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40 Cards in this Set
- Front
- Back
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What are the causes of primary and secondary malnutrition?
What are some other minor causes |
Primary malnutrition
Nutrients missing from diet Secondary malnutrition Malabsorption, impaired utilization or storage, excess loss and increased need. Other causes: Poverty, ignorance, chronic alcoholism, acute and chronic illnesses and self-imposed dietary restriction |
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Protein-energy maltnutrition - Marasmus
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Caloric deprivation.
Weight below 60% of normal for sex, height, and age. Loss of muscle mass and subcutaneous tissue. Extremities are emaciated Immune deficiency |
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Protein energy malnutrition - Kwashiorkor
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Protein deprivation.
Generalized or dependent edema Weight 60-80% normal Skin lesions: hypo/hyperpigmentation and desquamation “flaky paint” appearance. Hair changes Fatty liver Vitamin deficiencies Defects in immunity and secondary infections |
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Anorexia Nervosa
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Self induced starvation resulting in marked weight loss.
Amenorrhea Cold intolerance Bradycardia Constipation Change in skin and hair (lanugo) Dehydration and electrolyte abnormalities (hypokalemia) Decreased bone density Susceptibility to cardiac arrhythmia and sudden death |
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Bulimia
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Patient binges on food and then induces vomiting.
More common than anorexia nervosa and has a better prognosis. 1-2% of women and 0.1% of men, average onset 20 years of age. Amenorrhea <50% cases. Chronic use of laxatives and diuretics. Electrolyte imbalances (hypokalemia) predispose to cardiac arrhythmias. Pulmonary aspirate of gastric contents. Esophageal and stomach rupture. |
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Name the lipid soluble and water soluble vitamins
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Lipid soluble: A, D, E (Tocopherol), K
Water soluble: - Thiamin (vitamin B1) - Riboflavin (vitamin B2) - Niacin (Nicotinic acid, nicotinamide, vitamin B3) - Pantothenic acid (vitamin B5) - Vitamin B6 (pyridoxine, pyridoxal, pyridoxamine) - Biotin - Vitamin B12 (Cobalamin) - Folic acid (pteroyl-glutamic acid) |
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Name 3 characteristics of lipid soluble vitamins
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Apolar hydrophobic molecules.
Absorbed efficiently when normal fat absorption is taking place. Once absorbed, they are transported in the blood in lipoproteins or attached to specific binding proteins. |
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Name the features of Vitamin A
-where is it derived from? -what is needed for its absorption -is it converted into something and where? |
Retinol and retinol ester. Oxidized in vivo to retinal and retinoic acid.
Animal derived (i.e., liver, fish, eggs, milk, butter), and vegetable derived (i.e., carrots, squash, and spinach). Vegetables supply carotenoids the most important of these is beta-carotene. Bile, pancreatic enzymes, and antioxidant activity in the food is required for absorption. Retinol and β-carotene are absorbed in the intestine, where β-carotene is converted to retinol. Retinol is then transported to the liver for storage. More than 90% of the body's vitamin A reserves are stored in the liver. Retinol may be stored in peripheral tissues as retinol ester or be oxidized to form retinoic acid. Retinoic acid has important effects in epithelial differentiation and growth. |
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Name 3 functions of vitamin A
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Maintaining normal vision in reduced light.
Differentiation of specialized epithelial cells, mainly mucus-secreting cells. Enhancing immunity to infections, particularly in children. |
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Describe vitamin A deficiency
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Impaired vision: night blindness and xerophthalmia (dry eye).
Secondary pulmonary infections. Renal and urinary bladder stones. Follicular or papular dermatosis. Impairment of immunity leads to higher mortality rates from common infections such as measles, pneumonia, and infectious diarrhea (especially in children). |
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Vitamin A toxicity (hypervitaminosis)
Acute vs. chronic effects |
Acute effects: headache, vomiting, stupor, and papilledema (symptoms suggestive of brain tumor).
Chronic toxicity: weight loss, anorexia, nausea, vomiting, hepatomegaly with parenchymal damage and fibrosis and bone and joint pain. Synthetic retinoids used for the treatment of acne are teratogenic. |
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Describe 3 characteristics of Vitamin D
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Central role in calcium and phosphate metabolism.
Synthesis in the skin is the major source of vitamin D. Remainder (10%) is obtained from dietary sources (i.e, deep-sea fish, plants, and grains). 1,25 dihydroxyvitamin D (1,25 (OH)2D), is the biologically active form of vitamin D. |
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What are the 2 functions of vitamin D
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Intestinal absorption of calcium and phosphorus.
Collaborates with PTH in the mobilization of calcium from bone and reabsorption of calcium in the distal renal tubules. |
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Vitamin D deficiency
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Rickets in growing children and osteomalacia in adults. Associated to hypocalcemia.
Hypocalcemia increased PTH production which: (1) activates renal α1-hydroxylase; (2) mobilizes calcium from bone; (3) decreases renal calcium excretion; and (4) increases renal excretion of phosphate. Serum levels of calcium are restored to nearly normal, but hypophosphatemia persists, impairing mineralization of bone |
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Vitamin D toxicity
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Megadoses can lead to hypervitaminosis.
In children, it may take the form of metastatic calcifications of soft tissues such as the kidney. In adults it causes bone pain and hypercalcemia. |
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2 characteritics of vitamin E
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Antioxidant that scavenges free radicals formed in redox reactions throughout the body.
The nervous system is a particular target of vitamin E deficiency. |
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Vitamin E deficiency
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Cholestasis, cystic fibrosis, and primary small intestinal disease.
Infants with low birth weight with immature liver and gastrointestinal tract. Abetalipoproteinemia. Impaired vitamin E metabolism. Neurologic manifestations: Primary posterior columns of the spinal cord affected with depressed or absent tendon reflexes, ataxia, dysarthria, loss of position, vibration sense and pain sensation. Muscle weakness. |
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Name 2 protective effects that Vitamin E does.
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Protective effects against atherosclerosis and cancer, the two most common causes of death in the United States.
Atherosclerosis, it is suggested it may inhibit atheroma formation by reducing the oxidation of LDL. Cancer, antioxidants are postulated to scavenge free radicals, thereby preventing DNA damage and mutagenesis. |
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2 characteristics of vitamin K
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Required cofactor to convert glutamyl residues to gamma- carboxyglutamates needed for clotting factors VII, IX, X and prothrombin (factor II).
Activation of anticoagulant proteins C and S. |
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Vitamin K deficiency
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Biliary tract disease.
Ingestion of broad-spectrum antibiotics. Neonatal period, liver reserves are small, the bacterial flora is not yet developed, and the level of vitamin K in breast milk is low. Diffuse liver disease, hepatocyte dysfunction interferes with synthesis of the vitamin K-dependent coagulation factors. Full-term infants, by one week of age, endogenous flora provide sufficient vitamin K to correct any lingering deficit. Adults, bleeding diathesis may occur with hematomas, hematuria, melena, ecchymoses, and bleeding from the gums. Hemorrhagic disease of the newborn: intracranial, skin, umbilicus, and visceral hemorrhage. |
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Vitamin B1 (Thiamin) source and 3 functions
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Available in the diet, although refined foods such as polished rice, white flour, and white sugar contain small amounts.
Thiamin pyrophosphate has three major functions: - Synthesis of adenosine triphosphate (ATP). - Cofactor for transketolase in the pentose phosphate pathway. - Maintain neural membranes and normal nerve conduction (peripheral nerves). |
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Berberi heart disease (wet)
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Peripheral vasodilation, high-output cardiac failure, and eventually peripheral edema.
Heart may be normal, have subtle changes, or be markedly enlarged and globular (owing to four-chamber dilation), with pale, flabby myocardium. Dilation thins the ventricular walls. Mural thrombi are often present, particularly in the dilated atria. |
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Polyneuropathy (dry beriberi) - associted with thiamin deficiency
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Symmetric with myelin degeneration and disruption of axons involving motor, sensory, and reflex arcs.
The progressive sensory loss is accompanied by muscle weakness and hyporeflexia or areflexia. |
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What might you see in chronic alcoholics with thiamin deficiency?
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Wernicke-Korsakoff syndrome
Wernicke encephalopathy: ophthalmoplegia, nystagmus, ataxia of gait and stance, and derangement of mental function, characterized by global confusion, apathy, listlessness, and disorientation. Korsakoff psychosis: serious impairment of remote recall (retrograde amnesia), inability to acquire new information, and confabulation. |
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How would thiamin deficiency impact the central nervous system?
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affects mamillary bodies, periventricular regions of the thalamus, floor of the fourth ventricle, and anterior region of the cerebellum.
Hemorrhage and degenerative changes in the neurons are noted. |
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Where can riboflavin (B2) be found?
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Distributed in meat, dairy products, and vegetables as free riboflavin or riboflavin phosphate and is absorbed in the upper gastrointestinal tract.
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Where can riboflavin deficiency be found?
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Alcoholics, cases of chronic infections, advanced cancer, or other debilitating diseases.
Anorexia nervosa and in individuals who avoid dairy products, since milk is a good source of riboflavin. |
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Name some clinical manifestations of riboflavin deficiency
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Cheilosis or cheilitis (angles of the mouth)
Glossitis Superficial interstitial keratitis Greasy, scaling dermatitis Scrotal and vulvar lesions |
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Where can niacin (vitamin B3) be found?
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Niacin derived from the diet or synthesized endogenously.
Widely available in grains, legumes, seed oils and in much smaller quantities in meats. Pharmacologic doses of nicotinic acid lowers plasma LDL levels by reducing hepatic synthesis of VLDL (treatment of hypercholesterolemia). |
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What is the deficiency of niacin known as? What is the clinical syndrome classically identified as?
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Deficiency is known as pellagra (rough skin).
Clinical syndrome is classically identified as "three Ds“ for dermatitis, diarrhea, and dementia. |
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Describe where niacin deficiency can be found.
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Pellagra is encountered sporadically among alcoholics and persons suffering from chronic debilitating illnesses, including HIV infection.
Niacin in maize (corn), is bound, seen among native populations that subsist largely on maize. Protracted diarrheal states Diets deficient in protein Long-term administration of drugs such as isoniazid and 6-mercaptopurine |
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Where is vitamin B6 (pyridoxine) be found?
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Three closely related pyridine derivatives: pyridoxine, pyridoxal, and pyridoxamine and their corresponding phosphates.
Present in virtually all foods. |
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Describe where vitamin B6 deficiency is found? What are the causes?
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Secondary causes: long-term use of drugs that act as pyridoxine antagonists i.e., isoniazid, estrogens, and penicillamine.
Observed in alcoholics because acetaldehyde (alcohol metabolite) enhances pyridoxine degradation. Pregnancy is associated with increased demand. Associated with high levels of plasma homocysteine which is a risk factor for atherosclerosis. No evidence that vitamin B6 supplements reduce the risk of cardiovascular disease. |
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What are some clinical manifestations of vitamin B6 deficiency?
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Seborrheic dermatitis
Cheilosis Glossitis Peripheral neuropathy Convulsions |
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Sources and function of Vitamin C (ascorbic acid)
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Sources: milk and some animal products (liver, fish) and is abundant in a variety of fruits and vegetables.
Ascorbic acid functions by accelerating hydroxylation and amidation reactions, i.e, hydroxylation of procollagen. |
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What are the clinical manifestations of vitamin C deficiency.
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Bone disease in growing children, hemorrhage and healing defects in both children and adults.
Collagen (highest content of hydroxyproline) is most affected, particularly in blood vessels, accounting for the predisposition to hemorrhage. Purpura and ecchymoses in skin and gingival mucosa. Extensive subperiosteal hematomas and bleeding into joint spaces after minimal trauma. Retrobulbar, subarachnoid, and intracerebral hemorrhages may prove fatal. |
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Describe severe scurvy
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gingival swelling, hemorrhages, and secondary bacterial periodontal infection are common.
A distinctive perifollicular, hyperkeratotic papular rash (ringed by hemorrhage) often appears. Wound healing and localization of focal infections are impaired because of the derangement in collagen synthesis. Anemia is common, resulting from bleeding and from a secondary decrease in iron absorption. |
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Where can vitamin C deficiency be found?
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Elderly individuals
Alcoholics Peritoneal dialysis and hemodialysis patients. Food faddists. Infants maintained on formulas of processed milk without supplementation. |
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What vitamins are assumed to have anticarcinogenic effects and why?
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Vitamins C, E, β-carotene, and selenium have been assumed to have anticarcinogenic effects because of their antioxidant properties.
Retinoic acid promotes epithelial differentiation and is believed to reverse squamous metaplasia. |
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What factors determine nutrition-diet disease interactions?
When is cancer risk reduced regarding diet? |
Genetic factors determine nutrition-diet-disease interactions.
Cancer risk is reduced in populations with high fruit and vegetable intake and normal body mass index. Recommended to eat a nutritionally complete, varied diet that supports maintenance of normal weight, high in fruits and vegetables and moderate/low in red meat and fat. |
