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PHAR 303 (toxicology) > blood > Flashcards

blood Flashcards

final exam

1
Q

what is contained in blood?

A
  • 55% plasma: water, plasma proteins
  • 45%: formed elements: RBCs (99.9%), platelets and WBCs
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2
Q

hematopoisesis

A

the formation of formed elements (RBCs, WBCs, platelets) through formation of myeloid or lymphoid progenitor cells

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3
Q

what are the plasma proteins? (with relative abundances)

A
  • albumin (60%)
  • globulins (35%)
  • fibrinogen (4%)
  • others (1%)
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4
Q

what is serum?

A

plasma- fibrinogen

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5
Q

where do cells come from in the first 8 weeks, 3-7 months, and as an adult?

A
  • yolk sac
  • liver, spleen
  • bone marrow
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6
Q

hematotoxicology

A

the study of adverse effects of the exogenous chemicals on blood and blood-forming tissues (including drugs and non-therapeutic chemicals)

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7
Q

types of toxicity in hematotoxicity

A

primary, secondary

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8
Q

primary hematotoxicity

A

one or more blood component directly affected; common serious effects of xenobiotics

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9
Q

secondary hematotoxicity

A

toxicity because of other tissue injuries or systemic disturbances (sepsis, allergy, chronic inflammatory disease)

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10
Q

consequences of hematotoxicology (which cell does it target)

A
  • hypoxia (erythrocytes)
  • hemorrhage (platelets)
  • infection (immune cells)
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11
Q

erythron

A

all stages of the erythrocyte, including precursors in the bone marrow and circulating mature RBCs

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12
Q

targets of xenobiotics that affect erythrocytes

A
  • production
  • function
  • survival
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13
Q

what is a common effect of xenobiotics that effect erythrocytes?

A

anemia:
- reduction in proportion of RBCs
- A person’s level of hemoglobin within them is lower than a healthy person

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14
Q

anemia definition

A

a reduction in the oxygen carrying capacity of blood due to decreases in hemoglobin (Hb) concentration and red blood cell (RBC) volume.

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15
Q

symptoms of anemia

A

weakness, lethargy, dyspnea

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16
Q

which organs can be affected by anemia

A

all b/c interferes with oxygen delivery to peripheral tissue

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17
Q

3 groups of anemia

A
  1. caused by blood loss
  2. decreased or faulty RBC production/maturation
  3. increased destruction of RBCs
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18
Q

RBC production dependent on: ?

A

frequent cell division and high rate of Hb synthesis

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19
Q

Hb range in males and females

A

males: 14-18 g/dl
females: 12-16 g/dl

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20
Q

heme

A

a porphyrin ring surrounding a single ion of iron (can interact reversibly with oxygen molecule)

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21
Q

what does each Hb contain

A

2 α chains and 2 β chains (making up the Globin), each containing 1 heme

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22
Q

types of anemias

A

iron deficiency anemia, sideroblastic anemias, megaloblastic anemia

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23
Q

erythropoiesis process

A
  • proerythroblast from erythroid progenitor
  • Actively synthesize hemoglobin
  • Hemoglobin appears (day 3)
  • normoblast (Nuclei pyknotic)
  • reticulocyte (Still contains some RNA – ejected nucleus)
  • mature RBC (day 7-8)
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24
Q

steps to hemoglobin synthesis

A

in bone marrow:
- initial: in mitochondria, takes glycine and Succinyl-CoA and converts it – rate limiting step
- intermediate steps: in cytoplasm
- final steps: Incorporation of iron into the porphyrin ring (in mitochondria)

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25
Q

which step is altered in iron deficiency anemia?

A

final step where iron is incorporated into porphyrin ring to make heme

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26
Q

recommended intake of iron for male and female

A

male: 8 mg/day
female: 18 mg/day

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27
Q

what can cause iron deficiency anemia?

A
  • Inadequate iron consumption
  • Decreased iron absorption
  • Iron loss secondary to blood loss
  • drugs that contribute to bleeding (e.g. NSAIDs)
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28
Q

sideroblastic anemia definition

A

Abnormal utilization of iron

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29
Q

what characterized sideroblastic anemia

A

the presence of ring sideroblasts in the bone
marrow; Erythroblasts with iron-loaded mitochondria (caused by buildup of iron)

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30
Q

what are the causes of sideroblastic anemia

A

defections in the synthesis of the porphyrin ring by:
- hereditary causes
- Acquired due to exposure of toxic substance (more common)

31
Q

effect of lead (Pb)

A

interferes with the first, second and last step of heme synthesis:
- first (rate-limiting): Aminolevulinic acid synthase
(ALAS)
- second: δ-aminolevulinic dehydratase
(ALAD)
last: incorporation of iron in porphyrin ring by Ferrochelatase

32
Q

what does PLP do?

A

is a cofactor for ALAS activity

33
Q

what is PLP?

A

pyridoxal-5-phosphate, an active form of vitamin B6

34
Q

effect of Isoniazid

A

inhibits PLP, which inhibits ALAS activity

35
Q

megaloblastic anemia

A

low RBC count, characterized by RBC precursors called megaloblasts (in the bone marrow) that are larger than normal

36
Q

what causes megaloblastic anemia

A

Any defect that causes a slowing of DNA synthesis (inhibits nuclear division) such as folate or vitamin B12 deficiency or malabsorption (since needed for DNA synthesis)

37
Q

where does vitamin b12 and folate come from

A

vit. B12: all foods of animal origin
folate: many foods of plant origin

38
Q

path of dietary vitamin B12

A
  • ingested
  • combined with haptocorrin in stomach
  • trsnsferred to intrinsic factor by gastric parietal cells
  • goes down small intestine
  • complex binds to receptor in terminal ileum
  • then it enters circulation, where it can be utilized by cells or stored in the liver
39
Q

path of dietary folate

A
  • ingested
  • undergoes hydrolysis in GI
  • absorbed in duodenum and jejunum
  • enters enterocytes, where enters folate cycle (makes N5-methyl THF)
  • enters cell or stored in liver
40
Q

what nucleotide is rate-limiting factor for DNA synthesis, why?

A

thymidylate since requires folate and vit. B12, so it is the one that is made the least

41
Q

how does chronic alcohol consumption lead to megaloblastic anemia?

A
  • it damages the gastric mucosa and thus decreases production of intrinsic factor, which decreases vit. B12 absorption
  • its affects intestinal mucosa to interfere with absorption of folic acid (jejunum) and Vitamin B12 (ileum)
42
Q

what can cause drug-induced megaloblastic anemia?

A
  • fluorouracil (suicide substrates): inhibits thymidylate synthase
  • methotrexate: block metabolism of folate
43
Q

aplastic anemia definition

A

inability of stem cells in bone marrow to generate mature blood cells (bone marrow hypoplasia)

44
Q

forms of aplastic anemia

A
  • pancytopenia
  • reticulocytopenia
  • pure red cell aplasia: rare
45
Q

pancytopenia

A

deficiency in red cells, leukocytes and platelets

46
Q

reticulocytopenia

A

reticulocyte (aka immature RBCs) count < 0.2%

47
Q

Pure red cell aplasia

A

absent or infrequent erythroblasts

48
Q

what causes aplastic anemia?

A
  • genetic: mutations affects DNA repair
  • damage to bone marrow: immune-mediated or direct toxicity
49
Q

ways which you can acquire aplastic anemia (which specific chemicals)

A
  • Iatrogenic (caused by treatment): radiation, drugs
  • chemicals: pesticides, arsenic, benzene, mercury
50
Q

most common rout of exposure of benzene

A

inhalation

51
Q

where is benzene found/produced?

A
  • widely used in industries (plastic, resin, fibers, rubber, …)
  • in crude oil (gasoline)
  • cigarette
  • naturally by volcanoes and forest fires
52
Q

IARC classification of benzene

A

class 1

53
Q

how does benzene cause leukemia?

A
  • converted to benzene oxide then to hydroquinone by CYP2E1 in liver
  • it can go in bone marrow and become benzoquinone, which causes toxicity
54
Q

normal lifespan of eryhthrocytes

A

120 days

55
Q

hemolytic anemia definition

A

Increased destruction of erythrocytes

56
Q

forms of hemolytic anemia

A
  • immune
  • non-immune (aka oxidative hemolytic anemia)
57
Q

immune hemolytic anemia + cause(s)

A
  • Interaction of antibodies (IgM or IgG) against antigens on the RBC – Initiates destruction of the RBC through complement or phagocytic cells
  • rare complication of drugs – penicillin: Binds on RBC surface → immune response against drug-coated RBC
58
Q

oxidative hemolytic anemia + cause(s)

A
  • increase in ROS due to G6PD deficiency, which usually supplies NAPDH
  • X chromosome-linked recessive mutation (males more affected): most asymptomatic until exposed to hemolytic trigger
  • favism
59
Q

favism

A
  • is high in B-glucosides
  • undergoes conversion to divicine and isouramil in digestive tract, which are highly reactive
  • produces ROS
  • Detoxified in a normal cell but not in G6PD deficient cell, causing RBC destruction due to oxidative damage
60
Q

Methemoglobinemia definition

A
  • a condition where the iron in hemoglobin is oxidized from the ferrous to the ferric state
  • this is something that occurs normally, but the level of methemoglobin is kept very low (converted back by CYP450s)
61
Q

effect of methemiglobinemia

A
  • ferric hemoglobin not capable of binding and
    transporting oxygen, which reduces oxygen-carrying capacity of the blood
  • leads to anemia, tissue hypoxia, cyanosis
62
Q

what causes Methemoglobinemia?

A
  • congenital: rare, Cytochrome b5 reductase deficiency
  • acquired: food preservatives; sodium nitrate, nitrates in fertilizers (ground water/food)
63
Q

why are infants more susceptible to methemoglobinemia?

A
  • Have higher proportion of Fetal Hb (may be more rapidly oxidized to HetHb than adult Hb)
  • Infants have lower levels of MetHb reductase than adults: more sensitive to nitrate/nitrite toxicity
64
Q

what can be given to reverse methemoglobinemia? how does it work?

A

methylene blue
- acts as a substrate for NADPH MetHb reductase, so transfers its electrons to hemoglobin

65
Q

what are platelets, what are they important for?

A
  • small blood cells that form clots to stop bleeding
  • important for blood clotting
66
Q

where and by what are platelets produced?

A

in bone marrow by megakaryocytes

67
Q

life of platelet

A

9-12 days

68
Q

thrombocytopenia

A

abnormal depletion of platelets (too much destruction or inadequate production)

69
Q

thrombocytosis

A

excessive number of platelets

70
Q

effect of alcohol on platelets

A

causes destruction of megakaryocytes leading to thrombocytopenia

71
Q

what can cause thrombocytopenia?

A

drugs such as penicillin, which can cause immune-mediated platelet destruction, by acting as a hapten on platelets

72
Q

blood clot formation

A

need clotting factors that convert prothrombin to thrombin, which converts fibrinogen to fibrin, which acts as a net to form clots.

73
Q

effect of warfarin

A

interferes with the vitamin K cycle, limiting the amount in its active form, which decreases clotting since vitamin K is a cofactor for clotting factors IX, VII, X, and II

PHAR 303 (toxicology) (14 decks)

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