University of Guyana Nutrition Notes PDF

University of Guyana College of Medical Sciences School of Medicine NUTRITION MED 2110 - Pathology I Lecturer - Dr. Nancy Sitchao Presented by - Group 7  Group Members Tucquana Ault Kaden Conway Eleesha Henry Keresia King Cristiana Raj Tashana Ramnarine  P...

University of Guyana College of Medical Sciences School of Medicine NUTRITION MED 2110 - Pathology I Lecturer - Dr. Nancy Sitchao Presented by - Group 7  Group Members Tucquana Ault Kaden Conway Eleesha Henry Keresia King Cristiana Raj Tashana Ramnarine  Protein - Energy Malnutrition PEM is the condition of lack of energy due to deficiency of all the macronutrients and some micronutrients. In developing countries, it affects children who are not provided with calories and proteins In developed countries, it affects the older generation. PEM can be classified into primary and secondary PEM. Primary PEM is usually found in children and is of two types 1) Marasmus and 2) Kwashiorkor.  Marasmus This is a severe manifestation of protein - energy malnutrition caused by a result of calorie insufficiency. A child with marasmus has major growth retardation as well as loss of muscle mass as a result of catabolism and depletion of the somatic protein compartment. Muscle proteins and subcutaneous fat are mobilised and used as fuel as an adaptive response of the body. With losses of muscle mass and subcutaneous fat, extremities are emaciated; by comparison, the head appears too large for the body.  Etiology - Insufficient calorie intake Precipitating factors in children - Poverty - Maternal Education - Wasting diseases of mothers such as HIV/AIDS. Precipitating factors in adults - Reduced food intake with age; physiological anorexia - Depression - Dementa - Elder abuse/ neglect  Pathophysiology Protein-calorie deficiency Adequate response of adrenal cortex Muscle protein Optimal increase Inhibited growth mobilized in plasma hormone cortisol response Normal Normal plasma plasma-free amino acid fatty acid Growth retardation Normal No fat deposits lipoprotein in the liver synthesis Signs and Symptoms Sunken fontanelles as a result of dehydration Weight loss more noticeable in groin/axilla. Children are less than 60% of the weight for age. Visible wasting of fat and muscle. Prominent skeleton Head appears too large for body Face old and wizened Dry, loose skin (skin atrophy) Dry, brittle hair or hair loss Lethargy, apathy and weakness BMI less than 16  Complications 1. Susceptibility to infection - Immunosuppression: prolonged calorie restriction impares T- cell functions, reduces neutrophil activity and causes atrophy of lymphoid tissues, leading to compromised immune system. 2. Electrolyte Imbalances and Fluid Changes - Electrolyte Loss: due to nutrient deficiency and increased excretion. - Total Body Water Increase: due to depletion of protein stores. 3. Gastrointestinal Changes - Villous Atrophy and Enzyme Loss 4. Central Nervous System and Cognitive Impairment - CNS Changes 5. Cardiovascular Adaptations - Reduced Cardiac Output Diagnosis 1. Physical examination - Height or length of person’s body is measured - Circumference of upper hand - Height to age ratio is determined 2. Blood tests 3. Stool and Urine Samples  Treatment/ Management Treatment is given in three (3) stages: 1. Resuscitation and Stabilization. 2. Nutritional Rehabilitation 3. Follow up and prevention of recurrence Refeeding Syndrome - Children in treatment for marasmus are at risk for refeeding syndrome, a life threatening complication that can result when the undernourished body tries to reboot too fast - Therefore, nutrition should be delivered slowly and carefully.  Kwashiorkor Kwashiorkor is a disease of edematous malnutrition marked by severe protein deficiency and bilateral extremity swelling. It occurs when the diet is more deficit in protein than in calories. It is most prevalent in impoverished communities, Southeast Asia and Sub-saharan Africa. It primarily affects children between ages 1-5.  Etiology Protein deficiency: Lack of protein in the diet can occur due to many factors such as poverty, limited access to protein-rich foods, consuming a diet rich in carbohydrates but low in protein. Micronutrient deficiency: Lack of necessary vitamins and minerals contribute to the development of kwashiorkor. Weaning too early: When a child is weaned too early without proper nutritional compensation. Infections and gastrointestinal disease  Pathophysiology Plasma Protein → Hypoalbuminemia → Plasma Osmotic Pressure Aldosterone & ADH → Salt and Fluid Retention → Edema Low Plasma Amino Acid Decreased protein synthesis Increased Plasma GH Decreased lipoprotein synthesis Increase Free Fatty Acid Hepatomegaly  Pathophysiology Muscle wasting occurs as body breaks down muscles tissue for energy. Skin and hair changes occur and the immune system is weakened. Protein deficiency can disrupt metabolic processes such as energy metabolism and hormone production. There is a decrease of mitosis in small bowel, mucosal atrophy and loss of villi. Bone marrow may be hypoplastic due to decreased red blood cell precursor. Thymic and lymphoid atrophy can occur. Severe malnutrition causes organ dysfunction.  Clinical Manifestation Edema Bloated stomach with ascites Muscle wasting Skin lesions Dry brittle hair Fatty liver Stunted growth  Diagnosis A physical examination should record characteristic signs such as edema, hair and skin changes, muscles wasting. Taking a history of dietary intake and growth patterns. Laboratory tests such as: 1. Albumin levels 2. Liver function tests 3. CBC 4. Urinalysis  Treatment Nutritional rehabilitation: First a high calorie diet is taken to restore energy levels. Then protein-rich foods are gradually introduced to help repair tissue and increase muscle mass. Vitamin and mineral supplements are given. Restoring electrolyte balance and treating dehydration. Manage infections: Any infections should be treated appropriately; proper hygiene should be practiced to reduce risk of further infection. Monitoring: Vital signs and weight must be closely monitored and treatment adjusted accordingly. Psychological support is provided.  Complications & Prevention Organ damage due to Ensuring a balanced diet. malnutrition Exclusively breastfeeding for first Refeeding syndrome: six months of life and providing Starvation appropriate complementary Death feeding. Increased risk of infection Good sanitation and hygiene. Cardiovascular Nutritional education failure/hypovolemic shock Providing support and food Loss of immune function security to vulnerable Impaired cellular function populations. Proper healthcare access  Anorexia Nervosa Anorexia nervosa is a state of self-induced starvation resulting in marked weight loss. It is estimated to occur in 1% to 2% of women and 0.1% of men. Occurs primarily in previously healthy young women who have acquired an obsession with attaining or maintaining thinness.  Risk Factors Associated with Anorexia Behavioral, psychological, social, biological, and genetic elements may raise the risk of anorexia. Contributing factors may include: Social perspectives Influences from the family Genetics Chemical imbalances in the brain Developmental problems  Risk Factors Associated with Anorexia Participating in sports and activities that emphasize body size and shape may also put you at risk. These consist of: Ballet Modeling Gymnastics Figure skating etc.  Signs and Symptoms of Anorexia There are several ways that anorexia might show up. They may be related to weight or diet, or they might be physical or emotional. Symptoms associated with food or weight can include: A shift in body image Low weight A severe fear of gaining weight Ignoring hunger  Signs and Symptoms of Anorexia Among the physical symptoms are: Amenorrhea Anemia Cold intolerance Lymphopenia Bradycardia Hypoalbuminemia Constipation Hypokalemia Changes in the skin and hair Dehydration Sluggishness or excessive fatigue Being extremely thin Decreased bone density Bloating or pain in the stomach  Signs and Symptoms of Anorexia Among the emotional symptoms are: Withdrawal from social interactions Absence of desire for sex Grumpiness Changes in mood Depression  Diagnosis There are three criteria set out by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5): Restriction of calorie consumption that leads to weight loss or a failure to gain weight, resulting in a significantly low body weight based on your age, sex, height and stage of growth. Intense fear of gaining weight or becoming “fat.” Having a distorted view of yourself and the seriousness of the state of your health.  Diagnosis The physical effects of anorexia can also be assessed using tests: Complete blood count (CBC) Electrolyte panel Electrocardiogram (EKG) Urinalysis Bone density test Kidney function tests Liver function tests Thyroid blood test  Treatment Treatment for anorexia most often involves a combination of: Individual and group psychotherapy (talk therapy). Nutrition counselling Medication. Hospitalization.  Impact of Anorexia on Nutritional Health & Wellbeing Complications that can result from untreated anorexia include: Loss of bone mass (osteoporosis) and Insomnia tooth enamel erosion Anemia Kidney and liver damage Peripheral neuropathy Fatty liver disease (steatosis) Ventricular arrhythmia Rhabdomyolysis Mitral valve prolapse Delayed puberty and physical growth Cardiac arrest Infertility and menstrual problems Death  What is Obesity? Obesity is defined as a state of increased body weight caused by adipose tissue accumulation that is of sufficient magnitude to produce adverse health effects.  What is Obesity? Obesity is a disorder of energy balance. The LEP gene and its byproduct, leptin, are essential for maintaining this balance. Leptin is secreted by adipocytes and regulates energy intake and expenditure. The anorexigenic response of leptin is attenuated in obese states.  What is Obesity? Adiponectin, referred to as the "guardian angel against obesity" and a "fat-burning molecule" is also produced in adipose tissue. Fatty acids are transported to the muscle for oxidation by adiponectin, which also reduces the amount of fatty acids that enter the liver, lowers the amount of glucose that the liver produces, and increases insulin sensitivity. Obese people typically have lower serum levels.  What is Obesity? Ghrelin is produced by the stomach and the hypothalamic arcuate nucleus. It works by activating the NPY/AgRP neurons in the hypothalamus, which promotes food intake. When compared to people of normal weight, ghrelin levels are lower in obese people and rise as obesity decreases.  Risk Factors Associated with Obesity Obesity often results from a combination of causes and contributing factors: Family inheritance and influences Lifestyle choices Certain diseases and medication Social and economic issues  Signs and Symptoms of Obesity Acanthosis nigricans Difficulty in sleeping Stretch marks Back and/or joint pain Excessive sweating Swelling and varicose veins in the Intolerance to heat lower limbs Infections in skin folds Fatigue Body Mass Index (BMI) greater than Depression 30 kg/m2. Dyspnoea Waist circumference greater than 94 cm in men and 88 cm in women High blood pressure level > 140/90 mmHg.  Diagnosis The diagnosis of obesity is based on a few factors: Clinical history Physical examination Blood analysis and imaging tests  Treatment Treatment for obesity most often involves a combination of: Diet Physical exercise Pharmacological treatment Bariatric surgery (BC) Cognitive-behavioral psychological treatment of obesity  Impact on Health and Wellbeing Obesity is associated with an increased incidence of several diseases in humans, including: Type 2 diabetes (insulin-resistant) Increased risk of coronary artery disease Non-alcoholic fatty liver disease Cholelithiasis (gallstones)  Impact on Health and Wellbeing Cont’d Obesity is associated with an increased incidence of several diseases in humans, including: Hypoventilation syndrome Osteoarthritis Increased risk of developing cancer  What is Goitre? Enlargement of the thyroid gland, which occurs when the thyroid gland is unable to produce enough thyroid hormones, leading to compensatory hyperplasia and hypertrophy of the gland.  Etiology There are several factors responsible for Goitre: Iodine Deficiency ○ Most common cause Exposure to Goitrogens Chronic Auto-immune Thyroiditis Genetic Defects in Hormone Synthesis  Goitre: Types Goitre can broadly be categorized into two types: Diffuse Non-toxic Multi-nodular  Goitre: Diffuse non-toxic Known as a “simple” goitre Enlarged follicles are filled with colloid Causes enlargement of the entire gland without producing nodularity Occurs in both Endemic and Sporadic Distribution ○ Endemic Goitre Occurs in geographic areas where the soil, water, and food supply contain low levels of iodine. Most common in mountains ○ Sporadic Goitre Occurs in individuals without a clear geographical or environmental cause. There is a striking female preponderance and a peak incidence at puberty or in young adult life.  Morphology Two phases ○ Hyperplastic phase ○ Colloid involution phase In the hyperplastic phase, the thyroid gland is diffusely and symmetrically enlarged The follicles are lined by crowded columnar cells, which may accumulate and form projections Accumulations are not uniform throughout the gland, and some follicles If dietary iodine subsequently increases or if the demand for thyroid hormone decreases, the stimulated follicle epithelium involutes to form an enlarged, colloid-rich gland (colloid goiter). ○ Cut surface are usually brown, glossy and translucent  Goitre: Multinodular Recurrent episodes of hyperplasia and involution combine to produce a more irregular enlargement of the thyroid, termed multinodular goiter. These produce the most extreme thyroid enlargement and are more frequently mistaken for neoplasms than any other form of thyroid disease. Virtually all long-standing simple goiters convert into multinodular goiters.  Pathogenesis Multinodular goiters likely develop due to differences in how individual follicular cells respond to external growth signals. Some cells may gain a growth advantage, possibly due to genetic changes, leading them to grow independently and form nodules. Genetic mutations in the TSH (thyroid-stimulating hormone) signaling pathway have been identified in some autonomous thyroid nodules, which allows these nodules to grow without normal hormonal regulation. Over time, follicle overgrowth and increased colloid storage cause physical strain, leading to the rupture of follicles and blood vessels. This rupture can result in hemorrhaging, scarring, and calcification. The scar tissue and the gland’s natural structure then contribute to the nodular appearance of the goiter.  Morphology Irregularly shaped Large and uneven, often affecting one side more than the other Sometimes extends downward behind the sternum and clavicles, forming an intrathoracic or "plunging" goiter. Microscopically: ○ colloid-rich follicles lined by flattened, inactive epithelium ○ Areas of follicle hyperplasia accompanied by degenerative changes related to physical stress.  Morphology (A) Gross morphology demonstrating a coarsely nodular gland containing areas of fibrosis and cystic change. (A) Gross morphology demonstrating a (B) Photomicrograph of a hyperplastic coarsely nodular gland containing areas of nodule fibrosis and cystic change.  Signs and Symptoms Signs and symptoms of Goitre include: Dysphagia Change of voice Hypothyroidism ○ Cold intolerance ○ Weight gain Hyperthyroidism ○ Weight loss ○ Heat intolerance Breathing difficulties Visible swelling at the front of the neck  Diagnosis Diagnostic measures of Goitre include: Imaging Laboratory Tests Clinical Examinations  Treatment Treatment options include: Monitoring Surgical Intervention Iodine Supplementation Thyroid Hormone Supplementation  What is Hemochromatosis? Hereditary hemochromatosis is a genetic condition where the body accumulates too much iron, mainly in the liver, pancreas, and heart. There are at least four genetic variations of this disorder. The most common form is an autosomal recessive disease that appears in adulthood due to mutations in the HFE gene.  What are the causes of Hemochromatosis? Hereditary hemochromatosis results from genetic mutations that lead to excessive iron absorption. The most common form involves mutations in the HFE gene. Type 1 Hereditary Hemochromatosis Type 2 Hereditary Hemochromatosis Type 3 Hereditary Hemochromatosis Type 4 Hereditary Hemochromatosis  Pathophysiology The mechanism for iron overload in both HFE and non-HFE hemochromatosis is increased gastrointestinal absorption of iron, leading to chronic tissue deposition. Hepcidin, a liver-derived peptide, regulates iron absorption. Normally, elevated iron stores up-regulate hepcidin, which inhibits ferroportin (aiding in iron absorption), preventing excessive iron absorption and storage in normal individuals. Hemochromatosis types 1 through 4 share the pathogenic basis of hepcidin deficiency or inactivity and similar clinical features.  Pathophysiology Cont’d Tissue injury generally results from reactive free hydroxyl radicals generated by iron deposition, catalyzing their formation. Specific organ damage mechanisms include skin hyperpigmentation from increased melanin and iron accumulation. In the liver, iron-induced lipid peroxidation triggers hepatocyte apoptosis, activating Kupffer cells to release pro-inflammatory cytokines. These cytokines stimulate hepatic stellate cells to produce collagen, leading to liver fibrosis and an increased risk of hepatocellular carcinoma.  Pathophysiology Some other affected sites include: Pancreas: Fibrosis and atrophy. Heart: Cardiomyopathy due to hemosiderin deposition. Skin: Hyperpigmentation (↑ melanin + iron). Other: Pituitary, adrenal, thyroid, parathyroid, and joints affected.  Morphology Haemochromatosis Histology. Micrograph of hemochromatosis liver showing hepatocytes with coarse golden yellow granules of hemosiderin within the cytoplasm. These granules stain with Prussian blue stain.  Morphology Macroscopic view of Hemochromatosis progressing liver to cirrhosis and HCC  Signs and Symptoms/Complications Normal total body iron content is approximately 2.5 g in women and 3.5 g in men. Symptoms might not appear until iron accumulation is excessive (>10 to 20 g) In Type 1 hereditary (HFE) hemochromatosis, symptoms relate to the organs with the largest iron deposits. Liver disease Skin bronzing or hyperpigmentation Diabetes mellitus Cardiomyopathy  Diagnosis High serum iron and ferritin levels Exclude secondary iron overload Liver biopsy if indicated Screen relatives for causative mutations  Treatment Aims to reduce total body iron through interventions like phlebotomy and iron chelators. Patients diagnosed early and treated with regular phlebotomy can have a normal life expectancy. Iron chelators may be used to bind and remove excess iron from the body. It is also crucial to monitor and treat any complications, such as diabetes mellitus, cardiomyopathy, and other secondary manifestations. Patients should follow a balanced diet without restricting iron-containing foods and avoid vitamin C supplements to reduce iron absorption.  What is Gout? Gout is a painful form of inflammatory arthritis that is caused by excess uric acid. This causes monosodium urate crystals to form in joints and soft tissue. This results from serum uric acid levels exceeding the threshold of crystal formation ( typically > 6.8 mg/ dL)  What are the causes of gout? The etiology of gout involves a combination of genetic, metabolic, and lifestyle factors that lead to hyperuricemia (elevated serum uric acid levels). Overproduction of uric acid: caused by enzymatic abnormalities -Hyperactivity of phosphoribosyl pyrophosphate (PRPP) synthetase: Increases purine synthesis. -Deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT): Seen in Lesch-Nyhan syndrome. High cellular turnover Excessive purine consumption Genetic factors: SLC2A9 and ABCG2 Increased risk if close family members has gout Increased risk with health conditions such a obesity, diabetes, congestive heart disease and hypertension  What are the causes of gout? Alcohol consumption Under excretion of uric acid: caused by genetic predisposition or by renal impair and certain medications such as Diuretics (e.g., thiazides, loop diuretics), Aspirin (low doses), Cyclosporine, Pyrazinamide and ethambutol (used in tuberculosis treatment).  Epidemiology The prevalence of gout ranged 1–4% worldwide and incidence ranged 0.1–0.3%. Gout is more common in men vs. women by 3:1 to 10:1 ratio. Gout incidence and prevalence increased by each decade of life, with prevalence increasing to 11–13% and incidence increasing to 0.4% in people older than 80 years. Some racial minorities (Han Chinese, Māori e.g) have higher prevalence Pathophysiology  Pathophysiology Hyperuricemia: Purine metabolism produces uric acid. Increased uric acid is termed hyperuricemia, this is caused by excessive purine intake, enzyme abnormalities or underexcretion of uric acid from the body Increased serum uric acid causes the formation of monosodium urate crystals. These are deposited in joints, soft tissue and possibly kidney The crystals are recognized by the body’s immune cells (macrophages).Macrophages phagocytose the crystals, triggering activation of the NLRP3. This causes the release of IL-1β, a key pro-inflammatory cytokine and recruit of other immune cells to the joint such as neutrophils. The cytokines and ROS released by neutrophil manifest the cardinal signs of inflammation Repeated flares cause chronic gout which is identified via joint damage and deformity, tophi formation and chronic synovitis  Signs and Symptoms Intense joint pain Lingering discomfort Inflammation and redness Warmth Tenderness Limited range of motion Tophi formation  Diagnosis Gout can be diagnosed during a physical examination by inspecting joints and analyzing symptoms. Imaging techniques may be used to examine joints. These techniques include: X-rays. Ultrasound. Magnetic resonance imaging (MRI). A CT (computed tomography) scan — specifically a dual-energy CT scan. Other tests include: Blood test- to check uric acid levels Joint aspiration- removes a sample of fluid from joint  Treatment There is no cure, treatment focuses on managing attacks, preventing future flares and keeping uric acid levels low First- line medication Nonsteroidal Anti-inflammatory Drugs (NSAIDs): over the counter medication like Naproxen and Ibuprofen. Colchicine Corticosteroids.  Treatment Uric acid medication: Used to lower uric acid levels Allopurinol. Febuxostat. Pegloticase. Probenecid. A low purine diet may be advised to lower uric acid. The diet limits alcohol, high purine foods: red meats, shellfish etc, sugary beverages. Increase intake of low fat dairy and vegetables. Long term management Urate lowering therapy First line agents: Allopurinol and Febuxostat- lowers uric acid production  Questions Which clinical feature distinguishes marasmus from kwashiorkor? A) Edema B) Muscle wasting C) Hepatomegaly D) Skin lesions Which of the following is a hallmark feature of kwashiorkor? A) Severe fat wasting B) Hyperuricemia C) Peripheral edema D) Thyroid gland enlargement Which nutrient deficiency is most commonly associated with the development of a goiter? A) Vitamin D B) Iron C) Iodine D) Vitamin B12  Questions What is the primary pathological process in gout? A) Deposition of cholesterol in blood vessels B) Deposition of urate crystals in joints C) Autoimmune destruction of synovial joints D) Degeneration of cartilage in weight-bearing joints Which of the following conditions is commonly associated with obesity? A) Hyperthyroidism B) Type 2 diabetes mellitus C) Marasmus D) Kwashiorkor  References Anorexia nervosa. (2017, August 22). Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/9794-anorexia-nervosa Anorexia nervosa. (2024, May 13). Johns Hopkins Medicine. https://www.hopkinsmedicine.org/health/conditions-and-diseases/eating-disorders/anorexia-nervosa Kumar, V., Abbas, A. K., & Aster, J. C. (2012). Robbins basic pathology e-book. Elsevier Health Sciences. Meneses, L. F., Martí, A. A., & Alejos, S. C. (n.d.). Lilliam flores meneses. Clínic Barcelona. https://www.clinicbarcelona.org/en/assistance/diseases/obesity/symptoms Obesity - Symptoms and causes. (n.d.). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742 Titi-Lartey, O. A., & Gupta, V. (2023, July 24). Marasmus. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK559224/#:~:text=Marasmus%20is%20a%20severe%20manifestation,average%20for%20age%20or %20sex.