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Summer FDTN Exam 6 > Clotting disorders > Flashcards

Clotting disorders Flashcards

1
Q

How do platelets and clotting factors usually circulate

A

In inactive form

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2
Q

Vascular injury leads to

A

vascular spasm
Plt adhesion mediated by vWF
coagulation cascade

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3
Q

What are PT/INR measure

A

integrity of extrinsic (factor VII) and common pathway

Used for Warfarin check

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4
Q

What does PT represent

A

time in seconds for plasma to clot after you have added calcium and thromboplastin (activates the extrinsic pathway)

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5
Q

What causes a prolonged PT

A

Deficiencies or inhibitors of clotting factors within the extrinsic or common pathways

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6
Q

Why was INR created

A

to assess patient’s PT in comparison to a geometric mean of 20+ healthy males and females at THAT specific lab

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7
Q

What does aPTT measure

A

Integrity of intrinsic (VIII, IX, XI, XII)and common pathways of the coag cascade

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8
Q

What is PTT (partial thromboplastin time)

A

time in seconds it takes for patients plasma to clot after adding Calcium (phospholipid that activates the intrinsic pathway)

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9
Q

What is the clotting factor where intrinsic and extrinsic all come together

A

Factor Xa! It activates thrombin and causes a clot to form

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10
Q

What type of patient would we worry about if they have a deficient PT

A

Young, healthy patient; suspect something autoimmune, (liver disease, DIC)
Those are the patients you should prob preform a mixing study on
-Elderly with deficient PT you think, ok this might just be age related, or they could be on warfarin

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11
Q

What are the outcomes of a mixing study with aPTT

A
  • if PTT corrects when you add “normal blood”: Pt has a factor deficiency* present in intrinsic path (8, 9, 11, 12). Essentially, when you add normal blood, the deficiency corrects bc you add those deficient factors in!
  • If PTT stays prolonged: it must be something that is destroying any blood that comes in (drugs like heparin; AI hemophilia A; Lupus anticoagulant)
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12
Q

If PTT corrects and you determine it is 2/2 an intrinsic path factor deficiency, what should you do

A

Get a clotting factor assay to determine which factor is involved, and determine whether it is acquired or congenital

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13
Q

What is Lupus anticoagulant (LAC)

A

Prolonged PTT
MC in young females- do NOT have to have SLE!
Suspect if pt: No bleeding Hx or has a clot and baseline prolonged PTT before you started the anticoag
-AutoAbs are directed at phospholipid binding proteins, causes Ab mediated thrombosis

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14
Q

What are the outcomes of a mixing study with PT

A

PT corrects: deficiency in extrinsic path (factor 2, 7, 10, fibrinogen), liver disease
PT stays prolonged w/ prolonged PTT: inhibitor of extrinsic path, factor V inhibitor

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15
Q

Deficiencies in clotting factors found by PT or aPTT mixing studies are MCC by

A

Supratherapeutic warfarin (rat poison)

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16
Q

Etiologies that cause inhibition of all pathways found in PT/PTT mixing studies include (what causes to “stay prolonged”)

A

LAC
nonspecific factor inhibitors w/ lymphoproliferative d/o
monoclonal protein disorder (cause autoimmunity)

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17
Q

What is warfarin

A

Inhibits vitamin K dependent clotting factors (7, 9, 10, protein C&S)
Pregnancy category X

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18
Q

What can a supratherapeutic INR 2/2 warfarin lead to

A

elevated PTT

  • for every 1.0 increase in PT, 16-17 sec. increase in PTT
  • If pt comes in w/ an INR of 8 and they aren’t bleeding, hold dose then decrease
  • if pt comes in w/ INR 4, hold dose 1-2 days then continue at same dose
  • if pt comes in vomiting and can’t take warfarin, PR/INR will be high
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19
Q

2 MC reasons to use warfarin are

A
  1. AFIB (goal INR 2-3)
  2. VTE (goal INR 2-3)
  3. Mechanical valve replacement (goal INR 2.5-3.5)
20
Q

What is UFH

A

Thrombin (factor IIa) and Xa inhibitor

Large molecule NOT well absorbed subQ, and can cause HIT

21
Q

What is LMWH

A

Stronger Xa inhibit, only mild IIa (thrombin) inhibition w/ longer half life
Derived from UFH but defractionated to make a smaller molecule more well absorbed subQ
*SAFE for pregnancy= LOVENOX
(lovenox is dosed by weight)
-generally not good for those that are obese or w/ CKD/ESRD

22
Q

Do you need to get labs or monitor LMWH

A

No! no need
But if you want to monitor your pt, you can check efficacy with anti-Xa levels 3-4 hours after Lovenox
-The only people you may need to monitor are obese or very thin patients

23
Q

What is Fondaparinux

A

synthetic factor Xa inhibitor that causes ATIII to change in coag cascade. 17 hr half life
NO REVERSAL AGENT*

24
Q

What are DOAC’s

A

Rivaroxiban/Epixaban: direct anti-Xa

Dabigatran: oral direct thrombin inhibitor used for AFib and VTE

25
Q

What are reversal agents for anticoagulants

A

Heparin: protamine
Warfarin: vitamin K
Lovenox: Protamine wil only reverse 60%; give Plt, FFP, and DDAVP
Dabigatran (pradaxa): dialysis if bleeding in brain. if not, Idarucizumab
Xarelto: PCC
Arixtra: Novo 7 SSAVP
(know MC, use for life threatening bleeds)

26
Q

What are RF for VTE and hypercoagulable states

A

Virchows triad: venous stasis + trauma/endothelial injury + hypercoagulable state = increased VTE risk
Hypercoag: cancer, smoking, pregnancy, estrogen, OCP, HRT, Tamoxifen/chemo drugs

27
Q

List some common hypercoagulable states

A 
Protein C&S or ATIII deficiency 
Factor V Leiden mutation 
prothrombin gene mutation 
LAC 
hyperhomocysteinemia 
Anticardiolipin antibody 
Paroxsymal nosturnal hemoglobinuria
28
Q

What prevents over-clotting by regulating the coagulation cascade

A

Protein C&S, AT III

Deficiency in any can cause hypercoagulability

29
Q

What is an ATIII deficiency

A

Mutations reduce levels or functional capacity of ATIII

Can also be low 2/2 liver disease, nephropathy, or heparin

30
Q

What are Protein C&S

A

Vitamin K dependent proteins
Can be low in nephrotic syndrome or warfarin
If low, both carry increased risk for VTE

31
Q

What is Factor V Leiden mutation

A

Normally, factor V helps convert prothrombin to thrombin, fibrinogen to fibrin, and forms a clot. And Protein C shuts this off so you do not over clot.
With this mutation, factor V is resistant to protein C, so it does not get shut off, so you end up clotting more 2/2 high thrombin
Heterozygous is MC and risk is only 5x higher
Homozygous is rare and risk is 80x higher
MC in white

32
Q

What is the prothrombin gene mutation

A

Mutation of nucleotide substitution in 3’ untranslated region of prothrombin gene= greater fxn of prothrombin (factor II)
3x higher VTE risk

33
Q

What is Homocysteine

A

High levels of Homocystein increase risk for VTE (arterial), vascular injury, platelet aggregation, smooth muscle hypertrophy, intimal thickening, elastic lamina disruption, and impaired NO activity

34
Q

What is hyperhomocysteinemia

A 
MTHFR deficiency (valine replaces alanine)
Can be caused by B6, B12. and folic acid deficiency , smoking, fibrates, and nicotinic acid 
Can Tx with B12 and folate, but they don't reduce risk of VTE
35
Q

What is antiphospholipid Ab syndrome (APS)

A

Antibodies to phospholipids cause recurrent venous or atrial thrombosis, pregnancy morbidity/fetal loss
The associated Abs are LAC, anticardiolipin antibody, and anti-beta 2 glycoprotein

36
Q

How do you treat APS

A

Lovenox!

Stops you from forming clots that can lead to thrombi 2/2 autoantibodies

37
Q

LAC and anticardiolipin antibody are both diseases where

A

the body forms IgG or IgM against phospholipids

Phospholipids are involved in the coag cascade and cause more arterial clotting

38
Q

Sneddon syndrome causes

A

Livedo reticularis and neurologic abnormalities
Typical of patients that have very progressive Lupus, may cause tissue hypoxia leading to the bruise that looks like mottled skin

39
Q

S/Sx of a DVT are

A

Swelling
Erythema
Pain/ache
May be of LE (more common) or UE

40
Q

What tests are used to evaluate VTE

A

Doppler US**: can be falsely - below knee. if you are very susp and it comes -, repeat in 2-3 days
CT angio: PE
VQ scan: good if w/ renal insufficiency, pregnant, or allergic to contrast dye
D-dimer: + is acute clot, but - if chronic clot or no clot! only use if you are really susp and US is (-)

41
Q

Your patient comes in and you do a doppler and determine they have a DVT. How do you proceed

A

Do they have RF? (surgery, pregnant, cancer, HRT, travel)
Start UFH/LMWH (preventive) first, then warfarin (must run coag panel)
Or start on a DOAC
Wait until you d/c warfarin for 3 WKS before you run confirmatory tests

42
Q

Why do you start UGH/LMWH before warfarin?

A

Warfarin initially drops protein C&S levels and puts a patient at higher risk for VTE before it “thins” the blood
Start on UFH to provide blood thinning while warfarin gains efficacy

43
Q

How long should you be on anticoags if you’ve had a VTE

A

1st VTE: 3-6 months
1st VTE + hypercoagulable (RF): 3-6 months
Life threatening VTE: may need lifelong (controversial)
Recurrent VTE + hypercoag: Lifelong anticoags
Idiopathic VTE: may need lifelong, 90% re-thrombose

44
Q

What is tPA (tissue plasminogen activator)

A

Thrombolytic therapy! given IV vs catheter-directed
Indicated for pts w/ extensive, life threatening clot -OR- w/ PE causing significant hemodynamic instability and RV strain (saddle embolism!)

45
Q

What is an IVC filter

A

Umbrella placed into the IVC
Reserved for pts that can’t take anticoags and are high risk for LE DVT, to prevent propagation
Also used if you had a BIG PE to avoid future lung injury -OR- if high risk of bleeding complications

46
Q

If you have a permanent IVC filter, you need

A

Lifelong anticoag therapy!

47
Q

How do you treat SF thrombophlebitis

A 
NSAIDs/ASA + warm compress 
AC if: 
>5cm 
very symptomatic 
clot w/in 2cm of where SF vein enters deep vein 
if SF thrombosis occurs while on ASA

Summer FDTN Exam 6 (7 decks)

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