Inflammation Flashcards
Nonspecific, predictable response of living tissue to injury
Inflammation
Examples of chronic inflammation
- Rheumatoid arthritis
- Lupus
Noxious
Fever
Inflammation has a protective role/generally beneficial, but can be uncontrollable and be harmful. What’s an example of this?
Pulmonary TB, can erode pulmonary vessels and cause massive bleeding (hemoptysis)
How is inflammation helpful forensically?
Inflammation only occurs in living tissues. In forensics is a “vital reaction” and indicated injury occurred before death.
5 signs of inflammation
- Calor (heat)
- Rubor (redness)
- Tumor (swelling)
- Dolor (pain)
- Functio laesa (loss of function)
Represents the body’s first response to injury (inflammation)
Changes in blood flow
Acts as sphincters and regulate inflow of blood into capillaries when mechanical stimulus (burn) stimulates nerves
Smooth muscle cells on pre-capillary arterioles
Are precapillary sphincters normally open or closed?
Closed. They open with “acute inflammation” and dilation allows blood to flow to site causing (redness, warmth, swelling)
- What is the 1st response of arterioles to injurious stimuli? How long does it last?
- 2nd response?
- Vasoconstriction, a few seconds
- Vasodilation (relaxation of precapillary sphincters)
Hyperemia
Excess of blood in the vessels (which causes warmth)
Which vessels cannot actively regulate incoming blood flow. Why?
-Capillaries
-Venules
Because they only have endothelial layer and basement membrane
Increased pressure in capillaries/venules leads to what?
It forces plasma filtration thru vessel wall –> edema
Ex: blister filled w/ clear fluid (plasma w/o RBC or WBC)
Edema causes blood flow in the dilated capillaries/venules to be slow due to what?
Hemoconcentration, so RBC stack on top of each other
Sludged erythrocytes form stacks called what? What results?
“Rouleaux”
-Slows circulation even more
What happens after “rouleaux”
“Pavementing”
-WBCs marginate and attach to edge of endothelium and develop elongated protusions (become sticky) to adhere to endothetlial cells lining capillaries/venules
What squeezes through gap junction
Neutrophils, after squeezing through they are at the site to perform phagocytosis
Normally present on leukocytes and endothelial cell in an inactive form
Surface adhesion molecules
During inflammation, surface components of leukocytes/endothelial cells are activated by soluble mediators of inflammation which are normally present in blood. What are these called?
Interleukins
Derived in part from platelets and leukocytes
interleukins
One of the most important triggers for release of mediators of inflammation
Adhesion of leukocytes to endothelial cells
What substance initiates clotting which leads to fibrin strands which anchor leukocytes to the vessel wall?
Platelets
The increased permeability of vessel walls of capillaries/venules lasts how long?
hours to days
Leakage of fluid from vessels into interstitial spaces
edema
In acute inflammation, most of the cells are what?
Neutrophils (PMNs)
As inflammation evolves, PMNs are joined by which cells after how many hours?
- Monocytes (also phagocytic)
- Within 24 hours
Lifespan of neutrophils (PMNs)
2 to 4 days
As inflammation proceeds and the neutrophils die/become less prominent. What 3 are they replaced by?
Macrophages, lymphocytes, plasma cells
4 phases in which neutrophils emigrate thru vessel wall
- Adhesion of PMN to endothelium
- Insertion of cytoplasmic pseudopods between junctions of endothelial cells (squeeze thru gap junctions)
- Pass thru basement membrane
- Ameboid movement away from vessel towards cause of inflammation (bacteria)
Active movement of PMNs along a concentration gradient is called what? What are they moving towards?
“Chemotaxis”
-Chemoattractant (bacteria or tissues destroyed by inflammation) or activated compliment
To make tasty for neutrophils, monocytes, macrophages
Opsonization
When do PMNs lose their mobility?
When they reach the bacteria or other chemoattractant. Now is when they do phagocytosis
How do PMNs recognize bacterium as foreign?
Psedudopods extending from their surface
The ____ of the PMN attached to the ___ of the bacteria
- Cell membrane of PMN
- Cell wall of bacteria
What 2 things act as opsonins (make tasty)
What becomes opsonized?
-Immunoglobulins
-Complement
(facilitate attachment of PMN to bacteria)
-Bacteria becomes opsonized to be eaten
Many leukocytes/PMNs have receptors for what 2 things which mediate contact w/ bacteria?
-C3
-Fc
(receptors)
Engulfment of bacterium. Cytoplasm of PMN surrounds foreign particle, invagination of cell membrane
Phagocytosis
W/ phagocytosis, how is the bacteria killed?
Inside the phagocytic vacuole, bacteriocidal substances are released from cytoplasm of PMN
Specific granule
Secondary granule
Non-specific
Primary granule
What is discharged into lumen of phagocytic vacuole during phagocytosis?
Contents of “specific granules” from PMNs
Dead/dying PMNs along w/ tissue debris
Pus (viscous yellow fluid)
Inflammations dominated by pus formation
Purulent/supparative inflammations
Inflammation produces what 2 important clinical findings (typically)
- Fever (over 37C)
2. Leukocytosis
A fever is a typical response to acute inflammation. What 2 substances act on thermoregulator centers in the hypothalamus
- Interleukin I
- Tumor Necrosis Factor (TNF)
Serves as a thermostat
Hypothalamus
The fever is mediated by what 2 prostaglandins? released from what?
-IL-2
-TNF
(released from pyrogens)
Released from PMNs and macrophages during inflammation
Pyrogens
Normal blood has how many leukocytes (WBC)?
Less than 10,000
Mediators of inflammation act on what? Which stimulates rapid release of leukocytes
bone marrow
Blood has how many leukocytes to be considered (leukocytosis)
Over 12,000 to 15,000
What predominates in acute inflammation?
Neutrophils
5 non-specific sxs of leukocytosis
- weakness
- depression
- pain
- exhaustion
- no appetite
In what 3 settings can inflammation be seen by a medical professional?
- PE
- Surgery
- Autopsy
6 types of pathologic inflammation
- Serous
- Fibrinous
- Purulent
- Ulcerative
- Pseudomembranous
- Granulomatous
- Mildest form of inflammation
- Occurs in early stages of inflammation
Serous inflammation
Type of inflammation:
- viral infections (herpes)
- Autoimmune disorders
- 2nd degree burns w/ blisters
Serous Inflammation
Type of inflammation:
- bacterial infections (strep or PNA)
- Pericarditis
Fibrinous inflammation
Type of inflammation:
- Staph/Strept
- abscess
Purulent inflammation
Type of inflammation:
- occurs on body surfaces or mucosa of hollow organs (stomach/intestines)
- Defect involving epithelium
Ulcerative inflammation
Type of inflammation:
- form of ulcerative inflammation combined w/ fibrinopurulent exudation
- exudate of fibrin, pus, cell debris, mucous
- C. diff
Pseudomembranous inflammation
exudate of fibrin, pus, cell debris, and mucous forms what?
Pseudomembrane on surface of ulcers (can be scraped away which causes profuse bleeding)
Type of inflammation:
- special form of chronic inflammation that is not preceeded by acute inflammation
- can be caused by antigens which evoke cell mediated hypersensitivity rxn or that persist at site of inflammation
Granulomatous inflammation
Examples of granulomatous inflammation
- TB
- certain fungal diseases
