Solution Manual For Nutrition Therapy and Pathophysiology 4th Edition Nelms

Solution Manual for Nutrition Therapy and
Pathophysiology 4th Edition, Nelms
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Solution Manual for Nutrition Therapy and Pathophysiology 4th Edition, Nelms
1
Chapter 9: Cellular and Physiological Response to Injury: The Role of the Immune System
Chapter 9: Cellular and Physiological Response to Injury: The Role of the

Immune System
Chapter Outline
I. Introduction
II. The Disease Process
III. Cellular Injury
A. Mechanisms of Cellular Injury
B. Cellular Response to Injury
1. Cellular Accumulations
2. Cellular Alterations in Size and Number
3. Cellular Injury from Infection
4. Types of Microorganisms
5. Course of Infection
6. Cellular Death
C. Host Resistance to Infectious Cellular Injury
IV. Preventing Transmission of Infection
V. Foundations of the Immune System
A. Organs of the Immune System
B. Cells of the Immune System
1. Monocytes and Macrophages
2. Leukocytes
3. Other Cells Derived from the Myeloid Stem Cell
4. Lymphocytes
C. Major Histocompatibility Complex/Human Leukocyte Antigens
D. Communication between Immune Cells
1. Complement
2. Cytokines
VI. The Immune Response
A. Innate and Adaptive Immunity
1. Innate Immune Response
2. Inflammation and Healing
3. Nutrition and Wound Healing
4. Adaptive Immune Response
VII. Autoimmunity
VIII. Attacking Altered and Foreign Cells: Tumors and Transplants
A. Tumor Immunology
B. Transplantation Immunology
1. Transplant Rejection
2. Matching
3. Immunosuppression
4. Transplantation of Specific Organs and Tissues
IX. Immunization
A. Passive Immunity
B. Active Immunization
C. Types of Vaccines
X. Immunodeficiency
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license distributed with a certain product or service or otherwise on a password-protected website for classroom use.
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2
A. Malnutrition and Immunodeficiency

B. Inherited Immunodeficiencies
C. Acquired Immunodeficiencies
XI. Hypersensitivity (Allergy)
A. Overview of Hypersensitivity
1. Definition Hypersensitivity
2. Epidemiology
3. Etiology: Classifications of Allergic Reactions
4. Pathophysiology
5. Medical Diagnosis and Treatment
6. Additional Medical Interventions
7. Delayed Hypersensitivity
B. Adverse Reactions to Food
1. Definition
2. Epidemiology
3. Etiology
4. Pathophysiology
5. Medical Diagnosis
C. Nutrition Therapy for Food Allergy
1. Nutrition Implications
2. Nutrition Assessment
3. Nutrition Diagnosis
4. Nutrition Intervention
XII. Conclusion
Classroom Activities
Activity 9-1
Items needed: Table 9.5 Nutrition Intervention for Wound Healing for Adults and Nutrition Facts labels from
supplements marketed for wound healing
As a class, discuss the following scenarios and the appropriate nutrition therapy for each scenario to help students
better understand the nutrition recommendations for wound healing. Utilize Table 9.5 for suggested answers to these
scenarios.
• Which nutrition supplements would be contraindicated in a patient with kidney failure?

• Which vitamin or mineral deficiency can delay wound healing and would generally benefit from nutritional
supplementation?
• Decreased intakes of which nutrients are often seen in the elderly?
Using the Nutrition Facts labels from supplements for wound healing, discuss the costs and benefits of using
commercial products to promote wound healing.
Activity 9-2
Items needed: Internet access to the website http://www.foodallergy.org/
Instruct students to peruse the given website and specifically look at the “Common Allergens” link to explore
common food sources of allergens (milk, egg, peanut, soy, etc.). Utilizing handouts available on the website under
3
“Education and Awareness,” have students role-play a nutrition education session between a registered dietitian and
a client with a food allergy. Encourage students to bookmark this website as a valuable tool for their future practice
as registered dietitians.
Build the Bridge to Application
Cases from Medical Nutrition Therapy: A Case Study Approach, 4th edition (ISBN 1133593151), may be used in
conjunction with this chapter. All cases have application to nutrition assessment/nutrition care process information.
Many cases have application to basic pathophysiology. The cases listed here primarily emphasize the chapter
concept.
• Case 29 – Metabolic Stress and Trauma

• Case 34 – AIDS
Enrichment Materials1
The following enrichment handouts are included in this manual (at the end of this section):
• Enrichment Handout 9-1: Antibody Structure and the Antigen–Antibody Bond
• Enrichment Handout 9-2: Detecting a Single Antigen: Monoclonal Antibodies
• Enrichment Handout 9-3: So Many Antigens, So Little DNA to Make Antibodies
• Enrichment Handout 9-4: Clonal Selection: Many Are Called but Few Are Chosen
• Enrichment Handout 9-5: Negative and Positive Selection of B Cells and T Cells
• Enrichment Handout 9-6: Huffing and Puffing: Responding to Asthma
• Enrichment Handout 9-7: Pernicious Anemia
• Enrichment Handout 9-8: Antibody Diversity Generated by Multiple Genes and Recombination
• Enrichment Handout 9-9: Numbers of MHC Antigens Based on Serological and DNA Methods
• Enrichment Handout 9-10: Sources of Antigen in Allergic Pneumonitis
• Enrichment Handout 9-11: Gender Differences in Autoimmune Disease
• Enrichment Handout 9-12: MHC and Autoimmune Disease
Worksheet Answer Key
Worksheet 9-1: Cellular Response to Injury—Calculations

1. A. 25–35 kcal/kg; recent weight loss and poor intake
B. Overweight; actual weight; recently lost weight and current weight is close to normal weight.
C. 180/2.2 = 81.8 kg × 30 kcal/kg = 2454 kcal
2. A. 81.8 kg × 1.5 grams/kg = 122.7 (round to 123 grams protein); low albumin
B. 20% from protein; 123 grams × 4 kcal/gram = 492 kcals/2454 kcal = 0.20 or 20%
C. Yes.
3. A. 30 mL/kg × 81.8 kg = 2454 = 2.5 L; 1 L more than minimum
B. A history of urinary tract infections plus Stage III ulcer may indicate higher fluid needs.
Worksheet 9-2: Diet Prescription for Food Allergy

1. Suggest resolve knowledge deficit of mother initially as priority.
2. Students’ answers will vary and may include the following: Dietary Reference Intakes (DRI) based on age and
1 Contributed by Christina Lee Frazier, Ph.D. of Southeast Missouri State University.
4
American Dietetic Association Nutrition Care Manual.

3. Facility-approved diet manual and departmental policies and procedures for the provision of nutrition care
4. Students’ answers will vary and may include the following: current lab values, patient’s food preferences,
eating schedule, activity level, exposure to sunlight to further assess vitamin D, and evaluation of total diet
quality (i.e., protein, vitamin, and mineral intakes).
5. Students’ answers will vary. Answers can include the following goal: Patient will consume 2 cups of calcium-
and vitamin D-enriched soy beverage products daily.
6. Students’ answers will vary and should include the following: specific dietary recommendation individualized
to the client’s health condition and nutrition diagnosis and based on current guidelines. Example: Cow’s milk
protein-free diet that would provide 800 mg calcium and 200 IU vitamin D daily is recommended. Example:
Educate caregivers on cow’s milk protein-free diet that provides 800 mg calcium and 200 IU vitamin D daily as
appropriate.
7. Students’ answers will vary and may include the timing and content of meals and snacks, and the frequency of
follow-up education sessions with the mother.
8. Students’ answers may include resources such as Nutrition Diagnosis and Intervention: Standardized Language
for the Nutrition care Process and the American Dietetic Association.
9. Students’ answers may vary and may include references to reliable websites on allergies, support groups, etc.
5
Worksheet 9-1: Cellular Response to Injury—Calculations

Use Table 9.5 as guides to completing this worksheet.
R.T. is a 69-year-old paraplegic male with a history of frequent urinary tract infections and poor wound healing. He
is admitted to a hospital with Stage III pressure ulcer on his left ankle. He is 5 feet 11 inches tall and weighs 180
pounds; his BMI is 25.1. He is wheelchair-bound. His temperature on admission is 100.4°F. Labs indicate an
increased white cell count, C-reactive protein (CRP), and a low albumin level of 3.1. R.T.’s caregiver reports that he
has lost five pounds in the past month as a result of poor appetite and fatigue.
1. Consider the following to calculate R.T.’s recommended calorie intake:

A. Critical thinking: What is the range of kcalories per kilogram recommended in Table 9.5 to promote wound
healing? Why would the middle of this range be a reasonable starting place to calculate his calorie needs?
B. As per the information in Chapter 3, what is R.T’s weight status according to his BMI? Will you use his
actual weight or adjusted weight to calculate his estimated calorie needs? Give your reasons.
C. Calculate R.T.’s recommended calorie needs using the above information and 30 kcal/kg. Remember to
convert the weight in pounds to kilograms by dividing it by 2.2.
2. A. Use a factor of 1.5 to calculate R.T.’s protein needs. Round your answer to the nearest gram. What
indication do you have that R.T. may benefit from this higher protein level?
B. Critical thinking: What percentage of R.T’s total calorie needs will this level of protein provide?
Remember that one gram of protein provides 4 kcal per gram.
C. Is this a reasonable protein goal for wound healing?
3. A. Calculate R.T.’s fluid needs using 30 mL/kg. Compare this with the minimum requirement of 1.5 L.
6
B. Critical thinking: What factors may indicate that R.T. may need more than the minimum fluid needs?
7
Worksheet 9-2: Diet Prescription for Food Allergy

Use information from this chapter and Table 4.1 to complete this worksheet.
J.T. is a 4-year-old boy recently diagnosed with cow’s milk allergy and has been recommended outpatient nutrition
counseling. He is 39 inches tall and weighs 35 pounds. His diet contains limited sources of vitamin D. Food records
completed by his mother reveal an average intake of 300 milligrams of calcium per day. He currently takes no
medications or dietary supplements. J.T.’s mother states that she has substituted fruit juice with milk in J.T.’s diet
because of the fear that “milk substitute” beverages may contain cow’s milk.
Nutrition diagnoses:
• Inadequate calcium intake related to limited intake of high-calcium foods as evidenced by the food frequency
questionnaire and the 3-day food diary that reveals an average intake of calcium less than 50% of the
recommended requirements for age
• Food- and nutrition-related knowledge deficit related to recent diagnosis of cow’s milk allergy as evidenced by
inappropriate dietary restrictions, a limited intake of vitamin D, and an intake of calcium less than 50% of
recommended requirements for age
Plan the Nutrition Intervention

1. How would you prioritize the nutrition diagnoses for this patient; i.e., which problem would you work to
resolve first? On what do you base your decision?
2. Give at least one example of evidence-based guidelines that may be used to formulate a nutrition prescription
for the diagnoses above.
3. What policies or program standards within your department or facility will be important to guide your plan for
nutrition care?
8
4. Describe additional information you will need to help you plan an appropriate intervention.
5. Determine at least one goal and expected outcome for one of the diagnoses above. Are these goals
individualized to the patient’s needs?
6. Using the information you have gathered, write a nutrition prescription for this patient that concisely states his
recommended dietary intake of foods and/or nutrients based on his nutrition diagnosis.
7. Give one or two examples of how you might further define the care that will be provided to J.T. in terms of
timing and frequency.
8. Name one authoritative resource that will assist you in utilizing standardized language to describe your nutrition
interventions.
9. What additional resources or referrals may enhance your nutrition care for this patient and his family?
9
Enrichment Handout 9-1: Antibody Structure and the Antigen–Antibody

Bond
An antibody molecule must bind specifically to antigens from the pathogen, so part of the
molecule must be variable to react specifically with a large variety of antigens. Often, the
antibody must also recruit other cells or molecules to destroy the pathogen. Thus, part of the
antibody must be constant to be recognized by the cells or molecules. The basic antibody
monomer is Y-shaped; it consists of two identical longer protein chains, or heavy chains, and
two identical shorter protein chains, or light chains. The COOH end, or constant region, of each
heavy chain and light chain has an amino acid sequence that is very similar to the sequence in
other antibody molecules. This is the part of the molecule (the Fc) that reacts with other cells and
chemical mediators (e.g., complement). The NH3 ends, or variable region, of the heavy and light
chains are in the two branches of the Y-shaped molecule. They have highly variable amino acid
sequences and create the Fab, where the antigen binds to the antibody.
In the variable region, there are hypervariable regions that come together due to folding to form
the antigen-binding site. Binding does not result in irreversible changes in either the antigen or
the antibody, but there may be some change to produce a better fit. Interactions between antigen
and antibody binding sites are very specific but rather weak, so bonds form and break. Covalent
bonds play no role. Instead, multiple weak non-covalent bonds—including hydrogen bonds,
hydrophobic interactions, electrostatic interactions, and van der Walls interactions—combine to
form the bond. The interacting groups must be close to bond; if the electron clouds of the antigen
and antibody overlap, repulsive forces come into play. Thus, a complementary shape is key to
maximizing closeness without inducing repulsion, so both the shape and the charges of an
antigen influence strength of the bond with the antibody. Molecules with different antigenic
specificities can bind to an antibody by attaching to different subsites within the Fab. In addition,
antigens with shared or very similar epitopes can bind to the same antibody. Thus, an immune
response to one antigen (e.g., smallpox) may protect from closely related pathogens (e.g.,
monkey pox).
Key terms:
• Heavy chain (H chain)—the larger of the two types of immunoglobulin chains
• Light chain (L chain)—the smaller of the two types of immunoglobulin chains; there are
two forms: k and l
• Constant region (C region)—the carboxyl-terminal portion of an immunoglobulin or TCR
molecule that is similar from molecule to molecule
• Fc—the part of the antibody without antigen-binding sites made of the C-terminal or
constant domains of the immunoglobulin heavy chains
• Variable region—the part of an antibody or TCR that differs from one antibody or TCR to
another and produces a binding site for a specific antigen
10
• Fab—part of the antibody molecule containing one antigen-binding site; contains the
variable ends or N terminus of one light and one heavy chain
• Epitope—specific part of an immunogen that stimulates a specific immune response and
reacts with the resulting antibody or activated T cell; also called antigenic determinant
11
Enrichment Handout 9-2:

Detecting a Single Antigen: Monoclonal Antibodies
When a pathogen or large molecule is inoculated into an animal, a polyclonal antibody

preparation is produced. The polyclonal antibody preparation contains a mixture of antibodies,
each recognizing a different epitope or region of the antigen. The polyclonal antibody
preparation is produced as pathogens and most larger molecules contain multiple antigenic
determinants. Monoclonal antibody preparations, which have clinical, diagnostic, and basic
molecular biology uses, contain antibodies that react with a single antigenic determinant. They
are produced by fusing spleen cells from an animal immunized with the target multideterminant
antigen (to provide antibody genes) with myeloma cells, malignant plasma cells that cannot
make antibodies (to provide “immortality”).
Ttrastuzumab (Herceptin®) is a monoclonal antibody against growth factor receptor HER2. In

breast cancers, HER2 increases the aggressiveness of the tumor. When used in conjunction with
chemotherapy, the monoclonal antibody was associated with a lower rate of death at 1 year,
longer survival, and a reduction in the risk of death in women with metastatic breast cancer that
overexpressed HER2.
12

So Many Antigens, So Little DNA to Make Antibodies
The human immune system must respond to thousands of antigens to protect from all pathogens
to which humans are exposed and must recognize all the antigens that arise on tumors. The
human genome contains about 34,000 genes, but humans produce 1010 different antibody
molecules. This would require about 15% of the genomes if each was coded separately. Thus,
mechanisms are needed that use less DNA to generate sufficient diversity in the Fab to react with
all the antigens an individual might encounter. Mechanisms that generate diversity include
multiple genes coding for the variable region, somatic mutation, somatic recombination, and
imprecise junctions.
Variable regions of light chains comprise a variable (V) and joining (J) segment, while the region
of the heavy chain has variable, diversity (D), and joining segments. One of each is brought
together through V(D)J recombination. The genome contains many possible V segments for both
light and heavy chains and a few D and J segments. Additional diversity is generated by somatic
mutation as primordial V genes mutate during B-cell development, increasing the number of V
segments. During B-cell development, one V is joined with one J in the light chains and one V,
one J, and one D are joined in the heavy chain by somatic recombination. The kappa light chain
has 35 V segments and 5 J segments. Since any J segment can combine with any V, 175 different
VJ combinations can be made from the 40 segments. The heavy chain has 55 V genes, 30 D
genes, and 6 J genes that will produce 9900 different combinations from the 91 segments. Since
the Fab contains the variable regions of both the light and heavy chains, 1,732,500 different Fabs
can be generated from the 131 DNA segments. Thus, a small amount of DNA can give rise to
antibodies that can react with many different antigens. Imprecise junctions that occur when the V
and J or D segments join produce further diversity.
13

Clonal Selection: Many Are Called but Few Are Chosen
As a result of the random rearrangement of DNA to produce the antibody specificity for a given
B cell, B cells that can react with a large diversity of antigens are circulating at any time. During
a primary or initial infection, clonal selection occurs. In this process, a B cell specific for an
antigen on a pathogen or tumor cell reacts with the antigen via the B-cell receptor (BCR, a B-cell
receptor made of an antibody molecule and several auxiliary molecules), inducing an expression
of CD40 on the surface of the B cell. The B cell processes the antigen, and fragments are
presented to T cells on MHC II molecules on the surface of the B cell. The interaction of B and T
cells is facilitated by the costimulatory molecules CD40 ligand (CD40L) on the T cell and CD40
on the B cell. The T cell secretes cytokines that induce proliferation of the B cell and its
differentiation into a plasma cell or antibody-forming cell (AFC). As a result, the few cells
capable of responding to the antigen have become clones of numerous antibody-secreting cells.
Some progeny cells do not divide or become plasma cells. Instead, they revert to small
lymphocytes with the same BCR on their surfaces as the original cell and thus the same antigen
specificity, called memory B cells. These will produce a more rapid response upon repeated
exposure to the antigen.
14

Negative and Positive Selection of B Cells and T Cells
The DNA in B cell progenitors of the bone marrow rearranges so that one variation of each
segment is expressed, allowing the B cell to make antibodies that will respond to a specific
antigen. As a consequence of the need for great diversity, some cells will produce antibodies
capable of reacting with a person’s own tissue antigens, which could lead to autoimmune
diseases. The process of negative selection eliminates these self-reactive cells. During T cell
production, stem cells migrate to the thymus as a result of chemical signals emitted by this
organ starting at six to nine weeks of gestation, and then differentiate in the thymus. T cell
DNA rearranges, and T cell receptors form so that each cell is capable of responding to a
specific antigen. As with B cells, selection occurs in order to retain useful cells and remove
potentially self-reactive cells. About 95% of lymphocytes produced die. Some die because
they are self-reactive or they did not make a useful receptor, but many die because an excess
is produced in order to ensure there are enough of them.
The T-cell receptor (TCR) rearranges while immature T cells are in the cortex or outer part of
the thymus. In positive selection, the TCR reacts with self-antigens presented by MHC
antigens on thymus epithelial cells. If a TCR binds too strongly, indicating it would react
with self-antigens, or if it fails to bind, indicating TCR did not recognize self-MHC, the cell
is not rescued. Those that react, but not too strongly, move into the medulla where they react
to self-antigens presented by normal antigen-presenting cells (APC). Any reaction with the
self-antigen in this step, called negative selection, causes cells to go into apoptosis. Most
self-reactive T cells are removed by the resulting clonal deletion. A cell starts out with
neither CD8 nor CD4 on its surface and then goes through a period when it has both. As it
moves to the medulla, it stops making one and will be rescued only if it has CD4 and reacts
with one of the MHC II antigens or has CD 8 and reacts with a MHC I antigen.
Key terms:
• Negative selection—the process in which B and T cells that react to self molecules are
deleted or functionally inactivated during their development
• Positive selection—the rescue from apoptosis of T cells in the thymus that can recognize
self-MHC molecules
• Clonal deletion—a process by which contact with an antigen, usually self-antigen, early
in lymphocyte differentiation leads to cell death by apoptosis
15

Huffing and Puffing: Responding to Asthma
Inhalers or "puffers" deliver a measured dose of a medicine in aerosol or fine powder form. The
medication can either work rapidly to relieve symptoms by opening airways (blue inhalers), or
prevent the symptoms by reducing the inflammation in the airways. There are several types of
asthma medications.
• Leukotriene modifiers such as Zileuton (Zyflo), a 5-lipoxygenase inhibitor that inhibits

leukotriene formation, and Montelukast (Singulair) and Zafirlukast (Accolate), which are
selective and competitive leukotriene receptor antagonists of leukotriene D and E, are used to
control asthma symptoms by preventing the synthesis or action of leukotrienes. They are
recommended for prophylaxis and chronic treatment.
• Cromolyn sodium, which is used in mild persistent and moderate persistent asthma, prevents
histamine and SRS-A release because cells cannot degranulate. Antiserotonins are LSD
derivatives.
• Inhaled corticosteroids including flunisolide (AeroBid), beclomethasone dipropionate

(Vanceril), triamcinolone acetonide (Azmacort), and budesonide (Pulmicort) are used for
mild, moderate, or severe persistent asthma.
• Beta-adrenergic agonists such as albuterol (Ventolin, Proventil), salmeterol (Serevent),

bitolterol (Tornalate), and pirbuterol acetate (Maxair) are used to manage acute episodes of
asthma. They work by stimulating beta 2-adrenergic receptor sites in the sympathetic nervous
system, producing increased amounts of cyclic 3'5-adenosine monophosphate (cAMP),
which leads to bronchial smooth muscle relaxation and an inhibition of the release of
inflammatory mediators.
16

Pernicious Anemia
The body requires vitamin B12 for the production of red blood cells, since it is needed for
rapid DNA synthesis during cell division. B12 is also needed for the maintenance of the
myelin sheath of the nerves, because it is essential for the metabolism of fatty acids. B12
attaches to intrinsic factor, a glycoprotein secreted by parietal cells in the stomach lining, and
is taken to the intestines, where it is absorbed. Pernicious anemia results from a deficit in
functioning of the intrinsic factor, due to hereditary factors, surgical removal of portions of
the stomach, chronic inflammation of the stomach lining, atrophied parietal cells, or an
autoimmune disease. The disease is associated with MHC types A2, A3, and B7 and blood
type A. Three types of autoantibodies are associated with pernicious anemia, including one
that attaches to parietal cells and two types of anti-intrinsic factor antibodies. Type 1, also
called blocking, is found in 50–60% of cases and keeps vitamin B12 from attaching to the
intrinsic factor; type 2, or precipitating, present in 30% of cases, stops the attachment of the
vitamin B12–intrinsic factor complex to ileal receptors.
Pernicious anemia normally appears around age 60, but a juvenile form exists, and men and
women are affected equally. Symptoms including weakness, fatigue, lightheadedness,
dizziness, palpitations and rapid heartbeat, shortness of breath, bleeding gums, mouth sores,
impaired smell, nausea, poor appetite, weight loss, diarrhea, tingling and numbness of hands
and feet, loss of deep tendon reflexes, and personality changes (megaloblastic madness)
develop slowly. Diagnostic tests include measurement of the number and appearance of red
and white blood cells, level of B12, amount of methylmalonic acid, and levels of intrinsic
factor and parietal cell antibodies. The Schilling test employs two doses of vitamin B12, an
initial radioactive dose taken by mouth and a second nonradioactive dose injected 2–6 hours
later. Urine is tested over the next 24 hours to determine if vitamin B12 is absorbed normally.
Treatment includes regular B12 injections. B12 deficiency can also be caused by intestinal
parasites, bacterial overgrowth, celiac disease, Crohn’s disease, deficit of B12 in the diet
(rarely), and the use of drugs such as colchicine, neomycin, and para-amino salicylic acid.
17
Enrichment Handout 9-8: Antibody Diversity Generated by Multiple Genes

and Recombination
Antibody Chain V J D Combinations

λ 35 5 175
κ 29 7 203
Heavy 55 6 30 9900
Total heavy and λ 1,732,500
Total heavy and κ 2,009,700
Total 3,742,200
18
Enrichment Handout 9-9: Numbers of MHC Antigens Based on Serological

and DNA Methods
HLA Antigen DNA Serology

HLA-A 119 40
HLA-B 245 88
HLA-C 74 9
HLA-DRB1 201 80
HLA-DQB1 39 7
HLA-DPB1 84 (-)
19
Enrichment Handout 9-10: Sources of Antigen in Allergic Pneumonitis
Condition or Disease Source of Antigen Antigen

Farmer’s lung Moldy hay Thermoactinom esvulgaris
Mushroom worker's lung Compost Thermophilic antinomycetes
Bird fancier's lung Dry bird droppings Avian proteins
Laundry worker's lung Detergent Enzymes of Bacillus subtilis
Pigeon breeder's lung Pigeon dander or droppings Pigeon proteins
Maple bark pneumonitis Maple bark dust Cytptostroma corticale
Malt worker's lung Moldy barley Aspergillus cavatus
Wheat weevil disease Infested flour Sitophilus granarius
Sequolosis Moldy sawdust Graphium and Pullularia
species
Cheese washer's disease Cheese casings Penicillium caseii spores
20

Gender Differences in Autoimmune Disease
Autoimmune Disease Female-to-Male Ratio

Hashimoto’s thyroiditis 50:01
Systemic lupus erythematosus 9:01
Sjögren’s syndrome 9:01
Antiphospholipid syndrome 9:01
Primary biliary cirrhosis 9:01
Mixed connective tissue disease 8:01
Graves’ disease 7:01
Rheumatoid arthritis 4:01
Scleroderma 3:01
Multiple sclerosis 2:01
Myasthenia gravis 2:01
Type 1 diabetes mellitus 2:01
Solution Manual for Nutrition Therapy and Pathophysiology 4th Edition, Nelms
21
Enrichment Handout 9-12: MHC and Autoimmune Disease
Autoimmune Disease MHC Relative Risk

Ankylosing spondylitis B27 87.4
Multiple sclerosis DR2 4.8
Graves disease DR3 3.7
Myasthenia gravis DR3 2.5
SLE DR3 5.8
Type 1 diabetes mellitus DR3&4 3.2
Protective DR2
B8 3
DQ2 14
DQ2/B8 20
Rheumatoid arthritis DR4 4.2
DR1 6
Hashimoto’s thyroiditis DR5 3.2
Goodpastures Syndrome DR2 15.9
Addison’s Disease B8 4
DR3 7
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Chapter 9: Cellular and Physiological Response to Injury: The Role of the

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A. Malnutrition and Immunodeficiency

• Which nutrition supplements would be contraindicated in a patient with kidney failure?

Build the Bridge to Application

• Case 29 – Metabolic Stress and Trauma

Worksheet Answer Key

Worksheet 9-1: Cellular Response to Injury—Calculations

Worksheet 9-2: Diet Prescription for Food Allergy

1 Contributed by Christina Lee Frazier, Ph.D. of Southeast Missouri State University.

American Dietetic Association Nutrition Care Manual.

Worksheet 9-1: Cellular Response to Injury—Calculations

1. Consider the following to calculate R.T.’s recommended calorie intake:

C. Is this a reasonable protein goal for wound healing?

Worksheet 9-2: Diet Prescription for Food Allergy

Plan the Nutrition Intervention

Enrichment Handout 9-1: Antibody Structure and the Antigen–Antibody

Enrichment Handout 9-2:

When a pathogen or large molecule is inoculated into an animal, a polyclonal antibody

Ttrastuzumab (Herceptin®) is a monoclonal antibody against growth factor receptor HER2. In

Enrichment Handout 9-3:

Enrichment Handout 9-4:

Enrichment Handout 9-5:

Enrichment Handout 9-6:

• Leukotriene modifiers such as Zileuton (Zyflo), a 5-lipoxygenase inhibitor that inhibits

• Inhaled corticosteroids including flunisolide (AeroBid), beclomethasone dipropionate

• Beta-adrenergic agonists such as albuterol (Ventolin, Proventil), salmeterol (Serevent),

Enrichment Handout 9-7:

Enrichment Handout 9-8: Antibody Diversity Generated by Multiple Genes

Antibody Chain V J D Combinations

Enrichment Handout 9-9: Numbers of MHC Antigens Based on Serological

HLA Antigen DNA Serology

Enrichment Handout 9-10: Sources of Antigen in Allergic Pneumonitis

Condition or Disease Source of Antigen Antigen

Enrichment Handout 9-11:

Autoimmune Disease Female-to-Male Ratio

Enrichment Handout 9-12: MHC and Autoimmune Disease

Autoimmune Disease MHC Relative Risk

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