Hemat. Approach to Anemic Patient Flashcards

1
Q

Define Anemia

A
  • Reduction in RBC mass or blood hemoglobin concentration
  • more than 2 standard deviations below the mean for age/gender/population
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2
Q

6 factors affecting Hg levels

A
  1. age
  2. race
  3. gender
  4. sexual maturity
  5. genetics
  6. altitude
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3
Q

How do

age, race, gender, sexual maturity, genetics, altitude

affect Hg levels?

A
  1. Babies/ kids: small bodies mean small losses are a big deal
  2. African, Asian, Mediterranean at higher risk for anemia.
    1. Normal levels are based on Caucasians (go figure)
  3. Women need to make more blood for menstruation, but also have lower Hg than men
  4. Prepubescent lower than post
  5. if mom or dad have anemia, kid might
  6. Higher elevations make people produce more Hg so they can perfuse tissue with the lower oxygen levels…adaptive.
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4
Q

What’s the process erythropoiesis

A
  1. renal interstitial peritubular cells detect low O2 in blood
  2. They secrete EPO (erythropoietin) into blood
  3. EPO stimulates proliferation and differentiation of RBC progenitors into Reticulocytes and prevent apoptosis
  4. Retics differentiate increasing in number
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5
Q

why does anemia develop

A
  • RBCs not being made efficiently (Production)
  • Bleeding (Loss)
  • Extravascular and Intravascular Destruction
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6
Q

Red Flags for Anemia History/Intake

A
  • Neonatal jaundice in the 1st 24 hrs
  • Diet low in Fe, B12, Folate, Pica.
  • G6PD deficiency gene expression (x-linked)= destruction of RBC
    • triggered by fava beans, moth balls, aspirin, sulfadrugs, NSAIDS, severe stress, infection, nitrofurintoin,
  • Gallstones at early age (Hg stones)
  • splenomegaly and fam hx of splenectomy
  • hepatomegaly
  • pre disposition populations
  • dark urine
  • jaundice, fatigue… etc.
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7
Q

Physical Signs on Exam secondary to Anemia

A

Glossitis (red swollen tongue)

angular cheilitis (B12 deficiency)

Fe deficiency: spooning nails

Icterus esp in lower scerla (under lower eye lid)

frontal bossing of forehead (bone marrow expansion): Rickets, congenital syphilis, beta thalassemia,

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8
Q

Hyperproliferative Anemias and Hypoproliferative anemias

A

hyper: associated with increased destruction: dark urine, jaundice, splenomegaly, anemia when destruction overwhelms production
hypo: lower production, etiology usually localizes in marrow, typical symptoms of anemia

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9
Q

Hb/Hgb

A

the concentration of hemoglobin: oxygen carrying proteins

2 beta and 2 alpha chains. each chain has associated heme group and each heme group has a central iron which binds oxygen.

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10
Q

HCT (%)

A

Hematocrit percent (should be 3x hemoglobin)

% of blood volume occupied by RBC

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11
Q

what does MCV mean?

A

mean cell corpuscular volume:

tells us the average volume of RBCs collected.

relates to RBC size to tell if micro=<80, normo=80-100, or macrocytic >100

neonates 110 normal, 70 at 1 year old

if larger, it’s newer cells (macrocytic)

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12
Q

MCH

A

Mean cell hemoglobin: average Hb concentration of the RBCs

(when cell size change,

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13
Q

what is MCHC?

A

Mean [Hg] per ONE Red blood cell

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14
Q

What does a Reticulocyte Count mean?

How do you evaluate for Anemia?

A

a direct reflection of rate of RBC production

indirect reflection of rate of RBC destruction (elevated in disorders with more destruction)

(reported as % and an absolute number “ARC”)

Use ARC and %retic x RBC to get the whole picture

if pt has retic of 1% (normal) that’s fine unless their Hg is low, then retic should be high and compensating.

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15
Q

two classifications and 3 sub classifications of anemia

A

PATHOPHYSIOLOGIC:

  • decreased production
  • blood loss
  • increased destruction

MORPHOLOGIC

  • Macrocytic
  • Normocytic
  • Microcytic
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16
Q

What are disorders of erythrocyte production?

A
  1. Fe deficiency
  2. Lead poisoning
  3. Inflammation
  4. bone marrow failure syndromes
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17
Q

What are disorders with destruction probs

A

Hemoglobinopathies

RBC Membrane defects

enzyme deficiencies

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18
Q

What is RBC chromicity

A

clues on [Hg] : color or RBC

central palor: normal

MCH, MCHC can give clues, but Peripheral blood smear is more important

hyperchromic, normochromic, hypochromic, or polychromasia

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19
Q

What diseases are connected with these shapes, and what are these RBC shapes:

Target cells,

echinocyte

Acanthocyte

Spherocyte

A

Target cells: looks like a target: liver disease, HbC, HbD, HbE, Thalassemia

echinocyte: spiney like a sea urchin: Uremia, hypokalemia, artifact

Acanthocyte: irregularly shaped RBC with thorny projection: liver disease, PK deficiency

Spherocyte: sphere shaped, no central palor: HS Immune hemolytic anemia

20
Q

Microcytic Anemia causes

A

Fe deficiency anemia

thalassemias (alpha & beta)

Chronic disease/ inflammation

Pb toxicicty

21
Q

Most common anemia

A

Fe deficiency with 3% of young children in US

8-10% have Fe deficiency with out anemia

(pregnant women, adolescents, elderly)

(if Fe deficient and small bodied, a small blood loss could push them over the edge to become anemic)

22
Q

Etiology of Fe deficiency

A
  • Increased demand to make blood (infancy, adolescents, pregnant, making more rbcs)
  • malnutrition (vegetarians, vegans, junk food diets)
  • decreased absorption (gastrectomy, H. pylori, IBD, drugs)
  • GI bleeds benign or malignant, GU bleeding heavy periods, blood donors
  • drugs: NSAIDS, steroids
  • chronic kidney disease, IBD, heart failure, obesity
23
Q

Stages of Fe depletion, what labs would you order and why

A

1) Depleted iron stores (marrow iron/serum ferratin) 2-3+
2) Iron deficient erythropoiesis: Serum Fe <100ug/dl and %saturation is <30
3) Iron Deficient Anemia: HCT<40, RBC become microcytic and hypochromic

*don’t stop treatment too early, gotta build up stores! Serum Fe increases in one meal, Serum ferratin slower to build

24
Q

What does low Fe look like with labs?

A

Low: Hg, MCV, MCH, MCHC, RBC count

Low uncompensated retic count

Increased TIBC/transferin (nothing to bind them)

Low ferritin (deficiency: <10-12ng/L, depletion: 12-20ng/L

normal is 20-300ng/L

Inflammation can falsely elevate Ferratin even if you don’t have iron stores

25
Q

Problems with Fe Tx

A

Ferous sulfate tastes horrible.

Side effects include dyspepsia, constipation, nausea, abd pain,

Helps to take with food… decreases absorption, but some is better than not taking it at all.

Polysaccharide preparations sweeter

26
Q

Foods with high Fe

A

Liver, red meat

beans/ greens

iron-fortified cereals/ grains

heme: meat, non-heme: vegetarian

27
Q

therapeutic response to Fe treatment of deficiency

A

Tx works within 3 days.

see less hypochromia, increased RDW

increased reticulocytes in 2-3 days,

Hg & MCV goes up in a week

Serum iron 1-2 hrs

TIBC goes down: 2-3 weeks

Serum Ferritin goes up: 1-2 weeks, 3-4 to normal

28
Q

Why are they having Fe loss in the first place?

What would you look for?

A

GI Blood loss: guaiac (occult stool), if positive endoscopy

Urea breath test

Test Antibodies for H. pylori, anti-transglutaminase (celiac sprue if fails to respond to oral iron)

C-reactive protein: inflammation? neoplasm? especially in elderly

Metro/menorrhagia: evaluate for bleeding disorder

29
Q

Normal Treatment for Fe deficiency

A

Iron Salts 100-200mg elemental Fe in 2 doses

Ferrous Sulfate, Ferrous Gluconate Taken on empty stomach for best absorption, avoid coffee, tea, take with Vit C (acid helps absorption) Kids: 2-6mg/2 doses, NO MILK

**continue Tx 3mths to replenish serum ferritin***

30
Q

when oral Fe is contraindicated, or another method is indicated

A

IV iron therapy : for those who can’t take orally (gastrectomy, duodenal bypass, H. pylori, celiac, IBD, genetic IRIDA, or if needs to be immediate recovery (severe anemia in 2nd-3rd trimester, chronic renal disease, substitution for blood transfusion (religious reasons), chemo anemia (from ESA)

contraindicated: 1st trimester of pregnancy, iron allergy (hypersensitivity rx)

31
Q

What is anemia of Chronic Disease

A

Anemia from a chronic state of inflammation

(like cancer, chronic infection, lupus, RA, and other autoimmune disease, obesity, aging)

that causes impaired production of RBCs

32
Q

What’s the pathophysiology Anemia of Chronic Disease that has to do with iron levels?

A

Hepsiden ( regulatory hormone made in liver, excreted to urine) tells Macrophages to keep iron inside cells, and not let it into circulation, and tells duodenal and intestinal cells not to absorb more Fe. This is because it thinks it is being invaded, and Fe makes bacterial infections stronger.

We expect higher hepsiden in Fe overload, and infection

33
Q

lab findings in Anemia of Chronic Disease

A

mild-moderate anemia

MCV: normal to low

RDW: normal

Retic Count: low

Ferritin: normal to high (even if Fe is low)

34
Q
A
35
Q

treatment Anemia of Chronic Disease

A
  1. eradicate underlying disease
  2. if impossible,
    1. transfusions
    2. IV iron
    3. Erythropoesis Stimulating Agents
    4. New experimental approaches targeting IL-6 activity
36
Q

What is macrocytic Anemia? what’s it caused by

A

Larger RBCs

Caused by B12 or Folate deficiency (DNA synthesis: mismatch between how much cytoplasm to put in cell and membrane so cells larger)

Non-Megaloblastic causes: Phentoin, Bactrim, ART, Chemo, hypothyroid, liver disease, alcoholics, myelodysplasia, bone marrow failure, reticulocytosis

37
Q

What labs do we order if we suspect Macrocytic Anemia?

A

CBC with peripheral blood smear (hyper-segmented neutrophils/neutropenia)

reticulocyte count (to see if MCV 110-140 is bigger because more retics, also to see if production or destruction prob)

serum cobalamin, folate, and TSH

liver function test (alcoholics)

measure folate/cobalamin (needed for DNA synthesis including for RBCs)

38
Q

Signs and symptoms of macrocytic anemia

A

Both for B12 and Folate deficiency, see glossitis-smooth tongue, and dyspnea with exercise, pallor, etc.

For B12, neuropathies, ataxia, seizures, psychiatric probs, decreased sensations

39
Q

what causes B12 deficiency

A

pernicious anemia: (autoimmune) disease where autoantibodies destroy gastric parietal cells which produce intrinsic factor

malabsorption: IBS, chrons disease, celiac, bowel resection

Hemolytic anemia, excess blood loss

pregnancy: when more need is happening

40
Q

Lab results for Macrocytic Anemia from B12 deficiency

A

moderate -severe anemia

elevated MCV 110-140

low reticulocyte (not compensated)

hypersegmented neutrophils and macroovalecytes on smear

mild thrombocytopenia and/or neutropenia

low serum B12, <170 (when normal or 170-210, confirm with elevated methylmalonic acid or homocystine)

41
Q

Diagnosis for Pernicious Anemia

A

Anti-intrinsic factor antibodies (100%specific, but only 70% sensitive= false neg)

Anti-parietal cell antibodies (more sensitive, but less specific=false positive)

Shilling test (board answer)

42
Q

Tx for B12 deficiency

A

IM or subcutaneous injection of 100mcg B12

daily x 1 wk, then weekly x 1 month, then monthly for life

OR

sublingual 1mg/day for EVER

(folic acid also recommended for first few mths of B12 tx)

43
Q

Response to B12 Tx for Macrocytic Anemia

A

well-being in 1-2 days,

brisk retic increase in 3-4 days, and Hg in 10 days

***Hypokalemia can occur during early response because increased K+ use for RBC production*** monitor

neuropathies improve totally by 6 mths

44
Q

Labs for Folate Deficiency

A

Mod-severe anemia

elevated MCV

low retic

hypersegmented neutrophils/macro-ovalcytes on peripheral smear

mild thrombocytopenia/neutrophils

RBC folic acid levels (better than serum folate b/c reflects body stores <150 is deficient)

also measure B12.

45
Q

Tx of folate deficiency

A

daily oral folic acid 1 mg

Response is rapid wellbeing

retics in 5-7 days

total correction of hematologic abnormals in 2 mths

46
Q

Non-megaloblastic anemia causes and Tx

A

anti-retroviral drugs, antiseizure meds, chemo, bactrim

hypothyroidism

non-alcoholic liver disease

chronic alcohol use: stop alcohol use, blood returns rapidly

47
Q

Differential for Normocytic Anemia

A

+++Reticulocytes

hemolytic anemia

Post-hemorrhagic anemia

—Reticulocytes

acute hemorrhage

anemia of inflammation

renal/liver disease

marrow infiltration

myelodysplastic syndrome