MOD 1 Disease and Cellular Response Flashcards
How cells adapt in reaction to stimulus
change: size, number, and characteristics.
(usually reversed after stimulus has been withdrawn)
Homeostasis
Body’s ability to maintain a dynamic steady state of INTERNAL BALANCE or equilibrium
Hyperplasia
INCREASED NUMBER of cells. Cell replication results in more cells in an organ or tissue
Hypertrophy
INCREASED SIZE of cell due to increased workload (weight training to build muscle) or a pathological condition (cardiomyopathy = enlarged heart) most common in cardiac and skeletal muscle tissue
Atrophy
REDUCED SIZE of cell due to disuse, decreased blood flow, malnutrition, etc.
Metaplasia
REPLACEMENT of one cell type with another that can better endure the stress (usually doesn’t work as well as the original tissue). Caused by chronic inflammation or irritation, i.e. callous or scar tissue
Dysplasia
Abnormal cell growth of specific tissue resulting in ABNORMAL SIZE SHAPE OR APPERANCE. often precedes cancerous changes.
Cell injury agents (causes)
physical agents, mechanical forces, temp extremes, radiation, electricity, chemical toxins, biological agents, nutritional imbalances.
Three main methods of cell injury
Free radical injury
Hypoxic cell injury
impaired calcium function
Free radical injury
Highly reactive chemical molecules with an unpaired electron pulls electrons from healthy cell molecules: cell damage, cancers, or other disease
Hypoxic Cell injury
Cellular oxygen deprivation. Brain/heart/kidneys are high consumers of O2. lack of O2 causes inflammatory response (heart attack, blood clots, lung disease)
Impaired calcium function
Ca++ is an important signaling ion for many cell responses. If the cell is injured, calcium builds up inside the cell and many cell structures are damaged. Too much Ca inside the cell causes mitochondrial damage which leads to cell death
Reversible Cell injury
causes impaired cell function but NOT death. body can repair itself back to homeostasis if the injury is reversed in time before cell death results (excess water,lipids, calcium)
Injured/ stressed cells collect abnormal amounts of:
Water
lipids
calcium
Excess Water due to injured/ stressed cells caused by and causes
caused by: sodium build-up due to the breakdown of the sodium and potassium pump as sodium collects inside the cell and attracts water
causes: intracellular swelling. (usually due to hypoxic injury)
Excess calcium in the cell because of injure or stress to the cell is caused by and causes whay
caused by: cells Ca++ Mg++ pump breaking down
Causes: calcium to collect inside the cell and causes inappropriate activation of cellular enzymes which damages the cell internally
Excess Lipids due to injured/ stressed cells causes what
Lipid collecting in the cell causes impairment of cell functions which leads to “fatty liver” fatty changes are a more ominous sign of cell injury than swelling but can be reversed with dietary changes
Irreversible cell injury
permanent cell death
Two types of cell death
Apoptosis
Necrosis
Apoptosis
Controlled cell death (implosion). Cell membrane maintains integrity which means cell contents are not released into the extracellular space so there is no inflammatory response
Necrosis
Uncontrolled cell death (explosion). Cell membrane loses integrity meaning cell contents are released into extracellular space and triggers the inflammatory response
Telomeres
Outermost tails of the chromosome arms that are shortened during each replication of a cell. When the telomere is too short to replicate the cell dies because it cannot reproduce itself anymore = replicative senescence AKA aging: cells don’t work as they used causing cellular aging
ALSO helps prevent cancer (limits amount of replications a cell can do)
Examples of damaged caused by cellular aging and other factors
-Decrease in elasticity of blood vessels (atherosclerosis = hardening of the arteries) and high blood pressure
-Loss of bowl motility due to aging or medications (chronic constipation)
-loss of muscle mass due to aging, malnutrition, eating disorders, etc. creating muscle weakness and problems with balance
-loss of subcutaneous fat due to aging or extreme dieting, cancer, malnutrition, etc. creating problems regulating temp, and skin breakdown over bony areas especially if bed-bound
Inflammation
-body’s natural response to an injury, toxin, stress, or trauma
-necessary for proper tissue repair and recovery
-healthy unless it becomes chronic
CHRONIC INFLAMMATION can cause serious health issues that have a huge impact on the medical industry
Inflammation is an underlying process for
cardiovascular disease
stroke (neurological disease)
cancer
diabetes
autoimmune disease
alzheimers
lung (pulmonary) disease
arthritis
Organs of the immune system
Bone Marrow: source of all blood components (red, white blood cells, and platelets)
Thymus gland: produces T-cells from lymphocytes
Lymph nodes/ tonsils/ spleen
Cells of inflammation
Endothelial cells
Platelets (thrombocytes)
Leukocytes (white blood cells)
Endothelial cell characteristics
line the blood vessels and produce chemicals that:
-vasodilate or vasoconstrict
-causes blood thinning/prevents clotting (to keep vein open)
- allows entrance/ exit into and out of the blood vessel (vessel wall permeability
Platelets characteristics
-responsible for blood coagulation/clotting
-platelets release of over 300 potent inflammatory mediators
leukocytes characteristics
they are major cellular component of the inflammatory response
-leukocytosis = higher than normal production of white blood cells
WBC are classified as either Granulocytes or agranulocytes
SHARP (signs/ symptoms of inflammation)
Swelling
Heat
Altered function
Redness
Pain
Types of leukocytes
Granulocytes
Agranulocytes
Granulocytes
GRANpa B.E.N
Neutrophils: (60% of wbc), heightened in acute bacterial infection (first responder, arrived before lymphocytes)
ACTIVATED within minutes last 5-10 days
Eosinophils: elevated in allergic reaction and parasite infections
Basophils: elevated in allergic reaction
Agranulocytes
And Granma Loves Money
Lymphocytes: (30% of WBC) B & T cells heightened in viral and chronic infections
Monocytes: circulate in the bloodstream. When called into action they migrate into tissue to become macrophages (cells that eat foreign particles in a process called phagocytosis
Types of Lymphocytes
T cells
B cells
Types of T cells
T memory cells
helper t cells
killer t cells
natural killer cells (NK cells)
suppressor T cells
T memory cells
Remain in lymph nodes for many years after an infection. should the same pathogen enter the body again theses cells produce new clones of T cells to that a rapid response is possible
Helper T cells
activate/ regulate t and b cells
killer t cells
attack virus-infected cells and tumor cells. ingest antigens via phagocytosis
natural killer cells (NK cells)
Attack abnormal cells such as cancer cells. these are lymphoid cells that can destroy cancer cells (have different surface markers than killer T cells)
Suppressor T cells
Returns the functioning of the immune system to normal operation after infection; prevents autoimmunity
B cells characteristics
Back up response and Makes antiBodies - humoral immune response
-slower response time than t cells
-Produced from lymphocytes in the Bone marrow
-releases antibodies and assists activation of t cells
-it takes time to make antibodies in response to a specific antigen unless they were already made at a time of previous exposure to the same antigen
Antigen
antibody generator: triggers the body to make antibodies (pollen, toxins, etc.)
-antigens reside on the SURFACE of cells they are identifiers. Each cell in our body has an antigen that tells the immune system that it is part of us and should not be eliminated
-each antigen is specific to each cell
Tumor antigens used for what
Used clinically as markers to indicate the presence of progressive growth of cancer
Antibodies
Immunoglobulins, B-cell lymphocytes
-Each antigen has a specific complementary antibody
-When the antibody attaches to its complementary antigen, the cell the antigen is attached to can’t reproduce.
Acute inflammatory response
Shown by neutrophils being present
expected to resolve itself in days or weeks
-end result: tissue is healed by being replaced with normal functioning cells
Chronic inflammatory response
show by lymphocytes being present
-periods of exacerbations and remissions, things never get better. Weeks to months to years to lifetime
-end result: tissue is replaced with malfunctioning cells
Local inflammatory response
Localized to one area
identified by SHARP
which is caused by chemical mediators
Systemic inflammatory response
System-wide infection
heightened WBC, CRP, and Fever
Chemical mediators cause what
Histamine, Serotonin, Cytokines, and “kinins” cause:
-Vasodilation (heat and redness (erythema))
-capillary permeability
-blood flow to slow so clotting can happen
-WBCs to congregate to the area of damage (contributes to swelling)
Local acute inflammation results in:
resolves completely with minimal scaring
heals with substantial scaring or fibrosis
progresses to chronic inflammation
Systemic 3
Acute-phase proteins
-C-reactive protein (CRP) : can be a marker for myocardial infarction risk
Fever
-most common objective sign of systemic inflammation especially during the acute response phase
White Blood Cell response
-normal range is 5,000 - 10,000
-WBC with differential is a blood test that shows blood levels for all various leukocytes
Chronic inflammation caused by:
recurrent and persistent infections
persistent exposure
obesity
What does it mean when
Neutrophils are up
lymphocytes are up
eosinophils are up
if WBC is below normal
Neutrophils up = acute bacterial infection
lymphocytes up = chronic or viral bacterial infection
Eosinophils up = allergic reaction or parasitic infection
WBC down = overwhelming infection has exhausted the WBC supply or the bone marrow is not able to keep up production of WBCs
SIRS (sepsis)
Systemic Inflammatory Response Syndrome
-Worst case scenario of systemic inflammation
-can result with or without infection
-can be caused by trauma, inflammation, or infection that leads to the activation of the inflammatory cascade
Inflammatory cascade (SIRS)
massive generalized vasodilation (extremely low blood pressure)
Increased capillary permeability (fluid leaks from blood vessel into tissue)
Multiple organ failure (kidneys, heart, lungs do not receive enough blood)
Circulatory shock (not enough blood pressure to circulate blood through body)
Hyperthermia
Fever
caused by bacterial or viral infections
The most common objective sign of systemic inflammation especially during the acute phase
What chemically triggers a fever
Pyrogen
most common one being interleukin 1
fevers can also be caused by damage to the hypothalamus
Fevers physiologically is what
changing the body’s temperature “set point”
causing chills because blood is leaving extremities and going to warm up the core (chills w/o an elevated temp can still indicate infection)
Normal temp
97-99.5 F
clincally significant fever: 101 F or higher
Normal temp Exceptions
Children can tolerate higher fever up to 104 F
Elderly could have an infection without an apparent fever
-lower core temp
-immune response is weaker with age (less released cytokine)
Good things about fevers
enhance immune function
microbial agents can’t grow in elevated temp
can be an indicator of infection
Standard test to determine cause of elevated temp
CBC (state of rbc and wbc and platelets)
Blood cultures (is there a pathogen in blood)
urinalysis (test urine for presence of infection
chest x-rays (check for pneumonia)
lumbar puncture ( check spinal fluid for presence of bacteria)
