Pathology

Cellular Adaptations Important Notes

1. Terms

Cellular Adaptations Long Essays

Question 1. Hypertrophy
Answer:

Hypertrophy Definition: Hypertrophy is an increase in the size of parenchymal cells resulting in enlargement of the organ/tissue, without any change in the number of cells.

Hypertrophy Etiology:

Hypertrophy is caused by increased functional demand or by hormonal stimulation.

Hypertrophy Etiological types:

It may be classified into:

• Physiologic hypertrophy: Enlarge the size of the uterus in pregnancy.
• Pathologic hypertrophy: Hypertrophy of cardiac muscle: In cardiovascular disease.
  • Systemic hypertension
  • Aortic valve disease
  • Mitral insufficiency.
• Hypertrophy of smooth muscle:
  • Cardiac achalasia (in the esophagus)
  • Pyloric stenosis (in the stomach)
  • Muscular arteries in hypertension.
• Hypertrophy of skeletal muscle:
  • A hypertrophied muscle in athletes and manual laborers
• Compensatory hypertrophy: This may occur in an organ when the contralateral organ is removed.
  • After nephrectomy on one side in young patients there is compensatory hypertrophy of the kidney as well as nephrons on the other side.

Morphologic features:

• The affected organ is enlarged and heavy.
• There is an enlargement of muscle fibers as well as of nuclei

Question 2. Metaplasia
Answer:

Metaplasia Definition:

Metaplasia is defined as a reversible change of one type of epithelial or mesenchymal adult cells to another type of adult epithelial or mesenchymal cells, usually in response to abnormal stimuli.

Metaplasia Types:

Metaplasia is divided into the following two types.

1. Epithelial
2. Mesenchymal.

1. Epithelial Metaplasia:

• Squamous metaplasia There is a transformation of various types of epithelium into squamous epithelium due to chronic irritation
• For example:
  • In bronchus in chronic smokers.
  • In uterine endocervix in prolapse of the ureters and in old age.
  • In renal pelvis and urinary bladder in chronic infections.
• Columnar metaplasia: There is the transformation of various epithelia into columnar epithelium.
• For example:
  • Intestinal metaplasia in healed chronic gastric ulcer.
  • In Barrett’s esophagus, normal squamous epithelium changes to columnar.

2. Mesenchyme metaplasia: There is the transformation of an adult type of mesenchymal tissue to another.

• Osseous metaplasia: Osseous metaplasia is the formation of bone in fibrous tissue, cartilage, and myxoid tissue.
• For example:
  • In the arterial wall in old age (Monchkeberg’s medial calcific sclerosis]
  • In soft tissues in myositis ossifications.
  • In cartilage of larynx and bronchi in elderly people.
  • In fibrous stoma of the tumor.
• Cartilaginous metaplasia: In the healing of fractures, cartilaginous metaplasia may occur where there is undue mobility.

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Question 3. Hyperplasia
Answer:

Hyperplasia Definition:

• Hyperplasia is an increase in the number of parenchymal cells resulting in enlargement of the organ/tissue.
  • Hyperplasia occurs due to the increased recruitment of cells from the resting phase of the cell cycle to undergo mitosis when stimulated.
  • Hyperplasia persists as long as the stimulus in present.

Hyperplasia Etiology:

Hyperplasia may occur due to physiologic and path-logic causes.

1. Physiologic hyperplasia: The two most common types are.

2. Pathologic hyperplasia: Due to excessive stimulation of hormones or growth factors.

Cellular Adaptations Short Question And Answers

Question 1. Atrophy
Answer:

Atrophy Definition:

Atrophy may be defined as the decrease in the number and size of parenchymal cells of an organ or its parts which was once normal.

Atrophy Causes:

Question 2. Anaplasia
Answer:

Anaplasia Definition:

• Anaplasia is a lack of differentiation and is a characteristic feature of most malignant tumors.
• Depending upon the degree of differentiation, the extent of anaplasia is also variable i.e., poorly differentiated malignant tumors have a high degree of anaplasia.

Result of Anaplasia:

• Loss of polarity
• Pleomorphism
• N: C ratio changes from 1:5 to 1:1
• Anisonucleosis.
• Hyperchromatism.
• Prominent nucleolus
• Tumor giant cells
• Chromosomal abnormalities.

Hemodynamic Derangements Due To Obstructive Nature Important Notes

1. Virchow’s triad includes 

• Endothelial injury
• Alteration in blood flow
• Hypercoagulability of blood

2. Arterial thrombi

• They are white, firm, mural
• It produces ischemia

3. Venous thrombi

• They are red, soft occlusive
• Causes embolism
• It may arise from thrombi in veins of the lower legs, pelvic veins, veins of upper limbs, cavernous sinus of the brain and right side of the heart
• It leads to obstruction of pulmonary arterial circulation leading to pulmonary embolism

4. Infarcts

Hemodynamic Derangements Due To Obstructive Nature Long Essays

Question 1. Define thrombosis. Discuss etiopathogenesis of thrombus.
Answer:

Thrombosis:

• Thrombosis is a process of the formation of solid mass in circulation from the constituents of flowing blood.
• The mass itself is called a thrombus.

Thrombus Etiopathogenesis:

There are primary events that pre-dispose to thrombus formation. It is called as vir- chow’straid.

1. Endothelial injury:

The integrity of the blood vessel wall is important for maintaining normal blood flow.

• Vascular injury exposes the subendothelial connective tissue (For example. Collagen, elastin, fibronectin, calamine, and glycosaminoglycans) which are thrombogenic and thus play an important role in initiating hemostasis as well as thrombosis.
• Conditions and factors which cause endothelial injury and predispose to thrombogenesis are as follows:
  • Endocardial injury in myocardial infarction, myocarditis, cardiac surgery, prosthetic valves.
  • Ulcerated plaques in advanced atherosclerosis.
  • Haemodynamic stress in hypertension.
  • Arterial diseases
  • Diabetes mellitus
  • Endogenous chemical agents such as endotoxins, hypercholesterolemia
  • Exogenous chemical agents such as cigarette smoke.
• Following endothelial cell injury, platelets come to play a central role sequence of events are:
  • Platelet Adhesion: Platelets in circulation recognize the site of endothelial injury and adhere to exposed sub endothelial collagen (Primary aggre¬gation).
  • Platelet release reaction: Activated platelets then undergo a release reaction by which platelet gran¬ules are released to the exterior.
  • Platelet aggregation: Two main types of platelet granules are.
    • Alpha granules containing fibrinogen, fibronectin, platelet factor 4, and cationic pro¬teins.
    • Dense bodies – ADP (Adenosine diphosphate), 5 – HT (serotonin), histamine, epinephrine, ionic calcium.

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Following the release of ADP, potent platelet aggregating agent, aggregation of additional platelets takes place (secondary aggregation).

• This results in the formation of a temporary hemostatic plug.
• The stable hemostatic plug is formed by fibrin, thrombin, and thromboxane A2.
• The coagulation system is involved in both the hemostatic process and thrombus formation.
• The coagulation mechanism is the conversion of the plasma fibrinogen into a solid mass of fibrin.
• Pathways of the coagulation system and fibrinolytic system.

2. Alteration of blood flow:

• Normally, there is the axial flow of blood in which a rapidly moving central stream – consists of leu¬cocytes and red cells. Slow-moving laminar stream – adjacent to central stream – consists of platelets peripheral stream – consists of most slow-moving cell-free plasma.
• In thrombosis, turbulence and stasis occur. Where normal flow is disturbed when blood slow down, blood cells including platelets mar- migrate to the periphery and kind of pavement closed to the endothelium. (Margination and pave- meeting).
• Stasis allows a higher release of oxygen from the blood and initiates venous thrombi even without evidence of endothelial injury.
• Turbulence injures the endothelium resulting in the deposition of platelets and fibrin – facilitating the formation of arterial and cardiac thrombi.

3. Hypercoagulability of blood:

• Hypercoagulability of blood is loosely defined as any alteration of coagulation pathways that pre¬disposes to thrombosis.
• It is brought about by following changes in the blood composition.
• Increase in coagulation factors like fibrinogen, prothrombin, factor 7 a, 7 a, and Xa.
• Increase in platelet count and their adhesiveness
• Decreased levels of coagulation inhibitors like anti-thrombin 3, and fibrin split products.

Question 2. Mention types and discuss the fate of the thrombus.
Answer:

Types of Thrombi:

• Thrombi can develop anywhere in the cardiovascular system i.e., in cardiac chambers, on valves, or in arteries, veins/capillaries.
• The size and shape of the thrombus depend on the site of origin and the cause.

Various types of thrombi are as follows:

1. Mural thrombi:

• Thrombi occurring in the heart chambers or in the aortic lumen are known as mural thrombi.
• Abnormal myocardial contraction or endomyocar¬dial injury promotes cardiac mural thrombi.

2. Arterial thrombi:

• They are white or pale in color.
• Microscopically, distinct lines of Zahn composed of platelets, and fibrin with enlarged red and white blood cells are seen.
• Arterial thrombi produce ischemia and infarction.

3. Venous thrombi:

• Venous thrombi are red and occlusive
• Microscopically, distinct lines of Zahn with more abundant red blood cells are seen.
• Red (venous) thrombi have more abundant red cells, leucocytes, and platelets entrapped in fibrin meshwork. Thus, red thrombi closely resemble blood clots in vitro.
• Venous thrombi cause embolism.

4. Post mortum thrombi:

They are gelatinous with a dark red dependent portion where red cells have settled by gravity and a yellow chicken fat supernatant and they are usually not attached to the underlying wall.

5. Vegetation:

• Thrombi occurring on the heart valves are called vegetation.
• Bacterial or fungal blood-borne infections can cause valve damage, leading to large thrombotic masses.
• Sterile vegetation can also develop on non-infected valves in a hypercoagulable state, so-called non-bacterial thrombotic endocarditis.

The fate of Thrombus:

1. Resolution:

• Thrombus activates the fibrinolytic system with the consequent release of plasmin which may dissolve the thrombus completely resulting in resolution.
• Usually, lysis is complete in small venous thrombi while large thrombi may not be dis¬solved.

2. Organisation:

• If the thrombus is not removed, it starts getting organized phagocytic cells (neutro¬phils and macrophages) appear and begin to phagocytose fibrin and cell debris. Capillaries grow into the thrombus from the site of the attachment and fibroblasts start invading the thrombus.
• Thus, fibrovascular granulation tissue is formed which subsequently becomes dense and less vascular and is covered over by endothelial cells.
  • This way thrombus is excluded from the vascular lumen and becomes part of the vessel wall.
  • The new vascular channels in it may be able to re-establish the blood flow, called recanaliza¬tion.
  • The fibrosis thrombus may undergo hyalinization and calcification example phlebitis in the pelvic reins.

3. Propagation:

Thrombus may enlarge in size due to more and more deposition from the constitu¬ents of flowing blood. In this way, it may ultimately cause obstruction of some important ves¬sel.

4. Thrombo embolism:

Thrombi in the early stage and infected thrombi are quite friable and may get detached from the vessel wall. These are released in the bloodstream as emboli which produce ill effects at the site of their lodgement.

Question 3. Define embolism. Give an account of various types of embolism.
Answer:

Embolism: Embolism is the partial/complete obstruc¬tion of some part of the cardiovascular system by any mass carried in the circulation, the transported intravas¬cular mass detached from the site of origin is called an embolus.

Types of Emboli:

1. Depending upon the matter in the emboli.

• Solid
  • Example: Detached thrombi (thrombotic emboli), tissue fragments, parasites, and foreign bodies.
• Liquid
  • Examples: Fat globules, amniotic fluid, bone marrow.
• Gaseous
  • Example: Air, other gases

2. Depending upon whether infected or not.

• Bland – when sterile
• Septic – when infected

3. Depending upon the source of emboli.

• Cardiac emboli
  • Example: Bmboli originating from atrium and atrial appendages, infarct in the left ventricle.
• Arterial emboli
  • Example: In systemic arteries in the brain, spleen, kidney, and intestine.
• Venous emboli
  • Example: In systemic arteries in the brain, spleen, kidney, and intestine.
• Lymphatic emboli can also occur.

4. Depending upon the flow of blood.

• Paradoxical embolus: An embolus which is carried from the venous side of circulation to the arterial side/vice versa is called paradoxical/crossed em¬bolus.
• Retrograde embolus: An embolus which travels against the flow of blood is called retrograde em-bolus.

Question 4. Define infarction. Describe the pathology of the infarct.
Answer:

Infraction:

Definition: Infarction is the process of tissue necrosis resulting from some form of circulatory insufficiency, the localized area of necrosis of developed is called an “infarct.

Infarct Etiology:

• Interrupted arterial blood supply is called ischemic necrosis.
• Less commonly venous obstruct (stagnant hypoxia).
• Sudden complete and continuous occlusion by thrombosis/embolism produces infarcts.
• Also by mono occlusive circulatory insufficiency.
• Example: Incomplete atherosclerotic narrowing of coro¬nary arteries may produce myocardial due to acute coronary insufficiency.

Types of infarcts:

1. Acc to colour:

• Pale/Anaemic: due to arterial occlusion And are seen in compact organs example., In the kidneys, heart, and spleen.
• Read/Haemorrhagic: Seen in soft loose tissue And are caused either by pulmonary arterial obstruction (example, in the lungs) or by arterial/venous occlusion (example In the intestines)

2. Acc. to age:

• Recent/Fresh
• Old/healed.

3. Acc. to presence/absence of infection: Bland, when free of bacteria contamination septic, when infected.

Infarct Pathogenesis:

• Localized hyperemia occurs immediately after ischemia. Within a few hours, the affected part becomes swol¬len because of edema And hemorrhage.
• Early changes are cloudy swelling And degeneration. Pro-gressive autolysis of necrotic tissue And hemolysis of red cells follows.
• An acute inflammatory reaction And hyperemia appear in the. surrounding tissue. Blood pigments are deposited in the infarct.
• There is progressive ingrowth of granulation tissue. Finally, the infarct is replaced by a fibrous scar.

Gross Appearance:

• All infarcts tend to be usually wedge-shaped, the apex pointing towards the occluded vessel And the wide base on the surface of the organ.
• Infarct due to arterial occlusion is pale while those due to venous obstructions are hemorrhagic.
• The recent infarcts are generally slightly elevated over the surface while the old infarcts are shrunken And de-pressed under the surface of the organ.

Histologic Characteristics of Infraction:

• The dominant histologic characteristic of infarction is ischemic coagulative necrosis of the affected area.
• It generally contains the same amount of hemorrhage.
• At the periphery, there is inflammatory reactions pre-dominated by neutrophils initially later even macro¬phages and fibroblasts appear.
• Most infarcts are ultimately replaced by fibrous tissue, which at times may show calcification. The brain is an exception. In CNS, liquefactive necrosis takes place.

Question 5. Describe the morphology and microscopic structure of cardiac infarction.
Answer:

Cardiac infarction Morphology:

• Infarcts of solid organs are usually wedged shaped
• Apex points towards the occluded artery and base on the surface of the organ
• Infarcts due to arterial occlusion appear pale and due to venous obstruction are hemorrhagic
• Red cells are lysed
• Cerebral infarcts
  • Poorly defined
  • Central softening
• New infarcts appear slightly elevated over the surface
• Old infarcts are shrunken and depressed under the surface

Cardiac infarction Microscopic Structure:

• It shows coagulative necrosis of the affected area of tissue or organ
• Shows some amount of hemorrhage
• At the periphery inflammatory reaction is seen
• Cerebral infarcts show liquefaction necrosis
• Gliosis occurs later
• Initially
  • Neutrophils are predominately present
  • Other cells present are macrophages and fibro¬blasts
• Later
  • The necrotic area is replaced by a fibrous scar
  • May show dystrophic calcification

Hemodynamic Derangements Due To Obstructive Nature Short Essays

Question 1. Fat emboli
Answer:

• Obstruction of arterioles and capillaries by fat globules constitutes fat embolism.
• If the obstruction in the circulation is by fragments of adipose tissue, it is called a fat-tissue embolism.

Fat emboli Etiology:

1. Traumatic causes:

• Trauma to bones- a most common cause.
  • Example: In fractures of long bones leading to the passage of fatty marrow in circulation, after orthopedic surgi¬cal procedures, etc.
• Trauma to soft tissue
  • Example: Laceration of adipose tissue and in puerperium due to injury to pelvic fatty tissue.

2. Non-traumatic causes:

• Extensive burns
• Diabetes mellitus
• Fatty liver
• Pancreatitis
• Sickle cell anemia
• Decompression sickness
• Inflammation of bones and soft tissues
• Extrinsic fat/oils are introduced into the body.

Fat emboli Pathogenesis:

There are few mechanisms to explain the pathogenesis.

1. Mechanical theory: Mobilisation of fluid fat following trauma to bones or soft tissues Releases fat glob¬ules which may enter venous circulation.
2. Emulsion instability theory: In non-traumatic cases, fat emboli are formed by aggregation of plasma lipids due to disturbance in the natural emulsification of fat
3. Intravascular coagulation theory: In stress, the release of some factors activates intravascular coagulation (DIC) and aggregation of fat emboli.
4. Toxic injury theory: Blood vessels of the lungs are chemically injured resulting in increased vascular permeability and consequent pulmonary edema.

Fat emboli Consequences:

1. Pulmonary fat embolism: Widespread obstruction can result in sudden death.
2. Systemic fat embolism: Petechial skin rash, petechial hemorrhages, decreased glomerular filtration, renal insufficiency, etc.

Question 2. Caissons disease
Answer:

• Decompression sickness is a specialized form of gas embolism and is known as Caisson’s disease
• It occurs when individuals are exposed to sudden changes in atmospheric pressure
• As seen in the deep sea, in underwater construction workers, and in individuals in unpressurized aircraft

Fat emboli Pathogenesis:

Produced when the individual decompresses suddenly either from high atmospheric pressure to normal level or from normal to low level

Fat emboli Features:

• Formation of minute gas bubbles in
  • Skeletal muscles
  • Supporting tissues in and about the joints
• This creates bends
• In the lungs, edema, hemorrhage, and focal atelectasis or emphysema may appear
• It may lead to sudden respiratory distress called chokes

Fat emboli Treatment:

Place the individual in a compression chamber which permits slow decompression of the individual

Question 3. Air emboli
Answer:

• Air embolism occurs when air is introduced into venous or arterial circulation.
• Gas bubbles within the circulation can obstruct vascular flow.

Venous air embolism: Air may be sucked into systemic veins during.

• Operations on head and neck and trauma
• Obstetrical operations and trauma
• Intravenous infusion of blood and fluids
• Angiography.

Arterial air embolism: Entry of air into pulmonary veins or its tributaries may occur in the following conditions:

• Cardiothoracic surgery and trauma
• Paradoxicalair embolism
• Arteriography.

Hemodynamic Derangements Due To Obstructive Nature Short Question And Answers

Question 1. Atrial embolism
Answer:

 

Arterial emboli may lead to infarction, myocardial infarc¬tion, gangrene, and sudden death.

Question 2. Pulmonary embolism
Answer:

Definition: Pulmonary embolism is the most common and fatal form of venous thromboembolism in which there is occlusion of a pulmonary arterial tree by thrombotic emboli.

Pulmonary embolism Etiology:

Thrombi originating from large veins of lower legs are 95%, less commonly thrombi originate from varicosities superficial veins of legs, and pelvic veins.

Pulmonary embolism Pathogenesis:

Detachment of thrombi produces thrombo-embolus that flows through venous drainage into large veins draining into right side of the heart

Pulmonary embolism Consequences:

• Acute corpulmonale
• Pulmonary hypertension
• Pulmonary infarction
• Chroniccorpulmonale
• Pulmonary hemorrhage
• Sudden death.

Question 3. Thromboembolism
Answer:

A detached thrombus or part of a thrombus forms thromboembolism

Question 4. Causes of ischemia
Answer:

Ischemia is defined as a deficiency of blood supply to a part of a tissue.

Etiology: Various causes of ischemia are as follows.

1. Causes in the heart: Inadequate cardiac output may result from.

• Heart block
• Ventricular arrest
• Fibrillation.

This may lead to ischaemic injury to the brain.

2. Causes in the arteries: These are

• Luminal occlusion such as due to
  • Thrombosis
  • Embolism
• Causes in the arterial wall such as
  • Vaso spasm
  • Hypothermia
  • Arteriole sclerosis
  • Poly arteritis nodosa.
• Outside pressure on the artery such as ligature tour¬niquet torsion tight bandages.

3. Causes in the veins: Blockage of venous drainage may lead to engorgement and obstruction to arterial supply resulting in ischemia.

Examples:

• Luminal occlusion as in.
  • Thrombosis of mesenteric veins
  • Cavernous sinus thrombosis.
• Causes in vessel wall- varicose veins of legs.
• Outside pressure on the vein.
  • Strangulated hernia
  • Intussusceptions’.
• Causes in the microcirculation.
  • Luminal occlusion.
    • By red cells example In sickle cell anemia
    • By white cells example In chronic myeloid leu¬kaemia
    • By fibrin, for example, defibration syndrome o by fat embolism.
  • Causes in microvasculature walls such as.
    • Vasculitis example Arthus reaction and
    • Frostbite injures wall of small blood ves¬sels.
  • Outside pressure on microvasculature as in bed sores.

Hemodynamic Derangements Due To Deranged Volume Important Notes

1. Hyperaemia

• Increased volume of blood from arterial and arteriolar dilatation is called hyperemia
• It is seen in
  • Inflammation
  • Blushing
  • Menopausal flush
  • Muscular exercise
  • High-grade fever
• The affected organ is pink or red

2. Caissons disease

• It is a form of gas embolism
• It is produced when an individual decompresses suddenly either from high atmospheric pressure to normal level or from normal pressure to low atmospheric pressure

3. Lines of Zahn

• It consists of alternate layers of aggregated platelets within fibrin meshwork and red cells
• Lines of Zahn are distinct in arterial thrombi

4. In hypovolemic shock, kidneys conserve body fluids by

• Reducing GFR
• Releasing aldosterone and ADH – aldosterone increases renal retention of sodium and water

Hemodynamic Derangements Due To Deranged Volume Long Essays

Question 1. Define shock. Discuss classification, pathogenesis, and pathology of shock.
(or)
Discuss Etiology, pathogenesis, and pathology of shock.
Answer:

Shock: Shock is a life-threatening clinical syndrome of cardiovascular collapse characterized by:

• An acute reduction of effective circulating blood volume [Hypotension) and
• Inadequate perfusion of cells and tissues [Hypoperfusion).

Types Of shock:

Classification and etiology of shock:

1. Hypovolaemic Shock

• Acute hemorrhage
• Dehydration from vomiting, diarrhoea
• Burns
• Excessive use of diuretics
• Acute pancreatitis

2. Cardiogenic Shock

• Deficient emptying example
  • Myocardial infarction
  • Cardiomyopathies
  • Rupture of the heart, ventricle or papillary muscle
  • Cardiac arrhythmias
• Deficient filling example
  • Cardiac tamponade from haemopericardium
• Obstruction to the outflow example
  • Pulmonary embolism
  • Ball valve thrombus
  • Tension pneumothorax
  • Dissecting aortic aneurysm

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3. Septic Shock

• Gram-negative septicemia (endotoxic shock) example Infection with E. coli, Proteus, Klebsiella, Pseudomonas and Bacteroides
• Gram-positive septicemia (exotoxic shock) example Infection with streptococci, pneumococci

4. Other Types

• Traumatic shock
  • Severe injuries
  • Surgery with marked blood loss
  • Obstetrical trauma
• Neurogenic shock
  • High cervical spinal cord injury
  • Accidental high spinal anesthesia
  • Severe head injury
• Hypoadrenal Shock
  • Administration of high doses of glucocorticoids
  • Secondary adrenal insufficiency (example in tubercu¬losis, metastatic disease, bilateral adrenal hemorrhage, idiopathic adrenal atrophy)

Pathology of Shock:

• Shock is characterized by multi-system failure.
• The morphogenic changes in shock are due to hypoxia resulting in degeneration and necrosis in various or¬gans.
• Predominant morphologic complications in shock are as follows:

1. Hypoxic Encephalopathy:

• An altered state of consciousness may be produced by cerebral ischemia in compensated shock.
• In prolonged shock and cardiac arrest, the brain suffers from severe ischaemic damage with loss of cortical functions, coma, and a vegetative state.
• Dead and dying nerve cells are replaced by gliosis.

2. Heart in shock:

• The heart is more vulnerable to the effects of hypoxia than any other organ.
• 2 important morphogenic changes in the heart are Hemorrhages and necrosis – There may be small/large ischaemic areas of infarcts, particularly located in the subepicardial and subendocardial regions.
• Zonal lesions- these are opaque transverse con-traction bands in the myocytes near the intercalated disc.

3. Shock lung:

• Due to dual blood supply lungs are not affected by hypovolaemic shock but are affected by septic shock. The lungs become heavy and wet.
• Microscopically, changes of adult respiratory distress syndrome (ARDS) are seen. Briefly, the changes include congestion, interstitial and alveolar edema, lymphocyte infiltration, fibrin, and platelet thrombi in the microvasculature.

4. Shock kidney:

• Irreversible renal injury is one of the most important complications of shock.
• Acute tubular necrosis occurs in which there are tubular lesions.
• The end result is generally anuria and death.

5. Adrenal changes in shock:

• Adrenals show stress syndrome which includes the release of aldosterone, glucocorticoid, and catecholamines like adrenaline.
• In severe shock, adrenal high can occur.

6. Haemorrhagic Gastroenteropahty:

The hypoperfusion of the alimentary tract in conditions such as shock and cardiac failure may result in mucosal and mural infarction called hemorrhagic gastro- teropathy.

7. Liver in shock:

Due to hypoxia vasodepressor ma¬terial is released which causes vasodilation, focal necrosis, fatty liver, and impaired liver functions grossly, faint nutmeg appearance is seen.

8. Other organs: Other organs such as lymph nodes, spleen, and pancreas may also show foci of necrosis in shock.

Pathogenesis: There are 2 basic features in the pathogenesis of shock.

1. Reduced effective circulating volume: It may result in either.

• By actual loss of blood volume as in hypovolemic shock or.
• By decreased cardiac output without actual loss of blood as in cardiogenic and septic shock.

2. Tissue Anoxia:

• Following the reduction in effective cir¬culating blood volume, there is decreased venous return and hence Tsedcardic output.
• This leads to reduced 02 supply, hence tissue anoxia which sets in cellular injury.

3. Release of inflammatory mediators: In response to cellular injury, inmate immunity of the body gets ac¬tivated and there is the release of inflammatory media¬tors but eventually these agents themselves become the cause of cell injury.

Pathogenesis

Question 3. What are the factors leading to irreversible shock?
Answer:

Factors Leading To Irreversible Shock:

1. Progressive Vasodilatation

• Anoxia damages the capillary and venular wall
• Arterioles do not respond to vasoconstrictors
• This results in Vasodilatation and peripheral pool¬ing of blood

2. Increased vascular permeability

• Tissue damage occurs due to anoxia
• This releases inflammatory mediators
• Results in increased vascular permeability

3. Myocardial depressant factor

• Release of Myocardial depressant factor causes
• Fall in blood pressure
• Persistent reduced blood flow to myocardium a Coronal insufficiency
• Myocardial ischemia

4. Worsening pulmonary hypoperfusion Causes respiratory distress

5. Anoxic damage to the heart, kidney, and brain

• Due to anaerobic glycolysis, tissue anoxia causes
  • Severe metabolic acidosis
  • Release of inflammatory mediators
  • Ischaemic cell death

6. Hypercoagulability

• Tissue damage activates the coagulation pathway which causes
  • Release of clot-promoting factor, thromboplastin
  • Release of platelet aggregator
  • ADP
  • Slowing of bloodstream
  • Vascular thrombosis

Hemodynamic Derangements Due To Deranged Volume Short Essays

Question 1. Irreversible shock
Answer:

When the shock is so severe and no recovery takes place in spite of compensatory mechanism, therapy, and control of the etiologic agent which caused the shock, it is called decompensated/irreversible shock.

Irreversible shock Pathogenesis:

• Progressive vasodilation
• ↑Vascular permeability
• Myocardial depressant factor (MDF]
• Pulmonary hypoperfusion
• Anoxic damage
• Hyper coagulability

Irreversible shock Complications:

• Brain – hypoxic encephalopathy
• Heart – focal myocardial necrosis
• Lungs – ARDS
• Kidney – ATN
• GI – Haemorrhagic gastro enteropathy
• Liver – necrosis
• Blood-DIC.
• Adrenals – necrosis

Question 3. Chronic venous congestion of the liver.
Answer:

Liver Etiology:

• It is seen in
• Right heart failure
• Occlusion of inferior vena cava and hepatic vein

Liver Macroscopic Appearance:

• Enlarged liver
• The tensed capsule is present

Liver Cut Surface:

• Shows a nutmeg liver appearance
• It shows the red and yellow mottled appearance
• The red part corresponds to the congested center of lob¬ules
• The yellow part corresponds to the fatty peripheral zone

Microscopic Appearance:

• Centrilobular zone
  • Shows severe hypoxia
  • Distended central veins and adjacent sinusoids
  • Degeneration of hepatocytes
  • Hemorrhagic necrosis
  • Fibrosis and regeneration of hepatocytes in long-standing cases
• Peripheral zone
  • Less effected
  • Fatty change in hepatocytes is seen

Question 4. Septic shock.
Answer:

Septic shock Etiology:

• Severe bacterial infection – more commonly Gram-negative
• Septicemia

Septic shock Pathogenesis:

Septic shock Result:

• Produces more neutrophils which liberate free radical causing vascular injury
• Promotes NO synthase for vasodilatation and hypoten¬sion

2. Activation of other inflammatory response

Activation of other inflammatory response Results

Hemodynamic Derangements Due To Deranged Volume Short Question And Answers

Question 1. Stages of shock
Answer:

Deterioration of the circulation in shock is a progressive phenomenon and can be divided into the following 3 stages.

1. Initial nonprogressive stage: During this stage reflex compensatory mechanisms are activated and perfusion of vital organs is maintained.

2. Progressive stage: This stage is characterized by tissue hypoperfusion and the onset of worsening circula¬tory and metabolic imbalances.

3. Irreversible stage: It sets in after the body has in¬curred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible

Question 2.Anaphylactic shock
Answer:

Anaphylactic shock Definition:

• Anaphylaxis is a state of rapidly developing immune response to an antigen to which the individual is previously sensitized.
• Anaphylactic shock develops due to vasodilation and peripheral pooling of blood.

Anaphylactic shock Pathogenesis:

• IgE antibodies sanitize basophils of peripheral blood/most cells of tissue leading to the release of anaphy¬lactic mediators like histamine, serotonin, VIP, and chemotactic factors of anaphylaxis.
• The effects produced are increased vascular permeability, smooth muscle contraction, and early vasoconstriction followed by vasodilation and shock.
• Increased vascular permeability and vasodilation lead to peripheral pooling and blood. This results in a reduction of effective circulating volume and shock.
• Example: Systemic anaphylaxis due to administration of antisera drugs like penicillin.

Clinical features of systemic anaphylaxis include itching, erythema, contraction of respiratory bronchioles, pulmonary edema, shock, and death.

Question 3. Mechanism of shock in burns
Answer:

• Reduction in blood volume due to fluid loss in burns in¬duces hypovolemic shock.
• The major effects of hypovolemic shock are due to de¬creased cardiac output and low intracardiac pressure.
• Accordingly, clinical features are increased heart rate (Tachycardia), low blood pressure (hypotension), low urinary output, and alteration in mental state (agitated to confused to lethargic).

Question 4. End result in a shock
Answer:

• Acute respiratory distress syndrome
• Disseminated intravascular coagulation
• Acute renal failure
• Multiple organ dysfunction syndrome
• Stupor
• Coma
• Death

Question 5. Nutmeg liver.
Answer:

• It is seen in the cut surface of chronic congestion of the liver
• It shows the red and yellow mottled appearance
• The red part corresponds to the congested center of lobules
• The yellow part corresponds to the fatty peripheral zone

Question 6. Neurogenic shock.
Answer:

Neurogenic shock Pathophysiology:

Neurogenic shock Damage to Organs:

• Increase in myocardial contractibility
• ARDS
• Increase in blood pressure
• Toxaemia
• Bacteraemia
• Renal failure
• Upper GI bleeding

Neurogenic shock Management:

• Administration of oxygen
• Vasoactive drugs – Phenoxybenzamine
• Inotropic agents – Dopamine
• Corticosteroids – Prednisolonel5 mg/kg
• Mechanical ventilation
• Fluid replacement

Haemodynamic Derangements Of Body Fluids Important Notes

1. Oedema

• It is an abnormal and excessive accumulation of fluid in the interstitial tissue spaces and serous cavities
• Causes
  • Decreased plasma oncotic pressure
  • Increased capillary hydrostatic pressure
  • Increased capillary permeability
  • Lymphatic obstruction
  • Sodium and water retention

2. Transudate and exudate

Derangements Of Body Fluids Long Essays

Question 1. Define oedema. Discuss pathogenesis and causes of oedema,
(or)
Discuss etiopathogenesis of oedema.
Answer:

Oedema: Oedema may be defined as abnormal and exces¬sive fluid accumulation in interstitial tissue spaces and serous cavities.

Types of Oedema:

1. Three main types of oedema:

2. Subcutaneous oedema is of 2 types.

 

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3. Depending on oedema fluid.

Etiopathogenesis:

Oedema is the result of an increase in the forces that tend to more fluids from the intravascular compartment to the interstitial space

The following six mechanisms may be operating singly/in combination to produce oedema.

1. Decreased plasma oncotic pressure:

• Plasma oncotic pressure exerted by the total amount of plasma proteins tends to draw fluid into the vessels normally.
• A fall in the total plasma protein level/hypoproteinemia less than 5g/dl lowers plasma oncotic pressure and thus it cannot effectively counteract the hydrostatic pressure of blood.
• This results in Tsed outward movement of fluid from the capillary wall and anodised inward movement of fluid from the interstitial space causing oedema.
• Example: Oedema of renal disease: Nephrotic syndrome, acute glomerulonephritis.
• Ascites of liver disease: cirrhosis.

2. Increased capillary hydrostatic pressure:

• Capillary hydrostatic pressure is the force that normally tends to drive fluid through the capillary wall into interstitial space by counteracting the force of plasma oncotic pressure.
• A rise in the hydrostatic pressure at the venular end to a level more than the plasma oncotic pressure results in minimal/no reabsorption of fluid at the venular end consequently leading to oedema.
• Example: Oedema of cardiac diseases→ Congestive cardiac failure, constrictive pericarditis.
• Passive congestion → Mechanical obstruction due to thrombosis of veins of lower limbs, varicosities, pressure by interns, and tumours.

3. Lymphatic obstruction:

Normally the interstitial fluid in the tissue space escapes through lymphatic and thus obstruction to the outflow of the lymphatics causes localized oedema known as lymphoedema.

4. Tissue factors:

They can cause oedema when the oncotic pressure of the interstitial fluid is elevated due to increased vascular permeability and inadequate removal of proteins by lymphatics.

5. Increased capillary permeability:

• Intact capillary endothelium acts as a semipermeable membrane permitting free flow of water and crystalloids and allowing only a minimal passage of tissue proteins.
• Sometimes, capillary endothelium may be injured, in such cases there is development of gaps increasing the capillary permeability to plasma proteins.
• Thus, the oncotic pressure of plasma is reduced and that of interstitial fluid is elevated producing oedema.
• Example: Generalized oedema in systemic infections, poisonings localized oedema. Inflammatory oedema – infections, allergic reactions. Angioneurotic oedema.

6. Sodium and water retention:

• Excessive retention and decreased renal excretion of sodium and water occur in response to hypovoleamia.
• Example: Oedema of cardiac disease – congestive cardiac failure.
• Ascites of liver disease – cirrhosis.

Question 2. What are the types of exudation? Describe the sequelae of pyogenic abscesses.
Answer:

Exudate:

Exudate is inflammatory oedema which is protein-rich with a specific gravity usually greater than 1.020

Exudation Types:

Sequence of Pyogenic Abscess:

• Drainage
  • Abscess may be discharged to the surface due to increased pressure inside
• Healing by fibrous scarring
• Calcification
  • If the abscess is not drained, it gets organized by dense fibrous tissue

Question 3. Classify inflammatory exudate. Give example. What are the differences between exudate and transudate?
Answer:

Derangements Of Body Fluids Short Essays

Question 1. Angioedema
Answer:

• Angioedema is an autosomal dominant disorder which manifests as a form of local anaphylaxis
• It Is characterised by laryngeal oedema, oedema of eyelids, lips, tongue and trunk
• The response is mediated by humoral antibodies of IgE type
• It involves the release of
  • Histamine
  • Serotonin
  • Leukotrienes
  • Prostaglandin
  • Platelet-activating factors
• These act as anaphylactic mediators
• They are responsible for changes associated with angioedema

Derangements Of Body Fluid Short Question And Answers

Question 1. Renal oedema
Answer:

Generalised oedema occurs in certain diseases of renal origin such as

1. Nephrotic syndrome:

In nephrotic syndrome, there is persistent and heavy proteinuria, there is hypo-al-buminemia causing decreased plasma oncotic pressure resulting in severe generalised oedema.

2. Glomerulonephritis:

Nephritic oedema is usually mild as compared to nephrotic oedema. Nephritic oedema is due to excessive reabsorption of sodium and water in the renal tubules via the resin angiotensin-aldosterone mechanism.

3. Acute tubular necrosis:

Acute tubular injury following shock/toxic chemicals results in gross oedema of the body.

Question 2. Pulmonary oedema
Answer:

• Pulmonary oedema develops from left heart failure.
• There is fluid accumulation not only in tissue spaces but also in the pulmonary arteriole.
• It causes serious functional impairment

Etiopathogenesis: Can result from either elevation of pulmonary hydrostatic pressure/increased capillary permeability.

• Elevation of pulmonary hydrostatic pressure.
  • An increase in hydrostatic pressure of pulmonary capillaries and the resulting imbalance between palm hydrostatic press and plasma oncotic pressure causes excess fluid to move into the interstitium.
  • Interstitial oedema develops later with a prolonged elevation of hydrostatic pressure, alveolar lining cells develop and alveolar oedema results.
  • This mechanism is seen in left heart failure, mitral stenosis and thyrotoxicosis.
• Increased capillary permeability: Damage to alveolar-capillary membrane causes increased permeability so that excess fluid and plasma proteins leak out, initially into the interstitium and later into the alveoli.
• Example: Fulminant pulmonary infections, radiation injury, inhalation of ototoxic substances.

Infections And Infestation Short Essays

Question 1. Lab diagnosis of enteric fever
Answer:

Enteric fever Lab Diagnosis:

1. Isolation of bacilli.

• For isolation of bacteria, specimens are obtained from blood, faeces, urine, aspirated duodenal fluid, bile, bone marrow or rose spot.
• These specimens are then cultured.

2. Demonstration of Antibodies

1. Widal test.

It is an agglutination for the detection of agglutinins H and 0 in patients with enteric fever

Widal test Method:

• Equal volumes f0.4 ml) serial dilutions of serum from 1:10 to 1: 640 and H and O antigens are mixed.
• One control tube containing antigen and normal saline is used.
• All these tubes are incubated in a water bath at 37°C.

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Widal test Results:

Widal test Interpretation:

3. Demonstration of circulating antigen.

Done by counterimmunoelectrophoresis and ELISA.

Question 2. Urinary sediment
Answer:

Urinary sediment contains the following constituents

• It also contains
  • Crystals of
    • Calcium oxalate
    • Uric acid
    • Amorphous urate
    • Tyrosine
    • Calcium carbonate
  • Miscellaneous structures like
    • Spermatozoa
    • Parasite
    • Fungus
    • Tumour cells

Infections And Infestation Short Question And Answers

Question 1. Amoebiasis
Answer:

• Caused by entamoeba histolytica
• E. Histolytica can cause two types of pathological lesions as follows

• This condition is called as amoebic dysentery.
• These ulcers may be generalised (or) may be localised to the ileo-caecal (or) sigmoidorectal region.
• Occasionally ulcers may involve deeper tissues and may cause perforation (or) peritonitis.
• Erosion of blood vessels may lead to haemorrhage.
• The superficial lesions generally heal without scarring.
• Deep ulcers form scars leading to strictures, partial obstruction and thickening of gut wall.

2. Extra-intestinal amoebiasis (or) secondary (or) metastatic lesions.

Amoebic liver abscess:

Question 2. Candidiasis
Answer:

• Candidiasis is caused by Candida albicans and occasionally by other Candida species
• It is an opportunistic endogenous infection.

Candidiasis Predisposing Factors:

• Diabetes
• Immunodeficiency
• Malignancy
• Prolonged administration of antibiotics
• Patients on immunosuppressive drugs and intravenous catheters

Candidiasis Treatment:

• Removal of predisposing factors
• For superficial infections- Topical application of polyene and imidazole is used
• For systemic infections- Amphotericin B + 5- fluoroscopy- tosine is used

Question 3. Rhinosporidiosis
Answer:

Rhinosporidiosis is a chronic granulomatous disease.

Rhinosporidiosis Causative Organism:

Rhinosporidium seeberi.

Rhinosporidiosis Mode of Infection:

Frequent contact with stagnant water.

Rhinosporidiosis Features:

• Friable polyps
• Sites involved- nose, mouth and eye
• Oral manifestations are Oropharyngeal lesions
• They appear as soft red polypoid growth and spread to the pharynx and larynx.
• These lesions contains mucoid discharge and are vascular.

Rhinosporidiosis Diagnosis:

• H and E stained tissue sections shows a large number of endospores within the sporangia
• These are embedded in a stroma of connective tissue, and capillaries

Question 4. Cysticercus cellulose
Answer:

• Cysticercus cellulose is the larval stage of taenia solium
• It develops in the muscles of the pig which is intermediate host
• A mature cyst is an opalescent ellipsoidal body and the long axis of the cyst is parallel to the muscle fibre.
• A dense milky white spot is present at the side where the scolex with its hooks and suckers remains invalidated.
• The cyst develops further when ingested by man which is the definitive host
• It may develop in any organ but are usually present in the subcutaneous tissues and muscles.

Various features of cysticercosis:

• They causes palpable nodule in sub-cutaneous tissues and muscles
• In brain leads to epileptic attacks.
• Neurocysticercosis involving the nervous system is the most serious form

Question 5. Fungi infecting hair
Answer:

• Dermatophytes are the group of fungi affecting the hair.
• Favus is a chronic type of ringworm involving the hair follicles

Fungi infecting hair Features:

• Alopecia
• Scarring
• Sparse hyphal growth
• Formation of air spaces within the hair shaft

Fungi infecting Hair Types:

Question 6. Urinometer.
Answer:

• It is an equipment for determining urine specific gravity
• It is composed of
  • Float – It is air filled glass tube
  • Weight – It is a bulb filled with ball bearings
  • Stem – It has calibrated graduation and numbers marked off to indicate specific gravity measurements
• Urinometer is placed in a tube of urine and where the meniscus of the urine reaches displays the specific gravity of the urine

Diseases Of The Immune System Important Notes

1. Hypersensitivity reactions

Diseases Of The Immune System Long Essays

Question 1. Define hypersensitive reaction. Explain type IV hypersensitive reaction.
Answer:

• Hypersensitivity or allergy is defined as a state of exaggerated immune response to the antigen, which may lead to tissue damage, disease or even death following contact with specific antigens.
• Lesions of hypersensitivity i.e., immunologic tissue injury are produced due to the interaction between antigen and product of immune response.
• Depending upon the rapidity, duration, and type of immune response, hypersensitivity reactions are classified into.

1. Immediate type:

It includes 3 types.

1. Type 1 – Anaphylactic reaction.

• Example: Systemic anaphylaxis/local anaphylaxis.

2. Type 2 – Cytotoxic reaction.

• Example: Erythroblastosis fetal, leucopenia.

3. Type 3 – Immune complex-mediated reaction

• Example: Arthritis and skin diseases.

2. Delayed type:

Type 4- Hypersensitivity reaction.

Type 4/delayed hypersensitivity reaction is tissue injury by cell-mediated immune response without the formation of antibodies but is instead a slow and prolonged response of specifically sensitized T- lymphocytes.

Etiology and pathogenesis: Type 4 reaction involves the role of most cells and basophils, macrophages and CDQ + T cells. The mechanism of type 4 reaction is:

• The antigen is recognized by CDg + T cells (cytotoxic T cells) and is processed by antigen-presenting cells.
• Antigen-presenting cells migrate to the lymph node where antigen is presented to helper T-cells (CD4 + T cells).
• Helper T cells release cytokines that stimulate T cell proliferation and activate macrophages.
• Activated T cells and macrophages release pro-inflammatory mediators and cause cell destruction.

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Examples:

• Reactions against mycobacterial infection.
  • Examples: Tuberculin reaction, granulomatous reaction in tuberculosis, leprosy.
• Reaction against virally infected cells
• Reaction against malignant cells in the body.
• Reaction against organ transplantation example transplant rejection, graft versus heart reaction.

Diseases Of The Immune System Short Essays

Question 1. Anaphylaxis
Answer:

• Anaphylaxis or type I hypersensitivity is defined as a state of rapidly developing an immune response to an antigen (i.e., allergen) to which the individual is previously sensitized.
• The reaction appears within 15-30 min of exposure to antigen.

Anaphylaxis Etiology: Type I reaction is mediated by humeral antibodies of IgE type or regain antibodies in response to antigen.

The definite cause is not known, but the following may be responsible.

• Environmental pollutants
• Genetic basis
• Concomitant factors – Allergic response may be linked to the occurrence of certain viral infections of the upper respiratory tract.

Anaphylaxis Pathogenesis: Type 1 reaction includes the participation of B lymphocytes and plasma cells, mast cells and basophils, neutrophils, and eosinophil It mechanism is:

• During first contact, with antigen, sensitization takes place.
• During the second contact, IgE antibodies on the surface of mast cells – basophils are firmly bound to FQ receptors and set in cell damage and degranulation of mast cells occurs.
• Released granules contain important chemicals and enzymes with pro-inflammatory properties – histamine, serotonin, vasoactive, intestinal peptide, prostaglandins, platelet-activating factor, etc. The effects of these agents are.
  • Increased vascular permeability
  • Smooth muscle contraction
  • Vasoconstriction followed by vasodilation
  • Shock
  • Increased gastric secretion
  • Increased nasal and lacrimal secretions
  • Eosinophilia and neutrophilia.

Anaphylaxis Examples:

• Reactions against mycobacterial infection.
  • Examples: Tuberculin reaction, granulomatous reaction in tuberculosis, leprosy.
• Reaction against virally infected cells
• Reaction against malignant cells in the body.
• Reaction against organ transplantation example, transplant rejection, graft versus host reaction.

Diseases Of The Immune System Short Question And Answers

Question 1. Atopy
Answer:

• Atopy is a form of type I hypersensitivity reaction
• The antigens commonly involved in it are pollens, house dust, and food
• These induce IgE antibodies

Atopy Features:

• Atopy shows marked familial distribution
• Atopy sensitization is developed spontaneously following natural contact with opens
• The reaction occurs at the site of entry of antigen
• For example
  • Inhalation of pollens affects the lungs
  • Contact leads to local allergy

Atopy Manifestations:

• Conjunctivitis
• Rhinitis
• Bronchospasm
• GI symptoms
• Dermatitis
• Cutaneous eruptions

Question 2. B lymphocytes
Answer:

• Lymphocytes are of 2 major types. B lymphocytes (10 – 15% of T lymphocytes (75 – 80%).
• Lymphocytes undergo maturation and differentiation in the bone marrow and form B cells.
• B cells are involved in humeral immunity by inciting antibody response.
• On coming in contact with an antigen, B cells are activated to proliferate and transform into plasma cells.
• Depending upon the maturation stage of B cells, specific CD molecules appear on the cell surface which can be identified by CD markers, common B cell markers include CD 19, 20, 21, 23.
• These cells also possess B cells receptors for surface immunoglobulin (IgM and IgG) and FQ receptors for attaching to antibody molecules.

Question 3. Cell-mediated immunity
Answer:

• It is also known as type 4 delayed hypersensitivity re-action.
• It is defined as tissue injury by cell-mediated immune response without the formation of antibodies but is instead a slow and prolonged response of specifically – sensitized lymphocytes.
• The reaction occurs about 24 hours after exposure to antigen and the effects is prolonged which may last up to 14 days.

Question 4. Routes of transmission of HIV
Answer:

Routes of transmission:

The virus is present in the body fluids like blood, lymph, and genital fluids and gets transmitted when a healthy individual’s body fluids come in contact with an affected individual.

• Sexual transmission: This is the commonest form of transmission.
• Transmission via blood and blood products: Next commonest form.
• • Intravenous drug abusers: By sharing needles, syringes, etc.
  • Hemophiliacs: Who received large amounts of factor 8 concentrates.
  • Recipients of HIV: Infected blood and blood products.
• Perinatal transmission: It is also called vertical transmission, which occurs from the infected mother to the newborn during pregnancy or through breast milk.
• Occupational transmission occurs in workers engaged

Healing Of Tissues Important Notes

1. Sequence of events of wound healing

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

2. Primary and secondary intention of healing and their examples

3. Factors inhibiting wound contraction

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

4. Complications of fracture healing

• Fibrous union
• Nonunion
• Delayed union

5. Factors influencing healing

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

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Healing Of Tissues Long Essays

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

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

1. Regeneration:

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

2. Repair:

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

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

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

1. Primary union:

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

2. Secondary union:

More common type. Takes place in the following manner.

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

Causes of nonhealing of fracture :

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

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

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

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

The sequence of events in primary union:

1. Initial hemorrhage:

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

2. Acute inflammatory response:

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

3. Epithelial changes:

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

4. Organisation:

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

5. Suture tracks:

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

Differences between primary and secondary union.

Healing Of Tissues Short Essays

Question 1. Granulation tissues
Answer:

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

1. Inflammation:

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

2. Phase of clearance:

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

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

1. Neovascularisation.
2. Fibrogenesis

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

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

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

Question 2. Complications of wound healing
Answer:

Complications of wound healing:

1. Infection:

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

2. Implantation (epidermal) cyst:

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

3. Pigmentation:

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

4. Deficient scar formation:

• Due to inadequate formation of granulation tissue.

5. Incisional hernia:

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

6. Hypertrophied scars and keloid formation:

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

7. Excessive contraction:

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

8. Neoplasia:

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

Healing Of Tissues Short Question And Answers

Question 1. Healing of oral structures
Answer:

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

1. Primary union
2. Secondary union

1. Primary union:

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

2. Secondary union:

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

Question 2. Healing by secondary intention
Answer:

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

The sequence of events is as follows:

1. Initial hemorrhage:

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

2. Inflammatory phase:

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

3. Epithelial changes:

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

4. Granulation tissue:

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

5. Wound contraction:

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

6. Presence of infection:

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

Chronic And Granulomatous Inflammation Important Notes

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

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

2. Giant cells

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

3. Types of leprosy

4. Lepromin test

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

5. Types of syphilis

6. Types of tuberculosis

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

7. Fate of primary tuberculosis

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

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8. Fate of secondary tuberculosis

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

9. Ghon’s complex

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

Chronic And Granulomatous Inflammation Long Essays

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

1. Microscopy:

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

2. Serological tests:

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

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

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

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

Granuloma Etiology:

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

Evolution of tubercle:

Constituents of granuloma:

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

The fate of granuloma:

Question 3. Write briefly on cervicofacial actinomycosis.
Answer:

Cervicofacial actinomycosis is the commonest form of actinomycosis

Cervicofacial actinomycosis Causative Organism:

Site Involved:

• Cheek
• Submaxillary regions

Route of Infection:

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

Cervicofacial actinomycosis Features:

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

Cervicofacial actinomycosis Microscopic Features:

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

Cervicofacial actinomycosis Complications:

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

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

Granuloma Classification:

Granulomatous diseases are grouped into three groups as follows:

Tuberculosis Etiopathogenesis:

Tuberculosis Pathology:

1. Gross appearance

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

2. Microscopic appearance

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

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

Secondary pulmonary tuberculosis Complications:

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

1. Fibrocaseous tuberculosis:

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

Fibrocaseous tuberculosis Complications:

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

2. Tuberculosis caseous pneumonia:

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

3. Systemic military tuberculosis:

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

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

Common examples of granuloma:

1. Bacterial Tuberculosis,

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

2. Fungal

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

3. Parasitic

• Schistosomiasis

4. Miscellaneous

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

Effects of Tuberculosis:

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

Chronic And Granulomatous Inflammation Short Essays

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

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

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

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

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

Tuberculoid leprosy:

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

Question 2. Oral lesions of syphilis
Answer:

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

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

Mode of transmission:

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

1. Pulmonary component:

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

2. Lymphatic vessels component:

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

3. Lymph node component:

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

Diagnosis of tuberculosis is made by the following tests

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

Question 4. Primary tuberculosis.
Answer:

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

Chronic And Granulomatous Inflammation Short Question And Answers

Question 1. Gumma
Answer:

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

Question 2. Morphology of granuloma
Answer:

Granuloma consists of:

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

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

Examples:

Question 4. Actinomycosis
Answer:

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

Question 5. Primary complex
Answer:

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

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

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

Question 6. Congenital syphilis
Answer:

Congenital syphilis’s Major features are:

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

Question 7. Lepromatous leprosy
Answer:

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

Question 8. Pathological lesions of syphilis
Answer:

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

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

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

Question 13. Tuberculoid type of leprosy
Answer:

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

Question 14. Chancre
Answer:

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

Question 15. Giant cells
Answer:

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

Giant cells in inflammation:

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

Giant cells in tumors:

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

Question 16. Lepra reaction
Answer:

Lepra reaction/reactional leprosy:

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

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

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

1. Upgrading reaction:

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

2. Downgrading reaction:

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

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

Acute Inflammation Important Notes

1. Vascular events

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

2. Vasoactive amines

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

3. Interleukin – 1 (IL-1)

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

4. Metabolites

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

5. Bradykinin

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

6. Macrophages

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

Read And Learn More: Pathology Question And Answers

7. Neutrophils

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

8. Cellular events in inflammation

• Exudation of leucocytes
• Phagocytosis

Acute Inflammation Long Essays

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

Inflammation Definition:

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

Vascular changes of inflammation:

1. Haemodynamic changes:

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

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

2. Altered vascular permeability:

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

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

Cardinal Signs Of Inflammation:

There are four cardinal signs of inflammation as follows

1. Rubor- redness

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

2. Tumor- swelling

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

3. Calor-heat

• Vasodilatation is responsible for it

4. Dolor- pain

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

Lewis Experiment:

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

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

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

1. Exudation of leucocytes
2. Phagocytosis.

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

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

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

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

Rolling and adhesion:

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

Emigration:

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

Chemotaxis:

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

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

The main types of phagocytic cells are:

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

Phagocytosis consists of the following steps:

1. Recognition and attachment:

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

2. Engulfment stage:

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

3. Killing and degradation:

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

Acute Inflammation Short Essays

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

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

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

Chemical Mediators of Acute Inflammation:

1. Cell-Derived Mediators:

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

2. Plasma-derived mediators (Plasma Proteases)

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

Question 2. Chemotaxis:
Answer:

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

Acute Inflammation Short Question And Answers

Question 1. Lymphokines
Answer:

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

Question 2. Varieties of inflammation
Answer:

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

1. Acute inflammation:

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

2. Chronic inflammation:

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

Question 3. The vascular phenomenon in inflammation
Answer:

Vascular changes in inflammation:

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

Hemodynamic changes:

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

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

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

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

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

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

Environmental And Nutritional Disorders Important Notes

1. Vitamins

• Fat-soluble vitamins

• Water soluble vitamins

Environmental And Nutritional Disorders Long Essays

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

Vitamins:

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

Vitamins Classification: Vitamins are divided into 2 groups.

1. Fat-soluble vitamins – A, D, E, K

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

2. Water-soluble vitamins – B and C

• They are more readily absorbed from the small intestine.

Vitamin D: (Calcitriol):

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

Rickets:

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

Pathogenesis of rickets occurs in the following sequence:

1. Endochondral ossification is long tubular bones.

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

Read And Learn More: Pathology Question And Answers

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

Rickets Clinical Features:

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

Rickets Biochemical changes:

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

Environmental And Nutritional Disorders Short Essays

Question 1. Pellagra
Answer:

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

Question 2. Osteomalacia
Answer:

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

Question 3. Manifestations of vitamin A deficiency.
Answer:

Lesions in Vitamin A deficiency:

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

Question 4. Beriberi.
Answer:

Deficiency of Thiamine results in beriberi

Beriberi Symptoms:

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

Beriberi Types:

1. Wet beriberi

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

2. Dry beriberi

• Associated with neurological manifestations

3. Infantile beriberi

• Seen in infants

Environmental And Nutritional Disorders Short Question And Answers

Question 1. Microscopic picture of osteomalacia
Answer:

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

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

Question 3. Scurvy
Answer:

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

Following manifestations are seen in vitamin C deficiency.

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

Question 4. Kwashiorkor
Answer:

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

Kwashiorkor Clinical Features:

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

Question 5. Vitamin B12
Answer:

It is cyanocobalamine

Coenzyme Forms:

• 5′- Deoxyadenosyl cobalamin
• Methylcobalamin

Vitamin B12 Functions:

1. Synthesis of methionine from homocysteine

• Vitamin B12 is used as Methylcobalamin in this reaction

2. Isomerization of methymalonyl CoA to succinyl CoA

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

Vitamin B12 Dietary Requirements:

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

Question 6. Vitamin B12 deficiency
Answer:

A deficiency of vitamin B12 leads to

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

Question 7. Protein-energy malnutrition
Answer:

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

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

Causes of Vitamin D Deficiency:

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

Vitamin D Deficiency Investigations: