n440 unit three: clotting UPDATED
ACTUAL Exam Questions and CORRECT
Answers
labs - PT - CORRECT ANSWER - normal → 10-15 sec
therapeutic → 15-30 sec
*associated w Warfarin
labs - aPTT - CORRECT ANSWER - normal → 35-45 sec
therapeutic → 45-112 sec
*associated w Heparin
labs - PTT - CORRECT ANSWER - normal → 60-70 sec
therapeutic → 90-175 sec
*associated w Heparin
labs - INR - CORRECT ANSWER - normal → <2
therapeutic → 2-3
*associated w Warfarin
labs - Xa - CORRECT ANSWER - normal → <0.1
therapeutic → 0.3-0.7
,*associated w Heparin
clotting - overview - CORRECT ANSWER - - hemostasis → multi-step process that
requires constant monitoring by the body to prevent excessive blood loss & ensure body tissues
are adequately perfused
- systemic clotting → problem extends to entire body; is usually result of a significant
hematologic event
> ex: large wound, GI bleed
- localized clotting → problem is localized; is usually a problem in a vein/artery; either injury to
vessel or clot within a vessel
> ex: laceration
clotting - stopping abnormalities - CORRECT ANSWER - - mechanisms limit clotting to
only the area where clotting is needed
- breakdown clots when injury has healed
- deficiency in clotting factors → incr risk for PE, DVT
- plasmin → digests fibrin, fibrinogen, & prothrombin; controls size of fibrin clot
- fibrinolysis → dissolves fibrin clot
clotting - meds that slow/stop clotting - CORRECT ANSWER - - platelet inhibitors
- thrombin inhibitors
- vitamin K antagonists
- fibrinolytic drugs → aka clot busters
clotting - platelet inhibitors - CORRECT ANSWER - - stop plts from sticking together
- prevent formation of clots
- occurs high up in the clotting cascade
, - ex → aspirin, clopidogrel (plavix), & ticagrelor (brilinta)
clotting - direct thrombin inhibitors - CORRECT ANSWER - - prevent conversion of
prothrombin to thrombin, which disrupts cascade so fibrinogen can't convert to fibrin
- no fibrin clots
- ex → dabigatran (pradaxa), rivaroxaban (xarelto), & apixaban (eliquis)
clotting - indirect thrombin inhibitors - CORRECT ANSWER - - bind to and incr activity
of antithrombin III
- as a result, thrombin is reduced which prevents fibrinogen conversion to fibrin
- no fibrin clots
- ex → heparin, enoxaparin (lovenox)
clotting - vitamin K antagonists - CORRECT ANSWER - - vit K is required for liver to
create clotting factors
- these antagonists decr synthesis/absorption of vit K in GI tract which limits clotting factors
- ex → warfarin (coumadin)
clotting - fibrinolytic drugs - CORRECT ANSWER - - breaks down fibrin threads in
formed clots
- activates plasmin which destroys fibrin
- ex → alteplase (activase) & tenecteplase (TNKase)
> can have TNK drip
abnormal clotting - assessment questions - CORRECT ANSWER - - hx → age; gender (F
have incr risk); bone marrow fxn; immunity; liver fxn; current meds; bleeding disorders
- nutrition → current diet; Fe intake; protein intake; alcohol consumption
ACTUAL Exam Questions and CORRECT
Answers
labs - PT - CORRECT ANSWER - normal → 10-15 sec
therapeutic → 15-30 sec
*associated w Warfarin
labs - aPTT - CORRECT ANSWER - normal → 35-45 sec
therapeutic → 45-112 sec
*associated w Heparin
labs - PTT - CORRECT ANSWER - normal → 60-70 sec
therapeutic → 90-175 sec
*associated w Heparin
labs - INR - CORRECT ANSWER - normal → <2
therapeutic → 2-3
*associated w Warfarin
labs - Xa - CORRECT ANSWER - normal → <0.1
therapeutic → 0.3-0.7
,*associated w Heparin
clotting - overview - CORRECT ANSWER - - hemostasis → multi-step process that
requires constant monitoring by the body to prevent excessive blood loss & ensure body tissues
are adequately perfused
- systemic clotting → problem extends to entire body; is usually result of a significant
hematologic event
> ex: large wound, GI bleed
- localized clotting → problem is localized; is usually a problem in a vein/artery; either injury to
vessel or clot within a vessel
> ex: laceration
clotting - stopping abnormalities - CORRECT ANSWER - - mechanisms limit clotting to
only the area where clotting is needed
- breakdown clots when injury has healed
- deficiency in clotting factors → incr risk for PE, DVT
- plasmin → digests fibrin, fibrinogen, & prothrombin; controls size of fibrin clot
- fibrinolysis → dissolves fibrin clot
clotting - meds that slow/stop clotting - CORRECT ANSWER - - platelet inhibitors
- thrombin inhibitors
- vitamin K antagonists
- fibrinolytic drugs → aka clot busters
clotting - platelet inhibitors - CORRECT ANSWER - - stop plts from sticking together
- prevent formation of clots
- occurs high up in the clotting cascade
, - ex → aspirin, clopidogrel (plavix), & ticagrelor (brilinta)
clotting - direct thrombin inhibitors - CORRECT ANSWER - - prevent conversion of
prothrombin to thrombin, which disrupts cascade so fibrinogen can't convert to fibrin
- no fibrin clots
- ex → dabigatran (pradaxa), rivaroxaban (xarelto), & apixaban (eliquis)
clotting - indirect thrombin inhibitors - CORRECT ANSWER - - bind to and incr activity
of antithrombin III
- as a result, thrombin is reduced which prevents fibrinogen conversion to fibrin
- no fibrin clots
- ex → heparin, enoxaparin (lovenox)
clotting - vitamin K antagonists - CORRECT ANSWER - - vit K is required for liver to
create clotting factors
- these antagonists decr synthesis/absorption of vit K in GI tract which limits clotting factors
- ex → warfarin (coumadin)
clotting - fibrinolytic drugs - CORRECT ANSWER - - breaks down fibrin threads in
formed clots
- activates plasmin which destroys fibrin
- ex → alteplase (activase) & tenecteplase (TNKase)
> can have TNK drip
abnormal clotting - assessment questions - CORRECT ANSWER - - hx → age; gender (F
have incr risk); bone marrow fxn; immunity; liver fxn; current meds; bleeding disorders
- nutrition → current diet; Fe intake; protein intake; alcohol consumption
