TP d'anatomie pathologique
General Concepts of Inflammatory Pathology
The inflammatory process is defined as the set of reactional phenomena triggered in a multicellular living organism by the aggression of a pathogen. This process follows a sequence of stages in a specific order, heavily influenced by chemical substances known as mediators of inflammation.
Acute inflammation represents the immediate response to an aggressive agent. It is often characterized by a sudden onset and a relatively short duration. This type of inflammation can heal spontaneously or through medical treatment, although it may leave permanent sequels if the initial tissue destruction is significant. Morphologically, acute inflammation can manifest in several forms: congestive, edematous, fibrinous, fibrino-leukocytic, hemorrhagic, purulent, necrotizing, or gangrenous. The systematic progression of inflammation involves several distinct phases: the vasculo-exsudative phase, the cellular phase, the detersion phase, and finally, the cicatrization (healing) phase.
Acute Appendicitis
Acute appendicitis is a prime example of an acute inflammatory process occurring in the appendix. Macroscopically, the appendix appears tumefied. Microscopic examination reveals varying states of the mucosal lining; the mucosa may be conserved in some areas, while other zones show rupture or ulceration. Suquenze ulcérée is described as a loss of substance that is subsequently replaced by a fibrino-leukocytic coating. In a normal state, the appendix contains cylindrical epithelium and Lieberkühn glands (sometimes spelled as Glonde de Liberbuhn in laboratory records).
Under the microscope, specific colors and structures help identify the pathology. Fibrin deposits appear as pink (rose) material, while leukocytes are visible as blue dots (pointillés bleus). In diseased states, the cylindrical epithelium may be replaced or obscured by a fibrino-leukocytic block centered within the lumen. Lymphoid follicles are a characteristic feature, and their presence alongside the loss of substance is a definitive marker of appendicitis.
Chronic and Specific Inflammation
Chronic inflammation is distinguished by a prolonged evolution and the development of collagen fibrosis. The cellular infiltration in chronic cases typically consists of histio-monocytic and lympho-plasmocytic elements. This differs from specific inflammation, which presents lesions evocative of a particular cause or group of causes. Examples includes the caseous necrosis seen in tuberculosis or the presence of foreign body giant cells.
Tuberculosis Study
Tuberculosis is an infectious disease resulting from the penetration and proliferation of a mycobacteriosis, specifically the Koch's Bacillus (BK), within the organism. It is pathologically characterized by the formation of granulomas. These granulomas are composed of epithelioid cells and giant cells, organized with a specific architecture. A hallmark of tuberculosis is the presence of caseous necrosis, which appears macroscopically and microscopically as a pink, cracked circle surrounded by a lymphocytic crown or ring.
Microscopic observation at high magnification allows for the identification of epithelioid cells, characterized by pink cytoplasm and blue/violet dots representing the nuclei. Caseous necrosis is acidophilic (pink), anise (defined here as having no living cells), and cracked. The total structure of the tuberculous granuloma features a central area of caseous necrosis, surrounded by epithelioid cells and giant cells (Langhans type) arranged in a crown-like formation, which is then encircled by a ring of lymphocytes.
Tumoral Pathology: Mammary Adenofibroma
Mammary adenofibroma is the most frequent benign tumor in young women, typically observed in individuals aged between years. Anatomically, the lobule is a component of the lobe and consists of several acini; these lobules are separated by bands of collagen tissue. The fibroadenoma originates within the intra-lobular stroma.
Macroscopically, the tumor presents as a rounded or multinodular mass with a smooth, bosselated surface. It is well-limited, encapsulated, and may be unique or multiple. Its size is variable, typically ranging between , and it has a hard consistency. Upon opening, the mass appears firm and white-grayish, potentially containing mucoid foci, cysts, or calcifications. It is frequently described as having a "popcorn" aspect.
Microscopically, there is a double proliferation. The epithelial component consists of tubes bordered by a double layer of epithelial and myoepithelial cells, often presenting a characteristic "Chinese letter" (lettres chinoises) shape. The stromal component consists of loose fibrous tissue surrounding these epithelial canalicular structures.
Tumoral Pathology: Colonic Adenocarcinoma
The colonic and rectal wall is composed of five superposed layers: the mucosa, submucosa, muscularis, sub-serous layer, and the serosa. The normal mucosa contains cylindrical epithelium and many Lieberkühn glands, which feature muco-secreting cylindrical cells with an open mucous pole. These glands, characterized by goblet cells (cellules caliciformes), often present an aspect compared to daisies (en marguerites).
An adenocarcinoma is a malignant epithelial glandular tumor. In the colon, it is categorized by its level of differentiation. A well-differentiated Lieberkühnian adenocarcinoma maintains some recognizable glandular structures, whereas a poorly differentiated adenocarcinoma loses this organized morphology. Histological comparison between a normal colon and one affected by adenocarcinoma shows a stark transition from normal mucosal architecture to disorganized malignant growth.
Overload Pathology: Hepatic Cholestasis
Overload refers to the accumulation of a substance, either endogenously or exogenously, within or outside of cells. Hepatic cholestasis is histologically defined by the visible accumulation of bile in liver tissue. Bile is composed of bilirubin and bile acids. When bilirubin accumulates in the blood, it leads to jaundice (ictère), characterized by the yellow coloration of the tissues and skin.
Normal liver histology includes hepatocyte cords (travées), sinusoids (clear vascular slits), and centrolobular veins (VCL). In cases of cholestasis, the liver macroscopically appears large, soft, and green. It may appear nodular, raising questions about progression to cirrhosis. Histologically, bile deposits appear as brownish-green granular material within the hepatocytes. Additionally, biliary thrombi may form within the interhepatocytic canaliculi and the interlobular ducts located in the portal spaces. Diagnosis involves recognizing the liver architecture and identifying the biliary surcharge inside hepatocytes and canaliculi.
Gaucher Disease
Gaucher disease is a genetic disorder transmitted in an autosomal recessive manner. It is caused by a mutation in the gene coding for the enzyme glucocerebrosidase, leading to an enzymatic deficiency. Consequently, glucocerebrosides accumulate within macrophages, forming what are known as Gaucher cells.
This accumulation occurs in various organs, leading to specific clinical findings: the spleen (splenomegaly, which can reach a weight of ), the liver (hepatomegaly), lymph nodes, bone marrow, and the tonsils. Macroscopically, the affected organs increase significantly in volume. Microscopically, Gaucher cells are large, measuring approximately . They possess abundant eosinophilic cytoplasm with a tiered, fibrillar, or "crumpled paper" (papier froissé) appearance, and a regular, eccentric nucleus.
Vascular Pathology: Renal Infarction
An infarct is a circumscribed focus of ischemic necrosis caused by the sudden and complete cessation of blood circulation. There are two macroscopic types: the white ischemic (pure) infarct, occurring when arterial circulation is of the terminal type, and the red hemorrhagic infarct, linked to double circulation or a combination of arterial blockage and venous return obstruction.
Renal infarction is often caused by an embolic obstruction of a branch of the renal artery. Macroscopically, it appears as a white cortical, triangular, or cuneiform area with a subcapsular base. It is typically well-limited and pale (white-yellowish) with a congestive red border (liseré congestif) at the periphery. A recent infarct is soft and salient, lifting the capsule, whereas an old infarct becomes white, hard, and depressed, forming a retracted triangular scar. Microscopically, it is a focus of coagulation (ischemic) necrosis where tissue structures appear "mummified," leaving only silhouettes known as tissue ghosts (fantômes de tissus). Associated inflammatory lesions include edema, hemorrhage, and leukocytes.
Vascular Pathology: Arterial Thrombosis
Thrombosis is the coagulation of blood during life within a vascular cavity or the heart. The resulting product is termed a thrombus. It is caused by three primary factors: slowed blood flow, alteration of the vascular wall, and modification of blood coagulability factors. Thrombi can be classified as white (platelet or fibrino-platelet), red (fibrino-cruoric), or mixed. Evolution involves fibrinolysis or conjunctive organization.
Microscopically, one must distinguish the layers of the arterial wall: the intima, media (made of fine muscular fibers), and adventitia. An organized thrombus adheres to the arterial wall. In recent thrombosis associated with an atheroma plaque, an eosinophilic thrombus may obstruct the arterial lumen, often accompanied by cholesterol crystals. In cases such as the thrombosis of a renal artery branch, the thrombus is composed of fibrin and platelets.