Heme/ Anemia Flashcards
VOLUME of RBCs; tells you how big RBC is; allows for classification of anemia
Normal 80-100
Mean Corpuscular Volume (MCV)
Concentration of hgb in RBCs; tells you how colorful RBCs are (pale, dark, norm)
Normal 32-36
Mean Corpuscular Hemoglobin Concentration (MCHC)
baby RBCs
Marrow production of RBCs; differentiate if anemia is r/t decreased production or increased loss
Absolute retic: 25-70 x10/L
Normal: 0.5-2%
Reticulocyte count
Shows percentage of subclass of hgb Help to identify thalassemias
Hgb electrophoresis
RBC distribution with - tells you variance in size of RBCs (let us know if there are a lot of reticulocytes or not)
RDW
First level that becomes abnormal when iron stores are becoming depleted - total body iron stores
Serum ferritin
amount of iron bound to transferrin (plasma carrier protein)
serum iron
indirectly measures the amount of transferrin. indicates the availability of binding sites on the protein for iron transport
Total iron-binding capacity (TIBC)
calculated with TIBS and serum iron (Serum iron/TIBC) x 100
Transferrin Saturation Percentage (20-50%)
Normal Hgb Levels
Male 13.8-17.2; female 12.1-15.1
Normal Hct Levels
Male 41-50%; female 36-44%
Rule of thumb: 1 hgb for every hct
Normal RBCs
Male 4.7-6.1; female 4.2-5.4
General Anemia
Men Hgb
Men Hgb <13.6g/dL
Women <12 r/t menstruation
CM: gradual/vague until <6 typically; fatigue, malaise, HA, dyspnea, irritability, decrease in exercise tolerance
PE: resting tachycardia and dyspnea (severe); murmur, brittle nails (long term), glossitis, angular cheilitis, spoon-shaped nails. Pallor (nails, lips, mucous membranes, palmar creases), bruising
dx: with CBC
General Anemia
Classification of anemia- MCV <80, decreased MCHC
Microcytic, hypochromic
possible causes of Microcytic, hypochromic anemia
Iron deficiency anemia Thalassemia Lead poisoning Sideroblastic anemia Aluminum toxicity
Classification of anemia- MCV >80, normal MCHC
Macrocytic, Normochromic
possible causes of Macrocytic, Normochromic anemia
Vitamin B12 deficiency
Folate deficiency
G6PD
Classification of anemia- MCV 80–100, normal MCHC
Normocytic, Normochromic
possible causes of Normocytic, Normochromic anemia
Anemia of chronic disease
Acute blood loss
Early iron deficiency
what kind of anemia is common in children and pregnant women.
IDA
Kinds of anemia common in elderly
anemia of chronic disease (ACD), nutritional deficiencies (B12, folate)
what kind of anemia is common in the Mediterranean, Middle East, Southeast Asia, India, and Pakistan
thalassemia
normal MCV, normal MCH/MCHC, hgb >9g/dL
Normocytic
reduced transport of iron to erythroid precursors; decreased RBC survival time, blunted erythropoietin response to anemia
One of most common anemias
Seen in: hospitalized pts, elderly, chronic disorders (acute/chronic infections, malignancy, inflammatory disorders, HIV), CAN coexist with IDA or be confused with it
CM: mild and asymptomatic; cm usu r/t underlying disease process, Fatigue, tachycardia, pallor
Anemia of Chronic Disease
Lab findings for Anemia of Chronic Disease
low serum iron
Ferritin normal or elevated
How to tx Anemia of Chronic Disease
Treat the cause
1st line: recombinant human erythropoietin (rHuEPO)
Used to stim the bone marrow to create more RBCs at a higher rate (HIV, cancer, CKD)
Non-Pharm:
Patient education: regular lab draws; call provider if increase in sx
normal MCV 80-100, normal MCHC
Benign w/unknown cause, occurs in childhood in prev health children, first few years of life
Frequently follows viral infection (viral suppression or IgG, IgM, or cell-mediated autoimmune response)
Transient Erythroblastopenia of Childhood (TEC)
6mon-3years of age, usually after 1 yr
Develop over days or weeks & assoc with viral s/s (fever, malaise, lethargy, abdominal pain, upper respiratory symptoms)
Gradually increasing pallor
Decreased energy levels/fatigue
PE: overall normal presentation
Jaundice can appear (esp. If child has preexisting hemoglobinopathy)
Transient Erythroblastopenia of Childhood (TEC)
Dx and labs:
Anemia
⬇Hgb (6-8g/dL, can be as low as 2.5g/dL)
⬇reticulocyte
✔MCV for age (this value will help differentiate it from other congenital hypoplastic anemias)
✔WBC (some neutropenia in 20%)
✔ or ⬆ platelet count
⬆ serum iron level (reflects decreased utilization)
Erythroid hypoplasia in bone marrow aspiration
Transient Erythroblastopenia of Childhood (TEC)
How to tx Transient Erythroblastopenia of Childhood (TEC)
1st line: Ø specific treatment indicated
Severe: Transfusions may be required, possible REFERRAL to hematologist
Macrocytic, normochromic (MCV >80), normal MCHC)
Folate r/t: malabsorption disorders, pregnancy (neural tube defects), cancer, hyperthyroid, ETOH abuse, sickle cell anemia, dietary folate deficiency, B12 r/t: malabsorption (pernicious anemia, crohn’s dx, celiac dx, gastrectomy/bariatric sx), meds (GERD tx, long term H2 blocker use, PPI’s), strict vegetarians
Normal B12 intake 3-5mcg/day
Other causes: drug use, liver dx, hypothyroidism, myelodysplastic syndrome, chemo
Folate & Vitamin B-12 Deficiency
CM: few sx- GLOVE AND STOCKING (numbness and tingling) - classic. Can get nerve damage if you dont fix it, glossitis
PE:
B12: Sore mouth with loss of taste → smooth, red, shiny, large tongue (glossitis)
if severe- neurologic findings (decreased vibratory sensation, loss of proprioception, peripheral neuropathy, ataxia, hyperactive reflexes, Romberg sign)
Vitamin B-12 Deficiency
diagnostic Methylmalonic acid…
elevated in vitb12 deficiency, normal in folate deficiency
foods high in folic acid and B12
Folic acid→ fruits and vegetables, liver, green leafy veggies, peas, beans, avocados, eggs, milk. Fortified foods: pasta, flour, cereal, bread, rice
Vit. B12 → meat protein, dairy, egg
most prevalent cause of vitamin B12 deficiency…atrophy of parietal cells in stomach leads to loss of intrinsic factor (IF) → necessary to absorb b12
Pernicious Anemia
how to dx and tx Pernicious Anemia:
Dx: assay for anti-IF or anti-parietal cells antibodies
Tx: 1st line: parental Vitamin B12 injections (IM or subQ): 6 week replacement schedule then monthly injections for life
Most common anemia in the world, most common nutrient deficiency.
Mostly affects women of reproductive age and older adults
Iron Deficiency Anemia
CM include… Paresthesia, sore tongue, brittle nails, spoon-shaped nails, pica (starch, ice, or clay)
Pica→ paper, dirt, clay; pagophagia→ ice
Iron Deficiency Anemia
Lab Findings for IDA
Hgb: ⬇ Serum ferritin: ⬇; RDW is the earliest marker for FE deficiency (p.748) Serum iron: ⬇ TIBC: ⬆ Transferrin saturation: ⬇
IDA Patient education
take iron 30 mins before meals. Calcium inhibits iron absorption (no dairy or calcium 1-2 hrs after taking iron supplements)
SE: constipation, nausea (add stool softener, take at bedtime)
Stool may be dark tar color
Complex inheritance pattern as multiple genes involved
Affected people: SE Asia, India, China, Philippines
4 genes (two from each parent) involved
Alpha (α) Thalassemia
four genes affected, leads to premature births that are either stillborn or die shortly after birth → incompatible with life
Alpha thalassemia major (hydrops fetalis)
Autosomal recessive
Affected people: Mediterranean, Middle Eastern, African, Asian
2 genes (one from each parent) involved
Beta (β) thalassemia
Dx/Lab findings:
Anemia
⬇ MCV
✔ iron studies
Hemoglobin electrophoresis (⬆ levels of hemoglobin A2) >3.5%- p.751 (primary diagnostic)
Alpha globin DNA mutation (REFER for this if thalassemia is suspected, test not readily available)
Mentzer index <13
Beta (β) thalassemia
PE: only remarkable in beta intermedia and major (compatible with life + abnormal findings)
Short stature
Abnormal facies
Cranial marrow expansion - trying to make more RBCs
Pallor, jaundice, enlarged spleen, liver, or heart
LIFE THREATENING, bone marrow stem cell failure. Secondary to infection or exposure to toxins or medications, or immune mediated. - REFER!
Aplastic Anemia
CM: abnormal bleeding, infection, anemia. Sudden onset. Hx may reveal recent viral infection, chronic disease, medication, toxin
PE:
petechiae, ecchymosis, purpura, pallor of skin and mucous membranes. Mild lymphadenopathy in late stage.
Aplastic Anemia
How to tx Aplastic Anemia
IMMEDIATE HEME REFERRAL
>40 yo: immunosuppression therapy. HSCT (hematopoietic stem cell transplant) in younger pts
Non-pharm Receive all vaccinations and maintain healthy diet and exercise
Patient education: protection from infectious sources is essential
increased rate of RBC destruction (body making them fine, destroying them at very fast rate)
Labs
High retic (producing because its low)
Low H/H,
High LDH (direct cellular injury),
Haptoglobin (low)- binds to free hbg as RBC rupture. Low indicates intravascular hemolysis
High Bilirubin level (RBC destruction)
Hemolytic anemias
Meds or foods that can precipitate Hemolytic anemias
sickle cell, Hereditary Spherocytosis, G6PD (meds can precipitate/fava beans)- Normocytic Anemia
deoxygenated Hgb undergoes irreversible changes that give sickle shape. Sickle cells become trapped in microcirculation causing obstruction, ischemia, and infarct leading to severe pain and end-organ damage (sickle crisis). Most often occurs in joints, extremities, back, chest, ABD, lungs
African Americans most affected
CM: asymptomatic until in periods of crisis
Vaso-occlusive crisis: severe pain, can lead to organ damage
Acute chest syndrome! Or septicemia
PE: jaundice, scleral icterus, murmur along left sternal border, cardiomegaly
Sickle Cell Anemia: REFER- Can affect every ROS
Treatment for sickle cell
Hydroxyurea: decreases percentage of hgb S (that become sickled) started at 10-20mg/kg/day
Hematopoietic stem cell transplant is only cure
for crisis: NSAIDs or oral narcotics, hydration, rest, heat, massage
Patho: mild chronic hemolytic anemia; RBC membrane has a smaller surface area with a spherical shape.
CM: jaundice in newborn period. Splenomegaly by 2 years of age; chronic fatigue, malaise, and abdominal pain
Hereditary Spherocytosis
positive family hx and pathognomonic findings of peripheral blood smear. (many microspherocytes and elevated MCHC).
Peripheral smear: RBC are uniformly spherical in shape, smaller than normal
Severe forms may require splenectomy. Consider prophylactic cholecystectomy d/t high incidence of gallstones
Hereditary Spherocytosis
inherited erythrocyte enzyme deficiency; can result in acute hemolytic anemia.
G6PD-induced hemolysis is precipitated by infection or ingestion of oxidant drug or food.
Women are usually carriers and males affected, typically African american; tropical/subtropical regions (associated w/ malaria)
Fava beans, ingestion of mothballs, or severe infections (viral or bacterial)
G6PD Deficiency
G6PD Deficiency…
Drugs a/w acute hemolysis:
ASA, phenacetin, sulfonamides, nitrofurantoin, and primaquine (malaria tx) → oxidant drugs→ ask “have you been on ABX recently?
