Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PATHO > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What are BVs made of

A

epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

First step after BV is injured

A

Platelets circulate in the body and go to fill the injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fibrin

A

strands that join together at the injury and seal the plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fibrinogen

A

covers the active part of fibrin until converted at the site of injury so the fibrin does not clot in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes fibrinogen to turn into fibrin

A

proteins in the blood—thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

thrombin

A

active form that helps convert fibrinogen into fibrin; helps make plasmin from plasminogen; breaks up fibrin to prevent constant clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

tissue factor

A

Joins with VII to make factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

prothrombin

A

inactive form of thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is the extrinsic pathway activated?

A

by initial BV insult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

intrinsic pathway

A

workhorse that gets most of the cascade done

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is blood?

A

mostly plasma–water, also proteins and solutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

plasma proteins

A

most is albumin and globulins, clotting factors, electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

albumin

A

control water/solutes in BVs vs cellular space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

globulins

A

HDLs, prothrombin, hormone-transporting proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most plentiful clotting facto

A

fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where are most clotting factors made?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Natural killer cells

A

WBCs, defense against tumors and viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Serum

A

plasma w/o clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Primary activator of cascade

A

Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Platelet function

A

hemostasis, coag, release clotting factors; normally circulate as smooth platelets–inactive until find damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Platelets

A

not true cells–contain cytoplasmic fragments that can release adhesive pros, coag, and growth factors when they sense a vessel injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Thrombocytopenia

A

low platelets–under 100k; high risk for bleeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where are extra platelets stored?

A

spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Steps of activation of clotting system

A

inc platelet adhesion at site of injury (active dendritic platelets), platelet degranulation (active platelets release prothrombotic molecules like ADP, ADP binds and induces agg as platelet-vasc wall and platelet-platelet adherence inc, activation of clotting system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Thromboxone

A

helps recruit platelets to the site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

blood clot

A

meshwork of fibrin strands and platelets; plug damage and stop bleeding–hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hemostasis

A

stopped bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which pathway is thrombin more active in?

A

Intrinsic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Target of clot medication

A

thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does body know to stop the clot?

A

anti-thrombin 3 is a circulating thrombin inhibitor, tissue factor pathway inhibitor inhibits factor Xa after body is clotted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

fibrinolysis

A

natural removal of clot; b/d of fibrin; tissue plasminogen activator turns plasminogen into plasmin which b/d fibrin and releases the caught blood cells, breaking the mesh up into fibrin degradation products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

u-PA

A

Also tells plasminogen to activate plasmin and break up fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clot risk factors

A

DVT, immobility, afib, heart attack, heart failure, stroke history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

coag goals

A

prevent clot formation, break apart existing clot, help inc circ and perfusion, dec pain, prevent further tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

heparins and coags biggest concern and NC

A

bleeding–ext or int; monitor Hgb and HCT, need to know where your pt is at risk of bleeding from and why they are on an anti-coag, VS change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

sx of bleeding

A

tachy (first sign), dec BP, resp chx, bruising; bright blood after surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

antithrombotics

A

prevent clot/thrombus

37
Q

anticoags

A

prevent action of clotting factors and prevent clots

38
Q

antiplatelets

A

prevent platelet plugs from forming by dec platelet agg; best for preventing heart attack and stroke

39
Q

Heparin MOA

A

prevent clots by activating anti-thrombin which indirectly inactivates thrombin and factor Xa (and more clotting factors); inhibits fibrin formation

40
Q

enoxaparin (low molecular weight heparin)

A

prevents clots by inactivating factor Xa; takes large Hep mol and cleaves them into smaller mol that adhere to Xa and become more bioavailable with larger half life

41
Q

Giving Heparin

A

only IV or SQ; parenteral only; in 5000 unit injection 2-3x/day or as IV drip with bolus; wt based in kg ONLY

42
Q

Heparin indications

A

acts very fast and effectively so for condx that need prompt activity (evolving stroke, big DVT, heart attack, adjunct for dialysis); low dose SQ injection for prophylaxis against post-op DVT, DIC

43
Q

Protamine sulfate

A

Heparin and enoxaparin antidote that binds with Heparin and immediately stops it; give IV SLOWLY to avoid BP drop

44
Q

Heparin is HIGH RISK

A

check with other RN before giving, rate change or bolus; check labs first

45
Q

SE of Heparin

A

bleeding, hematoma, anemia, thrombocytopenia

46
Q

Bleeding sx

A

VS, bruising, petechiae (red dots on skin), hematomas, black tarry stool

47
Q

Heparin induced thrombocytopenia

A

sim to allergix rxn; low platelet count and inc dev of thrombi caused by antibody dev

48
Q

What to do if suspect HIT

A

monitor platelet count, STOP platelet immediately if count gets below 100k, switch to non-hep anticoag

49
Q

What is IV heparin dose based on?

A

Clotting times–anti-Xa or aPTT; drawn q6h, change rate based on response

50
Q

How to draw Hep labs

A

pause for several minutes and flush with saline before drawing blood

50
Q

Therapeutic dose for Heparin

A

When labs show that you don’t need a bolus 2x in a row–found therapeutic dose and only need to draw labs in the morning prob

51
Q

Enoxaparin indications

A

prophylaxis and tx

52
Q

Enoxaparin NC

A

can be given at home–pre-dosed; only SQ; DON’T give with heparin or other anticoagulants except oral warfarin when treating PE or DVT; do not expel the air bubble: will remain in plunger to ensure whole dose is given; slower onset of action compared to heparin but LONGER half-life; rotate injection sites

53
Q

Enoxaparin SE

A

bleeding, thrombocytopenia, HIT

54
Q

Black box for enoxaparin

A

potential spinal hematoma if patient has epidural catheter

55
Q

Warfarin (coumadin) MOA

A

Vitamin-K inhibitor; prevents the synthesis of four coagulation factors (VII, IX, X, prothrombin)

56
Q

Warfarin indications

A

prevention VTE/DVT/PE, thrombotic events for patients with afib or heart valves, reduce recurrence of TIA or MI

57
Q

Warfarin SE

A

bleeding, lethargy, muscle pain, purple toes

58
Q

Giving warfarin

A

ONLY given PO, once a day, usually at 5PM; Onset not until 24 hours! Duration 2-5 days

59
Q

Warfarin antidote

A

Vit K (IV); if doesn’t work–fresh frozen plasma (FFP) or whole blood

60
Q

Warfarin NC

A

NOT for preg or breastfeeding bc DVT risk; Monitor & TEACH for signs of bleeding, HOLD before surgeries, monitor prothrombin time/INR; monitor INR monthly when reach therapeutic; many drug intx; food intx, avoid alc; Wear medic alert bracelet, use soft bristle toothbrush, no electric toothbrush

61
Q

INR with warfarin

A

international normalized ratio; normally 1ish, with warfarin we want 2-3.5

62
Q

Warfarin food intx

A

avoid foods high in vit K–green leafy veg like lettuce, kale, cucumber, kiwi, cabbage, etc

63
Q

Apixaban (Eliquis) and Rivaroxaban (Xarelto) MOA

A

direct inhibitor of factor Xa

64
Q

Apixaban (Eliquis) and Rivaroxaban (Xarelto) indications

A

prevent strokes in patients with afib, post-op thrombo-prophylaxis, treat DVT & PE

65
Q

Apixaban (Eliquis) and Rivaroxaban (Xarelto) SE

A

bleeding, hematoma, dizziness, rash, gastrointestinal distress, peripheral edema

66
Q

Black box warnings for Apixaban and rivaroxaban

A

spinal hematomas if pt has epidural catheter, risk of thrombosis if drugs stop abruptly

67
Q

apixaban and rivaroxaban NC

A

Drug intx, don’t give with other coags, watch liver fxn, don’t stop taking abruptly

68
Q

apixaban and rivaroxaban inc effect of

A

CYP3A4 inhibitors (amiodarone, erythromycin, ketonazole, HIV meds, diltiazem, verapamil, grapefruit juice)

69
Q

apixaban and rivaroxaban dec effect of

A

Decreased effects: phenytoin, carbamazepine, rifampin, and st. johns wort

69
Q

apixaban and rivaroxaban antidote

A

andexxa (recombinant factor Xa, inactivated zhzo)

70
Q

aspirin (as anti-platelet)

A

Blocks prostaglandin synthesis through the COX
enzyme pathways; also BLOCKS PLATELET AGGREGATION; prevent platelet clumping

71
Q

aspirin indx

A

prevent/treat MI, prevent ischemic stroke

72
Q

How can you take aspirin?

A

given PO; can chew baby aspirin for acute event if not EC

73
Q

aspirin SE

A

GI N/V, drowsy, confused, bleeding

74
Q

aspirin NC

A

Reye’s sx, OTC but prescribed by dr for platelet fxn, don’t crush EC

75
Q

aspirin CI

A

thrombocytopenia, active bleeding, blood cancers, traumatic injuries, GI ulcers, vitamin K deficiency, recent hemorrhagic stroke

76
Q

DDAVP (desmopressin)

A

Antiplatelets antiode—clop, tica, aspirin

77
Q

clopidogrel (Plavix) and Ticagrelor (Brilinta) MOA

A

Antiplatelet ADP inhibitor; alters the platelet membrane so it doesn’t receive the signal to
aggregate

78
Q

Clopidogrel and ticagrelor indx

A

dec risk of stroke, prophylaxis of TIAs, post-MI

79
Q

Clopidogrel and ticagrelor CI

A

thrombocytopenia, active bleeding, blood
cancers, traumatic injuries, GI ulcers, vitamin K deficiency,
recent hemorrhagic stroke

80
Q

Clopidogrel and ticagrelor SE

A

chest pain, edema, flu-like symptoms, abdominal pain, diarrhea, nausea, epistaxis, rash, pruritus

81
Q

Clopidogrel black box warning

A

patients with certain genetic abnormalities, who may have higher rate of CV events due to reduced conversion to its active metabolite

82
Q

epistaxis

A

nose bleed

83
Q

What dec clopidogrel’s effectiveness?

A

amiodoarone, calcium channel blocker, NSAIDs, PPIs

84
Q

Ticagelor black box warning

A

inc bleeding risk with aspirin dose over 100mg

85
Q

Ticagelor antidote

A

DDAVP or platelet transfusion

86
Q

Argatroban/bivalrudin class MOA and indications

A

Thrombin (factor IIa) inhibitors; treat HIT, for pt undergoing PCI procedures and at high risk for HIT

87
Q

Thrombin inhibitors SE and NC

A

SE—bleeding; IV only, nursing implications—labs (anti-Xa, H&H, platelets), Argatroban—careful in pt with hepatic dysfunction

PATHO (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions