Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/87

Click to flip

87 Cards in this Set

  • Front
  • Back
Hemostasis
process by which bleeding is stopped , initiated by blood vessel injury
Stages of Coagulation
1. Platelet Plug Formation

2. Coagulation
Platelet Plug Formation
platelets activated when exposed to interstitial collagen from injury/injured blood vessel.

Platelets stick -> form platelet plug. (this is where antiplatelet drugs work)
Coagulation
•Reinforcement of platelet plug with fibrin.

•Coagulant factors- prothrombin- thrombin- fibrin. To prevent wide-spread coagulation - antithrombin.

•Removal of clots done by plasmin.
Thrombosis

Definition
blood clot formed within vessel or heart

3 types:
-arterial

-venous

-heart
Thrombosis

Meds
anticoagulants, antiplatelets, thrombolytics

—all work differently to solve same problem; different areas of coagulation
Arterial Thrombosis
caused by adhesion of platelets to arterial wall. Leads to occlusion
Venous Thrombosis
sites where blood flow is slow, or pooling of blood.
•Danger - emboli break off, travel through the circulation
Heart Thrombosis
form on heart valves, heart chambers because of pooling (esp. atrial fibrillation) or slow flow —

lead to emboli (stroke or pulmonary embolism)
Anticoagulants
-disrupt clotting cascade and affect production of fibrin

-prevent new clots from developing, don’t break clots up.

-Mainly used for venous thrombi

- MEDS: Heparin, LW Heparin, Warfarin/Coumadin
Heparin
rapid acting.

IV or SQ in Units.
Heparin

MOA
-enhances activity of antithrombin ->leads to inactivation of thrombin and factor Xa.

Fibrin is reduced
Heparin

IND
pulmonary embolism

deep vein thrombosis

renal dialysis

evolving stroke (not hemorrhagic, but embolic okay)

open heart surgery
Heparin

CI
-any condition which causes bleeding.

-Used with caution with liver or kidney- has to be monitored but can be used.

-GI bleeding, ulcerative colitis—no heparin
Heparin

AE
-hemorrhage- can cause bleeding anywhere in body (GI)
-hypersensitivity reaction
-heparin-induced thrombocytopenia (decreased in platelets)
Heparin

DI
other drugs that cause bleeding

- increase risk of bleeding (aspirin)
Heparin

antidote
protamine sulfate- binds with heparin
Heparin

Nursing considerations
•Lab monitoring: measure coagulation time- activated partial thromboplastin time (aPTT).

- aPTT Normal 40 secs.
Goal: 1.5-2x - 60-80 secs.
Measure q 4-6hrs, adjust dose as needed. Once therapeutic, check q day.

-SUMMARY: Baseline first—titrate heparin based on aPTT—increase or decrease

•Monitor for signs of bleeding
•Check vitals: if bleeding, increase in heart rate
•Will bruise easily
Low-molecular wt heparin
-SQ (2xday).

-Give loading dose (high dose)

•SQ, standard dose based on body weight

•Most common one: enoxaparin/Lovenox.

•Less likely to cause bleeding and decrease in platelets.

•Don’t require aPTT (lab monitoring), allowing pt to do at home.
Low-molecular wt heparin

MOA
-Inactivates clotting factor Xa –-fibrin reduced.

-Not as effective as heparin
Low-molecular wt heparin

IND
-treatment & prevention of

•DVT for patients who are on bedrest for more than 5 days, or immobile patients

•used following surgery especially with hip or knee
Low-molecular wt heparin

AE
bleeding, thrombocytopenia (less likely)
Warfarin/Coumadin
•PO

•delayed action, long-term prophylaxis once therapeutic
Warfarin/Coumadin

MOA
interferes with biosynthesis of Vitamin K dependent clotting factors – acts as an antagonist to vit K. (factors: VII, IX, X, prothrombin).

•Delayed onset, overlap with heparin.

•Doesn’t stop those that started, just prevents

•Takes 3-7 days, started at same time as heparin and stop heparin when it becomes therapeutic
Warfarin/Coumadin

IND
long-term prophylaxis:

-atrial fibrillation

-valve replacement

-pulmonary emboli

-reduce risk of recurrent MI.

-Some people take for life
Warfarin/Coumadin

AE
causes:

hemorrhage bruising

do not use in pregnancy

do not use while breastfeeding
Warfarin/Coumadin

CI
same as heparin.

Don’t give to pt w/history of bleeding disorders.

Can’t be taken during pregnancy or breastfeeding (crosses placenta and in breastmilk)
Warfarin/Coumadin

DI
meds that decrease effects of coumadin:

seizure meds,
oral contraceptives,
foods high in vit K

Drugs must be monitored if given together.

meds that increase effects of coumadin: aspirin, heparin, anti-fungals, some antibiotics (erthromyocin)
Warfarin/Coumadin

ANTIDOTE
vitamin K (IM) antagonizes effects of warfarin
Warfarin/Coumadin

Nursing Considerations
Lab monitoring:

prothrombin time (PT) and international normalization ratio (INR) is a standard, compares PT with standard solution

•Normal INR is 1. Target 2-3.5. . Want to take longer to clot

•Important to monitor bleeding

T/L: medic-alert bracelet, use soft toothbrush, electric razor, avoid contact sports
Antiplatelets
•inhibit platelet aggregation, prevent one or more steps in the clotting activity of platelets

•For prevention of arterial thrombosis.
MEDS:

- aspirin

- Adenosine Diphosphate (ADP) Receptor Antagonist

- Glycoprotein IIB/IIIA Receptor Antagonist
Aspirin

MOA
- causes inhibition of an enzyme, cyclooxygenase, required for platelet activation.

-Prevents platelet activation. Deactivation lasts for life of the platelet

•Low doses: 81-325mg
Aspirin

IND
prevent MI and stroke
Aspirin

AE
-GI upset- can prevent by taking with food or taking coated aspirin

-Bleeding; GI or hemorrhagic stroke
ADP Receptor Antagonist

MOA
- Blocks ADP receptors on platelets preventing aggregation – inactivates platelets permanently.

•For pts who can’t tolerate ASA or do not respond.

•More effective but more expensive
ADP Receptor Antagonist

IND
prevent strokes/CVA (good at this), MI

ex: Plavix/clopidogrel
ADP Receptor Antagonist

AE
similar to ASA but less bleeding
Glycoprotein IIB/IIIA
Receptor Antagonist

MOA
-cause reversible blockage of platelet receptors AND
-inhibits final step in platelet aggregation.
Glycoprotein IIB/IIIA
Receptor Antagonist

IND
acute short term use, for interventions:

•IV only to prevent ischemic events in pts with acute coronary syndrome

•coronary interventions: angioplasty

•not commonly used on the floor

EX: Abciximab/ReoPro
Glycoprotein IIB/IIIA
Receptor Antagonist

AE
Bleeding
Thrombolytics
break up clots, for severe thrombotic disease.
break up fibrin in clots (called fibrinolytics)

Types: end in “ase”:
MOST COMMON- streptokinase/Streptase

alteplase/tPA
reteplase/Retavase
tenecteplase/TNKase
urokinase/Abbokinase
Streptokinase

MOA
Protein converts plasminogen to plasmin which digests thrombi.

•Has to be given within 6 hours of symptoms.

•Given IV.

•Works quickly, deactivates quickly
Streptokinase

IND
acute MI

massive pulmonary embolism

DVT

used in clotted vascular catheters, not peripheral—central line catheters (subclavian, etc)
Streptokinase

AE
bleeding- cautiously given

intracranial hemorrhage

antibody production- allergic reaction
Anemia
decrease in RBC, hematocrit, hemoglobin.

-Caused by blood loss, impaired production of RBC or increase destruction of RBC (affecting tissue oxygenation).

•Production: regulated by cellular O2 requirements and hormone erythropoietin (created in kidneys and stimulates bone marrow).

•Influenced by nutrition
Iron Deficiency Anemia
•lack of iron - needed for hemoglobin.

•Most commonly used: ferrous sulfate.

•Most common cause is nutrition
Iron Deficiency Anemia

AE
GI upset: heartburn, nausea, changes in stool (black)

staining of teeth (for infants its liquid so must be diluted)

toxicity- can cause acidosis, shock
Iron Deficiency Anemia

DI
Calcium, antacids- affects absorption of iron

Antibiotics- iron affects absorption of ABX

Vit C- good b/c increases absorption of iron
Iron Deficiency Anemia

antidote
defuroxamine – absorbs it
Iron IV or IM – Iron Dextran
•Is painful, causes tissue discoloration

anaphylaxis from reaction to dextran- test doses given

Hypotension

cardiac arrest

HA
Iron IV or IM – Iron Dextran

IND
used when PO iron is ineffective, or cannot absorb PO
Vitamin B12 deficiency anemia

(pernicious anemia)
• Vitamin B12 needed for DNA synthesis leading to RBC maturation
•Most common cause -impaired absorption due to loss of intrinsic factor from gastric problems needed for absorption of B12

•Danger- nerve problems

•Vitamin B12 preparation: Cyanocobalamin.

oCan be PO, most require monthly IM
Vitamin B12 deficiency anemia

AE
hypokalemia: due to increase RBC production, rare
Folic acid deficiency anemia

definiton
•Folic acid needed for RBC maturation

•Most common cause: poor diet or malabsorption.

•Replacement therapy: folic acid, folate, pteroylglutamic acid- all do same thing
Folic acid deficiency anemia

AE
none, non-toxic even at high doses

Danger:

can mask Vitamin B12 deficiency b/c cells look same (pernicious or folic acid deficiency)
Hematopoiesis
blood cell production, regulated by growth factors - colony-stimulating factors.
Act on bone marrow to produce blood cells
Erythropoietic Growth Factors

MOA
•stimulate production of RBC.

•Most common: Epoetin Alpha/Epogen, Procrit.

•given IV or SQ, 3x week
Erythropoietic Growth Factors

IND
chronic renal failure

HIV pts who are taking antivirals that cause anemia

chemotherapy pts b/c bone marrow suppressed

surgical pts who are anemic
Erythropoietic Growth Factors

AE
HTN b/c increases RBCs
Erythropoietic Growth Factors

Nursing considerations
monitor hemoglobin level to see affects
do not shake vial b/c destroy protein
Leukopoietic Growth Factors
•stimulate production of WBC.

•Most common one:
Filgrastim (Granulocyte Colony-Stimulating Factor – G-CSF)/Neupogen.

•Given IV or SQ q day.
Leukopoietic Growth Factors

MOA
acts on cells in bone marrow to increase production of neutrophils

causes mature neutrophils to be more effective
Leukopoietic Growth Factors

AE
bone pain
Leukopoietic Growth Factors

IND
cancer pts on chemo

bone marrow transplant (BMT) pts

pts with severe chronic neutropenia
Leukopoietic Growth Factors

Nursing considerations
monitor WBC count
do not shake vial (denatures protein)
Thrombopoietic Growth Factors
•stimulate platelet production.

•Oprelvekin/Interleukin-11.

•Given SQ q day.

•Time course- 21 days maximum
Thrombopoietic Growth Factors

MOA
stimulates production of stem cells and megakaryocytes, precursors of platelets
Thrombopoietic Growth Factors

IND
cancer pts on chemo that causes bone marrow suppression
Thrombopoietic Growth Factors

AE
fluid retention/edema

cardiac dysrythmias
Thrombopoietic Growth Factors

Nursing Considerations
monitor platelet count – use until counts >50k but not to exceed 21 days.

•Be careful with preparations
Lipid-lowering agents
- HMG CoA Reductase Inhibitors (most commonly given)

- Bile-Acid Binding Resins

- Nicotinic Acid (Niacin)

- Fibric Acid Derivatives

-
very low density lipoproteins

(VLDLs)
transport triglycerides to tissues.
low-density lipoproteins (LDL)
transports cholesterol to tissues
high-density lipoproteins (HDL)
-transports cholesterol from tissues back to liver

-promotes cholesterol removal
HMG CoA Reductase Inhibitors

MOA
inhibits HMG CoA reductase, enzyme in cholesterol biosynthesis.

•Causes increase in LDL receptors in liver so removes more LDLs from blood.


•LDL decrease, HDL increase
HMG CoA Reductase Inhibitors

types
Types: end in “statin”
atorvastatin/Lipitor fluvastatin/Lescol
lovastatin/Mevacor pravastatin/Pravachol
rosuvastatin/Crestor simuvastatin/Zocor
HMG CoA Reductase Inhibitors

AE
HA

GI disturbances

Myopathy- injury of muscle tissue

hepatomegaly
HMG CoA Reductase Inhibitors

DI
avoid meds that inhibit hepatic microsomal enzymes: raise statin levels

•do not use during pregnancy
Bile-Acid Binding Resins

MOA
prevent absorption of bile acid, bind with bile acids in GI tract

If statin isn’t enough, add this

Also decrease LDLs, doesn’t effect HDLs
Bile-Acid Binding Resins

Types
cholestyramine/Questran

colesevelam/Welchol
colestipol/Colestid
Bile-Acid Binding Resins

AE
GI: constipation, bloating
Bile-Acid Binding Resins

DI
can decrease absorption of fat soluble vitamins or other meds (taken 1 hr before or 4 after)

can form complexes with other drugs and affect their absorption
Nicotinic Acid (Niacin)

MOA
decrease production of VLDL which then cause decrease LDL. Increase HDL

Not used frequently b/c of AE
Nicotinic Acid (Niacin)

AE
skin

GI

hepatotoxicity

hyperglycemia – not good for diabetics
Fibric Acid Derivatives

MOA
decrease triglyceride levels, increase HDL, no effect on LDLs

EX: Gemfibrozil/Lopid
Fibric Acid Derivatives

AE
GI, gallstones

Hepatotoxicity
Fibric Acid Derivatives

DI
statins, warfarin