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BPT Sadness 😔 > Haematology ❤️ > Flashcards

Haematology ❤️ Flashcards

1
Q

What is the MOA of dabigatran?

A

Direct thrombin (IIa) inhibitor

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2
Q

What is a leukaemoid reaction?

A

Lots of WCC due to causes other than leukaemia
- Causes left shift of neutrophils (increase in immature WBC)
- Physiological response to stress or infection

Raised leucocyte alkaline phosphatase

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3
Q

ITP in association with autoimmune haemolytic anaemia (AIHA) is called?

A

Evan’s syndrome

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4
Q

A 24-year-old male presented with a one-week history of episodic severe abdominal pain associated with vomiting 4 to 5 times a day and dark red urine. He then suddenly developed rapidly progressive weakness in all four limbs for 3 days before being hospitalised.

Given the likely diagnosis, which of the following urinary tests would be raised?

A

Urine porphobilinogen; acute intermittent porphyria

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5
Q

What is the MOA of vitamin K, and how long does it take to affect INR?

A

Vitamin K acts as a cofactor in the carboxylation of clotting factors (II, VII, IX, X); 4 hours

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6
Q

What staging system is used for HL/NHL?

A

Ann-Arbor

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7
Q

Reed-Sternberg cells are found in which haematological condition?

A

Hodgkin’s lymphoma
- Bimodal distribution, 30s and 70s

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8
Q

Which clotting factor is elevated in acute liver failure?

A

Factor VIII
- Acute phase reactant
- Produced both in liver AND endothelial cells

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9
Q

What does eculizumab (Soliris) target, what conditions does it treat and what is a rare but serious associated risk?

A

Complement C5 (inhibits cleavage of C5 into C5a and C5b > C5b-9)
- PNH
- HUS
- Myasthenia gravis
- NMO

Meningococcal infection
- Thus recommend meningococcal vaccination 2 weeks before starting therapy

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10
Q

What is the reversal agent of dabigatran?

A

Praxbind; idarucizumab

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11
Q

What does obinutuzumab target, and which conditions does it treat?

A

CD20
- CLL (+ chlorambucil)
- Follicular lymphoma (+ bendamustine)

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12
Q

What is chlorambucil/Leukeran used for, and how does it work?

A

Conditions:
- CLL
- HL
- NHL

MOA
- Alkylating agent
- Blocks formation of DNA and RNA

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13
Q

What is caplacizumab/Cablivi and what is it used for?

A

Acquired thrombotic thrombocytopenic purpura (aTTP), in conjunction with plasma exchange and immunosuppression
- Targets GP1bIXV receptor in platelets

Faster recovery but higher rates of bleeding

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14
Q

Howell-Jolly bodies on blood film are pathognomic of?

A

Splenic dysfunction
- Splenectomy, or
- Functional asplenia e.g. from sickle cell disease

As well as Pappenheimer bodies

Also seen in coeliac disease

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15
Q

Haemophilia A and B deficiency in which factors and what is bleeding pattern?

A

Haem A = deficiency in factor VIII = A sounds like eight (most common)
- 80% of haemophillias

Haem B = Christmas disease, deficiency in factor IX = ninght before Christmas

Bleeding pattern: muscle and joint

Levels
• Mild = >5
• Severe = <1

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16
Q

4 different types of sickle cell anaemia crises?

A
  1. Vaso-occlusive crisis
    - Caused by infection, dehydration, deoxygenation (high altitude
    - Diagnose CLINICALLY
    - Infarcts in organise incl. bones e.g. avascular necrosis of hip
    - Tx: rapid hydration, IV pain control
  2. Acute chest syndrome
    - Vaso-occlusion in pulmonary microvasculature > infarct in lung parenchyma
    - SOB, chest pain, pulmonary infilatrate on CXR, hypoxia
    - Usually occurs as complication of vaso-occlusive pain episode; also caused by PE or thrombosis
    - Tx: pain relief, O2 therapy, ABx, transfusion or exchange > improves oxygenation
    - Prevention: hydroxyurea, vaccination
  3. Aplastic crisis
    - Caused by infection by parvovirus B19
    - Sudden fall in Hb
    - BM suppression > reduced reticulocytes
  4. Splenic sequestration crisis
    - Sickling within organs esp. spleen > pooling of blood with worsening anaemia
    - Acute, painful enlargement of spleen due to intrasplenic trapping of red cells
    - Increased reticulocyte count
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17
Q

Positive urine haemosiderin suggests which type of haemolysis?

A

Intravascular haemolysis

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18
Q

Haemolysis types

A
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19
Q

Causes for positive DAT

A
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20
Q

IgG positive warm or cold haemolytic anaemia?

A

WARM
- IgG grandma

Examples
- SLE
- CLL
- Lymphoma

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21
Q

Treatment ITP?

A
  1. Short course prednisolone or dexamethasone <6/52
  2. IVIg - if severe thrombocytopaenia + life-threatening bleeding
  3. If relapse and/or refractory ITP:
    i. Rituximab
    ii. Thrombopoietin receptor agonists e.g. PO eltrombopag, SC romiplostim
    iii. IF >1 year post Dx and still refractory - splenectomy
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22
Q

Type I HIT is chill (non-immune mediated, within a few days).

What is the pathophysiology in type II HIT?

A

Immune-mediated thrombocytopaenia occuring 5-10 days after exposure
- Caused by Ab against platelet factor 4
- Usually Plt ~150; if high baseline, decrease >50% is concerning

Dx:
- 4T scoring system > ELISA for platelet 4 Ab, followed by either
- Serotonin release assay OR Heparin-induced platelet aggregation assay

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23
Q

Non-heparin anti-coagulants?

A

Fondaparinux, danaparoid, rivaroxaban

NOT warfarin - requires 3-5 days for anti-thrombotic effect
- Declining protein C increases thrombotic risk

Tx:
- Nil thrombosis > 2-3/2
- Thrombotic event > 3-6/12

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24
Q

Scoring system for suspicion of TTP?

A

PLASMIC

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25
Q

Drugs which can cause TTP?

A

• Quinine, cyclosporine, gemcitabine
• VEGF-I incl. bevacizumab
• Cocaine, ecstasy, morphine

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26
Q

Features of MAHA?

A

Elevated LDH, decreased haptoglobin, schistocytes on peripheral smear, negative DAT, thrombocytopaenia

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27
Q

Key test in TTP?

A

ADAMTS13 level <10%

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28
Q

WTF is Witskott-Aldrich syndrome?

A

Triad:
1. Eczema
2. Thrombocytopaenia
3. Immunodeficiency + recurrent bacterial infections (chest)
- Low IgM

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29
Q

Bite cells and Heinz bodies on blood film suggest…?

A

G6PD deficiency

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30
Q

Most common inherited thrombophilia?

A

Factor V Leiden
- Activated protein C resistance > resistance to activated protein C prevents the coagulation cascade from deactivating, resulting in increased clot formation
- Autosomal dominant

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31
Q

WTF is poikilocytosis?

A

Abnormal variation in RBC shape
- Found in severe anaemia, certain shapes are helpful diagnostically

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32
Q

Cabot ring in blood film (look like rings or figure 8s)

A

Megaloblastic anaemia + MDS

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33
Q

Most common hereditary haemolytic anaemias

A
  1. Spherocytosis: hereditary spherocytosis (especially northern European)
  2. Non-spherocytosis: G6PD deficiency

Spherocytosis is autosomal dominant

Dx: Eosin-5′-maleimide (EMA) binding test

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34
Q

C-MYC gene translocation - t(8:14) and EBV is associated with which malignancy?

A

Burkitt lymphoma
- EBV
- Starry sky appearance

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35
Q

Smudge/smear cells are associated with…?

A

CLL
- Diagnose with immunophenotyping and flow cytometry
- Most commonly CD5, CD19, CD20, CD23

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36
Q

Beta-2-microglobulin is associated with?

A

Plasma cell myeloma

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37
Q

Ring sideroblasts are seen in which condition?

A

Myelodysplasia, EtOH, lead, anti-TB Rx

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38
Q

Characteristics of systemic mastocytosis?

A

Systemic mastocytosis results from a neoplastic proliferation of mast cells

Features
• Urticaria pigmentosa - produces a wheal on rubbing (Darier’s sign)
• Flushing
• Abdominal pain
• Monocytosis on the blood film

Diagnosis
• Raised serum tryptase levels
• Urinary histamine

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39
Q

Unusually giant platelet cells, thrombocytopenia, and prolonged bleeding time - potential Dx?

A

Bernard-Soulier syndrome
- Rare inherited blood clotting disorder
- Affected individuals tend to bleed excessively and incur spontaneous ecchymoses
- Involves a defect of the GPIb-IX-V complex, an essential platelet receptor complex that principally binds with the von Willebrand factor (vWF)
- GPIb-alpha (GPIBA), GPIB-beta (GPIBB), and GPIX (GP9)

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40
Q

Splenomegaly + teardrop/dacrocyte cells suggestive of…?

A

Myelofibrosis

Teardrop cells
- may be seen in the setting of marrow infiltration (by fibrosis, granulomatous inflammation, hematologic or metastatic malignancy), splenic abnormalities, megaloblastic anemia, and thalassemia

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41
Q

TP53 mutation suggestive of?

A

Li-Fraumeni syndrome
- Rare genetic condition which can increase risk of Ca incl. breast cancer, leukemia and sarcomas

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42
Q

Most specific finding for APML?

A

FISH with translocation on chromosomes 15 and 17
- High risk DIC > thus needs early initiation with all transretinoic acid
- t(15;17) (q22;q21)

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43
Q

Type II HITT - Ab against what?

And what scoring system is used for possible HITT?

A

Platelet factor 4

4T scoring system (low risk = 0-3 points)
1. Thrombocytopaenia (Plt decrease <30% or nadir <10)
2. Timing of platelet count decrease (Plt decrease <4 days without recent exposure)
3. Thrombosis or other sequelae (no thrombosis/other sequelae)
4. Other causes of thrombocytopaenia apparent? (definite other processes)

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44
Q

HHT Dx?

A

There are 4 main diagnostic criteria. If the patient has 2 then they are said to have a possible diagnosis of HHT. If they meet 3 or more of the criteria they are said to have a definite diagnosis of HHT:

epistaxis : spontaneous, recurrent nosebleeds

telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)

visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM

family history: a first-degree relative with HHT

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45
Q

Coagulation cascade

A
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46
Q

Extrinsic pathway?

A

VII + tissue factor
- TISSUEF = 7 letters

PT extrinsic
- PT EXercise

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47
Q

AML risk stratification

A
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48
Q

Mantle cell lymphoma

A

t(11;14)

CyclinD1/IgH

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49
Q

Follicular lymphoma

A

t(14;18), IgH/BCL2

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50
Q

Gastric MALT

A

t(11;18), MALT1

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51
Q

Key investigation of CLL is immunophenotyping. What are the key markers?

A

CD19, CD20 (weak) with coexpression CD5, CD23

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52
Q

Poor prognostic factors CLL?

A
  • Male
  • Age >70 years
  • Lymphocytes >50
  • Raised LDH
  • CD38 positive
  • TP53 mutation > poor response to chemo-immunoTx > imbrutinib, venetoclax
  • del17p
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53
Q

Good prognosis CLL?

A
  • Female
  • del13q (most common)
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54
Q

Triad for acute intermittent porphyria?
- Autosomal dominant
- Defect in porphobilinogen deaminase > toxic accumulation of aminolaevulinic acid and porphobilinogen

A

20-40 female

Abdominal pain + vomiting
Motor neuropathy
Depression
HTN, tachycardia

Dx:
- Urine turns deep red on standing
- Raised urinary porphbilinogen
- Raised delta aminolaevulinic acid and porphobilinogen

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55
Q

Waldenstrom’s macroglobulinaemia characteristic traits?

A

AKA lymphoplasmocytic lymphoma

B cell lymphoma
- Organomegaly, bicytopaenia (Hb, Plt)

IgM paraprotein
- IgM associated with cold AIHA

Hyperviscosity symptoms (visual disturbance, headache)

MYD88

56
Q

Difference between Waldenstrom’s macroglobulinaemia and MM?

A

Both have M spike/hypergammaglobulinaemia
- WM: organomegaly, no lytic lesions
- MM: no organomegaly, present lytic lesions

57
Q

Blood film in IDA?

A
  • Target cells
  • “Pencil” poikilocytes
  • Anisocytosis
  • Microcyte
  • Elliptocyte, ovalocyte

Ferritin, iron, transferrin saturation low (hepcidin also low)

58
Q

What is Mentzer index useful for?

A

Differentiating between two causes of microcytic hypochromic anaemia
- Index >15 = IDA
- Index <11 = thalessaemia minor

Microcytosis is more marked in thalassaemia minor

59
Q

Causes of dry tap on bone marrow?

A
60
Q

Characteristics myelofibrosis?

A

Old person with anaemia, massive splenomegaly, hypermetabolic syndrome (LOW, night sweats)

Bloods:
- Anaemia
- High WBC and Plt early in disease
- Tear drop poikilocytes
- Dry tap BMB
- High urate and LDH
- JAK2 V617F mutation

61
Q

Methaemoglobinaemia characteristics and associations?

A

Normal pO2 but decreased SpO2! Chocolate brown blood

Causes congenital
- HbM, HbH
- NADH methaemoglobin reductase deficiency

Treatment
- Methylene blue: converts/oxidises Fe3+ into Fe2+ (oxygen-carrying ferrous state)

62
Q

Drugs to avoid in G6PD

A

Rasburicase
Primaquine
Ciprofloxacin/moxifloxacin/norfloxacin
Nitrofurantoin
Sulphur drugs (incl. gliclazide), methylene blue, dapsone

F`ava beans and moth balls, henna

63
Q

Parvovirus in which condition can lead to aplastic crisis?

A

Hereditary spherocytosis

64
Q

Long term treatment of hereditary spherocytosis?

A

Folate replacement, splenectomy

65
Q

Gallstones +/- jaundice + chronic anaemia (extravascular haemolysis) with splenomegaly should make you think?

A

Hereditary spherocytosis (OR G6PD)

66
Q

Causes of basophilic stippling?

A

Lead poisoning/heavy metal toxicity
- DDx thalassaemia major and minor

Microcytic anaemia, basophilic stippling on the blood film, and peripheral motor neuropathy

67
Q

Haemolysis by site

A
68
Q

Characteristics vWD?

A
  • Easy bruising usu. mucosal; rarely joint
  • Normal Plt, INR; PTT sometimes prolonged

Tx:
- Desmopressin

69
Q

Thrombocytopaenia, anaemia, low fibrinogen, raised PT + APTT + INR should make you think?

A

DIC

70
Q

Which blood product has the highest risk of bacterial contamination?

A

Platelets

71
Q

Prophylaxis drugs in sickle cell anaemia

A

Hydroxyurea + pneumococcal vaccine
- Penicillin if splenectomy

72
Q

CML characteristics and treatment?

A
  • Philadelphia chromosome; t(9:22), BCR-ABL
  • Decreased LAP
  • Increase in granulocytes at different stages of maturation +/- thrombocytosis
  • Splenomegaly
  • May undergo blast transformation AML (80%) and ALL (20%)

Treatment: imatinib

73
Q

Single most important factor determining use of cryoprecipitate in bleeding?

A

Low fibrinogen

74
Q

APLS in pregnancy

A

Aspirin + LMWH

75
Q

Features AML

A
  • Anaemia and thrombocytopaenia
  • Increased WCC which are non-functioning/immature
76
Q

Which type of vWD have qualitative defects?

A

Type 1 and 3
- von W1-ll-3brand

77
Q

Richter’s transformation signs?

A

Rapidly progressive LN
Raises LDH

78
Q

Most common type of HL?

A

Nodular sclerosing (70%)

79
Q

How to objectively score PET scan in HL?

A

Deuville score?

80
Q

HL and pregnant?

A

ABVD over escalated BEACOPP

81
Q

Mixing studies which fail to correct are suggestive of?

A

Inhibitor e.g. lupus anticoagulant

82
Q

Poor prognostic marker in AML?

A

FLT3 mutation

83
Q

Good prognostic marker in AML?

A

NPM1

84
Q

Reed Sternberg cell in HL?

A

CD15, CD30 positive
- CD45 negative

85
Q

What is elevated in Castleman’s disease?

A

IL-6

86
Q

Treatment of cytokine release syndrome?

A

Steroids + tocilizumab

87
Q

What blood product is used for hypofibrinogenaemia?

A

Cryoprecipitate

88
Q

Most specific test for APLS?

A

B2 glycoprotein

89
Q

Dabigatran and coagulation studies?

A

Prolonged APTT and TT

90
Q

Which pathogen most associated with post-transplant lymphoproliferative disorder (PTLD)?

A

EBV

91
Q

Which cluster of differentiation is associated with stem cells?

A

CD34

92
Q

Erlenmyer flask deformity with haematological malignancy, anaemia, thrombocytopaenia and splenomegaly makes you think? Which cells are associated with this?

A

Gaucher’s disease
- Gaucher cells - macrophages filled with lipid material

93
Q

Indications for CAR-T therapy?

A
  • Relapsed/refractory DLBCL
  • Transformed follicular lymphoma
  • B-cell ALL up to ages 25 years old
94
Q

CD associated with gemtuzumab ozogomicin?

A

CD33

95
Q

What percentage of blasts in CML to be considered blast phase?

A

Blasts >20%

96
Q

Mechanism behind thrombosis in factor V Leiden?

A

Activated protein C resistance

97
Q

What targets BCR-ABL?

A

Imatinib
Dasatinib
Nilotinib

98
Q

Treatment of aHUS?

A

Eculizumab +/- PLEx

Summary of TMA treatment
- Typical HUS (NB: incubation period 1-10 days) > supportive care
- AHUS: as above
- TTP: PLEx

99
Q

Treatment of relapsed/refractory AIHA?

A

Rituximab
- Preferred over splenectomy

Initial treatment of WAIHA
- Predisolone - because steroids reduce production of auto-Ab by B cells

100
Q

Fatty bone marrow makes you think of which diagnosis and what is the treatment?

A

Aplastic anaemia

Severity assessment: modified Camitta criteria
- Marrow cellularity; <25% = severe
- ANC; <0.5 = severe
- Plt; <20
- Retics <20

Treatment
- SCREEN FOR PNH
- Non-severe/no sibling HLA match: ATG/anti-thymocyte globulin + cyclosporine
- Severe and sibling HLA match <40: alloSCT
- Eltromopag (TPO mimetic) as adjunct

101
Q

What is the role of BCL2 proteins?

A

Regulation of intrinsic, mitochondrial APOPTOSIS
- Venetoclax is BCL2 inhibitor

102
Q

Excessive post-op bleeding, easy bruising, menorrhagia and epistaxis suggest which bleeding disorder?

A

Von Williband disease
- Type 1: low amount
- Type 2: quantitative
- Type 3: no vWF (mimics haem A)

103
Q

How to differentiate DIC vs. liver disease?

A

Factor VIII
- Factor VIII is NOT made in the liver so the levels are normal/high (as acute phase reactant)
- Low in DIC as all factors are consumed

104
Q

AIHA summary/serology

A
105
Q

Treatment of CLL?

A
  • Fit and young: FCR (fludarabine, cyclophosphamide, ritux)
  • Fit but old >65: obinuzumab (anti-CD20) + chlorambucil
  • Old with comorbidities: chlorambucil
  • P53 mutation (poor Px): imbrutinib, venetoclax +/- rituximab or ofatumumab
106
Q

Treatment of essential thrombocythaemia

A

JAK2 - higher risk than CALR or MPL

107
Q

MGUS associated with which Ig is associated with higher risk of progression to lymphoid disorder and shorter survival?

A

IgM

108
Q

HIT is associated with which immunoglobulin?

A

IgG

109
Q

Indication for treatment of ITP?

A

Consider if Plt <50
Plt <30
RF incl. HTN, PUD

Treatment
- Glucocorticoids (pred 1-2mg/kg for 2-4 weeks) and IVIg
- Consider TPO
- Aza as steroid-sparing
- Can also use cyclosporine, ritux, anti-RhD Ig

110
Q

Thalidomide MOA and comparison to lenolidomide and pomalidomide?

A

Cereblon E3 ligase modulators AKA immunomodulatory drug with imide
- Anti-IL6, anti-VEGF

111
Q

MM treatment

A

Anti-viral Px and PJP

Proteosome inhibitors
* Bortezomib
* Carfilzomib
* Ixazomib
Immunomodulatory drugs (IMId)
* Thalodomide
* Lenolidomide
* Pomalidomide
Mab
* Daratumumab (anti-CD38
* Elotuzumab (anti-SLAMF7)
Histone deacetylase inhibitor
* Panobinostat
Alkylating agents
* Melphalan
* Cyclophosphamide
* Bendamustine
Others
* Dexamethasone
* Prednisolone
* Cisplatin
* Etoposide
Doxorubucin

112
Q

Parvovirus with anaemia in CLL makes you think?

A

Pure red cell aplasia
- Normocytic, normochromic anemia
- Low retics
- Absent/infrequent erythroblasts in BM

Treat IVIg

113
Q

What is involved in the YEARS algorithm for PE in pregnant women?

A
  1. Clinical signs DVT
  2. Haemoptysis
  3. PE most likely Dx

D-dimer <1 is reassuring

114
Q

Elevated Hb and Hct with aquagenic pruritis makes you think?

A

Polycythaemia vera
- Aim Hct <45%

115
Q

ITP in pregnancy vs. gestational thrombocytopaenia?

A

ITP is earlier is pregnancy (1st trimester), Plt usually <70 and pre-pregnancy thrombocytopaenia

116
Q

Which is higher risk of relapse - therapy-related AML or de novo?

A

Therapy-related/secondary AML
- AlloSCT

117
Q

Alpha thalassaemia summary

A

Carrier: αα/α- (Hb electrophoresis is normal)
Minor/trait: α-/α- or αα/–
HbH (moderately severe): α-/–
Hydrops faetalis: –/–

Chromosome 16

Hb electrophoresis is usually normal

118
Q

Beta thalassaemia summary

A

Increase in HbA2 > abnormal electrophoresis

Haemolysis
Iron excess
Hypoxia > splenomegaly, frontal bossing/skull enlargement

Greece and Italy
Chromosome 11; non-sense mutation > stop codon

119
Q

What is the Khorana score?

A

Risk of VTE in cancer patients
- High risk ≥3 points

120
Q

When to treat superficial vein thrombosis?

A

• Thrombus is >/= 5 cm, or
• Close to the deep venous system or,
• If other thrombophilic risk factors

Anticoagulation for 42 days

121
Q

Treatment of MDS with 5q deletion?

A

Lenolidamide

122
Q

Most common types of myeloma

A

IgG (52%)
IgA (20%)
Kappa or lambda light chain (BJP) (16%)
IgD (2%)
IgM (0.5%) > Waldenstrom’s macroglobulinaemia

IgE - VERY RARE; may progress to plasma cell leukaemia

123
Q

What is Felty’s triad?

A

RA, splenomegaly and neutropaenia

124
Q

Primary malignancy which has the strongest associated with radiation exposure?

A

Leukaemia

125
Q

Imbrutinib MOA and SE?

A

BTK and atrial flutter/atrial fibrillation

126
Q

What CD is on plasma cells?

A

CD 138
CD 38

127
Q

Frequency of mutation in essential thrombocythaemia AKA ET

A

JAK2 V617 60%
CALR 25%
MPL 5%

Unknown/no mutation 10%

128
Q

Which gain of function mutatio is a common co-mutation with JAK2 in myeloid malignancies?

A

ASXL1
- Assoc. AML, CML, MDS
- Usually poor Px

129
Q

Examples of acquired inhibitors

A

Acquired haemophillia A or haemophillia B
- Prolonged APTT which does not correct on mixing studies
- Associated extensive cutaneous bleeding

130
Q

Dasatinib what type of drug and major SE?

A

2nd generation TKI to treat CML
- 30% risk pleural effusion > Tx with diuretics, steroids, drug hiatus; can rechallenge but change TKI if recurrence

131
Q

Nilotinib indication and SE?

A

CML, 2nd gen TKI
- CVS events, metabolic syndrome, LFT derangement

132
Q

Key mechanism behind coagulopathy in APML?

A

Excessive hyperfibrinolysis
- Promyelocytes in APML express Annexin II on surface > excessive activation of tPA > plasminogen to plasmin + degradation of fibrinogen to fibrin > prolongs APTT and PT/INR

133
Q

Which immunoglobulin associated with COLD 🥶 AIHA

A

IgM
- IgMURDER THE CELLS
- Less common

Examples
- IgM monoclonal gammopathy
- Waldenstrom macroglobulinemia
- Mycoplasma pneumonia

134
Q

Degrees of renal excretion for DOACs

A
  • Dabigatran 80-85%
  • Edoxaban 35%
  • Rivaroxaban 35%
  • Apixaban 25%
135
Q

Treatment of methotrexate toxicity

A

Glucarpidase
- Converts MTX to inactive metabolites > rapidly lowers MTX levels
- Use with follinic acid aka calcium follinate

136
Q

What is MOA of zanubrutinib?

A

Inhibits BTK
- Binding to its active site
- Inhibit the proliferation and survival of malignant B cells to reduce the tumour size

137
Q

Someone who has BG APLS and WH warfarin pre-operatively presenting with fever, thrombosis, skin rash, multiorgan failure makes you think?

A

Catastrophic antiphospholipid antibody syndrome (CAPS)
- Treat with anticoagulation, PLEx +/- steroids

BPT Sadness 😔 (20 decks)

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