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Pathology lectures > 10th lecture acute inflammation > Flashcards

10th lecture acute inflammation Flashcards

1
Q

what is the definition of inflammation.

A

Inflammation is a universal and ancient form of host defense.
its a protective immune response, it is non specific. That is to say that the inflammation will be the same no matter the type of bacteria is involved.
INFLAMMATION IS NOT A DISEASE.

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2
Q

what are the two types of inflammation?

A

chronic and acute.

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3
Q

when does the acute inflammation develop? and how long does it last?

A

Develops in minutes to hours and lasts hours to days.

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4
Q

what are the main characteristics for acute inflammation?

A

exudation of fluids and proteins

emigration of leukocytes.

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5
Q

what happens if the initial acute inflammation fails to clear the debris?

A

it progresses to a more chronic inflammation.

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6
Q

what is the relation between infection and inflammation? What causes inflammation?

A

inflammation does not always have to be caused by infection. it can be caused by other things too.
- radiation

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7
Q

what is the function of the innate immune system (4)

A
  1. delay the need for adaptive immunity
  2. recognizes infectous non self
  3. execution
  4. serves to alert the clonal, adaptive immune system (dendritic cells).
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8
Q

what are some of the stimuli for acute inflammation?

A
  • infections
  • physical
  • chemical
  • tissue necrosis (myocardial infraction)
  • foreign bodies (splinter, sutures)
  • immune “responses” or “complexes”

the last 2 can lead to chronic inflammation

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9
Q

hoe does the innate immunity recognize infectious items?

A

APC’s have receptors called (PRR) pattern recognition receptors. Such as the toll like receptors.
these receptors recognize PAMP (pathogen associated molecular patterns)

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10
Q

what are some examples of PAMPS (pathogen associated molecular patterns) that the innate immune system can recognize?

A
  • LPS
  • DNA
  • CpG
  • DAMPS: (damage associated molecular patterns) SUCH AS:
  • urica acid (product of DNA breakdown)
  • ATP (mitochondria is damaged)
  • reduces potassium levels within the cells. (membrane damage)
  • DNA (nucleus damage)

Complement system, mannose-binding lectin, collectins can also recognize and kill infectious agents.

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11
Q

what are the principle functions of the PRP’s?

A
  • activation of complement
  • coagulation
  • phagocytosis
  • pro inflammatory signaling cascades induction of apoptosis.
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12
Q

what is the word that describes inflammation of the tongue?

A

glossitis

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13
Q

what is the word that describes inflammation of the mouth and lips?

A

stomatitis

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14
Q

what is the word that describes inflammation of the cornea?

A

keratitis

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15
Q

what is the word that describes inflammation of the lung?

A

pneumonia (note how it does not end in …itis)

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16
Q

what is the word that describes inflammation of the stomach?

A

gastritis

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17
Q

what is the word that describes inflammation of the small intestine?

A

enteritis

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18
Q

what is the word that describes inflammation of the coecum?

A

typhlitis

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19
Q

what is the word that describes inflammation of the rectum?

A

proctitis

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20
Q

what is the word that describes inflammation of the testis?

A

orchitis

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21
Q

what is the word that describes inflammation of the vagina?

A

colpitis

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22
Q

what is the word that describes inflammation of the fallopian tube?

A

salpingitis

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23
Q

what is the word that describes inflammation of the belly button?

A

omphalitis

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24
Q

what is the word that describes inflammation of the breast?

A

mastitis

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25
Q

what is the word that describes inflammation of the adipose tissue?

A

panniculitis

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26
Q

what is the word that describes inflammation of the brain?

A

encephalitis

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27
Q

what are the 4 classical sings of inflammation?

as described in 3000BC

A 
rubor (redness), 
calor (heat), 
tumor (swelling), 
dolor (pain),
- loss of function
28
Q

what are the sequence of events of inflammation?
(think of inflammation as being a battlefield)

-acute inflammation can only occur with vascular tissue and not avascular tissues. avascular tissues can have vascularization occur and precede acute inflammation)

A 
PREPARING THE BATTLEFIELD:
- normal histology
- vasodilation
- increased vascular permeability
- leakage of exudate
SOLDIERS HAVE THE GO TO THE ENEMY
- margination, rolling, adhesion
- transmigration (diapedesis)
- chemotaxis
- PMN activation
- Phagocytosis (recognition and killing)
END RESULT (3 possible outcomes)
- 100% resolution, SCAR, or chronic inflammation.
29
Q

what are the 3 end results of inflammation?

A
  • 100% resolution (all bacteria killed)
  • SCAR formation (greater inflammation then expected)
  • chronic inflammation
30
Q

what is the purpose of the events of inflammation?

A

the inflammatory vascular reaction is to deliver the humoral and cellular factors to the site of defence reaction. THUS; there has to be a change in vascular flow and caliber.
the dilation of the arteries results in congestion in the capillaries.

31
Q

during inflammation there is a vasodilation which results in congestion in the capillaries which results in what?

A

The flow of blood will be slow there will be an increase in endothelial gaps.
The gaps can occur due to: Dilation of vessels, retraction of endothelial cells, or injury to the endothelial cells do to the toxins, and leukocytes injury, as well as the transcytosis can also cause the permeability to increase.

Overally there is a leakage of fluid called exudate (NOT transudate)
NOTE: transudate forms when high hydrostatic pressure or decreased colloid osmotic pressure)
EXUDATE: rich in protein and cells, occurs during inflammation.

32
Q

Is edema transudate or exudate?

A

BOTH, it just means fluid leakage somewhere and it can be both exudate or transudate.

in lab analysis of fluid, if its rich in protein it will be called EXUDATE.

33
Q

what do the cellular elements of inflammation do?

A

with the slow blood flow and vascular congestion during inflammation the cells can go close to the vessel wall.

34
Q

what are the cells that participate in acute inflammation?

A 
Eosinophil
granular basophils
mastcell
macrophages
endothel
firboblasts
thrombocyte, lymphocyte

NEUTROPHIL is the most important in inflammation (it has 3 lobed nuclei under microscope)

35
Q

what are the terms that mean neutrophil?

A
  • neutophil
  • polymorphonuclear leukocyte (PMN, PML)
  • granulocyte
  • neutrophilic granulocyte
  • polymorph
36
Q

what is the 4 step process of extravasation of the PMNs?

PMN = neutrophil

A
  • Margination (PMN’s go toward wall)
  • Rolling (tumbling and heaping) due to selectins that are normally intracellular but expressed during inflammation)
  • Adhesion (via: integrins)
  • Transmigration (diapedesis) (via: CD 31)
37
Q

where is the site of transmigration of leukocytes?

do they go through or between the cells?

A

occurs in the postcapillary venules, do the microcirculatory disorders (affecting capillaries)
They (neutrophils) go THROUGH endothelial cells! and NOT between them.
lymphocytes go out between endothelial cells.
CD-31 mediates the neutrophil transmigration. And go towards the inflammation site (chemokines).

going through the cells can cause injury to the endothelial cells.

38
Q

what mediates increased permeability in the vessels? both in postcapillary venules and capillaries during INFLAMMATION?

A

POSTcapillary permeability is do to histamine and sertanion initial, after which
tnf-a and IL-1 will mediate increased permeability in capillaries during inflammation.

39
Q

what signal is given to neutrophils to tell them where to go?

A

IL-8 expressed on the endothelial cells tells them where to start the rolling and transmigration.

40
Q

(soldiers at the battlefield) what happens when leukocytes arrive at the site of inflammation?

A

they have to get activated (offending trigger to leukocytes causes them to:

  • produce eicosanoids (arachidonic acid derivatives)
  • undergo degranulation to
  • secrete cytokines.

after this activation there is PHAGOCYTOSIS

41
Q

what are the 3 phases of phagocytosis in order?

A
  • recognition (between neutrophil and bacteria)
  • engulfment (surrounding bacteria)
  • killing (releasing the enzymes in the granules to chew up bacteria) oxigen dependent and independent mechanisms.
42
Q

what is an additional method of killing microbes?

A

NET-OSIS? the neutrophil looses its DNA and dies.

Chromatin will form a network.

43
Q

what are the humoral elements and mediators of inflammation?

  • vasoactive amines:
  • vasoactive peptids:
  • complement system:
A
  • vasoactive amines: histamine, serotonine (vasodilation, permeability, pain)
  • vasoactive peptids: bradykinin
  • complement system: MAC, vasodilation, permeability, chemotaxis, opsonisation.
44
Q

where do the chemical mediators come from? and what are their characteristics?

in general in terms of inflammation.
what role do they play as “mediators”

A

-plasma derived mediators (liver)
-cell derived mediators
CHARACTERISTICS?
-have triggering stimuli
-can cause a cascade
-are short lived.

45
Q

2 vasoactive amines in inflammation?

what role do they play as “mediators”

A

histamine and serotonin
HISTAMINE: mast cells and basophils make it and acts as the most powerful vasodilator. (found in fish if ill-prepared food will contain histamine causing poisoning; generalized vasodilation)
SERATONIN: made by tumor cells and enterchromaffin cells, not as powerful of a vasodilation. seratonin evokes NO synthesis from arginine (indirect dilation).

NOTE: seratonin regulates emotion.

46
Q

what is the end result of the complement system?

what role do they play as “mediators”

A

MAC (membrane attack complex) the end result is the lysis of the membrane of the bacteria.

47
Q

what is the kinin system involved in?

what role do they play as “mediators”

A

bardykinin; increased permeability and is a smooth muscle contractor. NON vascular!!!

involved in pain mediation.
WASP sting will inject bradykinin.

48
Q

eicosanoids (arachidonic acid derivatives)
they are part of cell membranes.
what role do they play as “mediators”.

A
  1. prostaglandins (thromboxanes): cause pain, fever, clotting (ASPIRIN blocks this)
  2. leukotrienes (chemotaxis, vasoconstriction, increased permeability)
  3. lipoxins. (inhibit chemotaxis, vasodilation, counteract leukotrienes)
49
Q

what is the function of PAF (platelet activating factor).

what role do they play as “mediators”

A
  • PAF is a phospholipid
  • comes from many cells like eicosanoids
  • powerful platelet activation.

low concentration = vasodilation and increased permeability
high concentration = vasoconstriction

50
Q

what are the roles of cytokine and chemokines?

what role do they play as “mediators”

A 
lymphocytes and macrophages make them but so do many cells.
leukocyte recruitment (adhesion and transcytosis)
51
Q

what are the lysomal constituents?

what does their granules contain?

A

PRIMARY: (azurophilic/non-specific granules) contain: myeloperoxidase, lysozyme, acid hydrolases
SECONDARY: (specific granules) contain lactoferrin, lysozyme, alkaline phosphatase, collagenase.
(collagenase helps pass throught the basement membrane)

FREE radicals can also be found in the cells granules

52
Q

what do NO do?

A

potent vasodilator

produced from the action of NO synthetase from arginine.

53
Q

what is the ACUTE phase response?

A

systemic reaction to TNF, IL-1 and IL-6. the systemic reaction is: fever leukocyte number increase.
Acute phase proteins: C-reactive proteins, Fibrinogen mediated by IL-6.
Erythrocyte sedimentation rate increases
in severe infection SEPTIC shock can occur, hypotension, and metabolic disturbances mediated by TNF and IL-1

54
Q

Classification of acute inflammation based on the exudate:

Serous?

A

common cold, pleuritis exs, burns ,catarrhal inflammation of mucous membranes.

exudate do to inflammation but it is able to resolve itself.
-blisters (skin exudeate inflammation)
Etiology:
-hypersensitivity
-bacterial viral tissue injury
-physical and chemical tissue injury
55
Q

Classification of acute inflammation based on the exudate:

Fibrinous?

A

Serous membranes; pleuritis/pericarditis sicca, peritonitis fibrinosa mucous membranes, diphtery, typhoid fever, dysentery.

increased permeability of vessels but also fibrinogen can pass and the end product of fibrinogen degradation is pyruvate.

56
Q

Classification of acute inflammation based on the exudate:

purulent?

A

purulent inflammation means that at the site of inflammation there is a lot of pus. It contains lots of neutrophils.

folliculitis: (hair follicle inflammation)
furuncule: boil (a painful infection that forms around the hair follicle can forms pus)
carbuncule: (multiple boil in the skin)

57
Q

Classification of acute inflammation based on the exudate:

Haemorrhagic?

A

plaque, smallpox, anthrax, flu

injury to blood vessels causing haemorrhagic of inflammation site.

58
Q

Classification of acute inflammation based on the exudate:

Gangraenous?

A

Failure of inflammation.

59
Q

morphology of serous inflammation?

A

depends on tissue type:

  • serosa: erythema and inflammatory swelling from effusion with large numbers of displaced serosal covering cells/macrophages
  • skin: erythema, swelling
  • mucus membrane: erythema and swelling leading to mucosal edema
  • parencyma: erythema and swelling are present with sparse leukocytic infiltrate.
60
Q

morphology of fibrinous inflammation?

A
  • firbin is the endpoint of coagulation
  • “bread and butter” heart (adhesion between the visceral and parietal layers)
  • fibrinous exudate may be degraded by fibrinolysis and removed by macrophages resulting in resolution.
  • incomplete removal of fibrin resulting in organization and scarring with fibrous adhesions of pleural or pericardial
61
Q

how does pseudomembrane form in fibrinous inflammation?

A

-Pseudomembrane: upper portion of mucous surface undergoes necrosis along with a fibrinous inflammation causing pseudomemebrane formation.

necrosis + fibrinous inflammation.

62
Q

what are the differences between:

  • abscess
  • empyema:
  • phlegmon:
A
  • abscess: circumscribed pus in parenchymal organs in organs (organs with non-preformed cavity: kidney liver and kidney)
  • empyema: circumscribed pus in preformed body cavity (thoracic cavity)
  • phlegmon: purulent inflammation spreading in tissue spaces.
63
Q

what causes hemorrhagic inflammation caused by?

A

damage to blood vessels causing blood to go into the exudate.

  • skin anthrax
  • variola vera
  • urocystitis acuta (the catheter can cause damage of the mucous surface of urinary bladder)
  • influenza virus infections (lungs)
64
Q

what is gangrenous inflammation?

A

failure of inflammation and is a combination of: necrosis inflammation and bacterial infection.

common in the legs since the circulation in the area could be bad (poor vascularization of tissue) thus inflammation will start but will lead to necrosis.
The edema of tissues can interfere with the circulation causing necrotising inflammation
- pneumonia gangrenosa (do to aspiration)

65
Q

what is Ulcerative inflammation?

A

ulcers = local defects on the surface of an organ produced by inflammation. can occur in stomach, duodenum, intestinal.

Pathology lectures (24 decks)

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