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CFoM > 03c: Hemostasis > Flashcards

03c: Hemostasis Flashcards

1
Q

What are the key steps to preventing blood loss?

A
  1. Vasoconstriction
  2. Platelet plug
  3. Fibrin clot
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2
Q

List the machinery involved in vasoconstriction.

A
  1. Neurogenic (fastest)
  2. Myogenic (fast)
  3. Humoral (slow)
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3
Q

Examples of neurogenic vasoconstriction:

A

Spinal reflex, pain response

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4
Q

Examples of myotonic vasoconstriction:

A

Smooth muscle contracts (response to trauma)

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5
Q

Examples of humoral vasoconstriction:

A

Substance (i.e. Serotonin) release locally

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6
Q

Once blood extravasates in vessel injury, which steps take place?

A
  1. Endothelial cells produce VWF factor
  2. VWF binds collagen
  3. Platelets stick to VWF
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7
Q

What’s the “release reaction”?

A

Platelet adhesion (bound to VWF) causes exocytosis of granule contents

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8
Q

(X) acts as a bridge in formation of platelet plug.

A

X = collagen

Between endothelial tissue and platelets

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9
Q

Release reaction involves in exocytosis of which substance(s)?

A
  1. Ca
  2. Serotonin
  3. ADP
  4. Enzymes targeting platelet phospholipids
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10
Q

Which substance released by (X) specifically aids in increasing platelet aggregation?

A

ADP released by

X = platelets

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11
Q

How does release reaction affect vasoconstriction?

A
  1. Serotonin promotes vasoconstriction

2. Enzymes act on platelet phospholipids and produce TA2 (thromboxane A2)

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12
Q

Thromboxane A2, released by (X), has which effect(s)

A

Not released directly by platelets, but formed by action of enzymes released by platelets;

  1. Vasoconstriction
  2. Increase platelet aggregation
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13
Q

What’s the reason behind platelet aggregation?

A

Platelets stuck to VWF change surface characteristics (express receptors) that bind other platelets

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14
Q

Easy bruising, without severe hemorrhagic issues, can be a sign of (excess/defecit):

A

Defecit in platelet adhesion due to decreased VWF (production issues)

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15
Q

What’s considered primary hemostasis?

A

Vasoconstriction and platelet plug formation

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16
Q

What’s considered secondary hemostasis?

A

Fibrin clot formation

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17
Q

What’s thrombocytopenic purpura?

A

Shortage of thrombocytes (platelets), resulting in medium-sized lesions under skin

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18
Q

Patients without primary hemostasis will show (X) on which part(s) of body?

A

X = lesions under skin

Usually legs/feet

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19
Q

Small lesions under skin are called:

A

Petechiae

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20
Q

Medium lesions under skin are called:

A

Purpura

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21
Q

Large lesions under skin are called:

A

Ecchymoses

22
Q

In secondary hemostasis, what substance is being produced by (X) to increase platelet aggregation?

A

Nothing produced to increase aggregation!

Endothelial cells secrete prostacyclins to DECREASE aggregation

23
Q

In clot formation, what prevents the platelet plug from continuing to spread and grow?

A

Prostacyclins produced by endothelial cells in secondary hemostasis

24
Q

What’s hemophilia?

A

Lack of secondary hemostasis (incapable of forming strong, firm clot)

25
Q

T/F: Fibrin is a plasma protein that’s always in the circulation.

A

False - fibrinogen is

26
Q

Describe process that converts (X) to fibrin.

A

X = fibrinogen

  1. Thrombin cleaves it into fibrin monomers
  2. Monomers spontaneously polymerize into long chains (fibrin polymer)
27
Q

T/F: Covalent bonds support the fibrin clot.

A

True

28
Q

(X) reinforces fibrin clot by inserting (Y) bonds.

A 
X = Fibrin Stabilizing Factor XIII
Y = covalent
29
Q

Thrombin is what kind of protein?

A

Protease

30
Q

T/F: Thrombin is a plasma protein that’s always in the circulation.

A

False - Prothrombin is

31
Q

Extrinsic clotting pathway stimulated by:

A

External trauma that causes blood to escape from the vascular system.

32
Q

Intrinsic clotting pathway stimulated by:

A

Trauma inside the vascular system

33
Q

Intrinsic pathway factors come from:

A

Already in blood

34
Q

Extrinsic pathway factors come from:

A

Endothelial cells

35
Q

Which post-translational modification of clotting factors must occur for successful coagulation?

A
  1. Addition of second COOH at all Glu residues
  2. Ionize to COO-
  3. Both bind Ca
36
Q

Describe MOA of Warfarin.

A

Vit K analog (non-functional) that inhibits enzyme responsible for clotting factor post-translational modification

37
Q

The (extrinsic/intrinsic) clotting pathway is faster.

A

Extrinsic

38
Q

Removal of Fibrin after healing is carried out by:

A

Plasmin

39
Q

Which cell(s) secrete(s) plasmin?

A

Not secreted by cell; inactive precursor (Plasminogen) circulates in blood.

40
Q

Which factor(s) facilitate breakdown of fibrin by (X)?

A

X = plasmin

  1. Tissue plasminogen activator (tPA)
  2. Urokinase
41
Q

tPA is used in the ER to treat:

A

Coronary thrombosis; enhances clearance of coronary artery clot

42
Q

Aspirin has which effect on clotting? How?

A

Reduce clotting; inhibits cyclooxygenase (no production of TA2) and slows platelet adhesion, aggregation, vasoconstriction

43
Q

Which ion is crucial for proper clotting? When taking blood samples, we prevent clotting by:

A

Ca; container has Ca chelator (EDTA/citrate) that binds all Ca and prevents clotting

44
Q

Prompt hemolysis of many RBC will cause (increase/decrease) in circulating bilirubin for the few days following.

A

Increase

45
Q

T/F: Sickle cell disease can cause hypo proliferative anemia.

A

False - RBC breakdown too fast

46
Q

T/F: Renal failure can cause hypo proliferative anemia.

A

True

47
Q

T/F: G6PD deficiency can cause hypo proliferative anemia.

A

False - RBC breakdown too fast

48
Q

T/F: Marrow damage (chemotherapy/radiation) can cause hypo proliferative anemia.

A

True

49
Q

(Thalassemia/hereditary spherocytosis) can cause hypo proliferative anemia.

A

Thalassemia

50
Q

What’s thrombomodulin? How does it affect clot formation?

A

Epithelial transmembrane receptor that binds Thrombin; reduces coagulation

51
Q

(X) is a protein that (stimulates/inhibits) coagulation by which mechanism? Its activity is enhanced over 1000x by (Y).

A

X = antithrombin III

Inhibits coagulation by binding and inhibiting thrombin

Y = heparin

52
Q

Protein C is activated by (X) and (stimulates/inhibits) coagulation.

A

X = thrombin (when bound to thrombomodulin receptor)

Inhibits

CFoM (18 decks)

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