HEMATOLOGY - alterations in erythrocyte function: anemia

Question 1

what are erythrocytes? what do they do? what is their lifespan?

Answer 1

erythrocytes = RBC
- tissue oxygenation
- 100-120 days

Question 2

what is erythropoiesis? what are the nutritional requirements? what happens when nutritional requirements lack?

Answer 2

the PROCESS of making RBCs – if any of theses lack the RBC production slows down –> ANEMIA
- protein = amino acids
- cobalamin = vit b12
- folate = folic acid
- vit b6 = pyridoxine
- vit b2 = riboflavin
- vit c = ascorbic acid
- vit e
- pantothenic acid
- niacin
- iron
- copper

Question 3

what is hemoglobin (Hgb)?

Answer 3

the oxygen carrying part of the RBC (erythrocyte)
- takes up O2 in the lungs –> exchanges for Co2 in tissues

Question 4

what is Hematocrit (Hct)?

Answer 4

a measure of packed cell volume of RBCs expressed as a percentage of total volume

Question 5

how are erythrocytes made?

Answer 5

erythropoietin (hormone made by kidneys) stimulates erythrocyte production –> erythrocytes come from hematopoietic stem cells of myeloid tissue (red bone marrow)
- WBCs & platelets also come from myeloid tissue

Question 6

how do you apply erythrocyte production to tissue hypoxia? what about normal oxygen levels?

Answer 6

tissue hypoxia –> stimulates kidney –> increase erythropoietin production –> more RBCs

if there are normal O2 levels –> decreased erythropoietin production

Question 7

what is anemia?

Answer 7

• a reduction in the total number of erythrocytes in blood
  OR
• decrease in quality/quantity of hemoglobin

Question 8

what kinds of labs would we see in anemia?

Answer 8

• low RBCs
• low Hgb
• low Hct

Question 9

what are the normal range of RBCs in an average adult?

Answer 9

• female: 4.2-5.4 x 10^6 / uL
• male: 4.7-6.1 x 10^6/uL

Question 10

what is the normal range of Hgb of a RBC in an average adult?

Answer 10

-female: 12-16 g/dL
- male: 14-18 g/dL

Question 11

what is the normal range of Hct in an average adult?

Answer 11

• female: 37-47%
• male: 42-52%

Question 12

what is the general rule of thumb when it comes to Hgb & Hct?

Answer 12

Hct is 3x more than Hgb
- Hgb of 10 = Hct of 30

Question 13

why do people rely of Hgb more when it comes to knowing what kind of treatment to give?

Answer 13

there are factors like hydration & RBC morphology that change Hct levels

Question 14

what are the 3 main causes of anemia?

Answer 14

• decreased RBC production
• blood loss
• increase RBC destruction

Question 15

how do we classify anemia?

Answer 15

“-cytic” = cell size
“-chromic” = hemoglobin content

Question 16

what are RBC indices? what are the different types of indices?

Answer 16

they are different tests to indicate RBC size & Hgb content
- mean corpuscular volume (MCV)
- mean corpuscular hemoglobin (MCH)

Question 17

what is mean corpuscular volume (MCV)? normal range? elevated? low?

Answer 17

the RBC indice in terms of SIZE
- the average volume of a single RBC
- normal range: 80-95 fL
- normal MCV = normoCYTIC
- elevated MCV = macroCYTIC
- low MCV = microCYTIC

Question 18

what is mean corpuscular hemoglobin? normal range? elevated? low?

Answer 18

the RBC indice in terms of hemoglobin content
- the average amount of Hgb in a RBC
- normal range: 27-31 pg
- normal MCH = normoCHROMIC
- low MCH = hypoCHROMIC
- elevated MCH = X

Question 19

why is there no label for elevated MCH?

Answer 19

bc hgb can NOT be macro/hyper chromic since there is a MAX of hgb that can FIT in to a RBC
- max = 37 g/deciliter
- if MCH is high there are other reasons: shape, clumps & hemolyzed blood specimen

Question 20

what is the main alteration of anemia? what are the symptoms based on? when would you see these symptoms?

Answer 20

reduced oxygen carrying capacity of blood –> tissue hypoxia
- severity
- acute or chronic
- body’s ability to compensate
- etiology
- comorbidities in CV & respiratory

usually see these symptoms when hgb is < 7

Question 21

what is the pathophysiology of how clinical manifestations pop up starting with anemia?

Answer 21

anemia –> hypoxemia –> tissue hypoxia –> 3 things:
1. ischemia –> pain in muscles –> pain in LE w/ activities
2. weakness + fatigue and pallor of skin, mucus, & membranes
3.
- changes in resp status (body is trying to increase o2 in tissues) –> increase RR & exertional dyspnea
- CNS effects: dizzy, faint, & lethargy (brain sensitive to decr. O2)
- fatty changes in liver (regulated lipid metabolism)

Question 22

what are the cardiac compensatory mechanisms for anemia?

Answer 22

cardiac compensatory mechs are for initial compensation – if they are prolonged –> heart failure

• movement of interstitial fluid into blood –> increases plasma vol –> helps maintain BV BUT viscosity (thickness) of blood decreases –> thinner blood –> THREE THINGS
  1. increased blood flow turbulence –> hyperdynamic circulatory state –> murmurs
  2. increased HR & SV
  3. increase myocardial oxygen demand –> if not met can lead to angina or chest pain
  ALL THREE THINGS LEAD TO – cardiac dilation & heart valve insufficiency if underlying problem is not corrected
• vasodilation of arterioles, capillaries & venules –> increase BF & peripheral BF –> increase HR & SV bc body is trying to maintain oxygenation WHILE preventing cardiopulmonary congestion DUE TO increased BF

Question 23

what are the renal compensatory mechanisms for anemia?

Answer 23

• RAAS activation –> increase sodium & water retention
• increase of bisphosphoglycerate (BPG, decreases hgb affinity for O2 –> allows O2 to be released in tissues) –> helps hgb release more oxygen to tissues

Question 24

what are the rules / thresholds when it comes to transfusion of blood?

Answer 24

• symptomatic, < 10 g/dL –> considering transfusion of packed RBCs
• hgb of < 7-8 g/dL –> receive transfusion (symptoms at risk)
• if actively bleeding –> decision based on V/S, pace of bleed, & ability to stop bleeding

Question 25

what are the different types of anemia?

Answer 25

• macrocytic-normochromic
• microcytic-hypochromic
• normocytic-normochromic

Question 26

what is macrocytic-normochromic anemia? what are its clinical name? what causes it? what is it characterized by?

Answer 26

large cells, normal hgb concentration = pernicious anemia (vit b12 anemia) & folic acid deficiency anemia
- decreased dietary intake
- lack of intrinsic factor
- long term alcohol use disorder

characterized by ERYPTOSIS (he suicidal death of erythrocytes) –> premature death
- bc cells are v large –> gets stuck in capillaries –> die prematurely

Question 27

why is lack of intrinsic factor a cause of macrocytic-normochromic anemia?

Answer 27

it is specific to pernicious anemia (vit b12 anemia)
- stomach releases intrinsic factor
- intrinsic factor helps B12 be absorbed in small intestine

if can’t be absorbed, lack of nutritional need for RBC

Question 28

why is long term alcohol use disorder a cause for macrocytic-normochromic anemia?

Answer 28

the direct toxins effect on bone marrow –> secondary anemia bc of poor nutritional intake

Question 29

what are the clinical manifestations of macrocytic-normochromic anemia?

Answer 29

• glossitis: sore, smooth, beefy red tongue
• sallow skin: lemon color that is a combination for pallor + jaundice color
• nerve demyelination from vit b12 anemia: paresthesias (feet & fingers) & difficulty walking

Question 30

what is the major difference between folic acid deficiency & pernicious anemia (vit b12)

Answer 30

pernicious anemia has IRREVERSIBLE neurologic manifestations bc of nerve demyelination

Question 31

how do we diagnose macrocytic-normochromic anemia?

Answer 31

a CBC shows elevated MCV & normal MCH
- decreased plasma B12 levels
- decreased folic acid levels
- treatments depends on cause

Question 32

how do we treat pernicious anemia (vit b12)?

Answer 32

we GIVE vitamin b12 (also to prevent neurologic effects)
- PO most common
- parenteral & intranasal used if pt has impaired GI absorption

if cause of deficiency is permanent, treatment is lifelong
- folic acid may be used bc it can reverse hematologic effects but NOT neurologic effects

Question 33

how do we treat folic acid anemia? what happens if we give folic acid for a long time?

Answer 33

we GIVE folic acid
- PO is most common
- parenteral used if pt has impaired GI absorption

long term –> increase risk of colorectal cancer & prostate cancer
- only use as long as necessary

Question 34

what is microcytic-hypochromic anemia? what is its clinical name? what are the causes?

Answer 34

small cells, low hemoglobin concentration = iron deficiency anemia (lack of iron FOR hgb production & low hgb LVL)
- dietary deficiency
- impaired absorption
- increased requirement of iron (seen w women w heavy menses)
- chronic blood loss (common in older adults): iron is storing faster than being replaced & chronic clow GI bleed

Question 35

what are clinical manifestations of microcytic-hypochromic anemia (iron deficiency)

Answer 35

• pale earlobes, palms, & conjunctivae
• koilonychia: spoon shaped fingernails
• cheilosis: scales & fissures of mouth
• stomatitis: inflam of mouth
• painful ulcerations of buccal mucosa
• glossitis

Question 36

how do we diagnose iron deficiency anemia? what is ferritin?

Answer 36

CBC shows low MCV & low MCH
- decreased iron serum levels
- decreased ferritin serum levels (major iron storage protein)

Question 37

how do we treat microcytic-hypochromic anemia (iron deficiency)?

Answer 37

main treatment: treat underlying cause

iron supplementation
- PO FERROUS SULFATE most common
- IV IRON DEXTRAN most common IV prep

Question 38

what are the adverse effects with ORAL FERROUS SULFATE? when is absorption best? when should you take it to lower GI distress?

Answer 38

primarily GI related
- nausea
- pyrosis: heartburn
- bloating
- constipation
- black stool: NOT DANGEROUS, educate on this
- liquid oral Ferrous Sulfate –> staining of teeth –> dilute with other liquid, drink w straw & rinse mouth after administration

• absorption is best = taken b/w meals
• GI distress lowest = taken WITH meals
  BOTH ARE SAFE, just monitor side effects

Question 39

what are the side effects of IV IRON DEXTRAN? why do some people use this instead of FERROUS SULFATE?

Answer 39

some people use IV IRON DEXTRAN bc they can not take it orally

side effects: mainly from the dextran part
- anaphylaxis –> test dose
- hypotension
- headache
- fever
- urticaria (hives)
- arthralgia (joint pain)

Question 40

what is normocytic-normochromic anemia? what’s its clinical name? what is the cause?

Answer 40

normal size cells, normal hemoglobin concentration = anemia of chronic disease (ACD) or anemia of inflammation (AI)
- pts with chronic systemic disease or inflammation –> decreased erythropoiesis & impaired iron utilization

examples:
- HIV
- bacterial, fungal parasitic
- cancers
- autoimmune disease: RA & Lupus
- chronic kidney disease
- chronic rejection of solid organ transplant

Question 41

what are the clinical manifestations of normocytic-normochromic (ACD or AI) anemia?

Answer 41

usually mild to moderate
- similar to iron deficiency anemia (microcytic-hypochromic)

Question 42

how do we diagnose normocytic-normochromic anemia (ACD or AI)?

Answer 42

an early CBC will show normal MCV & normal MCH

a later CBC will show low MCV & low MCH

Question 43

how do we treat normocytic-normochromic anemia?

Answer 43

• treating underlying disorder
• erythropoietic growth factors
• transfusion of packed RBCs

Question 44

what are the different medications of erythropoietic growth factors? what are the routes?

Answer 44

can be thru IV & subq
- EPOETIN ALFA (Erythropoietin)
- DARBEPOETIN ALFA (Erythropoietin, long acting)

Question 45

what does EPOETIN ALFA & DARBEPOETIN ALFA do? when should you stop giving them?

Answer 45

they stimulate erythrocyte production
- reduced or hel when Hgb is 11 g/dL
- use the lowest dose possible so there is a decr need for transfusions

Question 46

what are the risks of EPOETIN ALFA & DARBEPOETIN ALFA?

Answer 46

increase risk of
- stroke
- heart failure (HF)
- blood clots
- myocardial infarction (MI)
- death

for pts w cancer – it may shorten time of tumor progression (aka tumor grows faster) –> reducing survival

Question 47

when do we see initial effects of EPOETIN ALFA & DARBEPOETIN ALFA? when will they reach its max?

Answer 47

initial effects seen within 1-2 weeks
- Hgb will reach max at 2-3 months

Question 48

what is posthemorrhagic anemia?

Answer 48

a type of normocytic-normochromic anemia that is due to acute blood loss
- trauma is the main cause
- depends of rate of bleeding –> CV collapse, shock & death
- hemostasis = ability to stop flow of bleed –> reduces –> coagulopathy (can not make clots)

Question 49

how do we treat posthemorrhagic anemia (normocytic-normochromic anemia)?

Answer 49

• treat underlying cause
• using products to restore blood volume
• massive transfusion of blood products

Question 50

what are the different ways we can restore blood volume with posthemorrhagic anemia?

Answer 50

crystalloid IV fluids:
- 0.9% SODIUM CHLORIDE
- LACTATED RINGERS

plasma volume expanders:
- DEXTRAN
- albumin

fresh frozen plasma (fluid part of blood, has clotting factors)