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Heme - Wier/Pallera > Evaluation of a Bleeding Patient > Flashcards

Evaluation of a Bleeding Patient Flashcards

1
Q

What are the steps in platelet plug formation?

A

a. PLATELETS attach to exposed collagen
b. aggregation trigger (ADP and TXA2 release)
c. ADP attracts more platelets
d. TXA2 causes vasocontriction

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2
Q

Suppose you get a patient that clots after being cut then bleeds again in 6-9 hours. What should you consider?

A

Factor XIII mutation

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3
Q

What 4 types of bleeding are you likely to see with bleeding disorders?

A
  • Purpura
  • Petechiae
  • Ecchymoses
  • Hemarthroses
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4
Q

T or F: Portal HTN can be a sign of low platelets.

A

True

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5
Q

What nutritional defects have the potential to lead to thrombocytopenia?
• What are some things that should be in your ddx for thrombocytopenia?

A

Nutritional:
• B12 or Folate Deficiency

Others:
Bone marrow failure, Chemo/Rad Exposure, Marrow infiltration

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6
Q

What level of platelets is classified as thrombocytopenia?

A

Less than 150,000

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7
Q

You see large platelets on the peripheral smear and a patient is thombocytopenic. What is most likely the cause of the thrombocytopenia?

A 
Increased Consumption of Platelets: 
• ITP
• HIT
• HUS
• TPP
• DIC
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8
Q

How would you run through the DDx of a 75 yr old man who has macrocytosis, pancytopenia, and a low platelet count?

A

Nutritional - Run Tests
• B12, Folate

Alcohol or Medications - Get from Hx.

If all else is negative take a bone marrow biopsy to test for Myelodysplasias or other pathologies

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9
Q

At what percent platelet hypoaggregation do you begin to suspect qualitative disorders?

A

less than 20%

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10
Q

In what cases might a patient who is actually hypercoagulable present with a lower PTT?

A

Lower PTT:
• Lupus Anticoagulant - in vivo it promotes thombosis, but in vitro it blocks phospholipids that act as a platform for catalysis of promthrombin activation

Lower PTT:
• Factor XII deficiency in vitro causes Hypercoagulable state

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11
Q

What is hemophilia C?
• How is it inherited?
• Epidemiology?
• Prolonged PT or PTT?

A

Factor XI deficiency

Inherited as Autosomal Recessive in A. Jews

**PTT prolonged

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12
Q

How are Hemophilia A and B inherited?

A

X-linked Recessive

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13
Q

If von Willibrand’s disease is present will you see a change in PT or PTT?

A

PTT is prolongued but not always - this makes sense because vW being low would lead to Factore VIII being destabilized

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14
Q

If someone has an autoimmune disease, what types of bleeding disorders should you expect?

A

Things that are Antibody Mediated like ITP and Lupus Anticoagulant

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15
Q

What clotting factors would be depressed in:
• Liver Disease
• Vitamin K Deficiency
• DIC

A

Liver Disease:
• Decreased V, VII, X

Vit. K Deficiency:
• Decreased VII, X

DIC
• Decreased V, VII, VIII, X

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16
Q

When taking Warfarin, what happens to the PT and PTT in the short term and Long Term?

A

Short Term:
• HIGH PT (because of factor VII decrease)

Long Term:
• HIGH PTT and PT (because of

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17
Q

What clotting factors are Vit. K dependent?

A

• Factor II, VII, IX, X, protein C and S.

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18
Q

What are some factors that can cause a Vit. K deficiency?

A
  • Nutritional Deficit
  • Antibiotic Use
  • Fat Malabsorption
19
Q

How would you treat a vitamin K deficiency?

A

Mild:
• Vit K replacement

Severe:
• Fresh Frozen Plasma

20
Q

Is Vit. K replacement an effective way to treat Clotting Factor deficiencies caused by Liver Disease?
• What if fibrinogen is low?

A

NO, the liver can’t do anything with the Vit. K, you should give these patients Fresh Frozen Plasma (all clotting factors)

Low Fibrinogen
• Cryoprecipitate (with Fibrinogen, VIII, XIII, and vWF would do)

21
Q

What’s the idea behind giving a patient IVIG or anti-Rh?

A

IVIG:
• Throwing a dog a bone…Spleen will have to take up Ig therefore it won’t attack the platelets bound by ig

anti-Rh:
• Causes RBC lysis and the liver and spleen attack the remnants and it prevents them from attacking platelets

22
Q

What common bacteria is associated with ITP?

A

H. Pylori

23
Q

Why do you see elevated LDH in the microangiopathic hemolytic anemia/thrombocytopenia?

A
  1. Anoxic Injury - blood isn’t getting to the periphery so cells there die without oxygen
  2. RBC lysis - lots of LDH because all they can do is glycolysis

**Not Seen in Extravascular Hemolysis Diseases

24
Q

What are the effects of Hemoglobin that results from extravascular hemolysis?

A
  • HEMOSIDEROSIS in kidney’s
  • LOW Haptoglobin
  • HIGH Unconjugated/Direct Bilirubin
25
Q

Compare the following for extravascular and Intravascular hemolysis:
• LDH
• Bilirubin
•Haptoglobin

A

Intarvascular:
• LDH - VERY ELEVATED
• Bilirubin - Elevated
• Haptoglobin - ABSENT

Extravascular:
• LDH - elevated
• Bilirubin - elevated
• haptoglobin - Normal/absent

26
Q

Compare the following for extravascular and Intravascular hemolysis:
• Hemoglobinurea
• Free Hb
• Urine Hemosiderin

A

Intravascular:
• Hemoglobinurea - present
• Free Hb - present
• Urine Hemosiderin - present

Extravascular:
•Hemoglobinurea - absent
• Free Hb - Absent
• Ureine Hemosiderin - absent

27
Q

T or F: ITP causes microangiopathic Hemolytic Anemia

A

False, diseases like TTP, HUS, and DIC do this

28
Q 
Which of the following microangiopathic hemolytic anemias corrects on a mixing study? Explain. 
• HUS
• TTP
• DIC
• aHUS 
• SLE
A

ONLY DIC will correct in a mixing study because it is not antibody mediated and there will be enough factor to make a clot

• IN all the others the amount of antibody in the plasma will block clot formation

29
Q

What causes are some factors besides sepsis that can cause DIC?

A
  • Metabolic Stress
  • Obsterical Complication (pre-eclampsia/eclampsia)
  • Malignancies
  • Severe Burns
30
Q

What single lab test can tell you that someone is in DIC?

A

NONE, it takes SEVERAL lab tests to confirm DIC

31
Q

How do you treat DIC?

A

DIC is treated by treating the organism or disease that is causing DIC

32
Q

What should be on your differential for DIC?

A
  • Severe Liver Failure/Liver Disease
  • Vit. K Deficiency
  • TTP
  • Congenital Abnormalities of Fibrinogen
  • HELLP syndrome
33
Q

When is plasma Therapy given:

A

ONLY indicated in ACTIVE bleeding (or invasive procedures)

Avoid having to do this in procedures by choosing a tamponadable site (e.g. put a central line into the femoral artery instead of subclavian etc.)

34
Q

What is a good option to give your patient if they only need fibrinogen?

A

• Cryoprecipitate (provides vWF, VII, X, and fibrinogen)

35
Q

When do you give a whole blood transfusion?

• how much do you give?

A

Indication:

  • Active Bleeding
  • Loss of RBCs in hemolysis

1 unit/10kg

36
Q

Should you give heparin during DIC?

A

• Use is very controversial MAYBE implicated with evidence of fibrin deposition and a large clot

37
Q

When should you start getting suspicious of HIT?

A

ANYONE who has been in the HOSPITAL recently or has had a procedure done that may have required heparin.

38
Q

What is the pathophysiology of HIT?

A
  1. Heparin Binds to PF4 on the platelet
  2. Ab. binds the Heparin:PF4 combo after it dissociates from the surface
  3. Fc receptor on the platelet binds Fc region on Ab
  4. Macrophages in the Spleen Remove the Platelet
39
Q

T or F: everybody that has HIT associated antibodies needs to avoid heparin

A

FALSE, many people have HIT associated Abs. HOWEVER only a small portion of these patients will have the HIT syndrome itself

**30% of the population is positive for these abs. but only a small portion would ever experience HIT

40
Q

What test would you for sure want to use on a patient with an autoimmune disease if testing for HIT?

A

Serotonin Assay (aka Functional assay)

41
Q

How does the pyrimid model apply to HIT?

A

Thrombosis: only 0.2-1.0% of ppl.
Thrombocytopenia: only 1-3% of ppl.

30% are + for the Heparin Ab.

42
Q

**What are the 4 Ts of determining whether or not to run a Heparin Lab Assay.

A

Thrombocytopenia: >50% (2); 30-50% (1)

**Timing: 5-10 days or less than 1 with prior exposure

Thrombosis: New Thrombosis, Skin Necrosis

oTher cause: none (2); possible (1)

**test anyone with 5 or higher

43
Q

T or F: if someone has a weakly positive immunologic Heparin assay, you might still want to run a functional assay because they still might have HIT.

A

TRUE, this would happen if the clinical probability of them having the disease was high

(functional assay = serotonin assay)

44
Q

T or F: its still only to give Low Molecular Weight Heparin with HIT.

A

FALSE

Heme - Wier/Pallera (12 decks)

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