Quiz 2 Flashcards
Physiology of Coagulation
Ultimate goal: Hemostasis
Physiologic process by which bleeding is stopped:
- Formation of a platelet plug
- Coagulation/Reinforcement of platelet plug with fibrin
Two Pathways that converge at clotting factor X after which they employ the same final series of reactions- both are self sustaining upon initiaion
Extrinsic (PT)
Intrinsic (PTT)
Platelet Aggregation ( platelet plug formation)
- platelets come in contact with collagen on the exposed surface of a damaged vessel- adhere to the site- platelet activation is initiated.
- Platelet activation leads to platelet aggregation
- Platelet aggregation ends with formation of fibrinogen bridges between glycoprotein IIb/IIIa receptors on adjacent platelets
BLOOD CLOT!
Indications for Anticoagulants
- DVT
- Atherosclerosis
- Stroke
- Acute Coronary Syndrome
- Unstable angina, MI - PVD
- Oncologic Processes
- Genetic Predisposition
Lab Values
Complete Blood Count 1. RBC 4.1- 5.3 2. WBC 4,500- 11,00 3. Hgb men 13-17 women 11-5 4. Hct men 43-49% women 38-44% 5. Platelets 150,000-450,000
Prothrombin Time (PT) 11-12.5 seconds
Activated Partial Prothrombin Time (aPTT)
Normal: 40 seconds
Therapeutic: 60-80
International Normalized Ratio (INR)
Normal 1 sec
Therapeutic 2-3 seconds
Type & Screen:Identify blood type and RH factor
Type & Cross Match
Compare your blood with someone else’s blood to see if they are compatible ( prior to transfusion)- literally mixing together
Pharmacotherapeutics of Anticoagulants
Interrupt clotting cascade
Do NOT break down existing clots
Given IV, SQ, or PO
Pharmacotherapeutics of Anti-platelet agents
interfere with platelet membrane function and platelet aggregation
Pharmacotherapeutics of Thrombolytics
Lyse ( dissolve ) existing clots
Heparin
MOA: heparin binds to antithrombin in the blood which in turn inactivates factors II and factor X which STOP fibrinogin from transforming into fibrin.
Stops clot formation!
~High alert medication~
Used for:
Treatment for acute thrombotic events: DVT, PE, MI
also used prophylactically for pts. going into surgery, obesity and cancer pts.
Can be given IV, with intensive monitoring of PTT and plasma levels. Dosed in Units - GIve via Pump device, check drug compatabilities, have 2nd nurse check initial dose and dose changes
Low dose therapy- given Sub Q. -does not require monitoring
Hepatic metabolism and renal excretion
safe for pregnant women
Antidote: Protamine sulfate
Adverse Effects:
-Bleedings
( check for bloody nose, petechia, hematuria, bloody stool, loss of consciousness, decrease BP, increase HR, decrease in hcb or hct)
-Heparin induced thrombocytopenia ( paradoxical effect)
-hypersensitivity reactions (chills, fever, rash: uticaria)
-hyperkalemia
-osteoporosis in longterm use
Enoxaprin ( Lovanox)
Low molecular weight heparin
Increased bioavailability & longer half live
Predictable dose response
Administration Tips:
- Administered subcutaneously
- Proper needle gauge & length
- Do not expel the air bubble
- Do not massage/Avoid umbilicus
pre-filled injector
Warfarin
MOA: Inhibits Vitamin K synthesis in the liver ( vitamin K stops bleeding)
Used for: AFIB, DVT and PE prophylaxis
highly protein bound. Has a delayed onset of action 8-12 hours, peaks 3-5 days
-dose depends on the goal of therapy
Can be given IV and PO, and at the same time
Monitored by INR and PT
Antidote is Vitamin K
Adverse Effects:
Hemorrhage
Teratogenic( Don’t give to pregnant women)
Direct Thrombin Inhibitors
Think GATOR
Dabigatran etexilate (Pradexa)
MOA: Binds with thrombin ( Factor II) in the blood and directly inhibits it
Adverse Effects:
Bleeding
Therapeutic Uses
- Atrial fibrillation
- used in setting of heparin induced thrombocytopenia
Fewer drug interactions than warfarin
No monitoring
Newly approved antidote:
Praxbind
Rivaroxaban (Xarelto)
Factor Xa Inhibitor
MOA: Binds with factor Xa and inhibits production of thrombin
Adverse Effects
- Bleeding
- Use with caution in patients with renal impairment and hepatic impairment
- Unsafe in pregnancy
Therapeutic Uses
- Prevention of DVT and –Pulmonary embolism following total hip replacement (THR) surgery or knee replacement (TKR) surgery
- Prevention of stroke in patients with atrial fibrillation
- Fewer drug interactions than warfarin
No monitoring
No antidote
Asprin
Antiplatelet Agent
MOA :Inhibits cyclooxygenase ( enzyme needed for TXA2)
Permanently inhibits the clotting abilities of the platelets for the lifetime of the platelet ( 7 days)
-Salicyclate, irreversible antiplatelet effects
- Discontinue 5-7 days prior to elective surgery
- No risk of neutropenia
- Low dose therapy is 81 to 325 mg/day
Adverse Effects:
Increased risk of GI bleed
Therapeutic Uses: Ischemic stroke TIA Chronic stable angina Unstable angina Coronary stents Previous MI Preventing and MI
Chew aspirin in the setting of MI
clopidogrel bisulfate(Plavix)
Adenosine Diphosphate Receptor Antagonists
MOA: Pro-drug – undergoes metabolism to its active form
irreversible anti-platelet effects
Platelet function and bleeding times return normal 7-10 days after the last dose
Therapeutic Uses:
- Prevent blockage of coronary artery stents
- Prevention of thrombotic events (ischemic stroke, MI, and vascular death) in patients with Acute Coronary Syndrome
- In patients with Acute Coronary Syndrome combine with aspirin
Adverse Effects:
Bleeding
Thrombotic Thrombocytopenic Purpura (TTP)
Drug Interactions:
Proton Pump Inhibitors- PPIs inhibit P450 and may decrease metabolism of clopidgrel
recombinant alteplase
dugs that end in - ASE
Thrombolytics
MOA:
Catalyzes the conversion of plasminogen into plasmin
Plasmin digests the fibrin meshwork of clots
Therapeutic Uses:
MI
Ischemic stroke
Massive pulmonary embolism
Very HIGH risk of bleeding
Monitor for bleeding
All sites
Nursing interventions: -Obtain patient history for contraindications to therapy Monitor for: -Vital sign changes: -Fever occurs in 30% of patients. -Signs of bleeding -Blood work abnormalities (hematocrit, hemoglobin, platelets, PT, thrombin time, aPTT) -Arrhythmias -Respiratory difficulties
Antihemophilic Factor (Factor VIII)
Used to temporarily treat or prevent bleeding in hemophilia.
Made from pooled human sources:
Carries a slight risk of hepatitis and HIV transmission
Dosage is individualized to meet patient needs.
T
each patient to avoid injury and carry identification of hemophilia.
(Amicar) aminocaproic acid
Hemostatic Agents (opposite of anti-coagulation: Systemic hemostatic drug that stops blood loss by enhancing coagulation.
Administer with an IV pump.
Place patient on cardiac monitor to detect arrhythmias.
Common adverse effects: nausea, anorexia
Blood pressure
BP= CO ( cardiac output X SVR ( systemic Vascular resistance)
CO= Volume of blood leaving the LV with each beat, affected by HR, Contractility, venous return and blood volume
Peripheral resistance (PR) - determined by diameter and length of vessel and arteriolar constriction
Primary HTN
(Essential) Hypertension
-No identifiable cause
Secondary Hypertension
Identifiable causes: Renal disease Oral contraceptive use Reno-vascular disease Cushings syndrome Pheochromocytoma ( tumor of adrenal gland)
Consequences of HTN
- Myocardial Infarction
- Heart failure
- Angina
- Kidney disease
- Stroke
- Degree of injury related to degree of elevation/higher pressure higher risk
-Asymptomatic until long after injury has developed
Benefits of lowering BP
Decrease in:
morbidity
strokes
MI
Heart failure
Increase in LIFESPAN
Evaluate HTN patients for
Cushings, oral contraceptives and pheochromocytoma
Other factors that increase CV Risk
- target organ damage
- smoking
- obesity
- diabetes
- lack of exercise
Goal: decrease cv and renal morbidity and mortality without decreasing quality of life
Therapeutic intervnetions
Lifestyle changes
Antihypertensive drug therapy
Stepped Care Approach
The stepped-care approach to HTN is based on the patient’s response to therapy.
A patient’s therapy may be “stepped up” if non-responsive or “stepped down” if the patient shows signs of good BP control over time.
Step I: lifestyle changes
Step II: lifestyle changes and drug therapy
Step III: continue lifestyle changes, increase drug dose or substitute another drug or add a second agent from a different drug class
Step IV: add a second or third drug or a diuretic
Classes of Hypertensive Drugs
- Diuretics
- sympatholytics( Andrenergic Anatagonists)
beta-adrenergic blockers
alpha 1 blockers
alpha/beta blockers
centrally acting Alpha 2 Agonist
3. Other ACE inhibitors ARBs Calcium Channel Blockers Direct Acting Vasodilators
Beta Blockers (OLOL)
MOA: Block the sympathetic nervous system Beta adrenergic receptors ↓ HR ↓ force of contraction Slows conduction through the AV node
Therapeutic Uses: Angina Pectoris HTN Cardiac dysrhythmias MI Heart failure
Adverse Effects: Bradycardia ↓ cardiac output Precipitation of heart failure AV heart block Reflex tachycardia Bronchoconstriction inhibition of glycogenolysis
end in -OLOL
Propranolol
10000000 % going to be on the quiz
Nonselective beta adrenergic antagonist (Beta1 and beta2)
↓ HR, ↓force of ventricular contraction and slow impulse conduction through the AV node, suppress secretion of renin (Beta1) Bronchoconstriction (Beta 2) Inhibits glycogenolysis (Beta 2) -Breakdown of glycogen to glucose -Most detrimental to diabetics
Lipid soluble- crosses membranes easily
- well absorbed
- widely distributed
- hepatic metabolism
- excreted in urine
Drug Interactions:
- Calcium Channel Blockers
- Insulin
Metoprolol
Cardioselective (Beta 1 only)!!!
Therapeutic Uses:
HTN, heart failure and MI
Hepatic metabolism;Renal excretion
Adverse Effects:
Bradycardia, ↓ CO, AV block, rebound tachycardia with abrupt discontinuation
Alpha Blockers ( ZOSIN)
MOA:Block alpha receptors on blood vessels
Therapeutic Uses:
Essential Hypertension
Adverse effects: Orthostatic Hypertension Reflex tachycardia Nasal congestion Inhibition of ejaculation
