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PR3154 > IC3- Blood Dyscrasias > Flashcards

IC3- Blood Dyscrasias Flashcards

1
Q

What are the 3 types of anaemias we will talk about here?

A
  1. Nutritional deficiency anaemia
  2. Aplastic anaemia
  3. Haemolytic anaemia
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2
Q

Describe anaemia caused by nutritional deficit.

Which nutritional deficit leads to micro/macrocytic RBCs?

A

Vit B12, folate and iron deficiency.

  • Vit B12 and folate deficiency → macrocytic RBCs
  • Iron deficiency → microcytic RBCs
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3
Q

What Tx can we give for iron-deficient anaemia?

A

Oral Fe3+ salts [ferrous sulphate], parenteral (IV) [iron sucrose]

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4
Q

How is iron supplements eliminated? What must we be careful of?

A

Elimination: minimal elimination in faeces, bile, urine and sweat

Careful dosing to avoid toxicity

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5
Q

ADEs of iron supplements? (Acute: 1, Chronic: 1)

A

Acute:
- Necrotizing gastroenteritis (necrosis of GI tract) with vomiting, abdominal pain, bloody diarrhoea followed by shock, lethargy, dyspnea, metabolic acidosis, coma and death

Chronic:
- Haemochromatosis → iron deposited in heart, liver, pancreas, other organs → organ failure, death

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6
Q

What are the Tx of overdose of iron? (2)

A

Parenteral deferoxamine or oral deferasirox iron chelators

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7
Q

What Tx can we give for Vit B12-deficient anaemia?

A

Cyanocobalamin, parenteral [hydroxocobalamin]

Hydroxocobalamin preferred as more protein binding → retains longer in circulation

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8
Q

Why is Cyanocobalamin/ Hydroxocobalamin not given as oral agent?

A

Oral not usually effective → deficiencies usually caused by GI malabsorption

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9
Q

What is the elimination and elimination t1/2 of Cyanocobalamin/ Hydroxocobalamin?

A

E: bile and urine (excess stored in liver, normally 3 years supply stored)

E t1/2: 26 - 31h (IV)

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10
Q

ADEs of Cyanocobalamin/ Hydroxocobalamin?

A
  • Photosensitivity → avoid direct exposure to sunlight
  • Injection site pain
  • HTN, hot flushing, arrhythmias secondary to hypokalemia
  • GI disturbances
  • Dizziness, tremor, headache,
  • Paresthesia (tingling/ numbing)
  • Chromaturia (abnormal urine colour)
  • Acneiform, bullous eruptions, rash, itching
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11
Q

DDIs of Cyanocobalamin/ Hydroxocobalamin?

A

PPIs → reduce oral absorption

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12
Q

Absorption (F, time to peak plasma conc), metabolism (name the active metabolite) and excretion of folic acid?

A

A; rapidly absorbed, F ~100%, peak plasma conc: 1h
M; liver and plasma, converted to active metabolite 5-methyltetrahydrofolate (5MTHF) → enterohepatic circulation
E; urine

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13
Q

Contraindications of folic acid? (2)

A
  • Untreated cobalamin deficiency (including untreated pernicious anaemia or other causes eg lifelong vegetarians)
  • Malignant disease
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14
Q

Special precautions of folic acid use? (5)

A
  • Folate-dependent tumours, haemolytic anaemia, alcoholism
  • Women with pre-existing diabetes, obesity, family Hx of neural tube defects, previous pregnancy affected by neural tube defect
  • Not appropriate for monoTx in pernicious, aplastic, or normocytic anaemia when anaemia is present with vit B12 deficiency
  • Children
  • Pregnancy & lactation
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15
Q

ADEs of folic acid? (3)

A
  • GI disturbances: bitter/ bad taste, nausea, abdominal distension (swelling), flatulence
  • Immune system disorders (rare): allergic reactions (rash, pruritus, erythema, urticaria (hives), dyspnoea, shock), allergic sensitization
  • Metabolism and nutrition disorders: anorexia (rare)
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16
Q

DDIs of folic acid? (6)

A
  • ↓ plasma conc of anticonvulsants (phenytoin, phenobarbital, carbamazepine, valproic acid)
  • ↑ efficacy of lithium
  • ↓ therapeutic effect of methotrexate chemotherapy
  • ↑ elimination with aspirin
  • ↓ absorption with sulfasalazine and triamterene
  • Chloramphenicol and sulfamethoxazole + trimethoprim may interfere with folate metabolism
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17
Q

Name the 2 Erythropoiesis -Stimulating Agents (ESAs)

A

Darbepoetin alfa, epoetin alfa

18
Q

Contraindications of ESAs? (2)

A
  • *Uncontrolled HTN
  • Hypersensitivity (rare)
19
Q

Special precautions of ESAs? (6)

A
  • *HTN
  • *Hx of seizure
  • Ischaemic vascular disease
  • Hepatic impairment, renal impairment
  • Sickle cell anaemia
  • Pregnancy, lactation, children
20
Q

ADEs of ESAs? What are the ADEs specific to Epoetin alfa and Darbepoetin alfa?

A
  • *HTN, edema, ↑ platelet count, *thrombosis, stroke, hyperK, seizures, myalgia (muscle aches), arthralgia, limb pain, GI effects (n/v)
  • *Epoetin alfa: pruritus
  • *Darbepoetin alfa: dyspnoea, cough, bronchitis
21
Q

What are the 2 types of aplastic anaemia and drugs that cause them (ALL impt!)?

A
  1. Dose-dependent direct drug toxicity → cancer chemotherapies, chloramphenicol
  2. Idiosyncratic (toxic metabolites) → carbamazepine, phenytoin
22
Q

What is the management for aplastic anaemia? (6)

A
  1. Withdraw causative drug if possible
    *2. Immunosuppressants: glucocorticoids, ciclosporin, cyclophosphamide, azathioprine, antithymocyte immunoglobulin
  2. Transfusion of erythrocytes and platelets
  3. Symptomatic Tx for infections
    *5. GM-CSF (granulocyte-macrophage colony-stimulating factor), G-CSF (granulocyte colony-stimulating factor) [filgrastim, sargramostim], interleukin-14 may be given
  4. HSCT (haematopoietic stem cell transplantation) may be necessary
23
Q

What are the 2 types of haemolytic anaemia?

A
  1. Immune haemolytic anaemia
  2. Non-immune haemolytic anaemia
24
Q

What are the 3 types of immune haemolytic anaemia and drugs that cause it?

A
  1. Drug-induced true autoAb production → *methyldopa
  2. Innocent bystander (immune complex) autoAb production → quinine, *quinidine
  3. Hapten-induced haemolysis → *penicillins, *cephalosporins, *streptomycin
25
Q

What are the types of non-immune haemolytic anaemia and drugs that cause it (ALL impt!)?

A

Protein adsorption → cisplatin, oxaliplatin, β-lactamase inhibitors

26
Q

What is the management for haemolytic anaemia?

A
  1. Withdraw drug if possible
  2. RBC transfusion if VERY LOW Hb
  3. HD may be required for pts with acute renal failure
    *4. Steroids and immunoglobulins in serious cases (eg glucocorticoids, antithymocyte immunoglobulin)
    *5. For auto-immune haemolytic anaemia, rituximab (human anti-CD20 monoclonal Ab) can be used
27
Q

What are the type of drugs used for Tx of thrombocytopenias?

Name specifically the drug name also

A

Megakaryocyte growth factors/ Platelet-Stimulating Agents (PSAs)

  1. Recombinant IL-11 (oprelvekin)
  2. Fc-fusion protein thrombopoietin receptor agonist (romiplostim)
  3. Oral non-peptide thrombopoietin receptor agonists (eltrombopag) → higher dose for non-east asian pts (NOT chinese, koreans, japanese, taiwanese, thai)
28
Q

General ADEs of Megakaryocyte growth factors/ Platelet-Stimulating Agents (PSAs)? (esp for oprelvekin?)

A
  • *Thromboembolic events
  • *Oprelvekin: fluid rtn, peripheral edema, dyspnoea on exertion
29
Q

Special precautions of Megakaryocyte growth factors/ Platelet-Stimulating Agents (PSAs)?

A
  • *Pt with or Hx of cerebrovascular disease
  • *Risk factors for thromboembolism (eg. advanced age, prolonged immobilisation, malignancies, surgery/ trauma, bleeding, obesity, smoking, contraceptives and HRT)
  • *Oprelvekin: chronic HF/ at risk of developing HF/ susceptibility to develop fluid rtn
30
Q

What are the drugs that cause immune thrombocytopenia? (ALL impt!)

A

Heparin, sulfonamides, carbamazepine, phenytoin, GPIIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban)

31
Q

Management of immune thrombocytopenia?

A
  1. Withdraw causative drug if possible
    *2. Immunosuppressants: glucocorticoids, ciclosporin, cyclophosphamide, azathioprine, antithymocyte immunoglobulin
  2. Platelet transfusion
32
Q

What are the drugs used for treatment of neutropenia?

Name the specific drug names too

What is their MOA?

A

Myeloid growth factors (MGF):

  1. Recombinant G-CSF (filgrastim, pegfilgrastim (+ plerixafor))
  2. Recombinant GM-CSF (sargramostim)

MOA: stimulate myeloid progenitor cells

33
Q

General ADEs of MGF?

A
  • Potentially fatal (severe sickle cell crisis, capillary leak syndrome, respiratory failure or acute respiratory distress syndrome ARDS, (rare) splenic rupture)
34
Q

What are the special precautions for use of MGF in neutropenia?

A
  • Pts with premalignant or malignant myeloid condition, acute myeloid leukaemia, sickle cell trait or disease, recent Hx of pneumonia/ lung infiltrates, osteoporotic bone disease
35
Q

Contraindications of use of MGF in neutropenia?

A

AVOID IN chronic myeloid leukaemia or myelodysplastic syndrome

36
Q

In clinical practice, is G-CSF (-grastims) or GM-CSF (-gramostims) used more commonly?

A

G-CSF used first (better tolerated), if no response then GM-CSF

37
Q

Difference between MOA of G-CSF (-grastims) and GM-CSF (-gramostims)?

A

G-CSF (-grastims):
- Stimulates proliferation and differentiation of progenitors committed to neutrophil lineage
- Additionally activates phagocytic activity of mature neutrophils and prolongs survival in circulation

GM-CSF (-gramostims):
- Broader effects than G-CSF → stimulates proliferation and differentiation of early and late granulocytic, erythroid and megakaryocyte progenitors

38
Q

What is the difference between G-CSF filgrastim and pegfilgrastim?

A

Pegfilgrastim is filgrastim covalently conjugated with PEG to extend t1/2

39
Q

ADEs of G-CSF?

A

Bone pain (reversible if drug discontinued)

40
Q

ADEs of CM-CSF?

A
  • Fever, malaise, arthralgias, myalgias
41
Q

What are the types of neutropenia and what drugs cause them? (3)

A
  1. Direct drug toxicity → *thiamazole, chlorpromazine, ticlopidine, busulfan, zidovudine
  2. Toxic metabolite → *clozapine, *carbimazole
  3. Immune (hapten/ complement mediated) → *β-lactam antibiotics, propylthiouracil
42
Q

Management of neutropenia?

A
  1. Withdraw causative drug if possible
  2. *Prophylactic administration of haematopoietic growth factors such as G-CSF (filgrastim/ pegfilgrastim) or GM-CSF (sargramostim)
  3. Routine (weekly) monitoring of WBC, esp for pts treated with clozapine

PR3154 (11 decks)

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