10/8/22, 7:56 PM Anemia - AMBOSS

Anemia Last edited: Jun 24, 2022

QBANK SESSION CLINICAL SCIENCES CLINICIAN LEARNED

Summary

Anemia is defined as a decrease in the quantity of circulating red blood cells (RBC), represented by a reduction in hemoglobin concentration (Hb), hematocrit (Hct),
or RBC count. It is a common condition that can be caused by inadequate RBC production, excessive RBC destruction, or blood loss. The most common cause is iron
deficiency. Clinical features, if present, are mostly nonspecific and may include fatigue, dyspnea, conjunctival pallor, and tachycardia. Once anemia has been established,
the mean corpuscular volume (MCV) should be checked to distinguish between microcytic, normocytic, and macrocytic anemia and to determine the next diagnostic
steps. Reticulocyte count can also be used to evaluate the bone marrow response. Treatment depends on the form of anemia and underlying condition. Acute and/or
severe cases of anemia may require transfusion of packed red blood cells.

See “Basics of hematology,” “Transfusion,” and “Iron deficiency anemia” for more information.

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Definition

Definition: a decrease in the absolute number of circulating RBCs; exact cutoffs vary from source to source. 
WHO criteria for anemia [1]
Men: Hb < 13 g/dL
Women: Hb < 12 g/dL
Children
6–59 months: < 11 g/dL
5–11 years: < 11.5 g/dL
12–14 years: < 12.0 g/dL
Revised WHO/National Cancer Institute [2] 
Men: Hb < 14 g/dL
Women: Hb < 12 g/dL
American Society of Hematology [3]
Men: Hb < 13.5 g/dL
Women: Hb < 12 g/dL
US National Health and Nutrition Examination Survey: children aged 12–35 months: Hb < 11 g/dL

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Classification

Anemia may be classified into several subtypes based on the following methods:

RBC size and morphology [4]

The most widely used classification

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Classification of anemia by morphology

Microcytic anemia Normocytic anemia Macrocytic anemia

MCV (fL) < 80 80–100 > 100

Insufficient nucleus maturation relative to cytoplasm expansion due to

Decreased blood volume and/or
Mechanism Insufficient hemoglobin production Defective DNA synthesis
decreased erythropoiesis
Defective DNA repair

Hemolytic anemia
Intrinsic defects: e.g., hemoglobinopathies,
Megaloblastic anemia: impaired DNA synthesis and/or repair
Defective heme synthesis: e.g., IDA, lead poisoning enzyme deficiencies
Etiology of with hypersegmented neutrophils (e.g., Vitamin B12 or folate deficiency)
Defective globin chain (↓ Globin → ↓ hemoglobin → ↓ MCV): Extrinsic defects: e.g., AIHA, MAHA,
anemia Nonmegaloblastic anemia: normal DNA
e.g., thalassemia Nonhemolytic anemia: e.g., blood
synthesis without hypersegmented neutrophils (e.g., liver disease)
loss, aplastic anemia, anemia of chronic
disease

Both iron deficiency anemia and anemia of chronic disease can manifest with normocytic anemia in the initial phase and microcytic anemia later on.

Bone marrow failure (e.g., due to myeloproliferative malignancy, myelodysplastic syndrome) can manifest with microcytic, normocytic, or macrocytic
anemia.

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Severity  [1]
Mild anemia
Hb level: below normal range based on age and sex, but > 10–11 g/dL 
Presentation: usually asymptomatic; clinical features of anemia may be present
Moderate anemia
Hb level: ∼ 7–10.9 g/dL 
Presentation: clinical features of anemia may or may not be present.
Severe anemia
Hb level: ∼ 7–8 g/dL 
Presentation: clinical features of anemia typically present; hemodynamic compromise may be present.

Other classifications
Time course: acute vs. chronic
Inheritance: inherited vs. acquired
Etiology: primary vs. secondary
RBC proliferation: hypoproliferative (decreased RBC production) vs. hyperproliferative (increased RBC destruction or blood loss)

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Etiology

Microcytic anemia
Defective heme synthesis
Iron deficiency anemia (IDA): the most common
Lead poisoning 
Anemia of chronic disease (late phase)
Sideroblastic anemia
Defective globin chain: Thalassemia

The causes of microcytic anemia can be remembered with IRON LAST: IRON deficiency, Lead poisoning, Anemia of chronic disease, Sideroblastic

anemia, Thalassemia.

Normocytic anemia

Hemolytic anemia
Intrinsic defects
Hemoglobinopathies
Sickle cell anemia
HbC disease
Enzyme deficiencies
Pyruvate kinase deficiency
G6PD deficiency
Membrane defects
Paroxysmal nocturnal hemoglobinuria
Hereditary spherocytosis
Extrinsic defects
Autoimmune hemolytic anemia
Microangiopathic hemolytic anemia
Macroangiopathic hemolytic anemia
Infections
Mechanical destruction 

Nonhemolytic normocytic anemia
Blood loss
Aplastic anemia
Anemia of chronic kidney disease
Iron deficiency anemia (early phase)
Anemia of chronic disease (early phase)
Dilutional anemia of pregnancy  [5]

Macrocytic anemia

Megaloblastic anemia 
Vitamin B12 deficiency 
Folate deficiency 
Medications
Phenytoin 
Sulfa drugs
Trimethoprim 
Hydroxyurea
MTX 
6-mercaptopurine 
Fanconi anemia 
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Orotic aciduria

Nonmegaloblastic anemia
Liver disease 
Alcohol use 
Diamond-Blackfan anemia
Myelodysplastic syndrome
Multiple myeloma
Hypothyroidism

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Clinical features

Clinical features of anemia

Asymptomatic 
Exertional dyspnea and fatigue
Worsening of angina pectoris 
Pallor (e.g., on mucous membranes, conjunctivae)
Growth impairment (chronic anemia)

Accompanying features
Vary depending on underlying etiology

Clinical features of shock (if anemia is acute)

Features of IDA: pica (craving for ice or dirt), brittle nails, angular cheilitis, atrophic glossitis
Features of megaloblastic anemia: oral sores, mucosal bleeding, paresthesias, ataxia
Clinical features of hemolysis
Signs of hemorrhage: e.g., GI bleeding, menorrhagia (See also “Classification of hemorrhagic shock.”)
Features of hyperdynamic state
Bounding pulses
Tachycardia/palpitations
Flow murmur
Pulsatile sound in the ear
Possibly heart failure (anemia-induced heart failure)
Features of extramedullary hematopoiesis may be present in certain severe, chronic forms of anemia (e.g., thalassemia, myelofibrosis).
Hepatosplenomegaly
Paravertebral mass 
Widening of diploic spaces of the skull 

Tachycardia and narrowed pulse pressure are the first signs of hemodynamically relevant blood loss. [5]

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Diagnostics

CBC with differential

Initial test to confirm and classify anemia.

RBC indices: MCV is the most important parameter in the diagnostic workup of anemia.
Based on MCV, further testing should be performed to determine the underlying cause. 
Abnormalities in platelet count, WBC count, and WBC differential may provide signs of the underlying diagnosis. [6]
Abnormal leukocytes may suggest bone marrow failure or bone marrow malignancy (e.g., aplastic anemia, leukemia, myelodysplastic).
Pancytopenia can result from several etiologies (e.g., peripheral cell destruction or sequestration in hypersplenism, aplastic anemia, infection).

Microcytic anemia (MCV < 80 fL) [6][7]

Iron studies: initial investigation for microcytic anemia 
↓ Ferritin OR normal/↑ ferritin and ↑ TIBC: iron deficiency anemia (see diagnosis of iron deficiency anemia) 
Normal/↑ ferritin and ↓ TIBC: anemia of chronic disease [8]
Serum iron levels are decreased in iron deficiency anemia and anemia of chronic disease.
Peripheral blood smear (PBS), reticulocyte count, RDW: not routinely required to evaluate microcytic anemia because findings are often nonspecific 
PBS findings may suggest a specific etiology. 
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Reticulocyte count
Low reticulocyte count (< 2%): iron deficiency anemia, thalassemia trait, anemia of chronic disease, sideroblastic anemia, and lead poisoning
High reticulocyte count (> 2%): thalassemia
RDW: typically high in iron deficiency anemia and sideroblastic anemia
Hemoglobin electrophoresis: obtain if serum iron levels, TIBC, and TfS are normal or elevated
Normal hemoglobin A2: sideroblastic anemia, α-thalassemia trait
Increased hemoglobin A2: β-thalassemia trait
Other hemoglobinopathies (e.g., hemoglobin E, hemoglobin C)
Bone marrow biopsy: consider if the following are identified [7]
Ringed sideroblasts on PBS (see sideroblastic anemia, myelodysplastic syndromes)
Unexplained thrombocytopenia, leukocytopenia, or pancytopenia
Numerous immature forms of blood cells on CBC and/or PBS
Serum lead level: consider in patients with basophilic stippling but no ringed sideroblasts on PBS (see lead poisoning)

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Serum laboratory findings in microcytic anemia

Transferrin
Red cell distribution width
Iron Ferritin saturation Transferrin or TIBC Reticulocyte count

(RDW)
(TfS)

Iron deficiency ↓ ↓ ↓ ↑ ↓ ↑

Anemia of chronic disease ↓ ↑ Normal to ↓ ↓ ↓ Normal

Thalassemia Normal to ↑* Normal to ↑* Normal to ↑* Normal to ↓* ↑ Normal (occasionally ↑)

Sideroblastic anemia ↑ ↑ ↑ ↓ ↓ ↑

Pregnancy or use of oral contraceptive pills Normal to ↓ Normal ↓ ↑ Normal Normal

* If there is iron overload (e.g., due to multiple transfusions, ineffective erythropoiesis, increased GI iron absorption)

Iron deficiency anemia and thalassemia trait are the most common causes of microcytic anemia. [7]

Basophilic stippling on peripheral blood smear suggests lead poisoning or sideroblastic anemia. Because ringed sideroblasts are not usually seen in lead
poisoning, they can help to distinguish between this condition and sideroblastic anemia.

While decreased ferritin confirms the diagnosis of iron deficiency anemia, elevated serum ferritin does not rule it out.

Macrocytic anemia (MCV > 100 fL) [6][9][10][11]

Peripheral blood smear (PBS): initial investigation for macrocytic anemia to look for megaloblastic changes (hypersegmented neutrophils)
Hypersegmented neutrophils (> 5 lobes): megaloblastic anemia 
No hypersegmented neutrophils: nonmegaloblastic anemia

Evaluation of megaloblastic macrocytic anemia

Vitamin B12 and folate levels: obtain in all patients with megaloblastic changes on PBS. [12][13]
Vitamin B12 levels < 200 pg/mL: vitamin B12 deficiency (see “Diagnostics” in vitamin B12 deficiency for further workup)
Folate < 2 ng/mL: folate deficiency
Serum homocysteine and methylmalonic acid levels: obtain in patients with borderline serum vitamin B12 and/or folate levels 
Normal methylmalonic acid but ↑ homocysteine levels: folic acid deficiency 
↑ Methylmalonic acid, normal/↑ homocysteine: vitamin B12 deficiency [10]
Bone marrow biopsy: consider if any of the following are present [10]
Normal vitamin B12 and folate levels
Normal methylmalonic acid and homocysteine levels
Unexplained thrombocytopenia, leukocytopenia, or pancytopenia
Numerous immature forms of blood cells on CBC and/or PBS
Additional evaluation: consider urine orotic acid levels if orotic aciduria is suspected (extremely rare) 

Serum methylmalonic acid levels are normal in folic acid deficiency and elevated in vitamin B12 deficiency. Serum homocysteine levels are elevated in
both.

Evaluation of nonmegaloblastic macrocytic anemia [6][10]

Reticulocyte count: Obtain in all patients with nonmegaloblastic macrocytic anemia to evaluate bone marrow response.
Normal/low reticulocyte count (< 2%)
Obtain a detailed drug and alcohol use history.  [10]
Consider TSH, hepatic panel. 

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High reticulocyte count (> 2%) 

Reassess history for evidence of acute or chronic blood loss.
Check hemolysis labs: ↓ haptoglobin, ↑ LDH, ↑ unconjugated bilirubin suggest a hemolytic anemia 
Additional evaluation: consider the following if reticulocyte count and metabolic panels are normal and there is no history of drug/alcohol use
Hemoglobin electrophoresis: ↑ HbF level indicates Diamond-Blackfan anemia
Bone marrow biopsy
Hypercellular marrow with dysplasia of all three cell lines: myelodysplastic syndrome
Hypocellular fat-filled marrow : aplastic anemia
Absent or sparse erythroid precursors: pure red cell aplasia

The most common causes of macrocytosis are chronic alcohol consumption, vitamin B12 and/or folate deficiency, and certain medications. [10]

Normocytic anemia (MCV 80–100 fL) [6][9][11][14]

Reticulocyte count: in all patients with normocytic anemia to evaluate bone marrow response
Normal/low reticulocyte count (< 2%) indicates ineffective or decreased RBC production (hypoproliferative anemia)
Iron studies: to evaluate for iron deficiency anemia and/or anemia of chronic disease  (see microcytic anemia)
Vitamin B12 and folate levels  (see megaloblastic macrocytic anemia)
Basic metabolic panel (BMP), LFTs, thyroid studies: if iron studies and vitamin B12 and folate levels are normal  [6]
Serum erythropoietin levels: consider if BUN and/or creatinine levels are abnormal  [15]
High reticulocyte count (> 2%)  [11]
Reassess history for evidence of acute or chronic blood loss.
Check hemolysis labs: ↓ haptoglobin, ↑ LDH, and ↑ unconjugated bilirubin suggest a hemolytic anemia 
Bone marrow aspirate and biopsy: consider in hypoproliferative anemia with normal nutritional assays and metabolic panels [6]

Additional diagnostics
Bone marrow biopsy: manual examination of bone marrow aspirate sample under a microscope
Rarely used in the workup of anemia 
Indications include pancytopenia and/or abnormal cells on the CBC or peripheral blood smear (e.g., blasts)
Prussian blue staining if sideroblastic anemia is suspected (see above) 
Can be used to diagnose:
Aplastic anemia 
Myelodysplastic syndromes
Myeloproliferative neoplasm
Malignant invasion of the bone marrow
Imaging: not routinely indicated for the workup of anemia unless bleeding is suspected
Consider endoscopy and/or colonoscopy in patients with anemia and positive FOBT.
Consider abdominal ultrasound to evaluate for hypersplenism, liver disease, or renal disease. 
Consider CT and/or PET scan if malignancy is suspected.

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Treatment

Identify and treat the underlying causes of anemia

Blood transfusion: See “Indications for pRBC transfusion” for details. [16][17][18]
Severe anemia in any patient: e.g., Hb ≤ 7 g/dL; or Hb ≤ 8 g/dL in patients with perioperative or cardiac risk factors
Moderate anemia in high-risk or symptomatic patients. 
Consider bone marrow transplantation in select cases (e.g., aplastic anemia).

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Aplastic anemia

Description
Pancytopenia caused by bone marrow insufficiency [20]
Should not be confused with aplastic crisis, a condition in which erythropoiesis is temporarily suppressed (e.g., due to parvovirus B19 infection in patients with hemolytic
anemias)
Etiology
Idiopathic in > 50% of cases
Possibly immune-mediated
May follow acute hepatitis (hepatitis-associated aplastic anemia)
Medication side effects: carbamazepine, methimazole, NSAIDs, chloramphenicol, propylthiouracil, sulfa drugs, cytostatic drugs (esp. alkylating
agents and antimetabolites) 
Toxins: benzene, cleaning solvents, insecticides, toluene
Ionizing radiation
Viruses: HBV, EBV, CMV, HIV
Fanconi anemia  [21][22]

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Hereditary autosomal recessive disorder due to a DNA crosslink repair defect resulting in bone marrow failure

Skeletal and organ abnormalities: short stature, hypo- and hyperpigmentation, cafe-au-lait spots, microcephaly, developmental delay, thumb and
forearm malformations, kidney, GI, heart, eye, and ear abnormalities
Laboratory tests show pancytopenia and normocytic or macrocytic anemia.
∼ 50% of patients with Fanconi anemia will develop acute myeloid leukemia or myelodysplastic syndromes in early adulthood. [23]
Clinical features
Fatigue, malaise
Pallor
Purpura, petechiae, mucosal bleeding
Infection
Diagnostics
CBC:
Pancytopenia (in contrast to aplastic crisis characterized by anemia only)
Normocytic or macrocytic anemia
Reticulocyte count: low
EPO level: high
Bone marrow biopsy findings
Hypocellular fat-filled marrow (dry bone marrow tap) 
RBCs normal morphology
Treatment
Cessation of the causative agent
Supportive therapy
Treatment of infections
Blood transfusion
Platelet transfusion
Bone marrow stimulants (e.g., GM-CSF, eltrombopag)
Immunosuppressive therapy 
Cyclosporine
Antithymocyte globulin (ATG)
Tacrolimus
Alemtuzumab 
Consider hematopoietic cell transplantation (HCT) in young patients. [24]

Agents that can cause aplastic anemia: Can't Make New Blood Cells Properly

= Carbamazepine, Methimazole, NSAIDs, Benzenes, Chloramphenicol, Propylthiouracil

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Anemia of chronic disease

Description: anemia due to chronic inflammation

Epidemiology: second most common anemia [25] 
Pathophysiology: inflammation → increase in cytokines (esp. IL-6) and hepcidin → results in the outcomes listed below:
Reduced iron release from macrophages in the reticuloendothelial system and reduced intestinal iron absorption → reduced iron available systemically
Reduced response (of production) to erythropoietin (EPO) and relative reduction of EPO levels → reduced RBC synthesis
Reduced erythrocyte survival and lifespan
Etiology
Inflammation (e.g., rheumatoid arthritis, systemic lupus erythematosus)
Malignancy (e.g., lung cancer, breast cancer, lymphoma)
Chronic infections (e.g., tuberculosis)
Diagnostics
CBC: normocytic anemia (early phase) → microcytic anemia (later phase)
Low iron
Low iron saturation
Low total iron binding capacity (TIBC)
High serum ferritin
Low reticulocyte count
Treatment:
Treat the underlying cause
Blood transfusion if required (see transfusion for indications for blood transfusion)
EPO in chronic incurable diseases (e.g., chronic kidney disease)

References:[26]

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Sideroblastic anemia

Description: anemia caused by defective heme metabolism, which leads to iron trapping inside the mitochondria [27]

Etiology
Inherited: X-linked sideroblastic anemia due to a δ-ALA-synthase gene defect
Acquired
Vitamin B6 deficiency
Lead poisoning 
Alcohol use disorder
Drugs (e.g., chloramphenicol, isoniazid , linezolid)
Copper deficiency
Myelodysplastic syndrome
Malignancy
Diagnostics
CBC: microcytic anemia
Serum iron studies
High ferritin
High iron 
High transferrin saturation
Normal/low TIBC
Peripheral blood smear
Basophilic stippling of RBCs 
Normocytes/macrocytes (more common in acquired etiologies)
Prussian blue staining of bone marrow: ringed sideroblasts 
Treatment
Cessation of the offending agent
Pyridoxine (B6) supplementation (a cofactor for δ-ALA synthase)

References: [28]

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Pure red cell aplasia

General
Description: normocytic, normochromic anemia characterized by a severe reduction in circulating reticulocytes and marked reduction or absence of erythroid precursors
in the bone marrow [29]
Pathophysiology: thought to be related to abnormal T-cell function and IgG antibodies that target erythroblasts and erythropoietin 
Etiology
Acquired
Most often idiopathic
Possible associated conditions
Thymoma
Myelodysplastic syndrome
Adverse drugs effects (e.g., from phenytoin, chloramphenicol)
Parvovirus B19 infection
Autoimmune disorders (e.g., type 1 diabetes, thyroiditis, rheumatoid arthritis)
Congenital: Diamond-Blackfan anemia (DBA): see below
Diagnostics
Low reticulocyte count
Bone marrow biopsy shows marked reduction or absence of erythroid precursors.
Treatment
Treatment of the underlying cause (e.g., cessation of possible offending agents, thymectomy)
Red blood cell transfusion for symptomatic patients
Immunosuppressive and/or cytotoxic agents (e.g., glucocorticoids, cyclosporine, cyclophosphamide)

Diamond-Blackfan anemia [30]
Description
Intrinsic defect of erythroid progenitor cells → ↑ apoptosis
Usually autosomal dominant inheritance or associated with impaired ribosome synthesis mutations
Rapid onset of macrocytic (nonmegaloblastic) anemia in infancy (usually diagnosed within the first year of life)
Additional clinical features: physical abnormalities manifest in ∼50% of affected individuals
Fatigue, poor feeding
Short stature, webbed neck
Upper extremity malformations (e.g., triphalangeal thumbs) 
Microcephaly, micrognathia
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Hypertelorism, flat nasal bridge, cleft palate

Congenital cataracts or glaucoma
Atrial and ventricular septal defects
Diagnostics
Electrophoresis
Elevated HbF levels
Low total Hb levels
Specific laboratory findings
Elevated erythrocyte adenosine deaminase levels (eADA)
Increased expression of i antigen in RBCs
Treatment [31]
Corticosteroids (first-line treatment)
Chronic red cell transfusions: individuals who do not respond to corticosteroids
Hematopoietic stem cell transplantation
Complications
Increased risk of malignancy: acute myelogenous leukemia, myelodysplastic syndrome, solid tumors (e.g., colon cancer, osteogenic sarcoma)
Treatment-associated complications: iron overload due to repeated transfusions, corticosteroid-induced hyperglycemia
Endocrine dysfunction: adrenal insufficiency, hypogonadism, vitamin D deficiency

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Acute blood loss anemia

Description: acute anemia due to blood loss 

Etiology: any cause of bleeding can cause acute blood loss anemia 
Clinical features: May be asymptomatic or have symptoms of anemia (see above)  [14]
Diagnostics [6][14]
Laboratory studies
CBC: ↓ or normal Hb 
Usually normocytic anemia
Compare to prior studies, if available. 
Check platelets for thrombocytopenia.
Type and screen with crossmatching
Coagulation panel
Blood for potential further studies based on CBC should be drawn before blood transfusion (draw and hold). 
Imaging: Modality depends on the pretest probability of the suspected site of bleeding.
CT soft tissue if there is concern for intramuscular bleeding 
CT abdomen and pelvis if there is concern for intraabdominal bleeding 
CXR and/or CT chest if there is concern for a pulmonary source (see “Diagnostics” in pleural effusion and in hemothorax) 
Endoscopy and/or colonoscopy if there is concern for a GI bleed (see ''Diagnostics'' in gastrointestinal bleeding) 
Treatment
Identify and treat the underlying cause.
Emergency blood transfusion

Hemoglobin and hematocrit levels can initially be normal in acute hemorrhage, even if there has already been significant blood loss. They will eventually
decrease after plasma volume has been restored either spontaneously or via IV fluid resuscitation.

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Related One-Minute Telegram

One-Minute Telegram 31-2021-1/3: Bariatric surgery associated with very high risk of long-term anemia
Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

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2020 AGA Clinical Practice Guidelines on the Gastrointestinal Evaluation of Iron Deficiency Anemia

References

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