Liver Disease coagulopathy - Vitamin K Dieficiency and Hemorrhage Flashcards

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
Q

May correct the bleeding associated with nonfunctional des-􏰔-carboxyl factors II (pro- thrombin), VII, IX, and X

A

Oral or intravenous vitamin K therapy

25
Q

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

A

TACO

26
Q

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

A

less than 50mg/dL

27
Q

IS often associated with platelet dysfunction and mild to moderate mucocutaneous bleeding

A

Chronic Renal Failure

28
Q

Platelet adhesion to blood vessels and platelet aggregation are suppressed, perhaps because these compounds coat the platelets

A

Guanidinosuccinic acid or phenolic compounds

29
Q

Decreased RBC mass (anemia) and thrombocytopenia contribute to the bleeding so these treatment may correct these disorders

A

Dialysis, RBC transfusions, or erythropoietin therapy

30
Q

This syndrome deposits fibrin in the renal microvasculature which reduce glomerular function

A

Hemostasis activation syndromes

31
Q

Examples of hemostasis activation syndrome

A

DIC, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura

32
Q

May be deposited in renal transplant rejection and in the glomerulonephritis syndrome of systemic lupus erythematosus.

A

Fibrin

33
Q

Lab results for bleeding in renal disease

A

Bleeding time: Prolonged
PTT and PT are normal

34
Q

Temporarily activates platelets and may ultimately improve platelet function, particularly when anemia is well controlled

A

Renal dialysis

35
Q

May be administered intravenously (DDAVP) or intra- nasally (Stimate, Behring) to increase the plasma concentration of VWF high-molecular-weight multimers.

A

Desmopressin

35
Q

Patients with renal failure should not take _ ; because these drugs increase the risk of hemorrhage

A

Aspirin, clopidogrel, prasugrel, ticagrelor, or other platelet inhibitors

36
Q

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.

A

Nephrotic Syndrome

36
Q

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.

A

Vitamin K

37
Q

is fat soluble and requires bile salts for absorption, biliary duct obstruction (atresia), fat malabsorption, and chronic diarrhea may cause vitamin K deficiency.

A

Vitamin K

38
Q

Disrupt normal gut flora may cause a slight reduction because they destroy bacteria that produce vitamin K.

A

Broad-spectrum antibiotics

39
Q

Condition where the activity levels of factors II (prothrombin), VII, IX, and X are lower in normal newborns than in adults

A

Hemorrhagic disease of the newborn

40
Q

prolongs the deficiency because passively acquired maternal antibodies delay the establishment of gut flora

A

Breastfeeding

41
Q

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

A

y-carboxylation cycle of coagulation factors

42
Q

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

A

Proteins induced by vitamin K antagonists (PIVKA) factors.

43
Q

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

A

brodifacoum or “superwarfarin”

44
Q

The single most common reason for hemorrhage-associated emergency department visits.

A

Inadvertent Coumadin overdose