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ACUTE INFLAMMATION VS CHRONIC INFLAMMATION &

GRANULOMATOUS INFLAMMATION

ALI AASAM KHAN

CU-1774-2020

DEPARTMENT OF PHARMACY, CECOS UNIVERSITY OF IT & EMERGING

SCIENCES, PESHAWAR, KHYBER PAKHTUNKHWA, PAKISTAN

PATHOLOGY

PHARM-514

SUBMITTED TO: MAM SANA HAIDER

DATE: JANUARY 10, 2023

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Question No # 1: Write a brief note on Granulomatous Inflammation. How can Acute

Inflammation be differentiated from Chronic Inflammation (12-15 points)?

Answer: INFLAMMATION:

Is described as Inflammation is the dynamic process

by which living tissues react to an injury. It concerns vascular and connective tissues in

particular.

OR

Inflammation is a response of vascularized tissues to

infections and tissue damage that brings cells and molecules of host defense from the circulation

to the sites where they are needed, to eliminate the offending agents.

Serial PARAMETERS ACUTE INFLAMMATION CHRONIC INFLAMMATION

No

1- Definition It is defined as the immediate and early It is defined as the inflammation of

response to tissue injury which can be either prolonged duration (weeks to years) in

physical or microbiologic. which continuing inflammation, tissue

injury, and healing often by fibrosis

proceeds simultaneously.

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2- Causes The pathogen, Harmful stimulations, and Pathogens, Foreign particles, and also the

open wounds (damaged cells) allergens are present that keep triggering the

acute inflammation that ends up becoming

chronic

3- Immune cells The major immune cells which are The macrophages and lymphocytes are

responsible for the phagocytosis of harmful major immune cells responsible for the

pathogens are neutrophils. phagocytosis of harmful invaders. Although

neutrophils are also present, the main role is

of the above-mentioned cells.

4- Inflammatory The key inflammatory mediators are The key mediators in chronic inflammation

Mediators histamines and eicosanoids are cytokines, growth factors, reactive

oxygen species, and hydrolase.

5- Types of The responses in acute inflammation are The responses in chronic inflammation are

Responses immediate, fixed, and standard processes. delayed and ever-changing.

6- Duration The duration of acute inflammation ranges The duration of chronic inflammation ranges

from a few minutes to a few weeks from a few weeks to months or even a few

years

7- Signs There are five cardinal signs of acute The following are the signs of chronic

inflammation which are the following: inflammation:

Redness (Rubor) Abdominal pain

Swelling (Tumor) Chest Pain

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Heat (Calor) Fatigue

Pain (Dolar) Fever

Function loss (Functio laesa) Joint pain or stiffness

Mouth sores

Rashes

8- Symptoms Redness, swollen, Pain sensation & burning Growth of new blood vessels and fibroblast

which will lead to the formation of dry,

rough protective scab over the wounds

Body pain, arthralgia, myalgia.

Chronic fatigue and insomnia.

Depression, anxiety, and mood

disorders.

Gastrointestinal complications like

constipation, diarrhea, and acid

reflux.

Weight gain or weight loss.

Frequent infections.

9- Complications The possible complication of acute The possible complications associated with

inflammation is the following: chronic inflammation are the following:

Damage to normal tissue Damaging the healthy cells, tissues,

Obstruction of tubes and organs

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Compression of vital structures It can cause internal scarring, tissue

death, and damage to the DNA in

previously healthy cells

10- Mechanism Acute inflammation is characterized by the Chronic inflammation is characterized by the

following processes: following processes:

Vasodilation Infiltration

Fluid exudation Tissue Destruction

Neutrophil infiltration Healing

These processes are activated and

amplified by a series of intracellular

and extracellular factors that tightly

coordinate the inflammatory process.

The innate immune system responds

rapidly to infection or injury.

11- Stages Acute inflammation consists of two stages: Chronic inflammation consists of the

following stages:
Vascular phase

Cellular phase Chronic non-specific inflammation

Chronic granulomatous inflammation

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12- Possible The following are the possible outcomes of The following are the possible outcomes of

Outcomes acute inflammation: chronic inflammation:

Complete resolution - with total Continued chronic inflammation

repair and destruction of the Change in tissue function

insult.  Atrophy

Fibrosis  Metaplasia (Change in cell

scar formation type)

Resolution (Damaging stimulus is

removed, healing can occur)

Scarring with dysfunction (Cirrhosis

in viral hepatitis)

Catastrophe (Damaging stimulus

increases, tissue healing response

weakens and the tissue damage

worsens

Example: Perforated gastric ulcer

13- Local and Prominent Less prominent, less subtle

systemic signs

14- Tissue injury, Usually mild & self-limited Often severe and progressive

fibrosis

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15- Histology In acute inflammation polymorphonuclear In Chronic inflammation

neutrophils usually predominate macrophages and lymphocytes

16- Systemic Fever often high Low-grade fever

manifestations

17- Specificity Non-specific Specific (where the immune

response is activated)

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Question No # 2: Write a brief note on granulomatous inflammation?

Answer: Granulomatous Inflammation:

This is the term given to forms of chronic

inflammation in which modified macrophages (epithelioid cells) accumulate in small

clusters surrounded by lymphocytes. The small clusters are called granulomas.

Example:

The basic lesion in tuberculosis is a good example.

Granulomatous inflammation is a histologic pattern of tissue reaction which appears following

cell injury.

Granulomatous inflammation may be defined as a type of chronic inflammation in which a

compact collection of cells of the mononuclear phagocyte system 37, chiefly activated

macrophages and cells derived from them are predominant.

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These cells are aggregated into well-demarcated focal lesions and the designation granuloma

(granule + oma = tumor) derives from this peculiar aspect. In addition, granulomas usually

contain an admixture of other cells, especially lymphocytes and plasma cells, and, depending on

their stage, fibroblasts39. Eosinophils are usually present in parasitic and fungal granulomas.

The distinctive pattern of chronic inflammation. Cellular attempt to contain an offending agent

that is difficult to eradicate (i.e. Tb)

Protective response to chronic infection or foreign material, preventing dissemination and

restricting inflammation.

Persistent, low-grade antigenic stimulation

Hypersensitivity

GRANULOMA:

A granuloma is a microscopic aggregation of macrophages that are

transformed into epithelioid cells and giant cells surrounded by a collar of mononuclear

leukocytes, principally lymphocytes and occasionally plasma cells.

Causes of Granulomatous inflammation

INFECTIVE

Bacterial

Tuberculosis (Mycobacterium tuberculosis)

Leprosy (Mycobacterium leprae)

Syphilitic gumma (Treponema pallidum)

Parasitic

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Schistosomiasis (Schistosoma mansoni, S. haematobium,

S. japonicum)

Fungal

Histoplasma capsulatum

Blastomycosis

Cryptococcus neoformans

Coccidiodes immitis

Inorganic Metals or Dusts

Silicosis

Berylliosis

Foreign Body

Suture, breast prosthesis, vascular graft

Unknown

Sarcoidosis

CELLS IN GRANULOMAS

*Macrophages are almost all recruited directly from the bloodstream monocytes.

*Epithelioid cells have abundant pink cytoplasm, indistinct borders, and elongated

Granulomatous inflammation is a type of chronic inflammation in which aggregates of

macrophages, T cells and neutrophils form at a site of infection which result in granuloma

formation. The activated macro-phages may develop abundant cytoplasm and begin to resemble

epithelial cells, and are called epithelioid cells. Some activated macrophages may fuse, forming

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multinucleate giant cells. Granuloma formation is a cellular attempt to contain an offending

agent that is difficult to eradicate. In this attempt there is often strong activation of T

lymphocytes leading to macrophage activation, which can cause injury tonormal tissues.

Types of granulomatous inflammation

Immune granulomas are caused by a variety of agents that are capable of inducing a persistent T

cell– mediated immune response. This type of immune response produces granulomas usually

when the inciting agent cannot be readily eliminated, such as a persistent microbe or a self

antigen.

In such responses, macro-phages activate T cells to produce cytokines, such asIL-2, which

activates other T cells, perpetuating the response, and IFN-γ, which activates the

macrophages.

Foreign body granulomas are seen in response to relatively inert foreign bodies, in the absence

of T cell– mediated immune responses. Typically, foreign body granulomas form

aroundmaterials such as talc (associated with intravenous drug abuse), sutures, or other fibers

that are large enough to preclude phagocytosis by a macrophage but are not immunogenic.

Epithelioid cells and giant cells are apposed to the surface of the foreign body. The foreign

material can usually be identified in the center of the granuloma, particularly if viewed with

polarized light, in which it may appear refractile.

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Causes of Granulomatous inflammation

Granulomas form in response to chronic inflammation. Accordingly, the most common cause of

granulomas are infections. Caseating granulomas are formed by infections, such as tuberculosis

and fungal infections.

Noncaseating granulomas may be formed by an inflammatory condition (e.g., sarcoidosis and

Crohn’s disease), vasculitis, and exposure to foreign objects. The formation of granulomas is

characteristic of certain diseases. Most commonly, in chronic granulomatous disease (CGD), an

inherited genetic mutation reduces the ability of white blood cells to kill certain bacteria and

fungi, like Staphylococcus aureus and Aspergillus. Individuals with CGD are highly susceptible

to infections that lead to granuloma development throughout the body. Similarly, granuloma

annulare is a chronic skin disorder characterized by granulomas appearing as small red or yellow

bumps in a ring shape on the skin. Finally, granulomatosis with polyangiitis (GPA) is a rare

autoimmune-induced vasculitis characterized by granuloma formation, causing inflammation of

the blood vessels (primarily small-sized arteries) and, ultimately, affecting blood flow.

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Fig: BCG-induced granulomatous inflammation in patients with APDS. 1, Granulomatous skin

lesion in a 4-year-old at the site of BCG vaccination administered at 4 months of age. 2, Skin

biopsy specimen showing granulomatous inflammation.

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REFERENCES:

1-Acute Inflammation. Available from: CHAPTER 3 INFLAMMATION, HEALING AND

REPAIR. dokumen.pub_pathology-illustrated-8th-edition-9780702072031-9780702072048.pdf

https://pubmed.ncbi.nlm.nih.gov/32310543/#:~:text=Inflammation%20can%20divide%20into%2

0three,and%20subacute%20which%20is%20a

Last Accessed: DECEMBER 10, 2023

2- Chronic Inflammation. Available from: CHAPTER 3 INFLAMMATION, HEALING AND

REPAIR.

dokumen.pub_pathology-illustrated-8th-edition-9780702072031-9780702072048.pdf

Last Accessed: DECEMBER 10, 2023

3- Granulomatous Inflammation. Available from: Chapter# 3 Inflammation and Repair

Robbins_Basic_Pathology_10th_Edition.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC498378/pdf/jclinpath00512-0001.pdf

https://www.scielo.br/j/rimtsp/a/pWjmn6YMffmxJnRXDN8yRJD/?lang=en

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Last Accessed: December 10, 2023

4- Granulomatous Inflammation. Available from: https://www.researchgate.net/figure/BCG-

induced-granulomatous-inflammation-in-patients-with-APDS-1-Granulomatous-

skin_fig1_308360233 http://ilovepathology.com/granulomatous-inflammation/

Last Accessed: December 10, 2023

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