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Pathology > Bleeding DIsorders > Flashcards

Bleeding DIsorders Flashcards

1
Q

The platelet count will show (qualitative / quatitative) disorder of platelets? What is the normal value?

A

quantitative; 150,000 - 300,000 platelets/microliter (isnt it supposed to be 450,000???)

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2
Q

If the platelet count is normal, bleeding time will show (qualitative / quatitative) disorder of platelets?

A

qualitative

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3
Q

Abnormal clotting time shows an abnormality in?

A

Extrinsic, Intrinsic and Common coagulation factors

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4
Q

Prothrombin time (PT) assesses (intrinsic / extrinsic) pathway in addition to the common pathway? Enumerate factors involved.

A

Extrinsic factors; F V, VII, X, prothrombin, fibrinogen

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5
Q

Activated Partial Thromboplastin time (aPTT) assesses (intrinsic / extrinsic) pathway in addition to the common pathway? Enumerate factors involved.

A

Intrinsic; F V, VIII, IX, X, XI, XII, prothrombin, fibrinogen

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6
Q

Excessive bleeding can result from?

A

Increased fragility of vessels, platelet deficiency, derangement of coagulation

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7
Q

In bleeding diorders with vessel wall abnormality, platelet count, bleeding time, PT, PTT are all (increased/decreased/normal)

A

NORMAL

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8
Q

What are the common causes of vessel wall abnormality

A

Infections, drug reactions, scurvy, Ehler’s Danlos, Henoch-Schonlein purpura, Hereditary hemorrhagic telangectasia (Weber-Osler-Rendu Syndrome), Perivascular amyloidosis

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9
Q

Describe the vessels in hereditary hemorrhagic telangectasia (Weber-Osler-Rendu Syndrome). Most common sites of bleeding?

A

Dilated and tortuous with thin walls; mucous membranes of nose, tongue, mouth, eyes, GIT

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10
Q

What causes Henoch-Schonlein purpura?

A

deposition of circulating immune complexes within the vessels and glomerular mesangial regions

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11
Q

At what platelet level is considered thrombocytopenia?

A

less than 100,000 platelets/microliter

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12
Q

At what platelet level does spontaneous bleeding become evident?

A

less than 20,000 platelets/microliter

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13
Q

What is the most feared (hahaha wtf??) complication of thrombocytopenia?

A

intracranial bleed

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14
Q

Platelet levels of 20,000 - 50,000 can aggravate ________ bleeding

A

post traumatic

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15
Q

(T/F) You should transfuse a patient (not undergoing surgery) when platelets are <20,000

A

False, do not transfuse unless symptomatic b/c body might produce antibodies against transfused platelets

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16
Q

Bleeding from thrombocytopenia is associated with (increased/decreased/normal) PT & PTT and often involves small vessels

A

Normal

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17
Q

Causes of thrombocytopenia

A 
Decreased platelet production 
Decreased platelet survival
Sequestration
Massive transfusion / dilution
Ineffective megakaryopoesis
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18
Q

Heparin causes a _______in platelet count

A

decrease

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19
Q

An autoimmune disease producing antibodies against platelets wherein there is a normal bone marrow (or increased megakaryocytes)

A

Idiopathic Thrombocytopenic Purpura (ITP)

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20
Q

Differences in population affected between acute and chronic ITP

A

Acute is self-limited an seen in childrenof any gender 1-2 weeks after a viral infection; Chronic is seen in adults especially in pregnant wormen with autoimmune disorders

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21
Q

In Chronic ITP, autaoantibodies are directed against platelet membrane glycoprotein of this type

A

Gp IIb/IIIa or Ib-IX

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22
Q

What Ig class is usually seen in chronic ITP

A

IgG

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23
Q

In chronic ITP, what is the alternative treatment to steroids? How does it help?

A

splenectomy. Removal of the source of autoantibodies

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24
Q

(T/F) Platelet concentrate transfusion in patients with ITP is helpful

A

False. Antibodies will just destroy the platelets

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25
Q

What is the characteristic pentad of thrombotic thrombocytopenic purpura (TTP)

A

1) Microangiopathic hemolytic anemia
2) Decreased platelets
3) Fever
4) Transient neurologic defects
5) Renal failure (usually in females, 4th decade of life)

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26
Q

Morphology in TTP

A

Widespread hyaline microthrombi

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27
Q

What is the enzyme deficiency in TTP?

A

ADAMTS 13 or vWF metalloprotease

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28
Q

What is the function of the enzyme ADAMTS 13?

A

degrades vWF

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29
Q

What are the main functions of vWF?

A

Platelet adhesion

Carry factor VIII and improve its lifespan

30
Q

What is the treatment for TTP

A

Plasma exchange

31
Q

What would be a differential diagnosis for TTP? How do you differentiate?

A

Hemolytic Uremic Syndrome (HUS). HUS does not have associated neurologic manifestations & ADAMTS 13 levels are normal

32
Q

What is the etiology of HUS?

A

Bacterial toxin (EHEC) that stimulate platelet aggregation

33
Q

What is the cause of typical HUS?

A

O157:H7 elaborates shiga-like toxin that alters endothelial cell function when absorbed, causing platelet activation and aggregration

34
Q

What is the cause of atypical HUS?

A

Defect in complement factor H, CD46 or factor I

35
Q

Examples of inborn/congenital abnormalities in platelet function

A

Von WIlldebrand Disease, Bernard soulier Syndrome, Glanzmann Thrombasthenia, Disorders of platelet secretion

36
Q

Reasons for acquired abnormalities in platelet function

A

Aspirin or NSAIDS, Uremia

37
Q

What is the most common inherited bleeding disorder in humans?

A

Von Willdebrand disease

38
Q

aPTT & PTT is _____ in Von Willdebrand disease and platelet count is _______; Risotcetin aggregation test is _______

A

elevated; normal; reduced

39
Q

What is defective in Von Willdebrand disease

A

vWF causing defective adhesion

40
Q

Which types of Von Willdebrand disease are associated with reduced quantity of circulating vWF? Which one autosomal recessive and is associated with extremely low levels of vWF?

A

Type 1 and 3; Type 3

41
Q

Type 2 Von Willdebrand disease is characterized by ________ defect in vWF

A

Qualitative

42
Q

Type 1 Von Willdebrand disease is autosomal _______?

A

dominant

43
Q

In type 2 Von Willdebrand disease, ______ mutations cause defective multimer assembly

A

missense

44
Q

In Bernard Soulier Syndrome, defective adhesion is caused by the lack of ______?

A

GpIb

45
Q

Lack of GpIIb/IIIa in Glanzmann Thrombasthenia causes defective _______?

A

aggregation

46
Q

In acquired platelet abnormalities d/t uremia, the platelet count is ______ and the BT is ______

A

Normal; Elevated

47
Q

The complex pathogenesis In acquired platelet abnormalities d/t uremia involves defects in ____, _____ and ______.

A

aggregation, adhesion and granule secretion

48
Q

Increased clotting time with normal platelet and BT is indicative of abnormalities in ____?

A

Clotting factors

49
Q

Abnormalities in extrinsic pathway factors will show an elevated ______?

A

PT

50
Q

Abnormalities in intrinsic pathway factors will show an elevated ______?

A

PTT

51
Q

vWF is synthesized in by?

A

endothelial cells and megakaryocytes

52
Q

What is the most important function of vWF?

A

Promote adhesion of platelets to the subendothelial matrix

53
Q

vWF stabilizes factor ____

A

VIII

54
Q

factor VIII is an essential cofactor of factor

A

IX

55
Q

What is the most common hereditary disease that is associated with life-threatening bleeding?

A

Hemophilia A

56
Q

Hemophilia A is caused by a deficiency in factor ____

A

VIII

57
Q

Hemophilia B (aka Christmas disease) is caused by a deficiency in factor ____

A

IX

58
Q

Hemophilia ___ is associated with normal PT and prolonged PTT

A

A and B

59
Q

(T/F) Both hemophilia A & B are recessive x-linked traits

A

True

60
Q

What is required for the diagnosis of hemophilia?

A

Specific assays of factor levels

61
Q

Liver disease and Vitamin K deficiency affects the following factors

A

II, VII, IX, X

62
Q

Disseminated Intravascular Coagulation (DIC) is caused by

A

excessive activation of coagulation leading to the consumption of platelets, fibrin and coagulation factors

63
Q

DIC is not a primary disease, it is caused by complications of conditions such as:

A

Obstetric complications / difficult labor
Neoplasms
Infections/sepsis
Massive tissue injury

64
Q

Give some triggers of DIC

A

Release of tissue factor or thromboplastic substances into circulation and widespread injury to endothelial cells

65
Q

Widespread injury to endothelial cells can be seen in

A

Bacterial infections
Massive trauma
Obstetric conditions
Neoplasms

66
Q

Possible consequences of DIC

A

WIdespread deposition of fibrin and microangiopathic hemolytic anemia
Hemorrhagic diathesis

67
Q

In DIC, thrombi are usually seen in the

A

Kidneys, alveolar capillaries, CNS, adrenals, spleen, liver

68
Q

Waterhouse Friedrichsen Syndrome is d/t

A

massive adrenal hemorrages

69
Q

Widespread microthrombi in the placenta causing premature atrophy of the cytotrophoblasts and syncytiotrophoblast

A

Sheenhan postpartum pituitary necrosis

70
Q

What is the definitive treatment for DIC?

A

Removal or treatment of inciting cause

71
Q

DIC is characterized by

A 
microangiopathic hemolytic anemia
Dyspnea, cyanosis, renal failure
Convulsions, coma
Oliguria, acute renal failure
Sudden or progressive circulatory failure / shock

Pathology (7 decks)

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