blood Flashcards

(74 cards)

1
Q

coposition of blood

A

55% plasma, 45% cells

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2
Q

hematopoiesis

A

the formation of blood cellular components- stem from pluripoten matopoietic stem cell- split to lymphoid stem cells and trillineage stem cells

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3
Q

what is Hematopoietic System

A

Erythrocytes (RBCs) are ideally suited for
their primary function: transport of oxygen
from the lungs into the peripheral tissues.
• Hemoglobin is a complex molecule that
consists of four globin subunits each
containing a heme group that can carry an
oxygen molecule (or carbon monoxide)

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4
Q

synthesis require

A

Hemoglobin synthesis requires iron, vitamin
B12, vitamin B6
, and folic acid.
• Red blood cells survive in the circulation on
average for 120 days.

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5
Q

spleen

A

Spleen: contains phagocytic cells that digest
main components of RBC’s and release them
for reuse or excretion

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6
Q

anemia

A

Anemia is a reduction of hemoglobin in the blood to
below-normal levels.
• Normal levels are >130 g/L in males and >115 g/L in
females. Textbook is American so its units are
lower i.e. in g/dL
• This may be associated with the following:
– Appearance of abnormal hemoglobin
– Reduced number of red blood cells
– Structural abnormalities of red blood cells
Hypoxia-lack of oxygen to the tissues

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7
Q

what do cell counters do and what values do they give you

A

Complete blood count gives you a count of all
the cells present in the sample
• This instrument is also able to give you the
characteristics of the cells that are present
• The instrument will also give a value for the
total hemoglobin present and the hematocrit
(amount of RBCs by volume) i.e. a hematocrit
(Hct) of 40%

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8
Q

what mesurement are made

A

Objective measurements of red blood cell
parameters are done with instruments that
estimate the size of red blood cells and their
hemoglobin content.
– Mean corpuscular volume (MCV)-Mean corpuscular volume (MCV) =
• <80 fL: Microcytic Anemia fL= femtoliter =10 -15 one quadrillionth of a liter
• >100 fL: Macrocytic Anemia

– Mean corpuscular hemoglobin (MCH)-• Mean corpuscular hemoglobin (MCH) =
Normal Range 28-32 pg/cell. < 28: Hypochromic
– Mean corpuscular hemoglobin concentration
(MCHC) -Normal Range 320-360 g/L
• Low values: Hypochromic Anemia !!!!!!!!!!!!!!!!!!! be able to diferentiate

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9
Q

anemia occurs when

A

Anemia may be a consequence of:
– Decreased hematopoiesis ( production) (nutrient deficiency
– Abnormal hematopoiesis (sickle cell)
– Increased loss or destruction of red blood cells

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10
Q

know some deseases and what they are classified under

A

slide 23

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11
Q

Decreased Hematopoiesis

A

Bone marrow failure
– Aplastic anemia
– pancytopenia:: lack of all blood cells in peripheral blood
– Myelophthisic anemia: bone marrow cells may be damaged or
replaced by infiltrates of metastatic tumor cells
• Deficiencies of nutrients
– Deficiency of vitamin B12 and folic acid (megaloblastic anemia)
– Protein deficiency
– Iron deficiency: most common deficiency

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12
Q

Abnormal Hematopoiesis

A

Usually consequence of genetic
abnormalities
• Sickle cell anemia: substitution of a valine
for glutamic acid at position 6 of the Beta
chain of hemoglobin

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13
Q

Increased Loss and Destruction

of Red Blood Cells

A
• Bleeding: Dilutional Anemia
• Intrasplenic sequestration:
hypersplenism
• Immune hemolysis
• Infections (malaria): parasite
Plasmodium
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14
Q

• Normocytic, normochromic anemia: Dilutional Anemia”

A

Usually following massive blood loss (or surgery because they give them more fluid): because of the loss of blood
fluid shifts from interstitial to ECF fluid compartment. Within a few
weeks blood cells are replenished by bone marrow
so looks the same just diluted

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15
Q

• Microcytic, hypochromic anemia

A

– Small & pale, Iron deficiency or thalassemia (affecting synthesis of
Hb)

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16
Q

• Macrocytic, normochromic anemia (normal in color, but large)

A

Deficiency of vitamin B12 and/or folic acid also in liver disease

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17
Q

• Anemia’s characterized by abnormal red blood

shapes

A

– Elliptocytosis, spherocytosis, sickle cell anemia

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18
Q

hypersplenism

A

increase destruction of RBC and loss

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19
Q

aplastic anemia

A

A pancytopenia or generalized bone marrow failure
Two Types
1. Idiopathic (cause unknown)
2. Secondary: bone marrow suppression. Due to cytotoxic
drugs, radiation therapy or viral infection.
• . Reversible with elimination of causative agent
• depleted of hematopoietic cells and consists only of
fibroblasts, fat cells, and scattered lymphocytes
• Anemia, leukopenia, and thrombocytopenia
• Symptoms - Uncontrollable infections, bleeding tendency,
chronic fatigue, sleepiness, and weakness

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20
Q

iron deficiency anemia

A

Most common form of anemia!!!!!!!!!
• Hypochromic microcytic anemia
• Bone marrow shows normal hematopoiesis
• Etiology
– Increased loss of iron (chronic bleeding)
– Inadequate iron intake or absorption
– Increased iron requirements (childhood growth and
pregnancy)
– Iron supplements usually solves problem

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21
Q

megaloblastic anemia

A

• Caused by a deficiency of vitamin B12 or folic acid
• Deficiency of either of the two cause a delay in hematopoiesis
• Normoblasts do not mature but are transformed to megaloblasts
– Vitamin B12 deficiency
• Pernicious Anemia: Lack of the gastric intrinsic factor due to
atrophic gastritis
– Folic acid deficiency
• Inadequate intake in the diet or because of malabsorption caused by
intestinal disease

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22
Q

megaloblastic anemia pathology

A
Bone marrow
– Hypercellular, numerous megaloblasts
• Peripheral blood
– Decreased RBC that are macrocytic
• Hypersegmentation of neutrophils
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23
Q

Pathologic Conditions Contributing to

Megaloblastic Anemia

A
Vitamin Deficiency or Malabsorption
•Pernicious anemia
•Resection of stomach
•Celiac Disease
•Crohn’s disease
•Parasites
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24
Q

pernicious anemia

A

subheading of megoloblastic : Lack of the gastric intrinsic factor due to
atrophic gastritis- know how to diferentiate mega and iron deficient

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25
Megaloblastic Anemia | Clinical Features
• Fatigue, shortness of breath, weakness • Destruction of posterior and lateral columns in the spinal cord—results in a loss of the senses of vibration and proprioception, as well as loss of the deep tendon reflexes • Treatment Vitamin B12 injections or folic acid supplementation.
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Hemolytic Anemia
• Increased red blood cell Destruction (hemolysis) • Intracorpuscular defects – Structural abnormalities Sickle cell anemia, thalassemia, or hereditary spherocytosis • Extracorpuscular defects – Antibodies, infectious agents, or mechanical factors – Autoimmune hemolytic anemia, hemolytic disease of the newborn, transfusion reactions, malaria, hemolytic anemia caused by cardiac valve prosthesis, disseminated intravascular coagulation
27
sickle cell anemia
Pathogenesis Substitution of glutamic acid by valine in  chain • Synthesis of an abnormal beta chain of globin • HbA gets mutated to HbS • Low O2 tension causes deformities (sickling) • Hemolytic crisis (avoidance of strenuous exercise) • Aggregates cause tissue ischemia
28
sickle cell anemia does what
``` Multiple infarcts in various organs Neurologic defects; sharp pain in the bones, spleen (autosplenectomy), and extremities; retinal infarcts Hyperbilirubinemia and jaundice (bile stones). No definitive therapy, high mortality. Avoid conditions that cause sickling and combat infections ```
29
clinical features of sicke cell anemia
``` • Retarded intellectual development and neurologic deficits (TIAs, small infarcts, stroke) • Cardiopulmonary insufficiency (HF, MI, Pulmonary edema and PE) • Recurrent infections • HbS< 40% asymptomatic • HbS 40-80% mild to moderate disease • HbS>80% typical symptoms of disease • High mortality ```
30
thalassemia
Prevalent of people of the Mediterranean • Genetic defect in the synthesis of HbA that reduces the rate of globin chain synthesis • No abnormal hemoglobin produced • Quantitative rather than qualitative (rate of synthesis of normal is slower than we need it to be- so no abonormalities just lack of) • beta-Thalassemia—reduced synthesis of the beta chain of globin • alpha-Thalassemia—reduced synthesis of the alpha chain of globin • Thalassemia minor or thalassemia trait – Heterozygotes – Only one of the 4 chains is missing – Mild, nonspecific symptoms – Microcytic Hypochromic anemia – Requires no treatment
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b- thalassemia
lack of Hba and get Hbf (a lot)- spleen breakdown more RBC causes jaundice, large speen, inlarge liver, hemosideration, growth retardation , cardiorespiratory insufficiency
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thalassemia major
Thalassemia major – Homozygotes – Severe and serious disease • Splenomegaly, hemosiderosis, and hepatomegaly • Bone marrow—compensatory hyperplasia • Calvarium—“crew-cut” hair on radiographic study • Hyperbilirubinemia and jaundice • Chronic anemia that retards the growth of children • Impairment of normal intellectual development • Cardiorespiratory insufficiency • No treatment for thalassemia mEDETERANIAN
33
Hereditary Spherocytosis
• The primary defect in the genes encoding either ankyrin or alpha or beta chain of spectrin • The most common hereditary disease of red blood cells in Caucasians • Autosomal dominant disease • Peripheral blood—spherocytes, anisocytosis • Hemolytic or aplastic crises—splenomegaly, jaundice • Splenectomy- treatment but no cure- SPLEEN SEES ITS TOO SMALL SO DESTROYS THEM - hyperspleenism
34
Polycythemia
Erythrocytosis • Increased number of red blood cells • Primary polycythemia, or polycythemia vera – Clonal proliferation of hematopoietic stem cells – Uncontrolled production of red blood cells and an increased total red blood cell mass – Myeloproliferative disorder • Secondary polycythemia – Increased red blood cell volume owing to erythroid bone marrow hyperplasia caused by erythropoietin – Usually caused by prolonged hypoxia – Living at high altitudes, anoxia secondary to chronic lung disease, congenital heart disease, renal carcinoma-
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• Primary polycythemia, or polycythemia vera
Clonal proliferation of hematopoietic stem cells – Uncontrolled production of red blood cells and an increased total red blood cell mass – Myeloproliferative disorder
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• Secondary polycythemia
– Increased red blood cell volume owing to erythroid bone marrow hyperplasia caused by erythropoietin – Usually caused by prolonged hypoxia – Living at high altitudes, anoxia secondary to chronic lung disease, congenital heart disease, renal carcinoma
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symptoms of polycythemia
``` Hypertension • Dark red or flushed face • Headaches, visual problems, neurologic symptoms • Splenomegaly • Hypercellular bone marrow seenin smokers too ```
38
Leukopenia
• Reduction in white blood cell count to belownormal levels • Neutropenia (agranulocytosis) – Bacterial infections • Lymphopenia – Bacterial, viral, fungal, and parasitic infections Short-term treatment is with antibiotics (fatigue, light headed)
39
know diferences in R AND wbc deseases
know
40
Leukocytosis
• Increased number of white blood cells in the peripheral blood • Granulocytosis, or neutrophilia – Bacterial infection • Eosinophilic leukocytosis, or eosinophilia – Allergies and some skin diseases or parasitic infections • Lymphocytosis – Viral infections, chronic infections, some autoimmune disorders – Splenomegaly (septic spleen), lymphadenopathy (enlarged)
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• Granulocytosis, or neutrophilia
– Bacterial infection
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• Eosinophilic leukocytosis, or eosinophilia
– Allergies and some skin diseases or parasitic infections
43
deferentiate leukopenia and leukocytosis
know
44
Lymphocytosis
– Viral infections, chronic infections, some autoimmune disorders – Splenomegaly (septic spleen), lymphadenopathy (enlarged)
45
Malignant Diseases of | White Blood Cells
leukimia and lymphoma and multiple myeloma
46
leukimia
``` s—malignant disease involving white blood cell precursors in the bone marrow and peripheral blood (acute and chronic) – Myeloid – Lymphoid lymphocytic ```
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Lymphomas—lymphoid
—lymphoid cell malignant diseases predominantly involving the lymph nodes – Non-Hodgkin’s lymphoma – Hodgkin’s lymphoma
48
multiple myeloma
malignant disease of plasma | cells
49
Etiology and Pathogenesis | of lymphomas and leukemia
The causes of most lymphomas and leukemia's, like the causes of most other malignant tumors, are unknown. • Viruses – HTLV-1 (Human T-Cell leukemia virus 1) – EBV (Epstein Barr Virus) • Endogenous oncogenes – t(8 (is translocated to chromosome 14) ,14)—Burkett's lymphoma – t(9,22)—chronic myelogenous leukemia (Philadelphia chromosome)
50
Leukemia
Bone marrow is infiltrated with malignant cells. • Peripheral blood contains an increased number of immature blood cells. • Complications include anemia, recurrent infections, and uncontrollable bleeding. • 85% of all leukemia's affect children and are acute • Chronic leukemia's found mostly in adults
51
Acute Lymphoblastic Leukemia
• Most common form of leukemia in children< 5yrs most common leukemia in kids • Massive infiltration of the bone marrow and peripheral blood with immature lymphoid cells (blasts) • 20-30% of all leukemia's • Recurrent infections, generalized weakness, and bleeding into the skin and major internal organs • Enlarged lymph nodes and mild splenomegaly • Treatment—with modern chemotherapy, remission can be induced in 2/3 of all patients • Without chemotherapy it is lethal within 3-6 months
52
list the 4 leukemias:!!!!
Acute Lymphoblastic Leukemia. Acute Myelogenous Leukemia Chronic Myelogenous Leukemia Chronic Lymphocytic Leukemia
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Acute Myelogenous Leukemia
This is the most common form of acute leukemia in adults.!!!!!! • Has an acute course; without treatment patients die within 6 months of onset of symptoms • Chemotherapy can induce remission in 60% of patients • 15-30% remain disease free for 5 years • High dose irradiation + chemotherapy followed by bome marrow transplantation during the 1st remission have a 70% 3-year survival.
54
Chronic Myelogenous Leukemia
Malignant disease of pluripotent hematopoietic stem cells capable of differentiating into neutrophils (alll cell lines are affected) • Bone marrow and peripheral blood overgrown with malignant stem cells and their descendants • 15% of all leukemia's: Slow onset • Disease of adulthood, anemia and hypermetabolism (tired and prone to infection) • Three phases of the disease: – Chronic phase: (2 to 3 years) <10% bone marrow blasts – Accelerated phase: >10% bone marrow (nonfunctional) blasts & >20% basophils in peripheral blood; increasing unresponsive to therapy – Blast crisis:> 20% blast in bone marrow • Tyrosine kinase inhibitors: induce remission in 90% of patients (!!!!!!) • Philadelphia (Ph1) chromosome, with BCR/ABL gene rearrangement
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lymphona
It affects any age group. • All forms are malignant • Malignant cells often infiltrate the lymph nodes, spleen, thymus, or bone marrow, but they may also involve any other organ in the body. • Extranodal lymphoma: originating outside of lymph nodes; in solid organs, GI, brain, eyes and skin • There are two large categories: – Non-Hodgkin’s lymphoma (NHL) – Hodgkin’s lymphoma
56
know the names, the age catagory, the symptoms, the treatments
hi
57
bening
its not harmful- hasnt mastatised to the blood stream
58
malignants
attafhes to base membrane of the cell to the blood stream and spread and some go to specific organs, example prostate- goes to brain
59
Non-Hodgkin’s Lymphomas
• Two major categories B and T cell neoplasms and NK- cell neoplasms • Most have the B cell phenotype • Occur in all age groups but most common in adults • Malignant cells Can spill over into blood and present as leukemia • Involve lymph nodes, bone marrow, spleen and thymus but can also be Extranodal • Most common site of Extranodal is GI • Clinical features: lymph node enlargement; splenomegaly and lymphocytosis (increase) • fatigue, fever, weight loss, anemia, leukopenia infections
60
what are the 2 types of lymphomas
non and the hogkins lymphomas
61
Follicular Lymphoma
( non hogkins lymphomas) This is the most common form of lymphoma in the United States (45% of all lymphomas). • It is mostly seen in older people. • The tumor is slow growing. • Most patients present with long-standing enlargement of the lymph nodes and only mild symptoms. • Most patients survive 7 to 9 years after diagnosis of the disease.
62
Diffuse Large-Cell Lymphomas
This is the most common aggressive form of NHL. • Complete infiltration of large lymphoid cells that have irregular outline and prominent nuclei • Tissue is infiltrated with large lymphoid cells that have irregular nuclear outlines and prominent nucleoli. • Spread to major organs is common • With chemotherapy, complete remission can be induced in 75% of patients.
63
Burkitt’s Lymphoma
• This is a highly malignant tumor composed of small B cells. • Extranodal masses are often more prominent than enlarged lymph nodes. • Endemic variant: – Sub-Saharan Africa – Children infected with Epstein-Barr Virus (EBV) – Mandible and facial soft tissue involvement • Sporadic variant: – Children and young adults most often affected – Abdominal mass (e.g., ovarian or intestinal mass) • Most children and young adults can be cured. • Adriamycin and rituximab — a potent chemotherapy regimen given in the hospital about every three weeks.
64
Hodgkin’s Lymphoma
A form of malignant disease that is pathologically distinct from other lymphomas • Disease spreads from one set of lymph nodes to another • Usually central lymph nodes • Age distribution curve is bimodal, with one peak at 25 years and another at 55 years. • Classical Hodgkin’s Lymphoma; Reed-Sternberg Cells are present (Bilobed or multilobed nucleus and prominent nucleoli surrounded by a clear halo (derived from B lymphocytes) • Non Classical Hodgkin’s Lymphoma: Lymphocytic Cells with Popcorn Nuclei:
65
what are Reed-Sternberg Cells
s are present (Bilobed or multilobed nucleus and prominent nucleoli surrounded by a clear halo (derived from B lymphocytes)- present in hodkin lymphomas!!!!!!!
66
where are popocorn cells seen
NON classical hodkins lymphomas
67
classical
reed-sternberg
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Hodgkin’s Lymphoma
Lymph nodes are enlarged (neck and mediastinum). • Extranodal involvement and leukemic spread are rare. • Prognosis of the disease depends primarily on the clinical stage. – Stage I and II tumors are associated with an excellent prognosis and a high rate of cure (>90%) with chemotherapy. – Advanced disease has a less favorable prognosis.
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stage 1 Staging of Hodgkin’s Lymphoma
1: involvement of single lymphnode, 2È 2 or more site 3: deseases on both sides of daiphragm may include spleen or localized 4: widespread liver bone marrow, skin, lung
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multiple myeloma
Most patients older than 45 years of age • Malignant plasma cells typically proliferate in the bone marrow and destroy the surrounding bone (bone fractures) • Hypercalcemia • Renal failure • Anemia and leukopenia Malignant Disease: transformation of a single plasma cell • Clonal expansion leads to an overgrowth in bone marrow • Because theses cells are descendants from a single cell they are termed “monoclonal” • Plasma cells secrete immunoglobulins which can be detected in the serum • After malignant transformation of a single plasma cell the descendants of this malignant cell all secrete the same form of immunoglobulin • Diagnosis is based on the following: – X-ray studies (lytic lesions) – Serum electrophoresis (monoclonal spike) – Bone marrow biopsy (neoplastic plasma cells in increased numbers) – Bence Jones Protein in urine (first biochemical tumor marker) • Most patients die within 3 to 4 years, primarily of kidney failure or infection Most patients> 45 years • Malignant cells destroy bone marrow • Punch holes through blood forming bones • Hypercalcemia with deposition in the kidney • Chemotherapy ineffective • secondary Raynauds syndrome
71
what is the bence jones protein
– Bence Jones Protein in urine (first biochemical tumor marker)
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bone abnormalities
crue cut- thalasemia- dont confuse with bone leision of multiple myeloma
73
beta
medeteranina
74
hyper spleenism
increase rate of loss or destruction