Pathology

• Morphology Of Cell Injury Pathology Short And Long Essay Question And Answers
• Intracellular Accumulation Pathology Short And Long Essay Question And Answers
• Amyloidosis Pathology Short And Long Essay Question And Answers
• Genetic And Pediatric Diseases Pathology Short And Long Essay Question And Answers
• Environmental And Nutritional Disorders Pathology Short And Long Essay Question And Answers
• Pathology Acute Inflammation Short And Long Essay Question And Answers
• Pathology Chronic And Granulomatous Inflammation Short And Long Essay Question And Answers
• Pathology Healing Of Tissues Short And Long Essay Question And Answers
• Pathology Diseases Of The Immune System Short And Long Essay Question And Answers
• Pathology Infections And Infestation Short And Long Essay Question And Answers
• Pathology Derangements Of Body Fluids Short And Long Essay Question And Answers
• Pathology Hemodynamic Derangements Due To Deranged Volume Short And Long Essay Question And Answers
• Pathology Hemodynamic Derangements Due To Obstructive Nature Short And Long Essay Question And Answers
• Pathology Cellular Adaptations Short And Long Essay Question And Answers
• Pathology Neoplasia Short And Long Essay Question And Answers
• Pathology Common Specific Tumour Short And Long Essay Question And Answers
• Disorders Of Red Blood Cells Short And Long Essay Question And Answers
• Disorders Of Platelets Short And Long Essay Question And Answers
• Disorders Of White Blood Cells Short And Long Essay Question And Answers
• Diseases Of Oral Cavity And Salivary Glands Short And Long Essay Question And Answers
• Pathology Diabetes Mellitus Short And Long Essay Question And Answers
• Pathology Miscellaneous Short And Long Essay Question And Answers

Amyloidosis Important Notes

1. Congo red stain

• All amyloid types have an affinity for it
• It stains amyloid orange in colour and when viewed in polarized light shows apple green birefringence

2. Primary and secondary amyloidosis

• Primary amyloidosis
  • Most common form
  • Occurs most commonly in plasma cell dyscrasias
  • It occurs in the heart, skin and skeletal muscle
• Secondary amyloidosis
  • Occurs as a complication of chronic infection or non-infectious inflammatory conditions
  • Typically distributed in the kidney, liver, spleen and adrenals

3. Amyloidosis of the kidney

• The most common and most serious
• Affected kidneys may be normal-sized or enlarged
• The cut surface shows a pale, waxy and translucent appearance

4. Diagnosis of amyloidosis

• Biopsy
• FNAC of abdominal subcutaneous fat followed by Congo red staining
• Injection of congo red dye intravenously in a living patient
• Electrophoresis
• Bone marrow aspiration

Amyloidosis Long Essays

Question 1. Define amyloidosis. Discuss in detail the etiopathogenesis of amyloidosis. Add a note on its staining characteristics.
Answer:

Definition:

• Is the term used for a group of diseases characterised by extracellular deposition of fibrillar proteinaceous sub-stance called amyloid having a common morphological appearance, staining properties and physical structure but with variable protein composition.

Pathogenesis:

• Irrespective of the type of amyloid, amyloidogenesis in vivo, occurs in the following sequence.
  • The pool of amyloidogenic precursor protein is present in circulation or may be present in response to stimuli.
  • A nidus of fibrillogenesis is formed which stimulates the deposition of amyloid protein
  • Partial degradation or proteolysis occurs before the deposition of fibrillar protein

Staining characteristics of Amyloid:

Amyloidosis Short Essays

Question 1. Classification of amyloidosis
Answer:

1. Based on the cause:

• Primary – with unknown cause and deposition is in the disease itself.
• Secondary – As a complication of some underlying known disease.

2. Based on the extent of amyloid deposition:

• Syssniic (generalised) – Involving multiple organs.
• Localised – involving one/2 organs.

3. On histological basis:

• Peri collagenous-corresponding in distribution to primary amyloidosis.
• Perirectulin – corresponding in distribution to sec­ondary amyloidosis.

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4. Based on tissues:

• Mesenchymal – organs derived from mesoderm.
• Parenchymal – GFgafiS ueFiveu fFGfil ectoderm and

5. Clinicopathologic classification:

• Systemic (generalised) amyloidosis:
  • Primary (AL)
  • Secondary/reactive/inflammatory (AA)
  • Heradofamilial (ATTR, AA, others)
• Localised amyloidosis:
  • Senile cardiac (ATTR)
  • Senile cerebral (AB, APP)
  • Endocrine (hormone precursors)
  • Tumour forming (AL)

Question 2. Microscopy of sago spleen
Answer:

• Sago’s spleen is a form of amyloidosis of the spleen
• In it splenomegaly is not marked
• The cut surface shows translucent, pale and waxy nodules resembling sago grains
• Microscopically it shows amyloid deposits in the walls of arterioles of the white pulp
• Later these deposits replace follicles

Question 3. Pathological changes in amyloidosis
Answer:

Gross Changes:

• The organ is usually enlarged, pale and rubbery

Cut Surface:

• It shows firm, translucent and waxy parenchyma

Microscopic Changes:

• Amyloid deposits are found in the walls of small blood vessels
• Later these deposits produce large macroscopic changes in the blood vessels
• Produces pressure atrophy

Amyloidosis Short Question And Answers

Question 1. Amyloidosis of liver
Answer:

It occurs in about half of the cases of systemic amyloidosis

Amyloidosis of Liver Pathology:

1. Gross features

• Liver is
  • Enlarged
  • Pale
  • Waxy
  • Firm

2. Microscopic features

• Initially
  • Amyloid appears in the space of Disse
• Later
  • Deposits increase
  • It compresses cords of hepatocytes
  • Liver cells get shrunken
  • They become atrophic and are replaced by amyloid
  • Hepatic function is normal
• Portal tracts and Kupffer cells are involved rarely.

Question 2. Source and nature of amyloid
Answer:

Amyloid is composed of 2 main types of complex proteins:

1. Comprises about 95% of amyloid.

• Comprises about 95% of amyloid.
• This consists of a meshwork of fibril proteins which are delicate, randomly dispersed, non-branching and having an indefinite length.
• Chemically 2 major types of amyloid proteins were identified.
  • AL (Amyloid light chain) protein.
  • AA (Amyloid-associated) protein.
  • Other proteins which include Transthyretin
    • β-Amyloid protein.
    • Ap2 microglobulin.
    • Amyloid from hormone precursor proteins.
    • Immunoglobulin heavy chain amyloid (AH)

2. Non-fibrillae components.

• Comprises of about 5% of amyloid material.
• These include the amyloid P (AP) component
  • Aglipoprotein – E (apoE)
  • Sulphated glycosaminoglycans
  • α – 1 anti chymotrypsin
  • Protein X

Pathology Miscellaneous Long Essays

Question 1. Discuss the causes of hemorrhage and describe the complications.
Answer:

Causes of Hemorrhage:

Hemorrhage Complications:

• It depends on
• Amount of blood loss
• Speed of blood loss
• Site of hemorrhage

Pathology Miscellaneous Short Essays

Question 1. Thyrotoxicosis
Answer: Thyrotoxicosis is a syndrome resulting from an increased level of free thyroxin

Thyrotoxicosis Clinical Features:

• Hyperactivity
• Irritability
• Heat intolerance
• Palpitations
• Fatigue
• Weakness
• Weight loss
• Increased appetite
• Tachycardia
• Systolic hypertension
• Presence of tremors
• Cardiac arrhythmias
• Excessive sweating
• Exophthalmos

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Thyrotoxicosis Management:

1. General management:

• Rest
• Nutritious diet

2. Drug therapy:

• Carbimazole- Initial dose of 30 mg/day, maintenance dose of 10-20 mg/day is given
• Potassium perchlorate -800 mg/day in divided doses
• Sodium or potassium iodide 6-10 mg/day

3. Surgical treatment: Subtotal thyroidectomy

4. Radioiodine treatment: Iodine is given in doses of 8-10 millicuries

Question 3. Mention the diseases transmitted through blood transfusion and screening tests.
Answer:

Diseases Transmitted Through Blood Transfusion: The common diseases transmitted through blood transfusion are as follows:

• AIDS
• Hepatitis B and C
• CMV
• Syphilis
• Malaria
• Toxoplasmosis

Screening Tests:

• The usual screening TESTS performed before blood transfusion are
  • ELISA for HIV and Hepatitis B
  • VDRL for syphilis
  • PS for malarial parasites

Pathology Miscellaneous Short Question And Answers

Question 1. Antioxidants
Answer: Antioxidants are endogenous or exogenous substances

Antioxidants Importance:

• Inactivate free radicals
• Play an important role in net effect of free radical in-jury
• It influence the rate of elimination of free radicals

Antioxidants Examples:

• Vitamin E, A, and C
• Sulfhydryl-containing compounds like cysteine and glutathione
• Serum proteins- ceruloplasmin and transferrin

Question 2. Idiopathic hemochromatosis
Answer:

• A form of hemosiderosis in which there is excessive intestinal absorption of iron even when intake is normal, it is called idiopathic hemochromatosis
• It is an autosomal dominant disease associated with much more deposits of iron
• It is characterized by a triad of
  • Pigmentary liver cirrhosis
  • Pancreas damage resulting in diabetes mellitus
  • Skin pigmentation

Idiopathic hemochromatosis Synonyms:

• Hereditary hemochromatosis
• Bronze diabetes

Question 3. Immunization of rabies
Answer:

Rabies vaccines are two types

1. Neural
2. Non-neural

1. Neural Vaccines:

• Semple vaccine:
  • The most widely used vaccine
  • Developed by Semple at Central Research Institute, Kasauli.
  • It is a 5% suspension of infected sheep brain and inactivated by 5% phenol at 37°C leaving no residual live virus.
• Beta Propiolactone (BPL) Vacine:
  • Modified semple vaccine
  • Instead of phenol, BPL is used as inactivating agent.
• Infant brain vaccine:
  • Used widely in south America
  • Reduce neurological complications.
    • Vaccination Schedules:
      • Now a days not used.
      • In the past they were given subcutaneously on the anterior abdominal wall.
      • 7 – 14 injections depends on the degree of risk.

2. Non-Neural Vaccines:

• Duck Egg Vaccine:
  • BPL is used as an inactivating agent
  • It has poor immunogenicity so not used now.
• Tissue culture vaccines: Following cell culture vaccines are available in India.

1. Human diploid cell strain vaccine [HDCS]

• The HDCS vaccine is prepared by growing the rabies virus on human diploid cells and is inactivated with BPL.
• This vaccine is highly antigenic and free of side effects

2. Purified chick embryo cell vaccine [PCEC]

• PCEC is now widely used.
• It is cheaper
• It contains BPL inactivated flurry LEP strain
• 3. Purified Vero cell vaccine [PVC]
• This vaccine is under study

Question 4. Bombay blood group
Answer:

• Red blood cells of type 0 have large amounts of another antigen called H substance
• This is different from ABO
• It is the precursor of A and B antigens
• An O-group individual who inherits A or B genes but fails to inherit the H gene from either parent is called the Bombay blood group
• It contains anti-A, anti-B, and anti-H antibodies in serum
• But red cells are not agglutinated by them

Question 5. The specific gravity of urine
Answer:

• The specific gravity of urine is the ratio of the weight of 1 ml volume of urine to that of 1 ml of distilled water
• it depends upon the concentration of various particles or solutes in the urine

Urine Uses: Use to measure concentrating and diluting power of the kidneys

Urine Methods:

• It is measured by
  • Urinometer
  • Refractometer
  • Reagent strips

Urine Significance:

Question 6. Anticoagulants used in blood bank
Answer: Anticoagulants are substances which prevent or postponed the coagulation of blood

Anticoagulants Types:

• Natural anticoagulants
• Anticoagulants used in blood banks
• Anticoagulants used in laboratory
• Therapeutic Anticoagulants

Anticoagulants Used In Blood Banks: Anticoagulants used in blood banks are

• Acid citrate dextrose (ACD)
• Citrate phosphate dextrose (CPD)
  • They are used to store blood in the blood bank
  • Citrates combine with calcium ions in the blood to form a calcium citrate complex
  • This decreases ionic calcium levels and prevents coagulation

Diabetes Mellitus Important Notes

1. Etiology of Diabetes Mellitus

• Reduced insulin secretion
• Decreased glucose use by the body
• Increased glucose production

2. Complications of Diabetes Mellitus

• Ketoacidosis
• Nonketotic coma
• Hypoglycemia
• Atherosclerosis
• Nephropathy
• Neuropathy
• Microangiopathy
• Retinopathy
• Infections

Diabetes Mellitus Long Essays

Question 1. Define diabetes mellitus. Discuss laboratory diagnosis and complications of diabetes mellitus.
Answer:

Diabetes Mellitus Definition: Diabetes mellitus is defined as a heterogenous metabolic disorder characterized by the common feature of chronic hyperglycaemia with disturbance of carbohydrate, fat and protein metabolism

Diabetes mellitus Laboratory Diagnosis:

• Urine testing
  • Glucosuria
    • The Dipstick method is used
    • In this method, enzyme coated paper strip is used which turns purple when dipped in urine containing glucose
  • ketonuria
    • Rothera’s test is used to detect ketone bodies in urine
• Single blood sugar estimation
  • O-toluidine, Somogyi-Nelson and glucose oxidase methods are used
  • A fasting plasma glucose value above 126 mg/dl is certainly indicative of diabetes
• Screening by fasting glucose test
  • It is a screening test for type 2 diabetes mellitus
  • Done for individuals above 45 years
• Oral glucose tolerance test

Diabetes Mellitus Method:

• Intake of a high carbohydrate diet 3 days prior to the test
• Overnight fasting on the day of the test
• A fasting blood sugar sample is collected
• 75 gms of glucose dissolved in 300 ml of distilled water is given to the individual
• Blood and urine samples are collected at half-hour intervals for atleast 2 hours

Diabetes Mellitus Result:

Diabetes Mellitus Complications:

• Acute metabolic complications
  • Diabetic ketoacidosis
    • Develop in patients with severe insulin deficiency
    • Pathogenesis

• • • Diabetic ketoacidosis Clinical Features:
      • Nausea, vomiting, anorexia
      • Deep and fast breathing
      • Mental confusion
      • Coma
  • Hyperosmolar hyperglycaemia non-ketotic coma
    • It is a complication of type 2 diabetes mellitus
    • Caused by severe dehydration which leads to sustained hyperglycaemia diuresis
      • Hyperglycaemia non-ketotic coma Clinical Features:
        • High blood sugar
        • High plasma osmolality
        • Thrombotic and bleeding complications
  • Hypoglycaemia
    • Develop in type 1 diabetes mellitus
    • Occurs due to
      • Excessive administration of insulin
      • Missing a meal
      • Stress
    • It produces
      • Permanent brain damage
      • Worsening of diabetic control
      • Rebound hyperglycaemia

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• Late systemic complications
  • Atherosclerosis
    • Common in both type 1 and type 2 diabetes mellitus
    • Its contributory factors are
      • Hyperlipidaemia
      • Reduced HDL levels
      • Non-enzymatic glycosylation
      • Increased platelets adhesiveness
      • Obesity
      • Hypertension
    • Atherosclerosis may lead to
      • Myocardial infarction
      • Cerebral stroke
      • Gangrene of toes and feet
  • Diabetic microangiopathy
    • It is the basement membrane thickening of small blood vessels and capillaries of different organs and tissues
    • Occurs due to increased glycosylation of haemoglobin and other proteins
  • Diabetic nephropathy
    • It is a severe complication of diabetes mellitus
    • Occurs in both types
      • Diabetic nephropathy Features:
        • Asymptomatic proteinuria
        • Nephrotic syndrome
        • Progressive Renal failure
        • Hypertension
  • Diabetic neuropathy
    • Effects all parts of the nervous system
      • Pathological Changes:
        • Segmental demyelination
        • Schwann cell injury
        • Axonal damage
  • Diabetic retinopathy
    • It is the cause of blindness
    • Other retinal complications include
      • Glaucoma
      • Cataract
      • Corneal disease
  • Infections
    • Diabetic patients are more susceptible to infections like tuberculosis, pyelonephritis, otitis, carbuncles and diabetic ulcers

Diabetes Mellitus Short Essays

Question 1. Aetiopathogenesis of Diabetes Mellitus.
Answer:

1. Genetic susceptibility Diabetes mellitus involves inheritance of multiple genes

2. Autoimmune factors

• Presence of islet cell antibodies against insulin
• Occurrence of CD8+ T lymphocytes with a variable number of CD4+ T lymphocytes and macrophages
• Selective destruction of beta cells by T-cell mediated cytotoxicity or by apoptosis

3. Constitutional factors

• Obesity, hypertension and level of physical activity
• Presence of viral infection

4. Insulin resistance

• It leads to
  • Impaired glucose uptake by tissues
  • Increased glucose synthesis by the liver
  • Hyperglycaemia

5. Impaired insulin secretion

• In diabetes mellitus, initially, there is increased secretion of insulin
• Later beta cells fail to secrete adequate insulin

6. Increased hepatic glucose synthesis

• In diabetes mellitus gluconeogenesis process remains unaffected
• Thus there is increased glucose synthesis in the liver.

Diabetes Mellitus Short Question And Answers

Question 1. Glycosuria.
Answer:

• It is the condition of glucose excretion in urine.
• Glucose appears in urine when the plasma glucose concentration exceeds the renal threshold for glucose.

Glycosuria Types:

1. Renal glycosuria.

• It is a benign condition.
• Occurs due to a reduced renal threshold for glucose.
• It is unrelated to diabetes.

2. Alimentary glycosuria.

• In certain individuals, blood glucose rapidly Increases after meals which get excreted in the urine.
• This is known as alimentary glycosuria.
• It is observed in.
  • Normal individuals.
  • Individuals with.
    • Hepatic diseases
    • Hyperthyroidism
    • Peptic ulcer.

Diseases Of Oral Cavity And Salivary Glands Important Notes

1. Developmental defects of the tongue

• Macroglossia
• Aglossia
• Fissuredtonghe
• Hairy tongue
• Tongue-tie
• Bifidtongue

2. Leukoplakia is defined as a white patch or plaque on oral mucosa exceeding 5mm India meter which cannot be rubbed off nor can be classified into any other disease

3. Sequele of dental caries

• Pulpitis-acute, chronic
• Apicalgranuloma
• Apical abscess

Diseases Of Oral Cavity And Salivary Glands Short Essays

Question 1. Cancrum oris
Answer:

• Cancrum oris or noma or necrotizing stomatitis is an inflammatory disease of the oral cavity.
• It occurs more commonly in poorly nourished children like in kwashiorkor, infectious diseases such as measles, immune deficiencies, and emotional stress.
• The lesions are characterized by necrosis of the marginal gingiva and may extend onto oral mucosa, causing cellulitis of the tissue of the cheek.
• The overlying skin becomes inflamed, edematous, and finally necrotic, the commencement of gangrene is noted
• The appearance of blackening of skin and extremely foul odor.
• Patients may have a high temperature during the course of the disease, may suffer secondary infections, and may die from toxemia and pneumonia.
• Cancrum oris Treatment: Antibiotics should be administered before the patient reaches the final stages of the disease.

Question 2. Adenocarcinoma
(or)
Leukoplakia
Answer:

Leukoplakia Definition: Leukoplakia may be clinically defined as a white patch/plaque on the oral mucosa, exceeding 5 mm in diameter, which cannot be rubbed off nor can be classified into any other diagnosable disease.

Leukoplakia Etiology:

• Smoking especially pipe and cigar smokers
• Chronic friction example, ill-fitting dentures
• Local irritants like.
  • Alcohol
  • Very hot and spicy food.
  • Beverages

Leukoplakia Morphology:

• Lesions may appear white, whitish yellow, or red velvety of more than 5 mm in diameter and variable in appearance.
• Usually circumscribed, slightly elevated, smooth/wrinkled, speckled nodular.

Leukoplakia Histology:

Microscopic examination reveals two types:

1. Hyperkeratotic
2. Dysplastic type.

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

2. Dysplastic type:

• Shows irregular stratification of the epithelium, focal areas of increased and abnormal mitotic figures, hyperchromatism, pleomorphism, loss of polarity, and individual call keratinization.
• Subepithelial tissue shows inflammatory infiltration of lymphocytes and plasma cells.
• Mild dysplasia reverts to normal but severe dysplasia indicates progression to carcinoma.

Leukoplakia Treatment:

• Elimination of irritating factors and includes:
  • Administration of Vit A, Vit B, and estrogens.
  • X-ray therapy
  • Fulguration
  • Surgical excision
  • Topical chemotherapy.

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Question 3. Epulis
Answer:

• Epulis is also known as peripheral giant cell granuloma
• It is an unusual inflammatory lesion of the gingiva

Epulis Clinical Features:

• Age- young to middle-aged adults
• It begins during the middle trimester of pregnancy
• Nonpathological soft swelling of gums occurs
• Size-1-1.5 cm, hemispherical
• It is covered by intact or ulcerated mucosa
• On the cut section, it appears grey to brown

Epulis Microscopic Appearance:

• It shows an aggregation of multinucleated foreign bodies like giant cells separated by scanty fibro angiomatous stroma
• There may be foci of hemosiderin deposits or an inflammatory infiltrate secondary to mucosa ulceration

Epulis Differential Diagnosis:

• True central giant cell tumours
• Intraosseous reparative giant cell granuloma

Epulis Treatment:

• Removal of underlying etiology
• Surgical excision

Question 4. Ameloblastoma
Answer:

• Ameloblastoma is the most common benign but locally invasive epithelial odontogenic tumor.
• It occurs in both the maxilla and mandible, but the posterior mandible in the molar ramus is the most common location.
• Clinically ameloblastoma presents as slow enlarging, painless, bony hard swelling of the jaw.
• Histologically, ameloblastoma shows many distinct patterns.
  • Follicular pattern
  • Plexiform pattern
  • Acanthomatous pattern
  • Basal cell pattern
  • Granular cell pattern
• Treatment is complete surgical excision and long-term follow-up of the patient.

Question 5. Vincent’s angina
Answer:

Vincent’s infection primarily involves the free gingival margin, the crest of the free gingiva, and the interdental papillae, when such lesions spread to the soft palate and tonsillar areas it is known as Vincent’s angina.

Vincent’s Etiology: Vincent’s bacilli [fusiform bacilli) and borrelia vincentis are the causative organisms.

Vincent’s Clinical Features:

• This is a painful condition of the throat characterized by local ulceration of the tonsils, mouth, and pharynx.
• It is insidious in onset, with less fever and less discomfort in the throat.
• Membrane which usually forms over the tonsil can be easily removed revealing an irregular ulcer on the tonsil.
• It may occur as an acute illness with diffuse involvement of tissue/as a chronic illness consisting of ulceration of the tonsil.

Vincent’s  Treatment:

• In the early acute stage, superficial cleansing of the oral cavity.
• In many cases, prompt regression of diseases results even without medication.

Question 6. Pleomorphic adenoma
Answer: Pleomorphic adenoma also called the mixed salivary tumor is the most common tumor of major [60 – 75%) and minor [50%) salivary glands.

Pleomorphic Adenoma Clinical features:

• The parotid gland is most commonly affected.
• More common in women and the 3rd – 5th decades of life.
• A tumour is a solitary, smooth surface but sometimes nodular, painless, and slow-growing.
• Often located below and in front of the ear and does not show fixation.

Pleomorphic Adenoma Morphology:

• Grossly, it is circumscribed, pseudo-encapsulated, rounded
• It may be a multilobulated, firm mass, 2 -5 cm in diameter, with a bosselated surface.
• Consistency is soft and mucoid.

Pleomorphic Adenoma Histology features: Characterised by the mixed appearance in which there are epithelial elements present in a matrix of mucoid, myxoid, and chondroid tissue.

• Epithelial component: Forms various patterns like ducts, acini, tubules, sheets, and strands of cells of ductal/myoepithelial origin.
• Ductal cells are cuboidal/columnar
• Myoepithelial cells are polygonal/spindle-shaped.
• Focal areas of squamous metaplasia and keratitis- -station may be present.

Pleomorphic adenoma Treatment:

• Surgical excision
• However, recurrence is much more common due to
  • Incomplete surgical removal,
  • Multiple foci of tumor,
  • Pseudo encapsulation.

Diseases Of Oral Cavity And Salivary Glands Short Question And Answers

Question 1. Dentigerous cyst
Answer:

• A dentigerous cyst also called a follicular cyst arises from the enamel of an unerupted tooth
• Most commonly involved are mandibular 3rd molars and maxillary canines.
• Occurs more commonly in children and young individuals.
• Histologically, the dentigerous cyst is composed of a thin fibrous tissue wall lined by stratified squamous epithelium
• This cyst may resemble a radicular cyst, except that chronic inflammatory changes characteristic of radicular cyst, are usually absent in dentigerous cysts.

Dentigerous cyst Treatment:

• Large cysts are treated by marsupialization in young individuals
• Smaller lesions can be surgically removed entirely.

Question 2. Dental caries
Answer: Dental caries is the most common disease of dental tissues, destroying the calcified tissues of teeth.

Dental Caries Etiology:

• A diet rich in carbohydrates which is soft and sticky.
• If the plaque is not removed it leads to tooth decay.
  • Caries occur chiefly in pits and fissures of molars and premolars
  • The earliest change is the appearance of a small, chalky white spot on enamel which enlarges and becomes yellow/brown and forms various cavities.
  • Pulpitis and necrosis of the pulp take place.
  • If left untreated, caries may progress from pulpitis to apical granuloma and apical abscess.

Question 3. Cancrum oris
Answer:

• It occurs commonly in poorly nourished children or with immune deficiencies and emotional stress.
• Oral mucosae like marginal gingiva, lips, and cheeks are affected by necrosis and gangrene
• Patients may have high temperatures and may die from toxemia and pneumonia.
• Malnutrition must be treated and antibiotics may be useful in the early stages of the disease.

Question 4. Microscopic picture of Warthin’s tumor.
Answer:

• It is a benign tumor of the parotid gland comprising about 8% of parotid neoplasms, seen more commonly in men.
• Grossly, the tumor is encapsulated, round/oval with a smooth surface.
• The cut surface shows characteristic slit-like/cystic spaces, containing milky fluid and having papillary projections.

Microscopically, the tumour shows 2 components.

• Epithelial parenchyma and
• Lymphoid stroma
• Epithelial parenchyma: This is composed of glandular and cystic structures having papillary arrangement and is lined by characteristic eosinophilic epithelium.
• Lymphoid stroma is present under the epithelium in the form of prominent lymphoid tissue, often with germinal centers.

Question 5. Typhoid ulcer
Answer:

• Typhoid ulcer occurs in the jejunum and colon
• It is aligned with their long axis along the length of the bowel
• The base of the ulcer is black due to sloughed mucosa
• Margins are slightly raised due to inflammatory edema and cellular proliferation
• Regional lymph nodes are enlarged

Typhoid ulcer Complications:

• Perforation of ulcers
• Hemorrhages

Systemic Hypertension Important Notes

1. Values

• Systolic-140-159mmHg
• Diastolic-90-99mmHg

2. Effects of hypertension

• Nephrosclerosis
• Hypertensive heart disease
• Retinopathy
• Intracranial hemorrhage

3. Types of aneurysms affecting larger Intracranial arteries

• Berry
• Mycotic
• Fusiform

4. Features of hypertensive retinopathy

• Arteriolar narrowing
• Flame shaped hemorrhages
• Macular star
• Cotton wool spots
• Microaneurysms
• Arteriovenous nicking
• Hard exudates

Systemic Hypertension Short Essays

Question 1. Hypertension
Answer:

• Hypertension is the sustained resting blood pressure of more than 160/95 mm Hg.
• It is the most common cause of cardiac failure and a major risk factor for atherosclerosis and cerebral hemorrhage

Hypertension Classification:

1. Clinical classification

2. General classification

• Primary or essential hypertension
  • Occurs due to unknown cause
• Secondary hypertension
  • Occurs due to the presence of renal, endocrine, or other diseases

3. According to the clinical course

• Benign hypertension
  • Moderate elevation of blood pressure occurs
  • Rise is slow over the years
  • It is often asymptomatic
• Malignant hypertension
  • It is a marked and sudden increase in blood pressure
  • Occurs in patients with evidence of previous benign hypertension
  • Often results in severe and acute renal, retinal, and cerebral damage

4. Etiological classification

• Essential or primary hypertension
  • Hereditary
  • Racial and environmental factors
  • Risk factors modifying the course
• Secondary hypertension
  • Renal diseases
  • Endocrine disorders
  • Coarctation of aorta
  • Neurogenic

Effects of Hypertension:

• Nephrosclerosis
• Heart diseases
• Retinopathy
• Intracranial hemorrhages

Disorders Of White Blood Cells Important Notes

1. Types of leukemia

2. Syndromes associated with leukemia

• Down’s syndrome
• Bloom’s syndrome
• Klinefilter’s syndrome
• Wiskott-Aldrictis syndrome
• Fanconi’s anemia

3. Infectious mononucleosis or glandular fever

• Caused by Epstein Barr virus
• Characterized by atypical leukocytes consisting of
  • Oval or horseshoe nuclei
  • Irregular nuclear chromatin
  • Basophilic foamy or vacuolated cytoplasm

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• Diagnostic tests
  • Monospot test
  • Paul Bunnel test
    • The normal titer of agglutinin and hemolysin in human blood against sheep blood cells does not exceed 1:8
    •  In a positive Paul Bunnel test, the titer may rise to 1:4096

4. Agranulocytosis

• Mostly occurs due to the ingestion of drugs like
  • Amidopyrine
  • Barbiturates
  • Chloramphenicol
  • Quinine
  • Sulfonamides
• Features
  • Presence of infection in the oral cavity, GIT, genitourinary tract, respiratory tract, and skin
  • Oral manifestation
  • Necrotizing ulcerations of the oral mucosa, pharynx, tonsils
  • Rapid destruction of supporting tissues of the teeth

5. Cyclic neutropenia

• It is characterized by periodic cyclic diminution of leukocytes
• Cycle commonly occurs at every 3 weeks
• Loss of alveolar bone around the teeth is an important oral manifestation

6. Disorders of neutrophil count

7. Leukaemoid reactions

• It is defined as a reactive excessive leucocytosis in the peripheral blood resembling that of leukemia
• It may be myeloid or lymphoid
• The myeloid type is a more common form
• Myeloid leukemoid reactions are seen in
  • Infections like staphylococcal pneumonia, TB, meningitis, diphtheria, sepsis, endocarditis
  • Intoxication
  • Malignant diseases like multiple myeloma
  • Severe hemorrhage and hemolysis
• Lymphoid leukemoid reaction are seen in
  • Infections like infectious mononucleosis, cytomegalovirus infection, pertussis
  • Malignant diseases rarely produce it

8. Most commonly affected bones in multiple myeloma are:

• Skull
• Spine
• Ribs
• Pelvis

Disorders Of White Blood Cells Long Essays

Question 1. Classify leukemia. Describe the clinical picture, blood, and bone marrow findings in acute leukemia.
Answer:

Leukemia Classification:

1. Based on cell types predominantly involved.

• Myeloid
• Lymphoid.

2. Based on the natural history of the disease:

• Acute
• Chronic.

WHO classification of myeloid neoplasm:

1. Myeloproliferative Diseases:

• Chronic myeloid leukaemia (CML], {Ph chromo¬some t(9;22) (q34;ll), BCR/ABL-positive}
• Chronic neutrophilic leukemia
• Chronic eosinophilic leukemia/ hypereosinophilic syndrome
• Chronic idiopathic myelofibrosis
• Polycythaemia vera (PV]
• Essential thrombocythaemia (ET)
• Chronic myeloproliferative disease, unclassifiable

2. Myelodysplastic/Myeloproliferative Diseases: Chronic myelomonocytic leukemia (CMML)

3. Myelodysplastic Syndrome (MDS):

• Refractory anemia (RA)
• Refractory anemia with ring sideroblasts (RARS)
• Refractory cytopenia with multilineage dysplasia (RCMD)
• RCMD with ringed sideroblasts (RCMD-RS)
• Refractory anemia with excess blasts [RAEB-1)
• RAEB-2
• Myelodysplastic syndrome unclassified (MDS-U)
• MDS with isolated del 5q

4. Acute Myeloid Leukaemia (AML):

• AML with recurrent cytogenetic abnormalities
  • AML with t(8;21)(q22;q22)
  • AML with abnormal bone marrow eosinophils {inv(16][pl3q22]}
  • Acute promyelocytic leukaemia {tC15;17](q22;ql2)}
  • AML with llq23 abnormalities (MLL)
• AML with multilineage dysplasia
  • With prior MDS
  • Without prior MDS
• AML and MDS, therapy-related
  • Alkylating agent-related
  • Topoisomerase type 2 inhibitor-related
  • Other types
• AML, not otherwise categorized
  • AML, minimally differentiated
  • AML without maturation
  • AML with maturation
  • Acute myelomonocytic leukemia (AMML)
  • Acute monoblastic and monocytic leukemia
  • Acute erythroid leukemia
  • Acute megakaryocytic leukemia
  • Acute basophilic leukemia
  • Acute panmyelosis with myelofibrosis
  • Myeloid sarcoma

5. Acute Biphenotypic Leukaemia

Acute Leukemia: It is a leukemia characterized by predominant undifferentiated leucocytes precursors

Acute Leukemia Clinical Features:

Acute Leukemia Blood Picture:

• Moderate reticulocytosis
• Normochromic anemia
• Increased platelet count
• WBCs count is more than 100000 per microlitre

Acute Leukemia Bone Marrow Examination:

• Cellularity- Bone marrow is hypercellular
• It shows predominantly myeloblasts and premyelo¬cytes
• Leukemic cells are demonstrated by Romanowsky stains
• Erythropoiesis shows
  • Reduced erythropoietic cells
  • Dyserythropoiesis,
  • Megaloblastic features
  • Ring sideroblasts
  • Megakaryocytes

Question 2. Define leukemia. Describe the etiology, clinical features, blood, and bone marrow picture of chronic myeloid leukemia.
Answer:

Leukemia: leukemia are a group of disorders arising from the malignant transformation of hematopoietic cells leading to an increased number of white blood cells in blood and/or bone marrow.

Chronic myeloid leukemia:

Chronic myeloid leukemia Etiology: It is a myeloproliferative disorder.

• Occurs as a result of the malignant transformation of plea- potent stem cells leading to the accumulation of a large number of immature leukocytes in the blood.
• Radiation exposure and genetic factors have been implicated in the development of CML

Chronic myeloid leukemia Clinical features:

• Onset is usually slow, initial symptoms are often non-specific example: weakness, pallor dyspnoea, and tachycardia.
• Symptoms due to hypermetabolism such as weight loss, anorexia, and night sweats.
• Splenomegaly is almost always present and is frequently massive. In some patients, it may be associated with acute pain due to splenic infarction.
• Bleeding tendencies such as bruising, epistaxis, menorrhagia, and hematomas may occur.
• Visual disturbance, neurologic manifestations.
• Juvenile CML is more often associated with lymph node enlargement than splenomegaly.

Peripheral blood picture of CML:

• Leucocyte count is elevated often > 1,00,000 cells/pl.
• Circulating cells are predominantly neutrophils, metamyelocytes, and myelocytes but basophils and eosinophils are also prominent.
• A typical finding is an increased number of platelets (thrombocytosis).
• Anaemia is usually of moderate degree and is normocytic, normochromic in type. Normablasts may be present occasionally.
• A small portion of myeloblasts usually < 5% are seen.

Bone marrow examination:

• Cellularity – Hyper cellular with total/partial re-placement of fat spaces by proliferating myeloid cells.
• Myeloid cells -Myeloblasts are only slightly increased.
• Erythropoiesis -Normoblasts but there is a reduction in erythropoietic cells.
• Megakaryocytes – Conspicuous but are usually smaller in size than normal.
• Increase in number of phagocytes.

Disorders Of White Blood Cells Short Essays

Question 1. Leukocytosis
Answer:

Leukocytosis is an increase in the number of white cells & is common in a variety of reactive inflammatory states caused by microbial and non-microbial stimuli.

Leukocytosis Causes: Leukocytosisare relatively non-specific and can be classified on the basis of particular white cell series affected as follows:

Causes of Leukocytosis: Leukocytosis are relatively non-specific and can be classified on the basis of particular white cells series affected as follows:

1. Neutrophilic leucocytosis.

• Cute bacterial infections especially those caused by pyogenic organisms.
• Sterile inflammation caused by tissue necrosis (myocardial infarction, burns)

2. Eosinophylic leucocytosis (eosinophilia)

• Allergic disorders such as asthma, hay fever
• Allergic skin diseases, for example., pemphigus, dermatitis herpetiform.
• Parasitic infestations
• Drug reactions
• Certain malignancies, for example., Hodgkin’s disease and some non-hodking’s lymphomas.
• Collagen vascular disorders and some vasculitis.

3. Basophilic leucocytosis (basophilia): Rare often indicates CML.

4. Monocytosis.

• Chronic infections, ie.g., tuberculosis
• Bacterial endocarditis
• Rickettsiosis and malaria
• Collagen vascular diseases, for example., systemic lupus erythematosus (SLE)
• Inflammatory bowel diseases, for example., ulcerative coli¬tis

5. Lymphocytosis: Usually accompanies monocytosis in many disorders associated with it.

• Chronic immunologic stimulation, for example., tuberculo¬sis, brucellosis and
• Viral infections, for example., hepatitis A, cytomegalovirus, Epstein-Barr virus, and bordetella pertussis infections.

Question 2. Causes of neutrophilic leukocytosis
Answer:

• Acute bacterial infections especially those caused by pyogenic organisms.
• Sterile inflammation caused by tissue necrosis (myocardial infarction, burns)

Question 3. Agranulocytosis
Answer:

• The term agranulocytosis is used to describe a state of severe neutropenia.
• A reduction in the number of granulocytes in the blood is known as neutropenia.

Agranulocytosis Causes: Neutropenia can be caused by the following reasons.

• Drug-induced: Anti-cancer, antibiotics, anticonvulsants, antithyroid drugs
• Hematological disease: Aplastic anemia, acute leukemia, etc.
• Infections: Malaria, TB, typhoid,
• Autoimmune: Systemic lupus erythematosus
• Congenital: Cyclic neutropenia.

Agranulocytosis Clinical features:

• Initially patient develops malaise, chills, and fever, with subsequent marked weakness and fatiguability.
• Massive growth of microorganisms due to inability to produce leukocyte response.
• Infections are usually present as ulcerating, necrotizing lesions of the gingiva, the floor of the mouth, buccal mucosa, and other sites within the oral cavity known as agranulo¬cytic angina.
• Lymphadenopathy and hepatosplenomegaly may be present.

Agranulocytosis Treatment:

• Patients with neutropenia and fever must be sent to the hospital.
• In severe infections, neutrophil transfusion must be done.
• Broad-spectrum antibiotics and antifungal drugs are to be given.

Question 4. Leukemoid reaction
Answer:

• Leukaemoid reaction is defined as the reactive excessive leucocytosis in peripheral blood resembling that of leukemia in the subject who does not have leukemia.
• Leukaemoid reaction may be myeloid or lymphoid.

Myeloid leukemoid reaction:

• The majority of leukemoid reactions involve the granulocyte series.
• It may occur in infection, intoxication, malignant diseases, severe hemorrhages, and severe hemolysis.

Lymphoid leukemoid reaction: It is found in conditions such as infectious mononucleosis, whooping cough, chicken pox, measles, and tuberculosis.

Agranulocytosis Lab diagnosis:

• Leukocytosis
• Infective cases may show toxic granulation and Dohle bodies in the cytoplasm of neutrophils.

Question 5. Peripheral blood picture of acute lymphatic leukemia
Answer: Acute lymphatic leukemia shows

1. Anaemia:

• Normochromic
• Shows few nucleated cells

2. Thrombocytopenia: Platelet count decreases to 100000 cells

3. White blood cells:

• WBC count is variable
• It may exceed 100000 cells or may be less than that
• Leukocytes appear as blasts cells

Disorders Of White Blood Cells Short Questions And Answers

Question 1. Eosinophilia
Answer:

• An increase in the number of eosinophilic leukocytes is referred to as eosinophilia.
• The causes of eosinophilia are as follows:
• Allergic disorders: Bronchial asthma, urticarial, drug hypersensitivity
• Parasitic infestations: Trichinosis, echinococcosis, intestinal parasitism.
• Skin diseases: Pemphigus, dermatitis herpetiformis, erythema parasitism.
• Certain malignancies: Hodgkin’s diseases and some non-Hodgkin’s lymphomas.
• Pulmonary infiltration which eosinophilia syndrome
• Irradiation.
• Miscellaneous disorders: Sarcoidosis, rheumatoid arthritis, polyarteritisnodosa.

Question 2. Blood picture in chronic myeloid leukemia
Answer:

• Leucocyte count is elevated often > 1,00,000 cells/Bll.
• Circulating cells are predominantly neutrophils, metamyelocytes, and myelocytes but basophils and eosinophils are also prominent
• The typical finding is an increased number of platelets (thrombocytosis).
• Anaemia is usually of moderate degree and is normocytic, normochromic in type. Normablasts may be present occasionally.
• A small portion of myeloblasts usually < 5% are seen.

Question 3. Peripheral smear layer findings in acute leu¬kemia
Answer:

1. Anaemia:

• Always present generally severe, progressive, and normochromic.
  • A moderate reticulocytosisupto 5% and a few nucleated red cells may be present.

2. Thrombocytopenia:

• Platelet count < 50,000/pl
  • When the platelet count is below 20,000/01 serious spontaneous haemorrhagic episodes develop.
  • Acute promyelocytic leukemia may be associated with a serious coagulation abnormality called dis-seminated intravascular coagulation.

3. White blood cells:

• In advanced cases, WBC > 1,00,000/pl
  • The majority of leucocytes in the peripheral blood are blasts and there is often neutropenia due to mar¬row infiltration by leukemic cells.

Question 4. Burkitt’s lymphoma
Answer:

• Burkitt’s lymphoma is a rare type of non-Hodgkin’s lymphoma (NHL).
• Epstein-Barr virus (EBV) and HIV are associated with the development of Burkitt’s lymphoma.
• This is the most rapidly progressive tumor first described in African children.
• Most patients present with lymphadenopathy and abdominal mass.
• It has a tendency to metastasize to the CNS.
• Treatment should be initiated promptly with intensive chemotherapy. Prophylactic chemotherapy is also given. 70-80% of patients may be cured.

Question 5. Multiple myeloma
Answer: Multiple myeloma is a malignant disease arising from the neoplastic transformation of plasma cells of mono-clonal origin

Multiple Myeloma Clinical Features:

• Age- in older age
• Anaemia
• Bone pain
• Infections
• Pathological fractures
• Renal failure
• Spinal cord compression

Multiple Myeloma Investigations:

• Bence- Jones proteins in urine
• Reversal of serum albumin/globulin ratio
• Increase in total serum proteins

Multiple Myeloma Treatment:

• Radiotherapy
• Biphosphonates
• Autologous peripheral cell transplantation
• Administration of thalidomide and proteasome inhibi¬tors
• Chemotherapy includes:
  • Melphalan
  • Cyclophosphamide
  • Doxorubicin
  • Dexamethasone

Diseases Of Cardiovascular Disorders Important Notes

1. Clinical patterns of angina

• Stable or typical angina
• Prinzmetal’s variant angina
• Unstable or crescendo angina

2. Forms of Creatine phosphokinase

• CK-MM-Derived from skeletal muscle
• CK-BB-Derived from the brain and lungs
• CK-MB-Derived from cardiac muscle

3. TypesofischaemicheartdiseaseJHD

• Stable angina
• Unstable angina
• Chronic IHD
• Myocardial infarction
• Sudden ischaemic death

Diseases Of Cardiovascular Disorders Short Question And Answers

Question 1. Hyperlipidemia
Answer:

• Hyperlipidaemia is a major risk factor for atherosclerosis
• It occurs due to
  • Diabetes mellitus
  • Myxoedema
  • Nephritic syndrome
  • Von Gierke’s disease
  • Xanthomatosis
  • Familial hypercholesterolemia
• Dietary regulation and administration of cholesterol-lowering drugs have beneficial effects on reducing the risk of ischaemic heart diseases

Question 2. Atheromatous plaques
Answer: A fully developed atherosclerotic lesion is called atheromatous plaque

Atheromatous plaques Appearance:

1. Gross appearance

• Appear as white to the yellowish-white lesion
• Size-1-2 cm in diameter
• Appears raised on the surface

2. Cut surface

• Shows luminal surface as a firm, white fibrous cap
• The central core is composed of yellow to yellow-white soft material called atheroma

3. Microscopic

• The fibrous cap is covered by endothelium
• It is composed of smooth muscles, dense connective tissue, and extracellular matrix
• The cellular area contains macrophages, foam cells, lymphocytes and smooth muscle cells
• The deeper central soft core consists of extracellular lipid material, cholesterol cleft, Fibrin, neurotic debris, and lipid-laden foam cells

Disorders Of Platelets Important Notes

1. Partial thromboplastin time

• Used to measure the intrinsic factors as well as factors common to both intrinsic and extrinsic pathways
• The normal range is – 30-40 sec
• Causes of prolonged partial thromboplastin time are
• Parenteral administration of heparin
  • DIC
  • Liver disease
  • Circulating anticoagulants

2. Thrombin time

• It is a semi-quantitative test for fibrinogen deficiency
• Normal range – 20-30 sec
• Common causes of prolonged thrombin time are
  • Presence of heparin
  • DIC

3. Bleeding time

• Normal range – 3-8 min
• Prolonged in
  • Thrombocytopenia
  • Von Willebrand disease
  • Vascular abnormalities
  • Disorders of platelet functions

4. Clotting time

• Normal range – 4-9 min
• Prolonged in
  • Hemophilia
  • Vitamin K deficiency
  • Liver diseases
  • Anticoagulant administration

5. Von Willebrand disease

• It occurs due to qualitative defect in Von Willebrand factor in blood
• It is characterized by
  • Normal platelet count
  • Prolonged bleeding time
  • Defective platelet aggregation
  • Reduced factor 8 activity

6. DIC (Disseminated Intravascular Coagulation)

• It is characterized by systemic activation of the blood coagulation system
• Results in the generation and deposition of fibrin leading to Microvascular thrombi in various organs
• Severe bleeding complications occur
• It is seen in promyelocytic leukaemia

Disorders Of Platelets Long Essays

Question 1. What is disseminated intravascular coagulation? Describe its etiopathogenesis.
Answer:

Disseminated Intravascular Coagulation: Disseminated intravascular coagulation is a complex thrombo-hemorrhagic disorder occurring as a secondary complication in some systemic diseases

Disseminated Intravascular Coagulation Etiopathogenesis: Pathogenesis of DIC includes the following events

1. Activation of coagulation: Etiological factors like massive tissue injury, presence of infections, and endothelial damage cause activation of coagulation by the release of tissue factor

2. Thrombotic phase:

• Endothelial damage from various thrombogenic stimuli causes:
  • Generalized platelet aggregation
  • Platelet adhesion
  • Deposition of small thrombi and emboli throughout microvasculature

3. Consumption phase: Consumption of coagulation factors and platelets occurs

4. Secondary fibrinolysis:

• The fibrinolytic system is secondary activated
• This causes the breakdown of fibrin resulting in the formation of FDPs in circulation

Disorders Of Platelets Short Essays

Question 1. Bleeding time
Answer:

• Bleeding time (BT] is defined as the time lapse between skin puncture and the arrest of bleeding.
• BT is the time from the onset of bleeding to the stoppage of bleeding. The bleeding stops due to the formation of a temporary haemostatic plug.
• Procedure: Under aseptic conditions, give a deep finger prick and note the time. Then remove the blood drop every 15 s with a clotting paper (along the edges] at a different spot till the bleeding stops. Count the number of spots and calculate BT as follows:
• BT = Initial time + (number of spots – 1] x 15 s

Read And Learn More: Pathology Question And Answers

Bleeding Time Indications:

• It is a useful screening test in patients with a history of prolonged bleeding.
• In patients with bleeding disorders before any surgical procedures.

Bleeding Time Interpretation: An abnormal BT is usually the result of

• Abnormalities in the structure or ability of capillary blood vessels to contract or
• Abnormalities in the number or functional integrity of the platelets.

Question 2. Thrombocytopenia
Answer: Thrombocytopenia is defined as a reduction in the peripheral blood platelet count below the lower limit of normal i. e., below 1,50,000/microlitre

• Platelet counts in the range of 20,000 – 50,000 cells/microlitre are associated with an increased risk of post-traumatic bleeding.
• Spontaneous bleeding is evident when the count falls below 20,000 cells/microlitre

Thrombocytopenia Causes:

1. Impaired platelet production:

• Generalised bone marrow failure.
• Aplastic anaemia, leukaemia, megaloblastic anaemia, marrow infiltration.
• Selective suppression of platelet production.
  • Drugs (Anticancer, cytotoxic, alcohol], Infection (HIV, measles].

2. Accelerated platelet destruction:

• Immunologic destruction.
  • Autoimmune – ITP, SLE
  • Drug associated – Heparin, sulfa compounds.
  • Infections – HIV, cytomegalovirus infections.
• Non – immunologic destruction,
  • DIC
  • Gaint haemangiomas
  • TTP

3. Splenic Sequestration: Splenomegaly.

4. Dilutional loss: Massive transfusion of old stored blood to bleeding patients.

Thrombocytopenia Clinical features:

• Usual manifestations are petechial haemorrhage, purpura, easy bruising, epistaxis, mucosal bleeding such as menorrhagia in women, nasal bleeding, bleeding from gums, and haematuria.
• Intracranial haemorrhage is rare.
• Splenomegaly and hepatomegaly may also occur.

Thrombocytopenia Investigations:

• Low platelet counts,
• Prolonged bleeding times,
• Normal coagulation profile
• Abnormal long clot retraction time.

Thrombocytopenia Treatment:

• Platelet transfusion.
• Treatment of the underlying cause.

Question 3. Hemophilia
Answer:

• Haemophilia is an X-linked recessive disorder characterised by the deficiency of factor 8 (Haemophilia A] classic haemophilia]
• Whereas inherited deficiency of factor 9 (Christmas factor/plasma thromboplastin component] produces Christmas disease/haemophilia B (Christmas disease].

Hemophilia A: Pathogenesis: It is caused by quantitative reduction of factor 8 in 90% of cases while 10% have normal/increased levels of factor 8 but reduced activity.

Hemophilia A Clinical features:

• In severe cases -Bleeding is spontaneous.
• In mild disease – Bleeding is rarely spontaneous
• Bleeding occurs mainly in joints (Haemarthrosis), muscles (haematoma), and viscera/in retroperitoneum but can involve any organ system.
• Spontaneous intracranial haemorrhage and oro-pharyngeal bleeding are rare, but when they occur they are the most feared complications.

Hemophilia A Treatment: Factor 8 replacement therapy, consisting of factor 8 concentrates/plasma cryoprecipitates.

Haemophilia B:

• Haemophilia B is rarer than haemophilia A.
• Inheritance patterns and clinical features of factor 9 are indistinguishable from those of classic haemophilia but accurate laboratory diagnosis is critical since haemophilia B requires treatment with different plasma fractions.

Hemophilia B: Treatment: infusion of either fresh frozen plasma/plasma enriched with factor 9

Question 4. Von Willebrand’s disease
Answer:

Von Willebrand’s Disease: This is the most common hereditary coagulation disorder occurring due to qualitative/quantitative defects in Von Willebrand’s factor.

• Von Willebrand factor is a multimeric plasma glycoprotein synthesized by megakaryocytes and endothelial cells. It serves two major functions as follows.
• Acts as a carrier protein for factor 8.
• Helps in the adhesion of platelets to subendothelial collagen.

Von Willebrand’s Disease Clinical features:

• Spontaneous bleeding from mucous membranes and excessive bleeding from wounds.
• Gastrointestinal bleeding.
• Epistaxis, menorrhagia, and superficial bruises are present

Von Willebrand’s Disease Lab investigations:

• Prolonged bleeding time,
• Normal platelets count,
• Bleeding time increased,
• Reduced vWF levels, factor 8 activity reduced.

Von Willebrand’s Disease Treatment:

• Factor 8 and vWF concentrate transfusion,
• The bleeding episodes can be managed by giving vasopressin which increases the VWF levels.
• Persistent bleeding is treated with factor 8 concentrate.
• Cryoprecipitate transfusion
• Antifibrinolytic agent
• Example: Tanexamie acid is useful in conjunctive therapy during dental procedures.

Question 5. Pancytopenia
Answer: Pancytopenia means the occurrence of anaemia, leukopenia and thrombocytopenia together.

The causes of pancytopenia are as follows:

1. Aplastic anaemia

2. Pancytopenia with normal or increased marrow cellularity.

• Myelodysplastic syndromes
• Hypersplenism
• megaloblastic anaemia

3. Paroxysmal nocturnal haemoglobinuria

4. Bone marrow infiltrations.

• Haematologic malignancies (leukaemias, lympho-mas, myelomas)
• Nonhaematologic metastatic malignancies
• Storage diseases
• Osteopetrosis.

Question 6. Idiopathic Thrombocytopenic Purpura.
Answer: It is characterized by the immunologic destruction of platelets and normal or increased megakaryocytes in bone marrow

Idiopathic Thrombocytopenic Purpura Types:

1. Acute
2. Chronic

Idiopathic Thrombocytopenic Purpura Clinical Features:

• Usual manifestations
• Petechial haemorrhage
• Purpura
• Easy bruising
  • Epistaxis
  • Mucosal bleeding such as menorrhagia in women
  • Nasal bleeding
  • Bleeding from gums
  • Hematuria
• Intracranial haemorrhage is rare
• Splenomegaly and hepatomegaly may also occur

Idiopathic Thrombocytopenic Purpura Lab Diagnosis:

• Diagnosis can be made from the following findings
  • Thrombocytopenia
  • Microangiopathic haemolytic anaemia
  • Leucocytosis
  • Bone marrow aspiration shows increased megakaryocytes
  • Examination of biopsy shows typical microthrombi in arterioles, capillaries and venules

Disorders Of Platelets Short Question And Answers

Question 1. Prothrombin time
Answer:

• Prothrombin measures the extrinsic system factor 7 as well as factors in the common pathway
• In it, tissue thromboplastin and calcium are added to the test

Normal Time: 10-14 seconds

Prolonged In:

• Administration of oral Anticoagulants
• Liver disease
• Vitamin K deficiency
• Disseminated intravascular coagulation

Question 2. Screening tests for bleeding disorders
Answer:

Disorders Of Red Blood Cells Important Notes

1. Types of Anaemia

2. Morphological types of anaemia

3. Triad of Plummer-Vinson syndrome

• Iron deficiency anaemia
• Koilonychia or spoon-shaped nails
• Hysteric dysphagia

4. Disorders Of Red Blood Cells Terms

5. Thalassaemia

• α-thalassaemia is due to deficient synthesis of α chain
• β-thalassaemia is due to deficient synthesis of β chain
• heterozygous form of thalassaemia is called thalassaemia minor
• The homozygous form of thalassaemia is called thalassaemia major

Thalassaemia Features:

• • Occurs within the first two years of life
  • Siblings are commonly affected
  • Present as
    • Hypochromic and microcytic anaemia
    • Prominent cheekbones
    • Depression of nasal bridge
    • Prominent premaxilla
    • Protrusion of maxillary anterior teeth

Read And Learn More: Pathology Question And Answers

• Laboratory findings
  • Target cells, safety-pin cells and normoblasts are seen
  • Poikilocytosis, Anisocytosis present
  • Elevated serum bilirubin level
  • Bone marrow shows large immature RBC
• Radiographic findings
  • Crew-cut or hair-on-end appearance on the surface of the skull
  • Salt and pepper appearance of trabeculae pattern of maxilla and mandible

6. Hormones essential for RBC production

• Erythropoietin
• Androgens
• Thyroxine

7. Metals essential for RBC production

• Iron
• Cobalt
• Manganese

8. Vitamins essential for RBC production

• Vitamin B12
• Vitamin C
• Vitamin B6
• Vitamin E
• Vitamin B2

9. Types of haemoglobin

• Adult haemoglobin – HbA
  • Consists of 2 alpha chains and 2 beta chains
• Fetal haemoglobin – HbF
  • Consists of 2 alpha chains and 2 gamma chains

Disorders Of Red Blood Cells Long Essays

Question 1. Define and classify anaemia. Describe labora¬tory diagnosis and Clinical features of iron deficiency Anaemia.
Answer:

Anaemia: Anaemia is defined as haemoglobin concentration in blood below the lower limit of the normal range for the age and sex of the individual.

In an adult male 13 g/dl and for females 11.5 g/dl is taken as the lower lift of the normal haemoglobin range.

Classification of anaemias:

1. Pathophysiologic:

• Anaemia due to increased blood loss
  • Acute post-haemorrhagic anaemia
  • Chronic blood loss
• Anaemias due to impaired red cell production
  • Cytoplasmic maturation defects
    • Deficient haem synthesis: Iron deficiency anaemia
    • Deficient globin synthesis: Thalassaemic syndromes
  • Nuclear maturation defects
    • Vitamin B12 and/or folic acid deficiency: Megaloblastic anaemia
  • Defects in stem cell proliferation and differentiation
    • Aplastic anaemia
    • Pure red cell aplasia
  • Anaemia of chronic disorders
  • Bone marrow infiltration
  • Congenital anaemia
• Anaemias due to increased red cell destruction [Haemolytic anaemias).
  • Extrinsic (extracorpuscular) red cell abnormalities
  • Intrinsic (intracorpuscular) red cell abnormalities

2. Morphologic:

1. Microcytic, hypochromic
2. Normocytic, normochromic
3. Macrocytic, normochromic

Iron deficiency anaemia:

• Commonest nutritional deficiency disorder.
• Iron is mainly available from a diet rich in meat, liver, beans and green vegetables.
• Milk is a poor source of iron.
• The daily iron requirement is 1 mg in males and 2 mg in females.
• Absorption of iron is facilitated by the presence of acid in the stomach and vit. C, while antacids and calcium phosphates decrease it.

Anaemia Laboratory diagnosis:

• Serum iron and ferritin are low.
• Total iron binding capacity is increased
• Transferrin saturation is below 16%.
• Stool examination for parasites and occult blood is useful.
• Endoscopic and radiographic examination of the GI tract is needed to detect the source of bleeding.

Haematological findings: Examination of peripheral blood picture.

• Size: Microcytic anisocytosis
• Chromicity: Anisochromia is present.
• Shape: Poikilocytosis is often present, pear-shaped tailed variety of RBC, elliptical form common.
• Reticulocytes: Present, either normal / reduced
• Osmotic fragility: Slightly decreased
• ESR: Seldom elevated
• Absolute value: MCV, MCH and MCHC are reduced.

Bone marrow findings:

• Marrow cellularity – increased due to erythroid hy¬poplasia micronormoblast
• Marrow iron-reduce reticuloendothelial iron stores and absence of siderotic iron granules from developing normoblasts.

Anaemia Clinical Features:

1. Anaemia:

• Usual symptoms are weakness, fatigue, dyspnoea on exertion, palpitations, pallor of skin, mucous membranes and sclera.
• Older patients may develop angina and congestive cardiac failure.
• Women-menorrhagia is a common symptom.

2. Epithelial tissue changes:

• Nails (koilonychia or spoon-shaped nails)
• Tongue (Atrophic glossitis)
• Mouth (angular stomatitis)

Question 2. Describe in detail clinical fea¬tures, peripheral blood smear and bone marrow findings in megaloblastic anaemia.
Answer:

Megaloblastic anaemia Clinical Features:

• Aneamia,
• Glossitis,
• Neurological manifestations –
• Numbness,
• paraesthesia,
• weakness,
• Ataxia, dimihinshed reflexes.
• Others- mild jaundice,
• Angular stomatitis, purpura, malabsorption, Anorexia.

1. Blood picture:

• Haemoglobin concentration- falls.
  • MCV and MCH increases
  • MCHC decreases/remains normal,
• Reticulocyte count – is low
• Red blood cells – blood smear demonstrates aniso- cytosis, poikilocytes and presence of macroscale-cytes
• Leucocytes – total WBC count is less than c Thrombocytes – giant platelets are present.

2. Bone marrow findings:

• Marrow cellularity – hypercellular bone marrow with decreased myeloid: erythroid ratio,
• Erythropoiesis – erythroid hyperplasia is due to characteristic megaloblastic erythropoiesis.
  • Megaloblasts are abnormal, large, nucleated erythroid precursors, having nuclear cytoplas¬mic asynchrony. Nuclei are large, having fine re¬ticular and open chromatin,
  • Abnormal mitosis may be seen in megaloblasts.
• Marrow iron – increase in the number and size of the iron granules in erythroid precursors. Iron in reticulum cells is increased.

Disorders Of Red Blood Cells Short Essays

Question 1. Sings and Symptoms of Anaemia
Answer:

Signs and symptoms of anaemia :

1. CNS: Faintness, giddiness, headache, tinnitus, drowsiness, numbness, and tingling sensations of hands and feet.
2. Cardiovascular system: Hyperdynamic circulation may be present with tachycardia, collapsing pulse, cardiomegaly, and dyspnoea, in elderly with congestive heart failure.
3. Gastrointestinal system: Nausea, constipation, weight loss, anorexia, flatulence.
4. Renal system: Mild proteinuria.
5. Ocular: Retinal haemorrhages if there is associated vascular disease.
6. Reproductive system: Menstrual disturbances such as menorrhoea and menorrhagia, loss of libido.
7. General: Pallor (of mucous membranes, conjunctiva, skin), tiredness, weakness, easy fatiguability, leth¬argy, headache).

Disorders Of Red Blood Cells  Short Question And Answers

Question 1. ESR
Answer: If a sample of blood with an anticoagulant is allowed to stand in a vertical tube, the RBC settles down due to gravity as compared to plasma with a clear supernatant layer of plasma. The rate at which the cells settle down is called ESR.

Method of Estimation of ESR:

• There are two standard methods as follows:

1. Wintrobe’s and Landsberg’s method: ESR is meas-ured in undiluted blood in a haematocrit tube.
2. Westergren’s method: ESR is measured in venous blood diluted accurately with 31.3 g/L trisodium cit¬rate in the proportion of 1:4 (1 volume of 3.8% so¬dium citrate and 4 volume of blood).

• The conditions were ESR is markedly raised are as follows:

1. Infective: Tuberculosis, kala-azar, in most of chronic infections.
2. Inflammation: Rheumatoid arthritis, rheumatic fever, other connective tissue disorders.
3. Neoplastic: Multiple myeloma, lymphoma, parapro- anaemia.
4. Miscellaneous: Aplastic anaemia, autoimmune disorders, mixed connective tissue disorders.

Question 2. Thalassemia
Answer:

• Thalasemia are hereditary disorder characterized by quantitative abnormalities of globin chain synthesis, i.e., reduce production of globin chains.
• Reduction in alpha chain synthesis leads to alpha thalassemia and that of the beta chain leads to beta thalassemia.
• Beta thalassemia major (Cooley’s anaemia) is a severe disease and manifests in childhood. This condition is transfusion dependent and generally fatal by 30 years of age.
• Beta thalassemia minor is a mild disease, nontransfusion dependent and patients can live full normal lives.

Thalassemia Clinical features:

• The important clinical manifestations are anaemia, re-current mild jaundice and hepatosplenomegaly.
• The family history may be positive.
• Expansion of bones.
• Iron overload due to repeated blood transfusion.

Thalassemia Laboratory findings:

Tests such as

• Haemoglobin electrophoresis,
• Decreased osmotic fragility,
• Amniocentesis and chorionic villi biopsy are performed for prenatal diagnosis in inherited conditions like thalassemia.

Thalassemia Treatment:

• Supportive treatment in the form of packed cell transfusion may be needed. However, repeated transfusion may lead to iron overload which in turn may require treatment with chelating agents, deferoxamine. Folic acid, 5 mg daily is given to meet the increased demand.
• Bone marrow transplantation is curative in thalassemia.

Question 4. Aplastic anaemia
Answer:

Aplastic anaemia is characterized by

• Anaemia
• Leukopenia
• Thrombocytopenia
• Hypocellular bone marrow

Aplastic anaemia  Etiology:

• Idiopathic
• Secondary to drugs, viruses, pregnancy
• Hereditary

Aplastic anaemia  Clinical Features:

• Anaemia
• Excessive tendency to bleed
• Easy bruising
• Epistaxis
• Gum bleeding
• Heavy menstrual flow
• Petechiae
• Predisposition to infections

Aplastic anaemia  Investigations:

• Blood smear- shows normocytic, microcytic anaemia, decreased granulocytes and platelet count
• Chromosomal studies for inherited disorders

Aplastic anaemia  Treatment:

• Bone marrow transplantation
• Immunosuppressive therapy
• Packed red cell transfusions
• Granulocytes transfusions

Question 5. Pernicious anaemia
Answer:

• Also known as Addisonian megaloblastic anaemia.
• Pathogenesis – an autoimmune reaction against gastric parietal cells that causes atrophy of gastric mucosa.
• About 2 – 3% of cases of pernicious anaemia develop carcinoma of the stomach.

Pernicious anaemia Lab Diagnosis:

• Hyper gastrinemia,
• Biochemical tests reveal serum bilirubin,
• LDH, Hb, ferritin and iron.
• Hematologic findings in blood and bone marrow are the same as those of megaloblastic anaemia.

Pernicious anaemia Treatment:

• Parenteral Vit. B12 replacement therapy
• Symptomatic and supportive therapy such as physiotherapy for neurologic deficits and occasionally blood transfusion.

Question 6. PCV
Answer: Packed cell volume is defined as the ratio of the volume of RBCs to that of whole blood and is expressed as a percentage Also called as haematocrit.

Methods of estimation of PCV:

1. Macro (Wintrobe’s) method: Blood is centrifuged for half an hour at 3000 rpm.
2. Micro haematocrit method: Using a capillary tube, blood is centrifuged at 12,5000 rpm.
3. Electronic method: Employ automated counters, where the derivation of RBC count, PCV, and MCV are closely interrelated.

Three layers are observed after centrifugation.

1. Plasma layer: Top most, clay yellow/straw coloured.
2. Buffy coat: Middle layer of WBC and platelets about 1 mm thick.
3. Column of RBC: Bottom layer.

• Increased buffy coat: Severe degree of leucocyte- sis/leukaemia.
• Colour of plasma layer:
  • Red colour – Haemolysis,
  • Yellow colour – jaundice.
• Diseases causing raised PCV:
  • Polycythaemia,
  • Burns,
  • Shock
  • Dehydration due to severe vomiting, diarrhoea,
  • Profuse sweating.
• Diseases causing low PCV:
  • Anaemia,
  • Pregnancy.

Question 7. Sickle cell anaemia
Answer:

• Sickle cell haemoglobin is produced due to substitution of valine for glutamine at the 6th position of a beta-globin chain of normal adult haemoglobin. (HbA).
• In heterozygous form – 40% of Hb is HbS,
• In homozygous – 100% of Hb is HbS (Individual suffers from sickle cell anaemia).

Sickle cell anaemia Clinical features:

• Severe haemolytic anaemia.
• Impaired growth and development, increased susceptibility to infectious.
• The distorted shape of sickle cells blocks blood circulation and causes repeated vaso-occlusive episodes.
• Oral findings – generalised osteoporosis, loss of tribe- collation of jawbones.
• Radiographic findings – hair on end appearance OR skull, tower-shaped skull, generalised osteoporosis, enlarged medullary cavities.

Sickle cell anaemia Lab findings:

• Anaemia, a positive sickling test,
• Sickle cells and target cells are seen on blood film.

Question 8. Megaloblastic anaemia
Answer:

• Megaloblastic anaemias are disorders caused by impaired DNA synthesis and are characterised by a distinc¬tive abnormally in the haematopoietic precursors in the bone marrow in which the maturation of the nucleus is delayed relative to that of the cytoplasm.
• Defective DNA synthesis due to deficiency of Vit Biz/folic acid (folate)

Megaloblastic anaemia Treatment: Hydroxycobalamin IM injection 1000 micro¬gram for 3 weeks, oral folic acid tablets daily for 4 months.

Question 9. Hereditary spherocytosis
Answer:

• Hereditary spherocytosis is a common type of hereditary haemolytic anaemia in which red cell membrane is abnormal.
• It is inherited as an autosomal dominant disorder.
• Pathogenesis: Deficiency in the structural protein of the red cell membrane spectrin.
• Clinical features: Anaemia, jaundice, splenomegaly and pigmented gall stones.
• Laboratory findings.
  • Anaemia and reticulocytosis
  • Rlnnd film shows mirrosnherorvtps.
  • Osmotic fragility
  • Negative direct Coomb’s test
  • Spontaneous auto haemolysis.

Question 10. Lab diagnosis of anaemia
Answer: Laboratory diagnosis of anaemia includes

• Peripheral blood smear
  • It shows
    • Variations in size of RBCs- microcytic or macrocytic
    • Variations in the shape of RBCs- poikilocytosis
    • Spherocytosis- spindle-shaped RBCs
    • Nucleated RBCs
    • Inadequate haemoglobin formation
    • Presence of Howell-Jolly bodies
    • Irregularly contracted red cells

Haemoglobin content: Haemoglobin content decreases in anaemia

• Red cell indices are used like MCV, MCH, MCHC
• ESR estimation
• Bone marrow aspiration
• Leucocyte and platelet count
• Reticulocyte count

Question 11. Hemosiderin
Answer: Hemosiderin is formed by aggregates of ferritin

Hemosiderin Microscopic Appearance:

• Appears as golden yellow to brown granular pigment
• Seen within the mononuclear phagocytes of the bone marrow, spleen and liver

Hemosiderin Pathological Conditions:

• Excessive hemosiderin occurs in
  • In the presence of excessive breakdown of red cells
  • During systemic overload of iron
  • Thalassaemia
  • Sideroblastic anaemia
  • Alcoholic cirrhosis
  • Multiple blood transfusions

Hemosiderin Effects:

• Black eye
• Brown induration in lungs
• Parenchymatous deposition of hemosiderin
• Reticuloendothelial deposition

Question 12. Pancytopenia.
Answer: It is the simultaneous presence of anaemia, leucopenia and thrombocytopenia.

Pancytopenia Causes:

• Aplastic anaemia,
• Paroxysmal nocturnal haemoglobinuria
• Megaloblastic anaemia.
• Bone marrow infiltrations.

Question 13. Beta thalassemia major.
Answer: It is stated with either a complete absence of beta chain synthesis or only a small amount of beta chains are formed

Beta thalassemia major Clinical Features:

• Cooley’s anaemia
• Bony expansion
• Hepatosplenomegaly
• Retarded growth
• Delayed puberty
• Diabetes Mellitus
• Damage to the liver and heart

Pancytopenia Treatment:

• Repeated blood transfusion
• Use of folic acid supplements
• Chelation therapy
• Bone marrow transplantation

Common Specific Tumours Important Notes

1. Basal cell carcinoma

• It is locally invasive
• It rarely metastasize
• It is a slow growing tumour of middle age
• It occurs exclusively on hairy skin
• Common site: above the line of the tragus of the ear to the corner of the mouth

2. Squamous cell carcinoma

• It may arise from any parts of the skin and mucous membrane lined by squamous epithelium
• Predisposing factors are
  • Solar keratosis
  • Chronic ulcers
  • Draining sinus
  • Osteomyelitis
  • Chewing betel nuts
  • Tobacco
  • Radiation

3. Teratoma: They are complex tumours composed of tissues derived from more than one of the three germ layers – endoderm, mesoderm and ectoderm

4. Hamartoma: It is a mass of disorganised but mature cells indigenous to the particular site

5. Various tumours:

Common Specific Tumours Short Essays

Question 1. Teratoma
Answer:

• Teratomas are complex tumours composed of tissues derived from more than one of the three germ cell layers
• They are commonly seen in the gonads of males and females

Teratoma Types:

• They are classified into three types
  • Mature teratoma
  • Immature teratoma
  • Teratoma with malignant proliferation

Teratoma Morphology:

• Gross appearance
  • They appear as large, grey-white masses
  • It enlarges the involved testis
• Cut surface:
  • Shows grey-white solid areas, cystic and honey-combed areas
  • Foci of cartilage and bone are also seen
• Microscopic features:

Question 2. Basal cell carcinoma
Answer:

• Also called as rodent ulcer. Most common tumour.
• If is a locally invasive, slow-growing tumour of middle-aged individuals which rarely metastasizes.

Basal cell carcinoma Etiology:

• Prolonged exposure to strong sunlight
• UV rays
• Arsenic is used in skin ointments.
• Dysregulation of the PTCH pathway
• Inherited effects of PTCH gene causing BCC, gorlin syndrome.

Basal cell carcinoma Clinical features:

• The majority of lesions occur on the face, usually abore a line joining lobe of the ear and the angle of the mouth.
• Common sites are the inner and outer canthus of the eye, the eyelids bridge of the nose and around nasolabial fold.
• Most common pattern is a nodule-ulcerative lesion a slow-growing small nodule that undergoes central with pearly, rolled margins.
• Tumour enlarges in size by burrowing and by destroying the tissues locally like a rodent and hence the name”rodent ulcer.

Basal cell carcinoma Microscopic examination: A most common pattern is solid basal cell carcinoma in which the dermis contains irregular masses of basaloid cells having the characteristic peripheral palisaded appearance of the nuclei.

Basal cell carcinoma Treatment:

• Tumours are usually treated with complete local excision.
• BCC responds well to radiation. Radiation is indicated in elderly patients with extensive lesions, does – 4000 – 6000 gy units.

Question 3. Microscopic picture of osteosarcoma
Answer:

• Microscopic examination of osteosarcoma shows following features
  • Sarcoma cells
    • The tumour cells are anaplastic mesenchymal stromal cells
    • They show marked pleomorphism and polymorphism
    • Cells may be spindles, round, oval, polygonal or bizarre tumour giant cells
    • They show hyperchromatism and atypical mitosis
  • Osteogenesis
    • The anaplastic sarcoma cells form an osteoid matrix and bone directly
    • It lies interspersed between the areas of tumour cells

Question 4. Microscopic picture of Osteoclastoma
Answer:

• Microscopic examination of osteoclastoma shows
  • A large number of osteoclast-like giant cells which are regularly scattered throughout the stroma
  • Giant cells may contain as many as 100 benign nuclei and are similar to normal osteoclast
  • Stromal cells are mononuclear cells and are the tumour cells
  • They are uniform, plump, spindle-shaped or round to oval in shape
  • They may have varying degrees of atypia and mitosis

Question 5. Fibroma
Answer: Fibroma are uncommon tumours of soft tissues

Fibroma Types:

Based on microscopic appearance, fibroma are of three types

Common Specific Tumours Short Question And Answers

Question 1. Malignant melanoma
Answer: Malignant melanoma is a tumour arising from pigment-forming cells i.e., melanoblast which are desired from the neural crest.

Malignant Melanoma Etiology: Unknown but there is the role of excessive exposure of white skin sunlight.

Common site:

• Oral and anagenital mucosa,
• Oesophagus,
• Conjuctiva,
• Orbit,
• Leptomeninges.

Read And Learn More: Pathology Question And Answers

Malignant melanoma Clinical features:

• Flat/slightly elevated nerves which has variegated pigmentation, and irregular borders and have undergone secondary changes of ulceration, bleeding and increase in size.
• Depending upon the clinical course and prognosis, cutaneous malignant melanomas are of 4 types.
  • Lentigo maligna melanoma
  • Superficial spreading melanoma
  • Acral lentiginous melanoma
  • Nodular melanoma.
• Malignant melanoma Spread: Metastatic spread in very common via lymphatics.
• Malignant melanoma Treatment: Surgery – main modality.
  Palliative and supportive – other modalities.

Question 2. Carcinoma in situ
Answer: When the cytological features of malignancy are present but the malignant cells are confined to epithelium without invasion across the basement membrane, it is called as carcinoma in situ/intra epithelial neoplasia.

Common sites:

• • Uterine cervix at the junction of ecto and endocervix
  • Banen’s disease of the skin.
  • Actinic/solar keratosis.
  • Oral leukoplakia
  • Interlobular and intraductal carcinoma of the breast.
• The area involved may be single and small/multifocal.
• It may return to normal/may develop into invasive cancer.
• In cervical cancer, there is sequential transformation from squamous metaplasia, to epithelial dysplasia, to carcinoma in situ and eventually in invasive cancer.

Question 3. Premalignant lesions
Answer:

Premalignant lesions Definition: Pre-malignant lesions is defined as morphologically altered tissue in which cancer is more likely to occur than its apparently normal counterparts

Premalignant lesions Examples:

• Leukoplakia
• Erythroplakia
• Mucosal changes associated with smoking habits
• Carcinoma in situ
• Bowen’s disease
• Actinic keratosis

Question 4. Sequestrum
Answer:

• Sequestrum is a fragment of dead tissue, usually bone, that has separated from healthy tissue as a result of injury or disease
• It is avascular

Sequestrum Types:

• Primary sequestrum
  • A piece of dead bone that completely separates from sound bone during the process of necrosis
• Secondary sequestrum
  • A piece of dead bone that is partially separated from sound bone during the process of necrosis but may be pushed back into position

Question 5. Osteoporosis
Answer: Osteoporosis is a common clinical syndrome involving multiple bones in which there is quantitative reduction of bone tissue mass

Osteoporosis Features:

• Common in elder people
• Increased risk of fractures occurs
• Causes pain and deformity

Osteoporosis Types:

• Primary osteoporosis
  • Occurs without any underlying disease or medication
  • Occurs due to the following factors
    • Genetic factors
    • Reduced physical activity
    • Deficiency of sex hormones
    • Combined deficiency of calcitonin and estrogen
• Secondary osteoporosis
  • Occurs due to underlying diseases like
    • Chronic anaemia
    • Acromegaly
    • Hepatic disease
    • Hyperparathyroidism

Question 6. Osteomyelitis
Answer:

Osteomyelitis Definition: An infection of bone that results in inflammation of bone involving the periosteum and haversian system is called osteomyelitis

Osteomyelitis Etiology:

• Odontogenic infections
• Traumatic injury
• Periostitis
• Hematogenous spread

Predisposing Factors:

• Conditions reducing host defences
  • Diabetes
  • Malnutrition
  • Leukaemia
  • Alcoholism
• Conditions compromising vascularity
  • Radiation
  • Paget’s disease
  • Fibrous disease
  • Malignancy

Question 7. Pyogenic Osteomyelitis
Answer:

• Pyogenic osteomyelitis is usually caused by bacterial infections
• It occurs most commonly in the long bones of infants and young children

Pyogenic Osteomyelitis Etiological Agents:

• Staphylococcus aureus
• E. coli
• Pseudomonas
• Klebsiella
• Anaerobes

Pyogenic Osteomyelitis Features:

• Painful and tender limb
• Fever
• Malaise
• Leucocytosis
• Draining sinus tract

Pyogenic Osteomyelitis Complications:

• Septicaemia
• Acute bacterial arthritis
• Pathologic fractures
• Development of squamous cell carcinoma
• Secondary amyloidosis
• Vertebral osteomyelitis

Question 8. Ewing’s sarcoma.
Answer: It is a malignant small round cell tumour

Ewing’s sarcoma Variants:

• Classic Ewing’s sarcoma
• Soft tissue Ewing’s sarcoma
• Primitive neuroectodermal tumour

Ewing’s Sarcoma Clinical Features:

• Age – Between 5-20 years
• Sex – Common in females
• Site-
• Shafts and metaphysis of long bones
• Flat bones such as the pelvis and scapula
• Presentation
  • Pain, swelling, and tenderness of the affected area
  • Fever
  • Leucocytosis
  • Elevated ESR

Neoplasia Important Notes

1. Exfoliative cytology or Pap smear

• It involves the study of cells that spontaneously shed off from epithelial surfaces into body cavities or body fluids
• It is based on the principle that malignant cells are incohesive and loose
• Thus they shed off into the lumen
• The cells are obtained by scraping, brushing or washing mucosal surfaces

2. Metastasis

• It is used to distinguish benign and malignant tumours
• Malignant tumours can metastasize
• Carcinomas metastasize through lymphatics while sarcomas through blood vessels

3. Oncogenic viruses

• These are viruses which induce carcinogenesis
• They may contain either DNA or RNA

Examples:

Neoplasia Long Essays

Question 1. Define neoplasia. Give the difference between benign and malignant tumours. Add a note on the paraneoplastic syndrome.
Answer:

Neoplasia Definition:

Neoplasia is defined as a mass of tissue formed as a result of the abnormal, excessive, uncoordinated, autonomous and purposeless proliferation of cells even after cessation of stimulus for growth which causes it.

Differences between benign and malignant tumours:

Paraneoplastic Syndrome:

Para neoplastic syndromes are a group of conditions developing in patients with advanced cancer which are neither explained by direct and distant spread of the turn-over nor by the usual hormone elaboration by the tissue of origin of the tumour.

• They occur in 10% -15% of patients with cancer.
• Various clinical syndromes included in INS are.
  • Endocrine syndrome.
    • Hypercalcemia
    • Cushing’s syndrome
    • Polycythemia
    • Flypoglycacmia.

Read And Learn More: Pathology Question And Answers

• • Neuromyopathic syndromes
  • Haematologic and vascular syndrome
  • Gastrointestinal syndrome
  • Renal syndrome
  • Cutaneous syndromes
  • Amyloidosis.

Question 2. Define neoplasia. Classify tumours. Discuss the mode of spread of malignant tumours.
Answer:

Classification of Tumours:

Spread of Tumours: It is by 2 ways.

1. Local invasion/direct spread:

• Benign tumours:
  • Form encapsulated/circumscribed masses
  • These that expand and push aside the surrounding normal tissues without actually invading, in- filtrating/metastasising.
• Malignant tumours: They also enlarge by expansion.
  • These tumours invade via the route of least resistance
  • Often cancers extend through tissue spaces, via lymphatics, blood vessels, and perineural spaces and may penetrate bone.
  • More commonly, tumours invade thin-walled capillaries and veins than thick-walled arteries.

2. Metastasis/Distant spread:

• Metastasis is defined as the spread of tumours by inva¬sion in such a way that discontinuous secondary tumour mass/masses are formed at the site of lodgement.
• Benign tumours do not metastasise while all malignant tumours with a few exceptions like gliomas of the CNS and basal cell carcinoma of skin can me¬tastasis.

Routes of Metasis:

1. Lymphatic spread: In general, carcinomas metastasize by lymphatic route

Involvement of lymph nodes by malignant cells may be of two forms.

2. Haemategenous spread:

• Sarcomas spread through hematogenous spread
• The common site for blood-borne metastasis are
  • Lung,
  • Breast,
  • Thyroid,
  • kidney,
  • Liberate and
  • Ovary.
• Spread:

Various other routes:

Question 3. Define tumour. Write briefly about carcino¬gens. Describe gross and microscopic features of squamous cell carcinoma.
Answer:

• Tumour: Tumour is defined as a mass of tissue formed as a result of abnormal, excessive, uncoordinated, autonomous and purposeless proliferation of cells
• Carcinogens: The agents which can induce tumours are called carcinogens

Types of Carcinogens:

Squamous Cell Carcinoma Features:

• Age: common in older individuals
• Sites involved
  • Lower lip
  • Lateral tongue
  • The floor of the mouth
  • Soft palate
  • Gingiva
  • Alveolar ridge
  • Buccal mucosa
• Presentation
  • Initially asymptomatic lesion
  • Resembles leukoplakia
  • Appears as a white or red nodule or fissure over the mucosa
  • The advanced lesion appears as rapidly enlarging exo-phytic growth or ulcer or tumour-like mass
  • The ulcer has persistent induration around the periph¬ery with elevated and everted margins
  • May predispose candidal infections
  • May be a secondary infected

Squamous Cell Carcinoma Morphology:

Gross appearance:

• It appears as nodular or lucrative growth
• Shows fungating and polypoid mass without ulceration
• Margin- elevated and indurated

Cut section

It shows grey-white endophytic as well as exophytic tumours

Microscopic appearance

• It is characterised by malignant cells
• These cells show variable degrees of differentiation
• Cells invade through the basement membrane into the dermis

Arrangement

• Cells are arranged in concentric layers called epithelial pearls
• They contain keratin material in the centre of the cell masses
• Cells are separated by lymphocytes

Question 4. Discuss about injury caused by ionizing radiation.
Answer:

• Ionizing radiation like X-rays, alpha, beta and gamma rays can cause cancer
• Cancer caused by them are
  • Cancer of
    • Thyroid
    • Skin
    • Breast
    • Ovary
    • Uterus
    • Lung
    • Myeloma
    • Salivary glands
    • Leukaemia

Ionizing radiation Mechanism:

• It causes DNA damage by one of the following mechanism
  • Direct damage to cellular DNA
  • Dislodges ions from water and other molecules of the cell and result in the formation of highly reactive free radicals that causes damage

Effects of Radiation:

• Chromosomal breakage
• Translocation
• Point mutation

Factors effecting it

• Type of radiation
• Dose
• Dose rate
• Frequency
• Host factors
  • Age
  • Individual susceptibility
  • Immune competence
  • Hormonal influences
  • Type of cells irradiated

Question 5. Define carcinogenesis. Discuss in detail the chemical carcinogenesis.
Answer:

Definition

• Carcinogenesis means the mechanism of induction of tumours
• Agents that induce tumours are called carcinogens

Chemical carcinogenesis:

• Chemical carcinogens have highly reactive electrophile groups that directly damage DNA leading to mutations and eventually cancer.
• Depending upon the mode of action, they are classified as:
  1. Initiator carcinogens.
  2. Promoter carcinogens

1. Initiator carcinogens: They can initiate the process of neoplastic transformation.

• Direct-acting carcinogens: They do not require metabolic activation.
  • Alkylating agents: Anticancer drugs (Cyclophosphamide, busulfan, melphalan, nitrosourea),
  • β-propionolactone and episodes.
• Indirect-acting agents (Procarcinogens): They require metabolic activation.
  • Polycyclic and heterocyclic aromatic hydrocarbons: Benzathracenes, benzopyrene.
  • Aromaticamaines, amides and azo dyesmaphthylamine ([3-naphthylamine), Ben-zidine and azo dyes like 2 – acctylaminofluorene, dimethyl amino azo benzene (butter yellow)
  • Naturally occurring products: Chemical derived from plants and microbial sources i.e., aflatoxin Bl,
  • Others: Nitrosamines/Nitrosamides in gastric carcinoma, insecticides, fungicides etc.

2. Promoter carcinogens:

• It promotes further clonal proliferation and expression of initiated cells
• Examples Phorbol esters, phenols, hormones like estrogen

Question 6. Define neoplasia. Classify oncogenic viruses and explain the role of viruses in carcinogenesis.
Answer:

Neoplasia Definition:

Neoplasia is defined as a mass of tissue formed as a result of abnormal, excessive, uncoordinated, autono¬mous and purposeless proliferation of cells even after cessation of stimulus for growth which causes it

Oncogenic Viruses:

• They are associated with neoplasms
• Based on nucleic acid content, oncogenic viruses are divided into 2 groups:

1. DNA viruses
2. RNA viruses

Role Of Virus In Carcinogenesis:

Neoplasia Short Essays

Question 1. Characteristics of malignancy
Answer:

1. Rate of growth:

• Malignant tumour cells have increased mitotic rates and slower death rates i.e., cancer cells do not follow normal control in the cell cycle and are immortal.
• Also, the rate of growth is directly proportional to the degree of differentiation.

2. Clinical and gross features:

• Clinically, malignant tumours grow rapidly, ulcerate on the surface, invade locally into deep tissues, may spread to distant sites, produce weight loss, anorexia and anaemia.
• Grossly, irregular in shape, poorly circumscribed and extending into adjacent tissues secondary changes like haemorrhage, infarction and ulceration are seen more often.

3. Microscopic features:

• Malignant tumours have a poor resemblance to origin.
• Basal polarity is lost
• Pleomorphism is present hyperchromatism and abnormal mitotic figures are seen.
• The nucleocytoplasmic ratio is increased anisonucleo- sis is generally present
• Tumour giant cells are present with nuclear atypia.
• The function may be retained/lost/abnormal.

4. Local invasion:

• Tumours invade via routes of least resistance eventually most cancers recognize no anatomic boundaries.
• Cancers extend through tissue space, permeate lymphatics, blood vessels, and perineural spaces and may penetrate the bone by going through nutrient foramina.

5. Metastasis/Distance spread:

• Lymphatic spread – In general carcinomas metastasize by the lymphatic route.
• Hematogenous spread – Common route for sarcomas.
• Spread along body cavities and natural passages – Routes are trans coelom, epithelial lined surfaces, CSF, and implantation.

Question 3. Staging of tumours
Answer:

• Staging of cancer is determined by surgical exploration or imaging and is based on the size, local and regional lymph node spread and distant metastasis.
• Staging is a system to determine the prognosis and choice of treatment of malignant cancer.
• Important systems of staging which currently in use are as follows:
  • TNM system (T-primary tumour, N-regional lymph node involvement, M-metastases]
  • ATC (American Joint Committee) System.
• Both systems take into account the following criteria;
  • Size of the primary tumour
  • Nodal involvement
  • Metastasis

TNM Staging: For each of the 3 components T, N and M, numbers are added to indicate the extent of involvement as under:

• T₀ to T₄: In sites to the largest and most expensive primary tumour
• N₀ to N₃: NO nodal involvement to widespread lymph node involvement.
• M₀ to M₂: NO metastasis to disseminated haematoge- nous metastasis.

AJC system: Cancers are divided into stages 0 to 4 and take into account all the 3 components i.e., size, nodal spread and distant metastasis.

Neoplasia Short Question And Answers

Question 1. Oncogenes
Answer:

• Mutant versions of proto-oncogenes that function autonomously without a requirement for normal growth-promoting signals are known as oncogenes.
• A normal gene/proto-oncogene is converted / acti¬vated to an oncogene by.
  • Change in the structure of the gene
  • Change in regulations of gene expression.
• Oncogenes are activated by.
  • Point mutation and deletion
  • Chromosomal translocation
  • Gene amplification.

Question 2. Oncogenic viruses
(or)
Virus-related human tumours and examples.
Answer:

• Oncogenic viruses are associated with neoplasms.
• Based on nucleic acid content, oncogenic viruses are divided into 2 groups.
  • DNA viruses
  • KNA viruses.

DNA oncogenic viruses: DNA oncogenic viruses have direct access to the host cell nucleus and are incorporated to the genome of the host cell DNA.

Classified into 5 groups.

1. Pap ova virus: Responsible for skin warts (squamous cell papillomae and invasive cervical cancer.
2. Herpes virus: Epstein- ban virus (EBV] Burkitt’s lymphoma and human herpes virus 8 kaposi’s sar¬coma.
3. Adenovirus: Causes respiratory tract infections and pharyngitis
4. Poxvines: They cause moluscum contagiosum
5. Hepadna virus: Hepatitis B virus.

Question 3. Lab diagnosis of cancer
Answer:

Question 4. Burkitt’s lymphoma
Answer:

• It is a distinctive type of B-cell lymphoma caused by Epstein-Barr virus [EBV] infection.
• 3 sub-groups of Burkitt’s lymphoma are:

1. African endemic
2. Sporadic
3. Immunodeficiency associated.

Burkitt’s lymphoma Etiology – EBV infection and immune suppression.

Burkitt’s Lymphoma Features:

• The disease affects children and adolescents
• Involves extranodal sites, particularly the jaw, gas- tro intestinal tract and gonads.

Histological appearances: Tightly packed lymphoblasts interspersed with phagocytic macrophages which impart a starry-sky appearance in histological sections.

Question 5. Etiology of oral cancer
Answer:

Question 6. Ionizing radiation
Answer: Ionizing radiation like X-rays, alpha, beta and gamma rays can cause cancer

Ionizing radiation Mechanism:

• It causes DNA damage by one of the following mechanism
  • Direct damage to cellular DNA
  • Dislodges ions from water and other molecules of the cell and result in the formation of highly reactive free radicals that causes damage

Effects of Radiation:

• Chromosomal breakage
• Translocation
• Point mutation

Question 7. Tumour markers
Answer:

• Tumour markers are biochemical assays of products elaborated by the tumour cells in blood/other body flu¬ids.
• These methods clack sensitivity as well as specificity and can be used.
  • As an adjacent to pathologic diagnosis arrived at by other methods and not for primary diagnosis of can¬cer.
  • Can be used as prognostic and therapeutic purposes
• Tumour markers include:
  • Oncofetal antigens
    • Alpha foetoprotein
    • Carcinoembryonic antigen.
  • Enzymes
    • Prostrate acid phosphatase
    • Lactic dehydrogenase
  • Hormones
    • Human chronic gonadotropin
    • Calcitonin
    • Ectopic hormone production
    • Cancer-associated proteins.