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APA II > hematology and anesthesia-naglehout 34 > Flashcards

hematology and anesthesia-naglehout 34 Flashcards

1
Q

1) where is intima of vessel wall

2) what does it secrete

A

1) inner layer separates flowing blood from endothelial wall

2) procoagulants, anticoagulants, and fibrinolytics

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2
Q

describe von willibrand factor

A

important mediator that is a necessary cofactor for adherence of platelets to subendothelial layer

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3
Q

describe tissue factor

A

activates clotting cascade path when injury to vessel occurs

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4
Q

describe 2 mediators that cause vasoconstriction

A

1)thromboxane A2, 2)adenosine diphosphate

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5
Q

describe 2 mediators that cause vasodilation

A

nitric oxide and prostacyclin

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6
Q

how might an endothelial cell suppress activation of coagulation system

A

expression of tissue factor pathway inhibitor

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7
Q

what is the most important, simpelist function of the endothelial lining

A

forms a barrier that separates fluid content of blood from thrombogenic material (collagen, procoagulants) that lies beneath and within subendothelial space
the endothelial lining repels blood components away from vessel wall

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8
Q

describe the subendothelial layer

A

highly thrombogenic, contains collagen, a stimulus for platelet adhesion to damaged vessel wall and fibronectin, which facilitates anchoring of fibrin during formation of platelet plug

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9
Q

describe the adventitia

A

control of blood flow by influencing vessel contraction, produces nitric oxide (vasodilator)

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10
Q

describe the role of nitric oxide

A

inhibits platelet adhesion, aggregation, and binding of fibrinogen between glycoprotein IIb/IIIa complex
causes vasodilation by nitric oxide synthase which increases guanilate cyclase producing a 2nd messenger guanylate monophosphate, causing smooth muscle relaxation causing increase in blood flow which limits procoagulants by washing them away

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11
Q

describe prostacyclin

A

from prostaglandin, causes vasodilation, interferes with platelet aggregation and formation

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12
Q

describe the normal platelet count and lifespan of a platelet

A

150-300,000 8 -12 days

7.1x10^3 used each day

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13
Q

what do platelet alpha granules store

A

vWF, fibrinogen, fibronectin, platelet factor 4, and platelet growth factor

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14
Q

what do dense granules of platelet store

A

non proteins-serotonin ADP ATP histamine, epinephrine

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15
Q

what do platelet granules synthesize to enable platelets to promote vascular and local tissue reactions

A

prostaglandins

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16
Q

why do platelets make thrombin

A

activate some of the coagulation factors and influence recruitment of platelets to site of injury

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17
Q

after vessel injury from plaque dislodgement, surgical instrumentation, or trauma, what happens next five steps

A

1) vessel wall contracts, decreases blood flow via thromboxane A2 and ADP
2) adhesion-vWF from endothelial cell emerges, GpIb from platelets attach to vWF, and call other platelets to site of injury 3)TF causes platelet to become activated 4)from platelet GpIIb/IIIa emerge to link other platelets to form a platelet plug 5)platelets release alpha and dense granules, contractile granules, and thrombin to promote procoagulant activity
* this platelet plug is unstable, if this does not control issue activation of coagulation cascade is next

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18
Q

what coagulation factors are not enzymes? what is another word for coagulation factors

A

factor V, VIII

zygomens

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19
Q

how is extrinsic pathway activated, what is another name for it, and what are factors in it

A
  • activated by release of tissue factor when injury occurred outside the vessel wall
  • tissue factor pathway
  • III(tissue factor aka thromboplastin) and VII (proconvertin)
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20
Q

describe extrinsic pathway 8 steps

A

1)damage occurs outside of blood vessels, 2)tissue factor(III) converts proconvertin (VII) to activated VIIa. 3)VIIa activates factor X (stuart power factor) of common pathway which 4)forms a complex with factor V (proaccelerin) 5)activating factor II (prothrombin) which when active becomes 6)thrombin (IIa). 7)Thrombin activates factor I (fibrinogen) to form 8)activated fibrinogen (Ia)

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21
Q

describe the intrinsic pathway (contact activation pathway)

A

1)injury within blood vessel initiates prekallikrein, high molecular weight kininogen and by the activation of factor XII (Hageman factor). in the presence of calcium (factor IV). Factor XII (Hageman) activates facttor XI(plasma thromboplastin antecedent) which activates factor IX(christmas)which activates factor VIII (antihemophilic factor) and merges at the common pathway and activates factor X(stuart power factor) which forms a complex with factor V (proaccelerin) activating factor II (prothrombin) which turns into thrombin IIa (when active) which activates factor I (fibrinogen) to form activated fibrinogen (Ia)

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22
Q

which factor is important for both pathways, intrinsic and extrinsic

A

conversion of prothrombin to thrombin
thrombin assists in activating factors V(proaccelerin), VIII(antihemophilic factor), I (Fibrin) and XIII(fibrin stabilizing) and influences platelets to area of injury. Ample amounts of thrombin(prothrombin) must be present to activate adequate fibrin to form a stable clot

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23
Q

how does thrombin act as an anticoagulant (3 ways)

A

1) prevents runaway clot formation by releasing tissue plasminogen activator (tPA) fro endothelial cells
2) stimulates protein C and protein S to stop clot formation
3) forms a relationship with antithrombin II to interfere with coagulation

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24
Q

what is terminal pathway of coagulation cascade

A 
common pathway-factor X is activated by intrinisc and extrinsic pathways, and factor X needs factor V and calcium to contert factor II(prothrombin) to its active state factor IIa(thrombin), and IIa(thrombin) activates factor I(fibrinogen)to its active Ia (fibrin)
factor XIII (fibrin stabilizing factor) makes sure platelet plug will hold by forming cross linking mesh in platelet plug, and in conjunction with factor Ia (fibrin) secures a secondary plug until bleeding stops and as it contracts it weaves the vessel together healing the site of injury
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25
Q

Where are most of coagulation proteins synthesized

what about calcium and vWF

A

in liver
calcium from diet (needed to position clotting factors on surface of platelet so coagulation will occur)
vWF-endothelial cells

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26
Q

what factors are vitamin K dependent

A

II, VII, IX, X

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27
Q

what is the purpose of the fibrinolytic system

A

exists to degrade fibrin

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28
Q

what does tissue factor plasma inhibitor do

A

stops action of tissue factor

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29
Q

what do protein C and S do

A

inhibit factors III, V and VII

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30
Q

what does antithrombin III do

A

inhibits thrombin activity by sequestering factors XII(hageman), XI(plasma thromboplastin antecedent), IX(christmas), and X(stuart power), and is a mediator that takes unnecessary clotting factors away so that the clot manufactured is disrupted

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31
Q

what are the primary components of a clot

A

plasminogen, plasmin, fibrin, and fibrin degredation products

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32
Q

describe plasminogen

A

enzyme made in the liver, stored in inactive form, when clot is forming, plasminogen incorperates into clot, and with the assistance of tPA and urokinase plasminogen is activated to plasmin. Plasmin acts on fibrin causing finrin to degrade into fibrin and fibrin degradation products

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33
Q

name two important fibrinolytic mediators that stop process of fibrinolysis when clot has been digested

A

1)alpha antiplasmin and 2)tissue plasminogen activator inhibitor

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34
Q

questions to ask preoperatively

A

1)unusual bleeding or bruising 2)istory of previous bleeding with dental procedures 3)history of excess bleeding after a minor procedure or childhood trauma 4)familial bleeding tendancies exist 5)bleeding after surgical procedure that was not anticipated
complaints of hematomas, runaway bruising, oozing

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35
Q

what are possible etiologies of disruptions in hemostasis

A

1)platelet problem 2)factor deficiency, 3)inherited disorder of coagulation, 4)presence of circulating anticoagulants, or a 5)disturbance of the fibrinolytic system

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36
Q

describe vitamin K

what are the vitamin K factors, what clinical presentations can disrupt vitamin K synthesis

A

created from bacteria in the gut and necessary for formation of factors II, VII, IX, X
liver issues, malabsorption, failure to secrete bile can disrupt this

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37
Q

Describe aspirin effects on platelets

A

hold for 7-10 days prior to surgery, aspirin directly affects the life of the platelet by irreversibly inhibiting cyclooxygenase, resulting in decreased platelet function

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38
Q

describe NSAIDs effects on platelets

A

inhibit cyclooxygenase reversible, hold 24-48 hours to avoid bleeding

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39
Q

what are alternatives to blood transfusions if patient refuses transfusion

A

erythropoietin, acute normovolemic hemodilution, cell salvage, recombinant factor VII or VIII, and topical coagulants, amicar, TXA

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40
Q

if patient requires surgery non emergently, when can you give vitamin K

A

4-6 hours prior to surgery vit K non emergent

plasma, PRBCs, platelets, cryo for emergency surgery

41
Q

bleeding time

A

normal 3-7 minutes
measures platelet function, adhesion
altered by aspirin, NSAIDS

42
Q

platelet count

A

150-300,000

43
Q

PT

A

12-14 seconds use INR 1.5-2.5
prolonged in extrinsic pathway (III, VII), common pathway(X, V, II, I) disorder
altered by coumarin deriviatives

44
Q

APTT

A

25-32 seconds
prolonged with intrinsic pathway(XII, XI, IX, VIII) disorder, common pathway disorder (X, V, II, I) altered by heparin and lovenox

45
Q

thrombin time

A

common pathway 8-12 seconds measures fibrinogen to fibrin reaction

46
Q

activated clotting time

A

80-150 guides anticoagulation dosing

47
Q

fibrinogen

A

> 150 measures fibrinogen levels

48
Q

fibrinogen degradation products

A

measures byproducts of clot dissolution

49
Q

DDimer

A

measures degradation products secondary to fibrinolysis

50
Q

antithrombin III

A

80-120% decreased level may explain subtherapeutic heparin levels, severely depressed in DIC

51
Q

thromboelestogram (TEG)

A

measures clot formation over time evaluates platelet reactions, coagulation, fibrinolysis indicates clot strength, platelet number and function, intrinsic path defects, thrombin formation, rate of fibrinolysis

52
Q

why transfuse PRBCs

A

improve tissue oxygenation

53
Q

how much platelets to give

what is greatest risk of giving platelets

A

1 pack raises plt count 5-10000
give 1 pack per 10kg of patient weight
greatest risk of bacterial contamination
one unit good for 4-5 days

54
Q

why give FFP

A

microvascular bleeding, concentration of coag factors are deficient, inherited coagulopathy, reversal of warfarin, deficiency resulting in dilutional coagulopathy
do not use for volume replacement

55
Q

describe dilutional coagulopathy

A

when blood is diluted to at least 30%, or when a patient loses more than one volume of blood, indicates only a third of the coagulation factors are present
PT/PTT prolonged 1.5 times normal

56
Q

why give cryo

A

contains fibrinogen, factors VIII, XIII, and fibronectin
use for microvascular bleeding with FFP, vWD or hemophilia when concentrates are unavailable, and suspected factor deficiencies

57
Q

alternatives to allogenic blood transfusions preoperatively

A

autologus donation, acute normovolemic hemodilution, blood cell salvage, recombinant factor VII

58
Q

what is recombinant factor VII

A

for hemophilia A (factor VIII, and B (factor IX) off label use for coagulation insufficiencies with platelet disfuntion intracranial hemorrhage, prostate surgery, and trauma
-enhances thrombin generation by augmenting TF/VII at the site of vessel injury and the surface of the platelet, administration boosts thrombin to form fibrin for clot stabilization 20-45 mcg/kg
-will inverse prolonged INR but does not replace all clotting factors
when giving prevent acidosis and hypothermia (interrupt efficacy of drug)
-side effects-CVA, MI, pulmonary emboli, and arterial and venous thromboemboli

59
Q

monitoring the hemodynamic stability post operatively

A

1)color and mentation 2)trends in vitals 3)UOP 4)hypothermia 5)hemodynamic values such as CVP 6)labs 7)dressings, drain volumes

60
Q

what is most common inherited coagulation disorder

A

Von Willibrand disease

61
Q

what are two main functions of vWF

A

1) to facilitate platelet adhesion

2) behave as a plasma carrier for factor VIII of the coagulation cascade

62
Q

where is vWF made

A

in endothelial cells and megakaryocytes

63
Q

1) describe mild to moderate vWd findings

2) describe severe vWd findings

A

1) regular or spontaneous bleeding is not evident but is likely after surgery or when trauma occurs
2) spontaneous epistaxis, oral, GI, and GU bleeding

64
Q

what are laboratory findings in vWD

A

patients with vWD have prolonged bleeding times, deficiency if vWF and factor VIII, decreased vWF activity measured by ristocetin cofactor assay, and a decreased factor VIII coagulant activity(VIII:C)

65
Q

what are three treatments for vWD to combat bleeding before, during, and after surgery

A

supplementation with 1)recombinant factor VIII-vWF concentrate preoperatively and during surgery to raise levels of circulating VIII and vWF, you may use 2)cryo for factor VIII, but there is risk of viral transmission
giving 3)desmopressin acetate (DDAVP) is good for milder forms of vWD-helps increase plasma levels of vWF and augment platelet aggregation

66
Q

What is hemophilia

A 
X linked recessive hematological disorder causes unpredictable bleeding, affects mostly males but females are carriers
hemophilia A (factor VIII) or hemophilia B(factor IX)
67
Q

describe mild, moderate and severe hemophilia A

A

mild (excessive bleeding after trauma or surgery)
moderate (rarely have extensive, un provoked bleeding)
severe (absence of factor VIII in plasma)
hemophiliacs have spontaneous bleeding, muscle hematoma, bleeding into joints, and pain at joint sites

68
Q

Describe anesthetic management of a patient with hemophilia in terms of pre op labs and treatments for anticipated bleeding

A
  • preoperatively test pt/aptt, factor VIII, factor IX, fibrinogen, and an inhibitor test.
  • check response to a patient who has received factor VII.
  • type and crossmatch patient.
  • give factor VIII before surgery.
  • give DDAVP 0.3mcg/kg to increase factor VIII and vWF
69
Q

Describe Aspirin and NSAIDS, how long to hold before surgery

A

aspirin-irreversible anti platelet cox1-2 inhibitor, hold for 7 days before surgery
NSAIDS-reversible platelet inhibition, cox 1-2 inhibitor, hold for 24-48 hours before surgery

70
Q

describe Rofecoxib and Celecoxib

A

cox 1 inhibitors, no need to hold before surgery

71
Q

describe 4 ADP receptor antagonists
which ones are prodrugs
how long to hold each one before surgery

A

clopidogrel(7 days), ticlopidine(7 days), prasurgrel(2-3 days), and ticagrelor(24-48 hours)
clopidogrel and ticlopidine are prodrugs

72
Q

describe dipyridamole, what type of drug, hold how long before surgery

A

inhibition of platelet uptake of ADP (phosphodiesterase antagonist) hold for 24-48 hours, used for PVD

73
Q

describe 3 GpIIb/IIIa receptor antagonists, how long to hold before surgery
which one can be reversed by dialysis?

A

abciximab(72 hours), eptifatide(24 hours) and tirofiban(24 hours) all metabolized by kidney
tirofiban can be reversed by dialysis

74
Q

describe warfarin, how long to stop before surgery, what are reversal methods

A

vitamin K antagonist, hold 2-4 days, can be reversed by vitamin K, recombinant factor VII, prothrombin complex concentrate, FFP

75
Q

describe heparin, how long to hold before surgery, reversal

A

heparin is an antithrombin III catalyst (stops activated factors II, VII, IX, X, XI, and XII) hold for 6 hours before surgery, can be reversed by protamine

76
Q

describe LMWH, how long to hold before surgery, what is reversal

A

antithrombin III catalyst (stops activated factor II and X) stop 12-24 hours before surgery, partial reversal with protamine

77
Q

describe pentasaccharide (fondaparinux) how long to hold before surgery

A

antithrombin III catalyst, stops activated factor X hold for 4 days

78
Q

describe rivaroxaban and apixaban, how long to hold before surgery

A

rivaroxiban (24-48 hours) and apixaban (24-48 hours) stops activated factor X

79
Q

describe 4 direct thrombin inhibitors, which one can be reversed, and how long to hold before surgery

A

-argatroban give for HIIT type II hold 4-6 hours
-hirudin give for HIIT type II hold 8 hours can be reversed with dialysis, polymathy methacrylate
-bibalirudin HIIT hold 2-3 hours
dabigatran non valvular fib hold 1-4 days

80
Q

describe activated protein C medication

A

drotecogin alfa for severe sepsis hold for 12 hours

81
Q

describe 2 fibrinolytic medications, MOA, how long to hold before surgery, and how can you reverse them

A

tissue plasminogen activator (tPA) hold 1 hour, reverse with antifibrinolytics
streptokinase hold for 3 hours, reverse with antifibrinolytics
both promote conversion of plasminogen to plasmin

82
Q

what are two complications of coronary stent placment

A
  • acute stent thrombosis (occludes of coronary artery leads to MI) can occur with discontinuation of anti platelet therapy increased platelet adhesion, TXA2 activity, platelet aggregation, occur within the first 30 days after stent placement
  • stent restenosis slowly developing occlusion resulting from endothelial growth peaks 6-9 months after stent placement
83
Q

describe bare metal stents (BMS)

A

steel or cobalt allow, endothelialization takes 2-4 weeks

84
Q

describe drug eluting stents (DES)

A

endothelialization is slow, sometimes incomplete, drug in stent stops cell division and excessive endothelial growth
-acute stent thrombosis occurs more with DES because of delayed incomplete epithelialization

85
Q

what type of meds are patients with DES and BMS put on how long should individuals continue with their drugs for with each type of stent

A
  • aspirin and clopidogrel to prevent acute stent thrombosis
  • BMS 4 to 6 weeks
  • DES at least 12 months
86
Q

How long to hold elective surgery with BMS and DES

A

BMS 4 to 6 weeks
DES 12 months
after thienopyridine therapy is completed with both

87
Q

when surgery cannot be postponed with stents, what med should be continued

A

continue aspirin

in high risk patients continue dual anti platelet therapy (aspirin and clopidogrel)beyond recommended timeframe

88
Q

when considering preoperative anticoagulation, what should be considered (2 major things)

A

risk of bleeding related to surgery

patients risk for thromboembolism

89
Q
  • describe DIC

- describe steps of DIC (5)

A

activation of systemic inflammation and coagulation
thrombosis, hemorrhage, or both
thrombosis in microcirculation and depletion of procoagulant factors
increased fibrinolytic activity followed by release of plasminogenactivator inhibitor type I (PAI-I) which impairs fibrinolysis and leads to accelerated formation of clots in DIC. activated protein C mediates release of inflammatory cytokines such as tumor necrosis factor nd interleukins from endothelial cells, complement activation and kinin generation increase the coagulation response, leading to more vascular occlusion
1)intravascular deposition of fibrin 2)thrombotic microangiopathy 3)compromised blood supply to organs 4) multi system organ failure 5)use and depletion of platelets and coagulation factors

90
Q

what causes hyperthrombinemia in DIC

A

tissue factor-under normal circumstances TF and tissue factor pathway inhibitor (TFPI) regulate process of coagulation. During sepsis, liver impairment, capillary leakage, and release of endotoxins and proinflammmatory cytokines, mediators are altered.

91
Q

How is DIC diagnosed

A

clinical presentation in conjunction with platelet count, PT/APTT, fibrinogen fibrin degradation products, DDImer, anti-thrombin

92
Q

how is DIC treated

A

depends. activated protein C with sepsis as it inactivates factors Va and VIIIa, resulting in decreased thrombin formation
platelets, cryo, FFP
antithrombotics (antithrombin III)

93
Q

what pO2 will cause sickling with HbS trait?

with HbS?

A

20-30mmHG with HbS trait

30-40 with full HbS

94
Q

what triggers a sickle cell crisis

A

hypoxemia, infection, hypothermia, dehydration, venous stasis, and acidosis
causes chronic hemolytic anemia, intermittent vasoocclusion, severe pain, and end organ damage

95
Q

anesthesia considerations for sickle cell patients

A

adequate hydration, O2 sat, normothermia, acid base balance, proper patient positioning, supplying adequate analgesia
transfusion to replace surgical blood loss (avoid HGB more than 10-11)

96
Q

what is the most important immunologic complication of heparin therapy

A

heparin induced thrombocytopenia, approx 5% of patients who are receiving heparin or LMWH will develop with 50% of these patients developing HIT thrombosis

97
Q

what are clinical presentations of HIT

what medications are given

A

thrombocytopenia, resistance to heparin, thrombosis, positive HIIT tests
give agatroban or hirudin

98
Q

Describe type I HIT

A

type I-thrombocytopenia is non immune related, caused by direct heparin platelet aggregation
1-4 day onset
mild thrombocytopenia that resolves spontaneously even with subsequent heparin
occurs with high dose heparin administration
not associated with thrombosis

99
Q

describe type II HIT

A

thrombocytopenia with platelet factor 4, IgG and heparin
onset is 5-14 days after start of heparin therapy
severe thrombocytopenia, heparin must be discontinued
associated with thrombosis and serious clinical issues

APA II (4 decks)

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