Endocrine And Metabolic Diseases Long Essays

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Question 1. Describe the etiology, clinical features, and management of tetanus.

Answer:

Tetanus:

  • It is a disorder of neuromuscular excitability

Etiology:

  • It is caused by exotoxin, tetanospasmin liberated by clostridium tetani

Etiology Clinical Features:

  • Trismus
  • Dysphagia
  • Risussardonicus- in it eyebrows and corners of the mouth are drawn up due to spasms of the muscles of the face and jaw
  • Opisthotonus- rigidity of the muscles of the neck and trunk
  • Elevation of temperature
  • Rapid pulse
  • Cyanosis

Etiology Types:

  1. Acute tetanus
    • The incubation period is less than 10 days
  2. Chronic tetanus
    • The incubation period is about a month
  3. Delayed tetanus or latent tetanus
    • In it organism remains latent for many years
  4. Local tetanus
    • There is the presence of local contraction of muscles
  5. Cephalic tetanus
    • There is irritation or paralysis of the cranial nerves
  6. Bulbar tetanus
    • There is an extensive spasm of the muscles of deglutition and respiration
  7. Late tetanus
    • The inoculation period is prolonged
  8. Tetanus neonatorum
    • Recurrent tetanus

Etiology Management:

  1. Passive immunization
    • 1 Lac units of Anti-tetanus serum is given half intravenously and half intramuscularly
  2. Antibiotics
    • Penicillin injection of 10 lac units every 4 hours
    • Metronidazole
    • Tetracycline
  3. Wound care
    • Thorough cleansing and debridement
    • Removal of all necrotic tissues and foreign bodies
    • All stitches are removed
    • Blood clots, foreign bodies, and pus are cleared
    • The wound should be left open
  4. The patient is isolated to a quiet, dark, and well-ventilated room
  5. Further treatment depends on the severity of the cases
    • In mild cases
      • Prozac in -200 mg IM
      • Barbiturate, amylobarbitone, or injection diazepam-5-40 mg 4 times in a day
    • In moderate cases
      • Passage of nasogastric tube for feeding
      • Passage of self-retaining catheter to drain the bladder
      • Administration of intravenous fluid
      • Maintenance of intake and output chart
      • Tracheostomy
    • In very severe cases
      • Use of muscle relaxant, 40 mg turbo- marine initially 4 and then IM injections
      • Tracheostomy
      • Sedation with pentothal sodium
      • Nasogastric feeding
      • Elimination of visceral stimuli
      • Intravenous administration of fluid and electrolytes
      • Constant nursing

Question 2. Describe the etiology and clinical features of acromegaly with special experience in dental problems.

Answer:

Acromegaly:

  • Acromegaly occurs due to excess secretion of GH later in life after epiphyseal closure

Etiology:

  • Pituitary adenoma
  • Pancreatic islet cell tumors
  • Hypothalamic tumors
  • Bronchial carcinoid
  • Small cell carcinoma of Hung

Acromegaly Clinical Features:

  • Thick bones-larger hands and feet
  • Enlarged skull
  • Increased intracranial pressure
  • Headache
  • Photophobia
  • Visual disturbances
  • Hepatomegaly

Read And Learn More: General Medicine Question and Answers

  • Cardiomegaly
  • Osteoporosis
  • Arthralgia
  • Excessive sweating
  • Myalgia
  • Bowing of legs
  • Barrel shaped chest

Acromegaly Oral Manifestations:

  • Enlarged mandible
  • Class 3 malocclusion
  • Macroglossia
  • Thick lips
  • Proclination of teeth
  • Hypercementosis
  • Large nose, ears, and prominent eyebrows
  • Periodontitis
  • Enlargement of maxillary air sinuses

Endocrine And Metabolic Diseases Diagnosis

Question 3. Enumerate the proliferating factors, pathogenesis, investigations, and management of diabetic ketoacidosis.

Answer:

Diabetic Ketoacidosis:

  • It is a complication of diabetes mellitus

Diabetic Ketoacidosis Proliferating Factors:

  • Undetected or undiagnosed type 1 diabetes
  • Stress
  • Infection

Diabetic Ketoacidosis Pathogenesis:

Endocrine And Metabolic Diseases Diabetic Ketoacidosis Pathogenesis

Diabetic Ketoacidosis Investigations:

  • Diabetic ketoacidosis is confirmed by
    1. Hyperglycaemia
    2. Ketonaemia
    3. 1 leavy ketonuria
    4. Acidosis

Diabetic Ketoacidosis Management:

  1. Correction of hyperglycemia
    • Administration of regular insulin 0.1 U/k bolus followed by 0.1 U/kg/ hour by ccontnousIV infusion till the patient recovers
  2. Correction of dehydration
    • Normal saline infusion of 1 liter in the first hour
    • Then 1 litre over the next 4 hours
    • Then quantity is titrated
  3. Correction of acidosis
    • Use of sodium bicarbonate
  4. Potassium
    • 10-20 mEq/hour potassium chloride is added to the drip for rapid correction of hyperglycemia

Question 4. Classify diabetes mellitus. Discuss the complications and management of diabetes mellitus

Answer:

Diabetes mellitus

  • Diabetes mellitus is defined as a heterogeneous metabolic disorder characterized by the common feature of chronic hyperglycemia with disturbance of carbohydrate, fat, and protein metabolism

Diabetes Mellitus Classification:

  1. Primary diabetes
    • Type 1- IInsulin-dependentdiabete mellitus
      • IImmunemediated
      • Nonimmune mediated
    • Type 2- NNoninsulin-dependentdiabetes mellitus
      • Obese
      • Non-obese
  2. Secondary diabetes
    • Pancreatic diabetes
    • Hormonal or endocrinal abnormalities
    • DDrug-inducedInsulin receptors antibodies
    • Genetic syndromes

Diabetes Mellitus Complications:

  1. Acute metabolic complications
    • Diabetic ketoacidosis
      • Develop in patients with severe insulin deficiency
      • Clinical Features:
        • Nausea, vomiting, anorexia
        • Deep and fast breathing
        • Mental confusion
        • Coma
    • Hyperosmolar hyperglycaemia nonketotic coma
      • It is a complication of type 2 diabetes mellitus
      • Caused by severe dehydration which leads to sustained hyperglycemia diuresis
      • Clinical Features:
        • High blood sugar
        • High plasma osmolality
        • Thrombotic and bleeding complications
    • Hypoglycaemia
      • Develop in type 1 diabetes mellitus
      • Clinical Features:
        • Permanent brain damage
        • Worsening of diabetic control
        • Rebound hyperglycaemia
  2. Late systemic complications
    • Atherosclerosis
      • Common in both type 1 and type 2 diabetes mellitus
      • Atherosclerosis may lead to
        • Myocardial infarction
        • Cerebral stroke
        • Gangrene of toes and feet
    • Diabetic microangiopathy
      • It is the abasementmembrane thickening of small blood vessels and capillaries of different organs and tissues
      • Occurs due to increased glycosylation of hemoglobin and other proteins
    • Diabetic nephropathy
      • It is a severe complication of diabetes mellitus
      • Occurs in both types
      • Features:
        • Asymptomatic proteinuria
        • Nephrotic syndrome
        • Progressive
        • Renal failure
        • Hypertension
    • Diabetic neuropathy
      • Effects all parts of the nervous system
    • Diabetic retinopathy
      • It is the cause of blindness
      • Other retinal complications include
        • Glaucoma
        • Cataract
        • Corneal disease
    • Infections
      • Diabetic patients are more susceptible to infections like tuberculosis, pyelonephritis, otitis, carbuncles and diabetic ulcers

Diabetes Mellitus Management:

  1. Diet management
    • The daily energy requirement for an individual is calculated according to age, weight, height, and activity
    • Calorie requirement:
      • For men- 36 kcal/kg
      • For women-34 kcal/kg
  2. Lifestyle modification
    • Physical exercise
    • Reduction of weight
    • Avoid alcohol and smoking
    • Behavioural exercises
  3. Oral hypoglycaemic drugs
    • Sulphonylureas
    • Meglitinides
    • Biguanides
    • Thiazolidinedione derivatives
    • Alpha-glucosidase inhibitors
  4. Insulin

Question 5. Discuss the complication of systemic ccorticosteroidtherapy with special reference to dental practice

Answer:

Complications of Systemic Corticosteroids:

  1. Metabolic effects
    • Mood changes from euphoria to depression
    • Fluid retention and edema
    • Hypertension
    • Glucose intolerance
    • Osteoporosis
    • Increased susceptibility to infection
    • Reactivation of latent tuberculosis
    • Impaired wound healing
    • Gastric erosions
    • Masked perforation
    • HHemorrhagefrom stomach and duodenum
  2. Suppression of hypothalamic-pituitary-adrenal axis
    • It occurs with high-dose therapy
    • This makes it difficult to withdraw steroids

Measures to Reduce Side Effects:

  • Use of the lowest possible dose
  • Administer on alternate days rather than daily
  • Use of morning dose rather than any other time
  • Use of steroids for established cases
  • Monitor caloric intake to prevent weight gain and reduce sodium intake
  • Use of H2 receptor blockers or proton pump inhibitors
  • Provide high calcium intake and vitamin D

Question 6. Outline the conditions wthatproduce pigmentation of oral mucosa. Discuss the clinical features of Addison’s disease.

Answer:

Causes of Oral Pigmentation:

  • Autoimmune adrenalitis
  • Tubcrculousadrenalitis
  • Bilateral adrenalectomy
  • Drugs-ketoconazole
  • Metastases in the adrenal
  • Haemochromatosis
  • Amyloidosis
  • Histoplasmosis

Addison’s Disease:

  • It is due to progressive destruction of the three zones of the adrenal cortex and medulla with lymphatic infiltration

Oral Pigmentation Clinical Features:

  1. Glucocorticoid insufficiency
    • Weight loss
    • Nausea and vomiting
    • Malaise
    • Weakness
    • Anorexia
    • Diarrhea
    • Constipation
    • Postural hypotension
    • Hypoglycaemia
  2. Mineralocorticoid deficiency
    • Hypotension
  3. Loss of aandrogensReduction of pubic and axillary hair in females
  4. Increased ACTH secretion
    • Pigmentation of exposed areas, pressure areas, mucous membranes, conjunctivae, and recently acquired scars

Question 7. Define hypo- and hyperthyroidism. Discuss clinical features, investigations, and treatment of hypothyroidism.

Answer:

Hyperthyroidism Definition:

  1. Hypothyroidism
    • It is a clinical condition caused by low levels of circulating thyroid hormones
  2. Hyperthyroidism
    • It is a clinical syndrome that results from exposure of the body tissues to excess circulating free thyroid hormones

Hypothyroidism Clinical Features:

  1. In new bom
    • Cretinism
    • Mental retardation
    • Poor growth
    • Difficult to nurse a baby
    • Dwarfism
  2. During childhood or adolescence
    • Juvenile hypothyroidism
    • Child appears young
    • Mental deficiency
    • Abdominal distension
    • Umbilical hernia
    • Prolapse of rectum
  3. In adults
    • Fatigue
    • Weight gain
    • Skin becomes thickened and puffy
    • Muscle cramps
    • Paraesthesia
    • Impaired speech
    • Reduced cardiac output
    • Elevation of blood pressure
    • Shortness of breath
    • Abdominal distension
    • Aches and pains
    • Anaemia
    • Alopecia
    • Menorrhagia, infertility
    • Constipation

Hypothyroidism Investigations:

  • Serum T3 and T4 levels- low
  • Serum TSH- high
  • Thyroid peroxidase antibodies- present
  • Serum cholesterol triglyceride- high
  • ECG- shows bradycardia, low amplitude of QRS, and ST-T changes
  • Blood- macrocytic anemia
  • X-ray chest- shows cardiomegaly
  • Photomtogram- delayed ankle jerk

Hypothyroidism Treatment:

  • Replacement of thyroid hormones by L-thyroxine
  • Initial starting dose-50-100 micrograms daily as a single dose empty stomach in the morning for the first 3-4 weeks
  • The dose is increased to 150 micrograms daily
  • The maximum dose is 300 micrograms in a day
  • In older persons or persons with ischaemic heart disease, a low dose of L-thyroxine 25 microgram/day is started and gradually increased

Question 8. Discuss the etiology, clinical features, and management of thyrotoxicosis. Mention a note on thyroid function tests

Answer:

Thyrotoxicosis is a syndrome resulting from an increased level of free thyroxin

Thyrotoxicosis Clinical Features

  • Hyperactivity
  • Irritability
  • Heat intolerance
  • Palpitations
  • Fatigue
  • Weakness
  • Weight loss
  • Increased appetite
  • Tachycardia
  • Systolic hypertension
  • Presence of tremors
  • Cardiac arrhythmias
  • Excessive sweating
  • Exophthalmos

Thyrotoxicosis Management:

  1. General management
    • Rest
    • Nutritious diet
  2. Drug therapy
    • Carbimazole
    • Initial dose of 30 nag/ day, maintenance dose of 10-20 mg/day is given
    • Potassium perchlorate – 800 nag/day in divided doses
    • Sodium or potassium iodide 6-10 nag/day
  3. Surgical treatment
    • Subtotal thyroidectomy
  4. Radioiodine treatment
    • Iodine is given in ddosesof 8-10 millicuries

Thyroid Function Tests:

  1. Measurement of radioactive iodine uptake
    • The normal value is 30%
    • Higher values indicate thyrotoxicosis
    • It is no longer used because of
      • Lack of sensitivity
      • Lack of specificity
      • Time-consuming
      • Complicated procedures
  2. Measurement of total T3 and T4 in blood by radioimmunoassay
    • Widely used
    • Normal Values:
      • Serum T3 total- 70-200 ng/1
      • Serum T4 total- 5.5-13.5 microgram/1
    • Drawbacks:
      • Measure the total amount of hormone
      • Gets changed with the fluctuations in their binding protein
  3. Measurement of free T3 and T4 in blood
    • NORMAL VALUES
    • Serum free T3-1-2.6 nmol/1
    • Serum free T4-10-27 nmol/1
  4. Estimation of TSH
    • Normal value- 0.15-3.5 mIU/1
    • High levels of ooccurin primary hypothyroidism
    • Low levels ooccurin hyperthyroidism and hypopituitarism
  5. Ultrasound of thyroid
    • Measure the size and mass of the thyroid
    • Detects shape and nodularity of thyroid
  6. Thyroid scan
    • It is used to detect functioning and nonfunctioning nodules in the thyroid
    • I131 or 99mTc is used for
  7. Antithyroid antibodies
    • Detects autoimmune thyroid disorders
    • Stimulating antibodies and TSH receptor-blocking antibodies are raised in Grave’s disease
  8. Needle biopsy of thyroid
    • Detects malignancy

Question 9. Discuss ethe tiology, clinical features, and management of myxoedema

Answer:

Myxoedema:

  • Myxoedema indicates severe hypothyroidism

Etiology:

  1. Primary causes
    • Spontaneous atrophic hypothyroidism
    • Iodine deficiency
    • Following 1131 therapy
    • Post thyroidectomy
    • Hashimoto’s thyroiditis
    • Radiation
  2. Secondary causes
    • Destruction of the pituitary gland
    • Post-surgery
    • Post radiation
    • Tumour
    • Disorders of hypothalamus

Myxoedema Clinical Features:

  1. General symptoms
    • Age and sex- Middle-aged males are frequently affected
    • Weakness
    • Fatigue
    • Lethargy
    • Low blood pressure
    • Mental retardation
    • Dry coarse skin
    • Swelling of the face and extremities
    • Cold intolerance
    • Husky voice
    • Decreased sweating
    • Anorexia
    • Loss of memory
    • Hearing impairment
    • Arthralgia
    • Muscle cramps
    • Paraesthesia
  2. Oral manifestations
    • Peri-orbital puffiness
    • Loss of facial hair
    • Swollen tongue, lips, and eyelids
    • Difficulty in speech
    • Underdevelopment of maxilla and mandible

Myxoedema Management:

  • Replacement of thyroid hormones by L-thyroxine
  • Initial starting dose-50-100 micrograms daily as a single dose empty stomach in the morning for the first 3-4 weeks
  • The dose is increased to 150 micrograms daily the maximum dose is 300 micrograms every day
  • In older persons or persons with ischaemic heart disease, a low dose of L-thyroxine 25 microgram/day is started and gradually increased

Question 10. Describe etiology, clinical features, diagnosis, and treatment of hyperthyroidism.

Answer:

Hyperthyroidism:

  • It is a clinical syndrome that results from exposure of the body tissues to excess of circulating free thyroid hormones

Etiology:

  1. Common
    • Grave’s disease
    • Toxic nodular goitre
      • Multinodular
      • Solitary nodule
  2. Less common
    • Thyroiditis
    • Drug-induced
    • Self-induced
    • Iodine excess
  3. Rare causes
    • Pituitary or ectopic TSH
    • Thyroid carcinoma

Hyperthyroidism Clinical Features:

  1. Goitre
  2. Gastrointestinal symptoms
    • Weight loss
    • Diarrhea
    • Vomiting
  3. Cardiovascular symptoms
    • Sinus tachycardia
    • Exertional dyspnoea
    • Arrhythmias
    • Precipitation of angina
  4. Neuromuscular symptoms
    • Nervousness, irritability
    • Restlessness
    • Tremors of hands
    • Muscular weakness
    • Exaggerated tendon reflexes
  5. Dermatological symptoms
    • Increased sweating
    • Clubbing of fingers
    • Loss of hairs
    • Redness of palms
  6. Reproductive symptoms
    • Menstrual irregularity
    • Abortions
    • Infertility
    • Loss of libido
  7. Ophthalmological
    • Lid retraction
    • Wide palpebral fissures
    • Exophthalmos
    • Diplopia
    • Excessive watering of eyes
  8. Miscellaneous
    • Heat intolerance
    • Excessive thirst
    • Fatigue
  9. Oral manifestations
    • Early exfoliation of deciduous teeth
    • Premature eruption of permanent teeth
    • Alveolar bone atrophy
    • Increased susceptibility to oral infections

Hyperthyroidism Diagnosis:

  • T3 and T4 levels- elevated
  • TSH levels- low
  • 131I uptake is increased
  • Serum cholesterol level- low
  • ECG changes- shows tachycardia, arrhythmias, ST- T changes
  • USG- shows diffuse goitre
  • Increased BMR
  • Decreased urinary excretion of iodine

Hyperthyroidism Treatment:

  1. Drug therapy
    • Anti-thyroid drugs
      • Carbimazole
      • Propylthiouracil -100-150 mg
    • Beta-blockers
      • Propanolol-80-160 mg daily
      • Metoprolol-50 mg/ day
  2. Radioactive ablation of thyroid
  3. Subtotal thyroidectomy
  4. Treatment of relapse
    • Long-term drug therapy is used
    • Radioactive iodine therapy
  5. Management of ophthalmopathy
    • Use of 60 mg of prednisolone daily
  6. Management of dermopathy
    • Local betamethasone ointment or triamcinolone injection may be used

Question 11. What are the causes of hypocalcemia? Describe clinical features and outline the treatment of tetany

Answer:

Hypocalcaemia:

  • It is a condition of low levels of calcium

Causes Of Hypocalcaemia:

  • Sepsis
  • Burns
  • Acute pancreatitis
  • Acute renal failure
  • Alkalosis
  • Drugs like diuretics, protamine, heparin, and glucagon
  • Toxic shock syndrome
  • Hypomagnesaemia
  • Plasmapheresis
  • Extensive transfusion
  • Malignancy

Tetany:

  • It is a clinical condition characterized by low levels of ionized calcium leading to increased neuromuscular excitability

Tetany Clinical Features:

  1. In children
    • Characteristic triad- carpopedal spasm, stridor and convulsion
    • Carpopedal spasm- flexion at metacarpophalangeal joints and extension at interphase- large joints wwithotherposition of the thumb
    • Stridor- closure of the glottis
  2. In adults
    • Tingling sensation in peripheral parts of limbs or around the mouth
    • Painful carpopedal spasm
    • Rarely stridor and convulsions
  3. Signs
    • Trousseau’s sign
      • Raising the blood pressure above systolic level by inflation of the sphygmomanometer cuff produces carpal spasm within 3-5 minutes
    • Chvostek’s sign
      • A tap at the facial nerve at an angle of the aw produces twitching of facial muscles

Tetany Treatment:

  1. Treatment of hypocalcemia
    • Injection of 20 ml of 10% calcium gluconate
  2. Treatment of alkalosis
    • Intravenous administration of isotonic saline
    • Withdrawal of alkalies
    • Inhalation of 5% CO2in oxygen- to treat hyperventilation
    • Psychotherapy

 

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