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26 Cards in this Set
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- Hashimoto thyroiditis
Briefly describe the causes and clinical manifestations of the thyroid diseases |
- Most common cause of HYPOthyroidism in the world where iodine levels are insufficient.
- Characterized by gradual thyroid failure because of autoimmune destruction of the thyroid gland. - Prevalent between 45 & 65 yo. - Women > Men - Strong genetic correlation in first degree relatives. Clinical features: - Painless enlargement of thyroid (Usually bilaterally symmetrical) 20 to hypothyroidism - Often have other autoimmune diseases and are at ⇧ risks for development of B-Cell Non-Hodgkin lymphoma |
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- Most common cause of HYPOthyroidism in the world where iodine levels are insufficient.
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- Hashimoto thyroiditis
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- Characterized by gradual thyroid failure because of autoimmune destruction of the thyroid gland.
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- Hashimoto thyroiditis
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- Hashimoto thyroiditis
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- Most common cause of HYPOthyroidism in the world where iodine levels are insufficient.
- Characterized by gradual thyroid failure because of autoimmune destruction of the thyroid gland. - Prevalent between 45 & 65 yo. - Women > Men - Strong genetic correlation in first degree relatives. Clinical features: - Painless enlargement of thyroid (Usually bilaterally symmetrical) 20 to hypothyroidism - Often have other autoimmune diseases and are at ⇧ risks for development of B-Cell Non-Hodgkin lymphoma |
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- Graves disease
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- Autoimmune disorder (Three important pathologies)
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- TSH stimulating IgG antibody binds to TSH receptor and mimics the actions of TSH
- Thyroid Growth stimulating Ig’s have been implicated in the growth of Thyroid follicular epithelium. - TSH-binding inhibitor Ig. These Ig’s prevent TSH from binding to its receptors in epithelial tissues, presenting in Graves disease, spontaneous episodes of hyperthyroidism. |
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- Graves disease
additional details of causes and statistics |
- Most common cause of HYPERthyroidism.
- Peak incidence between 20 & 40 yo. - Very common, in 1.5% - 2% of women - Women are 7x more likely than men to acquire - Characterized by Triad of manifestations - Thyrotoxicosis (Systemic excess of Thyroxine) All patients - Exophthalmos = 40% of patients - Dermothopathy = a minority of cases see pretibial myxedema |
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- Diffuse and multinodular goiter
what is it? two types? |
- Most common manifestation of thyroid disease.
- Reflect impaired synthesis of thyroid hormone. - Most often caused by dietary iodine deficiency. - Impairment of thyroid synthesis leads to a compensatory rise in serum TSH levels, in turn, which causes Hypertrophy and hyperplasia of the thyroid follicular cells. This compensation is able to overcome the hormone deficiency. - Two different onset types - Endemic goiter, which is found in areas where soil, food, and water have decreased amounts of iodine, (Mountainous areas, ie Himalayas and Andes) - Sporadic goiter, -Unknown causes, possibly ingestion of certain substances and hereditary enzyme deficiency. -This is greater in Women than men, and found in puberty and young adult life when the physiological call for Thyroid hormone is the greatest for energy and growth. |
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Distinguish between thyroid adenomas and carcinomas, and identify the most common examples of each.
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- Thyroid adenomas (Benign)
- Thyroid carcinomas (malignant tumor) - Clinical suggestions of malignancy - Solitary tumors are generally less likely to be malignant - Younger pts are less likely to have malignancy - Males are less likely to have malignancy than females - Nodules that take up radioactive iodine (Hot nodules) are LESS likely to be malignant. - Hx of Rx therapy in head and neck has increased chances of malignancy. |
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- Clinical suggestions of malignancy for thyroid adenomas and carcinomas
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- Solitary tumors are generally less likely to be malignant
- Younger pts are less likely to have malignancy - Males are less likely to have malignancy than females - Nodules that take up radioactive iodine (Hot nodules) are LESS likely to be malignant. - Hx of Rx therapy in head and neck has increased chances of malignancy. |
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structure and functions of the parathyroid glands.
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- Small glands that lie in close proximity to the upper and lower poles of each thyroid lobe.
- The activity of the parathyroids is controlled by the level of free (ionized) calcium in the bloodstream rather than by hormones secreted by the hypothalamus and pituitary. - Parathyroid hormone, (PTH) produced by the Parathyroids 20 to decr. Calcium levels has a few effects. - Activates osteoclasts - Incr. Renal tubular absorption of calcium - increases Vit-D conversion to active form in kidney - Incr. urinary Phosphate secretion - Augments GI calcium absorption |
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structure of the parathyroid glands.
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- Small glands that lie in close proximity to the upper and lower poles of each thyroid lobe.
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controls of the parathyroid glands.
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- The activity of the parathyroids is controlled by the level of free (ionized) calcium in the bloodstream rather than by hormones secreted by the hypothalamus and pituitary.
- Parathyroid hormone, (PTH) = produced by the Parathyroids 20 to decr. Calcium levels has a few effects. |
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functions of the parathyroid glands.
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- Activates osteoclasts
- Incr. Renal tubular absorption of calcium - increases Vit-D conversion to active form in kidney - Incr. urinary Phosphate secretion - Augments GI calcium absorption |
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cause of primary and secondary hyperparathyroidism.
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-most common endocrine disorders,
-cause of hypercalccemia. - Main causes are sporadic Adenoma (75-80%), -primary hyperplasia (10-15%), and -parathyroid carcinoma (<5%) -Usually affects adults - Women to Men ration is 3:1 |
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manifestations of primary and secondary hyperparathyroidism.
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Primary Hyperparathyroidism:
- Most common manifestation is Hypercalcemia - Clinical manifestations include - Painful bones from osteoperosis - Renal stones from excess calcium build-up - Abdominal groans - Psychic moans enlargement of one or more of the parathyroid glands. This leads to too much parathyroid hormone, which raises the level of calcium in the blood. |
Secondary hyperparathyroidism is:
-body produces extra parathyroid hormone due to calcium low Ca levels. -This is seen when vitamin D levels are low or when calcium is not absorbed from the intestines. If the parathyroid glands continue to produce too much parathyroid hormone even though the calcium level is back to normal, the condition is called "tertiary hyperthyroidism." It occurs especially in patients with kidney problems. |
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cause of secondary hyperparathyroidism.
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-caused by any condition associated with chronic depression in the serum calcium level, which would result in an over production compensation of PTH.
- Renal failure= most common cause of secondary hyperparathyroidism. -chronic renal failure causes increased phosphate levels, decreasing serum calcium levels. |
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manifestations of secondary hyperparathyroidism.
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-renal insufficiency .
-- May see bone abnormalities, but changes are way more pronounced in primary hyperparathyroidism. |
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causes of hypoparathyroidism.
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- HYPOparathyroidism is far less common than hyperparathyroidism.
- Major causes are: - Surgical removal inadvertently while performing thyroidectomy. - Congenital absence. - Autoimmune disease that affects endocrine organs. |
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clinical manifestations of hypoparathyroidism.
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- referable to HYPOcalcemia and include:
-Incr. Neuromuscular irritability (tingling, muscle spasm, facial grimacing, and sustained carpopedal spasm.) - cardiac arrhythmias - on occasion, ICP and seizures. |
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Compare and contrast the causes and clinical features of type 1 and type 2 diabetes mellitus.
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- Diabetes type 1
- Autoimmune disease in which islet destruction is caused by T lymphocytes. Beta cells are attacked by self antigens. - Most commonly develops in childhood and progresses with age. - Genetic factors play a role - CLINICAL FEATURES - Onset <20 yo - Normal weight - Markedly decreased blood insulin - Antibodies to islet cells - Ketoacidosis common - Diabetes Type 2 - Pathogenesis of 2 is unknown, -risk factors are - Sedentary lifestyle, dietary habits, and Visceral obesity. - Genetic factors even more significant in type 2 than type 1, although still unknown why, 20-40% of people with 1st degree relatives with type 2 diabetes will acquire the disease. - Two metabolic defects that characterize type 2 diabetes are: - Decr. ability of tissues to respond to insulin (INSULIN RESTSTANCE) - Beta cell dysfunction that is manifested as inadequate insulin secretion and hyperglycemia. - In most cases, resistance is the primary event followed by increased Beta cell dysfunction. - CLINICAL FEATURES - Onset >30 yo - Obesity - Increased blood insulin (early)Normal to moderate Decr. (late) - No antibodies to islet cells - Ketoacidosis rare, nonketotic hyperosmolar coma |
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long-term complications of diabetes mellitus.
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- Diabetes is the leading cause of
-End stage renal disease, -Adult onset blindness, and - non-traumatic lower extremity amputations. - Cardiovascular events such as MI, Cerebrovascular accidents, -Accelerated atherosclerosis - Diabetic Nephropathy - Visual impairment, -retinopathy, -Incr. risk of glaucoma an -cataracts. - Diabetic neuropathy -Enhanced susceptibility to: -infections of the skin -TB, -Pneumonia and -pyelonephritis. |
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Hypercortisolism (Cushing syndrome)
Describe causes : |
- This disorder is caused by any condition that produces an elevation in glucocorticoid levels.
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Describe clinical effects of hypercortisolism (Cushing syndrome);
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- Cushing Disease - a non-cancerous tumor, a pituitary adenoma produces Excess ACTH, which in turn elevates cortisol levels
- In clinical practice, Cushing syndrome caused by administration of excessive exogenous glucocorticoids (Iatrogenic Cushing syndrome) remaining cases are caused by: -hypersecretion of ACTH - Primary adrenocortical hyperplasia or neoplasia (Adrenal cushing syndrome) - The secretion of ectopic ACTH by non-endocrine neoplasms (Parneoplastic Cushing syndrome). - Non-clinician related causes, over 50% are Primary Hypothalmic-pituitary diseases. - Women 5x more likely than men to acquire. - CLINICAL FEATURES (Exaggeration of the known actions of glucocorticoids) - HTN, Weight gain, Truncal obesity, Moon face, Buffalo hump |
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Chronic Adrenal Insufficiency
Causes: (Addison disease or Cushings). |
- Addison’s disease is chronic adrenocortical insufficiency. It is an uncommon disorder resulting from progressive destruction of the adrenal cortex.
- There are four causes that account for more than 90% of all cases. - Autoimmune adrenalitis (60-70%) - TB - AIDS - Metastatic cancers. |
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clinical effects of chronic adrenal insufficiency (Addison disease).
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- CLINICAL FEATURES
- In general, manifestations do not appear until at least 90% of the adrenal cortex has been compromised - Weakness and easy fatigability complaints - GI disturbances, ie: anorexia, nausea, vomiting, weight loss and diarrhea - Primary Adrenal insufficiency is also characterized by high levels of ACTH -skin hyperpigmentation |
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clinical features of pheochromocytoma.
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- HTN is the dominant clinical manifestation
- Classically described as an abrupt, precipitous, elevation in blood pressure, associated with tachycardia, palpitations, headache, sweating, tremor, and a sense of apprehension: -Such episodes may be associated with pain in the abdomen or chest, nausea, and vomiting. |
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