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Histology > Inflammation - Acute and Chronic > Flashcards

Inflammation - Acute and Chronic Flashcards

1
Q

What is inflammation and what is its purpose?

A

a response to tissue injury by mechanical trauma, toxins, ischemia, immune responses, tissue necrosis, infections…
purpose is to destroy or contain the damaging agent, repair, healing, regeneration

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2
Q

what are the three components of acute inflammation?

A

vascular dilation, endothelial activation, neurotrophil activation and migration

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3
Q

what are the three morphological variant types of acute inflammation?

A

suppurative/puruent inflammation
fibrinous inflammation
serous inflammation

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4
Q

What are common examples of purulent inflammation>

A

lobar pneumonia, bronchipneumonia, acute appendicitis

URIs can spread down the respiratory tract and lead to tracheobronchitis and bronchiolitis

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5
Q

what are typical pyogenic bacterias?

A

staph, strep, E coli, neisseria spp., N. meningitidis, gonorrhea

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6
Q

what does tracheobronchitis and or bronchitis (acute inflammatory Suppurative/purulent inflammations) usually present with?

A

productive cough - yellow or green sputum

it can progress to bronchopneumonia

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7
Q

where are fibrinous inflammation found?

A

in serous membrane-lined cavities

pleural, pericardial, peritoneal

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8
Q

what are serious inflammations divided into?

A

transudate and exudate

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9
Q

what is transudate?

A

low specific gravity (like water) and low protein content

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10
Q

what is exudate?

A

high specific gravity (much higher than water) high protein content

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11
Q

where is serous inflammation found?

A

seen in skin in response to burns

serous-lined membranes like pleural effusions

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12
Q

what are the cardinal signs of inflammation - Celsus?

A

redness (rubor) - hyperemia (increase blood flow)
swelling (tumor) - fluid exudation and hyperemia
heat (calor) - hyperemia (increase blood flow)
pain (dolor) - release of bradykinin and PGE2
*inflammatory mediators bind to pain n.
added by Galen:
loss of function (functio laesa) - combined effects, mainly swelling and pain

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13
Q

how are the outcomes of acute inflammation determined?

A

severity of tissue damage
capacity of stem cells within the tissue to replace the specialized cells required (regeneration)
the type of agent causing the damage

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14
Q

what are the 3 possible outcomes of acute inflammation?

A

resolution - seen in sunburns, pneumonia
fibrosis (scar formation)
chronic inflammation

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15
Q

when can resolution happen?

A

when CT framework is intact and the tissue has capacity to regenerate

sunburn, pneumonia

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16
Q

how does the heart heal?

A

fibrosis - which is good because if you had a hole in your heart that would suck. At least there is structural integrity that is being re-established

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17
Q

what is a common type of chronic inflammation?

A

abcess formation - from pyogenic bacteria!

acute to chronic

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18
Q

what inflammatory infiltrates are found in chronic inflammation

A

lymphocytes, macrophages and plasma cells

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19
Q

how does chronic inflammation usually heal?

A

by fibrosis

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20
Q

what are some examples that can contribute to immunological chronic inflammation

A 
low toxicity organisms = syphillis
infective organisms that grow in cells = virus
allergic reactions
autoimmune conditions (SLE)
fungal, protozal and parasit infections
21
Q

what are non-immulpogical examples that contribute to chonic inflammation?

A

foreigh body reactions, inert noxious materials - silica, talc, asbestos, beryllium

22
Q

what is an example of a non-granulomatous chronic inflammation?

A

hep. B virus infection = liver fibrosis

Idiopathic pulmonary fibrosis

23
Q

what is tissue damage due to in chronic inflammation?

A

due to inflammatory response rather than the virus itself

24
Q

what is an example of a granulomatous chronic inflammation?

A

Tb(caseous necrosis - cheesy appearance) crones disease, diverticulitis
granulomas = giant cell + epitheliod macrophages

25
Q

what do granulomatous chronic infections contain

A

giant cells + epitheliod macrophages + chronic inflammation cells

26
Q

Where are free plasma proteins found?

A

Components of the coagulation cascade
Acute phase reactants - increase secretion of blood proteins from liver during inflammation
Complement proteins
Circulating immunoglobulin aka antibodies

27
Q

What is opsonization?

A

Coating bacteria with immunoglobulin and complement proteins which together, increase phagocytize activity

28
Q

What is acute pericarditis?

A

Mt of fibrin coats the visceral layer of the serous pericardium

29
Q

What are hemosiderin and where are they commonly found?

A

They are the foamy appearance of a cytoplasm of macrophages which also contains brownish pigment granules that are iron containing pigmented found commonly after an MI near necrotic cardiac muscle tissue

30
Q

What are fibrolysins?

A

Break down fibrin strands during clean up

31
Q

What are the infiltrates of chronic inflammation?

A 
Plasma cells
Lymphocytes
Macrophages
Eosinophils
Fibroblasts
32
Q

What is bronchiectasis?

A

Chronic inflammation of the bronchi leading to progressive destruction of muscular and elastic components of the wall and permanent dilation - elastic and muscular components are replaced by granulation and fibrous tissue

33
Q

How are giant cells formed? What is their function?

A

Formed by the fusion of epitheliod macrophages.

They are secretory

34
Q

Usually central necrosis in granulomateous conditions form what kind?

A

Atypical mycobacterium infection - suppurative
Tb- caseous necrosis
Chrons - no necrosis

35
Q

what does vascular dilation equal in acute inflammation?

A

hyperemia = increase of blood flow to different tissues in the body.

36
Q

how are neutrophils attracted to inflammation sites?

A

chemotaxis

37
Q

what is the major thing in pus?

A

neutrophils

also..necrotic debris and fluid with some fibrin.

38
Q

what does the exudate in fibrrous inflammation have high content of ?

A

plasma protein

39
Q

what is the exudate in purulent inflammation rich in

A

neutrophils

40
Q

what is seen in serous inflammation?

A

transudate

41
Q

when healing by fibrosis, the defect is filled by an ingrowth of what?

A

granulation tissue called organization

42
Q

what is teh granulation tissue (organization) eventually replaced ith?

A

collagen to form a fibrous scar

43
Q

over years, when there is a progressive loss of capillaries, what happens?

A

scar deminishes

44
Q

what is a chronic access?

A

An abscess cavity encapsulated by granulation and fibrous tissue

45
Q

what are the types of chronic inflammation?

A

1) Non-specific-follows non-resolution of acute inflammation, e.g. chronic peptic ulcer, chronic abscess
2) Specific (primary) -response to certain specific types of injurious agents
a. Non-immune mechanism –either granulomatousor non-granulomatous
b. Immune mechanism –either granulomatousor non-granulomatous

46
Q

in non-specific chronic inflammation what goes on?

A

Tissue damage, acute inflammation, granulation tissue, tissue repair and chronic inflammation coexist, with active tissue damage and acute inflammation in one area and adjacent areas of fibrosis and chronic inflammatory infiltrates.

47
Q

what is a key feature of chronic inflammation?

A

activation of macrophages

48
Q

imune type granulomatous response like tb what is another name?

A

Immune type, delayed hypersensitivity response,

49
Q

what can chronic fibrosis lead to ?

A

can result in great morbidity and sometimes mortality

Histology (21 decks)

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