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Pocket MSRA - Book 1 > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the causes of a microcytic anaemia?

A

Fe deficiency
Thalassaemia
Chronic disease

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2
Q

What are the FBC/hematinic findings suggestive of Fe deficiency anaemia?

A

FBC - Hb low, MCV low, MCH low
Haem - Fe low, Ferritin low, transferrin high

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3
Q

How is Thalassaemia classified?

A

Alpha
Beta

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4
Q

What is Thalassaemia?

A

Gene disorder causing decreased/absent synthesis of a/b globin chains

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5
Q

What are the subtypes of alpha thalassaemia?

A

Vary depending on how many genes deleted
1 - minima
2 - minor
3 - HbH
4 - Bart’s

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6
Q

Describe alpha thalassaemia minima

A

aa/a-
Low Hb/MCV
Normal RDW
Asymptomatic

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7
Q

Describe alpha thalassaemia minor

A

aa/– OR a-/a-
cis deletions more common in asians –> risk hydrops
Low Hb/MCV
Raised RDW
Asymptomatic

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8
Q

Describe alpha thalassaemia HbH

A

a-/–
VERY low Hb/MCV
VERY raised RDW
Haemolytic anaemia after birth

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9
Q

How is thalassaemia diagnosed?

A

HPLC/electrophoresis

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10
Q

How is alpha thalassaemia HbH managed?

A

Fe transfusion
Splenectomy (splenomegaly)

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11
Q

Describe alpha thalassaemia Bart’s

A

–/–
severe intrauterine haemolytic anaemia
fetal hydrops
fatal in utero

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12
Q

What is the inheritance pattern of thalassaemia?

A

Autosomal recessive
2x alpha genes on Chr 16
1x beta gene on Chr 11

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13
Q

What are the subtypes of beta thalassaemia?

A

Minor/trait
Intermedia
Major

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14
Q

Describe beta thalassaemia trait

A

B2/-
Low Hb/MCV/MCH
Target cells
Clinically asymptomatic

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15
Q

Describe beta thalassaemia intermedia

A

B0/B2 OR B+/B-
High HbF
Low Hb
VERY low MCV/MCH
Splenomegaly, bone changes
Variable transfusion dependency

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16
Q

Describe beta thalassaemia major

A

B0/B0

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17
Q

Describe beta thalassaemia major

A

B0/B0
HbF >90%
VERY low MCV/MCH
Severe haemolytic anaemia
-chronic transfusion dependency
Hepatosplenomegaly, bone changes

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18
Q

How should beta thalassaemia be treated?

A

Folate supplementation
Chronic transfusion w/ desferroxamine chelation
Ascorbate (removes Fe in urine)
GH Tx for endocrine complications
Bone marrow transplant (curative)

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19
Q

Why is excess Fe problematic in thalassaemia?

A

Causes endocrinopathy
-diabetes
-thyroid/adrenal/pituitary problems

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20
Q

What are the major complications of thalassaemia?

A

Aplastic crises if Parvovirus B19 infection
Osteopenia

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21
Q

What causes anaemia of chronic disease?

A

Chronic inflammation –>
Fe sequestration in macrophage stores –>
Reduced erthyropoiesis

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22
Q

What are the FBC/hematinic findings suggestive of anaemia of chronic disease?

A

Can be micro (late) OR normocytic (initial)
LOW transferrin

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23
Q

How is anaemia of chronic disease treated?

A

Treat underlying cause
Exogenous EPO (cancer, CKD)
IV Fe (not PO)

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24
Q

What are the causes of a macrocytic anaemia?

A

Folate deficiency
B12 deficiency
EtoH
Hypothyroidism
Drug-induced
Myelodyplastic syndromes

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25
Q

What are the causes of Folate deficiency?

A

Poor diet (folate in foliage)
Increased demand (pregnancy, dialysis, liver disease)
Inhibited (antifolates)
Malabsorption (resection, coeliac)

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26
Q

What commonly prescribed drugs are antifolates?

A

MTX
Phenytoin
(EtoH)

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27
Q

What are the FBC/hematinic findings suggestive of Folate deficiency?

A

Megaloblastic anaemia
Folate low
B12 normal
Hypersegmented neutrophils on blood film

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28
Q

How is Folate deficiency treated?

A

Folate replacement w/ B12

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29
Q

What is the potential complication of folate replacement alone?

A

Precipitation of subacute combined degeneration of cord if B12 drops too low

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30
Q

In which patients should prophylactic folate replacement be considered?

A

Pregnancy
Long term MTX usage

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31
Q

What are the causes of B12 deficiency?

A

Pure vegan diet
Defect in processing pathway/malabsorption
-pernicious anaemia
-gastric bypass
-terminal ileitis (Chron’s)
-pancreatic insufficiency

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32
Q

What is Pernicious anaemia?

A

Autoimmune destruction of parietal cells
Associated autoimmune disease (vitilligo, Hashimoto’s)
Increased risk of gastric ca

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33
Q

How can B12 deficiency present clinically?

A

Glossitis + angular stomatitis
Sensory polyneuropathy
Cognitive impairment
Optic atrophy (nutritional)
SACD
Osteoporosis

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34
Q

What are the FBC/hematinic findings suggestive of B12 deficiency?

A

Megaloblastic anaemia
Folate normal
B12 low
Hypersegmented neutrophils

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35
Q

How should B12 deficiency be treated?

A

B12 img IM inj for life

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36
Q

What are the causes of a normocytic anaemia?

A

Haemolysis
Underproduction

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37
Q

How can haemolytic anaemias be distinguished from underproductive anaemias?

A

Corrected reticulocyte count <3% = underproduction
-would be elevated in haemolysis

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38
Q

What are the two types of haemolysis?

A

Intravascular
-RBCs broken down w/i vessels
Extravascular
-RBCs destroyed by reticuloendothelial system (macrophages liver/spleen/LN)

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39
Q

What is a major complication of intravascular haemolysis?

A

Tubular necrosis 2o haemosiderin

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40
Q

What is Hereditary Spherocytosis?

A

Autosomal dominant condition causing spherocytosis of RBC
-prone to haemolysis

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41
Q

Describe the presentation, ix, tx and cx of hereditary spherocytosis

A

Mild haemolytic anaemia, high unconjungated bilirubin
Ix - SDS-PAGE (electrophoresis)
Tx - Folate, splenectomy
Cx - B19 crisis

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42
Q

What is Sickle Cell disease?

A

Autosomal recessive mutations of B-chain Hb

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43
Q

What are the two types of Sickle cell disease?

A

SC trait
Sickle cell disease/anaemia

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44
Q

Describe Sickle Cell Trait

A

Heterozygous mutation
Generally asymptomatic
Protective against malaria

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45
Q

Describe Sickle Cell Anaemia

A

Homozygous mutation (can co-exist w/ B-thal)
Fragile cells –> haemolysis (both intra/extra)

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46
Q

How does Sickle Cell Anaemia present?

A

Facial/cranial bone abrormalities
Hepatomegaly
Autoinfarction of spleen
Aplastic crises (B19 risk)
Vaso-occlusive crisis

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47
Q

What is a Sickle Cell crisis?

A

Vaso-occlusion in microcirculation caused by extensive sickling
Precipitated by:
-hypoxia
-cold
-dehydration
-infection

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48
Q

How can sickle cell crises present?

A

Dactylitis
Avascular necrosis
Acute chest syndrome
Renal papillary necrosis
Pain
CNS infarct –> stroke/seizures
Priapism

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49
Q

How is priapism treated in sickle cell crises?

A

A-agonist OR blood aspiration OR saline irrigation

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50
Q

What is the acute chest syndrome in sickle cell crisis?

A

Vaso-occlusion in pulmonary microcirculation w/ 2o infiltrates
Presents with:
-fever
-cx pain
-SOB
-wheeze
-cough
-tachypnoea
-pain

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51
Q

What are the complications of acute chest syndrome in sickle cell crisis?

A

Acute - ventilation, death (MCC)
Chronic - fibrosis –> Pulm HTN –> cor pulmonale

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52
Q

How should an acute chest syndrome in sickle cell crisis be managed?

A

Bronchodilators
Abx
Transfusion
Ventilation
Exchange transfusion

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53
Q

What are the chronic complications of Sickle Cell Anaemia?

A

Auto-splenectomy/infarction
-increased risk of infection w/ encapsulated organisms
Sickle cell retinopathy
-non-proliferative OR proliferative

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54
Q

How is Sickle cell Retinopathy managed?

A

Non-proliferative - Hydroxyurea
Proliferative - anti-VEGF, lasers, surgery

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55
Q

What is a sequestration crisis?

A

Pooling of blood in spleen +/- liver –> severe anaemia + shock
-mainly occurs in children
-requires uregent transfusion

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56
Q

What are the FBC/hematinic findings suggestive of B12 deficiency?

A

Normocytic anaemia
Sickle cells w/ target cells on film
Howell-Jolly bodies on film
Bili high

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57
Q

How should Sickle Cell anaemia be ix?

A

HPLC/electrophoresis
PCR

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58
Q

How is Sickle cell anaemia treated?

A

Hydroxyurea (reduces f of crisis)
Immunization/PPx abx
Folate supplement
Transfusions
Bone marrow transplant CURATIVE

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59
Q

What is G6PD deficiency?

A

XLR deficiency of G6PD
Causes haemolytic crises

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60
Q

What are the precipitants for a G6PD crisis?

A

Drugs (aspirin, sulphonamides, quinine, dapstone)
Fava beans
Henna tattoo
Infections

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61
Q

How does G6PD present?

A

Sudden haemolytic crises
-anaemia
-jaundice
-flank pain (Hb nephrotoxic)

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62
Q

How should G6PD be ix?

A

Blood film - Heinz bodies, bite cells
Enzyme assay

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63
Q

How is G6PD managed?

A

Self limiting
Transfusion if severe

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64
Q

What is autoimmune haemolytic anaemia?

A

Ig directed RBC destruction
-mediated by macrophages
IgG or IGM disease

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65
Q

How should autoimmune haemolytic anaemia be ix?

A

DIRECT coomb’s test + agglutination
-warm = IgG
-cold = IgM

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66
Q

Describe IgG autoimmune haemolytic anaemia

A

WARM agglutinin
Extravascular, central body
Associated w/ autoimmune disease/drugs

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67
Q

How should IgG autoimmune haemolytic anaemia be managed?

A

Treat underyling cause
Steroids
IVIG
Splenectomy

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68
Q

Describe IgM autoimmune haemolytic anaemia

A

COLD agglutinin
Intravascular, peripheries
Associated w/ EBV, HBV, mycoplasma

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69
Q

What is Porphyria?

A

Inherited metabolic disorders caused by abnormal heam synthesis

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70
Q

How dose acute intermittent porphyria present?

A

20-40ys
Painful abdomen
Polyneuropathy
Port-wine urine on sunlight exposure
Psych disturbances
PPT by drugs (P450 inducers, EtOh, starvation)

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71
Q

How is acute intermittent porphyria treated?

A

Glucose
Heme

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72
Q

How does porphyria cutanea tarda present?

A

Photosensitive blistering milla
-slow to heal
-hyperpigmentation

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73
Q

How should porphyria cutanea tarda be ix and rx?

A

Ix - uroporphyinogen (deficient), pink fluorescence of urine, ferritin
Rx - Chloroquine, venesection

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74
Q

What are the potential reactions to a blood product transfusion?

A

Non-immune mediated (hypoCa, CCf, infection, hyper K)
Acute
-febrile reaction
-minor allergic
-anaphylaxis
-acute haemolysis
-TACO
-TRALI (ARDS)
Chronic (delayed haemolysis)
GVHD (ciclosporin)

75
Q

What are the common myeloproliferative disorders?

A

Chronic Myeloid Leukaemia
Polycythaemia Vera
Myelofibrosis
Essential thrombocytopenia

76
Q

What gene abnormality is high risk for CML?

A

Philadelphia t9:22

77
Q

How does CML present?

A

Fatigue
Wt loss
Night sweats
Priapism
Tinnitus
Maturing granulocytes

78
Q

How should CML be investigated?

A

FISH/karyotype/PCR
FBC
-WBC 50-400
-Plt normal/high
-Hb low
Film - <10% blasts
BM hypercellular

79
Q

What is the treatment for CML?

A

Imatinib (tyrosine kinase inhibitor)
Hydroxycarbamide

80
Q

What is the progression of CML?

A

Chronic –> accelerated –> blast crisis (ALL/AML)

81
Q

How does PV present?

A

Viscosity headache
Dizziness
CVA
Pruritis
Ruddy complexion
VTE
Bleeding
Hepatosplenomegaly
Gouty arthritis
Peptic ulcers

81
Q

What gene mutation is high risk for PV?

A

JAK2 (95%)

82
Q

What are the 2o causes of PV?

A

High altitude
RCC
Von Hippel-Lindau
PKD
COPD
Heart disease

83
Q

What is the progression of PV?

A

15% progress to MF

84
Q

How should PV be investigated?

A

Flow cytometry
FBC
-high Hb
-high platelets
-low neutrophils
Low EPO

85
Q

How is PV treated?

A

Venesction
Low dose aspirin
Hydroxycarbamide

86
Q

How does MF present?

A

Lethargy
Wt loss
Night sweats
Fever
Pallor
Hepatosplenomegaly
High urate

87
Q

How should MF be investigated?

A

FBC
-high platelets
-high WCC
BM biopsy
-fibrosis
-dry tap
Teardrop cells on film
High urate/LDH

88
Q

How is MF treated?

A

Hydroxycarbamide
Thalidomide

89
Q

How does ET present?

A

Thrombosis/bleeding
-digital ischaemia
-CVA
-budd-chiari

90
Q

How should ET be investigated?

A

Screen for JAK2 (50%)
High platelets (>500)
Calreticulin (20%)

91
Q

How should ET be treated?

A

a-interferon (avoided in pregnancy)
Hydroxycarbamide
Low dose aspirin
Anagrelide

92
Q

What are the common types of Leukaemia?

A

Acute Myeloid Leukaemia
Acute Lymphoblastic Leukaemia
Chronic Lymphocytic Leukaemia
Myelodysplastic Syndromes

93
Q

What is a Leukaemoid reaction?

A

Leukocytosis 2o stress/infection/haemolysis as opposed to Leukaemia

94
Q

How can a Leukaemoid reaction be distinguished from Leukaemia?

A

Clinical context
High Leukocyte Alanine Phosphatase
Dohle bodies
LEFT shift

95
Q

What are the risk factors for AML?

A

Down’s
Radiation
Benzene exposure (smoking, paints/solvents, gasoline)
Mutations
-t(15;17) - good prognosis
-trisomies - poor prognosis

96
Q

How is AML classified?

A

FAB classification (M0-M7)
-M3 = Acute promyelocytic
-M7 = Acute megakaryoblastic

97
Q

What are the key features of Acute promyelocytic leukaemia?

A

10% of AML
t(15;17)
can cause DIC
treated w/ retinoids
good prognosis

98
Q

How does AML present?

A

Older patients
Bone marrow failure
Pallor
Fatigue
Exertional SOB
Recurrent infection
Bleeding
Gum infiltrates (M5)

99
Q

How should AML be investigated?

A

Platelets (low)
Blood film
-Blasts >20%
-auer rods
Immunophenotyping

100
Q

How is AML treated?

A

CTX (80% remission)
Platelet/RBC tranfusion
Bone marrow transplant

101
Q

What are the two main subtypes of ALL?

A

Bcell-ALL (most common)
Tcell-ALL

102
Q

How does ALL present?

A

2-4yrs
Weakness
Bruising
Otitis media
Bone pain
Enlarged LN
Headache

103
Q

What factors are suggestive of poor prognosis in ALL?

A

FAB L3 type
T/B cell surface marker
Philadelphia t(9;22)
Age <2 or >10
Male
CNS involvement
Initial WBC >100
Non-caucasian

104
Q

What factors are suggestive of good prognosis in ALL?

A

FAB L1 type
Low initial WBC
del9p
t(12;21)
t(1;19)

105
Q

How is ALL treated?

A

4 phase CTX

106
Q

How does CLL present?

A

> 50 y/o
ASYMPTOMATIC
Constitutional sx
Immune thrombocytopenia (bleed)
Warm autoimmune haemolytic anaemia (10%)
Hypogammaglobulinaemia (infections)
Red cell aplasia
Angioedema

107
Q

What is Richter’s transformation?

A

Transformation of CLL into more aggressive large cell lymphoma
-3% of cases

108
Q

Which cell-line is most commonly implicated in CLL?

A

> 95% B-cell clonal

109
Q

What factors suggest a poor prognosis in CLL?

A

Male
>70 y/o
Lymphocyte >50
Prolymphocyte >12
Doubling of lymphocytes <12mo
Raised LDH
CD38, TP52, del17p

110
Q

What factors suggest a good prognosis in CLL?

A

Del13q
-most common mutation in CLL (50%)

111
Q

What findings suggestive of CLL can be seen on a blood film?

A

Lymphocytes +++
Smear/smudge cells

112
Q

How should CLL be treated?

A

Watch and wait
High WCC NOT an indication to treat
Treat when other cell lines start to fall
-Fludarabine
-Ciclosporin
-Rituzimab
-Ibrutinib

113
Q

What is Hairy Cell Leukaemia?

A

Subtype of CLL

114
Q

How does Hairy Cell Leukaemia present?

A

Pancytopenia
Splenomegaly
Skin vasculitis

115
Q

How should Hairy Cell Leukaemia be investigated?

A

Bone marrow biopsy
-dry tap
TRAP stain +ve

116
Q

How should Hairy Cell Leukaemia be treated?

A

CTX
Immunotherapy

117
Q

What is Myelodysplasia?

A

Dysplasia in 2 or more cell lines

118
Q

How does Myelodysplasia present?

A

Elderly
Anaemia
30% progress to AML

119
Q

How should Myelodysplasia be treated?

A

Supportive
CTX not effective

120
Q

When should an enlarged LN be investigated?

A

If LN >1cm present for >6/52 needs excision biopsy

121
Q

What staging system is used for lymphoma?

A

Ann-Arbor
1 - (single group)
2 - 2+ regions on one side of diaphragm
3 - Both sides of diaphragm
4 - Extralymphatic manifestations

122
Q

What are the two main types of Lymphoma?

A

Hodgkin’s (rarer)
Non-Hodgkin’s

123
Q

At what ages does Hodgkin’s lymphoma present?

A

Bimodal distribution
-15-35
->60

124
Q

What are the main histological subtypes of Hodgkin’s lymphoma?

A

Nodular sclerosing (70%, women)
Mixed cellularity (20%)
Lymphocyte predominant (5%)
Lymphocyte depleted (rare)

125
Q

What factors suggest a poor prognosis in Hodgkin’s lymphoma?

A

B sx
Age >45
Stage IV
Hb <10.5
Male
Albumin <40
WBC >15

126
Q

How should Hodgkin’s lymphoma be treated?

A

External beam radiation therapy
Brentuximab
ABVD chemo

127
Q

What are the common subtypes of Non-Hodgkin’s lymphoma?

A

Waldenstrom macroglobulinaemia
Follicular
Mantle cell
Marginal zone
Diffuse large B-cell
Burkitt

128
Q

How does Walendstrom macroglobulinaemia present?

A

> 50
Headache
Hepatosplenomegaly
Visual disturbance
Cold AIHA
Hyperviscosity
Raynauld

129
Q

How should waldenstrom macroglobulinaemia be treated?

A

Exchange therapy
Ciclosporin

130
Q

What are the key features of mantle cell lymphoma?

A

Presents >60 y/o
Widespread (LN/liver/GI)
Aggressive w/ poor prognosis

131
Q

What are the key features of marginal zone lymphoma?

A

Extranodal
-gastric MALT
-thyroid
-salivary nodes
-lungs
-spleen

132
Q

What are the key features of B-cell lymphoma?

A

V. common (40%)
Fast/high grade
B-sx
Spreads to GI/testis/bone
Can require surgical removal of masses

133
Q

What is Paraproteinaemia?

A

Group of related diseases characterized by excess proliferation of Ig secreting cells
Spectrum from MGUS to myeloma

134
Q

How does myeloma present?

A

CRAB sx
-hypercalcaemia
-renal failure
-anaemia (bone marrow failure, other penias)
-bone pain (lumbar spine)
Amyloidosis

135
Q

What are the sx of Amyloidosis?

A

Peripheral neuropathy
Macroglossia
Cardiomegaly
Carpal tunnel syndrome
Hyperviscosity
Encapsulated bacteria infection

136
Q

How should suspected myeloma be investigated?

A

Film - Roleaux formation, anaemia (norm/norm)
Raised ESR, hyperCa, AKI
SPEP (M-spike)
UPEP (10% no M-spike, Bence-Jones)
Serum free light chain
Bx/radiology

137
Q

How should myeloma be managed?

A

HyperCa - IVI, bisphosphonates
Anaemia - EPO
Plasma exchange, dialysis
Chemo/radiotherapy
Autograft stem cell therapy

138
Q

Which clotting factors affect APPT?

A

12, 11, 9, 8, 10 5, 2, 1 (intrinsic)

139
Q

Which clotting factors affect PT?

A

7, 10, 5, 2, 1 (extrinsic)

140
Q

What can prolong the Thrombin time?

A

Heparin
Fibrinogen deficiency

141
Q

What clotting factor does LMWH work against?

A

Factor Xa

142
Q

What are the common causes of thrombocytopenia?

A

Idiopathic thrombocytopenic purpura
Thrombotic thrombocytopenic purpura
Haemolytic Uraemic Syndrome
Heparin-induced thrombocytopenia
DIC

143
Q

What are the causes of ITP?

A

1o - IgG antibodies
2o - SLE, leukaemia, quinine, heparin, HIV, hep C, antiphospholipid syndrome

144
Q

What is Evans Syndrome?

A

Autoimmune condition causing ITP + AIHA

145
Q

How does ITP present?

A

Acute form (children)
-self-limiting post viral infection
Chronic form (adults)
-women of childbearing age
-purpura, epistaxis, menorrhagia

146
Q

How is ITP investigated?

A

Dx of exclusion
(low platelet and normal clotting)

147
Q

How is ITP treated?

A

Steroids
IVIg
Splenectomy
Rituximab (if refractory)
NOT platelet transfusion

148
Q

What is thrombotic thrombocytopenia purpura?

A

Congenital lack of VWF cleaving protein (ADAMTS13)
Leads to platelet microthrombi that shear RBC –> microangiopathic haemolytic anaemia

149
Q

How does TTP present?

A

Microangiopathic haemolytic anaemia
Thrombocytopenia
Neurological abnormalities
Fever
Renal dysfunction

150
Q

How is TTP treated?

A

Steroids
Plasma exchange
Rituximab
AVOID platelet transfusion

151
Q

What is Haemolytic Uraemic Syndrome?

A

Vasculitis common in children
-90% post E.coli (0157:H7 infection)
-10% atypical
Most common cause of AKI in paeds

152
Q

How does HUS present?

A

Profuse diarrhoea –> bloody stools 1-3/7 later
Abdo pain
Vomiting
Fever
Rash

153
Q

How is HUS treated?

A

Supportive therapy +/- dialysis

154
Q

What is DIC?

A

Consumptive coagulopathy
Microthrombi and bleeds

155
Q

How is DIC treated?

A

Platelet replacement
Cryoprecipitate (fibrinogen + factors 8, 13, VWF)
FFP
RBC

156
Q

How does thrombophilia present?

A

Thrombosis
-DVT
-CVA
-VST
-PE
-Budd-Chiari
-MI

157
Q

What are the inherited causes of thrombophilia?

A

Factor V LEiden
Prothrombin 20210A gene mutation
Protein C or S deficiency
Antithrombin III deficiency

158
Q

What are the acquired causes of thrombophilia?

A

Tamoxifen
Olanzapine
HRT
OCP

159
Q

What is Von-Willebrand’s disease?

A

AD inherited deficiency of VWF

160
Q

What are the subtypes of VWD?

A

Type 1 (80%) - partial deficiency
Type 2 - abnormal form
Type 3 - total lack of factor (AR)

161
Q

How does VWD present?

A

Mild mucosal/skin bleeding

162
Q

How should VWD be investigated?

A

APTT (high) but PT normal
Bleeding time increased
Ristocetin test

163
Q

How is VWD treated?

A

Desompressin (increases VWF release)

164
Q

What is the action of Von-Willebrand factor?

A

Promotes platelet adhesion to damaged endothelium
Stabilizes FVIII

165
Q

What is haemophilia?

A

X-linked deficiency of clotting factors

166
Q

What are the two main types of haemophilia?

A

A - lack of factor 8
B - lack of factor 9

167
Q

How does haemophilia present?

A

DEEP TISSUE BLEEDING
Haemarthroses
Haematomas

168
Q

How should haemophilia be investigated?

A

Prolonged APTT ONLY

169
Q

How should haemophilia be treated?

A

Minor - elevation, pressure, TXA
Severe - recombinant FVIII/FIX

170
Q

How does unfractionated heparin work?

A

Unfractionated - Inhibits Xa + IIa
LMWH - binds ATIII Xa

171
Q

What reversal agent is available for heparin?

A

Protamine sulphate
-UFH full reversal
-LMWH partial reversal
-Fondaparinux no reversal

172
Q

What are the s/e of heparin?

A

HIT (not Fondaparinux)
Osteoporosis
HyperK

173
Q

What are the indications for DOACs?

A

Non-valvular AF
VTE

174
Q

How are DOACs eliminated?

A

Dabigatran (renal)
Rivaroxaban (liver)
Apixaban (faecal)

175
Q

What drugs commonly interact w/ DOACs?

A

Antiepileptics
Anti-retrovirals
Anti-fungals
Rifampicin

176
Q

How do DOACs work?

A

Dabigatran - inhibits thrombin
Others - inhibit Xa

177
Q

What reversal agent is available for DOACs?

A

Beriplex (PCC)
Dabigatran - Idarucizumab

178
Q

How does Warfarin work?

A

Vit K antagonist
Reduces II, VII, IX, X, protein C

179
Q

What are the s/e of Warfarin?

A

Haemorrhage
Teratogenic (can be used in breastfeeding)
Skin necrosis
Purple toes

180
Q

What factors can cause a high INR in warfarin pts?

A

Change in diet
Liver disease
ODEVICES
-omeprazole
-disulfiram
-erythromycin
-valproate
-isoniazide
-cipro/cimetidine
-acute EtoH
-sulphonamide
PCBRAS inducers
Cranberry juice
NSAIDs
Foods high in Vit K (leafy greens)

181
Q

What reversal agents are available for Warfarin?

A

Vit K
4 factor prothrombin complex

182
Q

When should Warfarin be used instead of a DOAC, and vice-versa?

A

Warfarin - CrCl <30, extracranial bleeding, poor compliance, wt >120kg, arterial thrombosis
DOAC - non valvular AF, VTE, prev. ICH, polypharmacy, good control

Pocket MSRA - Book 1 (7 decks)

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