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Lecture 5 Theory 3

The lecture covers the morphologic patterns and outcomes of acute inflammation, as well as chronic and granulomatous inflammation. It details the systemic effects of inflammation, including the acute phase response and various clinical manifestations. Key differences between acute and chronic inflammation are also highlighted.

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Noor Farhan
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2 views

Lecture 5 Theory 3

The lecture covers the morphologic patterns and outcomes of acute inflammation, as well as chronic and granulomatous inflammation. It details the systemic effects of inflammation, including the acute phase response and various clinical manifestations. Key differences between acute and chronic inflammation are also highlighted.

Uploaded by

Noor Farhan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Inflammation-2

Lec: 5

Dr. Payman Anwar Rashid


7/11/2024

Faculty of Pharmacy
Fall Semester
General Pathology
Grade 3
Week - 5
Lecture Outline:

• Morphologic patterns of acute inflammation

• Outcomes of acute inflammation

• Chronic inflammation

• Granulomatous inflammation

• Systemic Effects of Inflammation


Morphologic patterns of acute
inflammation
1. Serous
• Watery, protein-poor effusion
• E.g. blister
2. Fibrinous
Fibrin accumulation
Either entirely removed or becomes fibrotic
E.g. fibrinous pericarditis
3. Suppurative
• Presence of pus
• Often walled-off if persistent
• E.g. acute appendicitis
4. Ulceration
•Necrotic and eroded epithelial surface
•Underlying acute and chronic inflammation
•Trauma, toxins, vascular insufficiency
•E.g. peptic ulcer
Outcomes of acute inflammation

• 1. Complete resolution
• Little tissue damage
• Tissue capable of regeneration
• 2. Scarring (fibrosis)
• In tissues unable to regenerate
• Excessive fibrin deposition organized into
fibrous tissue
• 3. Abscess formation occurs with some bacterial
or fungal infections.

• 4. Progression to chronic inflammation


Chronic inflammation

• Chronic inflammation is of longer duration (days


to years) and is characterized by:
• mononuclear inflammatory cell infiltration,
• vascular proliferation, and
• scarring (fibrosis).
Chronic inflammation

• Mononuclear cell infiltration e.g Lymphocyte,


macrophage, plasma cell
• Tissue destruction by inflammatory cells
• Attempts at repair with fibrosis and
angiogenesis (new vessel formation)
• Causes:
• Persistent injury or infection (ulcer, TB)
• Prolonged toxic agent exposure (silica)
• Autoimmune disease states (RA, SLE)
The dominant cellular player in chronic
inflammation is the tissue macrophage
Blood monocyte Tissue macrophage (RES)

migrate into
tissue
within 48 hours
after injury

and differentiate

- Kupffer cell (liver)


- Microglia (CNS)
- Histiocytes (spleen)
- Alveolar macrophages (lung)
Lymphocyte Plasma cell

* however mast cells and eosinophils are as well


involved in chronic allergic diseases
Granulomatous Inflammation
It is a distinctive form of chronic inflammation
characterized by granuloma formation which is
nodular collection of epithelioid cells (activated
macrophage) surrounded by a collar of lymphocytes.
Epithelioid macrophage may fuse to form
multinucleate giant cells and central necrosis may be
present e.g. in tuberculosis.
Granulomatous inflammation
Gross Appearance Lung caseating necrosis

Tuberculosis
Systemic Effects of Inflammation
It is called acute phase response or systemic
inflammatory response syndrome (SIRS) which
represent responses to cytokines produced either by
bacterial products or by other inflammatory stimuli
and include the following clinical and pathological
changes:
1. Fever.
2. Acute Phase Protein: these are plasma protein
synthesized in liver and increases in response
to inflammatory stimuli e.g C-reactive protein.
3. Leukocytosis
• Elevated white blood cell count:
Bacterial infection (neutrophilia).
Parasitic infection (eosinophilia).
Viral infection (lymphocytosis).
4. Other manifestations include:
- increased pulse and blood pressure.
- decreased sweating.
- rigors, chills.
- anorexia.
- malaise.
5. In severe bacterial infections may lead to
septic shock.
Features Acute Chronic
Inflammation Inflammation
Duration Short (hours - Long (weeks-
days) months)
Onset Acute Insidious

Cardinal Present Absent


clinical
signs

Fluid Present Absent


exudation
& edema
Vascular Active vasodilation New vessel formation
changes Increased (granulation tissue)
permeability

Inflamma- Neutrophils macrophages,


tory cells Lymphocytes, plasma
cells, fibroblasts .

Fibrosis Absent Present


Thank You

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