1
Q
What are the goals of inflammation?
A
- destroy injurious agents and remove them
- wall off and confine these agents so as to limit their effects on the host
- stimulate and enhance the immune response
- promote healing
2
Q
Four cardinal signs of inflammation
A
-heat
-redness
-swelling
-pain
(and loss of function)
3
Q
two types of inflammation
A
acute and chronic
4
Q
acute inflammation
A
- relatively short duration (mins to days)
- characterized by fluid and protein exudation (leakage)
- predominant WBC is neutrophil
- changes in circulation of blood (first, brief vasoconstriction and then vasodilation)
- increase in vessel wall permeability
- WBC (leukocyte) response (move out of vessels and into extracellular spaces)
- release of chemical mediators of inflammation
5
Q
Chronic inflammation
A
- longer duration (days to years)
- characterized by tissue destruction and tissue repair
- predominant WBC is lymphocyte and macrophage
6
Q
most important change that occurs in acute inflammation
A
the vasodilation step followed by an increase in the vessel wall permeability which protein can not get out of normally but they can get out of the inflamed vessels
7
Q
Hemodynamics
A
- 60% total body wt is water (2/3 intracellular (40%) and 1/3 extracellular (20%))
- extracellular comartment (3/4 interstitial (15%) and 1/4 plasma (5%))
8
Q
Loss of homeostasis regarding fluid balance
A
- loss of fluids (not enough fluid = dehydration)
- retention of fluids (too much fluid)
- redistribution of body fluids (in the wrong places)
- disruption of fluid circulation
9
Q
example of loss of fluids
A
-blood loss, severe vomiting/diarrhea, extreme sweating, or excessive renal excretion
10
Q
retention of fluid example
A
inadequate renal excretion
11
Q
example of redistribution of body fluids to wrong places
A
edema
12
Q
example of disruption of fluid circulation
A
- thrombi- / emboli-
- vessel trauma
13
Q
edema definition
A
-abnormal accumulation of fluid in interstitial spaces or body cavities
14
Q
edema occurs because of?
A
an imbalance between
-the forces that keep fluid in the vessels and the forces that draw fluid out of the vessels
15
Q
forces that keep fluid in the vessels?
A
- low hydrostatic pressure in the vessels
- high oncotic pressure in the vessels
16
Q
forces that draw fluid of the vessels?
A
- high hydrostatic pressure in the vessels
- low oncotic pressure in the vessels
17
Q
oncotic pressure
A
osmosis but when particles are proteins
18
Q
hydrostatic pressure
A
works to balance pressures
19
Q
Distribution of edema
A
- generalized
- localized
- gives clues to etiology
20
Q
generalized edema
A
- all over body
- gravity dependent
- more seen in loosely attached tissues
21
Q
localized edema
A
- involving a specific tissue
- like cerebral edema or periorbital edema
- accumulating in a body cavity (abdomen = ascites and thorax = hydrothorax)
22
Q
Mechanisms of edema formation
A
- Inflammatory edema formation
- Hydrostatic edema formation
- osmotic/oncotic edema formation
- obstructive edema formation
- hypervolemic edema formation
- multifactorial edema formation
23
Q
inflammatory edema formation
A
- vessel wall made more permeable by mediators of inflammation
- increased blood flow due to inflammation
24
Q
hydrostatic edema formation
A
- increased arterial blood pressure
- OR increased venous backpressure
25
osmotic/oncotic edema formation
- reducion in osmotic pressure of the plasma (fewer proteins) usually due to hypoalbuminemia / hypoproteinemia
- increased protein loss (proteinuria, albuminuria, feces, urine)
- decreased protein synthesis (liver production)
- protein starvation
26
Obstructive edema formation
- due to lymphatic obstruction by:
* tumor cells
* chronic inflammation
* scarring of lymphatic ducts
* filarial parasites (elephantitis)
27
hypervolemic edema formation
- caused by retention of sodium and water by the kidneys
| - disorders triggering the renin, angiotensin, and aldosterone system
28
multifactorial edema formation
- the cause of edema is often a combination
- CHF: (congestive heart failure) hydrostatic and hypervolemic
* not pumping efficiently
* so retains water (kidneys)
* even harder on heart
29
In the real world swelling vs edema?
```
swelling:
-4 cardinal signs
-inflammatory
-heat
-redness
-swelling
-pain
-exudates
edema:
-5 other types
-cool
-normal or bluish
-"pitting" (fingertip deal)
-non-painful
-transudates
```
30
edema clinical considerations
- the effects of edema may range from merely annoying to fatal (example is cankles to cerebral edema)
- the existence of edema often points to evidence of underlying disease
- inactive people get hydrostatic edema due to lack of use of skeletal muscle pump
- use specific gravity to determine if exudate or transudate
31
exudates
rich in protein and larger numbers of cells (seen w/swelling, inflammation and is increased specific gravity)
32
transudates
less protein and fewer cells
| -seen with edema (5 other types) and is a lowered specific gravity
33
changes in vascular flow in inflamed vessels
- arterioles near the site of injury briefly constrict, then vasodilation occurs
- capillaries become flooded with blood
- increased permeability in the capillaries allow plasma proteins through the capillary walls
34
formation of inflammatory edema (swelling)
- movement of protein-rich fluid into the interstitium (area outside of vessels and between cells)
* decreases the intravascular oncotic pressure and increases the extravascular oncotic pressure
- the net result is even more outflow of water and ions int the extravascular tissues
- sign 1: (tumor) swelling
35
results of vasodilation
- blood flows more slowly and becomes more viscous as plasma moves outward
- tissues become red and mildly swollen due to engorgement of blood
- hyperemia
- sign 2: (rubor) redness
36
hyperemia
area appears redder than normal
37
results of increased vascular permeability
- chemical mediators of inflammation stim. the endothelial cells lining the capillaries and venues to retract
- creates spaces at intercellular junctions, allowing proteins & WBC's to leave the vessels
38
Movement of leukocytes out of blood vessels
1. Margination
2. Rolling
3. Adhesion
4. Leukocyte transmigration
39
normal blood flow term
axial streaming
40
Margination
- blood flow in dilated capillaries is slow
| - leukocytes settle out of the central stream and float to the periphery of the vessels
41
Rolling
-leukocytes tumble along on the epithelial surface, briefly sticking along the way
42
Adhesion
leukocytes firmly adhere to the endothelial surface
- inactive cell adhesion molecules (CAMs) are normally present on the surface of leukocytes and endothelial cells
- these molecules become activated by chemical mediators of inflammation
43
Leukocyte transmigration
- leukocytes migrate between endothelial cells by diapedesis (squeezing in through cracks between endothelial cells)
- leukocytes then cross the basement membrane by focally degrading it with collagenases
44
Mast cell degranulation
degranulation triggered by antigen combining with IgE, physical injury, or chemical agents
45
Chemical mediators of inflammation
- histamine, serotonin, bradykinin
- WBC chemotactic factors
- cytokines: interleukins & chemokines
- leukotrienes
- prostaglandins
- thromboxane
- platelet activating factor
46
Histamine
- released from mast cells, basophils and platelets
- causes vasodilation and increased vascular permeability
- immediate, transient reaction (minutes)
47
Prostaglandins ( E, A, F, B)
- cause pain and many other roles in inflammation
- anti-prostaglandin drugs = NSAID's
- prostaglandins also -> mucus production by stomach
- COX-2 inhibitors
48
Chemotaxis
- chemotactic factors use a chemical gradient to attract a specific type o WBC to the site of inflammation
- chemotaxis is when a WBC moves toward the site of injury following along a chemical gradient
- some characteristic factors for leukocytes:
* bacterial products
* components of complement system
* various chemical mediators
49
Plasma protein systems (involved with inflammation)
- inflammation is mediated by three key plasma protein systems:
- complement system
- clotting system (also fibrinolytic system to counter-regulate clotting)
- kinin system
50
The complement system
- consists of at least 30 proteins (C1, C2, etc) which act on each other in a cascade
- the cascade is activated by antigen-antibody complexes OR bacterial endotoxins, fungi, snake venom etc
- complement enhances inflammation by
* opsonizing bacteria
* attracting WBC's by chemotaxis-
* causing degranulation of mast cells
* C6-C9 can also create pores in bacterial membranes
51
The clotting system
forms a fibrinous meshwork at the site of inflammation that traps exudates, bacteria, etc
-prevents spread to adjacent healthy tissue
-keeps pathogens at site of greatest phagocytic activity
-forms a clot to stop bleeding and begin repair
thrombin converts fibrinogen to fibrin and also:
-enhances WBC adhesion to endothelium
-increases vascular permeability
-is chemotactic for leukocytes
52
The Kinin system
- activation of the kinin system leads to formation of bradykinin which causes:
* increased vascular permeability
* vasodilation
* pain
* may increase WBC chemotaxis
* probably causes endothelial cell retraction
- effects are similar to those of histamine, but become evident at a slower pace
53
Phagocytosis
1. Adherence to the antigen (opsonization by antibodies or complement)
2. Engulfment (pseudopods extend around the pathogen and surround it (forming a "phagosome")
3. Fusion of lysosomes with the phagosome
4. Destruction of the target by lysosomal enzymes
54
What are the possible outcomes of acute inflammation?
- complete resolution (beautiful & perfect)
* tissues capable of regeneration and mild injury
- scarring or fibrosis (repair)
* tissues that do not regenerate, or after substantial tissue destruction (best that it could)
- abscess formation
- progression to chronic inflammation
55
Chronic Inflammation info
active inflammation, tissue injury and healing all take place simultaneously
56
causes of chronic inflammation
- injurious agent persists OR
| - there is interference in the normal process of healing
57
examples of chronic inflammation
- persistent infections by certain organisms
- prolonged exposure to harmful agents
- autoimmune diseases
Pathophysiology
flashcards
Decks in class (11)
# Cards
-
Quiz 187
-
Biology of Cancer (Quiz 2)90
-
Normal Immunology46
-
Alterations of the Immune system35
-
Autoimmune24
-
Inflammation57
-
Week 7 Quiz (Wound healing and alt. of Hematologic fx)57
-
Hematologic Alterations Cont.78
-
Alterations of cardiovascular function50
-
alterations of cardiovascular fx for week 1046
-
alterations of the heart for week 1016
