Patho- Understanding the Immune System Flashcards
Protection of the body depends on three major lines of defense:
Skin and mucous membranes
The inflammatory response
Immune response
-Our bodies are made to be strong, survive, and be healthy
Body has natural defense systems to fight back
Three most important
First line of defense
Skin Mucous membranes Blink reflex Lashes Tears
-Skin- intact, protects against environment-skin has bacteria on it but it is intact so it doesn’t harm us
Mucous membranes- chemical substances present that fight off bacteria
-blink reflex- -lashes-protect-keep things out -nasal hair- -acid in stomach-protects us and kills off what isn't supposed to be there -cilia-cough reflex -tears-chemical that kills whatever gets in eye, eye washes away what's in there- chemical neutralizes Healthier person is better defense mechanisms work
Second line of defense
Inflammatory mechanisms are activated
Vasodilation and increased capillary permeability cause erythema (redness) and edema (swelling)
Phagocytes move in to engulf and destroy harmful substances.
Inflammatory-comes into play if first line of defense doesn’t work
Isolates and rids bacteria or problem
How effective, depends on how healthy you are
Blood vessels dilate, to get blood to effected area, erythema (redness), edema-swelling-happens because of the permeability of weakened vessel, phagocytes move in (pac-man) clear all of the bacteria (if not heathy then a doctor has to act as a phagocyte and clear the dead tissue)
Third line of defense
Immune Response is activated
Immune cells recognize and destroy harmful substances. adequate response-resolution inadequate response-disease spreads.
Immune response comes into play when 2nd line of defense doesn’t work.
Last effort- cells recognize bad guys and destroy it—if it works person will get better—if it doesn’t work disease spreads or person dies
inflammatory response
Activated when the first line of defense is inadequate
Nonspecific
Process of the response is identical regardless of the cause of injury
Universal-nonspecific-same in everyone regardless injury-how persons body responds, whether it is effective or not
Acute inflammation
Triggered by tissue injury and is essential to healing
Injury is defined as any form of damage or alteration to cells or tissues
Injury can include:
Invasion by microorganisms
Cellular mutations
Hypoxia or anoxia
Nutritional deficiencies
Physical or chemical damage.
ACUTE-rapid onset-time limited-max 2 weeks
Symptoms are worse
Cells become mutated
Hypoxia-lack of oxygen to tissues and cells
Anoxia-absent of oxygen
Eschemia- reversable oxygen
Necroses-complete cell death
Nutrition deficiencies can cause inflamation
Acute inflammation process
The ability to recognize injury
Activate a response
Appropriately shut down the response when the injury has passed
Result is either tissue repair or regeneration or formation of scar tissue.
System has to recognize injury
- activates a response
- if cells in body made to recognize injury don’t work then the first thing doesn’t happen and it makes it harder
- cells-lets go fight
- time limited-once problem is resolved inflammation stops-complete tissue repair-or regeneration occurs-scar tissue develops
Goals of acute inflammation
3 major goals:
To increase blood flow to the site of injury, referred to as the vascular response
To alert the products of healing to attend to the site of injury, which is referred to as the cellular response
To remove the injured tissue and prepare the site for healing
vascular response
Tissue injury requires a response at the level of the blood vessel near the site of the injury
Clotting and healing must occur to prevent infection
Structure of the blood vessels must change:
Dilate (widen) to accommodate increased blood flow to the site of injury
Lining of the blood vessel becomes more permeable (loosens to allow cells to easily move from the vessel into the injured tissue).
VASCULAR RESPONSSE
Blood vessels dilate-to get blood to area-to give it oxygen
Blood has got to go to injury site
Alert all cells involved in healing
Cells-closes to site are first to respond
Clotting
Cellular response
PHAGOCYTOSIS HAS TO OCCUR
Get rid of old (dead) get ready for new
Vascular response-blood and fluid needed
- Blood is composed of cells active in phagocytosis
- Increased fluid dilutes harmful substances at the site of the injury
Exudate (watery fluid) that accumulates at the site of injury: high in protein and leukocyte concentration: sign that the vessels are more permeable and cells active in phagocytosis are present
Inflammatory mediators: facilitate the process of widening and loosening of the blood vessels at the site of injury; located in the blood plasma, platelets, mast cells, basophils, neutrophils, endothelial cells, monocytes and macrophages
Blood is composed of oxygen-but blood also brings cells involved of phagocytosis
Fluid comes to site from blood vessels dilating and becoming PERMIBLE
If you pop a blister-it will get rid of protein the body needs-so it bad
inflammatory mediators within cells
Most mediators are formed within the cell
Within cells, most of these are generated in the cell plasma membrane or are made up of proteins within the cell
Most commonly, it is the white blood cells that produce and release the mediators
Platelets, endothelial cells and injured tissue cells are also potential sources.
Mediator-helps you fix a situation-sent in to help a process
Most are in plasma membrane(made of protein within the cells)
Have to have a good source of protein-for good healing
Most important ones come from white blood cell
Blood cells
Mast cell: important inflammatory mediator
Are leukocytes in the connective tissues; near blood vessels
Location allows for rapid response directly at the site of injury
Responsible for the production and immediate release of inflammatory mediators
Basophil: white blood cell; contains granules; functions similar to the mast cell
Signals to trigger, enhance and discontinue the inflammatory response are generated within other white blood cells (lymphocytes, monocytes/macrophages
important to remember
Mast cell- inflammatory mediator-goes straight to site of injury-produces and releases other inflammatory mediators needed to be present/first responder/like (EMS)/closest to site will respond-
leucocytes-term for white blood cell-our protectors-respond to injury
Basophil-contains granulum-get inflamatory process going
Have to have sufficient amount of platelets to clot/needed to heal/forms a scab
inflammatory mediators within platelets
Active in generating and releasing mediators to promote vasodilation, clotting, attraction of white blood cells, ad healing of injured tissues
Histamine, found in white blood cells, housed in platelets
Serotin: causes vasodilation
Histamine-substance found in white blood cells-same as taking (allergy)-anti-histamine-HISTAMINE is present when injury takes place
Serotin: causes vasodilation-comes fast
inflammatory mediators within endothelial or injured tissue
Mediators can be released from these sources
Platelet-activating factor: key role in promoting vessel vasodilation, clotting and attracting infection-fighting white blood cells to the site of injury
Corticosteroids: anti-inflammatory drugs that decrease the inflammatory process and inhibiting the immune response
inflammatory mediators within plasma
Mediators circulate continuously within blood plasma
Pathways responsible for the activation and deactivation of inflammatory mediators that circulate in the plasma – summary on next slide
IMPORTANT
Proteins are triggered in liver -start process of mediating inflamation -clotting-starts clotting cascade Vasoactive inflammatory mediators -summary
important info
Leukocyte
When you have an inflammatory process you have leukocytosis-elevated white blood cells
White blood cells-body’s protector
Too many white blood cells- infection or even strenuous exersice
Decreased white blood cell count-means something serious! You will not be able to fight infection
Neutrophil-first white blood cell on scene-short lived! If present injury happened recently
White blood cell differential-breaks down type of WBC
Macrophage-bigger cell-lives longer-seen mostly in chronic infection-live longer-
Eryhtrocyte-carried in blood, carried oxygen, someone who doesn’t do well in surgery would be an anemic person… person has problems delivering oxygen to areas in blood
Platelets-BLEEDING-low platelet counts patient will bleed to death, needed for healing
three steps for successful cellular response
Chemotaxis: process of moving certain cells to the site of injury
Cellular adherence: blood cells constantly moving through the vascular system, attraction and binding is essential for effective phagocytosis
Cellular migration: the cellular response depends on the ability of cells, primarily leukocytes, erythrocytes and platelets, to migrate to the exact site of injury
-Chemotaxis-process of moving certain site
Cellular adherence- essentail for phagocytosis
Cellular migration-if cells have ability to move
B lymphocytes
Matured in the bone marrow
Essential in mediating adaptive humoral immunity
Production of antibodies/immunoglobins
Account for 10-20% of blood lymphocytes
Lymphocytes-form into two separate categories-T cells and B cells
Start in bone marrow- B cells are very important in HUMORAL IMMUNITY-important in forming anitbodies
cytokinesis
More than a hundred distinct cell proteins
Proteins found within the white blood cell
Vital role in regulating in regulating inflammation
Active from the onset of vasodilation and increased permeability to the resolution of the inflammatory response
Each released from a specific cell and serves a specific purpose
-Proteins found in WBC-vital role in inflammation
CYTO-active in process to beginning to resolution
EACH CELL RESPONDS IN A CERTAIN WAY TO A CERTAIN INJURY
inflammation summary
Tissue injury Blood vessel vasodilation Increased vascular permeability Activation of the clotting cascade Continued release of vasoactive inflammatory mediators -Vascular inflammatory-dilation and permeable REMEMBER Purpose of inflammatory mediators And how many are there
Leukocyte
Different types of white blood cells (WBCs):
Neutrophils
Monocytes
Macrophages
Mast cells
Basophils
Eosinophils
T and B lymphocytes
Neutrophil-first to arrive-initiates phagocytosis-cleans up area-short lived
Monocytes-come with neutrophil-matures into macrophage-if present process has started maybe a week old
Basophils-acts like mast cell but releases histamine into blood- if Present-possible allergy
Eosinophils-effective in parasites and possibly an allergy
two types of leukocytes
Granulocytes
nongranular
local manifestations of acute inflammatory response
Redness (erythema)- vasodilation; increased blood flow to the injured area
Heat- vasodilation; increased blood flow to the injured area
Incapacitation-loss of function is related to tissue damage from injury, pain and swelling at the site
Pain- Increased vascular permeability and accumulation of fluid causes compression in the tissues, inflammatory mediators can also directly elicit a pain response
Exudate and edema- extracellular fluid accumulation often in tissues because of increased vascular permeability
Local-means site of injury
Redness and heat from increased blood flow
Pain-increased permeability
Exudate-extrcellular fluid
lymphedema
Enlargement and inflammation of the nearby lymph nodes
Can occur as a function of filtering or draining harmful substances at the injury site
Filter-lymphnodes-spread throughout our body
Lymphnode swelling can be sign of cancer or infection draining
systemic manifestations
Pyrexia (fever): elevation of core body temperature: result of inflammatory mediators acting directly on the hypothalamus
Stimulates phagocytosis
Inhibit the growth of certain microorganisms
Leukocytosis: elevation in white bold cells (leukocytes), with a count usually above 10,000/mm
Demonstrates the increased circulation of WBCs to aid in healing
Plasma proteins are also increased
Things spread through lymph or blood
Pyrexia-fever
Fever is a bodies defense- you don’t want it to go untreated
Normal white blood count between 5,000-to 10,000
Treatment
Goal of treatment: minimize the damage to healthy, unaffected tissue and promote rapid healing
Drug therapy: most commonly block the action of inflammatory mediators: thereby reducing the swelling, pain, redness and warmth typical of inflammation
Initial treatment:
Reduce blood flow to the local area
Decrease swelling
Block the action of various inflammatory mediators
Decrease pain
Want to help person before injury causes too much damage
Prevent damage to tissue
Reduce blood flow to local area because you don’t want it to stay there
Local injury-put ice! Heat will stimulate inflammatory process-BAD
Resolution of acute inflammatory
Self-limited
Once offending agent has been destroyed and removed, feedback systems regulated by the tree plasma protein systems (clotting, complement and kinin) along with the relevant inflammatory mediators, deactivate the inflammatory response
Allow the tissue to heal
-Small lived-
Chronic inflammation
Persistent or recurrent state of inflammation
Lasts several weeks or longer
Occurs when the acute inflammatory and immune responses are unsuccessful
Can be related to a injury that will not heal; persistent infectious process or an autoimmune condition
Autoimmunity occurs when the immune system identifies self-cells as “foreign” and attacks these cells
Injuries or infections are usually subtle and slow growing
Enzymes
Slower onset- sometimes process of inflammation isn’t effective
Sometimes Strength of an organism is so strong that person may not be able to fight infection
Diabetics- get injured and don’t heal properly-have to do amputations
Enzymes-scaring
Chief cells
CHIEF CELL-neutrophils
Acute-less scaring
general manifestations
Similar to acute inflammation during a “flare-up” of symptoms (redness, heat, pain, swelling, loss of function)
Symptoms may lead to scarring in the affected area or granuloma formation
Other systemic symptoms: fever, malaise, anemia, fatigue, anorexia, weight loss, or weakness
Remission can occur ins some conditions: patient has no sysmtoms
Less obvious-last longer-compromised
Remission can occur in some conditions: some patients have no synmtoms
Treatment
Aimed at removing the source of injury
Managing the symptoms
Long term use of anti-inflammatory, analgesic or immune modifying drugs
Chronic infections as a source of chronic inflammation: antimicrobial drugs
Immunity
Process by which the body recognizes foreign substances and neutralizes them to prevent damage
Types:
Adaptive immunity
Cell mediated immunity
Immunology: study of the structure and function of the immune system
IMPORTANT
Process at which the body recognizes a foreign substance
Humoral immunity- involves production of antibodies in response to an antigen-B lyphocytes
Adaptive-very specific, immune cells target foreign invader, has memory
Cell mediated immunity-involves production of cytotoxic magrohphages, these macrophages activate natural killer cell, whole cell mediated immunity is mediated by T lyphocyte
structures of immune system
Peripheral Immune Structures Lymph nodes Contain lymphocytes Filter lymphatic fluid Spleen Largest immune organ Produces lymphocytes macrophages Lymph nodes-filter and drain, Breast cancer-will dissect lymph node to seek cancer cells Contain lymphocytes Spleen-large immune organ, filters antigens for blood, and reservoir for blood , produces lymphocyted and macrophages
Central Immune Structures: Bone Marrow Production of lymphocytes Maturation of B lymphocytes Thymus Differentiation and maturation of lymphocytes
Bone marrow- cells start as stem cells, produces lymphocytes, B lymphocytes go to bone marrow to mature
Thymus- as you age it doesn’t work anymore (ineffective) T-cells mature in thymus
Tonsils
Consist of lymphoid tissue
Produce lymphocytes
Tonsils-location helps guard against airborne invaders and ingested invaders
Primary cellular components
T lymphocytes Matured in thymus Essential in adaptive cell-mediated immunity Destruction of cellular antigens Promote Antibody production of B lymphocytes Account for 60% of blood lymphocytes
Respond directly to antigen
accessory cellular components
Macrophages: essential in mediating innate immunity
Neutrophil: bind invading microbes to cell surface receptors
Dendritic cells: process and present antigen to T and B lymphocytes stimulating adaptive immune response
Phagocytosis to prevent colonization, entry, and spread of microbes
Macrophages- immediate, helps immune process go on
Dendritic cell: * works with T and B lymphocytes-important with adaptive immunity
Lymphoid progenitor cells
White blood cells (WBCs); also known as leukocytes
Basic functional units of the immune system
Lymphocytes: account for 25-35% of leukocytes circulating in the blood; 99% are located in the lymph fluid
Three major categories of WBCs are derived from the lymphoid progenitor cells:
1. T lymphocytes
2. B lymphocytes
3. Natural killer cells
T Lymphocytes
Mature in the thymus Require contact with an antigen Proliferate and differentiate into the following classification of cells: Cytotoxic T lymphocytes Helper T lymphocytes Suppressor T lymphocytes
Cytotoxic T lymphocytes-attack cells effected with viruses
Helper T-activates other cells to help immune process
Suppressor T- has a job to inhibit both types of immune responses
B Lymphocytes
Develop in the bone marrow
Migrate to peripheral lymphoid tissues
Activated after contact with an antigen
Recognize specific antigens
Antibodies are released from the membranes of plasma cells
Secreted antibody is known as immunoglobulin (Ig)
Designed to detect and bind to specific antigens
Each play a different role in the immune response
Secrete antibodies know as antibodies
Natural killer cells
Large, granular
Not antigen specific
Circulate until they come in contact with cells they can recognize a threat, such as infected cells or tumor cells
Attach and kill these cells
Myeloid progenitor cells
Produce granulocytes and monocytes Granulocytes: phagocytic cells Monocytes also phagocytic cells able to engulf larger quantities of debris than granulocytes macrophages Neutrophils Eosinophils Basophils Dendritic cells
Immune processes
Innate immunity
First responder to an insult
Rapid
Initiated by many different pathogens without requiring prior exposure
Primary cells: macrophages, neutrophils and dendritic cells
Goal: prevent microbe colonization, entry and spread
Rapid response
immune processes-adaptive immunity
Adaptive immunity
Primary cells: B and T lymphocytes and dendritic cells
Stimulated by phagocytosis and activation of antigen-presenting cells
Specificity
Diversity
Memory
Self and nonself recognition
Slower response than innate immunity
When organism is reintroduced, immune memory leads to more rapid and intense response
immunity can be acquired in different ways
Immunity can be acquired in different ways:
Active
Development of antibodies in response to an antigen
Actually having a disease or vaccine
Passive
Immunity transfer
Mother to infant
Active-had chicken pox-so you have active immunity
Passive- occurs naturally but is temporary-mother transfers to baby-gamoglobolin
humoral immunity
Humoral immunity
Immunity involving antibodies
Antibodies are immunoglobulins that react with an antigen in a specific way
Each B lymphocyte carries a single, specific receptor that recognizes a unique antigen pattern
B cells proliferate into effector cells (plasma cells that secrete antibodies)
Apoptosis (programmed cell death)
Remaining cells: memory cells
immunoglobin
Five major classes: Immunoglobulin G (IgG) Immunoglobulin M (IgM) Immunoglobulin A (IgA) Immunoglobulin D (IgD) Immunoglobulin E (IgE)
- Makes up most 80-85%, apears in all body fluids, major antibacterial, and antiviral antibody
- First antibody produced during immune response, present only in vascular system,
- Found mainly in body secretions, saliva, sweat, tears, mucous, defends against things body fluids can get to
- Found in plasma, perdominant antibody on surface of b cells, acts mainly as an antigen receptor
- Involved in immediate hypersensitivity reactions, allergic reaction, stimulates release of mass cell
Antibodies
Protect cells:
Neutralization
Promotion of phagocytosis and destruction of the pathogen- opsonization
Activation of the compliment system
Antibodies-protects cell, binds to antibody, neutralizes
Compliment system
Part of humoral immunity: major mediator of the inflammatory response
Activated components can destroy pathogens directly
Consists of proteins circulating as functionally inactive molecules
The system causes inflammation by increasing:
Vascular permeability
Chemotaxis
Phagocytosis
Lysis of the foreign cell
An antigen-antibody reaction is necessary for the complement system to activate: process called the complement cascade
Cell mediated immunity
Cell mediated immunity:
Cytotoxic T lymphocytes primary cells
Results in the recognition and the destruction of cells caring nonself antigens
Detect pathogens inside the cells that cannot be recognized by antibodies
Specificity recognition of foreign antigens involves cell surgace markers
T lymphocytes
Display membrane surface molecules known as CD, contributing to cell specificity
CD molecules determine specific functions and responses of T cell subtypes
CD8 is expressed on the surface of cytotoxic T lymphocytes (CD8 T lymphocytes)
Helper T lymphocytes express CD4 on their surfaces (CD4 lymphocytes
-broken down into t helpers- and t supressors
Molecule on memebrane called CD
CD4 cells and CD8—will talk more later
infection
Definition: an infection is a host organism’s response to a pathogen, or disease-causing substance
State of cellular, tissue, and sometimes even organ destruction from invasion of microorganisms
Microorganisms enter and multiply
Minor illnesses
Life-threatening conditions
Close to inflammatory process
Host has become compromised- causes cellular damage and cellular disruption, minor illnesses, viruses, or life-threatening-sepsis…
microbes that cause infection
Four types of microorganisms: Viruses Bacteria Fungi parasites
Cause same symptoms- know treatment options. Treatment for one doesn’t work with other
barriers to infection
Immune mechanisms play a role in guarding against microorganism invasion and maintain homeostasis Eyes Lymph nodes Skin Respiratory tract Blood Bone marrow Liver Spleen Digestive system Urogenital track
infection process factors
Factors that create a climate for infection: Poor nutrition Stress Humidity Poor sanitation Crowded living conditions Pollution Dust Medications hospitalization
infection process
Enter Attach Spread Opportunistic infections Opportunistic-person is compromised and, infection takes advantage
pathogens enter:
Direct contact
Inhalation
Ingestion
Insect or animal bite
clinical manifestations
Local: pain, heat, redness, swelling, lymph node enlargement and tenderness, site dependent loss of function
Presence of exudate: purulent (containing pus)
Systemic: fever, malaise, weakness, anorexia, headaches, nausea
Microrganism is present in body
Pus in present-contains dead white blood cell
see blue slides—-
infection treatment
Antimicrobial drugs
Antibacterial drugs
Antifungal drugs
Symptomatic treatment
Challenges
Overuse or incomplete use of antimicrobial drugs has led to multiple drug-resistant microbes
Globalization has promoted the rapid spread of harmful microbes around the world
Importation and mass distribution of perishable food items has also contributed to infectious disease spread
acute infection
Exposure Incubation Prodromal Acute clinical illness convalescence
complications
Septicemia
Bacteremia
Septic shock
