Pharmacology Lecture 3

Front 1

Hemostasis

Back 1

process by which bleeding is stopped , initiated by blood vessel injury

Front 2

Stages of Coagulation

Back 2

1. Platelet Plug Formation

2. Coagulation

Front 3

Platelet Plug Formation

Back 3

platelets activated when exposed to interstitial collagen from injury/injured blood vessel.

Platelets stick -> form platelet plug. (this is where antiplatelet drugs work)

Front 4

Coagulation

Back 4

•Reinforcement of platelet plug with fibrin.

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

•Removal of clots done by plasmin.

Front 5

Thrombosis

Definition

Back 5

blood clot formed within vessel or heart

3 types:
-arterial

-venous

-heart

Front 6

Thrombosis

Meds

Back 6

anticoagulants, antiplatelets, thrombolytics

—all work differently to solve same problem; different areas of coagulation

Front 7

Arterial Thrombosis

Back 7

caused by adhesion of platelets to arterial wall. Leads to occlusion

Front 8

Venous Thrombosis

Back 8

sites where blood flow is slow, or pooling of blood.
•Danger - emboli break off, travel through the circulation

Front 9

Heart Thrombosis

Back 9

form on heart valves, heart chambers because of pooling (esp. atrial fibrillation) or slow flow —

lead to emboli (stroke or pulmonary embolism)

Front 10

Anticoagulants

Back 10

-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

Front 11

Heparin

Back 11

rapid acting.

IV or SQ in Units.

Front 12

Heparin

MOA

Back 12

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

Fibrin is reduced

Front 13

Heparin

IND

Back 13

pulmonary embolism

deep vein thrombosis

renal dialysis

evolving stroke (not hemorrhagic, but embolic okay)

open heart surgery

Front 14

Heparin

CI

Back 14

-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

Front 15

Heparin

AE

Back 15

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

Front 16

Heparin

DI

Back 16

other drugs that cause bleeding

- increase risk of bleeding (aspirin)

Front 17

Heparin

antidote

Back 17

protamine sulfate- binds with heparin

Front 18

Heparin

Nursing considerations

Back 18

•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

Front 19

Low-molecular wt heparin

Back 19

-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.

Front 20

Low-molecular wt heparin

MOA

Back 20

-Inactivates clotting factor Xa –-fibrin reduced.

-Not as effective as heparin

Front 21

Low-molecular wt heparin

IND

Back 21

-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

Front 22

Low-molecular wt heparin

AE

Back 22

bleeding, thrombocytopenia (less likely)

Front 23

Warfarin/Coumadin

Back 23

•PO

•delayed action, long-term prophylaxis once therapeutic

Front 24

Warfarin/Coumadin

MOA

Back 24

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

Front 25

Warfarin/Coumadin

IND

Back 25

long-term prophylaxis:

-atrial fibrillation

-valve replacement

-pulmonary emboli

-reduce risk of recurrent MI.

-Some people take for life

Front 26

Warfarin/Coumadin

AE

Back 26

causes:

hemorrhage bruising

do not use in pregnancy

do not use while breastfeeding

Front 27

Warfarin/Coumadin

CI

Back 27

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)

Front 28

Warfarin/Coumadin

DI

Back 28

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)

Front 29

Warfarin/Coumadin

ANTIDOTE

Back 29

vitamin K (IM) antagonizes effects of warfarin

Front 30

Warfarin/Coumadin

Nursing Considerations

Back 30

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

Front 31

Antiplatelets

Back 31

•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

Front 32

Aspirin

MOA

Back 32

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

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

•Low doses: 81-325mg

Front 33

Aspirin

IND

Back 33

prevent MI and stroke

Front 34

Aspirin

AE

Back 34

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

-Bleeding; GI or hemorrhagic stroke

Front 35

ADP Receptor Antagonist

MOA

Back 35

- 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

Front 36

ADP Receptor Antagonist

IND

Back 36

prevent strokes/CVA (good at this), MI

ex: Plavix/clopidogrel

Front 37

ADP Receptor Antagonist

AE

Back 37

similar to ASA but less bleeding

Front 38

Glycoprotein IIB/IIIA
Receptor Antagonist

MOA

Back 38

-cause reversible blockage of platelet receptors AND
-inhibits final step in platelet aggregation.

Front 39

Glycoprotein IIB/IIIA
Receptor Antagonist

IND

Back 39

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

Front 40

Glycoprotein IIB/IIIA
Receptor Antagonist

AE

Back 40

Bleeding

Front 41

Thrombolytics

Back 41

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

Front 42

Streptokinase

MOA

Back 42

Protein converts plasminogen to plasmin which digests thrombi.

•Has to be given within 6 hours of symptoms.

•Given IV.

•Works quickly, deactivates quickly

Front 43

Streptokinase

IND

Back 43

acute MI

massive pulmonary embolism

DVT

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

Front 44

Streptokinase

AE

Back 44

bleeding- cautiously given

intracranial hemorrhage

antibody production- allergic reaction

Front 45

Anemia

Back 45

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

Front 46

Iron Deficiency Anemia

Back 46

•lack of iron - needed for hemoglobin.

•Most commonly used: ferrous sulfate.

•Most common cause is nutrition

Front 47

Iron Deficiency Anemia

AE

Back 47

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

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

toxicity- can cause acidosis, shock

Front 48

Iron Deficiency Anemia

DI

Back 48

Calcium, antacids- affects absorption of iron

Antibiotics- iron affects absorption of ABX

Vit C- good b/c increases absorption of iron

Front 49

Iron Deficiency Anemia

antidote

Back 49

defuroxamine – absorbs it

Front 50

Iron IV or IM – Iron Dextran

Back 50

•Is painful, causes tissue discoloration

anaphylaxis from reaction to dextran- test doses given

Hypotension

cardiac arrest

HA

Front 51

Iron IV or IM – Iron Dextran

IND

Back 51

used when PO iron is ineffective, or cannot absorb PO

Front 52

Vitamin B12 deficiency anemia

(pernicious anemia)

Back 52

• 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

Front 53

Vitamin B12 deficiency anemia

AE

Back 53

hypokalemia: due to increase RBC production, rare

Front 54

Folic acid deficiency anemia

definiton

Back 54

•Folic acid needed for RBC maturation

•Most common cause: poor diet or malabsorption.

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

Front 55

Folic acid deficiency anemia

AE

Back 55

none, non-toxic even at high doses

Danger:

can mask Vitamin B12 deficiency b/c cells look same (pernicious or folic acid deficiency)

Front 56

Hematopoiesis

Back 56

blood cell production, regulated by growth factors - colony-stimulating factors.
Act on bone marrow to produce blood cells

Front 57

Erythropoietic Growth Factors

MOA

Back 57

•stimulate production of RBC.

•Most common: Epoetin Alpha/Epogen, Procrit.

•given IV or SQ, 3x week

Front 58

Erythropoietic Growth Factors

IND

Back 58

chronic renal failure

HIV pts who are taking antivirals that cause anemia

chemotherapy pts b/c bone marrow suppressed

surgical pts who are anemic

Front 59

Erythropoietic Growth Factors

AE

Back 59

HTN b/c increases RBCs

Front 60

Erythropoietic Growth Factors

Nursing considerations

Back 60

monitor hemoglobin level to see affects
do not shake vial b/c destroy protein

Front 61

Leukopoietic Growth Factors

Back 61

•stimulate production of WBC.

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

•Given IV or SQ q day.

Front 62

Leukopoietic Growth Factors

MOA

Back 62

acts on cells in bone marrow to increase production of neutrophils

causes mature neutrophils to be more effective

Front 63

Leukopoietic Growth Factors

AE

Back 63

bone pain

Front 64

Leukopoietic Growth Factors

IND

Back 64

cancer pts on chemo

bone marrow transplant (BMT) pts

pts with severe chronic neutropenia

Front 65

Leukopoietic Growth Factors

Nursing considerations

Back 65

monitor WBC count
do not shake vial (denatures protein)

Front 66

Thrombopoietic Growth Factors

Back 66

•stimulate platelet production.

•Oprelvekin/Interleukin-11.

•Given SQ q day.

•Time course- 21 days maximum

Front 67

Thrombopoietic Growth Factors

MOA

Back 67

stimulates production of stem cells and megakaryocytes, precursors of platelets

Front 68

Thrombopoietic Growth Factors

IND

Back 68

cancer pts on chemo that causes bone marrow suppression

Front 69

Thrombopoietic Growth Factors

AE

Back 69

fluid retention/edema

cardiac dysrythmias

Front 70

Thrombopoietic Growth Factors

Nursing Considerations

Back 70

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

•Be careful with preparations

Front 71

Lipid-lowering agents

Back 71

- HMG CoA Reductase Inhibitors (most commonly given)

- Bile-Acid Binding Resins

- Nicotinic Acid (Niacin)

- Fibric Acid Derivatives

-

Front 72

very low density lipoproteins

(VLDLs)

Back 72

transport triglycerides to tissues.

Front 73

low-density lipoproteins (LDL)

Back 73

transports cholesterol to tissues

Front 74

high-density lipoproteins (HDL)

Back 74

-transports cholesterol from tissues back to liver

-promotes cholesterol removal

Front 75

HMG CoA Reductase Inhibitors

MOA

Back 75

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

Front 76

HMG CoA Reductase Inhibitors

types

Back 76

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

Front 77

HMG CoA Reductase Inhibitors

AE

Back 77

HA

GI disturbances

Myopathy- injury of muscle tissue

hepatomegaly

Front 78

HMG CoA Reductase Inhibitors

DI

Back 78

avoid meds that inhibit hepatic microsomal enzymes: raise statin levels

•do not use during pregnancy

Front 79

Bile-Acid Binding Resins

MOA

Back 79

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

Front 80

Bile-Acid Binding Resins

Types

Back 80

cholestyramine/Questran

colesevelam/Welchol
colestipol/Colestid

Front 81

Bile-Acid Binding Resins

AE

Back 81

GI: constipation, bloating

Front 82

Bile-Acid Binding Resins

DI

Back 82

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

Front 83

Nicotinic Acid (Niacin)

MOA

Back 83

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

Not used frequently b/c of AE

Front 84

Nicotinic Acid (Niacin)

AE

Back 84

skin

GI

hepatotoxicity

hyperglycemia – not good for diabetics

Front 85

Fibric Acid Derivatives

MOA

Back 85

decrease triglyceride levels, increase HDL, no effect on LDLs

EX: Gemfibrozil/Lopid

Front 86

Fibric Acid Derivatives

AE

Back 86

GI, gallstones

Hepatotoxicity

Front 87

Fibric Acid Derivatives

DI

Back 87

statins, warfarin