HEME-Coagulation D/o Flashcards

1
Q

Who and what is Virchow Triad?

A

Rudulph Virchow-

  1. Venous Statis
  2. Vascular injury
  3. Hypercoagulabilty
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2
Q

What is the foundation of clotting?

A

Fibrin
Contained in a thrombus
Active form of FACTOR 1
Fibrinogen= precursor of fibrin COMMON PATH

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3
Q

What inhibits platelets by the endothelial lining of blood vessels? What activates platelets?

A

Inhibited- NO and ADPase-

Activate.- injury, von Willebrand’s Factor vWF- activate from exposure of collagen which release vWF

Activation of platelets-change shape form mesh

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4
Q

Does DEC in proteins such as vWF, factors, fibrongen cause issues with clotting?

A

NO- platelets don”t require a lot of protein. Only needed for aggregation. Little Damage=

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5
Q

What is a clot composed of?

A

erythrocytes, platelets, and fibrin.

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6
Q

What does Plasmin do?

A

THROMBOLYSIS- eat the fibrin web
Blood wavering btwn clotting and thrombolysis.

*Tissue Plasminogen active plasminogen to plasmin- TPA clot buster

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7
Q

What are 2 causes of bleeding excessive/repetitive at unusual sites?

A

Bleeding Disorders

  1. problems with platelets​- skin and mucosa
    A. epistaxis, gum bleeding, menorrhagia.
  2. clotting factor deficiencies-​ skin and muscles. A. hemathroses)
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8
Q
The following are part of what kind of bleeding d/o:
Vascular integrity
Platelet function
Fibrinolysis
Coagulation factors
A

Congenital -single defect​ - one protein​

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9
Q
The following are part of what kind of bleeding d/o:
 Cancer*
 infection, shock, 
obstetrics,
malabsorption, 
autoimmune disorders
drugs 
NSAIDs, aspirin, thiazides, anticoagulants
A

Acquired: liver, kidneys, collagen, immune

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10
Q

What compares PT to a standard;

0.9-1.2 is normal

A

INR = International Normalized Ratio

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11
Q

What measures rate of conversion between fibrinogen and fibrin?

A

Thrombin clotting time

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12
Q

Mr. Purple c/o of skin bruising. PE- petechiae, purpura in mount and skin. What is likely d/o?

A
Thrombocytopenia
● MCC for abnormal bleeding.
●DEC in platelets.
● Causes: impaired production,
 INC destruction, 
splenic sequestration-traped in spleen, gets large
 dilution.
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13
Q
Mr. Sklyer is a child post URI with the following work up:  what is DX?
■Plateles- 10K-20K
mild anemia
○ Peripheral smear-megathrombocytes
○ Coags Normal- PT, PTT, INR= N
A

ITP: Idiopathic Thrombocytopenic Purpura

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14
Q

What is difference btwn acute and chronic ITP?

A
Acute​: 
children, 
**self-limited, 
autoimmune,
recent viral URI.

● Chronic​: any age
women, w/ other
autoimmune

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15
Q

Mr. Purple petechia is mild. He has PMH of epistaxis and mouth bleeds? Is this chronic or acute?

A

CHRONIC ITP

Acute-abrupt petechiae, purpura, or even hemorrhagic bullae on skin and mucous membranes.

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16
Q

Which status of ITP requires treatment?

A

CHRONIC
high dose prednisone
■ IV immunoglobulin, stem cell therapy
■ Splenectomy

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17
Q

What d/o is in children where destruction of platelets L/T anemia, kidney failure d/t small vessel damage?

A

Hemolytic-uremic syndrome (HUS)​

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18
Q

What d/o is INC blood clots formed in blood vessels make it hard for O2 to reach organs, ie kidneys?

A

Thrombotic thrombocytopenic purpura (TTP)​
FATAL
RARE
WOMEN
IMC-HIV
Known cause genetic mutation L/T microvascular infarcts

19
Q

What d/o is bleeding in people with severe underlying

illness, sepsis, cancer?

A

Disseminated intravascular coagulation (DIC)

TX- all d/o tranfusion, steriods, plasmpheresis

20
Q

Are von Willebrand’s factor enzymes or binding factors?

A

​ NOT an enzyme- no catalyzing function​.

Binds to:

  1. collagen,
  2. platelets,
  3. ** Factor VIII.
21
Q

Mr. Von has prolonged bleeding in mucous membranes.
Labs- Low vWF+Factor VIII, prolonged INR
Which factor is import in Von Willebrand dz?

A

AD- Congenital
FACTOR VIII- binds to vWF
thrombin doesn’t have enough Factor VIII to activate, so Factor X doesn’t get activated as much.
DEC 8= DEC X=DEC Thrombin= NO Clots= INC Bleeding

22
Q

What endocrine hormone treats vWV dz?

A

Desmopression-vaospression-ADH

Transfusion Factor VIII

23
Q

This bleeding d/o affects MEN only. Risk include
a. epistaxis, intracranial bleeding, hematemesis, melena, microscopic hematuria.
What is hallmark sign of this condition?

A

Hemophilia A​8-X-linked AR-rare

HEMEARTHROSIS + FACTOR VIII deficiency

24
Q

What factor is related with Hemophilia B9?

A

Factor IX- X-linked AR

Rare

25
Q

What can be a treatment for a person with petechiae and/or purpura, mucosal bleeding, w/o any comorbid or genetic history?

A

INC Vitamin K- prevents protein degradation, Enough VK mean clotting protein will work. C, S, 2, 7, 9, 10
leafy greens

TX- plasma has all clotting factors

26
Q

Besides malnutrition diet what are causes of low Vit K?

A

liver failure, celiac, bypass surgery,

broad-spectrum antibiotics-sulfonamides

27
Q

What is work up for suspected VK defiency?

A

prolonged PT, prolonged PTT.
Normals results- fibrinogen,
+thrombin time+ platelet count.

28
Q

What reduce the risk of this scare condition, from inappropriate platelet aggregation (inactivates COX)

A

ASA baby aspirin 81mg
prevents
1. Venous Thromboembolic - clots
***2. Pulmonary embolism- silent killer, mis dx often. SCARY

29
Q

Why is hypercoagulability risky in Virchow triad?

A

Inc protein C, S, Anti thrombin.
Cancer
DVT-thrombi originating in the veins, LE, and traveling to the lungs-

30
Q

Which pose high risk of DVT, which if MC

  1. 37-year-old woman comes in with a swollen right leg.
  2. Flight in from Thailand.
  3. OCPS
  4. Smoke
A

Virchow’s Triad is still considered the primary **TOOL for DX DVT

***UL MC specific finding
Pain LC
Homan- not great EBM, may dislodge

31
Q

Which has highest indicator for DVT based off Wells score
<1 point,
1-2 points
>2 points

A

<1 point = 3%
1-2 points = 17%
**>2 points = 75%

Pain and TTP do not correlate w/ size, locatin or extent

32
Q

Mr. Von has well score of ≥2 and + D-dimer? What is next?

A

MUST get duplex ultrasonography.​

  • ALL patients with a positive D-dimer
  • ALL patients with Wells score ≥2

Proximal DVT- good Sensitivity and NPV- 90% PE from upper

33
Q

Will D-dimer assay confirm diagnose of DVT?

A

NO! ONLY RULE OUT DVT
D-dimer is fibrin fragment in fresh fibrin clot and cross-linked fibrin
NOT in non-cross-linked
D-dimers seen in acute, vs. chronic. THUS if seen= +DVT

● Elevated in trauma, cancer, sepsis, surgery.

34
Q

Mr. Von has ≥2 Wells, POS US? No D-dimer

A

TREAT for DVT

IF pos. US, NO D-DIMER needed

35
Q

Mr. Von has ≥2 Wells, NEG US, NEG D- DIMER?

A

RULED OUT DVT

36
Q

Mr. Von has ≥2 Wells, NEG US, POS D-DIMER?

A

REPAT US in a week

37
Q

Mr. Von has < 2 Wells, POS US?

A

TREAT FOR DVT!!!

38
Q

What are drugs of choice for treating DVT?

A

***ANTICOAGUALANTS,

THROMPLETICS

Heparin- inpatient setting

Warfarin (Coumadin)- VK antagonist PO, degrades based on factors half-life. IE Factor II 50-72half life= 5 days to clear

LMW heparin- SQ injection

ADE- narrow TI/TW

39
Q

Due to risk of bleeding what is tirated based off INR and takes a lot of work?

A
Warfarin
Added w/ Hep 4-5d
Gaol INR 2-3
1. 1 dose guess 50-70 3(6x)-6(3x)mg QD
2. 5mg start-INR QD, then few days, weekly
Start low, slow 5mg/day
3. TX 3-6m
ADE- significant bleeding, minor common, Reverse w Plasma

NOAC-safer, less expensive over time

40
Q

If INR is <2 what is step?

A

NO extra dose. INC weekly 5-20%

41
Q

If INR is 3-3.5 what is added?

A

no dose withheld. DEC weekly 5-15%

42
Q

If INR is 3.6-4 what is steps?

A

Withhold 1 dose. DEC weekly 10-15%

43
Q

If INR is >4 what is steps?

A

Withhold 1 dose. DEC weekly 10-20%