Pharmacology Lecture 3

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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

â€”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 â€”

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

-prevent new clots from developing, donâ€™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 colitisâ€”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: â€¢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 firstâ€”titrate heparin based on aPTTâ€”increase or decrease

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

-Give loading dose (high dose)

â€¢SQ, standard dose based on body weight

â€¢Most common one: enoxaparin/Lovenox.

â€¢Less likely to cause bleeding and decrease in platelets.

â€¢Donâ€™t require aPTT (lab monitoring), allowing pt to do at home.
Low-molecular wt heparin MOA: -Inactivates clotting factor Xa â€“-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 â€“ acts as an antagonist to vit K. (factors: VII, IX, X, prothrombin).

â€¢Delayed onset, overlap with heparin.

â€¢Doesnâ€™t stop those that started, just prevents

â€¢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.

Donâ€™t give to pt w/history of bleeding disorders.

Canâ€™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 â€“ inactivates platelets permanently.

â€¢For pts who canâ€™t tolerate ASA or do not respond.

â€¢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 â€œaseâ€:
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 peripheralâ€”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 â€“ absorbs it
Iron IV or IM â€“ Iron Dextran: ⬢Is painful, causes tissue discoloration

anaphylaxis from reaction to dextran- test doses given

Hypotension

cardiac arrest

HA
Iron IV or IM â€“ 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: â€¢stimulate production of WBC.

â€¢Most common one:
Filgrastim (Granulocyte Colony-Stimulating Factor â€“ G-CSF)/Neupogen.

â€¢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 â€“ use until counts >50k but not to exceed 21 days.

â€¢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 â€œstatinâ€
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 isnâ€™t enough, add this

Also decrease LDLs, doesnâ€™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 â€“ 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

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