BCSE Pathology

General Pathology – BCSE Study Guide

📅 March 28, 2026 ⏱ 30 min read

General pathology forms the foundation for understanding disease processes across all veterinary species.

Overview and Clinical Importance

General pathology forms the foundation for understanding disease processes across all veterinary species. This topic encompasses the fundamental mechanisms of cellular injury, death, inflammation, and repair that underlie virtually every clinical condition. Mastery of these concepts is essential not only for the BCSE but for clinical practice, as they provide the framework for understanding disease etiology, progression, and therapeutic intervention.

High-YieldGeneral pathology questions frequently test the differences between reversible and irreversible cell injury, types of necrosis, and the distinction between acute and chronic inflammation. Understanding these foundational concepts helps answer complex clinical scenario questions.

Adaptation	Definition	Examples
Hypertrophy	Increase in cell SIZE due to increased functional demand or hormonal stimulation	Cardiac muscle in hypertension; skeletal muscle with exercise; uterine smooth muscle in pregnancy
Hyperplasia	Increase in cell NUMBER in response to growth factors or hormones	Endometrial hyperplasia; prostatic hyperplasia; liver regeneration after partial hepatectomy
Atrophy	Decrease in cell SIZE due to reduced workload, nutrition, or trophic signals	Denervation atrophy; disuse atrophy; senile atrophy; endocrine atrophy
Metaplasia	Reversible change from one differentiated cell type to another	Respiratory epithelium to squamous (smoking); Barrett esophagus (columnar replaces squamous)
Dysplasia	Disordered cell growth with loss of uniformity and architectural orientation	Cervical dysplasia; precancerous changes in epithelium (potentially reversible but may progress to neoplasia)

1. Cell Injury and Adaptation

Cellular Adaptations

Cells respond to stress through adaptive changes that allow survival under altered conditions. These adaptations are reversible if the stimulus is removed.

MEMORY AID - HHAAM for Cellular Adaptations

Hypertrophy (bigger), Hyperplasia (more), Atrophy (smaller), Aplasia (absent), Metaplasia (different type). Remember: "Cells ADAPT by getting Bigger, More, Smaller, or Different!"

[Include Image: Figure 1. Cellular adaptations diagram showing hypertrophy, hyperplasia, atrophy, and metaplasia]

Reversible vs. Irreversible Cell Injury

Cell injury occurs when cells are exposed to stressful stimuli that exceed their adaptive capacity. The injury may be reversible if the damaging stimulus is removed before critical damage occurs, or irreversible leading to cell death.

Causes of Cell Injury

Hypoxia and ischemia (most common cause)
Physical agents (trauma, temperature extremes, radiation, electrical shock)
Chemical agents and drugs (toxins, therapeutic drugs, heavy metals)
Infectious agents (bacteria, viruses, fungi, parasites)
Immunologic reactions (hypersensitivity, autoimmune disease)
Genetic defects and nutritional imbalances

High-YieldThe TWO hallmarks of IRREVERSIBLE injury are: (1) inability to restore mitochondrial function and (2) profound membrane damage. Membrane damage is the POINT OF NO RETURN.

MEMORY AID - Nuclear Changes in Necrosis - PKK

Pyknosis (nuclear shrinkage/condensation) → Karyorrhexis (nuclear fragmentation) → Karyolysis (nuclear dissolution). Think: "PacKing up and Killing the nucleus!"

[Include Image: Figure 2. Reversible vs irreversible cell injury showing cellular swelling, fatty change, and necrotic changes]

Feature	Reversible Injury	Irreversible Injury
ATP Levels	Decreased but partially maintained	Severely depleted (required for apoptosis; complete loss leads to necrosis)
Cell Membrane	Intact but may show blebbing	Disrupted with loss of integrity (POINT OF NO RETURN)
Mitochondria	Swelling but functional	Severe damage, loss of membrane potential, calcium influx
Nucleus	Chromatin clumping (reversible)	Pyknosis, karyorrhexis, karyolysis
Cytoplasm	Cloudy swelling, fatty change	Increased eosinophilia, myelin figures, calcium deposits
Outcome	Cell survives if stimulus removed	Cell death (necrosis or apoptosis)

2. Necrosis and Apoptosis

Necrosis

Necrosis is uncontrolled cell death resulting from overwhelming cellular injury. It is characterized by cell swelling, membrane rupture, release of cellular contents, and an inflammatory response. Unlike apoptosis, necrosis is ALWAYS pathological and damages surrounding tissue.

Types of Necrosis

MEMORY AID - Types of Necrosis - "CLCFFG"

Coagulative (solid organs, ischemia), Liquefactive (brain, abscesses), Caseous (TB/cheese), Fat (pancreas), Fibrinoid (vessels), Gangrenous (limbs). Remember: "Coagulative Lives Casually, Fat Fiber Gets Gangrene" OR think of the organ: Heart/Kidney = Coagulative, Brain = Liquefactive, Lung TB = Caseous, Pancreas = Fat.

High-YieldEXCEPTION: Brain undergoes LIQUEFACTIVE necrosis in ischemia (not coagulative like other organs). This is because brain tissue has high lipid content and abundant hydrolytic enzymes. Remember: "Brain is LIQUID gold!"

[Include Image: Figure 3. Types of necrosis histopathology - coagulative, liquefactive, caseous, and fat necrosis comparison]

Apoptosis

Apoptosis is programmed cell death - an energy-dependent, genetically controlled process that eliminates unwanted, damaged, or aged cells without causing inflammation. It is essential for normal development, tissue homeostasis, and immune function.

Apoptosis Pathways

Intrinsic (Mitochondrial) Pathway: Triggered by DNA damage, growth factor withdrawal, or cellular stress. Involves BCL-2 family proteins (pro-apoptotic: BAX, BAK; anti-apoptotic: BCL-2, BCL-XL). Leads to cytochrome c release from mitochondria → apoptosome formation → caspase-9 activation → executioner caspases (3, 6, 7).

Extrinsic (Death Receptor) Pathway: Triggered by death ligands (Fas ligand, TNF-alpha) binding to death receptors (Fas, TNFR1). Activates caspase-8 → executioner caspases. Important in immune-mediated cell killing (cytotoxic T cells).

MEMORY AID - Apoptosis vs Necrosis - "SIPA vs SPIN"

Apoptosis = SIPA: Shrinkage, Intact membrane, Programmed, ATP-dependent. Necrosis = SPIN: Swelling, Plasma membrane rupture, Inflammatory, No ATP needed.

High-YieldCASPASES are the executioners of apoptosis. They cleave cellular substrates leading to the morphologic changes of apoptosis. Caspase-3 is the key executioner caspase. Remember: Caspases are "Cellular Assassins Starting Programmed Apoptosis - Silently Ending Survival."

Type	Characteristics	Mechanism	Examples
Coagulative	Tissue architecture preserved for days; firm texture; cells appear as "ghost outlines"	Protein denaturation predominates over enzyme digestion; enzymes denatured by ischemia	Myocardial infarction; renal infarction; splenic infarction (MOST COMMON type)
Liquefactive	Complete digestion of dead cells; liquid viscous mass; creamy yellow (pus)	Enzymatic digestion predominates (autolysis/heterolysis); high enzyme content	Brain infarcts; abscesses; bacterial infections (neutrophil enzymes)
Caseous	Soft, white, cheese-like ("caseous"); amorphous granular debris	Combination of coagulative and liquefactive; lipid-rich mycobacterial cell wall	Tuberculosis; some fungal infections (histoplasmosis, coccidioidomycosis)
Fat Necrosis	Chalky white deposits (saponification); calcium soaps	Lipases digest fat → free fatty acids bind calcium → calcium soaps	Acute pancreatitis (enzymatic); traumatic fat necrosis in mammary tissue
Fibrinoid	Bright pink, smudgy material in vessel walls on H and E	Fibrin and immune complexes deposited in vessel walls	Malignant hypertension; vasculitis; immune-mediated diseases
Gangrenous	DRY: mummified, black tissue. WET: liquefactive with bacterial superinfection	Dry = coagulative (arterial occlusion). Wet = coagulative + liquefactive (bacteria)	Diabetic foot; frostbite; intestinal volvulus; ergot poisoning

3. Inflammation (Acute and Chronic)

Inflammation is a complex protective response to injury involving vascular and cellular events designed to eliminate the initial cause of injury, clear necrotic debris, and initiate repair. The cardinal signs are rubor (redness), calor (heat), tumor (swelling), dolor (pain), and functio laesa (loss of function).

MEMORY AID - Cardinal Signs of Inflammation

Remember the 5 Latin terms: Rubor (Redness), Calor (heat/Celsius), Tumor (swelling), Dolor (pain/Dolorous), Functio Laesa (Loss of function). "Red Cats Tumble Down Flights of stairs!"

Acute Inflammation

Acute inflammation is the immediate, short-term response (minutes to days) characterized by vascular changes and neutrophil recruitment. It aims to deliver defensive elements to the site of injury.

Vascular Events

Transient vasoconstriction (seconds) followed by sustained vasodilation (histamine, NO)
Increased vascular permeability → protein-rich exudate → edema
Stasis of blood flow → allows leukocyte margination

Cellular Events - Leukocyte Recruitment

MEMORY AID - Leukocyte Extravasation - "MRAFTC"

Margination → Rolling (selectins) → Activation (chemokines) → Firm adhesion (integrins) → Transmigration (PECAM-1) → Chemotaxis. Think: "My Red Ants Fight The Comets!"

Chemical Mediators of Inflammation

High-YieldFEVER is mediated by IL-1, IL-6, and TNF-alpha acting on the hypothalamus to produce prostaglandins (especially PGE2). This is why NSAIDs (COX inhibitors) reduce fever. Remember: "Inflammatory cytokines Turn Up the Thermostat via PGE2!"

[Include Image: Figure 4. Acute inflammation showing neutrophil margination, rolling, adhesion, and transmigration]

Chronic Inflammation

Chronic inflammation is prolonged inflammation (weeks to years) in which active inflammation, tissue destruction, and repair occur simultaneously. It is characterized by mononuclear cell infiltration (macrophages, lymphocytes, plasma cells), tissue destruction, and fibrosis.

Granulomatous Inflammation

Granulomatous inflammation is a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages (epithelioid cells) often with multinucleated giant cells, surrounded by lymphocytes. It occurs when the inciting agent is difficult to eradicate.

Causes of Granulomatous Inflammation: Mycobacteria (TB, Johne's disease), fungi (blastomycosis, histoplasmosis), foreign bodies, sarcoidosis, and certain parasites.

MEMORY AID - Causes of Granulomas - "TB FUNGi are Foreign"

Tuberculosis and other mycobacteria, FUNGal infections (histoplasmosis, blastomycosis, cryptococcosis), and Foreign bodies all cause granulomatous inflammation.

Feature	Necrosis	Apoptosis
Cell Size	Enlarged (swelling)	Reduced (shrinkage)
Nucleus	Pyknosis → karyorrhexis → karyolysis	Fragmentation into nucleosome-sized pieces
Plasma Membrane	Disrupted with loss of integrity	Intact but altered; blebbing; phosphatidylserine externalization
Cellular Contents	Enzymatic digestion; leak into extracellular space	Intact; packaged into apoptotic bodies
Inflammation	Present (DAMPs released)	Absent (clean removal by phagocytosis)
Energy Requirement	No ATP required	ATP-dependent process
Pattern	Contiguous groups of cells	Individual scattered cells
Role	Always pathological	Physiological or pathological

4. Healing and Repair

Tissue repair follows injury and inflammation and involves regeneration (replacement by identical cells) or repair by connective tissue (scarring). The capacity for regeneration depends on the proliferative capacity of the tissue.

Cell Proliferative Capacity

High-YieldLiver has REMARKABLE regenerative capacity (stable cells). Up to 70% can regenerate after partial hepatectomy. However, cardiac muscle and neurons are PERMANENT - damage results in scarring, not regeneration. This is why myocardial infarction results in scar tissue.

Wound Healing Phases

MEMORY AID - Wound Healing Phases - "HIPR"

Hemostasis → Inflammation → Proliferation → Remodeling. Think: "Healing Is Particularly Rewarding!" Or "HIPPO Repairs" (Hemostasis, Inflammation, Proliferation, Put-back-together [Remodeling]).

Primary vs. Secondary Intention Healing

Primary Intention: Clean, opposed wound edges (surgical incision). Minimal granulation tissue; minimal scarring; rapid healing.

Secondary Intention: Large tissue defect with separated edges (ulcer, burn). Extensive granulation tissue fills defect; wound contraction; larger scar; slower healing.

Factors Impairing Wound Healing

Infection (most common cause of delayed healing)
Nutritional deficiencies (protein, vitamin C [collagen synthesis], zinc)
Diabetes mellitus (impaired neutrophil function, microangiopathy)
Glucocorticoids (inhibit collagen synthesis and inflammatory response)
Poor blood supply / ischemia
Foreign bodies
Mechanical factors (tension on wound, motion)

[Include Image: Figure 5. Wound healing by primary and secondary intention comparison]

Step	Process	Key Molecules
1. Margination	WBCs move to vessel periphery due to blood stasis	Result of hemodynamic changes
2. Rolling	Loose, transient adhesion to endothelium	Selectins (E-selectin, P-selectin) and their ligands (Sialyl-Lewis X)
3. Activation	Chemokines activate leukocyte integrins	Chemokines (IL-8, MCP-1) on endothelium
4. Firm Adhesion	Tight binding to endothelium; spreading	Integrins (LFA-1, MAC-1) bind ICAM-1, VCAM-1
5. Transmigration	Diapedesis through vessel wall (mostly venules)	PECAM-1 (CD31) at intercellular junctions
6. Chemotaxis	Directed migration toward chemotactic gradient	Bacterial products, C5a, LTB4, IL-8

5. Hemodynamic Disorders

Edema

Edema is the accumulation of excess fluid in the interstitial space or body cavities. It can be classified by location: anasarca (generalized subcutaneous), ascites (peritoneal), hydrothorax (pleural), hydropericardium (pericardial).

MEMORY AID - Edema Causes - "HOLD IT"

Hydrostatic pressure increased, Oncotic pressure decreased, Lymphatic obstruction, Damage to vessels (permeability), Inflammation, Too much sodium/water retention.

Hyperemia and Congestion

Hyperemia (Active): Increased blood flow due to arteriolar dilation. Tissue appears red and warm. Physiologic (exercise, blushing) or pathologic (inflammation).

Congestion (Passive): Decreased venous outflow leading to blood accumulation. Tissue appears blue-red (cyanosis). Chronic congestion leads to hypoxia, atrophy, and fibrosis (e.g., nutmeg liver in CHF).

Hemorrhage

Hemorrhage is extravasation of blood due to vessel rupture. Named by size: petechiae (1-2 mm, often platelet/vessel defects), purpura (3 mm to 1 cm), ecchymoses (greater than 1 cm, bruising), hematoma (localized collection).

MEMORY AID - Hemorrhage Size Classification

"PEtechiae are Tiny, PUrpura are Pea-sized, ECchymoses are big ECMs (bigger than 1 cm)." Also: Think of increasing size - P-P-E corresponds to 1-2mm, 3mm-1cm, more than 1cm.

Mediator	Source	Major Effects
Histamine	Mast cells, basophils, platelets	Vasodilation; increased vascular permeability; early phase
Prostaglandins	Mast cells, leukocytes (via COX pathway)	PGE2, PGD2: vasodilation, pain, fever. PGI2: inhibits platelet aggregation
Leukotrienes	Leukocytes (via lipoxygenase)	LTB4: chemotaxis. LTC4, D4, E4: bronchoconstriction, vascular permeability
Complement	Plasma (liver synthesis)	C3a, C5a: anaphylatoxins (mast cell degranulation). C5a: chemotaxis. C3b: opsonin. MAC: lysis
Cytokines	Macrophages, lymphocytes	TNF-alpha, IL-1: fever, acute phase proteins, endothelial activation. IL-6: acute phase proteins
Nitric Oxide	Endothelium, macrophages	Vasodilation; microbicidal (in macrophages)
Bradykinin	Kinin system (plasma)	Pain, vasodilation, increased vascular permeability

6. Shock

Shock is a life-threatening state of circulatory failure resulting in inadequate tissue perfusion and cellular hypoxia. If not corrected, it leads to irreversible cellular injury, multiorgan failure, and death.

High-YieldSEPTIC SHOCK (distributive) is the MOST COMMON type of shock in hospitalized patients. In veterinary medicine, hypovolemic shock from hemorrhage or GI losses is also extremely common. GDV in dogs causes OBSTRUCTIVE shock.

Stages of Shock

1. Compensated (Nonprogressive): Sympathetic activation maintains perfusion to vital organs. Tachycardia, vasoconstriction, reduced urine output. May appear normal. REVERSIBLE with treatment.

2. Decompensated (Progressive): Compensatory mechanisms fail. Tissue hypoperfusion, lactic acidosis, altered mentation. POTENTIALLY REVERSIBLE with aggressive intervention.

3. Irreversible (Refractory): Widespread cellular injury, multiorgan failure, lysosomal enzyme release. IRREVERSIBLE - death despite treatment.

MEMORY AID - Types of Shock - "CHOD"

Cardiogenic (pump failure), Hypovolemic (tank empty), Obstructive (pipe blocked), Distributive (pipes too wide). Think of it as a plumbing problem!

[Include Image: Figure 6. Pathophysiology of shock showing the four types and their mechanisms]

Feature	Acute Inflammation	Chronic Inflammation
Duration	Hours to days	Weeks to months/years
Onset	Rapid	Gradual or follows acute
Predominant Cell	Neutrophils	Macrophages, lymphocytes, plasma cells
Tissue Injury	Usually mild, self-limited	Often severe, progressive
Vascular Changes	Prominent vasodilation and exudation	Angiogenesis, fibrosis
Outcomes	Resolution, abscess, or progression to chronic	Fibrosis (scarring), tissue destruction, or resolution

7. Neoplasia Principles and Metastasis

Benign vs. Malignant Neoplasms

High-YieldThe ONLY absolute criterion distinguishing malignant from benign tumors is METASTASIS. Local invasion strongly suggests malignancy but is not definitive.

Metastasis

Metastasis is the spread of tumor to sites discontinuous with the primary tumor. It is the hallmark of malignancy and the major cause of cancer morbidity and mortality.

Routes of Metastasis

Lymphatic spread: Most common for CARCINOMAS. Regional lymph nodes affected first (sentinel node).
Hematogenous spread: Most common for SARCOMAS. Lung is most common site (systemic circulation). Liver common for GI tumors (portal circulation).
Transcoelomic (seeding): Spread across body cavities (peritoneal carcinomatosis).

MEMORY AID - Metastasis Routes - "Carcinomas Love Lymph; Sarcomas Seek Blood"

Carcinomas preferentially spread via lymphatics; Sarcomas preferentially spread hematogenously. Also remember: "CAR-LYMPH-noma" and "SARCO-BLOOD-ma"

Tumor Nomenclature

High-YieldEXCEPTIONS to naming rules: Melanoma, Lymphoma, Mesothelioma, and Seminoma are all MALIGNANT despite ending in "-oma". Remember: "MLMS are Malicious despite their innocent names!"

Cell Type	Proliferative Capacity	Examples
Labile Cells	Continuously dividing; high regenerative capacity	Epidermis, GI epithelium, bone marrow, respiratory epithelium
Stable (Quiescent) Cells	Low baseline division; can regenerate when stimulated (G0 phase)	Hepatocytes, renal tubular cells, fibroblasts, smooth muscle, endothelium
Permanent Cells	Cannot divide; repair only by scarring	Neurons (CNS), cardiac myocytes, skeletal muscle cells

8. Additional Topics

Genetic and Developmental Disorders

Congenital anomalies: Present at birth; may be genetic or environmental (teratogens)
Chromosomal abnormalities: Aneuploidy, deletions, translocations
Single gene disorders: Autosomal dominant, autosomal recessive, X-linked
Multifactorial inheritance: Combination of genetic predisposition and environmental factors

Nutritional Diseases

Protein-calorie malnutrition: Marasmus (overall calorie deficiency), Kwashiorkor (protein deficiency with edema)
Vitamin deficiencies: Vitamin A (night blindness, epithelial changes), Vitamin D (rickets, osteomalacia), Vitamin E (white muscle disease), Vitamin K (coagulopathy)
Mineral deficiencies: Calcium/phosphorus (metabolic bone disease), copper (swayback in lambs), selenium (white muscle disease)
Obesity: Most common nutritional disorder in companion animals; associated with diabetes, osteoarthritis, hepatic lipidosis

Immune-Mediated Diseases

MEMORY AID - Hypersensitivity Types - "ACID"

Type I = Anaphylactic/Allergic (IgE), Type II = Cytotoxic (antibody vs cells), Type III = Immune Complex, Type IV = Delayed (T cells). Or remember: "1 is fast (Anaphylaxis), 4 is slow (Delayed)"

High-YieldIMHA (Immune-Mediated Hemolytic Anemia) and IMTP (Immune-Mediated Thrombocytopenia) are TYPE II hypersensitivity reactions - antibodies target RBCs or platelets for destruction.

Phase	Timing	Key Events
1. Hemostasis	Immediate (minutes)	Vasoconstriction, platelet plug formation, fibrin clot (coagulation cascade), platelet-derived growth factors released
2. Inflammation	Hours to days (0-3 days)	Neutrophils infiltrate (peak 24-48 hrs) for debridement; macrophages arrive (48-72 hrs) for phagocytosis and growth factor secretion
3. Proliferation	Days to weeks (3-21 days)	Granulation tissue formation: fibroblasts produce collagen; angiogenesis; epithelialization; wound contraction by myofibroblasts
4. Remodeling	Weeks to months/years	Type III collagen replaced by Type I collagen; cross-linking increases; scar maturation; maximum tensile strength 80% of normal at 3 months

Mechanism	Pathophysiology	Examples
Increased Hydrostatic Pressure	Elevated venous pressure forces fluid into interstitium	Congestive heart failure, venous obstruction, portal hypertension
Decreased Oncotic Pressure	Low plasma proteins (especially albumin) reduce osmotic pull	Nephrotic syndrome, liver failure, protein-losing enteropathy, malnutrition
Increased Vascular Permeability	Endothelial injury allows protein-rich fluid leakage	Inflammation, burns, allergic reactions, sepsis
Lymphatic Obstruction	Impaired lymph drainage causes localized edema	Tumors, post-surgical, filariasis, lymphangitis
Sodium/Water Retention	Excessive salt/water retention expands plasma volume	Renal failure, heart failure (RAAS activation)

Type	Mechanism	Causes	Key Features
Hypovolemic	Decreased circulating blood volume → reduced preload and cardiac output	Hemorrhage, severe dehydration, burns, GI losses (vomiting/diarrhea)	Tachycardia, cold/pale skin, low CVP, concentrated urine
Cardiogenic	Pump failure → inadequate cardiac output despite adequate volume	Myocardial infarction, cardiomyopathy, arrhythmias, valvular disease	Elevated CVP, pulmonary edema, jugular distension
Distributive	Inappropriate peripheral vasodilation → relative hypovolemia despite adequate volume	Sepsis (most common), anaphylaxis, neurogenic (spinal injury)	Warm extremities (early sepsis), decreased SVR, may have normal/high CO initially
Obstructive	Mechanical obstruction to blood flow impairs cardiac filling or output	Cardiac tamponade, tension pneumothorax, pulmonary embolism, GDV	Elevated CVP, pulsus paradoxus (tamponade), absent breath sounds (pneumothorax)

Feature	Benign	Malignant
Differentiation	Well-differentiated; resembles tissue of origin	Variable; may be poorly differentiated or anaplastic
Growth Rate	Usually slow	Usually rapid; increased mitotic figures
Local Invasion	Expansile, well-circumscribed, often encapsulated	Infiltrative, poorly demarcated, invades surrounding tissue
Metastasis	Absent	Present (defines malignancy)
Necrosis	Rare	Common (outgrows blood supply)
Nomenclature	Suffix: -oma (adenoma, fibroma, lipoma)	Carcinoma (epithelial), Sarcoma (mesenchymal)

Tissue Origin	Benign	Malignant
Epithelial (glandular)	Adenoma	Adenocarcinoma
Epithelial (squamous)	Squamous papilloma	Squamous cell carcinoma
Fibrous tissue	Fibroma	Fibrosarcoma
Adipose tissue	Lipoma	Liposarcoma
Bone	Osteoma	Osteosarcoma
Cartilage	Chondroma	Chondrosarcoma
Blood vessels	Hemangioma	Hemangiosarcoma
Smooth muscle	Leiomyoma	Leiomyosarcoma
Lymphoid tissue	N/A	Lymphoma/Lymphosarcoma

Type	Mechanism	Mediators	Examples
Type I (Immediate)	IgE-mediated mast cell degranulation	Histamine, leukotrienes, prostaglandins	Anaphylaxis, atopy, allergic rhinitis, flea allergy dermatitis
Type II (Cytotoxic)	IgG/IgM against cell surface antigens	Complement, phagocytes, NK cells	IMHA, IMTP, transfusion reactions, pemphigus, myasthenia gravis
Type III (Immune Complex)	Antigen-antibody complexes deposit in tissues	Complement, neutrophils	Glomerulonephritis, SLE, serum sickness, Arthus reaction
Type IV (Delayed)	T cell-mediated (no antibody)	Cytokines (IFN-gamma, TNF), macrophages	Contact dermatitis, tuberculin skin test, granulomatous disease, transplant rejection

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General Pathology &ndash; BCSE Study Guide