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What is the pathophysiology of anemias of chronic disease?

Neoplasms and sepsis create Tumor Necrosis Factor and Interferon-Beta. TNF decreases Fe bioavailability and erythropoietin. INF-b inhibits erythroid proliferation. Chronic infection/inflammation produces Interleukin-1 and Interferon-gamma. IL1 acts like TNF, while INF-g acts like INF-b.


What are six conditions associated with anemia of chronic disease?

Chronic infections, chronic inflammatory diseases (rheumatoid diseases), malignancies (carcinoma, Hodgkin's disease, etc.), lead intoxication, renal insufficiency, and endocrine disorders (thyroid disorders, adrenal insufficiency).


What is the pathophysiology of anemia in lead intoxication?

Lead inhibits protoporphyrin synthesis and iron availability.   This leads to decreased heme group and hemoglobin formation.


What is the pathophysiology of anemia of renal insufficiency?

Loss of kidney function results in loss of erythropoietin, which decreases erythroid production and thus RBC production.


What are the clinical features of anemias of chronic infection, inflammation, or malignancies?

Dependent on specific underlying disease.  May include fever, arthralgias, arthritis, and fatigue.   For infections, symptoms and signs relate to the location.


What are the laboratory tests for anemias of chronic infection, inflammation, or malignancies?

Mild-moderate anemia (HGB 8-12g/dl) Severity proportional to underlying disease.   May be normochromic/normocytic or microcytic with some hypochromia.   Decreased serum Fe, norm to dec TIBC, norm to inc ferritin, dec EPO for HCT, dec Retic count.


What are the clinical features of anemia of lead intoxication?

Personality changes, irritability, headache, weakness, wt loss, abdominal pain, vomiting, presenting with insidious nature (insidious means no clear starting time of symptoms, developing over days or weeks).


What are laboratory test findings for lead poisoning anemia?

Mild to moderate anemia.  Decreased retic count.   Microcytosis and mild hypochromia.   Basophilic stippling.   Inc protoporphyrin.   May see concurrent iron deficiency confounding Dx.  Inc lead levels.


What laboratory finding distiguishes anemias of iron deficiency from anemias of chronic infection/inflammation?

Transferrin (TIBC) levels in iron deficiency go up.   In chronic infection/inflammation TIBC levels stay normal or go down.   Always test serum Fe and TIBC together. This is because in chronic infection, iron stores are bound inside cells, mostly due to hepcidin, thus the serum iron is low but transferritin levels are normal.


What is protoporphyrin?

The chemical structure into which iron atoms settle to then form hemoglobin.   It is generally increased in conditions of low iron because it is still being produced at a regular rate, but not converted to heme.


What are clinical features of anemia of renal insufficiency?

S/Sx may be integrated with those of renal dysfunciton: fatigue, pallor, decreased exercise tolerance, dyspnea, tachypnea, anemia may have other contributing factors.


What are laboratory test findings of anemia of renal insufficiency?

Usually don't see anemia until creatinine clearance of <40% of normal, or serum creatinine >2-2.5mg/dl.   Moderate to severe anemia.   HGB 5-9 g/dl.   Normochromic, normocytic.   Dec retic count, occassionaly abnormal morphology.   EPO deficiency, dec production.


What are the clinical features of anemia of endocrine disorder?

Hyper/hypothyroidism or adrenal insufficiency.   Hyper or hypoactivity, weight gain or loss, systematic symptoms, skin, nail, hair changes in hyper or hypothyroidism help suggest etiology.   Nausea, vomiting, dehydration, weakness, and circulatory collapse suggest adrenal insufficiency.


What are the laboratory test findings of anemias of endocrine disorders?

All endocrine disorder anemias have decreased reticulocyte count and index.   Hypothyroidism:  mild anemia, most normochromic, normocytic (but may be micro or macrocytic).   Hyperthyroidism: usually normocytic may be microcytic.   Adrenal: mild anemia, normocytic.


What is the treatment of anemia of chronic inflammation/infection/malignancy?

Treament of underlying disorder and of co-morbidities (iron deficiency).   Sometime with EPO.


What is the treatment for anemias of lead intoxication?

Chelation of lead


What is the treatment of anemias of renal insufficiency?

EPO and treatment of co-morbid conditions (iron def, vitamin def, aluminum intoxication, etc.)


What is the treatment of anemias of endocrine disorder?

Hormone replacement for specifc disorder.   Treatment for comorbidities.


When is treatment by blood transfusion or EPO appropriate?

Blood transfusions are only appropriate when the severity of the anemia is such that cardiovascular decompensation is a possibility.   EPO should only be used when there is an absolute deficiency or when a response to it has been documented.   EPO treatment has been linked with increased strokes.


What are three rarely seen types of anemia?

Sideroblastic anemia (impaired production of protoprophyrin or incorporation of iron).   Low affinity hemoglobin disease (decreased affinity for oxygen, leads to better O2 delivery in tissues).   Protein calorie malnutrition (rare in US, lack of protein and other nutrients).


What influence do folate and B12 deficiencies have on anemia?

Folate and B12 deficiencies profoundly effect the maturation process of red blood cell precursors.  RBC precursors increase in size, arrest in S-phase, and undergo destruction leading to ineffective erythropoiesis in marrow.   Anemia is the most common result, but some cases are also associated with neutropenia or thrombocytopenia.


Where are iron, folate, and B12 absorbed?

Iron is absorbed in the duodenum.  Folate is absorbed in the middle of the jejunum.   B12 is absorbed in the terminal ileum (only if bound to IF intrinsic factor) and transported to the liver bound to transcobalamin II.


What are the causes of B12 deficiency?

95% of the causes of B12 deficiency are related to absorption.   Auto-immune - The body produces antibodies to IF as we age.   Damage to terminal ileum.    IF deficiency, malabsorption, defective transport, and metabolic defects.


What are the causes of folate deficiency?

Dietary insufficiency, malabsorption, drugs and toxins, inborn errors of metabolism, increased demands, increasd loss or metabolism.


What are clinical and lab findings of folate and B12 deficiency?

Both result in megaloblastic anemia.   Folate deficiency progresses rapidly (weeks to months) and is more likely associated with alcohol abuse and malnutrition.   B12 deficiency develops more slowly, more likely associated with malabsorption.


What are some hematological changes (morphological) in folate and B12 deficiency?

Megaloblastic changes evident at any stage of any red or white cell precursor - larger, less mature nucleus, but normal cytoplasm.   Macrocytosis - MCV>97, Ovalocytes, hypersegmented nuclei of neutrophils, retic index <1.0


What is evident in B12 deficiency but not in folate deficiency?

Neurological defects.   May be unreversible.