Healing Question And Answers

Inflammation And Healing

 

Question 1. What are the various types of healing of tissues? Describe in detail the healing of the bone fracture.
Or
Write a brief on healing by second intention (secondary union).
Answer:

There are two types of healing of tissues, i.e.

• Healing by primary intention:
• Healing by secondary intention.

Healing by Secondary Intention

This is defined as the healing of wounds having the following characteristics:

• The wound is not approximated by surgical sutures and is left open
• Open with large tissue defects at times it is infected.
• Having extensive loss of cells and tissues.

Read And Learn More: Pathology Question And Answers

The Sequence of Events in Secondary Intention Healing

• Initial Hemorrhage: Due to injury wound space is filled with blood, fibrin clot is formed which gets dried.
• Inflammatory Phase: Initial acute inflammatory response followed by the appearance of macrophages that clear of debris.
• Epithelial Changes: The basal cells of the epidermis from both cut margins start proliferating and marginating towards incisional space in the form of epithelial spurs till they meet in the middle and re-epithelialize gap completely. Proliferating epithelial cells do not cover the gap completely until granulation tissue from the base starts filing wound space. In this way, the scab is formed which is cast off In time regenerated epidermis becomes stratified and keratinized.
• Granulation Tissue: Main bulk of secondary healing is by granulation. Granulation tissue is formed by the proliferation of fibroblasts and neovascularization from the adjoining viable elements. Newly formed granulation tissue is deep red, granular and fragile. With time scar on maturation become pale.
• Wound Contraction: Due to the presence of myofibroblasts in granular tissue wound contracts to one-third and one-fourth of its original size.
• Presence of Infection: Bacterial contamination of open wounds delays the process of healing because of bacterial toxins. Surgical removal of dead and necrosed tissue prevents bacterial infection of open wounds.

Question 2. Write short notes on the repair of wounds and bones.
Answer:

Repair of Wound

When the healing takes place by the proliferation of connective tissue elements resulting in fibrosis and scarring.

Two processes are involved in the repair:

• Granulation Tissue Formation
• Contraction of Wounds.

Granulation Tissue Formation

Granulation tissue is the proliferation of new small blood vessels which are slightly lifted on the surface by a thin covering of fibroblasts and young collagen.

The following 3 phases are observed in the formation of granulation tissue:

• The phase of Inflammation: Following trauma, blood clots at the site of injury. There is an acute inflammatory response with the exudation of plasma, neutrophils, and some monocytes.
• The phase of Clearance: Combination of proteolytic enzymes liberated from neutrophils, autolytic enzymes from dead tissue cells, and phagocytic activity macrophages clear of the necrotic tissue, debris, and blood cells.
• Phase of Ingrowth of Granulation Tissue: This phase consists of 2 main processes: angiogenesis or neovascularization, and fibrogenesis
  • Angiogenesis: The formation of new blood vessels at the site of injury takes place by the proliferation of endothelial cells from the margins of severed blood vessels. Initially, the proliferated endothelial cells are solid buds but within a few hours develop lumen and start carrying blood. The newly formed vessels are more leaky accounting for the edematous appearance of new granulation tissue. Soon, these blood vessels differentiate into muscular arterioles, thin-walled venules, and true capillaries.
  • Fibrogenesis: The newly formed blood vessels are present in an amorphous ground substance or matrix. The new fibroblasts originate from fibrocytes as well as by mitotic division of fibroblasts. Some of these fibroblasts have a combination of morphologic and functional characteristics of smooth muscle cells known as myofibroblasts. Collagen fibrils begin to appear by about 6th day. As maturation proceeds, more and more of collagen is formed while the number of active fibroblasts and new blood vessels decreases. This results in the formation of an inactive-looking scar known as cicatrization.

Contraction of Wound

The wound starts contracting after 2-3 days and the process is completed by the 14th day. During this period, the wound is reduced by approximately 80% of its original size. Contracted wound results in rapid healing since a lesser surface area of the injured tissue has to be replaced.

Repair of Bone

Question 43. Describe inflammatory cells.
Answer:

Following are the inflammatory cells i.e.

Circulating leucocytes, i.e. polymorphonuclear neutrophils, eosinophils, basophils, and lymphocytes

Plasma cells

Tissue macrophages.

Inflammatory cells Polymorphonuclear Neutrophils

• Commonly called neutrophils or polymorphs, these cells along with basophils and eosinophils are known as granulocytes due to the presence of granules in the cytoplasm.
• These granules contain many substances like proteases, myeloperoxidase, lysozyme, esterase, aryl sulfatase, acid and alkaline phosphatase, and cationic proteins.
• The diameter of neutrophils ranges from 10 to 15 µm and is actively motile.
• These cells comprise 40-75% of circulating leucocytes and their number is increased in blood (neutrophilia) and tissues in acute bacterial infections.
• These cells arise in the bone marrow from stem cells.
• The functions of neutrophils in inflammation are as follows:
  • Initial phagocytosis of micro-organisms as they form the first line of body defense in bacterial infection. The steps involved are the adhesion of neutrophils to vascular endothelium, emigration through the vessel wall, chemotaxis, engulfment, degranulation, killing, and degradation of the foreign material.
  • Engulfment of antigen-antibody complexes and nonmicrobial material.
  • The harmful effects of neutrophils are the destruction of the basement membranes of glomeruli and small blood vessels.

inflammatory cells Eosinophils

• These are larger than neutrophils but are fewer in number, comprising 1 to 6% of total blood leucocytes.
• Eosinophils share many structural and functional similarities with neutrophils like their production in the bone marrow, locomotion, phagocytosis, lobed nucleus, and presence of granules in the cytoplasm containing a variety of enzymes, of which major basic protein and eosinophil cationic protein is the most important which have bactericidal and toxic action against helminthic parasites. However, granules of eosinophils are richer in myeloperoxidase than neutrophils and lack lysozyme.
• High level of steroid hormones leads to a fall in the number of eosinophils and even disappearance from blood.
• The absolute number of eosinophils is increased in the following conditions and, thus, they take part in inflammatory responses associated with these conditions:
• • Allergic conditions
  • Parasitic infestations
  • Skin diseases
  • Certain malignant lymphomas.

Inflammatory cells Basophils

• Basophils comprise about l% of circulating leucocytes and are morphologically and pharmacologically similar to mast cells of the tissue.
• These cells contain coarse basophilic granules in the cytoplasm and a polymorphonuclear nucleus.
• These granules are laden with heparin and histamine.
• Basophils and mast cells have receptors for IgE and degranulate when cross-linked with antigens.
• The role of these cells in inflammation are:
• • In the immediate and delayed types of hypersensitivity reactions
  • Release of histamine by IgE-sensitised basophils.

Inflammatory cells Lymphocytes

• These cells are the most numerous of the circulating leucocytes (20-45%).
• Apart from blood, lymphocytes are present in large numbers in the spleen, thymus, lymph nodes, and mucosa-associated lymphoid tissue (MALT).
• They have scanty cytoplasm and consist almost entirely of a nucleus.
• Besides their role in antibody formation (B lymphocytes) and in cell-mediated immunity (T lymphocytes), these cells participate in the following types of inflammatory responses:
• • In tissues, they are dominant cells in chronic inflammation and late-stage acute inflammation.
  • In blood, their number is increased in chronic infections like tuberculosis.

Inflammatory cells Plasma Cells

• These cells are larger than lymphocytes with more abundant cytoplasm and an eccentric nucleus that has a cartwheel pattern of chromatin.

• Plasma cells are normally not seen in peripheral blood.
• They develop from lymphocytes and are rich in RNA and ?-globulin in their cytoplasm. There is an inter-relationship between plasmacytosis and hyperglobulinemia. These cells are most active in antibody synthesis.
• Their number is increased in the following conditions:
• • Prolonged infection with immunological responses, For Example. in syphilis, rheumatoid arthritis, tuberculosis
  • Hypersensitivity reactions
  • Multiple myeloma.

Mononuclear-Phagocyte System

Following is the role of macrophages in inflammation:

• Phagocytosis (cell eating) and pinocytosis (cell drinking).
• Macrophages on activation by lymphokines released by T lymphocytes or by non-immunologic stimuli elaborate a variety of biologically active substances such as:
  • Proteases like collagenase and elastase degrade collagen and elastic tissue.
  • Plasminogen activator which activates the fibrinolytic system.
  • Products of complement.
  • Some coagulation factors convert fibrinogen to fibrin.
  • Chemotactic agents for other leucocytes.
  • Metabolites of arachidonic acid.
  • Growth-promoting factors for fibroblasts, blood vessels, and granulocytes.
  • Cytokines like interleukin-1 and tumor necrosis factor.
  • Oxygen-derived free radicals.

Question 4. Write a short note on the tubercle.
Answer:

Tubercle is formed by the tubercle bacilli.

Following is the sequence of events for the formation of tubercle bacilli:

• As tubercle bacilli are ingested in the body they are lodged in pulmonary capillaries. Now neutrophils are evoked and they destroy the organisms.
• After 12 hours progressive infiltration of macrophages takes place.
• Macrophages start phagocytosing of tubercle bacilli and either kill bacteria or die. In the latter case, they further proliferate locally as well as there is increased recruitment of macrophages from blood monocytes.
• As a part of the body’s immune response, T and B cells are activated. Activated CD4+T cells develop the cell-mediated delayed-type hypersensitivity reaction, while B cells result in the formation of antibodies that play no role in the body’s defense against tubercle bacilli.
• In 2-3 days, the macrophages undergo structural changes as a result of immune mechanisms—the cytoplasm becomes pale and eosinophilic and their nuclei become elongated and vesicular. This modified macrophage resembles epithelial cells and is called epithelioid cells.
• The epithelioid cells aggregate into tight clusters or granulomas.
• Some of the macrophages form multinucleated giant cells by fusion of adjacent cells.
• Around the mass of epithelioid cells and giant cells is a zone of lymphocytes, plasma cells, and fibroblasts. The lesion at this stage is called a hard tubercle due to the absence of central necrosis.
• Within 10-14 days, the center of the cellular mass begins to undergo caseation necrosis, characterized by a cheesy appearance and high lipid content. This stage is called as soft tubercle which is the hallmark of tuberculous lesions.
• The soft tubercle which is a fully-developed granuloma with a caseous center does not favor the rapid proliferation of tubercle bacilli.

Question 5. Write a short note on granulomatous lesions.
Answer:

Classification of granulomatous lesions or diseases

Specific or Infective Type

• Bacterial
  • Tuberculosis
  • Leprosy
  • Syphilis
  • Granuloma inguinale
  • Brucellosis
  • Cat scratch disease
  • Tularemia
  • Glanders
  • Actinomycosis.
• Fungal
  • Blastomycosis
  • Cryptococcosis
  • Coccidioidomycosis
  • Histoplasmosis
  • Parasitic
  • Schistosomiasis.
• Non­-Specific
  • Sarcoidosis
  • Crohn’s disease
  • Silicosis
  • Berylliosis
  • Foreign body granuloma
  • Orofacial granulomatosis.

Question 6. Define inflammation. Give causes.
Answer:

Causes inflammation

1. Physical agents: Heat, cold, radiation, and mechanical trauma.
2. Chemical agents: Organic and inorganic poisons
3. Infective agents: Bacteria, virus, and their toxins
4. Immunological agents: Cell-mediated and antigen-antibody reactions.

Question 7. Write a short note on cervicofacial actinomycosis.
Answer:

Cervicofacial actinomycosis is a chronic granulomatous suppurative and fibrosing disease caused by anaerobic or microaerophilic, Gram-positive, non-acid fast, branched filamentous bacteria.

Cervicofacial actinomycosis Pathogenesis

The infection enters from the tonsils, carious teeth, periodontal disease or trauma following tooth extraction. A firm swelling develops in the lower jaw.

There is the presence of initial acute inflammation followed by a chronic indolent phase. The lesion appears as single Or multiple induration.

Cervicofacial actinomycosis Clinical Features

• Commonly seen in adult males.
• The submandibular region is commonly infected.
• Trismus is the common feature that is present.

Cervicofacial actinomycosis Laboratory Diagnosis

• Biopsy: Biopsy from the lesional tissue is taken and is assessed microscopically. On microscopic examination, the following features are seen:
  • There is the presence of a granuloma with central suppuration.
  • There is a formation of an abscess in the center of the lesion and at the periphery are seen chronic inflammatory cells, giant cells, and fibroblasts.
  • The center of each abscess contains a bacterial colony ‘sulfur granule’ characterized by radiating filaments with hyaline, eosinophilic, club-like representatives of secreted immunoglobulins.
• Microscopy: Pus from the lesion is collected. Pus is withdrawn with a capillary pipette. Granules may also be obtained by applying gauze pads over the discharging sinuses. The granules are white or yellowish and range in size from minute specks to about 5 mm. They are examined microscopically under a coverslip. They are crushed between the slides and stained by Gram stain and examined. The granules are bacterial colonies that are found to consist of dense networkofthinGram-positive filaments surrounded by a peripheral zone of swollen radiating club-shaped structures presenting a sun ray appearance. Clubs are Gram-negative, acid-fast, and are of host origin.
• Staining: By Gomori’s methenamine silver stain the organism stain positively.
• Culture: Sulphur granules or pus-containing actinomycetes are washed and inoculated into thioglycollate liquid medium or streaked on brain-heart infusion agar and incubated anaerobically at 37 °C. In thioglycollate, A bovis produces general turbidity whereas A. israelii grows as fluff balls at the bottom of the tube.

Question 8. Write short notes on the types and stages of syphilis.
Answer:

Syphilis is a sexually transmitted disease caused by Treponema pallidum.

Types of Syphilis

• Acquired.
• Congenital

Stages of Syphilis

Acquired syphilis is divided into three stages, i.e.:

• Primary
• Secondary
• Tertiary

Primary Syphilis

• Lesion of primary syphilis is chancre.
• Chancre appears on genital or at extragenital sites in 2 to 4 weeks after exposure to bacteria.
• Initially, lesion is a painless papule that ulcerates in the center and there is the development of a chancre which is indurated lesion.
• Regional lymphadenitis is present.
• Chancre heals without scarring.

Syphilis Pathological Features

• The chancre histologically presents the following features:
• Proliferative granulation tissue is present at the margin of the ulcer.
• Dense infiltrates of plasma cells, lymphocytes, and macrophages.
• Obliterative endarteritis with perivascular infiltration of chronic inflammatory cells.
• T. pallidum may be seen when immunofluorescence studies or silver staining are done.

Secondary Syphilis

• When primary syphilis is not treated patient undergoes mucocutaneous lesions and painless lymphadenopathy in 2 to 3 months.
• Mucocutaneous lesions are mucous patches on the mouth, pharynx, and vagina.
• This stage is highly infective and spirochetes are easily demonstrated in lesions.

Syphilis Pathological Features

• The macular lesion shows inflammatory cell infiltration and obliterative endarteritis.
• The papular lesion exhibits endothelial proliferation, swelling, and perivascular chronic inflammatory cell infiltration.
• Condyloma lata reveals hyperplastic epithelium with hyperkeratosis and acanthosis.
• Obliterative endarteritis may also be seen and there may be occasional presence of epithelioid cells.

Syphilis Tertiary Syphilis

• After the latent period of appearance of secondary lesions and after 2–3 years of initial exposure tertiary lesions appear.
• Lesions of this stage are of two types:
  • Syphilitic gumma: It is a solitary, localized, rubbery lesion with central necrosis seen in organs like the liver, testis, bone, and brain.
  • Diffuse lesions: Seen in nervous and cardiovascular systems. Cardiovascular syphilis involves the thoracic aorta. The wall of the aorta is weakened and dilated due to syphilitic aortitis which leads to an aortic aneurysm. Neurosyphilis manifests as meningioma vascular syphilis affecting the meninges; tabes dorsalis affecting the spinal cord; general paresis affecting the brain.

Syphilis Pathological Features

• The gumma microscopically presents a peripheral rim made up of fibroblasts, which surrounds a central zone of coagulative necrosis.
• Fibroblasts are plump and they often resemble epitheliod cells.
• The occasional presence of giant cells and the regular presence of chronic inflammatory cells like plasma cells, lymphocytes, histiocytes, etc.

Question 9. Write a brief on the role of macrophages in inflammation.
Answer:

Following is the role of macrophages in inflammation:

• Phagocytosis (cell eating) and pinocytosis (cell drinking).
• Macrophages on activation by lymphokines released by T lymphocytes or by non-immunologic stimuli elaborate a variety of biologically active substances such as:
  • Proteases like collagenase and elastase degrade collagen and elastic tissue.
  • Plasminogen activator which activates the fibrinolytic system.
  • Products of complement.
  • Some coagulation factors convert fibrinogen to fibrin.
  • Chemotactic agents for other leucocytes.
  • Metabolites of arachidonic acid.
  • Growth-promoting factors for fibroblasts, blood vessels, and granulocytes.
  • Cytokines like interleukin-1 and tumor necrosis factor.
  • Oxygen-derived free radicals.

Question 10. What is granuloma?
Answer:

Granuloma is defined as a circumscribed tiny lesion about 1 mm in diameter composed predominantly of a collection of modified macrophages known as epithelioid cells and rimmed at the periphery by lymphoid cells.

Question 11. Write briefly on complications of wound healing.
Answer:

The following are the complications of wound healing:

1. Wound infection due to bacteria causes delayed healing
2. Formation of implantation cyst because of the persistence of epithelial cells in the wound after healing.
3. Pigmentation: Healed wounds have rust-like color due to hemosiderin pigmentation. If some colored material is left inside the wound it can persist and provide color to the wound.
4. Deficient scar formation: It can occur due to inadequate formation of granulation tissue.
5. Incisional hernia: Weak scar after laparotomy can be the site of the bursting open of a wound.
6. Hypertrophied scar and keloid formation: Sometimes the scar formed is ugly, excessive, and painful. Excessive formation of collagen in healing may result in the formation of keloid. Hypertrophied scars are confined to the border of the wound while keloids are tumor-like projections of connective tissue.
7. Excessive contraction: Exaggeration of wound contraction leads to the formation of contractures or cicatrization.
8. Neoplasia: It is very rare that a scar may be the site for the development of carcinoma later.

Question 12. Write down the fate and complications of tuberculosis.
Answer:

Fate of Tuberculosis

The fate of tuberculosis is divided into two parts i.e.

• The Fate of primary tuberculosis
• The fate of secondary tuberculosis.

Fate of Primary Tuberculosis

• Lesions of primary tuberculosis of the lung do not progress and heal by fibrosis with time they undergo calcification and ossification.
• In some of cases, the primary focus in the lung continues to grow and caseous material becomes disseminated via bronchi to other parts of the same lung or the opposite lung. It is known as progressive primary tuberculosis.
• Sometimes bacilli enter the circulation via erosion of a blood vessel and spread to various tissues and organs:  This is known as primary military tuberculosis and lesions are seen in organs such as the liver, spleen, kidney, brain and bone marrow.
• In low resistance and increased hypersensitivity of the host, the healed lesions of primary tuberculosis get reactivated. Bacilli lying inactivated in acellular caseous material get activated and lead to progressive secondary tuberculosis.

Complications of Tuberculosis

• Aneurysms of patent arteries that cross the cavity lead to hemoptysis.
• Extension to pleura which produces bronchopleural fistula.
• Extension to pleura-producing bronchopleural fistula.
• Tuberculous empyema due to deposition of caseous material on pleural surface.
• Thickened pleura due to adhesion of parietal pleura.

Question 13. Write the differences between acute and chronic inflammation.
Answer:

Following are the differences between acute and chronic inflammation:

Question 14. Define inflammation. Describe the vascular and cellular events of acute inflammation.
Answer:

Inflammation is defined as the local response of living mammalian tissues to injury due to any agent.

It is a body defense reaction in order to eliminate or limit the spread of injurious agents as well as to remove the consequent necrosed cells and tissues.

Vascular Events of Acute Inflammation

Cellular Events of Acute Inflammation

1. Extravasation of Leucocytes

2. Phagocytosis

Extravasation of leukocytes has the following steps:

• In the lumen: Margination, i.e. peripheral orientation of leukocytes, rolling, i.e. weak attachment of leukocytes to endothelium detachment and binding again, causing
  a rolling movement, pavement or adhesion, i.e. activation of leukocytes and fim binding of leukocytes to the endothelium
• Transmigration across the endothelium (emigration or diapedesis): Emigration is facilitated by the local dissolution of the exposed basement membrane by leukocyte-derived collagenase.
• Migration in interstitial tissue towards a chemotactic stimulus, i.e. chemotaxis.

Question 15. Write briefly on the tubercular lymph node.
Answer:

The tubercular lymph node is mainly the hilar and tracheobronchial lymph nodes in the area drained.

• The affected lymph nodes are matted and show caseation necrosis.
• Nodal lesions are the potential source of reinfection later on.
• Lymphatics draining the lung lesion consist of phagocytes which contain bacilli and may develop beaded, military tubercles along the path of hilar lymph nodes.

Question 16. Write briefly on complications of secondary tuberculosis.
Answer:

The following are the complications of secondary tuberculosis:

• Aneurysms of patent arteries that cross the cavity lead to hemoptysis.
• Extension to pleura which produces bronchopleural fistula.
• Extension to pleura-producing bronchopleural fistula.
• Tuberculous empyema due to deposition of caseous material on pleural surface.
• Thickened pleura due to adhesion of parietal pleura.