Term
| About how much energy can be gained from 1 gram of fat? Protein? Carbohydrates? |
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Definition
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Term
| About what percentage of the following can be absorbed from the GI tract: fat, protein, carbohydrates? |
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Definition
1. about 95%
2. about 92%
3. about 98% |
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Term
| What is the approximate breakdown of dietary percentages for the following nutrients in an American diet: fat, protein, carbohydrates? |
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Definition
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Term
| About how much protein is needed per day (g)? About how much per kilogram or body weight? |
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Definition
1. 30-50 g
2. 0.8-1.2 g/kg, depending on the level of activity |
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Term
| What is the respiratory quotient for fat? Protein? Carbohydrates? What should the average respiratory quotient be? |
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Definition
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Term
| How can one determine how much protein a person has metabolized per day? |
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Definition
| about 16% of protein is nitrogen and neither fat nor carbohydrates contained nitrogen; 90% of excreted nitrogen is eliminated in the urine and 10% in the feces; if the nitrogen content is measured and multiplied by 6.25 (100/16), it will yield the total grams of protein that the person has metabolized in the day |
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Term
| Where in the brain is the feeding center? Where is the satiety center? What other important regulatory centers for feeding and satiety exist? |
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Definition
1. the lateral nuclei of the hypothalamus
2. the ventromedial nuclei of the hypothalamus
3. the paraaventricular, the dorsomedial, and the arcuate nuclei |
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Term
| Define: hyperphagia, inanition, aphagia, orexigenic, anorexigenic |
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Definition
1. voracious eating
2. extreme weight loss
3. refusal to eat
4. stimulating feeding
5. inhibiting feeding |
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Term
| What hormones decrease the stimulus to feed? |
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Definition
| α-MSH, leptin, serotonin, norepinephrine, CRH, insulin, CCK, glucagon-like-peptide, cocaine-and amphetamine-regulated transcript, and peptide YY |
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Term
| What hormones increase the stimulus to feed? |
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Definition
| neuropeptide Y, agouti-related protein, melanin-containing hormone, orexins A and B, endorphins, galanin, amino acids (glutamate and γ-aminobutyric acid), cortisol, ghrein, and endocannabinoids |
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Term
| What are the types of neurons in the arcuate nucleus related to feeding and satiety? |
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Definition
1. POMC neurons that produce α-MSH with CART -- activation of these neurons causes satiety and increases energy expenditure
2. neurons that produce neuropeptide Y and AGRP -- activation of these neurons causes increased food intake and decreased energy expenditure |
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Term
| What are the mechanisms by which hunger is downregulated short-term? |
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Definition
a. upper GI filling/distension inhibits feeding -- via inhibitory signals sent from the stomach and small intestine through the vagi
b. GI hormonal factors suppress feeding -- CCK released in the duodenum in response to protein and fat has a short-term affect of activating sensory nerves in the duodenum that send signals to the brain via the vagi;
peptide YY is released throughout the entire GI tract, but mainly in the ileum and colon in response to caloric intake (more secretion with more fat); injections in mice have been shown to decrease feeding short-term
glucagon-like peptide secretion is stimulated by the presence of food in the intestines and GLP stimulates the release of insulin, both of which suppress appetite |
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Term
| What are the mechanisms by which hunger is upregulated short-term? |
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Definition
a. ghrelin -- this hormone is secreted during fasting, peaks right before a meal, and drops shortly after eating, indicating it probably stimulates the feeling of hunger
b. oral receptors of some sort meter food intake and temporarily decrease the desire for food |
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Term
| How do the concentrations of glucose, amino acids, or fats in the blood affect hunger? |
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Definition
| a. high concentrations of glucose, amino acids, and lipids decrease hunger and increase satiety; a rise in glucose concentration increases the rate of firing of glucoreceptor neurons in the satiety center in the ventromedial and paraventricular nuclei of the hypothalamus and decreases the firing of glucosensitive neurons in the hunger center of the lateral hypothalamus; amino acids and fat work on the same or closely associated neurons |
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Term
| How does temperature affect food intake? |
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Definition
| in cold weather, one tends to take in more food, due to an interaction between the temperature-regulating system and the food intake-regulating system in the brain; this is helpful because cold increases metabolic rate and increased food will provide extra nutrients to make fat as energy and insulation |
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Term
| How does adipose tissue help regulate food intake? |
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Definition
| adipose tissue releases leptin, which travels to the brain, moves across the blood-brain barrier, and occupies the leptin receptors at multiple sites, including the POMC neurons of the arcuate nuclei and the paraventricular nuclei; activation of those receptors causes: 1. decreased production of NPY and AGRP; 2. activation of POMC neurons, causing release of α-MSH and activation of melanocortin receptors; 3. increased production in the hypothalamus of substances that decrease food intake (like CRH); 4. increased SNS activity; 5. decreased insulin activity, which decreases energy storage |
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Term
| If adipose tissue releases leptin and leptin inhibits feeding, why do some people continue to eat excessively? |
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Definition
| possible reasons include the social and cultural factors that encourage eating while socializing, etc, or activity of other systems (redundant systems); one theory is that people develop leptin resistance, so the high levels of leptin do not reduce feeding as much as they should |
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Term
| Where is fat typically stored? |
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Definition
| subcutaneously, in the intraperitoneal cavity, and, in obese individuals, in the liver and other organs |
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Term
| How might the hypothalamus affect obesity/feeding? |
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Definition
| the exact cause is unknown, but people with tumors encroaching on the hypothalamus often develop progressive obesity; it has been hypothesized that the satiety setting may become reset in obese individuals after long periods of overeating, causing them to feel extremely hungry if they don't eat large quantities; the hypothalamus may have something to do with this |
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Term
| What does calorie restriction in obese individuals cause neurogenically? |
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Definition
| increased formation of orexigenic substances such as NPY and decreased formation of anorexic substances such as leptin and α-MSH |
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Term
| About how many cases of obesity are due to genetic factors? In what ways can genes cause obesity? |
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Definition
1. about 20-25%
2. they can cause abnormalities in pathways that regulate feeding centers and those that regulate energy expenditure and storage |
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Term
| What are the monogenic causes of obesity? |
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Definition
| mutation in MCR-4, congenital leptin deficiency and mutation of the leptin receptor |
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Term
| What are some drugs have been prescribed to assist with weight loss? What are their mechanisms and significant side effects? |
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Definition
a. amphetamine derivatives - directly inhibits the feeding center of the brain; it can stimulate the SNS and raise blood pressure
b. sibutramine - reduces food intake and increased energy expenditure; can stimulate the SNS and raise blood pressure
c. orlistat - reduces the amount of fat absorbed from the blood, causing a reduction in absorption of calories; this can unfortunately cause bad GI side effects and will decrease the absorption of fat-soluble vitamins. |
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Term
| What are surgical procedures (not liposuction) that are used to treat obesity? Describe them. What are the downsides to these procedures? |
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Definition
1. a. gastric bypass surgery - involves the construction of a small pouch in the proximal stomach separated from the rest with of the stomach with staples; the pouch is then connected to the jejunum with a section of small bowel
b. gastric banding surgery - an adjustable band is placed around the stomach near its upper end, creating a small pouch that restricts the amount of food that can be eaten at each meal
2. these are major surgeries and it is not entirely certain if these procedures might negatively affect patients long-term |
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Term
| Define: anorexia, anorexia nervousa, cachexia |
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Definition
1. reduction in or lack of food intake due to a loss of appetite
2. a condition in which someone loses all desire to eat or becomes nauseated by food, resulting in severe inanition
3. increased energy expenditure leading to weight loss (greater than that caused by reduced food intake) |
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Term
| What hormonal factors are believed to be involved in anorexia and cachexia? How are the believed to work? |
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Definition
1. TNF-α, IL-6, IL-1β, and proteolysis-inducing factor
2. their mechanism is unclear, but they are believed to work on the melanocortin system in the hypothalamus |
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Term
| Describe the shifts of nutrient metabolism during starvation. |
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Definition
| after a meal is finished and blood glucose levels have normalized, glycogen is gradually broken down to maintain blood glucose levels while the body changes to different sources for energy; ready protein stores are released for gluconeogenesis and protein is rapidly consumed until those readily mobilized stores are used up and fat metabolism takes over; some fat is converted into keto bodies to provide usable substrates for the brain's use; when fat stores are used up, less readily accessible protein (such as muscle) is broken down to provide the last energy store for the body before death by starvation |
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Term
| Why do vitamin deficiencies occur so soon (a week or so) after starvation begins? |
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Definition
| water-soluble vitamins cannot be stored in large amounts, so they must be replaced regularly or the will be depleted in about a week |
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Term
| What are the required daily amounts of the following: vitamin a, thiamine, riboflavin, niacin? |
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Definition
1. 5000 IU
2. 1.5 mg
3. 1.8 mg
4. 20 mg |
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Term
| What are the required daily amounts of the following: ascorbic acid, vitamin d, vitamin e, vitamin k? |
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Definition
1. 45 mg
2. 400 IU
3. 15 IU
4. 70 μg |
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Term
| What are the required daily amounts of the following: folic acid, vitamin b-12, pyridoxine, pantothenic acid? |
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Definition
1. 0.4 mg
2. 3 μg
3. 2 mg
4. unknown |
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Term
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Definition
| 1. an organic compound needed for normal metabolism that cannot be synthesized in the cells |
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Term
| How long can vitamin stores of the following last: vitamin A, vitamin D, vitamin B12, vitamin B compounds, and vitamin C. |
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Definition
1. 5-10 months
2. 2-4 months
3. 1+ years
4. a few days to maybe a week
5. up to a few weeks |
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Term
| How is vitamin A attained in the diet? What is it biologically necessary for? What does its deficiency result in? |
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Definition
1. in animal tissues it is attained in the form of retinol; a provitamin form of beta-cartenoids may be attained through vegetables
2. retinal pigments to assist with peripheral vision/prevention of night blindness; it's also used for normal growth of most tissues
3. night blindness, scaliness of skin, failure of growth in young animals including cessation of skeletal growth, failure of reproduction and atrophy of germinal epithelium and/or interruption of the female sexual cycle, and keratinization of the cornea |
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Term
| What is the biological use of thiamine? What is thiamine (B3) deficiency called? What metabolic conditions can this cause? |
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Definition
1. assists in the decarboxylation of pyruvic acid and other α-keto acids
2. beriberi
3. the utilization of glucose by the nervous system is decreased 50-60% and is replaced with ketone bodies |
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Term
| What neurological conditions can thiamine deficiency cause? |
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Definition
| chromatolysis, swelling, disruption of CNS communication, degeneration of myelin sheaths in PNS and CNS, polyneuritis (pain radiating along one or more nerves due to increased nerve irritability), paralysis |
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Term
| What circulatory conditions can thiamine deficiency cause? |
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Definition
| peripheral vasodilation leading to increased venous return leading to cardiac overload, weakened heart muscle (primary and secondary), and possibly heart failure, which also causes peripheral edema and ascites |
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Term
| What GI conditions can thiamine deficiency cause? |
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Definition
| indigestion, severe constipation, anorexia, gastric atony, hypochlorydria; these are all presumably due to an inability of the smooth muscles to derive enough energy from carbohydrate metabolism |
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Term
| What is the biological (non-pharmaceutical) use of niacin? What is a deficiency of niacin called? What does a deficiency in niacin cause? |
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Definition
1. is it used as a coenzyme to transport electrons for the electron transport chain (NAD)
2. pellagra (humans) or black tongue (canines)
3. initially, muscle weakness and poor glandular secretion; later, in severe cases, tissue death, lesions in the CNS, permenant dementia, psychosis, skin cracking and pigmented scaliness in areas of mechanical irritation or sunlight (inability of the skin to repair itself), irritation and inflammation of mucous membranes of the mouth and other portions of the GI tract |
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Term
| What what can be converted into niacin in small quantities? |
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Definition
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Term
| What is the biological function of riboflavin (B2)? What does a riboflavin deficiency cause? |
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Definition
1. it is used is FAD and FMN as electron carriers for the electron transport chain in the mitochondria
2. (seen in experimental animals) severe dermatitis, vomiting, diarrhea, muscle spasticity that becomes muscle weakness, coma, decline in body temperature, and then death; in humans only the following have been often noted: digestive diisturbances, burning sensation of the skin and eye, cracking at the corners of the mouth, headaches, mental depression, forgetfulness, etc. |
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Term
| What is the biological function of vitamin B12? How is this vitamin distinct from other B vitamins? |
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Definition
1. it acts as a coenzyme for hydrogen acceptance and reduces ribonucleotides to deoxyribonucleotides, promotion of growth, promotion of RBC formation and maturation
2. it has a prosthetic group with a cobalt in it; it can also be stored for much longer than other B vitamins |
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Term
| What can vitamin B12 deficiency cause? What can cause this? |
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Definition
1. demyelination of large nerve fibers in the spinal cord, especially the posterior columns and occasionally the lateral columns; it can also cause loss of peripheral sensation, paralysis, and pernicious anemia
2. usually it is caused by a lack of intrinsic factor, making it difficult or impossible to absorb B12 |
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Term
| What is the biological function of folic acid? |
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Definition
| it is a carrier of hydroxymethyl and formyl groups; can be used to synthesize purines and thymine, making it important to DNA formation (and cellular formation by corollary); folic acid is also very important in the neurological development of fetuses |
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Term
| What condition can a deficiency in folic acid cause? |
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Definition
| macrocytic anemia; this is almost identical to pernicious anemia |
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Term
| What is the biological function of pyridoxine (B6)? |
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Definition
| it functions as a coenzyme for many reactions in amino acid and protein metabolism; it is also believed to be involved in transamination for the synthesis of amino acids and the transport of some amino acids across the cell membrane |
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Term
| What can a lack of pyridoxine in the diet cause? |
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Definition
| dermatitis, decreased rate of growth, a fatty liver, anemia, and evidence of mental deterioration; in children, deficiency has been known to cause seizures, dermatitis, and GI disturbances like nausea and vomiting |
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Term
| What is the biological function of pantothenic acid? |
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Definition
| it is incorporated in the body into coenzyme CoA, which has many roles including conversion of decarboxylated pyruvic acid into acetyl-CoA before its entry into the CAC or the degradation of FFAs into multiple acetyl-CoA molecules |
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Term
| What would a deficiency in pantothenic acid cause? |
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Definition
| depressed metabolism of both carbohydrates and FFAs, retarded growth, failure of reproduction, graying of the hair, dermatitis, fatty liver, and hemorrhagic-adrenocortical necrosis |
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Term
| What is the biological use of ascorbic acid (vitamin C)? |
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Definition
| it activates the enzyme prolyl hydroxylase, which promotes the hydroxylation of hydroxyproline, which is integral in collagen; |
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Term
What can vitamin C deficiency cause?
How is vitamin C deficiency diagnosed? |
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Definition
1. a loss of collagen fiber synthesis, resulting in problems with wound healing, problems with bone growth, cessation of bone healing, and fragility of blood vessel walls due to endothelial cells and vessel walls not being held together with collagen fibers; the fragility of the vessel walls causes petechial hemorrhaging throughout the body and purpuric blotches; severe deficiency can cause muscle cells to fragment, lesions of the mouth, loosening of teeth, infections in the mouth, vomiting of blood, blood stools, cerebral hemorrhaging, fever, and death
2. one can produce petechial hemorrhaging with the inflation of a blood pressure cuff |
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Term
| What is the biological function of vitamin D? What does its deficiency cause? |
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Definition
1. it increases the absorption of calcium in the gut, helps control the deposition on and reabsorption from the bones, and helps the production of calcium-binding protein
2. rickets or osteomalacia |
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Term
| What is the biological function of vitamin E? What does its deficiency cause? |
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Definition
1. it is believed to prevent oxidation of unsaturated fats, causing abnormal membrane structure and fluidity
2. degeneration of germinal epithelium in the testes causing male sterility, resorption of a fetus after conception, and degeneration of renal tubules and muscle cells |
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Term
| What is the biological function of vitamin K? What does its deficiency cause? How is vitamin K attained? |
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Definition
1. it is an essential co-factor to a liver enzyme that adds a carboxyl group to factors II, VII, IX, and X, all of which are important to blood coagulation
2. severe bleeding problems
3. bacteria in the gut produce it; if they are destroyed, probiotics will need to be taken and dark green vegetables can provide some dietary vitamin K |
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Term
| What is the daily dietary requirement for the following: sodium, potassium, chloride, calcium? |
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Definition
1. 3 g
2. 1 g
3. 3.5 g
4. 1.2 g |
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Term
| What is the daily dietary requirement for the following: phosphorus, iron, iodide, magnesium? |
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Definition
1. 1.2 g
2. 18 mg
3. 150 μg
4. 0.4 μg |
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Term
| What is the daily dietary requirement for the following: cobalt, copper, manganese, zinc? |
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Definition
1. unknown
2. unknown
3. unknown
4. 15 mg |
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Term
| What is the biological function of magnesium? What will high Mg++ cause? What will low Mg++ cause? |
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Definition
1. it is a required catalyst to many IC reactions, including carbohydrate metabolism
2. depressed nervous system function and muscle contraction, the latter of which can be blocked with calcium administration
3. increased nervous system irritability, peripheral vasodilation, and acute cardiac arrhythmias, especially after an AMI |
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Term
| What is the biological function of calcium? What can high levels of calcium cause? Low levels? |
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Definition
1. it functions as a second messenger, an integral part of of nervous system firing, a component of bones, etc
2. NS depression, hyperpolarization, calcification outside of the bones, and cardiac arrest
3. it can cause spontaneous discharge of nervous system firing, leading to tetany |
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Term
| What is the biological function of phosphorus? |
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Definition
| it is used in numerous metabolic processes, coenzymes, bone matrix, etc |
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Term
| What is the biological function of iron? |
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Definition
| it it incorporated in hemoglobin and myoglobin as a transport/holding molecule for oxygen molecules and in the incorporation of cytochrome enzymes |
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Term
| What is the biological function of iodine? Zinc? Fluorine? |
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Definition
1. it is used in thyroid hormone
2. it is used in many enzymes, including carbonic anhydrase, lactic dehydrogenase, and some peptidases
3. can protect against caries and bacterial attack in the teeth
3. |
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Term
| Describe the mechanism by which ghrelin affects hunger/food intake. |
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Definition
| ghrelin attaches to a receptor on the AGRP/NPY neurons in the arcuate nucleus, which communicates with the periventricular nucleus via Y1 receptors and MCR-4 receptors, resulting in increased food intake and stimulation of the nucleus tractus solitarius, yielding increased sympathetic activity and energy expenditure; the AGRP/NPY neurons also communicate with the POMC/CART neurons via Y1 receptors |
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Term
| Describe the mechanism by which leptin affects hunger/food intake. |
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Definition
| Leptin attaches to receptors on the AGRP/NPY neurons, inhibiting them, and also attach to the POMC/CART neurons in the arcuate nucleus, stimulating their action; these neurons can communicate with MCR-4 receptors on the neurons of the periventricular nucleus and inhibit food intake; the POMC/CART neurons also communicate with the AGRP/NPY neurons to regulate their activity; POMC/CART neurons communicate using axons with α-MSH |
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