Hematology Flashcards

1
Q

What 3 proteins make up plasma?

A

albumin, globulins, fibrinogen

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2
Q

blood is made up of what 3 cell types

A

Erythrocytes, leukocytes, platlets

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3
Q

Chief function of blood (5)

A

Carry O2 (RBC)
Delivery of substances needed for cellular metabolism
Removal of wastes
Defense against microorganisms and injury
Maintenance of acid-base balance (bicarbonate)

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4
Q

How much blood is in the body?

A

6 quarts

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5
Q

Plasma: Function of each
Albumins
Globulins
Fibrinogen

A

Albumins
Function as carriers (eg: medication) and control the plasma oncotic pressure

Globulins
Carrier proteins and immunoglobulins (antibodies)

Clotting factors
Mainly fibrinogen

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6
Q
Erythrocytes (RBCs)
composition
function
structure
life cycle
A

Floating bags of hemoglobin
Most abundant cell in the body
Responsible for tissue oxygenation
Biconcavity (increase surface area) and reversible deformity(can be squeezed)
120-day life cycle (3-4 month), do not go through cell devision

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7
Q
Erythropoietin (EPO): 
function
location of function
location of production 
what triggers production
A

EPO makes RBCs, work in the bone marrow
Produced by peritubular cells of the kidney (electrolyte, fluid, pH balance)
Hypoxic state in the kidney triggers production

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8
Q

Leukocytes (WBCs)
Granulocytes vs Agranulocytes
what type of WBC are each
function of each

A

Granulocytes:
phagocytes (neutrophils, eosinophils, and basophils).
Granules in cytoplasm contain enzymes that kill antigens.

Agranulocytes:
monocytes, macrophages, and lymphocytes—contain relatively fewer granules than granulocytes. Carry out inflammatory and immune functions, remove debris
.

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9
Q

Granulocytes:

Eosinophils- function

A

Eosinophils ingest antigen-antibody complexes
Induced by IgE hypersensitivity for immune fighting in parasitic infections
Histaminase to that help control inflammatory processes

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10
Q

Granulocytes:

Basophils- function

A

Central cell in inflammation, release histamine
Basophils = in blood
Mast cells = vascularized connective tissue (not WBC)

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11
Q

Lymphocytes are what 3 cell types?

A

T cells
B cells
Natural killer (NK) cells

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12
Q

Platlets
Structure
function

A

(Thrombocytes)
Disk-shaped cytoplasmic fragments
Essential for blood coagulation and control of bleeding

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13
Q
Thrombopoietin (TPO):
function
location of production 
location of function
what triggers production
LIfespan
A
  • Hormone that stimulates the production and differentiation of megakaryocytes and is the main regulator of the circulating platelet numbers.
  • TPO is primarily produced by the liver and induces platelet production in the bone marrow.
  • Release b/c of trauma.
  • Platelets circulate for 10 days before losing their functional capacity
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14
Q

Primary lymphoid organs

Secondary lymphoid organ

A

Bone marrow and thymus

Spleen, lymph nodes

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15
Q

All of the lymphoid organs link the hematologic and immune systems in that they:

A

Link hemo to immuno because of masses of lymphoid tissue containing macrophages, T cells, B cells.

Another way to say it: are sites of residence, proliferation, differentiation, or function of lymphocytes and mononuclear phagocytes (monocytes and macrophages)

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16
Q

Spleen:

function

A

Largest secondary lymphoid organ
filters blood
Phagocytosis of old, damaged, and dead blood cells are removed
Blood storage

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17
Q

Lymph nodes

function

A

Facilitates maturation of lymphocytes
Transports lymphatic fluid back to the circulation
Cleanses the lymphatic fluid of microorganisms and foreign particles

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18
Q

MPS
what cells is it made up of
function
organs (2)

A

(Mononuclear Phagocyte System)
Consists of monocytes/macrophages that differentiate without dividing and reside in the tissues for months or perhaps years

Cells of the MPS ingest and destroy microorganisms and foreign material

The MPS is mostly the liver and spleen

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19
Q

Hematopoiesis

A

the process of Erythrocytes (blood cell) production in the bone marrow

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20
Q

Two stages of Hematopoiesis

A

1) mitotic division (i.e., proliferation)

2) maturation (i.e., differentiation) into mature hematologic cells

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21
Q

what are Pluripotent stem cells

A

mother cells continuously going though cell division. Daughter cells mature into RBC (EPO); WBC/ Plat. (TPO)

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22
Q

Bone marrow
Proper name
red vs yellow
location

A

Called myeloid tissue
Red (active) and yellow bone marrow (fat storage)
Adult active bone marrow found in flat bones
Marrow located in: Pelvic bones, vertebrae, cranium and mandible, sternum and ribs, humerus, and femur

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23
Q

3 examples of when Hematopoiesis is stimulated

A

-Stimulus to increase WBC production: infectious exposure
WBC are getting used up
-Stimulus to increase plat. production: trauma and blood loss (TPO)
-Stimulus to increase RBC production: anemia reflected through hypoxia (EPO)

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24
Q

Erythropoiesis
What it is
what stimulates it
what occurs internally

A

the maturation of RBCs.
Stimulated by EPO during times of hypoxia.
In each step the quantity of hemoglobin increases and the nucleus decreases in size.

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25
Erythrocytes
a red blood cell that (in humans) is typically a biconcave disc without a nucleus. Erythrocytes contain the pigment hemoglobin, which imparts the red color to blood, and transport oxygen and carbon dioxide to and from the tissues.
26
Hemoglobin function how many per RBC Function of the Two pairs of protein subunits (globins)
Oxygen-carrying protein of the erythrocyte A single erythrocyte contains as many as 300-400 million hemoglobin molecules Each subunit contains iron-protoporphyrin complex (heme) each heme carries 4 oxygen molecules
27
Nutritional requirements for hemoglobin synthesis | deficiency can lead to what?
Vitamins B12, B6, B2, E, and C; folic acid; pantothenic acid; and niacin (deficiency in B12 and Folate leads to decreased life span of RBC)
28
Destruction of Aged RBCs who does the destroying where is it done (primary and secondary)
Aged red cells (senescent) are destroyed by macrophages of the MPS Primarily done in the spleen The liver takes over if the spleen is nonfunctioning/absent
29
when Porphyrin (heme) are broken down, what happens
Porphyrin is reduced to bilirubin (pigmented- yellow/green wast from the breakdown of heme), transported to the liver, and secreted in the bile
30
Leukopoeisis: Leukocytes and Agranulocytes where do each come from when are they released?
Leukocytes arise from stem cells in the bone marrow Leukocytes mature in the bone marrow Agranulocytes are released into the bloodstream before they fully mature
31
Thrombopoeisis
is the development of platelets. Platelets (thrombocytes) are derived from stem cells that differentiate into megakaryocytes. During thrombopoiesis, the megakaryocyte nucleus enlarges and becomes extremely polyploidy without cellular division.
32
Endomitosis:
The megakaryocyte undergoes the nuclear phase of cell division but fails to undergo division (googlie eyes) The megakaryocyte expands due to the doubling of the DNA and breaks up into fragments (platelets)
33
Hemostasis means:
the arrest of bleeding by formation of blood clots at sites of vascular injury.
34
Hemostasis requires (5):
``` 1- Platelet plug "the gum in the hole" 2-Clotting factors (leads to the production of fibrin "the cement over the gum") 3- Blood flow and shear forces 4- Endothelial cells 5- Fibrinolysis ```
35
Hemostasis: Result of Vascular Spasm/Vasoconstriction in response to injury
Spasm induces vasoconstriction that inhibits amount of blood flow through the damaged area and blood loss
36
Plateplet plug Process (5)
Platelet activation (Calcium is essential for activation) Adhesion to damaged vascular wall von Willebrand factor (vWF) makes platelets sticky Platelet degranulation Aggregation adherence increases Platelets to wall and each other Activation of the clotting system and development of an immobilizing meshwork of platelets and fibrin
37
the 4 most important proteins that make up the Common Pathway of Coagulation and how they effect each other
Factors X and V activate prothrombin into thrombin. Thrombin then converts fibrinogen into fibrin, which becomes a fibrin clot.
38
Clot retraction what it is what facilitates this end result
Fibrin strands shorten, become denser and stronger to approximate the edges of the injured vessel and site of injury Facilitated by large numbers of platelets within the clot and actin-like contractile proteins in the platelets Pulls wound/tissues together to facilitate repair
39
``` Lysis of blood clots = Fibrinolytic system (3) ```
(Fibrinolysis) Plasminogen and plasmin breakdown) Fibrin degradation products D-dimers (bi-product)
40
Hematology Evaluation (testing) (3)
``` bone marrow function Blood tests (main way to test for hemo. issues) Hematocrit: ratio of RBC to overall volume ```
41
-cytosis= Erythrocytosis Leukocytosis Thrombocytosis -cytopenia (-penia)= erythrocytopeniaa leukocytopenia thrombocytopeni
(increased cell count, too many) 1- erythrocytosis (polycythemia, the disorder)= too many RBC, changes viscosity making blood more thick= hypercoagulation 2- leukocytosis= too many WBC, not worrisome sign of normal protective response. Insanely high and abnormal is concerning b/c poss leukemia 3- thrombocytosis (thrombocythemia)= too many platelets, greater risk of forming clots= hypercoagulation (deficiency in the cell, not enough) 1- erythrocytopenia= anemia leading to tissue hypoxia 2- leukocytopenia= immune suppression (most often decrease in neutrophils) 3- thrombocytopenia= won't be able to make a clot, increased bleeding risk
42
What is Anemia?
Low RBCs
43
Anemia classifications based on Morphology and Hemoglobin concentrations -CYTIC/ -CHROMIC
Size (Morphology): Identified by terms that end in -CYTIC Macrocytic (too big in size), microcytic (too small), normocytic (just right in size) Hemoglobin content (how much hemoglobin): Identified by terms that end in -CHROMIC Normochromic (normal hemoglobin) and hypochromic (not enough hemoglobin). Cannot have "too much"! You can have: Macro Normo; Micro Hypo; Normo Normo
44
Anemia: Anisocytosis vs Poikilocytosis
Red cells are present in various sizes (rare) Red cells are present in various shapes Describing sickle cell
45
Anemia: Physiologic manifestations Classic anemia symptoms
Physiologic s/s: Reduced oxygen-carrying capacity Symptoms: Fatigue, weakness, dyspnea (SOB, turning up res. response), and pallor (pale)
46
What breaks down a clot
Plasmin
47
What is the bi-product of platelet break down?
D-dimer
48
Macrocytic-Normochromic Anemias (3) | what they are
Pernicious, megaloblastic, folate deficiency | The cell is too big but have an abundance of hemoglobin
49
``` Macrocytic-Normochromic: Pernicious anemia cause Results in Symptoms Treatment ```
Can be caused by a lack of intrinsic factor from the gastric parietal cells (most common) Required for vitamin B12 absorption Results in vitamin B12 deficiency due to absorption not often a lack of B12 in diet (B12 obtained from red meat and eggs) Typical anemia symptoms with possible neurologic manifestations. Nerve demyelination (poss. neuropathy) Others: Loss of appetite, abdominal pain, beefy red tongue (atrophic glossitis), icterus, and splenic enlargement Treatment: Parenteral or high oral doses of vitamin B12
50
Macrocytic-Normochromic: megaloblastic anemias cause Characterized by
Caused by deficiencies in vitamin B12 or folate (these vitamins gives RBC their life span, decrease will shorten life span) Characterized by defective DNA synthesis
51
Macrocytic-Normochromic: Folate deficiency anemia cause Symptoms Treatment
Not dependent on any other factor Absorption of folate occurs in the small intestine Similar symptoms to pernicious anemia except neurologic manifestations generally not seen Treatment requires daily oral administration of folate
52
Microcytic-Hypochromic Anemias (3) | what it is
Characterized by red cells that are abnormally small and contain reduced amounts of hemoglobin (sm. b/c not make enough hemoglobin) 1) Iron deficiency (Disorders of iron metabolism) 2) Sideroblastic (Disorders of porphyrin and heme synthesis, mitochondrial disfunction) 3) Thalassemia (Disorders of globin synthesis, genetic)
53
Microcytic-Hypochromic: Iron deficiency | symptoms
Most common type of anemia worldwide Nutritional iron deficiency Metabolic or functional deficiency causes: Brittle, thin, coarsely ridged, and spoon-shaped nails. Glossitius (A red, sore, and painful tongue)
54
Koilonychia
Brittle, thin, coarsely ridged, and spoon-shaped nails. Caused by iron deficiency
55
Microcytic-Hypochromic: Sideroblastic anemia cause Characterized by
Altered mitochondrial metabolism causing ineffective iron uptake and resulting in dysfunctional hemoglobin synthesis Ringed sideroblasts within the bone marrow are diagnostic
56
Ringed sideroblasts
Sideroblasts are erythroblasts that contain iron granules that have not been synthesized into hemoglobin
57
Microcytic-Hypochromic: Thalassemia what is it cause Characterized by
Genetic disorder that produces malformed hemoglobin chains Originated in the Mediterranean region Autosomal recessive trait Estimated ~80 million carriers worldwide Produce less hemoglobin and have low number of RBCs (life long)
58
Normocytic-Normochromic (5) | what it is
Characterized by red cells that are relatively normal in size and hemoglobin content but insufficient in number of them How you get it on following slides Aplastic, Posthemorrhagic, Hemolytic, Sickle cell, chronic inflammation
59
Normocytic-Normochromic: Aplastic
Pancytopenia- ("pan" encompasses all) all blood cells are deficient (bone marrow problem) Pure red cell aplasia- Due to low EPO (thus a disfunction in the kidneys)
60
Normocytic-Normochromic: Posthemorrhagic
Acute blood loss (probably due to trauma)
61
Normocytic-Normochromic: Hemolytic
Over destruction of red blood cells: due to spleen enlargement. Autoimmune hemolytic anemias (eg: lupus) Jaundice: wast of bilirubin from breakdown of RBC
62
Normocytic-Normochromic: Sickle cell
``` Autosomal recessive disorder that distorts hemoglobin proteins Causes RBC to “sickle” in shape Most often in times of hypoxia No biconcave disc! Risk of CVA ```
63
Normocytic-Normochromic: chronic inflammation
Mild to moderate anemia seen in: | AIDS, rheumatoid arthritis, lupus erythematosus, hepatitis, renal failure, and malignancies
64
Polycythemia
Too many red blood cells
65
Relative polycythemia
Result of dehydration (b/c it lowers the plasma volume) Fluid loss results in relative increases of red cell counts and Hgb and Hct values
66
Absolute polycythemia | cause
too many RBC Causes: Abnormality of stem cells in the bone marrow making too many RBC Polycythemia vera (PV) or Increase in erythropoietin (EPO) in response to chronic hypoxia (at the kidney). An inappropriate response to erythropoietin-secreting tumors
67
Leukocytosis
Leukocytosis is a normal protective physiologic response to stressors
68
Leukopenia
Leukopenia is not normal and not beneficial | A low white count predisposes a patient to infections
69
Infectious Mononucleosis (mono)
Acute, self-limiting infection of B-lymphocytes transmitted by saliva through personal contact Commonly caused by: Epstein-Barr virus (EBV) (85%) Cytomegalovirus (CMV), hepatitis, influenza, HIV Serious complications are infrequent Fever, sore throat, swollen cervical lymph nodes, increased lymphocyte count Splenic rupture is the most common cause of death
70
Leukemia
Cancers of excessive accumulation of leukemic cells in bone marrow
71
Lymphocytic (lymphoblastic) Myelogenous Acute leukemia (early maturation) Chronic leukemia (late maturation)
were going to be lymphocytes (T, B, NKC) were goingt to be RBCs, platelets, and granulocytes - Presence of undifferentiated or immature cells (appear like stem cells), usually blast cells. Early in differation - Predominant cell is more differentiated but does not function normally ALM pediatrics AML/ CML (chromosome 9, older adults)
72
Lymphadenopathy Local lymphadenopathy General lymphadenopathy
Enlarged (swollen) lymph nodes that become palpable and tender Local lymphadenopathy Drainage of an inflammatory lesion located near the enlarged node General lymphadenopathy Occurs in the presence of malignant or nonmalignant disease (lymphoma)
73
Lymphomas | Two major categories: Hodgkin lymphoma, Non-Hodgkin lymphomas
Malignant transformation of lymphocytes Hodgkin lymphoma Characterized by presence of Reed-Sternberg (RS) cells (googly eye cells) Non-Hodgkin lymphomas B-Cell Neoplasms T & NK cell Neoplasms
74
Burkitt lymphoma
Most common non-Hodgkin lymphoma in children Fast-growing tumor of the jaw and facial bones Lesions in submandibular lymph nodes Associated with EBV or HIV infection Viral
75
Thrombocytopenia | What can it cuase
Platelet count <150,000/mm3 1) hemorrhage from minor trauma 2) spontaneous bleeding 3) severe bleeding (spontaneous bleeding, potentially fatal)
76
von Willebrand factor deficiency: | what is causes
used to adhere clot, cause increased bleeding risk
77
Vitamin K deficiency what it is used for what is causes
Vitamin K is necessary in the liver for synthesis and regulation clotting factors and anticoagulants may not be about to make a clot, decreased coagulation Vit K: dark leafy greens
78
Liver disease | what is causes
Liver disease causes a broad range of hemostasis disorders Don't make clotting factors, Decrease in TPO Defects in coagulation, fibrinolysis, and platelet number and function
79
``` Hemophilia A Hemophilia B what is it how it is caused what is causes ```
Hemophilia A: deficiency in Clotting factor VIII Hemophilia B: deficiency in Clotting factor IX Christmas Disease Transmission of A & B is via recessive X linked inheritance 1/3 of cases occur due to new mutations after birth, not inherited All forms of hemophilia are relatively rare. Cannot make a clot.
80
Disseminated Intravascular Coagulation (DIC) "Death Is Coming"
widespread clotting within vessels (leading to ischemia), activation of clotting factor to breakdown clots leading to possible hemorrhage Complex highly fatal disorder in which clotting and hemorrhage simultaneously occur Endothelial damage is the primary initiator of DIC Most often from sepsis Fibrin degradation product (FDP) and D-dimer levels increase
81
Stem cells
cells with the potential to develop into many different types of cells in the body. They serve as a repair system for the body.
82
Zymogen
-zyme= enzyme; -ogen= inactive protein an inactive protein which is converted into an enzyme when activated by another enzyme