor VIII (type A) or factor IX (type B) concentrate given once daily.
64
Q

What is malaria?

A

A parasitic infection of the erythrocytes, usually caused by plasmodium falciparum.

65
Q

How is malaria transmitted?

A
  • Female mosquito bites.
  • Can also be transmitted via blood transfusion/organ transplant.
66
Q

What is the typical clinical presentation of malaria?

A
  • RECENT TRAVEL HISTORY.
  • Fever
  • Chills
  • Headache
  • Arthralgia/myalgia.
67
Q

What diagnostic testing is used for malaria?

A
  • Rapid diagnostic testing (skin-prick) is first line, as it is cheap and quick. However, only reliable in testing for P. Falciparum, not other types of plasmodium.
  • Light microscopy with giemsa stained blood film. GOLD STANDARD.
68
Q

What is the treatment for malaria?

A
  • Piperaquine infusion (anti-malarial drug).
69
Q

What is multiple myeloma?

A
  • Malignant disease of the bone marrow plasma cells.
70
Q

What is the clinical presentation of multiple myeloma?

A

REMEMBER “CRAB”:

  • hyperCalcaemia
  • Renal impairment
  • ANAEMIA
  • BONE PAIN
71
Q

What are the risk factors for MM?

A
  • Abnormal free light-chain ratio.
  • FH
  • Radiation exposure.
72
Q

What is the epidemiology of multiple myeloma?

A
  • Peak presentation at 70 years old.
73
Q

What are the investigations used for multiple myeloma?

A
  • Bone marrow biopsy. Will show plasma cell infiltration in the bone marrow (gold standard).
74
Q

What is the treatment for multiple myeloma?

A

Chemotherapy (Thalidomide) + dexamethasone (corticosteroids).

  • Stem cell transplant (if illegible).
75
Q

What are the two types of lymphoma and how are they differentiated?

A
  • Hodgkins lymphoma. Containts Reed-sternberg cells.
  • Non-hodgkins lymphoma. Doesn’t contain Reed-sternberg cells.
76
Q

What is the clinical presentation of lymphoma?

What are aspects of clinical presentation are specific to HL?

A

Low grade lymphoma may be asymptomatic.

Presentation:

  • LYMPHADENOPATHY.
  • Fever
  • Fatigue
  • Weight loss
  • Night sweats

Specific to HL:

  • Pruritus.
  • Alcohol-triggered lymph node pain.
  • MORE COMMON IN YOUNG ADULTS THAN NHL.
77
Q

What are the key investigations for suspected lymphoma?

A
  • FBC with differential. Thrombocytopenia (Low Platelets), leukocytosis (Increased WCC). LOW HAEMOGLOBIN IF HODGKINS.
  • Lymph node biopsy. Differentiates between HL and NHL.
  • Full body CT. Look for metastases.
  • Lactate dehydrogenase. Level of elevation is an important prognostic factor.
78
Q

What is the treatment for non-Hodgkins lymphoma?

A
  • Chemo with R-CHOP regimen.
  • Rituximab, cyclophosphamide, Doxorubicin, vinicristine and prednisolone.
79
Q

What is the treatment for Hodgkins lymphoma?

A
  • Chemo (ABVD regiment).
  • Radiotherapy.

Phase 2 v2 (14 decks)

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