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Haem Flashcards

1
Q

What risk assessment is used for stroke prevention (anticoagulants)?

A

CHA2DS2VASc

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2
Q

What does the CHA2DS2VASc score stand for?

A

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age >= 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1
S Sex (female) 1

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3
Q

What must a woman or man score in order to be considered for or offered anticoagulation?

A

Men - all men with a score = 1 are considered for anticoagulation

Female - women are offered anticoagulation if they have a score >= 2 (women score 1 for being female)

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4
Q

List direct factor Xa inhibitors (anticoaglants)

A

apixaban, rivaroxaban

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5
Q

What is the reversal agent for factor Xa inhibitor?

A

andedanex alfa

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6
Q

List direct thrombin inhibitor

A

dabigatran, argatroban

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7
Q

What is the reversal agent for the direct thrombin inhibitor dabigatran?

A

idarucizumab

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8
Q

What anticoagulant is used in pregnancy?

A

heparin rather than warfarin as none teratogenic

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9
Q

What are the 2 different types of heparin available?

A

unfractionated - contains both LMWH and HMWH

fractionated - contains only LMWH

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10
Q

What is dalteparin (LMWH) mechanism of action?

A

potentiates antithrombin so increased inhibition of thrombin and factor 10a

preferred over UFH as reduced risk of HIT - UFH also inhibits factor 10

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11
Q

What is the reversal agent for LMWH?

A

there isn’t one - in an emergency can use protamine (partial reversibility)

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12
Q

What is the reversal agent for UFH?

A

protamine

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13
Q

What is an important consideration to make when giving unfractionated heparin?

A

it requires APTR (activated partial thromboplastin time ratio) monitoring

this is because of the risk of HIT (heparin induced thrombocytopenia) - depletion of platelet count over 5-10 days, high risk of thrombosis (due to antibodies interacting with platelets and heparin)

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14
Q

What is the mechanism of action for warfarin?

A

it reduces the production of vit K dependent factors

inhibits epoxide reductase whoch reduces the production of active vit K (hydroquinone)

therefore, there is a reduction in clotting factors 2, 7, 9 and 10 (and protein C and S)

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15
Q

What is an important consideration to make when administering warfarin to a patient?

A

they require ongoing monitoring - use INR (PT - extrinsic pathway is important to look at)

PT is sensitive to changes in factor 7 which has the shortest half life

in warfarin patients, their PT should be double a normal patient

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16
Q

What to do with patients on anticoagulation in specific emergencies (high INR, bleeding, urgent surgery)?

A
  1. fully reverse the anticoagulant
  • if warfarin give vit K
  • if heparin or LMWH give protamine
  • if dabigatran give idarucizumab
  • if factor Xa inhibitor (apixaban, rivaroxaban) give andexanet alfa
  1. prothrombin complex cocentrate
  2. fresh frozen plasma
  3. don’t restart anticoagulants until INR <5
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17
Q

What are the different blood products?

A
  • packed red cells
  • fresh frozen plasma
  • platelets
  • cryoprecipitate
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18
Q

What suspension are red cells contained within in packed red cells?

A

SAGM ( saline, adenine, glucose, manitol)

Remember GASM

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19
Q

Where do platelet blood products come from?

A

adult pool of platelets from 4 donors

suspended in the plasma of 1 donor

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20
Q

what does cryoprecipitate contain?

A

factor 8, VWF, fibrinogen

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21
Q

what are the 4 different blood groups and what antibodies are present in the plasma?

A

A - contains A antigens, B antibodies

B - contains B antigens, A antibodies

AB - contains A and B antigens, no antibodies

O - contains no antigens, A and B antibodies

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22
Q

which blood group is the universal donor?

A

group O

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23
Q

which blood group is the universal acceptor?

A

group AB

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24
Q

what is the rhesus blood group?

A

describes the presence or absence of rhesus antigen on the surface of RBCs

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25
Q

can Rh -ve blood receive Rh +ve blood?

A

no as Rh -ve has abs against Rh

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26
Q

what blood group is emergency or flying blood?

A

O Rh -ve

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27
Q

what protocol is used for managing a massive haemorrhage?

A

CODE RED

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28
Q

what 3 criteria determine whether a code red needs to be declared?

A
  • systolic blood pressure <90 mmHg
  • unresponsive to fluid bolus
  • suspected or confirmed massive haemorrhage
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29
Q

what 2 blood products does the code red pack A contain?

A

packed red cells and FFP

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30
Q

what 4 blood products does the code red pack B contain?

A

packed red cells
FFP
platelets
cryoprecipitate

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31
Q

what is the difference in pack A and B blood products in code red vs trauma?

A

in trauma, RBC and FFP are in equal concentrations

whereas in code red - give 2 more units of RBC than FFP

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32
Q

What is a transfusion reaction and how can it be classified?

A

any adverse event that occurs because of a blood transfusion

timing:

  • acute (during or within 24 hours of blood transfusion)
  • delayed (occurring more than 24 hours after transfusion)
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33
Q

List the types of acute transfusion reactions

A
  • acute haemolytic
  • febrile non-haemolytic
  • urticarial
  • anaphylactic
  • transfusion-related acute lung injury (TRALI)
  • transfusion-associated circulatory overload (TACO)
  • acute hypotensive
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34
Q

List the types of delayed transfusion reactions

A
  • delayed haemolytic
  • post-transfusion purpura
  • graft-versus host disease (GVHD)
  • transmission of infectious diseases
  • iron overload
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35
Q

List the types of delayed transfusion reactions

A
  • delayed haemolytic
  • post-transfusion purpura
  • graft-versus host disease (GVHD)
  • transmission of infectious diseases
  • iron overload
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36
Q

What is an acute haemolytic reaction?

A

caused by alloantibodies against transfused red cells

most dangerous immunological complication of transfusion

often due to clerical error

high risk of morbidity and mortality (renal failure, DIC)

37
Q

What are febrile non-haemolytic transfusion reactions?

A
  • 1-2% patients develop a febrile reaction
  • due to abs in patient plasma reacting against proteins in donor blood
  • as a result blood is now leucodepleted
38
Q

how does someone with a febrile non-haemolytic reaction present and how to manage?

A

fever with/out rigors 30-60 mins after start of unit, with/out rash

stop transfusion and give antipyretic with/out piriton

39
Q

What reactions will usually present after a small volume of blood transfusion?

A

anaphylactic and haemolytic reactions

40
Q

what signs and sx indicate a mild acute transfusion reaction?

A

fever - 1-2 degrees
urticaria
rash
pruritus

41
Q

what signs and sx indicate a severe acute transfusion reaction?

A 
pyrexia, rigors 
hypotension
loin/back pain
resp distress 
dark urine 
severe tachy
DIC
42
Q

what to do in a severe transfusion reaction?

A
  • if patient has dyspnoea secure airway give O2 (nebulise and give b2 agonist if wheeze)
  • if hypotensive, keep patient supine and elevate leg
43
Q

what investigations should be organised for fever and rigors in transfusion reaction?

A

DAT, LDH, haptoglobin
blood cultures
coag screen

44
Q

what is transfusion related acute lung injury (TRALI)?

A
  • serious complication of blood transfusion
  • due to interaction of specific donor leucocyte abs with recipient leucocytes
  • onset: 1-2 hours after transfusion
  • full manifestation: at 1-6 hours
  • presents similarly to LVF, ARDS (SOB, hypoxia, Pulm Oed)
45
Q

How to manage TRALI?

A
  • admit to ICU
  • aggressive ventilatory support
  • haemodynamic support
  • due to microvascular injury
46
Q

what is transfusion associated circulatory overload (TACO)?

A

this is a serious transfusion related reaction where pulmonary oedema develops primarily due to volume excess or circulatory overload

it is associated with high mortality

47
Q

what is the TACO checklist?

A

a risk assessment for all patients over 50 receiving a blood transfusion

questions to ask include:

  • does the patient have HF, CCF, aortic stenosis, left ventricular dysfunction
  • does the patient have pulmonary oedema
  • does the patient have peripheral oedema or on fluids
48
Q

what can be given to a patient at risk of TACO but requires a blood transfusion?

A
  • transfuse one unit of red cells and review anaemia sx
  • measure fluid balance
  • give prophylactic abx
  • monitor vitals carefully and O2 sats
49
Q

What are the features of TRALI vs TACO?

A

TRALI = hypoxia, fever, hypotension

TACO = pulmonary oedema, hypertension

50
Q

What is disseminated intravascular coagulation?

A

describes uncontrolled haemostasis (increased clotting and increased bleeding)

there is activation of coagulation pathways leading to the formation of intravascular thrombi and depletion of platelets and clotting factors

thrombi formation leads to organ ischaemia and multi-organ failure

depletion of platelets and clotting factors leads to spontaneous bleeding

51
Q

what are the causes of DIC?

A
  • sepsis and severe infection
  • trauma
  • organ destruction pancreatitis
  • malignancy
  • obstetric complications - amniotic fluid embolism
  • vascular abnormalities - vascular aneurysm
  • toxic and immunological insults - snake bites
52
Q

how would someone with DIC present?

A
  • hypotension, oliguria, tachycardia
  • gangrene
  • delirium or coma
  • petechiae, ecchymosis, oozing or haematuria (bleeding in 3 unrelated sites)
53
Q

What is a critical mediator of DIC and why?

A

tissue factor which is not usually in contact with the general circulation

however, in DIC, there is vascular damage so TF is exposed and plays a role

once activated, it binds with coagulation factors and triggers the extrinsic pathway via factor 7 -> triggering of the intrinsic pathway of coagulation

54
Q

What blood results would you expect in a patent with DIC?

A

low platelets
low fibrinogen
prolonged PT&APTT - prolonged bleeding time
increased fibrinogen degradation products/d-dimer

55
Q

What would a blood film for a DIC show

A

schistocytes - fragmented RBCs due to red cell injury from damaged endothelium

characteristic feature microangiopathic haemolytic anaemia

56
Q

what is the management for DIC?

A

treat underlying cause

if patient bleeding - blood transfusion of platelet concentrates, FFP, cryoprecipitate and red cells

57
Q

what is anaemia?

A

haemoglobin (Hb) level two standard deviations below the mean for the age and sex of the patient

  • In men aged over 15years — Hbbelow 130 g/L
  • In non-pregnant women aged over 15years —Hb below 120 g/L.
  • In children aged12–14years—Hb below 120 g/L.
  • In pregnant women—Hb below 110 g/L throughout pregnancy. An Hb level of 110 g/L or more appears adequate in the first trimester, and a level of 105g/L appears adequate in the second and third trimesters.
  • Postpartum — below 100 g/L.
58
Q

how do we assess the size of RBCs in anaemia?

A

MCV

macrocytic >100

normocytic 80-100

microcytic <80

59
Q

what are the 3 main types of microcytic anaemia?

A
  1. fe deficiency
  2. thalassaemia (globin deficiency)
  3. anaemia of chronic disease
60
Q

what studies can be used to distinguish the different types of microcytic anaemia?

A

iron studies

  • serum fe
  • total fe binding capacity
  • ferritin levels
61
Q

what are the 2 categories of normocytic anaemia and how are they classified?

A

hypoproliferative (<2%) and hyperproliferative (>2%)

classified by looking at the reticulocyte count

62
Q

list the types of hypoproliferative normocytic anaemia

A

aplasia (BM bails to produce RBCs) - leukaemia
other BM failure syndromes
chronic renal failure

63
Q

list the types of hyperproliferative normocytic anaemia

A

haemorrhage

haemolytic anaemia

64
Q

what are the 2 types of macrocytic anaemia and how do we distinguish them?

A

megaloblastic and non-megaloblastic

blood smear

65
Q

what are the types of megaloblastic anaemia?

A

vit B12 deficiency

folate deficiency

66
Q

what are the types of non-megaloblastic anaemia?

A
  • myelodysplastic syndrome due to malignancy
  • reticulocytosis due to haemolysis
  • drug induced - methotrexate
  • liver disease
  • hypothyroidism (myxoedema)
67
Q

how is fe absorbed from the diet?

A

absorbed from duodenum via enterocytes into the plasma

then binds to transferrin where it is transported to BM

excess fe stored as ferritin (in liver, spleen and BM)

68
Q

what is hepcidin and ferroportin?

A

hepcidin = iron regulatory hormone

ferroportin = hepcidin receptor and ion channel

regulates fe absorption

69
Q

what happens if there is an increase in fe from duodenum?

A

here is an increase in hepcidin and therefore a decrease in fe absorption (as hepcidin causes ferroportin internalisation and degradation)

70
Q

what is fe deficiency anaemia?

A

diminished red blood cell production due to low iron stores in the body

itisthe most common cause of microcytic anaemia and hypochromic anaemia

71
Q

what would the blood film show in a patient with Fe deficiency anaemia?

A
  • anisocytosis (RBCs of unequal size)
  • poikilocytosis (RBCs of varying shapes)
  • elliptocytes
  • hypochromia (pale)
  • microcytosis (small)
72
Q

what are the signs and sx of iron deficiency anaemia?

A
  • Fatigue
  • Shortness of breath on exertion
  • Palpitations
  • Pallor
  • Nail changes: this includes koilonychia (spoon-shaped nails)
  • Hair loss
  • Atrophic glossitis
  • Post-cricoid webs
  • Angular stomatitis
73
Q

what are the causes of fe deficiency anaemia?

A

Not enough taken in

  • poor diet - vegans and veggies
  • malabsorption - coeliac disease
  • increased physiological needs (pregnancy, lactation)

Losing too much

  • chronic slow bleeding
    • menses
    • colon cancer - faecal occult blood test (suspect in men)
74
Q

how do we investigate someone with fe deficiency anaemia?

A
  1. thorough hx - diet, mhx, changes in bowel habit, weight loss, menstrual hx
  2. bloods - FBC, iron studies, film
  3. endoscopy to rule out malignancy
75
Q

what would FBC and iron studies show in iron deficiency anaemia?

A

low Hb, low MCV

low serum ferritin (but can be raised due to inflammation), high TIBC (low fe stores), high transferrin

76
Q

how to manage fe deficiency anaemia?

A
  • Identify underlying cause
  • Oral ferrous sulfate - keep taking for 3 months after iron deficiency has been corrected
    • SE: black stools, diarrhoea, constipation, abdo pain, nausea
  • Iron rich diet - dark green leafy veg, meat, iron fortified bread
77
Q

complications of fe deficiency anaemia

A
  • cognitive and behavioural impairment
  • impaired muscular performance
  • heart failure
  • in pregnancy - low birth weight, pre-term delivery
78
Q

what is bone marrow failure?

A

when the BM is not producing enough stem cells
OR
the stem cells are being destroyed

79
Q

is bone marrow failure more commonly acquired or congenital?

A

acquired

80
Q

how do we classify bone marrow failure?

A

congenital

  • stem cell failure/aplastic anaemia (faconi anaemia) = all lineages affected
  • single lineage failure

acquired

  • aplastic anaemia (idiopathic, chemicals, drugs) = stem cells produced but are destroyed
  • single lineage failure (pure red cell aplasia)
81
Q

Describe the 2 lineages that arise from haematopoetic stem cells and what cells develop from these?

A

Stem cells are haematopoetic

They split into the lymphoid and myeloid lineages

Lymphoid progenitors become lymphoblasts

  • Lymphocytes (T and B)
  • NK cells

Myeloid progenitors become

  • erythrocytes
  • megakaryocytes -> platelets
  • myeloblasts -> neutrophils, monocytes, basophils, eosinophils
82
Q

What is aplastic anaemia?

A

Pancytopenia with hypocellular BM
No abnormal cells
Generally acquired

83
Q

What are the acquired causes of aplastic anaemia?

A
  • immune attack on stem cells → functional reduction in red cells
  • auto-reactive cytotoxic T-cells → autoimmune reaction
  • idiopathic
  • drugs - cytotoxics, chloramphenicol, sulphonamides, phenytoin, gold
  • toxins - benzene
  • infections - parvovirus, hepatitis
  • radiation
84
Q

What is the severity criteria for aplastic anaemia (severe and very severe)?

A

Severe

  • platelets <20,000 = risk of life threatening bleed
  • neutrophils <0.5 = risk of developing neutropenic sepsis

Very severe
-neutrophils <0.2

85
Q

What would a FBC for aplastic anaemia show?

A

Pancytopenia - low red cells, low white cells, low platelets

86
Q

What would a bone marrow biopsy for aplastic anaemia show?

A

Empty bone marrow - very fatty, absence of cells

87
Q

What is the management for aplastic anaemia?

A

BM transplant - only curative

Immunosuppressive drugs

88
Q

What is the main complication of aplastic anaemia?

A

Neutropenic sepsis and bleeding from thrombocytopenia

89
Q

What is pancytopenia?

A

Low red cells, white cells and platelets

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