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Pathophysiology > Coagulation > Flashcards

Coagulation Flashcards

1
Q

what is PT? what coag factors is it associated with?

A

pro-time/prothrombin time test: this measures the extrinsic pathway (how quickly your blood clots)
-coag factors: VII, X, V, II, I

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2
Q

what is the path of the extrinsic pathway?

A

tissue factor –> VII –> X –> V –> II (prothrombin activator: prothrombin to thrombin) –> I (fibrinogen to fibrin)…

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3
Q

most of the coag factors are _____ synthesized ____

A

proteins, liver

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4
Q

5 stages of hemostasis

A
  1. vessel spasm 2. formation of platelet plug 3. blood coag (insoluble fibrin clot formed) 4. clot retraction 5. clot dissolution
    (spasm, primary and secondary hemostasis)
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5
Q

INR is what?

A

international normalized ratio: measures how well an anticoagulation medicine is working.
= PT patient / PT normal population

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6
Q

PTT is what? associated with what factors?

A

partial thromboplastin time (w/ PT, asses amount and function of clotting factors). Intrinsic pathway efficiency. Factors XII, XI, IX, VIII, X, V, II, I

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7
Q

what is the path of the intrinsic path?

A

XII –> XI –> IX –> VIII –>X –> V –> II (prothrombin activator: prothrombin to thrombin) –> I (fibrinogen to fibrin)…

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8
Q

what is a normal PT?

A

12.5-15.0

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9
Q

long bleeding time = ____ count

A

decreased platelet FUNCTION

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10
Q

normal platelet count

A

150,000 - 400,000

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11
Q

ristocetin cofactor activity

A

RcoF is the most sensitive and specific test for von Willebrand’s disease (tests binding of vWF to platelet glycoprotein, and is decreased in virtually all types of the disease

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12
Q

what enzyme turns fibrinogen to insoluble fibrin (I) ?

A

thrombin

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13
Q

what enzyme turns prothrombin (II) into thrombin?

A

prothrombin activator (from factor X and V)

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14
Q

what is the thrombin time test? (TT) what would it be affected by?

A

TT: how fast thrombin can convert fibrinogen to fibrin
-affected by the level and/or function of fibrinogen and the presence of inhibitors (e.g., heparin, fibrinogen/fibrin degradation products, direct thrombin inhibitor).

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15
Q

what is a D-Dimer and what does it’s presence tell you?

A

D-Dimer (2 D fragments of a fibrin joined by a crosslink) is a fibrin degradation/split product (FDP or FSP) - a small fragment present in the blood after a clot is degraded by fibrinolysis. *Presence used to help Dx Thrombosis (DVT) (endothelial damage).
*(NEGATIVE result will rule OUT thrombosis)

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16
Q

what two tests measure kidney function? decreased kidney function will cause what?

A

BUN and creatinine : both metabolic products excreted in urine
Decrease intrinsic kidney function or blood profusion to the kidney will cause varying elevation in their values in the blood.

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17
Q

what is thrombogenicity? normal endothelium is ____

A

tendency to produce a thrombus (clot)

non-thrombogenic

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18
Q

how do resting platelets in endothelium remain unclotted?

A
  1. healthy endothelium release prostocyclin into plasma
  2. prostocyclin –> binds platelet membrane receptors = cAMP synthesis
  3. cAMP inhibits 2B3A, inhibits release of platelet aggregation agents or Ca2+.
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19
Q

what is 2B3A?

A

activated platelets express this to allow fibrinogen to cross bridge

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20
Q

what is BUN? its normal level?

A

blood urea nitrogen .

normal level: 6-20 mg/dL

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21
Q

what is creatinine? normal level?

A

is derived from the metabolism of creatine in muscle. Normal Values 0.6-1.2 mg/dl.

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22
Q

what is the process of primary hemostasis?

A
  1. Platelets adhere to vWF
  2. Shape change
  3. Granule release: Platelets become activated; secrete ADP and thromboxane (TXa2)
  4. Recruitment: further platelet activation
  5. aggregation: plug formed

Platelets have receptor for ADP; self-activating/aggregating

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23
Q

Occurring at the same time as primary platelet plug formation is _____, which refers to the activation of the _______

A

secondary hemostasis

coagulation cascade: reinforces platelet plug into stable secondary plug

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24
Q

in vivo the _____ is responsible for coagulation

A

the extrinsic pathway

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25
Q

prolonged PT could mean…

A

deficiency of VII, X, V, II, I; or antibody to any of the above factors.

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26
Q

prolonged PTT could mean …

A

XII, XI, IX, VIII, X, V, II, I, or antibody to any of these factors.

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27
Q

prolonged PT, normal PTT

A

factor VII deficiency

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28
Q

normal PT, prolonged PTT

A

factor XII, XI, IX, or VIII deficiency

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29
Q

prolonged PT and PTT

A

factore X, V, II, or I deficiency

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30
Q

increased bleeding w/ platelet count < ______ spontaneous bleeding w/ platelet count < ______

A

increased: 50,000
spontaneous: 20,000

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31
Q

thrombocytopenia

A

is low platelet count; bleeding due to this would be secondary to a quantitative platelet deficiency. (frequent with chemo)

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32
Q

If the platelet count is normal but the patient has a prolonged bleeding time this represents a _____

A 
vWD or qualitative platelet defect
usually acquired (drugs or renal failure)
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33
Q

vWD looks similar to what other disorder?

A

qualitative platelet defect

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34
Q

vWD

A

von willendbrand’s disease: factor VIII deficiency
A. vWF is responsible for the initial platelet adhesion to subendothelium; therefore causes prolonged B.T. (bleeding time)
B. vWF also stabilizes factor VIII; without it factor VIII is quickly broken down= prolonged PTT

combination of prolonged BT and a PTT with normal PT would be vWD; although will frequently only present with prolonged BT

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35
Q

what is the most common hereditary bleeding disorder ?

A

vWD

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36
Q

what is the classic lab finding for vWD?

A

Failure of ristocetin to agglutinate platelets

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37
Q

txt for vWD?

A

Minor bleeding - DDAVP - desmopressin; [increases vWF level and factor VIII level]
Severe bleeding - replacement VIII (intermediate purity factor )
[VIII concentrates contains vWF.]

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38
Q

renal failure is a cause of _____

A

qualitative platelet defect. prolonged BT but all other (PT, PTT, pLt count) normal

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39
Q

factor IX deficiency, aka…

A

hemophilia B

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40
Q

factor VIII deficiency, aka …

A

hemophilia A or vWD

41
Q

what is a 1:1 mixing study?

A

a method to Dx cause of factor deficiency.

patient’s plasma is mixed with normal plasma with all the known clotting factors. Therefore the mixture has at least 50% of all coagulation factors, (30% of a coagulation factor will result in a normal aPTT).
In the absence of inhibitors, this mixture will produce a normal clotting time. When addition of normal plasma fails to correct the clotting time into the normal range, the cause of the abnormal test is likely an inhibitor. (an antibody interfering)

42
Q

lab tests for factor IX and XI deficiencies?

A

PT, platelet counts and BTs normal.
1: 1 mixing study corrects the prolonged aPTT.
Final diagnosis based on factor IX. or XI assay.

43
Q

txt for factor IX deficiency?

A

factor IX replacement

44
Q

txt for factor XI deficiency?

A

fresh frozen plasma (FFP)

45
Q

what are 3 anti-coagulation medication agents? and their MOAs?

A

aspirin: COX-1 inhib, prevents aggregation of pLts
clopridogrel (plavix): inhibits ADP activation of pLts
2B/3A inhibitors: inhibit fibrinogen binding to 2B/3A, prevents aggregation of pLts

46
Q

how does the vasculature prevent excessive clotting and occlusion? (natural fibrinolytic agents)

A

The endothelium adjacent to thrombus secretes plasminogen activator which converts plasminogen to plasmin which lysis the clot preventing excessive clot formation.

47
Q

what are two fibrinolytic agents that can be used to prevent excessive clotting? what are each used for?

A

both only really used for STEMIs

  1. t-PA (tissue plasminogen activator): STEMI and strokes w/in 3 hours
  2. fibrinolytic inhibitors: to reverse fibrinolytic bleeding
48
Q

three naturally occurring inhibitors of coag.

A
  1. protein C
  2. protein S
  3. Antithrombin
49
Q

what does protein C do?

A

inactivates factor Va (active factor V)

50
Q

what does protein S do?

A

aids protein C (a cofactor for it)

51
Q

what does antithrombin do?

A

inactivates thrombin and factor Xa

activated factor X

52
Q

hereditary deficiency in protein C, S or antithrombin will result in increased risk for …

A

DVT or PE

53
Q

what is LDH? what will an increase of it mean?

A

lactate dehydrogenase
LDH is an intracellular enzyme released from RBC when they are destroyed. Increase RBC destruction (hemolysis) results in an elevation of the serum LDH level.

54
Q

what is heparin? which do you need to monitor ?

A

therapeutic (or prophylaxis ) anticoagulant. It binds to antithrombin and increases it’s anti-coagulation ability
unfractionated- UFH: need to monitor
low molecular weight- LMWH: don’t need to monitor

55
Q

heparin does not _____ rather it ______

A

lyse clots, rather it prevents further clot formation

56
Q

what is protamine sulfate?

A

can be used to reverse (full reverse for UFH, only can partially reverse for LMWH) the effect of heparin in a bleeding patient. (potential advantage of UFH)

57
Q

anticoagulant for high bleeding risk?

A

UFH

58
Q

anticoagulant for DVT, PE or acute coronary syndrome

A

UFH or LMWH

59
Q

DVT in pregnancy? what anticoag will you use?

A

LMWH (can’t use coumadin/warfarin b/c it’s a teratogen)

60
Q

how does coumadin (warfarin) work?

A

inhibits Vitamin K from becoming activated

61
Q

what does vitamin K do?

A

required by factors II, VII, IX and X to be functional

62
Q

how long does it take coumadin to become therapeutically effective?

A

about 5 days

63
Q

when is coumadin used? who is contraindicated for it?

A

oral anti-coag, Usually given in 3 month course to txt DVT or PE. TERATOGEN (not for pregnant!).

64
Q

giving coumadin is essentially giving what kind of deficiency?

A

vit K

65
Q

when is heparin used prophylactically?

A

UFH or LMWH (enoxaparin) is frequently used in immobilized medical patients and surgical patients as prophylactic therapy to prevent DVT, PE

66
Q

what is heparin- induced thrombocytopenia? (HIT)

A

after on heparin for 5-14 days…platelet count drop of greater than 50% of base line or to less than 120,000
(more frequence w/ UFH than LMWH)

67
Q

txt for HIT?

A

STOP heparin, take direct-thrombin-inhibitor (Argotrobran)

* can’t just switch to LMWH b/c there is cross-reactivity

68
Q

what is Vit K deficiency: how do you get it and how to Dx it?

A

usually occurs secondary to combination of malabsorption (fat soluble vit) or poor dietary intake plus antibacterial administration (which destroys Vit. K producing bacteria in GI tract).
Dx: PT prolong more than the PTT
1 : 1 mixing study will correct prolonged PT in lab.

69
Q

classic vit K deficiency pt presents as ….

A

post-op, NPO, on abx

70
Q

txt for vit K deficiency?

A

mild: Vit K : takes 12-24 hours
severe: FFP
coumadin induced: FFP or PCC

71
Q

what is the timespan that FFP will help?

A

fresh frozen plasma. only will last 6 hours .. *might have to give more if body is still not making its own coag factors by then

72
Q

what is Kcentra?

A

PCC: prothrombin complex concentrates which contain factors II, VII, IX, X

73
Q

what is DDAVP?

A

Desmopressin (DDAVP®) is used to help stop bleeding in patients with von Willebrand’s disease or mild hemophilia A. DDAVP causes the release of von Willebrand’s antigen from the platelets and the cells that line the blood vessels where it is stored

74
Q

what is coagulation deficit secondary to liver disease?

A

Prolonged PT and a PTT, with PT being more sensitive.
Portal HTN –> thrombocytopenia due to splenomegaly.
Increased fibrinolytic activity
= increased fibrin split products (FSP).

75
Q

what is disseminated intravascular coagulation? (DIC)

A

Tf (tissue factor- from breach in endothelium) is exposed to circulation … starts up coag cascade …widespread microvasc thrombosis + fibrinolytic system
(consuming the clotting factors- we can’t make them as fast as they are being consumed)

76
Q

Dx and txt of DIC

A 
prolonged PT, prolonged a PTT, decreased platelets, decreased fibrinogen, increased fibrin split products (FSP), along with increased D-Dimer
Treatment: 
		1. underlying disease 
		2. fresh frozen plasma
		3. platelets
77
Q

What is immune thrombocytopenia purpura? dx?

A

Increase platelet destruction secondary to autoantibody production; shows petechiae
Dx: low platelet count, normal HCT and WBC
Peripheral smear: Antibody covered (IgG) platelets destroyed by mononuclear phagocytic cells predominantly in the spleen.

78
Q

txt for thrombocytopenia

A
  1. Steroids – prednisone 1-1.5mg/kg (paralyzes macrophages so they don’t recognize and kill)
  2. Splenectomy: Site of platelet destruction and antibody production.
79
Q

what is the MOA of pradaxa?

A

direct thrombin inhibitor

80
Q

what is the MOA of xarelto and eliquis?

A

factor Xa inhibitor

81
Q

what are your indications for pradaxa, xarelto and eliquis?

A

CVT, PE, Afib

82
Q

what is a major difference between pradaxa vs xarelto and eliquis (besides MOA)?

A

theres a reveresible agent for pradaxa but not the other two

83
Q

what is pancytopenia?

A

all blood cell levels are below normal range (WBCs, thrombocytes, and hemoglobin)

84
Q

leukopenia, anemia and thrombocytopenia : what levels constitute each ?

A

leukopenia: < 4,000 WBCs
anemia: < 12 -13 g hemoglobin
thrombocytopenia: < 100,000 thrombocytes

85
Q

what is aplastic anemia (AA)?

A

body stops producing enough new blood cells.

=feeling fatigued and with a higher risk of infections and uncontrolled bleeding.

86
Q

pathogenesis of AA?

A

hematopoietic stem cells (HSC) injury + pancytopenia + absence of bone marrow

87
Q

txt of AA?

A

stem cell transplantation in eligible patients, otherwise treatment is with immunosuppressive therapy.

88
Q

Thrombotic Thrombocytopenia Purpura: TTP

A

vWF – cleaving protease deficiency : unable to breakdown into manageable vWFs
These large multimers cause agglutination of platelets in the circulation –> clots in microcirculation.

89
Q

what is your key lab value to Dx TTP?

A

3 things:
-Microangiopathic hemolytic anemia (fragmented RBCs from destruction of them)
-thrombocytopenia
-increased LDH (lactate dehydrogenase)
[LDH is an intracellular enzyme released from RBC when they are destroyed. ]
Dx: requires the first two

90
Q

Txt for TTP?

A

plasma exchange

91
Q

what disorder is TTP very similar to?

A

HUS (hemolytic uremic syndrome)

92
Q

what is hemolytic uremic syndrome ?

A

condition caused by the abnormal destruction of red blood cells. The damaged red blood cells clog the filtering system in the kidneys, which can lead to life-threatening kidney failure

93
Q

what is the most common cause of acute renal failure in children?

A

HUS

94
Q

what is the classic presentation of HUS?

A

young children who develop thrombocytopenia with microangiopathic hemolysis with accompanying oliguria (low urine output), proteinuria and an increase in BUN and creatinine.

95
Q

txt for HUS?

A

supportive, dialysis for renal function

96
Q

Dx of HUS?

A
  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia
  3. increased BUN/creatinine
    ( last one is deciding factor between this and TTP)
97
Q

Thrombin Time test?

A

Thrombin added to test tube, converts soluble fibrinogen to insoluble fibrin (visible clot).

98
Q

what causes prolonged thrombin time? (TT)

A

Cause of prolonged TT (Thrombin Time) a quantitative or qualitative defect in fibrinogen, FSP, or thrombin inhibitors (such as Dabigatran.)

Pathophysiology (28 decks)

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