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CMT-dos > Hemostasis & Coag > Flashcards

Hemostasis & Coag Flashcards

1
Q

Hemostasis

general

A

Innate, stepwise processes within the body that occurs following vessel injury → clot formation and cessation of bleeding

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2
Q

hemostasis

steps
Primary and secondary

A

Primary hemostasis
Platelet adhesion, activation, and aggregation to the damaged vascular endothelium, forming a plug (weak) that stops the bleeding temporarily

Secondary hemostasis
Activation of the coagulation cascade resulting in the formation of a more stable plug (strong fibrin clot)

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3
Q

Vasoconstriction

general

A

The blood vessel transiently constricts tolimit blood flow to the area

Vessel wall injury and constriction:
1. Site of injury
2. Constriction caused by endothelin release
3. Exposed collagen fibers

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4
Q

what drives vasoconstriction

A

What drives vasoconstriction?
* Neural stimulation reflex:innate contraction of the vascularsmooth muscles upon injury
* Endothelin:a vasoconstrictorsecreted from the damaged endothelial cells
* Thromboxane A2: a vasoconstrictor released fromactivated platelets

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5
Q

Primary Hemostasis

A

Following an endothelialcell injury, the following processes occur with theplateletsto form a temporary platelet plug:
Adhesion
Activation
Aggregation
Secretion

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6
Q

Primary Hemostasis

Platelet Adhesion

A

Platelets adhere to the site of injury with exposure to subendothelial components

What drives adhesion?
Platelet Gplb receptors tightly bind von Willebrand factor (vWF) which is released from injured endothelial cells
Other adhesion interactions with collagen, glycoprotein receptors, and tyrosine kinase receptors leading to adherent “activated” platelets

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7
Q

primary hemostasis

von Willebrand factor

A

glycoprotein that serves as the initial stationary foundation for clot formation

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8
Q

primary hemostasis

platelet activation

A

Activatedplateletsenhance further platelet adhesion and aggregation, and stimulatesecretion

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9
Q

Primary Hemostasis - Platelet Activation

Platelet activators

potent and weak

A

Potent platelet activators:
Thrombin: produced in the coagulation cascade
Collagen: interacts withplatelets at the site of injury

Weaker platelet activators:
ADP: acts in an autocrine fashion → released byplateletsto help activate otherplatelets
Epinephrine

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10
Q

Primary Hemostasis - Platelet Activation

Activatedplatelets will..

A

Undergo shape change to become an elongated pseudopod → new shape is extremely adherent
Activate theirGpIIb/IIIareceptors
Release their granules (alpha and dense)

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11
Q

Primary Hemostasis -

Platelet Aggregation

A

GpIIb/IIIareceptorspresent on the activated plateletsbegin binding to fibrinogen
Fibrinogen
Symmetricalmolecule
Canbind2plateletssimultaneously forming bridges betweenplatelets → platelet aggregation and formation of aprimary hemostatic plug

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12
Q

Primary Hemostasis - Platelet Secretion

A

Activated platelets release their granules (alpha and dense)

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13
Q

Primary Hemostasis - Platelet Secretion

Functions of secreted substances from granules of platelets

A

Recruit and activate additionalplatelets
Stimulate expression of GpIIb/IIIa onplatelets→ enhancedaggregation
Promotevasoconstriction
Stimulate the process of vascular repair via fibroblast/smooth muscle cellrecruitment
Contribute to initiation of thecoagulation cascade

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14
Q
A
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15
Q

Secondary Hemostasis – Coagulation Cascade

general

A

Series of reactions that ultimately generates a strong, cross-linkedfibrinclot

A number ofcoagulation factors undergo sequential activation by 1 of the 2 pathways

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16
Q

Secondary Hemostasis – Coagulation Cascade

Extrinsic pathway

A

Extrinsic pathway: primarily responsible forinitiationof the cascade; activated by tissue factor (factor 3) released by injured endothelial cells

ends with factor 10.

17
Q

Secondary Hemostasis – Coagulation Cascade

intrinsic

A

Intrinsic pathway: primarily involved inamplificationof the cascade; activated by negatively charged collagen in the subendothelial matrix

starts with 12 ends with 10

18
Q

Secondary Hemostasis – Coagulation Cascade

Common pathway:

A

Common pathway:
The extrinsic and intrinsic pathways join together to form the final common pathway when factor X is activated
Formation of thefibrinclot occurs at the end of the common pathway

starts with 10
ends with factor 13 which is fibrin clot

19
Q
A
20
Q

where do the Factors come from?

A

The liver is responsible for the formation of most factors (hepatocytes)
Factors XIII, XII, XI, X, IX, VII, V, II, and I

Exceptions:
Factor III and VIII originate from endothelial cells
Factor IV (calcium ion) is freely available in plasma

there is no factor 6

21
Q

as zymogens

A

inactive form of factors for coagulation

Become activated → act as a catalyst to cleave the next zymogen
Zymogen to enzyme activation was denoted with the letter a – Example: XII → XIIa

22
Q

which factors belong to which pathways

A

Pathway Factors
Extrinsic pathway: III and VII
Intrinsic pathway: XII, XI, IX, and VIII
Common pathway: X, V, II, I, and XIII

23
Q

vitamin K

general

A

Lipid cofactor that is required for normal blood clotting

Primarily synthesized in the colon as a byproduct of bacteria
Activated by epoxide reductase in theliver

24
Q

Vitamin K-dependent factors:

A

Factors II, VII, IX, X
Undergo carboxylation to become functional

25
Q

Inhibition of Coagulation

general

A

The body produces several substances that inhibit platelet binding,aggregation, andsecretion = natural anticoagulants

26
Q

natural anticoagulants

Tissue factor pathway inhibitor (TFPI)

A

Inhibits the activation of factor X
Located primarily on the surface of microvascular endothelial cells

27
Q

natural anticoagulants

Antithrombin III

A

Natural circulating anticoagulant produced by theliver
Inhibits activated forms of factors II, IX, and X

28
Q

natural anticoagulants

ProteinsC and Protein S

A

C:
Vitamin K-dependent factors produced by theliver
Protein C cleaves and inactivates factors V and VIII

S:
Vitamin K-dependent factors produced by theliver
Augments the activity of protein C

29
Q

Fibrinolytic Phase

A

The fibrinolytic system functions to remove the clot after the vasculature is repaired
Prevents excessive fibrin deposition
This process is accomplished primarily by plasmin

30
Q

Fibrinolytic Phase

Plasmin

A

Plasmin
Cleaves fibrin fibers (fibrinolysis) to form fibrin-degradation products
Cleaves other clotting factors (V, VIII, IX and X)
Plasminogen is activated →converted to plasmin by:
Tissue plasminogen activator (tPA)
Urine plasminogen activator (uPA)aka urokinase
Both are secreted by endothelial cells

31
Q

Coagulation Studies

general

A

Group of hematologic studies that reflect the function of blood vessels,platelets, and coagulation factors

Uses of coagulation studies
Evaluation of abnormal bleeding orthrombosis
Pre-operative testing
Management ofanticoagulationtherapy
Assist inresuscitationmanagement during massive transfusions

32
Q

Prothrombin Time (PT)

A

Time taken for theplasma to clot when exposed totissue factor
Measures function of the extrinsic and common pathways
Normal range: ~11–13 seconds

33
Q

prothrombin time

elevated in:

A

Warfarintherapy
Vitamin K deficiency
Deficiency of factors II, V, VII, and X
Liverdisease
Disseminated intravascular coagulation(DIC)

34
Q

prothrombin time (PT)

International Normalized Ratio (INR)

A

International Normalized Ratio (INR)
A ratio comparing the patient’s PT to a reference PT
Measures function of theextrinsicandcommonpathways
Normal range: approximately 0.8–1.1

35
Q

Activated Partial Thromboplastin Time (aPTT)

A

Time taken for theplasmato clot when exposed to a negatively charged substance (which activates the intrinsic pathway)
Measures function of both the intrinsic and common pathways
Normal range: ~25–40 sec

36
Q

Activated Partial Thromboplastin Time (aPTT)

elevated in

A

Elevated in:
Heparin therapy
Hemophilia(abnormal factor VIII or IX)
von Willebrand disease(vWD)
Liverdisease
Disseminated intravascular coagulation(DIC)

37
Q

Bleeding time (BT)

A

Measures the time for bleeding to stop after a lancet incision
Indirect measure of platelet function
Normal range: 2–7 minutes

prolonged in:
Thrombocytopenia
Disseminated intravascular coagulation(DIC)
von Willebrand disease(vWD)
Renal failure
NSAIDand/oraspirinuse

38
Q

Laboratory Evaluation of Coagulation

Fibrinogen

A

Precursor tofibrin
Abnormally low levels can increase bleeding risk
Bleeding tends to occur when levels < 100 mg/dL
Normal range: 200–400 mg/dL

39
Q

Laboratory Evaluation of Coagulation

D-dimer

A

Primary fibrin-degradation product
Released upon cleavage of cross-linkedfibrinby plasmin
Indicates recent or ongoing coagulation and fibrinolysis
Normal range: < 500 ng/mL

Elevated in:
DVT/PE
Stroke
Disseminated intravascular coagulation(DIC)
Covid-19 infection

CMT-dos (95 decks)

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