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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 (50 cards)

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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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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
what are the different types of anemia?
- macrocytic-normochromic - microcytic-hypochromic - normocytic-normochromic
26
what is macrocytic-normochromic anemia? what are its clinical name? what causes it? what is it characterized by?
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
why is lack of intrinsic factor a cause of macrocytic-normochromic anemia?
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
why is long term alcohol use disorder a cause for macrocytic-normochromic anemia?
the direct toxins effect on bone marrow --> secondary anemia bc of poor nutritional intake
29
what are the clinical manifestations of macrocytic-normochromic anemia?
- 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
what is the major difference between folic acid deficiency & pernicious anemia (vit b12)
pernicious anemia has IRREVERSIBLE neurologic manifestations bc of nerve demyelination
31
how do we diagnose macrocytic-normochromic anemia?
a CBC shows elevated MCV & normal MCH - decreased plasma B12 levels - decreased folic acid levels - treatments depends on cause
32
how do we treat pernicious anemia (vit b12)?
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
how do we treat folic acid anemia? what happens if we give folic acid for a long time?
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
what is microcytic-hypochromic anemia? what is its clinical name? what are the causes?
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
what are clinical manifestations of microcytic-hypochromic anemia (iron deficiency)
- pale earlobes, palms, & conjunctivae - koilonychia: spoon shaped fingernails - cheilosis: scales & fissures of mouth - stomatitis: inflam of mouth - painful ulcerations of buccal mucosa - glossitis
36
how do we diagnose iron deficiency anemia? what is ferritin?
CBC shows low MCV & low MCH - decreased iron serum levels - decreased ferritin serum levels (major iron storage protein)
37
how do we treat microcytic-hypochromic anemia (iron deficiency)?
main treatment: treat underlying cause iron supplementation - PO FERROUS SULFATE most common - IV IRON DEXTRAN most common IV prep
38
what are the adverse effects with ORAL FERROUS SULFATE? when is absorption best? when should you take it to lower GI distress?
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
what are the side effects of IV IRON DEXTRAN? why do some people use this instead of FERROUS SULFATE?
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
what is normocytic-normochromic anemia? what's its clinical name? what is the cause?
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
what are the clinical manifestations of normocytic-normochromic (ACD or AI) anemia?
usually mild to moderate - similar to iron deficiency anemia (microcytic-hypochromic)
42
how do we diagnose normocytic-normochromic anemia (ACD or AI)?
an early CBC will show normal MCV & normal MCH a later CBC will show low MCV & low MCH
43
how do we treat normocytic-normochromic anemia?
- treating underlying disorder - erythropoietic growth factors - transfusion of packed RBCs
44
what are the different medications of erythropoietic growth factors? what are the routes?
can be thru IV & subq - EPOETIN ALFA (Erythropoietin) - DARBEPOETIN ALFA (Erythropoietin, long acting)
45
what does EPOETIN ALFA & DARBEPOETIN ALFA do? when should you stop giving them?
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
what are the risks of EPOETIN ALFA & DARBEPOETIN ALFA?
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
when do we see initial effects of EPOETIN ALFA & DARBEPOETIN ALFA? when will they reach its max?
initial effects seen within 1-2 weeks - Hgb will reach max at 2-3 months
48
what is posthemorrhagic anemia?
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
how do we treat posthemorrhagic anemia (normocytic-normochromic anemia)?
- treat underlying cause - using products to restore blood volume - massive transfusion of blood products
50
what are the different ways we can restore blood volume with posthemorrhagic anemia?
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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