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Healing Of Tissues Important Notes

1. Sequence of events of wound healing

• Formation of a blood clot
• Acute inflammatory response
• Organization

2. Primary and secondary intention of healing and their examples

3. Factors inhibiting wound contraction

• Infection
• Foreign bodies
• Poor blood supply
• Ionizing radiation
• Vitamin C deficiency
• Glucocorticoids
• Uncontrolled diabetes

4. Complications of fracture healing

• Fibrous union
• Nonunion
• Delayed union

5. Factors influencing healing

• Local factors
  • Infection – reduces healing
  • Poor blood supply – reduces healing
  • Foreign bodies – reduce healing
  • Movement-reduces healing
  • Ionizing radiation – reduces healing
  • UV light – facilitates healing
• Systemic factors
  • Age-healing is rapid in young
  • Nutrition- vitamin deficiency delays healing
  • Uncontrolled diabetes reduces healing
  • Hematologic abnormalities reduce healing
  • Glucocorticoids reduce healing

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Healing Of Tissues Long Essays

Question 1. Describe the healing of a fracture. Enumerate the causes for nonhealing of fracture
Answer:

• Healing: Is the body’s response to injury in an attempt to restore normal structure and function. Healing involves 2 distinct processes:

1. Regeneration:

• When healing takes place by the proliferation of parenchymal cells and usually results in the complete restoration of the original tissues.

2. Repair:

• When healing takes place by the proliferation of connective tissue elements resulting in fibrosis and scarring at times, both processes take place simultaneously.

Healing of fracture: Healing of fracture by callus forma¬tion depends upon whether the fracture is

• Traumatic/pathological
• Complete/incomplete like green stick fracture and
• Simple, comminuted/compound.
• Healing of fractures takes place by.

1. Primary union:

• Occurs in special situations when the ends of fracture are approximated by the application of compression clamps.
• Here, the bony union takes place with the formation of medullary callus without periosteal callus forma¬tion.

2. Secondary union:

More common type. Takes place in the following manner.

• Procallus formation:
  • Hematoma – Bleeding from torn blood vessels surrounding the fracture.
  • Local inflammatory response – Occurs at the site of injury with exudation of fibrin, polymorphs, and macrophages.
  • In the growth of granulation tissue – With neovascular- polarisation and proliferation of mesenchymal cells from periosteum and endosteum.
  • Calluses formed – composed of woven bone and cartilage.
  • This stage is called provisional callus/precalculus formation.
• Osseous callus formation:
  • Procallus acts as a scaffolding on which an osseous callus composed of lamellar bone is formed.
  • Woven bone is cleared away by osteoclasts, in their place, newly formed blood vessels and os¬teoblasts invade, laying down osteoid which is calcified and lamellar bone is formed by developing a haversian system concentrically around the blood vessels.
• Remodeling:
  • Osteoblastic laying and osteoclastic removal take place during the formation of lamellar bone remodeling the united bone ends.
  • External callus is cleared away compact bone (cortex) is formed in place of intermediate callus, and the bone marrow cavity develops in in¬ternal callus

Causes of nonhealing of fracture :

• Local factors:
  • Infection – the presence of infection delays wound healing.
  • Poor blood supply – delays wound healing
  • Foreign bodies like sutures – delay healing
  • Movement of the injured area – delays healing
  • Exposure to ionizing radiation delays granulation tissue formation.
  • Exposure to UV light – facilitates healing
  • The type, size, and location of injury determine whether healing takes place by resolution/organization.
• Systemic factors:
  • Age-wound healing is rapid in young and slow in aged and debilitated people.
  • Nutrition – nutritional deficiency delays healing
  • Systemic infection – delays wound healing.
  • Uncontrolled diabetes – delay in healing.
  • Haematologic abnormalities – delay wound healing.

Question 2. Describe the healing of a wound by the primary union. Mention the differences between primary and secondary unions.
Answer:

Primary union: Primary union is defined as the healing of a wound which is

• Clean and uninfected
• Surgically incised
• Without much loss of cells and tissue
• Edges are approximated by surgical sutures.

The sequence of events in primary union:

1. Initial hemorrhage:

• Immediately after injury, the space between the surfaces of the wound is Filled with blood which later clots and seals the wound against dehydration and infections.

2. Acute inflammatory response:

• Within 24 hours, polymorphs appear from the margin. By 3rd day, they are replaced by macrophages.

3. Epithelial changes:

• Within 48 hours basal cell layer of the epidermis starts proliferating and forms a layer which separates the viable dermis from the overlying clot and necrotic material. This forms a scab which is cast off. By the 5th day, a new multi-layered epidermis is formed.

4. Organisation:

• Fibroblasts invade the wound area and by the 5th day new collagen fibrils start forming.
• In 4 weeks, scar tissue is with scantly cellular and vascular elements, a few inflammatory cells, and epi trellised surface is formed.

5. Suture tracks:

• Each suture track is a separate wound and incites the same phenomena as in the healing of the primary wound.
• When sutures are removed around 7th day, much of the epithelioid suture track is avulsed and the remaining epithelium tissue in the track is absorbed
• Sometimes, the suture track gets infected (stitch abscess) or the epithelial cells may persist in the track (implantation or epidermal cysts).

Differences between primary and secondary union.

Healing Of Tissues Short Essays

Question 1. Granulation tissues
Answer:

• Granulation tissue is a newly proliferated tissue that is formed during the healing of a wound by secondary inten¬tion.
• It takes place in 3 steps:

1. Inflammation:

• After the injury, blood clot forms at the site. There is an acute inflammatory response with exu¬dation of plasma, neutrophils, and some monocytes within 24 hours.

2. Phase of clearance:

• Necrotic tissue, debris, and RBCs are removed from the site by proteolytic enzymes liberated from neutrophils, autolytic enzymes from dead cells, and phagocytic activity of macro¬phages.

3. Phase of ingrowth of granulation tissue: Consists of 2 processes.

1. Neovascularisation.
2. Fibrogenesis

1. Neovascularisation: Formation of new blood vessels at the site of injury takes place by prolifera¬tion of endothelial cells which develops lumen and start carrying blood. These blood vessels differentiate into muscular arterioles, thin-walled venules, and true capillaries.

2. Fibro genesis: New fibroblasts originate from fibrocytes and by meiotic division of fibroblasts.

• Fibrils begin to appear by about 6th day.
• As maturation proceeds, more and more of collagen is formed, and the number of active fibroblasts and new blood vessels decreases.
• This results in the formation of an inactive-looking scar known as cicatrization.

Question 2. Complications of wound healing
Answer:

Complications of wound healing:

1. Infection:

• Due to the entry of bacteria, wound healing may be delayed.

2. Implantation (epidermal) cyst:

• Due to the persistence of epithelial cells in the wound after healing, cyst formation may occur.

3. Pigmentation:

• Healed wounds sometimes may have rust-like color due to staining with haemosiderin. Some colored pigments may be left behind during healing that imparts color.

4. Deficient scar formation:

• Due to inadequate formation of granulation tissue.

5. Incisional hernia:

• A weak scar, especially after a laparotomy, may be the site of the bursting open of a wound or an incisional hernia.

6. Hypertrophied scars and keloid formation:

• Excessive formation of collagen in healing results in keloid (claw-like) formation. Hypertrophied scars are confined to the borders of the initial wound.

7. Excessive contraction:

• An exaggeration of wound contraction may result in information of contrac¬tures /cicatrization.

8. Neoplasia:

• Rarely, a scar may be the site for the development of carcinoma later.
• Example: Squamous cell carcinoma in Marjolin’s ulcer.

Healing Of Tissues Short Question And Answers

Question 1. Healing of oral structures
Answer:

• Healing is defined as the body’s response to injury in an attempt to restore normal structure and function.
• Healing can take place by.

1. Primary union
2. Secondary union

1. Primary union:

• Primary healing takes place in clean and uninfected and surgically incised wounds whose edges are approximated by sutures and also where much loss of cells and tissues is not present.
• The sequence of events in primary union are
  • Initial hemorrhage
  • Acute inflammatory response.
  • Epithelial changes
  • Organization
  • Suture tracks.

2. Secondary union:

• Second healing takes place in wounds with a large tissue defect and where there is extensive loss of cells and tissues
• The sequence of events in secondary union are
• Initial hemorrhage
• Inflammatory phase
• Epithelial changes
• Granulation tissue
• Wound contraction
• Presence of infection.

Question 2. Healing by secondary intention
Answer:

• This is defined as the healing of a wound which is
• Open with large tissue defect.
• Having extensive loss of cells and tissues.
• The wound is not approximated by surgical sutures but is left open.

The sequence of events is as follows:

1. Initial hemorrhage:

• Wound space is filled with blood and fibrin clot which dries.

2. Inflammatory phase:

• An initial acute inflammatory response is seen followed by the appearance of macro-phages which clear off debris.

3. Epithelial changes:

• Epithelial cells proliferate from the wound margins in the form of epithelial spurs till re-epithelialization occurs and the gap is closed completely.
• But, proliferation cells do not cover the gap till granu¬lation tissue from the base starts filling the wound space.

4. Granulation tissue:

• This forms the main bulk of sec¬ondary healing. It is formed by the proliferation of fibro¬blasts and new blood vessels.

5. Wound contraction:

• This is not seen in primary healing due to the action of myofibroblasts, the wound contracts to one-third to one-fourth of its original size.

6. Presence of infection:

• Delays the process of healing due to the release of bacterial toxins that provoke necro¬sis, suppuration, and thrombosis.

Chronic And Granulomatous Inflammation Important Notes

1. Chronic inflammatory lesions are infiltrated by mononuclear inflammatory cells like phagocytes, lymphocytes, and plasma cells

• Macrophages comprise the most important cells in chronic inflammation
• Chronic granulomatous inflammation is characterized by the formation of granulomas which are tiny circumscribed lesions composed predominantly of a collection of modified macrophages called epitheloid cells and are rimmed at the periphery by lymphoid cells

2. Giant cells

• They are multinucleated cells derived from monocytes or macrophages
• The nuclei may be arranged
  • In horseshoe pattern
  • Clustered at two poles – Langhans giant cells
  • Present centrally – foreign body giant cells
• Langhans giant cells occur mostly in granulomas

3. Types of leprosy

4. Lepromin test

• It involves intradermal injection of lepromin an antigenic extract of M.leprae
• It is used for classifying leprosy on the basis of immune response
• It reveals delayed hypersensitivity reactions in patients of tuberculoid leprosy
• Patients with lepromatous leprosy are negative for the test

5. Types of syphilis

6. Types of tuberculosis

• Primary tuberculosis/ Ghons complex/ Childhood tuberculosis
• Secondary tuberculosis/ Post-primary reinfection/ Chronic tuberculosis

7. Fate of primary tuberculosis

• The lesions commonly do not progress but instead, heal by fibrosis and in time undergo calcification and even ossification
• Continuous to grow and the caseous material is disseminated through bronchi to other parts of the same lung or opposite lung
• Bacilli may enter the circulation through erosion in the blood vessel and spread to other tissues and organs resulting in military tuberculosis
• Healed lesions of primary tuberculosis may get reactivated and cause progressive second tuberculosis

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8. Fate of secondary tuberculosis

• Lesions may heal with fibrous scarring and calcification
• Lesions may coalesce and produce progressive secondary pulmonary tuberculosis along with
  • Fibrocaseous tuberculosis
  • Tuberculous caseous pneumonia
  • Military tuberculosis

9. Ghon’s complex

• It consists of three components
  • Pulmonary component
    • Lesion of the lung is the primary focus
    • It is 1-2 cm solitary area of tuberculous pneumonia located peripherally under a patch of pleurisy
  • Lymphatic vessel component
  • Lymph node component
    • This consists of hilar and tracheobronchial lymph nodes in the area drained.
    • These affected lymph nodes are matted and show caseation necrosis

Chronic And Granulomatous Inflammation Long Essays

Question 1. Describe briefly the serological diagnosis of syphilis.
Answer:

1. Microscopy:

• It is useful in primary and secondary syphilis
• Direct fluorescent antibody test is used for T. pal¬lidum
• In this method, acetone fixed smear is subjected to fluorescently tagged anti-T, pallidum antiserum

2. Serological tests:

• Tests for antibodies reacting with cardiolipin anti¬gen
  • Standard tests for syphilis
    • Wassermann test
      • It is a complement fixation test
        • Serological tests Method:
          • The patient’s serum is inactivated by heating at 56° C for 30 minutes
          • Incubated with cardiolipin antigen and guinea pig antigen at 37° C for 1 hour
          • The indicator is added to detect the presence or absence of a complement
        • Serological tests Interpretation:
          • If hemolysis does not occur, it indicates that the complement is utilized
          • This is positive Wassmann’s reaction
          • If hemolysis takes place, it indicates the complement is not been utilized in the primary reaction but utilized by the indicator system
    • Kahn test
      • It is a tube flocculation test
        • Kahn test Method:
          • 0.15 ml of inactivated serum is taken in three test tubes containing 0.05, 0.025, and 0.0125 ml of freshly prepared antigen dilution
          • Tubes are shaken on Kahn’s shaken and examined
        • Kahn test Interpretation:
          • The negative test shows uniform opalescence
          • A positive test shows floccules
    • VDRL test
      • In this test, the inactivated serum is mixed with cardiolipin antigen on a special slide and rotated for 4 minutes
      • Uniform distribution of crystals in the drop indicates the serum is non reacting
      • The formation of clumps indicates it is reactive
• Tests for antibodies reacting with group-specific treponemal antigen
  • Reiter protein complement fixation test
    • In this method, lipopolysaccharide protein complex antigen derived from the cultivable Reiter’s stain is used
    • It is less sensitive
• Tests for specific antibodies to pathogenic treponema
  • Treponema pallidum immobilization test
    • It employs live T. pallidum
    • The test serum is mixed with actively motile Nichol’s strain of T. pallidum and incubated anaerobically
    • If antibodies are present, the treponemas are immobilized
  • Fluorescent treponemal antibody absorption
    • Test serum is preabsorbed with an extract of nonpathogenic treponemas to remove group-specific antigens
    • It detects IgM and IgG
    • It is the earliest test to become positive
  • Microhaemagglutination test for treponema pallidum
    • T. pallidum antigen is coated onto the surface of red cells
    • Tanned sheep RBCs are sensitized with an extract of T. pallidum
    • When these sensitized erythrocytes are mixed with the patient’s serum containing anti¬bodies, the erythrocytes clump together
  • Enzyme immunoassay
    • They have been developed using T. pallidum antigens and are available commercially

Question 2. Define granuloma. What are the causes and pathology of granuloma?
Answer:

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

Besides the presence of epitheloid cells and lymphoid cells, granuloma have giant cells, necrosis, and fibrosis.

Granuloma Etiology:

• Tuberculosis is an infection caused by a rod-shaped, non-spore-forming, aerobic bacterium called mycobac¬terium tuberculosis.
• The organism is spread by small airborne droplets generated by coughing, sneezing, and talking to a person with pulmonary/laryngeal tuberculosis.
• Introduction of M-tuberculosis into the lungs leads to infection of the respiratory system, however, they can spread to other organs such as the lymphatics, pleura, bones/joints, and meninges and cause extrapulmonary tu¬berculosis.

Evolution of tubercle:

Constituents of granuloma:

• Epitheloid cells,
• Lymphoid cells,
• Giant cells,
• Necrosis,
• Fibrosis.

The fate of granuloma:

Question 3. Write briefly on cervicofacial actinomycosis.
Answer:

Cervicofacial actinomycosis is the commonest form of actinomycosis

Cervicofacial actinomycosis Causative Organism:

Site Involved:

• Cheek
• Submaxillary regions

Route of Infection:

• Tonsils
• Carious tooth
• Periodontal disease
• Trauma following tooth extraction

Cervicofacial actinomycosis Features:

• Initially, a firm swelling appears in the lower jaw
• Gradually, the mass breaks down
• This leads to abscesses and sinus formation

Cervicofacial actinomycosis Microscopic Features:

• The pus contains typical tiny yellow sulfur granules
• Abscess is present in the center of the lesion
• Periphery contains inflammatory cells, giant cells, and fibroblasts
• Radiating filaments demonstrating ray fungus, actino- myocytes appears in the center
• These filaments are hyaline, eosinophilic with club-like ends
• These demonstrate secreted immunoglobulins

Cervicofacial actinomycosis Complications:

• Spreading of infection into adjacent soft tissues
• Destruction of bone

Question 4. Classify granuloma. Describe the etiopathogenesis and pathology of tuberculosis.
Answer:

Granuloma Classification:

Granulomatous diseases are grouped into three groups as follows:

Tuberculosis Etiopathogenesis:

Tuberculosis Pathology:

1. Gross appearance

• The tuberculous cavity is spherical
• It has a thick fibrous wall
• Around the wall, foci of solidification are seen
• The wall is lined by yellowish, caseous, necrotic mate¬rial.
• Lumen contains thrombosed blood vessels

2. Microscopic appearance

• Lesions consist of tuberculous granuloma with caseation necrosis
• The wall of the cavity shows eosinophilic, granular, caseous material
• The outer wall shows fibrosis
• Granulomas consist of epithelioid cells, Langhan’s giant cells, and lymphocytes.

Question 5. Write briefly about the etiopathogenesis of tuberculosis. Describe the complications of secondary pulmonary tuberculosis.
Answer:

Secondary pulmonary tuberculosis Complications:

• Localized, apical, secondary pulmonary tuberculosis may heal with fibrous scarring and calcification.
• Lesions may coalesce together to form a larger area of tuberculous pneumonia and produce progressive secondary pulmonary tuberculosis with the following pulmonary and extra-pulmonary involvements

1. Fibrocaseous tuberculosis:

• The tubercular cavity is spherical with a thick fibrous wall, lined by yellowish, caseous, necrotic material, and the lumen is transversed by thrombosed blood vessels.
• Microscopically, the wall of the cavity shows eosinophilic, granulancaseous material which may show foci of dystrophic calcification. Widespread coalesced tuberculous granulomas composed of epithelioid cells, Langerhan s giant cells, and peripheral mantle of lymphocytes having central caseous necrosis are seen the outer wall of the cavity showing fibrosis.

Fibrocaseous tuberculosis Complications:

• May produce hemoptysis
• Extending to the pleura produces bronchopleural fistula.
• Tubercular empyema
• Thickened pleura.

2. Tuberculosis caseous pneumonia:

• In an individual with a high degree of hypersensitiv¬ity, secondary pulmonary tuberculosis may spread to the rest of the lung, producing caseous pneumonia.

3. Systemic military tuberculosis:

• This is lymphohaematogenous spread to tuberculous infection from the primary focus/later stages of tuberculosis.
• Spread may occur to systemic organs/isolated organs.
• The spread is either by the entry of infection into the pulmonary vein producing disseminated/isolated organ lesions in different extrapulmonary sites (for example liver spleen, kidney) or into the pulmonary artery re¬stricting the development of military lesions within the lung.
• Military lesions are millet seed-size (1mm diameter), yellowish, firm areas without grossly visible caseation necrosis.

Question 6. List common examples of a granuloma, and describe the pathogenesis and effects of any one.
Answer:

Common examples of granuloma:

1. Bacterial Tuberculosis,

• Leprosy,
• Syphilis,
• Granuloma inguinale,
• Brucellosis,
• Cat scratch disease,
• Taularemia,
• Glanders

2. Fungal

• Actinomycosis,
• Blastomycosis,
• Cryptococcosis,
• Cocci diomycosis

3. Parasitic

• Schistosomiasis

4. Miscellaneous

• Sarcoidosis,
• Crohn’s disease,
• Silicosis
• Berylliosis,

Effects of Tuberculosis:

• Productive cough
• Haemoptysis
• Pleural effusion
• Dyspnoea
• Orthopnea
• Fever
• Night sweats
• Fatigue
• Loss of weight
• Loss of appetite
• Pulmonary insufficiency
• Pulmonary hemorrhage
• Sepsis
• Secondary amyloidosis

Chronic And Granulomatous Inflammation Short Essays

Question 1. Classify leprosy. Describe the pathology of tuberculoid leprosy.
Answer:

Leprosy: Leprosy/Hansen’s disease is a slow communicable disease caused by mycobacterium lepra.

• It can be classified into 2 types based on the resistance offered as follows.

1. Lepromatous leprosy (represents low resistance)
2. Tuberculoid leprosy (represents high resistance)

• Leprosy is classified into 5 clinicopathologic groups (modified Ridley and Jopling’s classifica¬tion).
  • TT – Tuberculoid polar
  • BT – Borderline tuberculoid
  • BB – Mid borderline (dimorphic)
  • BL – Borderline lepromatous
  • LL – Lepromatous polar.

Tuberculoid leprosy:

• Tuberculoid leprosy is characterized by asymmetrical skin lesions that are hypopigmented and erythematous macules.
• Nerve involvement is with the distinct sensory distribution.
• Histopathological features include hard tubercles similar to granulomatous lesions eroding the basal layer of the epidermis.
• Lepra bacilli are few and seen in destroyed nerves.

Question 2. Oral lesions of syphilis
Answer:

• Syphilis is a sexually transmitted disease caused by spirochaetes, treponema pallidum.
• Syphilis is divided into 3 stages depending upon the period after which the lesions appear and the type of lesions.
• They are primary, secondary, and tertiary.
• Oral lesions occur in secondary syphilis known as mucous patches, on the tongue, gingiva, etc. or as a split papule on lips, which are highly infectious.
• Tertiary/late syphilis/gumma is a granuloma with central necrosis, noninfectious, and is most common on the tongue and palate.
• Palatal perforation by ulcer after vigorous antibiotic use is known as the Herxheimer reaction.
• In congenital/prenatal syphilis, the most constant finding is relatively short roots of mandibular permanent 1st molars, short maxilla, Hutchinson triad (teeth, eye/ear involved), hypoplasia of incisors and molars i. e., notched incisors and mulberry molars.
• Treatment: Penicillin is the drug of choice.

Question 3. What is Ghon’s complex? Mention the lab diagnosis of tuberculosis.
Answer:

Mode of transmission:

• Usually direct by inhalation of air-borne organisms.
• By exposure to contaminated secretions of infected persons
• By drinking milk contaminated with Mycobacterium bovis.
• The most commonly involved tissues for the primary complex are the lung and hilar lymph nodes.
• Ghon’s complex in the lungs consists of 3 components as follows:

1. Pulmonary component:

• The lesion in the lung is primary focus) Ghon’s focus. It is a 1 – 14 cm solitary area of grey-white inflammatory consolidation.
• Tubercle bacilli either free/within phagocytes drain to the regional lymph nodes, which often caseate. This combination of parenchymal lesion and nodal involvement is referred to as Ghon’s complex.

2. Lymphatic vessels component:

• Lymphatics draining the lung lesions contain phagocytes containing bacilli and may develop beaded, military tubercles along the path of hilar lymph nodes.

3. Lymph node component:

• Consists of enlarged hilar and tracheobronchial lymph nodes in the area drained. The affected lymph nodes are matted and show caseation necrosis.

Diagnosis of tuberculosis is made by the following tests

• Positive Mantoux skin test.
• Positive sputum for AFB.
• Complete haemogram (lymphocytosis and raised ESR)
• Chest X-ray (characteristic hilar nodules and other parenchymal changes)
• Fine needle aspiration cytology of an enlarged peripheral lymph node is quite helpful for confirmation of diagnosis.

Question 4. Primary tuberculosis.
Answer:

• Primary tuberculosis or Ghon’s complex is the infection of an individual who has not been previously infected/ immunized
• It consists of 3 components
  • Pulmonary component
• It is a lesion in the lung
• It is 1-14 cm solitary area of grey-white inflammatory consolidation
• Tubercle bacilli either free/within phagocytes drain to the regional lymph nodes which often caseate
• This combination of parenchymal lesion and nodal in¬volvement is referred to as Ghon’s complex
  • Lymphatic vessel component
• Lymphatics draining the lung lesions contain phagocytes containing bacilli and may develop beaded, mili¬tary tubercles along the path of hilar lymph nodes
  • Lymph node component
• Consists of enlarged hilar and tracheobronchial lymph nodes in the area drained
• The affected lymph nodes are matted and show casea¬tion necrosis

Chronic And Granulomatous Inflammation Short Question And Answers

Question 1. Gumma
Answer:

• Syphilitic gumma is a lesion caused by tertiary syphilis
• It is a solitary, localized rubbery lesion with central necrosis seen in the original like liver, testis, bone and brain-associated scarring of hepatic parenchyma.
• Histologically, the structure of gumma shows the following:
• Central coagulative necrosis resembles caseation but is less destructive so that outlines of necrotic cells can still be seen.
• Surrounding zone of palisaded macrophages with lymphocytes, plasma cells, giant cells, and fibroblasts.

Question 2. Morphology of granuloma
Answer:

Granuloma consists of:

Question 3. Granulomatous inflammation
(or)
Chronic Granulomatous inflammation
Answer:

Granulomatous inflammation is a typical reaction to poorly digestible agents elicited by tuberculosis, lep¬rosy, fungal infections, etc.

Examples:

Question 4. Actinomycosis
Answer:

• Actinomycosis is a chronic suppurative disease caused by anaerobic bacteria, actinomycetes Israeli.
• The infection is always endogenous in origin. The or¬ganisms invade, proliferate and disseminate in favour¬able conditions.
• Based on the anatomical location of lesions, actinomycosis is of the following types:
  • Cervico facial
  • Thoracic
  • Abdominal
  • Pelvic.
• Of all the types, cervicofacial actinomycosis is the com¬monest from.
  • Microscopically, in all the types:
  • The inflammatory reaction is a granuloma with central suppuration.
  • The Centre of each abscess contains a bacterial colony ‘sulfur granule’ characterized by radiating filaments.
  • Bacterial strains reveal the organisms as nonacid, fast, gram-positive filaments.

Question 5. Primary complex
Answer:

• Primary complex/Ghon’s complex/childhood tubercu¬losis/ is the primary tuberculosis. Is the infection of an individual who has not been previously in- infected/immunized.
• It consists of 3 components:

1. Pulmonary component
2. Lymphatic vessel component
3. Lymph node component

• The most commonly involved tissues for the primary complex are the lung and hilar lymph nodes.
• Tubercle bacilli, either free/within phagocytes drain the regional lymph nodes, which often caseate.
• This combination of parenchymal lesion and nodal in¬volvement is referred to as Ghon’s complex.

Question 6. Congenital syphilis
Answer:

Congenital syphilis’s Major features are:

• Hutchinson’s triad – which includes.
  • Hutchinsons’s teeth – small, widely spaced, peg-shaped permanent teeth.
  • Notched central incisors
  • Intestinal keratitis with blindness and deafness from 8th cranial nerve injury.
• Saddle shaped nose
• Bony lesions like epiphysis and periostitis
• Mucocutaneous lesions of acquired secondary syphilis
• Diffuse fibrosis in the liver.

Question 7. Lepromatous leprosy
Answer:

• Leprosy caused by mycobacterium leprae is of 2 types of which lepromatous leprosy represents low resis¬tance and tuberculoid leprosy represents high resis¬tance.
• Lepromatous leprosy is characterized by multiple symmetrical skin lesions that are hypopigmented and erythematous maculopapular/nodular.
• Nerve involvement is present with less serve sensory distribution.
• Histopathology involves the collection of foamy macro¬phages/lepra cells in the dermis separated from the epidermis by a clear zone.

Question 8. Pathological lesions of syphilis
Answer:

1. Primary chancre
2. Regional lymphadenopathy
3. Maculopapular rash
4. Mucous patches
5. Snail track ulcers
6. Flat papules around the anus
7. Tertiary gumma
8. Meningitis
9. Cranial nerve palsies
10. Generalized paralysis of insane

Question 9. What is tuberculoid granuloma? Give three examples
Answer:

• Tuberculoid granuloma is defined as circumscribed, tiny lesion about 1 mm in diameter, composed predominantly of a collection of modified macrophages called epitheloid cells and rimmed at the periphery by lymphoid cells.
• It is caused by mycobacterium tuberculosis that has 5 pathogenic strains. Hominis, bovis, avian, murine, and cold-blooded vertebrate strains.
• Different organs may be affected by mycobacterium tuberculosis, which lung is the most common organ.
  • Pulmonary tuberculosis
  • Intestinal tuberculosis
  • Hyperplastic caecal tuberculosis.

Question 13. Tuberculoid type of leprosy
Answer:

• Tuberculoid leprosy is characterized by asymmetrical skin lesions that are hypopigmented and erythematous macules.
• Nerve involvement is with the distinct sensory distribution.
• Histopathological features include hard tubercles similar to granulomatous lesions eroding the basal layer of the epidermis.
• Lepra bacilli are few and seen in destroyed nerves.

Question 14. Chancre
Answer:

• Chancre is a typical lesion of primary syphilis that appears on genitals/at extragenital sites in 2-4 weeks after exposure to infection.
• Initially, the lesion is a painless papule which ulcerates in the center so that the fully developed chancre is an indurated lesion with central ulceration accompanied by regional lymphadenitis.
• Chance heals without scarring, even in the absence of treatment

Question 15. Giant cells
Answer:

• In chronic inflammation, when the macrophages fail to deal with particles to be removed, they fuse together and form multinucleated giant cells.
• Giant cells are normally seen in cells like osteoclasts of bone, trophoblasts in the placenta, and megakaryocytes in bone marrow.
• Morphologically different cells are seen in chronic in¬flammation and tumors.

Giant cells in inflammation:

• Foreign body giant cells: Chronic infective granuloma, leprosy, and TS.
• Langerhans giant cells: Sarcoidosis and tuberculosis.
• Taunton’s giant cells: Xanthoma
• Aschoffs giant cells: Rheumatic nodules.

Giant cells in tumors:

• Anaplastic cancer giant cells: Seen in carcinoma of the liver and various soft-tissue sarcomas.
• Reed – Sternberg cells: Hodgkin’s lymphoma.
• Giant cells tumor of bone: Uniform distribution of os¬teoclastic giant cells spread in the stroma.

Question 16. Lepra reaction
Answer:

Lepra reaction/reactional leprosy:

• There may be of 2 types
  • Type 1 (Reversal reactions),
  • Type 2 (Erythema, nodosumleprosum)

Type 1: The polar forms of leprosy do not undergo any change in the clinical and histopathological picture.

Borderline groups are unstable and may move across the spectrum in either direction with upgrading/downgrading of the patient’s immune state.

1. Upgrading reaction:

• Characterized by increased cell-mediated immunity and occurs in patients of border¬line lepromatous (BL) type on treatment who up¬grade/shift towards tuberculoid type.

2. Downgrading reaction:

• Characterized by lowering of cellular immunity and is seen in borderline tuber¬culoid (BT) type who downgrade/shift towards lepromatous type.

Type 2: Occurs in lepromatous patients after treatment. It is characterized by tender cutaneous nodules, fever, iridocyclitis, synovitis, and lymph node involvement.

Acute Inflammation Important Notes

1. Vascular events

• Hemodynamic changes
  • Transient vasoconstriction
  • Persistent progressive vasodilatation
  • Elevation of local hydrostatic pressure
  • Slowing or stasis of microcirculation
  • Leucocyticmargination and emigration
• Changes in vascular permeability

2. Vasoactive amines

• They mediate inflammation
• They are histamine and serotonin
• Histamine
  • It is released from mast cells, basophils, and platelets
  • The actions are
    • Vasodilation
    • Increased vascular permeability
    • Itching
    • Pain
• Serotonin
  • It is present in chromaffin cells of GIT, spleen, nervous tissue cells, and platelets
  • Actions are similar to histamine but less potent

3. Interleukin – 1 (IL-1)

• It is secreted by monocytes and macrophages
• It is also known as leucocyte leucocyte-activating factor
• Together with the tumor necrosis factor it
  • Increases chemotaxis
  • Phagocytic activity of leukocytes
  • Increases resorption of bone

4. Metabolites

• Metabolites of arachidonic acid
  • Prostaglandins, thromboxane A2, prostacyclin
  • Prostaglandin increases vascular permeability, vasodilation, and bronchodilation
• Metabolites of lipo-oxygenase pathway
  • 5-HETE and leukotrienes

5. Bradykinin

• It acts in the early stages of inflammation
• Actions:
  • Induces smooth muscle contraction
  • Vasodilation
  • Increased vascular permeability
  • Pain

6. Macrophages

• Present in tissues
• Originates from circulating monocytes
• Has the limited capacity to divide
• Forms giant cells
• Survives for long periods
• Macrophages in tissues are called histiocytes

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7. Neutrophils

• They are dominant cells in acute inflammation in the First 24 hours
• They are short-lived

8. Cellular events in inflammation

• Exudation of leucocytes
• Phagocytosis

Acute Inflammation Long Essays

Question 1. Describe briefly the vascular phenomenon of inflammation.
(or)
Define inflammation. Describe the various vas¬cular changes of inflammation.
Answer:

Inflammation Definition:

• Inflammation is defined as a protective response intended to eliminate the initial cause of cell injury as well as necrotic cells and tissues resulting from the original insult.

Vascular changes of inflammation:

1. Haemodynamic changes:

Changes in the vascular flow and caliber of small blood vessels in the injured tissue take place in a sequence of events as follows:

• Transient’Vasoconstriction of arterioles:
  • Duration: Immediately after the injury, lasting for about
    • 3-5 seconds in minor injuries
    • 5 minutes in more severe injuries
  • Significance: restores normal blood flow.
• Persistent progressive vasodilation: It mainly involves the arterioles and to a lesser extent venules and capillaries.
  • Duration: This lasts for about half an hour after injury.
  • Significance: This results in increased blood vol¬ume in the microvascular bed of the area that is responsible for redness and warmth at the site of acute inflammation.
• A rise in local hydrostatic pressure: Due to progres¬sive vasodilatation, there is an elevation of the local hydrostatic pressure
  • Result:
    • Transudation of fluid into the extracellular space.
    • Swelling at the local site of acute inflammation.
• Slowing/stasis of microcirculation:
  • Result: Increases concentration of RBCs, thereby viscosity of blood increases.
• Margination/peripheral orientation of leuko-cytes:
  • Stasis is followed by leukocytic margination along the vascular endothelium, leukocytes then move and migrate through the gaps between the endo¬thelial cells into the extravascular space. This phenomenon is known as emigration.

2. Altered vascular permeability:

• Initially, the escape of fluid occurs due to vasodilation and due to the increased volume of blood flow, there is an elevation of hydrostatic pressure
• This results in the movement of fluid from capillaries into tissues, this fluid is called transudate.
• Later the characteristic inflammatory edema, exudate, appears by increased vascular permeability
• This results in decreased intravascular osmotic pressure; and increased osmotic pressure of interstitial fluid resulting in excessive outward flow of fluid into the intersti¬tial compartment which is the inflammatory exudate.
• Fluid accumulation in extravascular spaces is called edema.

Question 2. What are the cardinal signs of inflammation?
Answer:

Cardinal Signs Of Inflammation:

There are four cardinal signs of inflammation as follows

1. Rubor- redness

• Due to Vasodilatation in the area of inflammation, there is increased blood volume
• This causes redness

2. Tumor- swelling

• Local hydrostatic pressure is increased
• This results in the transudation of fluid into the extracellular space
• This causes swelling

3. Calor-heat

• Vasodilatation is responsible for it

4. Dolor- pain

• These four signs were described by Celsus in the first century A.D.
• A fifth sign called function less- loss of function was later added by Virchow
• These signs were demonstrated by Lewis’s experience

Lewis Experiment:

• To elicit the signs of inflammation, Lewis induced the changes in the skin of the inner aspect of the forearm by firm stroking with a blunt point
• The reaction is called a triple response or red-line response
• It consists of:

Question 3. Discuss cellular events in acute inflammation.
Answer:

Cellular events: Cellular events in acute inflammation can be described by

1. Exudation of leucocytes
2. Phagocytosis.

1. Exudation of leucocytes: The escape of leucocytes from the lumen of the microvasculature to the interstitial tissue is the most important feature.

• In acute inflammation, polymorph nuclear neutrophils (PMNs) comprise the first line of body defense, followed later by monocytes and macrophages.
• The changes leading to the migration of leukocytes are as follows:

Margination: In the early stage of inflammation there is vasodilation, subsequently slowing/stasis of the bloodstream takes place/

• Due to stasis, changes take place in microcircu¬lation.
• Central steam of the cell widens and the peripheral becomes narrower, this phenomenon is known as margination.
• RBC’s leukocytes are present in central steam;
• peripheral there is a cell-free layer due to margination,
• Neutrophils come close to the vessel wall, which is known as pavement.

Rolling and adhesion:

• Peripherally marginated and pavemented neutrophils slowly roll over the endothelial cells lin¬ing the vessel’s wall this is called as rolling.
• This is followed by the transient bond between the leukocytes and endothelial cells becoming firmer known as adhesion.
• Selectins, integrins, vascular and intercellular adhesion molecules, etc. bring about rolling and adhesion.

Emigration:

• Neutrophils move along the endothelial surface between endothelial cells
• Here neutrophiles give out cytoplasmic pseudo-pods.
• Neutrophils get lodged between endothelial cells and the basement membrane
• It secretes collagenases which damage the basement membrane and they escape out into extravascular space phenomenon known as emigration.
• Simultaneous to the emigration of leukocytes, RBCs also escape through the gap known as diapedesis

Chemotaxis:

• After extravasating from the blood, leukocytes migrate toward the sites of infection/injury.
• Chemotaxis is defined as the chemotactic factor me¬diated transmigration of leukocytes after crossing several barriers to reach the interstitial tis¬sues
• These chemotactic agents are also called chemokines and they carry specific receptors.

2. Phagocytosis: Phagocytosis is defined as the process of engulfment of solid particulate material by the cells. The cells performing this function are called phagocytes.

The main types of phagocytic cells are:

• Poly morpho nuclear neutrophils (PMNs): They appear early in the acute inflammatory response. Also called macrophages.
• Macrophages: These are circulating monocytes and fixed tissue mononuclear phagocytes.

Phagocytosis consists of the following steps:

1. Recognition and attachment:

• The microorganism is to be phagocytosed and the phagocytic cell repel each other due to both having a negatively charged surface.
• To overcome this repulsion, the microorganism gets coated with a naturally occurring factor in the serum called opsonins and gets targeted for phagocytosis by a process called opsonization.
• The 2 main opsonins in the serum and their cor¬responding receptors on the cell surface are as follows.
  • IgG opsonin and its corresponding receptor is an Fc fragment of immunoglobulin on the sur¬face polymorphs and monocytes.
  • Cgb opsonins fragment of complement and corresponding receptor for 03^ on the phagocytic cell surface.

2. Engulfment stage:

• The opsonized particle bound to the phagocyte surface is engulfed by the formation of cytoplasmic pseudopods around the particle and enveloping it in a phagocytic vacuole
• Eventually, the membrane of the phagocytic vacuole breaks from the cell surface so that the membrane-lined phagocytic vacuole lies free in the cyto¬plasm.
• This is converted into phagolysosome/phagosome on its fusion with the lysosomes of the cell.

3. Killing and degradation:

• In this stage, microorganisms are killed by the antibacterial substances and digested/degraded by hydrolytic enzymes.

Acute Inflammation Short Essays

Question 1. Classify and discuss chemical mediators of acute inflammation.
Answer:

• Chemical mediators are also called permeability factors/ endogenous mediators of increased vascular permeability; these are large and increasing numbers of endogenous compounds that can enhance vascular permeability.
• The substances acting as chemical mediators of inflammation may be released from the cells, plasma, or the damaged tissue itself.
• They are broadly classified into 2 groups as follows:

1. Mediators are released by cells.
2. Mediators originated from plasma

Chemical Mediators of Acute Inflammation:

1. Cell-Derived Mediators:

• Vasoactive amines [Histamine, 5-hydroxyethyl- time, neuropeptides)
• Arachidonic acid metabolites (Eicosanoids)
  • Metabolites via cyclo-oxygenase pathway (prostaglandins, thromboxane A2, prostacyclin, re-solving)
  • Metabolites via lipo-oxygenase pathway (5- HETE, leukotrienes, lipoxins)
• Lysosomal components (from PMNs, macrophages)
• Platelet-activating factor
• Cytokines (IL-1, TNF-a, TNF-|3, IFN-y, chemokines)
• Free radicals (Oxygen metabolites, nitric oxide)

2. Plasma-derived mediators (Plasma Proteases)

• Products of:
  • The kinin system
  • The clotting system
  • The fibrinolytic system
  • The complement system

Question 2. Chemotaxis:
Answer:

• Chemotaxis is defined as the chemotactic factor medi¬ated transmigration of leucocytes after crossing several barriers (endothelium, basement membrane, perivas¬cular, myofibroblastic, and matrix) to reach the intersti¬tial tissues.
• This concept is well illustrated by Boyden’s chamber experiment.
• In this, a Millipore filter (20m pore size) separates the suspension of leucocytes from the test solution in a tissue culture chamber. If the test solution contains chemotactic agents, the leucocytes migrate through the pores of the filter toward the chemotactic agent.
• The following agents act as potent chemotactic substances) chemokines for neutrophils.
  • Leukotriene B4 is a product of the lipoxygenase pathway of arachidonic acid metabolites.
  • Components of complement system (C5a and C3a in particular)
  • Cytokines (Interleukins, in particular, IL-8)
  • Soluble bacterial products (such as formulated pep-tides)

Acute Inflammation Short Question And Answers

Question 1. Lymphokines
Answer:

• Cytokines are polypeptide substances that are produced by activated lymphocytes and monocytes.
• Those cytokines which are produced by activated lym¬phocytes are called lymphokines.
• These agents may act on ‘self cells producing them/on other cells.
• TNF-p and IFN-y are produced by activated T-cells.
• They act as mediators of inflammation.

Question 2. Varieties of inflammation
Answer:

Types of inflammation: Depending on the host immune levels of the duration of response, inflammation can be classified as acute or chronic.

1. Acute inflammation:

• Acute inflammation is a rapid repose to injury or microbes and other foreign substances that is designed to deliver leukocytes and plasma proteins to sites of injury.
• The outcome of acute inflammation may be the removal of the exudate with the restoration of normal tissue architecture, transition to chronic inflammation or extensive destruction of the tissue resulting in scarring.

2. Chronic inflammation:

• Chronic inflammation is inflammation of prolonged duration about weeks to months to years in which active inflammation, tissue injury, and healing pro¬ceed simultaneously. Examples: tuberculosis, leprosy, fungal infection.
• Chronic infection is characterized by.
  • Infiltration with mononuclear cells including macrophages, lymphocytes, and plasma cells.
  • Tissue destruction is largely induced by the products of inflammatory cells.
  • Repair, involving new vessel proliferation i.e., angiogenesis and fibrosis.

Question 3. The vascular phenomenon in inflammation
Answer:

Vascular changes in inflammation:

• Alteration in microvasculature i.e., capillaries, venules, and arterioles, is the first response to tissue injury.
• Alternations include Hemodynamic changes and changes in vascular permeability.

Hemodynamic changes:

• It is the earliest sign of inflammation, that results from changes in the vascular flow and caliber of small blood vessels in the injured tissue.
• It takes place as a sequence of events.
  • Transient vasoconstriction of arterioles
  • Persistent vasodilation of arterioles, venules, and capillaries
  • Rise in local hydrostatic pressure.
  • Slowing/stasis of microcirculation.
  • Stasis is followed by leukocytic margination/peripheral orientation of leukocytes along the vascular endothelium.
  • After sticking briefly to the vascular endothelium, the leukocytes migrate through the gap between the endothelial cells into the extravascular space, this is known as margination

Altered Vascular Permeability: Increased vascular permeability is seen during inflammation which may be due to.

• Contraction/retraction of endothelial cells.
• Injury to endothelial cells.
• Leakiness in neovascularization.

Question 4. Mention the role of histamine in inflammation
Answer:

• Role of histamine in inflammation:
  • Vasodilatation
  • Increases vascular permeability
  • Causes itching and pain

Question 5. What are Free Radicals? Give two examples.
Answer:

Environmental And Nutritional Disorders Important Notes

1. Vitamins

• Fat-soluble vitamins

• Water soluble vitamins

Environmental And Nutritional Disorders Long Essays

Question 1. Classify vitamins. Discuss the role of vitamin D in rickets.
Answer:

Vitamins:

• Vitamins are organic substances which cannot be synthesized with the body and are essential for the maintenance of the normal structure and function of cells.

Vitamins Classification: Vitamins are divided into 2 groups.

1. Fat-soluble vitamins – A, D, E, K

• They are absorbed from the intestine in the presence of the bile salts and intact pancreatic function.

2. Water-soluble vitamins – B and C

• They are more readily absorbed from the small intestine.

Vitamin D: (Calcitriol):

• Vitamin D is a fat-soluble vitamin, commonly known as anti-rachitic vitamin
• Deficiency of vitamin D results in
  • Rickets in children
  • Osteomalacia in adults

Rickets:

Rickets a clinical disorder seen in growing children from 6 months to 2 years of age due to a deficiency of Vit. D.

Pathogenesis of rickets occurs in the following sequence:

1. Endochondral ossification is long tubular bones.

• Overgrowth of epiphyseal cartilage due to proliferation of cartilage cells at the epiphyseal cartilage due to proliferation of cartilage cells at the epiphyses followed by inadequate provisional calcification/mineralization.
• Persistence and overgrowth of epiphyseal cartilage, deposition of osteoid matrix on inadequately mineralized cartilage resulting in enlargement and lateral expansion of the osteochondral junction.
• Deformation of the skeleton due to loss of struc-tural rigidity of the developing bones.
• Irregular overgrowth of small blood vessels in disorganized and weak bones.

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2. Intramembranous ossification in flat bones. Mesenchymal cells differentiate into osteoblasts with lying down of osteoid matrix which fails to get mineralized resulting in soft and weak feat bones.

Rickets Clinical Features:

• The gross skeletal changes depend on the severity of the rachitic process, its duration, and in particular the stresses to which individual bones are subjected.
• Craniotabes, the earliest bony lesion occurring due to small round unossified areas in the membranous bones of the skull.
• Harrison’s sulcus which occurs due to in drawing of soft ribs on inspiration.
• Pigeon chest deformity
• Bow legs occur in ambulatory children due to weak bones of the lower legs.
• Knocked knees may occur due to enlarged ends of the femur, tibia, and fibula.
• Lower epiphyses of the radius may be enlarged.
• Lumbar lordosis due to involvement of the spine and pelvis.

Rickets Biochemical changes:

• Lowered levels of active metabolites of vitamin D.
• Normal or slightly low plasma calcium levels, low plasma phosphate levels and raised plasma alkaline phosphatase levels.

Environmental And Nutritional Disorders Short Essays

Question 1. Pellagra
Answer:

• Niacin deficiency causes Pellagra i.e., rought skin.
• The cardinal manifestations of pellagra are referred to as the three D’s i.e., dermatitis, diarrhea, and dementia and if not treated may lead to 4th D i.e., death.
  • Dermatitis: Sun-exposed areas of skin developed erythema resembling sun-burn which may progress to chronic type with blister formation.
  • Diarrhea: This is seen along with stomatitis, glossitis, enteritis, nausea and vomiting.
  • Dementia: Degeneration of neurons of the brain of the spinal tract results in neurological symptoms such as dementia, peripheral neuritis, ataxia, and visual and auditory disturbances.
• Oral findings include:
  • The bald tongue of sandwich,
  • Raw beefy tongue
  • Mucosa becomes fiery red and painful
  • Profuse salivation.
• Chronic alcoholics are at high risk of developing pellagra because in addition to dietary deficiency, niacin absorption is impaired in them.

Question 2. Osteomalacia
Answer:

• Osteomalacia is the adult manifestation of Vit. D deficiency is characterized by failure of mineralization of the osteoid matrix.
• Due to failure of mineralization, excess of persistent osteoid is produced which is a characteristic of osteomalacia.
• The contours of the bone is not affected, but the bone is weak and vulnerable to fractures.
• Other clinical features include
  • Muscular weakness,
  • Vague body pains,
  • Fractures following trivial trauma,
  • Losser’s zones/pseudofractures at weak places in bones.
• Biochemical changes include
  • Normal/low serum calcium levels, low plasma phosphate levels, and raised serum alkaline phosphatase due to increased osteoblastic activity.

Question 3. Manifestations of vitamin A deficiency.
Answer:

Lesions in Vitamin A deficiency:

• Ocular lesions:
  • Night blindness,
  • Xerophthalmia, dry and scaly sclera, conjunctiva
  • Keratomalacia due to infections of corneal ulcers,
  • Bitot’s spots are focal triangular areas of opacities due to the accumulation of keratinized epithelium.
  • Blindness due to infection, scarring, and opacities.
• Cuntaneous lesions :
  • Xeroderma/toad-like appearance of skin because of papular lesions due to follicular hyperkeratosis and keratin plugging in the sebaceous glands.
• Other lesions:
  • Squamous metaplasia of
    • Respiratory epithelium,
    • Pancreatic ductal epithelium,
    • Urothelium
    • Long-standing metaplasia may progress to anaplasia.
    • Immune dysfunction.
    • Pregnant women may have an increased risk of maternal infection, mortality, and impaired embryonic development

Question 4. Beriberi.
Answer:

Deficiency of Thiamine results in beriberi

Beriberi Symptoms:

• Loss of appetite
• Weakness
• Constipation
• Nausea
• Mental depression
• Peripheral neuropathy
• Irritability
• Numbness in the legs

Beriberi Types:

1. Wet beriberi

• Characterized by edema of legs, face, trunk, and serous cavities

2. Dry beriberi

• Associated with neurological manifestations

3. Infantile beriberi

• Seen in infants

Environmental And Nutritional Disorders Short Question And Answers

Question 1. Microscopic picture of osteomalacia
Answer:

• Osteomalacia shows the following microscopic features
• Failure of mineralization of the osteoid matrix
• Decreased mineralization at the borders between osteoid and bone
• Osteoid remains unstained by von Kossa’s stain while calcified bone is stained black
• Increased osteoclastic activity and fibrosis of marrow is seen

Question 2. Mention two differences between Kwashiorkar and marasmus
Answer:

Question 3. Scurvy
Answer:

• Vitamin C deficiency results in scurvy.
• Lesions and clinical manifestations of Vit. C deficiency are seen more commonly in two extreme age groups i.e., early childhood and geriatric patients.

Following manifestations are seen in vitamin C deficiency.

• Hemorrhage diathesis – A marked tendency to bleed which is characteristic of scurvy. There may be
• Skeletal lesions – There is a deranged formation of the osteoid matrix but not deranged mineralization. Growing tubular bones as well as flat bones are affected.
• Delayed wound healing.
• Anaemia – Normocytic normochromic type.
• Skin rash – Hyperkeratotic and follicular rash may occur.
• Lesions in teeth and gums – Scurvy may interfere with the development of dentin. The gums are soft and swollen, may bleed easily, and get infected commonly.

Question 4. Kwashiorkor
Answer:

• Protein deficiency with sufficient calorie intake is called as kwashioker.
• There is an enlarged fatty liver and atrophy of different tissues and organs but subcutaneous fat is preserved.

Kwashiorkor Clinical Features:

• Occurs in children between 6 months and 3 years of age.
• Generalized/localized edema is present.
• Anaemia.
• Wasting of muscles.
• Growth failure.
• Hair changes – Overall loss of color.
• A flag sign is seen – alternate bands of light and dark hair.

Question 5. Vitamin B12
Answer:

It is cyanocobalamine

Coenzyme Forms:

• 5′- Deoxyadenosyl cobalamin
• Methylcobalamin

Vitamin B12 Functions:

1. Synthesis of methionine from homocysteine

• Vitamin B12 is used as Methylcobalamin in this reaction

2. Isomerization of methymalonyl CoA to succinyl CoA

• It occurs in the presence of vitamin B12 Coenzyme, deoxyadenosine cobalamin

Vitamin B12 Dietary Requirements:

• Adults- 3 micrograms/day
• Children- 0.5-1.5 micrograms/day
• During pregnancy and lactation- 4 micrograms/day

Question 6. Vitamin B12 deficiency
Answer:

A deficiency of vitamin B12 leads to

• Pernicious anemia
  • Characterized by low hemoglobin levels, decreased number of erythrocytes, and neurological manifestations
• Neuronal degeneration
• Demyelination of the nervous system

Question 7. Protein-energy malnutrition
Answer:

• It is the most common nutritional disorder of developing countries
• The two extreme forms of it are
  • Kwashiorkor
  • Marasmus

Question 8. Enumerate causes and investigations in vitamin D deficiency.
Answer:

Causes of Vitamin D Deficiency:

• Inadequate exposure to sunlight
• Dietary deficiency of vitamin D
• Malabsorption of lipids
• Derangement of vitamin D metabolism
• Resistance of end-organ to respond to vitamin D

Vitamin D Deficiency Investigations:

Genetic And Pediatric Diseases Important Notes

1. Syndrome and their chromosomal abnormalities

2. Structural abnormalities of chromosomes include

• Translocation
• Deletions
• Inversion
• Ring chromosome
• Isochromosome

Genetic And Pediatric Diseases Short Essays

Question 1. Down’s syndrome
Answer:

• Down’s syndrome/trisomy 21/mongolism affects approximately 1 in 1000 births.
• It is the most common chromosomal disorder and is the commonest cause of mental retardation.

Down’s syndrome Etiology:

• Late maternal age
• Nondisjunction of chromosome 21 during an early stage of embryogenesis.

Down’s Syndrome Clinical Features:

• Epicanthal folds and flat facial profile,
• Slanting eyes produce a mango-loid appearance.
• Hands are short with a transverse single palmar crease.
• Abnormalities of ears, trunk, pelvis, and phalanges
• Cardiac malformations
• Congenital malformations are common and quite disabling
• Risk of developing acute leukemias, especially mega-karyotypic leukemia.
• Oral manifestations:
  • Deficient maxilla – class 111 relation,
  • Open mouth,
  • Large tongue,
  • Caries free teeth due to excess salivation.

Read And Learn More: Pathology Question And Answers

Genetic And Pediatric Diseases Short Questions And Answers

Question 1. Chromosome mutations
Answer:

• Mutation refers to permanent changes in the DNA. The genetic disorders arising from chromosomal aberrations are a consequence of numeric or structural abnormalities in the chromosomes.
• General features of chromosomal disorders and specific examples of diseases involving changes in the karyotype are as follows:
  • Chromosomal disorders resulting from mutations may be associated with absences/excess of chromosomes.
  • Absence-monosomy
  • Excess – trisomy.
• Generally, the loss of chromosomes produces more severe defects than the gain of chromosomes.
• Excess chromosomal material may result from a complete chromosome as in trisomy or a chromosome as in Rebortsonian translocation.
• Imbalances of sex chromosomes are tolerated much better than similar imbalances of autosomes.

Question 2. Inborn errors of metabolism
Answer:

• Storage diseases or inborn errors of metabolism are biochemically distinct groups of disorders occurring due to genetic defects in the metabolism of carbohydrates, lipids, and proteins resulting in intracellular accumulation of metabolites.
• Based on the biochemical composition, storage diseases are classified into distinct groups.

1. Glycogen storage disease: There is defective glucose metabolism resulting in excessive intracellular accumulation of glycogen.

Example:

• Von Gierke’s disease,
• Pompe’s disease,
• Mcardle’s disease etc.

2. Mucopolysacchari doses:

This results from a deficiency of specific lysosomal enzymes involved in the degradation of mucopolysaccharides/glycosaminoglycan- cans and is therefore, a form of lysosomal storage disease.

3. Other types:

• Sphingolipidoses/gangliosidoses – accumulation of gangliosides
• Gaucher’s disease – accumulation of glucose- offside.
• Niemann-pick diseases-accumulation of sphingomyelin.

Question 3. Erythroblastosis fetalis.
Answer:

Erythroblastosis fetal/Haemolytic disease of the newborn results from the passage of IgG antibodies from the maternal circulation across the placenta into the circulation of fetal red cells.

HDN can occur in 2 ways.

1. Incompatibility of ABO or Rh blood group system.

• Severest from may result in intrauterine death from hydrops fetal.

2. HDN due to ABO incompatibility.

• Occurs most frequently in infants born to group O mothers who possess anti-A /anti-B IgG antibodies.

Intracellular Accumulations Important Notes

1. Endogenous pigments

• It includes lipofuscin, melanin, and certain derivatives of hemoglobin
• Lipofuscin is a yellowish-brown intracellular lipid pigment
• Found in
  • Atrophied cells of old age so-called wear and tear pigment
  • Myocardial fibres
  • Hepatocytes
  • Leydig cells of the testes
  • Neurons of senile dementia

Intracellular Accumulations Long Essays

Question 1. Mention types of degeneration. Discuss pathogenesis and macroscopic appearance of fatty liver.
Answer:

Degeneration Types:

Fatty Liver Pathogenesis:

In fatty liver: Intracellular accumulation of triglycerides can occur due to defect at one/ more of the following 6 steps:

• Increased entry of fatty acids into the liver.
• Increased synthesis of fatty acids by the liver.
• Decreased conversion of fatty acids into ketone bodies resulting in increased esterification of fatty acids to triglycerides.
• Increased a-glycerophosphate causes increased esterification of fatty acids to triglycerides.
• Decreased synthesis of lipid acceptor protein resulting in decreased formation of lipoprotein from triglycerides.
• Block in the excretion of lipoprotein from the liver into plasma.

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Macroscopic Appearance of Fatty Liver:

1. Gross appearance

• Size- liver is enlarged
• Color-yellow
• Capsule- tense and glistening capsule
• Margins are rounded

2. Cut surface

• It bulges slightly
• Color varies from pale yellow to yellow
• The surface is greasy to the touch

Question 2. Define and classify degeneration. Discuss etiopathogenesis and pathology of fatty liver,
(or)
Mention types of degeneration. Discuss patho¬genesis and microscopic appearance of fatty liver
Answer:

Degeneration Definition:

• Degeneration is a process by which a tissue deteriorates, loses its functional activity, and may become con¬verted into or replaced by other kinds of tissue.

Fatty Liver:

• Fatty liver or steatosis is the intracellular accumulation of neutral fat within parenchymal cells
• It is common in the liver as it plays a central role in fat metabolism

Microscopic Appearance:

• The fatty liver shows numerous lipid vacuoles in the cytoplasm of hepatocytes
• It is seen as a clear area that may vary from minute droplets to an extension of the entire cytoplasm

1. Initially

• Vacuoles are small
• They are present around the nucleus
• Centrilobular hepatocytes are affected

2. Later

• Vacuoles enlarge
• They push the nucleus to the periphery of the cells
• Fat accumulation involves the entire lobule
• Occasionally adjacent cells containing fat may rupture producing fatty cysts
• Rarely, lymphogranuloma may appear consisting of a collection of microphones, lymphocytes, and multi-nucleate giant cells

Intracellular Accumulations Short Essays

Question 1. What is fatty liver? What are its causes?
Answer:

• Fatty change/steatosis is the intra-cellular accumula¬tion of neutral fat within parenchymal cells.
• It is especially common is the liver as it plays a central role in fat metabolism,
• It may occur in other non-fatty tissues like the heart, skeletal muscles, kidneys, and other organs.

Fatty Liver Types:

• Fatty change may be
  • Mild and reversible
  • Severe and irreversible resulting in cell death.

Etiology: Fatty change in the liver results from.

Question 2. Wear and tear pigment
Answer:

• Lipofuscin is known as wear and tear pigment.
• Lipofuscin/lipochrome is a yellowish-brown intra-cellular lipid pigment.
• It is a hemoprotein-derived pigment

Site of Appearance:

• In atrophied cells of old age and Lence known as wear and tear pigment.
• It is seen in myocardial fibers, hepatocytes, Leydig cells of the testis, and neurons in senile dementia.

Significance:

• Lipofuscin represents the collection of indigestible material in the lysosomes after intra-cellular lipid peroxi¬dation and is therefore an example of residual bodies.

Microscopy:

• By light microscopy, the pigment is coarse, golden brown granular, and often.’ accumulates in the central part of the cells around the nuclei.
• In heart muscle, change is associated with wasting of the muscle and is commonly refered to as brown atrophy.
• By electron microscopy, lipofuscin appears. J as integrally- ribosomal electron-dense granules in perinuclear location. Granules are composed of did-protein complexes.

Question 3. Hemosiderosis
Answer:

Hemosiderosis Definition:

• Excessive storage of hemosiderin is called he-mosiderosis

Hemosiderosis Causes:

• Increased breakdown of red cells
• Systemic overload of iron due to
  • Primary causes
    • Idiopathic
    • Hereditary
  • Secondary causes
    • Thalassaemia
    • Sideroblastic anemia
    • Alcoholic cirrhosis

Hemosiderosis Effects:

1. Localized hemosiderosis

• Black eye occurs due to bilirubin and biliverdin
• Brown induration in the lungs occurs due to small hemorrhages

2. Generalized hemosiderosis

• Parenchymatous deposition of hemosiderin in the liver, kidney, pancreas
• Reticuloendothelial deposition in the liver, spleen, and bone marrow

Intracellular Accumulations Short Question And Answers

Question 1. Melanin pigment
Answer:

• Melanin is an endogenous pigment
• Melanin is a brown-black, non-hemoglobin-derived pigment normally present in the hair, skin, choroid of the eye, meninges, and adrenal medulla.

Melanin pigment Synthesis:

• It is synthesized in the melanocytes and dendritic cells

Melanin pigment Storage:

• Stored in the form of cytoplasmic granules in the phagocytic cells called as melanophores.

Melanin pigment Disorders:

Various disorders of melanin pigmentation cause gen¬eralised and localized hyperpigmentation and hypopigmentation.

1. Generalised hyperpigmentation is seen during.

• Addison’s disease
• Chloasma
• Chronic arsenal poisoning.

2. Focal hyperpigmentation.

• Cafe-au-lait spots in Albright’s syndrome.
• Peutz-Jeghers syndrome.
• Melanosis coli.
• Melanotic tumors
• Dermatopathiclymphadentis.

3. Generalised hypopigmentation.

• Albinism

4. Localised hypopigmentation.

• Leukodema
• Vitiligo
• Acquire focal hypopigmentation.

Question 2. Exogenous pigment
Answer:

Exogenous pigments are the pigments introduced into the body from outside such as by inhalation, ingestion, or inoculation.

Inhaled pigments:

• The most commonly inhaled substances are carbon/coal, dust, silica/stone dust, iron oxide, asbestos, and various other organic substances.
• These substances may cause occupational lung disease called pneumoconiosis.
• Extensive deposition of particulate material over many years provides low-grade inflammation, fibrosis, and impaired respiratory function.

Ingested pigments:

• Chronic ingestion of certain metals may produce pigmentation. E^/Argyria, chronic lead poisoning, melanosis coli.

Injected pigments:

• Examples of injected pigments are prolonged use of ointments containing mercury, dirt left accidentally in a wound, and tattooing by pricking the skin with dyes.
• In it pigment is taken by the macrophages and lies permanently in the connective tissue

Question 3. Fatty degeneration/ fatty change
Answer:

• Fatty degeneration or fatty change is the intracellular accumulation of neutral fat within parenchymal cells
• It occurs in the cytosol and represents an absolute increase in the intracellular lipids

Fatty change Types:

• Depending upon the cause and amount of accumulation, fatty change can be

1. Mild and reversible
2. Severe and irreversible- Causing cell death

Question 4. Causes of Ketonuria.
Answer:

• Metabolic abnormalities – diabetes, renal glycosuria
• Dietary conditions – starvation, fasting, prolonged vomiting, anorexia
• Hyperthyroidism, fever, pregnancy, lactation

Question 5. Ketone bodies.
Answer:

• Ketone bodies are water-soluble molecules – acetone, acetoacetate, and beta-hydroxybutyrate
• They are produced by the liver from fatty acids during low food intake, starvation, prolonged intense exercise, alcoholism or untreated diabetes mellitus
• Ketone bodies are readily picked up by the extrahepatic tissues and converted into acetyl CoA which enters the citric acid cycle
• It is oxidized in mitochondria for energy

Morphology Of Cell Injury Important Notes

1. Types of necrosis

2. Types of degeneration

• Cloudy swelling – a most common type
• Hydropic
• Hyaline
• Mucoid degeneration

3. Morphological forms of cell injury

• Reversible
  • Cellular Swelling
  • Fatty change
  • Hyaline change
  • Mucoid change
• Irreversible
  • Apoptosis
  • Autolysis
  • Necrosis

4. Apoptosis

• Apoptosis is physiological or programmed cell death
• It eliminates cells that are genetically altered or injured beyond repair without eliciting a severe host reaction
• It prevents the development of epithelial dysplasia by programmed cell death
• It is usually single-cell death and undergoes coagulative necrosis.

Morphology Of Cell Injury Long Essays

Question 1. Classify necrosis. Discuss its nuclear changes.
Answer:

Necrosis Classification:

Necrosis is classified into the following types:

1. Coagulative necrosis

• Caused by irreversible focal injury

2. Liquefaction necrosis

• Occurs due to ischaemic injury and bacterial or fungal infections

Read And Learn More: Pathology Question And Answers

3. Caseous necrosis

• Found in the center of foci of tuberculous infections

4. Fat necrosis

• Occurs at two anatomically different locations

5. Fibrinoid necrosis

• Deposition of fibrin-like material occurs

Nuclear Changes In Necrosis:

1. Pyknosis

• It is a condensation of nuclear chromatin

2. Karyolysis

• Undergo dissolution

3. Karyorrhexis

• Fragmentation

Question 2. Define necrosis. Classify and discuss different types of necrosis.
(or)
Define necrosis. Discuss etiopathogenesis and morphology of various types of necrosis.
Answer:

Definition:

Necrosis is defined as a localized area of death of tissue followed by degradation of tissue by hydrolytic enzymes liberated from dead cells, it is invariably accompanied by an inflammatory reaction

Necrosis Types:

There are five types of necrosis

1. Coagulative necrosis

• Causes:
  • Ischaemia
  • Bacterial infection
  • Chemical agents like mercuric chloride
• Pathogenesis
  • Irreversible cell injury
  • Results in sudden cessation of blood flow

2. Liquefaction necrosis

• Causes:
  • Ischaemia
  • Bacterial infections
• Pathogenesis
  • Bacterial and fungal infections produce hydro-lytic enzymes
  • This causes the degradation of tissue

3. Caseous necrosis

• Occurs in the center of foci of Tuberculous infections

4. Fat necrosis

• Occurs at two anatomically different locations
• Types
  • Acute pancreatic necrosis
  • Traumatic fat necrosis

5. Fibrinoid necrosis

• Deposition of fibrin-like material occurs

Morphology of types of Necrosis:

Question 3. Define and classify gangrene. Write the differences between dry and wet gangrene
Answer:

Definition:

• Gangrene is a form of necrosis of tissue with superadded putrefaction

Gangrene Classification:

• Gangrene is classified into two main types

1. Dry gangrene
2. Wet gangrene

Difference Between Dry and Wet Gangrene:

Question 4. Write about wet gangrene.
Answer:

Wet Gangrene:

Wet gangrene usually occurs in moist tissues and organs

Site Involved:

• Mouth
• Bowel
• Lung
• Cervix
• Vulva

Wet Gangrene Cause:

• Venous blockage

Wet Gangrene Pathogenesis:

• The affected part is filled with blood
• It favors the rapid growth of Putrefaction bacteria
• Formation of toxic products by bacteria
• Absorption of toxic products
• Causes septicemia
• Finally causes death

Wet Gangrene Features:

1. Gross features

• The affected part appears soft, swollen, putrid, rotten, and dark
• Part is stained dark

2. Microscopic features

• Coagulative necrosis is seen
• There is ulceration of the mucosa and intense inflammatory infiltration
• Lumen shows mucus and blood
• There is no line of demarcation present.

Morphology Of Cell Injury Short Essays

Question 1. Types of necrosis with examples
Answer:

Types of Necrosis:

Question 2. Dry gangrene
Answer:

Gangrene:

• Gangrene is a form of necrosis of tissue with super-added putrefaction

Dry Gangrene:

• It is a form of gangrene occurring due to Ischaemia

Dry Gangrene Causes:

• Ischaemia
• Atherosclerosis
• Buerger’s disease
• Raynaud’s disease
• Trauma
• Ergot poisoning

Dry Gangrene Features:

• Begins in the distal part of a limb
• Occurs in one of the toes which is farthest from the blood supply
• Here bacteria fail to grow in the necrosed tissue
• Gangrene spreads slowly upwards until it reaches an area with a good blood supply
• The line of demarcation is seen between the gangrenous part and the viable part

Dry Gangrene Gross Appearance:

• The affected part is dry, shrunken, and dark black
• It appears black due to the liberation of hemoglobin from hemolysed red blood cells which is acted upon by hydrogen disulfide produced by bacteria
• The line of demarcation is seen

Dry Gangrene Microscopic Appearance:

• Necrosis with smudging of the tissue is seen
• The line of demarcation contains inflammatory granulation tissue

Question 3. What is dystrophic calcification? Give two examples.
Answer:

Dystrophic calcification is the deposition of calcium salts in dead and degenerated tissues with normal calcium metabolism and normal serum calcium levels

Dystrophic Types:

1. Calcification in dead tissue: Examples

• Caseous necrosis in tuberculosis
• Liquefaction necrosis in chronic abscess
• Fat necrosis
• Gamma Gandy bodies in chronic venous congestion
• Infarcts
• Thrombi in veins
• Haematomas in bones
• Dead parasites
• Calcification in breast cancer
• Congenital toxoplasmosis

2. Calcification in degenerated tissues

• Stroma of tumors
• Atheromas
• Dense old scars
• Cysts
• Calcinosis cutis
• Senile degeneration

Dystrophic Pathogenesis:

1. Initiation

• Precipitates of calcium and phosphate begin to accumulate both intracellularly and extracellularly

2. Propagation

• Mineral deposits propagate to form mineral crystals

Question 4. Differences between Necrosis and Apoptosis.
Answer:

Morphology Of Cell Injury Short Question And Answers

Question 1. Irreversible cell injury
Answer:

• Cell injury is defined as a variety of stresses a cell en-. counters as a result of changes in its internal and external environment
• When such an injury is severe and persistent, cell death occurs
• Such an injury is called irreversible cell injury

Irreversible cell injury Features:

• The inability of the cell to reverse mitochondrial dysfunction
• Disturbance in cell membrane functions
• Reduction in ATP
• Continued depletion of proteins
• Reduced intracellular pH
• Leakage of lysosomal enzymes

Question 2. Etiology of cell injury
Answer:

Cell injury occurs due to the following causes:

1. Genetic causes

2. Acquired causes

• Hypoxia and ischemia
• Physical agents
• Chemical agents
• Microbial agents
• Nutritional derangements
• Immunologic agents
• Aging
• Iatrogenic factors
• Idiopathic

Question 3. Free radical injury
Answer:

• The free radical injury occurs in situations like ionizing radiation
• Oxygen free radicals are produced within the mitochondrial matrix
• They are:
  • Superoxide
  • Hydrogen peroxide
  • Hydroxyl radical

Free radical injury Effects:

• Lipid peroxidation
• Oxidation of proteins
• DNA damage
• Cytoskeletal damage

Question 4. Reversible cell injury
Answer:

• Cell injury is defined as a variety of stresses a cell encounters as a result of changes in its internal and external environment
• When the stress is mild to moderate, the injured cell may recover, it is called reversible cell injury

Question 5. Hyaline calcification
Answer:

• It describes the glassy, homogeneous, eosinophilic appearance of a material
• It is associated with pathological conditions that may be intracellular or extracellular

Question 6. Dystrophic and metastatic calcification.
Answer:

Question 7. Apoptosis
Answer:

Apoptosis is a form of coordinated and internally programmed cell death that has significance in a variety of physiologic and pathological conditions

1. Apoptosis in biological processes

• Organized cell destruction during the development of the embryo
• Physiologic involution of cells in hormone-dependent tissues
• Normal cell destruction

2. Pathologic process

• Cell death in tumors
• Cell death by cytotoxic T cells
• Cell death in viral infections
• Pathologic atrophy of organs