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”
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!
3
Q
Who is at most risk for developing Anemia in the US?
A
- Children under 2 yrs;
- Menstruating females;
- Pregnant females;
- Frail elderly;
- Female athletes;
- Obese children
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
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%)
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
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
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
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
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)
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!
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
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
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
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
16
Q
What is MCV (Mean Corpuscular Volume) (mcg/m3)?
A
Measures the average size of RBCs
17
Q
What is MCHC (Mean corpuscular hemoglobin concentration)?
A
–
18
Q
What is Serum Ferritin (mcg/L)?
A
-Iron STORAGE within the blood
19
Q
What is Serum transferrin (g/L)?
A
-Available to TRANSPORT Iron throughout the blood
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
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%
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.
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
24
Q
What are the clinical manifestations of iron def?
A
- Cold extremities;
- Pallor;
- Fatigue;
- Malaise;
- Tachycardia (heart rate > 100 bpm)
25
What are the classification of Anemia based on?
1. Cell size;
| 2. Hemoglobin content
26
What are the variations in cell size?
1. Macrocytic – abnormally LARGE cells;
2. Normocytic – normal sized cells ;
3. Microcytic – abnormally SMALL cells
27
What are the variations in Hemoglobin content?
1. Hypochromic – abnormally PALE in color upon visual inspection under a microscope → LOW hemoglobin ;
2. Normochromic – normal coloration
28
What are the standard treatments for iron def?
- 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
29
What is Hepcidin?
- 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
30
What causes Nutritional Anemias?
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
31
What are the types of Nutritional Anemias?
- Iron;
- Vitamin B12;
- Folic Acid;
- Pyridoxine;
- Vitamin C;
- Protein;
- Copper
32
What are the MACROCYTIC Anemia Deficiencies?
- Cyanocabalamin (B12);
- Folate;
- Thiamin;
- Pyridoxine
33
What are the MICROCYTIC Anemia Deficiencies?
- Protein;
- Iron;
- Ascorbate;
- Vitamin A;
- Pyridoxine;
- Copper;
- Manganese
34
What are the MICROCYTIC Anemia Toxicities?
- Copper;
- Zinc;
- Lead;
- Cadmium;
- Other heavy metals
35
What causes Hemolytic Anemia?
-Vit. E deficiency or toxicity
36
What is the effect of decreased IRON stores on absorption?
- 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
37
What is the effect of decreased FOLATE and B12 stores on absorption?
- Absorption is NOT increased when stores are decreased;
| - Note: adequate folate intake can mask Vitamin B12 deficiency until neuropathy develops
38
What are the Morphological classifications of anemia?
- Hypochromic OR normochromic;
| - Microcytic, normocytic, macrocytic
39
What defines Hypochromic, Microcytic anemia?
(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
40
What defines Normochromic, Normocytic anemia?
(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)
41
How does CRF and Cirrohosis cause Normochromic, Normocytic anemia?
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
42
What defines Marcocytic anemia?
(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
43
What are the stages of Iron Deficiency Anemia?
- 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.
44
What is the Early Dysfunctions seen with iron deficiency?
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
45
What is Pica?
Craving clay and paint chips
46
What is Pagophagia?
Craving ice
47
What are the Later, more sever problems associated with Iron deficiency anemia?
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
48
What is the Medical Dx for Iron Def. Anemia?
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
49
Why is Hgb NOT a good indicator for iron deficiency anemia diagnosis?
1. Not affected until later in disease process;
2. Cannot distinguish between iron deficiency and other anemias;
3. Values vary significantly between healthy individuals
50
What are the Medical Management techniques for Iron Def. Anemia?
- Treat UNDERLYING cause of anemia;
1. Oral supplements;
2. Parenteral Iron-Dextran
51
What are the considerations for Oral Supps in treating Iron def?
* *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)
52
Why is Ferrous iron a good supp?
- Better absorption;
| - Easier on GI tract
53
Why is the Chelated form a good supp?
- Better absorption;
- Less affected by iron absorption inhibitors;
- Easier on GI tract because needed in LOWER doses
54
What can inhibit iron absorption?
Phytates, Tannins, Oxalates, Calcium and other minerals (Tea, Coffee, Grains, Leafy Green Vegetables, Mineral supps)
55
How does Vitamin C effect iron absorption?
- Increases absorption (+);
| - Increases GI discomfort (-)
56
What is Parenteral Iron-Dextran for treating iron def?
* 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
What are the benefits/limitations of Parenteral Iron-Dextran?
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
What is included in the NCP Assessment for Iron Def. Anemia?
1. Diet Hx;
| 2. Med Hx
59
What should be considered in the Diet Hx?
**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
What should be included in the Med. Hx?
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
What is the Nutrition Diagnosis for Iron Def. Anemia based on?
- 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
What are some possible Nutrition Diagnoses from IDNT?
- 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
What is a possible PES statement for Iron Def. Anemia?
"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
What is the basis of Dietary Intervention for Iron Def. Anemia?
* 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
What is the Nutrition Prescription for Iron Def. Anemia?
* 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
What is the Dietary Intake Recommendations for repletion for Iron Def. Anemia?
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
Why should recommendations Encourage ↑ consumption of foods w/ ↑ amounts of heme iron?
1. Heme iron more bioavailable than non-heme iron;
| 2. Heme iron ~ 15% absorbable/ Non heme iron ~ 3-8% absorbable
68
Why should people Eat MFP with other foods to ↑ iron absorption?
-Presence of MFP in a meal allows iron from the entire meal to be absorbed better
69
What should be avoided avoided when trying to replete iron stores?
-Avoid large amounts coffee/tea especially with meals
70
What are possible OBJECTIVE outcomes to measure in Monitoring/Eval?
* Objective=
1. Physical findings (skin, nails, mouth, epithelium);
2. Lab values (what are these?);
3. Anthropometrics (children)
71
What are possible Food Intake Assessments in Monitoring/Eval?
- Actual Fe intake vs. reference standard;
| - Assess diet for high iron sources vs. behavioral goal
72
What are possible SUBJECTIVE Reports regarding iron deficiency anemia?
* 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
What is the Pathophysiology of Megaloblastic Anemia?
- Related to disturbed synthesis of DNA;
| - Both vitamin B12 and folic acid required for SYNTHESIS of thymidylate in DNA formation
74
What is the Morphology of Megaloblastic Anemia?
Large, immature, abnormal RBC
75
What are the main causes of Megaloblastic Anemia?
* *95% of cases Megaloblastic Anemia due to Folic acid or Vitamin B12 deficiency;
- Both vitamins needed for synthesis nucleoproteins = DNA
76
How quickly are Folic Acid and B12 stores deleted?
- Folic acid stores depleted more quickly (2-4 mos);
| - Vitamin B12 stores depleted more slowly (several years)
77
How do Folic Acid and B12 deficiency relate?
1. Folic Acid supplementation can mask Vitamin B12 deficiency until neuro-psychiatric damage → ;
- Vitamin B12 deficiency can lead to folic acid deficiency
78
How do Folic Acid Supps mask B12 deficiency?
- 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
How can B12 deficiency lead to Folic Acid deficiency?
* *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
What functions of the body require B12 methyl group transfers?
1-C transfers =
- DNA synthesis;
- Neurotransmitter synthesis;
- Other functions
81
What are the conversions of folate to the active form?
1. Pterolymonoglutamic acids (floats);
2. Tetrahydrofolate (active form);
3. 5-methyl THFA (= major circulating and storage form)
82
What are the etiologies (causes) of Folic Acid Def?
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
What can contribute to ALL possible causes of Folic Acid Def?
-Alcoholism!!
84
What is the “Methylfolate Trap”?
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;
5. While in the 5-methyl form, it CANNOT function in this role and therefore con activation occurs
85
What else is involved in the Methylfolate trap?
- 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
What is the progression of Folic Acid deficiency?
4 stages:
| DEPLETION progresses to DEFICIENCY = 2-4 month period
87
Stage 1 of Folic Acid Def.
Stage 1: serum folate decreased (early negative folate balance)
88
Stage 2 of Folic Acid Def.
Stage 2: RBC folate begins to decrease and continues to decrease through stage 4
89
Stage 3 of Folic Acid Def.
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
Stage 4 of Folic Acid Def.
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
What does RBC folate indicate?
RBC folate reflects ACTUAL body folate stores → vs. serum folate which reflects NEGATIVE balance at time blood is drawn
92
What is the diagnostic criteria for Folic Acid Def?
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
What is the diagnostic criteria for B12 Def?
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
Why is MMA a good indication of B12 def?
-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
Why are Positive Intrinsic Factor antibodies an indication of B12 def?
Intrinsic factor being destroyed and thus inadequate IF to release B12 from the food source
96
How does Elevated Homocysteine indicate B12 def?
Related to the inability to transfer the extra methyl group from the inactive form of folate to the active, bioavailable form
97
Why should you always consider a B12 def along with Folic Acid def?
- Detecting a folate deficiency CAN’T MISS a potential B12 deficiency!!
- Check for both as much as possible
98
What are the Clinical Signs/Symptoms of Folic Acid Def?
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
What is specific to Pernicious Anemia?
- Low serum Vit. B12;
| - Normal = 200-900 pg/mL
100
What are the etiologies (causes) of B12 def and Pernicious Anemia?
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
How does lack of Intrinsic Factor cause Megaloblastic Anemia with B12 def?
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
What causes decreased absorption and leads to Megaloblastic Anemia with B12 def?
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
How does H. Pylori exacerbate or cause the anemia?
- 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
What is the Medical Management of MEGALOBLASTIC Anemia (Folate and B12)?
1. Oral sups of Folate/B12;
| 2. Parenteral Vit. B12 (IM or Subcutaneous)
105
What is the Oral Supplementation for Megaloblastic Anemia?
* 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
What is the Parenteral Vit. B12 treatment for Megaloblastic Anemia?
* IM or Subcutaneous) ;
- 100mcg or more B12;
- Initially once/ week;
- Decreased to once/month
107
What is included in the Diet/Med Hx for Megaloblastic Anemia (Folate and B12 def)?
- 24 hour recall or FFQ to determine folate/B12 intake;
- Gastric condition causing ↓ absorption;
- Energy/ protein needs (1.5g/kg)
108
What are the mild CLINICAL signs of Megaloblastic Anemia (folate and B12 def)?
MILD =
- Fatigue
- Low BP/tachycardia
- Pallor
- Muscle weakness
- Shortness of breath
- Mild cognitive impairment
109
What are the moderate-severe CLINICAL signs of Megaloblastic Anemia (folate and B12 def)?
- MODERATE – SEVERE =
- Neuropathy
- Parasthesia – tingling in the fingers and toes
- Diarrhea
- Jaundice
- Glossitis
- Personality/memory changes
110
What are the possible IDNT diagnoses for Megaloblastic Anemia (folate and B12)?
- 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
What FOOD Interventions are used in treating Megaloblastic Anemia (folate and B12)?
- 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
What EDUCATION Interventions are used in treating Megaloblastic Anemia (folate and B12)?
- 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
What should be Monitored/Evaled with Megaloblastic Anemia (folate and B12)?
1. Supps/meds - monitor use;
2. Labs;
3. Diet;
4. GI Condition
114
What labs are monitored with Megaloblastic Anemia (folate and B12)?
- Serum B12
- Serum folate
- Urinary formiminoglutamic acid
- MMA
- Homocysteine
- Transcobalamin II
115
What about the diet should be monitored with Megaloblastic Anemia (folate and B12)?
- Monitor intake of foods high in B12, folate
- Monitor knowledge/ behavior;
- Fortified foods use ;
- ↓ intake of soft drinks
116
What is Sickle-Cell Anemia?
-Non-Nutritional Anemia = Chronic Hemolytic Anemia
117
What individuals are most affected by Sickle Cell?
- African and Mediterranean descent;
| - Also individuals from: India, Caribbean, Central America, South America, Hispanic American
118
What is the etiology (cause) for sickle cell?
- 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
What is the pathophysiology of sickle cell?
- Decreased oxygen carrying capacity due to abnormal Hgb and shape of cell;
- → early cell death
120
What are the Clinical signs and symptoms of Sickle Cell?
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;
5. Weight loss (Increased REE, Increased protein turnover);
6. Increased risk for bone disease
121
What is included in the Assessment for Sickle Cell?
* *Patient history
- Growth hx;
- Problem list;
- Hx of surgeries/procedures;
- Diet hx;
* *Needs Calculations are DIFFERENT with SICKLE CELL
122
What is the difference in ENERGY needs for adolescents with Sickle Cell?
Energy needs: 6% – 22% ↑than normal
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What is the difference in PROTEIN needs for adolescents with Sickle Cell?
Protein needs: 44% – 100% ↑ than normal 0.8 g/kg
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What are the REE calls for Sickle Cell in adolescents?
- 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!!!!
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What are the increased NEEDS for those with Sickle Cell?
- 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;
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What are the risks of IRON and Sickle Cell?
- Risk for iron OVERLOAD;
- Also risk for concurrent deficiency
* NOTE: normalizing nutrition status may decrease incidence of crisis
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What are the difference in ENERGY and PROTEIN for adults with Sickle Cell?
Energy and Protein =
-120% – 150% of DRI
- Fat =
- may exceed 30% of energy ;
- Encourage unsaturated fats
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What are good sources of fluid for those with sickle cell?
- Water;
- Milk;
- Juice;
- Soup;
- Sports drinks;
- Popsicles;
- Fruits;
- Vegetables
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What sups should be considered in treating Sickle Cell?
1. Consider High Calorie/ High protein liquid supplements;
2. Other supplements to consider:
- Glutamine
- Arginine
- Citrulline
- Possibly Zn and Magnesium
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What are the possible IDNT diagnoses for nutrition problems related to Sickle Cell?
* *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)
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Example PES Statements
- 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
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What should intervention with Sickle cell treatment be based upon?
Problems of the individual =
- weight loss
- poor growth
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What are the goals of intervention with Sickle cell nutrition therapy?
- Meet increased needs;
- Prevent malnutrition;
- Promote weight gain/ catch up growth in children;
- Prevent abnormalities with bone mineralization
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What should be Monitored/Evaled when treating Sickle Cell?
- Monitor patient’s nutritional status (Indicators??, Criteria??);
- Modify nutrition care plan if results are not adequate;
- Change intervention if disease state changes
