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MCHB full > Haematology > Flashcards

Haematology Flashcards

1
Q

INR of 5-8 with no bleeding - action?

A

Omit 1-2 doses warfarin, continue when INR under 5 and reduce subsequent dose

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2
Q

INR of 5-8 with minor bleed- action?

A

Omit warfarin, give Vit K IV, restart warfarin when INR is <5

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3
Q

INR of 5-8 with major bleed - action?

A

Any major bleed (regardless of INR)

= Stop warfarin, give IV vit K and either dried prothrombin complex concentrate or FFP

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4
Q

INR >8 with minor bleed - action?

A

Stop warfarin, give IV vit K (which may need repeating)

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5
Q

INR > 8 with no bleed - action?

A

Stop warfarin, give oral vit K, repeat vit K if still too high after 24 hours

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6
Q

What is the Chadsvasc score where treatment is indicated?

A

> 2 for females

>1 for males

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7
Q

Name 2 indications for LMWH?

A

Prophylaxis of VTE or treatment of thrombolytic events

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8
Q

Name 3 side effects of LMWH?

A

Haemorrhage
HIT (Heparin induced thrombocytopenia) - low platlets
Hyperkalaemia

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9
Q

What should be done about surgical procedures which carry a high risk of bleeding for patient taking warfarin?

A

Stop warfarin 5 days before

If high risk VTE then start LMWH (TREATMENT DOSE) bridging therapy

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10
Q

What should be done about surgical procedures which carry a low risk of bleeding for patient taking warfarin?

A

Can continue warfarin as normal if INR around 1.5-2

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11
Q

How should warfarin be restarted for a post op patient?

A

Restart LMWH and warfarin together
Continue LMWH until INR is in range for 48 hours

(This is done as warfarin gives a transient hypercoaguable state when first started)

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12
Q

What changes to use of LMWH should be considered in renal impairment?

A

Safe to use

LMWH is safest anti-coag in renal impairment

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13
Q

What patient consideration needs to be asked about when prescribing LMWH?

A

Are they able to self-inject?

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14
Q

What MCV is seen in thalassemia?

A

Low MCV (microcytic)

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15
Q

Anaemia of chronic disease and haemolytic anaemia both show what MCV?

A

Normocytic (normal MCV)

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16
Q

Pernicious anaemia shows what MCV/ Hb results?

A

Hb: Low
MCV: High (macrocytic)

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17
Q

What MCV is seen in (a) iron deficiency anaemia (b) folate/ vit B12 deficiency

A

(a) Low MCV (microcytic)

b) High MCV (macrocytic

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18
Q

A 57-year-old woman presents with breathlessness. On further questioning, she also notes fatigue and lethargy. This has been going on for the last year. On examination, the GP notices a lemon tinge to her skin as well as impaired vibration sense in her distal legs and feet.

Given her presentation what is the most likely diagnosis?

A

Pernicious anaemia

A lemon tinge to the skin is associated with pernicious anaemia

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19
Q

What are the features of acute haemolytic transfusion reaction?

A

Mismatched blood group + massive intravascular haemolysis

  • Mins after starting
  • Fever
  • Hypotension
  • Agitation, chest pain
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20
Q

How should acute haemolytic transfuion reaction be treated? (3)

A

Immediate termination of transfusion
Fluid resus
Inform lab

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21
Q

How does an anaphylactic transfusion reaction present?

A

Urticaria
Stridor
Hypotension
Angioedema

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22
Q

How should anaphylactic transfusion reaction be treated?

A

Simple urticaria: Stop transfusion, give antihistamine, resume once syx resolve

Severe: Permenantly stop, IM adrenaline, supportive care. Consider steroids

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23
Q

What is the difference between Haemophillia A and Haemophillia B?

A

A deficiency in FVIII (5x more common)

B deficiency in FIX

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24
Q

How is haemophillia inherited?

A

X-linked recessive (mainly male and NO male-male transmission)

Note acquired haemophillia is also possible

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25
Q

How does haemophillia present?

A

Deep muscle bleeds and haemarthrosis are characteristic

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26
Q

How do you diagnose haemophillia on bloods?

A

Low factor 8/9
Increased APTT

Normal bleed time (raised in vWB disease)
Normal prothrombin time (raised in vitK deficiency)
Normal platelets

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27
Q

How do you manage haemophillia, how does this change if the patient is bleeding?

A

Avoid NSAIDS and IM injections

Minor bleed - Pressure, elevation and DDVAP (desmopressin)
Mod - Replace F8/9 to 50% normal levels
Severe - Replace F8/9 to 100% normal levels

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28
Q

How do you distinguish between haemophillia, vitk deficiency and von willibrand disease on bloods?

A

All have raised APTT

Haemophillia - PT and bleed time are normal
VonWillibrand - PT normal but bleed time raised
VitK deficiency - PT raised but bleed time normal

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29
Q

What are the characteristics of vonWillibrand disease? (Inheritance and incidence)

A

Deficiency in vWFactor

Autosomal dominant!

Up- to 1% incidence, most common in females

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30
Q

What are the presenting features of vonWillibrand disease?

A

Bleeding from mucus membranes

(Epistaxis, post surgery, menorrhagia

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31
Q

How do you manage bleeding in a patient with vWD?

A

1) DDAVP (desmopressin)
2) vWF/ VIII concentrates

If minor bleed can use tranexamic acid

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32
Q

How does vWD show on bloods?

A

Raised APTT
Raised bleed time
Normal PT

Low FVIIIc (as VWF normally binds to FVIII)

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33
Q

Name three microcytic anaemia’s?

A

Iron deficiency
Thalassaemia
Sideroblastic anaemia

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34
Q

Name three normocytic anaemias?

A

Anaemia of chronic disease
Anaemia due to CKD
Aplastic anaemia
Haemolytic anaemia

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35
Q

Name three macrocytic anaemias?

A

B12 or folate deficiency (including pernicious)
Alcohol or liver disease
Anaemia of pregnancy
Hypothyroidism

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36
Q

What is Fanconi anaemia?

A

Autosomal recessive aplastic anaemia

  • Causes pancytopenic marrow failure
  • Increases cancer susceptibility
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37
Q

What is pernicious anaemia?

A

Antibodies to gastric parietal cells or intrinsic factor
- Don’t absorb B12
(Associated with other autoimmune like thyroid, diabetes, rheumatoid)

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38
Q

How is pernicious anaemia treated?

A

3 months of vitB12 injections

Folic acid suppliment may also be needed

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39
Q

What is sickle cell anaemia and how is it inherited?

A

Autosomal recessive

- Abnormal synthesis of HbS chain, more common in africans and presents in first 6 months or when exposed to hypoxia

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40
Q

How should iron deficiency anaemia be treated?

A

Ferrous sulphate for 3-6 months

200mg BD or TDS

41
Q

Name 3 complications of sickle cell anaemia?

A

Occlusion of microvessels (joint pain, tachypnoea, abdo pain)
Aplastic crisis - severe drop in Hb over 1 wk, commonly precipitated by parvovirus B19
Sequestation crisis - Sudden enlargement of spleen (low Hb and hypovolemic shock)

42
Q

How do you treat sickle cell anaemia?

A

Avoid cold, dehydration and exhuation

  • Transfusions
  • May need AB prophylaxis
  • May need marrow transplants
43
Q

What are the 4 main leukaemia’s?

A

ALL - Kids (2-5yrs) <20% blast cells in bone marrow
AML - Median age = 70. Most common acute leukaemia in adults
CML - Peak 60-65, associated with philedelphia chromosome
CLL- Peak 72 years. Most common leukaemia in the western world.

44
Q

Name 3 presenting features of a leukaemia?

A

Pancytopenia

  • Fatigue
  • Fevers and night sweats
  • Weight loss, enlarged spleen
  • Bone pain, lumps, swollen glands
  • Bruising and bleeding
45
Q

How are leukaemia’s diagnosed?

A

Blood film

Bone marrow aspiration

46
Q

How could you distinguish between an acute and a chronic leukaemia?

A

Acute tends to be more symptomatic with depleted white cells. Tend to have more blast cells

Chronic tends to be found incidentally with raised white cells

47
Q

How do lymphoma’s tend to present?

A

CANCER OF LYMPHOCYTES
Painless, slowly progressive lymphadenopathy (neck, groin, armpit, supraclavicular).
Possible SOB and cough from lymphadenopathy in chest

B symptoms (weight loss >10%, fever >38 or night sweats) - suggests higher grade

48
Q

What are the three main types of lymphoma?

A

(Usually B cell)
Hodgkins - Characterised by reed-sternberg cell. Age >70 is most common (better prognosis)
Non-hodgkins - 5x more common. Usually presents >50 although is a diverse group of diseases
Burkitt’s - Children (5-8 ) of afro-carribean most common.

49
Q

What is the most common type of hodgkin’s lymphoma?

A

Nodular sclerosing

50
Q

Which type of hodgkin’s lymphoma carries the best prognosis?

A

Lymphocyte predominant

51
Q

Which type of hodgkin’s lymphoma carries the worst prognosis?

A

Lymphocyte depleted

52
Q

What staging system is used for lymphoma’s?

A 
Ann Arbour 
S1- One LN group affected
S2- Two or more affected, same side of diaphragm
S3- Both sides of diaphragm
S4- Organ spread
53
Q

What is the best way to diagnose lymphoma?

A

Excisional biopsy of LN (better than FNA)

54
Q

What features of LN’s suggest a more sinister pathology?

A

> 1cm
Round and deep
Painless, hard, rubbery and non-mobile

55
Q

What is a myeloma? Who does it most commonly affect?

A

Proliferation of plasma cells
- 2nd most common haem malignancy (after lymphoma)

Most common >age70, in afro-carribean and in men

56
Q

Name 4 presenting features of a myeloma?

A 
CRAB
C- Calcium raised
R- Renal failure
A- Anaemia
B- Bone lesions (commonly back pain but also fractures)
57
Q

How is myeloma diagnosed?

A

(In GP do bence jones protein in urine)

1st: Serum electrophoresis
2nd: Bone marrow biopsy

58
Q

What protein is commonly found in the urine of patient’s with myeloma?

A

Bence jones protein

Can show Myeloma or Waldenstom’s macroglobulinaemia

59
Q

How is myeloma treated?

A

Tx of complications

  • Analgesia
  • Tranfusion if Hb <8
  • Give EPO if needed
  • Chemo can prolong life but often disease becomes refractory to Tx
60
Q

What is average life expectancy for a patient with myeloma?

A

3-4 years

Death commonly due to infection of renal failure

61
Q

Name 4 complications of myeloma?

A
  • Hypercalcemia (rehydrate w fluid then give bisphosphonates)
  • Spinal cord compression (give high dose dext and local radiotherapy)
  • Hyperviscosity (note reduced cognition, visual changes and bleeding)
  • Acute renal failure (fluids/ dialysis)
62
Q

What is MGUS, how does it present?

A

Monoclonal gammopathy of unknown significance
- Like a ‘pre-myeloma’, carries 1% annual risk of developing myeloma

Presentation: Low paraprotein (<30g/L), <10% bone marrow plasma cells. No organ or tissue damage

63
Q

What is DIC?

A

Innapropriate activation of thrombin and coagulation mechanism leading to thrombosis (and more commonly haemorrhage as clotting factors run out)

  • Usually happens 2ndary to another pathology rather than as a primary event
64
Q

Name 5 conditions which may be complicated by DIC?

A
  • Infections - i.e. meningococcal septicaemia
  • Malignancy (especially leukaemia)
  • Trauma/ burns
  • Pregnancy complications (abruption, HELP)
  • Incompatible blood transfusion
65
Q

How does DIC present?

A

Bleeding from at least three unrelated sites (ENT, GI, resp, cannula sites etc)
Confusion
Fevers
- Petechiae, purpura

66
Q

What are the 4 main investigations for DIC?

A

Prothrombin time (PT) - Low
APTT - Low
Platelets - Low
Fibrinogen - Low

(If 2 are +ve, diagnosis possible, 3= likely, 4 = extremely likely)

67
Q

How is DIC treated?

A

Correct underlying cause

  • FFP and platelets depending on how unwell they are
68
Q

What is in cryoprecipitate?

A

Cryoprecipitate contains factor VIII, fibrinogen, von Willebrand factor and factor XIII

69
Q

What is the biggest risk factor for Hodgkins lymphoma in teenagers?

A

Epstein barr virus

70
Q

What are the normal Hb reference ranges?

A

Men: 13.5-18
Women: 11.5-16

71
Q

What is the most common inherited thrombophillia?

A

Factor V Leiden

72
Q

What is the single most important factor in determining whether cryoprecipitate should be given?

A

Fibrinogen level (if low give cryo)

73
Q

Name 2 drugs which can cause a macrocytic anaemia?

A

Methotrexate
Trimethoprim
(Due to B12 deficiency)

74
Q

What blood results are seen in IDA?

A 
Low iron 
Low ferritin (as that stores iron in cells)
Low transferrin saturation (as trying to transport more)
High total iron binding capacity (as trying to make the most of iron which is there)
75
Q

What blood results are seen in haemochromotosis?

A

High iron
High transferrin saturation
High ferritin
Low total iron binding capacity

76
Q

What is ferritin? What is transferin?

A 
Transferin = transfers iron around the blood
Ferritin = stores iron in cells
77
Q

What blood results are seen in anaemia of chronic disease?

A

Raised ferritin

Normal iron, low transferin sat, low TIBC

78
Q

How is B12 deficiency treated?

A

Hydroxycobalmin

Given once every other day for 2 weeks, then 3 monthly for life

79
Q

What blood tests will be raised if there a haemolytic process occuring?

A

Raised reticulocytes
Raised bilirubin
Raised LDH

(Do a blood film)

80
Q

How is thalassaemia treated?

A

Minor - often asymptomatic

Major = Lifelong transfusions + desferrioxamine (binds excess iron) as repeated transfusions can cause iron overload

81
Q

How can bleeding disorders be characterised?

A

Vascular - CTD’s (ehler-danlos etc.)
Platelet - vWD, ITP, TTP (thrombotic thrombocytopenic purpura), DIC
Coagulation - Haemophillia (A+B), liver disease, vitK deficiency/ warfarin

82
Q

What do each of PT and APTT measure?

A

PT (INR) = Extrinsic pathway

APTT = Intrinsic pathway

83
Q

When is bleed time raised?

A

When platlets are affected (so bleed time is raised in vWD etc but NOT in haemophillia or warfarin)

84
Q

Haemophillia will raised which coagulation parameters?

A 
Raised APTT (as factor 8(A) and 9(B) which are just in the intrinisic pathway)
Normal PT (as the extrinsic pathway is completely unaffected)
Normal platelets and bleed time
85
Q

VonWillibrand disease will change coagulation parameters how?

A

Raised bleed time (as disorder of platelet agregation) and will give raised APTT (as also affect Factor 8)

  • Normal PT and normal platelets (as not low platelets, they just don’t clot properly)
86
Q

DIC will change coagulation parameters how?

A 
APTT, PT, BT all raised 
Platelets low (as all are being used up)

(Also D-dimer raised as lots of degradation products)

87
Q

How does ITP present?

A

Immune thrombocytopenic purpura
Often child with recent viral infection

Bloods: Low platelets and raised bleed time
(PT and APTT normal as only platelets affected)

88
Q

How is ITP treated?

A

Give steroids (not platelets as they are just been eaten up, unless life threatening).

89
Q

How does TTP present?

A

Thrombotic thrombocytopenic purpura - FATRN
(Low platlets with kidney or neuro involvement)
Fever,
Anaemia
Thrombocytopenia
Renal or
Neuro involvement

90
Q

When do you give a transfusion of RBC?

A

When Hb <70

Or when < 80 and cardiac disease

91
Q

Auer rods suggest what diagnosis?

A

AML (most common acute leukaemia in adults)

92
Q

Smudge cells suggest what diagnosis?

A

CLL (most common leukaemia in western world)

93
Q

How do you prevent tumour lysis syndrome, what is it commonly associated with?

A

Allopurinol

Most commonly associated with Burkitts lymphoma

94
Q

Name 3 common causes of splenomegaly?

A

Infection (EBV, malaria)
Malignancy (lymphoma, leukaemia)
Portal hypertension
Sickle cell disease

95
Q

Philadelphia chromosome is most commonly associated with which leukaemia?

A

CML

96
Q

In the context of anaemia, what does a raised LDH suggest?

A

Cell lysis

Therefore haemolytic anaemia

97
Q

What is polycythemia ruba vera and how does it present?

A

Polycythaemia vera is a neoplasm of the bone marrow which results in the production of excessive red blood cells. The classic symptom of this condition is intense itching which usually occurs after exposure to hot water or hot and humid weather.

98
Q

What is Factor V Leiden and how does it present?

A

Most common inherited thrombophillia (defect in Protein C)

  • Presents as recurrent venous thrombosis
99
Q

How does antiphospholipid syndrome present?

A

Venous + arterial thrombosis

Paradoxical rise in APTT (helps distinguish from Factor V Leiden etc)

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