Heme/ Anemia Flashcards

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1
Q

VOLUME of RBCs; tells you how big RBC is; allows for classification of anemia
Normal 80-100

A

Mean Corpuscular Volume (MCV)

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2
Q

Concentration of hgb in RBCs; tells you how colorful RBCs are (pale, dark, norm)
Normal 32-36

A

Mean Corpuscular Hemoglobin Concentration (MCHC)

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3
Q

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%

A

Reticulocyte count

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4
Q
Shows percentage of subclass of hgb
Help to identify thalassemias
A

Hgb electrophoresis

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5
Q

RBC distribution with - tells you variance in size of RBCs (let us know if there are a lot of reticulocytes or not)

A

RDW

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6
Q

First level that becomes abnormal when iron stores are becoming depleted - total body iron stores

A

Serum ferritin

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7
Q

amount of iron bound to transferrin (plasma carrier protein)

A

serum iron

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8
Q

indirectly measures the amount of transferrin. indicates the availability of binding sites on the protein for iron transport

A

Total iron-binding capacity (TIBC)

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9
Q

calculated with TIBS and serum iron (Serum iron/TIBC) x 100

A

Transferrin Saturation Percentage (20-50%)

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10
Q

Normal Hgb Levels

A

Male 13.8-17.2; female 12.1-15.1

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11
Q

Normal Hct Levels

A

Male 41-50%; female 36-44%

Rule of thumb: 1 hgb for every hct

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12
Q

Normal RBCs

A

Male 4.7-6.1; female 4.2-5.4

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13
Q

General Anemia

Men Hgb

A

Men Hgb <13.6g/dL

Women <12 r/t menstruation

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14
Q

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

A

General Anemia

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15
Q

Classification of anemia- MCV <80, decreased MCHC

A

Microcytic, hypochromic

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16
Q

possible causes of Microcytic, hypochromic anemia

A
Iron deficiency anemia
Thalassemia
Lead poisoning
Sideroblastic anemia
Aluminum toxicity
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17
Q

Classification of anemia- MCV >80, normal MCHC

A

Macrocytic, Normochromic

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18
Q

possible causes of Macrocytic, Normochromic anemia

A

Vitamin B12 deficiency
Folate deficiency
G6PD

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19
Q

Classification of anemia- MCV 80–100, normal MCHC

A

Normocytic, Normochromic

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20
Q

possible causes of Normocytic, Normochromic anemia

A

Anemia of chronic disease
Acute blood loss
Early iron deficiency

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21
Q

what kind of anemia is common in children and pregnant women.

A

IDA

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22
Q

Kinds of anemia common in elderly

A

anemia of chronic disease (ACD), nutritional deficiencies (B12, folate)

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23
Q

what kind of anemia is common in the Mediterranean, Middle East, Southeast Asia, India, and Pakistan

A

thalassemia

24
Q

normal MCV, normal MCH/MCHC, hgb >9g/dL

A

Normocytic

25
Q

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

A

Anemia of Chronic Disease

26
Q

Lab findings for Anemia of Chronic Disease

A

low serum iron

Ferritin normal or elevated

27
Q

How to tx Anemia of Chronic Disease

A

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

28
Q

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)

A

Transient Erythroblastopenia of Childhood (TEC)

29
Q

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)

A

Transient Erythroblastopenia of Childhood (TEC)

30
Q

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

A

Transient Erythroblastopenia of Childhood (TEC)

31
Q

How to tx Transient Erythroblastopenia of Childhood (TEC)

A

1st line: Ø specific treatment indicated

Severe: Transfusions may be required, possible REFERRAL to hematologist

32
Q

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

A

Folate & Vitamin B-12 Deficiency

33
Q

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)

A

Vitamin B-12 Deficiency

34
Q

diagnostic Methylmalonic acid…

A

elevated in vitb12 deficiency, normal in folate deficiency

35
Q

foods high in folic acid and B12

A

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

36
Q

most prevalent cause of vitamin B12 deficiency…atrophy of parietal cells in stomach leads to loss of intrinsic factor (IF) → necessary to absorb b12

A

Pernicious Anemia

37
Q

how to dx and tx Pernicious Anemia:

A

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

38
Q

Most common anemia in the world, most common nutrient deficiency.
Mostly affects women of reproductive age and older adults

A

Iron Deficiency Anemia

39
Q

CM include… Paresthesia, sore tongue, brittle nails, spoon-shaped nails, pica (starch, ice, or clay)
Pica→ paper, dirt, clay; pagophagia→ ice

A

Iron Deficiency Anemia

40
Q

Lab Findings for IDA

A
Hgb: ⬇
Serum ferritin: ⬇; RDW is the earliest marker for FE deficiency (p.748)
Serum iron: ⬇
TIBC: ⬆
Transferrin saturation: ⬇
41
Q

IDA Patient education

A

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

42
Q

Complex inheritance pattern as multiple genes involved
Affected people: SE Asia, India, China, Philippines
4 genes (two from each parent) involved

A

Alpha (α) Thalassemia

43
Q

four genes affected, leads to premature births that are either stillborn or die shortly after birth → incompatible with life

A

Alpha thalassemia major (hydrops fetalis)

44
Q

Autosomal recessive
Affected people: Mediterranean, Middle Eastern, African, Asian
2 genes (one from each parent) involved

A

Beta (β) thalassemia

45
Q

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

A

Beta (β) thalassemia

46
Q

PE: only remarkable in beta intermedia and major (compatible with life + abnormal findings)

A

Short stature
Abnormal facies
Cranial marrow expansion - trying to make more RBCs
Pallor, jaundice, enlarged spleen, liver, or heart

47
Q

LIFE THREATENING, bone marrow stem cell failure. Secondary to infection or exposure to toxins or medications, or immune mediated. - REFER!

A

Aplastic Anemia

48
Q

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.

A

Aplastic Anemia

49
Q

How to tx Aplastic Anemia

A

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

50
Q

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)

A

Hemolytic anemias

51
Q

Meds or foods that can precipitate Hemolytic anemias

A

sickle cell, Hereditary Spherocytosis, G6PD (meds can precipitate/fava beans)- Normocytic Anemia

52
Q

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

A

Sickle Cell Anemia: REFER- Can affect every ROS

53
Q

Treatment for sickle cell

A

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

54
Q

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

A

Hereditary Spherocytosis

55
Q

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

A

Hereditary Spherocytosis

56
Q

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)

A

G6PD Deficiency

57
Q

G6PD Deficiency…

Drugs a/w acute hemolysis:

A

ASA, phenacetin, sulfonamides, nitrofurantoin, and primaquine (malaria tx) → oxidant drugs→ ask “have you been on ABX recently?