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Current medical school curricula predominantly facilitate early integration of basic science principles into clinical practice to strengthen diagnostic skills and the ability to make treatment decisions. In addition, they promote life-long learning and understanding of the principles of medical practice. The Pathology Competencies for Medical Education (PCME) were developed in response to a call to action by pathology course directors nationwide to teach medical students pathology principles necessary for the practice of medicine. The PCME are divided into three competencies: 1) Disease Mechanisms and Processes, 2) Organ System Pathology, and 3) Diagnostic Medicine and Therapeutic Pathology. Each of these competencies is broad and contains multiple learning goals with more specific learning objectives. The original competencies were designed to be a living document, meaning that they will be revised and updated periodically, and have undergone their first revision with this publication. The development of teaching cases, which have a classic case-based design, for the learning objectives is the next step in providing educational content that is peer-reviewed and readily accessible for pathology course directors, medical educators, and medical students. Application of the PCME and cases promotes a minimum standard of exposure of the undifferentiated medical student to pathophysiologic principles. The publication of the PCME and the educational cases will create a current educational resource and repository published through Academic Pathology.
Becoming a competent physician requires the ability to gain a broad foundation of knowledge, skills, and attitudes essential for independent medical practice. Essential in this is the understanding of the normal and pathological processes of each organ system, the ability to apply disease mechanisms to describe the pathobiology, and the ability to continually improve the diagnostic acumen and optimal treatment decisions through lifelong learning. The initial project to develop pathology competencies was described in the article “National Standards in Pathology Education,”1 where over 60 pathology course directors and department chairs submitted pathology course objectives that were extensively revised and peer-reviewed, then posted on the Association of Pathology Chairs (APC) Website in 2014, where they were available for both course directors and medical students. A website externally linked from the APC Website was maintained where anyone could leave a comment regarding the competencies. This project, the pathology competencies for medical education (PCME), was initiated and supported by the Undergraduate Medical Education Committee of the APC.2
Most medical schools have transitioned to an integrated organ–based curriculum,1 where individual courses are no longer taught as distinct disciplines. The manner in which medical students are taught has also changed. The lecture format has largely been replaced with multiple types of active learning, including integrated small group discussions, team-based learning exercises, and flipped classrooms. Pathology course directors have a new challenge in education that has vastly transformed from the classic 1910 Abraham Flexner module of basic science education with individual basic science and clinical skills courses followed by 2 years of clinical practice apprenticeships3 to an integrated and interdisciplinary medical school curriculum. In this transformation, individual disciplines are no longer presented as stand-alone courses, and the exponential expanse of medical knowledge requires an ever-changing and comprehensive understanding of pathobiology by the competent practicing physician. The importance of understanding pathobiology is underscored by the significant amount of questions included on the current US Medical Licensing Examination (USMLE), where pathobiology is tested in both Steps 1 and 3 of the licensing examinations.4 Every medical student must master disease processes and therapeutics in order to become a competent intern, resident, and fully practicing physician. As stated in the current standard 7 of the Liaison Committee on Medical Education (LCME) publication “structures and functions of a medical school,”5 there are important elements that must be understood including: (1) recognize and interpret symptoms and signs of disease and (2) develop differential diagnoses and treatment plans.
Pathology has a central role to assist students and physicians in (1) understanding the mechanisms of disease that lead to the signs and symptoms that must be recognized in patients, (2) forming a differential diagnosis, and (3) applying laboratory medicine that allows physicians to rule in or out individual diagnoses and make appropriate diagnostic and treatment decisions. This is in line with the Carnegie Foundation’s report calling for a new reform of learning that is “learner centered”6 and for learning outcomes to be tied to competencies.
The goal of this endeavor is 3-fold: (1) to revise the previously Website-published pathology competencies as these must be a living document, meaning revised regularly to keep pace with current medical practice and understanding, to highlight the essential (or minimum) for all medical students to understand for the practice of medicine and remain current with medical practice; (2) to emphasize laboratory medicine, which is often not taught, or at best only superficially taught, in many medical school curricula; and (3) to develop a shared resource of pathology competencies and educational cases highlighting the competencies for pathology faculty, educators, and students, which are developed by or with pathologists, peer-reviewed, and represent foundational understanding of pathobiology essential for clinical practiec that can easily be adapted into any curriculum.
The PCME have detailed learning objectives under each goal that direct medical students and course directors to important facets of each learning goal that can be individually applied by learners. The competencies are divided into 3 sections—disease mechanisms and processes, organ system pathology, and diagnostic medicine and therapeutic pathology—and allow flexibility for each learning institution and learner to apply the learning goals and objectives in a way that can keep the unique design of each curriculum or learning plan. The competencies are purposefully kept broad as they represent the minimum requirements of what pathology course directors across the nation have agreed upon to prepare medical students for entry into any residency program and for the subsequent contemporary practice of medicine.1
The learning objectives of the competencies are meant to be a living document, being continually commented upon by pathologists, medical educators, and medical students, and revised accordingly after review by an editorial group. The topics, goals, and learning objectives, as well as the comments submitted on the PCME website before November 2016, have been extensively reviewed by the original editorial group to ensure the learning objectives are current with the changing and expanding medical knowledge. Compared with the original competencies, additional sections have been developed, learning objectives have been revised, the format has been standardized, and new introductions for each section have been added. The revised competencies are found in the following pages of this article.
Following publication of the original PCME, the Undergraduate Medical Educators Section (UMEDS) of APC began developing educational cases for the pathology competencies that are current, peer-reviewed, and highlight the pathology competencies in learning cases that can easily be adapted to multiple types of educational modalities. Some of the original cases were posted on the PCME website.
The format of the cases has evolved from the original cases posted on the PCME website to the present format of educational cases that are presented in this special edition of Academic Pathology. The educational cases reference the PCME from the following pages, and address at least 1 primary learning objective, but may have 1 or more secondary learning objective(s). The pathology competencies and learning objectives are clearly indicated in the beginning of each case so that the focus of the educational case is evident. Key elements of the current format include clinical presentation, discussion questions or points, learning points, and references. The clinical presentation may include images or laboratory data for the patient’s presentation. The discussion questions or points are questions or statements that promote clinical reasoning followed by detailed explanations of the pathology, medicine, or therapeutics brought up in the discussion point or question. The learning points at the end of the case highlight the main teaching points from the preceding discussion. Thus, the cases demonstrate the application of medical reasoning to clinical scenarios that allow the learner to understand and apply diagnostic principles, incorporating morphologic findings and laboratory values with discussion of the laboratory medicine essentials for accurate diagnosis and treatment. References are included in each case and will allow the reader to review the original sources used to create the learning case or gain additional in-depth information. Thus, the educational cases are written in a style that can be easily used or adapted to multiple educational formats, such as small group discussions or flipped classrooms.
Development of the PCME and the educational cases that support the individual learning objectives is a tremendous undertaking. On the broadest level, this effort supports the LCME standard 7, which requires all medical school curricula to prepare the undifferentiated medical student with sufficient breadth and depth of knowledge for the contemporary practice of medicine. This very broad view is the level at which the objectives were originally created, intended to be the minimum-level objectives course directors nationally felt were needed for adequate understanding for the practice of medicine. In addition, the PCME can be used by individual medical schools to gain leverage for additional curriculum development, especially in laboratory medicine, which is often only minimally taught, and to help expose students to pathology as a clinical specialty. Having a national repository of competencies that is peer-reviewed allows use of learning objectives and educational cases in individual curricula, potentially relieving some of the load on pathology course directors to continually update curricula to keep up with the exponential expanse of knowledge, laboratory testing, and treatment options. And lastly, a national repository of learning objectives and cases can potentially be used to support pathology exposure in integrated curricula to ensure exposure to a minimum amount of pathology for all students. We invite our audience to comment on the depth and breadth of the competencies found on the following pages.
The primary audience for the educational cases is our pathology educators, especially since not all pathology course directors are pathologists. The cases are peer-reviewed, appropriately referenced, and can be used as teaching material by faculty and students. Discussions that follow each discussion point should be broad enough to give faculty who may use these educational cases a deeper understanding of the pathobiology behind the learning objectives needed to teach or explain the concepts to the students. Here we emphasize that the discussions should explain the basic science and medicine behind each objective at a deeper level than the bare minimum of the objectives. As educators, we must be able to explain and build on basic knowledge concepts for our students, tying the information together in a tightly woven fabric across disciplines. In addition, the discussions should explain the clinical reasoning behind each of the discussion points. Thus the educational cases are not intended to be a bare-bones review, but rather a fuller discussion building on concepts and explaining the thought process that will allow our students to become critical thinkers and apply new knowledge in the future. Having said this, the cases may be adapted to different levels or types of learners during different parts of the curriculum. For example, a case may present a simple benign lesion at a basic level where the intent is to highlight histologic features that help to differentiate between benign and malignant processes, however, another case may cover that same lesion in a different scenario to highlight clinical or diagnostic aspects of that specific disease.
Examples of educational cases can be found in the following pages for a variety of objectives from the three pathology competencies. The educational cases allow for individual use of the cases as students for primary learning or inclusion in medical school curricula in an adaptable format for a variety of teaching venues including laboratories, small group discussions or Team-Based-Learning. The educational cases are intended to facilitate knowledge integration and retention essential for clinical practice. Moving forward, we invite the broader community to submit educational cases to Academic Pathology to grow this national resource.
The educational cases highlight principles of the 3 competencies—(1) disease mechanisms and processes, (2) organ system pathology, and (3) diagnostic medicine and therapeutic pathology—and are presented in a way to help the development of clinical reasoning and the application of basic science into medicine, as well as increase the diagnostic acumen and treatment of disease. Continuing to build and review the PCME and create educational cases to highlight what we as a pathology education community feel is essential knowledge for the practice of medicine requires broader input.
We encourage readers to comment on the pathology competencies to further shape what we as pathologists feel is essential for medical education. Comments regarding the PCME can be sent to Jen Norman, in the APC office, at gro.sdorpcpa@namronj. As stated above, the competencies are a living document requiring periodic updates. Comments will be reviewed and revised competencies will be published. In addition, we invite readers to submit educational cases directly to Academic Pathology, following the submission guidelines found on the Academic Pathology website.
We are grateful to Academic Pathology that the PCME and educational cases will be published as an easily accessible resource for educators and students.
A foundational knowledge of mechanisms of disease including the etiology, local or systemic responses to disease, consequences of disease, and cellular events involved in disease or adaptive changes is essential for understanding disease processes in organ system pathology and in patients.
There are 10 topics within this competency area. Each topic includes general learning goals and specific objectives that students should be able to meet before step 1 of the USMLE. Table 1 lists the topic areas and reference codes and shows the number of goals and objectives for each.
This topic includes a basic knowledge of genetic mechanisms of disease including inherited and somatic disorders with the resulting consequences leading to disorders of development, metabolism, aging, stem cell biology, immunology, and the development of cancer.
Apply knowledge of the genetic mechanisms of disease to discuss how changes in the genome can cause developmental and functional abnormalities at the cellular, tissue, and organism levels.
Describe different types of mutations that can occur in human disease, and discuss how each of these can produce abnormalities in DNA transcription and/or alterations in the type or amount of protein produced.
Compare and contrast the inheritance patterns of different types of Mendelian disorders and give examples of each type of pattern.
Provide examples of genetic diseases associated with abnormal enzyme function, and compare and contrast with genetic diseases that produce abnormal structural proteins or other nonenzyme proteins.
Discuss mechanisms that result in developmental abnormalities involving abnormal chromosomal number and provide examples of diseases associated with trisomies or chromosomal deletions.
Discuss and give examples of disorders associated with multifactorial inheritance and describe how environmental factors can interact with genetic factors to produce or modulate disease.
Describe the pathophysiologic mechanisms that result in disorders of a nonclassical inheritance and mitochondrial inheritance and give clinical examples of each.
This topic includes a basic understanding of characteristics of benign and malignant neoplasms, epidemiologic and environmental factors that influence neoplastic change, as well as an understanding of the molecular basis of neoplasia including oncogenes, tumor suppressor genes, carcinogenic agents, and host defense.
Apply knowledge of the genetic basis of neoplasia to explain how genetic changes are acquired, how functional alterations in these mutated genes lead to the development of cancer, and how these alterations can be exploited with therapy.
Discuss and provide examples of molecular genetic mechanisms that underlie cancers, including germline mutations (including point mutations, deletions, amplifications, and translocations) and epigenetic changes.
Explain the action of oncogenes and tumor suppressor genes in growth factor–initiated signal transduction in both normal and neoplastic cells and discuss how this information can be utilized for treatment.
Compare and contrast the actions of genes that promote cell growth in cancers with those that inhibit cell death and explain how this information influences the choice of therapeutic agents.
Describe how cells maintain DNA fidelity and discuss, with examples, how mutations in these pathways produce genomic instability and clonal evolution.
Apply knowledge of the environmental factors that influence neoplastic transformation.
Describe the prevalence of neoplastic diseases and discuss the environmental factors that influence patients as they move between geographical regions.
Describe the mechanisms by which exposure to radiation, tobacco, alcohol, or other environmental chemical agents can produce cancer.
Describe the mechanisms by which viruses and other microbiological agents can contribute to the development of cancer.
Describe environmental factors that influence the incidence of common tumors.
Apply knowledge of the characteristics of neoplasia to discuss the morphologic appearance, classification, biological behavior, and staging of neoplasms.
Describe the essential morphologic features of neoplasms and indicate how these can be used to diagnose, classify, and predict biological behavior of cancers.
Discuss the cellular capabilities of neoplasms that enable them to invade tissues and to metastasize and recognize how this differentiates benign from malignant neoplasms.
Discuss the dependence of cancers on stromal elements and ability to generate their own blood supply to maintain growth and explain how this information can be used to treat cancers.
Define and provide examples of paraneoplastic syndromes and describe how substances produced by cancers can produce systemic effects in the host.
Compare and contrast the basic grading and staging of neoplastic diseases and describe the tumor, (lymph) nodes, metastasis (TNM) classification for common tumors such as breast and colon carcinoma.
Etiologies including physical damage resulting from trauma, particles, extreme temperature, and radiation and chemical exposures to small molecules and biologic toxins. The mechanism of injury usually causes direct damage that initiates a host response that can lead to a range of results from the process of resolution to a chronic complicated pathologic state.
Apply knowledge of biochemistry and cellular physiology to describe the mechanisms leading to cell injury induced by exposure to external agents including radiation, environmental toxins, drugs of abuse, and therapeutic agents.
Compare and contrast different mechanisms of chemical injury, specifically agents that act by direct binding to and inactivation of cellular constituents with those that require metabolic activation to induce toxicity and discuss how genetic factors affect toxicity of different agents.
Discuss the pathogenesis of tobacco use and the resultant pathologic changes in affected organs.
Discuss the pathogenesis of alcohol abuse and the resultant pathologic changes in affected organs.
Describe the mechanism by which drugs of abuse induce central nervous system effects and discuss, with examples, toxicities associated with both chronic use and acute overdose of these drugs, and withdrawal effects.
Provide examples of industrial, occupational, or environmental exposures that produce disease, the resultant pathologic changes in these affected organs from chronic exposure, and indicate what organ systems are most commonly affected by which agents.
Discuss, with examples, how therapeutic drugs can produce toxic effects on different tissues, distinguishing between idiosyncratic and dose-dependent effects.
Discuss the mechanisms by which radiation damages cells and tissues and compare and contrast how ultraviolet radiation, therapeutic radiation, and acute radiation sickness produce different disease manifestations in different organ systems. Discuss which organs are susceptible and why.
Apply knowledge of biochemistry, anatomy, physiology, and mechanisms of cell injury to describe the pathogenic mechanisms of physical injury.
Compare and contrast the types of injuries associated with mechanical force (blunt vs. penetrating) with respect to effects on skin, blood vessels, and the directly affected organs and discuss systemic response to massive trauma.
Discuss thermal injuries, comparing and contrasting the direct and systemic effects of thermal burns, hyperthermia, and hypothermia and mechanism of injury at the cellular level.
This topic includes the etiologic mechanisms, host responses, and disease processes leading to impairment of absorption, transport, and utilization of nutrients and oxygen, storage disorders, and disposal of waste products.
Apply knowledge of biochemistry and cellular physiology to explain the pathogenic mechanisms resulting from nutrient deprivation or nutrient toxicity, and the resulting pathology at the cellular, tissue, and organism levels.
Compare and contrast sources of fat-soluble and water-soluble vitamins (dietary sources) with respect to absorption, metabolism, and potential toxicity.
List vitamins and minerals whose deficiency can be associated with defined pathologic states, and explain the mechanisms by which these deficiencies produce disease.
Discuss the etiology and pathogenesis of obesity, comparing and contrasting genetic and environmental factors, and describe common clinical consequences.
Discuss the pathologic consequences of nutritional deficiencies other than vitamin deficiencies, with emphasis on severe protein-energy malnutrition, and discuss the pathologic states that have a significant impact on nutritional requirements.
Discuss the effect of diet and nutritional state on systemic disease, emphasizing the role it plays in the development of atherosclerosis and cancer.
This topic includes the understanding of acute and chronic inflammation, patterns of inflammation, the cellular components, mediators, and systemic effects.
Apply knowledge of the biochemistry and cellular physiology to describe pathogenic mechanisms of acute and chronic inflammation, and the resulting pathology at the cellular, tissue, and organism levels.
Describe the time course of the vascular and cellular events responsible for the acute inflammatory response to injury, and discuss the receptors and ligands that are responsible for these events.
Describe phagocytosis and the molecular mechanisms of intracellular killing.
Discuss the chemical mediators of inflammation, classifying the mediators with respect to origins, targets, and mechanisms of action.
Describe systemic changes seen in inflammation, including metabolic consequences of changes in levels of serum proteins (acute phase reactants) and other inflammatory mediators.
Summarize the possible pathological outcomes of inflammation and discuss factors that determine what outcomes are seen under different circumstances.
Recognize and classify the major types of inflammatory lesions that can be present in histologic sections, and identify the cellular and protein constituents in these lesions.
Compare and contrast acute, chronic, and granulomatous inflammation with respect to the major cell type(s) involved in the processes, the types of etiologic agents that produce each of these, and the mechanisms of tissue injury seen with these different types of inflammation.
Classify types of extravascular fluids associated with injury based on their cellular and protein content, know the terminology used to define these, and provide examples of pathologic conditions in which these can be found.
This topic includes the understanding of normal and dysregulated innate and adaptive cellular immune responses resulting in inflammation, resolution, and disease.
Apply knowledge of basic mechanisms of immunology to explain how dysfunction can produce cellular injury, acute and chronic inflammation, autoimmunity, allergic reactions, and susceptibility to infection; how these changes affect organ function and the health of the organism; and how therapeutic intervention can mitigate these effects.
Compare and contrast innate and adaptive immunity with respect to the molecules and cells involved in the immune response, and the role of these systems in host defense.
Compare and contrast the roles played by T cells, B cells, Natural Killer (NK) cells, macrophages, and dendritic cells in the immune response.
Discuss, with examples, the production of different cytokines by different immune cells, the roles that cytokines play in effecting the immune response, and how knowledge of cytokine action can be exploited in the treatment of disease.
Compare and contrast the mechanisms of the 4 hypersensitivity reactions with respect to the situations in which each is triggered, mechanisms of injury, resulting pathologic effects on tissue, and the ultimate clinical consequences.
Discuss how the complement cascade is activated, the role its activation plays in both inflammation and cellular cytotoxicity, and how abnormalities in complement function can produce disease.
Define immunological tolerance, and describe the role that failure of tolerance plays in the development of autoimmune diseases.
Discuss the structure and function of human histocompatibility antigens and describe the role of this system in both transplantation and susceptibility to certain diseases.
Discuss the consequences of tissue transplantation, including mechanisms and pathophysiology of graft vs. host organ rejection, and the possible therapeutic interventions that can mitigate these effects.
Compare and contrast the genetic basis and inheritance patterns of the well-defined primary immunodeficiency syndromes, discuss the pathogenesis and clinical sequelae of these disorders, and describe therapeutic interventions that can mitigate or correct them.
Describe the etiology, mechanisms of action, and possible clinical consequences of secondary immune deficiencies.
This topic includes the mechanisms by which microorganisms, viruses, and parasites cause disease including virulence factors produced by microorganisms and host response.
Apply knowledge of biochemical and cellular physiology to describe the pathogenic mechanisms of infectious diseases including both pathogen and host factors, the resulting pathology at the cellular, tissue, and organism levels, and clinical manifestations.
Explain the human host barrier to infection and describe how organisms spread within the body once the barrier is broken.
Describe the general categories of infective agents including bacteria, viruses, fungi, and parasites and describe the morphologic patterns of infectious diseases and the general mechanisms by which each of these cause disease.
Compare and contrast host responses to different classes of infectious agents in terms of morphological features, mechanisms of action, and mechanisms of immune evasion.
Apply knowledge of biochemical and cellular physiology to describe pathogenic mechanisms; the resulting pathology at the cellular, tissue, and organism levels; and the clinical manifestations of viral, bacterial, fungal, and parasitic infections.
Compare and contrast the mechanisms by which RNA, DNA, and retroviral viruses enter and damage cells.
Compare and contrast viruses that result in acute transient, chronic latent, chronic productive and transformative infections and discuss how these differences result in different disease pathogenesis.
Compare and contrast the histopathological features of herpes virus, cytomegalovirus, human papilloma virus, and adenovirus in terms of nuclear features, inclusions, size of cells, and other unique characteristics; recognize these histopathological features of viral infections in images of different tissues.
Describe the mechanisms by which bacteria damage cells and tissues, comparing and contrasting mechanisms characteristic of infection with particular categories of bacteria.
Discuss the different patterns of transmission of bacterial diseases as a function of both the type of organism and the organ systems involved in the infection.
Describe the histologic patterns of tissue response to bacterial infection as a function of differences in the organisms involved, the specific organ affected, and the manner by which the bacterium enters the organ.
Recognize and compare morphology and cell wall features of bacteria using Gram stain, Warthin Starry (silver) stain, Acid Fast stain, Partial Acid Fast stain, and Periodic Acid Schiff stain, and correlate with diagnosis.
List the different types of fungal organisms that infect humans and compare and contrast the mechanisms by which they damage tissues, the inflammatory responses they induce, and the resultant diseases that arise.
Recognize histopathologic evidence of fungal infections and compare and contrast the histopathological features and staining characteristics of the following fungi: Candida albicans, Cryptococcus neoformans, Aspergillus, Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitis, Pneumocystis jiroveci, and Zygomycetes.
Compare and contrast the types of fungal infections that occur in immunosuppressed and immunocompetent patients with respect to the organisms involved, the mechanisms of organ damage, and the resultant clinical manifestations.
Describe classes of parasites that produce human disease, give examples of each class, and discuss their life cycle within humans and within other hosts.
Discuss the mechanisms of pathologic damage caused by different parasites in different tissues, and describe the diseases, complications, and possible outcomes associated with such infections.
Recognize tissues involved with parasitic infections and compare the histopathological features and staining characteristics of parasites producing the following parasitic diseases: toxoplasmosis, giardiasis, amebiasis, malaria, babesiosis, leishmaniasis, trypanosomiasis, strongyloidiasis, schistosomiasis, filariasis, and cestode infections.
This topic includes an understanding of the pathogenesis of cellular proliferation for regeneration of cells, including of stem cells, and tissue and signal mechanisms for the repair process.
Apply knowledge of biochemistry and cellular physiology to describe the pathogenic mechanisms of tissue regeneration, renewal, and repair, the resulting pathology at the cellular, tissue, and organism levels, and describe clinical manifestations.
Compare and contrast embryonic and adult (somatic) stem cells with respect to their ability to proliferate and differentiate into different cell types; define induced pluripotent stem cells and compare and contrast them with the other types of stem cells.
Describe the 5 stages of the cell cycle, and explain the role of cyclins, cyclin-dependent kinase, and other proteins in the regulation of progression through the cell cycle, and how disruption of the cell cycle can lead to disease with resultant pathology.
Discuss the signaling pathways involved in the regulation of cell growth, listing important cell surface receptors, and describing the mechanisms whereby engagement of receptors by growth factors leads to cell growth.
List the important proteins of the extracellular matrix, describe the role of cell–matrix interactions in cell growth and differentiation, and provide examples of how structural alterations of matrix proteins produce disease.
Describe the regulation of angiogenesis, discussing receptors on vascular endothelium as well as the role soluble and stromal factors play in the process, and describe the effect of aberrant angiogenesis in certain diseases.
Describe the phases of cutaneous wound healing, the mechanisms of healing by first intention (primary union) and second intention (secondary union) and possible clinical consequences of abnormal wound healing.
Explain the effects of anti-inflammatory medications on wound repair.
This topic includes a basic knowledge of edema, congestion, and shock as well as a basic understanding of the coagulation cascade to understand the pathogenesis of thromboembolic disorders.
Apply knowledge of the biochemical and cellular physiology to discuss the pathogenic mechanisms resulting in alterations in hemodynamics and shock. Describe the resulting pathology at the cellular, tissue, and organism level and describe clinical manifestations associated with these pathologic changes.
Describe the pathophysiologic categories of edema and compare and contrast, with examples, how edema can be produced as a result of changes in hydrostatic pressure or plasma oncotic pressure.
Explain the clinical, morphological, and physiological significance of hyperemia, congestion, and hemorrhage, with respect to the disease states that cause them.
Classify different types of shock according to etiology and compare and contrast the pathogenesis of these different types.
Apply knowledge of the biochemical and cellular physiology to discuss pathogenetic mechanisms that result in alterations in blood clotting or other disruptions to blood flow. Describe the resulting pathology at the cellular, tissue, and organism level and the clinical manifestations associated with these pathologic changes.
Discuss the vascular, cellular, and humoral events involved in blood clotting and provide examples of genetic or acquired factors that can lead to either excess clotting or bleeding.
Compare and contrast thrombosis in situ and thromboembolism with respect to sites of involvement, risk factors, and attendant pathologic and clinical consequences.
Compare and contrast the etiology and clinical consequences of different types of embolism.
This topic includes a basic understanding of the cellular responses to cellular stress, mechanisms of cellular injury, and differentiating necrosis and apoptosis.
Apply knowledge of membrane physiology, metabolism, signal transduction, and macromolecular synthesis to discuss cellular responses to injury at the cell, tissue, and organism levels; how these responses affect morphologic appearance; and how they can be used for diagnostic, prognostic, and therapeutic purposes.
Discuss the pathogenesis of hyperplasia, hypertrophy, atrophy, and metaplasia, and compare and contrast their possible physiologic and pathologic causes.
Define necrosis and compare and contrast the forms of necrosis produced in response to different etiologic agents with respect to their variable clinical and morphologic features.
Compare and contrast ischemia and hypoxia and discuss the time course of the molecular events that occur in a cell in response to lack of oxygen, emphasizing the events that distinguish reversible from irreversible injury.
Summarize the cell’s response to reperfusion injury emphasizing how reperfusion can exacerbate injury produced by ischemia.
Apply knowledge of biochemistry and cellular physiology to differentiate between pathogenic and physiologic mechanisms of cell death, the resulting morphologic appearance, and the physiologic and clinical settings in which these mechanisms are activated.
Contrast the etiology, mechanisms, and morphologic changes of apoptosis with those of necrosis. Discuss the circumstances in which dysregulation of apoptosis can produce disease, and circumstances that determine why cells undergo apoptosis vs. necrosis.
Apply knowledge of cellular physiology, metabolism, and macromolecular synthesis to discuss cellular and subcellular responses to sublethal injury or stress on cells; how these responses affect morphologic appearance at the cell and tissue level; and how they can affect organ function.
Discuss, with examples, the changes that occur in cellular organelles or cytoskeletal proteins of different cell types in response to environmental alterations.
Describe the mechanisms of intracellular accumulations and the morphologic and clinical consequences of these accumulations.
Once the student has mastered the fundamental mechanisms and processes for causing, sustaining, extending, or resolving injury, this knowledge can be integrated to understand how pathology in each organ system affects the initial pathologic site, multi-organ systems, and the overall function of the patient.
There are 23 topics within this competency area. Each topic includes general learning goals and specific objectives that medical students should be able to meet upon graduation from medical school. Table 2 lists the topic areas and shows the number of goals and objectives for each.
Cardiovascular disorders resulting from abnormal development, hypoxia, immune dysregulation, infections and smooth muscle changes as they relate to the blood vessels are enumerated.
Apply knowedge of immunologic principles, inflammation, and tissue repair to explain atherosclerosis and its complications.
Explain how environmental factors (including elevated cholesterol and LDL complexes, infection, and smoking) can contribute to endothelial cell injury.
Describe the positive feedback loop in which damaged endothelial cells cause further endothelial damage.
Predict the local and distant consequences that are likely to follow rupture of an atherosclerotic plaque and the resultant clinical presentation.
Describe the morphologic changes in atherosclerosis and discuss how atrophic changes in the vessel wall may result in aneurysm formation.
Apply knowledge of the cellular response to injury and basic hemodynamic principles to explain how defective or excessive inflammatory and reparative processes damage blood vessels and how this damage results in thrombus formation.
Discuss the steps in thrombus formation and its predisposing factors.
Compare and contrast aortic aneurysms and aortic dissections in terms of their predisposing factors, the sites of involvement, and patient populations likely to be affected.
Describe the clinical consequences of an abdominal aortic aneurysm.
Apply knowledge of microbiological principles and mechanisms of immunologically mediated disease to discuss the pathogenesis, clinical presentation, morphological features, and laboratory diagnosis of the different vasculitides.
Describe how a drug-induced vasculitis depends on a functioning immune system.
Compare and contrast the mechanisms by which an autoimmune disease can appear as a vasculitis in 1 specific organ or as a generalized disease in many organs.
Describe the vasculitides that occur in large, medium, and small vessels.
Cardiovascular disorders resulting from abnormal development, hypoxia, immune dysregulation, infections and intrinsic muscle disease as they relate to the heart are enumerated.
Apply knowledge of anatomy, physiology, and general pathophysiologic principles to describe the clinical presentation associated with heart failure.
Compare and contrast right heart versus left heart failure in terms of clinical features, pathologic features, and the short-term and long-term consequences.
Compare and contrast the clinicopathologic features of dilated, restrictive, and hypertrophic cardiomyopathies.
Apply knowledge of anatomy, physiology, and general pathophysiologic principles to explain how atherosclerosis leads to heart disease and death.
Explain how ischemic heart disease can progress while remaining entirely free of symptoms for many years.
Contrast the clinical, physiologic, and histologic differences between exercise-induced angina and unstable angina.
Contrast the behavior of the myocardium that has been subjected to chronic ischemia alone from that of reperfused myocardium following therapy for infarction.
Compare and contrast the gross and microscopic features of acute myocardial infarction and remote myocardial infarction, and at what point gross or microscopic pathology appears.
Describe the histologic features of acute myocardial infarction and explain the pathophysiology underlying the histologic changes from initial infarction through fibrosis and relate to the laboratory diagnosis of myocardial infarction.
Identify short-term and long-term complications of myocardial infarction.
Apply knowledge of embryologic principles to describe how improper development of the heart and blood vessels leads to cardiac dysfunction.
Name the most common forms of congenital heart disease and outline their clinical presentation, natural history, and long- and short-term complications.
Name several common genetic disorders associated with congenital heart disease, and describe the clinical presentation.
Describe a paradoxical embolus in terms of congenital heart disease.
Define the concepts of left to right shunt, right to left shunt, and shunt reversal, and correlate with clinical presentation.
Apply knowledge of immunological and microbiological principles to explain the role of infectious agents in myocardial dysfunction and describe the related clinical presentations.
Describe the major manifestations of rheumatic fever and its effect on the endocardium, myocardium, and pericardium.
Compare the effects of rheumatic fever and bacterial endocarditis on the endocardium, myocardium, and pericardium.
Describe the 2 major patterns of infective endocarditis and the pathologic changes seen in the cardiac valves.
Discuss the pathologic features of noninfective endocarditis on the cardiac valves.
Describe the clinicopathologic features of myocarditis.
Summarize the common causes of pericarditis and their pathophysiologic features.
Apply knowledge of the anatomy and physiology of heart valves to explain how valvular dysfunction leads to heart failure and describe the related clinical presentation.
Discuss the complications associated with aortic stenosis.
Describe the clinicopathologic features of mitral valve prolapse.
Apply knowledge of the mechanism of response of cardiac muscle to increased resistance to describe the clinical and pathologic changes seen in systemic and pulmonary hypertension.
Describe the gross and microscopic adaptive changes in the myocardium that result from pulmonary hypertension.
Discuss the pathogenesis of hypertension and the gross and microscopic adaptive changes in the myocardium that result from systemic hypertension.
Red blood cell disorders resulting from abnormal development, nutritional derangements, inherited disorders, and intrinsic disease as they relate to anemia are enumerated.
Apply knowledge of nutritional biochemistry, erythropoiesis, and red blood cell structure and function to a discussion of the behavioral, hereditary, developmental, and chronic causes of anemia.
Explain the contribution of iron to red blood cell development and function. Describe behaviors and conditions that lead to iron deficiency and contrast the morphology and laboratory parameters of normal red cells versus iron-deficient cells.
Discuss the pathophysiology of hereditary spherocytosis.
Discuss the role of hepcidin as an iron regulator and describe how different types of alterations in the hepcidin pathway can produce anemia of chronic disease or iron overload.
Discuss the role of vitamin B12 and folic acid in red cell development and describe the pathophysiology of anemia arising from B12 and folic acid deficiency.
Explain the mechanisms by which anemia is produced on the basis of shortened red cell survival, distinguishing between intrinsic and extrinsic causes of red cell destruction.
Compare and contrast congenital and acquired forms of aplastic anemia.
Describe the structural alterations and regulatory abnormalities associated with hemoglobinopathies and thalassemia, and discuss how these abnormalities give rise to the clinical manifestations of these diseases.
White blood cell disorders resulting from abnormal development, genetic mutations, infections, and intrinsic disease as they relate to reactive and neoplastic abnormalities are enumerated.
Apply knowledge of anatomy and physiology to describe the normal development of white blood cells and nonneoplastic conditions leading to increased or decreased numbers of white blood cells.
Describe the maturational pathway of white blood cells, naming and describing the morphology of the cells present at each stage for each white blood cell type.
Define the role of growth factors in the development and maturation of white blood cells.
Define leukocytosis, describe several etiologies leading to it, and contrast it with leukemoid reaction.
Compare and contrast the causes, mechanisms, and consequences of neutropenia and lymphopenia.
Describe the common causes for neutrophilia, lymphocytosis, monocytosis, eosinophilia, and basophilia.
Discuss the common causes for neutropenia, lymphopenia, and leukopenia and compare with pancytopenia.
Apply knowledge of general concepts of neoplasia to explain how genetic mutations can produce hematologic malignancies and how the clinical behavior of different malignancies can be explained by different mutations.
Explain the difference between germline and somatic mutations; give examples and explain how each mutation contributes to the development of hematologic malignancies.
Compare and contrast, with examples, translocations that result in malignancy by activation of oncogenes with those that produce fusion proteins.
Explain with examples how dysregulation of cell proliferation or of cell death can give rise to lymphomas, and compare and contrast diseases arising by each mechanism with respect to morphologic appearance and clinical behavior.
Describe how understanding the molecular pathogenesis of leukemia and lymphoma can suggest targets for therapeutic intervention and give examples of diseases currently treated by targeted therapy.
Describe the clinicopathologic features of multiple myeloma in terms of clinical presentation, laboratory findings, radiologic findings, histologic features, and prognosis.
Apply knowledge of hematopoiesis to discuss the pathophysiologic basis for the classification of leukemia and lymphomas.
Describe the morphologic features that characterize typical cases of acute leukemia and lymphoma.
Compare and contrast myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemia with respect to morphologic appearance, clinical features, and underlying pathophysiology.
Compare and contrast low-grade or indolent lymphomas and high-grade or aggressive lymphomas with respect to underlying pathophysiology that yields specific morphologic features and clinical behavior.
Discuss the morphologic appearance of a blast and be able to distinguish acute myeloid leukemia from chronic myelogenous leukemia.
Describe the histologic appearance of typical cases of follicular lymphoma, diffuse large B-cell lymphoma, small lymphocytic lymphoma/chronic lymphocytic leukemia, and Hodgkin lymphoma.
Compare and contrast Hodgkin lymphoma with at least 2 non-Hodgkin lymphomas with respect to age and clinical symptoms at presentation, sites and pattern of spread of disease, cell of origin, histologic appearance, and prognosis and response to therapy.
Discuss the clinical manifestations of hematolymphoid neoplasms including age distribution of different tumors, presenting symptoms and signs, disease complications, natural history, and response to therapy.
Identify the tumors of bone marrow most likely to present with anemia, leukopenia, or thrombocytopenia and discuss the presenting clinical features most likely to be associated with each.
Define B symptoms, list which lymphomas are most and least likely to be associated with them, and discuss the prognostic implications of B symptoms in these diseases.
Define staging as it applies to lymphoma and give examples of different lymphomas in which staging has different clinical implications.
Identify lymphomas most likely to present in or involve extranodal sites such as the gastrointestinal tract, bone marrow, blood, skin, or central nervous system.
Describe how stem cells give rise to the diverse cell populations seen in bone marrow and lymph nodes and discuss how knowledge of hematopoietic cell development can provide a framework for understanding hematolymphoid neoplasia.
Outline, with examples, the difference between the cell of origin of a neoplasm and the morphologic expression of that disease.
Discuss the evidence that supports the existence of stem cells in myeloid leukemias and list the features of chronic myeloproliferative neoplasms that suggest they are derived from stem cells.
Describe the morphologic and molecular changes that take place within a lymph node in response to B-cell activation and explain how these changes relate to different types of B-cell non-Hodgkin lymphoma.
Thymus Apply knowledge of the anatomy and function of the thymus to summarize how developmental anomalies, immune disorders, and malignant transformation of epithelial and lymphoid cells lead to immune dysfunction.
Compare and contrast thymoma from lymphoma and describe the clinicopathologic features of thymic neoplasms.
Explain how deficits in particular stages of thymic development can produce specific types of disease.
Apply knowledge of the anatomy and function of the spleen to explain how developmental anomalies, immune, and metabolic disorders neoplasia lead to splenic dysfunction.
Explain the contribution of normal splenic function to nonneoplastic diseases.
Describe the clinicopathologic features of neoplastic and nonneoplastic disorders leading to splenomegaly.
Platelet disorders resulting from abnormal development, inherited disorders, immune, and infectious diseases and their central role in blood clotting as they relate to coagulation and hemostasis abnormalities are enumerated.
Apply knowledge of platelet structure and function to discuss qualitative and quantitative disorders leading to abnormal bleeding.
Summarize the role played by platelets in hemostasis, including platelet adhesion, activation, and aggregation.
Identify the examples of each of the following pathogenetic categories of thrombocytopenia: decreased production, decreased platelet survival, sequestration, dilutional effect.
Compare and contrast the following thrombocytopenia syndromes: immune thrombocytopenic purpura, drug-induced thrombocytopenia, heparin-induced thrombocytopenia.
Compare and contrast thrombotic thromobocytopenic purpura with hemolytic uremic syndrome.
Explain the biochemical basis of the following congenital and acquired defective platelet disorders: Bernard-Soulier syndrome, Glanzmann thrombasthenia, storage pool disorders, aspirin-related dysfunction, uremia-related dysfunction.
Explain the bases of marrow aplasia/myelophthisis, nutritional deficiency, and myelodysplasia as causes of thrombocytopenia form of marrow failure.
Apply knowledge of normal hemostasis, interaction of platelets, and procoagulant and anticoagulant factors to describe qualitative and quantitative disorders leading to abnormal bleeding and thrombosis.
Distinguish among the following manifestations of hemorrhage: hematoma, petechiae, purpura, and ecchymoses.
Compare and contrast the following stages of hemostasis: vasoconstriction, primary hemostasis, secondary hemostasis, and antithrombotic counterregulation.
Outline the process of secondary hemostasis, in terms of intrinsic pathway, extrinsic pathway, common pathway, fibrin formation, and fibrinolysis.
Describe how particular proteins that regulate the proteases to activate the clotting cascade either promote or inhibit coagulation.
Compare and contrast the roles of endothelial injury, stasis, and alterations in the regulation of blood clotting in the development of the hypercoagulable state.
Give examples and discuss the pathophysiology of inherited versus acquired conditions that increase the risk of thrombophilia.
Discuss disseminated intravascular coagulopathy (DIC) in terms of etiologies, pathogenesis, clinical presentation, and course.
Discuss the pathogenesis and clinical and laboratory manifestations of hemophilia A and explain how it differs from hemophilia B.
Describe the pathogenesis and clinical and laboratory findings in liver disease and vitamin K deficiency.
Compare and contrast types I, II, and III von Willebrand disease and explain the quantitative or qualitative abnormalities and the laboratory features observed in each type.
Describe the pathogenesis and clinical and laboratory findings in antiphospholipid antibody syndrome.
Explain the mechanism of heparin-induced thrombocytopenia/thrombosis and describe its clinical presentation and approach to therapy.
Explain the risk of thrombophilia in cancer, describe the context of Trousseau syndrome, and give classic examples of malignancies associated with thrombophilia.
Respiratory disorders resulting from abnormal development, genetic mutations, immune, infections, and intrinsic disease as they relate to lung abnormalities are enumerated.
Apply knowledge of the structure and function of blood vessels to explain the pathogenesis, clinical manifestations, and pathologic findings in pulmonary embolism, pulmonary hypertension, and diffuse pulmonary hemorrhage syndromes.
Compare and contrast the clinical manifestations, radiographic and pathologic findings, and potential consequences of pulmonary embolism in terms of single versus multiple, and small versus large emboli.
Discuss the factors, including underlying conditions, which can impact the incidence and clinical significance of pulmonary embolism.
Describe the structural cardiopulmonary conditions that are frequently associated with pulmonary hypertension.
Explain how each of the following cardiopulmonary conditions contributes to pulmonary hypertension: increased pulmonary blood flow or pressure, increased pulmonary vascular resistance, or left heart resistance to blood flow.
Describe the pathogenesis of pulmonary hypertension in hereditary and secondary forms and the characteristic gross and microscopic morphologic features of each.
Compare and contrast the clinical manifestations, pathogenesis, and pathologic findings in Goodpasture Syndrome and granulomatosis with polyangiitis (Wegener Granulomatosis).
Apply knowledge of the local pulmonary defense mechanisms and systemic host resistance to infection to discuss pathogenesis, classification, clinical manifestations, and pathologic findings in lower respiratory tract infections in immunocompetent and immunocompromised hosts.
Discuss the common infectious agents that produce pulmonary disease that are generally associated with defects in innate, humoral, or cell-mediated immunity.
Describe the classification of pneumonias by clinical setting and name the common etiologic agents for each category.
Compare and contrast the clinical presentation and manifestations, gross and microscopic pathology, prognosis, and potential complications for each category of pneumonia.
Define bronchopneumonia, lobar pneumonia, and atypical pneumonia/interstitial pneumonitis and compare and contrast the common etiologic agents and pathologic findings for each.
Compare and contrast the clinical presentation and gross and microscopic findings in primary, secondary/reactivation, and miliary tuberculosis.
Define antigenic drift and antigenic shift in influenza viruses and discuss how these can result in epidemics and pandemics.
Compare and contrast the pathologic findings in upper and lower respiratory tract influenza infections.
Name risk factors for aspiration pneumonia and describe the pathology, prognosis, and potential complications.
Define lung abscess in terms of pathogenesis, typical microorganisms, clinical presentation and course, and pathologic findings.
Compare and contrast the causative agents, geographic locations, clinical presentation, and pathologic findings in chronic pneumonia caused by fungal organisms.
Discuss the differences in clinical presentation and etiologic agents of pneumonia in immunocompetent versus immunocompromised hosts.
Apply knowledge of the molecular basis of neoplasia to describe clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of lung neoplasms.
Describe the common locations for the different types of lung cancer.
Discuss key gross and histopathologic features that may help differentiate between small cell, adenocarcinoma, and squamous cell carcinoma.
Describe features that favor the diagnosis of metastatic carcinoma over a primary lung tumor.
Describe the contribution of specific genetic mutations that are found in particular lung cancers and explain how these mutations affect therapeutic decisions.
Explain the environmental factors that predispose to the development of lung cancer and illustrate how these factors interact with genetic factors in the development of cancer.
Apply knowledge of the genetic and environmental factors leading to cell injury to explain the clinical and pathophysiological consequences that result in obstruction to airflow.
Describe the role of smoking in emphysema; name the 4 different types of emphysema, which is most common, and which lobes of the lungs are most involved in centrilobular emphysema.
Explain the gross morphologic changes associated with bronchiectasis and name 2 diseases that may lead to bronchiectasis.
Describe the clinicopathologic features identified with common forms of pneumoconiosis.
Compare and contrast the clinicopathologic features and causes of asthma and describe the morphologic changes and consequences that result in airflow obstruction.
Head and neck disorders resulting from abnormal development, genetic mutations, immune, and intrinsic disease as they relate to salivary and upper respiratory abnormalities are enumerated.
Apply knowledge of the structure and function of the salivary glands to an understanding of the clinicopathologic features associated with disorders presenting with gland enlargement.
Describe the potential causes for obstruction of the salivary gland duct.
Discuss disorders arising from lymphocytic infiltration of the salivary glands and discuss their potential neoplastic complications.
Describe Sjögren syndrome and discuss how it relates to salivary gland dysfunction, its effect on multiple organ systems, complications, and long term risks.
Apply knowledge of the etiology, pathogenesis, morphological appearance; and classification of neoplasms involving the salivary glands, oral cavity, upper airways, and larynx to their diagnosis; and prediction of biological behavior, prevention, and treatment.
Distinguish the clinicopathologic features of the 2 benign tumors (pleomorphic adenoma or mixed tumor and Warthin tumor) from the malignant mucoepidermoid carcinoma.
Discuss the pathogenesis of squamous cell carcinoma of the oropharynx and the spectrum of histologic findings from normal mucosa to invasive disease.
Compare and contrast human papillomavirus (HPV)-driven and alcohol-/tobacco-driven development of squamous cell carcinoma including precursor lesions, tumor formation and progression, anatomic location, and survival rate.
Compare and contrast developmental lesions that present as masses in the neck (branchial cyst and thyroglossal duct cyst) from a paraganglioma including pathogenesis and morphologic features of each.
Gastrointestinal (GI) tract disorders resulting from abnormal development, genetic mutations, immune, infections, and intrinsic disease as they relate to the esophagus, small, and large intestine abnormalities are enumerated.
Apply knowledge of the embryology of the foregut, midgut, and hindgut to summarize the morphological features and clinical presentation of developmental anomalies.
Discuss the clinicopathological features of tracheoesophageal fistula, pyloric stenosis, intestinal atresia, Meckel diverticulum, and Hirschprung disease.
Apply knowledge of the gross anatomy of the GI tract and hemodynamic principles to discuss vascular disorders.
Explain the pathogenesis and clinicopathological features for common disorders of the GI tract that arise from hypoxia or ischemia.
Compare and contrast the pathophysiology of necrotizing enterocolitis from bowel infarction due to shock and atherosclerosis.
Apply knowledge of the molecular basis of neoplasia to explain the clinical presentation, inheritance risk, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of gastrointestinal neoplasms.
Discuss the precursor lesions, risk factors, and hereditary cancer syndromes that lead to GI neoplasia.
Summarize the molecular basis and clinicopathologic features, local and systemic, for esophageal cancer, gastric cancer, GI lymphoma, GIST, colon, and anal cancer.
Describe the location of adenocarcinomas versus squamous cell carcinomas of the esophagus and list the major risk factors for each.
Discuss the 2 most important prognostic factors for colon cancer and explain why they are most important.
Compare and contrast the different types of polyps and their risk of developing cancer.
Apply knowledge of the gross anatomy of the GI tract and its blood supply to describe presenting signs and symptoms and pattern of spread of gastrointestinal neoplasms.
Distinguish between carcinomas arising in the left and right colon in terms of symptoms and morphology.
Describe how colon cancers are staged and list the common sites of metastases.
Apply knowledge of immune system dysregulation to discuss specific immune-related disorders.
Compare and contrast the pathophysiology and clinicopathological features of inflammatory bowel disease.
Explain the pathophysiology of gliadin hypersensitivity (celiac disease).
Describe the distribution of Crohn’s disease, pathogenesis, and how transmural involvement is related to complications and compare and contrast Crohn’s disease with ulcerative colitis
Apply knowledge of gastrointestinal anatomy and physiology to summarize the clinicopathologic features, diagnostic criteria, and therapy of disorders presenting with malabsorption.
Compare and contrast the pathogenesis and clinicopathologic features of systemic disorders leading to malabsorption.
Outline disorders of the pancreas and bile acid metabolism, and discuss how they lead to malabsorption.
Explain how celiac disease, sprue, gastroenteritis, and inflammatory bowel disease lead to malabsorption.
Apply knowledge of common pathogens and principles of immunity to describe the morphological features and clinical presentation of infectious diseases affecting immunocompetent and immunocompromised patients.
Compare the underlying mechanism and clinicopathologic features of GI tract involvement by common bacterial, fungal, and parasitic pathogens.
Relate the clinicopathologic features of Helicobacter to chronic gastritis and ulcer formation.
Apply knowledge of GI anatomy and physiology to explain the clinicopathologic features, diagnostic criteria, and therapy of disorders resulting in acid reflux, abnormal GI motility, and gastrointestinal tract obstruction.
Describe the pathophysiology and clinicopathological features of disorders presenting with dysphagia.
Compare and contrast the pathophysiology of gastrointestinal disorders that present with GI obstruction, including disorders such as volvulus, hernias, adhesions, and intussusception.
Describe the pathogenesis and complications of diverticulosis.
Describe the clinicopathologic features of acute appendicitis and discuss the clinical differential diagnosis and potential complications of this disorder.
Hepatobiliary disorders resulting from abnormal development, genetic mutations, immune, infections, toxins, and intrinsic disease as they relate to liver and biliary abnormalities are enumerated.
Apply knowledge of pathogenic organisms infecting the liver and their transmission, natural history, pathogenesis, laboratory profiles, and histopathological patterns of injury to the prevention and diagnosis of hepatitis.
Explain the routes of transmission of different hepatotropic viruses and how they relate to the public health measures that have been implemented to prevent their transmission.
Compare and contrast the possible clinical outcomes of the major hepatotropic viruses with particular reference to the incidence of progression to chronic hepatitis and cirrhosis.
Describe the pathophysiology associated with the major hepatotropic viruses and explain how this knowledge can be used to assess the presence of hepatitis, and the management and prognosis of this disease.
Explain the pathogenetic mechanisms of injury that result in the histopathological findings observed in acute and chronic viral hepatitis.
Describe the etiology of hepatic abscesses and the pathways that infectious agents may take to reach the liver.
Classify types of cirrhosis, in terms of etiology, pathogenesis, morphologic pattern (gross and microscopic), and their relationship to neoplasia.
Apply knowledge of the cellular response to injury, the pathogenic mechanisms leading to disease and the biochemical alterations of hepatic function to explain the clinicopathologic features, prognosis, and treatment of disorders resulting from ethanol and other drugs and toxins.
Describe the clinicopathologic features of excessive ethanol ingestion, focusing on biochemical pathways and short- and long-term complications, and compare and contrast alcoholic with nonalcoholic fatty liver disease.
Describe the clinicopathologic features of excessive acetaminophen ingestion focusing on biochemical pathways and short- and long-term complications.
Discuss the clinicopathologic features of excessive iron absorption, focusing on biochemical pathways, genetic factors, and short- and long-term complications.
Apply knowledge of the molecular basis of neoplasia to describe the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of hepatic neoplasms.
Compare and contrast, in the context of geographic location, the epidemiological importance of the known etiologic agents associated with the development of hepatocellular carcinoma and suggest public health measures that might decrease its incidence.
Discuss the pathogenesis of hepatocellular carcinoma arising in the setting of hepatitis B and hepatitis C, chronic hepatitis, and cirrhosis.
Describe how the molecular basis of a hepatic adenoma contributes to the risk of malignant transformation.
Identify the major space-occupying lesions that may be seen on radiographic imaging of the normal and cirrhotic liver, and discuss the complications of cirrhosis.
Describe the factors that lead to metastasis to the liver and the features of metastatic disease that distinguish it from primary neoplasms.
Apply knowledge of the cellular response to injury, the pathogenic mechanisms leading to disease and the biochemical alterations of hepatic function to describe the clinicopathologic features, prognosis, and treatment of intrahepatic and extrahepatic biliary tract diseases.
Outline how autoimmune hepatitis, primary and secondary biliary cirrhosis, and primary sclerosing cholangitis differ regarding associated conditions, incidence, sex predilection, etiology, laboratory features, clinical features and prognosis.
Compare and contrast the etiology and treatment of biliary atresia and neonatal hepatitis.
Apply knowledge of the molecular basis of neoplasia to an understanding of the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of neoplasms involving the biliary tree.
Describe the epidemiology, morphology, and clinical features of gallbladder and extrahepatic biliary tract carcinoma.
Describe the presenting symptoms of cholangiocarcinoma and how the symptoms relate to the location.
Apply knowledge of both the embryonic principles of hepatic and bile tract development and mechanisms of fibro-inflammatory injury to an understanding of disorders due to maldevelopment and acquired abnormalities of the biliary tree.
Describe the inheritance, etiology, clinical and laboratory features, and prognosis of congenital hepatic fibrosis.
Describe the inheritance, etiology, clinical and laboratory features, and prognosis of polycystic liver disease.
Apply knowledge of general biochemical principles to an understanding of how gallstones develop, risk factors for their development, and their clinical presentation and complications.
Describe the risk factors, clinical features, complications, mechanisms, and composition of gallstones.
Differentiate the epidemiology, morphology, clinical features, and complications of acute and chronic cholecystitis.
Differentiate the etiology, pathogenesis, morphology, and clinical features of empyema and hydrops of the gallbladder.
Pancreas disorders resulting from abnormal development, genetic mutations, immune, infections and intrinsic disease as they relate to the exocrine pancreatic abnormalities are enumerated.
Apply knowledge of the structure and function of the pancreas to an understanding of the clinicopathologic features and diagnostic criteria of disorders resulting from cellular injury to the exocrine pancreas.
Compare and contrast acute and chronic pancreatitis in terms of etiology, pathogenesis, morphologic features, and complications.
Describe with examples genetic disorders that affect the function of the exocrine pancreas.
Apply knowledge of the molecular basis of neoplasia to an understanding of the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of pancreatic neoplasms.
Describe the major types of neoplasms affecting the exocrine pancreas.
Explain how the location of a pancreatic neoplasm determines its presenting symptoms and discuss the risk factors for pancreatic adenocarcinoma.
Describe clinicopathological features of neoplasms of the endocrine pancreas.
Kidney disorders resulting from abnormal development, genetic mutations, immune, infections, and intrinsic disease as they relate to renal abnormalities are enumerated.
Apply knowledge of the molecular basis of neoplasia to explain the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of renal neoplasms.
Compare and contrast the 3 major types of renal cell carcinoma (clear cell, papillary, and chromophobe) in terms of clinical presentation, diagnostic morphological features, and molecular pathogenesis.
Compare and contrast pelvic urothelial malignancies with renal cell carcinomas in relation to risk factors, microscopic appearance, and biological behavior.
Describe how renal cell carcinoma is graded and staged and discuss the factors that determine prognosis.
Describe the clinical and pathologic features and molecular basis for Wilms tumor and list the histologic features that are important to recognize in determining prognosis, and the etiology of Wilms tumor as part of different syndromes.
Apply knowledge of kidney structure and function to summarize how acquired and hereditary abnormalities of the renal tubules and interstitium cause acute and/or chronic renal dysfunction.
Describe the clinicopathological features and pathogenesis of tubulointerstitial diseases and discuss how their pathogenesis relates to treatment and outcomes.
Compare and contrast acute pyelonephritis, drug-induced interstitial nephritis, and lupus nephritis in terms of pathogenesis, clinical presentation, histopathological appearance, and treatment.
Compare and contrast ischemic and nephrotoxic forms of acute tubular injury, including typical clinical contexts, pathogenesis of renal failure, microscopic appearance, and expected outcome.
Compare and contrast chronic pyelonephritis and reflux nephropathy, including the organisms commonly associated with each.
Compare and contrast the common causes of renal vascular dysfunction in terms of size and types of vessels involved, characteristic gross and microscopic morphology, pathogenesis, and clinical presentation.
Compare thrombotic and embolic causes of renal arterial occlusions in terms of underlying pathogenesis, gross and microscopic pathological anatomy, and clinical presentation.
Discuss how the pathogenesis of hypertension leads to structural changes in the renal vasculature and how the characteristic pathological vascular lesions of the kidney seen in hypertension cause renal dysfunction.
Compare and contrast typical hemolytic uremic syndrome (HUS), atypical HUS, and thrombotic thrombocytopenic purpura (TTP) in terms of clinical presentation, renal histopathology, pathogenesis, and prognosis.
Apply knowledge of the embryologic principles of kidney and lower urinary tract development to explain developmental anomalies.
Compare autosomal dominant and autosomal recessive polycystic kidney disease in terms of pathological anatomy, molecular pathogenesis, and clinical presentation.
Apply knowledge of the structure and function of the kidney to describe the pathogenetic mechanisms, diagnostic criteria, and clinicopathologic features of glomerular diseases presenting with asymptomatic proteinuria, nephrotic and nephritic syndrome.
Describe the proliferative and proinflammatory pathologies of conditions presenting with nephritic syndrome.
Describe the pathophysiology and morphologic features of nephrotic syndrome, and contrast with nephritic syndrome.
Compare and contrast the mechanisms of immune complex and antibody-mediated glomerulonephritis.
Describe the pathogenesis of diabetic nephropathy and the associated clinicopathologic features.
Describe the pathogenesis of the nephropathies associated with dysproteinemia.
Bladder disorders resulting from abnormal development, genetic mutations, infections, obstructions and intrinsic disease as they relate to urothelial abnormalities are enumerated.
Apply knowledge of the molecular basis of neoplasia to describe the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of bladder neoplasms.
Compare and contrast the different precursor lesions of urothelial carcinoma in terms of architecture, cytologic features, molecular–genetic changes, and propensity for invasion/progression.
Relate the risk factors for urothelial carcinoma to general principles of carcinogenesis.
Describe the typical clinical presentation of urothelial carcinoma and the advantages and limitations of urine cytology in diagnosis and surveillance of urothelial carcinoma.
Relate stage of bladder cancer to prognosis and therapy, including the role of BCG, in the treatment of low-stage tumors.
Apply knowledge of innate and adaptive immunity, pathogenic organisms infecting the bladder and their transmission to explain the natural history, pathogenesis, diagnosis, laboratory profiles, histopathological features, and prevention of cystitis.
Discuss the typical clinical symptomatology of acute cystitis and the organisms commonly causing this disorder.
Describe the most common noninfectious causes of cystitis.
Describe examples in which cystitis may result in mass lesions or morphologic lesions of the urinary bladder, and describe the pathogenesis of the process.
Apply knowledge of the anatomy and physiology of the kidney to describe how disorders may lead to obstruction of urinary outflow.
Describe the pathogenesis of bladder diverticula, including congenital and acquired, and their potential role in infection, lithiasis, and obstruction and occult carcinoma.
List the different chemical types of nephrolithiasis, and explain the pathophysiologic mechanisms related to development and therapy/prevention of urinary stones.
Explain and give specific examples of several causes of urinary obstruction.
Prostrate disorders resulting from genetic mutations, infections, and intrinsic disease as they relate to prostate abnormalities are enumerated.
Apply knowledge of the molecular and cellular origins of prostate cancers, specifically adenocarcinoma, to summarize the epidemiology, clinicopathological features, natural history, and treatment strategies for this disease.
Outline the cellular phenotype of the typical adenocarcinoma cell and describe its molecular and immunohistochemical characteristics.
Define the histopathological diagnostic criteria for the diagnosis of adenocarcinoma.
Explain the epidemiology of prostate cancer with respect to age, race, and family history.
Compare and contrast the significance of “histological” adenocarcinoma versus a “clinically significant” adenocarcinoma.
Apply knowledge of the molecular and cellular origins of nonneoplastic disorders of the prostate, specifically prostatitis and nodular hyperplasia, to explain the epidemiology, clinicopathological features, natural history, and treatment strategy for these diseases.
Explain the molecular and hormonal origins of nodular hyperplasia, the area of the prostate affected, the natural history of the disease, various treatment strategies, and anticipated outcomes of treatment.
Describe the pathophysiologic basis for inflammatory conditions affecting the prostate, including the organisms causing this condition.
Testicular disorders resulting from abnormal development, germ cell lesions, infections, and intrinsic disease as they relate to testes abnormalities are enumerated.
Apply knowledge of the molecular and cellular origins of nonneoplastic disorders of the testis to explain the epidemiology, clinicopathological features, natural history, and treatment strategy for these diseases.
Name the structure through which the testes descend during fetal development and what is brought with the testes in the descent. Describe the complications observed for failure of the testes to descend (cryptorchidism).
Describe the clinicopathologic features that occur in the testis due to torsion of the spermatic cord.
Discuss several inflammatory conditions affecting the testis and the clinicopathologic features associated with each.
Apply knowledge of the molecular and cellular origins of the common types of testicular cancer to explain the epidemiology, clinicopathological features, natural history, and treatment strategies for this disease.
Describe the most important risk factors for development of a germ cell tumor of the testis and outline the clinicopathologic features for the different morphologic patterns seen.
Discuss a differential diagnosis for a testicular mass.
Breast disorders resulting from abnormal development, genetic mutations, immune mediated, infections, and intrinsic disease as they relate to breast abnormalities are enumerated.
Apply knowledge of the embryology, cellular responses to injury, underlying etiology, and biologic and molecular alterations to describe the clinical presentation, inheritance risk, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and therapy of nonneoplastic disorders of the breast.
Identify the most frequently diagnosed breast lesions by age of the patient, based on the most common clinical presentations in males versus females.
Discuss silicone breast implants in terms of the morphologic changes in the adjacent breast and the risk of subsequent autoimmune disease and cancer.
Compare and contrast reactive breast conditions in terms of etiology, pathogenesis, morphology, and clinical features.
Discuss the clinical significance of proliferative and nonproliferative fibrocystic change, with and without atypia, and describe how each of these changes and the family history affects the subsequent risk of developing breast cancer.
Apply knowledge of the molecular basis of neoplasia to describe the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of breast neoplasms.
Compare and contrast fibroadenoma and phyllodes tumor in terms of clinical features, morphologic findings, and prognosis.
Describe the proposed precursor-carcinoma sequence in breast cancer and name the characteristic morphologic changes.
Compare and contrast ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS) in terms of incidence, clinical presentation, morphology, biomarker expression, pattern of spread, natural history, treatment, and prognosis.
For the most common breast cancer susceptibility genes, describe the normal function of the gene product, incidence of gene mutation, reasons for its association with cancer, percentage of hereditary breast cancer, and risk of breast cancer by age 70.
Explain the major molecular classes of invasive ductal carcinoma of the breast identified by gene expression profiling, and describe how each correlates with prognosis and response to therapy.
Construct a table to compare and contrast invasive ductal carcinoma (NOS), invasive lobular carcinoma, medullary carcinoma, colloid (mucinous) carcinoma, tubular carcinoma, and metaplastic carcinoma of the breast in terms of incidence, age predilection, etiology, pathogenesis, clinical presentation, gross and microscopic morphology, grade, molecular classification, patterns of spread, clinical course, prognostic indicators, treatment options, and survival rates, and indicate which are more common in males versus females.
Explain the prognosis and likelihood of recurrence and response to therapy for breast cancer patients based on knowledge of molecular classification and/or gene expression profiling, morphologic classification, grade, prognostic marker studies, and other predictive factors.
Uterine disorders resulting from abnormal development, genetic mutations, infections, and intrinsic disease as they relate to uterine abnormalities are enumerated.
Apply knowledge of the molecular basis of neoplasia to describe the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of uterine neoplasms.
Compare and contrast common benign and malignant uterine neoplasms, including important clinicopathological features related to treatment and prognosis.
Compare and contrast the precursors, clinical setting, risk factors, pathologic findings and prognosis for type I and type II carcinomas of the endometrium.
Discuss the relationship of endometrial carcinoma to hereditary nonpolyposis colorectal carcinoma.
Discuss the natural history, clinical presentation, and management of benign smooth muscle tumors of the uterus and the risk for malignant transformation.
Apply knowledge of uterine physiology, endocrinology, and anatomy to compare and contrast the clinical presentation and pathology of common nonneoplastic uterine disorders.
Define endometrial hyperplasia and discuss its etiology, classification, and prognosis.
Identify the phases of the menstrual cycle and the major hormonal changes that occur, comparing normal menstruation to common causes of abnormal bleeding in adolescents, perimenopausal, and postmenopausal women.
Compare and contrast the pathology of adenomyosis with endometriosis.
Discuss causes of abnormal uterine bleeding including hormonal disturbances, acute and chronic endometritis, and endometrial polyps.
Apply knowledge of cervical physiology and anatomy to compare and contrast the clinical presentation and pathology of common cervical disorders.
Discuss the common human papillomavirus (HPV) types that affect the cervix and discuss the pathogenesis of cervical dysplasia and neoplasia, and cervical screening methods and prevention.
Apply knowledge of physiology and anatomy to compare and contrast the clinical presentation and pathology of common female genital tract disorders.
Discuss the common pelvic infections including those affecting the vulva, vagina, cervix, and fallopian tubes, and describe the pathogenesis of pelvic inflammatory disease, common organisms involved, and its complications.
Ovarian disorders resulting from abnormal development, genetic mutations, infections, immune, and intrinsic disease as they relate to the ovary are enumerated.
Apply knowledge of the molecular basis of neoplasia to describe the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of ovarian neoplasms
Describe the embryologic development and the histologic components of the ovary, including surface Müllerian epithelium, germ cells, and the sex-cord stromal cells.
Describe the risk factors, genetic associations, and molecular basis, including hereditary cancer syndromes, for ovarian neoplasms, including those derived from epithelium, sex-cord stromal as well as germ cell neoplasms.
Apply knowledge of infectious diseases, embryology, and immunology to explain the major pathologic features of processes affecting the ovary.
Describe the pathogens, bacterial, fungal, and parasitic that can cause ovarian disease and explain the underlying mechanisms, clinicopathologic features, and complications.
Explain the pathophysiologic basis of polycystic ovary syndrome.
Explain the mechanism(s) by which the dysregulation of the immune system gives rise to ovarian disease and describe the pathology observed.
Describe the clinicopathologic features of menopause and the basis for treatment.
Pregnancy disorders resulting from abnormal implantation, genetic mutations, hemodynamic, immune, infections, and intrinsic disease as they relate to gestational disease abnormalities are enumerated.
Apply knowledge of embryology, cellular responses to injury, hemodynamics, and molecular alterations to summarize the clinical presentation, morphologic appearance, classification, diagnosis, biologic behavior of and therapy for disorders of pregnancy.
Describe risk factors, characteristic morphologic findings, potential outcomes, and the medical/surgical options for management of ectopic pregnancy in relation to the pathogenesis and likelihood of adverse consequences.
List 2 fetal and 6 maternal causes for spontaneous abortion and indicate which is the most common.
Describe how disorders of late pregnancy can lead to effects that threaten the mother and/or fetus.
Discuss the ascending and hematogenous infections occurring during pregnancy in terms of etiology, pathogenesis, morphology, methods of diagnosis, prognosis, and treatment.
Explain the principal pathophysiologic aberrations of the placenta and maternal circulation in preeclampsia and eclampsia; the characteristic morphologic features in the placenta, liver, kidney, and brain; and how management is affected by gestational age and severity of disease.
Explain with specific examples how to differentiate forms of gestational trophoblastic disease based on etiology, pathogenesis, morphologic features, clinical features, and laboratory findings, including potential consequences and/or subsequent risks, treatment, and prognosis for each.
Describe the pathophysiologic effects of diabetes mellitus on the mother and fetus.
Endocrine disorders resulting from abnormal development, genetic mutations, immune, infections, and intrinsic disease as they relate to multiple endocrine organ abnormalities are enumerated.
Apply knowledge of pituitary physiology to describe the pathophysiology and clinicopathologic features of disorders associated with hyperpituitarism and hypopituitarism.
List several causes for destruction of the anterior pituitary and the clinicopathologic features associated with each.
Define Sheehan’s syndrome and discuss the clinicopathologic features associated with it.
Outline the clinicopathologic features associated with disorders affecting the posterior pituitary gland.
Apply knowledge of thyroid physiology to explain the pathophysiology and clinicopathologic features of disorders associated with hyperthyroidism and hypothyroidism.
Compare and contrast the causes of hyperthyroidism versus hypothyroidism.
Compare and contrast the clinicopathologic features of hyperthyroidism versus hypothyroidism.
Apply knowledge of immune system dysregulation to summarize immune-related disorders of the thyroid.
Compare and contrast the pathophysiology and clinicopathologic features of Graves’ disease, Hashimoto’s thyroiditis, and subacute lymphocytic thyroiditis.
Compare and contrast immune-mediated thyroid disease with subacute granulomatous thyroiditis (de Quervain’s thyroiditis).
Apply knowledge of adrenal physiology to describe the pathophysiology and clinicopathologic features of disorders associated with adrenocortical hyperfunction (hyperadrenalism) and adrenocortical insufficiency.
Compare and contrast the causes and clinicopathologic features of hypercortisolism (Cushing syndrome) and the pathophysiologic basis distinguishing between these causes and the management of this disease.
Compare and contrast the causes and clinicopathologic features of primary and secondary hyperaldosteronism.
Outline the clinicopathologic features of congenital adrenal hyperplasia.
Compare and contrast the causes of adrenocortical insufficiency, including the pathogenesis of primary acute and chronic adrenocortical insufficiency.
Apply knowledge of the molecular basis of neoplasia to explain the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of endocrine neoplasms.
Compare and contrast the clinicopathologic features of follicular adenomas, follicular carcinoma, and papillary thyroid carcinoma.
Describe the molecular basis and clinicopathologic features of medullary thyroid carcinoma.
Outline the clinicopathologic features of pheochromocytoma and compare and contrast the hereditary cancer syndromes associated with paragangliomas/pheochromocytomas.
Explain the clinicopathologic features of pituitary adenomas including their genetic mutations and their associated clinical syndromes.
Compare and contrast the clinicopathologic features of the pancreatic endocrine tumors including the genetic alterations and complications of each.
Apply knowledge of the structure and function of the endocrine pancreas and biochemical principles of carbohydrate metabolism to summarize the clinicopathologic features, diagnostic criteria, and therapy of disorders resulting from excess or decreased production of insulin and other islet cell hormones.
Compare and contrast the clinicopathologic features of type 1 and type 2 diabetes.
Outline the pathologic complications of diabetes mellitus.
Compare and contrast the clinicopathologic features of MEN 1 with MEN 2 and 3.
Skin disorders resulting from abnormal development, genetic mutations, immune, infections, and intrinsic disease as they relate to dermal abnormalities are enumerated.
Apply knowledge of histology, cell biology, inflammation, and neoplasia to an understanding of the clinical presentation, biologic behavior, morphologic appearance, and classification of diseases of the skin.
Describe the pathophysiologic basis for changes in the color, surface texture, swelling, temperature, and sensitivity of skin.
Apply knowledge of the anatomic and immunologic structure of the skin to discuss the role of skin in protecting against direct invasion of skin and appendages by pathogens.
Explain the anatomic basis for the skin as a barrier and the role of normal flora that colonize the skin in this function.
Describe common bacterial, viral, fungal, and parasitic agents that may cause cutaneous infections and the particular sites that they infect, and morphologic features and complications of these infections.
Apply knowledge of basic concepts in immunopathology and the key immunologic functions of components of the skin to understand the pathologic basis of disease caused by reactivity to exogenous agents versus immunologically driven disease with a genetic component.
Describe the clinical features and pathologic basis for skin manifestations to exogenous antigens including infectious organisms, drugs, chemicals, and environmental agents.
Describe the clinical features and pathologic basis for the following immunologically driven diseases with a genetic component: eczema, psoriasis, and vitiligo.
Apply knowledge of genetics, skin structure, and function and basic principles of pathology to an understanding of nonneoplastic inherited disorders of the skin.
Describe the genetic basis for blistering diseases affecting the skin.
Apply knowledge of the molecular basis of neoplasia to an understanding of the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and therapy of benign and malignant skin neoplasms.
Describe the clinical presentation and histopathologic findings of benign skin growths of the following cellular origins: basal cell, squamous cell, melanocytes, as well as neoplasms of dermal origin.
Describe the clinical presentation, precursor lesions, risk factors and hereditary cancer syndromes that lead to the following skin cancers: basal cell carcinomas, squamous cell carcinoma, and melanoma.
Identify the genetic disorders with high risk of skin cancers and explain the molecular basis of that risk as well as the genomic mutations involved.
Explain the role of ultraviolet light and other environmental factors in development of various skin cancers.
Describe the various clinical presentations of cutaneous T-cell lymphoma/mycosis fungoides and discuss the natural course of the disease.
Musculoskeletal disorders resulting from abnormal development, genetic mutations, nutritional, immune, infections, and intrinsic disease as they relate to lung abnormalities are enumerated.
Apply knowledge of the molecular basis of neoplasia to describe the clinical presentation, biologic behavior, morphologic appearance, classification, diagnosis, prognosis, and targeted therapy of bone neoplasms.
Describe examples of bone forming, cartilage forming, and other common bone tumors including the clinicopathologic features, radiological features, treatment, and prognosis of each.
Describe the most common benign and malignant bone forming tumors in children and adolescents in terms of clinical presentation, radiologic findings, histologic features, treatment, and prognosis.
Describe the most common benign and malignant cartilaginous tumor of bone in children and adolescents in terms of clinical presentation, radiologic findings, histologic features, treatment, and prognosis.
Describe the tumors that commonly metastasize to bone, the radiologic manifestations of metastatic lesion involving bone, and the difference between osteoblastic and osteolytic metastases.
Describe the common benign and malignant soft tissue tumors including the genetic contribution to tumor development and progression.
Apply knowledge of histology, immunology, microbiology, and biological and molecular alterations to discuss clinical presentation, biological behavior, morphological appearance, and natural history of nonneoplastic disorders of bones, joints, and skeletal muscle.
Compare and contrast osteomalacia and rickets with respect to pathogenesis and clinicopathologic features.
Discuss the pathogenesis of osteomyelitis, including predisposing factors, organisms involved, morphologic appearance, and complications.
Distinguish primary from secondary osteoporosis in terms of etiology, pathogenesis, and morphology.
Describe the common degenerative diseases of the spine.
Compare and contrast pathologic versus nonpathologic fractures including the potential for healing.
Discuss the clincopathologic changes of Paget Disease including the histologic phases, genetic changes, and complications of this disorder.
Compare and contrast rheumatoid and osteoarthritis including the etiology, pathogenesis, and morphology of each.
Nervous system disorders resulting from abnormal development, genetic mutations, vascular, immune, infections, and intrinsic disease as they relate to central nervous system (CNS) abnormalities are enumerated.
Apply knowledge of the pathological and molecular basis of common brain tumors to describe their clinical behavior, effects on the nervous system, and therapies.
Explain the pathophysiology underlying the signs and symptoms associated with brain tumors.
Compare and contrast the common types of brain tumors that affect the cerebrum, the cerebellum, the meninges, and the cranial nerves in adults and children; and outline their molecular basis and clinicopathologic features.
Describe the major hereditary tumor syndromes of the central nervous system, the genes responsible for each syndrome, and the spectrum of tumors associated with each syndrome.
Explain the pathophysiologic basis for grading primary brain tumors and discuss how grading relates to prognosis and governs patient management.
Describe several complications of brain tumors and give specific examples.
Discuss carcinomas that commonly metastasize to the central nervous system and describe the locations in which metastases may be seen.
Apply knowledge of clinical features, neuroimaging studies and location of lesion(s) to develop a differential diagnosis for CNS infection.
Compare and contrast the clinical, gross, and microscopic manifestations of common bacterial, viral, and fungal infections of the central nervous system.
Discuss 5 common opportunistic infections that involve the CNS of immunocompromised individuals and describe their pathologic features.
Describe the clinicopathologic features of progressive multifocal leukoencephalopathy (John Cunningham virus) and contrast them with infiltrative astrocytoma.
Describe the gross and microscopic features of acute suppurative meningitis and brain abscess; and name the organisms most commonly associated with each.
Apply knowledge of neuroanatomy, pathogenesis, and biologic behavior to develop differential diagnoses and determine appropriate therapy for disorders of the spinal cord.
Describe the importance of distinguishing ependymoma from infiltrative astrocytoma intraoperatively and list the histologic features of each.
Explain how examination of a spinal cord at autopsy is important for the diagnosis and classification of demyelinating and/or neuromuscular diseases.
Describe the pathogenesis, clinical presentation, and gross and microscopic pathologic features of multiple sclerosis.
Apply knowledge of clinical, anatomic, and neuropathologic principles to the diagnosis of neuromuscular disorders.
Describe the etiology, pathogenesis, and clinical features of amyotrophic lateral sclerosis.
Describe the etiology, pathogenesis, and clinical features of 2 types of mitochondrial diseases affecting muscle, and explain why it may be important to obtain fresh frozen muscle to aid diagnosis.
Apply knowledge of structure and function and general pathologic concepts to describe disorders where dementia is a component.
Define the essential underlying abnormalities of amyloid and tau proteins in the most common causes of dementia in the United States.
Describe the protein processing abnormalities responsible for multiple neurodegenerative diseases.
Describe the clinical features, gross pathology, and histopathology of Alzheimer’s disease and name 3 regions of the brain that are usually involved.
Discuss 3 genes in which mutations have been identified in patients with early onset Alzheimer’s disease.
Describe several diseases which involve the basal ganglia and describe how to distinguish among the diseases in terms of gross, microscopic, and clinical pathology.
Apply knowledge of the structure and function of the brain and general immunopathology concepts to summarize disorders that result in demyelination in terms of their etiology, pathogenesis, clinical and morphologic features, natural history, and therapeutic options.
Describe the autoimmune mechanism mediated by CD4+ T cells that react against self myelin antigens in multiple sclerosis and outline the clinicopathologic features of the disease.
Apply knowledge of the structure and function of the brain and general pathology concepts to discuss disorders resulting from altered blood supply and hypoxia to the brain.
Compare and contrast the 2 major mechanisms for stroke and how treatment differs for each.
Describe the pathologic findings seen in the most common causes of traumatic brain injury.
Compare and contrast the etiologies and clinical presentations of epidural, subdural, subarachnoid hemorrhages, basal ganglionic, and lobar hemorrhages.
Describe the mechanism of hypertensive hemorrhage and name 3 common locations in which this occurs.
Describe how embolic infarcts differ from atherothrombotic infarcts in pathologic appearance and name 3 sources of emboli.
Compare and contrast the gross and histopathologic appearance of acute versus remote brain infarction.
Nervous system disorders resulting from abnormal development, genetic mutations, vascular, immune, infections and intrinsic disease as they relate to peripheral nervous system (PNS) and ocular abnormalities are enumerated.
Apply knowledge of the structure and function of the peripheral nerves and general pathology concepts to discuss peripheral nerve disorders.
Describe the clinicopathologic features of antibody-mediated disorders of the neuromuscular junction such as myasthenia gravis and Lambert-Eaton myasthenic Syndrome.
Compare and contrast the clinicopathologic features of inflammatory neuropathies, autoimmune neuropathy, and infectious neuropathy.
Compare and contrast the clinicopathologic features of neurofibromatosis types 1 and 2.
Apply knowledge of the pathological and molecular basis of common PNS tumors to describe their clinical behavior, effects on the nervous system, and therapies.
Describe the major hereditary tumor syndromes of the peripheral nervous system, the genes responsible for each syndrome, and the spectrum of tumors, including the histology associated with each syndrome.
Compare and contrast the common benign from malignant PNS tumors, and outline their molecular basis and clinicopathologic features.
Apply knowledge of the structure and function of the eye and general pathology concepts to discuss common ocular disorders.
Describe the clinicopathologic features of common primary and secondary disorders of the eye including macular degeneration and uveitis.
Describe the clinicopathologic features of common neoplasms of the eye including ocular melanoma and retinoblastoma.
Diagnosis and patient management require the student to apply their knowledge of disease mechanisms and organ system pathology to achieve efficient and effective use of clinical laboratory testing. In addition, the student should learn the proper use of blood/blood product utilization to enable optional diagnosis, treatment, and patient care.
There are 10 topics within this competency area. Each topic includes general learning goals and specific objectives that medical students should be able to meet upon graduation from medical school. Table 3 lists the topic areas and shows the number of goals and objectives for each.
Every physician should have an appreciation for the preanalytical, analytical, and postanalytical phases of laboratory testing. In addition, physicians need an appreciation of the statistical treatment of data that underlies test utilization. This includes but is not limited to the ability to choose the correct test to make a diagnosis enabling treatment selection and to employ the appropriate testing paradigm to monitor patients with chronic diseases enabling optimal clinical management.
Apply knowledge of clinical medicine, pathology, and statistics to determine the utility of a laboratory test in making a diagnosis and in monitoring chronic disease management. Explain the interpretation and limitations of clinical laboratory assays.
Give examples of common sources of preanalytical and postanalytical errors and categorize errors when the following procedures are not properly followed: pairing patient/specimen identification with the requisition forms, using correct specimen containers/tubes for specific tests, and timing of collection, transport, and storage.
Evaluate the quality of an assay in differentiating disease versus nondisease states, including graphically presenting and interpreting the data. Determine the relationship between sensitivity and specificity for this assay.
Determine the value of an assay by evaluating the impact of differing pretest probabilities such as prevalence on the positive and negative predictive value of the test. Give examples of the laboratory tests used to evaluate clinical disorders where predictive values are used to develop screening, diagnostic, prognostic, and patient management protocols.
Describe the methods used to establish reference intervals and how the following conditions apply: the effect of demographics, treatments, or disease states on reference intervals variability; the difference between reference ranges and therapeutic ranges and why 5% of laboratory test results fall outside a reference range; analytical versus clinical sensitivity; and mixing test results in the clinical information system from different laboratories that use different methodologies.
Explain the difference between technical variability and biologic variability including how physical and chemical parameters, such as sample size, hemolysis, and lipemia, can affect test results. Define analytical uncertainty, precision, accuracy, and coefficient of variation, and describe factors that contribute to each.
Compare and contrast appropriate uses of “stat” and “routine” test priorities with discussion of critical values and the elements of “turn-around time.” Predict which elements affect turn-around time the most.
Explain the broad differences between Food and Drug Administration (FDA)-approved tests and laboratory-developed tests, including Clinical Laboratory Improvement Amendments (CLIA) waived and nonwaived tests, and discuss the regulatory issues involved in physician-office laboratories, home testing, and provider-performed microscopy.
Explain how “point-of-care” (POC) testing in the physician office, multispecialty clinic, and hospital can enable better patient and population management of acute and chronic disease and why values generated using POC methods could differ from values generated in a high-throughput laboratory.
Create a clinical scenario that begins with a patient diagnosis and monitors a chronic disease for years, taking into account the following aspects: a laboratory testing decision tree to make the diagnosis, a protocol for monitoring the patient, the use of test panels and individual tests, the impact on healthcare cost for overutilization of laboratory testing, and the potential impact on cost for underutilization both at the diagnostic stage and in the management of chronic disease.
Compare and contrast the cost of several common laboratory diagnostic tests, such as Complete Blood Count (CBC) and CBC with a manual differential. Discuss the cost of diagnostic testing and the impact on health-care costs.
Every physician needs an understanding of transfusion medicine which encompasses the transfusion of red blood cells, platelets, and plasma products in order to correct deficiencies in patients or remove offending antibodies. Transfusions are not without risk and knowledge of the pathophysiology of the disease and risks of transfusion are vital for physicians for optimal patient outcomes.
Apply knowledge of pathology, hematopoietic cell physiology and immunology to explain concepts of blood component transfusion and the therapeutic interventions in transfusion medicine.
Define the blood components and blood component substitutes available for clinical use; the evidence-based indications and dosing for transfusion of these components; and how the efficacy of transfusion may be monitored.
Compare and contrast the pathophysiology, presentations, prophylaxis, and acute management of the different types of transfusion reactions.
Discuss infectious disease risks of transfusion.
Explain the HLA system and its role in both transfusion and transplantation.
Explain the clinical role of therapeutic apheresis in the management of the following disorders: sickle cell anemia, thrombotic thrombocytopenia, acute and chronic inflammatory demyelinating polyneuropathy, myasthenia gravis, antiglomerular basement membrane disease, organ transplantation, plasma cell dyscrasias, leukemia, and lymphoma.
Explain the role of blood group testing in determining paternity identification.
Every physician needs a thorough understanding of one of the most common tests ordered from the laboratory, the complete blood count or CBC. Differentiating between tests needed for diagnosis and treatment of anemias and coagulation disorders is important for appropriate treatment and monitoring of these disorders.
Apply knowledge of biochemistry, pharmacology, and pathology to describe the basic cellular and molecular events associated with blood coagulation and explain laboratory tests for diagnosis and management of coagulation disorders.
Describe the process whereby platelets are activated and aggregate after blood vessel injury.
Explain the action and the clinical use of common platelet function inhibitor drugs including, but not limited to, aspirin and clopidogrel.
Describe the process of fibrin formation in terms of the initiation of coagulation reactions by the exposure of tissue factor and/or “contact activation” and the subsequent proteolytic interactions that involve coagulation factor proteins.
Explain the actions and clinical use of commonly used anticoagulants including warfarin, the heparins, and the new oral direct inhibitors of thrombin and factor Xa.
Apply knowledge of biochemistry, pharmacology, and pathology to describe the use of specific laboratory tests to diagnose and manage coagulation disorders.
Explain selection of appropriate tests for identifying the cause(s) of bleeding and to monitor therapeutic anticoagulation.
Explain platelet function testing and discuss how platelet function testing can be used to differentiate between disorders of low platelets versus abnormal function of platelets.
Identify the likely deficiency of clotting factor(s) using the prothrombin time and the partial thromboplastin time coagulation tests.
Compare and contrast the roles of the following in evaluating coagulopathies: clinical history, prothrombin time test, partial thromboplastin time test, d-dimer assay, platelet count, and platelet function tests.
Describe how to evaluate a bleeding patient with a hemorrhagic disorder, and explain how the history influences testing, including the uses and limitations of screening PT, PTT, and platelet counts.
Explain how bleeding occurs in patients with disseminated intravascular coagulation and in patients with severe liver disease using coagulation testing.
Describe the major hereditary and acquired risk factors for thrombosis and how coagulation testing is used to confirm the diagnosis.
Apply knowledge of red blood cell (RBC) structure/function and nutrient metabolism, the mechanisms of anemia, and the clinical and pathological features of common causes of anemia, to develop an appropriate differential diagnosis.
Summarize laboratory testing for key cellular structures and functions of the RBC.
Discuss the laboratory testing for specific nutrients including iron and vitamins to erythropoiesis.
Differentiate between the pathophysiology of acute and chronic blood loss.
Apply knowledge of RBC structure/function and nutrient metabolism, the mechanisms of anemia, and the clinical and pathological features of common causes of anemia, to develop a diagnostic decision tree and recommend appropriate intervention for a patient with anemia.
Describe the primary causes of anemia, compare and contrast the clinical features and mechanisms of each, and discuss the different testing strategies for normocytic, macrocytic, and microcytic anemia.
Use the CBC and explain the contribution of each of the measurements of the CBC, how they are derived, and how they can help diagnose blood cell disorders using specific examples.
Discuss the RBC and white blood cell morphology on a peripheral smear to develop a differential diagnosis for a patient with anemia.
Correlate the genetic, pathological, and clinical features in patients with common inherited anemias.
Compare and contrast the clinical features and pathophysiology acquired including mechanical trauma, toxic, and antibody-mediated anemias.
Discuss when specific interventions should and should not be used for patients with specific types of anemia.
Infectious diseases are extremely common and every physician needs to be able to correlate clinical findings with the appropriate testing needed. Some infectious disorders will require immediate organism identification, and susceptibility to pharmacotherapy, and understanding principles underlying the different types of microorganisms and their identification is essential. Many newer techniques have been recently implemented, including molecular techniques, that allow more definitive identification and specialized treatment for infectious organisms.
Apply knowledge of infectious organisms to explain the pathogenesis of disease and clinical syndromes, appropriate collection of patient samples, organism identification and classification, antibiotic choice, and selection of medical/surgical interventions.
Explain the types of preanalytical variables that affect diagnostic accuracy and discuss factors that affect length of turn-around time for microbiological workups.
Compare and contrast the interpretations of Gram stains for rapid diagnosis of causative bacterial agents from sterile and contaminated sites and discuss the clinical settings where recognition of bacteria is most meaningful.
Give examples of the types of testing, and their optimal usage, performed in microbiology to identify an infectious disease.
Explain how a process that coordinates identification of the infectious organism, antibiotic sensitivity susceptibility testing, and reporting to the pharmacy antibiotic steward team and treating physician will optimize patient care and reduce health-care costs.
Integrate knowledge of antimicrobial agents with bacterial culture and susceptibility testing results to guide treatment of infectious diseases.
Associate mechanisms of action with antimicrobial agents including the following: disruption of cell wall synthesis, inhibition of protein synthesis, inhibition of DNA synthesis, and antimetabolites.
State the spectrum of activity for common antimicrobial agents.
Describe mechanisms of resistance found in common pathogens including the following: Penicillinase and mecA in Staphylococcus subspecies, vanA and vanB in Enterococcus subspecies, extended spectrum β-lactamases and carbapenemases in Enterobacteriaceae.
Describe the standardized techniques used in antimicrobial susceptibility testing, why standardization is important, and the differences between a qualitative and quantitative result including disk diffusion, broth microdilution, and automated antimicrobial susceptibility testing systems.
Name the genetic element detected by extrapolate cefoxitin and oxacillin susceptibility tests and describe how the results for Staphylococcus subspecies are used to predict activity of other β-lactam antibiotics.
Describe how the microbiology laboratory determines if an isolate from a blood culture is susceptible or resistant. Describe how the pharmacokinetic (PK)/pharmacodynamic (PD) models may influence a clinician’s choice of antibiotics given the susceptibility of an organism using specific examples.
Outline the principles that guide an institution’s reporting cascade for the following: FDA indications, The Clinical and Laboratory Standards Institute (CLSI) guidance, site of infection, institution formulary, and antimicrobial stewardship.
Use the institutional antibiogram to prescribe therapy before susceptibility test results are available.
List examples of molecular tests that are commonly used in clinical microbiology, and explain how they have an important impact on clinical care.
Explain how the application of Matrix-assisted Laser Desorption/Ionizationtime of Flight (MALDI-TOF) mass spectrometry in the clinical microbiology laboratory can impact patient care.
Explain the role of urine studies, including culture, in selecting antimicrobial therapy for infectious cystitis.
Describe a testing strategy for a typical uncomplicated community acquired urinary tract infection (UTI) versus a nosocomial UTI in a patient with a Foley catheter and list the key microbiological tests in diagnosis of UTIs.
Explain the role of Venereal Disease Research Laboratory / rapid plasma reagin (VDRL/RPR) and Treponema-specific tests in the diagnosis and management of syphilis.
Integrate concepts of virology with diagnostic techniques including culture, molecular, and antigen diagnostics to identify viral infections and guide treatment.
Describe the laboratory findings that diagnose hepatitis and correlate with the different possible clinical outcomes for each of the major hepatotropic viruses.
Explain the diagnosis of influenza in terms of diagnostic tests used, major antigens present, and the implications of a major shift in these antigens.
Describe the role of serology, Polymerase Chain reaction (PCR), and culture in the diagnosis of viral infections and name which viruses are most rapidly identified by each.
Explain the testing strategy used to diagnose HIV and the role of viral load and CD4 count in monitoring HIV infection.
Describe the tests available to examine the response of an HIV virus to therapeutic agents, explaining how each test works.
Integrate concepts of mycobacteriology with diagnostic techniques including culture, molecular, and antigen diagnostics to identify mycobacterial infections and guide treatment.
Describe the diagnostic tests available for the identification of mycobacteria including culture methods and new molecular tests.
Compare and contrast the methods, culture, and molecular tests used to identify mycobacteria drug susceptibility and the time required for results by each method.
Integrate concepts of mycology with diagnostic techniques including culture, molecular, and antigen diagnostics to identify fungal infections and guide treatment.
Differentiate among filamentous fungi, dimorphic fungi and yeast, and describe the diagnostic approaches for each type.
Define sensitivity testing and describe its role and use in the management of yeast infections.
Explain the basis for the galactomannan and β-glucan tests and how they are utilized to detect fungi and Pneumocystis.
Integrate concepts of parasitology with diagnostic techniques including culture, molecular, and antigen diagnostics to identify parasitic infections and guide treatment.
Compare and contrast metazoan and protozoan parasites and the diagnostic approaches to each.
Explain the role of stool samples, including number examined, role of microscopy, and coproantigen detection in the diagnosis of parasitic disease.
Summarize the role of serology and serological tests to diagnose toxoplasmosis and assess the risk of transmission during pregnancy.
Contrast Plasmodium falciparum with other malaria species and babesiosis on a blood smear and explain the role of thick and thin smears in the diagnosis and management of malaria.
Name the rapid tests that do not require blood smears to identify malaria and explain how these tests work.
Every physician needs to be able to differentiate between multiple different chemical tests in order to confirm a diagnosis or to follow disease progression. An understanding of the major chemical tests, their relationship to pathophysiology of disease progression, and understanding of limitations of such tests is essential for treatment.
Apply knowledge of biochemistry, pharmacology, and pathogenesis of disease and clinical syndromes to describe the basic cellular and molecular events associated with diseases of specific tissues and organ systems, and the use of laboratory tests to diagnose and manage these diseases including the selection of medical/surgical interventions.
Discuss the clinical presentation and the pathophysiologic bases of thyroid diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Discuss the clinical presentation and the pathophysiologic bases of cardiac diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Discuss the clinical presentation and the pathophysiologic bases of other endocrine diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Discuss the clinical presentation and the pathophysiologic bases of liver and gastrointestinal diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Discuss the clinical presentation and the pathophysiologic bases of renal diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Discuss the clinical presentation and the pathophysiologic bases of lung diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Determine the value of testing for drugs and toxins accounting for the routes of administration, distribution and metabolism of the agent of interest, including the specimen source, the analytes to be detected given the medical questions, and the timing constraints for specimen collection.
Select and interpret appropriate tests for specific cancer diagnostics, including tumor markers and serum monoclonal protein analysis.
Every physician needs an understanding of specific laboratory tests to differentiate between inflammatory and immune-mediated diseases. Many newer techniques have been recently implemented that allow more definitive diagnosis and specialized treatment for these disorders.
Apply knowledge of immunology, biochemistry, and pathology to describe the basic cellular and molecular events associated with immune system diseases of specific tissues and organ systems and the use of laboratory tests to diagnose and manage these diseases.
Compare and contrast markers of inflammation in terms of the pathophysiologic basis and stages of the inflammatory response.
Select and interpret appropriate tests for workup and interpretation of autoimmune disease, immunodeficiencies, and allergy testing.
Discuss, with examples, the application of serological testing in infectious diseases to establish immune status and diagnose infection.
Discuss the clinical presentation and pathophysiologic bases of autoimmune diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.
Every physician needs an appreciation of the complex field of genomics including Mendelian inheritance patterns to the ever evolving molecular techniques that are essential for diagnosing diseases as accurately as possible, and for many diseases correlated with specific targeted immune or chemotherapy to maximize effectiveness of treatment, decrease side effects, and optimize patient survival.
Apply knowledge of genetics including the structure and organization of the human genome and regulation of gene expression, genetic variation, and inheritance patterns to basic disease processes.
Describe molecular testing of Mendelian inheritance including autosomal dominant, autosomal recessive, X-linked; non-Mendelian inheritance including mitochondrial and imprinting; unstable repeat expansions; and cytogenetic translocations.
Demonstrate how to take a 3-generation family history and draw a pedigree. Distinguish between a nonpathogenic polymorphism and a pathogenic mutation, and describe the mechanisms that produce different types of mutations.
Compare diagnostic testing of single-gene disorders to diseases with complex inheritance patterns and include the role of rare, high-risk variants, and common, low-risk variants.
Outline the principles that underlie genetic linkage analysis and association studies and how they are used to identify genes associated with diseases.
Define the concepts “founder effect” and “genetic drift” and explain how genetic variants are distributed within populations.
Explain how genetic risk is determined by carrier status and carrier frequency of a condition and determine carrier frequencies and incidence of recessive conditions using Hardy-Weinberg Laws.
Distinguish dominant and recessive phenotypes and alleles and describe how incomplete penetrance, variable expressivity, imprinting, and pleiotropy affect the phenotypic expression of diseases.
Describe the concept of a modifier gene and its contribution to phenotypic variability.
Define the following cytogenetic terms and nomenclature: karyotype, euploidy, aneuploidy, monosomy, trisomy, deletion, ring chromosome, inversion, isochromosome, translocation, balanced reciprocal translocation, Robertsonian translocation.
Define mosaicism and explain how it affects the phenotype of a chromosomal disorder.
Apply knowledge of genetics to explain the molecular basis of single-gene and nonneoplastic chromosomal disorders.
Describe the genetic and epigenetic causes, pathophysiology and clinical manifestations, and optimal laboratory tests used to diagnose the following specific genetic disorders: Mendelian, autosomal disorders (dominant and recessive), X-linked disorders, chromosomal disorders, and disorders of nonclassic inheritance.
Apply knowledge of genetics to explain the genetic basis for neoplasia, and the role of genetic testing in diagnosis and treatment of diseases.
Describe 3 mechanisms by which genes predispose to neoplasia: oncogenes, tumor suppressor genes, DNA repair genes.
Describe the molecular genetic mechanisms that underlie cancers: germline mutations; somatic mutations including point mutations, deletions, amplifications and translocations; epigenetic changes.
Explain the application of molecular testing for diagnosis, prognostication, and therapeutic follow-up of oncologic diseases.
Apply knowledge of genetics to explain the role of reproductive genetics and population screening.
Describe the role of preconception and prenatal carrier testing for genetic disorders depending upon family history and ethnic background.
Describe the rationale for newborn screening for genetic diseases and explain the difference between screening and diagnostic testing.
Apply knowledge of genetics to explain the role of genetic testing in diagnosis and treatment of diseases and in counseling of patients and families.
Explain the mechanisms involved in the treatment of genetic diseases: organ transplantation, manipulating metabolic pathways, correction of defective structural proteins or enzymes, modulation of RNA expression, alteration of DNA sequence, and alteration of gene expression.
Describe how genetic variation can predict response to medications, dosing, and risk for adverse effects.
Describe how modification of nongenetic factors can prevent or mitigate disease in genetically predisposed individuals.
Describe the role of genetic counselors in patient care and when to make appropriate referrals for genetics evaluations.
Autopsy is a division of anatomic pathology that encompasses the examination of a deceased person, either for medical or legal reasons. Understanding the value of the autopsy, both for scientific investigation of potential inherited disorders and for understanding the diseases that led to a patient’s demise will allow clinicians appropriately discuss this end-of-life medical evaluation.
Apply knowledge of clinical medicine and quality management to discuss the value of the autopsy and procedures for obtaining permission for postmortem examination.
Provide examples demonstrating the value of the autopsy toward improvement in clinical diagnosis and management, quality control, medical education, research, and elucidation of “new” diseases.
Identify the legal next of kin or individual authorized to consent when obtaining consent for an autopsy.
Describe how to approach a family to request consent for an autopsy, including a discussion of the autopsy procedure in language that the patient’s family can understand.
Discuss the psychosocial–emotional aspects of the autopsy experience, including its role in closure, and the importance of communication and professionalism among the health-care team.
Apply knowledge of quality management to discuss the utility of death certificates and proper approaches for completing them.
Describe the importance of death certificates for tracking and analysis of public health trends.
Discuss the key components of the death certificate; differences among immediate, intermediate, and underlying (proximate) cause of death based on disease process; and the role of mechanisms of death on a death certificate.
Explain how under- or overutilization of medical care, and incorrect diagnoses, therapeutics, or informed consent can lead to medical errors and give examples of how an autopsy can identify errors thereby improving health care and decision-making.
Apply knowledge of clinical medicine and postmortem examination to discuss the indications for medical examiner referral and special procedures in the forensic postmortem examination.
Define the role of a medical examiner in terms of public health and protection of legal rights.
Identify circumstances of death that need to be reported to the medical examiner/coroner.
Surgical pathology is the area of anatomic pathology where all tissues or hardware removed from a patient is evaluated. Specimens sent to surgical pathology may range from minute endoscopic biopsies to large organ resections. Special techniques are commonly used by pathologists in evaluating these specimens that allow for definitive diagnosis and the recommendation of appropriate treatment for both benign and malignant lesions.
Apply knowledge of clinical medicine and pathology to describe the roles cytology and surgical pathology play in diagnosis and treatment of benign and malignant disorders. Use specific examples from the most common diseases and forms of cancer.
Describe the procedures for obtaining a biopsy of a tissue lesion or mass in different sites, including superficial and deep soft tissues, solid organs, and tubular organs. Associate each procedure and specimen type to either cytology or surgical pathology and give examples of possible reasons and follow-up for false negative biopsies.
List the major differential diagnoses for each type of cytology or surgical pathology specimen derived from a lesion or mass and describe appropriate further studies, both special stains and immunohistochemistry.
After looking at slides of a tissue lesion or mass, the pathologist makes a diagnosis. List options for surgical and nonsurgical treatment and describe prognostic and therapy-guiding tests that may be performed on the tissue.
Describe the information that the pathologist obtains from a resected tissue specimen, how this information is reported, how it is combined with clinical information to stage the tumor, and how staging information is used to guide treatment.
Apply knowledge of clinical medicine and pathology to describe the roles cytology and surgical pathology play in diagnosis and treatment of inflammatory disease, in particular those with immune or infectious etiologies.
Give examples of specific sites and diseases in which specific pathologic diagnoses of inflammatory and/or infectious conditions are critical to treatment and prognosis.
Apply knowledge of clinical medicine and pathology to describe hereditary/malformative disorders, in terms of clinically useful information that anatomic pathology diagnosis can provide.
Define general terminology for pathologic features that are associated with hereditary/malformative disorders.
Apply knowledge of clinical medicine and communication skills to interpret pathology reports and communicate the results to patients in the context of risk assessment and patient prognosis. Determine appropriate action including additional testing and clinical evaluation.
Explain the results of a pathology report to a patient in language the patient can understand.
Apply knowledge of pathology and the application of diagnostic decision trees to discuss the classification systems of leukemia and lymphomas, and describe the relative roles of ancillary laboratory studies in classification.
Describe the roles of immunohistochemistry, flow cytometry, cytogenetics, and molecular diagnostics in the diagnosis and classification of lymphoma, and explain how, with examples, different techniques are most appropriate in diagnosis, staging, and management of disease.
Explain how the work up of lymph nodes at the frozen section bench differs from routine frozen sections, and how examination of touch preparations of slides are used to streamline use of additional special techniques.
Discuss how a pathologist can use a diagnostic decision tree to make a diagnosis efficiently, minimize the time to report results to the oncologist, and optimize treatment decisions.
Cytopathology focuses on the individual cellular components of disease. Cytopathological examination is an essential tool for its wide-ranging reach in screening, diagnostics, prognostics, and prevention of advanced disease states. Furthermore, the minimally and noninvasive nature of ascertaining most cytological specimens allows for immediate access to viable cellular material for advanced testing, molecular, and biochemical analyses.
Apply knowledge of general and systems pathology to understand the meaning and context of cytologic diagnoses.
Compare and contrast the 3 basic methods to obtain cytologic material for diagnosis, describe the settings in which these can be used to diagnose benign and malignant conditions, and discuss the limitations of each.
Compare and contrast the degree of diagnostic certainty applied to general categorization in cytologic diagnosis.
Describe the uses and limitations of cytology, with examples, in identifying common infectious diseases.
Describe how cytologic specimens can add valuable information for tumor staging.
Apply knowledge of clinical medicine, pathology, and health-care delivery to describe the advantages cytopathologic examination offers over conventional pathologic tissue examination.
Describe the principles of an effective screening test and the uses and limitations of cytology.
Describe how adjunct testing is used in conjunction with cytology examination.
Describe how to find and utilize current algorithms for management of cervical screening.
As editors of the PCME, we thank the 60 pathologists who contributed to the original project of the National Standards of Pathology Education, and also thank Priscilla Markwood, Jennifer Purcell, and Jen Norman for their generous support of the project, especially Jen Norman for her tremendous administrative support.
Authors’ Note: The opinions expressed are those of the authors and do not reflect the official positions of the Uniformed Services University, the US Army, Navy, Air Force, or DoD.
Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: The development of clinical cases for the Pathology Competencies for Medical Education as outlined in this article is supported by the Association of Pathology Chairs.