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AGPC 4 > Anemia > Flashcards

Anemia Flashcards

1
Q

What is anemia?

A

deficiency in the mass of circulating RBCs (inhibits the capacity to deliver oxygen to tissues)

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2
Q

How is anemia measured?

A

(1) RBC count
(2) Hgb concentration
(3) % of Hct - % of volume of RBCs in total volume of a blood sample

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3
Q

What is the normal value of Hgb?

A 
Hgb:Hct = 1:3
Males = 13.5-17.5 g/dL - < 14 suggests anemia
Females = 12-16 g/dL - < 12 suggests anemia
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4
Q

What are the symptoms of anemia (same regardless of cause)?

A

severity of anemia causes symptoms - not etiology:

(1) decreased oxygen-carrying capacity - tiredness, exercise intolerance, poor concentration, pallor, angina
(2) cardiac compensation (increased stroke volume and heart rate): palpitations, dyspnea on exertion, hemic murmur (innocent murmur due to increase in stroke volume and thinner blood moving faster)

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5
Q

How is anemia classified?

A

according to mean corpuscular volume (size of RBCs):

(1) micrcytic - MCV < 80 fL
(2) normocytic - MCV 80-100 fL
(3) macrocytic - MCV > 100 fL

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6
Q

What is the major factor affecting size of RBCs?

A

hemoglobin - 90% of RBC volume

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7
Q

What is hemoglobin?

A

Hgb = heme/iron (4 molecules) + globin (2 alpha and 2 beta chains)

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8
Q

What is iron’s role in Hgb?

A

binds oxygen

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9
Q

What are the sources of problems in microcytic anemia?

A

(1) problem due to heme/iron - iron deficiency anemia or anemia of chronic disease
or
(2) problem due to globin chains - Thalassemia

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10
Q

What is iron deficiency anemia (IDA)?

A

most common cause of anemia worldwide - deficiency may be due to:

  • diet (lack of meat, sunflower seeds, nuts, whole grains, dark leafy greens)
  • poor iron absorption in duodenum (Celiac disease, Crohn’s disease)
  • increased iron demands (pregnancy)
  • blood loss (most common cause in adults - GI bleed most frequently)
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11
Q

What are the manifestations of IDA?

A

iron deficiency: pica, restless leg syndrome

low Hgb: tiredness, generalized weakness, shortness of breath, pallor, hemic murmur

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12
Q

How is IDA diagnosed?

A
  • low Hgb/Hct
  • low MCV (< 80 fL)
  • low mean corpuscular hemoglobin concentration - amount of Hgb per unit volume = < 33 g/dl)
  • increased red cell distribution width (greater than normal variation in size of RBCs - cells are produced under different processes/older cells will be larger than younger cells) = > 15%
  • low reticulocyte (immature RBCs) count - lack of iron reduces production of RBCs (bone marrow unable to produce sufficient numbers of new RBCs)
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13
Q

What will you see in a blood smear with IDA?

A

low MCV - microcytosis (blood specimen/peripheral blood)
low MCHC - hypochromia (blood smear - microscopic examination of blood)
increased RDW - anysocytosis - lack of equal cell sizes (blood smear)

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14
Q

What is transferrin?

A

protein produced by liver that transports iron (binds with free iron to transport it to liver)

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15
Q

What is ferritin?

A

protein that stores iron in the liver - measure of iron storage (can be falsely elevated in inflammatory states - may mask IDA)

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16
Q

How is IDA diagnosed?

A
  • low serum iron (normal = 50-150 ng/dl)
  • low ferritin (normal = 20-300 ng/dl)
  • low % transferrin saturation (normal = 20-50) => decreases in IDA because more transferrin is being produced but there are low levels of iron available to bind
  • high Total Iron Binding Capacity (TIBC - normal = 25-450 ng/dl) => measures transferrin level (transferrin binds iron) - will increase in IDA (to provide more potential iron-binding sites
  • low reticulocyte count
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17
Q

How is iron excreted from the body?

A

there is no physiologic excretion mechanism

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18
Q

How is iron processed in the body?

A

10-20 mg of iron consumed daily => 1-2 mg iron/day is absorbed and transported via transferrin (75% to bone marrow, 15% to ferritin/stores in liver and heart, 10% other processes) => 1-2 mg iron/day lost via desquamation of epithelia

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19
Q

What are the stages of IDA?

A

(1) iron storage is depleted without causing anemia (decrease in ferritin, decrease transferrin saturation, increase TIBC) - asymptomatic
(2) normocytic anemia (decrease in Hgb) - asymptomatic or mild symptoms of anemia
(3) microcytic hypochromic anemia (low MCV, low MCHC, low reticulocyte count) - symptomatic anemia

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20
Q

What is the management of IDA?

A

(1) determine the source of iron deficiency and bleeding - menorrhagia, melena (upper GI bleed), hematochezia (lower GI bleed), hematuria => if no obvious source of bleeding, consider occult GI bleed (MUST sent PT for colonoscopy to r/o colon cancer)
(2) severely symptomatic PTs (myocardial ischemia) - RBC transfusion (1 pack = 1 g increase)
(3) all other patients - oral iron supplementation (IV if absorption problems or GI side effects intolerable)

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21
Q

What does the provider need to know about iron supplementation?

A
  • side effects: nausea, constipation, heartburn, black stool
  • absorption is best on an empty stomach (30 minutes before meals - absorption is reduced 40-50% if taken with food) and with ascorbic acid (orange juice) - but will increase gastric side effects
  • treat for 4-6 months or until ferritin level is normal
  • safe handling (in a locked cabinet) - iron supplements account for 30% of fatal medication overdoses in children
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22
Q

What factors decrease iron absorption?

A

antacids, caffeine, calcium, H2 blockers, PPIs

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23
Q

What is the expected response to iron supplementation?

A

(1) bone marrow response - increase in reticulocyte count (7-10 days)
(2) resolution of anemia - increase in Hgb (1-2 months)
(3) restoration of iron stores - increase in ferritin (4-6 months)

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24
Q

Who should be screened for IDA?

A

only pregnant women - CBC testing should be limited to diagnostic testing in all other patients

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25
Q

What is the appropriate iron supplementation for pregnant women?

A

(1) anemia on screening - 60-120 mg of oral iron daily
(2) no anemia - 30 mg/day as primary prevention
=> maximum amount absorbed per day = 4 mg
=> body has no effective way to excrete > 1 mg/day - can lead to iron overload and cause direct myocardial damage

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26
Q

What is the etiology of ACD?

A

inflammatory mediators keep iron in storage sites (primarily the liver) - iron is not available for production of RBCs (not absolute deficiency => functional deficiency)

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27
Q

What are the causes of ACD?

A

chronic infection (TB, HIV, osteomyelitis), cancer, chronic inflammation (RA, SLE), chronic kidney disease

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28
Q

How is ACD diagnosed?

A

initial test = CBC:

  • low or normal MCV
  • low Hgb/Hct
  • low MCHC
  • normal RDW (chronic disease has long-term effects on bone marrow so RBCs will all be affected)
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29
Q

What will iron studies show in a PT with ACD?

A
  • low serum iron (body is making less iron available to factors that consume it - e.g., bacteria)
  • elevated ferritin (hallmark of ACD) - body is storing iron at any sign of inflammation
  • low TIBC - decrease in transferrin
  • elevated transferrin saturation
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30
Q

What is the management for ACD?

A

treat underlying condition

31
Q

What is Thalassemia?

A

inherited genetic condition that causes underproduction of globins - two types:

(1) alpha - genes that code for alpha globin are affected (inadequate production of alpha chains)
(2) beta - genes that code for beta globin are affected (inadequate production of beta chains)

32
Q

What is the etiology of alpha Thalassemia?

A

alpha chains are encoded by 4 genes - 2 from mother and 2 from father => severity of anemia depends on number of deleted genes (1 asymptomatic, 4 incompatible with life) - populations most affected = African, Mediterranean, and Asian

33
Q

What is the etiology of beta Thalassemia?

A

beta chains are encoded by 2 genes (1 from mother and 1 from father) - autosomal (not on sex chromosome) recessive (need to have 2 faulty genes for disease to be present) => severity of anemia depends on number of genes affected (1 abnormal = Thalassemia minor/mild disease; 2 abnormal = Thalassemia major/moderate to severe disease) - populations affected = Mediterranean, Middle Eastern, and Asian

34
Q

What are the manifestations of Thalassemia major?

A

transfusion-dependent anemia, symptoms appear within first year of life: severe anemia, failure to thrive, irritability, pallor, bone hyperplasia, chipmunk face (bone medullar expansion - body trying to produce RBCs from any bone available) => average life expectancy = 17 years

35
Q

How is Thalassemia diagnosed?

A

(1) initial tests: very low MCV (disproportionate to Hgb - hallmark of Thalassemia), low Hgb, normal RDW, normal iron studies
(2) most accurate diagnostic test - Hgb electrophoresis (separate chains) to confirm => used to distinguish alpha and beta Thalassemias

36
Q

What is the management for Thalassemia?

A

minor - usually nothing/genetic counseling

major - transfusions 2X/week with chelation therapy to prevent iron overload

37
Q

What are the labs that distinguish the microcytic anemias?

A 
ICD = decreased ferritin
ACD = increased ferritin
Thalassemia = severely decreased MCV (disproportionate to Hgb)
38
Q

What are the features of macrocytic anemias?

A
  • MCV > 100 fL
  • problem of “bad DNA” - not enough material for DNA synthesis and replication
  • reticulocytes are larger
  • normal iron/Hgb synthesis is not affected (normochromic = normal MCHC)
  • RDW increased
39
Q

What are the major causes of macrocytic anemias?

A

(1) factors that affect DNA synthesis of RBCs
- folate deficiency
- B12 deficiency
(2) factors that directly affect bone marrow - will lead to a decrease in the number of RBCs
- alcoholism
- hypothyroidism

40
Q

What are dietary sources of Vitamin B12?

A

meat, fish, milk (only animal products) - deficiency more common in strict vegans => stores are large (3 years)

41
Q

What are dietary sources of folate?

A

green leafy vegetables, beans, fruits (bananas), mushrooms, yeast => stores are limited (3 months)

42
Q

What are the common causes of B12 deficiency?

A

malabsorption due to:

  • deficiency of intrinsic factor (pernicious anemia) => most common cause
  • gastric/bariatric/ileac surgery or Crohn’s disease
43
Q

What are the common causes of folate deficiency?

A
  • dietary lack (elderly, alcoholics, “tea and toast diet”) => most common cause
  • malabsorption in jejunum
  • increased demand (cancer, pregnancy)
  • drugs (methotrexate, antiepileptic drugs, Bactrim)
44
Q

What is pernicious anemia (B12 deficiency)?

A

autoimmune disease - destruction of parietal cells (intrinsic factor deficiency leads to B12 deficiency) => because B12 is efficiently stored, it takes 2-3 years to develop anemia

45
Q

What are the effects of folate deficiency in pregnancy?

A

teratogenic - leads to neural tube defects (spina bifida) => women should take 0.4-0.8 mg/d for 3 months prior to conception (continue through lactation)

46
Q

What are the manifestations of B12 deficiency?

A

weakness, fatigue, atrophic glossitis (deficiency affects cells with high turnover rates), angular stomatitis, neurological (affects both central and peripheral nerves - parasthesia first and most common), ataxia, loss of vibratory sense, + Romberg sign, dementia

47
Q

What are the manifestations of folate deficiency?

A

weakness, fatigue, atrophic glossitis, stomatitis

48
Q

How are B12 and folate deficiency diagnosed?

A

common factors:
- MCV > 100 fL, low RBCs, low reticulocyte count
B12 deficiency:
- low serum B12 (can be normal/elevated in inflammatory states), elevated serum methylmalonic acid
folate deficiency:
- normal level of serum methylmalonic acid

49
Q

What is the treatment for B12 deficiency (due to malabsorption)?

A

parenteral (IM) therapy weekly to monthly for the rest of life => watch for hypokalemia - hematologic response is rapid/full recovery takes 2 months (neurological changes are irreversible if prolonged)

50
Q

What is the treatment for folate deficiency?

A

oral folate replacement (1 mg PO daily) - hematologic response is rapid

51
Q

What factors distinguish B12 (cobalamin) from folate deficiency?

A

B12:
- due to malabsorption, takes years for onset of symptoms, neurological deficits, low serum B12, elevated methylmalonic acid, Tx = B12 IM monthly for rest of life
folate:
- due to dietary deficiency, takes months for onset of symptoms, low serum folate, oral folate supplement

52
Q

What are the characteristics of normocytic anemias?

A

normal MCV, normal iron studies, low RBC count, low Hgb, elevated reticulocyte count, elevated indirect bilirubin, elevated LDH (lactate dehydrogenase)

53
Q

What are the causes of normocytic anemias?

A

destruction of RBCs due to:

  • hemolysis (sickle cell anemia, autoimmune hemolytic anemia)
  • acute blood loss
54
Q

What are the symptoms of normocytic anemias?

A

weakness, tiredness, pallor, jaundice (destruction of RBCs leads to increase in unconjugated bilirubin)

55
Q

What is sickle cell disease?

A

abnormality of beta chain structure due to the inheritance of an abnormal gene of the beta chain of Hgb - autosomal recessive (requires 2 abnormal genes for disease, 1 abnormal gene = trait) => trait affects 1:500 African Americans (50% risk for each pregnancy), disease affects 1:800 African Americans (25% risk for each pregnancy) - life expectancy reduced by 25-30 years (death most often due to infection)

56
Q

What are the manifestations of sickle cell disease?

A

sickled RBCs (decrease in oxygen causes change in structure of RBCs - become rigid and sickle shaped), retinopathy, acute respiratory distress, cor pulmonale, hematuria, autosplenectomy, bone necrosis, leg uclers, jaundice, anemia, severe pain

57
Q

How is sickle cell disease diagnosed?

A

initial = blood smear to detect red blood sickle cells; most accurate = electrophoresis to detect HgS (sickled hemoglobin)

58
Q

What is the treatment for sickle cell disease?

A
  • exchange blood transfusions for serious complications
  • vaccinations (pneumococcal, meningococcal, H. influenza)
  • hydroxyurea (fetal Hgb)
  • painful crises: hydration, oxygenation, pain control
  • genetic counseling
59
Q

What is the effect of hydroxyurea on PTs with sickle cell disease?

A

hydroxyurea increases fetal hemoglobin

60
Q

What is the initial test to diagnose leukemia?

A

peripheral blood smear to examine cells:
=> proliferation of blast cells = acute leukemia
=> proliferation of mature WBCs = chronic leukemia

61
Q

What is the best test to confirm a diagnosis of leukemia?

A

=> bone marrow biopsy

=> Dx of CML requires identification of genetic abnormalities (Philadelphia chromosome) via genetic testing

62
Q

What is leukemia?

A

proliferation of abnormal WBCs in the bone marrow - can spread to other organs (lymph nodes) and can interfere with production of normal WBCs, RBCs, and platelets

63
Q

How is leukemia classified?

A
  • type of WBCs affected
    => neutrophils/basophils/eosinophils = myelogenous leukemia
    => lymphocytes = lymphocytic leukemia
  • maturity of WBCs affected:
    => immature cells/blasts = acute leukemia
    => more mature cells (morphologically/structurally more mature but functionally defective) = chronic leukemia (characterized by leukocytosis/increase in WBCs on CBC)
64
Q

What are the signs and symptoms of acute leukemia?

A

fever, infections (neutropenia), mucosal bleeding and bruising (thrombocytopenia), fatigue (anemia), splenomegaly, painless lymphadenopathy, leukocytosis OR leukopenia

65
Q

What are the signs and symptoms of chronic leukemia?

A

may be asymptomatic and discovered on a routine WBC (leukocytosis) or constitutional symptoms (fatigue, weight loss, fever), splenomegaly, painless lymphadenopathy, leukocytosis (mostly lymphocytes = CLL; mostly neurophils = CML), mucosal bleeding and bruising (thrombocytopenia), fatigue (anemia)

66
Q

What are the ages groups most commonly affected by leukemia and what is the prognosis?

A

=> ALL: children - 75% survive 5 years
=> AML: adults - > age 50 = poor prognosis
=> CLL: older adults - 85-90% survive 5 years
=> CML: adults - > age 50 = poor prognosis

67
Q

What is the treatment for leukemia?

A
  • acute leukemia: chemotherapy and possible bone marrow transplant (ALL and AML)
  • chronic leukemia: chemotherapy (CLL and CML) and possible bone marrow transplant (CML)
68
Q

What are the diagnostic tests for suspicious lymph nodes?

A
  • initial test: excisional biopsy to determine cancer diagnosis
  • tests to determine stage:
    => CT scans of chest/abdomen/pelvis/neck with contrast - to determine staging
    => bone marrow biopsy
    => PET scan
    => CBC (will be normal in most cases), chemistries, SED rate, LDH (lactate dehydrogenase)
    => MUGA scan (test using radioactive tracer and camera to take picture of heart as it pumps blood)
    => pulmonary function tests (PFTs)
69
Q

What is the hallmark of Hodgkin’s lymphoma?

A

presence of Reed Sternberg cells (on biopsy) - cells are not present in non-Hodgkin lymphoma

70
Q

What is lymphoma?

A

solid tumor of lymph nodes - characterized by proliferation of abnormal lymphocytes in lymph nodes and spleen (can spread to bone marrow)
=> Hodgkin’s is local (primarily cervical lymph nodes)
=> non-Hodgkin’s is disseminated

71
Q

What are the signs and symptoms of lymphoma?

A

painless lymphadenopathy - nodes are painless, firm/rubbery, and fixed (no redness or warmth)
=> B symptoms: fever, weight loss, drenching night sweats, pruritis with hot shower = poor prognosis
=> symptoms depend on tumor location (e.g., pressure on esophagus causes dysphagia)

72
Q

What is the Tx for lymphoma?

A
  • local disease (1-2 nodes affected) = local radiation

- advanced disease (multiple nodes affected) = chemotherapy

73
Q

What is the prognosis with lymphoma?

A
  • Hodgkin’s: > 88%

- non-Hodgkin’s: around 70%

74
Q

Which groups are affected by lymphoma?

A
  • Hodgkin’s: 30-40 years old (more male than female) - Epstein Barr virus may be associated
  • non-Hodgkin’s: > 60 years old

AGPC 4 (22 decks)

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