Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
42 Cards in this Set
- Front
- Back
|
Define Cachexia |
The complex metabolic syndrome with muscle loss and possibly fat loss characterised by weight loss |
|
|
In which three aspects can cancer affect nutritional status? |
Tumor presence Host response Anticancer treatment |
|
|
What's the benefit of assessing nutrition? |
Early recognition and intervention Increase life expectancy, life quality, reduce morbidity, Improve immune system in help fighting disease Aid treatment and help recovery Design individual diet |
|
|
What does cachexia come from? |
Chronic disease, eg. chronic heart, lung, kidney, sepsis diseases, cancer |
|
|
Symptoms of cachexia? |
Inflammation, anorexia, insulin resistance, anemia, hypogonadism, then lead to muscle and fat loss, then weight loss and strength loss and fatigue |
|
|
Cachexia result most predominantly from which types of cancer? What are their incidence? |
Upper GI cancer 80% Lung cancer 60% |
|
|
What are the other forms of malnutrition? |
Undernutrition 1 or more nutrient deficient Sarcopenia muscle loss without weight loss Malnutrition under or over nutrition Starvation deprivation of all nutrients |
|
|
Similarities and difference between starvation and cachexia |
Starvation decrease in fat first, then muscle. Cachexia mainly muscle loss: fat breakdown and packed in VLDL. Insulin resistance, high serum insulin and cortisol. Resting metabolic rate increase Cachexia: still eating, so less caloric decease |
|
|
What's the change in fat and muscle loss in cachexia? |
50-50 fat and non-fat loss (skeletal muscle) |
|
|
What's the change in anabolic and catabolic factors in blood in cachexia? |
Anabolic decrease: GH, Thyroid, IGH-1, insulin, testosterone Catabolic increase: cortisol, glucagon, proinflammatory citokines, tumor-derived factors. |
|
|
What's acute phase response? |
Body's adaptation to tissue damage caused by hydrolase that's released from injured cell, tumor cell or malignant cells |
|
|
What's acute phase proteins? |
Released from liver concentration rises or falls in blood after inflammation positive or negative |
|
|
Give examples of acute phase proteins |
Positive: C, F Complement system, coagulation, c-reactive, fibrinectin, ferritin, inflammatory response elements Negative: A, T Transferrin, albumin, IGF-1, factor 12 |
|
|
Who produce cytokine? |
Host or tumor cells |
|
|
What's the function of cytokines? |
Regulate acute phase response, regulate immunocompetent cells, eg. macrophage, lymphocyte |
|
|
Where to cytokines act on? |
On the cells that produce them(autocrine) On other distant cells(endocrine) |
|
|
What are the examples of proinflammatory cytokines? |
(Interleukins) IL-1, IL-6 (interferon) IFN-gamma (leukemia inhibitory factor) LIF (tumor-necrosis factor) TNF-alpha |
|
|
Cytokine effects? |
Inflammation Loss of appetite, food intake Loss of GI mobility: slower gastric emptying, mobility of intestine Decreased blood flow Inhibit LPL Inhibit GH and IGF-1 signalling insulin resistance
|
|
|
Who modulates acute phase proteins? |
Cytokines |
|
|
Explain host-humor interactions of cachexia? |
Tumor causes inflammation, cytokines, acute phase proteins, anorexia and insulin resistance, muscle protein breakdown, muscle wasting |
|
|
What does TEE REE stands for? PAL? |
total energy expenditure and resting energy expenditure, physical activity level. >2.4 and <1.4 are the limits. |
|
|
What is hypermetabolism? What is the case of PAL in cachexia? |
Increase in REE level. In cachexia, REE increase but TEE decreases, due to lower physical activity. PAL rises |
|
|
What's the metabolism of lipid in cachexia? |
Lipolysis increases, lipid packed in VLDL in blood Not reabsorbed, thus low LPL activity. Hyperglycemia |
|
|
What's the metabolism of glucose in cachexia? |
Insulin resistance causes lower glucose uptake Glucose is the fuel for tumor, goes through Cori cycle. The body cannot uptake glucose, thus breakdown the only available protein
|
|
|
What's the metabolism of protein in cachexia? |
Increased proteolysis in muscle to produce AA for gluconeogenesis Decreased protein synthesis since less building blocks More hepatic proteins synthesis as APP |
|
|
What's the occurrence of anorexia in cachexia? |
50% |
|
|
What are the reasons of anorexia in cachexia? |
Less appetite Less GI motility: slower gastric emptying Brain chemo/radiation therapy Pain Depression Malabsorption Constipation Brain hypothalamus of appetite receptors
|
|
|
Early satiety reasons? |
Less GI motility, Increased gastric emptying time. Autonomic nervous dysfunction, opioid analgesics. |
|
|
Reasons for nausea? |
Nausea: drug side effects, abdominal disease, intracranial metastases, metabolic derangements, GI stasis |
|
|
Types and reasons of chemosensory abnormalities? |
Taste and smell distortions: taste aversion, phantom smells, hypersensitivity, bad tastes. treatment side effects, nutrient deficiency |
|
|
What's the clinical detection for cachexia? |
Exclusion: depression, sarcopenia, starvation, malabsorption, hyperthyroidism. Criteria: loss of more than 5% of body mass in last 12 months or less. 3 of the following 5: Fatigue, Decreased muscle strength, Anorexia, Low fat-free mass index Abnormal biochemistry, incl. Low albumin, anemia index, inflammatory markers. |
|
|
What are the goals of the therapy for cachexia? |
Increase lean body mass. Increase the perception of wellbeing Increase effect of treatments Manage symptoms Increase immune response |
|
|
The basic principle for nutritional counselling? The adaptations to individual has which criteria? Which are the recommendations? |
Individual More omega FA and multivitamin diet and exercise Increase in energy (1.5 REE) and increase in protein(1.2-1.5g/kg/d) Appetite, rounds of therapy, accessible routes of ingestion, symptoms |
|
|
What are the routes of nutritional administration? Which people are suitable for which? |
Oral- able to eat Enteral- not able to eat, Parenteral- Enteral not available, but end stage cancer patients not suitable |
|
|
What's the benefit of the oral and enteral routes of nutritional administration? |
Oral- follow individual's appetite, preference Enteral- Keeps GI tract intact, keeps architecture, barrier, immune functions and gut permeability. |
|
|
How is the recommendation of eating omega-3 FA in cachexia patients? |
Proven to reduce APPR, decrease tumor activity and chemotherapy toxicity. But contrasting Not harmful if less than 3 grams ingestion per day. |
|
|
How is the recommendation of eating AA in cachexia patients? |
No side effects. Increase protein formation rate and decrease proteolysis rate. |
|
|
What's the benefit of exercising in cachexia treatment? |
-Helps in anabolism -Strength training and nutritional supplements increase lean body mass in elderly- proven -Exercise help protein synthesis and turn blunted anabolism into restored. |
|
|
Which drug doesn't need further clinical trial for treatment in cachexia? |
progestational Megace |
|
|
What could be a concern of anabolic agents? |
Might feed tumor growth |
|
|
When can excess muscle proteolysis be beneficial to the body? |
Acute phase response. Life-sustaining |
|
|
What are the drug therapies for cachexia? |
Appetite stimulator Megace Ghrelin Anti-inflammatory Anabolic agents: SARM Cytokine inhibitors eg. IL-1,IL-6 receptor antagonists Metabolic regulators: myostatin receptor antagonist |
