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nurs 366: pathopharm ii > HEMATOLOGY - alterations in erythrocyte function: anemia > Flashcards

HEMATOLOGY - alterations in erythrocyte function: anemia Flashcards

EXAM 2 content

1
Q

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

A

erythrocytes = RBC
- tissue oxygenation
- 100-120 days

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2
Q

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

A

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

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3
Q

what is hemoglobin (Hgb)?

A

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

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4
Q

what is Hematocrit (Hct)?

A

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

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5
Q

how are erythrocytes made?

A

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

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6
Q

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

A

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

if there are normal O2 levels –> decreased erythropoietin production

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7
Q

what is anemia?

A
  • a reduction in the total number of erythrocytes in blood
    OR
  • decrease in quality/quantity of hemoglobin
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8
Q

what kinds of labs would we see in anemia?

A
  • low RBCs
  • low Hgb
  • low Hct
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9
Q

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

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

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

A

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

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11
Q

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

A
  • female: 37-47%
  • male: 42-52%
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12
Q

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

A

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

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13
Q

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

A

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

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14
Q

what are the 3 main causes of anemia?

A
  • decreased RBC production
  • blood loss
  • increase RBC destruction
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15
Q

how do we classify anemia?

A

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

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16
Q

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

A

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

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17
Q

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

A

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

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18
Q

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

A

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

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19
Q

why is there no label for elevated MCH?

A

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

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20
Q

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

A

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

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21
Q

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

A

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)

22
Q

what are the cardiac compensatory mechanisms for anemia?

A

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
23
Q

what are the renal compensatory mechanisms for anemia?

A
  • 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
24
Q

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

A
  • 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
25
Q

what are the different types of anemia?

A
  • macrocytic-normochromic
  • microcytic-hypochromic
  • normocytic-normochromic
26
Q

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

A

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

27
Q

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

A

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

28
Q

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

A

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

29
Q

what are the clinical manifestations of macrocytic-normochromic anemia?

A
  • 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
30
Q

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

A

pernicious anemia has IRREVERSIBLE neurologic manifestations bc of nerve demyelination

31
Q

how do we diagnose macrocytic-normochromic anemia?

A

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

32
Q

how do we treat pernicious anemia (vit b12)?

A

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

33
Q

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

A

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

34
Q

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

A

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

35
Q

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

A
  • pale earlobes, palms, & conjunctivae
  • koilonychia: spoon shaped fingernails
  • cheilosis: scales & fissures of mouth
  • stomatitis: inflam of mouth
  • painful ulcerations of buccal mucosa
  • glossitis
36
Q

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

A

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

37
Q

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

A

main treatment: treat underlying cause

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

38
Q

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

A

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
39
Q

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

A

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)

40
Q

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

A

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

41
Q

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

A

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

42
Q

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

A

an early CBC will show normal MCV & normal MCH

a later CBC will show low MCV & low MCH

43
Q

how do we treat normocytic-normochromic anemia?

A
  • treating underlying disorder
  • erythropoietic growth factors
  • transfusion of packed RBCs
44
Q

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

A

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

45
Q

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

A

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

46
Q

what are the risks of EPOETIN ALFA & DARBEPOETIN ALFA?

A

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

47
Q

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

A

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

48
Q

what is posthemorrhagic anemia?

A

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)

49
Q

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

A
  • treat underlying cause
  • using products to restore blood volume
  • massive transfusion of blood products
50
Q

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

A

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

plasma volume expanders:
- DEXTRAN
- albumin

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

nurs 366: pathopharm ii (30 decks)

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