week 1-6 theory Flashcards

1
Q

Identify the Causes of Disease

A

Genetic: Diseases that are caused entirely by inherited or prenatally acquired genetic defects.
Multifactorial: Diseases that result from the interaction of both genetic and environmental factors.
Environmental: Diseases caused entirely by environmental factors, such as infections, toxins, and physical injury

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2
Q

Describe the Various Forms of Cellular Injury

A
  1. Chemical Injury:
    Direct injury: Toxins directly interact with cellular components (e.g., mercuric chloride).
    Indirect injury: Chemicals are converted to toxic metabolites that damage the cell (e.g., free radicals causing membrane damage).
  2. Physical Injury:
    Kinetic force: Trauma or injury caused by mechanical forces.
    Thermal injury: Damage due to extreme heat (burns) or cold (frostbite).
  3. Infective Injury: Caused by microorganisms such as bacteria, viruses, fungi, and parasites​
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3
Q

Describe the Physiological and Pathological Role of Apoptosis

A

Physiological Role: Apoptosis is a form of programmed cell death that helps regulate tissue homeostasis. It eliminates damaged or unwanted cells without triggering an inflammatory response.
Pathological Role: When apoptosis is deregulated, it can contribute to various diseases, including cancer (failure to undergo apoptosis) or neurodegenerative diseases (excessive apoptosis). Apoptosis can be triggered by external factors such as radiation, toxins, and free radicals

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4
Q

Identify and Describe the Types of Necrosis

A
  1. Coagulative Necrosis:
    Preserves the underlying tissue architecture. Common in hypoxic injuries to solid organs (e.g., heart, kidneys).
  2. Liquefactive Necrosis:
    Characterized by enzymatic digestion of dead cells, often seen in bacterial infections or ischemic infarcts in the brain.
  3. Caseous Necrosis:
    Creates a “cheesy” appearance and is most characteristic of tuberculosis.
    Fat Necrosis:
    Seen in acute pancreatitis, where pancreatic lipases digest fat, leading to the release of fatty acids and chalky white areas of fat saponification.
  4. Gangrenous Necrosis:
    A form of tissue death due to ischemia, often affecting soft tissues. It can be classified as dry or wet depending on the presence of infection
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5
Q

Define Ischemia and Infarction

A

Ischemia: A condition where there is impaired vascular perfusion, leading to a lack of oxygen and nutrients in tissues. This can result from conditions like thrombosis, embolism, or atherosclerosis​
Infarction: Refers to tissue death (necrosis) caused by ischemia. This results when the blood supply to a part of the body is completely cut off, leading to irreversible cell death​

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6
Q

Causes of Ischemia

A

Thrombosis: The formation of a solid mass of blood constituents in vessels, which can obstruct blood flow.
Embolism: A mass traveling in the bloodstream that can lodge in vessels and block blood flow.
Atheroma: Plaque formation in arteries, commonly due to atherosclerosis.
Vasculitis: Inflammation of blood vessels.
Vascular Spasm: Sudden contraction of blood vessel muscles.
Compression: External pressure on blood vessels (commonly in veins).
Hyperviscosity: Thickened blood impairing its flow, commonly due to blood disorders

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7
Q

Thrombosis occurs when…

A

Thrombosis occurs when blood clots form abnormally within a blood vessel. It can lead to infarction, embolism, or edema.

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8
Q

what is
Virchow’s Triad

A

Virchow’s Triad: Three factors that contribute to thrombus formation:
Endothelial injury.
Abnormal blood flow (stasis or turbulence).
Hypercoagulability

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9
Q

Signs of inflammation

A

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

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10
Q

Process of Inflammation

A

Vascular Phase: Increased blood flow and permeability of blood vessels.
Cellular Phase: Movement of immune cells, like neutrophils, from the blood to the tissue​(

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11
Q

Vascular Mediators of Inflammation

A

Vascular mediators: Histamine, prostaglandins, and nitric oxide cause vasodilation and increased vascular permeability.

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12
Q

cellular Mediators of Inflammation

A

Cellular mediators: Neutrophils, macrophages, and lymphocytes respond to injury by migrating to the site of damage.

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13
Q

chemical Mediators of Inflammation

A

Chemical mediators: Cytokines, bradykinin, and complement proteins act to stimulate the inflammatory response​

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14
Q

Acute inflammation

A

A short-term, immediate response to injury with the main goal of removing the causative agent and repairing tissue. Characterized by fluid accumulation, immune cell infiltration, and swelling.

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15
Q

Chronic inflammation

A

Prolonged inflammation resulting from persistent stimuli. It involves ongoing tissue destruction and repair processes, often leading to scarring or fibrosis. Chronic inflammation can be associated with diseases like rheumatoid arthritis or tuberculosis

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16
Q

Describe Oedema

A

Oedema is the abnormal accumulation of fluid in the interstitial spaces of tissues.

17
Q

oedema cause

A

It is caused by:
Increased vascular permeability (e.g., inflammation).
Increased hydrostatic pressure (e.g., heart failure).
Reduced oncotic pressure (e.g., hypoalbuminemia).
Lymphatic obstruction (e.g., lymphatic damage)​

18
Q

what are types of Systemic Oedema

A

Cardiac Oedema: Caused by heart failure, leading to increased venous pressure and fluid retention, often presenting as peripheral oedema or pulmonary oedema.
Renal Oedema: Results from nephrotic syndrome, causing protein loss in the urine and hypoalbuminemia, leading to fluid accumulation.
Nutritional Oedema: Seen in malnutrition (e.g., kwashiorkor) due to low protein levels leading to decreased oncotic pressure.
Liver Failure Oedema: Due to impaired synthesis of albumin, leading to hypoalbuminemia and ascites (fluid in the abdomen)​

19
Q

Define different types of cell and tissue growth

A

Multiplicative: Increase in the number of cells.
Auxetic: Growth by an increase in cell size.
Accretionary: Growth by the accumulation of extracellular substances.
Combined: A combination of these processes occurs in various tissues.

20
Q

Endocrine factors in growth disorders

A

Growth hormone (GH) plays a key role, released from the anterior pituitary and stimulates Insulin-like Growth Factors (IGFs). Conditions like dwarfism (due to GH deficiency) and gigantism (due to excess GH before puberty) highlight the importance of GH regulation.

21
Q

Genetic factors in growth disorders

A

Genetic factors: Parental characteristics like height are often inherited. Conditions like achondroplasia are due to a lack of fibroblast growth factor receptors, while Down syndrome (trisomy 21) affects growth.

22
Q

nutritional factors in growth disorders

A

Nutritional factors: Nutritional deficiencies, like those seen in kwashiorkor (protein deficiency) and marasmus (caloric deficiency), greatly impact growth.

23
Q

Environmental factors in growth disorders

A

Environmental factors: Maternal substance abuse, birth weight, and illnesses can interfere with normal growth.

24
Q

Describe normal and abnormal tissue growth:

A

Atrophy: A reduction in cell size or organ size due to decreased workload, aging, or poor nutrition.
Hypertrophy: Increase in cell size, usually in response to increased workload (e.g., muscle hypertrophy due to exercise).
Hyperplasia: Increase in the number of cells, often seen with hypertrophy (e.g., epithelial hyperplasia in response to hormonal stimulation).
Hypoplasia: Failure to reach normal size during development.
Metaplasia: Replacement of one differentiated cell type with another, often as a response to stress (e.g., squamous metaplasia in the lungs of smokers).
Dysplasia: Disordered growth, often precancerous, involving abnormal cell shapes and increased growth rates (e.g., in epithelial tissues).

25
Q

Neoplasia Terminology

A

Neoplasm: An abnormal growth of tissue (tumor).
Metastasise: Spread of cancer cells to distant sites in the body.
Cancer: Uncontrolled growth and division of abnormal cells.
Oncology: The medical field focused on the study and treatment of tumors.

26
Q

General Features of Neoplastic Cells

A

Neoplastic cells are less dependent on oxygen and better adapted to anaerobic conditions.
They experience autonomous growth, meaning they grow independently of normal cellular controls.
Loss of specialized function and contact inhibition are common features, resulting in unregulated growth.
Neoplastic cells may undergo anaplasia, showing a loss of cellular differentiation.

27
Q

Benign Tumors

A

Do not metastasize.
Often encapsulated.
Slow-growing and well-differentiated.

28
Q

Malignant Tumors

A

Can invade surrounding tissues and metastasize.
Poor differentiation, less uniform, and often more vascularized.
Rapidly spreading.

29
Q

Tumor Classification by Tissue of Origin

A

Sarcoma: Arises in bone, cartilage, fat, muscle, or blood vessels.
Carcinoma: Originates from epithelial cells lining the skin or internal organs, representing the majority of cancers.

30
Q

Carcinogenesis

A

Initiation: Mutation or genetic alteration of a cell.
Promotion: Proliferation of mutated cells.
Progression: Aggressive growth and spread of cancer.
Carcinogens: Factors causing cancer, including chemicals (e.g., tobacco), radiation, viruses (e.g., HPV), hormones, and some microbial agents.

31
Q

Metastasis

A

Lymphatic Spread: Common in carcinomas.
Hematogenous Spread: More typical in sarcomas.
Transcoelomic Seeding: Spread within body cavities.
Metastasis requires enhanced cell mobility, enzyme release for tissue invasion, and loss of cellular cohesion.

32
Q

Grading and Staging of Tumors

A

Grading: Measures how differentiated the tumor cells are. Grade I is the most differentiated.
Staging: Describes the size, spread, and lymph node involvement:
T: Size and extent of the primary tumor.
N: Spread to nearby lymph nodes.
M: Presence of distant metastasis.