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Biochemistry - Sarah > Erythrocyte clotting > Flashcards

Erythrocyte clotting Flashcards

1
Q

Life span of RBC

A

~120 days

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2
Q

Anemias caused by:

A

Iron deficiency, B12 deficiency, folate deficiency, thalassemia, RBC loss

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3
Q

Erythrocyte metabolism is dependent on ___.

They also require ___.

A

glucose (glycolysis) (because RBCs do not have mitochondria)

NADPH reducing equivalents for glutathione

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4
Q

Erythrocytes use ___ to reduce ferric iron to ferrous iron.

A

NADH (from glycolysis)

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5
Q

Erythrocytes use __ to modulate oxygen binding to hemoglobin, which stabilizes deoxy-hemoglobin.

A

2,3-bisphosphoglycerate

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6
Q

Glucose-6-phosphate dehydrogenase deficiency results in ___.

A 
hemolytic anemia
(NADPH keeps glutathione reduced, helps prevent buildup of ROS, low NADPH results in hemolysis, deficiency decreases NADPH)
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7
Q

What are some sources of oxidative stress for red blood cells?

A

primaquine for malaria, aspirin, sulfonamide antibiotics (folic acid inhibitors), and fava beans

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8
Q

What causes microcytotic anemia?

A

iron deficiency, lead poisoning, or thalessemia
(They cause impaired hemoglobin synthesis)

Microcytic anemia is also known as hypochromic anemia

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9
Q

What causes macrocytic anemia?

A

B12 or folate (B9) deficiency

This causes impaired DNA synthesis

Macrocytic anemia is also known as normochromic anemia

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10
Q

What causes normocytic anemia?

A

Severe bleeding, sickle cell anemia, pyruvate kinase deficiency, or glucose-6-phosphate dehydrogenase deficiency

This causes red blood cell loss

Normocytic anemia is normochromic anemia

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11
Q

Hemostasis

A

The process of clot formation and susequent dissolution

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12
Q

Four major events associated with hemostasis

A

Vascular constriction, Platelets activated by thrombin and aggregate at injury site, fibrin clot formation: intrinsic and extrinsic pathways, dissolution of clot: action of plasmin

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13
Q

Platelets are derived from ___.

A

megakaryocytes

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14
Q

Hormone that controls platelet formation

A

thrombopoeitin

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15
Q

True or false: Platelets contain mitochondria.

A

True

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16
Q

Life span of platelet

A

7-10 days

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17
Q

Platelet activation

A

Adhesion, aggregation, and activation

adhesion: At damaged site, glycoprotein IA (GPIa) binds collagen and GPIb binds VonWillebrand factor (vWF) that is attached to collagen

Aggregation: glycoprotein IIb/IIIa molecules on platelets bind other platelets through fibrin

Activation: Release of hemostasis chemicals from intracellular granules

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18
Q

Phospholipase A

A

Stimulation of platelet membrane receptors triggers activation of platelet membrane phospholipase A2 (PLA2)
Hydrolyzes membrane phospholipids, platelets release arachidonic acid

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19
Q

PGI2

A

prostacyclin, major arachidonic acid metabolite formed by vascular cells (potent vasodilator, inhibitor of platelet aggregation)

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20
Q

Platelet-related bleeding disorders

A

Congenital bleeding disorders:
Bernard-Soulier syndrome: GPIb-IX deficiency causes bleeding disorder

Acquired platelet disorders:
Thrombocytopenia (low platelet count): defective formation of platelets by megakaryocytes, bone marrow neoplasia; excessive destruction of platelets - anti-platelet antibodies

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21
Q

Platelet inhibition drugs

A

Plavix (inhibits ADP-induced platelet aggregation acting by direct inhibition of adenosine diphosphate (ADP) binding to its receptor and of the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex

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22
Q

Antiplatelet drugs (examples)

A

dipyridamole, ticlopidine, clopidogrel (plavix)

Less gastric bleeding than aspirin

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23
Q

Dipyridamole

A

inhibits uptake of adenosine, leading to increased platelet A2 receptor stimulation and suppression of ADP receptor action

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24
Q

Blood Clotting cascade (intrinsic)

A 
Prekallikrein -->Kallikrein
Factor XII --> Factor XIIa
Factor XI --> Factor XIa
Factor IX --> Factor IXa
Factor X ---> Factor Xa (uses VIIIa)
Factor II / Prothrombin --> IIa /Thrombin
Factor I / Fibrinogen --> Factor Ia / Fibrin and XIII ---> XIIIa
Crosslinked fibrin clot/XIIIa
25
Q

Blood Clotting cascade (extrinsic)

A

Factor VII –> Factor VIIa
Factor X —> Factor Xa (uses VIIIa)
Factor II / Prothrombin –> IIa /Thrombin
Factor I / Fibrinogen –> Factor Ia / Fibrin and XIII —> XIIIa
Crosslinked fibrin clot/XIIIa

26
Q

Fibrin is synthesize as ___ and cleaved by ___.

A

fibrinogen,

thrombin (A serine protease)

27
Q

What does Transglutaminase do?

A

Factor XIIIa (transglutaminase) links lysine side chains to glutamine side chains

28
Q

What activates Transglutaminase?

A

Factor XIIIa is activated by Factor IIa (thrombin)

29
Q

True or false: Factor XIIIa is a serine protease.

A

FALSE

30
Q

What is prothrombinase?

A

Factor Xa and V form it and it catalyzes the proteolysis of prothrombin to thrombin.

31
Q

What does thrombin do?

A

This thrombin catalyzes the activation of factors V, VII, VIII, and XIII (triggering VIII is key for starting the intrinsic path)

It also catalyzes the formation of fibrin from fibrinogen

32
Q

___ inhibits thrombin.

A

Hirudin from leeches

33
Q

Vitamin K is important for ___.

A

The synthesis of prothrombin and other clotting factors

Cofactor for the enzyme that carboxylates Glutamine

34
Q

Gamma-carboxyglutamate binds ___.

A

Calcium

35
Q

Antagonist of Vitamin K

A

warfarin

36
Q

Vitamin K dependent clotting factors

A

X, II, VII, IX

also regulatory factor protein C

37
Q

Activated partial thromboplastin time

A

Phospholipid and silica added (test of the intrinsic pathway)

Prolonged aPTT indicates a deficiency in VIII, IX, XI, XII (all except XIII and VII) (used to monitor IV heparin)

38
Q

Prothrombin time

A

Used to test the extrinsic pathway

Factor III added to plasma. Specific for reduced factor VII but also X and II (used to monitor warfarin)

39
Q

Common pathway for clotting (simplified)

A

10/5 = 2. Factor X goes to Factor V goes to Factor 2

40
Q

Pnemonic for remembering extrinsic pathway

A

You do PT outside at 7 AM

Prothrombin time = extrinsic, uses Factor VII, then common pathway

41
Q

Prothrombin time can reveal ___.

A

Acquired bleeding disorders:
Vitamin K deficiency
Oral anticoagulants (Warfarin)
and Liver disease (Reduced hepatic synthesis of Factor II, VII, IX, X)

42
Q

Activated prothrombin time can reveal ___.

A

Hemophilia A (Factor VIII)

43
Q

Hemophilia A is associated with ___.

A

Factor VIII

44
Q

Antithrombin II

A

Serine protease inhibitor: inhibits activity of thrombin, Factos IXa, Xa, and XIa

45
Q

What does heparin do?

A

It binds to antithrombin III and increases its affinity for thrombin (thereby reducing clotting)

46
Q

Where is antithrombin synthesized?

A

In the liver

47
Q

Deficiency of antithrombin can lead to __.

A

increased risk of venous thromboembolism

48
Q

Factor V Leiden

A

Factor V variant that is resistant to protein C (increases clotting)

49
Q

Thrombin binds ___ on the surface of endothelial cells and activates ___.

A

thrombomodulin,

protein C

50
Q

Protein C forms a complex with ___ and provides selective proteolytic degradation of ___.

A

protein S,

Factor Va and VIIIa

51
Q

____ (a serine protease), degrades fibrin clot.

A

Plasmin

52
Q

Converts plasminogen to activated plasmin

A

tPA (tissue-type activator)

53
Q

T-PA inactivators

A

Plasminogen activator-inhibitor types 1 and 2 (PAI-1, PAI-2)

54
Q

t-PA

A

converts plasminogen to activated plasmin, made by endothelial cells, Has Kringle domains (binds fibrin), low basal concentrations in plasma

55
Q

Hemophilia A

A

Classic hemophilia
Deficiency in factor VIII (cofactor activating Xa)
X-linked
prolonged bleeding from wounds, easy bruising
treat with human plasma or recombinant factor VIII

56
Q

Von Willebrand Disease

A

Defective platelet adhesion (prolonged bleeding time)
different forms with different severity
more common than Hemophilia A

57
Q

Antithrombin deficiency

A

Causes deep vein thrombosis and pulmonary embolism

58
Q

Pyruvate Kinase deficiency

A

Separate isoforms in humans (one for erythrocyte; active tetramer)
Reduced ATP production results in failure to maintain cation gradient, loss of potassium and water, cell dehydration, hemolytic anemia
Hemolytic anemia has symptoms less severe than expected due to increased 2,3-bisphospholgycerate (2,3-BPG), results in greater release of oxygen to tissues
Partial block of PK increases 1,3-BPG and therefore 2,3-BPG
Wide range of severity, from infant death to asymptomatic adults
Treatment: transfusions and possible splenectomy (to prevent hemolytic anemia)

Biochemistry - Sarah (12 decks)

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