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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
what are considered Granulocytes
neutrophils eosiniphils basophils mast cells
26
what are considered Agranulocytes?
Monocytes/Macrophages lymphocytes NK cells
27
Granulates contain enzymes that are capable of destroying
microorganisms
28
platelets
thrombocytes
29
how are platelets shaped?
disk shaped cytoplasmic fragments
30
are platelets true cells?
no
31
how are platelets formed?
by fragmentation of megakaryocytes
32
Platelets are incapable of mitotic division because
they lack a nucleus
33
Platelets are essential for_____ and ______
blood coagulation and control of bleeding
34
Platelets function for _____days before being removed by the ____
10 days; spleen
35
What are some lymphoid organs?
Spleen | Lymph Nodes
36
The Spleen is the largest _________
secondary lymphoid organ
37
What does the spleen consist of?
Splenic Pulp | Venous Sinuses
38
What is splenic pulp?
masses of leukocytes
39
what is the splenic pulp responsible for?
fetal hematopoiesis
40
What are the venous sinuses composed of?
Old phagocytes | damaged dead cells
41
what are the venous sinuses responsible for?
blood storage (300ml)
42
Lymph nodes are part of the ___ and ____ systems
immune and hematologic systems
43
Lymph nodes facilitate maturation of
lymphocytes
44
Lymph nodes transport ____ fluid back to ___circulation
they transport lymphatic fluid back to circulation
45
Lymph Nodes cleanse the lymphatic fluid of:
microorganisms and foreign particles
46
Lymph nodes are the first sight of contact between:
circulating antigen and nodal lymphocytes
47
What is hematopoiesis?
the process of blood cell production in adult bone marrow.
48
how many new blood cells do we need per day?
100
49
What are the two stages of cytokinesis?
mitosis-cytokinesis | maturation
50
when does mitosis-cytokinesis stop?
before the cell enters the peripheral blood
51
what is it called when you have too many cells?
Polycythemias
52
Anemias
when you have too few cells
53
What destroys RBC?
Resident macrophages in spleen and liver
54
unconjugted bilirubin is____
toxic
55
Some bilirubin in the intestine is converted to:
urobilinogen
56
What converts bilirubin to urobilinogen?
intestinal bacteria
57
Most urobilinogen is excreted by the body in the ___ and some is reabsorbed into the _____.
excreted in the fecal material or reabsorbed into the blood.
58
What is jaundice caused by?
excess bilirubin production due to RBC destruction. More than the livers ability to conjugate. or Decreased bilirubin excretion
59
what might cause decreased bilirubin excretion?
``` reduced hepatic uptake (hepatitis, cirrhosis) decreased conjugation (hepatitis, cirrhosis, enzyme deficiency) bile duct obstruction (tumor, stone) ```
60
hepatitis and cirrhosis cause
reduced hepatic uptake
61
decreased conjugation is caused by
hepatitis cirrhosis enzyme deficiency
62
Skin, nail beds and whites of the eye take on a yellow color because of
excess bilirubin accumulation in the body
63
bilirubin is very toxic to:
brain cells
64
what is the treatment for jaundice?
treat cause of condition blood transfusion sun
65
Location of the site of the cause of jaundice is determined by:
the color of feces and urine
66
what is the site of the problem if your feces is light or clay colored and your urine dark?
extrahepatic obstructive jaundice | obstruction of bile duct.
67
what is the problem if your feces is normal to light color and your urine is light?
intrahepatic obstruction jaundice | damaged hepatocytes.
68
where is the problem if your feces if dark and so is your urine?
hemolytic anemia
69
X-ray, CT scan, and l iver biopsy provide evidence of the presence of
a stone, tumor, hepatitis, or cirrhosis
70
Hematocrit is ____% or total blood volume
38-45%
71
what is normal hematocrit for males?
42-45%
72
what is a normal hematocrit for females?
38-42%
73
polycythemia
myeloproliferative disorder
74
what are hematocrit levels for males and females in polycythemis?
females: greater than 48% males: greater than 52%
75
what are the different types of polycythemia?
relative | absolute (primary and secondary)
76
relative polycythemia
dehydration
77
Primary absolute polycythemia
polycythemia vera | increased RBC synthesis
78
secondary absolute polycynthemia
hypoxemia kidney disease other disorders that increase erythropoietin
79
what are some disorders that increase erythropoietin?
high altitude living smokers COPD
80
what are clinical manifestations of polycythemia?
Liver and spleen congested with RBD increased blood viscosity (light headedness/visual disturbance) Ruddy Cyanosis bone marrow is hyperplastic
81
Ruddy Cyanosis of the face
pruritus (itch) hypertension congestive heart failure
82
hyperplastic bone marrow is presents in all types except
dehydration
83
how do we treat relative polycythemia?
rehydrate patient
84
how do we treat polycythemia vera?
``` bleed patient (young) low dose aspirin (young) 32P (old) ```
85
how do we treat secondary polycythemia?
treat the cause of the hypoxemia or remove the cause of the excess erythropoietin (remove kidney, tumor, etc)
86
Anemia
decreased oxygen-carrying capacity of blood
87
What are clinical manifestations of anemia?
``` decreased RBCs in blood weakness fatigue headache lack of color in skin, nail beds increased heart rate ```
88
how do you classify anemia?
according to the size of the RBC and the hemoglobin content
89
when classifying anemia, "-cytic" deals with
size
90
when classifying anemia, "-chromic" deals with
hemoglobin content
91
normocytic-normochromic anemia
cells of normal size and hemoglobin content | reduces RBC number must be the prob if still anemia
92
what are common examples of normocytic-normochromic anemia?
posthemorrhagic anemia Aplastic anemia hemolytic anemia anemia of chronic disease
93
posthemorrhagic anemia
result of blood loss
94
appears____hours following blood loss
48-72
95
how much blood do you lose when posthemorrhagic anemia appears?
over 20% of blood volume.
96
Aplastic anemia
reduced erythrocyte synthesis
97
What are clinical manifestations of aplastic anemia
decreased cells in blood and bone marrow and decreased reticulocytes
98
what are the two types of aplastic anemia
all types of blood cells reduced | only RBCs reduced
99
pancytopenia
all blood cells reduced in blood
100
mixed cell aplasia
all types of celled reduced in bone marrow
101
Aplastic anemia
only RBCs reduced in blood
102
what is the cause of aplastic anemia?
destruction of bone marrow
103
what can destroy bone marrow?
``` radiation exposure to drugs, toxins, or various chemicals kidney failure (lack of erythropoietin) infection autoimmune idiopathic ```
104
hemolytic anemia
increased erythrocyte destruction
105
What are clinical manifestations of hemolytic anemia?
``` general manifestations of anemia Jaundice and dark fecal material and urine splenomegaly and hepatomegaly may occur bone marrow normal or hyperplastic increased reticulocytes ```
106
what are causes of hemolytic anemia?
autoimmune | acquired: drugs, toxins (eg lead, arsenic), or trauma
107
What are some genetic diseases that change the shape of RBCs?
sickle cell syndrome thalassemias both are microcytic-hypochromic
108
Cells rupture easily and are destroyed in the spleen and liver because of
the abnormal shape of the RBC membrane
109
Sickle cell anemia is a genetic disease cause by an
autosomal recessive gene
110
sickle cell anemia is characterized as
microcytic-hypochromic
111
Sickle cell is more common in people of
the near east, mediterranean, african, and southern indian origin
112
What are the effects of sickle cell anemia ?
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
when is sickle cell anemia fatal by for males and females?
Males-42yo | females-48yo
114
How do we treat sickle cell anemia ?
``` reduced stress blood transfusions prevent infections hydroxyurea keep patient well hydrated correct any acid-base imbalances ```
115
Thalassemias is a genetic disease caused by
autosomal recessive trait.
116
Thalassemias causes impaired
synthesis of the alpha or beta chain of hemoglobin
117
Thalassemias is characterized as
microcytic-hypochromic anemia
118
in thalassemias hemoglobin precipitates in RBCs which makes them
very fragile and changes their shape
119
thalassemias causes the bone marrow to be
overstimulated
120
overstimulation that takes place during thalassemias causes
the bone to become thin and easily broken and enlargement of the face bone.
121
how do you treat thalassemias?
splenectomy | blood transfusion
122
what is the problem with transfusions
hemosiderosis
123
hemosiderosis
``` storage of excess iron in tissues such as the: liver lungs skin pancreas ```
124
what is the cause of anemia due to chronic disease
macrophages produce substances (cytokines) that disrupt the iron cycle, causes RBC destruction, and inhibits erythropoiesis
125
in anemia caused by chronic disease, hepcidin expression is _____ in the liver
increased
126
what are clinical manifestations of anemia caused by chronic disease?
anemia related to chronic disease
127
who do you treat anemia of chronic disease?
eliminate chronic disease | increase RBC synthesis with colony stimulating factors and/or erythopoietin
128
anemia of chronic disease is classified as
normocytic-normochromic anemia
129
iron deficiency anemia is classified as
microcyctic-hypochromic anemia
130
iron deficiency anemia is caused by:
low iron, which inhibits RBC synthesis
131
what is the most common anemia worldwide?
iron deficiency anemia
132
who is iron deficiency anemia common in?
young children due to rapid growth | women due to poor diet, low testosterone, and moderate decreases in iron due to menstruation
133
how do you treat iron deficiency anemia?
increased iron in diet food is better than pills risk of toxicity in children
134
leukopenia
deficiencies in the quality and quantity of leukocytes | leukopenia is always normal
135
leukocytosis
increased number of leukocytes
136
many hematologic disorders are
malignancies
137
nonhematologic malignancies metastasize to____ affecting _____production
bone marrow affecting leukocyte production
138
what happens in quantitative disorders?
increases or decrease in cell numbers bone marrow disorders or premature destruction of cells response to infectious microorganism invasion
139
qualitative disorders are
disruptions of cellular function
140
leukocytosis ca be a normal ______ physiologic response to stressors
protective
141
leukopenia results in low WBC count which
predisposes to infections
142
what are some tests that are done to test for leukocytes?
peripheral blood differential cell count bone marrow biopsy lymph node biopsy
143
what are non-malignant leukocyte abnormalities?
infectious mononucleosis | lymphadenopathy
144
what are malignant leukocyte disorders
leukemias multiple myeloma malignant lymphomas
145
what is the cause of infectious mononucleosis?
epstein-barr virus spread through oral mucous membrane contact
146
what are clinical manifestations of infectious mononucleosis
``` 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
how do you treat infectious mononucleosis?
bed rest analgesics anti-inflammatory steroids
148
lymphadenopathy causes
enlarged or swollen lymph node
149
what is lymphadenopathy causes by?
an infection near or in the lymph
150
what is lymphadenopathy usually the result of?
leukemia
151
leukemia
cancer of the blood forming organs resulting in excess production of poorly functioning leukocytes
152
what are the symptoms of leukemia?
``` fatigue bleeding fever that is often apparent as night sweats weight loss bacterial, viral, and fungal infections ```
153
what are clinical tests that are done do diagnose leukemia?
blood smear | bone marrow biopsy
154
what are the different types of leukemia?
acute leukemia | chronic leukemia
155
what are the different types of acute leukemia?
acute myelogenous leukemia | acute lymphocytic leukemia
156
What are the types of chronic leukemia?
chronic myelogenous leukemia | chronic lymphocytic leukemia
157
Acute Leukemia causes alterations in the leukocytes:
early in the differentiation process
158
what is produced in acute leukemia?
large numbers of rapidly proliferating stem cell-like leukocytes
159
what does the untreated individual rapidly die of?
infection or hemorrhage | in a matter of weeks
160
AML
Acute myelogenous leukemia
161
AML affects the _____ line
myelogenous
162
which cells are in the myelogenous line?
eosinophils neutrophils mast basophils
163
in AML you see an increase of myelogenous ______ cells in marrow and blood
precursor cells
164
ALL
Acute Lymphocytic leukemia
165
which cells does ALL affect?
cells leading to t-lymphocytes and b-lymphocytes
166
in ALL you have increase number of ________
lymphocyte precursor cells
167
ALL is most common in
children
168
How do you treat acute leukemia?
chemo radiation bone marrow transplant 60%-90% survive when treated early
169
what is chronic leukemia?
leukemia that causes alterations in he leukocytes late in the differentiation process so, they are not well differentiated.
170
what is produced in chronic leukemia?
slow proliferating mature leukocytes which exhibit decreased function
171
what do people usually die of in chronic leukemia?
infection ot hemorrhage | takes a few years.
172
how is chronic leukemia discovered?
by a random blood test because it is initially asymptomatic
173
CML
chronic myelogenous leukemia
174
CML results in an increase of
precursor cells for monocytes, basophils, eosinophils, neutrophils, megalokaryocytes and erythrocytes. they are poorly functioning as well.
175
95% of the time it is caused by
a marked shortening of chromosome 22
176
philadelphia chromsome
chrom 22
177
CLL
chronic lymphocytic leukemia
178
what is CLL?
a decrease in cells leading to T lymphocytes and B lymphocytes which leads to an increase of progenitors and lymphocytes
179
how do you treat chronic leukemia?
chemo radiation bone marrow transplant
180
what is the cure rate for chronic leukemia?
20%
181
what is multiple myeloma?
slow proliferation of malignant blood cells
182
what causes the slow proliferation of malignant blood cells in multiple myeloma?
ask alex
183
how do you diagnose Multiple myeloma?
C.R.A.B.
184
what are clinical manifestations of multiple myeloma?
highly fragiile bones hypercalcemia large amount of immunoglobulin(IgG) in the blood kidney failure due to IgG blocking glomeruli and nephrocalcinosis
185
how do you treat multiple myeloma?
chemotherapy radiation therapy generally fatal (3-4 years)
186
lymphomas
malignancy of lymph nodes
187
which lymph node tissue is generally involved in lymphomas?
secondary lymphoid tissue | in rare cases: bone marrow can also be involved
188
where do lymphomas often spread to?
non-lymphoid tissues like lungs, pleura, etc
189
what are clinical manifestations of lymphomas?
``` swelling of lymph nodes mild fever (often night sweats) weakness sudden weight loss anemia ```
190
hodgkin lymphoma
the presence of transformed lymphocytes in teh affected lymph nodes. reed sternberg cells (multipolar or mult nuclei)
191
sternberg cells produce
and inhibitor of T-cell function
192
non-hodgkin lymphoma
absence of reed-sternberg cells in affected lymph nodes.
193
in non-hodgkin lymphoma there is a _____ of ___ cell and _____ activity
decrease of B cell and macrophage activity.
194
non-hodgkin lymphomas are common amongst
immunosuppressed patients.
195
what is the treatment for hodgkin/non-hodgkin lymphoma?
removal of malignant tissues and lymph node chemotherapy radiation therapy
196
what is the cure rate for early stage hodgkin disease?
75%
197
what is the cure rate for non-hodgkin lymphoma?
30%
198
hemostasis
formation and removal of a blood clot
199
blood coagulation involved the interaction of which three events?
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
vascular spasm is generally ____ in duration
short (less than one minute)
201
What causes vascular spasm?
damage of the blood vessel histamine serotonin
202
blood coagulation is generally a ___ duration
longer
203
what are the four parts of blood coagulation?
formation of the platelet plug formation of fibrous clot clot retraction thrombolysis
204
what activates platelet adherence?
trauma | inflammation
205
what are the steps in the formation of the platelet plug?
1. platelet adherence 2. platelet activation and degranulation 3. platelet aggregation
206
platelet adherence due to trauma causes
exposure of subendothelial matrix
207
von Willebrand factor vWF
matrix (collagen) exposure due to trauma
208
platelet adherence due to trauma causes
narrowing
209
when endothelium exposure to inflammatory factors also releases vWF
it promotes platelet adherence to subendothelial matrix
210
what are inflammatory factors?
endotoxin inflammatory cytokines histamine serotonin
211
normal platelets are in a ____ state
anti-coagulative
212
what does platelet activation do to normal platelets?
converts then into a pro-coagulative state
213
helthy endothelium releases factors that
inhibit platelet activation
214
what does PGI2 do?
it binds to receptors on platelets and inhibits their activation
215
what does NO do to platelet activation?
directly inhibits it
216
what does ADPase do to platelet activation?
it breaks down the ADP released from activated platelets. If it can get rid of al of the ADP it can stop activation
217
platelet activation causes
degranulation
218
___ platelets release secretory granules
activated
219
what is the positive feedback that occurs during platelet activation?
when the platelets are activated they granulate which then causes further activation and this more granulating.
220
thrombin concerts fibrinogen to fibrin which
binds multiple platelets to form a mesh
221
fibrous clots
consist of a series of plasma proteins made by the liver, platelets and endothelium

Pathohysiology (16 decks)

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