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Heme Path > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

1
Q

inherited deficiency of the (1) receptor which normally binds (2) allowing platelet adhesion to the sub-endothelial matrix

A
  1. platelet GpIb 2. vWf refers to Bernard‐Soulier syndrome
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2
Q

Qualitative defects in vWF are measured by?

A

electrophoresis only

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3
Q

Describe type II von Willebrand disease

A

Qualitative defect due to defective assembly in vWF, resulting in loss of the most active form

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4
Q

Infections‐mechanisms include damage to the vessel integrity by (1)

A
  1. bacteria

refers to causes of petechiae or purpura

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5
Q

Where is factor VIII made?

A

liver

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6
Q

Syndromes which cause collagen defects of the vessel wall

A

“Scurvy Ehlers-Danlos Cushing’s syndrome”

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7
Q

What is hemophilia B?

A

X linked recessive disorder of factor IX deficiency

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8
Q

Prothrombin time measures effectiveness of?

A

extrinsic and common pathways

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9
Q

platelet count, PT, and PTT in hemophilias

A

platelet count and PT are normal PTT prolonged

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10
Q

What is hemophilia A?

A

X linked recessive disorder in factor VIII

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11
Q

BINDS PLATELETS AND PROMOTES INTERACTION of vWF AND GLYCOPROTEIN Ib ON PLATELET MEMBRANE; it is the basis for the assay of vWF

A

RISTOCETIN (antibiotic)

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12
Q

hereditary condition with tortuous dilated blood vessels that easily bleed

A

hemorrhagic telangiectasia; Weber‐Osler‐Rendu syndrome

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13
Q

Add kaolin and cephalin to plasma and determine clotting time

A

partial thromboplastin time

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14
Q

PT, PTT, and bleeding time for platelet dysfunction

A

PT and PTT normal bleeding time prolonged

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15
Q

Treatment of hemophilia A

A

infusions of recombinant factor VIII

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16
Q

How can bleeding in von Willebrand disease patients be avoided during procedures?

A

Prophylactic infusions of plasma concentrates containing factor VIII von Willebrand factor

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17
Q

ACTIVATES FACTOR X IN THE INTRINSIC SYSTEM

A

Factor VIII

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18
Q

Compare and contrast type I and type III von Willebrand disease

A

both are quantitative defects in amount of vWF type I - Autosomal Dominant; mild to moderate bleeding type III - autosomal recessive; severe bleeding, hemarthrosis (hemophilia like syndrome), very low levels of vWF

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19
Q

DIC is frequently seen in what infections?

A

sepsis Rocky Mountain Spotted Fever Aspergilosis Malaria Histoplasmosis

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20
Q

Drug induced petechiae or purpura involving skin and mucous membranes pathophysiology

A

“mechanism usually is immune complex deposition in capillaries and vascular damage”

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21
Q

Causes of bleeding from thrombocytopenia

A

caused by decreased platelet production, decreased platelet survival (often on an immune basis) or via platelet consumption as in DIC splenomegaly dilution thrombocytopenia

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22
Q

s/s of von Willebrand disease

A

mild bleeding post-procedure menorrhagia

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23
Q

What organs are typically affected by DIC?

A

capillaries of brain, adrenal spleen, lungs, liver

24
Q

ristocetin cofactor activity in von Willebrand disease

A

decreased

25
Q

Manifestations of Henoch-Schonlein purpura

A

“purpuric skin rash, abdominal pain, intestinal bleeding and renal dysfunction”

26
Q

What is dilution thrombocytopenia?

A

massive transfusions of blood and blood products (trauma, liver transplant or cardiac surgery) cause a dilution thrombocytopenia which will require platelet transfusion to correct

27
Q

Add tissue thromboplastin in the presence of calcium ions to plasma and determine clotting time

A

prothrombin time

28
Q

The von Willebrand factor binds to (1) in the circulation and allows for increased half‐life of (1). This is essential as unbound (1) has a half‐life of <3 hrs. It also is essential for platelet adhesion to sub endothelial (2) via platelet receptor (3)

A
  1. factor VIII 2. collagen 3. GpIb.
29
Q

DIC is associated with many conditions including?

A

adenocarcinomas of pancreas, lung, stomach acute promyelocytic leukemia Infections: Sepsis Rocky Mountain Spotted Fever Aspergilosis Malaria Histoplasmosis OB complications trauma burns severe tissue hypoxia acidosis shock snake bite Abdominal aortic aneurysm rupture Heat stroke Acute hemolysis

30
Q

s/s of hemophilias

A

bruise easily; major bleeding from trauma or surgery; hemarthrosis leading to fibrotic and deformed joints; petechiae are ABSENT

31
Q

CAUSES PLATELET ADHESION TO SUBENDOTHELIAL COLLAGEN

A

vWF

32
Q

defects in release of platelet (1) which are required for normal platelet function

A
  1. ADP and thromboxane refers to storage pool disease
33
Q

What is the inciting event of DIC?

A

due to abnormal activation of the coagulation system caused by release of tissue thromboplastin or endothelial damage

34
Q

DIC is characterized by?

A

widespread thrombosis leading to microangiopathic hemolytic anemia and organ dysfunction, followed by uncontrolled bleeding

35
Q

OB complications in which DIC is seen

A

abruption placentae septic abortion amniotic fluid emboli toxemia of pregnancy

36
Q

Thrombocytopenia may also be due to conditions causing (1) where there is sequestration of platelets in the enlarged organ

A
  1. splenomegaly (cirrhosis e.g.)
37
Q

Bleeding from conditions that alter blood vessel wall; normal labs:

Causes of petechiae or purpura involving skin and mucous membranes

A

Amyloidosis Vasculitis Vitamin C deficiency Infections Drug induced (Steroids) Collagen defects Henoch-Schonlein purpura Weber-Osler-Rendu syndrome

38
Q

Bleeding from conditions that alter the blood vessel walls results in?

A

petechiae or purpura involving skin and mucous membranes

39
Q

What are the manifestations of coagulation factor deficiencies?

A

“bleeding in GI and GU tracts hemarthrosis (bleeding into large joints) prolonged bleeding after procedures”

40
Q

Partial thromboplastin time measures effectiveness of?

A

intrinsic and common pathways

41
Q

What are the complications of DIC?

A

pulmonary, renal, circulatory failure and severe shock

42
Q

The effect of aspirin on (1) is irreversible and lasts up to (2) after discontinuing aspirin

A
  1. cyclooxygenase 2. one week
43
Q

inherited deficiency of (1) required to form bridges between platelets and (2) (platelet aggregation).

A
  1. Gp IIb‐IIIa 2. fibrinogen refers to Glanzman’s thrombasthenia
44
Q

Causes of acquired platelet defects

A

platelet dysfunction from use of plavix or aspirin and other non‐steroidal anti‐inflammatory drugs uremia

45
Q

Bleeding from conditions that alter blood vessel wall; normal labs:

Lab findings in petechiae or purpura involving skin and mucous membranes

A

normal platelet count, PT and PTT and bleeding time

46
Q

Treatment of hemophilia B

A

Recombinant factor IX concentrates

47
Q

How do factor VIII levels predict severity of bleeding in hemophilia A? What are the cutoffs?

A

Factor VIII levels 1% of normal –> severe bleeding Factor VIII levels 2-5% of normal —> mild bleeding

48
Q

septicemia secondary to meningococcal or rickettsia infection

A

infectious cause of petechiae or purpura involving skin and mucous membranes

49
Q

What is the purpose of vWf binding to factor VIII?

A

increases half-life essential for platelet adhesion

50
Q

Heterozygote females can also rarely acquire the disorder from inactivation of the remaining normal Xchromosome

A

Hemophilia A

51
Q

What are the coagulation factor deficiencies? Which are inherited and which are acquired?

A

Inherited: Factor VIII Factor IX von Willebrand disease Acquired: DIC

52
Q

Where is vWF made?

A

endothelial cells

53
Q

What are the s/s of platelet dysfunction?

A

“Petechiae Easy bruising Nosebleeds Menorrhagia”

54
Q

What are some of the acquired coagulation disorders?

A

vitamin K deficiency parenchymal liver disease (cirrhosis)

55
Q

Platelets, factor VIII, PTT in von Willebrand disease

A

platelet counts normal factor VIII decreased PTT prolonged in types I and III

Heme Path (21 decks)

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