NUTRITION CARE PLAN ON KNEE OSTEOARTHITIS: A CASE STUDY

Mesolis, Leslie Ann P.

SUBMITTED TO THE DEPARTMENT OF NUTRITION AND DIETETICS

COLLEGE OF HUMAN ECOLOGY, CENTRAL MINDANAO UNIVERSITY
IN PARTIAL FULFILLMENT FOR THE COMPLETION OF THE
COURSE NUTRITION THERAPY II (ND55)

JULY 2022
 TABLE OF CONTENTS

Content Page
TITLE PAGE i
TABLE OF CONTENTS ii
I. INTRODUCTION 1
II. GENERAL INFORMATION OF THE CASE 2
III. MEDICAL INFORMATION OF THE DISEASE
A. Etiology and Pathogenesis of the Disease 3
B. General Pathophysiology of the Disease 4
C. Case-Specific and Nutrition-Oriented
Pathophysiology of the Disease 5
D. Clinical Manifestation 6
E. Epidemiology 6
F. Prevention and/or Treatment 7
G. Prognosis 7
IV. NUTRITION CARE PROCESS (NCP)
A. Nutrition Problem 1 8
A.1. Nutrition Assessment 8
A.2. Nutrition Diagnosis 8
A.3. Nutrition Intervention 8
A.4. Nutrition Monitoring and Evaluation 9
B. Nutrition Problem 2 9
B.1. Nutrition Assessment 9
B.2. Nutrition Diagnosis 10
B.3. Nutrition Intervention 10
B.4. Nutrition Monitoring and Evaluation 10
C. Nutrition Problem 3 10
C.1. Nutrition Assessment 10
C.2. Nutrition Diagnosis 11
C.3. Nutrition Intervention 11
C.4. Nutrition Monitoring and Evaluation 11
V. APPENDICES
A. Nutrition Care Plan 12
B. Dietary Prescription, Food and Menu Plan 16
C. Nutrient/Food-Drug Interactions 18
 D. Nutrition Assessment Tools 19
E. Summary of the Nutrition Assessment
Findings and Indications 22
F. Documentation 23
VI. GLOSSARY OF TERMS 25
VII. REFERENCES 26
 I. INTRODUCTION

Osteoarthritis (OA) is a prevalent chronic health condition that causes a lot of pain and
disability in adults (Johnson & Hunter, 2014). Increased age is a well-known risk factor for
OA in the joints most commonly afflicted, such as the hands, hips, knees, and spine. The
knee is the most common site of osteoarthritis in medical care, followed by the hand and hip
(Turkiewicz et al., 2014).

Knee osteoarthritis (OA), commonly known as degenerative joint disease of the knee,
is caused by wear and strain and gradual articular cartilage loss. It affects the elderly the
most. Squatting, kneeling, rising from a chair, and getting in and out of a car were all
problematic for patients with knee OA (Deshpande et al., 2016; Rutherford et al., 2017).
Obesity and population aging are expected to increase the prevalence of OA. Around the
world, 18 percent of women and 9.6% of men over the age of 60 show symptoms of OA,
with a quarter of these people unable to conduct daily activities (WHO, 2016).

The case study aims to address knee osteoarthritis through Nutrition Care Process
and Medical Nutrition Therapy, specifically:

1. To understand the medical information of knee osteoarthritis;

2. To provide appropriate nutrition diagnoses; and
3. To formulate correct nutrition interventions, Nutrition Care Plan and Food Plan
 II. GENERAL INFORMATION OF THE CASE

Pseudonym : Lola Naring

Age : 71 years old

Sex : Female

Date of Birth : August 12, 1950

Date of Admission : N/A

Attending Physician : Dr. Manases C. Dumaguit

Admission Impression : N/A

Diagnosis : Knee osteoarthritis

 III. MEDICAL INFORMATION OF THE DISEASE

A. Etiology and Pathogenesis of the Disease

The likelihood of developing osteoarthritis appears to rise with age. Overweight

individuals tend to get osteoarthritis as well. Osteoarthritis is caused by cartilage
deterioration caused by injury or continuous usage of a joint. Other types of arthritis can
wreak on joints, leading to osteoarthritis (Johnson et al., 2014). Aging, gender, race, obesity,
congenital and acquired deformity, inheritance, injury, and joint use are all factors that have
been linked to the development of OA.

Lockwood (2021) stated OA is caused by age, joint and muscle alterations, hormonal
changes (particularly in women after menopause), excess body weight, congenital defects,
and past joint damage resulting in muscle weakening and joint instability. There is some
indication that the most commonly affected synovial joints, such as the knees and hips for
weight-bearing and the joints of the hands for pincer grip tasks, are under-evolved for the
activities they are habitually exposed to. This could be owing to increased stress, such as in
deformities that influence the level system around the joint, or a reduction in the articular
contact area, such as in joint incongruity or instability (Elahee, 2012)

In this case, the knee OA was highlighted. A knee OA is defined pathogenetically by

structural abnormalities in and around the knee joint. The loss of cartilage and the growth of
osteophytes are the most common structural abnormalities (Andriacchi et al., 2015). The
amount of joint space loss or a reflection of cartilage loss and the presence of osteophytes
are objective markers of disease severity based on the amount of joint space loss or a
reflection of cartilage loss and the presence of osteophytes. Furthermore, early-stage OA
subchondral bone sclerosis and this process, which may involve microfractures, have been
proposed as pathogenetic factors in cartilage deterioration (Chen et al., 2020). Knee OA
causes a range of changes in articular and periarticular soft tissue in addition to structural
hard tissue alterations. Synovial hyperplasia and joint effusions are two examples of these
conditions.

Figure 1. Risk Factors for Knee Osteoarthritis and Related Disability (Bennell et al., 2012)
 B. General Pathophysiology of the Disease

The extracellular matrix of cartilage is maintained by only one type of cell, the
chondrocyte. Increased biomechanical stress and/or biochemical stimuli early in the OA
process can activate the anabolic function of chondrocytes to repair early cartilage damage.
This anabolic activity fails over time, resulting in an imbalance that favors deterioration. The
degradative pieces of ECM proteins (e.g., fibronectin and collagen) will cause synovial
membrane inflammation, which will then release catabolic and inflammatory factors,
increasing the OA process (Vincent et al., 2012).

The cartilage is affected by synovial inflammation, which is caused primarily by the

release of cartilage products into the synovial fluid, and subchondral bone transformation,
which is caused by the release of soluble mediators. Catabolic and pro-inflammatory
chemicals are released by chondrocytes and synoviocytes in the synovial membrane
(Kapoor et al., 2011). Proteinases, which increase protein synthesis, as well as other
catabolic agents, break down the ECM of the articular tissues. Endogenous inhibitors, such
as tissue inhibitors of MMPs (TIMPs) and proinflammatory cytokine inhibitors, are quickly
destroyed by these factors. Furthermore, in OA, the loss of the osteochondral junction's
integrity is linked to microcracks and the invasion of articular cartilage by vascular channels
coming from the subchondral bone, indicating that the subchondral bone and cartilage have
a molecular cross-talk. As the ECM in the articular tissues continues to degrade, the
cartilage is unable to tolerate typical mechanical forces.

Figure 2. General Pathophysiology of Osteoarthritis (Berenbaum, 2008). The failure of the

articular tissues to maintain a homeostatic balance between collagen synthesis and
breakdown causes OA, which is a complex illness. Edema is a symptom of cartilage
remodeling, which is followed by deterioration and loss of the tissue. Synovial inflammation
and subchondral bone remodeling are linked to these changes

External causes such as trauma, as well as endogenous risk factors including age,
heredity, and a high BMI, can cause osteoarthritis (BMI). Following an initial period of
cartilage edema, cartilage degradation and loss occurs, which is linked to synovial
inflammation, osteophyte production, and subchondral bone remodeling (Li et al., 2013).
Pain, incapacity, and a lower quality of life result from these structural alterations. Education
about osteoarthritis, its progression, risk factors, weight loss (if necessary), injury prevention,
exercise, and pharmaceutical symptomatic treatment are all part of current osteoarthritis
treatments. Acetaminophen (paracetamol), nonsteroidal anti-inflammatory medications
(NSAIDs), opioids, intra-articular (IA) hyaluronate and corticosteroids, and symptomatic
slow-acting drugs are all common therapies (SYSADOA).

C. Case-Specific and Nutrition-Oriented Pathophysiology of the Disease

Knee osteoarthritis is a common musculoskeletal disorder that causes pain, physical

impairment, and a lower quality of life in older adults. Osteoarthritis is one of the most
common types of joint disease and a common source of pain and disability. Age, genetic
susceptibility, previous injury, persistent stress across the joint, and aberrant mechanical
forces, primarily induced by obesity, all contribute to the development of osteoarthritis. In this
case, age is one of the factors linked to the patient's knee OA. According to Pereira et al.
(2017), age is highly related with the development of OA. From one perspective, aging
cartilage has changed chondrocyte activity and reacts to cytokines and growth hormones
differently. On the other hand, the neuro-muscular activity's protective role in the joints has
weakened over time. Furthermore, the cumulative role of other risk factors increases as
people grow older.

In addition, the client is overweight. Obesity and overweight are common risk factors for
knee OA, particularly in modern times when most human bodies are subjected to long
periods of excessive energy consumption. The association between obesity and knee OA is
particularly harmful because it sets in motion a vicious cycle in which OA pain reduces
physical activity, promoting further weight gain and weakening of muscles that stabilize and
protect joints, which can increase pain and OA progression. According to Fowler-Brown et
al., (2015), leptin levels explain half of the relationship between high BMI (25 to 30 kg/m2)
and knee OA in older adults. A systematic study also discovered significant support for
increased serum cholesterol and moderate evidence for obesity as risk factors for knee bone
marrow lesions in people with asymptomatic pre-osteoarthritis and developed osteoarthritis
(Lim et al., 2014). As a result, the serum cholesterol discovery could be an important early
modifiable risk factor.

Reactive oxygen and nitrogen species may be involved in the pathophysiology of OA,
and thus suppressing these with antioxidants may delay its onset and progression (Grover et
al., 2016). The antioxidant vitamins A, C, and E have received the most attention in this
context, with vitamin C being particularly relevant due to its requirement for collagen
formation (Li & Schellhorn, 2007). Although vitamin D has a variety of biological functions, its
principal role is assumed to be in bone metabolism and calcium homeostasis (Mabey &
Honsawek, 2015). The vitamin D receptors (VDRs), a class of nuclear receptors that
regulate gene expression to which it binds with great affinity, are responsible for the majority
of its activity. As a result, patients with knee OA should take more antioxidant vitamins A, C,
and E, as well as vitamin D.
 Figure 3. Case-Specific and Nutrition-Oriented Pathophysiology of the Disease

D. Clinical Manifestation

During the clinical assessment, numerous indications of knee OA might be found. These
include limping due to joint pain, slowed walking speed, and shorter and more frequent
strides. For a patient with knee OA, squatting may have become difficult. Advanced knee OA
is usually indicated by a deformity of the knee joint. A late symptom of the condition is
clinically evident varus or malalignment instability in the knee joint. Coarse crepitus is
thought to signal a loss of joint congruency (Doherty et al., 2017).

The tenderness of the knee joint can be detected by palpating it. Point-tenderness away
from the joint-line indicates a periarticular lesion, while tenderness along the joint-line
indicates an intracapsular origin for pain (Hafez et al., 2014). Physical impairment is linked to
a reduced range of movement, which can be easily assessed with a goniometer.
Osteophytes, remodeling, and capsular thickening are the main causes of decreased ROM,
which can be exacerbated by soft tissue swallowing. Muscle atrophy and weakening can be
difficult to detect, although they can occur in knee OA (Loureiro et al., 2018). Synovitis in
knee OA is indicated by the usual indications of inflammation, such as heat, discomfort, and
effusion. Although laboratory tests are not used to diagnose knee OA, they can aid in the
differential diagnosis.

E. Epidemiology

OA is the most common articular disease, and it is the most common cause of joint pain
and the associated functional deficits, as well as a reduction in the quality and even the
length of life. OA is a huge burden for society, both in terms of the patients' suffering and in
terms of treatment costs. Furthermore, females have a higher frequency of knee OA than
males (Plotnikoff et al., 2015). A meta-analysis published recently highlighted the gender
difference in prevalence, finding evidence for higher risk of prevalent and incident knee OA
in women. Females have more severe knee OA radiographically assessed than males,
according to the meta-analysis, and gender disparities grow with age > 55 years (Silverwood
et al., 2015). The prevalence of OA will rise as the population ages, especially if the obesity
rate remains above 50% in the 45+ age group.

F. Prevention and/or Treatment

There is no cure for osteoarthritis, and all of the existing treatments are aimed at
symptomatic relief. However, primary and secondary prevention interventions are required to
avoid rising OA rates as a result of an aging population, rising obesity, and increased
physical inactivity (Durstine et al., 2013). Since of anatomical and other variations, strategies
developed for knee OA may not apply to other joints.

Primary prevention strategies aim to reduce the risk of specific diseases by changing
behaviors or exposures that can contribute to disease, or by increasing resistance to the
effects of disease agent exposure. Knee injury prevention and adolescent obesity prevention
are two examples of therapies that are important to knee OA. Secondary prevention is
recognizing and addressing progression risk factors in those who are already at risk. The
detection and monitoring of weight gain and impairments in proprioceptive acuity, dynamic
joint stability, and muscle function, as well as subsequent intervention with weight
management and targeted exercise therapy in those who have already sustained a knee
injury, are examples relevant to knee OA (Roos & Arden, 2016).

G. Prognosis

Patients with osteoarthritis have a prognosis that is determined by which joints are damaged,
as well as the severity of symptomatology and functional impairment (Dong et al., 2015).
Some patients with osteoarthritis are essentially unaffected, while others may endure severe
disability. Joint replacement surgery may be the best long-term solution in some
circumstances. Obesity, advanced age, numerous joint involvements, and the development
of varus deformity are all linked to the disease's rapid progression (Cooper et al., 2014).
Joint replacement patients generally have an excellent prognosis, with success rates
exceeding 80%. Most prosthetic joints, however, wear out after 10 to 15 years, necessitating
a second surgery (Rönn et al., 2011).
IV. NUTRITION CARE PROCESS

A. Nutrition Problem 1

ASSESSMENT

❏ Food/Nutrition-Related History

❏ 163% of calorie adequacy

❏ Physical inactive

❏ Biochemistry

❏ Anthropometric Measurements

❏ Current weight (67 kg)

❏ Height (157 cm)

❏ BMI (27.18 kg/m2 - overweight)

❏ Nutrition-Focused Findings

❏ Client History

NUTRITION DIAGNOSIS

Overweight related to excess energy intake as evidenced by BMI value of 27.18

kg/m2, report of physical inactive and 163% of calorie adequacy.

INTERVENTION

❏ Goal:

❏ To weight reduction of 10% of body weight over 6 months by

decreasing caloric intake of 500-calorie deficit and consequently aim
within heathy range of 18.525 kg/m2.

❏ To encourage the client to have a at least 60 minutes exercise in 3

days a week.

❏ Actions:

❏ Food/Nutrition Delivery (ND)

❏ Create a meal plan with daily 500-calorie deficit based from the
TER.

❏ Nutrition Counseling

❏ Weight reduction in the management of knee osteoarthritis.

 ❏ Nutrition Counseling

❏ Schedule the client for sessions tackling about goal setting, self-
monitoring, stress management, and stimulus control.

❏ Coordinate of Nutrition Care

❏ Refer to the client to a physical therapist for physical exercise

applicable to the condition of the client.

MONITORING AND EVALUATION

❏ To monitor the weight changes in body weight of the client at least 0.5
kg/week of weight loss.

❏ To monitor the energy intake of the client by making her record daily
food dairy.

❏ To have the client visit the clinic for submission of daily food diaries
weekly.

❏ Evaluate adherence to counseling through a short test or review.

❏ To monitor the progress of the client’s physical activity by making her

report signed by the physical therapist weekly.

B. Nutrition Problem 2

ASSESSMENT

❏ Food/Nutrition-Related History

❏ Snack of high simple sugar foods

❏ Consumption of high saturated fat foods

❏ Biochemistry

❏ Fasting blood sugar: 13.29 mmol/L (↑)

❏ Cholesterol: 8.82 mmol/L (↑)

❏ Anthropometric Measurements

❏ Nutrition-Focused Findings

❏ Client History
 NUTRITION DIAGNOSIS

Altered nutrition-related laboratory values (fasting blood sugar, and cholesterol)

related to snacking of high simple sugar foods and consumption of high saturated
fat foods as evidenced by elevated fasting blood sugar (13.29 mmol/L), and
cholesterol (8.82 mmol/L)

INTERVENTION

❏ Goal:

❏ To normalize blood sugar, cholesterol, and creatinine levels within 6

months by low-carbohydrate diet, and reducing SFA using TLC meal
plan

❏ Actions:

❏ Food/Nutrition Delivery (ND)

❏ Boost the same daily reduced-calorie meal plan with:

*Reducing SFA intake to <7% total energy.

*Daily intake of low-glycemic index

❏ Nutrition Counseling

❏ Educate the client about food sources of low-fat meats and low-
glycemic index.

MONITORING AND EVALUATION

❏ To monitor the levels of blood sugar, and cholesterol monthly.

❏ To monitor the cholesterol, and CHO intake of the client by making her
record daily food dairy.

C. Nutrition Problem 3

ASSESSMENT

❏ Food/Nutrition-Related History

❏ Poor intake of foods that contain omega-3

❏ Biochemistry

❏ Anthropometric Measurements

❏ Nutrition-Focused Findings
 ❏ Client History

NUTRITION DIAGNOSIS

Increased nutrient needs (omega-3) related to increased demand of knee

osteoarthritis as evidenced by report of intake of foods low in omega-3.

INTERVENTION

❏ Goal:

❏ To reduce the knee pain and improve the muscle of the client by
increasing her intake of omega 3 fatty acids.

❏ Actions:

❏ Food/Nutrition Delivery (ND)

❏ Boost the same daily reduced-calorie meal plan with omega-3

fatty acids food items:

*Flax seeds, chia seeds, salmon, fish, walnuts, firm tofu,

shellfish, canola oil, and avocado

❏ Nutrition Counseling

❏ Educate the client about food sources of omega-3 and benefits

for the condition of the client.

❏ Coordinate of Nutrition Care

❏ Incorporate physical exercise applicable to the condition of the

client.

MONITORING AND EVALUATION

❏ To monitor the omega-3 intake of the client by making her record daily
food dairy
 V. APPENDICES

A. Nutrition Care Plan

CENTRAL MINDANAO UNIVERSITY

COLLEGE OF HUMAN ECOLOGY
DEPARTMENT OF NUTRITION AND DIETETICS
CMU NUTRITION CLINIC

NUTRITION CARE PLAN

Patient/Client Name: Lola Naring Sex: Female Age: 71 years-old

Medical condition: Knee Osteoarthritis

Nutrition Nutrition Nutrition Intervention Nutrition

Assessment Diagnosis Monitoring and
Goals Actions/Strategies
Evaluation

1.) Anthropometry PES No. 1: Goal No. 1: For Goal No. 1: For Goal No. 1:
a. Current 1.) Food/Nutrient 1.) Anthropometry
weight (67 Overweight 1.) To weight Delivery (ND) (AD)
kg) related to excess reduction of 10% of a. Create a a. To monitor
b. Height (157 energy intake as body weight over 5 meal plan the weight
cm) evidenced by BMI months by with a daily changes
c. BMI (27.18 value of 27.18 decreasing the 500-calorie in body
kg/m2 - kg/m2, report of caloric intake of deficit based weight of
overweight) physical inactive 500-calorie deficit on the TER. the client
2.) Biochemistry and 163% of and consequently 2.) Nutrition Education every day
N/A calorie adequacy. aim within the (E) 2.) Biochemistry
3.) Nutrition-Focused healthy range of a. Weight (BD)
PF 18.5 to 25 kg/m2.A reduction in N/A
N/A the 3.) Nutrition-
4.) Food/Nutrition-RH Goal No. 2 management Focused PF (PD)
a. __% of 1.) To encourage of knee N/A
calorie the client to have at osteoarthritis. 4.) Food/Nutrition-
adequacy least 60 minutes of 3.) Nutrition RH (FH)
b. Physical exercise 3 days a Counseling (C) a. To monitor
inactive week. a. Schedule the the energy
5.) Client History client for intake of
N/A sessions the client
tackling goal by making
setting, self- her record
monitoring, daily food
stress diary.
management, b. To have
and stimulus the client
control. visit the
4.) Coordination of clinic for
Nutrition Care (RC) submissio
N/A n of daily
food
For Goal No. 2: diaries
1.) Food/Nutrient weekly.
Delivery (ND) c. Evaluate
 N/A adherence
2.) Nutrition Education to
(E) counseling
N/A through a
3.) Nutrition short test
Counseling (C) or review.
N/A
4.) Coordination of For Goal No. 2:
Nutrition Care (RC) 1.) Anthropometry
a. Refer to the (AD)
client to a N/A
physical 2.) Biochemistry
therapist for (BD)
physical N/A
exercise 3.) Nutrition-
applicable to Focused PF (PD)
the condition N/A
of the client. 4.) Food/Nutrition-
RH (FH)
a. To monitor
the
progress
of the
client’s
physical
activity by
making
her report
signed by
the
physical
therapist
weekly.
1.) Anthropometry PES No. 1: Goal No. 1: For Goal No. 1: For Goal No. 1:
a. Snack of 1.) Food/Nutrient 1.) Anthropometry
high simple Altered nutrition- 1.) To normalize Delivery (ND) (AD)
sugar foods related laboratory blood sugar, a. Boost the N/A
b. Consumptio values (fasting cholesterol, and same daily 2.) Biochemistry
n of high blood sugar, and creatinine levels reduced- (BD)
saturated fat cholesterol) within 6 months by calorie meal a. To monitor
foods related to low-carbohydrate plan with the levels
2.) Biochemistry snacking of high diet, and reducing of blood
a. Fasting simple sugar SFA using TLC *Reducing sugar, and
blood sugar: foods and meal plan.C SFA intake to cholestero
13.29 consumption of <7% total l monthly.
mmol/L (↑) high saturated fat energy. 3.) Nutrition-
b. Cholesterol: foods as *Daily intake Focused PF (PD)
8.82 mmol/L evidenced by of low- N/A
(↑) elevated fasting glycemic 4.) Food/Nutrition-
3.) Nutrition-Focused blood sugar (13.29 index RH (FH)
PF mmol/L), and 2.) Nutrition Education a. To monitor
N/A cholesterol (8.82 (E) the
4.) Food/Nutrition-RH mmol/L) N/A cholestero
N/A 3.) Nutrition l, and
5.) Client History Counseling (C) CHO
 N/A a. Educate the intake of
client about the client
food sources by making
of low-fat her record
meats and daily food
low-glycemic diary.
index.
4.) Coordination of
Nutrition Care (RC)
N/A
1.) Anthropometry PES No. 1: Goal No. 1: For Goal No. 1: For Goal No. 1:
a. Poor intake 1.) Food/Nutrient 1.) Anthropometry
of foods that Increased nutrient 1.) To reduce the Delivery (ND) (AD)
contain needs (omega-3) knee pain and a. Boost the N/A
omega-3 related to improve the muscle same daily 2.) Biochemistry
2.) Biochemistry increased demand of the client by reduced- (BD)
N/A of knee increasing her calorie meal N/A
3.) Nutrition-Focused osteoarthritis as intake of omega 3 plan with 3.) Nutrition-
PF evidenced by fatty acids.D omega-3 Focused PF (PD)
N/A report of intake of dietary food N/A
4.) Food/Nutrition-RH foods low in items: 4.) Food/Nutrition-
N/A omega-3. RH (FH)
5.) Client History *Flax seeds, a. To monitor
N/A chia seeds, the
salmon, fish, vitamin
walnuts, firm intake of
tofu, shellfish, the client
canola oil, by making
and avocado. her record
2.) Nutrition Education daily food
(E) diary.
N/A
3.) Nutrition
Counseling (C)
a. Educate the
client about
food sources
ofomega-3
and benefits
for the
condition of
the client.
4.) Coordination of
Nutrition Care (RC)
a. Incorporate
physical
exercise
applicable to
the condition
of the client.
References:
A
Thomas, S., Browne, H., Mobasheri, A., & Rayman, M. P. (2018). What is the evidence for a role for diet and nutrition in
osteoarthritis. Rheumatology, 57(suppl_4), iv61-iv74.
BRiecke, B. F., Christensen, R., Christensen, P., Leeds, A. R., Boesen, M., Lohmander, L. S., ... & Bliddal, H. (2010).
Comparing two low-energy diets for the treatment of knee osteoarthritis symptoms in obese patients: a pragmatic
randomized clinical trial. Osteoarthritis and Cartilage, 18(6), 746-754.
CSimopoulou, T., Malizos, K. N., Poultsides, L., & Tsezou, A. (2010). Protective effect of atorvastatin in cultured

osteoarthritic chondrocytes. Journal of Orthopaedic Research, 28(1), 110-115.

DRAYMAN, M. C., & Nutrition, A. (2006). Arthritis.

Prepared by:

Leslie Ann P. Mesolis, SND

Student Nutritionist-Dietitian
Date: April 23, 2022

Checked by:

WILMAR JUN O. ELOPRE, RND

Supervising Dietitian/Instructor
Date: _________________
 B. Dietary Prescription, Food and Menu Plan

Name: Lola Naring Height: 157 cm Weight: 67 kg

DBW: 51.3 kg TER: 1400 kcal

DIET PRESCRIPTION: 1400 Kcal, CHO: 193 g, CHON: 53 g, FAT 30 g

Table 1. Food Plan

Total
Number of Carbohydrate Protein Fat
Energy
Exchanges
Food Group (g) (g) (g) (Kcal)
Vegetable 4 12 4 0 64
Fruit 4 40 0 0 160

Milk (low fat) 1 12 8 5 125

Sugar 3 15 0 0 60
CHO partial sum 79
193 - 79 = 114/23 = 4.9 or 5 rice exchange
Rice A – Low
2 46 0 0 184
Protein
Rice B – Medium
3 69 6 0 300
Protein
CHON partial sum 18
53 - 18 = 38/8 = 4.3 or 4 meat exchange
Low Fat 2 0 16 2 82
Medium
Meat 2 0 16 12 172
Fat
Fat partial sum 19
30 - 19 = 11/5 = 2.2 or 2 fat exchange
Fat 2 0 0 10 360
Total 194 50 29 1507

Table 2. Distribution of exchanges per meal for Client B

Food Group Number of Breakfast Morning Lunch Afternoon Supper
Exchanges Snack Snack
Vegetable 4 ½ 2 1½
Fruit 4 1 1 1 1
Rice A – Low 1 1
Protein
Rice B – 3 1 1 1
Medium Protein
Rice C – High 1 1
Protein
Milk 1 1
Low Fat 2 1 1
Meat Medium 2 2
Fat
Fat 6 2 2 1½ 1½
Sugar 3 1½ 1½

Table 3. One-Day Menu for Client

Meals of Food Group Sample Menu Household
the Day List Number of Measure
Exchanges
B Banana and egg white boiled with tomatoes
R Fruit 1 Banana, latundan ½ pc
E MF meat 2 Egg, white 2 pc
A Vegetable ½ Tomatoes ¼ cup
K Fat 1 Oil, canola 1 tsp
F Rice C 1 Oatmeal 1 ¼ cup
A
S
T
Avocado in ice
AM Rice B 1 Puto, puti 1 slice
SNACK Fat 2 Avocado 1 cup
Sugar 1½ Condensed Milk 1 ½ tsp
Sinigang Salmon
LF meat 2 Salmon, fillet 2 slices
L Vegetable 2 Okra 1 cup
U Malunggay Leaves
N Eggplant
C Fat 2 Oil, canola 2 tsp
H Rice B 1 Boiled Brown Rice ½ cup
Fruit 1 Watermelon 1 slice
Kamote Cue
PM Rice A 1 Sweet potato, with 1 pc
SNACK Sugar 1½ sugar, fried 1 ½ tsp
Fruit 1 Lemon juice ½ cup
Law-uy
LF meat 2 Fried, maya-maya 2 slices
Vegetables 1½ Malunggay leaves ¾ cup
S Tomato
U Okra
P Kalabasa
P
Fat 1½ Oil, canola 1 ½ tsp
E
Rice B 1 Boiled Brown Rice ½ cup
R
Fruit 1 Apple 1 slice

Table 3.1 Estimated Nutrient Content of the Menu

Type of Food Ingredients HH Weight Energy CHO (g) Fat (g)
meal Items/Name measure in grams Content
of Dish ment (g) (kcal)
Breakfast Banana and Banana, 1 pc 80 84 19.2 0.24
egg white Latundan
boiled Egg, white 2 pcs 110 67 2.2 0.22
oatmeal with Tomatoes ¼ cup 20 5 1.12 0.02
 tomatoes Canola oil 1 tsp 5 40 0 4.5
Oatmeal 1 ¼ cup 30 118.2 23.37 1.41
Milk Low-fat milk 1 cup 30 108.6 14.4 0.24
AM Puto Puti 1 slice 50 107 24.95 0.15
Snack Avocado 2 slices 65 65.65 6.83 4.03
Condensed 1 ½ tsp 7.5 25.05 4.44 0.53
milk
Lunch Sinigang Salmon, fillet 2 slices 70 59.5 0 0.49
Salmon Okra ¼ cup 22.5 6.75 1.37 0.05
Malunggay ¼ cup 20 12.6 2.12 0.18
leaves
Eggplant ¼ cup 22.5 5.63 1.10 0.02
Canola oil 2 tsp 10 80 0 9
Rice Brown ½ cup 80 290 61.04 2.24
Watermelon 1 slice 150 46.5 10.8 0.3
PM Boiled sweet Sweet 1 pc 30 71.7 12.93 2.07
snack potato with potato, with
lemon juice sugar, fried
Lemon Juice ½ glass 65 16.25 5.61 0
Dinner Rice Brown 1 cup 160 290 61.04 2.24
Law-uy Squash ¼ cup 20 9.4 2.16 0.04
Eggplant ¼ cup 22.5 5.63 1.10 0.02
Okra ¼ cup 22.5 6.75 1.37 0.05
Malunggay ¼ cup 20 12.6 2.12 0.18
leaves
Tomato ¼ cup 20 5 1.12 0.02
Canola oil 1 ½ tsp 7.5 3.82 0 7.5
Fried Fish Maya-maya 2 slices 70 44.8 0 0.14
Apple, Green 1 slice 75 47.25 11.18 0.08
TOTAL 1635 242 36
ADEQUACY 117% 125% 77%

Table 3.2 Estimated Nutrient Content of the Menu

Type of Food Ingredients Fiber SFA PUFA MUFA
meal Items/Name of
Dish
Breakfast Banana and egg Banana, 2.24 0.08 0.06 0.02
oatmeal with Latundan
tomatoes Egg 0 0 0 0
Tomatoes 0.06 0.002 0.01 0.004
Canola oil 0 0.32 1.33 2.56
Oatmeal 3.15 0.28 0.52 0.47
Milk Low-fat milk 0 0.16 0.01 0.06
AM Snack Puto Puti 0.75 0.12 0.01 0.02
Avocado 3.12 0.79 0.67 2.21
Condensed 0 0.56 0.02 0.15
milk
Lunch Sinigang Salmon Salmon, fillet 0 0.70 0.12 0.16
Okra 0.59 0.01 0.01 0.01
 Malunggay 0.34 0.03 0.05 0
leaves
Eggplant 0.34 0.005 0.01 0.002
Canola oil 0 0.64 2.66 5.12
Rice Brown 2.24 0.46 0.82 0.83
Watermelon 0.6 0.03 0.11 0.08
PM snack Boiled sweet Sweet potato, 1.29 1.75 0.03 0.12
potato with with sugar,
lemon juice fried
Lemon Juice 0.26 0 0 0
Dinner Rice Brown 2.24 0.46 0.82 0.83
Law-uy Squash 0.002 0.008 0.02 0.004
Eggplant 0.34 0.005 0.01 0.002
Okra 0.59 0.01 0.01 0.01
Malunggay 0.34 0.03 0.05 0
leaves
Tomato 0.06 0.002 0.01 0.004
Canola oil 0 0.53 2.22 4.42
Fried Fish Maya-maya 0 0.03 0.05 0.03
Apple, Green 2.25 0.02 0.02 0
TOTAL 23 9 14 24
ADEQUACY 76% 78% 85% 78%

Prepared by:

Leslie Ann P. Mesolis, SND

Student Nutritionist-Dietitian
Date: April 23, 2022
 C. Nutrient/Food-Drug Interactions

Medications/Supplements Nutrition Interactions Signs/Symptoms

Herbal Supplements (Pain N/A N/A
Reliever)
 D. Nutrition Assessment Tools

NUTRITION AND DIATETICS SERVICE

MEDICAL NUTRITION THERAPY FORM
(Nutrition Care Plan)

Name of the Patient (Last, First, MI): Lola Naring Hospital: ________________ Age: 72 Gender: Female
Name of Attending Physician: ________________________ Date of Admission: ______________
Diagnosis: Osteoarthritis Religion: Roman Catholic

NUTRITION ASSESSMENT
Present Diet of Patient: Normal Diet… Height: 157 (cm) Weight: 67 (kg)
Usual weight: ___ (kg) BMI: 27.18 kg/m2
Weight change: ___% over ____ weeks/months
%IBW: 131%
_✓ No change Biochemical Data:
____ Mostly liquids Albumin: Hematocrit
____ Sub-Optimal BUN: Hemoglobin
____ Starvation Calcium: LDL:
Poor intake prior to Cholesterol: 7.07 Phosphate:
Food Intake: admission mmol/L (↑) Potassium:
Creatinine: Sodium:
Glucose: 12.53 Triglycerides:
mmol/L (↑) URR:
HbA1C: 13.9% (↑)
HDL:
Bedridden Others: N/A
Functional
_✓ Ambulatory BP: N/A Acid Base Gas (ABG): N/A
Capacity:
____ Needs Assistance
Chewing/Swallowing Difficulties: N/A Food Allergies: N/A
Constipation: N/A Diarrhea: N/A Food Intolerance: N/A
Nutrient & Drug Interactions: N/A
SCORING OF NUTRITIONAL RISK RELATED FACTORS
_✓ Screening criteria for potential nutritional risk Mechanical / Digestive Problem (1 point)
(1 point) Low Albumin (1 point)
_✓ <85% or >130% Ideal Body Weight (1 point) _✓ Significant Lab Result (1 point)
Unintentional Weight Loss ____% over _____ Other/s (1 point)
weeks/months (2 points) TOTAL POINTS: 3 points

A nutrition risk factor with the following total score indicates:

□ 1 Low Risk 🗹 2-3 Moderate □ >3 High risk
NUTRITIONAL STATUS
□ Normal □ Moderate Malnutrition □ Severe Malnutrition
NUTRITION DIAGNOSIS (PROBLEM, ETIOLOGY, SIGNS AND SYMPTOMS)
Overweight related to excess energy intake as evidenced by BMI value of 27.18 kg/m2, report of physical
inactive and 163% of calorie adequacy.
Altered nutrition-related laboratory values (fasting blood sugar, and cholesterol) related to snacking of high
simple sugar foods and consumption of high saturated fat foods as evidenced by elevated fasting blood
sugar (13.29 mmol/L), cholesterol (8.82 mmol/L), and creatinine (126.75 umol/L).
 Increased nutrient needs (omega-3) related to increased demand of knee osteoarthritis as evidenced by
report of intake of foods low in omega-3.

NUTRITION INTERVENTION
Total Energy Requirement (TER): 1400 kcal/day
Carbohydrates: 193 grams/day Protein: 53 grams/day Fat: 46 grams/day
Others (e.g., micronutrients):
NUTRITION MONITORING AND EVALUATION
□ Shift diet to: 🗹 Compliance to Diet
(✓) Calories (✓) Protein (_) Fluid 🗹 Weight Changes
□ GI Tolerance
Recommended by: Conforme (Attending Physician):

LESLIE ANN P. MESOLIS ___________________________

Registered Nutritionist-Dietitian Physician

24-hour Food Recall

Type of Food Ingredients HH Weight Energy CHO (g) SF (g)
meal Items/Na measurement in grams Content
me of (g) (kcal)
Dish
Breakfast Rice Brown 1 cup 160 581 122 0.91
Ginisang Chayote 1 cup 80 12.8 2.8 0
Sayote
Vegetable 1 tablespoon 15 134 0 12.86
oil
Tomato ¼ cup 20 5 0.84 0
Maya-maya 1 matchbox 30 19 0 0
Banana Latundan 1 pc 80 84 19.52 0.1
Milk Anlene 1 cup 30 110 20 0.6
AM Softdrink Royal 1 glass 250 50 13 0
Snack Cake Chocolate 2 slices 80 298 47 2.98
cake
Lunch Rice Brown Rice 1 cup 160 581 122 0.91
Ginisang Upo 1 cup 80 12.8 3.04 0
Upo Vegetable 1 tablespoon 15 134 0 12.86
oil
Maya-maya 1 matchbox 30 19 0 0
Tinola Chicken, 1 matchbox 30 45 0 0.63
hita
Upo ¼ cup 20 3.2 0.76 0
Banana Latundan 1 pc 80 84 19.52 0.1
PM Softdrink Royal 1 glass 250 50 13 0
snack Leche Flan 2 slices 80 182 33 1.8
Dinner Rice Brown 1 cup 160 581 122 0.91
Law-uy Squash ¼ cup 20 9 0.3 0.1
 Eggplant ¼ cup 20 5 0.98 0.20
Okra ¼ cup 20 6 1.22 0
Malunggay ¼ cup 40 25.2 2.12 0.10
leaves
Fried Fish Maya-maya 1 matchbox 30 19 4.7 0.1
Milk Anlene 1 cup 30 110 20 0.6
TOTAL 3160 568 36
 A. Summary of the Nutrition Assessment Findings and Indications

Indicator Actual Normal Indication Nutrition

Value/Observation Value/Observation Assessment
Domain
Energy Intake 2844 kcal/day 1660 kcal/day Excess FH

BMI 27.18 kg/m2 18.5-24.99 kg/m2 Overweight AD

Fasting Blood 12.53 mmol/L 4.20-6.40 mmol/L Above BD

Sugar

Cholesterol 7.07 mmol/L 0.00-5.20 mmol//L Above BD

Creatinine 168.07 umol/L 53-97 umol/L Above BD

HbA1c 13.9% 4% - 6% Above BD

B. Documentation

Figure 1. Actual Picture of Lola Naring

Figure 2 - 3. Dietary Assessment with Lola Naring.

Figure 4 - 5. Biochemical Results of Lola Naring
 VI. GLOSSARY OF TERMS

Arthritis. A condition in which one or more joints enlarge and become tender. Joint pain and
stiffness are the most common symptoms of arthritis, which normally worsen with age.
Osteoarthritis and rheumatoid arthritis are the two most frequent kinds of arthritis.

Clinical Manifestation. The physical manifestation of a sickness or infection is referred to

as a clinical manifestation. Clinical manifestations that can be objective when seen by a
doctor or subjective when experienced by the patient.

Dietary Intake. An individual's daily eating habits, including the foods and calories ingested,
as well as their relative amounts.

Edema. Swelling is referred to as edema. Edema occurs when fluid accumulates in the
tissue of a portion of the body, causing it to swell. The arms and legs are the most usually
affected areas. Peripheral edema is the medical term for this condition.

Epidemiology. The study of the causes and distribution of health-related states and
diseases in certain populations.

Etiology. In medicine, etiology refers to determining the cause of a disease or condition.

Knee Osteoarthritis. Wear and tear, as well as progressive loss of articular cartilage, are
the most common causes of degenerative joint disease of the knee. It affects the elderly the
most.

Osteoarthritis. Inflammation, disintegration, and eventual loss of cartilage in the joints

produce this type of arthritis. Degenerative arthritis is another name for this condition.

Overweight. Patient/Client having a BMI of 25 – 29.99 kg/m2

Pathogenesis. The development of a disease and the sequence of circumstances that lead
to it.

Pathophysiology. The study of abnormal changes in body functioning that occur as a result
of, or in conjunction with, illness processes.

Physical Impairments. Physical impairments are situations in which a person's ability to do

physical tasks, coordinate motions, and perform essential living activities is impaired.

Prognosis. A prognosis is a prediction of someone's or something's future, particularly

whether or not a patient will recover from an illness.

Synovial hyperplasia. A condition in which the cellularity of the synovial membrane

increases, resulting in synovial thickness, which is a typical radiographic characteristic in
synovitis
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