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Special pathomorphology.

1. Definition, classification and morphological characteristics of anemia?

Anemia is a blood disease of erythrocytes quantity or their hemoglobin saturation per unit blood volume. In addition,
there could be erythrocytes of different shapes circulating i.e. anisocytosis; erythrocytes of different sizes poikilocytosis
or poikilocythemia; different level of coloring i.e. hyper chromia, hypochromia

Classification of anemia: post hemorrhagic anemia which result from blood loss; anemia as a result of erythropoiesis
disturbance; hemolytic anemia which results from increased hemolysis.

1. Post hemorrhagic anemia:


a. acute post hemorrhagic anemia occurs because of bleeding of large vessels and death occurs faster than
morphological changes,
b. Chronic post hemorrhagic anemia: its manifestation includes pallor skin, mucous tunics and viscera.
Hyperplasia of red bone marrow of flat bones. Metaplasia of yellow bone marrow occurs turning red;
centers of extramedullary erythropoiesis in the spleen, thymus, lymph nodes and other tissues occur.
2. Disturbance of erythropoiesis: occurs due to deficiency of Iron, Vitamin B12 of folic acid.
a. Hypochromic anemia: due to reduced iron intake
b. Hyper chromic anemia: due to disturbance in absorption of exogenous Vitamin B12 or folic acid due to
stomach disease, characterized by megaloblastic cells
3. Hemolytic anemia: characterized by increased hemolysis which can be intravascular or extravascular.
a. Intravascular: occurs when hemolytic poison gets into the blood e.g. malaria, sepsis, blood transfusions
b. Extravascular (intracellular): mostly inherited

2. Name the changes in parenchymal organs at different forms of anemia. The complications at anemia and causes of
death.

3. Definitions, classification, morphological characteristic of thrombocytopenia and thrombocytopathy?

Thrombocytopathies are diseases in which morphologic, functional, biochemical thrombocytes impairment observed,
which causes hemorrhagic syndrome development in the vessels of microcirculatory channels. It can be congenital or
acquired. They are characterized by the disturbance of the formation of hemostatic thrombocyte plug including
adhesion, secretion and aggregation.

Thrombocytopenia decreased quantity of platelets in circulating blood. Normal is 150-450 Mega

4. Classification and morphological characteristic of coagulopathy?

Coagulation is a group of diseases connected with the disturbance of blood circulation system. Prolonged deficiency of
any coagulation factor causes hemorrhagic syndrome in the organism. It can be congenital i.e. hemophilia A (factor 7) or
hemophilia B (factor 9) or aquired i.e. vitamin k deficiency

5. Leukemia: types, clinical-anatomical and histologically-genetic classification. Change in the bone marrow and
parenchymal organs in leukemia?

6. Lymphogranulomatosis. Morphological characteristics of development stages of lymphogranulomatosis?

Lymphogranulomatosis (Hodgkin disease) is tumoral disease is the lymphatic system, characterized by malignant
hyperplasia of lymphoid tissue with the formation of lymphogranuloma in the lymph nodes and internal organs.
Lymphogranulomatosis (Hodgkin’s lymphoma): the development of malignant nodular swelling of lymph nodes in
various parts of the body. It is characterized by the presence of giant multi nucleated cells called Reed-Sternberg cells
and Hodgkin’s mononuclear cells.

7. Multiple myeloma: morphological characteristics of changes in the bones and internal organs.

8. Myocarditis: types, morphological manifestations and consequences.

9. Pericarditis: types and reasens of disease development, morphological manifestations and consequences.

10. Atherosclerosis: definition according to the WHO; etiology, pathogenesis, changes in the vascular wall according to
phase of its development?

Atherosclerosis us various combinations of changes of internal membrane of arteries, which show up as a focus laying of
lipids, difficult connections of carbohydrates, elements of blood and circulatory in it matters, the formation of the
connecting tissue and laying of calcium. It damages elastic and elastic muscular type of vessels

Pathogenesis: four stages involved:

1. The prelipid stage: damage to endothelial cells i.e. loss of glycocalyx, lipoprotein (mainly LDL- which countract
the conversion of macrophages to foamy cells)) penetrates from blood plasma into damaged epithelium causing
swelling
2. the stage of lipid spots:
3. Stage of fibrous plaque (atheroma)
4. Stage of complicated defeats (ulceration, calcinosis, thrombosis)

11. Ischemic myocardial dystrophy and its morphological manifestations.

12. Myocardial infarction: causes of development, clinical - morphological manifestations, consequences of pathology.

13. Morphogenesis of acute and chronic insufficiency of heart. Cardiosclerosis.

14. Atherosclerosis: etiology, pathogenesis, clinical - morphological forms and their manifestations?

Etiology:

MORPHOLOGIC FEATURES Early lesions in the form of diffuse intimal thickening, fatty streaks and gelatinous lesions are
often the forerunners in the evolution of atherosclerotic lesions. However, the clinical disease states due to luminal
narrowing in atherosclerosis are caused by fully developed atheromatous plaques and complicated plaques.

1. FATTY STREAKS AND DOTS. Fatty streaks and dots on the intima by themselves are harmless but may be the
precursor lesions of atheromatous plaques. Grossly, the lesions may appear as flat or slightly elevated and
yellow. They may be either in the form of small, multiple dots, about 1 mm in size, or in the form of elongated,
beaded streaks. Microscopically, fatty streaks lying under the endothelium are composed of closely-packed
foam cells, lipidcontaining elongated smooth muscle cells and a few lymphoid cells. Small amount of
extracellular lipid, collagen and proteoglycans are also present
2. GELATINOUS LESIONS. Gelatinous lesions develop in the intima of the aorta and other major arteries in the first
few months of life. Like fatty streaks, they may also be precursors of plaques. They are round or oval,
circumscribed grey elevations, about 1 cm in diameter. Microscopically, gelatinous lesions are foci of increased
ground substance in the intima with thinned overlying endothelium.
3. ATHEROMATOUS PLAQUES. A fully developed atherosclerotic lesion is called atheromatous plaque, also called
fibrous plaque, fibrofatty plaque or atheroma. Grossly, atheromatous plaques are white to yellowishwhite
lesions, varying in diameter from 1-2 cm and raised on the surface by a few millimetres to a centimetre in
thickness. Cut section of the plaque reveals the luminal surface as a firm, white fibrous cap and a central core
composed of yellow to yellow-white, soft, porridgelike material and hence the name atheroma.

15. Hypertensive illness: definition, risk factors, pathogenesis, clinical - morphological stages of hypertensive disease?

Hypertensive disease or essential hypertension is a chronic disease with increase of arterial pressure.

Secondary/ symptomatic hypertension occurs at diseases of nervous system, kidneys and vessels. E.g. nephrogenic,
renal vasculitis, Ichenko Cushing, primary aldosteronism, polycythemia.

Risk factors: age, smoking, obesity, sedentary life style, genetics, alcohol consumption

Clinical-morphological stages: there are 3:

1. preclinical or transient: hypertrophy of muscular layer and hyperplasia of elastic structures of arteriole.
Hypertrophy of left ventricle of heart.
2. stage of widespread changes of arteries: characterized by constantly increasing heart pressure, increase in
permeability in walls of small artery. Plasmorrhagia and development of hyalinosis and arteriosclerosis
3. stage of secondary changes i.e. organ stage: characterized by destructive, atrophic and sclerotic changes of
internal organs

16. Morphological changes in blood vessels and organs at Hypertensive diseases; causes of death?

stage of widespread changes of arteries: characterized by constantly increasing heart pressure, increase in permeability
in walls of small artery. Plasmorrhagia and development of hyalinosis and arteriosclerosis. Vascular wall becomes
thickened and lumen of arteriol becomes narrower. In large arteries elastofibrosis develops and atherosclerosis.
Elastofibrosis is a compensative process for hypertension as hyperplasia and the rupturing up of the internal elastic
membrane of vascular wall. The development of atherosclerosis is related to the destruction of the vascular wall,
accumulation of cholesterol and increased arterial pressure.

17. Rheumatic disease (Sokolsky-Bouillaud disease). Etiology and pathogenesis, morphological manifestations, phases of
development of rheumatic disorganization of connective tissue; consequences of disease?

Rheumatic diseases are a group of chronic diseases characterized by systemic lesions of connective tissue and blood
vessels. In their etiology a significant role is played by latent streptococci infection and allergic reaction of delayed and
immediate type. This leads to the development of progressive disorganization of connective tissues – mucous edema, a
fibrinoid edema and necrosis, cellular reaction (granulamatosis) and sclerosis.

18. Rheumatoid polyarthritis: etiology, pathogenesis, morphological manifestations?

Rheumatoid arthritis is a chronic disease based on progressive disorganization of connective tissue of synovial
membranes and articular cartilages. Its characteristic feature is the development of nonsuppurative proliferative
synovitis followed by articular deformations.

Rheumatoid arthritis is a chronic inflammatory disorder that mostly effect the joints but can involve other organs like
the skin or the lungs. Rheumatoid arthritis is an autoimmune process that is typically triggered by an interaction
between a genetic factor and the environment. Hence the environmental factors create modifications in our antibodies
i.e. IgG or proteins like Collagen 2 or vimentin.

Citrullination is a process that can modify collagen type 2 and vimentin. Citrullination is when the amino acid arginine
found in these proteins is converted into citrulline. Immune cells will no longer recognize these proteins as self antigens
and attack them.
Morphology: formation of Pannus i.e. thick swollen synovial membrane with connective tissue made up of fibroblasts,
inflammatory cells and myofibroblasts. Overtime the pannus can break down the hyaline cartilage and damage the
articulating bones.

19. Lupus erythematosus (Libman-Sacks disease): etiology, pathogenesis, morphological changes?

SLE is a systemic autoimmune disease that can be acute or chronic and is characterized by erythematosus (skin
reddening) and lesions of skin, vessels and kidneys.

Etiology: SLE typically occurs when antinuclear antibodies produced by plasma cells bind to nuclear antigens of
apoptosed cells forming antibody-antigen complexes. These complexes then are deposited onto vessel walls, organs and
other tissue initiating a local inflammation reaction. This causes damage due to the activation of the complement system
i.e. MAC – this damages tissues i.e. type III hypersensitivity.

SLE is more common in women and estrogen is thought to be the reason.

Morphology:

Vessels: fibrinoid changes in the walls of microcirculatory vessels with formation of vasculitis

Skin: reddening of skin (erythema) due to proliferation of vasculitis in the derma, lymphohistiocytic infiltration

Kidneys: deposition of immune complexes and capillary thickening. Fibrinoid necrosis foci, hyaline thrombi, hematoxylin
bodies

Heart:

20. Scleroderma: pathogenesis, morphological manifestations?

Systemic scleroderma (systemic sclerosis) is defined by the development of diffuse sclerosis and hyalonosis of
connective tissue in various organs and tissues. It is characterized by excessive deposit of collagen in the skin and organs.

Pathogenesis:

Heart: sclerosis and contraction of mitral valve cusps, subendocardial cardiosclerosis with the development of
cardiovascular collapse – sclerodermic heart

Coronary vessels: concentric sclerosis and hyalinosis. Around the vessels there is inflammatory infiltration with
lymphocytes, macrophages and plasmatic cells

Skin: diffuse or focal epidermal atrophy. Sclerotic transformations and hyalinosis of connective tissue, in dermal vessels
one can observe vasculitis and reduction of blood stream which can cause necrosis exulceration foci in the skin. The face
can become mask like.

Kidneys: progressive vasculitis, concentric thickening and thrombosis of interlobular arteries. Cortical necrosis and
infarcts. Parenchymal sclerosis with the development of renal insufficiency.

GI: sclerotic transformations of submucous and muscular layer, swallowing and absorption disturbance, slowing-down of
motility and development of cachexia (weakening and wasting away of body part)

21. Nodular periarteritis: pathogenesis, morphological manifestations?

Nodular periarteritis is a systemic necrotizing inflammation of blood vessels (vasculitis) affecting medium-sized muscular
arteries, typically involving the arteries of the kidneys and other internal organs but generally sparing the lungs
circulation. In polyarteritis nodosa, small aneurysms are strung like the beads of a rosary, therefore making "rosary sign"
an important diagnostic feature of the vasculitis. PAN is associated with infection by the hepatitis B or hepatitis C virus.
Grossly, the lesions of PAN involve segments of vessels, especially at the bifurcations and branchings, as tiny beaded
nodules.

Microscopically, there are 3 sequential stages in the evolution of lesions in PAN:

i) Acute stage—There is fibrinoid necrosis in the centre of the nodule located in the media. An acute
inflammatory response develops around the focus of fibrinoid necrosis. The inflammatory infiltrate is
present in the entire circumference of the affected vessel (periarteritis) and consists chiefly of neutrophils
and eosinophils, and some mononuclear cells. The lumen may show thrombi and the weakened wall may be
the site of aneurysm formation.
ii) Healing stage—This is characterised by marked fibroblastic proliferation producing firm nodularity. The
inflammatory infiltrate now consists mainly of lymphocytes, plasma cells and macrophages.
iii) Healed stage—In this stage, the arterial wall is markedly thickened due to dense fibrosis. The internal elastic
lamina is fragmented or lost. Healed stage may contain haemosiderin-laden macrophages and organised
thrombus.

22. Bronchopneumonia (lobular pneumonia): classification, etiology, pathogenesis and complications?

Bronchopneumonia or lobular pneumonia is infection of the terminal bronchioles that extends into the surrounding
alveoli resulting in patchy consolidation of the lung.

ETIOLOGY. The common organisms responsible for bronchopneumonia are staphylococci, streptococci, pneumococci,
Klebsiella pneumoniae, Haemophilus influenzae, and gram-negative bacilli like Pseudomonas and coliform bacteria.

MORPHOLOGIC FEATURES. Grossly, bronchopneumonia is identified by patchy areas of red or grey consolidation
affecting one or more lobes, frequently found bilaterally and more often involving the lower zones of the lungs due to
gravitation of the secretions. On cut surface, these patchy consolidated lesions are dry, granular, firm, red or grey in
colour, 3 to 4 cm in diameter, slightly elevated over the surface and are often centred around a bronchiole. These patchy
areas are best picked up by passing the fingertips on the cut surface.

Histologically, the following features are observed:

i) Acute bronchiolitis.
ii) Suppurative exudate, consisting chiefly of neutrophils, in the peribronchiolar alveoli.
iii) Thickening of the alveolar septa by congested capillaries and leucocytic infiltration.
iv) Less involved alveoli contain oedema fluid.

COMPLICATIONS. The complications of lobar pneumonia may occur in bronchopneumonia as well. However, complete
resolution of bronchopneumonia is uncommon. There is generally some degree of destruction of the bronchioles
resulting in foci of bronchiolar fibrosis that may eventually cause bronchiectasis.
23. Lobar pneumonia (croupous pneumonia): etiology, morphological manifestations of stages of development of lobar
pneumonia?

Lobar pneumonia is an acute bacterial infection of a part of a lobe, the entire lobe, or even two lobes of one or both the
lungs.

ETIOLOGY. Based on the etiologic microbial agent causing lobar pneumonia, following types of lobar pneumonia are
described: Pneumococcal pneumonia; Staphylococcal pneumonia; Streptococcal pneumonia; Pneumonia by gram-
negative aerobic bacteria

Stages: Lobar pneumonia into 4 sequential pathologic phases:

1. stage of congestion (initial phase- 1-2 days): The initial phase represents the early acute inflammatory response
to bacterial infection. Grossly, the affected lobe is enlarged, heavy, dark red and congested. Cut surface exudes
blood-stained frothy fluid. Histologically, typical features of acute inflammatory response to the organisms are
seen. Dilatation and congestion of the capillaries in the alveolar walls. ii) Pale eosinophilic oedema fluid in the air
spaces. iii) A few red cells and neutrophils in the intra-alveolar fluid. iv) Numerous bacteria demonstrated in the
alveolar fluid by Gram’s staining.
2. red hepatisation (early consolidation 2-4 days): The term hepatisation in pneumonia refers to liver-like
consistency of the affected lobe on cut section. Grossly, the affected lobe is red, firm and consolidated. The cut
surface of the involved lobe is airless, red-pink, dry, granular and has liver-like consistency. The stage of red
hepatisation is accompanied by serofibrinous pleurisy. Histologically, the following features are observed i) The
oedema fluid of the preceding stage is replaced by strands of fibrin. ii) There is marked cellular exudate of
neutrophils and extravasation of red cells. iii) Many neutrophils show ingested bacteria.
3. grey hepatisation (late consolidation 4-8 days): Grossly, the affected lobe is firm and heavy. The cut surface is
dry, granular and grey in appearance with liverlike consistency. The change in colour from red to grey begins at
the hilum and spreads towards the periphery. Fibrinous pleurisy is prominent. Histologically, the following
changes are present i) The fibrin strands are dense and more numerous. ii) The cellular exudate of neutrophils is
reduced due to disintegration of many inflammatory cells as evidenced by their pyknotic nuclei. The red cells are
also fewer. The macrophages begin to appear in the exudate. iii) The cellular exudate is often separated from
the septal walls by a thin clear space. iv) The organisms are less numerous and appear as degenerated forms.
4. resolution (begins at 8th to 9th day and last for 1 to 3 weeks): Grossly, the previously solid fibrinous constituent
is liquefied by enzymatic action, eventually restoring the normal aeration in the affected lobe. The process of
softening begins centrally and spreads to the periphery. The cut surface is grey-red or dirty brown and frothy,
yellow, creamy fluid can be expressed on pressing. The pleural reaction may also show resolution but may
undergo organisation leading to fibrous obliteration of pleural cavity. Histologically, the following features are
noted: i) Macrophages are the predominant cells in the alveolar spaces, while neutrophils diminish in number.
Many of the macrophages contain engulfed neutrophils and debris. ii) Granular and fragmented strands of fibrin
in the alveolar spaces are seen due to progressive enzymatic digestion. iii) Alveolar capillaries are engorged. iv)
There is progressive removal of fluid content as well as cellular exudate from the air spaces, partly by
expectoration but mainly by lymphatics, resulting in restoration of normal lung parenchyma with aeration
24. Chronic nonspecific (Interstitial) pneumonia; Chronic bronchitis; Pneumosclerosis – morphological manifestations of
listed diseases.

25. Lobar pneumonia complications; the causes of death at the lobar pneumonia?

COMPLICATIONS

1. Organisation. In about 3% of cases, resolution of the exudate does not occur but instead it undergoes organisation.
There is ingrowth of fibroblasts from the alveolar septa resulting in fibrosed, tough, airless leathery lung tissue. This type
of post-pneumonic fibrosis is called carnification.

2. Pleural effusion. About 5% of treated cases of lobar pneumonia develop inflammation of the pleura with effusion.
The pleural effusion usually resolves but sometimes may undergo organisation with fibrous adhesions between visceral
and parietal pleura.

3. Empyema. Less than 1% of treated cases of lobar pneumonia develop encysted pus in the pleural cavity termed
empyema.

4. Lung abscess. A rare complication of lobar pneumonia is formation of lung abscess, especially when there is
secondary infection by other organisms. 5. Metastatic infection. Occasionally, infection in the lungs and pleural cavity in
lobar pneumonia may extend into the pericardium and the heart causing purulent pericarditis, bacterial endocarditis
and myocarditis. Other forms of metastatic infection encountered rarely in lobar pneumonias are otitis media,
mastoiditis, meningitis, brain abscess and purulent arthritis.

26. Acute and chronic obstructive pulmonary emphysema and its relationship with bronchitis, bronchiolitis and
pneumosclerosis. Morphological manifestations of disease.

27. Bronchial Asthma: etiology, pathogenesis and morphological manifestations?

ETIOPATHOGENESIS AND TYPES. Based on the stimuli initiating bronchial asthma, two broad etiologic types are
traditionally described: extrinsic (allergic, atopic) and intrinsic (idiosyncratic, non-atopic) asthma. A third type is a mixed
pattern

1. Extrinsic (atopic, allergic) asthma: Hypersensitivity to various extrinsic antigenic substances or ‘allergens’ is usually
present in these cases. Most of these allergens cause ill-effects by inhalation e.g. house dust, pollens, animal danders,
moulds etc. There are increased levels of IgE in the serum and positive skin test with the specific offending inhaled
antigen representing an IgE-mediated type I hypersensitivity reaction which includes an ‘acute immediate response’ and
a ‘late phase reaction’:

 Acute immediate response is initiated by IgE-sensitised mast cells (tissue counterparts of circulating basophils)
on the mucosal surface
 Late phase reaction follows the acute immediate response and is responsible for the prolonged manifestations
of asthma. It is caused by excessive mobilisation of blood leucocytes that include basophils besides eosinophils
and neutrophils

2. Intrinsic (idiosyncratic, non-atopic) asthma. This type of asthma develops later in adult life with negative personal or
family history of allergy, negative skin test and normal serum levels of IgE. Most of these patients develop typical
symptom-complex after an upper respiratory tract infection by viruses. Associated nasal polypi and chronic bronchitis
are commonly present.

MORPHOLOGIC FEATURES. The pathologic changes are similar in both major types of asthma. The pathologic material
examined is generally autopsy of lungs in patients dying of status asthmaticus but the changes are expected to be similar
in non-fatal cases. Grossly, the lungs are overdistended due to over-inflation. The cut surface shows characteristic
occlusion of the bronchi and bronchioles by viscid mucus plugs.
Microscopically, the following changes are observed:

1. The mucus plugs contain normal or degenerated respiratory epithelium forming twisted strips called Curschmann’s
spirals.

2. The sputum usually contains numerous eosinophils and diamond-shaped crystals derived from eosinophils called
Charcot-Leyden crystals.

3. The bronchial wall shows thickened basement membrane of the bronchial epithelium, submucosal

28. Gastritis: types, morphological characteristic and complications?

The term ‘gastritis’ is commonly employed for any clinical condition with upper abdominal discomfort like indigestion or
dyspepsia in which the specific clinical signs and radiological abnormalities are absent. The condition is of great
importance due to its relationship with peptic ulcer and gastric cancer. Broadly speaking, gastritis may be of 2 types—
acute and chronic. Chronic gastritis can further be of various types.

Acute gastritis is a transient acute inflammatory involvement of the stomach, mainly mucosa. The mucosal injury and
subsequent acute inflammation in acute gastritis occurs by one of the following mechanisms:

1. Reduced blood flow, resulting in mucosal hypoperfusion due to ischaemia.

2. Increased acid secretion and its accumulation due to H. pylori infection resulting in damage to epithelial barrier.
3. Decreased production of bicarbonate buffer.

ETIOPATHOGENESIS: Diet and personal habits; Infections (Helicobacter pylori); Viral infections (Viral hepatitis); Drugs
(NSAID); Severe stress (trauma)

MORPHOLOGIC FEATURES. Grossly, the gastric mucosa is oedematous with abundant mucus and haemorrhagic spots.
Microscopically, depending upon the stage, there is variable amount of oedema and infiltration by neutrophils in the
lamina propria. In acute haemorrhagic and erosive gastritis, the mucosa is sloughed off and there are haemorrhages on
the surface.

Chronic Gastritis: The mechanism of chronic gastric injury by any of the etiologic agents is by cytotoxic effect of the
injurious agent on the gastric mucosal epithelium, thus breaking the barrier and then inciting the inflammatory
response.

ETIOPATHOGENESIS. In the absence of clear etiology of chronic gastritis, a number of etiologic factors have been
implicated. All the causative factors of acute gastritis described above may result in chronic gastritis too. Recurrent
attacks of acute gastritis may result in chronic gastritis. Some additional causes are as under:

1. Reflux of duodenal contents into the stomach; 2. Infection with H. pylori; 3. Associated disease of the stomach and
duodenum; 4. Chronic hypochromic anaemia; 5. Immunological factors

CLASSIFICATION. Based on the type of mucosa affected (i.e. cardiac, body, pyloric, antral or transitional), a
clinicopathologic classification has been proposed (Table 20.2).

MORPHOLOGIC FEATURES. Grossly, the features of all forms of gastritis are inconclusive. The gastric mucosa may be
normal, atrophied, or oedematous.

Histologically, criteria for categorisation are based on the following:

i) Extent of inflammatory changes in the mucosa (i.e. superficial or deep).


ii) Activity of inflammation (i.e. quiscent or active; acute or chronic).
iii) Presence of and type of metaplasia (i.e. intestinal or pseudopyloric).

Based on above, following simple morphologic classification has been proposed:

1. Chronic superficial gastritis: there is inflammatory infiltrate consisting of plasma cells and lymphocytes in the
superficial layer of the gastric mucosa
2. Chronic atrophic gastritis: there is inflammatory cell infiltrate in the deeper layer of the mucosa and atrophy of
the epithelial elements including destruction of the glands.
3. Gastric atrophy: there is thinning of the gastric mucosa with loss of glands but no inflammation though
lymphoid aggregates may be present.
4. Chronic hypertrophic gastritis (Ménétrier’s disease): characterised pathologically by enormous thickening of
gastric rugal folds resembling cerebral convolutions, affecting mainly the region of fundic-body mucosa and
characteristically sparing antral mucosa. The patients present with dyspepsia, haematemesis, melaena or
protein-losing enteropathy.
5. Uncommon forms of chronic gastritis.
29. Peptic ulcer disease: causes, clinical and morphological characteristics of acute gastric ulcer, complications,
consequences?

Peptic ulcers are the areas of degeneration and necrosis of gastrointestinal mucosa exposed to acid-peptic secretions.
Though they can occur at any level of the alimentary tract that is exposed to hydrochloric acid and pepsin, they occur
most commonly (98-99%) in either the duodenum or the stomach in the ratio of 4:1. Each of the two main types may be
acute or chronic.

Acute peptic ulcers or stress ulcers are multiple, small mucosal erosions, seen most commonly in the stomach but
occasionally involving the duodenum.

ETIOLOGY. These ulcers occur following severe stress. The causes are as follows:

i) Psychological stress
ii) Physiological stress as in the following:
a. Shock
b. Severe trauma
c. Septicaemia
d. Extensive burns (Curling’s ulcers in the posterior aspect of the first part of the duodenum).
e. Intracranial lesions (Cushing’s ulcers developing from hyperacidity following excessive vagal
stimulation).
f. Drug intake (e.g. aspirin, steroids, butazolidine, indomethacin).
g. Local irritants (e.g. alcohol, smoking, coffee etc).

PATHOGENESIS: possible hypotheses for genesis of stress ulcers are as under:

1. Ischaemic hypoxic injury to the mucosal cells.

2. Depletion of the gastric mucus ‘barrier’ rendering the mucosa susceptible to attack by acid-peptic secretions.

MORPHOLOGIC FEATURES. Grossly, acute stress ulcers are multiple (more than three ulcers in 75% of cases). They are
more common anywhere in the stomach, followed in decreasing frequency by occurrence in the first part of duodenum.
They may be oval or circular in shape, usually less than 1 cm in diameter.
Microscopically, the stress ulcers are shallow and do not invade the muscular layer. The margins and base may show
some inflammatory reaction depending upon the duration of the ulcers. These ulcers commonly heal by complete re-
epithelialisation without leaving any scars. Complications such as haemorrhage and perforation may occur.

30. Clinical and morphological characteristics of chronic ulcer of stomach; complications and consequences of disease?

Chronic Peptic Ulcers (Gastric and Duodenal Ulcers): Gastric ulcer. The pathogenesis of gastric ulcer is mainly explained
on the basis of impaired gastric mucosal defenses against acid-pepsin secretions. Some other features in the
pathogenesis of gastric ulcer are as follows:

1. Hyperacidity may occur in gastric ulcer due to increased serum gastrin levels in response to ingested food in an
atonic stomach.
2. However, many patients of gastric ulcer have low-tonormal gastric acid levels. Ulcerogenesis in such patients is
explained on the basis of damaging influence of other factors such as gastritis, bile reflux, cigarette smoke etc.
3. The normally protective gastric mucus ‘barrier’ against acid-pepsin is deranged in gastric ulcer. There is
depletion in the quantity as well as quality of gastric mucus. One of the mechanisms for its depletion is
colonisation of the gastric mucosa by H. pylori seen in 75-80% patients of gastric ulcer

MORPHOLOGIC FEATURES. Gross Gastric ulcers are found predominantly along the lesser curvature in the region of
pyloric antrum, more commonly on the posterior than the anterior wall. typical peptic ulcers are commonly solitary
(80%), small (1-2.5 cm in diameter), round to oval and characteristically ‘punched out’. Benign ulcers usually have flat
margins in level with the surrounding mucosa. The mucosal folds converge towards the ulcer. The ulcers may vary in
depth from being superficial (confined to mucosa) to deep ulcers (penetrating into the muscular layer)/

Microscopically, chronic peptic ulcers have 4 histological zones. From within outside, these are as under (Fig. 20.14):

1. Necrotic zone—lies in the floor of the ulcer and is composed of fibrinous exudate containing necrotic debris and a few
leucocytes.

2. Superficial exudative zone—lies underneath the necrotic zone. The tissue elements here show coagulative necrosis
giving eosinophilic, smudgy appearance with nuclear debris.

3. Granulation tissue zone—is seen merging into the necrotic zone. It is composed of nonspecific inflammatory infiltrate
and proliferating capillaries.

4. Zone of cicatrisation—is seen merging into thick layer of granulation tissue. It is composed of dense fibrocollagenic
scar tissue over which granulation tissue rests. Thrombosed or sclerotic arteries may cross the ulcer which on erosion
may result in haemorrhage
COMPLICATIONS. Acute and subacute peptic ulcers usually heal without leaving any visible scar. However, healing of
chronic, larger and deeper ulcers may result in complications. These are as follows:

1. Obstruction. Development of fibrous scar at or near the pylorus results in pyloric stenosis. In the case of healed
duodenal ulcer, it causes duodenal stenosis. Healed ulcers along the lesser curvatures may produce ‘hourglass’
deformity due to fibrosis and contraction.

2. Haemorrhage. Minor bleeding by erosion of small blood vessels in the base of an ulcer occurs in all the ulcers and can
be detected by testing the stool for occult blood. Chronic blood loss may result in iron deficiency anaemia. Severe
bleeding may cause ‘coffee ground’ vomitus or melaena. A penetrating chronic ulcer may erode a major artery (e.g. left
gastric, gastroduodenal or splenic artery) and cause a massive and severe hematemesis and sometimes death.

3. Perforation. A perforated peptic ulcer is an acute abdominal emergency. Perforation occurs more commonly in
chronic duodenal ulcers than chronic gastric ulcers. Following sequelae may result in acute peritonitis

4. Malignant transformation.

31. Appendicitis: etiology, pathogenesis, clinical - morphological forms. Complications of acute appendicitis?

Acute inflammation of the appendix,

ETIOPATHOGENESIS. The most common mechanism is obstruction of the lumen from various etiologic factors that leads
to increased intraluminal pressure. This presses upon the blood vessels to produce ischaemic injury which in turn
favours the bacterial proliferation and hence acute appendicitis.

The common causes of appendicitis are as under:

A. Obstructive: 1. Faecolith 2. Calculi 3. Foreign body 4. Tumour 5. Worms (especially Enterobius vermicularis) 6. Diffuse
lymphoid hyperplasia, especially in children.

B. Non-obstructive: 1. Haematogenous spread of generalised infection 2. Vascular occlusion 3. Inappropriate diet lacking
roughage.
MORPHOLOGIC FEATURES. Grossly, the appearance depends upon the stage at which the acutely-inflamed appendix is
examined. In early acute appendicitis, the organ is swollen and serosa shows hyperaemia. In welldeveloped acute
inflammation called acute suppurative appendicitis, the serosa is coated with fibrinopurulent exudate and engorged
vessels on the surface. In further advanced cases called acute gangrenous appendicitis, there is necrosis and ulcerations
of mucosa which extend through the wall so that the appendix becomes soft and friable and the surface is coated with
greenish-black gangrenous necrosis.

Microscopically, the most important diagnostic histological criterion is the neutrophilic infiltration of the muscularis. In
early stage, the other changes besides acute inflammatory changes, are congestion and oedema of the appendiceal wall.
In later stages, the mucosa is sloughed off, the wall becomes necrotic, the blood vessels may get thrombosed and there
may be neutrophilic abscesses in the wall. In either case, an impacted foreign body, faecolith, or concretion may be seen
in the lumen

Complications of acute appendicitis: ruptured appendix, peritonitis (pocket of pus forms in abdomen)

CLINICAL COURSE. The patient presents with features of acute abdomen as under: 1. Colicky pain, initially around
umbilicus but later localised to right iliac fossa 2. Nausea and vomiting 3. Pyrexia of mild grade 4. Abdominal tenderness
5. Increased pulse rate 6. Neutrophilic leukocytosis

COMPLICATIONS. If the condition is not adequately managed, the following complications may occur:

1. Peritonitis. A perforated appendix as occurs in gangrenous appendicitis may cause localised or generalised peritonitis.
2. Appendix abscess. This is due to rupture of an appendix giving rise to localised abscess in the right iliac fossa. This
abscess may spread to other sites such as between the liver and diaphragm (subphrenic abscess), into the pelvis
between the urinary bladder and rectum, and in the females may involve uterus and fallopian tubes.

3. Adhesions. Late complications of acute appendicitis are fibrous adhesions to the greater omentum, small intestine
and other abdominal structures.

4. Portal pylephlebitis. Spread of infection into mesenteric veins may produce septic phlebitis and liver abscess.

5. Mucocele. Distension of distal appendix by mucus following recovery from an attack of acute appendicitis is referred
to as mucocele. It occurs generally due to proximal obstruction but sometimes may be due to a benign or malignant
neoplasm in the appendix. An infected mucocele may result in formation of empyema of the appendix.

32. Acute toxic dystrophy of liver: etiology, pathogenesis and morphological characteristics?
33. Cirrhosis of the liver: classifications according to etiologic, morphologic and functional principles. Morphology of
clinical and anatomical variations of cirrhosis?

Cirrhosis of the liver represents the irreversible end-stage of several diffuse diseases causing hepatocellular injury and is
characterised by the following 4 features:

1. It involves the entire liver.

2. The normal lobular architecture of hepatic parenchyma is disorganised.

3. There is formation of nodules separated from one another by irregular bands of fibrosis.

4. It occurs following hepatocellular necrosis of varying etiology so that there are alternate areas of necrosis and
regenerative nodules. However, regenerative nodules are not essential for diagnosis of cirrhosis since biliary
cirrhosis and cirrhosis in haemochromatosis have little regeneration.

Classification according to morphology: There are 3 morphologic types of cirrhosis—micronodular, macronodular and
mixed. Each of these forms may have an active (continuing hepatocellular necrosis and inflammatory reaction) and
inactive form (no evidence of continuing hepatocellular necrosis and has sharply-defined nodules of surviving hepatic
parenchyma without any significant inflammation).

1. Micronodular cirrhosis. In micronodular cirrhosis, the nodules are usually regular and small, less than 3 mm in
diameter. There is diffuse involvement of all the hepatic lobules forming nodules by thick fibrous septa which
may be portal-portal, portal-central, or both
2. Macronodular cirrhosis. In this type, the nodules are of variable size and are generally larger than 3 mm in
diameter. The pattern of involvement is more irregular than in micronodular cirrhosis, sparing some portal tracts
and central veins, and more marked evidence of regeneration.
3. Mixed cirrhosis. In mixed type, some parts of the liver show micronodular appearance while other parts show
macronodular pattern. All the portal tracts and central veins are not involved by fibrosis but instead some of
them are spared.
Alcoholic Liver Disease and Cirrhosis: Alcoholic liver disease is the term used to describe the spectrum of liver injury
associated with acute and chronic alcoholism. There are three sequential stages in alcoholic liver disease:

1. alcoholic steatosis (fatty liver),


2. alcoholic hepatitis and
3. alcoholic cirrhosis.
34. Clinical and morphological manifestations of acromegaly and pituitary dwarfism (nanizm)?

Pituitary dwarfism (nanism): short stature with normal length of arms and legs; hyperpigmentation; hypoglycemia; salt
craving; abdominal pain

Acromegaly: hormonal disorder caused by hypersecretion of growth hormone symptoms: enlarged hands and feet;
enlarged facial features; oily thickened skin

Pituitary Adenomas: Adenomas are the most common pituitary tumours. They are conventionally classified according to
their H & E staining characteristics of granules into acidophil, basophil and chromophobe adenomas.

MORPHOLOGIC FEATURES. Grossly, pituitary adenomas range in size from small foci of less than 10 mm in size (termed
microadenoma) to large adenomas several centimeters in diameter. They are spherical, soft and encapsulated.
Histologically, by light microscopy of H & E stained sections, an adenoma is composed predominantly of one of the
normal cell types of the anterior pituitary i.e acidophil, basophil or chromophobe cells. These cells may have following 3
types of patterns:

1. Diffuse pattern is composed of polygonal cells arranged in sheets with scanty stroma.

2. Sinusoidal pattern consists of columnar or fusiform cells with fibrovascular stroma around which the tumour
cells are arranged.

3. Papillary pattern is composed of columnar or fusiform cells arranged about fibrovascular papillae.
35. Diabetes mellitus: etiology, pathogenesis, clinical and morphological forms; complications and causes of death?

Diabetes mellitus is a chronical disease which appears due to insulin insufficiency and it’s a companied by metabolic
dysfunction.

Morphological forms:

Pancreas: atrophy, lipomatosis, hyalinosis, sclerosis

Liver: fatty atrophy, decrease in glycogen content in liver hepatocyte

Vessels: diabetic macroangiopathy – characterized by affection of elastic and muscular elastic types of arteries. It is
displayed by progressive atherosclerosis with the progress of vessel necrosis and lower extremity gangrene. Diabetic
microangiopathy – characterized by affection to arterioles and capillaries of different organs and tissues, the plasmatic
dripping and the basal membrane., lipohyalinosis, dystrophic changes, proliferation of endothelium and perithelium,
atrophic changes of cells, inflammatory lymphohistiocytic seepage of the side

Retina of eye: 2 type of retinopathy can occur: Non-proliferative (simple diabetic)- provokes separate microaneurysms
(dotty extravasation). Proliferative – provokes capillary neoplasm, considerable extravasations, retina sclerosis,
sclerosis of optic nerve II papilla with progress of glaucoma.

Nervous system: symmetric affection of peripheral nerves especially in lower extremities, segmental demyelination,
edema, axon dystrophy.

Kidneys: glomerulonephritis and glomerulosclerosis, proliferation of mesangial cells in glomerulus and hyaline
degeneration of mesangial develops. Fibrin hats appear on the glomerulus, glucogenic infiltration, fatty dystrophy and
hydropic (vacuolar) degeneration in segments of nephron. The kidney decrease in size symmetrically, have small grained
surface and hard consistence, the glomerulosclerosis can be follicular (nodular), diffuse and mixed. Clinical symptoms –
high proteinuria, edema, arterial hypertension

Cause of death: gangrene of upper extremity then septic pyemia, myocardial infarction, uremia

36. Endemic goiter: reasons of development; morphological and clinical manifestations?

Found in regions where there is a lack of iodine that determines the decrease in synthesis of the thyroid gland, because
of that the compensatory hypertrophy of the thyroid gland occurs. Eventually hypothyroidism occurs. Adults have
myxedema and children have endemic cretinism (mental and growth retardation)

37. Graves' disease: etiology, clinical and morphological forms?

Occurs due to hyperthyroidism which can occur due to autoimmunization where the antibodies stimulate the cellular
receptors of the thyroticis. There is a genetic inclination for this disease
Clinical symptoms: growth of the thyroid gland, tachycardia, loss of weight, increased nervous excitability.

Morphological changes: thyroid gland grows diffusely, it has a soft consistency, prismatic follicles of the epithelium
change into cylindrical ones, pseudo papillae appear, rarefaction of colloid, lymphoplasmacytic seepage of stroma.

38. Endocrine diseases of adrenal glands: classification, clinical and morphological forms and their manifestations?

Disease of the adrenals are divided into disease of the adrenal cortex (glomerulus- mineral corticoids- aldostrone;
fasciculata- Glucocorticoid - cortisol; reticularis-androgens) and cerebral and it can be hyperfunction or hypofunction.

Hyperfunction of cortex:

 Cushing disease: is a cause of Cushing's syndrome characterised by increased secretion of adrenocorticotropic


hormone (ACTH) from the anterior pituitary (secondary hypercortisolism). This is most often as a result of a
pituitary adenoma (specifically pituitary basophilism) or due to excess production of hypothalamus CRH
(corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism) that stimulates the synthesis of
cortisol by the adrenal glands. Pituitary adenomas are responsible for 80% of endogenous Cushing's syndrome,
when excluding Cushing's syndrome from exogenously administered corticosteroids. Symptoms: moon face, red
face, weight gain, loss of muscles, high blood pressure, poor short-term memory, red stretch marks
 Hyperaldosteronism: appears on the basis of an adenoma (aldoseroma). It can be primary or secondary. Its
accompanied by hypernatremia and hypokalemia. Arterial hypertension, muscle asthenia, impaired cardiac
function
 Hyper androgenic: accumulation of androgenic hormones which provokes progress of viricides

39. Glomerulopathies: etiology, pathogenesis, morphology of acute, subacute and chronic glomerulonephritis?

Glomerulopathies can be malformed (primary) or acquired:

Primary: main pathomorphological changes develop in membrane structures of glomerulus. It causes disorder of
filtration and formation of primary urine. Examples include:

 Alport syndrome: characterized by early development of renal insufficiency, with deficiency of ear and sight.
Morphologically it is shown with hemorrhagic type of glomerulonephritis and infiltration of intersitium with
lipids.
 System nephritis with amyloidosis:

Acquired: glomerulonephritis, nephrotic syndrome, amyloidosis, diabetic glomerulosclerosis.’

 Glomerulonephritis: mostly infectious allergic disease where immune complexes are deposited in the
subendothelial, subepithelial or mesangial. This causes damage to basal membrane of glomerulus. This typically
occurs after B-hemolytic streptococcus (i.e. Quincy and scarlet fever).
 Glomerulonephritis can occur due to immune complex or nephrotoxical, it can be acute or chronic (delayed
type hypersensitivity)
 Clinical features: oliguria, hematuria, proteinuria, arterial hypertension and oedema

Acute glomerulonephritis: it begins from intracapillary (endothelial cells) exudative changes then to extracapillary
(bowman capsule) changes and last productive changes occur. Exudative intracapillar glomerulonephritis: immune
complexes deposited in subendothelial injuring membrane which causes plasmorrhagy and leucodiapedesis. This causes
oedema of mesangium and infiltration of it by leukocytes. Exudative extracapillar: accumulation of exudate (serous,
fibrous, hemorrhagic) in cavity of capsule. Proliferative: characterized with reproduction of endothelial and mesangial
cells

MORPHOLOGIC FEATURES. Grossly, the kidneys are symmetrically enlarged, weighing one and a half to twice the
normal weight. The cortical as well as sectioned surface show petechial haemorrhages giving the characteristic
appearance of flea-bitten kidney.
Glomeruli—The glomeruli are affected diffusely. They are enlarged and hypercellular. The diffuse hypercellularity of the
tuft is due to proliferation of mesangial, endothelial and occasionally epithelial cells (acute proliferative lesions) as well
as by infiltration of leucocytes, chiefly polymorphs and sometimes monocytes (acute exudative lesion). There may be
small deposits of fibrin within the capillary lumina and in the mesangium.

Subacute glomerulonephritis: rapid onset/ malignant. Growing endothelial cells of capsule, proliferation of cells
squeezes bowman capsule and capillaries leading to renal failure

MORPHOLOGIC FEATURES. Grossly, the kidneys are usually enlarged and pale with smooth outer surface (large white
kidney). Cut surface shows pale cortex and congested medulla.

Glomeruli—Irrespective of the underlying etiology, all forms of RPGN show pathognomonic ‘crescents’ on the inside of
Bowman’s capsules. These are collections of palestaining polygonal cells which commonly tend to be elongated.
Eventually, crescents obliterate the Bowman’s space and compress the glomerular tuft. Fibrin deposition is invariably
present alongside crescents. Besides the crescents, glomerular tufts may show increased cellularity as a result of
proliferation of endothelial and mesangial cells and leucocytic infiltration. Fibrin thrombi are frequently present in the
glomerular tufts
Chronic glomerulonephritis: ends with sclerosis and hyalinosis of capillary glomerules forming lesions in cavity of
capsule

MORPHOLOGIC FEATURES. Grossly, the kidneys are usually small and contracted weighing as low as 50 gm each. The
capsule is adherent to the cortex. The cortical surface is generally diffusely granular (Fig. 22.22). On cut section, the
cortex is narrow and atrophic, while the medulla is unremarkable.

Microscopically, the changes vary greatly depending upon the underlying glomerular disease. In general, the following
changes are seen (Fig. 22.23).

i) Glomeruli—Glomeruli are reduced in number and most of those present show completely hyalinised tufts,
giving the appearance of acellular, eosinophilic masses which are PAS-positive. Evidence of underlying
glomerular disease may be present.
ii) Tubules—Many tubules completely disappear and there may be atrophy of tubules close to scarred
glomeruli. Tubular cells show hyaline-droplets, degeneration and tubular lumina frequently contain
eosinophilic, homogeneous casts.
iii) Interstitium—There is fine and delicate fibrosis of the interstitial tissue and varying number of chronic
inflammatory cells are often seen.
iv) Vessels—Advanced cases which are frequently associated with hypertension show conspicuous arterial and
arteriolar sclerosis.
40. The primary (hereditary) tubulopathy: causes of development and morphological manifestations?

Primary tubulopathies are a group of diseases caused by disorder of enzyme systems and enshortiment and narrowing
of canal space of PCT (causes disorder of reabsorption of glucose, amino acids, phosphorus, bicarbonates). Clinical
symptoms: polyuria and nephrolithiasis, secondary infections (otitis, pneumonia) often occur

Polyurical tubulopathies: due to disorder of DCT, causes water and glucose absorption disorder. Disease accompanied
by polyuria, polydipsia, vomiting, acidosis, glucosuria

Nephrolithiasis tubulopathies: have a genetic base (autosome recessive). Aminoaciduria is observed (blue color urine)
hyperoxalaturia (calcium oxalate in kidney – can cause interstitial nephritis and nephrosclerosis)

41. Secondary (acquired) tubulopathies and Acute renal insufficiency: etiology, pathogenesis, morphological
manifestations, complications and consequences of pathology?

Acute renal insufficiency: is characterized by sudden decrease in glomerular filtration, hence kidney loses ability to
maintain water salt homeostasis of body.

42. Pyelonephritis: etiology, pathogenesis, morphological manifestations and complications?

Pyelonephritis is inflammation of the kidney, typically due to a pyogenic bacterial infection.

Acute Pyelonephritis: Interstitial tissue of all layers are edema and infiltrated by neutrophils. Micro abscesses and
hemorrhage often arise.

ETIOPATHOGENESIS. Most cases of acute pyelonephritis follow infection of the lower urinary tract. The most common
pathogenic organism in urinary tract infection (UTI) is Escherichia coli (in 90% of cases), followed in decreasing
frequency, by Enterobacter, Klebsiella, Pseudomonas and Proteus. The bacteria gain entry into the urinary tract, and
thence into the kidney by one of the two routes: ascending infection and haematogenous infection.

MORPHOLOGIC FEATURES. Grossly, well-developed cases of acute pyelonephritis show enlarged and swollen kidney
that bulges on section. The cut surface shows small, yellow-white abscesses with a haemorrhagic rim. These abscesses
may be several millimetres across and are situated mainly in the cortex. Microscopically, acute pyelonephritis is
characterised by extensive acute inflammation involving the interstitium and causing destruction of the tubules.
Generally, the glomeruli and renal blood vessels show considerable resistance to infection and are spared. The acute
inflammation may be in the form of large number of neutrophils in the interstitial tissue and bursting into tubules, or
may form focal neutrophilic abscesses in the renal parenchyma.

Complications: Papillary necrosis, formation of carbuncles, connecting of pyogenic cavities (pyenephrosis), transition of
inflammation into fibrous capsule (perinephritis)

Chronic pyelonephritis: tubules dystrophically changed and sclerosed, tubule filled with colloid (thyroid kidney),
epithelium flattened

Complications: nephrogenic arterial hypertension and chronic renal deficiency

43. Nephrolithiasis: morphological characteristics, complications and consequences of disease?

Nephrolithiasis or urolithiasis is formation of urinary calculi at any level of the urinary tract.

Types of urinary calculi:

Type Etiology Pathogenesis Morphology


Calcium Hypercalciuria Supersaturation of ions Calcium stones are usually small (less than a centimeter), ovoid, hard,
stones with or without in urine. Alkaline pH of with granular rough surface. They are dark brown due to old blood
hypercalcemia, urine, low urinary pigment deposited in them as a result of repeated trauma caused to
idiopathic volume. Oxaluria and the urinary tract by these sharp-edged stones.
hyperuricosuria
Mixed Urinary Alkaline urinary pH Struvite stones are yellow-white or grey. They tend to be soft and
infection with produced by ammonia friable and irregular in shape. ‘Staghorn stone’ which is a large, solitary
urea splitting from splitting of urea stone that takes the shape of the renal pelvis where it is often formed
organisms like by bacterially produced is an example of struvite stone
Proteus urease
Uric Hyperuricosuria Acidic urine (pH below Uric acid stones are smooth, yellowish-brown, hard and often
acid with or without 6) decrease solubility multiple. On cut section, they show laminated structure.
Stones hyperuricemia of uric acid and favors
its precipitation
(e.g. in primary
gout)
Cystine Genetically Cystinuria containing Cystine stones are small, rounded, smooth and often multiple. They
Stones determined least soluble cystine are yellowish and waxy.
defect in precipitates as cystine
cystine crystals
transport
Other Inherited Xanthinuria
types abnormalities
of amino acid
metabolism
Consequences: urinary obstruction, pain, haematuria

44. Nephrosclerosis and its species. Morphological characteristic of acute and chronic renal insufficiency?

Benign Nephrosclerosis: caused by chronic hypertension.

MORPHOLOGIC FEATURES. Grossly, both the kidneys are affected equally and are reduced in size and weight, often
weighing about 100 gm or less. The capsule is often adherent to the cortical surface. The surface of the kidney is finely
granular and shows V-shaped areas of scarring. The cut surface shows firm kidney and narrowed cortex

Microscopically, there are primarily diffuse vascular changes which produce parenchymal changes secondarily as a
result of ischaemia. The histologic changes are, thus, described as vascular and parenchymal (Fig. 22.36,A):

i) Vascular changes: Changes in blood vessels involve arterioles and arteries up to the size of arcuate arteries.
There are 2 types of changes in these blood vessels:

a) Hyaline arteriolosclerosis that results in homogeneous and eosinophilic thickening of the wall of
small blood vessels.

b) lntimal thickening due to proliferation of smooth muscle cells in the intima.

ii) Parenchymal changes: As a consequence of ischaemia, there is variable degree of atrophy of parenchyma.
This includes: glomerular shrinkage, deposition of collagen in Bowman’s space, periglomerular fibrosis, tubular
atrophy and fine interstitial fibrosis.

Malignant Nephrosclerosis: caused by acute hypertension

MORPHOLOGIC FEATURES. Grossly, the appearance of the kidney varies. In a case of malignant hypertension
superimposed on pre-existing benign nephrosclerosis, the kidneys are small in size, shrunken and reduced in weight and
have finely granular surface. However, the kidneys of a patient who develops malignant hypertension in pure form are
enlarged, oedematous and have petechial haemorrhages on the surface producing so called ‘fleabitten kidney’.* Cut
surface shows red and yellow mottled appearance.

Microscopically, most commonly the changes are superimposed on benign nephrosclerosis. These changes are as under

i) Vascular changes: These are more severe and involve the arterioles. The two characteristic vascular changes seen are
as under:

a) Necrotising arteriolitis develops on hyaline arteriolosclerosis. The vessel wall shows fibrinoid necrosis, a few
acute inflammatory cells and small haemorrhages.

b) Hyperplastic intimal sclerosis or onionskin proliferation is characterised by concentric laminae of proliferated


smooth muscle cells, collagen and basement membranes.

ii) Ischaemic changes: The effects of vascular narrowing on the parenchyma include tubular loss, fine interstitial fibrosis
and foci of infarction necrosis.
45. Prostatic hypertrophy: histological types, morphological changes in the urinal bladder?

Non-neoplastic tumour-like enlargement of the prostate, commonly termed benign nodular hyperplasia (BNH) or benign
enlargement of prostate (BEP), is a very common condition in men and considered by some as normal ageing process.

ETIOLOGY: not fully understood, few etiological factors include: Endocrinology; racial; inflammation and arteriosclerosis

MORPHOLOGIC FEATURES. Grossly, the enlarged prostate is nodular, smooth and firm and weighs 2-4 times its normal
weight i.e. may weigh up to 40-80 gm. The appearance on cut section varies depending upon whether the hyperplasia is
predominantly of the glandular or fibromuscular tissue. In primarily glandular BEP the tissue is yellow-pink, soft, honey-
combed, and milky fluid exudes, whereas in mainly fibromuscular BEP the cut surface is firm, homogeneous and does
not exude milky fluid. The hyperplastic nodule forms a mass mainly in the inner periurethral prostatic gland so that the
surrounding prostatic tissue forms a false capsule which enables the surgeon to enucleate the nodular masses. The left-
over peripheral prostatic tissue may sometimes undergo recurrent nodular enlargement or may develop carcinoma
later.

Histologically, in every case, there is hyperplasia of all three tissue elements in varying proportions—glandular, fibrous
and muscular:
 Glandular hyperplasia predominates in most cases and is identified by exaggerated intra-acinar papillary
infoldings with delicate fibrovascular cores. The lining epithelium is two-layered: the inner tall columnar mucus
secreting with poorly-defined borders, and the outer cuboidal to flattened epithelium with basal nuclei.
 Fibromuscular hyperplasia when present as dominant component appears as aggregates of spindle cells
forming an appearance akin to fibromyoma of the uterus.
 In addition to glandular and/or fibromuscular hyperplasia, other histologic features frequently found include foci
of lymphocytic aggregates, small areas of infarction, corpora amylacea and foci of squamous metaplasia.

Changes in urinary bladder: irritation, inflammation, swelling

46. Diseases of the uterus cervix, clinical and morphological forms?

47. Fibrocystic breast disease: clinical and morphological forms and their manifestations.

48. Prenatal pathology: periods and their characteristics.

49. The birth trauma: morphological characteristic of birth injuries.

50. Hemolytic disease of the newborn: forms and pathological anatomical changes.

Pathomorphology of infection.

51. Measles (morbilli, rubeola or red measles): etiology, pathogenesis, clinical and pathological manifestations of the
disease and its complications?

Measles (rubeola) is an acute highly contagious infectious disease, its causes a catarrhal inflammation. measles infects
epithelial cells in trachea and bronchi, eyes of conjunctiva and then gets into the blood with the development of viremia.
Virus has an ability to reduce the barrier function of epithelium, phagocytic activity, repress the immune system.

Measles is an airborne disease which spreads through coughs and sneezing, it may also spread through contact with
saliva and nasal secretion.

Pathmorphology: in mucus there is edema, plethora, secretion of mucus, lymphohistiocystic infiltration. Sometimes
there is vascular dystrophy in mucus membrane and necrotic changes
Definition / general

 Also called rubeola


 Infectious acute febrile illness characterized by upper respiratory infection symptoms and maculopapular rash
 Spread by aerosols and droplets from respiratory secretions or rarely fomites

Microscopic (histologic) description

 Epithelial giant cells with viral inclusions


 Nuclei may contain a single large Cowdry type A inclusion
 Reticuloendothelial (Warthin-Finkeldey) giant cells may be found in lymphoid tissue

Complications: infection of airways and lungs (pneumonia. Bronchitis and croup), eye infection (conjunctivitis), middle
ear infection (otitis media), diarrhoe and vomiting

52. Describe the characteristics of skin rash (exanthema) and mucous membrane rash (enanthema) at the measles?

Exanthema is a skin rash accompanying a disease/ fever. The characteristic measles rash is classically described as a
generalized red maculopapular rash that begins several days after the fever starts. It starts on the back of the ears and,
after a few hours, spreads to the head and neck before spreading to cover most of the body, often causing itching. The
measles rash appears two to four days after the initial symptoms and lasts for up to eight days. The rash is said to
"stain", changing color from red to dark brown, before disappearing. A maculopapular rash is a type of rash
characterized by a flat, red area on the skin that is covered with small confluent bumps. It may only appear red in
lighter-skinned people. The term "maculopapular" is a compound: macules are small, flat discolored spots on the surface
of the skin; and papules are small, raised bumps. It is also described as erythematous, or red.

Enanthem (Koplik spots): is a rash (small spots) on the mucous membranes. Kolpik spots are characterized as clustural
white lesions on the buccal mucosa (opposite the lower 1st and 2nd molar). Kolpik spots are ulcerated mucosal lesions
marked by necrosis, neutrophilic exudate and neovascularisation

53. The essence of unreal croup with measles?

54. Morphology characteristic of measles pneumonia?

Measles (Rubeola) Pneumonia: Transbronchic biopsies showing multigiant cells with viral intranuclear eosinophilic
inclusions (Warthin-Finkeldey giant cells) pathognomonic of measles pneumonia (H&E stain, ×40).
Morphology: in lung between alveolar partitions are infiltrated by lymphocytes, histiocytes, plasmatic cells. The
development of interstitial giant cell pneumonia is possible

55. Morphology of meningococcal meningitis?

Meningococcal infection manifests itself in 3 forms: Meningococcal nasopharyngitis; festering meningitis; meningococcal
sepsis

Meningococcal meningitis: begins from a basal surface by the serose inflammation on the first days, and then passes on
a hemisphere and in 2 – 3 days festering inflammation develops as rather yellow green cap, the fibrinous inflammation
joins in 5-6 days. Septic ependyma and pyocephalus, meningoencephalitis can develop. Making progress hydrocephaly
and atrophy of brain can develop during the organization of fibrin.

Etiology: Bacterial meningitis usually has three main stages. At first, the bacteria multiply in the nasal passages and
throat, often causing no painful symptoms. Next, they invade the blood, introducing toxic substances into the circulation
and causing fever; if the infection is caused by N. meningitidis, a rash may appear and develop into hemorrhagic spots
(petechiae and purpura) in severe cases. In the third stage, the bacteria multiply in the meninges, where they produce
intense inflammatory changes and an exudate of pus.

A characteristic of meningitis is the rapid onset of symptoms, which may result in death within only a few hours. The
first symptom of meningitis is usually vomiting. A severe bursting headache develops when the meninges have become
inflamed and the pressure of the cerebrospinal fluid has increased. Stiffness of the neck then develops, owing to
irritation of the spinal nerves supplying those muscles. Deep tendon reflexes are exaggerated, and convulsions may
occur in infants and small children. In more severe cases, the cerebrospinal fluid becomes so thickened by pus that the
passages between the ventricles (cavities) of the brain and the spaces in the spinal meninges become blocked, causing
fluid to accumulate. The accumulation of fluid in the ventricles may in turn result in hydrocephalus, which causes coma
and death unless relieved.

56. Morphological characteristics, consequences and causes of death in infectious mononucleosis?

Infectious mononucleosis (IM, mono), also known as glandular fever, is an infection usually caused by the Epstein–Barr
virus (EBV).

Death: caused by break of spleen, peripheral paralysis of breathing, secondary infection

Consequences:

 Neurologic complications are rare but may include encephalitis, seizures, Guillain-Barré syndrome, peripheral
neuropathy, viral meningitis, myelitis, cranial nerve palsies, and psychosis. Encephalitis may manifest with
cerebellar dysfunction, or it may be global and rapidly progressive, similar to herpes simplex encephalitis, but is
usually self-limited.
 Hematologic complications are usually self-limited. They include Granulocytopenia; Thrombocytopenia;
Hemolytic anemia
 Transient mild granulocytopenia or thrombocytopenia occurs in about 50% of patients; severe cases, associated
with bacterial infection or bleeding, occur less frequently. Hemolytic anemia is often due to anti-i-specific cold-
agglutinin antibodies.
 Splenic rupture can have severe consequences. It can result from splenic enlargement and capsular swelling,
which are maximal 10 to 21 days after presentation. A history of trauma is present only about half of the time.
Rupture is usually painful but occasionally causes painless hypotension. For treatment, see Splenic Injury :
Treatment.
 Respiratory complications include, rarely, upper airway obstruction due to pharyngeal or paratracheal
lymphadenopathy; respiratory complications may respond to corticosteroids. Clinically silent interstitial
pulmonary infiltrates occur mostly in children and are usually visible on x-rays.
 Hepatic complications include elevated aminotransferase levels (about 2 to 3 times normal, returning to
baseline over 3 to 4 wk); they occur in about 95% of patients. If jaundice or more severe enzyme elevations
occur, other causes of hepatitis should be investigated.

Path morphology:

 Liver: enlarged with infiltration of lymphoid, plasmatic, mononuclear cells in parenchyma


 Spleen: spleen is multiplied, capsule is tense, crimson coloured parenchyma
 Brain tunics: plethoric, infiltrated by histiocytes, mononuclear cells
 Mononuclear infiltrates lungs, endo and pericardium, myocardium, kidneys pancreas

Definition / general: Acute pharyngitis and tonsillitis with gray-white exudate, lymphadenopathy in neck Due to Epstein-
Barr virus infection

Microscopic (histologic) description: Tonsil: reactive lymphoid hyperplasia (polymorphous transformed lymphocytes)
with extensive immunoblastic proliferation in sheets and nodules, marked atypia resembling Reed-Sternberg cells

57. Morphological characteristics, complications, consequences and causes of death at mumps (epidemic parotitis)?
58. Morphological characteristics, complications, consequences and causes of death with diphtheria?

Diphtheria is an infection caused by the bacterium Corynebacterium diphtheriae. Diphtheria causes a thick covering in
the back of the throat. It can lead to difficulty breathing, heart failure, paralysis, and even death.

Pathogenesis: entry- the bacilli multiply locally in the throat and elaborate a powerful exotoxin which produce local and
systemic symptoms. Local lesions: exotoxins causes necrosis of the epithelial cells and liberates serous and fibrinous
material which forms a grayish white pseudo membrane. The membrane bleeds when being dislodged, the surrounding
tissue is inflamed and edematous.

Complications from diphtheria:

 Blocking of the airway


 Damage to the heart muscle (myocarditis)
 Nerve damage (polyneuropathy)
 Loss of the ability to move (paralysis)
 Lung infection (respiratory failure or pneumonia)

59. Morphological characteristics, complications, consequences and causes of death in scarlet fever (scarlatina (old
name))?

Scarlet fever is a syndrome characterized by exudative pharyngitis, fever, and bright-red exanthem. It is caused by
streptococcal pyrogenic exotoxins (SPEs) types A, B, and C produced by group A beta-hemolytic streptococci (GABHS)
found in secretions and discharge from the nose, ears, throat, and skin.

Morphology: every period of scarlet fever has its charactertic manifestations;

 First period/ allergisation: catarrhal quinsy with acute plethoric of tonsil and pharynx (blazing pharynx).

Complications: lymphadenitis; otitis; otogenic abscess of cerebrum; endocarditis; glomerulonephritis; arthritis; defects
of heart; cardiosclerosis

Death: is mainly caused by toxemia, festering septic complications, kidney and cardiac insufficiency

60. Morphological characteristics, complications, consequences and causes of death with Pertussis (whooping cough).

61. Morphological characteristics, complications, consequences and causes of death with poliomyelitis.

62. Influenza: etiology, pathogenesis, clinical-pathological changes and complications of disease.

63. Human Respiratory Syncytial Infection (HRSI): etiology and pathological anatomy.

64. Morphology changes in the lungs during the severe form of influenza with significant intoxication.

65. Adenovirus infection: etiology and morphological manifestations.

66. Viral hepatitis: etiology, pathogenesis, types. Pathological anatomy of viral hepatitis and its complications.

67. Typhoid fever: etiology, pathogenesis, pathological anatomy and complications.

68. Dysentery: etiology, pathogenesis, pathological anatomy and complications.


69. Morphological characteristics of stages of colitis at dysentery.

70. Cholera: etiology, pathogenesis and pathological anatomy.

71. Salmonellosis: etiology, pathogenesis, pathological anatomy and complications.

72. Pathomorphology of intestinal forms of salmonellosis.

73. Pathomorphology of septic forms of salmonellosis.

75. Plague: etiology, pathogenesis and pathological anatomy.

76. Anthrax: etiology, pathogenesis, pathological anatomy.

77. The epidemic cerebrospinal meningitis: etiology, pathogenesis and pathological anatomy.

78. Tuberculosis: etiology, pathogenesis and pathological anatomy of primary tuberculous complex.

79. Varieties of progression of primary tuberculosis (growth of primary effect; hematogenous,

lymphogenous and mixed forms of progression).

80. Morphology of Ghon focus.

81. Hematogenous tuberculosis: definitions and types of hematogenous tuberculosis.

82. Pathological anatomy of hematogenous tuberculosis with prevailing lesion of the lung; complications of disease.

83. Pathological anatomy of generalized hematogenous tuberculosis and its complications.

84. Pathological anatomy of hematogenous tuberculosis with prevailing extrapulmonary lesions; their complications.

85. Secondary tuberculosis: causes of development, clinical and morphological forms of disease.

86. Pathological anatomy of secondary acute focal tuberculosis. The causes of death.

87. Pathological anatomy of fibrous-focal tuberculosis.

88. Pathological anatomy of infiltrative tuberculosis.

89. What is a tuberculoma; its morphological features?

90. Pathological anatomy of caseous pneumonia.

91. Pathological anatomy of acute cavernous tuberculosis.

92. Pathological anatomy of fibro-cavernous tuberculosis.

93. Pathological anatomy of cirrhotic tuberculosis.

94. Sepsis: etiology and pathogenesis. Differences sepsis from other infectious diseases.

General and local changes in the body during sepsis.

95. Clinical and anatomical forms of sepsis. Pathological anatomy of septicemia, pyosepticemia and chronic sepsis.

96. Protracted septic endocarditis: etiology, pathogenesis, morphological changes in organs.

Morphological differential diagnosis of septic endocarditis with rheumatic endocarditis.

97. Acquired immunodeficiency syndrome: definition, etiology, ways of transmission and pathogenesis of disease.

98. Dynamics of morphological changes in the lymph organs depending on AIDS periods.
99. Morphological manifestations of opportunistic infections and Kaposi sarcoma at AIDS. Causes of death in AIDS.

100. Morphological changes in hematogenic organs in AIDS.

Pathology of dental system and oral cavity

101. Caries: morphogenesis of carious lesion, stages of clinical morphological manifestations?

dental caries causes the destruction of calcified tissues of teeth.

MORPHOLOGIC FEATURES. Caries occurs chiefly in the areas of pits and fissures, mainly of the molars and premolars,
where food retention occurs, and in the cervical part of the tooth. Grossly, the earliest change is the appearance of a
small, chalky-white spot on the enamel which subsequently enlarges and often becomes yellow or brown and breaks
down to form carious cavity. Eventually, the cavity becomes larger due to fractures of enamel. Once the lesion reaches
enamel-dentin junction, destruction of dentine also begins. Microscopically, inflammation (pulpitis) and necrosis of pulp
take place. There is evidence of reaction of the tooth to the carious process in the form of secondary dentin, which is a
layer of odontoblasts laid down under the original dentine

Stages:

1. white spot,
2. superficial (enamel): destruction of enamel within limits to the enamel dentine junction
3. middle: destruction of dentinal enamel junction, dentinal tubules broaden filled with microorganisms, toxic
dystrophy and necrosis occurs in odontoblast processes
4. Deep: expanding softened dentine, carious cavity spreads to the pulp. Pulpitis may develop

Carious destruction of dental hard tissues frequently produces pulpitis and other inflammatory lesions like apical
granuloma and apical abscess. Less common causes of these lesions are fracture of tooth and accidental exposure of
pulp by the dentist.

Theories of caries formation:

1. Acidogenic/ chemoparasitic: this theory is a combination of chemical and septic theories and states that dental
decay is a chemoparasitic process consisting of 2 stages: decalcification of softening of tissues due to acids
produced by fermentation of starches and sugars in retaining centres of teeth, followed by dissolution of the
softened residue.
2. Proteolytic: this states that the organic component is lost first by proteolysis followed by loss of inorganic
component that has been more susceptible to an acid attack
3. Proteolytic chelation: products of proteolysis of the tooth substance acquired pellicle and food substances act
as a chelating agents which remove calcium ions from the tooth by forming a complex.

102. Uncarious lesions of teeth: clinical and morphological forms and their manifestations?

 Wedge shaped defects: trophic violation of organic matter of enamel and dentine leads to development of
atrophy and sclerosis. The are defects of hard tissue of neck of the tooth.
 Fluorosis: it’s a defect of enamel due to excess consumption of fluorine
o 1st degree: very weak defeat. Less than 1/3 of expresses chalky spots and ribbons
o 2nd degree: weak defeat. Porcelainoid and chalky spots and ribbons occupy the areas of crown of the
teeth near a half. There are separate pigmentic spots, but destruction is localized only in an enamel;
o ІІІ degree - a defeat is moderato expressed. More than on the half of surface of teeth spots are placed
which meet between itself;
o IV degree is a heavy defeat. On-the-spot teeth separate and plural erosions of enamel of different form
appear. They can be colourless or pigmentovani (vid yellow brown to the black
 Fluorosis: Mild to moderate fluorosis ranges clinically from white enamel spots to mottled brown-and-white
discolorations. Severe fluorosis appears as pitted, irregular, and discolored enamel.
 Erosion: Erosions of teeth are making progress like cup forms of diminishing of enamel and dentine on the
vestibular surface of teeth, at first chisels, and then caninus tooth and premolar of maxilla. Reason of disease is
not known. Develops for the people of middle ages. The chronic ran across with the gradual defeat of all plenty
of teeth. Defects are very sickly.
 Acid necrosis of hard tissues of tooth is a professional disease which develops in peoples, which contact with
inorganic acids on the factories

103. Pulpitis: etiology, pathogenesis and pathological anatomy?

Pulpitis. Pulpitis may be acute or chronic.

Acute pulpitis is accompanied by severe pain which may be continuous, throbbing or dull, and is accentuated by heat or
cold. It is often accompanied by mild fever and leucocytosis.

Chronic pulpitis occurs when pulp is exposed widely. It is often not associated with pain. Chronically inflamed pulp
tissue may protrude through the cavity forming polyp of the pulp. It may be partly covered by implanted squamous
epithelium.

104. Pathological anatomy features of acute pulpitis; its complications and consequences.

105. Pathological anatomy features of chronic pulpitis; its complications and consequences.

Name the definition of "periodontitis". Classification of periodontitis?

Inflammation of gums and support structure of tooth i.e. periodontal ligaments. This can be due to bacterial infection,
inflammation, trauma or irritant/ chemical

Classification:

 Acute periodontitis:
 Granulating periodontitis: exudate inflammation, tissue or red colour in the periodont, granulation tissue (scar
tissue; hypertrophy increase of connective tissue
 Chronic granulomatous periodontitis: simple granuloma; complex (epithelial) granuloma; cysto granuloma;
fibrous granuloma

The destructive forms of periodontal disease, known as periodontitis, are characterized by inflammation and the loss of
the periodontal attachment apparatus in adolescents and adults Armitage (1999). The cardinal signs of periodontitis
include attachment loss, alveolar bone loss, periodontal pocketing, and gingival inflammation.

106. Etiology and pathogenesis of periodontitis?

Periodontitis is an inflammation and degeneration of the supporting tissues of teeth resulting in teeth loss is a common
condition. The disease begins as chronic marginal gingivitis, secondary to bacterial plaques around the teeth such as
due to calculus (tartar) on the tooth surface, impacted food, uncontrolled diabetes, tooth-decay and ill-fitting dental
appliances. The gingival sulcus acts as convenient site for lodgement of food debris and bacterial plaque leading to
formation of periodontal pocket from which purulent discharge can be expressed by digital pressure.

Microscopically, chronic marginal gingivitis is characterised by heavy chronic inflammatory cell infiltrate, destruction of
collagen, and epithelial hyperplasia so as to line the pocket. Untreated chronic marginal gingivitis slowly progresses to
chronic periodontitis or pyorrhoea in which there is inflammatory destruction of deeper tissues. At this stage,
progressive resorption of alveolar bone occurs and the tooth ultimately gets detached

Periodontitis is the common sequel to chronic gingivitis and is recognised histologically by evidence of damage to the
alveolar bone, associated with signs of chronic inflammation. The bone of the alveolar crest shows resorption as
demonstrated by the presence of Hownship’s lacunae sometimes still containing multinucleated osteoclasts. The
epithelial attachment that normally lies in contact with the tooth enamel has moved downwards to be partly opposite
the enamel and the root cementum or even entirely opposite the root cementum (Figs. 8.4a, b). Resorption of bone and
downward displacement of the epithelial attachment may continue until there is insufficient periodontal tissue left for
adequate fixation of the tooth in the jaw. Caries may add to the damage caused by periodontitis by attacking the
cementum covering the exposed root surface.

107. Acute periodontitis: etiology, pathomorphology, clinical manifestation and diagnosis?

Last 2/3 days to 2 weeks. Sharp abscess in apex of tooth, edema, diffuse infiltration, serosal inflammation.

108. Chronic periodontitis: etiology, pathomorphology, clinical manifestation and diagnosis?

Exudate inflammation tissue of red colour in periodont granulation tissue (scar tissue), hypertrophy i.e. increase in
connective tissue

109. Gingivitis: etiology, pathological anatomy, complications and consequences?

Gingivitis is inflammation of gingiva it can be local (allergy) or general (infection or endocrine). Acute or chronic

Histological classification: catarrhal (serous exudate covering the mucosa); hypertrophy (overgrowth of gingiva);
ulcerative (reduction in mucus membrane)

110. The essence of dental plaque and dental tartar?

Dental plaque is a biofilm or mass of bacteria that grows on surfaces within the mouth. It is a sticky colorless deposit at
first, but when it forms tartar, it is often brown or pale yellow.

Classification of dental plaque:

 Supragingival plaque
 Subgingival plaque

111. Periodontitis: definition, etiology, pathogenesis and pathological anatomy?

The name "periodontitis" means "means inflammation around the tooth." Microorganisms, such as bacteria, stick to the
surface of the tooth and in the pockets surrounding the tooth, and they multiply. As the immune system reacts and
toxins are released, inflammation occurs.

Untreated periodontitis will eventually result in tooth loss. It may increase the risk of stroke, heart attack, and other
health problems.

Bacterial plaque, a sticky, colorless membrane that develops over the surface of teeth, is the most common cause of
periodontal disease. If plaque it not removed, it can harden to form tartar, or calculus.

Most cases of periodontitis are preventable through good dental hygiene.

Gingivitis VS periodontitis
Gingivitis occurs before periodontitis. It usually refers to gum inflammation, while periodontitis refers to gum disease
and the destruction of tissue, bone, or both.

Gingivitis: Bacterial plaque accumulates on the surface of the tooth, causing the gums to become red and inflamed. The
teeth may bleed during brushing. The gums are irritated and bothersome, but the teeth are not loose. There is no
irreversible damage to bone or surrounding tissue. Untreated gingivitis can progress to periodontitis.

Periodontitis: The gum and bone pull away from the teeth, forming large pockets. Debris collects in the spaces between
the gums and teeth and infects the area.

The immune system attacks bacteria as the plaque spreads below the gum line into the pockets. Bone and connective
tissue that hold the tooth start to break down, because of toxins produced by the bacteria. Teeth become loose and can
fall out. The changes may be irreversible

112. The stages of severity of periodontitis depending on the depth of periodontal pockets?
113. Complications and consequences of periodontitis.

114. Determination of periodontal disease. Macro and microscopic signs of periodontal disease.

115. Characteristics of idiopathic progressive parodontolisis?

Typically occurs in young adults and share many features of generalized juvenile periodontitis such as bone loss and
depressed neutrophil functions

116. Definition and etiology of epulis; histological types of epulis.?

Epulis (inflammatory fibrous hyperplasia) is a tumor like enlargement situated on gingival or alveolar mucosa. It is a
localized fibrous growth in the soft tissue.

Histological types of epulis:

 Angiomatous Epulis
 Gigantic cell epulis: is a from of fibrous epulis seen more in women as reactive change to trauma, the lesion
shows numerous osteoclast-like giant cells and vascular stroma
 Fibrotic epulis

Etiology of epulis: s is multifactorial like irritative factors (poor oral hygiene, chronic gingivitis, periodontal diseases) and
hormonal changes. It can also be denture induced

117. The morphology of giant epulis?


118. Morphological characteristics of gingival fibromatosis?

Generalized gingival hyperplasia. Growth of connective tissue, increased collagenous tissue with varying cellularity.

Histopathology An abundance of collagen is noted. Fibroblasts are increased in number, and various degrees of chronic
inflammation are seen. In some cases, especially those in which hormonal changes are important, capillaries may be
increased and prominent. The overlying epithelium usually exhibits some hyperplasia. Occasionally, plasma cells
dominate the histologic picture. In leukemic enlargements, atypical and immature white blood cells, representing a
malignant infiltrate, may be found.

119. Etiology, pathological anatomy, complications and consequences of osteitis and periostitis.

120. Etiology, pathogenesis, classification of jaw osteomyelitis?

Osteomyelitis of the jaws is osteomyelitis (which is infection and inflammation of the bone marrow, sometimes
abbreviated to OM) which occurs in the bones of the jaws (i.e. maxilla or the mandible).

Etiology: OM is usually a polymicrobial, opportunistic infection, caused primarily by a mixture of alpha hemolytic
streptococci and anaerobic bacteria from the oral cavity such as Peptostreptococcus, Fusobacterium and Prevotella, (in
contrast to OM of the long bones, usually caused by isolated Staphylococcus aureus infection). These are the same as
the common causative organisms in odotonogenic infections. However, when OM in the jaws follows trauma, is the
likely cause is still staphylococcal (usually Staphylococcus epidermis.

121. Pathomorphological manifestations of jaw osteomyelitis?

MORPHOLOGIC FEATURES. Depending upon the duration, osteomyelitis may be acute, subacute or chronic. The basic
pathologic changes in any stage of osteomyelitis are: suppuration, ischaemic necrosis, healing by fibrosis and bony
repair. The sequence of pathologic changes is as under (Fig. 28.2):
1. The infection begins in the metaphyseal end of the marrow cavity which is largely occupied by pus. At this stage,
microscopy reveals congestion, oedema and an exudate of neutrophils.

2. The tension in the marrow cavity is increased due to pus and results in spread of infection along the marrow cavity,
into the endosteum, and into the haversian and Volkmann’s canal, causing periosteitis.

3. The infection may reach the subperiosteal space forming subperiosteal abscesses. It may penetrate through the
cortex creating draining skin sinus tracts (Fig. 28.3).

4. Combination of suppuration and impaired blood supply to the cortical bone results in erosion, thinning and infarction
necrosis of the cortex called sequestrum.

5. With passage of time, there is formation of new bone beneath the periosteum present over the infected bone. This
forms an encasing sheath around the necrosed bone and is known as involucrum. Involucrum has irregular surface and
has perforations through which discharging sinus tracts pass.

6. Long continued neo-osteogenesis gives rise to dense sclerotic pattern of osteomyelitis called chronic sclerosing
nonsuppurative osteomyelitis of Garré.

7. Occasionally, acute osteomyelitis may be contained to a localised area and walled off by fibrous tissue and granulation
tissue. This is termed Brodie’s abscess.

8. In vertebral pyogenic osteomyelitis, infection begins from the disc (discitis) and spreads to involve the vertebral
bodies (Fig. 28.4,A)

122. Complications and consequences of osteitis, periostitis and osteomyelitis of jaw?

COMPLICATIONS. Osteomyelitis may result in the following complications:

1. Septicaemia.
2. Acute bacterial arthritis.
3. Pathologic fractures.
4. Development of squamous cell carcinoma in longstanding cases.
5. Secondary amyloidosis in long-standing cases.
6. Vertebral osteomyelitis may cause vertebral collapse with paravertebral abscess, epidural abscess, cord
compression and neurologic deficits.

Complications of osteitis (inflammation of the substance of a bone):

Complications of periostitis (inflammation of the membrane enveloping a bone.):

123. Cysts of the jaw: classification, morphological characteristics of follicular (developmental cyst) and radicular
(inflammatory cyst) (basal) cysts?

Radicular Cyst also called as apical, periodontal or simply dental cyst, is the most common cyst originating from the
dental tissues. It arises consequent to inflammation following destruction of dental pulp such as in dental caries, pulpitis,
and apical granuloma. The epithelial cells of Mallasez, which are nests of odontogenic epithelium embedded in the
periodontium, proliferate within apical granuloma under the influence of inflammation, leading to the formation of an
epithelium-lined cystic cavity. Most often, radicular cyst is observed at the apex of an erupted tooth and sometimes
contains thick pultaceous material

Histologically, the radicular cyst is lined by nonkeratinised squamous epithelium. Epithelial rete processes may
penetrate the underlying connective tissues. Radicular cyst of the maxilla may be lined by respiratory epithelium. The
cyst wall is fibrous and contains chronic inflammatory cells (lymphocytes, plasma cells with Russell bodies and
macrophages) hyaline bodies and deposits of cholesterol crystals which may be associated with foreign body giant cells

DENTIGEROUS (FOLLICULAR) CYST. Dentigerous cyst arises from enamel of an unerupted tooth. The mandibular third
molars and the maxillary canines are most often involved. Dentigerous cysts are less common than radicular cysts and
occur more commonly in children and young individuals. These cysts are more significant because of reported
occurrence of ameloblastoma and carcinoma in them.

Histologically, dentigerous cyst is composed of a thin fibrous tissue wall lined by stratified squamous epithelium. Thus,
the cyst may resemble radicular cyst, except that chronic inflammatory changes so characteristic of radicular cyst, are
usually absent in dentigerous cyst

124. Jaw tumour diseases. Morphological characteristics of fibrous dysplasia, cherubism and eosinophilic granuloma.

125. Unodontogenic tumors of jaw. Clinical and morphological features of osteoblastoclastoma.

126. Morphological characteristics of malignant unodontogenic tumors of jaw: - osteosarcoma, chondrosarcoma,


malignant lymphoma, secondary metastatic tumors.
127. Histogenesis of odontogenic tumors. Structural features of odontoma?

Odontogenic tumours are a group of uncommon lesions of the jaw derived from the odontogenic apparatus. These
tumours are usually benign but some have malignant counterparts.

128. Tumors developed from odontogenic epithelium. Morphological structure of ameloblastoma, adenomatoid tumor
and odontogenic carcinoma?

Ameloblastoma

Ameloblastoma is the most common benign but locally invasive epithelial odontogenic tumour. The tumour originates
from dental epithelium of the enamel itself or its epithelial residues.

Grossly, the tumour is greyish-white, usually solid, sometimes cystic, replacing and expanding the affected bone.
Histologically, ameloblastoma can show different patterns as follows:

i) Follicular pattern is the most common. The tumour consists of follicles of variable size and shape and
separated from each other by fibrous tissue. The structure of follicles is similar to that of enamel organ
consisting of central area of stellate cells resembling stellate reticulum, and peripheral layer of cuboidal or
columnar cells resembling epithelium. The central stellate areas may show cystic changes
ii) Plexiform pattern is the next common pattern after follicular pattern. The tumour epithelium is seen to
form irregular plexiform masses or network of strands. The stroma is usually scanty. Microcyst formation
can occur in the stroma.
iii) Acanthomatous pattern is squamous metaplasia within the islands of tumour cells.
iv) Basal cell pattern of ameloblastoma is similar to basal cell carcinoma of the skin.
v) Granular cell pattern is characterised by appearance of acidophilic granularity in the cytoplasm of tumour
cells. Combination of more than one morphologic pattern may also be seen. Tumour cells in ameloblastoma
exhibit positive immunostaining for cytokeratin and laminin as are seen in developing tooth.
Odontogenic Adenomatoid Tumour (Adeno-ameloblastoma) This is a benign tumour seen more often in females in
their 2nd decade of life. The tumour is commonly associated with an unerupted tooth and thus closely resembles
dentigerous cyst radiologically. Unlike ameloblastoma, adenomatoid odontogenic tumour is not invasive nor does it
recur after enucleation.

Histologically, the lesion has extensive cyst formations. The wall of cyst contains scanty fibrous connective tissue in
which are present characteristic tubule-like structures composed of epithelial cells and hence the name ‘adenomatoid’
(gland-like).

Odontogenic Carcinoma

i) Malignant ameloblastoma is the term used for the uncommon metastasising ameloblastoma.
ii) Ameloblastic carcinoma is the term employed for the ameloblastic tumour having cytologic features of
malignancy in the primary tumour.
iii) Primary intraosseous carcinoma may develop within the jaw from the rests of odontogenic epithelium.
iv) Rarely, carcinomas may arise from the odontogenic epithelium lining the odontogenic cysts.

129. The odontogenic mesenchymal associated tumors: dentynoma, odontogenic myxoma, cementoma?

Odontogenic Myxoma (Myxofibroma) Odontogenic myxoma is a locally invasive and recurring tumour.

Microscopically, it is characterised by abundant mucoid stroma and loose stellate cells in which are seen a few strands
of odontogenic epithelium.

Cementomas are a variety of benign lesions which are characterised by the presence of cementum or cementum-like
tissue. Five types of cementomas are described:

i) Benign cementoblastoma (true cementoma) is a solitary lesion of jaw, characterised by features


comparable to those of osteoid osteoma and osteoblastoma.
ii) Cementifying fibroma consists of cellular fibrous tissue containing calcified masses of cementum-like tissue.
iii) Periapical cemental dysplasia (Periapical fibrous dysplasia) is most common and resembles cementifying
fibroma except that it contains more fibrous tissue as well as cementum-like tissue.
iv) Multiple apical cementomas are found on the apical region of teeth and detected incidentally in
postmenopausal women.
v) Gigantiform cementoma is a large lobulated mass of cementum-like tissue. Sometimes, there are multiple
such masses in the jaw.
Odontomas

Odontomas are hamartomas (is a benign (noncancerous) tumorlike malformation made up of an abnormal mixture of
cells and tissues found in areas of the body where growth occurs) that contain both epithelial and mesodermal dental
tissue components. There are 3 subtypes:

i) Complex odontoma is always benign and consists of enamel, dentin and cementum which are not
differentiated, so that the structure of actual tooth is not identifiable.
ii) Compound odontoma is also benign and is comprised of differentiated dental tissue elements forming a
number of denticles in fibrous tissue.
iii) Ameloblastic fibro-odontoma is a lesion that resembles ameloblastic fibroma with odontoma formation.

130. Morphological characteristics of benign odontogenic mixed genesis tumors: structure of ameloblastic fibroma,
fibroodontoma, odontogenic fibroma and odontoameloblastoma?

Ameloblastic Fibroma

This is a benign tumour consisting of epithelial and connective tissues derived from odontogenic apparatus. It resembles
ameloblastoma but can be distinguished from it because ameloblastic fibroma occurs in younger age group (below 20
years) and the clinical behaviour is always benign.

Histologically, it consists of epithelial follicles similar to those of ameloblastoma, set in a very cellular connective tissue
stroma.

131. Clinical and pathological features of malignant odontogenic mixed genesis tumors (odontogenic sarcomas)?

132. Etiology, pathological anatomy, complications and consequences of sialoadenitis?

SIALADENITIS Inflammation of salivary glands, sialadenitis, may be acute or chronic;

Etiology:

 Viral infections e.g. mumps in children


 Bacterial and mycotic infection:
 Autoimmune disease:
o Sjögren’s syndrome characterised by triad of dry eyes (keratoconjunctivitis sicca), dry mouth
(xerostomia) and rheumatoid arthritis
o Mikulicz’s syndrome is the combination of inflammatory enlargement of salivary and lacrimal glands
with xerostomia

MORPHOLOGICAL FEATURES Irrespective of the underlying etiology of sialadenitis, there is swelling of the affected
salivary gland, usually restricted by the fibrous capsule. Acute stage is generally associated with local redness, pain and
tenderness with purulent ductal discharge. Late chronic cases may be replaced by firm fibrous swelling.

Microscopically, acute viral sialadenitis in mumps shows swelling and cytoplasmic vacuolation of the acinar epithelial
cells and degenerative changes in the ductal epithelium. There is interstitial oedema, fibrinoid degeneration of the
collagen and dense infiltration by mononuclear cells (lymphocytes, plasma cells and macrophages). Chronic and
recurrent sialadenitis is characterised by increased lymphoid tissue in the interstitium, progressive loss of secretory
tissue and replacement by fibrosis.

133. Etiology, pathological anatomy, complications and consequences of sialolithiasis (salivary calculi)?

Sialolithiases is a condition where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the
submandibular gland (also termed "Wharton's duct").
Etiology: Initially, factors such as abnormalities in calcium metabolism, dehydration, reduced salivary flow rate, altered
acidity (pH) of saliva caused by oropharyngeal infections, and altered solubility of crystalloids, leading to precipitation of
mineral salts, are involved.

Complications of sialolithiasis include sialadenitis (salivary gland infection), salivary gland inflammation and duct
narrowing (stricture). If this condition is left untreated, it may further lead to fibrosis and eventually causes
degeneration of the gland parenchyma.

134. Morphological characteristics of monomorphic adenoma of salivary glands?

The adenomas of the salivary glands are benign epithelial tumours. They are broadly classified into 2 major groups—
pleomorphic and monomorphic adenomas.

These are benign epithelial tumours of salivary glands without any evidence of mesenchyme-like tissues Their various
forms are as under:

WARTHIN’S TUMOUR (PAPILLARY CYSTADENOMA LYMPHOMATOSUM, ADENOLYMPHOMA):

MORPHOLOGIC FEATURES. Grossly, the tumour is encapsulated, round or oval with smooth surface. The cut surface
shows characteristic slit-like or cystic spaces, containing milky fluid and having papillary projections.

Microscopically, the tumour shows 2 components: epithelial parenchyma and lymphoid stroma (Fig. 19.15): Epithelial
parenchyma is composed of glandular and cystic structures having papillary arrangement and is lined by characteristic
eosinophilic epithelium. Variants of epithelial patterns include presence of mucous goblet cells and sebaceous
differentiation. Lymphoid stroma is present under the epithelium in the form of prominent lymphoid tissue, often with
germinal centres.
135. Morphological characteristics of mucus-epidermal tumors of salivary glands?

Mucoepidermoid Carcinoma (Malignant salivary gland):

MORPHOLOGIC FEATURES. Grossly, the tumour is usually circumscribed but not encapsulated. It varies in size from 1 to
4 cm.

Microscopically, the tumour is classified into low, intermediate and high grade depending upon the degree of
differentiation and tumour invasiveness. The tumour is composed of combination of 4 types of cells: mucinproducing,
squamous, intermediate and clear cells. Welldifferentiated tumours have predominance of mucinous cells, while poorly
differentiated have more solid and infiltrative pattern (Fig. 19.16).

136. Carcinoma of the salivary glands: morphological characteristics?


Adenoid Cystic Carcinoma (Cylindroma) This is a highly malignant tumour due to its typical infiltrative nature, especially
along the nerve sheaths. Adenoid cystic carcinoma is histologically characterised by cribriform appearance i.e. the
epithelial tumour cells of duct-lining and myoepithelial cells are arranged in duct-like structures or masses of cells,
having typical fenestrations or cyst-like spaces and hence the name ‘adenoid cystic’. These cystic spaces contain PAS-
positive basophilic material (Fig. 19.17).

Acinic Cell Carcinoma

This is a rare tumour composed of acinic cells resembling serous cells of normal salivary gland. These cells are arranged
in sheets or acini and have characteristic basophilic granular cytoplasm. The degree of atypia may vary from a benign
cytologic appearance to cellular features of malignancy

Adenocarcinoma

Adenocarcinoma of the salivary gland does not differ from adenocarcinoma elsewhere in the body. It may have some
variants such as mucoid adenocarcinoma, clear-cell adenocarcinoma and papillary cystadenocarcinoma

Epidermoid Carcinoma

This rare tumour has features of squamous cell carcinoma with keratin formation and has intercellular bridges. The
tumour commonly infiltrates the skin and involves the facial nerve early.

Undifferentiated Carcinoma

This highly malignant tumour consists of anaplastic epithelial cells which are too poorly differentiated to be placed in
any other known category.

137. Morphological characteristics of pleomorphic adenoma of salivary glands?

MORPHOLOGIC FEATURES. Grossly, pleomorphic adenoma is a circumscribed, pseudoencapsulated, rounded, at times


multilobulated, firm mass, 2-5 cm in diameter, with bosselated surface. The cut surface is greywhite and bluish,
variegated, semitranslucent, usually solid but occasionally may show small cystic spaces. The consistency is soft and
mucoid.

Microscopically, the pleomorphic adenoma is characterised by pleomorphic or ‘mixed’ appearance in which there are
epithelial elements present in a matrix of mucoid, myxoid and chondroid tissue (Fig. 19.14):
 Epithelial component may form various patterns like ducts, acini, tubules, sheets and strands of cells of ductal
or myoepithelial origin. The ductal cells are cuboidal or columnar, while the underlying myoepithelial cells may
be polygonal or spindle-shaped resembling smooth muscle cells. The material found in the lumina of ductlike
structures is PAS-positive epithelial mucin. Focal areas of squamous metaplasia and keratinisation may be
present. Immunohistochemically, the tumour cells are immunoreactive for epithelial (cytokeratin, EMA, CEA) as
well as myoepithelial (actin, vimentin and S-100) antibodies.
 Mesenchymal elements are present as loose connective tissue, and as myxoid, mucoid and chondroid matrix,
which simulates cartilage (pseudocartilage) but is actually connective tissue mucin. the matrix of the tumour has
been characterised as a product of myoepithelial cells as seen by S-100 immunostain positivity. However, true
cartilage and even bone may also be observed in a small proportion of these tumours. The epithelial and
mesenchymal elements are intermixed and either of the two components may be dominant in any tumour.

138. Tumuor disease of salivary glands: lymphoepithelial destructions, sialosis, oncocitosis.

139. Cheilitis (cheilosis): definition, etiology, clinical and morphological characteristics of its forms?

Cheilitis is inflammation of the lips. This inflammation may include the perioral skin (the skin around the mouth), the
vermilion border, and/or the labial mucosa

Etiology: Vitamin B deficiency;

140. Glossitis: definition, etiology, clinical and morphological characteristics of its forms?

Glossitis is inflammation of the tongue.

Acute glossitis characterised by swollen papillae occurs in eruptions of measles and scarlet fever.

In chronic glossitis, the tongue is raw and red without swollen papillae and is seen in malnutrition such as in pellagra,
ariboflavinosis and niacin deficiency. In iron deficiency anaemia, pernicious anaemia and sprue,

there is chronic atrophic glossitis characterised by atrophied papillae and smooth raw tongue.

What causes glossitis? A few factors can cause inflammation of the tongue, including:
 Allergic reactions: Allergic reactions to medications, food, and other potential irritants may aggravate the
papillae and the muscle tissues of the tongue. Irritants include toothpaste and certain types of medications that
treat high blood pressure.
 Diseases: Certain diseases that affect your immune system may attack the tongue’s muscles and papillae.
Herpes simplex, a virus that causes cold sores and blisters around the mouth, may contribute to swelling and
pain in the tongue.
 Low iron levels: Not enough iron in the blood can trigger glossitis. Iron regulates cell growth by helping your
body make red blood cells, which carry oxygen to your organs, tissues, and muscles. Low levels of iron in the
blood may result in low levels of myoglobin. Myoglobin is a protein in red blood cells that’s important for muscle
health, including the tongue’s muscle tissue.
 Mouth trauma: Trauma caused by injuries to the mouth can affect the condition of your tongue. Inflammation
may occur because of cuts and burns on the tongue or dental appliances like braces placed on your teeth.

Types of glossitis: There are different types of glossitis, which include:

 Acute glossitis is an inflammation of the tongue that appears suddenly and often has severe symptoms. This
type of glossitis typically develops during an allergic reaction.
 Chronic glossitis is an inflammation of the tongue that continues to recur. This type may begin as a symptom of
another health condition.
 Atrophic glossitis, also known as Hunter glossitis, occurs when many papillae are lost. This results in changes in
the tongue’s color and texture. This type of glossitis typically gives the tongue a glossy appearance.

141. Stomatitis: definition, etiologic groups, clinical and morphological characteristics of its forms?

STOMATITIS. Inflammation of the mucous membrane of the mouth is called stomatitis. It can occur in the course of
several different diseases.

i) Aphthous ulcers (Canker sores) is the commonest form of oral ulceration. The etiology is unknown but may
be precipitated by emotional factors, stress, allergy, hormonal imbalance, nutritional deficiencies,
gastrointestinal disturbances, trauma etc. The condition is characterised by painful oral ulcers, 1 cm or more
in size. Recurrent aphthae may form a part of Behcet’s syndrome and inflammatory bowel disease.
ii) Herpetic stomatitis is an acute disease occurring in infants and young children. It is the most common
manifestation of primary infection with herpes simplex virus. The lesions are in the form of vesicles around
the lips. Similar lesions may appear on the genital skin. Recurrent attacks occur due to stress, emotional
upsets and upper respiratory infections.
iii) Necrotising stomatitis (Noma or Cancrum oris) occurs more commonly in poorly-nourished children like in
kwashiorkor; infectious diseases such as measles, immunodeficiencies and emotional stress. The lesions are
characterised by necrosis of the marginal gingiva and may extend on to oral mucosa, causing cellulitis of the
tissue of the cheek. The condition may progress to gangrene of the cheek.
iv) Mycotic infections commonly involving the oral mucosa are actinomycosis and candidiasis.
a. Cervicofacial actinomycosis is the commonest form of the disease developing at the angle of the
mandible (Chapter 6).
b. Candidiasis (moniliasis or thrush) is caused by Candida albicans which is a commensal in the mouth. It
appears as an opportunistic infection in immunocompromised host. There are erythematous lesions on
the palate and angular cheilitis

142. Leukoplakia (idiopathic keratosis) of oral mucosa: morphological characteristic; macroand microscopic signs?

Leukoplakia (white plaque) may be clinically defined as a white patch or plaque on the oral mucosa, exceeding 5 mm in
diameter, which cannot be rubbed off nor can be classified into any other diagnosable disease. The term ‘leukoplakia’ is
reserved for epithelial thickening which may range from completely benign to atypical and to premalignant cellular
changes. Its associated with smoking
MORPHOLOGIC FEATURES. Grossly, the lesions of leukoplakia may appear white, whitish-yellow, or redvelvety of more
than 5 mm diameter and variable in appearance. They are usually circumscribed, slightly elevated, smooth or wrinkled,
speckled or nodular

Histologically, leukoplakia is of 2 types:

1. Hyperkeratotic type. This is characterised by an orderly and regular hyperplasia of squamous epithelium with
hyperkeratosis on the surface

2. Dysplastic type. When the changes such as irregular stratification of the epithelium, focal areas of increased and
abnormal mitotic figures, hyperchromatism, pleomorphism, loss of polarity and individual cell keratinisation are present,
the lesion is considered as epithelial dysplasia. The subepithelial tissues usually show an inflammatory infiltrate
composed of lymphocytes and plasma cells. The extent and degree of the epithelial changes indicate the degree of
severity of the epithelial dysplasia. Usually, mild dysplasia may revert back to normal if the offending etiologic factor is
removed, whereas severe dysplasia indicates that the case may progress to carcinoma. Erythroplasia is a form of
dysplastic leukoplakia in which the epithelial atypia is more marked and thus has higher risk of developing malignancy. If
the epithelial dysplasia is extensive so as to involve the entire thickness of the epithelium, the lesion is called carcinoma
in situ which may progress to invasive carcinoma

143. Erythroplakia (erythroplasia) of oral mucosa: morphological characteristic; macro- and microscopic signs?

Erythroplakia refers to a red patch on oral mucous membranes with well defined margins. It does not indicate a
particular microscopic diagnosis, although after a biopsy most cases are found to be

severe dysplasia or carcinoma. The causes of this lesion are believed to be similar to those responsible for oral cancer.
Therefore tobacco use probably has a significant role in the induction of many of these lesions, as does heavy alcohol
consumption. Nutritional deficits and other factors may have modifying roles.

144. Epithelial tumors of the lips, tongue, soft tissues of oral cavity (papilloma, squamous cell keratinising and non-
keratinising carcinoma, carcinoma in situ); pathologic anatomy characteristic.
145. Name the phases of wound healing and their characteristic?
146. The anatomical and physiological features of the maxillofacial area.

147. Morpho-functional structure of gunshot wound.

148. Morphology of primary wound canal in gunshot wound.

149. Morphology of contusion zones (primary necrosis) in gunshot wound.

150. Morphology of shaking zone (secondary necrosis) in gunshot wound.