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30 Cards in this Set

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Physiology/Pathophysiology of Coagulation
Hemostasis bleeding stopped, initiated by blood vessel injury. Two stages:
1. Platelet Plug Formation: platelets activated when exposed to interstitial collagen from injury. Platelets stick -> form platelet plug.

2. Coagulation: reinforcement of platelet plug with fibrin. To prevent wide-spread coagulation - antithrombin. Removal of clots done by plasmin-enzyme that digests fibrin. Fibrin is a protein that is produced by coagulating cascade. Antithrombin deactivates clotting factors.
Thrombosis
blood clot formed within vessel or heart
Types of thrombosis
1. Arterial: caused by adhesion of platelets to arterial wall. Leads to occlusion- atherosclerosis affects blood flow to organ
2. Venous: develop at sites where blood flow is slow, or pooling of blood. Danger - emboli break off, travel through the circ
3. Heart: form on heart valves, heart chambers because of pooling, dysrhythmias
Meds for Thromboembolism
Anticoagulants
Antiplatelets
Thrombolytics
Anticoagulants
disrupt clotting cascade and affect production of fibrin.-mainly venous thrombi, prevents formation of new clots, does NOT break up old ones, will not inc size
Types of anticoagulants
Heparin
Low-molecular wt heparin
Warfarin/Coumadin
Heparin
rapid acting. IV or SQ in Units. Nat. anticoagulant in tissues, >=2 inj/day
MOA: enhances activity of antithrombin ->leads to inactivation of thrombin and factor Xa. Fibrin is reduced. Large molecule can’t be absorbed in stomach

IND: pulmonary embolism
deep vein thrombosis
renal dialysis-to prevent blood clots
evolving stroke –when having stroke (embolic)
open heart surgery-to prevent blood clotting during procedures

CI (Contraindications) : any condition which causes bleeding. Used with caution with liver (affects metabolism of drug) or kidney (affects excretion of drug), ulcerative colitis, GI bleed

AE(Adverse Effects): hemorrhage-can cause bleeding anywhere in body
hypersensitivity reaction-allergic, derived from pork/cow tissue
heparin-induced thrombocytopenia –immune disorder causing dec in platelets

DI(Drug Interactions): other drugs that cause bleeding - inc risk of bleeding, aspirin-inc risk of bleeding

antidote: protamine sulfate-binds with heparin

Nursing considerations: only affected w/ DVT if therapeutic
Lab monitoring: coagulation time: activated partial thromboplastin time (aPTT). Normal 40 secs. Goal 1.5-2x 60-80 secs. Measure q 4-6hrs, adjust dose as needed. Once therapeutic check q day.
Monitor for signs of bleeding-blood in stool, change in vitals, BP should be lower, HR inc,
want prolonged time, get baseline, loading dose, maintenance dose, can become therapeutic in about 24 hours
will bruise easily, may have HA-intracranial bleeding
Low-molecular wt heparin
similar to heparin. SQ. Most common one: enoxaparin/Lovenox.-pre-filled syringes, less SE, less likely to cause bleeding and dec in platelets, taught how to give themselves SQ injections,
MOA: Inactivates clotting factor Xa – fibrin reduced, not as effective mechanism of heparin

IND: treatment and 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-not up walking around a lot, paraplegics to prevent blood clots

AE: bleeding, thrombocytopenia
Warfarin/Coumadin
po. delayed action, long-term prophylaxis, once therapeutic then used for a long time
MOA: interferes with biosynthesis of Vitamin K dependent clotting factors – acts as an antagonist to vit K (blocks Vitamin K). (factors: VII, IX, X, prothrombin). Delayed onset, overlap with heparin, only affects production of new clotting factors

IND: long-term prophylaxis: atrial fibrillation-blood pools and clots develop, valve replacement, pulmonary emboli, reduce risk of recurrent MI

AE: hemorrhage
bruising
do not use in pregnancy
do not use while breastfeeding

CI: same as heparin-don’t want to give to someone w/ hx of bleeding DO,
Pregnant women-crosses placenta, breastfeeding

DI: meds that dec effects of coumadin: seizure meds, oral contraceptives, foods high in vit K, monitor more closely,meds that inc effects of coumadin: aspirin, heparin, anti-fungals, some antibiotics

Antidote: vitamin K

Nursing Considerations:
Lab monitoring: prothrombin time (PT) try to normalize it and international normalization ratio (INR) compares PT w/ standard solution. Normal INR is 1. Target 2-3.5. .
T/L: medic-alert bracelet, use soft toothbrush-gums will bleed easily, electric razor, will take longer to stop bleeding, change risk of getting clot
Antiplatelets
inhibit platelet aggregation, prevent one or more steps in the clotting activity. For prevention of arterial thrombosis, also used for thrombosis
Types of antiplatelets
Aspirin
Adenosine Diphosphate (ADP) Receptor Antagonist
Glycoprotein IIB/IIA Receptor Antagonist
Aspirin
MOA: causes inhibition of an enzyme, cyclooxygenase, required for platelet activation. Low doses: 81-325mg, prevents activation of platelets so won’t clot, affects for life of platelet, once deactivated will not be activated, low doses given
IND: prevent MI and stroke, stop platelets from aggregating, better for MI

AE: GI upset, irritation, enteric coated to prevent irritation
Bleeding; GI or hemorrhagic stroke
Adenosine Diphosphate (ADP) Receptor Antagonist
more effective than aspirin
MOA: Blocks ADP receptors on platelets preventing aggregation – inactivates platelets. For pts who can’t tolerate ASA or do not respond.

IND: prevent strokes, MI, CVA, more selective for strokes

Ex. clopidogrel/Plavix

AE: similar to ASA but less bleeding, more tolerable for pts
Glycoprotein IIB/IIA Receptor Antagonist
Reversible
MOA: cause reversible blockage of platelet receptors, inhibits final step in platelet aggregation.

IND: acute short term use, IV only to prevent ischemic events in pts with acute coronary syndrome, coronary interventions, on for some type of intervention, during MI

Ex. Abciximab/ReoPro

AE: bleeding-always a possibility w/ anticoagulants
Thrombolytics
: break up clots, for severe thrombotic disease
Fibrinolytics-break up fibrin
Types: end in “ase”:
streptokinase/Streptase
alteplase/tPA
reteplase/Retavase
tenecteplase/TNKase
urokinase/Abbokinase
given anticoagulant at same time bc still at risk for clots
MOA: Streptokinase converts plasminogen to plasmin which digests thrombi
Given w/in 6 hours of event otherwise ineffective
IND: acute MI
massive pulmonary embolism
DVT
used in clotted vascular catheters-central line catheters in subclavian, IV works quickly, deactivated quickly

AE: bleeding
intracranial hemorrhage
antibody production-antibodies can form against Streptokinase
dangerous drug bc of risk of bleeding
Anemia
. Definition: dec in RBC, hematocrit, hemoglobin. Caused by blood loss, impaired production of RBC or inc destruction of RBC. Production: regulated by cellular O2 requirements and hormone erythropoietin-produced in kidneys, RISK-hypoxia
Iron Deficiency Anemia
lack of iron - needed for hemoglobin-has to be taken until hemoglobin back to norm Most common-ferrous sulfate
AE: GI upset
staining of teeth
toxicity-can get a change in stool, black tarry stool, gastric necrosis, acidosis

antidote: defuroxamine – absorbs iron-binds with Fe, prevents toxicity

DI: Ca, antacids-dec absorption
Antibiotics-dec absorption, Fe affects absorption of antibiotics
Vit C-inc Fe absorption

Iron IV or IM – Iron Dextran: painful causes tissue discoloration, can cause tissue damage
IND: used when po iron is ineffective, or cannot absorb po

AE: anaphylaxis-shock from Dextran (allergic rxn)
hypotension, cardiac arrest
HA
Vitamin B12 deficiency anemia
– pernicious anemia-intrinsic factor needed for B12 absorption
Vitamin B12 needed for DNA synthesis leading to RBC maturation, most common cause -impaired absorption due to loss of intrinsic factor. Vitamin B12 preparation: Cyanocobalamin. Can be po, most require monthly IM
AE: hypokalemia: due to inc RBC production, uses up K
Folic acid deficiency anemia
Folic acid needed for RBC maturation, most common cause: poor diet or malabsorption. Replacement therapy: folic acid, folate, pteroylglutamic acid.
AE: none, non-toxic even at high doses.

Danger: can mask Vit B12 deficiency-cells look same, neurological deficits can continue
Hematopoietic Growth Factors
affect blood
Hematopoiesis
blood cell production, regulated by growth factors - colony-stimulating factors. Act on bone marrow to produce blood cells
Erythropoietic Growth Factors
stimulate production of RBC. Most common: Epoetin Alpha/Epogen, Procrit. given IV or SQ, supplemental epoeitin
MOA: stimulates bone marrow to produce RBC, give 3 x week

IND: chronic renal failure
HIV pts who are taking antivirals that cause anemia
chemotherapy pts-suppresses bone marrow
surgical pts who are anemic

AE: HTN-inc hematocrit (amount RBCs)

Nursing Considerations: monitor hemoglobin level-make sure therapeutic
do not shake vial-will 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.
MOA: acts on cells in bone marrow to inc production of neutrophils (needed for infxn), makes mature neutrophils more effective

IND: cancer pts on chemo-infxn
bone marrow transplant pts-stimulate bone marrow to start making more
pts with severe chronic neutropenia

AE: bone pain bc acting on bone, Tylenol good for bone pain, dose dependent

Nursing considerations: monitor WBC count
do not shake vial (denatures protein)
Thrombopoietic Growth Factors
stimulate production of stem cells-precursor to platelets, not used as often, used a lot w/ cancer pts bc of bone marrow suppression
stimulate platelet production. Oprelvekin/Interleukin-11. given SQ q day.
MOA: stimulates production of stem cells and megakaryocytes,

IND: cancer pts on chemo that causes bone marrow suppression

AE: fluid retention, edema-inc in plasma volume
cardiac dysrythmias-inc in plasma volume puts a lot of strain on heart

Nursing considerations: monitor platelet count – use until counts >50k but not to exceed 21 days bc of possible SE
Lipid-lowering agents
to dec LDLs
A. Cholesterol/Lipoproteins
1. Cholesterol - component of cell membranes, required for synthesis of hormones and bile salts, preventing CAD, atherosclerosis

2. Lipoproteins: function as carriers for transporting lipids. Types:
a. very low density lipoproteins (VLDL): transport triglycerides to tissues. b. low-density lipoproteins (LDL): transports cholesterol to tissues.
c. high-density lipoproteins (HDL): transports cholesterol from tissues back to liver – promotes cholesterol removal-good thing bc cholesterol removed from blood returned to liver
HMG CoA Reductase Inhibitors
MOA: inhibits HMG CoA reductase (needed for cholesterol synthesis). Causes inc in LDL receptors in liver so removes more LDLs from blood. LDL dec. HDL inc

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

AE: HA
GI disturbances
Myopathy-injures muscle tissue-weakness, muscle aches
Hepatomegaly-affects liver

DI: 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
Binding agents bind with bile acid prevents in body
Types: cholestyramine/Questran colesevelam/Welchol
colestipol/Colestid

AE: GI: constipation, bloating, discomfort

DI: can dec absorption of fat soluble vitamins, binds w/ things and dec absorption
can form complexes with other drugs and affect their absorption
. Nicotinic Acid (Niacin)-
not used as frequently bc of SE
MOA: dec production of VLDL which then cause dec LDL. Inc HDL

AE: skin
GI
hepatotoxicity
hyperglycemia-in DM pts
Fibric Acid Derivatives
MOA: dec triglyceride levels, increase HDL, no effect on LDLs

Ex. Gemfibrozil/Lopid

AE: GI, gallstones
Hepatotoxicity

DI: statins, warfarin
Types of cholesterol lowering agents
HMG CoA Reductase Inhibitors
Bile-Acid Binding Resins
Nicotinic Acid (Niacin)
Fibric Acid Derivatives