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Unit 3: LGS > Week 4 > Flashcards

Week 4 Flashcards

1
Q

3 qualities that you would find vital to hemostasis

A
  • Localized and precise
  • Rapidly responsive
  • Self-limited
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2
Q

Goal of hemostatsis

A

maintain blood flow

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3
Q

Types of hemostasis

A
  • Primary: platelet adhesion and aggregation, forming platelet plug
  • Secondary: cascade, clotting factors; Happens at same time as primary
  • Tertiary: clot resorption
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4
Q

Inactive Coagulation system

A
  • vWF: in collagen, platelet, or free floating in plasma
  • GPIa: active in resting state
  • GPIIb/IIIa: inactive in resting state
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5
Q

Steps of hemostasis

A
  1. Injury to site- collagen is exposed and tissue factor is released
  2. Endothelial and subendothelial cells release vFW which will unwind and go to collagen and tissue factor begins forming thrombin
    a. Thrombin: will activate platelets
    b. vFW: will activate platelets
  3. Activated platelets bind to vFW via GPIb
  4. Bound platelets expose GPIIb/IIIa
  5. Fibrinogen in blood will bind to GPIIb/IIIa of two platelets to cross link them and begin forming platelet plug
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6
Q

Activating platelet

  • what induces?
  • what is down stream effect?
A
  • by tissue factor and binding to vWF
  • induces exposure of GPIIb/IIIA
  • Undergo conformation change
  • Degranulate- will recruit more platelet to site of injury
  • Arachodonic acid is taken from phospholipid membrane and converted to thromboxane A2
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7
Q

Importance of conformational change in platelets

A

-from disc shape to spiny shape; important because it allows for increased surface area, because stuff happening in secondary hemostasis happens in membrane of platelet

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8
Q

Granules in platelets

A

-electron dense and specific granule

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9
Q

Electron dense granule

-secretions

A
  • ADP: activates more platelets

- Serotonin: localized vasoconstriction

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10
Q

Specific granule

-secretions

A
  • Fibrinogen: links two platelets together to form platelet plug
  • vWF: glue between platelets and collagen, draws platelet to site of injury
  • PDGF: will start repair
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11
Q

Secondary Hemostasis

A
  • Forms fibrin meshwork around platelet plug

- contributors: blood coagulation factors, platelets, calcium

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12
Q

Fibrin meshwork

A
  • Gives platelet plug stability

- Will permanently seal the site of injury

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13
Q

Blood coagulation factors

  • produced by:
  • types:
A
  • liver; already produced and present in blood, but inactive
  • Serine proteases (II, VII, IX, X, XI); break down proteins with serines
  • Cofactors: assist process by attaching to endothelium and collagen to help other enzymes bind
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14
Q

Coagulation factors I, II, III

-descriptive name, function/active form

A

I: fibrinogen, fibrin
II: prothrombin, serine protease
III: Tissue factor; cofactor

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15
Q

Extrinsic cascade

  • function
  • activation
  • pathway
A
  • produce small amount of Xa, to make small clot
  • Exogenous Tissue Factor (Factor III)- thromboplastin
  • Vascular injury–III (thromboplastin) + Ca–VII to VIIa (serine protease)–X to Xa (serine protease)
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16
Q

Intrinsic in-vitro

  • function
  • activated by
  • pathway
A
  • co-agulates blood outside of body
  • activated by contacting negatively charged surface; ex. Glas (Kininogen and kallirein)
  • produces large amount of Xa
  • XII to XiI a–XI to XIa–IX to IXa–IXa and Factor VIIIa converts X to Xa
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17
Q

Intrinsic in-vivo

  • function
  • activation
  • pathway
A
  • co-agulates blood in body by producing large amount of Xa
  • response to injury
  • Tissue Factor activates VII to VIIa, VIIa then binds to Tissue Factor; Thrombin activates XI to XIa; XIa and VIIa/TF combine to change IX to IXa; Thrombin activates VIII to VIIIa; IXa and VIIIa combine to make tenase; tenase then changes X to Xa
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18
Q

Common pathway

A
  • Xa + Va + Ca will activate prothrombin to thrombin; thrombin then activates fibrinogen to fibrin monomer and XIII to XIIIa; XIIIa then cross links fibrin monomers to make cross linked fibrin polymers (hard clot)
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19
Q

Thrombocytopenia

  • definition
  • based on
  • below in hospital patients
  • below in healthy patients
A
  • decreased number of platelets in blood
  • Defined based on reference range
  • Below 50,000 would be worried about spontaneous bleeding
  • In healthy patients 20,000 should be enough to stop spontaneous bleeding
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20
Q

Causes of thrombocytopenia

A
  • Destruction
  • Consumption: Decreased due to be used to make clot
  • Decreased production in the bone marrow
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21
Q

Chronic ITP thrombocytopenic purpura

-cause

A
  • Idiopathic (unknown cause) but it autoimmune mediated; Antibodies directed at platelets, Platelets destroyed in the spleen
  • Purpura: easy superficial bruising
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22
Q

Treatment for Chronic ITP thrombocytopenic purpura

A
  • Corticosteroid: Suppress immune response and decrease production of antibodies
  • Retuximab: Mono-clonoal antibody that targets b-cells making antibodies
  • Splenectomy: When nothing else works
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23
Q

Importance of history in bleeding disorders

A

-trying to figure out whether sxs are from genetic or acquired problem

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24
Q

What are we looking out for in PE for bleeding disorder

A

-collateral veins, bruising, redness, edema

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25
Q

Purpura

A

-superficial bleeding larger than 3 mm

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26
Q

Petichie

A

-superficial bleeding smaller than 3 mm, usually occurs in multiples

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27
Q

Labs ordered in patients with bleeding

A

CBC, PT, PTT

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28
Q

Labs for ITP

A

platelet: low
PT: normal
PTT: normal
peripheral blood smear: reduced amnt platelets and shows immature platelets

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29
Q

Von Willebrand Disease labs

A

platelet: normal
PT: normal
PTT: elevated
Platelet function assays

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30
Q

Clues that can distinguish between factor VIII/IX disorder and von Willebrand disorder

A

-von willebrand is included in primary and secondary clotting, so it will be seen in deep tissue and superficial bleeding

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31
Q

How is von Willebrand involved in secondary hemostasis?

A

It combines factor VIII and IX together to make tenays complex which will then activate factor X

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32
Q

Treatment for von Willebrand

A
  • Concentrated von Willebrand

- DDADP: vasopressin that causes endothelial cells to release all the von Willebrand factor that they have

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33
Q

Factor VIII deficiency labs

A
  • platelets normal
  • PT normal
  • PTT elevated
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34
Q

PTT mixing study

A
  • to detemine whether it is fator VII/IX deficiency or von Willebrand
  • will mix patients plasma with control plasma and repeat PTT, if PTT still elevated means that it is Factor deficiency
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35
Q

How to determine between factor VIII and factor IX deficiency

A
  • mix patients serum with serum of patient who has confirmed deficiency of one of the factors, then repeat PTT
  • If PTT is normal, then that patient has the opposite factor deficiency, if PTT remains elevated then that patient has that factor deficiency
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36
Q

Levles of Hemophilia A

A

Severe: only 1-2% of Factor VIII works
Moderate: 2-4% of factor VIII works
Mild: 4-30% of factor VIII works

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37
Q

Inheritance pattern of hemophilia A

A

-x-linked recessive

38
Q

Treatment of Factor VIII deficiency

A

-treat with concentrated Factor XIII pooled from plasma donations

39
Q

Vit K deficiency

A

-acquired form of bleeding problem, NOT hereditary

40
Q

Vit K deficiency labs

A
  • PT: elevated
  • PTT: elevated
  • Factor panels: II, VII, IX, X all low
41
Q

What does elevated PT and PTT mean?

A

-defect in common pathway OR in multiple factors

42
Q

Treatment for Vit K deficiency

A
  • Increase vitamin K in diet, dark/leafy greens
43
Q

Role of Vit K in hemostasis

A
  • helps to activate factors II, VII, IX, X (serine proteases)
  • Gammacarboxlyatin of glutamine residues: Helps with binding of Ca, which then helps to bind with negatively bound phosphomembrane and allows for factors to bind
44
Q

Types of vit K

A
  • Filoquinone (K1): green leafy veggies
  • Melaquinone (K2): from animals
  • Meladinone (K3): Has a lot of issues, not used often
45
Q

Filoquinone conversion

A
  • Filoqinone is converted to melaquinone through gut microbiota
  • Melaquinone is more active and stable form
46
Q

Causes of Vit K deficiency

A
  • antibiotics: would kill gut micro co plant vit K cannot be turned into stable more active form
  • Fat malabsorption: because kitamin k is fat soluble vitamin
  • New born babies: need vitamin k shots
47
Q

Tertiary hemostasis

A

will occur a few days after clot formation because it breaks down the clot

48
Q

Clot retraction

A
  • clot shrinks: will help to close wound by pulling ends together
  • Fibrinolysis: will degrade fibrin polymers
49
Q

Plasminogen

A

created in liver and in plasma, it’s the inactive form–activated to plasmin

50
Q

tPA and U-PA

A
  • activates plasminogen to plasmin
51
Q

Streptokinase

A
  • tPA produced by bacteria that can bind to plasminogen and create plasmin
52
Q

Plasmin

A
  • breaks down fibrin

- is in free and bound form

53
Q

a2- antiplasmin

A

-turns off free form of plasmin so that it will not degrade clot

54
Q

How is hemostatic cascade turned off?

A
  • Protein C-Protein S

- Serpins and anti-thrombin

55
Q

Protein C

A
  • Production: by the liver, inactive form in present in the blood and is activated by thrombomodulin
  • will destroy factor V and VIII so that pro-thrombulin complex cannot be made and prothrombin will not be activated into thrombin
56
Q

thrombomodulin

A

-receptor on endothelial membrane, will activate protein C once thrombin binds to receptor

57
Q

difference between bound thrombin and free thrombin

A
  • Free: would activate factor V - pro hemostasis

- Bound: would inactivate factor V through protein C-anti hemostasis

58
Q

Serpins

A

serine protease inhibitors; needed to deactivate proteases so they do not start breaking down random proteins in the body

59
Q

Anti-thrombin III

A
  • specific serpin
  • Binds to free thrombin and inactivates it
  • Will also inhibit thrombin production by inhibiting factor 12, 11, 10, 9
60
Q

Heparin

A

-Produced by mast cells; will bind to anti-thrombin to make it fit thrombin more tightly to inactivate thrombin better

61
Q

Thrombosis

A
  • Pathological formation of a clot; no injury occurs

- different from hemostasis because hemostasis clot formation is to help with injury

62
Q

Virchows triad

A

-endothelial injury, hypercoagilability and abnormal blood flow cause thrombosis

63
Q

Endothelial injury

A

-endothelium maintains balance b/w pro-thrombosis (clotting factors) and anti-thrombosis (turns off mechanism)

64
Q

Extrinsic thrombotic factors

A

Tissue factor (factor III)

65
Q

Intrinsic thrombotic factors

A
  • vWF (present in sub-endothelium as well)
  • Factor VIII
  • Endothelin
66
Q

Anti-thrombotic factors

A
  • tPA

- Thrombomodulin

67
Q

Causes of endothelial changes

A
  • Trauma, inflammation, plaques, free radicals (oxidative stress), toxins, infections
  • all of these will make epithelium hyperactive or dysfunctional; these change gene expression from anti-thrombotic to pro-thrombotic to prod. A diff. set of proteins that might be contributory towards the process
68
Q

Procoagulant changes

A
  • Prod. TPA inhibitor which won’t degrade the fibrin
  • Won’t express thrombomodulin so you have lots of free floating thrombin which is prothrombin
  • Might dec. internal heparin meaning anti-thrombin 3 won’t be activated
69
Q

stasis

A

slowing of blood flow

70
Q

causes of turbulence and stasis

A
  • Plaques or aneurysms
  • Ppl wit sickle cell anemia have abnormal blood cells that can get stuck in smaller blood vessels causing stasis leading to thrombosis
  • Polycythemia - Change in laminar blood flow damaging endothelium causing thrombotic effects
71
Q

Plaques

A

caused by cholesterol, calcium, and macrophages settling in blood vessel and being trapped in endothelial and being oxidized by free radicals

72
Q

Hypercoagulability

A

-Forming more blood clots that can be due to genetics (primary hypercoagulability) and acquired (secondary hypercoagulability)

73
Q

Factor V Leiden

A

• Point mutation in factor 5 gene
• Isn’t inhibited by protein C
• Another example of hypercoagulability: pro-thrombin (point mutation in regulatory region that leads to prod. Of a lot of clots)
-Anti-thrombin III deficiency

74
Q

Methionine

A
  • First a.a present in eukaryotic proteins
  • It has a thiol group so has sulfur
  • produces homocysteine through methylation by using SAM and B9
  • B12 helps B9 grab methyl group
75
Q

Homocysteine

A

-precursor to cysteine (transulfuration through vit B6) or can be reconverted to methionine

76
Q

Risk factors for CAD

A
  • Hypertension - endothelial damage that dep. On other secondary affects patient has from hypertension; basically having high pressure damaging endothelium
  • Elevated cholesterol - plaque formation which can cause turbulent blood flow and endothelial dysfunction
  • Smoking - causes endothelial damage
  • Inc. age: less elasticity in vessels
77
Q

Arterial thrombus

A

-caused by Atherosclerosis
-Composed of platelet aggregates
- high flow
endothelial damage both activate platelets to make a firm clot to withstand high blood flow
-use anti-platelet medications (aspirin)

78
Q

Venous thrombus

A

○ Has platelets but more rich in fibrin
○ Don’t have as much platelet involvement
○ more related to low blood flow conditions
loss of laminar flow b/c cells are just sitting there not flowing so can initiate contact and adhesion
-use anti-coagulant medications

79
Q

Aspirin

A
  • Irreversible cox 1 inhibitor so inhibits aracondonic acid
  • Has more of a platelet affect than other meds
  • If having outpatient elective surgery then patient should stop aspirin for a 7-10 days b/c that’s about how long platelets live for; should at least stop 5 days before b/c then would have at least a good amount of functional platelets; there are several tests that can test the functions of platelets w/ drug use
80
Q

How does myocardial infraction place the patient at an increased risk of cardiac thrombus formation?

A
  • fibrosis of wall: decreased motility

- potential focal thinning of wall: aneurysm formation

81
Q

Abciximab

A
  • Monoclonal antibody
  • 2b3a receptor blocker
  • 2b3a binds to fibrinogen and that allows for platelet aggregation
  • Given intravenously (IV form)
  • Limited to patients going in for percutaneous
  • Prevents additional thrombotic
82
Q

Clopidogrel

A

• Blocks ADP receptor which are in granules in platelets and when they become activated the platelets degranulate
• Used in combination w/ aspiring
-Delivered orally

83
Q

Lab test for DVT

A

D-dimer; ultrasound

84
Q

Treatment for DVT

A
  • Initial: Lovonox - low molecular weight only inhibits factor VIII (been cut up and only keeps parts that are active), subcutaneously; don’t give for kidney problems; Heparin - unfractioned molecular weight; given intravenously or subcutatenously; would give if need to act quickly and don’t know patient history
  • Long term: Warfarin - would give while still on heparin b/c protein C; vit. C has to be in the reduced form and it serves as a co-factor; has to be converted back into its reduced form but warfarin blocks it (2, 7, 9, 10); protein C and factor 7 have a very short half life
85
Q

Heparin MOA

A
  • unfactionate heparin: binds to anti-throbin III to inactivate thrombin and Xa
  • lower molecular (enoxaprin) and fondaparinux: inhibits prod. Of Xa from X; lower bleeding risk profile
86
Q

Rivaroxaban

A
  • Factor Xa inhibitor

- oral

87
Q

Dabigatran

A
  • Thrombin inhibitor

- oral

88
Q

Strokes

  • diagnosis
  • time importance
A
  • CT; check if hemorrhagic or ischemic stroke b/c if they’re bleeding you don’t want them to bleed more
  • tissue plasminogen needs to be given w/I 2 hrs
89
Q

Fibrinolytics

A

-More and more fibrin so starts to get more dense and has cross-linking

90
Q

TPA

A
  • breaks down fibrin

- not as effective after 3-4 hours because of fibrinolytics

Unit 3: LGS (7 decks)

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