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Para-Clinical Pathology Syllabus
Every chapter and topic of Pathology examined in Para-Clinical — 19 chapters, 72 topics and 173 sub-topics, plus 77 flashcards written against it.
Pathology syllabus — full chapter and topic list
Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pathology in Para-Clinical, not a summary of it.
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Cell Injury and Adaptation
4 topics- Cell Injury
- Types of Cell Injury
- Mechanisms of Cell Injury
- Reversible and Irreversible Injury
- Cell Death: Necrosis and Apoptosis
- Cellular Adaptations
- Hypertrophy
- Hyperplasia
- Atrophy
- Metaplasia
- Intracellular Accumulations
- Lipids
- Proteins
- Glycogen
- Pigments
- Pathologic Calcification
- Dystrophic Calcification
- Metastatic Calcification
- Cell Injury
-
Inflammation and Repair
3 topics- Acute Inflammation
- Vascular Changes
- Cellular Events
- Chemical Mediators
- Chronic Inflammation
- Causes
- Cellular Components
- Granulomatous Inflammation
- Tissue Repair
- Regeneration
- Healing by Connective Tissue
- Factors Affecting Healing
- Acute Inflammation
-
Hemodynamic Disorders
5 topics- Edema
- Pathophysiology
- Types of Edema
- Hemorrhage
- Causes
- Clinical Significance
- Thrombosis
- Pathogenesis
- Fate of Thrombus
- Embolism
- Types of Emboli
- Clinical Consequences
- Shock
- Types of Shock
- Pathophysiology
- Clinical Features
- Edema
-
Genetic Disorders
4 topics- Mendelian Disorders
- Autosomal Dominant Disorders
- Autosomal Recessive Disorders
- X-linked Disorders
- Chromosomal Disorders
- Numerical Abnormalities
- Structural Abnormalities
- Multifactorial Disorders
- Examples and Mechanisms
- Molecular Basis of Genetic Diseases
- Mutations
- Epigenetics
- Mendelian Disorders
-
Neoplasia
6 topics- Fundamentals of Neoplasia
- Definitions and Nomenclature
- Benign vs Malignant Tumors
- Molecular Basis of Cancer
- Genetic Changes in Cancer
- Oncogenes and Tumor Suppressor Genes
- Tumor-Host Interactions
- Local and Systemic Effects
- Paraneoplastic Syndromes
- Carcinogenesis
- Chemical Carcinogenesis
- Radiation Carcinogenesis
- Microbial Carcinogenesis
- Tumor Progression and Metastasis
- Invasion and Metastasis
- Angiogenesis
- Clinical Aspects of Neoplasia
- Diagnosis
- Grading and Staging
- Treatment
- Fundamentals of Neoplasia
-
Environmental and Nutritional Pathology
2 topics- Environmental Diseases
- Toxicology
- Chemical Injuries
- Physical Injuries
- Nutritional Diseases
- Malnutrition
- Vitamin Deficiencies
- Obesity
- Environmental Diseases
-
Infectious Diseases
5 topics- General Principles of Microbial Pathogenesis
- Host-Pathogen Interactions
- Mechanisms of Microbial Injury
- Bacterial Infections
- Pathogenesis and Examples
- Viral Infections
- Pathogenesis and Examples
- Fungal Infections
- Pathogenesis and Examples
- Parasitic Infections
- Pathogenesis and Examples
- General Principles of Microbial Pathogenesis
-
Immunopathology
5 topics- Basics of the Immune System
- Innate Immunity
- Adaptive Immunity
- Hypersensitivity Reactions
- Type I Hypersensitivity
- Type II Hypersensitivity
- Type III Hypersensitivity
- Type IV Hypersensitivity
- Autoimmune Diseases
- Mechanisms
- Examples
- Immunodeficiency Diseases
- Primary Immunodeficiencies
- Secondary Immunodeficiencies
- Amyloidosis
- Pathogenesis
- Classification
- Clinical Features
- Basics of the Immune System
-
Blood Vessels
1 topic- Vascular Disorders
- Atherosclerosis
- Hypertension
- Aneurysms
- Vasculitis
- Vascular Disorders
-
Heart
4 topics- Ischemic Heart Disease
- Pathogenesis
- Clinical Syndromes
- Hypertensive Heart Disease
- Left-sided Hypertensive Heart Disease
- Right-sided Hypertensive Heart Disease
- Valvular Heart Disease
- Rheumatic Heart Disease
- Infective Endocarditis
- Non-infective Endocarditis
- Myocardial Diseases
- Cardiomyopathies
- Myocarditis
- Ischemic Heart Disease
-
Respiratory System
4 topics- Obstructive Lung Diseases
- Chronic Obstructive Pulmonary Disease (COPD)
- Asthma
- Bronchiectasis
- Restrictive Lung Diseases
- Interstitial Lung Diseases
- Pneumoconiosis
- Pulmonary Infections
- Pneumonia
- Tuberculosis
- Fungal Infections
- Lung Tumors
- Primary Lung Cancer
- Metastatic Tumors
- Obstructive Lung Diseases
-
Gastrointestinal Tract
6 topics- Esophagus
- Esophagitis
- Barrett's Esophagus
- Esophageal Cancer
- Stomach
- Gastritis
- Peptic Ulcer Disease
- Gastric Cancer
- Intestines
- Inflammatory Bowel Disease
- Infectious Enterocolitis
- Colorectal Cancer
- Liver
- Hepatitis
- Cirrhosis
- Hepatocellular Carcinoma
- Gallbladder and Biliary Tract
- Cholelithiasis
- Cholecystitis
- Gallbladder Cancer
- Pancreas
- Pancreatitis
- Pancreatic Cancer
- Esophagus
-
Urinary Tract
2 topics- Kidneys
- Glomerular Diseases
- Tubulointerstitial Diseases
- Renal Tumors
- Ureters and Bladder
- Urolithiasis
- Bladder Cancer
- Kidneys
-
Reproductive System
3 topics- Male Reproductive System
- Prostate Diseases
- Testicular Tumors
- Female Reproductive System
- Cervical Diseases
- Endometrial Diseases
- Ovarian Tumors
- Breast
- Benign Breast Diseases
- Breast Cancer
- Male Reproductive System
-
Endocrine System
5 topics- Pituitary Gland
- Hyperpituitarism
- Hypopituitarism
- Thyroid Gland
- Hyperthyroidism
- Hypothyroidism
- Thyroid Tumors
- Parathyroid Gland
- Hyperparathyroidism
- Hypoparathyroidism
- Adrenal Gland
- Adrenocortical Hyperfunction
- Adrenocortical Hypofunction
- Adrenal Tumors
- Pancreatic Endocrine Tumors
- Insulinomas
- Gastrinomas
- Pituitary Gland
-
Nervous System
4 topics- Cerebrovascular Diseases
- Stroke
- Aneurysms
- Infections of the CNS
- Meningitis
- Encephalitis
- Neurodegenerative Diseases
- Alzheimer's Disease
- Parkinson's Disease
- Amyotrophic Lateral Sclerosis
- CNS Tumors
- Gliomas
- Meningiomas
- Cerebrovascular Diseases
-
Musculoskeletal System
3 topics- Bone Diseases
- Osteoporosis
- Osteomyelitis
- Bone Tumors
- Joint Diseases
- Osteoarthritis
- Rheumatoid Arthritis
- Gout
- Muscle Diseases
- Muscular Dystrophies
- Myopathies
- Bone Diseases
-
Skin
3 topics- Inflammatory Skin Diseases
- Eczema
- Psoriasis
- Acne
- Blistering Diseases
- Pemphigus
- Bullous Pemphigoid
- Skin Tumors
- Benign Tumors
- Malignant Tumors
- Inflammatory Skin Diseases
-
Pediatric Diseases
3 topics- Congenital Anomalies
- Types and Examples
- Perinatal Infections
- TORCH Infections
- Pediatric Tumors
- Neuroblastoma
- Wilms Tumor
- Congenital Anomalies
Pathology flashcards for Para-Clinical
24 of 77 cards from the Pathology deck — real questions with worked answers.
Define reversible cell injury and name its two key morphologic hallmarks.
Reversible injury is cell damage that can be corrected if the stimulus is removed, before a 'point of no return' is reached. The two hallmarks are cellular swelling (hydropic change, from failure of the $\ce{Na+/K+}$ ATPase pump) and fatty change (steatosis, accumulation of lipid vacuoles).
What are the two morphologic features that define IRREVERSIBLE cell injury (the 'point of no return')?
Severe mitochondrial dysfunction (inability to reverse, with mitochondrial permeability transition pore formation) and profound disturbance of membrane function (plasma membrane damage). Massive $\ce{Ca^{2+}}$ influx and marked amorphous densities in mitochondria are key signs.
List the principal biochemical mechanisms of cell injury.
(1) ATP depletion, (2) Mitochondrial damage, (3) Increased intracellular $\ce{Ca^{2+}}$ and loss of calcium homeostasis, (4) Accumulation of oxygen-derived free radicals (oxidative stress), (5) Defects in membrane permeability, and (6) Damage to DNA and proteins.
Name the three major reactive oxygen species (ROS) and the enzymes that neutralize each.
Superoxide ($\ce{O2^{.-}}$), neutralized by superoxide dismutase (SOD); hydrogen peroxide ($\ce{H2O2}$), neutralized by catalase and glutathione peroxidase; hydroxyl radical ($\ce{^{.}OH}$), the most reactive, scavenged by glutathione and antioxidants.
Contrast necrosis and apoptosis on: energy dependence, membrane integrity, and inflammation.
Necrosis: ATP-independent (passive), plasma membrane ruptures, contents leak causing inflammation. Apoptosis: ATP-dependent (active/energy-requiring), membrane remains intact (forms apoptotic bodies), and it does NOT elicit inflammation.
Match each necrosis pattern to its classic setting: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous.
Coagulative — ischemic infarcts of solid organs (except brain). Liquefactive — brain infarcts and abscesses. Caseous — tuberculosis. Fat — acute pancreatitis (enzymatic). Fibrinoid — immune vascular injury (vasculitis). Gangrenous — limb ischemia (clinical term).
Name the two major pathways of apoptosis and the key initiator caspases of each.
Intrinsic (mitochondrial) pathway — regulated by BCL-2 family, releases cytochrome c, activates caspase-9. Extrinsic (death receptor) pathway — triggered by Fas/FasL or TNF, activates caspase-8. Both converge on executioner caspases 3 and 6.
In the BCL-2 family, which proteins are pro-apoptotic and which are anti-apoptotic?
Anti-apoptotic (pro-survival): BCL-2, BCL-XL, MCL-1. Pro-apoptotic effectors: BAX and BAK (form mitochondrial pores). Pro-apoptotic sensors (BH3-only): BAD, BID, BIM, PUMA, NOXA.
Define the four types of cellular adaptation to stress with a defining feature of each.
Hypertrophy — increased cell SIZE (e.g., cardiac muscle). Hyperplasia — increased cell NUMBER (e.g., endometrium). Atrophy — decreased size/number (e.g., disuse). Metaplasia — reversible replacement of one differentiated cell type by another (e.g., Barrett esophagus).
What is metaplasia, and give the classic example of squamous and columnar metaplasia.
Metaplasia is the reversible change in which one adult (differentiated) cell type is replaced by another better suited to the stress. Squamous metaplasia: bronchial epithelium in smokers. Columnar (glandular) metaplasia: Barrett esophagus (squamous replaced by columnar intestinal-type epithelium due to acid reflux).
Distinguish physiologic from pathologic hyperplasia with an example of each.
Physiologic hyperplasia is hormonal (breast in puberty/pregnancy) or compensatory (liver regeneration after resection). Pathologic hyperplasia results from excessive hormonal/growth-factor stimulation (endometrial hyperplasia, benign prostatic hyperplasia) and can predispose to cancer.
List the major categories of intracellular accumulations.
(1) Abnormal amounts of normal substances (lipids, proteins, carbohydrates/glycogen), (2) Abnormal endogenous substances from defective metabolism/folding (e.g., storage diseases), (3) Exogenous pigments/materials not degraded (e.g., carbon, silica), and (4) Endogenous pigments (lipofuscin, melanin, hemosiderin, bilirubin).
Compare lipofuscin and hemosiderin: composition and significance.
Lipofuscin ('wear-and-tear' pigment) is yellow-brown, made of lipid-protein complexes from lipid peroxidation; a marker of aging/atrophy, harmless. Hemosiderin is a golden-brown iron-storage pigment (aggregated ferritin), stains blue with Prussian blue; excess (hemosiderosis/hemochromatosis) can cause organ damage.
What is dystrophic vs metastatic calcification? Give serum calcium status and typical setting for each.
Dystrophic calcification: occurs in DAMAGED/necrotic tissue with NORMAL serum calcium (e.g., atheromas, damaged heart valves, caseous TB). Metastatic calcification: deposition in NORMAL tissue due to HYPERCALCEMIA (e.g., hyperparathyroidism, vitamin D toxicity, bone destruction, renal failure).
Name the four main causes of hypercalcemia leading to metastatic calcification.
(1) Increased parathyroid hormone (primary hyperparathyroidism, PTHrP from tumors), (2) Bone destruction (myeloma, metastases, immobilization, Paget disease), (3) Vitamin D disorders (toxicity, sarcoidosis), (4) Renal failure (secondary hyperparathyroidism with phosphate retention).
List the five cardinal (clinical) signs of acute inflammation and their Latin names.
Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
Describe the vascular changes of acute inflammation in order.
Transient vasoconstriction, then vasodilation (increased blood flow → heat and redness), followed by increased vascular permeability (exudation of protein-rich fluid → edema), causing stasis and margination of leukocytes.
What are the sequential steps of leukocyte extravasation in acute inflammation?
(1) Margination and rolling (selectins), (2) Firm adhesion (integrins binding ICAM-1/VCAM-1), (3) Transmigration/diapedesis (PECAM-1/CD31), and (4) Chemotaxis toward the stimulus.
Name the adhesion molecule pairs for leukocyte rolling and firm adhesion.
Rolling: selectins — E-selectin (endothelium), P-selectin (endothelium/platelets), L-selectin (leukocytes) — bind sialyl-Lewis X. Firm adhesion: leukocyte integrins LFA-1 and VLA-4/Mac-1 bind endothelial ICAM-1 and VCAM-1.
List potent chemotactic agents for neutrophils.
C5a (complement), leukotriene $\ce{B4}$ (LTB4), bacterial N-formyl-methionyl peptides, and chemokines such as IL-8 (CXCL8).
Describe the three steps of phagocytosis.
(1) Recognition and attachment (aided by opsonins: IgG, C3b, collectins), (2) Engulfment (forming a phagosome that fuses with a lysosome → phagolysosome), and (3) Killing/degradation (via ROS from the respiratory burst, reactive nitrogen species/NO, and lysosomal enzymes).
What generates the oxidative burst in neutrophil killing, and what is chronic granulomatous disease?
NADPH oxidase converts $\ce{O2}$ to superoxide, then $\ce{H2O2}$; myeloperoxidase (MPO) converts $\ce{H2O2 + Cl^{-}}$ to hypochlorite ($\ce{HOCl}$), the most potent bactericidal agent. Chronic granulomatous disease results from an inherited NADPH oxidase defect, causing recurrent infections with catalase-positive organisms.
Classify the chemical mediators of inflammation into cell-derived vs plasma-derived, with examples.
Cell-derived: histamine, serotonin (preformed); prostaglandins, leukotrienes, PAF, ROS, NO, cytokines (TNF, IL-1), chemokines (newly synthesized). Plasma-derived: complement system (C3a, C5a, MAC), kinin system (bradykinin), and coagulation/fibrinolytic systems.
Which arachidonic acid metabolites cause vasodilation, vasoconstriction, and chemotaxis? Name the two enzyme pathways.
Cyclooxygenase (COX) pathway → prostaglandins ($\ce{PGI2/PGE2}$ vasodilation; $\ce{TXA2}$ vasoconstriction + platelet aggregation). Lipoxygenase pathway → leukotrienes ($\ce{LTB4}$ chemotaxis; $\ce{LTC4/D4/E4}$ bronchoconstriction and increased permeability, the 'SRS-A').
Planning Pathology for Para-Clinical
Pathology is about 36% of the Para-Clinical syllabus by topic count — 72 of 199 topics, spread over 19 chapters. At roughly 45 minutes per topic plus 12 minutes per sub-topic, a first pass runs to about 90 hours.
The heaviest chapters are Neoplasia (6 topics), Gastrointestinal Tract (6 topics), Hemodynamic Disorders (5 topics) . Front-load those while your energy is high; the short chapters are better revision filler later.
Work top-down: read the chapter, then tick topics off individually rather than marking the whole chapter done. Sub-topics are where silent gaps hide.
Pathology (Para-Clinical) FAQ
What is in the Para-Clinical Pathology syllabus?
Pathology is split into 19 chapters — Cell Injury and Adaptation, Inflammation and Repair, Hemodynamic Disorders, Genetic Disorders, Neoplasia and Environmental and Nutritional Pathology, and 13 more, containing 72 topics and 173 sub-topics in total.
How is Pathology structured in the Para-Clinical syllabus?
19 chapters. Pathology accounts for about 36% of the topics in the whole Para-Clinical syllabus (72 of 199).
How long should I spend on Pathology for Para-Clinical?
Budget around 90 hours for a first pass through Pathology — about 45 minutes per topic plus 12 minutes per sub-topic across its 72 topics. Add revision cycles on top.
Are there flashcards for Para-Clinical Pathology?
Yes — a 77-card Pathology deck. Sample cards are printed on this page, and the full deck is free in the Examius app with spaced repetition scheduling.