MNT Exam 4

Pathophysiology of cancer

abnormal/uncontrolled cell division and reproduction

carcinogenesis

origin or development of cancer

oncogenes

inhibit apoptosis

tumor suppressor genes

become deactivated in cancer cells

what percent of all cancers occur as a result of inherited mutations?

5-10%

top 10 cancers by rate of new cancers

1. breast

2. prostate

3. lung and bronchus

4. colon/rectum

5. corpus/uterus

6. skin

7. urinary

8. lymphoma

9. kidney/renal pelvis

10. leukemias

top 10 cancers by rates of death

1. lung/bronchus

2. prostate

3. breast

4. colorectal

5. pancreas

6. liver and bile duct

7. leukemias

8. ovary

9. corpus/uterus

10. lymphoma

nutrition related carcinogenesis

polycyclic aromatic hydrocarbons (surface of red meat)

alcohol - daily consumption of tow or more drinks

obesity - insulin-like growth factor-1 - second only to tobacco use

BPA

nutrition prevention of cancer

antioxidants/phytochemicals negate effects

omega-3s

protein foods - particularly soy protein

chemoprevention of cancer

antioxidants and bioactive compounds found in F/V

vitamin D

flavonoids and phytates - found in coffee and tea

phytochemicals - cruciferous veggies

vegetarian diets (adults only)

physical activity - decreases co-morbidities

goals of cancer treatments

cure - complete response to treatment

control - extend life when cure not possible

palliative - keep patient as comfortable as possible

MNT for curing cancer

adequate calories, PTN, micronutrients, supplements, monitor body weight (compare to pre cancer weight)

MNT to control cancer

maintain/replenish body weight - calories and PTN

MNT for palliative cancer treatment

food and drink for comfort and joy only

withdrawing nutrition support

managing discomfort

nutritional impact of chemotherapy/biotherapy/hormone therapy + MNT

diarrhea, nausea, vomiting

MNT - encourage fluids, smaller more freq meals, low fiber

nutritional impact of radiation + MNT

esophagitis, enteritis

MNT - nutrition support, modified textures

nutritional impacts of hematopoietic cell transplantation + MNT

immunosuppression

MNT - safe food handling to decrease infection risk

pre - cachexia

loss of appetite (anorexia)

impaired glucose intolerance

may precede involuntary weight loss

progression of pre-cachexia to cachexia depends on…

cancer type and stage

presence of systemic inflammation

low food intake

lack of response to anti cancer therapy

overview of cancer cachexia

poor nutrition coupled w/ effects of cancer treatment may lead to malnutrition

associated with

1. reduction in treatment tolerance

2. compromised response to therapy

3. poor quality of life

4. decreased duration of survival

pathophysiology of cancer cachexia

negative protein and energy balance driven by:

1. reduced food intake

2. abnormal metabolism

3. systemic inflammation

diagnosis of cachexia

weight loss >5%

body mass index <20 and weight loss >2%

sarcopenia and weight loss >2% (muscle wasting)

clinical symptoms and effects of cachexia

persistent loss of skeletal muscle w/ or w/o fat mass loss (fat more likely to be preserved)

anemia

malnutrition

diagnosis guidelines domains for cachexia

1. intake

2. clinical - swallowing difficulty, GI

3. behavior - environmental domain

energy needs for cancer

individualized to condition

• repletion/weight gain - 30-35kcal/kg

• hypermetabolic/stressed - 35 kcal;/kg

• hemapoteitic cell transplant - 35 kcal/kg

• sepsis - 20-30 kcal/kg

protein needs for cancer

individualized - 1.2-1.5 g/kg

fluid intake for cancer

20-40 ml/kg or 1ml/kcal

at least small sips w/ every meal and snack

supplements and cancer patients

be aware of alternative/complementary medicine approaches

ask why and who told pt to take supplement

concentrated green tea (anti-inflammatory) - negatively impacts drug function

alternative and complementary treatment of cancer

natural products - be mindful of liver toxicity

mind/body practice - meditation, yoga

placebo effect, helps mindset

epidemiology of HIV/AIDS

prevention - preexposure prophylaxis drugs (PREP)

transmission - non sterile syringes, pregnancy/breast feeding, blood transfusion, organ transplant, unprotected sex

side effects of PREP

gastric distress

diarrhea

headaches

weight loss

early HIV symptoms

flu like symptoms within 2-4 weeks of infection

often mild symptoms - mistaken for other illnesses

some individuals do not experience may symptoms in initial phase

pathophysiology of HIV

primary HIV infection invades genetic core of CD4+ cells, which are T-helper lymphocyte cells

4 stages of progression:

1. acute HIV

2. clinical latency

3. symptomatic HIV

4. AIDS

biomarkers: HIV RNA (viral load) and CD4+ cell count (check every 3-4mo)

seroconversion: detectable antibodies against HIV virus (3weeks - 3 months post infection)

medical management of HIV

ART - antiretroviral therapy

goal: stop viral replication, maintain viral suppression, prevent drug resistance

predictors of adherence to medical management of HIV

health literacy

neurocognitive impairment

psychosocial issues

substance use

stigma

denial

difficultly with taking medications

complexity of regimen

food insecurity

food and drug interactions for HIV

grapefruits and PIs compete for P450 enzyme

alcohol metabolism may be affected and increase risk of toxicity

many ART drugs need to be taken with a meal

nutrition related side effects of HIV

diarrhea, fatigue, reflux, nausea, vomiting

dyslipidemia, insulin resistance (due to inflammation)

HIV energy needs

asymptomatic: increase REE by 10%

opportunistic infections: increase REE by 20-50%

HIV protein needs

1-1.4 g/kg for maintenance

1.5-2 g/kg for increasing lean body mass

protein needs increase with CD4 <500

assessing anthros/body composition

HIV associated lipodystrophy syndrome - much less common now

wasting

reducing CVD risk and obesity

HIV associated lipodystrophy syndrome

metabolic and physiological changes

establishing baseline or history is important

gain or loss of fat mass

wasting in HIV

unintentional weight loss, fat loss, eventually muscle loss

highest risk is individuals not on ART

reducing CVD risk and obesity in HIV patients

omega 3 fatty acids

physical activity

general healthful diet

GI health in HIV

supplemental protein, probiotics, yogurt glutamine may help GI side effects

products with live and active cultures

pair with regular intake of prebiotics

Definition of inborn errors of metabolism

inherited traits which result int he absence or reduced activity of a specific enzyme or cofactor

goals of MNT for genetic metabolic disorders

maintain biochemical equilibrium

support typical growth and development

support social and emotional development

purpose of newborn screenings

prevent or reduce severe clinical illness, neurological impairment, intellectual disability

MNT interventions of inborn errors of metabolism

1. restricting available substrate

2. supplementing product

3. providing enzymatic cofactor

4. using a combination of above

disorders of AA metabolism

require low protein diet or diet absent of specific AA

PKU

Phe is not metabolized to Try because of deficiency of phenylalanine hydroxylase

tyrosine becomes conditionally essential

all states screen for PKU at birth

prevalence: 1:15,000

maple syrup urine disease (MSUD)

branched chain keto-acid decarboxylase complex

low protein - without leucine, isoleucine, valine

supplement thiamin

prevalence: 1:185,000

diagnosing PKU

blood Phe >6-10mg/dl (360-600 mmol/L)

tyrosine levels < 3mg/dl (165 mmol/L)

routine checks of blood Phe to make sure within range of 2-6 mg/dl

enzyme replacement therapy now available

MNT for PKU

phenylalanine free formula/medical food

low phenylalanine foods

supplement with tyrosine

adequate nutritional intake

regular monitoring of growth

family/patient education

Steps in PKU diet Rx

1. fluid requirements

2. establish dosing weight and energy requirements

3. calculate total protein needs

4. estimate phenylalanine requirement

5. estimate remaining protein intake considering tyrosine intake

6. meeting remaining kcal need from CHO and fat

7. consider vitamin and mineral requirements

8. calculate final Rx and develop meal plan

9. double check work

medical treatment of MSUD

peritoneal dialysis

maintain plasma leucine concentration

therapeutic liver tranplantation

MNT for MSUD

restrict the substrate: low protein formula

gradual introduction of BCAAs when plasma Leu concentrations are normal

disorders of organic acid metabolism

vast majority require low protein diet

examples: methylmalonic academia, propionic academia

risk and complications: seizures, metabolic acidosis, brain damage, hyperammonemia, coma, vomiting

for ketone utilization disorders: upper limit of protein 1.5g/kg/day and supplemental bicitra to reduce ketoacidosis

disorders of urea cycle metabolism

require low protein diet, formulas w/o nonessential AA

steps in designing low protein eating plan

1. determine protein tolerance based on age, diagnosis, growth

2. calculate the portion and energy needs

3. provide at least 70% of total protein as high-biological value protein from formula for infants from milk or dairy foods for older kids

4. provide energy and nutrient sources to meet basic needs

5. add water to meet fluid requirements

6. for older kids provide foods to meet food variety, texture, energy needs

7. provide adequate intake of calcium, iron, zinc, and other vitamins and minerals for age

disorders of carb metabolism

elimination of problematic carbohydrate sources

glycogen storage disease

symptoms

• enlarged liver (build up of glycogen)

• hypoglycemia

• impaired growth

inability to convert glycogen to glucose

normalize blood glucose/maintain euglycemia

GSD treatment (medical/MNT)

medical - need to monitor and normalize blood gluocse

MNT -provide glucose in the diet to maintain euglycemia

disorders of FA oxidation

requires low fat diet (<30%)

requires avoidance of fasting and high intake of CHO rich foods

supplements for disorders of FA oxidation

L-carntitine

MCT oil

MNT goals

tailoring dietary plans to match specific metabolic defects, ensure optimal growth and minis harmful effects of the disorder