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Heme/Onc Exam 2 > Bleeding conditions > Flashcards

Bleeding conditions Flashcards

1
Q

Platelet Function Assay

A

● Time it takes to clot a damaged vessel
● Measures platelet adhesion and aggregation
● Whole blood is passed over a membrane containing collagen and epinephrine or ADP
● Reported as the seconds required to close a small aperture in the membrane
● Less invasive, and more reproducible

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2
Q

Prothrombin time assesses function of the ____ and common pathway

A

extrinsic

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3
Q

Time required for a fibrin clot formation

A

Prothrombin time
Normally 11-15 seconds

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3
Q

Partial Thromboplastin Time is Used to assess the ____ and Common Pathway

A

Intrinsic

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4
Q

Prolonged if over 35 sec (normally 25-35 seconds)

A

Partial Thromboplastin Time

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5
Q

Coagulation Factor Assays (V, VII, VIII, IX, X, XI, XII)

A

● Used to detect specific coagulation factors
● Used to evaluate blood with abnormal PT and PTT
● Test is done by adding a factor, and watching for correction of the PT and PTT
● Various disease states hereditary or otherwise, contribute to clotting factor deficiencies

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6
Q

disorders of Primary Hemostasis are
those disorders that deal with ____

A

low platelet count or some
form of platelet dysfunction.

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7
Q

PT and PTT should be normal in disorders of ____ hemostasis

A

primary

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8
Q

Thrombocytopenia simply means low ____

A

Platelet count

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9
Q

Thrombocytopenia can be due to either

A

○ Decreased Platelet production
○ Enhanced Platelet destruction

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10
Q

Pathophysiology of thrombocytopenia - Examples of Decreased Production of Platelets-

A

■ Bone marrow failure (ex: Aplastic Anemia)
■ Malignant infiltration of the the bone marrow
■ Exposure to some meds, chemotherapy, or radiation
■ Significant nutritional deficiencies

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11
Q

Pathophysiology of thrombocytopenia - Examples of Increased Destruction of Platelets

A

■ Immune Thrombocytopenia (ex: ITP)
■ Heparin-Induced Thrombocytopenia
■ Disseminated Intravascular Coagulopathy (DIC)
■ Hypersplenism (ex: Related to cirrhosis, lymphoma)
■ Septicemia

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12
Q

Thrombocytopenia Exam and Lab Findings:

A

○ If significant Thrombocytopenia, Petechiae, Purpura, or
Ecchymosis may develop with little or no explanation.
○ Platelet count will be low on CBC.

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13
Q

____ are flat, red, pinhead-sized lesions
that can appear anywhere on the body
but more likely to be seen in dependent
areas. They do not blanch with pressure.

A

Petechiae

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14
Q

____ is the coalescence of
petechiae on the surface of the skin.
They are nonpalpable and are more of a
purple color. They also do not blanch.

A

Dry Purpura

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15
Q

The finding of purpura on mucous
membranes (rather than the skin) is
sometimes referred to as ____

A

Wet Purpura
This is generally considered to be a sign
for more serious bleeding as platelet
counts are typically very low in order for
wet purpura to occur.

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16
Q

Thrombocytopenia: Treatment and Management

A

○ Treatment obviously depends on the
underlying condition causing the
Thrombocytopenia.

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17
Q

An acquired autoimmune disorder characterized by isolated
thrombocytopenia, maybe without an apparent cause

A

ITP
● Immune Thrombocytopenic Purpura (previously called “idiopathic”)

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18
Q

What is this

A

Wet purpura

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19
Q

Epidemiology of ITP

A

● Occurs predominantly in young children; peak incidence is between 2 and 5 years of age.
● Can occur in adulthood as well, usually more insidious.
○ Usually between 20-50 years of age

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20
Q

ITP Pathophysiology

A

○ An antibody is inappropriately produced that binds to surface antigens GPIIb/IIa and others
○ The antibody-coated platelets are then bound by a splenic macrophage and destroyed in the spleen → Shortened half life
■ Thrombocytopenia occurs as a result of accelerated splenic destruction of the platelets.

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21
Q

Primary vs secondary ITP

A

Primary ITP: Acquired immune thrombocytopenia without an apparent
cause
Secondary ITP: ITP associated with another condition with an inciting event

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22
Q

ITP: Characteristic Signs and Symptoms

A

bleeding, spontaneous bruising, epistaxis,
gingival, with platelet counts 10,000 - 20,000/mcL
○ Adult women may have menorrhagia.
○ Intracranial hemorrhage is an infrequent occurrence, but it is
the most common cause of death among patients with ITP.

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23
Q

Diagnostic testing for ITP

A

○ Hallmark is Isolated Thrombocytopenia.
■ If other abnormalities on CBC, likely not ITP
■ If bleeding has occurred, sure, may have anemia
○ PT/INR and PTT are normal.
○ Bone Marrow biopsy may show increased number of Megakaryocytes

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24
Q

ITP Treatment:

A

○ Avoidance of trauma, NSAIDs, and Aspirin.
○ Childhood ITP is usually self-limited and often does not require treatment.
○ Short course of Steroids is usually the mainstay of treatment
○ Platelet transfusion can be given in severe hemorrhage
○ Relapse can occur, rituximab and TPO mimetics in refractory cases
○ Splenectomy reserved for persistent, chronic cases (risks?)

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25
Q

TTP

A

Thrombotic Thrombocytopenic Purpura (TTP)

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26
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A

● Uncommon condition that was mysterious and usually fatal only 15-20 years ago.
○ Can still be acutely life-threatening
● Characterized by Thrombocytopenia, Hemolytic Anemia, and Impairment of Renal function.
○ Considered a Microangiopathic Hemolysis

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27
Q

Pathophysiology of TTP

A

○ It’s believed the disease occurs due to the
presence of “high molecular weight
multimers of vWF.”
○ The high molecular weight vWF seems to
tether clumps of platelets to endothelial
surfaces sporadically.

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28
Q

Deficiency in the protease ADAMTS13 has
been identified with ___

A

TTP

29
Q

Characteristic Signs and Symptoms of TTP

A

○ Most patients present with fever.
○ Thrombocytopenia
○ Microangiopathic hemolytic anemia
○ Renal impairment
○ Neurologic dysfunction is characteristic of the disease, but not always present.

30
Q

TTP Additional diagnostic testing:

A

○ Anemia on CBC
○ Elevated Lactate Dehydrogenase (LDH)
○ Reticulocytosis
○ Schistocytosis
○ Thrombocytopenia
○ Elevated BUN/Creatinine

31
Q

TTP Treatment and Management

A

○ Mortality rate is greater than 95% without treatment!
○ Plasma Exchange is the primary treatment.
○ Platelet transfusion is contraindicated as the initial treatment
○ Glucocorticoids and rituximab- immunosuppressive
○ Caplacizumab for high risk- monoclonal binds to vWF
○ Hemodialysis
○ Sometimes blood transfusions are necessary to treat anemia.
○ With plasma exchange, 80-90% recover completely

32
Q

Hemolytic Uremic Syndrome classic triad

A

○ Hemolytic Anemia
○ Thrombocytopenia
○ Renal Dysfunction
(just like with TTP)

33
Q

What differentiates HUS from TTP?

A

Classically differentiated from TTP by absence of Neurologic symptoms. Although ¼ can get neurologic signs

34
Q

Hemolytic Uremic Syndrome pathophysiology

A

○ About 50% of cases are caused by an enteropathic strain of E coli
(O157:H7), which releases a Shiga-like toxin.
○ Primary lesions are of the endothelium of arterioles with formation of platelet thrombi, resulting in thrombosis and
necrosis of the intrarenal vessels. ↑urea in the blood.

35
Q

Hemolytic Uremic Syndrome Characteristic Signs and Symptoms

A

○ In young children, a history of recent and/or recurrent
diarrhea is classic for HUS. Often bloody dirrhea
○ Pallor is common.
○ Cutaneous or GI bleeds are possible.
○ Oliguria- Significant kidney injury
○ Abdominal pain
○ Nausea/vomiting
○ Neurologic symptoms are very rare in childhood HUS.
○ HUS in adulthood is a continuum of TTP and neurologic
symptoms are possible

36
Q

Hemolytic Uremic Syndrome diagnostic testing

A

○ Hemolytic anemia (less severe than TTP)
○ Thrombocytopenia (less severe than TTP)
○ Acute renal injury (more severe than TTP)
○ Elevated LDH
○ Reticulocytosis
○ Schistocytosis
○ Stool culture may be positive for E coli O157:H7
○ PT/INR and PTT will be normal

37
Q

Hemolytic Uremic Syndrome Treatment and management

A

○ Treatment for HUS is primarily supportive.
○ Most children with diarrhea-associated HUS recover within 2-3 weeks.
○ In severe cases, blood transfusions,
○ Eculizumab- Monoclonal antibodies when severe
○ Early hemodialysis improves outcome.

38
Q

von Willebrand’s Disease inheritence

A

Autosomal Dominant disorder that results from deficient or defective vWF and causes ineffective platelet adhesion.
○ von Willebrand’s Disease is the most common inherited bleeding disorder.

39
Q

von Willebrand’s Disease Pathophysiology

A

○ Normal vWF serves two main functions-
■ Molecule that adheres platelet to injured endothelium
■ Chaperone to Factor VIII, slowing its degradation

40
Q

Several types of vWD

A

■ Type 1 (75-80% of vWD): Common, Low levels of vWF
● vWF levels are perhaps 15-60% of normal
■ Type 2 (20-22%): Several subtypes
● vWF levels are normal, but vWF is defective
■ Type 3 (rare): Homozygous, very low levels of vWF
● vWF levels are less than 5% of normal, big concern for bleeding

41
Q

von Willebrand’s Disease Characteristic Signs and Symptoms

A

○ If there is bleeding, it is most commonly mild to moderate integument or mucosal bleeding
○ Common history is bleeding more than normal in childhood/teenager after surgery or trauma with parents reporting a similar problem when they were young.
○ Severe bleeding is less common- Type 2 vWD usually has moderate to severe bleeding in childhood.

42
Q
A
43
Q

von Willebrand’s Disease Diagnostic Testing:

A

○ Platelet count is normal; they are there and functioning.
○ Aggregation studies (Platelet Function assays) are normal except for Ristocetin assay
○ vWF levels are generally measured as low, esp Type 3.
○ Factor VIII levels are generally low as well.

44
Q

von Willebrand’s Disease Treatment and Management

A

○ Aspirin can significantly affect vWD patients.
■ Avoid Aspirin!
○ Most cases require no treatment unless having surgery.
○ Intranasal DDAVP (Desmopressin) can be given 30-90 minutes prior to surgery (Best for type 1).
■ Can be given after dental procedures (etc.) if oozing is occuring.
■ DDAVP causes release of vWF and Factor VIII from storage sites
(increasing vWF 2-7 fold).
○ In cases of significant bleeding (Type 3 usually), IV Humate-P (vWF/Factor VIII concentrate) can be given.

45
Q

disorders of Secondary
Hemostasis are those that deal with ____

A

Factor deficiencies or dysfunctions within the Coagulation Cascade

46
Q

Disorders of Secondary Hemostasis include

A

○ Hemophilia A
○ Hemophilia B
○ Liver Disease-Induced
○ Vitamin K Deficiency

47
Q

Hemophilia A

A

Hemophilia A is hereditary bleeding
disorder that is considered X-Linked
Recessive.

48
Q

___ is the most common severe bleeding disorder

A

Hemophilia A

49
Q

Hemophilia A Pathophysiology

A

○ The disorder leads to a deficiency in
Coagulation Factor VIII.
○ Factor IX is unable to activate Factor
X, so coagulation is dysfunctional
.

50
Q

Hemophilia A Characteristic Signs and Symptoms

A

○ Bleeds in deep tissue is characteristic.
○ Spontaneous Hemarthroses- Essentially diagnostic!
○ Can also bleed into muscles, GI tract, and base of tongue

51
Q

What is this called and indicative of?

A

Spontaneous Hemarthroses- Essentially diagnostic for hemophilia A

52
Q

Hemophilia A Diagnostic Testing

A

○ Because the Intrinsic Pathway is completely dependant
on Factor VIII, PTT is prolonged with Hemophilia A.
○ Coagulation Factor VIII Assay will show decreased levels.

53
Q

Hemophilia A Treatment and Management

A

○ Repeated hemarthrosis may lead to joint deformities.
○ Patients with Hemophilia should avoid any contact sports, Aspirin, and IM injections.
○ Recommended treatment is…
■ IV infusion of Factor VIII concentrate.
■ Severe cases get 2-3 x / wk prophylactically
■ Emicizumab- prophylaxis X→Xa
○ DDAVP may also be administered (no more than once every 48 hours)

54
Q

Hemophilia B differences from A

A

● Essentially the exact same disease as Hemophilia A, only a few specific differences.
● This X-Linked Recessive disorder is less common and is a deficiency of Factor IX
● Labs are the same, except it is Factor IX decreased on assay

55
Q

“Christmas Disease”

A

Hemophilia B

56
Q

Hemophilia B Treatment and Management

A

○ Factor IX concentrate is mainstay of treatment-
■ Most Factor IX concentrates also contain Factors II, VII, and X.
● Creates an increased risk of clotting when receiving treatment.
○ DDAVP is not used for Hemophilia B.
○ Otherwise, treatment and recommendations are the same for Hemophilia A and B

57
Q

Vitamin K Deficiency pathophysiology

A

Vitamin K deficiency bleeding disorder can be caused by…
■ Warfarin therapy
■ Poor diet
■ Malabsorption
● Antibiotic-related diarrhea
● Inflammatory bowel disease
■ Biliary obstruction

58
Q

Vitamin K Deficiency Diagnostic Testing

A

○ PT/INR and PTT are elevated.
■ PT is generally more affected than PTT (but both really)
○ Platelet level is generally normal.
○ Platelet function studies would be normal

59
Q

Vitamin K Deficiency treatment

A

○ Treatment depends on the etiology.
○ If poor diet or malabsorption problem, fix it.
○ If on Warfarin and PT/INR is too high, decrease dose.
○ If acute bleeding due to Vitamin K deficiency…
■ Vitamin K replacement (IV or PO; SQ is less predictable)
■ Administration of FFP may be indicated in emergencies

60
Q

The liver is responsible for
production of all coagulation
factors except____

A

VIII and vWF.

61
Q

Characteristic Signs and Symptoms of Liver Disease-Induced coagulation issues

A

○ Any type of bleeding is a possible
sign/symptom.
○ Assess for signs of liver failure
(jaundice, caput medusae, ascites, etc)

62
Q

Diagnostic Testing for Liver Disease-Induced coagulation issues

A

○ Characteristically shows prolonged PT and PTT.
■ Administration of Vitamin K will not correct this
○ May see Thrombocytopenia secondary to hypersplenism.

63
Q

Liver Disease-Induced Treatment and Management:

A

○ Treatment should be focused on optimizing liver function.
○ If in end-stage hepatic failure, treatment is difficult.
■ Transplantation will correct the coagulopathy
HEM-HEMOST-2
○ If there is an acute bleed, FFP can be
administered.

64
Q

DIC

A

Disseminated Intravascular Coagulation

65
Q

Disseminated Intravascular Coagulation

A

● Uncontrolled activation of coagulation
■ → depletion of clotting factors and fibrinogen
■ Thrombocytopenia as platelets are used up

66
Q

DIC Pathophysiology

A

○ The pathophysiology is very complex, but at the core is the extensive release of Tissue Factor.
■ Due to widespread tissue injury or endovascular damage
○ This leads to widespread Coag Cascade ignition in such a way that the coagulation factors are consumed.
● Leading to widespread Fibrin production
○ Platelets are activated and bind to endovascular tissue.
○ The presence of widespread fibrin chunks and microvascular coagulation
results in RBC hemolysis
○ Plasminogen is activated into Plasmin, which breaks down some of the Fibrin, so
degradation products are present

67
Q

DIC Diagnostic testing

A

○ Early Dz may show low normals ○ Thrombocytopenia ○ Elevated PT/INR ○ Elevated aPTT ○ Reduced fibrinogen levels ○ Elevated D-Dimer ○ Schistocytes on blood smear ○ Low levels of Coag Factors ○ Commonly see acute renal injury ■ Elevated BUN/Creatinine
○ As you can see, everything is off

68
Q

DIC Treatment and Management

A

○ Once DIC sets in, Mortality rates are 50-60%.
○ Most important part of treatment is first treat the underlying disease.
○ Admission to the hospital with hematology consult

69
Q

HELLP Syndrome can progress to DIC

A

Hemolysis, Elevated Liver enzymes, Low Platelets

70
Q

DIC as a complication of pregnancy

A

● HELLP Syndrome can progress to DIC
● Hemolysis, Elevated Liver enzymes, Low Platelets
● Kidney injury
● High mortality rate
● Treatment includes delivery

Heme/Onc Exam 2 (7 decks)

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