Cvt - Path Exam 2 Alterations In O2 Transport

Front 1

What is blood made of?

Back 1

45% cells
55% plasma

Front 2

How much blood is in the body?

Back 2

5-6 liters

Front 3

pH norm:

Back 3

7.35-7.45 (avg 7.4)
1/10th in changes

Front 4

T/F - Blood is made up of organic and inorganic components.

Back 4

True!

Front 5

Which is more accurate - Hgb or HCT?

Back 5

HCT

Front 6

What are the cellular components of blood?

Back 6

1. erythrocytes
2. leukocytes
3. platelets

Front 7

erythrocytes:

Back 7

=RBC
-transport O2 and CO2
-buffer blood pH
-Hgb carries O2
-live 80-120 days

Front 8

Why do RBC's only live about 100 days?

Back 8

no nucleus, cytoplasm or cell membrane

Front 9

leukocytes:

Back 9

=WBC
-phagocytosis of microorganisms
-5-10,000 normally
-live months to years

Front 10

In adults, where are most RBCs formed?

Back 10

iliac crest (most accessible) and sternum

Front 11

hematopoiesis:

Back 11

-development of all blood cells
-marrow converts from yellow (fatty) bone to red marrow when necessary

Front 12

What is bone marrow conversion stimulated by?

Back 12

erythropoietin

Front 13

What is needed for the production of RBCs?

Back 13

1. folic acid (forms RBCs)
2. Fe
3. B12 (division of RBCs)

Front 14

Where is Fe absorbed in the body?

Back 14

in the small intestines where it is either stored or used

Front 15

Which is more soluble - O2 or CO2?

Back 15

CO2 is 20 times more soluble than O2.

Front 16

Aplastic anemia:

Back 16

-worst type of anemia
-causes are chloramphenicol, benzene and radiation
-toxic, radiologic, or immunologic
-up to 75% morbidity
-best prognosis is from transplants

Front 17

What are some examples of aplastic anemia?

Back 17

leukopenia and thrombocytopenia

Front 18

What are the treatments for aplastic anemia?

Back 18

transfusions, bone marrow transplants and drugs to stimulate marrow

Front 19

4 diseases caused from decreased RBC production:

Back 19

1. aplastic anemia
2. anemia from CRF
3. vitamin B12 (folate) deficiency
4. iron deficiency anemia

Front 20

anemia from CRF:

Back 20

-decrease in erythropoietin production

Front 21

Name 3 causes for anemia from CRF.

Back 21

decrease in exccretion causing hemolysis, depression of bone marrow and blood loss in urine

Front 22

vitamin B12 deficiency:

Back 22

-aka Folate deficiency
-aka pernicious anemia
-lack of intrinsic factor and B12 is not absorbed
-an autoimmune disease
-can cause possible peripheral nerve degeneration or in spinal cord
-can cause achlorhydria

Front 23

achlorhydria:

Back 23

lack of sufficient gastric juice in the stomach

Front 24

iron deficiency anemia:

Back 24

-most common nutritional deficiency in the world
-very little lost except from bleeding
-can cause hypochromic and microcytic effects
-majority of pts are asymptomatic

Front 25

What is the treatment for iron deficiency anemia?

Back 25

Fe

Front 26

What is the treatment for folate deficiency?

Back 26

B12

Front 27

Name the anemias related to inherited disorders.

Back 27

1. thalassemia
2. sickle cell anemia
3. spherocytosis

Front 28

thalassemia:

Back 28

-anemia where RBCs produced are abnormal and prone to destruction
-in Asians and Mediterranean descent (familial in nature)
-skeletal deformities and organomegaly endocrine disorders
-Tx: blood tranfusions, drugs, splenectomy

Front 29

splenectomy:

Back 29

-surgery to remove all or part of the spleen
-this increases RBCs bc the destroying capacity has been destroyed

Front 30

sickle cell anemia:

Back 30

-prominent in the black race
-aka HbS where RBC decrease stability and solubility
-homozygous (HbS only) or heterozygous (HbA>HbS)

Front 31

What are the signs and symptoms of sickle cell anemia?

Back 31

1. vascular occlusion
2. thrombosis and emboli
3. acute episodes of "crisis" (hemolytic or vascular)

Front 32

spherocytosis:

Back 32

-abnormal membranes
-anemia manifestations
-splenectomy usually curative

Front 33

What are the 2 general causes of anemias?

Back 33

1. decreased production of RBCs
2. increased destruction of RBCs

Front 34

Types of transfusion therapy:

Back 34

1. whole blood
2. packed RBCs
3. fresh, frozen plasma (for low proteins)
4. pheresis

Front 35

pheresis:

Back 35

-transfusion of components of blood; for example, platelets, RBCs

Front 36

polycythemia:

Back 36

overproduction of RBCs
cause is unknown
increases blood viscosity causing occlusive vascular lesions, bleeding and florid expression
-muelosuppressive therapy (radioisotope)
-prognosis: 7-15 yrs with tx

Front 37

Types of polycythemia:

Back 37

1. polycythemia
2. secondary polycythemia
3. relative polycythemia

Front 38

secondary polycythemia:

Back 38

-increased RBCs secondary to tissue hypoxia
-inappropriate erythropoietin, androgens or steroid
-tx: treat underlying process

Front 39

relative polycythemia:

Back 39

anemia due to dehydration or stress related issues

Front 40

Which transfusion therapy is no longer common?

Back 40

whole blood transfusion

Front 41

What is considered acute blood loss?

Back 41

-20% loss (symptoms occur with exercise)
-40% loss (causes shock)
-blood replacement necessary

Front 42

What is a common treatment for polycythemia?

Back 42

phlebotomy (removing blood to reduce blood volume)

Front 43

Describe the hemoglobin synthesis:

Back 43

1. Fe is absorbed in the duodenum (jejunum)
2. RBC are formed
3. RBCs are stored as ferritin or synthesized heme

Front 44

hemolytic disease of newborn:

Back 44

-fetal RBCs cross the placenta and maternal antibodies destroy the fetal RBCs
-causes maternal ABO compatability or Rh factor
-causes anemia, reticulocytosis, jaundice
-CV neural changes and organomegaly

Front 45

hematopoesis:

Back 45

-development of all blood cells
-marrow converts from yeelow (fatty) bone to red when necessary
-marrow conversion is stimulated by erythropoetin

Front 46

Describe RBC production process:

Back 46

1. decrease in Hgb (means a decrease in O2 renal tension)
2. erythropoetin is stimulated by kidneys
3. eryth stimulates RBC production

Front 47

Describe RBC destruction process:

Back 47

1. heme converts to bilirubin
2. attaches to plasma proteins for transport
3. removed from blood by liver
4. excreted in bile
5. moves to small intestines
6. converts to urobilinogen
7. urob is either absorbed or excreted in feces

Front 48

RBC destruction:

Back 48

-digested by macrophages
-80-90% occurs in spleen and liver
-Fe breaks down, is used, released and stored
-bilirubin degradation of heme

Front 49

How much Hgb transports oxygen?

Back 49

97%

Front 50

Partial pressure of O2:

Back 50

-measurement of O2 in the blood
-high in the lungs where O2 binds easily
-low in the tissues where O2 is released
-80-100 in the arteries and 35-40 in the veins

Front 51

CO2 transport process:

Back 51

1. gas is dissolved in the blood as HCO3 ion
2. combines with Hgb

Front 52

reticulocytes:

Back 52

immature red blood cells

Front 53

Where are most plasma proteins found?

Back 53

in the liver

Front 54

Functions of plasma proteins:

Back 54

1. regulates blood volume
2. regulates fluid balance
3. contributes to blood viscosity for maintaining BP

Front 55

Types of plasma proteins:

Back 55

1. albumin
2. globulin
3. fibrinogen
4. misc-CHO, fats, amino acids, glucose, cholesterol, electrolytes

Front 56

What does globulin transport?

Back 56

1. bilirubin, lipids and steroids
2. Fe and Cu
3. antibody molecules

Front 57

Effects of sickle cell anemia:

Back 57

-a type of severe anemia
-increase of bilirubin form excessive breakdown of RBCs
-causes hemoglobinuria