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PAS 753 (Molecular Pathophysiology) > hematological disorders > Flashcards

hematological disorders Flashcards

1
Q

what is blood

A

dilute saline with dissolved chemicals and suspended cells

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2
Q

what are four dissolved components of blood

A

nutrients (glucose, vitamins)

Electrolytes (Na, K, Cl, Ca)

Hormones (insulin, T3/T4)

Proteins (albumen, carriers)

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3
Q

T/F drugs are also found dissolved in blood

A

true

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4
Q

differentiate between blood, plasma, and serum

A

blood is all the dissolved and suspended components

plasma is blood with the suspended components removed

serum has all the cell and clotting factors removed

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5
Q

four functional factors of red blood cells

A

Hemoglobin

size, shape

flexibility

longevity

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6
Q

what is the protein structure of hemoglobin

A

a protein tetramer with alpha and beta or alpha and gamma polypeptide chains and one oxygen carrying heme group

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7
Q

what is the structural difference between adult and fetal hemoglobin

A

adult hemoglobin has 2 alpha and 2 beta chains

fetal hemoglobin has 2 alpha and 2 gamma chains

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8
Q

why do RBCs need to flexible?

why is this relevant?

A

RBCs neet to fit through small vessles

as people get older RBCs are less flexible and more likely to clot

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9
Q

what components of blood come from the myeloid line

A

erythrocytes

megakaryocytes (platelets)

granulocytes (N, B, E-phils) and monocytes

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10
Q

what cells come from the lymphoid line

A

NK cells

dendritic cells

T & B lymphoctyes

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11
Q

granular leukocytes

A

basophiles

neutrophils

eosinophils

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12
Q

agranular leukocytes (mononuclear)

A

monocytes

lymphocytes

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13
Q

why do some RBCs appear “speckled”

A

they are reticulocytes that have remains of the endoplasmic reticulum remaining

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14
Q

how long do RBCs last before being broken down

A

100-120 days

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15
Q

what cells break down RBCs

A

reticuloendothelial cells found in the spleen and liver

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16
Q

what is the main byproduct of hemoglobin breakdown

A

bilirubin

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17
Q

bilirubin is an indicator of what

A

liver function

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18
Q

what causes jaundice

A

high levels of bilirubin

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19
Q

T/F a small number of RBCs are lost through the GI, Urine, Skin

A

true

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20
Q

anemia

A

pathological deficiency of oxygen carrying capacity of blood caused by a decrease in the number or function of RBCs

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21
Q

what is a normal blood volume

A

4-8 liters

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22
Q

T/F gamma hemoglobin production is turned off in adults

A

true

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23
Q

white pulp of the spleen

A

lymph tissue

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24
Q

red pulp of the spleen

A

tortuous sinsoids that weed out old RBCs or RBCs with antigens to be broken down

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25
Q

where do RBCs come from

does all bone marrow produce RBCs

A

bone marrow

no, mostly in the hips, sternum, long bones

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26
Q

erythropoetin

A

cytokine that stimulates the production of erythrocytes

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27
Q

what triggets the production of EPO

A

decreased oxygen saturation in the blood

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28
Q

where is erythropoietin produce

A

the juxtapoglomerular cells of the kidneys

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29
Q

band cells

A

immature neutrophils that are indicative of rapid production of neutrophils

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30
Q

why is neutrophil count important in cancer treatment

A

chemo decreases bone marrow function

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31
Q

Do RBCs have a nucleus?

why is that important in transfusion

A

no

because we don;t have to match HLA-1 antigens just blood type

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32
Q

what are reticulocytes indictive of

A

rapid production of RBCs

destruction of RBCs

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33
Q

recyclining function of RE macrophages

A

amino acids and iron from hemoglobin is recycled into the bone marrow to make new RBCs

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34
Q

CBC

A

complete blood count (RBCs, WBCs, platelets, hemoglobin and hematocrit)

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35
Q

on a CBC the hematocrit is generally how much higher than hemoglobin

A

3x

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36
Q

when you spin out blood what is the “buffy coat”

A

white blood cells

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37
Q

what are the signs of hypervolemia based on the amount of blood lost

A

10-15% initial signs of vascular instability

greater than 30% orthostatic hypertension

greater than 40% hypovolemic shock

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38
Q

hemoglobin content is dependent on what two factors

A

production of Hgb - loss of Hgb

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39
Q

reduced hgb production is indicative of what?

A

bone marrow issue

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40
Q

increasd hgb loss means

A

accelerated destruction or loss from vasculature

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41
Q

three questions to ask when considering bone marrow deficiency in anemia

A

enough stem cells

enough nutrients to make RBCs (iron, folate)

enough stimulation (EPO)

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42
Q

three systems that patients will often loss RBCs through (example of disoder)

A

GYN (heavy period)

GI (cancer, ulcer)

GU (cancer)

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43
Q

four problems that would lead to decreased erythropoesis in the RBCs

A

nutritional deficiencies

loss of stimulation

toxicity

neoplasm

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44
Q

two general nutrition deficiency that cause anemia

A

anemia of chronic disease

starvation

45
Q

three specifict nutrient deficiencies that will cause anemia

A

folate

b12

Iron

46
Q

four dietary sources of iron

A

meat, seafood, beans, spinach

47
Q

two histological descriptors of iron deficient anemia

A

microcytic (small)

hypochromic (pale colored)

48
Q

T/F pregnancy and lactation can caused anemia through loss of RBCs

A

false, they cause increased demand

49
Q

four steps to treat iron deficiecy

A

stop blood loss if there is any

improve diet

oral iron

parenteral iron

50
Q

what is the complication with oral iron supplements

A

compliance issues due to GI side effects

51
Q

what is the histological sign of B-12 and folate deficency

A

megaloblastic anemia

52
Q

megaloblastic anemia

A

Large RBCs, hypersegmented neutrophils caused by impaired DNA synthesis

53
Q

cobalamin

A

B 12

54
Q

B12 is important to the synthesis of what

A

nucleic acid synthesis

55
Q

where is B12 found

A

tightly bound to protein in meat

56
Q

what is needed to extract dietary b12

A

low gastric pH and intrinsic factor

57
Q

causes of b12 deficiency

A

dietary (strict vegan)

gastric dysfunction

GI malabsorption (ileal disease)

58
Q

three ways gastric disfunction can cause b12 deficiency

A

pernicious anemia

gastric atrophy

gastric surgery

59
Q

what causes pernicious anemia

A

auto antibodies against intrinsic factor

60
Q

what will be two signs of pernicious anemia

A

megaloblastic anemia and progressive neurological deterioration

61
Q

why is it dangerous to give folate to treat pernicious anemia

A

folate will correct the anemia but not the neurlogical damage

62
Q

treatment for b12 deficiency

A

large oral doses of B12

intramuscular B12

63
Q

folic acid is an essential cofactor in what

A

amino acid and DNA synthesis

64
Q

what is the effect of folic acid on fetal development

A

assist in neural tube development and decreases ther risk of anencephaly or spina bifida

65
Q

causes of folate deficincy

A

not enough fruits and veggies

increased demand (pregnancy, hemolytic anemia)

malabsorption of folate

66
Q

folate deficiency treatment

A

daily folic acid tablets

67
Q

if there is a coexisting B12 deficiency what will folate treatment do

A

correct anemia but not neurodegeneration

68
Q

how do chronic renal failure cause anemia

A

loss of EPO resulting in moderate anemia

69
Q

three causes of bone marrow toxicity

A

pharmacological

environmental

immunologic

70
Q

three environmental sources of bone marrow toxic substances

A

solvents

pesticides

radiation

71
Q

aplastic anemia

A

an autoimmune disorder that causes the loss of hemopoietic cells

72
Q

what are the three clinical manifestations of aplastic anemia

A

anemia

leukocytopenia (chronic infection)

thrombocytopenia (no clotting factors0

73
Q

treatment of aplastic anemia

A

immunosuppresion

bone marrow transplant

74
Q

what is the immunosuppressive treatment of aplastic anemia

how often is it successful

A

antilymphocyte or antithymocyte globulin

50-70%

75
Q

why is a good HLA match needed for bone marrow transplant

A

a poor match will produce graft versus host disease as the graft produces lymphocytes that react to antigens

76
Q

myeloproliferative disorders

A

cancers that will displace normal bone marrow

77
Q

types of myeloproliferative disorders

A

leukemia

lymphoma

multiple myeloma

polycythemia

thromocythemia

78
Q

two types of leukemia

A

myeloid (acute or chronic)

lymphoid (acute or chronic)

79
Q

two types of lymphoma

A

hodgkins

non-hodgkins

80
Q

what is the diffence between hodgkins and non-hodgkins

A
81
Q

polycythemia

A

overly productive bone marrow that produces too many blood cells

82
Q

risk of thrombocythemia

A

increased clotting

83
Q

classic GI causes of chronic bleeding

A

peptic ulcer or cancer

84
Q

classic cause of anemia from gyn

A

uterine (heavy period, leiomyoma

85
Q

classic urinary causes of anemia

A

renal cell carcinoma

bladder carcinoma

86
Q

causes of hemolysis

A

defect in RBC size shape or function

outside destructrion of normal RBCs

87
Q

hemoglobinopathy

two types

A

change in Hgb structure and function

sickle cell anemia

thalassemia

88
Q

what causes sickle cell anemia

A

autosomal recessive mutation of Hgb A

89
Q

what causes sickle cell disease

A

homozygous vs heterozygous Hgb A mutation

90
Q

T/F heterozygous Hgb is usually asymptomatic

A

true

91
Q

are the risks associated with sickle cell anemia

A

chromic hemolytic anemia

microinfarction due to clottin

92
Q

what will microinfarctions from sickle cell cause

A

leg ulcers

functional splenomegaly

shortened life span

93
Q

thalassemia

A

genetic defect in globin biosynthesis

classified as alpha or beta thalassiema

94
Q

describe the genetic characteristics of thalassemia

A

autosomal recessive

95
Q

differniate between homozygous and heterozygous thalassemia

A

homozygotes have signifcant disease (major)

heterozygotes are mildly anemia or asymptomatic

96
Q

what are the risks of major thalassemia

A

severe anemia

hepatosplenomegaly

growth abnormalities

97
Q

what is the treatment for severe anemia for major thalassemia

what is the risk

A

repeat transfusions

iron overload (hemosiderosis)

98
Q

what is the treatment for hepatosplenomegaly caused by thalassemia

A

eventually splenectomy, which will increase risk of infection

99
Q

why are growth abnormalities present in beta thalassemia

A

there is an overgrowth of bone marrow that can cause pathologic fractures or “chipmunk facies”

100
Q

two RBC enzyme deficiencies

A

G6pD

PKD

101
Q

T/F G6PD and PKD defiency are both autosomal dominant

A

false, they are autosomal recessive

102
Q

what is the evolutionary benefit to G6PD deficieny

A

heterozygotes have increase survival rate with malaria infection

103
Q

G6PD homozygotes are at risk for hemolysis triggered by what three factors

A

certain diseases (infection, diabetes)

certain foods (fava beans)

certain drugs (sulfa, aspirin)

104
Q

four other causes of hemolysis that arent sickle cell or

A
105
Q

important questions to ask in anemai

A

diet

menstruation

GI distress

medication

106
Q

normochromic, normocytic RBCs with normal reticulocytes, iron

but

pancytopenia

three things that top the DDx

A

aplastic anemia

bone marrow dysfunction

drug reaction

107
Q

DDx for

megaloblastic anemia

low reticulocytes

normal iron studies

A

folate deficiency

B12 deficiency

metformin

GI symptoms

108
Q

DDx for

Normal indices (red blood cell size)

Reticulocyte count high

Iron studies normal

Bilirubin level elevated

A

Hemolysis

Inheritied hemoglobin disorderd (thalassemia or sickle cell)

Autoimmune disorders (lupus)

G6PD

Pyruvate kinase deficiency

PAS 753 (Molecular Pathophysiology) (17 decks)

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