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Pathophysiology > Inflammation > Flashcards

Inflammation Flashcards

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
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2
Q

Four cardinal signs of inflammation

A

-heat
-redness
-swelling
-pain
(and loss of function)

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3
Q

two types of inflammation

A

acute and chronic

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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
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5
Q

Chronic inflammation

A
  • longer duration (days to years)
  • characterized by tissue destruction and tissue repair
  • predominant WBC is lymphocyte and macrophage
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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

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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%))
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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
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9
Q

example of loss of fluids

A

-blood loss, severe vomiting/diarrhea, extreme sweating, or excessive renal excretion

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10
Q

retention of fluid example

A

inadequate renal excretion

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11
Q

example of redistribution of body fluids to wrong places

A

edema

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12
Q

example of disruption of fluid circulation

A
  • thrombi- / emboli-

- vessel trauma

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13
Q

edema definition

A

-abnormal accumulation of fluid in interstitial spaces or body cavities

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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

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15
Q

forces that keep fluid in the vessels?

A
  • low hydrostatic pressure in the vessels

- high oncotic pressure in the vessels

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16
Q

forces that draw fluid of the vessels?

A
  • high hydrostatic pressure in the vessels

- low oncotic pressure in the vessels

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17
Q

oncotic pressure

A

osmosis but when particles are proteins

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18
Q

hydrostatic pressure

A

works to balance pressures

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19
Q

Distribution of edema

A
  • generalized
  • localized
  • gives clues to etiology
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20
Q

generalized edema

A
  • all over body
  • gravity dependent
  • more seen in loosely attached tissues
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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)
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22
Q

Mechanisms of edema formation

A
  1. Inflammatory edema formation
  2. Hydrostatic edema formation
  3. osmotic/oncotic edema formation
  4. obstructive edema formation
  5. hypervolemic edema formation
  6. multifactorial edema formation
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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
Q

osmotic/oncotic edema formation

A
  • 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
Q

Obstructive edema formation

A
  • due to lymphatic obstruction by:
  • tumor cells
  • chronic inflammation
  • scarring of lymphatic ducts
  • filarial parasites (elephantitis)
27
Q

hypervolemic edema formation

A
  • caused by retention of sodium and water by the kidneys

- disorders triggering the renin, angiotensin, and aldosterone system

28
Q

multifactorial edema formation

A
  • 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
Q

In the real world swelling vs edema?

A 
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
Q

edema clinical considerations

A
  • 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
Q

exudates

A

rich in protein and larger numbers of cells (seen w/swelling, inflammation and is increased specific gravity)

32
Q

transudates

A

less protein and fewer cells

-seen with edema (5 other types) and is a lowered specific gravity

33
Q

changes in vascular flow in inflamed vessels

A
  • 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
Q

formation of inflammatory edema (swelling)

A
  • 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
Q

results of vasodilation

A
  • 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
Q

hyperemia

A

area appears redder than normal

37
Q

results of increased vascular permeability

A
  • 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
Q

Movement of leukocytes out of blood vessels

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Leukocyte transmigration
39
Q

normal blood flow term

A

axial streaming

40
Q

Margination

A
  • blood flow in dilated capillaries is slow

- leukocytes settle out of the central stream and float to the periphery of the vessels

41
Q

Rolling

A

-leukocytes tumble along on the epithelial surface, briefly sticking along the way

42
Q

Adhesion

A

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
Q

Leukocyte transmigration

A
  • 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
Q

Mast cell degranulation

A

degranulation triggered by antigen combining with IgE, physical injury, or chemical agents

45
Q

Chemical mediators of inflammation

A
  • histamine, serotonin, bradykinin
  • WBC chemotactic factors
  • cytokines: interleukins & chemokines
  • leukotrienes
  • prostaglandins
  • thromboxane
  • platelet activating factor
46
Q

Histamine

A
  • released from mast cells, basophils and platelets
  • causes vasodilation and increased vascular permeability
  • immediate, transient reaction (minutes)
47
Q

Prostaglandins ( E, A, F, B)

A
  • cause pain and many other roles in inflammation
  • anti-prostaglandin drugs = NSAID’s
  • prostaglandins also -> mucus production by stomach
  • COX-2 inhibitors
48
Q

Chemotaxis

A
  • 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
Q

Plasma protein systems (involved with inflammation)

A
  • inflammation is mediated by three key plasma protein systems:
  • complement system
  • clotting system (also fibrinolytic system to counter-regulate clotting)
  • kinin system
50
Q

The complement system

A
  • 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
Q

The clotting system

A

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
Q

The Kinin system

A
  • 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
Q

Phagocytosis

A
  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
Q

What are the possible outcomes of acute inflammation?

A
  • 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
Q

Chronic Inflammation info

A

active inflammation, tissue injury and healing all take place simultaneously

56
Q

causes of chronic inflammation

A
  • injurious agent persists OR

- there is interference in the normal process of healing

57
Q

examples of chronic inflammation

A
  • persistent infections by certain organisms
  • prolonged exposure to harmful agents
  • autoimmune diseases

Pathophysiology (11 decks)

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