DIMS Lectures General Pathology PDF

🔬 Introduction to General Pathology

Definition & Importance: Pathology is the study of diseases, their causes, mechanisms, and effects on the body.
Branches of Pathology:
- General Pathology – Focuses on common disease mechanisms such as inflammation and cell injury.
- Systemic Pathology – Covers diseases affecting specific organ systems.
Application in Medicine:

Essential for diagnosing diseases through histopathology and laboratory analysis.
Guides treatment decisions and prognosis assessment.

🩸 Cellular Injury, Adaptations, and Death

Cellular Adaptations to Stress

Hypertrophy: Increase in cell size due to increased functional demand (e.g., heart muscle hypertrophy in hypertension).
Hyperplasia: Increase in the number of cells due to hormonal or compensatory stimulation (e.g., prostatic hyperplasia).
Atrophy: Decrease in cell size due to aging, disuse, or ischemia (e.g., muscle wasting in immobilization).
Metaplasia: Reversible change in cell type (e.g., squamous metaplasia in smokers' lungs).

Cell Injury and Death

Reversible Injury:
- Cellular swelling, membrane damage, and mitochondrial dysfunction.
- Can recover if stimulus is removed.
Irreversible Injury:
- Leads to necrosis or apoptosis.

Types of Necrosis

Coagulative Necrosis: Common in myocardial infarction.
Liquefactive Necrosis: Seen in brain infarcts and abscesses.
Caseous Necrosis: Typical in tuberculosis.
Fat Necrosis: Found in acute pancreatitis.

Apoptosis (Programmed Cell Death)

Controlled cell death mechanism.
Prevents cancer development by eliminating damaged cells.

Congenital Disorders: Born with a Twist

Some diseases start before birth due to genetic hiccups. The notes mention congenital disorders tied to chromosomal abnormalities—think Down syndrome from an extra chromosome 21. These conditions shape a patient’s life from day one, and understanding them is key for pediatrics.

Chromosomal Abnormalities: Genetic Mishaps

Speaking of chromosomes, the PDF lists specific glitches:

Microdeletion: Tiny DNA chunks vanish.

Macrodeletion: Bigger losses happen.

Ring Chromosome: Ends fuse into a loop.

Inversion: A segment flips backward.

Robertsonian Translocation: Two chromosomes merge.

Trisomy: An extra chromosome sneaks in.

These errors mess with DNA’s blueprint, causing syndromes you’ll see in exams.

Translocation: Chromosomes on the Move

Translocation—when chromosome parts swap places—gets its own spotlight. It’s a big deal in cancers like leukemia, where genes get shuffled into dangerous combos. Picture it as a genetic mix-up with serious consequences.

Free Radicals: Tiny Wrecking Balls

Free radicals are unstable molecules from metabolism, radiation, or smoking. They damage DNA, proteins, and cell membranes, speeding up aging or sparking cancer. The body fights back with antioxidants, but when radicals win, trouble brews.

Cell Death: The Endgame

When cells can’t recover, they die. The notes cover:

Necrosis: Uncontrolled, messy cell death (e.g., gangrene).

Apoptosis: Programmed, tidy death (e.g., shedding old skin cells).

Knowing the difference helps you spot disease patterns.

Apoptosis Mechanisms: How Cells Say Goodbye

Apoptosis isn’t random—it’s a precise process. The PDF hints at mechanisms like protein signals telling cells to self-destruct. It’s vital in development (shaping fingers) and stopping rogue cells (like early cancer).

Calcification: Hardening Trouble

Sometimes, calcium builds up where it shouldn’t—like in damaged tissues. This calcification can stiffen arteries or form stones, complicating conditions like atherosclerosis. It’s a sneaky pathology player.

Histamine: Inflammation’s Messenger

Histamine kicks off inflammation, causing swelling and redness. Released during allergies or injuries, it calls immune cells to the scene. Think bee stings—that itch and puffiness? Histamine’s doing.

Cytokines: Immune Chatter

Cytokines are proteins that coordinate immunity. They signal inflammation, healing, or fever—think of them as the body’s text messages. In chronic diseases, they can overdo it, causing harm.

Classical Pathway: Complement in Action

The complement system—a cascade of proteins—amps up immunity. The classical pathway, triggered by antibodies, punches holes in invaders (via the MAC, or membrane attack complex). It’s a star in fighting infections.

Complement System Activation: Defending the Body

Complement activation isn’t just classical—it has other paths too. It tags germs, calls immune cells, and lyses threats. The notes highlight its role in hypersensitivity reactions—crucial for case studies.

Diabetes (Diabetics): A Metabolic Mess

This condition ties to nutritional imbalance. Excess carbs, proteins, or fats can lead to obesity and diabetes mellitus—think insulin issues and high blood sugar wreaking havoc.

Immunopathological Disorders: Immunity Backfires

When immunity misfires, you get immunopathology. Cover autoimmune diseases (like lupus) and hypersensitivity—where the body attacks itself or overreacts to harmless stuff.

Antibodies: The Immune Arsenal

Antibodies (IgG, IgE, etc.) are proteins that tag invaders. The notes tie them to hypersensitivity types—IgE for allergies, IgG for cell destruction. They’re your exam’s immunology MVPs.

HLA Genes: Tissue Matchmakers

HLA genes control immune recognition—like a barcode for cells. They’re big in transplant rejection: mismatched HLA means the body says, “Nope, not mine!” and attacks the graft.

Types of Graft: Transplant Talk

Grafts come in flavors:

Autograft: Your own tissue (e.g., skin).

Allograft: From another person.

Xenograft: From animals.

Each type affects rejection risk—key for surgery questions.

Transplant Rejection: The Body Says No

Rejection happens when the immune system spots a graft as foreign. The notes link it to HLA mismatch—acute rejection can hit fast, while chronic takes time. A transplant’s fate hangs on this balance.

Inflammation: The Body’s Fire Alarm

Inflammation fights injury or infection. Acute (short-term) heals cuts; chronic (long-term) fuels diseases like TB. The PDF ties it to histamine and cytokines—core concepts for diagnosis.

Hypersensitivity Reactions (HSR): Immunity Overdrive

The four HSR types get detailed:

Type I: IgE-driven allergies (e.g., asthma).

Type II: IgG attacks cells (e.g., transfusion reactions, rheumatic heart disease).

Type III: Immune complexes clog tissues (e.g., SLE).

Type IV: T-cell delayed response (e.g., TB granulomas).

Immunity

Autoimmune Diseases: Rheumatoid arthritis, SLE, multiple sclerosis.
Immunodeficiency Disorders:
- HIV/AIDS, SCID (Severe Combined Immunodeficiency).

Examples like Goodpasture syndrome and Hashimoto’s thyroiditis make these stick.

Healing: Repairing the Damage

Healing splits into:

Primary Intention: Clean wounds, minimal scars.

Secondary Intention: Messy wounds (like RTAs) with tissue loss, inflammation, and delayed repair.

detail maximal loss of function in severe cases—exam gold.

Shock: Circulation Crisis

Shock—low blood flow to organs—includes septic shock (infection-driven). Stages matter: early compensation can save lives, but late shock is grim. A clinical must-know.

Oncogenesis: Cancer’s Origin Story

Cancer begins with oncogenesis. Key players:

Proto-oncogenes: Growth promoters turned oncogenes via mutations (e.g., point mutation, translocation).

Tumor Suppressor Genes: Brakes on growth—lose them, and cells go wild.

DNA Repair Genes: Fixers that fail, piling up mutations.

Anti-Apoptotic Genes: Stop cell death, letting tumors thrive.

Telomerase: Keeps cancer cells immortal.

Knudson’s two-hit hypothesis ties it together: two mutations for sporadic cancer, one inherited hit for familial cases.

Causes of Cell Injury: The Full List

Beyond the acronym, microorganisms and nutrition—stressing infections (bacteria, viruses) and diet (starvation or excess) as injury triggers. Obesity links to diabetes and heart disease here.

Nutritional Imbalance: Diet’s Dark Side

Too many carbs, proteins, or lipids? You’re on the obesity fast track, raising risks for diabetes and strokes. The notes connect this to pathology’s big picture.

Chromatin: DNA’s Resting Form

Chromatin is DNA’s coiled-up state in resting cells. The PDF hints at its structure—unraveling it during division is how genes get read. A genetics refresher!

Basement Membrane: Tissue Glue

Repeated in the notes, the basement membrane anchors cells—like glue between skin layers. Damage here (e.g., in kidney disease) disrupts function.

Metaplasia, Dysplasia, and Beyond

The neoplasia path:

Metaplasia: Cells swap types (e.g., smoking turns lung cells into tougher ones).

Dysplasia: Weird cell growth, pre-cancer.

Carcinoma in Situ: Cancer stuck in place.

Metastatic Carcinoma: Cancer on the move.

A progression you’ll see in oncology questions.

Type II HSR Pathogenesis: Cell Destruction

Type II HSR specifics:

Complement Activation: MAC lyses cells (e.g., RBCs in transfusion reactions).

Antibody-Dependent Cellular Cytotoxicity: Immune cells kill tagged targets (e.g., tumors).

Examples: erythroblastosis fetalis, leukopenia, and more.

Type III HSR: Immune Complex Chaos

Free immune complexes (IgG) clog tissues, sparking inflammation. Think lupus or post-strep glomerulonephritis—classic cases.

Type IV HSR: Delayed Damage

T-cells (CD4/CD8) drive this slow reaction via MHC presentation. TB’s granulomas? That’s Type IV in action.

🌍 Environmental & Nutritional Pathology

Toxic Exposures: Heavy metals, radiation, air pollution.
Nutritional Deficiencies:

Vitamin D Deficiency → Rickets/Osteomalacia.
Vitamin C Deficiency → Scurvy.

🧬 Genetic Disorders & Pediatric Pathology

Single-Gene Disorders:
- Cystic fibrosis, sickle cell anemia, hemophilia.
Chromosomal Abnormalities:
- Down syndrome (Trisomy 21), Turner syndrome.

🔬 Neoplasia (Cancer Pathology)

Benign vs. Malignant Tumors:
- Benign: Slow-growing, non-invasive, localized tumors.
- Malignant: Aggressive, metastasizing, and poorly differentiated.
Carcinogenesis (Cancer Development):

Genetic mutations in oncogenes (e.g., RAS, MYC) and tumor suppressor genes (e.g., TP53, RB1).
Risk factors include smoking, radiation, and viral infections (HPV, EBV)

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