Brainscape's Knowledge GenomeTM

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


See full index

MS1 FOM > Week 10 - clotting > Flashcards

Week 10 - clotting Flashcards

1
Q

What is primary vs secondary vs tertiary hemostasis?

A

Primary - platelet plug
Secondary - fibrin clot
Tertiary - clot stabilization

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

What are some potential DDx of primary hemostatic issues?

A

Decreased or dysfunctional platelets (liver disease, CKD), vascular disorders (Ehlers-Danlos, HIT)

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

What are some potential DDx of secondary hemostatic issues?

A

hereditary clotting factor deficiencies, acquired deficiencies, DIC

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

Compare petechiae vs purpura vs ecchymosis

A

Petechia: <2mm
Purpura: purple-coloured spots 3-5mm
Ecchymoses: aka bruising

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

What are the intrinsic, extrinsic, and common coagulation factors?

A

Intrinsic: F7
Extrinsic: F12,11,9,8
Common: F10,5,2,1

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

Name 6 different blood products available to patients

A
  1. blood transufsion
  2. platelet transfusion
  3. plasma transfusion
  4. fibrinogen concentrate
  5. cryoprecipitate
  6. prothrombin complex concentrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When do you give a blood transfusion?

A

Hb<70, massive bleeding, cardiac ischemia

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

When do you give platelet transfusions?

A

platelets <10

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

When are platelet transfusions contraindicated?

A

In those with TTP or HIT

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

What is in plasma transfusions?

A

coagulation factors and fibrinogen

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

When is fibrinogen concentrate indicated?

A

In those with fibrinogen deficiency

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

What is in cryoprecipitate?

A

Factors 8, 13, fibrinogen, and VWF

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

When is PCC indicated? What is in it?

A

Antidote for warfarin- contains Vitamin K dependent factors

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

What are the 4 zones of platelets?

A

Peripheral zone, sol-gel zone, organelle zone, membrane system

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

Describe platelet peripheral zone

A

Surface membranes with glycoproteins for adhesion

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

Describe platelet sol-gel zone

A

cytoskeleton

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

Describe platelet organelle zone

A

alpha granules containing adhesion proteins (fibrinogen, VWF) and delta granules containing ATP, ADP, Ca

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

What are the 4 steps of hemostasis

A
  1. arteriolar vasoconstriction
  2. exposure of ECM and platelet adhesion, aggregation, and activation
  3. TF release and coagulation cascade
  4. formation of permanent plug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe target of aspirin

A

targets COX to decrease production of thromboxane A2 and platelet activation

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

Describe target of Clopidrogel

A

targets P2Y12 receptor to prevent platelet activation

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

Describe target of Abciximab

A

targets glycoproteins to prevent platelet aggregation, also directly inhibit F10a

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

Describe target of heparin

A

enhances plasma protein antithrombin to prevent thrombin generation

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

Which coagulation factors are non-enzymes?

A

5 and 8

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

Compare hemophilia A and B

A

A- factor 8 def
B- factor 9 def

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

Describe role of VWF in clotting

A
  1. recruits platelets (involved in adhesion and aggregation)
  2. chaperone for F8 during secondary hemostasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the Vit K dependent factors?

A

2,7,9,10

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

What does the fibrinolytic system do?

A

Removes and regulates clots

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

Describe fibrinolytic system

A

tissue plasminogen activator activates plasminogen to plasmin, which targets and degrades fibrins

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

What inhibits tPA?

A

PAI-1

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

What does fibrin get degraded to?

A

D-dimers

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

Reasons for isolated elevated PT/INR?

A

F7 issue: Liver disease, warfarin, Vitamin K deficiency, congenital F7 deficiency

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

Reason for isolated elevated PTT?

A

Issue with intrinsic pathway: heparin, lupus anticoagulants, severe VWD (F8), congenital F12/11/9/8 deficiency

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

Reason for elevated PT/INR and PTT?

A

common pathway issue: DIC, severe liver disease, severe Vit K deficiency/warfarin, high dose heparin, new anticoagulants, congenital F10/5/2/1 deficiency

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

What are the next steps if you dont see any differences in PTT or PT/INR?

A

Look at VWD, factor 8 deficiency, platelet function disorder

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

How do you determine if a factor inhibitor is present?

A

Mixing study

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

How can types of bleeding be used to distinguish different hemostatic issues?

A

mucosal bleeds = primary hemostasis

joint/soft tissue bleeds = secondary hemostasis

delayed bleed after injury = tertiary hemostasis

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

What tools are used to distinguish between regular/pathogenic bleeds?

A

BAT

38
Q

What can caused thrombocytopenia?

A

decreased marrow production, increased destruction, sequestration

39
Q

What can cause a dysfunctional platelet plug?

A

IPD, VWD, drugs, CKD

40
Q

What can cause hyperfibrinolysis?

A

F13 deficiency/dysfunction, PAI-1 deficiency, a2 antiplasmin deficiency

41
Q

What causes acquired hemophilia A?

A

Sudden generation of autoantibodies against F8

42
Q

What are some things that can predispose one to acquired hemophilia A?

A

CLL, adenocarcinomas, postpartum, autoimmune disorders, dermatologic disorders, drugs

43
Q

Compare presentaiton of acquired vs hereditary hemophilia A

A

Acquired: Subcutaneous hematomas and muscle bleeding
Hereditary: joint bleeding

44
Q

Describe mixing study of hemophilia A

A

Does not correct

45
Q

What are 3 treatment strategies for acquired hemophilia A?

A
  1. manage bleeding with agents that bypass F8
  2. Remove autoantibody with immunosuppressive therapy
  3. treat underlying cause
46
Q

How do clotting factors differ in neonates?

A

vit K factors low, VWF and F8 high

47
Q

In the pediatric bleeding questionnaire, what score indicates a bleeding disorder?

A

> 2

48
Q

How does vit K deficiency affect factor 5, factor 7, factor 8, TT, platelet count, fibrinogen, and D dimer?

A

Factor 5: no effect
Factor 7: decrease
Factor 8: no effect
TT: no effect
Platelet count: no effect
Fibrinogen: no effect
D dimer: no effect

49
Q

How does liver disease affect factor 5, factor 7, factor 8, TT, platelet count, fibrinogen, and D dimer?

A

Factor 5: decrease
Factor 7: decrease
Factor 8: normal or increase
TT: increase
Platelet count: decrease
Fibrinogen: decrease
D dimer: normal

50
Q

How does DIC affect factor 5, factor 7, factor 8, TT, platelet count, fibrinogen, and D dimer?

A

Factor 5: decrease
Factor 7: decrease
Factor 8: decrease
TT: increase
Platelet count: decrease
Fibrinogen: decrease
D dimer: increase

51
Q

How does a congenital factor deficiency affect factor 5, factor 7, factor 8, TT, platelet count, fibrinogen, and D dimer?

A

Factor 5: decrease (depends)
Factor 7: decrease (depends)
Factor 8: decrease (depends)
TT: increase
Platelet count: no effect
Fibrinogen: decrease
D dimer: normal

52
Q

What can be administered to stop mucosal bleeding in patients with hereditary hemophilia?

A

Tranexamic acid

53
Q

Compare T1, T2, and T3 VWD

A

T1 and T3 are quantitative disorders: decreased VWD antigen (and proportionally decreased activity)
T2 is qualitative: decreased activity but normal antigen

54
Q

How is VWD managed?

A

prevent bleeds, use DDAVP to increase F8 levels, tranexamic acid, cryoprecipitate

55
Q

What are the 5 types of thrombocytopenia

A

ITP, HIT, and the TMAs: HUS, TTP and DIC

56
Q

What causes ITP?

A

Immune-mediated destruction of platelets due to autoantibody production in BM - idiopathic of from lymphoma, leukemia, infections

57
Q

How is ITP characterized?

A

Mucosal bleeds, purpura, history of autoimmune disorders

58
Q

How is ITP diagnosed?

A

Diagnosis of exclusion: platelet count low but other blood markers ok.

59
Q

How is ITP managed?

A

glucocorticoids as 1st line therapy to suppress immune system and then can do splenectomy if issue doesnt improve

60
Q

When do you infuse platelets with thrombocytopenias?

A

Only with DIC! Dont transfuse platelets with HIT, TTP, HUS or ITP

61
Q

What causes TTP?

A

primary or secondary- drugs, pregnancy, infection, stem cell transplant

62
Q

How is TTP diagnosed?

A

Schistocytes on blood film and low ADAMTS-13 levels

63
Q

What happens in TTP?

A

Low ADAPTS-13 levels means VWF multimers cant be cleaved so they accumulate and block blood flow

64
Q

How is TTP treated?

A

plasma exchange to remove and replace VWF monomers

65
Q

What is the pathophysiology of HUS?

A

Endothelial damage due to toxins (esp. Shiga toxin) or cancer, pregnancy, and autoimmune conditions causes acute kidney injury which leads to micro thrombosis

66
Q

How is HUS diagnosed?

A

Acute kidney injury, schistocytes, and normal ADAMTS-13 levels

67
Q

How is HUS managed?

A

Supportive: monitoring and IV fluids. Avoid antibiotics

68
Q

What is the pathophysiology of DIC?

A

Overactivation of coagulation cascade that causes small clots

69
Q

What can cause DIC?

A

Infection, cancers, trauma, obstetric issues

70
Q

How is DIC diagnosed?

A

Schistocytes, elevated INR (Key!!), elevated D-dimer, low fibrinogen

71
Q

How is DIC managed?

A

Supportive (IV fluids) and treat underlying condition

72
Q

What is the pathophysiology of HIT?

A

Immune/antibody-mediated ADR to heparin resulting in platelet activation and thrombosis WITHOUT bleeding

73
Q

How is HIT diagnosed?

A

Based on 4T score: thrombocytopenia, timing (acute/severe onset over 5-10d), thrombosis, and no other thrombotic causes

74
Q

How is HIT managed?

A

stop all heparin and start alternative anticoagulant

75
Q

What are risk factors for thrombosis?

A

Vichow’s triad: stasis, injury, and hypercoagulability

76
Q

what can cause hypercoagulability?

A

Cancer, certain drugs, hereditary or acquired hemostatic disorders

77
Q

How is thrombosis prevented?

A

Early mobilization after surgery

78
Q

What meds are given after surgery for low vs high thrombotic risk patients?

A

Low risk: 2500u dalteparin (LMWH) daily
High risk: 5000u dalteparin daily or heparin or a DOA

79
Q

What does DVT diagnosis require? Describe

A

Objective test not just clinical assessment: do D-dimer test and if its positive then do a compression ultrasound

80
Q

What is the clinical model for predicting DVT probability?

A

Wells rule: having active cancer, paralysis, stasis, tenderness, swelling, edema, Hx of thrombosis

81
Q

What are some symptoms of PE?

A

pleuritic chest pain, dyspnea, syncope, tachycardia, hemoptysis

82
Q

How is PE diagnosed?

A

With objective assessment: do V/Q scan and if theres a mismatch this is indicative of PE. Do a D-dimer test and if positive then do CT pulmonary angiogram

83
Q

What are the 2 main goals of venous thromboembolism (VTE) treatment?

A

alleviation of symptoms and prevention of death due to PE

84
Q

How is VTE treated?

A

Through anticoagluation: low mw heparin, warfarin, direct oral anticoagulants, etc.

85
Q

What are contraindications for heparin or DOAs? what do you give instead?

A

renal failure
Give warfarin instead

86
Q

What are contradictions for DOAs? What do you give instead?

A

Pregnancy and GI issues. Give LMWH instead

87
Q

Compare treatment direction for VTE in cancer patients, those with major risk factors, and idiopathic men/women

A

Cancer: 6m
Risk factors: 3m
idiopathic men: indefinitley
idiopathic women: 6m

88
Q

Are DVT and PE treated as outpatient or inpatient? Describe treatment of each

A

DVT: outpatient. Elevate limb, encourage activity, compression stockings, NSAID for pain

PE: inpatient. Activity as tolerated, NSAIDs, anticoagulants

89
Q

What are 5 causes of hereditary thrombophilia?

A
  1. Factor 5 Leiden
  2. prothrombin gene mutation
  3. Protein C deficiency
  4. Protein S deficiency
  5. Antithrombin deficiency
90
Q

What can cause acquired thrombophilia?

A

Antiphospholipid Ab/lupus anticoagulant

91
Q

What are 5 types of anticoagulants

A
  1. unfractionated heparin
  2. LMWH
  3. Vitamin K agonists
  4. Direct thrombin inhibitors
  5. direct oral anticoagulants

MS1 FOM (5 decks)

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