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Anatomical pathology > INFLAMMATION > Flashcards

INFLAMMATION Flashcards

1
Q

OVERVIEW OF INFLAMMATION

A

• A host response to local injury in vascularized tissues to
infection & damaged tissues
• Brings cells and molecules of host defense from the circulation
to eliminate the offending agents
• Not in itself a disease, but is usually a manifestation of
disease.
• Terminates when offending agent is eliminate

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2
Q

Stimuli of Inflammation

A
  • Infections (Bacterial, Viral, Fungal)
  • Trauma (Blunt/Penetrating)
  • Physical & Chemical agents (irradiation, burns, acids)
  • Tissue necrosis
  • Foreign bodies (Sutures)
  • Immune reactions
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3
Q

Classification of Inflammation

A

• Classified into:
• Acute - the initial & often transient series of tissue reaction to
injury.
• Chronic – the subsequent & often prolonged tissue reactions
following the initial response.
• Characterized by differences in the cell types taking part in the
inflammatory response

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4
Q

ACUTE INFLAMMATION

A

• Initial, rapid response: infections/tissue damage
• Within minutes/hours
• Short duration: several hours/ few days
• Exudation of fluid & plasma proteins (oedema)
• Emigration of leukocytes (neutrophils)
• When it fails to clear the stimulus: progress to a protracted phase
of chronic inflammation (CI).

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5
Q

Chronic Inflammation

A
  • It is of longer duration
  • Associated with more tissue destruction
  • Presence of lymphocytes and macrophages
  • Proliferation of blood vessels
  • Deposition of connective tissue

• A response of prolonged duration (weeks or months) in which
inflammation, tissue injury and attempts at repair coexist, in varying
combinations
• May precede AI
• Start insidiously as a low-grade, smoldering response

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6
Q

Cardinal Signs of Inflammation

A
  • Rubor (Redness)
  • Tumor ( Swelling)
  • Calor (Heat)
  • Dolor ( Pain)
  • Functio laesa(Loss of function)
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7
Q

Components of Acute & Chronic Inflammation

A

• Major participants: blood vessels & leukocytes
• Blood vessels dilate: slow down blood flow & increase their
permeability
• Characteristics of the endothelium lining change: leukocytes migrate
into the tissues.
• Leukocytes are activated: Ingest & destroy microbes and dead cells

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8
Q

Sequence Of Events

A

• Recognition of offending agent by host
cells in extravascular tissue
• Recruitment of leukocytes and plasma
proteins into the tissues
• Removal of the stimulus for inflammation
• Regulation of the response
• Repair of damaged tissue

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9
Q

the acute inflammatory response involves:

A

a) Vascular changes

b) Cellular events (leukocytes)

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10
Q

Vascular changes

A

Vasodilation
• Induced by the action of several mediators:
histamine on vascular smooth muscle
• Earliest manifestations of AI
• First involves the arterioles and then leads to
opening of new capillary beds in the area.
• Increased blood flow: heat & redness
(erythema)

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11
Q

Increased permeability of the microvasculature

A

• Contraction of endothelial cells: increased
interendothelial spaces
• outpouring of protein-rich fluid : extravascular
tissues

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12
Q

STASIS IN VASCULAR CHANGES

A

• Slower blood flow, concentration of red cells in small vessels,
and increased viscosity of the blood.
• Engorgement of small vessels
• Vascular congestion & localized redness
• Neutrophils, accumulate along the vascular endothelium
• Endothelial cells are activated by mediators: express increased
levels of adhesion molecules

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13
Q

Characteristics of Leaked Fluid (Exudation)

A

• Escape of fluid, proteins and blood cells from blood into tissue or
body cavities exudation.
• An exudate is an extravascular fluid that has a high protein
concentration & contains cellular debris.
• A transudate is a fluid with low protein content, little or no
cellular material, and low specific gravity
• Oedema denotes an excess of fluid in the interstitial tissue or
serous cavities & can be an exudate or a transudate.
• Pus - a purulent exudate: leukocytes, dead cells & microbes

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14
Q

Characteristics of Oedema

A

Exudate

Specific gravity ≥1.020
Protein content High
Cells & debris High
cause by inflammatory

Transudate

 Protein content low
Cells & debris low
 specific gravity <1.020
caused by Inflammatory & 
Others
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15
Q

Cellular Events in Acute Inflammation

A

• Recruitment of Leukocytes to sites of infection and injury
1. In the lumen: margination, rolling, & adhesion to
endothelium.
2. Transmigration across the endothelium (diapedesis)
3. Migration in interstitial tissues toward a chemotactic
stimulus

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16
Q

mechanism of margination

A

White blood cells are confined to a central axial column of the vessel.
• Due to stasis hemodynamic conditions change, & more white cells assume a peripheral position along the endothelial surface

17
Q

ROLLING AND ADHESION

A
  • Leukocytes tumble slowly along the endothelium & adhere transiently (rolling),
  • Finally coming to rest at some point where they adhere firmly (adhesion)
18
Q

diapedesis

A
  • Leukocytes insert pseudopods into the interendothelial junctions & squeeze through to assume a position between the endothelial cell & the basement membrane
  • Traverse the basement membrane & escape into the extravascular space
19
Q

Morphologic Patterns of Acute Inflammation

A

• Morphologic hallmarks - Dilation of small blood vessels & accumulation of
leukocytes and fluid in the extravascular tissue.
• Special morphologic patterns are often superimposed
- Severity of the reaction
- Specific cause
- Particular tissue and site involved
• Provide valuable clues about the underlying cause

20
Q

Serous inflammation

A

Exudation of cell poor fluid into spaces created by cell injury or into body cavities lined
• Increased vascular permeability) or from the secretions of mesothelial cells
• Transudate e.g. Skin blister from a
burn

21
Q

Fibrinous inflammation

A
  • Vascular leaks are large/there is a local pro-coagulant stimulus (e.g. cancer cells)
  • Fibrinogen leaks & Fibrin is formed
  • Characteristic of inflammation lining body cavities e.g. pericardium• Lead to scarring - organisation
22
Q

PURULENT (SUPPURATIVE) INFLAMMATION

A

• An exudate - neutrophils, liquefied debris of
necrotic cells, and edema fluid(pus).
• Bacterial infection (pyogenic)-staphylococci
• Produced by seeding of pyogenic bacteria
• Acute appendicitis

23
Q

ULCERS

A
  • A local defect of the surface of an organ
  • Produced by the shedding of inflamed necrotic tissue.
  • Peptic ulcer
  • Chronic = Fibroblasts, scarring and inflammatory cells
24
Q

Outcomes of Acute Inflammation

A

• Complete resolution - little tissue destruction & removal of
microbes
• Healing by scarring, or fibrosis in tissue incapable of
regeneration
• Chronic inflammation- persistence of agent or disturbance
in healing

25
Q

Mediators of Inflammation

A

• Substances that initiate & regulate inflammatory reactions
• Most important are vasoactive amines, lipid products (prostaglandins
and leukotrienes), cytokines (including chemokines), and complement
activation.
• Either secreted by cells/generated from plasma proteins
• The major cell types are the sentinels that detect invaders and tissue
damage
• Plasma derived mediators produced in the liver

26
Q

Causes of Chronic Inflammation

A

• Persistent infections e.g. Mycobacteria
• Hypersensitivity diseases - excessive activation of immune system/
unregulated immune responses against microbes or common
environmental substances
• Prolonged exposure to potentially toxic agents e.g. silicosis
• Sometimes takes specific pattern - granulomatous reaction
• Fibrosis may dominate the late stages

27
Q

MORPHOLOGY OF CHRONIC INFLAMMATION

A 
Infiltration with mononuclear cells; 
macrophages, lymphocytes & 
plasma cells 
• Tissue destruction
• Attempts at healing by connective 
tissue replacement of damaged 
tissue (angiogenesis & fibrosis)
28
Q

GRANULOMATOUS INFLAMMATION

A

Collections of activated macrophages(epithelioid cells)
• Epithelioid cells & multinucleated giant cells
• Foreign body granulomas (talc)
• Immune granulomas (cytokines e.g. IL2)

29
Q

Morphology of Granulomatous Inflammation

A

• Aggregates of epithelioid macrophages are surrounded by a collar
of lymphocytes
• In Mycobacterium tuberculosis a combination of hypoxia and free
radical–mediated injury leads to a central zone of necrosis
• Grossly, this has a granular, cheesy appearance and is therefore
called caseous necrosis
• Microscopically, appears as amorphous, structureless, eosinophilic,
granular debris, with complete loss of cellular details

30
Q

Differential of Granulomatous Inflammation

A
  • Limited number of conditions that cause it (some life-threatening)
  • TB granuloma, referred to as a tubercle
  • Leprosy
  • Syphilis
  • Disease of Unknown aetiology - Sarcoidosis
  • Crohn disease
31
Q

Systemic Effects of Inflammation

A

• Inflammation is associated with cytokine-induced systemic
reactions that are collectively called the acute-phase response:
- Fever
- Acute-phase proteins (C-Reactive Protein)
- Leukocytosis
• Other: ↑ pulse &BP, shivering, chills, anorexia, somnolence, and
malaise, probably because of the actions of cytokines on brain
cells

32
Q

fever

A
  • An elevation by 1° to 4°C
  • Substances that induce fever are called pyrogens
  • Caused by prostaglandins: hypothalamus
  • NSAIDs: inhibit prostaglandin synthesis
33
Q

Acute phase proteins

A

• Mostly synthesized in the liver
• Plasma concentrations: Increase several hundred-fold
• Three of the best-known of these proteins are
- C-reactive protein (CRP)
- Fibrinogen
- Serum amyloid A (SAA) protein

34
Q

Leukocytosis

A

• Leukocyte count ++ 15,000 /20,000 cells/mL > 100,000 cells/mL.
• Most bacterial infections = increase neutrophil count: neutrophilia
• Viral infections = increase in lymphocytes: lymphocytosis
• In some allergies and parasitic infestations = increase in
eosinophils: eosinophilia.
• Certain infections are associated with a decreased number of
circulating white cells leukopenia

35
Q

Other Systemic effects of Inflammation

A

• Disseminated Intravascular Coagulation (DIC)
• Hypotensive shock
• Metabolic disturbances (including insulin resistance and
hyperglycemia
• This clinical triad is known as septic shock

Anatomical pathology (13 decks)

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