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Fall 2014 > MNT — Exam #2 : Part 1 > Flashcards

MNT — Exam #2 : Part 1 Flashcards

1
Q

What is Anemia?

A
  • Deficiency in size or number of RBC’s or the amount of Hgb contained in RBC;
  • “abnormal blood constitutes resulting from various etiologies; anemia is a symptom and is often a result of the decrement in blood constitutes, although some forms of elevated blood components that are non-functional may be referred to as anemia”
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2
Q

What is the current trend for Anemia in the US?

A
  • Had been increasing, but finally leveled of and appears to be in a recent decline throughout the population;
  • Proportion of anemic elderly is increasing!
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3
Q

Who is at most risk for developing Anemia in the US?

A
  1. Children under 2 yrs;
  2. Menstruating females;
  3. Pregnant females;
  4. Frail elderly;
  5. Female athletes;
  6. Obese children
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4
Q

Why are young children at risk?

A
  • Mostly in the US between the ages of 1-2 (7%);
  • Mostly related to poor intake and/or absorption ;
  • Maternal milk contains lactoferrin which increase bioavailability to infants → Human milk and iron-fortified formula have DECREASED infant deficiency
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5
Q

What group has the highest iron deficiency rate in the US?

A

Deficiency in the US greatest among women ages 12-49 (12%)

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6
Q

Why are Pregnant Females at risk for anemia?

A
  • Needs are much greater during pregnancy;

- Fetus takes precedence over mother and thus maternal stores are quickly lost

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7
Q

What happens if a pregnancy anemia goes untreated?

A

Maternal problems range from pre-eclampsia to pica during pregnancy, and several post-partum issues such as depression, cognitive disturbances, and gallstones ;

  • Deficiency can Lead to premature birth, LBW, and other developmental disorders;
  • Iron supps and multi-nutrients are highly common during pregnancy
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8
Q

Why is iron deficiency increasing in the elderly?

A
  • Becoming increasingly common and rapidly increasing as more people are reaching the ages of 85 and beyond and naturally developing anemia → atypical presentation of anemia for this group;
  • “Graying of America” (aging of the population) will most likely create a much higher percent found among older, poorer, minority women deeming them a high-risk group
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9
Q

Why is anemia common in Female Athletes?

A

RBC losses with consistent, continuous high impact landings coupled with menstruation losses, poor oral intake of iron and increased needs fro oxygen carrying capacity with sports

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10
Q

Why is iron deficiency seen in Obese Children?

A

Due to IRON-POOR food choices that are high in fat but lack micronutrients are though to be the main cause → Lots of empty calorie consumption ;

  • Several other nutrient are also involved in heme-synthesis, so it might be due to a combo of deficiencies and not just a singular deficiency of iron itself ;
  • NHANES – children who are overweight are TWICE as likely to be iron deficient as those of a healthy weight;
  • Increased levels of body fat = increased levels of inflammatory cytokines which have been associated with anemia of chronic disease (ACD)
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11
Q

What is Hepcidin?

A
  • Hormone that regulates iron homeostasis;
  • -Iron def. with obesity with T2DM and metabolic syndrome is also studied with regard to hepcidin and/or ACD → Comorbid conditions!
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12
Q

Who is most at risk Worldwide for iron deficiency anemia?

A
  • Iron-deficiency anemia varies the most by SES → those in poor countries, and poor people in wealthy areas are much likely do develop deficiency;
  • Incidence and prevalence much higher among African American and Hispanic women than White women
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13
Q

What is Hemoglobin (g/dL)?

A

Concentration of oxygen carrying protein in RBC → the four-pyrrole ring compound in RBCs that contain iron centers and responsible for the transport of OXYGEN

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14
Q

What is Hematocrit (%)?

A
  • Measures the percentage of whole blood volume that is made up of RBC ; Dependent on the number of RBC and size;
  • Packed RBC volume expressed as a percentage of whole blood upon centrifugation
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15
Q

What is Serum Iron?

A

Represents the amount of iron in the BLOOD where it is bound to transferrin and available for RBC production

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16
Q

What is MCV (Mean Corpuscular Volume) (mcg/m3)?

A

Measures the average size of RBCs

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17
Q

What is MCHC (Mean corpuscular hemoglobin concentration)?

A

–

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18
Q

What is Serum Ferritin (mcg/L)?

A

-Iron STORAGE within the blood

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19
Q

What is Serum transferrin (g/L)?

A

-Available to TRANSPORT Iron throughout the blood

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20
Q

What is Total Iron binding capacity (TIBC) (mcg/dl)?

A

The capacity for the binding of iron by blood constitutes;

-A surrogate measure for TRANSFERRIN, since it binds most of the body’s iron

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21
Q

What is Transferrin Saturation (%)?

A

-Indicates extent to which transferrin is saturated with iron represents the amount of iron available to the tissues;
-(Serum iron ÷ TIBC) x 100 Normal: 20% – 50%;
—Stages I & II: Low – normal
— Stages III & IV: <16%

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22
Q

What is Soluble serum transferrin receptors (STFR’s)?

A

-INCREASE with iron deficiency;
-Transferrin binds iron and carries to bone marrow, epithelial cells (storage) and placenta.;
-Transferrin molecules generated on surface of RBC in response to need for iron.
→ With iron DEFICIENCY STFR’s break off surface of cell and float in serum
→ INCREASED levels indicate increased iron deficiency.

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23
Q

What are the Etiologies for Iron Def?

A

Lots of variation!;
-Can be from blood loss, inadequate iron intake, increased needs (pregnancy, athletes, during menstruation, etc.) poor absorption, excess or contaminates

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24
Q

What are the clinical manifestations of iron def?

A
  • Cold extremities;
  • Pallor;
  • Fatigue;
  • Malaise;
  • Tachycardia (heart rate > 100 bpm)
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25
Q

What are the classification of Anemia based on?

A
  1. Cell size;

2. Hemoglobin content

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26
Q

What are the variations in cell size?

A
  1. Macrocytic – abnormally LARGE cells;
  2. Normocytic – normal sized cells ;
  3. Microcytic – abnormally SMALL cells
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27
Q

What are the variations in Hemoglobin content?

A
  1. Hypochromic – abnormally PALE in color upon visual inspection under a microscope → LOW hemoglobin ;
  2. Normochromic – normal coloration
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28
Q

What are the standard treatments for iron def?

A
  • Continued iron-dense, nutrient-dense dietary intake, supps, and correction of underlying conditions causing deficit;;
  • Uncomplicated deficiencies have up-regulated proteins for enhancing iron absorption in the GI tract = transferring/hepcidin;
  • **Increasing nutrient density is the BEST option
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29
Q

What is Hepcidin?

A
  • Hepcidin (hormone/protein) regulates iron status and RBC needs per the SI to manage absorption;
  • Feedback mechanism allows increased absorption of heme and non-heme iron
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30
Q

What causes Nutritional Anemias?

A

Microcytic, macrocytic, hemolytic =
-Many anemias are caused by LACK OF NUTRIENTS required for normal erythrocyte (RBC) formation → Inability to make RBCs, which are MADE from Iron to CARRY Oxygen

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31
Q

What are the types of Nutritional Anemias?

A
  • Iron;
  • Vitamin B12;
  • Folic Acid;
  • Pyridoxine;
  • Vitamin C;
  • Protein;
  • Copper
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32
Q

What are the MACROCYTIC Anemia Deficiencies?

A
  • Cyanocabalamin (B12);
  • Folate;
  • Thiamin;
  • Pyridoxine
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33
Q

What are the MICROCYTIC Anemia Deficiencies?

A
  • Protein;
  • Iron;
  • Ascorbate;
  • Vitamin A;
  • Pyridoxine;
  • Copper;
  • Manganese
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34
Q

What are the MICROCYTIC Anemia Toxicities?

A
  • Copper;
  • Zinc;
  • Lead;
  • Cadmium;
  • Other heavy metals
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35
Q

What causes Hemolytic Anemia?

A

-Vit. E deficiency or toxicity

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36
Q

What is the effect of decreased IRON stores on absorption?

A
  • With decreased stores, increased absorption ;
  • → Less you have, the more you absorb!!;
  • If levels are adequate, will not absorb anymore because body does NOT need it
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37
Q

What is the effect of decreased FOLATE and B12 stores on absorption?

A
  • Absorption is NOT increased when stores are decreased;

- Note: adequate folate intake can mask Vitamin B12 deficiency until neuropathy develops

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38
Q

What are the Morphological classifications of anemia?

A
  • Hypochromic OR normochromic;

- Microcytic, normocytic, macrocytic

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39
Q

What defines Hypochromic, Microcytic anemia?

A

(MCV <31) =

  1. Iron Deficiency Anemia (chronic blood loss, inadequate diet/decreased absorption, increased demands) → Continuous loss coupled with low intake ;
  2. Thalassemia (disorder of globin synthesis, inherited);
  3. Pyridoxine responsive anemia
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40
Q

What defines Normochromic, Normocytic anemia?

A

(MCV 82-92; MCHC >30) =

  1. Recent blood loss → Large sudden loss of blood volume;
  2. Overexpansion of blood volume (pregnancy);
  3. Chronic disorders (Renal dx, cirrhosis of liver)
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41
Q

How does CRF and Cirrohosis cause Normochromic, Normocytic anemia?

A
  1. Chronic Renal failure leads to decreased production of Erythropoietin → Less RBCs are then produced leading to iron deficiency anemia
  2. Cirrohosis of Liver – Iron can actually become trapped in the liver and become toxic
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42
Q

What defines Marcocytic anemia?

A

(MCV > 94; MCHC >31) =

  • Megaloblastic – large immature RBCs (Vitamin B12 and Folic Acid deficiency);
  • Can be commonly attributed to chronic alcoholism;
  • Disorders of DNA synthesis
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43
Q

What are the stages of Iron Deficiency Anemia?

A
  • Stage 1: (moderate depletion of iron stores) = NO dysfunction;
  • Stage 2: (Severe depletion of iron stores) = NO dysfunction;
  • Stage 3: (Iron deficiency) = DYSFUNCTION;
  • Stage 4: (Iron deficiency) = DYSFUNCTION and ANEMIA;
  • *Labs are somewhat different in each stage.
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44
Q

What is the Early Dysfunctions seen with iron deficiency?

A
  1. Inadequate muscle function → decreased work performance & exercise tolerance;
  2. Neurologic involvement → fatigue, anorexia, pica- pagophagia, restless leg syndrome (could be attributed to depleted iron in the brain);
  3. Growth abnormalities/ Abnormal cognitive development in children;
  4. Decreased Immune function → frequent infections
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45
Q

What is Pica?

A

Craving clay and paint chips

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46
Q

What is Pagophagia?

A

Craving ice

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47
Q

What are the Later, more sever problems associated with Iron deficiency anemia?

A
  1. Defects in epithelial tissue → pallor of face, changes in tongue/ mouth, nails, stomach;
  2. Cardiac and respiratory changes → can lead to tachycardia, cardiac failure
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48
Q

What is the Medical Dx for Iron Def. Anemia?

A
  1. Need to include more than 1 method of evaluation → SO many factors account ;
  2. Most useful: serum ferritin, iron, and transferrin → affected the most readily; change more quickly than Hgb and Hct;
  3. Hemoglobin alone not appropriate for diagnosis
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49
Q

Why is Hgb NOT a good indicator for iron deficiency anemia diagnosis?

A
  1. Not affected until later in disease process;
  2. Cannot distinguish between iron deficiency and other anemias;
  3. Values vary significantly between healthy individuals
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50
Q

What are the Medical Management techniques for Iron Def. Anemia?

A
  • Treat UNDERLYING cause of anemia;
    1. Oral supplements;
    2. Parenteral Iron-Dextran
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51
Q

What are the considerations for Oral Supps in treating Iron def?

A
  • *Absorption and Affect on GI;
    1. Ferrous iron → Reduced form;
    2. Chelated form (combined with amino acids);
    3. Empty stomach = Better absorption, but GI side effects/discomfort;
    4. Vitamin C;
    5. Take separately from other mineral supplements (avoid competition)
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52
Q

Why is Ferrous iron a good supp?

A
  • Better absorption;

- Easier on GI tract

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53
Q

Why is the Chelated form a good supp?

A
  • Better absorption;
  • Less affected by iron absorption inhibitors;
  • Easier on GI tract because needed in LOWER doses
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54
Q

What can inhibit iron absorption?

A

Phytates, Tannins, Oxalates, Calcium and other minerals (Tea, Coffee, Grains, Leafy Green Vegetables, Mineral supps)

55
Q

How does Vitamin C effect iron absorption?

A
  • Increases absorption (+);

- Increases GI discomfort (-)

56
Q

What is Parenteral Iron-Dextran for treating iron def?

A
  • Iron infusion directly into the blood when oral supps are not adequate;
  • Indications for use:
    1. Patient not taking medication as prescribed;
    2. Excessive bleeding* (example);
    3. Poor absorption of supplemental iron
57
Q

What are the benefits/limitations of Parenteral Iron-Dextran?

A
  1. FASTER replacement of iron stores (+) — directly into the blood stream;
  2. More expensive than oral supplements (-);
  3. Not as safe as oral supplements (-)
58
Q

What is included in the NCP Assessment for Iron Def. Anemia?

A
  1. Diet Hx;

2. Med Hx

59
Q

What should be considered in the Diet Hx?

A

**Assess dietary Fe INTAKE (direct and indirect effect on iron status):
1. MFP → meat, fish, poultry
2. Vegetarianism → lack of heme-iron, competing nutrients in grains and veggies
3. Coffee/tea intake (tannins)/ (also phytates, oxalates) → inhibit
4. Supplement use → competition
5. Cooking w/ cast-iron cookware → helpful, but can make excessive
6. Low energy diet → less food, less nutrients
7. Too much fiber
8. Iron-fortified cereal
→ Compare to DRI

60
Q

What should be included in the Med. Hx?

A
  1. Medical conditions → leading to/causing iron deficiency;
  2. Menstrual cycle;
  3. Pregnant/lactating;
  4. Recent blood loss;
  5. Physical activity;
  6. Medications (ie: calcium containing antacids — can lower absorption of iron and compete)
61
Q

What is the Nutrition Diagnosis for Iron Def. Anemia based on?

A
  • Based on information obtained during nutrition assessment;
  • Most often related to =
    1. inadequate intake;
    2. imbalance of nutrients;
    3. altered nutrition-related labs (Hb);
    4. increased iron needs
62
Q

What are some possible Nutrition Diagnoses from IDNT?

A
  • Inadequate mineral intake (specify): NI-5.10.1;
  • Inadequate vitamin intake (specify): NI-5.9.1;
  • Increased nutrient needs (specify): NI-5.1;
  • Undesirable food choices: NB-1.7
63
Q

What is a possible PES statement for Iron Def. Anemia?

A

“Inadequate mineral intake (iron) RT limited access to high iron foods due to economic constraints AEB estimated iron intake from less than recommended intake, Hgb

64
Q

What is the basis of Dietary Intervention for Iron Def. Anemia?

A
  • GOAL = Repletion of iron stores;
  • FOCUS = search for true cause:
  • Dietary changes and/or sups;
  • Improve bioavailability through the use of complementary foods (plants food with complementary amino acids) - Bioengineering has increased some availability;
  • Continued nutrition education
65
Q

What is the Nutrition Prescription for Iron Def. Anemia?

A
  • Supplemental iron (RD can recommend/ may be able to prescribe);
  • 30 mg ferrous iron tid adults (Daily dose: 50-200mg);
  • Continue supplement for 3-5 months;
  • Monitor and follow up with patient on gastric irritation with supplement;
  • If not tolerated on empty stomach, can take with meals
66
Q

What is the Dietary Intake Recommendations for repletion for Iron Def. Anemia?

A
  1. Encourage ↑ consumption of foods w/ ↑ amounts of heme iron;
  2. Eat MFP with other foods to ↑ iron absorption;
  3. Use cast-iron cookware for acidic foods;
  4. INCREASE intake of vitamin C (source @ each meal);
  5. Include iron-fortified foods;
  6. Avoid large amounts coffee/tea especially with meals
67
Q

Why should recommendations Encourage ↑ consumption of foods w/ ↑ amounts of heme iron?

A
  1. Heme iron more bioavailable than non-heme iron;

2. Heme iron ~ 15% absorbable/ Non heme iron ~ 3-8% absorbable

68
Q

Why should people Eat MFP with other foods to ↑ iron absorption?

A

-Presence of MFP in a meal allows iron from the entire meal to be absorbed better

69
Q

What should be avoided avoided when trying to replete iron stores?

A

-Avoid large amounts coffee/tea especially with meals

70
Q

What are possible OBJECTIVE outcomes to measure in Monitoring/Eval?

A
  • Objective=
    1. Physical findings (skin, nails, mouth, epithelium);
    2. Lab values (what are these?);
    3. Anthropometrics (children)
71
Q

What are possible Food Intake Assessments in Monitoring/Eval?

A
  • Actual Fe intake vs. reference standard;

- Assess diet for high iron sources vs. behavioral goal

72
Q

What are possible SUBJECTIVE Reports regarding iron deficiency anemia?

A
  • From the patient!;
    1. Symptoms reported by patient-related to the anemia → ILLNESS;
  • Fatigue/ exercise tolerance;
  • Immune function(infections);
    2. Symptomsrelated to supplementation and/or diet changes → TREATMENT;
  • Nausea;
  • Constipation/diarrhea;
  • Heartburn
73
Q

What is the Pathophysiology of Megaloblastic Anemia?

A
  • Related to disturbed synthesis of DNA;

- Both vitamin B12 and folic acid required for SYNTHESIS of thymidylate in DNA formation

74
Q

What is the Morphology of Megaloblastic Anemia?

A

Large, immature, abnormal RBC

75
Q

What are the main causes of Megaloblastic Anemia?

A
  • *95% of cases Megaloblastic Anemia due to Folic acid or Vitamin B12 deficiency;
  • Both vitamins needed for synthesis nucleoproteins = DNA
76
Q

How quickly are Folic Acid and B12 stores deleted?

A
  • Folic acid stores depleted more quickly (2-4 mos);

- Vitamin B12 stores depleted more slowly (several years)

77
Q

How do Folic Acid and B12 deficiency relate?

A
  1. Folic Acid supplementation can mask Vitamin B12 deficiency until neuro-psychiatric damage → ;
    - Vitamin B12 deficiency can lead to folic acid deficiency
78
Q

How do Folic Acid Supps mask B12 deficiency?

A
  • Folic acid deficiency shows earlier signs/symptoms, so treating with folic acid can mask the ultimate B12 deficient;
  • **B12 def. can lead to severe neurological problems if goes untreated for an extended period of time
79
Q

How can B12 deficiency lead to Folic Acid deficiency?

A
  • *5-methyl tetrahydrofolate trap =
  • Methyl group must be able to be transferred to the B12;
  • Can ultimately stop DNA synthesis ;
  • Accumulation of uracil (can’t be converted to thymudilate);
  • Deficiency in RBC leading to large, immature RBCs ;
  • B12 1-Carbon transfers also used for neurotransmitter synthesis and other functions throughout the body
80
Q

What functions of the body require B12 methyl group transfers?

A

1-C transfers =

  • DNA synthesis;
  • Neurotransmitter synthesis;
  • Other functions
81
Q

What are the conversions of folate to the active form?

A
  1. Pterolymonoglutamic acids (floats);
  2. Tetrahydrofolate (active form);
  3. 5-methyl THFA (= major circulating and storage form)
82
Q

What are the etiologies (causes) of Folic Acid Def?

A
  1. Inadequate intake/ stores → Alcoholism, elderly, pregnancy;
  2. Poor absorption → Alcoholism, Celiac disease, drug interactions, congenital defects;
  3. Poor utilization → Alcoholism, Medications (anticonvulsants), Vitamin B12 & Vitamin C deficiency;
  4. Increased need → Alcoholism, Infancy, medications, increased hematopoiesis, inflammation;
  5. Inflammation → inflammatory cytokines contribute to increased cell turnover and increased use of nutrients and mobilization of LBM;
  6. Increased excretion → Alcoholism, Liver disease, kidney dialysis, Vitamin B12 Deficiency
83
Q

What can contribute to ALL possible causes of Folic Acid Def?

A

-Alcoholism!!

84
Q

What is the “Methylfolate Trap”?

A
  1. B12 is needed to receive a 1-C methyl group from the INACTIVE form of folic acid (5-methyl tetrahydrofolate)→ and create the active THFA form!!;
  2. Transfer required so 5-methyl tetrahydrofolate can be converted to ACTIVE form, TETRAHYDRAFOLATE;
  3. Normally THFA is a 1-carbon carrier, picking up 1-carbon units and bringing to other molecule;
  4. While in the 5-methyl form, it CANNOT function in this role and therefore con activation occurs
85
Q

What else is involved in the Methylfolate trap?

A
  • Also deals with HOMOCYSTEINE and METHIONINE ;
  • An inadequate intake of B vitamins, as well as genetic factors that affect the body’s absorption and use of folic acid, can lead to elevated homocysteine levels.→ INCREASED levels of homocysteine are related to increased risk of CVD
86
Q

What is the progression of Folic Acid deficiency?

A

4 stages:

DEPLETION progresses to DEFICIENCY = 2-4 month period

87
Q

Stage 1 of Folic Acid Def.

A

Stage 1: serum folate decreased (early negative folate balance)

88
Q

Stage 2 of Folic Acid Def.

A

Stage 2: RBC folate begins to decrease and continues to decrease through stage 4

89
Q

Stage 3 of Folic Acid Def.

A

Stage 3: Damaged folate metabolism with folate deficient erythropoiesis (creation of RBC) and slowed DNA synthesis (abnl deoxyuridine –dU suppression test – done in vitro – corrected with folates)

90
Q

Stage 4 of Folic Acid Def.

A

Stage 4: Clinical folate deficiency anemia!!;

  • MCV becomes elevated at this stage;
  • Decrease in Hemoglobin not seen until stage 4;
  • Serum folate very low (< 3ng/mL) and RBC folate < 140-160ng/mL.
91
Q

What does RBC folate indicate?

A

RBC folate reflects ACTUAL body folate stores → vs. serum folate which reflects NEGATIVE balance at time blood is drawn

92
Q

What is the diagnostic criteria for Folic Acid Def?

A
  1. Low serum folate
  2. Low RBC folate
  3. Elevated formiminoglutamic acid in urine;
    - -Folic acid is needed for the conversion of histamine to glutamate → Formiminoglutamic acid is an intermediate of this conversion → ELEVATED levels thus indicate cycle is not working and there is increased excretion of FIGLU;
  4. dU in peripheral blood lymphocytes → deoxyuridilate
93
Q

What is the diagnostic criteria for B12 Def?

A
  1. Low ser B12 (< 320 pg/mLà signs of def);
  2. Low B12 bound to transcobalamin II ;
  3. Elevated Methylmalonic acid (MMA) levels in serum or urine;
  4. Positive Intrinsic factor antibodies and parietal cell antibodies;
    - Elevated Homocysteine
94
Q

Why is MMA a good indication of B12 def?

A

-Elevated urine levels;
-** ONLY B12 deficiency assay that has been validated as screening tool;
→ MMA increases when B12 &/or folate not available to participate in specific metabolic pathways involved in homocysteine metabolism

95
Q

Why are Positive Intrinsic Factor antibodies an indication of B12 def?

A

Intrinsic factor being destroyed and thus inadequate IF to release B12 from the food source

96
Q

How does Elevated Homocysteine indicate B12 def?

A

Related to the inability to transfer the extra methyl group from the inactive form of folate to the active, bioavailable form

97
Q

Why should you always consider a B12 def along with Folic Acid def?

A
  • Detecting a folate deficiency CAN’T MISS a potential B12 deficiency!!
  • Check for both as much as possible
98
Q

What are the Clinical Signs/Symptoms of Folic Acid Def?

A
  1. Fatigue, Dyspnea
  2. Sore tongue, glossitis
  3. Diarrhea
  4. Irritability, forgetfulness → Neurological effects
  5. Anorexia, weight loss
  6. Fetal neural tube defects → RESULT of lack of adequate folate consumption prior to and during pregnancy
99
Q

What is specific to Pernicious Anemia?

A
  • Low serum Vit. B12;

- Normal = 200-900 pg/mL

100
Q

What are the etiologies (causes) of B12 def and Pernicious Anemia?

A
  1. Lack of Intrinsic Factor = technically cause of Pernicious Anemia;
  2. Decreased Absorption;
  3. Surgical resection of stomach;
  4. Inadequate intake ;
  5. Infants of mother’s with B12 deficiency
101
Q

How does lack of Intrinsic Factor cause Megaloblastic Anemia with B12 def?

A
  1. Involvement of parietal cells → provide the acidity to the stomach through the production of HCL;
  2. Role of HCL → detaches the B12 from the protein source so that it made me digested;
  3. Role of proteases → Breakdown the protein and detaching the B12 from the R-proteins so that it may bind to IF and continue into the small intestine ;
  4. Role of terminal ileum → Final absorption of B12 takes place in the later part of the small intestine; Must have a functional SI
    * *Only exceptionally large amounts of B12 can be absorbed in the lack of HCl and intrinsic factor
102
Q

What causes decreased absorption and leads to Megaloblastic Anemia with B12 def?

A
  1. Medications
  2. GI disorders
  3. Atrophic Gastritis, Peptic Ulcer disease r/t H. pylori;
  4. Celiac and Crohn’s disease → inadequately functioning small intestine greatly inhibits absorption;
  5. HIV;
  6. Excess bacteria in stomach that require B12 (w/aging)
103
Q

How does H. Pylori exacerbate or cause the anemia?

A
  • H. pylori will actually utilize some of the nutrients from foods and increase other needs as well as cause deficiencies ;
  • People over 50 need more readily available forms of B12 with decreased stomach acidity → Fortified breakfast cereal and supps and injections
104
Q

What is the Medical Management of MEGALOBLASTIC Anemia (Folate and B12)?

A
  1. Oral sups of Folate/B12;

2. Parenteral Vit. B12 (IM or Subcutaneous)

105
Q

What is the Oral Supplementation for Megaloblastic Anemia?

A
  • Oral supplementation Folate / Vitamin B12;
  • 1mg folate for 2-3 weeks;
  • Large doses of B12 (1000mcg daily) → Only way to get around a lack of intrinsic factor ;
  • May need to continue supplement when deficiency is complicated by alcoholism or other conditions;
  • *Folate and thiamine are extremely important to alcoholism
106
Q

What is the Parenteral Vit. B12 treatment for Megaloblastic Anemia?

A
  • IM or Subcutaneous) ;
  • 100mcg or more B12;
  • Initially once/ week;
  • Decreased to once/month
107
Q

What is included in the Diet/Med Hx for Megaloblastic Anemia (Folate and B12 def)?

A
  • 24 hour recall or FFQ to determine folate/B12 intake;
  • Gastric condition causing ↓ absorption;
  • Energy/ protein needs (1.5g/kg)
108
Q

What are the mild CLINICAL signs of Megaloblastic Anemia (folate and B12 def)?

A

MILD =

  • Fatigue
  • Low BP/tachycardia
  • Pallor
  • Muscle weakness
  • Shortness of breath
  • Mild cognitive impairment
109
Q

What are the moderate-severe CLINICAL signs of Megaloblastic Anemia (folate and B12 def)?

A
  • MODERATE – SEVERE =
  • Neuropathy
  • Parasthesia – tingling in the fingers and toes
  • Diarrhea
  • Jaundice
  • Glossitis
  • Personality/memory changes
110
Q

What are the possible IDNT diagnoses for Megaloblastic Anemia (folate and B12)?

A
  • Inadequate vitamin intake (specify);
  • Increased nutrient needs (specify) (look at reference sheets);
  • Altered nutrition-related lab values (specify);
  • *Remember – diagnosis is NUTRITION, NOT medical (i.e. nutrition dx isn’t “pernicious anemia”)
111
Q

What FOOD Interventions are used in treating Megaloblastic Anemia (folate and B12)?

A
  • Included in both inpatient and outpatient settings, but the major focus of inpatient when the intake will be constantly monitored and provided ;
  • Encourage ↓ intake of soft drinks;
  • Fortified breakfast cereal;
  • Encourage intake of animal products →B12 ONLY found in animal products and attached to the proteins ;
  • Folate rich foods (not cooked due to sensitivity of vitamin to heat);
  • With metformin, consider increased intake calcium (shown to reverse B12 malabsorption)
112
Q

What EDUCATION Interventions are used in treating Megaloblastic Anemia (folate and B12)?

A
  • Outpatient setting, some education needs to be provided;
  • Counseling;
  • Causes;
  • Folate and B12 rich food sources;
  • Food pairings;
  • LIfestyle factors that exacerbate;
  • Signs/symptoms to watch for reoccurrence
113
Q

What should be Monitored/Evaled with Megaloblastic Anemia (folate and B12)?

A
  1. Supps/meds - monitor use;
  2. Labs;
  3. Diet;
  4. GI Condition
114
Q

What labs are monitored with Megaloblastic Anemia (folate and B12)?

A
  • Serum B12
  • Serum folate
  • Urinary formiminoglutamic acid
  • MMA
  • Homocysteine
  • Transcobalamin II
115
Q

What about the diet should be monitored with Megaloblastic Anemia (folate and B12)?

A
  • Monitor intake of foods high in B12, folate
  • Monitor knowledge/ behavior;
  • Fortified foods use ;
  • ↓ intake of soft drinks
116
Q

What is Sickle-Cell Anemia?

A

-Non-Nutritional Anemia = Chronic Hemolytic Anemia

117
Q

What individuals are most affected by Sickle Cell?

A
  • African and Mediterranean descent;

- Also individuals from: India, Caribbean, Central America, South America, Hispanic American

118
Q

What is the etiology (cause) for sickle cell?

A
  • Inherited trait;
  • Substitution of VALINE for GLUTAMIC ACID in Hgb synthesis;
  • Fragile, distorted cell → hemolysis and blocks microvasculature;
  • Pain from vaso-occlusion;
  • Blood flow impeded
119
Q

What is the pathophysiology of sickle cell?

A
  • Decreased oxygen carrying capacity due to abnormal Hgb and shape of cell;
  • → early cell death
120
Q

What are the Clinical signs and symptoms of Sickle Cell?

A
  1. Severe pain crisis w/ fatigue → Sickle Cell Crisis; pt’s typically end up in the hospital;
  2. Increased risk for infection due to effect of sickle cells on spleen
    - -Especially bacterial infections such as salmonella, strep, pneumonia;
    - -Possible prophylactic penacillan through childhood;
  3. Weight loss (Increased REE, Increased protein turnover);
  4. Increased risk for bone disease
121
Q

What is included in the Assessment for Sickle Cell?

A
  • *Patient history
  • Growth hx;
  • Problem list;
  • Hx of surgeries/procedures;
  • Diet hx;
  • *Needs Calculations are DIFFERENT with SICKLE CELL
122
Q

What is the difference in ENERGY needs for adolescents with Sickle Cell?

A

Energy needs: 6% – 22% ↑than normal

123
Q

What is the difference in PROTEIN needs for adolescents with Sickle Cell?

A

Protein needs: 44% – 100% ↑ than normal 0.8 g/kg

124
Q

What are the REE calls for Sickle Cell in adolescents?

A
  • Boys: REE = 1305 + (18.6 x wt. in kg) – (55.7 x Hgb in g/dL);
  • Girls: REE = 1100 + (13.3 x wt. in kg) – (30.2 x Hgb in g/dL)
  • Multiple times activity factor!!!!
125
Q

What are the increased NEEDS for those with Sickle Cell?

A
  • Energy;
  • Protein;
  • Fluid;
  • Glutamine, Arginine;
  • Omega-3 fatty acids;
  • Magnesium, Zinc;
  • Vitamin E, Vitamin D, Vitamin A;
  • Vitamin B-6, Vitamin B-12, Folate, Riboflavin;
  • Vitamin C;
126
Q

What are the risks of IRON and Sickle Cell?

A
  • Risk for iron OVERLOAD;
  • Also risk for concurrent deficiency
  • NOTE: normalizing nutrition status may decrease incidence of crisis
127
Q

What are the difference in ENERGY and PROTEIN for adults with Sickle Cell?

A

Energy and Protein =
-120% – 150% of DRI

  • Fat =
  • may exceed 30% of energy ;
  • Encourage unsaturated fats
128
Q

What are good sources of fluid for those with sickle cell?

A
  • Water;
  • Milk;
  • Juice;
  • Soup;
  • Sports drinks;
  • Popsicles;
  • Fruits;
  • Vegetables
129
Q

What sups should be considered in treating Sickle Cell?

A
  1. Consider High Calorie/ High protein liquid supplements;
  2. Other supplements to consider:
    - Glutamine
    - Arginine
    - Citrulline
    - Possibly Zn and Magnesium
130
Q

What are the possible IDNT diagnoses for nutrition problems related to Sickle Cell?

A
  • *Make diagnoses related to nutrition problems resulting FROM sickle cell;
  • Increased energy expenditure (NI-1.2);
  • Inadequate mineral intake (specify) (NI-5.10.1);
  • Inadequate vitamin intake (specify) (NI-5.9.1);
  • Inadequate protein intake (NI-5.7.1)
131
Q

Example PES Statements

A
  • Increased energy expenditure RT physiological causes increasing nutrient needs AEB measured resting metabolic rate 200 calories greater than predicted;
  • Inadequate energy intake RT decreased ability to consume sufficient energy due to pain associated with sickle cell crisis AEB failure to gain (or maintain) appropriate weight
132
Q

What should intervention with Sickle cell treatment be based upon?

A

Problems of the individual =

  • weight loss
  • poor growth
133
Q

What are the goals of intervention with Sickle cell nutrition therapy?

A
  • Meet increased needs;
  • Prevent malnutrition;
  • Promote weight gain/ catch up growth in children;
  • Prevent abnormalities with bone mineralization
134
Q

What should be Monitored/Evaled when treating Sickle Cell?

A
  • Monitor patient’s nutritional status (Indicators??, Criteria??);
  • Modify nutrition care plan if results are not adequate;
  • Change intervention if disease state changes

Fall 2014 (8 decks)

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