The flashcards below were created by user
on FreezingBlue Flashcards.
Nutrition 5 - Protein Energy Malnutrition (PEM)
- proteins synthesized & secreted by the viscera (organs), primarily the liver (eg. albumin)
- in a healthy individual visceral proteins reflect nutritional status
- in an ill individual the level of visceral protein no longer reflects nutritional status
Acute Phase Proteins
- proteins whose plasma concentrations increase (positive) or decrease (negative) in response to inflammation or illness
- the response is called the acute-phase reaction
What are the two main causes of undernutrition?
- 1. restricted food intake (eg. starvation, anorexia, diet)
- 2. illness/pathology (eg. cachexia, sarcopenia)
- both can lead to protein energy malnutrition (PEM)
What happens when there is a decrease in energy intake?
- 1. reduced energy EXPENDITURE
- 2. increased reliance on FAs & ketones
- 3. less protein is used for gluconeogenesis
What happens when someone cuts down how much protein they eat?
- 1. they increase the recycling of AAs
- 2. the synthesis of visceral proteins is prioritized (makes a person vulnerable to infection)
Protein energy malnutrition (PEM)
- a condition caused by prolonged inadequacy of protein or energy required to meet the body's metabolic demands
- increases a persons risk of morbidity & mortality
- also called Protein Calorie Malnutrition (PCM)
- occurs when dietary intake of protein is insufficient to meet metabolic demands
- people who try to lose weight (“therapeutic dieting”) generally don't get PEM unless there is extended severe energy deficiency or inadequate protein intake
What are some causes of primary PEM?
- 1. social factors: poverty, limited access to food, famine, war, living alone w/ inability to get food
- 2. in children due to inappropriate feeding b/c of restrictive diets, inadequate feeding w/ illness, improper introduction of complementary foods
- 3. alcohol or drug abuse
- 4. food faddism/highly restrictive diets
- caused by acute or chronic illness (or its treatment) which:
- 1. impairs the intake or absorption of protein or energy (eg. oral cancer)
- 2. increases excretion of energy or protein (eg. diarrhea or urinary losses of protein)
- 3. increases protein or energy requirements (eg. fever or trauma)
- 4. increases metabolic losses or reduces metabolic efficiency (eg. futile cycling that accompanies some diseases)
Cachexia (Wasting Syndrome)
- loss of weight, muscle atrophy, fatigue, weakness, & loss of appetite in someone not trying to lose weight - there is a disproportionate loss of FFM compared to the FM lost
- the losses cannot be reversed nutritionally: even if the affected patient eats more calories, lean body mass will be lost, indicating a primary pathology
- the condition is mediated by inflammation, hormone cascades, & the CNS/SNS
What type of conditions are often accompanied by Cachexia?
- 1. Cancer --> inflammation (IL-6, TNF-alpha, IL-1Beta, IL-8)
- [Chronic obstructive pulmonary disease (COPD) also leads to inflammation & subsequent cytokine production]
- 2. End Stage Renal Disease or Chronic Kidney Disease (ESRD/CKD) --> catecholamines (epineph + norepineph)
- [congestive heart failure (CHF) also leads to catecholamine production]
- age-related degenerative loss of skeletal muscle mass, quality, & strength
- mediated by pro-inflammatory cytokines, growth hormone secretion, & input from a CNS that has fewer motor neurons
- a type of PEM that manifests as a primary deficiency of energy
- there is a loss of body mass but hepatic/visceral proteins (eg. albumin) are maintained
- is a chronic condition that progresses over weeks to months; body fat is lost to a greater extent than lean tissue (until fat stores are depleted)
- advanced marasmus is characterized by severe loss of fat + skeletal muscle, & in children a below average height for their age
Wasting caused by Marasmus manifests how in respect to data points?
- children: low weight for their height
- adults: unhealthily low BMI
What is the most obvious symptom of Marasmus?
loss of subcutaneous fat
In the FFM (fat free mass) category of people suffering from Marasmus, do people lose more muscle or more organ tissue?
More Muscle is lost than organ tissue
dietary protein deficiency with varying degrees of energy deficiency; can occur as a result of not enough protein or essential AA intake
What is the translation of Kwashiorkor?
"the sickness the [first] baby gets when the new baby comes"
What are characteristic symptoms of Kwashiorkor?
- 1. reduced circulating concentrations of proteins such as albumin
- 2. edema from a DECREASE in oncotic pressure
Which progresses more quickly, Marasmus or Kwashiorkor?
- Kwashiorkor's progression of is highly variable but is usually more rapid than marasmus
- if kwashiorkor persists, muscle wasting will become evident
What role does Insulin play in Kwashiorkor?
- it promotes/worsens the disease
- eating CHOs stimulate insulin secretion, which stimulates muscle protein anabolism & reduces muscle catabolism
- this results in fewer AAs released from muscle
- with fewer circulating AAs, the liver lacks substrates to synthesize visceral proteins (eg. albumin)
- albumin is a major contributor to oncotic pressure; decreased concentrations of it result in less fluid in the vasculature & more in interstitial spaces [EDEMA]
Besides edema (aka fluid retention in interstitial spaces), what else contributes to the abdominal distention characteristic of Kwashiorkor?
- a liver that is unable to package & export fat and therefore accumulates it, increasing in size
- insufficient AAs results in less hepatic synthesis of apoproteins that combine with lipid to be export from the liver
- TAG synthesis proceeds as a result of CHO feeding, but cannot be packaged into VLDL & exported
- occurs when there is combined energy AND protein deficiency, resulting in loss of fat, lean mass, & reduced circulating protein concentrations
- if marasmus occurs first, it increases susceptibility to further infections, which can result in a kwashiorkor-like syndrome that accompanies acute illness superimposed on marasmus (separate from Marasmic Kwashiorkor)
How can Marasmus be distinguished from Kwashiorkor?
- kwashiorkor (pregnant babies) is protein deficiency w/ adequate energy intake whereas marasmus (skeletons) is INadequate energy intake in all forms, including protein
- Marasmus: depletion of skeletal muscle protein (after a while), but maintenance of visceral protein (until late stage of the disease)
- Kwashiorkor: depletion of visceral protein (primarily), but maintenance of skeletal muscle protein (b/c of insulin)
What illness is sometimes characterized by the "flag sign"?
- flag sign = when the hair loses pigment, because pigment is produced by protein & there is insufficient protein in Kwashiorkor
What factors influence the outcomes of PEM?
- 1. *the duration of undernutrition affects the outcome
- 2. dehydration (is fatal in 1-2 weeks)
- 3. the degree to which PEM occurs
- 4. what type of diet is present
- 5. weight & body composition (initial & what's lost)
- 6. whether there's additional infection (accelerates M&M)
Complications of PEM
- 1. delayed growth & development
- 2. loss of productivity & play
- 3. infections (esp. respiratory & GI)
- 4. anema
- 5. cardiac arrhythmia
- 6. eventual loss of energy stores -> circulatory collapse, respiratory failure, coma
Death is associated with a loss of
- 40-50% of body weight
- 30-50% of fat free mass (FFM)
- 75-90% of FM (fat mass)
- a BMI of less than 11 for women, 13 for men
Why does Marasmus have a low BMI associated with mortality but Kwashiorkor has a high BMI associated with mortality?
- because there is no confounding variable in Marasmus, BMI is indicative of the actual ratio of weight to height; the lower the less healthy
- more severe Kwashiorkor is associated with severe edema, which confounds BMI; it's no longer actually representative of a person's weight to height, however a greater BMI = more edema = a more severe disease
refers to protein energy malnutrition (PEM) in acutely ill patients; micronutrient deficiency or excess may also be present
Due to the body's metabolic response to acute illness, PEM in acutely ill patients often resembles what?
- if illness or inadequate energy intake persists, marasmic kwashiorkor may result
- hospitalized patients may suffer from primary PEM, secondary PEM associated with chronic or acute illness, or both; acute PEM may be superimposed on chronic PEM
What features characterize the response to acute illness, sometimes called “the stress response”?
- 1. fever - increased resting energy expenditure (REE)
- 2. hormonal responses (insulin resistance, increased glucagon & cortisol)
- 3. activation of SNS & catecholamines
- 4. cytokine response (more acute phase than visceral proteins made)
integrated metabolic response to illness
- • Hypermetabolism: increased energy needs proportional to severity of illness and fever
- • Accelerated protein catabolism of muscle, albumin & other proteins
- • Altered hepatic protein synthesis (acute [ferritin] > visceral [albumin])
- • Gluconeogenesis even when blood glucose is normal or elevated
- • Hyperglycemia
- • Edema due to hypoalbuminemia, increased capillary “leakiness”, & water retention
- • Futile Cycles
What does glucose NOT do in acute illness?
it does NOT suppress muscle catabolism OR gluconeogenesis
What type of person is at risk for PEM-related complications?
- 1. someone with a BMI of less than 18.5
- 2. someone's who's lost 10% of body weight (especially if this is accompanied by a physiologic deficit)
- 3. someone who has already had PEM
- 4. someone w/ a history of poor nutrient intake
What is not a good indicator of malnutrition (esp. PEM) in a person who is hospitalized?
- low serum albumin concentration could have been normal prior to admission but is now low b/c of illness, NOT b/c of pre-existing PEM
- also changes in body fluid will dilute or concentrate protein concentrations - BAD MEASUREMENT of nutritional status
When should a hospitalized patient be fed?
- depends on their condition
- Well nourished: feed within 7-10 days
- Malnourished: feed within 3-5 days
- patients with pre-existing PEM should receive nutrition within 3-5 days (these patients have reduced “reserves” and are at greater risk for complications due to PEM)
- ICU: consider feeding within 1-2 days if hemodynamically stable
By what 2 means is nutrition support is provided?
- 1. enteral nutrition
- 2. parenteral nutrition
- use of the gut for feeding: tubes are placed
- into the stomach or through the stomach into the intestine by insertion through nose (nasogastric/nasoenteric tubes) or mouth (orogastric/oroenteric tubes)
- consists of a formula containing water, macronutrients, fiber, & micronutrients
- more permanent versions of enteral feeding are tubes placed through the abdominal wall into the stomach or small intestine
What are the benefits of enteral feeding?
- prevention/treatment of malnutrition
- minimizes complications of parenteral nutrition
- maintains the gut mucosa
- prevents bacterial translocation
- stimulates GALT
- reduces infection
- modulates stress response
What are some complications that may result from enteral feeding?
- 1. may be incorrectly placed outside the stomach (eg. lung or worse…brain)
- 2. aspiration pneumonia (lung infection)
- 3. diarrhea
- the gut is bypassed and patients are fed intravenously
- provision of nutrition into a central vein such as the vena cava is called total parenteral nutrition (TPN)
- provision into a smaller vein in the extremities or elsewhere is called peripheral parenteral nutrition (PPN)
- consists of a formula containing water, macronutrients (simplest forms), electrolytes, vitamins, & trace elements
What is more common with parenteral nutrition?
- 1. more calories are delivered
- 2. more hyperglycemia
- 3. more infections
- however overall in comparison with enteral nutrition, there is generally no difference in mortality or length of hospital stay
TPN v. PPN
- total parenteral nutrition: HIGH osmolarity requires nutrients be administered in vena cava; meets E & protein needs
- peripheral parenteral nutrition: LOW osmolarity due to risk of phlebitis; may NOT meet E & protein needs
What are some complications that may result from parenteral feeding?
- thrombosis (phlebitis)
- refeeding syndrome
- liver dysfunction
- incorrect central catheter placement (into lung causing pneumothorax)
What type of hospital patients are likely to benefit from nutrition support?
- pre-operative patients with moderate-to-severe PEM
- inpatients hospitalized with severe alcoholic liver disease
- patients about to undergo bone marrow transplantation
- any acutely ill patient w/ malnutrition who will be unable to meet at least 80% of their metabolic needs alone in the next 48 hr
- an acutely ill patient who is mildly malnourished or well-nourished but who is unlikely to meet >80% of their nutritional needs within the next 7-10 days
Why would lipids be included in enteral or parenteral (emulsified) nutrition support?
- because they're an energy source & they prevent essential FA deficiencies
- US lipid sources only have omega-6 FAs but treatment w/ parenteral IV fish oil has been shown to decrease infection, days attached to a ventilator, & a patient's length of stay
- IV fish oil also decreased or reversed cholestasis (bile blockage or synthesis defect) in TPN-dependent children
What are some complications that may result from lipids in nutrition support?
- arachidonic acid production (PG & LT precursor --> immunosuppression)
- bacteremia or fungemia (in blood)
- bacterial growth in IV lipid emulsions
- CDC recommends such an IV hang for less than 12 hours
- metabolic disturbances that occur as a result of reinstitution of nutrition to patients who are starved or severely malnourished (low BMI, low ion levels, alcohol or drug abusers, unintentional weight losers)
- can result in respiratory failure, aspiration (lung infection), hemolysis - side effects of electrolyte abnormalities & micronutrient (eg. thiamine) deficiencies
- preventable by providing all electrolytes PRIOR to providing nutrition
What electrolytes are PARTICULARLY important to restore normal levels of in a person to prevent refeeding syndrome?
What happens in the body when ____ is overfed:
- CHO: there is an increase in CO2 production, increasing the respiratory quotient, resulting in difficulty breathing; could also cause hyperglycemia
- Fat: gums up reticular endothelial system, which makes it difficult for leukocytes in the blood to move through endothelium to sites of infection --> difficulty fighting infection
- Protein: not much happens when protein is overfed