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Pathology > hemopoesis pt 2 > Flashcards

hemopoesis pt 2 Flashcards

1
Q

Hematopoietic System
responsible for?
components?

A

Blood cell forming system

composed of:
Lymph tissue
Bone Marrow
Red bone marrow
Yellow bone marrow

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2
Q

which marrow repsonsible?

hematopoesis

A

Process in which red and white blood cells are
produced
Red bone marrow

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3
Q

when does yellow marrow form

A

about 4 yrs old, will replace all reed aside from that in flat bones

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4
Q

Hematopoietic Bone Marrow locations in the Adult

A

Vertebrae
Ribs
Sternum
Ilia

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5
Q

Erythrocytes
 formed via?
 Formation Regulated by?
 __% of RBCs replaced daily
 Life span?

A

 Erythropoiesis
 Regulated by kidneys-Erythropoietin (released with decreased O2)
 1% of RBCs replaced daily
 Life span-120 days (4 months)

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6
Q

Development of Blood Cells from
Hematopoietic Stem Cell to Mature Cells diagram

A
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7
Q

Reticulocytes
 what is in cytoplasm?
 Normal range:
 Indicator of?
 Reticulocytosis?
 Reticulocyte count should be?

A

 Immature red blood cells
 Reticular network of RNA in cytoplasm
 Normal range: 0.5% to 1.5%
 Indicator of bone marrow activity
 Reticulocytosis – elevated number of reticulocytes in blood
 Reticulocyte count should be appropriate to the clinical situation

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8
Q

stages of erythropoesis?

A
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9
Q

normal values of RBC, platlets, WBC

peripheral blood examination

A

done via phlebotomy
 Erythrocytes – 4.0 – 5.5 million / mm3
 Thrombocytes – 150 - 400 thousand / mm3
 Leukocytes – 5 – 10 thousand / mm3

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10
Q

how should normal RBC appear on blood smear

A

biconcave and 7-8 microns

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11
Q

Hemoglobin and Hematocrit Values for males and females

A

Hematocrit - percent
Males 40 - 54%
Females 37 - 47%

Hemoglobin – grams per deciliter (100ml)
Males 14 - 18
Females 12 - 16

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12
Q

what is serum

A

plasma-clotting factors

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13
Q

blood components, %

A
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14
Q

hematocrit

A

measures RBC V as a % of the total V

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15
Q

RBC count

A

total number RBC in whole blood

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16
Q

hemglobin measure

A

measure Hb in blood which reflect RBCs

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17
Q

leukocytes measure

A

combined total of all types of WBC, can be broken down to individual cell types

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18
Q

Adult Hematopoietic Bone Marrow in the Adult can be used to?

A

examine potential dx: MM, leukemia and metastesis

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19
Q

Bone Marrow Aspiration
and Biopsy

A

Posterior superior iliac crest, sample stained and viewed

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20
Q

Hemoglobin strucutre components

A

heme and globin

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21
Q

Heme

A

non-protein portion of Hb
 Iron porphyrin - 4 pyrrole rings + iron

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22
Q

forms?

Globin

A

protein portion
HbA (Adult Hb) – 2 alpha, 2 beta
HbF (Fetal Hb) – 2 alpha, 2 gamma

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23
Q

normal adult RBC contain which form Hb mainly

A

HbA

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24
Q

what must Fe charge be in Hb

A

2+

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25
Q

Terminology for Reduction
in the Number of Cells
Erythrocytes
(Leukocytes
(Thrombocytes )

A

Erythrocytes – anemia, erythropenia
(Leukocytes – leukopenia)
(Thrombocytes - thrombocytopenia)

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26
Q

Descriptive Terms for Erythrocytes

A

cell size and hb content (chromic)

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27
Q

causes?

RBC cell size classes

A

Normocytic
Macrocytic – B12, Folate deficiency
Microcytic – Iron deficiency

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28
Q

Hemoglobin content classes

A

Normochromic
Hypochromic

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29
Q

most common anemia seen?

A

Fe def- microcytic hypochromic

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30
Q

Anemia
 A reduction in?
 oxygen carrying capacity?

A

 A reduction in the erythron – a reduction in the total red cell mass
below normal limits

 Reduction in the oxygen carrying capacity of the blood leading to
tissue hypoxia

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31
Q

anemia diagnosed based on?

A

 Usually diagnosed based on:
Inadequate numbers of erythrocytes (low hematocrit - the ratio of packed red cells to total blood volume)
Inadequate level of hemoglobin – the hemoglobin concentration of the blood

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32
Q

anemias can be due to a disbalance btwn?

A

RBC production and destruction

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33
Q

3 ways anemias occur

A

Increased RBC destruction
Decreased RBC production
Blood loss

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34
Q

Clinical Features of Anemia
skin
energy
breathing
cardio
nails
tongue
Cognitive
 extremities
 Headache

A

Pallor – pale skin and mucosa
Lethargy – lack of energy, fatigue, weakness
Dyspnea – labored breathing, SOB
Tachycardia, arrhythmia, chest pain
Koilonychia - spoon-shaped nails
Atrophic glossitis
Cognitive problems, dizziness
Cold extremities
Headache

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35
Q

why fatique with anemia?

A

a person with a low hematocrit cannot carry enough oxygen in the blood to meet energy demands.
Weakness, malaise, and easy fatigability.

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36
Q

why tachycarida with anemia?

A

Increased heart rate - compensates for the low oxygen carrying capacity of the blood

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37
Q

why SOB with anemia

A

 Shortness of breath / increased respiratory rate – compensates for the poor delivery of oxygen to the tissues.
Dyspnea on mild exertion.

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38
Q

why low bp with anemia

A

 Low blood pressure – a decrease in blood viscosity directly lowers total peripheral resistance to the flow of
blood, thus lowering mean arterial blood pressure

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39
Q

why pale skin with anemia

A
  • hemoglobin is bright red when oxygenated and less red when deoxygenated. Because the redness
    of skin is due to the redness of blood, the skin of an anemic person (who has less oxygen in the blood) will be
    less red (paler) than the average person
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40
Q

why headache with anemia

A

Central nervous system - hypoxia can cause headache, dimness of vision, and faintness

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41
Q

hw can anemia lead to cardiac failure

A

Cardiac failure can develop and compound the tissue hypoxia caused by the deficiency of O2 in the blood

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42
Q

Anemias of Increased Blood Destruction

A

Sickle cell anemia
Thalassemia
Erythroblastosis fetalis
G6PD deficiency
Malaria

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43
Q

dx vs trait? genetics?

Sickle Cell Anemia

A

 A hemoglobinopathy
 Inherited, mis-sense mutation of beta chain
 A single AA substitution of valine for glutamic acid
 Forms a new, abnormal hemoglobin, Hemoglobin S - HbS
 Sickle cell disease – homozygous HbS
 Sickle cell trait - heterozygous, a less serious condition

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44
Q

HbS homo vs hetero

A

 Individuals with sickle cell trait (heterozygous for HbS) have a survival
advantage in malaria-endemic areas
 Homozygous normal – increased mortality due to malaria
 Heterozygous HbS – survival advantage
 Homozygous HbS – increased mortality due to sickle cell disease
 About 8% of African Americans are heterozygous (sickle cell trait)
 1 in 600 African Americans are homozygous (sickle cell disease)

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45
Q

dif in hetero?

Behavior of HbS in
Hypoxic Conditions

A

 HbS molecules polymerize when deoxygenated, forming HbS aggregates
 Cytosol changes from a freely-flowing liquid to a viscous gel
 With continued deoxygenation, HbS aggregates form long, needle-like fibers that distort the red cell shape
 Sickle cell trait – HbA interferes with HbS polymerization in the heterozygous condition
 Red cells do not sickle except under conditions of profound hypoxia

46
Q

anemia? vascular? common locations? spleen?

Clinical Effects of Sickling
in Sickle Cell Anemia

A

 Hemolytic anemia - chronic hemolysis leading to jaundice and phagocytosis in spleen
 Microvascular occlusions - sickle cells becone arrested during transit through the microvasculature
 Vaso-occlusive crises (pain crises)-episodes of hypoxic injury and infarction that cause severe pain in the affected region: Commonly involved sites: bone, lung, liver, brain, spleen
 Autosplenectomy

47
Q

Clinical Consequences of
Splenectomy

A

Increased susceptibility to infection with encapsulated organisms
Pneumococcus pneumoniae and Hemophilus influenzae

48
Q

what can this be seen with?

A

hair on end radiograph, can be seen with sickle cell anemia and beta thalassemia major

49
Q

what radiogrpahic anomolies can be seen with SCA

A

hair in end and step ladder trabeculae

50
Q

Thalassemia

A

Group of inherited diseases
Quantitative problem - too few globins synthesized, A or B could be affected
Underproduction of normal globin proteins due to mutations in regulatory genes

51
Q

can lead to?

tx thalassemia

A

Regular transfusions – iron
overload – organ damage

52
Q

bones? spleen? growth? tx?

consequences of thalassemia

A

 Bone deformities – expansion
of marrow space
 Splenomegaly - splenectomy
 Impaired growth
 Bone marrow transplantation

53
Q

genetics? forms?

beta thalassemia

A

Two genes involved in making beta chain (one from each parent)
Severity depends on number of affected beta chain genes
One gene – beta-thalassemia minor - beta-thalassemia trait= Mild disease
Two genes – beta-thalassemia major (Cooley’s anemia)= Severe disease

54
Q

genetics? forms?

Alpha Thalassemia

A

 Four genes involved in making alpha chain (two from each parent)
 Severity depends on number of affected alpha chain genes

 One gene – asymptomatic carrier
 Two genes – alpha-thalassemia minor - alpha-thalassemia trait= Mild disease
 Three genes – hemoglobin H disease= Moderate to severe disease
 Four genes – alpha-thalassemia major – (lethal)

55
Q

what can happen in marrow of mid face with thalassemia

A

compensatory hyperplasia

56
Q

what can be seen radiograpically with thalassemia

A

hair on end like SCA

57
Q

ABO Blood Group Incompatibility leads to?

A

ABO mismatch leads to intravascular hemolysis
Antibody-coated erythrocytes destroyed by both complement-mediated lysis and by phagocytosis in spleen

58
Q

Ab, Ag

blood groups

A
59
Q

Blood Type Distribution ABO

A

Type O – 45%
Type A – 42%
Type B – 10%
Type AB – 3%

60
Q

Blood Type Distribution Rh

A

Positive - 85%
Negative - 15%

61
Q

Erythroblastosis Fetalis

A

Hemolytic Blood Rh-Mediated Hemolytic Disease of the Newborn

62
Q

if known mom - and baby + what can be done?

Erythroblastosis Fetalis:
1st Pregnancy at Delivery

A

 Rh- mom
 Rh+ fetus
 Fetal RBCs cross the placenta and
enter the maternal circulation
during birth trauma
 Prophylactic anti-Rh (D) immune
globulin (Rhogam) within 72 hours
of delivery
 Rhogam lyses fetal RBCs in the
maternal circulation – effectively
removing any available antigen,
so the mom doesn’t develop anti-
Rh antibodies
baby not harmed

63
Q

Erythroblastosis Fetalis:
2nd Pregnancy at Delivery

A

 Rh- mom, with anti-Rh from prior
pregnancy
 Rh+ fetus
 Anamnestic response rapidly
produces anti-Rh (IgG)
 Anti-Rh IgG crosses placenta
and lyses fetal RBCs
 Rh-mediated hemolytic disease

64
Q

prevention of Erythroblastosis Fetalis

A

Rhogam: Rhesus Immune Globulin - RhIg
Immunoglobulin
Administered to Rh-negative women after pregnancies in which they carried Rh-positive fetuses
Anti-D antibodies

65
Q

high levels of what are seen in fetus? can deposit where?

Erythroblastosis Fetalis effects in fetus

A

 Hemolytic anemia in utero
 Rh-negative mother develops antibodies against Rh-positive erythrocytes of fetus
 Antibodies cross placenta and hemolyze fetal erythrocytes
 High levels of bilirubin and biliverdin
 Deposition in developing teeth
 Only primary teeth affected

66
Q

abnromal cell in periphery? increased? brain? dental?

Clinical Features of Erythroblastosis Fetalis seen in fetus?

A

 Erythroblasts in peripheral blood
 Hyperbilirubinemia
 Kernicterus (bilirubin encephalopathy) if bilirubin reaches a high
levels
 Developmental dental defects reported- enamel hypo and staining

67
Q

genetic, demo, symptoms

Glucose-6-Phosphate
Dehydrogenase Deficiency

A

 X-linked disease; most common human enzyme defect (African-American male population)
 Most are asymptomatic; at risk for non-immune hemolytic anemia upon exposure to oxidative stress
 Oxidative stress: infections, drugs (aspirin)

68
Q

G6PD importance

A

 G6PD / NADPH / Glutathione pathway - maintains supply of reduced glutathione to scavenge free radicals (anti-oxidant)
 Red cells sustain damage from oxidizing free radicals (phagocytosed in spleen), decreased RBC

69
Q

individuals with what are G6PD def. (aside from mutation)

A

All individuals with Favism (hemolysis due to Broad Beans(fava)) are G6PD deficient

70
Q

G6PD can give a survival advantage where

A

endemic malaria environments

71
Q

superficial manifestation of G6PD def

A

juandice

72
Q

Malaria
 caused by? vector/resivoir?
Reproduction in? causes?
type of anemia?
morbidity, mortality?

A

Malaria
Protozoal disease – primarily Plasmodium falciparum
Female Anopheles mosquito vector, human reservoir
Reproduction in red cells – showers of organisms produce shaking, chills and fever
Hemolytic anemia
High morbidity, mortality

73
Q

Anemias of Decreased
Red Blood Cell production

A

Iron deficiency anemia -microcytic, hypochromic
Pernicious anemia (B12 deficiency) - macrocytic
Folic acid deficiency anemia - macrocytic
Aplastic anemia

74
Q

fe def anemia appearence on smear

A

microcytic and hypochromic

75
Q

Iron Deficiency Anemia
 Most common?
 Lack of Fe most common?
 RBC app
 Seen most often in? why?
 Treated with?
 When in males, suspect what?

A

 Most common anemia in US
 Lack of Fe most common nutritional
deficiency in the world
 Microcytic, hypochromic
 Seen most often in females – more iron lost in menses than replaced by nutrition
 Treated with iron supplements
 When in males, suspect internal
bleeding

76
Q

tongue with fe def

A

atrophic

77
Q

fe de f anemia most common presentation

A

middle aged female with profound anemia

78
Q

causes of fe def

A

Dietary lack
Impaired absorption
Increased requirement
Chronic blood loss

79
Q

how can infants be fe def

A

breat feeding

80
Q

how cna children be fe def

A

poor diet

81
Q

males and females

how can adults be fe def

A

Males - peptic ulcer
disease
Females - menorrhagia or
pregnancy

82
Q

developed vs undeveloped

elderly fe def causes

A

Colonic polyps / colon adenocarcinoma in Western world
Hookworm infection in developing world

83
Q

Laboratory Measurements of Iron Status

A

Serum ferritin
Total iron binding capacity (TIBC)
% saturation
Serum iron

84
Q

Serum ferritin measures reflect what?

A

Serum ferritin – reflects iron stores in bone marrow
macrophages and liver

85
Q

Total iron binding capacity (TIBC)

A

measure of transferrin
molecules in blood

86
Q

% saturation –

A

percent of transferrin molecules bound by
iron (nl = 33%)

87
Q

Serum iron

A

Serum iron – measure of iron in the blood

88
Q

demo? what is def? mucosa? esphogus? risk of/where?

Plummer-Vinson Syndrome

A

Scandinavian, Northern European women
Severe Fe-deficiency anemia
Mucosal atrophy - atrophic glossitis
Esophageal webs - dysphagia
Increased risk for squamous cell carcinoma: Esophagus, Oropharynx, Posterior Oral Cavity

89
Q

Macrocytic Anemia forms

A

Pernicious anemia (B12 deficiency) - macrocytic
Folic acid deficiency anemia - macrocytic

90
Q

what is def in pernicious anemia

A

B12

91
Q

absorption req? what is formed/absorbed where?

Vitamin B12 (Cobalamin) Metabolism

A

Absorption of vitamin B12 requires intrinsic factor, which is secreted by the
parietal cells of the stomach
Cobalamin – Intrinsic Factor complex
absorbed in the ileum

92
Q

type of dx? B12 req for?

Pernicious Anemia

A

Autoimmune disease
Not due to dietary deficiency of B12
A form of megaloblastic anemia caused by autoimmune gastritis and failure of intrinsic factor production leading to vitamin B12 deficiency
Loss of ability to absorb Vitamin B12
Vitamin B12 (cobalamin) required for normal folate metabolism and DNA synthesis

93
Q

food sources b12

A

milk, poultry, eggs, meat, shellfish

94
Q

B12 roles

A

maintenence CNS and RBC production

95
Q

tongue w pernicious anemia

A

atrophic and ulcerative

96
Q

lips/ventral tongue with pernicious anemia

A

red

97
Q

folate needed for?

folic acid def

A

Megaloblastic anemia
Dietary deficiency of folic acid
Folate required for DNA synthesis

98
Q

aplastic anemia

A

 Marrow aplasia secondary to supression of multipotent myeloid
stem cells (erythrocyte, leukocyte and thrombocyte series), resulting in pancytopenia

99
Q

what can cause aplastic anemia

A

 May be caused by known myelotoxic agents (eg. whole body radiation)
 Antineoplastic drugs (alkylating agents, antimetabolites)
 Benzene
 Chloramphenicol

100
Q

aplastic anemia pathogenesis may involve

A

T cell attack on myeloid stem cells

101
Q

prognosis aplastic anemia

A

unpredictable

102
Q

tx aplastic anemia

A

bone marrow transplant and transfusions

103
Q

anemias of blood loss

A

Gastrointestinal bleeding
Hemoptysis (coughing up blood)
Epistaxis (nosebleed)
Hematuria (blood in urine)
Menstrual blood loss

104
Q

vomiting? stool?

GI bleeding indications

A

Hematemasis (vomiting blood)
Melena (black stool)
Hematochezia (red blood in feces).

105
Q

Menstrual blood loss forms

A

Menorrhagia (excessive bleeding)
Metrorrhagia (irregular bleeding).

106
Q

Fecal Occult Blood Test – Stool Guaiac

A

Screening test for occult bleeding in GI tract

107
Q

forms?

Polycythemia (Erythrocytosis)

A

 An increase in the RBC mass
can be relative or absolute

108
Q

 Relative polycythemia

A

dehydration – decreased plasma volume with normal red cell mass

109
Q

 Absolute polycythemia

A

a true increase in red cell mass
can be primary or secondary

110
Q

 Primary absolute polycythemia (polycythemia vera)

A

 Erythropoietin-independent
 Acquired, clonal stem cell disorder (a chronic myeloproliferative disorder)

111
Q

EPO? response to? examples?

 Secondary polycythemia

A

 Erythropoietin-dependent
 Compensatory response to tissue hypoxia: Chronic lung disease, Cigarette smoking, Residence at high altitude, Paraneoplastic syndromes

Pathology (20 decks)

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