Quiz 4 Flashcards

1
Q

Heparin
Action
Use
Administration
Antidote

A

Bind with antithrombin III (inhibit clot formation, stops coagulation cascade)
Prevent venous thrombosis
SubQ: prevention
IV: treatment
Protamine sulfate

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2
Q

Adverse effects of heparin

A

Nosebleeds, blood urine and stool, bloody gums
Heparin-induced thrombocytopenia (low platelets caused by heparin)

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3
Q

Antidote of warfarin

A

Vitamin K

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4
Q

Direct Factor Xa
Antagonist
Prototype
Action
Use

A

Rivaroxaban (Xarelto)
Inhibits platelet activation
Prevention of VTE and stroke

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5
Q

Adverse reactions of alteplase
Antidote

A

Hemorrhage
Aminocaproic acid

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6
Q

3 factors the predispose pts to thrombosis

A

Stasis: blood slow = > cot
Vascular damage
Hypercoagulability: > chance of coagulation

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7
Q

Arterial clot formation vs venous clot formation

A

Arterial: damaged vessels
Venous: caused by circulatory stasis

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8
Q

Heparin lab (what is it)
Therapeutic

A

apTT: how long it takes for a clot to form (activated thromboplastin time)
45-70 sec

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9
Q

Enoxaparin (lovenox)
What is it?
Administration
Labs

A

Low-molecular-weight heparin (having a low molecular weight)
SubQ
Frequent lab monitoring not required

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10
Q

Contraindication of enoxaparin

A

renal impairment

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11
Q

Side effects of enoxaparin

A

lower risk of bleeding

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12
Q

Vitamin K antagonist
Prototype
Action
Use

A

Warfarin (Coumadin)
Inhibits hepatic synthesis of Vitamin K
Prevent thromboembolic events

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13
Q

Labs for warfarin

A

INR (international normalized ratio). Time it takes to clot
Therapeutic range: 2-3
(calculated from PT (prothrombin time))

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14
Q

Antiplatelet
Prototype
Action
Use
OTC

A

Clopidogrel (plavix)
Action: irreversibly suppresses platelets (platelet lifespan is 7-10 days)
Prevents new clots or prevent them from getting bigger
Aspirin

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15
Q

Thrombolytic
Prototype
Action
Use

A

Alteplase (Activase)
Bind to fibrin promoting conversion of plasminogen to plasmin (plasmin digests fibrin)
Disintegrates clots

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16
Q

When do we give alteplase

A

Severe cases where leg isn’t being perfused
Ischemic stroke

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17
Q

Erythropoiesis-stimulating agents
Prototype
MOA
Use

A

Epoetin alfa (procrit)
Mimics hormone erythropoietin. Only give if benefits > risk
Anemia secondary to chemotherapy or kidney disease

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18
Q

Granulocyte colony stimulating factor
Prototype
MOA
Use
Administration

A

Filgrastim (neupogen)
Tell bone marrow to make more neutrophils
Neutropenia secondary to marrow transplant or chemo
SubQ or IV

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19
Q

Adverse effects of filgrastim

A

Flu-like symptoms
Arthralgia (joint stiffness)
Splenomegaly

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20
Q

Interferons
Prototype
MOA
Use
Administration

A

Interferon alfa 2B
Antiviral, destroys viruses
Antineoplastic, boost immune response
SubQ or IM (3 times a week)

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21
Q

What are interferons
Functions

A

Proteins naturally occurring in the body (alpha, beta, gamma)
Slow growth of cancer cells, stimulate certain WBCs to fight cancer, antiviral effects

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22
Q

Black box warning on Epoetin alfa

A

Hemoglobin must be < 10 g/dl
Avoid if hemoglobin > 12g/dl = > blood clots

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23
Q

Epoetin alfa
Administration

A

SubQ, IV

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24
Q

Nursing interventions of filgrastim

A

Palpating abdominal in case of splenomegaly

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25
Q

Function of triglycerides

A

Store unused calories and provide your body with energy

26
Q

Nonpharmacological methods for cholesterol reduction

A

< saturate fats and cholesterol
< total fat intake to 30% or less of caloric intake
< cholesterol intake to 300mg/day or less
Exercise
Stop smoking

27
Q

HMG CoA Reductase Inhibitors
Prototype
Action
Use

A

Atorvastatin
Inhibit enzyme HMG CoA reductase (responsible for cholesterol biosynthesis)
Reduce amount of cholesterol the body makes. < LDLs, > HDL

28
Q

Side effects of HMG CoA reductase inhibitors

A

GI distress, constipation, fatigue, cataracts, liver impairment, muscle cramps, rhabdomyolysis (skeletal muscle destruction)
brown colored pee

29
Q

Bile acid sequestrants
Prototype
Action
Use

A

Cholestyramine
Binds with bile acids in the intestine to be excreted out
Remove bile (cholesterol) from the body. Causes cholesterol to be pooped out

30
Q

Side effects of bile acid sequestrants

A

Constipation, flatulance, cramping

31
Q

Fibrates
Prototype
Action
Use

A

Fenofibrate
Increases breakdown of fatty acids
Reduces triglycerides

32
Q

Adverse effects of fibrates

A

GI upset, liver dysfunction, gallstones

33
Q

Intervention of fibrates

A

Get liver checked out, labs

34
Q

Cholesterol Absorption inhibitor
Prototype
Action
Adverse effects

A

Ezetimibe
acts on the cells in the small intestine to inhibit cholesterol absorption
Diarrhea

35
Q

Misc. Antihyperlipidemics
Prototype
Action

A

Nicotinic acid/ Niacin/ Vitamin B
Reduces VLDL and LDL

36
Q

Side effects of Misc. Antihyperlipidemics

A

GI distress, flushing, hepatic dysfunction, hyperglycemia, hyperuricemia

37
Q

Nursing interventions for dyslipidemia medications

A

Blood lipid levels
Monitor lab values for liver function
Take several weeks before blood lipid levels decline
Instruct pt to have annual eye exams and report changes in visual acuity

38
Q

Function of cholesterol

A

Cell membrane
Steroid hormones
Bile salts: digestion of fats

39
Q

HDL vs LDL

A

High-density lipoprotein: removes cholesterol from blood–>liver for elimination
Low-density lipoprotein: Fat leaks out into bloodstream = plaque buildup

40
Q

Should you suddenly stop taking HMG CoA reductase inhibitors?

A

No, taper
Abrupt discontinuation may lead to rebound effect

41
Q

Interventions for bile acid sequestrants

A

Drink with water
Stay hydrate
Eat more fiber

42
Q

Why do we not want to administer antihyperlipidemics

A

Large doses are required
Leads to bad reactions/toxicity

43
Q

Nursing responsibilities for immunosuppressants

A

Monitor for infection

44
Q

Autoimmune disorders

A

Crohn’s Disease: bowel inflammation
Rheumatoid arthritis
Psoriasis: plaque lesions
Myasthenia Gravis

45
Q

Function of antigens

A

recognize self vs pathogens

46
Q

What happens after an organ transplant

A

Graft rejection reaction: fight the organ and rejecting it
Can lead to organ failure

47
Q

Why do clients that receive transplanted tissue require immunosuppressants?

A

So body doesn’t deny it

48
Q

Anti-rejection therapy
Drugs
MOA
Adverse effects
How long?

A

Mycophenolate Mofetil (CellCept), Cyclosporine
Suppress the immune system
Increase risk for infection
For life

49
Q

contraindications of cyclosporine

A

Grapefruit juice
Cause toxicity

50
Q

Administration of cyclosporine

A

Mix cyclosporine with juice to make it palatable

51
Q

Corticosteroids
Drugs
Use
How long?

A

Prednisone, hydrocortisone
Asthma, COPD, joint pain
Short term, Tapered

52
Q

Side effects of corticosteroids

A

Anti-inflammatory effects, immunosuppressive effects, moodswings, increased appetite
Long term: moon face, weight gain

53
Q

Antibody (immunoglobulin) preparations
Route
MOA
Drugs

A

Parenterally
Block cell receptors or inhibit inflammatory cytokines
Monoclonal antibodies
Polyclonal antibodies. Muromonab-CD3, infliximab, basiliximab

54
Q

Antibody (immunoglobulin)
preparations
Use
Side effects

A

Reduces damage caused by inflammation
Prevent rejection
Risk for infection

55
Q

How is antibody preparations preapred?

A

Make multiple antigens, put in a bottle, and given to redirect their immune system

56
Q

Side/Adverse effects of chemotherapy

A

Affects normal cells (rapidly growth tissues)
Alopecia, infertility, anemia, myelosuppression (< in WBC, platelets, RBC), dry/flaky skin, nosebleeds

57
Q

How long till the body starts feeling the effects of chemotherapy?

A

7-10 days
Try to avoid people because immunocompromised

58
Q

Anticancer drugs

A

Alkylating agents (prevent DNA replication)
Antitumor antibiotics
Hormones
Antimetabolites
Vinca alkaloids

59
Q

Function of combination chemotherapy

A

Enhances tumoricidal activity (destroys tumor cells)
> chance of affecting cancer cells in all phases of cell cycle
> synergestic effects to kill cancer cells
< drug resistance

60
Q

Why are 2 anticancer drugs used instead of just 1?

A

Synergistic effect when combined