- Published on
Pathology – Eczemas
Definition • A collection of inflammatory dermatoses clinically identified by an erythematous papulovesicular eruption and histologically defined by intraepidermal edema (spongiosis).
Atopic dermatitis • Chronic dermatitis prevalent in individuals with atopy. • A highly prevalent condition with incidence rates reaching up to 15%. • Generally manifests in newborns and children. • Clinically induces a pruritic erythematous papulovesicular eruption affecting the facial region and the extensor surfaces of the upper and lower limbs. Biopsies from acute lesions reveal epidermal spongiosis and dermal inflammation. Biopsies from subsequent lesions demonstrate epidermal thickening and hyperkeratosis accompanied by moderate spongiosis.
Contact dermatitis due to irritants • Inflammatory dermatosis induced by the direct toxic impact of an irritant. • A prevalent etiology of occupational dermatosis. • Clinically induces erythema accompanied by vesiculation. Biopsies reveal epidermal spongiosis and dermal inflammation.
Allergic contact dermatitis • Inflammatory dermatosis resulting from a delayed-type hypersensitivity response to an allergen to which the patient has been exposed. • A prevalent occupational dermatosis, notably documented among hairdressers. • Clinically induces pruritic papules and vesicles 12–48 hours post-exposure. • Frequent offenders comprise nickel, cosmetics, and edibles. Biopsies reveal epidermal spongiosis accompanied by vesicle development and an inflammatory infiltrate, typically including eosinophils.
Nummular dermatitis • Inflammatory dermatosis of indeterminate etiology. • Clinically presents as small papules and vesicles that merge into coin-shaped plaques. • Biopsies reveal epidermal spongiosis and inflammation in first lesions. Advanced lesions exhibit epidermal hyperplasia.
Seborrheic dermatitis • Prevalent inflammatory dermatological condition impacting 1–3% of the population. Evidence indicates it may stem from an atypical immunological response to Malassezia organisms, though this remains contentious. • Clinically presents with erythematous, scaly papules and plaques, occasionally exhibiting a greasy look, located on the scalp, ears, eyebrows, and nasolabial region. Biopsies reveal varied epidermal spongiosis and hyperplasia accompanied by overlaying parakeratosis centered on hair follicles.
Definition • A collection of inflammatory dermatoses clinically identified by an erythematous papulovesicular eruption and histologically defined by intraepidermal edema (spongiosis).
Atopic dermatitis • Chronic dermatitis prevalent in individuals with atopy. • A highly prevalent condition with incidence rates reaching up to 15%. • Generally manifests in newborns and children. • Clinically induces a pruritic erythematous papulovesicular eruption affecting the facial region and the extensor surfaces of the upper and lower limbs. Biopsies from acute lesions reveal epidermal spongiosis and dermal inflammation. Biopsies from subsequent lesions demonstrate epidermal thickening and hyperkeratosis accompanied by moderate spongiosis.
Contact dermatitis due to irritants • Inflammatory dermatosis induced by the direct toxic impact of an irritant. • A prevalent etiology of occupational dermatosis. • Clinically induces erythema accompanied by vesiculation. Biopsies reveal epidermal spongiosis and dermal inflammation.
Allergic contact dermatitis • Inflammatory dermatosis resulting from a delayed-type hypersensitivity response to an allergen to which the patient has been exposed. • A prevalent occupational dermatosis, notably documented among hairdressers. • Clinically induces pruritic papules and vesicles 12–48 hours post-exposure. • Frequent offenders comprise nickel, cosmetics, and edibles. Biopsies reveal epidermal spongiosis accompanied by vesicle development and an inflammatory infiltrate, typically including eosinophils.
Nummular dermatitis • Inflammatory dermatosis of indeterminate etiology. • Clinically presents as small papules and vesicles that merge into coin-shaped plaques. • Biopsies reveal epidermal spongiosis and inflammation in first lesions. Advanced lesions exhibit epidermal hyperplasia.
Seborrheic dermatitis • Prevalent inflammatory dermatological condition impacting 1–3% of the population. Evidence indicates it may stem from an atypical immunological response to Malassezia organisms, though this remains contentious. • Clinically presents with erythematous, scaly papules and plaques, occasionally exhibiting a greasy look, located on the scalp, ears, eyebrows, and nasolabial region. Biopsies reveal varied epidermal spongiosis and hyperplasia accompanied by overlaying parakeratosis centered on hair follicles.
- Published on
Pathology - Primary amyloidosis
Definition: A plasma cell neoplasm characterized by the accumulation of AL amyloid in several tissues.
Epidemiology • Uncommon ailment. The median age at diagnosis is 65 years, with a predominance of males.
Aetiology The majority of patients possess an underlying plasma cell neoplasm yet do not fulfill the diagnostic criteria for plasma cell myeloma. Pathogenesis • AL amyloid consists of immunoglobulin light chains produced by monoclonal plasma cells, which aggregate in diverse tissues in a β-pleated sheet configuration. • The deposited amyloid comprises both intact light chains and fragments of the variable NH2-terminal region.
Presentation • Clinical manifestations associated with amyloid accumulation in several organs. Commonly affected areas encompass the skin, kidneys, heart, liver, intestines, and peripheral nerves. Characteristic manifestations include purpura, peripheral neuropathy, cardiac insufficiency, nephrotic syndrome, and malabsorption.
Histopathology • Amyloid can be identified in several tissues as a pink, amorphous material. The Congo Amyloid exhibits red staining under ordinary light microscopy and 'apple green' under polarized light. Bone marrow biopsies generally reveal a little elevation in plasma cells, which may present as either normal or abnormal. The plasma cells exhibit monotypism for either kappa or lambda light chains.
Prognosis: • Dismal prognosis with a median survival of merely 2 years from diagnosis. The predominant cause of mortality is amyloid-related heart failure.
Definition: A plasma cell neoplasm characterized by the accumulation of AL amyloid in several tissues.
Epidemiology • Uncommon ailment. The median age at diagnosis is 65 years, with a predominance of males.
Aetiology The majority of patients possess an underlying plasma cell neoplasm yet do not fulfill the diagnostic criteria for plasma cell myeloma. Pathogenesis • AL amyloid consists of immunoglobulin light chains produced by monoclonal plasma cells, which aggregate in diverse tissues in a β-pleated sheet configuration. • The deposited amyloid comprises both intact light chains and fragments of the variable NH2-terminal region.
Presentation • Clinical manifestations associated with amyloid accumulation in several organs. Commonly affected areas encompass the skin, kidneys, heart, liver, intestines, and peripheral nerves. Characteristic manifestations include purpura, peripheral neuropathy, cardiac insufficiency, nephrotic syndrome, and malabsorption.
Histopathology • Amyloid can be identified in several tissues as a pink, amorphous material. The Congo Amyloid exhibits red staining under ordinary light microscopy and 'apple green' under polarized light. Bone marrow biopsies generally reveal a little elevation in plasma cells, which may present as either normal or abnormal. The plasma cells exhibit monotypism for either kappa or lambda light chains.
Prognosis: • Dismal prognosis with a median survival of merely 2 years from diagnosis. The predominant cause of mortality is amyloid-related heart failure.
- Published on
Pathology - Plasma cell myeloma
Definition: A diffuse neoplasm of plasma cells originating from bone marrow, characterized by the presence of paraproteins in serum and/or urine.
Epidemiology • Incidence ranges from 3 to 5 per 100,000 individuals. •
Manifestations are observed in older persons, with a mean diagnostic age of 70 years. • There is a masculine predominance of 1.5:1.
Aetiology • Unidentified.
Pathogenesis The neoplastic plasma cells produce cytokines that activate osteoclasts, resulting in lytic bone lesions. Circulating paraprotein inhibits normal immunoglobulin synthesis, hence elevating the susceptibility to infections. Free light chains traversing the kidneys contribute to renal failure.
Presentation: • Ostealgia and recurring infections. • Anemia, elevated ESR, hypercalcemia, and renal dysfunction are prevalent.
Histopathology A definitive diagnosis necessitates a bone marrow biopsy. • The bone marrow exhibits an abundance of monoclonal plasma cells organized in clusters, nodules, or sheets. • Clonality can be confirmed immunohistochemically by demonstrating kappa or lambda light chain restriction.
Prognosis • Myeloma is an incurable condition. • Average survival is 3–4 years post-diagnosis.
Definition: A diffuse neoplasm of plasma cells originating from bone marrow, characterized by the presence of paraproteins in serum and/or urine.
Epidemiology • Incidence ranges from 3 to 5 per 100,000 individuals. •
Manifestations are observed in older persons, with a mean diagnostic age of 70 years. • There is a masculine predominance of 1.5:1.
Aetiology • Unidentified.
Pathogenesis The neoplastic plasma cells produce cytokines that activate osteoclasts, resulting in lytic bone lesions. Circulating paraprotein inhibits normal immunoglobulin synthesis, hence elevating the susceptibility to infections. Free light chains traversing the kidneys contribute to renal failure.
Presentation: • Ostealgia and recurring infections. • Anemia, elevated ESR, hypercalcemia, and renal dysfunction are prevalent.
Histopathology A definitive diagnosis necessitates a bone marrow biopsy. • The bone marrow exhibits an abundance of monoclonal plasma cells organized in clusters, nodules, or sheets. • Clonality can be confirmed immunohistochemically by demonstrating kappa or lambda light chain restriction.
Prognosis • Myeloma is an incurable condition. • Average survival is 3–4 years post-diagnosis.
- Published on
Pathology - Mantle cell lymphoma
A mature B-cell neoplasm characterized by monomorphic, small to medium-sized lymphoid cells exhibiting uneven nuclear outlines and a CCND1 translocation.
Epidemiology • Constitutes 3–10% of all non-Hodgkin B-cell lymphomas. • Primarily occurs in adults, with a mean age of 60 years.
Aetiology: Unknown. Genetics • Nearly all instances exhibit a t(11;14) translocation involving the CCND1 (cyclin D1) and IGH genes. Deregulated expression of cyclin D1 leads to unrestrained proliferation of lymphoid cells.
Presentation: The majority of individuals exhibit lymph node involvement. The liver, spleen, bone marrow, or peripheral blood may also be affected. Extranodal areas, especially the gastrointestinal tract, may also be involved. Histopathology • Affected tissues are substituted by sheets of monomorphic, tiny to medium-sized lymphoid cells exhibiting irregular nuclear contours. • Hyalinized small blood arteries and dispersed epithelioid histiocytes are frequently observed. Immunophenotype: B-cell markers PAX5, CD20, and CD79a exhibit positivity. • CD5 and cyclin D1 exhibit positivity. • CD23 and CD10 are often negative.
Prognosis • Despite its unremarkable look, the prognosis is typically unfavorable, with a median survival of merely 3–5 years.
A mature B-cell neoplasm characterized by monomorphic, small to medium-sized lymphoid cells exhibiting uneven nuclear outlines and a CCND1 translocation.
Epidemiology • Constitutes 3–10% of all non-Hodgkin B-cell lymphomas. • Primarily occurs in adults, with a mean age of 60 years.
Aetiology: Unknown. Genetics • Nearly all instances exhibit a t(11;14) translocation involving the CCND1 (cyclin D1) and IGH genes. Deregulated expression of cyclin D1 leads to unrestrained proliferation of lymphoid cells.
Presentation: The majority of individuals exhibit lymph node involvement. The liver, spleen, bone marrow, or peripheral blood may also be affected. Extranodal areas, especially the gastrointestinal tract, may also be involved. Histopathology • Affected tissues are substituted by sheets of monomorphic, tiny to medium-sized lymphoid cells exhibiting irregular nuclear contours. • Hyalinized small blood arteries and dispersed epithelioid histiocytes are frequently observed. Immunophenotype: B-cell markers PAX5, CD20, and CD79a exhibit positivity. • CD5 and cyclin D1 exhibit positivity. • CD23 and CD10 are often negative.
Prognosis • Despite its unremarkable look, the prognosis is typically unfavorable, with a median survival of merely 3–5 years.
- Published on
Pathology - Classical Hodgkin lymphoma
A lymphoid tumor characterized by dysfunctional neoplastic B-cells, referred to as Hodgkin/Reed Sternberg (HRS) cells, situated amid a dense non-neoplastic inflammatory milieu.
Epidemiology • Bimodal age distribution, characterized by a high incidence between 15 and 35 years, and a secondary peak in later life. • Males are predominantly affected, except in the case of the nodular sclerosis variation, which exhibits equal incidence across genders.
Aetiology • Unknown; although, Epstein-Barr virus (EBV) infection has been associated with certain kinds.
Presentation • The majority of patients have localized lymphadenopathy. • Fever, nocturnal diaphoresis, and weight loss are prevalent (referred to as 'B symptoms').
Histopathology • Lymph nodes are infiltrated by varying quantities of neoplastic HRS cells amid a robust inflammatory milieu
The standard diagnosis The Reed-Sternberg cell is a substantial cell characterized by two prominent nuclei, each containing distinct eosinophilic nucleoli. Four histological subtypes are identified based on the quantity and characteristics of the HRS cells and the reactive background: nodular sclerosis, mixed cellularity, lymphocyte-rich, and lymphocyte-depleted. The immunophenotype of HRS cells is characterized by positivity for CD15 and negativity for CD30, exhibiting a distinctive membranous and Golgi staining pattern. PAX5 and MUM-1 are invariably positive in HRS cells, but CD20 and CD79a are typically negative or expressed at low levels.
Prognosis: Contemporary treatment protocols provide a cure rate over 85% for classical Hodgkin lymphoma. Nodular lymphocyte-predominant Hodgkin lymphoma Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is acknowledged as a unique subtype of Hodgkin lymphoma. NLPHL constitutes 75% of all Hodgkin lymphomas. It generally occurs in young to middle-aged adults between the ages of 30 and 50. The atypical B-cells, referred to as lymphocyte-predominant cells, are immunophenotypically differentiated from classical HRS cells; they generally do not express CD30 and CD15, while exhibiting significant expression of CD20 and EMA. The disease progresses slowly and is seldom lethal.
A lymphoid tumor characterized by dysfunctional neoplastic B-cells, referred to as Hodgkin/Reed Sternberg (HRS) cells, situated amid a dense non-neoplastic inflammatory milieu.
Epidemiology • Bimodal age distribution, characterized by a high incidence between 15 and 35 years, and a secondary peak in later life. • Males are predominantly affected, except in the case of the nodular sclerosis variation, which exhibits equal incidence across genders.
Aetiology • Unknown; although, Epstein-Barr virus (EBV) infection has been associated with certain kinds.
Presentation • The majority of patients have localized lymphadenopathy. • Fever, nocturnal diaphoresis, and weight loss are prevalent (referred to as 'B symptoms').
Histopathology • Lymph nodes are infiltrated by varying quantities of neoplastic HRS cells amid a robust inflammatory milieu
The standard diagnosis The Reed-Sternberg cell is a substantial cell characterized by two prominent nuclei, each containing distinct eosinophilic nucleoli. Four histological subtypes are identified based on the quantity and characteristics of the HRS cells and the reactive background: nodular sclerosis, mixed cellularity, lymphocyte-rich, and lymphocyte-depleted. The immunophenotype of HRS cells is characterized by positivity for CD15 and negativity for CD30, exhibiting a distinctive membranous and Golgi staining pattern. PAX5 and MUM-1 are invariably positive in HRS cells, but CD20 and CD79a are typically negative or expressed at low levels.
Prognosis: Contemporary treatment protocols provide a cure rate over 85% for classical Hodgkin lymphoma. Nodular lymphocyte-predominant Hodgkin lymphoma Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is acknowledged as a unique subtype of Hodgkin lymphoma. NLPHL constitutes 75% of all Hodgkin lymphomas. It generally occurs in young to middle-aged adults between the ages of 30 and 50. The atypical B-cells, referred to as lymphocyte-predominant cells, are immunophenotypically differentiated from classical HRS cells; they generally do not express CD30 and CD15, while exhibiting significant expression of CD20 and EMA. The disease progresses slowly and is seldom lethal.
- Published on
Pathology - Lichen planus
Definition • An inflammatory dermatosis characterized by pruritic purple papules clinically and a lichenoid response pattern histologically.
Epidemiology • Affects around 1% of the population. • Typically occurs in middle-aged people, with a slight prevalence in females. Aetiology: Unknown. Pathogenesis • Believed to signify a delayed-type hypersensitivity response to an unidentified epidermal antigen.
Presentation • The cutaneous lesions are diminutive, flat-topped, violaceous papules that are typically associated with acute pruritus. • Delicate white lines (Wickham’s striae) typically traverse the surface. • The lesions predominantly manifest on the flexor surfaces of the wrists, the extensor surfaces of the hands, and the forearms. • Oral involvement is prevalent (see p. 86), as are genital lesionsespecially in males.
Histopathology • A substantial band-like inflammatory infiltrate comprising lymphocytes and macrophages is observed beneath the epidermis. • The basal layer of the epidermis exhibits vacuolar damage accompanied by cytoid body formation and melanin leakage. • The epidermis demonstrates irregular acanthosis, hyperkeratosis, and wedge-shaped hypergranulosis.
Prognosis: In the majority of instances, the condition resolves autonomously over a variable duration ranging from weeks to one year.
Definition • An inflammatory dermatosis characterized by pruritic purple papules clinically and a lichenoid response pattern histologically.
Epidemiology • Affects around 1% of the population. • Typically occurs in middle-aged people, with a slight prevalence in females. Aetiology: Unknown. Pathogenesis • Believed to signify a delayed-type hypersensitivity response to an unidentified epidermal antigen.
Presentation • The cutaneous lesions are diminutive, flat-topped, violaceous papules that are typically associated with acute pruritus. • Delicate white lines (Wickham’s striae) typically traverse the surface. • The lesions predominantly manifest on the flexor surfaces of the wrists, the extensor surfaces of the hands, and the forearms. • Oral involvement is prevalent (see p. 86), as are genital lesionsespecially in males.
Histopathology • A substantial band-like inflammatory infiltrate comprising lymphocytes and macrophages is observed beneath the epidermis. • The basal layer of the epidermis exhibits vacuolar damage accompanied by cytoid body formation and melanin leakage. • The epidermis demonstrates irregular acanthosis, hyperkeratosis, and wedge-shaped hypergranulosis.
Prognosis: In the majority of instances, the condition resolves autonomously over a variable duration ranging from weeks to one year.
- Published on
Pathology - Extranodal marginal zone lymphoma
Definition: An extranodal mature B-cell neoplasm primarily consisting of tiny neoplastic marginal zone cells.
Epidemiology • Constitutes 7–8% of all non-Hodgkin B-cell lymphomas. • Primarily occurs in adults with a mean age of 60. Locations of engagement • The gastrointestinal system constitutes 50% of all instances, with the stomach as the predominant site. • Additional locations encompass the lung, salivary gland, skin, thyroid, and breast.
Etiology • Gastric instances are generally linked to Helicobacter pylori. • Additional implicated species comprise Campylobacter jejuni (jejunum) and Borrelia burgdorferi (skin). • Autoimmune illnesses are also linked, such as Hashimoto’s thyroiditis (thyroid) and Sjögren’s syndrome (salivary gland). Pathogenesis • The majority of cases are preceded by a chronic inflammatory condition that results in the accumulation of extranodal lymphoid tissue. • Extended stimulation of lymphoid proliferation ultimately culminates in the transition into a neoplastic process.
Presentation • Symptoms associated with a mass at the affected location.
Histopathology • Affected tissues comprise a diverse assemblage of small neoplastic B-cells that encircle and may infiltrate the underlying reactive lymphoid follicles. • The cellular composition includes marginal zone cells, monocytoid-like cells, small lymphocytes, and dispersed immunoblasts and centroblast-like cells. • In epithelial-lined tissues, the neoplastic lymphoid cells generally infiltrate and obliterate the epithelium, resulting in lymphoepithelial lesions. Immunophenotype: B-cell markers PAX5, CD20, and CD79a are expressed positively. CD5, CD10, CD23, and cyclin D1 are all absent.
Prognosis: Exhibits indolent behavior with extended periods of disease-free remission post-treatment.
Definition: An extranodal mature B-cell neoplasm primarily consisting of tiny neoplastic marginal zone cells.
Epidemiology • Constitutes 7–8% of all non-Hodgkin B-cell lymphomas. • Primarily occurs in adults with a mean age of 60. Locations of engagement • The gastrointestinal system constitutes 50% of all instances, with the stomach as the predominant site. • Additional locations encompass the lung, salivary gland, skin, thyroid, and breast.
Etiology • Gastric instances are generally linked to Helicobacter pylori. • Additional implicated species comprise Campylobacter jejuni (jejunum) and Borrelia burgdorferi (skin). • Autoimmune illnesses are also linked, such as Hashimoto’s thyroiditis (thyroid) and Sjögren’s syndrome (salivary gland). Pathogenesis • The majority of cases are preceded by a chronic inflammatory condition that results in the accumulation of extranodal lymphoid tissue. • Extended stimulation of lymphoid proliferation ultimately culminates in the transition into a neoplastic process.
Presentation • Symptoms associated with a mass at the affected location.
Histopathology • Affected tissues comprise a diverse assemblage of small neoplastic B-cells that encircle and may infiltrate the underlying reactive lymphoid follicles. • The cellular composition includes marginal zone cells, monocytoid-like cells, small lymphocytes, and dispersed immunoblasts and centroblast-like cells. • In epithelial-lined tissues, the neoplastic lymphoid cells generally infiltrate and obliterate the epithelium, resulting in lymphoepithelial lesions. Immunophenotype: B-cell markers PAX5, CD20, and CD79a are expressed positively. CD5, CD10, CD23, and cyclin D1 are all absent.
Prognosis: Exhibits indolent behavior with extended periods of disease-free remission post-treatment.
- Published on
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.
- Published on
Pathology - Parathyroid carcinoma
Definition: A malignant epithelial neoplasm originating from the parathyroid gland.
Epidemiology: Rare, constituting around 1% of primary hyperparathyroidism cases. • The majority manifest in individuals in their 40s and 50s, exhibiting no gender preference.
Aetiology • The cause remains unidentified, however anecdotal evidence suggests a connection with secondary hyperparathyroidism and previous neck irradiation. • Parathyroid cancer has not been associated with MEN 1.
Carcinogenesis • The most commonly observed aberration is the loss of genetic material at chromosome 13q.
Presentation • In contrast to individuals with parathyroid hyperplasia or adenoma, patients typically exhibit symptomatic primary hyperparathyroidism accompanied by a discernible neck mass. • Calcium concentrations are typically elevated (3.5–4mmol/L), accompanied by symptoms such as polyuria, polydipsia, weakness, renal colic, and ostealgia. Macroscopy: Parathyroid carcinomas are typically significantly larger than adenomas, averaging a weight of 12g. • They may exhibit well-defined margins or possess distinctly infiltrative borders.
Histopathology: Parathyroid carcinomas consist of sheets of epithelial cells that frequently appear deceptively benign. The development of follicles is atypical. • Tumors frequently possess a robust capsule and are interspersed with dense fibrous tissue bands that partition the tumor into several expansive nodules. • Capsular invasion, vascular invasion, tumor necrosis, and an elevated mitotic index are all strongly indicative of malignancy.
Prognosis • The 10-year survival rate is around 50%. • The majority of patients succumb to the unmanageable metabolic consequences of severe hyperparathyroidism caused by recurrent tumors.
Definition: A malignant epithelial neoplasm originating from the parathyroid gland.
Epidemiology: Rare, constituting around 1% of primary hyperparathyroidism cases. • The majority manifest in individuals in their 40s and 50s, exhibiting no gender preference.
Aetiology • The cause remains unidentified, however anecdotal evidence suggests a connection with secondary hyperparathyroidism and previous neck irradiation. • Parathyroid cancer has not been associated with MEN 1.
Carcinogenesis • The most commonly observed aberration is the loss of genetic material at chromosome 13q.
Presentation • In contrast to individuals with parathyroid hyperplasia or adenoma, patients typically exhibit symptomatic primary hyperparathyroidism accompanied by a discernible neck mass. • Calcium concentrations are typically elevated (3.5–4mmol/L), accompanied by symptoms such as polyuria, polydipsia, weakness, renal colic, and ostealgia. Macroscopy: Parathyroid carcinomas are typically significantly larger than adenomas, averaging a weight of 12g. • They may exhibit well-defined margins or possess distinctly infiltrative borders.
Histopathology: Parathyroid carcinomas consist of sheets of epithelial cells that frequently appear deceptively benign. The development of follicles is atypical. • Tumors frequently possess a robust capsule and are interspersed with dense fibrous tissue bands that partition the tumor into several expansive nodules. • Capsular invasion, vascular invasion, tumor necrosis, and an elevated mitotic index are all strongly indicative of malignancy.
Prognosis • The 10-year survival rate is around 50%. • The majority of patients succumb to the unmanageable metabolic consequences of severe hyperparathyroidism caused by recurrent tumors.
- Published on
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.