General Pathology and Hematology Crash Course

Dr. Priyanka Sachdev is conducting a crash course on high-yielding topics in General Pathology and Hematology, covering important topics in a concise manner.
The course aims to cover essential topics for exams like FMG, NEET PG, and NEXT, focusing on frequently asked questions.
The session is divided into General Pathology, Hematology, and Systemic Pathology, with a total duration of about 14-15 hours.
Dr. Priyanka Sachdev follows a teaching approach where she covers theory concisely, followed by solving MCQs related to the topic.
The course covers key concepts such as cell adaptation, cell injury, and cell death (apoptosis and necrosis).
In cell adaptation, cells try to survive unfavorable conditions through hypertrophy, hyperplasia, atrophy, metaplasia, and dysplasia.
The pregnant uterus serves as an example of both hypertrophy and hyperplasia during pregnancy and atrophy post-delivery.
Metaplasia involves the transformation of one mature cell type into another mature cell type, like squamous to columnar or vice versa.
The cervix exemplifies metaplasia, with the endocervix showing squamous metaplasia and the ectocervix showing columnar metaplasia.
Dysplasia is characterized by cellular changes including increased layers, disordered arrangement, loss of basal polarity, pleomorphism, hyperchromatism, altered NC ratio, and increased mitosis.
Apoptosis is a type of cell death where cells commit suicide in a regulated manner due to fulfilled function or irreparable DNA damage.
Apoptosis involves the activation of caspase enzymes that lead to the fragmentation of the cell into apoptotic bodies without leakage or inflammation.
Apoptosis can be triggered extrinsically (external signal) or intrinsically (internal signal), with caspase activation leading to cell degradation.
The extrinsic pathway involves ligand binding to death receptors (e.g., CD95) on the cell surface, leading to caspase activation via the formation of the FADD domain.- Caspase 8 and 10 are converted from inactive to active form during activation.
The initiation phase of the intrinsic pathway involves signals coming from inside the cell, particularly from the nucleus to the mitochondria.
Cytochrome C, present between the two membranes of the mitochondria, is normally prevented from leaking out by anti-apoptotic proteins (bcl2, bclx, mcl1).
When DNA is damaged beyond repair, p53 signals the mitochondria to initiate apoptosis by replacing anti-apoptotic proteins with pro-apoptotic proteins (bax, bak, bim).
In the intrinsic pathway, the signal for apoptosis comes from inside the cell (nucleus to mitochondria), leading to the activation of caspase-9 after cytochrome C leakage.- Chapter 1: Introduction to Necrosis*
Definition of Necrosis: Death of a group of cells, leading to inflammation.
Types of Necrosis (5):
Coagulative: Architecture preserved, but cytoplasmic and nuclear details lost (e.g., ischemia except brain)
Liquefactive: Semi-fluid gelatinous material, forming a gel (e.g., ischemia of brain, pyogenic infection)
Caseous: Granular debris resembling cheese (e.g., TB, syphilis, histoplasma, coccidiomycosis)
Fat: Death of adipose cells, leading to chalky white deposits (e.g., female breast, pancreas, mesentery)
Fibrinoid: Occurs in blood vessel walls, forming a pink ribbon-like material (e.g., vasculitis)
Chapter 2: Inflammation*
Acute Inflammation*
Definition: Protective response to harmful stimuli, consisting of five vascular and six cellular events.
Vascular Events (5):
Vasoconstriction (transient)
Vasodilation (persistent)
Increase in hydrostatic pressure
Increased vascular permeability (creates gaps)
Stasis
Cellular Events (6):
Margination: WBCs move to the periphery of blood vessels
Rolling: WBCs roll along endothelial lining
Adhesion: WBCs stop at gaps
Transmigration: WBCs come out of gaps
Chemotaxis: WBCs move towards chemical signals from bacteria
Phagocytosis: WBCs engulf bacteria
Chronic Inflammation (Granulomatous Inflammation)*
Definition: Prolonged inflammation with simultaneous injury and repair attempts.
Steps:
Antigen enters body (non-degratable)
Antigen presenting cells take antigen to helper T cells (Th1)
Th1 cells secrete three cytokines: interferon gamma, TNF alpha, interleukins 1 and 2
Formation of Granuloma:
Interferon gamma: converts macrophages to epithelioid cells and giant cells
TNF alpha: activates fibroblasts to form collagen
Interleukins 1 and 2: activate T lymphocytes
Cells arrange themselves in layers: epithelioid cells and giant cells in center, T lymphocytes in middle, fibroblasts in outer layer
Types of Giant Cells:
Foreign body: nucleus haphazardly scattered
Langhans: horseshoe-shaped nucleus
Totten: nucleus forming a ring with vacuoles in cytoplasm
Star-shaped Granuloma (Stellate Granuloma):
Granuloma with star-shaped appearance
Examples: cat scratch disease, lymphogranuloma venereum
Examples of Granulomatous Inflammation:
Bacterial: TB, leprosy, syphilis, cat scratch disease
Fungal: actinomycosis, blastomycosis, crypto mycosis, coccidium mycosis
Parasitic: cystosoma
Miscellaneous: sarcoidosis, Crohn's disease, foreign body granuloma