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Pathology - Follicular lymphoma
Definition: A mature B-cell neoplasm consisting of germinal center cells (centrocytes and centroblasts).
Epidemiology • Represents approximately 20% of all non-Hodgkin lymphomas. • Primarily impacts individuals aged 50 to 60.
Aetiology: Unknown. Genetics: 90% of cases exhibit a distinctive t(14;18) translocation, leading to the fusion of the BCL2 gene with the IGH locus. Deregulated synthesis of the anti-apoptotic Bcl-2 protein leads to clonal proliferation.
Presentation: Extensive lymphadenopathy and splenomegaly. • Patients are often asymptomatic.
Histopathology Nodal architecture is supplanted by contiguous neoplastic follicles. Neoplastic follicles are devoid of mantle zones and consist of haphazardly arranged neoplastic centroblasts and centrocytes. Tangible body macrophages are typically lacking. • Neoplastic cells typically exhibit interfollicular dissemination. Bone marrow involvement is defined by paratrabecular clusters of malignant centrocytes and centroblasts. Immunophenotype PAX5, CD20, and CD79a, which are B-cell markers, exhibit positivity. Bcl-2, Bcl-6, and CD10 are furthermore positive. • CD5, CD23, and cyclin D1 are absent.
Prognosis is contingent upon the severity of the disease and the grade of the tumor. Approximately 25% progression into a high-grade lymphoma, typically diffuse large B-cell lymphoma, correlating with a swift clinical deterioration and mortality.
Definition: A mature B-cell neoplasm consisting of germinal center cells (centrocytes and centroblasts).
Epidemiology • Represents approximately 20% of all non-Hodgkin lymphomas. • Primarily impacts individuals aged 50 to 60.
Aetiology: Unknown. Genetics: 90% of cases exhibit a distinctive t(14;18) translocation, leading to the fusion of the BCL2 gene with the IGH locus. Deregulated synthesis of the anti-apoptotic Bcl-2 protein leads to clonal proliferation.
Presentation: Extensive lymphadenopathy and splenomegaly. • Patients are often asymptomatic.
Histopathology Nodal architecture is supplanted by contiguous neoplastic follicles. Neoplastic follicles are devoid of mantle zones and consist of haphazardly arranged neoplastic centroblasts and centrocytes. Tangible body macrophages are typically lacking. • Neoplastic cells typically exhibit interfollicular dissemination. Bone marrow involvement is defined by paratrabecular clusters of malignant centrocytes and centroblasts. Immunophenotype PAX5, CD20, and CD79a, which are B-cell markers, exhibit positivity. Bcl-2, Bcl-6, and CD10 are furthermore positive. • CD5, CD23, and cyclin D1 are absent.
Prognosis is contingent upon the severity of the disease and the grade of the tumor. Approximately 25% progression into a high-grade lymphoma, typically diffuse large B-cell lymphoma, correlating with a swift clinical deterioration and mortality.
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Pathology - Phaeochromocytoma
A neoplasm originating from the chromaffin cells of the adrenal medulla.
Epidemiology: Rare, having a yearly incidence of 8 per million. Aetiology • The majority are irregular. Approximately 10% are linked to hereditary illnesses, including MEN 2, neurofibromatosis type 1, and von Hippel–Lindau disease. Hereditary tumors are more prone to manifest at a younger age and exhibit bilateral occurrence. Genetics • Sporadic tumors exhibit a significant prevalence of 1p loss of heterozygosity.
Presentation • Patients experience sudden episodes of pulsating headaches, diaphoresis, palpitations, thoracic pain, and abdominal discomfort resulting from elevated circulating catecholamines produced by the tumor. • Hypertension is frequently observed
Elevated urine catecholamines and their metabolites serve as a significant diagnostic tool.
Macroscopy • A well-defined tumor exhibiting a firm grey cut surface. • Average dimensions of 6 cm and a mass of 200 g.
Histopathology • Tumor cells exhibit distinctive clusters ('zellballen') interspersed with a fine vascular network. • The cells are polygonal, possessing granular basophilic cytoplasm. • Nuclei display a peculiar stippled chromatin pattern. • Scattered pleomorphic nuclei may be observed.
Prognosis • 90% exhibit a benign behavior. • Regrettably, histological analysis is not dependable in forecasting the 10% that may be malignant; however, concerning indicators include invasive development, necrosis, and elevated mitotic activity.
A neoplasm originating from the chromaffin cells of the adrenal medulla.
Epidemiology: Rare, having a yearly incidence of 8 per million. Aetiology • The majority are irregular. Approximately 10% are linked to hereditary illnesses, including MEN 2, neurofibromatosis type 1, and von Hippel–Lindau disease. Hereditary tumors are more prone to manifest at a younger age and exhibit bilateral occurrence. Genetics • Sporadic tumors exhibit a significant prevalence of 1p loss of heterozygosity.
Presentation • Patients experience sudden episodes of pulsating headaches, diaphoresis, palpitations, thoracic pain, and abdominal discomfort resulting from elevated circulating catecholamines produced by the tumor. • Hypertension is frequently observed
Elevated urine catecholamines and their metabolites serve as a significant diagnostic tool.
Macroscopy • A well-defined tumor exhibiting a firm grey cut surface. • Average dimensions of 6 cm and a mass of 200 g.
Histopathology • Tumor cells exhibit distinctive clusters ('zellballen') interspersed with a fine vascular network. • The cells are polygonal, possessing granular basophilic cytoplasm. • Nuclei display a peculiar stippled chromatin pattern. • Scattered pleomorphic nuclei may be observed.
Prognosis • 90% exhibit a benign behavior. • Regrettably, histological analysis is not dependable in forecasting the 10% that may be malignant; however, concerning indicators include invasive development, necrosis, and elevated mitotic activity.
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Pathology - Adrenal cortical adenoma
A nonmalignant epithelial tumor of the adrenal cortex. Epidemiology: The majority of instances manifest in adults, exhibiting no gender preference. The actual incidence figures remain unknown, mostly due to the difficulty in differentiating nodular adrenal hyperplasia from genuine neoplastic adenomas.
Aetiology • Predominantly unidentified in the majority of instances. Genetics • No consistent genetic anomalies have been identified. Presentation • The majority of non-functional tumors are identified accidentally during abdominal imaging conducted for unrelated purposes. Aldosterone-producing adenomas manifest as primary hyperaldosteronism (Conn’s syndrome), which is characterized by hypertension and, in certain patients, hypokalaemia. Cortisol-secreting adenomas manifest as Cushing's syndrome.
Macroscopy • The adrenal gland exhibits a well-defined tumor that may be encapsulated. The median tumor weight is 40 grams. Aldosterone-producing adenomas may exhibit a brilliant yellow coloration, whereas those linked to Cushing’s syndrome may range from yellow to tan. A limited quantity of adenomas exhibit a black coloration, referred to as 'black adenoma.'
Histopathology: The tumors consist of massive polygonal cells organized in nests and trabeculae, interspersed with a delicate vascular network. The cells have cytoplasm that is either transparent and microvesicular or dense and eosinophilic. The nuclei are typically spherical to oval in shape and generally have a bland appearance. • At times, pronounced nuclear pleomorphism may be observed; nevertheless, this does not imply malignant behavior. A compressed ring of normal adrenal cortex may be observed at the periphery.
Prognosis: Adrenal cortical adenomas are benign tumors that lack the potential for malignant behavior. The prognosis is mostly influenced by the severity of the endocrine effects of functional tumors.
Pathological staging of adrenal cortical carcinoma Primary tumour (T)
pT1: tumour 5cm or less in size, localized.
pT2: tumour > 5cm, localized.
pT3: tumour of any size, locally invasive, but not involving adjacent organs.
pT4: tumour of any size, involving adjacent organs.
Regional lymph nodes (N)
N0: no regional lymph node metastasis.
N1: regional lymph node metastasis
A nonmalignant epithelial tumor of the adrenal cortex. Epidemiology: The majority of instances manifest in adults, exhibiting no gender preference. The actual incidence figures remain unknown, mostly due to the difficulty in differentiating nodular adrenal hyperplasia from genuine neoplastic adenomas.
Aetiology • Predominantly unidentified in the majority of instances. Genetics • No consistent genetic anomalies have been identified. Presentation • The majority of non-functional tumors are identified accidentally during abdominal imaging conducted for unrelated purposes. Aldosterone-producing adenomas manifest as primary hyperaldosteronism (Conn’s syndrome), which is characterized by hypertension and, in certain patients, hypokalaemia. Cortisol-secreting adenomas manifest as Cushing's syndrome.
Macroscopy • The adrenal gland exhibits a well-defined tumor that may be encapsulated. The median tumor weight is 40 grams. Aldosterone-producing adenomas may exhibit a brilliant yellow coloration, whereas those linked to Cushing’s syndrome may range from yellow to tan. A limited quantity of adenomas exhibit a black coloration, referred to as 'black adenoma.'
Histopathology: The tumors consist of massive polygonal cells organized in nests and trabeculae, interspersed with a delicate vascular network. The cells have cytoplasm that is either transparent and microvesicular or dense and eosinophilic. The nuclei are typically spherical to oval in shape and generally have a bland appearance. • At times, pronounced nuclear pleomorphism may be observed; nevertheless, this does not imply malignant behavior. A compressed ring of normal adrenal cortex may be observed at the periphery.
Prognosis: Adrenal cortical adenomas are benign tumors that lack the potential for malignant behavior. The prognosis is mostly influenced by the severity of the endocrine effects of functional tumors.
Pathological staging of adrenal cortical carcinoma Primary tumour (T)
pT1: tumour 5cm or less in size, localized.
pT2: tumour > 5cm, localized.
pT3: tumour of any size, locally invasive, but not involving adjacent organs.
pT4: tumour of any size, involving adjacent organs.
Regional lymph nodes (N)
N0: no regional lymph node metastasis.
N1: regional lymph node metastasis
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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 - 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 - 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.
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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 - Diabetes mellitus
Definition • A metabolic condition characterized by persistent hyperglycemia resulting from insufficient insulin production.
Epidemiology • Highly prevalent, impacting approximately 2% of the population. • Increasing in prevalence.
Etiology Type 1 diabetes results from the autoimmune death of insulin-secreting beta cells by CD4+ and CD8+ T lymphocytes. Autoantibodies targeting beta cells and insulin may potentially be pertinent. Type 2 diabetes is closely associated with obesity and insulin resistance. Initially, the pancreas compensates for insulin resistance by augmenting insulin production; however, beta cells ultimately experience 'secretory exhaustion,' resulting in abnormally low insulin levels.
Pathogenesis
The absence of insulin induces the release of energy reserves from muscle, adipose tissue, and the liver
• Glucose accumulates in the bloodstream, resulting in hyperglycemia. • In the kidneys, the glucose reabsorption process reaches saturation, resulting in the presence of glucose in the urine. Glucose in renal tubules induces water reabsorption through osmosis, resulting in osmotic diuresis. The elevated plasma osmolality activates the thirst center. Diabetes progressively harms capillaries and significantly increases atherosclerosis.
Presentation: Polyuria and polydipsia are the hallmark symptoms of diabetes mellitus. Hyperglycemia also predisposes individuals to recurrent dermatological and urinary tract infections. Type 1 diabetics may acutely manifest with diabetic ketoacidosis. Biochemistry: Fasting plasma glucose exceeding 7.0 mmol/L or random plasma glucose above 11.1 mmol/L. Patients exhibiting borderline readings should undergo an oral glucose tolerance test.
Complications A variety of organ systems are jeopardized in diabetes
• Ischemic heart disease resulting from advanced coronary artery atherosclerosis. • Chronic kidney disease resulting from diabetic nephropathy• Vision impairment resulting from cataract development and diabetic retinopathy. • Peripheral vascular disease resulting from atherosclerosis. • Foot ulceration resulting from peripheral neuropathy and ischemia
Definition • A metabolic condition characterized by persistent hyperglycemia resulting from insufficient insulin production.
Epidemiology • Highly prevalent, impacting approximately 2% of the population. • Increasing in prevalence.
Etiology Type 1 diabetes results from the autoimmune death of insulin-secreting beta cells by CD4+ and CD8+ T lymphocytes. Autoantibodies targeting beta cells and insulin may potentially be pertinent. Type 2 diabetes is closely associated with obesity and insulin resistance. Initially, the pancreas compensates for insulin resistance by augmenting insulin production; however, beta cells ultimately experience 'secretory exhaustion,' resulting in abnormally low insulin levels.
Pathogenesis
The absence of insulin induces the release of energy reserves from muscle, adipose tissue, and the liver
• Glucose accumulates in the bloodstream, resulting in hyperglycemia. • In the kidneys, the glucose reabsorption process reaches saturation, resulting in the presence of glucose in the urine. Glucose in renal tubules induces water reabsorption through osmosis, resulting in osmotic diuresis. The elevated plasma osmolality activates the thirst center. Diabetes progressively harms capillaries and significantly increases atherosclerosis.
Presentation: Polyuria and polydipsia are the hallmark symptoms of diabetes mellitus. Hyperglycemia also predisposes individuals to recurrent dermatological and urinary tract infections. Type 1 diabetics may acutely manifest with diabetic ketoacidosis. Biochemistry: Fasting plasma glucose exceeding 7.0 mmol/L or random plasma glucose above 11.1 mmol/L. Patients exhibiting borderline readings should undergo an oral glucose tolerance test.
Complications A variety of organ systems are jeopardized in diabetes
• Ischemic heart disease resulting from advanced coronary artery atherosclerosis. • Chronic kidney disease resulting from diabetic nephropathy• Vision impairment resulting from cataract development and diabetic retinopathy. • Peripheral vascular disease resulting from atherosclerosis. • Foot ulceration resulting from peripheral neuropathy and ischemia
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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.
