USMLE Pathoma Quiz

Questions and Answers

What happens when there is an increase in stress on an organ?

Necrosis of cells

Decreased organ size

Increase in organ size (correct)

No change to organ size

Hypertrophy involves the production of new cells from stem cells.

False

What is the classic example of metaplasia?

Barrett esophagus

A decrease in stress leads to a decrease in organ size called ______.

atrophy Signup and view all the answers

What is the consequence of prolonged pathologic hyperplasia?

Dysplasia Signup and view all the answers

What condition occurs when ischemia leads to decreased oxygen delivery to tissues?

Hypoxia Signup and view all the answers

Metaplasia is an irreversible condition.

False Signup and view all the answers

What is the hallmark of reversible cellular injury?

Cellular swelling Signup and view all the answers

In cases of carbon monoxide poisoning, the appearance of the skin is described as ______.

cherry-red Signup and view all the answers

Which type of cellular injury results in a build-up of sodium and water inside the cell?

Hypoxia Signup and view all the answers

What results from lysosome membrane damage?

Hydrolytic enzymes leaking into the cytosol. Signup and view all the answers

What are the two mechanisms of cell death?

Necrosis and apoptosis. Signup and view all the answers

Which type of necrosis is characteristic of ischemic infarction of any organ except the brain?

Coagulative necrosis Signup and view all the answers

What histological appearance characterizes caseous necrosis?

Soft and friable, 'cottage cheese-like' Signup and view all the answers

The mechanism of necrotic adipose tissue resembles ______.

Fat necrosis Signup and view all the answers

What are apoptotic bodies?

Remnants of a cell that fall off during apoptosis. Signup and view all the answers

Apoptosis is always followed by inflammation.

False Signup and view all the answers

What is a significant consequence of free radical injury?

Peroxidation of lipids Signup and view all the answers

What appearance does amyloid have when stained?

Apple-green birefringence Signup and view all the answers

What is the characteristic of primary amyloidosis?

Systemic deposition of AL amyloid derived from immunoglobulin light chain. Signup and view all the answers

Which form of necrosis is characterized by necrotic tissue becoming liquefied?

Liquefactive necrosis Signup and view all the answers

At what age do most individuals with Down syndrome develop Alzheimer disease?

40 Signup and view all the answers

What deposits in joints cause dialysis-associated amyloidosis?

β2-microglobulin Signup and view all the answers

What hormone is produced by tumor cells in medullary carcinoma of the thyroid?

Calcitonin Signup and view all the answers

Acute inflammation is always characterized by the presence of lymphocytes.

False Signup and view all the answers

What leads to the activation of Toll-like receptors (TLRs)?

Pathogen-associated molecular patterns (PAMPs) Signup and view all the answers

Which mediators are responsible for vasodilation and increased vascular permeability during inflammation?

Histamine Signup and view all the answers

Which process is NOT involved in the dilation of blood vessels during inflammation?

Stimulation of macrophages Signup and view all the answers

What type of immunity does acute inflammation primarily involve?

Innate immunity Signup and view all the answers

Match the following inflammatory mediators with their roles:

Histamine = Vasodilation and increased vascular permeability Prostaglandins = Pain and fever mediation Leukotrienes = Attraction of neutrophils C3a = Triggering mast cell degranulation Signup and view all the answers

What leads to the production of bradykinin during inflammation?

Kinin system activation Signup and view all the answers

What are pregnant women with anti-SSA at risk for?

Delivering babies with neonatal lupus and congenital heart block. Signup and view all the answers

What is lymphocytic sialadenitis on a lip biopsy indicative of?

Diagnosing Sjögren's syndrome. Signup and view all the answers

What type of lymphoma is associated with increased risk in patients with autoimmune disorders?

Marginal zone lymphoma Signup and view all the answers

What is systemic sclerosis?

An autoimmune disorder characterized by sclerosis of skin and visceral organs. Signup and view all the answers

What is the classic prototype of limited systemic sclerosis?

CREST syndrome Signup and view all the answers

Diffuse systemic sclerosis has limited skin involvement.

False Signup and view all the answers

What characterizes mixed connective tissue disease?

Autoimmune-mediated tissue damage with mixed features of SLE, systemic sclerosis, and polymyositis. Signup and view all the answers

Healing is initiated when ______ begins.

inflammation Signup and view all the answers

What are the three types of tissues based on regenerative capacity?

Labile, stable, and permanent. Signup and view all the answers

What is granulation tissue?

The initial phase of repair consisting of fibroblasts, capillaries, and myofibroblasts. Signup and view all the answers

Keloids are characterized by normal type III collagen production.

False Signup and view all the answers

What is the leading cause of cancer death in adults?

Lung cancer. Signup and view all the answers

What is the most common cancer by incidence in adults?

Breast Signup and view all the answers

What initiates cancer formation?

Damage to DNA of stem cells. Signup and view all the answers

What characterizes the presence of lymphocytes and plasma cells in tissue?

Chronic inflammation Signup and view all the answers

Which of the following are stimuli for chronic inflammation? (Select all that apply)

Autoimmune disease Signup and view all the answers

Where do progenitor T cells further develop?

Thymus Signup and view all the answers

CD4+ T cells recognize antigens presented on __________ molecules.

MHC class II Signup and view all the answers

CD8+ T cells recognize antigens presented on __________ molecules.

MHC class I Signup and view all the answers

What provides the second activation signal for CD4+ helper T cells?

B7 on APC binds CD28 on CD4+ helper T cells Signup and view all the answers

Which cytokines does the TH2 subset secrete? (Select all that apply)

IL-5 Signup and view all the answers

What is a characteristic feature of granulomas?

A collection of epithelioid histiocytes Signup and view all the answers

What genetic mutation is associated with DiGeorge syndrome?

22q11 microdeletion Signup and view all the answers

Which deficiency is associated with X-linked agammaglobulinemia?

Bruton tyrosine kinase mutation Signup and view all the answers

What autoimmune disease is characterized by immune-mediated damage of self tissues?

Rheumatoid arthritis Signup and view all the answers

What is the first-line treatment for systemic lupus erythematosus?

Avoiding direct sunlight and glucocorticoids for flares Signup and view all the answers

Study Notes

Growth Adaptations

Homeostasis of organs is maintained under physiological stress; changes in stress can prompt growth adaptations.
Hypertrophy involves an increase in cell size, while hyperplasia involves an increase in cell number.
Permanent tissues, like cardiac and skeletal muscle, can only undergo hypertrophy due to their inability to proliferate.
Atrophy occurs when stress decreases, leading to a reduction in organ size through cell size and number decrease via apoptosis or cellular degradation mechanisms.
Metaplasia involves a change in cell type to adapt to stress, commonly seen as a transformation of one epithelial type to another; it is reversible if the stressor is removed.

Cellular Injury

Cellular injury occurs when stress surpasses the cell's adaptive capacity, influenced by stress type, severity, and cell type susceptibility.
Neurons are highly susceptible to ischemic injury, while skeletal muscle is more resilient.
Common causes include inflammation, nutrition imbalance, hypoxia, trauma, and genetic mutations.
Hypoxia, a key cause of cellular injury, is connected to inadequate oxygen delivery to tissues, affecting cellular energy production.

Hypoxia Mechanisms

Caused by ischemia, hypoxemia, and decreased oxygen-carrying capacity of blood; ischemia includes decreased arterial perfusion, venous drainage, and shock.
Hypoxemia is characterized by a low partial pressure of oxygen in the blood, leading to potential complications from high altitudes, hypoventilation, diffusion defects, or V/Q mismatch.
Decreased oxygen-carrying capacity can result from anemia or carbon monoxide poisoning; methemoglobinemia also impairs oxygen binding due to oxidized hemoglobin.

Cellular Injury Phases

Initial hypoxic damage is reversible, marked by cellular swelling and loss of cellular functions.
Long-term injury becomes irreversible, marked by membrane damage that leads to cell death; indicators of irreversible damage include enzyme leakage and mitochondrial dysfunction.

Cell Death Mechanisms

Cell death is identified by nuclear loss, manifested through nuclear condensation, fragmentation, and dissolution.
Two main mechanisms of cell death: necrosis (associated with inflammation and process-related damage) and apoptosis (programmed cell death without inflammation).
Necrosis can be categorized into various types based on tissue morphology and underlying pathologies.

Types of Necrosis

Coagulative necrosis retains tissue structure despite the absence of nuclei, primarily seen in ischemic infarcts of organs, with wedge-shaped and pale characteristics.
Liquefactive necrosis results from enzymatic destruction, often leading to pus formation and is typically associated with bacterial infections or cerebral infarcts.

Dysplasia and Metaplasia

Dysplasia involves disordered cellular growth, often a precursor to cancer, typically stemming from chronic irritation or pathology.
Underlying conditions such as endometrial hyperplasia or Barrett esophagus can lead to dysplasia progression to carcinoma if stress persists.

Aplasia and Hypoplasia

Aplasia refers to failure in cell production during embryonic development, while hypoplasia describes underdevelopment resulting in smaller organ size.

This structured overview provides a foundation for understanding key principles around growth adaptations, cellular injury, and cell death mechanisms critical in pathology.### Necrosis Types

Liquefactive Necrosis: Necrotic tissue turns liquid due to enzymatic lysis of cells and proteins.
- Brain Infarction: Proteolytic enzymes from microglial cells cause liquefaction.
- Abscess: Liquefaction happens due to neutrophil activity.
- Pancreatitis: Enzymes from the pancreas lead to the liquefaction of parenchyma.
Gangrenous Necrosis: Coagulative necrosis that appears mummified.
- Dry Gangrene: Caused by ischemia in lower limbs and gastrointestinal tract.
- Wet Gangrene: Results from superimposed infections on dry gangrene leading to liquefactive necrosis.
Caseous Necrosis: Soft, friable tissue resembling "cottage cheese".
- Combines features of coagulative and liquefactive necrosis.
- Common in granulomatous inflammation, especially from tuberculosis or fungal infections.
Fat Necrosis: Necrotic adipose tissue exhibits a chalky-white appearance due to calcium deposits.
- Associated with trauma to fat tissue, especially in the breast and pancreatitis, leading to saponification.
- Saponification: Calcium deposition on dead tissues due to fatty acids.
Fibrinoid Necrosis: Damage to blood vessel walls with protein leakage.
- Results in bright pink staining of vessel walls microscopically.
- Commonly seen in malignant hypertension and vasculitis.

Apoptosis

Definition: Energy-dependent, programmed cell death occurring in single cells or small groups.
- Examples: Endometrial shedding during menstruation, removal of cells during embryogenesis, and CD8+ T cell-mediated cell death.
Morphological Features:
- Shrinking of the dying cell with increased eosinophilia.
- Nucleus condensation and fragmentation; formation of apoptotic bodies removed by macrophages.
Mediators: Caspases activate proteases and endonucleases.
- Intrinsic Pathway: Involves Bcl2 inactivation and cytochrome c release.
- Extrinsic Pathway: Triggered by FAS ligand binding to FAS receptor and TNF binding to its receptor.
- Cytotoxic T cell Pathway: CD8+ T cells release perforins and granzymes leading to caspase activation.

Free Radical Injury

Definition: Free radicals are unstable molecules with unpaired electrons.
Physiological Generation: Occurs during oxidative phosphorylation; results in superoxide, hydrogen peroxide, and hydroxyl radicals.
Pathological Generation: Involves ionizing radiation, inflammation, metals, and certain drugs which produce free radicals that cause cell injury.
Effects: Free radicals damage cellular components through lipid peroxidation and DNA/protein oxidation.
Elimination Mechanisms:
- Antioxidants (vitamins A, C, E, glutathione).
- Enzymatic systems (superoxide dismutase, glutathione peroxidase, catalase).

Examples of Free Radical Injury

Carbon Tetrachloride (CCl4): Causes liver cell injury due to free radical formation, impairing protein synthesis.
Reperfusion Injury: Free radicals generated after blood supply returns to ischemic tissue can exacerbate injury, often seen with continued rise in cardiac enzymes after myocardial infarction.

Amyloidosis

Definition: Deposition of misfolded proteins in extracellular spaces leading to tissue damage.
Characteristics:
- Misfolded proteins form β-pleated sheets.
- Detection involves Congo red staining, showing apple-green birefringence under polarized light.
Systemic Amyloidosis:
- Primary: Involves AL amyloid from immunoglobulin light chains, associated with plasma cell disorders like multiple myeloma.
- Secondary: Involves AA amyloid from SAA protein, increased during chronic inflammation, associated with conditions like Familial Mediterranean Fever.
Clinical Findings: Organs can be affected, but classic signs include nephrotic syndrome (kidney), restrictive cardiomyopathy, and tongue enlargement.
Localized Amyloidosis: Generally affects a single organ, with examples like senile cardiac amyloidosis (transthyretin deposits) and Alzheimer's disease (Aβ amyloid deposits in the brain).### Inflammation Activation
Activated by tissue trauma, complement proteins C3a and C5a, or cross-linking of cell-surface IgE by antigen.
Immediate response includes release of preformed histamine, leading to vasodilation and increased vascular permeability.
Delayed response involves production of arachidonic acid metabolites, particularly leukotrienes.

Complement System

Comprises proinflammatory serum proteins that enhance inflammation.
Activation pathways:
- Classical pathway: C1 binds IgG or IgM complexed with antigen.
- Alternative pathway: Microbial products directly activate complement.
- Mannose-binding lectin (MBL) pathway: MBL binds to mannose on microorganisms.
All pathways produce C3 convertase, leading to C3a and C3b, and eventually C5 convertase (C5a and C5b).
C3a and C5a (anaphylatoxins) trigger mast cell degranulation, causing vasodilation and increased permeability.
C5a is chemotactic for neutrophils, while C3b acts as an opsonin for phagocytosis.
The membrane attack complex (MAC), formed by C5b with C6-C9, lyses microbes.

Hageman Factor (Factor XII)

Inactive proinflammatory protein produced in the liver.
Activated by exposure to subendothelial or tissue collagen, triggering coagulation, complement, and kinin systems.
Kinin system produces bradykinin, mediating similar effects to histamine, plus pain.

Cardinal Signs of Inflammation

Redness and Warmth (rubor and calor): Result from vasodilation and increased blood flow, mediated by histamine, prostaglandins, and bradykinin.
Swelling (tumor): Caused by fluid leakage from postcapillary venules into interstitial space, primarily through histamine and tissue damage.
Pain (dolor): Sensitized by bradykinin and PGE2 acting on sensory nerve endings.
Fever: Induced by pyrogens causing macrophages to release IL-1 and TNF, increasing hypothalamic PGE2 levels.

Neutrophil Arrival and Function

Margination: Vasodilation reduces blood flow, causing neutrophils to move to vessel peripheries.
Rolling: Selectins on endothelial cells interact with sialyl Lewis X on leukocytes, facilitating rolling due to P-selectin and E-selectin.
Adhesion: Cellular adhesion molecules (ICAM and VCAM) upregulated by TNF and IL-1 attract integrins on leukocytes, leading to firm adhesion.
Transmigration and Chemotaxis: Neutrophils traverse endothelial layers towards chemical signals like IL-8, C5a, and bacterial products.
Phagocytosis: Enhanced by opsonins (IgG and C3b); formation of phagolysosomes occurs via pseudopods of leukocytes.

Defects in Neutrophil Function

Leukocyte adhesion deficiency: Caused by integrin defects, resulting in recurrent infections and delayed umbilical cord separation.
Chediak-Higashi syndrome: Impairments in phagolysosome formation lead to increased infections and characteristic giant leukocyte granules.
Chronic Granulomatous Disease (CGD): NADPH oxidase defects hinder O2-dependent killing, causing susceptibility to catalase-positive organisms.
Myeloperoxidase (MPO) deficiency: Results in increased risk of Candida infections, but most patients remain asymptomatic.

Macrophages in Inflammation

Predominate after neutrophils, appearing 2-3 days post-inflammation onset.
Ingest organisms and manage inflammatory outcomes via cytokines:
- Resolution and healing through anti-inflammatory cytokines (IL-10, TGF-β).
- Continued inflammation through IL-8, attracting more neutrophils.
- Abscess formation, mediated by fibrosis.
- Chronic inflammation through antigen presentation to activate T cells.

Chronic Inflammation

Characterized by lymphocytes and plasma cells, with slower but more specific immune responses.
Common stimuli include persistent infections, autoimmune diseases, and foreign materials.

T Lymphocyte Function

Progenitor T cells produced in bone marrow and maturing in the thymus.
Activation requires binding of the antigen/MHC complex plus a second signal (e.g., CD28 on T cells binding B7 on APCs).
CD4+ helper T cells:
- Differentiate into TH1 and TH2 subsets, secreting cytokines that regulate immune responses.
CD8+ cytotoxic T cells: Activated by intracellular antigens, capable of inducing apoptosis in target cells via perforin and granzyme.

B Lymphocyte Function

Immature B cells mature in the bone marrow, expressing surface IgM and IgD.
Activation involves binding of antigens, leading to differentiation into plasma cells.
Helper T cells assist in B cell activation by cytokine release.

Granulomatous Inflammation

A chronic inflammation subtype marked by the formation of granulomas, composed of epithelioid macrophages and giant cells.
Granulomas can be either caseating (e.g., tuberculosis) or non-caseating (e.g., sarcoidosis).
Formed when macrophages present antigens to T cells, leading to IL-12 secretion and TH1 differentiation.

Primary Immunodeficiency

DiGeorge Syndrome: A developmental issue linked to microdeletion at chromosome 22q11, affecting T-cell production and function.

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Test your knowledge with this quiz based on USMLE Pathoma material. It encompasses various topics essential for understanding pathology concepts. Perfect for medical students preparing for the USMLE exam.