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My PANCE Decks > Hemostasis/Coagulopathies (Self-Made) > Flashcards

Hemostasis/Coagulopathies (Self-Made) Flashcards

1
Q

What is primary hemostasis?

A

Platelet plug formation

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2
Q

What factors are contained within the alpha granule of a platelet?

A
  • PDGF
  • Transforming growth factor Beta
  • Fibrinogen
  • VWF
  • PF4
  • Factor V
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3
Q

Where can vWF be found?

A
  • Endothelial cells
  • Platelets
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4
Q

What are the primary functions of vWF?

A
  • Binding to endothelium to promote platelet adhesion.
  • Plasma carrier for Factor VIII, preventing its degradation.
  • Binds to exposed collagen.
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5
Q

How does the extrinsic pathway of coagulation work?

A

7 => 10 => 5 => 2 => 1

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6
Q

How does the intrinsic pathway of coagulation work?

A

12 => 11 => 9 & 8 => 10 => 5 => 2 => 1

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7
Q

What is the driving force to convert prothrombin?

A

Prothrombin activator, which is Factor 10.

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8
Q

If I am vitamin K deficient, what factors/proteins are affected?

A

2, 7, 9, 10, protein C & S

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9
Q

What demograpic is especially susceptible to Vit K deficiency?

A

Newborns

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10
Q

What are the two ways the intrinsic pathway can be triggered for coagulation?

A
  • Trauma to the blood vessels themselves.
  • Exposure of blood to collagen.
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11
Q

What kind of chronic organ disease would impair blood coagulation? Why?

A

Liver disease, since prothrombin is manufactured by the liver.

Also affects fibrinogen production.

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12
Q

What is the most abundant coagulation protein?

A

Fibrinogen

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13
Q

What does heparin act on?

A

Anti-thrombin III

AT3 inactivates thrombin & 10a (Primary)
Also inactivates 9a & 11a (secondary)
AKA intrinsic pathway inhibition

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14
Q

What does a D-dimer measure?

A

The degradation products created from breakdown of fibrin by plasmin.

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15
Q

What does the protein C&S complex primarily inhibit?

A

Thrombin and 8a.

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16
Q

What compound inhibits coagulation of blood products?

A

Sodium citrate

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17
Q

What antibodies does a person with AB blood have? A blood?

A

AB: no antibodies present.
A: anti-B antibodies present.

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18
Q

Does Rh+ mean it has antigens or antibodies?

A

Antigens.

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19
Q

Why is a type and screen ordered? What is its function?

A
  • Determines the receipient’s ABO and Rh phenotype. (Type)
  • Identifies any antibodies that may directed against other antigens (Screen)
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20
Q

When is a cross-match not ordered? What is it?

A

Not ordered in emergency settings due to the time it takes.
Mixes donor blood with receipient blood to ensure a match.

Checks agglutination.

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21
Q

A patient presents to the ER with acute blood loss due to a 5cm laceration on their arm. The bleeding is controlled via applied pressure. They are mildly hypotensive, and CBC reveals a Hgb of 8.5. The patient has no other symptoms currently. Should they be transfused PRBCs? Why or why not?

A

No.
Given the lack of any other symptoms (esp. lack of CV symptoms) and her Hgb of 8.5, she is not indicated to require a PRBC transfusion.

If she was still having an ongoing bleed that was not stopping, PRBCs should be considered to stabilize her hemodynamically.

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22
Q

A patient presents to the ER with acute blood loss due to a 5cm laceration on their arm. The bleeding is not controlled via applied pressure. They are mildly hypotensive at the moment, and CBC reveals a Hgb of 7.5. The patient has no other symptoms currently. She is transfused 1 unit PRBCs, but during the transfusion, she begins to feel very chilly and starts itching her leg. Her temperature goes up to 38.3F from a baseline of 37C. What is the next step in her management?

A

Stop the transfusion, report it to the blood bank, and administer tylenol to bring her fever down.

Always stop transfusion if an acute reaction is suspected.

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23
Q

What is the benefit of whole blood transfusion and the primary reason it is not used commonly?

A

It offers the greatest oxygen affinity within its RBCs.

However, it is difficult to store due to RBCs requiring a temperature that platelets and clotting factors become degraded in.

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24
Q

A patient requires a unit of PRBCs for transfusion. They are noted to be immunodeficient and have a history of GVHD. What modification should be made to their PRBC transfusion order?

A

Irradiation of PRBCs.

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25
Q

What blood type is a universal receipient for plasma?

A

O blood type can receive any plasma from any blood type.

Plasma only has antibodies.

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26
Q

What is the chief advantange of cryoprecipitate over FFP?

A

Smaller volume overall, but high concentrations of vWF, F8, F13, and fibrinogen

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27
Q

For a patient with a platelet count of 140k, what would prompt us to transfuse them?

A

Ongoing bleeding + platelet dysfunction (disease or drug-induced)

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28
Q

What can reverse heparin?

A

Protamine sulfate.

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29
Q

How does DDAVP/Desmopressin work?

A

Increases plasma levels of vWF, F8, and tPA, shortening aPTT and bleeding time.

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30
Q

When is topical thrombin contraindicated?

A
  • Known sensitivity to bovine products
  • Massive bleeding
  • Large vessel bleeds
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31
Q

A patient is admitted to the hospital with a hx of ESRD on dialysis. The hospitalist wants you to order an anticoagulant for them. What would be the best option for a parenteral anticoagulant?

A

Unfractionated heparin, which is cleared hepatically.

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32
Q

What hypersensitivty reaction type is heparin induced thrombocytopenia?

A

Type 2 antibody-mediated.

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33
Q

What risk factors are associated with HIT?

A
  • Use of UFH in surgical patients
  • Females
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34
Q

What is the classic presentation of HIT?

A
  • A drop of platelet count > 50% from baseline or new onset thrombocytopenia 5-10 days after beginning heparin.
  • Acute systemic reactions
  • Necrotic skin lesion at heparin injection site.
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35
Q

After HIT is suspected, what steps should be taken?

A
  1. STOP heparin.
  2. Confirm HIT via HIPA, serotonin release assay, and Heparin-PF4 Ab ELISA.
  3. Switch to argatroban if AC still required.
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36
Q

What are the primary differences between UFH and LMWH?

A
  • UFH is hepatically cleared; LMWH is renally cleared.
  • UFH has broad activity and binds to 10a directly; LWMH has far higher inhibition of 10a by AT3 binding.
  • LWMH can be given SC in the abdominal wall.
  • LWMH must be monitored via anti-F10 levels, not aPTT.
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37
Q

If a patient is pregnant and requires AC, what is the best medication?

A

LMWH

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38
Q

A patient presents for elective surgery and is currently on warfarin. They have no cardiac history, other than afib. They have a history of HTN, HLD, and T2DM. Do they require bridging and why or why not?

A

They require bridging via lovenox to transition their warfarin due to their high stroke risk. Afib + HTN + HLD puts their coagulation at risk for embolism, as well as potentially narrowed arteries from HLD.

39
Q

How does argatroban differ from heparin?

A

Argatroban is a direct thrombin inhibitor. No effect on AT3.

Measured via aPTT.

40
Q

A patient with a history of liver cirrhosis on the telemetry unit has been on heparin for 5 days and suddenly developed HIT. They were taken off their heparin. They still require AC. What parenteral AC is best for them at this point?

A

They should be given bivalirudin/angiomax, given their inability to hepatically clear argatroban.

41
Q

What factors make warfarin preferred over DOACs?

A
  • Cost
  • No renal dosing required
42
Q

What factors make DOACs preferred over warfarin?

A
  • Far less drug-drug interactions.
  • DOACs show higher efficacy.
  • DOACs require very minimal diet adjustments or monitoring.
43
Q

A 55 year-old man who has been undergoing stable and successful anticoagulation with warfarin for recurrent DVT presents to the Emergency Department passing blood in his stool. What lab tests should be ordered?

A
  • CBC
  • CMP
  • PT/INR
44
Q

A 55 year-old man who has been undergoing stable and successful anticoagulation with warfarin for recurrent DVT presents to the Emergency Department passing blood in his stool. CBC reveals a Hgb of 5.1. What are the next steps in his management?

A

Begin IV vitamin K and PRBC transfusion.

45
Q

What is the only DOAC that primarily inhibits thrombin?

A

Dabigatran/Pradaxa

All the other 3 DOACs are F10a inhibitors. Xaban ending = 10a ban

46
Q

When are DOAC reversal agents indicated?

A

Emergent surgery or life-threatening/uncontrollable bleeding

47
Q

Which DOAC is mostly safe in a CKD patient?

A

None!

Warfarin is preferred in a patient with CKD that requires AC.

48
Q

What kind of therapy will irreversibly modify a platelet’s function for its lifespan?

A

Aspirin therapy.

49
Q

Which antiplatelet drugs are reversible?

A
  • Ticagrelor/Brilinta
  • Cangrelor/Kengreal
  • Eptifibatide/Integrilin
  • Abciximab/Reopro
50
Q

When is streptokinase contraindicated for therapy?

A

Ischemic stroke.

51
Q

What is the primary difference in mechanism of action between alteplase and streptokinase?

A
  • Alteplase selectively binds to bound plasminogen.
  • Streptokinase simply activates plasminogen in general.
52
Q

A 70 y/o female is diagnosed with nonvalvular atrial fibrillation. Her PMH is significant for CKD, with a moderately reduced renal function. All of the following anticoagulants would be expected to require a reduced dosage in the patient except:
a) Apixaban
b) Dabigatran
c) Rivaroxaban
d) Warfarin

A
53
Q

What does heparin bind to in order to exert its anticoagulant effect?

A

Antithrombin III

54
Q

Which of the P2Y12 ADP receptor antagonists REVERSIBLY binds the receptor?
a) Clopidogrel (Plavix)
b) Prasugrel (Effient)
c) Ticagrelor (Brilinta)
d) Ticlopidine (Ticlid)

A

C: Ticagrelor/Brilinta

55
Q

What is most appropriate treatment for reversing the anticoagulant effect of heparin?

A

Protamine sulfate

56
Q

If a patient has a PMH of GERD and takes omeprazole daily, which P2Y12 drug should be avoided?
a) Prasugrel (Effient)
b) Ticlopidine (Ticlid)
c) Clopidogrel (Plavix)
d) Congrelor (Kengreal)

A

C: Clopidogrel/Plavix

57
Q

What are the primary concerns with prescribing ticlopidine?

A

Life-threatening hematologic reactions.

58
Q

What are the hallmark signs of a coagulopathy?

A
  • Easy bruising
  • Abnormal bleeding
  • Prolonged bleeding post-dental work
  • Menorrhagia
  • Recurrent epistaxis
59
Q

If a patient presents with mucocutaneous bleeding, what is the most likely underlying etiology for a bleeding disorder?

A

Qualitative/quantitative platelet defects.

60
Q

If a patient presents with bleeding within their joints, what is the most likley underlyin etiology for a bleeding disorder?

A

Coagulation factor disorder.

61
Q

What does elevated INR suggest?

A

Higher bleed risk

62
Q

What is the mnemonic for PT and aPTT monitoring?

A

PT = play tennis (Extrinsic)
aPTT = play table tennis (Intrinsic)

Elevations in both imply common pathway defect.

63
Q

What is the most common X-linked genetic disease?

A

Hemophilia A

64
Q

A male patient presents with prolonged bleeding following his cholecystectomy. A CBC and coagulation panel are ordered, revealing the patient to have elevated aPTT, but all other lab studies are normal. What is the most likely underlying etiology and suggested course of treatment?

A

Mild hemophilia A, which can be treated with DDAVP or factor 8 concentrate.

Male = far more likely.
Elevated aPTT = intrinsic pathway deficiency.
Normal platelet count = factor dysfunction rather than platelet dysfunction.

65
Q

At what point in terms of factor 8 activity is hemophilia A considered severe?

A

< 1% activity present.

66
Q

What is the suggested course of treatment for someone presenting with hemophilia B?

A

Factor 9 concentrate is the only treatment option.

67
Q

What NSAID is typically ok for hemophilia patients to take? Why?

A

Celecoxib/celebrex is generally ok to treat any arthritis symptoms that develop.

It is a selective COX-2 inhibitor.

68
Q

What are the primary causes of death for someone with hemophilia?

A
  • Transfusion-obtained HIV/AIDS
  • Hepatitis/Cirrhosis
69
Q

What is the primary cause of death in terms of hemorrhage for a hemophilia patient?

A

ICH

70
Q

A 25-year male patient has recently been diagnosed with factor 8 deficiency, AKA hemophilia A. He has a mild case, characterized by prolonged bleeding after he gets hurt. What patient education should be given to him regarding managing his condition?

A
  • AVOID CONTACT SPORTS
  • Attend all your hematology appointments and blood transfusions.
71
Q

What is the most common inherited coagulopathy? How is it inherited?

A

vWD

Autosomally, either dominant or recessively.

72
Q

Which vWD type present clinically similar to hemophilia A? Why?

A

Type 3, due to the near absence of vWF, which results in a near absence of F8.

73
Q

A patient presents with recurrent nosebleeds and easy bruising. Additionally, they tend to stay in the dentist’s office for extended amounts of time due to prolonged bleeding. Lab studies are ordered, including a CBC and coagulation panel, but the only abnormal finding is a mildly prolonged aPTT. What is the probably underlying etiology and treatment options?

A

It is most likely vWD.
Treatment includes DDAVP, recombinant vWF< or vWF/F8 concentrates.

DDAVP is only indicated in mild bleeding.

74
Q

What ethnic group is most susceptible to Factor 11 deficiency? Treatment options?

A

Ashkenazi Jewish
Treated with F11 concentrate or FFP if not available.

75
Q

How does thrombocytopenia typically present on examination?

A
  • Mucous membrane bleeding
  • Epistaxis
  • Gum bleeding
  • GI bleeds
  • Petechiae
76
Q

A 5-year old child presents with a sudden onset of petechial rash. Their MHx includes a recent URI, resolve just a week ago. Basic labs are drawn, with only isolated thrombocytopenia noted. The patient has no other symptoms, but the mother is worried about the rash, which is non-blanchable. How should this patient be managed?

A

Watchful waiting.
Unless the patient’s condition worsens, no specific treatment is warranted.

Immune thrombocytopenic purpura (ITP)

77
Q

A 5-year old child presents with a sudden onset of petechial rash. Their MHx includes a recent URI, resolve just a week ago. Basic labs are drawn, with only isolated thrombocytopenia of 80,000 plts noted. The patient has no other symptoms, but the mother is worried about the rash, which is non-blanchable. After some monitoring for a week, the patient’s CBC is redrawn, showing a platelet count of 40,000. The mother also notes that the patient recently got a papercut and it took 30 minutes to stop the bleeding. What is the suggested course of treatment for this patient?

A
  1. Corticosteroids (First-line)
  2. IVIG
  3. Consider plt transfusion
  4. Consider splenectomy for thrombocytopenia > 6mo.

ITP

Also educate mother to have her child avoid contact sports.

78
Q

What is the primary mechanism responsible for drug-induced thrombocytopenia? What is the most common general drug class that causes it?

A

Immune-mediated, usually due to ABXs.

79
Q

What is more likely, an inherited platelet dysfunction disorder or an acquired?

A

Acquired or iatrogenic is far more common.

80
Q

What are the most common etiologies for iatrogenic platelet defects?

A

ASA or plavix therapy.

NSAIDs as well.

81
Q

What diagnostic study would be particularly useful in evaluating for a qualitative platelet disorder?

A

Peripheral smear.

82
Q

What defines a thrombic microangiopathy?

A
  • Thrombocytopenia
  • Microangiopathic hemolytic anemia due to shearing of erythrocytes in microcirculation.
83
Q

What is the hallmark finding for thrombotic thrombocytopenic purpura? (TTP)

A
  • Lack of ADAMTS13 molecule to breakdown large vWF multimers.
  • Antibodies against ADAMTS13
84
Q

What is the classic presentation of TTP?

A
  • Acute/subacute onset of symptoms.
  • Neurologic dysfunction (Stroke-like)
  • Anemia
  • Thrombocytopenia
  • Fever (50%)
  • Hemoglobulinuria
85
Q

What do lab values generally look like for TTP?

A
  • Mild-mod leukocytosis
  • Mild Hgb decrease
  • Plts 20k-50k
  • Mild-mod schistocytosis
  • Normal coag studies with elevated fibrinogen.
  • Negative direct Coomb’s
86
Q

What is the first-line treatment for TTP?

A

FFP exchange, aka therapeutic plasma exchange.

95% mortality if no plasma exchange occurs.

87
Q

What is the most common cause of renal failure in children?

A

Hemolytic-uremic syndrome (HUS)

88
Q

What is the classic presentation of a HUS patient?

A
  • Prodrome of fever and bloody diarrhea for 2-7d
  • Acute renal failure
  • Anuria
  • Young child
89
Q

What is the most commonly associated etiology with typical HUS?

A

Shiga-like toxin secondary to E.coli infection by serotype 0157:H7.

90
Q

A 2- year old patient presents with anuria, following a week-long period of fever and bloody diarrhea. The mother has been hydrating the patient well, but labs reveal an elevated BUN/creatine and anemia. Peripheral smear reveals schistocytosis. The child’s face is pale, and the mother admits that his urine was sometimes “dark red”. The child is considered to be in acute renal failure. What is the suggested course of treatment for this child and what other labs should be considered?

A

Supportive care, ensuring the patient does not bleed out.

Stool samples for E. coli and shigella can be ordered.

HUS

91
Q

What is the mnemonic for causes of DIC?

A
  • Sepsis
  • Trauma
  • Obstetric complications
  • Pancreatitis
  • Malignancy
  • Nephrotic Syndrome
  • Transfusion Reaction

STOP Making New Thrombi

92
Q

What are the hallmark signs and lab findings of someone in DIC?

A
  • Bleeding from multiple sites. (Purpura fulminans)
  • Elevated aPTT and PT
  • Thrombocytopenia
  • Elevated D-Dimer
  • Decreased Fibrinogen
93
Q

If a DIC patient has been treated with first-line therapy and is not improving, what should be considered second-line?

A

Heparin infusion

94
Q

What does an infusion of cryoprecipitate affect lab-wise in DIC? Infusion of FFP?

A

Cyroprecipitate will raise fibrinogen levels back up.
FFP will reduce aPTT and PT times.

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