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78 Cards in this Set
- Front
- Back
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Pathophysiology |
The study of changes in body function caused by disease |
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Etiology |
The cause of disease |
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Pathogenesis |
How the disease process develops and evolves |
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Risk factors |
Multiple factors that predispose someone to a particular disease |
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Idiopathic |
The disease has no known cause |
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Clinical course |
Evolution of a disease. Acute subacute and chronic |
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Epidemiology |
The study of disease in populations |
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Incidence |
The number of new cases occurring in a specific time period |
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Prevalence |
Number of existing cases within a population in a specific time period |
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Define and give examples of the terms sign and symptom |
A sign is a manifestation that is noted by an observer. For example elevated temperature, a swollen extremity, blood pressure, pulse rate. A symptom is a subjective complaint that is noted by the person with a disorder. Pain, difficulty breathing, nausea etc |
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Homeostasis |
The tendency toward us a stable equilibrium between interdependent elements |
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What is the purpose of cell adaptation |
Allows cells to survive and maintain function when faced with stresses that endanger its normal structure and function |
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Is cell adaptation permanent |
No a cell can return to its pre-adoptive state once the signal for adaptation is removed |
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Hypertrophy |
Increase in cell size. This is what happens when you lift weights the increase in muscle mass is increasing cell size |
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Atrophy |
Decrease in cell size. This can occur when your legs in a cast or you're unable to be active for a period of time. Muscles shrink as cell size decreases. |
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Hyperplasia |
Increase in cell number. This occurs with cells that can still undergo mitosis.. eg the liver can replace itself with new tissue. |
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Metaplasia |
Changes in cell type. Eg change from ciliated columnar epithelium to stratified squamous epithelium in the Airways of a smoker |
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Dysplasia |
Changes in cell size shape and organization. Can be due to chronic irritation or inflammation. It can be reversed if the irritant is removed. Thought to be a precursor to cancer. |
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Denervation |
Lack of innervation to a muscle. |
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Ischemia |
Lack of blood flow to a muscle |
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Types of agents that cause cell injury |
Physical agents--mechanical forces, temperature extremes, and electrical forces Radiation--sunlight, x-rays Chemical agents--drugs, lead toxicity, free radicals Biological agents--viruses, bacteria, fungi, protozoa Nutritional imbalance--hypoxia, malnutrition, reactions |
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Hypoxia cell injury |
Cells suffering from lack of oxygen which interrupts the production of ATP through aerobic respiration. Anaerobic glycolysis will take over until glycogen reserves are depleted. Cells such as those from brain and heart require a lot of oxygen and will suffer damage in 4 to 6 minutes of oxygen deprivation Can be caused by inadequate amount of oxygen in the air, respiratory disease, ischemia interruption of ATP production will lead to ionic imbalances and cellular swelling due to the failure of ATP dependant sodium potassium pump Cellular membranes will become leaky which will cause loss of enzymes and other proteins |
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Free radical injury |
Free radicals are highly reactive chemical species that can lead to cell injury by reacting with key cellular components or set off a chain reaction leading to widespread damage Preactions can lead to damage of cell membranes, cross-linking of proteins, inactivation of enzymes systems, or damage to the nucleic acids that make up DNA |
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How free radicals are formed |
1--during normal cellular reactions, including energy generation, breakdown of lipids and proteins and inflammatory processes 2--absorption of energy sources example UV light other radiation 3--enzymatic breakdown of exogenous chemicals / drugs |
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ROS |
Reactive oxygen species--molecular oxygen |
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Minimize free radical effects |
Vitamin c and e help to neutralize free radicals |
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Chemical injury |
Can be toxic mutagenic or carcinogenic.
Are absorbed through the respiratory, gastrointestinal, and integumentary systems Our body deals with harmful chemicals through detoxification enzymes or antioxidant system |
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Cell death |
Apoptosis or necrosis |
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What is the difference between apoptosis and necrosis |
Both are forms of cell death. Apoptosis is controlled cell death to eliminate worn-out cells, excess cells, improperly formed cells or cells with damaged DNA. Enzymes are activated to degrade cellular DNA and proteins. Plasma membrane is altered which leads to phagocytosis of dying cells. necrosis is a pathologic form of cell death resulting from irreversible cell injury. The cell basically swells and explodes. |
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Necrosis types |
Coagulative Liquefactive Caseous Gangrenous |
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Coagulative necrosis |
Most common Normally results from hypoxia Proteins coagulate formula solid Mass Occurs primarily and kidneys, heart, and adrenal glands |
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Liquefactive necrosis |
Commonly results from ischemia to neurons and glial cells in the brain Cells are digested by their own hydrolases, become soft and liquefy can also occur due to bacterial infections whereby neutrophils release hydrolases to kill bacteria and create an area of pus |
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Caseous necrosis |
Common in lungs during a primary tuberculosis infection Combination of coagulative and liquefactive necrosis dead cells disintegrate but the debris is not completely digested which leaves the tissue with a cheese like appearance Necrotic tissue is walled off from the rest of the tissue |
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Fat necrosis |
Occurs in breast, pancreas and other abdominal organs Cellular breakdown is due to powerful lipases free fatty acids combine with calcium, magnesium and necrotic tissue appears opaque and chalky white |
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Gangrenous necrosis |
Term used when mass of tissue undergoes necrosis Due to severe hypoxic injury because of arteriosclerosis or blockage of major arteries Hypoxia followed by bacterial invasion leads to necrosis |
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Types of gangrene |
Dry gangrene--form of coagulation necrosis. Area becomes dry and shrinks, skin wrinkles and colour changes to dark brown or black. Usually occurs in the extremities. Wet gangrene--form of liquefactive necrosis. Area becomes cold, swollen, skin is moist. Can occur on extremities or internal organs. foul odour is present due to bacterial invasion. release of bacterial toxins into bloodstream could be life threatening. Gas gangrene--due to infection of tissue by specific anaerobic bacteria that are commonly found in soil. Can occur during a compound fracture where dirt are embedded. Gas bubbles are formed in tissue and it's potentially fatal |
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What are the goals of inflammation |
To protect the body from a pathogenic invasion To limit the range of contamination And to prepare damaged tissue for healing |
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Signs and symptoms of inflammation |
Heat Pain Redness Swelling And sometimes loss of function |
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What are the vascular responses and chemical mediators that lead to the signs/symptoms of inflammation? |
Vasodilation leads to increased blood flow that produces the redness and heat permeability of capillaries increases which allows fluid to escape into the tissues and cause swelling pain and impaired function follow as a result of tissue swelling and release of chemical mediators |
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What is the importance of vasodilation and increase in capillary permeability during inflammation? |
Vasodilation leads to increased blood flow and produces redness and heat permeability of capillaries increases which allows fluid to escape into the tissue and cause swelling |
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What is the importance of clotting during the inflammatory response? |
The clotting system stops bleeding, localizes microorganisms, and provides a meshwork for repair and healing |
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How does fever develop in what does it's possible benefit? |
Fever is partially induced by specific cytokines released from neutrophils and macrophages. These cytokines are known as endogenous pyrogens which act directly on the hypothalamus to control the body's thermostat a fever can be beneficial because some microorganisms are highly sensitive the small increases in body temperature |
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Leukocytosis |
An elevated white blood cell count usually a sign of inflammation |
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Mast cells location and role |
Mast cells are found in connective tissue throughout the body most abundantly in the dermis of the skin and mucosa of the GI and respiratory tracts Releases chemical mediators including histamine and chemotactic factors Histamine dialates blood vessels and vascular permeability Chemotactic factors attract neutrophils and eosinophils to injured site |
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Neutrophils location and role |
Neutrophils are produced in the bone marrow and are the most abundant type of white blood cell They are first on the scene to clean up dead cells and destroy microbes. They only live 24 to 48 hours after arriving at an inflammatory site. |
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Monocytes location and role |
Monocytes are created in bone marrow and our type of white blood cell They usually follow neutrophils into the site of injury within 24 hours Monocytes mature into macrophages which lasts longer than neutrophils. They helped to destroy dangerous agent by phagocytosis. They also take part in activating specific immunity, resolving inflammatory response, and initiating healing |
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Natural killer cells |
Located in blood and lymph have the ability to kill cancer cells and virus-infected cells before the adaptive mechanisms are activated they attacked by identifying the lack of self cell surface receptors and recognizing cell surface carbohydrates on target cells They killed by releasing cytolytic chemicals called perforins. |
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Platelets |
Circulate in the bloodstream once an injury occurs they take part in clotting and releasing chemical mediators of inflammation |
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Responsive white blood cells |
Margination of white blood cells to capillary walls Emigration of white blood cells Chemotaxis Phagocytosis |
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Margination (pavementing) |
Leukocytes low their migration and then adhere to the endothelial cells via adhesion molecules |
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Emigration (diapedesis) |
immigration consists of leukocytes sending extensions through the permeable capillaries and moving through the walls and into the tissues in amoeboid fashion Emigration occurs after adherence of the phagocyte to the endothelial cell |
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Chemotaxis |
Leukocytes following chemical signals towards injured site |
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Phagocytosis |
Engulfing of bacterial and cellular debris by macrophages and neutrophils Consists of four processes adherence, engulfment, formation of phagosome, intracellular killing |
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Histamine |
Found in preformed granules in platelets basophils and mast cells causes vasodilation and increased permeability of caterpillar he's one of first mediators of inflammatory response |
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Prostaglandins |
Are ubiquitous lipid soluble molecule derived from cell membrane phospholipids Contribute to vasodilation, capillary permeability, neutrophil chemotaxis, pain and fever Aspirin reduces inflammation by inhibiting production of prostaglandins |
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Plasma proteins |
Include kinins, activated complement proteins, and clotting factors |
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Bradykinin |
Causes dilation a vessels, increased capillary permeability and pain |
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activated complement protein |
Consists of several proteins that take part in every part of inflammatory responseincluding killing microorganisms directly, hemo taxes, degranulation of mast cells, and opsonization |
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Clotting system |
Forms of fibrous mesh work at information site to trap exudate microorganisms and foreign bodies which A) prevent spread of infection and inflammation to adjacent tissues B) keeps microorganisms close to area of greatest amount of phagocytes C) forms of clot that stops bleeding and provides a framework for future repair and healing |
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Cytokines |
Small proteins produced by several cells including lymphocytes macrophages Include interleukins interferons and other related proteins Interleukin-1 and tumour necrosis factor tnf Alpha are major inflammatory cytokines that participate in many processes including inducing fever |
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Acute inflammation |
Rapid onset with minimal damage and rapid resolution Characterized by the formation of different types of exudate which is the stuff that leaks out of the capillaries |
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Types of exudate |
Serous exudate--watery with low protein usually seen with mild inflammation Hemorrhagic exudate--when there is severe tissue and blood vessel damage with leakage of red blood cells from capillaries Fibrinous exudate--contains large amounts of fibrinogen a form of thick and sticky mesh work due to severe inflammation example pneumonia Purulent exudate--contains pus. Degraded white blood cells protein and tissue debris caused by persistent bacterial infections |
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Chronic inflammation |
A response that last 2 weeks or longer
May develop due to an unsuccessful acute response or from a low-grade response that failed to evoke an acute response
Macrophages and lymphocytes instead of neutrophils are the major white blood cell moving to site Proliferation of fibroblasts also occurs which can lead to scarring and deformity 2 patterns of chronic inflammation are possible nonspecific chronic inflammation and granulomatous inflammation |
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Nonspecific chronic inflammation |
Involves a defuse accumulation of macrophages and lymphocytes at site of injury fibroblast proliferation occurs and leads to scar formation that replaces the normal CT or parenchymal tissue |
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Granulomatous lesion |
A granuloma is a small 1- 2 mm lesion where an infiltration of macrophages are surrounded by lymphocytes occurs as a result of contact with asbestos and microorganisms that cause tuberculosis or syphilis These substances are poorly digested and therefore hard to control. A mass of macrophages surround the foreign substance. dance membrane of connective tissue eventually encapsulates the legion and isolates it Tubercle is a granuloma in this inflammatory response to microbacterium tuberculosis infection |
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Difference between acute and chronic inflammation |
Acute usually comes on quickly and disappears quickly. Chronic takes awhile to manifest and causes scar tissue. Can be difficult to resolve Acute inflammation uses mainly neutrophils. Where chronic uses macrophages and lymphocytes |
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What is the self marker on your body cells |
Self marker is located on antigen presenting cells apc'sas well as all other nucleated cells and helps are lymphocytes determine what is self and what is foreign |
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What are the antigen presenting cells? What is their job? |
antigen presenting cells are heterogeneous group of immune cells that mediate the cellular immune response by processing and presenting antigens for recognition by certain lymphocytes such as t cells. Apc's include dendritic cells, macrophages, langerhans cells, and B cells |
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List examples of Central and peripheral lymphoid tissues organs |
Central--bone marrow and thymus. This is where lymphocytes mature Secondary lymphoid organs--spleen, lymph nodes. The site of lymphocyte activation by antigens |
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What are the effector cells for t & B lymphocytes |
Surface recognition molecules - clusters of differentiation. Eg cd4+ t helper cells (regulatory cell) - releases cytokines and help to activate B cells and other t cells Eg cd8+ t cytotoxic cells (an effector cell) kill tumour cells and virus-infected cells memory t and B cells that are produced during an immune response reside in the body for a long. Of time and are involved with the quicker and height and response to subsequent exposure to the same antigen |
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Where are macrophages found in the body |
They develop for monocytes as they migrated to various tissues they can be free and wander through up tissue looking for foreign invaders or fixed and permanent residents of a particular organ |
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Role of macrophages in the immune response |
They help digest foreign substances when coated with antibody Secrete cytokines to activate t and B cells act as antigen-presenting cells by presenting to t helper cells digested antigen with the MHC class II molecule can destroy virus-infected cells or tumour cells when appropriately stimulated by cytokines |
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Where are dendritic cells found in the body |
they're located in areas close to barriers of the body in order to be in the best position to encounter foreign invaders |
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What is the role of dendritic cells in the immune response |
There are star-shaped and act as APCs Dendritic cells found in the skin are called langerhans cells when they encountered antigen they can move to lymph nodes to present antigen to t lymphocytes |
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Mhs |
Major histocompatibility complex This is a cell surface molecule that help distinguish normal self cells and foreign invaders Each individual has a unique set of MHC proteins also known as human leukocyte antigens HLA because they were first discovered in white blood cells There are two classes of cells class 1 and class 2 |
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Class I |
Cell surface glycoproteins that interact with antigen receptors and the cd8 molecule on t cytotoxic cells contains a groove to bind peptide fragments to antigen. Binding of peptide fragments to the class one molecule will alert the immune system that a cell has been infected by a virus or has become cancerous t cytotoxic cells will be activated only after it binds with the MHS class 1 molecule antigen complex |
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Class 2 |
Interacts with CD4 t helper cells After phagocytosis, digested fragments are bound to class II MHC T helper cells recognize the class to antigen complex and become activated activated t helper cells release cytokines to enhance the response by other lymphocytes |
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B cell activation |
Step 1 bind to antigen Step 2 receive cytokine from th Step 3 differentiation into plasma cells making antibodies and memory cells for future immune response to be faster |
