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646 Test 2 > Anemia > Flashcards

Anemia Flashcards

1
Q

What is normal Hgb?

A

Women: 12-15 g/dL
Men: 13-17 g/dL

1-2 g/dL LOWER in women and AA men than white men

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2
Q

What is the prevalence of anemia?

A

~1 in 77 people

10-12% of people over 65
20% of people over 85
10% of nursing home residents

Common factor in chronic illness

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3
Q

What is the prevalence of symptoms in anemia?

A

MOST are asymptomatic
Acuity: may be rapid or chronic onset
Severity varies
Young vs. old patients

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4
Q

What are the symptoms of anemia?

A
  • Dyspnea
  • Chest pain
  • Palpitations
  • Dizziness/lightheadedness/syncope
  • Fatigue/weakness/exercise intolerance
  • Neuro changes (with profound anemia, you can see stroke-like symptoms…rare)
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5
Q

What are the signs of anemia?

A

Often NO signs
Vital sign changes:
Orthostasis/tachycardia after 30% blood volume loss
Hypovolemic shock after 40% blood volume loss

Conjunctival pallor
Scleral icterus (from hemolytic anemia, increased bili)
Angular chelitis (more with deficiencies)
Glossitis
Lymphadenopathy
Heart murmur, signs of HF
Splenomegaly
Peripheral neuropathy: abnormal vibration, proprioception
DOE with profound anemia because body senses decreased O2

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6
Q

What does the red cell size tell you about the pathology of anemia?

A

Microcytic anemia = MCV <80, indicating decreased production of RBCs (more older cells); is it a bone marrow issue or issue of not having the necessary ingredients?

Normocytic anemia = MCV 80-100

Macrocytic anemia = MCV >100, indicating majority of cells are immature, the problem is not related to the bone marrow

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7
Q

What are possibly pathogeneses of anemia?

A 
Decreased production (by the bone marrow)
Increased destruction
Sequestration
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8
Q

What is the differential of microcytic anemia (MCV<80)?

A
  • Iron deficiency (MOST COMMON)
  • Anemia of chronic disease - body cannot access the Fe
  • Thalassemia - genetic mutation on heme subunit so that cannot make normal Hgb for RBCs
  • Sideroblastic anemia - bone marrow makes ringed sideroblasts rather than normal RBCs
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9
Q

What is the differential of normocytic anemia (MCV 80-100)?

A
  • Anemia of chronic disease
  • Anemia of renal failure
  • Hemolysis
  • Hypothyroidism
  • Early blood loss
  • Primary bone marrow disorder (myelodysplasia, bone marrow infiltration, myeloma, aplastic anemia)…if this goes on long enough, can turn microcytic
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10
Q

What is the differential of macrocytic anemia (MCV>100)?

A

Megaloblastic (most common):

  • B12 deficiency
  • Folate deficiency

Non-megaloblastic

  • Liver disease
  • Medications
  • Myelodysplasia
  • Reticulocytosis
  • Alcohol
  • Hypothyroidism
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11
Q

What does the peripheral smear look like in megaloblastic macrocytosis anemia?

A
  • Large, oval RBCs

- Hypersegmented neutrophils that are packed with protein junk

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12
Q

What are elements of the HISTORY when evaluating possible anemia?

A

Possible sources of blood loss
-Menstrual history
-Hx/sx suggestive of GI bleeding (dark stool, emesis with blood)
-Urinary loss (hematuria)
-Pulmonary loss (hemoptysis)
PMH - chronic illnesses?
PSH - gastric bypass/bowel surgery like small bowel resection that decreases absorption?
Medications
-GI blood loss (NSAIDs)
-Hemolysis
-Bone marrow suppression
FH - anemia, thalassemia, sickle cell?
Diet - veggies/fruits? meats? access? alcohol? vegan?
Pregnancy - increases blood volume, so a relative low Hgb/Hct

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13
Q

What does the CBC tell you?

A 
WBC
Hgb/Hct
PLT
MCV
RDW
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14
Q

What is RDW?

A

Normal: 11-15%
Indicates the variety of cells present
Will be increased when the bone marrow is acting correctly in response to microcytic anemia
Use this in addition to MCV to make determination of cause of anemia

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15
Q

What is transferrin?

A
  • Made in the liver
  • Glycoprotein that reversibly binds to Fe and transports Fe from the blood to BM, spleen, and liver
  • High levels indicates possible IDA
  • Low levels may indicate liver disease or hemolytic anemia
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16
Q

What is TIBC?

A

Total Iron Binding Capacity
Measures the blood’s capacity to bind iron with transferrin

Transferrin sat = Serum Fe/TIBC x 100
When transferrin sat is low, indicates IDA

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17
Q

What are reticulocytes and how do you measure them?

A

Reticulocytes = immature blood cells

Retic count = the % of retics in your blood, so not an accurate assessment of bone marrow activity when you’re anemic

Reticulocyte Index (RI) is a more accurate measure of the reticulocytes because it adjusts the number according to pt’s Hct, a good marker of bone marrow response to anemia
If RI > 1, it is responding appropriately
If RI is very low, it is a chronic process

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18
Q

What will the CBC look like in a patient with IDA?

A

Low iron
High TIBC
Low ferritin (Note: ferritin is an acute phase reactant, so if the pt is older with lots of conditions, this may be increased 2/2 inflammation)
Fe/TIBC < 18%
MCV/RBC > 13 (helps differentiate between thalassemia)

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19
Q

What will the CBC look like in a patient with anemia of chronic disease (AOCD)?

A

High ferritin (because it is an acute phase reactant)
Low iron (cannot get it out of stores, so low in blood)
Low TIBC
Fe/TIBC > 18%

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20
Q

How do you approach the differential diagnosis in microcytic anemia?

A
  • Rule out IDA: look at ferritin, serum Fe, TIBC, transferrin sat (Fe/TIBC); MCV is usually 60s-70s
  • Consider thalassemia: MCV usually <50
  • Is there a cause for AOCD?
21
Q

What is the diagnostic approach to normocytic anemia?

A

Step 1: Rule out nutritional anemias (Ferritin, B12, Folate)
Step 2: Rule out anemia of renal insufficiency
-GFR < 60 (lack of erythropoietin)
-Normal peripheral smear
-Inappropriately normal serum erythropoietin
Step 3: Look for hemolysis (likely other s/sx with this)
-Increased LDH (cell destruction)
-Increased indirect bilirubin (Hgb catabolism)
-Increased reticulocytosis
-Decreased haptoglobin (serum protein that clears Hgb)
Step 4: Consider AOCD or bone marrow disorder

22
Q

What are the lab results in hemolysis?

A
  • Increased LDH (cell destruction)
  • Increased indirect bilirubin (Hgb catabolism)
  • Increased reticulocytosis
  • Decreased haptoglobin (serum protein that clears Hgb)
23
Q

What is the diagnostic approach to macrocytic anemia?

A

Step 1: Rule out meds that cause macrocytosis (alcohol, hydroxyurea, methotrexate, trimethoprim, AZT, 5-FU, chemo)
Step 2: Rule out nutritional causes
-Check B12, Folate, MMA, Homocysteine
Step 3: Look for bone marrow disease

24
Q

Why do you check Methylmalonic acid?

A

B12 helps convert MMA to Coenzyme A

Thus, increased MMA may indicate B12 deficiency
B12 levels may be normal, but checking MMA can indicate a deficiency

25
Q

What is the prevalence of IDA?

A

Highest in women of childbearing age:
12% in women 12-49
9% in women 50-69

Ethnic differences amongst women:
10% in non-hispanic whites
19% in AAs
22% in Mexicans living in US!!!

Much rarer in men (2-3%) and requires an intense workup

26
Q

What is the differential of IDA?

A 
Blood loss
-Menstrual
-GI
-Urinary, Pulmonary
Decreased absorption
-Malabsorption
-Partial gastrectomy
Increased requirements
-Pregnancy/Lactation
Decreased intake
-Children/Vegans
27
Q

What will a peripheral smear show in IDA?

A

Hypochromic RBCs

28
Q

How do you evaluate a patient with IDA?

A

GI evaluation: colonoscopy/EGD in men, postmenopausal women, or premenopausal women with symptoms

Menstruating women without localizing GI symptoms can be treated empirically with iron

29
Q

How do you treat IDA?

A 
Oral iron:
-Start daily and titrate to BID/TID
-Treatment duration for 4 months
Follow-up: 
-Re-check Hgb in 1 month (corrects in 6-8 weeks)

IV iron:

  • Iron dextran, ferric gluconate, or iron sucrose (venofer)
  • Used when pt unable to tolerate oral iron or malabsorption
  • SE: anaphylaxis (iron dextran)
30
Q

What are the SE of oral iron?

A

Constipation, abd pain, nausea, dark stools, interactions with other meds
Treat with stool softeners, take with food, titrate slowly

31
Q

What’s the deal with Alpha Thalassemia?

A

15% trait in AA and very common in SE Asian

Genotype and phenotype:
aa/aa = normal
-a/aa = silent carrier
-a/-a or --/aa = trait
--/-a = HbH disease
--/-- = hydrops fetalis
32
Q

What’s the deal with Beta Thalassemia

A

More common in Mediterranean, Greek, Italian, North African ethnicities

Genotype and phenotype:
B/B = normal
-/B = trait
-/- = homozygous

33
Q

How do you learn about the alpha and beta subunits in thalassemias?

A

Hemoglobin electrophoresis

34
Q

What will a peripheral smear in thalassemia look like?

A

Often will see target cells because of misfolded proteins

35
Q

How do you diagnose thalassemia?

A

Beta thalassemia is diagnosed with Hgb electrophoresis and will show increased HgbA2

Alpha thalassemia is diagnosed with genetic testing, it is severe and often diagnosed at childhood

36
Q

What is the treatment plan for thalassemia?

A

No treatment for thalassemia TRAIT
Genetic counseling provided if contemplating pregnancy
Do not supplement with iron

37
Q

What is involved in the differential diagnosis of B12 deficiency anemia?

A

Decreased intake
-Vegan, alcohol (decreases intrinsic factor levels), elderly

Malabsorption

  • PPI/H2 blockers that inhibit binding between B12 and intrinsic factor (cannot absorb B12)
  • Lack of intrinsic factor/parietal cells (pernicious anemia, atrophic gastritis, gastrectomy)
  • Other GI causes (sprue/celiac, ileal disease)
  • Biological competition (bacterial overgrowth, tapeworm)
38
Q

How do you evaluate a patient for B12 deficiency?

A
  • B12 level
  • Methylmalonic acid level (will be increased)
  • Homocysteine (will be increased)
  • Pernicious anemia (autoimmune issue where you cannot absorb B12): parietal cell antibody and intrinsic factor antibody levels
39
Q

What is the dosing schedule for B12 treatment?

A

Oral

  • Initial dose of 1,000-2,000 mcg/day for 1-2 weeks
  • Maintenance: 1,000 mcg/day for life

IM

  • Initial dose: 100-1,000 mcg/day for 1 week; then weekly for 1 month
  • Maintenance: 100-1,000 mcg every 1-3 months
40
Q

What are (red cell) intrinsic causes of hemolytic anemias?

A

Membranopathies - hereditary spherocytosis
Enzymopathies - G6PD deficiency
Hemoglobinopathies - Sickle cell disease

41
Q

What are (red cell) extrinsic causes of hemolytic anemias?

A

Immune-mediated: autoimmune or alloiummune (transfusion reaction)
Microangiopathic: TTP (Thrombotic Thrombocytopenic Purpura), HUS (Hemolytic-Uremic Syndrome), DIC (Disseminated Intravascular Coagulation), HELLP (Hemolysis, Elevated Liver Enzymes, Low Platelet count)
Infection associated

42
Q

What is involved in the diagnosis of hemolytic anemia?

A

Hemolysis Labs:

  • Increased retic
  • Increased LDH
  • Increased unconjugated bilirubin
  • Decreased haptoglobin

Peripheral smear:

  • Schistocytes
  • Spherocytes
  • Sickle cells
43
Q

What is the “Rule of Thirds” in older adults?

A

1/3 nutritional deficiency
1/3 anemia of chronic disease
1/3 unexplained anemia

44
Q

When should you refer an anemic patient?

A
  • Etiology is unclear
  • Need for bone marrow biopsy
  • Hemolytic anemias
  • Need for transfusion (symptomatic anemia or not responding to oral therapy)
45
Q

What is Rouleaux on a peripheral smear?

A

Shows stacks or aggregations of red blood cells

Present in multiple myeloma, macroglobulinemia, or artifact

46
Q

What is the significance of schistocytes in a peripheral smear?

A

Schistocytes = RBC fragments resulting from membrane damage when they pass through vessels; sometimes called “bite cells”

Occur in:
Microangiopathic Hemolytic Anemias (MAHA) (e.g., DIC, HUS, TTP)
Severe burns, uremia
Hemolytic anemia

47
Q

What is the significance of sickle cells on peripheral smear?

A

Crescent shaped cells that occur when sickle cell patients experience stressors like dehydration, infection, or low O2 supply

48
Q

What is the significance of target cells on peripheral smear?

A 
Seen in:
Sickle cell (HbC)
Thalassemia
Liver disease
Post-splenectomy
Severe IDA

646 Test 2 (8 decks)

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