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Year 4 - Toxicology > 19 - Blood > Flashcards

19 - Blood Flashcards

1
Q

Vital functions of blood

A
  • Transport oxygen
  • Transport drugs
  • Maintain fluid balance
  • Important part of immune system
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2
Q

What is hematopoiesis? Where does it occur?

A
  • Occurs in bone marrow in healthy adults
  • Stem cells stimulated (poietins or colony-stimulating factors) to differentiate into committed cells that further mature
  • The earlier the drug-induced hematological disorder (DIHD) occurs in the cascade of hematopoiesis (differentiation) the more severe the disorder
  • Incidence of DIHD difficult to ascertain (0.01% drug-induced agranulocytosis)
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3
Q

Which drugs suppress bone marrow?

A
  • Methotrexate
  • Cyclophosphamide
  • Colchicine
  • Azathioprine
  • Ganciclovir
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4
Q

What are the types of hematoxicity?

A
  • Primary
  • Secondary
  • Idiosyncratic
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5
Q

What is primary hematotoxicity?

A

Direct cytotoxic mechanism or immunological mechanism

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6
Q

What is secondary hematotoxicity?

A
  • Toxic effect a consequence of other tissue injury or systemic disturbances
  • Damage caused by reactive/ compensatory mechanisms
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7
Q

Lab findings of anemia

A

Decreased RBC (count or volume) or decreased hemoglobin

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8
Q

Lab findings of polycythemia

A

Increased RBC (count or concentration)

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9
Q

Lab findings of thrombocytopenia

A

Decreased platelets

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10
Q

Lab findings of leukopenia

A

Decreased WBCs

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11
Q

Lab findings of granulocytopenia

A

Decreased neutrophils, eosinophils, and basophils

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12
Q

Lab findings of neutropenia

A

Decreased neutrophils

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13
Q

Lab findings of agranulocytosis

A

Very decreased neutrophils

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14
Q

Lab findings of pancytopenia

A

Decrease in all blood cells

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15
Q

Lab findings of hypocoagulability

A

Decreased clotting factors

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16
Q

What are the ways in which drugs may alter RBCs?

A
  • Production
  • Function
  • Survival
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17
Q

How can drugs alter RBC production?

A
  • Cell division/ hematopoiesis
  • Hemoglobin synthesis => iron deficiency anemia
  • Sideroblastic anemia
  • Megaloblastic anemia
  • Aplastic anemia
  • Polycythemia
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18
Q

How can drugs alter RBC function?

A
  • *Through effects on hemoglobin

- O2/ CO2 transport – shifts in oxygen dissociation curve => methemoglobinemia

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19
Q

How can drugs alter RBC survival?

A
  • Normally ~ 120 days but shortened by oxidative injury, decreased metabolism, and/ or altered membrane => hemolytic anemia (immune-mediated or oxidative injury such as G6PD deficiency)
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20
Q

What is sideroblastic anemia?

A

Interference w/ heme synthesis

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21
Q

Causes of sideroblastic anemia? Is it reversible?

A
  • EtOH
  • Isonizaid (w/o vitamin B6 supplementation)
  • Chloramphenicol
  • Cycloserine
  • Linezolid
  • Zinc toxicity/ copper deficiency
  • Lead intoxication
  • Reversible w/ drug d/c
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22
Q

What is megaloblastic anemia?

A

Abnormal development of RBC precursors (megaloblasts)

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23
Q

What can cause megaloblastic anemia?

A
  • Drugs w/ effect on DNA synthesis

- Folate and/or vitamin B12 deficiency from inadequate dietary intake or drugs

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24
Q

Which drugs have an effect on DNA synthesis?

A
  • Anti-neoplastics
  • Immunosuppressants
  • Allopurinol
  • Antiretrovirals
25
Q

Which drugs cause folate and/or vitamin B12 deficiency?

A
  • Drugs that inhibit dihydrofolate reductase (TMP-SMX)

- Drugs that inhibit folate or vitamin B12 absorption/ increase folate catabolism

26
Q

Which drugs inhibit folate or vitamin B12 absorption and/or increase folate catabolism?

A
  • Phenytoin, primidone, phenobarbital
  • Estrogens/ oral contraceptives
  • PPIs/H2RAs
  • Metformin
  • Antibiotics (penicillins, tetracyclines, erythromycin, nitrofurantoin)
27
Q

What causes aplastic anemia?

A
  • Bone marrow failure
  • Injury to pluripotent stem cell in bone marrow
  • Drugs, radiation, pregnancy, viruses, immune disorders, idiopathic
28
Q

Which drugs cause aplastic anemia?

A
  • Anti-neoplastics
  • Bismuth
  • Mercury
  • Sulfonamides
  • Carbamazepine
  • Gold compounds
  • Phenytoin
  • Benzene
29
Q

Sx of aplastic anemia

A
  • Fatigue, weakness
  • Stomatitis
  • Easy bruising
  • Petechiae
  • Purpura
  • Recurrent infections
  • Bleeding
  • Death (sepsis/ hemorrhage) w/in 18 months
30
Q

Aplastic anemia treatment

A
  • Withdrawal of drug
  • Symptomatic tx of bleeding, infection
  • Immunosuppressive -> corticosteroids, cyclosporine, GM-CSF, IL-1, GCSF, antithymocyte globulin
  • Bone marrow transplant
31
Q

Sx of polycythemia

A
  • Chest/ abdominal pain
  • Myalgia/ weakness/ fatigue
  • Headache
  • Paresthesias
  • Blurred vision/ transient loss of vision
  • Poor mentation/ sense of depersonalization
  • Risk of VTE
32
Q

Mechanisms of polycythemia

A
  • Increased erythropoiesis
  • Decreased plasma volume
  • Combination of both (ex: smoking, which causes chronic hypoxia)
33
Q

Which drugs cause increased erythropoiesis?

A
  • Cobalt
  • Blood doping, self-injection of erythropoietin
  • Testosterone (especially ester injections), anabolic steroids
  • Chronic/occupational exposure to CO
34
Q

What is methemoglobin? Is the concentration normally high or low?

A
  • Heme iron oxidized to ferric state, therefore cannot bind/ transport O2
  • Normal control mechanisms maintain low methemoglobin concentration
35
Q

What is methemoglobinemia?

A
  • High methemoglobin concentration
  • Cyanosis appears when concentration > 5-10%
  • Life threatening at 70%
36
Q

What causes methemoglobinemia?

A
  • Oxidizing drugs

- Ex: nitrites, nitrates, nitroglycerin, topical anesthetics, street drugs

37
Q

Antidote for methemoglobinemia? What does it do?

A
  • Methylene blue

- Increases rate of methemoglobin reduction

38
Q

Antidote for methemoglobinemia? What does it do?

A
  • Methylene blue

- Increases rate of methemoglobin reduction

39
Q

What is a hapten?

A

Small molecule that binds to larger carrier and elicits an immune response

40
Q

Which drugs act as haptens?

A
  • Beta lactams
  • Tetracyclines
  • Anti-neoplastics
41
Q

Which drugs induce formation of auto-antibodies to cellular components?

A
  • Levodopa, methyldopa
  • Procainamide
  • Cimetidine
42
Q

Sx and onset of oxidative hemolysis

A
  • Jaundice
  • Pallor
  • Dark urine
  • Onset = 2-4 days
43
Q

What may cause oxidative hemolysis?

A

G6PD deficiency

44
Q

What can cause myeloid leukemias?

A
  • Alkylating agents (ex: melphalan, cyclophosphamide, busulfan, cisplatin)
  • Topoisomerase II inhibitors (ex: etoposide, doxorubicin, mitoxantrone)
  • Antimetabolites (ex: azathioprine, 6-mercaptopurine)
  • Radiation
  • Occupational exposure (benzene, formaldehyde)
  • Tobacco smoke
45
Q

What can cause lymphoid leukemias?

A
  • Radiation
  • Occupational exposure (paint, benzene, formaldehyde)
  • Tobacco smoke
  • Immunosuppression
46
Q

Difference between neutrophils vs. basophils and eosinophils

A
  • Neutrophils = mediate inflammation

- Basophils and eosinophils = modulate inflammation

47
Q

Which drugs affect neutrophil proliferation?

A
  • MTX
  • Cytarabine
  • Cyclophosphamide
  • Cisplatin
48
Q

Which drugs impair phagocytosis of granulocytes?

A
  • EtOH
  • Glucocorticoids
  • Radiocontrast dye
49
Q

Is clozapine neutropenia immune mediated?

A

Yes

50
Q

Many drugs that cause aplastic anemia can also cause ____

A

Toxic neutropenia/ agranulocytosis

51
Q

What is agranulocytosis?

A

Neutrophils < 500/mm3

52
Q

Clinical presentation of agranulocytosis

A
  • Oral ulcers +/- fever
  • Severe pharyngitis, fever, malaise, weakness and chills
  • Sepsis
53
Q

Tx of agranulocytosis

A
  • D/c any drug associated w/ agranulocytosis
  • Symptomatic tx (infections)
  • IV immune globulin
  • G-CSF
54
Q

What affect can drugs have on platelets?

A
  • Alter quantity (either production or survival)
  • Alter activation
  • Alter function (ex: antiplatelets)
55
Q

Clinical presentation of thrombocytopenia

A
  • Early sx = bruising, petechiae/ ecchymosis, epistaxis
    • May be initial manifestation of aplastic anemia
  • Fever, chills, pruritus, lethargy
  • Bleeding may be abrupt (life-threatening hemorrhage)
  • 7 days are required for the development of the immune response after the first exposure
  • Develops w/in 12 hours of a repeated exposure to a sensitizing agent
56
Q

What is heparin-induced thrombocytopenia?

A

Platelet count < 150,000 cells/mm3

57
Q

Types of heparin-induced thrombocytopenia

A
  • Type 1 (non-immune) = early onset, non-thrombotic, self-limiting
  • Type 2 (immune) = delayed onset, unless previously sensitized
58
Q

Tx of thrombocytopenia

A
  • D/c the drug
    • If HIT, start non-heparin anticoagulant (argatroban, DOACs)
    • Anti-coagulate at least 2-3 months if no thrombosis, 3-6 months if thrombosis occurred
  • Transfusions
  • Immunosuppressive therapy
59
Q

Tx for active bleeding w/ warfarin

A
  • Hold warfarin

- Give IV vitamin K and factor concentrates

Year 4 - Toxicology (22 decks)

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