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Fundamentals 3- Heme > The Bleeding Patient > Flashcards

The Bleeding Patient Flashcards

1
Q

What 11 diagnoses are associated with problems of primary hemostasis?

A
  1. pseudothrombocytopenia
  2. immune thrombocytopenia
  3. Bone marrow failure
  4. DIC
  5. Hypersplenism
  6. pharmacological agents
  7. vWF disease
  8. Uremia
  9. Scurvy
  10. Vasculitis
  11. Osler Weber Rendu Disease
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2
Q

What are the 6 clinical presentations associated with secondary hemostasis?

A
  1. Hemophilia A
  2. Hemophilia B
  3. Heparin
  4. Coumadin
  5. Vit K deficiency
  6. Liver disease
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3
Q

What is Osler-Weber-Rendu disease?

A

A hereditary disease with hemorrhagic telangiectasia (dilated vessels in mucous membranes and skin)

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4
Q

What is the Ristocetin cofactor assay?

A

Ristocetin induces aggregation of platelets in the presence of vWF

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5
Q

What is vWF?

A

Multimers that non-covalently link with factor 8, are necessary to allow adhesion of platelets to vasculature.
Deficiency is an autosomal dominant disease

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6
Q

What is the difference between a primary and secondary defect in hemostasis?

A

Primary- platelet type defect

Secondary- factors defect

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7
Q

What drugs could affect primary hemostasis?

What drugs could affect secondary?

A

Primary- NSAIDs, aspirin, quinine or quinidine

Secondary- Heparin, Coumadin (warfarin)

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8
Q

What four things should be discussed in the history when evaluating a bleeding patient?

A
  1. Stressors- dental, menses, surgery, labor
  2. Timing- “can’t stop bleeding” = primary. Went home and then later is started bleeding = secondary
  3. Family history of bleeding
  4. Drugs
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9
Q

What 5 things should you focus on for the physical exam during your evaluation of a bleeding patient?

A
  1. Petechiae- pathognomonic for thrombocytopenia
  2. Purpura
  3. Splenomegaly
  4. Lymph node examination
  5. Hemarthosis and hematoma (collections of blood/sudden swelling)
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10
Q

What is most concerning about mucousal hemorrhage in a patient with severe thrombocytopenia?

A

There is an increased risk of CNS hemorrhage

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11
Q

What are the initial laboratory screening tests for a bleeding patient?

A
  1. CBC with differential
  2. Peripheral smear
  3. PT/INR, PTT, TT
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12
Q

What are the characteristics of primary hemostasis?

onset, location of bleeds, smear characteristics

A
  1. Early bleeding
  2. Mucocutaneous bleeding (oral, gums, menses, GI)
  3. Abnormal platelet count, function, or morphology
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13
Q

What are the 3 MAJOR disorders of primary hemostasis?

A
  1. Platelets - thrombocytopenia OR platelet function disorders
  2. Vascular integrity
  3. vWF
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14
Q

Hemostasis will be normal above a platelet count of _____________________.
Platelet counts above __________ are good for most surgical procedures.
Spontaneous bleeding doesn’t really occur until a platelet count below ____________________.

A

100,000 is normal.
Surgery can be down with 50,000 and above
Platelet counts below 30,000 can cause spontaneous bleeds

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15
Q

What is pseudothrombocytopenia?

What should you do to test this if it is suspected?

A

Artifactual clumping of certain individual platelets in response to EDTA (an anti-coagulant) in the blood collection tube.
This can falsely lower the platelet count leading to an incorrect diagnosis of thrombocytopenia.
Smear and see if there is platelet clumping at the feathered edge. If yes, repeat the test using heparin or citrate instead of EDTA. No clumping should occur and you should get a true platelet count.

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16
Q

What does it mean if the MPV is low, normal or high?

A

Low: decreased production (older platelets)
Normal: abnormal distribution of platelets
High: increased destruction (because young platelets are large)

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17
Q

If you have an unexpected, isolated thrombocytopenia on a routine blood draw, what is the most likely cause? What should you do?

A

The platelets probably clumped due to thrombin production during a difficult needle stick.
Confirm by taking a second sample

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18
Q

What are four situations where you would get decreased production of platelets?

A
  1. Bone marrow infiltration- leukemia, metastatic cancer, infections like TB, CMV, HIV, or macrophage storage disorders
  2. End stage Cirrhosis- deficient thrombopoietin
  3. B12/folate deficiency, iron deficiency
  4. Overwhelming sepsis
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19
Q

Why might you see thrombocytopenia in a person with end stage cirrhosis?

What cell might you see on the smear?

A

The liver will be making less thrombopoietin so there will be a decrease in production of platelets

You will see spur cells on the smear.

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20
Q

What information would let you know that the decrease in platelet production is most likely due to a bone marrow infiltrate?

A

The production of RBC and WBC will decrease too so you will see pancytopenia

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21
Q

What are the two main causes of platelet destruction?

A
  1. Immune destruction- (ITP or idiopathic)
  2. Non-immune destruction - microangiopathy, DIC, thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS) or vasculitis
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22
Q

What are five non-immune causes of platelet destruction?

What cells might you see on the peripheral smear?

A
  1. Microangiopathy
  2. HUS
  3. TTP
  4. DIC
  5. vasculitis

You may see schistocytes on the smear

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23
Q

If you see normal MPV platelets with a thrombocytopenia, what is the most likely cause? What is it secondary to?

A

Hypersplenism secondary to cirrhosis.

This sequesters the platelets altering their distribution because they are pooled and trapped in the enlarged spleen.

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24
Q

When looking at the peripheral smear of thrombocytopenia, what 6 things should you be on the lookout for?

A
  1. clumping of platelets at the feathered edge (pseudothrombocytopenia)
  2. Schistocytes- increased destruction
  3. Teardrop RBC, nucleated RBC- marrow infiltrate
  4. Spherocytes/microspherocytes- autoimmune hemolytic anemia, immune thrombocytopenia
  5. Macrocytosis- clues you in to B12/folate deficiency which can be associated with liver disease or alcoholism. Liver problems decrease production of platelets (decreased thrombopoietin)
  6. Microcytosis/hypochromia- associated with Fe deficiency which can also be associated with thrombocytopenia
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25
Q

Describe what you would see on:
1. physical exam
2. CBC, smear, PT/PTT/TT
and any other findings that would help in the diagnosis of idiopathic immune thrombocytopenia (ITP)

What patients have a higher risk of ITP?

A

The physical exam will be normal except for petechiae and purpura.
The CBC, smear, PT/PTT/TT/D-dimers should be normal
If there is splenomegaly it is NOT ITP
Bone marrow should be considered in older patients

HIV+ patients have a higher incidence of ITP (antibodies against platelets)

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26
Q

What are three examples of primary autoimmune thrombocytopenias?

A
  1. Classic
  2. HIV-related
  3. Hep C related
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27
Q

What are three examples of secondary autoimmune thrombocytopenias?

A
  1. Lupus
  2. Lymphoproliferative disorders
  3. solid tumors
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28
Q

How is ITP treated in children? How does this differ from how it is treated in adults?

A

Children- ITP is self-limited and can remit without therapy
Adults- the goal is to maintain safe (not necessarily normal) platelet levels. Prednisone is the cornerstone of treatment (1/3 enter remission)

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29
Q

What are the treatment options for adults with ITP?

5- 3 short term, 2 if they fail

A
  1. Prednisone
  2. IVIG infusion inhibits the destruction of circulating platelets because the IVIG binds Fc on phagocytic cells (throwing a dog that’s attacking you a stick)
  3. Anti-RhD (WinRho) has a similar effect to IVIG and is used in Rh+ patients
  4. Splenectomy if short term therapies with steroids fail
  5. Immunosuppression with rituxan (anti-CD20)
30
Q

What are the major drugs that can cause thrombocytopenia?

A
  1. quinidine
  2. sulfa drugs
  3. penicillin
  4. ticarcillin
    Many others**
31
Q

What is HIT?

How is it diagnoses?

A

Heparin-induced thrombocytopenia- it is a virulent thrombocytopenia associated with risk of arterial and venous thrombosis.
Ab form against a platelet factor 4-heparin complex that causes a sustained pro-thrombotic state.
It is diagnosed by measuring these HIT Ab.

32
Q

What are signs and symptoms of acquired platelet functional defects (uremias, NSAIDs, ASA)?

How do you test for platelet function defects?

A

superficial eccymoses (bruising) on the extremities out of proportion to the level of trauma.

Test for defects using PFA-100.
(platelet aggregation is NOT commonly needed in acquired defects but can provide specific patterns to identify the defect)

33
Q

What are the three major things that cause acquired platelet disfunction?
What is the function/mechanism of each?

A
  1. Drugs - NSAIDS/ASA inhibit COX (no TXA2, decreased prostaglandins). Alter the entire life of exposed platelet (7-10 days)
  2. Chronic renal failure (Uremia)- retained organic acids
  3. Chronic liver failure- ??
34
Q

What are the four inherited QUALITATIVE platelet disorders?

A
  1. Glanzmann - GpIIb/IIIa
  2. Bernard-Soulier- GPIb- IX- V (“giant platelets”)
  3. Pseudo-vWF disease (GpIb)
  4. Storage pool deficiencies (grey platelet syndrome)
35
Q

What is Glanzmann thrombasthenia?

A

Autosomal recessive disorder that demonstrates the importance of GpIIb/IIIa complex.
Platelet count and morphology are normal but they are not able to aggregate or retract the clot

36
Q

What is Bernard-Soulier syndrome?

A

“Giant platelet syndrome” - autosomal dominant or recessive and is due to a defect in the GpIB-IX-V complex causing a defect in vWF-dependent platelet aggregation.

37
Q

What two types of platelets will not aggregate in the ristocetin test? How can you differentiate the two?

A
  1. vWF disease platelets (can’t aggregate due to loss of vWF on the endothelium)
  2. Bernard-Soulier platelets (missing GPIb on the platelet so can’t bind to vWF to aggregate)

Differentiate by adding vWF to the ristocetin. If they aggregate, it was a vWF disease defect.

38
Q

What are the two types storage pool deficiencies?

How are they diagnosed?

A
  1. Delta storage pool disorders- lack platelet dense granules (occurs with Wiscott Aldrich, Chediak-Higashi)
  2. Gray platelet syndrome- lack of platelet alpha granules

They are diagnosed with EM of the platelets and a PFA100.

39
Q

What are the two forms of PFA100?
Which one will be prolonged if the patient has taken aspirin?
What could prolong both?

A

The instrument measures the time it takes for a platelet plug to form in the presence of collagen:

  1. Epi- prolonged if the patient took aspirin
  2. ADP

Both are prolonged by platelet function disorders like vWF disease, glanzmann thrombasthenia, storage pool disorders, etc)

40
Q

What are the two major functions of vWF?

A
  1. bridges GPIb on the platelet to the subendothelium in platelet adhesion
  2. transports factor VIII (protecting it from inactivation and increasing its half life)
41
Q

Describe vWF disease.

  1. how does one get it?
  2. what is the problem?
  3. what is the physical presentation?
  4. what tests are abnormal?
A
  1. most common. Autosomal dominant
  2. abnormal quality OR quantity of vWF
  3. easy bruising, mucosal bleeds
  4. prolonged PTT (factor 8 issue)
42
Q

What is the difference between type 1 and type 2 vWF disease?

A

Type one is quantitiative (~80%)

Type 2 is qualitative (~20%)

43
Q

What are the lab tests for vWF disease?

What is the most sensitive and specific?

A
  1. PFA-100
  2. vWF antigen immunoassay
  3. Ristocetin cofactor assay (quantitative measure of activity) ** most sensitive/specific
  4. Ristocetin Induced platelet aggregation
  5. Multimer assay
44
Q

What are the four disorders associated with vascular integrity?

A
  1. Scurvy
  2. Leukocytoclastic vasculitis
  3. Henoch-Schonlein Purpura
  4. Osler-Weber- Rendu disease
45
Q

What is the clinical presentation of scurvy?

A

Unusual pattern of hemorrhage surrounding the hair follicles giving a stippling appearance.

46
Q

What is leukocytoclastic vasculitis?

A

Hemorrhage in the skin due to inflamed blood vessels.

“palpable purpura”- purple nodules or crust felt with the hand

47
Q

What is Henoch-Schonlein Purpura (HSP)?

A

leukocytoclastic vasculitis in children between 2 and 10 that presents with urticarial plaques on trunks, scrotum, and lower extremities

48
Q

What is Osler-Weber-Rendu disease?

A

autosomal dominant hemorrhagic telangiectasia with dermal and mucosal hemorrhage, frequent nosebleeds and mucosal bleeds due to fragility of vessels.

49
Q

Describe secondary hemostasis disorder in terms of time of onset and physical exam findings.

A

Delayed onset with bleeding in deep tissue, joints (hemarthrosis) and deep hematoma (muscle compartment and retroperitoneal)

50
Q

What tests are used to evaluate secondary hemostasis?

A
  1. PT (prothrombin time)
  2. PTT (partial thromboplastin time)
  3. TT (thrombin time)
51
Q

What triggers the extrinsic pathway?

A

Vascular injury exposes TF to the blood

52
Q

What activates the intrinsic pathway?

A

Thrombin activates factor 11

53
Q

What are the four functions of thrombin?

A
  1. cleaves fibrinogen to fibrin
  2. activates VIII and V
  3. activates platelets
  4. initiates termination of the clotting cascade by interacting with thrombomodulin
54
Q

The ___________pathway is assessed by PTT and the _____________ pathway is assessed by PT.

A

Intrinsic (12,11, 9, 8) are assessed by PTT

Extrinsic (TF, 7) is assessed by PT (or with warfarin INR)

55
Q

Where are all the clotting factors made?

What are the vit K dependent factors?

A

They are all made in the liver except 8 which is made by endothelial cells
vit K : protein C&S, 2,7,9,10

56
Q

What 3 situations would present with an abnormal PT/INR and normal PTT/TT?

A
  1. Liver disease/cirrhosis
  2. Warfarin/Coumadin/vitK deficiency
  3. Congenital factor 7 deficiency
57
Q

What clotting factor is the most warfarin sensitive?

A

Factor 7. Warfarin affects all the clotting factors that need vit K because it disrupts the generation of vit K.

58
Q

In what 3 patients could you see a vit K deficiency?

A
  1. malnourished patients
  2. patients on prolonged antibiotics that disrupt gut flora
  3. ICU patients
59
Q

What situations would cause abnormal PTT with normal PT and TT?

A
  1. Heparin
  2. Hemophilia A (8) and B (9)
  3. Lupus anticoagulant

Anything that causes a deficiency in 12,11,9,8, HMWK, prekallikrien

60
Q

What is the purpose of the 50/50 mix when testing a clotting factor deficiency?

A

If 50/50 mix of patient serum and “normal” serum corrects the problem, it was a clotting factor deficiency.
If the 50/50 does not correct, it is an inhibitor

61
Q

What is the inheritance pattern of hemophilia A and B?

Which factors are defiecient in each?

A

X-linked recessive so grandfather to grandson transmission
Hemophilia A = 8
Hemophilia B= 9

62
Q

What test is done for acquired inhibitors of the coagulation cascade?

A
  1. 50/50 mix will not correct
  2. dilute Russell viper venom will activate coagulation directly as is not sensitive to inhibitors except it is prolonged with lupus anticoagulant
63
Q

What does TT measure?

What situations would cause an abnormal TT (other tests can be abnormal or normal)?

A

It is thrombin time and measures fibrinogen quality or quantitiy. It is the time to form clot when thrombin is added directly to plasma.

  1. liver disease
  2. heparin
64
Q

What are potential causes when PT/INR and PTT are abnormal?

A
  1. Severe Vit K deficiency
  2. Coumadin overdose
  3. DIC
  4. Advanced liver disease
  5. congenital 2, 5, 10 deficiencies
65
Q

What allows you to distinguish between prolonged PT/PTT due to liver disease vs, DIC?

A

Factor 8 levels will be normal in liver disease and decreased in DIC

66
Q

What is DIC?

What type of cell can be seen to verify DIC?

A

Diseminated Intravascular Coagulation where there is an inappropriate co-existence of fibrin formation and fibrinolysis that results in a global consumption of clotting factors.
Schistocytes confirm microangiopathic hemolytic anemia which results because of the inappropriate fibrin strands that sheer RBC as they pass

67
Q

What would be the physical signs of DIC?

A
  1. bleeding from venipuncture and IV
  2. Conjunctival bleeding
  3. confluent purpura
68
Q

What are the clinical settings where you would see DIC?

A
  1. Sepsis
  2. Malignancies - APML
  3. Obstetrical disasters
  4. Trauma- crush injury, brain injury, burns
69
Q

What are the lab diagnoses of Acute DIC?

A
  1. platelet count (must be low)
  2. PT/PTT/TT
  3. fibrinogen
  4. fibrinogen degradation products (FDP) - sensitive but not specific
  5. D-dimers- specific but less sensitive
70
Q

What are the lab diagnoses for chronic DIC?
When is chronic DIC usually seen?
What is treatment?

A
  1. elevated fibrinogen degradation products (FDP)
  2. positive D-dimers
  3. mildly depressed platelet count

Seen in adenocarcinoma and obstetric patients with a dead fetus.
Treated with heparin

71
Q

What factor deficiency is associated with a normal PT/PTT/TT?
How is deficiency in this factor measured?

A

Factor 13 deficiency is associated with poor wound healing .
It is measured by increased solubility of fibrin clot in urea

72
Q

What is the physical presentation of amyloidosis?

What is the underlying problem?

A

Raccoon eyes and macroglossia.

It is usually a vascular problem but some may be due to inhibition of factor X

Fundamentals 3- Heme (19 decks)

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