Brainscape's Knowledge GenomeTM

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


See full index

ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn > Chapter 2 - Hematology > Flashcards

Chapter 2 - Hematology Flashcards

1
Q

What are the three initial responses to vascular injury

A
  1. vasoconstriction
  2. platelet adhesion
  3. thrombin generation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Intrinsic Pathway starts with?

A

exposed collagen, prekallikrein, HMW kininogen, factor XII

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

Intrinsic pathway steps?

A
  • collagen, prekallikrein, HMW kininogen + XII
  • activate XI
  • activate IX, then add VIII
  • activate X, then add V
  • convert prothrombin (factor II) to thrombin
  • thrombin converts fibrinogen to fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Extrinsic pathway starts with?

A

Tissue factor from incured cells + factor VII

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

Steps of extrinsic?

A
  • tissue factor + factor VII
  • activate X then add V
  • convert prothrombin to thrombin
  • thrombin then converts fibrinogen to fibrin
  • measured w/ PT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the prothrombin complex and what does it do?

A

X, V, Ca, PF-3, Prothrombin

forms on platelets

catalyzes the formation of thrombin

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

What is the convergence point for both intrinsic and extrinsic paths?

A

Factor X

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

What does the Tissue factor pathway inhibitor do?

A

Inhibits factor X

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

What does Fibrin do?

A

combines with platelets (GpIIb/IIIa) to form the platelet plug to create hemostasis

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

What does factor XIII do?

A

helps crosslink Fibrin

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

Why is thrombin the key to coagulation? What does it activate?

A

Thrombin

  • converts Fibrinogen to Fibrin and Fibrin split products
  • activates factors V and VIII
  • activates platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Protein C, what does it do?

A
  • Vitamin K-dependent anticoagulation factor
  • degrades factors V and VIII
  • degrades fibrinogen
  • Deficiency can lead to DVTs and Warfarin skin necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is protein S, what does it do?

A
  • Vitamin K dependent anticoagulation factor
  • cofactor of Protein C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TPA is released from where and does what?

A
  • released from endothelium
  • converts plasminogen to plasmin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Plasmin does what?

A
  • degrades factor V and VIII, fibrinogen, and fibrin
  • destruction of platelet plug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Alpha-2 antiplasmin?

A
  • natural inhibitor of plasmin
  • released from endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What factor has the shortest half life?

A

VII

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

What factors’ activity is lost in stored blood but not FFP?

A

V and VIII

labile factors

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

What factor is not synthesized in the liver? where is it synthesized?

A

VIII

synthesized in the endothelium (with vWF), released by ADH (DDAVP), labile factor (along w/ V, so activity is lost in stored blood, but not FFP), broken down by plasmin and protein C (works better w/ S), hemophilia A

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

What are the vitamin K dependent factors?

A

II, VII, IX, X, C and S

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

How long does it take for Vitamin K to take effect?

A

12 hours

Not adequate alone for emergency bleeding - need FFP too

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

How long does it take FFP to work and how long does it last?

A

immediately

lasts 6 hours

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

What is factor II?

A

Prothrombin

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

What is the normal half life of RBCs? Platelets? PMNs?

A
  • RBCs 120 days
  • platelets 7 days
  • PMNs 1-2 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is Prostacyclin (PGI2) released from and what does it do?

A
  • Endothelium
  • Epoprostenol, iloprost, cisaprost - decreases platelet aggregation and causes vasodilitation (antagonistic to TXA2)
  • Used to treat pulmonary arterial hypertension, Raynaud’s, possibly limb ischemia
  • Increases cAMP in platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Thromboxane (TXA2) - where is it released from, what does it do?

A
  • Platelets
  • Increases plt aggregation and promotes vasoconstriction
  • Triggers the release of Ca2+ in platelets → exposes GpIIb/IIIa recepter → platelet-platelet binding
  • platelet to collagen binding (GpIb)
  • activates PIP system to further release calcium
  • can be given in early (<3 hrs) trauma w/ fibrinolysis

The opposite of PGI2 (prostacyclin from endothel, vasodilates, stops aggregation)

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

What is in high concentration in cryoprecipitate and what is it used for?

A
  • high concentrations of vWf, VIII
  • use in von Willebrands disease and hemophilia A (VIII def)
  • contains fibrinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is in FFP?

A

High levels of all factors including V and VIII, C, S, AT-III

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

Why are DDAVP and conjugated estrogens used in the setting of coagulopathy?

*remember estrogen exposure increases DVT risk

A

Cause release of VIII and vWF from endothelium

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

What factors does PT measure?

A

II, V, VII, X, fibrinogen

best for liver synthetic function

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

What does PTT measure?

A

All but VII and VIII - Does not pick up VII deficiency

routine anticoag: measure q6h, keep at 60-90 sec

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

What is an ACT?

A

Activated clotting time

150-200 for routine anticoagulation

480 for Cardiopulmonary bypass. Also used for ECMO.

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

What level INR is a relative contraindication for surgical procedures?

A

>1.5

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

What level INR is a relative contraindication for central line, PCT biopsies, and eye surgery?

A

>1.3

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

What is the most common cause of surgical bleeding?

A

Incomplete hemostasis

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

What is the most common congenital bleeding disorder?

A

von Willebrands

MC Psx: epistaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the inheritance of von willebrand’s disease?

A

I and II are AD.

III is AR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does vWf do?

A

links GpIb receptor on platelets to collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

In von willebrand’s, what is the PT and PTT? Bleeding time?

A
  • PT normal
  • PTT normal or abnormal (VIII can be affected)
  • bleeding time long (ristocetin test)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

In these types of von willebrand’s disease there is a problem in vWf quantity. How do you treat?

A
  • I - reduced quantity of vWF, MC
  • III - complete deficiency, most severe bleeding
  • Tx: recombinant VIII, vWf, cryoprecipitate
    • DDAVP, conjugated estrogens works for I but not III (nothing to release)
41
Q

This type of Von willebrand’s disease has a problem in the quality of vWf

A

Type II

Tx: recombinant VIII:vWF, cryoprecipitate, DDAVP

42
Q

What is Hemophilia A and what is its inheritance?

MC symptom?

A
  • Factor VIII deficiency
  • Sex linked recessive
  • MC Sx: hemarthrosis
43
Q

Does factor VIII cross the placenta?

A

Yes. Circumcision may not cause bleeding in hemophila A pts.

44
Q

What is Hemophilia B and what is its inheritance?

A

Factor IX deficiency - Christmas disease. Sex linked recessive.

45
Q

What can cause an acquired thrombocytopenia?

A

H2 blockers, heparin

46
Q

What is Glanzmann’s thrombocytopenia?

A
  • GpIIb/IIIa receptor def - platelets cannot bind to each other
  • Fibrin normally links them together at this site
  • Tx: platelets
  • Like abciximab - GpIIb/IIIa inhibitor used in PCI
47
Q

What is Bernard Soulier?

A
  • GpIb receptor deficiency on platelets
  • Can’t bind vWF to collagen
  • Tx: platelets
48
Q

What does Uremia do to platelets and what is the treatment?

A
  • Inhibits platelet function by inhibiting vWF release
  • Labs: BUN >60-80
  • Tx: hemodialysis first, DDAVP for acute reversal, cryo for moderate/severe bleeding
49
Q

What does Ticlopidine do to platelets?

A
  • decreases ADP on platelet surface (fibrinogen can’t bind)
  • prevents exposure of GpIIb/IIIa (Glanzman like)
  • Tx: platelets
50
Q

What does Dipyridamole do to platelets?

A
  • inhibits cAMP phosphodiesterase, increases cAMP
  • decreases ADP induced platelet aggregation
  • Tx: platelets
51
Q

What does Pentoxifylline do to platelets?

A
  • inhibits platelet aggregation
  • Tx: platelets
52
Q

What does Clopidogrel do?

A
  • irreversibly inhibits P2Y12 receptor (ADP receptor)
  • Uses: in STEMI or NSTEMI, use plavix to load before PCI. Can be added w/ ASA in postop coronary stent.
  • Also used in PAD and stroke.
  • Tx: platelets
  • Similar mechanism to prasugrel and ticagrelor
53
Q

PCN/cephalosporins do what to platelets?

A
  • bind platelets
  • can increase bleeding time
54
Q

HIT is caused by what antibody?

A
  • IgG heparin-PF4 ab (anti-heparin ab) - causes platelet destruction
55
Q

What type of clot does HIT cause?

A

White clot

56
Q

How do you diagnose and manage HIT?

A
  • Suspect w/ heparin exposure >5 days (previous hospitalization)
  • >50% platelet drop, necrotic lesions at injection sites, thrombus, or anaphylaxis
  1. Stop all heparin
  2. Start direct thrombin inhibitor - argatroban, hirudin, ancrod, or dextran
  3. Send serotonin release assay (confirmatory test, ELISA for hep-ab)
  4. Avoid platelet transfusion (risk of thrombosis)
  5. If wanting to start warfarin, wait for platelets to recover (>150K), then bridge
57
Q

What are the lab findings in DIC?

A
  • decreased platelets (often initiated by tissue factor)
  • prolonged PT and PTT
  • low fibrinogen
  • high fibrin splits/high D-Dimer
  • Tx: underlying cause (eg sepsis)
58
Q

How many days before surgery should ASA be stopped?

A

7 days

  • inhibits COX in platelets
  • decreases TXA2 (vasoconstriction, platelet aggregation)
  • b/c platelets lack DNA, they can’t resynth COX
59
Q

How many days before surgery should coumadin be stopped?

A

5 days

  • consider starting heparin anticoag while warfarin wears off
  • 36 hrs half-life
  • if bleeding - give vit K and possibly FFP
  • if bleeding to death - can give IV vit K and PCC
60
Q

What should platelets be at before surgery? after surgery?

A

50k; 20k

61
Q

Prostate surgery has what effect bleeding?

A

can relase urokinase, activates plasminogen = thrombolysis

Treat with e-Aminocaproic acid (Amicar, inh fibrinolysis)

62
Q

Tooth extraction or tonsillectomy will pick up what percentage of Pt’s with a bleeding disorder?

A

99%

H&P best way to predict bleeding risk

63
Q

What is the most common cause of congenital hypercoagulability?

A

defect of factor V Leiden

  • resistance to activated protein C
  • Tx: heparin, warfarin
64
Q

What is the treatment of hyperhomocysteinemia

A

folic acid and B12 (10% of spontaneous DVT’s)

65
Q

What is the treatment for G20210 prothrombin gene defect?

A

heparin, warfarin (5% of spontaneous DVT’s)

66
Q

How does Antithrombin III deficiency develop and how is it treated?

A
  • can develop after previous heparin exposure
  • heparin will not anticoagulate these patients
  • Tx: recombinant AT-III or FFP THEN heparin/warfarin
67
Q

What antibody is the lupus anticoagulant, what does it do to PTT and to coagulation?

How is it diagnosed?

How is it treated?

A
  • Antiphospholipid antibodies - cardiolipin, lupus anticoagulant
  • Causes a procoagulant state - thrombi, loss of pregnancy
  • Not all have SLE
  • Labs: PTT prolonged (but hypercoag), not corrected by FFP
  • Dx: by positive russell viper venom time, false + RPR
  • Tx: heparin, warfarin
68
Q

What are some causes of acquired hypercoagulability?

A

Tobacco (#1), malignancy, inflammatory state, Inflammatory Bowel disease, oral contraceptives, pregnancy, rheumatoied, postop, myeloproliferative

69
Q

How does cardiopulmonary bypass cause hypercoagulable state and what is the prevention?

A

Causes factor XII activation. Prevent with heparin.

70
Q

What is the pathogenesis of warfarin skin necrosis?

A
  • Pts who don’t get heparin bridge
  • Protein C and S have short half life
  • Transient hypercoaculable state
  • Protein C deficiency especially susceptible
  • Tx: heparin
71
Q

What is Virchow’s Triad?

A

Stasis, Endothelial injury, hypercoagulable state

Leads to venous thromboses

72
Q

What is the key element in the development of an arterial thrombus?

A

endothelial injury

73
Q

How long must a pt be on warfarin for their 1st, 2nd, or 3rd DVT?

A
  • 1 = 6 months
  • 2 = 1 year
  • 3 or significant PE= lifetime
74
Q

What are the indications for a greenfield IVC filter?

A
  • contraindications to anticoagulation
  • documented PE on anticoagulation
  • free floating ileofemoral, IVC, or femoral DVT
  • pts s/p pulmonary embolectomy
75
Q

Patient has pulmonary embolism and is in shock despite massive ionotropes, what do you do?

A
  • OR - open embolectomy vs angiography w/ suction catheter
  • If not in shock, give heparin
  • thrombolytics not proven to increase survival
  • MC from ileofemoral region
76
Q

What percentage of positive V/Q scans have negative duplexes?

A

33%

77
Q

How does warfarin work?

A

prevents vitamin K-dependent decarboxylation of glutamic resudues on vitamin K-dependent factors (II, VII, IX, X)

protein<span> C and S also affected</span>

78
Q

How does Dextran work?

A

Inhibits platelets and coagulation factors - antiplatelet and anticoagulant

79
Q

How do SCD’s work?

A

improve venous return but also induce fibrinolysis with compression (TPA)

80
Q

How does Heparin work?

A

potentiates antithrombin III

81
Q

How is heparin reversed?

A

Protamine (1-1.5 protamine/100U heparin) follow PTT’s

82
Q

What is the half life of heparin and how is it cleared?

A

60-90 minutes

Cleared by retuculoendothelial system (spleen, macrophages)

83
Q

What are the long term side effects of heparin? Does it cross placenta?

A

osteoporosis, alopecia

no - okay for pregnancy, unlilke warfarin

84
Q

What are the problems/reactions of protamine?

A
  • cross reacts with NPH insulin or previous heparin exposure
  • 4-5% of patients get reaction - hypotension, bradycardia, decreased cardiac fxn
85
Q

How dies Hirudin work? is it reversible?

A
  • From leeches
  • Irreversible direct thrombin inhibitor (most potent)
  • Want PTT 60-90
  • High risk of bleeding
86
Q

How does Argatroban work?

Where is it metabolized?

What is the half life?

What is it often used for?

A
  • direct thrombin inhibitor
  • metabolized in liver
  • T1/2 50 mins
  • use for HITT
87
Q

How does Bivalirudin work? where is it metabolized? half life?

A
  • reversible direct thrombin inhibitor
  • metabolized by proteinase enzymes in the blood
  • half life 25-30 mins
88
Q

How does Ancrod work? where does it come from?

A
  • Malaysian pit viper venom
  • stimulates tPA release
89
Q

How does Amicar (e-aminocaproic acid) work?

A
  • Inhibiting plasmin → inhibits fibrinolysis (preserves clot)
  • Uses: DIC, persistent bleeding after cardiopulmonary bypass, thrombolytic overdose
90
Q

What are common thrombolytics? Which one has high antigenicity?

A
  • urokinase, tPA, streptokinase
  • streptokinase has high antigenicity
91
Q

What is required for thrombolytics to work?

A

Guidewire must get past obstruction

92
Q

What are acceptable Fibrinogen levels when using thrombolytics?

A
  • >100
  • <100 associated with increased risk/severity of bleeding.
93
Q

What are absolute contraindication to using thrombolytics?

A
  • active internal bleeding
  • recent CVA or NSGY (<3 months)
  • intracranial pathology
  • recent GI bleed
94
Q

Major (not absolute) contraindications to thrombolytics?

A
  • recent surgery (<10 days)
  • organ biopsy
  • left heart thrombus
  • active peptic ulcer
  • major trauma
  • uncontrolled HTN
95
Q

What is the key to anticoagulation? What does it do?

A

Antithrombin III

  • binds and inhibits thrombin
  • inhibits factors IX, X, and XI
  • Heparin upregulates ATIII up to 1000x normal activity
96
Q

How do you manage Hemophilia A peri-operatively?

A
  • needs levels 100% preop
  • keep 80-100% for 10-14 days after surgery
  • follow PTT q8h postop (psx w/ prolong PTT and nl PT)
  • Psx: epistaxis, ICH, hematuria
    • Tx: recombinant FVIII, cryo
  • Psx: hemarthrosis (MC psx)
    • Tx: don’t aspirate, ice, RoM exercise, FVIII, cryo
97
Q

How do you manage Hemophilia B peri-operatively?

A
  • need levels 100% pre-op
  • keep 30-40% 2-3 days postop
  • labs: PTT prolong, normal PT (like Hemophilia A)
  • Tx: recombinant IX, FFP
98
Q

How do platelet disorders present?

A

epistaxis, bruising, petechiae, purpura

ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn (51 decks)

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