1.

Describe the structure of platelets, its dimensions, normal count & life span

*Structure:*

Platelets, also known as thrombocytes, are small, irregularly-shaped cells that play a crucial
role in blood clotting. They are formed from the fragmentation of megakaryocytes in the bone
marrow.

*Components:*

1. *Plasma membrane:* A phospholipid bilayer that surrounds the platelet.

2. *Cytoplasm:* Contains various organelles, such as mitochondria, microtubules, and

granules.

3. *Granules:* Alpha-granules, dense-granules, and lysosomes, which store various chemicals

and proteins involved in clotting.

4. *Cytoskeleton:* Maintains platelet shape and structure.

*Dimensions:*

- Diameter: 2-3 μm (micrometers)

- Thickness: 0.5-1.0 μm

- Volume: 5-10 fl (femtoliters)

*Normal Count:*

- Adult: 150,000-450,000 platelets/μL (microliter) of blood

- Children: 150,000-500,000 platelets/μL

*Life Span:*

- Average life span: 8-12 days

- Circulating platelets are constantly being replaced by new ones produced in the bone marrow.

2.What are the functions of platelets?

Platelets play a vital role in maintaining hemostasis, which is the process of stopping
bleeding when a blood vessel is injured. Here are the main functions of platelets:

1. *Blood Clotting*: Platelets aggregate and form a platelet plug to seal the injured blood
vessel, which helps to stop bleeding.

2. *Adhesion*: Platelets adhere to the damaged blood vessel wall, which helps to initiate the
clotting process.

3. *Aggregation*: Platelets aggregate with each other, forming a platelet plug that helps to
seal the injured blood vessel.

4. *Release of Chemical Signals*: Platelets release chemical signals, such as adenosine

diphosphate (ADP) and thromboxane A2, which attract more platelets to the site of injury and
promote clotting.

5. *Formation of Fibrin Clot*: Platelets provide a surface for the formation of a fibrin clot,
which is a network of fibers that helps to strengthen the platelet plug and stop bleeding.

In summary, platelets play a crucial role in maintaining hemostasis by forming a platelet plug,
releasing chemical signals, and promoting the formation of a fibrin clot to stop bleeding.

3. Describe the steps of thrombopoeises & factors regulating it.

Thrombopoiesis is the process of platelet production, which involves the development of

megakaryocytes in the bone marrow and their eventual fragmentation into platelets. Here are
the steps of thrombopoiesis:

*Steps of Thrombopoiesis:*

1. *Megakaryoblast formation*: Hematopoietic stem cells differentiate into megakaryoblasts.

2. *Megakaryocyte formation*: Megakaryoblasts mature into megakaryocytes, which undergo

endomitosis (multiple rounds of DNA replication without cell division).

3. *Maturation*: Megakaryocytes mature and accumulate platelet-specific granules and

organelles.

4. *Fragmentation*: Mature megakaryocytes extend proplatelets, which break off into

platelets.

5. *Platelet release*: Platelets are released into the circulation.

*Factors Regulating Thrombopoiesis:*

6. *Thrombopoietin (TPO)*: A hormone produced by the liver and kidney that stimulates
megakaryocyte development and platelet production.

7. *Interleukin-3 (IL-3)*: A cytokine that supports the growth and development of

megakaryocytes.

8. *Interleukin-6 (IL-6)*: A cytokine that enhances megakaryocyte maturation and platelet

production.
9. *Stem cell factor (SCF)*: A growth factor that supports the growth and development of
hematopoietic stem cells, including megakaryocytes.

10. *Bone marrow microenvironment*: The bone marrow microenvironment, including stromal
cells and extracellular matrix, provides support and regulation for megakaryocyte
development.

These factors work together to regulate thrombopoiesis and maintain a steady-state platelet
count in the circulation.

4.What are the properties of platelets

Here are the key properties of platelets:

1. _Anucleate cells_: Platelets are small, irregularly-shaped cells that lack a nucleus.

2. _Small size_: Platelets are approximately 2-3 μm in diameter.

3. _Short lifespan_: Platelets have a short lifespan of 8-12 days.

4. _High surface-to-volume ratio_: Platelets have a high surface-to-volume ratio, allowing them
to interact with other cells and surfaces.

5. _Adhesive properties_: Platelets have adhesive properties, allowing them to stick to other
platelets, endothelial cells, and subendothelial surfaces.

6. _Aggregation properties_: Platelets can aggregate with each other, forming a platelet plug.

7. _Release of granule contents_: Platelets release granule contents, such as ADP, ATP, and
calcium, upon activation.

8. _Phagocytic activity_: Platelets have limited phagocytic activity, allowing them to engulf
small particles.

9. _Reactive shape change_: Platelets undergo a reactive shape change, becoming more
spherical and developing pseudopodia, upon activation.

10. _Membrane fluidity_: Platelets have a fluid membrane, allowing them to change shape and
interact with other cells.

These properties enable platelets to perform their critical functions in hemostasis, including
adhesion, aggregation, and clot formation.

5.What is haemostasis & what are its steps?

Hemostasis is the process by which the body stops bleeding after an injury. It involves a
complex interplay of cellular and molecular components to form a blood clot and prevent
excessive blood loss.

Here are the steps of hemostasis:

*Step 1: Vasoconstriction (0-30 seconds)*

- The injured blood vessel constricts, reducing blood flow to the area.

- This is mediated by the release of thromboxane A2 and other vasoconstrictors.

*Step 2: Platelet Adhesion (30 seconds-1 minute)*

- Platelets adhere to the injured blood vessel wall, forming a platelet plug.

- This is mediated by the release of von Willebrand factor and other adhesion molecules.

*Step 3: Platelet Activation and Aggregation (1-2 minutes)*

- Platelets become activated, releasing granule contents and expressing surface receptors.

- Activated platelets aggregate with each other, forming a platelet plug.

*Step 4: Coagulation Cascade (2-10 minutes)*

- The coagulation cascade is triggered, involving a series of enzyme-catalyzed reactions.

- The cascade results in the formation of fibrin, a protein that forms a blood clot.

*Step 5: Fibrin Clot Formation (10-30 minutes)*

- Fibrin monomers polymerize to form a fibrin clot.

- The clot is stabilized by the formation of cross-links between fibrin molecules.

*Step 6: Clot Retraction and Remodeling (hours-days)*

- The clot is retracted, pulling the edges of the injured blood vessel together.

- The clot is remodeled, with the formation of new tissue and the removal of dead cells and
debris.

Hemostasis is a critical process that prevents excessive blood loss and promotes healing
after an injury.

6.Enumerate the clotting factors

 Here are the 13 clotting factors, also known as coagulation factors, that play a crucial role in
the blood coagulation cascade:

1. *Factor I (Fibrinogen)*: Converted to fibrin, which forms the blood clot.

2. *Factor II (Prothrombin)*: Converted to thrombin, which activates other clotting factors.

3. *Factor III (Tissue Factor)*: Initiates the extrinsic pathway of coagulation.

4. *Factor IV (Calcium ions)*: Essential for the binding of clotting factors to phospholipid
surfaces.

5. *Factor V*: A cofactor for the conversion of prothrombin to thrombin.

6. *Factor VII*: Activates the extrinsic pathway of coagulation.

7. *Factor VIII*: A cofactor for the activation of factor X.

8. *Factor IX*: Activates the intrinsic pathway of coagulation.

9. *Factor X*: Activates the conversion of prothrombin to thrombin.

10. *Factor XI*: Activates the intrinsic pathway of coagulation.

11. *Factor XII (Hageman factor)*: Initiates the intrinsic pathway of coagulation.

12. *Factor XIII (Fibrin stabilizing factor)*: Stabilizes the fibrin clot.

13. *Von Willebrand factor (VWF)*: A protein that helps platelets adhere to the injured blood
vessel wall.

These clotting factors work together in a complex cascade to form a blood clot and stop
bleeding.

7.Describe the extrinsic pathway for clotting

The extrinsic pathway of blood coagulation is a rapid response to tissue damage, and it's
triggered by the release of tissue factor (TF) from damaged tissue cells.

Here's a step-by-step description of the extrinsic pathway:

1. _Tissue damage_: When tissue is damaged, tissue factor (TF) is released from the
damaged cells.

2. _TF binds to factor VII_: Tissue factor binds to factor VII, forming a TF-FVIIa complex.

3. _Activation of factor VII_: The TF-FVIIa complex activates factor VII to its active form, factor
VIIa.
4. _Activation of factor X_: Factor VIIa activates factor X to its active form, factor Xa.

5. _Activation of prothrombin_: Factor Xa activates prothrombin (factor II) to its active form,
thrombin (factor IIa).

6. _Fibrin formation_: Thrombin converts fibrinogen (factor I) to fibrin, which forms the blood
clot.

The extrinsic pathway is rapid and efficient, and it's triggered by tissue damage. It's also
known as the "tissue factor pathway".

Key players:

- Tissue factor (TF)

- Factor VII

- Factor X

- Prothrombin (factor II)

- Thrombin (factor IIa)

- Fibrinogen (factor I)

The extrinsic pathway converges with the intrinsic pathway at the level of factor X activation,
and from there, the common pathway takes over to form the blood clot.

8. Describe the intrinsic pathway

: The intrinsic pathway of blood coagulation is a complex process that involves the sequential
activation of several clotting factors, ultimately leading to the formation of a blood clot.

Here's a step-by-step description of the intrinsic pathway:

1. _Damage to the vascular endothelium_: The intrinsic pathway is triggered by damage to the
vascular endothelium, which exposes negatively charged surfaces.

2. _Activation of factor XII (Hageman factor)_: Factor XII comes into contact with the
negatively charged surface and becomes activated to factor XIIa.

3. _Activation of factor XI_: Factor XIIa activates factor XI to its active form, factor XIa.

4. _Activation of factor IX_: Factor XIa activates factor IX to its active form, factor IXa.

5. _Activation of factor X_: Factor IXa, in combination with factor VIIIa, activates factor X to its
active form, factor Xa.
6. _Activation of prothrombin_: Factor Xa activates prothrombin (factor II) to its active form,
thrombin (factor IIa).

7. _Fibrin formation_: Thrombin converts fibrinogen (factor I) to fibrin, which forms the blood
clot.

Key players:

- Factor XII (Hageman factor)

- Factor XI

- Factor IX

- Factor VIII

- Factor X

- Prothrombin (factor II)

- Thrombin (factor IIa)

- Fibrinogen (factor I)

The intrinsic pathway is slower than the extrinsic pathway but is still essential for maintaining
hemostasis. It's also known as the "contact activation pathway".

The intrinsic pathway converges with the extrinsic pathway at the level of factor X activation,
and from there, the common pathway takes over to form the blood clot.

9. What is haemophilia, its causes & treatment

Hemophilia is a rare genetic disorder characterized by the inability of blood to clot properly,
leading to prolonged bleeding.

*Types of Hemophilia:*

1. *Hemophilia A (Classic Hemophilia)*: Caused by a deficiency in factor VIII, a clotting factor.

2. *Hemophilia B (Christmas Disease)*: Caused by a deficiency in factor IX, a clotting factor.

*Causes:*

3. *Genetic mutation*: Hemophilia is caused by a mutation in the gene that codes for factor
VIII or factor IX.

4. *Inherited trait*: Hemophilia is usually inherited from one's parents, with the mutated gene
being passed down from mother to son.
5. *Spontaneous mutation*: In some cases, hemophilia can occur due to a spontaneous
mutation in the gene.

*Symptoms:*

6. *Prolonged bleeding*: Hemophilia patients experience prolonged bleeding after injuries,

surgeries, or even spontaneous bleeding.

7. *Joint pain and swelling*: Repeated bleeding into joints can cause pain, swelling, and
eventual joint damage.

8. *Bruising*: Easy bruising is common in hemophilia patients.

*Treatment:*

9. *Replacement therapy*: Infusing the missing clotting factor (factor VIII or factor IX) into the
bloodstream to promote clotting.

10. *Prophylactic treatment*: Regular infusions of clotting factor to prevent bleeding episodes.

11. *On-demand treatment*: Infusing clotting factor in response to a bleeding episode.

12. *Gene therapy*: Experimental treatment aimed at correcting the genetic mutation causing
hemophilia.

*Complications:*

13. *Inhibitor development*: Some patients may develop inhibitors, which are antibodies that
interfere with the replacement therapy.

14. *Joint damage*: Repeated bleeding into joints can cause permanent damage.

15. *Infections*: Hemophilia patients are at risk of contracting infections, such as HIV and
hepatitis, through contaminated blood products.

Early diagnosis and treatment can significantly improve the quality of life for individuals with
hemophilia.

10.What is fibrinolytic system?

The fibrinolytic system is a physiological process that helps to dissolve blood clots (fibrin)
and maintain vascular patency.

_Components of the Fibrinolytic System:_

1. _Plasminogen_: An inactive precursor molecule that is converted to plasmin.

2. _Plasmin_: A proteolytic enzyme that breaks down fibrin clots.

3. _Tissue plasminogen activator (tPA)_: An enzyme that converts plasminogen to plasmin.

4. _Urokinase_: An enzyme that also converts plasminogen to plasmin.

5. _Plasminogen activator inhibitors (PAI)_: Molecules that inhibit the activity of tPA and
urokinase.

6. _Alpha-2 antiplasmin_: A molecule that inhibits the activity of plasmin.

_Process of Fibrinolysis:_

7. _Activation of plasminogen_: tPA or urokinase converts plasminogen to plasmin.

8. _Degradation of fibrin_: Plasmin breaks down fibrin clots into smaller fragments.

9. _Inhibition of plasmin_: Alpha-2 antiplasmin inhibits the activity of plasmin.

_Regulation of Fibrinolysis:_

10. _Balance between activators and inhibitors_: The fibrinolytic system is regulated by a
balance between activators (tPA, urokinase) and inhibitors (PAI, alpha-2 antiplasmin).

11. _Feedback mechanisms_: The fibrinolytic system has feedback mechanisms to prevent
excessive fibrinolysis.

_Dysregulation of Fibrinolysis:_

12. _Thrombotic disorders_: Dysregulation of the fibrinolytic system can lead to thrombotic
disorders, such as deep vein thrombosis.

13. _Bleeding disorders_: Dysregulation of the fibrinolytic system can also lead to bleeding
disorders, such as hemophilia.

The fibrinolytic system plays a crucial role in maintaining vascular health and preventing
thrombotic disorders.

11. What are the functions of factor V, VIII Thrombin, von willibrands factor

Here are the functions of each:

*Factor V:*

1. _Cofactor for factor Xa_: Factor V serves as a cofactor for factor Xa, helping to activate
prothrombin to thrombin.
2. _Acceleration of prothrombin activation_: Factor V accelerates the activation of
prothrombin to thrombin, which is essential for fibrin formation.

3. _Regulation of coagulation_: Factor V helps regulate the coagulation cascade by interacting

with other clotting factors.

*Factor VIII:*

4. _Cofactor for factor IXa_: Factor VIII serves as a cofactor for factor IXa, helping to activate
factor X to factor Xa.

5. _Acceleration of factor X activation_: Factor VIII accelerates the activation of factor X to

factor Xa, which is essential for the coagulation cascade.

6. _Regulation of intrinsic pathway_: Factor VIII helps regulate the intrinsic pathway of
coagulation by interacting with other clotting factors.

*Thrombin (Factor IIa):*

7. _Conversion of fibrinogen to fibrin_: Thrombin converts fibrinogen to fibrin, which forms the
blood clot.

8. _Activation of factor XI and factor V_: Thrombin activates factor XI and factor V, which
helps to amplify the coagulation cascade.

9. _Regulation of coagulation_: Thrombin helps regulate the coagulation cascade by

interacting with other clotting factors.

*Von Willebrand Factor (VWF):*

10. _Adhesion of platelets to damaged vessels_: VWF helps platelets adhere to damaged
blood vessels, which is essential for hemostasis.

11. _Stabilization of factor VIII_: VWF binds to factor VIII, helping to stabilize it and regulate its
activity.

12. _Regulation of platelet function_: VWF helps regulate platelet function by interacting with
platelet receptors.

Each of these factors plays a critical role in the coagulation cascade, and deficiencies or
dysregulation can lead to bleeding or thrombotic disorders.

12. What is the role of vitamin K in haemostasis

Vitamin K plays a crucial role in hemostasis by facilitating the production of clotting factors in
the liver.

_Role of Vitamin K in Hemostasis:_

1. _Gamma-carboxylation_: Vitamin K is necessary for the gamma-carboxylation of glutamic

acid residues on certain proteins, including clotting factors II, VII, IX, and X.

2. _Activation of clotting factors_: The gamma-carboxylation process activates these clotting

factors, allowing them to bind to calcium ions and phospholipid surfaces, which is essential
for blood coagulation.

3. _Regulation of coagulation_: Vitamin K helps regulate the coagulation cascade by ensuring

that the clotting factors are produced in their active forms.

_Consequences of Vitamin K Deficiency:_

4. _Bleeding disorders_: A deficiency in vitamin K can lead to bleeding disorders, such as easy
bruising, nosebleeds, and bleeding gums.

5. _Increased risk of hemorrhage_: Vitamin K deficiency can increase the risk of hemorrhage,
particularly in newborns and individuals with liver disease.

_Food Sources of Vitamin K:_

6. _Leafy green vegetables_: Leafy green vegetables, such as spinach, kale, and broccoli, are
rich in vitamin K.

7. _Fermented foods_: Fermented foods, such as sauerkraut and cheese, are also good
sources of vitamin K.

8. _Fatty fish_: Fatty fish, such as salmon and tuna, are good sources of vitamin K.

Overall, vitamin K plays a critical role in maintaining hemostasis, and a deficiency in this
vitamin can have serious consequences.

13.Why blood does not clot in our body?

There are several reasons why blood doesn't clot inside the body:

1. _Intact endothelium_: The endothelium, a thin layer of cells lining blood vessels, prevents
platelet activation and clotting by releasing anti-thrombotic factors like nitric oxide and
prostacyclin.

2. _Anticoagulant proteins_: Anticoagulant proteins like antithrombin, protein C, and protein S

inhibit the coagulation cascade and prevent clotting.
3. _Fibrinolytic system_: The fibrinolytic system, which includes plasminogen and plasmin,
breaks down any clots that may form.

4. _Blood flow_: The constant flow of blood through vessels helps to prevent clotting by
washing away any activated clotting factors.

5. _Inhibitors of platelet activation_: Inhibitors like prostacyclin and nitric oxide prevent
platelet activation and aggregation.

6. _Thrombomodulin_: Thrombomodulin, a protein on the endothelial surface, binds to

thrombin and activates protein C, which inhibits coagulation.

These mechanisms work together to maintain blood fluidity and prevent unwanted clotting
inside the body.

14.: What is DIC/Disseminated Intravascular coagulation

Disseminated Intravascular Coagulation (DIC) is a complex and life-threatening disorder

characterized by widespread activation of the coagulation cascade, leading to:

1. _Widespread clotting_: Formation of microthrombi in small blood vessels throughout the

body.

2. _Consumption of clotting factors_: Depletion of platelets, fibrinogen, and other clotting

factors, leading to bleeding complications.

3. _Organ dysfunction_: Impaired blood flow to vital organs, causing damage and dysfunction.

_Causes of DIC:_

1. _Sepsis_: Severe infection, often caused by gram-negative bacteria.

2. _Trauma_: Severe injury, such as head trauma or multiple fractures.

3. _Cancer_: Certain types of cancer, like leukemia or lymphoma.

4. _Pregnancy complications_: Placental abruption, amniotic fluid embolism, or preeclampsia.

5. _Snake bites_: Certain snake venoms can trigger DIC.

_Symptoms of DIC:_

1. _Bleeding_: Easy bruising, nosebleeds, or bleeding gums.

2. _Thrombosis_: Formation of blood clots in small blood vessels.

3. _Organ dysfunction_: Impaired function of vital organs, such as kidneys, liver, or lungs.

_Diagnosis of DIC:_

1. _Laboratory tests_: Prothrombin time (PT), activated partial thromboplastin time (aPTT),
fibrinogen level, and platelet count.

2. _Imaging studies_: Ultrasound, CT, or MRI to evaluate organ damage.

_Treatment of DIC:_

1. _Supportive care_: Management of underlying condition, fluid resuscitation, and blood

transfusions.

2. _Anticoagulation therapy_: Heparin or low-molecular-weight heparin to prevent further

clotting.

3. _Fibrinolytic therapy_: Administration of fibrinolytic agents, like tissue plasminogen

activator (tPA), to dissolve clots.

DIC is a medical emergency that requires prompt recognition and treatment to prevent serious
complications and improve outcomes.

15. What is Thromboembolism & its causes

Thromboembolism is a condition where a blood clot (thrombus) forms in a blood vessel and
breaks loose, traveling through the bloodstream and lodging in another vessel, blocking blood
flow.

_Types of Thromboembolism:_

1. _Deep Vein Thrombosis (DVT)_: A clot forms in a deep vein, typically in the legs.

2. _Pulmonary Embolism (PE)_: A clot breaks loose and travels to the lungs, blocking blood flow.

3. _Arterial Thromboembolism_: A clot forms in an artery and breaks loose, traveling to another
artery and blocking blood flow.

_Cause of Thromboembolism:_

4. _Blood stasis_: Prolonged immobility, surgery, or trauma can cause blood to pool and clot.
5. _Hypercoagulability_: Conditions like cancer, genetic disorders, or medications can increase
the risk of clotting.

6. _Vessel wall damage_: Trauma, surgery, or conditions like atherosclerosis can damage blood
vessels and increase the risk of clotting.

7. _Cardiovascular disease_: Conditions like heart failure, atrial fibrillation, or myocardial

infarction can increase the risk of thromboembolism.

8. _Genetic disorders_: Conditions like factor V Leiden, protein C deficiency, or antithrombin

deficiency can increase the risk of thromboembolism.

9. _Medications_: Certain medications, such as birth control pills, hormone replacement therapy,
or chemotherapy, can increase the risk of thromboembolism.

10. _Other medical conditions_: Conditions like obesity, smoking, or chronic inflammation can
also increase the risk of thromboembolism.

It's essential to identify and manage risk factors to prevent thromboembolism.

16. Enumerate the test done to detect bleeding disorders along with their normal
values

Here are some common tests used to detect bleeding disorders, along with their normal
values:

1. _Complete Blood Count (CBC)_:

- Hemoglobin (Hb): 13.5-17.5 g/dL (male), 12-16 g/dL (female)

- Hematocrit (Hct): 40-54% (male), 37-48% (female)

- Platelet count: 150,000-450,000/μL

2. _Prothrombin Time (PT)_:

- Normal value: 11-14 seconds

- INR (International Normalized Ratio): 0.8-1.2

3. _Activated Partial Thromboplastin Time (aPTT)_:

- Normal value: 25-35 seconds

4. _Bleeding Time (BT)_:

 - Normal value: 2-7 minutes

5. _Platelet Function Tests_:

- Platelet aggregation: Normal aggregation curve

- Platelet adhesion: Normal adhesion to collagen or other surfaces

6. _Coagulation Factor Assays_:

- Factor VIII: 50-150% of normal

- Factor IX: 50-150% of normal

- Factor XI: 50-150% of normal

- Factor XII: 50-150% of normal

7. _Von Willebrand Factor (VWF) Assays_:

- VWF antigen: 50-150% of normal

- VWF activity (ristocetin cofactor): 50-150% of normal

8. _Fibrinogen Assay_:

- Normal value: 200-400 mg/dL

9. _Thrombin Time (TT)_:

- Normal value: 10-15 seconds

10. _Reptilase Time (RT)_:

- Normal value: 15-25 seconds

Note: Normal values may vary slightly depending on the laboratory and the specific test used.

17.Name the anticoagulants, their mechanism of action & use

Here are some common anticoagulants, their mechanism of action, and their uses:

1. *Warfarin*

- Mechanism: Inhibits vitamin K-dependent clotting factors (II, VII, IX, X)

- Use: Prevention and treatment of deep vein thrombosis, pulmonary embolism, and atrial
fibrillation

2. *Heparin*
 - Mechanism: Enhances antithrombin III activity, inhibiting thrombin and factor Xa

- Use: Treatment of acute coronary syndromes, deep vein thrombosis, and pulmonary
embolism

3. *Low-Molecular-Weight Heparin (LMWH)*

- Mechanism: Similar to heparin, but with more predictable anticoagulation

- Use: Prevention and treatment of deep vein thrombosis, pulmonary embolism, and acute
coronary syndromes

4. *Fondaparinux*

- Mechanism: Inhibits factor Xa

- Use: Prevention of deep vein thrombosis in patients undergoing major orthopedic surgery

5. *Rivaroxaban*

- Mechanism: Directly inhibits factor Xa

- Use: Prevention of deep vein thrombosis, pulmonary embolism, and stroke in patients with
atrial fibrillation

6. *Apixaban*

- Mechanism: Directly inhibits factor Xa

- Use: Prevention of deep vein thrombosis, pulmonary embolism, and stroke in patients with
atrial fibrillation

7. *Dabigatran*

- Mechanism: Directly inhibits thrombin

- Use: Prevention of deep vein thrombosis, pulmonary embolism, and stroke in patients with
atrial fibrillation

8. *Edoxaban*

- Mechanism: Directly inhibits factor Xa

- Use: Prevention of deep vein thrombosis, pulmonary embolism, and stroke in patients with
atrial fibrillation

9. *Argatroban*

- Mechanism: Directly inhibits thrombin

 - Use: Treatment of heparin-induced thrombocytopenia and as an anticoagulant in patients
with heparin allergy

10. *Bivalirudin*

- Mechanism: Directly inhibits thrombin

- Use: Treatment of acute coronary syndromes and as an anticoagulant in patients

undergoing percutaneous coronary intervention

Note: This is not an exhaustive list, and the uses of these anticoagulants may vary depending
on the specific clinical scenario and guidelines.

18.: How is Blood stored in Blood Banks? What is preservation injury?

Blood storage in blood banks involves several steps to ensure the quality and safety of the
blood components.

_Blood Collection and Processing:_

1. Blood is collected from donors into sterile bags containing anticoagulant-preservative

solutions.

2. The blood is then processed into various components, such as:

- Whole blood

- Red blood cells (RBCs)

- Plasma

- Platelets

- Cryoprecipitate

_Blood Storage:_

3. RBCs are stored at 2-6°C in refrigerators with a shelf life of up to 35-42 days.

4. Plasma is stored at -25°C or lower in freezers with a shelf life of up to 1 year.

5. Platelets are stored at 20-24°C in agitators with a shelf life of up to 5-7 days.

6. Cryoprecipitate is stored at -25°C or lower in freezers with a shelf life of up to 1 year.

_Preservation Injury:_

Preservation injury refers to the damage that occurs to blood cells during storage, leading to a
decrease in their viability and function.
_Types of Preservation Injury:_

1. _Metabolic changes_: RBCs undergo metabolic changes, such as a decrease in ATP and 2,3
-BPG levels.

2. _Oxidative damage_: RBCs are susceptible to oxidative damage, leading to hemolysis.

3. _Cell membrane changes_: RBCs undergo changes in their cell membrane, leading to a
decrease in deformability.

4. _Apoptosis_: RBCs can undergo apoptosis, leading to a decrease in their viability.

_Strategies to Minimize Preservation Injury:_

5. _Optimized storage conditions_: Maintaining optimal storage temperatures, humidity, and

agitation.

6. _Additives and preservatives_: Using additives and preservatives, such as adenine and
mannitol, to maintain RBC viability.

7. _Improved storage media_: Developing improved storage media that mimic the natural
environment of RBCs.

8. _Reducing storage duration_: Minimizing the storage duration of blood components to

reduce the risk of preservation injury.

19.Enumerate the Blood group systems along with their agglutinogens. What is the
importance of Blood groups?

Here are the main blood group systems, their agglutinogens, and the importance of blood
groups:

_Blood Group Systems:_

1. _ABO Blood Group System_

- Agglutinogens: A and B antigens

- Importance: Determines compatibility for blood transfusions

2. _Rh Blood Group System_

- Agglutinogens: RhD, RhC, RhE, Rhc, and RhE antigens

- Importance: Determines compatibility for blood transfusions and can cause hemolytic
disease of the newborn (HDN)

3. _Kell Blood Group System_

 - Agglutinogens: K1, K2, K3, and K4 antigens

- Importance: Can cause hemolytic transfusion reactions and HDN

4. _MNS Blood Group System_

- Agglutinogens: M, N, S, and s antigens

- Importance: Can cause hemolytic transfusion reactions

5. _Duffy Blood Group System_

- Agglutinogens: Fya and Fyb antigens

- Importance: Can cause hemolytic transfusion reactions

6. _P Blood Group System_

- Agglutinogens: P1 antigen

- Importance: Can cause hemolytic transfusion reactions

7. _Lewis Blood Group System_

- Agglutinogens: Lea and Leb antigens

- Importance: Can cause hemolytic transfusion reactions

8. _I Blood Group System_

- Agglutinogens: I antigen

- Importance: Can cause hemolytic transfusion reactions

_Importance of Blood Groups:_

1. _Blood Transfusions_: Blood groups determine compatibility for blood transfusions, and
mismatched transfusions can lead to severe reactions or even death.

2. _Pregnancy and Childbirth_: Blood groups can affect pregnancy and childbirth, particularly
in cases of Rh incompatibility, which can cause HDN.

3. _Forensic Medicine_: Blood groups can be used in forensic medicine to identify individuals
and solve crimes.

4. _Genetic Studies_: Blood groups can provide valuable information for genetic studies and
research.
5. _Transplantation_: Blood groups can affect the success of organ and tissue transplantation.

In summary, blood groups play a critical role in ensuring safe blood transfusions, preventing
hemolytic disease of the newborn, and providing valuable information for genetic studies,
forensic medicine, and transplantation.

20.What are agglutinogens, agglutinin their types & agglutination reaction?

How are agglutinogens formed

Excellent questions!

_Agglutinogens:_

Agglutinogens are antigens present on the surface of red blood cells (RBCs) that can trigger
an immune response, leading to the production of antibodies. These antibodies can then bind
to the agglutinogens, causing the RBCs to clump together, a process known as agglutination.

_Agglutinins:_

Agglutinins are antibodies that bind to agglutinogens, causing agglutination. There are two
types of agglutinins:

1. *Natural agglutinins*: These are antibodies that are present in an individual's blood without
any prior exposure to the corresponding antigen. Examples include anti-A and anti-B
antibodies in individuals with type O blood.

2. *Immune agglutinins*: These are antibodies that are produced in response to exposure to a
specific antigen. Examples include antibodies produced in response to blood transfusions or
pregnancy.

_Types of Agglutinins:_

There are several types of agglutinins, including:

1. *Isoagglutinins*: These are antibodies that react with antigens present on the surface of
RBCs from another individual of the same species.

2. *Heteroagglutinins*: These are antibodies that react with antigens present on the surface of
RBCs from a different species.

3. *Autoagglutinins*: These are antibodies that react with antigens present on the surface of
one's own RBCs.
_Agglutination Reaction:_

The agglutination reaction occurs when agglutinins bind to agglutinogens on the surface of
RBCs, causing the RBCs to clump together. This reaction can be observed in various
laboratory tests, such as:

1. *Blood typing*: To determine an individual's blood type (A, B, AB, or O).

2. *Cross-matching*: To ensure compatibility between the blood of a donor and a recipient.

_Formation of Agglutinogens:_

Agglutinogens are formed through the process of glycosylation, where carbohydrate

molecules (oligosaccharides) are attached to proteins or lipids on the surface of RBCs. These
carbohydrate molecules determine the specificity of the agglutinogen.

In summary, agglutinogens are antigens present on RBCs that can trigger an immune
response, leading to the production of agglutinins (antibodies). The binding of agglutinins to
agglutinogens causes agglutination, which can be observed in laboratory tests.

21.Where are agglutinogens & agglutinins present

Agglutinogens and agglutinins are present in various locations:

_Agglutinogens:_

1. _Red Blood Cells (RBCs)_: Agglutinogens are present on the surface of RBCs, specifically on
the membrane.

2. _Plasma_: Some agglutinogens, like the ABO blood group antigens, are also present in
plasma.

_Agglutinins:_

1. _Plasma_: Agglutinins are present in plasma, where they can bind to agglutinogens on RBCs.

2. _Serum_: Agglutinins are also present in serum, which is plasma with clotting factors
removed.

3. _Lymphoid tissues_: Agglutinins can also be produced by lymphoid tissues, such as the
spleen and lymph nodes.

_Specific locations for ABO blood group system:_

1. _A antigen_: Present on RBCs of individuals with A or AB blood type.

2. _B antigen_: Present on RBCs of individuals with B or AB blood type.

3. _Anti-A antibody_: Present in plasma of individuals with B or O blood type.

4. _Anti-B antibody_: Present in plasma of individuals with A or O blood type.

It's worth noting that agglutinogens and agglutinins can also be present in other bodily fluids,
such as saliva, urine, and semen, but their presence and significance in these fluids are less
well understood.

22.What is Landsteiners law

Landsteiner's Law, also known as the Landsteiner Rule, states:

"In an individual, the presence of an antigen on red blood cells (RBCs) is accompanied by the
absence of the corresponding antibody in the plasma."

In other words:

1. If an individual has a specific antigen on their RBCs (e.g., A antigen), they will not have the
corresponding antibody (anti-A) in their plasma.

2. Conversely, if an individual has a specific antibody in their plasma (e.g., anti-A), they will not
have the corresponding antigen (A antigen) on their RBCs.

This law was formulated by Karl Landsteiner, an Austrian-American biologist, in 1901, and it
forms the basis of the ABO blood group system.

Landsteiner's Law is essential for:

1. Blood typing: Determining an individual's blood type (A, B, AB, or O) based on the presence
or absence of specific antigens and antibodies.

2. Blood transfusions: Ensuring compatibility between the blood of a donor and a recipient to
prevent adverse reactions.

The law has been widely applied in transfusion medicine and has saved countless lives by
preventing incompatible blood transfusions.

23.What is Bombay Blood group

The Bombay blood group is a rare blood type that was first discovered in 1952 in Bombay
(now Mumbai), India.
Characteristics:_

1. *Lack of H antigen*: Individuals with the Bombay blood group lack the H antigen on their red
blood cells (RBCs).

2. *Lack of A and B antigens*: They also lack the A and B antigens, which are typically present
on RBCs of individuals with A, B, or AB blood types.

3. *Presence of anti-A and anti-B antibodies*: Despite lacking the A and B antigens, individuals
with the Bombay blood group have anti-A and anti-B antibodies in their plasma.

_Consequences:_

1. *Transfusion challenges*: Finding compatible blood for transfusions can be extremely

difficult, as the individual's immune system will react with any blood containing A or B
antigens.

2. *Rare occurrence*: The Bombay blood group is extremely rare, with only a few reported
cases worldwide.

_Genetic basis:_

The Bombay blood group is caused by a mutation in the FUT1 gene, which codes for the
enzyme responsible for adding the H antigen to RBCs.

In summary, the Bombay blood group is a rare and unique blood type characterized by the lack
of H, A, and B antigens, and the presence of anti-A and anti-B antibodies.

24.Name the components of Blood & in which conditions they can be transfused.

Here are the components of blood and the conditions in which they can be transfused:

1. _Whole Blood_:

- Transfusion conditions: Massive bleeding, trauma, surgery, or severe anemia.

- Shelf life: 21-35 days.

2. _Red Blood Cells (RBCs)_:

- Transfusion conditions: Anemia, chronic blood loss, or increased red blood cell destruction.

- Shelf life: 21-35 days.

3. _Platelets_:

- Transfusion conditions: Thrombocytopenia, bleeding disorders, or platelet dysfunction.

 - Shelf life: 3-5 days.

4. _Fresh Frozen Plasma (FFP)_:

- Transfusion conditions: Coagulopathy, bleeding disorders, or liver disease.

- Shelf life: 1 year.

5. _Cryoprecipitate_:

- Transfusion conditions: Hemophilia A, von Willebrand disease, or fibrinogen deficiency.

- Shelf life: 1 year.

6. _Granulocytes_:

- Transfusion conditions: Severe neutropenia or granulocyte dysfunction.

- Shelf life: 24 hours.

7. _Plasma Derivatives_:

- Albumin: Transfusion conditions: Hypoalbuminemia, shock, or liver disease.

- Immunoglobulins: Transfusion conditions: Immunodeficiency disorders or autoimmune

diseases.

These blood components can be transfused in various medical conditions, including:

- Trauma or surgery

- Cancer or chemotherapy

- Chronic anemia or bleeding disorders

- Organ transplantation

- Severe infections or sepsis

- Liver or kidney disease

It's essential to note that blood transfusions should only be performed under the guidance of
a qualified healthcare professional and with proper cross-matching and compatibility testing
to ensure safe and effective transfusion.

25.What is Rh incompatibility? How can it be prevented and how is it treated?

: Rh incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus. This can
lead to the production of anti-Rh antibodies in the mother's blood, which can cross the
placenta and attack the fetus's red blood cells.

_Causes of Rh Incompatibility:_

1. _Rh-negative mother_: The mother has Rh-negative blood, meaning she lacks the RhD
antigen on her red blood cells.

2. _Rh-positive fetus_: The fetus inherits the RhD antigen from the father, making it Rh-positive.

3. _Sensitization_: During pregnancy or childbirth, the mother's immune system is exposed to

the Rh-positive fetal red blood cells, leading to the production of anti-Rh antibodies.

_Consequences of Rh Incompatibility:_

1. _Hemolytic disease of the newborn (HDN)_: The anti-Rh antibodies can cross the placenta
and attack the fetus's red blood cells, leading to anemia, jaundice, and potentially life-
threatening complications.

2. _Fetal anemia_: The destruction of fetal red blood cells can lead to anemia, which can
cause fetal heart failure and other complications.

_Prevention of Rh Incompatibility:_

1. _Rh typing_: Determine the Rh status of the mother and father to identify potential
incompatibility.

2. _Rh immunoglobulin (RhIg)_: Administer RhIg to the mother during pregnancy and after
childbirth to prevent sensitization.

3. _Prenatal monitoring_: Monitor the mother's antibody levels and the fetus's well-being
during pregnancy.

_Treatment of Rh Incompatibility:_

1. _Intrauterine transfusions_: Transfuse compatible red blood cells to the fetus to treat
anemia.

2. _Exchange transfusions_: Perform exchange transfusions after birth to remove the baby's
Rh-positive red blood cells and replace them with Rh-negative cells.

3. _Phototherapy_: Use phototherapy to treat jaundice caused by HDN.

4. _Supportive care_: Provide supportive care, such as oxygen therapy and monitoring, to
manage complications.
In summary, Rh incompatibility can be prevented with proper prenatal care, Rh typing, and
administration of RhIg. If HDN occurs, treatment options include intrauterine transfusions,
exchange transfusions, phototherapy, and supportive care.

26.What are the types of WBC's? What are their normal values & functions? What do
the granules of various granulocytes contain & their functions?

Here's an overview of the types of white blood cells (WBCs), their normal values, functions,
and granule contents:

Types of WBCs:_

1. _Neutrophils_ (45-75% of total WBCs)

- Normal value: 1,800-7,000 cells/μL

- Function: Phagocytosis, bactericidal activity, and inflammation

- Granules: Primary (azurophilic) granules contain myeloperoxidase, lysozyme, and

defensins; secondary (specific) granules contain lactoferrin, collagenase, and gelatinase

2. _Lymphocytes_ (20-40% of total WBCs)

- Normal value: 1,000-4,800 cells/μL

- Function: Immune response, antibody production, and cell-mediated immunity

- No granules

3. _Monocytes_ (5-10% of total WBCs)

- Normal value: 200-900 cells/μL

- Function: Phagocytosis, antigen presentation, and cytokine production

- Granules: Contain lysozyme, acid phosphatase, and esterases

4. _Eosinophils_ (1-4% of total WBCs)

- Normal value: 50-500 cells/μL

- Function: Parasite destruction, allergy, and inflammation

- Granules: Contain major basic protein, eosinophil peroxidase, and eosinophil-derived

neurotoxin

5. _Basophils_ (0.5-1% of total WBCs)

 - Normal value: 20-100 cells/μL

- Function: Histamine release, inflammation, and allergy

- Granules: Contain histamine, heparin, and leukotrienes

_Granules of Granulocytes:_

1. _Primary (azurophilic) granules_: Contain enzymes, antimicrobial peptides, and acid

hydrolases

2. _Secondary (specific) granules_: Contain enzymes, receptors, and other proteins involved in
inflammation and immune response

3. _Tertiary (gelatinase) granules_: Contain enzymes involved in matrix degradation and tissue
remodeling

4. _Secretory vesicles_: Contain cytokines, chemokines, and other signaling molecules

In summary, WBCs play crucial roles in immune defense, inflammation, and tissue repair. Each
type of WBC has distinct functions, granule contents, and normal values, which are essential
for maintaining health and preventing disease.

27.What is monocyte macrophage system & types of macrophages? What is

phagocytosis & describe its steps?

Excellent questions!

_Monocyte-Macrophage System:_

The monocyte-macrophage system is a network of immune cells that play a crucial role in the
defense against infections, inflammation, and tissue repair. Monocytes and macrophages are
two types of cells that belong to this system.

1. _Monocytes_: Monocytes are immature cells that circulate in the blood and mature into
macrophages upon tissue migration.

2. _Macrophages_: Macrophages are mature cells that reside in tissues and play a key role in
phagocytosis, antigen presentation, and cytokine production.

_Types of Macrophages:_

There are several types of macrophages, each with distinct functions:

1. _Tissue-resident macrophages_: Found in various tissues, such as liver (Kupffer cells), lung
(alveolar macrophages), and brain (microglia).

2. _Inflammatory macrophages_: Recruited to sites of inflammation, where they play a key role
in phagocytosis and cytokine production.

3. _Wound-healing macrophages_: Involved in tissue repair and wound healing.

4. _Tumor-associated macrophages_: Found in tumor microenvironments, where they can

promote or inhibit tumor growth.

_Phogocytosis:_

Phagocytosis is the process by which cells engulf and internalize foreign particles, bacteria,
dead cells, or debris.

_Steps of Phagocytosis:_

1. _Recognition_: Phagocytic cells recognize foreign particles or microorganisms through

pattern recognition receptors (PRRs).

2. _Adhesion_: Phagocytic cells adhere to the foreign particle or microorganism.

3. _Engulfment_: Phagocytic cells extend their membranes to engulf the foreign particle or
microorganism.

4. _Internalization_: The engulfed particle or microorganism is internalized into a phagosome.

5. _Fusion with lysosomes_: The phagosome fuses with lysosomes, which contain digestive
enzymes.

6. _Degradation_: The foreign particle or microorganism is degraded by the digestive enzymes.

7. _Elimination_: The degraded material is eliminated from the cell through exocytosis.

In summary, the monocyte-macrophage system plays a vital role in immune defense,

inflammation, and tissue repair. Phagocytosis is a critical process by which cells eliminate
foreign particles and microorganisms, and its steps involve recognition, adhesion, engulfment,
internalization, fusion with lysosomes, degradation, and elimination.
28.What is leucocytosis. Leukopenia. Leukemia & Leukemoid reaction

Here are the definitions and explanations:

_Leucocytosis:_

Leucocytosis is an increase in the total number of white blood cells (WBCs) in the blood. This
can be a response to:

1. Infection (bacterial, viral, or fungal)

2. Inflammation

3. Trauma

4. Stress

5. Certain medications

Normal WBC count: 4,500-11,000 cells/μL

_Leukopenia:_

Leukopenia is a decrease in the total number of WBCs in the blood. This can be caused by:

1. Bone marrow failure

2. Chemotherapy

3. Radiation therapy

4. Infections (e.g., HIV, tuberculosis)

5. Autoimmune disorders

6. Certain medications

Normal WBC count: <4,500 cells/μL

_Leukemia:_

Leukemia is a type of cancer that affects the blood and bone marrow. It is characterized by:

1. Uncontrolled proliferation of abnormal WBCs

2. Disruption of normal blood cell production

3. Accumulation of malignant cells in the bone marrow, blood, and other organs
Types of leukemia:

1. Acute myeloid leukemia (AML)

2. Acute lymphoblastic leukemia (ALL)

3. Chronic myeloid leukemia (CML)

4. Chronic lymphocytic leukemia (CLL)

_Leukemoid Reaction:_

A leukemoid reaction is a benign condition that mimics leukemia, characterized by:

1. A marked increase in WBC count (>50,000 cells/μL)

2. Presence of immature WBCs (e.g., myeloblasts, promyelocytes)

3. Absence of malignant cells

Causes of leukemoid reaction:

1. Severe infection

2. Inflammation

3. Trauma

4. Stress

5. Certain medications

Key differences between leukemia and leukemoid reaction:

1. Malignancy: Leukemia is a malignant condition, while leukemoid reaction is benign.

2. WBC count: Leukemia often presents with a higher WBC count than leukemoid reaction.

3. Immature cells: Leukemia is characterized by the presence of malignant immature cells,

while leukemoid reaction shows immature cells that are not malignant.

29.What is Leukopoeisis & its steps? How is leukopoeisis regulated

Here are the explanations:

_Leukopoiesis:_

Leukopoiesis is the process of producing white blood cells (WBCs) in the bone marrow. It
involves the proliferation, differentiation, and maturation of hematopoietic stem cells into
various types of WBCs.

_Steps of Leukopoiesis:_

1. _Self-renewal of hematopoietic stem cells_: Hematopoietic stem cells divide to produce

more stem cells.

2. _Commitment to myeloid or lymphoid lineage_: Stem cells commit to either the myeloid
(granulocyte, monocyte, and platelet production) or lymphoid (lymphocyte production) lineage.

3. _Proliferation and differentiation_: Committed cells proliferate and differentiate into specific
types of WBCs.

4. _Maturation_: Immature WBCs mature into functional cells.

5. _Release into circulation_: Mature WBCs are released into the bloodstream.

_Regulation of Leukopoiesis:_

Leukopoiesis is regulated by a complex interplay of:

1. _Hematopoietic growth factors_: Cytokines and growth factors, such as granulocyte-colony

stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and
interleukin-3 (IL-3), promote proliferation and differentiation.

2. _Transcription factors_: Proteins that regulate gene expression, such as PU.1 and C/EBPα,
control the commitment to specific lineages.

3. _Stem cell niche_: The bone marrow microenvironment, including stromal cells, osteoblasts,
and endothelial cells, supports hematopoietic stem cell maintenance and differentiation.

4. _Negative regulators_: Inhibitory cytokines, such as tumor necrosis factor-alpha (TNF-α)

and transforming growth factor-beta (TGF-β), regulate leukopoiesis by inhibiting proliferation
and differentiation.

5. _Feedback mechanisms_: The production of WBCs is regulated by feedback mechanisms,

such as the inhibition of G-CSF production by mature neutrophils.

In summary, leukopoiesis is a complex process regulated by a network of growth factors,

transcription factors, stem cell niche, negative regulators, and feedback mechanisms.
30.Define & classify immunity. What is Antigen, complete Antigen & hapten?

Here are the definitions and classifications:

_Immunity:_

Immunity is the body's ability to defend itself against pathogens, such as bacteria, viruses, and
other foreign substances.

_Classification of Immunity:_

1. _Innate Immunity_: Non-specific, immediate defense against infection, including physical

barriers, phagocytic cells, and inflammatory responses.

2. _Adaptive Immunity_: Specific, acquired defense against infection, involving lymphocytes (T

cells and B cells) and the production of antibodies.

_Antigen:_

An antigen is a substance that can stimulate an immune response, resulting in the production
of antibodies or activated immune cells.

_Complete Antigen:_

A complete antigen is a substance that can:

1. Stimulate an immune response

2. React with the resulting antibodies

Examples of complete antigens include proteins, polysaccharides, and viruses.

_Hapten:_

A hapten is a small molecule that can:

1. Bind to an antibody

2. Stimulate an immune response only when attached to a larger carrier molecule

Haptens are typically small molecules, such as drugs or toxins, that are not immunogenic on

their own but can become immunogenic when attached to a carrier protein.

_Examples:_

1. Penicillin is a hapten that can stimulate an immune response when attached to a carrier
protein.

2. Pollen is a complete antigen that can stimulate an immune response on its own.

In summary, immunity is the body's defense against pathogens, and it can be classified into
innate and adaptive immunity. Antigens are substances that stimulate an immune response,
and they can be complete antigens or haptens.

31. What are the nonspecific defense mechanisms/innate immunity present in our
body

Here are the nonspecific defense mechanisms/innate immunity present in our body:

*Physical Barriers:*

1. *Skin*: Provides a physical barrier against external pathogens

2. *Mucous membranes*: Traps pathogens and prevents them from entering the body

3. *Eye lashes and tears*: Protects the eyes from pathogens

4. *Nose hairs and mucous*: Filters out pathogens from the air we breathe

*Chemical Barriers:*

5. *Lysozyme*: An enzyme in tears, saliva, and mucus that breaks down bacterial cell walls

6. *Acidic pH*: The acidic environment of the skin and stomach inhibits the growth of many
pathogens

7. *Antimicrobial peptides*: Small peptides that kill or inhibit the growth of pathogens

*Cellular Defense Mechanisms:*

8. *Neutrophils*: Phagocytic cells that engulf and kill pathogens

9. *Macrophages*: Phagocytic cells that engulf and kill pathogens, and also present antigens
to lymphocytes

10. *Dendritic cells*: Antigen-presenting cells that activate lymphocytes

11. *Natural killer cells*: Cells that recognize and kill infected cells or tumor cells

*Inflammatory Response:*

12. *Increased blood flow*: Brings white blood cells and nutrients to the site of infection
13. *Increased permeability*: Allows white blood cells to leave the bloodstream and enter the
infected tissue

14. *Chemical signals*: Cytokines and chemokines that attract white blood cells to the site of
infection

*Complement System:*

15. *A group of proteins*: That work together to help eliminate pathogens from the body

16. *Enhances phagocytosis*: Helps neutrophils and macrophages engulf and kill pathogens

17. *Lyses pathogens*: Directly kills pathogens by forming a membrane attack complex

These nonspecific defense mechanisms/innate immunity provide immediate protection

against infection and play a crucial role in activating the adaptive immune response.

32.What is acquired immunity and its types?

: Acquired immunity is a type of immunity that is developed after exposure to a specific

antigen, either through infection or immunization. It is also known as specific immunity.

_Types of Acquired Immunity:_

1. *Active Immunity*: The body produces antibodies in response to direct exposure to an

antigen, either through infection or immunization. Examples include:

- Recovery from an infectious disease (e.g., chickenpox)

- Vaccination (e.g., MMR vaccine)

2. *Passive Immunity*: Antibodies are transferred from one individual to another, providing
temporary protection. Examples include:

- Mother's antibodies passed to her baby through breast milk or placenta

- Administration of immunoglobulins (antibodies) to prevent or treat infections

3. *Cell-Mediated Immunity*: T cells (T lymphocytes) play a key role in recognizing and

eliminating infected cells or producing chemical signals that activate the immune response.

4. *Humoral Immunity*: B cells (B lymphocytes) produce antibodies that recognize and bind to
specific antigens, marking them for destruction.

_Characteristics of Acquired Immunity:_

1. *Specificity*: Acquired immunity is specific to the antigen that triggered the response.

2. *Adaptability*: The immune system can adapt to new antigens and remember previous
encounters.

3. *Memory*: Acquired immunity often involves immunological memory, allowing for a rapid
response to future exposures.

4. *Duration*: Acquired immunity can provide long-term protection, but its duration varies
depending on the antigen and individual factors.

In summary, acquired immunity is a specific and adaptive type of immunity that develops after
exposure to an antigen, and it can be categorized into active, passive, cell-mediated, and
humoral immunity.

33.: How are T and B lymphocytes processed

T and B lymphocytes, also known as T cells and B cells, are processed in the following ways:

*T Cell Processing:*

1. *Origin*: T cells originate from hematopoietic stem cells in the bone marrow.

2. *Migration*: Immature T cells migrate to the thymus, where they undergo maturation and
selection.

3. *Positive Selection*: T cells that recognize self-MHC (Major Histocompatibility Complex)

molecules are selected to survive.

4. *Negative Selection*: T cells that recognize self-antigens are eliminated to prevent

autoimmunity.

5. *Maturation*: T cells mature into naive T cells, which then circulate in the blood and
lymphoid organs.

6. *Activation*: Naive T cells are activated by antigen-presenting cells (APCs), such as

dendritic cells, which present antigens on their surface.

*B Cell Processing:*

7. *Origin*: B cells originate from hematopoietic stem cells in the bone marrow.

8. *Maturation*: B cells mature in the bone marrow, where they undergo V(D)J recombination
to generate a unique antibody repertoire.
9. *Selection*: B cells that produce self-reactive antibodies are eliminated to prevent
autoimmunity.

10. *Activation*: Naive B cells are activated by antigens, which bind to their surface antibodies.

11. *Class Switching*: Activated B cells undergo class switching, which allows them to
produce different classes of antibodies (e.g., IgG, IgA, IgE).

12. *Affinity Maturation*: Activated B cells undergo affinity maturation, which involves
somatic hypermutation and selection of high-affinity antibodies.

*Shared Processing Steps:*

13. *Antigen Presentation*: Both T and B cells require antigen presentation by APCs to
become activated.

14. *Co-Stimulation*: Both T and B cells require co-stimulation by APCs to become fully
activated.

15. *Cytokine Signaling*: Both T and B cells respond to cytokine signals, which help regulate
their activation, proliferation, and differentiation.

In summary, T and B lymphocytes undergo distinct processing steps, including maturation,

selection, activation, and differentiation. However, they also share common processing steps,
such as antigen presentation, co-stimulation, and cytokine signaling.

34.: What are thymus dependent and thymus independent antigens.

Thymus-dependent (TD) and thymus-independent (TI) antigens are classifications of antigens

based on their ability to stimulate an immune response with or without the help of T cells.

*Thymus-Dependent (TD) Antigens:*

TD antigens require the help of T cells to stimulate an immune response. Characteristics:

1. *Protein antigens*: Typically proteins or protein conjugates.

2. *T cell activation*: Require T cell activation to induce an immune response.

3. *Antibody class switching*: Induce class switching from IgM to IgG, IgA, or IgE.

4. *Immunological memory*: Induce immunological memory, allowing for a rapid response to

future exposures.

5. *Examples*: Tetanus toxoid, diphtheria toxoid, and most viral antigens.

*Thymus-Independent (TI) Antigens:*

TI antigens can stimulate an immune response without the help of T cells. Characteristics:

1. *Polysaccharide antigens*: Typically polysaccharides or lipopolysaccharides.

2. *B cell activation*: Directly activate B cells without T cell help.

3. *IgM production*: Primarily induce IgM antibody production.

4. *No immunological memory*: Do not induce immunological memory.

5. *Examples*: Pneumococcal polysaccharides, meningococcal polysaccharides, and

lipopolysaccharides from Gram-negative bacteria.

In summary, TD antigens require T cell help to stimulate an immune response, while TI

antigens can directly activate B cells without T cell help. This distinction is important for
understanding the mechanisms of immune responses and for developing effective vaccines.

35. What are the types of T Cells and their role in immunity

T cells, also known as T lymphocytes, play a central role in cell-mediated immunity. There are
several types of T cells, each with distinct functions:

1. *Cytotoxic T Cells (CD8+ T Cells)*:

- Recognize and kill infected cells or tumor cells.

- Release cytotoxins, such as perforin and granzymes, to induce cell death.

2. *Helper T Cells (CD4+ T Cells)*:

- Assist in activating B cells and other immune cells.

- Produce cytokines, such as IL-2 and IL-4, to coordinate immune responses.

- Subtypes:

- Th1 cells: Produce IFN-γ and promote cell-mediated immunity.

- Th2 cells: Produce IL-4 and promote humoral immunity.

- Th17 cells: Produce IL-17 and promote inflammation.

3. *Memory T Cells*:

- Remember specific antigens and can quickly respond to future infections.

- Can differentiate into effector T cells upon re-exposure to the antigen.

4. *Regulatory T Cells (Tregs)*:

- Suppress excessive or inappropriate immune responses.

- Maintain immune tolerance to self-antigens and prevent autoimmunity.

5. *Natural Killer T Cells (NKT Cells)*:

- Recognize lipid antigens presented by CD1d molecules.

- Produce cytokines and activate immune cells to fight infections.

6. *Gamma Delta T Cells (γδ T Cells)*:

- Recognize non-peptide antigens, such as lipids and phospholipids.

- Play a role in innate immunity and inflammation.

In summary, T cells are a diverse group of immune cells that play crucial roles in cell-mediated
immunity, including recognizing and killing infected cells, activating immune responses, and
regulating immune tolerance.

36. What are natural killer cells and their functions

Natural killer (NK) cells are a type of lymphocyte that plays a crucial role in the innate immune
system.

_Characteristics:_

1. _Large granular lymphocytes_: NK cells are characterized by their large size and granular
appearance.

2. _CD56+ and CD16+_: NK cells express the CD56 and CD16 surface markers.

3. _Non-MHC restricted_: NK cells do not require major histocompatibility complex (MHC)

molecules to recognize and kill target cells.

_Functions:_

1. _Tumor cell recognition and killing_: NK cells recognize and kill tumor cells that lack MHC
class I expression.

2. _Viral infected cell recognition and killing_: NK cells recognize and kill cells infected with
viruses, such as herpesvirus and cytomegalovirus.

3. _Bacterial infected cell recognition and killing_: NK cells recognize and kill cells infected
with bacteria, such as Listeria and Salmonella.
4. _Cytokine production_: NK cells produce cytokines, such as IFN-γ and TNF-α, which activate
immune responses.

5. _Antibody-dependent cellular cytotoxicity (ADCC)_: NK cells can kill target cells that are
opsonized with antibodies.

_Activation and regulation:_

1. _IL-2 and IL-15_: NK cells are activated by IL-2 and IL-15, which are produced by T cells and
dendritic cells.

2. _Inhibitory receptors_: NK cells express inhibitory receptors, such as KIR and NKG2A, which
regulate their activity.

3. _Activating receptors_: NK cells express activating receptors, such as NKG2D and CD16,
which activate their cytotoxic activity.

In summary, NK cells are a critical component of the innate immune system, recognizing and
killing tumor cells, virally infected cells, and bacterial infected cells, while also producing
cytokines and participating in ADCC.

37.Describe cell mediated immunity

Cell-mediated immunity (CMI) is a type of immune response that involves the activation of
immune cells, such as T cells and macrophages, to defend against infections and diseases.

_Characteristics:_

1. _Cellular response_: CMI involves the activation of immune cells, rather than the production
of antibodies.

2. _T cell-mediated_: T cells, particularly CD4+ and CD8+ T cells, play a central role in CMI.

3. _Antigen-specific_: CMI is specific to the antigen that triggered the response.

4. _Memory_: CMI can provide long-term immunity through the formation of memory T cells.

_Mechanisms:_

1. _Antigen presentation_: Antigens are presented to T cells by antigen-presenting cells

(APCs), such as dendritic cells and macrophages.

2. _T cell activation_: T cells recognize and respond to antigens presented by APCs, leading to
their activation and proliferation.
3. _Cytokine production_: Activated T cells produce cytokines, which coordinate the immune
response and activate other immune cells.

4. _Cell-mediated killing_: Activated T cells, such as CD8+ T cells, can directly kill infected cells
or produce cytotoxins to eliminate pathogens.

_Types of CMI:_

1. _Delayed-type hypersensitivity (DTH)_: A type of CMI that involves the activation of T cells
and macrophages to eliminate pathogens.

2. _Cell-mediated cytotoxicity_: A type of CMI that involves the direct killing of infected cells by
activated T cells.

_Importance:_

1. _Defense against intracellular pathogens_: CMI is essential for defending against

intracellular pathogens, such as viruses and bacteria.

2. _Tumor immunity_: CMI plays a crucial role in tumor immunity, with activated T cells
recognizing and eliminating cancer cells.

3. _Transplant rejection_: CMI is involved in transplant rejection, with activated T cells

recognizing and responding to foreign tissues.

In summary, cell-mediated immunity is a critical component of the immune system, involving

the activation of T cells and other immune cells to defend against infections and diseases.

38.What do you mean by T cell ontogeny

T cell ontogeny refers to the developmental process by which T cells mature from
hematopoietic stem cells in the bone marrow to become functional immune cells.

_Steps involved in T cell ontogeny:_

1. *Hematopoietic stem cell commitment*: Hematopoietic stem cells commit to the T cell
lineage.

2. *Pro-T cell formation*: Pro-T cells are formed in the bone marrow and begin to express T
cell-specific genes.

3. *Thymus migration*: Pro-T cells migrate to the thymus, where they undergo further
development.

4. *Thymocyte formation*: Pro-T cells differentiate into thymocytes, which undergo V(D)J
recombination to generate a diverse T cell receptor (TCR) repertoire.

5. *Positive selection*: Thymocytes that recognize self-MHC molecules are positively selected
to survive.

6. *Negative selection*: Thymocytes that recognize self-antigens are negatively selected to

undergo apoptosis.

7. *Maturation*: Surviving thymocytes mature into single-positive CD4+ or CD8+ T cells.

8. *Export to periphery*: Mature T cells are exported to the periphery, where they circulate and
respond to antigens.

_Key events in T cell ontogeny:_

1. *TCR gene rearrangement*: V(D)J recombination generates a unique TCR repertoire.

2. *Thymic selection*: Positive and negative selection shape the T cell repertoire.

3. *Maturation*: T cells mature and acquire functional competence.

_Dysregulation of T cell ontogeny:_

1. *Immunodeficiency*: Impaired T cell development can lead to immunodeficiency.

2. *Autoimmunity*: Abnormal T cell selection can contribute to autoimmunity.

3. *Cancer*: Dysregulation of T cell development can contribute to cancer.

In summary, T cell ontogeny is the complex process by which T cells develop from
hematopoietic stem cells to become functional immune cells.

39.What are cytokines, their types and functions

: Cytokines are small proteins released by cells that have a specific effect on the interactions
and communications between cells. They play a crucial role in the immune system, helping to
fight off infections and inflammation.
_Types of Cytokines:_

1. _Interleukins (IL)_: IL-1 to IL-38, involved in various immune responses.

2. _Interferons (IFN)_: IFN-α, IFN-β, and IFN-γ, involved in antiviral and antiproliferative
responses.

3. _Tumor Necrosis Factors (TNF)_: TNF-α and TNF-β, involved in inflammation and cell death.

4. _Colony-Stimulating Factors (CSF)_: Involved in the proliferation and differentiation of

hematopoietic cells.

5. _Chemokines_: Involved in chemotaxis, directing immune cells to sites of infection or

inflammation.

_Functions of Cytokines:_

1. _Immune cell activation_: Cytokines activate immune cells, such as T cells and
macrophages.

2. _Inflammation_: Cytokines promote inflammation, which helps to fight off infections.

3. _Cell growth and differentiation_: Cytokines regulate the growth and differentiation of
immune cells.

4. _Antiviral and antiproliferative responses_: Cytokines, such as interferons, help to fight off
viral infections and regulate cell growth.

5. _Immunomodulation_: Cytokines can modulate the immune response, either enhancing or

suppressing it.

_Examples of Cytokines and their Functions:_

1. _IL-2_: T cell growth and activation.

2. _IFN-γ_: Antiviral and antiproliferative responses.

3. _TNF-α_: Inflammation and cell death.

4. _IL-1β_: Inflammation and immune cell activation.

5. _IL-10_: Immunosuppression and anti-inflammation.

In summary, cytokines are essential signaling molecules that help to coordinate the immune
response, promoting inflammation, immune cell activation, and cell growth and differentiation.

40. What is MHC complex its types mechanism of action & significance.

The Major Histocompatibility Complex (MHC) is a group of genes that play a critical role in
the immune system.

_Types of MHC:_

1. _MHC Class I_: Expressed on the surface of almost all nucleated cells, presenting
endogenously synthesized peptides to CD8+ T cells.

2. _MHC Class II_: Expressed on the surface of antigen-presenting cells (APCs), presenting
exogenously derived peptides to CD4+ T cells.

3. _MHC Class III_: Not directly involved in antigen presentation, but encodes other immune-
related genes.

_Mechanism of Action:_

1. _Antigen Processing_: Proteins from inside the cell or from outside the cell are broken down
into peptides.

2. _Peptide Loading_: The peptides are loaded onto MHC molecules.

3. _MHC-Peptide Complex Formation_: The MHC molecule presents the peptide to T cells.

4. _T Cell Recognition_: T cells recognize the MHC-peptide complex through their T cell
receptor (TCR).

_Significance:_

1. _Transplant Rejection_: MHC mismatch between donor and recipient can lead to transplant
rejection.

2. _Autoimmune Diseases_: MHC molecules can contribute to autoimmune diseases by

presenting self-peptides to autoreactive T cells.

3. _Infectious Diseases_: MHC molecules play a crucial role in presenting peptides from
pathogens to T cells, helping to fight infections.

4. _Cancer_: MHC molecules can present tumor-specific peptides to T cells, helping to

eliminate cancer cells.
_Importance of MHC Diversity:_

1. _Protection against Infectious Diseases_: MHC diversity helps to protect against infectious
diseases by allowing the immune system to recognize and respond to a wide range of
pathogens.

2. _Reduced Risk of Autoimmune Diseases_: MHC diversity can reduce the risk of
autoimmune diseases by minimizing the presentation of self-peptides to autoreactive T cells.

In summary, the MHC complex plays a vital role in the immune system by presenting peptides
to T cells, helping to fight infections, and preventing autoimmune diseases.

41.What is primary & secondary immune response? How are memory cells formed?

Here are the explanations:

_Primary Immune Response:_

The primary immune response occurs when the body encounters a specific antigen for the
first time.

_Characteristics:_

1. _Slow response_: The primary response takes time to develop, typically 3-14 days.

2. _Low antibody levels_: The initial antibody response is weak and consists mainly of IgM
antibodies.

3. _Limited protection_: The primary response provides limited protection against the antigen.

_Secondary Immune Response:_

The secondary immune response occurs when the body encounters the same antigen again.

_Characteristics:_

1. _Rapid response_: The secondary response is faster, typically within hours or days.

2. _High antibody levels_: The secondary response produces higher levels of antibodies,
mainly IgG, IgA, or IgE.

3. _Improved protection_: The secondary response provides improved protection against the
antigen.
_Formation of Memory Cells:_

Memory cells are formed during the primary immune response and play a crucial role in the
secondary immune response.

_Memory B Cells:_

1. _Activated B cells_: During the primary response, activated B cells differentiate into memory
B cells.

2. _Long-lived_: Memory B cells are long-lived and can persist for years or even decades.

3. _Rapid response_: Upon re-exposure to the antigen, memory B cells rapidly differentiate into
antibody-producing plasma cells.

_Memory T Cells:_

1. _Activated T cells_: During the primary response, activated T cells differentiate into memory
T cells.

2. _Long-lived_: Memory T cells are long-lived and can persist for years or even decades.

3. _Rapid response_: Upon re-exposure to the antigen, memory T cells rapidly expand and
differentiate into effector T cells.

In summary, the primary immune response is the initial response to an antigen, while the
secondary immune response is a rapid and more effective response to the same antigen.
Memory cells, including memory B cells and memory T cells, are formed during the primary
response and play a crucial role in the secondary response, providing long-term immunity
against specific antigens.

42.Describe humoral immunity

Humoral immunity is a type of immunity that involves the production of antibodies by B cells
to fight infections.

_Characteristics:_

1. _Antibody-mediated_: Humoral immunity involves the production of antibodies, which are

proteins that recognize and bind to specific antigens.

2. _B cell-mediated_: B cells, also known as B lymphocytes, are the primary cells responsible
for producing antibodies.

3. _Specificity_: Humoral immunity is specific to the antigen that triggered the response.

_Mechanisms:_

1. _Antigen recognition_: B cells recognize antigens through their surface-bound antibodies.

2. _Activation_: Activated B cells differentiate into plasma cells, which produce large amounts
of antibodies.

3. _Antibody production_: Antibodies are produced in response to antigen stimulation and help
to neutralize or remove the antigen.

_Types of Antibodies:_

1. _IgA (Immunoglobulin A)_: Found in mucosal surfaces, such as the respiratory,

gastrointestinal, and genitourinary tracts.

2. _IgD (Immunoglobulin D)_: Found on the surface of mature B cells and plays a role in
antigen recognition.

3. _IgE (Immunoglobulin E)_: Involved in allergic reactions and parasitic infections.

4. _IgG (Immunoglobulin G)_: The most abundant antibody in the blood and provides long-term
immunity.

5. _IgM (Immunoglobulin M)_: The first antibody produced in response to an infection and
provides immediate protection.

_Functions:_

1. _Neutralization_: Antibodies neutralize pathogens by binding to them and preventing their

entry into host cells.

2. _Opsonization_: Antibodies mark pathogens for destruction by phagocytic cells.

3. _Complement activation_: Antibodies activate the complement system, which helps to

eliminate pathogens.

_Importance:_
1. _Protection against infections_: Humoral immunity provides protection against bacterial,
viral, and fungal infections.

2. _Long-term immunity_: Humoral immunity can provide long-term immunity against specific
pathogens.

In summary, humoral immunity is a type of immunity that involves the production of

antibodies by B cells to fight infections. It provides specific protection against pathogens and
can offer long-term immunity.

43. What are the types of antibodies/immunoglobulins released by plasma cells, their
types & functions? What is the mechanism of action of immunoglobulins

Here are the types of antibodies/immunoglobulins, their functions, and mechanism of action:

_Types of Immunoglobulins:_

1. _IgA (Immunoglobulin A)_: Found in mucosal surfaces, such as the respiratory,

gastrointestinal, and genitourinary tracts.

- Functions: Neutralizes pathogens, prevents adhesion to mucosal surfaces.

2. _IgD (Immunoglobulin D)_: Found on the surface of mature B cells.

- Functions: Antigen recognition, activation of B cells.

3. _IgE (Immunoglobulin E)_: Involved in allergic reactions and parasitic infections.

- Functions: Triggers allergic responses, activates eosinophils.

4. _IgG (Immunoglobulin G)_: The most abundant antibody in the blood.

- Functions: Neutralizes pathogens, provides long-term immunity.

5. _IgM (Immunoglobulin M)_: The first antibody produced in response to an infection.

- Functions: Provides immediate protection, activates complement system.

_Mechanism of Action of Immunoglobulins:_

1. _Neutralization_: Immunoglobulins bind to pathogens, preventing their entry into host cells.

2. _Opsonization_: Immunoglobulins mark pathogens for destruction by phagocytic cells.

3. _Complement Activation_: Immunoglobulins activate the complement system, which helps

to eliminate pathogens.
4. _Antibody-Dependent Cellular Cytotoxicity (ADCC)_: Immunoglobulins bind to target cells,
marking them for destruction by immune cells.

5. _Inhibition of Adhesion_: Immunoglobulins prevent pathogens from adhering to host cells.

_Structure of Immunoglobulins:_

1. _Heavy Chain_: Determines the class of immunoglobulin (IgA, IgD, IgE, IgG, IgM).

2. _Light Chain_: Contributes to the antigen-binding site.

3. _Variable Region_: Recognizes and binds to specific antigens.

4. _Constant Region_: Determines the effector functions of the immunoglobulin.

In summary, immunoglobulins are a crucial part of the immune system, providing protection
against pathogens through various mechanisms, including neutralization, opsonization,
complement activation, ADCC, and inhibition of adhesion.

44.What are the types of hypersensitivity reactions

Hypersensitivity reactions are excessive or inappropriate immune responses that can cause
tissue damage and disease. There are four main types of hypersensitivity reactions:

_Type I: Immediate Hypersensitivity (Anaphylactic Hypersensitivity)_

1. _Mediators_: IgE antibodies, histamine, and other chemical mediators.

2. _Mechanism_: IgE antibodies bind to mast cells, triggering the release of histamine and
other mediators, leading to increased vascular permeability, smooth muscle contraction, and
bronchospasm.

3. _Examples_: Anaphylaxis, allergic rhinitis, asthma, and food allergies.

_Type II: Antibody-Dependent Hypersensitivity (Cytotoxic Hypersensitivity)_

1. _Mediators_: IgG and IgM antibodies.

2. _Mechanism_: Antibodies bind to specific antigens on the surface of cells or tissues,

marking them for destruction by complement, neutrophils, or macrophages.

3. _Examples_: Hemolytic disease of the newborn, autoimmune hemolytic anemia, and

Goodpasture's syndrome.
_Type III: Immune Complex Hypersensitivity_

1. _Mediators_: IgG and IgM antibodies, complement.

2. _Mechanism_: Antigen-antibody complexes (immune complexes) form in the circulation,

deposit in tissues, and activate complement, leading to inflammation and tissue damage.

3. _Examples_: Systemic lupus erythematosus, rheumatoid arthritis, and serum sickness.

_Type IV: Delayed-Type Hypersensitivity (Cell-Mediated Hypersensitivity)_

1. _Mediators_: T cells, macrophages, and other immune cells.

2. _Mechanism_: T cells recognize antigens presented by antigen-presenting cells, leading to

the activation of immune cells, which then cause tissue damage and inflammation.

3. _Examples_: Contact dermatitis, tuberculin reaction, and transplant rejection.

In summary, hypersensitivity reactions are classified into four main types based on the
immune mechanisms involved and the timing of the response. Understanding these types is
essential for diagnosing and managing various allergic and autoimmune diseases.

45.Describe complement system & its mechanism of action

: The complement system is a group of proteins that play a crucial role in the immune system
by helping to eliminate pathogens from the body.

Components of the Complement System:_

1. _C1-C9_: These are the main complement proteins, which work together to form the
complement cascade.

2. _C3 convertase_: An enzyme that cleaves C3 into C3a and C3b.

3. _C5 convertase_: An enzyme that cleaves C5 into C5a and C5b.

4. _Membrane attack complex (MAC)_: A complex of proteins that forms pores in the
membranes of target cells.

_Mechanism of Action:_

1. _Activation_: The complement system can be activated through three main pathways: the
classical pathway, the alternative pathway, and the lectin pathway.

2. _C3 convertase formation_: The activation of the complement system leads to the
formation of C3 convertase, which cleaves C3 into C3a and C3b.

3. _C5 convertase formation_: The formation of C5 convertase leads to the cleavage of C5 into
C5a and C5b.

4. _MAC formation_: The formation of MAC leads to the formation of pores in the membranes
of target cells, causing cell lysis.

5. _Inflammation_: The complement system also contributes to inflammation by releasing pro-

inflammatory molecules, such as C3a and C5a.

_Functions of the Complement System:_

1. _Opsonization_: The complement system helps to opsonize pathogens, making them more
susceptible to phagocytosis.

2. _Lysis_: The complement system can lyse pathogens directly through the formation of MAC.

3. _Inflammation_: The complement system contributes to inflammation by releasing pro-

inflammatory molecules.

4. _Immune complex clearance_: The complement system helps to clear immune complexes
from the circulation.

_Regulation of the Complement System:_

1. _Regulatory proteins_: The complement system is regulated by several proteins, including

C1 inhibitor, factor H, and factor I.

2. _Cell surface receptors_: The complement system is also regulated by cell surface
receptors, such as CR1 and CR2.

In summary, the complement system is a complex system of proteins that play a crucial role
in the immune system by helping to eliminate pathogens from the body. Its mechanism of
action involves the activation of a cascade of proteins, leading to the formation of MAC and
the lysis of target cells.

46. How does immunologic tolerance to own tissues develop & what happens when it
fails?

Immunologic tolerance to own tissues, also known as self-tolerance, is the ability of the
immune system to distinguish between self and non-self, preventing an immune response
against the body's own tissues.

_Development of Immunologic Tolerance:_

1. _Central tolerance_: During fetal development, immature immune cells are educated to
recognize self-antigens in the thymus (for T cells) and bone marrow (for B cells).

2. _Negative selection_: Immature immune cells that recognize self-antigens are eliminated or
inactivated, preventing them from entering the peripheral immune system.

3. _Peripheral tolerance_: In the periphery, immune cells are regulated by various mechanisms,
such as anergy, suppression, and clonal deletion, to prevent responses against self-antigens.

_Mechanisms of Peripheral Tolerance:_

1. _Anergy_: Immune cells become unresponsive to self-antigens.

2. _Suppression_: Regulatory immune cells, such as Tregs, suppress responses against self-
antigens.

3. _Clonal deletion_: Immune cells that recognize self-antigens are eliminated.

_Failure of Immunologic Tolerance:_

1. _Autoimmune diseases_: Failure of immunologic tolerance leads to autoimmune diseases,

such as rheumatoid arthritis, lupus, and multiple sclerosis.

2. _Autoinflammatory diseases_: Failure of immunologic tolerance can also lead to

autoinflammatory diseases, such as psoriasis and Crohn's disease.

3. _Transplant rejection_: Failure of immunologic tolerance can lead to transplant rejection, as

the immune system recognizes the transplanted organ as foreign.

_Causes of Failure of Immunologic Tolerance:_

1. _Genetic predisposition_: Genetic mutations can affect the development and function of
immune cells.

2. _Environmental factors_: Environmental factors, such as infections and toxins, can trigger
autoimmune responses.

3. _Hormonal imbalances_: Hormonal imbalances can affect the immune system and lead to
autoimmune diseases.
In summary, immunologic tolerance to own tissues develops through central and peripheral
mechanisms, including negative selection, anergy, suppression, and clonal deletion. Failure of
immunologic tolerance can lead to autoimmune and autoinflammatory diseases, as well as
transplant rejection.

47. Why the foetus does not produce immune response & not rejected by the mother's
body

The fetus does not produce an immune response and is not rejected by the mother's body due
to several mechanisms that ensure immune tolerance:

_Reasons for immune tolerance:_

1. *Genetic similarity*: The fetus shares 50% of its genetic material with the mother, making it
less likely to be recognized as foreign.

2. *Placental barrier*: The placenta acts as a physical barrier, separating the fetal and
maternal circulations, and preventing direct contact between fetal and maternal immune cells.

3. *Immune suppression*: The placenta produces immune-suppressive factors, such as

prostaglandins and cytokines, which inhibit the maternal immune response.

4. *Fetal trophoblasts*: Fetal trophoblasts, which form the outer layer of the placenta, do not
express major histocompatibility complex (MHC) molecules, making it difficult for the
maternal immune system to recognize them as foreign.

5. *Regulatory T cells*: Regulatory T cells (Tregs) are present in the maternal-fetal interface
and help to suppress the maternal immune response.

6. *Cytokine balance*: A balance between pro-inflammatory and anti-inflammatory cytokines

maintains immune tolerance.

7. *Fetal-maternal tolerance*: The fetus produces factors that promote tolerance, such as
human chorionic gonadotropin (hCG), which inhibits the maternal immune response.

_Consequences of immune tolerance:_

1. *Successful pregnancy*: Immune tolerance allows for a successful pregnancy, as the fetus
is not rejected by the mother's immune system.

2. *Fetal development*: Immune tolerance enables the fetus to develop and grow without
being attacked by the maternal immune system.
In summary, the fetus does not produce an immune response and is not rejected by the
mother's body due to a combination of genetic similarity, placental barrier, immune
suppression, and other mechanisms that ensure immune tolerance.

48.What is the etiololgy of AIDS how does it spread & which type of WBCs are infected
in this diseases

AIDS (Acquired Immunodeficiency Syndrome) is a chronic and life-threatening condition

caused by the Human Immunodeficiency Virus (HIV).

_Etiology of AIDS:_

1. _Human Immunodeficiency Virus (HIV)_: HIV is a retrovirus that attacks and weakens the
immune system.

2. _Transmission_: HIV is primarily transmitted through:

- Unprotected sexual contact (vaginal, anal, or oral)

- Sharing contaminated needles or syringes

- Mother-to-child transmission during pregnancy, childbirth, or breastfeeding

- Blood transfusions from an infected donor (rare in developed countries due to screening)

_Spread of HIV:_

1. _Viral replication_: HIV replicates rapidly in the body, targeting immune cells.

2. _Immune system suppression_: HIV infects and destroys CD4+ T cells, weakening the
immune system.

3. _Opportunistic infections_: As the immune system weakens, opportunistic infections and

cancers take advantage, leading to AIDS.

_White Blood Cells (WBCs) infected in AIDS:_

1. _CD4+ T cells (T helper cells)_: HIV primarily infects and destroys CD4+ T cells, which play a
crucial role in coordinating the immune response.

2. _Macrophages_: HIV can also infect macrophages, which are immune cells that engulf and
digest foreign particles and microorganisms.
3. _Dendritic cells_: HIV can infect dendritic cells, which are antigen-presenting cells that help
activate T cells.

_Stages of HIV infection:_

1. _Acute HIV infection_: The initial stage, characterized by flu-like symptoms and high viral
loads.

2. _Clinical latency_: A asymptomatic stage, during which the virus continues to replicate and
the immune system gradually weakens.

3. _AIDS_: The advanced stage, characterized by severe immune system damage and the
occurrence of opportunistic infections and cancers.

In summary, AIDS is caused by the Human Immunodeficiency Virus (HIV), which primarily
infects and destroys CD4+ T cells, weakening the immune system and leading to opportunistic
infections and cancers.

49. What is Di-George syndrome

DiGeorge syndrome, also known as 22q11.2 deletion syndrome, is a rare congenital disorder
characterized by various physical, developmental, and immune system abnormalities.

_Causes:_

1. _Genetic deletion_: A deletion of a small segment of chromosome 22 (22q11.2) leads to the

syndrome.

2. _Inheritance_: The syndrome can be inherited in an autosomal dominant pattern, but most
cases are sporadic.

_Characteristics:_

1. _Congenital heart defects_: Abnormalities in the structure of the heart.

2. _Cleft palate_: A congenital split in the roof of the mouth.

3. _Immune system defects_: Thymic hypoplasia or aplasia, leading to reduced T-cell

production.

4. _Hypocalcemia_: Low levels of calcium in the blood.

5. _Developmental delays_: Delays in speech, language, and cognitive development.

6. _Facial abnormalities_: Characteristic facial features, such as a long face, almond-shaped

eyes, and a prominent nose.

_Immunological features:_

1. _T-cell deficiency_: Reduced T-cell production due to thymic hypoplasia or aplasia.

2. _Increased susceptibility to infections_: Patients are more prone to infections, particularly

those caused by viruses and fungi.

3. _Autoimmune disorders_: Some patients may develop autoimmune disorders, such as

autoimmune hemolytic anemia or thrombocytopenia.

_Diagnosis:_

1. _Genetic testing_: Fluorescence in situ hybridization (FISH) or chromosomal microarray

analysis to detect the 22q11.2 deletion.

2. _Imaging studies_: Echocardiogram, chest X-ray, and other imaging studies to evaluate
congenital heart defects.

3. _Immunological evaluation_: T-cell subset analysis and other immunological tests to

assess immune function.

_Treatment:_

1. _Surgical correction_: Surgery to correct congenital heart defects and other physical
abnormalities.

2. _Immunoglobulin replacement therapy_: Regular infusions of immunoglobulins to replace

deficient antibodies.

3. _Prophylactic antibiotics_: Antibiotics to prevent infections.

4. _Speech and language therapy_: Therapy to address developmental delays and speech
difficulties.

In summary, DiGeorge syndrome is a complex congenital disorder characterized by physical,

developmental, and immune system abnormalities. Early diagnosis and treatment can
significantly improve the quality of life for affected individuals.

50.What is immunization & what are the modes through which if can be achieved?

Immunization is the process by which an individual's immune system is stimulated to produce

a specific response to a particular disease-causing agent, such as a virus or bacteria. This can
be achieved through various modes:

_Modes of Immunization:_

1. *Active Immunization*: Exposure to a weakened or killed form of the disease-causing agent,

which stimulates the immune system to produce antibodies and immune cells.

- Examples: Vaccines, such as MMR, DTaP, and influenza vaccines.

2. *Passive Immunization*: Transfer of pre-formed antibodies from one individual to another,

providing temporary protection.

- Examples: Immunoglobulin injections, such as rabies immunoglobulin, and mother-to-child

transfer of antibodies during breastfeeding.

3. *Herd Immunity*: Indirect protection of a population from an infectious disease when a

sufficient percentage of individuals are immunized, reducing the spread of the disease.

- Examples: Community-wide vaccination programs, such as those for measles and

influenza.

_Types of Vaccines:_

1. *Inactivated Vaccines*: Contain killed or inactivated pathogens.

- Examples: Influenza, HPV, and Hepatitis A vaccines.

2. *Live, Attenuated Vaccines*: Contain weakened or attenuated pathogens.

- Examples: MMR, Varicella, and Rotavirus vaccines.

3. *Conjugate Vaccines*: Combine a weakened pathogen with a carrier protein.

- Examples: Hib, PCV, and MenACWY vaccines.

4. *Subunit Vaccines*: Contain only specific components of a pathogen.

- Examples: Hepatitis B and HPV vaccines.

5. *mRNA Vaccines*: Use messenger RNA to instruct cells to produce a specific protein.
 - Examples: COVID-19 vaccines, such as Pfizer-BioNTech and Moderna.

In summary, immunization can be achieved through active immunization using vaccines,

passive immunization through antibody transfer, or herd immunity through community-wide
vaccination programs. Various types of vaccines are available, each with its own
characteristics and advantages.