Nutritional Disorders PDF

NUTRITIONAL DISORDERS Edda Vuhahula, DDS, PhD (Path) Associate Professor  Nutritional Pathology – A branch is a branch of pathology that investigates how inadequate or excessive nutrion impacts health, leading to disease. It combines biochemistry, physiology and...

NUTRITIONAL DISORDERS Edda Vuhahula, DDS, PhD (Path) Associate Professor  Nutritional Pathology – A branch is a branch of pathology that investigates how inadequate or excessive nutrion impacts health, leading to disease. It combines biochemistry, physiology and clinical medicine Relevance – Chronic diseases like obesity, herat disease and diabetes are strongly influenced by diet – Likewise, nutritional deficiencies lead to significant conditions such as anemia, rickets and scuvy  Basic Principles of Nutrition Macronutrients Carbohydrates provides energy Proteins are essential for growth and repair Fats are vital for energy stirage and cellular structures Imbalance leads to either energy deficiencies (hypogycaemia or excess eg obesity Micronutrients Include vitamins( eg A,C,D,and B complex) Minerals (eg Ca, Fe and Mg) Deficiencies causes diseases like scuvy(Vit C def), Rickets (Vit D def) and anemia (iron deficiency) Water and Electrolytes imbalance- dehydration and electrolyte disturbances  MALNUTRITION A pathological state resulting from a relative or absolute deficiency or excess of one or more essential nutrients; clinically manifested or detected only by biochemical, anthropometric or physiological tests.  Forms of Malnutrition 1. Undernutrition: Marasmus 2. Overnutrition: Obesity, Hypervitaminoses 3. Specific Deficiency: Kwashiorkor, Hypovitaminoses, Mineral Deficiencies 4. Imbalance: Electrolyte Imbalance ETIOLOGY Marasmus  Common in the 1st year of life Etiology:  “Balanced starvation”  Insufficient breastmilk  Dilute milk mixture or lack of hygiene  Marasmus Clinical Manifestations: 3. Urinary hydroxyproline/ 1. Wasting gm crea low, early 2. Muscle wasting 4. Serum essential a.a. 3. Growth retardation index N 4. Mental changes 5. Anemia uncommon 5. No edema 6. Glucose tolerance 6. Variable-subnormal curves diabetic type temp, slow PR, good appetite, often 7. K+ deficiency present w/diarrhea, etc. 8. Serum cholesterol low 9. Diminished enzyme Laboratory Data: activity 1. Serum albumin N 10.Bone growth delayed 2. Urinary urea/ gm 11.Liver biopsy N or crea N atrophic Kwashiorkor  Between 1-3 yrs old Etiology:  Very low protein but w/calories from CHO  In places where starchy foods are main staple  Never exclusively dietary  Kwashiorkor Clinical Manifestations: C. Occasional Signs: A. Diagnostic Signs 1. Flaky-paint rash 2. Noma 1. Edema 3. Hepatomegaly 2. Muscle wasting 4. Associated 3. Psychomotor changes B. Common Signs Laboratory: 1. Hair changes 1. Decreased serum albumin 2. Diffuse depigmentation 2. EEG abnomalities of skin 3. Iron & folic acid 3. Moonface deficiencies 4. Anemia 4. Liver biopsy fatty or fibrosis may occur Kwashiorkor  Treatment of PEM 1. Severe PEM is an emergency, hospitalization 1-3 mo desirable 2. On admission, treat vitamin deficiencies, dehydration & associated infections 3. In the acute phase, feeding started as soon as rehydrated & when edema is lost, full- strength feeds given with maintenance calories & protein; recovery after 2-3 wks 4. Rehabilitation with high energy feeds (150- 200 kcal/kg/day) started once full-strength feeds tolerated; recovery expected within 4-6 wks on high energy feeds  Prognosis of PEM  Permanent impairment of physical & mental growth if severe & occurs early especially before 6 months old  First 48 hours critical, with poor treatment mortality may exceed 50%  Even with thorough treatment, 10% mortality may still occur  Some mortality causes are endocrine, cardiac or liver failure, electrolyte imbalance, hypoglycemia & hypothermia  Obesity 1. Definition: Generalized, excessive accumulation of fat in subcutaneous & other tissues 2. Classification according to “desirable” weight standard: Overweight ~ >10% while Obese ~ >20% 3. The Centers for Disease Control (CDC) avoids using "obesity" instead suggest two levels of overweight: 85th percentile of BMI ~ "at risk" level & 95th percentile of BMI ~ the more severe level 4. The American Obesity Association uses: The 85th percentile of BMI for overweight because ~ BMI of 25, overweight for adults and the 95th percentile of BMI for obesity because ~ BMI of 30, the marker for obesity in adults  Obesity  Appears most frequently in the 1st year, 5-6 years & adolescence Etiology:  Excessive intake of food compared w/ utilization  Genetic constitution  Psychic disturbance  Endocrine & metabolic disturbances rare  Insufficient exercise or lack of activity  Obesity Clinical Manifestations: 1. Fine facial features on a heavy-looking taller child 2. Larger upper arms & thighs 3. Genu valgum common (knock knees, ankles are apart) 4. Relatively small hands & fingers tapering 5. Adiposity in mammary regions 6. Pendulous abdomen w/ striae 7. In boys, external genitalia appear small though actually average in size 8. In girls, external genitalia normal & menarche not delayed 9. Psychologic disturbances common 10. Bone age advanced Obesity  Treatment of Obesity A. 1st principle: decrease energy intake 1. Initial med exam to R/O pathological causes 2. 3-day food recall to itemize child’s diet 3. Plan the right diet a. Avoid all sweets, fried foods & fats b. Limit milk intake to not >2 glasses/day c. For 10-14 yrs, limit to 1,100-1300 cal diet for several months 4. Child must be properly motivated & family involvement is essential B. 2nd principle: increase energy output 1. Obtain an activity history 2. Increase physical activity 3. Involve in hobbies to prevent boredom  Complication of Obesity Pickwickian Syndrome  Rare complication of extreme exogenous obesity  Severe cardiorespiratory distress & alveolar hypoventilation  Includes polycythemia, hypoxemia, cyanosis, CHF (congestive Heart Failure) High O2 conc dangerous in cyanosis  Weight reduction ASAP & quick  The Energy-Releasing Vitamins Thiamine, Riboflavin, Niacin, Pyridoxine are cofactors to enzymes in energy metabolism, hence, deficiencies show up in quickly growing tissues such as epithelium. Typical symptoms for the Nerve cells use lots of group include: energy, so symptoms  Dermatitis also show up in the nervous tissue:  Glossitis  Cheilitis  Peripheral neuropathy  Diarrhea  Depression  Mental confusion  Lack of motor coordination  Malaise  Thiamine (Vitamin B1) Deficiency Beriberi Pathology: Biochemically, there is accumulation of pyruvic and lactic acid in body fluids causing: 1. Cardiac dysfunction such as cardiac enlargement esp right side, edema of interstitial tissue & fatty degeneration of myocardium 2. Degeneration of myelin & of axon cylinders resulting in peripheral neuropathy and 3. In chronic deficiency states, vascular dilatation & brain hemorrhages of Wernicke’s Disease, resulting in weakness of eye movement, ataxia of gait and mental disturbance  Thiamine Deficiency (Beriberi) Three forms: 1. Wet beriberi: generalized edema, acute cardiac symptoms and prompt response to thiamine administration 2. Dry beriberi: edema not present, condition similar to peripheral neuritis w/ neurological disorders present 3. Infantile beriberi divided into: a. Acute cardiac - ages 2-4 months; sudden onset of cardiac s/sx such as cyanosis, dyspnea, systolic murmur & pulmonary edema w/ rales b. Aphonic - ages 5-7 months; insidious onset of hoarseness, dysphonia or aphonia c. Pseudomeningeal - ages 8-10 months; signs of meningeal irritation w/ apathy, drowsiness & even unconsciousness; occurs more often  Thiamine Deficiency (Beriberi) Diagnosis: Prevention: 1. Clinical manifestations not 1. Richest sources are meat, conclusive whole grain, enriched cereal 2. Therapeutic test w/ grains and legumes parenteral thiamine = 2. Improved milling of rice dramatic improvement conserve thiamine 3. Blood lactic & pyruvic acid 3. Excessive cooking of levels elevated after oral load vegetables or polishing of of glucose cereals destroy 4. Decreased red cell 4. In breast-fed infants, hemolysate transketolase prevention achieved by RDA: Infants 0.4mg maternal diet w/ sufficient Older children 0.6-1.2mg amounts Nursing mothers 1.5mg Treatment: Adults 1-1.3mg 1. Children: 10mg p. o. daily for several weeks 2. Adults 50mg Thiamine Deficiency (Beriberi) Thiamine Deficiency (Beriberi)  Riboflavin (Vitamin B2) Deficiency Functions: 1. Acts as coenzyme of flavoprotein important in a. a., f. a. & CHO metabolism & cellular respiration 2. Needed also by retinal eye pigments for light adaptation Clinical Manifestations: 1. Characteristic lesions of the lips, the most common of which are angular stomatitis and cheilosis 2. Localized seborrheic dermatitis of the face may result such as nasolabial seborrhea or dyssebacia and angular palpebritis 3. Scrotal or vulvar dermatosis may also occur 4. Ocular s/sx are photophobia, blurred vision, itching of the eyes, lacrimation & corneal vascularization  Riboflavin Deficiency Diagnosis: 1. Urinary riboflavin determination 2. RBC riboflavin load test RDA: Infants & children 10yrs 1.4-2mg depending on food intake Adults 0.025mg/gm dietary protein Prevention: 1. Best sources: eggs, liver, meat, fish, milk, whole or enriched ground cereals, legumes, green leafy vegetables 2. Impaired absorption in achlorhydria, diarrhea & vomiting Treatment: 1. Riboflavin 2-5mg p. o. daily w/ increased B complex 2. Parenteral administration if relief not obtained Riboflavin Deficiency  Niacin (Vitamin B3) Deficiency Pellagra Etiology: 1. Diets low in niacin &/or tryptophan 2. Amino acid imbalance or as a result of malabsorption 3. Excessive corn consumption Clinical Manifestations: 1. Start w/ anorexia, weakness, irritability, numbness & dizziness 2. Classical triad of dermatitis, diarrhea & dementia 3. Dermatitis may develop insidiously to sunlight or heat a. First appears as symmetrical erythema b. Followed by drying, scaling & pigmentation w/ vesicles & bullae at times c. Predilection for back of hands, wrists, forearms (pellagrous glove), neck (Casal’s necklace) & lower legs (pellagrous boot) 4. GIT s/sx are diarrhea, stomatitis or glossitis; feces pale, foul milky, soapy or at times steatorrheic 5. Mental changes include depression, irritability, disorientation, insomnia & delirium  Niacin Deficiency (Pellagra) Diagnosis: 1. History & manifestations of diet poor in niacin or tryptophan 2. In niacin deficiency, urinary levels of N-methyl- nicotinamide low or absent Differential diagnoses: Kwashiorkor, Infantile Eczema, Combination deficiencies of amino acids & trace minerals such as zinc RDA: Infants & children