Transcript File - Hayley Morgan

MNT For
Anemia
By: Hayley Morgan
By: Hayley Morgan
What is Anemia?
 Inability of blood to supply tissues with adequate
oxygen for proper metabolic function.
 Diagnosis made by patient history, physical exam,
signs and symptoms, and hematological laboratory
findings.
 Usually associated with decreased levels of hemoglobin or hematocrit (packed red cell volume) –
Abnormal hemoglobin may give appearance of
anemia (methemoglobin).
 Usually associated with decreased RBCs.
Types of anemia
Iron Deficiency Anemia
Megaloblastic Anemia
Pernicious Anemia
Anemia of Chronic Disease
Aplastic Anemia
Blood Loss Anemia
Fanconi Anemia
Hemolytic Anemia
Sickle Cell Anemia
Thalassemias (Cooley’s Anemia)
Types of Anemia
 Microcytic (<80 fL)
• Iron deficiency
• Thalassemia
• Anemia of chronic disease
 Macrocytic (>100 fL)
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Vitamin B12 deficiency
Folate deficiency
Myelodysplasia
Chemotherapy
Liver disease
Increased reticulocytosis
Myxedema
 Normocytic
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Anemia of chronic disease
Aplasia
Protein-energy malnutrition
Chronic renal failure
Post-hemorrhagic
Iron deficiency
anemia
 Iron Stores
• Humans contain ~2.5g of iron, with 2.0-2.5g circulating as part of heme in
hemoglobin.
• Another ~0.3g found in myoglobin, in heme cytochromes, and in Fe-S
complexes.
• Iron stored in body primarily as protein complexes (ferritin and hemosiderin.)
 Nutritional Iron Balance
 Intake
• Dietary iron intake
• Medicinal iron
• PRBC transfusions
 Excretion
• Gastrointestinal bleeding
• Menses
• Other forms of bleedings
• Loss of epidermal cells for
the skin and gut
Assessment
Signs and Symptoms
• Pale or yellow “sallow” skin
• Unexplained fatigue/ lack of energy
• Shortness of Breathe
• Headaches
• Picophagia, craving ice or clay
Physical Exam
• Cheilosis
• Fissures at the corner of the mouth
• Koilonychia
• Spooning of the
fingernails
Biochemical Findings
• Hypochromic (Low Hemoglobin)
• Microcytic Cells (Low MCV)
• Target Cells (Codocytes)
Treatment
MNT
Other
• Diet: beef, poultry, especially
organ meats. Fish; especially
shellfish, sardines, and
anchovies. Leafy greens like
the cabbage family, broccoli,
kale, and spinach. Legumes,
and iron enriched pastas.
• IV Iron; patient can not
tolerate oral
supplementation, severe iron
deficiency, chronic bleeding,
and patients receiving
supplemental
erythropoietin.
• Iron supplements: 50-200mg
of inorganic ferrous form
supplement. Vitamin C
supplement can increase
absorption.
• Blood Transfusions
Megaloblastic
Anemia
• Due to impaired DNA synthesis
• Affects cells primarily having relatively rapid turnover,
especially hematopoietic precursors and
gastrointestinal epithelial cells
• Cell division is sluggish, but cytoplasmic development
progresses normally, so megaloblastic cells tend to be
large, with an increased ratio of RNA to DNA.
• Megaloblastic erythroid progenitors tend to be
destroyed in the marrow
• Marrow cellularity is often increased but production of
red blood cells (RBC) is decreased
Assessment
• Vitamin B12 Deficiency
• Inadequate intake: vegans (rare)
• Malabsorption
• Defective release of cobalamin from food
• Gastric achlorhydria
• Partial gastrectomy
• Drugs that block acid secretion
• Inadequate production of intrinsic factor (IF)
• Pernicious anemia
• Total gastrectomy
• Disorders of terminal ileum
• Sprue
• Regional enteritis
• Intestinal resection
• Competition for cobalamin
• Fish tapeworm (Diphyllobothrium latum)
• Bacteria: "blind loop" syndrome
• Drugs: p-aminosalicylic acid, colchicine, neomycin
Assessment
• Hematologic
• High MCV
• High MCH
• Low RBC count
• Gastrointestinal
• Glossitis
• Anorexia
• Diarrhea
• Neurologic (found in 3/4th of individuals with pernicious anemia)
• Numbness and paresthesia in the extremities, Weakness, Ataxia
• Sphincter disturbances
• Disturbances of mentation
•
Mild irritability and forgetfulness to severe dementia or frank psychosis.
• Demyelination, Axonal degeneration, and then Neuronal death
•
Last stage is irreversible
Megaloblastic
Anemia
• Macrocytic RBC
• Hypersegmented Neutrophil
Vitamin b12
absorption
• Oral Phase
Vitamin b12
absorption
• Gastric Phase
Vitamin B12
absorption
• Intestinal Phase
Vitamin b12
deficiency
• Any interruption along this path can result in
cobalamin deficiency
• Gastrectomy results in low production of IF
• Terminal ileal resection (>100 cm), decreases the site
absorption of B12- IF complex
Pernicious anemia
• Most common cause of cobalamin deficiency
• Caused by the absence of IF
• Atrophy of the mucosa
• Autoimmune destruction of parietal cells
• Seen mostly in the elderly, average age of 60
Diagnosis of vitamin b12
deficiency
• Macrocytosis
• Peripheral blood smear
• Cobalamin levels
• Elevated serum methylmalonic acid and homocysteine
levels
• Schilling Test (rarely used)
Treatment of vitamin b12
deficiency
• Replacement therapy
• Parenteral treatment given weekly intramuscularly for 8
weeks, followed by intramuscularly every month for the rest
of the patients life
• Daily oral replacement therapy
Causes of megaloblastic
anemia
• Folate Deficiency
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Inadequate intake; unbalanced diet (common in alcoholics, teens, some infants)
Increased requirements
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Pregnancy
Infancy
Malignancy
Increased hematopoiesis (chronic hemolytic anemias)
Chronic exfoliative skin disorders
Hemodialysis
• Malabsorption
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Sprue – Celiac Disease
Drugs; Phenytoin, barbiturates, ethanol
• Impaired metabolism
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Inhibitors of dihydrofolate reductase; methotrexate, pyrimethamine,
triamterene, pentamidine, trimethoprim
Alcohol
Rare enzyme deficiencies; dihydrofolate reductase, others
Assessment
• More often malnourished than those with B12
deficiency
• Gastrointestinal manifestations
• More widespread and more severe than those of pernicious
anemia
• Diarrhea is often present
• Cheilosis
• Glossitis
• Neurologic abnormalities do not occur
Stages of folate
deficiency
1. Negative folate balance (decreased serum folate)
2. Decreased RBC folate levels and hypersegmented
neutrophils
3. Macroovalocytes, increased MCV, and decreased
hemoglobin
Diagnosis of folate
deficiency
• Peripheral blood and bone marrow biopsy look exactly
like B12 deficiency
• Plasma folate <3 ng/ml- fluctuates with recent dietary
intake
• RBC folate- more reliable of tissue stores <140 ng/ml
• Only increased serum homocysteine levels but NOT
serum methylmalonic acid levels
Treatment of folate
deficiency
• Replacement therapy
• Folate prophylaxis
• Women planning pregnancy are advised to take 400g folic
acid daily before conception and until 12 weeks of
pregnancy to prevent neural-tube defects (5mg/day for
women with a previous affected pregnancy)
• Folate fortification of cereal grains at 1-4 mg/kg has been
made mandatory in the USA as an additional method of
improving the folate status of the population
• Folate is also recommended in other states of increased
demand such as long-term hemodialysis and chronic
hemolytic disorders
Non-effective treatment of
pernicious anemia with folate
• Vitamin B12 deficiency anemia can be temporarily
correct by folate supplementation
• However, this does not correct the neurologic deficits
• Folate “draws” vitamin B12 away from neurologic systems
for RBC production and can exacerbate combined systems
degeneration.
Current research
Anemia of Chronic Disease
CHF, Oncology, & CKD
Anemia of chronic
disease (ACD)
• Most patients suffering from chronic infections, chronic
inflammations, or various malignancies develop a mild to
moderate anemia. This anemia, designated anemia of chronic
disease, is characterized by a low serum iron level, a low to
normal transferrin level, and a high to normal ferritin level.
However, the anemia appears to be caused, not by these changes
in iron metabolism, but, rather, by the effect of a number of
suppressor cytokines. Tissues injured by infections or
inflammation and neoplastic cells release cytokines, such as
interleukin-1, tumor necrosis factor, and interferon gamma,
known to reduce the production of erythropoietin in the kidney
and impair its action in the marrow. As such, the anemia is
probably caused primarily by a reduction in erythropoietingenerated red cell production. Therapeutic trials have revealed
that the anemia is indeed responsive to erythropoietin, and in
most cases, it can be ameliorated by the parental administration
of sufficient amounts of human recombinant erythropoietin.
Erythropoietin
In addition to cleaning the blood, kidneys perform other functions.
One of those functions is producing the hormone erythropoietin
(EPO). Erythropoietin signals bone marrow to produce red blood
cells. As renal disease progresses, the diseased kidneys cannot
produce enough erythropoietin, therefore, not as many red blood
cells are made.
chf
• The Use of Subcutaneous Erythropoietin and
Intravenous Iron for the Treatment of Anemia of
Severe, Resistant Congestive Heart Failure Improves
Cardiac and Renal Function and Functional Cardiac
Class, and Markedly Reduces Hospitalizations
• Journal of the American College of Cardiology
•
Silverberg, Donald S., Dov Wexler, Miriam Blum, Gad Keren, David Sheps, Eyal
Leibovitch, David Brosh, Shlomo Laniado, Doron Schwartz, Tatyana Yachnin,
Itzhak Shapira, Dov Gavish, Ron Baruch, Bella Koifman, Carl Kaplan, Shoshana
Steinbruch, and Adrian Iaina. "The Use of Subcutaneous Erythropoietin and
Intravenous Iron for the Treatment of the Anemia of Severe, Resistant Congestive
Heart Failure Improves Cardiac and Renal Function and Functional Cardiac Class,
and Markedly Reduces Hospitalizations." Journal of the American College of Cardiology
49.7 (2008): 1737-744. Print.
CHF
Objective: The study evaluated the prevalence and severity of anemia in
patients with CHF and the effect of its correction on cardiac and renal function
and hospitalization.
Methods: The prevalence and severity of anemia in patients with CHF was
studied through a retrospective study on 142 patients from a CHF clinic. An
intervention study was performed on 26 of these patients by administering
subcutaneous erythropoietin and iron sufficient to increase the Hb to 12g%.
The doses of CHF medications, except diuretics, were not changed during the
intervention period.
Results: The prevalence of anemia in the 142 patients increased with the
severity of CHF. 79% of 142 patients were found to have anemia. In the
intervention study, the anemia of 26 patients was treated for a mean of 7.2 +/5.5 months. The mean Hb level and mean left ventricular ejection fraction
increased significantly. The mean number of hospitalizations decreased 91.9%
compared with a similar period before the study. The doses of oral and
intravenous furosemide decreased, and the rate of fall of the glomerular
filtration rate slowed with treatment.
Oncology
• Darbepoetin Alfa for the treatment of Anemia in
Patients with Active Cancer not Receiving
Chemotherapy or Radiotherapy
• Smith, Robert E., Matti S. Appro, Heinz Ludwig, Tomas
Pinter, and Martin Smakal. "Darbepoetin Alfa for the
Treatment of Anemia in Patients with Active Cancer Not
Receiving Chemotherapy or Radiotherapy." Journal of
Clinical Oncology 26.7 (2008): 1040-050. Web.
Oncology
Objective: Test the efficacy and safety of synthetic erythropoietin,
Darbepoetin Alfa (DA) for treating patients with active cancer and
anemia not receiving or planning to receive cytotoxic chemotherapy
or radiotherapy.
Methods: Patients with active cancer and anemia not receiving
treatment were enrolled onto a phase III, multicenter, randomized,
placebo-controlled study. Patients received DA or placebo every 4
weeks for 16 weeks, with 2-year follow-up for survival.
oncology
Results: The incidence of transfusions between weeks 5 and 17 was
lower in the DA group but was not statistically significant compared
to placebo group. DA group was associated with an increased
incidence of cardiovascular and thromboembolic events and more
deaths during the initial 16-week treatment period. Long-term
survival data demonstrated statistically significant poorer survival in
patients treated with DA versus placebo.
Conclusion: DA was not associated with statistically significant
reduction in transfusion. Shorter survival with DA. This study does
not support the use of erythropoiesis-stimulating agents for this
group of patients.
Chronic kidney
Disease
• CKD has adverse consequences on almost all body systems. The kidney
participates in erythropoiesis. Anemia is prevalent in CKD with effects on
the cardiovascular system. It is mostly due to erythropoietin deficiency,
inhibition of erythropoiesis by uremic solutes, and reduction of RBC life
span.
• Endogenous erythropoietin dysfunction occurs when GFR falls below 2025 ml/min.
• Treating anemia of CKD is based on correction of iron deficiency and
replacement of decreased erythropoietin production by erythropoietin
stimulating agents (ESA’s)
• Health related quality of life in CKD patients can be improved by treating
anemia. Newly available ESA’s and newly developed epotinbiosimilars
are expected to lead to improvements in the management of CKD
CKD
• Epoetin in the management of anemia associated with
chronic kidney disease, differential pharmacology and
clinical utility
• Davis, Mary-lynn, Jun Wu, Katherine Downton, Emile
Ludman, and Virginia Noxon. "Epoetin in the
Management of Anemia Associated with Chronic
Kidney Disease, Differential Pharmacology and Clinical
Utility." Biologics 8 (2014): 155-67. Web.
CKD
Objective: Effectiveness of ESA’s in patients with renal anemia,
(Renal anemia is cauterized with a Hb level <13.0 g/dL in adult
males and <12.0 g/dL in adult females) secondary to Chronic
Kidney Disease.
Methods: Large scale study referencing previous studies on 165
name brands of ESA’s where the patients were being treated for
renal anemia after iron dosing failed to increased Hb levels.
Results: Dosage of epoetin of 93-97 IU/kg/week to treat anemia
resulted in significant stimulation of erythropoiesis and increased
levels of Hb >11.5g/dL
Conclusion: Patients with symptomatic renal anemia subsequent to
ESRD or CKD of at least stage 3 (est. GFR <60) whose Hb levels
are <10 g/dL should be considered for epoetin therapy.
Case Study 1
• Emma an 18yo female consulted her physician for weakness,
lethargy, and breathlessness. She revealed that she has been
experiencing excessive bleeding with menstruation.
• RBC count 3.5
• Hb 7g/dL
• Hct 30%
• Serum Iron – low
• MCV- low
• MCHC- low
• What type of anemia does Emma most likely have? What are some
physical symptoms she may have upon examination? What would
your recommendation be for nutrition intervention?
Case study 2
• Marg a 65yo female reports about 2 months of tiredness,
feeling faint from “getting up too fast”, and “memory
problems”.
• RBC count- low
• MCV- high
• MCH- high
• MCHC- normal
What type of anemia does Marg have? Are there other tests
that should be ordered? What would you recommend as a
nutrition intervention?
Pes statements
• Discuss
Questions?
•
http://www.hematology.org
•
https://www.nhlbi.nih.gov
•
Hark, Lisa, and Gail Morrison. Medical Nutrition and Disease: A Case-based Approach. Chichester, UK:
Wiley-Blackwell, Print.
•
Nahikian-Nelms, Marcia. Nutrition Therapy and Pathophysiology. Belmont, CA: Wadsworth, Cengage
Learning, 2011. Print.
•
Escott-Stump, Sylvia. Nutrition and Diagnosis-related Care. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins, 2012. Print.
•
Ludwig H, Van Belle S, Barrett-Lee, et al. The European Cancer Anaemia Survey (ECAS): a large,
multinational, prospective survey defining the prevalence, incidence, and treatment of anaemia in
cancer patients. Eur J Cancer 2004;40:2293-2306.
•
Caro JJ, Salas M, Ward A, et al. Anemia as an independent prognostic factor for survival in patients
with cancer: a systematic, quantitative review. Cancer 2002;94:2793-2796.
•
http://content.onlinejacc.org/article.aspx?articleid=1130180
•
Impacts of Recombinant Human Erythropoietin Treatment During Predialysis Periods on the
Progression of Chronic Kidney Disease in a Large-Scale Cohort Study
Thank you!
•
Silverberg, Donald S., Dov Wexler, Miriam Blum, Gad Keren, David Sheps, Eyal Leibovitch,
David Brosh, Shlomo Laniado, Doron Schwartz, Tatyana Yachnin, Itzhak Shapira, Dov
Gavish, Ron Baruch, Bella Koifman, Carl Kaplan, Shoshana Steinbruch, and Adrian Iaina.
"The Use of Subcutaneous Erythropoietin and Intravenous Iron for the Treatment of the
Anemia of Severe, Resistant Congestive Heart Failure Improves Cardiac and Renal Function
and Functional Cardiac Class, and Markedly Reduces Hospitalizations." Journal of the
American College of Cardiology 49.7 (2008): 1737-744. Print.
• Smith, Robert E., Matti S. Appro, Heinz Ludwig, Tomas Pinter, and
Martin Smakal. "Darbepoetin Alfa for the Treatment of Anemia in
Patients with Active Cancer Not Receiving Chemotherapy or
Radiotherapy." Journal of Clinical Oncology 26.7 (2008): 1040-050.
Web.
• Davis, Mary-lynn, Jun Wu, Katherine Downton, Emile Ludman, and
Virginia Noxon. "Epoetin in the Management of Anemia Associated
with Chronic Kidney Disease, Differential Pharmacology and
Clinical Utility." Biologics 8 (2014): 155-67. Web.