Anemia - Key Things To Remember

Front 1

What is erythropoiesis?

Back 1

the production of RBCs

Front 2

What is erythropoietin?

Back 2

a hormone
- secreted by the kidneys
- increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues.

Front 3

What is CBC?

Back 3

Complete Blood Count - count of all the cells in the bloodstream

Front 4

What is Hgb?

Back 4

Hemoglobin
- the amount of RBCs in a given WEIGHT of blood

Front 5

What is Hct?

Back 5

Hematocrit
- the percentage of RBCs in a given volume of blood

Front 6

What is MCV?

Back 6

Mean Corpuscular Volume
- cell size (cytic)
ex. normocytic, macrocytic, or microcytic

Front 7

What is MCHC?

Back 7

Mean Corpuscular Hemoglobin Concentration
- amount of hemoglobin in each RBC (chromic)

Front 8

What does normochromic mean?

Back 8

normal volume to hgb ratio

Front 9

What is anemia?

Back 9

a reduction in the total number of circulating erythrocytes or RBCs
and/or
a decrease in the quality or quantity of hub

Front 10

What causes anemia?

Back 10

1. ALTERED PRODUCTION of RBCs
2. blood LOSS
3. increased DESTRUCTION of RBCs
4. a combination of any or all 3

Front 11

What are the different types of anemia?

Back 11

1. iron deficiency anemia
2. pernicious (vitamin B12) anemia
3. folate deficiency anemia
4. post-hemorrhagic anemia
5. others (aplastic anemia, hemolytic anemia, and anemia of chronic disease)

Front 12

How does decreased hemoglobin lead to decreased ATP?

Back 12

decreased hgb --> decreased O2 carrying capacity --> decreased O2 at tissues --> decreased ATP (causing negative effects & compensation)

Front 13

What are the negative effects of decreased ATP?

Back 13

- decreased energy (overall) ex. fatigue
- decreased energy and function in the cell (ex. impaired wound healing)

Front 14

What compensation occurs as a result of decreased ATP?

Back 14

decreased ATP activates the HPA axis causing:
- increased RR - catecholamines stimulate respiratory control center (medulla) to increase RR
- increased HR - epinephrine stimulates SA node to increase firing rate --> increases HR
- increased SV - catacholamines cause dilation of the skeletal muscle vasculature and vasoconstriction of peripheral smooth muscle which shunts blood to the core and increases SV
- VSM constriction - catacholamines cause peripheral smooth muscle contraction which shunts blood to core, leaving the periphery pale and cool

Front 15

What are common signs and symptoms of all types of anemia?

Back 15

HPA effects:
- breathlessness
- pale/cool
- increased HR

Decreased ATP effects:
- loss of tissues function
- fatigue/lethargy
- dizziness
- fainting

Front 16

What causes iron deficiency anemia?

Back 16

1. blood loss: chronic small amounts (ex. menstruation, ulcers, bowel cancer, NSAID [non-steroidal anti-inflammatory disease]
2. decreased absorption of iron
3. low dietary intake

Front 17

Where is iron stored?

Back 17

iron is stored in the heme in hemoglobin
- also stored in bone marrow, liver and spleen

Front 18

What are serum ferritin levels?

Back 18

provides an indicator of iron stores in the body

Front 19

How does iron deficiency anemia develop?

Back 19

iron stores are depleted --> insufficient iron in the marrow for hgb synthesis --> altered RBC development --> hemoglobin deficient cells replace circulating normal RBCs --> hypochromic and microcytic cells

Front 20

What are Hypochromic cells?

Back 20

cells that have less hemoglobin per cell (low MCHC)

Front 21

What are microcytic cells?

Back 21

cells that are small in size
- they reduce their volume to maintain a normal volume to hgb ratio (Low MCV)

Front 22

If there are small RBCs circulating the bloodstream, how will that affect hgb and hematocrit levels?

Back 22

fewer formed, so low hgb and hct

Front 23

What are S&S of iron deficiency anemia?

Back 23

- fatigue
- weakness
- fainting
- pale/cool skin
- SOB

- specific:
- no iron for cell maintenance/repair --> brittle, thin and concave fingernails, sore, red tongue, stomatitis, esp. of corners of mouth

Front 24

How is iron deficiency diagnosed?

Back 24

- combination of:
- clinical manifestations
- blood work: CBC & serum ferritin levels

Front 25

How is iron deficiency treated?

Back 25

- stop blood loss
- dietary corrections (ex. red meats, legumes, iron fortified foods, etc.)
- iron replacement - higher amounts than multivitamin
- blood transfusions - depends on circumstances, benefit/risk ratio
- monitor - lab values & signs and symptoms
***just because hgb returns to normal does not mean that Fe deficiency anemia is cured!

Front 26

What causes vitamin B12 deficiency?

Back 26

- decreased dietary vitamin B12 or folate intake
- malabsorption of vitamin B12 [intrinsic factor is needed for B12 absorption; may be a congenital disease or atrophy of gastric mucosa]
- gastrectomy - surgical removal of a part or the whole of the stomach.
- small bowel disease or loss (ex. Chron's)

Front 27

How does vitamin B12/folate deficiency anemia develop?

Back 27

- both deficiencies interfere with DNA synthesis
- vitamin B12 converts folic acid to an active form --> active folic acid is a key component of nucleotides that make up DNA --> therefore, cell division is disrupted

Front 28

What is the pathway of a developing RBC?

Back 28

uncommitted stem cell --> [erythropoietin - hormone converts stem cell to committed proerythroblast --> [DNA synthesis occurs] --> normoblast cell is formed (nucleus shrinks and is reabsorbed) & hemoglobin is formed during the normoblast stage --> converted to reticulocyte (cell leaves marrow and enters bloodstream) --> converted to erythrocyte (cell achieves final size & shape - hemoglobin synthesis ceases)

Front 29

What is the result of Vitamin B12/folate deficiency?

Back 29

- macrocytic (large, abnormally shaped erythrocytes) - high MCV
- normochromic cells - hgb content of cells is normal (they may be hyperchromic or hypochromic) - MCHC usually normal or high
***when in circulation, these cells are defective and die prematurely - so low hct and low hgb [even though they are larger, they will not survive, causing low hgb)

Front 30

How does vitamin B12 deficiency affect MCHC?

Back 30

vitamin B12 deficiency does not affect MCHC

Front 31

What are the S&S of vitamin B12 deficiency?

Back 31

- fatigue
- weakness
- pale/cool
- confusion

specific S&S:
- parasthesia (numbness/tingling) of feet and fingers [b/c lack of normal myelin maintenance which surrounds nerves], difficulty walking, death

Front 32

What are the S&S of folate deficiency?

Back 32

same as B12 (EXCEPT)
- NO neurological symptoms R/T demyelination

Front 33

How is vitamin B12/folate deficiency diagnosed?

Back 33

- clinical manifestations
- blood work:
- CBC
- serum B12
- serum folate

Front 34

How is vitamin B12/folate deficiency treated?

Back 34

- dietary corrections
- oral supplementation
- SQ/IM injections of B12/folate MONTHLY

Front 35

What is post-hemorrhagic anemia?

Back 35

- loss of large amounts of blood (ex. hemorrhage)

Front 36

What are the signs and symptoms of post-hemorrhagic anemia?

Back 36

- same as hypovolemia, hypoxia and anemia

Front 37

What are the lab values of post-hemorrhagic anemia?

Back 37

hgb - low
hct - low
MCV - normocytic
MCHC - normochromic

Front 38

How is post-hemorrhagic anemia treated?

Back 38

- replace fluids
- blood transfusion
- give iron

Front 39

What are some other types of anemia?

Back 39

1. hemolytic - RBCs lysed or destroyed
2. Aplastic - stem cells destroyed (ex. leukemia)
3. Anemia of chronic disease (ex. altered iron recycling)

Front 40

What questions should always be answered regarding anemia?

Back 40

1. where does the defect occur?
2. what is the result to cell size and shape?
3. what is the result to total hgb & # of RBCs?