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Blood and Lymph > Exam 1 Part 2 > Flashcards

Exam 1 Part 2 Flashcards

1
Q

Methemoglobin - how do you get it?

A

acquired or genetic

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2
Q

Acquired Methemoglobin

A

acquired from drugs, well water with nitrates, cyto B5 reductase

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3
Q

Acquired methemoglobin treatment

A

removal of inciting drug or chemical, treat with methylene blue to reduce cyanosis and tachypnea

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4
Q

Genetic methemoglobin

A

AR or AD; cytochrombe B5 reductase deficiency, mutation in alpha or beta globin.

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5
Q

Cyto B5 Reductase

A

keeps iron in ferrous form, reduced in genetic forms of methemoglobin

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6
Q

Newborns and Methemoglobin

A

more suseptible due to th HbF more readily oxidized to ferric state and lower Cyto B5 reductase activity

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7
Q

Carbon Monoxide binding afinity

A

240X higher than oxygen

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8
Q

Carboxyhemoglobin

A

formed when Hb binds to CO instead of O

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9
Q

Symptoms of CO poisoning

A

headache, malaise, nausea, dizzines, seizures, coma, MI, loss of cognition, movement disorders. Cherry Red.

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10
Q

Treatment and diagnosis of CO poisoning

A

100% oxygen or hyperbaric oxygen, diagnosis by CO-oximetry

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11
Q

How is pulse ox measured?

A

two light emitting diodes at 660 nm and 940 nm that measures the deoxyhemoglobin and oxyhemoglobin absorbption by pulsatile flow.

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12
Q

Flaws in pulse ox?

A

movement, nail polish, deeply pigmented skin, shock, anemia, does measure CO.

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13
Q

Anemia

A

insufficient Red cell mass to adequates deliver oxygen to peripheral tissue

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14
Q

how do we define the existence of anemia - lab?

A

Hb concentration, Htc, RBC count

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15
Q

Variation of Hb with age?

A

At birth Hb is 17% and drops to child level by 3months - 5 yars. Children have less Hb than adults 12%

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16
Q

Routine lab tests in the CBC for anemia?

A

Hb, Hct, RBC count, MCV, RDW, RBC morphology, Retic Count

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17
Q

how long are retics in marrow

A

3 days

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18
Q

how long are retics in blood

A

1 day

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19
Q

normal retic count

A

0.4-1.7%

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20
Q

Absolute Retic Count

A

% * RBC count

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21
Q

Retic Index use

A

corrects for altered red cell concentration and stress reticulocytes

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22
Q

RI calculation

A

Pt Hb/Normal Hb * (1/Stress retic factor)

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23
Q

symptoms of anemia

A

shortness of breath, tachypnea, Dyspnea (labored breathing), fatigue, Rapid HR (tachycardia), dizziness, claudication, angina, pallor,

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24
Q

Claudication

A

pain in extremeities while moving

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25
Q

Dyspnea

A

labored breathing

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26
Q

where is Fe more soluble?

A

low pH

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27
Q

How is Fe balanced?

A

controlled by absorbion and NOT through excretion

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28
Q

How is Fe lost?

A

exfolication of skin, mucosal surfaces GI, urine, mestruation

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29
Q

Iron is mostly stored where?

A

65% in Hb; 13% ferritin, 12% hemosiderin 6% myoglobin 0.1% trabsferrin

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30
Q

Iron Absorption on apical membrane

A

DCYTP converts from Ferric to Ferrous (2+) and transports through DMTI

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31
Q

DCYTP

A

Cytochrome B like protein - converst Ferric to ferrous on apical surface

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32
Q

DMT1

A

divalent metal ion transporter, transports Ferrous iron into epithelial cell

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33
Q

Iron Absorption on BL membrane

A

Ferroportin transporters Ferrous iron out and Hephasetin converst to Ferric

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34
Q

Ferroportin

A

on BL membrane and trasnporter Ferrous iron out of cell

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35
Q

Hephaestin

A

on BL membrane and converts Ferrous to Ferric

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36
Q

Hepcidin

A

produced by liver due to high iorn intake, inflammation and infection; concentration decreases with anemi and hypoxia

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37
Q

increasing hepcidin_.

A

decreases the amount of ferroportin and decrease iron transfer from epithelial cells

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38
Q

How do we increase Fe absorption?

A

Amino acids, vit C, high iron diet, increase erythropoesis, low pH, increase gastroferrin

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39
Q

how do we decrease Fe absorption?

A

phytates and oxalates

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40
Q

Hemochromatosis

A

deficiency in hepcidin

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41
Q

Iron Cycle

A

Fe from GI, liver, macrophages binds to Transferrin in Ferric form. Tansferrin interacts with receptors to bring iron intracellularly for Ferritin storage or use.

42
Q

Ferritin vs Hemosiderin

A

both intracellular storage, but Ferritin binds reversibly to Ferric form

43
Q

how do transferrin boudn iron get into cell?

A

binds to receptor on cell surface and forms clatharin coated vesicle

44
Q

How does transferrin release iron onces encdocytosed?

A

opening of Proton pumps intracellularly.

45
Q

How does iron get into cytoplasm from intracllular vesicle?

A

through DMT1 channel

46
Q

Apo-Transferrin

A

Transferrin not boung to Fe

47
Q

Intraluminal factors for Fe absorbtion

A

Gastric factors (low pH, gastroferrin), protein, AA, Vit C, phytates, oxalates, iron ingested

48
Q

Extraluminal factors for Fe absorption

A

Erythropoietic activity

49
Q

Transferrin

A

plasma mprotein that binds 2 molds of Ferric iron; high binding affinity

50
Q

Ferritin vs Hemosiderin

A

Intracllular sotrage, mulimeric structure. Protein coat with center that contains feric.

51
Q

How do splenic macrophages affect iron?

A

ingest RBCs and isoalte iron and bidn to Ferritin, where is it converted to ferrous and transproted by ferroprotin in plasma to bind with transferrin.

52
Q

What converts Ferrous to Ferric on splenic macrophages

A

ceruloplasmin

53
Q

what converst ferric to ferrous in splenic macrophages

A

xanthine oxidase

54
Q

Hepcidin controls_

A

peptide produced by hepatocyte, negative regualtor for Fe absorption in GI, trasnprot by placent or release from macrophages.

55
Q

Inflammation and infection with hepcidin

A

inhibition of ferroportin – iron retetion in macrophages and continued anemia

56
Q

what lab tests are characteristic of iron depetion

A

low marrow Fe, slighly elevated transferrin IBC, low serum ferritin, increased iron absoprtion

57
Q

what lab tests are characteristic of Iron deficient erythropoesis?

A

0 marrow Fe, elevanted transferrin and iron abosrption, low Serum ferritin AND, low Serum iron, low transferrin sat, lo

58
Q

what lab tests are characteristic of iron deficient anemia

A

0 Marrow Fe, extremely elevanted Transferrin IBC, low serum ferritin, increased iron abs, low serum iron, low Trasnferrin saturation, microcytic cells

59
Q

Characteristics of Iron Deficiency

A

decreased hb syntehesis and cell proliferation, multiple sympoms based

60
Q

Iron deficient anema - nueromuscular defects

A

mild defects in performance, muerpsych dysfunction

61
Q

Fe def anemia - epithelial cahnges

A

ridges and koilonychia on nails, papillary atrophy on tongue

62
Q

Fe def anemia - GI

A

dysphagis, esophageal webs, gastritis, protein loosing enteropathy

63
Q

Immune system and Fe Deficiency

A

innate and adaptive immune dysfunction

64
Q

pica

A

eating things with iron to account for Fe deficiency

65
Q

what population is Fe deficiency most common?

A

9% in infants/toddlers, 11% adolesecent females

66
Q

what causes Fe deficiency?

A

decreased intake, increased loos, increased need (due to infancy, pregnancy, lactation)

67
Q

Fe Def anemia diagnosis

A

decreased Hb and Hct, decreased Retic count, microcytsosis, hypochormia, increase RDW; dec serum Fe and ferritin, increase TIBC and FEP

68
Q

Fe Deficient anemia treatment

A

oral iron 150-200 mg/day in 3 doses or 4-6 mg/kd/day in 3 doeses

69
Q

Iron overload

A

due to increase in diet, increased abosprtion due to HFE gene, and repeat transfusions.

70
Q

Iron overlad diagnosis

A

increased serum iron, infreased ferritin, invreased liver iron

71
Q

symptoms of iron overlad

A

cardiac failure, liver dysfunction and failure, diabetes

72
Q

treatment for hemochromatosis

A

therapeutic phlebotomy

73
Q

Hemosiderosis

A

iron chelators

74
Q

desferal

A

IV or SC infusion of iron chelator

75
Q

Exjade

A

oral iron chelator

76
Q

where does hematopoesis occur in embryonal state?

A

yolk sac

77
Q

where does hematopoesis occur in fetal stage?

A

liver/spleen (switches from yolk sac at 4-5 months)

78
Q

Post-natal hematopoiesis

A

at birth in marrow, including long bones. But as child ages switches to axial skeleton in vertebrae, pelivs, sternum, ribs,aand skull

79
Q

Platelet life span

A

8.5 days; 200 billion per average man/day

80
Q

how many RBC produced in average man

A

175 billion/day

81
Q

Nuetrophils/granulocytes life span

A

7 hours; 70 billion per average man/day

82
Q

myeloid

A

non-erythorid and non-lymphoid lineages - granulocytes, monocytes, megakaryoctes, platelets

83
Q

Lymphoid

A

T, B and NK cells lineages

84
Q

Self renew

A

production of daughter cell that are completely unchanged, capable of cell renewal or committed to differentiation.

85
Q

hematopoietic Stem cells

A

mother of all blood cells and grive rise to lymphoid and myeloid elements

86
Q

Pluripotent Stem cells

A

Colony Forming Units _ lymphoid or GEMM - granulocyte/erythroid,monocyte,megakaryocyte

87
Q

Progenitor Cells

A

self renewal is liminted; irreverisbly commit to differenitation along myleoid progenitage or burst forming erythroid

88
Q

Precursor Cells

A

maturing cells visible in the marrow; capable (somewhat of cell divison) but cannot self renew; give rise to mature functional cells in peripheral blood.

89
Q

Cortical bone

A

bone in between trabeculae which holds marrow

90
Q

Sinusoids:

A

leaky blood vessles to allow communication between marrow and periphery

91
Q

Erythropoietin

A

EPO made by kidney in response to hypoxia, promote erythropoiesis

92
Q

Thrombopoietin

A

TOP promotes megakaryopoiesis

93
Q

Granulocyte-Monocyte colony stimulaiting factor

A

promotes granulopoiesis and monopoiesis

94
Q

Granulocyte-colon stimulating factor

A

promotes grannulopoiesis

95
Q

Interleukin 5

A

promotes eosinophil production

96
Q

Interluekin 3

A

promotes basophil production

97
Q

pattern of erythropoeisis

A

progenitor –> proerythroblast –> basophilic erythroblast –> reticulocyte –> erythrocyte

98
Q

Function of EPO in erythropoiesis

A

differentiate and mature basophilic erythroblast and allows to leave marrow as reticulocyte

99
Q

Hypoxia

A

biggest driving factor of RBC production; triggers EPO activation to increase mitosis and maturation and Hb levles

100
Q

characteriscics of cell maturation

A

cells get slightly smaller with more condensed chromatin. Greyish cyto accumulates Hb.

101
Q

Mekagaryopoiesis

A

Thrombopoesis. Megakaryblast matures to mekakarycoyte –> platelet.

102
Q

treatment of G6PD deficiency

A

supportive care, avoid oxidant drugs/food, folate, transfusion if severe

Blood and Lymph (6 decks)

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