Anemia: Clinical Diagnosis and Management Flashcards

1
Q

What labs are clues to hemolysis?

A

lactate dehydrogenase (LDH), indirect (unconjugated) bilirubin, and haptoglobin

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2
Q

if hemolysis is occurring, what would the LDH level be?

A

high

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3
Q

if hemolysis is occurring, what would the indirect (unconjugated) bilirubin be?

A

high

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4
Q

if hemolysis is occurring, what would the haptoglobin be?

A

low

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5
Q

what four things are included in iron studies?

A

iron level, ferritin, transferrin, and transferrin saturation

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6
Q

what does ferritin measure/ what is ferritin?

A

iron storage protein, proportional to iron levels except during inflammatory cases and then it will be opposite the iron level

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7
Q

what is transferrin?

A

circulating iron transport protein (increased in iron deficiency anemia) (synonymous with total iron binding capacity (TIBC))

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8
Q

what is transferrin saturation (TSAT)?

A

iron stores/ capacity x 100

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9
Q

what are three things that could cause microcytic anemia?

A

IDA, thalassemia, sickle cell disease

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10
Q

what three things could cause normocytic anemia?

A

anemia of chronic disease, renal disease, and acute blood loss

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11
Q

what 4 things could cause macrocytic anemia?

A

Folate/B12 deficiency, hypothyroidism, EtOH, MDS

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12
Q

what would the iron studies look like in a patient with iron deficiency anemia?

A

ferritin will be low; transferrin saturation will be low

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13
Q

what is the earliest and most sensitive index that will change in iron deficiency anemia?

A

RDW

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14
Q

what are the indications that iron is low? (iron studies wise)

A

low serum iron and low serum ferritin

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15
Q

what are the indications that the body is just waiting for iron (compensating)?

A

increased total iron binding capacity (TIBC) and increased transferrin receptor (TFR)

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16
Q

in male patients or postmenopausal females, iron deficiency anemia should prompt an evaluation for what?

A

sources of gastrointestinal blood loss

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17
Q

what are the signs of anemia of chronic disease?

A

clinical suspicion for systemic inflammation, MCV: normal to low, low serum iron, normal to high ferritin levels, low transferrin, low transferrin saturation

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18
Q

what are the effects of inflammatory cytokines?

A

they decrease intestinal absorption of iron and they decrease erythropoietin production; they also increase hepcidin

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19
Q

what are the effects of hepcidin?

A

it decreases ferroportin, decreases transferrin, and increases ferritin

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20
Q

what are the signs of uncompensated blood loss?

A

normocytic anemia and a normal reticulocyte count

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21
Q

what are the signs of hypovolemic shock?

A

hypotensive, tachycardia, and weak pulses

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22
Q

coffee ground emesis is often an indication of what?

A

digested blood (upper GI bleed)

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23
Q

what can happen as a result of anemia from acute blood loss?

A

hypovolemia, myocardial ischemia, and renal failure

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24
Q

when do you screen pregnant women for development of Rh antibodies?

A

at 1st prenatal visit and at 28 weeks

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25
who is the universal blood donor?
O-
26
who is the universal plasma donor?
AB
27
who is the universal blood recipient?
AB+
28
what is the gold standard for diagnosing osteonecrosis of the femoral head?
MRI
29
How can you confirm the diagnosis of sickle cell anemia?
peripheral smear and hemoglobin electrophoresis
30
what will you see on a peripheral smear that will help you diagnose sickle cell anemia?
cell sickling and increased RDW
31
when diagnosing sickle cell disease, what does chromography allow you to do?
it allows you to quantify the level of disease
32
what might the chromography look like in sickle cell trait?
there would be 2 spikes- 1 at hemoglobin A and 1 at hemoglobin S
33
what is the inheritance pattern of sickle cell anemia?
autosomal recessive
34
The sickled red cells interact with inflammatory cells, platelets, and endothelial cells to promote what?
vaso-occlusion (aka microvascular occlusions)
35
What are three consequences of sickle cell disease?
chronic hemolysis, tissue damage, and microvascular occlusion
36
what is an example of a devastating consequence of vaso-occlusion in sickle cell anemia?
stroke
37
What is the most deadly consequence of sickle cell disease?
acute chest syndrome
38
what initiates acute chest syndrome?
vaso-occlusion caused by marrow emboli from necrosing bone; the vaso-occlusion travels to the lungs and is essentially a PE
39
To have acute chest syndrome, what 3 things must you have?
shortness of breath, hypoxemia, and fever
40
If you diagnose a patient with acute chest syndrome, how do you treat them?
you have to treat empirically for PNA and provide supportive care with oxygen; transfusions can assist these patients as well
41
How does vascular occlusion in sickle cell anemia affect the kidneys?
urine cannot be concentrated due to medullary damage (polyuria); hematuria is often a manifestation
42
what does fever + hip pain mean until proven otherwise?
osteomyelitis
43
where does avascular necrosis most often occur in sickle cell anemia patients?
femoral head
44
What is the spleen's involvement in sickle cell anemia?
there is a massive collection of sickled cells in the spleen which results in splenomegaly (sequestration); spleen could burst; patient could die due to hypovolemia; splenic infarct (occurs due to splenic congestion and poor blood flow secondary to sickle cell disease
45
Older folks with sickle cell disease often eventually autosplenectomize; what is significant about this?
they are at an increased risk for infections (encapsulated organisms) so they need to be immunized
46
What is the treatment plan for sickle cell anemia?
1. start patients on O2 to minimize deoxygenation and further sickling 2. control pain; avoid high altitudes; keep Hgb S low
47
what medication is used to keep Hgb S low?
Hydroxyurea: it decreases Hgb s and increased HbF
48
a patient comes in and you find that they have macrocytosis and pancytopenia. What should you suspect?
aplastic anemia
49
what is aplastic anemia?
pancytopenia with associated bone marrow hypocellularity
50
How do you treat aplastic anemia?
transfusion support or growth factor support; if no spontaneous resolution then possible stem cell transplant
51
What causes megaloblastic anemia?
impaired DNA synthesis
52
what are the identifiable morphological changes that occur in megaloblastic anemia?
megaloblasts, hyper-segmented neutrophils, macrocytosis
53
what is responsible for the majority of megaloblastic anemias due to impaired DNA synthesis?
vitamin B12 and folate deficiency
54
how might deficiency of vitamin B12 occur?
consumption issue or absorption issue: ask diet history, gastric bypass surgery or gastrectomy history, chron's disease history
55
What could cause an absorption issue to vitamin B12?
pernicious anemia, gastric bypass surgery, gastrectomy
56
what is pernicious anemia?
an autoimmune condition with antibodies against: intrinsic factor and gastric parietal cells
57
What is the metabolic testing for vitamin B 12 deficiency that will be consistent with a vitamin B12 deficiency?
methylmalonic acid (MMA) will be increased and homocysteine will be increased
58
how does folate deficiency occur?
consumption: selective diet or alcoholism; increased requirement: pregnancy; absorption: small intestine inflammation (celiac's disease or chron's) or by medication
59
what medication may cause folate deficiency?
methotrexate
60
pregnant women need how much folate daily?
400 mcg daily
61
how can you confirm low folate levels using metabolic testing?
methylmalonic acid (MMA) will be normal and homocysteine will be high for folate deficiency