General Pathology — MCQs
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A 4-year-old boy presents with extremely pliable skin, easy bruising, and joint hyperextensibility. Biochemical studies show a deficiency of lysyl hydroxylase. What cellular or tissue component abnormalities would most likely be revealed by ultrastructural examination of a skin biopsy from this patient?
What is the histologic hallmark of Langerhans cells?
Which of the following is NOT a cell cycle inhibitor?
Liquefactive necrosis on necrotic tissue results in which of the following?
Karyotype of Klinefelter syndrome is?
MHC restriction is a characteristic of all of the following except:
What is the earliest event in ischemic cardiac myocytes?
Which chromosome is associated with familial polyposis coli?
Which cells are primarily involved in humoral immunity?
Which of the following histological features are characteristic of shock?
General Pathology Indian Medical PG Practice Questions and MCQs
Question 841: A 4-year-old boy presents with extremely pliable skin, easy bruising, and joint hyperextensibility. Biochemical studies show a deficiency of lysyl hydroxylase. What cellular or tissue component abnormalities would most likely be revealed by ultrastructural examination of a skin biopsy from this patient?
- A. Actin-myosin filaments
- B. Collagen fibers (Correct Answer)
- C. Glycocalyx
- D. Intermediate filaments
Explanation: **Explanation:** The clinical presentation of hypermobile joints, hyperextensible skin, and easy bruising in a child is classic for **Ehlers-Danlos Syndrome (EDS)** [1]. The specific mention of a **lysyl hydroxylase deficiency** identifies this as the **Kyphoscoliotic type (Type VI)** of EDS. **Why Collagen fibers is correct:** Collagen synthesis is a complex multi-step process. Lysyl hydroxylase is an enzyme responsible for the hydroxylation of lysine residues in procollagen chains. This step is critical for the subsequent formation of **stable cross-links** between collagen molecules. Without these cross-links, collagen fibers lack tensile strength and structural integrity [1]. Ultrastructural examination (Electron Microscopy) would reveal fragmented, disorganized, or thinner-than-normal collagen fibrils within the dermis. **Why the other options are incorrect:** * **Actin-myosin filaments (A):** These are contractile proteins found in muscle cells (and the cytoskeleton), not the extracellular matrix. They are unaffected in EDS. * **Glycocalyx (C):** This is the carbohydrate-rich outer coating of the cell membrane involved in cell recognition and signaling, unrelated to connective tissue strength. * **Intermediate filaments (D):** These provide mechanical strength *inside* the cell (e.g., keratins, vimentin). While important for cellular integrity, they are not the primary defect in EDS. **NEET-PG High-Yield Pearls:** * **EDS Type IV (Vascular Type):** Defect in **Type III Collagen** (COL3A1). High risk of arterial or bowel rupture [1]. * **EDS Type VI (Kyphoscoliotic Type):** Defect in **Lysyl Hydroxylase**. Characterized by ocular fragility and severe hypotonia. * **Vitamin C connection:** Scurvy also involves defective hydroxylation (proline/lysine) because Vitamin C is a necessary cofactor for these hydroxylase enzymes. * **Copper connection:** Lysyl **oxidase** (different from hydroxylase) requires Copper; its deficiency leads to Menkes disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 154-156.
Question 842: What is the histologic hallmark of Langerhans cells?
- A. Dendritic cell processes
- B. Giant mitochondria
- C. Birbeck granules (Correct Answer)
- D. Eosinophilic granules
Explanation: **Explanation:** **Langerhans cells** are specialized dendritic cells (antigen-presenting cells) primarily found in the stratum spinosum of the epidermis [2], [3]. The histologic hallmark of these cells is the presence of **Birbeck granules**, which are pathognomonic [1]. 1. **Why Birbeck granules are correct:** Under electron microscopy, Birbeck granules appear as unique, rod-shaped, pentalaminar cytoplasmic organelles [1]. They often feature a bulbous end, giving them a characteristic **"tennis racket" appearance** [1]. They contain the protein **langerin** (CD207) and are involved in the endocytosis and processing of antigens [1]. 2. **Why other options are incorrect:** * **Dendritic cell processes:** While Langerhans cells do have dendritic processes to capture antigens, this is a feature shared by many other immune cells (like follicular dendritic cells) and is not a specific histologic hallmark [2]. * **Giant mitochondria:** These are seen in certain metabolic or toxic states (e.g., alcoholic liver disease) but have no specific association with Langerhans cells. * **Eosinophilic granules:** These are characteristic of eosinophils or cells undergoing specific types of degeneration, not the ultrastructural hallmark of Langerhans cells. **High-Yield Clinical Pearls for NEET-PG:** * **Immunohistochemistry (IHC) Markers:** Langerhans cells are positive for **S-100**, **CD1a**, and **CD207 (Langerin)** [1]. * **Langerhans Cell Histiocytosis (LCH):** A clonal proliferation of these cells. On biopsy, look for "coffee-bean" shaped nuclei with linear grooves [1]. * **Origin:** Unlike other skin cells, Langerhans cells originate from the **bone marrow** (monocyte-macrophage lineage). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 629-630. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 200. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1144.
Question 843: Which of the following is NOT a cell cycle inhibitor?
- A. P21
- B. P27
- C. P16/INK4a
- D. Cyclin D-CDK4 complex (Correct Answer)
Explanation: ### Explanation The cell cycle is strictly regulated by a balance between **Cyclins/Cyclin-Dependent Kinases (CDKs)**, which promote progression, and **CDK Inhibitors (CDKIs)**, which halt the cycle. **Why Cyclin D-CDK4 complex is the correct answer:** The **Cyclin D-CDK4 complex** is a **cell cycle promoter**, not an inhibitor [1]. During the G1 phase, Cyclin D binds to CDK4 (or CDK6). This active complex phosphorylates the Retinoblastoma (Rb) protein. Phosphorylated Rb releases the transcription factor E2F, which then triggers the expression of genes required for the S-phase [1]. Therefore, this complex acts as a "gas pedal" for cell division. **Analysis of Incorrect Options (The Inhibitors):** * **P21:** A member of the **Cip/Kip family**. It is induced by the **p53** tumor suppressor gene in response to DNA damage [2]. It inhibits multiple CDKs, preventing the cell from entering the S-phase. * **P27:** Another **Cip/Kip family** member. It responds to growth inhibitory signals (like TGF-β) and binds to Cyclin E-CDK2 complexes to cause cell cycle arrest in G1. * **P16/INK4a:** A member of the **INK4 (Inhibitors of Kinase 4) family** [3]. It specifically competes with Cyclin D to bind to CDK4/6, maintaining the Rb protein in its hypophosphorylated (active) state, thereby blocking the G1-S transition [1]. **NEET-PG High-Yield Pearls:** * **Two Families of CDKIs:** 1. **Cip/Kip family:** p21, p27, p57 (Broad spectrum; inhibit most CDKs). 2. **INK4 family:** p15, p16, p18, p19 (Selective for CDK4 and CDK6) [3]. * **p53 Connection:** p53 mediates G1 arrest primarily by transactivating **p21** [2]. * **Clinical Correlation:** Loss of **p16** is frequently seen in many cancers, including pancreatic carcinoma and melanoma [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 300-302. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 37-38.
Question 844: Liquefactive necrosis on necrotic tissue results in which of the following?
- A. Gangrene
- B. Embolism
- C. Infarct (Correct Answer)
- D. Caseation
Explanation: **Explanation:** The correct answer is **Infarct**. [2] **Understanding the Concept:** An **infarct** is an area of ischemic necrosis caused by the occlusion of either the arterial supply or the venous drainage. [2] In most solid organs (like the heart, kidney, or spleen), ischemia leads to **coagulative necrosis**. However, in the **Central Nervous System (CNS)**, hypoxic cell death uniquely results in **liquefactive necrosis**. [1] This is due to the high lipid content of the brain and the lack of a supportive connective tissue framework, leading to rapid enzymatic digestion of the tissue into a liquid viscous mass. [1] Therefore, an infarct in the brain manifests as liquefactive necrosis. **Analysis of Incorrect Options:** * **Gangrene (Option A):** This is a form of coagulative necrosis (dry) or coagulative necrosis with superimposed liquefaction by bacteria (wet). [3] While it involves liquefaction, it is a clinical term for limb/bowel necrosis rather than the primary result of liquefactive necrosis itself. * **Embolism (Option B):** This is a **cause** of an infarct, not a result of necrosis. [4] An embolus is a detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin. * **Caseation (Option D):** This is a specific form of necrosis characteristic of **Tuberculosis**. [4] It is a combination of coagulative and liquefactive necrosis, appearing "cheese-like" macroscopically, but it is not the standard result of liquefactive necrosis in ischemic tissue. **NEET-PG High-Yield Pearls:** * **Liquefactive Necrosis** is the hallmark of two specific conditions: **Brain Infarcts** and **Abscesses** (due to pyogenic bacterial/fungal infections). [1] * **Coagulative Necrosis** is the most common pattern of necrosis in all organs **except the brain**. [2] * In liquefactive necrosis, the architecture of the dead tissue is completely lost, [1] unlike coagulative necrosis where the cellular outline is preserved for a few days ("tombstone appearance"). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 148-149. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1268.
Question 845: Karyotype of Klinefelter syndrome is?
- A. 47XXY (Correct Answer)
- B. 45XO
- C. 46XXY
- D. 45XXX
Explanation: **Explanation:** **1. Why Option A is Correct:** Klinefelter syndrome is the most common cause of male hypogonadism, occurring in approximately 1 in 660 live male births [1]. It is characterized by the presence of two or more X chromosomes and one or more Y chromosomes. The classic karyotype is **47,XXY**, resulting from **meiotic non-disjunction** of sex chromosomes during gametogenesis (more commonly maternal than paternal). The presence of the Y chromosome ensures a male phenotype, while the extra X chromosome leads to testicular dysgenesis. **2. Why Other Options are Incorrect:** * **Option B (45,XO):** This is the karyotype for **Turner Syndrome**, characterized by a female phenotype with streak ovaries and short stature. * **Option C (46,XXY):** This is mathematically incorrect. A human karyotype with XXY sex chromosomes must have a total of 47 chromosomes. * **Option D (45,XXX):** This is mathematically impossible (Triple X syndrome is 47,XXX). A 45-chromosome count with three X chromosomes cannot exist. **3. High-Yield Clinical Pearls for NEET-PG:** * **Clinical Features:** Tall stature, eunuchoid body proportions (increased span-to-height ratio), small firm testes, gynecomastia, and female-type hair distribution. * **Hormonal Profile:** Low Testosterone, **High FSH and LH** (due to loss of feedback inhibition), and High Estradiol. * **Histopathology:** Hyalinization and fibrosis of seminiferous tubules with **Leydig cell hyperplasia** (apparent/relative). * **Complications:** Increased risk of **Male Breast Cancer** (20x higher than normal), Extragonadal Germ Cell Tumors (Mediastinal), and Autoimmune diseases (like SLE). * **Barr Body:** Patients with 47,XXY will show **one Barr body** on a buccal smear (Total X chromosomes minus 1). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 92-93.
Question 846: MHC restriction is a characteristic of all of the following except:
- A. Antiviral cytotoxic T cell response
- B. Antibacterial helper T cell and cytotoxic cell response
- C. Allograft rejection (Correct Answer)
- D. Autoimmune disorder
Explanation: ### Explanation **MHC Restriction** is the biological requirement that T cell receptors (TCRs) can only recognize and respond to foreign antigens when they are presented on the surface of self-MHC molecules [1]. CD8+ T cells are restricted to MHC Class I, while CD4+ T cells are restricted to MHC Class II. **Why Allograft Rejection is the Correct Answer:** In allograft rejection, the primary mechanism is **Direct Allorecognition**. Here, the recipient’s T cells directly recognize the *donor’s* intact MHC molecules on the surface of the graft's cells (passenger leukocytes) [1]. Because the T cells are reacting to **foreign (non-self) MHC**, the rule of "self-MHC restriction" is bypassed [1]. The T cell perceives the foreign MHC molecule itself as a "mimic" of a self-MHC molecule presenting a foreign peptide [1]. **Analysis of Incorrect Options:** * **Antiviral response:** Cytotoxic T cells (CD8+) must recognize viral peptides presented specifically on **self-MHC Class I** to kill infected cells. * **Antibacterial response:** Helper T cells (CD4+) recognize bacterial peptides on **self-MHC Class II** (on APCs), and Cytotoxic T cells recognize intracellular bacteria on **self-MHC Class I**. * **Autoimmune disorders:** These involve a breakdown of tolerance where T cells react to **self-antigens** presented on **self-MHC** molecules. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Present on all nucleated cells; presents endogenous antigens (viruses, tumors) to CD8+ T cells. * **MHC Class II:** Present on Professional APCs (Dendritic cells, Macrophages, B cells); presents exogenous antigens to CD4+ T cells. * **Direct Allorecognition:** Responsible for acute cellular rejection; bypasses MHC restriction [1]. * **Indirect Allorecognition:** Recipient APCs process donor MHC and present it on **self-MHC**; this follows the rule of MHC restriction and is involved in chronic rejection [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 240-241.
Question 847: What is the earliest event in ischemic cardiac myocytes?
- A. Microvascular injury
- B. Irreversible cell injury
- C. Loss of contractility (Correct Answer)
- D. ATP reduction to 50% of normal
Explanation: ### Explanation The correct answer is **Loss of contractility**. In the sequence of events following myocardial ischemia, the transition from aerobic to anaerobic metabolism occurs within seconds. This leads to a rapid depletion of high-energy phosphates (ATP) and the accumulation of lactic acid. The resulting intracellular acidosis and failure of the calcium pump lead to the **loss of contractility**, which occurs within **60 seconds** of onset [1][2]. This is a functional change that precedes any structural or irreversible damage [2]. **Analysis of Options:** * **ATP reduction to 50% of normal:** While ATP begins to fall immediately, it drops to 50% of normal levels at approximately **10 minutes**. Loss of contractility occurs much earlier (within 1 minute). * **Irreversible cell injury:** This occurs significantly later, typically after **20 to 40 minutes** of persistent ischemia, characterized by profound membrane damage and mitochondrial densities [2][3]. * **Microvascular injury:** This is a late-stage event associated with prolonged ischemia (usually >1 hour) and is a key component of the "no-reflow" phenomenon during reperfusion [3]. **NEET-PG High-Yield Pearls:** * **Earliest biochemical change:** Depletion of ATP (starts in seconds). * **Earliest functional change:** Loss of contractility (<1 minute) [1]. * **Irreversibility threshold:** 20–40 minutes (Myocardial Infarction begins) [2]. * **Light Microscopy (LM):** The earliest visible change is "wavy fibers" (1–3 hours). * **Electron Microscopy (EM):** The earliest visible changes are mitochondrial swelling and glycogen depletion (within minutes) [2]. * **Gross change:** Pallor is usually seen only after 12–24 hours. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 61-62. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 548-550. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 554-556.
Question 848: Which chromosome is associated with familial polyposis coli?
- A. Chromosome 5 (Correct Answer)
- B. Chromosome 6
- C. Chromosome 11
- D. Chromosome 13
Explanation: **Explanation:** **1. Why Chromosome 5 is Correct:** Familial Adenomatous Polyposis (FAP), also known as familial polyposis coli, is an autosomal dominant condition characterized by the development of hundreds to thousands of adenomatous colorectal polyps [1]. It is caused by a germline mutation in the **APC (Adenomatous Polyposis Coli) gene**, which is located on the long arm of **Chromosome 5 (5q21)**. The APC gene is a tumor suppressor gene that regulates the Wnt signaling pathway; its loss leads to the accumulation of β-catenin, promoting uncontrolled cell proliferation [1]. **2. Why the Other Options are Incorrect:** * **Chromosome 6:** Associated with the **HLA complex** (Major Histocompatibility Complex) and diseases like Hemochromatosis (*HFE* gene). * **Chromosome 11:** Associated with the **WT1 gene** (Wilms tumor) and the **β-globin gene cluster** (Sickle cell anemia, β-thalassemia). * **Chromosome 13:** Associated with the **RB1 gene** (Retinoblastoma) and the **BRCA2 gene** (Breast cancer). **3. Clinical Pearls for NEET-PG:** * **The "100% Rule":** If left untreated, the risk of progression to colorectal carcinoma in FAP patients is virtually **100%** by age 40-50 [1]. * **Gardner Syndrome:** A variant of FAP (also Chromosome 5) presenting with intestinal polyps plus extra-intestinal manifestations like **osteomas** (mandible), epidermal cysts, and desmoid tumors. * **Turcot Syndrome:** Association of colonic polyposis with **CNS tumors** (Medulloblastoma is associated with APC mutations; Glioblastoma with HNPCC/Lynch syndrome). * **Screening:** Proctosigmoidoscopy is recommended starting at age 10-12 years for at-risk family members. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 821-822.
Question 849: Which cells are primarily involved in humoral immunity?
- A. B-cells (Correct Answer)
- B. T-cells
- C. Helper cells
- D. Dendritic cells
Explanation: **Explanation:** **Humoral immunity** (also known as antibody-mediated immunity) is the aspect of the adaptive immune system mediated by macromolecules found in extracellular fluids. [3] * **Why B-cells are correct:** B-lymphocytes are the primary mediators of humoral immunity. [1] Upon encountering a specific antigen, B-cells differentiate into **plasma cells**, which secrete large quantities of **antibodies (immunoglobulins)**. [2] These antibodies circulate in the blood and lymph (the "humors"), where they neutralize pathogens, activate the complement system, and promote opsonization. [3] **Analysis of Incorrect Options:** * **T-cells:** These are the primary mediators of **Cell-Mediated Immunity (CMI)**. [1] They do not produce antibodies but instead interact directly with infected or abnormal cells. * **Helper cells (CD4+ T-cells):** While they play a crucial role in "helping" B-cells switch classes and mature via cytokine secretion, they are a subset of T-cells and do not produce antibodies themselves. [3] * **Dendritic cells:** These are professional **Antigen-Presenting Cells (APCs)**. Their primary role is to capture, process, and present antigens to T-cells to initiate the adaptive immune response. [2] **High-Yield Clinical Pearls for NEET-PG:** * **B-cell Maturation:** Occurs in the **bone marrow** (unlike T-cells, which mature in the thymus). [1] * **Markers:** CD19, CD20, and CD21 are characteristic surface markers for B-cells. * **Memory:** Both B and T cells create memory cells, providing long-term immunity. [4] * **Agammaglobulinemia:** A deficiency in B-cell maturation (e.g., Bruton’s Tyrosine Kinase deficiency) leads to a complete lack of humoral immunity and recurrent bacterial infections. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 579-580. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 206-207. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 161-162.
Question 850: Which of the following histological features are characteristic of shock?
- A. Acute tubular necrosis (ATN)
- B. Pulmonary congestion
- C. Depletion of lipids in adrenal cortex
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Shock is characterized by systemic hypoperfusion leading to cellular hypoxia and multi-organ dysfunction [3]. The histological changes reflect the vulnerability of specific tissues to ischemia [1]. * **Acute Tubular Necrosis (ATN):** The kidneys are highly sensitive to ischemia. In shock, the renal tubules (especially the proximal convoluted tubules) undergo necrosis due to reduced blood flow [2]. This is the most common cause of acute kidney injury in shocked patients. * **Pulmonary Congestion:** In cardiogenic shock (left-sided heart failure), blood backs up into the pulmonary circulation, leading to heavy, wet lungs and alveolar edema. In septic or traumatic shock, "Shock Lung" (Diffuse Alveolar Damage/ARDS) occurs, characterized by hyaline membrane formation. * **Depletion of Lipids in Adrenal Cortex:** Shock is a state of extreme systemic stress. The adrenal glands respond by rapidly synthesizing and secreting corticosteroids. This leads to the exhaustion of stored cholesterol (lipids) in the cortical cells, transforming the normally pale-yellow cortex into a lipid-depleted, reddish-brown appearance. **High-Yield Clinical Pearls for NEET-PG:** * **Brain:** Ischemic encephalopathy occurs; the most sensitive cells are **Pyramidal cells of the hippocampus** and **Purkinje cells of the cerebellum** [4]. * **Heart:** Shows subendocardial hemorrhage and contraction band necrosis. * **Liver:** "Nutmeg liver" (centrilobular necrosis) occurs due to passive congestion and hypoxia. * **GI Tract:** Hemorrhagic enteropathy (patchy mucosal necrosis) [3]. Since all the listed features are classic morphological manifestations of multi-organ damage in shock, **Option D** is the correct answer. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 150-151. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 149-150. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 144. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 140-142.
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