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Pathology – Malaria
Malaria
Pathogen
• Plasmodia protozoa: Plasmodium (P.) falciparum, P. vivax, P. ovale, P. malariae.
Epidemiology: Endemic in tropical regions of Africa, Asia, and South America. Approximately 10 million new infections annually. Approximately 1 million fatalities annually, predominantly due to P. falciparum. Transmission • Female Anopheles mosquitoes inject Plasmodium sporozoites during a blood meal.
Pathogenesis
• Sporozoites invade hepatocytes and grow into merozoites. • Merozoites infect and replicate within erythrocytes, resulting in hemolytic anemia. Sequestration of red blood cells significantly infected by P. falciparum results in acute renal failure and cerebral malaria.
Presentation
• A non-specific influenza-like disease characterized initially by headache, malaise, and myalgia. • Subsequently, fevers and chills ensue. Cerebral malaria manifests with confusion, seizures, and coma.
Diagnosis: Parasitized erythrocytes may be observed upon inspection of blood smears. Prognosis: Non-falciparum malaria exhibits a minimal death rate. Severe falciparum malaria can be fatal.
Adverse prognostic indicators encompass elevated parasitaemia, hypoglycaemia, disseminated intravascular coagulation (DIC), and renal dysfunction.
Malaria
Pathogen
• Plasmodia protozoa: Plasmodium (P.) falciparum, P. vivax, P. ovale, P. malariae.
Epidemiology: Endemic in tropical regions of Africa, Asia, and South America. Approximately 10 million new infections annually. Approximately 1 million fatalities annually, predominantly due to P. falciparum. Transmission • Female Anopheles mosquitoes inject Plasmodium sporozoites during a blood meal.
Pathogenesis
• Sporozoites invade hepatocytes and grow into merozoites. • Merozoites infect and replicate within erythrocytes, resulting in hemolytic anemia. Sequestration of red blood cells significantly infected by P. falciparum results in acute renal failure and cerebral malaria.
Presentation
• A non-specific influenza-like disease characterized initially by headache, malaise, and myalgia. • Subsequently, fevers and chills ensue. Cerebral malaria manifests with confusion, seizures, and coma.
Diagnosis: Parasitized erythrocytes may be observed upon inspection of blood smears. Prognosis: Non-falciparum malaria exhibits a minimal death rate. Severe falciparum malaria can be fatal.
Adverse prognostic indicators encompass elevated parasitaemia, hypoglycaemia, disseminated intravascular coagulation (DIC), and renal dysfunction.
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Pathology - Infectious mononucleosis
Pathogen: Epstein–Barr virus (EBV), a DNA herpesvirus. Epidemiology • The majority of patients are adolescents or young adults. • Absence of gender or racial bias.
• Transmission occurs via saliva or respiratory droplets from an individual infected with EBV.
• Incubation duration of 4–5 weeks.
Mechanism of Disease
Development EBV infects oropharyngeal epithelial cells through the C3d receptor and replicates within these cells. EBV infects B-lymphocytes, causing the linear genome to circularize and survive as an episome.
Viral persistence facilitates continuous multiplication within oropharyngeal epithelial cells and the secretion of infectious particles into saliva. Presentation: sore throat, fever, malaise.
Clinical examination may disclose lymphadenopathy, palatal petechiae, and splenomegaly.
Diagnosis: Lymphocytosis. • The peripheral blood film reveals big atypical cells, which are not specific to EBV. • Ninety percent possess heterophil antibodies (Paul–Bunnell; Monospot test). • EBV-specific IgM antibodies indicate a current infection.
Histopathology
• Lymph nodes and tonsils exhibit significant paracortical growth due to massive lymphoid blasts comprising a mixture of B- and T-cells. The EBV-LMP1 antigen can be identified immunohistochemically in some B-blasts.
Prognosis: In the majority of instances, the condition is self-limiting. • Uncommon consequences encompass meningitis, encephalitis, cranial nerve lesions, Guillain–Barré syndrome, depression, and fatigue.
Pathogen: Epstein–Barr virus (EBV), a DNA herpesvirus. Epidemiology • The majority of patients are adolescents or young adults. • Absence of gender or racial bias.
• Transmission occurs via saliva or respiratory droplets from an individual infected with EBV.
• Incubation duration of 4–5 weeks.
Mechanism of Disease
Development EBV infects oropharyngeal epithelial cells through the C3d receptor and replicates within these cells. EBV infects B-lymphocytes, causing the linear genome to circularize and survive as an episome.
Viral persistence facilitates continuous multiplication within oropharyngeal epithelial cells and the secretion of infectious particles into saliva. Presentation: sore throat, fever, malaise.
Clinical examination may disclose lymphadenopathy, palatal petechiae, and splenomegaly.
Diagnosis: Lymphocytosis. • The peripheral blood film reveals big atypical cells, which are not specific to EBV. • Ninety percent possess heterophil antibodies (Paul–Bunnell; Monospot test). • EBV-specific IgM antibodies indicate a current infection.
Histopathology
• Lymph nodes and tonsils exhibit significant paracortical growth due to massive lymphoid blasts comprising a mixture of B- and T-cells. The EBV-LMP1 antigen can be identified immunohistochemically in some B-blasts.
Prognosis: In the majority of instances, the condition is self-limiting. • Uncommon consequences encompass meningitis, encephalitis, cranial nerve lesions, Guillain–Barré syndrome, depression, and fatigue.
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Pathology- Human Immunodeficiency Virus
Pathogen
• Enveloped RNA virus with a single-stranded, positive-sense genome. • Belongs to the lentivirus genus within the retrovirus family.
Epidemiology
• Prevalent globally, particularly in Sub-Saharan Africa. • Designated as a pandemic by the World Health Organization (WHO).
Transmission
• Primary transmission pathways include unprotected sexual intercourse, infected needles, breast milk, and maternal transmission during childbirth
. • Transmission through transfused blood products has been nearly eradicated due to rigorous donor screening protocols.
Immunopathogenesis
• Infects CD4+ helper T lymphocytes, macrophages, and dendritic cells. • Extensive dissemination of lymphoid tissue transpires post-infection. • HIV-specific CD8+ cytotoxic T-cells initially manage the disease. • Subsequently, HIV evades immunological regulation via antigenic mutation. • Viral load escalates fast while CD4+ numbers decline sharply.
Presentation
• Acute seroconversion induces a flu-like disease characterized by fever, lymphadenopathy, pharyngitis, myalgia, rash, and oral ulcers. The latency phase subsequently ensues, typically remaining asymptomatic. The last phase is characterized by opportunistic infections and/or neoplasm. Common infections encompass bacterial pneumonia,pulmonary tuberculosis,Pneumocystis pneumonia, oesophageal candidiasis, cryptosporidiosis, Mycobacterium avium in the colon,cryptococcal meningitis, and cerebral toxoplasmosis.
Common neoplasms encompass cervical and anal warts, carcinoma, non-Hodgkin B-cell lymphomas, and Kaposi's sarcoma.
Histopathology
• Lymph nodes exhibit pronounced follicular proliferation accompanied by follicle lysis. Lymphomas are typically of the diffuse big B-cell variety.
• The bone marrow exhibits dysplasia characterized by disorganization of hematopoietic lineages and an elevated count of plasma cells.
• The skin may present with eosinophilic folliculitis, indicating infiltration of hair follicles by eosinophils. Cutaneous Kaposi's sarcoma exhibits an erratic proliferation of HHV-8-positive spindle cells inside the dermis, resulting in the formation of slit-like vascular gaps. Pneumocystis pneumonia is characterized by lymphocytic alveolitis accompanied by silver-positive organisms in the alveolar spaces. Prognosis: With contemporary anti-HIV medicine, numerous individuals can anticipate a lifespan approaching normalcy, resulting in death with HIV rather than from it.
Pathogen
• Enveloped RNA virus with a single-stranded, positive-sense genome. • Belongs to the lentivirus genus within the retrovirus family.
Epidemiology
• Prevalent globally, particularly in Sub-Saharan Africa. • Designated as a pandemic by the World Health Organization (WHO).
Transmission
• Primary transmission pathways include unprotected sexual intercourse, infected needles, breast milk, and maternal transmission during childbirth
. • Transmission through transfused blood products has been nearly eradicated due to rigorous donor screening protocols.
Immunopathogenesis
• Infects CD4+ helper T lymphocytes, macrophages, and dendritic cells. • Extensive dissemination of lymphoid tissue transpires post-infection. • HIV-specific CD8+ cytotoxic T-cells initially manage the disease. • Subsequently, HIV evades immunological regulation via antigenic mutation. • Viral load escalates fast while CD4+ numbers decline sharply.
Presentation
• Acute seroconversion induces a flu-like disease characterized by fever, lymphadenopathy, pharyngitis, myalgia, rash, and oral ulcers. The latency phase subsequently ensues, typically remaining asymptomatic. The last phase is characterized by opportunistic infections and/or neoplasm. Common infections encompass bacterial pneumonia,pulmonary tuberculosis,Pneumocystis pneumonia, oesophageal candidiasis, cryptosporidiosis, Mycobacterium avium in the colon,cryptococcal meningitis, and cerebral toxoplasmosis.
Common neoplasms encompass cervical and anal warts, carcinoma, non-Hodgkin B-cell lymphomas, and Kaposi's sarcoma.
Histopathology
• Lymph nodes exhibit pronounced follicular proliferation accompanied by follicle lysis. Lymphomas are typically of the diffuse big B-cell variety.
• The bone marrow exhibits dysplasia characterized by disorganization of hematopoietic lineages and an elevated count of plasma cells.
• The skin may present with eosinophilic folliculitis, indicating infiltration of hair follicles by eosinophils. Cutaneous Kaposi's sarcoma exhibits an erratic proliferation of HHV-8-positive spindle cells inside the dermis, resulting in the formation of slit-like vascular gaps. Pneumocystis pneumonia is characterized by lymphocytic alveolitis accompanied by silver-positive organisms in the alveolar spaces. Prognosis: With contemporary anti-HIV medicine, numerous individuals can anticipate a lifespan approaching normalcy, resulting in death with HIV rather than from it.
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Pathology- Antimicrobial agents
Antibacterial agents
Inhibitors of cellular wall biosynthesis • Disrupt peptidoglycan production. • Beta-lactams, such as penicillins and cephalosporins. • Glycopeptides, such as vancomycin and teicoplanin.
Protein synthesis inhibitors
• Bind to bacterial ribosomes and inhibit the elongation of protein chains. Aminoglycosides, such as gentamicin. • Tetracyclines, such as doxycycline. • Macrolides, such as erythromycin and clarithromycin.
Nucleic acid synthesis inhibitors
• Disrupt the production of DNA precursors or the process of DNA replication. • Sulfonamides, such as sulfamethoxazole. • Trimethoprim. • Quinolones, such as ciprofloxacin. • Rifamycins, such as rifampicin. • Nitroimidazoles, such as metronidazole.
Antiviral medications
Aciclovir is a guanosine analogue that undergoes phosphorylation by viral thymidine kinase. Aciclovir triphosphate is integrated into viral DNA, resulting in the cessation of chain replication. Ganciclovir is analogous to acyclovir, although exhibits more efficacy against cytomegalovirus (CMV). Contemporary HIV treatment employs a mix of reverse transcriptase inhibitors and protease inhibitors.
Antifungal medications
Azoles inhibit the formation of ergosterol, such as fluconazole. Polyenes disrupt the functionality of fungal cell membranes, such as amphotericin and nystatin.
Antibacterial agents
Inhibitors of cellular wall biosynthesis • Disrupt peptidoglycan production. • Beta-lactams, such as penicillins and cephalosporins. • Glycopeptides, such as vancomycin and teicoplanin.
Protein synthesis inhibitors
• Bind to bacterial ribosomes and inhibit the elongation of protein chains. Aminoglycosides, such as gentamicin. • Tetracyclines, such as doxycycline. • Macrolides, such as erythromycin and clarithromycin.
Nucleic acid synthesis inhibitors
• Disrupt the production of DNA precursors or the process of DNA replication. • Sulfonamides, such as sulfamethoxazole. • Trimethoprim. • Quinolones, such as ciprofloxacin. • Rifamycins, such as rifampicin. • Nitroimidazoles, such as metronidazole.
Antiviral medications
Aciclovir is a guanosine analogue that undergoes phosphorylation by viral thymidine kinase. Aciclovir triphosphate is integrated into viral DNA, resulting in the cessation of chain replication. Ganciclovir is analogous to acyclovir, although exhibits more efficacy against cytomegalovirus (CMV). Contemporary HIV treatment employs a mix of reverse transcriptase inhibitors and protease inhibitors.
Antifungal medications
Azoles inhibit the formation of ergosterol, such as fluconazole. Polyenes disrupt the functionality of fungal cell membranes, such as amphotericin and nystatin.
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Pathology – Microbes
Bacteria • Unicellular entities possessing double-stranded DNA that resides freely in the cytoplasm, encased by a cell membrane and cell wall. • Predominantly thrive in the presence of oxygen (aerobes), however are capable of growth in its absence (facultative anaerobes). Certain organisms proliferate exclusively under anoxic conditions (strict anaerobes). Gram-positive bacteria possess a robust cell wall comprised of peptidoglycan plus an additional polymer, frequently teichoic acid. Gram-negative bacteria possess a weaker peptidoglycan layer, which is covered by an outer lipid membrane consisting of lipopolysaccharide. Mycobacteria are a kind of bacteria characterized by a thick, waxy cell wall that can be stained using the Ziehl–Nielsen method.
Viruses are the smallest and most basic organisms, consisting of genetic material in the form of DNA or RNA encased within a protein shell known as a capsid. Certain viruses possess an external lipid membrane obtained from the host cell in which they originated. • Obligate intracellular entities that proliferate exclusively by infecting a host cell and commandeering its metabolic machinery. • Induce disease by damaging host cells (direct cytopathic effect) or as a result of the immunological response to the infection. • Certain viruses can induce latent infections, such as herpes simplex. • Some viruses are carcinogenic and contribute to the transformation of host cells and the onset of malignancy, for instance, HPV in cervical cancer and EBV in nasopharyngeal carcinoma.
Fungi possess DNA encased within a nucleus, feature a cell membrane that includes ergosterol, and have an external cell wall made of chitin. Yeasts are unicellular fungi that reproduce asexually through budding, such as Candida. • Moulds develop as branching filaments termed hyphae that intertwine to create a complex structure known as mycelium. Mycelia generate spores. • Certain fungi can survive in both yeast and mold forms, such as Histoplasma
Protozoa are unicellular creatures that can inhabit host cells or exist in the extracellular milieu. Intracellular protozoa obtain nourishment from the host cell (e.g., Plasmodium, Leishmania, Toxoplasma). Extracellular protozoa obtain nutrients through direct intake and/or the consumption of sloughed epithelial cells (e.g., Giardia, Trichomonas). Helminths • Complex multicellular parasitic worms that vary in size from tiny entities to colossal animals several meters long. • Numerous species possess intricate life cycles that involve multiple hosts. • Categorized as nematodes (roundworms), cestodes (tapeworms), and trematodes (flukes)
Bacteria • Unicellular entities possessing double-stranded DNA that resides freely in the cytoplasm, encased by a cell membrane and cell wall. • Predominantly thrive in the presence of oxygen (aerobes), however are capable of growth in its absence (facultative anaerobes). Certain organisms proliferate exclusively under anoxic conditions (strict anaerobes). Gram-positive bacteria possess a robust cell wall comprised of peptidoglycan plus an additional polymer, frequently teichoic acid. Gram-negative bacteria possess a weaker peptidoglycan layer, which is covered by an outer lipid membrane consisting of lipopolysaccharide. Mycobacteria are a kind of bacteria characterized by a thick, waxy cell wall that can be stained using the Ziehl–Nielsen method.
Viruses are the smallest and most basic organisms, consisting of genetic material in the form of DNA or RNA encased within a protein shell known as a capsid. Certain viruses possess an external lipid membrane obtained from the host cell in which they originated. • Obligate intracellular entities that proliferate exclusively by infecting a host cell and commandeering its metabolic machinery. • Induce disease by damaging host cells (direct cytopathic effect) or as a result of the immunological response to the infection. • Certain viruses can induce latent infections, such as herpes simplex. • Some viruses are carcinogenic and contribute to the transformation of host cells and the onset of malignancy, for instance, HPV in cervical cancer and EBV in nasopharyngeal carcinoma.
Fungi possess DNA encased within a nucleus, feature a cell membrane that includes ergosterol, and have an external cell wall made of chitin. Yeasts are unicellular fungi that reproduce asexually through budding, such as Candida. • Moulds develop as branching filaments termed hyphae that intertwine to create a complex structure known as mycelium. Mycelia generate spores. • Certain fungi can survive in both yeast and mold forms, such as Histoplasma
Protozoa are unicellular creatures that can inhabit host cells or exist in the extracellular milieu. Intracellular protozoa obtain nourishment from the host cell (e.g., Plasmodium, Leishmania, Toxoplasma). Extracellular protozoa obtain nutrients through direct intake and/or the consumption of sloughed epithelial cells (e.g., Giardia, Trichomonas). Helminths • Complex multicellular parasitic worms that vary in size from tiny entities to colossal animals several meters long. • Numerous species possess intricate life cycles that involve multiple hosts. • Categorized as nematodes (roundworms), cestodes (tapeworms), and trematodes (flukes)
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Pathology - Carcinogenesis
Definition • The series of events culminating in the formation of a malignant tumor.
Aetiology
• Radiation or chemicals that impair DNA, such as sunlight in skin carcinomas and cigarette smoke in lung carcinomas. Chronic inflammatory illnesses that induce sustained cellular proliferation, such as ulcerative colitis, increase the risk of colonic cancer
.• Elevated hormone levels induce the proliferation of hormonally responsive tissues, such as estrogens in breast and endometrial carcinomas. Oncogenic viruses synthesize proteins that facilitate unregulated cell proliferation, such as HPV in cervical cancer. Pathogenesis DNA damage to genes encoding proteins that govern cell division permits uncontrolled cellular proliferation. Genes regulating cell division are categorized into oncogenes and tumor suppressor genes. Oncogenes are mutated genes that facilitate cell division. Mutations typically lead to the overexpression of the gene product or the constitutive activation of the protein product. Examples of oncogenes frequently mutated in malignancies are KIT, RAS, and MYC.
Tumor suppressor genes
• Genes that encode proteins which typically decrease cellular proliferation. • Typically, the inactivation of both alleles is necessary for a tumorigenic impact. Examples of frequently altered tumour suppressor genes in malignancies include P53, CDKN2A, and RB
Metastasis
• The attainment of metastatic capability is a crucial occurrence in the progression of a neoplasm; dissemination to remote locations is a primary factor contributing to the mortality associated with malignant tumors. Malignant neoplasms disseminate through three primary pathways: hematogenous spread to distant organs (e.g., lungs, liver, bone, brain), lymphatic spread to regional lymph nodes (e.g., axillary lymph nodes in breast carcinomas), and transcoelomic spread, wherein malignant tumors adjacent to body cavities, such as the pleura or peritoneum, can infiltrate these spaces and propagate to other organs. Successful metastasis necessitates the malignant cells to surmount several obstacles: detachment from adjacent cells, degradation of the extracellular matrix, invasion of a vessel lumen, endurance in circulation while reaching a distant location, egress from the vessel, and effective implantation and proliferation at the new site.
Definition • The series of events culminating in the formation of a malignant tumor.
Aetiology
• Radiation or chemicals that impair DNA, such as sunlight in skin carcinomas and cigarette smoke in lung carcinomas. Chronic inflammatory illnesses that induce sustained cellular proliferation, such as ulcerative colitis, increase the risk of colonic cancer
.• Elevated hormone levels induce the proliferation of hormonally responsive tissues, such as estrogens in breast and endometrial carcinomas. Oncogenic viruses synthesize proteins that facilitate unregulated cell proliferation, such as HPV in cervical cancer. Pathogenesis DNA damage to genes encoding proteins that govern cell division permits uncontrolled cellular proliferation. Genes regulating cell division are categorized into oncogenes and tumor suppressor genes. Oncogenes are mutated genes that facilitate cell division. Mutations typically lead to the overexpression of the gene product or the constitutive activation of the protein product. Examples of oncogenes frequently mutated in malignancies are KIT, RAS, and MYC.
Tumor suppressor genes
• Genes that encode proteins which typically decrease cellular proliferation. • Typically, the inactivation of both alleles is necessary for a tumorigenic impact. Examples of frequently altered tumour suppressor genes in malignancies include P53, CDKN2A, and RB
Metastasis
• The attainment of metastatic capability is a crucial occurrence in the progression of a neoplasm; dissemination to remote locations is a primary factor contributing to the mortality associated with malignant tumors. Malignant neoplasms disseminate through three primary pathways: hematogenous spread to distant organs (e.g., lungs, liver, bone, brain), lymphatic spread to regional lymph nodes (e.g., axillary lymph nodes in breast carcinomas), and transcoelomic spread, wherein malignant tumors adjacent to body cavities, such as the pleura or peritoneum, can infiltrate these spaces and propagate to other organs. Successful metastasis necessitates the malignant cells to surmount several obstacles: detachment from adjacent cells, degradation of the extracellular matrix, invasion of a vessel lumen, endurance in circulation while reaching a distant location, egress from the vessel, and effective implantation and proliferation at the new site.
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Pathology – Neoplasia
Definitions
A neoplasm is an abnormal tissue mass characterized by unregulated growth and lacking any beneficial function. The term is frequently employed interchangeably with the term tumor, which denotes a swelling.
Benign neoplasms typically have a gradual development rate and remain localized to their site of origin. While benign neoplasms typically follow a harmless trajectory, they may pose risks if they exert pressure on essential adjacent structures or if they emit hormones indiscriminately.
Malignant neoplasms possess the ability to disseminate or metastasis to remote locations, resulting in new tumors known as metastases, which can proliferate independently of the initial tumor.
Cancer is an overarching word for any malignant neoplasm.
Nomenclature of neoplasms
Epithelial neoplasms
Benign neoplasms of squamous epithelium are termed acanthomas when flat and papillomas when exhibiting branching fronds.
Benign neoplasms of glandular epithelium are referred to as adenomas.
Epithelial malignancies are classified as carcinomas.
Carcinomas exhibiting squamous differentiation are termed squamous cell carcinomas. Carcinomas exhibiting glandular differentiation are termed adenocarcinomas. Carcinomas frequently follow a stage of epithelial dysplasia, characterized by the presence of neoplastic cells inside the epithelium, without penetration beyond the epithelial boundaries.
Neoplasms of connective tissue Lipoma is a benign adipose tissue tumor. • Leiomyoma is a benign neoplasm of smooth muscle. • Rhabdomyoma is a benign neoplasm of skeletal muscle. • Angioma is a benign vascular neoplasm. • Osteoma is a benign osseous neoplasm. Liposarcoma is a malignant tumor of adipose tissue. Leiomyosarcoma is a malignant neoplasm of smooth muscle tissue. • Rhabdomyosarcoma is a malignant neoplasm of skeletal muscle. • Angiosarcoma is a malignant neoplasm of vascular tissue. • Osteosarcoma is a malignant neoplasm of bone.
Alternative neoplasm classifications Lymphomas, leukemias, and myeloma are hematological malignancies originating from blood or bone marrow cells.
Malignant melanoma is a tumor of malignant melanocytes. Malignant mesothelioma is a neoplastic mesothelial tumor. Germ cell tumors constitute a heterogeneous category of neoplasms that typically originate in the testes or ovaries. Embryonal tumors are a category of malignant neoplasms primarily observed in children, characterized by highly undifferentiated cells, such as neuroblastoma and nephroblastoma.
Definitions
A neoplasm is an abnormal tissue mass characterized by unregulated growth and lacking any beneficial function. The term is frequently employed interchangeably with the term tumor, which denotes a swelling.
Benign neoplasms typically have a gradual development rate and remain localized to their site of origin. While benign neoplasms typically follow a harmless trajectory, they may pose risks if they exert pressure on essential adjacent structures or if they emit hormones indiscriminately.
Malignant neoplasms possess the ability to disseminate or metastasis to remote locations, resulting in new tumors known as metastases, which can proliferate independently of the initial tumor.
Cancer is an overarching word for any malignant neoplasm.
Nomenclature of neoplasms
Epithelial neoplasms
Benign neoplasms of squamous epithelium are termed acanthomas when flat and papillomas when exhibiting branching fronds.
Benign neoplasms of glandular epithelium are referred to as adenomas.
Epithelial malignancies are classified as carcinomas.
Carcinomas exhibiting squamous differentiation are termed squamous cell carcinomas. Carcinomas exhibiting glandular differentiation are termed adenocarcinomas. Carcinomas frequently follow a stage of epithelial dysplasia, characterized by the presence of neoplastic cells inside the epithelium, without penetration beyond the epithelial boundaries.
Neoplasms of connective tissue Lipoma is a benign adipose tissue tumor. • Leiomyoma is a benign neoplasm of smooth muscle. • Rhabdomyoma is a benign neoplasm of skeletal muscle. • Angioma is a benign vascular neoplasm. • Osteoma is a benign osseous neoplasm. Liposarcoma is a malignant tumor of adipose tissue. Leiomyosarcoma is a malignant neoplasm of smooth muscle tissue. • Rhabdomyosarcoma is a malignant neoplasm of skeletal muscle. • Angiosarcoma is a malignant neoplasm of vascular tissue. • Osteosarcoma is a malignant neoplasm of bone.
Alternative neoplasm classifications Lymphomas, leukemias, and myeloma are hematological malignancies originating from blood or bone marrow cells.
Malignant melanoma is a tumor of malignant melanocytes. Malignant mesothelioma is a neoplastic mesothelial tumor. Germ cell tumors constitute a heterogeneous category of neoplasms that typically originate in the testes or ovaries. Embryonal tumors are a category of malignant neoplasms primarily observed in children, characterized by highly undifferentiated cells, such as neuroblastoma and nephroblastoma.
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Pathology - Hypersensitivity reactions
Definition • A collection of disorders resulting from an aberrant immune-mediated response. • This response may target an exogenous antigen from the environment or a self-antigen, in which case it constitutes a kind of autoimmunity.
Type 1 hypersensitivity
• Defined by the synthesis of IgE antibodies in reaction to an antigen. • The cross-linking of surface IgE receptors on mast cells triggers the release of mediators, including histamine, which incite acute inflammation. • Characteristic of individuals with atopy, a hereditary predisposition to generate elevated levels of IgE in reaction to environmental antigens such as pollen and house dust mites. Anaphylaxis is a systemic type of acute hypersensitivity resulting from the extensive release of histamine. In its most extreme manifestation, it may result in anaphylactic shock. • Immediate hypersensitivity disorders impact over 20% of the population, and their prevalence is increasing.
Antibody-mediated (type 2) hypersensitivity is induced by IgG or IgM antibodies attaching to a fixed antigen within a tissue. The binding of antibodies can activate the complement system, resulting in cellular damage, as seen in bullous pemphigoid or induce alterations in cellular function, exemplified by TSH-receptor stimulating antibodies in Graves' disease.
Immune complex-mediated (type 3) hypersensitivity • Arises from circulating IgG or IgM antibodies that form immune complexes with antigens in the bloodstream, subsequently depositing in tissues and activating complement. • Preferred sites for immune complex deposition include small blood vessels, kidneys, and joints. • Reactions characterized by immune complex-mediated hypersensitivity often manifest as multisystem disorders, prominently featuring vasculitis, arthritis, and glomerulonephritis, as observed in systemic lupus erythematosus.
T-cell-mediated (type 4) hypersensitivity is induced by activated T-lymphocytes that damage cells through direct cytotoxicity or by secreting cytokines that stimulate macrophage activation. • T-cell responses are characterized by a latency of 1–2 days, hence the designation delayed-type hypersensitivity. • Illustrative cases encompass contact dermatitisHashimoto’s thyroiditis primary biliary cirrhosisand tuberculosis.
Definition • A collection of disorders resulting from an aberrant immune-mediated response. • This response may target an exogenous antigen from the environment or a self-antigen, in which case it constitutes a kind of autoimmunity.
Type 1 hypersensitivity
• Defined by the synthesis of IgE antibodies in reaction to an antigen. • The cross-linking of surface IgE receptors on mast cells triggers the release of mediators, including histamine, which incite acute inflammation. • Characteristic of individuals with atopy, a hereditary predisposition to generate elevated levels of IgE in reaction to environmental antigens such as pollen and house dust mites. Anaphylaxis is a systemic type of acute hypersensitivity resulting from the extensive release of histamine. In its most extreme manifestation, it may result in anaphylactic shock. • Immediate hypersensitivity disorders impact over 20% of the population, and their prevalence is increasing.
Antibody-mediated (type 2) hypersensitivity is induced by IgG or IgM antibodies attaching to a fixed antigen within a tissue. The binding of antibodies can activate the complement system, resulting in cellular damage, as seen in bullous pemphigoid or induce alterations in cellular function, exemplified by TSH-receptor stimulating antibodies in Graves' disease.
Immune complex-mediated (type 3) hypersensitivity • Arises from circulating IgG or IgM antibodies that form immune complexes with antigens in the bloodstream, subsequently depositing in tissues and activating complement. • Preferred sites for immune complex deposition include small blood vessels, kidneys, and joints. • Reactions characterized by immune complex-mediated hypersensitivity often manifest as multisystem disorders, prominently featuring vasculitis, arthritis, and glomerulonephritis, as observed in systemic lupus erythematosus.
T-cell-mediated (type 4) hypersensitivity is induced by activated T-lymphocytes that damage cells through direct cytotoxicity or by secreting cytokines that stimulate macrophage activation. • T-cell responses are characterized by a latency of 1–2 days, hence the designation delayed-type hypersensitivity. • Illustrative cases encompass contact dermatitisHashimoto’s thyroiditis primary biliary cirrhosisand tuberculosis.
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Pathology – Innate Immunity
innate immunity
Epithelial interfaces
Epithelial surfaces serve as the primary entry points for infections into the body. A continuous epithelial layer establishes a physical barrier to infection. The acidic pH of the skin and the presence of fatty acids in sebum suppress microbial proliferation.
The gastrointestinal system contains gastric acid, pancreatic enzymes, mucosal IgA, and normal colonic flora that function to inhibit the onset of infection. The respiratory tract produces mucus to capture organisms, while cilia facilitate their passage to the throat for swallowing. Continuous urination along the urinary system inhibits microbial adherence to the urothelium.
Phagocytes
Organisms penetrating epithelial surfaces meet tissue macrophages that identify infections and recruit neutrophils to the location
Macrophages and neutrophils are phagocytic cells that engulf bacteria through phagocytosis, forming a phagosome
The phagosome then merges with cytoplasmic lysosomes, which harbor enzymes and reactive oxygen species that eliminate the bacterium. Phagocytes identify species by pattern recognition receptors, such as mannose receptors, Toll-like receptors, and Nod-like receptors.
Acute-phase proteins
Cytokines generated by phagocytes prompt the liver to swiftly manufacture and discharge acute phase proteins. Mannose-binding lectin identifies microbial surface sugars and undergoes a conformational alteration, enabling it to attach to the protein MASP, thereby forming a complex that activates the complement system.
C-reactive protein attaches to the phosphorylcholine components of microbial lipopolysaccharides, facilitating their phagocytosis by macrophages.
Complement
• A assemblage of circulating proteins that aid the immune system in eliminating pathogens.
• Can be initiated by antibodies attached to a microbe (traditional pathway), automatically activated by bacteria devoid of a regulatory protein found on host cells (alternative pathway), or by mannose-binding protein (lectin pathway). A sequential cascade results in the formation of C3 convertase, an enzyme that cleaves many C3 molecules into C3b.
• Microbes coated with C3b are eliminated through phagocytosis or the membrane assault complex, a polymer of terminal complement components that creates pores in the microbial cell membrane.
• The complement system is stringently regulated to avert unregulated activation. Decay-accelerating factor impedes the binding of C3b to cellular surfaces, while membrane cofactor protein degrades C3b.
innate immunity
Epithelial interfaces
Epithelial surfaces serve as the primary entry points for infections into the body. A continuous epithelial layer establishes a physical barrier to infection. The acidic pH of the skin and the presence of fatty acids in sebum suppress microbial proliferation.
The gastrointestinal system contains gastric acid, pancreatic enzymes, mucosal IgA, and normal colonic flora that function to inhibit the onset of infection. The respiratory tract produces mucus to capture organisms, while cilia facilitate their passage to the throat for swallowing. Continuous urination along the urinary system inhibits microbial adherence to the urothelium.
Phagocytes
Organisms penetrating epithelial surfaces meet tissue macrophages that identify infections and recruit neutrophils to the location
Macrophages and neutrophils are phagocytic cells that engulf bacteria through phagocytosis, forming a phagosome
The phagosome then merges with cytoplasmic lysosomes, which harbor enzymes and reactive oxygen species that eliminate the bacterium. Phagocytes identify species by pattern recognition receptors, such as mannose receptors, Toll-like receptors, and Nod-like receptors.
Acute-phase proteins
Cytokines generated by phagocytes prompt the liver to swiftly manufacture and discharge acute phase proteins. Mannose-binding lectin identifies microbial surface sugars and undergoes a conformational alteration, enabling it to attach to the protein MASP, thereby forming a complex that activates the complement system.
C-reactive protein attaches to the phosphorylcholine components of microbial lipopolysaccharides, facilitating their phagocytosis by macrophages.
Complement
• A assemblage of circulating proteins that aid the immune system in eliminating pathogens.
• Can be initiated by antibodies attached to a microbe (traditional pathway), automatically activated by bacteria devoid of a regulatory protein found on host cells (alternative pathway), or by mannose-binding protein (lectin pathway). A sequential cascade results in the formation of C3 convertase, an enzyme that cleaves many C3 molecules into C3b.
• Microbes coated with C3b are eliminated through phagocytosis or the membrane assault complex, a polymer of terminal complement components that creates pores in the microbial cell membrane.
• The complement system is stringently regulated to avert unregulated activation. Decay-accelerating factor impedes the binding of C3b to cellular surfaces, while membrane cofactor protein degrades C3b.
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Pathology - Inflammation and Healing
Acute inflammation
• A swift, non-specific reaction to cellular damage
. • Coordinated by cytokines generated from damaged cells, such as histamine, serotonin, prostaglandins, leukotrienes, and platelet-activating factor. Cytokines stimulate endothelial cells, resulting in the development of an acute inflammatory exudate including fluid, fibrin, and neutrophils. Severe acute inflammation may result in a localized accumulation of pus within a necrotic cavity (abscess). Acute inflammation may resolve, heal with fibrosis, or advance to chronic inflammation.
Chronic inflammation is a sustained type of inflammation characterized by concurrent tissue damage and attempts at healing.
• May originate from acute inflammation or manifest from the onset.
• Defined by the presence of chronic inflammatory cells, specifically macrophages, lymphocytes, and plasma cells.
• More prone to healing with permanent scarring rather than resolution.
Granulomatous inflammation is a distinct form of chronic inflammation marked by the presence of activated macrophages referred to as epithelioid histiocytes. Collections of epithelioid macrophages are referred to as granulomas. Granulomatous inflammation is linked to foreign substances, chronic infections (such as mycobacteria), and conditions of indeterminate etiology (for instance, sarcoidosis).
Restoration
• The procedure of substituting necrotic and impaired tissue with viable tissue
. • May transpire via regeneration or repair. Regeneration (resolution) substitutes injured cells with identical cell types and represents the optimal outcome. This can only happen if the connective tissue framework is intact and if the tissue possesses regenerative capabilities. Repair initiates with the development of granulation tissue, subsequently transformed into a collagen-dense scar. While the structural integrity is preserved, the functionality of the damaged tissue is compromised.
Acute inflammation
• A swift, non-specific reaction to cellular damage
. • Coordinated by cytokines generated from damaged cells, such as histamine, serotonin, prostaglandins, leukotrienes, and platelet-activating factor. Cytokines stimulate endothelial cells, resulting in the development of an acute inflammatory exudate including fluid, fibrin, and neutrophils. Severe acute inflammation may result in a localized accumulation of pus within a necrotic cavity (abscess). Acute inflammation may resolve, heal with fibrosis, or advance to chronic inflammation.
Chronic inflammation is a sustained type of inflammation characterized by concurrent tissue damage and attempts at healing.
• May originate from acute inflammation or manifest from the onset.
• Defined by the presence of chronic inflammatory cells, specifically macrophages, lymphocytes, and plasma cells.
• More prone to healing with permanent scarring rather than resolution.
Granulomatous inflammation is a distinct form of chronic inflammation marked by the presence of activated macrophages referred to as epithelioid histiocytes. Collections of epithelioid macrophages are referred to as granulomas. Granulomatous inflammation is linked to foreign substances, chronic infections (such as mycobacteria), and conditions of indeterminate etiology (for instance, sarcoidosis).
Restoration
• The procedure of substituting necrotic and impaired tissue with viable tissue
. • May transpire via regeneration or repair. Regeneration (resolution) substitutes injured cells with identical cell types and represents the optimal outcome. This can only happen if the connective tissue framework is intact and if the tissue possesses regenerative capabilities. Repair initiates with the development of granulation tissue, subsequently transformed into a collagen-dense scar. While the structural integrity is preserved, the functionality of the damaged tissue is compromised.
