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Anemia Flashcards

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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
What is the appropriate iron supplementation for pregnant women?
(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
26
What is the etiology of ACD?
inflammatory mediators keep iron in storage sites (primarily the liver) - iron is not available for production of RBCs (not absolute deficiency => functional deficiency)
27
What are the causes of ACD?
chronic infection (TB, HIV, osteomyelitis), cancer, chronic inflammation (RA, SLE), chronic kidney disease
28
How is ACD diagnosed?
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)
29
What will iron studies show in a PT with ACD?
- 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
30
What is the management for ACD?
treat underlying condition
31
What is Thalassemia?
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
What is the etiology of alpha Thalassemia?
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
What is the etiology of beta Thalassemia?
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
What are the manifestations of Thalassemia major?
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
How is Thalassemia diagnosed?
(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
What is the management for Thalassemia?
minor - usually nothing/genetic counseling | major - transfusions 2X/week with chelation therapy to prevent iron overload
37
What are the labs that distinguish the microcytic anemias?
``` ICD = decreased ferritin ACD = increased ferritin Thalassemia = severely decreased MCV (disproportionate to Hgb) ```
38
What are the features of macrocytic anemias?
- 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
What are the major causes of macrocytic anemias?
(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
What are dietary sources of Vitamin B12?
meat, fish, milk (only animal products) - deficiency more common in strict vegans => stores are large (3 years)
41
What are dietary sources of folate?
green leafy vegetables, beans, fruits (bananas), mushrooms, yeast => stores are limited (3 months)
42
What are the common causes of B12 deficiency?
malabsorption due to: - deficiency of intrinsic factor (pernicious anemia) => most common cause - gastric/bariatric/ileac surgery or Crohn's disease
43
What are the common causes of folate deficiency?
- dietary lack (elderly, alcoholics, "tea and toast diet") => most common cause - malabsorption in jejunum - increased demand (cancer, pregnancy) - drugs (methotrexate, antiepileptic drugs, Bactrim)
44
What is pernicious anemia (B12 deficiency)?
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
What are the effects of folate deficiency in pregnancy?
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
What are the manifestations of B12 deficiency?
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
What are the manifestations of folate deficiency?
weakness, fatigue, atrophic glossitis, stomatitis
48
How are B12 and folate deficiency diagnosed?
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
What is the treatment for B12 deficiency (due to malabsorption)?
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
What is the treatment for folate deficiency?
oral folate replacement (1 mg PO daily) - hematologic response is rapid
51
What factors distinguish B12 (cobalamin) from folate deficiency?
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
What are the characteristics of normocytic anemias?
normal MCV, normal iron studies, low RBC count, low Hgb, elevated reticulocyte count, elevated indirect bilirubin, elevated LDH (lactate dehydrogenase)
53
What are the causes of normocytic anemias?
destruction of RBCs due to: - hemolysis (sickle cell anemia, autoimmune hemolytic anemia) - acute blood loss
54
What are the symptoms of normocytic anemias?
weakness, tiredness, pallor, jaundice (destruction of RBCs leads to increase in unconjugated bilirubin)
55
What is sickle cell disease?
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
What are the manifestations of sickle cell disease?
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
How is sickle cell disease diagnosed?
initial = blood smear to detect red blood sickle cells; most accurate = electrophoresis to detect HgS (sickled hemoglobin)
58
What is the treatment for sickle cell disease?
- exchange blood transfusions for serious complications - vaccinations (pneumococcal, meningococcal, H. influenza) - hydroxyurea (fetal Hgb) - painful crises: hydration, oxygenation, pain control - genetic counseling
59
What is the effect of hydroxyurea on PTs with sickle cell disease?
hydroxyurea increases fetal hemoglobin
60
What is the initial test to diagnose leukemia?
peripheral blood smear to examine cells: => proliferation of blast cells = acute leukemia => proliferation of mature WBCs = chronic leukemia
61
What is the best test to confirm a diagnosis of leukemia?
=> bone marrow biopsy | => Dx of CML requires identification of genetic abnormalities (Philadelphia chromosome) via genetic testing
62
What is leukemia?
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
How is leukemia classified?
- 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
What are the signs and symptoms of acute leukemia?
fever, infections (neutropenia), mucosal bleeding and bruising (thrombocytopenia), fatigue (anemia), splenomegaly, painless lymphadenopathy, leukocytosis OR leukopenia
65
What are the signs and symptoms of chronic leukemia?
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
What are the ages groups most commonly affected by leukemia and what is the prognosis?
=> 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
What is the treatment for leukemia?
- acute leukemia: chemotherapy and possible bone marrow transplant (ALL and AML) - chronic leukemia: chemotherapy (CLL and CML) and possible bone marrow transplant (CML)
68
What are the diagnostic tests for suspicious lymph nodes?
- 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
What is the hallmark of Hodgkin's lymphoma?
presence of Reed Sternberg cells (on biopsy) - cells are not present in non-Hodgkin lymphoma
70
What is lymphoma?
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
What are the signs and symptoms of lymphoma?
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
What is the Tx for lymphoma?
- local disease (1-2 nodes affected) = local radiation | - advanced disease (multiple nodes affected) = chemotherapy
73
What is the prognosis with lymphoma?
- Hodgkin's: > 88% | - non-Hodgkin's: around 70%
74
Which groups are affected by lymphoma?
- 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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