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Fundamentals for Understanding Veterinary Pathology
理解獸醫病理學的基本原則

Margaret A. Miller and James F. Zachary
瑪格麗特·A·米勒和詹姆斯·F·扎卡里

Key Readings Index 關鍵閱讀索引

Information Fundamental for Effective Use of this Book, 1
有效使用本書的基本資訊，1
Diagnoses in Veterinary Pathology, 2
獸醫病理學診斷，2
Language of Veterinary Pathology, 3
獸醫病理學語言，3
Recognition and Interpretation of Lesions, 4
病變的識別與解釋，4
Pattern Recognition in Gross
在粗糙中的模式識別
(Macroscopic) Examinations, 4
（宏觀）檢查，4

Abstract 摘要

Specular Highlights, 4 Colors of Normal Tissues and Organs, 7 Evaluation of Lesions Affecting Tissues and Organs, 9
鏡面高光，正常組織和器官的 4 種顏色，影響組織和器官的病變評估 7，9

Key Element 1: Distribution of Lesions, 9
關鍵要素 1：病變的分佈，9
Key Element 2: Quantity of Lesions, 9
關鍵元素 2：病變數量，9
Key Element 3: Colors of Lesions, 9
關鍵元素 3：病變的顏色，9
Key Element 4: Shapes of Lesions, 11
關鍵元素 4：病變的形狀，11

Key Element 5: Sizes of Lesions, 11
關鍵要素 5：病變的大小，11Key Element 6: Firmness (Density) of
關鍵元素 6：堅固性（密度）Lesions, 12 病變，12Key Element 7: Surface Texture of
關鍵元素 7：表面質感的Lesions, 12 病變，12Diagnostic Pathology, 12 診斷病理學，12Macroscopic (Gross) Reports, 12
宏觀（粗略）報告，12Microscopic Reports, 12 顯微報告，12

Veterinary pathology is a medical specialty that studies the lesions and mechanisms of diseases affecting animal species. Veterinary pathologists in North America, after receiving their degree in veterinary medicine (DVM, VMD), train in the specialty for an additional 3 to 5 years and are certified by examination as (1) anatomic pathologists, who investigate lesions observed on the postmortem floor and with a microscope, or as (2) clinical pathologists, who study the cytologic, microscopic, and biochemical alterations of blood, bone marrow, urine, and other body fluids and/or aspirates. Similar certification programs also exist in Europe and Japan. Although there is some overlap in subject matter between anatomic and clinical pathology, the focus of this book is on anatomic pathology. Clinical pathology is taught separately in most veterinary curricula, and there are excellent books covering this subject matter.
獸醫病理學是一個醫學專業，研究影響動物物種的病變和疾病機制。北美的獸醫病理學家在獲得獸醫學位（DVM, VMD）後，需再接受 3 到 5 年的專業訓練，並通過考試獲得認證，成為（1）解剖病理學家，研究在屍檢和顯微鏡下觀察到的病變，或（2）臨床病理學家，研究血液、骨髓、尿液及其他體液和/或抽取物的細胞學、顯微鏡和生化變化。歐洲和日本也有類似的認證計劃。雖然解剖病理學和臨床病理學之間的主題有些重疊，但本書的重點在於解剖病理學。臨床病理學在大多數獸醫課程中是單獨教授的，並且有優秀的書籍涵蓋這一主題。
In the practice of veterinary pathology, the goal is to answer a question or solve a problem. The question depends on the nature of the investigation. In diagnostic pathology, an autopsy (syn: necropsy/ postmortem examination) may be performed to (1) determine the cause of death of an individual animal or multiple animals in a herd, flock, kennel, or cattery or (2) explain decreased production within these groups. Surgical pathology involves sampling a tissue by biopsy or fine needle aspirate (i.e., cytology) and using the information acquired from evaluating the specimen to establish a diagnosis, prognosis, and therapy for the living animal. In forensic pathology, the purpose of an autopsy is to determine the cause of death from a legal perspective. Lastly, experimental pathology occurs in research settings where the pathologist designs laboratory studies with the goal of correlating morphologic lesions with clinical, functional, genetic, immunologic, and/ or biochemical information to elucidate the pathogeneses of diseases.
在獸醫病理學的實踐中，目標是回答一個問題或解決一個問題。問題取決於調查的性質。在診斷病理學中，可能會進行屍檢（同義詞：剖檢/ 死後檢查）以（1）確定單一動物或一群、群、犬舍或貓舍中多隻動物的死亡原因，或（2）解釋這些群體中的生產下降。外科病理學涉及通過活檢或細針抽吸（即細胞學）取樣組織，並利用從評估標本中獲得的信息來確立診斷、預後和對活體動物的治療。在法醫病理學中，屍檢的目的是從法律角度確定死亡原因。最後，實驗病理學發生在研究環境中，病理學家設計實驗室研究，目的是將形態學病變與臨床、功能、遺傳、免疫和/或生化信息相關聯，以闡明疾病的發病機制。
Although veterinary pathologists may have differing practice specializations, they have a common goal of sharing their expertise with veterinary students through classroom and laboratory teaching, conducting pathology rounds and seminars, and writing chapters in textbooks as examples. Most veterinary school graduates will practice internal medicine or surgery rather than pathology; nevertheless, pathology is an integral part of veterinary education and practice. Pathology is the link between basic sciences, such as anatomy and physiology, and the clinical sciences and is the foundation for a lifetime of learning, diagnosing, and understanding disease in living and dead animals. The practicing veterinarian and the veterinary pathologist also form a team at the forefront of animal and public health.
儘管獸醫病理學家可能有不同的專業實踐，但他們有一個共同的目標，就是通過課堂和實驗室教學、進行病理查房和研討會，以及撰寫教科書章節等方式，與獸醫學生分享他們的專業知識。大多數獸醫學校畢業生將從事內科或外科，而非病理學；然而，病理學是獸醫教育和實踐中不可或缺的一部分。病理學是基礎科學（如解剖學和生理學）與臨床科學之間的聯繫，並且是終身學習、診斷和理解活體及死體動物疾病的基礎。執業獸醫和獸醫病理學家也組成了一個在動物和公共健康最前沿的團隊。

Information Fundamental for Effective Use 致病機轉 of this Book
有效使用本書的基本資訊 致病機轉

Pathology is the investigation of disease. It encompasses the recognition and interpretation of structural and functional alterations (i.e., lesions) of cells, tissues, and organs, as well as the microbial, parasitic, biochemical, genetic, and molecular mechanisms that cause disease. As an effort to make understanding this information straightforward, this book has been divided into two sections. The first section contains 6 chapters covering general pathology (Cellular and Molecular Mechanisms of Disease); the second section contains 15 chapters covering systemic pathology (Pathology of Organ Systems). Lastly, there is an extensive online E-section that contains 11 appendices that discuss and illustrate the fundamentals of veterinary diagnostic pathology, such as Appendix C, Postmortem Examination (Autopsy) of Domestic Animal Species and Appendix D, Recognition and Interpretation of Macroscopic (Gross) Lesions.
病理學是對疾病的研究。它包括對細胞、組織和器官的結構和功能變化（即病變）的識別和解釋，以及導致疾病的微生物、寄生蟲、生化、遺傳和分子機制。為了使理解這些信息變得簡單明瞭，本書分為兩個部分。第一部分包含 6 章，涵蓋一般病理學（疾病的細胞和分子機制）；第二部分包含 15 章，涵蓋系統病理學（器官系統的病理學）。最後，還有一個廣泛的在線電子部分，包含 11 個附錄，討論和說明獸醫診斷病理學的基本原理，例如附錄 C，家畜的死後檢查（屍檢）和附錄 D，宏觀（粗大）病變的識別和解釋。
The section on general pathology is an examination of the responses of cells and tissues to injury with a focus on the causes of and processes involved in these responses. Chapters in this section cover cellular adaptations (degenerative, regenerative, or restorative), vascular disorders, inflammation, and neoplasia as well as mechanisms of infectious diseases and disorders of immunity. These categorizations simplify the teaching and learning of general pathology. In the living body, however, cell injury provokes a variety of vascular, inflammatory, and immune-mediated responses in addition to disturbances of growth that occur concurrently or in rapid succession over time.
一般病理學的部分是對細胞和組織對損傷反應的檢視，重點在於這些反應的原因和過程。本部分的章節涵蓋細胞適應（退行性、再生性或修復性）、血管疾病、炎症和腫瘤，以及傳染病和免疫障礙的機制。這些分類簡化了一般病理學的教學和學習。然而，在活體中，細胞損傷引發各種血管、炎症和免疫介導的反應，此外還伴隨著同時或迅速發生的生長障礙。
Table I 1  I  1 " I "1\mathbf{\text { I }} 1 表格 I 1  I  1 " I "1\mathbf{\text { I }} 1 Types of Diagnoses 診斷類型
Type of Diagnosis 診斷類型 Information Used to Make the Diagnosis
用於診斷的信息		 Actual Diagnosis 實際診斷
Clinical diagnosis 臨床診斷 臨床診斷 Signalment, history, and physical examination
信號、歷史和身體檢查

前腹痛 輕度黃疸
Anterior abdominal pain
Mild icterus
Anterior abdominal pain Mild icterus| Anterior abdominal pain | | :--- | | Mild icterus |
肉眼診斷 Liver disease 肝病
Gross (macroscopic) diagnosis
粗略（宏觀）診斷

身體檢查、內窺鏡檢查、探查手術或屍檢結果
Physical examination, endoscopic examination,
exploratory surgery, or autopsy findings
Physical examination, endoscopic examination, exploratory surgery, or autopsy findings| Physical examination, endoscopic examination, | | :--- | | exploratory surgery, or autopsy findings |
 Multifocal necrotizing hepatitis
多灶性壞死性肝炎
{
Morphologic diagnosis 型態診斷
Differential diagnosis 區別診斷
Morphologic diagnosis 型態診斷 Differential diagnosis 區別診斷| Morphologic diagnosis 型態診斷 | | :--- | | Differential diagnosis 區別診斷 |
}
{型態診斷 型態診斷 區別診斷}		 Autopsy findings (macroscopic and microscopic lesions)
屍檢結果（宏觀和微觀病變）		 Acute multifocal necrotizing hepatitis
急性多發性壞死性肝炎
Autopsy findings, signalment, and history
屍檢結果、信號、和歷史

泰澤氏病 肝部沙門氏菌病 病毒性肝炎
Tyzzer's disease
Hepatic salmonellosis
Viral hepatitis
Tyzzer's disease Hepatic salmonellosis Viral hepatitis| Tyzzer's disease | | :--- | | Hepatic salmonellosis | | Viral hepatitis |
Definitive diagnosis 絕對診斷 Autopsy findings, plus the results of ancillary tests
驗屍結果，加上輔助檢測的結果		 Tyzzer's disease 泰澤氏病
Etiologic diagnosis 病因診斷
病因診斷

微生物學測試結果，加上解剖發現的資訊
Microbiology test results, plus information from autopsy
findings
Microbiology test results, plus information from autopsy findings| Microbiology test results, plus information from autopsy | | :--- | | findings |
Clostridial hepatitis or Clostridium piliforme
hepatitis
Clostridial hepatitis or Clostridium piliforme hepatitis| Clostridial hepatitis or Clostridium piliforme | | :--- | | hepatitis |
Table " I "1 Types of Diagnoses Type of Diagnosis Information Used to Make the Diagnosis Actual Diagnosis Clinical diagnosis 臨床診斷 Signalment, history, and physical examination "Anterior abdominal pain Mild icterus" 肉眼診斷 Liver disease Gross (macroscopic) diagnosis "Physical examination, endoscopic examination, exploratory surgery, or autopsy findings" Multifocal necrotizing hepatitis {"Morphologic diagnosis 型態診斷 Differential diagnosis 區別診斷"} Autopsy findings (macroscopic and microscopic lesions) Acute multifocal necrotizing hepatitis Autopsy findings, signalment, and history "Tyzzer's disease Hepatic salmonellosis Viral hepatitis" Definitive diagnosis 絕對診斷 Autopsy findings, plus the results of ancillary tests Tyzzer's disease Etiologic diagnosis 病因診斷 "Microbiology test results, plus information from autopsy findings" "Clostridial hepatitis or Clostridium piliforme hepatitis"| Table $\mathbf{\text { I }} 1$ | Types of Diagnoses | | | | :---: | :---: | :---: | :---: | | Type of Diagnosis | | Information Used to Make the Diagnosis | Actual Diagnosis | | Clinical diagnosis 臨床診斷 | | Signalment, history, and physical examination | Anterior abdominal pain <br> Mild icterus | | | 肉眼診斷 | | Liver disease | | Gross (macroscopic) diagnosis | | Physical examination, endoscopic examination, <br> exploratory surgery, or autopsy findings | Multifocal necrotizing hepatitis | | {Morphologic diagnosis 型態診斷 <br> Differential diagnosis 區別診斷} | | Autopsy findings (macroscopic and microscopic lesions) | Acute multifocal necrotizing hepatitis | | | | Autopsy findings, signalment, and history | Tyzzer's disease <br> Hepatic salmonellosis <br> Viral hepatitis | | Definitive diagnosis 絕對診斷 | | Autopsy findings, plus the results of ancillary tests | Tyzzer's disease | | Etiologic diagnosis 病因診斷 | | Microbiology test results, plus information from autopsy <br> findings | Clostridial hepatitis or Clostridium piliforme <br> hepatitis |
*Tyzzer’s disease (Clostridium piliforme) used as an example.
Tentative diagnosis 暫時性診斷
Systemic pathology is the study of disorders that affect a “system,” meaning one or more organs of the body of the entire animal. It is not a separate discipline from general pathology but a different approach to studying disease, in which the principles of general pathology are applied at the level of a tissue, organ, or the entire body. The section on systemic pathology is organized for teaching purposes by grouping materials into chapters based on traditionally defined “organ systems.” Nevertheless, students must remember that disease seldom, if ever, affects only one tissue or organ. It also helps to remember that most tissues and organs respond in similar ways to a particular type of injury. As a result, there is value in mastering the concepts of general pathology before studying systemic pathology. There is no optimal order in which to teach individual organ system chapters in systemic pathology, so this subject matter may be taught in different sequences in veterinary curricula.
The goal of understanding and learning information discussed and illustrated throughout this book is based on the assumption that students have acquired and retained information in other courses that will contribute to making this aim successful. However, to ensure this outcome, such prerequisite materials are summarized in the sections that follow.

Diagnoses in Veterinary Pathology

Diagnosis is a common and important goal in veterinary practice and in veterinary pathology (Table I.1).
  • Clinical Diagnosis: A clinical diagnosis is based mainly on the signalment (e.g., age, sex, breed), history, and findings of the physical examination. Even with data from clinical pathologic analyses or diagnostic imaging, the clinical diagnosis may only be tentative or presumptive.
  • Gross (Macroscopic) Diagnosis: The establishment of a gross a a ^(a){ }^{a} (i.e., macroscopic) diagnosis results from information obtained from a physical examination, endoscopic examination, exploratory surgery, or autopsy and is based on the ability of the clinician or prosector b b ^(b){ }^{\mathrm{b}} to recognize and interpret macroscopic lesions in tissues and organs. In some cases, the gross diagnosis is a definitive diagnosis (e.g., bone fractures and other traumatic injuries). An experienced pathologist can diagnose certain infectious, nutritional, or neoplastic diseases with accuracy at the macroscopic level; however, most
DDDEMT: Examples of the Nomenclature Table I. 2 Used to Construct a Morphologic
Diagnosis
Degree 程度 Minimal ⋅ ⋅ *\cdot Mild ⋅ ⋅ *\cdot Moderate ⋅ ⋅ *\cdot Marked (severe)
Duration 病程 Acute ・ Subacute ⋅ ⋅ *\cdot Chronic ⋅ ⋅ *\cdot Chronic-active
Distribution 分布
Focal ⋅ ⋅ *\cdot Multifocal ∙ ∙ ∙\bullet Locally extensive ⋅ ⋅ *\cdot Diffuse
(interstitial) ∙ ∙ ∙\bullet Cranioventral † † ^(†){ }^{\dagger}
Focal * Multifocal ∙ Locally extensive * Diffuse (interstitial) ∙ Cranioventral ^(†)| Focal $\cdot$ Multifocal $\bullet$ Locally extensive $\cdot$ Diffuse | | :--- | | (interstitial) $\bullet$ Cranioventral ${ }^{\dagger}$ |
Exudate 渗出液 渗出液  ^("渗出液 "){ }^{\text {渗出液 }}渗出液
Serous ・ Catarrhal ⋅ ⋅ *\cdot Fibrinous ・ Suppurative
- Granulomatous ⋅ ⋅ *\cdot Pyogranulomatous
Serous ・ Catarrhal * Fibrinous ・ Suppurative - Granulomatous * Pyogranulomatous| Serous ・ Catarrhal $\cdot$ Fibrinous ・ Suppurative | | :--- | | - Granulomatous $\cdot$ Pyogranulomatous |
Modifier ‡ ‡ ^(‡){ }^{\ddagger} 修飾性
詞語
Modifier ^(‡) 修飾性 詞語| Modifier ${ }^{\ddagger}$ 修飾性 | | :--- | | 詞語 |
Necrotizing ⋅ ⋅ *\cdot Bronchointerstitial ⋅ ⋅ *\cdot Hemorrhagic
- Embolic
Necrotizing * Bronchointerstitial * Hemorrhagic - Embolic| Necrotizing $\cdot$ Bronchointerstitial $\cdot$ Hemorrhagic | | :--- | | - Embolic |
Tissue ‡ ‡ ^(‡){ }^{\ddagger} 組織
Cystitis ・ Encephalitis ・ Enteritis ・ Hepatitis
- Nephritis ⋅ ⋅ *\cdot Pneumonia § § ^(§){ }^{\S}§
Cystitis ・ Encephalitis ・ Enteritis ・ Hepatitis - Nephritis * Pneumonia ^(§)| Cystitis ・ Encephalitis ・ Enteritis ・ Hepatitis | | :--- | | - Nephritis $\cdot$ Pneumonia ${ }^{\S}$ |
Degree 程度 Minimal * Mild * Moderate * Marked (severe) Duration 病程 Acute ・ Subacute * Chronic * Chronic-active Distribution 分布 "Focal * Multifocal ∙ Locally extensive * Diffuse (interstitial) ∙ Cranioventral ^(†)" Exudate ^("渗出液 ") "Serous ・ Catarrhal * Fibrinous ・ Suppurative - Granulomatous * Pyogranulomatous" "Modifier ^(‡) 修飾性 詞語" "Necrotizing * Bronchointerstitial * Hemorrhagic - Embolic" Tissue ^(‡) 組織 "Cystitis ・ Encephalitis ・ Enteritis ・ Hepatitis - Nephritis * Pneumonia ^(§)"| Degree 程度 | Minimal $\cdot$ Mild $\cdot$ Moderate $\cdot$ Marked (severe) | | :---: | :---: | | Duration 病程 | Acute ・ Subacute $\cdot$ Chronic $\cdot$ Chronic-active | | Distribution 分布 | Focal $\cdot$ Multifocal $\bullet$ Locally extensive $\cdot$ Diffuse <br> (interstitial) $\bullet$ Cranioventral ${ }^{\dagger}$ | | Exudate ${ }^{\text {渗出液 }}$ | Serous ・ Catarrhal $\cdot$ Fibrinous ・ Suppurative <br> - Granulomatous $\cdot$ Pyogranulomatous | | Modifier ${ }^{\ddagger}$ 修飾性 <br> 詞語 | Necrotizing $\cdot$ Bronchointerstitial $\cdot$ Hemorrhagic <br> - Embolic | | Tissue ${ }^{\ddagger}$ 組織 | Cystitis ・ Encephalitis ・ Enteritis ・ Hepatitis <br> - Nephritis $\cdot$ Pneumonia ${ }^{\S}$ |
*This table provides examples of how nomenclature can be used to construct a morphologic diagnosis. It is not intended to be all inclusive and may vary from patterns used in other veterinary colleges or schools. 
+Used only for diseases of the lungs. 
The terms listed in the row to the right of this word are provided as examples. There are many additional terms that are explained and used throughout this book. §Pneumonia is recognized as the term to characterize inflammation of the lung. 
gross examinations are followed by microscopic (i.e., histologic) examinations c c ^(c){ }^{c} to establish morphologic diagnoses. 
  • Morphologic Diagnosis: A morphologic diagnosis is a clear and concise naming of a pattern of structural changes observed in a gross or microscopic lesion. Pathologists develop morphologic diagnoses by recognizing and interpreting gross lesions observed at autopsy or in biopsy specimens and microscopic lesions in histologic sections or cytologic preparations. A morphologic diagnosis names and categorizes lesions based on the following observations of the injury: degree, duration, distribution, exudate, modifiers, and tissue (DDDEMT). The nomenclature of each of these DDDEMT injury observations is listed in Table I. 2. 
A morphologic diagnosis can be based on gross or histologic lesions. It should categorize the lesion-as degeneration or necrosis, a vascular disturbance, inflammation, or as a disturbance of growth—and indicate the affected tissue(s) and/or organ(s). As an example, the word necrosis is often a part of a morphologic diagnosis that categorizes a lesion; however, it needs one more word (e.g., hepatic) to identify the affected tissue. Thus, hepatic necrosis is a complete morphologic diagnosis, although it may need a modifier or two for explanatory purposes (see Table I.2). For example, multifocal (randomly distributed) hepatic necrosis (i.e., multifocal hepatic necrosis) implicates an infection, whereas lobular hepatic 
necrosis (e.g., centrilobular hepatic necrosis) is usually the result of ischemic, metabolic, or toxic injury. Additional modifiers for descriptive purposes could include, for example, the degree of severity and the duration of injury. In some settings, the morphologic diagnosis is the end point (i.e., definitive diagnosis). More often, it is the basis for the formulation of a differential diagnosis. 
  • Differential Diagnosis: A differential diagnosis is a list of diseases or conditions and their morphologic diagnoses that could cause the clinical findings or observed lesions. The list (descending rank order [most likely → → rarr\rightarrow least likely]) should not be exhaustive, but rather should contain those diseases (usually three to five disease entities) that are most likely to have caused the lesions in an animal with the recorded signalment and history. Generally, the list is initially developed from the clinical findings and then focused as more diagnostic information becomes available based on the results of a postmortem examination or surgical biopsy and the results of other supporting laboratory tests. 
  • Definitive Diagnosis: The ultimate goal in the examination of a specimen is establishing a definitive diagnosis. The definitive diagnosis identifies the specific disease or condition causing the lesions. In some situations, a morphologic diagnosis is a definitive diagnosis (e.g., naming of a neoplasm). More often, especially in infectious diseases, the morphologic diagnosis is the starting point. For example, if a morphologic diagnosis of multifocal hepatic necrosis or multifocal necrotizing hepatitis suggests an infectious disease, then the identification of the microbial agent that causes the disease will serve to establish the definitive diagnosis. Ancillary tests, such as microbiology, parasitology, chemical analyses, and immunohistochemistry can be essential in refining a differential diagnosis to reach the definitive diagnosis. Ancillary tests are selected based on the nature of the disease. For example, a poorly differentiated mast cell tumor might necessitate obtaining more information from histochemistry, immunohistochemistry, or perhaps even molecular diagnostics, such as polymerase chain reaction (PCR) amplification of nucleic acids, whereas evaluation of a hematoxylin and eosin (H&E)-stained histologic section may suffice for a well-differentiated mast cell tumor. 
Neoplastic diseases are one of a few situations in which a morphologic diagnosis (i.e., the name of the tumor) is also the definitive diagnosis. Lesions caused by trauma (e.g., fractures, hemorrhages) are additional examples in which morphologic diagnoses are also definitive diagnoses. Lesions of nutritional deficiencies or toxic diseases are seldom so specific and generally implicate chemical injury without incriminating a particular substance; thus, a definitive diagnosis is unlikely, and a differential diagnosis is more likely. Infectious diseases, unless the lesions are highly specific, also result in a list of potential bacteriologic, mycologic, virologic, or parasitologic causes (i.e., differential diagnosis). Microbiologic analyses are then required for identification of a particular cause (e.g., genus and species of the etiologic agent) to establish a definitive diagnosis. 
  • Etiologic Diagnosis: An etiologic diagnosis emphasizes the cause, rather than the morphologic features, of a disease. For example, in a foal with Tyzzer’s disease, the morphologic diagnosis of acute multifocal necrotizing hepatitis could be replaced or supplemented with an etiologic diagnosis of clostridial hepatitis once the cause (Clostridium piliforme) is identified. Importantly, an etiologic diagnosis of clostridial hepatitis does not implicate a particular species of Clostridium, and so it is less useful than the definitive diagnosis of Tyzzer’s disease (C. piliforme infection). 

Language of Veterinary Pathology 

Throughout this book, students will use terminology in common with the vocabulary used in other veterinary courses; however, they will also encounter new terminology that is essential to understanding veterinary pathology. The acquisition and use of this new terminology are based on having a clear understanding of the meaning of five essential terms: 
  • Cell: The smallest component of an animal’s structure that is capable of independent survival and function. 
  • Tissue: A term used to identify structural groupings of cells within an animal’s body. There are four main types of tissue: connective, muscle, nervous, and epithelial. Epithelial tissue contains the largest number of specific cell types within this classification system and includes, as examples, cells of the skin (e.g., keratinocytes), intestinal villi (e.g., enterocytes), and liver (e.g., hepatocytes). 
  • Organs/organ systems: The end-product of embryologic development is the arrangement of cells and tissues into functional units (i.e., organs/organ systems) that serve a need within an animal’s body. 
  • Structure: The configuration, organization, and physical (or physiologic) roles of cells, tissues, and organs/organ systems in homeostasis d d ^(d){ }^{\mathrm{d}} and in response to injury and disease. 
  • Function: The metabolic, biochemical, and genomic/molecular processes of cells, tissues, and organs/organ systems in homeostasis and in response to injury and disease. 
    Students should also remember that pathology is the study of disease and that the word pathology is not equivalent to the word lesion. A lesion is a structural abnormality in a tissue or organ. All too often, the phrase “no pathology is observed” is heard in a lecture, seminar, or medical rounds or is read in a journal article or clinical report. This phrase would be more correctly expressed or written as “no lesion is observed.” Likewise, all lesions by definition are pathologic, so it is a mistake or redundant at best to refer to pathologic lesions. Additionally, although the vocabulary of pathology is common to that used in other veterinary courses, certain words mean one thing in one course or subject area, such as a tissue, and something quite different when used in another course or in describing a different tissue. Indeed, the precise meaning-and precision is the object in writing or speaking about pathology-of a word depends very much on the context. For example, the word malacia, which literally means softening, implies a lack of mineralization when applied to bones, but when applied to the brain, it means liquefactive necrosis. Finally, the term necrosis is a particularly important word used in this book, and it is discussed and illustrated extensively in Chapter 1, Mechanisms and Morphology of Cellular Injury, Adaptation, and Death. It means death or, more precisely, the structural changes that follow death, not of the animal, but of cells within tissues and organs in the animal. The basis for recognizing and interpreting many of the lesions discussed and illustrated in this book is the result of necrosis of cells in tissues and organs. 
Throughout this book, students will also study many disorders involving inflammatory, noninflammatory, degenerative, and proliferative processes, as well as many other types of responses to injury. The grammatic structure used to identify and link these processes to specific types of injury are rooted historically in Greek terminology employing noun-combining forms. The most common noun-combining forms used in this book are: 
  • itis: inflammatory diseases or disorders in tissues or organs (e.g., steatitis, bronchitis, or hepatitis). 
  • opathy: noninflammatory diseases or disorders in tissues or organs (e.g., neuropathy, hepatopathy, lymphadenopathy). 
  • -osis: noninflammatory conditions (e.g., hepatosis), degenerative conditions (e.g., steatosis), ongoing processes (e.g., cirrhosis), or existing states (e.g., calcinosis) in tissues or organs. 
  • omegaly: enlargement of tissues or organs (e.g., splenomegaly, hepatomegaly). 
  • ectasis: dilation or distention of tubular structures (e.g., bronchiectasis, lymphangiectasis). 
  • -penia: a deficiency (e.g., osteopenia, cytopenia). 
  • -plasia: formation, growth, or cellular multiplication (e.g., aplasia, hypoplasia, hyperplasia). 
  • -trophy: nourishment, development (e.g., atrophy, hypertrophy). 
  • -genesis: beginning, development, or production of something (e.g., agenesis, osteogenesis, carcinogenesis, pathogenesis). 
  • -cele: a distended space or sac within a tissue or organ (e.g., meningocele, hematocele). 
  • -oma: a mass or tumor, such as a granuloma or fibroma/fibrosarcoma, respectively. 

Recognition and Interpretation of Lesions 

Veterinarians who enter the field of anatomic pathology often do so because they enjoy the challenge of solving a problem (a mystery), much like detectives or investigators. The pathologist obtains a history, develops a diagnostic strategy, and evaluates a surgical biopsy specimen or performs a postmortem examination. Recognition and interpretation of lesions and the results of other nonmorphologic laboratory tests are part of the evidence that the pathologist collects to evaluate and solve the case. Such nonmorphologic techniques include, as examples, the isolation and identification of infectious agents or toxicants, quantification of chemical deficiencies or excesses, and the detection of genetic abnormalities. In most cases, the evidence fits into a pattern that establishes a definitive diagnosis and thus contributes to providing an answer and/or closure for livestock and pet owners. In some cases, however, a definitive diagnosis eludes pathologists and their collaborators. 
Information acquired from a postmortem examination is based, in part, on the recognition and interpretation of morphologic changes, specifically of the macroscopic and microscopic lesions that develop in injured cells, tissues, organs, and organ systems. There are many causes of cellular dysfunction and injury, and they are discussed in detail in Chapter 1, Mechanisms and Morphology of Cellular Injury, Adaptation, and Death and in all the chapters of this book. 
In veterinary school, students will learn to recognize, evaluate, and interpret lesions at the macroscopic level because as practicing veterinarians they will observe tissues and organs through physical, endoscopic, otoscopic, and ophthalmoscopic examinations as well as through exploratory surgery and postmortem examinations. Achieving these goals is dependent on acquiring a knowledge base from courses in anatomy and pathology during the veterinary curriculum and concurrently learning how to express this information verbally and in writing to colleagues in practice settings during clinical rotations and to clients in clinical practice. 
Lesions are changes in the normal morphologic characteristics of cells in a tissue, organ, or organ system. They most commonly arise from cellular dysfunction or injury that alters cellular homeostasis. There are approximately 220 types of somatic cells in an animal’s body. Each of these cell types has an established “normal” morphology for the individual cell and for how these cells are arranged into groups that form the structure of tissues, organs, or organ systems. Additionally, each tissue type has a unique microcirculation (i.e., microvasculature e e ^(e){ }^{\mathrm{e}} ) and 
waste products between blood and extravascular tissue (for more detail see Chapter 2, Vascular Disorders and Thrombosis). vascular/lymphatic drainage pattern that also contribute to their color. Therefore, every tissue, organ, or organ system has an established morphologic pattern that is considered normal for macroscopic and microscopic observations. During macroscopic (gross) evaluations, a clinician or pathologist/prosector must (1) recognize the structure and appearance (i.e., gross morphology) of normal tissues and organs and, most importantly, (2) recognize morphologic changes (i.e., patterns) in these tissues and organs that would be interpreted as lesions. 

Pattern Recognition in Gross (Macroscopic) Examinations 

During a postmortem examination, veterinary pathologists methodically examine all the tissues, organs, and organ systems of the animal and identify and characterize the gross (macroscopic) lesions. They recognize that specific diseases or disease processes (mechanisms) have lesions that occur consistently with a particular disease or disease process and thus the lesions are pathognomonic (i.e., distinctively characteristic of a particular disease) for a specific disease or disease process. This recognition-interpretation-correlation process is termed pattern recognition. Veterinary pathologists over the last century have documented patterns of lesions that are consistent with and diagnostic of a wide array of diseases and mechanisms of disease occurring in animals. These patterns, in part, serve as the basis for materials that are discussed and illustrated in the pathology of organ systems courses in veterinary school curricula. Pattern recognition is an analytic process used to develop morphologic diagnoses and/or determine the mechanism of injury (pathogenesis), and is based on the morphologic characteristics of the gross lesions observed during the postmortem examination. These characteristics include distribution, quantity, color, shape, size, firmness (density), and surface texture. In addition, the signalment (e.g., species, age, sex, breed) of the affected animal is also valuable information in recognizing a potential pattern. Specific lesion patterns have been documented for specific diseases such as, for example, (1) feline infectious peritonitis, (2) Johne’s disease (paratuberculosis), (3) end-stage liver (cirrhosis), (4) porcine pleuropneumonia, and (5) congestive and hypertrophic cardiomyopathies. Patterns have also been documented for specific mechanisms of injury, such as (1) chronic pulmonary congestion and edema, (2) chronic passive hepatic congestion (nutmeg liver), (3) hydrothorax, (4) hydronephrosis, and (5) herniation of the parahippocampal gyri. The thought processes of pattern recognition are summarized and illustrated in Table I.3. Additionally, lesion patterns can occur in a single tissue or organ, suggesting a targeted disease, or be more extensive and involve a collection of tissues or organs, suggesting a systemic disease. 
For students, the ability to recognize and interpret patterns of lesions will be acquired in veterinary school and refined during their careers. There are numerous diagnostically useful patterns that will be reinforced throughout the Pathology of Organ Systems chapters of this book. Recognition of patterns exhibiting acute versus chronic changes, focal or multifocal versus diffuse changes, and active/primary versus passive/secondary processes, as examples, will also be very useful. Pattern recognition is covered in greater detail in Appendix D, Recognition and Interpretation of Macroscopic (Gross) Lesions. The colors of tissues and organs and the key characteristics of lesions that serve as the basis to recognize and interpret patterns in veterinary practice are discussed in the sections that follow; however, students must first recognize the appearance of specular highlights in gross photographs. 

Specular Highlights 白點 

Specular highlights are bright white areas of varied sizes and shapes that occur on the surfaces of tissues and organs in photographs. This 

Example 2 
Example 3 
鞏固的 ・ Cranioventral lung consolidated and firm ( n n nn, normal parenchyma) 
充血的 - Cranioventral hyperemic (dark red to purple) areas from acute lobular inflammation (arrows) 
  • Cranioventral areas of chronic inflammation (dark pink to gray-tan areas, arrowheads) 
Young adult male cat 
Peritoneal and pleural cavities filled by amber-colored fluid (asterisks) 
Older adult female dog 
Example 3 § 3 § 3^(§)3^{\S}§ 

sal surfaces and (arrows) involving sero kidney, and liver 
  • Contracted kidney with pitted and nodular (white arrowheads) cortical surface 
  • Strands of gray-white fibrin span peritoneal and pleural surfaces (arrowheads) 
  • Thickened and opaque (fibrosis) capsule (asterisks) adhered to cortex 不透明的 
  • Gray-white fibrosing (chronic) inflammation at cortical surface (arrows) and in renal interstitium (black arrowheads) 

Elements 

Distribution 
Locally extensive cranioventral (cranioventral lung lobes) 
Quantity 
Two-thirds of cranioventral lung lobes affected; approximately half of total lung volume affected 
Color Red to dark-red to gray-tan 
Shape Lobular pattern matches the shape of lung lobules 
Size 
Firmness (density) 
Surface texture 
Example 1 小葉 
Area of the cranioventral lung lobes 

-

 
Morphologic
diagnosis
Morphologic diagnosis| Morphologic | | :--- | | diagnosis |
 Suppurative and lobular bronchopneumonia 
 
Common
name for
the disease
Common name for the disease| Common | | :--- | | name for | | the disease |
 Porcine enzootic pneumonia 
 
Causative
agent
Causative agent| Causative | | :--- | | agent |
 Mycoplasma hyopneumoniae 
 
Mechanism
(patho-
genesis
pathway)
Mechanism (patho- genesis pathway)| Mechanism | | :--- | | (patho- | | genesis | | pathway) |
 
Inhalation of bacteria → → rarr\rightarrow bronchial and bronchiolar mucosa
→ → rarr\rightarrow lysis of ciliated epithelial cells → → rarr\rightarrow loss of function
(mucociliary apparatus) → → rarr\rightarrow dependent (cranioventral)
settling → → rarr\rightarrow terminal bronchioles and alveoli → → rarr\rightarrow
bronchointerstitial pneumonia → → rarr\rightarrow acute and chronic
inflammation with hyperplasia of bronchus-associated
lymphoid tissue → → rarr\rightarrow suppurative bronchopneumonia
Inhalation of bacteria rarr bronchial and bronchiolar mucosa rarr lysis of ciliated epithelial cells rarr loss of function (mucociliary apparatus) rarr dependent (cranioventral) settling rarr terminal bronchioles and alveoli rarr bronchointerstitial pneumonia rarr acute and chronic inflammation with hyperplasia of bronchus-associated lymphoid tissue rarr suppurative bronchopneumonia| Inhalation of bacteria $\rightarrow$ bronchial and bronchiolar mucosa | | :--- | | $\rightarrow$ lysis of ciliated epithelial cells $\rightarrow$ loss of function | | (mucociliary apparatus) $\rightarrow$ dependent (cranioventral) | | settling $\rightarrow$ terminal bronchioles and alveoli $\rightarrow$ | | bronchointerstitial pneumonia $\rightarrow$ acute and chronic | | inflammation with hyperplasia of bronchus-associated | | lymphoid tissue $\rightarrow$ suppurative bronchopneumonia |
"Morphologic diagnosis" Suppurative and lobular bronchopneumonia "Common name for the disease" Porcine enzootic pneumonia "Causative agent" Mycoplasma hyopneumoniae "Mechanism (patho- genesis pathway)" "Inhalation of bacteria rarr bronchial and bronchiolar mucosa rarr lysis of ciliated epithelial cells rarr loss of function (mucociliary apparatus) rarr dependent (cranioventral) settling rarr terminal bronchioles and alveoli rarr bronchointerstitial pneumonia rarr acute and chronic inflammation with hyperplasia of bronchus-associated lymphoid tissue rarr suppurative bronchopneumonia"| Morphologic <br> diagnosis | Suppurative and lobular bronchopneumonia | | :---: | :---: | | Common <br> name for <br> the disease | Porcine enzootic pneumonia | | Causative <br> agent | Mycoplasma hyopneumoniae | | Mechanism <br> (patho- <br> genesis <br> pathway) | Inhalation of bacteria $\rightarrow$ bronchial and bronchiolar mucosa <br> $\rightarrow$ lysis of ciliated epithelial cells $\rightarrow$ loss of function <br> (mucociliary apparatus) $\rightarrow$ dependent (cranioventral) <br> settling $\rightarrow$ terminal bronchioles and alveoli $\rightarrow$ <br> bronchointerstitial pneumonia $\rightarrow$ acute and chronic <br> inflammation with hyperplasia of bronchus-associated <br> lymphoid tissue $\rightarrow$ suppurative bronchopneumonia |

Example 2 

Perivascular pattern with linear streaks following blood vessels in serosa, peritoneum, and pleura (see arrows in previous figure) 
Numerous nodules and plaques; abundant fibrinous Entire capsule and > 75 % > 75 % > 75%>75 \% cortical interstitium affected exudate (see figure) 
Gray-white to yellow (see arrows in figure) 
Nodules, plaques, and linear streaks (see distribution and arrows in figure) 
Varied sizes, nodules ( mm in diameter) (see arrows in figure) 
Firm nodules; soft plaques and strands of fibrin 
Shaggy (abundant fibrin) and nodular (granulomas) Mostly smooth with patchy roughening because of fibrinous exudate 

STEP 4: BASED ON OBSERVATIONS IN STEPS 2 AND 3, INTERPRET THE LESIONS AND DEVELOP MORPHOLOGIG DIAGNOSES AND DIAGNOSTIC REPORTS.
Example 2 

Fibrinous and granulomatous peritonitis, pleuritis, and vasculitis 
Feline infectious peritonitis 
Feline infectious peritonitis virus (alphacoronavirus) 
Ingestion of virus → → rarr\rightarrow infection of small intestinal villous epithelial cells → → rarr\rightarrow viral mutation → → rarr\rightarrow infection of and replication in macrophages → → rarr\rightarrow regional and systemic trafficking → → rarr\rightarrow macrophage activation and targeting to veins → → rarr\rightarrow immune recognition of virus-infected macrophages → → rarr\rightarrow pyogranulomatous phlebitis → → rarr\rightarrow pyogranulomatous vasculitis and polyserositis 

Example 3 

Capsule and cortical interstitium (fibrosis) 
Gray-white bands (fibrous tissue) Gray-white nodules and poorly demarcated areas of fibrosis and inflammation Nodular to conical or irregularly shaped patches and bands 
Varied sizes, nodules ( mm in diameter) 
Fibrous bands and areas of fibrosing inflammation are firmer than normal renal parenchyma 
Smooth (mature fibrous tissue in capsule), but nodular because of fibrous contraction of cortical parenchyma 

Example 3 

Chronic tubulointerstitial nephritis 
Chronic interstitial nephritis 
Bacterial or viral septicemias 
Toxins 
Immune complexes 
Septicemia/viremia/toxemia/immune complexes → → rarr\rightarrow injury of interstitial endothelial cells → → rarr\rightarrow cell death → → rarr\rightarrow inflammation and fibrosis → → rarr\rightarrow injury of proximal tubular epithelial cells → → rarr\rightarrow cell death → → rarr\rightarrow inflammation and fibrosis → → rarr\rightarrow interstitia fibrosis → → rarr\rightarrow chronic tubulointerstitial nephritis 
∗ ∗ ^(**){ }^{*} Gross lesions (also known as: macroscopic lesions) are the morphologic changes observed visually (by sight using unaided eyes) in tissues and organs during a postmortem examination 
† † ^(†){ }^{\dagger} Image courtesy Dr. A. López, Atlantic Veterinary College. 
#Image courtesy Dr. H. Gelberg, College of Veterinary Medicine, Oregon State University. 
SImage courtesy Dr. M.D. McGavin, College of Veterinary Medicine, University of Tennessee 
book uses over 1000 photographs to describe and illustrate the processes involved in the recognition, interpretation, and diagnosis of gross (macroscopic) lesions, and specular highlights will frequently be observed in many of these images. In postmortem environments, photography of gross lesions, in part, involves using a light source such as the sun, room lights, studio lights, and/or camera flash units to fully and properly illuminate the colors of the gross specimen and to create shadows on its surface to reveal its modeling and texture (for more information on lighting and specimen photography, see Appendix B, Photographic Techniques in Veterinary Pathology). As a result of this lighting, many of these photographs will have specular highlights on the surfaces of the tissues and organs. They will occur on tissues and organs whose surfaces are normal and on surfaces with lesions. Students must be able to (1) recognize specular highlights in gross photographs and (2) differentiate them from gross lesions. 
Because specular highlights are white spots (or areas) of varied shapes and sizes, they must be differentiated from whitish-gray to light yellow lesions, such as those caused by fibrin, fibrosis, acute or chronic inflammatory exudates, or surface mineralization. Specular highlights are “bright” (always the same color) white (i.e., RGB 255 , 255 , 255 255 , 255 , 255 255,255,255255,255,255 ) and assume a wide array of sizes (millimeters to centimeters) and shapes (pinpoint to circular to elliptical) based on the morphology of the surface of the affected specimen (Fig. I.1). Surfaces that are smooth (flat) and “shiny,” such as those covered by serosae (e.g., pleurae [lung] and peritonea [intestine]), can have large specular highlights (centimeters at the widest point; see Fig. I.1, A-C). In addition, highlights can be more prominent when the surfaces are wet (water or other bodily fluids) or have a convex shape. Surfaces that are roughened and/or granular can have pinpoint to small highlights (millimeters at the widest point; see Fig. I.1, D − F D − F D-FD-F ). Roughened surfaces of tissues and organs usually result from a variety of types of specific cell injury (see Chapter 1, Mechanisms and Morphology of Cellular Injury, Adaptation, and Death) and from inflammatory responses, such as active hyperemia, fibrinogenesis, suppuration, granulation tissue, and fibrosis (healing; see Chapter 3, Inflammation and Healing). 
Additionally, roughened surfaces can also occur when an organ, such as the liver or kidney, is sectioned with a knife or scalpel blade and the “cut” surface is illuminated and photographed (see Fig. I.1, E). The cut surface exposes internal structures, such as glomeruli, renal tubules, microvessels, hepatic lobules, bile canaliculi, and/or nodular aggregates of leukocytes (neoplasia or inflammation), that may project irregularly outward and give the cut surface a roughened appearance (see Fig. I.1, D and F). This internal structure may be “normal” or may be caused by injury or inflammation of the tissue or organ; however, in either case, specular highlights may be present on gross images. Lastly, in many instances, specular highlights are a blend of the two basic types (solid vs. dots) previously discussed with the central area of the highlight being solid and the periphery consisting of pinpoints to small dots (see Fig. I.1, B, C, and F). This outcome occurs when the surface has intermixed smooth and roughened areas and/or there is convex curvature of the surface, such as occurs with intestines. 
For more information on specular highlights and the physics of why they occur on the surfaces of specimens, see https://www. physicsclassroom.com/class/refln/Lesson-1/Specular-vs-DiffuseReflection. 

Colors of Normal Tissues and Organs 

Throughout this book, students will find numerous photographs of gross lesions that occur in diseases of domestic animals (horses, cattle, sheep, goats, pigs, dogs, and cats). They will learn how to recognize, evaluate, and interpret changes in tissue and organs and to recognize the characteristics of the lesions that assist in establishing morphologic diagnoses. Thus, recognizing the colors of normal tissues and organs is an essential first step in this process. f f ^(f){ }^{f} To begin, the basic colors of normal tissues and organs are a mixture of color densities (light to dark) arising from the hues and/or shades of the five colors listed: 
  • white to gray, attributable to proteins, minerals, and lipids that contribute to the structure of the cells; 
  • yellow, attributable to substances such as lipids, carotene pigments, cytochromes, lipochromes, bilirubin, amyloid, and hemosiderin; 
  • red, attributable to blood (i.e., erythrocytes) flowing through or trapped within the circulatory system and microcirculation of the tissue or organ; 
  • brown, attributable to melanin pigments, myoglobin, cytochromes, bilirubin, hemosiderin, and hematin; and 
  • black, attributable to melanin pigments and hematin or other exogenous pigments. 
    The natural colors of cells and thus of tissues and organs are determined by molecules that contribute to the structure of the cell and by substances that are synthesized by or accumulate within the cell. Secondly, the colors of tissues and organs are also influenced by the number of erythrocytes within them. Each of these tissues and organs has a unique structurally defined microcirculation that facilitates the exchange of nutrients and waste products between erythrocytes and extravascular tissue. Thus, the natural color of each tissue and organ is also blended with colors of the red spectrum that are contributed by erythrocytes, which flow through the microcirculation of these tissues and organs. These relationships are explained in greater detail as follows: 
  • Colors of Molecules/Substances Contained within Normal Cells: In homeostasis, the overall color of a tissue or organ is determined by the color of the cells that make up the tissue and organ. As a general rule, parenchymal and stromal cells (also leukocytes) appear white to light yellow because the molecules that make up the structure of these cells are predominately proteins and lipids. Nevertheless, cells can have a range of inherent colors if they, in homeostasis, have inborn, synthesized, or accumulated pigments, such as melanin (e.g., skin [light brown to brown-black]); myoglobin (e.g., skeletal and cardiac muscle [red to red-brown]); cytochromes (e.g., liver, kidney, and endocrine glands [dark red to brown]); bilirubin and iron (e.g., liver [dark red-brown]); lipochromes/lipofuscin (e.g., liver, heart, brain [yellow to light brown]); and carotenes/carotenoids (e.g., fat [yellow]). 
  • Colors of Erythrocytes and the Microcirculation: Erythrocytes and their interactions with the microcirculation also play a key role in determining the color of tissues and organs. Erythrocytes contain hemoglobin, an iron-protein complex (i.e., hemoprotein) that transports and exchanges oxygen and carbon dioxide throughout the body. Well-oxygenated hemoglobin gives erythrocytes their normal red color; poorly oxygenated hemoglobin gives erythrocytes a dark red to red-brown color or even the blue color of venous blood. Consequently, well-oxygenated erythrocytes give tissues and organs a faint pink to red color. The degree of pink to red coloring is also influenced by the quantity of erythrocytes retained in the tissue or organ as regulated by the microcirculation, which serves as the conduit to move erythrocytes 
Figure I. 1 Examples of Specular Highlights. A, Scrotal hernia, scrotum, pig. The arrows identify several areas of specular highlights of varied sizes on “normal” smooth shiny and wet surfaces (serosae [peritoneum]). t t tt, Testis. B, Chronic passive congestion, liver, dog. The arrows identify several areas of specular highlights on smooth shiny surfaces (serosae [peritoneum]). These areas should not be confused with areas of capsular fibrosis (asterisks) or acute inflammation and/or fibrin accumulation (not shown here). Note that the areas of capsular fibrosis show variations in shape, size, texture, and color (whitish-gray). C, Kidney, capsular surface, granulomatous nephritis, dog. Specular highlights occur most commonly and intensely on smooth shiny surfaces (solid bright white areas [arrows]) such as the capsule of the kidney. Note the pinpoint or spotlike circular to elliptical white highlights haphazardly arranged singularly or in small groups around the central large areas of solid white highlights. Lastly, there are multiple subcapsular, cortical, whitish-gray-red, raised granulomas (arrowheads) caused by migrating ascarid larvae; they look distinctly different from the specular highlights. D, Emphysema, urinary bladder mucosa, cow. Multiple mucosal swellings (asterisks) have formed as a result of gas bubbles that have expanded the mucosa and are secondary to bacterial infection of the lower urinary tract. Inset: Note that the swellings contain numerous smaller bubbles (arrowhead) that have roughened (raised) the mucosal surfaces. Pinpoint specular highlights have formed on the surfaces of most of these bubbles (arrow). E, Proliferative glomerulonephritis, kidney, dorsal section, dog. Numerous bright white pinpoint to spotlike specular highlights of varied, but usually small, sizes (arrows) occur on roughened surfaces (boxes with black dashed lines) caused by enlarged glomeruli. Affected glomeruli are small, yellow-tan, ovoid raised foci (boxes with white dashed lines) that project outward from the cut surface of the cortex. A few of these glomeruli have pinpoint bright white specular highlights on their surfaces. F, Uremic pneumopathy from chronic renal failure, lung, 4-year-old dog. All of the lung lobes are gray-white-red because of extensive mineralization of alveolar walls and contiguous pleura. This lesion has “roughened” the pleural surface of the entire lung. Specular highlights (asterisk and box with black dashed lines) are most prominent on the convex surfaces of the caudal and middle lung lobes. The more uniform convex surface of the middle area of the caudal lobe favors the formation of uniform solid specular highlights (asterisk), whereas the more roughened texture of the pleural surface of the middle lung lobe (box with black dashed lines) favors the formation of pinpoint or spotlike circular to elliptical white specular highlights haphazardly arranged singularly or in small groups. Uniform solid specular highlights may have pinpoint or spotlike circular highlights at their periphery (asterisk) as the result of roughened or uneven surfaces. Lastly, it is important to notice the areas (boxes with white dashed lines) of extensive gray-white-red mineralization of alveolar walls and contiguous pleura and the absence of specular highlights in these areas even when the pleural surface is uneven/roughened. In the photographic process, these areas receive ambient light and are not directly exposed to light rays from the light source. For more information on specular highlights and the physics of why they occur on the surface of specimens, see https://www.physicsclassroom.com/class/refln/Lesson-1/Specular-vs-Diffuse-Reflec tion. (A courtesy Dr. H. Gelberg, College of Veterinary Medicine, Oregon State University. B courtesy College of Veterinary Medicine, North Carolina State University. C courtesy Dr. W. Crowell, College of Veterinary Medicine, The University of Georgia; and Noah’s Arkive, College of Veterinary Medicine, The University of Georgia. D and D insetcourtesy Dr. M.D. McGavin, College of Veterinary Medicine, University of Tennessee. E courtesy Dr. S.J. Newman, College of Veterinary Medicine, University of Tennessee. F courtesy Dr. A. López, Atlantic Veterinary College.) 
through these tissues and organs. Thus, acting together, erythrocytes and the microcirculation determine, in part, the colors of normal tissues and organs by means of (1) the oxygenation status of erythrocytes, (2) the oxygen-carrying capacity of erythrocytes, (3) the quantity and distribution of the microcirculation, (4) the number of erythrocytes in the microcirculation, and (5) the rate of flow of erythrocytes into, through, and out of the microcirculation. 

Evaluation of Lesions Affecting Tissues and Organs 

The key elements used to evaluate lesions and develop morphologic diagnoses are: 
  • Distribution 
  • Quantity 
  • Color 
  • Shape 
  • Size 
  • Firmness (density) 
  • Surface texture 
Individually, each of these key elements is similar to a single piece of a picture puzzle and has limited diagnostic value. When all of the pieces (key elements) of the puzzle are assembled into a finished puzzle, however, the picture can be evaluated and interpreted within the context of the case materials and morphologic and definitive diagnoses established. The basic components of each of these key elements will be described in the sections that follow; however, the processes involved in analyzing and interpreting all of the key elements in a diagnostic context are beyond the scope of this introduction. Such processes are covered in detail in the chapters of this book and in Appendix D, Recognition and Interpretation of Macroscopic (Gross) Lesions. 

Key Element 1: Distribution of Lesions 

Lesions in organs are most commonly distributed in one of four patterns: involvement of the entire organ (diffuse), a single focus, a locally extensive focus (i.e., a larger single focus), or multiple foci (see Fig. 3.16). Involvement of the entire organ is usually suggestive of (1) injury originating within the inborn metabolic processes of the parenchymal cells (e.g., storage diseases, lipidosis); (2) injury arising from hematogenous spread of microbial or other toxins to the organ via the cardiovascular system (e.g., septicemia, toxemia); (3) injury arising from changes in vascular flow through the organ attributable to dysfunction of the heart and/or vascular system (e.g., passive congestion); or (4) a highly infiltrative neoplasm (e.g., hematopoietic origin). 

Key Element 2: Quantity of Lesions 

A lesion occurring as a single focus in an organ is usually the result of (1) inborn alterations affecting one cell or one focus of cells (e.g., neoplasia); (2) a solitary embolus (e.g., microbial, parasitic, or neoplastic); (3) a direct extension pathway (e.g., parasitic larval migration); or (4) traumatic injury (e.g., penetrating wound). A lesion that occurs as a locally extensive focus is usually a lesion that began as a small focus that has grown larger over time. Lastly, lesions occurring as multiple foci can develop in the targeted organ (e.g., infectious or neoplastic disease) or reflect embolization of microbes or metastasis of a neoplasm from a primary site in distant tissue or organ. In most cases, lesions occurring as multiple foci in an organ are morphologically similar to each other, but this may vary in key element parameters to some degree. Nevertheless, if intermingled with these multifocal lesions are other foci with a strikingly different appearance, then a second cause for these additional lesions must be considered. 
Lastly, in rare cases (e.g., hepatocellular carcinoma), primary tumors can appear as multiple foci (nodules or masses) in one organ. That is to say, some tumors metastasize only within the organ in which the primary tumor originated. In most cases, the largest mass is the primary tumor; the smaller masses are the metastases. 

Key Element 3: Colors of Lesions 

Most of the colors of lesions shown throughout this book arise from variations in the five basic colors previously discussed (see Colors of Normal Tissues and Organs). When injured, the normal color of a tissue or organ can become lighter or darker (i.e., change in color density), or the normal color can be mixed with or replaced by a new color(s) from one or more of the five basic colors previously listed, depending on the pathogenesis and/or duration of the disease. As an example, a normal lung will be pale pink (red color group; Fig. I.2, A); however, in animals with congestive heart failure, the affected lung will be red/darker red (see Fig. I.2, B) because of the accumulation of erythrocytes, which are likely poorly oxygenated, in the pulmonary microcirculation. If the congestive heart failure progresses to chronic passive congestion, the color of the lung will change from red/darker red to intermixed areas of red/darker red and yellow (see Fig. I.2, C) because of the accumulation of hemosiderin (see Yellow, Pigmentation later) in pulmonary macrophages from effete erythrocytes. With a longer duration of chronic passive congestion, the intermixed red/darker red and yellow areas may change to intermixed red/darker red and yellow/brown areas (see Fig. I.2, C; also see Brown, Pigmentation later). In another example, animals with pulmonary calcification (pulmonary calcinosis) will have normal pale pink lungs (see Fig. I.2, A) that will change with time to pinkish-white and/or pinkish-whitish-gray (see Fig. I.2, D; see White to Gray, Mineralization later) because of the accumulation of calcium in cells and tissues in the lung. 
Thus, lesions can vary in color and color density depending on the pathogenesis and duration of the disease. Only the more common lesions of the five basic color groups are listed. See E-Table D. 3 and Appendix D, Recognition and Interpretation of Macroscopic (Gross) Lesions for more detailed discussions of the colors of lesions, including the colors of pigments produced by specific bacteria in inflammatory exudates (also see E-Table D.4). 
  • White to gray 
  • Amyloid 
  • Anemia 
  • Atrophy 
  • Cell swelling 
  • Healing (fibrosis/granulation tissue) 
  • Hyperplasia 
  • Infarction 
  • Inflammation 
  • Mineralization (calcium/calcification) 
  • Necrosis 
  • Neoplasia 
  • Storage diseases 
  • Yellow 
  • Amyloid 
  • Chyle 
  • Congestion, chronic passive 
  • Edema fluid (hydroabdomen/hydroperitoneum/hydropericardium/hydrothorax) 
  • Fat necrosis/saponification 
  • Fatty change/steatosis (lipids) 
  • Pigmentation (bilirubin, carotene, ceroid, lipofuscin, hemosiderin) 
  • Storage diseases 
Figure I. 2 Examples of Color Changes in Lungs. A, Normal lung, dog. Pale pink lung. B, Acute pulmonary congestion, lung, dog. Red to darker red lung. C, Chronic pulmonary congestion, pulmonary hemosiderosis, lung, 5-year-old dog. Intermixed areas of red to darker red and yellow-brown lung. D, Uremic pneumopathy, pulmonary calcinosis, chronic renal failure, lung, 4-year-old dog. Pinkish-white to pinkish-white-gray lung. (Courtesy Dr. A. López, Atlantic Veterinary College.) 
  • Reds 
  • Congestion, acute passive 
  • Congestion, chronic passive 
  • Erosions/ulcerations 
  • Hemorrhage 
  • Hyperemia 
  • Infarction 
  • Inflammation 
  • Necrosis 
  • Thrombosis 
  • Brown 
  • Congestion, chronic passive 
  • Pigmentation (melanin, bilirubin, hemosiderin, hematin) 
  • Black 
  • Endogenous pigmentation (melanin, hematin) 
  • Exogenous pigment (carbon, excretory pigment of Fascioloides magna) 
    Some lesions caused by bacteria may contain pigments synthesized and deposited in the lesions by the bacteria. These colors include pink, black, blue-green, yellow-green, red-brown, red, and gold. For more detail, see E-Table Appendix D.4, Colors of Pigments Produced by Common Bacteria. 
Mechanisms Involved in Alterations of the Colors of Tissues and Organs. Alteration in the normal color of a tissue or organ can involve the entire tissue or organ or specific areas, regions, or zones within the tissue or organ. Mechanisms involved in alterations of the normal colors are summarized in the following points. 
  • Alteration in Normal Color Affecting the Entire Tissue or Organ: Alteration in the normal color of an entire tissue or organ is usually observed early in a postmortem examination (or during other means of examination), when, for example, the thoracic and abdominal cavities are opened and the organs are observed in situ (i.e., in their natural/original positions). Depending on the cause, tissues and organs can appear pale to almost white (e.g., anemia, hypovolemia, poor tissue perfusion), dark red to purple (e.g., poorly oxygenated erythrocytes, reduced venous flow, passive congestion), or bright red or brown (e.g., chemically induced alteration of hemoglobin) compared with normal tissues and organs. 
As an example of changes in color, the lung is an organ in which parenchymal and stromal cells are white. In homeostasis, however, the lung is pink (light red) because it is a highly vascular organ with an extensive microcirculation that contains numerous properly oxygenated erythrocytes. Unlike more “solid” organs (see the last paragraph in this section discussing the liver and kidney), the lung is unique in that it inflates and deflates during respiration. The blood/air density of lung parenchyma at the time of death can vary, which, in turn, will influence the intensity of pink color of the lung on gross examination. Thus, inflated lung will be faintly pink, whereas partially or fully deflated lung will be darker pink. 
If the lung is faint pink to white, the color change may indicate anemia, hypovolemia, cardiac dysfunction, or microvascular dysfunction. If the lung is dark red to purple, the color change may indicate poor oxygenation of erythrocytes in the lung (e.g., cyanosis, chronic obstructive pulmonary disease [COPD], acute or chronic lung disease) or reduced cardiac output and/or perfusion through the microcirculation (e.g., heart or vascular disease, 
gNote that the lesions listed as examples for red can result from (1) blood retained within the vascular system in tissues and organs, (2) blood that is released into tissues and organs from an injured vascular system, and/or (3) a combination of both mechanisms. 
考慮肺表面肋骨壓是否正常? 
passive congestion). In cases in which the lung is yellow, the color change usually indicates icterus attributable to hyperbilirubinemia. Because icteric blood plasma is yellow, the degree of yellow staining of lipids in parenchymal and stromal cells depends on the duration and severity of the hyperbilirubinemia. The lung can also be bright red (e.g., carbon monoxide poisoning) or brown (e.g., methemoglobinemia). These color changes are caused by chemically induced alterations in the oxygen-carrying capacity of hemoglobin in erythrocytes in the microcirculation. In addition, the color of the lung is influenced by diseases that alter respiration or affect the pulmonary microcirculation, interstitium, or alveolar spaces. 
Organs such as the kidney and liver are “solid” in consistency and red-brown to brown in color because of the structure and density of their parenchymal cells and the endogenous pigments within their cytoplasm. When erythrocytes are retained in these organs (e.g., passive congestion) because of cardiac or vascular dysfunction, they can appear darker with the retention of poorly oxygenated erythrocytes in the microcirculation. Conversely, such organs can also appear “pale” in their entirety (i.e., color change from brown to tan). Causes for pale kidneys or liver usually involve reduced microvascular perfusion or reduced number of erythrocytes (e.g., anemia). In addition, pale kidneys, liver, or other organs can occur with disease processes that affect most of the cells in the organ. These processes include, but are not limited to (1) cell swelling and/or necrosis and (2) the accumulation of endogenous or exogenous substances in cells or tissues, such as glycogen, fat, or amyloid. 
  • Alteration in Color Affecting Areas, Regions, or Zones within a Tissue or Organ: The major colors of lesions that affect areas, regions, or zones in a tissue or organ are white to gray-white (e.g., necrosis [infarction], cell swelling, inflammation, cell proliferation [neoplasia]); yellow (e.g., icterus, amyloid, bilirubin, lipid [accumulation of fat/steatosis], hemosiderosis/hemosiderin); red (e.g., congestion, hemorrhage, thrombosis, necrosis [hemorrhagic infarction]); and tan to brown (e.g., bilirubin, hemosiderosis/hemosiderin). Such colors will usually be distributed in patterns that are characteristic of specific anatomic structures in the affected organ, such as lobules, tubules, or alveoli. 
Lastly, most neoplasms are initially recognized as a “mass” (i.e., solitary) or as “masses” (i.e., multiple) within an area, region, or zone within a tissue or organ. They most commonly appear as white to off-white (gray) to light pink to yellow (i.e., fat content) masses on gross examination. As previously discussed, this appearance is attributable to the proteins and fats that make up the majority of the structure of these proliferating cells and to the absence of the synthesis of pigments and other tinted molecules within these cells. In addition, neoplasms are often highly vascular, so the tissue may have a light pink to pink appearance. Exceptions to these general rules are melanomas and hemangiosarcomas. Melanomas have cells that can produce melanin pigments and make the cells brown to black; however, some melanomas can be “amelanotic.” Hemangiosarcomas are composed of malignant endothelial cells that form haphazardly arranged vascular channels that are congested with poorly oxygenated and slow-flowing erythrocytes, which make the tumor appear dark red to blue-purple. 

Key Element 4: Shapes of Lesions 

Shape and size of lesions are usually evaluated concurrently because, under most circumstances, a change in shape will usually cause a change in size, and vice versa. It must be remembered that shape is only one of the seven key elements used to establish a morphologic diagnosis for a lesion. Shapes of lesions in tissues and organs are assessed in two ways. First, the “relative” shape of the entire organ is estimated. Is the shape of the organ normal? Changes in the shape of the entire organ can occur with acute or chronic vascular congestion, infiltrative neoplasms, and accumulations of substances, such as lipids, sugars, or amyloid, in cells or tissues. Secondly, and most commonly, lesions within the tissue or organ can assume a variety of shapes, some distinct, some not so distinct, and some a mixture of several shapes. These shapes are described as follows: 
  • Nodules/nodular/mass (circumscribed/well-circumscribed/spaceoccupying) 
有明確界線的 
  • Solid nodules or masses, such as tumors, granulomas, and neoplastic or microbial emboli 血栓pl. embolus 
  • Sacs of fluid or exudate, such as cysts or abscesses, respectively, 膿腫 that can have the external appearance of a nodule or mass 
  • Hematomas 
  • Noncircumscribed/poorly circumscribed 
  • Tumors, especially malignant types, hematopoietic diseases, inflammation, healing (fibrosis/granulation tissue) 
  • Depressions, erosions, ulcerations 
  • Trauma, stress, lytic microbes, chemical (acid reflux)/physi cal / cal / cal//\mathrm{cal} / environmental agents 
  • Elevated/raised/plaquelike 
  • Microbes, parasites, some tumors, healing (fibrosis/granulation tissue) 
  • Wedge-shaped/rhomboidal 
  • Infarcts 

Key Element 5: Sizes of Lesions 

Sizes of lesions in tissues and organs are assessed in two ways. First, the “relative” size of the entire organ is estimated. Is the organ “larger or smaller” than normal? Organ enlargement occurs with acute or chronic vascular congestion hypertrophy or hyperplasia, infiltra-慢性血管疲 tive neoplasms, and accumulations of substances. Shrunken organs (atrophy) are usually obvious on gross examination and attributable to alterations in vascular flow (e.g., vascular shunts), loss of principal cells (e.g., lymphoid atrophy), or metabolic changes (e.g., loss of trophic hormone or loss of growth factor stimulation). 
Second, wher one or morelesions (foci) are visible in the organ, the size of the lesions are measured to establish a size range! The size range can be used as a “relative” indicator of the age of a lesion. Small lesions, usually in the 1 to 3 mm in diameter range, are usually foci of acute cell swelling, cellular necrosis, and/or acute inflammation and classified as acute lesions. These lesions are characterized by substantial destruction of parenchymal and stromal cells. h h ^(h){ }^{h} Small lesions, depending on the cause, can be hours to days old, whereas larger lesions can range from days to weeks or longer in age. 
In general, the of a lesion can be estimated by the “healing/reparative” responses of parenchymal and stromal cells in the lesion and by the responses of unaffected cells adjacent to the lesion. Lesions that are hours old tend to consist of injured and necrotic cells, exudates, and peripheral vascular responses (active hyperemia) and tend to appear soft to gel-like on cut surface. Lesions that are days old tend to show healing/reparative responses, such as early fibroplasia at the interface between the lesion and adjacent normal cells. Lesions that are weeks old tend to show healing/reparative responses with more abundant fibrosis and/or the formation of granulomas or bony metaplasia. Much of this information is acquired by slicing the lesion with a knife or scalpel blade and grossly evaluating the characteristics of its content. The size of lesions is usually nonspecific, whereas their pattern of distribution and their color, shape, surface characteristics, and texture can be very diagnostic. 
There are also a few situations in which the relative size of nodules/masses may be useful information. A solid uniform solitary mass, if large ( > 2 cm > 2 cm > 2cm>2 \mathrm{~cm} in diameter), is usually interpreted as a benign tumor. Benign tumors are usually solitary, well-defined, and grow slowly. Malignant tumors can also be solitary but are poorly defined, invasive, and grow rapidly. Exceptions to these general rules do occur. In the context of neoplasia, multiple masses that have similar sizes (e.g., 1 to 2 cm in diameter) and similar structural characteristics (e.g., solid mass, color, shape,) and that are distributed at random (vascular pattern) in an organ are most likely tumor metastases. 

Key Element 6: Firmness (Density) of Lesions 

Some lesions are softer or firmer than normal or thicker or thinner than normal. The softness or firmness of a lesion is determined by its structural components. Lesions that are soft to the touch are areas of acute cellular necrosis, acute inflammation, hemorrhage, fluid, or fat. Lesions that are firmer than normal may contain connective tissue (e.g., fibrosis), granulation tissue, swollen cells, chronic (e.g., granulomatous) inflammation, proliferating cells (i.e., hyperplasia or neoplasia), amyloid, bone, or mineralization. 腫㿎細胞不可用增生形容, 
用大量增長可以(原理L無法控制) 

Key Element 7: Surface Texture of Lesions 

Some lesions have unique external surface changes, such as a fibrillar overlay (e.g., fibrin), roughened or granular surface (e.g., connective tissue), capsule (e.g., connective tissue), confined or encapsulated 
無秩序的・隨意的edges (e.g., benign neoplasm), invasive and haphazardly arranged edges (e.g., malignant neoplasm), or a depressed surface (e.g., erosion/ulceration from superficial necrosis; areas of necrosis within a malignant neoplasm), that are characteristic of a specific cause or mechanism of injury. Because the skin, mucocutaneous junctions, and mucosal surfaces cover or line large areas of an animal’s body, they also must be carefully examined in a postmortem examination for lesions, especially for erosions and ulcerations. 

Diagnostic Pathology 

Diagnostic laboratories affiliated with veterinary schools provide an important component of the knowledge base taught in veterinary school curricula. Much of the information discussed and illustrated throughout this book arose from clinical cases evaluated by veterinary students in diagnostic laboratories settings. In such settings, students acquire experience in recognizing, evaluating, and interpreting lesions at macroscopic and microscopic levels. As practicing veterinarians, they will observe tissues and organs through physical, endoscopic, otoscopic, and ophthalmoscopic examinations as well as through exploratory surgery and postmortem examinations. Thus, students and practicing veterinarians will spend a majority of their “pathology time” evaluating and interpreting macroscopic lesions. They will also obtain experience using a microscope through coursework and through cytologic and fecal examinations, but except for certain specialties (e.g., dermatology and theriogenology), practicing veterinarians may be unlikely to evaluate specimens prepared for histopathologic examination. Nevertheless, practicing veterinarians will consult with veterinary pathologists and read pathology reports i i ^(i){ }^{\mathrm{i}} on a regular basis and therefore will need to be familiar with the key elements used in these reports. The key elements, as discussed in earlier sections, for macroscopic and microscopic reports are listed in the following sections and are also covered in much greater detail in the systemic pathology chapters of this book, in Appendix C, Postmortem Examination (Autopsy) of Domestic Animal Species, 
and in Appendix D, Recognition and Interpretation of Macroscopic (Gross) Lesions. 

Macroscopic (Gross) Reports 

As previously mentioned, practicing veterinarians will recognize, evaluate, and interpret lesions, most commonly at the macroscopic level. Recognition and interpretation of gross (macroscopic) lesions are based on morphologic characteristics that can include changes in color, size, shape, texture, surface topography, specific anatomic location(s), distribution, and density. This information serves as the basis for practicing veterinarians or pathologists to name a lesion, determine its potential cause, and establish a definitive diagnosis for the disorder. Additionally, the process of describing these lesions and developing morphologic diagnoses is based on the use of positional terminology. Thus, positional planes and directions, such as lateral, medial, dorsal, and ventral, should be clearly understood because they are used throughout all chapters in this book and are illustrated in Fig. I.3. Finally, students should remember that lesions exist in three-dimensional space. They have width ( x ), height ( y ), and depth ( z ) ( z ) (z)(z) dimensions. Photographs of gross lesions in books tend to show the x and y dimensions very well but rarely the z z zz dimension (depth), so students must initially estimate (based on experience) the depth of most gross lesions. 
Evaluation of macroscopic (gross) lesions includes: (1) identifying the suspected lesion (there may be more than one); (2) sampling the lesion using “sterile” procedures, if needed, for additional analysis (e.g., microbial culture); (3) examining the “intact” lesion(s) in situ; (4) slicing the lesion for internal evaluation and measurement; and (5) sampling the lesion for histopathologic evaluation of its microscopic features. Morphologic characteristics (i.e., key elements) used by pathologists to recognize, interpret, and describe macroscopic (gross) lesions in pathology reports include: 
  • Anatomic location and, if informative, the positional plane of the lesion (see Fig. I.3, Directional Labels and Planes of the Animal Body) 
  • Colors of tissue(s) making up the lesion and of adjacent normal tissue(s), especially at the interface of the lesion and the normal tissue 
  • Touch/feel (palpable characteristics) of the lesion 
  • Surface characteristics, especially color and texture, of the lesion 
  • Size of the lesion 
  • Shape of the lesion 
  • Density and distribution of the lesion(s) 
  • Structural arrangement of tissues and/or substances in the lesion (also the relationship to adjacent normal tissue, especially at the interface of the lesion and the normal tissue) 
  • Expected “normal” materials (e.g., bile) in the lesion 
  • Unexpected “abnormal” materials (e.g., fibrin or amyloid) in the lesion 
  • Smell (e.g., ammoniacal odor in animals with uremia) of the lesion 

Microscopic Reports 

Morphologic characteristics (i.e., key elements) used by pathologists to recognize, interpret, and describe microscopic lesions in pathology reports include: 
  • Anatomic location of the lesion 
  • Size/volume and shape of affected cells and their nuclei 
  • Density and distribution of the cells 
  • Structural arrangement of the cells 
  • Characteristics of nuclear (DNA) and cytoplasmic (RNA) chromatin 
  • Mitotic activity 
Figure I. 3 Directional Labels and Planes of the Animal Body. (Courtesy and modified from Dyce KM, Sack WO, Wensing CJG: Textbook of veterinary anatomy, ed 4. W.B. Saunders Company.) 
  • Tinctorial features (with H&E, eosin = red and hematoxylin = blue) of the cells 
  • Expected “normal” materials (e.g., bile within hepatic canaliculi and bile ducts) or cells (e.g., lymphocytes in Peyer’s patches of the small intestine) 
  • Unexpected “abnormal” materials (e.g., fibrin or amyloid), cells (e.g., inflammatory or neoplastic cells), or microbes (e.g., bacteria) Greater detail on the morphologic characteristics of lesions occurring in specific disorders of domestic animals are discussed and illustrated in all chapters of this book and are organized based on the organs and organ systems involved and the animal species affected by the disorder. 

In Conclusion 

For many students, veterinary pathology will be a challenge. New vocabulary, different approaches to learning, numerous disorders with complicated mechanisms, and so forth, will test students’ capabilities and endurance. Nevertheless, students will be rewarded not only by mastering knowledge useful in the practice of veterinary medicine but also by acquiring skill sets applicable to descriptive writing, problem solving, time management, data organization, and effective decision making. Additionally, students will learn that most of the skills acquired through studying veterinary pathology will readily extrapolate to and be useful in all areas of veterinary medical practice and are applicable to companion animals, equids, production animals, and wildlife, exotic, or zoo animals. 
  1. a a ^(a){ }^{a} The word “gross” as applied herein is an adjective that means “visible to the naked or unaided eye” and is used in pathology in medical terms such as gross lesions, gross findings, or gross examination, as examples. The term “macroscopic” is synonymous with the term “gross.” 
    b b  ^("b "){ }^{\text {b }} The individual who conducts the dissection, examination, and evaluation of the animal during an autopsy. 
  2. 'Examination of tissues or organs using a microscope, most commonly a light microscope. 
  3. d d ^(d){ }^{\mathrm{d}} The existence of cells, tissues, and organs/organ systems in a physiologic condition that is considered normal for each type of cell, tissue, and organ/ organ system. 
  4. fF fF ^("fF"){ }^{\text {fF}} For photographs of the colors of normal organs see Appendix E-Table D.1, Colors of Normal Tissues and Organs. 
  5. h h ^(h){ }^{\mathrm{h}} Small lesions could also be a primary tumor or tumor metastases. These lesions are usually solid and firm. 
  6. i i ^(i){ }^{\mathrm{i}} Also see Online Appendix A, Communication, Collaboration, and Consultation in Veterinary Pathology. 
  7. Suggested Readings are listed at www.expertconsult.com.