Chapter 29 Flashcards

1
Q

Thrombocytopenia

A

Platelet count of less than 100,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can occur with a platelet count of < 50,000

A

Hemorrhage from minor trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can occur with a platelet count of < 15,000

A

Spontaneous bleeding without apparent trauma resulting in petechiae, ecchymosis, larger purpuric spots, or frank bleeding from mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can occur with a platelet count of < 10,000

A

Severe bleeding that can be fatal if it occurs in the GI tract, respiratory system, or CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Heparin-Induced Thrombocytopenia (HIT)

A
  • An adverse drug reaction caused by IgG antibodies against the heparin-platelet factor 4
  • leads to increased platelet consumption and a decrease in platelet counts beginning 5-10 days after administration of heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Clinical Manifestations of Heparin-Induced Thrombocytopenia (HIT)

A
  • low platelet count (a decrease of approximately 50% in the platelet count is seen)
  • risk for venous (DVT and PE) or arterial (acute limb ischemia) thrombosis
  • bleeding is uncommon, even with low platelet counts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment for Heparin-Induced Thrombocytopenia (HIT)

A
  • stop the heparin
  • do NOT switch to low-molecular-weight heparin OR warfarin until symptoms of HIT are gone due to increased risk of skin necrosis
  • the chance of spontaneous blood clots can be diminished using thrombin inhibitors (lepirudin, argatroban)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Congenital alterations in platelet function can be categorized into several types of disorders (5)

A
  1. Adhesion between platelets and the vessel wall
  2. Platelet-platelet adhesion
  3. Platelet granule secretion
  4. Arachidonic acid pathway activity
  5. Membrane phospholipid regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Drugs that affect platelet function

A
  1. Aspirin irreversibly inhibits cyclooxygenase function for several days after administration
  2. NSAIDs also affect cyclooxygenase but it is reversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Systemic disorders that affect platelet function

A
  1. Chronic renal disease
  2. Liver disease
  3. CABG
  4. Severe deficiencies of iron or folate
  5. Presence of antiplatelet antibodies associated with autoimmune disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hematologic disorders that cause platelet dysfunction

A
  1. Chronic myeloproliferative disorders
  2. Multiple myeloma
  3. Leukemias
  4. Myelodysplastic syndromes
  5. Dysproteinemias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes disorders of coagulation?

A
  • caused by defects or deficiencies of one or more of the clotting factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Impaired Hemostasis

A
  • inability to promote coagulation and the development of a stable fibrin clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can cardiovascular abnormalities trigger coagulation inappropriately?

A
  • any abnormality that alters normal blood flow by accelerating, decelerating, or obstructing it can result in spontaneous coagulation within the vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can vasculitis trigger coagulation inappropriately?

A

Vasculitis, or inflammation of the blood vessels, as well as vessel damage, activates platelets, which in turn activates the coagulation cascade
- in extensive or prolonged vasculitis, clot formation can suppress mechanisms that normally control clot formation and breakdown, leading to clogging of the vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does a vitamin K deficiency contribute to impaired hemostasis?

A
  • vitamin K is necessary for synthesis and regulation of prothrombin, procoagulant factors (7, 9, 10) and proteins C and S (anticoagulant regulators)
17
Q

Causes of Vitamin K Deficiency

A
  • the most common cause is parenteral nutrition in combination with broad-spectrum antibiotics that destroy normal gut flora
    -rarely is a deficiency caused by lack of dietary intake
18
Q

Clinical Manifestations of Vitamin K Deficiency

A

Ranges from laboratory abnormalities to significant hemorrhage

19
Q

Treatment for Vitamin K Deficiency

A

Parenteral administration of vitamin K
- FFP may be administered but is usually reserved for patients with life-threatening hemorrhages or who require emergency surgery

20
Q

How does liver disease contribute to impaired hemostasis?

A

The hepatic parenchymal cells produce most of the factors involved in hemostasis. Thus damage to the liver frequently results in diminished production of factors involved in clotting.
- can cause a broad range of hemostatic disorders (defects in coagulation, fibrinolysis, and platelet number and function)

21
Q

Treatment for liver disease associated disorders of coagulation

A

Fresh frozen plasma (FFP)

22
Q

Consumptive Thrombohemorrhagic Disorders

A
  • heterogenous group of conditions that range from hemorrhagic and thrombotic pathologic conditions
  • Example: Disseminated intravascular coagulation (DIC)
23
Q

Cause of DIC

A

Caused by a variety of clinical conditions that release tissue factor
- causes an increase in fibrin and thrombin activity in the blood
- produces augmented clot formation and accelerated fibrinolysis

24
Q

DIC is characterized by what functions?

A

Characterized by a cycle of intravascular clotting, followed by active bleeding
- is caused by the initial consumption of coagulation factors and platelets
- results from abnormally widespread and ongoing activation of clotting
- hemorrhage: is secondary to the abnormally high consumptions of clotting factors and platelets
- deposition of fibrin clots in the circulation interferes with blood flow, causing widespread organ hypoperfusion (organ ischemia)

25
Q

Clinical Manifestations of DIC

A
  1. Bleeding from venipuncture sites
  2. Bleeding from arterial lines
  3. Bleeding from surgical wounds
  4. Purpura, petechiae, and hematomas
  5. Symmetric cyanosis of the fingers and toes
26
Q

DIC Treatment

A
  • restore hemostasis
  • maintain organ function
  • control thrombosis
  • replacement therapy (platelets, FFP, cryoprecipitate)
  • replace anticoagulants
27
Q

How to maintain organ function in DIC

A

Maintenance of organ function is achieved by fluid replacement to sustain adequate circulating blood volume and to maintain optimal tissue and organ perfusion
- fluids may be required to restore blood pressure, cardiac output, and urine output to normal parameters

28
Q

Replacement Therapy for DIC

A
  1. Platelets for thrombocytopenia
  2. FFP provides volume and replaces clotting factors
  3. Cryoprecipitate replaces fibrinogen