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NURS 2500 > CLASS 8 - PLATELETS, CLOTTING, AND RELATED THERAPIES > Flashcards

CLASS 8 - PLATELETS, CLOTTING, AND RELATED THERAPIES Flashcards

1
Q

What is a thrombus?

What is an embolus?

A

Thrombus: Formed clot in the vascular system
Embolus: Thrombus that has moved from one part of the vascular system to another

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2
Q

What is hemostasis?

A

How blood clots

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3
Q

What is the defference between a clot and a thrombus?

A

Clot is good, stops bleeding.

Thrombus is bad bc it is a clot within a blood vessels + blocks it.

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4
Q

What is the coagulation cascade?

A

Sequence of interactions between proteins that cause fibrin deposition at the location of tissue injury.

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5
Q

What are the 2 pathways involved in the coagulation cascade? What is the role of each pathway?

A

Intrinsic (contact) + Extrinsic
Intrinsic: important for the amplification of the cascade
Extrinsic: important for initializing the coagulation cascade

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6
Q

what are the roles of prothrombin, thrombin, fibrinogen and fibrin in the coagulation cascade?

A

prothrombin converts to thrombin. Thrombin converts fibrinogen to fibrin, and fibrin forms a mesh at the site of tissue injury to help form the clot.

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7
Q

what are the signs of altered perfusion in the body due to clotting?

A
  • dizziness
  • chest pain
  • shortness of breath
  • skin tenderness / warmth
  • swelling
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8
Q

what is the function of anticoagulant medications?

A

interfere w the coagulation cascade

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9
Q

what is the difference in the MOA between antiplatelets and anticoagulants and thrombolytics?

A

Antiplatelets and anticoagulants prevent clots from getting formed in the first place
Thrombolytics act on the existing clot and dissolve it either by direct or indirect inactivation of the conversion of plasminigen to plasmin.

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10
Q

What is thrombocytopenia?

A

Reduction in platets below normal.

* remember platelets are thrombocytes

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11
Q

Which platelet count indicates thrombocytopenia? Which indicates prolonged bleeding? Which indicates severe, spontaneous bleeding?

A

thrombocytopenia: below 150 x 10^9 / L

prolonged bleeding: 50 X 10^9 / L

severe, spontaneous bleeding: 10 x 10^9 / L

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12
Q

What are the clinical manifestations of thrombocytopenia?

A
  • Often asymptomatic
  • bleeing
  • petechiae
  • ecchymoses
  • prolonged bleeding after procedures
  • hemorrhage
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13
Q

what is the difference between immune and non-immune thrombocytopenia?

A

immune: antibodies mark platelets for destruction and remove them in the spleen

non-immune: platelets taken out of circulation, decreased platelet prouction due to disease or diet

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14
Q

what are the 4 major etiologies of thrombocytopenia?

A
  • ITP (Immune Thrombocytopenic purpura)
  • TTP (thromboti thrombocytopenic purpura)
  • HIT (heparin induced thrombocytopenia)
  • Acquired Thrombocytopenia from decreased platelet production
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15
Q

what is the difference between acquired and inherited causes of thrombocytopenia?

A

Inherited thrombocytopenia are genetic predispositions to thrombocytopenia(like pancytopenia).
Most thrombocytopenia are acquired due to foods, herbs, and drug rxns.

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16
Q

Describe Immune Thromocytopenic Purpura (ITP)

- how is the clinical manifestation of ITP different in children than older adults?

A

Most common form of thrombocytopenia

  • acquired / immue
  • platelets are mistakenly coated with antibodies when they reach the spleen and are destroyed by macrophages w/in 1-3 days (platelets notmally survive 8-10)
  • manifests as an acute condition in children and chronic in older adults
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17
Q

Describe thrombotic thrombocytopenic purpura (TTP). Why is this considered to be a medical emergency?

A

Acquired / Non-immune

  • typically has an underlying cause such as infection
  • enhanced agglutination of platelets which form microthrombi that deposit in arterioles and capillaries.
  • this is a medical emergency because bleeding and clotting occur simultaneously.
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18
Q

Describe Heparin Induced Thrombocytopenia (HIT). When should you expect HIT?

A

Acquired / Non-Immune

  • body begins to attack platelets as a result of heparin therapy.
  • thrombocytopenia develops 5-10 days after heparin therapy is started.
  • Expect HIT if a patient’s platelet count falls by more than 50% of their baseline platelet count OR if it falls below 150 x 10^9 / L
  • Venous thrombosis and arterial thrombosis can develop
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19
Q

Describe Acquired Thrombocytopenia from decreased platet production

A

Acquired / Non-Immune

  • body does not produce as many platelets bc there is an external factor inhibiting production (disease or drug)
  • common cause is chemotherapy
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20
Q

Which drug class would be used to stop bleeding due to thrombocytopenia?

A

Antifibrinolytics.

21
Q

What is the purpose of a platelet count on a complete blood count?

A

Low platelet counts can indicate thrombocytopenia.

22
Q

Why would megakaryocytes be elevated while the destruction of circulatinf platelets is occurring in the body?

A

platelets produced in megakaryocytes - so increased megakaryotes could be to compensate for the loss of platelets.

23
Q

What treatments would be used to treat ITP?

A
  • corticosteroids
  • IVIG
  • Platelet transfusion
  • immunosuppressive therapy
  • splenectomy
24
Q

What treatments would be used to treat TTP?

A
  • identify + treat cause
  • plasmapheresis
  • high dose corticosteroids
  • splenectomy
  • chemotherapy, immunosuppressive agents
25
Q

What treatments would be used to treat HIT?

A
  • discontinue heparin
  • direct or indirect thrombin inhibitors
  • plasmapheresis
  • thrombolytic agents
26
Q

What treatments would be used to treat acquired thrombocytopenia from decreased platelet production?

A
  • identify + treat cause
  • corticosteroids
  • platelet transfusions
27
Q

Define the 3 major factor deficiency disorders:

  • Hemophilia A
  • Hemophilia B
  • Von Willibrand Disease
A
  • Hemophilia A: Factor 8 (VIII) deficiency - 80% of all cases
  • Hemophilia B: Factor 9 (IX) deficiency
  • Von Willibrand Disease: deficiency of vWF.
28
Q

What are the clinical manifestations of Hemophilia / Von Willebrand Disease?

A
  • Slow, persistent, prolonged bleeding from minor trauma and small cuts
  • Delayed bleeding after minor injuries
  • Uncontrollable hemorrhage after dental extractions / brushing teeth
  • Epistaxis
  • GI bleeding
  • Hematuria
  • Ecchymosis / subcut hematomas
  • Neurological signs
  • Hemarthrosis (bleeding in the joints)
29
Q

How is hemophilia acquired? Is it more common in females or males?

A

Sex-linked recessive, more common in males.

30
Q

What would the following lab results look like in a patient with hemophilia:

  • activated partial thromboplastin time (aPTT)
  • prothrombin time (PT)
  • platelet count
  • thrombin time
A
  • activated partial thromboplastin time (aPTT): PROLONGED due to deficiency of intrinsic clotting factor
  • prothrombin time (PT) - NORMAL
  • platelet count: NORMAL
  • thrombin time: NORMAL
31
Q

What is Von Willebrand disease?

A

deficiency of vWF.
vWF carries factor 8.
Most common blood disorder, affects 1/1000 Canadians.

32
Q

Describe the laboratory results of a patient w von willebrand’s disease

A

prolonged aPTT -prolonged bleeding time due to deficiency of intrinsic clotting factor
normal PT, Platelet count, and thrombin time.

33
Q

What is the function of antifibrinolytic agents such as aminocaproic acid?

A
  • inhibit breakdown of fibrin by inhibiting the formation of plasmin from plasminogen (plasmin breaks up clots).
  • Helps to keep bleeding episodes under control
  • most useful for preventing recurrent bleeding, less helpful in stopping ongoing bleed.
34
Q

What are Factor 8 + 9 concentrates made from?

A

made from donor plasma.

35
Q
  • Outline the formula for factor 8 (XIII) replacement

- Outline the formula for factor 9 (IX) replacement

A

FACTOR 8- (Patient’s weight x Target Activity Level) ÷ 1

FACTOR 9- (Patient’s weight x Target Activity Level) ÷ 2

36
Q

Calculate Factor VIII and IX replacement for a 35 kg pediatric patient

A

Target activity level 40-60%
Factor 8 - 35x 40 = 1400/ 1
- 35 x 60 = 2100
factor 8 btwn 1400 and 2100 u

Factor 9 btwn 700 and 1050 u

37
Q

A pediatric client becomes resistant to factor replacement. What might be happening in the body?

A

The patient developed antibodies to the factor replacement therapy

38
Q

What is phlebitis?

Which type of therapy is this common in?

A

Inflammation (redness, tenderness, warmth, mild edema) of a superficial vein w/o the presence of a thrombus
This is very common w IV therapy.

39
Q

What is a Venous Thrombo-Embolism (VTE)

* also called venous thrombosis

A

vein inflammation w a resulting thrombus

40
Q

What is a superficial vein thrombosis? Is it usually located in the arms or legs? What are the assessment findings?
What can it cause if left untreated?

A

thrombus in a vein near the skin surface.
usually in superficial leg veins, sometimes in the arms.
Results in tenderness, rubor, warmth, pain, and inflammation along the vein.
Vein appears as a palpable cord.
If left untreated, can result in DVT.

41
Q

What is Deep Vein Thrombosis (DVT)? What is a life threatning risk associated with DVT?
What are the assessment findings for DVT?

A

Thrombus in a deep vein, most commonly in the iliac and femoral veins. Potential life-threatnening risk is the embolus breaking away and travelling to the lung causing a pulmonary embolism.
Assessment findings: deep veins of arms, legs, pelvis, and pulm systems; tenderness or pressure over involved vein, induration of overlying muscle, venous distension, edema, pain, deep rubor, increased temp, HTN, post-thrombotic syndrome may occur

42
Q

What are varicose veins?

A

abnormally swollen + twisted veins w defective valves. most often seen in the legs.

43
Q

What is post-thrombotic syndrome? Why does it occur? What are the symptoms?

A

Results from chronic venous hypertension caused by destruction of valves, stiffness and noncompliance of vein walls, and persistent venous obstruction.

  • pain
  • aching
  • sensation of “heaviness”
  • swelling
  • cramps
  • itching
  • tingling
  • edema
  • eczema
44
Q

What is Virchow’s Triad?

A

Virchow’s triad identifies the 3 important etiological factors of venous thrombo-embolism formation, including:

  1. Venous stasis
  2. Hypercoagulability
  3. Trauma to a vessel
45
Q

What is venous stasis?

A

slow blood flow caused by dysfunctional vein valves, inactive extremity muscles, change in unidirectional blood flow

46
Q

How can venous stasis, endothelial damage, and blood hypercoagulability result in thrombus formation?

A
  • venous stasis
  • endothelial damage leads to release of clotting factors and activation of platelets
  • hypercoagulability leads to an increase in fibrin production.

platelets aggregate, clotting factors stimulated to produce fibrin, and firin entraps blood cells and adheres to vein wall = THROMBUS

47
Q

what is a pulmonary embolism?

A

blockage of pulmonary arterires by a thrombus, fat or air embolus, or tumor tissue.

48
Q

what are the clinical manifestations of a pulmonary embolism?

A

dyspnea, sudden chest pain, tachycardia, low BP, tachypnea, low O2 sat, cyanosis

49
Q

which drug classes would be used to treat a pulmonary embolism?

A

anticoagulants, thrombolytics, antiplatelets

NURS 2500 (22 decks)

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