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Patho: pulmonary; cardi; hemo; GI; Urinary > Hematology > Flashcards

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
Q

Erythrocytes

A

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.

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26
Q

Hemoglobin
function
how many per RBC
Function of the Two pairs of protein subunits (globins)

A

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

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27
Q

Nutritional requirements for hemoglobin synthesis

deficiency can lead to what?

A

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)

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28
Q

Destruction of Aged RBCs
who does the destroying
where is it done (primary and secondary)

A

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

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29
Q

when Porphyrin (heme) are broken down, what happens

A

Porphyrin is reduced to bilirubin (pigmented- yellow/green wast from the breakdown of heme), transported to the liver, and secreted in the bile

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30
Q

Leukopoeisis: Leukocytes and Agranulocytes
where do each come from
when are they released?

A

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

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31
Q

Thrombopoeisis

A

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.

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32
Q

Endomitosis:

A

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)

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33
Q

Hemostasis means:

A

the arrest of bleeding by formation of blood clots at sites of vascular injury.

34
Q

Hemostasis requires (5):

A 
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
Q

Hemostasis: Result of Vascular Spasm/Vasoconstriction in response to injury

A

Spasm induces vasoconstriction that inhibits amount of blood flow through the damaged area and blood loss

36
Q

Plateplet plug Process (5)

A

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
Q

the 4 most important proteins that make up the Common Pathway of Coagulation and how they effect each other

A

Factors X and V activate prothrombin into thrombin. Thrombin then converts fibrinogen into fibrin, which becomes a fibrin clot.

38
Q

Clot retraction
what it is
what facilitates this
end result

A

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
Q 
Lysis of blood clots = 
Fibrinolytic system (3)
A

(Fibrinolysis)

Plasminogen and plasmin breakdown)
Fibrin degradation products
D-dimers (bi-product)

40
Q

Hematology Evaluation (testing) (3)

A 
bone marrow function
Blood tests (main way to test for hemo. issues)
Hematocrit: ratio of RBC to overall volume
41
Q

-cytosis=
Erythrocytosis
Leukocytosis
Thrombocytosis

-cytopenia (-penia)=
erythrocytopeniaa
leukocytopenia
thrombocytopeni

A

(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
Q

What is Anemia?

A

Low RBCs

43
Q

Anemia classifications based on Morphology and Hemoglobin concentrations
-CYTIC/ -CHROMIC

A

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
Q

Anemia: Anisocytosis vs Poikilocytosis

A

Red cells are present in various sizes (rare)

Red cells are present in various shapes
Describing sickle cell

45
Q

Anemia:
Physiologic manifestations

Classic anemia symptoms

A

Physiologic s/s: Reduced oxygen-carrying capacity

Symptoms: Fatigue, weakness, dyspnea (SOB, turning up res. response), and pallor (pale)

46
Q

What breaks down a clot

A

Plasmin

47
Q

What is the bi-product of platelet break down?

A

D-dimer

48
Q

Macrocytic-Normochromic Anemias (3)

what they are

A

Pernicious, megaloblastic, folate deficiency

The cell is too big but have an abundance of hemoglobin

49
Q 
Macrocytic-Normochromic: Pernicious anemia
cause
Results in
Symptoms 
Treatment
A

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
Q

Macrocytic-Normochromic: megaloblastic anemias
cause
Characterized by

A

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
Q

Macrocytic-Normochromic: Folate deficiency anemia
cause
Symptoms
Treatment

A

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
Q

Microcytic-Hypochromic Anemias (3)

what it is

A

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
Q

Microcytic-Hypochromic: Iron deficiency

symptoms

A

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
Q

Koilonychia

A

Brittle, thin, coarsely ridged, and spoon-shaped nails. Caused by iron deficiency

55
Q

Microcytic-Hypochromic: Sideroblastic anemia
cause
Characterized by

A

Altered mitochondrial metabolism causing ineffective iron uptake and resulting in dysfunctional hemoglobin synthesis

Ringed sideroblasts within the bone marrow are diagnostic

56
Q

Ringed sideroblasts

A

Sideroblasts are erythroblasts that contain iron granules that have not been synthesized into hemoglobin

57
Q

Microcytic-Hypochromic: Thalassemia
what is it
cause
Characterized by

A

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
Q

Normocytic-Normochromic (5)

what it is

A

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
Q

Normocytic-Normochromic: Aplastic

A

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
Q

Normocytic-Normochromic: Posthemorrhagic

A

Acute blood loss (probably due to trauma)

61
Q

Normocytic-Normochromic: Hemolytic

A

Over destruction of red blood cells: due to spleen enlargement.

Autoimmune hemolytic anemias (eg: lupus)

Jaundice: wast of bilirubin from breakdown of RBC

62
Q

Normocytic-Normochromic: Sickle cell

A 
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
Q

Normocytic-Normochromic: chronic inflammation

A

Mild to moderate anemia seen in:

AIDS, rheumatoid arthritis, lupus erythematosus, hepatitis, renal failure, and malignancies

64
Q

Polycythemia

A

Too many red blood cells

65
Q

Relative polycythemia

A

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
Q

Absolute polycythemia

cause

A

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
Q

Leukocytosis

A

Leukocytosis is a normal protective physiologic response to stressors

68
Q

Leukopenia

A

Leukopenia is not normal and not beneficial

A low white count predisposes a patient to infections

69
Q

Infectious Mononucleosis (mono)

A

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
Q

Leukemia

A

Cancers of excessive accumulation of leukemic cells in bone marrow

71
Q

Lymphocytic (lymphoblastic)

Myelogenous

Acute leukemia (early maturation)

Chronic leukemia (late maturation)

A

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
Q

Lymphadenopathy
Local lymphadenopathy
General lymphadenopathy

A

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
Q

Lymphomas

Two major categories: Hodgkin lymphoma, Non-Hodgkin lymphomas

A

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
Q

Burkitt lymphoma

A

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
Q

Thrombocytopenia

What can it cuase

A

Platelet count <150,000/mm3

1) hemorrhage from minor trauma
2) spontaneous bleeding
3) severe bleeding (spontaneous bleeding, potentially fatal)

76
Q

von Willebrand factor deficiency:

what is causes

A

used to adhere clot, cause increased bleeding risk

77
Q

Vitamin K deficiency
what it is used for
what is causes

A

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
Q

Liver disease

what is causes

A

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
Q 
Hemophilia A
Hemophilia B
what is it
how it is caused
what is causes
A

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
Q

Disseminated Intravascular Coagulation (DIC) “Death Is Coming”

A

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
Q

Stem cells

A

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
Q

Zymogen

A

-zyme= enzyme; -ogen= inactive protein

an inactive protein which is converted into an enzyme when activated by another enzyme

Patho: pulmonary; cardi; hemo; GI; Urinary (10 decks)

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