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Pathohysiology > Hematological Disorders--exam 3 > Flashcards

Hematological Disorders--exam 3 Flashcards

1
Q

what is the composition of blood?

A

90% water
10% solutes
plasma
serum

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2
Q

how many liters of blood to be have?

A

~5.5L

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3
Q

Plasma

A

50-55% of the blood volume

organic and inorganic elements

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4
Q

Serum

A

Plasma that has been allowed to clot to remove fibrinogen (may interfere with diagnostic tests)

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5
Q

Protein make up how much of the plasma’s weight?

A

7%

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6
Q

Where are the majority of plasma proteins synthesizes?

A

in the liver

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7
Q

which plasma proteins are NOT synthesized in the liver? Where are they synthesized?

A

Immunoglobulins and they are made by B cells

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8
Q

What are different plasma proteins?

A

Albumin
Globulin
Clotting Factors

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9
Q

Albumin

A

carrier molecule that controls plasma oncotic pressure

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10
Q

Globulins

A

carrier proteins and immunoglobulins

antibodies

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11
Q

Clotting Factors

A

mainly fibrinogen

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12
Q

What the plasma protein classifications by function?

A

Clotting
defense
Transport
regulation

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13
Q

Clotting Plasma Protein

A

Fibrinogen and Fibrin

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14
Q

Defense Plasma Protein

A

Antibodies

completment

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15
Q

Transport plasma proteins

A

proteins

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16
Q

regulation plasma proteins

A

Enzymatic inhibitors

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17
Q

Erythrocytes

A

Red blood cells

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18
Q

which cell is the most abundant cell in the blood?

A

Erythrocytes

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19
Q

Erythrocytes lack a _____

A

nucleus

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20
Q

Which cell is responsible for tissue oxygenation

A

Erythrocytes

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21
Q

What is the shape of Erythrocytes?

A

biconcavity and reversible deformity

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22
Q

how long is the life cycle of an Erythrocyte?

A

120 days

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23
Q

What do Leukocytes do?

A

they defend the body against infection and remove debris

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24
Q

What are the different types of leukocytes?

A

Granulocytes

Agranulocytes

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25
Q

what are considered Granulocytes

A

neutrophils
eosiniphils
basophils
mast cells

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26
Q

what are considered Agranulocytes?

A

Monocytes/Macrophages
lymphocytes
NK cells

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27
Q

Granulates contain enzymes that are capable of destroying

A

microorganisms

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28
Q

platelets

A

thrombocytes

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29
Q

how are platelets shaped?

A

disk shaped cytoplasmic fragments

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30
Q

are platelets true cells?

A

no

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31
Q

how are platelets formed?

A

by fragmentation of megakaryocytes

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32
Q

Platelets are incapable of mitotic division because

A

they lack a nucleus

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33
Q

Platelets are essential for_____ and ______

A

blood coagulation and control of bleeding

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34
Q

Platelets function for _____days before being removed by the ____

A

10 days; spleen

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35
Q

What are some lymphoid organs?

A

Spleen

Lymph Nodes

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36
Q

The Spleen is the largest _________

A

secondary lymphoid organ

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37
Q

What does the spleen consist of?

A

Splenic Pulp

Venous Sinuses

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38
Q

What is splenic pulp?

A

masses of leukocytes

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39
Q

what is the splenic pulp responsible for?

A

fetal hematopoiesis

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40
Q

What are the venous sinuses composed of?

A

Old phagocytes

damaged dead cells

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41
Q

what are the venous sinuses responsible for?

A

blood storage (300ml)

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42
Q

Lymph nodes are part of the ___ and ____ systems

A

immune and hematologic systems

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43
Q

Lymph nodes facilitate maturation of

A

lymphocytes

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44
Q

Lymph nodes transport ____ fluid back to ___circulation

A

they transport lymphatic fluid back to circulation

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45
Q

Lymph Nodes cleanse the lymphatic fluid of:

A

microorganisms and foreign particles

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46
Q

Lymph nodes are the first sight of contact between:

A

circulating antigen and nodal lymphocytes

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47
Q

What is hematopoiesis?

A

the process of blood cell production in adult bone marrow.

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48
Q

how many new blood cells do we need per day?

A

100

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49
Q

What are the two stages of cytokinesis?

A

mitosis-cytokinesis

maturation

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50
Q

when does mitosis-cytokinesis stop?

A

before the cell enters the peripheral blood

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51
Q

what is it called when you have too many cells?

A

Polycythemias

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52
Q

Anemias

A

when you have too few cells

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53
Q

What destroys RBC?

A

Resident macrophages in spleen and liver

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54
Q

unconjugted bilirubin is____

A

toxic

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55
Q

Some bilirubin in the intestine is converted to:

A

urobilinogen

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56
Q

What converts bilirubin to urobilinogen?

A

intestinal bacteria

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57
Q

Most urobilinogen is excreted by the body in the ___ and some is reabsorbed into the _____.

A

excreted in the fecal material or reabsorbed into the blood.

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58
Q

What is jaundice caused by?

A

excess bilirubin production due to RBC destruction. More than the livers ability to conjugate.
or
Decreased bilirubin excretion

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59
Q

what might cause decreased bilirubin excretion?

A 
reduced hepatic uptake (hepatitis, cirrhosis)
decreased conjugation (hepatitis, cirrhosis, enzyme deficiency) 
bile duct obstruction (tumor, stone)
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60
Q

hepatitis and cirrhosis cause

A

reduced hepatic uptake

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61
Q

decreased conjugation is caused by

A

hepatitis
cirrhosis
enzyme deficiency

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62
Q

Skin, nail beds and whites of the eye take on a yellow color because of

A

excess bilirubin accumulation in the body

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63
Q

bilirubin is very toxic to:

A

brain cells

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64
Q

what is the treatment for jaundice?

A

treat cause of condition
blood transfusion
sun

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65
Q

Location of the site of the cause of jaundice is determined by:

A

the color of feces and urine

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66
Q

what is the site of the problem if your feces is light or clay colored and your urine dark?

A

extrahepatic obstructive jaundice

obstruction of bile duct.

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67
Q

what is the problem if your feces is normal to light color and your urine is light?

A

intrahepatic obstruction jaundice

damaged hepatocytes.

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68
Q

where is the problem if your feces if dark and so is your urine?

A

hemolytic anemia

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69
Q

X-ray, CT scan, and l iver biopsy provide evidence of the presence of

A

a stone, tumor, hepatitis, or cirrhosis

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70
Q

Hematocrit is ____% or total blood volume

A

38-45%

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71
Q

what is normal hematocrit for males?

A

42-45%

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72
Q

what is a normal hematocrit for females?

A

38-42%

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73
Q

polycythemia

A

myeloproliferative disorder

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74
Q

what are hematocrit levels for males and females in polycythemis?

A

females: greater than 48%
males: greater than 52%

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75
Q

what are the different types of polycythemia?

A

relative

absolute (primary and secondary)

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76
Q

relative polycythemia

A

dehydration

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77
Q

Primary absolute polycythemia

A

polycythemia vera

increased RBC synthesis

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78
Q

secondary absolute polycynthemia

A

hypoxemia
kidney disease
other disorders that increase erythropoietin

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79
Q

what are some disorders that increase erythropoietin?

A

high altitude living
smokers
COPD

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80
Q

what are clinical manifestations of polycythemia?

A

Liver and spleen congested with RBD
increased blood viscosity (light headedness/visual disturbance)
Ruddy Cyanosis
bone marrow is hyperplastic

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81
Q

Ruddy Cyanosis of the face

A

pruritus (itch)
hypertension
congestive heart failure

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82
Q

hyperplastic bone marrow is presents in all types except

A

dehydration

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83
Q

how do we treat relative polycythemia?

A

rehydrate patient

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84
Q

how do we treat polycythemia vera?

A 
bleed patient (young)
low dose aspirin (young)
32P (old)
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85
Q

how do we treat secondary polycythemia?

A

treat the cause of the hypoxemia or remove the cause of the excess erythropoietin
(remove kidney, tumor, etc)

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86
Q

Anemia

A

decreased oxygen-carrying capacity of blood

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87
Q

What are clinical manifestations of anemia?

A 
decreased RBCs in blood 
weakness
fatigue 
headache 
lack of color in skin, nail beds
increased heart rate
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88
Q

how do you classify anemia?

A

according to the size of the RBC and the hemoglobin content

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89
Q

when classifying anemia, “-cytic” deals with

A

size

90
Q

when classifying anemia, “-chromic” deals with

A

hemoglobin content

91
Q

normocytic-normochromic anemia

A

cells of normal size and hemoglobin content

reduces RBC number must be the prob if still anemia

92
Q

what are common examples of normocytic-normochromic anemia?

A

posthemorrhagic anemia
Aplastic anemia
hemolytic anemia
anemia of chronic disease

93
Q

posthemorrhagic anemia

A

result of blood loss

94
Q

appears____hours following blood loss

A

48-72

95
Q

how much blood do you lose when posthemorrhagic anemia appears?

A

over 20% of blood volume.

96
Q

Aplastic anemia

A

reduced erythrocyte synthesis

97
Q

What are clinical manifestations of aplastic anemia

A

decreased cells in blood and bone marrow and decreased reticulocytes

98
Q

what are the two types of aplastic anemia

A

all types of blood cells reduced

only RBCs reduced

99
Q

pancytopenia

A

all blood cells reduced in blood

100
Q

mixed cell aplasia

A

all types of celled reduced in bone marrow

101
Q

Aplastic anemia

A

only RBCs reduced in blood

102
Q

what is the cause of aplastic anemia?

A

destruction of bone marrow

103
Q

what can destroy bone marrow?

A 
radiation exposure to drugs, toxins, or various chemicals
kidney failure (lack of erythropoietin) 
infection 
autoimmune 
idiopathic
104
Q

hemolytic anemia

A

increased erythrocyte destruction

105
Q

What are clinical manifestations of hemolytic anemia?

A 
general manifestations of anemia 
Jaundice and dark fecal material and urine 
splenomegaly and hepatomegaly may occur
bone marrow normal or hyperplastic 
increased reticulocytes
106
Q

what are causes of hemolytic anemia?

A

autoimmune

acquired: drugs, toxins (eg lead, arsenic), or trauma

107
Q

What are some genetic diseases that change the shape of RBCs?

A

sickle cell syndrome
thalassemias
both are microcytic-hypochromic

108
Q

Cells rupture easily and are destroyed in the spleen and liver because of

A

the abnormal shape of the RBC membrane

109
Q

Sickle cell anemia is a genetic disease cause by an

A

autosomal recessive gene

110
Q

sickle cell anemia is characterized as

A

microcytic-hypochromic

111
Q

Sickle cell is more common in people of

A

the near east, mediterranean, african, and southern indian origin

112
Q

What are the effects of sickle cell anemia ?

A

low oxygen carrying capacity
acidosis (reduced buffering capacity)
RBC membrane becomes rigid, leading to ruptured cells
the sickle shaped cells also do not pass through small capillaries
increased RBC synthesis causes bone changes

113
Q

when is sickle cell anemia fatal by for males and females?

A

Males-42yo

females-48yo

114
Q

How do we treat sickle cell anemia ?

A 
reduced stress
blood transfusions 
prevent infections
hydroxyurea
keep patient well hydrated 
correct any acid-base imbalances
115
Q

Thalassemias is a genetic disease caused by

A

autosomal recessive trait.

116
Q

Thalassemias causes impaired

A

synthesis of the alpha or beta chain of hemoglobin

117
Q

Thalassemias is characterized as

A

microcytic-hypochromic anemia

118
Q

in thalassemias hemoglobin precipitates in RBCs which makes them

A

very fragile and changes their shape

119
Q

thalassemias causes the bone marrow to be

A

overstimulated

120
Q

overstimulation that takes place during thalassemias causes

A

the bone to become thin and easily broken and enlargement of the face bone.

121
Q

how do you treat thalassemias?

A

splenectomy

blood transfusion

122
Q

what is the problem with transfusions

A

hemosiderosis

123
Q

hemosiderosis

A 
storage of excess iron in tissues such as the:
liver 
lungs
skin 
pancreas
124
Q

what is the cause of anemia due to chronic disease

A

macrophages produce substances (cytokines) that disrupt the iron cycle, causes RBC destruction, and inhibits erythropoiesis

125
Q

in anemia caused by chronic disease, hepcidin expression is _____ in the liver

A

increased

126
Q

what are clinical manifestations of anemia caused by chronic disease?

A

anemia related to chronic disease

127
Q

who do you treat anemia of chronic disease?

A

eliminate chronic disease

increase RBC synthesis with colony stimulating factors and/or erythopoietin

128
Q

anemia of chronic disease is classified as

A

normocytic-normochromic anemia

129
Q

iron deficiency anemia is classified as

A

microcyctic-hypochromic anemia

130
Q

iron deficiency anemia is caused by:

A

low iron, which inhibits RBC synthesis

131
Q

what is the most common anemia worldwide?

A

iron deficiency anemia

132
Q

who is iron deficiency anemia common in?

A

young children due to rapid growth

women due to poor diet, low testosterone, and moderate decreases in iron due to menstruation

133
Q

how do you treat iron deficiency anemia?

A

increased iron in diet
food is better than pills
risk of toxicity in children

134
Q

leukopenia

A

deficiencies in the quality and quantity of leukocytes

leukopenia is always normal

135
Q

leukocytosis

A

increased number of leukocytes

136
Q

many hematologic disorders are

A

malignancies

137
Q

nonhematologic malignancies metastasize to____ affecting _____production

A

bone marrow affecting leukocyte production

138
Q

what happens in quantitative disorders?

A

increases or decrease in cell numbers
bone marrow disorders or premature destruction of cells
response to infectious microorganism invasion

139
Q

qualitative disorders are

A

disruptions of cellular function

140
Q

leukocytosis ca be a normal ______ physiologic response to stressors

A

protective

141
Q

leukopenia results in low WBC count which

A

predisposes to infections

142
Q

what are some tests that are done to test for leukocytes?

A

peripheral blood differential cell count
bone marrow biopsy
lymph node biopsy

143
Q

what are non-malignant leukocyte abnormalities?

A

infectious mononucleosis

lymphadenopathy

144
Q

what are malignant leukocyte disorders

A

leukemias
multiple myeloma
malignant lymphomas

145
Q

what is the cause of infectious mononucleosis?

A

epstein-barr virus spread through oral mucous membrane contact

146
Q

what are clinical manifestations of infectious mononucleosis

A 
lymph node enlargement
splenomegaly 
sore throat 
mild fever
fatigue, malaisem headache 
rash on trunk 
increases number of lymphocytes with 10-20% of the cells having abnormal shapes 
antibodies against the virus present in the blood (late in the disease)
147
Q

how do you treat infectious mononucleosis?

A

bed rest
analgesics
anti-inflammatory steroids

148
Q

lymphadenopathy causes

A

enlarged or swollen lymph node

149
Q

what is lymphadenopathy causes by?

A

an infection near or in the lymph

150
Q

what is lymphadenopathy usually the result of?

A

leukemia

151
Q

leukemia

A

cancer of the blood forming organs resulting in excess production of poorly functioning leukocytes

152
Q

what are the symptoms of leukemia?

A 
fatigue 
bleeding 
fever that is often apparent as night sweats 
weight loss
bacterial, viral, and fungal infections
153
Q

what are clinical tests that are done do diagnose leukemia?

A

blood smear

bone marrow biopsy

154
Q

what are the different types of leukemia?

A

acute leukemia

chronic leukemia

155
Q

what are the different types of acute leukemia?

A

acute myelogenous leukemia

acute lymphocytic leukemia

156
Q

What are the types of chronic leukemia?

A

chronic myelogenous leukemia

chronic lymphocytic leukemia

157
Q

Acute Leukemia causes alterations in the leukocytes:

A

early in the differentiation process

158
Q

what is produced in acute leukemia?

A

large numbers of rapidly proliferating stem cell-like leukocytes

159
Q

what does the untreated individual rapidly die of?

A

infection or hemorrhage

in a matter of weeks

160
Q

AML

A

Acute myelogenous leukemia

161
Q

AML affects the _____ line

A

myelogenous

162
Q

which cells are in the myelogenous line?

A

eosinophils
neutrophils
mast
basophils

163
Q

in AML you see an increase of myelogenous ______ cells in marrow and blood

A

precursor cells

164
Q

ALL

A

Acute Lymphocytic leukemia

165
Q

which cells does ALL affect?

A

cells leading to t-lymphocytes and b-lymphocytes

166
Q

in ALL you have increase number of ________

A

lymphocyte precursor cells

167
Q

ALL is most common in

A

children

168
Q

How do you treat acute leukemia?

A

chemo
radiation
bone marrow transplant
60%-90% survive when treated early

169
Q

what is chronic leukemia?

A

leukemia that causes alterations in he leukocytes late in the differentiation process
so, they are not well differentiated.

170
Q

what is produced in chronic leukemia?

A

slow proliferating mature leukocytes which exhibit decreased function

171
Q

what do people usually die of in chronic leukemia?

A

infection ot hemorrhage

takes a few years.

172
Q

how is chronic leukemia discovered?

A

by a random blood test because it is initially asymptomatic

173
Q

CML

A

chronic myelogenous leukemia

174
Q

CML results in an increase of

A

precursor cells for monocytes, basophils, eosinophils, neutrophils, megalokaryocytes and erythrocytes.
they are poorly functioning as well.

175
Q

95% of the time it is caused by

A

a marked shortening of chromosome 22

176
Q

philadelphia chromsome

A

chrom 22

177
Q

CLL

A

chronic lymphocytic leukemia

178
Q

what is CLL?

A

a decrease in cells leading to T lymphocytes and B lymphocytes which leads to an increase of progenitors and lymphocytes

179
Q

how do you treat chronic leukemia?

A

chemo
radiation
bone marrow transplant

180
Q

what is the cure rate for chronic leukemia?

A

20%

181
Q

what is multiple myeloma?

A

slow proliferation of malignant blood cells

182
Q

what causes the slow proliferation of malignant blood cells in multiple myeloma?

A

ask alex

183
Q

how do you diagnose Multiple myeloma?

A

C.R.A.B.

184
Q

what are clinical manifestations of multiple myeloma?

A

highly fragiile bones
hypercalcemia
large amount of immunoglobulin(IgG) in the blood
kidney failure due to IgG blocking glomeruli and nephrocalcinosis

185
Q

how do you treat multiple myeloma?

A

chemotherapy
radiation therapy
generally fatal (3-4 years)

186
Q

lymphomas

A

malignancy of lymph nodes

187
Q

which lymph node tissue is generally involved in lymphomas?

A

secondary lymphoid tissue

in rare cases: bone marrow can also be involved

188
Q

where do lymphomas often spread to?

A

non-lymphoid tissues like lungs, pleura, etc

189
Q

what are clinical manifestations of lymphomas?

A 
swelling of lymph nodes 
mild fever (often night sweats) 
weakness
sudden weight loss
anemia
190
Q

hodgkin lymphoma

A

the presence of transformed lymphocytes in teh affected lymph nodes.
reed sternberg cells (multipolar or mult nuclei)

191
Q

sternberg cells produce

A

and inhibitor of T-cell function

192
Q

non-hodgkin lymphoma

A

absence of reed-sternberg cells in affected lymph nodes.

193
Q

in non-hodgkin lymphoma there is a _____ of ___ cell and _____ activity

A

decrease of B cell and macrophage activity.

194
Q

non-hodgkin lymphomas are common amongst

A

immunosuppressed patients.

195
Q

what is the treatment for hodgkin/non-hodgkin lymphoma?

A

removal of malignant tissues and lymph node
chemotherapy
radiation therapy

196
Q

what is the cure rate for early stage hodgkin disease?

A

75%

197
Q

what is the cure rate for non-hodgkin lymphoma?

A

30%

198
Q

hemostasis

A

formation and removal of a blood clot

199
Q

blood coagulation involved the interaction of which three events?

A

activation of blood coagulation
inhibition of blood coagulation
dissolving of blood clot
the bottom two balance the top one out so its doesn’t clot too much.

200
Q

vascular spasm is generally ____ in duration

A

short (less than one minute)

201
Q

What causes vascular spasm?

A

damage of the blood vessel
histamine
serotonin

202
Q

blood coagulation is generally a ___ duration

A

longer

203
Q

what are the four parts of blood coagulation?

A

formation of the platelet plug
formation of fibrous clot
clot retraction
thrombolysis

204
Q

what activates platelet adherence?

A

trauma

inflammation

205
Q

what are the steps in the formation of the platelet plug?

A
  1. platelet adherence
  2. platelet activation and degranulation
  3. platelet aggregation
206
Q

platelet adherence due to trauma causes

A

exposure of subendothelial matrix

207
Q

von Willebrand factor vWF

A

matrix (collagen) exposure due to trauma

208
Q

platelet adherence due to trauma causes

A

narrowing

209
Q

when endothelium exposure to inflammatory factors also releases vWF

A

it promotes platelet adherence to subendothelial matrix

210
Q

what are inflammatory factors?

A

endotoxin
inflammatory cytokines
histamine
serotonin

211
Q

normal platelets are in a ____ state

A

anti-coagulative

212
Q

what does platelet activation do to normal platelets?

A

converts then into a pro-coagulative state

213
Q

helthy endothelium releases factors that

A

inhibit platelet activation

214
Q

what does PGI2 do?

A

it binds to receptors on platelets and inhibits their activation

215
Q

what does NO do to platelet activation?

A

directly inhibits it

216
Q

what does ADPase do to platelet activation?

A

it breaks down the ADP released from activated platelets. If it can get rid of al of the ADP it can stop activation

217
Q

platelet activation causes

A

degranulation

218
Q

___ platelets release secretory granules

A

activated

219
Q

what is the positive feedback that occurs during platelet activation?

A

when the platelets are activated they granulate which then causes further activation and this more granulating.

220
Q

thrombin concerts fibrinogen to fibrin which

A

binds multiple platelets to form a mesh

221
Q

fibrous clots

A

consist of a series of plasma proteins made by the liver, platelets and endothelium

Pathohysiology (16 decks)

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