NExT Pathology, Pharmacology and Microbiology (Para-clinical Sciences) Syllabus

Pathology, Pharmacology and Microbiology (Para-clinical Sciences) syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pathology, Pharmacology and Microbiology (Para-clinical Sciences) in NExT, not a summary of it.

1. 1

   General and Systemic Pathology

   5 topics

   • Cell Injury, Inflammation and Repair
     • Necrosis, apoptosis, acute and chronic inflammation
   • Neoplasia
     • Carcinogenesis, tumor markers, metastasis
   • Hemodynamic Disorders
     • Thrombosis, embolism, infarction, edema
   • Immunopathology and Amyloidosis
   • Systemic Pathology Correlations
     • Organ-specific lesions across systems
2. 2

   Hematology and Clinical Pathology

   3 topics

   • Laboratory Hematology
     • Peripheral smear, CBC interpretation
   • Coagulation and Transfusion Medicine
     • Blood grouping, cross-matching, transfusion reactions
   • Urinalysis and Body Fluid Examination
3. 3

   General Pharmacology and Pharmacokinetics

   4 topics

   • Pharmacokinetics and Pharmacodynamics
     • Absorption, distribution, metabolism, excretion
     • Receptor theory, dose-response, agonist/antagonist
   • Adverse Drug Reactions and Pharmacovigilance
   • Routes of Administration and Drug Interactions
   • Rational Drug Use and Essential Medicines
4. 4

   Systemic and Clinical Pharmacology

   5 topics

   • Autonomic Nervous System Drugs
     • Cholinergics, adrenergics and antagonists
   • Cardiovascular and Renal Pharmacology
     • Antihypertensives, diuretics, antianginals
   • CNS Pharmacology
     • Sedatives, antiepileptics, antipsychotics, opioids
   • Antimicrobial Chemotherapy
     • Antibiotics, antivirals, antifungals, AMR
   • Chemotherapy and Hormonal Agents
5. 5

   General Microbiology and Immunology

   3 topics

   • Bacterial Structure, Sterilization and Disinfection
   • Immunology
     • Innate and adaptive immunity, hypersensitivity
     • Vaccines and immunodiagnostics
   • Host-Parasite Relationship and Infection Control
6. 6

   Systematic Microbiology

   4 topics

   • Medical Bacteriology
     • Gram-positive and gram-negative pathogens
     • Mycobacteria and spirochetes
   • Virology
     • Hepatitis viruses, HIV, respiratory viruses
   • Mycology and Parasitology
     • Systemic mycoses, protozoa, helminths
   • Clinical Microbiology and Lab Diagnosis

Pathology, Pharmacology and Microbiology (Para-clinical Sciences) flashcards for NExT

18 of 51 cards from the Pathology, Pharmacology and Microbiology (Para-clinical Sciences) deck — real questions with worked answers.

1. What are the two main types of cellular adaptation involving size, and how do they differ?

   Hypertrophy is an increase in cell size (and organ size) due to increased synthesis of structural components, occurring in non-dividing cells like cardiac/skeletal muscle. Hyperplasia is an increase in the number of cells, occurring only in tissues capable of division (e.g., endometrium, liver).

2. What is the key biochemical difference between reversible and irreversible cell injury?

   Reversible injury shows ATP depletion, cellular swelling, and ribosomal detachment but intact membranes. Irreversible injury is marked by severe membrane damage (mitochondrial, lysosomal, plasma) and profound mitochondrial dysfunction with massive calcium influx; the two hallmarks are inability to reverse mitochondrial dysfunction and membrane function loss.

3. Name the morphological patterns of necrosis and a classic example of each.

   Coagulative (ischemia/MI), liquefactive (brain infarct, abscess), caseous (TB), fat necrosis (acute pancreatitis), fibrinoid (immune vasculitis/malignant hypertension), and gangrenous (limb ischemia).

4. What are the two pathways of apoptosis and their key triggers?

   The intrinsic (mitochondrial) pathway is triggered by cell stress/DNA damage via Bcl-2 family proteins releasing cytochrome c. The extrinsic (death receptor) pathway is triggered by ligands like FasL/TNF binding death receptors (Fas/TNFR1). Both converge on executioner caspases (3, 6, 7).

5. What is the difference between dystrophic and metastatic calcification?

   Dystrophic calcification occurs in damaged/necrotic tissue with normal serum calcium levels (e.g., atheromas, TB lesions). Metastatic calcification occurs in normal tissue due to hypercalcemia (e.g., hyperparathyroidism, vitamin D toxicity, renal failure).

6. What are the five cardinal signs of acute inflammation and their Latin terms?

   Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

7. List the sequential steps of leukocyte extravasation in acute inflammation.

   Margination and rolling (selectins), adhesion (integrins binding ICAM-1/VCAM-1), transmigration/diapedesis (PECAM-1/CD31), and chemotaxis toward the injury (e.g., C5a, LTB4, IL-8, bacterial products).

8. What are the major chemical mediators of vasodilation and increased vascular permeability in inflammation?

   Vasodilation: histamine, prostaglandins (PGI2, PGE2), and nitric oxide. Increased permeability: histamine, bradykinin, leukotrienes (C4, D4, E4), and substance P.

9. Distinguish healing by primary intention from secondary intention.

   Primary intention: clean, approximated wound edges (e.g., surgical incision) with minimal tissue loss, little granulation tissue, and a thin scar. Secondary intention: large gaping wounds with extensive tissue loss, abundant granulation tissue, significant wound contraction, and a larger scar.

10. What growth factor is most important in angiogenesis, and which cell deposits collagen in repair?

    VEGF (vascular endothelial growth factor) drives angiogenesis. Fibroblasts (and myofibroblasts) deposit collagen and extracellular matrix; myofibroblasts also mediate wound contraction.

11. What is the difference between a benign and malignant neoplasm in terms of nomenclature suffixes?

    Benign tumors generally end in '-oma' (e.g., adenoma, lipoma). Malignant tumors of epithelial origin are 'carcinomas' and those of mesenchymal origin are 'sarcomas.' Exceptions like lymphoma, melanoma, and seminoma are malignant despite the '-oma' suffix.

12. Define anaplasia and list its cytologic features.

    Anaplasia is lack of differentiation, a hallmark of malignancy. Features: pleomorphism (variation in cell/nuclear size and shape), hyperchromatic nuclei with high nuclear-to-cytoplasmic ratio, prominent nucleoli, abnormal/atypical mitoses, and loss of polarity.

13. What is the difference between an oncogene and a tumor suppressor gene, with an example of each?

    Oncogenes are mutated proto-oncogenes that promote growth and are dominant (one allele mutation suffices), e.g., RAS, MYC. Tumor suppressor genes inhibit growth and are typically recessive (both alleles must be lost—'two-hit hypothesis'), e.g., TP53, RB.

14. Define metastasis and name the most common routes of spread for carcinomas versus sarcomas.

    Metastasis is the spread of tumor to discontinuous distant sites, the most reliable marker of malignancy. Carcinomas typically spread via lymphatics; sarcomas typically spread hematogenously (via blood).

15. List the steps of the metastatic cascade.

    Invasion of basement membrane → loosening of cell-cell contacts (E-cadherin loss) → degradation of ECM (matrix metalloproteinases) → migration → intravasation into vessels → survival in circulation → extravasation → formation of micrometastasis → colonization at the distant site.

16. What are the key differences between an exudate and a transudate?

    Exudate: high protein (>2.9 g/dL), specific gravity >1.020, high LDH, cloudy, due to inflammation/increased vascular permeability. Transudate: low protein, specific gravity <1.012, clear, due to hydrostatic/oncotic pressure imbalance (e.g., heart failure, hypoalbuminemia).

17. What is Virchow's triad for thrombosis?

    The three factors predisposing to thrombus formation: (1) endothelial injury, (2) abnormal blood flow (stasis or turbulence), and (3) hypercoagulability.

18. Differentiate a red (hemorrhagic) infarct from a white (anemic) infarct.

    Red infarcts occur in loose tissues with dual blood supply or venous occlusion (e.g., lung, intestine), with hemorrhage into necrotic zone. White infarcts occur in solid organs with end-arterial supply (e.g., heart, spleen, kidney) where dense tissue limits hemorrhage.

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