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Pathology - Hashimoto's thyroiditis
Definition: An autoimmune thyroid disorder marked by generalized thyroid enlargement and elevated levels of thyroid autoantibodies.
Epidemiology • Prevalent, impacting approximately 1% of the population. • Primarily manifests in middle-aged women. Aetiology • Unidentified.
Pathogenesis • Activated CD4+ helper T-cells enlist CD8+ cytotoxic T-cells that annihilate thyroid follicular epithelial cells. • Anti-thyroid autoantibodies generated by activated B-cells may also play a role.
Presentation: Diffuse firm goiter accompanied by characteristics of hypothyroidism.
Biochemistry • Thyroid-stimulating hormone (TSH) and thyroxine (T4). • Autoantibodies against thyroglobulin, thyroid peroxidase, and TSH receptor are typically present. It is important to note that the latter antibody differs from that observed in Graves' illness, as it inhibits the TSH receptor instead of activating it.
Macroscopy • The thyroid exhibits diffuse enlargement and nodularity. • The cut surface is typically soft and white, suggesting lymphoid tissue. Cytopathology • Aspirates are cellular, comprising numerous lymphoid cells and few follicular epithelial cells exhibiting Hurthle cell transformation. • Hurthle cells include ample granular cytoplasm and expanded nuclei with vesicular chromatin.
Histopathology • The thyroid has extensive lymphoid infiltration accompanied by the establishment of germinal centers. • Thyroid follicles are atrophic and demonstrate widespread Hurthle cell transformation, marked by copious eosinophilic granular cytoplasm and nuclear expansion.
Prognosis: Favorable with thyroxine replacement therapy. 2 The incidence of thyroid lymphoma, typically extranodal marginal zone B-cell lymphoma, has risen.
Definition: An autoimmune thyroid disorder marked by generalized thyroid enlargement and elevated levels of thyroid autoantibodies.
Epidemiology • Prevalent, impacting approximately 1% of the population. • Primarily manifests in middle-aged women. Aetiology • Unidentified.
Pathogenesis • Activated CD4+ helper T-cells enlist CD8+ cytotoxic T-cells that annihilate thyroid follicular epithelial cells. • Anti-thyroid autoantibodies generated by activated B-cells may also play a role.
Presentation: Diffuse firm goiter accompanied by characteristics of hypothyroidism.
Biochemistry • Thyroid-stimulating hormone (TSH) and thyroxine (T4). • Autoantibodies against thyroglobulin, thyroid peroxidase, and TSH receptor are typically present. It is important to note that the latter antibody differs from that observed in Graves' illness, as it inhibits the TSH receptor instead of activating it.
Macroscopy • The thyroid exhibits diffuse enlargement and nodularity. • The cut surface is typically soft and white, suggesting lymphoid tissue. Cytopathology • Aspirates are cellular, comprising numerous lymphoid cells and few follicular epithelial cells exhibiting Hurthle cell transformation. • Hurthle cells include ample granular cytoplasm and expanded nuclei with vesicular chromatin.
Histopathology • The thyroid has extensive lymphoid infiltration accompanied by the establishment of germinal centers. • Thyroid follicles are atrophic and demonstrate widespread Hurthle cell transformation, marked by copious eosinophilic granular cytoplasm and nuclear expansion.
Prognosis: Favorable with thyroxine replacement therapy. 2 The incidence of thyroid lymphoma, typically extranodal marginal zone B-cell lymphoma, has risen.
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Pathology - Graves' disease
Definition: An autoimmune thyroid disorder marked by thyrotoxicosis and widespread hyperplasia of the thyroid gland.
Epidemiology • Prevalent, impacting up to 1% of the population. • The highest frequency occurs in young adults aged 30 to 40. • Women are disproportionately impacted compared to men.
Aetiology • Synthesis of antibodies that stimulate the TSH receptor. Pathogenesis TSH receptor-stimulating antibodies attach to the TSH receptor, activating it and prompting hyperplasia of the thyroid follicular epithelium along with unregulated release of thyroid hormones.
Presentation • individuals exhibit thyrotoxicosis accompanied by a diffuse goitre. • Certain individuals may additionally manifest a kind of orbital disease referred to as Graves' ophthalmopathy.
Macroscopy • The thyroid exhibits diffuse enlargement with a firm, red cut surface. • Following treatment, the thyroid may present a nodular morphology. Cytopathology: Aspirates exhibit significant cellularity with minimal colloid and many follicular epithelial cells demonstrating hyperplastic alterations. 2 Aspiration is seldom conducted in instances with active Graves' disease, as the clinical diagnosis is typically clear-cut. This is advantageous, as the highly cellular aspirates can readily be misidentified as a neoplastic process by the inattentive.
Histopathology • The thyroid exhibits diffuse hyperplasia characterized by colloid depletion and significant hyperplastic alterations of the follicular epithelium. • A heterogeneous lymphoid infiltrate, with or without germinal centers, is typically observed.
Prognosis: Excellent with adequate thyroid ablative therapy.
Definition: An autoimmune thyroid disorder marked by thyrotoxicosis and widespread hyperplasia of the thyroid gland.
Epidemiology • Prevalent, impacting up to 1% of the population. • The highest frequency occurs in young adults aged 30 to 40. • Women are disproportionately impacted compared to men.
Aetiology • Synthesis of antibodies that stimulate the TSH receptor. Pathogenesis TSH receptor-stimulating antibodies attach to the TSH receptor, activating it and prompting hyperplasia of the thyroid follicular epithelium along with unregulated release of thyroid hormones.
Presentation • individuals exhibit thyrotoxicosis accompanied by a diffuse goitre. • Certain individuals may additionally manifest a kind of orbital disease referred to as Graves' ophthalmopathy.
Macroscopy • The thyroid exhibits diffuse enlargement with a firm, red cut surface. • Following treatment, the thyroid may present a nodular morphology. Cytopathology: Aspirates exhibit significant cellularity with minimal colloid and many follicular epithelial cells demonstrating hyperplastic alterations. 2 Aspiration is seldom conducted in instances with active Graves' disease, as the clinical diagnosis is typically clear-cut. This is advantageous, as the highly cellular aspirates can readily be misidentified as a neoplastic process by the inattentive.
Histopathology • The thyroid exhibits diffuse hyperplasia characterized by colloid depletion and significant hyperplastic alterations of the follicular epithelium. • A heterogeneous lymphoid infiltrate, with or without germinal centers, is typically observed.
Prognosis: Excellent with adequate thyroid ablative therapy.
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Pathology - Nodular Goitre
Definition • Nodular hypertrophy of the thyroid gland.
Epidemiology • Extremely prevalent. • Clinically evident nodular goitre impacts up to 5% of the population.
Etiology Numerous instances are believed to result from minor genetic anomalies in the components of the thyroid hormone synthesis machinery.
Pathogenesis
Decreased thyroid hormone levels prompt the anterior pituitary to secrete TSH. Repetitive cycles of stimulation and involution lead to the formation of numerous nodules in the thyroid.
Presentation • A distinctly enlarged, nodular goitre. • The majority of individuals are euthyroid.
Macroscopy
The thyroid gland is hypertrophied and multinodular. Slicing exposes several unencapsulated nodules of diverse sizes, typically filled with copious colloid. • Regions exhibiting cystic alteration, hemorrhage, and calcification are prevalent.
Cytopathology
Aspirates exhibit a high concentration of colloid with minimal thyroid follicular epithelium. • Macrophages containing haemosiderin may be present as a result of prior bleeding. Foamy macrophages frequently signify cystic transformation within a lesion.
Histopathology: The thyroid has many nodules of diverse dimensions, accompanied by regions of cystic alteration and hemorrhage. The follicles within the nodules exhibit varied characteristics. Some are significantly distended with colloid, some exhibit hyperplasia, while others are diminutive and densely arranged, creating cellular 'adenomatoid' nodules.
Prognosis • Nodular goitre is a benign disorder with no documented elevated risk of thyroid carcinoma. • The primary potential complication is the compression of adjacent tissues, such as the trachea, due to a significantly larger nodular goitre.
Definition • Nodular hypertrophy of the thyroid gland.
Epidemiology • Extremely prevalent. • Clinically evident nodular goitre impacts up to 5% of the population.
Etiology Numerous instances are believed to result from minor genetic anomalies in the components of the thyroid hormone synthesis machinery.
Pathogenesis
Decreased thyroid hormone levels prompt the anterior pituitary to secrete TSH. Repetitive cycles of stimulation and involution lead to the formation of numerous nodules in the thyroid.
Presentation • A distinctly enlarged, nodular goitre. • The majority of individuals are euthyroid.
Macroscopy
The thyroid gland is hypertrophied and multinodular. Slicing exposes several unencapsulated nodules of diverse sizes, typically filled with copious colloid. • Regions exhibiting cystic alteration, hemorrhage, and calcification are prevalent.
Cytopathology
Aspirates exhibit a high concentration of colloid with minimal thyroid follicular epithelium. • Macrophages containing haemosiderin may be present as a result of prior bleeding. Foamy macrophages frequently signify cystic transformation within a lesion.
Histopathology: The thyroid has many nodules of diverse dimensions, accompanied by regions of cystic alteration and hemorrhage. The follicles within the nodules exhibit varied characteristics. Some are significantly distended with colloid, some exhibit hyperplasia, while others are diminutive and densely arranged, creating cellular 'adenomatoid' nodules.
Prognosis • Nodular goitre is a benign disorder with no documented elevated risk of thyroid carcinoma. • The primary potential complication is the compression of adjacent tissues, such as the trachea, due to a significantly larger nodular goitre.
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Pathology - Follicular adenoma
Definition: A benign, encapsulated thyroid neoplasm with follicular differentiation.
Epidemiology: The predominant thyroid neoplasm. • The actual incidence is challenging to assess because of inconsistent criteria for differentiating follicular adenomas from cellular adenomatoid nodules in nodular goiters.
Aetiology: Associated with radiation exposure and iodine deficiency. Genetics • Chromosomal trisomies, especially trisomy 7, represent the predominant category of genetic anomalies. Presentation • The majority appear with a singular thyroid nodule, either detected by the patient or identified incidentally through imaging. Spontaneous hemorrhage within an adenoma may result in severe discomfort and an increase in nodule size. Macroscopy • The thyroid has a distinctly defined, thinly encapsulated solid nodule characterized by a gray, tan, or brown sliced surface. Cytopathology • Aspirates exhibit cellularity, comprising many follicular cells with minimal colloid. • The follicular cells are observed both in a dissociated state and in minute microfollicular configurations. 2 It is important to recognize that cytology cannot differentiate between follicular adenoma and follicular cancer. This may solely be accomplished histologically. Histopathology • Follicular adenomas are encapsulated epithelial tumors exhibiting follicular differentiation. • By definition, there is an absence of capsular or vascular penetration.
Prognosis: Follicular adenomas are benign neoplasms that are resolved with surgical excision.
Definition: A benign, encapsulated thyroid neoplasm with follicular differentiation.
Epidemiology: The predominant thyroid neoplasm. • The actual incidence is challenging to assess because of inconsistent criteria for differentiating follicular adenomas from cellular adenomatoid nodules in nodular goiters.
Aetiology: Associated with radiation exposure and iodine deficiency. Genetics • Chromosomal trisomies, especially trisomy 7, represent the predominant category of genetic anomalies. Presentation • The majority appear with a singular thyroid nodule, either detected by the patient or identified incidentally through imaging. Spontaneous hemorrhage within an adenoma may result in severe discomfort and an increase in nodule size. Macroscopy • The thyroid has a distinctly defined, thinly encapsulated solid nodule characterized by a gray, tan, or brown sliced surface. Cytopathology • Aspirates exhibit cellularity, comprising many follicular cells with minimal colloid. • The follicular cells are observed both in a dissociated state and in minute microfollicular configurations. 2 It is important to recognize that cytology cannot differentiate between follicular adenoma and follicular cancer. This may solely be accomplished histologically. Histopathology • Follicular adenomas are encapsulated epithelial tumors exhibiting follicular differentiation. • By definition, there is an absence of capsular or vascular penetration.
Prognosis: Follicular adenomas are benign neoplasms that are resolved with surgical excision.
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Pathology - Thyroid carcinomas
Definition • A collection of malignant epithelial tumors originating in the thyroid gland. Four principal kinds are identified: papillary, follicular, medullary, and anaplastic.
Epidemiology • Rare, constituting around 1% of all cancers in wealthy nations. The average age of diagnosis is mid-40s to early 50s for the papillary type, 50s for the follicular and medullary forms, and 60s for the anaplastic type. Aetiology • Radiation exposure is a recognized risk factor for thyroid carcinoma, particularly papillary carcinoma. Iodine deficiency is also a contributing factor, especially in follicular carcinomas. Approximately 25% of medullary carcinomas are associated with inherited disorders, specifically multiple endocrine neoplasia (MEN) types 2A and 2B, as well as familial medullary thyroid cancer (FMTC).
Carcinogenesis: RET and TRK mutations are characteristic of papillary carcinomas. Follicular carcinomas typically exhibit RAS mutations. TP53 mutations are prevalent in anaplastic carcinomas. Presentation: Most well-differentiated thyroid carcinomas manifest as a solitary thyroid nodule. Thyroid function is typically normal.
Anaplastic carcinoma typically manifests as a swiftly expanding cervical mass; encroachment on adjacent structures results in hoarseness, dysphagia, and dyspnea. Macroscopy: Papillary carcinomas typically present as firm, grey-white lumps with uneven boundaries. They are frequently multifocal.
Follicular carcinomas are typically encapsulated, spherical solid tumors exhibiting a tan to brown hue.
Medullary carcinomas are solid grey-white to tan tumors, frequently characterized by a gritty texture.
Anaplastic carcinomas are substantial necrotic tumors that typically supplant the thyroid and extensively infiltrate surrounding tissues.
Cytopathology
Papillary carcinoma aspirates comprise papillaroid fragments of follicular epithelial cells exhibiting the distinctive nuclear characteristics of papillary carcinoma, such as powdered chromatin, thick nuclear membranes, nuclear grooves, and nuclear pseudoinclusions. Multinucleated giant cells, psammoma bodies, and dense colloid may be observed.
Follicular carcinoma aspirates are cellular, comprising follicular epithelial cells found individually and in microfollicular configurations. It is important to note that these appearances are indistinguishable from follicular adenomas; cytological analysis cannot differentiate between these entities
Medullary carcinoma aspirates are cellular, with loosely cohesive epithelial cells that may be either round or spindle-shaped. Certain cells may have eccentric nuclei, resulting in a plasmacytoid morphology. The nuclei have coarsely granular chromatin. Amyloid fragments may be observed.
Anaplastic carcinoma aspirates have considerable cellularity, with significantly abnormal malignant cells.
Histopathology
Papillary carcinoma is characterized by distinct nuclear features: oval form, overlapping, chromatin clearance, nuclear grooves, and pseudoinclusions. While the majority of tumors exhibit a papillary form, this characteristic is not essential for diagnosis.
Follicular carcinoma is an invasive follicular tumor devoid of the nuclear characteristics associated with papillary thyroid carcinoma. Follicular carcinomas are categorized into two primary types: slightly invasive and broadly invasive.
Minimally invasive tumors have restricted capsular invasion and/or vascular invasion.
Extensively invasive tumors exhibit extensive infiltration of the thyroid and/or vascular structures.
Medullary carcinoma exhibits sheets, nests, or trabeculae of rounded or spindle-shaped neoplastic cells characterized by granular cytoplasm and nuclei containing coarse chromatin. Amyloid deposits may be observed. The diagnosis can be validated by immunoreactivity for calcitonin.
Anaplastic carcinomas consist of extremely pleomorphic epithelioid and spindle-shaped cells. Significant necrosis is observed, and vascular blockage by tumor is prevalent.
Prognosis: Papillary carcinomas and less invasive follicular carcinomas are low-grade malignancies characterized by an excellent prognosis. Extensively invasive follicular carcinomas and medullary carcinomas are intermediate-grade neoplasms associated with an elevated risk of metastasis and mortality. Anaplastic carcinomas are exceedingly malignant and nearly usually result in death within months of diagnosis.
TNM 7 pathological staging of thyroid carcinomas Primary tumour (T)
pT1a: tumour d 10mm in size, limited to the thyroid.
pT1b: tumour d 20mm, but > 10mm in size, limited to the thyroid.
pT2: tumour > 20mm, but d 40mm in size, limited to the thyroid.
pT3: tumour > 40mm in size, limited to thyroid, or any tumour with
minimal extrathyroid extension.
pT4a: tumour of any size extending beyond the thyroid capsule to
invade subcutaneous soft tissues, the larynx, trachea, oesophagus, or
recurrent laryngeal nerve.
pT4b: tumour invades the prevertebral fascia, mediastinal vessels, or
encases the carotid artery.
2 Note that all anaplastic tumours are considered T4.
Regional lymph nodes (N)
pN0: no regional lymph node metastasis.
pN1a: metastases in level VI cervical lymph nodes.
pN1b: metastases in levels I–V cervical, retropharyngeal, or superior
mediastinal lymph nodes
Definition • A collection of malignant epithelial tumors originating in the thyroid gland. Four principal kinds are identified: papillary, follicular, medullary, and anaplastic.
Epidemiology • Rare, constituting around 1% of all cancers in wealthy nations. The average age of diagnosis is mid-40s to early 50s for the papillary type, 50s for the follicular and medullary forms, and 60s for the anaplastic type. Aetiology • Radiation exposure is a recognized risk factor for thyroid carcinoma, particularly papillary carcinoma. Iodine deficiency is also a contributing factor, especially in follicular carcinomas. Approximately 25% of medullary carcinomas are associated with inherited disorders, specifically multiple endocrine neoplasia (MEN) types 2A and 2B, as well as familial medullary thyroid cancer (FMTC).
Carcinogenesis: RET and TRK mutations are characteristic of papillary carcinomas. Follicular carcinomas typically exhibit RAS mutations. TP53 mutations are prevalent in anaplastic carcinomas. Presentation: Most well-differentiated thyroid carcinomas manifest as a solitary thyroid nodule. Thyroid function is typically normal.
Anaplastic carcinoma typically manifests as a swiftly expanding cervical mass; encroachment on adjacent structures results in hoarseness, dysphagia, and dyspnea. Macroscopy: Papillary carcinomas typically present as firm, grey-white lumps with uneven boundaries. They are frequently multifocal.
Follicular carcinomas are typically encapsulated, spherical solid tumors exhibiting a tan to brown hue.
Medullary carcinomas are solid grey-white to tan tumors, frequently characterized by a gritty texture.
Anaplastic carcinomas are substantial necrotic tumors that typically supplant the thyroid and extensively infiltrate surrounding tissues.
Cytopathology
Papillary carcinoma aspirates comprise papillaroid fragments of follicular epithelial cells exhibiting the distinctive nuclear characteristics of papillary carcinoma, such as powdered chromatin, thick nuclear membranes, nuclear grooves, and nuclear pseudoinclusions. Multinucleated giant cells, psammoma bodies, and dense colloid may be observed.
Follicular carcinoma aspirates are cellular, comprising follicular epithelial cells found individually and in microfollicular configurations. It is important to note that these appearances are indistinguishable from follicular adenomas; cytological analysis cannot differentiate between these entities
Medullary carcinoma aspirates are cellular, with loosely cohesive epithelial cells that may be either round or spindle-shaped. Certain cells may have eccentric nuclei, resulting in a plasmacytoid morphology. The nuclei have coarsely granular chromatin. Amyloid fragments may be observed.
Anaplastic carcinoma aspirates have considerable cellularity, with significantly abnormal malignant cells.
Histopathology
Papillary carcinoma is characterized by distinct nuclear features: oval form, overlapping, chromatin clearance, nuclear grooves, and pseudoinclusions. While the majority of tumors exhibit a papillary form, this characteristic is not essential for diagnosis.
Follicular carcinoma is an invasive follicular tumor devoid of the nuclear characteristics associated with papillary thyroid carcinoma. Follicular carcinomas are categorized into two primary types: slightly invasive and broadly invasive.
Minimally invasive tumors have restricted capsular invasion and/or vascular invasion.
Extensively invasive tumors exhibit extensive infiltration of the thyroid and/or vascular structures.
Medullary carcinoma exhibits sheets, nests, or trabeculae of rounded or spindle-shaped neoplastic cells characterized by granular cytoplasm and nuclei containing coarse chromatin. Amyloid deposits may be observed. The diagnosis can be validated by immunoreactivity for calcitonin.
Anaplastic carcinomas consist of extremely pleomorphic epithelioid and spindle-shaped cells. Significant necrosis is observed, and vascular blockage by tumor is prevalent.
Prognosis: Papillary carcinomas and less invasive follicular carcinomas are low-grade malignancies characterized by an excellent prognosis. Extensively invasive follicular carcinomas and medullary carcinomas are intermediate-grade neoplasms associated with an elevated risk of metastasis and mortality. Anaplastic carcinomas are exceedingly malignant and nearly usually result in death within months of diagnosis.
TNM 7 pathological staging of thyroid carcinomas Primary tumour (T)
pT1a: tumour d 10mm in size, limited to the thyroid.
pT1b: tumour d 20mm, but > 10mm in size, limited to the thyroid.
pT2: tumour > 20mm, but d 40mm in size, limited to the thyroid.
pT3: tumour > 40mm in size, limited to thyroid, or any tumour with
minimal extrathyroid extension.
pT4a: tumour of any size extending beyond the thyroid capsule to
invade subcutaneous soft tissues, the larynx, trachea, oesophagus, or
recurrent laryngeal nerve.
pT4b: tumour invades the prevertebral fascia, mediastinal vessels, or
encases the carotid artery.
2 Note that all anaplastic tumours are considered T4.
Regional lymph nodes (N)
pN0: no regional lymph node metastasis.
pN1a: metastases in level VI cervical lymph nodes.
pN1b: metastases in levels I–V cervical, retropharyngeal, or superior
mediastinal lymph nodes
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Pathology - Parathyroid hyperplasia
Definition: An augmentation of parathyroid cell mass without an identifiable trigger.
Epidemiology • Rare, constituting around 20% of primary hyperparathyroidism. • Women are impacted more significantly than men, at a ratio of 3:1.
Aetiology • The majority of patients exhibit sporadic hyperplasia without a discernible etiology. • Approximately 20% of cases are attributed to family illness, predominantly Multiple Endocrine Neoplasia (MEN). 1.
Pathogenesis • Parathyroid hyperplasia results in excessive secretion of parathyroid hormone (PTH). Elevated PTH levels induce hypercalcemia via enhancing calcium absorption from the gastrointestinal tract and kidneys, as well as by augmenting osteoclastic activity in bone.
Presentation • individuals exhibit primary hyperparathyroidism, a biochemical illness characterized by hypercalcemia and an abnormally normal or elevated PTH level. • Numerous individuals are asymptomatic when this condition is identified accidentally. • Some individuals may exhibit nonspecific symptoms such as tiredness, nausea, constipation, polyuria, and arthralgia.
Macroscopy • All parathyroid glands exhibit hypertrophy, with weights exceeding 60 mg and dimensions surpassing 6 mm, but with variability among the glands.
Histopathology • The principal characteristic is an augmentation of cellular mass within the gland, correlated with a reduction in adipose content. • Typically, there is an elevation in both primary and oncocytic cell types. Secondary fibrosis and hemorrhage are prevalent observations.
Prognosis: Excellent after subtotal parathyroidectomy.
Definition: An augmentation of parathyroid cell mass without an identifiable trigger.
Epidemiology • Rare, constituting around 20% of primary hyperparathyroidism. • Women are impacted more significantly than men, at a ratio of 3:1.
Aetiology • The majority of patients exhibit sporadic hyperplasia without a discernible etiology. • Approximately 20% of cases are attributed to family illness, predominantly Multiple Endocrine Neoplasia (MEN). 1.
Pathogenesis • Parathyroid hyperplasia results in excessive secretion of parathyroid hormone (PTH). Elevated PTH levels induce hypercalcemia via enhancing calcium absorption from the gastrointestinal tract and kidneys, as well as by augmenting osteoclastic activity in bone.
Presentation • individuals exhibit primary hyperparathyroidism, a biochemical illness characterized by hypercalcemia and an abnormally normal or elevated PTH level. • Numerous individuals are asymptomatic when this condition is identified accidentally. • Some individuals may exhibit nonspecific symptoms such as tiredness, nausea, constipation, polyuria, and arthralgia.
Macroscopy • All parathyroid glands exhibit hypertrophy, with weights exceeding 60 mg and dimensions surpassing 6 mm, but with variability among the glands.
Histopathology • The principal characteristic is an augmentation of cellular mass within the gland, correlated with a reduction in adipose content. • Typically, there is an elevation in both primary and oncocytic cell types. Secondary fibrosis and hemorrhage are prevalent observations.
Prognosis: Excellent after subtotal parathyroidectomy.
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Pathology - Parathyroid adenoma
A nonmalignant epithelial tumor of the parathyroid gland.
Epidemiology: Common, constituting approximately 80% of primary hyperparathyroidism. • Peak incidence occurs between the ages of 50 and 60 years. • Women are impacted more significantly than men, at a ratio of 3:1
Aetiology • The underlying causes are inadequately comprehended, however previous irradiation of the neck seems to elevate the risk. The pathogenesis involves the autonomous secretion of parathyroid hormone (PTH) from the adenoma, resulting in hypercalcemia due to uncontrolled calcium mobilization from the bone and increased calcium absorption in the kidneys and gastrointestinal tract.
Presentation • Patients exhibit primary hyperparathyroidism, characterized by hypercalcemia accompanied by an abnormally normal or elevated PTH level. • A multitude of patients are asymptomatic when this is identified inadvertently. • Some individuals may exhibit nonspecific symptoms such as tiredness, nausea, constipation, polyuria, and arthralgia.
Macroscopy: A solitary parathyroid gland exhibits enlargement, measuring over 6mm in size and over 60mg in weight. The adenoma is often smooth, firm, soft, and light brown in hue. Histopathology: The parathyroid gland exhibits a well-defined, often encapsulated mass comprised of parathyroid epithelial cells devoid of adipose tissue. A compressed rim of normal parathyroid tissue frequently exists at one margin. Chief cells typically dominate, however an interspersing of oncocytic cells is also occasionally observed. The cells might be organized into solid sheets, trabeculae, or follicles. Stromal edema, fibrosis, and hemorrhage are frequently observed.
Prognosis: Parathyroid adenomas are benign tumors that can be effectively treated with surgical removal.
A nonmalignant epithelial tumor of the parathyroid gland.
Epidemiology: Common, constituting approximately 80% of primary hyperparathyroidism. • Peak incidence occurs between the ages of 50 and 60 years. • Women are impacted more significantly than men, at a ratio of 3:1
Aetiology • The underlying causes are inadequately comprehended, however previous irradiation of the neck seems to elevate the risk. The pathogenesis involves the autonomous secretion of parathyroid hormone (PTH) from the adenoma, resulting in hypercalcemia due to uncontrolled calcium mobilization from the bone and increased calcium absorption in the kidneys and gastrointestinal tract.
Presentation • Patients exhibit primary hyperparathyroidism, characterized by hypercalcemia accompanied by an abnormally normal or elevated PTH level. • A multitude of patients are asymptomatic when this is identified inadvertently. • Some individuals may exhibit nonspecific symptoms such as tiredness, nausea, constipation, polyuria, and arthralgia.
Macroscopy: A solitary parathyroid gland exhibits enlargement, measuring over 6mm in size and over 60mg in weight. The adenoma is often smooth, firm, soft, and light brown in hue. Histopathology: The parathyroid gland exhibits a well-defined, often encapsulated mass comprised of parathyroid epithelial cells devoid of adipose tissue. A compressed rim of normal parathyroid tissue frequently exists at one margin. Chief cells typically dominate, however an interspersing of oncocytic cells is also occasionally observed. The cells might be organized into solid sheets, trabeculae, or follicles. Stromal edema, fibrosis, and hemorrhage are frequently observed.
Prognosis: Parathyroid adenomas are benign tumors that can be effectively treated with surgical removal.
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Pathology - Addison's disease
Definition: Primary adrenocortical insufficiency. Epidemiology • Uncommon, with an estimated annual incidence of 1 in 100,000 individuals. • The majority of instances occur in young to middle-aged adults. • Women are disproportionately impacted compared to men.
Etiology • Autoimmune degradation in industrialized nations. • Disseminated TB in underdeveloped nations. • Alternative etiologies, such as adrenal metastases, are infrequent.
Pathogenesis • Addison's disease results in a significant deficiency of glucocorticoid and mineralocorticoid synthesis by the adrenal cortex.
Clinical manifestations do not become apparent until approximately 90% of the gland has been obliterated.
Presentation: Fatigue, lethargy, and debilitation. • Anorexia, nausea, emesis, and diarrhea. • Weight loss may be significant.
The clinical appearance is frequently subtle and non-specific, complicating the diagnosis.
Biochemistry • Sodium and potassium levels. • Urea concentration resulting from dehydration. • As much as fifty percent of patients have hypoglycemia. • Circulating anti-adrenal autoantibodies are frequently observed. Diagnosis • Individuals suspected of having Addison’s disease should undergo dynamic adrenal cortex testing via a Synacthen test. This entails an intramuscular injection of synthetic adrenocorticotropic hormone (ACTH). The typical response is an elevation in plasma cortisol levels. In Addison's disease, there is either an absence of cortisol elevation or merely a negligible increase.
Prognosis: Favorable if diagnosis is established and lifetime replacement medication is initiated with synthetic glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone). It is essential for patients to comprehend the necessity of augmenting their hydrocortisone dosage throughout any concurrent illness. 3 Untreated or inadequately treated Addison's disease may lead to abrupt adrenal failure ('Addisonian crisis'), characterized by a perilous combination of hypovolemic shock, significant hypoglycemia, and hyponatremia
Definition: Primary adrenocortical insufficiency. Epidemiology • Uncommon, with an estimated annual incidence of 1 in 100,000 individuals. • The majority of instances occur in young to middle-aged adults. • Women are disproportionately impacted compared to men.
Etiology • Autoimmune degradation in industrialized nations. • Disseminated TB in underdeveloped nations. • Alternative etiologies, such as adrenal metastases, are infrequent.
Pathogenesis • Addison's disease results in a significant deficiency of glucocorticoid and mineralocorticoid synthesis by the adrenal cortex.
Clinical manifestations do not become apparent until approximately 90% of the gland has been obliterated.
Presentation: Fatigue, lethargy, and debilitation. • Anorexia, nausea, emesis, and diarrhea. • Weight loss may be significant.
The clinical appearance is frequently subtle and non-specific, complicating the diagnosis.
Biochemistry • Sodium and potassium levels. • Urea concentration resulting from dehydration. • As much as fifty percent of patients have hypoglycemia. • Circulating anti-adrenal autoantibodies are frequently observed. Diagnosis • Individuals suspected of having Addison’s disease should undergo dynamic adrenal cortex testing via a Synacthen test. This entails an intramuscular injection of synthetic adrenocorticotropic hormone (ACTH). The typical response is an elevation in plasma cortisol levels. In Addison's disease, there is either an absence of cortisol elevation or merely a negligible increase.
Prognosis: Favorable if diagnosis is established and lifetime replacement medication is initiated with synthetic glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone). It is essential for patients to comprehend the necessity of augmenting their hydrocortisone dosage throughout any concurrent illness. 3 Untreated or inadequately treated Addison's disease may lead to abrupt adrenal failure ('Addisonian crisis'), characterized by a perilous combination of hypovolemic shock, significant hypoglycemia, and hyponatremia
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Pathology - Neuroblastoma
Definition • A malignant pediatric tumor originating from neural crest-derived cells of the sympathetic nervous system. Most originate in the adrenal medulla or paraspinal sympathetic ganglia.
Epidemiology: The third most prevalent malignant neoplasm in pediatric populations. • Incidence of 1 in 10,000 live births annually. • Predominantly occur throughout the first four years of life.
Aetiology: Unknown. Genetics • Tumor genetics possess significant prognostic consequences. Amplification of MYCN, diploidy, and deletions on chromosome 1p are all correlated with a worse prognosis. Presentation • The majority of children exhibit symptoms of illness characterized by weight loss, fever, watery diarrhea, and a discernible abdominal mass. Biochemistry • Elevated urinary levels of catecholamines and their metabolites, vanillylmandelic acid (VMA) and homovanilic acid (HMA), serve as a significant diagnostic tool. Macroscopy • A lobulated, soft, gray tumor mass of approximately 6–8 cm, closely associated with the adrenal gland or sympathetic chain.
Histopathology • Neuroblastoma is classified into four categories based on the degree of development of primitive neuroblasts into ganglion cells. • Undifferentiated neuroblastoma consists of undifferentiated neuroblasts lacking any signs of ganglionic differentiation. They resemble several other 'small round blue cell tumors' of childhood, necessitating other procedures to confirm the diagnosis (e.g., antibody for brain markers such as CD56 and synaptophysin). Poorly differentiated neuroblastoma exhibits minimal ganglionic differentiation (<5% of cells) and comprises neurofibrillary stroma. • differentiated neuroblastoma numerous ganglionic cells (> 5%, but
Definition • A malignant pediatric tumor originating from neural crest-derived cells of the sympathetic nervous system. Most originate in the adrenal medulla or paraspinal sympathetic ganglia.
Epidemiology: The third most prevalent malignant neoplasm in pediatric populations. • Incidence of 1 in 10,000 live births annually. • Predominantly occur throughout the first four years of life.
Aetiology: Unknown. Genetics • Tumor genetics possess significant prognostic consequences. Amplification of MYCN, diploidy, and deletions on chromosome 1p are all correlated with a worse prognosis. Presentation • The majority of children exhibit symptoms of illness characterized by weight loss, fever, watery diarrhea, and a discernible abdominal mass. Biochemistry • Elevated urinary levels of catecholamines and their metabolites, vanillylmandelic acid (VMA) and homovanilic acid (HMA), serve as a significant diagnostic tool. Macroscopy • A lobulated, soft, gray tumor mass of approximately 6–8 cm, closely associated with the adrenal gland or sympathetic chain.
Histopathology • Neuroblastoma is classified into four categories based on the degree of development of primitive neuroblasts into ganglion cells. • Undifferentiated neuroblastoma consists of undifferentiated neuroblasts lacking any signs of ganglionic differentiation. They resemble several other 'small round blue cell tumors' of childhood, necessitating other procedures to confirm the diagnosis (e.g., antibody for brain markers such as CD56 and synaptophysin). Poorly differentiated neuroblastoma exhibits minimal ganglionic differentiation (<5% of cells) and comprises neurofibrillary stroma. • differentiated neuroblastoma numerous ganglionic cells (> 5%, but
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Pathology- Iron deficiency anemia
Definition: A decrease in hemoglobin (Hb) concentration resulting from insufficient iron availability.
Epidemiology The predominant etiology of anemia. Etiology Chronic gastrointestinal blood loss is the predominant etiology. • Globally, this is typically associated with hookworm infection. • Frequent causes in affluent nations encompass peptic ulcers, gastric cancer, sigmoid diverticular disease, and colorectal carcinoma. Excessive menstrual bleeding in women may result in iron deficiency. Gastrointestinal disorders that lead to iron malabsorption can result in iron deficiency, such as celiac disease. 1 Excluding a gastrointestinal tract malignancy is essential in any adult patient presenting with unexplained iron deficiency anemia. Pathogenesis Iron is a vital component of the heme group in hemoglobin. Chronic iron deficiency disrupts the final stage in heme production.
Presentation • May be asymptomatic and identified with routine complete blood count. • Symptoms encompass fatigue and dyspnea during activity. • Certain cases may present with additional manifestations such as koilonychia, angular cheilitis, and glossitis. Complete blood count • reduced Hemoglobin. • reduced Mean corpuscular volume (MCV). • Decreased serum ferritin, decreased serum iron, decreased transferrin saturation, increased total iron binding capacity (TIBC).
Peripheral blood smear • Microcytic red blood cells. • Hypochromic pale red cells. • Heterogeneity in erythrocyte dimensions (anisocytosis) and morphology (poikilocytosis). • Elongated elliptical red blood cells, commonly referred to as 'pencil cells,' are frequently observed.
Bone marrow
Mild to moderate erythroid hyperplasia. • Lack of detectable iron
Definition: A decrease in hemoglobin (Hb) concentration resulting from insufficient iron availability.
Epidemiology The predominant etiology of anemia. Etiology Chronic gastrointestinal blood loss is the predominant etiology. • Globally, this is typically associated with hookworm infection. • Frequent causes in affluent nations encompass peptic ulcers, gastric cancer, sigmoid diverticular disease, and colorectal carcinoma. Excessive menstrual bleeding in women may result in iron deficiency. Gastrointestinal disorders that lead to iron malabsorption can result in iron deficiency, such as celiac disease. 1 Excluding a gastrointestinal tract malignancy is essential in any adult patient presenting with unexplained iron deficiency anemia. Pathogenesis Iron is a vital component of the heme group in hemoglobin. Chronic iron deficiency disrupts the final stage in heme production.
Presentation • May be asymptomatic and identified with routine complete blood count. • Symptoms encompass fatigue and dyspnea during activity. • Certain cases may present with additional manifestations such as koilonychia, angular cheilitis, and glossitis. Complete blood count • reduced Hemoglobin. • reduced Mean corpuscular volume (MCV). • Decreased serum ferritin, decreased serum iron, decreased transferrin saturation, increased total iron binding capacity (TIBC).
Peripheral blood smear • Microcytic red blood cells. • Hypochromic pale red cells. • Heterogeneity in erythrocyte dimensions (anisocytosis) and morphology (poikilocytosis). • Elongated elliptical red blood cells, commonly referred to as 'pencil cells,' are frequently observed.
Bone marrow
Mild to moderate erythroid hyperplasia. • Lack of detectable iron
