blood Flashcards

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
Q

Megaloblastic Anemia

Clinical Features

A

• 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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26
Q

Hemolytic Anemia

A

• 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

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27
Q

sickle cell anemia

A

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

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28
Q

sickle cell anemia does what

A
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
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29
Q

clinical features of sicke cell anemia

A
• 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
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30
Q

thalassemia

A

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

31
Q

b- thalassemia

A

lack of Hba and get Hbf (a lot)- spleen breakdown more RBC causes jaundice, large speen, inlarge liver, hemosideration, growth retardation , cardiorespiratory insufficiency

32
Q

thalassemia major

A

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
Q

Hereditary Spherocytosis

A

• 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
Q

Polycythemia

A

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-

35
Q

• Primary polycythemia, or polycythemia vera

A

Clonal proliferation of hematopoietic stem cells
– Uncontrolled production of red blood cells and an increased total red
blood cell mass
– Myeloproliferative disorder

36
Q

• Secondary polycythemia

A

– 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

37
Q

symptoms of polycythemia

A
Hypertension
• Dark red or flushed face
• Headaches, visual problems, neurologic
symptoms
• Splenomegaly
• Hypercellular bone marrow
seenin smokers too
38
Q

Leukopenia

A

• 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
Q

know diferences in R AND wbc deseases

A

know

40
Q

Leukocytosis

A

• 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)

41
Q

• Granulocytosis, or neutrophilia

A

– Bacterial infection

42
Q

• Eosinophilic leukocytosis, or eosinophilia

A

– Allergies and some skin diseases or parasitic infections

43
Q

deferentiate leukopenia and leukocytosis

A

know

44
Q

Lymphocytosis

A

– Viral infections, chronic infections, some autoimmune
disorders
– Splenomegaly (septic spleen), lymphadenopathy
(enlarged)

45
Q

Malignant Diseases of

White Blood Cells

A

leukimia and lymphoma and multiple myeloma

46
Q

leukimia

A
s—malignant disease involving white
blood cell precursors in the bone marrow and
peripheral blood (acute and chronic)
– Myeloid
– Lymphoid lymphocytic
47
Q

Lymphomas—lymphoid

A

—lymphoid cell malignant diseases
predominantly involving the lymph nodes
– Non-Hodgkin’s lymphoma
– Hodgkin’s lymphoma

48
Q

multiple myeloma

A

malignant disease of plasma

cells

49
Q

Etiology and Pathogenesis

of lymphomas and leukemia

A

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
Q

Leukemia

A

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
Q

Acute Lymphoblastic Leukemia

A

• 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
Q

list the 4 leukemias:!!!!

A

Acute Lymphoblastic Leukemia.
Acute Myelogenous Leukemia
Chronic Myelogenous Leukemia
Chronic Lymphocytic Leukemia

53
Q

Acute Myelogenous Leukemia

A

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
Q

Chronic Myelogenous Leukemia

A

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

55
Q

lymphona

A

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
Q

know the names, the age catagory, the symptoms, the treatments

A

hi

57
Q

bening

A

its not harmful- hasnt mastatised to the blood stream

58
Q

malignants

A

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
Q

Non-Hodgkin’s Lymphomas

A

• 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
Q

what are the 2 types of lymphomas

A

non and the hogkins lymphomas

61
Q

Follicular Lymphoma

A

( 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
Q

Diffuse Large-Cell Lymphomas

A

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
Q

Burkitt’s Lymphoma

A

• 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
Q

Hodgkin’s Lymphoma

A

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
Q

what are Reed-Sternberg Cells

A

s are present
(Bilobed or multilobed nucleus and prominent nucleoli surrounded by a
clear halo (derived from B lymphocytes)- present in hodkin lymphomas!!!!!!!

66
Q

where are popocorn cells seen

A

NON classical hodkins lymphomas

67
Q

classical

A

reed-sternberg

68
Q

Hodgkin’s Lymphoma

A

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.

69
Q

stage 1 Staging of Hodgkin’s Lymphoma

A

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

70
Q

multiple myeloma

A

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
Q

what is the bence jones protein

A

– Bence Jones Protein in urine (first biochemical tumor marker)

72
Q

bone abnormalities

A

crue cut- thalasemia- dont confuse with bone leision of multiple myeloma

73
Q

beta

A

medeteranina

74
Q

hyper spleenism

A

increase rate of loss or destruction