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nur 326 exam 1b > Disorders of RBCs > Flashcards

Disorders of RBCs Flashcards

1
Q

role of Hgb

A

–reversibly binds oxygen and CO2 for transport
–adequate Hgb necessary for oxygen delivery to the tissues

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2
Q

RBC/Bus analogy

A

Bus = RBC
Seats = Hgb
What seats are made of = Iron
Passengers = Oxygen

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3
Q

All diseases of RBCs mean … ?

A

less oxygen is able to be transported to the tissues

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4
Q

anemia type d/t abnormal Hgb

A

sickle cell

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5
Q

name for abnormally large, regular Hgb concentration RBCs

A

macrocytic, normochromic

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6
Q

what anemias have macrocytic, normochromic RBCs?

A

B12 and folate deficiencies

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7
Q

name for abnormally small, low Hgb concentration RBCs

A

microcytic, hypochromic

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8
Q

what anemia has microcytic, hypochromic RBCs?

A

iron deficiency anemia

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9
Q

name for normal size, normal Hgb concentration RBCs

A

normocytic, normochromic

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10
Q

what conditions have normocytic, normochromic RBCs?

A

–blood loss
–sickle cell
–aplastic anemia

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11
Q

relationship between microcytic and MCV

A

microcytic = decreased MCV

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12
Q

relationship between macrocytic and MCV

A

macrocytic = increased MCV

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13
Q

effect of B12/folate deficiencies on RBCs

A

negatively affects DNA synthesis in RBCs

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14
Q

normal Hgb levels

A

Male: 14-18
Female: 12-16

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15
Q

mild anemia Hgb levels

A

Male: 10-13.5
Female: 10-12

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16
Q

moderate anemia Hgb level

A

8 - <10

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17
Q

severe anemia Hgb level

A

< 8

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18
Q

why are anemia symptoms present?

A

due to decreased oxygen carrying capacity

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19
Q

mild-moderate anemia symptoms

A

–fatigue
–weakness
–tachycardia
–dyspnea

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20
Q

moderate-severe anemia symptoms

A

–increased HR and RR
–hypotension, pallor, faintness
–CV symptoms (esp. with exertion)

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21
Q

pathophys cause of weakness in anemia

A

decreased oxygen to muscles

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22
Q

pathophys cause of fatigue in anemia

A

decreased energy production

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23
Q

pathophys cause of pallor in anemia

A

blood redistribution away from skin and toward major organs (compensatory mechanism)

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24
Q

pathophys cause of increased HR, palpitations in anemia

A

increased cardiac output (compensatory)

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25
Q

pathophys of bone pain in anemia

A

increased secretion of erythropoietin

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26
Q

pathophys of chest pain/heart failure in anemia

A

decreased oxygenation of cardiac muscle

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27
Q

pathophys of dyspnea/increased RR in anemia

A

decreased overall oxygenation

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28
Q

demographic factors of iron deficiency anemia

A

–elderly
–teenager
–female
–immigrant
–aborigine
–widower

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29
Q

dietary factors of iron deficiency anemia

A

–low iron, haem iron
–low vitamin C
–excess phytate
–excess coffee/tea
–fad diets

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30
Q

social/physical factors of iron deficiency anemia

A

–poverty
–poor dentition
–candle burning
–alcohol abuse
–GIT disease
–depression

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31
Q

etiologies of iron deficiency anemia

A

–decreased INTAKE of iron
–impaired ABSORPTION of iron
–increased DEMAND for iron
–excessive loss (GI bleed, menstruation)

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32
Q

symptoms of iron deficiency anemia

A

–general symptoms of anemia
–smooth tongue/glossitis/mouth ulcers/cheilosis
–koilonychia (“spoon nails”)
–pica

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33
Q

megaloblastic anemia

A

condition in which the bone marrow produces unusually large, structurally abnormal, immature RBCs

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34
Q

leading cause of megaloblastic anemia

A

B12 and folic acid deficiency

35
Q

why are B12 and folic acid needed in RBCs?

A

DNA synthesis

36
Q

who is most likely to have megaloblastic anemia?

A

elderly

37
Q

atrophic gastritis

A

stomach lining has thinned causing decreased intrinsic factor

38
Q

what do parietal cells produce?

A

acid (iron absorption) and intrinsic factor (B12 absorption)

39
Q

most common cause of B12 deficiency

A

pernicious anemia (autoimmune)

40
Q

what are some diseases that can cause a reduction of IF?

A

–Crohn’s
–celiac
–bacterial growth
–parasite

41
Q

symptoms of B12 deficiency

A

–symptoms of anemia
–neuropathy
–ataxia
–glossitis
–dementia/psychosis

42
Q

what is a folate deficiency caused by (broadly)?

A

decreased intake and increased need

43
Q

examples of decreased intake for folate deficiencies

A

–alcoholism
–diet
–cirrhosis

44
Q

example of increased need for folate

A

pregnancy

45
Q

where is folate stored?

A

liver

46
Q

main etiology of chronic kidney disease

A

impaired erythropoietin production

47
Q

what is erythropoietin?

A

what is released to tell our bone marrow to make RBCs

48
Q

relevance of Hgb/Hct in chronic kidney disease

A

correspond with the degree of kidney insufficiency

49
Q

symptoms of chronic kidney disease

A

s/s of anemia

50
Q

aplastic anemia

A

–primary condition of bone marrow stem failure
–rare
–autoimmune is most common

51
Q

what is aplastic anemia characterized by?

A

pancytopenia

52
Q

what is pancytopenia?

A

decreased RBCs, leukocytes, and platelets

53
Q

treatment of aplastic anemia

A

–blood transfusions
–bone marrow transplant
–immunosuppressants
–corticosteroids
–drugs to stimulate erythropoiesis

54
Q

causes of aplastic anemia

A

–idiopathic (majority)
–high dose exposure to toxic agents (radiation, chemo, insecticides)
–autoimmune mechanisms (complication of infection)

55
Q

acquired hemolytic anemia

A

premature destruction of RBCs caused by some external agent

56
Q

common causes of acquired hemolytic anemia

A

–autoimmune attack
–blood incompatibilities
–drug reactions
–physical agents (severe burn)
–microangiopathies

57
Q

what happens with acquired hemolytic anemia?

A

–formation of immune complexes
–lysis = cell death

58
Q

symptoms of acquired hemolytic anemia

A

–low hemoglobin
–increased reticulocyte count
–mild jaundice
–hemoglobinuria

59
Q

sickle cell anemia

A

inability to bind Hgb normally; genetic

60
Q

hemoglobin S

A

–sickle cell; distorts shape, especially when oxygen is low
–fragile sickle-shaped cells deliver less oxygen to the tissues

61
Q

cause of pain in sickle cell anemia

A

misshapen RBCs easily clog blood vessels and break into pieces that disrupt blood flow, leading to ischemia and necrosis

62
Q

symptoms of sickle cell anemia

A

–s/s of anemia
–swelling of hands and feet with fever
–painful episodes

63
Q

pain crisis triggers with sickle cell

A

–dehydration
–stress
–high altitudes
–fever
–extreme temps

64
Q

treatment for sickle cell

A

–O2
–hydration
–pain management
–infection control measures
–blood transfusions
–bone marrow transplants
–genetic counseling and treatment

65
Q

medication for sickle cell

A

hydroxyurea

66
Q

thalassemia

A

genetic; abnormal Hgb makes erythrocytes microcytic, hypochromic, and of carrying size

67
Q

treatment for thalassemia

A

–blood transfusions
–bone marrow transplants
–splenectomy

68
Q

patho of thalassemia

A

–genetic disorder occurring mostly in persons of Mediterranean descent
–abnormal Hgb (lack of alpha and beta globin)

69
Q

symptoms of thalassemia

A

–delayed growth
–fatigue
–dyspnea
–hepatomegaly
–splenomegaly
–bone deformities
–jaundice

70
Q

causes of anemia from blood loss

A

–gross
–occult

71
Q

rate of blood loss and anemia

A

–IMPORTANT!
–unable to compensate
–slow = less symptoms

72
Q

risk factors for polycythemia

A

–chronic hypoxia
–living at high altitudes
–long-term cigarette smoking
–familial and genetic predisposition
–long-term exposure to CO2

73
Q

relative polycythemia

A

isolated decrease in plasma volume, elevating the Hgb, Hct, and RBC count

74
Q

etiology of relative polycythemia

A

severe dehydration

75
Q

primary polycythemia

A

polycythemia vera
–typically > 60 years
–most often in males (2x)

76
Q

patho of polycythemia vera

A

a single stem cell mutates into a cell that overproduces all blood cells except for lymphocytes

77
Q

symptoms of polycythemia vera

A

–HA
–fatigue
–weight loss
–dyspnea
–HTN
–clotting problems
–ruddy color
–intense/painful itching made worse by heat or exposure to water (aquagenic pruritis)

78
Q

biggest concern with polycythemia vera

A

CV events (stroke/MI)

79
Q

etiology of secondary polycythemia

A

adaptive (compensatory) response to tissue hypoxia

80
Q

purpose causing secondary polycythemia

A

provide more O2 carriers by increasing RBC production

81
Q

effects of increased blood viscosity and blood volume in secondary polycythemia

A

–HTN (HA, concentration issues, ruddy, cyanosis)
–decreased blood flow issues (DVT, hemorrhage. angina)

82
Q

effects of hypermetabolism in secondary polycythemia

A

–night sweats
–weight loss

83
Q

effects of increased RBCs and H&H in secondary polycythemia

A

–itching
–pain in fingers and toes

84
Q
A

nur 326 exam 1b (9 decks)

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