Unit 3 - Formative 7 D3

Front 1

Composition of whole blood

Back 1

Plasma 55%
Buffy Coat (white blood cells/platelets, trapped between plasma and RBC) <1%
Red Blood Cells 45%

Front 2

Hematocrit of an individual w/ anemia

Back 2

10-15%

Front 3

Hematocrit of an individual with polycythemia

Back 3

60-65%

Front 4

Hematocrit

Back 4

Proportion of blood volume occupied by red blood cells

Front 5

Plasma

Back 5

Contains water, proteins, lipids, electrolytes/nonelectrolytes, clotting factors which can be removed if the blood is allowed to clot and the fluid portion is removed (serum)

Front 6

Serum

Back 6

Plasma with clotting factors removed

Front 7

Cation electrolye composition of plasma

Back 7

Extracellular: Na+/Ca
Intracellular: K/Mg

Front 8

Anion electrolye composition of plasma

Back 8

Extracellular: Cl, Hc03
Intracellular: P04, Protein

Front 9

Why is there is a small difference betwen the sodium concentration in the plasma vs interstitial fluid

Back 9

Proteins that are held back primarily in the plasma have a negative charge and attract a small portion of the sodium molecules and retain them in the plasma slightly above what is seen in the interstitial space (Donnan effect)

Different charged substrates unable to pass through the membrane can create an uneven electrical charge

Front 10

What is the glucose concentration in plasma?

Back 10

100 mg/dl

Front 11

What is the normal urea to creatinine ratio in plasma

Back 11

Urea: 15
Creatinine: 1.5

10:1 is the normal ratio, can be altered in some diseases

Front 12

Buffy Coat

Back 12

Contains white blood cells and paltelets
Usually less than 1% of blood

Front 13

What are the dominant type of WBC in the buffy coat?

Back 13

Neutrophils: 62%
Lymphocytes: 30%

Front 14

What is the lifespan of a RBC

Back 14

120 days; this means we must have a mechanism in place to replace blood cells that die of old age or are lost due to a laceration or menstruation

Front 15

Where are erythrocytes derived from?

Back 15

Pluripotent hematopoietic stem cell

Front 16

In an older individual, in what bones does erythrocyte production dominantly take place?

Back 16

Vertebra, sternum, rib

Front 17

In younger individuals, in what bones does erythrocyte productoin dominantly take place

Back 17

Tibia/Femur (shaft of long bones)

Front 18

Erythropoietin

Back 18

Released in response to low tissue oxygenation; stimulates hematopoietic stem cell to increase production of RBC and increase oxygen delivery

Front 19

What is the function of loose bonding of oxygen to iron in hemoglobin?

Back 19

O binds loosely so it can be easily distributed to tissues


CO binds irreversibly to iron; is deadly even in relatively low concentrations

Front 20

Transportation of iron

Back 20

Iron is absorbed from small intestines where it is carried in the plasma by transferin which carries iroin to different tissues and is predominantly bound as ferritin in tissues; allows a constant source of free iron that can move back in forth between tissues and plasma

Front 21

What is the relationship between blood viscotiy and hematocrit

Back 21

Increased hematocrit exponentially increases the viscocity of whole blood

Front 22

Blood Loss Anemia

Back 22

After hemorrhage plasma is replaced more rapidly then erythrocytes

Front 23

Aplastic Anemia

Back 23

Lack of functioning bone marrow

Front 24

Megaloblastic Anemia

Back 24

Lack of vitamin B12, folic acid, or intrinsic factor result in low number of erythrocytes

Front 25

Hemolytic anemia

Back 25

Heredity anemias including sickle cell and erythroblastosis fetalis

Front 26

Secondary Polycythemia

Back 26

Exposure to high altitude results in increased levels of 2,3-BPG, which increases the production of RBCs

Front 27

Polycythemia Vera

Back 27

Genetic aberration in the hemocytoblastic cells that allows the continued production of RBC's even though an adequate number already exist

Front 28

Rule of three

Back 28

RBC = approximately FIVE x 10^6/mm^3
hemoglobin = approximately 15g/dl
HCT = approximately 45%

RBC value x 3 = hemoglobin
hemoglobin x 3 = HCT

Front 29

Red Top Blood Collection Tubes

Back 29

No anticoagulant; used to collect serum for chemistry; some red topped tubes have clot activators; clot time is approximately 30 min

Front 30

Green Top Blood Collection Tubes

Back 30

Contain heparin; heparin helps prevent cell breakdown and thus the release of K+ from RBC (remains as plasma and won't become serum since clot will not form)

Heparin used when you need an accurate potassium level

Front 31

Light Blue Top Blood Collection Tubes

Back 31

Sodium citrate (1 part to 9 parts blood); tube must be completely filled to maintain correct dilution

Front 32

What are the two major products of the pentose phosphate pathway?

Back 32

NADPH and ribose-5-phosphate

Front 33

What is the purpose of the HMP shunt/pentose phosphate pathway?

Back 33

Provide a source of NADPH from an abundantly available glucose-6-phosphateNADPH is required for reductive reactions like glutathione reduction inside RBC);

Front 34

In the pentose phosphate pathway what is the generated NADPH used for?

Back 34

Fatty acid synthesis; glutathione reduction; other rxns

Front 35

In the pentose phosphate pathway, what is the generated ribose 5-phosphate used for?

Back 35

Nucleotide biosynthesis

Front 36

What is the general rule differentiating NADPH and NADH?

Back 36

NADPH: anabolic reactions (cholesterol biosynthesis, fatty acid biosynthesis)
NADH: catabolic reactions (glycolysis, TCA cycle)

Front 37

Gloucose 6 phosphate dehydrogenase deficiency

Back 37

G6P generates NADPH which is necessary to reduce glutathione, which detoxifies free radicals and peroxides; decreased NADPH in RBCs leads to hemolytic anemia due to poor RBC defense against oxidizing agents (fava beans, sulfonamides, primaquine, antiTB drugs)

Front 38

Epidemiology of glucose 6 phosphate dehydrogenase deficiency

Back 38

Most common enzyme deficiency in world; 1/10 african americans carry a mutation in G6PD (associated with resistance to malaria)
Individuals often asyptomatic until provoked by illness or exposure to drugs

Front 39

Function of glutathione

Back 39

Protects cells against oxidative damage

CYSTEINE residues between two glutathione molecules can form DIFULSIDE BONDS and be used as a site of oxidation and reduction

Front 40

When might an individual with glucose-6-phosphate dehydrogenase deficiency run into problems?

Back 40

Whenever there is an increase in reactive oxygen species; caused by medications, infections or FAVA BEANS

Front 41

What is the result of severe oxidative damage in an erythrocyte?

Back 41

Hemolysis

Front 42

Heinz Bodies

Back 42

Oxidized/denatured hemoglobin precipitated within RBC

Front 43

Bite cells

Back 43

Result from the phagocytic removal of Heinz bodies by macrophages

Front 44

Phosphofructokinase enzyme deficiency (glycolysis) clinical presentation

Back 44

Rhabdomyolysis and myoglobinuria, exercise intolerance, increased glycogen storage, hemolytic anemia, hyperuricemia
Classified as a glycogen sotrage disease type VII (similar to McArdles Type V)

Front 45

Pathogenesis of phosphofructokinase enzyme deficiency (glycolysis)

Back 45

Catalyzes F6P -> F16BP which is a regulatory step for glycolysis

no glycolysis -> no ATP -> Na/K ATPase shutdown -> hemolysis
ADP buildup -> increased AMP -> increased uric acid synthesis

3 isoforms of PFK: muscle, liver, platelet (M form is affected, RBC have both M and L form)

Front 46

Pyruvate Kinase Deficiency (glycolysis) clinical presentation

Back 46

Second most common deficiency (after G6PDH)
Hemolytic anemia doesn't usually present till later in life; heterozygote asymptomatic
PK mutations linked to increase malarial resistance

Front 47

Pyrovuate Kinase Pathogenesis (glycolysis)

Back 47

PK catalyzes PEP -> Pyruvate
ATP made in this step
Deficiency -> decreased ATP

Some compensation by because of increase in 2,3-BPG (decreased affinity of Hb for 02)

Front 48

Methemoglobin Reductase (cytochrome B5 reductase) (methemoglobin reductase pathway) clinical presentation

Back 48

Makes people blue; causes anemia

Front 49

Methemoglobin Reductase (cytochrome B5 reductase) (methemoglobin reductase pathway) pathogenesis

Back 49

MeR uses NADH from glycolysis to reduce ironb Fe3+(ferric heme - aka methemoglobin) to Fe2+ (ferrous heme) and ONLY ferrous heme binds oxygen; so knocking out MeR decreases the ability of oxgey binding = hemolytic anemia

Deficiency from MeR deficiency, genetically acquired mutant Hb allele or drugs
Deficiency -> decreased oxygen carrying capacity

Front 50

2,3-Biphosphoglycerate Mutase (Rapoport-Luberin Shunt) clinical presentation

Back 50

Deficiency rare; causes anemia

Front 51

2,3-Biphosphoglycerate Mutase (Rapoport-Luberin Shunt) pathogenesis

Back 51

BPGM catalyzes 1,3-BPG -> 2,3-BPG

2,3 - BPG is an allosteric effector of Hb (decreased Hb affinity for 02 - right shifts sat curve)

Front 52

Difference between ferric and ferrous state of hemoglobin?

Back 52

Ferric: methemoglobin, can't bind oxygen

Ferrous: Can bind oxygen

The reaction between the two is catalyzed by methemoglobin reductase (MeR), also called cytochrome b5 reductase

Front 53

What two things can you give to treat methemoglobinemia?

Back 53

Methylene blue and ascorbic acid, which function as reducing agents to reduce ferric (Fe3+) to ferrous (Fe2+)

Front 54

Methemoglobinemia

Back 54

A deficiency in methemoglobin reductase (most severe form, present at birth)

Front 55

What is the function of 2,3-BPG?

Back 55

Decreases the affinity of hemoglobin for oxygen so it can be delivered to tissue sites with an increase oxygen requirement (high altitude, congestive heart failure)

Shifts Hb-oxygen saturatoin curve to the right