Class 2 - Inflammation Flashcards
Inflammation is regarded as a ______ and ______ response to injury
vascular
cellular
The purpose of inflammation is _______
- removal of an injurious agent
- cleaning of debris and repair
List types of inflammation and their etiologies
Acute - infection or tissue necrosis/infarction
Chronic - non-healing acute process, foreign material in body, auto-immune reaction
The classic signs of inflammation are __________
redness (rubor) swelling (tumor) heat (calor) pain (dolor) loss of function (functio laesa)
List vascular events of acute inflammation
1) brief constriction of arterioles
2) following dilatation of arterioles
3) increased blood flow to the area
4) hyperemia
5) increased hydrostatic pressure - edema
6) venous stasis of blood - heat
In terms of vascular event of acute inflammation, why is there pain?
increased hydrostatic pressure in area leads to accumulation of fluids in interstitial space, putting pressure on sensory receptors
The major cells of acute response to inflammation are _____ aka ________
PMNs - polymorphonuclear leukocytes
neutrophils
The process of leukocyte accumulation is called ______
margination
List sequence of cellular stage of acute inflammation
1) Margination and adhesion to endothelium
2) Transmigration across endothelium (Diapedesis)
3) Chemotaxis
4) Activation and phagocytosis
Leukocyte adhesion and transmigration across endothelium is facilitated by _________ on the leukocyte and endothelial surfaces.
complementary adhesion molecules (e.g. selectins, integrins)
Chemotaxis is ___________
locomotion oriented along a chemical gradient
Band cells are _______. They are released from _____ when __________
immature neutrophils with horseshoe (band) shaped nuclei
bone marrow
there is excessive demand for phagocytes (acute inflammation)
Phagocytes are attracted to inflamed tissues through a process called _______.
chemotaxis
High Neutrophil count can be attributed to _____
Bacterial infection, burns, stress, inflammation
High Lymphocyte count can be attributed to ______.
Viral infection, leukemia
High Monocyte count can be attributed to _________.
Viral or fungal infection, chronic diseases
High Eosinophil count can be attributed to _____
allergic reaction, parasites, autoimmune disorder
High Basophil count can be attributed to_______
allergic reaction, cancers, hyperthyroidism
Histamine and serotonin are released from (which type of cells)______ during acute inflammation
basophils, mast cells, platelets
Describe function of histamine and serotonin in acute inflammation.
Cause vasodilation and increased vascular permeability (fluid escape into interstitial space). Also cause bronchoconstriction
Prostaglandins and cytokines are derived from _________
arachidonic acid (both are chemical mediators of inflammation)
Prostaglandins function to _________
induce vasodilation and bronchoconstriction
pain
(chemical mediators of inflammation)
Cytokines function to _______
“kines” to move
activate immune response by other blood cells, attraction of neutrophils, thrombosis, activate liver
LV makes blood more viscous so it’s easier to prevent by localizing
(chemical mediators of inflammation)
PAF stands for ______. Describe its function.
Platelet aggregating factor -
it activates neutrophils, acts a eosinophil attractant, and stimualates histamine and serotonin release leading to vasodilation and bronchoconstriction
Describe role of LV in inflammation response.
LV is a major supplier of active phase proteins which makes the blood compartment more viscous, keeping acute inflammation localized
What are expected outcomes of acute inflammation?
elimination of injurious agent via phagocytosis
List cells that mainly participate in chronic inflammation
macrophages, lymphocytes, plasma cells,
The two types of chronic inflammation are _______
diffuse (nonspecific)
granulomatous
Describe diffuse chronic inflammation
accumulation of macrophages at site of injury lead to fibroblast proliferation, with subsequent scar formation that replaces normal tissue
Describe granulomatous inflammation
macrophages aggregate around foreign body forming granulomas
A granuloma is ________
a lesion in which there is a massing of macrophages surrounded by lymphocytes
Capacity for healing depends on _______
tissue type, cell type, immunocompetence, age, retention of debris, underlying chronic conditions, lifestyle, risk factors, environment, quality of health care
The two types of wound healing are __________
primary and secondary intention
Describe primary intention wound healing
wound margins are close together, injured tissues composed of labile cells, typically found in clean surgical wounds, minimal scarring
Describe secondary intention wound healing
extensive wounds where tissues are composed of permanent cells, granulation leads to scarring, possible adhesion
What tissues usually heal by primary intention?
Tissues composed of labile cells
What tissues usually heal by secondary intention?
Tissues composed of permanent cells
Labile cells are those that __________
continue to divide and replicate throughout life, e.g.epithelial cells of skin, oral cavity, vagina, cervix
Stable cells are those that ________
normally stop dividing when growth ceases unless appropriately stimulated, e.g. LV, KD, smooth muscle, vascular endothelial cells
Permanent cells are those that _______
cannot undergo mitotic division, e.g. nerve cells, skeletal muscle, cardiac muscle
Adhesions often occur _________
as a natural part of the body’s healing process after surgery
CRP stands for _____. Its function is to _________
C-Reactive Protein
assists in increasing viscosity of blood
ESR stands for _______. How will ESR change during inflammation? Why?
Erythrocyte Sedimentation Rate
ESR will increase since CRP along with complement proteins and fibrin increase blood viscosity
List vascular components of inflammation
increase in vascular permeability
vasodilatation
endothelial injury
List cellular components of inflammation
neutrophils extravasate (let force of fluids out) from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release
Describe acute inflammation
neutrophil, eosinophil, and antibody mediated
acute inflammation is rapid onset (sec to min), lasts min to days. outcomes incl. complete resolution, abscess formation, and progression to chronic
Describe chronic inflammation
mononuclear cell and fibroblast mediated; characterized by persistent destruction and repair. associated with blood v. proliferation, fibrosis. granuloma: nodular collections of epithelioid macrophages and giant cells. outcomes include scarring and amyloidosis.
Compare dystrophic calcification
vs
metastatic calcification
both types of calcification consist of calcium phosphate crystals. differ is that dystrophic calcification (post mi) occurs in damaged tissue, and metastatic calcification occurs in normal tissue in the setting of hypercalcemia
dystrophic = damaged
List the chemical mediators of inflammation ___. They are derivatives of ____?
- prostaglandins - vasodilatation, pain
- prostacyclins - vasodilatation, platelets inhibition
- thromboxane A2 - vasoconstriction, increase platelet activity
- leukotrienes - promotes chemotaxis (encourage WBC)
- cytokines - activate immune response by other blood cells …
- PAF “platelet aggregation factor” activates platelets to release histamine, serotonin
they are derivatives of ARACHIDONIC ACID
What inhibits chemical meditators of inflammation?
anti-inflammatory drugs
fat free food (chemical garbage)
List non-specific markers of inflammation from LV
CRP - C reactive protein
Fibrin - increases ESR
Chronic inflammation is organized by which cells?
macrophages (in tissue), lymphocytes (b-in blood t-in thymus), plasma cells
List 2 types of chronic inflammation
- interstitial/diffuse ie. asthma, COPD
2. granulomatous (granuloma/cellular rosette) ie. TB, Crohn’s
What is the outcome of inflammation?
- complete resolution: most common
- scar formation & partial or complete loss of fx (less common)
- ulcer
- fistula
- peritonitis
- abscess
- becoming more general/ extensive rather than local
When is cellular injury reversible?
cellular and organelle swelling is reversible
ie. increase cranial pressure due to edema of brain
Describe irreversible cellular injury
- disintegration of cellular & organelle membranes (ribo, mtio, nucl)
- nuclear pyknosis: shrinking necleus
- karyorrhexis: nucleus and chromatin are broken to pieces
- karyolysis: nucleus disappears (autodigested by cellular enzymes)
Describe granulation
healing of inflammation often involves ingrowth of capillaries and fibroblasts
ie MI
