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SBL > Anemia: Clinical Diagnosis and Management > Flashcards

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
Q

who is the universal blood donor?

A

O-

26
Q

who is the universal plasma donor?

A

AB

27
Q

who is the universal blood recipient?

A

AB+

28
Q

what is the gold standard for diagnosing osteonecrosis of the femoral head?

A

MRI

29
Q

How can you confirm the diagnosis of sickle cell anemia?

A

peripheral smear and hemoglobin electrophoresis

30
Q

what will you see on a peripheral smear that will help you diagnose sickle cell anemia?

A

cell sickling and increased RDW

31
Q

when diagnosing sickle cell disease, what does chromography allow you to do?

A

it allows you to quantify the level of disease

32
Q

what might the chromography look like in sickle cell trait?

A

there would be 2 spikes- 1 at hemoglobin A and 1 at hemoglobin S

33
Q

what is the inheritance pattern of sickle cell anemia?

A

autosomal recessive

34
Q

The sickled red cells interact with inflammatory cells, platelets, and endothelial cells to promote what?

A

vaso-occlusion (aka microvascular occlusions)

35
Q

What are three consequences of sickle cell disease?

A

chronic hemolysis, tissue damage, and microvascular occlusion

36
Q

what is an example of a devastating consequence of vaso-occlusion in sickle cell anemia?

A

stroke

37
Q

What is the most deadly consequence of sickle cell disease?

A

acute chest syndrome

38
Q

what initiates acute chest syndrome?

A

vaso-occlusion caused by marrow emboli from necrosing bone; the vaso-occlusion travels to the lungs and is essentially a PE

39
Q

To have acute chest syndrome, what 3 things must you have?

A

shortness of breath, hypoxemia, and fever

40
Q

If you diagnose a patient with acute chest syndrome, how do you treat them?

A

you have to treat empirically for PNA and provide supportive care with oxygen; transfusions can assist these patients as well

41
Q

How does vascular occlusion in sickle cell anemia affect the kidneys?

A

urine cannot be concentrated due to medullary damage (polyuria); hematuria is often a manifestation

42
Q

what does fever + hip pain mean until proven otherwise?

A

osteomyelitis

43
Q

where does avascular necrosis most often occur in sickle cell anemia patients?

A

femoral head

44
Q

What is the spleen’s involvement in sickle cell anemia?

A

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
Q

Older folks with sickle cell disease often eventually autosplenectomize; what is significant about this?

A

they are at an increased risk for infections (encapsulated organisms) so they need to be immunized

46
Q

What is the treatment plan for sickle cell anemia?

A
  1. start patients on O2 to minimize deoxygenation and further sickling 2. control pain; avoid high altitudes; keep Hgb S low
47
Q

what medication is used to keep Hgb S low?

A

Hydroxyurea: it decreases Hgb s and increased HbF

48
Q

a patient comes in and you find that they have macrocytosis and pancytopenia. What should you suspect?

A

aplastic anemia

49
Q

what is aplastic anemia?

A

pancytopenia with associated bone marrow hypocellularity

50
Q

How do you treat aplastic anemia?

A

transfusion support or growth factor support; if no spontaneous resolution then possible stem cell transplant

51
Q

What causes megaloblastic anemia?

A

impaired DNA synthesis

52
Q

what are the identifiable morphological changes that occur in megaloblastic anemia?

A

megaloblasts, hyper-segmented neutrophils, macrocytosis

53
Q

what is responsible for the majority of megaloblastic anemias due to impaired DNA synthesis?

A

vitamin B12 and folate deficiency

54
Q

how might deficiency of vitamin B12 occur?

A

consumption issue or absorption issue: ask diet history, gastric bypass surgery or gastrectomy history, chron’s disease history

55
Q

What could cause an absorption issue to vitamin B12?

A

pernicious anemia, gastric bypass surgery, gastrectomy

56
Q

what is pernicious anemia?

A

an autoimmune condition with antibodies against: intrinsic factor and gastric parietal cells

57
Q

What is the metabolic testing for vitamin B 12 deficiency that will be consistent with a vitamin B12 deficiency?

A

methylmalonic acid (MMA) will be increased and homocysteine will be increased

58
Q

how does folate deficiency occur?

A

consumption: selective diet or alcoholism; increased requirement: pregnancy; absorption: small intestine inflammation (celiac’s disease or chron’s) or by medication

59
Q

what medication may cause folate deficiency?

A

methotrexate

60
Q

pregnant women need how much folate daily?

A

400 mcg daily

61
Q

how can you confirm low folate levels using metabolic testing?

A

methylmalonic acid (MMA) will be normal and homocysteine will be high for folate deficiency

SBL (14 decks)

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