Term
| Acute vs chronic inflammation? |
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Definition
acute is sudden onset, resolves quickly. lasts minutes to days
Chronic is longer duration, about 3 months or longer. |
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Term
| Characteristics of inflammation? |
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Definition
Tumor (swelling),
Rubor (red)
Calor (heat)
Dolor (pain)
functio laesa (loss of function. |
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Term
| What are the vascular changes of inflammation? |
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Definition
Vasodilation - Increase vascular permeability, increased blood flow, increase pressure, transudation (movement of fluid from the vessels to the tissue), exudation (movement of proteins from vessels to tissue), margination/rolling of white blood cells, adhesion via selectins and integrins, Transmigration of white blood cells to the site of injury due to chemotaxis.
Refer to notes for more details. |
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Term
| What are the cellular changes invovled with inflammation? |
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Definition
Neutrophils involved with pyogenic, macrophages involved with chronic,
opsinization (putting relish on bacteria/foreign object), and degranulation and killing. |
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Term
| What are the preformed mediators of the inflammatory process? |
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Definition
histamine,
seratonin,
lysozomal enzymes |
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Term
| What are the newly synthsized mediators? |
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Definition
| prostaglandins, leukotrienes, platelet activating factors, activated oxygen species, nitric oxide, cytokines. |
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Term
| Define the role of histamine in the inflammatory process |
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Definition
It is a vasoactive amine found predominantly in mast cells and basophils and platelets.
It is widely distributed throughout the body.
MAIN EFFECT: increased vascular permeability. Causes vasodilation, and itching as well. |
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Term
What is, and where do you find seratonin?
When is it released? |
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Definition
it has effects similar to histamine. found in platelets.
It is released during platelet aggregation. |
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Term
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Definition
| Proteolytic enzymes. These degrade endocytosed molecules. These can be a problem when you have a messy eater! |
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Term
What are the 2 pathways of arachadonic acid production?
What are the enzymes used? |
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Definition
COX pathway via cyclooxygenase: prostaglandins, thromboxanes, prostacyclins
LOX Pathway via lipoxygenase enzyme: Luekotrienes - Lopogynase and Lipoxin. |
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Term
What are the roles of:
1. prostaglandins?
2. Thromboxane?
3. Prostacyclin |
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Definition
1. vasodilation and edema, pain, heat, fever
2. Cause vasoconstriction and promote platelet aggregation
3. These inhibit platelet aggregation. Cause vasodilation. |
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Term
What are the roles of:
1. Leukotrienes?
2. Lipoxin? |
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Definition
1. Chemotaxis, Bronchospasm, vasoconstriction
2. Vasodilation, inhibit neutrophil chemotaxis, stimulate monocyte adhesion. |
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Term
| What are platelet activating factors? |
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Definition
| They cause platelet aggregation and adhesion. They induce vasodilation and increased permeability, stimulate synthsis of AA metabolites, and chemotaxis. |
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Term
What are cytokines (in general).
Name the cytokines we've discussed so far: |
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Definition
They modulate the functions of other cells.
Produced largely by lymphocytes and macrophages.
Interleukin-1, Interleukin-8, Tumor necrosis factor-alpha, and Interferon-gamma. |
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Term
| What is the role of interleukin 1? |
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Definition
It is produced by activated macrophages, causes endothelial activation for adhesion of white cells. They increase thrombogenicity, AA and Nitric Oxide production, and they cause fever, lethargy, and dereased appetite.
Responsible for making you feel like crap. |
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Term
| What is the role of interleukin-8 |
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Definition
chemoattractant.
Activates PMNs |
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Term
| Tumor necrosis factor-alpha causes? |
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Definition
aggregation and activation of neturophils.
Release of proteolytic enzymes from mesenchymal cells
Activates fibroblasts
Fever, lethargy, decreased appetite. |
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Term
| What is the role of interferon-gamma? |
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Definition
| activates macrophages and neutraphils, stimulates the synthsis of nitric oxide, protects agaisnt viral infection. |
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Term
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Definition
a short-lived, soluble, free radical gas.
It is inovlved with regulating neurotransmitter rlease and blood flow, vasodilation, microbiocidal, antagonizes platelet activation, decreases leukocyte adhesion. |
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Term
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Definition
At low levels, they amplify inflammatory mediators,
at higher levels they are tissue damaging. |
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Term
| What are the 2 major systemic mediator events? |
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Definition
1. Complement activation:
2. Activation factor 12: stimulates kinin cascade and coagulation |
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Term
| What is the main roles of the complement system? |
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Definition
1. Lysis of cells
2. Generation of mediators that attract phagocytes
3. Opsonization
4. Increases vascular permeabilty by degranulation of mast cells. |
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Term
| The kinin cascade. What is cause? |
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Definition
vascular permeabilyty, vasodilation and increased permeabiltiy
Bronhcial constriction
Pain |
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Term
| What does the clotting cascade do? |
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Definition
enhance leukocyte adhesion to endothelium,
generate fibrinopeptides that increase vascular permeability,
genereate insoluble fibrin clot and
concurrently activates fibrinolytic system to prevent irrevocable clotting of the entire vasculature! |
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Term
| What are the outcomes of acute inflammation? |
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Definition
Complete resolution and tissue returns to normal,
healting with scarring after substantial damage,
Abscess formation with pygenic organisms,
Progression to chronic. |
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Term
| What are some characterisitcs of chronic inflammation / what can result in a chronic inflammatory cascade? |
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Definition
Tissue destruction
fibroblastic, rather than exudative
less toxic than acute
Initiated as primary process
Persistent infections
prolonged exposure to non-degradable matter
Autoimmune diseases. |
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Term
| What type of cells are involved with chronic inflammation? Stages? |
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Definition
macrophages.
Innocent little macrophage, doing its thing > T-cell thug comes along, talking trash > innocent macrphage gets activated by T-cell, and will do damage.
T-cell activated macrophage will do damage!! If they could, they would set a fire! [Hallmark of chronic inflmamation = these t-cell activated macrophages] they fight off infection, but also do damage to surrouding tissues. |
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Term
| What cells do macrophages activate? |
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Definition
| lymphocytes. Release mediators. continue attacking until foreign thing is taken care of. |
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Term
| In addition to activated lymphocytes, what other cells are involved with inflammation? |
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Definition
Plasma cells - produce antibodies.
Mast cells - histamine
Fibroblast proliferation - scarring. can cause function loss. |
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Term
| What is a granulomatous inflammation? |
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Definition
specific type of chronic inflammation - accumulation of macrophages (epitheloid cells?); macrophags surorunded by lymphocytes and plasma cells;
Characteristic of type IV hypersensitivity. |
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Term
| Granulomatous can be caused by: |
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Definition
Bacteria,
fungi,
inorganic materials |
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Term
| The 2 types of granulomatous inflammations? |
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Definition
FB granulomas
Immune granuloma |
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Term
Drug Classes we should know! (what do they do?)
1. Antihistamines
2. Mast cell stabilizers
3. NSAIDs
4. Corticosteroids |
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Definition
1. block action of histamine by binding to receptor,
2. inhibit mast cell release of histamine
3. Inhibition of COX and thereby prostaglandins.
4. stops inflammatory cascade. |
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Term
| What is a hypersensitivity? |
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Definition
A abnormal or excessive sensitivity to a thing that doesnt deserve a harsh response!
"Diseases resulting from immune mediated tissue-damaging reactions)."
The immune response is more damaging than the antigen would ever be.
EG: pollen. Does it deserve that big of a response? |
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Term
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Definition
Example: pollen - get conjuctivitis.
Anaphylactic reaction.
Treat with anti-histamine |
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Term
| Type II Hypersensitivity: |
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Definition
"Ab-dependant"
EG: Mooren ulcer - antibody complement that has affixed itself to cornea; mounting an immune response because macrophages come to eat it up. vomit.
EG: Myasthenia gravis: antibodies towards Ach receptors.
Graves disease: antibodies towards thyroid stimulating hormone. |
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Term
| Type III hypersensitivity: |
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Definition
"Immune-complex-mediated"
EG:
SLE retinopathy
Sjogren's syndrome - severe dry mouth and eye. antigen antibody fall into salivary and lacrimal gland and destroy the glands. |
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Term
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Definition
"cell-mediated"
-EG:
Rh arthiritis - you get scleritis or episcleritis.
TB - you get uvitis
Diabetic - retinopahty. |
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Term
| What are some causes of cell death |
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Definition
hypoxia,
physical agent,
chemical agent/drugs
infectious agent
immunologic agent
Genetic derangement
nutritional imbalance. |
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Term
| What is the cellular response to injury? - what are the 6 ways cells may adapt? |
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Definition
Adapt or die.
Up to a point, cell injury is reversible.
Ways cells adapt:
1. Atrophy
2. Hypertrophy
3. Hyperplasia
4. Metaplasia
5. Dysplasia
6. Neoplasia |
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Term
| What is atrophy? are cells dead? |
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Definition
THe shrinkage of cells, due to loss by substance, so that cell can adapt.
the cell is smaller, but still viable. it requires less energy to remain viable. |
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Term
Hypertrophy:
What are the 3 types? |
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Definition
increase cell size. "increased ultra-structural synthesis without cell division"
1. Hormonal = transient, EG breasts during pregnancy
2. Compensatory = kidney enlargement when one is removed
3. Adaptive= muscle enlargement with exercise. |
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Term
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Definition
Increase number of cells.
1. Physiologic (HORMONAL - like changes during pregnancy or COMPENSATORY EG liver- if you destroy part of it, it will grow back!)
2. Pathologic (epithelial hyperplasia from papilloma virus) |
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Term
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Definition
Replacement one cell type with another.
You must have genetic reprogramming of stem cells.
1. Epithelial metaplasia =
EG: ciliated columnar epithelium replaced with stratified squameous in smokers!
2. Mesenchymal metaplasia = fibroblasts to osteoblasts. |
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Term
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Definition
disorderly, non-neoplastic proliferation of cells.
Lose uniformity of individual cells.
Tremendous variation in cell shape and size
In epithelia, when entire thickness of tissue is dysplastic, that is called a CARCINOMA IN SITU |
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Term
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Definition
new, autonomous growth.
Benign neoplasm:
Well-differentiated cells - look and act like forbearers. Encapsulated, but they can still kill you if they get big enough!!!!
Malignant neoplasm: anaplasia possible, can be invasive and metasticize. Can definitely kill you! |
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Term
Is cell death reversible?
what is it characterized by? |
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Definition
Yes. Up to a certain point.
Characterized by inability to reverse mitochondiral dysfunction, Cell membrane damage, Ca2+ influx, and free radicals. |
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Term
| Decreased production of ATP in cells allow for influx of? |
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Definition
| Calcium! Calcium is a big killer. |
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Term
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Definition
Necrosis happens after premature cell death. necrotic cells cant maintain membrane integrity, so cellular contents leak out and result in greater tissue damage.
Necrotic cells dont send the normal chemical signals to the immune system - therefore - preventing or decreasing normal phagocytosis of deceased cells. |
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Term
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Definition
Programmed cell death.
The "physiologic" way for a cell to die.
Cells shrink. but membrane does not rupture. |
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Term
| What is the difference between repair and healing? |
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Definition
Repair means teh tissue is able to regenerate itself and it restors general architecture and function.
Healing, on the other hand, occurs when the cell lacks regenerative ability, and we get fibrosis and scar formation. |
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Term
| Cells that proliferate include: |
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Definition
| -remnants of the injured cells, vascular endothelial cells, and fibroblasts |
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Term
| Proliferation is triggered by |
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Definition
| Growth factors, hormones, cytokines, and extracellular matrix signals. |
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Term
| what are labile tissues? Examples? |
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Definition
continuously dividing cells
EG:
- surface epithelia: skin, cornea, GI
tract.
- Bone marrow: RBC, WBC, platelets |
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Term
| What are stable tissues? Examples? |
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Definition
| limited capacity to regenerate. They will regenerate, but slower and not as completely. Exception: LIVER. livers grows back! |
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Term
| What are permanent tissue? Examples? |
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Definition
Non-proliferative cells , post-mitotic.
EG: cardiac and neuronal. |
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Term
| What is symmetric replication/self-renewal of stem cells? |
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Definition
| Stem cells generate new stem cell. |
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Term
| What is asymmetric replication of stem cells? |
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Definition
| Generation of "committed cells" that go on to produce differentiated cells that make up parenchyma or whatever tissue. |
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Term
| What are embyonic stem cells? |
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Definition
| Pluripotential cells - can generate multiple cell lines. |
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Term
| What are adult stem cells? |
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Definition
| They are bone marrow stem cells taht can generate fat, bone, muscle, and cartilage. |
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Term
| What tells cells when to proliferate or how to do it? |
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Definition
Growth factors.
Growth factosr are released to the cells to increase mitotic activity. they increase cell size, increase cell division, and protect from apoptoic death!!! |
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Term
| What are the 3 signaling mechanisms for growth factors? |
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Definition
1. Autocrine: same cell signals that it needs growth -- EG liver hyperplasia, lymphocyte proliferation.
2. Paracrine: neighboring cells - recruit inflammatory cells - wound healing.
3. Endocrine: hormone secreted into bloodstream from EG thyroid/adrenal gland. |
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Term
| What is soo cool about the extracellualr matrix? |
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Definition
it is a dynamic constantly remodeling network that surrounds cells. it includes
1. intracellular matrix: present in spaces between the cells
2. Basement membrane : plate-like mesh around epithelial, endothelial, and smooth muscle cells. |
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Term
| What are some good properties of the ECM? |
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Definition
| The ECM has collagen, elastin, and all kinds of stuff that give it form, strength and rigidity. Its the tissue upon which cells exist. It tells the cells how they are going to grow and how they’re going to organize themselves. If the ECM is damaged, you will get healing, but not good repair. |
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Term
| What are some functions of teh ECM? |
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Definition
Mechanical support
Control of cell growth by regulating cell proliferation
Maintenance of cell differentiation
Scaffolding for tissue renewal
Storage of regulatory molecules (growth factors)
An intact ECM is required for tissue regeneration, and if it is damaged, repair can only be accomplished by scar formation |
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Term
| When tissue injury is chronic or severe, what happens? |
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Definition
We get the the formation of granulation tissue
Pink, granular appearing tissue seen under scab
Proliferation of fibroblasts and delicate capillaries
Granulation tissue then accumulates connective tissue
A scar is born |
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Term
| Describe the process of primary union (Cutaneous wound healing) |
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Definition
primary union of tissues: is the best way to have it happen. This is because its planned, via EG surgery. Clean cut, We don’t have lots of debris. And it is closed by a suture/dermabond/whatever you decide to close it with – which brings wound to apposition where it closes cleanly.
Focal disruption of tissue with death of few cells. By one month, the site is covered by normal epithelial cells
Wound strength is about 80% at 3 months
Only about 10% when sutures are removed at 1 week |
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Term
| Describe the process of Healing by second intention (secondary union) |
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Definition
Larger wounds with extensive tissue loss
Seen in abscesses, ulceration, and infarction
More intense inflammation
Wound contraction
Action of myofibroblasts
Large scar formation |
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Term
| What are some factors that can cause delayed wound healing? |
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Definition
Infection
Poor nutrition (particularly vitamin C deficiency)
Poor perfusion
Mechanical pressure or torsion to wound
Glucocorticoids
Foreign bodies |
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