General Pathology and Hematology Crash Course

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10 Questions

Which organ exemplifies both hypertrophy and hyperplasia during pregnancy and atrophy post-delivery?

Uterus

Which type of cell adaptation involves the transformation of one mature cell type into another mature cell type?

Metaplasia

Which cellular change is NOT characteristic of dysplasia?

Basal polarity maintained

In which part of the cervix does squamous metaplasia occur?

Endocervix

What mechanism do cells utilize to survive unfavorable conditions through changes like hypertrophy and hyperplasia?

Adaptation

What is the main function of caspase enzymes in apoptosis?

Lead to cell fragmentation

Which pathway of apoptosis involves signals coming from inside the cell?

Intrinsic pathway

What is the role of cytochrome C in the intrinsic pathway of apoptosis?

Signals mitochondria to initiate apoptosis

Which type of necrosis leads to death of adipose cells and chalky white deposits?

Fat necrosis

What is the main cellular event in acute inflammation where WBCs move towards chemical signals from bacteria?

Chemotaxis

Study Notes

  • 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

Join Dr. Priyanka Sachdev for a comprehensive crash course on key topics in General Pathology and Hematology, focusing on essential concepts frequently asked in exams like FMG, NEET PG, and NEXT. Covering areas like cell adaptation, cell injury, necrosis, inflammation, and more, this course provides a concise overview followed by MCQs to enhance understanding.

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