Haematology physiology Flashcards
14676 – Erythropoiesis is
1: subject to feedback control
2: a feature of acclimatisation to altitude
3: inhibited by a rise in the circulating red cell level to supernormal values
4: controlled by erythropoietin produced by erythrocytes
TTTF
Refer to Ganong, 19th Ed, Ch 27, page 508 and following
4 - kidney produces EPO
10104 – Fetal haemoglobin (haemoglobin F)
1: has less affinity for O2 than adult haemoglobin (HbA)
2: binds 2-3 DPG less effectively than HbA
3: at birth is 20% of the circulating Hb
4: at four months is 10% of the circulating Hb
FTFT
Ganong, 19th ed, Ch 27, 32 and 35
15296 – S: Complications commonly arise when an Rh negative mother carries an Rh positive baby during her first pregnancy because R: small amounts of foetal blood leak into the materal circulation
S is false and R is true
Refer to Ganong, 19th Ed, Ch 27, page 515
8657 – A child who is group O Rh negative can have a parent who is
1: group B Rh positive
2: group O Rh positive
3: group A Rh positive
4: group AB Rh positive
TTTF
Ganong, 19th ed, Ch 27
7114, 18316 – Plasma for group A blood will agglutinate
A. only group AB blood
B. only group B blood
C. group B blood and group AB blood
D. group AB blood, group B blood and group O blood
E. group B blood and group O blood
C
See commentary in STEM Module: Peri-operative Care and Complications (Q18).
Plasma from group A blood contains anti-B antibodies and will thus agglutinate both group B blood and group AB blood (C).
20547 – S. Haemoglobin has a greater buffering capacity than plasma proteins at physiological pH BECAUSE R. according to the Henderson-Hasselbach equation, the buffering capacity of a system is greatest when pH=pK
S is true, R is true but not a valid explanation of S
Ganong 13th Ed. Ch. 35 P. 554
12524 – Of the following, the safest combination for packed red cell transfusion in an emergency would be
A. donor type A recipient type O
B. donor type AB recipient type B
C. donor type B recipient type O
D. donor type B recipient type AB
E. donor type AB recipient type O
D
People with Type AB red cells have no iso-agglutinins. It is therefore safe to transfuse B cells (in the absence of atypical anti-red blood cell antibodies in the recipient). If whole blood were transfused (Group B), the donor alpha-agglutinin may haemolyse recipient AB cells dependent on the donor agglutinin titre.
13090 – Thrombocytopenia sometimes complicates the repeated transfusion of large quantities of blood because
1: the patient’s platelets are diluted by the transfusion
2: anti-platelet antibodies may be produced by the recipient
3: the platelets in stored blood are non-viable
4: the transfused plasma sometimes contains anti-platelet antibodies
TTTT
After a massive haemorrhage (which will have preceded the repeated transfusion of large quantities of blood) the patient will have lost functional platelets, only to have them replaced by non-viable platelets in the transfused blood (A and C true). The transfusion of serum or blood always carries the risk of transferring unwanted antibodies (D true). The production of anti-platelet antibodies is a well recognised phenomenon which can occur in a variety of circumstances (B true).
9953 – The delivery of O2 from blood to tissues would be increased by an increase in the tissue capillaries of
1: the 2,3-DPG (diphosphoglycerate) content of the red blood cells
2: blood pCO2
3: blood temperature
4: blood pH
TTTF
Ganong, 19th ed, Ch 35
27240 – S:Heparin and warfarin have significant similarities in mechanism of action but the action of aspirin is different because R:platelets have no influence on the clotting cascade.
S is true and R is false
Heparin acts to potentiate antithrombin III, which inhibits several serine proteases in the intrinsic clotting cascade (naturally occurring inhibitor of activated Factor X, but not actually thrombin; the name is misleading). Warfarin, the vitamin K antagonist, blocks the conversion of six clotting factors, including prothrombin, to their active form by inhibiting a process essential to their activation: namely, conversion of glutamate residues to gammacarboxyglutamate.
Thus heparin and warfarin, despite their differences in route of administration, time course of activation, and clinical uses, do have a final common pathway of action: they block the clotting cascade. Aspirin acts to inhibit cyclo-oxygenase in platelets, and thus inhibit platelet aggregation. Platelets have multiple inputs to their aggregation cascade, including contact with collagen and mediators such as ADP released from other platelets. The assertion in the question is a true statement. The proposed reason identifies platelets as the target of action of aspirin, but the proposition that platelets have no influence on the clotting cascade is incorrect. In fact, platelet phospholipids are essential cofactors in several steps of the clotting cascade, which occur on the surface of the platelet. Clotting can occur without red cells or leucocytes, but not without platelets. Thus, the reason given is a false statement.
8645 – S: The formation of the platelet plug after vessel injury is inhibited by anticoagulation with Heparin because R: Heparin inhibits platelet aggregation because of its strong antithrombin effect
both S and R and false
Ganong, 19th ed, Ch 27
12662 – S: Aspirin inhibits platelet aggregation by inhibiting cyclooxygenase activity because R: cyclo-oxygenase converts arachidonic acid to endoperoxides PGG2 and PGH2
S is true, R is true and a valid explanation of S
Cyclo-oxygenase converts arachidonic acid to endoperoxides PGG2 and PGH2 some of which is converted by thromboxane synthetase to thromboxane A2 in the platelets (R true and valid explanation of S). This promotes both vasoconstriction and platelet aggregation. Nonsteroidal antiinflammatory drugs such as Aspirin inhibit cyclo-oxygenase activity and thus the amount of endoperoxides PGG2, PGH2 and thromboxane A2 which are produced. Thus they decrease platelet aggregability (S true).
12644 – S: 5000 Units of Heparin given subcutaneously twice daily perioperatively reduces the incidence of post-operative deep vein thrombosis because R: Heparin, in sub-therapeutic dosage, potentiates anti-thrombin activity
S is true, R is true and a valid explanation of S.
The high incidence of postoperative venous thrombosis has been shown in many studies to be significantly reduced by the administration of heparin subcutaneously in a low dosage of 5000 units bd (S true). In the vast majority of people this is a sub-therapeutic dose of anticoagulant which does not change parameters such as activated partial thromboplastin time and which produces minimal bleeding. The subtherapeutic prophylactic dose of heparin exerts its effect by potentiating the action of the naturally occurring inhibitor of activated Factor X, known as antithrombin III (R true and is a valid explanation of S).
15137 – Following injury to a small artery, the formation of a temporary platelet plug is
1: unaffected by therapeutic doses of heparin
2: unaffected by therapeutic doses of dicoumarol
3: associated with local vasoconstriction
4: followed by the conversion of insoluble plasma fibrinogen to insoluble fibrin
TTTF
Refer to Ganong, 19th Ed, Ch 27, page 516 and following
13584 – Erythropoietin
1: is closely linked to the renin-angiotensin system
2: increases differentiation of stem cells to proerythroblasts
3: is a glycoprotein
4: cannot be formed in humans in the absence of the kidney
FTTF
Erythropoietin is a circulating glycoprotein with a molecular weight of about 23,000 (C true). Much of it comes from the kidneys although some comes from other organs (D false). In the foetus, erythropoietin causes certain stem cells in the bone marrow to be converted to proerythroblasts (B true). The erythropoietin system is quite separate from the renin-angiotensin system. Angiotensin II has no erythropoietic effect and erythropoietin has no effect on blood pressure of aldosterone secretion (A false).
