Blood Physiology MCQS (for FCPS Part 1)

Blood Physiology MCQs for FCPS Part 1

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These MCQs are taken from the book “FCPs Pretest Series – Physiology”. To purchase this book, click here (the link will open in anew tab)

fcps pretest series physiology

1. Vitamin k is not involved in the synthesis of clotting Factor

A. IX

B. VII

C. X

D. Fibrinogen

E. Prothrombin

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Ans. D

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CLOTTING FACTORS

 

These are the factors that take part in blood clotting (coagulations); these include:.

  1. Fibrinogen
  2. Prothrombin
  3. Tissue thromboplastin
  4. Calcium
  5. Labile factor
  6. Accelerin (functionless)
  7. Stable factor
  8. Antihemophilic factor A
  9. Christmas factor or antihemophilic factor
  10. Stuart prower factor
  11. Plasma thromboplastin antecedent
  12. Hageman factor
  13. Fibrin-stabilizing factor
  14. Prekallikrein
  15. High molecular weight kininogen
  16. Platelets

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    ROLE OF VITAMIN K IN BLOOD COAGULATION

    .

    Vitamin K is needed for the formation of:.

  • Factor II (Prothrombin)
  • Factor VII (antihemophiliv factor A)
  • Factor IX (Christmas factor/antihemophilic factor B)
  • Factor X (stuart prower factor)
  • Protein C and protein S

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2. Antivitaminosis k causes decreased production or Decreased plasma concentration of the following Except

A. Factor IX

B. Factor VII

C. Fibrinogen

D. Prothrombin

E. Steuart- prewer factor

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Ans. C

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3. Most important feature of the platelets is:

A. Count changes after splenectomy

B. Form hemostatic plug when bind to collagen fibers

C. Formed from precursor cells in the bone marrow

D. Granules in their cytoplasm

E. Non-nucleated

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Ans. B (NOTE: The process of hemostasis is important and is frequently tested in exam).

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HEMOSTASIS

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DEFINITION: Prevention of blood loss is called hemostasis.

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STAGES: Hemostasis occurs in two stages: (i) Primary hemostasis (ii) Secondary hemostasis

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  1. Primary hemostasis forms a weak platelet plug and is mediated by interaction between platelets and the vessel wall.
  2. Secondary hemostasis stabilizes the platelet plug and is mediated by the coagulation cascade (extrinsic and intrinsic pathways)

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PRIMARY HEMOSTSIS

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STEP 1: TRANSIENT VASOCONSTRICTION OF DAMAGED VESSEL

 

Transient vasoconstriction of the blood vessel occurs due to endothelin released from the damaged blood vessel (to minimize blood flow and blood loss).

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STEP 2: PLATELET ADHESION TO SURFACE OF DISRUPTED VESSEL

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Von willebrand factor (vWF) binds to the exposed subendothelial collagen.

Platelets bind vWF.

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STEP 3: PLATELET DEGRANULATION

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Adhesion of platelets to vWF induces the release of thromboxane A2 (TXA2) which promotes “platelets aggregation”.

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STEP 4: Platelets Aggregation

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Platelets aggregate at the site of injury by using fibrinogen as a linking molecule, resulting in formation of a weak platelet plug, which is stabilized by secondary hemostasis.

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SECONDARY HEMOSTASIS

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The whole mechanism of secondary hemostasis can be divided into three parts:

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          1. Formation of prothrombin activator (via extrinsic and intrinsic pathways)

          2. Prothrombin activator converts prothrombin into thrombin

          3. Thrombin converts fibrinogen into fibrin threads, which join together to form fibrin meshwork,                which finally converts to a blood clot

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(A) FORMATION OF PROTHROMBIN ACTIVATOR

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Prothrombin activator is formed by two pathways:

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  1. Extrinsic pathway
  2. Intrinsic pathway

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  • EXTRINSIC PATHWAY: Uses factor 7 (MNEMONIC: Extrinsic – sEven)
  • INTRINSIC PATHWAY: Uses factors 8, 9, —–, 11, 12

 

intrinsic and extrinsic pathways

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(a) EXTRINSIC PATHWAY

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  • This pathway is begins with trauma to the vessel wall; the damaged tissue releases tissue thromboplastin (factor 3).

So, it’s important to note that it’s the “tissue thromboplastin” which initiates “extrinsic pathway” (as well as “DIC” – Disseminated intravascular coagulation).

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  • Tissue thromboplastin activates factor 7
  • Activated factor 7 activates:

    .

  • Factor 9 – which activates intrinsic pathway.

Factor 10 – which complexes with phospholipid (of factor 3) and factor 5 to form prothrombin activator.

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(b) INTRINSIC PATHWAY

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  • This pathway begins with trauma to the blood itself or exposure of the platelets to the subendothelial collagen due to damage to the vascular wall. Any of these conditions lead to activation of factor 8 (Hageman factor).

    .

So, it’s important to note that it’s the “factor 8” which initiates “intrinsic pathway”..

  • Activated factor 8 activates factor 9
  • Activated factor 9 activates factor 10
  • Activated factor 10 combines with phospholipid and factor 5 to form prothrombin activator.

    .

It’s important to note that extrinsic and intrinsic pathways converge on factor 10.

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(B) CONVERSION OF PROTHROMBIN TO THROMBIN

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The prothrombin activator converts prothrombin into thrombin.

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(C) CONVERSION OF FIBRINOGEN INTO FIBRIN THREADS

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  • Thrombin acts as a proteolytic enzyme on fibrinogen, resulting in formation of fibrin threads; many fibrin threads join together to form fibrin meshwork.
  • In the early stages, the fibrin threads in fibrin meshwork are held together by weak hydrogen bonds, so the resultant clot is weak and can easily be broken apart.
  • Clotting factor 13 (fibrin stabilizing factor) is present in plasma which causes the formation of strong covalent bonds between the fibrin threads, thus giving tremendous strength to fibrin mesh work, making it more stable.

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FORMATION OF CLOT: Clot is composed of a meshwork of fibrin threads, which entrap platelets, blood cells, and plasma.

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4. Platelet aggregation occurs by

A. Thromboxane A2

B. Prostaglandin

C. Prostacyclin

D. Complement system

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Ans. A

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5. Which of following factor stabilizes fibrin

A. X

B. XI

C. IX

D. III

E. XIII

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Ans. E.

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6. Intrinsic system of the blood clotting:

A. Involves activation of factor VII

B. Involves activation of factor XII by exposure of the blood to the Colleges fibers

C. Is less rapid

D. Is triggered by the release of tissue thromboplastin

E. Requires calcium ions

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Ans. B

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7. Plasma fibrinogen:

A. Concentration affects erythrocyte sedimentation rate

B. Concentration changes in liver diseases

C. Controls movement of fluid across the capillary wall

D. Is involved in the blood clotting

E. Is synthesized in the reticulo-endothelial cells

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Ans. D. Fibrinogen is clotting “factor 1” and is involved in blood clotting.

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8. The following are present in circulating Blood except

A. Prothombin

B. Fibrinogen

C. Thrombin

D. Albumin

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Ans. C. Normally, the blood contains prothrombin (and not thrombin). When coagulation cascade is activated, only then prothrombin is converted into thrombin.

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9. Clotting factor present in both plasma and serum is

a. Factor VIII

b. Thrombin

c. Factor V

d. Factor VII

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Ans. D

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DIFFERENCE BETWEEN PLASMA AND SERUM

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  • The fluid part of the blood is called plasma
  • The fluid which expresses out after clotting of plasma due to clot retraction is called serum. So, in contrast to plasma, serum do not contain clotting factors because it if formed after clotting (clotting factors have been utilized during clotting):

    .

    Serum = Plasma – clotting factors

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  • The only clotting factor present in serum is clotting factor 7

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10. First factor to be lost from stored blood is

A. 2,3 DPG

B. ATP

C. Factor V

D. Factor VII

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Ans. A. Old outdated blood is usually deficient in 2,3-DPG.

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11. Life of platelets is

A. 10 days

B. About 1 week

C. 2-4 days

D. About 1 month

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Ans. A. Life span of RBCs is 120 days, while that of platelets is 10 days. That’s why RBCs last longer than platelets after blood has been transfused into a patient.

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12. Regarding platelets, the following are correct except

A. Are produced by fragmentation from the cytroplasm of the megakaryocytes

B. Interleukin-3 (i1-3) and (i1-6) have thrombopoietic activity

C. Megakaryocytes arise from haemopoietic stem cell

D. Normal platelet life is 120 days

E. Stem cell to platelet production takes 10 days

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Ans. D

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13. Inappropriate for platelets

A) In normal person 20% platelets are abnormal

B) Circulating life span is 33 days

C) On bone marrow megakaryocytes seen

D) Contain ADP and serotonin

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Ans. B

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14. Which of the following statements regarding functions Of the plasma proteins is not correct

A. Albumin serves as carrier for bilirubin

B. Fibrinogen is essential for the blood clothing

C. Plasma colloid osmotic pressure depends mainly upon globulins

D. These act as a buffer

E. These take part in the transport of co2

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Ans. C. Albumin is the most abundant protein in the blood, and hence, plasma colloid osmotic pressure depends mainly upon albumin.

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15. If blood samples from two people are mixed, very often The erythrocytes clump, a process known as Agglutination, as a result of an antigen-antibody Reaction. A woman of blood group 0 rhesus negative

A. Could be a universal recipient

B. Could not have a child that would be affected by rhesus incompatibility

C. Has neither antigen A nor antigen B on the red cells

D. Has no antibodies to the ABO system in her blood

E. Has the most common blood type

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Ans. C

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AGGLUTINOGENS

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DEFINITION: The antigens present on the cell membrane of RBCs, that cause agglutination (blood clotting) on combining with corresponding antibodies (agglutinin), are called agglutinogens.

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TYPES: Agglutinogens are of two types:

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       1. Agglutinogen A

        2. Agglutinogen B

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AGGLUTININS

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DEFINITION: The antibodies (immnoglobulins – IgM or IgG) present in plasma, that cause agglutination on combining with the corresponding agglutinogens, are called agglutinins.

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TYPES: They are of two types:

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               1. Anti-A agglutinin

2. Anti-B agglutinin

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RULES OF ABO BLOOD GROUP NOMENCLATURE

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        RULE 1: The blood groups are named according to the antigens present on RBCs. For example:.

  1. BLOOD GROUP A: A person with blood group A will have antigen A on his RBCs.
  2. BLOOD GROUP B: A person with blood group B will have antigen B on his RBCs.
  3. BLOOD GROUP AB: A person with blood group AB will have both antigens A and B on his RBCs.
  4. BLOOD GROUP O: A person with blood group AB will have neither antigen A nor antigen B on his RBCs.

    .

    RULE 2: Same antigen and its corresponding antibody never exist in blood of the same person (because an antigen reacts with its corresponding antibody, resulting in agglutination, i.e., blood clumping). A person will always have a different antibody to his antigen. For example:

    .

        1. BLOOD GROUP A: A person with blood group A will have antibody B in his plasma.

        2. BLOOD GROUP B: A person with blood group B will have antibody A in his plasma.

        3. BLOOD GROUP AB: A person with blood group AB will have neither antibody A nor antibody B                                                in his plasma.

         4. BLOOD GROUP O: A person with blood group O will have both antibodies A and antibodies B                                                 in his plasma..

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TRANSFUSION REACTIONS

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DEFINITION: Reactions occurring in blood of recipient due to mismatched blood transfusion are called transfusion reactions.

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CONSEQUENCES: Transfusion reaction may result in:.

  1. Agglutination
  2. Hemolysis
  3. Jaundice
  4. Acute kidney shutdown

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    AGGLUTINATION

    .

    DEFINITION: Aggregation of RBCs together into a clump is called agglutination.

    .

    MECHANISM: IgG antibodies has two binding sites and IgM has ten. So, a single antibody can attach two or ten RBCs, thereby causing RBCs to aggregate into a clump.

    .

    RULE FOR AGGLUTINATION: The rule is “antibodies of the recipient will react with it’s corresponding antigens of the donor to cause agglutination”. For example:.

          1. A person with blood group A can be transfused with blood group A because the recepient has                  antibodies B while the donor has antigen A; antibody B will not react with antigen A.

          2. A person with blood group A can not be transfused with blood group B because the recipient h                 as antibodies B while the donor has antigen B; antibodies B will react with antigens B.

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UNIVERSAL RECEPIENT

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Persons with blood group AB are called universal recepients, because they do not have any circulating antibodies in the blood to cause agglutination of the donor’s antigens.

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UNIVERSAL DONOR

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Persons with blood group O are called universal dOnors, because they have no antigens on their RBCs which can react with antibodies of the recipient.

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Table: Blood group antigens and antibodies

Blood group

Antigen (agglutinogen)

Antibody (agglutinin)

A

A

B

B

B

A

AB

AB

O

AB

 

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Rh Factor

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Antigens present on RBCs surface that cause agglutination on mixing with anti-Rh serum are called Rh factors.

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Rh BLOOD TYPES

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There are two types of Rh blood:

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  1. Rh POSITIVE: A person who has Rh D antigens (Rh factor D) on his RBCs (and has no Rh D antibodies in his plasma) is called Rh positive.
  2. Rh NEGATIVE: A person who does not have Rh D antigens on his RBCs (but have Rh D antibodies in this plasma) is called Rh negative.

    .

    Phenotype

    Rh D antigens

    Rh D antibodies

    Rh+

    Present

    Absent

    Rh-

    Absent

    Present

    .

    .

    Rh TRANSFUSION REACTIONS

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    RULE OF Rh TRANSFUSION REACTION: Rh antibodies of the recipient will react with Rh antigens of the donor.

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    Rh POSITIVE RECEPIENT: An Rh positive person has no Rh D antibodies in his blood (to react with Rh antigens), so he may be given both Rh positive and Rh negative blood.

    .

    Rh NEGATIVE RECEPIENT: When Rh positive blood is given to “Rh negative person”, transfusion reaction will occur between Rh antigens of the donor and Rh antibodies of the recipient. This is an example of erythroblastosis fetalis, in which “Rh negative mother” is exposed to Rh positive blood of the fetus.

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    16. Universal recepient

    A. A+ve

    B. AB+ve

    C. AB-ve

    D. 0+ve

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Ans. B

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16.. The Universal donor group is:

A. Awe

B. A -ve

C: AB -ve

D. 0 –ve

E. AB .ve

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Ans. D

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17. In the plasma of blood group ‘A’ person. there are

A. Anti A antibodies

B. Anti AB antibodies

C. Anti B antibodies

D. IgG antibodies

E. No antibodies

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Ans. C. A person with blood group A will have antigen A and antibodies B.

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18. regarding red blood cells following statements are true Except

A. Are formed in yolk sac in early embryonic life

B. Contain agglutinin on their cell membrane

C. Contain haemoglobin which is an important buffer

D. Have a life span of 120 days

E. In reticulocyte stage are stained with cresyle blue

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Ans. B. RBC contain agglutinogens (antigens) on their cell membrane. Agglutinin (antibodies) circulate freely in plasma.

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19. Blood transfusion reaction is likely to occur when a Person having blood group A+ is transfused with blood Of group

A. A+

B. A-

C. AB-

D. O-

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Ans. C. The rule is “antibodies of the recipient will react with antigens of the donor”. Blood group A+ will have antibodies B and no Rh antibodies.

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[Option A] – A+ blood group has antigen A and Rh antigen, which will not react with antibodies B of the recipient.

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[Option B] – A- blood will have antigen A and no Rh antigens, so it will not react with antibodies B.

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[Option C] – AB- blood will have antigens A and B, and no Rh antigen, so antigen B of the donor will react with antibodies B of the recipient.

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[Option D] – O- Blood (universal donor) has no antigens at all, so it will not react with blood of the recipient.

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20. A young woman in the labor room requires blood Transfusion. Her blood samples sent to the laboratory for “group & cross match”. The laboratory technician reports That “her red cells are agglutinated by antisera – A & D While her serum is agglutinating B cells”. The most suitable Blood donor for her would be

A. Blood group A negative

B. Blood group A positive

C. Blood group AB positive

D. Blood group 0 negative

E blood group 0 positive

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Ans. B. ABO BLOOD GROUP: If the patient’s blood is agglutinated by antibodies (antibodies are also called anitisera) A, it means that the patient’s blood contain antigen A. A person having antigen A will have blood group A.

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Rh BLOOD GROUP: If the patient’s blood is agglutinated by antibody D (Rh antigen), it means that the patient has Rh antigen (Rh factor D). A person having Rh antigen is Rh positive.

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21. A male with A+ (Ao,DD) Blood group, married to a female having B+ (Bo,Dd ) blood group. Children can have all blood groups except

a. AB +ve

b. AB -ve

c. A + ve

d. B +ve

e. 0 +ve

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Ans. B

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GENETIC DETERMINATION OF ABO BLOOD GROUPS

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– There are three types of genes which determine antigens of the ABO blood group system:

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  • GENE o: Type o gene does not produce any antigen
  • GENE A: Type A gene produces antigen A.
  • GENE B: Type B gene produces antigen B.

– Every person gets two genes, one from the father and one from the mother.

– There are six possible combinations of genes.

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Gene A

Gene B

Gene o

Gene A

AA

AB

oA

Gene B

AB

BB

oB

Gene o

oA

oB

oo

..

So, the six possible combinations of genes are:

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  • GENOTYPE AA: Genotype AA produces antigen A → Person having antigen A will have blood group A.
  • GENOTYPE AB: Genotype AB produces antigens A and B → Persons having antigens A and B will have blood group AB.
  • GENOTYPE oA: Genotype oA produces antigen A → So, the person will have blood group A.
  • GENOTYPE BB: Genotype BB produces antigen B → The person will have blood group B.
  • GENOTYPE oB: Genotype oB produces antigen B → The person will have blood group B.
  • GENOTYPE oo: Genotype oo does not produce any antigen → The person will have blood group O.

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Genotype

Antigen

Blood group

AA

A

A

AB

AB

AB

oA

A

A

BB

B

B

oB

B

B

oo

No antigen

O

.

.

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GENETIC DETERMINATION OF Rh BLOOD GROUP SYSTEM

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–  There are two types of genes which determine antigens of the Rh blood group system:
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  • Gene D
  • Gene d

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– Every person gets two genes, one from the father and one from the mother.

– There are three possible combinations of genes.

Gene D Gene d
Gene D DD Dd
Gene d Dd dd

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So, the three possible combinations of genes are:

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  • GENOTYPE DD: Genotype DD produces Rh D antigens → A person having Rh D antigen is Rh+
  • GENOTYPE Dd: Genotype Dd produces Rh D antigens → The person will be Rh+
  • GENOTYPE dd: Genotype dd does not produce Rh D antigens → The person will be Rh-

    .

    .

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Gene D

Gene d

Gene D

DD

Dd

Gene d

Dd

dd

 

Genotype

Rh D antigen

Blood group

DD

Present

Rh+

Dd

Present

Rh+

dd

Absent

Rh-

 

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EXPLANATION OF MCQ

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ABO BLOOD GROUP: Father has genotype Ao, while mother has genotype Bo; so, the following combinations are possible in their babies:

.

.

Gene A

Gene o

Gene B

AB

oB

Gene o

oA

oo

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So, their babies may have the flowing genotypes and blood groups:

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  1. Genotype AB → Blood group AB
  2. Genotype oB → Blood group B
  3. Genotype oA → Blood group A
  4. Genotype oo → Blood group O

    .

    Rh BLOOD GROUP: Gnenotype of father is “DD” while that of mother is “Dd”; so the following combinations are possible in their children:

    .

    .

    So, their babies may have the following genotypes and blood groups:

    .

    1. Genotype DD → Rh
    2. Genotype dD → Rh+

    .

    22. Blood group antigens are

    A. Are attached to the haemoglobin molecule

    B. Inherited as recessive characteristic;

    C. Inherited characteristics carried by the autosome

    D. Not found in !issues other than the blood

    E. To be present in plasma

    .

    Ans. C

    .

    23. Transfusion reaction will not occur in a patient if we transfuse the

    a. Group A with 0

    b. Group A with AB

    c. Group AB with A

    d. Group B with 0

    e. Group 0 with B

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Ans. C. Option A, C, and D are correct (there may be problem with the recall).

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24. In Rh-blood group, Rh-agglutinins

A. Are always present in Rh-negative blood

B. Are predominantly 1 gm

C. Are present on red cell membrane

D. Develop in Rh-negative woman pregnant with Rh-positive fetus

E. Do not cross the placenta in the first trimester of pregnancy

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Ans. D

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ERYTHRBLASTOSIS FETALIS

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DEFINITION: It is disease of the fetus and newborn infants, characterized by agglutination and hemolysis of RBCs due to incompatibility between child’s and mother Rh factors.

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MECHANISM

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  • If an Rh- woman marries an Rh+ man, some of their children may inherit Rh+ blood group from their father.
  • If some of the RBCs of the Rh+ baby (which has Rh D antigens) pass through placenta into the circulatory system of the mother, it initiates the formation of Rh D antibodies against the Rh D antigens of the baby’s RBCs.
  • The first baby is born safely but if the second fetus is also Rh+, the blood of mother containing Rh D antibodies will clump the blood of fetus containing Rh D antigens.
  • The clumped RBCs are then hemolyzed by macrophages, releasing hemoglobin → The macrophages breakdown this hemoglobin into bilirubin → The skin color of the baby becomes yellow (jaundice), and hence, the baby is born with severe jaundice.

    .

    25. First child of blood group negative Mother and blood group positive father has hepatosplenomegaly. Now 2nd child has (erythroblastosis fetales). Baby has which blood group

    a. 0+ve

    b. 0-ve

    c. B-

    d. A-

.

Ans. A. In case of erythroblastosis fetalis:

.

  • The mother will always be Rh- (only Rh- person can be sensitized to make Rh D antibodies).
  • The father will always be Rh+ (to transmit Rh+ blood group to the child; for the child to be Rh positive, at least one parent should be Rh positive.)
  • The child will always be Rh+ (only Rh+ blood can sensitize the Rh- mother to make Rh D antibodies).

    .

26. Baby has hemolytic disease and blood group is B positive. With which blood you will do exchange transfusion

a. B negative

b. 0

c. AB

d. B+

e. Any Rh + blood

.

Ans. A

.

TREATMENT OF ERYTHROBLASTOSIS FETALIS

.

  • Mother has already transmitted Rh D antibodies to the cute baby (which can react with RH D antigens of any Rh+ blood).
  • So, the baby should always be infused with 400ml of “Rh- Blood” (which do not have Rh D antigens, for reaction with Rh D antibodies present in the baby’s blood).
  • After six weeks, when Rh D antibodies are destroyed in the baby’s body, Rh- blood in the baby is replaced by baby’s own Rh positive blood.

    .

    27. A baby with erythoblastosis fetalis needs exchange transfusion. Baby is A+ . Which blood group should be transfused :

    a. A+

    b. A-

    c. AB

    d. 0+

.

Ans. B. A baby suffering from eryhtroblastosis fetalis should always be transfused with Rh negative blood.

.

28. Rh agglutinin

A. Is present on the surface of rbcs

B. Is present in Rh+ve blood groups

C. Is produced in Rh-ve mother when she Conceives an Rh+ve baby

D. Rh negative individual has D antigen

.

Ans. C. RBCs of Rh+ baby goes to body of Rh- mother to induce the formation of Rh agglutinins (antibodies).

.

29. The best way to prevent Rh Isoimmunisation in a woman who has Given birth to Rh positive fetus is

A. Blood transfusion

B. Platelet transfusion

C. Serum

D. Rh immunoglobulins

.

Ans. D. Rh D antibodies (Rhogam injection) should be given to Rh- mother after each delivery of an Rh+ baby; these antibodies destroy the Rh D antigens which have come to the mother’s body from the baby via placenta.

.

30. Patient with blood group A should not be given

a. A+

b. A-

c. O

d. AB

e. 3 days old blood

.

Ans. D. Blood group A will have antibodies B. Blood group Ab will have antigens A and B. So, antigen B of the donor will react with antibody B of the recipient.

.

31. True about Rh blood group antigen:

A. Will not be found in any tissue other than the blood.

B. Will be inherited by Autosomal recessive pattern

C. Found only in GIT

D. Found on Hb.

.

Ans. A

.

32. Father’s Blood group is AB+ve. Their child can not Have which of the following blood group:

A. 0+

B. A+

C. B+

D. AB+

.

Ans. A

.

  • If the father’s blood group is AB positive, it means that father has genes A and B.
  • A child receives one gene from the father and one from the mother.
  • So, the child will receive either gene A or gene B from the father, resulting in any one of the following blood groups:

    .

  • Blood group A
  • Blood group B
  • Blood group AB

    .

  • A child with blood group O will have genotype OO, which means that one “gene o” will have to come from father, and another “gene o” will have to come from mother. Here, in this case, the father do have “gene o”, its impossible for the chile to inherit blood group from a father whose blood group is AB.

    .

    33. Transfusion reaction will occur in a patient if we transfuse the

    A. Group A with 0

    B. Group A with AB

    C Group B with 0

    D Group 0 with B

.

Ans. D. Group O has antibodies A and B. Group B has antigens B. So, antigen B of the donor will react with antibodies B of the recipient.

.

34. Regarding Rh blood transfusion to the Anemic baby, true is

A. Crossmatch blood to baby’s plasma

B. Crossmatch blood to mother’s plasma

C. Crossmatch blood to mother’s blood

D. Give WBC depleted transfusion

E. Give red cell concentrates Crossmatched with fetal blood

.

Ans. A

.

35. Which among the following will produce Severe reaction during transfusion

A. A- to A+

B. O+ to AB

C. A+ to AB

D. O- to AB+

.

Ans. A???

.

36. Rh incompatibility occurs in a mother if She has:

A. Rh negative fetus

B. Rh positive fetus

C. If she has Rh positive blood group

D. None of above

.

Ans. B

.

37. After multiple blood transfusion, which Occur

A. Hypokalemia

B. Hypernatremia

C. Hypocalcemia

D. Raised blood urea nitrogen

.

Ans. C

.

BLOOD TRANSFUSION RISKS

.

  • Transmission of infection (e.g., hepatitis C)
  • Transfusion reactions
  • Agglutination
  • Hemolysis
  • Acute kidney shutdown
  • Iron-overload (due to “repeated” transfusions, e.g., in patient of thalassemia), resulting in hemochromatosis (Hemochromatosis means “organ damage caused by iron overload)
  • Hypocalcemia (stored blood units contains citrate which is a calcium chelator) due to “massive” blood transfusion, resulting in tetany.
  • Hyperkalemia (RBCs contain K+; RBCs may lyse in old blood units, thus releasing K+)

    .

    38. Rapid infusion of citrated blood causes

    A. Tetanus

    B. Tetany

    C. Flaccid paralysis

    D. Bleeding

.

Ans. B. Refer to the above MCQ

.

39. A 40 year old male after road traffic Accident had received massive blood Transfusion. He is expected to have all Except

A. Hypocalcaemia

B. Hypokalemia

C. Hypothermia

D. Left shift of Oxyheamoglobin Dissociation curve

E. Metabolic acidosis

.

Ans. B. Refer to the above MCQ

.

40. RBC’s are

a. Biconvex

b. Nonfragile

c. Have nucleus

d. Largest of all cells

e. Have glycolytic enzyme activity

.

Ans. E. RBCs have no nucleus, mitochondria and endoplasmic reticulum but they can still survive because they do have enzymes of glycolysis and hexose-monophosphate shunt to utilize glucose for ATP production.

.

41. Stimulus for erythropoiten secretion is:

A. Hypoxia

B. Hyperventilation

C. CO2

D. 02

.

Ans. A

.

  • Tissue oxygenation is the basic regulator of RBC production.
  • (1) ↓Blood volume (2) ↓Blood flow (e.g., due to thrombosis) (3) ↓Hb (anemia) (4) Failure of diffusion of oxygen from alveoli to pulmonary capillaries ↓Tissue oxygenation (hypoxia) → Hypoxia is the most potent stimulant for erythropoietin secretion form kidneys → Erythropoietin stimulates RBC production in the bone marrow.
  • The most potent stimulant for erythropoietin secretion is hypoxia; so, the most potent stimulant for RBC production is also hypoxia.

    .

    42. Stimulation of RBC production in bone marrow is Due to

    A: Erythropoietin

    B. Spectrin

    C. Ankyrin

.

Ans. A

.

43. The last factor which will returned to Normal in hemorrhagic shock

A. Heart rate

B. Blood pressure

C. Cardiac contractility

D. Rbcs in peripheral smear

E. Pulse pressure

.

Ans. D. RBCs take time for synthesis.

.

44. ESR decreases with increase in:

A. Cholesterol in blood

B. Increase globulin

C. Plasma albumin

D. Fibrinogen

E. Temperature

.

Ans. C

.

ERYTHROCYTE SEDIMENTATION RATE (ESR)

.

        DEFINITION

.

  • In the presence of an anticoagulant, rate of settling-down of RBCs in a specimen of blood which is allowed to stand in a glass tube is called ESR.
  • RBCs settle-down because they are heavier than plasma.

    .

    READING OF ESR

    .

  • Height of supernatant fluid in mm, which is separated out at the top of vertical column of blood after one hour, is noted; this gives reading of ESR.
  • So, if reading is more, less RBCs have settled down, and vice versa.

    .

    FACTORS AFFECTING ESR

    .

  • ESR is increased by rouleux formation; rouleaux formation is “aggregation of RBCs with each other or filing up of RBCs upon each other”. After rouleux formation, RBCs fall at a faster rate.

    .

  • Products of inflammation (e.g., fibrinogen) coat RBCs and prmote rouleaux formation, thus increasing ESR.

.

Table Factors affecting ESR

.

↑ESR

↓ESR

RBCs

Most Anemias (RBCs are less, so aggregating factors are more concentrated)

  • Sickle cell anemia (altered shape)
  • Polycythemia (↑RBCs “dilute” aggregation factors)

Diseases

  • Cancer, e.g., multiple myeloma)
  • Autoimmune disorders (e.g., SLE)

CHF

Infection/ inflammation

  • Infections (due to proteins that enter circulation from site of infection)
  • Inflammation (e.g., temporal arteritis) due to fibrinogen

↑Albumin

Physiological factors

  • Pregnancy (due to fibrinogen)
  • Old age

.

.

45. A hematocrit of 41% means:

A. 41% of formed elements in blood are Rbcs

B. 41% of blood is plasma

C. 41% of blood is serum

D. 41% of formed elements in blood Comprises of rbcs, wbcs and platelets

E. 41°%, of rbcs contain hemoglobin

.

Ans. D

.

HEMATOCRIT

.

DEFINITION: Percentage of blood which is cells, i.e., RBCs, WBCs, and platelets, is called hematocrit.

.

NORMAL VALUE: 45%

.

WHY FORMED ELEMENTS SO CALLED: RBCs, WBCs, and platelets are called formed elements because they have shape and form.

.

46. Iron is stored in the form of

A. Ferritin

B. Transferrin

C. Apoferritin

D. Ferrous

E. Hemosiderin

.

Ans. A

.

STORAGE OF IRON

.

FERRITIN: Excess of iron combines with apoferritinto form ferritin (soluble) which is stored especially in liver.

.

HEMOSIDERIN: Small quantities of iron are stored in insoluble form called hemosiderin when apoferritin pool is saturated.

.

As most of the iron is normally stored in the form of ferritin, so the best answer here is “ferritin”.

.

47. Haemoglobin molecule has

A. 4 atoms of Fe

B. 2 atoms of Fe

C. 1 atom of Fe

.

Ans. A

.

  • Each hemoglobin chain contains one iron.
  • Each hemoglobin molecule contains four hemoglobin chains (2 alpha chains + 2 beta chains).
  • So, one hemoglobin molecule contains four atoms of iron.

    .

    STEPS OF FORMATION OF HEMOGLOBIN

    .

  • 2 Succinyl- CoA + Glycine → Pyrrole

    .

  • 4 pyrroles → Protoporphyrin IX

    .

  • Protoporphyrin + Fe+2 → Heme

    .

  • Heme + Polypeptide (globin) → Hemoglobin chain (α or β)

    .

  • 2 Alpha + 2 Beta cahians → Hemoglobin A

    .

48. The intrinsic and extrinsic blood coagulation pathways converge at the formation of activated

A. Hageman factor Xlla

B. Stuart factor Xa

C. Antihemophilia factor VII a

D. Fibrin la

E. Thrombin Ila

.

Ans. B. The intrinsic and extrinsic pathways converge on activated factor X.

.

49. Plasma fibrinogen

A. Concentration increases in liver diseases

B. Has a molecular weight of 39,000

C. Is converted into fibrin during blood clotting

D. Is mainly responsible for the plasma colloid oernotic pressure

E. Is normally filtered through the glomerular membrane

.

Ans. C

.

BASIC THEORY OF COAGULATION (BLOOD CLOTTING)

.

(A) FORMATION OF PROTHROMBIN: First of all prothrombin activator is formed by extrinsic and intrinsic pathway in response to damage to vessel or damage to blood.

.

(B) CONVERSION OF PROTHROMBIN TO THROMBIN: The prothrombin activator then catalyzes the conversion of prothrombin to thrombin.

.

(C) CONVERSION OF FIBRINOGEN TO FIBRIN: Thrombin then catalyzes the conversion of fibrinogen to fibrin threads that enmeshes platelets, blood cells, and plasma to form blood clot.

.

50. Fibrinogen is

A. A low molecular weight protein

B. Converted into fibrin in the absence of thrombin

C. Excreted through kidney

D. Formed in the liver

E. Mainly found in interstitial fluid

.

Ans. D

.

51. In the lymphatic system, antibodies for circulation in the Serum are produced by

A. All macrophages

B. B lymphocytes that have been transformed into plasma cells

C. Macrophages that have ingested antigen or fragments of antigen

D. Reticulocytes in the spleen and bone marrow before they lose their Nuclei and become circulating erythrocytes

E. T lymphocytes in the lymph node

.

Ans. B. B lymphocytes mature into plasma cells which then make antibodies.

.

52. In order for heparin to be an effective anticoagulant, a Naturally occurring inhibitor of clotting is required. The Most likely inhibitor is

A. Antithrombin III

B. Factor v

C. Factor xii

D. Plasminogen

E. Protein c

.

Ans. A

.

WHY BLOOD DOES NOT COAGULATE IN BODY

.

Blood is prevented from coagulation intravascular system due to

.

  • Endothelial surface factors:

    .

  • Smoothness of endothelium
  • A layer of glycocalyx adjacent to endothelium, repels clotting factors and platelets
  • Thrombomodulin present on endothelium binds thrombin.

    .

  • Rapid blood flow
  • The presence of intravascular anticoagulants:

    .

  • Heparin
  • Antithrombin III
  • Fibrin threads
  • Alpha2-macroglobulins

    .

    53. Natural anticoagulant in body

    A) Warfarin

    B) Heparin

    C) Heparin and Warfarin

    D) All of them

    .

    Ans. B. Heparin is natural anticoagulant (prevents formation of blood clot), while plasminogen is natural thrombolytic/antithrombotic (causes lysis of the blood clot).

    .

    54. Heparin is released from which connective tissue:

    A. Fibroblast

    B. Mast cells

    C. Chromatepherc

    D. Neutrophils

    .

    Ans. B

    .

    872- Natural antithrombotic released in body

    A. Warfarin

    B. Heparin

    C. Vit C

    D. Plasminogen

    .

    Ans. D

    .

    53. The blood in the vessels normally does not clot because:

    a. Vitamin K antagonists are present in plasma

    b. Thrombin has positive feedback on plasminogen

    c. Sodium citrate in plasma chelates calcium ions.

    d. Vascular endothelium is smooth and coated with glycocalyx

.

Ans. D

.

54. Antithrombin III is a circulating protease inhibitor that

A. Binds to the valine protease in the coagulation system

B. Has same structure as that of thrombin

C. Is chelated out by free calcium

D. Is produced in the kidney

E. When binds to serine protease, it’s action is facilitated by heparin

.

Ans. E

.

55. All are involved in clotting except

A. Factor VIII

B. Factor XIII

C. Factor IX

D. Protein C

E. Antithrombin III

.

Ans. E. In contrast to thrombin which promotes blood clotting, Antithrombin III inhibits blood clotting.

.

56. Platelets

A. Are small 4-8 micron in diameter

B. Contain alpha granules which secrete serotonin

C. Contain dense granules which secrete platelet drive growth factor

D. Count increases after splenectomy

E. Have normally a half life of about 10 days

.

Ans. D. Platelets are removed from the body by spleen; therefore, splenectomy causes increase in platelets count.

.

57. Regarding platelets, following statements are true except

A. Count is decreased by splenectomy

B. Count when is normal, purpura may also occur

C. Count when log causes deficient clot retraction

D. Have a half life of about 4 days

E. Have both .actin grid myosin in their cytoplasm

.

Ans. A. Platelets count increases after splenectomy.

.

58. In normal human blood

A. The eosinophil is the most common type of white blood cells

B. The iron is mostly in haemoglobin

C. There are more lymphocytes than neutrophils

D. There are more platelets than red cells

E. There are more white cells than the red cells

.

Ans. B

.

IRON DISTRIBUTION IN THE BODY

.

  • Hemoglobin contains 65% of total iron.
  • Reticuloendothelial system and liver contains 15 – 30% of total iron.
  • Myoglobin contains 4% of total iron.
  • Various heme compounds contain 1% of total iron.

    .

    59. Secondary polycythemia is caused by excess of

    A. Erythropoietin

    B. Haemosiderin in liver

    C. Serum folic acid

    D. Serum iron

    E. Vitamin b12

.

Ans. A

.

POLYCYTHEMIA

.

DEFINITION: Increase in RBC count is called polycythemia.

.

TYPES: Two types

.

        (A) SECONDARY POLYCYTHEMIA

.

  • Secondary polycythemia occurs secondary to other causes, e.g., hypoxia due high altitude of due to cardiac failure.
  • High altitude or cardiac failure → Tissue hypoxia → Hypoxia is a stimulus for erythropoietin secretion from kidneys → Erythropoietin stimulates RBCs production by bone marrow → ↑RBC count

    .

    (B) PRIMARY POLYCYTHEMIA (POLYCYTHEMIA VERA)

    Tumor in bone marrow → Excessive production of RBC → ↑RBC count

    .

    60. A young soldier aged 24 reports to the CMH, on his way back From high altitude region he was on duty for about 6 Months. He complains of headache & blueness of fingertips. On Examination, he is found to have moderate splenic enlargement, BP = 150/95 mmhg and PCV = 60%. He is most likely suffering from

    A. methemoglohinernia

    B. Mild hypertension

    C. polycythemia vera

    D. secondary polycythemia

    E. Sickle cell anemia

.

Ans. D. Signs and symptoms are typical of secondary polycythemia (induced by low oxygen tension at high altitude).

.

61. Polycythemia can result from excess Intake of

A. Cobalt

B. Iron

C. Copper

D. Zinc

.

Ans. A???

.

62. The most common plasma protein is

A. Albumin

B. Globulin

C. Keratin

D. Fibrinogen

.

Ans. A

.

63. Normal albumin globulin ratio in plasma Is

A. 2:1

B. 1:1

C. 1:2

.

Ans. A

.

64. A person doing journey from rawalpindi to abbotabad, is worried about his fingertips that are blue. What is the probable cause?

A. Primary polycythemia

B. Secondary polycythemia

C. Burger’s disease

D. Poly arteritis nodosa

.

Ans. B. Abottabad is at high altitude. At high altitude, atmospheric pressure is low which results in hypoxia. Hypoxia in turn causes secondary polycythemia.

.

Polycythemia causes cyanosis because ↑RBC count increases blood viscosity → Increase in blood viscosity decreases blood flow → Greater than normal amount of oxygen is deoxygenated before the blood can enter from capillaries to veins →The blue color of this deoxygenated hemoglobin masks the red color of oxygenated hemoglobin → The skin color becomes blue (cyanosed).

.

65. Erythrocytes in adults

A. Are broken down when aged in the spleen

B. Are more in females

C. Develop directly from polychromatophilic erythroblast

D. Have a life span of about three weeks

E. When fully formed stain basophilic

.

Ans. A. Old RBCs are broken down by spleen.

.

66. After completion of a normal life span, the RBCs are mainly Degraded in the

A. Bone marrow

B. Kidneys

C. Liver

D. Lymph nodes

E. Spleen

.

Ans. E

.

67. Which of the following is correct about Red blood cells

A. Destroyed in spleen

B. Life span of 60 days

C. Can easily pass through blood capillaries

D. They have aerobic metabolism

E. They are biconvex in shape

.

Ans. A

.

68. Heme is converted to bilirubin mainly in:

A. Kidney.

B. Liver

C. Spleen

D. Bone marrow

.

Ans. C

.

69. The important function of the plasma fibrinogen is:

A. Blood clotting

B. Its role in the humoral immunity

C. Major contribution in plasma colloid osmotic pressure

D. Transport of carbon dioxide

E. Transport of hormones

.

Ans. A

.

70. Regarding haemoglobin following statements are true except

A. Binds four molecules of oxygen per molecule

B. Has a theoretical oxygen carrying capacity of 1.39 ml/g

C. Is a mucopolysaccharide

D. Is catabolised in the reticulo-endothelial system (res)

E. Offers an important buffering system in the blood

.

Ans. C

.

71. One of the following substances is vital to the mechanism of Blood coagulation

A. Ca ions

B., k ions

C. Mg ions

D. Na ions

E. P ions

.

Ans. A. Except for the first two steps in extrinsic and intrinsic pathways, Ca+ ions are required for all reactions. So, blood clotting will not occur in the absence of Ca+.

.

72. Following are the components of hemostasis except

A. RBC

B. Blood vessel

C. Coagulation factors

D. Fibrinolytic system

E. Platelets

.

Ans. A. Prevention of blood loss is called hemostasis. RBCs have no role in hemostasis.

.

73. Hemoglobin A consists of

A. Two alpha and two beta chains

B. Two alpha and two delta chains

C. Two alpha and two gamma chains

D. Two beta and two delta chains

E. Iwo beta and two gamma chains

.

Ans. A

.

Table Types of Hb and their chains

Types of Hb

Chains

Hb A (adult Hb)

2 Alpha + 2 Beta

Hb A2

2 Alpha + 2 Delta

Hb F (fetal Hb)

2 Alpha + 2 Gamma

.

74. Adult Hb is composed of

A. 2 alpha + 2 beta

B. 2 alpha + 2 gamma

C. 2 alpha + 2 delt

.

Ans. A

.

75. Hemoglobin concentration is highest in

A. Basophilic erythroblast

B. Orthochromatic erythroblast

C. Polychromatic erythroblast

D. Proerythroblast

E. Reticulocyte

.

Ans. E. STAGES OF ERYTHROPOIESIS: CFU-E stem cell in bone marrow → Pro-erythroblast → Basophil erythroblast (very little Hb) → Polychromatophil erythroblast (enough Hb) → Orthochromatic erythroblast (very large amount of erythroblast) → Reticulocyte (cytoplasm filled with 34% Hb) → Mature erythrocyte

.

76. Which of following can cause haemolysis

A. Copper

B. Zinc

C. Lead

D. Chromium

.

Ans. C

.

77. The type of hemoglobin that has least Affinity for 2,3 diphosphoglycerate (2,3- DPG) or (2,3-BPG) is:

A. Hg A.

B. Hg F.

C. Hg B.

D. Hg A2.

.

Ans. B

.

78. Regarding thrombocyte’s function in clotting

A. Adhere to fibroblast

B. Release platelet factors which start coagulation

C. Clot expansion

.

Ans. B

.

79. Factor VIII is produced in

A. Bone marrow

B. Endothelial cells

C. Hepatocytes

D. Kupffer’s cells

E. Lymph node follicles

.

Ans. B. LIVER: Liver synthesizes clotting factors 1 (fibrinogen), 2 (prothrombin), 7, 9, 10.

.

ENDOTHELIAL CELLS: Endothelial cells of the blood vessels synthesizes factor 8.

.

80. Factor VIII is formed by

A. Hepatocytes

B. Kupfur cells

C. Bone marrow

D. Spleen

E. Thymus

.

Ans. A

.

81. Lymphocytes

A) Increase in cushing syndrome

B) Defense against cancer

C) Unaffected by hormones

D) Interact with Esinophils to produce platelets

E) Originate from bone marrow only

.

Ans. E. Both B and T lymphocytes are synthesized in the bone marrow.

.

82. Thrombolytics control bleeding by

A) Adhering to fibroblast

B) Initiating clotting process by platelet factor

C) By clot extension

D) Secreting heparin

E) Contraction caused by bradykinnin

.

Ans. A

.

83. Monocytes

A. Have common origin with neutrophils

B. After passing to tissue, reenter blood

.

Ans. A

.

84. Transfusion reaction will not occur in a pt if we transfuse the

A. group A with 0

B. group A with AB

C. group AB with A

D. group B with 0

E. -group 0 with B

.

Ans. C

.

85. Adult hemoglobin is a conjugated protein that contains:

A. Two alpha & two gamma chains

B. Iron in ferrous form

C. Carries CO2

D. It provides more oxygen as compared to fetal hemoglobin

.

Ans. B

.

.

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