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38 Cards in this Set
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Describe the clinical features of disorders due to Growth hormone excess
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GH stimulates skeletal and soft-tissue growth. It produces gigantism in children (if acquired before Epiphyseal fusion) and acromegaly in adults.
-.Agromegaly - appears in adults. Bones grow broader and heavier, resulting in enlargement of hands, feet and face. Facial features enlarge and protruding mandible with large tounge is common. Gigantism - excess GH prior to puberty resulting in lateral bone growth and tall stature. Signs – diabetes, hypertension, may be present. - It can also lead to heart failure, oedema, hypertension, Arthropathy, proximal myopathy, glycosuria |
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Describe the function of two hormones produced by hypothalamus and stored in posterior pituitary. Also describe how to investigate possible suspected ADH hyposecretion
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Oxytoxcin - important for females, stimulates uterine myometrial contraction and milk ejection. Possible 'love' hormone!
ADH - aka vasopressin, controls thirst and water regulation. ADH stimulates receptors in the kidney allowing the collecting tubule to become more permeable to water thus reasorption occurs reducing diuresis and increasing water retention. Reg. blood vol and pressure. ADH release increased by increased osmolarity, hypovolemia, hypotension, nausea, AGTII, Cortisol, antidepressants. ADH decreased by decreased osmolarity, HTN, ethanol. Deficiency or insensivity leads to polyuria, nocturia and polydipsia - leading to dehydration & severe thirst. Diabetes Insipidus. investigation include water depreviation test - fasting and no fluids overnight, monitor urine and serum osmolarity, urine volume and wt for up to 8 hours. Electrolyte levels can be useful guides. – Levels of calcium and potassium |
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List any five (5) presentations of hypothalamic and pituitary diseases and discuss the investigations and management of hypothalamic and pituitary diseases in detail
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1. Pituitary lesions and tumours
2. Posterior pit dysfunction - diabetes insipidus 3. Ant pit overactivity - hyperprolactinaemia, acromegaly 4. Ant pit underactivity - hypopituitarism e.g. Kallmans, Sheehans, Empty stella Investigations for: Presence of a tumour - xray, US, MRI, biopsy Hormone levels - serum blood tests using radioimmunoassay, measuring effectiveness of the hormone to reflect the activity. 24 hr urine tests. Hypo or hyperfunction - stimulation or supression tests. Management - depends on the cause: Hormone defiency - replacement therapy e.g. insulin in DM Hormone excess - supression drugs, radioiodine & surgery (hyperthyroidism) Adenomas - removed surgically and/or radiation therapy, replacement therapy may then be required if gland function affected. |
Hypothyroidism, hyperthyroidism, acromegaly, gigantism, dwarfism, diabetes insipidus, hyperprolactinaemia, hypogonadism, Cushing’s syndrome, etc. Students may write down signs and symptoms of any of these conditions.
Investigations: - Investigations of any space occupying lesions and tumours - Detailed history of cause, origin, onset and progress of any condition - Lateral skull X-ray to show enlargement of the fossa, - Visual field - MRI of the pituitary - Is there a hormonal excess? - Is there a deficiency of any hormone? Management and treatment: - Removal and control of tumour - Reduction of excess hormone secretion - Replacement of hormone deficiencies, - Rule out differential diagnosis |
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Name and give a short description of the aetiological mechanisms common to most of the endocrine disorders
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AI Dx - organ specific dx can affect every major endocrine organ, characterised by the presence of specific AB in the serum. Conditions more common in women with strong genetic link.
Endocrine tumours - hormone secreting tumours most commonly seen in pituitary, thyroid and parathyroid. Most commonly benign. Enzymatic defects - def or abnormal enzymes can lead to reduced production of secreted hormone - mild symptoms due to partial and can be evidient only under stress, more severe if onset noted early in life. Receptor abnormalities - hormones work by activating cellular receptors, secretion and control are normal but receptors defective. Drugs - can induce endocrine Dx e.g. steroids - cushings syn/diabetes, insulin -hypoglycemia, Iodine - hyperthyroidism. |
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Name three particular syndromes related to hypopituitarism. Discuss the aetiology, clinical features, investigations, treatment and management of anterior pituitary hypo functioning
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Kallmans syn - gonadotrophin (GnRH) defiency, often familial gene mutation. CF -decreased or absence of smell, colour blindness, cleft palate.
Sheehans syn - pituitary infarction following postpartum haemorrhage. Rare. Empty stella syn - pituitary stella turnica is devoid of tissue. CF -depend on extent of defiencies, presenting the same as the symptoms of primary def of the endocrine gland. |
Aetiology:
- Due to pituitary/ hypothalamic dysfunction/hypo function eg. Tumour, surgery, head trauma. - Congenital - Infective - Vascular - Immunological - Neoplastic - Traumatic - Infiltrations - Functional and others Clinical features - Signs and symptoms depend upon the axis involved and would be similar to the hypo functioning of the other endocrine glands - Hypothyroidism – slowness of thoughts, action, dry skin and cold intolerance - Hypoadrenalism – hypotension, hyponatraemia, cardiovascular collapse during stressful illness - Hypogonadism – loss of libido, loss of secondary sexual hair, amenorrhoea and impotence are symptoms of gonadotrophin and thus gonadal deficiencies - Hyperprolactinaemia - GH deficiency – dwarfism in children - Weight increase/decrease - Pan hypopituitarism – classic picture of pallor with hairlessness. Investigation - Each axis requires separate investigation - Use of hormone levels/measurement - CT/MRI possible use of biopsies Treatment - Replacement therapy for steroid / thyroid hormones. - Surgery for non-secreting macroadenoma - Lifelong replacement therapy of hormones. |
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Classify and give examples of causes of primary hypothyroidism
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Congenital – agenesis/ ectopic thyroid remnants
Defects of hormone synthesis – iodine deficiency, dyshormonogenesis, anti-thyroid drugs Autoimmune – atrophic thyroiditis, Hashimoto’s thyroiditis, postpartum thyroiditis Infective – post subacute thyroiditis |
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Hashimoto’s thyroiditis - define and describe cause
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Hashimoto’s thyroiditis: This form of autoimmune thyroiditis is more common in women in late middle age. It produces atrophic changes with regeneration, leading to goitre formation. The gland is usually firm and rubbery but may range from soft to hard. TPO antibodies are present, often in very high titres (>1000IU/L) patient may be hypothyroid or euthyroid, though may go through initial toxic phase.
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Spontaneous atrophic hypothyroidism
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Spontaneous atrophic hypothyroidism: most common cause of hypothyroidism and is associated with anti-thyroid antibodies leading to lymphoid infiltration of the gland and eventual atrophy and fibrosis. It is associated with other autoimmune diseases such as pernicious anaemia, vitiligo, and other endocrine deficiencies. In some cases, intermittent hypothyroidism occurs with recovery, antibodies which block the TSH receptor may sometimes be involved in the aetiology
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Subacute thyroiditis - define and describe
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Subacute thyroiditis: This is transient hyperthyroidism from an acute inflammatory process, probably viral in origin. Apart from the toxicosis, there is usually fever, malaise and pain in the neck with tachycardia and local thyroid tenderness. Hypothyroidism usually transient may follow after a few weeks.
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Postpartum thyroiditis - define and describe
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Postpartum thyroiditis: usually a transient phenomenon observed following pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. It is believed to result from the modifications to the immune system necessary in pregnancy. Histologically it is lymphocytic thyroiditis.
Investigations for all the thyroid disorders includes the thyroid function tests. Estimating the levels of T3, T4 and TSH. Sometimes, testing for presence of specific antibodies (anti-thyroid antibodies) and a complete blood count may be used. Levels of TRH give us the idea about hypothalamic functions. |
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Give the clinical features of any two varieties of disorders due to increased activity of the thyroid gland
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- Graves disease
- Toxic multi-nodular goitre - Post-partum thyroiditis - Subacute thyroiditis - Low iodine uptake hyperthyroidism - De Quevain’s thyroiditis - Factitious hyperthyroidism |
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Thyroid gland produces two classes of the hormones - 3 hormones, 2 actions - what are they and how do they work?
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Thyroid gland produces Thyroxine (T4), Tri-iodotyrosine (T3) and Calcitonin. T3 and T4 control the metabolic rate of many tissues while Calcitonin regulates the calcium metabolism.
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What is goitre? Give the classification of Goitre.
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Enlargement of thyroid is called goitre. It is more common in women than in men.
Classification: Diffuse goitre - Simple goitre - Autoimmune thyroid disease - Thyroiditis - Iodine deficiency (endemic goitre) Nodular goitre - Multinodular goitre - Solitary nodular goitre - Fibrotic goitre - Cysts |
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Hyperthyroidism - CF
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Hyper activity of the thyroid gland can cause increased metabolic rate. This would lead to increased heart rate, hypertension, restlessness and rapid weight loss. The patient may as well present with tachycardia, tremors, palpitations, hyperkinesis, excessive sweating, warm peripheries, and cardiac failure.
Overactivity of thyroid causes exopthalmos, lid lag and stare –look of the eyes. Female patient would present with oligomenorrhoea and premenstrual syndromes with irritability and restlessness, malaise, stiffness of joints and muscle weakness. |
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Hypothyroidism - CF
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Hypothyroidism may produce many symptoms including the accumulation of muco-polysaccharide in the subcutaneous tissues.
Due to lack of the activity of thyroid hormone, the patient would present with unexplained weight gain, cold intolerance, bradycardia and constipation. The hair would become dry, brittle and the skin becomes thick. It may also affect the menstrual cycles in females, leading to irregular menses and long periods of amenorrhoea. The lack in activity and metabolic rate would lead to mental slowness and slow –relaxing reflexes. Obesity would have its own complications as a result of hypothyroidism. Its effects on cardiac tissue may cause cardiac enlargement and pericardial effusion in some patients. |
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Abnormalities of Adrenal Glands - Addisons
CF? |
Addison’s disease - hypo Symptoms Weight loss, anorexia, malaise, weakness, fever, depression, impotence, amenorrhoea, diarrhoea, nausea/vomiting, confusion, syncope from postural hypotension, abdominal pain, constipation, myalgia, joint or back pain.
Signs - Pigmentation, esp. of new scars and palmar creases, buccal pigmentation, postural hypotension, loss of weight, general wasting, dehydration, loss of body hair, vitiligo. |
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Abnormalities of Adrenal Glands - Cushings
CF? |
Cushing’s syndrome - hyper
Weight gain (central), change of appearance, depression, insomnia, amenorrhea, oligomenorrhoea, poor libido, thin skin, easy bruising, hair growth, acne, muscular weakness, growth arrest in children, back pain, polyuria/polydipsia, psychosis Signs - Moon face, plethora, hirsutism, acne, frontal balding (female), thin skin bruising, hypertension, pathological fractures, striae (red/purple) |
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Cause of Addisons?
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Autoimmune disease, tuberculosis, surgical removal of the gland, haemorrhage/infarction, infiltration – malignant destruction, Amyloid, Adrenal leucodystrophy
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Cause of Cushings?
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ACTH-dependent disease Ectopic ACTH producing tumours, ACTH administration. Alcohol induced pseudo – Cushing’s syndrome Non –ACTH dependent disease Adrenal adenoma, adrenal carcinoma, glucocorticoid administration
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Define and compare Type I and Type II diabetes
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I - insulin dependant, younger age onset.
Autoimmune disease. Islet cell autoantibodies, Insulitis Diseases that show B cell destruction Insulin deficiency. May develop ketoacidosis. Always need insulin II - non-insulin dependant, usually >30yo. No-immune disturbance. Insulin Resistance Partial insulin deficiency. May develop hyperosmolar state. Many need insulin in later stages. |
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Type 1 DM definition
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Type I: results from insulin deficiency. It is prominent diabetes of childhood, reaching a peak incidence around the time of puberty. A slow-burning variant with slower progression to insulin deficiency. Causes considerable weight loss, hyperglycaemia which fails to correct with diet and tablet treatment, presence of strong ketonuria and presence of auto-antibodies.
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Type II DM definition
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Type II: relatively common diabetes in all populations enjoying an affluent lifestyle. The four major determinants are increasing age, obesity, ethnicity and family history. This is the non-insulin dependent diabetes. More relevant to life-style rather than genetic
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Clinical presentation of DM?
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Clinical presentation
- Acute presentation: polyuria, thirst, weight loss - Ketonuria in young people and may progress to Ketoacidosis. - Subacute presentation: could be over several months or years, particularly in older patients. - Lack of energy, visual blurring, or Pruritus vulvae - Balanitis due to candidia infection - Complications as the presenting feature: staphylococcal infection, retinopathy, polyneuropathy, erectile dysfunction, arterial disease, resulting in myocardial infarction or peripheral gangrene. - Sometimes, the only presentation may be Glycosuria or raised blood sugar. |
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Psychological implications of diabetes -
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- Most patients experience periods of not coping, helplessness, denial and acceptance often fluctuating over time.
- It is impossible to take a holiday from diabetes - Concessions or sympathy are often denied - The treatment is complex and demanding - Embarrassing loss of control over personal behaviour or consciousness can occur in insulin-treated patients - Risk-taking behaviour - Poor self-image - Eating disorders - Insulin omission |
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Diabetes insipidus - affected gland?
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posterior pituitary
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Acromegaly affected gland?
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anterior pituitary - hyper
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Hashimoto’s thyroiditis – affected gland?
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thyroid - hypo
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Myxoedema coma affected gland?
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thyroid - hypo
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Cushing’s syndrome – affected gland?
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adrenal - hypo or
Addison’s disease – affected gland? adrenal - hyper |
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SIADH –affected gland?
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hypothalamus / post. Pituitary - hypo
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Gynaecomastia affected gland?
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anterior pituitary - hyper
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Kallmann’s syndrome – affected gland?
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anterior pituitary - hypo
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Grave’s disease – affected gland?
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thyroid - hyper
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Name the endocrine glands and the hormones produced by them, which regulate the normal body calcium metabolism.
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The thyroid gland produces Calcitonin and the parathyroid gland produces para-thyroid hormone. Both these hormones regulate the calcium metabolism by their effects on the bone cells (osteoclasts and osteoblasts).
Hypercalcaemia is the presence of excessive calcium in the blood |
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The major causes of hypercalcaemia are:
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1. Excessive parathormone secretion
a. Primary hyperparathyroidism b. Secondary hyperparathyroidism c. Tertiary hyperparathyroidism 2. Malignant diseases 3. Excess action of vitamin D 4. Excessive calcium intake 5. Thyrotoxicosis and Addison’s disease 6. Long term immobility 7. Familial hypocalciuric hypercalcaemia 8. Drugs like Thiazide diuretics, vitamin D , lithium |
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Signs and symptoms of hypercalcemia?
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- Tiredness, malaise, dehydration and depression
- Renal colic from stones, polyuria and nocturia, haematuria and hypertension - Mild nephrogenic diabetes insipidus - Bone pains, hyper parathyroidism mainly affects the cortical bone and bone cysts and locally destructive brown tumours. - Sometimes may present with abdominal pains - Corneal calcification |
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Ix of hypercalcemia?
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Investigations and differential diagnosis
Biochemistry - Several fasting calcium and phosphate samples - Serum PTH - Hyperchloraemic acidosis - Renal function tests - Protein electrophoresis - Serum TSH - Serum ACE - Hydrocortisone suppression test Imaging using abdominal X rays to show renal calculi or Nephrocalcinosis - USG, CT scan or MRI - Radioisotope subtraction scanning for parathyroid tissue |
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Rx of hypercalcemia?
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- Medical management
- Surgical - Management of emergency hypercalcaemia. |
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