Liver Disease coagulopathy - Vitamin K Dieficiency and Hemorrhage Flashcards

(47 cards)

1
Q

Enlarged and collateral esophageal vessels are called

A

Esophageal varices

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2
Q

Occurs in liver disease–associated thrombocytopenia, often accompanied by decreased platelet function.

A

Mucocutaneous Bleeding

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3
Q

Consequence of procoagulant dysfunction and deficiency.

A

Anatomic Bleeding

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4
Q

May suppress the biosynthetic function of hepatocytes, reducing either the concentrations or activities of the plasma coagulation factors to less than hemostatic levels (<40 units/dL)

A

Hepatitis, cirrhosis, obstructive jaundice, cancer, poisoning, and congenital disorders of bilirubin metabolism

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5
Q

In liver disease these seven factors are produced in their des-y-carboxyl forms, which cannot participate in coagulation

A

Factors II (prothrombin), VII, IX, and X and control proteins C, S, and Z.

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6
Q

On the onset of liver dse, this factor has the shortest plasma half-life at 6 hours, is the first coagulation factor to exhibit decreased activity.

A

Factor VII

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7
Q

Is a more specific marker of liver disease than deficient factors II, VII, IX, or X because this factor is non-vitamin K dependent

A

Factor V

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8
Q

Acute phase reactant that frequently becomes elevated in early or mild liver disease.

A

Fibrinogen

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9
Q

A condition called __ is characterized by moderately and severely diseased liver produces fibrinogen that is coated with excessive sialic acid,

A

Dysfibrinogenemia

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10
Q

Causes generalized soft tissue bleeding associated with a prolonged TT and an exceptionally prolonged reptilase clotting time.

A

Dysfibrinogenemia

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11
Q

This condition will make the fibrinogen level fall to less than 100 mg/dL, a mark of liver failure

A

End-stage liver disease

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12
Q

Are acute phase reactants that may be unaffected or elevated in mild to moderate liver disease.

A

VWF and factors VIII and XIII

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13
Q

VWF is produced from

A

Endothelial cells and megakaryocytes

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14
Q

occurs in one-third of patients with liver disease. Platelet counts of less than 150,000/􏰀L may result from sequestration and shortened platelet survival associated with portal hypertension and resultant hepatosplenomegaly

A

Moderate thrombocytopenia

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15
Q

A significant complication of liver disease that is caused by decreased liver pro- duction of regulatory antithrombin, protein C, or protein S and by the release of activated procoagulants from degenerating liver cell

A

Chronic or compensated Disseminated Intravascular Coagulation

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16
Q

May also produce nonspecific procoagulant substances that trigger chronic DIC, leading to ischemic complications

A

Hepatocytes

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16
Q

T/F: The failing liver cannot clear activated coagulation factors.

A

TRUE

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17
Q

PT, PTT, and TT are pro- longed, the fibrinogen level is reduced to less than 100 mg/dL, and D-dimers are significantly increased

A

Acute, uncompensated DIC

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18
Q

A hallmark of unregulated coagulation and fibrinolysis.

A

D-dimer assay value

19
Q

Are used to characterize the hemostatic abnormalities in liver disease

A

PT, PTT, TT, fibrinogen concentration, platelet count, and D-dimer concentration

20
Q

Factors that may be may be used in combination to differentiate liver disease from vitamin K deficiency.

A

Factor V and VII

21
Q

Test that is occasionally may be useful to confirm dysfibrinogenemia

A

Reptilase time test

22
Q

Venom of reptile __ is substituted for the thrombin reagent. It triggers fibrin polymerization by cleaving fibrinopeptide A

A

Bothrops atrox (common lancehead viper)

23
Q

Is unaffected by standard unfractionated heparin therapy and can be used to assess fibrinogen function even when there is heparin in the specimen

A

Reptilase time test

24
May correct the bleeding associated with nonfunctional des-􏰔-carboxyl factors II (pro- thrombin), VII, IX, and X
Oral or intravenous vitamin K therapy
25
This is likely to occur when 30 mL/kg has been administered, but it may occur with even smaller volumes in patients with compromised cardiac or kidney function
TACO
26
If the fibrinogen level is less than __g/dL, spontaneous bleeding is imminent and cryoprecipitate or fibrinogen concentrate (RiaSTAP, CSL Behring) may be selected for therapy
less than 50mg/dL
27
IS often associated with platelet dysfunction and mild to moderate mucocutaneous bleeding
Chronic Renal Failure
28
Platelet adhesion to blood vessels and platelet aggregation are suppressed, perhaps because these compounds coat the platelets
Guanidinosuccinic acid or phenolic compounds
29
Decreased RBC mass (anemia) and thrombocytopenia contribute to the bleeding so these treatment may correct these disorders
Dialysis, RBC transfusions, or erythropoietin therapy
30
This syndrome deposits fibrin in the renal microvasculature which reduce glomerular function
Hemostasis activation syndromes
31
Examples of hemostasis activation syndrome
DIC, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura
32
May be deposited in renal transplant rejection and in the glomerulonephritis syndrome of systemic lupus erythematosus.
Fibrin
33
Lab results for bleeding in renal disease
Bleeding time: Prolonged PTT and PT are normal
34
Temporarily activates platelets and may ultimately improve platelet function, particularly when anemia is well controlled
Renal dialysis
35
May be administered intravenously (DDAVP) or intra- nasally (Stimate, Behring) to increase the plasma concentration of VWF high-molecular-weight multimers.
Desmopressin
35
Patients with renal failure should not take _ ; because these drugs increase the risk of hemorrhage
Aspirin, clopidogrel, prasugrel, ticagrelor, or other platelet inhibitors
36
A state of increased glomerular permeability associated with a variety of conditions, such as chronic glomerulonephritis, diabetic glomerulosclerosis, systemic lupus erythematosus, amyloidosis, and renal vein thrombosis.
Nephrotic Syndrome
36
Required for normal function of the vitamin K- dependent prothrombin group of coagulation factor, is ubiquitous in foods, especially green leafy vegetables, and the daily requirement is small, so pure dietary deficiency is rare.
Vitamin K
37
is fat soluble and requires bile salts for absorption, biliary duct obstruction (atresia), fat malabsorption, and chronic diarrhea may cause vitamin K deficiency.
Vitamin K
38
Disrupt normal gut flora may cause a slight reduction because they destroy bacteria that produce vitamin K.
Broad-spectrum antibiotics
39
Condition where the activity levels of factors II (prothrombin), VII, IX, and X are lower in normal newborns than in adults
Hemorrhagic disease of the newborn
40
prolongs the deficiency because passively acquired maternal antibodies delay the establishment of gut flora
Breastfeeding
41
This is interrupted by coumarin-type oral anticoagulants such as warfarin (Coumadin) that disrupt the vitamin K epoxide reductase and vitamin K quinone reductase reactions
y-carboxylation cycle of coagulation factors
42
In this situation the liver releases dysfunctional des-y-carboxyl factors II (prothrombin), VII, IX, and X and proteins C, S, and Z; these inactive forms are called
Proteins induced by vitamin K antagonists (PIVKA) factors.
43
Often used as a rodenticide, lasts for weeks to months, and treatment of poisoning with this substance requires repeated administration of vitamin K with follow-up PT monitoring
brodifacoum or “superwarfarin"
44
The single most common reason for hemorrhage-associated emergency department visits.
Inadvertent Coumadin overdose