Study Guides for Week 3 and 4 (complete - looked up unsure ones) Flashcards
What is atrophy?
-Cells revert to a smaller size in response to changes in metabolic requirements or their environment
What is the difference between the MHC classes (I, II, III)?
II. cell surface receptors that help the immune system identify and eliminate abnormal cells. They are found on the surface of most nucleated cells, as well as platelets. (from online)
I: expressed on APC (From Khan Academy: Bind to bad proteins found INSIDE the cell and present them so cytotoxic T cells can kill them)
III: complement system
What are the effects on the cells/tissues when exposed to extremes in temperature?
-Shivering becomes ineffective
-When body temp is less than 87.8 degrees (Confusion, stupor, lethargy, and Arrhythmias (J waves, A-Fib))
What are antibodies? Describe production, (immunoglobulins)
- are complex (Y-shaped) glycoproteins
- produced by mature B lymphocytes
- specifically recognize and bind to a foreign antigen
Types of of Antibodies
GAMED
5 types:
- IgG
- IgM
- IgA
- IgE
- IgD
Functions of antibodies
Functions:
- directly impede the function of the pathogen
- neutralize secreted toxins and enzymes
- facilitate the removal of antigens by phagocytic cells
- participate in cell-mediated immunity
- activation of opsonization (tagging)
- activation of inflammation
What cells indicate a transition from innate to adaptive immunity?
Antigen-presenting cells (APCs)
- these begin the transition from innate to adaptive immunity (change from non-specific to specific)
APCs include:
- macrophages
- B lymphocytes
- dendritic cells
What is special about neutrophils?
In acute inflammation
- account for about 60-70% of WBCs
- non-specific
- phagocytosis
- very mobile, get to the injury site in 90 minutes
- short life span (24-48 hours)
What are Peyers Patches?
- lymphoid tissues in the GI, respiratory, and urogenital tracts (small intestines)
- only contain B cells
- not encapsulated
What does the term “intracellular accumulations” refer to?
- Buildup of substances that cells cannot immediately use or eliminate
- May be abnormal or stored products from other parts of the body
- Substances may accumulate transiently or permanently
– Normal body substances (i.e. Lipids)
– Abnormal exogenous Products, from errors in metabolism
– Exogenous products that cannot be broken down by the cell
What are lymph nodes?
- vessels provide lymph: protein-rich fluid
Function:
- filter foreign material from the lymph before it enters the blood
- centers for the growth and response of immune cells
- located throughout the body
Plasma derived mediators (coagulation system); what do they do?
- the main role is the formation of the fibrin clot
- traps exudate, microorganisms, and foreign bodies
- send chemotactic signals to neutrophils
- triggers kinins (and kinin triggers this)
What is herd immunity?
think COVID vaccine
- a bunch of people getting vaccine and collectively get herd immunity to a disease (just writing in my own words)
What is the role of dendritic cells in innate immunity?
- found in nose, lungs, mucosal lining of the GI tract and skin
- migrate through the lymphatic system
- provide major link between innate and adaptive immunity
– takes the organism to the B and T lymphocytes (antigen-presenting cell)
– some can produce interferon to suppress viral replications - also involved in cell-mediated immune reactions (e.g. allergic type IE contact dermatitis)
What types of cells are included in innate immunity?
- neutrophils
- monocytes/macrophages
- natural killer cells
- Dendritic
What is inflammation?
Reaction to injury to the cells or the actual death of a cell
Production and release of the inflammatory mediators
An innate, natural immune response to cell injury or invading microorganisms by:
- neutralizing harmful agents
- removes damaged and dead tissue
- generates new tissue
- promotes healing
How is body temperature regulated in the brain?
-Hypothalamus
-Involves: Sweating, Vasodialation, Erector muscles constrict, shivering, vasoconstriction
How does acetaminophen/ibuprofen lower fever?
The synthesis of prostaglandin E2 (PGE2) depends upon the enzyme cyclooxygenase (pathway for prostaglandins).
- The basis for cyclooxygenase is arachidonic acid released from the cell membrane
- This release is the rate-limiting step in the synthesis of PGE2
- Inhibitors of cyclooxygenases (either COX-1 or COX-2) are potent antipyretics
How does the body generate heat?
Derived from metabolic activity in the muscles and liver
SNS neurotransmitters play a role (I.e. epinephrine and norepinephrine)
Released when an increase in body temp needed—so heat production rather than energy generation
What are the primary organs associated with the immune system? What do these organs do (split between cards for each) (5)
- spleen
- thymus
- tonsils
- peyers patches
- appendix
- lymph nodes
(5)
Identify types of barriers of the first line of defense
(Physical, Mechanical, Chemical)
Physical barriers
- skin
- mucous membranes
Mechanical barriers
- coughing
- sneezing
Chemical barriers
- tears
- sweat
- stomach acid
Activation of complement system
What role do leukotrienes play in the inflammatory response?
- slower and last longer than histamine
- permeability, adhesion of endothelial cells, chemotaxis of neutrophils, eosinophils, monocytes
- LTD4: causes slow and sustained constriction of bronchioles - asthma
Where are cell-derived mediators produced?
produced by the cells
i think produced by these:
- macrophages (monocytes)
- mast cells (basophils)
- endothelial cells
- leukocytes
- platelets
at the site of inflammation or tissue injury, by various immune cells
Special NSAIDs (Ketorolac and Indomethacin)
Ketorolac (Toradol):
- GIVE PO, IV, AND IM
- CAN BE USED AS AN ALTERNATIVE TO OPIOID THERAPY
- SHOULD NOT BE USED FOR MORE THAN 5 DAYS
- USUALLY WEANED TO ORAL
- NO PEDIATRIC USE
Indomethacin:
- USED FOR PERICARDITIS AND GOUT
- VERY IRRITATING TO THE GI TRACT
Plasma derived mediators: the complement system
- consists of over 30 plasma proteins
- make the inflammatory response work better and stronger:
– cell lysis: allows for granules to be released
– opsonization: recognizing and tagging
– chemotaxis: signaling - anaphylation:
– degranulation of mast cells
– release of histamine
– vasodilation and increase vascular pemeability
What is the difference between hormonal and compensatory hyperplasia? Example of each?
Pregnancy
Vs
liver regeneration
What is the role of chemokines in innate immunity?
Are a subgroup of cytokines produced by the thymus and lymphoid tissue
Control the movement and positioning of immune cells (T cells, B cells, dendritic cells) in tissues and critical for function on innate immune system
warn other host cells of danger
- signaling
Too many can cause damage to cells and tissues
Cell recruitment
What is special about eosinophils?
“The ER team”
In acute inflammation
- 2-3% of WBCs; move like neutrophils
- mildly phagocytic
- react slower, arrive 2-3 hours after injury
- live longer
- play a role in allergic reactions (work with basophils in allergic rhinitis and asthma)
What is the role of adaptive immunity? Why is it considered to be the second line of defense? (she wrote second on study guide, but slides say third line and there’s a second line in innate)
- Characterized by antigen-specific response: has to be activated to work
- considered to be third line of defense
- relies on previous exposure to an antigen
– stronger
– more prolonged
Has three types:
- humoral
- cell-mediated
- regulatory T cells
First line of defense: epithelial barriers
- closed packed cells, layers, constant shedding and protective layer of keratin
– salty acidic environment inhibit colonization - lysozyme makes cells easier for phagocytosis
Mucous membranes: tight epithelial cells; mucus traps and washes away along with saliva
Cilia: moves microbes towards the throat so can be expelled by coughing
Surfactants in respiratory tract “opsonize” or tag the cells which need to have phagocytosis
GI tract –> goblet cells secrete mucin –> hydrated form: mucus; traps pathogens for destruction
What is special about mast cells?
in acute inflammation
- activate inflammation
– membrane permeability
– leukocyte chemotaxis (signaling injury and response of other WBC) - when activated: release several pro-inflammatory mediators
– histamine
– heparin
What happens to the temperature set point during a fever?
During a fever, the body’s temperature set point increases due to the hypothalamus resetting itself to a higher level, causing the body to actively try to maintain a higher core temperature than usual
What is an antigen? What part of the antigen works with other adaptive immunity cells?
Substances which generate the response from the host (trigger an immune response)
- aka immunogens
- can be bacteria, viruses, parasites; even pollen, poison ivy, bee stinges
Epitopes work with other adaptive immune cells?
What happens during the cellular stage? Identify the 4 phases and what occurs (splitting this into other cards)
Margination and Adhesion
Transmigration
Chemotaxis
Phagocytosis
What are the effects on the cells/tissues when exposed to chemicals?
Online: When cells and tissues are exposed to chemicals, potential effects include: cell death, damage to cell membranes, disruption of cellular processes, DNA mutations, impaired protein synthesis, inflammation, tissue damage, and depending on the chemical and exposure level, even cancer development; the specific effects depend on the type of chemical, concentration, exposure duration, and the tissue involved.
What is the role of macrophages in innate immunity?
are in both innate and adaptive; in first line defense in innate immunity
- scavenger; final clean up
- go to all tissues; long lived
What is the difference between physiologic and compensatory hypertrophy? Examples of each?
Physiologic: exercise
Compensatory: Donating a Kidney
What is exudate? Examples?
Vary based on fluid type, plasma protein content and the +/- of certain cells
Serous exudate: watery protein low in protein content
Serosanguinous: RBCs that leak from capillary injury
Purulent exudate: pus is filled with neutrophils protein and tissue debris
What is white pulp in the spleen?
contains concentrated areas of the T and B lymphocytes, dendritic cells
What steps take place after initial response in innate immunity?
Not sure on this?
Second line of defense:
- inflammatory response
- antimicrobial proteins
- phagocytosis
What cells are phagocytic?
- neutrophils
- dendritic cells
- monocytes/macrophages
- natural killer cells
Drug interactions for NSAIDs
- anticoagulants
- corticosteroids
- alcohol
- ACE inhibitors
- ASA and other anti-platelets
- lithium: NSAIDs increase levels
- many herbals will increase the antiplatelet effects:
– chamomile
– ginkgo
– ginseng
– ginger
– garlic
–dong quai
Cellular Stage: Phase 2 Transmigration
Transmigration
- leukocytes migrate through the vessel wall
What are contraindications of aspirin (ASA)?
- allergy (watch closely in asthmatics)
- bleeding abnormalities
- renal dysfunction
- NEVER GIVE TO CHILDREN UNDER AGE 18, CAUSES REYE SYNDROME
- no pregnancy: may see it though in those with coagulation issues
Functions of antibodies (immunoglobulins)
Functions:
- directly impede the function of the pathogen
- neutralize secreted toxins and enzymes
- facilitate the removal of antigens by phagocytic cells
- participate in cell-mediated immunity
- activation of opsonization (tagging)
- activation of inflammation
What is the importance of cyclooxygenase-2 (COX-2)?
- associated with inflammation
- pain
- edema
- muscle contractions
Can dysplasia lead to canncer?
It may cause cancer.
What is the role of the thymus?
maturation of functional T-cells
- atrophies with age and replaced by fat, around puberty
What is the importance of nitric oxide?
- potent vasodilator
- helps keep endothelial cells healthy and smooth
- blocking of nitric oxide production in normal promotes the leukocyte rolling and adhesion
- decreases leukocyte recruitment: reduces inflammation
– inflammation in endothelial cells leads to no blockage
Immunoglobulin M (IgM)
- accounts for 6-10%
- first one to appear in response to bacterial or viral infections
- largest of the immunoglobulins
- when IgM present: usually sign of acute infection
- activates complement system
Immunoglobulin A (IgA)
- immunity at mucosal surfaces/body fluids
– saliva, tears, breast milk, bronchial, prostate, GI, vaginal secretions) - primary defense against local infections in mucosal tissues
- prevents attachments of microbes to epithelial cells
Interleukins: IL-6
- cause liver to produce proteins and colony stimulating factors (blood production)
work to improve protein catabolism
make the liver produce the acute phase reactants which also include complement, clotting factors and protease inhibitors (idk if this point is for IL-1 and TNF-A or all interleukins because of her ppt set up)
What are the effects on the cells/tissues when exposed to infections?
Online: When cells and tissues are exposed to infections, they can experience direct damage from the invading pathogen, including cell death, altered cellular functions, and disruption of tissue integrity, often accompanied by an inflammatory response from the immune system, which can further contribute to tissue damage in some cases; the specific effects depend on the type of pathogen and the tissue involved.
What are the classic signs of inflammation?
- redness
- swelling
- heat
- pain
- loss of function
HARPS
Cytotoxic T (killer) cells and their CD protein
- express the CD 8 protein
- once activated, they search out and destroy antigens
- are able to differentiate what are normal and what are bad
- cause apoptosis or programmed death
Cellular Stage: Phase 3 Chemotaxis
- guide leukocytes to the site of injury
- are mediated by proteins released from the local immune cells
– cause neutrophils to squeeze through endothelial cells
endothelial cells help this process by releasing nitric oxide
Why is inflammation good? Bad?
Good:
- important in understanding everything that happens to our bodies
- is a normal necessary function that occurs to:
– fight off infection
– heal from an injury
- basis of research in many disease states and helps determine treatment
Bad:
- inflammatory processes in:
– coronary disease and MI
– emphysema, asthma, and chronic bronchitis-inflammatory process
– allergic rhinitis
- can become chronic
- inflammation = “itis”
What are the different mechanisms of heat loss? How do they work?
-Shivering
-“goose bumps”
-Non-shivering heat production by liver
-Exertion
Or
Occurs through 5 processes:
Radiation: (Most common)
Transfer of heat from one place to another
Conduction: requires direct contact
Convection: Requires fluid flow, such as air or water
Evaporation (Sweat)
Respiration (insensible)
Cellular Stage: Phase 1 Margination and Adhesion
Margination and Adhesion
- contact of leukocytes with the endothelial tissue
- cytokines cause the endothelial cells to give off cell adhesion molecules (selectin)
– slows flow and causes leukocytes to roll along the endothelial surface
– neutrophils secrete integrins and stick to endothelium
- accumulation of leukocytes which occurs when there is decreased volume
What is the difference between active and passive immunity? How are they different if naturally acquired vs artificially acquired
Chat gpt response:
Active Immunity:
- The body produces its own antibodies in response to exposure to an antigen.
- It provides long-term or even lifelong protection because the immune system develops memory cells.
Naturally Acquired Active Immunity:
- Occurs when a person is exposed to a pathogen naturally (e.g., getting infected with a virus or bacteria).
- Example: A person gets chickenpox, recovers, and develops immunity.
Artificially Acquired Active Immunity:
- Occurs when a person is exposed to an antigen through vaccination (without actually getting the disease).
- Example: Receiving the measles, mumps, and rubella (MMR) vaccine stimulates the immune system to create antibodies and memory cells.
Passive Immunity:
- The body receives antibodies from an external source, rather than making its own.
- Provides short-term protection because the body does not develop memory cells.
Naturally Acquired Passive Immunity:
- Occurs when antibodies are passed from mother to baby through the placenta (IgG antibodies) or breast milk (IgA antibodies).
- Example: A newborn receiving maternal antibodies provides protection for a few months.
Artificially Acquired Passive Immunity:
- Occurs when antibodies are injected into a person from an external source (e.g., through an injection of immune globulin).
- Example: A person exposed to rabies receives rabies immune globulin (RIG) to provide immediate but short-term protection.
What are the major types of cells in the immune system?
B cells, T cells, natural killer cells, APCs, dendritic cells, neutrophils, monocytes/macrophages
What happens during the vascular stage?
increased blood flow:
- starts with transient vasoconstriction followed by rapid vasodilation
- injured tissue secretes nitric oxide and histamine
- causes heat, redness, and pain
Increased vascular permeability:
- causes leakage into the extravascular space and then into the tissues
- swelling and pain
As fluid moves out, the blood thickens and stagnates so clotting occurs
Involves changes to the microcirculation in the capillaries, arterioles, and venules
Where does aspirin and NSAIDs impact the inflammatory process?
they both impact COX 1 and 2
What do free radicals do?
What is the role of B cells?
B lymphocytes -> plasma cells -> antibodies
Designated as plasma/memory cells by the helper T cells
- cells transform into antibody secreting plasma cells or memory B cells
Plasma cells bind and remove the unique antigen – lead to opsonization or tagging of cells that need to have phagocytosis
Memory cells go to the peripheral cells for the next time the body has exposure to this antigen
How do NSAIDs work?
- work by inhibiting prostaglandin synthesis
- inhibits COX-1 and COX-2
- suppress inflammation
- pain relief
- anti-pyretic
- can inhibit platelet aggregation
Black box warning: increase risk of cardiovascular events/stroke
Avoid use in patients with:
- HTN
- heart and/or kidney disease
- diabetes
All inhibit COX 1 and COX2 by blocking synthesis of prostaglandins
- can have non-selective COX inhibitors
- there is one COX-2 inhibitor: celebrex
What are the indications for NSAIDs?
All inhibit COX 1 and COX2 by blocking synthesis of prostaglandins
- can have non-selective COX inhibitors
- there is one COX-2 inhibitor: celebrex
Second line of defense - innate immunity
- inflammatory response
- antimicrobial proteins
- phagocytosis
What are the phases of a fever?
*Prodrome
- Non specific complaints (i.e. aches, pain, etc.)
*Chill
- Shivering, which causes the core temperature to rise
- Complaints of “Freezing to death”
- Vasodilatation caused red flushed skin Once the set point has been reached
*Defervescence (Fever breaks)
- complains of “Burning up”
- Diaphoresis
What are key side effects of aspirin (ASA)?
Toxicities:
-Tinnitus
-Can progress to sweating, fever, dehydration, metabolic acidosis and LOC changes
-REYES
-Excess bleeding, upset stomach
Give a common example of dysplasia
atypical cervical cells that precede cervical cancer
What is special about basophils?
In acute inflammation
- less than 1% of WBC
- release histamine and heparin in areas of tissue damage
– also releases serotonin
Toxicities with ASA (signs)
- tinnitus!
- can progress to:
– sweating
– fever
– dehydration
– metabolic acidosis
– LOC changes - medical emergency if OD
What are the nursing considerations for aspirin (ASA)?
same as NSAIDs:
- administer with food
- assess for gastritis, ulcers, GI bleed
- long term use may have PPI (proton pump inhibitor) or H2 blocker use as well
- watch creatinine and BUN
- assess for CV risk
- stop at least one week before surgery
- assess for fluid retention/weight gain
- IV ibuprofen should be administered over 30 minutes
- be certain well hydrated
do not stop ASA without confirming with prescribing provider!
Patient education with ASA
- similar to NSAID
- do not combine with NSAID
- be careful with bleeding
- soft toothbrush, good oral care
- careful with razors
Cellular Stage: Phase 4 Phagocytosis
- attachment of leukocyte to offending agent
- engulfment:
– cytoplasm move around and enclose the particle in a phagosome - phagosome fuses with lysosome which contains antibacterial molecules
- kills and degradation of the bacteria
What is the role of cell-derived mediators in the inflammatory process?
Work on endothelial cells and capillary permeability?
Explain what happens in dysplasia
- Characterized by “deranged” cell growth of a specific tissue which results is cells of all shapes and sizes
- Often results from irritation or inflammation and can be a be precursor of cancer
- It is adaptive meaning once the irritation is gone, the dysplasia can resolve or progress to cancer in situ
Nonselective Cox Inhibitors (non-selective NSAIDs)
ASPIRIN (NOT AN NSAID)
IBUPROFEN
NAPROXEN
DICLOFENAC
MELOXICAM
INDOMETHACIN
KETOROLAC
What are the three types of adaptive immunity?
- humoral
- cell-mediated
- regulatory T cells
Describe the hematopoietic cascade. What are the two major categories developed from hemocytoblasts?
Stems initially from multipotential hematopoietic stem cell (hemocytoblast)
Two major categories:
- Common myeloid progenitor – RBC, WBC, platelets
- Common lymphoid progenitor: lymphocytes
Helper T cells and their CD protein
- express the CD4 protein
- direct B and lymphocytes and macrophages
- secrete cytokines, chemokines
– kill the infected dead cells and stimulate new macrophages - play a role in the amplifying and activation of the humoral response
How do cells become atrophic?
- When cells are not being used there is decreased demand…the cells will go back to a smaller size and function at a level that is compatible for survival.
– These cells reduce the oxygen consumption and cellular functions by decreasing the number of organelles
Give an example of metaplasia
When the stratified squamous cells are replace the ciliated columnar cells in the in the trachea and large airways.
-EX. Reflux of stomach acid into the esophagus over a prolonged period can cause the lining of the esophagus to change from stratified squamous epithelium to columnar epithelium.
EX. Changes in pH, acid base changes, hormones, smoking, alsochol
What is opsonization?
Tagging of cells
- needing to have phagocytosis
- antibodies tag antigen
Where do corticosteroids impact the inflammatory process?
- affect arachidonic acid and stop it before COX 1 and 2 and lipooxygenase can be made
- work higher up on the arachidonic acid cascade than NSAIDs
- has anti-inflammatory and immunosuppressant properties
- metabolized in the liver and excreted via kidneys
Numerous side effects:
- increase risk of infection
- psychiatric effects
- adrenal suppression
- diabetes
- osteoporosis
Medications:
- prednisone
- methyl prednisone
- hydrocortisone
What is the importance of chronic inflammation?
- inflammation that has gone haywire
- occurs due to:
– unsuccessful resolution of acute inflammation
– low-grade/long-lasting state
– obesity - presence of macrophages and lymphocytes
- can be asymptomatic
Examples: lung disease, CAD, IBD
(numerous disorders related)
What is red pulp in the spleen?
where old or damaged RBCs are destroyed
What are chemokines?
They are best known for their ability to stimulate the migration of cells, most notably white blood cells (leukocytes).
What are cytokines? (as cell-derived inflammatory mediators)
- produced by macrophages and lymphocytes, endothelial cells
- help regulate immunity
- tumor necrosis factor (TNF) and interleukin-1 and 6: responsible for most of symptoms experienced
- weight loss and cachexia
– cachexia: a metabolic syndrome that causes involuntary weight loss and muscle wasting - cause fever, hypotension, increased HR, increase cortisol levels, decreased appetite
Why is humoral immunity necessary in adaptive immunity?
Process of making B cells
Works to rid the body of microbes and toxins
- antigen-antibody complexes
- clumping of cells
- neutralization of toxins, bacteria, viruses
- destruction of pathogens
- adherence of the antigen to immune cells
- phagocytosis
- complement activation
Has primary and secondary responses
What are the effects on the cells/tissues when exposed to radiation?
Online: When exposed to radiation, cells and tissues can experience a range of effects, including DNA damage, cell death, impaired function, and potential mutations that can lead to cancer, depending on the radiation dose and the type of tissue involved; high doses can cause immediate effects like skin burns, while lower doses may increase the risk of long-term health issues like cancer.
How does aspirin (ASA) work?
Actions:
- anti-pyretic
- analgesia
Inhibit prostaglandin production:
- reduce swelling and/or pain
- lower fever
Also inhibits platelet aggregation by stopping thromboxane A and prostacyclin
Platelet inhibition within 15-20 minutes if not enteric-coated
Describe the pathophysiology of an abscess
Acute inflammatory response
Core surrounded by neutrophils
A) Inflammation: capillary dilation, fluid exudation, neutrophil migration
B) Suppuration: development of suppurative or purulent exudate containing degraded neutrophils and tissue debris
C) abscess formation: walling off of the area of purulent exudate to form an abscess
What are contraindications for NSAIDs?
- no pregnancy (Pregnancy Category C)
- history of PUD or GI bleed
- bleeding disorders
- allergies
- renal insufficiency
- hx of HTN, heart failure, diabetes
What is the importance of histamine? What role does it play in the inflammatory process?
- a principle inflammatory mediator in acute response
- found in all the tissues; highest concentration in mast cells, basophils and platelets
- causes vasodilation and increased vascular permeability
- binds to H1 receptors on the endothelial cells (especially on bronchi and causes bronchoconstriction [lungs])
- binds to H2 receptors; is anti-inflammatory (found in large number in stomach and produces acid [GI tract])
What is cell-mediated immunity? What are the major cells associated?
Functions against microbes, parasites, bacteria, viruses which replicate inside cells where they can not be destroyed by antibodies
T cells are the major player
Cytotoxic T cells: attack and destroy the target cells
Helper T cells (CD4): work to control cells where the pathogen grows in the phagosomes of the macrophages
- CD4 cells: secrete interferon – stimulates microcidal substance in the macrophage which kills the cell
What are adaptive cellular changes?
- Changes that occur due to disease process, altered cell function or environmental influences.
- Changes occur when extracellular signals and cues “turn on” signaling mechanisms inside the cell identifying some thing needed by the cell
- These signals send chemical messengers that alter gene expression
– increase work demand or threats to survival by changing cell size, number, or form
– Serve as a protective mechanism, to prevent cellular and tissue damage - When the reason for cell adaptation is removed, the need for changing gene expression stops and in some instances the cell will go back to normal
What is hyperplasia?
- Increase in the # of cells in an organ or a tissue
- Occur in tissues which have mitotic division such as the epidermis, intestinal epithelium and glanddular tissue.
-Normal adaptive process which occurs from a stimulus. Likely genes responding to messengers in the cell to increase replication. - It is controlled
- Usually stops when the stimulus is removed
Interleukins: IL-10
- is anti-inflammatory and helps deactivate the macrophages when the event is over
work to improve protein catabolism
make the liver produce the acute phase reactants which also include complement, clotting factors and protease inhibitors (idk if this point is for IL-1 and TNF-A or all interleukins because of her ppt set up)
What is hypertrophy?
An increase in cell size and a resulting increase in the amount of functioning tissue
- increased workload that is placed usually on the cardias and skeletal muscle
- Just can not make more cells
- Causes an increase in size. Does not increase # of cells.
How do older adults respond to a fever?
Not unusual for a sick older adult to not have a fever or to be very sick with a small elevation
- May present with confusion
- temperature of 99 may be concerning
- Confusion and other symptoms may indicate illness
What is the role of the spleen?
- largest of the lymph organs
- red and white pulp
What are nursing considerations for NSAIDs?
- administer with food
- assess for gastritis, ulcers, GI bleed
- long term use may have PPI (proton pump inhibitor) or H2 blocker use as well
- watch creatinine and BUN
- assess for CV risk
- stop at least one week before surgery
- assess for fluid retention/weight gain
- IV ibuprofen should be administered over 30 minutes
- be certain well hydrated
What are the differences between B and T lymphocytes?
B lymphocytes (B cells):
- mature in the bone marrow
- play a major role in humoral immune response
- differentiate into:
– plasma cells and produce antibodies (immunoglobulins)
– memory cells
T lymphocytes (T cells):
- leave bone marrow early; go to the thymus where they mature
- play a major role in cellular-mediated immunity
- types of T cells:
– helper
– cytotoxic (killer)
– regulatory
CD proteins - what does it mean? Types?
Clusters of Differentiation
- are cell surface markers/receptors
- expressed by the cells at different stages of maturation and activation
- over 370 different CD markers
Helper T cells: CD4 protein
Cytotoxic T (killer) cells: CD8 protein
What is the role of the complement system in innate immunity?
Are groups of circulating plasma proteins that help defend against microorganisms
- Serve as a bridge between innate and adaptive immunity
When activated: sets in to play a series of events which end in lysis of pathogens
- Three stages:
– initial activation phase
– amplification of inflammation
– late-stage membrane attack response
— CELL LYSIS
Help in the disposal of immune complexes and by-products associated with inflammation
Plasma derived mediators: fibrinolysis system
- acts in opposition to the coagulation system
- main inflammatory mediator is plasmin
- plasmin:
– breaks down fibrin clot which increases permeability
– plays role in complement cascade - when clot breaks down, results in FDP’s which increases vascular permeability
What is acute inflammation?
- immediate reaction to injury to blood vessels and tissues
- triggered by many different stimuli:
– injury
– infection
– foreign bodies
– malignancies
– immune reactions - help to remove the “intruder”
Two stages of inflammatory response:
- vascular stage
- cellular stage
Explain what occurs when the cellular membrane is damaged
(NOT SURE) Could lead to necrosis of tissue?
Online: When a cellular membrane is damaged, it loses its ability to selectively regulate what enters and exits the cell, leading to an imbalance in the cell’s internal environment, often causing vital components to leak out and ultimately resulting in cell death; this is because the membrane acts as a barrier, maintaining the cell’s homeostasis, and damage disrupts this crucial function.
What are key side effects of NSAIDs?
Gastrointestinal:
- pain, heartburn, nausea
- gastric mucosa damage
- GI bleeding
Kidneys:
- major cause of renal disease and renal failure
- increased in those with HTN, heart failure, DM and in older adults
electrolyte imbalance
Pregnancy: category C
Describe innate immunity
- non-specific part of the immune system (broad spectrum defense)
- no memory
- plays a role in the inflammatory process, which can actually lead to disease
Immunoglobulin D (IgD)
- antigen receptor to begin the differentiation of B lymphocytes
- least understood
– known to play a role in activation of mast cells and basophils
Can metaplasia lead to cancerous changes?
No. But it can progess to Dysplasia.
COULD Be precancerous Ex. Barretts esophagus
What are five mechanisms of atrophy? Give an example of each
-Disuse: decreased skeletal muscle use
-Denervation: Occurs when limb is paralyzed
-Loss of endocrine stimulation: –Menopause
-Inadequate nutrition
-Ischemia: from decreased oxygen to tissues
-Aging
What are the two types of inflammatory mediators?
Plasma-derived mediators
Cell-derived mediators
Why is opsonization important for memory cells?
Tags cells; memory cells go to peripheral cells for the next time body has exposure to the antigen and can react stronger
Immunoglobulin E (IgE)
- important in allergic and parasitic infections
- binds to the mast cells/basophils
– binding of IgE to these triggers histamine to be release and the rest of the inflammatory response and allergic reactions
What happens during metaplasia?
– Conversion of normal cells to a different cell type often following an injury or insult from outside stimuli
-Replaces the original cells with ones that can better tolerate conditions
-Keeps the same tissue types
What is the role of histamine in innate immunity?
unsure
from online:
Histamine plays a key role in innate immunity by acting as a pro-inflammatory mediator, primarily released by mast cells, which triggers a cascade of responses including vasodilation, increased vascular permeability, and recruitment of immune cells to the site of infection or injury, essentially facilitating the body’s initial response to pathogens or allergens.
What is the role of platelets?
play an integral role in both the inflammatory response and immune response
- help recognize foreign invaders
- secrete cytokine and chemokines
- suppress pro-inflammatory mediators
- express MHC during infections
What role does arachidonic acid play in the inflammatory response?
- found in phospholipids; release of arachidonic acid leads to eicosanoid mediators
- make prostaglandins and leukotrienes (promote inflammatory response)
- thromboxane A: helps with platelet aggregation and constriction
What are the indications for aspirin (ASA)?
-Anti-pyretic
-Analgesia
-Inhibits prostaglandin production (reduces swelling/pain and Lowers fever)
-Also inhibits platelet aggregation
Immunoglobulin G (IgG)
- most abundant of the circulating immunoglobulins (75-80%)
- the only one which crosses the placenta and transfer immunity from mother to baby “starter immune set”
- protects against bacteria, viruses, and parasite infections
- activates complement system
- enhances phagocytosis
What is the importance of serotonin? What role does it play in the inflammatory process?
- similar to histamine; not as potent
- also similar to basophils
- found in platelets, mast cells, certain cells in GI tract, spleen and nerve cells
- have a receptor for IgE
- along with histamine -> increases vascular permeability and vasodilation
What is the role of cytokines in innate immunity?
Are proteins produced and secreted by most cells in the body
- interleukins (IL), interferons (IFNs), and tumor necrosis factor (TNF)
- can be pro-inflammatory (TNF, IL-1, IL-6) or anti-inflammatory (IL-10)
Act as chemical messengers; aiding in the communication among cells; are secreted and bind to receptors on targeted cells
- play a role in both innate/adaptive immunity
- not stored and are short livers
- pleiotropic: can act on different cells, not just one
Produce colony stimulating factors to induce different cell types in the bone marrow
Plasma derived mediators: kinin system
- increase capillary permeability and stimulate pain receptors
- factor XII in the coagulation cascade can activate this system
- when the system is activated, leads to the formation of bradykinin which:
– binds with beta 1 and beta 2 receptors
– increases dilation and vascular permeability
– smooth muscle contraction
– works with prostaglandin
What is special about endothelial cells?
should be nice and smooth, but is rough with inflammation idfk
Interleukins: IL-1 and TNF-A
- typically cause the fever
- IL-1 stimulates the release of neutrophils causing neutrophilia
work to improve protein catabolism
make the liver produce the acute phase reactants which also include complement, clotting factors and protease inhibitors (idk if this point is for IL-1 and TNF-A or all interleukins because of her ppt set up)
Macrophages and adaptive immunity
- gets rid of pathogens and infected cells through the adaptive system
- APC: bind the antigen to the lymphocytes
- acts like a recruiter: produces signaling proteins that active other immune cells
– release cytokines/chemokines - scavenger: perform the final clean up
What are 3 examples of the plasma-derived mediators and what role do they play in the inflammatory response? (roles split into other cards)
Examples/types:
- kinin system
- coagulation system
- complement system
- fibrinolysis system
these are non-reactive until activated
Primary response of humoral immunity
Primary response: cell waiting for antibody to be detected; clonal selection occurs
- B cells differentiate into plasma cells which create the antibodies
- activation takes 1-2 weeks and many get better during primary stage
– IgM is produced in large amounts then IgG
What is the role of natural killer cells in innate immunity?
- first line of defense: constantly roaming body
- can recognize and kill bacteria, viruses, stressed, or tumor cells
- release cytotoxic granules (performin and granzyme) resulting in apoptosis
- solicit help from other types of immune cells by releasing proteins in the blood (cytokines)
are a subclass of granule-filled (granular) lymphocytes
innate immune system
What is the importance of cyclooxygenase-1 (COX-1)?
“good guys”
- found in most tissues
- macrophage differentiation
- platelet aggregation
- renal function
also gastric mucus, clotting, stickiness of platelet
What do prostaglandins do?
- inflammatory mediators
- made from arachidonic acid by the action of COX
- strengthen histamine
- increase vascular permeability
- neutrophil chemotaxis
- causes pain by a direct effect on nerves
What are the effects on the cells/tissues when exposed to electricity?
Online:
When cells and tissues are exposed to electricity, the primary effects can include disruption of cell membranes through electroporation (creating temporary pores), causing changes in ion balance, potential damage to cellular components, heat generation due to electrical resistance, and depending on the intensity, can lead to cell death, tissue damage, muscle contractions, and nerve stimulation, all depending on the voltage, current density, and duration of exposure.
Why do people experience pain/redness after they step on a rusty nail? Why do they have swelling after the injury?
because of the increased blood flow: increased pain and redness
because of increased vascular permeability: swelling
What is the role of antigen-presenting cells (APC)? Which cells are involved?
Are a group of immune cells that mediate the cellular response by processing and present antigens for recognition by certain lymphocytes (T cells)
- begins the transition from innate to adaptive immunity
- express the MHC molecules on their membrane
- involved in T-cell activation
- “present” the antigen to the immune system
APCs include: (they chop up the antigen and move it to the surface for the MHC complex)
- macrophages
- B lymphocytes
- dendritic cells
What is special about monocytes/macrophages?
are agranulocytes
- monocytes account for 3% of WBCs
- play a role in both inflammatory response and immune response
- as they mature, become macrophages: live longer and better phagocytosis
- assist in producing inflammatory mediators
- live longer so they can maintain chronic inflammation
What cells are involved in the inflammatory response?
Leukocytes:
- Granulocytes [poly nucleated]:
– neutrophils
– eosinophils
– basophils
– mast cells
- Agranulocytes [single nucleus]:
– monocytes
– macrophages
– lymphocytes
– these tend to have a bigger role in immune response than in inflammation
What is an epitope?
Part of an antigen that binds to a specific antigen receptor on the surface of a B or T cell that triggers a cellular immune response
What is special about lymphocytes?
- lymphocytes are the smallest leukocytes
- work with macrophages and work in chronic inflammation
- plasma cells develop from B lymphocytes
Secondary response of humoral immunity
Secondary response: occurs with repeated exposure
- recognition occurs faster
- minimal IgM but large amounts of IgG
titers, booster shot
Discuss the role of major histocompatibility (MHC) complexes
Enables the t-lymphocytes to determine “healthy vs unhealthy” cells
- recognition of self/non-self
Person’s MHC proteins are unique and impact immune responses and susceptibility to certain disease
- human leukocyte antigen (HLA): on chromosome 6; are proteins on cell surface and define a person’s tissue type
- proteins involved in antigen presentation
- encode for parts of complement system
Are large cluster of genes on chromosome 6 (3 classes: I, II, III
Why is non-physiologic hyperplasia different from physiologic hyperplasia?
Non-physiologic hyperplasia, also called pathological hyperplasia, is different from physiologic hyperplasia because it refers to an abnormal increase in cell production within a tissue or organ, often caused by excessive hormonal stimulation or other abnormal stimuli, while physiologic hyperplasia is a normal, controlled increase in cell numbers that occurs as a natural response to a physiological need, like during pregnancy or puberty.
What are tonsils?
- collection of lymph located at entrance to digestive and respiratory tracts
- no afferent lymphatic vessels
