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Pathology - Thyroid Carcinoma
Linked to radiation exposure to the head/neck or a genetic tendency for thyroid cancer.
Thyroid: Firm nodules present.
Microscopic: Four histological kinds. (1) Follicular: tiny, homogeneous follicles packed with colloid. (2) Papillary thyroid cancer: accounts for 75%-80% of cases, characterized by papillae made of cuboidal cells, Orphan Annie nuclei, and psammoma bodies; (3) Medullary thyroid cancer: originates from C cells, forming nests of cells surrounded by amyloid deposits; (4) Anaplastic thyroid cancer: has pleomorphic large cells, spindle cells, and small anaplastic cells.
Presence of a painless lump in the neck, which may cause difficulty swallowing or hoarseness due to local pressure; thyroid function tests often show normal results.
Papillary cancer spreads to nearby lymph nodes.
Follicular cancer spreads to the lung and bone through the bloodstream.
Medullary gland secretes calcitonin and is linked to Multiple Endocrine Neoplasia type IIA and IIB.
Treatment options include thyroidectomy, lobectomy, and radioactive iodine treatment.
Papillary thyroid cancer has a favorable prognosis, while anaplastic thyroid cancer has a notably unfavorable prognosis.
Thyroid adenomas are prevalent. Microscopically, they consist of consistent follicles filled with colloid, although having different histologic variations. They are not deemed precancerous and typically do not perform any function.
Linked to radiation exposure to the head/neck or a genetic tendency for thyroid cancer.
Thyroid: Firm nodules present.
Microscopic: Four histological kinds. (1) Follicular: tiny, homogeneous follicles packed with colloid. (2) Papillary thyroid cancer: accounts for 75%-80% of cases, characterized by papillae made of cuboidal cells, Orphan Annie nuclei, and psammoma bodies; (3) Medullary thyroid cancer: originates from C cells, forming nests of cells surrounded by amyloid deposits; (4) Anaplastic thyroid cancer: has pleomorphic large cells, spindle cells, and small anaplastic cells.
Presence of a painless lump in the neck, which may cause difficulty swallowing or hoarseness due to local pressure; thyroid function tests often show normal results.
Papillary cancer spreads to nearby lymph nodes.
Follicular cancer spreads to the lung and bone through the bloodstream.
Medullary gland secretes calcitonin and is linked to Multiple Endocrine Neoplasia type IIA and IIB.
Treatment options include thyroidectomy, lobectomy, and radioactive iodine treatment.
Papillary thyroid cancer has a favorable prognosis, while anaplastic thyroid cancer has a notably unfavorable prognosis.
Thyroid adenomas are prevalent. Microscopically, they consist of consistent follicles filled with colloid, although having different histologic variations. They are not deemed precancerous and typically do not perform any function.
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Pathology - Diabetes Insipidus
Diabetes Insipidus
Central diabetes insipidus is characterized by a lack of ADH secretion from the posterior pituitary. It can be either idiopathic or result from damage to the hypothalamus, such as from neoplastic or traumatic causes, or histiocytosis.
Nephrogenic diabetes insipidus is characterized by faulty ADH receptors in the kidney. It can be caused by hereditary deficiency, certain medicines (such as lithium and demeclocycline), hypercalcemia, or tubulointerstitial renal disease.
Insufficient ADH or the kidney's inability to detect ADH leads to the inability to retain water, causing excessive urine production. Insufficient water retention causes a rise in serum osmolality, triggering the activation of thirst receptors in the brain and the posterior pituitary gland to secrete additional ADH.
Clinical Symptoms and Signs
Symptoms include excessive thirst and urination, seizures, headaches, and indications of dehydration.
Laboratory results: Elevated serum osmolality, high levels of sodium in the blood, and reduced urine specific gravity.
Desmopressin treatment for central diabetic insipidus.
Low-sodium diet and thiazide diuretic prescribed for nephrogenic diabetic insipidus.
Diabetes Insipidus
Central diabetes insipidus is characterized by a lack of ADH secretion from the posterior pituitary. It can be either idiopathic or result from damage to the hypothalamus, such as from neoplastic or traumatic causes, or histiocytosis.
Nephrogenic diabetes insipidus is characterized by faulty ADH receptors in the kidney. It can be caused by hereditary deficiency, certain medicines (such as lithium and demeclocycline), hypercalcemia, or tubulointerstitial renal disease.
Insufficient ADH or the kidney's inability to detect ADH leads to the inability to retain water, causing excessive urine production. Insufficient water retention causes a rise in serum osmolality, triggering the activation of thirst receptors in the brain and the posterior pituitary gland to secrete additional ADH.
Clinical Symptoms and Signs
Symptoms include excessive thirst and urination, seizures, headaches, and indications of dehydration.
Laboratory results: Elevated serum osmolality, high levels of sodium in the blood, and reduced urine specific gravity.
Desmopressin treatment for central diabetic insipidus.
Low-sodium diet and thiazide diuretic prescribed for nephrogenic diabetic insipidus.
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Pathology - Hashimoto Thyroiditis
Hashimoto Thyroiditis is an autoimmune illness.
Incidence is higher in middle-aged women, persons with a family history of Hashimoto or other autoimmune disorders, and those who are HLA-DRS- and BLABS-positive.
Pathology
Gross: Symmetrical thyroid hypertrophy resulting in a goiter.
The thyroid gland shows infiltration by lymphocytes and plasma cells, development of germinal centers, atrophic follicles, and Hurthle cells (epithelial cells with eosinophilic cytoplasm) under microscopic examination.
Symptoms and signs
Temporary excessive thyroid hormone levels, then decreased thyroid hormone levels.
Laboratory results: Autoantibodies target TG, thyroid peroxidase, TSH receptors, and/or iodine receptors.
Therapy: Synthetic levothyroxine.
Riedel thyroiditis is an uncommon form of thyroiditis marked by gradual fibrosis of the thyroid gland that spreads into other structures in the neck. The condition presents as a painless goiter that is firm, accompanied by difficulty swallowing or hoarseness. Approximately 30% of people will also experience hypothyroidism. Treatment involves partial thyroidectomy and corticosteroids.
Hashimoto Thyroiditis is an autoimmune illness.
Incidence is higher in middle-aged women, persons with a family history of Hashimoto or other autoimmune disorders, and those who are HLA-DRS- and BLABS-positive.
Pathology
Gross: Symmetrical thyroid hypertrophy resulting in a goiter.
The thyroid gland shows infiltration by lymphocytes and plasma cells, development of germinal centers, atrophic follicles, and Hurthle cells (epithelial cells with eosinophilic cytoplasm) under microscopic examination.
Symptoms and signs
Temporary excessive thyroid hormone levels, then decreased thyroid hormone levels.
Laboratory results: Autoantibodies target TG, thyroid peroxidase, TSH receptors, and/or iodine receptors.
Therapy: Synthetic levothyroxine.
Riedel thyroiditis is an uncommon form of thyroiditis marked by gradual fibrosis of the thyroid gland that spreads into other structures in the neck. The condition presents as a painless goiter that is firm, accompanied by difficulty swallowing or hoarseness. Approximately 30% of people will also experience hypothyroidism. Treatment involves partial thyroidectomy and corticosteroids.
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Pathology - Cretinism and Myxedema
Cretinism is a kind of hypothyroidism that occurs during infancy. It can be caused by iodine insufficiency, congenital thyroid malformation, or a loss of enzymes responsible for synthesizing thyroid hormones.
Myxedema is a condition of hypothyroidism that typically affects middle-aged women. It can be caused by factors such as iodine shortage or surgical/radiation damage to the thyroid gland.
Thyroid: Moderate gland hypertrophy.
Soft tissues show an accumulation of glycosaminoglycans and hyaluronic acid.
Cretinism is characterized by symptoms of hypothyroidism, which include delayed development of the musculoskeletal and nervous systems leading to low stature, bloated abdomen, and mental retardation. Other common features are goiter, edematous face, and a big tongue.
Myxedema is a condition characterized by symptoms of hypothyroidism, including goiter, thickening of facial features, periorbital edema, pale skin. In extreme cases, myxedema coma can occur, leading to hypotension, bradycardia, hypothermia, and respiratory depression.
Therapy: Synthetic levothyroxine.
Cretinism has become less common due to the widespread inclusion of iodine to diets and screening of neonates for hypothyroidism.
Cretinism is a kind of hypothyroidism that occurs during infancy. It can be caused by iodine insufficiency, congenital thyroid malformation, or a loss of enzymes responsible for synthesizing thyroid hormones.
Myxedema is a condition of hypothyroidism that typically affects middle-aged women. It can be caused by factors such as iodine shortage or surgical/radiation damage to the thyroid gland.
Thyroid: Moderate gland hypertrophy.
Soft tissues show an accumulation of glycosaminoglycans and hyaluronic acid.
Cretinism is characterized by symptoms of hypothyroidism, which include delayed development of the musculoskeletal and nervous systems leading to low stature, bloated abdomen, and mental retardation. Other common features are goiter, edematous face, and a big tongue.
Myxedema is a condition characterized by symptoms of hypothyroidism, including goiter, thickening of facial features, periorbital edema, pale skin. In extreme cases, myxedema coma can occur, leading to hypotension, bradycardia, hypothermia, and respiratory depression.
Therapy: Synthetic levothyroxine.
Cretinism has become less common due to the widespread inclusion of iodine to diets and screening of neonates for hypothyroidism.
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Pathology - Graves Disease
Resulting from the production of thyroid-stimulating immunoglobulin and thyroid growth immunoglobulin.
Prevalent in women between the ages of 20 and 40, as well as in individuals who test positive for HLA-DR3 and HLA-B8.
Thyroid-stimulating immunoglobulin binds to TSH receptors on thyroid follicles, leading to the stimulation of thyroid hormone synthesis. Thyroid growth immunoglobulin also induces glandular hyperplasia and hypertrophy.
Study of diseases
Enlargement of the thyroid gland in a symmetrical manner.
Microscopic findings include hypercellularity with tiny, closely packed follicles containing minimal colloid. The interstitium may show infiltration of lymphocytes.
Clinical Symptoms
Symptoms of hyperthyroidism include exophthalmos (protrusion of the eyes), thicker edematous nodules on lower extremities, and a bruit around the thyroid gland.
Imaging: A radioactive iodine scan will show a widespread increase in absorption.
Laboratory results: Decreased TSH; elevated free T4 and free T3 levels.
Therapy
Treatment options include radioactive iodine, antithyroid medications such as propylthiouracil to limit thyroid hormone synthesis, thyroidectomy, and the use of beta-blockers like propranolol to manage tachycardia.
Resulting from the production of thyroid-stimulating immunoglobulin and thyroid growth immunoglobulin.
Prevalent in women between the ages of 20 and 40, as well as in individuals who test positive for HLA-DR3 and HLA-B8.
Thyroid-stimulating immunoglobulin binds to TSH receptors on thyroid follicles, leading to the stimulation of thyroid hormone synthesis. Thyroid growth immunoglobulin also induces glandular hyperplasia and hypertrophy.
Study of diseases
Enlargement of the thyroid gland in a symmetrical manner.
Microscopic findings include hypercellularity with tiny, closely packed follicles containing minimal colloid. The interstitium may show infiltration of lymphocytes.
Clinical Symptoms
Symptoms of hyperthyroidism include exophthalmos (protrusion of the eyes), thicker edematous nodules on lower extremities, and a bruit around the thyroid gland.
Imaging: A radioactive iodine scan will show a widespread increase in absorption.
Laboratory results: Decreased TSH; elevated free T4 and free T3 levels.
Therapy
Treatment options include radioactive iodine, antithyroid medications such as propylthiouracil to limit thyroid hormone synthesis, thyroidectomy, and the use of beta-blockers like propranolol to manage tachycardia.
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Pathology - Craniopharyngioma
Originating from residual tissue of Rathke's pouch, the embryonic precursor of the anterior pituitary gland.
Typically happens in childhood.
Pituitary craniopharyngioma typically presents as a cyst with calcification, containing layers of stratified squamous or columnar epithelium with keratin development.
Symptoms and signs
Bitemporal hemianopsia or other visual problems may occur due to potential constriction of the optic chiasm, leading to growth retardation, diabetes insipidus, or other pituitary deficits.
Imaging: Radiographs can identify calcified lesions in the brain.
Procedure Surgically excising the adenoma.
Originating from residual tissue of Rathke's pouch, the embryonic precursor of the anterior pituitary gland.
Typically happens in childhood.
Pituitary craniopharyngioma typically presents as a cyst with calcification, containing layers of stratified squamous or columnar epithelium with keratin development.
Symptoms and signs
Bitemporal hemianopsia or other visual problems may occur due to potential constriction of the optic chiasm, leading to growth retardation, diabetes insipidus, or other pituitary deficits.
Imaging: Radiographs can identify calcified lesions in the brain.
Procedure Surgically excising the adenoma.
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Pathology - Syndrome of Inappropriate ADH ( SIADH)
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) can be caused by pulmonary disorders (such as COPD and pneumonia), intracranial issues (like trauma, hemorrhage, and stroke), certain medications (such as antipsychotics and chemotherapy), or pain. It can also result from abnormal ADH production by tumors like small-cell bronchogenic carcinoma.
Pathology
Heightened ADH secretion leads to water retention in the collecting duct of the nephron.
Water retention results in the dilution of serum electrolytes, particularly sodium, leading to lower levels of electrolytes and serum osmolality.
Clinical Symptoms and Signs
Fatigue and confusion resulting from low levels of sodium in the blood and normal fluid volume.
Laboratory results: Low sodium levels, reduced serum osmolality, elevated urine osmolality.
Treatment includes fluid restriction, demeclocycline, and hypertonic saline for severe hyponatremia.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) can be caused by pulmonary disorders (such as COPD and pneumonia), intracranial issues (like trauma, hemorrhage, and stroke), certain medications (such as antipsychotics and chemotherapy), or pain. It can also result from abnormal ADH production by tumors like small-cell bronchogenic carcinoma.
Pathology
Heightened ADH secretion leads to water retention in the collecting duct of the nephron.
Water retention results in the dilution of serum electrolytes, particularly sodium, leading to lower levels of electrolytes and serum osmolality.
Clinical Symptoms and Signs
Fatigue and confusion resulting from low levels of sodium in the blood and normal fluid volume.
Laboratory results: Low sodium levels, reduced serum osmolality, elevated urine osmolality.
Treatment includes fluid restriction, demeclocycline, and hypertonic saline for severe hyponatremia.
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Pathology - Acromegaly and Gigantism
Resulting from a pituitary somatotropic adenoma.
Pituitary adenoma consists of many acidophilic cells that carry secretory granules filled with growth hormone (GH).
Pathophysiology: Elevated growth hormone leads to heightened release of insulin-like growth factor from the liver.
Symptoms and signs
Gigantism in children is characterized by excessive height due to the presence of an adenoma before the closure of the growth plates.
Acromegaly is a condition that occurs in adults due to the presence of an adenoma after the closure of the epiphyses. It is characterized by the enlargement of hands, feet, skull, and mandible, weight gain, insulin resistance leading to high blood sugar levels, hypertension, enlarged heart, heart failure, and possibly hypogonadism with symptoms like amenorrhea or reduced sex drive.
Patients may experience bitemporal hemianopsia or other visual abnormalities as a result of potential compression of the optic chiasm by an adenoma.
Laboratory results: Hyperglycemia is characterized by increased levels of growth hormone (GH) and insulin-like growth factor 1.
Treatment involves the use of octreotide, a somatostatin analog that reduces GH release by feedback inhibition, and surgical excision of the adenoma.
Resulting from a pituitary somatotropic adenoma.
Pituitary adenoma consists of many acidophilic cells that carry secretory granules filled with growth hormone (GH).
Pathophysiology: Elevated growth hormone leads to heightened release of insulin-like growth factor from the liver.
Symptoms and signs
Gigantism in children is characterized by excessive height due to the presence of an adenoma before the closure of the growth plates.
Acromegaly is a condition that occurs in adults due to the presence of an adenoma after the closure of the epiphyses. It is characterized by the enlargement of hands, feet, skull, and mandible, weight gain, insulin resistance leading to high blood sugar levels, hypertension, enlarged heart, heart failure, and possibly hypogonadism with symptoms like amenorrhea or reduced sex drive.
Patients may experience bitemporal hemianopsia or other visual abnormalities as a result of potential compression of the optic chiasm by an adenoma.
Laboratory results: Hyperglycemia is characterized by increased levels of growth hormone (GH) and insulin-like growth factor 1.
Treatment involves the use of octreotide, a somatostatin analog that reduces GH release by feedback inhibition, and surgical excision of the adenoma.
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Pathology - Acute Renal Failure
Prerenal causes include reduced effective arterial volume (e.g., congestive heart failure, hypovolemia, systemic vasodilation such as in sepsis) or renal vasoconstriction due to medications like NSAIDs, ACE inhibitors, or the renin-angiotensin system.
Intrarenal causes include acute tubular necrosis, acute interstitial nephritis, glomerulonephritis, and thrombotic microangiopathy.
Postrenal causes include kidney stones, benign prostatic hyperplasia (BPH), neurogenic bladder, and neoplasia.
Prerenal conditions occur when there is reduced blood flow to the kidneys, leading to a decrease in glomerular filtration rate (GFR) and causing the retention of salt and water.
Intrarenal: Defined by patchy tubular necrosis causing tubule blockage, fluid backflow through the necrotic tubule, and subsequent reduction in GFR.
Postrenal conditions occur only when there is bilateral outflow blockage, leading to increased ureteral pressure that affects nephrotubules and reduces glomerular filtration rate (GFR).
Oliguria, azotemia, and hyperkalemia.
Lab results: (1) Prerenal: low urinary Na+ (< 10), high urine osmolality (> 500), fractional excretion of Na+ (Fe Na+) < 1%, BUN/Cr ratio > 20; (2) Intrarenal: low urine osmolality (< 350), Fe Na+ > 2%, presence of urinary epithelial/granular casts; (3) Postrenal: high urinary Na+ (> 40), Fe Na+ > 4%, BUN/Cr ratio > 20.
Pre- and intrarenal: Manage fluid and electrolyte levels; address underlying cause; consider dialysis if needed.
Postrenal: Managing blockage.
Prerenal causes include reduced effective arterial volume (e.g., congestive heart failure, hypovolemia, systemic vasodilation such as in sepsis) or renal vasoconstriction due to medications like NSAIDs, ACE inhibitors, or the renin-angiotensin system.
Intrarenal causes include acute tubular necrosis, acute interstitial nephritis, glomerulonephritis, and thrombotic microangiopathy.
Postrenal causes include kidney stones, benign prostatic hyperplasia (BPH), neurogenic bladder, and neoplasia.
Prerenal conditions occur when there is reduced blood flow to the kidneys, leading to a decrease in glomerular filtration rate (GFR) and causing the retention of salt and water.
Intrarenal: Defined by patchy tubular necrosis causing tubule blockage, fluid backflow through the necrotic tubule, and subsequent reduction in GFR.
Postrenal conditions occur only when there is bilateral outflow blockage, leading to increased ureteral pressure that affects nephrotubules and reduces glomerular filtration rate (GFR).
Oliguria, azotemia, and hyperkalemia.
Lab results: (1) Prerenal: low urinary Na+ (< 10), high urine osmolality (> 500), fractional excretion of Na+ (Fe Na+) < 1%, BUN/Cr ratio > 20; (2) Intrarenal: low urine osmolality (< 350), Fe Na+ > 2%, presence of urinary epithelial/granular casts; (3) Postrenal: high urinary Na+ (> 40), Fe Na+ > 4%, BUN/Cr ratio > 20.
Pre- and intrarenal: Manage fluid and electrolyte levels; address underlying cause; consider dialysis if needed.
Postrenal: Managing blockage.
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Pathology - Chronic Kidney Disease
Linked to diabetes, hypertension, glomerular illnesses such as RPGN, vasculitides like Wegener granulomatosis, renal artery stenosis, medicines such as lithium and sulfa drugs, infections, or autoimmune diseases like SLE.
As glomerular filtration rate decreases, the kidney's ability to regulate electrolyte balances, such as potassium excretion leading to hyperkalemia, and sodium and water handling causing volume overload, diminishes. Additionally, the kidney's capacity to maintain pH balance is compromised, resulting in metabolic acidosis due to insufficient ammonia production to bind with endogenous acid and be excreted as ammonium. Anemia occurs due to reduced production of erythropoietin by malfunctioning kidneys.
Clinical Symptoms
Initially asymptomatic, chronic kidney disease (CKD) advances to cause symptoms such as edema, dyspnea due to volume overload, fatigue, and weakness.
Possible complications consist of cardiac arrhythmias due to electrolyte imbalances, encephalopathy, platelet dysfunction, renal osteodystrophy, and pericarditis.
Laboratory results indicate anemia, increased blood urea nitrogen (BUN) and creatinine levels, metabolic acidosis, low calcium levels (hypocalcemia), high phosphate levels (hyperphosphatemia), and high potassium levels (hyperkalemia).
Prescribe ACE inhibitors and diuretics, check electrolytes, administer phosphate binders, manage underlying disease. Advanced stages may necessitate dialysis or transplant.
Individuals undergoing long-term dialysis for chronic kidney disease have a 5-year survival rate of 35%.
Reasons to start dialysis in chronic kidney disease include metabolic imbalances such as acidosis and hyperkalemia, controlling excess fluid, advancing uremic encephalopathy, and managing symptoms of uremia such malnutrition, pericarditis, or pleuritis.
Linked to diabetes, hypertension, glomerular illnesses such as RPGN, vasculitides like Wegener granulomatosis, renal artery stenosis, medicines such as lithium and sulfa drugs, infections, or autoimmune diseases like SLE.
As glomerular filtration rate decreases, the kidney's ability to regulate electrolyte balances, such as potassium excretion leading to hyperkalemia, and sodium and water handling causing volume overload, diminishes. Additionally, the kidney's capacity to maintain pH balance is compromised, resulting in metabolic acidosis due to insufficient ammonia production to bind with endogenous acid and be excreted as ammonium. Anemia occurs due to reduced production of erythropoietin by malfunctioning kidneys.
Clinical Symptoms
Initially asymptomatic, chronic kidney disease (CKD) advances to cause symptoms such as edema, dyspnea due to volume overload, fatigue, and weakness.
Possible complications consist of cardiac arrhythmias due to electrolyte imbalances, encephalopathy, platelet dysfunction, renal osteodystrophy, and pericarditis.
Laboratory results indicate anemia, increased blood urea nitrogen (BUN) and creatinine levels, metabolic acidosis, low calcium levels (hypocalcemia), high phosphate levels (hyperphosphatemia), and high potassium levels (hyperkalemia).
Prescribe ACE inhibitors and diuretics, check electrolytes, administer phosphate binders, manage underlying disease. Advanced stages may necessitate dialysis or transplant.
Individuals undergoing long-term dialysis for chronic kidney disease have a 5-year survival rate of 35%.
Reasons to start dialysis in chronic kidney disease include metabolic imbalances such as acidosis and hyperkalemia, controlling excess fluid, advancing uremic encephalopathy, and managing symptoms of uremia such malnutrition, pericarditis, or pleuritis.
