Oral Aspects of Metabolic Disorders Short Notes

Oral Aspects of Metabolic Disorders Short Notes

Question 1. What is the normal blood potassium level?
Answer. The normal potassium level in the blood is 3.5–5.0 milliequivalents per liter (mEq/L).

Question 1a What are the functions of potassium in the body?
Answer.

• Structural development of nerve cells
• Controlling the normal function of nerves and muscles.

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Question1b. What is hypokalemia?
Answer. Fall in the blood potassium level below normal.

Question 1c. Name the effects of hypokalemia.
Answer.

• Muscle weakness and cramps
• Palpitation and cardiac arrhythmia.

Question 1d. What is hyperkalemia?
Answer. Elevated level of potassium in blood is called hyperkalemia.

Question 1e. What are the effects of hyperkalemia?
Answer.

• Nausea, fatigue and muscle weakness
• Tingling sensations
• Slow heart beat and cardiac arrest in extreme cases.

Question 1f. Which mineral is present highest in amount in human body?
Answer. Calcium.

Question 1g. What is the total amount of calcium present in an average adult human body?
Answer. There is about 1 to 2 kg of calcium present in average adult human body.

Question 2. How the total calcium is distributed throughout our body?
Answer.

• About 98 percent is in the skeleton in the form of calcium phosphate salts
• Some amount is present in the plasma, bound to albumin
• Rest is present in ionic form.

Question 3. What is the plasma concentration of calcium?
Answer. In normal adults, the plasma concentration of calcium is about 8.8 to 10.4 mg/dL.

Question 4. The concentration of calcium in plasma is controlled by which hormone?
Answer. The concentration of calcium in plasma is critical and is subjected to tight hormonal control through parathyroid hormone.

Question 5. How parathyroid hormone maintains the plasma calcium level in blood?
Answer. When the plasma calcium level is low, this hormone supply calcium ions into the plasma by resorbing bone from skeleton (our bone serves as the most important storage of calcium).

Question 6. How excess calcium leaves blood plasma?
Answer. Calcium leaves the plasma via the following routes:

• Secretion into the gastrointestinal tract
• Urinary excretion
• Sweating
• Re-deposition into bone minerals.

Question 6a. What is calmodulin?
Answer. It is a small calcium binding protein that modifis the activity of many enzymes and other proteins in response to changes in serum concentration of calcium.

Question 7. Name the factors affecting the absorption of calcium into the body from diet.
Answer.

• Vitamin-D increases the absorption of calcium from the intestine
• Reduction in the level of parathyroid hormone in blood causes increased calcium absorption
• Chemicals like citrates or oxalates decrease calcium absorption
• Pathological condition like Sprue also cause decreased calcium absorption.

Question 8. What are the effects of decreased calcium levels in plasma?
Answer.

• Increased neuromuscular irritability
• Tetany—characterized by peri-oral muscular spasm and carpopedal spasm
• Convulsions and laryngospasms
• Defective blood coagulation
• Disturbance in normal heart rhythm
• Irregularity in normal membrane permeability
• Defective formation of bones and teeth
• Bone resorptions and increased osteoporosis.

Question 8a. What is carpopedal spasm?
Answer. A spasmodic contraction of the muscles of the hands and feet or especially of the wrists and ankles in disorders such as alkalosis and tetany.

Question 8b. What is convulsion?
Answer. Convulsion is a medical condition where body muscles contract and relax rapidly and repeatedly, resulting in an uncontrolled shaking of the body.

Question 9. What is the function of calcitonin?
Answer. Calcitonin helps in the incorporation of calcium into the bone (opposes the action of osteoclasts).

Question 9a. What are the effects of increased calcium levels in plasma?
Answer.

• Anorexia, nausea, vomiting, constipation, depression and lethargy, etc.
• Depressed nerve conductivity and muscle rigor Coma
• Deposition of solid calcium and phosphorus stones, within the blood vessels, mucous membrane, skin and kidney, etc.

Question 9b. Hypercalcemia associated with malignancy is most often mediated by what?
Answer. It is mediated by parathyroid hormone related protein.

Question 9c. Name the common causes of osteoporosis of bone?
Answer.

• Hyperparathyroidism
• Long-term steroid therapy
• Thyrotoxicosis.

Question 9d. What is the best method of diagnosis in osteoporosis?
Answer. Dual energy X-ray absorptiometry.

Question 10. What is pathologic calcifiation?
Answer. Pathologic calcifiation is the abnormal deposition of calcium in various tumors and organs of the body.

Question 11. What are types of pathologic calcifiations?
Answer.

• Dystrophic calcifiation
• Metastatic calcifiation
• Calcinosis type of calcifiation.

Question 12. What is dystrophic calcifiation?
Answer. It is a type of pathologic calcifiation in which calcium salts are deposited in the dead or degenerating tissue of the body.

Question 13. Is dystrophic calcifiation related to increased calcium levels in the blood?
Answer. It is not associated with increased levels of serum calcium but related to the change in the local environment, e.g. increased local tissue alkalinity, etc.

Question 14. Give some examples of dystrophic calcifiations.
Answer.

• Pulp stones
• Calcifiation of the gingival tissue, tongue and buccal mucosa
• Calcifiation of the tuberculous lymph nodes
• Blood vessel arteriosclerosis
• Calcifiations within tumors and cysts, e.g. calcifying epithelial odontogenic tumor,ossifying firoma and calcifying epithelial odontogenic cyst, etc.

Question 15. What is metastatic calcifiation?
Answer. Abnormal deposition of calcium in the tissue due to increase in the amount of serum calcium is known as metastatic calcifiation.

Question 16. Name the conditions in which metastatic calcifiations may occur.
Answer.

• Hyperparathyroidism
• Hypervitaminosis –D.

Question 17. Metastatic calcifiations often occur in which tissues?
Answer. Calcifiation usually involves tissues, e.g. lung, kidney, GI tract, blood vessels, oral mucosa and jawbones.

Question 18. What is calcinosis?
Answer. Abnormal deposition of calcium under or within the skin or epithelium is known as calcinosis.

Question 19. Name the disease in which, calcinosis may occur?
Answer.

• Scleroderma
• Dermatomyositis.

Question 20. Describe the functions of phosphorous in our body?
Answer.

• Formation of bone and teeth
• It helps in the metabolism of carbohydrates and fat by the process of phosphorylation.
• It forms phosphoproteins, nucleoproteins and nerve phsophatides, etc.
• It helps in the formation of adenosine triphosphate (ATP), which is the energy resource for various biologic functions of the body.

Question 21. What is the normal plasma concentration of phosphorus?
Answer. Normal plasma concentration of phosphorus is about 2–4 mg/dl.

Question 22. What is hypophosphatemia?
Answer. Decrease in the phosphorus levels of plasma below 2.5 mg/dL is called hypophosphatemia.

Question 23. What are the causes of hypophosphatemia?
Answer.

• Renal failure with increased excretion
• Heavy metal poisoning
• Starvation
• Respiratory alkalosis
• Sepsis.

Question 24. Describe the clinical features of hypophosphatemia.
Answer.

• Anorexia and bone pain
• Muscular weakness with waddling gait
• Defective growth in children
• Thrombocytopenia decreased WBC formation and hemolytic anemia.

Question 25. What is hyperphosphatemia?
Answer. An increased phosphorus level in plasma (above 4.5 mg/dL) is called hyperphosphatemia.

Question 26. What is the effect of hyperphosphatemia in the body?
Answer. It may cause in abnormal calcifiation in different parts of the body.

Question 27. Name the causes of hyperphosphatemia.
Answer.

• Renal failure with decreased excretion of phosphorus
• Hypoparathyroidism
• Excess phosphorus given in IV injections.

Question 28. What is hypophosphatasia?
Answer. Hypophosphatasia is a hereditary disorder characterized by defiiency of alkaline phosphatase in the blood and in the tissues.

Question 29. What are the primary effects of hypophosphatasia?
Answer. The condition causes defective bone mineralization and there is also defective cementogenesis in teeth.

Question 30. Describe the dental features of hypophosphatasia.
Answer.

• Premature loss of primary teeth
• Enlarged pulp chambers of the primary teeth
• Lack of cementum formation on the root surface
• Hypoplasia of enamel
• Inadequate mineralization of the long bones with rickets-like change
• Premature exfoliation of permanent teeth (sometimes it is the only manifestation of the disease).

Question 31. What is the main function of iron in the body?
Answer. Formation of hemoglobin in RBC.

Question 31a. In which form, iron is absorbed in the body?
Answer. Iron is absorbed as ferrous or ferric salts from the upper part of duodenum.

Question 32. What are the causes of iron defiiency?
Answer.

• Chronic blood loss due to worm infestations
• Decreased absorption of iron
• Increased hepatic sequestration of iron.

Question 33. Describe the clinical features of chronic iron defiiency.
Answer.

• Esophageal web in Plummer–Vinson’s syndrome
• Spooning of nails and loss of color of the facial skin
• Oral ulceration and sore tongue
• Fissuring in the angle of the mouth.

Question 34. What is hemochromatosis?
Answer. Hemochromatosis is a condition resulting from increased iron absorption in the body.

Question 35. What are the clinical manifestations of hemochromatosis?
Answer.

• Pigmentation of skin and mucosa due to excessive iron deposition
• Red, raw fisured tongue
• Tongue can also be pale with smooth atrophic and depapillated surface.

Question 35a. What is the function of iodine in the body?
Answer. Synthesis of thyroxin hormone.

Question 35b. What is the role of cobalt in the body?
Answer. Formation of vitamin B

Question 35c. What is the function of chloride in the body?
Answer. Maintenance of acid-base balance in the blood.

Question 36. What are the functions of magnesium in our body?
Answer. Magnesium helps in phosphorilation process and it acts as a co-factor in certain enzymatic activity especially for phosphatase and co-carboxylase enzyme, etc.

Question 37. Name the features of magnesium defiiency in the body.
Answer.

• CNS depression
• Anorexia
• Nausea
• Vomiting
• Corpopedal spasm.

Question 38. Name the functions of zinc in our body.
Answer.

• Wound healing
• To improve bone growth
• Proper keratinisation of oral mucosa
• Prevents free radical injury.

Question 39. What is a vitamin?
Answer. Vitamins are a group of powerful organic substances,essential for normal body metabolism; these are often present in the natural foodstuffs in minute quantities or may be produced synthetically.

Question 39a. What is a pro-vitamin?
Answer. Provitamin is an organic substance present in food, which after consumption in the body transform into a vitamin. Example—Beta–carotine is provitamin of vitamin A and 7-Dehydrocholesterol is a provitamin of vitamin-D.

Question 39b. What is an anti-vitamin?
Answer. Antivitamin or vitamin antagonist is a chemical substance, which is structurally similar to a vitamin but it doesn’t function as a vitamin in the body, rather prevents or spoils the action of a vitamin. Example- Galactoflvin in an antivitamin of Ribolflvin (vitamin B2).

Question 39c. What is a pseudovitamin?
Answer. A chemical substance, which has structural similarity to a vitamin but has no functional value as vitamin, is called a pseudovitamin.

Question 39d. In which category vitamin-D belongs to?
Answer. Vitamin D belongs to the category of fat soluble vitamins and it chemically behaves like a hormone or pro-hormone in many instances.

Question 39e. What is the actual name of vitamin D?
Answer. Calciferol.

Question 39f. Why vitamin D is also called antiricketic factor?
Answer. Because of its power to prevent Rickets.

Question 40. What is the active form of vitamin D?
Answer. The active form of vitamin D is known as 1-25 dihydroxycholecalciferol

Question 41. How do we get vitamin D in our body?
Answer. It can either be produced in the sun-exposed skin or can be absorbed in the intestine as dietary vitamin D.

Question 42. Name the functions of vitamin D.
Answer.

• Growth of the body
• Maintenance of blood and bone calcium level
• Absorption of calcium and phosphorus from the foods in intestine
• It helps in calcium and phosphorous metabolism
• Promotes mineralization of bone, cartilage and teeth
• Induces immunomodulatory functions and promotes phagocytosis
• Antagonistically acts against the action of parathyroid hormone
• Increases the renal reabsorption of calcium and phosphorus.

Question 43. What are the effects of excessive vitamin D in the body?
Answer. Very high levels of vitamin D in the body can cause the following problems:

• Increased bone resorptions
• Can cause high blood pressure
• Anorexia, nausea, vomiting followed by polyurea and polydipsia
• Weakness, nervousness, pruritus (itching)
• Renal failure and increased risk of ischemic heart disease.

Question 44. Name the features of vitamin D defiiency?
Answer.

• Rickets in children and osteomalacia in adults (both are bone softening diseases)
• Increased risk of colon and breast cancer
• Increased risk of heart attack in men
• Increased susceptibility to periodontal disease, multiple sclerosis and tuberculosis, etc.
• Increased risk of osteoporosis.

Question 45. What is osteoporosis?
Answer. Osteoporosis is a common disease characterized by gradual loss of mineral content in the bone.

Question 46. What are the causes of osteoporosis?
Answer.

• Low intake of calcium and the minerals
• Oral Aspects of Metabolic Disorders 357
• Lack of intestinal absorption of minerals
• Decreased estrogen levels in blood leading to demineralization of bone
• Increased urinary loss of calcium
• Hyperparathyroidism
• Stress
• Long-term steroid therapy
• Tetracycline and anticonvulsant therapy.

Question 46a. Describe the clinical features of osteoporosis.
Answer.

• It is frequently seen in post–menopausal women and men over the age of 80 years.
• Spontaneous fracture of bone especially femoral neck fracture
• Loss of lamina-dura of alveolar bone with increased tooth mobility and tooth exfoliation
• Increased incidences of jawbone fracture.

Question 47. What is rickets?
Answer. It is a hereditary disorder transmitted as X-linked dominant trait and is characterized by decreased levels of calcium and phosphorous in the body in childhood; coupled with decreased renal reabsorption and increased renal excretion of the minerals.

Question 48. What are the clinical manifestations of rickets?
Answer.

• Wide fontanells of skull and frontal bossing
• Decrease in the body length
• Bowing of legs as the bones are soft and weak
• Increase incidence of bone fracture
• Muscular weakness.

Question 49. Name the oral manifestations of rickets.
Answer.

• Formation of globular hypocalcifid dentin in tooth
• Wide band of predentin in tooth
• Large pulp horns in tooth, which may be extending up to the dentinoenamel junction
• Periapical lesions in multiple teeth
• Delayed eruption of teeth
• Abnormal cementum formation
• Loss of lamina-dura.

Question 50. Does the caries susceptibility of the patient increases in rickets?
Answer. Generally there is no increase in the caries susceptibility seen.

Question 51. What is the actual name of vitamin A?
Answer. Retinol.

Question 51a. Which vitamin is also known as a anti-xerophthalmic factor?
Answer. Vitamin A, because it prevents blindness.

Question 51b. Vitamin A is fat soluble or water soluble?
Answer. It is a fat soluble vitamin.

Question 51c. How many types of vitamin A are found?
Answer. Two types—vitamin A1 and A2; they are structurally almost similar to each other but A 1 is functionally more potent than A2.

Question 51d. Name the functions of vitamin A.
Answer.

• Helps in general growth of the body
• Vitamin A helps in the maintenance of the structure and function of specialized epithelium
• It produces photosensitive pigments (rhodopsin) in the eye
• It prevents the growth of epithelial malignant tumors
• It maintains the normal skeletal growth
• Maintenance of lysosomal stability and synthesis of glycoprotein.

Question 51e. What is the function of rhodopsin?
Answer. It is a photosensitive pigments present in the retina of our eye; function of this pigment is to create visual excitation in presence of light.

Question 52. Describe the effects of vitamin A defiiency.
Answer.

• Night blindness and impaired vision
• Bitot’s spot—a gray, triangular, elevated spots in the cornea or conjunctiva
• Xerophthalmia—(dry, red conjunctiva) with corneal ulceration
• Keratomalacia—damage to the cornea with formation of thick layer of keratin over it (cataract)
• Xerostomia
• Follicular keratosis of the skin with loss of sweat and sebaceous glands
• Squamous metaplasia of the columnar epithelium
• Hyperkeratosis of the oral mucosa and gingivitis.

Question 52a. What is night blindness and how it is related with vitamin A?
Answer. Vitamin A helps in synthesis of ‘rhodopsin’, the photosensitive pigment, which helps us to see in the dim light or even in darkness. A person is unable to see at night (night blindness) due to lack of synthesis of rhodopsis in absence of vitamin A.

Question 52b. What are the oral changes seen in vitamin A defiiency?
Answer.

• Hyperkeratosis of oral mucosa
• Xerostomia
• Abnormal formation of ameloblasts and odontoblasts leading to poor formation of tooth enamel and dentin.

Question 53. Name the effects of hypervitaminosis A.
Answer.

• Effects in children:
• Cortical thickening of bone
• Retarded bone growth with fragility
• Hemorrhage and bulging of the fontanells
• Effects in adults:
• Fatigue, headache, drowsiness with anorexia
• Weight loss, bone pain
• Skin pigmentations and alopecia
• Sexual hypofunction
• Fall of prothrombin level in blood plasma with hemorrhage.

Question 54. What is the full name of Vitamin E?
Answer. Tocopherol (antisterilitic factor).

Question 54a. Name the important functions of vitamin E.
Answer.

• Maintain sexual function and prevent sterility
• Acts as an antioxidant.

Question 54b. What are the manifestations of vitamin E defiiency?
Answer.

• Haemolytic anemia due to increased fragility of RBC ,and leukocytosis
• Muscular dystrophy,
• Posterior column abnormalities
• Cerebellar ataxia.

Question 54c. What is the actual name of vitamin B1 and which disease develops due to its defiiency?
Answer. Thiamine, it plays an important role in carbohydrate metabolism and its defiiency produces the disease called beriberi.

Question 55. Describe the oral manifestations of vitamin B1 defiiency (beriberi)?
Answer. The oral manifestations of beriberi include edema of the tongue, loss of its papillae and glossodynia.

Question 56. What is the function of niacin? Its defiiency causes which disease?
Answer. Niacin (nicotinic acid) plays an important role in the intracellular oxidation process and its defiiency causes pellagra.

Question 57. Describe the main clinical features of pellagra.
Answer. The disease pellagra is clinically summarized by 4Ds:

• Dementia
• Dermatitis
• Diarrhea
• Death.

Question 58. What are the oral manifestations of pellagra?
Answer.

• Generalized stomatitis with burning sensation, swelling, redness, pain and ulceration in the oral mucosa
• The tongue becomes red, enlarged and depapillated, with a bald surface
• The tongue may coated with a grayish pigmentation and may have deep ulcerations
• Gingival margins are often red, swollen and ulcerated
• Painful lips and angular cheilitis often develop.

Question 59. What is the scientifi name of vitamin B2?
Answer. The scientifi name of vitamin B 2 is riboflvin.

Question 60. Name the common oral manifestations of riboflvin defiiency?
Answer. Angular cheilitis, glossitis, cheilosis (swelling and cracking at the angle of lip), angular stomatitis, etc.

Question 61. Give the clinical appearance of angular stomatitis.
Answer. Inflmmation of oral mucosa at the angle of mouth; in this condition, the lips exhibit reddening with fisures, painful cracks, dry scaling along with maceration at the corner of the mouth.

Question 62. What is magenta glossitis?
Answer. Magenta glossitis is a peculiar form of glossitis, which occurs due to riboflvin defiiency;in this disease the tongue is magenta in color and its surface appears granular or ‘pebbly’due to flttening and mushrooming of the papillae.

Question 63. Describe the clinical manifestations of folic acid defiiency.
Answer.

• Loss of filiform and fungiform papilla of tongue; which results in a smooth, shiny appearance
• Defective keratinization and increased susceptibility to infection in the oral mucosa Gingivitis and oral ulceration

Question 63a. What is vitamin B12 and what are its functions?
Answer. Vitamin B 12, also called cobalamin, is a water-soluble vitamin with a key role in the normal functioning of the brain and nervous system; it helps in the formation of blood. It is used to treat pernicious anemia.

Question 63b. Enumerate the function of vitamin B12.
Answer.

• Helps in structural development and maturation of RBC
• Stimulates the bone marrow and helps in formation of WBC and platelets
• Helps in activation of some areas of central nervous system.

Question 63c. Name the effects of vitamin B12 defiiency.
Answer. Optic atrophy, myelopathy (pernicious and megaloblastic anemia) and peripheral neuropathy.

Question 63d. What is pernicious anemia?
Answer. It is the type of anemia, which occurs due lack of absorption of vitamin B12 because of absence of the intrinsic factor in the stomach. The RBC cells remain immature in this anemia.

Question 63e. What is megaloblastic anemia?
Answer. This anemia is characterized by the formation of abnormally large, nucleated and immature RBC cells (megaloblasts) in the blood; it develops due to defiiency of vitamin B12 and B6.

Question 64. What is the scientifi name of vitamin C?
Answer. The scientifi name of vitamin C is ascorbic acid.

Question 65. What are the functions of vitamin C?
Answer.

• Synthesis of collagen
• Synthesis of osteoid and dentin
• Helps in the synthesis of neurotransmitter nor-epinephrine
• Synthesis of carnitine, a molecule that helps in transport of fat to mitochondria to produce energy
• Metabolism of cholesterol
• Highly effective antioxidant
• Helps in absorption of iron from intestine and also helps in maturation of RBC
• Decreases the risk of cardiac diseases, strokes and cancer, etc
• Decreases the oxidative stress and thereby reduce the risk of diabetes mellitus.

Question 65a. Enumerate the defiiency symptoms of vitamin C.
Answer.

• Scurvy
• Increased capillary fragility and hemorrhage
• Abnormal bone formation with increased brittleness of bone
• Disturbance in blood coagulation
• Disturbed carbohydrate metabolism
• Increased susceptibility to infection.

Question 66. Name the most important disease produced due to defiiency of vitamin C.
Answer. Scurvy, which is the clinical manifestation of vitamin C defiiency.

Question 66a. Deprivation of vitamin C for how many weeks can lead to scurvy?
Answer. About 20 to 30 weeks.

Question 67. Describe the clinical manifestations of scurvy and other related symptoms of vitamin C defiiency.
Answer.

• Petechiae and ecchymosis in the oral mucous membrane
• Painful swelling of gingiva with excessive bleeding and bad breath
• Mild to marked loosening of teeth with premature exfoliations
• Retardation of wound healing
• Defective function of odontoblast and osteoblast cells
• Abnormality in tooth formation
• Disturbed bone growth in children due to defective collagen synthesis and osteoid matrix formations
• Fatigue due to defective fat metabolism
• Bruising, premature loss of hair, joint pain and swelling.

Question 68. What is follicular hyperkeratosis?
Answer. Follicular hyperkeratosis is a skin condition characterized by excessive synthesis of keratin in the hair follicles; which results in rough, cone-shaped, elevated papules in the skin.

Question 69. What is vitamin H (vitamin B8)?
Answer. Vitamin H or biotin is a water soluble vitamin, which helps in pyruvic acid metabolism in liver and its defiiency can cause muscle pain, anorexia, weight loss and neural weakness, etc.

Question 69a. What is the actual name of vitamin K?
Answer. Phylloquinone (antihemorrhagic factor).

Question 69b. What is the chief function of vitamin K?
Answer. Vitamin K helps in the synthesis of prothrombin, which is factor II for blood coagulation; it also helps in synthesis of other clotting factors, e.g. proconvertin, factor VIII, IX and X, etc.

Question 69c. What is the role of vitamin E tooth and bone mineralization?
Answer. Vitamin E helps in activation of osteocalasin and other similar proteins in the bone as well as in the enamel or dentin matrix; the process helps in calcium deposition in bone and tooth.

Question 70. How vitamin K is made available in the body?
Answer. Most of Vitamin K may be synthesized by intestinal micro flra in humans and some amount of it can be available from natural fruits.

Question 70a. Why the chances of hemorrhage may increase in long-term antibiotic therapy?
Answer. Such therapy kills intestinal flra, which produces vitamin K and defiiency of the vitamin K increase the risk of hemorrhage.

Question 71. Describe the effects of vitamin K defiiency.
Answer.

• Decreased prothrombin levels in blood with increased tendency for hemorrhage and bruising
• Increased bleeding after tooth extraction and following minor surgical interventions.

Question 72. What are amyloids?
Answer. Amyloids are abnormal firillar proteins, which have a peculiar homogenous, translucent appearance and a characteristic staining property.

Question 73. What is amyloidosis?
Answer. Amyloidosis is a pathological condition characterized by the extracellular deposition of amyloids within the tissue.

Question 74. What are the types of amylodoisis?
Answer. Amyloidosis are of two types: Primary (idiopathic) and secondary (reactive).

Question 75. What is primary or idiopathic amylodoisis?
Answer. Primary (idiopathic) type of amyloidosis arises as a result of derangement of immunoglobulin synthesis and consists of fragments of IgG molecules in the tissues.

Question 76. What is secondary (reactive) amyloidosis?
Answer. Secondary (reactive) amyloidosis occurs as a complication of chronic destructive inflmmatory disease like rheumatoid arthritis, tuberculosis, sarcoidosis or osteomyelitis and it also occurs in some malignant conditions.

Question 77. Name the sites in the oral cavity where amyloidosis may occur.
Answer. Tongue, gingiva, oral mucosa, salivary glands and muscles, etc.

Question 78. Describe the clinical features of localized amyloidosis in mouth.
Answer.

• Macroglossia with a pale or purplish color of tongue; the lateral border of tongue often shows indentations of teeth.
• Gingival swelling with petechiae, ecchymosis and mucosal hemorrhage with ulcerations Salivary gland swelling with xerostomia.

Question 79. Name one odontogenic tumor, in which large amounts of amyloid tissue are found.
Answer. Pindborg’s tumor.

Question 80. How amyloid tissues appear histologically within the tissue?
Answer. In the tissue amyloids appear as weakly eosinophilic, homogenous, amorphus hyaline materials.

Question 81. Inside the tissue where these amyloid materials are often seen?
Answer. These are mostly seen in the perivascular regions as well as within the submucous connective tissue.

Question 82. Name the special stains used in the detection of amyloids.
Answer. Congo red and crystal violet stains.

Question 83. How amyloid materials appear in Congo red stain?
Answer. When stained with Congo red, amyloids in the tissue produce a typical apple-green birefringence, when viewed with polarized light.

Question 84. How amyloid materials appear in crystal violet stain?
Answer. Crystal violet stain exhibits red colored amyloid materials in the tissue.

Question 85. What is porphyria?
Answer. Porphyria is an inborn error of porphyrin metabolism and is characterized by overproduction of uroporphyrin and other related substances in the body.

Question 86. What are the types of porphyrias seen?
Answer. Porphyria is commonly of two types: Erythropoietic porphyria and hepatic porphyria.

Question 87. Name the clinical features of erythropoietic porphyria.
Answer. The erythropoietic porphyria is characterized by red urine, photophobia, hairy face and reddish or brownish colored teeth. There may be occasional presence of vesiculobullous skin lesions.

Question 88. Why tooth discoloration occurs in porphyria?
Answer. The tooth discoloration occurs due to deposition of porphyrins in enamel, dentin and cementum, etc. The discoloration is more intense in deciduous teeth with both enamel and dentin is affected; discoloration is less severe in permanent teeth.

Question 89. What is Hurler syndrome?
Answer. Hurler syndrome is a disturbance of carbohydrate metabolism and is characterized by elevated mucopolysaccharide levels in urine. The disease is somewhat fatal in nature and it commonly affects children.

Question 90. Name the common symptoms of Hurler syndrome.
Answer. Mental retardation, dwarfim, hypertelorism, puffy eyelids and corneal clouding and hepatosplenomegaly, etc.

Question 91. Describe the oral manifestations of Hurler’s syndrome.
Answer.

• Deformed face with short and broad mandible and coarse, thick lips
• Large tongue, open mouth
• Lack of tooth eruption or delayed eruption and microdontia
• Gingival hyperplasia and diestema formation.

Question 92. Name the major types of disturbance in lipid metabolism.
Answer. Disturbance in lipid metabolism are classifid into two broad groups—Histiocytosis ‘X’ and lipid reticuloendotheliosis.

Question 93. Name the diseases which come under the histiocytosis-X group.
Answer. Mainly three diseases are included in this group:

• Hand-Schuller-Christian disease
• Eosinophilic granuloma
• Letterer-Siwe disease.

Question 94. Name the diseases which come under lipid reticuloendotheliosis group.
Answer. The lipid reticuloendotheliosis includes two diseases -Gaucher’s disease and NiemannPick disease.

Question 95. What is a growth hormone?
Answer. Growth hormone or somatotrophic hormone is secreted from the anterior pituitary and helps in normal growth of the body (e.g. general body growth, bone and muscle growth,growth of body cells,etc)

Question 95a. What happens in hyposecretion of growth hormone during infancy?
Answer. Hyposecretion in infancy leads to dwarfim, in which the patients usually have a much shorter but well-proportioned body.

Question 96. What are the causes of hyposecretion of growth hormone?
Answer. It might occur due to the following causes:

• Tumor of pituitary, e.g. craniopharyngioma
• Hypophyseal firosis
• Supracellar cyst
• Destruction of pituitary gland by trauma

Question 97. Describe the clinical features of dwarfim.
Answer.

• Short body stature with sparse hair on the head and other hairy regions
• Generalized atrophy of all body organs with childish face
• Wrinkled atrophic skin, hypogonadism, impotence and amenorrhea.

Question 98.Describe the oral manifestations of dwarfim.
Answer.

• Small face in comparison to the skull
• Delayed exfoliation of deciduous teeth
• Delayed completion of tooth roots
• Delayed eruption of permanent teeth
• Crowning of teeth
• Underdevelopment of maxilla and mandible
• Smaller crown size of the teeth and smaller root length
• Lack of development of third molars.

Question 99. Name one important fiding in the blood in dwarfim.
Answer. Hypoglycemia.

Question 100. Describe the clinical features of growth hormone insuffiiency in adults.
Answer.

• The person looks much older than that of his genuine age
• Easy fatigability and muscle weakness, hypotention with lack of resistance to cold Irregular menstrual cycles in females
• Failure of lactation,dry and wrinkled skin.

Question 101. What is diabetes insipidus?
Answer. Diabetes insipidus is a disorder of water metabolism, caused by the defiiency of vasopressin, the anti-diuretic hormone (ADH) secreted by the posterior pituitary.

Question 102. What are the causes of diabetes insipidus?
Answer. It can be either idiopathic or can be secondary to head trauma, neoplasm, surgical ablation or irradiation of pituitary gland.

Question 102a. How much flid is fitered every day by our kidneys?
Answer. About 170 liters; in normal situation 168.5 liters of water is reabsorbed in the body while 1.5 liter is excreted as urine.

Question 102b. How the urinary output level changes in diabetes insipidus?
Answer. In diabetes insipidus, urinary output is severely increased (may be up to 40 liters in a day) and it happens due to decreased water reabsorption from kidney because of low vasopressin secretion.

Question 103. Describe the clinical features of diabetes insipidus.
Answer.

• Marked polyurea—daily output of 5 to 40 liters of urine
• Polydipsia (increased thrust)—4 to 40 liters of flid required daily
• Patients have a craving for cold water
• Dehydration, headache, fatigue and irritability
• Xerostomia (dry mouth) is the most signifiant oral manifestation
• Sialosis or non-inflmmatory swelling of the parotid gland.

Question 104. Name the important laboratory fidings in diabetes insipidus.
Answer.

• Increase in plasma osmolarity
• Low specifi gravity of urine (1.001–1.005).

Question 105. What is flid deprivation test in diabetes insipidus?
Answer. In Diabetes insipidus patients usually have low specifi gravity of urine (1.001–1.005); if flid intake is restricted in a person for 8–12 hours and even after that there is no increase in the specifi gravity of urine, the case should be diagnosed as diabetes insipidus.

Question 106. What is the treatment of diabetes insipidus?
Answer. Administration of vasopressin and chlorpropamide.

Question 107. Name the causes of hypersecretion of growth hormone?
Answer.

• Hypersecretion of growth hormone due to functional pituitary adenoma
• Increased function of anterior pituitary, which regulates the secretion of growth hormone.

Question 108. What is the effect of hypersecretion of growth hormone in infants?
Answer. Hyperpituitarism or increased production of growth hormone from the anterior pituitary leads to gigantism in infants (before the fusion of bone epiphyses).

Question 109. What is the effect of hypersecretion of growth hormone in adults?
Answer. Hyperpituitarism causes acromegaly in adults (after the fusion of bone epiphyses).

Question 110. Describe the clinical features of pituitary gigantism.
Answer.

• Generalized symmetric overgrowth of the body with extreme body height (above 7 feet) with long extremities
• Hyperglycemia
• Genital underdevelopment and defective vision
• Headache, lassitude, joint pain, excessive perspiration and muscle pain.

Question 111. What are the oral manifestations of gigantism?
Answer.

• Enlarged maxilla and mandible with severe growth of the facial soft tissues
• Marked increase in the vertical dimension of face
• Large size of teeth (true generalized macrodontia) and early eruption of teeth
• Macroglossia and hypercementosis of teeth.

Question 112. What is acromegaly?
Answer. The disease occurs due to hypersecretion of growth hormone in adults after the closure of epiphyseal end plates.

Question 113. What are the general manifestations of acromegaly?
Answer.

• Thick bones with larger hands and feet; which often have a ‘spade – like’ appearance.
• Enlarged skull with increased intracranial pressure often causing headache,photophobia and visual disturbances, etc.
• Nose and forehead are enlarged
• Patients often suffer from hypertension, cardiac problems and peripheral neuropathy,etc.

Question 113a. What is the basic difference in the abnormal bone growth pattern in gigantism and acromegaly?
Answer. In gigantism, the bones grow excessively in length while in acromegaly the bones grow in width.

Question 114. What is the most signifiant change in the orofacial region in acromegaly?
Answer. Overproduction of growth hormone in adults causes activation of condylar growth center in mandible with abnormal increase in the size of mandible.

Question 115. Describe the oral manifestations of acromegaly.
Answer.

• Large mandible with development of class III malocclusion
• Macroglossia with indentations of teeth on the lateral border of tongue
• A typical coarse facial features due to abnormal soft tissue growth
• Thick lips, which often produce a Negroid appearance to the patient
• Proclination of teeth with diastema formation due to abnormal growth of jaws after the eruption of teeth
• Hypercementosis in tooth
• Hypertrophy of tissues of soft palate, which often causes disturbance in sleep.
• Large nose, ears and prominent eyebrows
• Increased incidences of periodontitis
• Poor fiting of old prosthesis due to large size of the jaw (especially lower the lower one)
• Enlargement of maxillary air sinuses.

Question 115a. Which hormone has no cell surface receptor?
Answer. Thyroxin.

Question 116. What is hypothyroidism?
Answer. Hypothyroidism refers to decreased levels of thyroid hormone in the body, which causes decreased metabolic rate and results in retardation of growth, differentiation and function of the entire body systems.

Question 117. What is cretinism?
Answer. During childhood, hypothyroidism produces a disease called cretinism.

Question 118. What is myxedema?
Answer. Hypothyroidism in adults produces the disease called myxedema.

Question 119. What are the possible causes of hypothyroidism?
Answer.

• Autoimmune disease
• Congenital absence of the thyroid gland
• Lack of iodine in food
• Decreased secretion of TSH (necessary for secretion of thyroid hormone) by pituitary gland
• Atrophy, damage or surgical removal of the thyroid gland
• Congenital absence of thyroid gland.

Question 120. Describe the systemic manifestations of cretinism.
Answer.

• A short, poorly developed and mentally retarded child with neonatal jaundice, horsecry, delayed development of speech and walking capability
• The child is often obese, dwarf, stocky and pot bellied
• The child often exhibits large skull, generalized non-pitting edema, coarse dry skin and sparse brittle hair
• Hypotension, protuberant abdomen with umbilical hernia and atrophy of the sweat glands are also seen.

Question 121. Mention the oral manifestations of cretinism?
Answer.

• Dull, expressionless face of the child, broad flt face and delayed development of speech.
• Delayed eruption and exfoliation of deciduous teeth and malocclusion
• Underdevelopment of mandible, macroglossia with protruding tongue and thick lips.
• Diffiulty in swallowing due to extremely large tongue
• Constant drooling of saliva from the mouth.

Question 121a. What is the common age of development of myxedema?
Answer. It frequently develops among the middle-aged males.

Question 122. Describe the systemic manifestations of myxedema.
Answer.

• Weakness, weight gain, fatigue, cold intolerance, low blood pressure and mental retardation
• Patients often sleep on an average about 12 to 14 hours in a day
• Dry coarse skin with loss of hair, swelling of the face and extremities
• Husky voice, decreased sweating and anorexia
• Loss of memory, hearing impairment, arthralgia, muscle cramps and paresthesia.

Question 123. Describe the oral manifestations of myxedema.
Answer.

• Dull expressionless face with periorbital puffiess and loss of hair
• The tongue, lips and eyelids, etc. are edematous (non-pitting type) and swollen
• The large tongue often interferes with speech
• Underdevelopment of maxilla and mandible.

Question 124. What is hyperthyroidism?
Answer. Hyperthyroidism is the disease, which is caused by excessive production of thyroid hormone in the body.

Question 125. What are the causes of hyperthyroidism?
Answer.

• Hyperplasia of thyroid gland with increased function (goiter)
• Increased secretion of thyroid hormone due to benign tumor in the gland.
• Increased TSH secretion due to pituitary over-secretion.

Question 126. Hyperthyroidism occurs more often at what age and in which sex it is more common?
Answer. The disease mostly occurs in 3rd and 4th decade of life and it shows a defiite female predilection.

Question 127. Describe the general clinical features of hyperthyroidism.
Answer.

• Hypertension, weight loss despite increased appetite and palpitations (tachycardia)
• Widened pulse pressure (increased systolic and decreased diastolic pressure)
• Increased risk of cardiovascular disease, tremors and nervousness
• Emotional instability with easy tearing, photophobia, warm smooth skin
• Exophthalmos, osteoporosis and excessive sweating.

Question 128. What are the oral manifestations of hyperparathyroidism?
Answer.

• Early exfoliation of deciduous teeth
• Premature eruption of permanent teeth
• Alveolar bone atrophy
• Increased susceptibility to oral infections.

Question 129. Which patients will have higher risk of developing cardiac emergency during dental treatment—hypothyroidism or hyperthyroidism?
Answer. Hyperthyroidism patients often have diffiulty in undergoing dental extractions or other dental surgical procedures because of the cardiac abnormality. Whereas hypothyroidism patients are often safely negotiated in this regard.

Question 130. What is the function of parathyroid hormone?
Answer. The primary function of parathormone is to maintain the normal calcium and phosphorus levels in blood.

Question 131. What is hyperparathyroidism?
Answer. Excessive concentration of parathormore in the blood is known as hyperparathyroidism.

Question 132. What are the types of hyperparathyroidism?
Answer. Hyperparathyroidism is of two types: (i) primary hyperparathyroidism and (ii) secondary hyperparathyroidism.

Question 132a. What is the primary effect of parathyroid hormone?
Answer. The main function of hormone is to maintain the calcium and phosphate balance in blood.
It helps in maintaining blood calcium by intestinal absorption, controls renal excretion and supplies calcium to blood by bone resorption in case of defiiency. It stimulates the osteoclast cells to resorb the bone to release calcium ions from the skeleton when there is a fall in the blood calcium level. It helps in reducing the phosphate level in blood.

Question 132b. Which hormone has the action just opposite to parathyroid hormone?
Answer. Calcitonin (it inhibits the osteoclast cells).

Question 133. What is primary hyperparathyroidism?
Answer. The primary hyperparathyroidism occurs due to excessive parathormore production in the body. It occurs as a result of adenoma, hyperplasia or functional carcinoma of the parathyroid glands.

Question 134. What is secondary hyperparathyroidism?
Answer. Secondary hyperparathyroidism occurs as a result of hyperplasia of the parathyroid gland secondary to some disease, like end-stage of renal disease, osteomalacia and multiple myeloma, etc.

Question 135. Hyperparathyroidism commonly affects which category of people?
Answer. The disease occurs more commonly among the middle-aged females (postmenopausal).

Question 136. Describe the general symptoms of hyperparathyroidism.
Answer.

• The early symptoms include fatigue, weakness, anorexia, polyurea, thirst, and constipation, etc.
• Depression, insomnia, loss of memory of recent events
• Increased incidence of peptic ulcers and itching sensations in the skin
• Hypertension and CVS due to renal damage
• Vomiting, stone formation in the kidneys (due to increased excretion of calcium) and joint stiffness.

Question 137. What are the common oral manifestations of hyperparathyroidism?
Answer. The common oral manifestations are loosening and mobility of teeth, pathological fractures of the jaw, etc.

Question 138. Describe the radiological features of hyperparathyroidism.
Answer.

• Generalized osteoporosis with loss of lamina dura around the roots of teeth.
• In severe cases multiple, well defied, unilocular or multilocular radiolucent areas may be seen in the jawbones, which often resemble cysts or tumors (osteitis firosa cystica)
• Decrease in the trabacular density and blurring of normal trabacular pattern often produce a typical ‘ground-glass’ appearance in the jawbone.

Question 139. What is the typical radiographic fiding seen hyperparathyroidism with lateral skull radiograph?
Answer. Lateral skull radiograph in hyperparathyroidism often reveals a typical “salt and pepper” effect.

Question 140. What is brown tumor or brown nodules?
Answer. In case of hyperparathyroidism, the gross tissue specimen often has a reddish-brown appearance due to the blood pigments and hence the lesion is often referred to as the “brown tumor or brown nodules”.

Question 141. Describe the histological features of hyperparathyroidism.
Answer. Histology reveals the following:
Osteoclastic resorptions of bone with proliferation of extremely vascular granulation tissue showing large number of blood capillaries and endothelium-lined spaces within the bone

• There are some areas of excessive hemorrhage and hemosiderin pigmentations within the tissue with presence of multiple multinuclead osteoclast type of giant cells.

Question 142. Hyperparathyroidism histologically resembles which lesion?
Answer. Central giant cell granuloma.

Question 143. How hyperparathyroidism can be distinguished from central giant cell granuloma?
Answer. Multiple bone involvement and raised serum calcium level, which are commonly seen in heperparathyroidism, are not seen in giant cell granulomas. Moreover, parathormone assay helps in differentiating these two lesions accurately.

Question 144. Describe the laboratory investigations in hyperparathyroidism.
Answer.

• Serum calcium level may be as high as 15 to 17 mg/dL (normal is 9–12 mg/dL)
• Serum alkaline phosphatase and urinary hydroxy-proline levels are not elevated
• unless the condition is extremely severe
• Serum phosphate level is reduced (may be as low as 2.5 mg/dL)
• Urinary calcium and phosphate levels are elevated
• USG, CT-scan etc are done to detect the tumor in the gland
• Serum parathormone level is elevated (could be detected by immunoassay).

Question 144a. Why serum phosphate level is low in hyperparathyroidism?
Answer.Due to decreased renal reabsorption of phosphste.

Question 145. What are the treatments of hyperparathyroidism?
Answer. Excision of the parathyroid tumor, administration of Vitamin D and dietary phosphate supplements.

Question 146. What is hypoparathyroidism?
Answer. Hypoparathyroidism refers to the defiiency of parathyroid hormone levels in the body and it is a much more rare entity as compared to hyperparathyroidism.

Question 147. What are the causes of hypoparathyroidism?
Answer.

• If parathyroid gland is mistakenly removed during surgical intervention of the thyroid
• Autoimmune damage of the parathyroid gland
• Rare diseases like Di-George syndrome or endocrine candidosis syndrome.

Question 148. Describe the general clinical manifestations of hypoparathyroidism.
Answer. Hypoparathyroidism often causes hypocalcemia in the body, which produces the following features:

• Increased neuromuscular excitability if the calcium level falls below 7 to 8 mg/dL.
• Tetany with carpopedal spasm occurs if serum calcium level falls below 5 to 6 mg/dL.

Question 148a. Why neuromuscular excitability increase in hypoparathyroidism?
Answer. In this disease the blood calcium level goes down and simultaneously blood sodium and potassium levels goes up; the later ions in higher concentrations often cause increased neuromuscular excitability.

Question 149. What are the oral manifestations of hypoparathyroidism?
Answer.

• Positive Chvostek’s sign
• Aplasia or hypoplasia of teeth with failure of eruption.
• Short roots of teeth but thick lamina dura
• Incompletely mineralized dentine
• Enamel hypoplasia (pitting type)
• Chronic persistent candidiasis in young people.

Question 150. What is Chvostek’s sign?
Answer. Chvostek’s sign is an important fiding associated with hypocalcemia; which is characterized by twitching of the upper lip when the facial nerve is tapped just below the zygomatic process.

Question 151. Describe the laboratory fidings in hypoparathyroidism?
Answer.

• Decreased level of parathormone in blood as seen in radioimmunoassay
• Decreased serum calcium concentration
• Decreased serum phosphate level
• Normal renal functions initially.

Question 152. What is the treatment of hypoparathyroidism?
Answer. Administration of vitamin D precursor (ergocalceferol).

Question 153. What are the parts of the Adrenal gland?
Answer. The adrenal gland is made up of two parts—adrenal cortex and adrenal medulla.

Question 154. Name the hormones liberated by adrenal cortex.
Answer. The adrenal cortex liberates three hormones:

• Mineralocorticoids for example aldosterone
• Glucocorticoids for example cortisol
• Sex hormones for example adrenal androgens.

Question 155. Name the hormones liberated by adrenal medulla.
Answer. The adrenal medulla produces two hormones—epinephrine and nor-epinephrine.

Question 156. What are the functions of mineralocortocoid hormones?
Answer. These hormones are concerned with sodium and water retentions and potassium excretions in the body.

Question 157. What are the functions glucocorticoid (steroid) hormones?
Answer.

• To antagonize the action of insulin (promotes gluconeogenesis, which provides glucose)
• Increases breakdown of protein and fatty acids
• Suppresses inflmmation, inhibits scar formation
• Blocks allergic reactions
• Decreases the number of circulating eosinophils and leukocytes
• Exerts a permissive action on functioning of CNS
• Inhibits release of adrenocorticotropins.

Question 158. Name the indications of steroid therapy.
Answer. Steroid therapy is done in the following conditions:

• Hormone disorder: Addison’s disease
• Rheumatic condition: Rheumatoid arthritis and Acute rheumatic fever
• Blood disorders: ITP (Idiopathic thrombo-cytopenic purpura), leukemia and hemolytic anemia
• Allergic conditions: Bronchial asthma, allergic rhinitis
• Oral Aspects of Metabolic Disorders 373
• Dermatologic conditions: Drug rashes, giant hives, lichen planus, dermatitis
• Ocular diseases: Conjunctivitis, uveitis
• Collagen disorders: Lupus erythematosus and periarteritis nodosa
• Gastrointestinal problems: Ulcerative colitis
• Organ transplant patients: As an immunosuppressive drug
• Neurological problems: Cerebral edema
• Miscellaneous conditions: Gout, multiple sclerosis, etc.

Question 159. Name the common side effects of long-term steroid therapy.
Answer.

• Suppression of adrenocortical function with risk of circulatory failure
• Suppressed inflmmatory response with impaired wound healing
• Increased osteoporosis
• Immunosuppression with increased susceptibility to opportunistic infections
• Depressed protein metabolism
• Sodium and water retention in the body with moon face
• Raised blood sugar (steroid diabetes).

Question 160. Glucocorticoids are administered in which conditions?
Answer.

• Status asthmaticus.
• Acute adrenal insuffiiency
• Anaphylactic reaction (only after adrenaline has been given).

Question 161. What are the functions of steroid or glucocorticoid hormones?
Answer. The steroid hormone plays an essential role in maintaining life because it performs important metabolic activity of the body. It provides the capacity to resist all types of noxious stimuli and environmental changes.

Question 162. Secretion of steroid hormone is controlled by which hormone?
Answer. The secretion of steroid hormone is controlled by the pituitary hormone called the adrenocorticotropic hormone (ACTH).

Question 163. What is steroid crisis?
Answer. If a person undergoing long-term steroid therapy stops taking the drug abruptly, he or
she may go into severe shock when exposed to some kinds of stress or strain; such type of situation is known as steroid crisis.

Question 164. Why steroid crisis occurs?
Answer. If a patient takes steroid (cortisol) from outside sources for a longer duration, the function of his or her adrenal cortex becomes diminished. Such exogenous steroid dependent person if stops taking the drug abruptly, he or she may go into severe shock, which is often known as “steroid crisis”.

Question 164a. How steroid crisis can be avoided?
Answer. To avoid steroid crisis in long-term steroid-dependent persons, the drug should never be stopped abruptly; rather the therapy should be ended by gradually tapering the dose of steroid.

Question 164b. What are the functions of adrenaline or epinephrine?
Answer.

• Increases heart rate and cardiac out-put
• Vasoconstrictions
• Bronchodialatations and increases respiratory rate
• Increases BMR.

Question 164c. Why adrenaline is called the hormone of emergency?
Answer. In cases of emergency (e.g.extreme fear or anger), this hormone is secreted and it helps us to survive the situation by increasing the heart rate, respiratory rate and the blood pressure, etc.

Question 165. What is the most important hormone in mineralocorticoid group?
Answer. Aldosterone.

Question 166. Mineralocorticoid hormone is produced in which part of the adrenal gland?
Answer. It is a steroid hormone of mineralocorticoid group produced by the outer section (zona glomerulosa) of the adrenal cortex in the adrenal gland.

Question 167. What is the function of mineralocorticoid hormone?
Answer. It acts on the kidney nephrons to conserve Na+ ion and secrete K+ ions in order to maintain the flid balance in the body and the blood pressure.

Question 168. What is primary hyperaldosteronism?
Answer. Primary hyperaldosteronism is the condition, which occurs due to over secretion of aldosterone by an adrenal adenoma.

Question 169. What are the manifestations of Primary hyperaldosteronism?
Answer. It is characterized by hypokalemia, alkalosis, muscular weakness, polyuria (multiple urination), polydipsia (excessive thirst) and hypertension, etc.

Question 170. What is secondary hyperaldosteronism?
Answer. It occurs due to extra-adrenal stimulation of aldosterone; usually associated with nephritic syndrome, cirrhosis liver, heart failure and malignant hypertension, etc.

Question 171. What is conn’s syndrome?
Answer. When hyperproduction of aldosterone (primary hyperaldosteronism) occurs due to a solitary benign aldosterone-secreting adenoma of the adrenal gland, the condition is known asconn’ssyndrome. Itischaracterized byincreased plasmasodium and potassium levels and decreased plasma calcium level; which result in muscle contractions, fatigue and high blood pressure, etc.

Question 172. How acute adrenocortical insuffiiency may occur?
Answer. It may occur either due to surgical removal of adrenal gland or due to destruction of the adrenal gland by injury or infection.

Question 173. What are the features of acute adrenocortical insuffiiency?
Answer. The features of acute adrenocortical insuffiiency include the following:

• Headache
• Nausea
• Vomiting
• Abdominal pain
• Low blood pressure.

Question 174. What is Waterhouse-Friderichsen syndrome?
Answer. Waterhouse-Friderichsen syndrome occurs as aresultofacute adrenocortical insuffiiency,in association with infection by Meningococci, Streptococci, Pneumococci, etc.

Question 175. What happens in Waterhouse-Friderichsen syndrome?
Answer. In this disease patients often develop rapidly fulminating septicemia with purpura; and death occurs within 48 to 72 hours.

Question 176. What is Addison’s disease?
Answer. It is a debilitating and potentially fatal condition, which occurs due to chronic insuffiiency of the adrenocortical hormone.

Question 176a. Addison’s disease is related to adrenal cortex or the pituitary gland?
Answer. Adrenal cortex.

Question 177. Describe the clinical manifestations of Addison’s disease.
Answer.

• Postural hypotension with fatigue, irritability, weight loss and vomiting
• Brown hyperpigmentations of skin including orofacial region ( bronzing pigmentation)
• Small and feeble pulse
• Chronic mucocutaneous candidiasis.

Question 178. Why hyperpigmentations occur in Addison’s disease?
Answer. It occurs due to increased level of beta-lipoprotein or increased ACTH, both cause stimulations to the melanocytes to produce more melanin in the skin or mucosa.

Question 179. What is Cushing’s syndrome?
Answer. Cushing’s syndrome is the hormonal disorder, which results from hypersecretion of gluccocorticoid hormone due to over-activity of the adrenal glands.

Question 180. How Cushing’s syndrome can occur?
Answer. Cushing’s syndrome occurs due to the following reasons:

• Administration of high dose of ACTH or increased ACTH production in a pituitary tumor
• Administration of high dose of corticosteroids
• Adrenocortical hyperplasia with over production of glucocorticoids
• Adenoma or carcinoma of the adrenal cortex
• Ectopic ACTH syndrome.

Question 180a. What is the earliest manifestation of Cushing’s syndrome?
Answer. Loss of diurnal (pertaining to the daytime) variation.

Question 181. Describe the clinical features of Cushing’s syndrome?
Answer.

• Persistent hyperglycemia (steroid diabetes)
• Severe osteoporosis
• Potassium depletion leading to hypokalemia, arrhythmias.
• Sodium and water retention which causes hypertension and edema
• Abnormal fat deposition in the orofacial region produces a puffy and bilateral
• edematous swelling of the face (“moon facies”).
• Development of abnormal fat pad on the neck (buffalo-hump).
• Generalized obesity and lowered resistance to stress
• Decreased immunity with increased susceptibility to infection (especially opportunistic infections).
• Poor wound healing.

Question 182. What is steroid diabetes?
Answer. Steroid diabetes or “steroid-induced diabetes” refers to the prolonged hyperglycemia due to glucocorticoid therapy for another medical condition.

Question 183. Why steroid diabetes occurs?
Answer. Steroid diabetes occurs because glucocorticoid hormones oppose the action of insulin and cause increase in blood sugar level either by decreasing the peripheral uptake of sugar or by increasing the process of gluconeogenesis in liver.

Question 184. Name the glucocorticoid hormones, which can cause steroid diabetes.
Answer. Prednisolone and dexametheasone.

Question 185. What is diabetes mellitus?
Answer. Diabetes mellitus is metabolic disorder characterized by increased levels of glucose in the blood (hyperglycemia) caused by an imbalance between insulin supply and insulin demand in the body.

Question 186. What is insulin?
Answer. Insulin is a natural hormone, which is secreted by the beta cells of the islets of Langerhan’s of pancreas.

Question 187. What is the function of insulin?
Answer. Insulin is a natural hormone which helps in transporting or carrying the glucose (sugar) from bloodstream to the cells (cells need glucose as it is the primary fuel for energy) and thus controls the level of glucose in blood.

Question 187a. Why glucose level increases in blood in diabetic patients?
Answer. In absence of insulin:

• Tissue utilization of glucose is reduced and
• There is more entry of glucose into the blood due to more glycogenolysis (breakdown of stored glycogen into glucose)
• Both mechanisms cause excess glucose levels in blood (hyperglycaemia).

Question. 188. What happens to the glucose once it reaches to the cells from the bloodstream?
Answer. The cells might use glucose for production of energy as it is the main fuel for the body or it is sent to the liver for preservation, in the form of glycogen.

Question 189. Name the other functions of insulin, besides controlling the blood sugar.
Answer.

• Stimulates lipogenesis
• Diminishes lipolysis
  Increases amino acid transport into cells
• Modulates transcription
• Altering the cell content of numerous mRNAs
• Stimulates growth
• DNA synthesis
• Cell replication.

Question 189a. Why floride is used during collection of blood samples for blood sugar estimation?
Answer. It inhibits the enzyme enolase.

Question 190. What are the different types of diabetes?
Answer. There are two main types of diabetes mellitus:

1. Insulin-dependent diabetes mellitus (IDDM)/type 1 diabetes/juvenile onset diabetes.
2. Non-insulin-dependent diabetes mellitus (NIDDM)/type 2 diabetes/adult onset diabetes.

Question 191. What is insulin-dependent diabetes mellitus (IDDM) or Type 1 diabetes?
Answer. This diabetes occurs if the beta cells produce little or no insulin.

Question 192. What is non-insulin-dependent diabetes mellitus (NIDDM) / Type 2 diabetes?
Answer. In this type of diabetes there is insulin production in the body but the body cells do not respond correctly to insulin and as a result hyperglycaemia occurs. This is also called insulin resistance.

Question 193. Name the most common symptoms of diabetes mellitus.
Answer. There are four cardinal signs of diabetes mellitus:

• Polyuria (frequent urination)
• Nocturia –disturbance in sleep at night due to repeated urination
• Polydypsia (increased thirst)
• Polyphagia (increased hunger)
• Presence of glucose in urine
• Dehydration of intra and extracellular flid
• Weight loss

Question 194. Name the other important features of diabetes mellitus.
Answer. Blurry vision, irritability, tingling or numbness in the hands or feet, frequent infections,poor wound healing, extreme unexplained fatigue, etc.

Question 194a. What is glycosuria?
Answer. Presence of glucose in urine is called glycosuria.

Question 194b. Glycosuria will occur if the blood glucose level goes above?
Answer. 180 mg/dL or more.

Question 194c. Why there is increased thrust or polydypsia in diabetes?
Answer. In diabetes, the viscosity of blood increases with the increase in the level of glucose; which causes increase in the osmotic pressure in blood. As a result of this intracellular and extracellular flids are dawned into the blood and then get excreted via urine,leading to dehydration. Tissue dehydration not only increases the urinary output but also causes polydypsia (excessive feeling of thrust).

Question 194d. What is atherosclerosis and why does it occur diabetic patients?
Answer. Atherosclerosis is a pathological condition, in which an artery wall thickens as a result of the accumulation of fatty materials, such as cholesterol and triglyceride. In diabetic patients, utilization of glucose is decreased due to lack of insulin; this causes increased breakdown of fat in liver, which often produces more cholesterol and ketone bodies in blood. Excess cholesterol gets deposited on the inner wall of blood vessels leading eventually to atherosclerosis.

Question 195. Describe the oral manifestations of diabetes mellitus.
Answer.

• Gingival hyperplasia with pain and gingival bleeding
• Severe rapidly destructive periodontitis
• Dry mouth due to polyuria and dehydration
• Delayed healing of oral wounds
• Unusually prolonged oral candidiasis
• Burning mouth syndrome
• Increased prevalence of “dry socket” after tooth extraction
• Loss of taste sensation or altered taste sensations (dysgeusia)
• Increased incidence of enamel hypoplasia
• Atypical dental pain.

Question 196. Describe the diabetic investigations.
Answer. Common diabetes blood tests are as follow:

• Fasting blood glucose level—diabetes is diagnosed if it is higher than 126 mg/dL two times
• Hemoglobin A1c test—
• Normal: Less than 5.7%
• Pre-diabetes: 5.7–6.4%
• Diabetes: 6.5% or higher
• Random blood sugar level: It is diabetes if sugar is higher than 200 mg/dL
• Oral glucose tolerance test: Diabetes is diagnosed if glucose level is higher than 200 mg/dL after 2 hours.
• Urinary glucose estimation: If the level is above 10–20 mg/dL, diabetes should be suspected.

Question 197. Name the periodic investigations, needed to monitor diabetes and prevent problems caused by it.
Answer.

Skin and bones on the feet and legs: Regular check-up of the skin and bones on the feet and legs; to check if the feet are getting numb

• Blood pressure: Blood pressure should be checked at least every year (blood pressure should be within130/80 mm/Hg)
• Hemoglobin A1c (HbA1c) test: Checking of hemoglobin A1c test (HbA1c) to be done every 6 months if the diabetes is well controlled; otherwise, every 3 months
• Cholesterol and triglyceride levels: Estimation of cholesterol and triglyceride levels to be done annually (desired LDL cholesterol levels should be below 70-100 mg/dL)
• Renal function test: Annual renal function test (microalbuminuria and serum creatinine) to make sure that the kidneys are working well
• Eye check up: Eye check up at least once a year, or more often if there are signs of diabetic eye problems.
• Dental check up: Dental check up every 6 months for a thorough dental cleaning and exam.

Question 197a. In diabetic patients HbA1c level in blood indicates what?
Answer. Long term status of blood sugar levels.

Question 197b. What is diabetic ketoacidosis ?
Answer. Diabetic ketoacidosis is a life-threatening problem in diabetes mellitus (mostly type 1) where the insulin level is very low or absent.

Question 197c. What is happens in our body in diabetic ketoacidosis?
Answer. Normally our body produces energy by metabolism of glucose (the main fuel) with the help of insulin. In severe insulin defiiency when the body cannot use sugar (glucose) as a fuel to make energy, it tries to breakdown body fat to produce energy, which results in formation of ‘ketones’ (byproduct of fat breakdown) in the blood. More production of ketones in the blood makes it acidic and toxic; and the condition is called diabetic ketoacidosis.

Question 198. Why diabetic ketoacidosis is a matter of serious concern?
Answer. It often leads to coma and death if not treated promptly.

Question 199. What are the features of diabetic ketoacidosis?
Answer.

• Deep, rapid breathing
• Dry skin and mouth with flshed face
• Fruity breath odor
• Nausea or vomiting, inability to keep down flids Stomach pain.

Question 200. What is gestational diabetes?
Answer. Gestational diabetes is the high blood sugar level that starts or is fist diagnosed during pregnancy.

Question 201. Why gestational diabetes occurs?
Answer. It occurs because the action of insulin is often blocked by some pregnancy hormones and as a result glucose levels may increase in a pregnant woman’s blood. This is also called contrainsulin effect.

Question 202. Name the pregnancy hormones, which might produce gestational diabetes by inhibiting the action of insulin.
Answer. Estrogen, cortisol, and human placental lactogen.

Question 203. During which stage of pregnancy gestational diabetes develops?
Answer. It usually begins about 20 to 24 weeks into the pregnancy.

Question 204. What is the fate of ‘gestational diabetes’?
Answer. All symptoms of diabetes completely subside after the delivery.

Question 205. What is steroid diabetes?
Answer.Steroid diabetes or “steroid-induced diabetes” refers to the prolonged hyperglycemia due to glucocorticoid therapy given for some other medical condition the patient is suffering from.

Question 206. Name the general complications of diabetes.
Answer.

• Diabetic ketoacidosis
• Diabetic neuropathy
• Diabetic nephropathy
• Diabetic retinopathy
• Ischemic heart disease
• Hypoglycaemic coma and death

Question 207. What is hypoglycemia?
Answer. When the blood sugar level falls below 70 mg/dL the condition can be called hypoglycaemia. It may develop quickly in people with diabetes who are receiving insulin.

Question 208. Describe the features of hypoglycemia.
Answer.

• Headache, hunger and nervousness
• Rapid heartbeat (palpitations), shaking and sweating
• Severe weakness.

Question 209. What is progeria?
Answer. Progeria is a disease of unknown etiology and it is characterized by dwarfim and premature senility.

Question 210. What are the clinical features of progeria?
Answer. The affected infants exhibit alopecia, skin pigmentation, atrophic skin, high-pitched voice, smaller mandible, muscular atrophy and joint deformity, etc. The patients usually have an above normal IQuestion and they resemble a “wizened little old person”.

Question 211. What are the oral manifestations of progeria?
Answer.

• Delayed eruption of teeth
• Excessive secondary dentin formation in teeth.

Question 212. Describe the oral manifestations occurring due to alteration in the sex hormone levels in the body.
Answer.

Puberty: Hyperplastic gingivitis and gingival bleeding

Pregnancy: Gingivitis, gingival bleeding and pregnancy tumor

Menstruation: Transitory gingivitis and cyclical oral ulcerations

Menopause: Desquamative gingivitis, dry mouth and glossodynia.