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Medicine II > coagulation disorders > Flashcards

coagulation disorders Flashcards

1
Q

i. Platelets are actively inhibited by

A

the endothelial lining of blood vessels (via NO and ADPase)

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2
Q

Endothelial injury exposes collagen and releases ________, which activates platelets

A

Endothelial injury exposes collagen and releases von Willebrand’s Factor (vWF), which activates platelets

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3
Q

using GP Ia, actin, and myosin platlets _____ toexposed collagen

A

platlets adhere to exposed collagen with myosin GP Ia, actin,

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4
Q

Platelets aggregate, using

A

vWF and fibrinogen

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5
Q

a blood clot is composed of

A

Fibrin
platlets
erythrocytes

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6
Q

these proteins work to inactivate clotting factors

A

b. Protein C (activated by Protein S) and antithrombin work to inactivate clotting factors

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7
Q

TFPI inhibits

A

tissue factor pathway inhibitor

inhibits Xa and thrombin

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8
Q

this is the enzyme that converts plasminogen to plasmin

A

tPA

tisse plaminogen activator

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9
Q

bleeding disorders can be

A

due to a platelet issue
due to a clotting issue
congenital or aquired

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10
Q

these types of bleeding disorders usually effect the skin and muscles

A

clotting

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11
Q

this type of bleeding disorder usually involves the skin and mucosa

A

platelet disorders

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12
Q

congenital bleeding disorders usually effect

A 
vascular integrity 
platelet function
fibrinolysis 
or 
coagulation factors
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13
Q

types of acquired bleeding disorders

A

involves multiple systems: liver, kidney, collagen, immune)

i. Cancer, infection, shock, obstetrics, malabsorption, AI disorders
ii. Drugs (NSAIDs, aspirin, thiazides, anticoagulants)

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14
Q

laboratory studies that can be done to assess bleeding disorders

A

Platelet count, peripheral smear, bleeding time
Prothrombin time (PT), partial
thromboblastin time (PTT), activated
PTT, or INR
1.0 is normal INR
The higher the PT time, the less likely we are to clot normally

Thrombin clotting time (measures rate of conversion between fibrinogen and fibrin)
iv. Some problems may require more specialized studies

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15
Q

The most common cause of abnormal bleeding

and what is it

A

Thrombocytopenia

Abnormal decrease in the number of platelets

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16
Q

what causes thrombocytopenia

A

impaired production, increased destruction, splenic sequestration, dilution

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17
Q

usual presentation of thrombocytopenia

A

d.Usual presentation is petechiae and/or purpura on the skin and mucous membranes

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18
Q

ITP: Idiopathic Thrombocytopenic Purpura

what populations do we see with this acutely

A

Acute: most commonly in children, self-limited, autoimmune, associated with a recent viral URI

Abrupt appearance of petechiae, purpua, or even hemorrhagic bullae on skin and mucous membranes

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19
Q

ITP: Idiopathic Thrombocytopenic Purpura

what type of chronic dz do we see

A

Chronic: any age (20-50 most commonly), more common in women, often associated with other autoimmune disorders

Usually milder (petechiae only)

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20
Q

lab findings ITP

A 
"	Decreased platelets
o	Acute: 10,000 - 20,000/uL
o	Chronic: 25,000 - 75,000/uL
"	Possible mild anemia
"	Peripheral smear shows megathrombocytes
"	Coags (PT, PTT, INR) are normal
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21
Q

Treatment of ITP

A 
"	Acute: usually self-limited, resolves spontaneously (May require steroids or splenectomy)
"	Chronic: Rarely resolves spontaneously
o	Initial tx: high dose prednisone
o	IV immunoglobulin, stem cell therapy
o	Splenectomy
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22
Q

disorders of platelet function are most commonly

A

May be congenital (many possible causes) or acquired (drugs - ASA or other NSAIDs, clopidogrel/Plavix - uremia, alcoholism, hypothermia, malnutrition)

More commonly it is acquired

this is not an issue of too few like in ITP but rather funky guys

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23
Q

rare but often fatal. Occurs in previously healthy patients, between 20-50, more often in women, sometimes in people w/ HIV

A

a. Thrombotic thrombocytopenic purpura (TTP

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24
Q

is like TTP but found in children

i. Can be fatal

A

b. Hemolytic-uremic syndrome (HUS)

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25
Q

causes generalized bleeding in people w/ severe underlying illness (e.g., sepsis, cancer)
i. When people go into shock or septic, their entire clotting system can collapse

A

disseminating intravascular coagualtion

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26
Q

pathophys of disseminating intravascular coagulation

what is the treatment

A

Caused by abnormal aggregation of platelets, which both impairs their ability to function normally, AND can cause microvascular infarcts (losing fingers, losing end of their nose, losing their penis)

Transfusion, steroids, plasmapheresis(filters out their blood - abnormal platelets, etc)

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27
Q

Autosomal dominant, congenital bleeding disorder

and the most common type

A

c. Von Willebrand’s Disease
iii. There are six different types. Type I accounts for 80% of all cases. Most cases are mild

Factor VIII is bound to vWF while inactive in circulation
Factor VIII degrades rapidly when not bound to vWF

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28
Q

what does vWF do

A

Binds to collagen, binds to platelets, and binds to Factor VIII

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29
Q

factor VIII is released from vWF by

A

v. Factor VIII is released from vWF by the action of thrombin

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30
Q

what is the defect seen with vWF

A

The defect in von Willebrand’s factor means thrombin doesn’t have enough Factor VIII to activate, so Factor X doesn’t get activated as much

31
Q

Clinical features

A

bleeding in mucous membranes. Bleeding is exacerbated by ASA

32
Q

tx of vWF

A

is w/ desmopressin, or transfusion of Factor VIII

In patients w/ homozygous disease, symptoms are much more severe - can be life threatening

33
Q

Hemophilia A

A

seen only in men has to do with a defieicney in VIII

AAAAEIGHT

34
Q

Hemophilia B

A

It’s deficiency of Factor IX

X-lined recessive, about 1 in 30,000 US male births

35
Q

hallmark sign of hemophilia B

A

c. The hallmark sign is hemarthrosis

little boy with sad elbow

36
Q

CM of hemophilia

and the Tx

A

XIII. Bleeding into joints (can be both A and B)

Can also have epistaxis, intracranial bleeding, hematemesis, melena, microscopic hematuria
Tends to present in childhood
Symptoms can range from very severe to mild

Treatment is Factor VIII (or IX)

37
Q

b. These are the most common acquired coagulopathies

A

vitamin K deficiencys

38
Q

how does vitamin K work

A

d. Vitamin K works by modifying certain proteins, preventing them from degradation

39
Q

vitamin K dependent factors

A

coagulation cascade, including prothrombin, Protein C and Protein S, and Factors VII, IX, and X.

40
Q

why would someone present with a vitamin K deficiency

A

May be due to poor diet, liver failure, malabsorption, malnutrition, or use of broad-spectrum antibiotics (e.g., sulfanomides)

41
Q

lab findings with a acquired coagulopathy like vitamin K deficiency

A

” Prolonged PT
“ Sometimes prolonged PTT
“ Normal fibrinogen, thrombin time, and platelet count

42
Q

tx of vitamin K deficiency

A

the underlying cause (which is usually obvious)
“ Parenteral Vitamin K
“ Plasma to treat acute bleeding
“ Address malnutrition & malabsorption

43
Q

virchows

A

stasis
hypercoagulopathy
injury

44
Q

CM of DVT

A

” Unilateral edema = most specific finding
“ Leg pain occurs in 50%
“ Homan’s sign has no + or - predictive value, and may dislodge clot
“ Leg tenderness may be present in 75% of pt’s w/ DVT “ However, it’s also found in 50% of pt’s w/o DVT
“ Pain & tenderness do not correlate w/ size, location, or extent of thrombus
“ Clinical findings of DVT (or PE) occur in just 10% of patients w/ DVT (or PE)

45
Q

what helps evaluate risk for DVT

A

xiii. The Wells Score
1. <1 point = 3%
2. 1-2 points = 17%
3. >2 points = 75%

46
Q

D-dimer assays what are they

A

D-dimer fibrin fragments are present in fresh fibrin clot and cross-linked fibrin, but NOT in non-cross-linked fibrin or fibrinogen

47
Q

how can D-dimer assays be used

A

b. Elevated in trauma, cancer, sepsis, surgery

c. Therefore, the D-dimer assay can rule out a DVT, but shouldn’t be used to confirm the diagnosis

48
Q

when can we rule out DVT with D-dimer

A

e. Negative test in a low-mod risk patient w/ a Wells score <2 rules out a DVT

49
Q

when would you do a diagnostic study for DVT suspicion

A
  1. All patients w/ a positive D-dimer and all patients w/ Wells score >2 require a diagnostic study
50
Q

ULS sensitivity is best for what type of DVT

A

a. Proximal DVT: Sensitivity 97%, NPV 99%
i. NPV = negative predictive value
b. Distal DVT: Sensitivity 73%
c. Over 90% of acute PE are from proximal, rather than distal DVT

51
Q

Wells >2 and US pos

tx or nah?

A

treat

52
Q

wells >3 uls negative ?

A

rule out with D dimer

53
Q

wells >2 ULS Neg D dimer postitive

A

repeast ULS in week

54
Q

wells <2 ULS positive

A

treat

55
Q

wells>2 ULS neg

A

rule out DVT D dimer

56
Q

goals of DVT tx

A
  1. Goals of therapy -
    a. Prevent clot extension
    b. Prevent acute PE
    c. Prevent recurrence of DVT
57
Q

what is the standard for DVT Tx

A
  1. Anti-coagulation therapy, as opposed to thrombolytic therapy, is the norm, although thrombolytics may be used in some cases
58
Q

recommedned rx for DVT and limitations

A

a. Heparin, Warfarin (Coumadin), LMW heparin

b. Heparin and Warfarin are effective, but have 2 major limitations
i. Narrow therapeutic window
ii. Highly variable dose response among individual patients
iii. This means intensive lab monitoring

59
Q

when would we use heparin

A

best in inpatient for rapid anticoagualtion

60
Q

goal with heparin tx

A

i. Goal is achieving a PTT between 1.5-2.5 times upper range of normal; hospitals have predetermined protocols to achieve this

61
Q

when do we use warfarin and what is the goal

A

ii. Warfarin is usually started with heparin therapy; goal INR is 2.0-3.0 for 2 consecutive days

62
Q

advantages of LMWH

A

Advantages

Can be given SQ (will bypass the gut)

Longer duration, can be given once or twice daily

No monitoring necessary; response correlated w/ body weight

Lower risk of thrombocytopenia

63
Q

disadvantage of LMWH

A

Disadvantages
“ Cost
“ Cannot be easily reversed if bleeding occurs

64
Q

i. The oral anticoagulant of choice

A

e. Warfarin

65
Q

how does warfarin work

A

ii. It is Vitamin K agonist. Thus, it effectively induces Vitamin K deficiency in the patient
iii. Inhibits prothrombin, Proteins C and S, and Factors VII, IX, and XI

66
Q

how do we use heparin and warfarin together

A

Heparin is continued for 4-5 days to counteract warfarin’s initial hypercoagulability effect

Like heparin, warfarin’s effect is highly variable among individual patients

67
Q

how do anticoagulants work for DVT if they are not thrombolytic

A

vi. B/c its effect is passive (i.e., allowing clotting factors to degrade), its effect is dependent on the half-life of clotting factors - and there are MANY factors involved

68
Q

main clotting factor that we are waiting for with anticoagulant therapy

A

vii. The main one is prothrombin (Factor II), which has a half-life of 50 hours, and may take up to 5 days to clear completely

69
Q

average daily dose of warfarin

A

ii. The first dose should be the clinician’s best estimate of pt’s required daily dose

Avg daily dose in a 50 yo is 6.3mg/day

Avg daily dose in a 70 yo is 3.6mg/day

Start at 5mg/day. Check INR daily, then every few days, titrate dose, until steady state

70
Q

risk of fatility and bleeding with warfain

A

viii. 1% risk of fatality annually (closely related to age and control of INR)
ix. “Minor bleeds” are common, w/ approx. 15% annual incidence

71
Q

INR <2

A

increase weekly dose 5-20%

72
Q

INR 3-3.5

A

decrease weekly 5-15%

73
Q

INR 3.6-4

A

withold 1 dose

decrease weekly 10-15%

74
Q

INR>4

A

withold 1 dose

decrease weekly 10-20%

Medicine II (21 decks)

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