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Hematology (C) > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What is hemostasis?

A

A complex physiologic process that keeps circulating bld in a fluid state and then, when an injury occurs, produces a clot to stop the bleeding, confines the clot to the site of injury, and finally dissolves the clot as the wound heals

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2
Q

What are the aims of hemostasis?

A
  1. To make bld flow smooth once the injury has been healed
  2. Stops the bld from going out of the bld vessels / minimizing bld loss via the fomation of clot
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3
Q

What is the detailed process of hemostasis?

A

Once injury is present / occur -> bld vessels will detect the injury and send signal so that the body can send commands to minimize bld loss (minimizing bld loss is done via vasoconstriction wherein the affected bld vessel and its lumen will become more narrow -> resulting for the bld to flow in other adjacent bld vessels and only minimal bld will flow in the affected bld vessel = minimized bld loss) -> but bld loss is still present, hence, PLTs (w/c comes from the bld that flows in the affected bld vessel) will activate themselves -> once PLTs activate themselves, they will become sticky -> then, PLTs will form a temporary PLT plug (only temporary because this PLT plug is unstable: because under minimal stress, it can be easily dislodged / removed) in the site of injury via sticking themselves w/ 1 another -> to make the temporary plug stronger, PROs (specifically coagulation factors) will take action -> the coag factors will activate 1 anohter and create an end product called as fibrin clot / mesh (w/c is made of fibrin strings / polymers that sticks to 1 another | where PLTs, RBCs, and WBCs will be trapped | w/c will stay for several days depending on the severity of the injury as the wound heals) -> when such various cells are trapped in the mesh, the bleeding will be stopped -> the stable fibrin clot must be removed when the wound is already healed (because if the clot is not removed, the affected bld vessel will be obstructed -> resulting for the bld flow to not be smooth) -> hence, the clot must be removed via the process of fibrinolysis

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4
Q

What are the steps that occur in hemostasis?

A
  1. Vasoconstriction
  2. Primary hemostasis
  3. Secondary hemostasis
  4. Fibrinolysis
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5
Q

What are the main players in vasoconstriction?

A
  1. Smooth muscle (in the bld vessel)
  2. Brain (for issuing impt commands)
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6
Q

What is the main player in primary hemostasis?

A

PLTs

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7
Q

What is the end product in secondary hemostasis?

A

Formation of stable fibrin clot

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8
Q

What is fibrinolysis?

A

Breaking down of fibrin clot

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9
Q

What is the main player in fibrinolysis?

A

Plasmin

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10
Q

What is the fxn of plasmin?

A

Inhibits clotting by destroying the formed clots

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11
Q

Where does plasmin come from?

A

Plasminogen (when plasminogen is activated, it becomes plasmin)

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12
Q

Hemostasis comes from what Greek words?

A
  1. Haima: bld
  2. Stasis: to stop
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13
Q

What are the 3 main layers of bld vessel?

A
  1. Tunica adventitia / Vascula adventitia / Tunica externa
  2. Tunica media / Vascula media
  3. Tunica intima/e / Vascula intima / Tunica interna
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14
Q

Where are the ff layers of the bld vessel located:

  1. Tunica adventitia
  2. Tunica media
  3. Tunica intima/e
A
  1. External
  2. Middle
  3. Internal
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15
Q

What are the cells present in tunica adventitia?

A
  1. Collagen / subendothelial collagen (SEC)
  2. Fibroblasts
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16
Q

What are the cells present in tunica media?

A
  1. Smooth muscles (main)
  2. Elastic tissues
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17
Q

What is the cell present in tunica intima/e?

A

Endothelial cells

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18
Q

What is the characteristic of endothelial cell and its purpose?

A

It has a non-reactive surface

W/c makes bld flow smooth as possible

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19
Q

What is the fxn of endothelial cells?

A

Secretes a lot of substances that makes sure that PLTs will not be activated

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20
Q

What is the fxn of smooth muscles?

A

For movement (vasoconstriction and vasodilation)

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21
Q

What is vasoconstriction?

A

Narrowing of bld vessels

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22
Q

What is the purpose of vasoconstriction?

A

To minimize bld loss when there’s an injury

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23
Q

How long does vasoconstriction take place?

A

Occurs within 1st few secs after 1st few mins of injury, hence, it’s an immediate short-lived rxn (depending on the severity of injury)

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24
Q

What is vasodilation?

A

Lumen of bld vessels enlarges

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25
Q

When does vasodilation occur?

A

After vasoconstriction

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26
Q

What is the purpose of vasodilation?

A

To ensure that the site of injury is free from bacteria -> this is done via sending WBCs by the bld (to hasten the process of sending WBCs in the site of injury, vasodilation will occur [bigger lumen = more WBCs])

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27
Q

What are the fxns of collagen?

A
  1. To protect bld vessel from surrounding outside structures
  2. Prevents smooth muscles from overextending (during vasodilation)
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28
Q

How can hemostasis make sure that there is smooth bld flow in the absence of injury?

A

Via the action of endothelial cells w/c secretes a lot of substances called antithrombotic factors

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29
Q

True or False

Antithrombotic factors, procoagulants, vasoconstrictors, and vasodilators present in balance

A

True

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30
Q

What continuously secretes antithrombotic factors, procoagulants, vasoconstrictors, and vasodilators in the absence of injury?

A

Endothelial cells

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31
Q

Once injury is present, what will be increased?

A
  1. Procoagulants
  2. Vasoconstrictors
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32
Q

What are the 2 classifications of antithrombotic factors?

A
  1. Antiplatelets
  2. Anticoagulants
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33
Q

What is the fxn of antiPLTs?

A

Inhibits primary hemostasis

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34
Q

What is the fxn of anticoagulants?

A

Inhibits 2ndary hemostasis

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35
Q

What are the exs of antithrombotic factors?

A
  1. Thrombomodulin
  2. Antithrombin
  3. Prostacyclin
  4. Plasminogen activator
  5. Heparin

TAPPH

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36
Q

What is the fxn of thrombomodulin?

A

Influences / modulates thrombin (factor IIa) to become anticoagulant

If thrombin is procoagulant (w/c promotes / supports coagulation) -> w/ the presence of thrombomodulin, it will influence thrombin to become an anticoagulant (because 1 of the special features of thrombin is to become either a procoagulant / anticoagulant)

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37
Q

What is the fxn of antithrombin?

A

Primary inhibitor of thrombin

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38
Q

What is the fxn of prostacyclin?

A

Inhibits the activity of PLTs / inhibits PLT activation

Instead of the PLTs being activated, the process of activation is inhibited by prostacyclin -> to ensure that there is a smooth bld flow (because an activated PLT is sticky -> hence, even w/out injury, it can adhere in the surfaces of the bld vessel)

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39
Q

What is the fxn of plasminogen activator?

A

Plasminogen activator is an enzyme that activates plasminogen to plasmin

Plasmin is a PRO that dissolves fibrin -> reason why it’s considered an antithrombotic factor

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40
Q

What are the fxns of heparin?

A
  1. Anticoagulant
  2. Inhibits factors II and X
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41
Q

What are procoagulant factors?

A

Factors that promote coagulation

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42
Q

What are the exs of procoagulant factors?

A
  1. von Willebrand factor (vWF)
  2. Plasminogen activator inhibitor-1 (PAI-1)
  3. Platelet activating factor
  4. Thromboxane A2
  5. Thromboplastin

vPP(pepe)TT(tite)

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43
Q

What is the fxn of vWF?

A

It serves as a bridge for PLTs to adhere to bld vessels

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44
Q

What is the fxn of PLT activating factor?

A

Activates PLT

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45
Q

What is the fxn of PAI-1?

A

Inhibits plasminogen activator

Hence, if plasminogen activator is absent, plasminogen will not be activated to plasmin -> if plasmin is absent, there will be no fibrinolysis

PAI-1 is the opposite of plasminogen activator

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46
Q

What is thromboplastin and its fxn?

A
  1. It is a compound derived from cell membranes
  2. It’s other name is tissue factor -> but this is a misnomer because thromboplastin is a combination of tissue factor + phospholipids

Enhances activity of factor X

Thromboplastin is sort of the opposite of heparin

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47
Q

What is the fxn of thromboxane A2?

A

Supports the activation of PLTs

Thromboxane A2 is the opposite of prostacyclin

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48
Q

Enumerate the antithrombotic factors and their procoagulants counterparts and explain why

A
  1. Prostacyclin and thromboxane A2
    -> Prostacyclin: inhibits activity of PLTs / inhibits PLT activation
    -> Thromboxane A2: supports PLT activation
  2. Plasminogen activator and PAI-1
    -> Plasminogen activator: activates plasminogen to become plasmin
    -> PAI-1: inhibits activation of plasminogen
  3. Heparin and thromboplastin
    -> Heparin: inhibits factors II and X
    -> Thromboplasin: enhances activity of factor X
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49
Q

What is the fxn of vasodilators?

A

Dilates bld vessels

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50
Q

What are the exs of vasodilators?

A
  1. Nitric oxide
  2. Prostacyclin

NP

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51
Q

What are the vasodilators?

A
  1. Nitric oxide
  2. Prostacyclin

NP

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52
Q

What are the fxns of nitric oxide?

A
  1. Inhibits via interruption of PLT adhesion and aggregation
  2. Stimulates disaggregation of preformed PLT aggregates

If clot is present in a sp site -> nitric oxide can disaggregate the clot

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53
Q

What is the fxn of prostacyclin?

A

Inhibits PLT aggregation

54
Q

What are the exs of vasoconstrictors?

A
  1. Thromboxane A2
  2. Angiotensin converting enzyme (ACE)
  3. Leukotrienes
  4. Endothelin

vasoCONSTRICTors = TALE

55
Q

What are the fxns of thromboxane A2?

A

Vasoconstrictor (and also a procoagulant)

Vasoconstrictor + procoagulant

56
Q

What is the fxn of ACE?

A

Enhances PLT aggregation

ACE is the opposite of prostacyclin and nitric oxide (sort of)

57
Q

What are leukotrienes and its fxn?

A

They are vast of substances

Can be a vasoconstrictor / vasodilator
-> but in hemostasis, most of leukotrienes are vasoconstrictors

58
Q

What are the characteristics of endothelin?

A
  1. Most potent vasoconstrictor in hemostasis
  2. Secreted by endothelial cells
59
Q

What are the phases that occur during hemostasis upon injury?

A
  1. Vascular phase
  2. Primary hemostasis
  3. Secondary hemostasis
  4. Fibrinolysis
60
Q

How does fibrinolysis differ from other events that happen during hemostasis upon injury?

A

All of the phases that occur during hemostasis upon injury will start simultaneously upon getting injured, however, fibrinolysis will be completed after a few days -> hence, the activation of plasminogen will occur when an injury occurred (but the process will be very slow) -> the activation of plasminogen needs to be very slow because plasminogen must not be activated within a few mins, no clot will be formed

61
Q

What are the detailed events that happen during hemostasis upon injury?

A

Vascular phase
1. Brain will send signals / electrical impulses to smooth muscles (because there are neurons [sensory nerve endings] in bld vessels for vasoconstriction / vasospasm
2. Substances such as serotonin (w/c is a happy hormone by it can also serve as a vasoconstrictor | along w/ dopamine, endorphins, and oxytocin | w/c is secreted by PLTs -> w/c means that there are serotonin hormones in the plasma) will ensure that the vasoconstriction that happened will occur continuously (for a few / several mins) and will not occur quickly because the electrical impulses will not be enough

Primary hemostasis
3. PLTs will start to crowd the affected area
4. PLTs will form a temporary PLT plug in the site of injury

Secondary hemostasis
5. Coag factors will enhance the temporary PLT plug
6. Once fibrin clots are present, it will maintain its state for a few days while the tissues in the affected area are healing

Fibrinolysis
7. After a few days, plasminogen will be converted into plasmin

62
Q

What is the characteristic of vasoconstriction?

A

Shortest process (can only last for secs to a few mins [no std time: because the severity of injury is not std] | large injury = longer vasoconstriction | small injury = shorter vasoconstriction)

63
Q

What are the events that happen in vasoconstriction (in hemostasis)?

A
  1. Bld vessels have sensory nerve endings -> when they detect an injury -> they will send signal to the brain -> then, brain will send series of commands to make sure that the smooth muscle will contract (continuous contraction is called vasospasm)
  2. Then, primary hemostasis will occur

Bld vessels will send signals to the brain -> brain will send series of command to conduct vasospasm -> primary hemostasis will occur

64
Q

What is the characteristic of PLTs?

A

Unnucleated fragments

65
Q

What are the characteristics of inactivated PLTs in a normal / healthy state?

A
  1. Disc-shaped
  2. Not sticky
66
Q

What will happen to inactivated PLTs once they are activated and why?

A

They will shrink because they need to secrete various substances

67
Q

What are the characteristics of activated PLTs?

A
  1. Irregularly shaped
  2. Sticky
68
Q

Are PLTs present in the bone marrow? Why and why not?

A

No, because megakaryocytes are present in the bone marrow, not PLTs

69
Q

What are the characteristics of megakaryocytes?

A
  1. Biggest WBC
  2. Capable of producing up to 4,000 PLTs
70
Q

How are PLTs produced?

A

When megakaryocytes mature (where they began to have appendages w/c will detach overtime) -> these detached fragments are called as PLTs w/c are seen in the bld vessels

71
Q

What are the 3 main steps / stages of primary hemostasis?

A
  1. PLT adhesion
  2. PLT aggregation
  3. PLT secretion

In other references, the order of steps / stages are: 1. PLT adhesion, 2. PLT secretion, and 3. PLT aggregation
-> after secretion of granules (in PLT secretion) -> other PLTs will aggregate to form clumps

72
Q

What happens in PLT adhesion?

A

Step in w/c PLTs bind to non-PLT surfaces such as SEC
-> where adhesion of PLTs to bld vessel happen (specifically in the SEC)

73
Q

What happens in PLT aggregation?

A

Step in w/c PLTs bind to 1 another to form aggregates (w/c are clumps)

74
Q

What happens in PLT secretion?

A

Step in w/c PLT release their granules

75
Q

What is the characteristic of the step of PLT secretion?

A

Happens simultaneously w/ PLT adhesion and aggregation

76
Q

What is the key player in PLT adhesion?

A

GP1b

77
Q

What are the characteristics of vWF?

A
  1. Suspended in the plasma
  2. Secreted by:
    a. Endothelial cells
    b. PLTs
  3. Have an affinity to SEC
  4. Attracted to:
    a. PROs
    b. GP Ib/IX/V (w/c is present in the surface of PLTs)

Endothelial cells and PLTs secrete vWF -> hence, vWF is suspended in the plasma

78
Q

What are the detailed events that happen in PLT adhesion?

A
  1. In healthy state, endothelial cells secrete nitric oxide and prostacyclin w/c fxns as vasodilators and keep the PLTs from adhering to surface of endothelial cells
  2. Upon injury to the endothelial cells, the production of nitric oxide and prostacyclin will be interrupted, thus allowing PLTs to adhere to the endothelial cells
    -> hence, if there are no nitric oxide and prostacyclin -> PLTs will become activated and they will become free to adhere to the surface of bld vessels -> such PLTs are mostly attracted to the site of injury because they are more attracted to endothelial cells than endothelial collagen
  3. Upon injury, the vWF (suspended in the plasma: because it is secreted by endothelial cells and PLTs | have an affinity to SEC -> hence, vWF will adhere to the SEC | they are also attracted to PLTs [they are attracted to PROs and various substances seen in the PLTs, 1 of w/c is GP Ib/IX/V w/c is present on the surface of PLTs -> hence, vWF binds to the SEC and GP Ib/IX/V and acts as a bridge between collagen and PLT]) that is secreted by the endothelial cells will adhere to the SEC
  4. The GP1b (specifically GP Ib/IX/V w/c is made up of 3 glycoPROs such as glycoPRO Ib, V, and IX) expressed on the surface of the PLTs will adhere to the vWF that is attached to the SEC
  5. PLT activation will then take place, altering the shape of the PLT by forming pseudopods
    -> once PLT is activated -> PLT aggregation will then be activated

Endothelial cells secrete nitric oxide and prostacyclin -> upon injury, the production of nitric oxide and prostacylcin will be interrupted -> resulting for PLTs to adhere to the endothelial cells -> vWF will be suspended in the plasma -> vWF will adhere to SEC and GP Ib/IX/V and acts as a bridge between collagen and PLT -> GP1b will adhere to vWF that is attached to the SEC -> PLTs will be activated

79
Q

What is the dse / condition called if there is a reduction / total absence of GP1b resulting from the inability of PLTs to adhere on the vessel walls?

A

Bernard-Soulier syndrome (BSS)

80
Q

What are the symptoms of pts w/ BSS?

A
  1. Easy bruising
    -> since PLT adhesion will not occur -> temporary PLT plug will not occur -> resulting to easy bruising (because the bld will go outside the bld vessels and then will be stuck between tissues | easy bruising will occur especially if the bld vessel is shallow enough)
  2. Nosebleeds
  3. Menorrhagia
    -> abnormally strong / profuse bleeding in females during menstruation
  4. Gastrointestinal bleeding
    -> occassionally occurring only
    -> depends on severity of BSS
81
Q

What are the physical findings in a pt w/ BSS?

A
  1. Increased bruising
  2. Purpura
  3. Petechial rash
82
Q

What is the key player in PLT aggregation?

A

GP2b/3a

83
Q

What are the events that happen in PLT aggregation?

A
  1. After adhering to the SEC, PLTs will then secrete adenosine diphosphate (ADP) in order to activate glycoPRO IIb/IIIa (GP2b/3a)
  2. GP2b/3a will then bind to the vWF that is present in the plasma
  3. GP2b/3a of other PLTs will then bind to the opposite side of the vWF
  4. Such steps mentioned above will result to the formation of a temporary PLT plug

Other rationale of events that happen in PLT aggregation:
1 end of vWF will bind to the subunits of the SEC and the other end is bounded to the GP1b found on the surface of PLTs (multiple layers must be present to ensure that clot is durable w/c is done via the production of PLTs) -> GP2b/3a has an affinity w/ vWF (if GP1b is only capable to binding w/ vWF, GP2b/3a can bind to vWF and fibrinogen) + GP2b/3a of other PLTs will also bind to the vWF = formation of aggregates

84
Q

What is GP2b/3a?

A

A glycoPRO that can bind to both vWF and fibrinogen

85
Q

What is the other term of fibrinogen?

A

Factor I

86
Q

What is the dse / condition called if there is an abnormality w/ GP2b/3a resulting to an inability of PLTs to form aggregates?

A

Glanzmanns thrombasthenia

87
Q

What are the symptoms of pts w/ Glanzmanns thrombasthenia?

A
  1. Easy bruising
  2. Nosebleeds
  3. Menorrhagia
  4. Gastrointestinal bleeding (occasional)
88
Q

What are the physical findings from a pt w/ Glanzmanns thrombasthenia?

A
  1. Increased bruising
  2. Purpura
  3. Petechial rash
89
Q

What are alpha and dense granules?

A

Mostly procoagulants

90
Q

What are being secreted in PLT secretion and their fxns?

A
  1. Alpha granules
    a. Fibrinogen
    -> serve as bridge for receptors such as GP2b/3a and GP Ib/IX/V
    b. vWF
    -> serve as bridge for receptors such as GP2b/3a and GP Ib/IX/V
  2. Dense granules
    a. Serotonin
    -> vasoconstrictor
    b. ADP
    -> aids in PLT activation
    c. Ca
    -> cofactor needed for 2ndary hemostasis
  3. Other contents
91
Q

What is the characteristic of PLT secretion?

A

Happens simultaneously during PLT adhesion and aggregation, w/ most secretion occurring during the aggregation phase

92
Q

What are the substances that promotes coagulation?

A
  1. High molecular weight kininogen (HMWK)
  2. Fibrinogen
  3. Factor V
  4. Factor VIII: vWF / factor VIII
    -> factor VIII is written as factor VIII: vWF because factor VIII is a labile factor (meaning, it is easily broken down) -> in order to protect factor VIII, it has to bind w/ vWF
93
Q

What is the source of the substances that promotes coagulation?

A

Alpha granules

94
Q

What is the fxn of HMWK?

A

Contact activation of intrinsic coag pathway

95
Q

What is the fxn of fibrinogen?

A

Converted to fibrin for clot formation

96
Q

What is the fxn of factor V?

A

Cofactor in fibrin clot formation

97
Q

What is the fxn of factor VIII?

A

Assists PLT adhesion to SEC to provide coagulation on surface

98
Q

What are the substances that promotes aggregation?

A
  1. ADP
  2. Ca
  3. Platelet factor 4
99
Q

What are the sources of:

  1. ADP
  2. Ca
  3. PLT factor 4
A
  1. Dense granules
  2. Dense granules
  3. Alpha granules
100
Q

What is the fxn of ADP, Ca, and PLT factor 4?

A

Promote PLT aggregation

101
Q

What are the substances that promotes vasoconstriction?

A
  1. Serotonin
  2. Thromboxane A2
102
Q

What are the sources of:

  1. Serotonin
  2. Thromboxane A2
A
  1. Dense granules
  2. Membrane phospholipids
103
Q

What is the fxn of serotonin and thromboxane A2?

A

Promotes vasoconstriction at site of injury

104
Q

What are the substances that promotes vascular repair?

A
  1. PLT derived growth factor
  2. Beta thromboglobulin
105
Q

What is the source of PLT derived growth factor and beta thromboglobulin?

A

Alpha granules

106
Q

What is the fxn of PLT derived growth factor?

A

Promotes smooth muscle cell growth for vessel repair

107
Q

What is the fxn of beta thromboglobulin?

A

Chemotactic for fibroblasts to help in vessel repair

108
Q

What are the substances that affects other systems?

A
  1. Plasminogen
    -> / plasmin
    -> produced by the PLTs within the same day
    -> process of converting plasminogen to plasmin will take days
  2. Alpha 2-antiplasmin
109
Q

What is the source of plasminogen and alpha 2-antiplasmin?

A

Alpha granules

110
Q

What is the fxn of plasminogen?

A

Precursor to plasmin w/c induces clot lysis

111
Q

What is the fxn of alpha 2- antiplasmin?

A

Major inhibitor of plasmin (hence, it will inhibit clot lysis)

112
Q

What are the fxns of prostacyclin and nitric oxide?

A
  1. Vasodilators
  2. PLT receptor blockers
  3. Prevent PLT activation
113
Q

What is the meaning of CD?

A

Cluster of differentiation

114
Q

What is CD 39?

A

Enzyme produced by endothelial cells that metabolizes ADP and ATP in PLTs thereby impeding its fxn

115
Q

What is the importance of ATP?

A

Needed by cells (serves as energy) for them to fxn

116
Q

What is the fxn of aspirin and non-steroidal anti-inflammatory drugs (NSAIDS)?

A

Prevents formation of thromboxane A2 (TxA2)

117
Q

What are the tests for assessing vascular integrity (in primary hemostasis)?

A
  1. Bleeding time
  2. Capillary fragility test
118
Q

What is the general characteristic of the tests for vascular integrity?

A

Tests to determine if the bleeding present is caused by a problem in the bld (coag factors and PLTs) / a problem of fragile veins (/ bld vessels)

119
Q

What are the tests under capillary fragility test?

A
  1. Rumpel-Leede test / Tourniquet test / Hess test / Positive pressure technique
  2. Petechiometer method / Suction cup method / Negative pressure method
120
Q

What is the general aim of tests for quantitative evaluation of PLTs?

A

Tests to determine the # / quantity of PLTs

121
Q

What are the tests for quantitative evaluation of PLTs?

A
  1. Direct method
    a. Rees and Ecker
    b. Tocantin’s method
  2. Indirect method
    a. Founyaun’s? method
  3. Unopette system
  4. Automated counting machine
    a. Flow cytometry
122
Q

What is the general aim of the tests for qualitative evaluation of PLTs?

A

Tests to determine the fxn of PLTs

123
Q

What are the categories of tests for qualitative evaluation of PLTs?

A
  1. Tests for PLT adhesion
  2. Tests for PLT aggregation
124
Q

What are the tests for PLT adhesion?

A

Bleeding time
1. Duke’s method
2. Ivy’s method
3. Adelson-Crosby method and Macfarlane method
4. Copy-Lalitch method

125
Q

What are the tests for PLT aggregation?

A
  1. Turbidimetry
  2. Nephelometry
    a. ADP
    b. Collagen
    c. Epinephrine
    d. Snake venom
    e. Thrombin
    f. Ristocetin

ADP downwards are agents / agonists that are used to aggregate PLTs

126
Q

What are agonists?

A

Substances that promote either aggregation / adhesion

127
Q

What is the characteristic of Duke’s method (of bleeding time)?

A

Most practical method (only needs lancet, cotton, filter paper, and a timer)

128
Q

How is Duke’s method (of bleeding time) done?

A

Pt is pricked using a lancet on the fingertip / earlobe -> time is then measured from the time of pricking up to the time when bleeding stops

129
Q

What is the characteristic of Ivy’s method (of bleeding time)?

A

Better than Duke’s method

130
Q

How is Ivy’s method (of bleeding time) done?

A

Constant pressure is applied (via the use of pressure cuff) -> puncture forearm w/ BP cuff set at 40 mmHg using a lancet -> time is then measured from the time of pricking up to when bleeding stops

Hematology (C) (1 decks)

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